12.1 Primary Dermatologic Lesions, Inflammatory Dermatoses & Cutaneous Malignancies
Key Takeaways
- Primary skin lesion taxonomy provides the essential diagnostic foundation: macules/patches are flat circumscribed color changes (<1 cm vs >=1 cm); papules/plaques are palpable solid elevations (<1 cm vs >=1 cm); vesicles/bullae are fluid-filled blisters (<1 cm vs >=1 cm); wheals represent transient dermal edema.
- Plaque psoriasis is an immune-mediated papulosquamous disease driven by the IL-23/Th17/IL-17 inflammatory axis, characterized by well-demarcated erythematous plaques with silvery-white micaceous scale, the Auspitz sign, and the Koebner phenomenon; systemic oral corticosteroids are strictly contraindicated due to the risk of precipitating fatal generalized pustular or erythrodermic psoriasis flares upon withdrawal.
- Melanoma screening utilizes the ABCDE criteria (Asymmetry, Border irregularity, Color variegation, Diameter >=6 mm, Evolving) and the 'ugly duckling' sign; any suspicious pigmented lesion mandates a full-thickness narrow-margin (1-3 mm) excisional biopsy down to subcutaneous fat, as superficial shave biopsies that transect the base prevent accurate Breslow depth measurement, which is the single most critical histological prognostic determinant.
- Autoimmune bullous diseases are differentiated by blister architecture and Nikolsky sign: Bullous Pemphigoid produces tense, subepidermal blisters with negative Nikolsky sign (autoantibodies against hemidesmosomal BP180/BP230), whereas Pemphigus Vulgaris produces flaccid intraepidermal blisters and severe mucosal ulcerations with a positive Nikolsky sign (autoantibodies against desmoglein 1/3).
- Severe cutaneous adverse reactions (SCAR)—including Stevens-Johnson Syndrome (SJS, <10% BSA detachment), SJS/TEN overlap (10-30% BSA), and Toxic Epidermal Necrolysis (TEN, >30% BSA)—are medical emergencies driven by medication triggers (sulfa drugs, allopurinol, aromatic anticonvulsants, NSAIDs), demanding immediate cessation of the culprit drug, transfer to a burn intensive care unit, and avoidance of silver sulfadiazine.
Last updated: August 2026
Primary Dermatologic Lesions, Inflammatory Dermatoses & Cutaneous Malignancies
Cutaneous complaints represent over 15% of all primary care encounters in adult and geriatric medicine. For the Adult-Gerontology Primary Care Nurse Practitioner (AGPCNP), clinical competency requires mastery of standard dermatologic taxonomy, systematic lesion interrogation, evidence-based management of chronic inflammatory dermatoses, rapid identification and biopsy selection for cutaneous malignancies, and immediate triage of life-threatening dermatologic emergencies.
1. Dermatologic Physical Diagnosis & Lesion Morphology
Accurate diagnosis begins with precise anatomical nomenclature. Dermatologic lesions are categorized into primary (direct result of the disease process) and secondary (modifications caused by trauma, scratching, infection, or chronicity).
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| TAXONOMY OF PRIMARY SKIN LESIONS |
| |
| FLAT, NON-PALPABLE LESIONS (Color Change Only): |
| * Macule: Flat, circumscribed area of discoloration <1.0 cm (e.g., freckles/ephelides, petechiae)|
| * Patch: Flat, non-palpable area of discoloration >=1.0 cm (e.g., vitiligo, melasma, café-au-lait)|
| |
| PALPABLE, SOLID ELEVATED LESIONS: |
| * Papule: Solid, elevated, palpable lesion <1.0 cm (e.g., elevated nevi, molluscum, acne) |
| * Plaque: Elevated, flat-topped, palpable plateau >=1.0 cm (e.g., psoriasis, lichen planus) |
| * Nodule: Solid, palpable, circumscribed lesion >=1.0 cm with deep dermal/subcutaneous depth |
| (e.g., rheumatoid nodule, lipoma, erythema nodosum) |
| * Wheal (Urtica): Transient, elevated, compressible edematous plaque resulting from dermal |
| mast cell histamine degranulation; typically resolves within 24 hours without scarring. |
| |
| FLUID-FILLED (CYSTIC / BLISTERING) LESIONS: |
| * Vesicle: Circumscribed, elevated lesion containing serous fluid <1.0 cm (e.g., HSV, VZV) |
| * Bulla: Large circumscribed blister containing serous or seropurulent fluid >=1.0 cm |
| (e.g., bullous pemphigoid, second-degree burn, severe contact dermatitis) |
| * Pustule: Circumscribed superficial cavity filled with purulent exudate (pus) (e.g., acne, |
| folliculitis, pustular psoriasis) |
| * Cyst: Encapsulated fluid-filled or semi-solid cavity lined by true epithelium in dermis |
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Secondary Lesions and Surface Changes
- Scale (Desquamation): Heaped-up, horny keratinized cells; flaky skin shedding (e.g., psoriasis, seborrheic dermatitis, tinea).
- Crust ("Scab"): Dried exudate of serous blood or purulent fluid on the skin surface (e.g., impetigo honey-colored crusts).
- Lichenification: Visible and palpable thickening of the epidermis with exaggerated skin markings, caused by chronic rubbing or scratching (e.g., lichen simplex chronicus, chronic atopic dermatitis).
- Erosion: Focal loss of part or all of the epidermis; moist, shallow, non-scarring (e.g., ruptured herpes vesicle).
- Ulcer: Full-thickness loss of epidermis extending into the dermis or subcutaneous fat; heals with scarring (e.g., venous stasis ulcer, pyoderma gangrenosum).
- Fissure: Linear cleavage or crack through the epidermis into the dermis with sharp walls (e.g., chapped lips, athlete's foot, palmoplantar eczema).
- Atrophy: Thinning of the skin surface (epidermal) with loss of skin markings, or loss of dermal collagen/subcutaneous fat leading to a depression (e.g., prolonged topical fluorinated steroid use, aging skin, discoid lupus).
- Excoriation: Linear or punctate epidermal loss caused by mechanical scratching (e.g., neurotic excoriations, prurigo nodularis).
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| LESION CONFIGURATION & MORPHOLOGY PATTERNS |
| |
| * Annular: Ring-shaped with central clearing (e.g., Tinea corporis, Erythema annulare centrifugum)|
| * Linear: Arranged in a straight line (e.g., Poison ivy / Rhus contact dermatitis, scratch marks)|
| * Grouped / Herpetiform: Clustered vesicles on an erythematous base (e.g., HSV-1/2, VZV) |
| * Reticular: Net-like, lace-like pattern (e.g., Livedo reticularis, erythema ab igne) |
| * Targetoid / Iris: Concentric rings with 3 distinct zones (e.g., Erythema multiforme) |
| * Dermatomal / Zosteriform: Distributed along a unilateral sensory nerve dermatome (e.g., Shingles)|
| * Guttate: Drop-like, small dispersed papules (e.g., Guttate psoriasis post-streptococcal) |
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2. Inflammatory & Papulosquamous Dermatoses
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| PAPULOSQUAMOUS & INFLAMMATORY DERMATOSES MATRIX |
| |
| DISEASE KEY CLINICAL FEATURES DISTINGUISHING SIGNS FIRST-LINE MANAGEMENT |
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| Plaque Psoriasis Well-demarcated, erythematous Auspitz sign (pinpoint Topical Class I/II |
| plaques with silvery-white bleeding upon scale corticosteroids + |
| micaceous scales on extensor removal); Koebner Calcipotriene (Vit D3).|
| surfaces (elbows, knees, phenomenon; nail Severe (>10% BSA): |
| scalp, lumbosacral). pitting, oil-drop sign. Biologics (TNF/IL-17/23)|
| |
| Atopic Dermatitis Intense pruritus ("the itch Flexural lichenification Emollient barrier |
| (Eczema) that rashes"), ill-defined (antecubital, popliteal creams; topical |
| erythematous papules/plaques fossae, neck); Dennie- steroids (hydrocortisone|
| with weeping, xerosis. Morgan folds; allergic on face; triamcinolone |
| shiners. on body); Dupilumab. |
| |
| Contact 1. Allergic (Type IV delayed Urushiol (poison ivy) Allergen avoidance; |
| Dermatitis hypersensitivity): nickel, presents with LINEAR high-potency topical |
| neomycin, poison ivy. vesicles; intense itch. steroids. Severe: Oral |
| 2. Irritant: soaps, chemicals, Irritant lacks vesicle prednisone 2-3 week |
| water friction (80% of cases). spread; burning pain. slow taper (no rebound)|
| |
| Seborrheic Greasy, yellowish, unctuous Associated with Topical Ketoconazole |
| Dermatitis scaling on erythematous base; Malassezia furfur; high 2% cream/shampoo; |
| scalp, nasolabial folds, prevalence in severe selenium sulfide, zinc |
| eyebrows, chest. Parkinson's & HIV/AIDS! pyrithione; low-potency|
| steroid for flares. |
| |
| Pityriasis Begins with solitary 2-5 cm Follows Langer's skin Self-limiting (6-8 wks);|
| Rosea HERALD PATCH; 1-2 weeks later cleavage lines in supportive (antihist- |
| secondary eruption of small "CHRISTMAS TREE" amines, emollients); |
| oval salmon-colored plaques. distribution on back. RPR test to rule out |
| Collarette of scale. Secondary Syphilis! |
| |
| Lichen Planus The 6 P's: Pruritic, Polygonal, WICKHAM'S STRIAE (lacy High-potency topical |
| Planar, Purple, Papules, white oral lines); corticosteroids |
| Plaques. Volar wrists, shins. STRONG ASSOCIATION WITH (clobetasol); check |
| HEPATITIS C VIRUS (HCV)!Hepatitis C serologies!|
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Plaque Psoriasis: Pathophysiology & Management Nuances
- Pathogenesis: Hyperproliferation of epidermal keratinocytes (epidermal transit time reduced from normal 28 days to 3–5 days) driven by dendritic cell secretion of IL-23, stimulating Th17 and Th22 cells to release IL-17A, IL-17F, and IL-22.
- Phenotypes:
- Chronic Plaque Psoriasis: Extensor distribution (elbows, knees, presacral, scalp).
- Guttate Psoriasis: Abrupt onset of small "raindrop" papules across the trunk, classically triggered by Group A Streptococcal pharyngitis (obtain throat culture / ASO titer).
- Inverse Psoriasis: Involves intertriginous skin folds (axillae, inframammary, inguinal, gluteal cleft); lacks visible scale due to friction/maceration, appearing as smooth, glistening red plaques.
- Pustular Psoriasis & Erythrodermic Psoriasis: Severe, life-threatening generalized exfoliative conditions with high risk of high-output heart failure, hypothermia, sepsis, and protein-losing enteropathy.
- Critical Board Warning (Systemic Steroids): Never administer oral systemic corticosteroids (such as prednisone or methylprednisolone Medrol Dosepaks) for psoriasis! While initial improvement may occur, systemic steroid taper or withdrawal predictably precipitates catastrophic, life-threatening generalized pustular psoriasis (von Zumbusch) or erythrodermic psoriasis.
- Topical Corticosteroid Potency Ladder (Classes I to VII):
- Class I (Ultra-High Potency): Clobetasol propionate 0.05%, Betamethasone dipropionate augmented 0.05%. Used for thick plaques on palms, soles, scalp, trunk. Limit use to <2–4 consecutive weeks to prevent skin atrophy, telangiectasias, striae, and HPA-axis suppression.
- Class II/III (High Potency): Fluocinonide 0.05%, Triamcinolone acetonide 0.5%.
- Class IV/V (Medium Potency): Triamcinolone acetonide 0.1%, Hydrocortisone valerate 0.2%. Body and extremities.
- Class VI/VII (Low Potency): Desonide 0.05%, Hydrocortisone 1%–2.5%. Mandatory for face, eyelids, intertriginous folds, and groin to prevent severe atrophy and steroid-induced rosacea/glaucoma.
3. Acneiform Disorders & Hidradenitis Suppurativa
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| ACNE VULGARIS vs. ROSACEA vs. HIDRADENITIS |
| |
| FEATURE ACNE VULGARIS ACNE ROSACEA HIDRADENITIS SUPPURATIVA|
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| Primary Lesions Comedones (open/blackheads, Erythema, telangiectasias, Deep painful nodules, |
| closed/whiteheads), papules, pustules. sinus tracts, "tombstone|
| inflammatory papules, cysts.NO COMEDONES! double comedones", scars|
| |
| Distribution Face, chest, upper back, Central face (cheeks, Apocrine gland zones: |
| shoulders (pilosebaceous). nose, chin, forehead). axillae, groin, perineum|
| |
| Vascular Component Absent Prominent flushing, Absent |
| telangiectasias. |
| |
| Pathophysiology Cutibacterium acnes, Neurovascular hyper- Follicular occlusion of |
| follicular hyperkeratin- reactivity, Demodex apocrine gland units, |
| ization, androgen sebum. folliculorum mites. sinus tract fibrosis. |
| |
| Systemic / Variant PCOS, hyperandrogenism. Rhinophyma (phymatous), Hurley Stages I - III. |
| Features Ocular rosacea (blepharitis). |
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Stepwise Management Protocols
Acne Vulgaris Stepwise Approach:
- Mild Comedonal: Topical Retinoid (Adapalene 0.1% or 0.3%, Tretinoin 0.025%–0.1%, or Tazarotene) applied at night.
- Mild-to-Moderate Inflammatory: Topical Retinoid + Benzoyl Peroxide (BPO 2.5%–5%) + Topical Clindamycin 1% (always combine topical antibiotics with BPO to prevent bacterial resistance).
- Moderate-to-Severe Inflammatory / Refractory: Add Oral Tetracycline Antibiotic (Doxycycline 100 mg BID or Minocycline 100 mg BID) for a limited 3-to-4 month course. In adult females: add Spironolactone (50–100 mg/day) or combined oral contraceptives (COCs) to block androgen receptors.
- Severe Nodulocystic / Scarring / Refractory: Oral Isotretinoin (Accutane). Highly teratogenic (craniofacial, cardiac, CNS defects); mandates enrollment in the FDA iPLEDGE program, 2 negative pregnancy tests prior to initiation, monthly pregnancy tests, 2 forms of contraception, and regular monitoring of fasting lipid panels and hepatic transaminases.
Acne Rosacea Subtypes & Management:
- Subtypes: (1) Erythematotelangiectatic (flushing, persistent central redness), (2) Papulopustular (red bumps and pus lesions without comedones), (3) Phymatous (sebaceous hyperplasia, bulbous nasal enlargement / rhinophyma), (4) Ocular (grittiness, blepharitis, conjunctival injection).
- Triggers to Avoid: Sun exposure, hot beverages, spicy foods, alcohol (especially red wine), emotional stress, extremes of temperature.
- Pharmacotherapy:
- Topical Agents: Metronidazole 0.75%–1.0% gel/cream, Azelaic acid 15%, Ivermectin 1% cream (targets Demodex mites).
- Oral Therapy (for inflammatory pustules): Subantimicrobial-dose Doxycycline (40 mg modified-release daily; anti-inflammatory without antibacterial selective pressure) or standard Doxycycline 50–100 mg daily.
- Persistent Erythema: Topical alpha-adrenergic agonists (Brimonidine gel, Oxymetazoline cream) for temporary vasoconstriction.
Hidradenitis Suppurativa (Hurley Staging & Management):
- Hurley Stage I (Isolated abscesses without sinus tracts): Topical Clindamycin 1% lotion BID, oral zinc gluconate, intralesional triamcinolone for acute flares.
- Hurley Stage II (Recurrent abscesses with sinus tract formation and scarring): Oral Tetracyclines or combination Clindamycin (300 mg BID) + Rifampin (300 mg BID) for 10–12 weeks; surgical punch debridement/unroofing of sinus tracts.
- Hurley Stage III (Diffuse, confluent involvement with extensive interconnected sinus tracts): Biologic therapy (Adalimumab 160 mg at week 0, 80 mg at week 2, 40 mg weekly starting week 4, or Secukinumab); wide surgical excision of affected apocrine-bearing tissue.
4. Cutaneous Malignancies & Premalignant Neoplasms
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| CUTANEOUS NEOPLASMS: CLINICAL & PATHOLOGICAL SPECTRUM |
| |
| NEOPLASM CLINICAL PRESENTATION RISK FACTORS & BIOPSY TREATMENT & PROGNOSIS |
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| Actinic Keratosis Rough, gritty, erythematous Chronic UV radiation; Liquid nitrogen cryo- |
| (AK) papule with yellow-brown scale; cumulative sun damage. therapy (solitary); |
| feels like "SANDPAPER"; on Premalignant precursor Field therapy with |
| face, scalp, ears, dorsal hands.to Squamous Cell CA. topical 5-FU 5% or |
| Imiquimod cream. |
| |
| Basal Cell Pearly, translucent papule or Sun exposure, fair skin. Shave or punch biopsy. |
| Carcinoma (BCC) nodule with ROLLED BORDERS, Most common skin cancer Electrodesiccation & |
| central ulceration ("rodent (~80%). Slow growing; curettage (ED&C), |
| ulcer"), and TELANGIECTASIAS. metastasis is <0.1%. surgical excision, or |
| Mohs surgery for face. |
| |
| Squamous Cell Hyperkeratotic, firm, indurated UV exposure, HPV, Punch or excisional |
| Carcinoma (SCC) erythematous plaque or nodule, chronic wounds/scars biopsy. Wide surgical |
| often with central ulceration (Marjolin's ulcer). excision or Mohs. |
| and thick adherent crust. TRANSPLANT PATIENTS Check regional lymph |
| Lower lip, ears, scalp, hands. HAVE 65X HIGHER RISK! nodes for metastasis. |
| |
| Malignant ABCDE criteria: Asymmetry, UV exposure, blistering Excisional biopsy with |
| Melanoma Border irregularity, Color childhood sunburns, 1-3 mm margins! |
| variegation, Diameter >=6mm, dysplastic nevi, family BRESLOW DEPTH is the |
| Evolving. "Ugly Duckling" sign. history, CDKN2A/BRAF. key prognostic factor! |
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Clinical Melanoma Subtypes
- Superficial Spreading Melanoma (~70%): Most common subtype; characterized by a prolonged radial (horizontal) growth phase before vertical invasion; appears on sun-exposed trunk in men and lower legs in women.
- Nodular Melanoma (~15%): Aggressive, early vertical growth phase without preceding horizontal spread; appears as a rapidly enlarging dark blue-black or amelanotic (flesh-colored) nodule.
- Lentigo Maligna Melanoma (~10%): Occurs in elderly individuals on chronically sun-damaged facial skin; evolves from in situ precursor (lentigo maligna) over decades.
- Acral Lentiginous Melanoma (~5%): Most common melanoma in dark-pigmented individuals (African, Asian, Hispanic descent); occurs on palms, soles, and subungual nail beds (Hutchinson's sign = longitudinal melanonychia with pigment extending onto the proximal or lateral nail fold); not related to UV radiation.
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| MELANOMA BIOPSY & SURGICAL MARGIN DECISION TREE |
| |
| [SUSPICIOUS PIGMENTED LESION (ABCDE (+) / Ugly Duckling)] |
| | |
| v |
| [DEFINITIVE BIOPSY MODALITY] |
| - FULL-THICKNESS EXCISIONAL BIOPSY with 1 to 3 mm normal margins down to subcutaneous fat. |
| - If lesion is extremely large on face/cosmetic area: Deep Punch Biopsy of darkest/thickest area.|
| - NEVER PERFORM A SUPERFICIAL SHAVE BIOPSY! (Transects the base and destroys Breslow depth). |
| | |
| v |
| [PATHOLOGY REPORT: BRESLOW THICKNESS DETERMINATION] |
| * In Situ Melanoma ------------------------> Wide Local Excision with 0.5 cm margin |
| * Breslow Depth <= 1.0 mm ------------------> Wide Local Excision with 1.0 cm margin |
| * Breslow Depth 1.01 - 2.0 mm --------------> Wide Local Excision with 1.0 - 2.0 cm margin + |
| Sentinel Lymph Node Biopsy (SLNB) |
| * Breslow Depth > 2.0 mm -------------------> Wide Local Excision with 2.0 cm margin + SLNB |
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5. Autoimmune Bullous Diseases & Dermatologic Emergencies
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| AUTOIMMUNE BULLOUS DISORDERS: COMPARATIVE PROFILE |
| |
| FEATURE BULLOUS PEMPHIGOID (BP) PEMPHIGUS VULGARIS (PV) |
| --------------------------------------------------------------------------------------------- |
| Typical Patient Elderly adults (age >= 70 years) Middle-aged adults (age 40 - 60 years) |
| Target Antigens BP180 (Type XVII collagen) & Desmoglein 3 (mucosa) and |
| BP230 in HEMIDESMOSOMES. Desmoglein 1 (skin) in DESMOSOMES. |
| Blister Level SUBEPIDERMAL (thick, sturdy roof) INTRAEPIDERMAL (flaccid, fragile roof) |
| Blister Character TENSE, firm bullae on normal or FLACCID bullae that rupture easily, |
| erythematous/urticarial base leaving painful, raw, bleeding erosions|
| Mucosal Involvement Rare / Mild (<20% of cases) PROMINENT (>90%); oral mucosal |
| ulcers precede skin lesions by months! |
| Nikolsky Sign NEGATIVE (lateral pressure does POSITIVE (lateral friction sloughs |
| not dislodge normal skin) normal-appearing epidermis) |
| Direct Immuno- Linear IgG and C3 deposition along Intercellular IgG deposition in "fish- |
| fluorescence (DIF) the DERMAL-EPIDERMAL JUNCTION. net" or "chicken-wire" pattern. |
| Mortality / Severity Moderate; responsive to topical HIGH MORTALITY if untreated (fluid |
| clobetasol or oral steroids. loss, severe sepsis, shock). |
| First-Line Therapy High-potency topical Clobetasol High-dose systemic Prednisone + |
| cream or oral Prednisone. Rituximab (anti-CD20 monoclonal). |
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Life-Threatening Severe Cutaneous Adverse Reactions (SCAR)
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| SEVERE CUTANEOUS ADVERSE REACTIONS (SCAR) |
| |
| [STEVENS-JOHNSON SYNDROME (SJS) & TOXIC EPIDERMAL NECROLYSIS (TEN)] |
| - Pathophysiology: Massive cytotoxic T-cell / NK-cell mediated keratinocyte apoptosis via |
| Fas/FasL and Granulysin pathways triggered by drug exposure. |
| - Common Drug Triggers: S - Sulfa antibiotics (TMP-SMX); A - Allopurinol; A - Anticonvulsants |
| (Carbamazepine, Lamotrigine, Phenytoin); N - NSAIDs (Oxicams); P - Penicillins/Cephalosporins.|
| - Latency: 1 to 3 weeks following initial drug exposure. |
| - Classification by Body Surface Area (BSA) of Epidermal Detachment: |
| * SJS: <10% BSA detachment with mucosal involvement. |
| * SJS/TEN Overlap: 10% to 30% BSA detachment. |
| * TEN: >30% BSA detachment (extensive sheet-like scalded epidermal sloughing). |
| - Clinical Features: Prodromal fever/flu-like illness -> Dusky, purpuric, coalescent targetoid |
| macules -> Flaccid bullae -> Sheet-like epidermal sloughing (+ Nikolsky sign) -> Severe |
| MUCOSAL INVOLVEMENT (>=2 mucous membranes: hemorrhagic crusting of lips, eyes, urethra). |
| - Management: |
| 1. IMMEDIATE DISCONTINUATION of all potential offending medications! |
| 2. Immediate transfer to a regional BURN INTENSIVE CARE UNIT (BICU). |
| 3. Aggressive fluid/electrolyte resuscitation and strict barrier warming (hypothermia risk). |
| 4. Strict avoidance of silver sulfadiazine (contains sulfa!). |
| 5. Urgent Ophthalmology consultation (prevents symblepharon and permanent corneal blindness). |
| 6. Immunomodulatory therapy: Cyclosporine, IVIG, or Etanercept. |
| |
| [DRUG REACTION WITH EOSINOPHILIA & SYSTEMIC SYMPTOMS (DRESS SYNDROME)] |
| - Pathophysiology: Delayed drug hypersensitivity associated with Human Herpesvirus 6 (HHV-6) |
| reactivation. |
| - Latency: Long latency (2 to 8 WEEKS post drug initiation; e.g., Allopurinol, Dapsone). |
| - Clinical Triad: High fever (>38.5°C), diffuse morbilliform/edematous exanthem (facial edema), |
| and INTERNAL ORGAN INVOLVEMENT (HEPATITIS in 80%, acute interstitial nephritis, pneumonitis). |
| - Hematology: Marked peripheral EOSINOPHILIA (>=1500/mcL) and atypical lymphocytosis. |
| - Management: Discontinue culprit drug; systemic corticosteroids (Prednisone 1 mg/kg/day) with |
| slow taper over 2 to 3 months to prevent fatal rebound myocarditis/hepatitis. |
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6. Geriatric Dermatologic Syndromes
- Xerosis (Asteatosis) & Asteatotic Eczema (Eczema Craquelé): Loss of epidermal ceramides, sebum, and natural moisturizing factor in older adults leads to severe dry, scaly skin. Asteatotic eczema presents as fine fissuring resembling "cracked porcelain" or "dry riverbeds" on the pretibial shins. Management: lukewarm brief showers, immediate post-bath application of thick ceramide-based ointments/creams (petrolatum, Aquaphor), and low-potency topical steroids.
- Actinic (Senile / Bateman's) Purpura: Benign, non-palpable, well-demarcated ecchymotic macules and patches on the sun-damaged extensor forearms and dorsal hands of older adults. Pathophysiology: loss of dermal collagen and elastic support around dermal microvessels, allowing minor shearing trauma to cause red blood cell extravasation without a primary coagulopathy. Normal platelet count and coagulation profile.
- Pressure Injury Staging (NPUAP Guidelines):
- Stage 1: Non-blanchable erythema of intact skin over a bony prominence.
- Stage 2: Partial-thickness skin loss with exposed dermis (shallow open ulcer, pink/red wound bed, or intact/ruptured serum-filled blister).
- Stage 3: Full-thickness skin loss; adipose (subcutaneous fat) is visible, but bone, tendon, and muscle are NOT exposed. May have epibole (rolled edges) and slough.
- Stage 4: Full-thickness skin and tissue loss with directly exposed or palpable bone, tendon, cartilage, or muscle. High risk of osteomyelitis.
- Unstageable: Full-thickness loss where the base is completely obscured by slough (yellow, tan, gray) or eschar (brown, black); depth cannot be determined until debrided.
- Deep Tissue Pressure Injury (DTPI): Persistent non-blanchable deep red, maroon, or purple discoloration, or epidermal separation revealing a dark wound bed or blood-filled blister.
7. Board-Yield Summary & Clinical Pearls
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| ANCC AGPCNP CLINICAL EXAM PEARLS |
| |
| - Never prescribe Oral Systemic Corticosteroids for Plaque Psoriasis! Withdrawal triggers |
| catastrophic, life-threatening Generalized Pustular Psoriasis (von Zumbusch) or Erythroderma.|
| |
| - For any suspicious pigmented lesion concerning for Malignant Melanoma, perform an Excisional |
| Biopsy with 1-3 mm margins! Avoid superficial shave biopsies that transect the base and prevent|
| accurate determination of Breslow Depth (the primary prognostic determinant). |
| |
| - Differentiate Blistering Emergencies: Tense bullae with negative Nikolsky sign in an elderly |
| adult = Bullous Pemphigoid (hemidesmosomes). Flaccid bullae with positive Nikolsky sign and |
| severe oral mucosal ulcerations = Pemphigus Vulgaris (desmoglein). |
| |
| - Seborrheic Dermatitis that is unusually severe, explosive, or refractory to therapy warrants |
| screening for HIV/AIDS and evaluation for Parkinson's Disease. |
| |
| - Lichen Planus (the 6 P's + Wickham's striae) mandates screening for Hepatitis C Virus (HCV). |
| |
| - In SJS/TEN: Transfer immediately to a Burn ICU, discontinue offending drugs, and NEVER use |
| Silver Sulfadiazine cream, as it contains a sulfonamide moiety that perpetuates the reaction. |
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Test Your Knowledge
A 64-year-old male presents to the primary care clinic with a 6-month history of a slowly enlarging, asymptomatic pigmented lesion on his upper back. Physical examination reveals an asymmetric 8 mm macule with irregular, scalloped borders and variegated coloration ranging from light tan to dark brown and focal blue-black areas. The lesion is distinctly different from his other surrounding benign-appearing nevi. Which of the following diagnostic procedures represents the most appropriate next step in clinical management?
A
B
C
D
Test Your Knowledge
A 48-year-old male with a 10-year history of moderate plaque psoriasis presents to the clinic reporting a sudden, severe flare of his skin disease. Two weeks ago, he was treated with a 6-day oral methylprednisolone dose pack by an urgent care provider for acute lumbar back strain. Upon completing the steroid taper, he developed acute generalized erythroderma covering 90% of his body surface area, accompanied by thousands of pinpoint non-follicular pustules, severe skin pain, rigors, and a temperature of 38.8°C (101.8°F). What is the AGPCNP's most accurate interpretation of this clinical presentation?
A
B
C
D
Test Your Knowledge
A 78-year-old female presents with a 3-week history of severe, generalized pruritus followed by the eruption of large, firm, tense fluid-filled blisters on an erythematous and urticarial base across her lower abdomen, thighs, and flexor forearms. She denies any pain or ulcerations in her mouth. On physical examination, firm lateral pressure applied to the normal-appearing perilesional skin does not induce epidermal detachment or blister extension (negative Nikolsky sign). Direct immunofluorescence of a perilesional punch biopsy reveals linear IgG and C3 deposition along the basement membrane zone. Which of the following is the most likely diagnosis?
A
B
C
D