Ultimate Exam Guide: Dermatology

Lecture 1: Viral Skin Diseases (5 MCQs)

Herpes Simplex Virus (HSV) Infections
  • Herpetic Whitlow: Infection of the pulp of a finger tip. Primarily occurs in children with oral herpes (due to thumb sucking) and in dentists (occupational hazard).
  • Herpetic Keratoconjunctivitis: Begins as marginal keratitis or corneal ulcer. Extremely dangerous as it may end in blindness.
  • Recurrent Erythema Multiforme Minor: Usually caused by recurrent Herpes Simplex Virus Type 1 (HSV-1) orolabial disease. Characterized by typical target (iris) lesions on the palm, elbow, knee, and oral mucosa.
  • Disseminated Herpes Simplex Infection: Occurs especially in premature newborns, malnourished infants, and immunocompromised persons.
  • Eczema Herpeticum: Occurs in patients with Atopic Dermatitis, may lead to rapid spread of the virus throughout the eczematous area.
  • Diagnosis: Clinical. Tzanck Smear (Non-specific, positive for both HSV and VZV showing multinucleated giant cells). Direct Fluorescent Antibody Test (DFAT), Viral culture, Polymerase Chain Reaction (PCR), Biopsy.
  • Treatment: Aim is to shorten the attack, manage symptoms, and prevent recurrence (but NOT to cure). Acyclovir 200mg 5 times daily for 5 days for acute attacks. Acyclovir 400mg twice daily for recurrent lesions.
Varicella Zoster Virus (VZV): Chickenpox & Shingles
  • Transmission: The virus can spread 2 days BEFORE the rash develops and continues until blisters fully crust over. Spreads through contact for at least 15 minutes, touching blisters, or respiratory secretions. A susceptible person can get Chickenpox by touching Shingles lesions.
  • Varicella (Chickenpox) Treatment: Bland antipruritic lotion, cool wet compresses, antipyretics. Acyclovir in the first 24 hours of illness provides better symptomatic relief.
  • Herpes Zoster (Shingles): Caused by Varicella Zoster Virus which remains latent in the sensory dorsal root ganglion cells after natural infection.
  • Clinical Presentation: Unilateral dermatomal distribution of erythematous papules and plaques (mainly thoracic, cranial, and lumbar). Preceded by several days of severe pain.
  • Complications (High-Yield):
    • Disseminated Herpes Zoster: Defined as more than 20 lesions outside the primary affected dermatome. Mostly seen in old/debilitated individuals.
    • Ophthalmic Zoster: Causes uveitis or keratitis.
    • Motor nerve neuropathy.
    • Post-Herpetic Neuralgia (PHN): Defined as persistent pain ONE month after the onset of zoster infection.
  • Treatment: Bed rest, gentle pressure/heat to reduce pain. Acyclovir 800 mg FIVE times daily for 7 days.
Molluscum Contagiosum
  • Organism: Molluscum Contagiosum Virus (MCV), a double-stranded DNA virus related to the poxvirus. Crucially, it does NOT develop latency like herpes viruses.
  • Clinical Appearance: 2-5mm firm, dome-shaped pearly white papules with a highly characteristic central umbilication.
  • Transmission & Site: Direct skin-to-skin contact. In children, affects face, trunk, extremities. Crucial Point: If restricted to the genital area in a child, sexual abuse MUST be considered. In adults, it is a Sexually Transmitted Disease (STD) favoring the lower abdomen, thighs, and genitalia.
  • Disease Course: Individual lesions last 2-8 weeks. Autoinoculation causes new lesions; total infection duration can be up to 8 months.
  • Diagnosis: Microscopic exam of core material treated with Potassium Hydroxide (KOH) preparation shows inclusion bodies within keratinocytes.
  • Treatment: Curettage (avoid in cosmetic areas), Cryotherapy, Podophyllotoxin 0.5%, Salicylic acid, Trichloroacetic Acid (TCA) peel 35%, Immunomodulator (Imiquimod 5% cream/Aldara applied 3 times/week for 4 weeks), Oral Cimetidine 30mg/kg/day.
Warts (Verruca & Human Papillomavirus - HPV)
  • Planter Warts (HPV-1): Generally appear at pressure points on the ball of the foot. Sometimes grouped to form a mosaic wart. May be confused with corns or calluses, but plantar warts have a soft central core and black dots (thrombosed capillaries) that calluses lack.
  • Genital Warts (Condylomata Acuminata): The most common sexually transmitted disease.
    • HPV types 6, 11 result in Benign lesions.
    • HPV types 16, 18, 31, 33, 35 are strongly associated with Anogenital Dysplasia & Squamous Cell Carcinoma (SCC) (High-risk oncogenic types).
  • Transmission & Presentation: Transmitted via sexual contact and microabrasions allowing virions into the basal cell layer. Can be transmitted from mother to neonate causing laryngeal papillomatosis. Appears as gray/pink lobulated papules or cauliflower-like mass.
  • General Treatments for Warts: Depends on type, age, and previous therapy. Options include:
    • Topical salicylic acid (with or without lactic acid).
    • Topical 5-Fluorouracil (5-FU) cream.
    • Light Cryotherapy or CO2 laser destruction.
    • Local Bleomycin injection.
    • Oral Cimetidine (30-40 mg/kg/day) for immunomodulatory effect.
    • Podophylline 10-25% or Trichloroacetic Acid (TCA) / Bichloroacetic acid 35-85% (caustic agents).
Human Immunodeficiency Virus (HIV) & AIDS
  • Pathogenesis: HIV belongs to Retroviruses (an RNA virus converted to DNA in the host cell under the effect of the Reverse Transcriptase Enzyme). It infects Human CD4+ T-helper cells leading to progressive immunodeficiency.
  • AIDS Definition: End-stage disease occurs when the CD4+ T-lymphocyte count reaches less than 200 cells per ml.
  • Cutaneous Manifestations (3 Groups):
    1. Infections (Opportunistic): Chronic Herpes Simplex Virus (HSV) ulcers, Chickenpox, Disseminated Herpes Zoster, Molluscum Contagiosum, Warts, severe Candidiasis, Dermatophytosis, and Syphilis.
    2. Inflammatory Dermatoses: Severe Seborrheic Dermatitis, Atopic Dermatitis, Psoriasis, Ichthyosis, Xeroderma, and adverse drug reactions.
    3. Neoplasms: Highly associated with HIV/AIDS, including Kaposi Sarcoma, Superficial Basal Cell Carcinoma of the trunk, Squamous Cell Carcinoma (cervix/anal canal), and Extranodal B-cell Lymphoma.
  • Unique HIV conditions: Oral hairy leukoplakia, eosinophilic folliculitis, bacillary angiomatosis.
  • Diagnosis & Monitoring: Clinical signs. CD4+ T lymphocyte count is used to monitor the degree of immunodeficiency. HIV/AIDS RNA (Viral Load) is used to monitor response to therapy.
  • Treatment: Since HIV destroys helper T cells, effective treatment reverses the natural history using combinations of anti-retroviral agents called HAART (Highly Active Anti-Retroviral Therapy).
💡 High-Yield Hints for Lecture 1
  • Dentists presenting with painful fingertip vesicles? Think Herpetic Whitlow.
  • A patient presenting with multinucleated giant cells on a Tzanck smear has an active Herpes (HSV or VZV) infection, but it doesn't specify which one.
  • Acyclovir shortens attacks but does NOT cure the latent herpes virus.
  • Plantar warts have black dots (thrombosed capillaries), distinguishing them from calluses.
  • Molluscum Contagiosum Virus (MCV) uniquely does NOT establish latency in nerve ganglia.
  • A CD4+ count dropping below 200 cells/ml officially diagnoses AIDS.

Lecture 2: Bacterial Skin Infections (5 MCQs)

Skin Flora & Basic Infections
  • Resident Flora (Normal/Harmless): Consists mainly of Staphylococcus epidermidis, Corynebacterium, Propionibacterium acnes, and Pityrosporum ovale (a monocellular yeast). Only cause disease in immunocompromised/AIDS patients.
  • Transient Flora: Includes most pathogenic bacteria.
  • Treatment of bacterial infections: Localized: Antiseptics (Potassium permanganate), Topical antibiotics (Mupirocin/Bactroban, neomycin, fusidic acid). Widespread: Systemic antibiotics (flucloxacillin, 3rd generation cephalosporin).
  • Ecthyma: An ulcerative DEEP Staphylococcal or Streptococcal pyoderma. Nearly always occurs on the shins or dorsal feet. Heals after a few weeks leaving SCARS. Predisposing factors: uncleanliness, malnutrition, trauma.
Cutaneous Tuberculosis (Mycobacterium tuberculosis)
  • Caused by Mycobacterium tuberculosis. Classified into 4 categories: Exogenous inoculation, Endogenous spread, Hematogenous spread, and Tuberculids (allergic reaction, no pathogen in lesion e.g., Erythema Induratum/Bazin's disease).
  • Lupus Vulgaris (Hematogenous spread): Single plaque composed of grouped red-brown papules. Key Diagnostic Sign: When blanched by diascopic pressure (glass slide), it shows a classic Apple Jelly Color. Occurs on head/neck in persons with high immunity. Slowly progressive, destructive, leaves deformed scars.
  • Scrofuloderma (Endogenous spread): Direct extension from underlying tuberculous lymphadenitis (most frequently cervical Lymph Nodes). Multiple nodules drain to form sinuses/ulcers. Heals with characteristic cord-like scars.
Leprosy (Hansen's Disease)
  • Diagnosis: Clinical (skin & nerve involvement). Biopsy of skin/nerve stained with Fite-Faraco stain. Slit skin smear of cooler areas (earlobes, elbows, knees) stained with Acid-Fast Stain.
  • Lepromin Test: NOT used for diagnosis. It is a classic test for Cell-Mediated Immunity to help classify a given case (Prognostic/Classificatory tool).
  • Treatment (Highly Tested):
    • Paucibacillary (TT - Tuberculoid): Rifampicin 600mg + Dapsone 100mg daily for 6 months. Then Dapsone monotherapy for 3 years.
    • Multibacillary (BB, BL, LL): Rifampicin 600mg + Dapsone 100mg + Clofazimine 50mg for 3 years.
💡 High-Yield Hints for Lecture 2
  • Unlike Impetigo, Ecthyma is deep and heals with SCARS.
  • Apple jelly nodules upon diascopy = Lupus Vulgaris (Cutaneous TB).
  • Scrofuloderma specifically heals with cord-like scars.
  • Fite-Faraco stain is specific for skin/nerve biopsies in Leprosy.
  • Never use the Lepromin test to diagnose Leprosy; use it only to classify the type/immunity level.

Lecture 3: Fungal Infections of the Skin (4 MCQs)

Dermatophytosis (Tinea Infections)
  • Tinea Capitis (Scalp):
    • Inflammatory (Kerion): Scaly erythematous papular eruption with loose/broken-off hairs. Develops into a boggy, painful swelling with multiple pustules (Kerion). Results in scarring and permanent alopecia.
    • Favus: Diffuse foul-smelling yellow crustation surrounding hairs in a cup-shaped crust called Scutula. May end in scarring alopecia. Rare in Iraq.
  • Tinea Barbae (Beard): Affects bearded area in males. Mostly unilateral. Deep nodular suppurative or superficial crusted patches with folliculitis. Painful and tender.
  • Tinea Corporis (Body): Affects trunk/limbs (excluding hands, feet, groin). Annular (ring-shaped) lesion with an erythematous, scaly, sharply circumscribed active inflamed border and central clearing/scaling. Mainly caused by Trichophyton rubrum.
  • Tinea Cruris (Groin/Jock Itch): Men > Women. Risk factors: hot humid climate, occlusion, obesity, chronic use of topical steroids. ALWAYS associated with Tinea Pedis. Sharply demarcated red scaly plaque with active border.
  • Tinea Faciae (Face): Affects face in females, and non-bearded areas in males.
  • Tinea Unguium (Onychomycosis): Superficial or deep nail infection. Affects free edge causing yellow discoloration, ridging, subungual hyperkeratosis, and onycholysis. Extremely difficult to treat.
  • Tinea Manuum (Hands): Usually unilateral fine powdery scales on palmar creases. Pathogen: Trichophyton rubrum. Highly associated with Tinea Pedis.
  • Tinea Pedis (Athlete's Foot): Age 20-50. 4 clinical types:
    1. Interdigital: Commonly between 4th and 5th interdigital web spaces. Maceration, fissuring.
    2. Moccasin: Confined to the heel. Well-demarcated erythema with minute papules on margin, scaling, hyperkeratosis.
    3. Inflammatory Bullous: Vesicles/bullae in web spaces/instep. Pus if Staphylococcus aureus superinfection. May be associated with Id reaction.
    4. Ulcerative: Interdigital space extending to plantar/dorsal surfaces.
    Organisms: Trichophyton rubrum, Trichophyton mentagrophytes, Epidermophyton floccosum.
  • Tinea Incognito: Misdiagnosed tinea treated with potent topical steroids, causing loss of characteristic fungal features. Most common in Tinea Cruris, Faciae, and Manuum.
Diagnosis & Treatment of Fungal Infections
  • Diagnosis:
    • Wood's Light (Ultraviolet light 365 nm): Extremely useful for Microsporum species which give a Green Fluorescence in a dark room.
    • Skin Scraping: Direct microscopy using 10-20% Potassium Hydroxide (KOH) shows spores and hyphae.
    • Culture: Sabouraud's glucose agar for 7-14 days.
  • Topical Treatment: Imidazoles (Clotrimazole, Miconazole), Tolnaftate, Whitfield's ointment (3% salicylic acid + 6% benzoic acid). Apply for 4 weeks (continue 1 week after clearing, apply 3 cm beyond margin). Crucial MCQ: Topical treatments are INEFFECTIVE for Tinea Capitis, Tinea Barbae, and Tinea Unguium (Nails).
  • Systemic Treatment: Required for Capitis, Barbae, Unguium, inflammatory tineas, and extensive/hyperkeratotic Tinea Pedis.
    • Terbinafine: Inhibits fungal squalene epoxidase. Fungicidal, but NOT effective against Candida or Pityriasis Versicolor.
    • Ketoconazole / Itraconazole / Fluconazole: Imidazole group acting on cytochrome P-450. Broad spectrum (effective against Candida & P. Versicolor). Side effects: hepatitis, teratogenicity.
Candidiasis (Candida albicans)
  • Pathogenesis: Unicellular yeast, normal commensal in GIT/anogenital area. Opportunistic.
  • Oral Thrush: Newborn infants (vaginal tract transmission) or immunocompromised/AIDS. White patches on buccal mucosa/tongue. Scraping leaves a raw bleeding area.
  • Angular Cheilitis (Perleche): Bilateral at angles of mouth. Common with ill-fitting dentures.
  • Candidal Vulvovaginitis / Balanitis: Sore, itchy, macerated wet erythema. Risk factors: Diabetes, HIV, pregnancy, uncircumcised males. Symptoms: pruritus, discharge, dyspareunia. Recurrent Vulvovaginal Candidiasis (VVC) is defined as THREE or more episodes per year.
  • Candidal Intertrigo: Moist glazed macerated erythema with characteristic Satellite Pustules on opposing skin surfaces (groins, axillae, inframammary).
  • Napkin (Diaper) Candidiasis: Involves the skin folds with satellite lesions (differentiates it from irritant diaper dermatitis which spares folds).
  • Erosio Interdigitalis Blastomycetica: Oval white macerated skin on the web spaces of fingers.
  • Chronic Paronychia: Mixed Candidal & Bacterial (Staph, Pseudomonas) infection of fingernails. Common in housewives due to continuous use of detergents causing cuticle loss.
  • Congenital Cutaneous Candidiasis: Passage through birth canal. Manifests hours after delivery. Spares oral cavity and diaper area.
  • Diagnosis: Swab for KOH shows spores and pseudohyphae. Test Blood Sugar for recurrent cases.
  • Treatment: Gentian violet (drying), Nystatin (effective ONLY against Candida, not dermatophytes), Imidazoles like Clotrimazole (effective against BOTH Dermatophytes and Candida).
Pityriasis Versicolor
  • Pathogen: Chronic commensal yeast infection caused by Malassezia furfur (the pathogenic phase of Pityrosporum orbiculare/ovale, a resident skin flora).
  • Clinical: Hypo- or hyper-pigmented macules and patches with fine scaling on the trunk. Asymptomatic or mild itching. Common in young adults with high sebum secretion.
  • Triggers: Warm climate (summer), hyperhidrosis, oily skin, glucocorticoids, immunodeficiency.
  • Diagnosis:
    • Wood's Light: Yellow / Lemon color fluorescence.
    • Skin Scraping (KOH): Shows classic Spaghetti and Meatball appearance under microscope.
💡 High-Yield Hints for Lecture 3
  • Tinea Cruris is almost always linked to a concurrent Tinea Pedis. Always check the feet!
  • Applying topical steroids to a fungal infection modifies its appearance, known as Tinea Incognito.
  • Terbinafine is excellent for Dermatophytes but useless for Candida and P. Versicolor.
  • Nystatin cures Candida but is useless for Dermatophytes. Imidazoles cure both!
  • Satellite pustules involving the skin folds in a baby = Candidal Diaper Dermatitis (Irritant dermatitis spares folds).
  • "Spaghetti and Meatballs" on KOH = Malassezia furfur (Pityriasis Versicolor).

Lecture 4: Diseases of Hair (9 MCQs)

Normal Hair Physiology & Cycle
  • Anagen Phase: Growing hairs. Lasts about 3 years (1000 days). Makes up 85%-90% of scalp hair.
  • Catagen Phase: Transitional phase. Lasts 1-2 weeks. Growth ceases, formation of club hair begins.
  • Telogen Phase: Resting phase (club hairs). Lasts 3-4 months (about 100 days) before shedding. Makes up 10-15% of scalp hair.
  • General Facts: Scalp has ~100,000 hairs. Daily shed: 100-150 hairs. Shaving/menstruation has NO effect on growth rate.
  • Hair Types: Lanugo (fine fetal hair), Vellus (fine unpigmented on child face/arms), Terminal (coarse, thick, dark on men's face/chest).
Alopecia Areata (Non-Cicatricial Focal Alopecia)
  • Rapid, complete hair loss in round/oval, uninflamed, non-scaly patches.
  • Hallmark Sign: At the periphery of the bald patch, loose broken hairs show a tapered attenuated bulb called Exclamation Marks (!).
  • Histology: Helper T-cell dominant lymphocytic infiltration at the peribulbar area of anagen follicles. Drives follicle into abnormal catagen. (Autoimmune T-cell mediated).
  • Poor Prognostic Factors (MCQ): Early childhood onset, Association with atopy, Down syndrome, autoimmune disease, Widespread involvement, Positive family history, Ophiasis (band-like hair loss at scalp periphery), Onychodystrophy (nail involvement), Duration more than 5 years.
  • Treatment: Intralesional steroid injection (for localized like eyebrows), high strength topical steroids, Topical Anthralin 1% (15-20 min contact), Topical Minoxidil. For extensive cases: Induction of contact sensitivity (Dinitrochlorobenzene - DNCB), PUVA, high-dose oral Prednisolone for rapidly progressive cases.
Androgenetic Alopecia & Diffuse Shedding (Effluviums)
  • Androgenetic Alopecia: Gradual hair loss from vertex and frontotemporal regions (bitemporal recession). Parietal and occipital areas spared.
    • Pathogenesis: Polygenic inheritance. Adequate androgen stimulation. Key mechanism: Increase in 5-alpha reductase enzyme in the bald area (converts testosterone to DHT). Lengthening of telogen and shortening of anagen leads to follicle miniaturization.
    • Treatment: 2-5% Topical Minoxidil solution (best for duration <10 yrs, area <10cm). Finasteride 1 mg/day (Type 2 5-alpha reductase inhibitor, lowers DHT in scalp/serum, used 6-12 months). Hair transplant (minigraft from occipital to anterior).
  • Telogen Effluvium: Excessive loss of normal club (telogen) hairs. Diffuse shedding.
    • Triggers: Surgery, parturition (childbirth), high fever, severe stress, rapid weight loss. Drugs: Metoprolol, Captopril, Propranolol, Bromocriptine.
    • Pathology: Precipitates anagen hairs prematurely into catagen/telogen. Stops spontaneously once trigger is removed.
  • Anagen Effluvium: Hair loss occurring in the anagen phase, frequently following Chemotherapy (antimetabolites, cyclophosphamide). Apparent 1-2 months after starting drugs. Reversible upon stopping.
Cicatricial Alopecia, Hirsutism & Hypertrichosis
  • Cicatricial (Scarring) Alopecia: Tissue destruction, inflammation, atrophy.
    • Primary: Systemic Lupus Erythematosus (SLE), Lichen Planopilaris, Pseudopelade of Brocq, Dissecting Folliculitis, Acne Keloidalis Nuchae.
    • Secondary / Congenital: Post-trauma, post-infection (e.g. Kerion/Favus).
  • Hirsutism: Male-pattern terminal hair growth in women (androgen-dependent).
    • Causes: 1. PCOS (Stein-Leventhal syndrome): Menstrual irregularity, acne, androgenetic alopecia. Check Luteinizing Hormone / Follicle Stimulating Hormone (LH/FSH) ratio.
      2. Ovarian tumors (Arrhenoblastoma, Leydig cell).
      3. Adrenal causes (Congenital Adrenal Hyperplasia, Adenoma/Carcinoma -> Virilization).
      4. Pituitary (Cushing's, Acromegaly, Prolactinoma).
      5. Drugs (Phenothiazine, high progestin, birth control).
    • Investigations: Total Testosterone & DHEA-S (mild hirsutism). Overnight dexamethasone suppression (Cushing's). 17-hydroxyprogesterone & ACTH stimulation (late-onset CAH).
    • Treatment (Antiandrogens): Cimetidine (weak), Ketoconazole (hepatotoxic risk), Cyproterone acetate + ethinyl estradiol, Spironolactone (strong anti-androgen, 75-200 mg daily).
  • Hypertrichosis: Overgrowth of hair NOT localized to androgen-dependent areas.
    • Generalized Congenital: X-linked dominant. Entire body covered with fine villous hair (spares palms/soles). Causes: Fetal Hydantoin Syndrome, Fetal Alcohol Syndrome, maternal Minoxidil use.
    • Generalized Acquired: Secondary to drugs (Minoxidil, Cyclosporine, Danazol, Corticosteroids).
💡 High-Yield Hints for Lecture 4
  • Patchy hair loss with no scaling and no inflammation + Exclamation mark hairs = Alopecia Areata.
  • Hair loss 3 months after childbirth or major surgery is due to Telogen Effluvium.
  • Finasteride works by inhibiting Type 2 5-alpha reductase, stopping the conversion of Testosterone to DHT.
  • Hirsutism follows a male pattern and is androgen-driven; Hypertrichosis is generalized/localized overgrowth independent of androgens.
  • Hair loss immediately following Chemotherapy is Anagen Effluvium.

Lecture 5: Bullous Diseases of the Skin (4 MCQs)

Levels of Blisters & Pemphigus (Intra-epidermal)
  • Sub-corneal bullae: Bullous impetigo, miliaria crystallina, Staphylococcal Scalded Skin Syndrome (SSSS).
  • Intra-epidermal bullae: Pemphigus, acute eczema, viral vesicles.
  • Sub-epidermal bullae: Bullous Pemphigoid, Pemphigoid Gestationis, Dermatitis Herpetiformis, Epidermolysis Bullosa, Bullous erythema multiforme/SLE/Lichen planus, Linear IgA disease.
  • Pemphigus (Autoimmune):
    • Affects young people in Iraq (30-40 years), elderly elsewhere.
    • Types: Superficial (Pemphigus foliaceus, Pemphigus erythematosus). Deep/Suprabasal (Pemphigus vulgaris, Pemphigus vegetans).
    • Pathogenesis: Autoantibodies of Immunoglobulin G (IgG) type directed against the desmosomes between keratinocytes. Specifically binds to Desmogleins (transmembrane glycoproteins). Causes keratinocytes to split (Acantholysis) forming INTRA-epidermal vesicles.
    • Prognosis: Antibody titer correlates directly with severity. Very high titers are lethal.
    • Clinical: Easily ruptured flaccid bullae. Fluid becomes hemorrhagic/seropurulent. Ruptures into painful erosions covered with crustations. Because they are superficial, patients often present with generalized crustations rather than intact bullae.
    • Diagnosis: Skin biopsy shows intra-epidermal vesicles & acantholysis. Direct Immunofluorescence (DIF): shows IgG deposition around keratinocytes (fish-net pattern). Indirect IFT uses patient serum on normal skin.
    • Treatment: Prolonged daily baths, systemic/topical steroids. Immunosuppressives (steroid-sparing): Azathioprine (2-3 mg/kg), Methotrexate (25-35 mg/week), Cyclophosphamide, Mycophenolate mofetil. Plasmapheresis (to reduce antibody titers). High-dose Intravenous Immunoglobulin (IVIG). Rituximab (anti-CD20 monoclonal antibody).
Bullous Pemphigoid & Pemphigoid Gestationis (Sub-epidermal)
  • Bullous Pemphigoid:
    • Affects Elderly patients (65-70 years). Starts as severe pruritic dermatitis -> Urticarial lesions -> Large TENSE Sub-epidermal bullae.
    • Pathogenesis: IgG circulating anti-basement membrane antibodies directed against Lamina Lucida. Key difference from Pemphigus: NO correlation between antibody titer and disease activity.
    • Self-limiting disease within 5-6 years. Mortality is low.
    • Treatment: Lower dose steroids (50-100mg Prednisolone), Azathioprine, Dapsone/Methotrexate (safe in elderly/mild cases), Tetracycline + Nicotinamide.
  • Herpes Gestationis (Pemphigoid Gestationis):
    • Intensely pruritic bullous disease of pregnancy. Onset during Second Trimester (average 21 weeks) or post-partum.
    • Urticarial plaques/vesicles around umbilicus and extremities. Spares the face, scalp, and oral mucosa.
    • Flares a few days after delivery, remits spontaneously. Recurs in subsequent pregnancies, menses, or with Oral Contraceptive Pills (OCPs).
    • Histology: Sub-epidermal blister. Heavy linear deposition of Complement 3 (C3) (and IgG in 30%) along the basement membrane zone (lamina lucida).
    • Treatment: Topical steroids (mild), Systemic steroids 40mg/day (severe).
Dermatitis Herpetiformis (DH) & Childhood Bullous Disease
  • Dermatitis Herpetiformis:
    • Chronic, relapsing, SEVERELY pruritic disease. Symmetrical grouped polymorphous papulovesicular/bullous lesions.
    • Scratching leads to bleeding and scarring. Predilection for extensor surfaces: Scalp, nuchal area, forearms, post-axillary folds, back, buttocks. Age 20-40, equal sex ratio.
    • Diagnosis: Circulating Immunoglobulin A (IgA) antibodies against smooth muscle endomysium (70% of patients). Direct Immunofluorescence (DIF): IgA deposition (granular pattern) at the TIPS of the dermal papillae. Sub-epidermal bullae.
    • Treatment: Dapsone and Sulfapyridine (50-300 mg daily). Monitor for side effects: Hemolytic anemia, methemoglobinemia, agranulocytosis, peripheral neuropathy.
  • Chronic Benign Bullous Disease of Childhood:
    • Preschool age, self-limiting within 2-3 years. Large tense bullae around mouth, pelvis, limbs.
    • DIF shows Linear IgA deposition at the dermo-epidermal junction.
    • Treatment: Dapsone with/without steroids.
Erythema Multiforme & Epidermolysis Bullosa
  • Erythema Multiforme (EM):
    • Self-limiting (1-4 weeks), young adults in spring. Two types: EM Simplex (Minor) and Stevens-Johnson Syndrome (SJS - Major/severe with mucosal involvement).
    • Lesion Morphology: Target or Iris lesion consisting of 3 zones: 1) Central dusky purpura/blister, 2) Elevated edematous pale ring, 3) Surrounding macular erythema.
    • Etiology (Crucial MCQ):
      1. Infections: Herpes Simplex Virus Type 1 (HSV-1) Labialis is the most common cause of EM Minor (lesions appear 5 days after HSV).
      2. Drugs: Sulfonamides, NSAIDs, Allopurinol, Anticonvulsants -> usually cause Stevens-Johnson Syndrome (SJS).
      3. Inflammatory Bowel Disease (Crohn's, UC), Sunlight, Radiation.
    • Treatment: Systemic steroids (High dose 1100mg daily + Intravenous fluids for SJS).
  • Epidermolysis Bullosa (EB):
    • Hereditary EB: Mechanobullous disease (blisters follow minor trauma). 3 groups: EB Simplex, Junctional EB, Dystrophic EB.
    • Dystrophic EB: Blistering below the basal lamina, heals with scarring and MILIA formation. Due to mutation in anchoring fibril Type VII (7) Collagen.
    • EB Acquisita: Chronic sub-epidermal blistering due to Autoimmunity to Type VII collagen in anchoring fibrils. Mechanobullous type heals with scars/milia. Refractory to treatment.
  • Bullous Diabeticorum: Common in Iraq. Huge bullous lesions affecting the feet in Diabetes Mellitus patients. Heals with rest/supportive care.
💡 High-Yield Hints for Lecture 5
  • Acantholysis + Intra-epidermal blister + Fish-net DIF = Pemphigus Vulgaris.
  • Tense bullae + Sub-epidermal blister + Elderly patient = Bullous Pemphigoid.
  • Intensely itchy grouped vesicles + IgA at dermal papillae tips = Dermatitis Herpetiformis.
  • Bullous disease forming in the second trimester + spares face/oral mucosa = Herpes Gestationis.
  • Target/Iris lesions typically follow a recent HSV-1 cold sore infection (Erythema Multiforme).
  • Severe drug reactions (Sulfonamides, Anticonvulsants) trigger Stevens-Johnson Syndrome (SJS).

Lecture 6: Sexually Transmitted Diseases (STDs) (3 MCQs)

Organisms & Classifications
  • Bacterial: Chlamydia trachomatis L-types (L1, L2, L3) causes Lymphogranuloma venereum (LGV). Haemophilus ducreyi causes Chancroid. Treponema pallidum causes Syphilis. Neisseria Gonorrhoeae causes Gonorrhea.
  • Protozoal: Trichomoniasis (Trichomonas vaginalis), Giardiasis (Giardia lamblia), Amebiasis (Entamoeba histolytica).
  • Fungal: Vulvovaginal candidiasis (Candida albicans).
  • Parasitic: Scabies (Sarcoptes scabiei), Pediculosis (Phthirus pubis).
  • Viral: HPV (Genital Warts), HSV-2 (Genital Herpes), HIV/AIDS.
Bacterial STDs: Syphilis & Chancroid
  • Syphilis: Human infectious disease caused by Treponema pallidum (spirochete bacterium). Can infect any organ.
    • Transmission: Direct contact with primary/secondary lesions, transplacental (in utero), birth canal, blood products.
    • Stages:
      • Primary Syphilis: Incubation ~21 days. Papules undergo necrosis forming a PAINLESS, clean, hard INDURATED ulcer (Chancre) with painless, discrete regional lymphadenopathy. Heals in 3-6 weeks.
      • Secondary Syphilis: Systemic spread (skin rash, condylomata lata).
      • Early Latent Syphilis: Duration < 1 year (infectious). Documented seroconversion (VDRL/RPR) without active disease symptoms.
      • Late Latent Syphilis: Duration ≥ 1 year.
      • Tertiary (Late) Syphilis: Occurs in untreated patients. Characterized by Gumma (ulcerative, nodular granulomas that heal with scarring), Neurosyphilis (CSF abnormality, reactive VDRL), Cardiovascular syphilis (endarteritis obliterans). Note: Gumma is allergic, no pathogen in ulcer.
      • Congenital Syphilis: Residual stigmata include Hutchinson's teeth, frontal bossing, saddle nose, poorly developed maxilla, saber shin.
    • Diagnosis: Dark Field Microscopy (positive in primary chancre). Serology: Non-treponemal tests (Rapid Plasma Reagin - RPR, Venereal Disease Research Laboratory - VDRL). Prozone Phenomenon: If antibody titer is too high, test may give a false negative. Treponemal tests (FTA-ABS) remain reactive for life.
    • Treatment: Benzathine Penicillin G. No proven alternative; allergic patients must be desensitized.
  • Chancroid:
    • Caused by Haemophilus ducreyi (Gram-negative bacilli). Rule: "Croi > Cry > Pain". Cofactor for HIV.
    • Clinical: Incubation 4-7 days. Tender papules evolve into a Tender, sharply bordered, undermined, NON-indurated PAINFUL ulcer with yellowish exudate. Associated with highly diagnostic Painful Suppurative Lymphadenopathy.
    • Diagnosis: Clinical, Dark Field & Syphilis serology (to exclude T. pallidum), Culture on special media.
    • Management: Azithromycin 1g single dose, or Ceftriaxone 250mg IM single dose, or Ciprofloxacin 500mg bid x 3 days.
Chlamydia Trachomatis (NGU & LGV)
  • Obligate intracellular bacteria. Most common bacterial STD in every population.
  • Localized CT Infection:
    • Non-Gonococcal Urethritis (NGU): Urethral discharge, dysuria, itching in men.
    • Proctitis: Mild rectal pain, mucous discharge, tenesmus.
    • Mucopurulent Cervicitis: Asymptomatic or vaginal discharge / intermenstrual bleeding.
    • Pelvic Inflammatory Disease (PID): Lower abdominal pain, silent salpingitis leading to fallopian tube scarring, ectopic pregnancy, and infertility.
  • Invasive CT Infection (Lymphogranuloma Venereum - LGV):
    • Presents as acute LGV (genital lesion + suppurative regional lymphadenitis). Can cause hemorrhagic proctitis in women, and long-term genital elephantiasis, strictures, and fistulas of penis, urethra, and rectum.
  • Diagnosis: Polymerase Chain Reaction (PCR) is the most sensitive and specific. Direct Fluorescent Antibody (DFA), ELISA, Culture.
  • Management: Azithromycin 1g single dose, or Doxycycline 100mg daily for 7 days.
Genital Herpes (HSV-2)
  • Recurrent lifelong STD caused by Herpes Simplex Virus Type 2 (HSV-2) more than HSV-1. Characterized by symptomatic and asymptomatic viral shedding.
  • Risk factors: Lifetime sexual partners, male homosexuality, history of STDs.
  • Primary Infection: 90% asymptomatic. Symptomatic: fever, headache, myalgia, dysuria, vaginal/urethral discharge, and Tender Inguinal Lymphadenopathy. Erythematous plaques -> vesicles -> pustules -> eroded painful ulcers. Heals in 2-4 weeks.
  • Recurrent Infection: Milder symptoms, smaller eroded plaques, heal in 1-2 weeks.
  • Diagnosis: Must be confirmed by Viral Culture and Direct Fluorescent Antibody Test (DFAT) or serology (due to atypical presentations and asymptomatic shedding).
💡 High-Yield Hints for Lecture 6
  • Treponema pallidum (Syphilis) creates a PAINLESS, hard chancre.
  • Haemophilus ducreyi (Chancroid) creates a PAINFUL, soft, purulent ulcer with suppurative lymphadenopathy.
  • A patient with high antibodies for Syphilis might test negative on VDRL due to the Prozone Phenomenon (requires serum dilution).
  • Chlamydia Trachomatis is the leading cause of PID and ectopic pregnancy/infertility due to silent salpingitis.
  • Genital ulcers (Syphilis, Chancroid, HSV) are major co-factors that heavily increase the transmission risk of HIV.

Ultimate Comparisons (High-Yield MCQs)

1. Pemphigus Vulgaris vs. Bullous Pemphigoid
Feature Pemphigus Vulgaris Bullous Pemphigoid
Blister Level Intra-epidermal (Acantholysis) Sub-epidermal
Target Antigen Desmogleins (Desmosomes) Lamina Lucida (Basement Membrane)
Blister Morphology Flaccid, easily ruptured, painful erosions Large, Tense, thick-roofed bullae
Antibody Titer Correlates with disease severity Does NOT correlate with severity
DIF Pattern IgG intercellular (Fish-net pattern) IgG/C3 linear at basement membrane
Age Group Younger/Middle-aged (30-40 in Iraq) Elderly (65-70 years)
2. Syphilitic Chancre vs. Chancroid
Feature Syphilitic Chancre (Primary Syphilis) Chancroid
Causative Organism Treponema pallidum (Spirochete) Haemophilus ducreyi (Gram -ve Bacilli)
Pain Painless Highly Painful ("Croi > Cry > Pain")
Ulcer Base & Edges Clean base, hard Indurated edges Purulent yellow exudate, Undermined non-indurated edges
Lymphadenopathy Painless, hard, discrete Painful, Suppurative (Diagnostic)
Treatment Benzathine Penicillin G Azithromycin / Ceftriaxone / Ciprofloxacin
3. Alopecia Areata vs. Androgenetic Alopecia
Feature Alopecia Areata Androgenetic Alopecia
Type Focal, Non-scarring Patterned decline, Non-scarring
Pathogenesis Autoimmune T-cell mediated (peribulbar) Genetic + Androgens (5-alpha reductase converts Testosterone to DHT)
Clinical Hallmark Sudden round/oval bald patches with Exclamation marks Gradual bitemporal recession & vertex loss. Hair miniaturization.
Treatment Intralesional/Topical steroids, Minoxidil, Dinitrochlorobenzene (DNCB) Topical Minoxidil (2-5%), Finasteride 1mg
4. Tinea Corporis vs. Pityriasis Versicolor
Feature Tinea Corporis Pityriasis Versicolor
Causative Organism Dermatophytes (Mainly Trichophyton rubrum) Yeast (Malassezia furfur / P. ovale)
Clinical Appearance Annular (ring) lesions with active inflamed red scaly border and central clearing. Hypo/hyper-pigmented macules with fine scaling. No inflamed border.
KOH Preparation Spores and branching hyphae Spaghetti and Meatballs appearance
Wood's Light Usually Negative (unless Microsporum) Yellow / Lemon fluorescence
5. Tinea Capitis: Kerion vs. Favus
Feature Inflammatory Tinea Capitis (Kerion) Favus
Clinical Appearance Boggy, painful swelling with multiple pustules. Cup-shaped yellow crustations (Scutula) surrounding hair base.
Odor Not specifically foul-smelling. Distinctive Foul-smelling crusts.
End Result Scarring and permanent alopecia. Scarring alopecia (Rare in Iraq now).
6. Primary vs. Secondary Cicatricial Alopecia
Feature Primary Cicatricial Alopecia Secondary Cicatricial Alopecia
Pathology Location Inflammatory process directly targets and destroys the hair follicle. Follicle is destroyed as a "bystander" due to a wider disease/trauma.
Common Causes Systemic Lupus Erythematosus (SLE), Lichen Planopilaris, Pseudopelade of Brocq. Trauma, deep burns, severe infections (Kerion, Favus, Lupus Vulgaris).
7. Hirsutism vs. Hypertrichosis
Feature Hirsutism Hypertrichosis
Definition Male-pattern terminal hair growth in women. Overgrowth of hair anywhere on the body.
Androgen Dependency Strictly Androgen-Dependent. NOT localized to androgen-dependent areas.
Common Causes Polycystic Ovary Syndrome (PCOS), Adrenal Tumors, CAH. Drugs (Minoxidil, Cyclosporine), Fetal Alcohol Syndrome.
Treatment Approach Antiandrogens (Spironolactone, Cyproterone acetate). Remove offending drug/trigger, physical hair removal.