Dermatology

Notes
5th year/ Faculty of Medicine

By: AMJAD SAMARA

Additional notes added by:

Laith Abu Snouber

2015
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CONTENTS:

1. Infections :
A. Bacterial skin infections
1. Impetigo
2. Cellulitis
3. Syphilis
4. Gonorrhea
B. Viral skin infections
1. Herpes simplex
2. Herpes zoster
3. Orf
C. Fungal infections
D. Infestations
1. Leishmania
2. Scabies
3. Pediculosis

2. Papulosquamous skin diseases

2.1 Pityrisais Rosea
2.2 Psoriasis
2.3 Lichen Planus

3. Bullous Skin Diseases

3.1 Pemphigus
3.2 Bullous Pemphigoid

4. Allergic skin diseases

4.1 Urticaria
4.2 Contact Dermatitis
4.3 Angioedema

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5. Sebaceous Gland Disorders :
5.1 Acne Vulgaris
5.2 Acne Rosacea

6. Skin Tumors :
6.1 Basal Cell Carcinoma ( BCC )
6.2 Squamous Cell Carcinoma ( SCC )
6.3 Malignant Melanoma ( MM )

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 Introduction:

Skin anatomy and histology:

The skin is composed mainly of 3 layers:
1. Epidermis
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.

11th week of gestation – Nails take the final shape.

17th week of gestation – Finger tips take the final shape.

4.5 months of gestation – skin growth is completed.

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.

The epidermis is composed of 3 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.

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 B. Prickle Cell layer (stratum spinosum): in addition to keratinocytes, it also
contain Langerhans cells which are dendritic shaped, antigen presenting
cells (APC).
C. Granular cell layer ( stratum granulosum )
D. Flat cell layer ( stratum corneum )

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.

2. Dermis:

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.

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 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
stratum granulosum. It is usually seen in skin disease with high turnover
like: psoriasis.

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3. Acanthosis: a skin condition characterized by increased thickness of
stratum spinosum.

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:

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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.

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Bacterial skin infections:

I. Impetigo:

It is a superficial bacterial skin infection that

affects only the epidermis. It is caused by
staphylococci (most commonly), streptococci
or both together.
It is mostly seen in children younger than 12
yrs, affecting mainly exposed areas like the
face, hands, and lower limbs.

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.

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 Treatment include:
1. Broad spectrum systemic antibiotics (dicloxacilin or cephalexin).
2. Topical antibiotics (gentamycin and fusidic acid).

II. Cellulitis:

It is a bacterial skin infection that is frequently compared to other

condition called erysipelas.
Unlike erysipelas, cellulitis is caused by streptococci but in 10%-20% of the
cases staphylococci are also present. Other organisms may also be the
cause. Erysipelas is a pure strep infection.
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).

III. Gonorrhea:

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.

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The clinical presentation is variable. In males, urethra is mainly infected
and patients are presented with yellowish urethral discharge, and dysuria.
In female patients, the cervix is the affected part and patients are
presented with lower abdominal pain, bloody vaginal discharge, and
dysuria.
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.
 In Gonorrhea history taking, important to ask about sexual activity history and allergy to
penicillin.

Complications of gonococcal infection could include: chronic septic

arthritis. Specific complications that occur in males are: 1. chronic orchitis.
2. Epididymitis 3. Infertility that may necessitate IVF. In females,
complications include: 1. Pelvic inflammatory disease that may lead to 2.
Ectopic pregnancy or 3. Infertility.
Treatment is, either:
1. One single shot of ceftriaxone 1 g IM or,
2. Oral ciprofloxacin (2 tablets 500mg X2). If the patient is allergic to ceftriaxone ( note it’s a
drug used for UTI)
All partners should be treated at the same time.

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

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 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.

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 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)
10- Bowen’s disease (risk of malignant transformation). (SCC in situ)

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 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.

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 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)

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).

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  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.

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)

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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.

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 Viral Infections

I. Herpes simplex virus infection:

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:

It is caused by herpes virus varicella zoster (the same virus that causes
chickenpox). An attack is the result of the reactivation, usually for no
obvious reason, of virus that has remained dormant in a sensory root
ganglion. Reactivation is sometimes associated with trauma, surgery,
stress, drug ingestion, or conditions which weaken normal defense
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.

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 III. Viral Warts:

Warts are caused by human papilloma virus (HPV). Infections occur when
wart virus in skin scales comes into contact with breaches in the skin or
mucous membranes.
Warts adopt a variety of patterns:
1- Common warts (verruca vulgaris).
2- Plantar warts: usually confused with plantar corns. Often multiple,
plantar warts can be painful.
3- Mosaic warts.
4- Plane warts (flat warts or verruca plana): most commonly on the face
and head.
5- Anogenital warts (Condyloma acuminata)
6- Verruca vegetante ( cauliflower shaped)
7- Line shaped warts.

Treatment modalities include: (medications and procedures)

1- Salicylic acid (topical keratolytic)

2- Higher concentrations of salicylic acid preparations (podophyllin) for
hospitalized patients.
3- Topical imiquimod.
4- Intralesional injection of interferon or 5-fluorouracil
5- Electrocautery
6- Cryotherapy with liquid nitrogen.
7- Surgical curettage.
(Note: some of these medications and procedures are used for
treatment of premalignant lesions that will be discussed later).

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 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)

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 V. Molluscum contagiosum:

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

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Fungal infections:
Dermatophyte infections (ringworm):
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
the former, bacterial infection is suspected and the lesion is called Kerion
(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:
1. Systemic antifungal medications: 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:
- < 20 kg: 62.5 mg/day,
- 20-40 kg: 125 mg/day,
- > 40 kg: 250 mg/day (adult dose).

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
Treatment :

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
 Parasitic infestations:
I. Leishmania:
Leishmania organisms are
protozoa whose life cycle:

- The container: rattus rattus

‫الوبر الصخري‬
‫ لكن مع شق‬، ‫ لذا كان منتشرا في منطقة اريحا فقط‬، ‫ يعيش الحيوان في المغارات‬: ‫مالحظة‬
‫اإلحتالل للطرق اإللتفافية زاد تعرض السكان للحيوان واآلن هو موجود في مدن فلسطينية مثل‬
‫ الخ‬،، ‫ طولكرم‬، ‫ رام هللا‬، ‫نابلس‬

- The vector: female

sandflies.
- Incubation period 3-4 weeks

Different species in different geographical areas cause different clinical
pictures:
1. Leishmania tropica is found around the Mediterranean coast and in
southern Asia; it causes chronically discharging skin nodules (cutaneous
leishmaniasis)

2. Leishmania donovani causes kala-azar (visceral leishmaniasis), a

disease characterized by fever, hepatosplenomegaly and anemia. The
skin may show an irregular darkening, particularly on the face and
hands.

3. Leishmania mexicana and braziliensis are found in South and Central

America cause (mucocutaneous leishmaniasis).

(The discussion below is all about cutaneous type!)

In cutaneous leishmaniasis: the primary skin lesion is papule or nodule.

Then it may be infected, crusted, or ulcerated. Patient may be presented in
any stage.

27
The most affected areas are sun exposed areas like the face. Transmission
from human to human is not documented.

Diagnosis starts with goo history (residency, occupation ...), physical

examination, and confirmed via a laboratory test. Laboratory tests for
diagnosis of leishmaniasis include:

- Microscopic examination of a smear of the fluid obtained from the

lesion. Giemsa stain is used and Leishmania bodies are detected.

- Leishmania intradermal skin test (similar to PPD test). It gives 50% false
positive results (not specific).

- Skin biopsy (the definitive diagnosis)

(Note: types of skin biopsy are: 1. Fine needle aspirate 2. Punch biopsy
3. Excisional biopsy 4.shaving biopsy )

Differential diagnosis of cutaneous leishmaniasis include:

1. Pyogenic granuloma (capillary rich lesion, red nodule, easy to bleed,

sometimes treated with embolization).

2. Keratoacanthoma

3. Basal cell carcinoma

4. Squamous cell carcinoma

5. Viral warts

6. Pyoderma gangrenosum

Note: important to include 1, 5, 6 and 2 in acute cases (ie 3 weeks history) while
3,4 are chronic ( years).

28
Treatment of cutaneous leishmaniasis:

1. If the lesion is solitary:

- Intralesional Pentostam (Sodium stibogluconate), up to 2.5 cc in the

margin of the lesion. Follow up in 2-3 week.

- Cryotherapy with liquid nitrogen.

- Never go for surgery as it leaves a large scar, so it’s not seen
any more – but you can see it in old patents above 80.

 2. If multiple lesions: Pentostam is given IM (extremely painful though)

 6ml/day for 10 days.
 ‫ تأتي هذه الجهود ألن‬، ‫ هذا الدواء غير متوفر في الصيدليات ويحصل عليه المريض مجانا من وزارة الصحة‬: ‫مالحظة‬
 ‫المرض يؤثر على الدخل القومي للبلد النه يصيب المزارعين بشكل رئيسي مما يؤدي إلى انخفاض اإلنتاجية الزراعية‬
 ala-azar / visceral leishmaniasis is also treated with Pentostam IM

Cryotherapy (using liquid nitrogen, painful, causes necrosis of the lesion
 and healing) is contraindicated in the some cases: a lesion that is around
 the eyes or mouth, infected lesions, hemangiomas, pyogenic granuloma,
 BCC, and SCC.

Old treatment methods (out dated) include: electrocautery, surgical
excision. The lesions are usually self-limiting (BUT it takes years and leads
to scar formation).

29
 II. Scabies:
It is a highly contagious disease caused by the mite Sarcoptes scabiei
hominis. It is transmitted from person to person through close body
contact.

Once on the skin, fertilized female mites burrow through stratum corneum
(subcorneal space). It is more active at night hence the classical
presentation “night itching”. It is also more active in hot and wet
environment. The primary skin lesion in scabies is burrow (C or V shaped).
Clinically, it can be seen as a small line starting with a vesicle. Burrows are
best seen in elderly and children; because they have thin skin.

- The patent suffers from itching due to foreign body reaction against the eggs.
- Burrows are like tunnels, so recognized by entrance site vesicle at the beginning of the

C or V shaped burrow.

 DDx of burrow is furrow, it’s like a groove not a tunnel , it got no roof.

The
 life cycle of the acarus is about 30 days.
 Fertilized female may Produce 1-2 eggs every day.
Classical clinical presentation: itching, often affecting several people and
being particularly severe at night. On examination, urticarial popular rash
may be seen on the trunk, around the nipples, armpits, interdigital spaces
and umbilicus. On infants and children palmoplanter sides may be
involved. Other skin lesion that can be detected: burrows, scratching
marks, popular urticarial rash.
Diagnosis is based on history and physical examination.
History: night itching? Location of itching and timing? Travel? Other
family members itching ?

Differential diagnosis:

1. Contact dermatitis
2. Psychological stress
3. Other medical conditions: renal or liver failure (pruritis), obstructive
jaundice.

4. Drug reaction.

30
 5. Duhring’s disease: (or dermatitis herpetiformis, despite the name, it is
not related to herpes virus!). It is a specific manifestation of celiac
disease (CD).

6. Mycosis fungoides: is the most common form of cutaneous T-cell

lymphoma. Obviously, it is not a fungal infection and it is not
contagious.

7. Other causes of itching (different presentation than scabies): Hodgkin’s

lymphoma, leukoplastic vasculitis, lichen simplex chronicus
(neurodermatitis), diabetes, tenia versicolor, acute urticaria

Treatment of scabies:

- All family members, including the patient of course, should be treated

at the same time. Keep in mind that the incubation period of scabies is
30 days.
- The drug of choice is permethrin 1% (lotion, or cream). It is safe to be
used for infants and pregnant. The topical preparation is applied below
the neck for 12 -24 hours twice to ensure cure.
Apply over the entire body, if neonate apply over face and hands (it’s safe)

- Other options include: crotamiton, Gamma- benzylhexachloride, and

benzyl benzoate. (There is a concern about neurotoxicity in some of
these drugs!)

Medications to control itchiness include antihistamine and anti-

inflammatory agents.

- Underwear clothes got mates so advice the patient:

 Wear the same ones all the treatment period or
 Wash- them, boil them in hot water and then iron them )‫ ( كي المالبس الداخلية‬or
Keep them in closed nylon bags for 1 – 2 days (mites can’t live without a lost so die)
 For travelers, tourists and cloth traders use them once, dispose and buy new ones.

 Note: rare type of scabies called Norwegian scabies is seen with

immunocompromised AIDS patients, present as non-itchy, all over the body
scales that look like psoriasis clinically.

31
 III. Lice infestations (Pediculosis):
Lice are flattened wingless insects that suck blood. Their eggs attached to
hairs or clothing, are known as nits.

There are 3 clinical forms:

1. Head lice (pediculosis capitis).

2. Body lice (pediculosis corporis)

3. Pubic lice (pediculosis pubis)

The clinical presentation: itching is the first presentation. Scratching and

secondary infections may follow. In body lice, the presentation is quite
similar to scabies. The main difference is that burrows are not seen in PE.

Nits Vs. Dandruff? Nits are closely attached to hair shaft and hard to remove, dandruff is
removed easily.

Treatment is the same as scabies
- For head lice in a shampoo form, it dissolves the keratin that forms the cell wall of the
eggs/nits, apply shampoo for 15 – 20 min then the hair is combed with a special comb
with narrow spaced teeth, antihistamine reduces itching, and it’s important the treat
all the surrounding children to prevent re-infection.
- For body lice same as scabies. ( clinical presentation same as scabies but with no
burrow on physical exam)

- Shaving of pubic hair is of benefit in pubic lice.

Look for other STDs : AIDS, syphilis, Gonorrhea, genital warts ,,etc.

32
 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
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).

34
 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.
 II. Pityrisais Rosea:
 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).

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.

37
 III. Lichen planus:
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
- 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.
 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.

* 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
 DDx of skin lesions in PV includes: burns, epidermolysis bullosa, erythema
multiforme, Steven Johnson syndrome (SJS), dermatitis herpetiformis,
drug reaction, bullous impetigo, or herpes zoster. Mouth ulcers can be
mistaken for aphthae, lichen planus, Behcet disease, trauma, or drug
reaction.

Diagnosis is made based on history and physical examination. Usually

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)
(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.

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

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.

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.

Differential diagnosis: tinea versicolor, pityrisais rosea, guttate psoriasis,

drug reaction, or secondary syphilis.

Diagnosis is based on history, physical examination, lab tests including:

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.
 - 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.

Special types of urticaria:

- 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
II. Contact dermatitis:
It is a type of skin inflammation results from exposure to allergens (allergic
contact dermatitis) or irritants (irritant contact dermatitis).

Common causes of allergic contact dermatitis: metals like nickel and

chromium. Common causes of irritant contact dermatitis include: solvents,
detergents, cleaning products, latex, and certain foods and drinks.

Signs and symptoms of both types of contact dermatitis are very similar.
The first sign is usually the presence of rash or skin lesion at the site of
exposure. Other symptoms may include itching, skin redness or
inflammation, localized swelling and the area may become more tender or
warmer. These symptoms are more prominent in irritant contact
dermatitis.

In allergic contact dermatitis; once an individual has developed a skin

reaction to a certain substance it is most likely that they will have it for the
rest of their life, and the symptoms will reappear when in contact with the
allergen. The reaction may be generalized.

The diagnosis is based in history and physical examination. Patch testing is

the method used to identify the specific cause of allergy; a substance
causing a delayed type hypersensitivity reaction.

Treatment of irritant contact dermatitis includes topical steroids and local

antihistamines. Treatment of allergic contact dermatitis includes topical
steroids and systemic antihistamines.

III. Atopic dermatitis:

Also known as eczema is a type of dermatitis, a chronic inflammatory,
relapsing, non-contagious and itchy skin disorder. The cause is believed to
involve a number of factors including: genetics, immune system
dysfunction, environmental exposures, and difficulties with the

45
 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:

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

(day)

The optimal dose is reached by the end of the treatment period as 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
 Skin cancer:

There are three main types of skin cancer: basal cell carcinoma (BCC),
squamous cell carcinoma (SCC) and melanoma. The first two together
along with a number of less common skin cancers are known as
nonmelanoma skin cancer (NMSC).

Greater than 90% of cases are caused by exposure to ultraviolet radiation

from the Sun. This exposure increases the risk of all three main types of
skin cancer.

I. Basal cell carcinoma (BCC):

It is one of the most common

cancers(70%-80%of
nonmelanoma skin cancer). It
rarely metastasizes or kills, but it is
still considered malignant. It is also
known as rodent ulcer.

It originates for basal cells of the

skin in sun exposed areas, most head and neck. The nose is the most
common site and sun exposure is the most common risk factor.

 Basal-cell carcinomas may be divided into the following types:

1- Nodular basal-cell carcinoma: This is the most common form of BCC.
2- Superficial basal-cell carcinoma
3- Cystic basal-cell carcinoma
4- Pigmented basal-cell carcinoma
5- Nevoid basal-cell carcinoma

54
6- Sclerosing basal-cell carcinoma

Diagnosis of Basal cell carcinoma (like other skin cancer) is based on

history and physical examination. Skin biopsy is used to confirm the
diagnosis. As a general role, the more the lesion close to mucocutaneous
junction, the less likely to be basal CC and more likely to be squamous CC.

The differential diagnosis of BCC (which is similar to SCC) includes:

Leishmania, pyogenic granuloma, acanthoma, warts, and malignant
melanoma.

Although basal-cell carcinoma rarely metastasizes, it grows locally with

invasion and destruction of local tissues. The Prognosis is excellent if the
appropriate method of treatment is used in early primary basal-cell
cancers.

In general, the treatment modalities used for premalignant lesions are:
sunlight protection, 5-fluorouracil, imiquimod, and intralesional interferon
injection. In malignant lesions: Cryotherapy, electrotherapy and surgery
are used. Radiotherapy and chemotherapy are used in some cases of skin
cancers (especially when metastasized).

Mohs surgery is a procedure in which the tumor is surgically excised and

then immediately examined under a microscope. The base and edges are
microscopically examined to verify sufficient margins before the surgical
repair of the site.

55
II. Squamous cell carcinoma (SCC):

It arises from epithelial cells; squamous cells. It

is one of the major forms of skin cancer,
however, it also occurs in lining of digestive
tract, lungs and other areas of the body (sun
exposed and unexposed areas). Most common
SCC of the skin arises close to mucocutaneous
junction, like upper and lower lips.

Squamous cell carcinoma metastasized to the adjacent lymph nodes, with

distant metastasis is less likely.

Squamous cell carcinoma may arise from a premalignant skin conditions

including:

1- Solar keratosis (also known as actinic keratosis): with untreated lesions

have up to a 20% risk of progression to squamous cell carcinoma.

2- Leukoplakia: appear as firmly attached white patches on the mucous

membranes of the oral cavity.

3- Skin affected by radiation or chronic ulcers including burns, keloid scars.

4- Ulcerative lichen planus

5- Bowen's disease (also known as "squamous cell carcinoma in situ").

6- Keratoacanthoma: is a low grade skin tumor may be considered a

variant of SCC.

56
Marjolin's ulcer refers to an aggressive ulcerating squamous cell
carcinoma presenting in an area of previously traumatized, chronically
inflamed, or scarred skin.

III. Melanoma:

Is a type of skin cancer which forms from

melanocytes. These cells predominantly
occur in skin, but are also found in other
parts of the body, including the bowel
and the eye.

The primary cause of melanoma is

ultraviolet light (UV) exposure in those
with low levels of skin pigment.

Distant metastasis is not unusual with most common sites of metastasis

are: brain, bone, liver, lungs, distant lymph nodes and the abdomen.

Melanoma is classified clinically into the following types:

1- Superficial spreading melanoma (which is the most common type)

2- Nodular melanoma

3- Lentigo melanoma

4- Acral melanoma

57
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.

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

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

58