Dermatology, Lecture Notes on some Common & Serious Skin & Venereal Diseases.pdf

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Dermatology
Lecture Notes on some Common & Serious Skin & Venereal Diseases
Prepared by
Dr. Adnan A. Kamal
(M.B., B.Ch.,D.V.D, Cairo)
Assistant Clinical Professor of Dermatology, Faculty of Medicine & Dentistry, Al-
Quds University-Jerusalem
President of Dermatology Society-Jerusalem Center
Lecturer of Anatomy, Physiology, Dermatology & Venereology, L.W.F Nursing
School-A.V.H-Jerusalem (Previously)
Specialist of Dermatology, Venereology, Sexology and Andrology in Jerusalem
Consultant Dermatologist to the Makassed Islamic Charitable Hospital, Augusta
victoria Hospital, St. Joseph Hospital and Red Crescent Hospital
Jerusalem

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Introduction
Dermatology is the science which deals with the various skin disorders; their etiology,
incidence (age and sex), methods of transmission, sites of election, clinical picture (signs and
symptoms), predisposing and precipitating factors, differential diagnosis, prognosis,
complications, prophylaxis treatment, etc... .
The skin is an important system in the body and must be thought of in the same way we
think of the cardiovascular and other systems in the body. It is the protective covering of the
whole body, the main sensory organ of the body, of the main secretory organs; which regulates
body temperature and supplies it with vitamin D.
It is said that the skin is the mirror of the Soma and Psyche as from the expression of the
face you can guess if the patient is happy or sad, angry or satisfied … etc and from the color of
the skin you can have an idea about the state of the internal organs & systems; you can say that
the patient is anemic if the skin color is pale, jaundiced if the color is yellow, cyanosed if blue …
etc. also you can tell if the patient is young or old and the state of nutrition and hydration from
the health and elasticity of skin.

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Chapter I
Anatomy & Physiology of the Skin
The skin consists of two main layers:
I. The Epidermis ( derived from the Ectoderm) which consists of four layers:
1. The horny layer (Stratum Corneum).
2. The Stratum Lucidum (Only in the palms and soles).
3. The Granular layer (Stratum Granulosum).
4. The Germinatve layer (Stratum Malpighii), which consists of:
-The Brickle cell layer.
- The Germinal layer.
o Normally, it takes the Brickle Cell 27 days to be keratinized and shed from the surface.
o The melanocytes are dendritic cells found as a network at the plan of Epidermo-dermal
junction and produce melanin.
II. The Dermis, the true skin (derived from the Mesoderm), consists of two layers:
1. The Papillary layer: contains the nerve endings, blood vessels and the lymphatic
channels.
2. The Reticular layer: contains the sweat glands, the sebaceous glands, the hair follicles
and the arrector pili muscles.
The Hypoderm: a transitional layer between the skin and the sebaceous tissue containing fat cells,
connective tissue and the roots of the hair follicles and the sweat glands.
The Sweat glands: each consists of a glomerulous (seceting) part and a duct which opens on the
surface by the pore.
The sweat glands are of two types:
1. Eccrine sweat glands: secret ordinary sweat.
2. Apocrine sweat glands: open in the hair follicle and serve a sexual function.
The Sweat: a colorless fluid made up of 99% water and the remaining is salt, mainly NaCl.
The Sebaceous glands: are holocrine glands which secret sebum. Their function is to lubricate the
skin and hair.
- The Meibomian glands of the eyelids, the Tyson’s glands of the penis, the Cicuminous glands of
the ears and the Mammary glands of the breasts are modified sebaceous glands.
- Androgens and thyroxin cause the sebaceous glands to enlarge and secret more, while estrogens
do the opposite.

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The blood supply of the skin is derived from two arterial four venous plexuses.
The nerve supply of the skin is mainly sensory but motor fibers are also present.
The skin appendages:
1) The Hair: each arises in a follicle which is an invagination of the epidermis, it is made of three parts:
a) The Cuticle.
b) The Cortex.
c) The Medulla.
The arrector pili muscle is anchored to the hair follicle and causes erection of the hair on contraction.
The hair growth is cyclic and is affected by the various toxemias and endocrine disturbances.
The average daily rate of scalp hair growth is 0.35 mm and the hair continues growing from 2-6 years
before falling.
Types of hair: there are three: a) Scalp hair.
b) Lanugo hair.
c) Sexual hair.
The average number of the scalp hair is 100,000 and the usual daily loss is 20-150.
2) The Nails: each is composed of three parts: a) The nail blade.
b) The nail matrix.
c) The nail bed.
Abnormalities of the nails are either due to severe illness, trauma, anemia, toxemia or are congenital.
The average growth rate of a nail is 0.1 mm daily, the finger nail takes about 100-150 days to
reproduce itself and the toe nail three times longer.
Functions of the skin:
1. Protective covering of the body.
2. Regulates body temperature.
3. The main sensory organ of the body.
4. Acts as an excretory organ.
5. Has self-disinfection mechanism.
6. Supplies vitamin D to the body.
7. Protects against cancerous and precancerous conditions.

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Chapter II
The Dermatological Lesions
I. The primary lesions: which are formed during the early stages of the disease:
1. The Macule: circumscribed alternation of skin color.
2. The papule: solid elevation of the skin, 1-5 mm.
3. The Nodule: larger lesion, deeply seated.
4. The Tumor: a huge mass which may be fungating or ulcerating.
5. The Plaque: flat circumscribed area of abnormal skin.
6. The Vesicle (Blister): circumscribed collection of fluid in the epidermis.
7. The Bulla: a larger vesicle containing serum, sero-pus or hemorrhagic fluid.
8. The Wheal: evanescent edematous elevation of skin, whitish in color and surrounded by a
red halo.
9. The Bunow (Furrow): irregular, short, linear, grayish, beaded elevation of the horny
layer.
10. The Comedo (Comedone): small plug of laminated horny cells and sebum blocking the
pilo-sebaceous orifice.
11. The pustule: small epidermal collection of pus.
12. The Scales: partially separated laminated masses of the horny layer.
II. The secondary lesions: result from trauma or bacterial invasion or alteration in the primary lesions
of the skin.
1. The Excoriations (Abrasions): superficial linear discontinuations of the skin.
2. The Fissures: deep linear discontinuations of skin.
3. The Crusts: masses of dries exudates.
4. The Ulcers: localized loss of substance of skin.
5. The Scars: fibrous tissue replacement of skin substance.

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Some pathologic terms:
 Lichenification: thickening, hyperpigmentation and exaggeration of the skin markings.
 Hyperkeratosis: thickening of the normal horny cell layer.
 Parakeratosis: thickening of the horny cell layer with persistence of nuclei.
 Spongiosis: extracellular edema of the brickle cell layer.
 Dyskeratosis: abnormal keratinization of the horny cells.
 Acanthosis: hyperplasia of the stratum Malpighii.
 Acantholysis: detachment of the epidermal cells from each other.
 Dermatitis: skin disease of inflammatory nature.
Some dermatologic procedures
 Patchy testing: is done in contact dermatitis to detect the nature of the sensitizer.
 Tzanck test: is done in vesicular and bullous diseases for cytology.
 Intradermal test: e.g. Tuberculin, Leishmanin, Trichophytin… etc. to confirm diagnosis.
 Skin biopsy: in which a piece of skin is taken and sent for histopathological examination.
 Intralesional injection: in which the drug is injected intradermally e.g. corticosteroids in some
chronic skin diseases.
 Electrocautary: by which tissue fulguration, desiccation or coagulation is done as a treatment of
certain skin conditions e.g. warts.
 Diascopy: is to press the lesion under glass slide to clear off the masking erythema and detect the
nature of the underlying lesion.
 Cryosurgery: in which cold is used to induce necrosis of the lesion e.g. CO2 snow and NO2
liquid.

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Chapter III
General Principles of Treatment of Skin Diseases
I. Removal of the cause.
II. External applications:
1. Powders: used on slightly moist areas to dry the skin and prevent friction e.g. talc
powder.
2. Lotions: a) Simple lotion (only salt and water) e.g. Boric acid lotion.
b) Shaky lotions, a mixture of POWDER + GLYCERINE + WATER, used as a
covering for weeping lesions in acute and subacute inflammations e.g. Calamine lotion.
Rx:
Calamine powder 4.0
Zinc oxide 5.0
Glycerine 6.0
Aqua rosea 15.0
Aqua calcis 120.0
3. Creams: greasy preparations containing WATER + GRAEASE + inert POWDER, used
in weeping and inflamed areas e.g. ZnO cream
Rx:
Zinc oxide 32.0
Lanolin 12.0
Aqua clacis ad. 100.0
4. Liniments: emulsions made up of POWDER suspended in OLIVE OIL and AQUA
CALCIS e.g. Calamine liniment.
Rx:
Prepared calamine 5-8
Zinc oxide 5-8
Olive oil 100.0
Aqua calcis 100.0
5. Ointments: greasy-like substances used in chronic scaling lesions e.g. Whitefield oint.
Rx:
Salicylic acid 3.0
Benzoic acid 6.0
Lanoline 20.0
Vaseline ad. 100.0

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6. Pastes: preparations half of which is inert POWDER and the other half is GREASE, used
in subacute and slightly moist lesions e.g. Lassar’s paste:
Rx:
Zinc oxide 25.0
Starch 25.0
Vaseline 50.0
7. Poultices: used for removal of thick crusts e.g. Boric acid and Starch Poultices.
8. Fomentations: used for septic skin lesions e.g. antiphlogestine fomentation.
9. Baths: e.g. Bran bath, Potassium Permanganate bath and Sodium Bicarbonate bath.
10. Paints: used in areas where creases exist e.g. Castellani paint.
III. Physical agents:
1) Cold: e.g CO2 snow in treatment of warts.
2) Heat: e.g. cautery in removal of naevi.
3) Radiation: e.g. UV light, X-ray and LASER.
IV. Antibiotics: e.g. tetracyclines, gentamycin… etc. but not binicillins or sulpha as they are
potential sensitizers.
V. Antihistamines: e.g. Benadryl, Lorastine… etc, and it should be noted that all of them have
hypnotic side effects and shouldn’t be given to drivers or to those running machines or students
during their work.
VI. Antimalarias: e.g. Resochin, Aralen… etc. they act also as sun screens and are very beneficial in
some skin diseases in which the Sun plays a role in its etiology.
VII. Cortisone and Allaied steroids: used in severe skin disease systemically e.g. exfoliative
dermatitis but can be used locally in many other skin diseases except those caused by a virus or
T.B. bacillus as they cause flaring of the lesions.

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Chapter IV
Classification of Skin Diseases
I. Congenital anomalies (Genodermatosis) e.g.:
1. Ichthyosis.
2. Naevi.
II. Primary irritant dermatitis e.g.:
1. Housewife eczema.
2. Diaper dermatitis.
III. Infective group:
1. Bacterial skin diseases (pyogenic infections) e.g.:
- Impetigo contagiosum.
- Intertigo.
- Erysipelas.
- Sycosis.
- Furuculosis.
- Carbuncles.
2. Viral skin diseases e.g.:
- Herpes simplex.
- Herpes zoster.
- Verrucae (warts).
- Mollaseum contagiosum.
- Variola (smallpox).
- Varicella (chickenpox).
- Vaccinia (cowpox).
3. Fungal skin diseases (Mycoses) e.g.:
- Deep mycoses.
- Superficial mycosis.
- Moniliasis.
4. Skin diseases caused by animal parasites e.g.:
- Scabies.
- Pediculosis.
- Bed bugs.
- Flea bites.
- Cutaneous leishmaniasis.

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5. Bacillary skin diseases e.g.:
- T.B. of skin (T.B Chancre, Lupus vulgaris, Bazin’s disease… etc).
- Leprosy.
6. Spirochetal skin diseases e.g. Syphilis.
IV. Seborrhoeic dermatoses:
1. Seborrhoeic dermatitis.
2. Acne Vulgaris.
3. Acne Rosacea.
V. Allergic group:
1. Urticaria.
2. Eczema.
3. Erythemata.
VI. Scaly erythematous dermatoses: e.g.:
1. Psoriasis.
2. Lupus erythematosus.
3. Lichen Planus.
4. Pityriasis Rosea.
5. Pityriasis Rubra Pilaris.
VII. Deficiency skin diseases:
1. Pellagra.
2. Scurvy.
3. Perleche.
VIII. Vesiculo-Bullous skin diseases e.g.:
1. Pemphigus.
2. Dermatitis herpetiformis.
IX. Hair disorders:
1. Alopecias.
2. Hypertrichosis.
X. Pigment disorders:
1. Melasma.
2. Vitiligo.
XI. Psycho-somatic skin diseases:
1. Dermatitis artifacta.
2. Acne Excriee.
3. Trichtellomania.

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XII. Degenerative skin diseases:
1. Corns.
2. Callosities.
XIII. Precancerous and cancerous skin conditions:
1. Leukoplakia.
2. Senile keratosis.
3. Basal cell carcinoma.
4. Malignant melanoma.
5. Squamous cell carcinoma.
6. Mycosis fungoides.
XIV. Disorders of the subcutaneous fat:
1. panniculitis.
2. Insulin lipodystrophy.
XV. Errors of metabolism:
1. Xanthomatosis.
2. Histocytosis.
3. Amyloidosis.
4. Porphyria.

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Chapter V
Congenital Anomalies of the Skin (Genodermatosis)
A. Ichthyosis.
Synonyms: fish skin.
Definition: a genetic disease usually appearing not before the end of the 1st
year.
Description: the skin is dry, rough, scaly and very sensitive.
the hair is thin and the nails are brittle.
Etiology: unknown.
Pathology: abnormal keratinization and defective sweat and sebaceous secretions.
Site of election:
- Mild form (Xeroderma) affects the extensor surfaces of the limbs but the whole body may be
affected except the flexor surfaces of big joints.
- Severe form (Harlewuin Foetus) affects the whole body.
Prognosis:
- Mild cases slightly improve at puberty.
-Moderate cases remain stationary.
-Severe cases may prove fatal.
Prophylaxis: prevention of marriage between relatives, especially those who have a positive family
history.
Treatment is symptomatic:
1. Keep the skin moist and lubricated (warm and moist Climate)
2. Vitamin A 300000 IU daily.
3. Kertolytic agents as salicylic acid 2-5%.
4. Emollients e.g. olive oil/glycerine ratio 3/1.
5. Thyroid extracts and nicotinic acid may be used.

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B. Naevi
They are localized cutaneous abnormalities due to hyperplasia of the vascular epidermal or connective
tissue elements of the skin, which may be hard or soft.
They appear at birth or later on. They may disappear spontaneously or persists.
They are benign tumors and are removed only for cosmetic purposes.
Treatment is by either a) CO2 snow.
b) Electrocautary.
c) Plastic surgery.

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Chapter VI
Primary Irritant Dermatitis
A. House Wife Eczema
Clinical signs:
It is a common skin disease due to, or at least mediated by, excessive and prolonged exposure to soaps
or detergents and water.
- The eruption usually develops with dryness and redness of the fingers.
- Dry scales with peeling are evident at the tips of the fingers.
- Chapping is seen on the back of the hands
- Erythematous hardening of the palms with fissures.
- Frequently, these persons complain of dermatitis around and under the rings.
The defatting action and maceration produced by prolonged immersion or frequent washing of the
hands may be seen in many other types of workers such as bar-tenders, food handlers, chefs, physicians
and dentists; all of whom wash their hands frequently.
Etiology:
Myriads of factors may contribute
- There may be allergic sensitization to
1. Food stuffs handled in the kitchen as garlic, onion, tomato, spinach, grape fruit, orange,
figs, parsnip and cheese.
2. Rubber gloves, plastic articles, house plants as Philodendron, to metals as nickel, to dyes
as paraphenylenediamine and numerous other contactants.
- Candidiasis may develop especially in the interdigital webs.
- Feuerman believes that potassium dichromate sensitivity plays a major role in House-Wife
eczema.
Diagnosis:
It is mainly done by exclusion of the offending substances. The alkali in the soap and cleansers isn’t
true sensitizers; patch testing won’t elicit a true allergic reaction to alkali. However, it must be
remembered that perfumes and antibacterial materials that are allergic may be incorporated in the
substances. Photosensitization to some of the antiseptic soaps may occur.

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Patch testing to soap is performed with 2% aqueous solution placed on the skin for 48 hours. The
reaction isn’t allergic but irritant. It shows redness and a burned appearance to the point of vesiculation.
Patch test to other substances should be performed simultaneously to determine possible multiple
sensitization that may occur.
N.B.: during cold weather, frequent hand washing without proper drying will cause “Chapping” which
is probably a defatting and dehydration of the skin.
Treatment:
In most cases it is impossible for the patient, especially the young mother, to discontinue soap and
water exposure. Frequently, a halt in the use of chlorine bleaches and ammonia may bring remarkable
improvements.
Rubber gloves should be worn, especially when strong detergents are used. However, the possibility of
the development of sensitivity to rubber must be kept in mind. Rubber gloves shouldn’t be worn for more
than a few minutes because of the maceration action of the accumulated perspiration in the gloves. If
white cotton gloves are worn most of the time, the patient is deterred from frequent wetting of the hands.
The various corticosteroids creams are beneficial. They should be applied lightly every two to three
hours. For inflamed, swollen, oozing and weeping dermatitis, compresses of iced cold milk or Burrow’s
1:20 solution applied for 20 minutes every 4 hours. After using the compress, corticosteroid cream
(without neomycin) should be applied.
B. Diaper Dermatitis
It is a common dermatitis of the diaper area in the infants, also known as Napkin Psoriasis. It is an
erythematous and papulo-vesicular dermatitis distributed over the lower abdomen, the genitalia, the thighs
and the convex surfaces of the buttocks.
The intertrigenous areas often remain unaffected. Erythematous patches sometimes spread to the legs
and heels from contact with the wet diaper
In severe cases, there may be superficial ulceration. The tip of the penis may become irritated and
crusted with the result that the baby urinates frequently and spots of blood appear on the diaper.
The condition occurs most frequently in infants whose diaper isn’t changed all the night.

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In some instances the eruption has a well demarcated often polycystic and elevated psoriasiform
patches with micaceous scales.
Diaper dermatitis has been attributed to the alkaline irritative effects of ammonia formed in the wet
diaper by the splitting of urea by the ammonia forming bacillus in feces.
Diaper dermatitis must be differentiated from intertrigenous fungus infection usually caused by
Candida albicans and frequently seen in conjunction with diaper dermatitis. Toilet dermatitis may be due
to reaction to paint, shellac or plastic seats. The use of strong bleaches and strong soaps in laundering
diapers may also contribute to diaper rash.
Treatment is closely connected with prophylactic measures. The frequent changing of diaper is the best
measure. Thorough cleansing of the skin when diapers are changed should be done mainly with baby or
olive oil and a minimum of soap and water. The diaper if laundered at home should have a final rinse in
vinegar water (one ounce of vinegar to each gallon of water). Diaperene may also be used accourding to
instructions of the manufacturer.
Disposable diapers, especially those with synthetic liners, tend to minimize contact of the skin with
urine.
Topical corticosteroids applied lightly at the time of diaper change are not only effective but also safe
since there is little or no absorption.
For those who want to avoid the use of corticosteroids completely, 1-2-3 ointment is excellent.
Rx:
Barrow’s solution. 1 part.
Anhydrous lanoline. 2 parts.
Lassar’s Paste (without salicylic acid). 3 parts.
Dispense 120 grams.
M.Sig. apply when changing the diaper.

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Chapter VII
Pyogenic Infections of the Skin
A. Impetigo Contagiosum
Etiology: streptococci and to lesser extent Staphylococci (impetigo neonatorum) or both.
Age incidence: more common among children.
Sites of election: exposed area (face, scalp, hands, feet, legs and forearms) but may affect any part. The
course is 2-3 weeks.
Types:
- Primary: when Streptococci gain access to the epidermis through an abrasion.
- Secondary: to an itchy disease e.g. scabies, urticarial, eczema, pediculosis… etc.
Description:
The primary lesion is red spot macule that soon becomes a small vesicle which ruptures rapidly and
the fluid contents coagulate and dry to form a crust. Other vesicles soon form. The crust becomes dry and
darkens till it falls leaving a pigmented spot (macule) that fade gradually.
Sometimes the regional lymph glands are enlarged.
Predisposing causes: 1. Lack of cleanliness.
2. Itchy disease of the skin.
3. Presence of discharging ear of sinus.
4. Exposure to contagious.
Treatment:
1. Look for predisposing cause and treat it.
2. Local treatment:
 Antiseptic cleansing and drying lotions e.g. potassium permanganate 1/5000 – 1/10000,
boric acid lotion 3% … etc.
 Gentle removal of crusts by warm water, oil or starch and boric acid poultices.
 Antiseptic ointments e.g. gentamycin, tetracycline… etc. (but NOT penicillin or sulpha).

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C. Systemic antibiotics: only in the following conditions:
a) Septicemia, indicated by rise of temperature.
b) Regional lymphadenitis.
c) Extensive lesions
d) Impetigo Neonatorum.
D. Pus culture and sensitivity test in resistant cases.
Complications: rare but serious e.g. glomerulonephritis, endocarditis, arthritis… etc.
N.B. when impetigo comes in an area where there is skin fold it is called “Intertrigo”. Intertrigo may be
Streptococcal, Monilial, Seborrhoeic or due to other causes or mixed infections.
B. Erysipelas
Etiology: Streptococcus pyogenes.
Age incidence: all ages.
Sex incidence: both sexes.
Sites of election: face and legs (affecting skin and subcutaneous tissues).
Description: organisms enter through an abrasion in the skin. Their toxins cause an inflammatory
reaction with dilatation of the capillaries resulting in redness, hotness, swelling and pain in the affected
area which has a well-defined margin.
Incubation period: 2-5 days.
Course: 1-2 weeks, after which eruption stops spreading, temperature falls down, redness and swelling
subsides with slight degree of desquamation.
Complications:
1. Suppuration and gangrene.
2. Nephritis.
3. Meningitis.
4. Pneumonia.
5. Septicemia.
6. Acute infective endocarditis.

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Treatment:
1. Complete bed rest.
2. Penicillin procaine 800,000 IU daily till all signs and symptoms disappear then continue with
400,000 IU daily for another 5 days to guard against recurrence.
N.B. patients sensitive to penicillin can be given broad spectrum antibiotics e.g. tetracycline,
erythromycin … etc.
3. Local treatment in the form of 50% ichthyol solutionin water as a paint to relieve pain.
4. Symptomatic treatment for pain and fever in the form of aspirin, novalgin … etc.
N.B. the disease is very contagious and fatal but rare nowadays.
C. Sycosis
Types:
1) Sycosis Barbae (Barber’s rash).
2) Sycosis Nuchae (Acne Keloidales).
Etiology: S. aureus.
Lesion: folliculitis and perifolliculitis.
Age incidence: adults.
Sex incidence: males.
Sites of election: beard area, upper lip and back of the neck.
Description: disease commences as isolated discrete papulo-pustules from which hairs protrude. The
pustules rupture and the adjacent are then infected.
Predisposing causes:
1. Blepharitis and dacryocystitis.
2. Infected razors, shaving brushes or towels.
3. Seborrhoeic patients are more affected.
4. Anemia, avitaminosis, eczema and hygienic conditions.

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Treatment:
1) Eradication of septic foci in nose, nasal sinuses, tonsils and lacrimal sac.
2) Stop shaving and epilate hair with forceps and remove crusts.
3) Antiseptic lotions e.g. potassium permanganate 1/8000.
4) Local antibiotics as erythromycin with neomycin ointment.
5) Systemic antibiotics for 6 weeks, changed every 2 weeks.
6) Pus culture and sensitivity test for chronic and resistant cases.
7) Tonics, vitamin B complex, regulation of bowel motion … etc.
D. Furunculosis
Synonyms: boils, micro abscess.
Definition: acute painful circumscribes infection of the pilo-sebaceous follicle.
Etiology: staphylococci.
Description: commences as a small tender nodule which rapidly increases in size forming a conical
projection. In few days suppuration occurs and a tiny pustule forms at the apex of the conical nodule. The
center of the lesion then soften and the skin weakens and the pus escapes followed few days later be the
CORE which is formed of necrosed tissue, pus and cocci, then the cavity is filled with granulation tissue
and the lesion heals with a small scar left.
1. May appear on healthy skin.
2. May complicate a pruritic skin lesion as scabies, sweat-rash … etc.
3. In occurs in diabetics and prediabetics ( so urine examination, FBS and blood sugar tolerance curve are
important).
4. Patients with chronic nephritis, seborrhoeic states.
Treatment:
1) Personal cleanliness (frequent baths).
2) Treatment of predisposing cause.
3) Eradication of septic foci.
4) Penicillins and sulphonamides or broad spectrum antibiotics.
5) Local ointments.
6) Yeast, vitamin B complex and auto-vaccination.

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E. Carbuncles
Definition: a mass of confluent boils.
Etiology: virulent strain of cocci.
Predisposing factors are debilitation and diabetes mellitus.
Sites of election: back of the neck and trunk.
Lesion: deep extensive necrotizing folliculitis and perifolliculitis.
Description: the affected hair follicle and the surrounding tissue in deep part of the dermis form a
continuous slough bathed in pus and surrounded by a dense phlegmonous (gangrenous) inflammation of
the dermis and subcutaneous tissue.
Numerous pustules appear at the orifice of the pilo-sebaceous follicles,
Treatment:
1. Rest in case of large carbuncles or bad general health.
2. Diabetes should be controlled urgently if present.
3. Sulphonamides, penicillin or broad spectrum antibiotics.
4. Vitamins especially vitamin B complex, fluids and alkalis.
5. Urine examination to exclude nephritis.
6. Local antiseptics.
7. Surgical interference with cruciate incision.
8. Pus culture and sensitivity in resistant cases.
F. Pyogenic Granulaoma
In some cases of pyogenic infections which aren’t adequately treated and in some predisposed
persons who have tendency to granulation tissue formation, a small fragile tumor, very vascular, and
bleeds on touch is formed.
Such tumors usually don’t respond to local or systemic antibiotics and needs electocautary to destroy
the granulation tissue and stop bleeding.

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Chapter VIII
Viral Skin Diseases
A. Herpes simplex
Synonyms: Herpes labialis, Herpes Orificalis, Herpes Progenitalis …etc.
Sites of election: around body orifices e.g. the mouth, nose, eyes, ears, external urinary meatus, anus …
etc.
Description:
Commences by sudden appearance of a slightly swollen red patch in which the patient feels heat and
itching.
Few hours later, vesicles appearing containing clear fluid which rapidly becomes turbid.
The vesicles run in each other, then rupture and form yellowish crust which dries, darkens and falls
after few days leaving slightly reddened patch which disappears later without scarring.
Course: 1-2 weeks, but is recurrent.
Predisposing factors: 50-60% of normal people are carriers to the virus.
1) Fevers, e.g. influenza, tonsillitis, pneumonia.
2) Minor local injury or irritation.
3) Strong sunlight or UV light.
4) Excessive coitus and nervous irritability.
5) Pregnancy and menstruation.
6) Vaccines and drugs especially sulphonamides.
Treatment:
1. Locally:
- Antiviral cream e.g. acyclovir cream.
- Drying lotion and antiseptic powders e.g. calamine lotion with phenol or ichthyol.
- Local antibiotics in case of secondary infections e.g. gentamycin ointments.
2. Internally:
- Analgesics and antipyratics e.g. aspirin, salicylates … etc.
- Vitamins especially vitamin B complex.
- Nicotinic acid.

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3. Smallpox vaccine 4 times at 15 days interval was given previously to prevent frequency of recurrence.
4. Acyclovir 1gm daily for 5 days in recurrent cases.
Prognosis:
- The attack is self-limited.
- When secondary infected, may develop into impetigo.
- If affects the cornea, keratitis and panophthalmitis occurs and may lead to blindness.
B. Herpes zoster
Synonyms: zoster, zona, shingles.
Etiology: virus related to that of Varicella (chickenpox), there is a cross immunity and cross infectivity
between both.
Site of election: skin, mucous membrane and nerve structures (the posterior nerve root ganglion of the
cutaneous nerves).
It is unilateral and may affect the cranial nerves.
Age incidence: more in adults than in children.
Description: occurs in groups of vesicles or bullae, on a red edematous base, which is usually preceded
by pain along one or more of the sensory nerves in one side of the body 7-15 days before (preherpetic
neuralgia).
Regional lymph nodes are enlarged and there may be slight fever.
The vesicles run along the course of a cutaneous nerve and contain first clear fluid which soon becomes
turbid. Then the vesicles rupture and crusts are formed. When these fall they leave a reddish spot.
Course: 10 days to 3 weeks, longer and more painful in elderly.
Prognosis: usually occurs once in life and give permanent immunity.
- Herpes zoster ophthalmicus may lead to loss of vision.
- The younger the age, the better the prognosis.
-
Precipitating causes:
1. Trauma to the spine.
2. Vaccinations and drugs such as arsenic.
3. Fever and blood diseases such as Hodgkin’s disease, leukemia … etc.
4. Tebes dorsalis, pott’s diseases or malignancy.

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Complications:
1) Secondary infections.
2) Ulceration and gangrene.
3) Post herpetic neuralgia.
4) Paretic and paralytic phenomena with muscular atrophy.
5) Myelitis, meningitis, encephalitis … etc.
6) Eye complications, eye blindness.
7) Alopecia.
Treatment:
1. Acyclovir 4g daily for 7 days, if the patient was seen within the 1st
3 days of the disease (to avoid
postherpetic neuralgia).
2. Analgesics: novalgin, aspirin, codeine … etc.
3. Antibiotics: achromycin, erythromycin … etc in case of secondary infections.
4. Corticosteroids in combination with antibiotics in case of Hepes zoster ophthalmicus.
5. Vitamin B complex, liver extract, pituitrin and ergot preparations for postherpetic neuralgia
(don’t give to hypertensives and pregnants).
6. Irradiation of the spine with infra-red rays or injection of local anesthesia for post herpetic
neuralgia.
7. Dusting powder or calamine lotion with collodion to prevent infection or use tetracycline
ointment 3%.
C. Verrucae
Synonym: warts.
Etiology: filterable virus.
Description: small tumors of the skin, irregular in size and shape, hard and sessile projections, rough in
the surface and mamillated and of variable color from the skin.
They are symptomless except the plantar warts which are painful. They bleed on scrapping in sports.
They begin as pin-point to pin-head papules that grow gradually. Daughter lesions develop around the
mother wart.
The base isn’t infiltrate and the lesions are multiple (differentiation from malignant tumors).
Site of election: the dorsal surfaces of the fingers and hands, the palms, the face and the scalp but may
appear on any part of the body.

25
Treatment:
1) Chemical agents as glacial acetic acid.
2) Electrocautary.
3) X-ray therapy for plantar warts.
4) CO2 snow or NO2 liquid.
5) Podophylin resin 25% in liquid paraffin for venereal warts (Condylomata Accuminata).
6) Suggestion i.e. reassurance given by the treating physician.
N.B. - The adjacent skin should be protected carefully during treatment (by Vaseline)
- Local or general anesthesia may be needed.
D. Mollascum Contagiosum
Etiology: filterable virus.
Description: small, pearly, white, rounded papules, sessile, multiple and varying in size.
The surface is smooth and umblicated in the center.
On squeezing, a white, cheesy material can be expressed.
They are symptomless unless secondarily infected.
Site of election: face, neck, thighs, genitalia and forearms.
Treatment:
- Curettage and cauterization with carbolic acid.
- Electrocautary may be done.

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Chapter IX
Fungal Skin Diseases
A. Deep Mycoses
These are primarily systemic diseases, affecting the lungs, liver, spleen … etc with ocassional
involvement of the skin or mucous membranes.
These include: Actinomycoses, Blastomycoses, Histoplasmoses, Madura Foot … etc.
They need systemic treatment such as: Amphotricin-B, Terbinafine, Itraconazole, Fluconazole … etc
but not Griseofulvin.
B. Superficial Mycoses
Fungi are vegetable organisms that can live in nature as nonpathogens (saprophytes) on animals or
human beings. They can provoke dermatoses when circumstances favor their growth e.g. excessive heat
or sweating. The most important of these are:
1. Tinea Capitis:
Synonym: ringworm.
Etiology: fungi (varying in type: Microsporons, Trichophytons … etc), the animal types and more
dangerous than the human types.
Age incidence: children more than adults.
Clinical types:
 Scaly type.
 Black-dot type.
 Suppurative type (Kerion)
Methods of transmission:
1. From child to child.
2. From barber’s shop.
3. From animals as cats, dogs … etc.
Lesion: any scaly patch in a child with loss of hair (alopecia) should be considered ringworm till proven
otherwise.
Diagnosis:
1) Demonstration of florescent hair under Wood’s light, it’ll give a greenish-blue florescence.
2) Spores and hyphae can be seen under the microscope after adding 20% KOH solution to the hair.
3) Trichophytin test will be positive.
4) The clinical picture.

27
Treatment:
1. Griseofulvin 12.5mg/Kg/day in 2-4 divided doses for 4-6 weeks or Terbinafine:
- 62.5mg daily for children weighing 0-20 Kg.
- 125 mg daily for children weighing 20-40 Kg.
- 250 mg daily for children weighing over 40 Kg.
2. Wash scalp with soap and water twice weekly.
3. Rub daily with whitfield ointment.
2. Favus (Tinea Favosa)
Definition: chronic fungus infection.
Site of election:
1) Mainly scalp.
2) May affect the body.
3) Rarely the nails.
Characteristic lesion: sulphur cups scutula which may coalesce to give honey-comb appearance.
Description:
- The scalp has a mousy odor.
- The hair is lusterless, brittle and may split into two.
- The disease is patchy but the whole scalp may be affected.
Prognosis: the disease destroys the hair follicles leading to cicatricial alopecia in neglected cases.
Treatment: the same as ringworms.
3. Tinea Circinata (Corporis)
Site of election: glabrous (hairless) skin.
Age incidence: more in children.
Description: the lesion is circular patches which spread out peripherally with healing in the center. The
active edge is red, scaly and there may be minute vesicles, pustules or crusts. The center is usually clear
but may be slightly scaly. There is usually mild itching.
Treatment:
1) Search for the primary lesion and treat.
2) Tri-iodine 2-3% t.d.s. for 1 week followed by Whitfield ointment once by night for another week
is usually sufficient OR local antimycotic creams or ointments as Miconazole 2% may be used
for at least 2 weeks.

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4. Tinea Cruris
Site of election:
- Upper and inner parts of the thighs.
- Ano-genital region.
- Pubic region and lower abdomen.
Description: the same as in Tinea Circinata.
Treatment:
1) Search for the primary focus (as Tinea Capitis, Tinea Pedis … etc) and treat as it may be due to
an auto infection or contracted from another object or animal.
2) Locally as in Tinea Circinata but Castellani’s paint is very effective here.
3) Griseofulvin (not more than 6 tablets daily for adults) for 3-4 weeks in resistant cases.
4) Under-clothes should be boiled and ironed.
5. Tinea Pedis
Synonym: Athlete’s foot.
Definition: fungus infection of the horny layer of the foot but the nails may be involved.
Description:
- The skin between the toes, especially the 4th and 5th or the 3rd and 4th, is fissured, whitish and
sodden. Desquamation reveals a red, raw, shiny base.
- Itching may be present and secondary infection is common.
- The affected foot may have a bad smell in the neglected cases.
Treatment:
a) Prophylactic:
1. Avoid walking bare-footed beside swimming pools.
2. Dry the feet thoroughly after path or washings.
3. Sandals and well-ventilated shoes are preferred during summer.
b) Curative:
1. In acute cases use soaks of Boric acid or potassium permanganate 1/8000 solution.
2. When inflammation subsides, Castellani’s paint (half dilution) or Tr. Iodine 1-2% are
very useful.
3. Whitfield ointment may be used.
4. Griseofulvin is given in adequate doses and for relatively long time for resistant cases.
5. Stockings should be sterilized and shoes should be formalin-fumigated.

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6. Tinea Barbae
Definition: chronic infection of the bearded area of the cheek and face.
1) Infected towels.
2) In barber’s shop.
3) From animals to farmers.
Treatment:
1) Griseofulvin in adequate doses.
2) Worm fomentations of 1-2% Resorcin in water.
3) Application of week solutions of Tr. Iodine or Whitfield ointment.
4) Infected hair should be removed by forceps.
7. Tinea Versicolor (Pityriasis Versicolor)
Definition: very superficial fungus infection affecting the stratum corneum only.
Sites of election: neck, trunck, upper parts of the extremities but rarely on the face or whole body.
Clinical types:
1) Hyperpigmented type.
2) Hypopigmented type.
3) Mixed type, which is the commonest.
Description: macular lesions, well-defined, varying in size and brownish or yellowish in color with slight
scaling.
Season: more in summer with spontaneous remission in winter.
- Swimming pools.
- Clothes and beddings.
Treatment:
1) Daily paths and scraping with a brush.
2) Clothes and bedding should be boiled and ironed.
3) 30% sodium hyposulphite in water applied every morning after bath for one month.
4) Whitfield ointment or ointment containing 2% sulphur and 2% salicylic acid may be applied by
night.
5) Selenium sulphide 2% shampoo may be used as paint before bath.

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8. Onychomycosis
Description:
- The fungus spores and mycelia are located under the nail plate. Masses of keratin and fungal
elements accumulate under the nail lifting it up from its bed.
- The nail plate is brittle and opaque.
Treatment:
1) Avulsion of the nails is no more needed.
2) Prolonged griseofulvin therapy was used (3-6 months for finger nails and 12-18 months for toe
nails with a lot of gastrointestinal troubles and liver and kidney dysfunctions).
3) Terbinafine is now given ( 6 weeks for finger nails and 12 weeks for toe nails in a small dose
with less GI, liver and kidney troubles).
4) Itraconazole may also be given as pulse therapy (given for 1 week and rest for 3 weeks).
5) Fluconazole may also be given.
C. Moniliasis
Definition: a group of eruptions of the skin and the mucus membranes caused by a yeast-like organism.
Etiology: Candida albicans.
Classification:
1) Localized e.g. monilial intertrigo, onychia and paronychia, perleche (angular stomatitis), thrush
(superficial glossitis), monilial vaginitis, proctitis … etc.
2) Generalized with buccal and intestinal infection.
3) Systemic, affecting internal organs.
4) Monilidis (allergic eruptions).
Predisposing factors:
1. Diabetes mellitus.
2. Prolonged corticosteroid therapy.
3. Prolonged antibiotic therapy.
4. Chronic alcoholism.
5. Obesity and hyperhiderosis.
6. Debilitation and vitamin deficiency.
Treatment:
1) Nystatin sulphate is the specific drug (applied locally or taken by mouth).
2) Castellani’s paint or 1-2% gentian violet for the cutaneous forms.
3) For intestinal moniliasis, nystatin sulphate 6-8 tablets/day are given.
4) For vaginal moniliasis give vaginal tablets of nystatin.

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Chapter X
Skin Diseases due to Animal Parasites
A. Scabies
Definition: a contagious skin disease, characterized by severe itching which is usually worse by night
because the parasite is stimulated by warmth.
Etiology: the female Acarus mite called “Sarcoptes scabiei hominis”.
Description:
- After impregnation, the female burrows itself horizontally in the horny layer of the epidermis.
This results in a burrow in which the female lays its eggs.
- This burrow is pathognomonic, it is a small grayish elevated line, about 0.5 cm in length, it is
usually tortuous, curved and beaded. A little pearly vesicle may be seen at the end of the burrow. The
burrows are only seen early in the disease then disappear due to scratching which removes their roofs.
- There may be also multiple eruptions of itchy, small, red papules, excoriations and vesicles.
- Erythematous macules, inflamed follicles, urticarial wheals and eczematous patches may be seen
also.
- Pyogenic infection is common in the form of pustules, ulcers, boils … etc.
1. Infected persons as what happens when infected children sleep with each or with their mothers.
2. During sexual intercourse when infection starts on the genitalia then spreads to the whole body.
3. Contact with infected animals as camels, cats, dogs … etc.
4. Indirect contact through the clothes, beddings or towels of infected persons or through seats of
water closets.
Sites of election: lesions are symmetrical and generalized
1) Interdigital webs and sides of the fingers.
2) The flexors of the wrists about the ulnar border.
3) The medial sides of the forearms.
4) The points of the elbows.
5) The anterior axillary fold.
6) Round the nipples in women.
7) The lower abdomen and external genitalia.
8) The sides of the natal cleft and the lower parts of the buttocks.
9) The medial aspects of the thighs and legs.
10) Round the ankles and dorsal surfaces of the feet.

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Complications:
1. Impetigo and ecthyma.
2. Boils and furuncles.
3. Lymphadenitis.
4. Acarophobia; fear of infection with Acarus.
5. Irritation due to abuse of sarcopticides.
6. Sensitization to drugs used.
Treatment:
- All the family, colleagues and animals of the infected person should be examined and those who found
to be infected should be treated at the same time.
- All the clothes and beddings should be disinfected by boiling and ironing.
- A hot bath with soap and brush should be made before the application of the sarcopticide and the skin
should be dried.
1) Sulphur ointment is the best and most effective (5-10% for adults and 3-5% for children). The
whole body from the neck to the feet is rubbed for 4-5 successive nights. 15% ZnO may be added
due to the bad odor of sulphur and the possibility of causing allergic dermatitis. 5% balsam of
Peru may also be added.
2) Benzyl benzoate, 25%emulsion in soft soap and alcohol for adults, 12.5% for children, is also
effective. It is a one night treatment (two applications may be applied at the same night).
3) Mitigal 10% in liquid paraffin for 3 successive nights is a clean and effective preparation.
4) Crotamiton 10% lotion is used for two successive nights.
5) Gamma benzene hexachloride (Lindane) 1-2% cream is a one night treatment and is very
effective.
6) Permethrin 5% cream is applied for 8-12 hours, it is very effective but very expensive.
7) Antihistamines may be used to alleviate itching.
8) Local or systemic antibiotics are recommended in case of secondary infections.

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B. Pediculosis
Types:
a) Pediculosis Capitis (Head Louse).
b) Pediculosis Corporis (Body Louse).
c) Phtheriasis Pubis (Crab Louse).
1. Pediculosis Capitis:
Sites of election: mainly on the back and sides of the head amongst the hair are found the parasite while
the eggs (nits) are attached to the hair.
Description: the parasite causes severe irritation due to its bites in order to suck blood for its
nourishment. This leads to scratching and secondary infection leading to impetigo and pustular lesions
with enlargement of the cervical lymph glands.
Age incidence: more common in children.
Sex incidence: more frequent in girls due to the long hair.
Treatment: in heavy infestation in the boy, the hair is cut short while in girls and adults treatment should
be done in the presence of long hair.
1) Benzyl benzoate emulsion 10% is highly recommended. This is applied by night and washed the
second morning.
2) Lethane 384 or Lindane is curative and prophylactic for 1 week.
3) Sulphur ointment 3% may be used in cases of secondary infections.
4) Antibiotics are also used in cases of regional lymphadenitis.
5) Antihistaminics are used to alleviate itching.
6) Other sarcopticides e.g. Crotamiton 10% or Permethrine 5% may be used.
N.B. another courses of treatment after 3 weeks (incubation period for hatching of nits) may be necessary
in heavily infested persons to eradicate the second generation.

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2. Pediculosis Corporis:
Age incidence: adults, especially elderly.
Description: it is the largest of all varieties of lice. It isn’t found on the body except for few instances in
which the parasite may be seen crawling among the hair on the shoulders and neck but commonly seen on
the clothes especially about the seams.
As all pediculi, it feeds on the blood of the patient. This causes itching and scratching of the skin with
excoriations and the appearance of pigmented lesions.
Regional lymph nodes are enlarged.
N.B. the body louse is very dangerous because it conveys Typhus, Trench, and Relapsing fevers.
The condition is common during wars and strarvation especially among the elderly who neglect
bathing and frequent clothes changing.
Treatment:
- All clothing and beddings must be disinfected and thoroughly dusted with 10% D.D.T in
Talc powder.
- Dusting may be carried out without undressing the patient by means of a special powder
blower.
- A simple method is to boil and iron all clothing after being turned inside out, especially
those in direct contact with the skin.
- Simple ZnO cream or ointment may be used for treatment of excoriations on the skin.
Also White precipitate ointment.

35
3. Phtheriasis pubis:
Description: it is caused by the crab louse which short but broad, it fixes its nits to the hair near the skin
and it is very difficult to get away from the hair.
Sites of election: it affects hair of the pubic region, around the arms, axillae, chest or limbs of hairy
person. The eye brows and eye lashes are sometimes affected.
N.B. parts of the parasite may be sometimes buried in the skin at the mouth of the hair follicle and leave
bluish spots.
Methods of transmission: the disease is usually contacted during sexual intercourse but rarely as an
accidental infection.
Signs and symptoms: the bites of the parasite cause severe itching and every case of Pruritus Ani or
Vulvae the existence of phtheriasis Pubis should be excluded.
Treatment:
1) Hair in the pubic and affected areas should be shaved before applying the White precipitate
ointment.
2) 10% Crotamiton cream or lotion may be applied for 5 days.
3) 10% Benzy benzoate emulsion is very effective.
4) 1-2% Gamma benzene hexachloride is the best.
5) In case of infestation of the eye lashes, the parasite should be removed with a forceps and 1%
yellow oxide of mercury eye ointment should be applied.

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C. Leishmaniasis
Synonyms: oriental sore, Jericho boil, Allepo boil, Baghdad boil, Lahur boil … etc.
Definition: infection caused by a parasite called “Leishmania tropica” which is transmitted by a sand fly
called “Phlebotomus papatasii” which is the natural vector for the disease.the reservoir animal is the rat
and certain other rudents (Ratus ratus).
Types:
1. Leishmania tropica (Cutaneous Leishmaniasis).
2. Leishmania donovani (Kala-Azar, Visceral Leishmaniasis).
3. Leishmania braziliensis (Espundia, Muco-Cutaneous Leishmaniasis).
Sites of election: usually the uncovered area (face, nose, forehead, cheeks, ears, hands, forearms and lips)
but any other area that get exposed to the bite of the fly may be affected. The lesion may be single or
multiple according to the number of bites.
N.B. once the patient has the disease, permanent immunity develops.
The primary lesion is an indolent, red, flat papule that is free of pain and tenderness then develops
onto nodule then ulcer then a disfiguring scar after 12-24 months.
Diagnosis:
1) A history of an ulcerating granulomatous nodule of less than two years duration is suggestive of
the disease especially in the endemic area.
2) A smear from the non-ulcerating lesion stained with Giemsa stain often shows the organism.
3) Leishmanin test is positive.
Treatment:
a) Pentavalent antimony is the drug of choice, it is given Intralesional, IM or IV.
b) Amphotericin B has been found to be effective.
c) Electrocautary may be done in small lesions.
d) Cryotherapy with NO2 may also be used in small lesions.
e) Irradiation with infra-red rays may also help in small lesions.
f) Ketoconazole and metronidazole aren’t effective.

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Chapter XI
Bacillary Skin Diseases
A. Primary Tuberculous Complex (TB Chancre)
Definition: it is the first TB infection of the body. It takes the cutaneous route instead of the pulmonary
route (Ghon’s focus).
Age incidence: mostly in children.
Sites of election:
- The face especially the lip region.
- The upper limbs especially the fingers.
- It may affect the mucus membranes of the nose and mouth.
Description:
After 2-3 weeks from exposure, a papule and more often a nodule develops which is slowly
progressive and resistant to treatment.
Ulceration often occurs and extending lymphangitis and lymphadenitis are present which constitute
the primary complex.
The ulcer lasts for 1-2 months then heals by scaring or leaves a tuberculous nodule and Lupus
Vulgaris may develop at the site.
Tuberculin reaction is negative at first, after 3-4 weeks immunity develops and it turns strongly
positive and lymph glands disappear.

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B. Lupus Vulgaris (L.V.)
Definition: a chronic and usually localized slowly progressive tuberculous affection of the skin.
Age incidence: 50% occurs in children below 15 years of age and 80% below the age of 20 years.
Description: the primary lesion is known as the lupus nodule or the apple-jelly nodule which is soft and
reddish-yellow in color if pressed with a glass slide (i.e. diascopy) as it is usually masked by erythema.
The nodule increases in size and the disease may extend by peripheral deposition of fresh nodules and
coalescence of the old ones thus a plaque is formed. The center of the patch either regress, fibrose and
forms a scar or ulcerates and ultimately heals by a scar tissue.
N.B.
1. The nodule is avascular and doesn’t bleed on piercing by a probe. This is a diagnostic test.
2. Lupus patches are long standing, usually for years.
3. The scar tissue is thick and contractile and it is never healthy (this is a characteristic of TB).
Modes of infection:
1) Direct infection through an abrasion in the skin especially in children’s buttocks during creeping.
2) Extension to skin from infected mucous membranes of the nose or mouth.
3) Extension to the skin from a TB gland or a TB sinus through lymphatics.
4) Rarely hematogenous infection during fever.
Disfigurements caused by the contractile scar:
1. Ectropion of one of both eyelids.
2. Parrot peak like nose, due to eating up of the cartilaginous portion of the nose.
3. Simian nose due to eating up of the central portion and alae nasi.
4. The lobules of the ears may be eaten.
5. Microstoma.
6. Pseudo-ankylosis of the joints.
Complications:
1) Frequent attacks of erysipelas.
2) TB meningitis and dactylitis.
3) Pulmonary TB (rare).
4) Squamous cell carcinoma.

39
Treatment: in addition to the anti-tuberculous measures involving hygiene, diet, vitamins … etc, the
followings should be done:
1. Isoniazid (I.N.H) 5 mg/Kg/day for 9-12 months.
2. Streptomycin 1 gm twice or three times weekly in combination with I.N.H.
3. P.A.S. is much less effective in the treatment,
4. Calciferol or vitamin D2 is very effective in daily doses of 150,000 I.U. orally or 600,000 I.U.
twice weekly IM. It works through calcification. The duration of treatment is several weeks to
few months.
5. CO2 snow application improves scar healing.
6. X-ray irradiation is better avoided because of risk of epithelioma.
C. Erythema Induratum (Bazin disease):
Definition: erythema nodosum-like lesions.
Sites of election: posterior aspects of the legs and thighs.
Age and sex incidence: girls and middle-aged women.
Description:
- The skin over such lesions is usually violaceous because the peripheral circulation is very poor.
- The lesions are dark red nodules, which are painful, deep and hypodermic.
- They may undergo necrosis and ulcer formation. The patient is usually anemic and of the
chilblain diathesis. He lives indoor life with a good deal of standing as nurses, housekeepers …
etc.
Prognosis: healing of the ulcers occurs after months into a pigmented depressed scar but the lesion may
recur every cold season.
Treatment:
- In addition to the general measures e.g. care of the general health, hygiene and nutrition, certain
tonics A Cod-liver oil, vitamin D2 and I.N.H. are advised.
- Local measures to stimulate the circulation and overcome the venous stasis are advised in the form
of adhesive elastic bandages, radiant heat, infra-red irradiation, short waves … etc.
- Bed rest in advanced cases.
- The ulcers should be dressed by dyes or antiseptics.

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D. Leprosy
Synonyms: Hanseniasis, Lepra, Hansen’s disease.
Definition: chronic, systemic infectious disease caused by Mycobacterium leprae.
Manifestations: granulomatous lesions in skin, mucus membranes, nerves, bones and viscera.
Classification: is based on clinical, bacteriological, immunological and histopathological criteria:
1) Tuberculoid leprosy (TT): maculo-anaesthetic patches, loss of the outer third of the eye brows,
nerve enlargement (ulnar nerve), paralysis and wasting.
2) Borderline tuberculoid leprosy (BT): smaller lesions, numerous, less hair loss, nerves are slightly
enlarged.
3) Borderline leprosy (BL): only skin and nerve involvement.
4) Borderline lepromatous leprosy (BL): numerous lesions even nodules, nerve lesions appear rare.
5) Lepromatous leprosy( LL): infiltration of the skin, loss of eye lids known as “Leonine Facies”.
Diagnosis:
1. Demonstration of the acid-fast bacilli in the skin smear (Zeihl-Nelsen’s stain).
2. Histamine test, flare won’t appear if the nerve is damaged.
3. Methacholine sweat test in dark skinned people.
4. Skin biopsy.
5. Skin sensory test.
6. Lepromin test (Mitsuda reaction).
Treatment: isn’t completely satisfactory.
1) DDS (dapsone or avlosulfon) is the treatment of choice.
2) SU-1906 (Ciba).
3) B-663 (Giegy).
Prophylaxis:
1. BCG vaccination.
2. DDS, small doses for exposed children.

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Chapter XII
Spirochetal Skin Diseases
A. Syphilis
Definition: an infectious skin disease due to a spirochete called Treponema pallidum and is characterized
by great chronicity. It may involve every structure in the body and simulate many diseases in
dermatology, medicine and surgery and that is why it is called “Great Simulator and Great Immitator”.
Classification:
a) Acquired syphilis:
I. Early syphilis, within 2 years of infection, includes:
1) Chancre.
2) Secondary lesions.
3) Early latent syphilis.
II. Late syphilis, after 2 years of infection, includes:
1) Late latent syphilis.
2) Gummatous reactions in
- Skin, subcutaneous tissue and mucous membranes.
- Bones, joints, muscles … etc.
- Viscera.
3) Cardiovascular syphilis and neurosyphilis.
b) Congenital syphilis:
I. Early.
II. Late.
III. Stigmata.
Chancre
This is the primary lesion of syphilis and is due to tissue reaction to inoculation of the treponemas. It
appears after the incubation period of, usually 2-4 weeks but may vary from 9-90 days. It beins as a red,
dull macule which becomes papular and enlarges peripherally. The surface soon becomes eroded, giving
rise to an ulcer 0.5-1.0 cm in diameter. The ulcer is circular or oval, regular and well-defined.
The surface is smooth, eroded with adherent crusts.
The floor consists of dull red granulation tissue.
The base is indurated and gives the feeling of a button embedded in the tissues.
The lesion is painless unless secondary infection has occurred. It is usually single but multiple
simultaneous chancers rarely occur.

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In the male, the chancer usually occurs in the coronal sulcus, glans penis, prepuce, frenulum preputii,
the external urinary meatus or the shaft of the penis. Intrameatal chancer may occur.
In the female, it may occur on the cervix, uterus, labium majus, fourchette, labium minor, clitoris or
near the urethral orifice.
Extragenital chancers are found on the lips, tongue, tonsils, fingers, eyelids, nipples, anus or anal
canal.
The regional lymph nodes become enlarged within a week form the appearance of the chancer. They
are discrete, painless and of a firm, rubbery consistency. In genital chancers, the lymph node enlargement
is bilateral usually while in extragenital, it may be unilateral.
The chancer heals spontaneously after 3-8 weeks leaving a thin atrophic scar.
Secondary Syphilis
6-8 weeks after the beginning of the primary stage, signs and symptoms of the secondary stage may
appear. They may appear earlier and so the secondary stage begins while the chancer is still present.
Occasionally they are delayed even for a year.
This stage is characterized by constitutional symptoms as malaise, anorexia, headache, low grade
fever, cutaneous rash, mucosal lesions, adenitis, nail and hair changes, aching pains especially in the long
bones, muscles and joints.
The skin eruption has the following characteristics:
1) Absence of itching.
2) Pleomorphism.
3) Nonvesicular.
4) Usually associated with muco-membranous lesions.
It may be macula rash (Roseolar Syphilid), papular or pustular. Moist papules and condylomata lata
may also appear in the intertrigenous areas, they swarm with treponemas and are the most infectious
lesions of syphilis.
Syphilitic leukoderma on the back and sides of neck may be evident in women and dark-skinned
individuals.
The mucous membrane lesions may appear in the form of mucous patches or snail track ulcers.

43
Late Syphilis
The most characteristic lesion is the localized Gumma. Diffuse gummatous infiltration also occurs. It
affects every organ but commonly involves:
1. The skin and subcutaneous tissue, mucous membranes and submucous tissue.
2. The bones, joints, muscles … etc.
The cutaneous gummata may appear clinically in the form of nodular lesions or subcutaneous gummata.
Congenital Syphilis
There is no chancer in congenital syphilis. The treponemas pass to the fetus from the mother’s blood,
usually after the 4th
month when the placenta has developed.
a) Early congenital syphilis:
1) The cutaneous lesions:
- The bullous eruption, especially on the palms and soles.
- The papular and papulo-squamous eruptions on the trunk.
- The condylomata lata in the moist areas.
- The rhagades at the angles of the mouth.
- The Café-au0lait pigmentation of the skin.
- The loss of hair on the scalp.
- The syphilitic onychia.
2) The mucous membrane lesions: mucous patches in the mouth and on the muco-
periosteum of the nasal cavity, giving rise to syphilitic rhinitis (Syphilirtic Snuffles).
b) Late congenital syphilis: the skin and mucous membrane lesions are similar to those of late
acquired syphilis, consisting of gummata of the soft tissues. They commonly begin in the
subcutaneous or submucous tissues.
Diagnosis of Syphilis:
I. The primary stage:
1) The dark field examionation to demonstrate the T. pallidum in the serum taken from the
chancre.
2) The standard serological tests e.g. the Wassermann or Kahn tests for V.D.R.L.
II. The secondary and later stages:
1. The standard serological tests.
2. The specific tests e.g. the Treponema immobilization test and the Reiter’s protein
complement fixation test.

44
Treatment of Syphilis:
I. Early syphilis (primary, secondary and early latent syphilis): 600,000 I.U. of procaine penicillin in
aqueous solution or with 2% aluminum monostearate may be given E.O.D. for 10 injections (total
dose 6 million units).
II. Late syphilis (benign gummatous and late latent syphilis): benzathine penicillin G is give in doses of
3 million units at 7 days interval (total dose 10 million units).
N.B. to avoid the Jarish-Hexheimer reaction, start the treatment with IM injection of 0.2-0.3 gm of
bismuth weekly for 3-4 weeks before starting penicillin.
III. Congenital syphilis:
a) Early (less than 2 years): total dose of penicillin is 450,000 I.U./Kg body weight, giving in
divided doses over a period of 10 days.
b) Late (over 2 years): treatment and follow up as the ;ate acquired syphilis.
Follow up Syphilis:
In case of early syphilis:
Clinical inspection and two quantitative serologic tests (as Wassermann and Kahn) should be done
monthly for 6 months then at 3 months interval for a year. If only one spinal fluid examination is to be
done, the preferred time is 12 months after the treatment. This examination includes: serological tests,
cells, proteins and colloidal gold curve.
In case of relapse, the treatment should be repeated giving DOUBLE the ordinary dose.
In case of late syphilis, quantitative standard serologic tests should be done at 6 months interval for 2
years.
A static or falling titer may be considered satisfactory.
Persistence of positive serologic tests after adequate treatment is considered as a sign of immunity
and not necessarily as a sign of resistance.
In case of congenital syphilis, the follow up is as for the early acquired syphilis.

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Chapter XIII
Seborrhoeic Dermatoses
A. Seborrhoeic Dermatitis
Definition: seborrhea means a state of excessive production of sebum which is altered in both quantity
and quality (i.e. excessive in amount and more acidic due to presence of hyperlipidemia) and the fatty
acids are excreted through the skin.
Seborrhoeic dermatitis is a chronic scaly erythematous eruptions due to over activity of the sebaceous
glands.
Etiology:
- May be caused by endocrinal dysfunction.
- Organisms (especially Microsporon ovale) seem to play an important role in the production of the
inflammatory phase of the disease.
Types:
1) Dandruff is the mildest form. It occurs on the scalp in the form of small whitish, dry scales
encircling the hair follicles without redness of inflammation.
2) In severer cases, the patient complains of itching which is relieved by washing the head.
3) In more severe cases, the seborrhoeic areas (eyebrows, nasolabial folds, retroauricular sulci,
external auditory meatus, the prestrenal area and the interscapular region) are affected and
blepharitis is common.
4) In more marked forms, diffuse erythema and greasy scales appear on the face, scalp and
nasolabial folds. Oval or annular patches appear on the prestrenal and interscapular areas.
5) In more extensive cases, the axillae, the ano-genital region and the umbilicus are affected.
Lacerations may occur and monilial is found in abundance. Sometimes pyogenic infection may
supervene causing exudation, crusting and inflammation.
Age incidence: it usually starts at puberty and in the pre-pubertal age (9-11 years).
Associations: usually associated in men with baldness (hair recedes at the temples and disappears at the
vertex  seborrhoeic alopecia). It seems to be hereditary and hormones play an important role here.

46
Treatment:
a) Local:
1. Repeated washing of the scalp (daily of E.O.D.) to remove the scales and alleviate
itching.
2. Alcoholic drying lotions containing salicylic acid 3-4%, resorcin 2-4%, mercuric
chloride 1-2/10,000 always help.
3. Sometimes better results are obtained if the treatment is begun by an ointment (used
daily for 1 week, the E.O.D. for 2 weeks, then once weekly for 6-7 weeks). The scalp
should be washed in the next morning and hair lotion used.
N.B. ointments containing castor oil makes it more saponinifiable and easily washable.
4. Selenium sulphide 1-2% shampoo 1-2 teaspoons are applied to the scalp after washing
with soap and warm water then rinsing, it makes a lather, allowed to remain for 5
minutes then the hair is thoroughly rinsed. It is applied twice weekly for 2 weeks, then
once weekly for another 2 weeks, then once every 3 -6 weeks.
N.B. crude coal tar or ketoconazole may also be used instead of selenium sulphide.
5. For acute disease, 2% sulphur in Calamine lotion is helpful.
6. 3% vioform ointment and cream are helpful in selected cases.
b) Systemic:
1) Diet free of excessive fats and carbohydrates.
2) Broad spectrum antibiotics and corticosteroids.
3) Antihistaminics for itching.
4) Short courses of corticosteroids may be needed.
N.B. milk crust which appears on the scalp of infants as a thick yellowish oily crust and may spread to the
face, neck or the whole body is a type of seborrhoeic dermatitis common among newborns.

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B. Acne Vulgaris
Definition: chronic inflammatory disease of the sebaceous glands and the pilo-sebaceous follicles.
Associations: seborrhea (oily skin).
Age incidence: puberty, 12-30 years.
Sites of election: face, neck, shoulders, chest and upper parts of the back.
Description:
- The primary lesion id the comedo or comedone (black head) which is a plug of keratin and sebum
blocking and dilating the pilo-sebaceous follicle.
- The surface if the comedone is black (due to slow oxidation and accumulation of melanin
granules) and the lower portion is white.
- Papules, nodules, pustules, deep abscesses, sinuses or cysts may develop. All of them may be
present at the same time (Acne Conglobata).
- Superficial acne lesions may involute without forming pustules but as a role, the apex of the
lesion suppurates then forms papulo-pustules which break down within few days. After
evacuation of pus, the lesion involutes within a week.
- If suppuration involved only the sebaceous glands and follicles, no would follow but if the
connective tissue surrounding the glands participated in the Suppurative process, a scar would
result  pitting.
Etiology: is still a matter of discussion but the following theories are considered:
1. The infecting organisms: (Corynebacterium acne, Staphylococcus albus epidermidis,
Microsporon ovale and Durnidix folliculorum) play a great role in the development of acne.
2. It is believed that androgens play a great role in the follicular stimulation leading to
hyperkeratosis if the orifices and ducts causing comedo formation.
N.B. castrated patients don’t develop acne.
3. The hereditary factor is well known.
4. The constitutional factor is important. The seborrhoeic skin is more susceptible.

48
5. The dietary factor is still questionable but indulgence in taking fats and carbohydrates and
irregularity in feeding encourages acne formation.
6. The environmental factor such as indoor life, the lack of exercise, lack of sleep, worry and
overwork.
7. Drugs such as bromides and iodides and lack of vitamins especially vitamin A cause
exacerbation of preexisting acne.
8. Sex hormones may be considered as exiting factors (acne increases during menstruation).
Treatment:
1) Thorough medical examination and treatment of gastrointestinal upset, constipation, septic foci,
anemia and avitaminosis.
2) Cleansing: washing several times per day with any soap ad any water to reduce the bacterial flora
and remove excessive secretions.
3) General hygiene: plenty of fresh air, exercise, sun and sea bathing. The lack of sleep, emotional
tension and anxiety should be relieved.
4) Diet: should be regulated, chocolates, nuts excess of milk, ice creams, iodides and bromides
should be avoided.
5) Local treatment:
a) Comedo extraction: by comedo extractor and not by hand. Pustules should be evacuated and
deep lesions drained through a minute incision.
b) Topical treatment:
- Alcoholic shaky lotions containing sulphur helped many patients. They are apllied 2 or 3
times daily.
- Local antibiotics e.g. erythromycin, gentamycin, tetracycline or clindamycin may be
used.
- Benzyl peroxide 5-10% cream or gel.
- Vitamin A acid 0.025-0.05% cream or gel.
- Combination of antibiotics with comedolytic agents as benzamycin cream.

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N.B.
- Emollients (nourishing creams) shouldn’t be used.
- Medicated creams (with neomycin or corticosteroids) may be indicated to alleviate dryness caused by
drying lotions.
- Intralesional corticosteroids are only indicated in cystic acne.
6) Systemic treatment:
a. Antibiotics in pustular lesions e.g. oxytetracyclines, doxycycline, minocycline, erythromycin
… etc.
b. Vitamins, especially A and B-complex.
c. Steroids (10 mg prednisolone daily for short period in special cases).
d. Estrogen and thyroid extracts are rarely used.
e. Isotretinoin (vitamin A acid) 0.5-1 mg/Kg/day. For at least 4 months in very severe and
resistant cases after doing liver and kidney function which should be repeated every month.
The drug should be stopped at any time there is liver or kidney dysfunction and shouldn’t be
given to pregnant women and females shouldn’t get pregnant at least 2 months after finishing
the treatment as the drug is teraotgenic.
N.B. some cases of nodular acne might need certain surgical procedures as dermabrasion which should be
done in hospital by a clever plastic surgeon otherwise, the results will be very disappointing.

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C. Acne Rosacea
Definition: chronic erythematous and papulo-pustular eruption of the face.
Age incidence: middle age.
Sex incidence: more in women.
Sites of election: middle third of the face.
Description: four stages may be seen if the patient isn’t treated
a) Stage of recurrent transient erythema of the flush area of the face, evoked by drinking hot fluids
or alcohol, exposure to heat or eating spicy food.
b) Stage of persistent erythema.
c) Stage of telangiectasia and pustulation about the nose, cheeks and chine become prominent.
d) Stage of rhinophyma in which hypertrophy of the nose will result (potato nase).
1. Seborrhoeic dermatitis and acne vulgaris.
2. Gastrointestinal disturbances e.g. hypochlorhydria.
3. Nervous instability and menopausal changes.
Treatment:
1) Eliminate coffee, alcohol, hot drinks and spicy foods from meals.
2) Avoid exposure to extremes of hot and cold.
3) Reduce emotional tension by tranquilizers.
4) Antibiotics especially tetracycline for pustulation.
5) Short term corticosteroid therapy.
6) Topical treatment in the form of sun screens and sulphur in Calamine lotion.
7) Vitamin B-complex especially B6.
8) Telengiectatic vessels may be destroyed by electrolysis.
9) Rhinophyma is treated by plastic surgery.

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Chapter XIV
Allergic skin diseases
A. Urticaria
Definition: acute skin disease characterized by sudden appearance of wheels which last from hours to few
days then fade away.
Sites of election: any area of the skin but more common on covered areas as the trunk, buttocks an chest.
Description:
- The patient first feels an intense irritation followed by the appearance of red blotches which rapidly
develop into raised wheals with red halos, which may be few in number or numerous and closely
grouped together.
- Subjective symptoms are usually marked but depend on the sensitivity of the patient. Itching, burning
or bricking are the main complaint.
- There is slight rise of the temperature.
Age incidence: all ages but more in children.
Types:
1) Allergic type, due to food, drugs … etc.
2) Non-allergic type, due to emotional factors.
Etiology:
1. Food as eggs, cheese, milk, fishes, lobsters, strawberries, bananas, canned food, chocolates, meat,
vegetables … etc.
2. Absorption of some abnormal protein fractions, owing to digestive upset.
3. Drugs as aspirin, salicylates, penicillin, sulphonamides, codeine, morphine … etc.
4. Sera as A.T.S.
5. Inhalants like pollens, dust, perfume, feathers … etc.
6. Intestinal parasites.
7. Septic foci in teeth, tonsils, nasal sinuses and UTI.
8. External irritants as bites or stings of mosquito, bees, lice, flees, bedbugs and scabies giving rise
to papular urticaria.
9. Physical agents as cold, heat, pressure causing physical urticaria.

52
10. Associated with other diseases as malaria and obstructive jaundice, leukemia, purpura and
Hodgkin’s disease.
11. Neurotic or psych-somatic factors.
Treatment:
1) Search for the cause and remove it if possible. This needs exhaustive history with particular stress
on foods, drinks, and drugs. Careful examination of septic foci, GI upset, parasitic infestation and
emotional stress.
2) In acute urticaria due to food as fish, egg … etc. a purgative may help to remove the remains of
toxic material from the intestine.
3) Anti-histamines are very helpful 2nd
and 3rd
generations as telfast and lorastine are give to patients
who need alert during their work as drivers and students. Sedative ones (1st
generation) as cidalin,
benedryl, Phenergan are given to the others.
4) Adrenaline in 1/1000 solution, SC, in doses of 0.2-0.5 ml is helpful in severe cases and in cases
associated with edema of the glottis.
5) Corticosteroids may be given but better be kept for severe cases associated with edema of the
glottis.
6) Calcium gluconate 10% IV may help.
7) Autohemotherapy was used in some chronic Cases.
8) Local treatment: any soothing lotion or powder.
9) Desensitization: in case you can’t avoid the cause.

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B. Eczema
Definition: superficial allergic inflammation of the skin in which the diagnostic lesion consists of minute
vesicles.
Clinical picture:
- Characterized by severe itching and polymorphic eruption in the form of vesicles and papules on an
erythematous and edematous base.
- Oozing and crusting are principal features of some types of eczema.
Etiology:
 Eczema is due to an antigen-antibody reaction where shock tissue is in the epidermis.
 It depends on two factors:
1. A general hypersensitive state (internal factor).
2. An external irritating factor.
 The first factor may be inherited or acquired.
Predisposing factors:
a) Local factors:
1. Dryness of the skin as seen in winter times, in elderly with senile skin or in certain skin
diseases as ichthyosis and xeroderma.
2. Excessive moisture: as in summer where there is excessive sweating leading to friction, heat
and macerations especially in the skin folds.
3. Exposure to irritants and chemicals especially in certain occupations where there is continuous
exposure and increased concentration  occupational dermatitis.
4. Overgreasing and degreasing e.g. frequent washing with bad soap and water, much use of
disinfectants as alcohol.
5. Venous congestion: especially about the lower limbs as in venous stasis and varicosity 
varicose eczema.
b) General factors:
1) Hereditary hypersensitive state which may be familial or acquired,
2) Age: eczema is more frequent in infants and elderly (i.e. the two extremes of age) but it
may affect any age and any sex.
3) Body and nervous debility e.g. worry, fatigue, overwork, insomnia and emotions.
4) Food factor which is most manifest in urticaria but overindulgence in offending foods
may predispose to eczema formation.

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Types of eczema:
1. Atopic dermatitis, which includes:
a) Infantile eczema.
b) Flexural eczema of childhood (Pesnier’s Prurigo).
c) Disseminated nerodermatitis.
2. Contact dermatitis.
3. Discoid eczema.
4. Varicose eczema.
5. Infection eczematoid dermatitis.
Infantile eczema
Age incidence: 2 months – 2 years.
Site of election: starts principally on the cheeks but may later extend over the entire face. In severe cases,
the process extends to the scalp, limbs (particularly flexural surfaces) and the trunk.
Description:
- The usual clinical picture shows erythematous and edematous small papules or papulo-vesicular,
oozing, crusting and scaling lesions.
- Secondary infection is usually marked.
- The condition is usually accompanied by intensive itching. The child who is usually well-nourished is
irritable, rubs his/her face against a pillow, rolls the head from side to side and moves the heals up
and down on the legs.
Etiology: milk, eggs, wheat, wool and silk are the common allergens but the internal heridetary
hypersensitive state plays a great role.
Prognosis: affected children, after repeated remissions and exacerbations, grow out of their eczema
before the end of the second year, and only a minority carries on their eczema which may persists with
less tendency to oozing and crusting but in the form of itchy lichenified plaques affecting mainly the
flexor surfaces of the limbs especially the anti-cubital and popliteal spaces.
The condition may disappear or recur after several years in the adolescents and adult age
(disseminated neurodermatitis) where the lesions are drier and thicker  formation of large lichenified
areas and plaques.
Management of atopic dermatitis:
1) Change of environment: as hospitalization may bring about marked improvement in many cases
even without treatment. This may be due to elimination of the host dust.
2) Avoid exposure to irritants as wool, dust, detergents … etc.
3) Elimination of food allergen in diet, if possible, e.g. cow’s milk, wheat or other cereals, eggs,
citrous fruits, spinach, peas, tomatoes, fish and fish products.

55
4) Local treatment:
a) Crusts should be removed by boric acid lotion or diluted potassium permanganate
solution or warm olive oil.
b) Local application in the form of calamine lotion, liquor aluminum acetate, liniments or
pastes with ichthyol or tar 2-5% are helpful.
c) Local corticosteroids (lotions and creams) are very helpful. In the dry scaly stage,
ointments containing tar together with corticosteroids may be used.
d) Antibiotics may be needed locally if the lesions are infected (neomycin and bacitracin
may be the drugs of choice).
5) Systemic corticosteroids especially in severe and wide spread affections and during
exacerbations are indicated to bring the case under control.
6) Antihistaminics, given orally are of great help. They effectively minimize itching.
7) Barbiturates for sedation are especially indicated in these patients.
8) Systemic antibiotics for secondary infection (penicillin, streptomycin and sulpha preparations
are better avoided).
9) Stop the use of soap and water because they aggravate the condition.
Contact Dermatitis
Definition: an acute allergic inflammation of the skin with edema, vesicles and sometimes bullae which is
associated with itching and burning sensation.
Etiology: it is caused by external application of certain agents to which the skin has acquired sensitivity,
which are called SENSITIZERS. These sanitizers don’t cause visible cutaneous changes on the first
contact but repeated contacts will provoke the formation of the antibody against the sensitizer.
Sites of election: may affect any part of the skin coming in contact but areas of the thin skin as the
eyelids, neck and genitalia are more affected than thick skin as palms and may lead to swelling and
edema.
N.B. drugs which cause local sensitization to the skin may lead to contact dermatitis at the same site if
they are taken systemically due to the fact that antibodies formed become fixed to the skin.
Nature of the sensitizer:
1. Cosmetics as hair dyes, eye-liners, lip-sticks, nail polish, creams, powders … etc.
2. Metals as chromium in cement, leather, watch back, ear rings, rings, bands, suspenders … etc.
3. Plastics as in foot wears, watch straps … etc.
4. Rubber as in shoes, gloves, suspenders … etc.
5. Fabries due to dyes or formaldehyde and other chemicals used in the process of finishing cloth.

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Chapter XV
Scaly Erythematous Dermatitis
A. Psoriasis
Definition: scaly erythematous skin disease characterized by chronicity and persistence affecting 1-2% of
the general population. It represents 2-3% of the skin diseases in the Arabian countries while 8% in
Scandinavian countries.
Age incidence: usually starts at the age of ten years (but may be below) and is more common in children
than adults.
Primary lesion: a dry, scaly, red papule, about the size of pin head or larger.
Diagnosis: on scrapping the lesion, the silvery appearance of the scales becomes more obvious and as
scrapping is continued, a thin membrane is reached (Buckly’s membrane). Further scrapping will lead to
bleeding from certain points (Auspitz’ sign) and this is pathognomonic of psoriasis.
Description: lesions start by palpules which increase in size to form plaques which may be many
centimeters in diameter. The plaque is dry, round and has a well-defined margin. The center of the plaque
may clear and the lesion appears circinate. Adjacent plaques may coalesce and result in polycyclic or
serpiginous outline.
Types:
1) Punctate psoriasis (pin-point size).
2) Guttate psoriasis (rain drop size).
3) Discoid or nummular psoriasis (coin-shaped).
4) Circinate psoriasis.
5) Gyrate or geographical psoriasis.
6) Linear psoriasis (following scratch, injury … etc) “Koebner’s phenomena.
7) Flexural psoriasis.
8) Pustular psoriasis and Zumbuch’s psoriasis.
9) Psoriasis of palms and soles.
10) Psoriasis of the scalp.
11) Psoriasis of the nails.
12) Psoriasis of the mucous membranes (doubtful).
Sites of election: on the pressured points and covered areas.
1. Extensor surfaces of the limbs.
2. The back of the elbow and front of the knees.
3. The scalp.
4. The sacral area.
5. The genitalia.
6. The chest and abdomen.

57
Etiology: still unknown but it is neither infectious nor contagious and it is believed now that it is
multifactorial.
Precipitating factors:
1) Trauma.
2) Streptococcal infection.
3) Psychological upset.
4) Other factors:
a) Light deficiency.
b) Relation to rheumatic diathesis.
c) Autoimmune disease.
d) Endocrine dysfunction.
Treatment: local treatment in most cases but in certain conditions, systemic treatment is a must which
includes the following:
1. Exfoliative dermatitis.
2. Extensive lesions (generalized psoriasis).
3. Acute febrile pustular psoriasis (Zumbuch’s psoriasis).
4. Cases resistant to local treatment.
1) Local treatment:
1. During acute attacks, mild local applications are allowed e.g. 1-2% salicylic acid ointment
OR 2-5% ichthyol ointment.
2. In the flexural psoriasis, 1% hydrocortisone may help.
3. In chronic cases, the following may be applied:
a) Crude coal tar: used as 2-5% ointment or may be applied as it is to the lesion. It is very
effective but is refused by some patients because of its unpleasant odor and color and it may
cause irritation to the skin.
b) Combination of tar and UV irradiation (Goekermann Regimen) is very effective. On the
first evening, all patches of psoriasis are covered with the tar ointment, the next morning, the
skin is irradiated with UV rays or exposed to the sun. This is followed by a warm soap bath,
the skin is dried and the tar ointment is reapplied. This treatment should be continued for 2-3
weeks.
c) Tar may be combined with salicylic acid and ammoniated mercury in an ointment and
applied by night.
d) Chrysarobin 3-10%.
e) Anthralin 0.1-0.5% or even 2% (short contact therapy).
f) Local potent corticosteroids.
g) Local retinoid (vitamin A acid preparation).
h) UV irradiation.
i) Vitamin D3 lotion or ointment.
N.B. X-ray shouldn’t be used in psoriasis.

58
2) Systemic treatment:
- Low fat, low protein diet, vitamins, heavy metals were tried but without benefit.
- Corticosteroids, especially triamcinolone clear the lesions but after stoppage, the lesions
recur with wider spread.
- Aminopterin (folic acid antagonist).
- Isotretinoins (vitamin A acid preparation).
- Antimitotic drugs as cyclosporine, methotrexate … etc.
- Photochemotherapy (PUVA) in which a photosensitizer drug as psoralen is given orally
and after 2 hours the patient is exposed to the sunlight or UV light.
3) Psychotherapy.
Prognosis:
Psoriasis tends to persist for many years and may be for life-time. It may show spontaneous
exacerbations and remissions which may vary from months up to years. Exacerbations usually occur
during winter and remissions during summer.
B. Pityriasis Rosea
Definition: a mild inflammatory disease characterized by macules and maculo-papular lesions which are
slightly scaly and formed mostly on the trunk.
Age incidence: appears at any age but is commoner in young adults.
Etiology: unknown but may be one of the following:
a. Virus.
b. Spirochetal infection.
c. A special mild exanthema.
Symptoms:
Usually there are no symptoms but sometimes headache and malaise and occasionally some itching.
The onset is sudden with the appearance of a solitary macular lesion, known as “Medallion” or “Herald
patch” which persists on the trunk for one or two weeks before the other lesions appear.
When other lesions appear which are oval in shape, their long axis run along the lines of cleavage of
the skin, their edges are quit well-defined and the surface is always scaly.
In older lesions, the scales are marked on the edge forming a delicate collarette.

59
Varieties:
1- The usual type: in which the lesions appear mainly on the trunk and upper parts of the
extremities.
2- The abortive type: in which the Herald patch is not followed by the generalized eruption.
3- The inverted type: where the lesions appear on the extremities, mainly on the forearm and legs.
The arms and thighs are also affected but to a lesser degree. The trunk remains free.
Coarse: it is a self-limiting disease with duration usually of 4-6 weeks, rarely up to 12 weeks.
Diagnosis: by the character and distribution of the lesion.
Prognosis: excellent.
Treatment:
1) There is spontaneous cure within 4-6 weeks in the untreated cases.
2) Soothing powders and creams may be enough in mild cases.
3) The excess use of soap should be avoided to diminish the irritation and itching.
4) Antihistaminic drugs may be necessary in the moderate cases.
5) Rarely, a short course of oral &/or local corticosteroids may be indicated in severe eczematized
cases.
6) Exposure to UV light rays is believed by some to shorten the duration of the disease.
C. Lupus Erythematosus
I. Discoid Lupus Erythematosus:
Synonym: chronic localized lupus erythematosus.
Definition: a chronic inflammatory scaly and scarring disease that affects the face and follows a
prolonged course.
Age incidence: commonest between 20-40 years of age.
Sex incidence: females are more than males 2:1
Sites of election; sun exposed areas are most affected.
Clinical picture:
1- Persistant localized erythema.
2- Adherent scales related to dilated follicles.
3- Follicular plugging leading to Stippling appearance.
4- Redness and telangiectasia of the border.
5- Atrophy and scarring of the center.
The lesions are symptomless but the main complaint is disfiguring.
Course: it is usually very chronic and ends by scarring and deformity, 6% of cases may pass to SLE.

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II. Systemic Lupus Erythematosus
Definition: a progressive and fulminating disease of great medical importance. It is a collagen disease
that involves the entire vascular tree with manifestations in every organ of the body including the skin.
The cutaneous signs are present only in 50% of cases.
Laboratory findings:
1) Blood: leukopenia, thrombocytopenia, anemia and high ESR.
2) Urinary findings: albuminuria, hematuria and casts.
3) Positive LE phenomenon in the peripheral blood and LE cells in the bone marrow.
Etiology is still unknown but the followings are suggested:
1. Hypersensitivity to infection.
2. Allergy to drugs as sulpha, penicillin … etc.
3. Photosensitivity.
4. Virus.
5. Autoimmune disease.
Treatment:
a) DLE (Discoid lupus erythematosus):
1- Protection from sunlight by the use of sunscreen.
2- Eradication of the septic foci.
3- Oral anti-malarials.
4- Local Intralesional (IL) injections of corticosteroids.
5- Freezing by CO2 snow or NO2.
b) SLE (Systemic lupus erythematosus):
1) Systemic steroid therapy is the backbone of treatment.
2) Oral anti-malarials may be used.

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D. Lichen Planus
Synonyms: Lichen Ruber Planus.
Definition: an inflammatory disease of the skin and mucous membranes of unknown origin.
Etiology: unknown but the following may be accused:
a) Emotional stress.
b) Familial tendency.
c) Drug eruption.
d) Virus mycoplasma.
Primary lesion:
- Small, flat, polygonal, glistening violaceous papules with a network of striae on the surface,
known as Wickham’s striae which leave deep pigmentations after disappearance.
- Mucous membrane lesions are seen on the inner sites of the cheeks as whitish patches or network
which may ulcerate and malignant changes may occur.
Associations: Bullous Lichen Planus and internal tumors.
Sites of election: flexor aspects of the limbs, volar aspects of the wrists and medial sides of the thighs,
flexor surfaces of the forearms, lumbar area, vulva and anus.
Clinical picture:
- Pruritus is an outstanding symptom.
- Koebner’s phenomenon is present.
Treatment is symptomatic
1. Corticosteroids, corticotropins, tranquilizers and antihistamines.
2. Local corticosteroids with or without tar.
3. Intralesional injections of corticosteroids.

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E. Pityriasis Rubra Pilaris (P.R.P)
Definition: chronic skin disease characterized by small follicular papules and disseminated yellowish
pink scaly patches.
Etiology: unknown, but may be:
a) Familial.
b) Vitamin deficiency disorder, especially vitamin A.
Age incidence: childhood and adults (51-55 years).
Sex incidence: both sexes but more in males than females.
Clinical picture:
1. Scaliness of the scalp.
2. Hyperkeratosis of the palms and soles.
3. Follicular hyperkeratosis of proximal phalanges.
4. Psorisiform patches.
5. Small islands of normal skin.
Treatment is symptomatic
1) Topical olive oil and bland emollient.
2) Starch bathing.
3) Methotrexate.
4) Vitamin A in high doses.
5) Penicillin V.
6) Corticosteroids and ACTH.
Prognosis:
- Unpredictable.
- Childhood is better than adulthood P.R.P.
- Remissions are common.

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Chapter XVI
Vesiculo-Bullous Skin Diseases
Pemphigus
Definition: a chronic skin disorder characterized by recurrent bullae of the skin and the mucous
membranes.
Types:
1) Pemphigus vulgaris with its variant pemphigus vegetans.
2) Pemphigus foliaceous and its variant pemphigus erythematosus.
Etiology: still unknown but may be due to:
1. Salt retention.
2. Autoimmune mechanism.
3. Inhibition or activation of certain enzymes.
4. Virus.
Clinical picture:
- Insidious onset.
- The bullae are at first tense, round and contain clear serum which soon becomes purulent as the
bullae become flaccid.
- The skin around the bullae is normal.
- The bullae soon rupture and leave raw areas on the skin or mouth which are extremely tender as
crusts form.
- The size of bullae varies, they may be as big as the palm.
- Any site may be involved, the oral lesions are often the first signs of the disease.
- The patient’s general condition deteriorates rapidly in accordance with the severity of the skin
lesions.
- Nikolsky’s sign is present. This means when firm pressure with the finger is exerted on normal
skin the epidermis glides over the dermis owing to generally poor attachment of the Brickle cells
(Acantholysis).
- Eosinophilia and leukocytosis sometimes occur. The lesions occur in waves and sometimes quite
long periods of remission occur.
- Tzanck test is positive, in which scrappings from the bottom of the bullae show acantholysis of
the cells.

64
Treatment:
1) Steroid treatment can save the life of these patients although death can occur in spite of this
treatment. Huge doses may have to be given at first to improve the clinical condition, namely up to
200 mg prednisolone daily. Then the dose is decreased in a logarithmic manner and the patient is kept
on a maintenance dose 5-10 mg daily. Anytime there is recurrence this dose or any dose the patient on,
is doubled or even tripled till the condition improves.
2) ACTH should also be considered.
3) Anti-mitotic drugs can also be given especially to those who can’t tolerate high doses of
corticosteroids e.g. cyclophosphamide and cyclosporine. They enable us to reduce the dose of
corticosteroids and its complications.
4) To avoid complications of corticosteroids also, anatcids, aabolics, calcium, high protein diet and
vitamins may be given.
5) Antibiotics may be given to avoid secondary infections.
6) The patient must be kept in bed or isolated at hospital.
7) Locally mouth care with local antifungal treatment, local antibiotics or local anesthetics may be
used to clear secondary infection and to enable the patient to eat.
8) Locally the eroded areas of the skin may be treated with potassium permanganate or eusil
dressing. In difficult and generalized lesions potassium permanganate baths are very helpful to get rid
of the bad odor of the lesions and to clear the secondary infection.
Prognosis:
- Depends greatly on the response to steroid treatment.
- It is neither infectious nor contagious.
- It affects both sexes, M:F is 3:1.
Differential diagnosis:
Other vesiculo-bullous skin diseases, mainly pemphigoid in which the bullae are subepidermal while
in pemphigus they are intraepidermal.
Acantholysis is evident in pemphigus but absent in pemphigoid.

65
Chapter XVII
Hair Disorders
A. Hypertrichosis
Excessive growth of hair which may be:
a) Congenital e.g. hairy navus.
b) Endocrinal due to pituitary, adrenal, ovarian and thyroid dysfunction.
c) Iatrogenic due to Dilantin, ACTH, corticosteroids and hexachlorobenzene, testosterone,
monoxidil … etc.
d) Idiopathic: racial, genetic or familial … etc.
Treatment: look for the cause and treat if possible e.g. corticosteroids in cases of adrenal involvement
which will suppress adrenal secretion of androgens or use anti-androgen (17-α-methyl-B-nortestosterone).
1. Shaving: not favored by many ladies as there is rapid regrowth of hair but it doesn’t increase the
coarseness or amount of hair as it is believed by some.
2. Epilating waxes and poultices: are preferred by many ladies as regrowth of hair takes
considerable time. It also doesn’t coarsen subsequent growth.
3. Depilatories containing barium sulphide which may be irritant and corrodes only the projecting
hair shaft but has o destructive effect on the intrafollicular growing portion.
4. Bleaching with hydrogen peroxideor equal parts of it and water of ammonia makes dark hair less
noticeable and corrodes the finger hair.
5. Electrolysis: high frequency or galvanic current is a safe method but has 20-35% recurrence when
performed by experts. Scarring and infections are the only dangers.
6. X-ray: causes permanent epilation but has the danger of radiodermatitis, skin keratosis and
cancer.
7. LASER: is the most recent and was thought to cause permanent epilation but proved to have
recurrences after few years.

66
B. Alopecia (Hair Falling)
Definition: partial or total loss of scalp or body hair which may be congenital or acquired.
1) Congenital alopecia is more rare and may be due to:
a) Congenital ectodermal defect.
b) Congenital cicatrisation defect.
2) Acquired alopecia which may be cicatricial or non-cicatricial
a) Cicatricial due to:
- Favus.
- Lupus erythematosus.
- Burns.
b) Non-cicatricial: which may be:
- Diffuse, may be:
1. Senile (most common).
2. Post-febrile or secondary to severe illness as diabetes mellitus, anemia,
toxemia … etc.
3. Syphilitic.
4. Traumatic.
5. Seborrhoeic.
6. Alopecia totalis.
7. Alopecia universalis.
8. Iatrogenic e.g. anti-mitotic drugs and isotretinoins.
9. Physiological e.g. during pregnancy and lactation.
- Focal, may be:
1) Alopecia areata.
2) Syphilitic (moth-eaten).
3) Fungal (black-dot).
Alopecia Areata
Definition: sudden complete loss of hair in circumscribed areas of the scalp, it may involve the beard area
or the eyebrows or lashes.
Clinical picture:
The condition isn’t preceded by any symptoms. The patch may be rounded or oval, small or large,
usually single but may be multiple.
The periphery which expands may show some characteristic hair (exclamation mark hair).
The vertex and the occipital region are the common sites but other areas of the scalp and body may be
affected. The skin is normal.

67
In case of alopecia universalis, hair loss occurs all over the body surface BUT in alopecia totalis, the
whole scalp hair, beard area, eyebrows and eyelashes only fall.
After a viable period (few weeks to few months) the hair regrows, which are at first downy and light
in color then become normal. At the same time, new patches of alopecia may develop.
Age and sex incidence:
- It is common between 10-35 years of age but may occur at any age.
- It is more common in males but females are affected.
Etiology: the cause is unknown but there may be responsible factors:
1. Septic foci: hair regrows after eradication of such foci.
2. Reflexes: eye-strain or mal-erupting teeth.
3. Psychosomatic disorders: following sudden shocking news, nervous strain or states of stress
during wars or students’ examinations.
4. Endocrinal dysfunction and trophoneurosis.
Prognosis is good and hair regrowth may occur after 2-3 months, sometimes 6-9 months, rarely after
several years.
Treatment:
1) Careful examination of teeth, eyes, ears and eradication of septic foci.
2) Reassurance is very important.
3) Psychotherapeutic measures are sometimes beneficial.
4) Thyroid extracts are given in some cases.
5) Prolonged courses of corticosteroids are ACTH are helpful in some cases of alopecia totalis or
universalis but recurrences are common after stoppage of treatment.
6) Local treatment:
a) Application of local irritants.
b) UV irradiation twice weekly in doses leading to slight erythema.
c) Intradermal injection of triamcinolone diluted in distilled water 1:4.

68
Chapter XVIII
Disorders of Pigmentation
Normal pigmentation of skin is influenced by the amount of melanin, the degree of vascularity, the
presence of carotene and the thickness of the horny and fatty layers of the skin.
A. Hyperpigmentation
1. Congenital e.g. pigmented naevi.
2. Neoplastic e.g. melanoma.
3. Physical agents e.g. sunburn, pressure, friction, heat … etc.
4. Dermatoses with hyperpigmentation e.g. L.P., D.H., X.P. … etc.
5. Metabolic disorders e.g. Gaucher’s disease, Neimann-Pick disease, alkaptonuria … etc.
6. Iatrogenic e.g. ateprine, arsenic, gold, silver, bismuth … etc.
7. Industrial, in coal miners, anthracite worker and pitch workers.
8. Hormonal: increased MSH of pituitary during pregnancy and menopause.
9. Systemic diseases e.g. syphilis, malaria, pellagra, diabetes, Addison’s disease.
Melisma
Synonyms: cloasma, mask of pregnancy.
Sites of election: malar prominenceis and forehead, the upper lip, nipples, and about the external
genitalia.
Incidence:
- During pregnancy and at menopause.
- In case of ovarian disorders.
- With contraceptive pills.
Clinical picture: starts form 1-20 months after beginning the contraceptive therapy.
Treatment:
1) Bleaching creams containing hydroquinone 2-4%.
2) Sunscreens, opaque base are also used.
3) Mild peeling by 95% phenol and neutralization by isopropyl alcohol.
Prognosis:
 Melisma of pregnancy usually clears in few months after delivery.
 Cessation of the contraceptive pills rarely clears the hyperpigmentation.

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B. Hypopigmentation
1. Congenital e.g. nevus, albinism.
2. Occupational:
- Rubber industry, wearing gloves containing antioxidants or monobenzyl ether of
hydroquinone.
- Women dressing shields, rubber garters.
- From condoms.
3. Post-inflammatory e.g. P.R., Ps., H.Z, secondary syphilis.
4. Post-burns and scarring.
5. Idiopathic e.g. vitiligo.
Vitiligo
Synonym: leucoderma.
Definition: a condition in which a pigment disappears from the skin in patches so that they become milky
white in color.
Etiology: unknown but the following may be accused:
1) Structural changes.
2) Neurogenic factors.
3) Autoimmune mechanism.
- There is sometimes a familial history and dark people are commonly affected.
Age and sex incidence: both sexes and any age.
Associations:
1. Hyperthyroidism.
2. Diabetes mellitus.
3. Pernicious anemia.
Clinical features:
- The onset is sudden.
- The patches assume various sizes and shapes and are most common on the face, neck, hands,
wrists, abdomen and thighs.
- The hair also becomes white.
- All these patches are sensitive to sunlight.
Course: the condition may remain static for months or years and only occasionally clears spontaneously.

Dermatology, Lecture Notes on some Common & Serious Skin & Venereal Diseases.pdf

Dermatology, Lecture Notes on some Common & Serious Skin & Venereal Diseases.pdf

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