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Table of contents :
Skin Infections
Bacterial infections
Viral infection
Fungal infections
Parasitic infections
Scaly Erythematous Eruptions
Pityriasis Rosea
Lichen Planus
Lupus Erythematosus
Allergic Dermatoses
Drugs Eruption
Erythema Multiforme
Disorders Of Melanocytes: Vitiligo
Disorders Of Sebaceous Glands : Acne
Disorders Of Hair Follicles: Alopecia
Cutaneous Manifestation Of Internal Disorders
Tables, Rapid Revision, MCQs

Citation preview

DERMATOLOGY made EASY Supported by ■ Video 1^ e s s on s in CD m


Mahmoud Sewilam Kasr Al-Ainy School of Medicine Cairo University

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

Dermatology Made Easy Supported By NEW UPDATED Video Lessons On CD


Mahmoud Sewilam

Kasr Al-Ainy School of Medicine

Cairo University

Fourth Edition

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬





InfectionsH^H^^^I Bacterial infections


Viral infection


Fungal infections


Parasitic infections




Scaly Erythematous Eruptions^^^^l Psoriasis


Pityriasis Rosea


Lichen Planus

Lupus Erythematosus


Allergic Dermatoses^^^^^^^H Eczema




Drugs Eruption Erythema Multiforme



Disorders Of Melanocytes:


Vitiligo Disorders Of Sebaceous


Glands: Acne

Disorders Of Hair Follicles:


Alopecia Cutaneous Manifestation Of


Internal Disorders

Tables, Rapid Revision, MCQs

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

Introduction To Dermatology The Skin :

The skin is the LARGEST organ of the body ,


Epldtnnli It weighs 1/7 of body with surface are of 1.75 Cutaneous findings can be clue to internal diseases e.g. 0«fmn psoriasis may be associated with arthritis Management of the skin : — HypoPermli Complaint. History skin and non skin related. Examine skin, hair, nails, and mucous membranes, mainly the oral mucosa in good light.


Investigations e.g. Biopsy and fungal scraping.

1. 2.

5. Treatment.

Function of the skin :

1. 2.

Vitamin D formation from precursor under the effect of sunlight Sensory function, temperature , pain , pressure ,touch .

3. Sweat excretion 4. 5.

Immunological function via Langerhans cells

Temperature control through vasodilatation , vasoconstriction and vaporisation of sweat from the skin surface.



Protection against physical injury ,thermal injury , invading micro-organisms and UVR


Prevention of water & electrolyte loss Skin is composed of 3 main layers :

Epidermis, dermis, hypodermis

spWermia dermis eccrine

gland axternal root sheath



arrector pill muscle sebaceous gland Internal root shealb

I cuticle hair 1 cortex I medulla

Skin appendages : matrix


Nails ; contain keratin


Hair follicles: contain keratin


Sebaceous glands: discharge their sebum content into hair follicles.

blood vessel

conneciive tissue papilla

Together with hair , they form the pilosebaceous units

Sweat glands : open on the surface of the epidermis through sweat ducts : Eccrine sweat glands all over the body surface

Apocrine sweat glands at body flexures only

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 1

Structure Of Skin

❖ Skin is composed of 3 main layers : equame about to



v^^,,^ake off surface



keratlnlzed squsmes


granule cell

layer prickle cell

layers basal

cell layer divtdiiiQ cell

Merkel/ cell

A. Epidermis




B. Dermis

It is the most outer layer of

It is present below the

the skin.

basement membrane

C. Hypodermis (subcutaneous fat) It is the lowest layer of the skin.

It rests on the basement membrane It is formed of cells :

Kerationcytes(KCs): For formation of keratin ,the

covering protein layer of the skin.

It is composed of: • Collagen, elastic

It is composed of:

fibers and matrix of

glycosaminoglycans ^ It contains:

KCs are arranged as ;

Kerationous(horny) cell

layer; upper most component ; composed of dead cell(with no nuclei




Granular cell layer; cells contain keratohyaline granules. Squamous(prickle) cell layer above the basal cell layer. Basal cell layer; lower most layer ,for formation of KCs. Melanocytes : for formation of melanin , skin color contributor.

Lobules of Fat cells ,

separated by Fibrous septa composed of collagen and large blood vessels Blood vessels ;

arterioles , capillaries and venules Nerve fibers


Langerhans cells(LCs): for immune function of the skin

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

Cutaneous Signs I.

Primary Lesions:

• These are the initial lesions of skin diseases(first to appear)

Papule :a circumscribed solid elevation of skin less than 0.5 cm in diameter e.g. Psoriasis and lichen planus. Nodule: a circumscribed solid elevation of skin more than

0.5 cm in diameter . It is Deep lesion that represents a Dermal or subcutaneous pathology E.g. Lepromatous leprosy

2. Plaque: an area of change of texture or consistency of the skin. It may be elevated or depressed under the surface of the skin. An elevated lesion may originated de novo or as a

result of confluence of multiple papules. It occupies a large surface area in comparison with its height in contrast to the



Vesicle :an elevation of skin containing fluid less than 0.5 cm in diameter

Bulla: an elevation of the skin containing fluid more than 0.5 cm in diameter .

A cyst differs from vesicle or bulla by having a wall. 4. Macule: a circumscribed area of skin discoloration less

than 1 cm in diameter . It could be hypopigmented , hyperpigmented or erythematous , e.g. brown macule in pityriasis versicolor & white macule in vitiligo. • Patch : A macule more than 1 cm in diameter.

5. Comedo :the primary lesion of acne. There are two types ; • Closed comedo or White head which is vellowish papule.

• Open comedo or hlack head which is a flat or slightly

elevated papule with dilated central opening filled with blackened keratin. Closed

6. Wheal: the primary lesion of urticaria. • Evanescent(transient) Edematous Elevations of the skin of variable sized.

• Itching is usually present 7. Burrow:the primary lesion of scabies. • A linear elevation of epidermis tunneled by female sarcoptes scabiei mite.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬


Secondary Lesions

These occur as a result of modification of primary lesions 1. Pustule : a small elevation of skin

containing purulent material . It may originate as a pustule or may develop from a papule or vesicle(Iry or 2ry)

Scale:Dry or greasy laminated masses of keratin.

3. Crust: dried materiai on the skin as

serum , pus ,or blood.

Excoriation & abrasions : superficial discontinuation of the skin; only Epidermal

Excoriations are caused by scratching with fingernails Abrasions are due to mechanical trauma or constant friction.

5. Erosion : a partial or total loss of the Epidermis ,not reaching not involving the dermis so heal without scar.

Ulcer: a rounded or irregularly shaped excavations that result from total loss

of the epidermis plus some portion of the dermis.

7. Fissure (crack): a linear cleft through the epidermis extending into the dermis.

8. Furrow : A deroofed burrow caused

by scratching of a burrow

❖ SKIN INFECTIONS: 1. Bacterial Infections

2. Viral Infections

3. Fungal Infections 4. Parasitic Infections

5. Leprosy

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ beard area

Upper part of

Primary predisposed to by poor hygiene and moisture Secondary due to insect bites,scabies or pediculosis capitis infestation IQ


3. Circinate impetigo It occurs as an extension of ordinary impetigo or secondary to rupture of bullous impetigo 4. Ulcerative impetigo( ):it occurs on legs lesion have thick crusts and heal with scar.

newborn infants.

2. Bullous Impetigo: • It is caused by Staphylococci. Primary lesion is a bulla. It characteristically occurs in newborn infants, though it may occur in any age. It accompanied by constitutional symptoms and might be fatal in

symptoms and it resolves within a few days.


drainage Systemic

Incision and

TTT: by

intertriginous areas

beard area

It occurs on the back

, neck,

Follicular pustules and papules in the

Follicular red papules



Treatment of predisposing factors Topical antiseptics as Povidone iodine or Potassium Permanganate 1/ 8000- 1/10,000 Topical antibiotics as fusidic acid ,gentamycin or bacitracin Systemic antibiotic given if infection generalized , associated with fever or lymphadenopathy and in cases of bullous impetigo or ecthyma .

Treatment of ALL :

Complications of Impetigo Contagiosum:: Spread of infection to other sites & children. Post streptococcal glomerulonephritis in 2-5 % of cases affected by nephrotogenic strains

the disease begins with 2 mm ^pustules erythematous macules which shortlj develop in vesicles. These rupmre with seropurulent discharge which dries to form loosely stratified Golden yellow Crusts . It occurs on scalp as a complication of pediculosis capitis. ,face , hands , genitalia. There are NO constitutional


Obesity and diabetes

Moisture, poor hygiene and shaving

poor hygiene



Moisture and






follicle with central


Multiple deep boils that open on the surface by multiple

Deep infection in Lower part of hair

= Boil




Staphylocoeeus Staphylocoeeus aureus

Infection could be:

hair follicle

Folliculitis of the


Infection in

Cocci-type bacteria ; Streptococci and staphylococci

Superficial infection of the Skin

Types I 1. Ordinary impetigo :



I- BACTERIAL INFECTIONS: A)Impetigo Contagiosum B)Folliculitis C)Sycosis barbea = impetigo of


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ J

episodes • Systemic antibiotics as penicillin or

with fine Scales in intertriginous areas; axillae, groins, submammary areas. • Wood's light shows coral red fluorescence due to porphyrin.

1- Topical therapy


or tetracycline

2- Systemic therapy : as erythromycin

Antifungals as azole deratives (although it's a diphtheroid bacteria)

Antibiotics as Fusidic acid

o Lymphedema occurs from recurrent

• Dry Scaly reddish brown


Staphylococcus aureus & Streptococcus pyogenes

lower dermis & SC tissue

Suppurative inflammation of





Erythromycin is given for several

Benzathine - Penicillin or

organism is streptococcus. - Dicloxacillin, Rifampicin,

- Aggressive Antibiotic Therapy

Swollen, Tender ,Erythematous , Constitutional symptoms include malaise and fever, chills. Sharp border. o Ill-defined border. Extensive cases blisters may be

• For resistant cases ,confirm that

o o o o




DM., Obesity, Debilitating Diseases


Beta - hemolytic streptococci.



Corynebacterium minutissimum

Suppurative inflammation of UPPER

Superficial infection of intertriginous






1. 2. 3. 4.

Herpes Simplex(HS)caused by herpes simplex virus(HSV). Herpes Zoster(HZ)caused by varicella zoster virus(VZV ). Warts(Verrucae)caused by human papilloma virus(HPV ), Molluscum contagiosum caused by Pox virus. B)Herpes Zoster(HZ)

A)Herpes Simplex(HS) C

It is the most common viral infection.

It caused by varicella zoster virus(


It is caused by herpes simplex virus(HSV) DNA virus of two types ;




HSV type I which leads to herpes labialis


and other non - genital infections and, HSV type H which leads to herpes progenitalis. ^X MOT:


Skin to skin Skin to mucous membrane contact IP

7-10 days > CHICKEN POX(Varicella)

2-5 days




t o

It occurs in patient who is infected for the


first time 0



e n e



It causes primary herpetic gingivostomatitis Infection is usually subclinical and passes unnoticed in about 90


% of cases o


It is characterized by small superficial vesicles on the oropharynx that rupture

quickly leaving painful denuded areas . These are accompanied by fever, swollen gums ,lymphadenopathy , sore throat,

It occurs in patient who is exposed to the virus for the first time.

malaise ,loss of appetite

It is a relatively mild childhood disease with generalized but selflimiting vesicular eruption that

Lesion heal within 2 weeks. Recurrent attacks


Following resolution of primary infection, virus is not eliminated from the body. HSV has a special predilection for neural tissue. It migrates to dorsal root ganglia and

leads to the formation of brownish crust.

❖ A.

Lesions heal within 10 days. After the attack , virus resides in

posterior root ganglia.

remains dormant. o

If reactivated , viral particles migrate along peripheral nerves to the skin and mucous membranes causing recurrent HS at or near the primary site.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

PDF for reactivation

PDF for reactivation :

Fatigue ,Fever , Trauma, UVR ,stress ,


Fever ,Trauma

Menstruation, GIT disturbances


Decreased resistance ,Drugs(

Altered immune status

corticosteroids and

or immunosuppressives

immunosuppressive agents), Diseases of the spine(TB and metastatic deposits)and malignant Diseases(lymphoma and Hodgkin's disease)


Sites of Recurrent attacks

Reactivation of infection

Lips(Herpes Labialis): usually bilateral (may be unilateral) grouped vesicles on erythematous base on the lips usually preceded or associated with burning or tingling sensation. Within a few days, vesicles dry up forming o


Herpes Zoster

crusts and fall off. o

Lesions heal without a scar

Face :(herpes facialis): around | w (/J other orifices as eyes, nose, cheeks& ears o Onset is accompanied or preceded Special variants of HSV type I one week before by pain, o Ocular mucosa :It needs o Strictly Unilateral(not crossing prompt ophthalmologic midline, linear, along a dermatome consultation —> comeal opacity. )groups of vesicles on o Finger or hand (herpetic whitlow): erythematous and edematous base , along the distribution of one or o

more sensory nerves ,local LNs

may be enlarged o Vesicles usually dry up without

It occurs on the finger as a result of direct inoculation of HSV into abraded skin, it is

very painful with vesicles, edema and redness > HSV TYPE 11

(Herpes Progenitalis) Primary infection :

o It is transmitted by sexual contact o It involves genitalia of both males and females,



o Recovery occurs after 2-4 weeks, o It may leave scars. Special variants A. Abortive type of HZ presents with only pain and some redness without vesicular eruption. B. Bloody: Hemorrhagic in which

o It is characterized by painful grouped vesicles contain blood. superficial vesicles on an erythematous base C. Gangrenous or Generalized in followed by erosion or genital ulceration immunocompromized patients. o Herpes progenitails in a pregnant woman at o Disease is not recurrent; one the time of delivery is a strong indication attack gives Permanent solid for Caesarian section as neonatal infection immunity is serious Recurrent attacks

o Less severe than the primary infection.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬






P 1 i c



ti 0

Secondary infection Eye complications e.g. keratitis and comeal ulcers Erythema mnltiforme due to recurrent HSV type I

CNS complications e.g. encephalitis and meningitis; rare but serious, occur especially in infants and children

n s

5. Cancer cervix due

to recurrent cervical HSV type II


Secondary infection Eye complications; HZ ophthalmicus


CNS complications;


post-herpetic neuralgia where pain persists for several months after healing of lesions. It occurs in 10-20% of the patients , especially in elderly patients or due to delay in starting antiviral therapy Cicatriciai



1. Clinical picture

NB :


2. Tznak smear using

*t* HZ may be a manifestation of


g n

Giemsa stain 3. Viral culture

internal malignancy if: o Very old Age


4. Serological tests; HSV antibody titers against Type I and II

o Gangrenous type


5. PCR

o Recurrent


A. Avoid precipitating factors if possible to



prevent recurrence

B. Avoid direct sexual contact during the attack in genital herpes C. TOPICAL THERAPY :

I. Drying antiseptic lotions: They are given in early vesicular stage. o

o Bilateral affection

a) TOPICAL THERAPY : in vesicular stage : 1) Drying antiseptic lotions:

2) Antivirals: acyclovir cream in very early stage 5 times daily may minimize the duration of the attack

b) SYSTEMIC THERAPY : 1) Antivirals : o Potassium Permanganate 1/8000 - 1/10,000 . 2. Antiviral: o Acyclovir, SOOmg tablets 5 times Effective when given early in the course of o daily(every 4 hours)for 7 days the diseases (better in prodromal stage). Valacyclovir , 1000 mg 3 times o ( o Acyclovir cream applied 5 times daily daily for 7 days every 4 hours)for 5 days. o Famcyclovir , 500 mg 3 times daily o It reduces period of the attack and duration for 7 days of viral shedding. 3. Idoxuridine(IDU) given for Eye lesions 2) Analgesics ,Carbamazepine And D. SYSTEMIC THERAPY: antivirals Gabapentin For Pain o




10 % Aluminum Acetate.

It should be given early, within 48-72 hours from the appearance of the eruption. Acyclovir, 200 mg 5 times daily(every 4 hours)for 5 days is administrated in : Severe episodes or for

immunocompromized patients.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

The Most Important Points In Herpes Simplex And Herpes Zoster Herpes simplex Cause

o HSV-I^ orofacial

Herpes zoster o Varicella - zoster virus

o HSV- II —^ genital herpes Recurrence

o + ve

Primary lesion

o Bilateral grouped vesicles on erythematous base

o -ve ,one attack gives solid immunity o Unilateral grouped vesicles on erythematous


o Periorificial

o Along distribution of





Unilateral or bilateral

o 2-5 days with tingling, burning or itching which precede or accompany eruption


o Strictly unilateral(not crossing midline, linear, along a dermatome) o 7-10 days; pain precedes or accompanies the eruption & severity

increases with age or delay treatment Lymphadenopathy



o Secondary infection o Eye complications E.g. Keratitis and comeal ulcers o Erythema multiforme o CNS complications e.g. Encephalitis and meningitis o


-ve or -i-ve



o Secondary infection o Eye complications; HZ ophthalmicus o CNS complicatios; Post-herpetic neuralgia o Cicatricial alopecia

Cancer cervix

1. Topical therapv:

1. Topical therapv :

o Drying antiseptic lotions; o Acyclovir cream o IDU for eye lesions

o Drying antiseptic lotions; o Acyclovir cream 2. Systemic therapv

2. Systemic therapy


o Antivirals : Acyclovir, 200 mg 5 times daily(every 4 hours)for 5 days

1- Acyclovir, 800mg tablets 5 times daily(every 4 hours )for 7 days 2- Valacyclovir, 1000 mg 3 times daily for 7 days 3- Famcyclovir ,500 mg 3 times daily for 7 days B.Analgesics, Carbamazepine And Gabapentin For Pain


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ filiformis): Long thin Pedunculated skin growths

6. Digitiform warts(verruca digitata): Papillomatous , thin projections with finger like processes having a common stem

Phenomenon (isomorphic response)

verrucous papules.

5. Filiform warts(verruca

Occur more in children & shows Koehner's

Asymptomatic skin colored &

2. Common warts(verruca 3. Plane warts(verruca plana): vulgaris): Asymptomatic skin colored flat-topped papules.


■ Spontaneous involution may occur within 2 years ■ Treatment of a few warts may induce regression of other warts

o Course of infection :

o Complications of HPV infection : oncogenicity; may predispose to cervical dysplasia or cancer cervix


4. Planter warts (verruca plantaris): Involves sole of foot, tender, thick & growing

1. Genital warts(Condyloma acuminata): Involves skin of genitals in both sexs. In mucous membranes ,they are; soft pinkish, moist foul smelling outgrowth that bleed easily with a cauliflower appearance ,



o These are eommon , infectious , benign , epithelial growth caused by human papilloma virus(HPV) 0 They involve both skin and mucous membrane, Mode of infection : Direct or indirect contact o IP: 1- 6 Months ,Types of warts :

C)Warts = Verrucae


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 4. Laser treatment by Pulsed dye laser or Co2 laser 5. Podophyllin resin 25 % in alcohol, liquid paraffin or tincture benzoin co for treating venereal warts. It is painted twice weekly and should be washed after 6-8 hours. It is contraindicated in pregnant females and in large bleeding

4. Laser treatment.

1. Electrocautery 2. Chemical cautery with phenol after removal with curette. 3. Cryotherapy






IP: 2-6 Weeks

Mode ofinfection : Direct or indirect contact

It is caused by pox virus

Shiny, pearly white Smooth Surface dome shaped ^^^h Central umhilication. Squeezing the lesion —> White Cheesy material can be expressed from the central punctum. It involves non-genital or genital skin; the later is considered a sexually transmitted diseases(STDs)



D)Molluscum Contagiosum

2. Chemical Cautery; cell destruction by caustics such as carbolic acid (phenol), glacial acetic acid, trichloroacetic acid 40 %,salicyclic acid 40 % or lactic acid 40% warts. 3. Cryotherapy; cell destruction by freezing • Recently, imiquimod cream may be used in the treatment of effect of liquid nitrogen venereal warts by stimulating local interferon production 6. Resistant Planter warts treated by Radiotherapy.

effect under anesthesia

1. ElectroCautery; cell destruction by heat


placebo application.

warts after

disappearance of




♦♦♦ Fungus is a kind of plant defective in ehlorophyll.

❖ Fungal skin diseases are either superficial affecting skin only or deep affecting internal organs

Superficial fungal infections : These are among the most common dermatologic disorders :

|l) Dermatophytes = ring worm = tinea^^l111) Yeasts o Microspora ,trichophtya , epidermophyta o Involve skin and skin appendages(hair and nails)

o Malassezia furfur , Candida species

o Mode of infection : direct contact or

indirect contact from barbershops or patient's fomites

Dermatopliytes := ring worm = tinea

Tinea capitis = Ringworm of scalp

Tinea Circinata

Tinea Cruris =

(Tinea corporis)=

Ringworm Of Groin

Ringworm of hairless skin

f i;' mJN A' ( Tinea Axillaris

iJ Tinea Barbae =

Tinea Pedis =

Ringworm Of Beard

Athlete's Foot





Tinea Mannum


Tinea Unguium = Onychomycosis


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

1- Tinea capitis:= ringworm of scalp ,types ; Black- dot



"V ' "






Children only


Children and

Children and



Single or multiple

Hairs break off at the surface of

Boggy swelling

Scales / loose hairs


to hair follicles

Yellow cupbald patches on studded with shaped sulfur the Scalp, with fine the skin giving follicular pustules crust(scutula) grayish white picti licture of HfflS ,pus is localized of mousy odor that break off

that form around loose hairs and lead to diffuse

Stumps about 3 mm long that can be easily pulled out Alopecia areata




Children only

SL Clinical


loss hair replaced by fibrous tissue Abscess


Seborrheic dermatitis Course

No scar

No scar



alopecia (if not treated early)


• Diagnosis of Tinea capitis: 1. Clinical examination

2. Wood's light: microspore gives wmffiBTescencS 3. Direct microscopic examination using 15 % potassium hydroxide to identify hyphae and spores 4. Culture on Sabouraud's agar medium for two weeks • TTT of Tinea capitis : I- Topical therapy : USELESS IF USED ALONE

a. Tincture iodine 1- 2%, Tolnaftate cream, whitfleld ointment, azole derivatives.

b. Shampooing with selenium sulphide suspension or ketoconazole shampoo twice weekly renders the patient non- infectious early II- Systemic therapy :

o Griseofulvin, 12.5 mg/kg/day after meals, for 6- 8 weeks 2 divided doses.(one tablet / 10 kg body weight with a maximum of6 tablets)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 14

2. Tinea Circinata(Tinea corporis)= ringworm of hairless skin

•Caused by trichophyta and microspora •Clinical picture :

• Single or multiple • Itching is a common symptom. • Well defined annular active red patches

with healing center & vesicular scaly edge. • Coalesce to form Polycyclic Patterns

• It occurs on exposed surfaces of the body as Face or arms • DP : Herald patch of pityriasis rosea • TTT :

- For localized cases : topical antifungal twice daily - For extensive or resistant cases, GAA; Griseofulvin for 3 weeks ,Azoic derivatives or Allylamines.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 15


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬





Tinea Cruris =

Tinea Barbae = Tinea Pedis =

firiseofulvin for 3 weeks , Azole derivatives or ^llylamines

c) For extensive or resistant cases , GAA:

b) For loealized cases : topical antifungal twice daily

a) Avoid PDF

Candidiasis ,flexural psoriasis , seborrheic dermatitis and erythrasma

common in most cases.

glands. Itching is

secretions of sebaceous

antifungal effect of fatty


to tinea circinata or


NOT involved due to

face. Lesions are similar

occurring in the shows pustules like

one sided on the neck or

Involvement is mostly


buttocks. Scrotum is

occurring in the crural area, it might extend into the gluteal folds and the

It is a tinea circinata

friction, maceration, heat.

Excessive sweating, obesity,



barber's instruments


nails of digits or toes may be

One or more


weeks for toe nails B.Itraconazole

fmgemails and 12

weeks for

250 mg daily for 6

A. Terbinafine:

theranv :

❖ Svstemic


asymmetrical if

unilateral and

o Usually


leading to

or brittleness

greenish coloration o With thickening

Yellowish or

Epidermophyta and Trichophyta

Tinea Unguium = Onychomycosis

only in extensive

seated pustules with itchy sensation

Occurs unilaterally on the palm as a welldefined area of multiple vesicles and deeply

Tinea Mannum


3. Systemic therapy

1-2 %

2. Topical therapy e.g. tincture iodine

1. Avoid PDF


(narrowest interdigital

and Fifth in Feet,

Lesion Bilateral, particularly the Fourth


Reeurrences are

white with bad odor.

sodden, macerated,

Skin between toes

wet floor boards

Source of infection :


excessive moisture of

excessive sweating and

Epidermophyta and Trichophyta

Source of infection:

Athlete's Foot

farm animals or

Ringworm Of Beard


It is a tinea

Tinea Axillaris

Epidermophyta and

Ringworm Of Groin




= Tinea Versicolor


o It is very common superficial mycotic infection, more in tropical climates and summer time,

o It occurs in young adults with a familial predisposition, o It is caused by lipophilic yeast Malassezia furur ; the pathogenic (mycelial) form of pityrosporum

o It is caused by Candida albieans : a dimorphic organism: - Yeast(Y)form (commensal; in mouth, gut and vagina)

- Mycelial(M)form (pathogenic) PDF:

o Under certain conditions organism is shifted from its commensal to its

mycelial pathogenic form; this shift is predisposed to by thefollowing:

orbiculare which is a normal

commensal yeast of human hair follicles which under certain

1- Moisture and Sweating

conditions, tums to the pathogenic mycelial form.

2- Trauma, e.g. friction from obesity 3- Drugs as corticosteroids , cytotoxics and antibiotics

4- Debilitating diseases as malignancy or AIDS

5- Conditions associated with Decrease

resistance, e.g. anemia, pregnancy,

cushing's syndrome, diabetes mellitus. ❖ Clinical Types Of Candidiasis 1-Mucosal candidiasis : A. Whitish Psendomembrane

(Oral Thrush ); in the mouth occurs in infants and debilitated adults

B- Vulvo-Vaginitis(Thrush

pruritus vulvae with





Usually starts on neck, upper parts of

White vaginal discharge. Creamy, Thick; commoner in pregnancy

chest, back of arms.

C-Balanitis :

In extensive cases it spreads to abdomen and other parts of body.

in uncircumcised males

2- Cutaneous candidiasis:

Symptomless , but itching may be •'0

present. o


Recurrences are common in Summer 9

due to Heat and Humidity



Primary lesion : Sharply demarcated MACULE,byperpigmented or

hypopigmented covered by fine branny Scaling.


Vesicles that coalesce and rupture giving well defined, red eroded areas with white fringed edge and forerunners (Satellites).

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 17

Diagnosis Of Pityriasis Versicolor

A- Paronvchia And Onychia: ❖ Occupation is very important predisposing factor, e.g. housewives & cooks.

^ V'. M

'Hs '■ I ■ f' Ji m o


Nail fold is swollen, red and slightly tender. Nail plate shows discoloration, transverse ridging and corrugation, DD: Pyogenic paronychia (in Candida paronychia : the condition is chronic with no throbbing or pointing)

> Groins ,axillae and under breasts


> Erosio -interdigitalis blastomycetica;

o 1. Clinical examination

2. Wood's light gives yellow fluorescence.

Maceration with sodden skin between finger webs. It commonly affects the space between the Ring and Middle fingers(3rd&4th)(narrowest Space)

> Angular cbeilitis (perlecbe);

3. Parker ink stain shows

Mycelia and Spores (Meat balls & Spaghetti appearance) in Skin Scrapings of Scales. o

Streptococcal infection and riboflavin deficiency may also have a role(DD)

^ Napkin dermatitis;


Creases "Satellite" affected lesions Maceration and erythema with sharp border beyond which are satellite papules and vesieles that occur in diaper area of newboms and infants. Depth offlexures are usually affected. (differentiates iffrom dermatitis due to contact with napkins where the depths of flexures are spared

(diaper rash)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 18



Tinea Versicolor




o It is the backbone of treatment because


drugs are secreted in sweat, so they can reach the fungus of contaminated areas all over the body, drugs include : a. Ketoconazole 200 mg , one tablet daily for 10 days


A- Dyes; castellani paint and gentian


violet 1-2 %

b. Itraconazole

B- Nystatin creams, A-Mycostatin: oral powders and vaginal suspension

c. Fluconazole 150 mg, capsules , 2 capsules / week for 2-3 weeks



I. Imidazole derivatives, shampoo, cream, spray, or lotion.

C- Imidazole

B- Azotes;


ketoconazole and

2. Tincture iodine 1-2 %;causes skin



3. Sodium hyposulphite 30 % aqueous

C- Amphotericin B


IV in severe cases

4. Selenium sulphide 2.5 % suspension or shampoo 5. Whitfield lotion or ointment

6. Zinc pyrithione incorporated in shampoo HI. TO PREVENT RELAPSE:

1) Selenium Sluphide shampooing once weekly 2) Ketoconazole tablets 3 days per month

NB: Griseofulvin is not used in treatment, because it is not effective for treatment of


for 6 month

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 19




• Tincture iodine 1- 2 % is effective

against dermatophytes, but ineffective against Candida • Gentian violet is effective against Candida, but ineffective against dermatophytes

• CasteUani paint is effective against both Candida and dermatophtyes

A.Griseofulvin :

• Derived from penieillium

• Dose : 12.5 mg/kg body weight given after meals in two divided doses(

maximum daily dose is 6 tablets) • Duration of treatment is 3-6 weeks

• Fungistatic, effective against Dermatophytes, but not against yeasts • Tablets (125 mg)or syrup (125 mg /5ml)

B-Solutions : sodium hyposulphite 30 % for tinea versieolor

• Contraindication In Hepatic diseases & Pregnancy • Side effects include Hepatotoxicity , Photosensitivity and Bone marrow depression

B.Allylamines:terbinafme : effeetive (salicylic acid 3 ,benzoic acid 6 , lanoline 12 against dermatophytes only ,side effects are minimal and Vaseline add to 100) C-Ointment: whitfield's ointment

D.Creams:Broad spectrum Antifungals : Allylamines as terbinafine Azoles as clotrimazole and miconazole

C.AzoIes: Broad spectrum Against dermatophytes and yeast. ♦> Ketoconazole :

• Active imidazole derivative

• Given in a dosage of 200 mg daily with food for 10 days • Contraindicated in Pregnancy

• Side effects include Hepatotoxicity ❖ Triazoles:

Itraconazole 200 mg/day for one week Fluconazole 150 mg once/week till cure; side effects are minimal

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 20

IV)PARASITIC INFECTIONS 1. Scabies. t> pes > Human scabies > Animal scabies 2. Pediculosis.

❖ Human scabies:

1. Def.: It is a contagious disease ofthe skin caused by the pregnant female ofthe mite, sarcoptes scabiei

2. Incubation period :2 weeks

Mites burrow under


the skin and iay eggs

3. Life cycle:fertilized female mite invades the epidermis. It digs a sloping burrow where it deposits two-three eggs/day to reach a total of 10-25 eggs. The female mite dies and eggs hatch. Nymphs come out to the surface ofthe skin. After maturation, copulation occurs between males and females. Pregnant females start a new cycle. 4. Mode of infestation :

- Direct by close contact with human cases

- Indirect spread by clothes or bedding (less important) • Mite cannot survive for more than few days away from skin 5. PDF:poor hygiene , overcrowdness and sexual promiscuity(STDs); however scabies

ignores all social and economic barriers; anyone can contract scabies regardless of age , sex or race .

6. Clinical picture:



Itching is the most common manifestation; increases at night Lesions are polymorphic; the primary lesion is the burrow Burrows are linear elevations of the skin, 5-15 mm long. Other lesions include :furrows, scratch marks, papules, and pustules • They are seen in-between fingers, wrist area, medial sides of forearms, anterior axillary folds, breast in females, lower abdomen,,genitalia in males and medial aspect of thighs and buttock. Head, neck,

palms, soles and upper back are spared (diagnostic sign )



‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 21

7. Post-scabietic nodules:

Incidence: Rare condition

Inflammatory nodules that occur as a

hypersensitivity reaction to the parasite Itchy Indurated , reddish brown fltWiiaMmanfnuCT in color and up to 12 mm in diameter Persist for Weeks or Months after scabies has been treated

Treatment is by Intralesional steroids 8. Special variants of scabies : Norwegian scabies

Scabies in children and infants


incognito o



Has atypical distribution; scalp , head , neck , back , palm and soles (because thin skin) Secondary bacterial infection and eczematous changes occurs If we suspect scabies in an infant, we should examine the





Occurs in

immunocompromized and mental retarded patients Presents by erythroderma (generalized erythema and scales) Itching is absent in spite of presence of millions (1-2)of


Caused by steroid

application o

Difficult to


mites o

Surrounding normal persons may suffer from ordinary scabies.

9. Complication of scabies: 1- Secondary INfections 2- INsomnia and exhaustion

3- Acarophobia 10.Diagnosis of scabies : I-Clinical:

1- Noctumal pruritus

2- Positive family history 3- Morphology and distribution of lesions 4- Spared sites Il-Investigations :

1-Mite can be extracted and examined under the microscope 2-Skin biopsy

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 22

Treatment of scabies: /- General


II- Topical treatment

• Sulphur

Treatment of all family members at the same time Disinfection of clothes and beddings After a hot bath, in which the skin is thoroughly scrubbed, the scabiecide is applied careful y to all the skin below the neck • Crotamiton • Benzyl • Permethrin • Gamma


cream or







hexachloride lotion

5 % for




25 % preparation

5 % preparation

1% preparation

Applied for 1 night, may be repeated after

Applied for 1 night and repeated after

1 week

1 week

It is non-specific, non-diagnostic. It is used for : B- Prognosis of leprosy

A- Classification of leprosy

o Strongly positive : suggests tuberculoid

o Shift of test from -ve to +ve indicates

efficacy of therapy given to the patient


o Weakly negative: suggests borderline tuberculoid(BT)

o -

Negative :could mean borderline leprosy(BB), borderline lepromatous leprosy(BL) or lepromatous leprosy(LL)

o NB :If normal person in an endemic area is lepromin negative, he is liable to contract leprosy due to absence of cell mediated immunity.

Nerve Involvement In Leprosy Common

Peioneal Nerve

Normal Foot

Leprosy involves superficial nerves e.g. ulnar, lateral popliteal and great auricular nerves. Involved nerves are thickened, tender & beaded

Sensory nerves affection leads to glove and stock anesthesia with loss of pain leading to repeated injuries of hands & feet and trophic changes Motor nerves affection causes facial palsy (facial), claw hand (ulnar), ape hand( median) or dropped foot (lateral popliteal)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 26

❖ Clinical Types Of Leprosy : 1)Tuberculoid Leprosy

Disease of

2)Lepromatous Leprosy

Nerves & skin & systemie

Nerves & skin




Lepromin test Bacteriology

Strongly Positive No or Paucibacilliary

No immunity Negative Multibacilliary

Clinical picture • Maculoanaethetic patch with hypopigmented Center. • Skin dry , hairless, insensitive

• Glistening Erythematous or skin-colored papules, NODULES and plaques • Ear ^ thickened & nodular

• Thickening of Ears ,face & skin of forehead + nodule on nose +

deepening of natural lines gives the picture of "Expression: Leonine Facies" • Eyebrows^ alopecia of outer 1/3 Nerves

Involved early; may lead to glove and stocking anesthesia



• Edema & ulceration the legs. Late anesthesia leading to loss of Temperature, Light touch. Pain then Deep touch ^ trophic changes Spontaneous bleeding from nose


Nodules & ulcers of nasal septum


Cartilage destruction ^ nose deformity Larynx, bones, muscles and testes Intercurrent infections


Very slow course

3)Borderline leprosy: according to patient's immunity, could be BT,BE or BL. Patient exhibits elinical features of either TT or LL, often with a prevalence of either one or the other

❖ Reactions in leprosy: These are acute episodes that occur during the chronic course of multibacilliary leprosy. They may occur spontaneously or may be precipitated by (infection, treatment,, vaccination),(physical stress, injury , operation),(pregnancy & parturition)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 27

o Types of reactions: type I reaction & type II reaction. Type II Reaction

Type 1 Reaction

Type of reaction r

Acute inflammation of existing

Type III immune complex Erythema nodosum leprosum +


Edema of hands & feet


Swelling with pain & tendemess paralysis

Mild nerve damage



Fever , malaise , iritis , dactylitis , Arthritis , neuritis and myositis

Type of immunity Type IV cell mediated Skin

disturbances D

1. Clinical picture


2. Skin smear from ear lobes , elbows, knees and any visible lesion thenstained with modified Ziel-Neelson stain.

g n


is T


3. Skin biopsy 4. Nerve sheath biopsy 5. Polymerase chain reaction(PGR)


w Dapsone

; 100 mg


^Nwmter :

CatatOQ No: RF-O*


Health care ,Patient education & rehabilitation




Clofazlmine ASt«>».63.9i

Voiuimi: SO

Data: tWSOSO

Multidrug therapy is administered to avoid resistance of bacilli: • Rifampicin 600 mg / day is administered at first for two weeks to decrease number of Bacilli and render the Patient non-infectious

• Dapsone is the cheapest and most important drug (the backbone) • Clofazlmine is Bacteriostatic and Anti-Inflammatory > Treatment of paucibacilliarv leprosv :

• Rifampicin 600 mg every month (2 capsules at the doctor's office) • Dapsone 100 mg daily

> Treatment of multibacillarv leprosv:

Given for at least 6 months

• Follow up is 2 years after the end of therapy

• Rifampicin 600 mg and clofazimine 300 mg every month • Dapsone 100 mg and clofazimine 50 md daily Given for at least 2 years • Follow up is 5 years after the end

of therapy > Treatment of reactions :

• • • •

Avoid predisposing factors. Physical and mental rest is essential. Anti-leprosy treatment should be continued in a lower dose Anti-Inflammatory agents as corticosteroids , clofazimine 300 mg daily and aspirin

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 28

Scaly Erythematous Eruptions

1. Psoriasis

2. Pityriasis Rosea 3. Lichen planus 4. Lupus Erythematosus 1)PSORIASIS

o It is common uou-infectious scaly erythematous skin disease, o It is less severe in summer than in winter Patho

o Increased rate of division of basal cell layer which leads to increased rate of

epidermal turnover with decrease of turnover time from 28 days to 7 days

geuesi Etiolo

I) Genetic predisposition


II)Provocation factors:



Lack of exposure to Ultraviolet rays; the disease exacerbates in winter, mainly affected covered parts and occurs in Scandinavian countries more than in tropical areas.


Infection: hemolytic streptococcal infection may cause guttate psorias^ asis

3. 5.

Drugs as hypertensive drugs, NSAIDs and anti-malarial drugs Metabolic; hypocalcaemia may precipitate pustular psoriasis Endocrinak e.g. Pregnancy may precipitate psoriasis


Psychogenic factors


Trauma; the disease usually starts on pressure points as elbows, knee and sacral



area; also trauma elicits disease in uninvolved skin; Koebner's Phenomenon

(isomorphic response) Clinic al





Auspitz sign

Primary lesion is a well-defined erythematous PAPULE covered by Shiny Silvery dry /poi'.e/y.attached Scales. Papules coalesce to give Plaques. Removal of the scales will lead to the appearance of bleeding spots

corresponding to the tips of dermal Papillae (Auspitz sign)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 29


I) Psoriasis Vulgaris: most common type


A. Skin Psoriasis :


Bilateral Symmetrical Involves tongue, extensors or upper and lower limbs, nails, elbows ,knees ,lumbosacral, flexures& glans and


Annular, Punctate, Circinate, Discoid, Linear or Guttate.

B. Scalp Psoriasis : Erythematous plaques and scales

Should be differentiated from scales of seborrheic dermatitis :

Psoriatic scales












C. Flexural Psoriasis

o Involves intertriginious areas e.g. axillae , groin, submammary fold and gluteal folds. Has the same clinical features , but scaling is reduced or absent due to moisturefrom friction D. Nail Psoriasis

o occurs with All types of psoriasis or alone o usually Bilateral affection of both hands and feet

o Pitting ,Subungual hyperkeratosis , Onycholysis or Ridges.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 30

II) Erythrodermic Psoriasis

o Involves more than 90 % of the body surfaee area, o It starts de novo or on top of psoriasis or vulgaris III) Pustular Psoriasis;

o Sterile pustules are formed(no organism , only PMNLs) o It may be generalized or localized to bands and feet IV) Arthropathic Psoriasis

o Involves distal interpbalangeal joints

o occurs with All types of psoriasis or alone o usually Bilateral affection of both bands and feet o Pitting ,Subungual byperkeratosis , Onycbolysis or Ridges.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 31


❖ Reassurance and emotional support stressing in the non-contagious and benign nature of psoriasis Treatment depends upon age, sex, occupation, and the type and the extent of psoriasis I)LOCAL THERAPY : FOR MILD &



- For extensive psoriasis vulgaris, pustular, erythrodermic or arthropathic psoriasis a) Acitretin = retinoids:

A. Anthralin(dithranol)0.1 - 0.5 %

irritant and leaves brown staining of skin

o Vitamin A derivative o Side effects include :

B.Phototherapy_: o PUVA;topical photosensitizer (Psoralen )followed by UVA o Narrow band UVB in hepatic cirrhosis and extensive skin involvement.

1. Teratogenicity(Pregnancy should be avoided during and for two years after the end of the treatment course) 2. Increase Cholesterol and triglyceride level 3. Dryness of skin and mucous membrane o Dose ; 0.5 - 1 mg / kg / day b) Phototherapy: o PUVA; oral photosensitizer ; psoralen followed in 2 hrs by UVA o Given 3 times weekly till clearance followed by maintenance c) Corticosteroids:

C. Corticosteroids: o For localized areas

o Ointment, cream or lotion; action

o for generalized pustular and erythrodermic psoriasis in case of

increases under occlusion

o intra-lesional injection(by dermojet)for

resistance to other medications

o start by a high loading dose till

nail psoriasis

improvement, and then taper gradually until reaching the lowest maintenance dose

D. Calcipotriol: o a vitamin D3 analogue that induces

d) Cyclosporine : - Potent immunomodulatory agent used

differentiation of keratinocytes and inhibits T-cell proliferation

primarily for prevention of transplant

E. Coal tar 2-5 %

rejection - Dose is 3 mg / kg / day

o followed by Sun exposure

- Side effects are dose-related hypertension

o should not be used on face, genitalia or

and renal toxicity e) Methotrexate: o Antimitotic effect; decreases rate of


o should not be used in pustular psoriasis F. Laser:

o Dye laser or Excimer 308 nm may help in some cases

division ofBasal cell layer by inhibition of dihydrofolate reductase enzyme —^ inhibit DNA proliferation, o Side effects are Bone marrow depression and Cytotoxic on the liver .

G.Salicylic acid 5%: o Ointment removes scales

o Dose is 0.2- 0.4 % mg / kg / week

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 32

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

Well-defined ,Planar {Flat topped), Polyangular , Purple

DD: Tinea Circinata(Tinea corporis)

- ringworm of hairless skin.

After the lesion subsides.

Post lichen hyperPigmentation occurs.


❖ It usually starts on one side of the trunk with its longitudinal axis parallel to the ribs

Koebner's Phenomenon (isomorphic response) can occur; trauma to skin produces characteristic

primary lesions on traumatized sites

healing center 3. Inner clear zone

2. An intermediate zone with a collarette of scales and

1. An outer erythematous zone,

scratching, since scratching produces more Pain in lesions

❖ Single oval lesion that shows three zones;

> Primary lesions: Herald Patch:

Lesions involves oral mucosa ,Flexor surfaces espeeially wrists ,flanks , medial thighs ,shins of tibia & glans penis. Pruritus may be severe and occurs in Paroxysms . Patients responds by rubbing the lesions rather than

surface and adherent Scales.

(violaceous) and Pruritic (itchy)[^3553 with Shiny

Primary lesion is a:



1-Psychological Stress; many cases are preceded by stress 2-Liver disease; hepatitis C virus may be associated 3- Sun rays cause actinic lichen planus 4-Drugs as antimalarial, gold and NSAID

Viral etiology It is caused by human herpes(HHV)- 6 and -7

prevalent in spring and autumn Etiology

o It is inflammatory non-infectious scaly erythematous eruption. It represents an exanthematous reaction to an upper respiratory viral infection. It is highest between 15-40 years and more

o It is a Pruritic non- infective scaly erythematous disease of skin, hair, and mucous membranes of unknown etiology

• Still unknown : however, theories are ;




Pify riasis Rosea(PR)

Lichen Planus(LP)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬






Lesions exacerbate in Summer and remit in winter

cicatricial alopecia

Hyperkeratotic follicular papules, which lead to

III) LP of scalp = Hypertrophic LP :


- Occurs on Sun exposed areas; forehead, butterfly area, lower lip , V-shaped are of chest and dorsa of hands - Characterized by Annular lesions or classical Papules

II) Actinic LP(LP tropicus)= Annular LP

I) Ordinary LP

Lichen Planus(LP)

Recurrences are not common

2- Inverted PR: occurs on distal parts of extremities

1- Ordinary PR.


- Lesions are usually asymptomatic except in 30 % of cases , itching may be present - Spontaneously heal within 4-8 weeks


o Occurs after 1-2 weeks from the onset of herald patch o Lesions are similar to herald patch ,but smaller and multiple o They are distributed along the long axis of ribs forming Christmas tree pattem of distribution, o Lesions are usually located on the trunk and proximal parts of the limbs; flannel area giving the picture ofjacket with short

Pityriasis Rosea(PR) > Secondary eruption:

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬




1- Patient reassurance that eruption is self-limiting and noninfectious.



Systemic photoprotectives e.g. Chloroquine 200-400mg/day





4- For itching, oral antihistamines , mild topical corticosteroids and

2- Avoid skin irritation by avoiding skin rubbing or hot bath

Avoid sun exposure Topical si/nscreens

3- Soothing lotions e.g. calamine lotion

Steroids, topical, systemic &





5- Flexural PR : eruption is limited to flexures as axillae and groins

young children

4- Papular PR:lesions are more elevated . It usually occurs in

3- Abortive PR: only herald patch, not followed by secondary eruption




Mucous membrane lesions are chronic. 1- Avoid the cause If possible. 2- For pruritus sedative and antihistamines 4- Systemic 6- Mucosal 5- Actinic lesions 3- Local therapy therapy lesions

months-2 years leaving characteristic post lichen hyperpigmentation; recurrences may occur.

V Most lesions undergo spontaneous healing in 6

> Course of LP:

Lesions are Resistant to treatment


Characterized by Reticulate white Streaks forming a network, Pinpoint Papules or ulcerative lesions, which are Painful and may change into Squamous cell

More common in the inner sides ofthe cheeks

IV) Mucosal LP = Atrophic LP:

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬


Stippling sign



It occurs in early life with a female : male ratio of8:1

kidney,joints and vasculature.

Alopecia, diffuse and non-cicatricial

dorsa of hands)

Malar Rash; erythematous ,non-scarring patches on light exposed areas (butterfly area offace, V-shaped are of chest &

Discoid lesions resembling those of DLE

❖ Skin manifestations of SEE :


Borders of plaque show telangiectasia . Purpura, vasculitis and ulcerations ,urticaria in the course of several months , Erythema multiform lesions flatten leaving a thin atrophic scar; Raynaud's phenomenon therefore scalp lesions end up with permanent cicatricial alopecia 1- Avoid sun exposure and use sun-screen creams or lotions 2- Systemic photoprotectives e.g. Chloroquine 200-400 mg/day 3- Corticosteroids; Topical, Intralesional & Systemic for resistant cases.

dilated pilosehaceous orifices(stippling sign) i? ^

Characterized by well-defined erythematous PLAQUES covered with adherent scales; lying underneath are

Adherent scales

dorsa of hands

Lesions involves sun-exposed areas; forehead, butterfly area of face, nose, ears, lower lip, scalp , V-shaped area of the chest and

abnormalities and pathological changes .

It involves a number of organs and systems, particularly skin,


with a female : male ratio of 2: 1

It is a systemic disease characterized by immunological

Systemic lupus erythematosus

confined to the skin. It occurs in the third and fourth decades

o It is chronic inflammatory scaly erythematous eruption

Discoid lupus erythermatosus

3. Systemic lupus erythematosus(SEE)

It is an autoimmune collagen disease. It occurs in three forms : 1. Discoid lupus erythematosus(DUE) 2. Subacute lupus erythematosus(SCLE)


1- Eczema. 2- Urticaria. 3- Drugs eruption. 4- Erythema multiforme. I) ECZEMA(dermatitis) Def.: It is one of the allergic diseases.

- It is characterized by Ill-defined erythema, Itching and vesicle formation at one stage. CLINICAL TYPES


B. Chronic Eczema :lichenification

(thickening of skin and exaggeration of

A. Acute Eczema : erythema, swelling, vesicles, oozing with subsequent crusting

skin markings), excoriations and

hyper-or hypopigmentation

C. Subacute Eczema:features of both acute and chronic forms MAIN TYPES OF ECZEMA

I) Contact Dermatitis

A- Primary Irritant Dermatitis:

B- Allergic Contact Dermatitis

Affects any individual(not allergic), previous contact is non-required for the

Immunological reaction that develops in genetically susceptible individuals after exposure to the

eczema to develop


Dermatitis occurs soon after exposure Caused by direct damage by strong

Presentation of allergen occurs by LCS to T-cells (type IV reaction). On re-exposure to the same antigen, lesions develop in sensitized

acids and alkalis or due to cumulative

damage by mild irritant, e.g. Frequent washing

individuals at sites of contact.

Susceptible individuals are compulsive washers, dishwashers,, housewives, nurses and surgeon Common agents are soaps, detergents,

vegetables or solvents

Common allergens are glues, nickel ,chromate , cleansers, eosmetics, rubber, resins, and medications(

sulfa powder, penieillin ointment and local antihistamines)

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 37

*t* Photodermatitis :

o A photo - allergic reaction occurring as a result of


activation of a chemical, local or systemic by light.

o Lesions appear on light exposed skin and presents with acute eczema.

Diagnosis Of Contact Dermatitis :


1. History

2. Clinical picture


3. Histopathology


4. Patch testing;


Eczema develops at site(s) of causative allergen(s) II) Discoid Eczema :

extensorsurfacesofextremities,^j|^ ^ ^j|


'i 1

' » »






Calculated amounts of common allergens are applied to skin of back and kept for 48 hrs.

1 ' '


III) Stasis Eczema

chronic venous insufficiency,


which leads to rupture of small hemosedrin deposition

in skin and secondary dermatitis. Involves medial side of one or both lower

legs above medial malleolus followed by edema, oozing, vesiculation , crusting, itching and pigmentation. Ulceration may follow.

V)Seborrheic Dermatitis:

IV),Atopic Eczema:

o Atopy is a genetic hereditary predisposition o It is scaly erythematous dermatitis to develop allergic rhinitis, atopic dermatitis bronchial asthma & hay Fever, o Family history is positive 50-70% of patients.

❖ Pathogenesis : o Triggering factors will lead to T-helper cell proliferation, excessive inflammatory cytokine production with subsequent pathological and clinical changes.

o It is caused by lipophilic yeast Malassezia furur; the

pathogenic (mycelial)form of pityrosporum orbiculare

❖ Precipitating factors : o Irritants, allergens(house- dust mite) o Excessive washing, food o Staphylococci, viruses

o Cold weather and lack of humidity

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 38

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬

Acute eczema

2 years


0 Only 10 % of cases of atopic dermatitis of infancy or childhood persist to adulthood.


o And sides of the

popliteal fossae

antecubital and


o Or may involve whole


particularly the

o Involve the flexures

0 Groups of itchy papules

And dorsa of hands

0 In cheeks


o Age is from 2 months- o Age is from 4-12

k ^


A. Infantile Phase(

B. Childhood Phase

rV)Atopic Eczema:



childhood type accompanied by hyperpigmentation and

Lesions are similar to

o Age is over 12 years

C. Adult Phase

erythematous patches

localized scalv

o Diffuse or

androgen on sebaceous glands months.

subsides after 3

with genetic susceptibility due

Affects individuals

to effect of



mother to infant;

hormone from

0 Caused by transfer of androgen

and interseapular

areas, antestemal

o Usually on scalp, o Involving hairy intertriginous folds areas and body (retro-auricular areas, flexures (scalp, neck, groins)& nasolabial folds, diaper area retroauricular


o Greasy yellowish

-10 months

o Age is from 2 weeks

V)Seborrheic Dermatitis: a) Infants: b) Adults :


A-Avoid the causative agent C-Chronic Eczema :

B- Acute Eczema :

Local therapy :

I) o

Drying antiseptic lotions (the best) as

o Local corticosteroids ointments

aluminum acetate, potassium

because skin surface is intact

permanganate 1/8000 or normal saline . o

Corticosteroids Creams; have Hydrous base which does not irritate the eroded surface like ointments which have a Vaseline base


Systemic therapy: o Corticosteroids

o Corticosteroids o Antihistamines

D)Management Of Special Types:

I)Primary Irritant Dermatitis : protection e.g. by gloves, rest and lubrication.

Ill) Stasis Eczema :Limb elevation Management of varicose veins

II) Atopic dermatitis : o Education of patient and family avoid stress, cold, dryness, and irritants

IV)Seborrheic dermatitis:

o Frequent application of moisturizers and

o Antidandruff shampoos containing selenium sulflde, zinc pyrithione or

o Olive oil infantile scalp lesions o Corticosteroid creams and lotions


o Topical immunomodulators especially in children to avoid long term corticosteroid

ketoconazole .

therapy o Narrow band UVB in severe cases

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 40



Def.: It is common allergic skin disease caused by type I hypersensitivity reaction. o It is characterized by the release of histamine, which leads to vasodilatation with local

increase of permeability and development of transient edema of the skin; wheal. It is usually accompanied by an itchy sensation. ETIOLOGY OF URTICARIA

l)Exogenous Causes : A.Ingestants :

2)Endogenous Causes :

1. Pregnancy

- Foods as fish, food preservatives, milk, 2. Internal Malignancies : lymphoma or eggs, chocolates, nuts, strawberry& banana GIT cancer - Drugs as penicillin, salycilates , 3. Medical disorders : SLE ,liver sulfonamides and NSAIDs diseases, malaria and thyrotoxicosis B. Injectants :

- Drugs e.g. Penicillin, other antibiotics and

5. Intestinal Parasites : protozoal and



4. Local Microbial infections : bacterial, viral or fungal helminthic infestations

Blood elements

- Insect bites e.g. mosquitoes, fleas and ants

C.Inhalants : grass pollens ,mould spores and perfumes

* Autoimmune Etiology is suspected in some cases of chronic urticaria.(Autoantibodies against receptors on mast cells). PATHOGENESIS OF URTICARIA

- Onfirst antigen exposure, IgE antibodies are formed and these bind to IgE receptors on mast cells

- On second exposure {after one week or more)to the same antigen or antigenticallyrelated compound, antigen-antibody reaction occurs on the surface of mast cells. This is followed by degranulation of mast cells and release of chemical mediators (histamine, prostaglandins, heparin) CLINICAL PICTURE OF WHEALS WHEAL

o Sudden appearance of whitish or reddish slightly elevated edematous lesions o Size of wheal varies from few mms to several cms

o o o o

Involves any area of mucous membranes or skin surface Lesions are more commonly generalized or localized Lesions are evanescent (transient); they lastly only for few hours If lesions continue to erupt for more than 3 months, it is called chronic urticaria

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 41

I) Ordinary Type :described before

V)Physical Urticarial:

II) Angioedema :

Wheals appear at site of exposure to physical agents TYPES:

VD involves large size blood vessels of the deep dermis and hypodermis leading to solid edema which persists for a few days It occurs in soft tissue as , eyelids, lips and genitals If involves the larynx, it may lead to

Solar urticaria : on Sun exposure parts

Pressure urticaria : after prolonged pressure Cold urticarial on exposure to cold Heat urticaria on exposure to heat VI)Papular Urticaria :

edema of vocal cords and suffocations

III)Factitious Urticaria :

Very mild trauma leads to wheal formation corresponding to site oftrauma to increase in - It occurs in response to insect bites It usually affects infants and children (up to triple response. IV)Cholinergic Urticaria :

7 years)

- Involves exposed areas if due to flying insects (mosquito)or covered areas due to non-flying insects( ants and fleas) A wheal appears at the site of the bite.

- Acetylcholine is the mediator^ - Patient is sweating then he feels prickly and itchy sensation (due to muscular effort, nervous excitation or overheating) - Small wheals may be observed

Within one or two days, an itchy erythematous papule appears at the center of the wheal and stays for few days. Lesions occur in groups or lines representing the tract of the responsible

corresponding to Sweat glands. - Lesions involve scalp, neck and upper chest more than other body areas. - Lesions subside usually within one hour - The Condition is Self-limiting within few


Insect injects more than one antigen. This leads to two types of allergic reactions; type I when an antigenic substance leads to wheal formation and type IV in which another antigen leads to lymphocytic cell

months with Seasonal recurrence.

infiltration and papule formation.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 42


1- Careful history and skin tests to determine the cause of urticarial, usually reachable in 50 % of cases

2.Body examination to detect:

■ Subtype of lesion; papular urticarial, dermographism or ordinary ■ Sites : on exposed parts, asymmetrical or peripherally distributed ■ Associated Systemic diseases as SLE

■ Degree of Severity to decide type oftreatment TREATMENT OF URTICARIA :

I) Avoid the cause if known

II) Local therapy

Ill) Systemic therapy : according to the severity, start by:

A. Cold compresses cause vasoconstriction

B. Calamine lotion has a soothing effect C. Corticosteroids in localized forms as japular urticaria

a) Oral antihistamines(HI antagonists ); - Sedating as chlorpheniramine maleate and hydroxyzine (Hypnotics). - Non-sedating as loratidine and cetrizine

b) Parental antihistamines ,IM or IV


c) Oral corticosteroids d) Parental corticosteroids

CAlAll/.Vf lonav

>i«na>u I

e) Adrenaline, 0.2- 0.5 ml of 1 : 1000

solution, SC or IM (never IV ). It is life saving in severe cases and angioedema, contraindicated in cardiac patients. (hnimcfll

Treatment Of Papular Urticaria : 1. Control of the cause as use of

insect repellents 2. Topical corticosteroids 3. Other lines of treatment of urticaria.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 43

Ill) Drug eruptions

Def.: Drug's Adverse effects on the skin may manifest in several form which may mimic any

skin disease. It differs by having an Acute onset, Atypical distribution, more inflammation and subsidence After stoppage of the causative drug. Common drug reactions include :

1- Angioedema & Urticaria.

2- Acneform Eruptions; most commonly caused by corticosteroids

3- Photosensitive Drug Reactions

4- Erythroderma (Exfoliative Dermatitis)


5- Fixed Drug Eruption;

Most commonly caused by sulfonamides and NSAIDs Called fixed because it is fixed to the drugs and fixed to the site Characterized by macule or patch which may progress to vesicles or bullae followed by rupture and formation of an erosion May involve and part of the skin or mucous membranes, but the most common sites ate the lips and genitalia.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 44

IV) Erythema Multiforme(EM )

Def.: It is hypersensitivity syndrome affecting skin, mucous membranes and internal organs. It is characterized by multiforme eruption with a special target (iris) lesion. The disease is frequently caused by infection or drugs where a T-cell response is seen in the skin

leading to epidermal eel! death CAUSES

1. Genetic factors 2. Autoimmune diseases e.g. SLE

^ 4L


3. Drugs as sulfonamides , NSAlDs, Anticonvulsants and Allopurinol 4. Infections; HSV(most common cause), mycoplasma pneumonia, EB virus ,HEY and HIV

5. Intemal malignancy as carcinoma and lymphoma CLINICAL PICTURE Skin lesions

Mucosal involvement


May be mild or severe affecting conjunctival, oral, nasal, genital, or anal mucosa

PAINFUL hemorrhagic bullae and

Lesions are bilateral and symmetrical, commonly affecting the limbs especially


dorsal surfaces of hands and feet. The


most characteristic lesion is the


Pain in severe eases is agonizing that it may interfere with eating and/or micturition

erythematous, annular ring with central vesicle or hyperpigmented known as target (iris) lesion . Other skin lesions inelude erythematous macules,papules, vesicles and bullae

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 45


b. EM major

a. EM minor :

More wide spread; severe lesions are seen The mild form of the disease with only

with extensive mueosal involvement and

limited skin affection, no or mild mueosal involvement and no systemic affection. It

may be systemic affection in the form of pneumonia, sepsis, renal tubular necrosis

lasts for 1-4 weeks and could be recurrent.

and death. TTT

1-Avoid The Cause if possible e.g. antiviral drugs for HSV,stop offending drugs and

treatment of associated systemic diseases. 2- Local Therapy

3-Systemic Therapy

a) Corticosteroids in severe cases b) Antibiotics to control sepsis c) Antihistamines

Antibiotics for blisters and erosions

Antiseptics and Anaesthetics for oral erosions

Cold compresses Calamine lotion has a soothing effect Treatment of EM major: Hospitalization in severe cases Consult an ophthalmologist for ocular

Corticosteroids creams or ointments


Management of any systemic


‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 46

Disorders of melanocytes Vitiligo Definition

It is a common, non-infectious, genetically determined disorder characterized by loss of melanocytes.

Primary lesion

o Primary lesion is a well circumscribed milky white macule or patch, o It affects any part of the skin even scalp, lips, or nipples leading to whitening of hairs.

Etiology 1- Autoimmune Theory : 1

o Antimelanocytes antibodies cause destruction of melanocytes. o This theory is proved by the association of vitiligo with autoimmune diseases as DM, thyroid disease and pernicious anemia o Precipitating factors include psychological or mechanical trauma 2-Neurogenic Theory

o Melanocytotoxic substances released from the nerve endings cause destmction of melanocytes o It starts at finger tips and is resistant to treatment 3- Contact Or Chemical Theory:

o Melanocytotoxic substance(Phenolic derivatives) in gloves, slippers and film developers cause disease in specially predisposed persons 4- UV Rays: o

Excessive exposure to UV rays may lead to vitiligo of exposed parts m some



o Melanocytes( melanin forming cells)are destroyed and disappear (Absent)from epidermis; no melanin is produced leading to appearance of milky white macule or patch.

‫اﺷﺗري ﻧﺳﺧﺗك إذا ﻧﻔﻌك اﻟﻛﺗﺎب وادﻋم ﺗﺣدﯾﺛﮫ ﺑﻧﯾﺔ ﻧﺷر اﻟﻌﻠم‬ 47

Clinical Types 2. Unilateral vitiligo

1. Focal vitiligo

i 4. Universal vitiligo

3. Generalized vitiligo

Differential diagnosis: 1. Pityriasis Alba

2. Pityriasis (Tinea) Versicolor 3. Post Inflammatory Hypopigmentation e.g. Tubereuloid Leprosy. Treatment:

1-Phototherapy :

• Stimulates residual melanoeytes in hair follicles for repigmentation