Skin – Chapter 8 Comprehensive Notes

Anatomy of the Skin

• Three principal layers (superficial ➜ deep)

  • Epidermis: thin, avascular; site of keratinocyte maturation, melanocytes, Langerhans (immune) cells

  • Dermis: dense connective tissue; houses blood vessels, sensory nerves, sweat glands, hair follicles, sebaceous glands

  • Hypodermis / Subcutaneous layer: loose areolar + adipose tissue; functions in insulation, energy storage, shock absorption

• Accessory / adnexal structures

  • Hair shaft, hair bulb, associated arrector pili muscle

  • Sweat pore opening ➜ eccrine & apocrine sweat glands deeper in dermis

  • Cutaneous nerves (sensory & autonomic) interwoven throughout dermis

  • Vascular network: superficial veins, arteries, capillaries supplying nutrients & facilitating thermoregulation

• Functional overview

  • Physical/mechanical barrier, immune surveillance, thermoregulation, vitamin D synthesis, sensory perception

  • Clinical significance: pathology often tied to which layer is involved (e.g.
    burn depth, skin cancers)

Common Skin Lesions & Other Alterations - can be both primary and secondary (primary would be like a freckle) ( secondary would be like a cut)

• Primary Lesions (initial pathological change) - IMPORTANT FOR EXAM

  • Macule: flat, ≤ 1\text{ cm}, clearly defined edge (e.g.
    freckle)

  • Papule: small, solid elevation, < 0.5\text{ cm} (e.g.
    wart)

  • Nodule: firm, raised, deeper than papule, > 0.5\text{ cm}

  • Vesicle: fluid-filled blister, < 1\text{ cm} (e.g.
    chickenpox)

  • Pustule: raised, purulent exudate (e.g.
    acne)

  • Plaque: broad, plateau-like elevation, often scalelike surface (e.g.
    psoriasis)

• Secondary Lesions / Skin breaks

  • Ulcer: cavity/erosion into dermis ➜ risk of infection, scarring

  • Fissure: linear crack (e.g.
    athlete’s foot)

• Pigmentation Disorders

  • Albinism -suncreenale skin uses suncreen long sleeves sunglasses Acquired, patchy destruction/loss of melanocytes ➜ hypopigmented macules Acquired, patchy destructimelhypopigmented maculested maculested macules

  • vates UV damage risk

  • Vitiligo - MIcheal Jackson disease

  • Acquired, patchy destructimelhypopigmented maculested maculested macules; autoimmune association

• Symptomatic descriptor

  • Pruritus: itch sensation; mediated by histamine, serotonin, cytokines; common to many dermatoses

Inflammatory Skin Disorders

• Contact Dermaement (Allergic/irritant) - could be an example likcalcineurinng

  • Type IV hypersensitivity → erythema, edema, vesicles at contact calcineurin

  • ement: remove allergen, topical/systemic steroids, barrier creamscalcineurin

• (Hives)

  • IgE-mediated mast-cell degranulation → transient wheals; risk of ancalcineurinaphylaxis in severe allergy

• Atopic Dermatitis (Eczema)

  • Chronic, relapsing; genetic filaggrin defect + allergiecalcineurin lichenified plaques in flexures

  • Long-term care: moisturizers, avoid triggers, topical steroids, calcineurin inhibitors

Psoriasis (Immune-Mediated Hyper-proliferation) Presents as a silvery plaque

• Multifactorial: polygenic predisposition + triggers (trauma, infection, stress)

• Pathophysiology

  • Aberrant T-cell activation ➜ cytokine release (TNF-α, IL-17/23) ➜ keratinocyte hyper-turnover (~3–4 days vs normal 28 days) ➜ thickened epidermis + retention of nuclei in stratum corneum (parakeratosis)

• Clinical picture

  • Well-demarcated erythematous plaques with overlying silvery scale (classic on extensor surfaces)

  • Auspitz sign: pinpoint bleeding on scale removal

  • Koebner phenomenon: lesions at trauma sites

  • Course: periods of remission & exacerbation; pruritus common

• Therapies

  • Topical high-potency steroids, vitamin D analogues (calcipotriol), coal tar

  • Phototherapy (UVB, PUVA) stimulates controlled cell turnover & immunomodulation

  • Systemic: methotrexate, cyclosporine, biologics (anti-TNF, anti-IL-17/23) for moderate–severe disease

Selected Skin Infections

Acute Necrotizing Fasciitis (“Flesh-Eating”) Common in diabetic patients. Spreads very rapidly hours not days

• Polymicrobial; Group A \beta-hemolytic Streptococcus pyogenes frequent culprit, sometimes with anaerobes (e.g.
  Clostridium)

• Rapid spread along fascial planes; toxins → vascular occlusion, tissue necrosis, systemic sepsis

• Hallmarks

  • Severe, disproportionate pain, erythema → violaceous → black gangrene

  • Rapid onset, edema, bullae, systemic toxicity (fever, tachycardia, hypotension)

• Urgent management - These patients require a lot of antibiotics

  • carbapenemtrum IV antibiotics (e.g.
    carbapenem + clindamycin), surgical debridement; may require amputation

  • Hyperbaric oxygen adjunct

Leprosy (Hansen’s Disease- attacks nerves and muscles) Curable in eaerly stages

• Mycobacterium leprae; obligate intracellular; requires prolonged exposure, mainly affects immunocompromised or genetically susceptible

• Clinical spectrum: tuberculoid (paucibacillary) vs lepromatous (multibacillary)

• Findings: hypopigmented/erythematous macules, loss of sensation due to peripheral nerve involvement, facial deformity (“lion-like facies”)

• Treatment: multidrug therapy (dapsone + rifampin ± clofazimine) for 6–24 months

Herpes Simplex Virus (HSV)- Asymptomatic viral shedding (can spread without an active sore)

• HSV-1 (orolabial-cold sores), HSV-2 (genital spread via sexual contact) — but overlapping sites possible

• Latency in sensory ganglia (trigeminal or sacral)

• Prodrome: burning/tingling neuralgia ➜ grouped vesicles on erythematous base ➜ crusting

• Ocular involvement → keratitis, vision threat

• Chronic with recurrences; triggered by stress, UV, illness

• Management: oral or topical antivirals (acyclovir, valacyclovir) initiated at prodrome to reduce severity

• Appears with fever, sickness, and stress

Tinea (Dermatophytosis)

• Fungal infection (Trichophyton, Microsporum, Epidermophyton)

• Classification by site

  • Tinea capitis (scalp): alopecia patches; often in children - “cradel cap”

  • Tinea corporis (body): “ringworm” annular plaques with central clearing

  • Tinea pedis (feet): interdigital scaling, fissures (“athlete’s foot”)

• Transmission: human-human, animal-human, fomites

• Signs: itchy, erythematous rings, vesicles/papules at advancing border

• Therapy: topical azoles/allylamines; oral griseofulvin/terbinafine for scalp or refractory disease

Skin Cancers

Squamous Cell Carcinoma (SCC)- caused by sun exposure

• Malignant proliferation of keratinocytes in epidermis

• Etiology: cumulative UVB radiation (sun-exposed sites); risk factors—actinic keratoses, immunosuppression, chronic wounds

• Lesion characteristics

  • Painless, scaly, hyperkeratotic, reddish plaque or nodule with irregular border; may ulcerate

  • Generally slow-growing, localized; metastasis risk if lip, ear, or immunosuppressed

• Management: surgical excision with clear margins; Mohs micrographic surgery for high-risk locations; radiation if unresectable

Malignant Melanoma - the most serious, fast growing

• Neoplasm of melanocytes; most deadly cutaneous cancer

• Risk factors: intermittent intense sun exposure, blistering sunburns, fair skin, numerous/atypical nevi, genetic mutations (e.g.
  BRAF, CDKN2A), hormonal influence (pregnancy, estrogen therapy)

• May arise de novo or from pre-existing nevus

• Red-flag evolution summarized by ABCDE (see below)

• Biological behavior

  • Radial growth phase → vertical growth invading dermis → metastasis via lymphatics & blood

• Treatment

  • Wide local excision (depth guided by Breslow thickness) extending into dermis/subcutaneous fat - Surgery

  • Sentinel lymph-node biopsy for staging

  • Adjuvant: immunotherapy (checkpoint inhibitors), targeted therapy (BRAF/MEK inhibitors), radiation for metastasis

ABCDE Criteria: Benign vs Malignant Mole Assessment

• A — Asymmetry

  • Benign: symmetrical; Malignant: halves unequal

• B — Border

  • Benign: smooth, even; Malignant: irregular, scalloped, poorly defined

• C — Colour

  • Benign: uniform brown/tan; Malignant: varied shades (black, red, white, blue)

• D — Diameter

  • Benign: usually < 6\text{ mm}; Malignant: may exceed 6\text{ mm}, but size alone not diagnostic

• E — Evolving

  • Benign: stable; Malignant: changes in size, shape, colour, elevation, or new symptoms (itching, bleeding)

Clinical Pearl: When a patient removes socks and skin flakes disperse (xerosis or hyperkeratotic scaling), examine for tinea pedis, psoriasis, or chronic eczema, and evaluate environment (low humidity) & footwear hygiene.

Inter-disciplinary Connections & Implications

• Dermatologic signs often mirror systemic disease (e.g.
  psoriasis association with psoriatic arthritis, metabolic syndrome)

• Prompt recognition of necrotizing fasciitis or melanoma greatly alters prognosis—emphasizing collaborative care and public education on sun safety & early warning signs.

• Ethical obligation: counter stigma (leprosy, HSV) by providing accurate contagion facts and supporting affected patients.