PASS MMed (FM) – by Yi Bing, Vanessa, Hui Ting, Chara (NHG

Batch of 2018)
ADMIN/ID GASTRO
1. Ethics Summary 3 1. Abdominal Distension 139
2. STIs 14 2. Diarrhea 141
3. Dyspepsia 145
CARDIO 4. Dysphagia 151
1. Atrial Fibrillation / Warfarin 15 5. Hepatitis B - Acute or Chronic 154
2. Calf pain / PAD 26 6. Jaundice 159
3. Chest pain 31 7. Lower BGIT 162
4. Hyperlipidemia 35 8. Raised ALT/AST 164
5. Hypertension 40 9. Vomiting and Nausea 169
6. Palpitations 46
7. Syncope 50 GERIATRICS
8. CCF 55 1. Memory Loss 171
9. IHD 61 2. Falls 175
10. LL swelling 64 3. Urinary Incontinence 180

DERMATOLOGY GENERAL SURGERY

1. Acne Vulgaris 69 1. Colonoscopy screening 183
2. Atopic Dermatitis 73 2. Gynecomastia 184
3. Alopecia 75
4. Rash 78 HAEMATOLOGY
5. Urticaria 82 1. Anaemia 185
2. Bleeding/Bruising 189
ENDOCRINE
1. Approach to Weight Gain 85 NEUROLOGY
2. Hyperthyroidism 89 1. Approach to Tremors 195
3. Hypothyroidism 97 2. Chronic post stroke 202
4. Osteoporosis 101 3. Difficulty Walking 205
5. Primary Obesity 104 4. Headache 207
6. Steroids / 2’ adrenal insufficiency 106 5. One sided weakness 213
7. Type 1 DM 107 6. Paraesthesia 216
8. Type 2 DM 110 7. Parkinson’s Disease 219

ENT NON-SPECIFIC
1. Approach to Ear Pain 118 1. Abnormal screening tests*
2. Approach to Tinnitus 120 2. Fatigue 223
3. Epistaxis 123 3. Immunocompromised pts, Immunosuppressants 229
4. Hearing loss 126 4. Loss of weight 230
5. Hoarse voice 129 5. Nocturnal leg cramps 233
6. Neck lump 130 6. Dizziness 235
7. Audiogram interpretation* 7. Prolonged Fever 237

EYE GYNAE
1. Approach to red eye 132 1. Abnormal Pap Smear 241
2. Double Vision 134 2. Approach to AUB 247
3. Loss of Vision 136 3. Contraception 258
4. Dysmenorrhoea 268
5. Infertility 272
6. Menopause 275
7. Atrophic vaginitis 283
8. Vaginal discharge 283
OBSTETRICS Paeds General
1. Abortion 285 1. Approach to developmental delay 390
2. Antenatal care 289 2. Autism 393
3. Antenatal Down Syndrome and General Advice 292
4. DM Pre-conception 293 PSYCHIATRY
5. Gestational Diabetes 297 1. ADHD 395
6. Hypertension in Pregnancy 298 2. Anorexia 398
7. Nausea and Vomiting in Pregnancy 300 3. Anxious / Worry 409
8. Post-Natal Care 303 4. Insomnia 413
9. Thalassemia Counselling 306 5. Depression ± Bipolar 416
6. Psychiatric Conditions Summary 419
ORTHOPAEDICS
1. Ankle and Foot Pain 307 RENAL
2. Back Pain 308 1. Adult Polycystic Kidney Disease 426
3. Hip Pain 312 2. Approach to AKI 420
4. Knee Pain 314 3. Approach to CKD 421
5. Neck Pain 317 4. Approach to Hyperkalemia 436
6. Shoulder Pain 318 5. Approach to Hypokalemia 438
7. Hand 320 6. Approach to Hyponatremia 440

PAEDIATRICS RESPI
Paeds Endocrine 1. Asthma 434
1. Approach to abnormal growth centiles 324 2. Bronchiectasis 448
2. Approach to pubertal delay 330 3. COPD 450
3. Approach to short stature 334 4. Approach to cough 457
4. Down syndrome 340 5. Approach to Hemoptysis 460
5. Noonan syndrome PE 343 6. Approach to SOB 463
6. Turner Syndrome 345 7. Approach to wheeze 466
7. Approach to T1DM (long case) 347 8. Smoking cessation 468
8. Failure to thrive 350 9. Spirometry 472

Paeds Gastro RHEUMATOLOGY

1. Abdominal pain 353 1. Approach to Joint Pain 476
2. Gout 488
Paeds Hemato 3. Psoriasis 492
1. Counselling on hemophilia 352
2. Approach to bleeding and bruising 359 UROLOGY
3. Thalassemia song 366 1. Approach to Lower Urinary Tract Symptoms (LUTS)
486
Paeds Neurology 2. Approach to urethritis in males 500
1. Febrile seizure 367 3. Approach to erectile dysfunction 502
4. Approach to hematuria 506
Paeds Ortho 5. Approach to nocturia 509
1. Approach to Limping child 371

Paeds Renal
1. Nephrotic syndrome 370
2. Nocturnal enuresis 382
3. Renal - UTI 384

Paeds Respi
1. Approach to wheeze 388
2. Paeds Asthma 394

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ADMIN/ID 1. ETHICS SUMMARY
Summary
1. 4 box approach
2. Principles and professional obligations
3. Possible scenarios
a. Driving license
b. Fitness for work
c. Pregnancy
d. Collusion
e. Harm to others
f. Abuse
g. Collegiality
4. Collusion
5. Breaking bad news
6. Admin
a. AMD
b. LPA
c. Infectious disease act
d. Sample driving license form

3
4 PILLARS OF MEDICAL ETHICS
Beneficience Do what is in the patient’s best interests

Non-maleficience Not to cause harm and to seek to prevent harm

Autonomy Respect the right of the individual to make choices about his or her
own life
Choices reached after much deliberation as to what is in his/her best
interests
Considering the respect for others too ie medical stuff

Justice To treat all patients fairly and without discrimination

4 PROFESSIONAL OBLIGATIONS
1) Patient’s best interests
2) Fidelity (Faithful or loyal) - promise keeping, the need to maintain pt- dr rs
3) Truth-telling – Informed consent, Obligation to tell pt the truth/ avoid collusion, maintain pt-dr rs
4) Confidentiality

POSSIBLE ETHICS
DRIVING LICENSE**
Not fit to drive ● Epilepsy vocational: fit free 10 years;
Eg epilepsy personal: fit free 3 years and no medicines
for at least 1 year

Temporarily not fit to drive ● Post stroke: clearance by neuro after DARP
Eg post stroke, uncontrolled BP ● BP personal: can continue
● BP vocational: unfit if SBP>=200 or

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 DBP >=110, resume when BP stable
controlled

Giddiness (Meniere, vertigo, labyrinthine disorders) ● Vocational: stop until symptom free 1 year
● Personal: stop until symptom free 3/12

OSA

Drinker who wants to drive vocationally (CAGE 2

and above)
FITNESS FOR WORK
Bloodborne illnesses in Healthcare workers ● Okay if not exposed to blood or operating
or possible needlestick
PREGNANCY
Underage teenager ● <16: call 999/ make police report
● <14 ● Cannot break confidentiality ie can't tell
● 14-16 parents but ask patient to tell parents or
ask if you can tell on her behalf
● 16-21: No need to report but encourage to
tell parents
○ Gillick competency

FDW ● If here to sign statutory form = no choice,

● Want to keep must declare
● Want to TOP ● If not here to sign form:
[Manage pregnancy] → get employer to
*once form is signed (ie UPT positive, FDW has to terminate work permit, return home to
be deported and will not be able to return to deliver then come back again to work
Singapore again) or
** form has to be submitted within 1 month [Safe abortion] → get FDW to tell
employer, undergo TOP in a safe
environment, repeat UPT within 1 month
and have form signed
COLLUSION
Cancer diagnosis
HARM TO OTHERS
Psychiatric illnesses

Harm to self

Surgeon with blood borne illness ie hepatitis B , ● Advised pt to inform SMC himself and
employer and change job scope
● If pt refuses, In view of duty to protect
others from harm, need to inform SMC

Doctor with substance abuse with near misses or

actual misses ● Determine if any actual or near harm to
patient
● Determine if patient goes to work under
drug influence
● Advised to stop substance abuse and if

5
 difficulty stopping, advise to stop practising
first and report SMC himself
● If pt refuses, inform SMC and employer
● Above reportable to SMC
ABUSE
Child, elder (no mental capacity) ● Neglect vs Abuse?
● Send to ED
○ 999 if guardian refuse

Spousal ● Safety netting: hotline, pave centre etc

COLLEGIALITY / MEDICAL ERROR [ABC]

NURSE
Naming: “I can see that this makes you feel very worried”
Understanding: “This has been a hard time for you.” “This makes sense to me”
Respecting: “You have been through a lot.” “It must be a lot of stress to deal with___”
Supporting: “I want to help in any way I can.”
Exploring: “How are you coping with this?”

1. Acknowledge error
a. “I am sorry that this information should have been informed to you earlier.”
b. “ I am sorry that you have been given a medication that you are allergic to.”
c. I am not able to comment on his management as I was not present during the consult.
He may have his rationale for managing the condition this way, and to confirm, I will
need to check with him. Be assured we take your feedback seriously, will bring it up to
our management, and will try to improve our workflow.
2. Bring patient back to check on them clinically and to update them about “investigation and plan
for improvement”
3. Check with colleague about what happened once he is back. Institute safety measures.
a. Ensure drug allergy always checked
b. Ensure abnormal reason always flagged and highlighted

At this point in time, I would also like to help you get better and feel more comfortable.

REFUSAL OF TREATMENT (mentally competent) URWC first

Explain the medical indication, risk and benefits

HIPOCRATES
H: WHy is pt refusing?
I: Involve others
P: Psychologically able to make decision? U R W C
O: Offer referral for 2nd opinion
C: Certainty – is pt certain about information? Sufficient information?
R: Risks vs Benefits of treatment vs non-treatment
A: Autonomy - we respect your decision
T: Take a stand – Accept or reject pt decision , explain that this is against medical advice
E: Ensure continuity of care, support pt - ie memo, medications
S: State that pt can change his mind

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 ** Strongly reinforce that your medical advice is to go ED, however if pt strongly refuse after many tries,
in pt’ best interests, you will have to assist pt with memo , medications

COLLUSION
Possible Scenarios:
a) Family member instructs you not to disclose diagnosis to a patient for fear of patient’s reaction
towards the bad news.

BREAKS (you must break the collusion)

Before meeting the patient, set the stage ꈸ What is the patient’s personality like? How does he/she
right with the family by explaining usually take bad news?
patient’s autonomy while respecting need ꈸ Do you think the patient would have like to know what is
to do no harm. going on?
ꈸ Once I have ascertained that pt has low risk of harming
himself, if he/she wants to know, it is his/her right to know
what is going on with her body

Reasoning that ꈸ Pt has been experiencing these symptoms for a while and
● Patient may have an idea of the not getting better
diagnosis ꈸ He may have an idea of his diagnosis and may want to
● Patient may not react the way know what is happening to his body especially if we are
family thinks he might starting treatment. He may have unfulfilled wishes that he
● Patient will need to know the wants to fulfil if he were to know his diagnosis
diagnosis for management ꈸ Pt may not react the way we think he might
planning

Explore patient’s perceptions ꈸ What do you understand about your condition so far?
ꈸ Some people may or may not want to know about their
diagnosis, will you want to know about your diagnosis ?

Assess patient’s likelihood of acting in ꈸ Assess suicide risk

ways harmful to them ꈸ Different people may cope with stress or bad news
differently. Have you had bad experiences previously and
how did you react to them?

Knowledge sharing (fire pre warning) ꈸ

Support emotionally (pt and family) ꈸ We will be here to walk with you and provide you with
assistance wherever necessary.

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 BREAKING BAD NEWS
Steps POSSIBLE SCENARIOS
(SPIKES)
Cancer Newly Diagnosed HIV
Setting ● Is there anyone who came with you Confirm the result given, locally using 4th generation EIA
today? with western blot confirmation test.
● Would you like them to be present?
Setting:
Ensure privacy, avoid distraction/interruption, involve
significant others, sit down, and connect with the patient
(eye contact)
Perception ● Summarise what patient has been ”What is your understanding of the blood test?”
through and experienced so far “What do you already know about HIV infection/AIDS?”
● Do you have any ideas what may have
caused your __[insert symptom]___?
Invitation to ● Would you like me to tell you the results, “How much information would you like to receive at this
share or would you prefer to have your family time?”
here with you when I tell you about the “Do you prefer to receive the information in stages or all
results? at once?”
Knowledge Fire warning shot first Fire warning shot first
sharing ● I have just reviewed your __[insert “Unfortunately I have some bad news. PAUSE. Your blood
invx]__, and it does not look too good. test is positive for HIV infection”
__PAUSE___ “I’m sorry to inform you that…”
● Share the information: There is a growth
on the scan, and it looks potentially
cancerous.
● If lab results, can say factually that
normal range is between __ to __. Your
results show that it is __, __x the normal
range.
____PAUSE____
Empathize After giving patient time to absorb… Response to patient’s emotion with empathy
● How are you feeling right now? Naming: “I can see that this makes you feel very worried”
● NURSE the emotion Understanding: “This has been a hard time for you.”
○ Name “This makes sense to me”
○ Understand Respecting: “You have been through a lot.” “It must be a
○ Respect lot of stress to deal with___”
○ Support Supporting: “I want to help in any way I can.”
○ Empathise Exploring: “How are you coping with this?”

Try to explore:
● Symptoms of acute seroconversion and
manifestations of AIDS
● Previous history of STIs
● Risk factors of STIs/HIV (IV Substance use,
promiscuity)
● Previous HIV/STI screening
● Explore patient occupation (healthcare personal)
Support ● Moving forward, how can I help you? PE
○ Emotion → call family? Refer T, Height, Weight, BMI (loss of weight)
psychologist? Link up with Eye jaundice (Hepatitis), eye signs of CMV infection

8
 support group? Throat: thrush, cold sore
○ Medically → Refer to relevant Palpable generalized LN
specialty Lung: (TB, PCP)
Abdomen: hepatosplenomgaly
Genitalia: signs of other STI infection
Skin rash

Management
Discuss management options, if the patient’s emotion
ready, to maintain hope and future-oriented outlook.
● Referral to Infectious disease specialist (early) for
blood test and KIV antiviral therapy
● Enquire details for MOH disease notification
● Adequate MC and job relocation
● Explained that it is compulsory by law to inform
partner of HIV status, contact tracing, Importance of
partner screening
● STI screening if not done e.g. Hepatitis B, C
● Reinforced safe sexual practice – barrier method

ADVANCED MEDICAL DIRECTIVE (AMD)

● Allows a person of sound mind who is above 21 years of age to make an advance medical directive
authorizing the withdrawal and withholding of extraordinary life-sustaining treatment in the event
of his suffering from a terminal illness.
● Criteria for an AMD:
○ Terminal illness – an incurable condition from which there is no reasonable prospect of a
temporary or permanent recovery
○ Extraordinary life-sustaining treatment – excluding palliative care, any medical procedure
that merely prolongs the dying process when death is imminently inevitable.
○ Mentally incompetent / incapable of exercising rationale judgment

History Taking
- Pt must be above 21
- Need to ensure pt is voluntary , no coercion
- Ensure pt is mentally competent
- Explain what AMD/LPA means to pt, check if pt understand, retain, weigh, communicate a decision

- Need to have two people witness when pt sign the AMD in your presence. One witness must be the
doctor. The second witness must be 21 years or above and can be the doctor’s nurse, or any other suitable
person and no vested interests in your demise ( ie not your beneficiary)
- AMD can be revoked at anytime
- Hospital staff do not know if pt has AMD, it is confidential and they are not allowed to ask pt

LASTING POWER OF ATTORNEY

● The LPA is a legal document which allows a person who is at least 21 years of age('donor'),to
voluntarily appoint one or more persons ('donee(s)') to make decisions and act on his behalf should
he lose mental capacity one day. A donee can be appointed to act in the two broad areas of
personal welfare and property & affairs matters.

● Requirements to qualify to make a LPA

○ You must be at least 21 years old
○ You must have mental capacity to make LPA

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 ○ You must not be an undischarged bankrupt if you wish to make LPA for property or affairs
matters

● You can revoke your LPA anytime when you have the mental capacity
● It is up to a medical professional to decide when a patient has lost their capacity and the person with
LPA should step in.
● Any perceived neglect or abuse of power by nominated LPA “caretakers” will be addressed by the
Office of the Public Guardian.

Personal welfare matters

● where the donor should live,
● who the donor should live with,
● day to day care decisions (e.g. what to wear and eat),
● what social activities to take part in,
● handling the donor’s personal correspondence, and
● whom the donor may have contact with.

Property & affairs matters

● dealing with property – buying, selling, renting and mortgaging property,
● opening, closing and operating bank accounts,
● receiving dividends, income, or other financial entitlements on behalf of the donor,
● handling tax matters,
● paying the rent, mortgage repayments and household expenses,
● investing the donor’s savings, and
● purchasing a vehicle or other equipment the donor needs

History Taking
- Pt must be above 21
- Need to ensure pt is voluntary , no coercion
- Ensure pt is mentally competent
- Explain what LPA means to pt, check if pt understand, retain, weigh, communicate a decision

HIV AND INFECTIOUS DISEASE ACT

Under the Infectious Diseases Act, it is an offence for persons who know that they are infected with HIV not
to inform their sex partners of their HIV status before sexual intercourse.A person who is unaware of his/her
HIV status but has reason to believe that he/she has HIV/AIDS should inform his/her partner of the risk and
use a condom with his/her partner.
If you believe that you have HIV/AIDS or are at risk of contracting it, you must take reasonable precautions
to protect your sexual partner (e.g. by using condoms or go for HIV testing to confirm that you are HIV-
negative or inform your partner of the risk of contracting HIV

10
11
Even if there is a fail criteria, must continue to screen for the rest
Class of license
Vocational vs personal car
Any accidents/ Near misses / Hypoglycemia symptoms
Any evidence of drug intoxication

12
PMHX / Surgical Hx/ Drug Hx
Social hx - Smoking and alcohol (CAGE)

P/E
Alert BP HR , regular
H: S1S2 no murmur
L: Clear
ROM of C- Spine (Turn neck left and right) / lumbar spine (bend forward to touch toes)/ Abduction of
shoulders
Gait

MX
- arrange for further review to ensure resolution of hypoglycaemia episodes before certify fitness to drive
- explain reasons for not certifying his driving assessment in professional manner and shows empathy
- offer financial counselling

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ADMIN/ID 2. STI SUMMARY
SEXUAL HISTORY
Partners
Practices
Protection from STD
Past history of STD
Prevention of pregnancy
Age of first SI | Last SI | Total lifetime sexual partners | Protection – each modality

GONOCOCCAL
● Diagnosis of Neisseria gonorrhoeae should be by identification of the organism at infected sites by
direct microscopy, culture or NAATs. Serology is NOT useful for screening of N. gonorrhoeae due to
the lack of sensitivity and specificity.
● Test of cure after 14/7 post-gonococcal urethritis with urethral smear
● Serologic tests for syphilis and HIV should be performed; if negative they should be repeated at 3
months after the last risky exposure

I. Uncomplicated N gonorrhea infections {urethral, endocervical, rectal, pharyngeal}

● IM Ceftriaxone 500mg once + PO Azithromycin 1g once
● 3rd gen cephalosporins
● Co-treatment of Chlamydia for concurrent infection AND slow possibility of development of
cephalosporin resistance
● NB: Fluoroquinolones contraindicated
II. Disseminated gonococcal infection (DGI)
● Hospitalisation!
● IV Ceftriaxone 1g daily + PO Azithromycin 1g once
● 24-48 hours after improvement begins, and can be converted to an oral cephalosporin therapy for
a total of 7 days
● Anti-chlamydia therapy should be given at the same time
III. Gonococcal infection in pregnancy
● Cephalosporins in the recommended dosages are safe and effective in pregnancy
● Simultaneous treatment for chlamydial infection with Azithromycin 1g stat or Erythromycin 500 mg
orally qid x 7 – 14 days

AIDS defining illness and tx

Oral thrush / candidiasis - Nystatin 400,000-600,000 units 4 times/day; swish in the mouth
and retain for as long as possible (several minutes) before
swallowing
- 7- 14 days

Seborrheic dermatitis of scalp - Topical ketoconazole shampoo 2x / week

- Topical betamethasone valerate 0.1% scalp lotion 1 applic BD

Seborrheic dermatitis of face - Topical steroid cream BD

- Topical azole BD

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CVM 1. ATRIAL FIBRILLATION

AF NHG CPG
Complaint (acute Palpitation / syncope
cases/ symptomatic) Chest pain / SOB / fatigue / diaphoresis
Cause (in acute cases) Cardiac disease: IHD, valvular
Ppt causes: Sepsis,Hyperthyroidism, Alcohol
Control INR level
Heart rate
Compliance to tx Compliance to warfarin
Any new drugs
Consistent intake of green leafy vegetables
Any change in diet

Warfarin Tablet Soil, Sky, Sun

1 mg – Brown
3 mg – Blue
5 mg – Red/ Pink
Complications from AF Heart failure – PND /Ortho/ PND / LL swelling
Stroke – weakness/ numbness/ BOV / Slurred speech / facial droop / dysphagia
Complications from tx Bleeding
Competency In administration of meds
Crisis Mx
Co-morbids Other chronic conditions
DM HTN HLD IHD Smoking Alcohol Obesity etc

P/E BP HR (time for one min)

Alert vs confused
(Go to the bed)
Any bruising, pallor
Pronator Drift (Stroke)
H S1 S2, any murmur or prosthetic heart sound
L Clear
Pedal edema (Any CCF)
Gait (Any CI to warfarin / stroke)

KIV Thyroid exam if new onset AF

Ix ECG, INR, CXR

FBC, TFT, Electrolytes
2D echo

15
 Mx If new onset ⇒ ED
1) Rate control
- HR <80 at rest, <110 during moderate exercise
- ßB (bisoprolol, propranolol, metoprolol, atenolol), or CCB (diltiazem, verapamil)
- Digoxin for HF pts, IV Amiodarone for acute Mx

2) Rhythm control
- Acute AF within 48 hrs

3) Anti-coagulation: Warfarin vs NOAC

- CHA2DS2VASc & HASBLED
sex cat not counted in CHA2DS2VASc

INR Targets when using Warfarin

🜻 INR range 2-3
- A fib, AVR without risk factors, VTE (DVT, PE), post-MI
🜻 INR range 2.5-3.5
- Metallic MVR or
- Metallic AVR with risk factors (AF, low EF, previous embolism, hypercoagulable
state):
🜻 INR target of 1.6 – 2.5
In elderly patients >75 years of age, or in those deemed to be at higher bleeding
risk, a lower INR may be chosen instead, balancing the risks and benefits of
anticoagulation
Indications for referral Patients with serious acute underlying medical conditions, such as suspected
myocardial ischaemia or infarction, or heart failure;
▪ Patients who are symptomatic or present with impaired haemodynamic status
as a result of AF;
▪ Patients with a fast ventricular response rate, or in whom pre-excitation
through an accessory conduction pathway is suspected;
▪ Patients who develop a complication of AF, such as an embolic stroke or a
systemic embolic event; and
▪ Patients with acute onset of AF within the preceding 48 hours who are judged
to be candidates for urgent cardioversion

* OTHER REASONS WHY PATIENTS MIGHT BE ON WARFARIN: DVT, PE, AF, MVR/AVR, MI with or without
stent, Antiphospholipid syndrome

16
17
HAS-BLED Score: score of ≥ 3 indicates high bleeding risk, with ≥ 4 bleeds per 100 patients per year.

18
 Possible scenarios
1) Subtherapeutic Non pharmacological
INR due to non - To take consistent amount of vegetables
compliance to - Avoid certain food ie cranberry juice, TCM, alcohol
warfarin - Inform doctors if you make any changes in your diet and medications

Pharmacological
- Restart warfarin at same dose!
- Reinforce on compliance

Education
- Red flag – symptoms of stroke, AMI or bleeding , to return immediately

Follow up
Depends on INR levels, usually within 1-2 weeks

2) Non pharmacological
Supratherapeutic/ - To take consistent amount of vegetables
subtherapeutic - Avoid certain food ie cranberry juice, TCM, alcohol
INR due to drug- - Inform doctors if you make any changes in your diet and medications
drug interaction - Education: red flag – symptoms of stroke, AMI or bleeding , to return immediately

Pharmacological
- Stop the precipitating drug if possible
- Adjust dose of warfarin based on INR levels ( See below)

Follow up
- Repeat INR every 1 to 2 weeks for every dose adjustment.
- When target INR is achieved, next INR may be checked after 4 weeks and subsequently every 8
to 12 weekly.
- INR of >5.0 is a critical lab result,
o Direct access referral to cardio or neuro if clinically stable
o Refer A&E via ambulance if pts have signs or symptoms of bleeding or haemodynamically
compromised (i.e. low blood pressure, altered conscious state etc)

3) Reinitiation of For reinitiation after a procedure

warfarin after a - Check latest INR. Exclude development of any new contraindications to warfarin
procedure / - Restart patient on last known warfarin dose that maintained patient at therapeutic range
Initiation of - Re-initiation in polyclinic should not be attempted for cases that require low molecular weight
Warfarin heparin during procedure. Cases requiring rapid anticoagulation with concurrent heparin/ low
molecular weight heparin should be referred to hospitals for management.

For initiation
- Check baseline INR before initiation of warfarin. If INR >1.2, to consider evaluation for
coagulopathy before initiating warfarin
- For initiation, a fixed dose of 2-5mg/day (2-3mg for Chinese / Malays and 4-5mg for Indians) is
recommended

For both reinitiation and initiation

- Check INR on day 3 after initiation/re-initiation and every 1-2 days till 2 consecutive readings of
target INR have been achieved
● Generally doses will be adjusted by 0.5mg to 1mg
● Steady state is expected at least after 5 days

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 ● Thereafter check INR weekly for the first month, then 4 weekly and finally 8 to 12 weekly
once INR readings stable
● Adjust INR accordingly via the intranet warfarin calculator if not at therapeutic range
after 1-2 weeks post initiation

4) Dental ● INR within 24h prior to procedure

● Continue Warfarin

5) On treatment ● Change to Nitrofurantoin

for UTI

20
21
 Warfarin management issues
Stem
1. Patient on warfarin for a chronic illness (e.g. AF, antiphospholipid syndrome) with an acute
complaint which requires you to start a medication (which may affect INR).

Diet and warfarin ● Increases vitamin K

● Reduces

Drugs and warfarin ● Antibiotics

(refer to NHGP chart) ○ UTI: nitrofurantoin ok
○ Skin infection: Augmentin/amoxicillin/cephalexin/cloxacillin
still ok
● Analgesia
○ Codeine and orphenadrine ok
○ Paracetamol not exceeding 2g/day ok
○ NSAID generally not so ok
● Antidepressants

⚲ Consider repeating INR soon after medication given to ensure it

remains within therapeutic range.
⚲ Be aware that INR can be affected in infection as well, which can
justify INR level on the same day.

Improving warfarin ● Difficulty with halving tablet

compliance (eliminating ○ Try pill cutter
half tablets) ○ Calculate total weekly dose and round off to whole number
and give whole tablets. For example, 2.5mg daily= 17.5 ~ 18 =
3/2/3/2/3/2/3

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4) Bg AF with high mCHA2DS2Vasc score, Need to offer warfarin vs NOAC
- Explain indication for anti-coagulation: To prevent stroke and systemic embolism
- Explain Risks of bleeding - assess risk factors ie hx of ICH/ GI bleed/ Bleeding tendencies - low
platele , high INR

Choice of oral anticoagulant is based on

- Bleeding risks
- Age
- Co-morbids
- Renal and Liver function
- Concomitant drugs
- Drug tolerability
- Cost and individual preference

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 Warfarin NOACs - Rivaroxaban, Dabigatran,
apixaban
Indication ⟐ Non valvular AF ⟐ Non valvular AF
⟐ All Valvular AF ⟐ Specific valvular AF - AS , AR, MR
⟐ AF with Mechanical heart valves EXCEPT MS!
⟐ AF with Moderate to severe mitral stenosis
Benefits ⟐ Cheap ⟐ No need for INR monitoring
⟐ Can reverse with vitamin K, frozen plasma, ⟐ A/w with fewer intracranial
prothrombin complex haemorrhages compared to warfarin
⟐ Can be used in renal and liver impairment
Disadvantages ⟐ Frequent drug-drug / drug-food interaction ⟐ Expensive
⟐ Need frequent blood tests and INR monitoring, ⟐ Only dabigatran has reversal agent
ie at baseline, D3, every 1-2 days until therapeutic (idarucizumab), the rest does not
INR then weekly then 4 weekly then 8-12 weekly have
⟐ A narrow therapeutic range Less preferable in patients with high
⟐ Need for 6 out of 10 INR readings to be within bleeding risk
therapeutic range ⟐ Not recommended for pts with
⟐ A delayed onset and offset anticoagulation CrCl< 30ml/min and severe liver
which may require bridging therapy impairment
Factors ⟐ Can maintain at least 6 out of 10 therapeutic INR ⟐ Unable to maintain at least 6 out
favouring this ⟐ CrCl < 30 and severe liver impairment of 10 therapeutic INR
agent ⟐ Unable to tolerate NOAC side effect ie epigastric ⟐ Difficult access to INR monitoring
discomfort due to lab access or venous access
⟐ Has significant drug drug interaction with NOAC ⟐ Pt reluctant to have frequent INR
monitoring

Rivaroxaban
⟐ Rivaroxaban 20mg ON (CrCl ≥50), 15mg ON for (CrCl <50)
⟐ Need to check LFT and RP before initiation
⟐ Check renal panel at least annually and 6 monthly for pts with renal impairment CrCl 30-60 ml/min ,
contraindicated in CrCl < 30

Lab tests to do prior to initiation of NOAC: FBC, LFT / RP, KIV INR

24
Warfarin-Food Interactions
Foods rich in Vitamin K decrease effect of warfarin: green leafy vegetables (e.g. spinach, broccoli, lettuce,
brussels sprouts), certain legumes, some vegetable oils (e.g. soybean oil) animal livers, some fermented
foods (e.g. cheese), green tea. Chronic alcohol intake can increase metabolism of oral anticoagulants

Foods with anti-platelet effect(increase bleeding): garlic, foods containing salicylates (fruits, vegetables,
spices, teas, certain flavoured candies)

Others: Avocado (decrease effect of warfarin), Vit E (potentiate effect of warfarin), dietary supplements
(arnica, bilberry, butchers broom, cat’s claw, dong quai, feverfew, forskolin, garlic, ginger, ginkgo, horse
chestnut, inositol hexaphosphate, licorice, melilot (sweet clover), pau d’arco, red clover, St John’s wort,
sweet woodruff, turmeric, willow bark, wheat grass, alcohol (continuous heavy drinking stimulates hepatic
enzymes, increasing metabolism of warfarin, decrease effect of warfarin)

25
CVM 2. APPROACH TO CALF PAIN/ CLAUDICATION

Differentials
Acute (<2 weeks) Chronic (>2 weeks)
1) Acute limb ischemia (<2 weeks) (Trauma, 1) Vascular claudication/ PAD –Chronic (>2weeks)
Embolism ie AF/ AMI , thrombosis, dissecting (Critical limb ischemia vs non critical limb ischemia)
aortic aneurysm) 2) Neurogenic claudication/ Spinal stenosis
2) DVT 3) Lumbar radiculopathy ie PID or foraminal stenosis
3) Cellulitis 4) Venous claudication / Chronic venous insufficiency
4) Trauma ----------------------------------------------------
5) OA hip/knee
6) Diabetic neuropathic pain
7) Muscular pain
8) Symptomatic Baker cyst
9) Chronic compartment syndrome

Important things in vascular claudication

1) Differentiate vascular from neurogenic
● Vascular: shop window to shop window, pain on walking, relieved by standing, constant claud
distance, worse walking uphill, CVRF, pulses diminished
● Neurogenic: park bench to park bench, pain on walking, relieved by sitting and bending forward,
variable claud distance, worse walking downhill, pulses diminished
2) Acute vs Chronic (Critical vs non critical limb ischemia)
● Acute Limb Ischemia: Pain, paraesthesia, pallor, perishingly cold, pulseless, paralysis
● Critical Limb Ischemia: Rest pain requiring opioid analgesia, ulcer or gangrene
3) Claudication distance: if < 200m and not responding to medical therapy ⇒ Refer
4) Level of claudication: Aorta (AAA), Aortoiliac (Buttock, thigh and impotence), Femoral or popliteal (Calf),
Tibial and peroneal (Foot)
5) Palpate all the pulses!

HISTORY
Complaint: Leg pain
● Site: Unilateral/bilateral, which part of the leg (level of vessel involvement)
● Onset and progression: Acute (<2 weeks) vs chronic (>2 weeks)
● Characteristic: Aching pain (Vascular/ Neurogenic Claudication), Sharp and shooting pain
(Radiculopathy), Bursting/ Tight (Venous/compartment)
● Radiation: Back pain to the leg (PID)
● Timing: Duration (<10 mins vascular, slow in neurogenic), how often, is it getting worse (suspect
thrombosis)
● Exacerbating: Walking/ climbing up slope (Vascular), Standing/ walking/ Climb down slope/ bending
backwards (Neurogenic), Standing /Walking/Sitting (venous), Sitting down (radiculopathy/PID)
● Relieving factors: Standing alone (Vascular), Sit down/ bending forward (Neurogenic)
● Severity: Claudication distance – Fixed claudication distance (Vascular), Variable claudication
distance (Neurogenic), if vascular claud < 200m and not amenable to medical therapy -> Refer
● Rest pain?

Cause
● Rule out red flags
o Chest pain / Palpitations / SOB (Embolic - AF/AMI)
o Rest pain, ischemic ulcers, gangrene (Critical limb ischemia)
o (Acute limb ischemia (5Ps), critical limb ischemia if rest pain > 2 weeks and require regular
opioids, ulcer or gangrene)
o Trauma to calf and back

26
 o Fever, redness, pain (cellulitis)
o Painful swelling, Hx of cancer, hx or family hx of clotting problems, Recent surgery /
immobilization > 3 days, pregnancy, OCP (DVT)
● If acute / critical limb ischemia:
o Level of claudication: Abdominal pain (AAA), Buttock and erectile dysfunction (Aortoiliac),
Thigh, Calf
o Rest pain aggravated by raising limb, improved by lowering, duration of opioids needed
o Precipitating cause of ulcers ie numbness, poor fitting shoes, any complications of local and
systemic infection ie fever, chills, rigors
● Back pain, leg weakness, numbness (Neurogenic / Lumbar radiculopathy)
● Leg swelling with darkening of skin or itch over LL (Venous)
● Hip/ knee pain (Hip/ knee arthritis)
● Poorly controlled DM / numbness (Diabetic neuropathic pain)
● Swelling at the back of the knee, pain on exercise and at rest (Symptomatic Baker’s cyst)
● Recent exercise (Ligamentous/ MSK strain)
● Heavy muscled athletes (chronic compartment syndrome)

Course
● Previous similar episodes?
● Tried what treatment?
● Seen other doctors for it?

Complications
● Functional ! Occupation!
● For chronic PAD: any Bleeding on DAPT, any falls

Chronic conditions/ PMHX - RF control – Control, compliance, complications, competency ,checking

● DM / HLD / HTN / IHD / Stroke

Drug Hx
● Aspirin, Statins, Drug Allergy

Family Hx
● DM / HLD / HTN / IHD / Stroke

Social Hx
● Smoking/Alcohol
● Occupation – Physical demands at work
● Social support - Stays with who
● Environment - ie any lift landing, need to climb stairs?

Psy Hx

PHYSICAL EXAMINATION
T BP HR Wt BMI
Pulse for atrial fibrillation! (possible embolism)
Lie patient supine
Look:
● Shiny skin, loss of hair, nail dystrophy, lift foot up to look at ball of foot /toes / lateral part of foot
for punched-out ulcers (arterial), part the toes for ulcers/ infection in PAD (hyperpigmentation,
venous ulcers, stasis eczema in CVI)
● Redness, open wounds
● Varicosities. Hyperpigmentation over gaiter region
● Look at popliteal fossa for Baker’s cyst

27
Feel:
Temperature, cap refill < 2s, ALL the pulses, Ulcer
● Dorsalis pedis – 1/3 down the line joining midpoint of malleolus and 1st toe web space
● Posterior tibial pulse – 1/3 down the line joining medial malleolus and heel
● Popliteal pulse – Ask patient to bend 60-90 degrees, palpate deeply in popliteal fossa with fingers
of one hand pressing the fingers of the other
● Femoral pulse – mid point of the line joining ASIS and pubic symphysis, just below inguinal ligament
Palpate abdomen for AAA and listen for abdominal bruit
Sensation: painful numbness/ tingling in ischemic neuropathy
Calves: tenderness, erythema, non supple, measure the calf circumference 10cm below tibial tuberosity
and compare both sides

Move:
Spine ROM
Power LL
Gait

KIV Buerger’s test

KIV SLR

5 signs of acute limb ischemia: pain, pallor, pulseness, parathesiae, paralysis

INVESTIGATION
● ABPI in bilateral legs, if 0.5-0.9 ⇒ PAD
○ If ABPI > 1.4 → order TBI
○ ABPI <0.5 ⇒ Critical Limb Ischemia
○ Normal = 0.9-1.2
● KIV ECG if suspecting thrombosis
● KIV XR

28
 MANAGEMENT

PAD Non pharmacological: (CPG guidelines)

- Control of CVRF
● Smoking cessation
● Diet and exercise
● DM: HbA1c < 7% as appropriate
● Hypertension:
○ Non-DM and non-CKD < 140/90
○ DM and CKD < 130/80 * Beta-blockers are not contraindicated
● Hyperlipidemia: LDL < 2.1 (Shld be <2.1 based on HLD guidelines)
- Exercise to improve collateral blood flow: Continue walking until maximum pain tolerated, rest for a
while till pain free then restart again. Should try 3x /week for at least 30-45mins each time. Aim to
increase claudication distance
- When claudication improves, advise to slowly increase duration and intensity of exercises

Pharmacological
- Aspirin: Anti-platelet effect by preventing platelet aggravation, hence reduce risk of thrombosis ->
prevent AMI/Stroke (DOES NOT HELP WITH THE PAIN OF CLAUDICATION)
- Statin: Stabilize cholesterol plagues, less tendency to rupture and reduce inflammation of the vessels
-> prevent AMI /Stroke
- 2nd line KIV Cilostazol (100mg BD): try for 3/12 and assess symptoms
- ACE-inhibitors: reasonable for symptomatic patients with lower extremity PAD (reduces risk adverse
cardiovascular events) (Ramipril has benefits for PAD)

(BAD CALFS: BP control / Aspirin / DM / Cessation of smoking / ACE / Lifestyle / Footcare / Statin)

Education / Crisis Management

- If develop rest pain, darkening of toes, ulcers, to return immediately

Follow-up
- Follow up with monitoring of claudication distance and regular ABPI
- Try at least 6 months of conservative treatment first
- If fail conservative & indications for referral → refer for CT angiogram, Angioplasty (usu for focal
stenotic lesions, large vessels if aortoiliacs), Bypass grafting

When to refer
- Critical limb ischaemia (rest pain, ischaemic ulcers, gangrene)
- Acute limb ischemia – pain, pulselessness, paraesthesia, pallor, paralysis (5 P’s)
- ABI < 0.5 even in absence of symptom
- Claudication distance < 200 m & pain unresponsive to medical therapy, with limitation of daily
activity (even if ABI > 0.5)
- Other vascular causes of lower limb ischaemia (eg. arterial embolism, dissection, trauma, aneurysm)

- Some patients assessed to be in possible need of revascularization but where ABI may be falsely
normal e.g. in diabetics (due to calcified arteries)

29
Critical
Limb
Ischemia

Neurogenic - Non-pharm: Physiotherapy is the mainstay of treatment. Improve posture, increase lumbar
claudication flexion and reduce lordosis by strengthening abdominal muscle.
- Pharm: NSAID, opioids etc.

30
CVM 3. APPROACH TO CHEST PAIN

Possible scenarios
1) Pt presents with chest pain with Acute ACS / Unstable Angina
2) Pt with angina came for fitness to drive
3) Pt with known angina but suboptimal control
4) GERD
5) Panic attack

DDx:
1. Cardiac:
a. Aortic dissection
b. AMI / Unstable Angina
c. Arrhythmias
d. Pericarditis/myocarditis
2. Respiratory:
a. Pneumothorax
b. Pulmonary embolism
c. Pneumonia
d. Pleural effusion
e. Lung cancer
3. Abdominal:
a. GERD
b. Pancreatitis
c. Esophageal rupture
4. Musculoskeletal/skin
a. Costochondritis
b. Zoster
c. Rib fracture/tumors
5. Psychogenic ie panic attack

Initial approach: exclude 6 life-threatening causes of chest pain

● § Aortic dissection
● § Acute myocardial infarction
● § Unstable angina
● § Pneumothorax
● § Pulmonary embolism
● § Esophageal rupture

HISTORY
● Chest pain
o Site
o Onset How long? Intermittent? Chronic?
o Nature? Severity? Radiation?
o Exacerbating esp on exertion?
o Pleuritic?
o Worse on palpation?
o Relieving factors: Improved with sitting forward (pericarditis), nitrates (angina)
● Effort tolerance, before and current
● SOB
o Exertional?
● LL swelling/ abd swelling/ Orthopnea/ PND (Congestive heart failure)
● Palpitations? (Arrhythmias)
● Numbness / weakness (Aortic dissection)
31
● Epigastric discomfort, nausea, vomiting, burping, burning sensation/acid brash (GERD)
● Binge drinking, coffee ground vomitus (Oesophageal rupture)
● Pain that radiates to the pain and improves on sitting forward, nausea, vomiting (pancreatitis)
● Fever, cough (Chest infection)
● Haemoptysis, unilateral LL swelling, personal history of DVT, risk factors for DVT (PE)
● LOW/ LOA, haemoptysis, cervical lymphadenopathy (lung cancer)
● Anxiety (Psychogenic)

Paeds:
- Developmental
- Vaccination

Course:
● Treatments tried?

PMHx:
● Known IHD
o Compliance to meds esp aspirin/ Clopidogrel
o Causes: supply vs demand (any sepsis, hyperthyroidism, anemia, uncontrolled hypertension)
o EF?
o Any residual lesions?

Drug history + compliance

FHx:
● Sudden cardiac death or premature CAD (less than 55 yo in men and less than 65 yo in women)
● Thrombophilia, DVT/ PE

Social history: smoking, alcohol

Psy Hx

PHYSICAL EXAMINATION
BP HR SpO2 RR KIV Temp
{seated} Inspection: Respiratory distress, diaphoresis, pallor, rashes?
Peripheries: weak pulse, RR delay, cool and clammy
{lie 45deg} Neck: raised JVP, KIV tracheal deviation
Heart: S3, new murmur ie AR
Lungs: bibasal creps, KIV chest expansion, percussion if lung case
KIV Abdo: tenderness in pancreatitis
Pedal edema / unilateral leg swelling from DVT KIV measure

INVESTIGATIONS
● ECG
● CXR: PTX, pneumonia, widened mediastinum
● KIV blood tests: FBC, UECr, lipid profile, fasting glucose
● Oesophageal-gastro-duodenoscopy
● 24 hour oesophageal pH monitoring

MANAGEMENT

32
AMI - Non pharm: Monitor vitals, Bed rest, elevate head of bed to 45 degrees
(NSTEMI/STEMI) - Pharm: MONA therapy - Oxygen supplementation (Keep SpO2 > 90), Aspirin 300mg
Stat is pt is not already on aspirin, Sublingual GTN (CI in Severe aortic stenosis,
Concurrent use of sildenafil (Viagra), RV infarct)
- Send patient to A&E via ambulance

Unstable Angina - If ST changes and unable to differentiate from NSTEMI -> Mx as per AMI
- If no ST changes but suggestive hx -> Send pt to A&E via ambulance

IHD stable ABCDE

- Aspirin and ACEi and anti-angina
- Beta blocker and BP (target depends on other comorbid)
- Cholesterol (LDL below 2.1 with statins) and cigarette
- DM and diet advice (DASH and maybe fluid restrict)
- Exercise

Hx of angina, Class 1, 2 and 3 licences

assess fitness to Angina – Not fit until angina is satisfactorily controlled.
drive Myocardial infarction, coronary artery bypass graft, unstable angina – Not fit for at
least 1 month after episode.
Coronary angioplasty – At least 1 week off driving; resume driving if recovery
satisfactory.

Class 4, 5 and vocational licences

Completion of exercise stress test required so will need cardiologist certification

Pneumonia CURB-65, CRB-65

Clinical factor Points

Confusion 1

Blood urea nitrogen > 19 mg 1

per dL

Respiratory rate ≥ 30 breaths 1

per minute

Systolic blood pressure < 90 1

mm Hg or
Diastolic blood pressure ≤ 60
mm Hg

Age ≥ 65 years 1

Total points:

* Urea ≥7.0 mmol

For CURB65: ≥2 → Inpatient Mx
For CRB65: ≥1 → Inpatient Mx ( But if 1 point is due to age and no other co-morbids,
can consider outpt tx)

33
GERD - Non pharm: Weight loss, Wait for 2-3 hours after food before lying down, Elevate
head of bed, Avoid food triggers, stop smoking and alcohol, small frequent meals
- Pharmacological: Antacids, Omeprazole
- Red flag advice to return
- Review for improvement of symptoms
- KIV OGD if persistent

Panic attack - Refer to psych notes

Gastritis - Refer to dyspepsia notes

Zoster - Refer to zoster notes

PE Wells criteria for PE

Wells Criteria for PE: Don't Die Tell The Team To Calculate Criteria
Don’t (DVT symptoms) 3 points Die (Diagnosis most likely PE) 3 points Tell
(Tachycardia) 1.5 points The Team (Three days [at least] of immobilization, or surgery
in the past Thirty days) 1.5 points To (Thromboembolism in the past [DVT or PE]) 1.5
points Calculate (Coughing up blood [hemoptysis]) 1 point Criteria (Cancer) 1 point
This is what the scores mean:
6 High probability of PE 2-6 Moderate probability of PE < 2 Low probability of PE
The modified Wells Criteria is a bit simpler: > 4 PE is likely ≤ 4 PE is unlikely

34
CVM 4. HYPERLIPIDAEMIA

DDx:
1. Primary
a. Familial
2. Secondary
a. Alcohol
b. Hypothyroidism
c. Diabetes
d. Nephrotic syndrome / renal failure
e. Primary biliary cirrhosis
f. Drugs: OCP, Steroids, beta blockers, diuretics, HAART (NNRTI)

Ddx 2
Primary Secondary
● Lifestyle factor OILY PD
● Familial Obesity
hypercholesterolemia* Intoxication (CAGE)
Low thyroid (hypothyroid)
Protein (nephrotic syndrome)
Your drugs (OCP, beta blockers, diuretics, atypical antipsychotics,
HAART)
Primary biliary cirrhosis
DM

HISTORY
Complaint: Hyperlipidaemia
● How long? Progression?
● Treatment? Compliance

Complications
o IHD: angina, exertional dyspnea, previous MIs, IHD
o PVD: claudication pain, gangrene, foot ulcers
o Stroke / TIAs
o Abdominal pain, nausea, vomiting → Pancreatitis
o High TG >10 → Pancreatitis
● Dietary history
● Lifestyle: exercise, alcohol

Causes
● Frothy urine, UL/LL/facial/periorbital edema → nephrotic syndrome
● Pruritus, jaundice, hyperpigmentation, easy bruising → primary biliary cirrhosis
● Lethargy, weight gain, cold intolerance, constipation, menorrhagia → hypothyroidism

PMHx:
● Metabolic syndrome: DM, HTN, gout
● Renal disease
● Liver disease (PBC)
● Hypothyroidism
● HIV / AIDS

Drug history:
● HAART (NNRTI)
35
 ● Diuretics, beta blockers
● Oestrogens
● Atypical antipsychotics

Family history:
● Hyperlipidaemia
● DM, HTN
● Thyroid disease

Social history:
● Smoking / Drinking (KIV CAGE)

P/E
BP HR BMI
Waist circumference
● Eyes: xanthelasma, jaundice
● Tendon xanthomas: hands, feet, achilles tendon
● Cream and peaches appearance, goitre, dry skin, brittle hair – hypothyroidism
● Neck - goitre
● Hyperpigmentation, jaundice, excoriation marks – primary biliary cirrhosis
● Abdomen - tenderness in pancreatitis, hepato/splenomegaly in PBC

INVX
Bloods:
● Urine dipstick for nephrotic syndrome
● Lipid panel
● Fasting glucose for diabetes
● Urea creatinine electrolytes for renal impairment
● Thyroid function test for hypothyroidism
● Liver function test, CK as baseline
● Anti mitochondrial antibody for PBC

Imaging:
● US HBS for liver cirrhosis if suspecting PBC

Others:
● Urine protein creatinine ratio: >3.5g / day → nephrotic syndrome

MX
High TG ᐉ Non pharm: Exclude acute pancreatitis, Stop precipitating cause ie alcohol or
tx underlying cause, Exercise, Diet, Wt loss, avoid conc sugar
ᐉ Pharm: TG > 4.5
○ Fenofibrate 100mg OM
○ Omega 3 Fish Oil 4 - 12 g daily
● Consider adding fibrate in high risk DM pts when TG is between 2.3-
4.5mmol/L, in the presence of low HDL-C (<1.0mmol/L).
ᐉ Red flag advice for symptoms of acute pancreatitis
ᐉ F/up for rpt lipid panel / ast /alt

If liver - Stop statin therapy if serious liver injury with clinical symptoms and/or
enzymes > 3x hyperbilirubinemia or jaundice occurs during treatment. If an alternate etiology
upper limit is not found, the statin should not be restarted.

36
 while on statin - If there is an alternative etiology, Stop therapy first. Treat the underlying cause.
Statin therapy may be re-started at lower doses if the levels returned to normal.

Nephrotic - Treat the underlying nephrotic syndrome first

Syndrome - If LDL still not better → Add ACEi/ARB
- If LDL still not better → Add Statins
- KIV ED if acute onset nephrotic syndrome

Alcoholism - CAGE questionnaire

Have you ever felt like you should cut down on your drinking
Has anyone annoyed you by criticizing you for drinking
Have you ever felt bad or guilty about your drinking?
Have you ever had a drink first thing in the morning to steady your nerves or get
rid of a hangover (eye-opener)?

- Gradual reduction in alcohol

- PO thiamine 100mg OM
- Refer to NAMS, Red flag advice for alcohol withdrawal symptoms

FH - Screening of all first degree relatives of diagnosed familial FH patients is

recommended, start from age 2 years
- Start pt on statin ie Atorvastatin
- Refer to endocrinologist for what?
o Genetic testing – heterozygous vs homozygous
▪ Homozygous treatment likely high dose statin, Ezetimibe
± PCSK9 inhibitor
- New drug: PCSK9 inhibitor – monoclonal antibody; Repatha (SC dosing
monthly)
- Can add Ezetimibe
o IMPROVE-IT trial: Ezetimibe 10mg daily as second line therapy –
should lower by 20-30%
o Follow above with PCSK9 inhibitor as per FOURIER trial
▪ PCSK9 inhibitor lowered risk of non-fatal MI/stroke
although no decrease in risk of cardiovascular death
rd
- 3 line therapy: lipoprotein apheresis, liver transplant, ileal bypass
surgery, portacaval anastomosis
- Treatment target to lower LDL to <2.1 or reduction of ≥20%
- KIV Aspirin in v/o high risk CAD

Appendix

37
38
39
CVM 5. HYPERTENSION
Potential cases
1) Young and thin patient noted to have raised BP over past few clinic visits
2) Middle aged male whose BP remains poorly controlled despite being on 3 anti HTN including a
diuretic
3) Young HTN (<30yo)
4) Pt taking TCM for knee pain presenting with HTN
5) Pt with morning headaches and recent increase in BP, previously BP well controlled
6) Pt on bg of polycystic kidney disease presents with LL swelling and raised BP

Main issues for HTN case:

1) Primary vs Secondary HTN esp in young population
2) Complications of HTN
3) Co-morbids
Ddx 1 for secondary causes (TRACK PPAADS)
Thyrotoxicosis
Renovascular disease
Acromegaly
Aorta coarctation
Cushing’s syndrome
Kidney disease
Pheochromocytoma
Pre-eclampsia↑
Aldosteronism
Acromegaly
Drugs
Sleep apnea

Ddx 2 (RENAL)
Renal (GN, APKD, RAS), Endocrine (Conn’s, Cushing’, pheo, thyroid, toxicemia of pregnancy), Neurogenic
(OSA), Aortic (coarctation), Labile (stress, insufficient sleep)

DDx 3 for HTN

1. Primary hypertension
2. Secondary causes of hypertension
a. Renal: Renal artery stenosis, chronic renal disease, polycystic kidney disease, chronic
pyelonephritis
b. Endocrine: Thyrotoxicosis, Cushing’s syndrome, pheochromocytoma, Pregnancy
(preeclampsia), acromegaly, hyperaldosteronism
c. Neuro: Raised ICP
d. Cardiorespiratory: Coarctation of aorta, OSA
e. Drugs!
3. Drug induced
a. Flu medications: drugs containing ephedrine/ pseudoephedrine
b. NSAIDs (sodium retention and resistance to hypertension treatment)
c. Oral contraceptives
d. Anabolic steroid use
e. Illicit drugs: amphetamine, cocaine
f. Cyclosporine
4. White coat hypertension

40
HISTORY
Complaint:
● Hypertension
○ Duration, onset, progress
○ BP reading?
○ Home BP check?
○ Headache, visual blurring, nausea/vomiting
Course:
● If on anti-HTN, have more than 3 been used?
● Has it been previously stable, then only recently worsened?

Complications: End organ involvement

● Cardio - AMI / Acute pulmonary edema/ CAD with angina:
o Chest pain, exertional SOB, orthopnea /PND, ankle swelling
● Peripheral vascular disease:
o Claudication, cold extremities
● Neuro - Stroke:
o Visual disturbances, neuro deficit
● Renal Failure:
o Decreased urine output, nausea, lethargy, pruritus, ankle swelling
● Eye:
o Blurring of vision

Causes: [Rule out secondary causes of hypertension]

Suspect 2o HTN if: severe or resistant HTN, acute rise in previously stable BP, age of onset before puberty,
<30 with no FHx and no obesity
● Thyrotoxicosis: heat intolerance, weight loss, tremor, anxiety, diarrhea
● Acromegaly: Change in facial appearance, ring cannot fit or tight, increased shoe size, headache,
visual field disturbance
● Chronic renal failure (as above): Reduced urine output, Frothy urine, lethargy, pruritus, ankle
swelling
● Cushing’s syndrome: weight gain, easy bruising, thin skin, striae, proximal myopathy
o 2’ TCM, exogenous steroids
● Polycystic kidney disease: haematuria, abdominal pain, dysuria
● Pheochromocytoma: headache + palpitations + sweating, flushing, weight loss, paroxysmal ↑BP
● Preeclampsia: LMP, h/o pre-eclampsia, headache, BOV, abdominal pain, vomiting
● ↑Aldosteronism: unexplained hypoK
● Obstructive sleep apnea: snoring at night/witnessed apnea, daytime somnolence, fatigue
● Raised ICP: Hx of cancer, neurological deficits
● White coat hypertension

PMH
● If already known to have hypertension
o How long, Control thus far?
o Medications and Compliance
o Complications - as above
o Checking - Home BP monitoring
o Competency
● Co-morbids: Other CVRF: DM, hyperlipidaemia, ischemic heart disease
● Sec causes of hypertension: kidney disease, thyroid

Family History
● HTN

41
 ● Premature IHD in 1st degree relative: Male <55yr - Female <65 yr (CPG)
● Autoimmune conditions – predispose to thyrotoxicosis, pheochromocytoma (in MEN2)

Drug History
● Compliance to medications, SE
● OTC meds: NSAIDs, nasal decongestants
● Illicit drugs, stimulants
● Oral contraceptives, antidepressants, steroids

Social History
● Smoking, drinking

PHYSICAL EXAMINATION
BP HR (take BP properly: pt seated both feet on ground (not crossed); check pulse while
inflating cuff)
Wt Ht BMI Waist circumference (>90cm for male, >80cm for female)
[Seated]
● Inspect: Cushingnoid, goitre, acromegaly features
● Eyes: thyroid eye dz, xanthelasma ● etiology
● UL: Hand tremors, prox myopathy, spade-like hands, pronator drift

[45 deg]
● Neck: JVP
● Feel pulse and any radial-radial or radial-femoral delay
● CVS: palpate apex beat, auscultate for murmurs ● complications

[sit up]
● Lungs: creps
● complications
[supine]
● Abdo: Ballot kidneys. auscultate for renal bruit.
● LL: DM dermopathy
● etiology
[complete]
Offer fundoscopy

INVESTIGATIONS
● Stat tests:
○ ECG: LVH/AMI
○ Urine dipstick for HTN urgency
● Tests for chronic f/u
○ uACR, Na/K/Cr, fasting glucose, lipid panel
● KIV 24 hour BP monitoring if BP labile / suspected white coat hypertension
● Other Investigations
○ Renal Function and Electrolytes
■ Raised creatinine in chronic renal impairment
■ Rise in creatinine more than 30% after initiating ACE-I/ARB
■ Hypokalemia in hyperaldosteronism
○ Thyroid function test
○ UFEME w dipstick: proteinuria, casts
○ US Kidneys: Discrepancy in kidney sizes of more than 1.5 cm

Investigations done in SOC to Evaluate Secondary Hypertension

42
 ■ Reno-vascular disease → US Renal Arteries
■ Aorta → CT Angiogram in adults, 2DE in children
■ Cushing’s Syndrome → Low dose dexamethasone test
■ Pheochromocytoma → 24h urine metanephrines and catecholamines, CT Adrenals with
contrast
■ Aldosteronism → plasma aldosterone concentration / plasma renin activity, salt loading tests
■ OSA → 24h BP, sleep study

MANAGEMENT
1) Resistant Hypertension (BP remains >140/90 mmHg despite concurrent use of three antihypertensive
agents of different classes at adequate doses, one of which should be a diuretic)
⤿ Rule out secondary HTN (as above)
⤿ Confirm resistant HTN with 24 hour BP monitoring
Non-pharmacologic therapies
● Low salt diet, exercise
● Weight loss
● Smoking cessation, reduce alcohol, reduce stress

Pharmacological
● Triple combination of ACEi/ARB, long acting dihydropyridine CCB and a long acting thiazide diuretic
is often effective and well tolerated
● Add Spironolactone as a fourth agent if eGFR ≥45
● Replace thiazide with loop diuretic for patients with renal impairment
● Consider referral to a hypertension / vascular medicine specialist if BP still remains elevated despite
6 months of intensive treatment

Education
● Home BP monitoring , target home BP < 135/85 mmHg
● Target BP (CPG)
General:
< 140/90 mmHg in patients age < 80 yrs.
< 150/90 mmHg in patients age ≥ 80 yrs (do not decrease diastolic BP to < 60 mmHg).
Special conditions:
< 140/80 mmHg in patients with diabetes mellitus.
≤ 130/80 mmHg in patients with proteinuria (both diabetic and non-diabetic patients).
< 150/100 mmHg in pregnant patients without target organ damage (do not decrease diastolic BP
to < 80 mmHg).
< 140/90 mmHg in pregnant patients with target organ damage.
< 220/120 mmHg during 1st 24 hrs of acute stroke (lower with care by 10-15%).
Lower by 10/5 mmHg if BP >140/90 mmHg after acute phase of stroke.
< 160/90 mmHg for acute intracranial bleed

2) Secondary Hypertension
● Indications to evaluate for secondary hypertension
1) Sudden rise in patient with previously stable readings
2) Age of onset before puberty
3) Age of onset before 30 in non obese patients with no family hx of HTN
4) Malignant or accelerated hypertension
5) Severe or resistant HTN
● Some scenarios:
○ Age <30 with grade 1 HTN, no obvious clinical features suggestive of 2o HTN & normal initial
investigations → can treat as essential hypertension.

43
 ○ Age <30 with grade 2 HTN (or higher), no obvious clinical fts & normal initial investigations
→ follow-up closely and repeat tests, and refer for further evaluation if blood pressure
remains high despite patient being on 2 medications.

ჲ eg Acromegaly
● Lower the IGF-1 concentration to within the normal range for the patient's age and gender, control
adenoma size and reduce mass effects, improve symptoms, and reverse metabolic abnormalities
such as diabetes mellitus
● Soft tissue overgrowth recede but bony abnormalities do not regress, jt symptoms usu persist

3) Hypertensive Emergencies
● BP >180/110mmHg a/w end organ damage, impending or progressive organ damage
○ Eg: major neurological changes, HTN encephalopathy, CVA, ICH, acute LV failure, APO,
aortic dissection, renal failure, eclampsia.
● Refer to the Emergency Department

4) Hypertensive Urgencies
● Isolated large blood pressure elevations without acute target organ damage.
● Often associated with treatment discontinuation/reduction as well as anxiety.
● Exclude acute target organ damage through history (symptoms), physical examination including
fundoscopy, urinalysis (for proteinuria/haematuria) ± serum creatinine.
● Can be treated by reinstitution or intensification of drug therapy and treatment of anxiety.
● BP may not settle within 1 to 2 hrs, both due to pharmacokinetics/onset of action of drugs as well
as patients’ anxiety/impatience while waiting in the clinic
● Once target organ damage has been excluded, consider sending home (with home BP monitoring if
available), with scheduled review on the following day or within the next few days.
● Advise patient to proceed to Emergency Department if symptomatic.

5) White Coat Hypertension

Suggested by:
● Markedly elevated clinic blood pressure readings in the absence of documented end-organ
damage. Normal ambulatory blood pressure readings taken at work or at home.
● Unusual variability of blood pressure readings.
● Symptoms suggesting episodes of hypotension.
● Blood pressure seemingly resistant to treatment.
● Ambulatory or home blood pressure monitoring useful for identification and monitoring.

OTHER NOTES
Definitions of HTN
Severe Hypertension: >180mmHg / >120mmHg and have no acute end organ injury
Malignant Hypertension: >180mmHg / >120mmHg with end organ injury
Accelerated Hypertension: recent significant increase over baseline BP that is associated with target organ
damage
Resistant Hypertension: hypertension that persists despite three adequate antihypertensive medications,
including one diuretic

44
Secondary HTN

45
46
CVM 6. PALPITATIONS

Possible Scenarios
1) Middle Aged Female presenting with palpitations and
2) Young Female with palpitations and chest tightness

DDx:
1. Cardiac conditions causing arrhythmias
a. Regular tachycardia: SVT i.e WPW, sinus tachycardia, atrial flutter with 2:1 block,
ventricular tachycardia
b. Irregular tachycardia: AF, atrial flutter with variable block, ventricular ectopics
c. Bradycardia
2. Appropriate sinus tachycardia: Anaemia, dehydration
3. Pulmonary embolism
4. Endocrine
a. Hyperthyroidism / Hypothyroidism
b. Phaeochromocytoma
c. Hypoglycaemia
5. Drug induced eg Ventolin use, sympathomimetics, coffee/ tea, thyroxine
6. Anxiety disorder
7. Physiological: exercise, pregnancy (haemodynamic changes)

DDx:

History:
Complaint: Palpitations
● How long, how many episodes, how long each lasted. Abrupt onset and abrupt abortion.
● Circumstances under which palpitations occurred
● Relieving and exacerbating factors
o Exercise precipitates VT and polymorphic VT
o Coffee, alcohol
● Regular or irregular
● Previous episodes

Causes:
● Leg swelling, recent immobilization / surgery
● Bleeding: BGIT, PV bleeding, coagulopathy

47
 ● Heat intolerance, weight loss, good appetite, diarrhea, tremors – hyperthyroidism
● Cold intolerance, weight gain despite normal appetite, lethargy, constipation – hypothyroidism
● Hunger, sweating, skipped meal – hypoglycaemia
● Headache, sweating, high BP, flushing – phaeochromocytoma
● Has feelings of anxiousness, impending doom, SOB – anxiety disorder

Complications:
● Giddiness, SOB, weakness, syncope, chest pain
● Exertional symptoms, angina, LL swelling, orthopnea, PND → IHD or CHF

PMHx:
● IHD, structural heart disease, other CVRF
● Thyroid diseases
● Conditions that would require use of beta-agonist drugs eg asthma, COPD
● Depression, anxiety

FHx:
● IHD, structural heart disease, arrhythmia
● Thyroid conditions

Drug history:
● Ventolin
● Sympathomimetics: pseudoephedrine used for URTI
● Illicit drugs

Psy Hx: GAD2 (ANEW)

Social history:
● Alcohol, coffee/tea

PHYSICAL EXAMINATION
BP HR (rate, rhythm/ regularity)
[Seated]
Inspect: pallor, hydration status, CRT
Neck – Look for neck swelling and swallow, Feel for goitre
KIV thyroid exam if suspecting thyroid
Hand: tremours

[45o]
JVP – elevated in heart failure, abnormal in AF/ flutter
Heart sounds /murmur
KIV Lungs if suspecting CCF
KIV Abdo, DRE if BGIT
KIV PV/speculum if PV bleeding
KIV Pedal edema if suspecting CCF
Calves for DVT

KIV Mental State Exam if anxious

INVESTIGATIONS
STAT tests that are available: FBC, ECG, Hypocount; CXR, UPT for pregnancy
Offer: TFT, fasting glucose and lipids, UECr
KIV CXR for signs of congestive heart failure
Others: ECG looking for arrhythmia, 24hr continuous electrocardiogram monitoring, echocardiogram
looking for any structural heart disease

48
MANAGEMENT
Hyperthyroidism - Rule out thyroid storm , If Bursch Wartofsky score > 45 -> Refer to ED
- If not thyroid storm, tx with propanolol 20mg BD
- Check for CI: Asthma, Heart Block
- Send for TFT, TRAb, Review in 1/52
- Give Red Flag advice to return

Panic Attack - Check for panic disorder and other a/w psych conditions
- Refer to Psych notes

WPW - Non pharmacological: Vagal maneuvers

- Pharmacological: Not available in primary care
- Red flag advice
- Disposition:
- If in active SVT – Refer to ED
- If patient is not in active SVT, refer to cardio direct access for radiofrequency
ablation/ pharmacological therapy
- Give anti-arrhythmic drugs ie flecainide, propafenone
- DO NOT GIVE BETA BLOCKERS, CCB, Adenosine, Digoxin that will block the
AV node if unsure of diagnosis!

Anemia - Treat underlying cause

● BGIT ● Hemodynamically unstable = ED

● Menorrhagia ● Iron + Vit C supplementation

● Menorrhagia: Tranexamic acid 500mg TDS

49
Other Notes

Panic Disorder
Panic attack: PANICS D (4 out of 13)
P – Palpitations
A – Abdominal distress – Nausea, diarrhoea, sick stomach
N – Numbness (parasthesia)
I – Intense fear of death / losing control / going crazy
C – Chest tightness/ Choking / Chills
S – Shortness of breath / Sweating / Shaking
D – Dizziness / depersonalisation (feeling detached from oneself) / derealisation (feeling of not in reality)

50
CVM 7. APPROACH TO SYNCOPE

Mr Roy is a player in a soccer club. He was seen in my clinic 2/7 ago for brief episode of syncope with loss
of consciousness. Please kindly see and advise accordingly.

DDx
1. Cardiac
a. Arrhythmias (sick sinus syndrome, heart blocks, WPW, prolonged QT)
b. Structural heart disease (HOCM, aortic stenosis)
c. Carotid sinus hypersensitivity -> if causes syncope -> Carotid sinus syncope
d. Orthostatic Hypotension: Autonomic failure: DM, Parkinson’s, MSA
e. Vasovagal
f. AMI
2. Neuro:
a. Seizures
b. Stroke/TIA
3. Endocrine / Metabolic:
a. Hypoglycaemia
b. Anemia
c. Hypocortisolism
d. Alcohol-related
e. Dehydration
f. Electrolyte imbalances: Potassium, sodium, calcium, magnesium
4. Resp:
a. Pulmonary embolism
5. Drugs:
a. CNS depressants, diabetic drugs

HISTORY
Complaint:
Characterize the “syncope” first. Exclude vertigo/disequilibrium/seizures. Classically described as darkening
of vision/softening of sound with LOC.

Related to syncope itself (WITNESSED OR UNWITNESSED)

● What were you doing at that time?
o Any change in posture – orthostatic
o Any prolonged standing, loud noises, emotional distress
o Any triggers for seizures like flashing lights
o Neck movements, shaving, wearing a tight collar – carotid sinus hypersensitivity
● Pre ictal symptoms
o Chest pain, SOB, palpitations – cardiac cause
o Focal neurological weakness, giddiness – TIA/ stroke
o Sudden onset of headache with neck stiffness – SAH
o Aura – seizure
o Nausea, light headedness, blurred vision, exposure to noxious stimuli – vasovagal
syncope
o Nausea, hunger, palpitations, light headedness – hypoglycaemia
● Syncope itself: “did you lose consciousness”
o How long?
o Any jerking of limbs: which limbs, which part of face, where did it start and where did it
spread to?
o Any incontinence, biting of tongue, uprolling of eyes, frothing of mouth?
● Post ictal

51
 o Any weakness or numbness? BOV? Slurring of speech? Difficulty swallowing?
o Confused or alert?
o Headache?
● Triggers
o Recent illnesses/stress
o Anemia, causes of anemia eg BGIT
Course: previous episodes or first
Complications of syncope:
● Head injury
● Other trauma

PMHx:
● IHD / heart problems / arrhythmias
● Fits: how long, treatment and compliance, follow up, what is cause, last fit
● Parkinson’s, MSA
● DM: how long, treatment, follow up, complications, ANY PREVIOUS EPISODES OF HYPOGLYCAEMIA,
SMBG – what is reading usually

Drug history:
● Illicit drugs important! / TCM
● Insulin and OHGAs
● Anti hypertensives

Family history:
● DM, epilepsy, heart problems (both IHD and things like HOCM)

Social history:
● Work
● Alcohol history important

PHYSICAL EXAMINATION
T BP HR POSTURAL BP
Cardio
Pallor
Tongue for hydration
Carotid bruit
Palpate pulse for regularity and pulsus parvus et tardus, collapsing pulse
Heart: Cardiac murmur (AS?)

Neuro
Pronator drift. Screen power.
Gait

INVESTIGATIONS
● Blood tests:
○ FBC looking for any anaemia
○ KIV Hypocount
● ECG
● KIV RP/ LFT

52
MANAGEMENT
Arrhythmia Refer to ED Stat

Seizure / TIA / Stroke Refer to ED Stat

Aortic stenosis (newly [Link]

diagnosed) symptomatic-aortic-
stenosis?search=aortic%20stenosis&source=search_result&selectedTitl
e=3~150&usage_type=default&display_rank=3#H8

Vasovagal Syncope a. Disposition: keep in primary care

b. Non drug: Avoid precipitating factors: avoid prolonged standing
c. Drugs: usually none needed
d. Educate: Assure about benign nature of reflex syncope but warn
about potential of injury due to fall. Practical tips (stool to sit on if
cannot avoid prolonged standing), when symptom set in to sit down
or lie down with legs raised or tense lower limb muscles, prop leg up
e. Follow up: if recurrent, more frequent or red flag symptom present
to return KIV tilt table test

Carotid Sinus Non pharm / Education: Avoid accidental mechanical manipulation of

hypersensitivity the carotid sinuses (neck) if they receive medical or chiropractic
(Pause duration of >3 treatments to the neck area or wear tight collars.
seconds or drop in BP >50
mmHg during carotid sinus For CSS: Permanent cardiac pacing, may need Vasoconstrictor drugs ie
massage, may or may not midodrine
be associated with
symptoms) Disposition: ? Refer to ED vs Cardio same day

Carotid Sinus Syncope (CSH

with syncope)

Orthostatic Hypotension 2o ⊛ Non pharm: Hydration, stop precipitating drugs, pressure stockings in
to autonomic dysfunction the daytime, Exercise, Elevate head of bed and get up slowly, cross your
legs when sitting
- Pharmacological
§ 1stline Fludrocortisone – cause salt and water retention to increase
intravascular volume.
§ - SE: fluid overload, hypertension & hypokalemia
§ - Start at 50mcg once/day to max 200-300mcg/ day
§ 2ndline or add on: Midodrine
§ Ergotamine – cause vasoconstriction
If pt has supine hypertension and postural hypotension: give anti-
hypertensives at night, fludrocortisone in the morning

Anemia Address underlying cause

Hypoglycemia ● Address underlying cause

● Hypoglycemia advice (15-15 rule)
● KIV adjust DM meds

53
Brugada Syndrome (Slides) - Type 1 Brugada Syndrome, pt presents with syncope
ECG abnormalities for Type 1 ECG: Coved ST segment elevation >2mm in >1 of V1-V3 followed by a
negative T wave

Symptoms: Syncope, Dizziness, Palpitations, SOB

Ix: ECG , Echocardiogram, Cardiac Stress Test

Mx:
Refer to ED STAT
Implantable cardioverter – defibrillator
Antiarrhythmic drug to reduce the frequency of ICD shocks ie amiodarone , quinidine
Radiofrequency ablation

Note:
This Type 1 ECG abnormality must be associated with one of the following clinical criteria to make the
diagnosis of Brugada syndrome
● Syncope
● Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
● Family history of sudden cardiac death at <45 years old .
● Coved-type ECGs in family members.
● Inducibility of VT with programmed electrical stimulation
● Nocturnal agonal respiration
For patients with the Brugada ECG pattern who are otherwise asymptomatic and have none of the criteria
that would suggest Brugada syndrome, → No treatment needed

54
55
CVM 8. CONGESTIVE CARDIAC FAILURE

Stem
1. Worsening CCF to evaluate cause (ADHF)

DDx for acute decompensated heart failure 1

Reduced pumping Increased demand

- Coronary heart disease: Stable angina, - Arrhythmias

Unstable angina, NSTEMI, STEMI - Sepsis
- Myocarditis - Hyperthyroid
- Valvular heart disease - Anemia:BGIT?
- Non compliance to fluid restriction
- Drugs: cardiodepressant (NSAID)

DDx for acute decompensated heart failure 2

Cardiac Non cardiac

ᐉ AMI a) Non compliance to medications, fluid and salt

ᐉ Arrhythmias restriction
ᐉ Papillary muscle rupture b) Suboptimal tx – ie not on ACEi / diuretics
(CP / SOB / diaphoresis / Palpitations / syncope / c) Renal dysfunction, Pulmonary embolism,
giddiness) anemia, hyperthyroidism, infection ie UTI,
pneumonia
d) Concomitant medications ie NSAIDS, CCB

HISTORY Eg CCF follow-up

Complaint: SOB, PND, Orthopnea, LL swelling, decreased effort tolerance
**rule out other causes of dyspnea
● Severity and triggers of SOB/fatigue – determine NYHA class
○ NYHA class 1-4 → no limitations, limitations iADL, limitations bADL, symptomatic at rest

Course
● Investigations done (Last 2DE Ejection fraction?), Coronary angiogram/CT angiography
● Hospitalisations

Control
● Medical comorbidities control: BP target <130/80, HbA1c <7%, LDL <2.1

Checking
● Weight trend
● Home BP monitoring, SMBG if relevant

Compliance to fluid restriction, sodium restriction, medications

Complications of disease
● Affect Function?
● Hypotension

Complications of treatment
● AKI

56
 ● Hyperkalemia (due to ACEi, spironolactone)
● Bleeding if on antiplatelets

Co-morbids

Crisis Mx: Does pt know what to do if

Social Hx
Psy Hx

Function: bADLs/iADLs, PU/BO

Preventive Health
● Vaccines: flu, pneumococcal

PHYSICAL EXAMINATION
T BP HR RR
Ht Wt BMI
Conjunctival pallor
Hand tremours
Goitre
[Lie 45o]
Neck: Raised JVP
Praecordium: Displaced apex beat, parasternal heave, S3, murmurs
Lungs: Bibasal creps
LL: Pedal edema

INVESTIGATIONS
● Stat tests:
○ ECG, CXR
○ FBC (anemia)
○ Urine dipstick (proteinuria)
● RP (Renal impairment), CaMgPO4, TFT, LFT with albumin (third spacing), glucose, lipid panel
● 2DE for initial evaluation

MANAGEMENT
Chronic management CCF ABCDEF
ACEi / ARB, Aldosterone antagonist, Aspirin
Beta-blocker, BP management
Cholesterol, Cigarette cessation
Diuretics, Diet, DM control, Digoxin
Exercise, education of patient
Flu vaccination annually

ADHF ● Refer ED for IV diuretics

HFrEF ● ACEi/ARB/ARNI + ßblocker (± Spironolactone) to reduce morbidity

and mortality
○ ACEi beneficial for pts with prior/current symptoms of
HFrEF to reduce morbidity and mortality
○ ARB if intolerant to ACEi (cough or angioedema)
○ Chronic symptomatic HFrEF NYHA II/III who tolerate
ACEi/ARB → recommend replacement with ARNI (eg

57
 Entresto) to further reduce morbidity and mortality
● Ivabradine can be beneficial to reduce HF hospitalization for
patients with symptomatic (NYHA class II-III) stable chronic HFrEF
(LVEF ≤35%) who are receiving max medical tx, including ß-blocker
at max tolerated dose, and who are in sinus rhythm with a heart
rate of 70 bpm or greater at rest

HFpEF ● Diuretics for symptom relief from volume overload

● BP control with ßblocker, ACEi/ARB
● In some pts with EF ≥45%, elevated BNP levels or HF admission
within 1 year, eGFR>30, Cr<221µmol/L, K<5.0), aldosterone
receptor antagonists might be considered to decrease
hospitalizations
Non pharm
● Restrict dietary sodium <2g/day; fluid restriction 800ml-2000ml
● Monitor weight and BP
● Mx risk factors
○ Screen for DM; HbA1c <7%
○ HTN: aim BP <130/80mmHg {2017 ACC/AHA guideline} (stage A HF or pts w increased cardiovascular
risk ie age >75, established vascular disease, CKD, or Framingham Risk Score >15%)
○ HLD: LDL <2.6, TG <2.3, HDL >1.15
○ CKD
○ Smoking cessation
○ Diet, Exercise
○ Weight reduction for BMI ≥25
● Vaccinations - flu / pneumococcal
● Psychosocial factors eg support
● Pt education: dz management

Pharm
● If systolic heart failure, ensure pt on beta-blocker, ACEi, KIV add on Spironolactone
● Frusemide for symptomatic relief
● Anemia
○ In patients with NYHA class II and III HF and iron deficiency (ferritin <100 ng/mL or 100 to
300 ng/mL if transferrin saturation is <20%), IV iron replacement might be reasonable to
improve functional status and QoL

Education
● Crisis Mx: Red flags to return

58
2017 ACC/AHA Focused Update on 2013 Guidelines for HF

2013 ACC/AHA Guidelines

59
60
61
CVM 9. ISCHEMIC HEART DISEASE

HISTORY
Complaints: Angina (retrosternal chest pain, exacerbated by exercise or emotion, relieved by rest or GTN).
Rule out unstable angina/NSTEMI/STEMI.
*Rule out other causes of chest pain
Course: Medical management vs PCI vs CABG. Any ICD.
Causes:
- Supply reduced: Atherosclerotic disease from underlying DM/HTN/HLD/smoker
- Demand increased: Sepsis/thyroid/anemia
Control:
- Any chest pain? If yes, distance before chest pain comes on: Stable or reduced.
- Diet/ Exercise
- DM hba1c <7%? LDL <2.1?
Compliance
- Non pharm
- Pharm
Complications of disease:
- Limitation of activities
Complications of treatment:
- Antiplatelet side effects: BGIT
- Statin side effects: muscle aches

Medical Hx: IHD, DM, HTN, HLD

Drug Hx: ABCDE (ACEI/ARB and angina meds like nitrate and aldosterone antagonist if EF <40%), Beta
blocker and BP meds, Cholesterol meds, Diuretics and DM meds
Fhx: Sudden cardiac death?
Preventive: Flu and pneumococcal vaccines.

Psy: PHQ2. GAD2.

Social: Work. Finances? Smoking? Alcohol? Home environment? Exercise? Diet?
Function: DEATH AND SHAFTTT affected?

PHYSICAL EXAM
BP HR BMI (<25) KIV waist circumference.
[seated] Pallor
Cardio exam: Pulse rate. Conj pallor. JVP. Apex beat. Murmurs. Basal crepitations. LL edema.

INVX
- ECG
- If suspecting other causes, FBC, TFT

62
MANAGEMENT (stable angina)
Risk factor management Plaque stabilizing Antianginal Heart failure
(antiplatelet/statins) management

- DM - Antiplatelet - Sublingual GTN ABCDEF

- HTN - Statin - Beta blocker
- HLD first line
- Smoking PCI/CABG as indicated - Then… CCB/long
- Obesity acting nitrates

Worsening angina/ New - Determine etiology (any reversible causes)

onset angina = Unstable - Rest angina, crescendo angina considered unstable angina.
angina Technically disposition is ED for chest pain protocol.
- If patient declines referral to ED, may need to optimize angina
medications while awaiting CVM appt.

Bleeding symptoms while - Risk of bleeding: Superficial site (skin, anterior epistaxis) vs
on DAPT (e.g. BGIT, deeper (BGIT/hematuria)
epistaxis, hematuria) - If unable to stop bleeding, consider ED referral.

Dental procedure while on - DAPT should not be interrupted especially before 30 days of
DAPT bare metal stent and 6 months of DEB. If need to interrupt,
consult cardiologist if not able to defer.
- Memo to dentist to avoid NSAID class of analgesia

Worsening CKD (stage 4

eGFR<30) or hyper K while
on aldosterone
antagonist/ACEi

Can stop DAPT? - Risk of stopping DAPT

- Less than 30 days high risk of stent thrombosis
- 6 months and above generally ok to discontinue plavix
- Between 1-6 months is debatable

63
64
CVM 10. APPROACH TO LL SWELLING

Differential Diagnoses
Unilateral
1. Cellulitis
2. Deep Vein Thrombosis
3. Trauma - Acute compartment syndrome
4. Lymphedema
- Pelvic tumour / Malignancy/ Inguinal lymph nodes
- Lymph node dissection
- Trauma
- Radiation affecting lymphatic drainage
5. MSK - Muscle sprain, Baker’s cyst rupture
6. Complex regional pain syndrome

Bilateral
1. Congestive heart failure / Cor pulmonale
a. Valvular heart disease
b. Congenital heart disease
c. Ischemic heart disease
d. Tachy-arrhythmias
e. Cor pulmonale secondary to pulmonary hypertension (primary or secondary)
2. Renal failure/Nephrotic syndrome
3. Chronic liver disease
4. Protein losing enteropathy / Malabsorption
5. Chronic venous insufficiency
6. Hypothyroidism / Pretibial myxedema
7. Pregnancy
8. Obstructive sleep apnea resulting in pulmonary hypertension
9. Drugs eg amlodipine, fenfluramine
10. Dependent edema
11. Extrinsic venous compression
12. Lymphedema

65
 Ddx 3
● Due to increased arterial pressure 3rd spacing
○ Increased hydrostatic pressure: CCF, Cor pulmonale, Renal failure,
○ Reduced oncotic pressure: Nephrotic syndrome, liver failure, protein losing enteropathy
● Due to reduced venous drainage: CVI, DVT
● Due to reduced lymphatic drainage: Pelvic organ enlargement (e.g. tumor, pregnancy)
● Acute trauma: Compartment syndrome
● Due to skin swelling: Cellulitis, myxedema
● Drugs: Amlodipine

HISTORY
Complaint
● LL swelling
○ Unilateral vs Bilateral?
○ Painful or painless?
○ Onset: Sudden onset (<72 hrs) vs Gradual
○ Duration
○ Progression: stable, improving, worsening, intermittent?
○ Relieving and exacerbating factors
■ Worse at end of day and better with elevation → Chronic venous insufficiency, Cardiac
■ Better at end of the day → Renal
○ Up to which part of leg?
● A/w swelling in other parts of body (Systemic causes)
○ Abdominal distension
○ UL edema
○ Facial swelling/ periorbital edema

Cause
Red flags:
● Risk factors for deep vein thrombosis - TOM IS POPE
○ Trauma, Obesity, Malignancy, Inherited thrombophilia eg family hx of blood clot in the
legs/lungs, Recent surgery/ Immobilization / Long flight in last 4 weeks, Previous DVT/PE, OCP
pill, Pregnancy, Elderly
● Weight Loss / Abdominal distension/ mass/ hx of pelvic surgery with lymph node dissection or radiation
(Lymphedema)
● Trauma / fall (Acute compartment syndrome)
● Fever, pain, redness, open wounds on the leg (Cellulitis)
● Recent exercise / posterior knee pain, knee stiffness, swelling or a mass behind the knee (MSK)

● Chest pain/ SOB (esp exertional), orthopnea, PND, palpitations? (congestive heart failure)
● Recurrent cough/ sputum production/ haemoptysis/ SOB/ pleuritic chest pain? (chronic lung diseases
→ cor pulmonale)
● Frothy urine / decrease in urine volume? (nephrotic syndrome/ renal failure)
● Jaundice, pruritus, easy bruising, haematemesis ± risk factors for CLD (chronic liver disease)
● Weight gain, cold intolerance, constipation, menorrhagia? (hypothyroidism)
● LMP! (Pregnancy)
● Night pain/pain that wakes pt up at night, rest pain, constitutional symptoms (Malignancy)
● Any new medications that you took recently that caused this ankle swelling, usually initiation or change
in dose (Drug induced)

Course
- Previous similar episodes?
- Tried what treatment?

66
 - Seen other doctors for it?

Complications
- If suspecting DVT, rule out PE: SOB / Palpitations / Effort tolerance
- If just benign leg swelling: Function affected? Job?

PMHx
● Hx of cancer / DVT /PE / Clotting problems
● Hx of IHD / CCF / Liver disease / Renal disease
● Thyroid problems

Family history
● IHD
● Clotting problems (leading to recurrent pulm emboli → cor pulmonale)
● Thyroid problems

Drug Hx DRUG ALLERGY?

● Calcium channel blockers: amlodipine, nifedipine
● Thiazolinediones (pioglitazone)

Social Hx
● Smoking - increases risk of DVT
● Alcohol
● Occupation - prolonged standing can predispose to CVI
● Function affected? Finances?

Psy Hx

PHYSICAL EXAMINATION
Temp BP HR
Ht Wt BMI
Standing
● Inspection of the leg
○ Erythema, Varicose Veins, CVI changes ie hyperpigmentation, venous ulcers,
lipodermatosclerosis (CEAP)
○ Swelling at the back of the knee → Baker’s cyst

Lie 45o
● Heart: S1 S2, S3 in CCF

Lie supine
● Face: pallor, jaundice, sallow complexion
● Neck:
○ Raised JVP → CCF
○ Goitre
● Lungs: crepitations
● Abdomen: pelvic masses, organomegaly, hernia, lymph nodes, ascites (shifting dullness)
● Peripheries: chronic stigmata of liver or renal disease, AVF
● Feel for warmth, tenderness, level of pitting edema, DP/PT
● Measure the calf circumference 10cm below the tibial tuberosity: significant if >3cm than the other
leg, entire leg swollen and only confined to one leg → Well score for DVT HIGH

INVESTIGATIONS

67
 ● Stat tests
○ Urine dipstick/Urine PCR
○ CXR: cardiomegaly, signs of congestive heart failure
○ KIV XR: fracture
○ KIV ECG: arrhythmia, right axis deviation in cor pulmonale
● Bloods: RP, Albumin with Liver function test, thyroid function tests
● US Venous doppler if suspecting DVT

Specialist level
Ultrasound of hepatobilary system: cirrhosis
Computer tomography of thorax if suspecting chronic lung conditions
Echocardiogram for congestive heart failure, look for right ventricular dilatation in cor pulmonale
Cardiac catheterization to look for pulmonary hypertension and exclude cardiac shunts

MANAGEMENT
1) Acute DVT
→ Calculate Well’s criteria → Refer to A&E for US Venous Doppler, will have to start anti-coagulation
*** Postthrombotic syndrome is characterized by chronic leg swelling, pain, cramping, and skin changes
including telangiectasias, which occur in 20% to 50% of patients within five years of a thrombotic event. In
addition to anticoagulation, compression stockings should be used after a DVT to prevent postthrombotic
syndrome

68
Wells Score for DVT: C3P2O + R2D2
C (3):
ꈸ Cancer (active)
ꈸ Collateral superficial veins visible
ꈸ Calf diameter increase >3 cm
P (2):
ꈸ Pitting oedema
ꈸ Previous DVT documented
O: Oedema of the whole leg
+: Tenderness of the calf
R (2):
ꈸ Recent surgery
ꈸ Recent immobilization
D2:
ꈸ Different diagnosis more likely (subtract 2 points)

Score negative to 0: low probability

Score 1-2: Mod risk of DVT (Need to refer for D-dimer)
Score 3 and above: likely DVT (Need to refer for US Doppler)

2) Medication induced
- Stop the offending medication, replace with another drug if necessary

Advice
● Watch your symptoms
● Keep your legs elevated
● Avoid standing for long periods
● Wear covered footwear to protect against trauma and infection

3) CVI
● CEAP
● KIV compression stockings if pulses normal

4) Cellulitis
● Cloxacillin
● Review within 1/52

69
DERM 1. APPROACH TO ACNE VULGARIS

CLINICAL FEATURES
Lesions are seen on the face, chest, back, shoulder, upper arms.
Lesions seen are:
1. Non-inflamed lesions: comedones, consisting of blackheads (open comedones), in which the black colour
is due to melanin (not dirt) and whiteheads (closed comedones)
2. Inflamed lesions: may be superficial papules and pustules or deep (pustules, nodules and cysts)
3. Scars: hypertrophic scars, keloids, ice-pick scars, depressed fibrotic scars, atrophic macules

Important points to cover

1) Extent of acne and severity
2) Triggers for acne
3) Secondary causes for acne
4) Treatment tried so far
4) Impact of acne on psychosocial/function
5) Medications, S/E and plan for pregnancy
6) Follow up

HISTORY
Complaint: Acne
- Distribution: face, trunk, back, arms, shoulders
- Type and severity: comedonal, inflammatory papules/ pustules, nodulocystic, number

Cause
- Triggers: Stress, High glycemic index diet with dairy products, Hormones (increase in androgens during
puberty)
● What facial wash do you use, is it non-comedogenic and oil-free
- Secondary causes:
● External: Makeup, new facial wash / cream that are comedogenic, Occupational exposure to
oil/coal tar
● Drugs: Steroids (topical and systemic) / TCM , anti-epileptics ie phenytoin, anti TB ie isoniazid
● PCOS: LMP! Menstrual history and oligomenorrhoea, facial hair, chest hair
● Cushing’s syndrome: rounded facies, easy bruising, weak when you try to comb hair or climb stairs,
striae on abdomen

- Differential diagnosis (not acne)

● Rosacea: Photosensitive, telangiectasia
● Perioral dermatitis
● Folliculitis
● Keratosis pilaris

Course
- Seen any doctors, tried what treatment

Complications
- Fever / facial pain – cellulitis
- Depression

PMHX
Drug Hx – as above
Gynae Hx ***: LMP / Plan for pregnancy!
Social Hx ***: Impact on psycho-social /function – How has your acne affected you ? Work / School/ Self
Esteem
70
Occupation exposure as above / Relationship/ Smoking /Alcohol

Family Hx
Psy Hx: PHQ-2 and GAD-2

PHYSICAL EXAMINATION
BP HR BMI Ht Wt
Face – acne , rounded facies in Cushing’s , facial hair in PCOS
Trunk – acne , supraclavicular fat pad, chest hair
Back – acne, dorsal fat pad
Abdomen – any striae
Test shoulder abduction for proximal myopathy (Cushing’s)

MANAGEMENT
Possible Scenarios Management

Acne Lifestyle Mods

ꄗ Avoid high glycemic index diet and excessive dairy products
ꄗ Reinforce to use only non-comedogenic and oil-free cosmetics
ꄗ Avoid use of any abrasive cleansers or excessive cleansing that may cause
skin irritation

1) Mild Acne Comedonal → Tretinoin 0.025% cream ON or Adapalene 0.1% gel ON

ᐉ Comedonal (non- (keratolytic and anti-inflammatory)
inflammatory) acne + ● Apply thin layer to affected areas and areas that are prone to acne
few superficial ● Common side effects: skin irritation, dryness and flaking, most
inflammatory lesions notable during first month of therapy (should apply this with facial
moisturizer and sunblock)

Inflammatory lesions → topical Benzoyl peroxide (2.5%, 5%) gel OM ±

topical Clindamycin (solution/gel) OD
● Apply to affected areas, not just on each spot
● Do not apply together with Tretinoin cream as it oxidizes Tretinoin
● Side effects: skin irritation, stinging, tightening, burning sensation
● Topical antibiotics should not be used as monotherapy!
● Better treatment efficacy when combined with retinoids or BPO. Also
decreases occurrence of bacterial resistance

2) Moderate Acne ꄗ Add on topical retinoids or benzoyl peroxide to oral antibiotics

ᐉ Inflammatory lesions ꄗ Oral ABx: Doxycycline 100 mg OM/BD or Erythromycin 500 mg BD
(ie papules, pustules) ● Duration of treatment: 3-6 months
● Review 6-8 weeks post initiation for improvement
● Reduce/stop oral antibiotics when inflammatory lesions clear
● Doxycycline & Erythromycin side effects: nausea, vomiting, diarrhea,
abdominal pain
● Maintenance therapy following initial successful therapy: Even if acne
cleared, continue to use topical retinoids at night, with or without the
additional use of benzoyl peroxide in the morning.

3) Severe Acne ꄗ Refer dermatologist for systemic isotretinoin

ᐉ Nodulocystic ● Indication: Severe recalcitrant nodular acne, tx resistant, scarring
acne, acne fulminans, significant psychologic distress, abx-induced
gram neg folliculitis

71
 ● Dose : Initiated at a dose of 0.5 mg/kg/day for the first month of
therapy, and is subsequently increased to 1 mg/kg/day. Taken once
or twice daily with food. Continue until cumulative dose of 120 to
150 mg/kg is achieved. Typically reached over four to six months.
● S/E:
○ Teratogenic
○ Elevated liver enzymes
○ Increased LDL / TG
○ Mucocutaneous: dry mouth, dry skin, cheilitis, photophobia,
Stevens-Johnson syndrome
○ Psy: low mood, depression, suicide
○ Myalgias, visual changes, idiopathic intracranial hypertension
● Monitoring:
○ LFT and lipid panel prior to initiation, repeat 4-8/52 after
initiation
○ UPT prior and every month until 1 month after cessation
○ Two forms of birth control for at least one month prior to
starting isotretinoin therapy, during therapy, and for one
month after therapy.

4) Pregnant woman with ● Suitable for pregnancy: oral erythromycin, topical clindamycin,
acne flare topical azelaic acid (Pregnancy class B drugs)
● CI: oral isotretinoin, Doxycycline, topical retinoids (BZP is class C in
pregnancy)

When to Refer ● Unsatisfactory response to treatment after 2 months of oral

antibiotics
● Nodulocystic acne
● Acne Scars
● Severe psychological distress from acne (besides referral to
dermatologist consider referral to psychologist)
● Diagnostic uncertainty
● Patients failing to respond to multiple therapeutic interventions

72
73
DERM 2. APPROACH TO ATOPIC DERMATITIS

HISTORY
Complaint: Rash, itch (consider other ddx as well)
- Location: Is it typical of eczema? Neck, elbow and knee flexures
- Characteristic: Dry/vesicular/lichenified/purulent
Control
Triggers:
- House dust mite
- Environment: grass, low humidity
- Food allergy *** - common: cow’s milk, egg white, soy, wheat
- Stress
- Neutral to alkaline soap

Compliance
● Non-pharm: Skin care(soap, bath,moisturizer, scratch), avoidance of triggers
● Pharm (Address ICE: e.g. steroid phobia)

Complications
● Secondary bacterial infection – discharge, formation of crust, warmth, redness, fever
● Eczema herpeticum
Competency - how is the application, who applies the creams, apply where and when
Co-morbids- Food allergy, AR , Allergic conjunctivitis, Asthma
Crisis Mx - How to recognize symptoms of infx

PMHX, Drug Hx, Allergy

Family - Atopy
Psycho – PHQ-2 and GAD -2
Social – QoL – Education, activities, friends, marriage partners , Finances

Management (Resource : NSC Atopic Dermatitis PDF)

Maintenance when not in Educate:
flare - Explained diagnosis of atopic dermatitis - inflammation of skin , skin is dry ,
red and itchy
- It can be improved with avoidance of triggers, compliance to good skin care,
medications
- Skin care involves
1) Daily moisturizer TDS, especially after bath and swimming to prevent drying
of skin
2) Use gentle soap. Soap substitute (emulsifying ointment for bath).
3) Limit shower duration to 3-5 minutes, with room temperature water to
prevent drying of skin
4) Avoid scratching by relieving itch with antihistamines, keep fingernails
short and wear thin and loose clothings
- Avoidance of triggers
1) Reduce dust: Sun and vacuum mattress at least once a week. Wash
bedsheets and pillowcases in hot water (60 degree celsius) for 1 hour once
per week, use dust mite impermeable pillow covers
2) Wipe away sweat immediately to avoid aggravation of eczema, and keep in
cool surroundings
3) Avoid food triggers, stress reduction

Treatment of exacerbation of Will require HIGH DOSE topical steroids to reduce inflammation
eczema - Use a fingertip unit of steroid cream

74
 - Use a potent corticosteroid BD during exacerbation then gradual taper down
to less potent corticosteroid 2x/week to prev affected areas

S/E of topical steroid : thinning of skin, striae, purpura, aggravate cutaneous

infection, steroid acne/folliculitis, cataract

Concerns about topical steroids affecting growth: little systemic absorption

into bloodstream, less likely to affect growth whereas poorly controlled
eczema can affect growth. Will monitor closely for side effects of steroids

For adult only : Consider short course of prednisolone: (UTD) : 40 to 60

mg/day for three to four days, then 20 to 30 mg/day for three to four days)

Treatment of infection: - Oral antibiotic (target staph aureus/ strep) : cloxacillin, cephalexin (500mg
QDS adults x 5/7)
- PP wash for exudative conditions
- Stop steroid cream over the infected area

Indications to refer to dermatology (CPG)

● Suspicion of Allergic Contact Dermatitis
● Unsatisfactory response to topical steroids
● Eczema/Dermatitis affecting more than 10% BSA (Body Surface Area)
● Patients where phototherapy or systemic treatment ie immunotherapy (azathioprine, ciclosporin is indicated
(E.g. Requiring more than 2 courses of oral prednisolone in a year)
● Severe atopic dermatitis significantly affecting quality of life or causing psychological trauma
● Presence of steroid side effects

Food allergy – skin prick test , food elimination and challenge

75
DERM 3. APPROACH TO ALOPECIA

CAUSES
Scarring - Discoid Lupus
- Lichen Planus
- Tinea Capitis
- Morphoea
- Radiation
- Burns
- Surgery

Non-Scarring

Patterned - Trichotillomania
- Androgenetic Hair Loss
- Female Pattern Hair Loss

Focal - Alopecia Areata

- Syphilis
- Pressure Induced
- Traction Alopecia

Diffuse - Telogen Effluvium (drugs*, medical

disorders**, poor diet)
- Anagen Effluvium (chemotherapy)
*common drugs:
o Anti-thyroid drugs (carbimazole, PTU)
o Anticoagulants (heparin, warfarin)
o Anti-convulsants
o Anti-mitotic drugs (bleomycin, doxorubicin, vincristine)
o Captopril
o Lithium
o Retinoids
o OCPs
o Propranolol
**medical disorders:
● major illnesses/surgery
● major psychological stress
● childbirth
● thyroid disorders (hyper or hypo)
● significant weight loss
● chronic iron deficiency
● poisoning from eg. arsenic, mercury or thallium

Name/Age/Sex

BIOLOGICAL

ACUTE CHRONIC ILLNESS MEDICAL HISTORY

Complaint: Hair Loss Cause ● Medical/

76
 ● Site Course Surgical Hx
● Onset Control ● Drug Hx/
● Character: itching, prickling, tenderness (scarring) Compliance Drug
● Duration Complications allergies
● Severity: affecting mood/ QOL Checking ● Medication
Cause Competency List
● Recent catastrophic ● TCM/OTC
illnesses/childbirth/psychological stress Comorbidities
● Hyper/Hypothyroid symptoms Crisis management
● Associated rash (secondary syphillis), atopic
dermatitis, psoriasis, seborrheic dermatitis
● Habitual hair pulling
● Recent medications
● Recent surgeries
Course
● Previous treatments
● Previous medical consultations

Complications
● Function: work/school, mood, relationship with
others

DISEASE PREVENTION FAMILY HISTORY

- Vaccinations Androgenetic hair

- Cancer prevention: loss

PSYCHOLOGICAL

PHQ-2 I
GAD-2 C: Affecting
work/life?
E

SOCIAL

Home/Environment – triggers?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sleep

PHYSICAL EXAMINATION ***HAND RUB***

T BP HR
● Goitre
● Examine hair - note pattern of hair loss, scarring vs non scarring
● Associated rash
● Hair pull test (to determine active hair loss → 6 or more hair fibres are extracted)

INVESTIGATIONS
● FBC to screen for anaemia
● TFT: hypothyroid vs hyperthyroid

77
MANAGEMENT
Treat underlying cause

Alopecia Areata
● 1st line: Intralesional or Topical steroids (for children and adults who are unable to tolerate
intralesional steroids)
i. betametasone valerate 0.1% scalp lotion BD
● 2nd line: Minoxidil
ii. dose dependent effect ie. 5% generate more hair growth than 2%
iii. less efficacious
Prognosis
○ No definitive treatment for cure, therapies only help to stimulate hair growth
○ Chance of recurrence is high

Androgenetic Hair Loss

● 1st line: Finasteride
a. 1mg daily
b. Most efficacious
● 2nd line: Minoxidil 2% or 5% BD
● Prognosis
○ Generally good response to above therapies, however must continue for at least 12 months
before assessment of efficacy can be made

78
DERM 4. APPROACH TO RASH

Differential diagnosis - DISEAS OF SKIN (Mnemonic)

Primary skin condition Eczema
Psoriasis
Seborrheic dermatitis

Infections Viral exanthem

- Varicella
- Herpes Zoster
Bacterial
- Meningococaemia
Parasite
Many Many

Drug induced Allergy - Steven’s Johnson, TENS, DRESS

Drug eruption
Lupus

Food induced Food allergy

Chemicals / Occupational exposure Irritant Contact dermatitis

Allergic contact dermatitis

Environment / Exposure (Travel) Insect bites

Tick bites

Sexually transmitted Syphilis

HIV

Autoimmune SLE
Rheumatoid arthritis
Scleroderma
Dermatomyositis

D - Drug induced allergy

I - Infection
S - Skin conditions ( primary)
E - Environment / Exposure / Travel
A - Autoimmune
S - Sexually transmitted diseases

O - Occupational exposure
F - Food allergy

Name/Age/Sex

BIOLOGICAL

ACUTE CHRONIC MEDICAL HX

Complaint : Rash Cause ● Medical/

79
 ● Site: Areas affected Course Surgical
○ Skin folds → may be fungus / eczema Control Hx
○ Flexures → Eczema Compliance ● Drug Hx/
○ Scalp + nails + extensor → Psoriasis Cx Drug
○ Palms + soles → HFMD, Scabies, Syphillis, Checking allergies
Gonorrhoeal! Competenc ● Med List
● Onset: When did it start , relation of rash to the drug y ● TCM/OT
● Character of rash C
● Associated symptoms: Comorbids
○ Anaphylaxis - SOB, Wheezing, Eye swelling Crisis Mx
○ Steven’s Johnson’s/TENS / HFMD / Herpes simplex
- Oral ulcers
○ Fever +/- URTI / GE symptoms
○ Environmental hx/ Travel - Dust exposure,
Surrounding construction, Recent Travel and
activities ie hiking ( bites), water activities
○ LOW / LOA / Joint pains / Red Eye
Cause
● Drug History (anaphylactic reactions, drug eruptions)
● SJS/TENS (oral ulcers, blistering skin lesions)
● HFMD (contact history)
● Post infectious exanthem (fever/infective symptoms)
● Autoimmune (joint pains, LOA/LOW, conjunctivitis)
● Contact dermatitis (travel/chemical exposure/occupation)
● STDs (sexual history/high risk behaviour)
Course
● Duration of illness
● Previous treatments
● Previous medical consultations
Complications
● Function: work/school, mood, relationship with others

DISEASE PREVENTION FAMILY HISTORY

- Vaccinations Androgenetic
- Cancer prevention: hair loss

PSYCHOLOGICAL

PHQ-2 I
GAD-2 C: Affecting
work/life?
E

SOCIAL

Home/Environment – triggers?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sleep

PHYSICAL EXAMINATION

80
T BP HR
MSE
Hoarseness of voice
Eyes for angioedema if suspecting allergy
Cervical lymph nodes if suspecting infection
Mouth for oral ulcers if suspecting SJS
Lungs if suspecting drug allergy
Body involvement of rash - Head to toe - Scalp, face, mouth / mucous membranes,extensor or flexor
surfaces of extremities, palms, soles, trunk , back, limbs

Eczema - face, neck flexures, cubital fossa, hands and palms, popliteal fossa

If signs of atopy → Check for enlarged nasal turbinates , listen to the lungs

Psoriasis - Scalp, Nails , Joints, Extensor Surfaces

INVESTIGATIONS
1. FBC
○ Leukocytosis or thrombocytopenia or eosinophils esp in DRESS
○ Eosinophils in parasites!
2. Skin Scrape for fungal infection

MANAGEMENT - DEF
Non pharmacological
Pharmacological
Education
Follow-up

81
82
DERM 5. APPROACH TO URTICARIA

CAUSES
Immunologic ● Type I hypersensitivity
● Complement-mediated urticaria
● Immune contact urticaria

Physical ● Dermographism (When skin is stroked)

● Cold urticaria
● Solar urticaria
● Cholinergic urticaria (sweating)
● Pressure angioedema
● Vibratory angioedema

Drugs ● Mast cell-releasing agents, pseudoallergens, ACE

inhibitors
● NSAIDs

Idiopathic

Vasculitic (a/w autoimmune causes) ● Usually lasts > 24hrs , purplish lesions , painful

Infection ● Bacterial infections, H pylori (association

unknown)
● Viral infections (Hepatitis A, B, C)
● Parasite

Thyroid ● Hypothyroidism

Distinct angioedema (± urticaria) ● Hereditary angioedema

syndromes ● Angioedema-urticaria-eosinophilia syndrome

Name/Age/Sex

BIOLOGICAL

Acute Chronic Medical History

illness

83
Acute vs Chronic Cause ● Medical/
● Acute <6/52, chronic >6/52 Course Surgical
Control Hx
Complaint: Urticaria Compliance ● Drug Hx/
● Site Complication Drug
● Onset s allergies
● Character: Itch Checking ● Med List
● Residual hyperpigmentation? Painful? (vasculitic fts) Competency ● TCM/OTC
● Duration: 6/52? Each wheal <24h?
● Triggers Comorbiditie
● Relieving factors: antihistamines s
● Severity: Affecting function/QoL Crisis
management
Cause
● TRO red flags: angioedema, SOB, wheeze
● New food/exposures/contacts?
● Drugs particularly NSAIDs
● Dermographism
● Heat, cold, sun, water, sweat, pressure, vibration
● Rashes, joint pain, LOA/LOW, hair loss? (autoimmune)
● Cold intolerance, constipation, wt gain (hypothyroidism)
● Fever, URTI/GE (infections)
● Family history (hereditary)

Course
● Previous treatments?
● Seen other doctors for it?

Complications
● Function
○ Sleep, mood
● Secondary infections?

Disease Prevention Family Hx

● Vaccinations NA
● Cancer prevention:

PSYCHOLOGICAL

PHQ-2 I
GAD-2 C:
E

SOCIAL

Home/Environment – triggers?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sleep

84
PHYSICAL EXAMINATION ***HAND RUB***
T BP HR KIV SpO2
● Angioedema? Stridor?
● Goitre
● Examine skin
● Lungs: rhonchi

INVESTIGATIONS
● FBC: screen for infection? eosinophils?
● TFT: hypothyroid?
● KIV ESR, UFEME, RP if suspect vasculitis

MANAGEMENT
❖ Non-pharmacological
● Avoid triggers
❖ Pharmacological
● 1st line: Second generation H1 antihistamines
○ Eg Loratadine 10mg OD, Cetirizine 10mg OD
○ Dose daily up to 4x normal dose
○ Duration: at least 2 months BUT can TCU 2/52 to review clinically
● If 1st line not controlling symptoms within 1-2/52, consider step 2
● Topical placebo effect – don’t need!
❖ Prognosis
● Spontaneous remission of chronic idiopathic urticaria ~50% within 3 years, but physical
urticaria remission only in 16% of patients
● Some pts may experience repeated episodes through life

85
ENDO 1. APPROACH TO WEIGHT GAIN

DIFFERENTIAL DIAGNOSES
Fat ● Primary obesity (Net calorie increase)
○ Depression/SAD
○ Overeating
○ Sedentary lifestyle
● Secondary
○ Endocrine
■ Hypothyroidism
■ Cushing’s syndrome
■ PCOS
■ Hypothalamic (ACTH secreting tumor)
■ Insulinoma
○ Drugs
■ Sulfonylurea, insulin
■ Steroids
■ Antipsychotic
■ Anti epileptic
■ Antidepressants (TCA)
■ OCP
○ Nicotine withdrawal

Fluid Cardiac
Renal: CKD, nephrotic syndrome
Liver
Malabsorption

Fetus

Feces, Flatus

Filthy large mass Abdominal mass

Pelvic / O&G mass

86
HISTORY
» Complaint: Weight gain
● How much over how long?
● Quantity: 10% over 6 months
● Distribution: truncal (>likely Cushing’s) vs limbs (>likely if fluid gain) vs face (angioedema)
● Triggers
● Change in diet/physical activity

» Cause:
– Fat gain
● TCM use, thin skin, easy bruising, acne, hirsutism, striae, prox myopathy → Cushing’s
● Cold intolerance, somnolence, wt gain despite decreased appetite, constipation, dry skin, hoarse
voice, neck swelling → Hypothyroidism
● Oligomenorrhea, acne oily skin, hirsutism, male pattern baldness → PCOS
● Early morning headache, projectile vomiting, BOV, polydipsia, polyuria, nocturia, recent HI →
Hypothalamic
● Episodes of extreme hunger, blackout, sweating, palpitations, seizures → Insulinoma
● Drugs
○ New drugs, recent increased dose?
○ Repeated courses of steroids eg for poorly controlled asthma/COPD, rheum or derm
conditions, OCPs
– Fluid gain
● Orthopnea, PND, LL swelling → Cardiac
● History of renal dz, facial and limb swelling, pruritus, frothy urine, oliguria/anuria → Renal
● Jaundice, easy bruising, abdo distension, LL swelling, sleep-wake reversal → Liver
● Chronic diarrhea → Protein-losing enteropathy

– Fetus: LMP?

– Tumour
● Constitutional symptoms
● Headache, visual symptoms → Hypothalamic
● Constipation, obstructive urinary symptoms, unilateral limb/scrotal swelling → Pelvic mass
● IMB, PMB → Gynae

– Functional
● Diet/activity change: “Describe a typical diet for you in a day”. Activity level. Elicit ICE.
● Low mood, anhedonia

» Complications
● Cardiovascular RF : DM/ HTN/ HLD / IHD / Stroke

Past Medical History

● Cardiac
● Renal
● Liver

Drug History

Family History
● Thyroid disorders
● Malignancies

87
Social History
● Smoking
○ Cessation can cause weight gain
● Alcohol
○ Liver failure
● Occupation
● FUNCTION affected?

PHYSICAL EXAMINATION *** HAND RUB ***

T BP HR Ht Wt BMI
● General inspection
○ Distribution of weight gain
○ Respiratory distress? → fluid gain, pulm mets
○ Face: Jaundice? Sallow appearance?
○ AVF?
○ Cushingoid features?
○ Stigmata of chronic liver disease?
● JVP raised?
● Goitre?
● Heart: S1 S2, S3 in CCF
● Lungs: creps?
● Abdomen/Pelvic
○ Organomegaly? Ascites? Fetus?
● Pedal edema

INVESTIGATIONS
● RP, LFT, TFT, lipid panel, glucose
○ If hypothyroid, next step = anti-TPO Ab, TRAb
● uPCR / Udipstick / UFEME: proteinuria
● CXR: CCF features

MANAGEMENT
Lifestyle modifications

Primary obesity Refer to obesity document

● Exercise (FITT)
○ Frequency (5 and more days per week)
○ Intensity (75-90% MHR for fit people, 60-75% MHR for less fit)
○ Time
○ Type of exercise (250 mins aerobic exercise to LOSE weight,
150 mins aerobic exercise to MAINTAIN)
● Diet (healthy plate concept)
● Pharm: Orlistat 120mg TDS with fatty meal

If hypothyroid ● Thyroxine replacement: 1.6mcg/kg BW, increase by 25mcg every 3-

4/52
○ 12.5 mcg - 25 mcg OM for elderly patients or patients with
coronary heart disease
○ 25 mcg - 50 mcg OM for adult patients or patients without
coronary heart disease
○ Take on empty stomach, separate 1-2h from calcium/iron/soy
products, Omeprazole

88
 ● Repeat TFT 3-4/52

If Cushing’s 2’ steroid ● Do not stop TCM, refer to Endocrine direct access ,explain that
eventually need to stop TCM with tapering dose of steriods to prevent
adrenal insufficiency
● 2nd option: Block & Replace: Stop steroid, replace with Hydrocortisone
tapering dose
○ Eg 10mg BD → 10mg OM + 5mg ON → 5mg BD
● Refer Endocrine
● WARN: adrenal insufficiency, sick day advice. If lethargy , giddiness
(hypotension), LOA , n/v , confusion , go ED immediately

89
ENDO 2. APPROACH TO HYPERTHYROIDISM

Possible Cases
Presenting with symptoms of hyperthyroidism (eg ﹡ Approach to palpitations
palpitations)
﹡ Ix: TFT

Lab showing deranged hyperthyroidism, pt ﹡ Ix: FBC, LFT baseline + TRAb, anti-TPO Ab
symptomatic
﹡ Discuss CBZ including ADRs, ensure no
contraindications
﹡ KIV Propranolol

Hyperthyroidism in pregnancy ﹡ Treat with PTU instead of CBZ in 1st trimester

due to risk of neonatal aplasia cutis
﹡ Convert to CBZ in 2nd and 3rd trimester due to
risk of PTU hepatotoxicity
﹡ Refer OG

Differential Diagnoses
Increased de-novo synthesis Increased release of Increased
preformed thyroxine exogenous
thyroxine

Primary Secondary Subacute thyroiditis Drug induced

hyperthyroidism hyperthyroidism
(TSH low, T4 high) (TSH high, T4 high)

Graves’ TSH-producing pituitary Postpartum thyroiditis

hyperthyroidism adenoma

Hashitoxicosis Thyroid storm

Toxic adenoma
Toxic MNG

HISTORY
Complaints
➔ Hyperthyroid in blood test
➔ Thyrotoxic symptoms
◆ CNS: nervousness, irritability, insomnia
◆ CVS: palpitations, tachycardia, Exertional SOB, LL edema
◆ Heat intolerance, tremors
◆ GE: LOW despite good appetite, Diarrhea/inc BO frequency
◆ NL: muscle weakness
◆ OG: dec menstrual flow
◆ Eye: diplopia
◆ Derm: alopecia

Causes
● Family history of thyroid disease, smooth neck swelling, eye swelling, double vision, shin swelling,
⇒ Grave’s

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 ● Nodules in neck ⇒ toxic MNG
● Headache, visual defects ⇒ TSH-producing pituitary adenoma
● Pain in neck, recent or current viral illness ⇒ subacute thyroiditis
● Recent delivery ⇒ postpartum thyroiditis
● Any drugs from doctors/OTC etc ⇒ exogenous source

Course
● Any investigations done?
● Bloods: Thyroid profile, ultrasound neck

Complications
● Cardio: Atrial fibrillation, Heart failure symptoms (e.g. orthopnea/PND/lower limb swelling)
● KIV Osteoporosis: fragility fractures
● KIV Compression: SOB, dysphagia, hoarseness of voice
● Hypokalemic periodic paralysis
● Eye: Diplopia, red and painful eye from exposure keratitis, BOV from keratitis/ optic nerve
compression
● Thyroid storm
» Fever
» CNS: agitation, lethargy / delirium / psychosis, seizure / coma
» GE/HPB: abdo pain / nausea / vomiting / diarrhea, jaundice
» CVS: tachycardia, AF
» CCF: pedal edema, bibasal creps, pulm edema
» Precipitant history

Co-morbid autoimmune conditions: Type 1 DM, Pernicious anemia, Myasthenia Gravis, Vitiligo, adrenal
insufficiency

Medical Hx: History of pituitary adenoma?

Drug Hx:
● Exogenous thyroxine
● Amiodarone (hypo/hyper), Lithium (usually hypo), Iodine
● Asthma, COPD – for treatment in event pt req Propranolol
Family Hx: Thyroid disorder
Social Hx: Smoking? ⇒ can worsen thyroid eye disease
Gynae Hx: LMP! Sexually Active? Planning to have a baby?

PHYSICAL EXAMINATION
T BP HR
Ht Wt BMI
Inspection
● Does the patient look thin, nervous/agitated, excess sweating
● Tremors
● Is a neck lump present and does it move with swallowing?
● Eye signs, EOM
○ Exophthalmos, periorbital and conjunctival edema, ophthalmoplegia, pretibial myxedema
only in Graves pts
○ Look from side and behind/top

Palpation
● Pulse (rate and rhythm especially for AF), warm peripheries, sweaty palm/skin
● Neck (from behind): type of thyroid swelling, single nodule (toxic adenoma) or multinodular (goiter
or Graves) or diffusely enlarged (Graves), is the swelling tender (thyroiditis) and is it mobile, any
cervical or supraclavicular lymph nodes palpable

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 Percussion
● For retrosternal extension (if so, do Pemberton’s)

KIV Auscultation
● For bruit (if present =Graves)

Others
● Complete by checking pretibial myxedema (=Graves), proximal myopathy & reflexes (should be
hyper), check BP, check for visual field defects or diplopia

INVESTIGATIONS
● TFT
● TSH receptor antibody, anti-TPO Ab
● FBC, LFT ⇒ baseline prior to initiating ATD
● ECG for AF / Sinus tachycardia

MANAGEMENT
1) Graves’ Disease ● Education
○ Anti-thyroid drugs take 12-24 months, duration of
treatment at least 12-18 months
○ Consequences of non-treatment, stopping treatment
■ Especially in reproductive females, impact on
fetus
○ Treatment options: medical vs RAI vs surgical
○ Aim to achieve clinical and biochemical euthyroid, may
take 3-6 months

● Non-pharmacological
○ Smoking cessation (esp for ophthalmopathy)

● Pharmacological
○ Beta blockers (Propranolol 20mg BD or Atenolol 25mg
OM) to alleviate thyrotoxic symptoms – tachycardia,
tremors
■ Contraindicated if asthma, COPD
○ Carbimazole 20mg-40mg/day (eg CBZ 20mg OM)
■ Warn about ADRs especially agranulocytosis (to
return if T>38 with sore throat / rash / mouth
ulcers / bruising / malaise for FBC KIV refer ED),
jaundice, abdo pain, nausea/vomiting, acholic
stools or dark urine, arthralgia
■ Other ADRs: abnormal sense of taste, pruritus,
urticaria, fever, arthralgia
■ Rare but serious ADRs: hepatitis,
agranulocytosis (incidence of few cases per
thousand), cholestatic jaundice,
thrombocytopenia, lupus-like syndrome
○ PTU if first trimester pregnancy 150-200mg/day (eg PTU
50mg TDS)
■ 2nd trimester onwards, switch to CBZ
■ CBZ a/w aplasia cutis of neonate
■ PTU a/w hepatotoxicity

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 ■ CBZ to PTU, multiply Red by 10
○ Baseline FBC, LFT prior to initiation of ATD
○ TCU 2-4/52 with TFT 1/52 prior

○ Advise on contraception when pt is still thyrotoxic

○ Advise pt to come back immediately if she is pregnant as
need to switch to PTU
○ If low dose CBZ and well controlled Graves’, can
consider trial off CBZ in pregnancy

● Ophthalmopathy
○ Eye drops, sunglasses
○ Tape eyelids close or wear goggles when sleeping
○ Stop smoking
○ Surgery if severe orbital edema leading to optic nerve
compression

● Cessation of treatment ie after 12-18 months (if TRAb, TSH

normal)
○ Consider repeating TRAb before cessation
■ If TRAb is still very high, continue treatment x
6/12
○ Repeat TFT 3/12, 9/12 post-treatment, thereafter 1 year
later
○ Educate re: chance of relapse 50%
○ Prognosis when trial off CMZ
- 50% chance of relapse 1st trial
- 75% chance of relapse 2nd trial

● Referral criteria
○ Pregnancy at any trimester
○ If thyroid storm ⇒ ED

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 ○ Cx eg AF, heart failure, eye Cx (exposure keratitis, loss of
vis4ion from optic n compression,
diplopia/ophthalmoplegia)
○ Solitary nodule / MNG / tender goitre / suspected
malignancy ⇒ FNAC/US
○ Pt on drugs that can affect TFT eg Amiodarone
2) Hashimoto’s thyroiditis (initial ● Will become hypothyroid very quickly after initiation of anti-
thyrotoxic phase) thyroid drugs
3) Subacute thyroiditis (UTD) Management
● Px: Neck pain, diffusely enlarged ● Relief of pain
goitre. Pain may radiate to the jaw , ○ NSAIDs: pain should resolve by 2-3 days
throat, upper chest, ears. ○ If not better, trial of prednisolone
○ Preceded by URTI; transient ● Monitoring
mild hyperthyroidism symptoms ○ Monitor TFT every 2-8 weeks to check for hyperthyroid
due to release of thyroxine and hypothyroid phase
stored within thyroid follicles ● Hyperthyroid / hypothyroid symptoms if necessary
● Sequelae: Hyperthyroidism x 6- ○ Symptomatic tx - If pt presents with tremors/
8/52 → Transient euthyroid → palpitations, can give propranolol
Hypothyroidism x 6-8/52 → ○ No need for thioamides because hyperthyroidism is not
Euthyroid or remain hypothyroid caused by excess thyroid hormone synthesis.
● Ix: It is a clinical diagnosis! ○ Usually if there is initial hyperthyroidism symptoms, will
○ TFT be transient.
○ ± FBC (TRO acute infectious ○ If symptomatic mod- severe hypothyroidism or TSH >10
thyroiditis) mU/L, tx with 50 or 100 mcg of levothyroxine for six to
○ ± TRAb (negative, TRO graves) eight weeks (with a goal TSH in the normal range). The
○ ± Radioiodine uptake test will T4 should then be discontinued, and the patient
show low uptake (TRO graves) reevaluated in four to six weeks to be sure that the
○ ± US thyroid will show diffusely hypothyroidism is not permanent.
enlarged, hypoechoic thyroid
4) Post partum thyroiditis (UTD/ Mx of Hyperthyroid/ Hypothyroid symptoms
Endocrine Society and the American ● Tremors/ palpitations: Symptomatic tx with Propranolol 40 - 120
Thyroid Association) mg (peripheral beta-blocker)
● Definition: An abnormal TSH level ● No need for anti-thyroid meds because the hyperthyroid phase
within the first 12 months of postpartum thyroiditis is caused by autoimmune destruction
postpartum in the absence of a of the thyroid, resulting in release of stored thyroid hormone
toxic thyroid nodule or TRAb ● Most women recover and are euthyroid within one year
(thyroxine receptor antibodies) postpartum. Some have permanent hypothyroidism or goitre
○ Affects 1.1% to 21.1% of ● If symptomatic hypothyroidism or TSH >10 mU/L - treat with
women. levothyroxine (typically approximately 50 to 100 mcg/day), aim
● Px: Hyperthyroidism, fatigue for normal TSH. Also Treat women who are breastfeeding or
● Clinical course varies : 25% who wish to become pregnant. When T4 is instituted in these
hyperthyroidism,> circumstances, the goal is a normal TSH.
hypothyroidism > then recovery;
43% present with symptoms of Follow up
hypothyroidism; and 32% present ● Monitor every 4 -8 weeks to confirm resolution or detect
with hyperthyroidism. development of severe hypothyroidism
● Ix: TFT, Trab (negative) ● Screen annual TFT for women with a history of postpartum
○ Radioactive iodine uptake scan thyroiditis as they are at increased risk of permanent
- postpartum thyroiditis (low hypothyroidism
uptake) from Graves disease
(high uptake), but is
contraindicated in

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 breastfeeding women.
Patients must limit close
contact with others for a time
after the study.
5) Pre-pregnancy hyperthyroidism How would you counsel a young woman with thyrotoxicosis who
Thyroid physiology — To meet the wishes to be pregnant?
increased metabolic needs during a ● Ideally, pregnancy should be avoided (Take contraception) until
normal pregnancy, there are changes in hyperthyroidism is adequately treated because the rate of fetal
thyroid physiology that are reflected in loss is high
altered thyroid function tests. The major ● Advise euthyroid state 3 months before conception. Avoid
changes in thyroid function during conception 3 months after RAI
pregnancy are: ● Treat with Carbimazole. Patient needs to inform if intending to
●An increase in serum thyroxine- be pregnant → switch to PTU
binding globulin (TBG) ● Aim TSH <2.5 in pregnancy
●Stimulation of the thyrotropin ● If it occurs or recurs during pregnancy, then
(thyroid-stimulating hormone [TSH]) o Treat with PTU in first trimester, switch to CMZ in 2nd
receptor by human chorionic trimester
gonadotropin (hCG) ▪ Lowest dose possible such that fT4 is at the
upper range of normal
▪ CMZ a/w aplasia cutis congenita, esophageal
and choanal atresias in first trimester
▪ PTU higher risk of hepatotoxicity
▪ Can also be safely treated with surgery in the
second trimester (indicated for obstructive
symptoms/ failure of medical therapy, non
compliance)
▪ If very low dose (e.g. CMZ 2.5mg OM, can stop
and rpt early)
o In the 3rd trimester, TSI (thyroid stimulating
immunoglobulin) levels declines and remission of
hyperthyroidism occurs; stopping medications is
possible then
o Will require serial growth scans 28,32,36 to look for
foetal goiter and assess infants for hyperthyroidism
after birth
o Measure Trab at 28 weeks – if high, high risk of foetal
thyroid dysfunction and neonatal thyrotoxicosis
o up to 750mg/d PTU or 20mg CMZ can be safely used in
lactating mothers

Complications of poorly controlled thyrotoxicosis

Foetal Maternal
Miscarriage Pregnancy induced
IUGR (Intrauterine growth restriction) hypertension / preclampsia
Preterm labour Heart failure
Placental abruption
Increased prenatal mortality/ Still
birth
Foetal /neonatal thyrotoxicosis
6) Rash after initiation of CMZ/PTU ● Determine severity of rash, rule out angioedema/severe
features
● Can continue with medication, cover with antihistamines

95
● Red flag advice

96
Burch Wartofsky Score

97
98
ENDO 3. APPROACH TO HYPOTHYROIDISM

Possible Cases
Presenting with symptoms of hypothyroidism ﹡ Approach to symptoms
﹡ Ix: TFT
Lab showing hypothyroidism, pt symptomatic ﹡ Anti-TPO Ab
﹡ Initiate Thyroxine
Subclinical hypothyroidism ﹡ Identify cause
ᗎ Eg 2’ drug-food interaction, suboptimal dosing ﹡ Adjust administration
Suboptimal TSH for post-thyroidectomy for CA ﹡ Explain lower target TSH (<0.1 mU/L)

DIFFERENTIAL DIAGNOSES
Primary Hypothyroidism ᗎ Hashimoto’s
ᗎ Iatrogenic
❖ Post thyroidectomy
❖ Post RAI
❖ Post External neck irradiation
ᗎ Iodine deficiency
ᗎ Drugs: Lithium, Amiodarone, immunotherapy
ᗎ Infiltrative dz: Reidel’s, leukemia, scleroderma, sarcoidosis
ᗎ Postpartum thyroiditis
ᗎ Subacute thyroiditis
(Central) Secondary, Tertiary ᗎ Pituitary tumour
Hypothyroidism ᗎ Postpartum pituitary necrosis (Sheehan)

HISTORY PMH
Complaints ● **Ask about aetiology for
● Hypothyroidism in labs hypothyroidism!**
● Subclinical hypothyroidism ● Type 1 DM
● Pernicious anemia
Control: Symptoms of hypothyroidism ● Vitiligo
● Lethargy/ depression/ psychosis ● Addison's disease
● Constipation ● Alopecia areata
● Weight gain ● SLE/ RA
● Cold intolerance ● Previous radiation to head & neck
● Menorrhagia ● IHD (for treatment)
● CTS
● Skin, hair changes Drug Hx
● Amiodarone, lithium, sunitinib
Causes ● Calcium, iron supplements, PPI, OCP,
● Recent viral illness / pain over goitre Sucralfate, anticonvulsants
● Changes in diet or New drugs
● Family history O&G Hx
● LMP
Complications
● **Beware myxedema coma**
● Heart failure

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 ● Effusions: SOB
● Dyslipidemia , Insulin resistance
● Infertility
● Dementia
● Anemia
● Symptoms of compression w goitre
○ Hoarseness of voice
○ SOB / stridor
○ Dysphagia

Compliance to meds
● Takes meds 2h apart from soy products,
calcium, caffeine, food
● Takes at same time of the day
ICEKAPS Issues
WASHED
Mood PHYSICAL EXAMINATION
Depression BP HR BMI
Anxiety ᕯ Inspection: coarse facial features/ periorbital
edema, dry skin, fine brittle hair with loss of outer
Function third of eyebrow, obesity, hoarseness of voice
ᕯ Scar from previous thyroidectomy
Preventive ᕯ Mouth : Macroglossia
ᕯ Neck: swallow, palpate for goitre
ᕯ Peripheries: pulse (bradycardia), proximal
myopathy, delayed ankle tendon reflexes , CTS,
ᕯ CVS/Respi: effusions/ CCF
ᕯ Neurological system for cerebellar signs (offer)
Offer screening for dementia
INVESTIGATIONS
● TFT
● Autoantibodies: thyroglobulin and peroxidase
antibodies

● ECG: sinus bradycardia, low voltages, flat T

waves
● Full blood count for anaemia (where relevant)

● Lipid panel for high cholesterol

● Electrolytes for hyponatraemia (where
relevant)

MANAGEMENT
1) Hashimoto’s thyroiditis
● Anti-TPO Ab usually present
● Levothyroxine replacement
○ 1.6mcg/kg/day
● Lower starting dose if advanced age or high IHD risk
● Repeat TFT in 3-4/52 , 6-8/52 for subclinical hypothyroidism after initiation

2) Post-thyroidectomy for CA

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American Thyroid Association guidelines:
● Aim TSH suppression 0.1-0.5mU/L for low risk CA
○ Aim TSH suppression <0.1mU/L for high risk CA
● Lifelong suppression

3) Pregnancy
● The increase in levothyroxine requirements occurs as early by 5th week of gestation and plateaus by
16 to 20 weeks
● Need to increase total thyroxine by 30-50% at the time of positive pregnancy test and adjusted to
achieve trimester specific TSH Goal (low T4 increases risk of miscarriage)
○ Women on fixed doses of levothyroxine to take 9 doses weekly (one extra dose on 2 days
of the week) once the pregnancy is confirmed
○ Ie once pregnant, increase dose of Thyroxine
● TSH Goals
○ First trimester: 0.1 – 2.5 uIU/ml
○ Second trimester: 0.2 – 3.0 uIU/ml
○ Third trimester: 0.3 – 3.0 uIU/ml
● Checking: TFT should be assessed every 4 weeks to protect the health of the mother and fetus
and to avoid pregnancy complications
○ If above goal, need to check every 2-3 weeks
● Refer to Endocrine
● Concerns:
Foetal Maternal
Miscarriage Pregnancy induced hypertension /
Neurodevelopmental delay especially if treatment preeclampsia
delayed in first trimester Post natal depression
Leads to mental retardation, delay in growth
“cretinism”

4) Subclinical hypothyroidism
● Ddx
○ Adherence
○ Medication administration with foods
○ Medication interaction with other drugs
● Tx if TSH ≥10 mU/L
● Tx is individualized if TSH is between 5 to 10mU/L
○ TSH 7.0-9.9 mU/L, age <65 ⇒ ꑙ TREAT ꑙ
■ Age ≥65 ⇒ Treat only if symptomatic
○ TSH above normal to <7.0 → Symptomatic or high anti-TPO Ab or goitre ⇒ ꑙ TREAT ꑙ
● Benefit of T4 treatment in reducing ischemic heart disease events and overall mortality in younger
individuals with subclinical hypothyroidism (hence treat if age <65 and TSH ≥7.0 mU/L)
● Tx is generally given in the presence of a) positive anti-TPO, b) goitre or a c) strong family history of
autoimmune thyroid disease

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 ● TSH >10 ⇒ TREAT
● TSH 5-10:
(1) An thing to point towards Hashimoto’s (anti-TPO, goitre, fhx of thyroid disease). If so
treat.
(2) If not, any CVRF (smoker, personal hx of IHD, DM, HTN, HLD). If so treat.
(3) If not, is patient below 65 years old. If so treat.
(4) Otherwise… watch.

5) TSH abnormal due to concomitant medications ie calcium/ phosphate binder in ESRF pts
ie Calcium acetate 2 tab TDS dosing with Thyroxine 50mcg OM
● Take thyroxine at bedtime, preferably 4 hours after dinner (ie space apart 4 hours)
● For ESRF pts requiring phosphate binder with every meal:
○ Take a diet history, avoid phosphate content in breakfast, take calcium acetate / phosphate
binder with lunch and dinner instead.
○ Food high in phosphate: Dairy pdts, Meat, Animal organs, Seafood, Coke/Beer/Chocolate
○ Non-calcium binders ie sevelamer carbonate can affect thyroxine absorption as well
● Memo to Renal physician

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ENDO 4. APPROACH TO OSTEOPOROSIS

Possible Cases
1. Presented with fragility fracture
2. Newly diagnosed Osteoporosis
3. Male Osteoporosis
4. Experienced side effects to bisphosphonates
5. Recurrent fracture despite on bisphosphonates and treatment failure

DDx
Primary Secondary

1. Post menopausal woman; 1. Endocrine

contributed by dietary and lifestyle a. Cushing’s syndrome
factors b. Thyrotoxicosis
a. Low calcium in diet c. Hyperparathyroidism
b. Inactive lifestyle d. Hypogonadism
c. Smoking and alcohol use 2. Rheumatoid arthritis
3. Chronic diseases eg chronic renal failure, liver
failure
4. Drugs
a. Steroids
b. Anti epileptics
c. Anti retroviral drugs (NRTI)
5. GI
a. Malabsorption diseases eg celiac
disease
b. Primary biliary cirrhosis
c. Eating disorders eg anorexia nervosa
6. Malignancy
a. Multiple myeloma
7. Infections eg HIV

HISTORY
Complaint: Osteoporosis
● How was it diagnosed? Based on fragility fracture? Or based on BMD?
● If BMD, T score initially was? Z score?

Causes
● Cushing’s syndrome: weight gain, thin skin, easy bruising, central fat deposition, purple striae,
acne, hirsute, exogenous steroids.
● Thyrotoxicosis: weight loss, heat intolerance, good appetite, tremors, diarrhea, amenorrhea, eye
abnormalities, rash over shin
● Hypogonadism: (for both genders) loss of libido; (in females) amenorrhea, acne, hirsutism; (in
males) loss of morning erection, erectile dysfunction, gynaecomastia, diminished hair growth
● Rheumatoid arthritis: joint pains, stiffness, deformities
● PMH: CKD, chronic liver disease
● Malabsorption diseases:
o Steatorrhea, stools difficult to flush
o Abdominal discomfort especially after eating certain kinds of food (eg wheat, rye, barley –
celiac disease)
● Eating disorders: dietary history, self image, weight

103
 ● Multiple myeloma: bone pain, weight loss

Course:
● BMD done?
● Investigations done for secondary causes: TFT, ESR, Vit D levels, PTH, renal panel, testosterone
levels

Complications
● Fracture, Fall hx
● Pain from osteoporotic fracture

PMHx:
● Ask abt above conditions
● Any dysphagia, GERD, dental problem, CKD → contraindications to bisphosphonates

Drug history: Steroids, anti epileptics

FHx: history of osteoporosis – at what age?

Social history:
● Smoking/ Drinking
● Occupation
● Lifestyle – inactive
● DIET History: Calcium and vit d?

Function
● Fall screen

PHYSICAL EXAMINATION
BP HR BMI
● Obvious spot diagnoses
o Cushing’s syndrome
o Neck: swallow to look for goitre → Thyrotoxicosis
o Rheumatoid arthritis
● Dental: Caries
● Spine to look for step deformities suggesting of previous vertebral fractures
● Gait

INVESTIGATIONS
Confirm osteoporosis
● Bone mineral density scan
○ T score: - 1 to – 2.5: osteopenia
○ T score: – 2.5 or worse: osteoporosis
○ If young, look at Z score instead of T score

Blood tests: FBC, TFT, 25-Vit D, calcium, phosphate, Cr, KIV LFT, ESR

MANAGEMENT
1) Treat underlying aetiology
Non-pharm:
● Encourage active lifestyle, quit smoking and drinking, eat high calcium diet (milk, cheese, nuts,
green leafy vegetables), sunlight exposure (morning/ evening sun at least 15mins)
● Weight bearing and strengthening exercise
● Fall precaution advice/ Home safety/ foot wear: non slippery shoes, non slip mats, grab bars,
sufficient lighting

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 ● EASE programme for home modification
● Stop smoking and alcohol

Pharm:
● Bisphosphonates – Alendronate, Risedronate
○ SE: reflux esophagitis, osteonecrosis of the jaw, atypical fractures
○ Ensure vit D replete
○ Refer to dental for dental clearance within 1 month of initiation of bisphosphonates
● Bisphosphonates – IV Zoledronic acid (yearly)
● Denosumab: human monoclonal antibody (6 monthly)
○ SE: hypocalcemia, infections of respiratory and urinary tract, rash, constipation, cataracts
● Vit D replacement (ensure > 30mg/ml if osteoporotic): Cholecalciferol (3,000–5,000 IU) daily for at
least 6–12 weeks then maintenance dose of cholecalciferol 1000-2000 IU per day
○ KIV Ergo x 8/52 then Lynae maintenance
● Calcium supplements

2) Osteoporosis treatment failure

Defined as either one of the following
A) 2 or more fractures at typical osteoporosis site
B) 1 fracture PLUS significant decline in BMD or No significant change in bone turnover markers
C) Significant decline in BMD PLUS No significant change in bone turnover markers
Significant decline in BMD defined as
Interval change / % change in BMD: -4% at femur, -5% at lumbar spine

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ENDO 5. APPROACH TO OBESITY

Definitions: BMI: 23 (mod CVS risk), 27.5 (high CVS risk)

- Percentage body fat – 25% or less for males, 33% or less for females
- Waist circumference – 90cm or less for males, 80cm or less for females

Important pts
- Ascertain true significant weight gain
- Rule out secondary causes, stop precipitating cause if present
- Assess readiness for change and previous weight loss efforts
- Check for complications / comorbids
- Mx: Non pharm, set realistic targets, when to offer pharm and bariatric

HISTORY
Complaint:
- Assess Weight hx/growth history
- Define weight gain, ______kg to ________kg over a duration of ____________.
- Distribution of weight gain – Truncal only ? Truncal and limbs? Abdominal distension?
- Triggers of weight gain - significant life events, job change and smoking cessation, new medications
- Family weight history
- ICE: Assess stage of change (precontemplation, contemplation, preparation, action, maintenance/relapse)

Cause:
- Rule out secondary causes: Fluid overload causes, Endocrine (Hypothyroid, Cushing’s, PCOS, insulinoma),
Drugs! (OCP, steroids, antidepressants, anti-psychotics)
- Hypothyroidism: weight gain despite poor appetite, cold intolerance, constipation
- Cushing’s syndrome: rounded facies, hirsutism, acne, proximal weakness (combing hair, getting up from a
chair), abdominal purple striae (stretch marks), easy bruising, poor wound healing, alopecia, cataracts,
- PCOS: irregular menses, hirsutism
- Insulinoma: Lightheadedness, blackouts, sweating, palpitations
- Hypothalamic dz: Headache, visual disturbance

Primary obesity: Diet, Exercise (Social reasons for eating more or exercising less)

Course: Check previous weight loss trials and outcome

Complications/Co-morbids
- CVRF: HTN, HLD, DM, IHD, Stroke
- NAFLD/ Gallbladder dz, OSA, Depression
- PCOS in females

PMHx: as above
Family Hx: obesity, CVRF
Social Hx: alcohol, smoking, occupation (sedentary vs active), function ie OA knees
Psycho Hx: PHQ-2/ GAD -2, Body image affected?
Menstrual Hx: For females and desire for fertility / PCOS
Preventive Health!

PHYSICAL EXAMINATION
BP HR Ht Wt BMI Waist circumference
Face – Rounded facies, xanthelasma, acne, hirsutism
Neck – Goitre, Acanthosis nigricans, bruising
Heart/ Lung - ? Pulmonary HTN in OSA
Abdomen – Hepatomegaly in NAFLD
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INVESTIGATIONS
- TFT, FPG, lipid panel, LFT,
- Other test depending on suspect etiology

MANAGEMENT [Link]
o
- Rule out and treat 2 causes (like depression causing binge eating) , stop meds that causes obesity

Education
- Inform overweight / obese patients of their condition. Explain that the greater the BMI, the greater the
risk of cardiovascular (CV) disease, DM, HTN, HLD, and all-cause mortality

Non pharm
- Realistic weight loss should not exceed 0.5 -1 kg a week. Aim to lose 10% of initial weight over 6/12.
- Long-term goals should continue in the same vein as the short-term goals, and the patient should be
encouraged to lose more weight if possible (e.g. 10–20% of initial body weight).
- Diet: Avoid Sugar-sweetened beverages . Maintain a diet that is higher in vegetables, legumes, fruits and
whole grains, and lower in sugar and refined carbohydrates. Adequate amounts of low energy density, lean,
high-protein foods (e.g. chicken breast, fish, egg white, beans and tofu). In paeds, remove junk food.
- Exercise: At least 250 mins/week mod intensity exercise to lose weight, 150 mins to maintain weight
- In pediatric patients target is to reduce rate of weight gain AND NOT WEIGHT LOSS, ESPECIALLY IF
THEY HAVE NOT REACHED ADULT HEIGHT.

Pharm
Indication for drug therapy: BMI 27.5–29.9 kg/m2 in Asians with comorbidities or complications of obesity
such as hypertension, T2DM
● Phentermine and mazindol may be used for weight management for the short-term (6–12 months).
○ MOA of phentermine: sympathomimetic – reduces appetite by stimulating release of
norephinephrine
○ S/E of phentermine: hypertension, palpitations, tachycardia, headache , insomnia
○ Mazindol: stimulant drug that acts as appetite suppressants
● Liraglutide may be used for weight management up to 2 years while Orlistat(Xenical) may be used
as an anti-obesity drug for long-term therapy (up to 4 years)
○ Orlistat MOA: inhibit pancreatic lipase, decreases fat absorption from GIT . 120mg TDS
(taken with each meal that includes fat or up to 1 hr after each meal)
○ S/E: Steatorrhoea, soft stools, flatulence with discharge, bowel incontinence rare report of
severe liver injury /nephrolithiasis / oxalate nephropathy with renal failure , decreased
absorption of fat soluble vitamins ie A,D,E,K
○ CI: in chronic malabsorption syndrome, cholestasis, Inflammatory bowel disease
○ Monitoring: Need to Monitor Renal function, LFT, give daily multi vitamin supplement
containing fat soluble vitamins
● Acupuncture may be considered as a short term anti-obesity therapeutic option on a case by case
basis

Surgical treatment
Indication: Patients with BMI above 40kg/m2 or above 35kg/m2 with at least one obesity-related
comorbidity, especially if difficult to control with lifestyle and pharmacological therapy, may be considered
for bariatric surgery as a medical treatment
● Female patients should avoid getting pregnant post bariatric surgery until weight loss is stabilized .
Appropriate contraceptive device should be given
● Bariatric surgery: Gastric banding and Roux en Y
○ S/E malabsorption, vitamin deficiency, dumping syndrome, surgical risk

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108
ENDO 6. STEROIDS → Secondary Adrenal Insufficiency

Patients with HPA Suppression

a. HPA suppression likely
● Glucocorticoid dose equivalent to Prednisolone >20mg/day x >3/52 (ie >80mg
Hydrocortisone)
● ON dose of Prednisolone ≥5mg for more than few weeks
● Any patient with Cushingoid appearance
b. HPA suppression unlikely
● A patient who has received any dose of glucocorticoid for less than three weeks
● Patients treated with alternate-day Prednisone at a dose of less than 10 mg (or its
equivalent)
c. Intermediate/uncertain risk
● Those taking 10 to 20 mg of Prednisone per day for more than three weeks
● Any patient who has taken any dose less than 10 mg of Prednisone per day for more than a
few weeks (provided that it is not taken as a single bedtime dose)

Investigations: Low dose ACTH stimulation test

Corticosteroid Conversion

Glucocorticoid Withdrawal
● 5-10 mg/day every one to two weeks from an initial dose above 40 mg of Prednisone or equivalent
per day.
● 5 mg/day every one to two weeks at prednisone doses between 40 and 20 mg/day.
● 2.5 mg/day every two to three weeks at prednisone doses between 20 and 10 mg/day.
● 1 mg/day every two to four weeks at prednisone doses between 10 and 5 mg/day.
● 0.5 mg/day every two to four weeks at prednisone doses from 5 mg/day down. This can be
achieved by alternating daily doses, eg, 5 mg on day one and 4 mg on day two.

Glucocorticoid Replacement for Adrenal Insufficiency

● Hydrocortisone short-acting, given TDS to mimic day curve
○ Or BD with ⅔ dose in morning and ⅓ dose in afternoon to simulate normal circadian
rhythm
○ Eg Hydrocortisone 10mg OM + 5mg OA

Stress Dose
● 3 x 3 rule: Increase dose to 2-3 times the dose for 3 days – for minor illnesses eg URTI

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ENDO 7. TYPE 1 DM

HISTORY
Acute complaints?

Chronic review
Cause: autoimmune destruction of pancreatic islet cells
Course: who is following up with you? Next TCU?
Control
- HbA1c <7.5%
- Home blood glucose monitoring
- Fasting 4.4-7.2
- 2 hours postprandial <10
Compliance
- Non pharm
- Diet: Try not to overly restrict if <12 years old (so that they have experience with different
kinds of food, and hence will know their correction unit)
- Exercise: at least 150mins physical activity per week moderate to intense
- Pharm
- Insulin: injection technique (injection site, FB away from umbilicus or bruise, eject bubbles
prior to injection, storage of insulin), carb count and carb exchange awareness if on basal
bolus regime
- Barriers to compliance: rushing, forgetting, stigmatization
Complications
- from disease
- Retinopathy, nephropathy, neuropathy, ihd, stroke, PVD (DRP - screen 5 years from onset
of disease)/DFS/renal panel and UACR)
- Acute hyperglycemia > DKA symptoms, ketone monitoring
- From treatment: hypoglycaemia symptoms, bruising or lipodystrophy
Co-morbidities
- other autoimmune conditions eg hypothyroid
Crisis management
- hypergly awareness
- Hypoglycaemia awareness (rule of 15)
- Sick day advice (SICK)
Disease prevention

Psycho: PHQ2, address ICE

Social: find out implications of disease on family, school, activities, finances (any place in school to store
insulin, is teacher aware of her condition)

PHYSICAL EXAMINATION
BP HR BMI *** plot centiles if paediatrics***
LIE DOWN ON COUCH
palpate abdomen for lipodystrophy (must offer deltoid/buttock if patient injects in those areas)
LIE ON COUCH (must part toes and lift up heel)
Foot examination: inspect for trophic skin changes, diabetic dermopathy, ulcers. Feel for coolness,
reduction in pulses. Check sensation with monofilament 10 points.

INVESTIGATIONS
Hypocount (fasting)
HbA1c
DRP

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MANAGEMENT
- Non pharm: dietary advice, carb counting assessment, exercise
- Pharm: Ensure compliance
- Education on hyper/hypo/sick day advice
- TCU: Ensure patient has upcoming specialist appointment, arrange dietician for carb counting if
appropriate

Possible scenarios/RFE Points to cover

T1DM wants to travel Refer T2DM notes

T1DM pre participation assessment (e.g.

sports CCA/run marathon)

Pre employment as driver

Driving license renewal

111
Other notes (NHG CPG)

112
ENDO 8. TYPE 2 DM

Stems
1. Poorly controlled Type 2 DM due to poor compliance
2. DM with hypoglycemia symptoms, or hypoglycemia unawareness
3. DM on insulin acutely unwell (sick day advice)
4. Social: T2DM to travel
5. T2DM keen for pregnancy
6. Secondary cause of DM - ie Cushing’s syndrome, chronic pancreatitis

Primary Secondary Causes of DM

Type 1 vs Type 2 DM Endocrine: Cushing’s syndrome, Thyrotoxicosis, Acromegaly
Drugs: Steroid ingestion, Diuretics,
Surgery: Post Pancreatectomy, Chronic pancreatitis

HISTORY
Complaints
● Poor diabetic control ie Foot ulcer
● Hypoglycemia: (Due to intake of insulin + skipped meals / long acting insulin)
● Hyperglycemia: polyuria/ oliguria, polydipsia, polyphagia, LOW, fatigue (DKA / HHS)

Cause
Primary Secondary

Due to lifestyle ● Endocrine: Cushing’s syndrome,

Thyrotoxicosis, Acromegaly
● Drugs: Steroid ingestion, Diuretics
● Surgery: Post Pancreatectomy

Course (initial diagnosis of DM)

● Age of Diagnosis
● Type I / II Diabetes
● Presenting complaints - polyuria/ oliguria, polydipsia, polyphagia, LOW, fatigue
● Investigations done to confirm diagnosis : RSL/ OGTT

Control & Compliance & Competency

● Recent HbA1c ?
○ On Follow Up ? – Who, frequency, compliance
● Medications
○ OHGAs: started immediately after diagnosis? Type, Dosage, Frequency, any changes
recently
○ Insulin (suggest more severe): When started, Indications for starting, Type, Dosage,
Frequency, who injects it (impt if eye problems), injection site + rotation, any changes
recently
● Lifestyle modification
○ Diet: Meal contents (What do you usually eat in a day), Number of meals
○ Exercise: Type of exercise, duration, frequency
○ Smoking / Alcohol
● Any recent illness ie cellulitis / OTC meds ie steroids, cough syrup

Checking

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 ● SMBG? Range of usual values pre/post-prandial? (aim premeal 4-7 , post meal 5-10 unless frail)

Complications of Meds and Disease

● Symptoms of Hypoglycemia: giddiness, palpitations, tremors, diaphoresis, extreme hunger
● DKA/HHS: abdominal pain and vomiting, metabolic acidosis (Kussmaul breathing)

Macrovascular
● IHD/ AMI: Previous angina/AMI, chest pain, SOB, palpitations, diaphoresis, giddiness, syncope ,
nausea, vomiting
● CVA: Previous stroke/ suddenly paralysed
● PVD: Diabetic foot ulcers, abscess, gangrene, amputation, cellulitis, poor wound healing, Vascular
claudication (Shop bench to shop bench), Leg pain while walking, relieved when stop walking,
claudication distance, skin changes over the lower limbs, Footcare education, Annual Foot
Screening

Microvascular
● Nephropathy: Renal failure, polyuria/oliguria, frothy urine, hypertension, swelling,
● Neuropathy (motor, sensory, autonomic): numbness, parathesia , gloves and stocking
distribution,weakness, postural hypotension, gastroparesis (early satiety, nausea, vomiting),
dysphagia, urinary retention, impotence
● Retinopathy: Cataracts, Blurring of Vision, Previous Laser Operation, Annual Diabetic Retinopathy
Screening, Follow- Up with Ophthalmologist

Crisis Mx
● Hypoglycemia Management (15-15 rule)
● Sick day advice if on insulin

Co-morbids
● Ensure BP, LDL, uACR, BMI on Target etc
● Hba1c < 7% or <8%
● BP < 140/80 or < 130/80 if nephropathy / retinopathy
● LDL < 2.6 or < 2.1 if ASCVD, CKD
● BMI < 23

Family History of Diabetes

Past Medical History

Gestational DM, HTN, HLD, CKD, IHD, AMI, CVA,, cancer
Past hospitalizations & surgeries

Drug History
Drug allergies , Current Medications
Any TCM / Steroids/ OTC meds

Social History
WASHED, caregiver
***Occupation (Affect medication regimen)
Functional status
Address social factors that are barrier to DM control ie work stress – How are you coping with your new
promotion, is it affecting your diet and time to exercise

Psycho Hx
PHQ-2 , GAD- 2

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PHYSICAL EXAMINATION
BP HR BMI
ᐉ Lie down supine to examine abdomen for lipodystrophy
ᐉ Offer Fundoscopy: look for retinopathy changes
ᐉ Foot examination
● INSPECTION:
○ Look at the front/nails, soles (pressure ulcers), part the toes (fungal infection)
○ Pallor, shiny skin, loss of hair, ulcer, pressure sores, callus, nail changes , cellulitis , fungal
infection
● PALPATION
○ Temperature (Cold)
○ Capillary return
○ Pulses: posterior tibial artery, dorsalis pedis artery
● TEST: (3)
○ Proprioception or Vibration
○ Pin prick sensation: Check sensation over chest as reference, test sensation by dermatome;
if numb distally, check distal to proximal for stocking distribution of numbness

○ Sensation with monofilament (10g)

■ Perpendicularly until they bend for about one second. If patients fail to sense the
monofilament after it bends, the test site is considered to be insensate.
○ Offer ABI or TBI (if suspicious of PVD) ABI <0.5 and TBI <0.7 is considered severe

INVESTIGATIONS

MANAGEMENT
Non pharmacological / Education
- Diet, Exercise
- Compliance to meds
- Monitoring home CBG and titration (HOW FREQUENT TO MONITOR IN TYPE 2 DM): Use pre lunch and pre
dinner hypocount as surrogate for breakfast and lunch post prandial
- Hypoglycemia advice
- Sick day advice
- Complications of DM
Macro – Stroke / AMI / PVD
Micro – nephropathy , retinopathy, neuropathy

Pharmacological

115
- Able to recognize need for insulin and start insulin
- Advise on starting dose
- Teach how to inject insulin & rotate site
- Titrate other OHGAs
- Educate on side effects

Follow up [Link]
T2DM on basal + OHGA ● Home BGM frequency: Daily pre-BF hypocount? Aim 4-7.
(e.g. glargine 24U ON + ● If HbA1c >7%, fasting hypocount<7 → likely post prandial spike
metformin 850mg TDS + ● Check premeal TDS + bed time H/C, if pre-lunch, pre-dinner,
glipizide 5mg BD) bedtime h/c > 10, (surrogate for post bf, post lunch, post dinner
prandial spikes), can increase glipizide, or to start bolus insulin.

T2DM on basal plus ● BGM frequency

T2DM on basal bolus

T2DM on premixed insulin

Specific scenarios
1) Diabetic patient on insulin and travel [Link]

Air travel
- Adjustment of medication schedule is not needed when travelling north or south (e.g. Singapore to
Thailand) or when travelling across fewer than 5 time zones (e.g. Singapore to Asian countries,
Australia or New Zealand).
- Travelling across 5 or more time zones (1 time zone = 2 hours)
● Generally when travelling westward across 5 or more time zones, an additional meal with
change of dose of anti-DM medication may be needed due to “lengthening of the day” (e.g.
Singapore to Europe).
● When travelling eastward across 5 or more time zones, a patient may need to omit a meal
and reduce dose of anti-DM medication due to “shortening of the day” (e.g. Europe to
Singapore).

- History taking:
○ Time of departure and time of arrival at transit and destination country with different time
zones
○ Duration of air flight and time interval spent at transit
○ Estimated meal times
○ Planned activity and diet when overseas
○ Brief check on control, compliance, complications, checking, competency

- P/E: Vitals and abdomen for lipodystrophy

Management:
Non pharmacological
- Diet – Check with airlines for diabetic-friendly meals. Patient to bring healthy snacks ie nuts and
sandwiches on the plane instead of taking of sweet snacks on the the plane. Need to watch diet
when overseas to prevent diabetic emergencies
- On board plane - Write a memo to the airline stating her condition and the need to carry insulin,
needles, syringes, test strips and sweets and CBG monitoring machine onto hand carry luggage on
the plane. Also carry pharmacy-labelled pill bottles/packets and insulin vials. This will help with
security clearance at

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check in.
- Storage of insulin Avoid keeping insulin in check in luggage as the cold may damage the insulin
- Crisis Mx - Give a memo to the patient stating her condition in case she turns ill on the plane
- Hypoglycemia / hyperglycemia advice – To bring sweets with her at all times in case she develops
hypoglycemic symptoms. Ensure adequate hydration during flight to prevent DKA/HHS
- Hypoglycemia management advice (15g glucose check 15 minutes later)

Pharmacological
- Check diabetes travel website
- GENERAL RULE: NO HYPO DURING TRAVEL (½ basal before travel, the other ½ 12 hours later; next full
dose will be based on other country’s time as long as 12 hours have lapsed since 2nd ½ dose). Bring 2
watches, one singapore time for meds admin, the other the destination country time.
- Consider adding rapid acting insulin to cover with meals on board as meal times may be irregular.
- Oral medication timings can follow Singapore time while on board (and time with meals), but OK to omit
next dose if timing is too close upon arrival at New York

Education (as above)

Follow up

2) DM pt on insulin with acute illness (ACG) SICK DAY ADVICE

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 ● Blood glucose levels usually rise when pt is ill due to stress hormones. Appetite may be reduced
during illness. Blood glucose turns erratic as a result.
● Advised to continue insulin and check CBG more regularly (e.g. every 4 hours)
● Encourage to keep hydrated
● Avoid skipping meals but to take small frequent meals ie drinking sweetened juices or liquid
supplements if their appetite decreases

3) DM pt who wants to fast for Ramadan and exercise (NHGP Ramadan Guidelines and ACG)
● Assess suitability to fast – High risk or low risk
● Ask about DM crisis, hypogly, LMP/Pregnancy, co-morbids, intense physical labour

Very high risk (must not fast) High risk (should not fast)
Hypoglycemia in the following situations: ● Type 2 DM with sustained poor glycemic
● Severe hypoglycemia within 3 months prior control
to Ramadan ● Well controlled Type 1 DM
● History of recurrent hypoglycemia ● Well controlled Type 2 DM on multi dose
● History of hypoglycemia unawareness insulin or mixed insulin
● Pregnant Type 2 DM or GDM controlled
Hyperglycemia by diet alone or Metformin
● Diabetic ketoacidosis within 3 months prior ● CKD stage 3
to Ramadan ● Stable microvascular complications
● Hyperosmolar hyperglycemia coma within ● Other comorbid conditions that present
previous 3 months with additional risk factors
● People with diabetes performing intense
Poorly controlled Type 1 DM physical labour
● Acute illness ● Treatment with drugs that can affect
● Chronic dialysis or CKD stage 4 & 5 mentation
● Pregnancy in pre-existing diabetes or GDM
treated with insulin or SUs

Advanced macrovascular complications

● Old age with ill health

Non pharmacological / Education

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 ● Discuss regarding risks of fasting ie hypoglycemia, hyperglycemia ,DKA / HHS and address any
problems encountered previously during fasting
● Monitor SMBG more regularly (1-2 x /day or more)
● Advise to maintain healthy and balanced diet when they break their fast (healthy plate)
● Avoid vigorous exercise during fasting
● Recognize signs and symptoms of hypo and hyperglycemia and management or go A&E if in
diabetic emergency or refractory hypoglycemia

Pharmacological
Medication Before Ramadan During Ramadan
Metformin Metformin TDS 1/3 daily dose at predawn meal
2/3 daily dose at sunset meal
Sulphonylurea Sulphonylurea OM Sulphonylurea ON at sunset meal
Sulphonylurea BD ½ the morning dose at predawn meal
Usual dose at sunset meal
Alpha glucosidase No change in dose
inhibitors, incretin-based (exception: if acarbose is given three times a day,
therapies e.g. DPP4 change to twice a day, to be taken at sunset &
inhibitors predawn meals)

Insulin Before Ramadan During Ramadan

Basal Single dose a day Change basal insulin to be given at bedtime.
eg Glargine
Single basal + OHGA *Reduce basal insulin dose by 20 to 30 % to avoid hypoglycemia
Basal + pre meals bolus May need to increase dose of pre- dinner bolus to avoid post-
prandial hyperglycemia & decrease pre-BF bolus to avoid
hypoglycemia.
Omit pre-lunch bolus insulin.
Pre mixed Premix BD Reverse doses
eg insulin ● At sunset meal, give usual morning dose
30/70 ● At predawn meal, give reduced evening dose (reduce by 20
to 50%)
Premix twice a day + As above & omit pre- lunch bolus insulin
bolus insulin pre lunch NB: Consider changing to long acting or intermediate insulin in the
evening & short acting or rapid acting insulin with meals.
(see above for dose adjustment under basal + pre meals bolus)

4) DM patient with inconsistent diet (ACG)

● Advise patient regarding healthy eating habits
● Skipping or delaying meals or changing the amount or type of food can affect their blood glucose
levels
● Advise patients who are on fixed insulin doses that they need consistent intake of carbohydrate
● Refer patient to a dietician

5) Insulin administration and storage

● Inspect insulin to ensure that it looks as it should (cloudy vs clear)
● Do not use if clumping or precipitation or frosting
● Inject insulin subcutaneously into the abdomen, thighs, arms or buttocks. Avoid areas with bruise,
scar tissue, near groin, umbilicus or groin. Absorption rate varies from site to site, be consistent. Do
not massage injection sites
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 ● Rotate insulin sites regularly within one area to avoid lipodystrophy
● If unopened, keep insulin at 2-8oC, do not freeze
● If opened, keep at room temperature below 30oC and keep up to 4-6 weeks
● Discard used syringes and pen needles in a puncture resistant container. Do not reuse them

6) Young DM keen for pregnancy (Refer to OG document)

7) Special things to discuss for screening for GDM – Read the ACG guidelines!

8) DM patients with hypoglycemia, or even hypoglycemia unawareness

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ENT 1. APPROACH TO EAR PAIN

Primary Otalgia Secondary Otalgia

Infection TMJ disorder

** Malignant otitis externa in DM / Skull base
osteomyelitis
Rhinosinusitis

Trauma Dental disorder

Foreign Body Trigeminal neuralgia

Impacted cerumen Temporal arteritis

Head and neck cancer - oropharyngeal region

(soft palate, posterior pharyngeal wall, palatine
tonsil or tongue base)

HISTORY
Complaint
Unilateral Ear pain
- Onset / Duration – Sudden/ gradual
- Character – sharp/ shooting , dull ache
- Radiation
- Aggravating – chewing in TMJ Disorders
- Relieving factors -

Cause
Red flags:
LOW, odynophagia, dysphagia, dysphonia, haemoptysis, smoking -> H&N cancer / Skull base osteomyelitis
(CN involvement)
Progressive or sudden hearing loss
Loss of vision, black spots, headache -> Temporal arteritis
Immunosuppression or DM in a patient with infection -> Malignant otitis externa/ skull of base
osteomyelitis

Ear discharge, hearing loss, vertigo, aural fullness and tinnitus -> Primary Otalgia
Runny nose / blocked nose / facial fullness -> Rhinosinusitis
Trauma / FB entry
Exacerbation of pain associated with chewing, clicking sound on opening jaw -> TMJ
Tooth/ Gum Pain/ Hx of tonsil infections
Facial pain, unilateral attacks of pain that commence abruptly, last up to two minutes and are extremely
excruciating -> Trigeminal neuralgia

Course:
Complications:

121
PMHX: DM / Immunocompromising conditions
Drug Hx:
Family Hx: Cancer esp H&N
Social Hx: Smoking, Alcohol
Psycho Hx: Any stressors, PHQ-2 , GAD -2 in TMJ disorder

P/E
General inspection of the external ear including pre-auricular and mastoid
Otoscopic examination of the auditory canal and viewing the tympanic membrane
Cranial nerve exam if abnormal otoscopy
TMJ joint – Tenderness on palpation , Opening and closing the mouth may reveal trismus, as well as audible
or palpable crepitus suggestive of a TMJ abnormality.
Palpate temporal region for palpable temporal artery and tenderness
Oral cavity -> Dental problems, Tongue, soft palpate , posterior pharyngeal wall and tonsils
Neck lymphadenopathy

MANAGEMENT
1) TMJ joint dysfunction
- Non pharm : Avoid triggers ie teeth grinding/ nail biting/ pen chewing , CBT
in the long run to prevent recurrent attacks, refer to psychologist for review

- Pharmacological : Analgesia (NSAIDs/muscle relaxant/tricyclic anti-depressant) for acute setting, but will
need some

- Kiv maxillofacial dental surgeon review for refractory cases, additional management options include
surgery, trigger point muscle injections, botulinum toxic injections, intra-articular injections.

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ENT 2. APPROACH TO TINNITUS

Ddx
Subjective Objective (rare less than 1%)

Hearing loss Eustachian tube

- conductive
- Cerumen Vascular: arterial bruit, venous hum, vascular
- Otitis media tumor
- Cholesteatoma
- Sensorineural muscular disorder: palate spasms
- Presbycusis
- Noise induced hearing loss
- Meniere’s
- Acoustic neuroma
- Infective cause
- Ototoxic drugs*

History
Complaint: Tinnitus
- Site: Unilateral or bilateral
- Onset: Abrupt or gradual
- Character: Pulsatile? High pitched?
- Precipitating events?
- Worsen with swallowing? Neck movement?
- Time course: Progressive vs static. Duration >3 weeks?
- Severity
Causes
- Hearing loss?
- Wax/digging ears
- Ear discharge?
- History of otitis media?
- Loud noise exposure?
- Vertigo and aural fullness? → Meniere
- Unilateral weakness/numbness/slurred speech/gait problem
- New medications? (see appendix below)
Course
- Any investigation done? E.g. audiometry
Complications
- Impact on function → eg. driver cannot hear road noise

Medical hx
Drugs: Ototoxic drugs

Psy: PHQ2. GAD2. Associated with tinnitus

Social: Occupation and hobbies

Physical Exam
Otoscopy → cerumen/infective otitis/cholesteatoma
Weber and rinne test → determine if sensory or conductive
Neurological exam with cerebellar exam and gait

123
Investigations Don’t think there is any in primary care

Management
Pulsatile tinnitus - Direct access to ENT for imaging
- Red flag advice

Sensorineural hearing - Acute <72 hr

loss - Neurological deficits
- Send to ED for urgent imaging

Sensorineural hearing - Send to ENT for audiometr

loss - May need hearing aid
- chronic - Advise to avoid loud noise exposure, stop offending drugs

Conductive hearing loss - If cerumen seen, olive oil ear drops and syringing. Reassess after.
- If otitis externa, tx with topical abx and steroids. Reassess after.
- If otitis media, oral amoxicillin. Reassess after.

124
125
ENT 3. APPROACH TO EPISTAXIS

Ddx
Local Systemic

● Tumours: Nasopharyngeal cancer (adults), hemangioma, nasal ● Causes of generalized

polyp bleeding
● Trauma: Nose-picking, FB a. Thrombocytopenia
● Mucosal irritant: Allergic rhinitis, Rhinosinusitis (URTI), dry air b. Coagulopathy
● Poorly controlled hypertension (adults) c. Vessel defect
● Other rare causes: HHT (Hereditary haemorrhagic telengiectasia
(Osler Weber Rendu), Vasculitis: Wegener’s granulomatosis

HISTORY
Complaint
● Epistaxis:
o Onset, duration, progression
o How often? How severe: quantity of blood loss?
o Exacerbating factors: frequent nose picking, environmental: air conditioned places
o Relieving factors
o How do you stop the bleeding?

Cause:
● Rule out other sites of bleeding first (r/o causes of generalized bleeding)
o Gum bleeding , petechiae (small red dots on the body), easy bruising, CNS bleeding,
menorrhagia, Haematemesis, PR bleeding, malaena, haematuria,
o Joint bleeding, muscle hematomas
o If generalized → refer to notes on purpura
o Any bleeding during previous tooth extraction, surgery, delivery
● Neck lump, hearing loss, diplopia, difficulty swallowing, facial numbness or weakness, LOW/ LOA,
anosmia → nasopharyngeal cancer (adult)
● Lumps in the nasal cavity → nasal polyps
● Recent injury or trauma / Nose picking / FB
● Hx of allergic nose, fever, rhinitis, cough, sore throat → rhinosinusitis

Rare:
● Telengiectasia over face, mouth, hands; SOB, chest pain (lung AVM), abdominal swelling or mass (liver
AVM), PR bleeding, malaena (GI AVM), UL/ LL weakness (CNS AVM) → HHT
● Rash, haematuria, frothy urine, cough, runny nose → Wegener’s granulomatosis

Complications:
● Cx of anaemia: SOB, exertional symptoms, postural giddiness, lethargy

PMHx:
o NPC (adults)
o Allergic Rhinitis
o Nasal polyps

Drug Hx: Anti platelets, anti coagulants

FHx:
o Recurrent epistaxis – HHT

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ISTH BAT - Bleeding Assessment Tool
Screening for congenital bleeding disorder
A. Abnormal cut-offs
1. Men >3
2. Women >5
3. Children >2

* Consultation only: the patient sought medical evaluation and was either referred to a specialist or offered
detailed laboratory invx

MANAGEMENT

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Acute epistaxis ● First aid measures

● Red flag advice

Prevention of recurrent ● Rule out causes that needs further evaluation

epistaxis ○ Coagulopathy, thrombocytopenia
● Manage benign causes
○ Humidify air: Humidifier, normal saline nasal spray
○ STOP INTRANASAL STEROIDS. CAN SWITCH TO
ANTIHISTAMINES
○ Educate first aid
○ Red flag advice

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 ENT 4. APPROACH TO HEARING LOSS

DIFFERENTIAL DIAGNOSIS
Conductive Sensorineural

Obstruction of external auditory canal: Infection (e.g. meningitis, labyrinthitis)

Cerumen; foreign body; debris from otitis externa; large Trauma (e.g. temporal bone fracture)
exostoses, osteomas Neoplasm (e.g. acoustic neuroma, invasive NPC)
Meniere disease (Triad of hearing loss, vertigo,
tinnitus)

Age-related hearing loss;

Noise induced hearing loss
Medications

Autoimmune disease

Impairment of tympanic membrane function

Perforated tympanic membrane; tympanosclerosis

Middle ear conditions

Otitis media with effusion; otosclerosis; cholesteatoma;
disarticulation of ossicular chain; glomus tumors

BIOLOGICAL

Acute Chronic illness Medical History

Complaint: Hearing loss Cause ● Medical/

● Site: Right? Left? Both? Course Surgical
● Onset: Sudden or gradual (within <72 hours?) Control Hx
● Character: Distorted sound? Loss of high pitch? ● Home ● Drug Hx/
● Precipitating: Loud noise? Drugs (aminoglycosides etc)? Toxic ● Clinic Drug
chemicals (toluene?) Compliance allergies
● Timing: Lasts for seconds? Minutes? Hours? Days ● Non ● TCM/OT
Cause pharm C
● Rule out red flags ● Pharm
○ Fever/headache/neck stiffness → meningitis Complications ● Travel /
○ Vertigo/weakness/numbness/slurred speech/dysphagia/ gait ● Disease Contact
difficulty → CP angle tumor ● Treatmen Hx
○ Trauma t
○ Unilateral Checking ● Birth Hx
● Recent URTI → labyrinthitis Competency ● Immuniz
● Tinnitus/ Vertigo → Meniere’s triad ation
● Ear pain/discharge/digging ears → otitis externa Comorbidities history
● History of tympanic membrane perforation/OM Crisis ● Develop
● Environment/ Occupation: Chronic loud noise exposure/toxic management mental
chemical Hx
● Drug Hx: Ototoxic drugs/ new drugs
Course
● Previous similar episodes?
● Tried what treatment?
● Seen other doctors for it?

129
Complications

Disease Prevention Family Hx

- Vaccinations Hearing loss

- Cancer prevention

PSYCHOLOGICAL

PHQ-2 ICE
GAD-2

SOCIAL

Activities / Environment Function

Employment
Drugs (Smoking, alcohol, illicit drugs) Bladder and
Sleep bowel

Eye, ear and

swallowing

PHYSICAL EXAMINATION ***HAND RUB***

T BP HR
1. Ear exam: Tenderness over tragus. Otoscopy to inspect EAC for FB/erythema/slough/TM.
2. Do Weber before Rinne’s (For Rinne, V parallel to ear, not perpendicular)
3. Neuro: Cranial nerve and cerebellar exam as indicated TRO CPA
4. Cervical lymph node exam if SNHL pattern especially if unilateral TRO NPC

130
INVESTIGATIONS
Audiogram
● 0-20 dB: Normal
○ 20-40 dB: Mild hearing loss
○ 40-70: Moderate
○ 70-90: Severe
○ 90-120: Profound hearing loss
● Conductive hearing loss will have air-bone gap (>10dB difference between AC BC, but AC usually
above 60dB)
● Otosclerosis: Carhart notch at 2kHz
● Noise-induced SNHL: worst at 3-6kHz, typically notch at 4kHz
● Meniere’s SNHL: early on = low tone SNHL → low and high tone SNHL → “flat” 50dB SNHL

MANAGEMENT
1. Acute sudden sensorineural hearing loss (SSNHL)
a. Disposition: Direct access ENT as up to 16% have serious underlying pathology. Usually will
need MRI Brain + audiogram. If patient presents with vertigo as well and unable to rule out
stroke → Refer ED
b. Pharm: Prednisolone 1mg/kg (max 60mg) x 10-14 days with PPI cover, KIV extend
additional 10 days if partial response
i. Antivirals? AAO-HNS suggest NOT treating with antivirals due to lack of evidence
for efficacy and medication ADRs
c. Follow up audiogram 6/12 of initial diagnosis

2. Unilateral SNHL
a. **Tumor until proven otherwise, esp in elderly Chinese male. Refer for neuroimaging.
(can be acoustic neuroma, invasive NPC)

3. Infective otitis externa

a. Disposition: Outpatient. Rule out malignant otitis externa esp in immunocompromised /
DM
b. Non-pharm: Aural toilet to clean out debris to facilitate ear drop penetration
c. Pharm: Cipro/hydrocortisone topical ear drops 3 drops BD x 1/52
d. Educate: If patient is immunocompromised, or has skin condition predisposing to recurrent
otitis media, advise use of ear plug to avoid water entering ear, dry ears after water
entering ear.
e. Follow-up: TCU 1-2 weeks.

4. Ear cerumen
a. Disposition: Outpatient tx
b. Non-pharm: Avoid digging ears with cotton bud
c. Pharm: Olive oil ear drops and warm water irrigation

131
5. TM Perforation → Conductive HL
a. Most acute TM perforations heal themselves

6. Cholesteatoma
7. Presbycusis
a. KIV referral for hearing aid

8. Noise-induced SNHL

132
ENT 5. APPROACH TO HOARSE VOICE

DDx:
1. Laryngeal carcinoma
2. Lung cancer with involvement of left recurrent laryngeal nerve
3. Overuse laryngitis
4. Laryngeal polyp
5. Infective laryngitis
a. Acute: viral
b. Chronic: Candida
6. Hypothyroidism
7. GERD
8. Previous trauma to vocal cords: FB, previous intubation

Questions:
Hoarseness of voice:
● How long
● Worsening, stable, improving
● Intermittent or chronic
● Onset: gradual or sudden (was it after a bout of viral laryngitis)

● LOW/ LOA
● SOB, pleuritic chest pain, haemoptysis, neck lumps? (lung cancer)
● Use voice often? (overuse laryngitis)
● Sore throat, fever (chronic infective laryngitis: candida; acute viral laryngitis)
● Hypothyroid symptoms: cold intolerance, weight gain, loss of appetite, constipation, swelling
● Acid brash/ Water brash with epigastric discomfort, chest discomfort when lying down flat? (GERD)
● Previous intubation? (Vocal cord injury)

PMHx:
● GERD, thyroid, recent URTI
● Asthma/ COPD requiring use of steroid inhalers

Drug history:
● Steroid inhalers: overuse, technique, use of spacer, gargle after use?

Social history:
● Smoking

Investigations:
Blood tests: TFT for hypothyroidism
Imaging: CXR to look for lung cancer
Others: ENT referral to do laryngoscopy to look for polyps, masses, signs of inflammation, 24hr esophageal
pH monitoring for GERD

133
ENT 6. APPROACH TO NECK LUMP

DDx:
1. Malignancy
a. Lymphoma/ Leukaemia
b. Head and neck tumour eg NPC
c. Other malignancies: lung, GI, breast
2. Infections
a. Acute infections: recent URTI (CMV/ EBV) / tonsillitis
b. Viral: HIV
c. Bacterial: TB, Meliodosis
3. Inflammatory, infiltrative
a. Sarcoidosis
b. SLE
4. Thyroid swelling
5. Congenital: branchial, thyroglossal, dermoid cysts
6. Vascular: carotid artery aneurysm
7. Salivary gland disease: parotitis, submandibular calculi, neoplasms

Questions:
Neck lump:
● Where – midline or at the side
● Getting bigger/ smaller/ stable
● Painful or painlessbgd
● Firm or soft or hard
● How did you first notice it?
● Mobility
o Can move the lump under the skin?
o Does lump move with swallowing?
● Aggravating factors
o Alcohol making pain worse – Hodgkin’s lymphoma
o Pain worse before or during eating – salivary gland pathology
● Other lumps elsewhere

● LOW/ LOA, fever, night sweats – TB, lymphoma

● Abdominal masses or other swollen lumps – Lymphoma / Leukaemia
● Epistaxis, hoarse voice; haemoptysis, SOB, cough; change in bowel habit, PR bleeding/ malaena,
tenesmus, change in caliber of stool – Head and neck tumour and other malignancies
● Fever, sore throat, runny nose, ear d/c, ear pain – recent URTI
● Dental problems, dental pain
● Recent URTI, tonsillitis
● Rash, cough, eye problems – sarcoidosis
● Photosensitivity, rash, alopecia, oral ulcers – SLE
● Complications:
o SOB or stridor caused by large neck mass
o Dysphagia caused by large neck mass
● Risk factors for HIV
o Sexual history
o Previous blood transfusions
o IVDA

PMHx:
134
 ● Cancer anywhere
● TB, HIV
● Recurrent URTI or tonsillitis
● SLE

Drug Hx:
● Drugs that can cause lymphadenopathy: Allopurinol, phenytoin

FHx:
● Tuberculosis
● Cancer

Social history: Smoking

Investigations:
Blood tests: FBC looking for raised total white cell count, HIV screen, TFT, PBF, ESR, LFT
Imaging: CXR to rule out lung cancer and tuberculosis and sarcoidosis
Others: fine needle aspiration of neck lump to send for acid fast bacilli smear and culture, gram stain and
culture and cytology, core biopsy

135
EYE 1. APPROACH TO RED EYE

DIFFERENTIAL DIAGNOSES
V – Vascular - Subconjunctival haemorrhage
I – Infection – Conjunctivitis – viral (ie Adenovirus, HSV, VZV, Chlamydia ), bacterial, gonorrhoeal chlamydia,
(STDs)
T - Trauma - Physical / chemical burn, corneal abrasion, foreign body
A – Autoimmune – Siogren’s syndrome, episcleritis (usu idiopathic) , scleritis / Allergy – ie Allergic
conjunctivitis
M – Hyperthyroidism, menopausal
I – Inflammatory – keratitis, iritis, blepharitis / Increased ocular pressure in glaucoma
N – Neoplastic – ie haemorrhage due to orbital mass
C – Contact lens related **
D – Dry Eyes
Drugs: Anti-cholinergics → antihistamines, amitriptyline
Others – Glaucoma , Blepharitis

Think of layers of the eye!

Cornea – keratitis, corneal abrasion, foreign body, chemical burn, physical trauma
Sclera – scleritis, episcleritis ,
Conjunctiva – conjunctivitis – viral/ bacteria/ allergic
Subconjunctival – Subconjunctiva haemorrhage
Uveitis/ Iritis
Vitreous – Glaucoma ( increased intra-ocular pressure)
Contact lens related, Dry Eyes
Blepharitis
Neoplastic – ie haemorrhage 2 to orbital mass

HISTORY
Complaint:
● Duration, onset
● Triggers:
● Worse at the end of the day/ work
● Exacerbating factors : ie allergen
● Relieving factors
● Progression
● Pain?
● Contact lens use?
● Other eye symptoms : Pain, Discharge, BOV
Cause:
● TRO infection: URTI symptoms (Viral) purulent discharge (bacterial/ STD) , high risk behavior + dysuria
+ urethral d/c (gonorrhea/chlamydia)
● Trauma: physical contact/sports, exposure to chemical splashes
● TRO metabolic: hyperthyroid symptoms, menopause symptoms: hot flushes, bodyaches, fatigue
● TRO autoimmune:dry mouth, O/E fever, joint pains, rashes, oral ulcers, personal history of
connective tissue disorders
● Headache / vomiting / retro-orbital pain
● Neoplastic: early morning nausea and vomiting, headaches, double vision
● Any evidence of anticholinergics usage
Course: Tried any meds so far
Complications: Affected function ?

Physical Examination
136
T BP
[seated] Fundoscopy
Pupillary reflex
Rash - malar rash, skin tightening
Oral ulcers
Goitre, tremors, reflexes
Cranial nerves

137
EYE 2. APPROACH TO DOUBLE VISION

DDx:
(a) Binocular
1. Orbital lesions
a. Orbital fractures
b. Cellulitis
c. Tumours
2. Muscle disease
a. Grave’s opthalmopathy
b. Orbital myositis
c. Genetic myopathy: chronic progressive external opthalmoplegia (CPEO), Kearns-Sayre
syndrome (triad of CPEO, pigmentary retinopathy and onset before age 20)
3. Neuromuscular junction
a. Myasthenia gravis
b. Botulism
4. Nerve
a. Causes of 3rd, 4th, 6th nerve palsies
b. Grouped – cavernous sinus syndrome, superior orbital fissure/ orbital apex syndrome, base of
skull/ meningitis
5. Brain
a. CVA (infarct, haemorrhage), tumour, abscess, demyelinating (Multiple sclerosis)
(b) Mono ocular – refer to blurring of vision notes

Questions:
● Is it double vision (two images) or blurring of vision (one image but blur) or loss of vision (which visual
fields)
● Mono ocular , binocular (double image disappear on covering one eye)
● Double vision
o Onset: sudden or gradual, progression
o Character: overlap horizontal, vertical or oblique
o Exacerbating factors
▪ Worse at end of the day – myasthenia gravis
▪ Worse on looking at which direction or multiple directions, or does it vary
o Relieving factors
▪ Better at start of the day and after some rest
● Visual acuity, loss of colour vision – involvement of CN II
● Pain on moving eye
● Recent fall / trauma – orbital fractures
● Fever, redness around the eye – cellulitis
● Headache with features of raised intracranial pressure, LOW / LOA – tumour
● UL / LL weakness, slurring of speech, dysphagia – stroke
● Previous similar episodes that resolved – multiple sclerosis
● History of thyroid prob, heat intolerance, weight loss despite good appetite, agitation, tremors, goitre,
diarrhea – Grave’s disease
● Lethargy that gets worse at end of the day, ptosis, variable strabismus and opthalmoplegia, proximal
weakness – myasthenia gravis
● Numbness over face – cavernous sinus lesions / superior orbital fissure syndromes

138
PMHx:
● Previous facial surgery
● Thyroid disease
● Myasthenia gravis
● Old stroke and other CVRF (DM, HTN, hyperlipidaemia)
● Intracranial aneurysm
● Cancer

FHx:
● Thyroid, MG

Social history:
● How is double vision affecting your life?
● Job: does double vision affect job
● Driving

P/E
Neck for goitre
Ptosis
CN exam + lid lag exam + eyelid fatiguability test
Arms fatiguability test for proximal myopathy
UL - pronator drift, dysmetria
Hands extended - Tremors, acropachy
Gait

Mx
1) Ocular MG
- Refer to Neuro direct access
- If Systemic MG -> Refer to ED

139
EYE 3. APPROACH TO LOSS OF VISION

Differential Diagnosis
Media Retina Neural visual pathway Others

ᐉ Keratitis ᐉ Retinal artery ᐉ Optic nerve problems ᐉ Psychogenic

ᐉ Corneal edema occlusion ● Ischemic optic neuropathy ᐉ Trauma
ᐉ Hyphema ᐉ Retinal vein occlusion ● Optic neuritis
ᐉ Lens changes ᐉ Retinal detachment ● Papilledema
ᐉ Glaucoma ᐉ Maculopathy ᐉ Chiasmal disorders (pit
apoplexy)
ᐉ Vitreous
hemorrhage ᐉ Retrochiasmal disorders
ᐉ Uveitis (Cortical, subcortical)
● Homonymous hemianopia
● Cortical blindness

HISTORY
Complaint: Loss of vision
● Laterality: Monocular or binocular?
○ Bilateral suggests chiasmal, retrochiasmal visual pathway disorder
● Total or subtotal
● Timing/Onset
● Duration
● Progression: stable or progressive or spontaneously resolved
● Painful or painless?
○ Pain → keratitis, glaucoma, optic neuritis, endophthalmitis
● Redness
● Trauma
● Diplopia, floaters, photopsia
● TRO neglect

Cause
● Retina causes: CVRF
● CVA: Numbness, weakness, dysphagia, dysarthria, diplopia
● SOL/ Glaucoma: Headache, vomiting, LOA, LOW (in SOL)
● Vasculitis: GCA causing CRAO or ION: temporal headache, jaw claudication, scalp tenderness, fever,
LOW, fatigue
● Fever

Complications
● Falls, RTA

Past Medical History

● Vascular disease: HTN, DM, CAD, hypercoagulability
● Refractive status – high myopia or hyperopia?
● Contact lens wear
● Eye surgery
● Medications

Family Hx
● Glaucoma , CVRF

Social History
140
 ● Smoking
● Job
● Function eg driving

PHYSICAL EXAMINATION
BP HR HR regular?
Ht Wt BMI

VA , Pupillary reaction / RAPD , EOM

Visual fields
Fundoscopy
Cranial nerves

Pronator drift
Gait
Brief neuro exam: reflexes, power
H: murmur?
Carotid bruit

INVESTIGATIONS
● KIV ECG if suggestive of arrhythmia eg AF causing embolic stroke

MANAGEMENT
1. Homonymous hemianopia 2’ occipital stroke (embolic from new AF)
● Refer ED

2. Request glaucoma screening

● Primary Open Angle Glaucoma vs Acute Angle Closure Glaucoma (usually symptomatic)
● Hx
○ Risk factors: age (≥70s), 1o relative with glaucoma, increased IOP, black race
○ No hard evidence: Myopia, DM
● PE
○ PEARL
○ Fundoscopy: cup disc ratio
○ VA
○ Confrontational visual fields
No risk factors + PE normal Monitor, discharge

No risk factors + PE abnormal Refer Eye (urgency dependent on PE findings)

Risk factors Refer Eye for screening

● Eg automated VF testing

141
142
GASTRO 1. APPROACH TO ABDOMINAL DISTENSION
Ddx: Fat, Fluid, Faeces, Flatus, Foetus, Filthy large tumor (6F)

DDx of ascites:
● Chronic liver disease with cirrhosis
o Chronic ethanol ingestion
o Hepatitis B and C
o Non alcoholic steatohepatitis
o Cardiac failure
o Autoimmune hepatitis
o Primary biliary cirrhosis
o Wilson’s disease
o Haemochromatosis
o Budd Chiari syndrome
● Malignancy - GI, ovarian
● Nephrotic syndrome/ Chronic renal failure
● Congestive heart failure/ Constrictive pericarditis
● Tuberculous
● Protein losing enteropathy
● Hypothyroidism

HISTORY
● Abdominal swelling
o How long? Sudden/ Slow onset? Progressively worse/ Stable?
o Which part of the abdomen?
● Bowel habits: Diarrhea or constipation? Passing flatus?
● Nausea or vomiting?
● Abdominal pain?
● LOA/ LOW? – malignancy

● History of liver cirrhosis?

o Jaundice, pruritus, easy bruising, haematemesis
● Risk factors for liver cirrhosis
o Chronic ethanol ingestion
o History of hepatitis B or C
o Previous blood transfusions (also secondary haemochromatosis)
o Intravenous drug use
o Severe pruritus (PBC)
● Cough? Fever? Chills and rigors? (TB)
o Contact history and travel history
● Night sweats? (TB, Lymphoma/ Leukaemia)
● Swollen lymph nodes (TB, Lymphoma/ Leukaemia, other malignancy)
● SOB/ exertional symptoms/ orthopnea/ PND (Congestive heart failure)
● LL edema, UL edema, facial swelling, periorbital edema (anasarca suggestive of nephrotic syndrome)
● Menstrual Hx
● Frothy urine, decrease in urine volume (nephrotic syndrome, chronic renal failure)
● Weight gain, cold intolerance, lethargy, constipation, menorrhagia, LL edema (hypothyroidism)
● Sexual history for Hep B

PMHx:
o History of liver cirrhosis
o Cancer
o Hep B or Hep C
o Heart failure, renal disease
143
Drug history:
o Drug use like methotrexate, amiodarone or isoniazid
o OTC meds

Social history:
o Alcohol
o How function is affected

PHYSICAL EXAMINATION **** HAND RUB ****

T BP HR
Ht Wt BMI
{seated} Inspection: pallor, cachexic, jaundiced
Cervical LNs
{lie flat} Abdo: masses, ascites
Inguinal LNs
Pedal edema
Offer DRE, PV

INVESTIGATIONS
Ascitic tap:
● fluid albumin and protein, cell counts, gram stain and culture, cytology, acid fast bacilli smear
and culture
● Serum ascitic albumin gradient:
o > 10g/L portal hypertension: liver cirrhosis, cardiac failure/ constrictive pericarditis,
Budd Chiari syndrome
o < 10g/L: nephrotic syndrome, malignancy, tuberculous, protein losing enteropathy
Blood tests:
● FBC (raised TW suggestive of SBP), urea creatinine and electrolytes (rule out renal failure), liver
function test, thyroid function test, albumin level
● Urine protein creatinine ratio (nephrotic syndrome)

Imaging: chest radiograph looking for signs of congestive heart failure, computer tomography of the
abdomen to confirm the diagnosis and looking for aetiology, ultrasound of the abdomen to confirm
presence of ascites, check for aetiology such as liver cirrhosis, chronic renal failure

144
GASTRO 2. APPROACH TO DIARRHEA

Chronic diarrhea = ≥3 loose or watery stools per day for ≥4 weeks

DDx:
1. Infection: bacterial, TB, protozoan, parasitic
2. Malabsorption
a. Pancreatic disease – chronic pancreatitis
b. Lactose intolerance / Post enteritis secondary lactose intolerance
c. Food allergy/ intolerance
d. CMPI (Cow’s milk protein intolerance) esp in neonate
e. Celiac disease
3. Inflammatory bowel disease (Crohn’s, ulcerative colitis)
4. Colorectal cancer
5. Irritable bowel syndrome
6. Hyperthyroidism
7. Drugs: laxatives
8. Others: GI fistulas, radiation colitis

Ddx 2: LAOSAII

145
HISTORY
Complaint: Diarrhea
● How long? Onset? Any nocturnal diarrhoea (if absent, may be non-organic ie IBS)
● Progression? Frequency , Consistency
● What was the stool pattern before this?
● Nature of stools: bloody, steatorrhea, oily/ floats in water, , mucoid stools
● Watery, inflammatory or fatty?
o If watery → osmotic, secretory (continues even when food intake is stopped) or functional
● Exacerbated by intake of certain types of food? / Stress
o Eg for celiac disease: wheat, barley, rye
o Eg for lactose intolerance: dairy products
● Relieved by defecation / loperamide
● Severity -> complications

Causes
● ⚐ Mass symptoms: nausea, vomiting, abdominal pain, constipation w spurious diarrhea
● Full travel history including intake of food at foreign lands, any street food or intake of
contaminated water (tap water/ river water etc)
● Joint pain, rash, mouth ulcers, malaise → inflammatory bowel disease
● Change in bowel habit, change in caliber of stool, tenesmus → colorectal cancer ⚐
● Hyperthyroid symptoms
● Contact history: diarrhea, TB
● Osmotic symptoms → DM
● Abdo pain a/w defecation, a/w change in stool form and frequency, stressors → IBS

Course
● Tried any medications? Altered diet? Any improvement?
● Invx or scopes done?

Complications
● Dehydration: Dizziness, reduced urine output, lethargy
● Malnutrition
● If paeds/adolescent, consider failure to thrive/developmental delay
● Anemia symptoms, IO if CA

PMHx:
● Previous GI surgery, radiation therapy
● TB
● Lactose intolerance
● Thyroid, DM

Drug history:
● Recent use of antibiotics, laxatives, colchicine, metformin, TCM/OTC

Family Hx: eg if CA, IBD

Social: Work (especially if dealing with food), Alcoholism (CAGE, exceeds recommended alcohol intake),
Smoking

Psy Hx: GAD2, PHQ2

PHYSICAL EXAMINATION
T BP HR

146
Ht Wt BMI
{seated} Inspection: pallor, jaundice, cachexic
Mucous membrane, CRT <2s
Neck: goitre, cervical LNs
Mouth: oral ulcers
Hands: fine finger tremors, Dupuytren’s
{lying flat} Stigmata of CLD
Skin: rashes for IBD
Abdo: masses and tenderness, BS
Offer DRE
Mental State Examination

INVESTIGATIONS
● Stat tests
○ FBC, random glucose
● Other blood tests:
○ UECr, LFT, amylase, iron panel (iron deficiency anaemia commonly seen in celiac disease),
folate/ B12 and calcium panel, TFT
● Stool tests: gram stain and culture, ova cysts and parasites, clostridium difficile toxin, leucocytes,
occult blood
● Others: barium enema for crohn’s disease, colonoscopy, small bowel biopsy
○ Auto antibodies for celiac disease (endomysial antibodies)

MANAGEMENT
Chronic Pancreatitis ● Pain Mx:
○ Gradual reduction in alcohol intake, watch for alcohol withdrawal
symptoms
○ Stop smoking
○ Hydration and small frequent low fat meals
● Steatorrhea:
○ Restrict fat intake, <20g/ day
○ Pancreatic enzyme supplementation
○ Vitamin supplements (Fat soluble vitamin analogues ADEK)
● Glucose intolerance: Screen for DM
● Alcoholism: Thiamine 100mg OM, Refer to NAMS
● Red flag advice: Symptoms of acute pancreatitis!
Diarrhoea in a ● Consider stool cultures/OCP, FBC, RP
returned traveller ● If mild-moderate symptoms ⇒ ORS, diet and hydration advice, symptomatic
tx (can use loperamide or diphenoxylate).
● If symptoms persistent or severe ⇒ can use Azithromycin or
Fluoroquinolone
○ Azithro 500mg daily x 3/7
○ Cipro 500mg BD x 3/7
● IF BLOODY PLEASE DON’T GIVE ABX. CAN BE DUE TO EHEC, AND IF ABX
GIVEN, CAN CAUSE HUS ESPECIALLY IN CHILDREN.
● If very dehydrated or unstable ⇒ to ED
IBS-diarrhea ● Diagnosis of exclusion, still need to refer for scopes!
predominant ● Pain management
{Rome IV} ○ Anti-spasmodics: Buscopan
○ If doesn’t work, consider TCA like Amitriptyline or SSRI
● Diarrhoea management
○ Non-pharm: Low FODMAP food*
○ Antimotility: Loperamide 45 mins before meals TDS

147
 ● Psy: CBT
● Exercise
● KIV treat concomitant GAD/MDD
Inflammatory ● Refer Gastro for confirmation with scopes
bowel disease ● Rx: ASA (topical if mild, topical and oral if more severe) ± oral steroids
● Ask about pt’s crisis management plan given by GE, if any
Drug-induced ● Try to stop. Otherwise reduce dose if possible.

Appendix

148
GASTRO 3. APPROACH TO DYSPEPSIA

DIFFERENTIAL DIAGNOSIS
Esophagus Esophagus cancer
GERD
Stomach Stomach cancer
Peptic ulcer disease
H pylori
Functional dyspepsia, IBS
Gastroparesis
Intestines Malabsorption (lactose etc)
Duodenitis
Biliary tract Gallstone disease
Pancreas Pancreatitis

Cardiac AMI
Systemic Diabetes (gastroparesis)
Hypothyroid
Hypercalcemia
Pregnancy (early)
Food allergy
Medications Acarbose, Metformin
NSAIDS, COX 2 inhibitors
Steroids
Bisphosphonates
Antibiotics
Psychiatric Panic attack
GAD
IBS

HISTORY
Dyspepsia: Epigastric pain / Abdo bloating / Heartburn / Belching and flatulence
● Site: Epigastrium
● Onset: Gradual vs sudden (AMI)
● Character: Burning, Dull and Constant, Colicky
● Radiation: Tip of right shoulder blade (Gallstone), back(Pancreatitis/esophagitis), chest
● Exacerbating: Oily food, post meals, supine position, exertion
● Relieving factor: After BO (IBS)
● Time: Progressively worsening

Cause
● ⚐ Esophageal/Gastric CA: Dysphagia, hematemesis, melena, PR bleeding, LOW, LOA, early satiety,
vomiting, FHx of CA
● ⚐ AMI: Associated SOB, diaphoresis, angina, change in effort tolerance
● GERD: Heartburn, acid brash/bitter taste in mouth, regurgitation esp lying down at night
● Peptic ulcer: Hx of NSAIDS/steroids intake, h/o ulcer
● Gallstones: Jaundice, pale stools, dark urine, colicky pain
● Pancreatitis: Associated nausea/vomiting, preceding alcohol binge
● Hypothyroid: Cold intolerance, lethargy, constipation
● DM: Control of DM
● Medication chart review
149
Course
● Investigations done: OGD, H pylori testing (stool antigen/urea breath test or biopsy), US HBS
● Tried what medications
○ If H pylori +ve, triple therapy or quadruple therapy? UBT repeated after treatment to
document clearance?

Complications
● Malnutrition, dehydration
● Anemia symptoms eg UBGIT

PMH
● GERD, Peptic Ulcer, Gallstones, Cancer, Diabetes, Hypothyroid, HLD
● Previous OGD / H pylori infection with incomplete eradication

Drug Hx
● NSAIDS, steroids, TCM, OTC, Drug Allergy

Family Hx
● Cancers, H pylori

Social Hx
● Smoking, Alcohol (esp pancreatitis)
● Diet, Exercise
● Occupation

Psy Hx: GAD2, PHQ2

Travel/Contact Hx

PHYSICAL EXAMINATION
T BP HR
Ht Wt BMI
{seated} General inspection: Cachectic? Jaundiced? Pallor?
Tongue for hydration
Neck: Supraclavicular LN, goitre
{lie flat} Abdomen exam: masses, tenderness, guarding/ Murphy’s
Diabetic dermopathy
KIV DRE
Mental State Examination if Psy

INVESTIGATIONS
● STAT: FBC, ECG, H/C
------------------------------------------
● LFT, RP
● US HBS: gallstones
● OGD

150
 MANAGEMENT
1. Ulcer dyspepsia ᐉ Non-pharm: Avoid NSAID/steroids. Stop smoking. Limit alcohol max 1 drink per
day.
ᐉ Pharm: PPI has better cure rate than H2RA
ᐉ Test for H pylori, and treat if positive:
A. 1st line (triple therapy): Amoxicillin 1g BD + Clarithromycin 500mg BD +
Omeprazole 20mg BD } x 2/52
➔ If penicillin-allergic, switch Amoxicillin to Metronidazole 500mg TDS
B. 2nd line (quadruple therapy): Metronidazole 500mg QDS + Tetracycline
500mg QDS + Bismuth subsalicylate 525mg QDS + Omeprazole 20mg BD }
x 2/52
➔ Tetracycline can be substituted for Doxycycline 100mg BD
ᐉ May need repeat OGD to ensure gastric ulcer healed
ᐉ Methods of diagnosing Helicobacter pylori infection:
● Non-invasive: Urea breath test, Helicobacter stool antigen detection
● Invasive: Rapid urease testing from endoscopic biopsies, Histology
2. Functional dyspepsia ᐉ Non-pharm: Rule out H pylori infection. Treat as for GERD wrt lifestyle
i) Postprandial distress syndrome ᐉ Pharm: 8 weeks of PPI OD
(PDS): Meal-induced dyspeptic symptoms A. If fail, try TCA, start low dose (eg Amitriptyline 10mg ON)
suggestive of motility disturbance
B. If still fail, try prokinetic agents 30mins pre-meal (eg maxolon or
ii) Epigastric pain syndrome (EPS): domperidone)
Epigastric pain/burning that may not be
triggered with food, may occur with fasting
iii) Overlap PDS-EPS

3. GERD (ACG guidelines) Non pharmacological

● Weight loss, smoking cessation, reduce alcohol
● Head of bed elevation: 20-30cm
● Avoidance of meals 2–3 h before bedtime if nocturnal GERD
● Small and frequent meals (not evidence based)
● Avoid food that can trigger reflux eg fatty foods, chocolate, caffeine,
alcohol, acidic, spicy foods (not evidence based) & gaseous drinks

Pharmacological
● PPI: Starting with once a day dosing 30-60mins before meal, titrate to BD
or increase dose if partial response x 4/52
● Consider prokinetic agents
● Consider H pylori eradication if present
● Antacids eg Gaviscon PRN or 1.5-2h pre-meal and bedtime
**In presence of red flags or refractory to optimal dose of PPI → Refer for OGD
4. Irritable Bowel Syndrome (1) IBS-C with predominant constipation (i.e., >25% of bowel movements with
Bristol stool form types 1 or 2 and <25% of bowel movements with Bristol stool
form types 6 or 7)
(2) IBS-D with predominant diarrhea (i.e., >25% of bowel movements with Bristol
stool form types 6 or 7 and <25% of bowel movements with Bristol stool form types
1 or 2)

151
 (3) IBS-M with mixed bowel habits (i.e., >25% of bowel movements with Bristol
stool form types 1 or 2 and >25% of bowel movements with Bristol stool form types
6 or 7)
(4) Unclassified IBS-U describing those patients who meet diagnostic criteria for IBS
but whose bowel habits cannot be categorized into any of the three previous
groups.

ᐉ Dietary modification
● May benefit from exclusion of gas-producing foods ie low fermentable
oligo-, di-, and monosaccharides and polyols (FODMAP) diet ± lactose and
gluten avoidance
● Insufficient evidence to support food allergy testing
● Role of fiber controversial but in IBS-C: can consider fiber eg psyllium
ᐉ Physical activity
ᐉ Adjunct pharmacotherapy: for moderate to severe symptoms that impair QoL
● IBS-C pts who fail psyllium → PEG (improves constipation but not abdo
pain)
○ Persistent constipation despite PEG in IBS-C women →
Lubiprostone
● IBS-D pts: Loperamide 2mg 45mins pre-meal (improves diarrhea but not
abdo pain/IBS symptoms)
○ NB: Use only in limited doses/PRN if mixed constipation and
diarrhea
○ Persistent diarrhea despite Loperamide → Cholestyramine
● Abdo pain and bloating: antispasmodics PRN only if persistent pain despite
constipation
○ Persistent pain despite antispasmodics → Antidepressants such as
TCAs eg Amitriptyline 10-25mg ON
○ If depression cofactor → Antidepressants such as SSRI/SNRIs

Appendix

152
153
154
ACG/CAG Clinical Guideline: Management of Dyspepsia
[Link]

155
GASTRO 4. APPROACH TO DYSPHAGIA

Mechanical Neuromuscular
● Extrinsic compression ● Brain
○ Goitre ○ CVA
○ Mediastinal mass ○ Parkinson
● Luminal wall ○ Pseudobulbar/Bulbar palsy
○ Esophageal cancer ● Nerve
○ Gastric cancer ○ Achalasia
○ Esophagitis ● Neuromuscular Junction
■ Reflux ○ Myasthenia Gravis
■ Drug, caustic injury ● Muscle
■ Infective ○ Scleroderma
● Intraluminal ○ Myositis
○ Foreign body

HISTORY
» Complaint: Dysphagia
First differentiate between oropharyngeal dysphagia and esophageal dysphagia
● Onset: sudden or gradual
● Duration
● Characterise
o Any difficulty initiating swallowing? → oropharyngeal (neuromuscular)
o Nasal regurgitation? → oropharyngeal “Does food ever come back up your nose when you
swallow?”
o Any coughing or choking after swallowing? → esophageal (structural)
o Liquids or solids worse?
o Liquids worse in oropharyngeal, solids worse in esophageal “Where does the food
get stuck?”

156
 ● Time: constant, worst at end of day?
● Stable or progressively worse

» Causes
Structural vs Functional; Oropharyngeal vs Esophageal
● Red flags:
o LOW, LOA, haematemesis, melena, early satiety , fatigue, malaise (CA)
o Fever, night sweats, neck lump, hoarse voice (Mediastinal mass/ ext comp)
o UL/LL weakness, slurred speech, numbness (Stroke)
o Mets symptoms: eg early AM headache, bone pain, back pain, jaundice
● Any pain on swallowing
o Odynophagia suggest esophagitis or esophageal infection
● Pain in between meals (esophageal spasm, cancer)
Chest pain when swallowing
o Diffuse esophageal spasm, achalasia, systemic sclerosis
● Abdominal pain, nausea, vomiting
● Acid or water brash
● History of swallowing foreign body
● Tightening of skin, skin nodules, Raynaud’s phenomenon, finger ulcers (scleroderma)
● Ptosis; tremor, bradykinesia (Neuromuscular causes)

» Course: previous treatments, invx?

» Complications:
● Aspiration pneumonia: fever/cough with phlegm
● Malnutrition, dehydration

PMHx
● Gastritis/GERD
● MG, Parkinson’s, Multiple sclerosis, old strokes
● Scleroderma
● Malignancies, previous radiotherapy to thorax

Drug history
● NSAIDs, Aspirin, Doxycycline, Bisphosphonates, Nitrates, calcium channel blockers
● TCM, supplements

FHx
● AI conditions: MG, thyroid etc
● CTDs: RA, scleroderma
● Malignancies

Social Hx
● Alcohol and smoking
● Sexual history for HIV risk

PHYSICAL EXAMINATION **HAND RUB**

T BP HR
Ht Wt BMI
{seated down}
● Speech: Dysarthric?
● General Inspection
○ Cachexic
○ Scleroderma features over hands/face, mask like facies? Pill-rolling tremors?
● Eyes: Pallor

157
 ● Mouth: oral thrush, esophageal candidiasis, hydration
● Neck: inspect for goitre, palpate cervical lymph nodes (esp supraclavicular for GI malignancy)
● Neuro exam
○ Pronator drift
○ Tone: Parkinsonism
○ Lower CNs exam (9, 10, 11, 12) KIV proceed → bulbar/pseudobulbar palsy
○ KIV lid or proximal muscle weakness with fatigability, proximal>> distal weakness to suggest myopathy
{Gait}
{supine}
● Abdo for masses
OFFER: Bedside swallow test, DRE

INVESTIGATIONS
● STAT: FBC, CXR
------------------------------------------------------------------------------------------------------
● Blood tests:
○ FBC looking for anaemia
○ KIV RP, glucose
● Imaging: CXR looking for possible aspiration pneumonia related to dysphagia, barium swallow
where characteristic findings of achalasia, esophageal spasm and tumours can be seen
● Others: OGD to confirm diagnosis and exclude tumours

MANAGEMENT
1) Acute dysphagia TRO CVA → ED

2) Direct access gastro

158
GASTRO 5. HEPATITIS B – ACUTE OR CHRONIC

Important points
- Check for symptoms
- Complications ie liver failure
- Cause –Sexual Hx! Occupation
- Counselling:
● Course of dz chronic hep b > cirrhosis /HCC , follow up with repeat HbsAg, crisis management
● Prevent transmission, contraception, inform and protect partner/ family members, screen STD
- Report acute Hep B to CD lens
- Vaccination

Hepatitis B
Definition:
- DNA virus transmitted via sexual contact of body fluids
- Risk of developing chronicity higher the younger the person is , 5% of adults fail to clear the acute
infection
- 5 stages of infection – Immune tolerance -> Immune active/clearance -> Inactive chronic infection ->
Chronic disease -> Recovery (in most patients phase 2 goes straight to phase 5)
- Chronic Hep B = HepBsAg +ve over a period of 6 months with absence of HepBsAb
- In chronic disease low HBV DNA load and absence of HbeAg are prognostic factors for improved clinical
outcome
- At any point in time, patient can develop high viral replication/ infectivity ie Hb e-antigen positive
- Co-infection with Hep C/D increase risk of cirrhosis/HCC

HISTORY
Complaint
Symptoms of acute hep B : Typically mild, Jaundice, RHC pain, Nausea/vomiting, Anorexia, low grade fever,
myalgia, fatigability, **Aversion to food/cigarettes**
Complications: Chronic Hepatitis B/ liver failure(ABCDE)/ Cirrhosis/ HCC
Cause: Sexual contact, IVDA, blood transfusion, sharing of needles, tattooing ,

Course: What ix done, mx

Sexual Hx:
● Currently sexually active, last sexual intercourse, with who, oral/ anal/vagina, any barrier used,
men/women/both, how many sexual partners, casual sex, personal or partner hx of STD.
● Symptoms of STD: dysuria, urethral d/c, rashes, oral or perianal symptoms
Family Hx : Hepatitis B/C, liver disease / jaundice
PMHX:
Drug Hx: Steroids / TCM
Social Hx: Occupation, Alcohol , Smoking
Psych Hx:
Preventive Health: Vaccinations !

PHYSICAL EXAMINATION
Jaundiced in some acute cases
Peripheral stigmata of chronic liver dz
Abdomen: tender enlarged liver in acute hepatitis, enlarged spleen in cirrhotic liver with portal
hypertension, ascites
Edema

INVESTIGATIONS

159
 1. Acute – Serologic tests for Hep A/B/C, Liver function test, u/s abdomen
2. Chronic – 6 monthly LFT + AFP, Yearly u/s abdomen + HBeAg, if transaminitis occurs check
HepBeAg/Hep B DNA quantification, KIV refer to gastro for further management if HepBeAg +ve with
persistent transaminitis

MANAGEMENT
st
1 time HbsAg positive ● TRO acute hepatitis vs chronic carrier → symptomatic hepatitis?
LFT normal ○ Acute hepatitis ⇒ ED
● F/u: Explain the need to repeat in 6 months to see if infection resolves or
becomes chronic infection
● If pt got the infection in adulthood, most will clear the infection. If pt got the
infection as a child, more likely to become chronic infection
● Safety: Ask patient to Inform sexual partner regarding Hep B infection and
advise them to go for screening
● Explain risk of transmission, advise on contraception or abstinence unless
partner is immune
● Refer to DSC clinic for screening of other STDs
● Legal: Report MOH CD lens for acute hepatitis B
1st time HbsAg positive ● If AST/ALT >3x ULN ⇒ refer Gastro
LFT abnormal ● If <3x ULN ⇒ review 3 to 6 months with US HBS, recheck HbsAg for
seroconversion after 6 months
○ If positive then the usual Hep B carrier screen
Known Hep B carrier ● If AST/ALT >3x ULN ⇒ refer Gastro then repeat US HBS earlier
Mild LFT elevation ● If <3x ULN ⇒ repeat LFT / US HBS in 3 months, refer if AST/ALT persistently
raised/ signs of cirrhosis
● Remove other possible hepatotoxic substances eg alcohol/TCM
Known Hep B carrier, ● Refer Gastro regardless of LFT
HBeAg positive ≥40 yo
Known Hep B carrier, ● Repeat HBeAg annually
HBeAg positive <40 yo ● If transaminitis ⇒ refer
Known Hep B carrier ● Screen partner for hep B status KIV vaccinate
who wants to get ● Baby will get routine Hep B vaccination 1st dose + IVIg, and repeat hep B
pregnant status screening at 9 months
Hep B carrier chronic ● Explain that chronic hep B is usually asymptomatic and symptoms occur late
f/u ● Screen hep A KIV vaccinate
● Chronic hep B can progress to liver cirrhosis and HCC , importance of
compliance to follow up , 6monthly LFT, AFP and yearly US HBS and HbeAg
● Red flag symptoms to return
● Advise family to check status; if non immune to get vaccinated.
Lifestyle Advice for both Acute and Chronic Hep B
● Avoid alcohol/ smoking / steroids /TCM
● Do not share razor blade or tooth brush, cover your wounds
● Contraception with condoms (unless partner is Hep B immune)
● Get everyone who stays with pt, family members esp sexual partner to go for
hep B screening
● Vaccinations: Vaccinate patient against Hep A, Vaccinate sexual partners
against Hep A/B, Immediate Hep B IgG and vaccination of newborn if mother
is Hep B carrier
● Preventive Health - screen for concomitant STDs (HIV, VDRL)

160
 When to refer Gastroenterologist
Any of the following:
● Clinical signs - Jaundice, hepatomegaly, splenomegaly, ascites, pedal edema,
palmar erythema, spider naevi present
● Laboratory results abnormal - ALT / AST persistently raised over 3
months,AFP raised OR rising trend OR HBe Ag +ve at age 40 and above , Low
albumin, raised bilirubin level, Low platelet level
● U/S HBS suspicious for cirrhosis, HCC or abnormal lesions for which CT is
recommended
Hep B carrier with ● Direct access Gastro
elevated AFP ● Rule out liver failure
● Explain to patient that AFP can be elevate due to HCC, but can also be
elevated due to other reasons:
○ Chronic or acute hepatitis
○ Pregnancy
○ Other tumors: germ cell tumour, gastric cancer
Hepatitis B vaccination ● Individuals who do not respond to the initial vaccine series should complete a
non responders second vaccine series with a single-antigen vaccine (usu successful in 50-70%
of pts)
● Retest for anti-HBs 1-2 months after the second vaccination series.
● Nonresponders to the second course of vaccine should be tested for HBsAg or
HB core Ag, as some may have had undiagnosed chronic HBV infection / HB
core mutant ( does not exhibit s Ag)
● Individuals who fail to respond after 2nd vaccination series are unlikely to
benefit from further vaccination. They should be educated on how to prevent
HBV infection

Causes of vaccine nonresponders:

1) Undiagnosed chronic HBV vaccination -> check HBsAg or HB core antibody
(Hep B Core mutant who does not exhibit s antigen)
2) Patients with underlying medical conditions, such as chronic kidney disease
and immunosuppressed states, they should receive a higher dose of the
conventional hepatitis B vaccine
3) Healthy individuals who ack a dominant response gene that controls the
production of anti-HBs.
4) Technical errors due to wrong administation or storage of vaccines

Ways to enhance immunogenicity of vaccine

● Recombinant Hep B vaccine
● DNA vaccine
● Intradermal innoculation

If previously developed antibodies after vaccination and subsequently lost the

antibodies -> Considered immune, No need to revaccinate or check antibodies again

Pharmacological for Hep B

- Alpha interferon – risk of aggravating neuropsychiatric disorders (especially depression),
myelosuppression, hepatotoxicity
- Lamivudine – nucleoside analogue, risk of potentially fatal lactic acidosis, pancreatitis in paeds
- Entecavir – guanosine analogue inhibitor, lactic acidosis, discontinuation may cause hepatitis
exacerbation
- Surgery – removal of gallstones (if obstruction), Liver transplant if Cirrhotic, Surgery if HCC occurs

161
Recommendations for doctors to follow
- Add in HBeAg yearly to panel for Hep B carrier
- Do not discharge but continue to monitor seroconverted Hep B carriers (HBs Ag +ve → HBs Ag -ve & Anti
HBs +ve) at least with annual panel for Hep B carrier & US HBS. Remind these patients to inform their
specialists the risk of Hep B flare up should they develop any malignancy or autoimmune disease requiring
chemotherapy or long term steroid or immunosuppressant
- Refer to Gastro all Hep B carriers if HBeAg is still positive at 40 yrs old, regardless of status or ALT
- Refer Gastroenterology if there is persistent elevation of ALT 1-2x ULN (upper limit of normal) or signs of
cirrhosis from US HBS irregardless of positive or negative HBeAg
- Consider A&E referral if suspicious of acute Hep B flare with clinical evidence of jaundice and laboratory
finding of transaminitis.

162
163
GASTRO 6. APPROACH TO JAUNDICE

DIFFERENTIAL DIAGNOSES
1. Pre-hepatic
a. Haemolysis (G6PD deficiency, Hypersplenism, Drugs, autoimmune etc)
2. Hepatic
a. Primary HCC / secondary hepatic metastases
b. Hepatitis
i. Infections: Viral (hepatitis), bacterial, parasitic
ii. Alcoholic
iii. NASH
iv. Drugs
1. Anti TB drugs
2. Statins
3. Paracetamol
c. Chronic liver disease (many causes)
d. Hereditary: Gilbert’s syndrome
e. Vascular: Budd chiari syndrome
f. Intra-hepatic cholestasis of pregnancy
3. Post-hepatic
a. Gallstones
b. Cholangiocarcinoma
c. Pancreatic cancer
d. Cholangitis

HISTORY
» Complaint: Jaundice
● How was it noticed?
● Onset: sudden, gradual
● Course/Progression
o Recurrent: gallstones, Gilbert’s disease
● Painful or painless?
o Painful → infective, gallstones, liver abscess
● Colicky RHC pain → gallstones
● Steady RHC pain → hepatitis
● Spiking fever, chills, rigors → cholangitis
o Painless → Worry about malignancy
● Duration
● Exclude hypercarotenemia: taking a lot of orange food, scleral involvement

» Cause:
● Fatigue, exertional SOB, palpitations, non-vertiginous giddiness → Haemolysis
● Abdominal distension, pain → hepatosplenomegaly
● Pale stools and tea coloured urine, pruritus → obstructive jaundice
● LOW/LOA → malignancy
● Pruritus, bruising, ascites → chronic liver disease
● Fever + RHC pain + jaundice = Charcot’s triad for cholangitis
● Risk factors:
o Seafood (Hep A)
o Sexual history (Hep B) – MSM
o Previous blood transfusions, tattoos, IVDA (Hep B and C)
● Alopecia, dry eyes/mouth, mouth ulcers, red painful eye, rashes, jt pain → Autoimmune
● Pregnant?
● Nausea, vomiting, haematemesis
164
 ● PR bleeding, malena, BO habit

» Complications of cirrhosis (if suspicious)

● Melena or haematemesis
● Albumin: LL swelling
● Coagulopathy: easy bruising, epistaxis, gum bleeding, melena, hematochezia
● Ascites
● Encephalopathy: confusion, sleep-wake reversal
● Fatty diarrhea/Steatorrhea: pale, bulky, foul-smelling, oily, difficult to flush

PMH
● Liver disease, cancer, recent anaesthesia, blood transfusions, other autoimmune conditions
● G6PD deficiency, Thalassemia, blood disorders
● Cardiac valvular surgery, previous biliary surgery

Drug History
● Statins, antibiotics, paracetamol, NSAIDs, AEDs, antipsychotics, Methotrexate, anti-TB drugs, TCM
● Recent immunosuppression leading to hepatitis flare
● Previous Hep A and B vaccinations

FHx
● Hep B
● Jaundice (Gilbert’s syndrome)

Travel/ Contact Hx
● Hep A

Social History
● Full alcoholic history: type, amount, duration of use, CAGE
● Occupation

Psycho Hx

PHYSICAL EXAMINATION
T BP HR
Ht Wt BMI
● General inspection
○ Pallor, scleral icterus, cachexia
○ Respiratory distress
● Peripheries
○ Scratch marks, stigmata of CLD, tattoos/IVDA
○ Portal HTN: caput medusae, splenomegaly, periumbilical venous hum
● Abdomen
○ Scars
○ Hepatomegaly, splenomegaly
○ Ascites
● DRE for pale stools
● IDC: tea coloured urine?

INVESTIGATIONS
● Stat bloods:
○ FBC for anaemia and raised TW and thrombocytopenia (possible liver cirrhosis with
thrombocytopenia)
○ INR to look for coagulopathy

165
 ● Non-stat:
○ LFT to look for derangements
○ UECr
○ Glucose
○ AFP
● Others: Viral hepatitis screen
● Others @ hospital: LDH, haptoglobin
● Imaging: US HBS looking for any biliary obstruction and whether any SOL

MANAGEMENT
Diagnosis dependent
1) Hemolysis from G6PD – hemodynamically stable?
● Stop offending drug
● Aggressive hydration
● KIV transfusion for severe anemia

2) Cholangitis/Malignancy
● Cholangitis, malignancy → ED

166
GASTRO 7. APPROACH TO LOWER BGIT

DDx:
Vascular ● Hemorrhoids
● Angiodysplasia

Infective /Ischemic ● EHEC, shigella, salmonella, C diff

● Ischemic colitis

Traumatic ● Diverticular bleed

● Anal fissure

Autoimmune ● Inflammatory bowel disease (UC, Crohn’s)

Iatrogenic ● Drugs (Anti platelets, anti coagulants, NSAIDs)

Neoplastic ● Polyp
● Colorectal CA

Systemic 1. Causes of thrombocytopenia

2. Causes of coagulopathy
3. Vasculitis

HISTORY
Rectal bleeding:
● How long, intermittent/constant
● On wiping/toilet paper, mixed in stools, end of defecation
● Fresh blood or melena or dried blood or blood clots
● Any mucus, spurious diarrhea
● Previous episodes

Causes
● Other GI symptoms: Nausea/vomiting, abdominal pain, jaundice
● Diarrhea, constipation, tenesmus, change in stool caliber, bowel habits, abdo mass, LOW/LOA →
Malignancy
● Fever, Travel/ Contact Hx, Recent ABx use → Infection
● Straining, constipation, rectal lumps or masses, prev history or PR bleeding, mass prolapsing out
from anus → Haemorrhoids
● Recurrent diarrhea, PR bleeding, abdominal pain, joint pain, rash → IBD
● Other bleeding elsewhere → Drugs, systemic disorders

Course: Tx tried, previous OGD/colonoscopy

Complications
● Dehydration
● Anemia symptoms
● IO from tumour

PMHx:
● CRC, haemorrhoids, colonic diverticuli or polyps
● Other CAs
● Other conditions requiring use of NSAIDS, anti platelets etc
● Atrial fibrillation/arrhythmia/ CVRF

167
Drug History:
● Antiplatelets, anticoagulants
● NSAIDs, iron and bismuth
● Antibiotics
● TCM, supplements

Social Hx: W A S H E D

FHx:
● Colorectal carcinoma, inflammatory bowel disease, polyps

PHYSICAL EXAMINATION
T BP HR SpO2 Wt BMI
[seated down]
- Eyes: conjunctival pallor
- Mouth: oral ulcers
- Rash: erythema nodosum, pyoderma gangrenosum
- Pulse regular?
- Supraclavicular LN

[lying down supine]

- Abdo for masses, organomegaly, tenderness
- DRE

INVESTIGATIONS
● STAT tests: FBC, INR
● Others: RP, ECG if suspect AF, barium enema, colonoscopy

MANAGEMENT
Hemorrhoids ● Lifestyle mods: high fibre diet, exercise, adequate hydration
● Daflon
○ 2 tabs TDS x 3/7 then 2 tabs BD x 3/7 then 2 tabs OD x 3/7
OR
○ 2 tabs BD x 1/12
● Fybogel
● Proctosedyl ointment
● KIV colonoscopy for band ligation
● Thrombosed piles within 3/7 → can I&D
C difficile diarrhea ● Stool CD toxin
● Stop offending antibiotics
● Metronidazole 400mg TDS x 10/7
● Hand hygiene: handwashing (alcohol rub NOT effective)
Inflammatory bowel ● Rule out other causes of BGIT
disease ● MUST DO FBC
● Co-manage with gastro. Direct access or ED.

● Mild
● Mod: 4-6 bloody diarrhea, mild anemia, low grade fever
● Severe: >6 bloody diarrhea, fever, anemia, tachy, rapid weight loss
Diverticulosis ● Refer colorectal for colonoscopy
● Refer ED if haemodynamically unstable

168
GASTRO 8. APPROACH TO TRANSAMINITIS

CAUSES: Pre hepatic vs Hepatic vs Post-hepatic

Mild transaminitis - VITAMIN
Infection Chronic viral hep B, C
Acute Hep A
Any acute viral infection
Toxins / Alcohol
Drugs Acute: Statins, Allopurinol, Aspirin, Augmentin, INH, Lisinopril, Losartan, NSAIDs, Risperidone,
Valproate
Chronic: OCP
Autoimmune Autoimmune hepatitis, PBC
Metabolic NAFLD, NASH
Pregnancy (pre-eclampsia, acute fatty liver)
Endocrine Thyroid disorders: hypothyroid, hyperthyroid
Adrenal insufficiency
Ischemia Ischemic hepatitis in AMI / CCF
Neoplastic HCC
Mets
Muscle Myopathy
Strenuous Exercise / Rhabdomyolysis

Name/Age/Sex

BIOLOGICAL

Acute Chronic illness Medical History

Complaint: Raised ALT/AST Cause ● Medical/

Course Surgical Hx
Cause Control ● Drug Hx/
● Abdominal pain, Vomiting Compliance Drug
● Jaundice Complications allergies
● Tea-coloured urine, pale stools, Pruritus ● Medicatio
● New drugs/changes in dose Comorbidities n List
○ Statin, Paracetamol toxicity ● HLD ● TCM/OTC
● TCM, supplements? ● DM
● Alcohol? ● Obesit
● Fever/ URTI/ GE symptoms (non hepatic viral infection) y
● Recent blood transfusions, Tattoos, IVDA ● Thyroi
● Sexual Hx: casual sex, multiple sexual partners, unprotected, d
hx of STD Crisis Mx
● Travel (hepatitis A endemic areas) or contaminated
water/food
● Contact (with persons with jaundice)
● FHx of hepatitis B or liver disorders (vertical transmission or
autoimmune)
● Pregnancy

169
 ● Thyroid symptoms
● Chest pain /SOB/ LL swelling (AMI/CCF)

Course: Full LFT? US HBS?

Complications
● Liver failure (ABCDE)
○ Hypoalbuminemia → LL swelling
○ Bilirubin → Jaundice
○ Coagulopathy → Bruising
○ Ascites → Abdo distension
○ Encephalopathy
● NAFLD → at higher risk of cardiovascular dz, screen for CVRF

Disease Prevention Family Hx

↣ Vaccinations: Hep B, Hep A ↣ Malignancy

↣ Cancer prevention: ↣ Hepatitis B

PSYCHOLOGICAL

PHQ-2 ICE
GAD-2

SOCIAL

Drugs (Smoking, alcohol, illicit drugs) Function

Sexual Hx (partners, protection, prev STI, )

PHYSICAL EXAMINATION ***HAND RUB***

BP HR Ht Wt BMI
{seated} General inspection: Jaundice?
Stigmata of chronic liver disease
Neck: cervical LNs
{lying flat} Abdomen: Hepatomegaly? Splenomegaly? HSM? Ascites
JVP, pedal edema, Heart S1 S2 (for suspected hepatic congestion from CCF/AMI)

INVESTIGATIONS
● FBC (to calculate NAFLD score)
● LFT with GGT
● Hep B, C, Hep A screen
● US HBS
● Lipid panel / Fasting glucose if fatty liver
● KIV TFT
● KIV TIBC, Ferritin – haemochromatosis

MANAGEMENT
Scenarios
1) Fatty Liver Non-pharmacological
● Weight loss is the mainstay of treatment: Aim to lose 5-10% of body-weight over 6
months or / 0.5 - 1kg per week or 2kg per month

170
 ● Lifestyle modification for weight loss: Low-fat , low-carbohydrate, or Mediterranean
diet, avoid fructose-containing beverages and foods
● Avoid all alcohol consumption( associated with disease progression)
● Hep A & B vaccination
● Screen / Control other CVRF: DM , HTN, HLD
● Calculate NAFLD score to predict risk of fibrosis
Pharmacological
● Stop offending agent
Education
● Explain risk of progression to Non alcoholic steatohepatitis (NASH) (liver inflammation)
which can progress to cirrhosis and HCC
● Go ED if develop severe abdo pain / Vomiting / jaundice
Follow-up
● Repeat LFT (3-6 months)
● Refer if
○ ALT persistently > 120IU OR
○ AST increasing trend OR
○ Low albumin OR
○ Low platelet OR
○ Elevated total bilirubin/ globulin OR
○ US shows cirrhosis/ coarse or nodular echotexture
○ LFTs not better with weight loss

2) Recalled for ● If obvious cause for raised LFT >3x ULN → no need to refer, remove the underlying
abnormal LFT cause, hold off statins temporarily KIV restart when LFT improves
● 3 months after starting/increasing statin, ALT/AST raised but <3x ULN → continue
statin
● After starting/increasing statin, ALT/AST raised but >3x ULN → stop statin
● Pt’s ICEKAPS about statin vs liver injury

3) Drug ● Stop the offending cause

induced ● If AST/ALT >3x upper limit, stop statins first even if it is not the cause of transaminitis
as you will be concerned about problems with statin metabolism when there is liver
injury

4) 2o to ● CAGE questionnaire: 2 points or more → Screening test positive for alcohol use
alcohol intake problem
● Gradual reduction in alcohol intake to prevent alcohol withdrawal
● Thiamine 100mg OM
● Refer to NAMS

A standard alcoholic drink contains 10 grams of alcohol. This roughly equates to:
● A can (330 ml) of regular beer with 5% alcohol content
● Half glass (100 ml) of wine with 15% alcohol content (glass height = 15cm)
● A shot (30 ml) of spirits with 40% alcohol content
Recommended alcohol limits
Men should drink no more than two standard drinks per day
Women not more than one standard drink per day.

5) Patterns of liver test abnormalities – LFT abnormalities can often be grouped into one of
several patterns: hepatocellular, cholestatic, or isolated hyperbilirubinemia

AST:ALT ratio

171
An AST to ALT ratio of 2:1 or greater - alcoholic liver disease, particularly in the setting of an
elevated gamma-glutamyl transpeptidase
ALT > AST : Other causes ie viral hepatitis

172
Appendix

173
174
GASTRO 9. APPROACH TO VOMITING AND NAUSEA

Gastrointestina Hepatobiliary
l Cholecystitis/ Cholangitis Fever, Abdominal pain, Jaundice
Hepatitis
Pancreatitis

Intestinal Reflux
GERD Diarrhoea, abdo pain , LOA
Gastroenteritis / Colitis /Appendicitis Constipation, abdo distension
Intestinal obstruction / Gastric obstruction (Head
of pancreas CA, gastric CA)

Genitourinary Pyelonephritis Dysuria, increased urinary

Uremia frequency, urgency
Flank pain, high fever

Neurological Meningitis Rash, neck stiffness, fever

Head injury Hx of HI
Raised ICP - SOL / ICH Headache, neuro deficits

Metabolic DKA/HHS Bg of poorly controlled DM

Thyrotoxicosis Tremors, heat intolerance

Otology Otitis Media / Meniere /Vestibular dysfunction Ear pain, hearing loss, vertigo

Systemic Pregnancy! / Pre-eclampsia LMP !

Drug Hx / alcohol / chemotherapy Drug Hx / alcohol / chemotherapy
Fever
Sepsis CP, SOB
AMI

HISTORY
- Complaint: Nausea / Vomiting
● Contents of vomitus: Undigested food / digested food / liquid, gastric secretions, bilious fluid
● Colour of vomitus: yellow bilious liquid , coffee ground vomitus , fresh blood
● Timing: >1hr after meal (GOO, gastroparesis), early morning (raised ICP, pregnancy)
● Projectile: pyloric stenosis, raised ICP
- Cause: Rule out differential diagnosis as above
- Complications ie dehydration / hypovolemia/ electrolyte imbalance, ability to take orally -> Decide
whether can manage outpatient or need hospitalization
** Drug Hx
** Pregnancy – last LMP

PHYSICAL EXAMINATION
T BP HR Postural BP!
BMI
Jaundice (hepatobiliary)
Tongue dry, capillary refill
Goitre

175
Abdomen: scars (adhesion I/O), distension (obstruction), hernias (obstruction), tenderness, BS (ileus)
Succussion splash
KIV Neuro exam / Otoscopy

INVESTIGATIONS
Stat tests
● FBC – infection
● UPT ! – women of childbearing age
● KIV AXR: mechanical obstruction

Other tests
● Renal Panel ( Na, K, Cr , Ur) – electrolyte imbalance
● LFT – For upper abdominal pain , jaundice
● TFT – If symptoms of hyperthyroidism

Further tests: OGD – Refer specialist

MANAGEMENT

176
GERI 1. APPROACH TO MEMORY LOSS
Possible Scenarios
1) New onset memory loss ﹡Hx: TRO delirium, depression, reversible
causes of dementia
﹡Mx: Dementia labs

2) Memory loss and request for AMD/ LPA

3) Alzheimer’s dementia on f/up with OPS

Differential Diagnosis: 3D
DEMENTIA DSM 4 criteria (see below): Amnesia + agnosia/aphasia/apraxia/executive function
loss

Reversible causes of dementia similar to delirium (DEMENTIA: Drugs, Emotion,

Metabolic (hypothyroid, hypercalcemia, vit b12 def), Eyes and Ears, NPH, Tumor,
Infections, Anemia and Alcohol)
Irreversible: alzheimer’s , vascular , frontotemporal dementia, lewy body , PD with
dementia

DEPRESSION If present, MUST exclude

- Bipolar
- Psychosis

DELIRIUM (AICD) Acute and fluctuating

Inattention
Conscious level changes
Disorganized thinking

Causes - DELIRIUMS: Drugs, Ears and Eyes, Low oxygen, Infection, Retention of
urine/stools, Intracranial ie stroke /infection/SOL/, Under hydration, Metabolic
(hypoglycemia, vit B12 def, hypothyroidism), Surgery/Sleep

HISTORY
Complaint: Memory loss
● Did anyone come with you today
● Duration: Acute vs chronic (6/12)
● Onset: Sudden, stepwise, gradual, any precipitating events?
● Characterize: STML or LTML. Give examples.
● Time: Progressively worsening, stable, or fluctuates
Causes
● Rule out depression: PHQ2 → if positive → PHQ9
● TRO Delirium: Ask for acute and fluctuating course, inattention, disordered thinking (ie irrelevant
speech, illogical flow of ideas), altered mental status, sleep wake issues etc (best from
collaborative history)
○ If positive , Ask for possible causes of delirium: Drugs or withdrawal, infection symptoms,
hypoglycemia, vision or hearing difficulty, urinary or bowel retention, chest pain
● Dementia: Check aphasia, agnosia, apraxia, loss of executive functioning
○ Irreversible: Alzheimer, Vascular, Frontotemporal, Lewy body dementia

177
 ○ REVERSIBLE SECONDARY CAUSES OF DEMENTIA : hypothyroid symptoms, vision, hearing,
hx of CA, feet numbness, urinary incontinence. Any head HI, one sided weakness/
numbness, change in personality, visual hallucinations
Course
● Any ix done
● Timeline of symptoms, speed of progression
Complications
● Any safety issues ie leave the stove on, got into accidents while driving
● Affected function? bADL, iADL -DEATH and SHAFT
● BPSD in dementia

Med Hx: Any hx of strokes, dementia, depression

Drugs: Any recreational drugs/ OTC/TCM/ anti-histamines/ anti cholinergic/ anti-psychotics / OHGAs
Family history: dementia, depression
Preventive

Psycho: PHQ2? GAD2? bipolar / psychosis (if found to have depression), Hx of psychiatric illness
ICE:
Social
● Work
● $
● Smoking/alcohol/drugs
● Home environment
● Exercise
● Diet
● Caregiver stress
● *** AMD and LPA
Function
● bADL, iADL: DEATH SHAFT, How is patient getting food? How is patient managing medications?
● Falls
● Cognition
● Bladder/bowel
● Eye/ENT/swallowing

PHYSICAL EXAMINATION
SHORT CASE LONG CASE
T BP HR T BP HR
Head: Head:
ᐉ AMT score: PARTY x 2 (education level?) ᐉ AMT score: PARTY x 2 (education level?)
Place and Prime minister Place and Prime minister
Age and Address Age and Address
Recall and Recognize Recall and Recognize
Time and Twenty to one Time and Twenty to one
Year now and Year of birth Year now and Year of birth

178
 ᐉ Eyes: pallor
ᐉ Neuro UL: ᐉ KIV neck: goitre (can omit if no thyroid
● Pronator drift symptoms)
● Dysmetria
● Tone: lead-pipe rigidity, cogwheeling Gait (to bed):
● Proprioception ᐉ Parkinsonism? Broad-based? Ataxic?

Stand: Lie on bed:

ᐉ Romberg ᐉ Lying postural BP
ᐉ Neuro UL:
Gait: ● Pronator drift
ᐉ Parkinsonism? Broad-based? Ataxic? ● Dysmetria
● Tone: lead-pipe rigidity, cogwheeling
Mental state exam: Depression ● Reflexes
● (KIV power if there’s time)
● Proprioception

Stand: (take further social Hx)

ᐉ Romberg
ᐉ Standing postural BP

Mental state exam: Depression

Offer: Offer:
● MMSE ● MMSE
AMT
● 7 and below is FAIL
○ 0-6 years education: must get 7/10
○ >6 years education: must get 9/10
○ Unadjusted: must get 8/10

INVESTIGATIONS
● Stat: FBC
● RP, LFT, CaMgPO4, TFT, Vit B12, glucose, (KIV Syphilis screen with VDRL/RPR, HIV screen)
● ECG

MANAGEMENT
● Delirium: Treat underlying cause
● Depression: Ensure not actively suicidal to allow outpatient treatment. CBT, supportive therapy.
SSRI. follow-up.
● Dementia (see geriatric giant notes): Correct reversible causes of dementia first

Counselling followed by ABCDEF

Counselling - Progressive disease, pt may eventually require greater level of care
- Aim to slow down the rate of progression but not cure

Activities of daily living - Find out his goals of care

- Keep him as active as possible within safe limits , do not restrict them from
doing activities, can worsen cognitive decline
- Regular exercise

179
 BPSD - Screen for depression, anxiety, wandering, sleep- wake reversal , agitation

Cognition - Monitor with MMSE

Drugs - Avoid polypharmacy and meds that can affect cognition

Environment / Social - Caregiver stress

- Financial difficulties
- Elder abuse !!
- Community resources available:
● Home: Home medical, HNF, meal on wheels, FDW levy concession,
Home Help services (Pack Medication, personal hygiene)
● Community: Senior activity centre, Dementia Day care, Social day care,
Day rehab centre

Functional/ Rehab - Home safety, driving safety

Needs - bADL/iADL, Falls, Bladder, Bowel, Eyes, Ear, Throat (Swallowing, Nutrition)
- Fall risk assessment

Indications for CT brain (no consensus) for evaluation of dementia

- Unusual features
o Age <60
o Rapid decline in cognition (<2/12)
o Dementia of short duration (<2 years)
o Unusual or atypical cognitive symptoms (e.g. progressive aphasia)
- Likely to find a bleed
o Recent significant head trauma
o New onset severe headache, seizures
o Use of anti-coagulants
o History of bleeding disorder
- Likely to find a SOL
o History of CA (with potential for brain METS)
o New-onset focal neurologic deficits
- Likely to find NPH
o Urinary incontinence and gait disturbance early in dementia

180
GERI 2. FALLS IN THE ELDERLY
Possible Scenarios:
1. Multifactorial causes for falls in elderly ie Polypharmacy, OA knees, Visual Impairment
2. Recurrent falls with multiple bruises secondary to elder abuse

HISTORY – PRECIPITATING, PREDISPOSING, COMPLICATIONS

History of fall Prefall – (does pt remember?)
● Mechanism/ Circumstances / Location (What were you doing, Were you
getting up from the bed ie postural related, Where were you), any witness,
time of day
● Associated symptoms – giddiness, chest pain , SOB , one sided weakness,
numbness , unsteady gait, fever, vomiting, diarrhoea, bleeding GI
During the fall – any HI/ LOC , jerking of limbs
After the fall – any injuries and ability to get up, incontinence/ Todd’s paralysis
Causes Vascular - CNS (strokes/TIA), CVM (MI/dissecting aneurysms), GI (anaemia 2’
bleeding GIT)
Infections - urosepsis, pneumonia
T
A
Metabolic - electrolyte imbalance (dehydration/GI losses), hypoglycemia,
hyperglycemia
Iatrogenic - medications (postural hypotension, sedatives)
N

Predisposing CNS Cognitive impairment / Dementia / Confusion/

factors Depression
(INTRINSIC)
Neuromotor Parkinson’s disease
Cervical / Lumbar Myelopathy
Cerebellar degeneration / Stroke

Proprioception Peripheral neuropathy

Vision Cataracts
Glaucoma
Senile macular degeneration

Vestibular BPPV

Musculoskeletal Arthritis
Deformities
Muscle weakness

Predisposing 1. Poor lighting

Factors 2. Inappropriate eyewear/foot wear
(EXTRINSIC) 3. Uneven flooring, Loose carpets / clutter
4. Inappropriate furniture height
Precipitating ❏ Any Previous falls, is it recurrent falls (≥2 within 6 months), what were the
factors circumstances surrounding those falls?
❏ Acute or chronic medical problems
Complications Complications of Falls
from fall ● Fractures: hip, vertebral, others
● Head injuries
● Soft tissue injuries, lacerations, haematomas

181
 ● Fear of falling → self imposed restriction in mobility/activities → fnal decline
Complications of Immobility
● Soft tissue / MSK: Muscle wasting, bed sores
● ARU
● Constipation
● Hypostatic pneumonia
● DVT / PE
● Postural hypotension
● Aggravation of osteoporosis
● Depression
PMHX/ Surgical Hx
● Ask what was being done
● Medication changes
● Complications
Drug Hx (see above)
● Any drug allergies
● OTC/TCM
● Polypharmacy → try to cut down on unnecessary medications
● Any meds that can predispose to falls ie anti-histamines, cough/flu meds, anti-HTN,
benzodiazepines
Family Hx
Social Hx/ Functional Hx – 4 + 4 C
Work
Accounting
Smoking, Alcohol
Home: married/single, children (how often do they visit?), who do you stay with
Exercise
Diet
Coping, Safety concerns
Capability: bADL DEATH, iADL SHAFT (esp in elderly, falls, osteoporosis pt); PU, BO; Eye, Ear, Swallowing
Cognition
Care: self, Caregiver
Community

Home Assessment
What kind of housing do you stay in? HDB, any lift landing?
Any steps to enter your house or in your house / uneven flooring?
An difficulties moving around in your house?
Any grab bars in the toilet?
Is there enough lighting at home?

Psychiatric Hx: PHQ2 / GAD2

Preventive Health: Cancer Screen, Consider Vaccination

PHYSICAL EXAMINATION (HEAD TO TOE)

1. Look at the patient overall for any injuries and ask for pain: scalp hematoma, bruises, swollen joints,
bleeding
2. MSE: Cognition, Mood
3. KIV Neck (if dementia suspected): inspect for goitre
4. Pronator Drift
5. UL: Dysmetria, Tone (cogwheeling?), Power (prox shoulders + distal fingers)
{Stand up} 6. KIV Timed Up And Go (normal <10s)

182
{Lie 45o} 7. CVS exam: HR, Palpate apex beat, Auscultate (arrhythmias, bradycardia, murmurs
(AS?))
{Lie Supine} 8. Postural BP + HR: supine + HR
9. Lower Limbs: » Sensory (dermatome + KIV glove and stocking)
» Proprioception
10. Knee or Hip exam or Feet exam: joint line tenderness, ROM, crepitus
{Stand up for 3 mins}
11. Romberg’s
12. Eyes: Visual acuity / Cataracts / Pallor (KIV Snellen chart)
13. Tongue: hydration
14. Postural BP + HR: standing BP + HR (Take social Hx while pt is standing)
● Drop of systolic ≥20mmHg and diastolic ≥10mmHg
● Do you feel giddy and is it the same as how you felt before you fall
15. KIV screen mental status: AMT (PARTY x2)
16. Look at footwear

INVESTIGATIONS
● Bloods: FBC, UECr, Glucose, vit B12, TFT, vitamin D
● BMD assessment
● ECG – for arrhythmias!
● Other tests depending on hx and results eg neuroimaging, EEG, ambulatory cardiac monitoring

MANAGEMENT – MULTIDISCIPLINARY
1. Treat underlying cause e.g. AMI, sepsis, osteoporosis
2. Medication Review: Eliminate drug, reduce dose or substitute
Medications that increase risk of falls
Drowsiness / unsteadiness / Central acting drugs Tranquilizers
giddiness BZDs
TCAs
phenothiazines
Antihistamines
Codeine containing mixtures
Analgesics / Narcotics
Postural hypotension Vasodilators Anti-hypertensives
Anti-psychotics CVS drugs
Anti-parkinsons
Anti-depressants
Anti-cholinergics
Extrapyramidal effects Anti-psychotics Haloperidol, risperidone
Metoclopramide
Vestibular toxicity Aminoglycosides Gentamicin
High dose loop diuretics
Electrolyte abnormalities Diuretics HCTZ, Frusemide

3. Modify predisposing factors: Treat postural hypotension / correct vision / Vit D def / Osteoporosis
Postural Hypotension
Causes Idiopathic
Drugs induced
Hypovolemia (Dehydration, Anemia)
Autonomic failure due to neurological dz ie parkinsonism, DM or medications

183
 Treatment Non pharmacological
● Review medications
● Correct hypovolaemia – encourage hydration
● Pressure stockings (Check pulses first before prescribing!)
● Abdominal binder
● Behavioural modifications eg exercise, drink cup of water before getting out of
bed
● Elevate head of bed and get up slowly, cross your legs when sitting
Pharmacological
● 1st line Fludrocortisone: salt and water retention to increase intravascular
volume
○ SE: fluid overload, supine hypertension, hypokalemia
○ Start at 0.05mg once/ day to max 0.2-0.3mg/day
nd
● 2 line or add on: Midodrine
● Ergotamine – cause vasoconstriction
● If pt has supine hypertension and postural hypotension, give anti-
hypertensives at night + Fludrocortisone in the morning

Vision Impairment: 3 components of vision

I. Visual acuity – cataracts, glaucoma
II. Contrast sensitivity – e.g. problems recognizing edge of steps
III. Depth perception

Osteoporosis / Vit D Deficiency

● Vit D: 15-20 mins of sunlight daily, need 800-1000 IU/day
● KIV bisphosphonates or Denosumab
● Calcium supplements: 1000mg for general population, 1200mg if osteoporotic

4. Treat complications
5. Cognition and mood
a. Poor safety awareness
b. Judgemental errors
c. Overestimation of capacity
d. Failing to remember limitations and impairments
e. Hallucinations, restlessness causing wandering, delusions
f. Visuospatial dysfunction
g. Agnosia
h. Apraxia
i. Loss of proprioception, gait and balance

Management
Environmental manipulation ● Reducing amount of furnishings
● Appropriate furniture height
● Safety equipments e.g. grab bars
Behavioural strategies ● Provide activity to counteract inactivity
● Identify cause of wandering e.g. stress, noise, hunger
Supervision and personal protection ● Alarm systems
● Protective garments e.g. hip protectors

6. Physiotherapy: Exercises for neuromuscular strengthening ie resistance band, taichi, walking

★ Problems with: balance, strength, endurance, and gait

184
 ★ Treat underlying disorder e.g. Parkinson’s dz, cervical myelopathy
★ Rehabilitation: gait and balance training, vestibular rehab, exercise
★ Assistive devices & training in their usage: walking sticks / frames
7. Occupational therapy: for home modification
★ Home assessment by occupational therapist and appropriate modifications
★ HDB Ease programme
★ Modify clutter, stairs, walking aids and footwear
★ Improve lighting, add grab bars, correct furniture height, avoid use of restraints, padded
flooring materials
8. Podiatry: Footwear modification
★ Ill-fitting shoes? Recommend shoes with low heel height, high surface contact area may
reduce risk for falling
9. Fear of falling / Education of risk taking behaviours
★ Climbing stairs, standing on unsteady chairs, wearing poor fitting shoes, walking in socks, not
using mobility devices prescribed

COMPLICATIONS
Complications of Falls
● Fractures: hip, vertebral, others
● Head injuries
● Soft tissue injuries, lacerations, haematomas
● Fear of falling causing self imposed restriction in mobility/activities – leads to functional decline

Complications of Immobility
● Muscle wasting
● ARU
● Constipation
● Bed sores
● Hypostatic pneumonia
● DVT / PE
● Postural hypotension
● Aggravation of osteoporosis
● Depression

Gait disorders classified by sensorimotor levels

Low Peripheral · Unsteady uncoordinated gait
sensory
Peripheral motor Arthritic · Antalgic gait ± Trendelenburg’s sign
Myopathic / · Prox. Myopathy – waddling gait and foot
neuropathic slap
weakness · Distal myopathy – foot drop resulting in
high steppage gait & foot slap
High Spasticity Hemiplegia, Unilateral circumduction, knee hyperextension,
hemiparesis talipes equinovarius, ± lack of arm swing
Paraplegia, Bilat circumduction, scissoring, short shuffling and
paraparesis scarping steps
Parkinsonism Small shuffling steps, festination, propulsion,
retropulsion, turning en bloc, absent arm swing,
hesitation

185
Cerebellar ataxia Wide based gait with trunk sway, irregular stepping
Cautious gait Widened base, shortened stride, decreased velocity,
en bloc turns

186
GERI 3. URINARY INCONTINENCE

Transient causes Delirium

(DIAPPERS) Infection
Atrophic vaginitis
Pharmaceuticals – anticholinergics (urinary retention), diuretics
Psychiatric – depression
Endocrine – diabetes mellitus, diabetes insipidus, hypercalcaemia
Restricted mobility
Stool impaction

Established Functional problem ▪ Impaired cognition (dementia)

causes (Anatomy is normal) ▪ Environmental (unfamiliar env, restraints, inaccessibility of
toilet)
▪ Mobility problem e.g. hemiplegia, PD
▪ Increased urine production e.g. diuretics

Failure to store 1. Detrusor overactivity

(Urge or stress ▪ Stroke
incontinence) ▪ Parkinson’s disease
▪ Spinal cord injury
▪ Lower tract irritation e.g. tumour

2. Outlet incompetence
▪ Weak pelvic floor
▪ Intrinsic urethral weakness

Failure to empty 1. Detrusor underactivity

(Overflow ▪ Stroke
incontinence) ▪ Spinal cord disease
▪ Autonomic neuropathy – DM
▪ Chronic distension
▪ Primary detrusor hypocontractility

2. Outlet obstruction
▪ Detrusor-sphincter dyssynergia
▪ BPH, urethral strictures (urethral obst)
▪ Bladder stone, tumour (vesical obst)
▪ Pelvic organ prolapse

Name/Age/Sex

BIOLOGICAL

ACUTE CHRONIC ILLNESS MEDICAL Hx

Complaint: Urinary Incontinence Cause Medical/ Surgical

● Type: Course Hx
○ Stress (urine leaks on coughing, sneezing, Control
laughing, change of posture) Compliance Drug Hx/ Drug
○ Urge (feel like going to toilet but urine leaks out Complications allergies
before reaching) Checking

187
 ○ Overflow (leak occurs spontaneously without Competency Medication List
triggers) ● Diuretics
● LUTS: Comorbidities
○ Irritative (UTI, bladder stone, tumour) ● BPH TCM/OTC
○ Obstructive (BPH, stricture) ● Stroke
Cause ● Parkinson’
● Any behavioural change/confusion (delirium) s
● Fever/infective symptoms (infection) ● Spinal
● Pruritus/dryness over perineal region (females → cord
atrophic vaginitis) disease
● Any new medications/medications list (pharmaceutical) ● Obstetric
● Low mood/crying (psychological) history
● Polyuria/polydipsia/polyphagia (endocrine → DM, Crisis
diabetes insipidus) management
● Recent surgeries/strokes/falls/fractures (restricted
mobility)
● Constipation (stool impaction)
Course
● Duration of incontinence
● Previous treatments
● Previous medical consultations
Complications
● Function: mood, BADLs
● Sexual dysfunction
● Sleep disturbances

DISEASE PREVENTION FAMILY HISTORY

- Vaccinations
- Cancer prevention:

PSYCHOLOGICAL

PHQ-2 I: part of aging

GAD-2 C: Affecting life?
E: Medications to
relieve symptoms

SOCIAL

Home/Environment – triggers?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sleep

PHYSICAL EXAMINATION
T BP HR
[seated] Mental state exam
AMT
[supine] Abdominal exam
DRE
Neurological examination (if suspicious for stroke/parkinson’s/spinal cord disease]

188
 PV if female

INVESTIGATIONS
● UFEME / urine dipstick TRO infection
● AXR: fecal loading

MANAGEMENT
Non pharmacological
○ Decrease intake of caffeine and alcohol
○ Decrease fluid intake in general (to 1.5-2L per day)
○ Prevent constipation
○ Bedside urinal, diapers, catheterisations
○ Home modifications
○ Behavioural strategies:
Cognitively impaired
● Prompted voiding - bring patient to toilet just before voiding
● Scheduled voiding - get patient to void at fixed time intervals
Cognitively intact
● pelvic floor exercises
● urge inhibition (squeeze pelvic muscles and keep still with deep breathing and wait for urge
to subside)
● Stress adaptation (brace pelvic muscles before coughing, sneezing, laughing or carrying
heavy objects)

Pharmacological
● Anticholinergics: oxybutynin, tolteridine
● Typical estrogens: premarin cream, vagifem → useful for atrophic vaginitis
● Alpha-adrenergic antagonists: prazosin, terazosin, alfuzosin → useful for benign prostatic
hyperplasia
● Surgery for bladder outlet obstructions eg BPH

189
GS 1. COLONOSCOPY SCREENING GUIDELINES

190
GS 2. GYNAECOMASTIA

CAUSES:
1. Hypogonadism/ Testicular conditions
a. Tumours
b. Infections (mumps, HIV)
c. Trauma/ Torsion
d. Previous radiotherapy
2. Tumours
a. Adrenal tumours
b. Bronchial tumours – producing hCG
3. Chronic liver disease
4. Drugs: Frusemide, Sprinolactone, Digoxin, oestrogens, finasteride, marijuana
5. Endocrine: Acromegaly, Hyperthyroidism
6. Alcohol excess – toxic to Leydig cells
7. Congenital
a. Klinefelter’s syndrome (47 XXY)
b. Kallman’s syndrome
8. Hypopituitarism

Questions:
Gynaecomastia
● Unilateral or bilateral
● How long, onset, duration

● Hypogonadism:
o Loss of libido, lethargy, low mood, infertility, erectile dysfunction, diminished hair growth,
smaller muscle bulk, small testes
o Abnormal growth at testes? Loss of weight?
o Testicular pain, erythema, swelling? – current and previous
o Trauma to testes
o Previous radiotherapy to testes
● Tumours: loss of weight, loss of appetite
● History of liver problems?
o Jaundice, pruritus, easy bruising
● Acromegaly: change in facial appearance, change in shoe size, change in size of hands and feet
● Hyperthyroidism: Heat intolerance, weight loss, increased appetite, tremors, diarrhea
● Hypopituitarism: (GH, then FSH/LH, prolactin, TSH, ACTH)
o Lack of GH: central obesity, dry skin, weakness, decreased exercise ability
o Hypothyroidism symptoms
o Hypocortisolic symptoms: fatigue, postural giddiness, nausea, vomiting

PMHx: Conditions above; conditions requiring use of medications that cause gynaecomastia
Drug history:
● Frusemide, Spironolactone, Digoxin
● Oestrogens
● Finasteride
● Marijuana
Social history: Ethanol ingestion

191
 HAEM 1. APPROACH TO ANEMIA
Definition
- Microcytic: <80 fL vs Normocytic: 80-96 fL vs Macrocytic: >96 fL
- Anaemia: WHO criteria <13 in men and <12 in women
- Ferritin: Using threshold <30 to diagnose iron deficiency has good sensitivity and specificity.

Ddx
Microcytic Normocytic Macrocytic

Iron deficiency Cancer associated anemia B12 deficiency

Thalassemia CKD Folate deficiency

Hemolytic anemia Alcoholic

Acute blood loss Liver disorders

Anemia of chronic disease Myelodysplastic / Leukaemia

Hypothyroidism (Both normo and macro)

Name/Age/Sex

BIOLOGICAL

Acute Chronic illness Medical History

Complaint: Anaemia Cause ● Medical/ Surgical

● Symptomatic or asymptomatic? Course Hx
Cause Control - GI surgery ,
● GI: BGIT? Scopes done? LOW/LOA/altered bowel habits/ PR ● Home malabsorption
bleed/ melena/ haematemesis? ● Clinic
● PV: Menorrhagia? Compliance ● Drug Hx/ Drug
● Hematuria? ● Non pharm allergies
● Dietary iron intake? Vegetarian? ● Pharm - Blood thinners

192
 ● Bleeding disorder? Complications - NSAIDS/ Steroids
● Family history of thalassemia? Any thalassemia screen? ● Disease - TCM/OTC
● History of renal failure? ● Treatment
● History of cancer? Checking ● G6PD def
● History of hypothyroidism? Cold intolerance, constipation? Competency
● History of liver disorders?
● Alcoholic? Comorbidities
● Jaundice? Triggering drugs in G6PD pt? Crisis management
Course
● Any investigations done before?
● OGD/colono/ Iron studies, renal panel, LFT, TFT, FOBT
Complications
● SOB/ Chest Pain / Giddiness / Reduced effort tolerance
● AMI/ CCF symptoms

Disease Prevention Family Hx

- Vaccinations Fhx of malignancy

- Cancer prevention: FOBT, PAP smear, MMG if relevant Fhx of thal

PSYCHOLOGICAL

PHQ-2 I
GAD-2 C
E

SOCIAL

W bADL (DEATH)
A iADL (SHAFTTT)
S Cognition
H Bladder and bowel
E Eye, ear and
D swallowing

PHYSICAL EXAMINATION ***HAND RUB***

T BP HR Postural BP
[seated]
1. General inspection: Pallor, jaundice. Angular cheilitis, koilonychia, atrophic glossitis
2. Neck: Lymph node. Goitre.
[supine]
3. Abdominal exam: Stigmata of chronic renal failure/ liver disorders. Supraclavicular LN, abdomen for
masses.
a. Offer DRE to look for SOL.
4. ± Cardiovascular exam: Auscultate for murmurs (flow murmurs)
5. ± Pelvic exam (if history of menorrhagia)

INVESTIGATIONS
Depends on what is suspected:
● Iron studies, thalassemia screen, B12, folate
● TFT, renal panel
● OGD/colonoscopy
● US pelvis for fibroids

193
MANAGEMENT
1. Iron deficiency
anaemia

Non-pharm:
● Dietary iron: eggs, oysters, lean red meat, dark leafy greens + vit C
● Treat underlying cause (e.g. menorrhagia, BGIT). For pre-menopausal
woman, can try iron replacement and check for correction. If not
corrected with iron supplementation, investigate for occult BGIT.
Pharm: Oral iron supplementation* Maintain 3/12 from Hb normalization
Gluconate>Sulfate>Fumarate
● Disposition: Threshold for transfusion is <7 for most, <8 if cardiac
conditions

● Followup:
○ FBC: Expect increase of 1g/dL per month

2. CKD anaemia ● Target Hb 10-11.5g/dL (uptodate)

Non pharmacological
● If Fe deficient → usual workup for Fe def ie Stool occult blood test /
colonoscopy / OGD and treat any underlying cause
● Advice on diet with iron: spinach, legumes
● Check FBC/ Ferritin Annually

Pharmacological
● If Fe deficient → Give Fe supplements

194
 ● If Hb < 10 and Fe replete (transferrin saturation (TSAT) is >25 percent
and ferritin >100 ng/mL) → offer ESA
● Refer to Renal for ESA
● Side effects of ESAs: Hypertension, Testicular cancer, pure red cell
aplasia, flu-like symptoms
● Cost of EPO can be offset by Medishield

Education (as above): Red flags

F/u: TCU in 4/52 (time required to see an improvement in Hb after starting
ESA)

3. B12 deficiency anemia ● Symptomatic patients: Initial parenteral administration (vitamin B12
or folic acid) is suggested for those who have symptomatic anemia or
neurologic findings. If appropriate, these individuals can be switched
to oral therapy after symptoms resolve.
● Impaired absorption: Parenteral vitamin B12 replacement is often
used for those who do not have the capacity to absorb oral
replacement (eg, pernicious anemia, intestinal blind loop). The
parenteral route is usually well-tolerated, and medication adherence
is assured. However, high-dose oral (or sublingual) vitamin B12
therapy can also be effective for those with impaired absorption,
provided that the dose is sufficient and medication adherence is
good and a response is documented
● Dietary deficiency: Oral replacement is adequate
● If due to metformin and necessary meds , can continue the same
meds and replace Vit B12
● Remove unnecessary medications that contributes to vit B12 def ie
stop PPI if not indicated, if indicated , can continue
● If no obvious cause found, ?pernicious anemia → Refer for anti-IF/
anti-parietal cell, if confirmed pernicious anemia, will need OGD TRO
atrophic gastritis which has increased risk of gastric CA

Appendix

195
196
HAEM 2. APPROACH TO BLEEDING & BRUISING
DIFFERENTIAL DIAGNOSES
Platelet REDUCED NUMBER REDUCED FUNCTION

Reduced production ● Platelet dysfunction

● Aplastic anemia • Drugs: Aspirin, NSAIDs
● Myelodysplastic syndrome - • Von-Willebrand dz
Infiltration of bone marrow • Renal failure
● Drugs (BM suppression): AZT, MTX • Multiple myeloma
Increased destruction (Calcium Renal impairment
● Immune-mediated Anemia Bone lesions - CRAB)
○ Auto-immune: SLE, ITP
○ Infections: HIV, EBV, CMV,
viral
○ Drugs: Heparin, Rifampin,
Quinidine, Quinine,
Sulfonamides, Sulfonylureas,
Penicillins
● Non-immune –
○ Sepsis
○ DIC, TTP, HUS
○ HELLP (hypertensive disorder
of pregnancy - hypertension,
elevated liver enzymes, low
platelet)
Sequestration
● Hypersplenism
○ Liver cirrhosis with portal
HTN
○ Myelofibrosis
○ RA with Felty’s syndrome
(triad: RA + low TW +
splenomegaly)
○ Storage diseases

Clotting factors Congenital Acquired

● Hemophilia Liver cirrhosis
Vitamin K deficiency (ask about
malabsorption syndromes,
steatorrhea)
DIC – sepsis/consumptive
coagulopathy
Drugs – anti-coagulants, warfarin,
NOACs, heparin

197
 Vessel/Connecti ● Hereditary Hemorrhagic · Connective tissue disease:
ve Tissue Telangectasias ● Marfan’s, Ehler Danlos
diseases ● Cushing’s, Vit C deficiency
● Infections: meningococcus,
gonococcus, bacterial
endocarditis
● Vasculitis: HSP, SLE,
polyarteritis nodosa,
cryoglobulinemia
● Amyloidosis (AA/AL)
● Drugs: steroids,
sulfonamides, penicillins,
thiazides

Inorganic Non-accidental injuries

Another way of classification:

DDx:
1. Rule out NAI / Trauma
2. Platelet defect
● Malignancy: Lymphoma/ Leukaemia / Multiple Myeloma
● Infections: Meningococcaemia, Dengue, Chikungunya, viral infections, malaria
● Autoimmune: HSP, ITP , SLE , RA with hypersplenism
● Drugs: carbamazepine, valproate, DMARDs eg methotrexate, azathioprine
● Chronic liver disease with hypersplenism
● Uraemia
● Prosthetic valves
● HUS (Triad: MAHA, Thrombocytopenia, AKI, triggered by Ecoli) / TTP (Pentad: Fever, Neuro
abnormalities, MAHA, Thrombocytopenic purpura, Renal dz)
● DIC
● Aplastic anaemia
3. Coagulation disorders
● Congenital: Haemophilia A and B, Von Willebrand’s disease
○ Chronic liver disease
○ DIC
○ Vitamin K deficiency
○ Drugs: heparin, warfarin
4. Capillary defect
● Steroid use
○ Vasculitis: Churg Strauss vasculitis, Wegener’s granulomatosis, PAN
○ Congenital: Ehlers-Danlos syndrome, Pseudoxanthoma elasticum

Name/Age/Sex

BIOLOGICAL

Acute Chronic illness Medical History

198
Complaint: Bleeding and bruising Cause ● Medical/ Surgical
● Site: Course Hx
● Skin petechiae/ purpura, gum bleed/epistaxis Control ● Hx of bleeding
-> Plt ● Home disorder
● Ecchymoses, Joint bleeding or hematomas -> ● Clinic ● Age dx-ed ,
coagulopathy Compliance presentation, ix,
● PR bleed/ melena/ haematemesis/ ● Non mx , f/up ,
Menorrhagia/CNS bleed pharm compliance, prev
● Onset: Acute or bleeding since birth ● Pharm admissions
(congenital) Complications
● (immediately after trauma -> Plt , delayed ● Disease ● Drug Hx/ Drug
bleeding ie hrs -> coagulopathy) ● Treatme allergies
nt ● Medication List
● Precipitating: Trauma/ NAI Checking (any antibiotics,
● Time course: How frequent? Competency OCP, antiplatelets,
anticoagulants),
● Severity: Quantify amount of bleeding. Assess Comorbidities TCM/OTC
how quickly bleeding takes to stop (e.g. nose Crisis
bleed resolved with anterior pressure?) management

Causes
● LOW/ LOA/ bone pain / lumps around
neck/armpit/groin (malignancy )
● Any recent fever, URTI, GE symptoms or
vaccination (ITP is preceded by__, viral
infections/ vaccination)
● Travel history (malaria)
● Recent trauma
● Possibility of abuse in the family!
● Recent new drugs
● Fam hx of bleeding disorders

● Rash, joint pain oral ulcers, alopecia (SLE)

● Hx of liver dz / kidney dz

● Hx of valve replacement
● Dietary history especially Vitamin C containing
fruits and vegetables
Course
● Tried what treatment?
● Seen other doctors for it?
Complications
● Anemia
● BGIT, Intracranial hemorrhage

Disease Prevention Family Hx

● Vaccinations: Bleeding problems ie

● Cancer prevention: X-linked recessive
Hemophilia - male relatives
affected
Von willebrand disease

199
 PSYCHOLOGICAL

PHQ-2 I
GAD-2 C
E

SOCIAL

Environment Function

Home bADL (DEATH)

Employment/education: High risk jobs iADL (SHAFTTT)
Activities: Contact sports?
Drugs (Smoking, alcohol, illicit drugs) Cognition
Sex and relationship with others: Number of sex partners. Man,
woman or both. Bladder and bowel
Suicide
Sleep Eye, ear and swallowing

Finance
Exercise
Diet

PHYSICAL EXAMINATION ***HAND RUB***

General inspection: Conjunctival pallor, look at hands for pallor
Vital signs
T BP HR
1. Mucosa exam: Nose inspection, oral cavity exam
2. Skin exam: Inspect for petechiae, bruises, hematoma
3. Joint exam: Look for haemarthrosis / arthropathy from recurrent haemarthrosis
4. Abdominal exam: Palpate for hepatosplenomegaly. LN exam (check cervical, axillary, inguinal
nodes).
5. Neuro exam***for evidence of ICH
Offer DRE to assess for BGIT.

INVESTIGATIONS
FBC: Platelet <100 for ITP
PT/PTT/INR
KIV PBF, LFT
BM aspirate is not routinely done for ITP unless there is suspicion of malignancy / BM failure

MANAGEMENT
1) ITP
● Characterized by Isolated thrombocytopenia (platelet count <100,000/microL)
● Autoimmune mediated - Ab bind to platelet and cause splenic destruction of platelet
● Common between 2 -10 years old
● Presentation: Widespread petechiae, purpura, ecchymosis , epistaxis, gum bleeding, less commonly
GI bleed/CNS bleed , absence of systemic symptoms
● Acute ITP: Self limiting, Resolves in 3-6 months with or without treatment, Occurs 1-4 weeks after
viral illness ie VZV, Measles, EBV, vaccinations
● Chronic ITP: thrombocytopenia > 12 months, usu > 10yrs old, exclude SLE, platelet production
disorder via BM exam

200
Acute ITP ⇒ ED
● Avoid high risk activities (e.g. contact sports) and trauma (eg, football, hocke, soccer, skiing, or gym)
● Avoid NSAIDS that can worsen ITP.
● For postmenarchal female patients, hormonal therapy (typically with a progesterone-based
treatment) may be warranted to control or inhibit menses and prevent severe menorrhagia.
● Educate on when to seek help ie life threatening bleeding, if develop symptoms of severe bleeding
(eg, severe headache, hematuria, melena, heavy menstrual bleeding), to return immediately

Treatment of children with newly diagnosed ITP is based upon the severity of bleeding symptoms, the
degree of thrombocytopenia, and additional risk factors. Depending on individual patient characteristics,
appropriate initial management may be either "watchful waiting" or pharmacologic intervention
Disposition:
● If plt > 20 and no or mild mucosal bleeding, watchful waiting, refer to paeds hemato direct access.
● If Plt <10-20 or active life threatening bleeding ie (ICH, GI bleeding with hemodynamic instability,
pulmonary hemorrhage with cardiopulmonary compromise), refer to ED for platelet transfusion,
IVIG, oral steroids , IV anti-D IG
● Monitor platelet counts once weekly initially.

Platelet threshold for surgery

In general can proceed if plt > 50K

2) Haemophilia (X-linked recessive)

Presentation:
● Severe - Spontaneous bleeds - haemarthrosis, hematomas, haematuria
● Moderate - bleeds with traum
● Mild - bleeds after surgery ie prolonged oozing after dental extraction
Complications of dz
● Haemarthrosis - knees/ elbows/ ankles/ shoulders, resulting in arthritis, joint instability and
ankylosis (Joint pain / stiffness/ giving way)
● Neurological problems - ICH, Haemorrhage into vertebral canal (neck and back pain followed by
ascending paralysis) . Peripheral nerve compression
● LIfe threatening hemorrhages - retropharyngeal, retroperitoneal
Complications of Tx

3) Non-accidental injury
● Suspect NAI early on if: multiple bruises of different ages, hx from parent inconsistent with injuries,
hx is vague, hx of bruising in a child not cruising
● “I ask this for all my pts with bruising: Is there any possibility that your child might be abused?”
● How were the injuries sustained
● If child abuse suspected, request to speak to child alone (parental refusal to allow child to be
interviewed alone is considered red flag for abuse)
● Is the injury witnessed, events preceding trauma, mechanism of injury, subsequent actions and
symptoms of patient (usually unwitnessed)
● Social hx ***VERY IMPT: who stays with the child, who is the main caregiver, who is around when
main caregiver is away, are parents married, any family problems? How does the patient behave
with certain people ie very quiet / refuse to follow someone

Examination:
● Examine with all the clothes removed sequentially
● Trunk , back, arms , legs , perineum (sexual abuse!)
● Retinal hemorrhages, hemotympanum, mouth (frenulum tears or palatal petechiae)
● Signs of neglect (malnourishment , poor hygiene)

201
 ● Multiple fractures in various stages of healing or co-existing with bruises, burns and fractures
● Injuries consistent with method of infliction - slap, belt, loop of cord, cigarette, iron
● Fractures: long bone # in pts who cannot walk, rib fracture, hollow viscus injury < 4 yo , subdural
hematoma
● Bruises: Bruises in children who cannot cruise, trunk, ear and neck

Mx:
● Non accusatory language that emphasizes need for further evaluation: “ This is more injury than
what we would expect from the event that you are describing. We should be careful to determine
whether there is something medical going on, or if someone might be hurting your child”
● OR “ sometimes when we see injuries like these, there are other injuries that may put patient at
risk and we need to test for them”
● Refer MSW
● Report Police
● Evaluate other siblings for abuse
● Need for hospitalisation:
● Tx of burns. Ingestion, intracerebral injury
● Child is considered unsafe in the care of the parents
● A protective environment where the child can be evaluated needs to be provided

202
NEURO 1. APPROACH TO TREMORS

DEFINITIONS
Resting Tremors: occurs in a body part that is relaxed and completely supported against gravity, typically
diminishes with voluntary movement

Action Tremors: occur with voluntary contraction of a muscle

1. Kinetic: associated with any voluntary movement and includes intention tremor
2. Postural: present while maintaining a position against gravity
3. Isometric: occurs with muscle contraction against a rigid stationary object
4. Intention tremor is produced with purposeful movement toward a target, such as lifting a finger to
touch the nose. Typically the tremor will become worse as an individual gets closer to their target.

Resting Tremor Parkinsonism

- Primary
- Parkinson plus
- Secondary

Action Tremor Neuro

⦿ Cerebellar Intention Tremor
⦿ Essential Tremor
- AD inheritance
- Peaks at 70 years of age (worsened gradually) but tremors present in
midlife

Endocrine
⦿ Thyrotoxicosis
⦿ Hypoglycemia

Systemic
⦿ Drug Tremour
● Alcohol withdrawal/DT
● Parkinson’s: Anti psychotics, anti emetics
● Cerebellar: Phenytoin, lithium, sodium valproate
● Exaggerated physiological tremor: beta agonists, thyroxine, flu
meds
⦿ Psychogenic Tremor / Anxiety
⦿ Enhanced Physiological Tremor: Caffeine use

⦿ Wilson’s Disease
- AR inheritance
- Associated liver disease
- ‘Wing beating’ tremor

⦿ Dystonic Tremor
- Rare, usually jerky tremors

203
 NAME/SEX/AGE
BIOLOGICAL
ACUTE COMPLAINT CHRONIC DZ MEDICAL HISTORY
Complaint: Tremours Cause Medical/ Surgical Hx
● Sites involved: Hands ± arms, head, jaw, legs, voice Course ● Parkinson’s Dz
○ Unilateral or bilateral (unilateral more PD) Control ● Thyroid/ DM
● Onset (sudden vs progressive) Compliance ● Conditions that req
○ Progressive = parkinson more likely Complications ßdrugs eg COPD
○ When does it occur ie hungry, stop alcohol Checking
● Character: Worse with movement, occurs at rest? Competency Drug Hx / Drug allergies
○ TRO chorea (involuntary, purposeless, restless, ● Illicit drugs
fidgety) Comorbidities particularly
● Duration, progression Crisis Mx amphetamines
● Exacerbating factors ● Caffeine Ingestion
● Alleviating factors: Alcohol in ET ● Salbutamol /
● Severity: affecting mood/ QOL/function Thyroxine
● Hand dominance Medication List
TCM/OTC
Cause
● Bradykinesia, Rigidity, Unsteady Gait
○ Slowness of movement, stiffness, difficulty turning
over in bed, postural instability, difficulty walking,
dribbling of saliva, loss of memory or attention
● Recent stroke disease, difficulty walking, nausea, vomiting,
vertigo, staccato speech → Cerebellar
● Heat intolerance, weight loss, diarrhea, insomnia →
Hyperthyroid
● Cold sweats, hunger pangs, missed meals, DM meds →
Hypoglycemia
● Anxiety
● Drugs
● Family history in ET/ WD

Course
● Tried any meds? Seen anyone? Progressively worse/more
areas?

Complication
● FUNCTION: work/school, mood, relationship with others
(examples of function: drinking water, handwriting, putting
on makeup etc)
DISEASE PREVENTION FAMILY HISTORY
- Vaccinations Essential Tremors
- Cancer prevention: Wilson’s Disease
PSYCHOLOGICAL
PHQ-2 I
GAD-2 - psychogenic tremor C: Affecting work/life?
E: Condition curable,
prognosis?
SOCIAL

204
Occupation: job affected?
Alcohol ?withdrawal
Home/Environment – triggers?
Sleep

PHYSICAL EXAMINATION ***HAND RUB***

BP HR KIV postural BP
● Inspection: Masked like facies/ pill rolling/ tremor, anxiety, Thyroid eye dz, Jaundice in WD
● Neck: Goitre (ask pt to swallow)
● Tremors on outstretched hand, place paper on hands to demonstrate, acropachy
● Pronator drift, dysmetria (no need to do full neuro exam)
● KIV UL screen: tone and reflexes
● Parkinson features: cogwheeling, lead pipe rigidity, bradykinesia
● CN: Eye EOM for Parkinson’s plus
● Gait: stooped posture etc
Assess function: Open cap, take out coin. Ask patient to write their name on a paper.

INVESTIGATIONS
● Stat tests: Random glucose
● Other tests: TFT for hyperthyroidism, LFTs for Wilson’s disease
● KIV CT/MRI if suspicious of cerebellar lesion

MANAGEMENT
1) Benign Essential ● Non pharm: avoid caffeine, overuse of sympathomimetics
Tremor ● Trial of Propranolol 60mg TDS - 320mg TDS
● Ensure BP tolerable and no significant POSTURAL drop
● S/E of ßblocker: Giddiness, bradycardia, fatigue, erectile
dysfunction
● Check for CI for ßblocker: arrhythmias, asthma, PVD, DM
● TCU to review

2) Parkinsonism likely PD ● Refer to Parkinson document

3) Thyrotoxicosis ● Refer to thyroid document

4) Drug-induced tremors ● Stop offending drug

205
SUMMARY FLOW CHART

206
NEURO 2. POST STROKE CASE

HISTORY
Important Issues to address
1) Pre and post-morbid function, especially in relation to job and role in the family
- bADLs & iADLs – DEATH SHAFT
- “ How has your stroke affected your daily routine?”
- “ How has your stroke affected your work”
- “ Do you need any help with your daily activities?”

2) Financial situation given chronic disability

3) Home environment, toilets, stairs
4) Family support, caregiver competence and stress

5) Any post stroke depression / memory loss

6) Control of Cardiovascular Risk Factors/ Predisposing factors – DM/ HTN/HLD/ Obesity / Smoking/Alcohol
/ Atrial fibrillation

7) Complications from stroke and treatment

=======================================================================================
Focus on how has pt been POST-stroke
Complaint: Post stroke (neuro deficits patient presented with and how it has been since)
Cause/Course: How did he present, what ix done, what was the cause of the stroke, management, any
physio (Bleed vs ischemia, cardioembolic - mx AF / murmur vs atherosclerosis)
Compliance:
Complications of disease: See Social Hx. Immobility - Falls, DVT/PE, Bed sores, Pneumonia / AMI
Complications of treatment: Bleeding symptoms from NSAID, SSRI side effect if on fluoxetine

Social Hx:
- Alcohol/Smoking
- Married/Single/ Children
- Occupation/ Financial situation given chronic disability

- Pre and post-morbid function, especially in relation to job and role in the family
- Handedness, mobility, walking aids, falls
- bADLs & iADLs – DEATH SHAFT
- Cognition
- Bladder/ Bowel Incontinence
- Eye, ENT, Swallowing

- Home environment: type of housing, lift landing, toilets, stairs, grab bars
- Family support, caregiver competence and stress

Psycho Hx: Any post stroke depression / memory loss

Control: CVRF, Diet, Exercise, HbA1c, BP, LDL, INR level

Compliance: Meds ,Check dose of medications
Competency: In taking medications , anyone helps with meds administration
Checking: BP/ Home CBG
Complications: Complications from CVRF and treatment: Ie hypo/hyperglycaemia, DFS, DRP,
hypo/hypertension, Bruising in the case of anti-coagulation, aspiration pneumonia from NG Tube feeding
Co-morbids: CVRF: DM/ HTN/HLD/ Obesity / Smoking/Alcohol / Atrial fibrillation
Crisis Mx: How to recognize another stroke (FAST)
207
PMHx: CVRF
Drug Hx:
Social Hx: As above
Psych Hx: As above
Family Hx: Of CVRF

PHYSICAL EXAMINATION
BP HR (check for atrial fibrillation)
BMI Ht Wt
{Seated}
- Functional assessment : Unbutton your shirt, pretend to comb your hair, pick up the coin, open the bottle
- Pronator drift, Power of UL / LL , KIV CN if obvious facial droop/swallowing impairment
- Gait

{Walk to the bed and lie down}

- Heart : S1 S2 if in AF , carotid bruit
- Lungs for aspiration pneumonia if swallowing impairment/ immobility
- Check for diapers if incontinence and sacral sores , tube feeding
- Pallor, bruising in AF
- DM dermopathy, xanthelesma

INVESTIGATIONS
● Stat: INR, HbA1c, FBC when on aspirin/warfarin, ECG
● Chronic labs: Hba1c, Lipid panel, RP, Urine acr, INR
MANAGEMENT
General management for post stroke
● Control CVRF:
○ Diet, Exercise
○ Quit smoking/ alcohol
○ Home BP / CBG monitoring
■ Target BP <140/90 post stroke (~3 days)
○ Adjust medications for CVRF
○ Arrange for DFS /DRP
○ Assist in improving compliance to meds: try to reduce need to halve medications → can try
to change dose to use full pill; if unable to, and concerned about halving pill equally can use
pill cutter
● Rehab to improve functional outcomes:
○ PT for strengthening exercises
○ OT for ADL/ iADL and to assess home environment
○ Swallowing with speech therapist (Avoid too many referrals during exam though)

● Optimize environment:
○ Grab bars, anti slip treatment to bathroom, ramp from corridor to home entrance. If in
wheelchair, assist in applying for handicap carpark label. ie EASE programme (Enhancement
for active seniors - provides subsidies for home enhancement)
○ Daytime activities: social day care, Day rehab centre
● Caregiver training, caregiver stress management
● Vaccinations

Acute stroke

208
- For hemorrhage may need craniotomy to evacuate bleed
- For infarct if <3 hours, tPA has proven to be beneficial, if 3-4.5 hours tPA is also beneficial but less so than
for patient with infarct <3 hours, SG guideline
- Blood pressure control <185/110 for tPA candidates, for non tPA candidates 220/120 is acceptable
threshold

Different scenarios
1) Post stroke with AF
- CHA2DS2VASC score ≥ 1 → Start warfarin / NOAC, check for CI, discuss risk and benefits (refer to AF mx)
- Generally target INR 2-3 target 2.5- 3.5 for MVR, AVR with AF or other complications
- Sub or supratherapeutic INR → adjust accordingly

2) Post stroke depression

- Consider psychologist referral
- Discuss regarding starting SSRI (in patients with recent stroke, fluoxetine for 3 months may promote the
recovery of neurological functioning, improve independence in activities of daily living and reduce the
incidence of depression post-stroke

209
NEURO 3. APPROACH TO DIFFICULTY WALKING

DDx

First establish whether it is global, proximal or distal.

Then establish if there is sensory involvement – if yes, less likely myopathy
1. Spinal cord compression (global)
a. Extradural: neoplastic (metastatic), PID, spondylosis, spondylolisthesis, vertebral abscess
b. Extramedullary: Meningioma, Neurofibroma, Ependymoma
c. Intramedullary: Glioma, ependymoma
2. Neuropathy (If more distal)
a. Alcohol
b. B12 deficiency
c. Carcinomatous
d. Renal failure
e. DM
f. Drugs: isoniazid, ethambutol, chemotherapy
g. AIDP/ CIDP
3. Myopathy (if more proximal)
a. Endocrine: Thyroid, Cushing’s, Acromegaly
b. Dermatomyositis, Polymyositis
c. Myasthenia gravis
d. Carcinomatous
e. Drugs: Steroids, Statins
f. Myositis: viral, bacterial
g. Electrolytes imbalances
4. Ataxia
a. Cerebellar disease
b. Alcohol
c. NPH
d. Old stroke (ataxic hemiparesis)
5. Parkinsonism

HISTORY
Difficulty walking:
● Unilateral, bilateral

210
 ● Global, distal or proximal: Difficulty getting up from sitting or squatting position, difficulty walking
up stairs
● How long?
● Stable, improving, worsening
● Intermittent or constant: worse at night or as day progresses

Rule out spinal cord compression!

● Loss of sensation: if present, to what level
● Any upper limb weakness
● Any urinary or faecal incontinence
● Back pain – spinal artery occlusion, PID, vertebral abscess, spinal stenosis
● Numbness over lower limbs – peripheral neuropathy
o To which level
o Any hand numbness?
● Difficulty swallowing, slurring of speech, blurring of vision – stroke
● Tremor, shuffling gait, slowness of movements – Parkinson’s disease
● Headache
● Giddiness
● Loss of weight, loss of appetite – malignancy

Complications
● Any previous falls? Cx of falls?

PMHx:
● Spinal prob
● DM, neuromuscular disorders, thyroid problems, cancer, renal prob
● CVRF for stroke
● Parkinson’s disease

Drug history: steroids, statins

FHx: DM, neuromuscular disorders, thyroid problems

Social history:
● Alcohol
● *FUNCTION affected? Work/school

PHYSICAL EXAMINATION
BP HR
{seated} Pronator drift
Inspect back/neck
Gait
KIV cranial nerves
{lie on bed} LL: Tone, Reflexes, Power, Sensation + proprioception

INVESTIGATIONS
● Stat tests
○ FBC
○ Random glucose
○ KIV XR LS Spine
● Other tests
○ Renal panel, TFT, B12 level and folate, ESR, autoimmune profile, CK level, syphilis serology,
HIV screening
● Further tests: MRI spine, CT head/ MRI head; Lumbar puncture

211
NEURO 4. APPROACH TO HEADACHE

HISTORY
Patient’s profile
Young patient with no red flags → migraine / tension
Elderly with DM/ HTN → Stroke, Giant Cell Arteritis
Overweight → OSA / Benign intracranial hypertension
Pregnant → preeclampsia, cerebral venous thrombosis, meningitis
Primary Secondary (Intracranial) Secondary Others
(Eye/Ear/Nose/Neck/Teeth)

Migraine Vascular: ICH, cerebral venous thrombosis, Eye: Glaucoma Medication

Poorly controlled HTN, Giant cell arteritis overuse
headache
Tension Infective: Meningitis, Encephalitis, Brain ENT: Sinusitis
headache abscess

Cluster Trauma Tooth: Dental caries/abscess

headache

Autoimmune: TMJ dysfunction

Metabolic: OSA, Pregnancy (Preeclampsia) Neck: Cervicogenic headache (cervical

spondylosis / whiplash injury)

Iatrogenic

Neoplasm: Meningioma, pituitary, 2’

metastasis

212
Name/Age/Sex
BIOLOGICAL
Acute Chronic illness Medical History
Complaint: Headache Cause ● Medical/ Surgical Hx
● Site: Unilateral/bilateral Course ○ HTN
● Onset and progression: Time to max pain within Control ● Drug allergies
minutes/hours? ● Home ● Medication List
● Character: Throbbing, tight, thunderclap ● Clinic ○ Analgesia
● Timing: Compliance history,
○ Each episode: Lasts minutes? Hours? Days? ● Non response to
○ Frequency: How many times per month? pharm painkillers
● Exacerbating: Lying flat/morning headache? Worse on ● Pharm ● TCM/OTC
coughing, sneezing? Worse with loud noise/bright lights? Complications
Worse with exertion? ● Disease ● Travel / Contact Hx
● Relieving factors: painkillers, lying down, avoiding bright ● Treatme
light and noise nt If paeds/adolescent:
● Severity: Worst headache of your life, pain score Checking ● Birth Hx
● Trauma/HI, fall Competency ● Immunization Hx
● Developmental Hx
Cause Comorbidities
● Rule out red flags Crisis
○ Fever/neck stiffness/altered personality → management
Meningitis/Encephalitis
○ LOW/LOA/focal neuro deficits → SOL
○ Pain worse on waking up in the morning? Worse
on coughing, sneezing? → SOL
○ Pain over temporal area, jaw claudication/transient
loss of vision, pain when eating (a/w Polymyalgia
Rheumatica) → Temporal arteritis
○ Eye pain/pressure/redness/BOV/nausea →
Glaucoma
● Snoring, tiredness, apnea, elevated BP, obese→ OSA
● Photophobia, phenophobia, N&V, Prodromal symptoms:
visual symptoms of flashing lights and blind patches,
gastrointestinal, numbness or weakness of limbs, aura
preceding lasting <1 hour → Migraine
● Eye involvement: eye pain, eye injection with runny or
stuffy nose and congestive symptoms on one side of the
face → Cluster headache
● Long periods of time when headache free? → Cluster
headache
● With pericranial muscle tenderness → Tension headache
● With chronic analgesia use → Medication overuse
headache
● Pregnancy → Pre-eclampsia
● Change in facial appearance, increase in shoe size, hands
and feet bigger → Acromegaly (pit tumour)
● Pain over cheekbones/ sinuses, runny nose, fever →
Sinusitis
● Pain on neck movement, sustained or awkward neck
postures, palpation of suboccipital, C2, C3 or C4 regions;

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 limited ROM of neck with neck stiffness → Cervicogenic
headache

Course
● Previous similar episodes?
● Tried what treatment?
● Seen other doctors for it?

Complications
● Drowsiness
● Confusion
● Loss of coordination
● FUNCTION: how is it affecting you? ⚐ Does it wake
you up at night?

Disease Prevention Family Hx

- Vaccinations
- Cancer prevention
PSYCHOLOGICAL
PHQ-2 I
GAD-2 C: Affecting work/life?
E
SOCIAL
Work bADL (DEATH)
Account iADL (SHAFTTT)
Smoking, Alcohol
Home Cognition
Exercise Bladder and bowel
Diet Eye, ear and swallowing

PHYSICAL EXAMINATION ***HAND RUB***

GCS T BP BMI
Neuro
● PEARL
● Pronator drift
● Dysmetria
● Power of UL (prox and distal)
● Gait
● Ophthalmoscopy for papilloedema
● Cranial nerves
Neck circumference (OSA)
Mouth mallampati score (OSA)
Palpate in front of tragus for temporal artery pulse, temporal region for tenderness in GCA !
Palpate sinuses for tenderness (index and middle fingers together, tap over frontal x 2, cheek x 2)
Palpate frontalis/temporalis/trapezius for muscle tenderness, C-spine for tenderness, assess ROM of
cervical spine

INVESTIGATIONS
● Stat tests
○ FBC: raised Tw
○ XR Cervical spine if pt has neck pain
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 ● Other tests: ESR for giant cell arteritis
● KIV at tertiary centre
○ CT brain looking for evidence of space occupying lesion or bleed or MRI brain
○ Others: Lumbar puncture for meningitis

MANAGEMENT
1) Migraine (UTD) Non pharm:
Cardinal features ● Avoid triggers, sleep hygiene, regular meal and
● Headache: Throbbing in quality. Usually exercise, stress reduction
but not necessarily unilateral. Increases in
intensity over hours. Lasts 4-72 hours. Pharm: Abortive
● Nausea/vomiting ● Mild: Oral paracetamol/NSAID
● Photophobia/phonophobia ● Moderate-severe
● Improvement in dark, quiet room or with ○ No nausea: Oral triptan ie sumatriptan
sleep. 50-100mg or Oral triptan-naproxen
● Aura preceding headache: Commonly ○ Nausea: Non-oral sumatriptan, IV
visual aura (can be sensory presenting as maxolon
tingling, lasting no more than 1 hour.
Scotoma/bright spots/lines etc Pharm: Preventive
● Postdrome: Post headache sudden ● Indications:
movement of head causes pain in location ○ Frequent or long lasting migraine
of antecedent headache. headaches (no strict definition, usually > 4
headaches per month or headaches >12h)
PE ○ Migraine attacks that cause significant
● Neurological exam TRO focal neuro deficits disability or diminished quality of life
→ suggests alternate causes despite appropriate acute treatment
○ Contraindication to acute therapies /
Diagnosis Failure of acute therapies/ Serious
● Clinical diagnosis by ICHD3 criteria adverse effects of acute therapies
○ Subdivides into migraine without ○ Risk of medication overuse headache
aura, migraine with aura, migraine ○ Menstrual migraine
with typical aura ● Amitriptyline, beta blocker (metoprolol,
propranolol), topiramate

2) Tension headache (UTD) Investigations: not necessary for diagnosis

History
● Headache: Bilateral, non-throbbing. Diagnosis
“Band-like”. May be ppt by stress. Lasts ● ICHD3 criteria
from 30mins to 7 days.
● May have pericranial muscle tenderness Treatment
(e.g. frontal, temporalis, masseter, SCM, ● Abortive
trapezius) ○ Mild: Simple analgesia
(paracetamol/NSAID)
PE ○ Combination caffeine with brufen
● Neuro exam TRO focal deficits ○ Aim to prevent medication overuse!!
● Can try to elicit pericranial muscle ● Preventive (ensure got indication)
tenderness: Use 2nd and 3rd finger, with ○ Non-drug: Stress management
rotating movement palpate for tenderness ○ Drug: Amitriptyline
over frontalis, temporalis, masseter,
trapezius

3) OSA Investigations
ᐉ Cardinal symptoms ● Lipid, glucose

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 ● Daytime sleepiness ● TFT (differential for symptoms)
● Unrefreshed sleep Refer ENT for polysomnography
● Snoring
● Apnea episodes / Nocturnal choking and Management
gasping for air ᐉ Non-pharm:
● Morning headaches ● Lose Weight - Diet and Exercise
ᐉ STOP BANG (0-2: low risk, 3-4: intermediate ● Avoid alcohol and medications that inhibits CNS ie
risk, ≥5: high risk) sedating medications such as BZD, anti-
● Snoring, Tiredness, Observed apnea, histamines, opiates, sedating anti-depressants
Pressure, BMI>35, Age>50, Neck ● Avoid supine position -> Sleep in lateral position
circumference > 40cm, Gender male (tennis ball in shirt)
ᐉDifferentials : Thyroid disease (due to neck mass ᐉ Education
compressing) ● Risk factors and consequences of OSA. Warned
> Associated with: DM, HTN, HLD, Obesity about the increased risk of accidents with
untreated OSA and the potential consequences of
ᐉ Complications: driving or operating other dangerous equipment
● Safety: Driving and accidents, Operating while sleepy
heavy machinery Refer to ENT for sleep study
● Metabolic: DM, HTN, HLD, Obesity, Fatty
liver
● Cardiovascular risk: Coronary artery
disease, Stroke
● Cognition / Mood: Cognitive dysfunction,
Mood disorders
ᐉ Psychosocial: Function at work, PHQ2, smoking
and alcohol

Physical Examination
● BP, BMI
● Neck circumference (17 inch men, 16 inch
women)
● Palate: Tonsil Hypertrophy, Mallampati
score (Open mouth and stick out tongue,
do not say “Ah” )
● Nasal septum
● CVM exam: pulmonary hypertension (loud
or palpable p2, parasternal heave, JVP
elevation, pedal oedema)

4) Giant Cell Arteritis (Vasculitis of large and Investigations: FBC, ESR

medium sized vessels)
ᐉ Cardinal symptoms Management
● Occurs in age > 50 yo, peaks in 7th decade ● Medical Emergency! Refer to ED stat due to high
● Pain over temporal aspect risk of stroke and vision loss
● Jaw claudication ● Rheum likely to do temporal artery biopsy and
● Visual disturbances ie transient give prednisolone
monocular vision loss (amaurosis fugax):
abrupt partial field defect or temporary
curtain effect
● Unexplained fever and constitutional
symptoms (fatigue, weight loss)

216
 ● Branches of the external carotid artery
may be affected: Facial swelling, Maxillary
and dental pain, Throat pain, Tongue pain
ᐉ Associated with: Polymyalgia Rheumatica
(aching and morning stiffness about the shoulder
and hip girdles, in the neck, and in the torso)

PE
● BP - Bilateral BP, HR (may have unequal BP
or HR due to vessel involvement)
● BMI
● Palpate temporal region: tender and
thickened vessels (immediately in front of
the tragus of the ear and up along the
temple)
● CN exam/ Pronator drift/ upper limb
power / Gait (as part of examination for
headache) (at the same time checking for
shoulder pain/ hip pain or stiffness in PR)
● Pulses: Carotid, brachial, radial, femoral,
and pedal pulses
● Bruit: Carotid, supraclavicular areas;
axillary, brachial, or femoral arteries,
abdominal aorta
● CVS exam: Aortic regurgitation (secondary
dilation of aortic valve due to
development of ascending aortic
aneurysm)

5) Cluster Headache Management

● Beta blockers or Lithium

6) Medication Overuse Headache Mx:

History (Definition: ICHD-3) ● Patient education abt detrimental effects of
● Headache ≥15days/month in pt w pre- analgesia overuse , during the period of analgesic
existing headache, as a consequence of withdrawal, the headaches are likely to
overuse of headache medications > 3 exacerbate before subsequently improving
months ● Abrupt discontinuation of offending medication
● Regular intake for ≥10 days/month ● Bridging therapy with medication of another class
(paracetamol / NSAIDS) or ≥15 ie NSAIDs/Steriods
days/month (other analgesia) for >3/12 ● Consider preventive therapy ie for migraine
● Usually resolves after the overuse is ● Follow up
stopped.
● Absence of red flags!

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NEURO 5. APPROACH TO ONE SIDED WEAKNESS

DDX
Neurological Systemic

1. Cortex / Sub-cortical/ Brainstem lesion Hypoglycemia

- Vascular:
- Stroke / TIA (infarct or haemorrhagic)
- Hemiplegic migraine
- Infection (abscess)
- Tumour
- Seizure: Post-ictal todd’s paralysis
- Demyelinating ie multiple sclerosis

2. Spinal cord lesion

- Trauma
- Infarct
- Tumour (Primary / Secondary)
- Myelitis
----------------------------------------------------------------
If only involves arm and not leg…
3. Brachial plexus lesion
- Trauma
- Compression: tumour, abscesses
4. Neuropathy
- Compression

HISTORY
Complaint
One sided Weakness
● Arm and leg or only arm
● How long? Onset – sudden or gradual? Progression? first episode?
o Need to establish exact timing as it will affect thrombolysis if acute stroke
o Duration < 10 mins, 10- 59 , > 60
● Associated numbness?
● Recovery: complete, partial
o If multiple episodes of weakness which resolves – multiple sclerosis

Causes
Red flags
● Associated facial weakness, LL weakness, slurring of speech, difficulty swallowing, blurring of
vision/ double vision
● Headache/ Early morning vomiting/ LOW / LOA Hx of cancer – space occupying lesions
o Nature of headache: worse when waking up in the morning, worse on coughing and
sneezing
● Fever/ neck stiffness/rash/ confusion - infection
● Any abnormal jerking movements/ tongue biting/ urinary incontinence? – Todd’s paralysis
● Visual aura/photophobia/phenophobia/ hemiplegia usually only lasts < 24hrs - paralytic migraine
● DM & hypoglycemia symptoms
● Back pain – spinal cord pathology
● Urinary retention or incontinence, constipation or bowel incontinence - spinal cord
● Any trauma or injury to shoulder area or arm prior? - brachial plexus injury

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PMHx:
● CVRF: HTN, DM, hyperlipidaemia, old strokes/ TIA, IHD
● AF
● Multiple sclerosis
● Malignancy
● Epilepsy

Social Hx:
● Smoking/ drinking
● Occupation
● HANDEDNESS: right or left handed?
● FUNCTION: how has it affected you?

Drug history:
● Anti platelets or anti coagulants – haemorrhagic stroke

FHx: CVRF, strokes

PHYSICAL EXAMINATION
T BP HR (irregularly irregular in AF in stroke) BMI Ht Wt
Pupils equal and reactive to light, CN 7, KIV CN exam if deficits present
Pronator drift
Cerebellar
Power
Gait

Heart - murmur
Radial radial delay - for ascending aortic dissection
Carotid bruit - carotid stenosis
Xanthelesma, DM dermopathy

INVESTIGATIONS
● Stat: Hypocount, ECG, FBC (infection, hb before starting aspirin)
● Chronic: Fasting glucose, fasting lipid panel

MANAGEMENT
Stroke - Refer to Emergency department
Acute Management:
- For hemorrhage may need craniotomy to evacuate bleed
- For infarct if < 3 hours, tPA has proven to be beneficial, if
3-4.5 hours tPA is also beneficial but
less so than for patient with infarct < 3 hours
- Blood pressure control <185/110 for tPA candidates, for
non tPA candidates 220/120 is acceptable threshold

TIA - Send to Direct access (same day) or ED regardless of TIA score

- Load aspirin 300mg stat if not on aspirin yet

219
Epilepsy with Todd - First time seizure -> ED
Paralysis
- Known epilepsy with breakthrough seizure
- -> If no obvious trigger -> refer ED
- -> If obvious trigger -> refer neuro direct access
- Identify and reverse triggers : Non-compliance to AED, drug
interactions with AED resulting in lower AED levels, lack of sleep,
stress, concurrent illness, alcohol abuse

- Seizure First Aid advice:

Place pt in recovery position or on his/her side,
Remove hazards, Do not place any object in the individual's mouth,
Give BZD if seizure > 5mins

- Home and Workplace Safety:

- Avoid Activities and sports which involves heights, water, or
aggressive physical contact, soak in prolonged bath
- Minimize exposure to open fires and sharp instruments, discourage
operation of heavy machinery

220
NEURO 6. APPROACH TO PARAESTHESIA

DDx:
Brain Unilateral ● Vascular: CVA, TIA
● Trauma: ICH
● Neoplastic: SOL, mets

Bilateral ● Meningitis
● Multiple sclerosis

Spinal cord ● Spinal stenosis

Nerve root ● PID, Radiculopathy

Plexus UL: Brachial plexus

LL: Lumbo-sacral plexus

Peripheral nerve Conforming to a Peripheral neuropathy (AABCCDD)

peripheral nerve ● Alcohol , AIDP (GBS)
distribution ● B12 deficiency
● Cancer, Chronic Renal failure, CIDP, CMT, HSMN
● DM
● Drugs (isoniazid and ethambutol, metronidazole)

Mononeuropathy like entrapment neuropathy (Carpal tunnel

syndrome, ulnar neuropathy)
● Risk factors for entrapment
○ Repetitive strain, use of vibration tools, previous
trauma
○ Acromegaly, hypothyroidism, obesity
○ Pregnancy
UL

- Median: carpal tunnel → acromegaly, hypothyroidism,

obesity, pregnancy, RA, drugs
- Ulnar: Guyon canal
- Radial
LL

Others ● Mononeuritis multiplex

● Migraine ± aura
● PVD
● Hypoglycemia
● Anxiety, panic attacks

HISTORY
Complaint: Pins and needles over bilateral hands
● Nature:
o Positive: pain – burning, electric shock like, shooting, stabbing?
o Negative: loss of sensation or numbness?
● Site: Which limbs, and if hands involved, which distribution? (does it correspond to any peripheral
nerve distribution)
● If both UL and LL, in glove and stocking distribution (peripheral neuropathy)
● How long each time, progression and severity

221
 ● Radiation - from neck
● Exacerbating factors : Any triggers ie worse after using vibration tool, worse at night and on waking
(CTS), on neck turning (C- spondylosis)
● Relieving factors (better on shaking hand suggestive of entrapment neuropathy)

Course
● Any ix done , mx

Cause
● Any associated weakness or muscles wasting? – motor component involved too - one sided or
bilateral
● Slurred speech, dysphagia, diplopia (CNS)
● Hx of cancer/ brain infx
● Hx of trauma / pain in neck/ back (Spinal cord/ Nerve roots)
● Alcohol/ Recent URTI/ Vegetarian/ Hx of DM/RF / Drug Hx (Peripheral neuropathy)
● Repetitive straining? Previous trauma? Use of vibration tools? (Mononeuropathy)
● Hypothyroid symptoms: Cold intolerance, lethargy, weight gain, edema, constipation
● Acromegaly symptoms: Change in facial features, change of glove and shoe size, headache
● LOW/ LOA (for paraneoplastic peripheral neuropathy)
● Migraine symptoms
● Anxiety

Complications
● ** MUST ALWAYS ASK IF PT IS LEFT OR RIGHT HANDED IF UL INVOLVED
● Function!

PMHx:
● Aetiologies of peripheral neuropathy: DM, renal failure, cancer, vitamin deficiencies
● Hypothyroidism, Acromegaly
● Previous wrist fractures

Drug history:
● Anti TB drugs (Isoniazid, ethambutol) or metronidazole

FHx:
● Hereditary neuropathies (HSMN)

Social history:
● Alcohol use for peripheral neuropathy
● Occupational history

PHYSICAL EXAMINATION
T BP HR BMI
{seated} Inspection: Acromegalic facies, Goitre, Anxiety
Examine every peripheral nerve: median, ulnar, radial nerve (Wasting, Sensation, Power,
Special tests)
Examine upper limb tone, reflexes, power, sensation pinprick and proprioception
esp C6, C7 to ddx from median nerve , C8 to ddx from ulnar nerve
Any duptyren’s contracture, parotidomegaly in alcoholism, DM dermopathy
Palpate C -spine for tenderness, C-spine ROM, Spurling’s test

INVESTIGATIONS
Stat tests
● Random glucose

222
 ● XR C spine, XR LS spine

Other tests
● TFT, RP, B12 levels, fasting glucose
● MRI of cervical spine

Others @ tertiary
● Nerve conduction study (in carpal tunnel syndrome), will show reduced or absent median sensory
nerve action potential (SNAP) from the index finger and prolongation of latency

MANAGEMENT
1) Carpal tunnel syndrome
Non pharmacological:
- Activity modification, reduce repetitive wrist movements
- Wrist splint at night

Pharmacological
- Neurobion
- Steroid injection

Surgical
- Carpal tunnel release

Other notes:
Mononeuritis multiplex - painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy
involving isolated damage to at least 2 separate nerve areas. It is actually is a group of disorders, not a true,
distinct disease entity. Typically, associated with
● DM
● Vasculitis
● Amyloidosis
● Direct tumor involvement - Lymphoma, leukemia
● Polyarteritis nodosa
● Rheumatoid arthritis
● Systemic lupus erythematosus
● Paraneoplastic syndromes

223
NEURO 7. APPROACH TO PARKINSON’S DISEASE

DDx
Primary PD Parkinson-Plus Syndromes Secondary Parkinsonism

Parkinson VITMTDD
Disease V Vascular: Strokes
I Infective: post encephalitis, HIV
T Trauma: head injury
Metabolic: MPTP neurotoxin, CO,
ethanol
T Tumour, NPH
Drugs! Dopamine receptor
blockers (Anti-psychotics, anti
emetic, lithium, methyldopa)

Degen
- Huntington’s disease
- Wilson’s disease

Parkinson’s disease is a progressive neurodegenerative disorder

Aetiology – loss of dopaminergic neurons in substantia nigra and other dopaminergic and non
dopaminergic areas of the brain

UKPDS Brain Bank Clinical diagnostic criteria for Parkinson’s Disease

Factors predicting against Primary Parkinson’s Disease

- Symmetry of motor signs
- Lack of tremors
- Poor response to levodopa (Response to levodopa is an important factor in distinguishing Parkinson’s
disease from other Parkinsonian syndromes)
- Falls early in course

224
 - Autonomic dysfunction early in course (urinary/fecal incontinence, urinary retention, postural
hypotension)
- Rapid disease progression
- Truncal rigidity more suggestive of Parkinson + (limb rigidity more suggestive of Parkinson Disease)

Factors predicting rapid rate of motor progression

- Older age at onset as an initial symptom
- Rigidity/hypokinesia as an initial symptom

HISTORY
1. Complaint /Control - Assess patient’s current Parkinsonian symptoms
- TRAP – Tremors, rigidity, akinesia (needed for diagnosis), postural instability
- One sided vs bilateral
- Any improvement in symptoms with the meds, any stiffness / involuntary movements prior to next dose

2. Cause
● Parkinson disease
● Secondary parkinsonism
○ - Repeated stroke with stepwise progression
○ - Definite encephalitis
○ - Repeated head injury
○ - Drug / neuroleptic treatment - metoclopramide, prochlorperazine, chlorpromazine, Toxin
exposure - MPTP (methyl-phenyl- tetrahydropyridine)
○ - Family hx of Parkinsonism - Huntington's disease /wilson’s disease
● Parkinsonism plus syndrome

3. Course
- When was the diagnosis made
- What was the initial presentation
- Progression of symptoms, f/up where, meds and mx

4. Compliance to medications
- Which meds, when started, any recent changes
- Need to taking at fixed and regular timings, take on empty stomach 30-60 mins bef meals

5. Complications of tx
Levo-dopa (dopamine precursor) – DOPA (See below)
D – Dystonia/ peak dose dyskinesia (need to lower the dose)/Depression
O – On-off phenomenon (rapid fluctuation between akinetic and choreoathetoic movements) / Wearing off
phenomenon (will need to increase dose/frequency of dosing)
Postural hypotension
A – Abdomen: Nausea, Vomiting, constipation

Dopamine agonist ie bromocriptine, ropinirole, pramixepole – hallucinations, psychosis , nausea

Enzyme inhibitors to prevent breakdown of dopamine - MAO-B inhibitors , COMT
Anti-cholinergics for tremors ie benzhexol – dry mouth, dizziness, urinary retention, BOV

6. Complications of dz [Hoehn-Yahr staging]

Motor:
- Recurrent falls
- Swallowing difficulty

Non-motor:
225
- Sleep disturbances ie REM sleep disorder
- Neuropsychiatric Symptoms: Depression, Dementia, Psychosis
- Autonomic Dysfunction: Orthostatic hypotension/ postural giddiness, Constipation, Vomiting, reduced
gastric motility, urinary retention with overflow incontinence, erectile dysfunction

PMH
- DM/HTN/ HLD/ IHD/ Stroke → vascular cause
- Schizophrenia on anti psychotics
- Hx of liver disease (Wilson’s)

Drug Hx
- Anti-psychotics (haloperidol), anti-emetics (metoclopramide, prochlorperazine, lithium

Family Hx
- Hx of parkinsonism, hx of liver disease (Wilson’s)

Psych Hx:
- PHQ-2, GAD-2
- Assess patient’s ICE : Progressive nature of disease

Social Hx:
Alcohol/ Smoking/ Married / Children / Occupation / Finances

Function
- Effect on patient’s life : Daily function (ADL/IADL)
- Mobility, Falls
- Cognition
- Bladder / Bowel
- Eye / ENT/ Swallowing

- Interactions with family and friends

- Type of housing, lift landing, home modification
- End of life plans in advanced Parkinson’s Disease
- Caregiver stress

PHYSICAL EXAMINATION
Postural BP (Do right at the start, do before taking social hx then ask social hx while standing)
→ supine, check BP
→ standing, pronator drift, dysmetria, leadpipe rigidity, cogwheeling, index to thumb tap, EOM ROM
(3mins)
→ pt’s gait (stooped posture, festinating gait, turning en bloc, reduced arm swing)

INVESTIGATIONS
1. No specific investigation, diagnosis is based on history and clinical examination
2. Trial of levodopa with good response indicates higher likelihood of primary Parkinson’s disease

MANAGEMENT
Non pharmacological
- Educate on progressive nature of dz , aim to control symptoms, improve QOL
- Encourage physical activity , fall prevention
- Refer to physiotherapy, occupational therapy to maintain mobility and independence of IADL and ADL
- Mobility aids as required (rollator, walking frame etc)
- Refer to speech therapy for speech quality
- Palliative care in end stage disease
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Pharmacological (as below)
- After initiation of pharmacotherapy, TCU in 1-2 weeks to review treatment, control of symptoms with
pharmacological therapy

Common SE Description Management

madopar
DOPA

Dyskinesia Choreiform involuntary Reduce dose and increase frequency instead

movement of face/arms 30-90
mins from dose of meds

Wearing off Freezing symptoms less than 4 Increase frequency of medications

phenomenon hours from last dose of maintaining same or lower doses each time
medications (higher dose has risk of dyskinesia)
BD to TDS dose

Sudden off No apparent relation to stiffness Confirm it is truly noted related to dose time
and levodopa dose (patient may not appreciate the dose time to
wearing off relation)
Avoid protein meals 30-60 minutes from the
dose.

Akinesia Sudden exacerbation of PD and Search for other causes and reverse
responses poorly to parkinson Given wrong dose
medications Anti-dopamine meds given (e.g. maxolon)

Postural hypotension Non-pharm [ABCDEF]:

Abdo binder
Bed up (head of bed). Bolus of water.
Countermaneouvres: compression stocking
daytime, leg crossing, squatting
Drugs
Education, Exercise
Fluids and salt: increase salt intake

Pharmacological
● 1stline Fludrocortisone: cause salt and
water retention to increase intravascular
volume.
○ SE: fluid overload, hypertension &
hypokalemia
○ Start at 50mcg once/day to max 200-
300mcg/ day
○ 2nd line or add on: Midodrine
10mg/day
○ Ergotamine: cause vasoconstriction
● If pt has supine hypertension and
postural hypotension: give anti-
hypertensives at night, fludrocortisone in
the morning

227
Abdomen: N/V, Domperidone to counter n/v
constipation Lactulose

228
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230
231
NON-SPECIFIC 2. APPROACH TO TIREDNESS

DDx
1. Cardio - Postural hypotension, CCF
2. Respi - Obstructive sleep apnea
3. Endocrine
a. Hypothyroidism
b. Adrenal insufficiency
4. GI - Anaemia
5. Neuro - Myasthenia gravis
6. Chronic end stage diseases: heart failure, renal failure, malignancy, liver disease
7. Chronic infections: TB
8. Rheumatological conditions: RA, SLE, Dermatomyositis
9. Chronic fatigue syndrome
10. Alcohol
11. Drugs: Betablocker, sedatives, anti-histamines
12. Depression

HISTORY
Complaint: Tiredness
● What do you mean by fatigue?
● How long?
● Whole day or worse as day progresses (myasthenia gravis)
● Exacerbating and relieving factors, better with rest (myasthenia gravis)

Cause
● Snoring at night, apneic episodes noted by partner, daytime somnolence, morning headaches,
feeling of poor sleep quality, restlessness at night (OSA)
● Weight gain, constipation, edema, cold intolerance (hypothyroidism)
● Postural giddiness, loss of appetite (hypoadrenalism)
● Exertional symptoms, postural giddiness, any bleeding/BGIT (anaemia)
o Source of bleeding: GI? PV? Chronic illness? Nutritional deficiency?
● Orthopnea/PND, LL swelling, SOB, chronic cough, poor urine output, jaundice, abdominal swelling,
LOW/LOA (renal failure, heart failure, chronic lung disease, liver failure, malignancy)
● Droopy eyelids, weakness that is worse with exercise and worse as day progresses (MG)
● Joint pain, alopecia, photosensitivity, oral ulcers, back pain, SOB (Rheumatological)
● Joint pain, muscular aches, sore throat, headache (chronic fatigue syndrome)
● Low mood, anhedonia, loss of motivation and concentration, insomnia (depression)

Complications
● How it affects daily living
o Does it pose any danger to pt? Eg falling asleep while driving

PMHx:
● Renal/heart/ liver failure, malignancy, DM

Drug history:
● Sedatives, anti-histamines, other drugs that can cause drowsiness
● Illicit drugs

Social Hx: Alcohol (taken near bedtime? CAGE)

PHYSICAL EXAMINATION
BP HR BMI
232
General appearance
Eyes: conjunctival pallor in anemia, Fatiguability of eyelids in MG
Nose/Mouth: Enlarged tonsils in OSA, nasal turbinates
Neck circumference, retrognathia, narrow oropharyngeal opening for OSA
Palpate neck for goitre in hypothyroid
Proximal myopathy and fatiguability in MG

H S1 S2
L
Pedal edema
Mental state exam

INVESTIGATIONS
● Blood tests: FBC, U/E/Cr, LFT, TFT, fasting glucose/lipid for CVRF
● Others: sleep study
● STOPBANG screening for OSA

MANAGEMENT
1) OSA [Link]
ᘇ ∂∂: neck masses, hypothyroidism, AR
ᘇ Refer for sleep study/polysomnography = diagnostic standard
◆ Apnea-hypopnea index ≥15/hour (or ≥5/hour if CVS comorbids present) = OSA
ᘇ Risk of progression causing R heart failure
ᘇ Can monitor with Epworth Sleepiness Scale
Treatment Options
ᘇ Lifestyle mods and weight reduction
◆ Sleep in lateral position eg tennis ball sewn into back of shirt
◆ Poor long-term compliance with positional therapy, hence not routinely recommended
over standard positive airway pressure therapy
◆ Avoid alcohol esp near bedtime, smoking cessation
● If taking alcohol, offer Thiamine
ᘇ Positive airway pressure eg CPAP
◆ Improves QoL and sleep indices
◆ Lowers BP, lowers risk of CVA and arrhythmia, improves LVEF in CCF pts, improves rates of
fatal and nonfatal CVS events
ᘇ Oral appliance therapy
◆ Mandibular advancement devices > Tongue-retaining devices
◆ But CPAP superior in improving sleep indices although QoL indices similar
ᘇ Surgery
◆ Insufficient evidence to support surgery
233
 ◆ Bariatric surgery in obese pts with OSA
✱✱ Things to consider: fitness to drive if dozing off?

2) Hypothyroidism
3) Depression
4) Anemia – cause?

234
NON-SPECIFIC 3. Evaluation and management of immunocompromised pts presenting to OPS for
infective symptoms ±fever
- Do FBC for all immunocompromised pts presenting with infective symptoms regardless of
presence of fever
- Do relevant ix for each complaint ie CXR for cough

Neutropenia - ANC < 1500 cells/microL Or Send ED immediately

Lymphocytopenia - ALC <1000 cells/microL for adults

If Fever > 38 Send ED

If Fever < 38 or no fever, pt clinically well, labs NAD Close f/up

Immunosuppressants and their side effects

Immunosuppressant Side Effects

Steroids Cushing, cataracts, osteoporosis, glaucoma

MTX Myelosuppression, liver toxicity, Pulmonary

fibrosis

Sulfasalazine Myelosuppression, nausea, rash, oral ulcers,

decreased sperm count

Azathioprine Myelosuppression, nausea, raised LFTs

Ciclosporin Gum hypertrophy, renal impairment, Nausea,

tremor,

Hydroxychloroquine Rash, retinopathy. Will need review by Eye

Biological agents Re-activation of TB, increase risk opportunistic

infections

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NON-SPECIFIC 4. APPROACH TO LOSS OF WEIGHT

DDx:
1. Malignancy
a. Females: breast, lung, colorectal
b. Males: lung, colorectal, prostate
2. End stage illnesses
a. End stage heart failure
b. End stage lung disease: COPD
c. ESRF
3. Malabsorption eg celiac disease, chronic pancreatitis
4. Other GI disorders
a. Oesophageal disease causing dysphagia
b. Gastroduodenal disease causing vomiting or abdominal pain
5. Endocrine
a. Hyperthyroidism
b. Poorly controlled DM
c. Hypocortisolism
6. Chronic infections eg HIV, TB
7. Depression/ Anxiety
8. Drugs
9. Poor dietary intake (social circumstances etc)

HISTORY
LOW
● How long
● How much weight lost (more than 5% over one year is significant)
● Did friends notice weight loss, clothes getting looser?
● Is weight loss intentional? Eg dieting, exercise, laxatives, diuretics

● Any change in appetite

o Involuntary weight loss with preserved appetite: thyrotoxicosis, poorly controlled DM,
malabsorption
o Involuntary weight loss with loss of appetite: malignancy, end stage diseases, GI conditions,
HIV, depression
● Screen for malignancy
o Females: any breast lumps, SOB/ cough/ haemoptysis, change in bowel habit/ malaena
o Males: SOB/ cough/ haemoptysis, change in bowel habit/ malaena, obstructive urinary
symptoms
o Bony pain – metastatic spread or primary
● LL swelling, orthopnea, PND, exertional symptoms – end stage heart failure
● SOB, poor effort tolerance – COPD, end stage lung disease
● Pruritus, fatigue, nausea, vomiting – ESRF
● Abdominal pain, steatorrhea, diarrhea – malabsorption
● Dysphagia, vomiting, early satiety – GI disorders
● Heat intolerance, diarrhea, anxiety, palpitations, tremor, eye symptoms – hyperthyroidism
● Nausea, postural giddiness, fatigue – hypocortisolism
● Low mood, anhedonia, loss of motivation and loss of concentration – depression
● Polyphagia, polyuria, polydipsia – DM
● Dietary history with assessment of intake

Alternative Differentials/ History

V–
I – Infection – TB, HIV ( Sexual hx and contact hx )
236
T –Tumour (Systemic symptoms, Female - Breast, colorectal ca, lung, Male - Lung, colorectal cancer,
prostate
A – Autoimmune (rash and joint pain)
M – Metabolic (DM, hyperthyroidism,phaechromocytoma, Addison’s) ,Malabsorption states ie IBD , celiac
disease
I – intestinal - Oesphageal dz ie gerd, dysphagia (obstruction vs neuromuscular) gastroduodenal dz ie
peptic ulcer, gastritis, gastric cancer
N–
C – Chronic diseases ie chronic heart failure, COPD , chronic kidney failure
D – Diet, Depression

TB Fever, night sweats, haemoptysis, cough, travel/contact hx

HIV (Sexual Hx) Take a Sexual hx (sensitive!) – how many sexual partners , social escorts,
homo/ heterosexual, protection, anal/ oral /vaginal /any history of
sexually transmitted diseases or partner hx

Tumour Hx of malignancy, neck/ groin lumps

Females: any breast lumps, SOB/ cough/ haemoptysis, change in bowel
habit/ malaena

Males: SOB/ cough/ haemoptysis, change in bowel habit/ malaena,

obstructive urinary symptoms

Bony pain – metastatic spread or primary

Autoimmune Rash, joint pain

Diabetes Polydipsia, polyuria, hyperphagia

Thyroid Tremors, heat intolerance, anxiety , insomnia, diarrhoea, palpitations,

sweating

Phaechromocytoma Headache, flushing

Malabsorption Chronic diarrhoea , bloody diarrhoea, vomiting

Intestinal - - Painful mouth lesions

Oropharynx - - Dysphagia/ Odynophagia
Esophagus / - LOA/ LOA / Early satiety / Abdominal bloating / obstructive symptoms ie
Stomach vomiting / Melena/ Haematemesis
-Change in bowel habit, PR bleed , symptoms of anemia

Chronic diseases Heart failure

(PMHX) COPD/ Asthma
Chronic liver dz – jaundice, abdo /leg swelling
Chronic kidney disease – oligouria, leg swelling, lethargy

Diet / drugs (Drug Appetite, slimming pills, thyroxine , Polypharmacy

Hx)

Depression/ Anxiety
(Psychosocial Hx)

PMHx:

237
 ● GI disorder, cancer, DM, thyroid disorders
● Heart, lung, renal disorders

FHx:
● DM, cancer, thyroid disorders

Drug history:
● Drugs that contribute to poor appetite: SSRIs, metformin
● Drugs with GI side effects: anticholinergics causing dry mouth, metformin causing nausea

Social history:
● Smoking / Drinking
● Sexual history for HIV
● Travel history

Sexual Hx for HIV! :

PHYSICAL EXAMINATION
BP / HR / Temp
Cachexia
Conjunctival pallor/ jaundice
Tongue - oral ulcers
Goitre
A Masses, organomegaly , DRE for anemia
Cervical LN / other LN if applicable

H S1 S2, S3 JVP raised

L decreased air entry
Peripheries
KIV Breast examination
Mental State examination

INVESTIGATIONS
FBC, H/C
CXR: rule out lung malignancy (esp if pt is a smoker)

TFT for hyperthyroidism

Fasting venous glucose to check for DM
Urea creatinine electrolytes to look for electrolyte imbalances that can be result of poor dietary intake, LFT
8am cortisol or Synacthen test

FOBT
OGD, colonoscopy

MANAGEMENT
If suspicious of malignancy -> Refer

If baseline evaluation is unremarkable, a three- to six-month observation period is justified.

Treatment focuses on the underlying cause. Nutritional supplements and flavor enhancers, and dietary
modification that takes into account patient preferences and chewing or swallowing disabilities may be
considered. Appetite stimulants may increase weight but have serious adverse effects and no evidence of
decreased mortality.

238
239
NON-SPECIFIC 5. APPROACH TO NOCTURNAL LEG CRAMPS

DIFFERENTIAL DIAGNOSES
Primary Secondary

● Idiopathic Medications
● HCTZ → electrolyte disturbances
● Statin, red yeast
● LABA
● ARB
● BZD
● OCP

Metabolic - HypoNa, HypoK , Hypocalcemia

● GI losses - vomiting/ diarrhoea
● Skin losses - Excessive sweating
● HypoMg in pregnancy
● Removal of fluid during HD

Endocrine
● DM/ Hypogly, hypothyroidism, Metabolic myopathies, alcoholism

Dehydration

Neurologic
● Restless leg syndrome
● Parkinson’s dz
● Radiculopathies, neuropathies, motor neuron dz

Structural / Mechanical
● Flat feet, genu recurvatum, and the hypermobility syndrome
● Prolonged sitting, inappropriate leg position during sedentary activity,
living/working on concrete floor

Others: Peripheral vascular disease, venous insufficiency

Other medications that may cause cramps include other beta agonists, beta blockers with intrinsic
sympathomimetic activity, angiotensin II receptor antagonists, benzodiazepines, teriparatide,
pyrazinamide, raloxifene, donepezil, neostigmine, tolcapone, clofibrate, cisplatin, vincristine, oral
contraceptives, and intravenous iron sucrose

HISTORY
Complaint: Cramp
- Site: Calf?
- Onset
- Aggravating: Walking? Stairs → claudication
- Relieved by: Rest?
- Severity: Affecting sleep?

Causes:
- Ddx: Rule out claudication stuff: Pallor/pale, pulselessness
- Medications: Diuretics
- Neurological: Sciatica/numbness or weakness

240
Course
- Maneuvers or medications tried

O/E
BP HR BMI
Neck: thyroid
Gait
LL: pulses

INVX
● RP

241
NON-SPECIFIC 6. APPROACH TO DIZZINESS AND GIDDINESS

DIFFERENTIAL DIAGNOSIS
Peripheral Central CVS GI Metabolic Others

BPPV CP angle Valvular Anemia Hypoglycemia Medications

tumor disease (?cause)

Vestibular Stroke or TIA Arrhythmia Postural Panic attacks

Neuronitis hypotension
(dehydration,
autonomic dysfn,
hypocortisol, drugs)

Meniere disease MI Electrolyte

disturbances

Carotid sinus
hypersensitivity

DDx:
1. Postural hypotension
a. Drugs
b. Autonomic dysfunction
c. Dehydration
d. Hypocortisolism
2. Stroke/ TIA
a. Posterior circulation insufficiency
3. Cerebellar syndrome
4. Electrolyte imbalances/ Metabolic
a. Sodium, potassium etc
b. Low sugar
c. Alcohol
5. Anaemia
6. Cardiac
a. Arrhythmias
b. AMI
7. Carotid sinus hypersensitivity, carotid sinus stenosis
8. Peripheral cause: BPPV, vestibular neuronitis, Meniere’s disease, otitis media/ externa

HISTORY
Complaint: Dizziness
● Character: Vertiginous? Lightheadedness ie Pre-syncope or syncope (tunnel vision) ?
Dysequilibrium (veering?)
o If non-vertiginous, can likely skip symptoms of peripheral causes
● Onset: Sudden or gradual. Episodic (peripheral) or continuous (central)?
● Timing: seconds vs minutes vs hours
● Precipitating factors: standing up from seated position, head movement/rolling in bed, movement
of neck (carotid sinus hypersensitivity), prolonged hunger, exertion
● Relieving factors: Lying down, sitting down

Associated symptoms
● UL/LL weakness of numbness → stroke, TIA

242
 ● Diplopia/dysphagia/dysarthria → post circulation stroke, TIA
● Tremor, difficulty coordinating, difficulty walking → cerebellar syndrome

Causes
● History of low sugar or low blood counts, hunger, generalised weakness → Hypoglycemia
● Exertional chest pain and SOB: PR bleeding, malena, haematemesis, haemoptysis or menorrhagia
→ Anaemia (?BGIT ?PV)
o Menstrual Hx: __ days menses, __ day cycle
o Complications of anemia
● Palpitations, chest pain, SOB, diaphoresis → Arrhythmias / AMI
● Tinnitus, hearing loss, ear discharge or pain, aural fullness → Peripheral causes
● Associated severe headache?
● Any vomiting / diarrhoea

Course
● Previous episodes
● Tried what treatment?
● Seen other doctors for it?

Complications
● Fall and its associated injuries

Function: How is this affecting you?

PMHx:
● DM, stroke, HTN, hyperlipidaemia
● Heart problems
● Ear problems

Drug history:
● Anti hypertensives
● Diuretics that can cause electrolyte imbalances
● Insulin, OHGAs

FHx:
● CVRF or heart problems

Social history:
● Alcohol

PHYSICAL EXAMINATION
BP (± postural BP) HR
Standing: Romberg
Gait (tandem gait)
Eyes: pallor, PEARL, EOM, nystagmus, hearing (no need weber’s / rinne’s if hearing normal)
Pronator drift, dysmetria (ataxic hemparesis)
KIV power
H: murmurs
Abdomen if suspect abdo masses, PV source
KIV offer DRE if suspect PR bleed, PV if suspect PVB
Otoscopy
Specific ENT exam: Dix Hallpike maneuver. HINTS test (Head Impulse, Nystagmus, Test of Skew) to ddx
vestibular neuronitis vs stroke

243
INVESTIGATIONS
Postural blood pressure monitoring
Bloods:
● FBC for anaemia
● BSL for hypoglycemia
● UECr for any electrolyte imbalances

Imaging:
● CT brain to rule out structural lesions and stroke → to ED
Others:
● ECG for arrhythmia, bradycardia
● 24Hr continuous ambulatory electrocardiogram monitoring for arrhythmia
● Echocardiogram for structural heart diseases
● Tilt table testing
● Carotid artery ultrasound for carotid artery stenosis

MANAGEMENT: ED or not?
Peripheral causes
● BPPV:
○ Treatment is Epley maneuver in clinic. Can teach Brandt-Daroff home exercises / self-
repositioning manouevres
○ NO ROLE for pharmacotherapy
○ Stemetil - vestibular suppressant (suppress the giddiness)

● Vestibular neuronitis:
○ Vestibular rehabilitation
○ Antiemetics/anti-nausea medications for no more than 3 days
○ Educate that it will spontaneously improve
● Meniere disease
○ Limit dietary salt intake to <2g per day. Reduce caffeine and alcohol.
○ Vestibular exercises
○ KIV thiazide diuretics
○ May need to refer to ENT if presentation were acute sensorineural hearing loss

Central causes
● Suspected stroke/TIA
● Suspected CP angle tumor
● Suspected arrhythmia/valvular heart diseases
● Anemia – hemodynamically unstable = ED
○ Consider iron studies if NCNC or folate/B12 if MCHC
○ Due to BGIT
■ Consider scopes
○ Due to menorrhagia
■ TV US to look for fibroids
■ Consider Progesterone to stop bleeding
■ Consider early referral

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Dix-Hallpike

If rotational, downward nystagmus or giddiness reproducible -> Positive

Epley’s maneuver

Brandt Daroff exercises (self treatment of vertigo)

To do the Brandt-Daroff exercise:

● Start in an upright, seated position.
● Move into the lying position on one side with your nose pointed up at about a 45-degree
angle.
● Remain in this position for about 30 seconds (or until the vertigo subsides, whichever is
longer). Then move back to the seated position.
● Repeat on the other side.
People who use this exercise usually are instructed to do multiple repetitions of the exercise at least twice a
day.

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AAFP

246
NON-SPECIFIC 7. APPROACH TO PROLONGED FEVER

Diagnosis of pyrexia of unknown origin

Fever ≥38 degree celsius for ≥3 weeks without etiology despite evaluation of at least three outpatient visits
or three days in inpatient care (Revised in 1991)

DIFFERENTIAL DIAGNOSES
INFECTION Viral
- Infectious mononucleosis EBV Sore throat , Fever, tonsillar ulcers
- CMV

- HIV!!! Fever, Lymphadenopathy, Rash, oral ulcers, non

specific lethargy, malaise

RF:
Blood related: previous tattoos, blood transfusions,
surgeries, IVDA Sexual transmission: Rem the 4Ps
(partners, practices, protection, previous STDs)
Bacterial
- CVS – Infective endocarditis Chest pain, SOB
- Respi – Tuberculosis , lung abscess Haemoptysis, night sweats, LOW, cough, chills and
- Hepatobiliary – Liver abscess rigors, runny nose, sore throat
- Gastrointestinal Abdominal pain , jaundice ,vomiting
Vomiting, diarrhea, seafood or raw food intake
- Genitourinary Irritative Urinary symptoms, Flank pain, Vomiting
- Skin Rashes

Parasite Travel Hx

Malignancy Lymphoproliferative,
myeloproliferative disorders
Leukaemia
Metastatic disease

Autoimmune Systemic Lupus Erythematosus

Rheumatoid Arthritis
Scleroderma
Still’s Disease
Inflammatory Bowel Disease
Polymyalgia rheumatica
Giant cell arteritis / temporal
arteritis

Others Drug-induced
Thromboembolic
Thyroiditis

HISTORY
Complaint: Fever
● No. of days
● What was peak Temperature?

247
 ● Did fever occur daily, or intervening afebrile days?
● What was response to antipyretics?

Cause
● Infection - Localising symptoms from head to toe
● Malignancy - LOW, LOA, night sweats, neck or armpit lumps, lethargy
● Autoimmune - Rashes, joint pain, oral ulcers, photosensitivity, red eyes, bloody diarrhoea

Travel history and Contact Hx

● Fresh water exposure – Leptospirosis
● Animal exposure – Dogs / rodents / rats (Leptospirosis), Cats (toxoplasmosis), farm animals
(brucellosis)
● Camping or travel in wooded areas

Sick contacts/ recent hospitalization: TB, Nosocomial infection

Sexual Hx: STDS! HIV infection! hx of transfusion – hep B, C, HIV

PMHx / Surgical Hx
● Cancer, autoimmune, HIV, TB, Malaria
● Previous operation ie presence of prosthesis → Osteomyelitis
Drug Hx: Immunosuppressives1
Family Hx: TB, Cancer, Autoimmune disease
Social Hx: Occupational exposure, Intravenous Drug Abuse (endocarditis), osteomyelitis

PHYSICAL EXAMINATION
T BP HR
Wt – LOW?
Eyes: injected conjunctiva, pallor, jaundice
Oral cavity: ulcers (HIV, viral infection), oral thrush, enlarged tonsils and exudates
Neck: cervical lymph nodes (offer axillary and inguinal lymph nodes too)
Heart: murmur?
Lungs
Abdomen: hepatosplenomegaly
Skin: rashes?
Joint pain / swelling
Genitalia (in HIV): ulcers, skin changes, discharge

INVESTIGATIONS
● Labs: FBC (look for neutropenia [ANC count])
○ ESR, CRP
○ KIV renal panel, LFT
● KIV CXR
● KIV UFEME, urine c/s

MANAGEMENT
AAFP: Empiric trials of antibiotics or steroids rarely establish a diagnosis and are discouraged in the
management of patients with FUO, unless there are clinical indications. Consultation with a subspecialist
(e.g., infectious disease specialist, rheumatologist, hematologist/oncologist) is appropriate at any point in
the evaluation.

Specific scenarios

1
HPA suppression if: glucocorticoid dose ≥20mg x >3/52 OR Pred ON ≥5mg for more than few weeks OR any pt who appears Cushingoid

248
1) Acute HIV infection
● Incubation period: 4-6 weeks after exposure
● Period of rapid viral replication, high viral load and infectivity
● Presentation: Prolonged fever, lymphadenopathy, rash, oral ulcers, malaise, arthralgia, myalgia
● Even if HIV test is pending, can assume it first!

Management:
● If hemodynamically stable, symptomatic tx for the fever and pain
● Refer to infectious disease direct access!
● Advise on screening for other STDs
● Advise on risk of transmission to sexual partners during period of high viral load, advised on
abstinence until treatment is initiated, alternative is condoms but risks of condom breakage etc

2) Fever secondary to newly diagnosed lymphoma ⇒ Refer to ED

Immunocompromising conditions
Congenital conditions
Congenital conditions most commonly affect the fetus and newborn. Classes of congenital conditions
include the following:
● Syndromes
● B-cell defects
● Combined B-cell and T-cell defects
● T-cell defects
● Macrophage, cytokine, and miscellaneous defects
● Phagocyte deficiency or dysfunction
● Complement deficiencies

Acquired conditions
These conditions may interfere directly with the immune system or may disrupt barrier function. Types of
acquired conditions include the following:
● Malnutrition
● HIV infection
● Trauma
● Medical conditions

List of immunosuppressants
Azathioprine (Imuran)
Mycophenolate mofetil (Cellcept)
Cyclosporine (Neoral, Sandimmune, Gengraf)
Methotrexate (Rheumatrex)
Leflunomide (Arava)
Cyclophosphamide (Cytoxan)
Chlorambucil (Leukeran)
Nitrogen mustard (Mustargen)

Definition of neutropenia
Neutropenia is defined as an absolute neutrophil count (ANC) <1500 cells/microL
(<1.5 x 109/L) in an adult.
Severe neutropenia is usually defined as an ANC <500 cells/microL (<0.5 x 109/L)

Fever in neutropenia
Fever (ie, a single oral temperature >38.3°C [101°F] or >38.0°C [100.4°F] sustained for >1 hour) should
always be presumed to be due to infection regardless of the presence of these other findings

249
Fever in a patient with neutropenia due to chemotherapy, HCT, or bone marrow suppression from any
cause is a medical emergency because such patients are at risk of sepsis and death from overwhelming
infection.

Management
The need for hospitalization depends upon the degree of neutropenia and the severity of infection (table
3). In general, patients with an ANC >1000 cells/microL can be managed on an outpatient basis, while those
with an ANC of <500 cells/microL and bone marrow aplasia require inpatient treatment with parenteral
antibiotics. Patients with an ANC between 500 and 1000 cells/microL can occasionally be managed on an
outpatient basis. We have a low threshold for hospital admission if the patient does not respond to
outpatient therapy. Routine reverse isolation procedures are of no benefit and serve to decrease contact
with medical personnel

Neutropenic fever - International guidelines advocate the administration of empiric antibacterial therapy
within 60 minutes of presentation in all patients presenting with a neutropenic fever

Treatment with empiric broad-spectrum antibiotics, including coverage for gram negative organisms
(including Pseudomonas species) should be initiated rapidly

If an immunocompromised patient (ie on immunosuppressants) has fever, ALWAYS DO A FBC !

CXR: mediastinal lymph nodes in lymphoma

250
GYNAE 1. NHGP/NUP ABNORMAL PAP SMEAR GUIDELINES

251
Endometrial Cells

NHGP Pap smear interpretations

List of terms in Pap smear reports: Clarification
Term Meaning Management
Atrophic smears with reactive Reactive, negative smear Routine
changes

Benign reactive changes

a) without atypia Reactive Routine

b) associated with atypia Atypia, probably reactive Earlier repeat

Endometrial cells We cannot always tell of

a) Is it stated that these are endometrial cells are benign or Correlate with age, LMP +
benign or abnormal abnormal. Pap smear not meant to clinical
endometrial cells seen? diagnose or screen for uterus (Please Annex A)
pathology. Within cycle OK to see
b) within or out of cycle endometrial cells. Out of cycle
needs clinical correlation.

Endocervical cells
a) reactive endocervical cells Reactive, negative Routine

b) no endocervical cells seen Endocervix not sampled Repeat in 1 year.

At 2nd Pap smear, use
endocervical brush.
If no endocervical cells seen in 2
consecutive smears, refer O&G.

252
Bacterial Flora Clinical correlation kiv treat
As far as pap smear is concerned
a) Excessive bacterial flora or Non specific for epithelial abnormalities à
neutrophils negative
b) Partially obscuring bacteria Routine
flora
Term Meaning Management
Intermediate cells As far as epithelial abnormalities
Descriptive terms à negative
a) superficial Not as well estrogenised à routine
intermediate cells Could be post-natal or peri-
b) intermediate cells menopausal

Inflammatory
a) inflammatory exudate As far as epithelial abnormalities
b) inflammatory changes More inflammatory cells scan, à negative
c) obscuring inflammation depends on time of cycle, clinical
d) reactive cellular changes finding Treat if symptomatic.
associated with inflammation In peri menopause/menopausal
women, kiv course of local
estrogens.

Repeat smear earlier . If 3

consecutive smears are
inflammatory, refer O&G.
Limited by obscuring blood Limited view but still satisfies If clinically NAD → routine
criteria for satisfactory smear
Lymphocytic cervicitis Severe chronic inflammation Earlier repeat
Metaplastic cells, Routine
a) reactive metaplastic cells Transition zone sampled
b) Squamous metaplastic
cells
Neutrophils
a) Moderate or large a) Descriptive, depends on time of Routine
number of cycle clinical findings
neutrophils without
atypia b)Inflammation with epithelial Early repeat
atypia Treat if there is cause clinically
b) Moderate or large
number of neutrophils with
atypia
Term Meaning Management
Parabasal cells
a) superficial If large numbers Routine
parabasal cells à poor estrogenisation, post natal,
b) parabasal cells menopausal
State consistent with HPV Suspect HPV Either repeat earlier or
colposcopy if previous abnormal

253
smear

254
GYNAE 2 . APPROACH TO ABNORMAL UTERINE BLEEDING
~ A normal cycle starts when pituitary FSH induces ovarian follicles to produce estrogen. Estrogen stimulates
proliferation of the endometrium. A LH surge prompts ovulation; the resultant corpus luteum produces
progesterone, inducing a secretory endometrium. In the absence of pregnancy, estrogen and progesterone
levels decline, and withdrawal bleeding occurs 13 to 15 days postovulation. Disruption of normal physiology,
anatomic changes in the endometrium, or endometrial CA may result in AUB.
~ Normal menstrual cycle: 21- 35 days with menstrual flow lasting 2-7 days

Definition of AUB: Any menstrual bleeding from the uterus that is either
⇨ Abnormal volume (excessive duration >7 days or heavy flow >80ml per cycle) OR
⇨ Irregular OR
⇨ Abnormal timing (delayed or frequent) OR
⇨ Non-menstrual bleeding such as IMB or PCB

Categories of AUB
Anovulatory bleeding Ovulatory
Irregular or infrequent periods, with flow ranging Occurs at regular intervals (every 24 to 35 days),
from light to excessively heavy but with excessive volume or duration of more
than seven days.

DIFFERENTIAL DIAGNOSES – PALM COEIN + Systemic Causes!

Think of the more likely causes based on the age! eg older pts think of perimenopausal, TRO malignancy!
Structural
P - Polyps
A – Adenomyosis
L – Leiomyoma
M – Malignancy & hyperplasia

Non-structural
C – Coagulopathy
O – Ovulatory dysfunction (refer below)
E – Endometrial dysfunction: endometritis, PID
I – Iatrogenic: IUCD
Not otherwise classified

Systemic causes
- Pregnancy
- Hypo/Hyperthyroidism
- Drug induced (Hormonal contraceptives ie Depo provera, post pill, anti-depressants, anti-psychotics,
AEDs)

Branch out under Ovulatory dysfunction

Hypothalamic Pituitary Ovarian Uterine Causes
(↓likely in perimenopause)
Excessive wt loss/gain Prolactinoma PCOS Asherman syndrome
Excessive exercise Sheehan’s Premature ovarian (adhesions and fibrosis of
Emotional or physical stress syndrome failure endometrium)
Severe illness Craniopharyngiom Resistant ovarian
a syndrome
Perimenopausal!

** IMB can be due to endometrial (polyps, hyperplasia/ carcinoma, endometritis/ PID) or cervical
conditions (polyps, cancer, cervicitis, ectropion) or vaginal conditions

255
** PCB usually due to cervical conditions
** Usually bleeding from cervix and vagina will be less than bleeding from the uterus

HISTORY
Acute Medical History

Complaint Gynaecological Hx
1) AUB – is it from endometrium/ cervix/ vagina ? - G_P_ ( previous mc/ abortions)
- Menstrual Hx: - Contraception – on OCP / PID?
- LMP (rule out pregnancy!) - Pap smear
- Frequency (ask for the exact dates of each menses)
- Duration Sexual Hx
- Amount of blood loss: no. of pads, heavy first few days, lighter flow - Relevant in PID
subsequently, any blood clots, menstrual diary
- Previous menstrual pattern Medical/ Surgical Hx
- Any IMB / PCB - Hx of fibroids / endometriosis /
adenomyosis / endometrial
Cause hyperplasia
- Hx of bleeding disorders / hypo
or hyperthyroidism

256
Red flag for older pts: LOW / LOA/ PMB/ Family hx of gynaecological
cancers (Risk factors for endometrial CA: Obesity BMI > 35, Use of Drug Hx/ Drug allergies
Tamoxifen, Hx of endometrial hyperplasia) Antiplatelet / anti coagulants
● Adenomyosis/Endometriosis: Dysmenorrhoea/ Dyspareunia/ Hormonal contraceptives ie depot
dyschezia, Bladder and bowel function (due to mass effect) provera, post pill, anti-
● Leiomyoma depressants, anti-psychotics, anti-
● Ovulatory: epileptics
○ Hypothalamus: Excessive wt gain/loss/ exercise /
Stress/ severe illness Ask for CI to NSAIDS (asthma,
○ Prolactinoma: headache, BOV, milky discharge from renal impairment, gastric
breast problems)
○ Sheehan: Heavy bleeding post delivery
○ PCOS: facial/ chest hair, hoarseness of voice, acne,
obesity
● Menopause: Perimenopausal symptoms – Flushing, Night
sweats, Palpitations, Insomnia, Mood swings, Irritability
● Endometrial:
○ PID: Fever / Pelvic pain / Vagina discharge
● Systemic:
○ Symptoms of hypo/hyperthyroidism: cold or heat
intolerance
Course
- Seen any doctors?
- Tried any medications / ix or mx done
Complications
- Anemia symptoms, Fertility
- Endometrial hyperplasia TRO malignancy if persistent anovulation

Disease Prevention Family Hx

● Vaccinations: HPV vaccine? Cancers / HNPCC/ Bleeding

● Cancer prevention: PAP smear? MMG if relevant. disorders/ thyroid

PSYCHOLOGICAL

How have you been coping? I

PHQ-2 C
GAD-2 E

SOCIAL

Impact on employment / education /activities / rs / sex / sleep Function

Drugs (Smoking, alcohol, illicit drugs) Bladder and bowel
Sex and relationship with others: Number of sex partners. Man,
woman or both.
Suicide
Sleep
Finance
Exercise
Diet

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PHYSICAL EXAMINATION ***HAND RUB***
T BP HR BMI
● Eyes: Conjunctival pallor
● Neck: goitre
● KIV look for chest hair and acanthosis nigricans in PCOS, Milky nipple discharge in Prolactinoma
● Abdominal exam: Scars, Abdominal tenderness, uterine enlargement, adnexal masses
● PV exam:
○ VE: Bimanual palpation of uterus and adnexal region
○ Cervical excitation/ Adnexal tenderness
○ KIV offer pap smear
● Speculum: check for cervical lesion/ polyp/ discharge / IUCD thread

INVESTIGATIONS
● Stat tests
○ UPT ****
○ FBC, KIV PT/aPTT/ INR for menorrhagia
● Other bloods
○ TFT, Serum prolactin, FSH, LH, Estradiol / Testosterone (Premature ovarian failure)
○ Serum testosterone in PCOS
● US Pelvis, If Age >40 yo, refer for Transvaginal US and Endometrial sampling/D&C , Swabs if suspect
Gonorrhoea/Chlamydia

MANAGEMENT
1) NSAIDS for analgesia Mefenamic acid 500mg TDS
2) Tranexamic acid 1g TDS x 3/7, risk of venous thrombosis
3) Combined OCP pill
4) Cyclical progesterone 5-10mg BD x 10-14 days up to 21 days
(anovulation: no corpus luteum to produce progesterone. Oral progesterone helps to stop proliferation of
lining, maintain lining and withdrawal of progesterone allows shedding of lining)
5) Mirena / levonorgestrel-releasing intrauterine system
- releases 20ug of LNG daily
- lasts 5 yrs, 50% amenorrhoea after 1 yr, 20% intermittent spotting in first 6 mths, lower risk of PID and
ectopic compared to copper IUCD
6) Depot provera – IM 150mg every 3 monthly
- Irregular bleeding the first 3 months, S/E : abdo bloating, breast tenderness, weight gain, depression,
water retention

APPROACH TO PRIMARY AMENORRHOEA

Definition: Absence of menses by age 16
Usually due to genetic condition ie Turner’s or anatomal condition ie Mullerian Agenesis

APPROACH TO SECONDARY AMENORRHOEA

Definition: Absence of menses for 6 months in a woman who was previously menstruating

258
INVX
Test Utility
1) UPT r/o pregnancy
2) TFT Hypo/hyperthyroidism
3) FSH / LH - Suggests ovarian failure if FSH > 30IU/L
- Low levels suggests hypothalamic / pituitary dysfunction
- Reversal of LH/FSH ratio > 3:1 suggests PCOS
4) Prolactin levels Prolactinoma
5) Estradiol/ Testosterone Ovarian failure
6) Progesterone challenge test - Ensure not pregnant
- Give norethisterone 5mg BD x 5/7
- If there is withdrawal bleeding with progesterone, means
there is presence of oestrogen, pt will need cyclical
progesterone for withdrawal bleeding to protect endometrium
from endometrial hyperplasia and carcinoma
7) Oestrogen and progesterone - If progesterone challenge test fails, combined progesterone
challenge test (if progesterone and oestrogen will be needed for added oestrogen
challenge test fails)

MX
Refer to O&G for workup of secondary amenorrhoea after excluding pregnancy
Prolonged amenorrhoea in women causes bone loss, consider ca/vit d supplements

For Secondary Amenorrhoea

1. Hypothalamic amenorrhea (hypogonadotropic hypogonadism) ie weight loss, stress, excessive exercise
● Disruption of pulsatile hypothalamic GnRH secretion → decreased pulses of gonadotropins, absent
midcycle surges in LH secretion, absence of normal follicular development, serum concentrations of
FSH are low or normal, and they often exceed those of LH, similar to the pattern in prepubertal
girls. → anovulation, and low serum estradiol (E2) concentrations.
● Female athlete triad: low energy availability + menstrual dysfunction + low bone density
● TRO eating disorders, mood disorders
● Mx:

259
 ○ Lifestyle changes: Need for adequate caloric intake to match energy expenditure
sometimes results in increased caloric intake or reduced exercise, followed by resumption
of menses.
■ Nonathletic women who are underweight or who appear to have nutritional
deficiencies should have nutritional counseling, and they can be referred to a
multidisciplinary team specializing in the assessment and treatment of individuals
with eating disorders.
○ CBT
○ Management of low bone density

2. Hyperprolactinemia — The management of women with amenorrhea due to hyperprolactinemia

depends upon the cause of the hyperprolactinemia and the patient's goals (eg, pursuing fertility or not).
This topic is reviewed in detail separately.

3. Primary ovarian insufficiency (premature ovarian failure) — Women with primary ovarian insufficiency
(POI) should receive estrogen therapy for prevention of bone loss. This can be either an oral contraceptive
(if the patient is having intermittent ovarian function and does not wish to become pregnant) or
replacement doses of estrogen and progestin. Regimens for the latter are reviewed separately. Age <40

4. Intrauterine adhesions — Therapy of Asherman syndrome (intrauterine adhesions) consists of

hysteroscopic lysis of adhesions followed by a course of estrogen treatment to stimulate regrowth of
endometrial tissue [10].

5. Polycystic ovary syndrome

ᐉ Definition: Rotterdam criteria: 2 out of 3
❖ Oligomenorrhea/ anovulation: <8 menstrual cycles/year
❖ Clinical hyperandrogenism (Ferriman Gallwey score) or biochemical hyperandrogenism (total
testosterone)
❖ Polycystic ovaries on US: ≥12 follicles in at least 1 ovary measuring 2-9mm in diameter or total
ovarian volume greater than 10ml
AND exclusion of other etiologies (eg CAH, androgen-secreting tumours, Cushing syndrome)
ᐉ Important points:
- Menstrual Hx / Hirsutism
- Desire for fertility?
- Metabolic syndrome
- Need to induce withdrawal bleed
ᐉ History
- Menstrual Hx: Oligomenorrhoea (from anovulation)
- Hyperandrogenism: facial hair, chest hair, acne, male pattern hair loss, voice deepening
- Gynae / Obs Hx: Infertility / Desire for fertility
- Obesity and metabolic syndrome: BMI, BP, DM, HLD
- Co-morbids: OSA/ NASH

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ᐉ DDx: Hypothyroidism, Cushing’s syndrome, drugs induced (steroids, androgen, progestins), other causes
of oligomenorrhea!
ᐉ Complications:
- Infertility
- Increase CVD/CVA risk
- Increase LDL and insulin resistance (leading to increase risk of DM)
- Increase risk of endometrial hyperplasia and cancer (need to induce withdrawal bleed at least 3-4
monthly)
- Depression and anxiety
ᐉ Physical Examination
- BP elevated, High BMI, Obesity (waist circumference >80cm)
- Face: Hirsutism and acne (as above), male pattern hair loss, deepening voice
- Neck: Acanthosis nigricans
- Abdomen: Usually unremarkable
- Others: increase muscle mass, clitoromegaly
ᐉ Invx: To exclude other disorders that can cause irregular menses and hyperandrogenism
- UPT, TFT
- US pelvis
- FG / lipids
(Others in tertiary centre: Serum prolactin (TRO pit tumor) LH and FSH (3:1), Testosterone levels
Urine cortisol and low dose dexa suppression test (r/o Cushings), Serum IGF1 (r/o acromegaly))
ᐉ Management
● Anovulation and Infertility
○ 1st line = lifestyle mods if overweight → calorie-restricted diet
○ Lifestyle mods + weight loss reduce insulin resistance and can significantly improve
ovulation
○ Ovulation induction: Clomiphene
○ Metformin impact is controversial in improving infertility
○ For those NOT desiring fertility
● 1st line: OCP to induce regular menses and reduce hyperandrogenism and
contraception (to protect endometrium from hyperplasia)
○ Ask for contraindications to OCP pills (CI in body mass index [BMI]
≥30 in >40 yo)
○ Alternative: progestin only pills, mirena, cyclic progestin therapy
● 2nd line: Metformin for menstrual regularity / ovulation, insulin resistance
and DM and reduce androgen levels
● Non-pharm / Lifestyle modification:

261
 ○ Diet, exercise and weight loss (2-5%, aim BMI <25) can help restore ovulatory cycles and
cause ovulation
○ Stop smoking
● Spironolactone 50-100mg BD for anti-androgen effect (teratogenic and can cause GI discomfort and
irregular menstrual bleed)
● Others:
○ Acne: Topical benzoyl peroxide, topical and oral antibiotics and topical retinoids for acne
○ HLD: Statins
● Surgical Intervention:
○ Aimed at restoring ovulation
○ Previously wedge resection used but risk of post op adhesions
○ Currently lap ovarian drilling → Cx eg formation of adhesions and ovarian atrophy
○ Concerns about long term effect of drilling on ovarian function

262
6. Perimenopausal
ᐉ Presenting symptoms:
● Vasomotor: Hot flushes, night sweats
● Psychological: depressive symptoms; anxiety, irritability; sleep disturbance; overall diminished well-
being; reduced memory
● Physical: sleep disturbance; fatigue; headaches; muscle and joint pain; crawling sensations on skin
(formication)
● Urogenital and sexual: vaginal itching, burning; dryness and dyspareunia; PU frequency, urgency
ᐉ Diagnosis: straightforward if a woman is >45 years and reports cessation of menstruation for over 12
months, ± symptoms.
● Challenging situations, in terms of diagnosis, include:
○ women who have had an endometrial ablation
○ women who have a progestin-releasing IUCD
○ women who are using systemic hormonal contraception (oestrogen plus progestin oral,
transdermal or vaginal ring or implanted, depot progestin)
○ women who have symptoms and are less than 45 years old
ᐉ Invx: Usually don’t need hormonal tests to diagnose menopause. To rule out other causes: UPT, TFT,
prolactin. KIV FBC / DM for fatigue

ᐉ Management
● Non pharmacological

263
● Pharmacological
○ Hormonal therapy

● Non hormonal for Vasomotor Symptoms

○ Selective serotonin reuptake inhibitors (SSRI)
○ Clonidine
○ Gabapentin
○ Pregabalin
○ Hypnosis
○ Cognitive behaviour therapy
○ Weight loss for obese women
○ Stellate ganglion blockade (for severe resistant symptoms)

264
Other Conditions
Cervical polyps
[Link]
● Cervical polyps commonly occur during the reproductive years, especially after age 40 years.
● Polyps should be removed when symptomatic (eg, bleeding, excessive discharge), large (≥3 cm), or
appearing atypical.
● Malignancy is rarely found in a cervical polyp; however, polyps which are removed should be
submitted to the laboratory for histological study.

Adenomyosis
[Link]
● Adenomyosis refers to a disorder in which endometrial glands and stroma are present within the
uterine musculature (uterine adenomyomatosis).
● Symptoms: menorrhagia and dysmenorrhea with a uniformly enlarged uterus) in the absence of
endometriosis or leiomyomas. MRI / TVUS
● Endometrial biopsy is often normal because the abnormality is in the myometrium, not the
endometrium. A definitive diagnosis of adenomyosis can only be made from histological
examination of hysterectomy specimens.
● Treatment:
○ Fertility desired: Medical: Progestogens
○ Fertility not desired: Hysterectomy is the treatment of choice for women with significant
symptoms. Ovaries can be conserved.

Sheehan syndrome
Also called postpartum hypopituitarism due excessive blood loss and hypotension during childbirth. Can
occur slowly, after a period of months or even years
Have too little of the hormones the pituitary gland controls: TSH thyroid, ACTH adrenal, Prolactin breast
milk production and FSH/LH menstrual function hormones.

Symptoms:
● Difficulty breast-feeding or an inability to breast-feed
● No menstrual periods (amenorrhea) or infrequent menstruation (oligomenorrhea)
● Inability to regrow shaved pubic hair
● Slowed mental function, weight gain and difficulty staying warm as a result of an underactive
thyroid (hypothyroidism)
● Low blood pressure (hypotension)
● Low blood sugar (hypoglycemia)
● Fatigue
● Irregular heartbeat
● Breast shrinkage

265
GYNAE 3. CONTRACEPTION

Possible Scenarios
Contraception initiation ● Family planning
○ Initiate COC

Troubleshooting contraception ● Missed pills

Emergency contraception

Natural Family Planning

Unintended pregnancy

Overview of contraception methods

Contraception methods
- Irreversible
- Vasectomy
- Tubal ligation
- Reversible
- Hormonal
- Oral: COC, POP
- Injectables: IM medroxyprogesterone (depot provera)
- IUD: Mirena (etonorgestrel)
- Others: Implanon, Patch, vaginal rings
- Non-hormonal
- Condoms, diaphragms, spermicides
- Copper IUD
- Natural
- NFP
- Lactational amenorrhoea

266
267
FAMILY PLANNING CONSULT
Consider patient characteristics, contraception method characteristics and timeframe for return to fertility.

HISTORY
Age: Above or below 35 years old
O&G history
- G_P_ or Gynae code [age] / [years married] / [previous pregnancies] / [no of pregnancies >28/52]
- Breastfeeding now?
- Postpartum week__? ⇒
- Progestin only pills generally safe post partum; theoretical concern about impaired
lactogenesis. Only to start after 30 days postpartum
- As a result of conflicting data regarding impact of estrogen-progestin contraceptives on
lactation, we advise avoiding estrogen-progestin contraceptives in breastfeeding women
who are less than 30 days postpartum. This practice is in accordance with guidance from
the Centers for Disease Control and Prevention. Breastfeeding women who are at least 30
days postpartum and do not have additional risk factors for thromboembolic events can
reasonably begin estrogen-progestin contraceptives.
- BUT locally: generally no COCP for breastfeeding mothers
- Recent abortion?
- Completed family? If not, is there any wish to return to fertility within 1 year? ⇒ if desires fertility
within 1 year, consider short-acting reversible methods.

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Medical History
- Any history of HTN, DM, Migraine with aura, smoker, DVT, IHD/stroke
- Obesity BMI ≥35
- Current STI/PID ⇒ Excludes IUD
- Fibroids causing distortion of uterine cavity -> excludes IUD
- Breast cancer/undiagnosed breast lumps
- Liver problems ie cirrhosis. liver tumours
- Undiagnosed vaginal bleeding

Drug history:
- Any previous use of hormonal methods and did patient experience any side effects?

Sexual History
- Number of sexual partners
- High risk behavior ⇒ Not suitable for IUD. Barrier method on top of regular contraception to
protect against STI.

Social History
- Religious beliefs ⇒ May preclude all methods except natural family planning
- Costs ⇒ May preclude implants, mirena etc.

PE
BP BMI
Supine
- Peripheral stigmata of chronic liver disease
- Eyes for jaundice
- Breast exam for lumps/nipple changes
- Abdo exam for liver masses
- Offer bimanual examination and PAP smear

INITIATING COCP
- Indication: Contraception
- Contraindication excluded
- Exclude pregnancy
- Clinically exclude (see table below)
- UPT exclusion ( at least 2 weeks from last SI)
- Exclude medical risk factors (Thrombosis risk, cancer risk)
- CA breast
- VTE
- CVA
- IHD
- Migraine with aura (stroke risk)
- HTN
- Smoker ≥35yo
- Recent surgery with immobilisation
- Liver disease (severe cirrhosis, hepatoma, hepatocellular adenoma)
- SLE with antiphospholipid Abs
- Solid organ transplant
- Valvular heart disease (arterial thrombosis)
- Vascular disease
- Precautions: Ensure not breastfeeding, not pregnant
- Monitor BMI and weight prior to initiation

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 - Drugs: Lamotrigine, Rifampicin, anticonvulsants (eg topiramate, phenytoin), some anti-
retrovirals
- Cost/compliance
- Adverse reactions explained:
- (Common) Nausea, vomiting, bloating, weight gain, breakthrough bleeding, breast
tenderness
- (Important) Thromboembolism/ stroke, increased risk of breast cancer with prolonged use ,
worsen migraine and increase BP
- Dose/duration/directions
- Dosing instruction (see below)
- See missed pill protocol below
- Beware of drug-drug interactions

270
Contraindications to postinor/ progesterone pills
- Pregnancy
- Undiagnosed vaginal bleeding
- Liver problems
- Breast Cancer
- For postinor: if <72 hours from last sexual intercourse
Special situations
Pt has epilepsy on lamotrigine
Cannot give COC due to risk of reducing the lamotrigine levels causing breakthrough seizure
Best option: IUD/IUCD
? Can give POP / Implanon /Depot Provera

Epilepsy on phenytoin / carbamazepine/ topiramate

Cannot give COC and POP
Best option: IUD/IUCD
? Can give Implanon /Depot Provera

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MISSED PILLS PROTOCOL

Questions:
What missed pill advice would you give?
What if she missed pill on 1stweek? Or 3rd week?
When would she need emergency contraception? When would she need additional contraception?
[Link]

What should I do if I miss a pill (combined pill)?

If you're on the combined contraceptive pill and you miss a pill, what you need to do depends on:
1) how many pills you've missed (you've missed a pill when it's more than 24 hours since you should have
taken it)
2) when you missed your pill (where you are in the pack)
3) the type of combined pill you are taking

What if I've missed one pill?

If you've missed one pill anywhere in the pack or started a new pack one day late, you're still protected
against pregnancy. You should:
272
 · take the last pill you missed now, even if this means taking two pills in one day
· carry on taking the rest of the pack as normal
· take your seven-day pill-free break as normal or, if you're on an everyday (ED) pill, take your
dummy (inactive) pills
If pills were missed in the LAST week of hormone pills (days 15 to 21 of a 28-day pack), the patient
should skip the hormone-free week (days 22 to 28). Finish the last week of hormone pills (week 3), then
skip week 4 (placebo pills), and immediately move on to a new pill pack the next day. If she is unable to
start a new pack, back-up contraception should be used until hormonal pills from a new pack are taken
for seven consecutive days.
You don't need to use extra contraception.

What if I've missed two or more pills?

If you've missed two or more pills anywhere in the pack or started a new pack two or more days late (48
hours or more), your protection against pregnancy may be affected. You should:
- Take the last pill you missed as soon as possible and continue with the usual pill taking schedule.
- Depending on when she remembers, she may take two pills at different timing (the moment of
remembering and her regular time) or two pills at the same time
leave any earlier missed pills
- If two or more pills are missed in the first week of the cycle and unprotected intercourse occurs during
this week, use of emergency contraception could decrease the risk of pregnancy.
- use extra contraception such as condoms for the next seven days

Additional things
If you are in the first week of taking the pills
> Need emergency contraception if you had unprotected sex within the last 7 days (need 7 consecutive
days of contraception before it is effective)
If you are in the second week of taking pills (7 or more pills left)
· Same. finish the pack, take your seven-day pill-free break as normal, or take your inactive pills
before you start your next pack
If you are in the third week of taking pills (less than 7 pills left)
· Finish the pack and start a new pack the next day; this means missing out the pill-free break or not
taking your inactive pills

EMERGENCY CONTRACEPTION
Scenario: Woman comes for morning after pill in clinic
Indication: For unprotected SI (due to failure to use/condom slip) within last 72 hours (or 120 hours if
choosing ulipristal)
Contraindications: Exclude pregnancy, and contraindications to pills/IUD
Available methods:
- Levonorgestrel aka postinor (1 dose vs split 2 doses)
- Ulipristal
- Yuzpe method (COC)
- Copper IUD

Method Administration

Levonorgestrel aka postinor (1 dose vs split 2 - 0.75mg now, and 0.75mg 12 hours later OR
doses) - 1 dose: 1.5mg STAT
● <72 hours

Ulipristal acetate aka Ella - 30mg STAT

● Up to 5 days

273
 Yuzpe method with COC (100mcg of ethinyl - 1 tab now, and 1 tab 12 hours later
estradiol and 0.5mg levonorgestrel)

Copper IUD - Insert in office

● Within 5 days

● Counsel on effectiveness, possible failure, need to exclude pregnancy if missed period after
emergency contraception.
● Counsel on regular contraception use.

If Emergency contraception is vomited

● If levonorgestrel is vomited within 3 hours of ingestion and no anti emetic given -> can give anti
emetic agent and repeat the levonorgestrel
● If estrogen- progestin is vomited within 1 hr of ingestion and no anti emetic given -> can give anti
emetic and estrogen-progestin dose repeatred , however it will be better to switch to
levonorgestrel alone method for the subsequent dose since there is less associated emesis
● If Uilipristal is vomitted within 3 hrs -> given anti-emetic and uilipristal repeated
● Alternative -> Offer placement of copper IUCD instead of emergency contraception

274
NATURAL FAMILY PLANNING

275
GYNAE 4. DYSMENORRHOEA

DIFFERENTIAL DIAGNOSES
Primary No pelvic pathology , usually in Recurrent during menses , caused by
perimenarche intense uterine contractions causing
ischemia
First D1-2 of menses
a/w nausea, diarrhoea, fatigue,
headache

Secondary Pelvic Inflammatory disease *** Fever, Foul smelling vaginal

discharge , urethritis, proctitis

Endometriosis Changes in timing and intensity of the

pain or dyspareunia may suggest
endometriosis,
Non midline pelvic pain
Dyspareunia and dyschezia
(less likely to have menorrhagia)

Adenomyosis (age after 35, non cyclic Abnormal uterine bleeding –

chronic pelvic pain) menorrhagia, intermenstrual
Fibroids (rare in adolescent, common by bleeding, oligomenorrhoea
35 PLUS Non midline pelvic pain
Dyspareunia and dyschezia

Cervical Stenosis
Pelvic congestion syndrome

Serious must Ectopic pregnancy LMP

rule out Miscarriage

Name/Age/Sex

BIOLOGICAL

Acute Chronic Medical History

276
Complaint Gynaecological Hx
Dysmenorrhoea ● - LMP
· Site – midline vs iliac fossa ● - Menstrual Flow
· Onset / Duration – sudden + new (ectopic) vs ● - G_P_ (previous mc/
gradual , occurs every menstrual cycle + similar abortions)
nature ● - Hx of ectopic pregnancy /
· Character PID / fibroids/
· Radiation – back ( occurs in both primary and endometriosis /
secondary causes) adenomysosis
· Timing – ● Contraception
· Exacerbating factors -
· Severity – Sexual Hx
o Relevant in PID
Cause
- Associated symptoms Medical/ Surgical Hx
· Foul smelling vaginal d/c or fever If menorrhagia -> bleeding
· Menstrual flow - ? menorrhagia, IMB , Post coital diathesis
bleeding
· Dyspareunia, Dyschezia Drug Hx/ Drug allergies
· Irritative urinary symptoms/ bowel function If menorrhagia -> blood thinners
· Abdominal distension Ask for CI to NSAIDS- asthma, renal
** if menorrhagia – check for hypothyroidism impairment, gastric problems
Course
● Tried what treatment? Medication List(any antibiotics,
● Seen other doctors for it? OCP), TCM/OTC
Complication
● Fertility concerns
● If menorrhagia -> anemia

Disease Prevention Family Hx

● Vaccinations: HPV vaccine? Endometriosis

● Cancer prevention: PAP smear? MMG if relevant If menorrhagia -> bleeding
disorders

PSYCHOLOGICAL

How have you been coping with the pain I

PHQ-2 C
GAD-2 E

SOCIAL

Impact on employment/ education /activities/ rs /sex / sleep Function

Environment
Home Bladder and bowel
Employment/education bADL (DEATH)
Activities iADL (SHAFTTT)
Drugs (Smoking, alcohol, illicit drugs)
Sex and relationship with others: Number of sex partners. Man, Cognition
woman or both.
Suicide Eye, ear and swallowing
Sleep
Finance

277
 Exercise
Diet

Physical Examination ***HAND RUB***

T BP ( hypotension in ectopic) HR
Abdominal exam: Palpate for abdominal tenderness, uterine enlargement, adnexal masses.
PV exam:“I will need to examine your private area”
Equipments: Double pair of gloves. Lubricating jelly. Speculum. Swab stick.
Cervical excitation.
Adnexal tenderness
Speculum (Show patient speculum, I will be inserting this plastic speculum to better visualize the vagina and
cervix). Check for discharge

Investigations
UPT, FBC/ TFT if menorrhagic, KIV ufeme
HVS if vaginal d/c
Transvaginal US

MANAGEMENT
1. Primary Dysmenorrhoea
Non pharmacological
- Heat to lower abdomen
- Exercise

Pharmacological
- NSAIDS
- COCP : suppress ovulation, endometrium atrophy, reduces menstral flow and uterine contractions
- Extended/continuous administration better relief vs cyclical eg 24/4 formulation
- POP, depo-povera (amenorrhea,return of fertility delayed), Mirena, implanon
Education
Follow up

2. Adenomyosis
Conservative
- NSAIDs, TXA
- IUD mirena ( not copper IUCD as it will worsen dysmenorrhoea)
- ( dont give OCP due to limited data on efficacy of ocp for adenomyosis according to uptodate)

Surgical
- Hysterectomy
- Fertility preserving : Uterine artery embolization

3. PID
Indications for hospitalization

278
Pharmacological Outpatient therapy :
A single dose of IM ceftrixacone 250mg + PO doxycycline 100 mg BD for 14 days)
KIV add metronidazole 500mg BD x 14 days for women with gynecologic instrumentation within the past
two to three weeks for anaerobic coverage.
An alternative to doxycycline is azithromycin 1g once per week for 14 days
An alternative to metronidazole is clindamycin 450mg QDS for 14 days

Counselling
- To refrain from sexual activity until they have completed therapy, their symptoms have resolved
- Screen for other STD
- Future safe sex practices
- Vaccinations - Hep B and HPV
- Male sex partners of women with PID should be examined and treated if they had sexual contact
with the patient during the 60 days prior to the patient's onset of symptoms, regardless of the
woman's STI test results. Regimens should include antibiotics with activity against N. gonorrhoeae
and C. trachomatis, such as ceftriaxone (250 mg) intramuscularly plus either azithromycin (1 gram)
orally as a single dose or doxycycline (100 mg) orally twice daily for seven days.

Followup: TCU within 48 to 72 hours

279
GYNAE 5. INFERTILITY

Differential diagnoses
Male factor Female factor

Anovulation Ovulating

Erectile Hypothalamus Pituitary Ovarian Systemic Structural

dysfunction
Stress Prolactinom PCOS Hypothyroid 1. Tubal obstruction
Sudden weight a Premature 2. Uterine adhesions/
loss ovarian fibroids/
failure endometriosis/
adenomyosis
3. Cervix pathology

HISTORY
Complaint: Infertility
- Confirm infertility: Regular (every 1-2 days SI or at least 2-3x/week after cessation of each
menstrual cycle), unprotected, vaginal intercourse for >12 months without conception
- Duration of infertility

Causes
● Female factor:
○ Gynae Hx :
○ Menstrual history: Focus on regularity of menses (irregular menses suggests anovulation)
■ How many menstrual cycles a year? <8 cycles/year → PCOS
○ G_ P_ (previous miscarriages/abortion), contraception, pap smear
○ Psychological stress
○ Weight changes
○ Headache, nipple discharge and visual field → prolactinoma
○ Fatigue, hair loss, cold intolerance → hypothyroid
○ Acne, hirsutism. Previous US ovaries done? → PCOS
○ Previous pelvic inflammatory disease/surgeries that can cause adhesions

● Male factor:
○ Alcohol usage
○ Smoking
○ Obesity
○ Psychological: stress, inability to sustain ejaculation, premature ejaculation
○ Erectile dysfunction
● Combination factor: Sexual History: protection, erectile dysfunction, penetration, ejaculation

Course
● Any hormone tests done? Day 21 progesterone levels?
● US scans?

Complications
● Rs between husband and wife?
● Mood? PHQ 2

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Medical History: Chronic illness that needs to be controlled before conception? (e.g. DM suboptimal should
be <6.5%)

DA:
Medication: Any chronic medications that needs to be altered to be pregnancy safe? (e.g. glipizide, statins,
carbimazole),
OTC/TCM

Family history
Preventive: HPV vaccines, vaccines that should be received by pregnant woman
Psychological: PHQ2, GAD2. ICE: Worried about permanent infertility?
Social:
● Work
● Finance: Fertility treatment may be expensive
● Smoking? Alcohol? → should stop
● SEXUAL HISTORY (protection, erectile dysfunction, penetration, ejaculation)
● Home
● Exercise
● Diet

PHYSICAL EXAMINATION
BP HR BMI
Inspection: Hirsutism? Acne? Obese? Too thin?
Neck: Goitre / Hypothyroid signs
Abdominal exam
Vaginal Examination: Cervical excitation? Adnexal masses? Palpable uterus?
KIV Pap smear

INVESTIGATIONS
UPT
TFT
US pelvis: TV/TA
Blood test for androgen, Day 21 progesterone
CVRF screening

MANAGEMENT
Likely PCOS desiring Non-pharm:
pregnancy ● Weight loss
● Abstain from smoking, alcohol
● Aim BMI <30
● Regular coitus ≥3x/week
● Screen for rubella ± varicella immunity, vaccinate if not immune,
thal screen
Educate: Cysts in ovary due to under- developed follicles.
Pharm
● Maybe metformin
● Optimise chronic medical conditions
● Start folic acid
● Refer for evaluation, clomiphene
● Refer fertility specialist

When to refer (KKH O&G book)

- Woman’s age > 35 yo

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 - Woman’s age > 30 yo and trying for > 1 yr
- Woman’s age < 30 yo and trying for > 2 yrs
- Duration of subfertility > 3 yrs
- Known hx of reproductive pathology ie amenorrhoea, PID Known hx of infertility ie premature
ovarian failure, tubal ligation/ vasectomy
- Structural abnormalities ie fibroids / endometriosis
- Sexual dysfunction
- Presence of male problems ie hx of urogenital surgery, varicocele , significant systemic illness

What specialist may do

- Scans: TVUS, hysterosalphingogram (look at fallopian tubes)
- Blood tests - check for hormonal levels Mid progesterone level (7 days before expected period <
30nmol -> ovulation dysfunction) FSH D2-3 / LH/ Prolactin / Testosterone / TFT
- Seminal analysis , check for hypospadias, scrotal varices, genetic syndrome for male partner
- Tx: clomiphene citrate, metformin, gonadotropins, laproscopic ovarian drilling for PCOS , In vitro
fertilisation (IVF)

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GYNAE 6. MENOPAUSE

Summary
● Natural menopause is defined as the permanent cessation of menstrual periods, determined
retrospectively after a woman has experienced 12 months of amenorrhea without any other
obvious pathological or physiological cause
● It occurs at a median age of 51.4 years in normal women, and is a reflection of complete, or near
complete, ovarian follicular depletion, with resulting hypoestrogenemia and high follicle-
stimulating hormone (FSH) concentrations
● Menopause before age 40 years is considered to be abnormal and is referred to as primary ovarian
insufficiency (premature ovarian failure)
● The menopausal transition, or perimenopause, begins on average four years before the final
menstrual period (FMP), and includes a number of physiologic changes that may affect a woman’s
quality of life. It is characterized by irregular menstrual cycles and marked hormonal fluctuations,
often accompanied by hot flashes, sleep disturbances, mood symptoms, and vaginal dryness
● In addition, changes in lipids and bone loss begin to occur, both of which have implications for long-
term health.
● Virtually all women experience the menstrual irregularity and hormonal fluctuations prior to clinical
menopause, up to 80 percent develop hot flashes (the most common menopausal symptom), but
only 20 to 30 percent seek medical attention for treatment.
● Much of the available information about the endocrine and clinical manifestations of the
menopausal transition comes from a number of longitudinal cohort studies of midlife women. The
largest of which, the Study of Women’s Health Across the Nation (SWAN), has followed a
multiethnic, community-based cohort of over 3000 women ages 42 to 52 years for 15 years

STRAW Staging System

Based upon data from the cohort studies, a staging system was developed that is now considered to be the
gold standard for characterizing reproductive aging from the reproductive years through menopause. The
Stages of Reproductive Aging Workshop (STRAW) staging system includes definitions for the late
reproductive years, the menopausal transition, perimenopause, menopause, and postmenopause –
symptoms, laboratory, and menstrual bleeding characteristics.

Although the STRAW system has been used primarily for women’s health research, it is helpful in the
clinical setting for patients and clinicians for assessing fertility potential, contraceptive needs, and potential
need for hormone therapy.

The typical menstrual cycle and hormonal changes that women experience as they traverse from the
premenopausal or reproductive years through the postmenopausal years includes the following:
⚘ Late reproductive years (STRAW -3a)
1. Women usually in their 40s,
2. Fertility potential declines
3. Follicular phase shortens – hence intermenstrual period shortens
4. Serum inhibin B decrease, FSH slightly increases, estrogen levels preserved, but luteal phase
progesterone decreases

⚘ Menopausal transitions/ Perimenopausal (STRAW -2 to -1)

1. Occurs average at 47 years old
2. Early transition - Change in intermenstrual interval – lengthening (40 to 50 days)
3. Late Transition - Progresses to skipped cycles, amenorrhea, increasing frequency of anovulatory
cycles
a. More dramatic fluctuations in FSH and estrogen
b. Drop in ovarian reserves – defined as decreased serum inhibin, AMH and AFC (antral follicle
count), defined as follicles measuring 2 to 10mm in diameter on TV US, declines steadily

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⚘ Menopause: permanent cessation [dx retrospectively 12 months after Final Menses Period (FMP)]
1. Serum FSH sustained near FMP then increases over several years before decreasing
2. Prediction of FMP in study now, as cardiovascular and bone loss risk
a. SWAN Study model – under validation
b. Calculation using BMI, age, AMH, smoking
c. Previous data suggest women who had at least 3 months of amenorrhea can expect FMP
within the next 4 years

Menopausal Symptoms – FLUSH

Flush Non-pharm
○ 80% women experiences it - Keep to cool ambient temperature
○ Most commonly at night (night - Wear light layer of clothes
sweats) - Avoid coffee and alcohol
○ Initially cluster around menses
during late reproductive years, and Pharm
become more common during the - Best is CHT if no contraindications
menopause transition - estrogen and progesterone
○ Sudden sensation of heat centered contraindications
on upper chest and face, that - Paroxetine
rapidly becomes generalized
○ Last 2- 4 mins, a/w profuse
sweating and palpitation

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 occasionally, and at times chills and
shivering, and anxiety
○ Frequency varies from few to
numerous in a day
○ Most stops within 4 to 5 years,
some prolonged

Lubricants (vaginal dryness) - KY jelly

- Topical Premarin

Unhappy → depressed or anxious - KIV treat (refer Psy notes)

Sex affected -

Hard to fall asleep - Sleep hygiene advice

- Refer insomnia notes

1. Hallmark symptoms of perimenopause and early postmenopausal is the HOT FLUSHES (HOT
FLASHES/ Vasomotor symptoms)
○ 80% women experiences it
○ Most commonly at night (night sweats)
○ Initially cluster around menses during late reproductive years, and become more common
during the menopause transition
○ Sudden sensation of heat centered on upper chest and face, that rapidly becomes
generalized
○ Last 2- 4 mins, a/w profuse sweating and palpitation occasionally, and at times chills and
shivering, and anxiety
○ Frequency varies from few to numerous in a day
○ Most stops within 4 to 5 years, some prolonged

2. Others
○ Vaginal dryness, itch, discharge, dyspareunia – progressive, worsen with time
○ Sleep disturbance
○ New onset mood disorders – depression and anxiety
○ Reduced sexual function
■ Multi-factorial – reduced blood flow to vaginal and vulva, reduced vaginal
lubrication, mood issues
○ Less clear for joint pain (WHI showed reduction in jt pain for those on HRT) and memory
loss (not shown in SWAN)
○ Breast pain – common in early transition then diminishes in late transition, likely due to
serum estrogen fluctuations

Long Terms Consequences of Estrogen Deficiency

1. Osteoporosis – highest during 1 year before and 2 years after FMP
2. Cardiovascular disease – increases after menopause, increased LDL
3. Dementia – limited support for hypothesis that estrogen preserves overall cognitive function (WHI
demonstrated no benefits)
4. Degenerative arthritis – limited data
5. Body composition – gain fat, lose lean mass
6. Skin changes – reduced collagen content leads to increased aging and wrinkling, limited data
suggest collagen changes in menopause minimised with estrogen

APPROACH
HISTORY
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 1. Assessment of the woman’s menstrual cycle history (ideally with a menstrual calendar),
2. Detailed history of any menopausal symptoms (hot flashes, sleep disturbances, depression, vaginal
dryness).
3. All women with symptoms of vaginal dryness, dyspareunia, or sexual dysfunction should have a
pelvic exam to evaluate for vaginal atrophy
4. Diagnosis of perimenopause
a. Older women 45 onwards
i. The age at onset of the menopausal transition is variable, and women over age 45
years who present with characteristic menopausal signs and symptoms are more
likely to be in the menopausal transition than to have a new endocrine disorder →
no further diagnostic evaluation may be necessary in light of typical symptoms
ii. Change in menstrual bleeding patterns more predictive than serum FSH (which
can be confusing)
iii. FSH not needed to make diagnosis
iv. Check HCG if suspect pregnancy
v. Endocrine testing (eg, prolactin and TSH) only needed if any suggestive features of
hyperprolactinemia or thyroid disease
b. Younger women 40 – 45 years old with irregular menstrual cycles with or without
menopausal symptoms → should be worked up for amenorrhea first
c. Women < 40 years → should not be diagnosed with menopause or perimenopause, need
work up for amenorrhea (consider Primary ovarian failure)
d. Diagnosis in Special groups
i. Women with menstrual cycle disorders – difficult. Need measurement of FSH for
diagnostic purpose
ii. Women on oral contraceptives – need to measure FSH 2 to 4 wks after stopping
pill, or stop pill at 50 to 51 years provided no contraindications
iii. Post hysterectomy or endometrial ablation – cannot use menstrual bleeding
criteria, FSH levels needed
e. Always consider if MENOPAUSE or HYPERTHYROID

TREATMENT (ACOG Practice Bulletin Jan 2014)

1. Approach – individualise for all women regardless of age, discuss risk and benefits, lowest effective
dose for the shortest duration
2. Consider the following factors
a. Symptom intensity and frequency
b. Medical history – is the patient a candidate for HT
c. Personal choice – is the patient interested in HT
d. Coexistence of other menopausal symptoms such as depression
3. Pharmacological or non-pharmacological tx

I) Pharmacological
1. Systemic HT (estrogen alone or in combination with progestin) = most effective therapy for
vasomotor symptoms
a. Well tolerated in most women, though standard doses may cause adverse effects such as
breast tenderness, vaginal bleeding, bloating and headaches
a. Low dose i.e. 0.5mg/d estradiol and ultra-low dose effective – validated by Heart Outcomes
Prevention Evaluation (HOPE) Trial
b. Administered oral or transdermal
c. Transdermal may have less VTE risks (based on observational trials) – bypass enterohepatic
circulation and thus less effect on clotting factors, TG and globulins
d. Side effects
i. Estrogen – breast soreness, minimised with lower doses
ii. Progestin - Mood symptoms and bloating, vaginal bleeding in cyclic E+P and
common in early months of continuous regime

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 e. Duration should be the shortest effective duration, usually 2- 3 years, no more than 5
years
f. Insufficient evidence to recommend abrupt or tapering discontinuation of HT as better –
though taper may be more pragmatic for those with severe vasomotor symptoms to
prevent abrupt rebound (reduce 1 pill per wk)
g. ACOG recommend against routine discontinuation of systemic estrogen at age 65
h. Women using oral contraceptives (OC)
i. Transit to lower estrogen doses (20mcg of ethinyl estradiol) between age 40 to 50
to reduce VTE risk
ii. Contraindications for OC use – smoking, HTN, migraine
iii. Transit to postmenopausal estrogen regime at age 50 or 51
i. Managing recurrence of symptoms
i. If mild, observe to see if improve or resolve
ii. If no improvement or recurrent, consider non-estrogen alternative
iii. If ineffective, restart estrogen
j. F/u: KIV increase dose after 8/52 after evaluating effectiveness
4. SERMS/Oestrogen Combination
a. Alternative to using progestin for preventing endometrial hyperplasia
b. Can reduce vasomotor and increase BMD
5. Bioidentical Hormone Therapy – not recommended (ACOG CO 532 Aug 12, AACE CE 2011)
a. Evidence is lacking to support superiority claims of compounded bioidentical hormones
over conven- tional menopausal hormone therapy.
b. Customized compounded hormones pose additional risks. These preparations have variable
purity and potency and lack efficacy and safety data.
c. Because of variable bioavailability and bioactivity, both under-dosage and over-dosage are
possible.
d. Conventional hormone therapy is preferred over compounded hormone therapy given the
available data.
e. Despite claims to the contrary, evidence is inadequate to support increased efficacy or
safety for individualized hormone therapy regimens based on salivary, serum, or urinary
testing.
6. Non-hormonal eg SSRIs
a. Low dose Paroxetine is the only non-hormonal medication approved by FDA to treat hot
flashes
i. Contraindication: Tamoxifen (hepatic enzyme inhibition)

II) Non pharmacological

7. Behavioural and lifestyle changes (no evidence that these improve hot flushes)
a. Layering of clothes
b. Maintain lower ambient temperature
c. Consuming cool drinks
d. Avoid alcohol and caffeine
8. Clinical hypnosis (5 x 45 min sessions weekly) reduced hot flashes by 74%
9. Alternatives (no consistent evidence)
a. Omega-3 fatty acid supplementation, black cohosh, yoga, red clover, herbal medicine,
acupuncture, exercise, stress reduction, relaxation therapy

HRT – risks, benefits, and contraindications for use

➿Benefits of HT
1. Benefits mostly outweigh the risk for most symptomatic women < 60 years old or < 10 years from
menopause
2. When counseling women about HT, the clinician should provide estimates for the absolute risks
and benefits for up to five years of treatment in young postmenopausal women (eg, <10 years

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 postmenopausal, or ages 50 to 59 years). Data used for estimates was from the intervention phase
of the WHI
3. Women should be reassured that the absolute risk of complications for healthy, young
postmenopausal women taking HT for 5 years is very low
4. In WHI and HERS trials, no differences in total mortality between the HT and placebo groups,
however when WHI was reanalyzed by age, a significant 30% mortality reduction was seen in
women <60 years
5. Data from WHI
a. E+P
i. Reduced risk of Fractures and colon cancer
1. Colon cancer HR 0.56, 95% CI 0.38-0.81
2. Fractures: Reduced at the hip (hazard ratio [HR] 0.67, unadjusted 95% CI 0.47-0.96) and at the
vertebrae and wrist (HR 0.65, unadjusted 95% CI 0.46-0.92; and HR 0.71, 95% CI 0.59-0.85, respectively)
b. E only
i. No increased risk of CHD or breast cancer
1. WHI reported an HR for CHD of 0.95 (95% CI 0.70-1.16)
2. WHI reported an HR for Breast cancer of 0.77, 95% CI 0.59-1.01
ii. Reduced fractures
1. Hip fracture (HR 0.61, 95% CI 0.41-0.91) and vertebral fracture (HR 0.62, 95% CI 0.42-0.93)
6. CVS
a. Awaiting more trials to determine CVS benefits (ELITE)
b. Estrogen
i. Have benefit effects on lipid (off set by progestin)
ii. Negative effect on TG
iii. Little effect on BP
iv. Neutral to beneficial on fat distribution
v. Neutral to beneficial for body weight
7. OTHER POSSIBLE BENEFITS
a. Recurrent urinary tract infection
b. Health-related quality of life
c. Falls
d. Skin
e. Eyes
f. Other

➿Risks
1. WHI Study (Large RCT of health menopausal women aged 50 to 77 years) demonstrated
a. Combined E+P (after average of 5 years)
i. Slight increased risk (study involving 16,000 women discontinued three years early
due to an increased risk of breast cancer, stroke, CHD, and venous
thromboembolism (VTE) over an average follow-up of 5.2 years)
1. Breast cancer (from 4th year of Rx)
2. CHD
3. Stroke
4. VTE (2-5x)
5. Non significant increase in ovarian cancer
ii. Increased risk of Gallbladder disease
1. Secondary WHI data analysis HR 1.67
2. Cholecystitis HR 1.80
3. Increased likelihood of cholecystectomy HR 1.93
b. E only
i. Study involving 11,000 women discontinued (one year early), due to an increased
risk of stroke and a calculation that suggested no overall health benefit
ii. Increased risk of stroke
iii. Increased risk of VTE (1.2 to 1.5x)
iv. Increased risk of Gallbladder disease

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 c. Difficult to generalize to younger women who are recently menopausal because WHI was
aimed at assessing HT for primary CHD prevention, hence many women were already past
menopausal transition (mean age of participants in WHI trial was 63 years old)
d. In a combined analysis of the two WHI HT trials, women who started MHT closer to
menopause appeared to have a lower risk of CHD compared with women further from
menopause (timing hypothesis)
2. OTHER POSSIBLE RISKS
a. Urinary incontinence
b. Bronchospasm
c. Systemic lupus erythematosus
d. Uterine leiomyomas
e. Epilepsy
f. Dry eye syndrome
g. Nephrolithiasis
3. Progestin alone therapy not first line for concern of increased breast cancer risk attributed to
progestin
4. Progestin attenuate the beneficial lipid effects of estrogen
5. Natural progesterone may have less VTE risk than synthetic progestins
6. HT no proven benefits for dementia prevention
7. Primary and secondary disease prevention (CVS & Bone)
a. ET or HT should not be used as the risk outweighs the benefits
b. USPSTF Recommendations for primary prevention of chronic disease: D
c. Insufficient Evidence of benefits
d. ACOG recommends against HT for primary and secondary prevention of CHD
i. Recent data suggest HT does not increase CHD risk for healthy women who
recently experienced menopause
ii. Some evidence support “timing hypothesis” which posits that CVS benefits may be
derived when ET or HT is used close to menopause
iii. Awaits further results from Early Versus Late Intervention Trial with Estradiol –
ELITE trial

➿Contraindications
1. History of breast CA
2. Undiagnosed PV bleeding
3. VTE
4. Severe liver disease

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290
GYNAE 7. ATROPHIC VAGINITIS

Introduction
● Menopause leads to a dramatic reduction in estrogen production, with an approximately 95
percent decline in estradiol concentration from the premenopausal to postmenopausal state
● This drop in estrogen concentration, exacerbated by the normal aging process, is responsible for
many of the adverse changes seen with vaginal atrophy
● These changes usually develop gradually, over a period of years, and, for many women, persist
unless they are treated. Hypoestrogenic changes include:
1. Thinning of the top layer of superficial epithelial cells, which may be entirely lacking in women with
severe atrophy
2. Loss of elasticity of the vaginal epithelium
3. Increased subepithelial connective tissue
4. Loss of rugae
5. Shortening and narrowing of the vaginal canal, with loss of distensibility
6. Reduction in vaginal secretions from 3 to 4 g/four hours to 1.7 g/four hours
7. Increase in vaginal pH to ≥5
● Thinning of the vaginal epithelium makes it more susceptible to trauma, leading to bleeding,
petechiae, and ulceration with any pressure, including the performing of a Pap smear
● Urinary tract structures are derived from the same embryologic origin as the genital tract and also
contain estrogen receptors. Thus, the bladder, urethra, pelvic floor musculature, and endopelvic
fascia are affected by a hypoestrogenic state. Possible consequences of atrophy of the urinary tract
include urethral discomfort, urinary frequency, hematuria, dysuria, and an increased frequency of
urinary tract infection
● Vaginal atrophy occurs primarily in women who are peri- or postmenopausal. Conditions or
medications that induce a transient or chronic hypoestrogenic state can also cause atrophic vaginal
changes.

Etiologies of vaginal atrophy include:

1. Natural menopause
2. Bilateral oophorectomy
3. Spontaneous premature ovarian failure
4. Ovarian failure due to radiation therapy, chemotherapy, or an adverse consequence of uterine
artery embolization; these may be temporary or permanent
5. Premenopausal use of medications with anti-estrogenic effects, such as tamoxifen, danazol,
medroxyprogesterone acetate, gonadotropin-releasing hormone agonists (eg, leuprolide, nafarelin,
goserelin) or antagonists (eg, ganirelix)
6. Postpartum reduction in estrogen production, particularly during lactation
7. Prolactin elevation due to hypothalamic-pituitary disorders with secondary reduction of estrogen
secretion by the ovary
8. Hypothalamic amenorrhea or amenorrhea in the setting of severe systemic lupus erythematosus or
rheumatoid arthritis (due to hypothalamic hypogonadism or primary ovarian insufficiency)
combined with glucocorticoid therapy. The combined suppression of ovarian and adrenal activity
(loss of adrenal androstenedione reduces estradiol synthesized through extraovarian
aromatization) results in extremely low estradiol levels.

Factors other than low estrogen levels can modulate the degree of atrophy. For example, cessation of coital
activity, vaginal nulliparity, and vaginal surgery may intensify vaginal atrophy symptoms.

Cigarette smoking causes relative estrogen deficiency and may reduce vaginal perfusion

Abstinence from sexual activity exacerbates atrophic changes, whereas sexual activity helps preserve the
vaginal epithelium, presumably by increasing blood flow and tissue elasticity.

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CLINICAL MANIFESTATIONS — Symptoms of urogenital atrophy include
1. Vaginal dryness
2. Vaginal burning or irritation
3. Decreased vaginal lubrication during sexual activity
4. Dyspareunia, including vulvar or vaginal pain (at the introitus or within the vagina)
5. Vulvar or vaginal bleeding (eg, postcoital bleeding, fissures)
6. Vaginal discharge (leukorrhea or yellow and malodorous)
7. Pelvic pressure or a vaginal bulge
8. Urinary tract symptoms (eg, urinary frequency, dysuria, urethral discomfort, hematuria)

Diagnosis
1. Usually clinical
2. Based on typical history and symptoms, and physical findings
3. Laboratory usually not necessary, other than for exclusion of other cause
a. Vaginal pH and Maturation index
b. Vaginal FEME
c. Pap smear
d. Serum hormones to confirm hypoestrogenic state (<20pg/mL)
e. TV US to characterize endometrial thickness
4. Differentials
a. Vaginal infections
b. Local reactions – dermatitis
c. Vulvovaginal lichen planus
d. Vulva lichen sclerosis
e. Genital tract ulcers or fissures as part of systemic disease
5. Treatment
a. Non-hormonal
i. Topical lubricants and moisturisers are first line Tx
ii. Mechanical
1. Sexual activity
2. Vaginal dilators
iii. Lifestyle
1. Stop smoking
b. Hormonal
i. Vaginal (tablet, ring, cream) or systemic estrogen
1. Beneficial effect on urinary tract
ii. SERMS (ospemifene) – side effects hot flushes

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GYNAE 8. VAGINAL DISCHARGE

Causes
Physiological Depends on time of menstrual cycle

Infective

● Vaginitis Vagina candidiasis

Bacterial vaginosis
Trichomonas

● With cervicitis Gonorrhoea

Chlamydia

Non-infective

● Atrophic vaginitis

● Irritant

Acute Chronic illness Medical History

Complaint Cause ● Gynae hx

Vagina discharge Course ● Medical/
● Onset Control Surgical Hx
● Character: Malodorous? Curd-like/thin? ● Home ● Drug Hx/ Drug
grey/green and purulent? Precipitating causes: ● Clinic allergies
Sexual partner? Recent antibiotics use? Compliance ● Medication List
● Time course: Related to menstrual cycle ● Non (any antibiotics,
● Associated symptoms pharm OCP), TCM/OTC
● Fever and abdominal pain ● Pharm
● Burning or irritation Complications ● Travel / Contact
● Itchy ● Disease Hx
Cause ● Tx ● Sexual Hx
Checking ● Psychiatric Hx
Competency
Course ● Birth Hx
● Tried what treatment? Comorbidities ● Immunization
● Seen other doctors for it? Crisis history
Complications management ● Developmental
● Associated STD Hx
● PID/tubo-ovarian abscess

Disease Prevention Family Hx

- Vaccinations: HPV vaccine?

- Cancer prevention: PAP smear? MMG if relevant

PSYCHOLOGICAL

PHQ-2 I
GAD- C
E

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 SOCIAL

Environment Function

Home bADL (DEATH)

Employment/education iADL (SHAFTTT)
Activities
Drugs (Smoking, alcohol, illicit drugs) Cognition
Sex and relationship with others: Number of sex partners. Man, woman or
both. Bladder and bowel
Suicide
Sleep Eye, ear and swallowing

Finance
Exercise
Diet

Physical Examination ***HAND RUB***

T BP HR
Abdominal exam: Palpate for abdominal tenderness, masses
PV exam: “I will need to examine your private area”
Equipments: Double pair of gloves. Lubricating jelly. Speculum. Swab stick.
Cervical excitation.
Adnexal tenderness
Speculum (Show patient speculum, I will be inserting this plastic speculum to better visualize the vagina and
cervix). Check for fistula/malignancy.

Investigations
Swab sample to take → send discharge for microscopy, pH testing, Nucleic acid amplification

Management
● Vagina candidiasis: Perineum hygiene. Clotrimazole pessary 100mg ON x 6/7 or 500mg ON once
dose. Educate on r/s with abx use.
● Bacterial vaginosis
● Trichomonas: Screen associated STI. Tx with Metronidazole 400mg BD x 7 days
- Notify CDlens
- Treat sexual partner for trichomonas even if asymptomatic
- Advise to avoid sexual intercourse until both pt and their partner is treated
● Chlamydia: Screen associated STI. Tx with Azithromycin 1g single dose or Doxycycline 100mg BD x 7
days
○ Notify CDlens for contact tracing.
○ Treat sexual partner for chlamydia even if asymptomatic
○ Advise to avoid sexual intercourse until both pt and their partner is treated
● Gonorrhoea: Screen associated STI. Tx with IM ceftriaxone 250mg 1 dose
○ Notify CDlens for contact tracing.
○ Treat for chlamydia empirically with azithromycin 1g single dose
○ Treat sexual partners from the past 60 days for both gonorrhoea and Chlamydia even if
asymptomatic
○ Advise to avoid sexual intercourse until both pt and their partner is treated

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OBS 1. ABORTION

Termination of Pregnancy Act

● There is no defined minimum or maximum age for the abortion procedure in Singapore
● There is no legal requirement for parental consent for minors (under 16).
● Abortion is prohibited after 24 weeks (6 months) of pregnancy unless the mother’s life is in danger.
(The duration of the pregnancy shall be calculated from the first day of the last normal
menstruation of the pregnant woman to the end of the 24th week.)

Legal Restrictions on Foreigners

Foreigners are only eligible for abortion in Singapore if they meet one of the four conditions below:
● They have been residing in Singapore for 4 months or more; or
● They are married to a Singapore citizen or have PR status; or
● They hold/are the wife of a holder of a work permit pass (not a temporary work permit) or EP; or
● An abortion is immediately necessary to save the life of a pregnant woman.

Procedure
1. Mandatory counselling
● Mandatory pre-abortion counselling is required before the procedure for all patients seeking
abortions. Your doctor will direct you to the counselling service after your consultation.
● Girls below 16 years of age need to be counselled at the Health Promotion Board Counselling
Centre (except for rape victims). Mentally disabled patients require certification by a psychiatrist
that continuation of the pregnancy will be harmful to the mother before medical procedures can be
done.

2. Waiting period: Mandatory of 48 hours after the counselling is conducted before the procedure can be
done.

3. Records
● Patients choosing to terminate a pregnancy are required to sign a declaration of marital status,
educational level, and number of living children. The Ministry of Health maintains a register of all
treatments to terminate pregnancy that records the patient’s name, date of procedure, and
method of termination.
● Patients will normally undergo post abortion counselling after the procedure and may be required
to return a week later to check for any complications.
● Because of the risk of infection, some doctors may advise that you should not have sex for up to
two weeks after your procedure.

Types of Abortion
First Trimester Surgical Abortion — (8 to 12 Weeks) If the pregnancy is more than eight weeks gestation,
the preferred method is a vacuum aspiration. In this procedure, forceps are inserted into the vagina. A local
anesthetic is inserted into the cervix. The cervix is then carefully dilated. A thin tube is passed through the
cervix and into the uterus. A tube is attached and used to suction the tissue out of the uterus. A curette is
then used to ensure the complete removal of pregnancy tissues
Second Trimester Surgical Abortion — (12 to 24 weeks) This process is more complicated and hospitalisation
is usually required for a day or two. Medicine is inserted into the vagina to induce natural expulsion of the
pregnancy. After the foetus and placenta are aborted, the womb is cleared by vacuum aspiration as above.
Cost: $800 to $5000

Risks
The medical risks associated with abortions are:
● Haemorrhage (excessive bleeding) – occurs in about one in every 1,000 abortions

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● Damage to the cervix (the entrance of the womb) – occurs in no more than 10 in every 1,000
abortions
● Damage to the womb – occurs in up to four in every 1,000 abortions during surgical abortion, and
less than one in 1,000 medical abortions carried out at 12-24 weeks

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OBS 2. ANTENATAL CARE

Profile
Age (< 18 years old or ≥35 advanced maternal age)
BMI (≥30 risk for GDM)

Obstetric Hx:
LMP : Calculate gestational Age
EDD :
G____P______
Gravida – total no. of pregnancies
Para – no. of live births at any gestation / stillbirths after 24 weeks
Any abortions/ miscarriages
1st baby – NVD /LSCS, Full term, Birthweight, any complications post birth
2nd baby -
Antenatally – any Preclampsia/ PIH/ Gestational DM
Postnatally – any depression / post 6 week OGTT results

Gynae Hx:
Menstrual regularity, occurs every month, duration of menses etcetc
Any prev gynae problems ie fibroids , PCOS , infertility
Pap smear
Contraception

PMHX/ Past surgeries

DM, HTN, HLD, DVT/PE , Thyroid disorders

Social HX:
Smoking, alcohol
Family support – Married for how many years, relationship
Occupation

Current pregnancy:
Planned vs unplanned
Any reduced foetal movements ( > 20 weeks) (Normal: At least 10 movements within 12 hours)
Any PV bleed
Any leaking liquor (>20 weeks)
Any contractions ( > 20 weeks)
Common symptoms:
Nausea/ vomiting
Anemia
Backache
Dysuria, urinary frequency
Constipation
Abdominal pain
Danger symptoms: PV bleeding, Leaking liquor in 3rd trimester, severe abdominal pain,
High Risk Pregnancy - Screen and Refer at First Visit

Present Pregnancy
1. Age < 18 years or ≥ 35 years at time of delivery (EDD)
2. Uncertain dates
3. Late booking (presenting at ≥ 20 weeks gestation)
4. Primary or secondary subfertility

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5. Substance abuse
6. Cervical incompetence

Past Obstetric History

1. Recurrent spontaneous abortion
2. Uterine rupture
3. Molar pregnancy
4. Grand multiparity (Parity ≥ 5)
5. Previous severe pregnancy induced hypertension
6. Low birth weight (< 2,500 g)
7. Macrosomia (> 4,000 g)
8. Previous infant with congenital or genetic disorders
9. Previous intrauterine death / stillbirth / early neonatal death

Medical or Surgical Conditions

1. Pre-existing hypertension
2. Pre-existing diabetes mellitus
3. Systemic diseases, e.g. cardiac disease, thyroid disorders, autoimmune disorders, renal disease
4. Past surgery, e.g. myomectomy, pelvic and uncertain abdominal operations
5. Psychiatric disorders
6. Deep vein thrombosis
7. Fibroid (past or present)

Examination and
Gestation History Plan
Investigations
< 12 weeks History taking Physical examination Explain and offer:
• LMP • Parameters To be done at NUH
• Current (height, weight, • Dating scan
gestation by BP) • First Trimester Screening (11 -
LMP • Auscultate 13+6 weeks)
• Maternal age heart and lungs To be done at NUP
• Obstetric and • Abdominal • Antenatal blood tests (FBC,
gynaecological exam HBsAg, anti-HBs Ab, Syphilis, HIV,
history ABO and Rhesus status)
• Past medical Routine investigation at • Thalassemia screen for all
history each visit pregnant women with unknown
• Family history • Urine dipstick test Thalassemia status
• Lifestyle: (glucose, protein) • OGTT for patients at high risk for
Smoking GDM as early in pregnancy as
• Symptoms in feasible (see Women at High Risk
current for GDM) and to repeat at 24 -
pregnancy 28 weeks if the test is normal

Medication :Folic acid 5 mg OM

High risk pregnancy -
Advice to patient
Refer to Obstetric
• Healthy lifestyle
• Advise to go ED if she has
abdominal pain or vaginal
bleeding

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≥ 12 weeks History taking Physical examination Explain and offer:
• LMP / EDD • Parameters (height,
* 1st visit • Current gestation weight, BP) To be done at NUH
• Maternal age * • Auscultate heart • Dating scan *
• Obstetric and and lungs • First Trimester Screening (11 -
gynecological • Abdominal exam 13+6 weeks) or Triple test
history * • Symphyseal fundal screening (15 - 20 weeks)
• Past medical history height • Screening scan for foetal
* • Doptone (fetal heart abnormalities at 18 - 22 weeks
• Family history * beat) To be done at NUP *
• Lifestyle: Smoking • Antenatal blood tests (FBC,
• Symptoms in Routine investigation at HBsAg, anti-HBs Ab, Syphilis, HIV,
current pregnancy each visit ABO and Rhesus status)
• Review results of • Urine dipstick test • Thalassemia screen for all
previous (glucose, protein) pregnant women with unknown
investigations and Thalassemia status
scans at NUP and • OGTT at 24 - 28 weeks for all
SOC pregnant women

Medication: Obimin 1 tab OM

High risk pregnancy -
Advice to patient
Refer to Obstetric
• Healthy lifestyle
• Advise to go ED if she has
abdominal pain or vaginal
bleeding

≥ 20 weeks History taking Physical examination Explain and offer:

• LMP / EDD • Parameters (height,
* 1st visit • Current gestation weight, BP) To be done at NUH
(late • Maternal age * • Auscultate heart • Screening scan for foetal
booker) • Obstetric and and lungs abnormalities at 18 - 22 weeks
gynaecological • Abdominal exam • Growth scan (28 - 32 weeks)
history * • Symphyseal fundal
• Past medical history height To be done at NUP
* • Doptone (foetal • OGTT at 24 - 28 weeks for all
• Family history * heart beat) pregnant women
• Lifestyle: Smoking
• Symptoms in Refer to Obstetric if SFH Medication
current pregnancy is larger or smaller than
• Obimin 1 tab OM
• Foetal movement dates by 2cm
• Review results of
Advice to patient
previous Routine investigation at
investigations and each visit • Advise to go ED if she has
scans at NUP and abdominal pain, vaginal
• Urine dipstick test
SOC bleeding, leaking liquor or
(glucose, protein)
decreased foetal movements
* All pregnant
women presenting at ≥
20 weeks gestation at
first visit:
Refer to
Obstetric early

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 Investigations at SOC Antenatal
Investigation Results
Investigation
6 - 12 weeks - Dating scan Full blood count Note Hb and MCV
11 - 13+6 weeks - Nuchal translucency • Also consider iron studies
and First trimester serum screening if Hb < 11 g/dL, MCV < 80
15 - 20 weeks - Triple test fl
18 - 22 weeks - Screening scan Thalassemia Include Thalassemia screen
(Foetal abnormality scan) screening for all pregnant women with
28 - 32 weeks - Growth scan unknown Thalassemia status
• Refer to Obstetric if newly
diagnosed Thal
• KIV FBC and Thalassemia
Frequency of Antenatal Follow-up at NUP
screen for spouse
HBsAg, anti-HBs If HBsAg negative and not
Less than 28 weeks of gestation -
Ab immune, recommend Hep B
4 weekly
vaccination postnatally
More than 28 weeks of gestation -
2 weekly
If HBsAg positive, refer to
More than 32 weeks of gestation -
Gastro for follow-up
Refer to Obstetric to continue follow-up
If positive, refer to DSC and
Syphilis screening
Obstetric
HIV screening Refer to CDC if positive
ABO blood group Refer to Obstetric if Rh
Women are at high risk for GDM if they have: and Rhesus status negative and partner is Rh
positive
1. BMI > 25.0 kg/m2 • Needs anti-D
2. First-degree relative with Diabetes immunoglobulin
3. Personal history of previous GDM or prophylaxis
large babies > 4 kg 75 g OGTT Refer to Obstetric if
4. Previous poor obstetric outcomes diagnosed with GDM or DM
usually associated with Diabetes in pregnancy
Refer to ED stat if a pregnant woman presents
Perform OGTT for these patients in the with:
first trimester and repeat at 24 -28 weeks • Vaginal bleeding, abdominal pain of uterine
if the test is normal. origin, leaking liquor, and/or decreased foetal
movement

Possible scenarios in Obstetrics

1) Vomiting in pregnancy
- Refer to the other document

2) UTI in pregnancy
- Acute cystitis: Dysuria, urinary freq and urgency
- Pyelonephritis: Fever and chills, flank pain, and costovertebral angle tenderness
- Rule out pregnancy complications from the UTI (pre-term labour, chorioamnionitis, placenta abruptio)
Intraamniotic infection: presentation with premature rupture of membranes, uterine
tenderness and/or foul odor of the amniotic fluid, and the absence of bacteriuria
Placenta abruptio: Back pain, vaginal bleeding, absent fever. Uterus firm, rigid and tender

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- IX: UFEME and urine culture

- MX:
- Cystitis :
- Augmentin for 5 -7 days , fosfomycin single dose , cephalexin for 5- 7 days
(note that Bactrim& nitrofurantoin - avoid first trimester and near term, avoid nitrofurantoin and
fosfomycin if pyelonephritis suspected)
- Increase fluid intake, perineal hygiene ( wipe from front to back)
- F/up with repeat urine c/s in 1 week

-Recurrent cystitis:
- Antimicrobial prophylaxis for the duration of pregnancy : daily or postcoital prophylaxis with low
dose nitrofurantoin (50 to 100 mg PO postcoitally or at bedtime) or cephalexin (250 to 500 mg PO
postcoitally or at bedtime) can be used.

- Pyelonephritis:
- Refer to ED for parenteral antibiotics. Antibiotic therapy can be converted to an oral regimen tailored to
the susceptibility profile of the isolated organism following clinical improvement. KIV tocolytics and steroids
before 34 weeks gestation

3) Asymptomatic bacteriuria
- guidelines from the Infectious Diseases Society of America that recommend screening all pregnant women
for asymptomatic bacteriuria at least once in early pregnancy
- Must treat! Untreated bacteriuria has been associated with an increased risk of preterm birth, low birth
weight, and perinatal mortality
- Mx: Abx and f/up same as cystitis

4) Frequency
- Assess fluid intake, exclude DM and UTI. If all the above are normal, consider the possibility of pelvic tumour

5) Proteinuria:
- Consider causes including UTI, hypertension, renal disease, contamination and orthostatic (by exclusion)
- Check ufeme, urine c/s, creatinine , Check BP , OR repeat early morning sample (diagnosis of exclusion)

6) Backache in pregnancy
- Usually diffuse ache with absence of red flags , no weakness/ numbness
7) Down Syndrome Screening
- Refer to document
8) Thalassemia Screen
- Refer to document
9) HTN in pregnancy
- Refer to document
10) GDM
- Refer to document

11) Air Travel

- In the absence of obstetric or medical complications, occasional air travel is safe for pregnant
women. (Safest in the 2nd trimester, try to avoid travelling in 1st and 3rd trimester if possible as
most common obs emergencies occur in 1st and 3rd trimester but not CI)
- Most commercial airlines allow pregnant women to fly up to 36 weeks of gestation (Single
pregnancy) , up to 32 weeks of gestation (Multiple pregnancy)
- Some airline require memo from doctors for certification to fly in third trimester ie 28 weeks or
more (jetlines)

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 - Potential risk : changes in cabin pressure and low humidity with physiological changes of pregnancy
can result in increase heart rate and blood pressure and decrease in aerobic capacity , DVT , LL
edema
- Preventive measures: use of support stockings and periodic movement of the lower extremities,
avoidance of restrictive clothing, occasional ambulation, and maintenance of adequate hydration,
preventive antiemetic
- For most air travelers, the risks to the fetus from exposure to cosmic radiation are negligible

11) Vaccinations
- Offer influenza vaccine (usually after the 1st trimester)
- Tdap vacccine between 16 - 32 weeks

12) Nutrition Advice

- Folate supplementation 400mcg/day ideally 4 weeks prior
o If hx of fetus with neural tube defects / taking folate antagonists – 4mg/day
- Reduce artificial sweeteners
- Caffeine: 150-300mg /day
- Caloric intake 300-400 more
- Avoid unpasteurized dairy – Toxoplasma / Listeria
- Avoid delicatessen food like cured meats / pate – Listeria
- Avoid raw eggs – salmonella
- Wash fruits/vegetables, cutting boards washed with hot soapy water after
- Avoid tea containing chamomile, peppermint, liqorice, raspberry leaf
- Thoroughly reheat leftover food – listeria
- Avoid undercooked meat or excessive liver / liver products(Vit A toxicity)
- Fish : avoid shark, swordfish, tilefish, tuna. Limit other fish to 12oz/week – mercury

13) Other advice

- Exercise – 30mins most days of the week. Caution falls / abdominal injury
- Routine counting of fetal movements NOT recommended - increases anxiety
- Avoid hair treatment (early preg), heavy metals, certain herbal therapies (gingko, ephedra, ginseng)
- Avoid hot tubs / saunas in 1st trimester(increased neural tube defects / miscarriage)

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OBS 3. DOWN SYNDROME

What is down syndrome: Baby has an extra copy of gene (chromosome 21) in body and will be born with
abnormal face, organs

Risk of Down Syndrome increases with maternal age

Age Risk
25yo 1 in 1000
35yo 1 in 300
45yo 1 in 100

SCREENING tests (expresses the chances of your child having down syndrome)
Test Trimester Detection Rate
First trimester screening (FTS) 11-13 weeks + 6 90%
- Nuchal translucency ultrasound days
- Maternal serum: ßhCG and PAPP-A 5% false positive
Triple / Quadruple Test 15-20 weeks 70-80%
- ßHCG, AFP, uE3, ± inhibin A
5% false positive
Non-invasive prenatal test (NIPT) After 10 weeks 98-99%
- Analysis of baby’s DNA in mother’s blood to
look for chromosomal abnormalities

NIPT
● OSCAR (One Stop Clinical Assessment of Risk) = FTS = NT + ßhCG + PAPPA
● Harmony: screens for trisomy 21, 18, 13
○ ± fetal sex, 22q11.2 microdeletion, sex chromosome aneuploidies
○ Can be used in singleton, twin pregnancies
○ Most sensitive test for Down syndrome screening

If screening results shows high risk >1 in 250 or >1 in 300→ offered confirmatory test
Confirmatory (can tell you with greater than 99% certainty whether your child has a chromosomal
abnormality)
Test Trimester Miscarriage Rate
Amniocentesis 16-20th week 0.3-0.5%
th
Chorionic villous sampling 10-12 week 0.5-1%

Pros and Cons of screening test:

Pros: non invasive , Cons : false positive and false negative

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OBS 4. DM PRE-CONCEPTION / YOUNG DM PT KEEN FOR PREGNANCY

History
● Duration and type of diabetes (type 1 or type 2)
● Acute complications, including history of infections, ketoacidosis, and hypoglycemia
● Chronic complications, including retinopathy, nephropathy, hypertension, atherosclerotic vascular
disease, and autonomic and peripheral neuropathy
● Diabetes management, including insulin regimen, prior or current use of oral glucose-lowering
agents, SMBG regimens and results, medical nutrition therapy, and physical activity
● Concomitant medical conditions and medications, thyroid disease in particular for patients with
type 1 diabetes
● Gynae Hx: LMP ( Rule out pregnancy!) Menstrual hx , contraceptive use
● Obs Hx: Previous pregnancy, any cx ie worsening of DM related complications, preclampsia
● Social Hx: Support system, including family and work environment

P/E
● BP , HR, BMI
● Cardiovascular exam for evidence of cardiac or peripheral vascular disease. (If found, patients
should have screening tests for CAD before attempting pregnancy to assure they can tolerate the
increased cardiac demands)
● +/- Neurological exam, including examination for signs of autonomic neuropathy
● Ensure DRP and DFS exam are uptodate , consider foot exam if DFS not done yet

Ix: UPT to rule out pregnancy, usual DM panel to screen for complications

Management
1) Counseling about the impact of glycemic status on maternal-fetal outcome, the risk of development or
progression of preexisting complications of diabetes, and the types and risks of adverse maternal, fetal, and
neonatal outcomes. Explain high risk pregnancy and return immediately if pregnant
2) Helping the patient achieve good glucose control, target Hba1c pre-conception ≤ 6.5 % (NICE, ADA)
3) Adjusting medications as needed for fetal safety
● Metformin is safe
● Change other OHGAs to insulin
○ NPH/Insulatard or Detemir (Glargine can cause macrosomia)
4) Evaluating for comorbidities and complications of diabetes
5) Initiating treatment of comorbidities and complications or optimizing status of existing medical
conditions
6) Discussion and provision of effective contraception to avoid unplanned pregnancy
7) Folic acid pre-conception
8) 7 point SMBG 2 days/week
● Pre-meal 4.4-5.5mmol/L
● Post-meal 5.5-6.6mmol/L

1) Maternal and Fetal risks

Fetal and Neonatal Risks Maternal
1st trimester Maternal Medical risks
- Congenital malformations - Progression of microvascular disease –
- Higher risk of miscarriage diabetic retinopathy, kidney disease
- Higher risk of Cardiovascular disease
- Autonomic neuropathy – gastroparesis can
increase risk of hyperemesis gravidarum
- Diabetic ketoacidosis
- Increased risk of severe hypoglycemia

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 3rd trimester Obstetric complications
- Macrosomia - Miscarriage
- Polyhydraminos - Preclampsia and gestation hypertension
- Growth restriction - Caesearean delivery if macrosomia
- Shoulder Dystocia - Preterm delivery
- Increased risk of preterm birth
- Perinatal mortality
Post delivery
- Neonatal complications

2) Glucose targets and monitoring

The following preconception glucose targets are reasonable to achieve:
●A1c <6.5 percent
●Fasting capillary blood glucose concentration 80 to 110 mg/dL (4.4 to 6.1 mmol/L)
●Two hour postprandial glucose concentration <155 mg/dL (8.6 mmol/L)
Since it takes two to three months to turn over A1c, women with diabetes should be encouraged to allow a
minimum of six months to achieve optimal glucose control before trying to conceive

3) Diet, Weight, Exercise

4) Medication and control of co-morbids and screen for complications

Medication management
Glucose control — We recommend insulin for women with type 1 or type 2 diabetes planning to conceive.
Insulin remains the standard drug for glucose management during pregnancy and should be used prior to
conception to provide continuity.
Medications suitable for pregnancy: Metformin, insulatard (NPH) , Levemir .
With combination of lispro or aspart insulin (novorapid) (actrapid also can but less satisfaction compared to
ultra short acting)
Glargine not ideal - can cause macrosomia, Stop other OHGAs

Blood pressure control — The prepregnancy blood pressure goal is <130/80 mmHg , which may be relaxed
to 120 to 160/80 to 105 mmHg in pregnancy. Stop Ace-I/ARB . Start labetalol or long-acting calcium channel
blocker or Methyldopa

Lipid control — Stop statins due to increased risk of birth defects with first trimester exposure.. Restart
after delivery/breast feeding.

5) Folic acid supplementation

6) Contraception (UK MEC and US MEC guidelines)

Type 1 or 2 DM only without any micro/macrovascular cx :
No CI.
Can use Condom, Estrogen-progestin and progestin-only contraceptives (POP, Implanon, IUS ) , IUD

Type 1 or 2 DM with nephropathy, retinopathy, neuropathy, other vascular disease, or diabetes >20 years :
Estrogen-progestin and Depot Provera not recommended due to higher rate of thromboembolic events
Can use Condom, POP , Implanon , IUS , IUD

Type 1 or 2 DM with multiple risk factors for cardiovascular disease ie obesity , smoking, hypertension,
hyperlipidemia
Estrogen-progestin and Depot Provera not recommended
Can use Condom, POP , Implanon , IUS , IUD

Hypertension only
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( well or poorly controlled ) -> Estrogen-progestin pill not recommended
≥Grade 2 hypertension or vascular dz -> Estrogen-progestin pill and depot provera not recommended

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6) Special things to discuss for screening for GDM – Read the ACG guidelines!

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OBS 5. GESTATIONAL DIABETES (ACG)

Guidelines for screening

● 1ST trimester → Screen all the high risk women for pre-existing DM using 2-point OGTT (pre-
pregnancy threshold)
○ If negative, to re-evaluate again at 24-28 weeks
*can screen before conception as well
● 24 to 28th weeks → Screen all pregnant women with 3 point OGTT (phase coincides with increase in
gestational insulin resistance)

Women at high risk of pre-existing diabetes – 2 + 2 + 2

Profile – 2 PMHX -2 Gynae Hx -2
Age ≥ 40 Polycystic ovarian syndrome Hx of GDM
Pre-pregnancy BMI > 30 Pre-diabetes hx Previous baby ≥4 kg

oGTT cut off

2 point OGTT 3 point OGTT (diagnosed GDM
if any of the 3 pt diagnostic
criteria is met)
O hour ≥ 6.1 ≥ 5.1
1 hour 7.8 – 11.0 ≥ 10.0
2 hour ≥ 11.1 ≥ 8.5
If first trimester diagnosed with pre-diabetes/ diabetes based on 2 pt OGTT, manage as per pre diabetes /
diabetes

Counselling for gestational DM

- Gestational diabetes is diabetes diagnosed in the 2nd and 3rd trimester of pregnancy
- Risk of GDM
Maternal Foetal
Pre-eclampsia Macrosomnia
Increased lifetime risk of diabetes and Shoulder Dystocia
cardiovascular disease

Management of gestational DM
- Refer to Specialist
- Start lifestyle intervention and lifestyle modification
- Advise on home CBG targets

Home CBG targets

● 7 point monitoring, 2 days/week
○ Aim fasting 4.4-5.5, 2h postprandial 5.5-6.6
Fasting glucose ≤5.2
1 hour post prandial ≤7.7
2 hour post prandial ≤6.6

After delivery
● Repeat 2 point OGTT 6 weeks post delivery
● Screen for DM every 1-3 years (annually if high risk)

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OBS 6. HYPERTENSION IN PREGNANCY

Preeclampsia-eclampsia – Preeclampsia refers to the syndrome of new onset of hypertension and

proteinuria or new onset of hypertension and end-organ dysfunction with or without proteinuria most
often after 20 weeks of gestation in a previously normotensive woman
Eclampsia is diagnosed when seizures have occurred.

BP ≥140/90 beyond 20 weeks gestation on 2 occasions at least 4 hrs apart and

● Proteinuria (urine dipstick 1+ or PCR>30 or UTP 24 hour >0.3g) or
● EOD (CLAMP)
CLAMP
● Cr double
● Liver enzyme double
● Abnormal platelet <100
● My head hurts
● Pulmonary edema
** If BP >160/90, confirmation within mins is sufficient

Chronic (preexisting) hypertension – Chronic hypertension is defined as hypertension that antedates

pregnancy, is present before the 20th week of pregnancy, or persists longer than 12 weeks postpartum.

Preeclampsia-eclampsia superimposed on chronic hypertension – Preeclampsia-eclampsia superimposed

upon chronic hypertension is diagnosed when a woman with chronic hypertension develops worsening
hypertension with new onset proteinuria or other features of preeclampsia (eg, elevated liver chemistries,
low platelet count).

Gestational hypertension – Gestational hypertension refers to elevated blood pressure first detected after
20 weeks of gestation in the absence of proteinuria or other diagnostic features of preeclampsia.

HELLP syndrome
Haemolysis, elevated liver enzymes, low platelet

Symptoms of pre-eclampsia
Severe headache, blurred vision, photopsia, and/or scotomata (dark areas or gaps in the visual field)
Right upper quadrant or epigastric pain, vomiting
SOB

Investigations
Urine dipstick / Urine pcr
FBC, LFT, Renal Panel

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Management (NUP /NHGP CPG)
1) Refer to hospital SOC if:
● BP ≥ 140/90 mmHg, or
● A rise of systolic BP ≥ 30 mmHg or diastolic BP ≥ 15 mmHg from previous readings (2 readings taken
4 hours apart)
2) In the presence of elevated blood pressure, refer to ED if the following red flags occur:
● Severe hypertension (systolic BP ≥ 160 mmHg or diastolic BP ≥ 110 mmHg on two occasions at least
four hours apart or only once if treated), persistent and/or severe headache, visual abnormalities,
upper abdominal or epigastric pain, nausea and vomiting, dyspnoea, retrosternal chest pain, altered
mental status, seizures

HTN target (NHGP CPG)

● < 150/100 mmHg in pregnant pts w/o target organ damage (do not decrease diastolic BP to < 80
mmHg).
● < 140/90 mmHg in pregnant pts with target organ damage, HLD, DM, Maternal age > 40, perinatal
loss

Anti hypertensives suitable in pregnancy (NHG CPG)

- Nifedipine (long-acting)
- Labetolol
- Methyldopa
- Hydralazine.

- Low dose aspirin (60-150mg/day) can be used from the end of the first trimester until the baby is born in
women with type 1 or type 2 diabetes to lower the risk of preeclampsia.

Drugs to avoid in pregnancy

- ACEi, ARB
- Mineralcorticoid receptor antagonist ie spironolactone
- Nitroprusside
- Statins/ Fibrates

Anti hypertensives suitable for breastfeeding

- Labetalol, propranolol, metoprolol (NOT ATENOLOL)
- Methyldopa
- Sustained release nifedipine , diltiazem, nicardipine, verapamil
- Hydralazine
- Hydrochlorothiazide
- Captopril and enalapril may be used but newborns may be more susceptible to the hemodynamic effects
of these drugs, such as hypotension, and sequelae such as oliguria and seizures.

Delivery
Uptodate and the American College of Obstetricians and Gynecologists (ACOG) suggested the following
approach for delivery of women with chronic hypertension and no superimposed preeclampsia, fetal
growth restriction, or abruption (past or current pregnancy):
•38+0 to 39+6 weeks of gestation for women not requiring medication
•37+0 to 39+6 weeks for women with hypertension controlled with medication
•36+0 to 37+6 weeks for women with severe hypertension difficult to control

Risks of hypertension in pregnancy

- Abruptio placentae
- Fetal growth restriction
- Preterm birth
- Perinatal death

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- Superimposed pre-eclampsia

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OBS 7. APPROACH TO NAUSEA AND VOMITING IN PREGNANCY

Main task
- Rule out other causes other than morning sickness
- Check for complications of current pregnancy
- Check for severity of hyperemesis gravidarum and complications : dehydration/ hypotension/ electrolyte
imbalance

Differentials
Gastrointestinal GERD
Gastroenteritis
Acute appendicitis
Intestinal obstruction

Hepatobiliary Pre-eclampsia! (third trimester) HELLP

Acute fatty liver of pregnancy
Cholecystitis / Cholangitis
Hepatitis/ Pancreatitis

Genitourinary Urinary Tract infection

Pyelonephritis

Endocrine Diabetic ketoacidosis

Gynae Hyperemesis Gravidarum

Ovarian Torsion
Degenerating Fibroid

Central nervous system / Neuro Meningitis

Migraine
Raised intracranial pressure ie tumours / ICH

Vestibular Meniere
Vestibular neuritis / labyrinthitis

HISTORY
Complaint
Vomiting
- Onset:
- Character: bloody/ bilious / undigested food contents
- Timing: early morning in pregnancy
- Exacerbating factors: Fatty meals (biliary disease), a few hrs after meals (ulcer, gastric obstruction), food
smells (pregnancy)
- Severity Able to tolerate orally?

Course:
- Duration
- What has been tried so far

Cause:
Red flags:
- Fever/ abdominal pain esp RIF/ RHC pain (acute appendicitis/ cholecystitis/ pancreatitis)
- Jaundice (cholangitis/hepatitis)
- Headache/ BOV/ RHC pain (Pre-clampsia – 3rd trimester)

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- Neck stiffness/ rash (meningitis)
** For pregnancy: Any vaginal bleeding, foul smelling vaginal discharge, leaking liquor (in 3rdtrimester)

- Diarrhoea/ Travel or contact hx (GE)

- Reflux/ Bloating esp after meals and on lying down (GERD)
- Constipation/ Abdominal distension (Intestinal obstruction)
- Dysuria/ urinary frequency / urgency/ Flank pain (UTI/ pyelonephritis)
- Hx of kidney stones
- LMP (pregnancy) / Hx of fibroid/ ovarian problems
- Photophobia/ phenophobia/ visual aura (migraine)
- Bg of poorly controlled DM / Hyperthyroidism (DKA , Thyrotoxicosis)
- Vertigo / Hearing loss/ Tinnitus (Meniere’s/ Vestibular Neuritis/ Labyrinthitis)

Complications:
- Unable to tolerate orally/ Dizziness/ generalised weakness/ Decreased urine volume (dehydration/
electrolyte imbalance)

PMHX: DM
Drug Hx/ Drug Allergy:
Gynaecological /Obstetric Hx: (impt in pregnancy case)
- LMP (pregnancy), gestation,
- Menses regular
- G_P_ , prev abortions/ miscarriages
- Details of delivery.. boy/girl , weight, gestation
- Prev hx of preclampsia, GDM
- Hx of gynaecological problems
- (if applicable): Contraception/ Pap smear/MMG
Family Hx:
Social Hx:
- Alcohol intake / Smoking
- Occupation/ Function -> How has it affected u so far ?
Psy Hx: PHQ-2, GAD -2 (Prenatal depression/anxiety)
Vaccination Hx:

PHYSICAL EXAMINATION
BP , HR , Temp , Ht , Wt , BMI KIV postural BP (CALCULATE WEIGHT LOSS, >5% of pre-pregnancy weight)
Alert/ Confused
Tongue hydration, Cap refill
Rash
Abdomen: Distension, Tenderness, mass, organomegaly, bowel sounds, Gravid uterus (SFH), fetal doptone
Neck stiffness
KIV Neuro examination
Pap smear !

INVX
Urine ketones, Renal panel
KIV FBC, Liver function test (HELLP), thyroid function test

MANAGEMENT
1) Early morning sickness
● 1st line = Pyridoxine + Doxylamine
● 2nd line = Metoclopramide, Ondansetron

2) Hyperemesis gravidarum = ≥5% loss of weight (from pre-pregnancy) AND urine ketones +ve

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May present with orthostatic hypotension, laboratory abnormalities (eg, electrolyte, thyroid, and liver
abnormalities), and physical signs of hypovolemia, and often require hospitalization for stabilization.
ᐉ When to admit for IV hydration and antiemetic
- If cannot tolerate liquids without vomiting and has not responded to outpatient management
- If hypovolemia (eg, lassitude, postural dizziness, thirst, tachycardia, decreased PU volume and
frequency)

ᐉ Outpatient management
Non pharmacological
- Small frequent meals
- Fluids should be consumed at least 30 minutes before or after solid food to minimize the effect of a full
stomach
- Eliminating coffee and spicy, odorous, high-fat, acidic, and very sweet foods, and substituting
snacks/meals that are protein-dominant, salty, low-fat, bland, and/or dry (eg, nuts, pretzels, crackers,
cereal, toast)
- Women with nausea should eat before, or as soon as, they feel hungry to avoid an empty stomach, which
can aggravate nausea ie A snack before getting out of bed in the morning and snacks during the night
- Avoid triggers: Stuffy rooms, odors (eg, perfume, chemicals, food, smoke), heat, humidity, noise, and
visual or physical motion (eg, flickering lights, driving)
- Ginger can reduce nausea but not vomiting

Pharmacological
- 1st line: Pyridoxine (vitamin B6) 10-25mg TDS PRN / Doxylamine – pyridoxine (FDA Class A)
- 2nd line: Antihistamines ie Dimenhydrinate (FDA Class B) , diphenhydramine (FDA Class B) (need to stop
first line if 1stline not working)
- 3rd line: Dopamine agonists ie metoclopramide (FDA Class B) , promethazine (FDA Class C) ,
prochlorperazine
Consider initiation of antiemetic therapy before the onset of nausea and vomiting symptoms to reduce
severity of symptoms

ᐉ Education: Serious symptoms of dehydration / hypovolemia

ᐉ Followup: One week after initiation of meds

Maternal and Fetal Outcomes

In pregnancies with uncomplicated nausea and vomiting, there is a decreased risk of miscarriage, as well as
lower rates of preterm delivery, fetal death, and growth restriction.14,15 However, infants of women who
lost weight early in the pregnancy, particularly in the setting of hyperemesis gravidarum, are at increased
risk of growth restriction or low birth weight.16 Women with nausea and vomiting that is refractory to
treatment or complicated by weight loss have increased risks of fetal growth restriction and fetal death, as
well as preeclampsia and maternal complications associated with vomiting (e.g., esophageal rupture,
retinal hemorrhage, Mallory-Weiss syndrome, pneumothorax)

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OBS 8. POSTNATAL CARE

Additional Hx:
Breastfeeding, breast engorgement or pain
Any abdominal pain / fever / foul smelling vaginal d/c
Lochia flow
How is the episiotomy wound site
**** Contraception and Pap smear VERY IMPT*****
Family Planning/Contraception - Have you completed your family planning, when do you want to have a
next baby

Social Hx
Married?
Staying with who
Who helps out with the baby
How is the baby doing?
Occupation
Finances

PHYSICAL EXAMINATION
Temp BP HR SpO2 BMI
Pallor?
MSE
Breast examination for engorgement and mastitis
Abdominal examination: Soft non tender
Perineal examination: inspect the episiotomy wound, ask pt to cough to check for urine leakage and pelvic
organ prolapse
VE: Bimanually palpate the uterus to ensure that the uterus is well contracted
Speculum: Any abnormal vaginal discharge or bleeding

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Possible Scenarios
1) Peurperal fever
- Defined as fever on 2 occasions from the 2nd day to 10th day post partum
- TRO DVT, PE, endometritis, mastitis
- OE: look for source
- Invx: KIV FBC, UFEME, CXR

2) Post natal blues

- Resolves within 2 weeks after delivery
- Review + safety netting

3) Post natal depression

- Occurs at first month to 1st year after delivery
- TRO self harm, harm to baby
- TRO unipolar depression vs psychosis vs bipolar
- Social support, safety netting
- Do not need to discontinue breastfeeding if they initiate anti depressants
- If breastfeeding: sertraline (50-100mg/day), paroxetine, venlafaxine (37.5-75mg /day)
- If not breastfeeding: fluoxetine (20-40mg/day), sertraline, escitalopram, venlafaxine
- Fluoxetine is linked to irritability, sleep disturbance and poor feeding in some infants exposed to it
in breastmilk

4) HTN and breastfeeding

Anti hypertensives suitable for breastfeeding
- Selective ßblockers: labetalol, propranolol, metoprolol
- Nifedipine
- Captopril and enalapril may be used but newborns may be more susceptible to the hemodynamic effects
of these drugs, such as hypotension, and sequelae such as oliguria and seizures.

(Methyldopa a/w increased risk of post natal depression. Diuretic increases thirst)

5) Contraception suitable for breastfeeding post partum

⇨ Implanon, IM Depot provera, POP
⇨ IUCD (mirena/ copper) if more than 4 weeks post partum or 0-48hours post partum
⇨ (Lactational amenorrhea method (LAM) for first 6 months post partum if total breastfeeding and
amenorrheic)

As a result of conflicting data regarding impact of estrogen-progestin contraceptives on lactation, we advise

avoiding COCP in breastfeeding women who are less than 30 days postpartum. Breastfeeding women who
are at least 30 days postpartum and do not have additional risk factors for thromboembolic events can
reasonably begin estrogen-progestin contraceptives (UTD) (Some sources state that COCP may reduce
breastmilk supply)

Contraception suitable for non-breastfeeding post partum

> 6 weeks post partum → can use all including OCP pill
< 6 weeks post partum → progestin options (Implanon, IM depot provera, POP, IUCD)

Effectiveness of Breastfeeding as contraception (lactational amenorrhea method (LAM))

98% effective in preventing pregnancy, provided
- Fully or nearly fully breastfeeding AND
- Less than 6 months post partum AND
- No menses since childbirth

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In postpartum women who do not breastfeed, ovulation returns at a mean of 39 days postpartum (earliest
ovulation reported 25 days after delivery)
Women who exclusively breastfeed typically have a delay in resumption of ovulation postpartum due to
prolactin-induced inhibition of pulsatile gonadotropin-releasing hormone release from the hypothalamus.

Interval between pregnancy

Advised to avoid conception for a least 18 months. <18 months interval between pregnancies a/w
increased risk of poor perinatal outcome after a live birth.
For advanced maternal age, An IPI of only 12 months may be a reasonable approach for women of
advanced maternal age, as it balances the increasing risk of subfertility and infertility with advancing age
and the increased risks of pregnancy complications associated with a very short (<6 months) IPI

6) GDM (refer to GDM approach)

7) Infective mastitis
● Frequent breastfeeding/pumping. Can continue feeding.
● Abx: cephalexin/cloxacillin; clindamycin if allergic 10-14 days
● If abscess forms or worsening symptoms early return
● See 48-72h

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OBS 9. THALASSAEMIA COUNSELLING

What is Thalassaemia
- Thalassaemia is an inherited blood disorder which is caused by an abnormal gene. A person with
thalassaemia is unable to produce normal, functioning haemoglobin in the blood.
- Haemoglobin carries oxygen from the lungs to all parts of the body. When the body is not able to produce
normal, functioning haemoglobin, the affected person suffers from anaemia.
- Thalassaemia is passed on from parent to child and can affect both males and females. In Singapore,
about 3% of the population are carriers of the thalassaemia gene.

What Are The Types Of Thalassaemia?

There are two types of thalassaemia:
1. Thalassaemia minor (thalassaemia trait).
2. Thalassaemia major.
- A person who has inherited one thalassaemia gene is said to have thalassaemia minor (thalassaemia
trait).He or she is healthy and leads a normal life. Most people with thalassaemia minor do not know that
they have it. However, the affected persons can pass on the abnormal gene to their children.
- Thalassaemia major is a severe form of anaemia. The affected person has inherited two thalassaemia
genes, one from each parent. He or she may look normal at birth but within 1 - 2 years of life, will suffer
from severe anaemia, which leads to poor growth and development as well as a shorter lifespan.
- The affected person will need blood transfusion every month to sustain life. At present, a bone marrow
transplant is the only hope of possible cure for thalassaemia major.

How Is Thalassaemia Inherited?

If only one parent has thalassaemia minor, the following can occur:
● 50% chance of having a child with thalassaemia minor
● 50% chance of having a normal child
● None of the couple’s children will get thalassaemia major

If both parents have thalassaemia minor, the following can occur:

● 25% chance of having a child with thalassaemia major
● 50% chance of having a child with thalassaemia minor
● 25% chance of having a normal child
The chances are the same with each pregnancy, no matter how many children the
couple may have.

Who Should Go For Thalassaemia Screening?

Since thalassaemia can be passed on from one generation to another, you and your partner should go for a
thalassaemia screening if you are:
● Planning to get married
● Starting a family

Thalassaemia screening involves a simple blood test and is available at all polyclinics.

What Should I Do If I Have Thalassaemia Minor?

- If you or your partner has thalassaemia minor, both of you should see a doctor for genetic counselling
before you plan to get married or have a child. The doctor will explain the risks and discuss the choices you
have. He may refer you to the National Thalassaemia Registry for further counselling.
- The National Thalassaemia Registry provides genetic counselling for people with thalassaemia and
screening for their families. The staff at the Registry will be able to answer your questions about this blood
disorder.

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ORTHO 1. ANKLE AND FOOT PAIN

Deformities Hallux Valgus

Hallux rigidus
Flat foot
Pes Cavus

Generalised dz Gout
RA/OA

Plantar fasciitis ● Contributing cause: tight Achilles tendon with limited ankle
dorsiflexion, pes planus / cavus, overpronation, leg-length
discrepancy,
● Passive dorsiflexion of toes or stand on tiptoes and toe walk
(windlass test) -> Reproduce the pain of plantar fasciitis

Ankle/ Foot Fracture

Enthesitis ie tendoachilles
tendon

Haemarthrosis

Hallux Valgus
- Signs: lateral deviation and rotation of hallux, bunion from hypertrophy of medial part of metatarsal head
and overlying bursa, KIV hammer toe, callosities, pes planus
- RF: Idiopathic, hereditary, enclosed footwear with narrow toe box
- Mx:
● Conservative: Footwear modification (deep toe boxes, low heels), physio
● Operative:
○ Indications: pain, function, cosmesis
○ Bunionectomy, corrective osteotomy of 1st metatarsal + soft tissue balancing

Ankle and Foot Fracture - Ottawa Ankle and Foot rule

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ORTHO 2. BACK PAIN

Ddx
Extraspinal Spinal

Pancreatitis V
Abdominal aortic Infection: TB, abscess
aneurysm Trauma: Fracture. Spondylolisthesis. PID.
Nephrolithiasis Autoimmune: seronegative spondyloarthropathies (RAPE: reactive
Retroperitoneal abscesses arthritis, AS, psoriatic arthropathy, enteropathic arthropathy)
Metabolic: Paget’s disease of spine. (Osteoporosis vertebral compression
#)
Iatrogenic
Neoplastic: tumours

HISTORY
Complaint: Back pain
● Characterize back pain
o Which part of back? Any abdominal pain? (R/O referred pain)
o Onset: sudden or gradual? Trigger
o Character?
▪ Dull, sharp, shooting, electric shock like, stabbing, burning
o Radiation?
▪ Radiating down the LL, esp below the knees – PID
o Relieving and exacerbating factors?
▪ Inflammatory2 or mechanical?
▪ Worse with movement or rest, morning stiffness ? – inflammatory vs mechanical
▪ Worse on standing and walking, climbing down hill, variable claud distance – spinal
stenosis / Neurogenic claudication
▪ Worse on sitting - PID
▪ Tried any analgesics
o Severity? Pain score

● Associated symptoms
o Rule out red flags:
▪ Fever, night sweats
▪ Weight loss
▪ History of malignancy
▪ Night pain, rest pain
▪ Trauma (mechanical)
▪ Neurological symptoms (TRO cauda equina)
● Numbness in limbs, trunk and abdomen
● Lower limb weakness
● Urinary retention or incontinence or constipation or bowel incontinence
● Difficulty walking
o Any other joint involvement or rash ? – inflammatory arthropathies
o Started after lifting heavy weights / numbness or weakness of LL – PID
o Any fever / chills / rigors / open wound over LL/ IVDA (bacteraemia) - infective causes
o Any associated abdominal pain ? – referred pain

2
Inflammatory = age <40, insidious onset, improvement with exercise, no difference with rest, pain at night (improved
on getting up)
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● If inflammatory arthropathies:
o Which other joints involved?
o Enthesitis?
o Morning stiffness? And better on movement / exercise?
o Red eye, painful eye, blurred vision? – uveitis
o SOB - ILD
o Rash? Nail changes? – psoriasis
o Bloody diarrhoea – enteropathic arthropathy, IBD
o Recent fever, dysuria, eye redness or pain, cough and other infective symptoms - reactive
arthritis
o Sexual history! (esp if suspecting reactive arthritis)
(Inflammatory pain - IPAIN - Insidious onset, Pain at night, Age of onset < 40, Improved with exercise/hot
water, No improvement with rest. a/w morning stiffness

● If mechanical:
o Back getting more stooped? – vertebral compression fracture
o If suspect osteoporosis – primary or secondary?
▪ Primary: age of menarche, age of menopause, dietary, lifestyle, weight
▪ Secondary: symptoms of hyperthyroidism, symptoms of Cushing’s syndrome,
symptoms of hypogonadism, symptoms of malabsorption, LOW / LOA for malignancy
o If weakness or numbness of LL
▪ Which part of LL?

● If referred pain:
o Abdominal:
▪ Any nausea, vomiting?
▪ Any loin to groin pain? Passing out of stones? Dysuria, cloudy urine, foul smelling
urine?
o Cardiac:
▪ Exertional symptoms?

PMH
▪ Cancer – vertebral metastases
▪ Tuberculosis – common cause of bone infection
▪ Arthropathies
▪ Psoriasis, IBD
▪ Osteoporosis: Previous hip fractures or wrist fractures? Previous vertebral compression fractures?
▪ Nephrolithiasis
▪ IHD

Drug Hx
● Drug allergy
● Steroids/TCM – secondary osteoporosis
● Anti epileptics – secondary osteoporosis
● HIV drugs – secondary osteoporosis
● Letrozole for breast cancer

Family Hx
▪ Arthropathy
▪ Parental fracture (RF for osteoporosis) (how old?)

Social Hx
▪ Smoking / Drinking?
▪ Sporting activities

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▪ Occupation
▪ Environment set-up
▪ How has back pain affected your life?

PHYSICAL EXAMINATION
Ht Wt BMI
Look Palpate spine / paravertebral muscles
ROM
SLR / lasegue/ bowstring
Neuro exam: tone, reflexes, power (sensation)
Gait
Pulses
Per-rectal exam
Offer to examine hip joint /sacroiliac joint/ Abdominal exam
Special tests for AS: FABER test for sacroiliac joint, Schober test, Head to Occiput test, Chest expansion

INVESTIGATIONS
Blood tests:
▪ FBC looking for leukocytosis
▪ ESR and CRP in Autoimmune dz
▪ Urea creatinine and electrolytes looking for renal impairment as this would affect the type of
analgesics that patient can be given, hypercalcaemia in multiple myeloma
Imaging tests:
▪ Radiograph of cervical/ thoracic/ lumbar spine looking for any degenerative changes,
compression fractures, lytic lesions, spondylolisthesis, decreased intervertebral space
▪ Plain radiograph of sacroiliac joints for sacroilitis in AS
▪ MRI of lumbosacral looking for any nerve compression
▪ Bone scan in suspected metastatic bone disease
▪ Bone mineral density scan for osteoporosis

MANAGEMENT
1. Neurogenic claudication/ Spinal stenosis
● Pathology: Narrowing of spinal canal (DDD, facet joint arthropathy, thickened ligamentum flavum)
resulting in compression of cervical cord or cauda equina
● Presents with Posterior thigh, calf , buttock pain cramping pain ( travel down leg) , weakness,
numbness or parathesiae (leg pain >>>>> back pain unless back pain due to underlying pathology)
● Occurs on standing or walking or climbing down hill, relieved on sitting down and bending forward
● Compared to vascular claudication, neurogenic claud has variable claud distance as it is position
dependent, worse on walking downhill,, no night pain/ CVRF
● PE: Kemp sign - unilateral radicular pain from foraminal stenosis made worse by extension of back,
usually no neurological deficits on examination , only present when pt is in extension and
ambulating
● Diagnosis usually based on hx alone. PE is usually unremarkable
● Mx
○ Conservative: education on back posture, pain control, physiotherapy, corticosteroid
injections
○ Operative: wide laminectomy +/- segmental fusion

2. Prolapsed intervertebral disc

● PE: Listing, midline tenderness, pain worse on flexion, SLR positive if nerve root compression
present, cross SLR if large central disc protrusion, loss of reflexes, sensory and motor loss at the
specific myotome

Mx

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 ● Rest followed by progressive activity as tolerated, physical therapy
● Anti-inflammatory medications
● Surgery for if persistent disabling pain lasting more than 6 weeks that have failed nonoperative
options / cauda equina
● **Differentials for radiculopathy: PID, spondylosis (facet joint hypertrophy, bone spurs, narrowing
of neural foramen), spondylolisthesis
● Management

3. Spondylodiscitis / Vertebral Abscess

⇒ Refer to ED for IV ABx cos likely pt has bacteraemia and spread to the spine

4. Vertebral Compression fracture

● Refer to osteoporosis mx
● Analgesia
● Physiotherapy
● Rest till pain improves and gradual return to usual activities, refrain from bed rest

5. Ankylosing Spondylitis
- Suspect in young adult with recurrent inflammatory back pain
- Follow Ortho Spine exam
- Special features: Occiput to wall, Schober’s test , FABER test, Chest Expansion
- Extra-articular: Anterior uveitis, Atlanto-axial sublux, Aortic Regurg, Apical Interstitial lung disease,
Enthesitis
- A/w: Reactive arthritis, Psoriatic arthropathy, IBD
- Mx:
PT/OT
Regular NSAIDs for 4 weeks at least
Sulphasalazine only for peripheral arthritis ie knees, ankles, not for axial dz
Refer to Rheumatologist for long term anti-inflammatory medications such as anti-TNF alpha antagonist

Neurogenic vs vascular claudication

Neurogenic Vascular

Exacerbating vs relieving factors Worse on extension (standing, Worse on walking/ uphill

walking, down hill) Relieved by standing / sitting
Improved on flexion (Sitting ,
uphill)

Claudication distance Variable depending on position Fixed

Cardiovascular RF absent present

Pulses present absent

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ORTHO 3. APPROACH TO HIP PAIN

Differential diagnosis
Joint disorder V – Avascular necrosis of the hip: (TCM use/ Perthes Disease)
I – Infection eg TB, Septic arthritis
T – Trauma
A – Autoimmune (RA)
M – Malignancy (primary, mets)

C – Congenital: SCFE, DDH

D – OA / Degenerative

Hernia
Referred pain Lumbar spine discogenic causes
True hip pain referred to the knee
Peri-articular Trochanteric Bursitis
Synovitis
Tendinitis – ITB
Hernia

Important points
- Rule out red flags
- Assess function and impact on occupation / function / social

HISTORY
Complaint
● Site: location and referred location – back pain, knee pain
○ ⚐ Hip pain (anterior) — usually at groin
○ ⚐ Pain at gluteal region (posterior) — usually lumbar pathology
● Onset/Duration : when the pain appears, How long each time, Similar previous episode or pain, is
it getting worse
● Timing:
○ Early morning pain- inflammation
○ Relieved at night- mechanical in nature
○ Night pain- implies severity, malignancy, infx
● Character: shooting (nerve), cramping
● Radiation
● Aggravating factor: Movement (mechanical) , rest ( inflammatory)
● Relieving factor: Medications (include analgesics and TCM), posture
● Severity: pain score, How far can you walk before resting

Cause
⚐ Red flags:
● LOW, LOA, persistent pain, night pain, night sweats
● Fever, swelling, redness of joint, recent injection
● Trauma
● Any hx of TCM / Steroid use
● Morning stiffness >30mins, worse on rest, relieved by movement, rash, other joints involvement
● Any back pain, numbness, weakness, urinary or bowel incontinence, erectile dysfunction

Course: Seen any doctors, any ix done,mx

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Complications: Falls, Function affected

PMH:
Drug Hx: TCM/ Steroids very impt !
Social Hx: Occupation, Family support, Smoking, alcohol
Functional Hx:
● “How has your hip pain affected your daily routine”, “premorbid status - How was your daily
routine like before the hip pain started”
● bADLS, iADLs
● PU
● BO
Psy Hx:

PHYSICAL EXAMINATION
Gait
- Hip examination
- Wasting
- Tenderness on palpation of hip joint
- ROM of hip joint
- Power and tone of LL
- SLR
- DP/PT
- Any spinal tenderness

Short case:
Walk
Trendenlenburg
Measure limb length discrepancy
Fixed flexion deformity
ROM of hip

INVX
XR pelvis, XR Hip (AP/Lat)

MANAGEMENT
1) AVN of hip - Stop TCM
- The goal of therapy is to preserve the native joint for as
long as possible
- The three main therapeutic options include nonoperative
management, joint-preserving procedures, and joint
replacement. Factors influencing the choice of therapy
include the presence (or absence) of symptoms, the degree
of involvement, the stage of the lesion, and the
comorbidities.

2) OA Hip ● Analgesia
● Maintain function
● Physio

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326
ORTHO 4. KNEE PAIN

Scenarios :
Elderly with bilateral mechanical knee pain -> OA knees
Young Athlete with sudden knee swelling and pain -> ACL tear

Ddx
Anterior Medial Lateral Posterior

● Patellofemoral pain ● OA knees ● Lat meniscus ● Baker

syndrome ● MCL ● LCL cyst
● Patellofemoral OA ● Medial meniscus ● Iliotibial band ● PCL
● Osgood Schlatter injury syndrome
● Patella subluxation ● Pes anserine
● Patella tendonitis bursitis

● Septic arthritis
● Crystal arthropathy: Gout
● Inflammatory: Reiter syndrome, RA
● Haemarthrosis
● Fracture

Referred pain from hip

Fixed flexion deformity of knee - OA/RA

Locked knees - torn meniscus / loose body

HISTORY
Complaint: Knee pain
- Site: Anterior/medial/lateral/posterior
- Onset: Sudden or gradual
- Characteristic: Rest pain or mechanical pain
- Radiation: Any hip pain also? → referred pain
- Time: Worse in the morning, worse at end of day
- Exacerbated by stairs and squatting, getting up from prolonged seating
- Pain score

Causes
- Fever -> Septic arthritis
- Trauma -> Haemarthrosis / fracture

327
 - Sudden swelling of knee → fracture, haemarthrosis
- Gradual swelling and redness / Hx of gout -> Gout / OA flare
- Stiffness >30mins, swelling, rashes → Inflammatory arthropathy
- Locking symptoms → meniscus
- Popping sound during injury, knee giving way → ligament

Course: Investigations done. Management tried

Complications: Impact on function (How far can you walk before you experience the pain / iADLs)

Med Hx: Known arthropathy, hemophilia

Surgical Hx
DA
Drug Hx: Beware of contraindication for NSAID use
OTC/TCM
Family Hx
Preventive

Psy: PHQ2. ICE?

Social: Impact on work. Home environment (Home with lift landing). Exercise (Find out if doing any quads
strengthening exercise)

PHYSICAL EXAMINATION
Temp BMI
Look
- Gait: Antalgic gait. Varus thrust.
- Effusion or deformity
- Knee sag
- Popliteal swelling
Feel
- J sign (lateral tracking as patient extends knee while seated on edge of bed)
- Warmth
- Effusion
- Joint line Tenderness

Move
- Active and passive ROM of knee
- Comment on crepitus

Special tests: Depends. Varus, Valgus stress test , Lachmann, mcmurray, posterior drawer, patella
apprehension

INVX
- X-rays
- Blood: FBC, ESR

MANAGEMENT
OA knees

Ligament injuries ie ACL - XR TRO fracture

tear - RICE
- Physio
- Refer for MRI knee

328
 IT band injury - Acute: Rest, Ice, Analgesia
- Subacute: Exercise strengthening therapy
- Graduated return to sports

Pes anserines

Osgood schlatter - Ice, analgesia

- Can continue physical activity
- If refractory, surgery is after closure of proximal tibial growth
plate

OA knee exercises

329
ORTHO 5. Neck pain

Scenarios:
Patient presents with frequent falls -> Cervical myelopathy
Pain and numbness over one arm -> Cervical spondylosis with radiculopathy

330
ORTHO 6: SHOULDER PAIN

DDx
Fracture/dislocations Others

● GH joint
○ OA shoulder
○ Septic arthritis
○ Inflammatory arthritis: RA
○ Labrum tear

● Around the GH joint

○ Frozen shoulder

● Muscles
○ Rotator cuff tendonitis
○ Rotator cuff tear
○ Bicep tendonitis
○ Polymyalgia rheumatica
○ Myositis: e.g. statin induced

● Referred pain from C-spine radiculopathy

● AMI referred pain

HISTORY
Complaint: Shoulder pain
- Site: Point
- Onset: Preceding trauma? Sudden or chronic
- Character: At rest or mechanical. Shooting pain?
- Radiate: From heart? From neck?
- Exacerbating: Overhead movement? On walking?
- Relieving
- Pain score

Causes
- Limited ROM?
- Swelling, stiffness, redness, fever, rashes, other joint involvements → RA
- Recent new medications?
- With headache, jaw claudications?
Course
Complications
- Function affected?

PHYSICAL EXAMINATION
T BP HR BMI
- Look
- Feel
- Move
- Special tests
- Check other systems as relevant: e.g. c-spine, heart, RA exam

INVESTIGATIONS
- XRay

331
 - FBC, ESR

MANAGEMENT
1) Rotator cuff tear Non-pharm
∆∆ TRO CVA ● Physio exercises

Pharm
● Analgesia

KIV surgery for maintenance of function

2) Frozen shoulder Non-pharm

Physiotherapy for frozen shoulder

1. Pendulum stretch
Do this exercise first. Relax your shoulders. Stand and lean over slightly, allowing the affected arm to hang
down. Swing the arm in a small circle — about a foot in diameter. Perform 10 revolutions in each direction,
once a day. As your symptoms improve, increase the diameter of your swing, but never force it. When
you're ready for more, increase the stretch by holding a light weight (three to five pounds) in the swinging
arm.

2. Towel stretch
Hold one end of a three-foot-long towel behind your back and grab the opposite end with your other hand.
Hold the towel in a horizontal position. Use your good arm to pull the affected arm upward to stretch it.
You can also do an advanced version of this exercise with the towel draped over your good shoulder. Hold
the bottom of the towel with the affected arm and pull it toward the lower back with the unaffected arm.
Do this 10 to 20 times a day.

332
ORTHO 7: HAND CONDITIONS

333
PHYSICAL EXAMINATION
Screening
{Hands on pillow}
● Inspect: wasting, scars, wide carrying angle of the elbows
{Hands off pillow}
● Wrist + finger extension → if unable, consider radial nerve palsy
● Make fist → look for Benediction sign
● O sign → median nerve
● Cross fingers → ulnar nerve
● Thumbs up → radial nerve
● Inspect elbows: rheumatoid nodules, gouty tophi, scars

{Hands on pillow}
Median nerve
● Confirm median nerve: thumb abduction (APB)
○ ± Oppose thumb to little finger (try to pry apart)
● Assess level of lesion:
○ Check DIPJ flexion of radial 2 fingers for FDP

Ulnar nerve
● Confirm ulnar nerve: Froment’s sign
● Assess level of lesion
○ Check DIPJ flexion of ulnar 2 fingers for FDP

Radial nerve {Hands palm down on pillow}

● Confirm radial nerve:
○ Extend fingers against resistance
● Assess level of lesion
○ Wrist extension against resistance

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 ○ Elbow extension against resistance

Sensation
● Dermatomes: C5 C6 C7 C8 T1
● 1st dorsal webspace
● If C6/C7 (fingertips) numb → check sensation over thenar eminence + split finger sign
● If C8 (fingertip) numb → check split finger sign + sensation over hypothenar eminence + ulnar 1.5
aspect of dorsum of hand

CAUSES OF NERVE PALSY

Surgical : Compression, Trauma , fracture
Medical: Mononeuritis multiplex, Infection(Leprosy)

MEDIAN NERVE
Level of Lesion Motor Loss Sensation Loss

@ wrist: Carpal Tunnel ● Thumb abduction ● Lateral 3.5 fingers gone

Syndrome ● ±oppose thumb to little ● (Split finger sign)
finger (try to pry apart) ● (Thenar eminence
spared)

Just proximal to wrist ● As above ● As above

● + thenar eminence gone

Proximal to wrist (forearm and ● As above ● As above

above) ● + FDP lateral 2 fingers
gone

Special Tests
- Carpal tunnel: Tinel and phalen
- Cubital fossa: Tinel sign

Differentials:
- C6/7 nerve root lesion : Weakness in Biceps & Triceps, Hyporeflexia at biceps & triceps

ULNAR NERVE
Level of Lesion Motor lost Sensation

@ wrist: Guyon canal - Froment sign positive ● Hypothenar eminence numb

● Ulnar 1.5 fingers numb
● Medial dorsum of hand intact

Just proximal to wrist As above ● As above

● DBUN lost (medial dorsum of
hand lost)

At elbow As above As above

Ulnar 2 finger FDP weak

Special Tests
- Cubital tunnel: Tinel sign

Differentials
- C8 & T1 nerve root lesion: Wasting of thenar eminence and Sensory loss over T1 dermatome

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 (above medial epicondyle)

RADIAL NERVE
Level of Lesion Motor Sensation

In forearm PIN loss NO loss if only PIN palsy

(Distal to elbow) ● Fingers extension weak (see above diagram)
● ± thumb extension weak
● NO wrist drop (extensor carpi radialis
longus intact, can still effect
extension)

● Fingers extension weak ● Loss over 1st dorsal

● ± thumb extension weak webspace
● NO wrist drop

Prox to elbow, Lower ⅓

distal to axilla ● As above
Middle ⅓ (saturday night palsy)
● As above
● Loss of muscle bulge with elbow
flexion when arm is at 90 degrees
(brachioradialis)
Upper ⅓
● As above

@ axilla: ● As above
(crutch palsy) ● Triceps

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337
 PAEDS ENDO 1. APPROACH TO ABNORMAL GROWTH CENTILES
INCREASED WEIGHT Endocrine
● Hypothyroidism
● Cushing’s
● Pituitary/Thalamic disorders
Genetic
● Down Syndrome
● Prader-Wili Syndrome
● Laurence-Moon Syndrome

DECREASED WEIGHT ● Malnourished, Psychosocial Deprivation

● Hyperthyroidism
● Inflammatory bowel dz
● Major organ failure (cardiac, renal, pulmonary, gastrointestinal)
● Inborn errors of metabolism
● Fe/ Zinc deficiency
● HIV infection
● Immune deficiencies
● Lead toxicity

INCREASED HEIGHT ● Hyperthyroidism

● Marfan’s syndrome
● Klinefelter’s syndrome
● Excessive production of growth hormone
● Homocystinuria

DECREASED HEIGHT ● Major organ failure (cardiac, renal, pulmonary, gastrointestinal)

● Hypothyroidism
● Turner’s syndrome
● Chronic anaemia
● Decreased production of growth hormone
● Skeletal dysplasia/rickets
● Psychosocial deprivation

INCREASED OFC Hydrocephalus

● Primary
● Secondary: Arnold-Chiari Malformation
Megalencephaly
● Primary (familial)
● Secondary: NF, Tuberous Sclerosis, Krabbe’s Disease (metabolic
storage disease)

DECREASED OFC Craniosynostosis (premature fusion of fontanelles)

Prenatal Insult
● Maternal infections (TORCH)
● Maternal alcohol/drug abuse
● Pregnancy/birth complications

NAME/AGE/SEX
BIOLOGICAL
ACUTE ANTENATAL/POSTNATAL/ DRUG HX
VACCINATIONS
Complaint: referred from nursing room for abnormal Antenatal History Allergies

338
weight centiles ● Maternal health: Long term meds
● Onset: sudden vs progressive DM/GDM, HTN, TCMs/supplemen
● Associated: abnormal height centiles and OFC infections, ts/OTCs
centiles? hypo/hyperthyroid
● Developmental milestones: achieved or delayed ● Drug/Alcohol abuse
● Premature rupture of
Cause membranes
● Diet history (3 days or last 24 hours)
● Hyper/hypothyroid symptoms Post-Natal History
● Recent catastrophic illnesses ● Birth history:
● Recent travel history (tapeworms) complications, drugs
● Chronic diarrhea, bloody diarrhea (IBD) given
● Lower limb swelling, generalised edema,
haematuria (renal) Developmental History
● Shortness of breath, decreased effort tolerance
(cardiac/pulmonary) Vaccinations

Course
● Seen any doctors for above
● Any interventions done

Complications
● Participation in school activities
DISEASE PREVENTION FAMILY HISTORY
- Vaccinations Parents
- Cancer prevention height/head size
Siblings
PSYCHOLOGICAL
PHQ-2 | GAD-2 ICEKAP
SOCIAL
Home/Environment – triggers?
Financial

PHYSICAL EXAMINATION ***HAND RUB***

General appearance (any presence of dysmorphism)
● Growth charts: Plot mid-parental height
● Developmental assessment
● Relevant CVS/Respi/Abdo examination
● Tanner staging

INVESTIGATIONS
● FBC: to screen for anaemia
● TFT: hypothyroid vs hyperthyroid
● RP + UFEME: renal problems
● LFTs

MANAGEMENT
Treat underlying causes (refer algorithms)

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Normal weight gain: infants (2x BW at 4/12 old, 3x BW at 1 year old) then 2kg per year between 2 years old
and puberty
Normal height velocity: 0-6 months 2.5cm/year, 6 months - 1 year 1.25cm/year, 1-2 years 10cm/year, 2-3
years 8cm/year 3-4 years 7cm/year
Normal OFC growth: 1cm/month up till 4 years old

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PAEDS ENDO 2. DELAYED PUBERTY

Definition: Absence of pubertal development by 12 yo in girls (no breast buds), 14 yo in boys (no increase in
testicular size).
GnRH deficiency → defective secretion of gonadotropins (LH and FSH) → inadequate steroid secretion by the
gonads.

Ddx
FSH and LH will be low FSH and LH will be high

Hypothalamic (GnRH) Pituitary (LH/FSH) Gonadal (Testosterone, estradiol,

progesterone)

ᐉ Constitutional delay of growth and puberty ᐉ Metabolic: Chromosomal disorders:

(Most common) ● Haemochromatosis ᐉ Turner syndrome,
ᐉ Congenital/Isolated GnRH deficiency ● Iron deposition from Klinefelter syndrome
(Genetic mutations ie Kallmann syndrome) blood transfusion ᐉ Gonadal dysgenesis
ᐉ Metabolic “Functional”: ᐉ Neoplastic: Pituitary
● Chronic illness: IBD adenoma Gonadal injury from orchitis/
● Under-eating ie AN or over-exercising ᐉ Trauma torsion/ cryptorchidism /
chemo/radiotherapy

Hypothyroidism

HISTORY
Complaint: Delayed puberty
● Onset: Beyond 12 yo for Female, beyond 14 yo for Males
● Time: Start and stalled vs never started
● Characterize:
○ Testes size? Secondary characteristics like voice change, pubic hair?
○ Breast size? Menarche? Hair growth?

Causes
● Constitutional delay→ Positive family hx of puberty delay.
● Weight loss/dieting?
● Chronic illnesses?
● Hx of haemochromatosis? Regular transfusion (“secondary haemochromatosis”)
● Headache and visual field changes?
● Hypothyroid → cold intolerance, weight gain, constipation
● Known genetic diseases e.g. turner, kline-felter
● Previous mump, undescended testes, irradiation to testes
● Anosmia → Kallman syndrome

Course
Complications: Emotional disturbances

Med Hx: Genetic disease? Hypothyroid? Hemochromatosis? Previous mumps or undesc testes?
DA
Drug Hx: OTC/TCM
FHx: Delayed puberty? Hemochromatosis?
Psy Hx: PHQ2. ICE?
Social: HEADSSS assessment

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PHYSICAL EXAMINATION
Plot growth paras on growth chart: Ht Wt BMI (AN)
Arm Span [arm span >ht by 5cm → delayed epiphyseal closure 2 to hypogonadism]
US/LS Ratio : High [immaturity and delay], < 1 [prolonged delay and true defect]
General inspection:
● Dysmorphic features (ie Turner’s)
● Bronzed appearance in Haemochromatosis (ie Thalassemia pts)
Goitre, thyroid status
Systemic review for chronic illnesses
Offer Tanner Staging. Request for Visual field (Pituitary adenoma), Sense of smell (Kallmann)

Stages of pubic hair development in boys:

Stage 1: Prepubertal, with no pubic hair.
Stage 2: Sparse, straight pubic hair along the base of the penis.
Stage 3: Hair is darker, coarser, and curlier, extending over the mid-pubis.
Stage 4: Hair is adult-like in appearance, but does not extend to thighs.
Stage 5: Hair is adult in appearance, extending from thigh to thigh.

Stages of external genitalia development in boys:

Stage 1: Prepubertal.
Stage 2: Enlargement of testes and scrotum; scrotal skin reddens and changes in texture.
Stage 3: Enlargement of penis (length at first); further growth of testes.
Stage 4: Increased size of penis with growth in breadth and development of glans; testes and scrotum
larger, scrotal skin darker.
Stage 5: Adult genitalia.

Stages in breast development in girls:

Stage 1: Prepubertal, with no palpable breast tissue.
Stage 2: Development of a breast bud, with elevation of the papilla and enlargement of the areolar
diameter.
Stage 3: Enlargement of the breast, without separation of areolar contour from the breast.
Stage 4: The areola and papilla project above the breast, forming a secondary mound.
Stage 5: Recession of the areola to match the contour of the breast; the papilla projects beyond the
contour of the areola and breast.

Stages of development in pubic hair in girls:

Stage 1: Prepubertal with no pubic hair.
Stage 2: Sparse, straight hair along the lateral vulva.
Stage 3: Hair is darker, coarser, and curlier, extending over the mid-pubis.
Stage 4: Hair is adult-like in appearance, but does not extend to the thighs.
Stage 5: Hair is adult in appearance, extending from thigh to thigh.

342
INVESTIGATIONS
● XR of left hand /wrist for bone age (check skeletal maturity)
● FBC
● Other tests: ESR, RP, LFT for chronic illnesses, TFT
● Further tests:

343
 ○ LH, FSH, Testosterone, Estradiol, Prolactin, Insulin Growth-like factor
○ Serum transferrin saturation and ferritin (Haemochromatosis)

MANAGEMENT
1) Constitutional delay of growth and puberty or ● Either "watchful waiting" with reassurance
isolated gonadotropin-releasing hormone (GnRH) and psychological support for the patient
deficiency (difficult to differentiate) and family
● Or short-term hormonal therapy, with
testosterone in boys and estrogen in girls.
2) Specific cause of delayed puberty ● Tx underlying disorder
ie hypothyroidism, IBD

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PAEDS ENDO 3. APPROACH TO SHORT STATURE

Definition: Height less than 3rd percentile on the growth chart or for his / her community

DDx
Normal (80%) Pathological (20%)
ᐉ Familial Proportionate (US/LS abnormal) Disproportionate
short stature Prenatal Postnatal ᐉ Rickets (vit C
ᐉ ᐉ IUGR (TORCH, ᐉ Nutritional deficiency (usu deficiency)
Constitutional fetal alcohol) affects wt too) ᐉ Achrondroplasia/
growth delay ᐉ Chromosomal ᐉ GIT malabsorption: IBD Hypochrondroplasia
abn (Down, Turner) ᐉ Endocrine: ᐉ Skeletal dysplasias
ᐉ Other genetic ● Type 1 DM ᐉ Osteogenesis
disorders ● Hypothyroidism imperfecta
● Growth hormone def ᐉ Spinal defects
● Cushing syn (scoliosis, kyphosis)
● Congenital Adrenal
hyperplasia
● Hypopituitarism
● PseudohypoPTH
ᐉ Chr dz (Chronic Heart, Lung,
Renal dz, hematological)
ᐉ Psychosocial - Child abuse
ᐉ Iatrogenic (steroids, radiation)
● Proportion depends on US/LS ratio.
● Normal infants US:LS ratio = 1.7 : 1
○ 3 yo = 1.33 ⇒ 5 yo = 1.19 ⇒ By 10 years of age ratio 1:1
● US/LS ratio increased, decreased AS → short limbs
○ Proximal: rhizomelic dwarf (most common)
○ Middle: mesomelic dwarf
○ Distal: acromelic dwarf
● US/LS ratio decreased, AS N → disorders affecting spine

● IUGR defined as BW below the 10th percentile for gestational age

● Percentiles on growth chart: 3, 10, 25, 50, 75, 90, 97th
● BW for term babies:
○ 2.3 - 3.7kg (3rd to 97th percentile) on health booklet
○ 2.5kg - 10th percentile

HISTORY
Presenting complaint: short stature = Ht <3rd percentile
● Establish when growth failure occurred: refer to growth charts
○ Prenatal (IUGR, low birth wt) vs Postnatal (Plot trend and drop in height percentiles after birth)
■ If prenatal → Look at antenatal hx
■ If post natal → Determine whether proportionate vs disproportionate by calculating
US/LS Ratio

If proportionately short
● Familial short stature → Fhx of short stature , Ht within range of MPH
● CGD → FHx of growth delay, puberty delayed but eventually reaching potential
● Nutritional def → Inadequate feeds (but usually affects weight too)
● GIT/IBD → Bloody diarrhoea / abdo pain / vomiting

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● Chronic dz → Cyanosis, SOB, Chronic Cough, Lethargy, Facial/ LL swelling, Poor urine output, Bruising,
frequent blood transfusions
● Endocrine → polydipsia/polyuria/LOW, Cold intolerance/ constipation/wt gain

If disproportionately short
● Rickets → Bowing of legs ,bone pain, teeth problems
● OI → Brittle bones, Frequent fractures

PMH
● Chr dzes: CHD, CF, severe asthma, IBD, GI malabsorption, celiac dz, CRF
● Endocrine dzes: Type 1 DM, Hypothyroidism, hypopit, hypothyroid, GH def
● Bony dzes: OI, rickets…

Antenatal Hx
● IUI eg. TORCH (Exposure to cat litter, Rash , Flu-like illness, Jaundice)
● IUGR, extreme prematurity
● Chr abn - ie Down’s
● Maternal drugs : Foetal alcohol syndrome

Drug Hx
● Long term high dose steroids
● Radiation

FHx: FSS/CGD
Psychosocial Hx: Neglect, abuse…
Developmental Hx

PHYSICAL EXAMINATION
General inspection
● Dysmorphism (Down, foetal alcohol, Russell-Silver, Noonan), skeletal dysplasia
● Short + obese → endocrine, syndromal causes
● Short + thin → malabsorption, undernutrition, chronic dz
WISH LIST
Offer to lie patient down to measure
● US:LS ratio : proportionate vs disproportionate
○ LS = pubic symphysis to plantar surface of foot
○ US = Height – LS
● Request parents’ hts, calculate MPH
● Tanner staging

If dysmorphic
{CHILD STANDING UP} “ Stand opposite me and mirror my movements.”
● Stand, palms together, arms out straight, legs together: asymmetry→ Russell-Silver syndrome
● Carrying angle increased → Turner syndrome
● Touch tips of thumbs to tips of shoulders
○ Overshoot → rhizomelic dwarf (achondroplasia, hypochondroplasia)
○ Do not reach shoulders: mesomelic / acromelic
● Hands:
○ Simian crease → Down syndrome
○ Fist: shortening of 4th metacarpal → Turner’s, pseudohypoparathyroidism
● Stand and bend down to touch toes → scoliosis, kyphosis
-----------------------------------------------------------------------------------------------------------------------
● Eyes: Blue eyes in osteogenesis imperfecta, Down’s features, pallor / jaundice in chronic conditions

346
 ● Ears: low set ears
● Mouth: High arched palate, crowding of teeth in OI
● Head: flattened occiput in Down’s
● Back of neck: thick neck fold in Down’s; low hairline, webbed neck in Turner’s
● Chest: wide spaced nipples, scars from prev congenital heart op
● Cardio: murmurs ?
○ AVSD, ASD, VSD, TOF → Down’s
○ CoA , ASD → Turner’s
○ PS → Noonan’s
○ Supravalvular AS → Williams Syndrome

ꄗ Abdomen low yield unless dysmorphism with known organ problems

ꄗ Tailor the rest of PE according to suspected causes of short stature

Osteogenesis Down [ROSEOLA] Turner [CLOWNS] Noonan [The SUN BURNS at

Imperfecta refer to down’s syndrome PE Cardiac abnormalities: NOON]
document coarctation of aorta, It is difficult to look high in the sky at
Eyes - blue sclera bicuspid, aortic dissection noon, therefore everything is down in
NOONan: Low set ears, downslanting
Scoliosis Round face Lymphedema eyes, Low posterior hairline, Low levels of
Increased laxity of Occipital flattening Ovaries underdeveloped IGF- 1, short stature.
the ligaments and Speckled iris (brushfield Webbed neck Short stature
skin spots) Nipples widely spaced Unusual facies (Ocular
# - humerus, Epicanthal folds Short stature hypertelorism, low set ears)
olecranon Open mouth with protruding Neck is webbed
Skull deformities tongue Bleeding disorders
Hearing loss Low set ears Unusual chest shape (sunken
Easy bruisability Almond eyes chest)
RAS MAPK mutation
Nose is flat
Stenosis (Pulmonic stenosis)
Noonan syndrome!

If no dysmorphism
Face: Rounded facies, acne in Cushing’s , any cyanosis / resp distress
Neck: Goitre

INVESTIGATIONS
Test Indications
Blood:
FBC, PBF Chr dz, anemia
ESR Infx, asympt IBD
U/E/Cr Chr renal dz
Fasting BG DM
Ca, PO4, ALP Rickets hypophosphatasia
LFT CLD, nutritional def
Ant-gliadin titre Celiac dz
TFT, TSH Hypothyroidism
Karyotype Turner syndrome (do karyotype in all short girls)
GH stimulation test GH deficiency
LH, FSH, PL, E2, Hypoganodism
testosterone
Dexa supp test Cushing syndrome
Sweat conductivity CF

347
 Imaging:
Bone age Maturational delay, precocious puberty, hypothyroidism,
Skeletal survey hypopituitarism
SXR Skeletal dysplasias
CT/MRI brain Craniopharyngioma
Intracranial tumour

MANAGEMENT
● Rx is dependent on cause.
○ Systemic dz: rx underlying dz
○ Psychosocial dwarfism: MSW, counselling, nutrition
○ CGD: no rx (normal variant)
○ Genetic syndromes: untreatable, genetic counselling
● Indications for GH
○ GH deficiency
○ CRF
○ Turner syndrome

Other Notes
● If BW is low → pts towards intrauterine / antenatal cause
● If BW is normal, then drops off → pts toward systemic dz
● If proportionately short and whose weight percentile is more than height percentile may have
endocrinopathy ie GH def, hypothyroidism, cushing’s syndrome
Familial Short Stature Constitutional Growth Delay
● Low BW ● N BW
rd
● Growth near / below 3 percentile by 1 yr ● Ht velocity slows down till 1 yr, when ht
<3rd percentile
● Fhx of short stature ● Similar fhx
● Puberty at normal age ● Puberty delayed
● Bone age normal ● Bone age delayed
● Ht falls w/i range for MPH ● Sexual dev N, eventually target ht is
reached.

Normal growth
● Ht/lt
● newborn: 50 cm
● 1st yr: gains 25 cm
● 2nd yr: gains 12.5 cm
● pre-pubertal: 4cm / yr
● puberty: 8.5 cm (girls), 9.5 cm (boys) / yr
● OFC: fr occiput to glabellar / supraorbital ridge (reflects brain growth, bone/water/SOL)
● newborn: 35 cm
● growth: 6, 3, 2, 1 cm for each quarter of 1st yr
● closure of fontanelles: 9-18 mths (ant), 1st few mths (post)
● Wt
● BW regained by 2 wks
● 1st 6 mths: 20 g/d
● next 6 mths: 15 g/d
● 4 mths: double BW
● 1 yr: triple BW
● 2 yrs: quadruple BW
● Bone age
● XR L wrist (~ 1 carpal bone/yr)
● In NN, XR knees and ankles
348
● Puberty
● breast dev 1st sign in females
● testicular enlargement > 4ml 1st sign in males

Mid parental height

● Target range = target ht ±7.5 cm

● Plot the target range at 18yo mark and see if child’s growth percentile falls within the range

349
 Child is Short
(Ht, Wt, COH plotted, pubertal assessment) ± BA

Parents’ height plotted → → Normal for his

↓ parents with
● Normal
Short for his parents growth
↓ velocity
● BA = CA
Looks normal Looks abnormal = Familial short
● Measure standing vs sitting stature
height
● Skeletal proportion

↙ ↘ ↙ ↘
Normal growth Low growth velocity
velocity

Constitutional ↙ ↘ Dysmorphic Disproportionate

delay in growth Wt < Ht Ht < Wt features short stature
and puberty Chronic illness ● Endocrine ● Turner’s ● Achondroplasi
⋇ Male, ± ● CHD causes ● Noonan a
FHx, ● CF ● GH ● Down’s ● Hypochondro
healthy ● GIT: celiac, deficiency ● Russel-Silver’s plasia
⋇ Delayed Crohn’s ● Hypothyroi ● Pseudohypop ● MPS
BA, ● CKD dism arathyroidism
growth ● Neuro ● Cushing’s
⋇ Subnormal disorders syndrome
height ● Hypopituita
velocity Psychosocial/ rism (if a/w
⋇ Present at emotional delayed
early deprivation puberty)
adolescen → Catch-up
ce, growth in
spontaneo nursery
us pick-up environment
second
half of
puberty

350
PAEDS ENDO 4. DOWN SYNDROME

Genetic counselling
- Down syndrome is a condition whereby an individual is born with characteristics(abnormal) facial
features, organ abnormalities and developmental delay
- All of us have 23 pairs of chromosomes, half of which are inherited from each parent. Down syndrome
occurs when an individual has an extra copy of chromosome 21
- Occurs in 1:650 births
- Risk increases with maternal age, maternal age 30 (1:1000), maternal age 40 (1:100)

Genetics/ Different types of Down syndrome

ꈸ Non-dysjunction (95%) of homologous chromosomes
ꈸ Translocation(4%)
ꈸ Mosaicism (1%) - mix of normal and trisomy 21 cells, higher functioning

○ Incidence: 1:600 births (1:200 risk of recurrence if mother < 35yo)

35 yo 1:400
37.5 yo 1:200
40 yo 1:100
43 yo 1:50
○ Clinical features:
○ general: floppy infant (hypotonia), small stature, hyperflexible jts
○ CNS: dev delay, MR
○ face/head: brachycephaly, mild microcephaly, epicanthic folds, prominent nuchal fold,
protruding tongue, dental hypoplasia
○ eyes: upslanting palpebral fissures (Mongolian slant to eyes), myopia, acquired cataracts,
Brushfield spots, squints/pseudosquints
○ skin: loose neck folds (infant), dry skin, folliculitis (adolescents), cutis marmorata (infant)
○ hair: soft fine hair, straight pubic hair
○ hands/feet: short fingers, 5th finger clinodactyly, simian crease, sandal gap
○ cardiac: AVSD, VSD, PDA, valve prolapse > 20yo, ASD
○ genitalia: small penis, testicular volume, infertility common
○ Associations:
○ immune: recurrent resp infx, increased R ALL
○ GI: imperforate anus, umbilical hernia, duodenal atresia (10%), Hirschsprung dz (3%)
○ endocrine: hypothyroidism
○ CNS: Alzheimer’s dz
○ Mx:
○ of problems/cx
○ genetic counselling
○ antenatal dx

PHYSICAL EXAMINATION: Look and Proceed

Head to Toe
Inspection (pt to stand)
● Head: feel for flat occiput
● Eyes: upslanting palpebral fissures, prominent epicanthal folds, hypertelorism, strabismus, cataract
● Flat nasal bridge
● (lift up hair) Low set ears
● Open mouth with protruding tongue
● Neck
○ Thickened posterior neck folds
○ Look for goitre KIV proceed with thyroid exam

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 ● Hands: Simian crease, clinodactyly, brachydactyly
● Feet: widened sandal gap
● Gait

Palpation
● CVS exam
○ Possibly: VSD, ASD, AVSD, Repaired TOF with midline scar with PS murmur
● KIV thyroid
● Abdo exam
○ Scars (for previous GI atresia)
○ Masses for: myeloproliferative, lymphoproliferative

Complete
● Developmental assessment
● Growth charts for Down’s syndrome children
● Formal vision and hearing assessment
● Otoscopy: OME
● Lymph node exam
● Labs: Glucose to look for DM, TFT, FBC

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PAEDS ENDO 5. NOONAN SYNDROME
○ Genetics: AD, new mutations, variable penetrance
○ Clinical features
○ general: short stature, abn body proportions,
○ face: broad forehead, ptosis, hypertelorism, epicanthic folds, down-slanting eyes, low-set ears,
flat nasal bridge
○ body: webbed neck, pectus carinatum, kyphoscoliosis, cubitus valgus
○ heart: right-sided lesions
○ genitals: cryptorchidism
○ Associations: R sided heart defects esp pul artery stenosis, also TOF (Turner’s a/w L sided heart defects)
○ MR may occur
○ May have hypertrophic CMP
○ Variable fertility

Physical Exam
General inspection
● Short stature
● Lymphedematous
● Mutiple brown spots.
● Scoliosis

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Head and neck
● Triangular face (inverted triangle) Wide forehead and small chin.
● Eyes: Hypertelorism. Down-slanting eyes. Droopy eyelids. Strabismus. Amblyopia
● High nasal bridge
● Low set ears
● Short and webbed neck

Chest
● Pectus excavatum. Can be pectus carinatum

CVS
● Pulmonary stenosis
● HOCM

Abdo
● Hepatosplenomegaly

Genital
● Undescended testes

Wish List
- Offer audiogram (Progressive SNHL)
- Ask seizure history

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PAEDS ENDO 6. TURNER SYNDROME
○ Genetics: 45 XO, non-disjunction, majority of foetuses abort spontaneously, mosaicism (only viable
monosomy in humans)
○ Incidence: 1: 2500
○ Clinical features:
○ general: short, loose neck folds (infants), generalised lymphoedema (newborn)
○ CVS: biscuspid aortic valve, CoA, AS, MVP
○ renal: horseshoe kidney, double renal pelvis
○ CNS: mild dev delay, IQ usu N, hearing impairment, essential HPT
○ gonads: ovarian dysgenesis -> infertile, no 2’ sexual characteristics
○ nails: narrow hyperconvex nails
○ skin: multiple pigmented naevi
○ skeletal: broad ‘shield’ chest, widely-spaced nipples, cubitus valgus, short 4th MC bone
○ craniofacial: prominent ears, narrow maxilla, small mandible, short webbed neck, low posterior
hairline
○ Dx: karyotype, lack of Barr body, low FSH, LH, E2
○ Associations:
○ CoA
○ AS
○ VSD
○ ASD
○ horseshoe kidneys
○ increased incidence of AI dz eg. AI thyroiditis, IBD
○ Mx:
○ E2 for dev of 2’ sexual characteristics, and till menopause for prevention of early onset OP (to
maintain BMD)
○ GH: for attaining appropriate ht
○ mosaic with Y chromosome: gonads to be removed (high R of neoplasia)
○ genetic counselling (pt sterile)

Physical Exam Mnemonic: CLOWNS

CLOWNS - Cardiac, lymphedema, ovaries underdeveloped, webbed neck, nipples widely spaced, short
stature
Instruction: “Look and proceed.”
General Inspection:
● Short stature.

355
 ● Brown spots on skin.
● Lymphedematous appearance.

STANDING UP
Head and neck
● Epicanthic folds. Strabismus. Droopy eyelids. Cataracts.
● Low set ears
● Mouth: High-arched palate
● Low hairline
● Goitre
● Short and webbed neck

Upper limb
● Wide carrying angle
● Short 4th metacarpal

LIE DOWN
Chest
● Shield-chest
● Wide spaced nipple

CVS
● AS (bicuspid aortic valve) - ESM at RUSE radiates to carotids
● Coarctation aorta - Radial/radial or radio-femoral delay , ESM radiates to the back

Wish list
- Growth centiles
- Tanner staging
- BP (offer BP both arms due to coarctation causing secondary HTN)
- Otoscopy and hearing test
- Labs: TFT.

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PAEDS ENDO 7. APPROACH TO TYPE 1 DM

NAME/AGE/SEX

BIOLOGICAL

ACUTE CHRONIC ILLNESSES DRUG HISTORY

Complaint Cause Allergies

Cause ● Family history of Type 1 DM? Other autoimmune diseases Long term medications
Course (Grave’s, celiac disease) TCMs/supplements/O
Cx Course TCs
● How did patient present, what symptoms/complications
did patient have
● Followed up with whom? How often?
Control
● What is the latest HbA1c? (toddlers: 7-8%, pri school -
puberty <7%)
● Any blood glucose monitoring at home?
● Hypocount diary
Compliance
● Who does injections of insulin, how many units, how
often?
● Any recent need to change insulin dosages?
● How many hospitalisations for DKA?
● How many episodes of hypoglycemic symptoms?
Complications
● CVRF: HLD, HTN
● Grave’s disease
● Nephropathy (screen with UACR) and retinopathy (DRP)
● To screen above once patient reaches pubertal age or 5
years after age of diagnosis whichever comes first
● Hypoglyecmic symptoms/episodes, any hypoglyecmia
unawareness? Carbohydrate counting and insulin
mismatch (intake lower than calculated OR output more
than expected → exercise)
● DKA hospitalisations
Checking
Competency
● Knows doses of insulin (basal - insulatard, glargine, lantus)
(very short acting - novorapid, apidra) some patients may
be on insulin pump but these are very rare
● CARBOHYDRATE counting (to match post-prandial insulin
with carbohydrate intake/output) → many tools to do this,
electronic apps usually, nutrition labels on foods
Comorbidities
● Thyroid disease
● THINK obesity:
1. Metabolic
○ Fatty liver
○ PCOS
○ HTN
○ HLD

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 ○ OSA
2. Mechanical
○ OA knees
○ SCFE in kids
3. Psychological
○ School bullying
Crisis management
Sick day protocol:
a. Hyperglycemia ppt. DKA
b. Hypoglycemia 2’ poor oral intake
● Always ensure basal insulin is given as patients are INSULIN
DEPENDENT
● Frequent hypocount checks to see if more hypo or hyper,
titrate insulin accordingly
● Encourage hydration

Hypoglycemia
● Hypocount <4
● Rescue with 15g of simple sugars (ie ½ cup milo, coke,
orange juice, 4 pieces of sweets)

DISEASE PREVENTION FAMILY HISTORY

- Vaccinations Type 1 DM
- Cancer prevention Celiac Disease
Grave’s Disease

PSYCHOLOGICAL

PHQ-2 ICE
GAD-2

SOCIAL

Home/Environment – triggers?
Check especially for school bullying, taunting
Body image (especially adolescent females as insulin causes weight gain)
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sleep

PHYSICAL EXAMINATION ***HAND RUB***

General appearance (any presence of dysmorphism)
BP HR
● Growth centiles/BMI
● Developmental assessment for toddlers
● Examine injection sites
● Quick DFS screening

INVESTIGATIONS
● Hba1c
● TFT (screening)

MANAGEMENT

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As per chronic diseases

359
PAEDS ENDO 8. APPROACH TO FAILURE TO THRIVE

Possible stem:
Came for well child visit. Falling centiles noted weight>>height>>OFC.

DIFFERENTIAL DIAGNOSES
Insufficient caloric intake ● Not enough food offered
due to... ○ Poor knowledge of nutritional needs
○ Neglect
● LOA / food aversion
○ Behavioural causes
○ Organic causes
■ Hypothyroidism
■ Malignancy
■ Autoimmune, inflammatory condition
■ Renal failure
■ IEMs
■ Chronic illnesses
● Affected ability to swallow
○ Abnormal craniofacial structures/esophagus (eg cleft lip)
○ Swallowing dysfunction (eg CP, muscular dystrophy)
○ Causes of respi distress
● Recurrent vomiting
○ GERD
○ Hiatal hernia
○ Pyloric stenosis
○ Malrotation
● Abnormal food transit, abnormal digestion/absorption
○ GIT malformation eg TOF, hiatal hernia
○ IBD
○ Cow’s milk protein allergy
○ Celiac disease
● Increased metabolic demand
○ CCF
○ Chronic respi failure/distress
○ Hyperthyroidism
○ Recurrent/chronic infxns
○ Chronic illness
○ Increased activities/exercise
Other Conditions ● Anemia
● Malignancy
● Metabolic disorders eg DM, DI, IEMs
● Placental insufficiency, asymmetrical IUGR, SGA
● Teratogens
● Genetic conditions
Familial

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HISTORY
1. Failure to thrive:
a. Onset
b. Confirm duration over which centiles dropped (Ask for health booklet)
c. Significant? (more than 2 centiles)
d. Pattern: Proportional or disproportional (Globally dropped vs weight predominant)
❖ Wt only → most common inadequate caloric intake
e. Mid-parental height and target height range
2. Ascertain etiology
a. Diet history to find out inorganic cause. “Describe a typical meal for your child.”
b. Assess for any screen time during meal time, and whether family eats meals together.
c. Child’s feeding and behaviour during meals
d. Caloric requirement of child
Age Kcal per kg per day
0 to 3 months 102
3 to 6 months 82
6 to 12 months 80
1-3 yo 82
3-5 77
5-7 72
7-9 67

e. CVM: Exertional dyspnea, orthopnea, lower limb swelling

f. Respiratory: Chronic cough, sputum
g. GI: Coughing post meals, bloody diarrhoea, steatorrhoea, jaundice, history of liver disease;
a/w food taken
h. Renal: Frothy urine, facial swelling, hematuria, history of renal failure
i. Rheumato: Rashes, joint swelling, fever
j. Endocrine: Heat intolerance, neck swelling
k. AMS, LOC
l. Recurrent or frequent infxns
3. Ascertain course: What have parents tried? Visited other doctors? Investigations done?
4. Complications: Development delay?

Medical Hx: Any hx of chronic illness?

Drug Hx: If any
Birth Hx: Especially if very young. Intrauterine growth restriction? BIRTH WEIGHT. Perinatal course
Immunization Hx: Ensure up to date
Development Hx: Quick screen. GFSS
Family Hx: Respi or GI dz
Social Hx: Main caregiver? Family dynamics?

PHYSICAL EXAMINATION
Wt Ht OFC (If less than 2yo) Plot centile and compare with previous centiles on health booklet
T BP HR RR
General inspection:
- Dysmorphism?
- Cleft lip/palate, drooling
- Hydration status, nutrition status (Wasting, sunken eyes, tongue moist, capillary refill time)
- Pallor
- Observe mother child interaction (especially if inorganic cause suspected)

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 - Look for signs of neglect

Cardio: heart sounds, murmurs, signs of fluid overload

Lungs: Crepitations, clubbing
Abdomen: Jaundice, stigmata of chronic liver disease. Abdominal scars. Hepatosplenomegaly
Endocrine: Observe for goitre
Rheum: Look for arthritis, skin rashes

INVESTIGATIONS (as directed by history)

TFT
LFT/RP
FBC
Renal panel

MANAGEMENT
1. Inorganic failure to thrive
- Advise on balanced nutrition diet, can refer to dietician.
- Increase caloric intake
- No screen time during meals. Family to eat together.
- Follow-up in 3 months to monitor growth.

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PAEDS GASTRO 1. APPROACH TO ABDOMINAL PAIN

DIFFERENTIAL DIAGNOSES
ACUTE Abdominal Pain (<2 months)
Surgical Causes
GIT Gynae Others Intra-abdominal solid
● Appendicitis ● Ovarian torsion ● Testicular organ
● Meckel diverticulitis ● Ruptured ovarian torsion ● Laceration of liver,
● Perforated viscus cyst spleen etc
● Malrotation with ● Ruptured ectopic
midgut volvulus pregnancy
● Incarcerated inguinal
hernia
● Adhesions with IO
● Intussusception
● Bowel
ischemia/gangrene
Non-surgical Causes
GIT HPB Uro Gynae
● Constipation ● Hepatitis ● UTI ● Dysmenorrhea
● GE ● Cholecystitis ● Urinary calculi ● Mittelschmerz
● Gastritis, PUD ● Cholelithiasis ● Distended ● PID
● GERD ● Cholangitis bladder ● Threatened
● Lactose intolerance ● Liver abscess ● Obstructive abortion
● Malabsorption ● Pancreatitis hydronephrosis ● Ectopic pregnancy
● Bowel ischemia ● Labour
● Acute mesenteric ● Endometriosis
ischemia
● Mesenteric adenitis
● Primary bacterial
peritonitis
Others Poisoning
● DKA ● Lead
● HSP ● Iron
● Pneumonia
● Sickle cell crisis
● Myocarditis
● MSK
● Hypovolemic shock
● First episode of chronic
abdominal pain

CHRONIC Abdominal Pain (>2 months)

Organic Causes
GIT HPB Uro
● PUD ● Chronic hepatitis ● UTI
● Gastritis / Hpylori ● Cholelithiasis ● Hydronephrosis
● GERD ● Chronic cholecystitis ● Urinary calculi
● IBD/ Autoimmune ● Chronic pancreatitis
● Lactose intolerance
● Food allergy/intolerance
● Malabsorption

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 ● Celiac disease
● Constipation
Gynae Others
● Dysmenorrhea ● Porphyria
● Mittelschmerz ● Tumours, malignancy
● PID
● Endometriosis
Functional Causes
Functional abdominal pain Primary constipation and its related
(functional dyspepsia, abdominal colic
migraine, IBS, functional abdominal
pain syndrome)

HISTORY
Complaint: Abdominal pain
● Acute or chronic
● Location of pain
● Duration
● Nature of pain [SOCRATES], onset of pain, radiation of pain
○ Epigastric or periumbilical pain radiating to back/scapula → pancreatitis
○ Epigastric pain ± nausea/vomiting/hematemesis/melena → gastritis, PUD
○ RHC pain ± jaundice → hepatitis, cholangitis, cholelithiasis, cholecystitis
○ LHC pain → gastritis, splenic cause
● Aggravating factors -> Particular food -> food allergy
● Relieved with BO?
● Severity - Wake up at night due to pain (Red flag)

Causes
● Fever, cough → Pneumonia
● Vomiting – blood, bilious , GI bleed
● Reflux
● Change in stools: diarrhea, constipation, BGIT
○ Diarrhea, flatulence, bloating a/w food → Food/lactose intolerance, malabsorption, IBS
● LOW, LOA
● Jaundice
● Rash, Joint pain
○ Purpuric rash on LL → HSP
● Dysuria, frequency
● Testicular swelling
● Menstrual history
● Polydipsia, polyuria, LOW, polyphagia → DM TRO DKA
● Trauma

Red flags
● IO symptoms
● Bilious vomiting
● Bloody vomitus
● LOW or poor growth
● Pain that wakes child up at night
● Chronic abdo pain that is not central/umbilical

Course
● Seen any doctors so far, ix, mx
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Complications
● Dehydration
● Shock, low blood pressure
● BGIT

Travel Hx
Contact Hx

PMH
● H/o nephrotic syndrome or CLD with ascites → TRO primary bacterial peritonitis, hypovolemic
shock

Medication Hx
● Recent drugs (eg NSAIDs, antibiotics) or TPN

Family Hx
● Gastritis / H-pylori / IBD / Celiac dz

Social Hx
● How has it affected school, activities, friends, family (finances)

PHYSICAL EXAMINATION
Growth charts
T BP HR
Pallor, jaundice
Abdomen

INVESTIGATIONS
● KIV Udipstick/UFEME if UTI suspected

MANAGEMENT
Chronic abdominal pain
● ‘KIV refer for consideration of scopes
● Tummy pain diary

Food Allergy
- Avoid triggers
- Read labels on packaged foods/ medications/ vaccines. prepare safe meals at home, avoid food
allergens in restaurant meals. Exposure to allergen-containing saliva may occur during kissing or
sharing of utensils, craftwork, cosmetic s
- May grow out of it
- Challenge test at older age

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366
PAEDS HAEM 1. HEMOPHILIA – X LINKED RECESSIVE

- Women are carriers of hemophilia and around 20% of them can have bleeding problems, most commonly
heavy menstrual bleeding. They can also pass down the defective X chromosome to their offspring.
- Many carriers have a clotting level between 30% and 70% of normal and do not usually suffer from severe
bleeding, although they may suffer from the most common symptom – heavy menstrual bleeding.
However, some carriers have less than 30% of the normal level of factor VIII or IX. These women are
considered to be mild hemophiliacs.
- Carriers have one normal X chromosome and one abnormal X chromosome. The normal X chromosome
produces a certain amount of factor VIII or IX clotting factor. This protects carriers from the most severe
form of hemophilia in which the level of clotting factor is less than 1%.
- However, the variation in clotting factor levels among carriers is very wide. In some carriers the level is
much below normal. In other carriers, the level is closer to normal. This is because the two X chromosomes,
one of which carries the hemophilia gene, are not equally functional. If the hemophilia X chromosome
happens to be functional in most cells, then the carrier will have a very low level of clotting factor activity.
It is not known how many carriers of hemophilia A and B have bleeding problems. Estimates vary up to
60%.

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368
PAEDS HAEM 2. APPROACH TO BLEEDING & BRUISING

DIFFERENTIAL DIAGNOSES
Platelet REDUCED NUMBER REDUCED FUNCTION
Reduced production ● Platelet dysfunction
● Aplastic anemia • Drugs: Aspirin, NSAIDs
● Myelodysplastic syndrome -Infiltration of • Von-Willebrand dz
bone marrow • Renal failure
● Drugs (BM suppression): AZT, MTX • Multiple myeloma (Calcium
Increased destruction Renal impairment Anemia Bone
● Immune-mediated lesions - CRAB)
○ Auto-immune: SLE, ITP
○ Infections: HIV, EBV, CMV, viral
○ Drugs: Heparin, Rifampin,
Quinidine, Quinine, Sulfonamides,
Sulfonylureas, Penicillins
● Non-immune –
○ Sepsis
○ DIC, TTP, HUS
○ HELLP (hypertensive disorder of
pregnancy - hypertension,
elevated liver enzymes, low
platelet)
Sequestration
● Hypersplenism
- Liver cirrhosis with portal HTN
- Myelofibrosis
- RA with Felty’s syndrome (triad: RA +
low TW + splenomegaly), Storage diseases

Clotting Congenital Acquired

factors - Hemophilia Liver cirrhosis
Vitamin K deficiency
DICL sepsis/consumptive coagulopathy
Drugs: anti-coagulants, warfarin,
NOACs, heparin

Vessel/Conn ● Hereditary Hemorrhagic Telangectasias Connective tissue disease

ective Tissue ● Marfan’s, Ehler Danlos
diseases ● Cushing’s, Vit C deficiency
● Infections: meningococcus,
gonococcus, bacterial
endocarditis
● Vasculitis: HSP, SLE,
polyarteritis nodosa,
cryoglobulinemia
● Amyloidosis (AA/AL)
● Drugs: steroids, sulfonamides,
penicillins, thiazides

Inorganic NAI

DDx:
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 1. Rule out NAI / Trauma
2. Platelet defect
a. Malignancy: Lymphoma/ Leukaemia / Multiple Myeloma
b. Infections: Meningococcaemia, Dengue, Chikungunya, viral infections, malaria
c. Autoimmune: HSP, ITP , SLE , RA with hypersplenism
d. Drugs: carbamazepine, valproate, DMARDs eg methotrexate, azathioprine
e. Chronic liver disease with hypersplenism
f. Uraemia
g. Prosthetic valves
h. HUS (Triad: MAHA, Thrombocytopenia, AKI, triggered by Ecoli) / TTP (Pentad: Fever, Neuro
abnormalities, MAHA, Thrombocytopenic purpura, Renal dz)
i. DIC
j. Aplastic anaemia
3. Coagulation disorders
a. Congenital: Hemophilia A and B, Von Willebrand’s disease
b. Chronic liver disease
c. DIC
d. Vitamin K deficiency
e. Drugs: heparin, warfarin
4. Capillary defect
a. Steroid use
b. Vasculitis: Churg Strauss vasculitis, Wegener’s granulomatosis, PAN
c. Congenital: Ehlers-Danlos syndrome, Pseudoxanthoma elasticum

Name/Age/Sex

BIOLOGICAL

Acute Chronic illness Medical History

Complaint: Bleeding and bruising Cause ● Medical/ Surgical Hx

● Site: Course - Hx of bleeding disorder
● Skin petechiae/ purpura, gum Control - Age dx-ed ,
bleed/epistaxis -> Plt ● Home presentation, ix , mx ,
● Ecchymoses, Joint bleeding or hematomas ● Clinic f/up , compliance, prev
-> coagulopathy Compliance admissions
● PR bleed/ melena/ haematemesis/ ● Non
Menorrhagia/CNS bleed pharm
● Onset: Acute or bleeding since birth ● Pharm ● Drug Hx/ Drug allergies
(congenital) Complications ● Medication List (any
● (immediately after trauma -> Plt , delayed ● Disease antibiotics, OCP,
bleeding ie hrs -> coagulopathy) ● Treatment antiplatelets,
● Precipitating: Trauma/ NAI Checking anticoagulants),
● Time course: How frequent? Competency TCM/OTC
● Severity: Quantify amount of bleeding.
Assess how quickly bleeding takes to stop Comorbidities
(e.g. nose bleed resolved with anterior Crisis
pressure?) management

Causes
● LOW/ LOA/ bone pain / lumps around
neck/armpit/groin (malignancy )

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 ● Any recent fever, URTI, GE symptoms or
vaccination (ITP is preceded bv__, viral
infections/ vaccination)
● Travel history (malaria)
● Recent trauma
● Possibility of abuse in the family!
● Recent new drugs
● Fam hx of bleeding disorders
● Rash, joint pain oral ulcers, alopecia (SLE)
● Hx of liver dz / kidney dz
● Hx of valve replacement
● Dietary history especially Vitamin C
containing fruits and vegetables
Course
● Tried what treatment?
● Seen other doctors for it?
Complications
● Anemia
● BGIT, Intracranial hemorrhage

Disease Prevention Family Hx

- Vaccinations: Bleeding problems ie

- Cancer prevention: X-linked recessive Hemophilia -
male relatives affected
Von willebrand disease

PSYCHOLOGICAL

PHQ-2 ICE
GAD-2

SOCIAL

Home Function
Employment/education: High risk jobs
Activities: Contact sports? bADL (DEATH)
Drugs (Smoking, alcohol, illicit drugs) iADL (SHAFTTT)
Sex and relationship with others
Suicide Cognition
Sleep
Finance Bladder and bowel
Exercise
Diet Eye, ear and swallowing

PHYSICAL EXAMINATION ***HAND RUB***

General inspection: Conjunctival pallor, look at hands for pallor
T BP HR
1. Mucosa exam: Nose inspection, oral cavity exam
2. Skin exam: Inspect for petechiae, bruises, hematoma
3. Joint exam: Look for haemarthrosis / arthropathy from recurrent haemarthrosis
4. Abdominal exam***: Palpate for hepatosplenomegaly. Lymph node examination (check cervical,
axillary, inguinal nodes).
5. Neuro exam***for evidence of ICH

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Offer DRE to assess for BGIT.

INVESTIGATIONS
FBC: Platelet <100 for ITP; PT/PTT/INR
KIV PBF, LFT (BM aspirate is not routinely done for ITP unless there is suspicion of malignancy / BM failure)

MANAGEMENT
1) ITP:
- Characterized by Isolated thrombocytopenia (platelet count <100,000/microL)
- Autoimmune mediated - Ab bind to platelet and cause splenic destruction of platelet
- Common between 2 -10 years old
- Presentation: Widespread petechiae, purpura, ecchymosis , epistaxis, gum bleeding, less commonly
GI bleed/CNS bleed , absence of systemic symptoms
- Acute ITP: Self limiting, Resolves in 3-6 months with or without treatment, Occurs 1-4 weeks after
viral illness ie VZV, Measles, EBV, vaccinations
- Chronic ITP: thrombocytopenia > 12 months, usu > 10yrs old, exclude SLE, platelet production
disorder via BM exam

Acute ITP ⇒ ED
● Avoid high risk activities (e.g. contact sports) and trauma (eg, football, boxing, lacrosse, and hockey,
baseball, soccer, skiing, or gymnastics)
● Avoid NSAIDS that can worsen ITP.
● For postmenarchal female patients, hormonal therapy (typically with a progesterone-based
treatment) may be warranted to control or inhibit menses and prevent severe menorrhagia.
● Educate on when to seek help ie life threatening bleeding, if develop symptoms of severe bleeding
(eg, severe headache, hematuria, melena, heavy menstrual bleeding), to return immediately.
Treatment of children with newly diagnosed ITP is based upon the severity of bleeding symptoms, the
degree of thrombocytopenia, and additional risk factors (algorithm 1). Depending on individual patient
characteristics, appropriate initial management may be either "watchful waiting" or pharmacologic
intervention
● Disposition:
● If plt > 20 and no or mild mucosal bleeding, watchful waiting, refer to paeds hemato direct access.
● If Plt <10-20 or active life threatening bleeding ie (ICH, GI bleeding with hemodynamic instability,
pulmonary hemorrhage with cardiopulmonary compromise), refer to ED for platelet transfusion,
IVIG, oral steroids , IV anti-D IG
● Monitor platelet counts once weekly initially.

Platelet threshold for surgery

In general can proceed if plt > 50K

2) Haemophilia (X-linked recessive)

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Presentation:
- Severe - Spontaneous bleeds - haemarthrosis, hematomas, haematuria
- Moderate - bleeds with traum
- Mild - bleeds after surgery ie prolonged oozing after dental extraction
Complications of dz
- Haemarthrosis - knees/ elbows/ ankles/ shoulders, resulting in arthritis, joint instability and
ankylosis (Joint pain / stiffness/ giving way)
- Neurological problems - ICH, Haemorrhage into vertebral canal (neck and back pain followed by
ascending paralysis) . Peripheral nerve compression
- LIfe threatening hemorrhages - retropharyngeal, retroperitoneal

Complications of Tx

3) Non-accidental injury
- Suspect NAI early on if
- Multiple bruises of different ages, hx from parent inconsistent with injuries, hx is vague , hx of
bruising in a child not cruising
- “I ask this for all my pts with bruising: Is there any possibility that your child might be abused?”
- How were the injuries sustained
- If child abuse suspected, request to speak to child alone (parental refusal to allow child to be
interviewed alone is considered red flag for abuse)
- Is the injury witnessed, events preceding trauma, mechanism of injury, subsequent actions and
symptoms of patient (usually unwitnessed)
- Social hx ***VERY IMPT- who stays with the child , who is the main caregiver , who is around when
main caregiver is away, are parents married, any family problems ? How does the patient behave
with certain people ie very quiet / refuse to follow someone

Examination:
- Examine with all the clothes removed sequentially
- Trunk , back, arms , legs , perineum (sexual abuse!)
- Retinal hemorrhages, hemotympanum, mouth (frenulum tears or palatal petechiae)
- Signs of neglect (malnourishment , poor hygiene)
- Multiple fractures in various stages of healing or co-existing with bruises, burns and fractures
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 - Injuries consistent with method of infliction - slap, belt, loop of cord, cigarette, iron
- Fractures: long bone # in pts who cannot walk, rib fracture, hollow viscus injury < 4 yo , subdural
hematoma
- Bruises: Bruises in children who cannot cruise, trunk, ear and neck

Mx:
- Non accusatory language that emphasizes need for further evaluation: “ This is more injury than
what we would expect from the event that you are describing. We should be careful to determine
whether there is something medical going on, or if someone might be hurting your child”
- OR “ sometimes when we see injuries like these, there are other injuries that may put patient at
risk and we need to test for them”
- Refer MSW
- Report Police
- Evaluate other siblings for abuse
- Need for hospitalisation:
- Tx of burns. Ingestion, intracerebral injury
- Child is considered unsafe in the care of the parents
- A protective environment where the child can be evaluated needs to be provided

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PAEDS HAEM 3. THALASSEMIA SONG
I will like to complete my examination by
- Plotting her growth parameters on a growth chart
- Tanner Staging
- Bedside hypocount
- CVS examination for flow murmur and dilated cardiomyopathy
- Thyroid Status
- Vision and Hearing assessment for desferal ophthalmo-toxicity and ototoxicity

My patient is a young Malay girl who has thalassemia. She appears short and thin for her age.

On inspection, her skin is bronzed, and she has thalassemic facies such as frontal bossing, maxillary
hyperplasia. She is pale and mildly jaundiced. There are scars on her arms suggesting previous cannula
insertion possibly for blood transfusion.

On examination of her abdomen, there are hyperpigmented marks on her abdomen suggesting iron
chelation therapy.

There is hepatomegaly which measures ____ cm below right costal margin, the edge is regular, the surface
is smooth and it is firm in consistency. It is non tender and there is no hepatic bruit
There is massive splenomegaly extending 10cm from the left costal margin, which is firm and non-tender.
The kidneys are not enlarged and there is no shifting dullness to suggest ascites. There was no
lymphadenopathy or cachexia.

As for the complications,

There is no peripheral stigmata of chronic liver disease such as clubbing of fingers, leukonychia, palmar
erythema, spider naevi. There are no distended superficial abdominal veins to suggest portal hypertension
(from cirrhosis). There are no abdominal scars to suggest splenectomy or cholecystectomy.

There are no prick marks on her fingertips to suggest glucose monitoring for diabetes.

On cardiac examination, her apex beat was not displaced and located in the 5th left ICS in the mid clavicular
line, and she did not have any flow murmurs.

In summary,
My patient is a young malay girl with thalassemia major on regular transfusion complicated by iron
overload

My differential diagnosis include

1) Other haemolytic anemia such as hereditary spherocytosis, G6PD
2) Chronic liver disease cx by portal hypertension
3) Myelo/lymphoproliferative disorders

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PAEDS NEURO 1. FEBRILE SEIZURE

Stem:
1. First presentation of febrile seizure
2. Known febrile fit, came for an episode of febrile seizure

Definition:
Febrile seizures are seizures that occur between the age of 6 and 60 months with a temperature of - >38 °C,
that are not the result of central nervous system infection or any metabolic imbalance, and that occur in
the absence of a history of prior afebrile seizures.

History
1. Seizure
Complaint:
Seizure history
(exclude complex seizure characteristics >15 minutes, non generalized fits, recurrence of fits in <24 hours,
todd paralysis post ictal)

Pre-ictal and post ictal events. Witnessed?

Pre-ictal - What was the patient doing
Ictal - Duration of fits, focal vs generalised, LOC, Stiffening, jerking, tongue biting, incontinence , Any
recurrence of fits
Post-ictal- Drowiness, any todd’s paralysis , duration

Causes: Ensure due to fever only.

Exclude other causes like meningitis, head injury, space occupying lesions, electrolyte imbalances ie
hypoglycemia, pseudoseizures (breath holding, rigors), Epilepsy, Drug induced

Course: What did parents do during seizure? Appropriate vs inappropriate seizure management

Complications: Head injuries? Other injuries sustained?

2. Fever
- Ascertain fever pattern, cause of fever, course and complications from the illness
- Drowiness, change in behaviour , Headache , rashes -> meningitis
- Vomiting, diarrhoea, LOA -> Electrolyte imbalance
- In non-verbal children , rule out UTI ! (urine bag in OPS, if positive-> send ED for in-out, if negative, less
likely UTI)
- Foul smelling urine , urinary frequency
- Ear discharge/ ear pain
- RN / Cough/ Sore throat / Oral ulcers
- Abdo pain

Medical Hx: Previous febrile fits, Hx of epilepsy,, neurocutaneous syndromes ie neurofibromatosis

Drugs Hx:

Birth and Developmental history - any perinatal insult , delayed milestones

Family Hx: Febrile Fits, Epilepsy, Neurocutaneous syndromes, Mental retardation / Developmental delay

Physical Examination:

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Vital signs : Temp , BP , HR , Growth percentiles
Inspection:
Toxic looking/ Drowsiness in meningism
Neurocutaneous stigmata
Rashes / vesicles / petechiae in infection
Neck stiffness: Kernig's sign, Brudzinski’s sign in meningism
Neurological examination: Moving all 4 limbs and running around in the consult room?
Opportunistic neuro examination if possible
Examination for fever!
Heart
Lungs
Cervical LN
Abdomen
Palms and Soles
Otoscopy
Throat

Investigations
Serum Electrolytes and Hypocount only for pts with history of poor oral intake
Urine bag to rule out UTI if fever in pre-verbal children

Management
1) Stop the seizure
2) Treat the underlying infection
3) Fever Management - Fever control is symptomatic and does not play a part in preventing further
febrile seizures
4) Encourage hydration
5) Standby Rectal diazepam - give if seizure > 5 mins
6) Seizure first aid/ Recovery Position
7) Red flag advice (below)
8) Education on long term outlook

Red flag advice - Bring the child to Children’s emergency if

▪ The seizure lasts more than 15 minutes or does not abort with rectal Diazepam
▪ There were two or more seizures in a row without the child regaining consciousness
▪ The child did not wake up from the seizure even after the seizure has stopped (post- ictal drowsiness
usually lasts about 30 min)
▪ The child develops new neurological deficits e.g. focal weakness

Education
- ⅓ of children may get 2nd febrile seizure (30%)
- ⅓ of children with 2nd febrile seizure may get a 3rd febrile seizure (10%)
- Risk of epilepsy is the same as the general population
- Does not affect intellectual performance
- 15-20% of children have family hx of febrile seizure

Seizure First Aid

• Lie the child on a flat surface
• Turn the child to the side to keep the airway clear
• Remove nearby hazards or sharp objects
• Place something soft and flat under the child’s head
• Loosen the clothing (e.g. collar)
• DO NOT try to hold the child’s tongue down with a spoon or any objects
• DO NOT try to bring the child around by throwing water on him, slapping or shaking him

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• DO NOT give the child anything to drink
• DO NOT hold the child down or restrain him in any way
• Stay with the child until his breathing is normal and the child is awake again
• Time the seizure. If the seizure lasts more than 5 minutes non stop, give rectal Diazepam to abort the
seizure

When to refer
- Complex Febrile Seizure
- First Febrile Fit in < 18 months old
- Afebrile Seizure
- Intracranial infection

NUH guidelines on management of febrile seizure

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PAEDS ORTHO 1. APPROACH TO LIMPING CHILD (NUH CE guidelines)

Definition:
Limp is defined as an uneven, jerky, or laborious gait, usually caused by pain, weakness, or deformity.

** Common cause: growing pain (btw 4-5yo and during puberty) dx of exclusion
**bilateral pain → myositis with recent viral illness

V – Vasculitis – HSP
I – Infections (Septic arthritis/ Osteomyelitis) / Transient synovitis (preceded by infection)/ STDs
T – Trauma / Tumour (includes ALL/AML!) / Hemophilia
A – Autoimmune – JIA / SLE
M – Metabolic / Neuromuscular disease – Hypothyroidism/obesity -> SCFE
I – Increased activity - 0veruse /exercise/ sprain/ Osgood schlatters
N–
- Non joint problems -> Referred pain from testicles, appendicitis , metabolic diseases
- NAI –> non accidental injury
- Normal -> Growing pain

C – Congenital - Developmental dysplasia of hip

Others: Perthes’ dz

HISTORY
Complaint
- Child is limping / refuse to weight bear on one limb/ painful limb

- Site of limping/ pain ie ankle,knee, hip,back , any other joints involvement( inflammatory disorders)
- Onset: Sudden vs gradual, Duration, What was the patient doing when pain started
- Character: constant severe pain (#, infection) vs intermittent less severe,
pain occur at night or wake child up (cancer), painless (DDH, neuromuscular disorders)
- Radiation: If knee pain -> rule out referred pain from hip
- Exacerbating factors: worse with movement (#, overuse injury, hypermobility syndrome)

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- Relieving factors: improve with movement (Inflammatory joint pain)
- Severity: Unable to bear weight (#, infection), able to bear weight (inflammatory + others)

Course
- Any ix done, mx, f/up where

Cause
Trauma Fracture, Contusion, Hemarthrosis
(haemophilia)
Fever , Night Pain ,Rest Pain Septic arthritis (Bacterial, TB, Gonorrhoeal)
Osteomyelitis , Malignancy
LOW, Anorexia, Night pain Malignancy, TB
Recent URTI Transient synovitis
Back pain Discitis, meningitis, vertebral osteomyelitis
Rashes, Joint pain HSP(LL), JIA, Leukaemia (Petechiae)
Morning stiffness, constitutional symptoms as Rheumato ie JIA, SLE
above: Fever, LOW, Rash, Red eyes, SOB
Family hx of autoimmune dz
Hypothyroidism, Obesity SCFE
Painless, weakness Neuromuscular
Activity in sports and pain worsens with activity Stress fracture, overuse syndromes, Osgood
Schlatter
Sexually active teenager Gonorrhoeal arthritis, reactive arthritis
Psychosocial issues Non accidental injury , complex regional pain
syndrome
Referred pain: Testicular pain; RIF pain, Testicular torsion, Appendicitis
vomiting, LOA

Complications; Impairment of school activities / function

PMHX: Autoimmune diseases, Joint problems
Drug Hx, drug allergies:
Family Hx: Cancers, autoimmune disorders
Social Hx: rule out NAI!, find out pt’s hobbies, CCA, school, level of activity
Psycho Hx:
Birth / Antenatal Hx:
Developmental Hx:
Immunisation Hx:
Sexual Hx in teenager !

PHYSICAL EXAMINATION
Temp BP HR
⊷General inspection
● Toxic looking -> Septic/ cancer
● Bruises -> NAI / Petechiae in leukaemia
● Rash -> HSP , SLE , Rheumatic fever
● Gait -> Able to weight bear?
⊷ Examine whole affected leg: redness, swelling, warmth, tenderness
⊷ Assess all joints for passive and active movements
● Effusion in hip will make internal rotation and abduction painful
⊷ FABER test
⊷ Limb length discrepancy
** Complete refusal to bear weight or severe reduction in movement of joints are red flags that need to be
noted

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INVESTIGATIONS
● FBC, ESR, CRP – for febrile patients or afebrile with several hx of limping but normal XR
● XR pelvis and lateral hip or relevant joint
● US Hip: if XR normal but suspicion of septic arthritis is high

TRANSIENT SYNOVITIS
- Relatively common problem (most common cause of limp in children)
- 3- 10 yo, Boys 2X> girls
- Usually self-limiting within approximately one week.
- Rapid onset of unilateral hip pain and limping in an otherwise well child , lasts for 1- 2 weeks
- Child usually will not have high fever
- There may be a history of preceding viral illness in past 1-2 weeks
- The prognosis usually is excellent, with full recovery to be expected. Recurrence rates from 4 to 15
percent have been reported. A small percentage (1 to 2 percent in most series) may go on to develop Legg-
Calvé-Perthes disease (LCP) with avascular necrosis of the ipsilateral femoral head

- P/E:
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- Hip held in flexion and abduction, limitation of internal rotation, usually able to bear some weight
- Tenderness on palpation even during passive movement
- Only mild limitation of ROM (severe reduction more suggestive of septic arthritis)
- Ix: XR no changes
- Mx: NSAIDS, Heat/ Massage, Able to weight bear with analgesia, Return to normal activity as tolerated,
Red flag advice, (Consider referring to ED if unable to weight bear or severe pain), Reassurance that
condition is self limiting

GROWING PAIN
- Diagnosis of exclusion
- Usually between 4-5 yo and during puberty
- Pain occurs at the end of the day , relieved with massage / after a good night rest
- Bone growth faster than rate of increase in length of muscle and tendon

SEPTIC ARTHRITIS
- Infection of joint that can destroy a joint within 24 hours.
- Child will usually have marked pain/spasm, high fever, systemic symptoms
- Acute onset of limp, REFUSAL to weight bear, examination usually very reduced ROM of hip joint
- Features suggestive of septic arthritis vs transient synovitis
ESR>40 CRP>20 Fever > 38.5 Non weight bearing WBC > 12000
- Remember that not all of the features may be present and that the younger the child, the more subtle the
presentation can be!
- Septic arthritis requires urgent aspiration +/- arthrotomy and washout.
- Will also require early IV abx commenced early (try to obtain joint fluid for analysis and culture first)

SLIPPED CAPITAL FEMORAL EPIPHYSIS

- Displacement of the capital femoral epiphysis from the femoral neck
- Tends to occur in 10 – 15 year olds
- Often with body weight above the 90th centile
- Boys are affected slightly more often than girls
- There may or may not be a history of some trauma
- Diagnosis is radiological.
- 25% may be bilateral
- AP views alone may miss subtle changes therefore bilateral ‘frog view’ is required
- Usually requires urgent operative reduction and pinning

PERTHE'S DISEASE
- Osteonecrosis of the femoral head (avascular necrosis of capital femoral epiphysis)
- Tends to be found in the age group of 4 to 12 years
- Diagnosis is radiological but x-ray changes may be absent early in the illness.
- Boys:Girls=4:1
- 15% may be bilateral
- Usually no systemic features
- Treatment of Perthes includes orthosis/bracing, no weight bearing, use of crutches, analgesia and close
orthopaedic follow up.

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8 yo Boy presents with Right hip pain , Referred pain to the knee, Shortened right leg

Describe:
- Right hip flattened epiphysis with sclerosis
- Widening of joint space
Dx: Perthes’ Disease
Pathophysiology :Avascular necrosis of femoral head in childhood
Mx:
Acute: NSAIDs, Casting/ bracing if ROM limited or deformity present, No weight bearing during acute pain,
use of crutches
Refer to Ortho direct access

Chronic :
2-6 years old - > Physiotherapy, avoid high impact activities ie running and jumping , use crutches, close
orthopaedic follow up.
> 6 yo and > 50% femoral head involved > surgical osteotomy of femur / pelvis

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13 yo boy with right hip pain , referred to the knee , shortened limp

Describe: Femoral head is seen displaced, posteriorly and inferiorly in relation to the femoral neck and
within the confines of the acetabulum.
Diagnosis: Slipped capital femoral epiphysis
CX: Avascular necrosis . Secondary OA
Associations in bilateral SCFE : Hypothyroidism, hypogonadism, hypopituitarism

MX: Refer to ED stat, will require emergency reduction and fixation to prevent avascular necrosis

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PAEDS RENAL 1. NEPHROTIC SYNDROME

Stem:
1. Came in with edema. (likely long case if to reach nephrotic syndrome and rule out other causes)
2. Came in to follow-up labs which points towards nephrotic syndrome
3. Came in with fever and worsening swelling, bg of nephrotic syndrome on steroids
4. Travel advice in known NS child

DIFFERENTIAL DIAGNOSES
Primary (95%) Idiopathic nephrotic syndrome: MCD (80%), FSGS
● Steroid-responsive vs steroid-resistant

Secondary ie a/w systemic dz or 2’ process that causes glomerular injury

● Without nephritis/glomerular inflammation on biopsy
○ Membranous nephropathy
○ Secondary FSGS (due to nephron loss from renal scarring/hypoplasia)
● With nephritis/glomerular inflammation on biopsy
○ Post-infectious GN, IE ie post-strep GN
○ SLE
○ Vasculitides eg IgA vasculitis (HSP)
○ Sickle cell (usually a/w 2o FSGS)
○ Hemolytic uremic syndrome

DEFINITION
1. Massive proteinuria: UPCR >3-3.5mg/mg or 300-350mg/mmol, or 24h UTP >3-3.5g/day
2. Albumin <25g/l
3. Raised cholesterol, TG, LDL, VLDL
4. Edema: clinical evidence of peripheral edema
ᐉ Remission: loss of edema, urine dipstick –ve/trace for 3 consec days
ᐉ Infreq relapsing: <2 episodes w/i first 6 mths, or <4 episodes w/i any subsequent 1 yr period
ᐉ Freq relapsing: >2 episodes w/i first 6 mths, or >4 episodes w/i any subsequent 1 yr period
ᐉ Steroid dependent: freq relapsers w 2 consec relapses while on steroids, or w/i 2 wks of cessation of
steroids
ᐉ Steroid resistant: fail to achieve remission despite 6 wks of daily high dose (60mg/m2/day)
prednisolone therapy

HISTORY
Complaint:
● Edema. Distribution of edema (Facial, LL/ankle, Abdominal, Scrotal)
● Rule out other causes of edema: CCF, Chronic liver disease, Renal failure. Ensure edema is gravity
dependent.
● Frothy urine, mild hematuria, oliguria
● SOB
● Weight gain
● Lethargy

Cause
● Nephrotic syndrome to confirm: Confirm urine protein excretion ≥50mg/kg/day. Reduced serum
albumin <30 ± oedema ± hyperlipidemia
● Most common cause: minimal change disease
● Check for secondary causes of nephrotic syndrome:

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 ○ Recent fever, URTI symptoms -> Post Strept GN
○ Malar rash, joint pain, oral ulcers, photosensitivity -> SLE
○ Purpuric rash, joint pain, abdominal pain → HSP
○ Drug induced
● If known nephrotic syndrome but worsening edema -> Check for triggers for relapse ie recent
infections/compliance to meds
● Differentiate from nephritic -> nephritic involves HTN, gross hematuria, less proteinuria

Course
● First dx, presenting symptoms, no of episodes, past hospitalisations
● Is pt steroid sensitive (infreq or freq relapses) or steroid dependent or steroid resistant
● Request for investigations done: Serum albumin, lipid panel, urine protein, urine microscopy,
creatinine, any renal biopsy done (unlikely in minimal change dz)
● Management so far, f/up with who/where

Complications: from disease and from treatment

● From third spacing: Hypovolemia symptoms, ascites and if ascites present, SBP
● From losing immunoglobulins: Frequent infections
● From losing antithrombins: Clotting symptoms (DVT, stroke symptoms), thromboembolism

Mnemonic: NEPHROTIC
ꄗ Nephrotic
ꄗ Edema, SOB from pleural effusion (not common)
ꄗ Proteinuria
ꄗ Hypovolemia, Hyponatremia (Seizures), Hyperlipidemia
ꄗ Renal failure (not common in nephrotic syndrome) → Reduced urine output
ꄗ O - Growth affected
ꄗ Thrombosis (sagittal sinus thrombosis, DVT) → confusion, headache painful leg swelling
ꄗ Infections esp encapsulated bacteria ie pneumococcus (spontaneous bacterial peritonitis) →
Fever/ Abdominal pain/ Vomiting / UTI / Skin infection
ꄗ Complications from tx a) steroids: Cushing’s Syndrome, b) other immunosuppressants

For chronic case

● Current symptoms
○ General health: anorexia, wt gain/loss, lethargy, growth charts
○ Edema: periorbital (often 1st sign), ankle, ascites, scrotal
○ Urinary: h’turia, oliguria, conc urine
○ Other: infx, abdo pain, HPT
● Control: How frequent are relapses/ hospitalizations, triggers, how treated, Does parent know what
to do if relapse, get the nephrotic diary!
● Is pt steroid sensitive (infreq or freq relapses) or steroid dependent or steroid resistant
● Compliance to meds: steroids and immunosuppressants , any change in meds
● Course: first diagnosis; no of episodes, hospitalisations, current treatment
○ Ask for nephrotic diary!
● Complications as above
● Checking: Weight monitoring, Urine dipstick for proteinuria
● Competency: Meds administration
● Co-morbids
● Crisis Mx: If develop fever, abdominal pain, confusion, to return immediately
● **Level of understanding of child and parent?
PMHx
Drug Hx
Family Hx of kidney disease ie glomerulonephritis

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Immunization: Avoid live vaccines while on pred, give flu and pneumoccocal
Birth / Antenatal/ Developmental Hx
Social Hx
● Dx impact on child: sick days, schoolwork, body image
● Family: marital problems, overprotective mother
● Financial
● Social support, help groups
● Psy Hx: coping with dz

PHYSICAL EXAMINATION
Growth charts / Ht Wt T BP HR
ᕯ Inspection:
● Facial, periorbital edema
● Etiology: Look for HSP signs like purpuric rash in lower limb. Look for malar rash of SLE.
● Cushingoid appearance (Cx of tx)
○ Facial acne
○ Eyes: cataract, glaucoma
● Signs of CKD
ᕯ Lungs for pleural effusion
ᕯ Abdomen: distension, striae, scars from renal bx, ascits, pain (SBP), sacral edema, scrotal edema
ᕯ Inspecting limbs for equal movement, no pronator drift from strokes
ᕯ Limbs: edema, proximal myopathy, purpura (HSP) ᕯ Calves supple, no DVT

INVESTIGATIONS
● Urine dipstick/UFEME: protein more than 3+
● Early morning UPCR >300mg/mmol or 24 hour UTP >3.5g/day (or >50mg/kg/day)
● LFT: Albumin <30
● Lipid panel: high TC, TG, total lipid
● UECr (less likely to have renal impairment in nephrotic syndrome), BUN
● C3
● Hepatitis B, C (tro GN), ANA (if ≥10yo or signs of SLE)
● FBC (Hb should be normal)
● Renal biopsy for children ≥12yo

MANAGEMENT
1. Newly diagnosed possible nephrotic syndrome
ᐉ Disposition: If stable, probably direct access to paediatrics
ᐉ Management
● Non-drug:
○ Diet: Low salt diet if edematous. No fluid restriction. No evidence for high protein diet.
○ Activity: No activity restriction. Avoid crowded places to prevent infection.
○ Vaccinations: No live vaccinations ie VZV, MMR, Oral polio, BCG. Give pneumococcal
vaccination.
● Drug: Explain paediatrics will probably start high dose oral steroids if minimal change disease.
○ Acute tx inpatient may include diuretics with albumin for gross oedema
○ Mainstay = Prednisolone (eg start with 60mg/kg/m2/day [max 80mg] x 4/52)
○ KIV cytotoxic drugs if unacceptable steroid toxicity, steroid resistant, steroid dependent
ᐉ Educate: Follow-up with weight and urine protein. Educate to look out for symptom of relapse and
complications like fever, severe abdominal pain, dizziness.
ᐉ Prognosis:
● Good prognosis in minimal change dz
● Recurrence: ⅓ will not recur, ⅓ will recur infrequently, ⅓ will recur frequently
ᐉ Complications

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 ● Infxn: cellulitis, peritonitis (2’ urinary loss of Ig, loss of factor B, loss of transferrin, T cell abn, steroid
therapy, immunosupp drugs)
● Thromboembolism: a/w hypercoagulability (2’ increased plasma fibrinogen, clotting factors V, VIII,
urinary loss of anti-thrombin III)
● HypoCa and bone demineralisation: loss of vit D-binding ptn in urine
● -ve nitrogen balance: loss of ptn in urine, poor intake (fr n, LOA)

2. Fitness to travel eg to India

● PMHX impt: steroid sensitive / dependent / resistant
● If currently symptomatic → cannot travel due to high risk of thrombosis
● Check whether parent / pt knows what to do in event of relapse. Educate on what to do
● Bring adequate medications
● Red flag advice: As pts on steroids are immunocompromised, if develop fever → to seek medical
attention immediately, avoid crowded places
● Standby letter stating his condition
● Advise to avoid live vaccines while on Prednisolone

3. Fitness to travel / mountain climbing

● As above
● Food: need to bring water purifier tablets
● No CI to acetazolamide
● Vaccination Hx: check whether pt had chickenpox before /varicella vaccination prior to onset of
nephrotic syndrome.
● If pt develops chickenpox and on Prednisolone → half the dose of prednisolone and start PO
acyclovir or PO valacyclovir (better)
● If pt develops chickenpox and on immunosuppressants → refer for IV acyclovir , specialist may stop
the immunosuppressants to allow pt to recover from chicken pox and prevent disseminated infx

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PAEDS RENAL 2: NOCTURNAL ENURESIS

Stem:
1. Not achieving urinary continence by 5 years of age
2. Started bedwetting again after achieving continence

DIFFERENTIAL DIAGNOSES
Commonly classified into monosymptomatic (aka no other symptoms besides incontinence), non
monosymptomatic, and complex enuresis (which means child has daytime incontinence as well).
Primary (no organic pathology) Secondary
Primary enuresis ● UTI
(Never achieved continence by 5 yo) ● Constipation
- Fluid intake ● Diabetes mellitus
● Spinal pathology
Secondary enuresis
● OSA
(Achieved continence for 6 months then wet)
- Recent stressful events

HISTORY
Complaint: Nocturnal incontinence
- Monosymptomatic vs non monosymptomatic ! -> any daytime incontinence
- Onset: Never achieved continence before vs achieved for more than 6 months before
- Precipitating events: Stressful events such as parental divorce
- Severity of episodes: ___x/week
- Does patient have voiding diary? (If following up and told to fill up)

Causes
- Drinking habits (drinking more in late afternoon/evening, what kind of drinks ie sugar drinks)
- Family history of nocturnal enuresis
- Dysuria/frequency of urine/daytime symptoms/foul-smelling urine
- Weak stream, straining on PU
- Polydipsia and polyuria, family history of diabetes
- Stooling pattern:
- History of spinal pathology? Lower limb weakness and back pain?

Course
- What has family tried?

Complications
- Affecting school? Self esteem?

Med Hx: DM
Drug: Diuretics
Birth Hx: Spina bifida
Development history! Ensure not delayed in other domains

PHYSICAL EXAMINATION
Growth centiles: Height and weight
Temperature (UTI)
BP (HTN signifies possible kidney disease)

Oral cavity: Adenotonsillar hypertrophy → OSA

Abdomen: Palpable bladder. Palpable stools?
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Genitalia: Phimosis, discharge
Back: Look for tuft of hair, sacral dimpling
Gait / Screen lower limb strength

INVESTIGATION
UFEME and urine dipstick (including specific gravity)

Depending on scenario:
- AXR if suspecting constipation
- XR LS spine if suspecting spinal pathology

MANAGEMENT
1) Primary enuresis Non-pharm
(no organic pathology) ● Timed daytime voiding. Void before bedtime
● Avoid high sugar, caffeinated beverages.
● Drink 80% of total daily fluid by 5pm. 20% after 5pm.
● Motivation chart (a sticker on calendar for each dry night achieved,
a book for 7 consecutive nights free of bedwetting). Penalty is
counter productive!
● Bed alarm (a special moisture sensor placed in the child's pajamas
triggers a bell or buzzer to go off at the start of urination. The alarm
is designed to awaken the child so he or she can get to the toilet and
finish urinating)
Pharm: If deemed necessary (failed conservative tx), can explain that
paediatrician may initiate desmopressin
Educate
● Reinforce that bedwetting is not the child nor the parent’s fault
● Explain that it is common (15% of children do not achieve continence
by 5 years old) and majority will resolve on its own
● Ways to reduce impact:
○ Room deodorizer
○ Using disposable bedsheets

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PAEDS RENAL 3: UTI IN CHILDREN

Clinical Presentation
- Lower UTI: Frequency, cloudy or foul-smelling urine, dysuria, suprapubic pain
- Upper UTI: As above, plus fever, loin pain, vomiting and constitutional symptoms

HISTORY
Complaint (as above)

Cause
● Hx of structural abnormalities: Complicated UTI
● Phimosis
● Constipation
● Poor perineal hygiene - wipe from back to front
● Holding of urine/ infrequent voiding
● Inadequate fluid intake
● Neuro symptoms

Course
● 1st episode or recurrent episode
● Seen any doctors
● Tried any treatment

Complications
● Toxic → not tolerating well orally, poor activity, poor urine output

PMH
● VUR?

Birth Hx / Developmental / Immunisation / Family hx / Social Hx

PHYSICAL EXAMINATION
T BP HR
Hydration status
Abdomen: Suprapubic or renal tenderness. Ballotable kidneys?
Genital: Phimosis in boys / labial adhesions in girls

INVESTIGATIONS
● UFEME
○ KIV urine culture (but should be sterile culture from in out catheterisation)
● FBC if febrile

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MANAGEMENT
Disposition

● Refer to ED if upper tract infection + < 3months OR upper tract ≥3 months + toxic
● Indication to refer renal medicine SOC for workup:
■ Under 6 months old with lower UTI
■ Febrile UTI regardless of age
■ Recurrent UTI (defined as 3 or more episodes of lower UTI, 2 or more episodes of
pyelonephritis, 1 episode of pyelonephritis and at least 1 episode of lower UTI)
○ Ultrasound kidneys will be done → KIV DMSA, MCUG, MAG3
● Review in 3 days’ time for review of symptoms

Non-pharm
● Perineum hygiene: Wipe front to back. Keep perineum dry. Cotton underwear.
● Timed voiding
● Treat constipation
○ KIV Lactulose 0.5mg/kg Q12-24H
○ Positive reinforcement strategies, reward system
○ Adequate hydration and fibers (prune, pear, apple juice)
● If tight foreskin:
- 1% hydrocortisone cream applied once daily after bath with gentle pressure, for 3 to 4
weeks for tight foreskin.
- The prepuce should be retractable after 4 to 6 weeks.
- Do not forcefully retract as this will irritate the foreskin.
- Do not use steroids for more than 3 months, as this may predispose lichen chronicus et
atrophy.

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Pharm
● If unable to tolerate orally or unwell → ED for IV abx
● If able to tolerate orally and well → oral antibiotics

For upper tract infection: Empirical ABx (1 week)

- PO Cephalexin 50mg/kg/day divided into 8hourly dose or
- PO Augmentin 50mg/kg/day divided in 12hourly dose

For lower tract infection: Empirical ABx (<12 yrs: 7-10 days, ≥12 yrs: 3 days)
- PO cephalexin (G6PD deficient patients)
- PO bactrim

Education: Red flags advice if unwell, cannot tolerate orally etc to seek medical attention

Follow-up: TCU 2 days to review pt and urine c/s especially if febrile and review abx sensitivity.

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UTI in child with known vesico-ureteric reflux (VUR)
[Link]

HISTORY
Complaints: UTI symptoms
Cause: Vesico-ureteric reflux -- Grade __?

Course: Who is following up? What investigations? Previous urine culture results and abx? Current
treatment?
Control: How many UTI this year?
Compliance
● Non pharm: Practising timed voiding? Avoiding constipation? Perineum hygiene?
● Pharm: If on prophylactic abx usually bactrim or nitrofurantoin (especially Grade 3 and above), is
patient compliant?
Complications
● Of disease: Evidence of renal failure like HTN, proteinuria
● Of treatment: Side effects of antibiotics like diarrhoea, rashes, nausea/vomitting?
Co-morbidities

PHYSICAL EXAMINATION
T BP HR
Growth chart -- plot height and weight centiles
Abdo exam: Tenderness. Renal punch

INVESTIGATIONS
● Urine culture is mandatory

MANAGEMENT
● If breakthrough UTI occurs while on antibiotics prophylaxis

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PAEDS RESPI 1. WHEEZING IN CHILDREN

Common scenarios
- Under 5 years with recurrent wheeze with strong atopy RF
- More than 5 years old with recurrent wheeze
- Wheezing after feeding

Most Dangerous / Common:

Anaphylaxis
Foreign Body
Recurrent Viral Infections – Bronchiolitis, bronchitis
Asthma
GERD
Tracheomalacia/ Bronchopulmonary dysplasia
Congenital Heart Dz

Approach to Wheeze

Respiratory CVM GI Others

Cardiac
Intrinsic Extrinsic wheeze/Congenital Heart GERD Vocal cord dysfunction
Dz

Acute Chronic Mediastinal mass

Anaphylaxis Asthma

Chronic
Foreign Body obstruction
Rhinosinusitis/PND

Viral induced wheeze - Tracheomalacia

Bronchitis
Bronchiolitis

Bronchopulmonary
Foreign Body
dysplasia

Immunodeficiency

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HISTORY
Complaint: Wheezing
● Confirm wheezing
● Onset: From birth (congenital), Acute (Anaphylaxis/FB/ infection), Chronic,
● Recurrent wheezing under what circumstances
● Character – Persistent (congenital), Episodic / worse at night or early morning (asthma)
● Exacerbating / Relieving factor
● NIE ---- distinguishes frequent viral induced bronchitis from asthma (nocturnal, interval
symptoms, exercise induced symptoms)

Course
● No of episodes, Required hospitalisations/ intubations, Ix done, Mx so far , F/up where
● Response to salbutamol

Cause
● Eye swelling, Rashes → Anaphylaxis
● Foreign body aspiration, choking → FB
● URTI symptoms, fever, no symptoms in betw infection → Viral induced wheeze
● Blocked / Runny nose / Facial tenderness → Chronic Rhinosinusitis
● Cough, Diurnal variation – worse in the morning / night, Occurs with exercise/laughing/ crying in
absence of respiratory infection/ smoke/pollutants, Triggers, Atopy, Fam Hx of atopy , good
response to ICS and PRN SABA, Reduced activity → Asthma

● Prematurity, occurs since birth → Tracheomalacia, BPD

● Noisy breathing when eating or crying , Worsens or improves with change in position →
Tracheomalacia
● Cough when feeding, vomits after feeds → GERD
● Hx of Congenital Heart Dz
● Recurrent fever and infection → Immunodeficiency / ciliary dysfunction
● LOW / Poor growth/ Lymphadenopathy → Tumour / Mediastinal masses

Personal Hx: Hx of congenital heart dz, multiple respiratory illness

Drug Hx:
Family Hx : Atopy
Developmental Hx: Is growth affected
Birth Hx: Prematurity, Low BW, Required mechanical ventilation postnatally → BPD
Antenatal /Immunisation

Social Hx: Any triggers for asthma

Psych Hx:

PHYSICAL EXAMINATION
Temp BP HR RR SPO2 Growth percentiles
● Inspection: Respiratory distress: Tachypnea, retractions, use of accessory muscles, pursed-lip
breathing, cyanosis, stridorous in FB aspiration
● Structural abnormalities: Increased anteroposterior (AP) diameter associated with chronic
hyperinflation, pectus excavatum, scoliosis complicated by airway compression.
● Atopic features: red, watery eyes, allergic shiners
● Neck: JVP raised in CCF, cervical LN
● Pale and swollen nasal turbinates in AR
● Lung exam: Tracheal deviation, Auscultation (focal wheeze or generalised)
● Heart: any S3, Murmurs
● Pedal edema
● Skin for eczema

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INVESTIGATIONS
● CXR TRO FB, Tuberculosis, structural abnormalities ie vascular rings
● Pulmonary function test for age ≥5 years old
● Methacholine challenge testing and exercise testing ≥5 years old can confirm airway hyperreactivity in
patients for whom the diagnosis of asthma still is in question despite doing spirometry
● Skin prick test for atopy
● FBC: for pts with chronic or systemic symptoms and may reveal anemia, leukocytosis, or
leukopenia. Eosinophilia supports an underlying allergic process or parasitic infection.
● 24-hour esophageal pH monitoring is suggested in infants and children with recurrent wheezing, particularly in children
<2 years of age with recurrent wheezing who are unresponsive to bronchodilators or inhaled or systemic glucocorticoids
Trial of treatment for at least 2 weeks with as needed SABA and regular low dose ICS (useful for <5 years
old >5 years old) . Response should be evaluated by symptom control (day & night time) and frequency of
wheezing and exacrbations. Marked clinical improvement during tx and deterioriation when tx is stopped
support a diagnosis of asthma

A positive response to empiric therapy (acid suppression) may be used to support a presumed diagnosis of
GERD

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400
For asthma in patients age 6 years and above

401
402
RESPI 2. PAEDS ASTHMA

HISTORY
Complaint: Wheezing, coughing, shortness of breath.
Course: How was diagnosis made? Previous hospitalizations? Previous ICU stay or intubation?
Control:
● Patient based: ACT <20 not good
● Clinic assessment based on GINA 2018: Well controlled, partly controlled, uncontrolled

Compliance
● Non pharm
○ Allergen avoidance: Dust mites? Animal danders?
○ Irritant avoidance: Smoking? Passive smoking?
● Pharm
○ Inhaler compliance
Competency
● Inhaler and spacer competency
Complications
● Of disease: School missed?
● Of treatment: Cushing? Growth affected?
Crisis management
● WAAP?
Co-morbidities
● Allergic rhinitis, eczema

Disease Prevention: Flu and pneumococcal vaccines? Annual influenza vaccine recommended. If never
received pneumococci before recommended for children if asthma requires chronic oral glucocorticoid.

Psychological

PHYSICAL EXAMINATION
T BP HR RR SpO2: Must keep >95% on room air
Growth centiles to plot
General inspection
● Respi status, respi effort, cyanosis
● Cushingnoid features – Cx of treatment
● Associated atopy: allergic shiners, atopic features
Nasal turbinates
Mouth: thrush?
Respiratory exam: Hyperinflated lungs? Rhonchi?

INVESTIGATIONS
- Usually not needed
- Spiro
● FEV1/FVC reduced at least once (children normal 0.90)

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 ● Post bronchodilator FEV1 increases by ≥12% AND
○ FEV1 / FVC increase by 200ml = bronchodilator reversibility

MANAGEMENT
- Non-pharm
● Allergen avoidance
○ House dust mites
■ Wash linen in hot water >60oC
■ Keep room well-ventilated
○ Cigarette smoke
■ Strongly discourage household smoking
● Passive smoking is bad
● Poor role-model to impressionable child
○ Avoid soft toys, fur and feathered pets at home
- Pharm (Maintain 3 months good control before stepping down. Step down by first removing add on
therapy, then halving steroids, before eventually stopping)

Follow Beclometasone dipropionate (HFA) - in polyclinic

404
- Education on WAAP

405
 - Follow-up
- After acute exacerbations: 2 weeks
- Otherwise if stable, see every 3 months

Asthma Predictive Index eg children <5yo

Asthma Predictive Index

Strict Criteria:
● ≥3 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria
Loose Criteria:
● <3 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria
Results:
● 59% of children with a positive loose index had active asthma at school age (defined at 15 years).
● 76% of those with a positive strict index had active asthma at school age (defined at 15 years).

Modified API
Positive mAPI defined by:
● ≥4 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria

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PAEDS GENERAL 1. APPROACH TO DEVELOPMENTAL DELAY

Possible cases
1. Parental concern about speech delay
2. Parental concern about behavior in school or social functioning.
3. Parental concern about possible autism

Definitions:
● 4 domains: Gross motor, fine motor, speech (receptive and expressive) and hearing, social
● Typical milestone charts plot 50 centile, red flags refer to when 90% of child acquires the skill.
● Isolated vs global developmental delay

Ddx
Language delay Social delay

● Primary (not due to another medical

condition): Hearing impairment, lack of
stimulation, Expressive language disorder.
Receptive language disorder
● Secondary
○ Autism
○ Cerebral palsy (spastic tongue)
○ Intellectual disability
○ Dysarthria

HISTORY
Complaint: Language delay Complaint: Social skill delay
- Expressive: How many words? Phrases?
Sentences?
- Receptive: Able to obey commands?
- Duration.
- Any regression of previously learnt skills

Causes
- Associated social skill problems.
Stereotyped behaviors.
Course

Complications

Complaint: Social or language delay.

Developmental History
– Any regression in milestones
- Any prolonged screen-time resulting in inadequate stimulation

Gross Motor

Fine Motor/Vision

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 Hearing/ Speech/ Language (Expressive and Receptive)
- Was his hearing screen normal? Hx of recurrent otitis media with effusion
- Does he let you know what he wants or needs? Does he points at objects or use gestures
- Language may be characterized by abnormal tone and prosody (pitch, intonation, stress, and rhythm used
in speech “echolalia” (repeating or “echoing” words for phrases), or “scripting” (e.g., repeating lines from a
favorite TV show).

Personal/ Social
- Does he have joint attention
- Does he make eye contact
- Does he play with other children in school?
- Does he smile at other people or share an object with someone (a lack of “shared affect” e.g., through a
smile) and “showing” behaviours (bringing an object over to another to share their interest in it with them).

- Does he have repetitive unusual behaviour such as hand-flapping, rocking, spinning

- Does he keep playing the same things such as lining toys up or spinning or mouthing objects.
- Does he adhere to strict routines in their daily lives and will often have a tantrum when the routine is
disrupted.
- Any preoccupation and attachment with atypical objects, such as a piece of paper or string
- Any hypersensitivity to sounds or fascination with lights

Behavioural History
- Any behavioural problems ie hyperactive , doesn’t follow instructions, throw tantrums that involve
injurious behavior

Birth History
– Any prematurity -> GDD

Family Hx of Autism

Social Hx
– Who is the main caregiver, language used at home. First child? Any family stressor

PHYSICAL EXAMINATION
- Growth percentiles including OFC and plot it on growth chart
- Any dysmorphic features
- Any neurocutaneous signs
- Social interaction, Any eye contact, Responds to name, Joint attention
- Play skills
- Use of language
- Presence of atypical behavior/ stereotype

- Hydration normal
- Red reflexes normal PEARL, full EOM
- Ears normal: nil effusion, TM normal (IMPT)
- Heart and lung normal
- Abdomen – no organomegaly, umbilicus normal
- Can walk steadily

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MANAGEMENT
Domains affected Management

Gross motor

Fine motor

Speech delay - Rule out hearing loss

- Refer to Paeds ENT for hearing assessment
- Reduce Screen time
- Encourage more exposure to reading
- Refer to Child Development Unit

Social skills

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PAEDS GENERAL 2. AUTISM
M-CHAT

AUTISTIC mnemonic for DSM V criteria

Abnormal social-emotional reciprocity “Do you or other people find it hard to have a conversation
with your child?
Does the child understand when you tell him or her to do
something?
Understanding nonverbal cues Do you find that your child has difficulty understanding
gestures. For eg, If you point at an object across the room,
does he look at it?
When you smile at your child, does he smile back
Turning acquaintances into friends Does your child play with other children
Insistence on sameness Does he have to keep to the same routine everyday ie take

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 the same route or eat the same food
Does he have difficulties with changes
Stereotypical movements/ use of obj or Does he keep doing the same movements ie lining up toys,
speech (orderly, echolalia) spinning toys, echolalia
Trains (fixated interest) Pre-occupation with an object
Increased/Decreased sensitivity to noises Does your child get upset by everyday noises
Child

DSM 5: Autism Spectrum Disorder

A. Persistent deficits in social communication and social interaction across multiple contexts, demonstrated by
deficits in all 3 of the following
1. Deficits in social-emotional reciprocity, ranging, for example, from abnormal social approach and failure of
normal back-and-forth conversation; to reduced sharing of interests, emotions, or affect; to failure to initiate or
respond to social interactions.
2. Deficits in nonverbal communicative behaviors used for social interaction, ranging, for example, from poorly
integrated verbal and nonverbal communication; to abnormalities in eye contact and body language or deficits in
understanding and use of gestures; to a total lack of facial expressions and nonverbal communication.
3. Deficits in developing, maintaining, and understanding relationships, ranging, for example, from difficulties
adjusting behavior to suit various social contexts; to difficulties in sharing imaginative play or in making friends; to
absence of interest in peers.
Specify current severity: based on social communication impairments and restricted repetitive patterns of behavior
B. Restricted, repetitive patterns of behavior, interests, or activities, at least 2 of the following
1. Stereotyped or repetitive motor movements, use of objects, or speech (e.g., simple motor stereotypies, lining
up toys or flipping objects, echolalia, idiosyncratic phrases).
2. Insistence on sameness, inflexible adherence to routines, or ritualized patterns or verbal nonverbal behavior
(e.g., extreme distress at small changes, difficulties with transitions, rigid thinking patterns, greeting rituals, need
to take same route or eat food every day).
3. Highly restricted, fixated interests that are abnormal in intensity or focus (e.g, strong attachment to or
preoccupation with unusual objects, excessively circumscribed or perseverative interest).
4. Hyper- or hyporeactivity to sensory input or unusual interests in sensory aspects of the environment (e.g.,
apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or
touching of objects, visual fascination with lights or movement).
Specify current severity:based on social communication impairments and restricted, repetitive patterns of behavior
C. Symptoms must be present in the early developmental period(but may not become fully manifest until social
demands exceed limited capacities, or may be masked by learned strategies in later life).
D. Symptoms cause clinically significant impairment in social, occupational, or other important areas of current
functioning.
E. These disturbances are not better explained by intellectual disability (intellectual developmental disorder) or
global developmental [Link] disability and autism spectrum disorder frequently co-occur; to make
comorbid diagnoses of autism spectrum disorder and intellectual disability, social communication should be below
that expected for general developmental level.
Note: Individuals with a well-established DSM-IV diagnosis of autistic disorder, Asperger’s disorder, or pervasive
developmental disorder not otherwise specified should be given the diagnosis of autism spectrum disorder.
Individuals who have marked deficits in social communication, but whose symptoms do not otherwise meet criteria
for autism spectrum disorder, should be evaluated for social (pragmatic) communication disorder.
Specify if:
With or without accompanying intellectual impairment
With or without accompanying language impairment
Associated with a known medical or genetic condition or environmental factor
With catatonia

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PSYCHIATRY 1. ATTENTION DEFICIT HYPERACTIVITY DISORDER

Stem
1. Parents receiving feedback about child not following class rules, or disruptive behavior in school.

DETAILS OFF
Details: fails to give close attention to details
Easily distracted
Task Avoidance
Instructions not followed
Loses things
Sustaining attention
Organising tasks and activities
Forgetful in daily activities
Fails to finish tasks, chores, duties

RAPID GIRL
Runs about or climbs excessively
Answers blurted out before questions completed
Plenty of talk
Interrupts others
Difficulty awaiting turn
Go: always on the go
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Impatient
Restless
Loud or noisy during quiet activities

HISTORY
Complaint: DETAILS OFF and RAPID GIRL
- Onset, course, and functional impact of ADHD symptoms
Occur often
●Be present in more than one setting (eg, school and home)
●Persist for at least six months
●Be present before the age of 12 years
●Impair function in academic, social, or occupational activities
●Be excessive for the developmental level of the child

Cause:
- Rule out differentials:
- Hearing and Visual impairment
- Learning disabilities, Language or communication disorders
- Autism spectrum disorders (ASD)
- Medical disorders:
CNS : Seizure, Head trauma
Endocrine: Hyperthyroidism
Sleep disorders: ie obstructive sleep apnea, restless leg/periodic limb movement disorder
Medication : salbutamol, substance abuse disorders

Complications:
- Impairment in School work and Home
- Injuries

Co-morbids./ Psychological :
- Emotional and behavioral disorders – Anxiety disorder, mood disorders, oppositional defiant disorder,
conduct disorder, obsessive-compulsive disorder, posttraumatic stress disorder, and adjustment disorder.

Birth Hx:
Prenatal exposures (eg, tobacco, drugs, alcohol)
Perinatal CNS infection, head trauma, recurrent otitis media, and medications

Family hx: ADHD

Developmental milestones esp language milestones

Environmental factors:
- High frequency digital media use
- Inappropriate educational setting
- Stressful home environment
- Parent-child temperament or "personality" mismatch and parental mental health conditions

Social
- School absences/ grades
- Relationships

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Diet:
- Avoid high sugar food
- Reduce screen time
- Avoid stimulants

AUTISTIC mnemonic for DSM V criteria

Abnormal social-emotional reciprocity Do you or other people find it hard to have a conversation
with your child?
Does the child understand when you tell him or her to do
something?
Understanding nonverbal cues Do you find that your child has difficulty understanding
gestures. For eg, If you point at an object across the room,
does he look at it?
When you smile at your child, does he smile back
Turning acquaintances into friends Does your child play with other children
Insistence on sameness Does he have to keep to the same routine everyday ie take
the same route or eat the same food
Does he have difficulties with changes
Stereotypical movements / use of obj or Does he keep doing the same movements ie lining up toys,
speech (orderly, echolalia) spinning toys, echolalia
Trains (fixated interest) Pre-occupation with an object
Increased/Decreased sensitivity to noises Does your child get upset by everyday noises
Child

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PSYCHIATRY 2. ANOREXIA

Stem
1. Brought in by parent due to concern about weight loss and restricted eating behavior.

Differential diagnoses
Primary Secondary
● Anorexia nervosa Rule out other causes of weight loss:
○ Restrictive - DM, hyperthyroidism
○ Purging aka bulimia nervosa - Malabsorption, inflammatory bowel disease
● Female athlete triad - Malignancy
○ Amenorrhea
○ Osteoporosis
○ Disordered eating

HISTORY
Complaint: Weight loss and restricted eating
- Onset
- Duration
- Triggers?
- Characterize: Restrictive eating? Binge eating with subsequent purging?
- Severity: Amount of weight loss?/ BMI
- Any vigorous physical activity?
- If amenorrhoea → Ask about sexual hx and KIV other causes of amenorrhoea

Causes
- DSM 5 criteria for anorexia nervosa: Low weight in relation to age/gender, intense fear of gaining
weight despite being underweight, distorted perception of body shape/weight with undue
influence on self worth. Any precipitating events like unkind comments? (SCOFF question; 2 or
more is positive)

S - Sick | C - Control | O - Lost 6.35kg in 3/12 | F - Fat | F - Food

- Polydipsia, polyuria
- Heat intolerance, tremors, palpitations, neck swelling
- Steatorrhoea, loose stools, bloody diarrhoea
- Fhx of malignancy, lymph node swelling, prolonged fever, LOA

Course
- What have parents tried?

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Complications
- CVS: Bradycardia, hypotension or postural drop. Arrhythmia
- Metabolic: Electrolyte imbalance Risk of refeeding syndrome
- OG: Amenorrhoea/oligomenorrhoea
- Osteoporosis/ fractures
- Derm: Hair loss, dry skin

PMH:
DA
Drugs: OTC/TCM, tried weight loss pills?
Birth Hx
Immunization Hx
Development Hx

Psychiatric: PHQ2. GAD2

Social: HEADSSS assessment: home environment, education, activities, drugs, sex, suicide, sleep

PHYSICAL EXAMINATION
T BP HR (bradycardia) ** postural drop (SBP>20, DBP>10 or HR >20 change)
BMI (plot and compare centiles) BMI classify severity → 17, 16, 15, below 15
Cardiovascular: May have mitral valve prolapse, pitting oedema (hypoalbuminemia)
Skin exam: Brittle hair and nails, dry skin

INVESTIGATIONS
- UPT may be needed if amenorrhoea
- ECG (look for bradycardia, prolonged QTc)
- Renal panel
- LFT with albumin
- Calcium, Mg, Phosphate
- Bone mineral density if amenorrhoea >9 months

MANAGEMENT
● Disposition: ED for hospitalization vs outpatient anorexia clinic direct access
● Non-drug:
○ Weight gain goal: 90% of weight expected for an average person matched to age and
gender
○ Strenuous physical activity should be restricted
○ Psychologist for psychotherapy. Family based therapy, group based therapy.

416
 ○ Dietician: Daily menus should include three full meals and a structured snack schedule that
is monitored by parents or the school nurse. A multivitamin plus vitamin D and calcium
supplements are recommended.
● Drug: +/- SSRI helps with comorbid depression but not weight gain. Some case report suggests
benefit with olanzapine.
● Education
● Follow-up: Monitor progress based on weight gain, resumption of menses

Questions to ask about AN :

Can you take me through your diet habit on a typical day and how often do you exercise?
What is your current weight and weight over the past 2 years?
Are you worried about gaining weight or being fat?
Your BMI is only 10, what do you feel about it ?
How do you feel when you look into the mirror

Avoidance of food vs binge eating and purging

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PSYCHIATRY 3. APPROACH TO ANXIETY/WORRY

Differential Diagnoses
Psychiatry ● GAD
● Panic disorder
● Adjustment disorder
● Agoraphobia
● Social anxiety disorder
● OCD
● PTSD

Organic

Cardio ● Arrhythmia
● Angina

Respi ● Pulmonary Embolism

● COPD/ Asthma

Endocrine ● Hyperthyroidism
● Pheochromocytoma
● Hypoglycemia

Neuro ● Stroke

Drugs/withdrawals ● Caffeine, alcohol withdrawals

● Salbutamol, thyroxine, decongestants

Name/Age/Sex

BIOLOGICAL

Acute Chronic Medical

illness History

Complaint: Anxiety Cause ● Medical/

● Onset: Abrupt onset peaking in 10 minutes → PD , constant Course Surgical Hx
floating → GAD Control - Thyroid
● Duration: At least 6 months → For GAD Compliance disorders,
● Precipitating events? Cx CVRF
○ Identifiable stressor (new environment/job/loss of loved Checking ● Psychiatric
ones) within last 3 months that triggered anxiety → Competency disorders
adjustment disorder
○ Various domains (e.g. home, work, interpersonal, health) Comorbids ● Drug Hx/
→ GAD Crisis Mx Drug
○ Unexpected → Panic attack/disorder allergies
● Severity: Affecting function/QoL - See above
● TRO concomitant panic disorder, agoraphobia if panic, social
anxiety disorder, substance abuse disorder, depression, psychosis, ● Medication
PTSD, List
○ **Panic attack vs panic disorder** ● TCM/OTC

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 Cause (associated symptoms)
● GAD DSM criteria (3 of 6 other symptoms; ANDICREST)
● PD DSM criteria (4 or more of symptoms) with accompanying
maladaptive behavior for at least 1 month after panic attack to
avoid or excessive worry about getting future episodes
● Agoraphobia: Do you fear being in a crowded place / public
transport whereby you can’t escape in event of a panic attack ?
● Social phobia: Do you worry about social situations where you are
the focus of attention
● Caffeinated drinks? Thyroxine pills? Ventolin inhalers? Heavy
alcohol use?
● Weight loss, tremors, diarrhoea, neck swelling → Hyperthyroid
● Headache, sweating, tachycardia → Pheochromocytoma
● If panic attacks: ask for differentials for each presenting symptom
ie chest pain worse on exertion/ diaphoresis/syncope, CVRF,
haemoptysis, LL swelling / recent immobilization/ wheeze, GI
bleed, one sided weakness/numbness

Course
● Previous treatments?
● Seen other doctors for it?

Complications
● **FUNCTION
○ Sleep, mood
○ Interpersonal relationship

Disease Prevention Family Hx

- Vaccinations Psychiatric
- Cancer prevention: disorders

PSYCHOLOGICAL

PHQ-2 (screen for comorbid depression) I

GAD-2 C: Affecting
work/life?
E

SOCIAL

Home/Environment – triggers?
Employment: Is work affected?
Activities: Hobbies?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sex and r/s with others?
Sleep

PHYSICAL EXAMINATION ***HAND RUB***

T BP HR KIV SpO2
● Mental State Exam

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 ● CVS: Examine pulse
● Thyroid exam

INVESTIGATIONS
● FBC, BSL, ECG, TFT

MANAGEMENT Of GAD, panic disorder (± agoraphobia)

Non-pharmacological
● Avoid triggers: Caffeine, stress, smoking, alcohol, stimulant drugs
● Promote exercise (exercise at 60-90% of maximal heart rate for 20 minutes 3x/week), yoga
● Improving sleep quantity and quality: Sleep hygiene advice
● Stress reduction strategies
○ Deal with negative thoughts
○ Diaphragmatic breathing
○ Progressive muscle relaxation
● CBT
● Involve family members, community/social resources

Pharmacological
● 1st line: SSRI
○ Eg Fluoxetine 20mg OM, Fluvoxamine 50mg ON, Paroxetine, Sertraline, Escitalopram 5mg
OM
○ Initiation: Titrate upwards slowly. Should not consider ineffective till titrated to higher end
of dose and maintained for at least 4 weeks
○ Duration of tx: At least 12 months before tapering downwards
○ ADRs: GI (Nausea, constipation), Weight gain, sexual dysfunction, Headache, nervousness,
insomnia (fluoxetine) , SIADH/hypoNa
○ Caution in: elderly, renal/hepatic impairment, pregnancy
● MINIMIZE BZD (technically can use benzodiazepine to tide over crisis, but long term use can result
in dependence. If needed long term, consider intermediate to long acting BZD like clonazepam.)

Follow-up
● 1-2 weekly for first 2-3 sessions → monthly to 2 monthly
● Acute treatment: 8-12/52
● Maintenance: 6-12/12 symptom-free

Deep Breathing Exercises

- Breathing exercises can help you to feel more relaxed. They should be done twice a day or
whenever you find your mind dwelling on upsetting thoughts or when you are experiencing pain.
- Place one hand on your chest and one hand on your tummy
- Take a slow deep breath in through your nose , feel your tummy moving outwards, and hold it for
a count of 7 (or as long as you are able)
- Slowly exhale through your mouth for a count of 8, feel your tummy moving inwards
- Repeat the cycle four more times for a total of 5 deep breaths

Progressive Muscle Relaxation

- Systematically tense different muscle groups in your body. Next, you release the tension and notice
how your muscles feel when you relax them. Done twice a day
- Take a slow deep breath and squeeze your hand as hard as you can for 5 seconds
- Next, breathe out and relax your hand. Let all the tightness flow out of the tensed muscles
- Remain in this relaxed state for about 15 seconds, and then move on to the next muscle group and
complete all the muscle groups

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Panic Disorder - Panic attack - PANICS D (4 out of 13)
P – Palpitations
A – Abdominal distress – Nausea, diarrhoea, sick stomach
N – Numbness(parathesia)
I – Intense fear of death / losing control / going crazy
C – Chest tightness/ Choking / Chills
S – Shortness of breath / Sweating / Shaking
D – Dizziness / depersonalisation (feeling detached from oneself) / derealisation (feeling of not in reality)

421
PSYCHIATRY 4. APPROACH TO INSOMNIA

Differential Diagnoses
Psychiatry ● PRIMARY SLEEP DISORDER
● GAD
● Depression
● Adjustment disorder
● Panic disorder

Organic
Drugs/withdrawals ● Caffeine, alcohol withdrawals, pseudoephedrine
Endocrine ● Thyroid disorder
● Uncontrolled DM (osmotic symptoms with polyuria)
Cardio ● Arrhythmia
● CCF (PND, orthopnea)
Respi ● OSA
● Asthma
● COPD
GI ● GERD
GU ● BPH (causing frequent nocturia)
Others ● Menopause
● Chronic Pain

Name/Age/Sex

BIOLOGICAL

Acute Chronic Medical History

Complaint: Insomnia Course ● Medical/

Confirm the symptoms: Control Surgical Hx
● Open-ended question to confirm what patient mean by insomnia? Complianc ● Drug Hx/
Determine the chief sleep symptoms = difficulty in initiating sleep, e Drug
frequent awakening and un-refreshing sleep Cx allergies
● Onset Checking ● Medicatio
● Precipitating factors n List
● Duration (chronic if >3weeks) Comorbids ● TCM/OTC
● Frequency Crisis Mx
● Total hours of sleep
● Quality of sleep
● Have patient tried anything to improve the sleep?

Cause (Primary insomnia or Secondary insomnia?)

● Evaluate sleep hygiene – coffee, tea, excessive water intake before
sleep, prolonged daytime nap, prolonged screen time before sleep

422
 ● Are there any life events that have affected your sleep? (birth,
death, job changes, move, work stress, new bed partner, financial
stress)
● Medication (diuretic) and substance use history
● Collateral history from spouse for symptoms to OSA = snoring,
observed apnea, daytime somnolence
● Urine symptoms to rule out DM, BPH in male
● Unstable angina = nocturnal chest pain
● Poor controlled asthma/COPD, decompensated CCF = breathless,
orthopnea, PND
● Psychiatric disorder = assess mood, anhedonia, panic symptoms,
suicidal ideation ± symptoms for biologic causes

Course
● Medications tried
● Assess for addiction if patient was given benzodiazepines

Complications
● How bad the insomnia affecting the social, occupation function
and family?
● Impaired daytime function
○ Fatigue/malaise, poor attention/concentration, social or
vocational/educational dysfunction, mood
disturbance/irritability, daytime sleepiness, reduced
motivation or energy, increased errors or accidents,
behavioural problems, ongoing worry about sleep

Co-morbid
● Restless leg syndrome

Disease Prevention Family Hx

- Vaccinations NA
- Cancer prevention:

PSYCHOLOGICAL

PHQ-2 (screen for comorbid depression) / PHQ 9 I

GAD-2 / GAD 7 C: Affecting
work/life?
E

SOCIAL

Home/Environment – triggers?
Employment: Is work affected?
Activities: Hobbies?
Drugs (Smoking, alcohol, illicit drugs)
Suicide
Sex and r/s with others?
Sleep

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PHYSICAL EXAMINATION ***HAND RUB***
BP HR KIV SpO2 RR
Height Weight BMI
● Mental state exam: Anxious?
● Throat for hypertrophic tonsil, micrognathia if OSA
● Neck circumference if OSA
● Goitre
● Hands for tremor/ acropachy
● Heart and lungs + pitting edema if CCF, COPD
● Abdomen if urinary symptoms, offer DRE for BPH

INVESTIGATIONS
● TFT if panic disorder
● PHQ9 or GAD7 if psychiatric disorder
● Epworth sleepiness scale if OSA
● UFEME if LUTS
● Urine dipstick and BSL if DM
● CXR if suspect fluid overload

MANAGEMENT
Predisposed by… | Precipitated by… | Perpetuated by… |
Protected by…
1. Sleep hygiene advice
- No water after 6pm (if nocturia)
- No coffee/tea after lunch/caffeinated drinks (red bull, coke)
- PU before sleep
- No screens before sleep
- Regular exercise and avoid nap at daytime
- Consider sleeping earlier and waking up earlier to do work where necessary
- Adjust bed environment to reduce stimuli
- Bed only sleep and sexual intercourse
2. Counseling to stop smoking and alcohol
- Start exercising regularly but not in evening/before bedtime
- No alcohol near bedtime (late afternoon/evening)
3. Pharmacological
- Sedative antihistamines eg Hydroxyzine 10-25mg ON PRN, Chlorpheniramine 4mg ON PRN
- ± 5 days of benzodiazepines Lorazepam 0.5 mg- 1mg ON PRN or Zolpidem (WARN patient its not
for long-term usage) x 2-4 weeks THEN REVIEW
- Melatonin
- Sedating SSRIs (Fluvoxamine 25mg - 50mg ON, Trazodone), antipsychotics low dose, Gabapentin,
BZD, Z drugs
- Trazodone ADR: priapism
4. If OSA, lifestyle modification esp. weight reduction and exercise, refer for sleep study
5. Manage accordingly if underlying CCF, asthma, COPD, BPH, DM
6. If MDD/Panic disorder – non pharmacological and pharmacological
7. Consider psychologist
8. APPROPRIATE FOLLOW UP FOR ALL
9. SAFE NETTING FOR ALL

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PSYCHIATRY 5. APPROACH TO DEPRESSION
- Unipolar depression
- Bipolar depression
- Bipolar 1 (Got mania)
- Bipolar 2 (No mania, got depression and hypomania)
2 weeks duration!

425
Assessment of suicide risk
- Risk factors :
- Duration of suicidal feelings
- Previous suicide attempts , what are the triggers, what did the pt do (lethality and frequency)
- Assess current suicide intent, Any suicide plan (When,Where,How), Expectation of outcome of
suicide attempt
- Plans for other after death: suicide notes, changes to will, consequences

- Protective factors:
- Are there things in life that you look forward to
- Who are the people supporting you in this moment
- Religion
- How do you usually cope

426
427
PSYCHIATRY 6. SUMMARY OF COMMON PSYCHIATRIC CONDITIONS

1. GAD
2. MDD
3. Panic Disorder vs Panic Attack
4. Agoraphobia
5. Social Anxiety
6. Acute Stress Reaction, PTSD
7. OCD

3Ps Approach
Predisposing factors
Precipitating factors
Perpetuating factors

Mental State Exam – ASEPTIC

Appearance and behavior

Speech
Emotions (Affect and Mood)
Perception (Any hallucinations or illusions)
Thought content and process
Insight and judgment
Cognition (consider AMT)

GENERALISED ANXIETY DISORDER

● Treatment
○ 1st line = SSRIs
○ CBT

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PANIC DISORDER vs PANIC ATTACK
Panic ATTACK
● DSM V
○ An abrupt surge* of intense fear or intense discomfort that reaches a peak within minutes,
and during which time four or more of the following 13 symptoms occur:
■ Palpitations, pounding heart, or accelerated heart rate
■ Sweating
■ Trembling or shaking
■ Sensations of shortness of breath or smothering
■ Feelings of choking
■ Chest pain or discomfort
■ Nausea or abdominal distress
■ Feeling dizzy, unsteady, light-headed, or faint
■ Chills or heat sensations
■ Paresthesias (numbness or tingling sensations)
■ Derealization (feelings of unreality) or depersonalization (being detached from oneself)
■ Fear of losing control or "going crazy"
■ Fear of dying
○ * The abrupt surge can occur from a calm state or an anxious state.
○ Note: Culture-specific symptoms (eg, tinnitus, neck soreness, headache, uncontrollable
screaming or crying) may be seen. Such symptoms should not count as one of the four
required symptoms.
● Can occur with other disorders eg PTSD with panic attacks

Panic DISORDER
● Definition = recurrent, unexpected panic attacks along with one month of either worry about future
attacks or the consequences of attacks (eg, medical concerns), OR a significant change in behavior
due to the attacks (eg, phobic avoidance or repetitive seeking of medical evaluations).

Panic Disorder
● Panic attack - PANICS D (4 out of 13)
● P – Palpitations
● A – Abdominal distress – Nausea, diarrhoea, sick stomach
● N – Numbness(parathesia)
● I – Intense fear of death / losing control / going crazy
● C – Chest tightness/ Choking / Chills
● S – Shortness of breath / Sweating / Shaking
● D – Dizziness / depersonalisation (feeling detached from oneself) / derealisation (feeling of not in
reality)

● Management: a) psychotherapy vs b) medication

○ No evidence of robust differences in effectiveness between these modalities in panic
disorder
○ a) Psychotherapy
■ 1st line = CBT
■ Others: Diaphragmatic breathing (1 hand on chest, 1 hand on abdomen),
Progressive muscle relaxation
○ b) Medication
■ 1st line = SSRI
● 2nd line = SNRIs, TCAs, MAOIs, BZD
■ Time to onset of clinically meaningful action varies by pt but average 4/52
■ Eg Fluvoxamine 25mg ON x 1/52 → self uptitrate to 50mg ON x 1/52 → review 3-
4/52 after initiation
■ ADRs: initial agitation, GI, ED

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AGORAPHOBIA
DSM-5 criteria for agoraphobia are described below:
A. Marked fear or anxiety about two or more of the following situations:
1. Using public transportation (eg, automobiles, buses, trains)
2. Being in open spaces (eg, parking lots, marketplaces, bridges)
3. Being in enclosed places (eg, shops, theaters, cinemas)
4. Standing in line or being in a crowd
5. Being outside of the home alone
B. The individual fears or avoids these situations because of thoughts that escape might be difficult or help might
not be available in the event of developing panic-like symptoms or other incapacitating or embarrassing symptoms
(eg, fear of falling in the elderly or fear of incontinence).
C. The agoraphobic situations almost always provoke fear or anxiety.
D. The agoraphobic situations are actively avoided, require the presence of a companion, or are endured with
intense fear or anxiety.
E. The fear or anxiety is out of proportion to the actual danger posed by the agoraphobic situations and to the
sociocultural context.
F. The fear, anxiety, or avoidance is persistent, typically lasting for six months or more.
G. The fear, anxiety, or avoidance causes clinically significant distress or impairment in social, occupational, or other
important areas of functioning.
H. If another medical condition (eg, inflammatory bowel disease, Parkinson's disease) is present, the fear, anxiety,
or avoidance is clearly excessive.
I. The fear, anxiety, or avoidance is not better explained by the symptoms of another mental disorder and are not
related exclusively to:
● A specific situation, as in specific phobia, situational type
● Social situations, as in social anxiety disorder
● Obsessions, as in obsessive-compulsive disorder

430
 ● Perceived defects or flaws in physical appearance, as in body dysmorphic disorder
● Reminders of traumatic events, as in posttraumatic stress disorder
● Fear of separation, as in separation anxiety disorder
● Treatment
○ UTD: Based on current evidence, treatment of agoraphobia independent of panic disorder
should follow recommendations for agoraphobia in the context of panic disorder

SOCIAL ANXIETY

Last 6 months or more

Mx:
● SSRI, CBT

Acute Stress Disorder vs PTSD

Acute Stress Disorder
A. Exposure to actual or threatened death, serious injury, or sexual violation in one (or more) of the following ways:
1. Directly experiencing the traumatic event(s)
2. Witnessing, in person, the event(s) as it occurred to others
3. Learning that the event(s) occurred to a close family member or close friend
Note: In cases of actual or threatened death of a family member or friend, the event(s) must have been
violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (eg, first
responders collecting human remains, police officers repeatedly exposed to details of child abuse)
Note: This does not apply to exposure through electronic media, television, movies, or pictures, unless this
exposure is work-related.
B. Presence of nine (or more) of the following symptoms from any of the five categories of intrusion, negative
mood, dissociation, avoidance, and arousal, beginning or worsening after the traumatic event(s) occurred:
● Intrusion symptoms
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).

431
 (Note: In children, repetitive play may occur in which themes or aspects of the traumatic event(s) are
expressed.)
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the
event(s).
(Note: In children, there may be frightening dreams without recognizable content.)
3. Dissociative reactions (eg, flashbacks) in which the individual feels or acts as if the traumatic event(s)
were recurring. (Such reactions may occur on a continuum, with the most extreme expression being a
complete loss of awareness of present surroundings.)
(Note: In children, trauma-specific reenactment may occur in play.)
4. Intense or prolonged psychological distress or marked physiological reactions in response to internal or
external cues that symbolize or resemble an aspect of the traumatic event(s).
● Negative mood
5. Persistent inability to experience positive emotions (eg, inability to experience happiness, satisfaction, or
loving feelings).
● Dissociative symptoms
6. An altered sense of the reality of one's surroundings or oneself (eg, seeing oneself from another's
perspective, being in a daze, time slowing).
7. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative
amnesia and not to other factors such as head injury, alcohol, or drugs).
● Avoidance symptoms
8. Efforts to avoid distressing memories, thoughts, or feelings about or closely associated with the
traumatic event(s).
9. Efforts to avoid external reminders (people, places, conversations, activities, objects, situations) that
arouse distressing memories, thoughts, or feelings about or closely associated with the traumatic event(s).
● Arousal symptoms
10. Sleep disturbance (eg, difficulty falling or staying asleep, restless sleep)
11. Irritable behavior and angry outbursts (with little or no provocation), typically expressed as verbal or
physical aggression toward people or objects
12. Hypervigilance
13. Problems with concentration
14. Exaggerated startle response
C. Duration of the disturbance (symptoms in Criterion B) is three days to one month after trauma exposure.
Note: Symptoms typically begin immediately after the trauma, but persistence for at least three days and up to a
month is needed to meet disorder criteria.
D. The disturbance causes clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
E. The disturbance is not attributable to the physiological effects of a substance (eg, medication or alcohol) or
another medical condition (eg, mild traumatic brain injury) and is not better explained by brief psychotic disorder.
● Treatment
○ 1st line = Trauma-focused CBT
■ 6 weekly sessions of 60-90 mins
■ ≥2/52 after exposure
○ Pharmaco
■ SSRIs not found to reduce ASD symptoms compared to placebo, but efficacious for
PTSD
● NB: If symptoms last >1/12, may be PTSD

PTSD
A. Exposure to actual or threatened death, serious injury, or sexual violence in one (or more) of the following ways:
1. Directly experiencing the traumatic event(s).
2. Witnessing, in person, the event(s) as it occurred to others.
3. Learning that the traumatic event(s) occurred to a close family member or close friend. In cases of actual
or threatened death of a family member or friend, the event(s) must have been violent or accidental.
4. Experiencing repeated or extreme exposure to aversive details of the traumatic event(s) (eg, first
responders collecting human remains; police officers repeatedly exposed to details of child abuse).

432
Note: Criterion A4 does not apply to exposure through electronic media, television, movies, or pictures, unless this
exposure is work related.
B. Presence of one (or more) of the following intrusion symptoms associated with the traumatic event(s), beginning
after the traumatic event(s) occurred:
1. Recurrent, involuntary, and intrusive distressing memories of the traumatic event(s).
(Note: In children older than six years, repetitive play may occur in which themes or aspects of the
traumatic event(s) are expressed.)
2. Recurrent distressing dreams in which the content and/or affect of the dream are related to the
traumatic event(s).
(Note: In children, there may be frightening dreams without recognizable content.)
3. Dissociative reactions (eg, flashbacks) in which the individual feels or acts as if the traumatic event(s)
were recurring. (Such reactions may occur on a continuum, with the most extreme expression being a
complete loss of awareness of present surroundings.)
(Note: In children, trauma-specific reenactment may occur in play.)
4. Intense or prolonged psychological distress at exposure to internal or external cues that symbolize or
resemble an aspect of the traumatic event(s).
5. Marked physiological reactions to internal or external cues that symbolize or resemble an aspect of the
traumatic event(s).
C. Persistent avoidance of stimuli associated with the traumatic event(s), beginning after the traumatic event(s)
occurred, as evidenced by one or both of the following:
1. Avoidance of or efforts to avoid distressing memories, thoughts, or feelings about or closely associated
with the traumatic event(s).
2. Avoidance of or efforts to avoid external reminders (people, places, conversations, activities, objects,
situations) that arouse distressing memories, thoughts, or feelings about or closely associated with the
traumatic event(s).
D. Negative alterations in cognitions and mood associated with the traumatic event(s), beginning or worsening
after the traumatic event(s) occurred, as evidenced by two (or more) of the following:
1. Inability to remember an important aspect of the traumatic event(s) (typically due to dissociative
amnesia and not to other factors such as head injury, alcohol, or drugs).
2. Persistent and exaggerated negative beliefs or expectations about oneself, others, or the world, for
example:
-"I am bad''
-"No one can be trusted''
-"The world is completely dangerous"
-"My whole nervous system is permanently ruined"
3. Persistent, distorted cognitions about the cause or consequences of the traumatic event(s) that lead the
individual to blame himself/herself or others.
4. Persistent negative emotional state (eg, fear, horror, anger, guilt, or shame).
5. Markedly diminished interest or participation in significant activities.
6. Feelings of detachment or estrangement from others.
7. Persistent inability to experience positive emotions (eg, inability to experience happiness, satisfaction, or
loving feelings).
E. Marked alterations in arousal and reactivity associated with the traumatic event(s), beginning or worsening after
the traumatic event(s) occurred, as evidenced by two (or more) of the following:
1. Irritable behavior and angry outbursts (with little or no provocation) typically expressed as verbal or
physical aggression toward people or objects.
2. Reckless or self-destructive behavior.
3. Hypervigilance.
4. Exaggerated startle response.
5. Problems with concentration.
6. Sleep disturbance (eg, difficulty falling or staying asleep or restless sleep).
F. Duration of the disturbance (Criteria B, C, D, and E) is more than one month.
G. The disturbance causes clinically significant distress or impairment in social, occupational, or other important
areas of functioning.
H. The disturbance is not attributable to the physiological effects of a substance (eg, medication, alcohol) or
another medical condition.
● Treatment
○ 1st line = trauma-focused psychotherapy that includes exposure

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○ Pharmaco: SSRIs

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OBSESSIVE-COMPULSIVE DISORDER

Is there any thought that keeps bothering you that you would like to get rid of but cannot?
Do you think the thoughts are excessive and making you anxious/distressed ?
Do you have impulses that you cant control ie wash or clean or check a lot ?
Are you concerned about putting things in a special order?
Why do you need to do them? What happens if you do not perform them -> feel anxious
Do your daily activities take a long time to finish ie > 1 hr per day
How has it affected your work and rs with other ppl or health ie irritant contact dermatitis from excessive
washing
Insight: What is your view of the current problem? Do you think the beliefs are true ?

Need to rule out organic causes for anxiety and other psychiatric conditions

MANAGEMENT
- CBT
- Exposure and response prevention
- Higher SSRI dose needed and tx response time is longer
- Refer to psychiatry

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RENAL 1. ADULT POLYCYSTIC KIDNEY DISEASE

Possible scenarios
1. ADPKD pt with gross hematuria
2. ADPKD pt with abdominal pain
3. Middle aged pt with recurrent UTI and high BP
4. ADPKD pt with other comorbids and ADPKD with HTN/ HLD

Definition:
- Autosomal Dominant
- Affects kidney, liver, pancreas, spleen
- Up to 50% of patients require renal replacement therapy by 60 years of age
- Chromosome 16 80-90% APKD1, Chromosome 4 10-15% APKD2
- APKD1 (ESRF mean 53 years) more severe than PKD2 (ESRF mean 74 years)
- Inverse association between size of polycystic kidneys and level of glomerular filtrate
- Poor prognostic factors for ESRF: Large kidneys, episodes of gross hematuria, severe and frequent
kidney infection, hypertension, males, multiple pregnancies
- Clinical features usually begin in 3rd-4th decade of life: cyst detectable in childhood and in utero

HISTORY
Complaint
● Renal: Hypertension, Hematuria, Proteinuria (Mild), UTI, Cyst Cx, Nephrolithiasis, Acute or chronic
flank and abdominal pain, Anaemia, Concentrating defect, RCC
● Hematuria – 2 to bleeding cyst, nephrolithiasis (usu microscopic)
● Flank/ Abdominal pain – UTI, nephrolithiasis, rupture of cyst, bleeding cyst, hepatic cysts
● Chronic kidney pain –stretching of the capsule or traction on the renal pedicle
● Concentrating defect - increased thirst, polyuria, nocturia, and urinary frequency
● Renal cell carcinoma – LOW / LOA

Extra-renal
● Cardiac: MVP, AR, MR
● Neuro: SAH from intracranial aneurysm
● GI: Hepatic and pancreatic cyst, Diverticulitis (80% of APKD patients on dialysis)
● Thoracic artery aneurysm

Course: What ix was done, Mx, f/up where

Complications: ESRF - Reduced urine output, LL swelling, pruritus, lethargy
Checking: Home BP monitoring
Co-morbids: (extra renal manifestations)SOB / Chest Pain/ One sided weakness/ numbness/ jaundice/ PR
bleed
Crisis Mx:
PMHx/Drug Hx
Family/ Social Hx: ? Genetic Counselling
Psych Hx:

PHYSICAL EXAMINATION
BP HR
Inspection: sallow? Respiratory status
Arms: AVF/AVG, perm cath
Pronator drift
CVS: murmurs
Abdo:

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Pedal edema

INVESTIGATIONS
Stat tests
● FBC, UFEME
Other tests
● Renal panel/GFR, cCa/PO4, LFT
● U/S Abdomen
@ tertiary: MRI/MRA to screen for aneurysm ; MRI to differentiate RCC from cysts; CT to distinguish cystic
wall calcifications and calculi; 2DE exclude Mitral valve prolapse ; Colono for diverticulitis

MANAGEMENT
Chronic Mx
Hypertension - Control BP <130/80 with ACE or ARB
- Low salt diet < 2g/day
CKD / ESRF - Low protein diet
- Correct electrolyte imbalance/ fluid overload
- Avoid NSAIDS
- PD/HD/Transplant in renal failure
Concentrating defect early on (polyuria, - Encourage a liberal fluid intake should be
urinary freq, nocturia) encouraged, with >3 L/day fluid intake recommended
unless in fluid overload in CKD
Counselling - Avoid contact sports with risk of trauma to back or
abdomen
Acute Mx
Acute pyelonephritis and/or cyst infection Send ED for IV ABx
who have marked systemic symptoms (eg,
high fever, flank pain, nausea, and vomiting)
Infected cyst with minimal or no systemic Oral ciprofloxacin or Bactrim
symptoms (difficult to differentiate from
pyelo)
Gross Hematuria Send ED
Abdominal pain 2 to enlarged kidneys, Avoid NSAIDS
excision of cyst etc

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RENAL 2. AKI/AOCKD

Differential Diagnoses
Pre-renal ● GI losses: Diarrhoea/vomiting
● Diuretics
● Insensible losses: Heat stroke

Renal ● Vasculitis (e.g. HUS)

● Renal vein thrombosis
● Pyelonephritis
● Autoimmune
● Iatrogenic: NSAIDS
● Multiple myeloma
● APKD

Post-renal ● Obstructive nephropathy - Stones , BPH

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RENAL 3. CHRONIC KIDNEY DISEASE

Possible scenarios
1. Follow-up CKD patient routinely
2. CKD patients with acute K>5.5
3. CKD patients with poorly controlled blood pressure
4. CKD patients with anemia
5. CKD patient who has refused dialysis, had AMD signed, comes to you for acute complaints
related to CKD

HISTORY
ꈸ Complaint
● Eg SOB, fatigue, palpitations, LL swelling/fluid overload

ꈸ Control (stage __ CKD)

● eGFR
● uACR/uPCR
● Weight

ꈸ Cause (of CKD)

● DM
○ HbA1c target <7%, SMBG, hypoglycemic symptoms
○ DRP, DFS
● HTN
○ HBPM, target <130/80
○ Symptoms
● ADPKD
● GN

ꈸ Cause (of AoCKD)

● Pre-renal
○ Dehydration
○ Drugs eg ACEi, NSAIDs
● Renal
○ Infection eg UTI, pyelo
○ Drugs causing ATN/AIN
● Post-renal
○ Obstruction eg BPH
○ Stones, strictures

ꈸ Course
● F/u Renal? Plans for RRT/already on RRT? Any biopsy done
● Admission/hospitalisations

ꈸ Comorbids
● LDL <2.1

ꈸ Compliance
● Lifestyle
○ Fluid restriction
○ Sodium restriction <2g/day
○ Renal diet: low K, low protein, low phosphate
● Medications

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ꈸ Complications (of disease)
● Fluid overload: SOB, LL swelling, facial swelling,
● Uremia: Pruritus, n/v
● Anemia: fatigue, reduced effort tolerance, syncope, giddiness
● Hyperkalemia: palpitations, muscle weakness
● Hyperphosphatemia/hypercalcemia

ꈸ Complications (of treatment)

● ACEi: cough
● Diuretics: electrolyte imbalances

ꈸ Crisis Management

Drug Hx
● NSAIDs, New/ increased ACE-I

Family Hx
● Kidney diseases - ie Polycystic kidney dz, GN

Psy Hx: PHQ2 GAD2

Social Hx: WASHED

Preventive Health
● Flu vaccine
● Pneumococcal vaccine
● FOBT
● KIV MMG, pap smear

Function
● iADL, bADL
● PU
● BO

PHYSICAL EXAMINATION
T BP HR
Ht Wt BMI
SHORT LONG CASE
● Inspection ● Inspection
○ Pallor, sallow ○ Pallor, sallow
● KIV neck for JVP if c/o SOB ● Hands
● AVF? ○ Leukonychia, Terry nails
● Abdo ○ AVF
○ PD scars ○ Uremic flap, scratch marks
○ Ballotable kidneys? ● Neck
○ Ascites ○ Perm cath
○ Lipodystrophy if on insulin ● Lungs: creps
○ DRE (if patient anaemic) ● Abdo
● Lungs: creps ○ PD scars
● Legs ○ Ballotable kidneys?
○ Pedal edema ○ Ascites
○ DM dermopathy ○ Lipodystrophy if on insulin

440
 ● KIV Heart exam if hyperkalemia ○ DRE (if patient anaemic)
● Legs
○ Pedal edema
○ DM dermopathy

INVESTIGATIONS
● Stat: FBC, Udipstick/UFEME, CXR, KIV XR KUB
● RP, uACR/uPCR

MANAGEMENT
1) Management of CKD patients
Eliminate reversible causes ● Hydration adequate
(AKI) ● No nephrotoxic drugs: NSAIDs
● Treat any obstructions: Stones/BPH

Slow progression of renal ● HTN: Tx with anti-HTN aim <130/80

disease ● Proteinuria: Tx with acei/arb, low protein diet <0.8g/kg/day
● DM: HbA1c target to meet
● Smoking cessation
● Other causes: SLE, primary GN, APKD

● NHG CPG : CKD 1-2: HbA1c <7%

● If advanced CKD 3-5, frail, elderly: HbA1c between 7.0 to 8.5%

Treat complications of disease ● Fluid overload: Na restriction, fluid restriction

● Hypertension: acei/arb with diuretics
● HyperK: low K diet**, Diuretics, may need to lower acei/arb
● Hyperphosphatemia: Phosphate binder. Low PO4 diet**.
● Acidemia: Sodium bicarb
● Anemia: Exclude iron deficiency, if ferritin<100.. EPO if ferritin
replete. Aim Hb 10-11.5. Watch SE.

Identify urgent RRT indication ● Acidemia

(AEIOU) ● Electrolyte (hyperK)
● Intoxication
● Overload
● Uremia

Refer for RRT discussion Stage 4 CKD onwards

Preventive health Vaccinations

● Pneumococcal
○ <65: PPSV23 first, then PCV13 at 65yo + repeat PPSV23 5
years after previous dose
● Influenza

AMD / ACP

441
2) Hyperkalemia in CKD patients
● Check Vital Signs
● Exclude spurious results ie specimen hemolysed
● Stat ECG if K > 5.5
● K 5.1-5.5
○ K diet reduced
○ Interchange atenolol to bisoprolol
○ Diuretics
● K5.5-6.4 (if asymptomatic and no ECG changes)
○ Resonium 15g TDS (no of days depends on eGFR)
○ Reduce ACEI/ARB
○ Renal referral if no improvement with above

● If there is no ECG changes, no need for ECG monitoring, can manage patient in primary care
● ** K ≥ 6.5 considered hyperkalemic emergency and need to send to ED (UTD)
● If there is ECG changes, pt has to be referred to A&E for ECG monitoring and IV insulin and dextrose
and IV calcium gluconate
● IV soluble insulin 5-10U with IV dextrose 50% 40ml SLOW over 5 mins

442
 ● IV Ca gluconate 10% 10ml over 2-3 min (not advisable to give in OPS cos need to check hourly
hypocount!)

ᐉ Symptoms of hyperkalemia: muscle weakness/paralysis, giddiness, palpitations (cardiac conduction

abnormalities, and cardiac arrhythmias). These manifestations usually occur when K ≥7 mEq/L with chronic
hyperkalemia, or possibly at lower levels in patients with an acute rise in serum
potassium and/or underlying cardiac conduction disease.

ᐉ ECG changes

● Tall SYMMETRICALLY peaked T wave >2 big squares (10mm) in precordial leads and >1 sqaure
(5mm) in limb leads
● Widened QRS complex
● Prolonged PR interval (sometimes missing P wave as it has merged with the QRS complex)
● There are several characteristic electrocardiogram (ECG) abnormalities associated with
hyperkalemia. A tall peaked T wave with a shortened QT interval is the earliest change, followed by
progressive lengthening of the PR interval and QRS duration

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3) CKD anaemia
● Target Hb 10-11.5g/dL (uptodate)

Non pharmacological
● If Fe deficient -> usual workup for Fe def ie Stool occult blood test / colonoscopy /OGD and treat
any underlying cause
● Advice on diet with iron
● Check FBC/ Ferritin Annually

Pharmacological
● If Fe deficient → Give Fe supplements
● If Hb <10 and Fe replete (transferrin saturation (TSAT) is >25 percent and ferritin >100 ng/mL),
Offer ESA (refer to renal for initiation)
● Side effects of ESAs: Hypertension, Testicular cancer, pure red cell aplasia, flu-like symptoms
● Cost of EPO can be offset by Medishield

Education: Red flags

Followup: TCU in 4/52 (time required to see an improvement in Hb after starting ESA

444
445
RENAL 4. APPROACH TO HYPERKALEMIA

Differential Diagnoses
Increased release of K from cells Reduced excretion of K by kidney

Pseudohyperkalemia: Due to hemolysis during AKI/CKD

venepuncture

Hypoinsulinemic state Reduced aldosterone secretion or action

Metabolic acidosis Reduced distal sodium delivery

Beta blockers
● Atenolol
● Propranolol
● Labetalol

Increased tissue catabolism

● Trauma
● Tumor lysis syndrome (hemato
malignancies with recent chemo)
***Increased potassium intake in itself rarely causes hyperkalemia.

HISTORY
Complaint: Abnormal K on blood test
- (Determine if hemolysed sample)
- Determine eGFR to find out if AKI/CKD
- Ask for symptoms of HyperK: giddiness, palpitations, muscle weakness

Causes:
- Any history of cancer (hemato malignancies with recent chemo) or muscle injury, recent strenuous
exercises?
- Any beta blockers?
- Type 1 or insulin dependent DM defaulted meds?
- Any risk factor for AKI/CKD: Dehydration? NSAIDS. DM/HTN/HLD/APKD?
- Any adrenal disease e.g. addison disease

Course

Complications

PHYSICAL EXAMINATION
BP HR RR
[supine]
- Stigmata of chronic renal failure: Terry’s nail, pallor, AVF/perm catheter, bruising, sallow
- Abdomen: Ballotable kidney? Renal bruit?

INVESTIGATIONS
{STAT Labs}
FBC (NCNC anaemia)
ECG (widened QRS complexes, tall tented T waves)
KIV hypocount if considering giving insulin

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{Other Labs}
Renal panel, phosphate, calcium, uric acid, creatinine kinase
US KUB

MANAGEMENT
If suspicions of ongoing tumor Refer ED for close monitoring of K levels
lysis/muscle injury

If due to CKD Hyperkalemia in CKD patients

● Check Vital Signs
● Exclude spurious results ie specimen hemolysed
● Stat ECG if K > 5.5
● K 5.1-5.5
○ K diet reduced
○ Interchange atenolol to bisoprolol
○ Diuretics
● K5.5-6.4 (if asymptomatic and no ECG changes)
○ Resonium 15g TDS (no of days depends on
eGFR)
○ Reduce ACEI/ARB
○ Renal referral if no improvement with above

447
 RENAL 5. HYPOKALEMIA

Differential diagnoses
Reduced intake Increased GI losses Increased urinary potassium losses Cellular exchange

This alone almost - Vomit - Loop or thiazide diuretics - Hyperinsulin state

never causes - Diarrhoea - Hyperaldosteronism - ß2 agonist
hypoK. - Hyperthyroidism - Metabolic alkalosis
- HypoMg

HISTORY
Complaint: HypoK
- Acute or chronic
- K 3.0-3.4, 2.5-2.9 or below 2.5
- Muscle weakness, lethargy, paralysis

Causes
- Vomiting or diarrhoea?
- Medication review - diuretics
- Associated hypertension (Conn’s syndrome)
- Any high dose insulin
- Any recent salbutamol usage
- Hyperthyroid symptoms

Course:
- Any workup previously

Complications
- Weakness
- Palpitations
- Paralysis
- Decreased mentation

Med Hx: Chronic diarrhoea | Conn’s syndrome | Asthma or COPD | DM on high dose insulin |
Hyperthyroidism poorly controlled
Drug Hx: Look for diuretics, laxatives, insulin, ß2 agonist
Social Hx: Diet → Potassium sufficient? (vegetable or fruit juice, starchy vegetables, kiwi/jackfruits)

PHYSICAL EXAMINATION
BP HR
General: Hydration status
Neck: goitre
Tremors, acropachy, hyperreflexia, thyroid eye signs, pretibial myxedema
Neuro: Myopathy weakness
Cardiac: Pulse rate, regularity
Respi: wheeze/rhonchi

INVESTIGATIONS
[STAT labs] BSL
ECG

448
 [Other
labs] Renal panel, Thyroid Panel, Magnesium

MANAGEMENT High risk patients: elderly, heart failure, patients on arrhythmic drugs - consider referring
Acute
K <2.5 Refer to ED for intravenous replacement

K 2.5 - 2.9 with ECG changes and symptomatic Refer to ED for intravenous replacement

K 2.5 - 2.9 without ECG changes and asymptomatic Consider replacement with Potassium Chloride
outpatient and review within the next 3/7

K > 2.9 Replace with Potassium Chloride and repeat K

within 3/7

Chronic
Refer to SOC (General Medicine for further workup of persistent hypokalemia)

449
 RENAL 6. HYPONATREMIA

Serum osmolality = (2 x Na) + glucose + urea

● Normal= 275-295
● Hypoosmolar: <275
● Hyperosmolar: >295
Rule out spurious: High glucose, high lipid, high protein

Differential Diagnoses
Hypovolemia Euvolemia Hypervolemia

● GI losses: Diarrhoea ● SIADH ● Cardiac failure

and vomiting ○ Drugs - escitalopram (SSRI) ● Cirrhosis
● Renal losses: Thiazide ○ Infection (e.g. pneumonia) ● Renal failure
diuretics, loop diuretics ○ Malignancy
○ CNS disorder
○ Surgery
○ Hypothyroid
○ Adrenal insufficiency (secondary)
● Primary polydipsia
● Reduced solute intake

HISTORY
Complaint: Hyponatremia
- Known or newly discovered
- If previously known, any workup done? E.g. SIADH workup with serum and urine osmolality,
sodium.

Causes:
- Nausea/vomiting → GI losses
- Any medications like diureitcs → Renal losses
- Orthopnea/PND/lower limb swelling/reduced effort tolerance → Cardiac failure
- History of renal failure on dialysis? Reduced urine output? → renal failure
- History of liver failure/cirrhosis?
- Excessive fluid intake → Primary polydipsia
- Cold intolerance, weight gain, constipation, neck swelling → Hypothyroidism
- New medications → Drug causes of SIADH
- LOW/LOA/known malignancy? Recent surgery? → SIADH

Course

Complications
● Nausea/vomiting/lethargy/seizure/obtundation or less profound like lethargy/muscle cramps/gait
disturbances

Med Hx: SIADH? Hypothyroid?

Drug Hx: SSRI?
Social: Low solute diet? Fluid intake excessive?

PHYSICAL EXAMINATION
BP HR
[seated]

450
 - Hydration status: Tongue, capillary refill time, skin turgor
- Goitre
[45 deg]
- JVP elevation. Lower limb pitting oedema.

INVESTIGATIONS
- Serum glucose, urea to calculate osmolality.
- Urine sodium and osmolality (SIADH: urine Na > 40 and urine Osm > 100)
- TFT

MANAGEMENT
1) Hypovolemia ● Acute symptomatic hyponatremia has to be referred for IV sodium replacement
under close monitoring
● Manage underlying cause: If drug cause, attempt to stop and replace with
alternative drugs. Manage cause of diarrhoea/vomiting. Hydration to replace
volume

2) Hypervolemia (e.g. ● Manage underlying cause: Manage cardiac failure. Diuretics, fluid restriction.
CKD, CCF) Optimize cardiac failure regime.

3) SIADH ● Treat underlying cause: e.g. tx pneumonia, stop offending drugs

● Fluid restriction aim <800ml/24 hr
● KIV sodium tablet

451
RESPI 1. APPROACH TO ASTHMA

HISTORY
Complaint: SOB/cough/wheezing/reduced effort tolerance. Diurnal variation. Episodic usually with triggers.
-----> If complaint does not sound like asthma, consider other differentials.

Course: How and when asthma was diagnosed? If >5 years old, any spirometry done to confirm airflow
reversibility? Prev hospitalization / intubation?

Cause:
● Underlying cause: Family or personal hx of atopy?
● Precipitating causes: {ACDE-I}
○ A - Allergen avoidance (dust mites, pets, carpets), Allergic Rhinitis
○ C - Cigarettes, Cold air/drinks, Construction
○ D - Drugs ie NSAID, beta blocker
○ E - Exercise, Emotion, Environment (incense smoke, mould)
○ I - Infection ie URTI
Medication, AR, GERD, Food, Infection, temp Cold, mould, dust, smoke, work, emotion, exercise,
mould, pets or carpets

Control: ACT score (Adult and Paeds version 19 and below are considered poor for both version). Recent
exacerbations, time off work and school due to asthma.

Compliance
Competency: Check inhaler technique. If using spacer, check spacer technique.

Complication
- Disease - Days off school or work? Development delay?
- Treatment - Growth, Oral Thrush, Cushing’s (less likely)

Crisis Mx: Does patient have written asthma action plan?

Comorbidities: Allergic rhinitis, atopic dermatitis, allergic conjunctivitis

Psychological: Any depression/anxiety due to illness?

Social:
- Occupation worsening asthma? (Asthma better when off work/ on weekends)
- How has asthma impacted work, school, hobbies?

PHYSICAL EXAMINATION
BMI T BP HR RR SpO2: <95% not good
IN PAEDS CASES, REMEMBER TO PLOT GROWTH CHARTS (age and gender appropriate)
Respi exam:
- Well thrived ? in paeds

452
 - Signs of respi distress: Cyanotic? Accessory muscles, speaking in sentences/phrases.
Agitated/lethargic?
- Other atopic features: Eczematous skin (dry, lichenified skin especially over flexors, necks), allergic
shiners
- Look at mouth/tongue: Thrush due to poor inhaler technique
- Features of Cushing’s
- Lung hyperinflated? Harrison’s sulcus? Wheeze/prolonged expiratory phase?

INVESTIGATIONS
- Spirometry (if never done before, or as part of monitoring to see FEV1 or FVC trend)
** in a well controlled asthma, you may see a normal spirometry. No obstruction and hence no reversibility
- FEV1/FVC reduced at least once (children normal 0.90)
● Post bronchodilator FEV1 increases by ≥12% AND
○ FEV1 / FVC increase by 200ml = bronchodilator reversibility

MANAGEMENT
1) Acute asthma exacerbation - Assess severity of attack
- Initiate nebulization in clinic (dry vs wet neb)
- Prednisolone 30mg OM x 5 days
- Assess response post nebulization; if adequate can discharge outpatient with
steroids, stepped up dose of inhalers, and review early with red flag advice
- If suboptimal response post nebulization, can consider repeat nebulization keep
in view ED referral.
- Give tcu in 1-2 weeks to review symptoms.

2) Chronic follow-up with - Non-pharm: Reinforce allergen avoidance. If drug cause, try to stop offending
control suboptimal drugs. Smoking cessation advice.
- Allergen avoidance
- House dust mites
- Wash linen in hot water >60oC
- Keep room well-ventilated
- Cigarette smoke
- Strongly discourage household smoking
- Passive smoking is bad
- Poor role-model to impressionable child
- Avoid soft toys, fur and feathered pets at home
- Assess which step patient is on based on GINA ladder and step up accordingly.
After stepping up and control achieved, maintain at least 3/12 before
considering stepping down.
- Educate on
i) Inhaler technique
ii) WAAP!!
- Follow-up TCU
- Vaccinations

3) Difficult to control asthma - Try to assess for other triggers. Otherwise, revisit diagnosis
despite optimized therapy and - If Spirometry: FEV1/FVC 50%, FEV1 Post bronchodilator increase by 7% and
compliance 100mls ->> inadequate reversibility in an obstructive airway dz , this patient
does not have asthma

453
4) Pt request to be excused - Ascertain why pt requests to be excused
from PE - Assess what activities she can do
- Is it truly exercise induced ie unable to do all activities , unable to do outdoor
activities or unable to do one sport only
- Any underlying social reason - HEADSSS
- If truly exercise induced w gd overall control → 2puff Salbutamol 15 min pre
exercise
- If overall poor asthma control with other additional triggers → Step up therapy
+ salbutamol puff before exercise

5) Occupational Asthma - Explain to patient diagnosis of occupational asthma likely related to exposure to
allergen at workplace
- Avoid triggers
- Smoking cessation counselling
- May need to discuss with employer possibility of change of role or may need to
consider other job options. May impact on finances/ lifestyle
- Refer to Respiratory Clinic who will notify MOM
- Pharm: Same Mx as usual asthma. Salbutamol inhaler for symptomatic relief
- KIV Step up to ICS or ICS/LABA if persistent

● In children, prefer to step up the ICS dose to med to high dose before adding LABA
● In adults, prefer to add LABA to low dose ICS

454
● Follow Beclometasone dipropionate (HFA) - in polyclinic
● Potency of fluticasone in children and adults same

455
Asthma Predictive Index eg children <5yo

Asthma Predictive Index

Strict Criteria:
● ≥3 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria
Loose Criteria:
● <3 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria
Results:
● 59% of children with a positive loose index had active asthma at school age (defined at 15 years).
● 76% of those with a positive strict index had active asthma at school age (defined at 15 years).

Modified API
Positive mAPI defined by:
● ≥4 episodes of wheezing per year, AND
● ≥1 major criteria OR ≥2 minor criteria

456
RESPI 2. BRONCHIECTASIS

Causes
● Focal
○ Luminal blockage – FB, broncholith
○ Arising from the wall – mitotic lesion of the lung
○ Extrinsic – enlarged LNs esp middle lobe from TB/fungi; displacement of airways post lobar
resection
● Diffuse
○ Post infectious conditions
■ Bacteria – Pseudomonas, Hemophilus, Pertussis
■ TB
■ Aspergillus (for upper lobe or proximal bronchiectasis) as in allergic
bronchopulmonary aspergillosis from type III immune complex reactions.
■ Virus – adenovirus, measles, influenza
○ Congenital conditions
■ Cystic fibrosis; Alpha 1 Antitrypsin deficiency; Kartagener’s syndrome of immotile
ciliary syndrome; Hypogammaglobulinemia
○ Rheumatic conditions
■ RA (1-3% of patients)
■ SLE
■ Sjogren’s
○ Others
■ Yellow nail syndrome (yellow nails, bronchiectasis, pl effusion and lymphedema)
■ Young’s syndrome(secondary ciliary dyskinesia from mercury intoxication)
■ Inflammatory bowel disease (UC or Crohn)
■ Congenital kyphoscoliosis
■ Idiopathic (50%)

HISTORY
Complaint: cough with sputum, hemoptysis, SOB, wheeze → consider other ddx as well
Course: How was it diagnosed? (HRCT is gold standard; CXR usually got some changes) management thus
far? Previous hospitalisations/ Intubations
Cause (BronChiEcTaSis): bronchial obstruction (tumour/fb/ln) , ciliary dysfunction (kartagener’s),
eosinophilic lung disease, TB, suppurative lung disease
OR BCREST - R for rheumatoid conditions
Control: frequency of exacerbation per year
Compliance: if on preventive abx therapy, compliant?
Complications of disease: Cor pulmonale (LL swelling), Sinusitis, Brain abscess, Lung abscess
Complications of treatment
Crisis management: aware of exacerbation symptoms?

Psy Hx: PHQ2. GAD2. ICE.

Social: work, finance, smoke/alcohol, home.
**Function?
Prev: Flu? Pneumococci?

PHYSICAL EXAMINATION
Temp BP HR RR SpO2
{45 deg} Clubbing. RA hands? SLE rash?
Lungs: coarse creps. Parasternal heave. LL oedema.
Sputum Mug

INVX
457
 ● STAT- FBC, CXR
HRCT , Sputum culture

MANAGEMENT Usually cannot tx underlying cause.

Acute ● ABx: amoxicillin/augmentin/ macrolides. Levofloxacin or cipro (if
exacerbation pseudomonas)
● Duration 10-14 days

Preventive ● Non pharm: Education, smoking cessation, physio

● Pharm
○ Prophylactic abx for recurrent exacerbation: oral azithromycin 250
mg once daily or 500 mg 3 times weekly for recurrent exa
○ Bronchodilators - short or long (improve FEV1 and reduce sputum
volume but no benefit on mortality)
○ Mucolytics
○ Inhaled glucocorticoids generally NOT recommended unless
concomitant asthma/ aspergillosis
● Surgery: Surgical resection of affected lung segments, Lung Transplant
● Vaccinations

Bronchiectasis exacerbation based on Hill et al:

Deterioration in three or more of the following key symptoms for at least 48 hours:
❏ cough
❏ sputum volume and / or consistency
❏ sputum purulence
❏ breathlessness and / or exercise tolerance
❏ fatigue and / or malaise
❏ haemoptysis
AND a clinician determines that a change in bronchiectasis treatment is required.
Definition of recurrent bronchiectasis exacerbation: ≥2 exacerbations per year

458
 RESPI 3. APPROACH TO COPD

Defined as:
- Disease of chronic airway inflammation with poor reversibility of symptoms with bronchodilator
therapy
- Consider in any pt w SOB, chronic cough or sputum production, ± h/o exposure to risk factors of disease
- Spirometry needed for definitive diagnosis
- Post-bronchodilator FEV1/FVC <0.7
- Airflow limitation: Grade 1-4 (FEV1≥80% predicted | ≤50-<80% predicted | ≤30-<50% predicted | <30%
predicted)

HISTORY
Complaint Acute exacerbation
● Increased dyspnoea
● Increased sputum volume
● Increased sputum purulence (thickness or tenacity)
● Increased cough/wheeze

Differential diagnosis of Chronic SOB / Cough

- Lung CA (LOW / Haemoptysis / Night sweats)
- TB
- Bronchiectasis
- CCF
- Anemia

Acute SOB/cough (must exclude)

- Acute coronary syndrome/CCF
- Pneumothorax/Pulmonary embolism
- Pneumonia/Pleural effusion

Course ● Any recent exacerbations/ hx of prev intubation NIV / hospitalisations

● How was it diagnosed, Ix done, Mx
● Latest spirometry results

Cause - Underlying cause of COPD: smoking, occupational inhalation of noxious particles, alpha 1
anti trypsin deficiency
- Cause of acute flare
● 70% infection: viral and bacterial
● 30% other causes environmental pollution, pulmonary embolism, or have an unknown
etiology

Control Stage into Gold A/B/C/D.

CAT Score (8) –

459
 Cough | Phlegm | Chest tightness | Walk up hill or climb stairs | Limitation of activities | Confident
of leaving home | Sleep soundly | Energy level

Triggers: Smoking, URTI, Occupation, Environmental factors ie second hand smoke, construction
work

Compliance To inhalers

Competenc Usage of inhalers (preventer vs rescue)

e

Cx Of Dz
● Cor pulmonale: Orthopnoea/ PND / LL swelling
● Pneumothorax: sudden onset of SOB
● Lung CA: LOW, LOA
Of Tx
● Inhaled corticosteroids/ oral steroids: Oral thrush, Cushing’s syndrome
● Anti-cholinergics: Dry mouth, URTI, urinary retention, constipation

Crisis Mx What to do in acute exacerbation

Co-morbids Smoking cessation!

CVD, osteoporosis, depression/anxiety, skeletal muscle dysfunction, metabolic syndrome, lung
cancer)

PMHx
Drug Hx: Any beta-blocker
Family Hx
Psy Hx: PHQ2, GAD-2
Social Hx
- Smoking, Alcohol
- Occupation (and past occupation)
- Marital status and children
- Financial
- House: any floor landing
Function: ADLs – activities limitation?
Preventive Health: Vaccinations! FOBT

PHYSICAL EXAMINATION (do a full respi exam! remb to examine for cor pulmonale! )
T BP HR RR SpO2 target 88 - 92%
{Seated} Pallor, cyanosis, polycythaemia
Respi status: tachypnoea, use of accessory muscles, hyperinflated chest
Peripheries: asterixis for respiratory failure, bounding pulse for CO2 retention
Cervical LNs
{Lie 45o} Cricosternal distance < 3cm
Raised JVP in Cor Pulmonale
Parasternal heave, loud P2 (Pulmonary HTN)
Reduced chest expansion
Hyperresonant on percussion
Auscultate: wheeze, creps in cor pulmonale, quiet b/s over bullae or PTX from ruptured
bullae
LL pedal edema in cor pulmonale

460
INVESTIGATIONS
Stat tests
- CXR r/o infection/CA
- FBC to screen for infection/anemia/ polycythaemia
- ECG to r/o CCF
Other tests: Spirometry for definitive diagnosis if not already done
@ tertiary: sputum culture and AFB smear ; CT lungs or ABG as required

MANAGEMENT
Acute COPD exacerbation* ● Supplemental oxygen (low flow, keep spO2 88 -92%)
(Anthonisen criteria ⅔) need to ensure respiratory drive preserved),
● Oral steroids: PO Prednisolone 30mg OM x 5-7 days
● Antibiotics x 1/52, treat underlying cause of the
exacerbation (e.g. ciprofloxacin 750mg BD)
● TCU 2 days to review symptoms

Chronic follow-up COPD 1) Educate on disease

2) Smoking Cessation
3) Exercise / Pulmonary Rehabilitation (in hospital)
4) Pharmacotherapy
● Depends on Patient Group ( See below)
● LAMAs have greater effect on exacerbation reduction
compared with LABAs, and decrease hospitalisations
● Regular treatment with ICS increases risk of pneumonia
5) Vaccinations
ᗎ Influenza: Annual
ᗎ Pneumococcal
● Age ≥65
○ No previous PCV13/PPSV23: PCV13 → 1 dose PPSV23
(≥12/12 after PCV13)
○ PPSV23 given before 65yo: PCV13 (≥12/12 after PPSV23) →
1 dose PPSV23 (>12/12 after PCV13 and ≥5 years after
PPSV23)
○ PPSV23 given at 65yo: PCV13 (≥12/12 after PPSV23)
○ PCV13 given before 65yo: PPSV23 (≥12/12 after PCV13)
○ PCV13 and PPSV23 given before 65yo: 1 dose PPSV23
(≥12/12 after PCV13 and ≥5 years after PPSV23)
● Age <65
○ No previous vaccine: 1 dose PPSV23
6) Follow up – spiro / CAT
7) Oxygen therapy >15 hours per day if required (if
PaO2<55mmHg or SpO2 <88% or pulmonary
HTN/CCF/polycythemia)
8) Lung reduction surgery /Lung transplant

APPENDIX

461
Typical organisms : Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae in most
patients)
Advanced COPD pts can also havePseudomonas aeruginosa and Enterobacteriaceae

462
463
464
New LAMA inhaler

465
 RESPI 4. APPROACH TO COUGH

DDx
1. Asthma
2. COPD/ bronchitis
a. Occupational
b. Toxins: cooking fumes
3. GERD
4. Allergic rhinitis
5. Infections:
a. Tuberculosis, NTM
b. ABPA
6. Drug induced
a. ACE inhibitors
b. Other drugs that can cause pneumonitis: Amiodarone, Bleomycin, Methotrexate
7. ILD
8. Bronchiectasis
9. Lung cancer
10. Sarcoidosis
11. Inhalation of foreign body
12. Vasculitis (GPA, Churg Strauss)

Ddx 2
Respi Cardio GI Medications

Upper Lower airway ● Cardiac ● GERD ● ACE inhibitor

airway ● Parenchyma: ILD, Cancer, failure ● Beta blocker
● URTI TB, pneumonia ● Nitrofurantoin
● PND ● Airway: Asthma, COPD, ● MTX
● AR bronchitis, bronchiectasis ● Amiodarone
● Vessel: Pulmonary
Embolism

HISTORY
Complaint: Cough
● How long (<3 weeks, 3-8 weeks, >8 weeks)
● Acute onset, gradual onset
● Progressively worse, stable, getting better
● Constant or intermittent
● Character: dry, purulent, amount, blood
● Worse in early morning or night (diurnal variation)
● Precipitating factors or relieving factors
o Precipitated by eating or drinking or lying down → GERD
o Precipitated by dust, pollen, cigarette, vapours, cold weather, exercise → asthma, AR

Causes
● Recent runny nose/sore throat/fever → post infectious cough
● Any wheezing/history of eczema or allergic rhinitis
● Any fever, chills or rigors, night sweats; contact history with TB pt or chronic cough? → TB
● Any hemoptysis/LOW/LOA → lung CA
● Any other atopy (eg AR, AC, AD) / fam hx of atopy → asthma
● SOB/orthopnea/PND/lower limb swelling → CCF

466
 ● Any acidic taste in mouth, water brash, abdominal discomfort → GERD
● New medications ie ACEi/ARB
● Exposure to asbestosis, silica, baking flour, toxic fumes
● Any rashes on body → vasculitis and sarcoidosis

Course
● Spiro/peak flow diary done?
● Previous episodes and response to bronchodilators?

Complications
● Function affected? ± development delay if paeds
● Anemia symptoms if hemoptysis

Control
● If COPD/asthma: inhaler technique, + WAAP if asthma
○ Previous hospitalisations / ICU HD / intubations NIV
○ Known triggers?

PMHx
● Asthma, AR, Eczema, COPD, GERD, TB, bronchiectasis
● Conditions that require the use of ACE inhibitors or other drugs that can cause pneumonitis

Drug history
● ACE inhibitors, Amiodarone, Methotrexate, Nitrofurantoin etc
● Check inhaler technique if using inhaler

Family history
● History of asthma, AR, eczema
● Cancer

Social history
● Smoker
● Occupation: any exposure to toxic fumes/ asbestos/ baking flour etc

Travel history

PE
Vitals: T, BP, HR, RR, SpO2
[seated]
● Respi distress?
● Head: Allergic shiners. Inferior nasal turbinates. Sinus tenderness to palpation percussion
● Cervical LNs

[45o]
● Hands: Clubbing, (asterixis). Gottron papules. RA hands.
● Neck: JVP elevated
● Heart: Deviated apex beat (S3?)
● Lungs: Wheeze, crepitations
● Pitting edema

INVESTIGATIONS
STAT tests
● Bloods: FBC

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 ● CXR to look for pneumonia, TB, foreign body, tumour
-------------------------------------------------------------------------------------
Spirometry: cough variant asthma
Imaging:
● CT thorax to look for pneumonia or SOL
Others:
● Serial peak flow monitoring to look for diurnal variation and peak flow diary
● Methacholine challenge test for asthma
● 24hr oesophageal pH monitoring for GERD
● Bronchoscopy

COPD exacerbation based on Anthonisen criteria: (⅔)

❏ Increased SOB
❏ Increased sputum volume
❏ Increased sputum purulence

Bronchiectasis exacerbation based on Hill et al:

Deterioration in ≥3 of the following key symptoms for at least 48 hours:
❏ cough
❏ sputum volume and / or consistency
❏ sputum purulence
❏ breathlessness and / or exercise tolerance
❏ fatigue and / or malaise
❏ haemoptysis
AND a clinician determines that a change in bronchiectasis treatment is required.

MANAGEMENT
1. Pneumonia
2. COPD: Acute exacerbation vs New diagnosis
3. Asthma: Acute exacerbation vs New diagnosis

468
 RESPI 5. APPROACH TO HEMOPTYSIS

DDx:
First distinguish true haemoptysis from bleeding from nasopharynx or upper gastrointestinal tract
Respi (VITTA) Cardiac Systemic

● Vascular ● Congestive heart ● Drugs: anti-platelets,

○ Pulmonary embolism failure anticoagulants
○ Pulmonary hypertension – which ● Mitral stenosis ● Bleeding disorders
of the 5 types?
● Infection
○ Pneumonia/ Bronchitis
○ Tuberculosis
○ Lung abscess
○ Bronchiectasis
● Trauma
● Tumour / Neoplastic
○ Primary: lung cancer
○ Secondary metastases
● Autoimmune
○ Wegener’s granulomatosis /
granulomatosis with polyangiitis,
Goodpasture’s syndrome

HISTORY
Complaint: Haemoptysis → “I would like to make sure it is not due to bleeding from nose or stomach.
Have you noticed any black, tarry stools? Have you noticed any nose bleeding?”
● Onset: sudden or gradual?
o Sudden onset – pulmonary embolism, pulmonary haemorrhage
● How long? How many episodes?
● Volume of each haemoptysis
o Massive if ≥50 ml per episode or ≥200ml/24 hours
● Character:
o Fresh blood
o Pink: small amt of blood
o Brown / Rusty: mucopurulent – pneumonia, bronchiectasis
o Clots?
● Increasing in frequency and volume

Causes
● Cough, productive or non productive
● Sputum: copious amounts – bronchiectasis
● Chest pain, pleuritic
● SOB
● LOW, LOA – malignancy, tuberculosis
● Hoarseness of voice – malignancy
● Night sweats, travel/ contact hx – tuberculosis
● Fever – pneumonia, tuberculosis
● Unilateral leg swelling or pain – deep vein thrombosis / pulmonary embolism
● Recent plane travel, immobility, surgery, previous blood clots – pulmonary embolism

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 ● Trauma to chest – Haemothorax
● Orthopnea/ PND, LL swelling – congestive heart failure
● Any other bleeding sites: epistaxis, PR bleeding, malena, haematemesis, easy bruising
● Rash, joint pain – vasculitis

Course

Complications
● Symptoms of anaemia: exertional SOB or chest pain, postural giddiness, palpitations
● cardiac failure symptoms
● cachexia from malignancies
● PHQ2 and GAD 2 for malignancies

PMHx
● Malignancy: Stage, treatment
● Tuberculosis
● Deep vein thrombosis
● Bronchiectasis, childhood lung infections, recurrent chest infections
● Heart failure or valve problems
● Bleeding disorders

Drug history
● Anti platelets or anticoagulants
● Oral contraception – pulmonary embolism

Family history
● Malignancy ie Lung CA, NPC
● Tuberculosis
● Bleeding disorders

Social history
● Smoking – malignancy
● Job – asbestosis → mesothelioma

PHYSICAL EXAMINATION
T BP HR RR SpO2
[90 deg]
● Conjunctival Pallor
● Cervical lymphadenopathy – how many, nature
○ Hard and matted – malignancy
○ Firm – infection / tuberculosis

[45 deg]
● Lungs:
o Crepitations – bronchiectasis
o Findings suggestive of mass lesion – malignancy
o Consolidation – pneumonia / malignancy / pulmonary embolism
o Clubbing – malignancy or bronchiectasis
● Cardiovascular
o Loud pulmonary component of the second heart sound – pulmonary hypertension or
pulmonary embolism
o MDM of mitral stenosis
o Raised JVP, bibasal creps, bipedal edema – congestive heart failure
● LL for any swelling, calves supple – deep vein thrombosis

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INVESTIGATIONS
STAT tests:
● FBC: Leucocytosis for infection, anaemia from haemoptysis, thrombocytopenia leading to
haemoptysis
● CXR: infxn, TB, bronchiectasis, malignancy, pulmonary congestion
● ECG, INR
---------------------------------------------------
Blood tests:
● Urea electrolytes creatinine: pulmonary-renal syndromes
● ESR raised in vasculitis
● ANCA for vasculitis
Imaging:
● Computer tomography pulmonary angiogram for pulmonary embolism
● Contrasted CT thorax for malignancy
● HRCT for bronchiectasis
Others:
● Sputum gram stain and culture for infection
● Sputum acid fast bacilli smear and culture for pulmonary tuberculosis
● Bronchoscopy for biopsy of lesion
● Radiologically guided biopsy of lesion

MANAGEMENT
Pulmonary Embolism ● ED. Send tx room. Monitor vital signs.
● Supplemental oxygen

TB ● TBCU direct access

● AFB smear/ c/s
● Isolate at home and start treatment, DOT
● Airborne precaution, check who is pt staying with
● TBCU to do contact tracing

Hemodynamically stable → consider Respi direct access

Hemodynamically unstable → refer ED after stabilising

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RESPI 6. APPROACH TO DYSPNEA

CHRONIC DYSPNEA {AAFP}

SYSTEM TYPE POSSIBLE DIAGNOSIS
Pulmonary Alveolar Bronchoalveolar carcinoma, TB, chronic pneumonia
Interstitial ILD - Drugs (e.g., methotrexate, amiodarone) or radiation
(DISCO STAR) therapy, lymphangitic spread of malignancy, passive congestion
Obstructive Asthma/bronchitis/bronchiectasis, bronchiolitis obliterans,
COPD, intrabronchial neoplasm, tracheomalacia
Restrictive Kyphoscoliosis, obesity, pleural disease/effusion,
(extrinsic) pneumothorax
Vascular Chronic pulmonary emboli, idiopathic pulmonary hypertension
Cardiac Arrhythmia Atrial fibrillation, inappropriate sinus tachycardia, sick sinus
syndrome/bradycardia
Myocardial Cardiomyopathies, coronary ischemia, CCF
Restrictive Constrictive pericarditis, pericardial effusion/tamponade
Valvular Aortic insufficiency/stenosis, congenital heart disease, mitral
valve insufficiency/stenosis
GI Dysmotility Gastroesophageal reflux disease/aspiration, neoplasia
Psychological Anxiety/ hyperventilation
Neuromuscula Metabolic Acidosis
r
Neurogenic Amyotrophic lateral sclerosis, muscular dystrophies, phrenic
nerve palsy, poliomyelitis
Systemic Anemia

HISTORY
Shortness of breath
● Duration
● Onset
● Exacerbating – worse on exertion, worse after contact with certain allergen, worse in morning/
night, severity
● Relieving factors
● Severity/ Effort tolerance

Associated symptoms
● Fever, Cough, sputum, colour of sputum
● LOW, Haemoptysis, Chronic smoker
● Night Sweats, Prev TB, Contact / Travel hx
● Wheeze, atopic features, hx of asthma
● Chronic smoker, hx of COPD
● Recent immobilization, LL swelling, surgery
● Joint pain, rash

● Chest Pain / Palpitations / Giddiness

● Orthopnea / PND, ankle swelling

● GI bleed / GU / Menorrhagia

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 ● Reflux
● Anxiety / other a/w somatic symptoms ie numbness
● Muscle weakness

Course
● Number of exacerbations, intubations/hospitalisations/ICU admissions

Complications
● Cardiac failure/renal failure/liver failure symptoms
● Work and school life
● Syncope for anaemia
●

PMHx:
● Rheumatological conditions, TB, vasculitis
● Heart failure

Drug history: As above that can cause pulmonary fibrosis

Psycho: GAD-2, PHQ-2

Social history: Smoking (COPD)

Occupation: Any exposure to asbestos, coal, silica – self and close family/ friends, improvement during
weekends / off-days?

PHYSICAL EXAM **HAND RUB**

T BP HR RR SpO2 BMI
{seated} Cervical LN
Hands: clubbing, RA, scleroderma, Gottron’s papules of DM
Conjunctival pallor / Icterus
{45o} JVP
H: dilated apex beat, any murmurs
L: crepitations (fine or coarse), wheeze – distribution, radiation marks
Ankle swelling, KIV DRE / abdo exam if anemia
KIV mental state exam

INVESTIGATIONS
● STAT tests
● CXR
Pulmonary fibrosis: reticulonodular infiltrates
Bronchiectasis: thickened airways, tramlines/ ring shadows
Congestive heart failure
Hyperinflated lungs in COPD
● ECG
● FBC for anaemia
--------------------------------------------------------------------------------------------------
● Spirometry:
○ Restrictive pattern for pulmonary fibrosis
○ Obstructive pattern for COPD, bronchiectasis, asthma (reversible)
● HRCT:
○ Pulmonary fibrosis: reticular abnormalities, ground-glass changes and honeycomb
changes in the lungs, look at distribution
○ Bronchiectasis: widening of the airways compared to the adjacent vessel (>1.5x),
signet ring sign; distribution and complications

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 ● ABG for respiratory failure
● CTPA for PE
● Renal panel
● Liver panel

MANAGEMENT
● Dependent on diagnosis
○ TRO PE → refer ED
● Preventive
○ Flu, pneumococcal vaccine
○ Smoking cessation

APPENDIX

Well’s criteria for PE: Don't Die Tell The Team To Calculate Criteria
Don’t - (DVT symptoms) 3 points
Die (Diagnosis most likely PE) 3 points
Tell (Tachycardia) 1.5 points
The Team (at least 3 days of immobilization, or surgery in the past 30d) 1.5 points
To (Thromboembolism in the past [DVT or PE]) 1.5 points
Calculate (Coughing up blood [hemoptysis]) 1 point
Criteria (Cancer) 1 point

The modified Wells Criteria

> 4 PE is likely
≤ 4 PE is unlikely

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RESPI 7. APPROACH TO WHEEZE
Differentiate wheeze (expiratory) from stridor (inspiratory)

Ddx 1
Lung Cardiac GI
● Intraluminal: FB ingestion ● CCF ● GERD
● Luminal: Asthma, COPD, Bronchitis
● Extraluminal: Extrinsic compression from lymphadenopathy

DDx 2
1. Occupational asthma
2. Asthma (non occupational)
3. COPD
4. Bronchitis
5. Heart failure
6. Foreign body ingestion
7. Extrinsic compression of airways from lymphadenopathy

HISTORY
Wheeze:
● Ask patient to demonstrate or clarify what he means by wheezing
● How long? Progression? Onset?
● Worse in the day or at night? Diurnal variation? Or when lying down?
● Is onset related to any particular triggering factor? ACDE-I for asthma
(keep in mind that occupational asthma can occur years after first exposure)
● Any exacerbating or relieving factors?

Causes
● A/w respiratory symptoms: cough, haemoptysis, SOB, chest pain, rhinorrhea
● Fever, recent URTI (bronchitis)
● NIE - Nocturnal symptoms, interval symptoms, exercise induced (Asthma)
● Foreign body ingestion?
● Rash, renal problems (Churg Strauss vasculitis)
● Orthopnea/ PND/ exertional symptoms (heart failure)
● Reflux, regurgitation (GERD)
● LOW/ LOA, other lymphadenopathy (extrinsic compression of airways)
● FULL OCCUPATIONAL HISTORY
o Nature of job
o What allergens pt is exposed to at work?
o Are symptoms worse at work and better on weekends and holidays?

Course
● Previous spiro?
● Previous treatments?

Compliance
Complications: Function limitation

PMHx:
● Asthma (full asthma history ie risk assessment)
o Onset and progression
o Medications: on what inhalers or oral meds, compliance and assess inhaler technique

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 o Triggering factors
o How many attacks a year? How often using Ventolin inhaler?
o Previous intubation or MICU admission for asthma?
o Any a/w eczema, allergic rhinitis, allergic conjunctivitis
o Any pets at home, carpets, soft toys
● Heart failure/ IHD

Drug Hx: ßblocker/ NSAIDS

FHx: Asthma, allergic rhinitis, eczema
Social history: Smoking (for COPD), Occupation, Hobbies – any possible allergens, anyone smokes at home
Psy Hx: PHQ2, GAD2

PHYSICAL EXAMINATION
T BP HR RR SpO2 Wt (impt in CCF)
{Seated} Pallor, respiratory distress
Head: allergic shiners, nasal turbinates, sinus tenderness
Neck: cervical LNs
{45deg} JVP elevated
H: apex beat, murmurs
L: bibasal creps, rhonchi
Pedal edema

INVESTIGATIONS
Stat tests
● FBC: raised total white cell count in bronchitis, eosinophilia in asthma, ABPA, Churg Strauss
vasculitis
● CXR: FB and signs of heart failure, lymphadenopathy, cardiomegaly
● KIV ECG if CCF

Other tests
● Urea creatinine and electrolytes for impaired renal function in Churg Strauss vasculitis
● Others: Metacholine challenge test for asthma, serial peak flow monitoring at work q2hrly to look
at variation during exposure and post exposure, spirometry

MANAGEMENT
Asthma exacerbation refer to asthma

COPD exacerbation refer to COPD

Undiagnosed obstructive airway disease

Cardiac wheeze refer to CCF

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RESPI 8. SMOKING CESSATION

Check reasons for smoking

Check for complications of smoking: IHD, COPD , PAD

HISTORY
5A approach
1. Ask:
a. Do you smoke?
b. If yes, how many sticks per day? How many years have you been smoking?
2. Advise: Inform on adverse effects of smoking. If patient has a chronic condition, relate patient’s
smoking with disease.
3. Assess: Evaluate stage

4. Assist (see non pharm and pharm management below)

5. Arrange follow-up

PMHX: CVRF, Seizure, Mental Health illness

Vaccinations: Flu / Pneumoccocal

Physical Examination
BP HR BMI (baseline weight)
Look for complications of smoking incl lung cancer

Investigations: Usually not necessary

Management

477
Non pharm
● Set target quit date
● Optimize social environment
● 4D
○ Distract (Stay away from friends who smoke)
○ Delay (ask patient to wait for 5 minutes when you feel urge to smoke)
○ Drink water
○ Deep breathing
● Anticipate with patient possible roadblocks
○ Nicotine withdrawal symptom (irritable, anxious, restless): Peaks in 1 week duration up to 4
weeks. NRT can be helpful (see below on how to give)
○ Depression:
○ Weight gain: Advise exercise, diet.
Pharm
● NRT (2 NRT products)

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RESPI 9. HOW TO READ SPIROMETRY
Look at FEV1/FVC first then FEV1 % change and volume change

COPD - post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation with no
reversibility in FEV1 post bronchodilator

Asthma– FEV1/FVC < 0.70 (pre/post) with positive bronchodilator response

> 12% increase in FEV1 AND
> 200mls increase in FEV1 or FVC
post bronchodilator challenge

481
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484
RHEUM 1. APPROACH TO JOINT PAIN

Possible cases
1) Gout
2) Psoriatic Arthropathy
3) Rheumatoid Arthritis of Hands
4) Osteoarthritis of Knee
5) Dermatomyositis / SLE / Polymyalgia Rheumatica
6) Acute (less likely to come out) : Disseminated Gonorrheal infection

Ddx 2
VITAMIN CD
Vascular: Avascular necrosis
Infection: Septic arthritis → TB, Gonorrhoea
Traumatic: Haemarthrosis, fracture
Autoimmune: RA, dermatomyositis, SLE, {Seronegative Spondyloarthritis - RAPE (Reactive arthritis,
Ankylosing Spondylitis, Psoriatic arthropathy, Enteropathic arthritis ( IBD) }
Metabolic: Gout and pseudogout
Iatrogenic
Neoplastic: Tumor (primary and secondary)

Congenital: Developmental dysplasia of the hip

Degenerative: OA

485
*** Rmb Gonococcal !!!!

** Night and Rest Pain impt

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** Constitutional Symptoms

** RA : Red eyes, SOB, neck pain/ numbness/ weakness from cervical myelopathy or CTS)

PMHx: Arthritis, CTDs, skin disorders

Drug history:
- Drug allergy: esp to NSAIDs as it is mainstay therapy in RA
- Thiazides / Indapamide ppt gout
- Procainamide or hydralazine causing drug induced lupus
- Betablockers/ ARB /ACE-I precipitating psoriasis

Family Hx RA or CTDs

Sexual Hx:
- Especially if suspecting gonococcal arthritis!!!
- Previous STIs? Previous STI screening for self, for partners?

Social history/ Functional Hx

- WASHED
- Handedness/ ambulation status
- ADLS - DEATH, SHAFT
- Effect on occupation/Finances/ Family Planning
- Occupational or leisure activities that may predispose to joint pains (housemaid’s knee)

Psych Hx:
Preventive Health:

PHYSICAL EXAMINATION
Refer to template below

INVESTIGATIONS (From IM notes)

Blood test:
FBC (looking for raised total white cell count or anaemia of chronic disease,
ESR / CRP
Rheumatoid factor (70% of people with RA will be positive) / Anti-CCP / ANA
Renal Panel
LFT (for drug of choice ie methotrexate and monitoring)
Imaging:
● X-rays of the joints (in RA looking for soft tissue swelling, juxta-articular osteopenia, decreased
joint space, then as disease gets more severe, erosions, subluxation, joint destruction)
● C- spine for Altantoaxial subluxation in RA
Others: joint aspiration if there is effusion present

MANAGEMENT
Septic Arthritis - Refer to A&E for joint aspiration and IV abx
(including - Synovial fluid cell count, gram stain, bacterial culture, crystals (WBC >
disseminated 50k -> suspicious of bacterial infx)
gonorrhoea)
- Check for other STD , STD prevention advice
- Contact tracing for partners within last 60 days of contact and tx
- Notify MOH via CD Lens

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Seronegative - PT/OT
Arthropathy - NSAIDS 1st line regular for 4 weeks
(RAPE: - Intraarticular corticosteroids for mono/oligoarthritis only, limited role
Reactive Arthritis for systemic steroids
Ankylosing Spondylitis - Refer to rheumatologist
Psoriatic Arthropathy - DMARDS ie MTX and Sulphasalazine for peripheral arthritis /uveitis/
Enteropathy extra-articular, NO ROLE FOR AXIAL DZ
associated) - Anti-TNF (monoclonal antibody ie infliximab) for both axial and
peripheral
** Refer to Psoriasis for Mx of Psoriasis

Rheumatoid Arthritis PT/OT

NSAIDs and Prednisolone
Refer to Rheumato for DMARDs, Immunomodulators or biologics (anti-
tumour necrosis factor, Rituximab)

SLE Acute flare of SLE -> Refer ED

NSAIDS
Topical steriods, Sunblock for rashes
Refer to Rheum for DMARDS, Immunomodulators or biologics

Dermatomyositis Non-pharm: Sun avoidance and sunblock for skin mx

PT/OT – to maintain joint function and reduce risk of contractures

Pharm: Consider steroids

Refer to Rheum
Need to screen for malignancy
Muscle disease – Steroids, DMARDs, IVIG and Biological Agents
Skin – Hydroxychloroquine and MTX
Calcinosis – Diltiazem, Bisphophonates, Surgery

Suspect ankylosing
spondylitis

KIV FBC, ESR

Refer for w/u

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Specific Conditions
1) Rheumatoid Arthritis
● Extra-articular changes:
○ Eyes: conjunctiva pallor in anemia, episcleritis, scleritis, keratoconjunctivitis sicca, cataracts
from steroids, Ophthalmoplegia from mononeuritis multiplex or myasthenia due to
penicillamine
○ Lungs: interstitial lung disease, pleural effusion, pneumonitis, pneumothorax, bronchiolitis
obliterans with organizing pneumonia
○ Heart: AR
○ Abdomen: Splenomegaly in Felty Syndrome
○ Neurological: Cervical myelopathy due to atlantoaxial subluxation, peripheral neuropathy,
nerve entrapment ie carpal tunnel, mononeuritis multiplex, proximal myopathy due to
steroids
● 5 causes of anemia in RA: Anemia of chronic disease, Fe Deficiency (GI bleed from NSAIDS),
Pernicious anemia, Hypersplenism from splenomegaly in Felty Syndrome, Aplasia due to
Gold/Penicillamine
● Acute: in RA flare, pt might require course of steroids and NSAIDS
● Chronic:
○ Multidisciplinary
○ Non pharmacological / Education
■ Patient education regarding disease progression
■ Physiotherapy, occupational therapy, use of splints
● Pharm: NSAIDs, DMARDs (refer below), Immunomodulators or biologics (anti- tumour necrosis
factor, Rituximab (ANTI CD20)
○ DMARDs can take up to 6 – 12 weeks for symptomatic benefit
○ Methotrexate and sulfasalazine are typical first line choices and may be used together
○ Methotrexate: avoid in liver disease, pregnancy and if alcoholic. SE: oral ulcers, nausea,
myelosuppression, hepatotoxicity, pneumonitis. Give concurrently with folic acid
○ Sulfasalazine: SE: myelosuppression, nausea, rash, oral ulcers, decreased sperm count
○ Penicillamine: SE: myelosuppression, renal toxicity, loss of taste, oral ulcers, MG-like
syndrome
○ Hydroxychloroquine: Least toxic but probably least effective. SE: Rash, retinopathy. Will
need review by Eye
○ Azathioprine: SE: myelosuppression, nausea, raised LFTs
○ Ciclosporin: SE: nausea, tremor, gum hypertrophy, renal impairment
● Surgical: Surgery for joint replacement

2) Ankylosing Spondylitis
- Follow Ortho Spine exam
- Special features: Occiput to wall, Schober’s test, FABER test, Chest Expansion
- Extra-articular: Anterior uveitis, Atlanto-axial sublux, Aortic Regurg, Apical Interstitial lung disease,
Enthesitis
- A/w: Reactive arthritis, Psoriatric arthropathy, IBD
- Mx:
● PT/OT
● Regular NSAIDs for 4 weeks at least
● Sulphasalazine only for peripheral arthritis ie knees, ankles, not for axial dz
● Refer to Rheumatologist for long term anti-inflammatory medications such as anti-TNF alpha
antagonist

3) SLE
SLICC criteria for the classification of systemic lupus erythematosus

489
(4 of 17 criteria, including at least one clinical criterion and one immunologic criterion;¶ OR biopsy-proven
lupus nephritisΔ)
Clinical criterion: A RASH POINT MD
A - Arthritis - non erosive peripheral joint
R - Renal Disorder - proteinuria >0.5g/day or 3+ on urine dipstick
A - ANA (Under immunologic criterion)
S - Serositis (pericaridis, pleuritis)
H - Haematological - hemolytic aenmia, leukopenia , lymphopenia , thrombocytopenia
P - Photosensitivty
O - Oral Ulcers
I - Immunological criterion (refer below)
N - Neurological disorder - seizure, psychosis
M - Malar Rash - spare nasolabial folds compared to dermatomyositis
D - Discoid Rash

Immunologic criterion: ANA, Anti-dsDNA, anti-S,. anti phospholipid ab

4) Reactive arthritis due to STI ie Chlamydia

● If no fever, less likely septic arthritis -> just treat underlying STI
● STI prevention advice

5) Disseminated gonococcal infection

● 2 forms
○ Triad of tenosynovitis, polyarthralgia, rash (gray pustules with erythematous base on
extremities and trunk
○ Purulent arthritis ± associated findings
● Invx: Blood c/s x2, swabs from mucosal sites, synovial fluid joint aspiration
○ Also screen for other STIs: Chlamydia, syphilis, hepatitis B, HIV
● Diagnosis made on N gonorrhea isolated on specimen of blood/tissue/synovial fluid/skin/non-
mucosal site
● Refer ED
○ IV Ceftriaxone 1g OM + PO Azithromycin 1g once
○ Tenosynovitis, dermatitis, polyarthralgia → ABx ≥7/7
■ Once initial clinical improvement with IV Ceftriaxone 1g OM for 24-48h, can change
to IM Ceftriaxone 250mg Q24H
○ Purulent arthritis → IV ABx until response seen (usually 7-14/7 IV ABx)
● STI prevention advice
● Partner management: contact, offer testing, treat presumptively (IM ceftriaxone 250mg OM + PO
azithromycin 1g
● Notification once gonorrhea confirmed but can be anonymous!

6) Dermatomyositis
Definition: Idiopathic systemic disease with characteristic cutaneous findings and inflammation of the
muscles, with proximal myopathy. (Polymyositis = Dermatomyositis without cutaneous findings)

Diagnostic Criteria (rash + 3⁄4):

- Symmetrical proximal muscle weakness (with or without dysphagia or respiratory muscle involvement) -
Elevated skeletal muscle enzyme (CK and aldolase)
- Abnormal EMG
- Abnormal muscle biopsy

490
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Add in request or do the additional steps for the different rheumatological conditions

493
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RHEUM 2. APPROACH TO GOUT
Stem:
1. Newly diagnosed gout with frequent attacks or tophi
2. Chronic gout with poor control due to diet/drugs/non-compliance (frequent attacks, suboptimal
uric acid)
3. Chronic gout with poor control in a CKD patient

HISTORY
Complaint Joint pain/swelling
(acute) Tophus complaint
Loin to groin pain from uric acid renal stone
**Always ascertain that it is truly gout (clinical history: acute usually occurring at night
onset of maximal pain intensity within 24h with improvement and complete resolution
within 2-3/7, joint aspiration proven, XR proven - punched out ‘moth eaten’ appearance
juxtapositioned to articular regions (usually small joints), examination - presence of
tophi) before proceeding
Cause ⇾ Rule out differentials for joint pain: Fever/ Trauma/ Recent injections/Rashes
⇾ Primary vs secondary gout
Primary
● Diet:
○ Animal purine rich food (animal organs, shellfish, red meat)
○ Alcohol
○ High fructose corn syrup (soft drinks)
○ NO need to avoid soy, beans, legumes (plant purine rich) NUS study
Secondary
● Medication induced:Diuretics
● Lymphoproliferative / myeloproliferative disorders
● Psoriasis
● Hemolytic anemia
● CKD
Course - Who is following up?
- What treatment are you on?
Control - Uric acid level (target 360 or 300)
- Clinical flare up: >2 per year, or > 1 per year in CKD stage 2 and above
- Gouty tophi
- History of stones
Compliance - Low purine diet
- Drug compliance: any change in medication dosage
Complication - Disease Cx: Renal impairment (urate nephropathy), Kidney stones
- Treatment Cx: Rashes (ADR including DRESS, TENS and SJS)**, Transaminitis
(Allopurinol), AoCKD (NSAID Cx), Cushingoid features (2o chronic steroid use)
** DRESS = type 1 hypersensitivity (occurs immediately within a few days)
TENS and SJS = delayed hypersensitivity (occurs up to 4/52 after starting medication)
Competency - Medication administration
Co-morbids - Risk factors for gout: Obesity, IHD, CKD, Smoking
- HTN
- Alcohol: CAGE

497
 Other Hx PMHX: CVRF, secondary causes as above
Drug Hx : above
Social Hx / Function Hx : Alcohol, Smoking, Occupation , How has your gout pain
affected your daily routine / work
Psych Hx:
PHYSICAL EXAMINATION
T BP HR BMI
Foot exam (Look, Feel, Move), Achilles Tendon, Gait
Hand exam (including hand function: open cap, take out coin)
Ears and elbow: tophi, extensor nodules
INVESTIGATIONS
- Depends on scenario
- If initiating - AST ALT FBC Uric Acid Creatinine UFEME
- FPG, lipid panel
MANAGEMENT
Non-drug
- Low purine diet counselling: LImit animal organ, shellfish, alcohol
- Control CVRF - exercise, lose weight
Drug
- ACUTE FLARE: EITHER NSAIDS (if kidney normal) or PREDNISOLONE (if kidney function poor);
COLCHICINE (renal dose adjusted if need be)
- INDICATIONS FOR URATE LOWERING THERAPY (ULT): >/=3 attacks per year, tophi, erosions on
XR
- START ULT even in acute flares with adequate prophylaxis (based on new guidelines by NUH
rheum)
- Colchicine prophylaxis 500mcg daily (if no renal impairment), EOD (if some renal impairment)
- Titrate ULT till target uric acid is achieved (generally no ceiling dose for allopurinol but mention
800mg as part of CPG and conventional guidelines)
- S/E of allopurinol: Rash, fever, oral ulcers (SJS), DRESS
- S/E of colchicine: diarrhoea
- Caution with statins ೱ
- If taking colchicine TDS with statin for acute flare of gout -> Stop statins temporarily
- If taking colchicine OM with statin for prophylaxis -> Monitor for muscle weakness, red urine

Education
- Educate on disease complications if not well controlled: Joint deformities with impaired
function. Educate on kidney stone risk which can hurt kidneys.
- Educate on crisis management: take Colchicine at first sign of flare
Follow-up
- Review in 2/52 for FBC, ALT/AST then 4/52 to assess response then 3/12 to ensure target UA
reached
- UA at target? How many flares?
- Check other comorbids - ie FG/ lipid panel
Crisis
- Colchicine 500mcg OM prophylaxis when initiating or increasing Allopurinol
- + Colchicine 500mcg TDS during gout flare x 3-5 days
- + NSAIDs during gout flare x 3-5 days (prednisolone if CKD)

Allopurinol: 1st line for gout as proven to have cardiovascular and renoprotective effect
● High risk for ADR if: initiation dose too high, Han Chinese female

498
Probenecid: alternative if allopurinol is not suitable, contraindicated if presence of renal stones or renal
impairment eGFR <30
Losartan, Fenofibrate, Atorvastatin = moderate uricosuric effect (can consider switching to these meds in
patients with IHD)

ೱ NHGP:
Statins Duration of Duration of Recommendation
Macrolide Colchicine
On Statins < 2 weeks Withhold statin while taking macrolide is taken, resume after the macrolide
has been stopped.
On Statins < 2 weeks Withhold statin while taking Colchicine is taken, resume after colchicine has
been stopped.
On Statins > 2 weeks Consider continuing statins and colchicine concurrently, while monitoring
e.g. gout for symptoms and signs of rhabdomyolysis/myopathy and creatinine kinase
prophylaxis (CK).

Consider checking patient’s CK after 2 weeks of taking statin and colchicine

concurrently. Assess at review if further monitoring of CK is required. (e.g. 6
weeks)
On/off Any duration Any duration AVOID prescribing colchicine and macrolide antibiotics together due to
Statins reported fatal interactions, and consider prescribing an alternative
combination.

NHGP Low Purine Diet pamphlet:

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RHEUM 3. APPROACH TO PSORIASIS

Important points in the Hx:

- Nature / Distribution/ Course of a rash on bg of psoriasis + ddx for rash
- Triggering factors
- Complications affecting other organ systems in psoriasis + ddx for joint pain
- CVRF screen
- Psychosocial + Function/ Occupation!
- Treatment plan – topical, supportive mx, consider referral for immunosuppression and psychosocial
support
===========================================================================
Definition: Multi-factorial chronic relapsing inflammatory skin disorder that can also involve nails and
joints, involves hyperproliferation of keratinocytes in the epidermis with increase in epidermal cell turnover
rate.

The patient’s palm can be approximated to be 1%. Mild psoriasis has <3% of body surface area
involvement. Moderate psoriasis involves 3-10% of the body surface area. Severe psoriasis involves more
than 10% of body surface area.

HISTORY
● Skin – Chronic plaque, Guttate, Generalised pustular, GED/erythrodermic (scalp, elbows, knees,
sacrum)
● Arthropathy + enthesitis/ tendinopathy– SORIA – Spondylitis ± sacroilitis , Oligoarthropathy with
dactylitis, RA type, Distal IPJ, Arthritis mutilans
○ (Ask which hand joints involved, any back pain/ hip pain /heel pain in TA)
● Nail changes – PSORIA – Pitting, Subungal plaque creating oil spot sign, hyperkeratosis, Onycholysis
an dystrophy, Ridging, Increased thickness (subungal hyperkeratosis)
● Eyes – Uveitis/ conjunctivitis, keratitis, blepharitis, sicca

Course:
- When diagnosed, f/up where, any ix done , any creams or medications tried ie DMARDS like methotrexate

Cause / Triggers for psoriasis:

- Stress
- Strep throat infection
- Trauma (Koebner’s phenomenon)
- Drugs!!!: ßblocker, ACEi/ARB, NSAIDs, steroid withdrawal, Li, anti-malarials, tetracycline, gemfibrozil,
terbinafine
- Autoimmune / genetic : HLA B27 (seronegative spondyloarthropathy), immune mediated
- Worsen psoriasis: smoking, alcohol , obesity

Differential Diagnosis:
● IBD arthropathy / Reactive arthritis / RA (bloody diarrhoea, dysuria, red eye, arthropathy sparing
DIPJ, mainly MCPJ/ PIPJ
● Eczema /Lichen planus/Lichen simplex chronicus /Lupus

Control: How frequent are the flares

Compliance to meds
Complications of disease:
- CVRF: DM/ HTN/HLD / IHD / CKD
- Others: Increased risk of lymphoma, crohn’s disease
- Psychosocial: depression, anxiety, financial difficulty
- Function / Occupation: destruction of joints, ADLs, Pain on squatting and getting up from squatting
position in sacroilitis
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Complications of Tx
NSAIDS :Gastritis/BGIT/Renal impairment)
Topical steroid : thinning of skin, easy bruising

PMHx: Any CVRF

Drug Hx : (Important for triggers!)
Family Hx : Psoriasis/ autoimmune conditions
Social/Function: As above

PHYSICAL EXAMINATION
- Inspection for extent of rash, Hand examination
1. Skin – well demarcated plaques with silvery scales found typically over extensor surfaces of
scalp/retroauricular/elbows/umbilical/lumbosacral/genital/perineal/knees

2. Arthritis
- RA type involves DIPJ (RA does not), with NAIL PITTING or other nail changes (oil spot sign, onycholysis
and dystrophy, ridging, hyperkeratosis)
- Dactylitis (sausage fingers from uniform inflammation of flexor tenosynovium)
- Arthritis mutilans – severe deformity with telescoping of fingers/toes (from reabsorbing of bone)
- Ankylosing spondylitis/ sacrolitis – Schober’s test, Faber’s test

3. Activity of Arthritis
- Skin: Koebner’s phenomenon, increased size of plaques, new plaques

4. FUNCTION

INVX (lab results are non specific in psoriatic arthritis)

- FBC (also can r/o reactive post infectious arthritis)
- ESR
Pre treatment bloods: FBC, renal and liver panel, TB screen, hepatitis screen (especially if starting biologics)
- RF/ANA – usually negative (rule out differentials)
- Skin biopsy
- Synovial aspirate – inflammatory picture
- XR – pencil in cup deformity (marginal bone erosions), joint space narrowing with ankylosis or joint space
increase due to destruction, unilateral sacroilitis, soft tissue swelling, syndesmophytes with sparing of
segments (in vertebral XRs)

MANAGEMENT
Education/ Non pharm
- Educate patient on the chronic relapsing nature of psoriasis
- Stop aggravating drugs
- Stress mx
- Avoid scratching
- Counsel on support groups (Psoriasis Association of Singapore)
- Lifestyle modification for associated CVRF and preventive health

Pharmacological
1) Stable Chronic Plaque Psoriasis
- Topical coal tar 10% ON or BD
- Topical Steroids (Low-moderate potency)
- Emollients
- Topical vitamin D and/or retinoid (must avoid sun)

502
- Oral retinoids (cannot get pregnant, decrease night vision, cataracts, corneal opacities, blephraritis, dry
eyes, GI discomfort)
- TNF alpha antagonist – reactivation of TB, increase susceptibility to infections, injection site and infusion
reactions, lupus like illness
- MTX and other DMARDS (marrow toxicity, toxicity to liver, renal damage for cyclosporine)

2) Scalp Psoriasis
- Coal Tar Shampoo 10% ON or BD
- Betamethasone 0.1% Scalp Lotion BD

3) Psoriatic arthritis
- If mild → NSAIDS (GI bleed, renal impairment)
- If severe, refer for
● DMARDS - MTX and other DMARDS (marrow toxicity, toxicity to liver, renal damage for
cyclosporine)
● Intra-articular steroids
● TNF alpha antagonist (reactivation of TB, increase susceptibility to infections, injection site and
infusion reactions, lupus like illness)
- PT/OT for maintenance of ROM

4) Uveitis/other eye complications

- Use topical steroids/lubricants and refer eye

5) Misc
- Treat depression if present (increase risk due to chronic disease) - Explore work environment, teach
stress management

When to refer for Specialist Consultation

- Unsatisfactory response to topical treatments such as steroids or coal tar
- Psoriasis affecting more than 10% BSA (Body Surface Area)
- Patients who may benefit from phototherapy or systemic therapy
- Guttate / Pustular / Erythrodermic Psoriasis
- Psoriatic Arthropathy

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504
 UROLOGY 1. APPROACH TO LOWER URINARY TRACT SYMPTOMS (LUTS)

Possible Cases
UTI / Pyuria - Exclude STI
- Ensure no prostatitis/ abscess
- Refer to Urethritis document!

BPH - Exclude other causes of obstructive symptoms

- IPSS scoring regarding severity
- Discuss PSA testing
- Non-pharm and pharm mx and s/e

DDx:
Luminal Mural Extraluminal Systemic
● Distal ● Urethral Stricture ● Faecal impaction ● Neurogenic
urethral ● BPH, Prostate CA ● Pelvic tumour bladder
Stone ● UTI - Urethritis / Prostatitis/ ● Diabetes
● FB Cystitis/ Epididymitis ● Drugs
● OAB, Detrusor over or under
activity

HISTORY
Voiding symptoms Storage symptoms
- Dysuria - Frequency
- Hesitancy - Urgency
- Interrupted flow - Nocturia
- Sensation of incomplete emptying - Incontinence
- Weak flow
- Dribbling
- Double voiding

- Duration of symptoms
- Other associated symptoms: Fever with loin pain and vomiting , cloudy urine, abdominal pain
Gross haematuria, acute retention of urine,
- Urethral d/c , Sexual History (Urethritis)
- LOW, back pain , fam hx of prostate ca ( prostate ca)
- Constipation
- Abdominal mass
- Saddle anaesthesia, bowel continence, previous back trauma (neurogenic bladder)
- Past medical history: DM, CCF, Parkinson’s
- Past surgical history: Procedures like indwelling catheter, cystoscopy, bladder stones, TURP
- Medication list: Diuretics, anti-psychotics, Traditional medications, Supplements
- Social History: Coffee, tea, alcohol drinking, smoking, occupation affected LUTS
- Family hx: Prostate Ca

PHYSICAL EXAMINATION
BP HR
Inspection: cachexia
[supine]
Abdominal: Mass, Palpable distended bladder, Inguinal hernia

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DRE: Prostate size, consistency, median sulcus, tenderness
**Red flags: Irregular, hard, nodules, Rectal mass, poor anal tone
Penis: Phimosis, Hypospadius
Others: Motor and sensory function of perineum and lower limbs, gait.

INVESTIGATIONS
- UFEME to screen for pyuria, hematuria, proteinuria or other pathology
- Urine culture if UFEME abnormal.
- KIV Baseline PSA

- IPSS scoring for BPH (in the exam charts)

Scoring interpretation: IPSS 0-7 = Mild | 8-19 = Moderate | 20-35 =
Severe
QOL <3 not bother ≥3 bothered

MANAGEMENT
Urethritis / Refer to urethritis symptoms document
Prostatitis/
Epididymitis
BPH Non pharmacological
o Cut down fluid intake at night, avoid caffeinated drinks, timed or organised
voiding
o Lifestyle advice: stop smoking, Lose weight if BMI is high, mx co-morbids

Pharmacological: Start if IPSS score ≥8 and QOL score ≥3 (Bothered)

1) Alpha-blockers ie alfuzosin, tamsulosin
● Relax the muscle around prostate and bladder neck
● Improvement in symptoms in weeks to months
● S/E – postural hypotension, giddiness, infertility due to retrograde ejaculation

Combination therapy with 5-alpha reductase if IPSS >20

2) 5- alpha reductase inhibitors ie finasteride (Refer to urologist)
● Reduce the size of prostate, take at least 6/12 to work
● Only use if prostate volume > 30g or PSA > 1.5 ng/dL and if BOO symptoms
and OAB
● S/E: Decreased libido, Erectile dysfunction, Ejaculatory disorders, Mastalgia,
Gynaecomastia.

F/up
- TCU in 4 weeks after initiation of alpha blockers, assess S/E
- TCU in 3 months for alpha reductase inhibitors, assess S/E
- Assess IPSS score for improvement, yearly PSA
Overactive Bladder Non pharmacological advice
● Limit fluids to 1.5L /day, cut down fluids after 6pm, stop last drink 2 hrs before
bedtime . limit caffeine/ alcohol intake to 2 cups before 2pm
● Avoid voiding at first sensation; distract yourself, prolong urge interval, timed
voiding
● If a/w urge/stress/involuntary urinary incontinence → Pelvic floor exercises:
Kegel’s exercises

Pharmacological

506
 ● Anticholinergic ie detrusitol (tolterodine) 1mg ON or oxybutynin to reduce
detrusor hyperactivity
● S/E : dry mouth, dry eyes, drowsiness, sedation, constipation, can worsen
cognitive impairment

Other Notes
Discussion with patient regarding testing of PSA
- Not recommended for screening
- Discuss with pt if symptomatic or if pt is keen and between 54 -69yo

There is a blood test called PSA that can tell us whether your condition is more likely to be cancer
If PSA > 4, higher possibility that it may be a cancer related problem , will need to send you to the urine
specialist for scan and needle biopsy
If PSA < 4, less likely to be cancer , more likely enlargement of prostate. We will monitor your conditions, If
any dangerous symptoms arise , we need to re-evaluate again.
● Locally we follow AUA guidelines, based on large PLCO (Prostate Lung Cancer Ovary) trial
○ Based in US: no CA prostate mortality benefit even after 15 years of follow up
■ No evidence that screening could be beneficial in any subgroups (comorbidity, age,
pretrial PSA testing)
■ But negative results discounted due to methodological flaws
● AUA guidelines
○ <40: Recommends against PSA screening
○ 40-54yo: Does not recommend routine screening in men at average risk (eg no positive
FHx)
○ 55-69yo: Shared decision-making – weigh benefits of preventing CA prostate mortality (1
men per 1,000 men screened over a decade) VS risks of known potential harms of
screening and treatment
○ To reduce harms of screening, routine interval of ≥2 years preferred
○ ≥70yo or any man with <10-15yrs life expectancy: Not recommended
● European association disagrees: ERSPC (European Randomized Study of Screening for Prostate
Cancer)
○ 180,000 men 50-74yo → PSA every 4 years vs no screening
○ CA prostate diagnosed more frequently but 27 additional cases of prostate cancer would
need to be detected by screening to prevent one death from prostate cancer after 13 years
○ All-cause mortality in the core group was not reduced with screening. Prostate cancer
mortality was also reduced in the entire cohort of men ages 50 to 74.
● 2010 meta-analysis and 2011 Cochrane meta-analysis:
○ Screening with PSA vs no screening did not statistically reduce death from CA prostate, but
increased cancer diagnosis
● BUT CA prostate ∆∆x of BPH hence reason to do to evaluate chances of CA rather than as primary
screen
● PSA can precede clinical disease by 5-10 years
○ Also elevated in benign conditions: BPH, prostatitis, subclinical inflammation, prostate
biopsy, cystoscopy, TURP, urinary retention, ejaculation, DRE, perineal trauma
● Harm from screening
○ Prostate biopsy
● CA prostate
○ 3rd in SG (2010-2014)

Kegel’s exercises
o Find your pelvic floor muscles – squeeze the ring of muscles around your anus as though you are
trying to avoid passing motion and wind (Can put your finger into the vagina and ask pt to squeeze)
Steps

507
1) Fast twitch – squeeze and hold for 1 second – repeat 5 times
2) Slow twitch – squeeze and hold for 5 second – repeat 5 times
3) Step 1 + 2 = 30 seconds = 1 cycle
4) To do 5 cycles (2-3 minutes) for 3-4 times a day (7-10mins)

Causes of pyuria
- Infection
- interstitial cystitis
- Cancer
- polycystic kidney dz
- Drugs – NSAIDS, diuretics, penicillin abx , PPI

Sterile pyuria
- Infection - STI ie gonorrhoea, TB , Viral infection, Interstitial cystitis, prostatitis
- Stones
- Tumours
- Polycystic kidney disease

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UROLOGY 2. URETHRITIS SYMPTOMS IN MALE

Definition: Dysuria, or discomfort with urination, is usually the chief complaint in men with urethritis and
is reported in the majority of men with gonorrhea and over half of patients with nongonococcal urethritis
(NGU). Other complaints include pruritus, burning, and discharge at the urethral meatus.

Urethritis = dysuria + discharge

DDX
Urethritis Cystitis Prostatitis Epididymitis

- Gonococcal urethritis
- Non-gonococcal
urethritis (NGU)

HISTORY
Acute
Complaint: Dysuria/pruritus/discharge
- Onset
- Duration
- Character: Brown/purulent/clear discharge
Causes
- Urethritis: associated eye redness/joint swelling or pain/fever. Sexual history.
- Cystitis: Urinary frequency/urgency/cloudy urine/abdominal or loin pain/fever
- Prostatitis: Similar to UTI symptoms/fever with chills and malaise.
- Epididymitis: Testicular/scrotal pain
Course
- Previous episodes and investigations with swab?
Complications

Sexual history
Med Hx: previous STI
Drug allergies
Drug history
Preventive: PEP/PrEP.
Psy: PHQ2. GAD2.
Social: Occupation especially if suspecting HIV. Smoking/alcohol/recreational drugs.

PHYSICAL EXAMINATION
T BP HR
General inspection: Eyes for conjunctivitis. Joint swellings/redness (septic arthritis). Rashes.
Abdomen→ palpation for tenderness. Renal punch.
Look for rashes/ulcerations/discharge. KIV offer swab if discharge seen.
Scrotal palpation for tenderness
Offer DRE for prostate nodules or tenderness and edema.

INVESTIGATIONS
- Urethral swab → gram stain to look for WBC (≥2 is positive) and gram neg diplococci
- FBC (especially if known HIV)
- First morning void of urine for Urine dipstick, UFEME, culture and nucleic acid amplification →
dipstick leukocyte +, UFEME ≥10 WBC
- Blood test: Look for HIV, syphilis.

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MANAGEMENT
Urethritis (GU - IM Ceftriaxone 250mg STAT and either Azithromycin 1g STAT or Doxycycline
and GNU) 100mg BD x 10-14 days
- Screen other STD → offer to send to DSC (syphilis, HIV, gonorrhea, chlamydia)
- Advise male pt to inform his sexual partners within last 60 days to go for
screening (female - within 90 days)
- Notify CD lens under infectious diseases act (for non-HIV conditions, no need
to give patient details, info still confidential)
- Tx sexual partners last 60 days. Advise to abstain from sexual activity at least
7 days from treatment and till asymptomatic.

Prostatitis - For patients with acute prostatitis who can take oral medications, we suggest
Trimethoprim-sulfamethoxazole (960mg orally every 12 hours) or a
fluoroquinolone (Ciprofloxacin 500 mg orally every 12 hours or Levofloxacin
500 mg orally once daily) as empiric therapy. Antibiotics should be
administered for six weeks to ensure eradication of the infection.
- Urine culture must be obtained
- If ARU occurs, suprapubic catheterize (NOT IDC)
- Refer Urology direct access

Cystitis - Nitrofurantoin 50-100mg QDS x 7/7 OR

- Trimethoprim-sulfamethoxazole (TMP-SMX) 960mg BD x 3/7 OR
- Fosfomycin single dose
- Beta-lactams
- If there are severe cystitis symptoms or concern about early involvement of
the prostate → fluoroquinolone x 5/7 (eg Ciprofloxacin 500mg BD x 1/52)
- Refer Urology direct access

510
UROLOGY 3. APPROACH TO ERECTILE DYSFUNCTION

CAUSES - VITAMN
Vascular ● HTN
● HLD
● Smoking
Iatrogenic ● Anti-HTN (beta blockers, CCB, diuretics [thiazide, spironolactone])
● Anti-depressants (SSRIs)
● Anti-psychotics
● Anti-convulsants
● Alcohol
● Opioids, illicit drugs
● CA chemotherapy
Trauma ● Trauma
● Pain
● Previous prostate surgery/irradiation
Anxiety ● Anxiety
● Depression
● Interpersonal relationship/conflict
● Stress
Metabolic ● DM
● Hypothyroidism
● Hypogonadism (testosterone deficiency)
● Obesity / Metabolic syndrome
● OSA
Neurologic ● Parkinson’s
● Multiple sclerosis
● Spinal cord injury

Ejaculatory Disorder
Psychological ● Performance anxiety
factors ● Depression
● History of sexual abuse
● Impaired self-body image

● Penile hypersensitivity

HISTORY
- Differentiate between: Decreased libido vs ED vs Ejaculatory disorder
- Any morning erections / erections when watching porn (if able to get these erections → think of
psychological / rs issues with wife causing ED)

Name/Age/Sex
BIOLOGICAL
Acute Chronic illness Medical History
TRO decreased libido vs ED vs ejaculatory disorder Cause ● Medical/
Course Surgical Hx
Complaint: Erectile Dysfunction Control ● Drug Hx/

511
 ● Onset: Sudden or gradual ● HTN Drug
● Character: difficulty obtaining vs maintaining? ● DM allergies
● Duration? Compliance ● Medication
● Triggers, precipitating events Complications List
● Frequency: every time, some of the time Checking ● TCM/OTC
● Any morning erections/ erections when watching porn (If Competency
able to get these erections → think of psychological / rs
issues with wife causing ED) Comorbidities - Sexual Hx
Crisis Mx (In general)
Complaint: Ejaculatory dysfunction for sexual
● Onset: previously normal or never had normal ejaculation disorders :
before Check for STD and
● Duration / Frequency safe sex!
● Timing of ejaculation - within 1 min of vaginal ejaucation
● Triggers/precipitating factors No. of sexual
● Any pain ? (Vaginismus) partners , tgt for
● Cause: Anxiety , Tension with partner how long, sexually
Cause active for how
● CVRF: BP control, HLD, DM, smoking long,
● Drug screen: previous anti-androgen drugs, new drugs, TCM, oral/ anal/ vaginal
alcohol sex
● Trauma, pain, prev urinary tract surgery Any protection
● Endocrine: thyroid symptoms, DM symptoms, decreased used
libido/ loss of body hair/ fatigue Any hx of STDs
● Weakness/numbness/ spinal cord injury
● PSY: PHQ2, GAD2
Course
● Tried what treatment?
● Seen other doctors for it?
● Sexual Hx
Complications
● Screen for IHD symptoms eg angina
● Psychological stress/relationship with partner
Disease Prevention Family Hx
- Vaccinations NA
- Cancer prevention
PSYCHOLOGICAL
PHQ-2 ICE
GAD-2
SOCIAL
WASHED Bladder and bowel

PHYSICAL EXAMINATION ***HAND RUB***

BP BMI Waist circumference
KIV Mental state exam
● Goitre?
● External genitalia:testicular atrophy, loss of hair in hypogonadism. Circumcised? (if circumcised,
then more sensitive → predisposes to premature ejaculation)
● Local factors over penile region causing pain
● If numbness/ weakness → LL neuro exam

512
 ● KIV DRE for prostate saddle anaesthesia / anal tone

INVESTIGATIONS
● UFEME
● ** ECG - screen for Q waves/ LVH (ED is a sign of vascular dz)
● Fasting glucose, lipid panel if not previously done
● TFT if symptomatic

MANAGEMENT
Erectile Lifestyle modifications
Dysfunction ● Stop smoking, alcohol
● Lose weight
● Exercise
● Control CVRF
● Target triggers eg stress
Pharmacological
● PDE5 inhibitor Sildenafil: PO 50mg daily, administer 30 mins to 1h before sexual
activity, max 100mg/day
○ Contraindications: if pt on nitrates
○ Monitor BP, HR, pulmonary edema KIV ECG
○ ADR: headache, flushing, hypotension, dyspepsia, visual disturbance,
epistaxis

Premature Non Pharmacological

ejaculation ● Use condoms - Durex performa (condom with anesthetics)
● Psychotherapy:improve self confidence and communication in rs thereafter
increase ejaculation latency
● Increase frequency of sexual intercourse
Pharmacological
● Topical Anaesthetics to glans 5 mins before SI
● Oral analgesics: tramadol
● SSRIs: Paroxetine 10-40mg/day, Fluoxetine 20-40mg/day, Escitalopram 10-
20mg/day

Premature ejaculation
Defined as
- Ejaculation that always or nearly always occurs prior to or within~1 min of vaginal penetration,
either present from the first sexual experience or following a new bothersome change in
ejaculatory latency;
- The inability to delay ejaculation on all or nearly all vaginal penetrations; and
- Negative personal consequences, such as distress, bother, frustration, and/or the avoidance of
sexual intimacy

Causes
- Uncertain or obscure in most cases
- Psychological factors such as a history of sexual abuse, impaired self-body image, depression, and
performance anxiety
- Possible negative conditioning and penile hypersensitivity

513
Case scenario: Erectile dysfunction 2 to SSRI
1) Depressed patients who are both unresponsive to SSRIs and troubled by SSRI induced sexual
dysfunction are typically switched to non-SSRI antidepressant such as bupropion 100 mg BD; after 3
days may increase to the usual dose of 100 mg TDS (UTD) , write memo to primary psychiatrist
regarding change in medication
2) For Depressed patients who respond to SSRIs but suffer sexual dysfunction include
- Decrease dose of SSRI and waiting for spontaneous remission of sexual impairment
- Switch to a non-SSRI antidepressant or a different SSRI
- Using a second drug to offset the adverse effects such as Viagra

514
 UROLOGY 4. APPROACH TO HEMATURIA

Differential diagnoses: Cyst, Infection, Stone, Cancer, Trauma, Systemic, GN

Sites of bleed Conditions
Pre-renal causes ● Arterio-venous malformation
● Renal artery disease: hypertension, thrombosis
● Renal vein disease: renal vein thrombosis
Renal causes ● Polycystic kidney disease, kidney cysts (eg ADPKD)
● Pyelonephritis
● Renal cell carcinoma
● GN:
○ Post streptococcal glomerulonephritis
○ Lupus nephritis
● Henoch Schonlein purpura, IgA nephropathy
Post-renal causes ● Ureters: Ureteric stones
● Bladder: bladder stones, cystitis, bladder cancer
● Prostate: prostatitis, BPH, prostate cancer
● Urethritis
Systemic causes ● Any cause of easy bleeding: thrombocytopenia, coagulopathy, vasculitis
● Anti-platelets, anti-coagulants

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HISTORY
Complaint: Haematuria
● Character: Frank blood, mixed with urine, brown, clots
● Duration, onset
● Present at which part of stream?
o Throughout (bleeding from bladder or above)
o Beginning of micturition and clears towards end of stream (bleeding from urethra)
o End of micturition (prostate or bladder base)
● Painless or painful
● Severity, progression

Causes/associated symptoms
● LOW / LOA (Cancer) (RCC: abdo pain and mass, Bladder Ca: painless)
● Fever, Dysuria, frequency, urgency (UTI)
● Loin to groin pain, History of calculi? (Stone)
● Voiding symptoms: difficulty initiating, poor stream, terminal dribbling, frequency (Urethritis /
Prostatitis/ Obstruction)
● Urethral discharge (Urethritis)
● Any recent URTI symptoms: sore throat, cough, fever (Post streptococcal glomerulonephritis)
● Oral ulcers, rash, alopecia, joint pain (lupus nephritis)
● UL/LL swelling, joint pain, rash (HSP)
● Previous trauma
● Any other bleeding tendencies: GI, BO, PV, epistaxis
● Hearing loss (Alport’s syndrome)

Complications
● Anaemia: Exertional chest pain, SOB, orthopnea, PND, LL swelling
● Acute retention of urine from blood clot: anuria, abdominal pain

** Sexual history **

PMHx:
● Kidney cysts, renal stones / bladder stones / urinary tract instrumentation

Drug history:
● Anti-platelets or anti-coagulants

FHx:
● Polycystic kidney disease
● Cancer
● Hearing loss (Alport’s syndrome)

SHx:
● Smoking (RF for bladder CA)
● Occupation - hairdresser with exposure to dyes (RF for bladder Ca)

PHYSICAL EXAMINATION
T BP HR
{seated} Eyes: Conjunctival Pallor
Mouth: Hydration
{lie flat} Abdomen: Tenderness, Ballotable kidneys, Renal bruit
Renal Punch
Offer DRE for prostatitis/ prostate cancer
KIV look at joints for swelling/ rash for autoimmune

516
INVESTIGATIONS
ᐉ Stat tests
● Urine dipstick, UFEME
● XR KUB
● FBC, INR

ᐉ Other tests
● Urine c/s
● U/E/Cr

ᐉ @ Tertiary:
● Urine cytology
● Urine phase contrast microscopy to differentiate between glomerular cause and non glomerular
cause of haematuria
● US kidneys
● Cystoscopy, CT urogram

MANAGEMENT
Hemodynamically stable?
● Bleeding kidney cyst in ADPKD patient → ED
● Pyelonephritis → Can treat outpatient if vitals stable, tolerating well orally, otherwise refer ED

Simple UTI → Can treat outpt and direct access Uro

● PO Nitrofurantoin 100mg QDS x 1/52
● PO Bactrim 960mg TDS x 3/7

Complicated UTI (structural abnormalities) → Refer ED for intravenous abx

● AAFP: uncomplicated UTI = premenopausal, nonpregnant woman with no known urologic
abnormalities or comorbidities

Urethritis – refer STI notes

517
UROLOGY 5. APPROACH TO NOCTURIA

- Definition of nocturia - Waking at night to void, where each micturition is preceded and followed by sleep,
clinically meaningful if void 2-3 times nightly
- Definition of polyuria - >/=3 litre of urine in a 24 hour period
- Definition of nocturnal polyuria – urinary volume at night >/= 33% of 24hour urine volume

DDx
Low-volume ● Overactive bladder
bladder void ● Bladder outlet obstruction ie Benign
prostate hyperplasia, Prostate CA
Increased night Polyuria
time urinary ● Intake of water (Primary polydipsia)
volume ● Diabetes
● Diabetes insipidus
CCF & edematous states causes third spacing of
Nocturnal polyuria- fluids. Assumption of the supine position
permits mobilization of some of the edema fluid
● Congestive Cardiac Failure into the vascular space and leads to a solute
● Edematous states ie nephrotic diuresis)
syndrome , chronic venous insufficiency
● Parkinson’s disease Autonomic dysfunction in parkinson’s disease
results in urinary sodium excretion
Age-related changes in secretion of arginine
vasopression (AVP) AVP usually secreted to target urine
concentration and normal diurnal variation
involves increase AVP at night to reduce
nighttime urine but the diurnal variation is
absent in elderly)

Sleep Obstructive sleep apnea Release of atrial natriuretic peptide (ANP) due
disturbance to negative intrathoracic pressure and
stretching of the myocardium -> inhibit
Primary sleep disorders (restless leg syndrome, aldosterone
periodic limb movements at night)
Hormonal changes related to sleep-disordered
breathing or due to patient misperception of
the reason for awakening

Obesity
Depression

Name/Age/Sex

BIOLOGICAL

Acute Chronic illness Medical History

Complaint Cause Medical Hx

"On average, how many times do you wake up at night to Course - DM, CCF, parkinsons dz,
void?" Control OSA
● Home
Nocturia ● Clinic Surgical Hx (if obstructive
● Onset/ Duration Compliance urinary symptoms)
Complications

518
 ● Character: Daily / Intermittent , Passing small Checking Bladder stones,
(overactive bladder) or large amounts (other causes) Competency instrumentation of
each time Comorbidities urinary tract
● Time course: Getting worse Crisis
● Associated symptoms management Drug Hx / Drug allergies:
o obstructive and irritative urinary symptoms - Diuretics, Betablockers,
o haematuria cholinesterase inhibitors
o urinary incontinence / retention / for dementia, TCM, OTC
constipation

Cause
● Lifestyle – 24 hr fluid intake, Timing of fluid intake esp
at night, Caffeine intake
● BPH - Obstructive urinary symptoms
● Red flags : Haematuria/ LOW/ LOA / night sweats/
intractable pain/ back pain in prostate cancer
● OAB - Irritative urinary symptoms- frequency ,
urgency , storage symptoms
● Hx of diabetes, polydipsia, polyphagia, LOW
● SOB/Orthopnoea/ LL swelling
● OSA symptoms – Snoring, daytime somnolence,
observed apnea
● Depression/ Obesity
Course
● Seen other doctors for it?
● Tried what treatment?

Complications
● If BPH – Acute retention of urine, UTI ie fever/ loin
pain , haematuria
● Falls / Fracture from getting up at night
● Morning fatigue and daytime sleepiness due to
disrupted sleep

Disease Prevention Family Hx

● Vaccinations Prostate Cancer/ DM

● Cancer prevention

PSYCHOLOGICAL

*** How much do the symptoms bother you and how much do they affect I
your quality of life – ideally should do IPSS Score for BPH C
Screen PHQ-2 for Depression E
GAD-2

SOCIAL

Diet / Exercise as above Function

Alcohol / Smoking
Affect work & sleep

519
PHYSICAL EXAMINATION
T BP HR , postural BP prior to initiation of alpha blockers (no time), BMI
Tongue: Hydration
Abdominal exam: Palpate for abdominal masses, inguinal hernia, palpable bladder
DRE: Enlarged prostate – number of FB , hard/ firm , prostate nodules , tenderness
Neuro - perianal sensation and anal tone , motor and sensory of lower limbs , gait

JVP
Heart: H S1 S2, any S3
Lungs: creps
Pedal edema

INVESTIGATIONS
- UFEME, Fasting glucose , KIV renal panel
- PSA for BPH (Need to discuss with patient and explain risk of false positive and false negative results and
need for prostate biopsy/ US if results positive )
- Frequency – volume chart/ Voiding diary - Helps to identify patients with isolated nocturnal polyuria or
excessive fluid intake which are common in ageing males.

520