Diseases, Disorders, and Injuries of the Integumentary System

Core Concepts

The language of skin lesions

Lesions are primary (initial change) or secondary (later changes such as crust or scar). Commonly taught primary lesions include:

• Macule — flat, color-only change (freckle); no elevation
• Papule — small, raised, solid bump (wart)
• Plaque — larger, flat-topped raised area (psoriasis)
• Vesicle — small fluid-filled blister (chickenpox, herpes); bulla = large blister
• Pustule — raised bump containing pus (acne, impetigo)
• Nodule — deeper solid mass; wheal — transient itchy raised area (hives)

Secondary changes include scale, crust, erosion, ulcer, and scar. Separating "what I see" (observation) from "what it means" (interpretation) is the discipline this guide emphasizes.

Bacterial skin infections

Bacteria cause common skin problems:

• Impetigo — superficial infection, most common in children, often around the nose and mouth, classically with honey-colored crusts; commonly associated with staphylococcal and streptococcal bacteria.
• Folliculitis, furuncles (boils), carbuncles — infections of hair follicles and surrounding tissue, usually staphylococcal; a boil is a deeper, painful collection.
• *MRSA (methicillin-resistant Staphylococcus aureus)* — a resistant strain causing skin and soft-tissue infections; a major healthcare concern because many antibiotics don't work against it. Prevention: hand hygiene and wound care.

Viral skin infections

• Warts — caused by human papillomavirus (HPV); benign keratinocyte growths on hands and feet (plantar warts).
• Herpes simplex virus (HSV) — recurrent cold sores (oral) and genital lesions; the virus can lie dormant in nerve cells and reactivate.
• Herpes zoster (shingles) — reactivation of the varicella-zoster virus (chickenpox virus); a painful, blistering rash along a single nerve pathway (dermatome).
• Molluscum contagiosum — poxvirus; small, firm, dome-shaped bumps, most often in children.

Fungal skin infections

• Tinea (ringworm) — despite the name, caused by fungi (dermatophytes), not worms. Named by site: tinea pedis (athlete's foot), tinea capitis (scalp), tinea corporis (body); the name comes from the ring-shaped, red, scaly patch it produces.
• Candidiasis (yeast infection) — caused by Candida yeasts, which overgrow in warm, moist areas (skin folds, mouth, diaper area); the healthy microbiome usually keeps them in check.

Inflammatory and immune-related conditions

• Acne vulgaris — begins when a follicle plugs with sebum and dead keratinocytes, forming a comedo (blackhead or whitehead). Follicle bacteria (commonly taught as Cutibacterium acnes) can proliferate in the plug, and the immune response produces inflammation. Puberty hormones drive increased sebum; acne is not caused by dirt alone — it is a multifactorial follicular disorder.
• Eczema (atopic dermatitis) — a chronic, itchy condition with dry, red, sometimes weeping patches; classically linked to a defective skin barrier and an overactive immune response to triggers. It often begins in childhood and can run in families.
• Psoriasis — immune-mediated, with dramatically accelerated keratinocyte turnover producing thick, silvery-scaled plaques over red bases on elbows, knees, scalp, and lower back; nail pitting can accompany it.
• Contact dermatitis — skin inflammation from direct contact with an irritant (harsh chemicals) or an allergen (the urushiol oil in poison ivy), producing red, itchy, sometimes blistering patches at the contact site.

Pigment disorders

• Vitiligo — melanocyte loss in well-defined white patches; an immune attack on melanocytes is the commonly taught mechanism.
• Albinism — inherited reduction or absence of melanin production, causing very light skin and hair and increased UV sensitivity.
• Age-related pigment changes — freckles, sun spots, and other accumulations from cumulative UV exposure; any changing pigmented lesion deserves professional evaluation.

Skin cancer

The three most commonly taught types:

• Basal cell carcinoma (BCC) — the most common skin cancer; arises from basal keratinocytes, grows slowly, rarely spreads but can invade locally; often a pearly, sometimes ulcerated bump on sun-exposed areas.
• Squamous cell carcinoma (SCC) — arises from keratinocytes of the stratum spinosum; can metastasize if untreated; often a scaly, crusted, or ulcerated patch on sun-exposed skin.
• Melanoma — arises from melanocytes; the most dangerous form because of its ability to spread; often (not always) develops from or resembles a mole. The ABCDE screening mnemonic — Asymmetry, Border irregularity, Color variation, Diameter ~6 mm, Evolving — prompts professional evaluation; it is not a diagnostic tool.

Prevention centers on reducing UV exposure: shade during peak sun, protective clothing, and sunscreen — general public-health guidance.

Injuries: burns

Burns are classified by depth (commonly taught system):

• Superficial (first-degree) — damage limited to the epidermis; red, painful, no blistering (classic sunburn).
• Partial-thickness (second-degree) — epidermis plus part of the dermis; painful blisters, red or mottled skin.
• Full-thickness (third-degree) — entire epidermis and dermis destroyed, possibly deeper; may appear white, brown, or charred and can be painless because nerve endings are destroyed — a counterintuitive exam point.

Burn extent is commonly estimated with the rule of nines (adult): the body surface divides into regions worth multiples of 9% (head 9%, each arm 9%, anterior trunk 18%, posterior trunk 18%, each leg 18%, perineum 1%). Larger burns threaten fluid balance, temperature control, and infection risk. Emergency burn care is a professional clinical procedure; first-aid education is public safety information, not a treatment protocol.

Wound healing (brief overview)

Healing follows a commonly taught sequence: inflammatory (clotting; immune cells clean the wound), proliferative (new tissue and vessels form), and remodeling (collagen reorganizes, scar matures). Healing time depends on wound size, depth, and infection.

How It Works / Step-by-Step Process

Describing a skin finding like a clinician (educational walkthrough):

1. Inspect: note the lesion's type (macule, papule, vesicle…), color, size, shape, and borders.
2. Locate: record where it is and its distribution (localized vs. widespread; follows a nerve path?).
3. Classify: primary lesion (initial) or secondary (crust, scale, ulcer)?
4. Gather context: onset, itching/pain, fever, exposures, family history.
5. Reason, don't diagnose: connect the description to possible categories (infection? inflammation? injury?) — diagnosis and treatment require a licensed clinician.

Burn assessment in the same spirit: determine depth (which layers are damaged), estimate extent (rule of nines), and consider which functions are lost — protection, thermoregulation, sensation — to explain why the injury is dangerous.

Common Confusions