NOTE: Highlighted in bold are the important key info!
Topics are arranged in order of most to least commonly tested
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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.
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.
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.
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.
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).
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.
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.
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.
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.
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).
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.