differential of celluliti :

crythema
Herpes zosten Prochomal
nodosum/AVT ·

Phase :
painful without lesion
Genorrhea
Imp
.

Syphilis very Important

=

Introduction:
is not done any more it
Surgery
· as

Scar
leaves a
very large

Skin anatomy and histology:

The skin is composed mainly of 3 layers:
1. Epidermis Differential for tinea versicolor
2. Dermis
3. Subcutaneous tissue

1. Epidermis :

It is the upper most skin layer and it varies in thickness from less than 0.1
mm on the eyelids to nearly 1 mm on the palms and soles.
Embryology notes: 7th week of gestation – It starts to form. ectode · :

no blood vessels /newes

takes blood supply by
11th week of gestation – Nails take the final shape. from
diffusion
17th week of gestation – Finger tips take the final shape. underlying blood vessels

4.5 months of gestation – skin growth is completed.

G
The epidermis is ectodermal in origin. It contains no blood vessels and no
nerves. The epidermal cells are supplied by DIFFUSION from the underlying
blood vessels. is the main
Keratinocyte
cell in all cellular (3)
of the skin
The epidermis is composed of 3 layers : layers
A. Basal cell layer: it is a single layer that lies on the basement membrane.
It contains the following types of cells :
1. Keratinocytes: the main cell type in all 3 cellular layers of the skin.
2. Melanocytes: (10% - 15%), dendritic shaped, responsible for the
formation of Melanin (skin pigment).
3. Merkel Cells: receptor cells responsible for the sense of light touch
discrimination of shapes and textures.
-

4
 Gives the skin
B. Prickle Cell layer (stratum spinosum): in addition to keratinocytes, it also It's strength and
-
contain Langerhans cells which are dendritic shaped, antigen presenting
-
flexibility
cells (APC). is the
Part of Keratin production (which
C. Granular cell layer ( stratum granulosum ) ->
of the skin)
main component
D. Flat cell layer ( stratum corneum )
* stratum luciclum is
-
an additional layer present finger tips Soles of feet and hands
on .
.

dead cells

Skin turnover cycle (Transepidermal cycle): is the time required for

cellular maturation starting from the basal layer till the corneum layer
&
which last for 28 days in normal skin. flatcellly inPalms and detee
.corneum
.
Lucidum)

Stratum Spinosum
· (Prickle)
contains Karatin langerhans cells
2. Dermis: +

Basal (Keratinocytes + melanocytes ,

Meckel cells
·

Mesodermal in origin, and varies in thickness form 0.4 -0.6 mm.

Embryology notes: 12th week of gestation – the beginning of dermis
formation.
Unlike the epidermis, it DOES CONTAIN blood vessels and nerves.
The dermis is attached to the epidermis by hemi-desmosomes.

5
 There is 5x106 hair in the whole body, 1x105 hair in the scalp of an
adult
The growth rate of hair is 0.5mm/24hour. While the growth rate of
nails is 0.1/24hour.
Hairs are classified into 3 types: Lanugo hairs (Fine long hairs
covering the fetus), Vellus hairs (Fine, short hairs covering much of
the body surface), and Terminal hairs (long, course hair seen in the
scalp and public regions).
The hair cycle: there are three phases of follicular activity: Anagen
-

(the active phase of hair production), Catagen (a phase of conversion

-

from active growth to the resting phase), and Telogen (a resting

-

phase).

The dermis is a connective tissue and it consists of: cells, fibers and
amorphous ground substance.
The main cells in the dermis are the fibroblasts (responsible for synthesis
of collagen and elastin fibers and ECM glycosaminoglycans, giving the
shape, elasticity and strength of the skin), but there are also small number
of macrophages, lymphocytes and mast cells.
The dermis consists of 2 layers: superficial papillary layer and deep
reticular layer.

Histological changes of the skin:

1. Hyperkeratosis: is thickening of stratum corneum often associated with

excessive keratin. The skin appears dry, thickened, fissured and solid.
For example: skin thickening is lichen planus and chronic eczema.

2. Parakeratosis: is a mode keratinization characterized by retention of

stratum corneum nuclei and it is associated with loss or thinning of

2.
-

stratum granulosum. It is usually seen in skin disease with high turnover

like: psoriasis.
Retained nuclei in Keratinocytes
as a
Sign ofelayed naturation

6
3. Acanthosis: a skin condition characterized by increased thickness of
stratum spinosum. (Prickle cell
layer (

4. Acantholysis: is the loss of intercellular connections, such as

desmosomes, resulting in the separation of skin cells. It is seen in
pemphigus vulgaris.

5. Dandruff: excessive shedding of dead skin usually dry and oily,

associated with seborrhoeic dermatitis.

6. Excoriation: is superficial loss of skin caused by scratching.

* So itching is a symptom, excoriation or scratch mark is a clinical sign.
7. Scales: a small piece of the outermost layer of the skin, the epidermis.

8. Expholiation: is complete sloughing and separation of the epidermis. It

is associated with skin conditions like: pemphigus vulgaris, pemphigus
Pemphigoid, Stevens–Johnson syndrome, burns, toxication, and staph
scalded skin syndrome (SSSS).

Primary vs. Secondary skin lesions:

1. Primary skin lesions: are the lesions that appear first in the disease
process and progress to secondary lesion if it is not treated. The table
below explains examples of primary skin lesion:

7
 elevated skim lesion > 2 midth
·

Plaque : cm in

2. Secondary skin lesions: these evolve form primary skin lesion :

A. Scale: is a flake arising from the horny layer.

B. Crust: it may look like a scale but is composed of dried blood or
tissue fluid.
C. Ulcer: when the whole of the epidermis and at least the upper part
of the dermis has been lost. If epidermis is the only part that is
involved there will be no bleeding. Usually, ulcers heal forming scars.
One example of this skin lesion is the chancre seen in syphilis.
D. Fissure: is a slit in the skin.
E. Atrophy: is a thinning of skin caused by diminution of the epidermis,
dermis or subcutaneous fat.

Examples on primary and secondary skin lesions:

1. Syphilis primary skin lesion is papule >> secondary skin lesion is

ulcer.
2. Chicken pox primary skin lesion is vesicle.
3. Scabies primary skin lesion is Burrow.
4. Pityrisais Rosea primary skin lesion is Herald patch.

8
 Impetigo Subtypes
· non-bollus Bollus
·

Ecthyma Impetigo
The most common
caused by S .
aureus - ulcerative lesions with

vesicles that Progres a crusting

·

papulesthatProgress flaccid bullae with

clear Yellow
time
erythematis fluid that darkens
over
base

Bacterial skin infections:

Purulent infection
contageous Superficial
,
caused
by Stres .
(GAS) or S .
aureus

infectiom of stratum of the eidermis

I. Impetigo:
corneum
·

Honey-crusted lesions

on an erythematis base

It is a superficial bacterial skin infection that

affects only the epidermis. It is caused by
staphylococci (most commonly), streptococci
or both together.
Risk factors : I It is mostly seen in children younger than 12

yrs, affecting mainly exposed areas like the

face, hands, and lower limbs.
3 Poor warm/humid
2 .

crowding .

hygiene
%

Lesions are usually multiple and characterized

by Golden yellow crusts.
It is highly contagious disease and transmitted
through direct contact and sharing items like
towels and clothing.
It tends to clear slowly even without treatment leaving a scar.
Complications include: poststreptococcal glomerulonephritis, and arthritis
(not rheumatic fever!).

Treatment should be directed to prevent the spread (including

hematogenous spread), and decrease the risk of complications.
Differential diagnosis: impetigo may resemble scabies especially when it is
infected. Bullous type may look like pemphigus blisters. Other lesions like
Herpes simplex may become impetiginized too. This should be considered
in the differential.
The diagnosis is done clinically and treatment must not be held up until
culture results are obtained.
:
Management Soaks
crusts Salina compress + anti Serstic
Limited Turgeligo-a Remove
+

Fusiclic acid
-

Topical : Retaramulinx Murzinocin +

Extensive/ecthyma oral Penicillin/claw

-

9
 Epidermis (ectoderm)
Bacterial Skin Infections
I
Thickness :
corneum /Flat cell layer)
·
·

and soles
·

Granular
cells
·

prickle : contains Keratinocytes and langerhans

spinosum
·
Basilar :
Keratinocytes (main cell types +
melanocytes
meckel cells (Sensation)

Treatment include:
Hemi-Desmosomes Both ?
Dermis
-

superficial Parsillary 1. Broad spectrum systemic antibiotics (dicloxacilin or cephalexin).

-
Deera Reticular 2. Topical antibiotics (gentamycin and fusidic acid).

Both cellulits and crysipelas are usually

Indolent
II. Cellulitis: The skin Resembles effective
·

·
course a
very
unilateral and occur in lower limb tissue and
and unset locurs
Skin infection Involving deep dermis physical barrier between soft
over
days) anch Subcutaneous adipose tissue environment ,
in the case of cellulitis
·
localized Symptoms It is a bacterial skin infection that is frequently compared to other
:
there's a breach causing entery of bacteria
Regional Lymphadenopathy condition called erysipelas. ·
Skin Trauma , eczema , Fungal nail infection
skin ulcers
Unlike erysipelas, cellulitis is caused by streptococci but in 10%-20% of the other risk factors include
pasilent
non-Parulent
·

3-hemolytic S cureus
.
cases staphylococci are also present. Other organisms may also be the edema due insufficient lymphatic decimage
strep .

cause. Erysipelas is a pure strep infection. alsoGolden-yellow obesity Immunosuppression ·

- crusting be Present may

Clinical picture is characterized by local signs of inflammation (warmth,

redness, swelling, and tenderness), usually presented in the lower limbs.
Erysipelas frequently affects the face. Signs of generalized illness can also
be present.
Both cellulitis and erysipelas are deep skin infections but skin inflammation
occurs at a deeper level in cellulitis, where the subcutaneous tissue is
involved. (So unlike impetigo, cellulitis is a DEEP infection)
Another difference is that in cellulitis the erythema is less marginated than
in erysipelas. (This is the most important difference)
Treatment of cellulitis: is systemic penicillin (oral or IM). If the patient is
allergic, ceftriaxone is the drug of choice. (Note: penicillin is not usually
given by intravenous infusion because it is frequently a cause of
anaphylaxis).
Erysipelas : Skin infection thatInvolves the mper dermis and superficial lymphatics Differential cellulitis :

dermis
exidermis and the urpren layer of Rosacea
acute unset /fever chills and malaise) always Proculent Penicillin
management Systemic
·
. nor
,
:

·
clear demarcation and often raised ·

If there's ear involvement then it is enysipelas

Milian's ear
Sign
Recurrent cellulitis :
obesity Immunosuppression
, ,
chronic vascular insufficiency , lymphatic insufficiency
·

complications Osteomyelitis :
,
Bacteremia ,
encocarditis , Sepsis ,
Toxic Shock Syndrome
Transmission via Sexual contact or vertical hansmission
III. Gonorrhea: Second
occurs

most common STD

It is a bacterial infection and a sexually transmitted disease (STD). It is

caused by Neisseria Gonorrhea. In microscopic examination, the causative
organism appears as intracellular gram negative diplococci.
*
obligate Inlacellular pathogen
·
Some strains are Sensetive to Serum compliment System (Serum- Sensitive
10
and some are Resistant (Serum - Resistant Strains)
 ·

Infects mucus membranes (lower hact

urgential Pharynx , ,
arus/Return
, conjunctival
uses pilli to adhere to epithelial cells
they also proteins for aherance
use and invasion
,
ope
of ergithelial cells ,
may use host cell complement receptors type 3
* male to female Transmission 50.70 % Per contact (that's because N Gonorrhea .
uses lipoligosaccharide
J to attach to sperm)
Female to male 20 % for transmission Purpose

Incubation Period
The clinical presentation is variable.Gr In males, urethra is mainly infected Lurethritis)
·

1 -
14
days
Patient is infected
(the
and patients are presented with yellowish urethral discharge, and dysuria. then The discharge at first is serious

experiencing but
volume and increases in
- cervicitie
Purulent
not In female patients, the cervix is the affected part and patients are becomes more

Symptoms Yet) presented with lower abdominal pain, bloody vaginal discharge, and
dysuria. vaginal discharge the most initial
Symptom (Prudent
is oclorous/ common ,
thin and may be

Dysparennia Intermenstrual Post-coital Post-menopausal bleeding or

Diagnosis starts with history and physical examination. It is confirmed by

,
,

examination of a smear obtained from the urethra 2 cm form the external

urethral meatus or midstream urine catch specimen in males, and by
cervical swab (not vaginal swab) in females. This way, the possibility of
contamination is reduced.
 Histological preparation of smear includes gram staining, Gonorrhea appear as
intracellular gram negative (i.e. pink color in opposite to gram + which appear blue)
diplococci. diagnosis could be done by Nucleic acid amplification Test (NAAT/PCR)
or

 In Gonorrhea history taking, important to ask about sexual activity history and allergy to
penicillin. Rectal Gonorrhea Primitis rectal * : ,

Pain ,
Tenesmus

Complications of gonococcal infection could include: chronic septic ophthalmia neonatorum neonatal
transmission during delivery
* :

arthritis. Specific complications that occur in males are: 1. chronic orchitis. These patients for are at risk

2. Epididymitis 3. Infertility that may necessitate IVF. In females, Systemic gonorrhea

Disseminated Gonococcal
complications include: 1. Pelvic inflammatory disease that may lead to 2. *

infection 1 : Vare %

Ectopic pregnancy or 3. Infertility. likely to be infection ·

more
an

Treatment is, either:

with Serum-Resistant strain

fever Rash
migratory Polyarthritis , ,

1. One single shot of ceftriaxone 1 g IM or, Tendonitis meningitis encocarditis , ,

2. Oral ciprofloxacin (2 tablets 500mg X2). If the patient is allergic to ceftriaxone ( note it’s a
drug used for UTI) Azithromycin is also added
·

Impiric treatment for chlamydia is they as an co-occur

All partners should be treated at the same time. together usually


IV. Syphilis:

It is a bacterial infection and a sexually transmitted disease, too.
Treponema pallidum is the causative organism (detected by dark-field
microscopy).

G-ve
negative Bacterium outside the human body'
·
,
an
obligate parasite I can't Survive

affects skin and mucus membranes (external genitalic and month) .

It belongs to Spirochetes which are a group
of bacteria that have endoflagella protein filaments) spiral
, in sharge and move
by Spinning

11
 The incubation period ranges between 9-90 days from the time of -

exposure. The average is 21 days. The clinically presentation can be

classified in 4 distinct stages and the disease is contagious in all stages.
These stages can be summarized in the figure below.

·
DDX for chancre : HSV ,
chancroid , Pemihigus
Bowen's SCC
5 signs of syphilis
,

choudyloma
& oral ulcer (
, chondyloma lata (differential is accreta

mouth eaten alopecia, chancre appears

IDBX discoid Lupus) SyphilitiaT
·

after .

pallidum lands on

the
the skin and Destroys

days /
Tissue
is 21
Laverage

In this stage
the
Spirochetes enter
blood stream causing
ISpirochetemia)
Disseminated Stage
-
The most contageous
stage wants caused by human
:
anogenital
Papilloma virus 6 , 11 16 18
, ,

Smooth white
and Painless want like lesions

asymptomatic Stage (Spirochetes

are found within small
and organs)
capillaries
Liver Joints and
,

Testis

Few
Spirochetes ,
but cause
Type IV
hypersensitivity
reaction /Severe Immune Response lead by T cells)

(Gummy tumors
.

lipoma lupus vulgaris (manifestation

,

of TB

12
 1. Primary syphilis:

The primary skin lesion is a small papule. It lasts for 7-12 days. After that,
a superficial ulcer (chancre) appears at the site of inoculation as a
secondary skin lesion. (In some cases the papule disappears spontaneously
and does not continue to the following stages).
 Many doctors think that primary skin lesion is chancre not papule because the patient
seeks medical attention for chancre not papule as it’s underestimated.
A typical chancre is ulcerated, although NOT painful, button like lesion
(with central umbilication or look like a volcano, spongy texture) that is up to 1.5 cm in
diameter accompanied by local painless lymphadenopathy. If untreated it
lasts for 4-6 weeks and then clears spontaneously.
Differential diagnosis for genital ulcers include:
1- Syphilis ( painless ulcer)
2- Behcet disease (painful oral and genital ulcers).
3- Blistering skin disease like pemphigus.
4- Fixed drug eruption: may appear as ulcerated blue colored lesion. It
recurs at the same site with each exposure to each particular
medication. Drugs causing fixed drug eruption: some NSAIDs and
antibiotics.
5- Herpes simplex: a painful vesicle or ulcer.
6- Candida infection: desquamated ulcer and burning sensation. In males
it could present as balanitis (infection of the glans penis)
7- Contact dermatitis: could be ulcerating but a wider lesion (3-4cm) with
erythema, scaling and itchy.
8- Chancroid: it is caused by a bacterial infection, too. It differs from
chance in: It could be multiple; it is painful, and accompanied by painful
adenopathy. It’s caused by the bacteria- Haemophilus ducreyi
9- Squamous cell carcinoma (SCC)
C10- Bowen’s disease (risk of malignant transformation). (SCC in situ)

13
 2. Secondary Syphilis:

It is characterized by the following features:

1- Non-itchy macular rash (localized or generalized)
2- Mucous membrane involvement (oral ulcers or erosions)
3- Condyloma lata (a smooth flat plaque around the anus)
4- Allopacia (partial multiple hair loss of the scalp < 5mm) also called moth
-

-
eaten allopacia.
Note that the chancre disappears in this stage.
Differential diagnosis of different features of secondary syphilis:
A. Non itchy macular rash:
1. Urticaria ( itchy skin rash in this case)
2. Drug reaction.
3. Pityrisais Rosea
4. Guttate psoriasis (if partially treated).
5. Tinea versicolor.

B. Mucous membrane involvement:

1. Behcet disease.
2. Pemphigus vulgaris
3. Drug reaction
4. Candida infection
5. Squamous cell carcinoma
6. Trauma
7. Ulcerative lichen planus (chronic mucocutaneous disease with risk of
malignant transformation to SCC).
8. Leukoplakia: patches of white keratosis firmly attached to oral
mucosa usually in heavy smokers. It is also premalignant.
9. Recurrent aphthus ulcers associated with stress or PUD or Crohn’s disease.

Note: what is the difference between lesion and rash?

Number, Rash is all over the body/area, so uncountable involvement; examples include
chickenpox and drug interaction.

14
 C. Condyloma lata:
1. Condyloma acuminata: genital warts caused by HPV infection.
2. Other viral infections (painful, raised, and irregularly shaped)
D. Allopacia:
1. Allopacia Areata:
2. Discoid lupus (associated with scar formation)
3. Seborrhoeic dermatitis
4. Tinea Capitis
5. Psoriasis
6. Lichen planus
7. Trichotillomania (psychiatric disorder).
(Note: discoid lupus and lichen planus cause permanent hair loss)
cicatrical alopecia

3. Latent Syphilis:

Is the hidden stage where there is positive serological tests and no clinical
symptoms and signs. (All previous 4 features disappear)
It is divided to two phases:
1. Early latent syphilis ( <2 years from first exposure)
2. Late latent syphilis (>2 years from first exposure)
-

4. Tertiary syphilis:

It may occur after 3 to 15 years after the initial infection and may be
divided into 3 different forms:

1. Gummatous syphilis: multiple nodular lesions with have the same color
as the skin called Gumma. (Note: the differential includes lupus vulgaris
of TB but this condition is characterized by apple juice color and lipomas).
2. Cardiovascular syphilis: CVS involvement particularly aortic aneurysm
(requires investigation with echocardiography). May lead to sudden death.
3. Neurosyphilis: LP and CSF analysis show (increased protein, decreased
Glucose, pleocytosis (increased WBCs), and + VDRL).

15
 Diagnosis not Treponemal Tests
These tests are

Non-Treponemal
T
pallidum Particle agglutination
Tests
specific for
Syphilis
·
.
-

absorbed
·

Rangid Plasma Regain as they detect anti-cardiolipin · fluoroscent herponemal antibody

·
veneral Disease Research antibodies (Reagin) >
-
These tests detect antibodies that

laboratory Tests (VDRL) which is alsoPositive in Pasients with specifically Tanget T.

pallidum
hypersensitivity Reactions

  Syphilis History talking must include: sexual activity (usually the patient denies), travel
 history, occupation, allergy to penicillin and you must ask about related STDs like AIDS,
 genital warts, Gonorrhea)

 In general, the diagnosis of syphilis is based on good history (history of sexual contact,
travel history, drug allergy like penicillin since it is the treatment of choice), good
physical examination (examination of the skin, scalp, oral cavity and genital areas), and
the diagnosis is confirmed by laboratory tests.
 Lab tests for diagnosis of syphilis include:
1. VDRL (venereal disease research laboratory): a serological test used for
screening of syphilis (it has high sensitivity, but more specific tests are
used for diagnosis). False positive test may be seen in: leprosy, TB,
connective tissue diseases like SLE and sarcoidosis, measles, certain
malignancies like lymphomas, and pregnancy.
So if a pregnant lady had +VDRL ask her detailed history then do the specific test.

2. TPHA (treponemal pallidum particle agglutination) and FTA-Abs

(fluorescent treponemal antibody absorption) are used for the diagnosis
(more specific). These tests are more expensive.
Plasma Reagain Test (RPR)
.
3 Raid
Treatment of syphilis remains the same regardless of the clinical stage at
the time of diagnosis. (Treatment for late infection is actually different).
The drug of choice is Benzathine Penicillin – Benzathine penicillin G (IM).
- Total dose is 2.4 million international units. This means 2 vials of 1.2 M
IU prepared with procaine 1% in 3 cc, a total of 5 cc (because it’s painful). The total dose is
given in two shots at the same time (vial to each buttock). The treatment is repeated after
one week.
- If the patient is penicillin allergic: the drug of choice could be:
1. Ceftriaxone (3rd generation cephalosporin) 1 g/ daily for 5 days.
2. Erythromycin: 2 g daily for 15 days.
3. Doxycycline: 200 mg daily for 15 days
- Repeat VDRL and physical examination after 1 month, 6 and 12 months.
o you must tell the patient husband/partner and report ministry of health (number not
name)

16
Jarisch-Herxheimer reaction: is one of the potential side effects of
treatment. It frequently starts within 1 hour and lasts for 24 hours, with
symptoms of fever, muscle pain, headache and tachycardia. It is caused by
cytokine release caused by immune reaction against bacterial toxins not a
reaction against penicillin. Treatment is a single pill of NSAIDs.

Congenital syphilis: the transmission occurs during pregnancy or during

delivery. Affected infants are usually asymptomatic. The symptoms appear
in the first year of life in most cases, including: Hepatosplenomegaly, rash,
fever, and characteristic finding like Hutchinson teeth. Delivery must be
through CS.
Diagnosis is
by looking at the baby and the mother's

Serological tests together

17
 Viral Infections
·
topical acyclovir + antihistamine
+
analgesic
I. Herpes simplex virus infection: · To decrease Recurrence :
Systemic
a
cyclonic 400 my X10 days

The presentation is usually vesicular,

painful skin rash. It has been separated
into two types (this distinction is not
absolute) :
1. HSV type I: is usually extragenital
frequently affects the lips and face.
- High recurrence rate.
- If a lady got type I you must send her for OBGYN
For speculum exam of cervix for type II.

2. HSV type II: mainly on the genitals. It

presented as rapidly ulcerating vesicle that increases the risk for&
SCC.
 More in females, found on cervix as ulcer not external genitalia, presents with pain
and vaginal bleeding, OBGYN do a speculum exam followed by cauterization of the
ulcer and treatment, if recurrent of non-resolving go for pap smear, biopsy and if
carcinoma is detected go for hysterectomy.

Treatment: may include topical acyclovir, systemic antihistamine, and

analgesic.

o In the last year, treatment changed to systemic acyclovir 400 mg once daily for 10 days

to decrease recurrence in addition to topical acyclovir, antihistamine and analgesia.


 II. Herpes zoster:

unilateral
It is caused by herpes virus varicella zoster (the same virus that causes dermatomal
chickenpox). An attack is the result of the reactivation, usually for no pattern
obvious reason, of virus that has remained dormant in a sensory root
Sensory Root
ganglion. Reactivation is sometimes associated with trauma, surgery,
stress, drug ingestion, or conditions which weaken normal defense
ganglic
mechanisms.
Clinical presentation: when it is reactivated the skin lesions will have a
dermatomal distribution characteristically unilateral. It is rarely bilateral
and affecting multiple dermatomes.
Prodromal phase precedes the skin rash; local parasthesia and burning
pain in dermatomal distribution, too. It is easily missed diagnosed as (differential diagnosis of
prodromal phase) :
- Acute myocardial infarction if left sided thoracic 18
- Appendicitis if lower abdominal distribution.
 - Disc prolapse or sciatica if back pain is the presentation
- Migraine headache if the face is affected
- Cholecystitis if RUQ pain is the chief complaint.

- Pancreatitis rarely in case of bilateral dermatomal pain (band

like).
To prevent misdiagnosis: take good history, do thorough PE, and order
CBC, ECG, and CXR. Start the treatment once the diagnosis is suspected DO
NOT wait for the skin rash to appear.
The most common form is Thoracic. But the most painful and worst
prognosis is when the ophthalmic division of trigeminal nerve is affected.

 The Differential diagnosis of the clinical phase include the blistering diseases like
pemphigus vulgaris, pemphigoid, drug reaction, burns, dermatitis herpatiformis,
 erythemia multiform, bullous impetigo

Treatment:
1. Systemic acyclovir (oral):-
800 mg x 5 times daily for 5 days. It is given to
reduce the incidence of postherptic neuralgia and it is ONLY effective in
the first 72h form the onset of skin rash appearance.
2. Analgesic like NSAIDs.
3. Topical acyclovir to promote healing and epithelialization.

 If you detect it in the prodromal phase give only systemic acyclovir, after that if
 vesicles appear give topical.

To estimate the time of lesions onset:
- Intact blisters (filled with plasma or even blood) < 24 hours.
- Ruptured and necrotic lesions (dark brown and crusted) > 72 hours.
(Systemic acyclovir is not given in this case since it is ineffective).
Complications:
- Post-herptic neuralgia, it may last for 3-6 months. Give gabapentin
- Active infection during pregnancy increases the risk for congenital
malformations (like cleft palate and hydrocephalus).
Acyclovir is completely safe during pregnancy.

19
 IV. Orf:

Its cause is parapox virus that can be transmitted to those handling

infected animals (zoonotic disease), like shepherds, butchers, and vets. It is
not transmitted from infected patients.
It is presented as asymptomatic single or multiple papule or nodule; no
pain and no itching, usually in the hands.
It could be associated with erythema multiform (examine the whole
body). And specially the oral cavity.
NO active treatment is required except in severely symptomatic patients.
It usually resolves spontaneously within 4-6 weeks.
 Advice patient to wear gloves at work, give psychological support that these
are self-limited, give ointment or moisturizer.

Note: erythema multiform can affect skin and also mucous membranes of bronchi
and oropharynx leading to bleeding or dyspnea so it’s an emergency that may
necessitate ICU admission.
Causes:
Infections, drug interaction, Stevin Johnson syndrome (emergency)

skin lesions + mucous membranes

Crythema multiform Involvement

k
·
SIS
DDX

che a

21

erythema multiforme
Steven Johnson Syndrome
·
 distribution :
waen
V. Molluscum contagiosum: caused by pox Chest and neck
mostly
,

in children
A viral infection presented as skin lesions. Individual lesions are shiny, causes Severe
white or pink, and hemispherical. A central punctum, which may contain a
cheesy core, gives the lesions there characteristic umbilicated look. itching
Treatment: many simple destructive measures include squeezing out the
lesions with forceps. Liquid nitrogen may also be helpful.
+topical Retinoic acid

22
 Fungal infections:
only
Dermatophyte infections (ringworm):
survivea
in
peri
Dermatophytes invade keratin only (this is why they are only superficial infections, no
keratin in lungs or heart for them to survive). Visceral fungal infections are not
Dermatophytes. In general zoophilic fungi (those transmitted to humans
by animals) cause a more severe inflammation than anthropophilic ones
(spread from person to person).

The presentation depends upon the site:

I. Tinea of the scalp (tinea capitis):

This is usually a disease of children (<12yr). The affected area is scalp hair
and skin (dermaomicrosporum).
They actually invade the hair NOT the skin, spores are seen in the hair shafts not around the
hair.

 It is characterized by: partial alopecia, scaling, and broken hair.
Fungi coming from animal sources (zoophilic fungi) induce more intense
inflammation than those spread from person to person (anthropophilic). In Bacterial
Tinia carits
the former, bacterial infection is suspected and the lesion is called Kerion > Inflammatory
-

(wet tinea capitis). So +KOH and + bacterial culture, give antibiotics and antifungal together.

Differential diagnosis include: alopecia areata (complete hair loss, with no

scaling, or broken hair), psoriasis (silver colored skin lesions with no hair
loss), seborrhoeic dermatitis, discoid lupus (hair loss and scar formation),
lichen planus, impetigo, carbuncle, abscess and trichotillomania.

 Lichen planus and discoid lupus cause special type of hair loss with scarring called
 cicatricial alopecia, it’s permanent irreversible hair loss as the hair follicles become
 atrophic.
Diagnosis is confirmed by microscopic examination of skin scraping,
containing hair, treated with 10% KOH solution. The test will be positive
when branching hyphae are seen. Spores can also be detected.
  Dry samples of skin/hair are taken by scrubbing
  If the lesions got fluids go for a smear
  Why KOH ? to dissolve the keratin
  Spores appear black colored cocci (like bacteria), and are seen in the hair shafts not
-

 around the hair.

 23
Treatment includes:
 dermis the dermis
Hair follicle is within the when
using tropical antifungal it doesn't reach
.

The vascularised part of skin is dermis

that's
why given Systemic

1. Systemic antifungal medications: E Griseofulvin is the drug of choice

(12.5 mg/kg/day for 6 weeks). The dose can be increased up to 20
mg/kg/day.
 It’s in syrup form so may cause GI disturbances, if so switch to Terbinafine for
patient compliance.
 If the patient is compliant but after 2 weeks there is bad outcome you have 2
choices: either you increase the dose to 20 mg/kg/day or switch to Terbinafine.
.
2. Topical antifungal preparations: (Topical ketoconazole and
moisturizers) the main goal is prevent the spread of infection (highly
contagious). So can use anything that prevent spread like vaseline, antihistamine ..etc
If it’s highly contagious, do we prevent the child from going to school for 6 weeks ? No,
just use topical preparations, wear a hat or any head cover, and tell the teachers/
principle to keep him away from other children as possible.
3. Follow up in 2 weeks to cheek the progression and compliance.

4. An alternative treatment is: Terbinafine tablets. The dose is according

to body weight:
·
branching hyphae
- < 20 kg: 62.5 mg/day,
- 20-40 kg: 125 mg/day, spores black: cocci

- > 40 kg: 250 mg/day (adult dose). like bacterial

II. Other types of tinea infections include: (Note: The treatment for the
following conditions is topical preparations except for tinea
unguium. All are confirmed by KOH test, you can also add antihistamine).

1. Tinea corporis (also called tinea circinata) affects arms and legs. DDx
includes: drug reaction, urticaria, secondary syphilis, guttate psoriasis,
p.rosea.
2. Tinea versicolor: affects the trunk and proximal extremities. DDx vitiligo
(only color change), 2nd ary syphilis.
3. Tinea manuum of the hands. DDx: contact dermatitis, psoriasis.

4. Tinea cruris of the groin. DDx includes: contact dermatitis, urticaria,

erythrasma (bacterial infections requires antibiotic treatment).

5. Tinea pedis (athlete’s foot). DDx: psoriasis, contact dermatitis,

pustulodermatitis.

6. Tinea faciei of the face.

24
 7. Tinea barbae of the beard.

8. Tinea unguium of the finger nails (discussed later).

Clinically, all of the forms have reactive margin, ie the disease is

expanding in course as dermatophytes are looking for more
keratin.
III. Onychomycosis: ( tinea unguium)

It is a fungal infection of the fingernails frequently affects one nail in
patients above 12years. It includes: superficial, proximal and distal
subtypes.
It is clinically characterized by:

1. Nail discoloration (black or brown)

2. Deformity of nail shape.

3. Thickening of the nail up to 5mm (normal thickness is 0.01-0.5mm).

Differential diagnosis includes:

1. Psoriasis (in this case most of the nails are affected not only one nail, also psoriasis is
likely to affect other areas).
2. Contact dermatitis

3. Lichen planus

4. Trauma

5. Malignant melanoma (L-shaped with the proximal and lateral boarders

show brown or black discoloration/ Hutchinson sign).

6. Atopic dermatitis
7. Paronychia (see below)

25
Side-effects of Systemic antifungal :
herpatotoxic causes slight elevation in herratic enzymes +

Reversibla
nail Growth Rate is

0 .

1mm/day

Treatment : Discontinued when both clinical signs resolve and

↑ Kolt results are
negative
Systemic antifungal: Terbinafine 250 mg/day. It is given till signs of
clinical (normal nail shape) and mycological (negative KOH) cure are
noted. This may take 6-12 months (the time for the nail to be
completely replaced).
 Note: remember that nail growth rate is 0.1mm/day, if it was the proximal type,
after 1 month, the nail is still covered by skin (of nail bed) and you need at least
 2 months to see initial results
  After nail appearance, advice monthly follow ups with KOH test each time, stop
 medication when the test is negative.

One of the dermatological conditions that affects the nails and it is
included in the differential diagnosis of Onychomycosis is Paronychia. It is
a bacterial and fungal (usually staph and candida) infection of hand or foot
where the nail and skin meet and the sides of base. It is presented either
acutely or chronically and often painful. Acute paronychia presents with
redness, swelling, and pain. It is managed with antibiotics and drainage if
abscess is present. Analgesics are given if pain is present. Chronic
paronychia presents with scaling, dryness, pain and swelling and it is
managed with topical antifungal and systemic antibiotics.

26
 Papulosquamous skin diseases:
I. Psoriasis:
It is a chronicnon infectious
Inflammatory skin disease,
Characterized by well-defined
erythematous plaques bearing large
adherent silvery scales. Usually, it
appears between the ages of 15 and 40.
The prevalence ranges between 1% and
3%.

There are 10 different clinical forms of

psoriasis:

1. Psoriasis vulgaris (common psoriasis) affects about 85%-90% of patient

with psoriasis. The plaques are most commonly found on extensor
surfaces (knees and elbows), back and scalp.
Note: lichen simplex chronicus: neurodermatitis is found on the occipital parts of scalp, see
the picture below
2. Punctate psoriasis, lesions appear like a skin rash.
3. Guttate psoriasis (1-1.5 cm lesions)

4. Plaque psoriasis (5-10 cm lesions)

5. Palmoplanter pustular psoriasis (PPPP)

6. Generalized pustular psoriasis

7. Nail psoriasis
Note: Paronychia: seen in a house wife with water use, composed of fungal and bacterial
infections; Candida and staph. Treated with systemic antibiotics and topical antifungal.

8. Psoriatic arthropathy
9. Flexural psoriasis (inverse psoriasis) affects skin folds.
10. Erythrodermic psoriasis (the worst prognosis, with risk of cardiac
failure). 33
 ⑤
Nail psoriasis is characterized with pitting of nails involved you can also see furrow ( in atopic
dermatitis, contact dermatitis)

How to differentiate onychomycosis and psoriasis ? Only one nail or multiple? And KOH test


Diagnosis of psoriasis is based on:

1. History: ask about family history (genetic predisposition, autosomal

dominant inheritance in some cases), and environmental triggers,
including: tonsilar inflammation or URI, drugs (antimalarials, beta
blockers, lithium, or NSAIDs).
Upper respiratory tract infection specially in children, tonsillectomy not necessarily to
resolve the psoriasis.

2. Physical examination: examination of the lesion to determine clinical

subtype. Specific signs that can be noted include: Kobner phenomenon
(if psoriasis is active, lesions can appear in skin damaged by scratches or
surgical wounds), and Auspitz sign (pinpoint bleeding when a scale is
removed.. caused by elongated dermal papillae).

(Note: Kobner phenomenon is positive in other conditions like: warts, lichen

planus, vitiligo, and atopic dermatitis). Kobner phenomenon can happen of scratch marks or on
surgical or other scars.

3. Skin biopsy to confirm the diagnosis: histopathological examination

shows the following changes: hyperkeratosis, Parakeratosis, elongated
dermal papillae, PMN infiltrate and microabscesses and T cell infiltrate
 in the upper dermis.

 DDx for Guttate psoriasis: scabies, secondary syphilis, drug reaction,
 Pityrisais Rosea, and tinea versicolor.
Treatment of psoriasis
1. Topical treatment if the affected area is <20% of body surface area.
Apply therapy until normal texture is reached, this can be after hours, days, weeks, and
this is for each individual lesion independently.

This include:
1- Topical steroids (it has anti-inflammatory effects)
2- Keratolytic preparations (lactic acid and salicylic acid preparations)
3- Systemic antihistamine
4- Dithranol (decrease energy supply by the mitochondria, and
decrease cell proliferation that occurs in psoriatic plaques).
steroid
Systemic causes
questi on Psoriasis 34
rebound effect
triggers
question
* on what we see on biopsy
I not only for Psoriasis
 5- Vitamin D3 preparations - Vit.D decreases DNA replication

6- Local phototherapy.

2. Systemic treatment if the affected area is >20%.

1- Ultraviolent (phototherapy): It works by increasing the time

required for DNA replication thus increasing the transepidermal
cycle (already shortened in psoriasis). (Note: UVA is used for
treatment of skin conditions. UVB causes skin burns after prolonged
sun exposure. UVC used for sterilization).

2- Photochemotherapy (PUVA): Psoralin (oral pills) is added to

increase the efficacy of phototherapy. One hour session for 3 times
every week is the standard. Eye exposure is minimized by wearing
special glasses for 6 hours after the procedure. PUVA is
contraindicated for children < 10 years.

3- Retinoic acid plus PUVA (RE/PUVA)

4- Immunosuppressive therapy: methotrexate is the drug of choice,

single dose 5-30mg weekly. Hepatotoxicity and nephrotoxicity are
probable side effects.

5- Biological Treatment: TNF inhibitors like adalimumab and

etanercept.
TNF factor inhibitors side effects include malignancies like leukemia and lymphoma. they
only improve life quality, not radical treatment.

Systemic corticosteroids are contraindicated in the treatment of psoriasis.

Rebound reaction happens when they are discontinued (generalized,
severe reaction including Erythrodermic psoriasis)

35
 Complications of long-term use of topical steroids include:

1- Skin atrophy (loss of the epidermis) 2- Telangiectasia

3- Erythema (redness) 4- Changes in pigmentation

In Erythrodermic psoriasis, start the treatment with immunosuppressive

and biologics.

PUVA is also used for treatment of: vitiligo, atopic dermatitis, allopacia
areata, lichen planus, and mycosis fungoides.
RE/PUVA is indicated for psoriasis only, not other diseases treated by PUVA.
** Causes of skin atrophy/dermal atrophy:

- Chronic topical steroids use and after steroidal injections

- ACNE vulgaris (as a complication you get skin atrophy, ie depressed area on skin)

- Burns - Discoid lupus

- Localized scleroderma (Morphea) - Lichen planus.

** How to prevent skin atrophy with steroids?

Use pulse (sequential) therapy method, to give steroids for 1 week followed by 3 weeks free.

** About ultraviolet light spectrum (mentioned by the doctor, numbers and details from Roxburgh’s common
skin diseases)

UVA light - long wave length 320-400 nm

UVB light - medium wave length 280-320 nm

UVC - short wave 250 - 280 nm (not found in nature, used for sterilization purposes in operation rooms)

UVB (around 290 nm) causes sun burn, sun tan, and skin cancer; it only penetrates as far as basal layer of
epidermis.

UVA: penetrates the dermis causing dermal degeneration known as solar keratosis, causes skin aging, cancer
and photosensitivity.

So PUVA means psoralin + UVA light.

** Contraindications for PUVA

- Renal / liver failure - for the chemotherapeutic agent psoralen - age less than 10 - photosensitivity. -
erythrodermic psoriasis, as the patent is severely ill and too weak to stand in the machine, he can fall down and
damage the machine (which is very very expensive)

** Why visiting areas like Jericho and Dead Sea improves the patients? - Jericho is lowest area on earth 36
so
UV-light is concentrated, like it's a natural PUVA. - Psychological support.
 acute
·

non-contageous
Parpulosquamous skin disease

Drugs Infection
II. Pityrisais Rosea:
,

Stress
 It is an acute, non-contagious,
papulosquamous skin disease frequently
affecting the trunk (chest, abdomen, and
back). It has usually a sudden onset but it is
associated with certain triggers, including:

1. Infections

2. Drugs

3. Psychological stress (the most common

trigger accounting for 90% of cases).

Most patients develop one plaque (Herald

patch) before the other (a primary lesion). It
is larger than later lesions, and is rounder, redder, and more scaly. After
several days many smaller plaques appear. The configuration is usually
characteristic; the longitudinal axes run parallel to the spine, and along the
lines of the ribs (Christmas tree). what the DDX for Christmas hee
is

urticaria seboic dermatitis

,

management spontaneously resolve

: within

The diagnosis is based on history taking and physical examination. The

illness is usually self-limiting with the eruptions last for 2-10 weeks
(average of 4 weeks) and then resolve spontaneously. DDx is similar to
secondary syphilis.

NO treatment is curative, and active treatment is seldom needed.

Moderately potent topical corticosteroids and systemic antihistamine will
help the itching. In some cases, a trial of antidepressants for 2-3 weeks
may decrease the stress and can be useful. See pictures very
Important
Types of Basal cell concinoma * Lichmania
·

Piteyasis Rosea psoriasis) Stateel

·

gutate
·
Timia carpitis ·
Rituximab (for pemphigus
* T-cell
Lymphoma
needs hospitalization)
anti CD20
·
contact decmatitis

Red
intimals are Given only within
Pemihisoid comes
·

on
7) hores of
·

37
Skin vesicles appearance not guien
,

Tinea versicularis * Spagetti after because

.
they become
and meatballs inefective (the inflammation is
what causes
Symptoms after 72 his
not the
ninus)
 leshmania ,
Scabies (no questions

Treatment
III. Lichen planus:
not in exam

The precise cause of lichen planus is unknown, but the disease is thought
to be related to some immunological process. It is still considered a chronic
papulosquamous skin disease.

Typical lesions are polygonal, or lilac

colored, intensely itchy, flat topped
papular skin rash. It usually arises in the
abdomen and extremities, particularly
the inner aspects of the wrist and legs.
On a close look, a whitestreaky
pattern on the surface of papules can
be seen (Wickham’s straie).

Lichen planus may affect: skin, nails

(10% of cases show changes ranging from fine longitudinal grooves to
destruction of nail fold and bed), and mucous membranes of oral cavity.
When it affects the scalp it causes irreversible allopacia called (cicatritial
allopacia).

A usual presentation is itching resistant to antihistamines. Regarding

Examination, as in psoriasis, Kobner phenomenon may occur. Skin biopsy
is indicative to confirm the diagnosis although the diagnosis is usually
obvious clinically.

Very characteristic to lichen planus that it's a rash that don't respond to antihistamines.

(Dermatitis herpatiformis is also like this; antihistamine resistant)

DDx of lichen planus: scabies, tenia versicolor , D.herpatiformis, contact dermatitis, drug
reaction.
4 places affected in lichen planus :

- Skin: polygonal, dry, itchy, scaly, lilac colored, transverse lines/wickham's striae

- nail : grooving, destruction

O
- mucous membranes : ulcers that if not treated can turn SCC.

- scalp : cicatritial allopecia. 

Treatment
 can be difficult. Treatment modalities include: potent topical
38
 steroid, systemic steroid courses, and Photochemotherapy (PUVA).
The most serious complication is that ulcerative form of lichen planus in
the mouth may lead to squamous cell carcinoma.
 [
Biological site of Pemphigus
deposition
·

Side effect ·
Pemiphigoid
Dermaliti herpetiformis
·

Bullous skin diseases:

I. Pemphigus:

 It is a chronic, severe and potentially

life threatening disease that affects the
skin and mucous membranes.

 It is an autoimmune disease in which

pathogenic IgG antibodies bind to
antigens within the epidermis (Type 2
hypersensitivity reaction). The main
antigen in pemphigus vulgaris is desmoglein; it is a cell adhesion molecule
found in desmosomes. The antigen–antibody reaction interferes with
adhesion, causing the keratinocytes to fall apart (Acantholysis). In
pemphigus, the level of separation is suprabasal and can be detected by
direct immunofluorescence staining.
* Desmosomes are important for skin shape preservation.

O
* IgG mostly, some textbooks mention little IgA and IgM.

(NOTE: the appearance of the blister is determined by the level at which it

forms and can be seen in different conditions. Subcorneal separation is
seen in IgA dermatosis and herpes simplex. Sub-epidermal separation is
characteristic of bullous pemphigoid).
Factors/elements for immunocomplex reaction to take place: antigen, antibody,
complement system, site/environment (in pemphigus it's supra-basal area)


 Clinical presentation is characterized by flaccid blisters of the skin and
mouth and, after the blisters rupture, by widespread painful erosions.
Usually, the blisters range between 2cm and 7cm in diameter. Most
patients develop the mouth lesions first, and mucous membrane
involvement may be the only clinical manifestation. Positive Nickolsky’s
sign is characteristic for& pemphigus vulgaris. The sign is present when
slight rubbing of the skin results in exfoliation of the outermost layer or
expansion of the bullae.

- Note Pemphigus oral ulcers are nonresponding to treatment.

- Patient got bad fishy smell due to fluids infection from blisters
39
 dermatitis herpetiformis
bilateral and
symmetrical
GI
Lymphoma
associated
DDx of skin lesions in PV includes: burns, epidermolysis bullosa, erythema when
with celica
multiforme, Steven Johnson syndrome (SJS), dermatitis herpetiformis,
drug reaction, bullous impetigo, or&
herpes zoster. Mouth ulcers can be defenctive Diagnosis
·

mistaken for aphthae, lichen planus, Behcet disease, trauma, or drug is

biopsy Perilesional - a

reaction. 3 above lesion IgA cm

is found Perilesional
Bapsone
Diagnosis is made based on history and physical examination. Usually management
affected patients are middle aged females. Information of disease duration
and past medical history of diabetes, hypertension, osteoporosis, and
peptic ulcer disease are also important to be obtained (since the treatment
would be high dose steroids!).

Skin biopsy shows that the& vesicles are intraepidermal, with rounded
keratinocytes floating freely within the blister cavity (acantholysis). Direct
immunofluorescence of adjacent normal skin shows intercellular
epidermal deposits of IgG and C3. Serum antibodies detected by indirect
immunofluorescence can be used to confirm the diagnosis. (NOTE: Tzanck
test, also known as Tzanck smear, is scraping of ulcer base to look for
Tzanck cells; multinucleated giant cells). Tzank test show acantholysis cells - giant
multinucleated cells.
* Immunofluorescence: direct for diagnosis, indirect for screening and follow up.

(The fluorophore allows visualization of the target distribution in the sample under a fluorescent microscope
(e.g. epifluorescence and confocal microscopes). We distinguish between two IF methods depending on
whether the fluorophore is conjugated to the primary or the secondary antibody:

- Direct IF uses a single antibody directed against the target of interest. The primary antibody is directly
conjugated to a fluorophore.

- Indirect IF uses two antibodies. The primary antibody is unconjugated and a fluorophore-conjugated
secondary antibody directed against the primary antibody is used for detection.)

Life threatening complications of PV include: infection of blisters

complicated by sepsis, or massive fluid loss resulting in hypovolemic shock
and electrolyte disturbances. Most deaths occur in the first few years of
the disease, with average survival rate 1.5 year even with treatment.

Treatment: (usually the patient needs admission for some time)

1. High dose systemic corticosteroids (80-120 mg prednisolone daily)
T

(Note: low dose steroid is 20mg, moderate dose is 60-80mg, and high dose 80-
120mg). 40

2. Immunosuppressive drug (steroid sparing agents) like methotrexate or

azathioprine (100mg daily).
 3. If present, control hypertension and diabetes by increasing the dose of
medications and protect against PUD; give Ranitidine.

4. Consider tapering the dose when: old lesions heal by crusting and no
new lesions appear. Prednisolone is tapered in a rate of 5-10mg every
2-3 days till a level of 40 mg daily is reached. Lifelong prednisolone
(10mg) is usually required. Immunosuppressive drug can be reduced to
half the dose initially and then stopped.

li
·
Treatment details:
#
Single dose per day, at morning time after breakfast (for lowest level of cortisol level
according to cortisol cycle in body), use prednisolone as it's short acting and not
hydrocortisone or other steroids

Give 3 tablets 40 mg and 100 mg immunosuppressive like azathioprine.

Patent is hospitalized for close follow up for a week - 10 days for biopsy, labs,
education and daily examination for healing of previous blisters and no new blisters
formation.

When this is reached (healing of previous blisters and no new blisters formation.)
decrease prednisolone 5 -10 mg every 2-3 days, immunosuppressive is kept 100.

When prednisolone reaches 40, we lower the azathioprine to 50

O
Keep patient at 10 prednisolone lifelong.

If it's stopped, rebound effect will happen; blistering become worse and we have to
start all over again! (From hospitalization to 10 mg prednisolone!)

41
Allergic skin diseases:
Introduction:

Hypersensitivity is exaggerated or inappropriate immunoreaction. The four

main types of hypersensitivity reaction are:

1. Type I: immediate hypersensitivity reactions: it is an IgE mediated

immune reaction. Urticaria and angioedema are examples of this kind
of reaction.

2. Type II: humoral cytotoxic reactions: It is an antigen antibody reaction

mediated by IgG or IgM. It is involved in certain autoimmune skin
diseases such as pemphigus and pemphigoid.

3. Type III: immune complex-mediated reactions: antibody antigen

complexes are formed and the compliment is activated. An example is
serum sickness (antibodies against blood vessel wall i.e. Vasculitis, with petechial and
purpural rash on skin.

4. Type IV: cell-mediated immune reactions: delayed type, T- cell

mediated reaction. It is important in granulomas, and allergic contact
dermatitis.

I. Urticaria
Urticaria is a common type I hypersensitivity reaction pattern in which
pink, itchy, or burning swelling (wheals) can occur anywhere on the body.
Traditionally, urticaria is divided into acute and chronic forms, based on
the duration of the disease rather than of individual wheals.

Urticaria that persists for more than 6 weeks is classified as chronic.

Patients with acute urticaria have a known cause in 95% of the cases. On
the contrary, chronic urticaria patients have no obvious cause in 95% of
the cases.

42
 Urticaria is believed to be caused by a reaction between antigens
(bacteria, drug or certain chemicals) and antibodies (frequently IgE) on the
surface of mast cells. This reaction causes the mast cells to degranulate
and release heparin, histamine and other inflammatory mediators.
Triggers of urticaria may include: infections, drugs, or even psychological
stress.
Mast cells are found in the dermis near blood vessels like the police in streets.
& nerves and have follicles

Effects of histamine release may include: vasodilation with increased

capillary permeability, itching, bronchoconstriction and dyspnea, nausea,
vomiting and abdominal pain.
Note: Urticaria in an infant can be very challenging to diagnose, moreover it’s an urgent case
that may lead to sudden death.
Hints that the infant is having bronchoconstriction:
- Intermittent loss of consciousness.
- Vomiting right after feeding with no obvious cause.
- Other clinical signs of respiratory distress (cyanosis, tachypnea, using excess muscles, flaring
of nostrils, etc.)

Clinical presentation: Most types of urticaria share the sudden appearance

of pink itchy wheals, which can come up anywhere on the skin surface.
Other symptoms may include: itching, dyspnea, abdominal pain, nausea
and vomiting.
Urticaria is characterized of bleaching when a pressure is induced over the lesion with a slide
(this is called diascopy), Vasculitis don’t disappear with pressure.
* diascopy
Differential diagnosis: tinea versicolor, pityrisais rosea, guttate psoriasis,
urticaria
drug reaction, or secondary syphilis.
disappears with
Pressure
Diagnosis is based on history, physical examination, lab tests including:
O
CBC, UA, ASOT (Anti-streptolysin O Titer), and CXR. Elevated serum IgE level is nonspecific.

Treatment: the first step in the treatment is to identify the cause and then
to eliminate it.

- Antihistamines are the mainstays of symptomatic treatment. H1

histamine antagonists (act as mast cell stabilizer) are used first and
they are sufficient for treatment in 70%-80% of the treatment. If it did
not work, the dose of H1 antagonists can often be increased and still
tolerated. In 20%-30% of cases, H2-blocking antihistamines (e.g.
cimetidine) may add benefit if used in conjunction with an H1 histamine 43
antagonist.
These percentages correlate to the percentage of each receptor type on the mast cell, i.e.
mast cells have 70-80% H1 receptors and 20-30% H2 receptors.
 .

Diascopy
· daiertest

- Systemic steroids are a must in children (even if no dyspnea) and in patients complaining
of dyspnea. It can also be used in angioedema with abdominal pain and
N&V. The dose may reach 40-60 mg/day in cases of laryngeal edema.
- Treat underlying condition like infection, stress, drugs, etc.

Note: sometimes urticarial rash (wheals) is not obvious on skin, so we use what is called
Darier test (rubbing of the lesion – with a wooden stick- leads to linear urtication and
erythema ( liner wheals) over and around the suspected area of hidden urticarial, this is
called Darier sign or Dermographism. This condition is called: Urticaria pigmentosa (UP)
and it’s a form of mast cell disorders.
Darien test
dermographism-surticaria
Special types of urticaria: Dismentosa
- Cold urticaria.
- Pressure urticaria.
- Cholinergic urticaria. (Appears when a person is sweating like exercise, bathing,
staying in a heated environment, or emotional stress.)
- Autoimmune urticaria (Associated with other autoimmune diseases specially
thyroid diseases)

Angioedema is a variant of urticaria (but with more histamine release) that primarily
affects the subcutaneous tissues, so that the swelling is less demarcated and less red
than an urticarial wheal. Angioedema most commonly occurs at junctions
between skin and mucous membranes (e.g. peri-orbital, peri-oral and
genital). It may be associated with swelling of the tongue and laryngeal
mucosa. Treatment is systemic corticosteroids and antihistamines.

44
 permeability of the skin. It is also associated with alteration of normal flora
-
populating the skin with staph species increasing to 70%.

The prevalence is 7%-17% in children with most people out grow it. 70% of
the patients have family history of atopy. 40% of the cases are associated
with food allergy too.

Note:
40% of patients with atopic dermatitis also have food allergy.
Top 5 foods causing food allergy: egg, milk, fish, Soybean and wheat (all 5 of them can be
found in Cerelac!)
Diagnosis can be done by Patch test, Elisa test for specific IgE subtypes.
Treated with diet restriction if possible and trails of desensitization can be done.

There are 3 clinical phases of the disease:

1- Infantile phase (<2 years): where it may affect the entire body with
erythema and scaling appear in the face as well. In 50% in the case it
disappears by the age around 2 years ( 18 months).
2- Childhood phase (2 years – 11 years): it affects the flexural areas.

3- Adult phase (>12 years): affects extensor sides, external genitalia and
-

hands.

Triggers of atopic dermatitis may include:

1- Psychological and emotional stress

2- Climate changes.
3- Certain types of food
4- Infections

The diagnosis of Atopic dermatitis is a clinical one. There is no specific

histological or laboratory finding that confirm the diagnosis.

The diagnosis of atopic dermatitis using the following criteria (Hanifin and
Rajka criteria) requires that patients have at least 3 of the 4 major criteria
-

and 3 of the 23 minor criteria.

-

46
 - Major criteria are:

1. Pruritus

2. Dermatitis affecting extensor surfaces in adults and the face in

infants (specific distribution)

3. Chronic or relapsing dermatitis

4. Personal or family history of cutaneous or respiratory atopy.

- Minor criteria are (can be divided into 4 categories)

1. Facial features: facial pallor, facial erythema, hypopigmented

patches, infraorbital darkening, infraorbital folds (Dennie-Morgan
folds), cheilitis, recurrent conjunctivitis, anterior neck folds.

2. Triggers: foods, emotional factors, environmental factors, skin

irritants

3. Complications: susceptibility to cutaneous infections, impaired cell-

mediated immunity, immediate skin-test reactivity, elevated IgE,
keratoconus, anterior subcapsular cataracts.

4. Other: early age of onset, dry skin, ichthyosis, hyperlinear palms,

keratosis pilaris, hand and foot dermatitis, nipple eczema, white
dermatographism, pityriasis alba, perifollicular accentuation.

There is no known cure for AD, although treatments may reduce the
severity and frequency of flares. Treatment modalities may include:

1. Moisturisers, systemic antihistamine, and topical steroids are first line.

Topical preparations of nonsteroidal anti-inflammatory drugs are also
used.
2. Tacrolimus (0.1% preparations) used to replace topical steroids after 2
weeks. Systemic or topical antibiotics are added in cases of infections.
3. In resistant cases, systemic corticosteroids,
systemic immunosuppressant drugs and phototherapy can be used.

Treatment notes according to phase:

- Infantile phase use topical steroids and topical NSAIDS.
- Childhood stage: the patient may have bad staph. infections due to
scratching, so it’s better to give systemic steroids and topical/systemic 47
antibiotics.
- Adults: systemic antihistamine, immunosuppressant, phototherapy and if
resistant give systemic steroids.
 Sebaceous Gland Disorders
I. Acne vulgaris (or simply acne)

Acne is a chronic disorder of the pilosebaceous apparatus (sebaceous

gland and hair follicle) characterized by comedones, papules, pustules,
cysts and scars. Nearly all teenagers have some acne (acne vulgaris) at
some point. It usually affects the seborrhoeic areas of the body including:
face, chest, neck, shoulders and back. Genetic and familial pattern is
estimated to be the cause of 70%.

Many factors combine to cause acne (pathophysiological changes):

1. Overproduction and secretion of sebum
2. Hyperkeratosis of sebaceous gland duct
3. Overproduction of inflammatory mediators
4. Over-colonization of normal skin flora Propionibacterium acnes

Risk factors include: hormonal disturbances especially during puberty,

increased levels of androgens in females, infections, psychological stress,
and certain drugs like corticosteroids, fatty foods and familial patterns.
(Note: there is no link between hyperlipidemia and acne vulgaris)
SO History in acne case: family predisposition, fatty foods, fatty hair type, menstrual
regularity, drug history, drug allergy, psychological stress.
Variants of acne include:

1. Infantile acne may follow transplacental stimulation of a child’s

sebaceous glands by maternal androgens passing through the placenta.
2. Drug-induced acne; corticosteroids most commonly. Steroid induced
acne are characterized by pustular lesion (with no comedones)
distributed all over the body rather than just seborrhoeic areas, homogenous lesions; all
are papules (this is a general role for drug reactions; they cause one type of lesions)

Note: you will never see food allergy presenting with solitary lesions

3. Acne associated with hormonal disturbances: like acne associated with

virilization and acne accompany polycystic ovarian syndrome (PCOS).
48
 4. Stress acne: it can start at any age with characteristic distribution over
the mandible.
5. Occupational acne: associated with specific occupations, appear over
the face and hands.
6. Cosmetics acne!

Differential diagnosis of acne vulgaris:

1. Stress folliculitis
2. Acne rosacea
3. Seborrhoeic dermatitis
4. Complications of medications
5. Contact dermatitis
6. Photosensitivity

Many different treatments are used for acne. The drug of choice depends
on the severity and type of skin lesion:

1. If the patient has only comedones (comedo-papular type): local

treatment is enough for most patients. Topical preparation like
keratolytics (salicylic acid, lactic acid...), and topical retinoic acid
preparations are used.
2. In case of papulopustular type of acne (where the skin lesions are
mostly pustules and papules), topical antibiotic (frequently
clindamycin) and systemic antibiotics are used. Commonly used
systemic antibiotic is tetracycline like doxycycline. Other alternatives
are: erythromycin, azithromycin, and cephalosporins.

49
 3. In nodulocystic type of acne; and if the above treatment regimens did
not work, oral retinoids are used. Isotretinoin (Accutane) is very
effective. It reverses the four pathophysiological changes that occur in
acne vulgaris (see above). Isotretinoin is given in a standard dose
related to body weight (0.5-1 mg/kg/day). The estimated dose is
calculated by this equation:
weight optimal
close
Bo X

days of treatment
Dose = Body weight (Kg) x optimal dose (mg/kg) / duration of treatment
(day)

The optimal dose is reached by the end of the treatment periodEas 120
mg/kg. The duration of the treatment is as much as 5 months (150-

days). Improvement is typically seen after one to two months of use.

When to use/ indications to use isotretinoin / keratan

- Unresponsive case to topical treatment

- Nodulocystic changes

- Social cases : people who need a good looking face, i.e. lecturer, secretary ,,etc.

- Acne Rosacea, even that it’s not a sebaceous glands pathology.

- Side effects of Isotretinoin include:

1- Increased lipid levels in the blood (triglycerides and cholesterol).
2- Increased liver enzymes.
3- Dry skin; specially perioral, and photosensitivity.
4- Nose bleeds (epistaxis)
5- Arthritis and muscle pain
6- Psychiatric side effects like depression and suicidal thoughts
7- Drug-drug reaction: tetracyclines must be stopped before starting
retinoids (pseudotumor cerebri: increased ICT, severe headache). It shouldn’t also be
used with vitamin A because this combination causes alopecia.
8- Isotretinoin is also teratogenic (increases the risk of congenital
abnormalities especially cleft lip, spina bifida, and hydrocephalus).
Birth control (e.g. OCP) is required for women of child bearing age.
Pregnancy is safe 1-2 months after discontinuation of the drug.

- Patients who are to start on isotretinoin should sign a consent form.

Other recommendations include: low fat diet, screening for liver
50
 enzymes and lipid profile, moisturizers for dry skin and OCP for women
of child bearing age.
- Standard dose of isotretinoin (0.5-1 mg/kg/day) is given for 5 months. It
is decreased to low dose (0.25-0.5 mg/kg/day); if the patient cannot
tolerate the drug and side effects appeared. If the patient continued to
have side effects the drug is stopped for 1 week before getting back to
the standard dose. Intermittent treatment (one week of standard dose
and 3 weeks off) is proved to be of no benefit.
Complications of untreated acne vulgaris include:
1. Hyperpigmented or hypopigmented skin spots
2. Scar formation (hypertrophic or keloid)

Patient preparation for isotretinoin:

1- LFT, KFT, cholesterol and TAG, and pregnancy tests, in addition to blood pressure
for HTN.
If one of the tests is abnormal don’t give Keratan, ask the patent to fix the problem
first, or you will face DVT/PE, atherosclerosis, MI, pancreatitis, etc.
2- Tell the patient about the drug and it’s side effects ( specially the ones he/she will
has immediately like epistasis, photosensitivity, dry skin, arthritis, keratitis)
3- The patient signs a special consent form.
4- Give the patient these warnings:
- No pregnancy after stopping the drug for at least 1 month ( the drug is given
for 5 months and 1 month after so no pregnancy after 6 months of starting
the drug)
- Low fat diet
- Decrease sun exposure and use sun screens.

Q- You started the treatment, then the patent developed jaundice or dark urine, what
to do?
Re-do the tests, if elevated, stop the treatment for 7 – 10 days, redo them then, if back
to normal continue the drug.
If no improvement after 7 -10 days, use low dose treatment (0.3-0.4 mg/kg/day)

Q- Both standard dose and low dose treatments share the same efficacy, compliance,
same cost effect.
So why not using the low dose from start? Less cumulative dose (you need 120 mg
cumulative dose in 5 months for optimal results).

Hormonal therapy:
When to consider hormonal therapy?
Clinical signs like hirsutism, obesity, acne, DM  you send the patent to do
ultrasound for the ovaries and check hormones levels.
Q- What if the US was normal and normal hormone levels? Give the hormonal
therapy even with normal tests with clinical signs; this is most likely target tissue
hypersensitivity.

Problem in increased levels of free testosterone and/or DHEA, so we give:

- Low dose estrogen and progesterone – Diane 35 (OCP like combination) for 21 days51
a month for 6 – 12 months.
Note it’s notn real contraceptive and won’t prevent pregnancy.
Give baby aspirin to decrease the hypercoagulable effect of estrogen.
- Andro q to decrease DHEA
 II. Acne Rosacea:

Acne rosacea is a chronic skin condition

characterized by facial redness, small
↑
and superficial dilated blood vessels on
facial skin, papules, pustules, and
swelling (unlike acne vulgaris, there is
no comedones! The pathology is not
related to the sebaceous glands).

Rosacea typically begins as redness on

the central face across the cheeks, nose, or forehead, but can also less
commonly affect the neck, chest, ears, and scalp.

Rosacea affects both sexes, but is almost three times more common in
women. Yet, complications are more common in men. Rosacea is
commonly found in people between the ages of 30 and 50 and is more
common in those of Caucasian descent.

Diagnosis: there is no single, specific test for rosacea! In most of the cases
the diagnosis is based on history and physical examination. A trial of
common treatments is useful for confirming a suspected diagnosis.
History of acne rosacea: does the redness increase with sun, pathing with hot water,
heat exposure ?

On physical examination: Telangiectasia, papules and pustules, no comedons, affects only

face not shoulders, back and chest.

The differential diagnosis of acne rosacea includes: acne vulgaris,
photosensitivity, flushing caused by emotional stress, Cushing syndrome,
carcinoid tumor (causes flushing), systemic lupus erythromatosis (SLE),
contact dermatitis or seborrheic dermatitis.

DDx of Telangiectasia: chronic steroids use, aspirin/ heparin use, liver disease and cirrhosis,
alcoholic persons.

Mild cases of acne rosacea are not treated and therapy for the treatment
is not curative. The two primary modalities of rosacea treatment are
topical and oral antibiotic agents.
52
 1- Topical metronidazole (1%) cream is used to produce vasoconstriction.
2- Oral antibiotics of the tetracycline class such as doxycycline are also
commonly used to reduce papulopustular lesions.
3- Because sunlight is believed to be a common trigger, some people
benefit from sun protection and avoiding sunlight.
4- Antimalarial medications are no longer used. Side effects may include:
- psoriasis, G6PD, and night blindness.
5- Isotretinoin by mouth is used in some cases.
6- Laser embolization and interventional radiologic procedures.
7- Systemic and topical steroids may worsen the condition and are
contraindicated.

Using drugs side effects in treatment:

- Using vasoconstrictor side effect of metronidazole in treating Acne rosacea

- Using minoxidil side effect of hirsutism for treating alopecia.

Complications of acne rosacea are:

1. Rhinophyma: is a large, bulbous, ruddy nose caused by granulomatous

infiltration.
2. Blepharitis: chronic inflammation of the eyelid.

53
A popular method for remembering the signs and symptoms of melanoma
is the mnemonic "ABCDE":

- Asymmetrical skin lesion.

- Border of the lesion is irregular.

- Color: melanomas usually have multiple colors.

- Diameter: moles greater than 6 mm are more likely to be melanomas

than smaller moles.

- Enlarging: Enlarging or evolving.

Diagnosis of melanoma (like other skin cancer) is based on history and

physical examination. Skin biopsy is used to confirm the diagnosis.
Radiology like CT scan is done to detect the present of distant metastasis.

The prognosis of melanoma is generally bad and may be affected by

several features

- If the thickness is less than 1 mm (with no distant metastasis) >> the

prognosis is better; 90% - 100% 5 year survival rate.
8. distenced
- If the thickness is more than 4 mm or distant metastasis is present >>
the prognosis is bad; <50% 5 year survival rate. bladden
. Severe
9 hypoxemia
Radiology 10 ·
cause hypotension
1. Fracture colle's /Smith II
.
ASA device

-MRI with or without

contrast

4. salter harris Type III

5 .
site of hemorrhage (basal ganglia)
58
Ischemia
.
6 MRI for acute

.
7 subclual origin of bleeching
 092345113
A popular method for remembering the signs and symptoms of melanoma 113
is the mnemonic "ABCDE":

- Asymmetrical skin lesion.

- Border of the lesion is irregular.

- Color: melanomas usually have multiple colors.

- Diameter: moles greater than 6 mm are more likely to be melanomas

than smaller moles.

- Enlarging: Enlarging or evolving.

Diagnosis of melanoma (like other skin cancer) is based on history and

physical examination. Skin biopsy is used to confirm the diagnosis.
Radiology like CT scan is done to detect the present of distant metastasis.

The prognosis of melanoma is generally bad and may be affected by

several features

- If the thickness is less than 1 mm (with no distant metastasis) >> the

prognosis is better; 90% - 100% 5 year survival rate.

- If the thickness is more than 4 mm or distant metastasis is present >>

the prognosis is bad; <50% 5 year survival rate.

58