MRCP 2-Practice Questions-Book.2 PDF
MRCP 2-Practice Questions-Book.2 PDF
AÿEIQ rons
Book 7
Cardiology
Respiratory- Dermatology
Medicine
Endocrinology
& Metabolism
Gastroenterology
Psychiatry
RenalMedicine
PASTEST
Dedicated to your Success
Contributors vii
Acknowledgements viii
Introduction ix
Dermatology 1
Questions 3
Gastroenterology 65
Questions 67
Psychiatry 11 1
Questions 113
Index 225
v
Dermatology
Virginia Hubbard MBBS MRCP
Consultant Dermatologist, The Whittington Hospital, London.
Endocrinology and Metabolism
Philip Kelly MBBS MRCP
Department of Diabetes and Metabolism, Royal London Hospital,
London.
Gastroenterology
Peter Irving MA MRCP
Specialist Registrar in Gastroenterology, Whipps Cross University
Hospital, London.
Psychiatry
Neil Harrison MRCP MRCPsych
Clinical Research Fellow, Institute of Cognitive Neuroscience and
Honorary Specialist Registrar, Neuropsychiatry, National Hospital,
Queen Square.
Renal Medicine
Ravi Rajakaria BSc(Hons) MBChB MRCP
Experimental Medicine and Nephrology, William Harvey Research
Institute, London.
vii
I would like to express my gratitude to the team al PasTest particularly
Amy Smith and Cathy Dickens for their unswerving support and tolerance
during the preparation of this book and series. Many patients have been
gracious enough to contribute to our ongoing education by allowing their
images to be used in these volumes. The series would have been
impossible without the help of the following: Dr Ed Seward, The
Middlesex Hospital, London for his comments on the gastroenterology
chapter; Drs. S Whitely, N Power and O Chan, Radiology; Dr R Feakins,
Pathology; Dr R Marley, Hepatology, BartsandThe London NHS Trust; Dr
R Makins, Homerton University Hospital NHS Trust and Dr J Mawdsley,
Barts and The London, Queen Mary School of Medicine and Dentistry;
Medical Photography, Radiology and Medicine, King George Hospital,
llford; Medical Illustration at Barts and The London School of Medicine
and Dentistry and The Department of Diabetes and Metabolism at The
Royal London Hospital. Special thanks are due to Dr Alexandra Nanzerfor
her considered and helpful criticisms and delightful encouragement.
Philip Kelly
VII
The MRCP (UK) Part 2 written examination consists of two 3-hour papers,
each with up to 100 multiple choice questions; they are either one from
five (best of 5) or 'n' from many, where two answers are chosen from ten.
Each question will have a clinical scenario and might contain
investigations to interpret; many might also contain an image. There is a
pass-mark agreed by the examiners but a candidate's performance is also
assessed in relation to other candidates.
This three-book series provides practice questions with extensive
explanations to aid candidates preparing for the examination. The authors
are all clinicians writing sections in their chosen fields and as such have
been chosen for their clear understanding of the required knowledgebase
for this important exam. The breadth of knowledge for this exam is vast
and they have attempted to cover the 'syllabus' as completely as possible.
Great care has been taken to explain areas that cause difficulty as
thoroughly as possible. No apology is made where the format of the
questions differs slightly from the exam. These books are not merely
practice papers but educational aids and where a topic can be best
explained by diversion from the strict format of the exam, for the sake of
understanding, this has been done.
This book covers dermatology, endocrinology and metabolism,
gastroenterology, psychiatry, and renal medicine and is best taken - in
concert with its partners within the series - as a supplement to a thorough
clinical grounding, the general medical texts and the core clinical
journals.
Any comments or suggestions on this book or the series will be gratefully
received.
ix
DERMATOLOGY - QUESTIONS
Case 1
-4 42-year-old woman presented with a 6-month history of this
appearance:
3
DERMATOLOGY - QUESTIONS
Case 2
1 Which of the following would typically cause this pattern of hair loss?
ÿ Discoid lupus erythematosus
A
ÿ Dissecting cellulitis of the scalp
B
C3 C Tinea capitis
O D Hypothyroidism
ÿ E Alopecia areata
4
DERMATOLOGY - QUESTIONS
Case 3
5
DERMATOLOGY- QUESTIONS
Case 4
This 67-year-old man with hypertension and epilepsy developed this rash
while on holiday in southern Spain.
1 Which of his drugs is the most likely culprit in this pattern of drug rash?
ÿ A Atenolol
ÿ B Bendroflumethiazide
ÿ C Codeine phosphate
ÿ D Phenytoin
ÿ E Aspirin
6
DERMATOLOGY - QUESTIONS
Case 5
7
DERMATOLOGY - QUESTIONS
Case 6
A 31-year-old man returned from a holiday in Florida with this rash on his
right shin. The rash spread at a rate of approximately 1cm per day. He was
systemically well.
8
DERMATOLOGY - QUESTIONS
Case 7
9
DERMATOLOGY - QUESTIONS
Case 8
10
DERMATOLOGY - QUESTIONS
Case 9
11
DERMATOLOGY- QUESTIONS
Case 10
12
DERMATOLOGY - QUESTIONS
Case 11
13
DERMATOLOGY - QUESTIONS
Case 12
14
DERMATOLOGY - QUESTIONS
Case 13
15
DERMATOLOGY- QUESTIONS
Case 14
16
DERMATOLOGY - QUESTIONS
Case 15
A 54-year-old woman presented with weight loss. These are her hands.
She was ANA-negative.
17
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 1
21
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 2
You are referred a lady with thyrotoxicosis and exophthalmos. She has a
moderate sized nodular goitre. The CI' has already started her on
carbimazole and this is her thyroid function while taking 5 mg once daily.
FreeT4 15.1 pmol/L
TSH 2.1 mU/L
Urine p-HCG Negative
She has a neck scan and a CT orbit to assess the exophthalmos:
RT L.T
T
*19 ii
9 THYROID SCON 23 Nov 1988 at 14:59
22
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
23
ENDOCRINOLOGY AND METABOI ISM - QUESTIONS
Case 3
25
endocrinoi ogy and metaboi ism questions
Case 4
26
ENDOCRINOI OCY AND METABOLISM - QUESTIONS
27
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 5
You are called to see a 68-year-old retired nurse who collapsed while
having a lipoma removed from his back under a general anaesthetic. In the
past he had Osgood Schlatter's disease. He is on no medication. His
mother has type I diabetes, his two sisters are well.
On examination he is 1.88 m, weighs 80 kg, the pulse is 70 bpm, |VP 4 cm
and blood pressure 1 10/70 mmHg with no postural drop. His capillary
glucose was 1 .8 mmol/L during the collapse but he came round within
10 minutes after having 25 g intravenous glucose.
Urinalysis Ketones ++
Prudently, some bloods were taken before the glucose was given. They are
as follows:
FBC Normal
Glucose 1.9 mmol/L
Sodium 135 mmol/L
Potassium 4.9 mmol/L
Bicarbonate 20 mmol/L
Chloride 104 mmol/L
Urea 3.5 mmol/L
Creatinine 70 pmol/L
LFTs Normal
Cortisol 315 nmol/L
28
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
29
ENDOC RINOLOGY AND METABOLISM - QUESTIONS
Case 6
You see a 36-year-old lady III hours after her admission after palpitations
which self-terminated. She is a gardener for the Royal Horticultural
Society, smokes one or two cigarettes a week anddrinks one bottle of wine
every 2 days. She has no past medical history. She suffers with aches and
pains all over which predate this presentation.
On examination the muscles are not tender and apart from being
proximally weak - she cannot rise from a squat - the neurological
examination, including the deep tendon reflexes, is normal; examination
of the respiratory and abdominal systems are normal. The J VP is 4 cm and
shows couplets of cannon waves and the BP is 1 40/94 mmHg.
Urinalysis pH 6.1
Protein trace
Blood trace
Specific gravity 1 .010
The ECG shows U waves, but is otherwise entirely normal.
Her investigations are shown:
EBC Normal
ESR 5 mni/h
CRP <1 mg/L
Sodium 1 44 mmol/L
Potassium 2.2 mmol/L
Bicarbonate 6 mmol/L
Chloride 1 25 mmol/L
Urea 7.8 mmol/L
Creatinine 100 umol/L
Calcium 2.2 mmol/L
Phosphate 0.7 mmol/L
Albumin 40 g/L
ALP 129 U/L
AST 22 U/L
ALT 15 U/L
Bilirubin 9 umol/L
The ward house officer was concerned about some abdominal pain and
requested the abdominal film shown opposite:
30
ENDOCRINOLOGY AND METABOLISM - QUE ST IONS
31
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 7
32
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 8
33
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 9
34
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 10
36
FNDOCRINOLOCY AND METABOLISM QUESTIONS
Case 11
37
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
38
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 12
}9
ENDOCRINOLOGY AND MFTABOI ISM - QUESTION'S
40
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 13
A 55-year-old man who is asymptomatic has on two separate occasions
shown the following venous plasma biochemistry:
Random glucose 6.1 mmol/L
75-g glucose tolerance test:
T+0 6.0 mmol/L
T + 120 1 1 .0 mmol/L
41
ENDOCRINOLOGY AND MFTABOI ISM - QUESTIONS
Case 14
You arc asked to see a 70-year-old lady on the Orthopaedic Ward who
fractured her hip. She is 24 hours post-op from a dynamic hip screw
insertion under general anaesthesia and is mildly nauseatedbut able to
keep water down. She has COPD, well controlledon inhalers, andtakes
aspirin anda nitrate for mildstable angina - which has not troubledher for
'years'.
On examination she is orientated, pale, apyrexial, pulse 96 bpm, BP 90/50
mmHg lying and 96 bpm and 90/50 mmHg standing, and the JVP is 3 cm.
Her chest is clear.
Hb 9.9 g/dL
MCV 90 fL
Platelets 604 x 107L
Sodium 124 mmol/L
Potassium 5.1 mmol/L
Bicarbonate 22 mmol/L
Chloride 100 mmol/L
Urea 3.1 mmol/L
Creatinine 50 [tmol/L
Calcium 2.4 mmol/l
Phosphate 1.1 mmol/L
Albumin 40 g/1
t4 15.1 pmol/L
TSH 2.1 U/L
Cortisol 120 nmol/L
Glucose 4.3 mmol/L
Urine osmolality 180 mosmol/kg
Plasma osmolality 271 mosmol/kg
42
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 15
Investigations reveal:
Hb 12.0 g/dL
WCC 12.0 x 109/L
Platelets 397 x 107L
ESR 68 mm/h
Case 16
You are asked to see a 44-year-old Irish lady who is under investigation foi
colicky abdominal pain, nausea and vomiting, and lassitude which all
come andgo somewhat. She is a university lecturer who has been unwel
with these symptoms over the last 9 monthsbut has continuedto work; she
has lost 10 kg.
On examination she is 1.70 m tall and 57 kg and looks unwell. The pulse is
90 bpm, BP 120/80 mmHg lying and 90/52 mmHg standing, |VP 2 cm.
Examination of the breasts, respiratory, abdominal and neurological
systems is normal.
44
ENDOCRINOLOGY AND MFTABOI ISM QUESTIONS
45
ENDOCRINOLOGY AND METABOl ISM - QUESTIONS
Case 17
A 32-year-old lady is seen in the Diabetes Clinic for 6-monthly review. She
has had type Idiabetes mellitus ( T 1DM) for the last 15 years. She is treated
with insulin aspart 8-12 units pre-meal and human Insulatard® 18 units at
10 pm. She monitors frequently and while some days can be good with
fasting capillaryglucose in the range of 4.5-6.5 mmol/L andpost-prandial
levels of no higher than 9.5 mmol/L,she can wake with lasting sugars
around 12-15 mmol/L andthen the whole day is erratic. She always has a
bedtime snack andshe suspects she is having nocturnal hypoglycaemia.
The HbAic is 7.2% andshe has no demonstrable complications. She is
having no meter or pen problems.
On examination her weight is stable at 70 kg and she has a BMI of
22 kg/rrr; the injection sites are fine.
Investigations reveal:
Tissue transglutamase antibodies Negative
9-am Cortisol 400 nmol/L
p-l ICG < 5 U/L
46
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 18
A gentleman has been investigated for hip/thigh pain. This is his pelvic
X-ray:
47
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 19
This gentleman's foot is warm, swollen and red, but is not painful.
On examination the skin is intact - there is no ulceration. The foot is not
tender. Peripheral pulses are present.
Investigations reveal:
Plasma glucose 15 mmol/L
Urate 400 mmol/L
48
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
49
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 20
This 45-year-old lady is seen in the Diabetes Clinic. She is currently only
taking metformin Ig bd, rosiglitazone 4 mg once daily and amlodipine
10 mg once daily. She does not smoke.
On examination her BMI is 32 kg/m2 and she has a blood pressure of
150/90 mmHg. Examination of the praecordium, respiratory and
abdominal systems is normal.
50
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
51
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 21
52
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 22
53
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 23
A CP refers you a 65-year-old gentleman with breathlessness which has
been present and slowly worsening for the last few weeks. The CP is
concernedthat there is something he is missing. The patient is not wheezy
but has hada cough productive ofgreen sputum for the last 2 days that has
not responded to amoxicillin as well as normally; the CP had treated him
for several infections, including pneumonia twice and urinary tract
infections over the preceding months. He normally has a cough
productive of white sputum. He has lost 5 kg in weight over the last 3
months and on direct questioning says he lost his appetite, is not sleeping
and is feeling frankly miserable. There have been no night sweats. No
prescription medication is taken but he takes magnesium trisilicate several
times daily for a very troublesome hiatus hernia; he is married with two
grown-up children, recently retired as a bank clerk, drinks approximately
30 units of alcohol a week and keeps no pets.
On examination he is thin, pale and looks a little unwell. His respiratory
rate is 24 breaths per minute, the chest is clear and there is no wheeze. The
pulse is 96 bpm, BP 130/70 mmHg and the heart, abdomen and nervous
system are normal.
Investigations:
Hb 8.8 g/dL
MCV 84 fL
WCC 3.1 x I07L
Neutrophils 1.1 x I07L
Lymphocytes 2.0 x IO'VL
Platelets 120 x 10'VI
ESR 1 10 mm/h
Sodium 1 39 mmol/L
Potassium 4.9 mmol/L
Bicarbonate 19 mmol/L
Chloride 106 mmol/L
Urea 19.1 mmol/L
Creatinine 180 umol/L
Calcium 2.7 mmol/L
Phosphate 1 .8 mmol/L
Albumin 26 g/L
ALP 90 U/L
Total protein 78 g/L
54
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
55
ENDOCRINOLOGY AND METABOLISM QUESTIONS
Case 24
56
ENDOCRINOLOGY AND METABOLISM QUESTIONS
Case 25
57
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 26
58
ENDOCRINOLOGY AND METABOLISM QUESTIONS
Case 27
59
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 28
60
ENDOCRINOI OGY AND METABOLISM QUESTIONS
Case 29
61
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 30
62
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Chest X-ray, 5 months ago
63
ENDOCRINOLOGY AND METABOLISM - QUESTIONS
Case 31
64
GASTROENTEROLOGY - QUESTIONS
Case 1
67
GASTROENTEROLOGY - QUESTIONS
Case 2
68
GASTROENTEROLOGY - QUESTIONS
Case 3
69
GASTROENTEROLOGY - QUESTIONS
Case 4
70
GASTROENTEROLOGY - QUESTIONS
Case 5
A 64-year-old lady presented with a 2-day history of melaena and
epigastric pain. She had a history of osteoarthritis for which she took
diclofenac.
On admission she had a pulse of 125 bpm. Her blood pressure was 1 10/70
mmHg lying and 1 00/50 mmHg when sitting. She was resuscitated with
intravenouscolloid. At endoscopy, she was found to have a stricture in the
mid-oesophagus which prevented passage of the endoscope. She
continued to have melaena and accordingly had angiography performed
which is shown below.
71
GASTROENTEROLOGY - QUESTIONS
Case 6
72
GASTROENTFROLOGY QULSTIONS
Case 7
A 28-year-old woman of Irish descent was referred to hospital with a
history of malaise and tiredness for 6 months. She complained that her
bowels had always been erratic but were more so recently; she hadbeen
passingsemi-formed stools three times a day for the last few months. There
was no history of foreign travel and, other than the oral contraceptive pill,
she was on no regular medications.
Examination revealed that she was pale and undernourished. Her
laboratory investigations were as follows:
Hb 9.6 g/dL
MCV 74 fL
WCC 6.2 x 109/L
Platelets 22! x 107L
Sodium I 39 mmol/L
Potassium 3.7 mmol/L
Urea 2.8 mmol/L
Creatinine 76 umol/L
Albumin 33 g/L
Calcium 1 .76 mmol/L
Bilirubin 5 umol/l.
AST 23 U/L
ALP 94 U/L
Anti-endomysial Ab negative
73
GASTROENTEROLOGY - QUESTIONS
Case 8
74
GASTROENTEROLOGY - QUESTIONS
Case 9
7.5
GASTROENTEROLOGY- QUESTIONS
Case 10
76
GASTROENTEROLOGY - QUESTIONS
Case 11
77
GASTROENTEROLOGY - QUESTIONS
Case 12
78
GASTROENTEROLOGY - QUESTIONS
Case 13
79
GASTROENTEROLOGY - QUESTIONS
Case 14
80
GASTROENTFROLOGY QUESTIONS
Case 15
A 52-year-oldgentleman was admitted with a history of haematemesis. He
haddrunk ten cans of strong lager a day for the last 10 years.
Examination revealed that he was lachycardic (1 1 0 bpm) and hypotensive
(95/60 mmHg supine). He was jaundiced and had multiple spider naevi on
hischest wall. His spleen was palpable on inspiration and shifting dullness
was detectable.
Blood results were as follows:
Hb 8.6 g/dl
MCV 104 f L
WCC 4.8 x 10'VL
Platelets 77 x IO'/L
PT 28 s
Sodium 129 mmol/L
Potassium 4.4 mmol/L
Urea 1 .4 mmol/L
Creatinine 78 umol/L
Albumin 23 g/L
Bilirubin 35 pmol/L
AST 245 U/L
ALP 256 U/L
81
GASTROENTEROLOGY - QUESTIONS
Case 16
A 19-year-old Bangladeshi man was referred to Outpatients with a history
of slight weight loss, crampy abdominal pain and, occasionally bloody
diarrhoea. He smoked 20 cigarettes a day, drank 14 units of alcohol per
week and worked as a mechanic. There was no past history of note. He
hadstarted taking ibuprofen for his abdominal pain and loperamide for his
diarrhoea.
On examination he was well, apyrexial and not tachycardic. He had mild
tenderness in his right iliac fossa but no masses were palpable in his
abdomen. His barium follow-through is shown below.
1 Which three of the following are most appropriate as part of your initial
management?
ÿ A Mesalazine ÿ F Infliximab
ÿ B Stop smoking ÿ G Vitamin B|_. injections
ÿ C Stop ibuprofen ÿ H Methotrexate
ÿ D Increase loperamide dosage ÿ I Parenteral hydrocortisone
ÿ E Azathioprine ÿ I Surgery
82
GASTROENTEROLOGY - QUESTIONS
Case 17
83
GASTROENTEROLOGY - QUESTIONS
Case 18
A 19-year-old woman was brought into hospital by her mother who had
recently returnedhome to find that her daughter was unwell. Two days
previously,the daughter had split up from her boyfriend andhadtaken
about 50 paracetamol tablets after drinking a quarter of a bottle of spirits.
She was not known to be a heavy drinker and had no past history of liver
disease. Other than the oral contraceptive pill, she was on no regular
medications.
On examination, her temperature was 37.1 °C. She was tearful and
withdrawn, but alert and orientated. Aggressive fluid resuscitation and
treatment with N-acetylcysteine were initiated.
1 Which one of the following tests, taken the following day, should prompt
referral to a specialist liver unit?
D A I'aracetamol level 50 mg/L
ÿ B AST 856 U/L
ÿ C Albumin 22 g/L
ÿ D pH 7.25
D E Creatinine 185 pmol/L
84
GASTROENTEROLOGY - QUESTIONS
Case 19
85
GASTROENTEROLOGY- QUESTIONS
Case 20
86
GASTROENTEROLOGY QUESTIONS
Case 21
Ilepatitis serology:
I lepatitis A IgM negative
I lepatitis A IgG negative
HBsAg positive
HBeAg positive
Anti-HBc antibody positive
Anti HBe antibody negative
87
GASTROENTEROLOGY - QUESTIONS
Case 22
88
GASTROENTEROLOGY - QUESTIONS
Case 23
89
GASTROENTEROLOGY - QUESTIONS
Case 24
90
GASTROENTEROLOGY QUESTIONS
91
GASTROENTEROLOGY - QUESTIONS
Case 25
92
GASTROENTEROLOGY - QUESTIONS
Case 26
93
GASTROENTEROLOGY - QUESTIONS
Case 27
1 Which of the following drugs that she is taking is least likely lo be the
cause?
ÿ 6-mercaptopurine
A
ÿ Phenobarbital
B
O C Prednisolone
0 D 5-aminosalicylic acid
0 E Sodium valproate
94
GASTROENTEROLOGY - QUESTIONS
Case 28
-4 79-year-old man was referred by his GP with a 4-month history of
dysphagia. He was unable to pinpoint the site of his symptoms accurately
but noted that his dysphagia worsened as he ate. At times he would
regurgitate food during his meals, which would temporarily relieve his
symptoms. According to his GP, who had weighed him, he had lost Ikg in
weight over the past 2 months. His medications included
bendroflumethiazide for hypertension and ranitidine, which he took
intermittently for symptoms of gastro-oesophageal reflux disease.
95
GASTROENTEROLOGY - QUESTIONS
Case 29
On examination she was pyrcxial at 39.2 "C and tachycardic at 105 bpm.
I ler abdomen was diffusely tender with guarding in the right upper
quadrant. Bowel sounds were reduced. A painful erythematous rash was
noted on the lower limbs.
Urinalysis Blood +
Hb 13.6 g/dL
MCV 85 fL
WCC 14.8x10'VL
Platelets 387 x 10"/L
CRP 55 mg/L
(S-HCG < 5 U/L
96
GASTROENTEROLOGY - QUESTIONS
Case 30
Her blood tests were checked 72 hours after initiating TPN and were as
follows:
Sodium 137 mmol/L
Potassium 2.9 mmol/L
Urea 2.4 mmol/L
Creatinine 69 gmol/L
Corrected Ca2+ 2.2 mmol/L
Phosphate4 0.2 mmol/L
Magnesium 0.4 mmol/L
97
GASTROENTEROLOGY- QUESTIONS
Case 31
Case 32
99
GASTROENTEROLOGY- QUESTIONS
Case 33
1 What are the changes on his hands most likely due to?
ÿ A Vitamin B,. deficiency
ÿ B Vitamin C deficiency
ÿ C Thiamine deficiency
ÿ D Niacin deficiency
ÿ E Riboflavin deficiency
100
GASTROENTEROLOGY - QUESTIONS
Case 34
101
GASTROENTEROLOGY- QUESTIONS
Case 35
102
GASTROENTEROLOGY -QUESTIONS
Case 36
A 42 -year-old man presented to his CP complaining of lethargy, pruritus,
right upper quadrant discomfort and dry mouth and eyes. Otherwise he
was asymptomatic andhad no previous history of note. He drank 24 units
of alcohol per week.
On examination, he had two-finger hepatomegaly and his spleen was just
palpable. No signs of chronic liver disease were present.
103
GASTROENTEROLOGY - QUESTIONS
Case 37
A 65-year-old woman is brought to A&E by her husband, complaining of
upper abdominal and lower chest pain radiating to the back. As part of
their fortieth wedding anniversary celebrations, they hadbeen out for a
large meal at which they hadconsumed more alcohol than they were
normally usedto. On returning home, she hadbecome nauseatedandhad
vomited three times. Concurrently, she developed upper abdominal and
lower chest pain and, subsequently, shortness of breath.
On examination, she was tachycardic at 105 bpm, tachypnoeic at 25
breaths per minute and was pyrexial at 37.8 °C. She had firmness in the
upper abdomen and a plain chest X-ray confirmed the clinical findings of a
left pleural effusion.
104
GASTROENTEROLOGY - QUESTIONS
Case 38
1 05
GASTROENTEROLOGY QUESTIONS
Case 39
Her blood results were as follows (RDW, red cell distribution width):
Mb 5.6 g/dl
MCV 90 II
WCC 5.8 x 107L
Platelets 387 x 1071
RDW 22%
Sodium 138 mmol/L
Potassium 4.4 mmol/L
Urea 4.4 mmol/L
Creatinine 99 (.rmol/L
Albumin 32g/L
Corrected Ca2+ 2.0 mmol/L
Bilirubin 30 nmol/L
106
GASTROENTEROLOGY - QUESTIONS
107
GASTROENTEROLOGY - QUESTIONS
Case 40
II.1 11.4
Died 53 years
colorectal colonic
cancer doIvds
aged 36
years
108
GASTROENTEROLOGY - QUESTIONS
Case 41
109
PSYCHIATRY - QUESTIONS
Case 1
Hb 1 1.9 g/dL
MCV 1 03 fF
wcc 4.5 x 107F
Platelets 1 05 x 10'VL
AFT 74 U/L
Albumin 32 g/L
Sodium 129 mmol/l.
Urea 3.1 mmol/l.
113
PSYCHIATRY - QUESTIONS
114
PSYCHIATRY - QUESTIONS
Case 2
A23-year-old Swedish student was brought to A&E by her boyfriend who
was concernedthat she hadbeen acting strangely for 48 hours. She had
become increasingly agitated and restless, claiming that her flatmate was
monitoring herbehaviour and trying to steal her identity. She hadnot slept
for 2 nights. On two occasions she hadbecome unresponsive, staring
blankly ahead, following which she appeared confused anddisorientated.
She hadvomited twice and was complaining of severe abdominal pain
that she ascribed to menstruation. She had had two similar though less
severe episodes around the time of menstruation in the last 2 months. She
hadbeen well until (> months previously, when she hadbecame depressed
at the time of her end-of-year exams andhadbeen prescribedfluvoxamine
by her CP.
On examination she appeared confused and was disorientated to time.
Abdominal examination revealed central tenderness without guarding.
Other than sinus tachycardia, the respiratory and cardiovascular
examinations were unremarkable. Neurological exam revealed reduced
sensation distally and reduced power on shoulder abduction bilaterally.
115
PSYCHIATRY - QUESTIONS
116
PSYCHIATRY - QUESTIONS
Case 3
I 17
PSYCHIATRY - QUFSTIONS
118
PSYCHIATRY - QUESTIONS
Case 4
119
RENAL MEDICINE - QUESTIONS
Case 1
1 Which one of the following medications is the most likely cause of his
acute renal failure?
ÿ Didanosine
A
ÿ Stavudine
B
Q Indinavir
C
L) D Atorvastatin
ÿ E Trimethoprin-sulfamethoxazole
123
RENAL MEDICINE- QUESTIONS
124
RENAL MEDICINE - QUESTIONS
Case 2
125
RENAL MEDICINE - QUESTIONS
126
RENAL MEDICINE - QUESTIONS
Case 3
127
RENAL MEDICINE - QUESTIONS
128
RENAL MEDICINE - QUESTIONS
Case 4
129
RENAL MEDICINE - QUESTIONS
Case 5
130
RENAL MEDICINE - QUESTIONS
Case 6
>
,
_ . /?
KV 120
HA 240
II 0.75
CI 0.0
M 5.0/7.5
202 11/33
AC 50 io « n r. W 420
121 1020 C 41
131
RENAL MEDICINE - QUESTIONS
132
RENAL MEDICINE - QUESTIONS
Case 7
133
RENAL MEDICINE - QUESTIONS
Case 8
Hepatitis serology:
B e antigen Negative
B core IgG antibody Positive
B surface antigen Positive
C antibody Negative
Renal biopsy was performed and is shown opposite.
134
RENAL MEDICINE - QUESTIONS
135
RENAL MEDICINE - QUESTIONS
Case 9
136
RENAL MEDICINE - QUESTIONS
Case 10
Investigations:
Creatinine 1 62 pmol/L
LFTs Normal
FBC Normal
Urine microscopy Red cell casts
ANCA Negative
ASOT Normal
Hepatitis B/C Negative
137
RENAL MEDICINE - QUESTIONS
Case 11
Her investigations:
Creatinine 96 umol/L
Calcium 2.48 mmol/L
Phosphate 1.02 mmol/L
Albumin 40 g/L
Urine protein 0.5 g/24 h
Creatinine clearance 68 mL/minute
24-h urine calcium 10 mmol (NR < 7.5 mmol)
24-h urine oxalate 1 .4 mmol (NR < 0.36 mmol)
24-h urine urate 3.2 mmol (NR < 4.5 mmol)
138
RENAL MEDICINE - QUESTIONS
1 What is the most likely diagnosis?
CD A Primary hyperoxaluria
CD B Primary hyperparathyroidism
CD C Secondary hyperparathyroidism
CD D Nephrogenic diabetes insipidus
CD E Surreptitious antacid ingestion
139
KLNAL MEDICINE - QUESTIONS
Case 12
140
RENAL MEDICINE QUESTIONS
Case 13
141
RENAI MEDICINE QUESTIONS
Case 14
142
RENAL MEDICINE QUESTIONS
Case 15
1 43
DERMATOLOGY - ANSWERS
Case 1
1 B Hypocalcaemia
This patient has lupus pernio, a cutaneous feature of sarcoidosis. Lupus
pernio causes violaceous infiltrated nodules and plaques, usually on the
nose. There may he associated swelling and ulceration and crusting of
the nasal vestibule.
Cutaneous features of sarcoidosis can be classified as acute, subacute or
chronic:
• Acute changes:
erythema nodosum
papular eruption
scar sarcoid - sarcoid localises to previous sites of trauma
• Subacute changes:
annular sarcoid
nodular sarcoid
angiolupoid sarcoid - rare; usually occurs in women; periorbital,
soft, domed, orange-red swellings
• Chronic changes:
plaque sarcoid
lupus pernio
scarring alopecia.
Lupus pernio lends to be associated with other forms of chronic fibrotic
sarcoidosis. These include:
• Bone cysts - radiolucent, usually in the hands and feet
• Chronic polyarthritis - usually involving ihe small bones of the hands
and feet
• Respiratory tract sarcoidosis - classically this causes a restrictive
pattern on pulmonary function tests
• Lacrimal gland swelling - Mikulicz syndrome, ie bilateral swelling of
the lacrimal and salivary glands. Sarcoid is one cause of this
• Renal sarcoid
• Hypercalcacmia.
Case 2
1 A Discoid lupus erythematosus
This is a picture of scarring alopecia.
146
DERMATOl OGY - ANSWERS
Case 3
1 D Pernicious anaem ia
This is vitiligo - an acquired disorder of depigmentation characterised by
147
DERMATOLOGY - ANSWERS
Case 4
1 B Bendroflumethiazide
This is the distribution of a photosensitive drug eruption. The most
common photosensitising drugs are:
• Thiazide diuretics
• Phenothiazines egchlorpromazine, promethazine
• Sulphonamides
• Oral hypoglycemics- tolbutamide, chlorpropamide
• Tetracyclines
• Griseofulvin
• Amiodarone- chronic use leads to slate-grey pigmentation.
Beta-blockers, lithium and NSAIDs may exacerbate psoriasis.
Codeine phosphate can cause a fixed drug eruption. This is a round itchy
erythematous oedematous patch, with or without blistering, which fades
to leave a brown discoloration of the skin. Re-challenge with the drug
will cause the rash to recur in the same place. Other drugs which
commonly cause a fixed drug eruption are:
148
DERMATOLOGY - ANSWERS
• Barbiturates
• Sulphonamides
• Tetracyclines
• Salicylates
• NSAIDs.
Phenytoin commonly causes a drug rash. It is a frequent cause of
erythema multiforme. In addition, it may cause the phenytoin
hypersensitivity syndrome. This is characterised by a rash (often
non-specific or morbilliform), fever, lymphadenopathy, hepatomegaly,
eosinophilia and abnormal LFTs. Phenytoin hypersensitivity can be fatal,
and there is cross-reactivity with carbamazepine, gabapentin and
phenobarbital. The only 'sate' anti-epileptic drug to use in this situation
is sodium valproate. In addition, first-degree relatives have a higher
chance of developing the syndrome with these drugs.
Case 5
1 A Phenytoin treatment
This is a fissured/scrota Itongue. It is associated with:
• Geographical tongue - common and a normal variant. It affects 1% of
the population; 50% also have a fissured tongue
• Granulomatous infiltration:
Sarcoid
Crohn's disease
Melkersson-Rosenthal syndrome -triad of labial oedema, fissured
tongue and recurrent unilateral facial palsy
Trisomy 21 .
Phenytoin and ciclosporin characteristically cause gingival hyperplasia.
Case 6
t E Ankylostoma braziliense
This is a picture of cutaneous larva migrans. This is a self-limiting
cutaneous eruption caused by the larvae of roundworms. Ankylostoma
braziliense is the most common agent. Cutaneous larva migrans has a
worldwide distribution but is especially prevalenl in Central and
Southern America. Dogs and cats carry the roundworm. Beaches are a
common reservoir.
Eggs are passed in the faeces of infected animals and then hatch in soil or
sand. The larvae easily penetrate skin, often causing a non-specific itchy
dermatitis at the time. Migration of larvae usually occurs within a week,
with the production of a wandering, thread-like, intensely pruritic,
149
DERMATOLOGY - ANSWERS
Case 7
1 A Spironolactone
This woman has facial hirsutism. Hirsutism is the abnormal growth of
terminal hair in androgen-sensitive areas such as the moustache and
beard regions. The causes of this arc:
• Ovarian:
PCOS
ovarian hyperthecosis
ovarian tumours
• Adrenal:
congenital adrenal hyperplasia
Cushing's disease
adrenal tumours
• I lyperprolactinaemia
• Acromegaly
• Androgen therapy, eg anabolic steroids
• Idiopathic - can be racial variation.
Appropriate investigations include:
• Testosterone and sex hormone-bindingglobulin
150
DERMATOLOGY - ANSWERS
• LH/FSH
• Androstenedione
• Dehydroepiandrosterone sulphate (DHEAS)
• Follicular phase 17-hydroxyprogesterone
• Prolactin
• Fasting glucose
• Ultrasound ovaries.
151
DLRMATOLOGY - ANSWKRS
Case 9
1 B Dermatomyositis
These are Gottron's papules, a pathognomonic sign in dermatomyositis.
Other typical cutaneous manifestations of dermatomyositis include:
• Heliotropic (violaceous) inflammatory rash of the eyelids. There may
also be periorbital oedema
• Erythema of the face, neck and upper trunk, which is often
photosensitive
• Calcinosis
• Raynaud's phenomenon.
Extracutaneous features of dermatomyositis are:
• Muscle weakness - proximal myopathy, dysphagia, dysarthria
• Pulmonary fibrosis and pulmonary hypertension
• Myocarditis and myocardial fibrosis - conduction defects, cardiac
failure
• Associated malignancy (in 10-50% cases) - lung, breast, ovarian,
stomach, renal, testis.
Diagnosis is confirmed by:
• Skin biopsy
• Muscle biopsy
• Muscle MRI, which can replace the need for muscle biopsy and can
identify patchy involvement (which can lead to a false-negative
muscle biopsy).
• EMG
• ANA-positive in > 90% and anti-Jo- 1 in 40%.
Other useful investigations include:
• EGG
• CXR.
This patient also requires chest CT and/or bronchoscopy.
The rash improves when an underlying malignancy is treated. Other
152
DERMATOLOGY - ANSWERS
therapies include:
• Systemic corticosteroids
• Hydroxychloroquine
• Methotrexate
• Intravenous immunoglobulin
• Sun protection.
Case 10
1 C Pulsed intravenous methylprednisolone
This is a classic picture of pyoderma gangrenosum. Pyoderma
gangrenosum is a destructive, necrolising, non-infective ulceration of the
skin. It presents as an ulcer with an undermined, overhanging purple
edge. There may be associated surrounding inflammation and necrosis.
Most cases of pyoderma gangrenosum are associated with an underlying
disease process. These include:
• Gastrointestinal disease - ulcerative colitis, Crohn's disease, peptic
ulcer disease
• Liver disease chronic active hepatitis, primary biliary cirrhosis,
sclerosing cholangitis
• Joint disease- rheumatoid arthritis, ankylosing spondylitis,
osteoarthritis, polychondritis, Behcet's syndrome
• Blood disorders - leukaemias, myelomas, lymphomas
• Neoplasia - carcinoma of the colon, prostate, breast or bronchus and
neuroendocrine tumours (carcinoids).
Case 11
1 D Cutaneous leishmaniasis
This is a typical ulcer of cutaneous leishmaniasis. Leishmaniasis is
transmitted by the sandfly. It can be cutaneous or visceral. Cutaneous
leishmaniasis can be of 'Old World' or 'New World' types.
1 53
DtRMATOI OCY - ANSWERS
Case 12
1 E Lichen planus
This is lichen planus. It characteristically causes small, flat-topped,
violaceous papules over the wrists, ankles and genitalia. White lacy lines
called 'Wickham's striae' are often seen within lesions. Oral
involvement is common - usually white patches or plaques on the
buccal mucosa, but sometimes erosive changes are seen. Nails typically
have pitting, longitudinal ridging and distal splitting. Scalp involvement
can be seen, with scarring alopecia which is then known as 'lichen
planopilaris'.
Risk factors for lichen planus include:
154
DERMATOI OGY - ANSWERS
Case 13
1 D Leprosy
The combination of a hypopigmenled patch and ulnar nerve palsy is
compatible with a diagnosis of leprosy, of borderline type.
Tuberculoid leprosy (TL) -> borderline leprosy -> lepromatous leprosy (LL)
Skin lesions:
• Sharply defined plaques
• Hypopigmented
• Anaesthetic skin lesions
• Symmetrical nodules or plaques
• May be hyperaesthetic.
Nerve lesions:
• Nerves near lesions may be enlarged
• Nerve trunk palsies
• Nerve palsies variable
• Distal symmetrical anaesthesia common.
Lepromin skin test:
Positive -> negative — negative.
ÿ
155
DERMATOLOGY - ANSWERS
Acid-fast bacilli:
Rare (paucibacillary) -> some -> lots (multibacillary).
Leprosy is endemic in Asia, Africa, the Pacific Basin and Latin America.
The average incubation period is 5 years. Transmission is probably via
nasal droplets.
Treatment:
It needs to be more intensive in the multibacillary lepromatous type
compared with the tuberculoid type
Dapsone + rifampicin + clofazimine for multibacillary LL
Dapsone + rifampicin for paucibacillary TL.
Complications:
1 Reversal reactions these occur when treatment is initiated in patients
with borderline disease. The disease shifts towards TL, existing lesions
may become inflamed and tender, and new 'satellite' lesions may
occur. Painful nerve trunk palsies may occur.
2 Erythema nodosum leprosum- this occurs in half of patients with LL. It
usually develops within the first few years after treatment is initiated. It
can affect any part of body and is self-limiting. There is associated
fever, malaise, anorexia and anaemia.
Case 14
1 C Withdraw carbamazepine
This is toxic epidermal necrolysis. There is extensive full-thickness
attachment of the epidermis. It is the most severe form of erythema
multiforme. Typically the rash starts as poorly defined macules with
darker centres. There is then sheet-like loss of the epidermis. Mucous
membrane involvement is present in 95% of patients, with involvement
of the oropharynx, eyes, genitalia and anus. I ligh fever is usual.
Most cases are related to an adverse drug reaction. The commonest
culprits are sulphonamides (eg co-lrimoxazole), aromatic
anticonvulsants (eg phenytoin, phenobarbital, carbamazepine), some
NSAIDs (eg phenylbutazone, piroxicam) and allopurinol. The incidence
is increased in patients with HIV infection. There is a high morbidity and
mortality (30%) associated with this condition.
Complications:
• Fluid loss - replace with an extra 3-4 litres per day
• Infection - the main cause of death in these patients
• Impaired thermoregulation
• Increased energy expenditure.
156
DERMATOLOGY ANSWERS
Management:
• Withdraw any suspect drug
• Avoid skin trauma, including large intravascular lines
• Fluid replacement
• Needs ITU/burns unit bed
• Sterile handling of the patient
• Non-adherent skin dressings
• Nasogastric tube and high-protein diet
• Raise environmental temperature to 30 32 "C
• Ophthalmology examination daily.
Case 15
1 8 Rheumatoid arthritis
These pictures show two features nail-fold infarcts and a symmetrical
polyarthropathy with swelling of the MCP joints.
Nail-fold infarcts are seen in association with small-vessel vasculitis.
They are characteristically seen in rheumatoid arthritis, SLE, scleroderma
and dermatomyosilis.
Only 30°/) of patients with rheumatoid arthritis are ANA-positive
(cf SLE, 85%).
157
ENDOCRINOLOGY AND METABOI ISM - ANSWERS
Case 1
1 E Familial dysbetalipoproteinaemia
There is a combined hyperlipidaemia with striate palmar xanthomas.
Palmar xanthomata are almost diagnostic of familial
dysbetalipoproteinaemia, (synonyms are broad-bela disease, remnant
removal disease or type III hyperlipidaemia (Fredrickson/WHO
classification)). Tuberoeruptive xanthomas also occur and may coalesce
to form tuberous xanthomas. Untreated, there is a marked increased
incidence of coronary heart disease and peripheral vascular disease. It is
rare; treatment is with diet, fibrates or statins. In the absence of palmar
xanthomas it cannot be distinguished from familial combined
hyperlipidaemia (type lib) or lipoprotein lipase deficiency (type V or I
hyperlipidaemia) on simple lipid measurement alone. Most (90%) of the
patients are homozygous for apolipoprotein E e2. DNA testing for this is
troublesome because it may identify the presence of e4 which is linked
with early-onset Alzheimer's disease; this information should not be
openly available in the patient's notes without their consent. Plasma can
also be examined by ultracentrifugation for the presence of (S-VLDL
(hence broad-beta), typical of familial dysbetalipoproteinaemia.
About 1% of the population have the e2/e2 phenotype; they have
cholesterol- enriched VI DL and low LDL, but do not have type III
dysbetalipoproteinaemia, whose expression requires the co-existence ot
a further abnormality affecting lipid metabolism. Examples of this are
hypothyroidism and obesity. Note that the total cholesterol is not made
up of LDI and this suggests elevated IDL which is characteristic ol
dysbetalipoproteinaemia. The disorder responds to weight reduction,
fibrates and statins. The high triglycerides confer an elevated risk of
pancreatitis.
Patients with familial mixed hyperlipidaemia have increased VLDL
(triglycerides) and LDL and typically low HDL; they are prone to
coronary artery disease, stroke and peripheral vascular disease.
Treatment is with diet and weight loss, statins, nicotinic acid and fibrates.
The hyperlipidaemia of diabetes most closely resembles this.
Patients with familial hypercholesterolaemia have increased LDL due to
a defect in the LDL receptor inherited in an autosomal dominant manner.
Heterozygosity is present in the UK in ~1 :450 people; their LDL-receptor
activity is reduced by -50%. The commonest presentation, unless picked
158
ENDOCRINOLOGY AND METABOLISM - ANSWERS
Case 2
1 C Referral to an ophthalmic surgeon
There is a 1 .5-2-cm soft-tissue-density retro-orbital mass arising from
within the right orbit, from either the greater wing of the sphenoid, the
fronto or the zygomatic bones. The orbit itself is proptosed. An
ophthalmic surgeon should be consulted in case the lesion is malignant
or there are compressive problems; benign retro-orbital tumours can
grow very slowly and just be kept under observation. Note that the
medial rectus muscles are of normal size - these are characteristically
involved in Craves' ophthalmopathy.
The thyroid scan shows several signal voids within the gland, suggesting
a multinodular gland. If this is in keeping with the exam findings, then
she could be followed up clinically or with ultrasound. The use of
fine-needle aspiration cytology depends on local practice.
There is little evidence that suppressive doses of thyroxine help suppress
the growth of goitres. Lack of evidence of benefit does not equate to
evidence of no benefit - many thyroidologists therefore still use
suppressive thyroxine. However, there is evidence that patients with a
suppressed TSH have adverse morbidity and mortality.
Case 3
1 C Cranial diabetes insipidus
Considering the problem of polyuria, the following diagnoses need to be
considered:
• Diabetes mellitus
• Diabetes insipidus (Dl):
cranial
nephrogenic
• Primary polydipsia (PP)
• Polyuric phase of renal failure.
159
ENDOCRINOLOGY AND METABOLISM ANSWERS
Case 4
1 E Primary hyperparathyroidism (PHP)
The baseline biochemistry shows hypercalcaemia, the corrected calcium
is 3.0 mmol/L (albumin is 41 g/L), the phosphate is low and there is a
normal anion gap metabolic acidosis. The 24-hour calcium is elevated,
highly suggestive of PHP. PTH increases serum calcium by mobilising it
from bone and increasing proximal tubular resorption and increases both
phosphate and bicarbonate excretion by preventing their resorption in
the proximal tubule.
The PTI I is not suppressed, suggesting one of three diagnoses:
• Primary hyperparathyroidism (PHP)
160
ENDOCRINOLOGY AND METABOLISM - ANSWERS
Case 5
1 B Anterior pituitary function
In the presence of hypoglycaemia there is an inadequate serum Cortisol.
Therefore one can confidently say that hypoadrenalism exists. A short
letracosactrin test will give no more useful information - the patient has
essentially had an insulin tolerance test.
The next question is whether it is primary or secondary hypoadrenalism.
161
ENDOCRINOLOGY AND METABOLISM ANSWERS
Case 6
1 B Distal renal tubular acidosis - RTA (type I)
The clinical details are of an arrhythmia in a well young lady who has
some aches and pains and a proximal myopathy. The investigations
show a normal anion gap metabolic acidosis with marked
hypokalaemia.
The causes ol a normal anion gap metabolic acidosis include:
• Distal renal tubular acidosis (type 1) - hypokalemic
• Distal renal tubular acidosis (type 4) - hyperkalaemic:
Addison's disease
minera locorticoid res ista nee
hyporeninaemia:
autonomic failure (Shy-Drager)
diabetes mellitus
• Proximal renal tubular acidosis (type 2).
The abdominal X-ray shows nephrocalcinosis, the causes of which are
summarised in the list at the lop of the next page.
162
ENDOCRINOLOGY AND METABOI ISM - ANSWERS
163
ENDOCRINOLOGY AND METABOI ISM - ANSWFRS
chronic obslruclion
renal Iransplantation
• Inherited:
autosomal dominant or, rarely autosomal recessive
sickle cell anaemia
medullary sponge kidney
• Drug-related:
analgesic nephropathy
amphotericin L5.
In this case the other features to note are a mild renal impairment
consistent with volume contraction, which exacerbates the secondary
hyperaldosteronism. There is perhaps a clue to the aetiology in this
youngish lady with a high ALP -primary biliary cirrhosis- or this could
represent the osteomalacia that frequently complicates the acidosis. The
autosomal dominant form can present in adulthood but more normally it
presents in childhood with failure to thrive.
In proximal RTA (type 2) nephrocalcinosis is almost never present; there
are usually multiple defects of tubular function and the urine pH can
become normal with a severe acidosis.
Case 7
1 C MRI pituitary
164
ENDOCRINOLOGY AND MFTABOLISM ANSWERS
on its own would nol ho the correct answer. Nolo the CSF glucose is
low and if it is 70% of the plasma, then there is a low plasma glucose
too.
Case 8
1 C Langerhans' cell histiocytosis (LCH)
The calculated serum osmolality, (2 x [Na + K] + (glucose + urea) is
304 mosmol/kg, yet the urine is dilute, suggesting a failure of urinary
concentrating ability. The patient is being investigated for diabetes, but
has not lost any weight; one can assume that polyuria and/or polydipsia
raised the possibility of diabetes - the plasma glucose is normal -
therefore diabetes insipidus is almost certainly present.
There are lucencies on the skull vault, the cause which may be:
• LCH
• Metastases
• Hyperparathyroidism
• Burr hole
• Neurofibroma
• Multiple myeloma
• I'aget's disease
• I Hemangioma
• Infective, eg tuberculosis.
The patient also has a rash, unsuccessfully treated as seborrhoeic
eczema. A rash is the most frequent feature of LCH, but it is often
overlooked. This, together with skull lucencies and diabetes insipidus,
makes Langerhans' cell histiocytosis the only correct answer. A tissue
biopsy should ideally be performed to confirm this. Full anterior pituitary
function tests should be performed. The disease can remit spontaneously
and il it is not causing any trouble, can be observed.
The lucencies were present in childhood, making metastases unlikely;
the patient is too young for myeloma. It is not the pepper-pot skull of
165
ENDOCRINOLOGY AND METABOLISM - ANSWERS
Case 9
1 A Primary aldosteronism - bilateral adrenal hyperplasia
There is hypertension and evidence of mineralocorticoid (MC) excess -
an alkalosis with the potassium in the lower part of the normal range. Up
to 40% of patients with surgically confirmed primary aldosteronism have
normal serum potassium; the alkalosis reflects intracellular potassium
depletion.
The next step in the investigation is to look at the plasma renin.
Suppression is compatible with primary aldosteronism; if it is not
suppressed, primary aldosteronism is very unlikely. To increase the
predictive value of this test, it is best performed on a diet with at least
100 mmol sodium per day, though this is a matter of diagnostic finesse
rather than a critical fact for MRCP purposes.
One would normally expect to see that the aldosterone is elevated as the
most likely diagnosis is primary aldosteronism (Conn's syndrome).
Conn's syndrome is an acceptable term for primary aldosteronism
caused by either unilateral adenoma or bilateral adrenal hyperplasia.
Considering mineralocorticoid hypertension more formally, the causes
are as follows:
• Normal MC receptor, normal ligand:
primary aldosteronism
glucocorticoid-remediable hyperaldosteronism (GRA)
• Normal receptor, abnormal ligand:
apparent MC excess (AME):
11 p-hydroxysteroiddehydrogenase (HSD) deficiency
I 1 p-HSD inactivation (glycyrrhetinic acid - liquorice,
carbenoxolone)
deoxycorticosterone (DOC) excess:
adrenal tumour - DOComa
congenital adrenal hyperplasia:
11-hydroxylase deficiency
1 7-hydroxylase deficiency
• Constitutive activation of receptor
progesterone- (P2)- induced hypertension (autosomal dominant
inheritance)
• Increased post-receptor activation:
kiddle's syndrome.
In our case the aldosterone is raised, confirming primary aldosteronism.
166
LNDOCRINOLOGY AND METABOLISM - ANSWERS
Case 10
1 E The statin should be discontinued
One would consider a rise in the transaminases of over three times the
upper limit of normal as a reason to discontinue the statin; otherwise,
they ought not to be discontinued. Increasing evidence shows that statins
are safe to initiate early after myocardial infarction (Ml), and clinical
practice in the UK would be not to stop.
The management of Ml in diabetes (of whatever type) is along standard
lines for non-diabetics. Retinopathy does not preclude thrombolysis.
Patients with diabetes have a worse prognosis after Ml than
non-diabetics but have a greater benefit from thrombolysis and should
always receive thrombolysis (or primary angioplasty) whatever the stage
of retinopathy.1
The absolute benefit of ACE inhibitors post-infarct is clear from several
trials and neither the renal impairment nor proteinuria preclude their
use. The presence of a third heart sound, even in the absence of
pulmonary oedema, is a clear indication of left ventricular dysfunction,
which one would expect in anterior infarction.
Beta-blockers are not contra indicated after Ml in diabetes and they
reduce mortality, sudden cardiac death and re-infarction after Ml. The
loss of hypoglycaemic awareness is inconsequential. Intravenous
p-blockade is more difficult, the evidence is contradictory but, on
balance, they are probably beneficial, although the effect may be smaller
than previously thought.2 In the presence of hypertension that precludes
thrombolysis, [S-blockers will lower the BP and allow thrombolysis to be
given. The matter in this question is easier as the systolic pressure
precludes intravenous |:i-blockade.
' Aiollo IP, Cahill MT, Wong |S. 2001.Systemic considerations in the management of
diabetic: retinopathy. American Journal of Ophthalmology, 132, 760 776.
2
Borrello F, Beahan M, Klein L, Gheorghiade M. 2003. Reappraisal of beta-blocker
therapy in the acute and chronic post-myocardial infarction period. Review of
Cardiovascular Medicine, 4(suppl 3): SI 3-S24.
167
ENDOCRINOLOGY AND METABOLISM ANSWERS
Case 11
1 C Chronic pancreatitis
The image shows pancreatic calcification across the abdomen at the
level of the first lumbar vertebra, which is almost diagnostic of chronic
pancreatitis. Intermittent, boring pain through to the back is
characteristic and the suggestion (hat he stopped drinking because of
abdominal pain is evidence of the aetiology. There is a mild anaemia
and a faint macrocytosis this could be due to Bi> deficiency, which is
occasionally found in chronic pancreatitis. The capillary glucose is
7.9 mmol/L and although we do not know whether the patient had eaten
recently, this must make one think of either diabetes mellitus or impaired
glucose tolerance - the appropriate diagnostic samples must be taken. A
mild obstructive jaundice is a frequent finding; malabsorption of fat-
soluble vitamins is common, but clinical manifestations such as
osteomalacia are rare.
Carcinoma of the head of the pancreas is a possibility but the pain is
more relentless, weight loss more of a feature, and the jaundice occurs
earlier in carcinoma; pancreatic calcification is less of a feature - but
chronic pancreatitis can develop in the pancreas proximal to an
obstructing carcinoma. Pancreatic carcinoma has a mean age of onset of
55 years, and the duration of symptoms is less than 6 months in half of
patients; the average duration of symptoms before death is between 4
and 10 months.
There is nothing to suggest metastases or tuberculous adrenal disease.
Case 12
1 D McArdle's disease
This patient's history goes back to childhood and he is now an
underweight adult with proximal wasting and normal reflexes
(MRCP-speakfor a myopathy).
The causes of myopathy are:
• Endocrine:
hypocalcaemia
hypokalemia
hypomagnesaemia
hypo- or hyperthyroidism
Cushing's syndrome
glycogen storage disorders
lipid storage diseases
mitochondrial diseases
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ENDOCRINOLOGY AND METABOLISM ANSWERS
periodic paralyses
• Inflammalory:
polymyositis
dermatomyositis
• Toxic:
corticosteroids
statins
colchicine
amiodarone
alcohol
penicillamine
halolhane- malignant hyperpyrexia
vincristine
chloroquine.
There is blood in the dipstick urinalysis but no cells or casts are seen on
microscopy, suggesting myoglobinuria. This occurs in muscle injury or
damage, as in:
• Trauma/compression
• Exercise
• Burns and electric shocks
• Viral myositis
• Sepsis - gas gangrene, tetanus, Legionnaires', shigellosis
• Malignant hyperpyrexia
• Coma
• Seizures
• Metabolic myopathies:
hypokalemia
glycogen storage disorders
mitochondrial diseases
lipid storage disorders
defects of carbohydrate metabolism
• Drugs/toxins - AZT, slat ins, ethylene glycol, isopropyl alcohol,
phencyclidine
• Snake bites.
The metabolic myopathies present with exercise intolerance and cramps
and myoglobinuria. Cramps and muscle discomfort may occur after brief
exercise (as in this case) or prolonged activity. Glycogen is the main
source of energy during brief exercise, while fatly acids are more
important in prolonged exercise. These cramps occurring early favour
glycogen storage disease.
There are several glycogen storage diseases. Pompe's usually presents in
children but can rarely present in an adult with a limb-girdle dystrophic
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ENDOCRINOLOGY AND METABOLISM - ANSWERS
Case 13
1 C Impaired glucose tolerance
This question requires a practical knowledge of the diagnostic criteria for
normality, impaired fasting glucose (IPG), impaired glucose tolerance
(IGF), and diabetes mellitus (DM). While these are complex, they must
be simplified to be practically useful. They are important as we are
habitually faced with interpretingglucose levels.
One must identify normality and identify when normality is not present.
Furthermore one must identify who to investigate more intensively (or
suggest that the GP investigates further) with surveillance, repeat testing
or, rarely, an oral glucose tolerance test (OGTT).
The importance of diagnosing diabetes mellitus is apparent. However,
the importance of diagnosing both impaired fasting glucose and
impaired glucose tolerance is often overlooked. IPG and IGT identify
patients who are at increased risk of developing diabetes; some 5% per
year, or 30% at 1 0 years. They also identify patients who are at increased
risk of developing macrovascular disease. Prospective data is sparse but
it seems that the risk of progression to DM and macrovascular disease is
greater with IGT than with IFG. Their other macrovascular risk factors
must be addressed.
There is no substitute for looking at the full WHO guidelines on the
diagnosis of diabetes but they are cumbersome.' The following points
must be taken with the proviso that samples must be repeated in
asymptomatic individuals; hyperglycaemia must be interpreted with
extreme caution in those with acute infective, traumatic, circulatory or
other stress as it may be transitory.
It is helpful to remember that, broadly speaking:
On fasting venous plasma samples:
ÿ6.0 mmol/L suggests normality;
>7.0 mmol/L suggests diabetes;
in-between is IFG.
After a 75 g glucose load:
>11.1 mmol/L suggests diabetes;
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ENDOCRINOLOGY AND METABOLISM - ANSWERS
1
http://www.diataes.org.uk/infocentre/carerec/newdiagnotK.htm
Case 14
1 D Hydrocortisone 100 mg intravenously stat and 20 mg orally tds
The clinical scenario is hyponatraemia. There is a major clue to a
possible aetiology in that she takes inhalers for mild COPD, possibly
suggesting steroids.
The first part of establishing the aetiology is establishing the volume
status of the patient. The following table outlines the possible causes
based on the volume.
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