Structure and Function of the SKIN

1- Epidermis: "cellular components only, thickness 0.4 to1.5mm, formed of

Keratinocytes that are organized in 4 layers and dendritic cells, dendritic cells
include indeterminate dendritic cells melanocytes Langerhans cells "
a. Basal Layer (Stratum Germinatium): Attached to the basement
membrane, contains melanocytes and single layer of columnar mitotically
active cells.
b. Spinous Layer (Stratum Spinosum): Its position is within mid-
epidermis, Supra-basal cells are polyhedral in shape+ rounded nucleus+
spine-like cell margins, Supra-basal cells move upwards through epidermis
and become progressively flatter.
c. Granular Layer (Stratum Granulosum): Named for presence of
basophilic kerato-hyaline granules within the cells at this layer.
NB. Clear cell Layer (stratum lucidum): present in the lower portion of
horny layer in palms and soles, cells are not nucleated nor granular "clear".
d. Horney Layer (Stratum Corneum): Stocked layer of a-nucleated
flattened cornified cells. The layer provides mechanical protection, barrier
to water and permeation of soluble substances.
2- Dermis: Composed of fibrous matrix and cellular CT elements and
contains nerve and vascular networks, dermis is arranged in two regions the
upper papillary dermis and the deeper reticular dermis, the papillary dermis
takes the contour of epidermis, reticular dermis takes the bulk of dermal tissue
and composed of "collagen fibrils" organized into large bundles with branching
elastic fibers surrounding the bundles.
3- Hypodermis(subcutis): Composed of adipose tissue. "It insulates
the body, reserve energy supply, Protects the skin, allows for its mobility over
the underlying structures, cosmetic effect in molding body contours. "look the
table p2"

Primary skin Lesions "with which skin disease begin"

• Not raised: 1- Macule: a circumscribed area less than 1cm of change in skin
color+ no elevation nor depression, e.g. Vitiligo and Pityriasis versicolor.
2- Patch: a macule greater than 1cm e.g. Vitiligo and tuberculoid
leprosy.
• Raised: 1- Papule: a dome shaped elevated solid lesion, less than 1cm
e.g. Papular urticaria, Warts and lichen planus.

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2- Nodule: Solid lesion, more than 1cm, deeper than papule "to dermis!".
e.g. Lupus vulgaris- Lepromatous leprosy- erythema nodosum.
3- Plaque: a plateau-like elevation+ large surface area relative to its height,
formed by confluence of papules. e.g. discoid lupus erythematosus, psoriasis
and lichen planus.
4- Vesicle: a circumscribed, thin-walled, elevated lesion+ less than 1cm+
containing serous fluid. e.g. H. Simplex and Zoster.
5- Pustule: like vesicle but contains pus. e.g. Pustular psoriasis and acne
vulgaris.
6- Bulla: a cystic swelling like vesicle but greater than 1cm. e.g. 2nd degree
burn, bullous impetigo, pemphigus.
7- Comedo: a plug of keratin and sebum in a dilated pilosebaceous orifice
leading to formation of black heads. It's the 1ry lesion of acne vulgaris.
8- Wheal "weal": an evanescent, edematous plaque+ peripheral
redness+ usually pruritus + it lasts only a few hours. It is the 1ry lesion of
urticaria.
• Burrow: a greyish irregular small tunnel in the horny layer that houses
"Sarcopts scabiei", it is characteristic for scabies.
• Scales: flakes or plates that represent compacted desquamated layers of
stratum corneum. e.g. scales of psoriasis, ichthyosis.

Secondary skin Lesions 13

- May evolve from primary or may be caused by external forces such as scratching,
trauma, infection or healing process.

Pustules: from 2ry infection of vesicles or papules.

Scales: 2ry here due to peeling of skin following superficial inflammation as
eczema or scarlet fever.

Crust: It results from drying of plasma or exudate on the skin. e.g. crusted
impetigo and eczema.

Excoriation: superficial abraded or traumatized skin by scratching or

rubbing.

Erosion: slightly depressed areas in which part or all epidermis has been lost.

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Fissure: Linear cleavage of skin extends to dermis. e.g. fissured heel, lips.
Ulceration: necrosis of epi, dermis, may SC T. e.g. chancre, varicose U.
Scar: permanent fibrotic changes on skin following damage to dermis.
Eschar: hard darkened plaque covering an ulcer implying extensive necrosis,
infarct or gangrene.

Keloids: Extensive fibrosis extends beyond edges of the wound due to

exaggerated connective tissue response of injured skin.

Lichenification: thickened of the epidermis+ hyperkeratosis+

hyperpigmentation+ exaggeration of normal skin lines, due to chronic rubbing or
scratching of an area. e.g. chronic eczema.

Atrophy: thinning or absence of epi, dermis or S.C fat e.g. atrophic lichen
planus, lichen sclerosus et atrophicus.

Petechiae, Purpura and Ecchymoses: Bleeding in the skin+ don't

blanch when pressed. Petechiae= smaller, purpura& ecchymoses= larger, purpura
may be palpable.

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Bacterial SKIN Diseases
Impetigo contagiosa
- Contagious superficial B skin infection. The organism enters through damaged
skin and is transmitted by direct contact.
1. Non bullous Impetigo: by Staph. aureus. Intra-epidermal, thin walled
vesiculopustular, on erythematous base, very fragile& rupture early. leaving a
crusted exudate "honey or yellowish-brown color" over superficial erosion, the
crusts dry and separate leaving erythema "fades without scarring". Around nose
and mouth, at scalp& limbs. Common in children who are affected at any site
especially on top of atopic dermatitis.
2. Bullous impetigo: by Staph., group A β hemolytic Streptococci. The organism
secretes exotoxin- sloughing of epidermis. Flaccid fragile bullae, bullae are less
rapidly rupture- larger, fluid is clear then become turbid. Thin brownish crusts are
formed after rupture, central healing with peripheral extension- circinate lesions,
face is commonly affected+ sites of pre-existing skin disease as miliaria, 90% in
children younger than 2 Y.

NB: Circinate impetigo: Central healing and peripheral extension of the bulla in
bullous type or is formed by more than one lesion arranged in circular P.

Crusted impetigo: thick yellowish crust covering the lesion "on the scalp".

Predisposing factors:
• Pre-existing skin disease as scabies, atopic dermatitis, miliaria, trauma,
pediculosis "Crusted impetigo", insect bite.
• Lack of cleanliness, over-crowding and poor hygiene.
• Warm and humid temperature.

Complications: Post-streptococcal acute GN/ Scarlet fever/ cellulitis, urticaria,

erythema multiform.

Treatment: (good hygiene- removal of crusts with saline soaks-

treatment of predisposing causes- topical treatment in localized infection-
systemic antibiotics in widespread & complicated cases)

- Topical: Potassium permanganate 1/10000 lotion 4 times daily "antiseptic"

Antibiotic creams: Gentamycin, neomycin, fucidic acid twice daily.
- Systemic antibiotics: Dicloxacllin 250mg every 8hours for 10 days, cephalexin
250mg every 8 hours.
Penicillinase resistant antibiotics "amoxicillin+ clavulanic acid" 20mg/kg/day
every 8hours for 10 days.

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Erythromycin 40mg/kg every 8hours for 10 days. Or azithromycin
Ecthyma
A deep form of impetigo "until dermis" forms adherent crusts beneath which
ulceration commonly occurs.
Aetiology: group A beta hemolytic Streptococci, Staph. or both.
Predisposing f.: poor hygiene - overcrowded - Hot& humid climate - sites of
sustained tissue injury as excoriations, malnutrition, immunocompromised patients.
Clinical features:
1- Sites: legs, buttocks& thighs.
2- It begins as a vesicle or pustule overlying erythematous base.
3- Transforms into a dermal ulceration with overlying crusts.
4- The crust is dark brown& bloody. It's thicker, harder& more adherent than crust
of impetigo.
5- When crust is removed= Ulcer: shallow, punched-out& raised indurated border.
"may increase, remain fixed or decrease in size".
6- Ecthyma heals slowly with a scar &/or hyperpigmentation.
7- Regional lymphadenopathy is common.

Treatment: "The same as impetigo but for longer period- Nutrition"

Cellulitis and Erysipelas

Cellulitis Erysipelas
Acute, subacute or chronic The same but more superficial+ sharp
bacterial inflammation of loose border. It may be deep also so two
C.T in S.C tissue. "coexist" processes "C&E" coexist mainly.
Causes: by Group A beta hemolytic streptococci "S. pyogenes"+ B, C+
Staph+ H. They begin with minor incidence as scratch, burn.
Commonest site is leg then face, arm.
Clinical Picture: 1- Dusky red 1- Shiny bright surface erythema with
erythema with diffused ill-defined raised well demarcated edge. 2- vesicles&
edge. 2- no blisters. bullae are common.
3- Hotness, swelling and pain or tenderness.4- Fever& chills.
5- Spreading hot tender plaque*.
Complications: "Lymphangitis and lymphedema, elephantiasis in recurrent
cellulitis with lymphedema, septicemia& GN& endocarditis.
NB: Pure erysipelas is present in areas where there is little subcutaneous
tissue e.g. the head and face. "Penicillin is treatment of choice".

Treatment:
1- Rest and cool compresses but avoid bandage.
2- Symptomatic for pyrexia and pain.
3- Oral antibiotics in mild cases and IM or IV for severe cases:

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a. Benzyl penicillin I.V 600-1200 mg, 4 times for 10 days.
b. Benzathine penicillin "G" I.M 600,000 units twice daily till signs& symptoms
disappear then continue for a week.
c. Erythromycin 500 mg, 3 times for 10 days.
d. Long-term penicillin is used as prophylaxis for recurrent cases.

Folliculitis: is an inflammation of hair follicles. The follicles are damaged by

shaving or scratching then infection then inflammation.

- By staph aureus.
- Types: Superficial folliculitis "upper parts of a hair follicle":
C/P minute erythematous pustules, crust later without involving the surrounding
skin, mostly in scalp& extremities.
Deep folliculitis "the whole of the hair follicle"
C/P peri-folliculitis, bearded men are more prone to sycosis barbae.
- Complications: hyper-pigmentation, scar, cellulitis, permanent hair loss
"cicatricial alopecia".

Furuncle: "boil" is an acute necrotic staph infection of a follicle+ involvement

of S.C tissue. "single or in crops".

- Site: Hairy parts& areas exposed to friction, e.g. face, neck, buttocks.
- Present as small follicular inflammatory nodule then becomes pustular then
necrotic, healing after discharge of necrotic core, leaving violaceous macule.

Carbuncle: A deep infection of a group of contagious follicles with staph

aureus+ intense inflammation in the surrounding and underlying C.T, more in men.

- Predisposing factors: DM, malnutrition, prolonged steroids& I. therapy, HF.

- Swelling "red, painful, indurated, large, multiple draining sites& necrosis of
intervening skin forming a yellow slough", Single lesion.
- Site on the back of neck& shoulders, hips& thigh.
- Constitutional symptoms: high fever, malaise.

Treatment: Flucloxacillin "full prolonged course+ control of underlying

condition "in carbuncle", Topical antibiotics reduce contamination of the
surrounding skin.

Erythrasma: Mild chronic localized superficial infection of the skin by aerobic

coryneform bacteria "Corynebacterium minutissimum".

Clinical picture: Patches "reddish brown, sharply margined, irregular, fine scales,
coral red fluorescence under wood's light".

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– on groin, axillae, intergluteal& sub-mammary flexures, toe".

Treatment: Topical as imidazole derivates "miconazole, clotrimazole for 2 weeks"

Systemic as erythromycin 1 gm/ day for 10 days.

Mycobacterial Skin Diseases

Cutaneous Tuberculosis Depends on rout of infection& immunity
Classification:

1- Inoculation tuberculosis: "Exogenous"

– Tuberculous chancre 1ry complex: from direct inoculation of TB "facultative
anerobic" into skin or mm, not previously infection with TB, Inflammatory
papule develops in 2-4 weeks, turns into ulcer firm non tender undermined
shallow+ granulomatous base, lymphadenopathy painless regional, ulcer heals
leaving scar
– Warty TB "TB verrucose cutis": from direct inoculation of TB, individual is
previously infected, has high degree of immunity, lesion is purplish or brownish
-red warty, site in knees& elbows& hands& feet, may clear up without
treatment, if lymphadenopathy present it is due to 2ry infection not TB.
– Lupus vulgaris "some cases": persistent& progressive, individual has
moderate or high immunity, lesion is sharply defined red-brown soft plaque
composed of deep-seated nodules+ gelatinous consistency "apple jelly nodules",
lesion becomes elevated& infiltrated& shows peripheral extension& heals with
thin unhealthy contractile scar.
Diascopy test: Individual nodules appear as brownish yellow spots "apple
jelly app." If they are pressed with a glass slide "to eliminate the vascular
component of inflammation"
Clinical varieties: plaque form, Ulcerative form, Popular& nodular forms,
Tumor like form, vegetating form.
Complications: Disfigurement "ectropion- microstomia- parrot beak nose by
eating up of nasal cartilage while intact central portion+ remaining ala nasi-
pseudo ankylosing of joints", Recurrent erysipelas due to 2ry strept.,
Tuberculous meningitis or pulmonary TB, Squamous cell carcinoma.
2- 2ry TB: "endogenous" Contagious spread
– scruofuloderma: by direct extension of TB infection to the skin from
underlying lymph node, bone or joint "TB focus", lesion is firm painless bluish
red nodules then they break down to form one or more ulcers "bluish irregular
under minded edge+ granulating base+ discharging caseous purulent exudate+
may heal without treatment leaving an unsightly puckered scar".

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– Autoinoculation cutis orificialis: lesion is formed By shedding of large
number of TB and inoculate into the skin and mm of orifices "nose, M, urinary
meatus", In young adults with severe visceral TB due to large number, lesion is
red papule evolve into painful soft ragged shallow ulcer+ under minded edge+
purulent necrotic floor+ no spontaneous healing, Site of inoculation is
determined by trauma, TB test is variable& anergic in late cases -v e.
3- Hematogenous:
– Acute miliary TB:TB Infection that has spread from internal TB site "mostly
lung" to tissue and organs via blood stream, Affects children or
immunocompromised, skin Lesions are crops of small "millet size" bluish
papules "vesicles or pustules", it develops into Ulcers, TB Test is -v e, bad
prognosis.
– Tuberculous gumma: Results from blood dissemination from a 1ry focus
during periods of low resistance, It Affects children or immunocompromised,
Lesion is firm subcutaneous nodule or fluctuant abscess, breaks down to form
undermined Ulcer and/or sinuses, Site extremities more than the trunk, S or M.
– Lupus vulgaris "some cases"
4- Eruptive TB "Tuberculides":
Generalized exanthema in an individual with good health+ moderate to high
immunity to TB.
– Nodular: Erythema induratum "Bazin disease": recurrent lump on the back of
legs in women, may ulcerate and heal without scar.
– Popular: Papulonecrotic Tuberculides: recurrent crops of crusted red papules,
on knees legs buttocks lower trunk, heals with scarring after 6 months.
– Micropapular: Lichen scrofulosorum: eruption of small perifollicular brownish
papules, on the trunk, they heal without scarring.

Diagnosis: History, C/P, TB test, 3specimens on three successive days stained with
ZN, skin biopsies with ordinary& acid fast, culture "Lowenstein-Jensen medium",
PCR, Postero-A chest radiology.

Treatment: "2 or 3 drugs simultaneously for 6 to 12 months"

1- Isoniazid 5mg/kg in adult, 10gm/kg in children, 300mg.
2- Rifampicin 10mg/kg in adult, 20gm/kg in children, not more than600.
3- Streptomycin 15mg/kg in adult, 30mg/kg in children IM, not more than 1gm.
4- Pyrazinamide 15-30mg/kg/day in adult& children, not more than 2gm.
5- Ethambutol 15-25mg/kg in adult& children.

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Leprosy "obligate intracellular"
Incubation Period: 6 months to 40 years, average 2-3 years.
Classification:
Indeterminate Leprosy: mild prodrome,

Early type- Lesion is 1 to few macules "hypopigmented or erythematous, few cm

in diameter, poorly defined age"- hair& sensation are normal- most cases evolve
to other form of leprosy depending on patient immunity- lepromin test is variable.

Tuberculoid leprosy "TT":

Affect only nerves& skin, may be purely neural, it affects good immune persons,
Skin lesion is few asymmetrical erythematous plaques with raised clear cut edge
sloping towards a flattened& hypopigmented center, the surface is dry hairless&
anesthetic, Nerve lesion is marked and localized to ulnar G auricular leads to
wasting/ paralysis/ anesthesia& trophic ulcers/ nerve 7 leads to eye damage.

Borderline Tuberculoid Leprosy "BT": similar tuberculoid but smaller, numerous,

less enlarged nerve, disease can remain or progress to BL or LL or back to TT.

Lepromatous Leprosy "LL":

Skin lesions are bilateral& symmetrical 1- macules "small ill-defined

erythematous or hypopigmented", 2- Papulo-nodular type,

3- Nodules " numerous skin colored pink or coppery+ shiny surface face and ear
lobes are common sites"="infiltrations" which with deepening of face lines leads
to leonine face,

Hair loss "late" of outer third of eyebrows eyelashes then the whole body,

Nerve lesion is late, bilateral& symmetrical, gloves& stock anesthesia, flattening

of hypothenar.

Other organs: Kidneys, hepatomegaly, lymphadenopathy, stridor& hoarseness,

muscles, osteomyelitis, keratitis, iridocyclitis nasal mucosa is hyperemic+
ulcerated+ bleeds easily= epistaxis. Lepromin test is negative.

Borderline Lepromatous Leprosy "BL": Lesions are numerous, less symmetrical,

macules& papules& nodules+ plaque, anesthesia is moderate or absent, may
regional adenopathy, may remain progress or regress.

Borderline Leprosy "BB":

Skin lesions are intermediate in number between LL/TT, asymmetrical, plaques

with punched out appearance are characteristic- Nerve lesion is early,

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asymmetrical, several nerves are affected, bacilli are present in slit skin smears but
less than LL- Lepromin test is negative.

Tuberculoid Lepromatous
Number of lesions 1-10 hundreds
Distribution Asymmetrical Symmetrical
Definition& clarity Defined age, markedly Vague edge, slightly
hypopigmented hypopigmented
Anesthesia Early, markedly defined, Late, ill defined,
localized to skin lesion extensive over cool
or peripheral nerves areas, initially slight
Autonomic loss Early in skin& nerve Late extensive
Nerve enlargement Marked in few nerves Slight but widespread
Mucosal& systemic Absent Common
Number of M. leprae Not detachable Numerous

Diagnosis:
1- Clinical diagnosis:

Typical skin lesions, anesthesia of them "order of loss of temperature then fine
touch then pain then deep touch sensation", thickened nodular tender nerves.

* Lap diagnosis: 2- Slit skin smear test: An incision is made in the lesion after
gripping it firmly to become blood free, its base is scraped to obtain fluid form it,
the fluid is placed on glass slide, fixed over a flam then stained by Ziehl-Neelson
acid fast method to count the bacilli.

3- Skin biopsy: for morphologic features and present of bacilli.

4- Nerve biopsy.

5- Lepromin test: determines type of leprosy, indicates host resistance to M, it is

prognostic not diagnostic, prepared by injection of bacilli intradermally, strongly
positive in TT= good cell mediated immunity, weakly +v e in BT, -v e in LL BL
BB.

Medical classification& Treatment of leprosy:

1- Paucibacillary leprosy "PB": by counting the skin patches= five patches or less,
two drugs for 6 months, Rifampicin 600mg monthly, Dapsone 100mg daily.
2- Multibacillary leprosy "MB": more than five patches, two or more drugs for
1.5 to 2 years, Rifampicin 600mg and Clofazimine "Lamprene" monthly,
Dapsone 100mg and Clofazimine 50mg. "Ofloxacin and minocycline good"
NB. If the smear is +v e classify the patient as MB whatever the number of skin patches.

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Lepra reactions: During acute course of leprosy acute episodes "reactions" may occur.
Type 1 Type 2
Type of leprosy affected TT and BT LL and BL
Mechanism Alteration of cell M. I. Immune complex Mech.
C/P Redness, swelling of Erythema nodosum
skin& nerve lesions, leprosum "painful red
tenderness, loss of nodules", malaise, joint
sensory, motor "facial &bone pain, PN, iritis,
palsy& dropped feet" no change of existing
lesions
Histopathology Increased bacilli, Few fragmented bacilli
vacuolated macrophages Vasculitis
in untreated patients. Poly morpho nuclear
Treated patients: infiltrate
reduced bacilli,
increased lymphocytes,
epitheloid and giant cells
Timing of attack After starting treatment Spontaneously or whilst
or during puerperium under treatment
Treatment of lepra reactions:
1- General: Rest with appropriate sedation, early diagnosis, early initiation of
anti-inflammatory drugs, continue MDT "therapy".
2- Precipitating factors should be removed.
3- Symptomatic treatment.
4- (a)Clofazimine 300mg for a month then gradual withdrawal.
(b)Systemic corticosteroids in severe cases as neuritis "40-60mg/kg for type1
20-40mg/kg for type 2".
(c)Thalidamide 400mg "teratogenic" but "good for ENL" Erythema nodosa 2.

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Fungal Skin Disease
Classification: *Superficial fungi: affects skin primarily. A) Dermatophytes
B) Yeast like fungi *Deep fungi: affects internal organs then affects skin 2ry to it.

A)Dermatophytes
They are called ringworm infection, microscopically "septate hyphae", three genera of
them affect the man named Microsporum "skin& hair" Trichophyton "skin, hair, nail"
Epidermophyton "skin, nail" acc to genus AND M. Canis T. rubra acc to species.

NB: when animal fungi causes human infections, they usually provoke a severe
inflammatory reaction.

Mode of infection: Direct contact, Indirect "capping, bedding, towels and combs".

Clinical forms of Dermatophytes:

1- Ringworm of the scalp: "Tinea capitis" affects children
a) Scaly type: scaly well-defined erythematous patches, perforated by lusterless
brittle broken off hair, caused by T. violaceum and M. Canis.
b) Black dot type: small blade patches, infected hair becomes thinned then
breaks off leaving dark stamps in the hair follicles "Black dot appearance",
caused by T. violaceum.
NB: Resolution in scaly& Black dot is not followed by scar.
c) Kerion: deep inflammatory reaction produces a raised boggy swelling
"seropus" on the scalp, Kerion shouldn’t be incised, it is caused by animal type
of fungi "T. violaceum, m. Canis".

NB: In severe cases there is cicatricial alopecia "small circumscribed areas of

baldness and scars.

NB: Differentiated from abscess by loss of hair, boggy surface, no pain& cystic
fluctuation.

NB: Any scaly patch+ loss of hair in child's scalp should be considered
ringworm till proved otherwise.

d) Tinea favosa "favus": Sulphur Crust raised concave yellowish called the
scutulum on the scalp, caused by T. schoenleini, in its coalescence= may
involves the whole scalp+ mousy odor+ honey comp+ cicatricial alopecia
"coconut hair".
2- Ringworm of the hairless skin: "Tinea Circinata or corporis":
Infection of non-hairy skin cause by most species, asymptomatic or pruritic.

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Lesion: erythematous macule or papule then develops to annular& arciform,
advanced active borders& healing centers, usually on exposed surface of body.
3- Ringworm of the beard area: "Tinea barbae" by infected barber's instruments.
Infection in beard area& moustache= adult man, (a)Superficial type= Tinea
corporis, (b)Deeper type: pustular folliculitis& Kerion+ the angle of the jaw.
4- Ringworm of the Palms and soles: "Tinea Manum and pedis"
Tinea Manum: hyperkeratotic& erythematous scaly sheets, circumscribed
vesicular and red papular areas, on the dorsum of the hand, Accentuation of the
flexural creases of the hands.
Tinea Pedis: "Athlete's foot" it takes three forms: 1) interdigital scaling
macerations& fissures between 4th& 5th toes "the most common", 2)vesico-bullous
type occurs on the side of the toes& the dorsum of the foot, 3)hyperkeratotic
scaling type "scales" on the sides of the feet& lower heel, well defined polycyclic
scaling border. Caused by T. interdigital, T. rubrum and Epidermophyton
floccosum.
5- Ringworm of nails: "onychomycosis or Tinea Unguim" Caused by Tichophyton
and Epidermophyton. Discoloration and opacity of nail plate then thickening and
cracking, subungual hyperkeratosis, onycholysis finally.
6- Ringworm of groin: "Tinea cruris" "T. axillae if in axilla" Symptoms are intense
pruritus and discomfort. Lesion: Erythematous papules or papulo-vesicles, they
extend and form scaly patches+ well-defined raised borders.

NB: Tinea incognito or steroid modified tinea:

A fungus infection modified by wrongly applied corticosteroids. The clinical P. is
suppressed: scaling and itching only, the case relapse rapidly with more aggressive
picture, repetition of steroids relieve the condition again and so on.

Diagnosis of dermatophytes:
Clinical picture, Examination of skin scrapings "10% KOH is added to the
specimens then it is warmed to dissolve the keratin then examined under microscope
for detection of hyphae and spores", Wood's light examination gives "pale green
fluorescence" in T. schoenleini and "green fluorescence" in Microsporum,
Culture: on Sabouradu's agar medium.

Treatment of Dermatophytes:
A) Local therapy: 1- Imidazole derivatives: Ketoconazole2%, Miconazole2%,
Econazole1%, Salconazole.2- Terbinafine "5 weeks for Tinea capitis& 2weeks
for Tinea corporis cruris pedis", Whitfield's ointment "Salicylic acid3, Benzoic
acid6, Lanoline12, Vaseline100", (for Dermatophytes only). 3- Magenta paint
for inflamed T. pedis.
B) Systemic therapy: 1- Itraconazole 200mg "for one week in Tinea cruris,
corporis, pedis" and bid for one week every month "for 2 month in fingernail and
3 months in toenails". 2- Fluconazole150mg/week "for 4 weeks in Tinea cruris,
corporis, pedis" "for 3 months in fingernails & 6 months in toenail. 3-

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Griseofulvin 12.5mg/kg is fungistatic "7weeks for Tinea capitis, 3weeks for
Tinea cruris corporis pedis, 6months for fingernail& 12months for toenail. 4-
Allylamines250mg fungicidal as Terbinafine.

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B) Yeast "Pityriasis versicolor"

Chronic fungal infection by Malassezia furfur and globose yeasts, predisposed by
warm humid climate immunosuppression and pregnancy.

Clinical Picture: Lesions vary from hyperpigmented pink to brown or

hypopigmented, coalescing macules& patches+ fine scales, present in trunk& neck,
hypopigmented lesions are noted by patients during summer and sun.

Diagnosis: a) KOH preparation "smear" reveals short straight angular hyphae+

clusters of thick-walled, round, budding yeast "spaghetti and meat balls".
b) Wood's light: gold to orange fluorescence.
Treatment*Topical: Na thiosulphate30%, Na hyposulphite30%, selenium sulphate2%
Topical azole derivatives "Keto, Mi, e, salconazole" and ketoconazole shampoo,
Alcoholic Whitfield lotion.
*Systemic: Itraconazole200mg for 7 days, Fluconazole150mg/week for 4 weeks.

Yeast "Candidiasis or moniliasis"

Candida albicans is a Commensal yeast like fungus but it can change to a pathogen
"mycelial form" not "yeast form". Predisposed by Warm humid climate,
immunosuppression, pregnancy "CCP", prolonged systemic corticosteroids
"antibiotics", maceration.

Clinical picture:
1-Candidal intertriginous or flexural lesions: are moist glazed red surface peeling
border and surrounded by satellite erythematous papules or pustules in obese.
2-Erosion inter-digitalis blastomycetica: maceration between middle& ring fingers.
3-Onychia and paronychia: nail folds are red, swollen, tender, in housewives "wet".
4-Oral thrush& superficial glossitis: white curd-like pseudo-membrane of4 in mouth.
5-Angular cheilitis: "perleche" erythema, soreness& cracking at angle of mouth.
6-Monalial proctitis, vulvovaginitis.
7-Systemic candidiasis: bad general condition, organism may spread to organs.

Treatment: Topical: nystatin cream, imidazole D, gentian violet2%, Castellani's P.

Systemic: Fluconazole150mg once, Itraconazole200mg twice daily for a day,
Nystatin500.000units 3 times/day for candida reservoir.

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Viral Skin Diseases
Herpes simplex
Virus may recurrent. It predisposed to trauma, immunosuppression, systemic steroids,
cytotoxic drugs, decreased cell mediated immunity "congenital or HIV, lymphoma,"

Clinical picture:"1ry infection"

Incubation period is 4-5 days, Lesion is vesicles on erythematous base on skin or mm,
they rapidly rupture or form pustule which rupture to leave ulcers cover with crusts.
A-Herpetic gingivostomatitis: most common with type 1, affects children, gums are
red swollen and vesicle on the tongue b. mucosa then yellowish ulceration+ fever&
malaise& LN. B-Herpes progenitalis: infection with type 2, vesicles and painful
ulcers on glans penis, shaft of penis, prepuce or vulva, vagina, cervix.

Complications: a-Keratoconjunctivitis: purulent+ ulceration of conj. Edematous

eye lids. b-Inoculation herpes simplex: Direct inoculation of the virus in abrasion or
normal skin gives large bulla& vesicles "deep vesicles coalesce to form honey-comb
appearance or form large bulla".
c-Eczema herpeticum: A widespread cutaneous infection with HSV occurs in patient
with pre-existing skin disease as atopic eczema, icthyosis vulgaris, Haily-Haily, there
is severe constitutional symptoms and LN.
d-Disseminated or systemic infection: in immunocompromised and neonates not
protected by maternal antibodies, "encephalitis, aseptic meningitis, hepatitis, arthritis.

Clinical picture: of "recurrent infection"

More commonly with type 2, precipitated by trauma, febrile illness, RTI, surgery,
menstruation.
It differs from 1ry by being milder, smaller, no fever, healing without scarring.

Treatment:
1- Topical: acyclovir cream 5 times daily.
2- Systemic: acyclovir200mg oral 5 times daily, for 5 days.
3- In pregnant: cesarean section is needed to avoid neonatal viremia.

15
Varicella (chickenpox)
By varicella zoster virus, incubation period is 9-23.

Clinical picture:
Constitutional symptoms fever, malaise for 2 days, lesion is multiple papules then
turn to tense clear vesicles then to pustules surrounded by red areolae, finally dry
crust which separates without scar. Lesions are more common on face scalp
"centripetal" and all stages can be seen at the same time.

Complications: secondary bacterial superinfection as impetigo, cellulitis

hemorrhagic varicella, keratitis, encephalitis, varicella pneumonia.

Treatment: In mild cases: Rest, analgesics, soothing antiseptic lotions as gentian

violet, K permanganate 1/10000, antibiotics.
In severe cases: Acyclovir oral 400mg 5times for 7 days or IV 10mg/kg 3times.

Herpes zoster "Shingles"

A result of reactive of residual latent varicella zoster virus in sensory ganglion,
precipitated by trauma, surgery, radiotherapy, immunosuppression, uncommonly
exposure to exogenous source of the virus may trigger reactivation.

Clinical features: firstly, pain is involving a dermatome, the lesion is rash of

closely grouped red papules then they turn to vesicles then pustules over background
of erythema, along affected dermatome, mucous m is involved, must be unilateral, LN
are enlarged and tender.

Clinical presentation: 1-Ordinary type. 2-Disseminated type "more than one

dermatome and may be fatal". 3-trigeminal nerve zoster "if vesicles are on side of
the nose= nasociliary Hutchinson sign, on uvula and tonsillar bed= maxillary, ant part
of the tongue& buccal mucosa= mandibular nerve".
4-Herpes zoster oticus "vesicles and pain on ear pinna and meatus, tonsillar fossa+
pain= Ramsay Hunt= facial nerve affection, may taste or hair loss".

Complications: 1-Post herpetic neuralgia: commonest complaint so better

considered clinical manifestation. 2-Occular: uveitis, keratitis, conjunctivitis,
scarring of eyelid. 3-Hemmorrhagic, bullous or gangrenous lesion. 4-Encephalitis
or meningoencephalitis in disseminated type, elderly or immunocompromised.

Treatment:1-Analgesics, antiseptic lotions. 2-Systemic acyclovir800mg 5times

for 10Days. 3-For ophthalmic, Ramsay-Hunt S.: prednisolone60mg for 2weeks+
Acyclovir10mg/kg IV for 7days. 4-Post H neuralgia: Analgesics, prednisolone+
Carbamazepine, TCA as amitriptyline75mg, Topical capsaicin 0.025%.

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Warts (Verruca)
Incubation period: from weeks to months.

Clinical Picture:
1-Common warts "V vulgaris": firm skin-colored papules+ rough horny cauliflower
surface, 1mm to1cm and may coalesce= large plaques, present on dorsum of the hand
fingers feet, new warts develop at the site of trauma= "Kobner's phenomenon".

2-Planter warts: sharply defined, rounded with rough keratotic surface surrounded
by smooth thick keratin layer. At pressure points: heel- toes- metatarsal heads. Painful.

3-Plane warts: flat, smooth, skin-colored or greyish yellow. On the face, hands.
Koebner's present. Usually affects the children.

4-Digitiform warts: finger-like projection arises from common papule, on scalp and
beard in males. 5-filiform warts: slender soft thin finger-like projections arising
separately, common in males on the neck and face.

6-Anogenital warts: "condylomata accuminata" Soft pink elongated pedunculated

masses, sexually transmitted, grows on moist intertriginous areas as penis and
scrotum/ vagina and labial mucosa+ urethral meatus and perianal.

Treatment: 1-Keratolytic agent "salicylic acid5-20%" in flexible collodion, salicylic

acid plaster. 2- 5-flurouracil5% topical. 3-Caustics "silver nitrate, trichloroacetic acid".
4-Formalin 2% for plantar warts. 5-Topical retinoic acid: plane warts. 6-Podophyllin
resin 25% in alcohol for anogenital warts, left for 4h then washed every week, not in
pregnancy. 7-Destruction by electrodessication. 8-Cryocautery with liquid nitrogen or
CO2 snow. 9-CO2 laser. *Intralesional bleomycin. *some resolve spontaneously.
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Molluscum contagiosum
By pox virus, direct contact or sexual, incubation period is 2weeks to 6months.

Clinical picture:
Discrete, shiny, pearly-white, hemispherical papules with central umbilication. 1-
5mm. More in children on face and trunk but on genitalia in adults.

Treatment:
1-Topical retinoic acid. 2-Podophyllin cream. *Expression of the contents by forceps.
3-Electrodessication "electrocautery". 4-Cryocautery with liquid nitrogen. 5-CO2 laser.
*Some lesions resolves spontaneously.

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Parasitic skin infections
Popular urticaria

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19
Eczema (Dermatitis)
Inflammation of the skin: itching, redness, scaling, clustered papulo vesicles.
Atopy is genetic or familial, but allergy is acquired and augmentation of the reaction.

Stages of eczema: 1-Acute eczema: Erythema, minute papules and vesicles

which may rupture leading to oozing and crusts, may undergoes 2ry infection. 2-
Subacute eczema: Papules, erythema and scales are predominant, but vesicles are
less apparent. 3- Chronic eczema: no oozing or crusts, skin is dry, scaly, fissured,
pruritis may leads to Lichenification of the skin.

Classification of eczema: "Exogenous 2 and Endogenous 6"

1-Contact dermatitis Exogenous
Caused by contact of the skin with irritant or allergic sensitizer. Predisposed by very
young age, atopic tendency, low humidity.

Allergic contact dermatitis: *Immunological process "hypersensitivity",

*results from exposure of sensitized individual to allergens as nickel- chromium-
plastics- cosmetics- some topical drugs, *Acute or subacute and bilateral, not limited
to site of contact, diagnosed by the patch test.

Irritant contact dermatitis: *No immunological inflammatory reaction,

* results from exposure of the skin to external irritant agent as alkalis- acids- solvents-
fiberglass, *varied morphology and limited to the site of the contact, *Acute or
subacute or chronic "severe= acute, repeated mild= subacute of chronic.

2-Infective eczematoid dermatitis "infective Eczema"

Exogenous

It is an inflammatory reaction of the skin adjacent to the site of oozing pyogenic

infection as purulent otitis or ulcer.

*It is caused by microorganisms or their products and clear when organisms are
eradicated.

*Lesion is erythematous patches well defined oozing crusting.

*It differs from infected eczema "2ry infection of eczema".

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1-Atopic eczema Endogenous
Chronic or chronically relapsing condition characterized by itchy papules which
become excoriated and lichenified, may be associated with other atopic condition.

Stages according to age: 1-Infantile atopic dermatitis "2m to 2Y": lesion is

erythema, scaling of checks and may extend, edematous papules and superficial
vesicles may present, intense pruritus. 2ry infection& lymphadenopathy are common.
2-Childhood atopic dermatitis "2 to 12Y": less exudative than above, may be lichenified.
located in cubital and popliteal fossae, flexor wrists and ankles, sides of the neck.
3-Adulthood atopic neurodermatitis: exudative plaques, more Lichenification but
lesion is drier and thicker. *localized eczematous patches may occur in the nipple of
young women. *Young adults are like the above "2". *In older adults the distribution
is less characteristic "chronic hand eczema may predominate, sometimes eruption
may be confluent and generalized with accentuation in the flexures".

NB: Sometimes lesion involves extensors or flexors and extensors.

NB: Localized neurodermatitis (lichen simplex chronicus): In some cases, one

area is affected with severe itching and rubbing leading to circumscribed lichenified
plaques. Sites: hands, feet, anus, vulva or scrotum.

Diagnosis of atopic dermatitis: "Hanifin-Rajka criteria"

Major criteria: Pruritus, typical morphology, chronic or relapsing dermatitis,
personal or family history.

Minor criteria: skin infection, nipple dermatitis, hand dermatitis, dry skin, facial
pallor or erythema, cheilitis, recurrent conjunctivitis, orbital darkening, whit
dermographism, pityriasis alba, keratosis pilaris, Dennie-Morgan infraorbital fold.

2-Seborrhoeic eczema Endogenous

Seborrhea means excessive production of sebum. Seborrheic eczema: A chronic
condition with a characteristic red sharply margined lesions cover by greasy scales,
present in areas rich in sebaceous glands "scalp- face- upper trunk".

Clinical picture: 1-On the scalp: yellowish white greasy scales, it may extend
beyond frontal hail line = "corona seborrhoieca". 2-On the face: there is scales and
erythema. Present on nasolabial fold, retro auricular "axilla, groins also". May
blepharitis.

3-Discoid (Nummular) eczema Endogenous

Lesion is coin shaped, well-defined eczematous plaques of vesicles "minute,
closely-set, thin-walled", on an erythematous base, rupture easily leading to oozing

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and crusting, some are dry+ scaling, chronic and relapsing. Site is back of the hands,
fingers extensor aspect of forearm and legs.

4-Gravitational eczema (Venous- Varicose- Stasis)

Endogenous *Secondary to venous hypertension and stasis.

Lesion: erythematous scaly exudative eruption. Site: around the ankle and lower leg
"medial malleoli". May ass. with varicose vein, edema, hemosiderosis atrophic
changes, ulceration. It is often modified by infection and rubbing. In middle age.

5-Asteatotic eczema (Winter- Senile eczema) Endogenous

Lesion: the skin is dry, scaly and surface broken in a crisscross fashion. Site: on
dorsa of the hands, extensor aspects of limbs. Associated with decrease in skin surface
lipids due to "dry cold winds, old age, low humidity, malnutrition, solvents on hand".

6-Pompholyx Endogenous
Type in which sudden attacks of crops of deep clear vesicles with no erythema and
may preceded by heat, irritation sensation. Site: on palms, fingers, soles. *It subsides
spontaneously but usually recurrent.

Treatment of eczema: all types

1-Correction of predisposing factors: avoid solvents& sensitizers, treatment of
varicose veins& foci of infection.
2-Broad spectrum antibiotics in cases of 2ry infection.
3-oral antihistamines. 4-short course of systemic steroids in acute severe cases.
5-Topical corticosteroids: twice daily for 10-21days "creams for acute& S but
ointment for dry chronic cases.
6-Topical immunomodulators: tacrolimus 0.03% ointment.
7-Topical emollients: Vaseline for dry skin and chronic.
8-Ultraviolet rays' therapy with PUVA and narrowband UVB "NBUVB".

22
Urticaria and Angioedema
Urticaria: Attacks of itchy well-demarcated, reddish, evanescent swelling of the
skin, ass. With pruritus and burning sensation. It may be acute "continuously or
intermittently for less than 6weeks" or chronic "if present more than 6weeks".

Angioedema: swelling of deep dermal and subcutaneous "or submucosal" tissues.

Swellings are painful rather than itchy, poorly defined, pale or skin colored.

Causes of urticaria:
1-Food: additives, preservatives, fishes, eggs, banana.
3-Contact urticaria: pollens, dust of animal fur. 4-Septic foci: in teeth, tonsils or UT
5-Intestinal parasites. 6-Insect bites or stings: causes papular urticaria.
7-Medical causes: hepatitis, H. pylori, obstructive jaundice.
8-Drugs: NSAIDs, antibiotics as penicillin. 9-Stress. 10-Serum sickness.

Pathophysiology: 1-Allergic: histamine is important mediator in urticaria, mast

cells are the major histamine releasing cells in the skin etc. 2-Non allergic: direct
degranulation of mast cell occurs without antigen antibody reaction due to the effect
of substances as "Aspirin, NSAIDs, neuropeptide, rifampicin, ciprofloxacin, vancomycin".
3-Physical urticaria: physical causes as heat, water, or pressure.

a. dermographism: sharply localized edema or wheel surrounding by erythematous

flare occurring within seconds after the skin has been stroked.

b. Solar urticaria: urticaria develops after few minutes of exposure to sunlight.

c. Cold urticaria: urticaria develops on exposure to cold.

d. Cholinergic urticaria: small wheels associated with sweeting due to heat or

emotional stress.

Treatment:

1-treatment of the cause. 2-AntiH1 antihistamines "classic as chlorpheniramine

maleate" and "non-sedating as cetirizine hydrochloride, loratadine". 3-AntiH2 may be
needed in addition to antiH1 "cimetidine, ranitidine".
4-Systemic steroids in severe cases Prednisolone 1mg/kg.
5-Epinephrine 1/1000 in solution subcutaneously 0.5ml in cases associated with
edema of the glottis. 6-locally: calamine lotion for soothing pruritis.

23
Reactive Erythema
Erythema multiforme
An immune-mediated disease characterized by target lesions on the hands and feet.

Causes:
1. Idiopathic 50%. 2. Viral: HSV. 3. Bacterial: streptococci. 4. Fungal:
coccidioidomycosis. 5. Drugs: penicillin, sulfonamide. 6. Others: pregnancy,
malignancy, LE.

Clinical picture:
lesion is red rings with central pale, site is on the hands and feet, may involve oral
conjunctiva or genital mucosa, if it is severe "Stevens Johnson's" it may be
generalized with extensive blistering.

Treatment: 1. Treatment of the cause. 2. Antihistamines. 3. Systemic steroids.

Erythema nodosum
It is an inflammation of subcutaneous fat, consisting of tender red nodules on the
edges.

Causes:
Idiopathic 20%. Viral: as cat scratch fever. Bacterial: streptococci, leprosy, TB.
Fungal: deep fungal as coccidiomycosis. Drugs: sulfonamides, CCPs.

Clinical picture:
Deep firm and tender reddish-blue nodules 1-5 cm, on claves and shins. Joint pain
and fever may occur.

Treatment: NSAIDs.

24
Papulo squamous Diseases
Psoriasis
It is a chronic inflammatory and proliferative skin disease, affects about 1-2%.

Cause: genetic predisposition with triggering factors:

Trauma "chemical, physical… etc. can elect psoriatic lesions as Koebner's
phenomenon", Weather "worse in winter, Infection "streptococcal", Drugs
"NSAIDs, antimalarial, beta blockers, ACE I", Endocrinal F "hypoparathyroidism
leads to hypocalcemia which triggers pustular psoriasis, Emotional stress.

Histopathology: Epidermis: parakeratosis "accelerated incomplete keratinization

of horny cell with retention of nuclei", absent granular cell layer, regular acanthosis
and elongation of club shaped rete ridges, supra-pupillary thinning of epidermis,
Munro micro-abscesses in stratum corneum, Spongiform pustules.

Dermis: Elongation and edema of dermal papillae, Dilated tortuous capillaries in the
upper papillae, perivascular inflammatory infiltrate "monocytes and neutrophil" in
upper dermis.

Pathogenesis: Epidermal keratinocyte hyperproliferation, Mitotic rate is many

times higher than normal, the time of epidermal cell maturation in psoriatic skin is 3-4
days "normal 26-28 days", T-cell mediated inflammatory process "T h1 cell".

Koebner phenomenon: Development of isomorphic= "having the same form"

pathologic lesions if the normal skin exposed to trauma in patients with psoriasis.

NB: Reverse Koebner reaction is clearance of existing psoriasis following injury.

NB2: Diseases displaying Koebner: Psoriasis, Lichen planus, Pityriasis rubra pilaris,
vitiligo, warts, molluscum contagiosum.

Clinical picture: 1ry Lesion is a full rich red "salmon pink" papule covered with
silvery laminated scales "can be removed easily", Papules may enlarge or coalesce
forming plaques. Site: extensor surfaces of limbs "elbows, knees", scalp and nails.
Grattage test: scraping of psoriatic lesion "with edge of a glass slide" results in
removal of scales layer after layer+ accentuation of silvery appearance until a smooth
glossy red membrane is finally left.
Auspitz sign: On scratching this membrane pinpointing hemorrhage appears.

Morphological patterns according to size and shape of lesions:

1- Punctate psoriasis "pin-point size". 2- Guttate psoriasis "size of drops".

25
3- Discoid psoriasis "coin shaped". 4- Annular p. "ring shaped produced by involution
of the center of the lesions".
5- Geographic P. "curved patterns produced on a large areas of the back". 6-Linear
psoriasis.

Clinical varieties: 1-psoriasis of scalp: scaly erythematous plaques, not crossing the
hair line, "DD from seborrheic dermatitis". 2-Flexural psoriasis: lesions are itchy
pink glaze with no scales due to continuous friction. 3-Psoriasis of palms and soles:
may be either "Typically scaly plaques, Thick fissured plaques like hyperkeratotic
eczema, Pustular" 4- Psoriasis of nails: pitting, yellowish discoloration, central area
of discoloration "oil drop", onycholysis. 5-Erythrodermic type: generalized
erythema and scaling. 6-Arthropathic psoriasis: arthritis, negative rheumatoid
factor.
7-Pustular psoriasis: the 1ry lesion is a sterile pustule.

Treatment:

A-Topical: 1-Tar: crude coal tar2-5%. 2-Salicylic acid: 3-5% keratinolytic.

3-Corticosteroids ointment. 4-Intralesional corticosteroid injection: triamcinolone
acetonide in localized resistant plaques, less effective in nail.
5-Calcipotriol ointment: "vit D analogue" It inhibits keratinocyte proliferation.
6-Anthralin 1%.

B-Systemic: 1-Methotrexate: 5mg/12hours for 3 doses every week, indicated in

erythrodermic and pustular psoriasis. 2-Cyclosporin A: 5mg/kg/day for severe cases.
3-Retinoids: acitretin 1mg/kg/day in severe cases. 4-photochemotherapy: (PUVA)
psoralens 0.6mg/kg 2hous before exposure to UVA rays 3 times weekly.
5-Phototherapy: narrowband UVA rays (NBUVA).

NB: Diseases treated by photochemotherapy and phototherapy: Psoriasis, Lichen

planus, Pityriasis rubra pilaris, vitiligo, pompholyx "eczema".

NB: Indications for intralesional injection of corticosteroids: Keloid, Hypertrophic

lichen planus, Discoid lupus, Post scabietic nodules, Localized chronic persistent
eczema, Alopecia areata, Cystic acne vulgaris.

NB: Disease treated by PUVA only: Alopecia areata.

NB: Disease treated by NBUVB rays only: Pityriasis Rosa.

26
Lichen planus
Itchy chronic inflammatory disease which affects skin and mucus membranes.

Pathogenesis: Genetic predisposition. Autoimmune. Hepatic c infection "strong

association". Emotional stress.

Histopathology: 1-Compact hyperkeratosis. 2-Focal hyper granulosis. 3-Irregular

acanthosis "thickened inner layer of the skin" and irregular elongation of rete ridges.
4-Liquefactive degeneration of basal layer. 5-Band like inflammatory infiltrate.

Clinical picture:
1-Primary lesion is pruritic shiny violaceous flat-topped papule which retains the
skin lines and shows white streaks (Whickham's striae). Site: on ankles, wrist, shin in
hypertrophic type but annular type located in lumbar region and glans penis.
2-Papules may coalesce into plaques or show linear distribution as apart of Koebner
phenomenon. Annular lesions are formed by arranged papules or single large papules.
3-Mucous membrane lesions are very common and may occur alone.
4-After disappearance of the lesions deep pigmentation is left for several months.

Clinical varieties of lichen planus:

1-Atrophic lichen planus "fading annular". 2-Hypertrophic. 3-Linear. 4-Annular
"glans penis". 5-Lichen planus bullous. 6-Lichen planus pigmentosus.
7-Lichen planus of the nails "linear ridges, groves and thinning of nail plate*.
8-Lichen planus of palms and soles "non itchy papules". 9-Lichen planus of mucus
membrane "may be white streaks on the buccal mucosa, white plaques on the tongue
or ulcerative". 10-lichen planus actinicus on sun exposed areas " annular in shape-
violet brown center +hypopigmented edge". 11-Lichen Plano-pilaris "follicular
papules result in cicatricial alopecia.

Treatment:
1-Avoide stress. 2-Topical: fluorinated steroid ointment, Intra-lesion steroids "in
hypertrophic type", tacrolimus.
3-Systemic: Antihistamines, systemic steroids (20mg/day for 6weeks in severe cases/
ulcerative mucus membrane or lichen Plano pilaris to prevent cicatricial alopecia),
Cyclosporine A, NBUVB and PUVA, Retinoids, Antimalarial for actinic L.P.

27
Pityriasis Rubra pilaris
A chronic disease characterized by follicular hyperkeratosis, orange red erythema,
branny scales, palmoplantar keratoderma.

Etiology: Unknown, it may be dominantly inherited or vitamin A deficiency.

Clinical picture: 1-Patches showing keratotic follicular papules. 2-Erythroderma

with islands of normal skin. 3-Follicular hyperkeratosis of proximal phalanges of
fingers and toes+ hyperkeratosis of palms& soles. 4-Nails are rough& dystrophic.
5-Scaly erythematous areas simulating Psoriasis+ scales of scalp.

Types:
1-Classical adult 55%. 2-Classical juvenile 10%. 3-Atypical adult 5%.
4-Atypical juvenile 5%. 5-Circumscribed juvenile 25%.

Treatment:
1-Emollients to reduce scaling. 2-Topical steroids& salicylic acid ointment.
3-Methotrexate 25mg/week. 4-Oral vit A 300000 IU/day. 5-NBUVB.
6-PUVA. 7-Topical vitamin D analogues.

Pityriasis Rosea
Acute, self-limited disorder characterized by superficial scaly lesion on the trunk.
Common on spring and autumn.

Etiology: Virus "HHV6-7", autoimmune, drug induced as captopril

&metronidazole& barbiturates.

Clinical picture: 1-primary lesion is herald patch, rosy-red, round or oval patch
covered by collarette of scales, site: trunk& knee& UL. 2-after 15 days it become
multiple, the long axes follows lines of cleavage& parallel to ribs in Christmas tree
pattern. 3-the eruption fades within 4-8 weeks.

Types: 1-Classical "more on the trunk& neck& UL". 2-Inverted "more in face&
extremities not the trunk". 3-Localized "limited to one region of the body". 4-Abortive
"no secondary eruption follows the herald patch".

Treatment:
1-Reassurance. 2-Calamine lotion. 3-Antihistaminics. 4-Narrow band UVB.

28
Lupus Erythematosus
Chronic cutaneous LE

29