Dermatology Final

1. Connective Tissue Diseases / Cutaneous Manifestations of Systemic Diseases

• Lichen Planus (LP)
  • Nail changes:
    • Pterygium (hypertrophy and distal proliferation of nail fold).
    • Other changes include thinning, dystrophy, longitudinal ridging.
    • Onycholysis can occur; pitting is less typical than in psoriasis.
    • Nail thickening is NOT typical (usually thinning).
  • Mucosal involvement: Buccal mucosa is the most common site if mucosa is involved.
  • Symptoms: Itching is a characteristic feature.
  • Histology: Hypergranulosis, sawtooth rete ridges, band-like lymphocytic infiltrate, Civatte bodies. (Hypogranulosis is NOT typical).
  • Primary lesion: Papule (not macule).
  • Course: Often self-limiting; 50% of cases may clear within 18 months, but chronicity can occur, especially with mucous or hypertrophic lesions.
  • Features: Wickham's striae are characteristic.

• Lupus Erythematosus
  • Discoid Lupus Erythematosus (DLE):
    • Can cause patchy scarring alopecia.
    • Histology: Destruction of basal cell layer (liquefaction degeneration).
    • Progression to Systemic Lupus Erythematosus (SLE) occurs in 5-10% of cases.
  • Systemic Lupus Erythematosus (SLE):
    • Commonest cutaneous eruption: Malar (butterfly) rash; photosensitive erythema is also common.
    • Neonatal lupus: Only a small percentage of babies born to mothers with Ro/La antibodies develop SLE later in life.
  • Photosensitivity: A girl with photosensitivity and an ANA titer of 1:32 may require further investigation (e.g., repeat ANA, anti-dsDNA, ENA) and photoprotection.

• Dermatomyositis
  • Associations:
    • Frequently associated with underlying malignancy in adults.
    • Childhood dermatomyositis is frequently associated with Calcinosis.
  • Clinical Signs:
    • Heliotrope rash (pathognomonic).
    • Gottron's sign/papules.
    • Proximal muscle weakness.
    • Ragged cuticles and nail fold telangiectasias.
  • Demographics: More common in females.
  • Risk: Calcinosis can occur in adults, though more common in juvenile form.

• Morphea (Localized Scleroderma)
  • Tissue involvement: Can include epidermis, subcutaneous tissue, muscles, and bones. All layers can be affected depending on type/depth.
  • Muscular atrophy: Can be associated with linear morphea (e.g., en coup de sabre).
  • Course: May or may not improve with time; can progress or stabilize.
  • Features: Presents with well-defined patches; not caused by UV light.

• Erythema Multiforme (EM)
  • Most common cause: Herpes simplex virus (HSV), especially for EM minor.
  • Other causes: Drugs, Mycoplasma.
  • Ulceration: Can occur, particularly in EM major / Stevens-Johnson Syndrome.

• Erythema Nodosum (EN)
  • Causes: Streptococcal infections, sarcoidosis, drugs, TB, pregnancy.
  • Association with malignancy: Can occur.
  • Ulceration: Erythema nodosum leprosum (Type 2 Lepra reaction) can ulcerate.
    • Typical EN lesions classically do not ulcerate. This distinction should be clearer to avoid confusion

• Erythema Gyratum Repens
  • Strongly associated with underlying internal malignancy (often lung cancer); considered pathognomonic.
  • NOT typically precipitated by streptococcal throat infection.

• Dermatitis Herpetiformis (DH)
  • Associations: Chronic autoimmune disease, frequently associated with celiac disease (gluten-sensitive enteropathy).
  • Histopathology: Subepidermal blisters with neutrophilic and eosinophilic microabscesses at the tips of dermal papillae. The prickle cell layer is NOT the primary abnormal layer.
  • Treatment: Dapsone (diamino-diphenyl sulfone).

• Vitiligo
  • Pathophysiology: Results from the destruction of melanocytes, leading to DEpigmented (not hypopigmented) patches.
  • Melanocytes: Number of melanocytes is decreased or absent in affected areas.
  • Associations: Significantly associated with autoimmune thyroid disease (hypo- or hyperthyroidism), pernicious anemia, Addison's disease, alopecia areata. Reticulosis is NOT a typical association.
  • Demographics: Affects males and females equally; onset usually in 20s and 30s.

• Piebaldism
  • Inheritance: Autosomal dominant.

• Post-Inflammatory Hypopigmentation
  • Causes: Can occur after psoriasis, lichen planus, and other inflammatory conditions.

• Chloasma (Melasma)
  • Treatment of choice: Topical hydroquinone-containing ointments (e.g., Eldoquin).

• Hodgkin's Disease
  • Commonest cutaneous lesion: Often secondary to pruritus (e.g., excoriations, lichenification); specific skin infiltrates are less common.

2. Fungal Infections

• General Principles
  • Tinea capitis: Usually requires systemic antifungal treatment.
  • Tinea pedis: Usually treated topically.
  • Pityriasis versicolor: Can recur.
  • Chronic paronychia: Often caused by mixed yeast and bacterial infection.

• Tinea Capitis
  • Epidemics: Often caused by anthropophilic fungi like Microsporum audouinii.
  • Causative organisms: Microsporum species (e.g., M. audouinii, M. canis), Trichophyton species (e.g., T. tonsurans, T. schoenleinii, T. violaceum, T. verrucosum).
  • Fluorescence: Apple green fluorescence under Wood's lamp is seen with some Microsporum species (e.g., M. canis, M. audouinii).
    • T. rubrum does NOT fluoresce.
    • T. schoenleinii may show dull blue under Wood’s-lamp examination.
  • Inflammatory Tinea Capitis (Kerion): Often caused by zoophilic fungi like T. verrucosum and T. mentagrophytes.
  • Ectothrix infection: Caused by fungi like T. mentagrophytes, M. canis. (T. schoenleinii is typically endothrix/favic).
  • Acquisition from cattle: Trichophyton verrucosum.
  • Treatment: Oral Griseofulvin is a first-line treatment.

• Griseofulvin
  • Pharmacokinetics: Absorption is better after a fatty meal.
  • Side effects: Headache is a common side effect.
  • Contraindications: Contraindicated in pregnancy.
  • Interactions: Phenobarbitone may reduce its effectiveness.

• Tinea Pedis
  • Prevalence: Commonest fungal infection in adults.
  • Causative organisms: T. rubrum, T. mentagrophytes, E. floccosum.

• Tinea Corporis
  • Lesion appearance: Typically annular with slightly elevated scaling margins and central clearing.

• Tinea Versicolor
  • Causative agent: Malassezia species.
  • Clinical features: Hypo- or hyperpigmented patches or plaques with fine scaling.
  • Wood's lamp: Shows yellowish-gold or coppery-orange fluorescence (NOT apple green or cherry red).

• Onychomycosis (Tinea Unguium)
  • Infection site: Primarily affects the nail plate.
  • Clinical features: Nail discoloration, onycholysis.
  • Treatment: Oral antifungal agents are usually required for toenail onychomycosis.
  • Causative organisms: T. rubrum is common.
  • Duration of treatment: Prolonged treatment is often necessary.

• Candidiasis
  • Cutaneous candidiasis: Presents as erythema with satellite pustules, especially in body flexures.
  • Sites: Interdigital areas, paronychial (proximal nail fold), angular cheilitis (corners of mouth), oral mucosa (thrush), genital area.
  • Skin colonization: Candida albicans is a commensal but not as ubiquitously colonizing healthy skin as Staphylococci.
  • Affected tissues: Skin, mucous membranes, nails. Hair is not typically affected.

3. Eczema (Dermatitis)

• General Histology
  • Acute eczema: Characterized by spongiosis (intercellular edema in the epidermis).
  • Subacute/Chronic: Parakeratosis, acanthosis. Normal or thickened granular layer (unlike psoriasis where it's reduced/absent).

• Atopic Dermatitis (AD)
  • Pathophysiology: T helper cells (Th2 predominant in acute) play a major role.
  • Infantile AD:
    • Onset: Typically begins after 2 months of age, not at birth.
    • Distribution: Extensor surfaces and face are common sites in infants. (Flexural involvement is more typical in older children/adults).
  • Adult AD Associations: Pruritus ani, asthma. Hair fall is NOT a direct association.
  • Investigations: Elevated serum IgE levels are common.
  • Lymphocytes: Bear greater than normal amounts of IgE on their surface.

• Seborrheic Dermatitis
  • Age of onset: Can occur in infants (cradle cap) and adults.
  • Distribution: Scalp, face (nasolabial folds, eyebrows), post-auricular areas, presternal. Flexural/intertriginous areas, not extensors, are common body sites.
  • Association: Linked to Malassezia yeast.
  • Prognosis: Generally better prognosis than atopic dermatitis.

• Contact Dermatitis
  • Mechanism: Usually a Type IV cell-mediated hypersensitivity reaction.
  • Diagnostic test: Patch test is pathognomonic for allergic contact dermatitis.
  • Common allergens:
    • Nickel is a very common cause of allergic contact dermatitis.
    • Primula (plant) can cause severe, even bullous, contact dermatitis.
    • Perfumes and hair dyes can cause pigmented contact dermatitis.
  • Site specific:
    • Nail varnish dermatitis: Commonest site is the face and neck (transfer from fingers).
    • Clothing dermatitis: Commonest site is body flexures.
  • Timing: Develops 12-72 hours after exposure to the allergen.

• General Eczema Features
  • Lichenification: Thickening and hardening of the skin with exaggerated skin markings, seen in chronic eczema.
  • Blisters (vesicles/bullae): Can occur in acute eczema. Chronic eczema typically does not cause blisters.
  • Unilateral hand eczema: KOH examination of skin scrapings is important to rule out tinea manuum.
  • Pityriasis alba: Appears hypopigmented under Wood's light.

4. Psoriasis

• Histopathology
  • Key features: Parakeratosis (retention of nuclei in stratum corneum), hyperkeratosis, acanthosis with elongated rete ridges, suprapapillary epidermal thinning, Munro's microabscesses (neutrophils in stratum corneum). Epidermal atrophy is NOT a feature (epidermis is thickened).

• Nail Psoriasis
  • Commonest manifestation: Pitting.
  • Other signs: Onycholysis, subungual hyperkeratosis, discoloration ("oil drop" sign).
  • Cause of nail pitting: Loss of parakeratotic cells from the nail surface due to involvement of the proximal nail matrix.
  • Clubbing is NOT a characteristic feature of psoriasis nails.

• Clinical Types and Triggers
  • Guttate psoriasis: Often triggered by streptococcal infection.
  • Exacerbating factors: Infections, stress, certain drugs (e.g., lithium, beta-blockers, antimalarials, NSAIDs, withdrawal of systemic corticosteroids), hypocalcemia, alcohol, smoking. Hypercalcemia is NOT an exacerbating factor.

• Psoriatic Erythroderma
  • Complications: Temperature dysregulation, dehydration, sepsis, high-output cardiac failure.

• Treatment Considerations
  • Systemic treatments: Methotrexate, cyclosporine, acitretin (systemic retinoid), biologic agents (TNF-alpha blockers). PUVA (Psoralen + UVA). Azathioprine is a second-line agent.
  • Isotretinoin is NOT typically used for psoriasis (used for acne).
  • Antimalarials are generally NOT used and can exacerbate psoriasis.
  • Topical Vitamin D analogues are used.
  • Oral steroids are generally avoided for chronic plaque psoriasis due to risk of rebound flares; may be used short-term for erythrodermic or pustular psoriasis.

• Inheritance
  • Pattern: Complex, polygenic. Often described as autosomal dominant with incomplete penetrance, not autosomal recessive.

• Associated Conditions
  • Psoriatic arthritis.
  • Metabolic syndrome.

5. Viral Infections

• Herpes Simplex Virus (HSV)
  • Recurrent HSV: Herpes labialis (cold sores) is the commonest form.
  • Herpes genitalia: Viral shedding and contagion can occur even when asymptomatic.

• Varicella-Zoster Virus (VZV) - Herpes Zoster (Shingles)
  • Clinical features:
    • Pain may precede the rash.
    • Rash is vesicular, typically unilateral and dermatomal (NOT commonly bilateral).
    • More serious in elderly and immunocompromised individuals.
  • Complications: Postherpetic neuralgia can last for months.
  • Treatment: Systemic antiviral treatment (e.g., acyclovir, valacyclovir, famciclovir) is indicated for patients >50 years, immunocompromised, or with severe/ophthalmic involvement. Topical acyclovir has limited efficacy for acute zoster.

• Pityriasis Rosea
  • Etiology: Associated with Human Herpesvirus 6 (HHV-6) and/or HHV-7.
  • Clinical features:
    • Herald patch (a single larger lesion) often precedes the generalized eruption.
    • Generalized rash consists of oval, erythematous, slightly raised patches with fine scales, often arranged in a "Christmas tree" pattern on the trunk. Collaret scales.
    • Itching is variable, usually mild to moderate.
    • Self-limiting, typically resolving in 6-8 weeks.
  • Diagnosis: Primarily clinical; family history is not typically relevant.
  • Appearance: Primarily a papulosquamous eruption, not macular.

• Molluscum Contagiosum
  • Causative agent: Poxvirus.

• Warts (Verrucae)
  • Causative agent: Human Papillomavirus (HPV), a double-stranded DNA virus. (NOT HHV-6).
  • Plain warts (Verruca plana):
    • Flat-topped papules, often on the face and hands.
    • Koebner phenomenon can occur.
    • Often resolve spontaneously.
    • Flat-topped, not spiky.
  • Common warts (Verruca vulgaris):
    • Rough, hyperkeratotic papules.
    • Do NOT typically transform into skin cancer.
    • Often resolve spontaneously.
  • Filiform/Digitate warts: Often affect body flexures, face.
  • Plantar warts: On soles of feet, can be painful. Surface can be rough/hyperkeratotic.
  • Treatment: Cryotherapy, salicylic acid, 5-fluorouracil (5-FU). Topical steroids are NOT a treatment for viral warts and can worsen them.
  • Genital warts (Condylomata acuminata):
    • Treatment options include podophyllotoxin, trichloroacetic acid, cryotherapy, imiquimod.

• Viral Exanthems
  • Roseola infantum (Exanthem subitum - HHV-6/7), Slapped cheek syndrome (Erythema infectiosum - Parvovirus B19), Rubella are viral.
  • Scarlet fever eruption is caused by a bacterial toxin (Streptococcus pyogenes).

6. Skin Tumors

• Nevi (Moles)
  • Nature: Developmental disorders resulting from abnormal proliferation of melanocytes.
  • Malignant degeneration: Junctional nevi (and compound, dysplastic nevi) have a higher potential for malignant transformation to melanoma.
  • ACTH: Nevi do not typically increase in size or number after ACTH injection.

• Actinic Keratosis (AK)
  • Nature: Premalignant lesion that can progress to squamous cell carcinoma (SCC). It is not malignant itself.
  • Clinical features: Fine scaled erythematous plaques on sun-exposed skin, especially in fair-skinned individuals.

• Seborrheic Keratosis
  • Nature: Benign epidermal tumor.

• Basal Cell Carcinoma (BCC)
  • Most common type: Nodular (or noduloulcerative) BCC.
  • Clinical features (Nodular BCC): Pearly papule or nodule with telangiectasia, often on the face (e.g., nose).
  • Prognosis: Generally good, as BCC is slow-growing and rarely metastasizes. Not always associated with a bad prognosis.
  • Metastasis: Rare, but if it occurs, regional lymph nodes are the most frequent site.
  • Demographics: More common in Caucasians.

• Squamous Cell Carcinoma (SCC)
  • Commonest site: Sun-exposed areas like the face, lower lip, ears, hands.
  • Growth rate: Can be faster growing than BCC.
  • Origin: Can arise from actinic keratosis.
  • Location: Approximately 75% of SCC lesions occur on the head and neck.

• Melanoma
  • Prognosis:
    • Nodular melanoma generally has the worst prognosis and is associated with early metastasis.
    • Key prognostic factors: Breslow thickness (measured from granular layer or ulcer base to deepest point of invasion), ulceration, mitotic rate, lymph node status.
    • Gender can be a factor (females often have better prognosis).
  • Origin: Can arise de novo or from a pre-existing nevus (estimates vary, around 20-40% from nevi).
  • Clinical features (ABCDEs): Asymmetry, Border irregularity, Color variegation, Diameter >6mm, Evolving.
  • Commonest type: Superficial spreading melanoma.

• Eccrine Sweat Gland Tumors
  • Example: Syringoma (benign).

• Paget's Disease of the Breast
  • Presentation: Unilateral, eczematous rash of the areola.
  • Next step: Skin biopsy is crucial to confirm diagnosis and rule out other conditions.

• Metastasis to Skin
  • Most frequent primary tumors metastasizing to skin: Breast cancer in women, lung cancer in men. Melanoma itself can also metastasize to skin.

7. Normal Skin Structure and Function

• Epidermis
  • Stratum corneum: Devoid of nuclei.
  • Basal layer: Mitotic cells (cell division) are primarily limited to this layer.
  • Melanocytes:
    • Located in the basal layer.
    • Connect to approximately 36 surrounding keratinocytes (epidermal melanin unit).
    • Appear as clear, larger cells relative to surrounding keratinocytes under a microscope.
    • Number of melanocytes is similar across different skin phototypes; differences in skin color are due to the size, number, and packaging of melanosomes, and rate of melanin degradation.
  • Langerhans cells: Dendritic, antigen-presenting cells found in the epidermis.
  • Merkel cells: Mechanoreceptor cells, dendritic in appearance, located near nerve endings in the basal layer.

• Dermis and Subcutis
  • Pacinian corpuscles: Mediate sensation of deep pressure and vibration.
  • Meissner's corpuscles: Mediate sensation of light touch. Located in dermal papillae.

• Glands
  • Sebaceous glands:
    • Originate from ectoderm.
    • Holocrine glands.
    • Controlled by androgens.
    • NOT normally found in buccal mucosa or glabrous skin (palms/soles). Found on face, scalp, upper back, vermilion of lip, areola of nipple.
    • Meibomian glands of the eyelids are modified sebaceous glands.
  • Sweat glands:
    • Controlled by neurons (autonomic nervous system).
    • Eccrine sweat glands: Cholinergic innervation.
    • Apocrine sweat glands: Characterized by decapitation secretion; adrenergic innervation.

• Glabrous Skin (Palms and Soles)
  • Characteristics: Thick epidermis, dermatoglyphics (fingerprints), presence of encapsulated sensory organs.
  • Absence of sebaceous glands and hair follicles.

8. Acne and Rosacea

• Acne Vulgaris
  • Pathophysiology:
    • Follicular plugging (comedone formation) is the first step.
    • Increased sebum production (androgen-mediated).
    • Proliferation of Propionibacterium acnes (now Cutibacterium acnes).
    • Inflammation.
    • Epidermal edema is not a primary pathogenic feature.
  • Lesions:
    • Comedones (open and closed) are the primary non-inflammatory lesions.
    • Inflammatory lesions include papules, pustules, nodules, cysts.
    • Vesicles are NOT typical lesions of acne vulgaris.
  • Precursor of large inflammatory lesions: Papules (which arise from comedones).
  • Factors: Greasy cosmetics may cause/worsen acne.
  • Flare-ups: Can be caused by steroids, certain antimalarial drugs, Vitamin B12. Estrogens (in OCPs) often improve acne.
  • Chloracne: Comedones predominate.
  • Treatment:
    • Isotretinoin is very effective for severe cystic acne.
    • Metronidazole is used for rosacea, NOT commonly for systemic treatment of acne vulgaris.

• Oral Isotretinoin
  • Side effects: Teratogenicity (Pregnancy Category X), dry lips (cheilitis is very common), dry skin/mucosa, elevated triglycerides, elevated liver enzymes, potential for hair loss. Increased intracranial pressure (rare).
  • Monitoring: Blood tests (lipids, LFTs, pregnancy test) are required before and during treatment.
  • Pregnancy: Strict contraception is mandatory during and for at least one month after stopping treatment.
  • Scarring alopecia and infertility are NOT typical side effects.

• Acne Rosacea
  • Clinical features: Persistent facial erythema, telangiectasias, papules, pustules. Rhinophyma can occur in severe, long-standing cases.
  • Age of onset: Typically affects adults (30-50s), not primarily teenagers.
  • Distinction from Acne Vulgaris: Rosacea lacks comedones. Rosacea has more prominent telangiectasias and persistent erythema.

9. Bullous Diseases

• Pemphigus Vulgaris
  • Pathophysiology: Autoimmune disease with antibodies against desmogleins (Dsg1 and Dsg3) leading to acantholysis.
  • Blisters: Intraepidermal (suprabasal), flaccid bullae, often on skin and mucous membranes (painful oral erosions are common).
  • Prognosis: Associated with significant morbidity and mortality if untreated.
  • Demographics: More common in middle-aged to elderly individuals, and in certain ethnic groups (e.g., Ashkenazi Jews).

• Bullous Pemphigoid
  • Pathophysiology: Autoimmune disease with antibodies against hemidesmosome components (BPAG1/BP230 and BPAG2/BP180/Collagen XVII) at the dermoepidermal junction.
  • Blisters: Subepidermal, tense bullae.
  • Immunofluorescence: Linear deposits of IgG and C3 along the basement membrane zone.
  • Prognosis: Generally less severe than pemphigus vulgaris.

• Differentiating Pemphigus and Pemphigoid
  • Blister location: Pemphigus = intraepidermal; Pemphigoid = subepidermal.
  • Blister type: Pemphigus = flaccid; Pemphigoid = tense.
  • Mortality: Pemphigus generally has higher morbidity/mortality if untreated.

• Epidermolysis Bullosa (EB)
  • General: Group of inherited disorders characterized by skin fragility and blister formation.
  • Mucous membrane involvement: Can be extensive in severe forms, particularly dystrophic EB.
  • Scarring:
    • Dystrophic EB heals WITH scarring.
    • Epidermolysis bullosa simplex typically heals WITHOUT scarring.

• Other Blistering Conditions
  • Generalized blistering can be caused by Pemphigus gestationis (Herpes gestationis).
  • Impetigo, dermatitis herpetiformis can cause epidermal bullae.
  • Chronic eczema does NOT typically cause epidermal bullae (acute eczema can).

• Diagnostic Aids
  • Immunofluorescence (direct and indirect) is highly valuable in differentiating autoimmune bullous diseases like bullous pemphigoid from other conditions like erythema multiforme.

10. Hair, Scalp, and Nail Disorders

• Hair Cycle and Growth
  • Anagen phase (growing): Approximately 85% of scalp hair follicles are in this phase. Lasts 2-6 years.
  • Telogen phase (resting): Resting stage of hair. Lasts 2-3 months.
  • Growth rate: Approximately 1 cm/month.
  • Hair characteristics: Genetically determined.

• Alopecia (Hair Loss)
  • Traumatic alopecia: Caused by traction, pressure, trichotillomania.
  • Alopecia Areata:
    • Non-scarring alopecia, often patchy.
    • Can occur in children and is often recurrent.
    • Does NOT fluoresce under Wood's lamp.
  • Telogen Effluvium:
    • Diffuse non-scarring hair shedding, occurring a few months after a trigger (e.g., childbirth, surgery, severe illness, crash diet, drugs like heparin).
    • Wood's lamp does NOT aid in diagnosis.
  • Anagen Effluvium:
    • Diffuse hair loss due to interruption of anagen phase, classically caused by cytotoxic drugs (chemotherapy).
  • Non-cicatricial (non-scarring) alopecia causes:
    • Diffuse: Telogen effluvium, anagen effluvium, endocrine dysfunction (e.g., hypothyroidism), nutritional deficiencies, hereditary hair shaft abnormalities.
    • Patchy: Male/female pattern hair loss, alopecia areata, secondary syphilis (moth-eaten alopecia).
    • Trichotillomania causes patchy, irregular non-scarring alopecia, not typically diffuse.
  • Cicatricial (scarring) alopecia causes:
    • Morphea (if scalp involved), DLE, lichen planopilaris, severe infections, sarcoidosis (if cutaneous lesions involve scalp).

• Nail Structure
  • Nail cuticle (eponychium): Formed by the dorsal layer of the posterior nail fold.
  • Nail matrix disorders: Can result in changes in nail shape, longitudinal ridging, and thickened nails.

• Specific Hair Disorders
  • Netherton's syndrome: Characteristic hair lesion is trichorrhexis invaginata ("bamboo hair").

11. Sexually Transmitted Diseases (STDs)

• Syphilis
  • Treatment: Benzathine penicillin G is the treatment of choice for all stages (except neurosyphilis, where aqueous crystalline penicillin G is used).
  • Diagnosis:
    • Early diagnosis: Dark field microscopy of chancre exudate. Serological tests like FTA-ABS (or other treponemal tests like TPPA/TPHA) become positive later but are very sensitive and specific.
    • Follow-up: Non-treponemal tests (VDRL/RPR) are used to monitor treatment response as titers decrease. FTA-ABS typically remains positive for life.
  • Primary Syphilis:
    • Chancre: Typically painless, single, indurated ulcer at the site of inoculation, rich with treponemes.
    • Dark field microscopy: If negative from chancre, aspirate from regionally enlarged lymph node can be examined.
  • Secondary Syphilis:
    • Onset: Lesions usually appear 2-12 weeks after infection.
    • Rash: Maculopapular or papulosquamous rash, often involving palms and soles. Typically generalized and can be itchy (variable). NOT commonly vesicular.
    • Condylomata lata: Highly infectious, moist, flat-topped papules in intertriginous areas.
    • Moth-eaten alopecia: Patchy non-scarring alopecia.
    • Other: Mucous patches, generalized lymphadenopathy (usually non-painful), constitutional symptoms. Auditory neuritis, periostitis can occur.
  • Treponema pallidum survival: Dies within approximately 48-72 hours in blood stored at normal refrigerator temperature (+4°C).

• Gonorrhea
  • Causative agent: Neisseria gonorrhoeae, a Gram-negative diplococcus.
  • Symptoms: Many females (up to 50%) can be asymptomatic.
  • Site of infection: Columnar epithelium is a predilection site (e.g., endocervix, urethra).
  • Best swab site (female): Endocervical swab.
  • Treatment: Penicillin resistance is widespread; current guidelines recommend combination therapy (e.g., ceftriaxone plus azithromycin or doxycycline). Old low-dose, long-term penicillin regimens are NOT effective.

• Chancroid
  • Causative agent: Haemophilus ducreyi.

• Non-Gonococcal Urethritis (NGU)
  • Treatment: Doxycycline (a tetracycline) or Azithromycin are drugs of choice.

12. Bacterial Infections

• Impetigo
  • Nature: Most superficial bacterial skin infection.
  • Causative agents: Staphylococcus aureus and/or Streptococcus pyogenes.
  • Commonly affected: Infants and children.

• Ecthyma
  • Nature: Deeper, ulcerative form of impetigo, extending into the dermis. It is NOT a superficial infection.
  • Common cause: Streptococcus pyogenes.
  • Predisposing factors: Immunocompromised individuals.

• Erysipelas
  • Clinical features: Well-defined, erythematous, indurated plaque with a raised border, often on the face or lower limbs. Fever and constitutional symptoms can occur.
  • Causative agent: Primarily Streptococcus pyogenes. Staphylococcus aureus is NOT the primary cause (though it can cause cellulitis or secondary infection).
  • Treatment: Penicillin is the drug of choice.

• Erythrasma
  • Causative agent: Corynebacterium minutissimum.
  • Wood's light examination: Shows a characteristic coral-red fluorescence.

• Staphylococcus aureus Carriage
  • Main local source contaminating the skin: Anterior nares (nose).

13. Urticaria and Angioedema

• Primary Lesion of Urticaria
  • Wheal: An edematous, erythematous, transient plaque that blanches with pressure. Very itchy.
  • Does NOT typically leave a hypopigmented scar.

• Pathophysiology
  • Main cells involved: Mast cells (release of histamine and other mediators).

• Acute Urticaria
  • Treatment of choice: Antihistamines.
  • Oral steroids are NOT first-line treatment; reserved for severe or refractory cases.

• Chronic Urticaria
  • Cause: In up to 90% of chronic cases, the cause is unknown (chronic idiopathic urticaria).

• Cold Urticaria
  • Characteristics: Can be familial or acquired, may be transferable in serum (passive transfer test), and can result in systemic reactions (e.g., unconsciousness if swimming in cold water).

• Cholinergic Urticaria
  • Diagnostic test: Provocation with exercise and heat challenge is most reliable. Intradermal methacholine test can also be used.

• Treatment
  • Antihistamines: Both sedating and non-sedating antihistamines are used.
    • For day-time use (less sedating): Second-generation antihistamines (e.g., piperidines like loratadine, cetirizine, fexofenadine).
  • Topical antihistamine ointments are generally NOT effective for widespread urticaria.

• Contact Sensitivity
  • Degree of sensitivity is influenced by: Amount of allergen, frequency of exposure, and route of exposure.

14. Ichthyosis

• Ichthyosis Vulgaris (Simplex)
  • Prevalence: Most common type of ichthyosis.
  • Clinical features: Fine, white scales, typically involves extensors, spares flexural areas. Often associated with keratosis pilaris and atopy.
  • Onset: Usually presents after 3 months of age, not at birth.

• X-linked Ichthyosis
  • Cause: Steroid sulfatase deficiency.
  • Associations: May be associated with corneal opacities, cryptorchidism. Congenital ichthyosis with renal agenesis/hernia is a severe manifestation potentially linked.

• Bullous Ichthyosiform Erythroderma (Epidermolytic Ichthyosis)
  • Inheritance: Autosomal dominant.

• Non-bullous Ichthyosiform Erythroderma (e.g., Lamellar Ichthyosis, Congenital Ichthyosiform Erythroderma)
  • Inheritance: Autosomal recessive.

• Ichthyosis Hystrix
  • Clinical features: Severe form with prominent hyperkeratosis, leading to thickening of all skin layers.

• Defective Keratinization
  • Common feature in various ichthyoses, psoriasis, epidermolytic hyperkeratosis. Lichen sclerosus et atrophicus involves epidermal atrophy and dermal changes, less primarily a keratinization defect in the same context.

15. Pruritus and Scabies

• Pruritus
  • Biliary obstruction: Pruritus is most directly related to the accumulation of bile salts in the skin.

• Scabies
  • Causative agent: Sarcoptes scabiei var. hominis.
  • Transmission: Typically by prolonged close personal contact. Can spread by simple handshake if prolonged.
  • Pruritus onset: After initial infestation, pruritus (due to sensitization) typically develops in 2-6 weeks.
  • Clinical features:
    • Intense itching, characteristically worse at night.
    • Burrows are pathognomonic lesions (best yield for scrapings).
    • Commonly affected sites in adults: Finger webs, wrists, axillae, areolae, umbilicus, genitalia. Back is usually spared in adults.
    • Infants: Can affect face, scalp, palms, and soles (sites often spared in adults). May present with acral pustules. Family history of itching IS usually present.
  • Treatment:
    • Permethrin 5% cream is a first-line treatment.
    • All household members and close contacts should be treated simultaneously.
    • Itching may persist for weeks even after successful treatment (post-scabetic pruritus).
    • Benzoyl benzoate is a topical treatment; benzoyl peroxide is for acne and not used for scabies. Systemic treatment is ivermectin.

16. Drug Rashes

• Acne Medicamentosa (Acneiform Eruption)
  • Causative drugs: Phenytoin, B12, corticosteroids, lithium, isoniazid.
  • Azelaic acid is a treatment for acne, not a cause of acne medicamentosa.

• Stevens-Johnson Syndrome (SJS) / Toxic Epidermal Necrolysis (TEN)
  • Nature: Severe, life-threatening mucocutaneous reactions.
  • Most common cause: Drugs (e.g., sulfonamides, anticonvulsants, NSAIDs, allopurinol), not infection.
  • Clinical features: Prodrome of fever/malaise, followed by painful skin, widespread blistering and epidermal detachment, mucosal erosions (oral, ocular, genital).
    • SJS involves <10% BSA detachment, SJS/TEN overlap 10-30%, TEN >30% BSA detachment.
    • Absence of oral erosions would NOT be typical for TEN.
  • Management: Requires intensive care unit (ICU) management due to high fatality rate.

17. Miscellaneous Dermatological Conditions and Principles

• UV Light and Skin
  • Penetration: UVA penetrates deeper into the skin than UVB. UVC is mostly absorbed by the ozone layer.
  • Intensity:
    • UVA intensity is relatively constant throughout the day.
    • UVB intensity peaks around midday.

• Sunscreens
  • Mechanism: Physical sunscreens (e.g., zinc oxide, titanium dioxide) reflect UV radiation. Chemical sunscreens absorb UV radiation.
  • SPF (Sun Protection Factor): Measures protection against UVB.
  • UVA protection: Indicated by ratings like PA system (PA+, PA++, etc.) or UVA star rating.
  • Efficacy: The actual level of sun protection achieved is often less than specified on the bottle due to inadequate application by users.

• Corticosteroids
  • Topical Corticosteroids (Side Effects of Prolonged Use):
    • Skin atrophy, telangiectasia, striae.
    • Hypopigmentation or hyperpigmentation.
    • Perioral dermatitis/rosacea-like eruptions.
    • Hypertrichosis (overgrowth of hair).
    • Cataracts or glaucoma (if applied near eyes).
  • Systemic Corticosteroids:
    • Indications: Systemic vasculitis, severe drug eruptions (e.g., SJS/TEN, DRESS), severe urticaria with angioedema, widespread acute eczema.
    • Generally NOT indicated for widespread chronic plaque psoriasis (risk of rebound).
    • Uses in acne: May be used for severe inflammatory acne (e.g., acne fulminans) or severe acne medicamentosa. Not for ordinary or nodular acne vulgaris.

• Phthirus Pubis (Pubic Lice)
  • Transmission: Can be transmitted from pubic hair to eyelashes (phthiriasis palpebrarum), axillary hair, chest hair. Less commonly to scalp hair.

• Erythroderma (Exfoliative Dermatitis)
  • Definition: Generalized erythema and scaling involving >80-90% of the skin surface.
  • Complications: Hypothermia (due to heat loss), dehydration, electrolyte imbalance, secondary infection, high-output cardiac failure. Hyperthermia is NOT a feature.
  • Associations: Can be caused by pre-existing dermatoses (e.g., psoriasis, eczema), drugs, malignancies (e.g., Sézary syndrome, mycosis fungoides), congenital ichthyosis. Lichen planus rarely causes erythroderma.
  • Investigation: Biopsy is usually done to help determine the underlying cause.

• Placental Transfer of Immunoglobulins
  • IgG is the only immunoglobulin that significantly crosses the normal placenta.

• Dermatoscope
  • Uses: Examination of pigmented lesions (nevi, melanoma), alopecia areata (e.g., exclamation mark hairs), vascular patterns. It is a hand-held tool.
  • NOT used for directly visualizing fungal hyphae and spores (this requires KOH preparation and microscopy).

• Cutaneous Leishmaniasis
  • Transmission: Transmitted by the bite of infected sandflies (not mosquitoes).
  • Clinical presentation: Often a painless ulcer on exposed skin (e.g., face in a child from an endemic area like the Jordan Valley).
  • Causative species for Leishmaniasis recidivans: L. tropica.
  • Pathology: Infection of reticuloendothelial (RE) cells (macrophages).
  • Treatment: Antimonials (e.g., sodium stibogluconate, meglumine antimoniate) are drugs of choice for many forms.

• Leprosy (Hansen's Disease)
  • Eye involvement: Can occur in intermediate and lepromatous leprosy.
  • Treatment duration (Lepromatous): Multidrug therapy is continued for at least 2 years (WHO recommendation), and often lifelong or until skin smears are consistently negative, depending on guidelines and response.

• Hyperpigmented Lesions
  • Evaluation of a growing, hyperpigmented lesion on the face:
    • Initial step: Dermoscopic examination.
    • If suspicious: Biopsy (excisional if possible for suspected melanoma, or incisional if very large). Chemical peeling is a cosmetic procedure and not for diagnosis of potentially malignant lesions.