Skin Disorders Study Guide - Sensory 2

Skin Disorders Study Guide — Sensory 2 (Ch. 56 & 57) Built from your instructor's slide deck, with mechanism-level detail added only where the slides assume background knowledge. Page numbers (e.g., p.1143) match the Linton Med-Surg text. Each condition is compartmentalized the way you like, and ends with a Clinical Pearl / NCLEX-style prompt. Quick Skin Anatomy Refresher (foundation for everything below) Epidermis — outermost, avascular; contains melanin (pigment/UV protection) and keratin. Normal turnover ≈ 28 days. Dermis ("true skin") — collagen, blood vessels, nerve endings, hair follicles + arrector pili, sebaceous (oil) glands, sudoriferous (sweat) glands, Pacinian corpuscles (pressure). Subcutaneous / hypodermis — fat + connective tissue; insulates, cushions, stores energy. Functions — protection (#1 barrier), temperature regulation, sensation, excretion, absorption, vitamin D synthesis. Thinnest skin = eyelids; thickest = soles of feet. Why this matters for the exam: burn depth, cancer type, and infection severity are all defined by which layer is involved. 1. Pruritus (p.1143) Pathophysiology / why it happens Itching is a symptom, not a disease. Sensory nerve endings in the dermis are stimulated by histamine and other mediators (released in allergy, dry skin, inflammation), or by systemic causes (liver/kidney disease, diabetes, lymphoma, drug reactions). Scratching damages the skin barrier → more inflammation → more itching = the itch–scratch cycle. Clinical presentation Excoriations (scratch marks), thickened/lichenified skin in chronic cases, possible secondary infection. Symptoms Itching (localized or generalized), often worse at night. Diagnostic tests / findings History & physical to identify the underlying cause; labs if systemic cause suspected (LFTs, BUN/creatinine, glucose, CBC). Treatment & nursing interventions - Treat the cause (this is the key teaching point). - Topical/oral corticosteroids, antihistamines, local anesthetics. - Cool environment, tepid baths, keep nails short, mild fragrance-free moisturizers, loose cotton clothing, distraction. Side effects to know Antihistamines (diphenhydramine) → sedation, anticholinergic effects (dry mouth, urinary retention, confusion in elderly). Long-term topical steroids → skin thinning/atrophy. Complications Secondary bacterial infection, scarring, sleep disturbance. Risk factors Dry skin (xerosis), elderly, allergy, systemic disease. Clinical Pearl: Generalized pruritus without an obvious rash is a red flag for a systemic cause — think liver disease (bile salts), renal failure (uremia), or hematologic malignancy. Don't just treat the skin; look deeper. 2. Dermatitis (p.1143) Pathophysiology / why it happens Inflammation of the skin from contact with irritants/allergens or from immune dysregulation. Three forms on your slides: - Contact — direct skin contact with an irritant (chemicals, soaps) or allergen (poison ivy, nickel, latex, cosmetics, pet dander). Allergic contact = type IV (delayed) hypersensitivity — reaction shows up 24–72 hrs after exposure. - Atopic (eczema) — chronic, relapsing; linked to a personal/family history of allergies, asthma, hay fever ("atopic triad") and a defective skin barrier (type I/IgE associated). - Seborrheic — overgrowth of Malassezia yeast in oily areas (scalp = dandruff, eyebrows, nasolabial folds). Clinical presentation Skin becomes red, inflamed, with papules; weeping/crusting; scaling in chronic cases; well-demarcated borders in contact dermatitis (often matches the shape of the exposure). Symptoms Burning, itching, pain, edema. Diagnostic tests / findings History & physical; patch testing to identify allergens in allergic contact dermatitis. Treatment & nursing interventions - Remove / avoid the cause (most important). - Antihistamines and anti-inflammatories (topical corticosteroids). - Cool compresses, emollients, avoid scratching. Side effects to know Topical steroid overuse → atrophy, striae, telangiectasias; antihistamine sedation. Complications Secondary infection from scratching, lichenification, chronic relapsing course. Risk factors Atopic history (asthma/allergies), occupational irritant exposure, family history. Clinical Pearl: Contact dermatitis distribution tells the story — a linear/streaky rash = poison ivy; a rash exactly where a watchband, necklace, or glove sits = nickel/latex. On the NCLEX, the right answer for prevention is almost always "identify and avoid the offending agent." 3. Acne (Acne Vulgaris) (p.1146) Pathophysiology / why it happens A disorder of the pilosebaceous unit (hair follicle + sebaceous gland). Androgens (puberty, menses, hormones) increase sebum production; the follicle plugs with sebum and dead keratin → comedone (blackhead/whitehead). Cutibacterium acnes (formerly P. acnes) bacteria multiply in the plug → inflammation → papules, pustules, nodules, cysts. Clinical presentation Comedones (open = blackheads, closed = whiteheads), papules, pustules, nodules, cysts on face, chest, back. Symptoms Visible lesions; tenderness with inflammatory/cystic lesions; psychosocial distress. Diagnostic tests / findings Clinical diagnosis by visual inspection. Treatment & nursing interventions - Topical retinoids (vitamin A derivatives), benzoyl peroxide, topical/oral antibiotics. - Isotretinoin (Accutane) for severe/cystic acne. - Teach gentle (not harsh) cleansing, non-comedogenic/oil-free cosmetics, don't pick/squeeze. Side effects to know (HIGH YIELD) - Isotretinoin = potent teratogen → requires two forms of contraception + the iPLEDGE program; monitor triglycerides/lipids and LFTs; causes severe dryness of skin/lips/eyes; linked to mood changes/depression. - Benzoyl peroxide → dryness, bleaches fabric. - Topical retinoids → photosensitivity, irritation. Complications Scarring, hyperpigmentation, psychological/self-esteem effects. Risk factors Adolescence, hormonal changes (menses, oral contraceptives can worsen or help depending on type), oil-based cosmetics, family history, certain medications (steroids). Clinical Pearl: Before starting isotretinoin in any female of childbearing age, the nurse must confirm a negative pregnancy test and enrollment in iPLEDGE. A patient on Accutane reporting worsening mood is a red flag worth escalating. 4. Fungal Infections — Dermatophytes / Tinea (p.1147) Pathophysiology / why it happens Dermatophytes are fungi that feed on keratin in skin, hair, and nails. They thrive in warm, moist environments. Named by location: - Tinea capitis — scalp (ringworm of scalp) - Tinea corporis — body (classic ring-shaped lesion) - Tinea cruris — groin ("jock itch") - Tinea pedis — feet ("athlete's foot") - Tinea unguium / onychomycosis — nails Clinical presentation Red, scaly, ring-shaped patches with a raised, advancing border and central clearing; macerated/cracked skin between toes; thickened discolored nails. Symptoms Itching, burning, scaling. Diagnostic tests / findings - KOH (potassium hydroxide) prep of skin scraping → shows fungal hyphae under microscope. - Wood's lamp — some fungi fluoresce. - Fungal culture. Treatment & nursing interventions - Topical antifungals (clotrimazole, terbinafine, ketoconazole, nystatin for candidal areas). - Oral antifungals (terbinafine, griseofulvin especially for scalp/nail) for widespread or resistant cases. - Keep skin clean and dry, change socks, don't share towels/combs, treat the full course. Side effects to know Oral antifungals (terbinafine, griseofulvin, ketoconazole) → hepatotoxic — monitor LFTs; griseofulvin → photosensitivity, GI upset, avoid alcohol. Complications Secondary bacterial infection, spread to others, chronic nail involvement. Risk factors Decreased immune response, diabetes mellitus, poor circulation, corticosteroid use, extremes of age, communal showers, sweating. Clinical Pearl: A ring-shaped lesion with central clearing and a scaly active border = classic tinea corporis ("ringworm" — it's a fungus, not a worm). Oral antifungal therapy → watch the liver (LFTs). 5. Psoriasis (p.1149) Pathophysiology / why it happens A chronic autoimmune/inflammatory disease. T cells are abnormally activated → trigger massive overproduction of epidermal cells (6–9× normal). Skin that should take ~26–28 days to turn over is shed in 3–4 days, so immature cells pile up → thick scaling plaques. Clinical presentation Red, raised plaques topped with silvery-white scales; common on scalp, elbows, knees, lower back, genitalia, and nails (pitting). May crack and bleed. Symptoms May or may not itch; pain/cracking; significant psychosocial impact (depression). Diagnostic tests / findings Clinical appearance; biopsy if uncertain. Auspitz sign — pinpoint bleeding when a scale is lifted off. Treatment & nursing interventions - Avoid precipitating factors. - Salicylic acid (removes scale), topical corticosteroids, vitamin D analogs. - Phototherapy / UV light. - Immunosuppressants — methotrexate, cyclosporine (slow cell growth). - Biologics — etanercept (Enbrel) and other TNF/IL inhibitors. Side effects to know (HIGH YIELD) - Methotrexate → hepatotoxicity, bone marrow suppression, mouth sores; give folic acid, monitor CBC/LFTs, avoid alcohol, teratogenic. - Biologics (Enbrel) → increased infection risk (TB reactivation) — screen before starting. - Long-term potent topical steroids → skin atrophy. Complications Psoriatic arthritis, secondary infection, profound psychosocial distress/depression. Risk factors / triggers Genetics; stress, trauma (Koebner phenomenon), infections, hormonal changes, certain medications; typical onset age 10–35. Chronic — improves and recurs. Clinical Pearl: Silvery scales on red plaques over elbows/knees/scalp = psoriasis. Lifting a scale → pinpoint bleeding = Auspitz sign. Any patient starting methotrexate needs baseline CBC + LFTs and must avoid alcohol and pregnancy. 6. Intertrigo (p.1150) Pathophysiology / why it happens Inflammation where two skin folds rub together (under breasts, abdominal folds, groin, axillae). Heat + friction + trapped moisture break down the skin barrier; warm moist folds then become an ideal home for Candida (yeast) and bacteria. Clinical presentation Red, weeping, raw skin in the fold; satellite vesicles and pustules (suggests candidal infection). Symptoms Burning, itching, soreness, odor. Diagnostic tests / findings History & physical; skin scraping/culture or biopsy to confirm organism. Treatment & nursing interventions - Topical corticosteroid + antifungal — nystatin, ketoconazole, clotrimazole. - Keep folds clean and dry, separate skin surfaces (soft cloth/absorbent dressing), promote air circulation, manage moisture. Side effects to know Prolonged topical steroid in folds → skin atrophy (folds are thin/occlusive, so absorb more); be cautious with potency and duration. Complications Secondary bacterial/fungal infection, skin breakdown. Risk factors Obesity, diabetes, heat/humidity, immobility, incontinence, excessive sweating. Clinical Pearl: "Satellite lesions" (small pustules just beyond the main red patch) in a skin fold = candidal (yeast) intertrigo — treat with an antifungal and, most importantly, keep the area dry. 7. Herpes Simplex Virus — HSV (p.1152) Pathophysiology / why it happens A virus spread by direct contact. After the first infection, HSV travels up nerves and goes dormant (latent) in the nerve ganglia. Stress, illness, fever, sunlight, or immunosuppression reactivate it → recurrent lesions in the same spot. - HSV-1 — face/upper body (cold sores/fever blisters). - HSV-2 — genital. Clinical presentation Cluster of small vesicles on a red base that rupture, weep, then crust; commonly on lips/perioral or genital area. Symptoms Tingling/burning prodrome before lesions appear, pain, itching. Diagnostic tests / findings Exudate (fluid) from a lesion for viral culture; Tzanck smear or PCR. Treatment & nursing interventions - Acyclovir (Zovirax) — oral/topical antiviral; valacyclovir/famciclovir. - Cold sores OTC → docosanol (Abreva). - Teach: contagious when lesions present, don't share utensils/lip products, hand hygiene, avoid touching eyes (herpetic keratitis), avoid known triggers; sunscreen on lips. Side effects to know Acyclovir → nephrotoxicity with IV/high doses (push fluids, monitor renal function), GI upset. Complications Recurrent outbreaks, herpetic whitlow (fingers), ocular involvement (keratitis → blindness), neonatal herpes if active during delivery, spread to immunocompromised. Risk factors Stress, fatigue, illness/fever, UV/sun exposure, immunosuppression, sexual contact (HSV-2). Clinical Pearl: A patient describing "tingling and burning before the blister appears" is reporting the prodrome — antivirals work best when started at the first sign, before vesicles fully form. 8. Herpes Zoster — Shingles (p.1153) Pathophysiology / why it happens Caused by reactivation of the varicella-zoster virus (VZV) — the same virus as chickenpox. After childhood chickenpox, VZV lies dormant in a dorsal root (nerve) ganglion. When immunity drops (age, illness, stress, immunosuppression), it reactivates and travels down a single sensory nerve → rash in that nerve's dermatome. Clinical presentation Unilateral rash that follows a nerve pathway (does NOT cross the body's midline), most often on the trunk; progresses from rash → grouped vesicles → ooze → crust. Symptoms Pain, burning, tickling, tingling, or numbness BEFORE the rash appears; flu-like symptoms (usually without fever); severe pain described as burning/stabbing/needles. Diagnostic tests / findings Clinical (dermatomal pattern is classic); H&P; viral culture/PCR of vesicle fluid if needed. Treatment & nursing interventions - Acyclovir (best within 72 hours of rash onset), anti-inflammatories, analgesics, gabapentin (Neurontin) for nerve pain. - Contact precautions while vesicles/drainage present (can give chickenpox to non-immune people, including pregnant women and immunocompromised). - Keep lesions clean/dry; cool compresses. Side effects to know Gabapentin (Neurontin) → dizziness, drowsiness, ataxia (fall risk); acyclovir → renal caution/hydration. Complications - Postherpetic neuralgia (PHN) — persistent nerve pain after the rash heals (the most common complication). - Ophthalmic zoster — involvement near the eye/nose tip (Hutchinson sign) → can threaten vision; medical emergency. - Secondary bacterial infection. Risk factors / prevention Age >50, immunosuppression, illness, stress, prior chickenpox. Prevention: shingles vaccine (recombinant zoster vaccine) recommended after age 50. Rash typically heals in 2–4 weeks. Clinical Pearl: A painful, unilateral, blistering rash that stops at the midline = shingles. If lesions appear on the tip of the nose or near the eye, suspect ophthalmic involvement → urgent ophthalmology referral to prevent vision loss. Lingering pain after healing = postherpetic neuralgia. 9. Cellulitis (p.1155) Pathophysiology / why it happens An acute, usually bacterial infection (often Streptococcus or Staphylococcus, including MRSA) of the dermis and subcutaneous tissue. Bacteria enter through a break in the skin (cut, insect bite, blister, burn, dry/cracked skin, ulcer) and spread through soft tissue, triggering inflammation. Clinical presentation Skin red, warm, edematous, painful, with poorly defined (spreading) borders; abscess may form. Symptoms Pain/tenderness, fever, headache, nausea, malaise, itching. Diagnostic tests / findings - H&P; mark the borders to monitor spread. - Blood cultures (if sepsis suspected), CBC (↑ WBC), wound culture. - Bone scan (rule out osteomyelitis), CT/MRI; ultrasound to rule out DVT (mimics cellulitis). Treatment & nursing interventions - Antibiotics (oral or IV depending on severity). - Incision & drainage (I&D), debridement if abscess. - Warm moist compresses, elevate the affected part, rest, mark and monitor margins, pain control. Side effects to know Antibiotic-related → GI upset, allergic reactions, C. difficile with broad-spectrum use, nephrotoxicity with vancomycin (monitor levels/renal function). Complications Sepsis (life-threatening), abscess, osteomyelitis, tissue necrosis, recurrence. Risk factors Elderly, diabetic, peripheral vascular disease (PVD), immunocompromised, lymphedema, any break in skin integrity. Clinical Pearl: Always outline the red margins with a pen and note the time — if the redness extends beyond the marked line, the infection is spreading and the provider needs to know. New fever + rapidly advancing redness = think sepsis. 10. Skin Cancer (p.1155) Pathophysiology / why it happens UV radiation damages DNA in skin cells, causing uncontrolled growth. Cumulative sun exposure (and tanning beds, radiation, chronic scars/ulcers) drives this. By age 65, about half of Americans will have had some form of skin cancer. Prompt removal decreases the risk of metastasis. Three types (know how to tell them apart) Type Key features Behavior Basal cell carcinoma Most common, slow-growing, waxy/pearly border Rarely metastasizes Squamous cell carcinoma Rough, scaly; often on tongue/lip, sun-exposed areas Can metastasize to internal organs Malignant melanoma Coal-black/blue, irregular border, asymmetric Highly malignant — spreads rapidly; most deadly Clinical presentation / symptoms (general) A new growth, or a change in a mole or scar. Use ABCDE: - Asymmetry Border (irregular) Color (varied/multiple) Diameter (> 6 mm) - Evolving (changing over time) Diagnostic tests / findings Visual inspection + biopsy (definitive). Treatment & nursing interventions - Removal: surgical excision, Mohs surgery (layer-by-layer, tissue-sparing — used for face/high-risk), cryotherapy, laser. - Radiation; wide surgical excision for melanoma; chemotherapy/immunotherapy in advanced melanoma. - Follow-up every 3–6 months. Teach sun protection (SPF, protective clothing, avoid peak sun/tanning beds) and monthly skin selfexams. Side effects to know Radiation → skin breakdown/fatigue; chemo/immunotherapy for melanoma → fatigue, immune-related effects, myelosuppression. Complications Metastasis (especially melanoma → other organs), disfigurement, recurrence. Risk factors Repeated/prolonged UV exposure, fair skin that freckles/burns, red or blond hair, blue/green eyes, family history, history of sunburns, indoor tanning, radiation exposure, certain moles, immunosuppression. Clinical Pearl: Melanoma = ABCDE. A mole that is asymmetric, has an irregular border, multiple colors, > 6 mm, or is changing must be evaluated. "Pearly/waxy" = basal cell; "rough/scaly on the lip" = squamous cell; "dark, irregular, fastchanging" = melanoma (the dangerous one). 11. Burns (p.1161) Pathophysiology / why it happens Tissue destruction from thermal, chemical, electrical, or radiation energy. Severity depends on depth, % body surface area (TBSA), location, age, cause, and comorbidities. Damaged capillaries leak fluid → massive fluid shift out of the vasculature → risk of hypovolemic (burn) shock early on. Depth classification Degree Layers involved Appearance Pain First (superficial) Epidermis only (e.g., sunburn) Red, dry Painful, swelling Second (partial thickness) Epidermis + dermis Red, blistering, moist Very painful, edema Third (full thickness) Through dermis into subcutaneous/muscle Gray, white, or black, leathery (eschar) No pain in the full-thickness area (nerves destroyed) — but painful at surrounding edges Severity assessment - Rule of Nines estimates % TBSA (head 9%, each arm 9%, each leg 18%, anterior trunk 18%, posterior trunk 18%, genitalia 1% in adults; infants/children weighted toward the head). - Worse outcomes with: infants and elderly; burns to head, genitalia, hands; greater TBSA; full thickness; comorbidities (diabetes, cardiac, respiratory). First aid / immediate priorities STOP THE BURN. Thermal: cool water for superficial/partial burns — NO ice, NO butter, NO oils. Cover with clean/sterile dressing. Chemical: brush off dry chemical first, then flush — some chemicals are activated by water. Electrical: look for entry AND exit wounds; runs deep; high risk of cardiac arrhythmias → cardiac monitoring; requires immediate medical attention. Prevent shock; protect the airway/respiratory status — look for soot around mouth/nares, singed nasal hairs (inhalation injury), and assess for carbon monoxide poisoning. Treat associated injuries. Phases of burn management Phase Time frame Focus Emergent / resuscitative Onset → complete fluid resuscitation (≈72 hrs) Airway, fluid resuscitation (Lactated Ringer's), central line/Foley, IV morphine for pain Acute Diuresis → complete wound closure Wound care, infection prevention, nutrition, grafting Rehabilitation Wound closure → optimal function PT/OT, contracture prevention, reconstruction, psychosocial counseling, vocational rehab Treatment & nursing interventions - Airway first; fluid resuscitation (LR; Parkland-type formula); Foley to monitor output; central line; IV opioids (morphine) — never IM/SQ in the emergent phase (poor absorption from edematous tissue). - NGT for paralytic ileus; tetanus prophylaxis + antibiotics; reverse (protective) isolation for large burns; sterile technique. - Wound care: debridement/removal of eschar, whirlpool, open or closed dressings; topical antimicrobials. - Escharotomy — surgical incision through eschar to relieve constriction and restore circulation when tight eschar + edema compromise perfusion. - Grafts: autograft (self — best), homograft (human donor), heterograft (animal). Full-thickness grafts → best appearance/function (face, hands); partial-thickness → large areas. Donor site: special covering left in place, allowed to air dry; bed cradle keeps sheets off. - Nutrition: high calorie (2,000–6,000)/TPN, high protein, vitamins A, C, E, calcium, iron (hypermetabolic state needs fuel for healing). Side effects to know (HIGH YIELD topical agents) - Silver sulfadiazine (Silvadene) → avoid in sulfa allergy; can cause leukopenia (transient drop in WBC). - Mafenide (Sulfamylon) → painful on application and can cause metabolic acidosis (carbonic anhydrase inhibitor) — monitor acid–base. - Silver nitrate → stains black, can cause electrolyte loss (hyponatremia). Complications - Infection/sepsis — the MOST COMMON CAUSE OF DEATH in the acute period. - Curling's ulcer (stress ulcer of the stomach/duodenum after major burns). - Hypovolemic shock (early), then fluid overload during diuresis; kidney failure, anemia, contractures/scarring, decubitus ulcers, respiratory complications, paralytic ileus. - Psychological: pain, fear, disfigurement, separation, immobilization, helplessness, depression. Risk factors Open flame/scald exposure, occupational chemical/electrical exposure, smoking, age extremes, impaired mobility/sensation. Clinical Pearl: Two burn red flags to memorize: 1. Soot around the nose/mouth, singed nasal hair, hoarseness = inhalation injury → protect the airway before it swells shut (airway is always priority #1). 2. Full-thickness (3rd-degree) burns are painless in the burned area because nerve endings are destroyed — a patient with a white/leathery, painless burn is more severely injured than one screaming in pain from a partial-thickness burn. Don't be falsely reassured by lack of pain. Bonus lab/value pearl: in the emergent phase expect hyperkalemia (potassium leaks from damaged cells) and hemoconcentration; during the diuretic/acute phase watch for hypokalemia. Best early indicator of adequate fluid resuscitation = urine output (~30 mL/hr in adults). Appendix — Aesthetic Surgeries (p.1169–1172, reading assignment) Brief reference only (your slide lists these as a reading, not a tested disorder): - Rhytidectomy — face lift - Blepharoplasty — eyelid lift - Rhinoplasty — nose reshaping - Breast augmentation / reduction One-page "if you only review this" cheat list Auspitz sign → psoriasis Satellite lesions → candidal intertrigo KOH prep + hyphae → tinea (fungal) Prodrome tingling before vesicles → herpes (HSV) Unilateral rash that stops at midline + PHN → shingles (VZV reactivation) Mark the borders → cellulitis (watch for spread/sepsis) ABCDE → melanoma Pearly/waxy → basal cell; scaly on lip → squamous cell No pain in the burn = full thickness (worse, not better) Sepsis = #1 cause of death in acute burn phase Curling's ulcer = stress ulcer after burns Airway is always the first burn priority (soot, singed hairs = inhalation injury) Isotretinoin/methotrexate = teratogenic + need lab monitoring