Clinical Medicine and Surgery I · Exam 1

How to use this guide

Dr. Carter’s Clin Med Pro Study Tip (Hypotension deck, slide 7) lists what to learn for every condition. Each card below answers those ten fields:

Name of Condition
Definition
Etiology (cause)
Epidemiology (who)
Risk Factors
Pathology
Clinical Manifestation
Diagnosis
Treatment/Therapy
Mortality ★

Every field comes from the lecture slides only. Where a deck is silent the card says Not covered in the lecture rather than filling the gap from elsewhere (308 of 1420 fields in this exam; Mortality alone: 128 of 142). Slide numbers follow each field. Cards open closed; tap one to read it.

The ★ on Mortality is on the original study-tip slide: fill it when a figure exists. A ★ highlighted phrase inside a field is a fact the professor emphasized in the lecture recording, carried over from this exam’s study guide.

Lecture 2 · General Dermatology I

Monique Jaquith, DMSc, PA-C · 18 conditions · source: 2. General Dermatology I.pptx

Atopic dermatitis★ Professor emphasized1 not covered

Name of Condition: Atopic dermatitis (also: eczema) Slides 46, 51
Definition: Chronic, relapsing, intensely pruritic inflammatory dermatosis with known triggers and a personal or family history of atopy; the most common type of eczema. Slides 46, 51
Etiology (cause): Epidermal-barrier impairment (notably reduced filaggrin) plus immune dysregulation, genetic susceptibility, altered skin microbiome and environmental triggers. Slide 51
Epidemiology (who): Often begins in infancy or childhood; affects 20% of children worldwide; more common in males; adult onset rare. Atopic triad (with asthma, allergic rhinitis): about 80% have at least one. Slides 51–52
Risk Factors: Personal or family atopy; elevated IgE (immunoglobulin E); allergens (pollen, dust mites, molds, pet dander, foods); xerosis; irritants; heat and sweat; stress; infection; overbathing. Slides 51–52
Pathology: Reduced filaggrin (normally packs keratin fibers and forms the skin's natural moisture) weakens the barrier. Eczema evolves acute (edema, vesicles, oozing) → subacute (scale, excoriation) → chronic (lichenification). Slides 46, 51
Clinical Manifestation: Dry skin, severe pruritus. Infants: weeping, crusted patches on cheeks, scalp, extensors. Children: ill-defined plaques in antecubital and popliteal fossae, wrists, ankles. Adults: flexures, hands, neck, eyelids. Flares last >6 weeks; lichenification when chronic. Slides 53–55
Diagnosis: Usually clinical (atopy, recurrent rash; IgE not routinely tested). Patch test if atypical, adult-onset or resistant; biopsy if atypical or refractory; culture crusted or pustular lesions; herpes simplex PCR (polymerase chain reaction) for painful monomorphic erosions. Slide 56
Treatment/Therapy: Emollients plus site-appropriate topical steroid: ★ low potency (hydrocortisone) for the face, low–medium for the body, applied sparingly; tacrolimus or pimecrolimus for face and eyelids; crisaborole; wet wraps for severe flares; hydroxyzine for itch; refer severe disease (phototherapy, systemic therapy). Slides 42, 57–58, 185
Mortality ★: Not covered in the lecture

Dyshidrotic eczema3 not covered

Name of Condition: Dyshidrotic eczema (also: dyshidrotic dermatitis, pompholyx, palmoplantar eczema) Slide 64
Definition: Chronic, relapsing condition of intensely pruritic vesicles on the hands and feet. Slide 64
Etiology (cause): Unknown. Slide 64
Epidemiology (who): Not covered in the lecture
Risk Factors: Irritant triggers: detergents, solvents, hair lotions or dyes, acidic foods. Slide 66
Pathology: Not covered in the lecture
Clinical Manifestation: Pruritus of palms, lateral and dorsal fingers or soles, then intensely pruritic "tapioca" vesicles that may coalesce into bullae; vesicles persist weeks, then dry and desquamate (peel); later scaling fissures and lichenification. Slides 61, 65
Diagnosis: Clinical. Slide 66
Treatment/Therapy: High-potency topical corticosteroid first line (e.g. clobetasol propionate 0.05%); systemic corticosteroids if severe. Avoid irritants; lukewarm water, soap-free cleanser, dry hands thoroughly, emollient right after. Slide 66
Mortality ★: Not covered in the lecture

Nummular eczema3 not covered

Name of Condition: Nummular eczema (also: discoid eczema, nummular dermatitis) Slides 68, 72
Definition: Eczema with intensely pruritic, coin-shaped ("nummular" is Latin for coin) scaly plaques. Slides 68, 72
Etiology (cause): Not fully understood; likely some degree of skin-barrier dysfunction. Slide 71
Epidemiology (who): More common in men and in adults over 50, though it can occur at any age. Slide 71
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Round, light pink, scaly, thin 1–10 cm plaques, mostly on the extremities (sometimes trunk); acute lesions dull red, exudative and crusted, becoming drier and scalier; uniform, without central clearing. Slides 69, 72
Diagnosis: Clinical. Main differential is tinea corporis (has central clearing). KOH (potassium hydroxide) preparation if tinea cannot be ruled out; bacterial culture if secondarily infected; patch testing if chronic or recurrent. Slides 73–74
Treatment/Therapy: Medium–high potency topical corticosteroid first line (e.g. triamcinolone acetonide 0.1%); emollients to restore the barrier and prevent recurrence; hydroxyzine or diphenhydramine for itch; treat secondary bacterial infection. Slide 74
Mortality ★: Not covered in the lecture

Irritant contact dermatitis1 not covered

Name of Condition: Irritant contact dermatitis Slides 79–80
Definition: Most common form of contact dermatitis: a response to chemicals or friction that disrupt the normal skin barrier. Slides 79–80
Etiology (cause): Irritants: acids and alkalis > soaps and detergents; friction. Concentrated agents can cause chemical burns and necrosis. Slide 80
Epidemiology (who): Frequently occupational, e.g. healthcare and janitorial workers who wash their hands often. Slide 80
Risk Factors: Frequent handwashing, occupational exposure, gloves, makeup, masks. Slides 80–81
Pathology: Direct disruption of the skin barrier by chemicals or friction; may coexist with allergic contact dermatitis. Slides 79–80
Clinical Manifestation: Mild irritants (soap): subacute, over weeks; acids/alkalis: minutes to ≥24 h. Well-demarcated, glazed, with erythema, edema, blistering, scaling; hands and forearms (gloves, handwashing), eyelids and face (makeup, masks). Slide 81
Diagnosis: Clinical: known irritant exposure plus obvious demarcation and unnatural distribution; in insidious cases a diagnosis of exclusion. Slides 79, 82
Treatment/Therapy: Avoid exposure; repair barrier with emollients; heavy emollient (petroleum jelly) under cotton gloves overnight; hydroxyzine or diphenhydramine for itch. Slide 82
Mortality ★: Not covered in the lecture

Allergic contact dermatitis2 not covered

Name of Condition: Allergic contact dermatitis (also: Rhus dermatitis (urushiol)) Slide 85
Definition: Cell-mediated, delayed type IV hypersensitivity reaction to contact with a specific allergen. Slide 85
Etiology (cause): Urushiol of Toxicodendron (poison ivy, oak, sumac) is most common; nickel (most common metal); perfumes; topical neomycin and bacitracin; adhesives. Slides 85–86
Epidemiology (who): About 50–75% of people in the United States are allergic to Toxicodendron plants. Slide 85
Risk Factors: Not covered in the lecture
Pathology: Driven by T cells and macrophages rather than antibodies; symptoms typically appear 48–72 h after exposure. Slide 85
Clinical Manifestation: Intensely pruritic rash (stinging, burning) at the contact site, shaped like the object (bandage, jewelry). Urushiol: linear vesicles, papules, bullae in multiple stages, onset 4–96 h, lasting up to 3 weeks; scratching can cause cellulitis; not contagious, but oil left on skin or clothing spreads it. Slides 86–87
Diagnosis: Clinical: history plus linear vesicles in multiple stages of healing (urushiol) or a well-demarcated rash at the contact site; patch testing diagnoses it; varicella-zoster PCR (polymerase chain reaction) if shingles (never crosses midline) is possible. Slides 35, 88–89
Treatment/Therapy: Soothing measures (oatmeal baths, cool wet compresses, astringents such as Burow's solution); limited area: high-potency topical steroid; extensive: high-dose oral corticosteroid tapered over 2–3 weeks (stopping early causes rebound). Slide 89
Mortality ★: Not covered in the lecture

Seborrheic dermatitis1 not covered

Name of Condition: Seborrheic dermatitis (also: dandruff (scalp)) Slide 93
Definition: Common, chronic, relapsing inflammatory condition of sebum-rich skin. Slide 93
Etiology (cause): Overgrowth of Malassezia, a normal skin-flora yeast that feeds on skin oils. Slides 93, 187
Epidemiology (who): Most common in males 20–50 years old. Slide 93
Risk Factors: Stress, immunosuppression, cold weather. Slide 93
Pathology: Not well understood; thought to involve interacting hormonal, environmental and immune (response to antigens) factors. Slide 93
Clinical Manifestation: Poorly demarcated, pruritic erythematous plaques 5–20 mm with greasy yellow scale on scalp, eyebrows, beard, nasolabial creases, forehead, behind ears, ear canal; itch worse with sweat; may look lighter on darker skin; petaloid (petal-shaped) variant in skin of color. Slides 92–94
Diagnosis: Clinical. Slide 95
Treatment/Therapy: Topical antifungal (ketoconazole) is the mainstay: ketoconazole or selenium sulfide shampoo for scalp, ketoconazole cream for face; short low-potency steroid early for inflammation; repeated long-term use often needed. Slides 95, 187
Mortality ★: Not covered in the lecture

Perioral dermatitis2 not covered

Name of Condition: Perioral dermatitis (also: periorificial dermatitis) Slide 98
Definition: Acneiform inflammatory eruption around the mouth (papules and pustules without the comedones of acne). Slide 98
Etiology (cause): Incompletely understood; topical corticosteroid exposure is the most important modifiable association. Slide 98
Epidemiology (who): Mostly women about 20–45 years old. Slide 98
Risk Factors: Topical corticosteroids; cosmetics, occlusive moisturizers, sunscreens, irritating skin care, certain toothpaste ingredients. Slide 98
Pathology: Not covered in the lecture
Clinical Manifestation: Grouped, monomorphic erythematous or skin-colored papules, papulovesicles or papulopustules around the mouth, nose or eyes, sparing a narrow rim at the vermilion border; burning, tightness, dryness, mild itch. Slide 99
Diagnosis: Clinical. KOH (potassium hydroxide) preparation if tinea or Candida suspected; culture if infected; patch test if allergic contact suspected; biopsy if atypical. Differential: rosacea, seborrheic dermatitis, acne (comedones). Slides 100–101
Treatment/Therapy: Stop facial topical corticosteroids (warn of temporary flare) and nonessential cosmetics; simplify skin care. Mild: topical metronidazole, erythromycin, pimecrolimus or azelaic acid. Extensive: oral tetracycline or doxycycline. Slides 102, 188
Mortality ★: Not covered in the lecture

Diaper dermatitis★ Professor emphasized2 not covered

Name of Condition: Diaper dermatitis Slide 105
Definition: Anatomic reaction pattern in the diaper area rather than a single diagnosis; irritant contact dermatitis is the most common form. Slide 105
Etiology (cause): Excess hydration, friction, maceration and prolonged urine/feces contact; raised pH boosts fecal enzymes that damage the barrier. Candida is the most common infectious complication. Slides 105–106
Epidemiology (who): Not covered in the lecture
Risk Factors: Diarrhea, antibiotic exposure, infrequent diaper changes, tight diapers, irritating wipes or cleansers. Slide 106
Pathology: Barrier disruption permits secondary infection with Candida or bacteria. Slide 106
Clinical Manifestation: Irritant: erythema, scale, papules, erosions on convex surfaces, folds spared. Candidal: beefy erythema involving folds, peripheral scale, satellite papules or pustules. Bacterial: bullae, crusting, pus, sharply demarcated perianal erythema. Slides 105, 107
Diagnosis: Clinical; fold involvement separates candidal from irritant. KOH (potassium hydroxide) preparation if Candida suspected (budding yeast, pseudohyphae); bacterial culture for purulence, bullae or crusting. Slides 105, 108
Treatment/Therapy: Frequent changes, gentle cleansing, air exposure, superabsorbent diapers; thick zinc oxide or petrolatum barrier each change; brief ★ low-potency topical corticosteroid (hydrocortisone) for significant inflammation; add topical antifungal for Candida; antibiotics only for proven bacterial infection. Slides 42, 109
Mortality ★: Not covered in the lecture

Stasis dermatitis★ Professor emphasized3 not covered

Name of Condition: Stasis dermatitis Slide 112
Definition: Inflammatory skin disorder of the lower legs caused by chronic venous hypertension. Slide 112
Etiology (cause): Most commonly chronic venous insufficiency: incompetent valves, venous obstruction or impaired calf-muscle pump raise venous pressure. Slides 112–113
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: High venous pressure → capillary leak of fluid, proteins and erythrocytes → edema, hemosiderin deposition, fibrosis, lipodermatosclerosis (hardened, narrowed lower leg), venous ulcer risk. Slide 113
Clinical Manifestation: Pruritic erythematous, violaceous or hyperpigmented patches in the gaiter region; acute: scale, weeping, crusting; chronic: brown hemosiderin, induration, atrophie blanche, ulcers. ★ Darker skin: erythema looks violaceous, gray or deep brown; palpate for warmth and edema. Slide 114
Diagnosis: Clinical (leg dermatitis with edema and venous disease); key is excluding cellulitis. Ankle-brachial index or toe pressure before compression if arterial disease suspected; venous duplex ultrasound for reflux, obstruction or deep venous thrombosis. Slides 112, 115–116, 186
Treatment/Therapy: Compression once arterial circulation is adequate; elevation, walking, calf exercises, weight management; fragrance-free emollients; short topical steroid course; refer (dermatology, vascular surgery, wound care) if refractory or ulcerated. Slide 117
Mortality ★: Not covered in the lecture

Bullous pemphigoid1 not covered

Name of Condition: Bullous pemphigoid Slide 122
Definition: Relatively benign autoimmune blistering disease of the epithelial basement membrane, causing subepithelial blisters; usually remits in 5–6 years. Slide 122
Etiology (cause): Autoimmune: antibodies against the basement membrane zone. Slides 122, 124
Epidemiology (who): Twice as common in men as women; usually after age 60. Slide 122
Risk Factors: Not covered in the lecture
Pathology: Subepithelial split; neutrophils aligned in a straight row at the dermal-epidermal junction; no acantholysis. Slides 124, 131
Clinical Manifestation: Prodrome of pruritic urticarial or edematous lesions for weeks to months, then 1–3 cm tense bullae (thick-walled, hard to rupture) on trunk, flexures, axillae, groin; mouth in 10–35%; erosions heal without scarring; Nikolsky sign negative. Slides 123, 131
Diagnosis: Biopsy lesion for histopathology plus perilesional skin for DIF (direct immunofluorescence); serum indirect immunofluorescence or ELISA (enzyme-linked immunosorbent assay) for anti-basement membrane antibodies. Slide 124
Treatment/Therapy: Mild: ultrapotent topical steroids. Moderate–severe: oral prednisone or doxycycline; dapsone for mucosal disease; low-dose methotrexate with folic acid. Refractory: methotrexate, azathioprine, biologics, IVIG (intravenous immunoglobulin). Slide 125
Mortality ★: Doxycycline carries lower mortality than oral prednisone, though prednisone clears blisters faster. Slide 125

Pemphigus1 not covered

Name of Condition: Pemphigus (also: pemphigus vulgaris, pemphigus foliaceus, pemphigus vegetans) Slide 129
Definition: Life-threatening autoimmune blistering disorder with intraepithelial blisters in skin and mucous membranes. Slide 129
Etiology (cause): Autoantibodies to keratinocyte adhesion molecules. Slide 129
Epidemiology (who): Rare. Vulgaris: common in Jewish and Mediterranean descent. Foliaceus: endemic in rural Brazil. Slide 128
Risk Factors: Not covered in the lecture
Pathology: Acantholysis (loss of keratinocyte-to-keratinocyte adhesion) produces intraepithelial blisters. Slides 129, 131
Clinical Manifestation: Insidious flaccid bullae that rupture, weep and bleed, leaving painful erosions and crusts on scalp, face, chest, axillae, groin, umbilicus; vulgaris begins in the mouth; Nikolsky sign positive (top skin layers slip off when rubbed). Foliaceus: superficial, scaly, rare mucosal. Vegetans: vegetating plaques in skin folds. Slides 128, 130–131
Diagnosis: Biopsy shows acantholysis; immunofluorescence and serum ELISA (enzyme-linked immunosorbent assay) for pathogenic antibodies confirm. Slide 132
Treatment/Therapy: Urgent: rituximab or high-dose oral prednisone (with azathioprine or mycophenolate to wean off steroid); antibiotics as needed; cleansing baths, wet dressings, topical/intralesional steroids; correct fluid and electrolytes. Slide 133
Mortality ★: Life-threatening; needs urgent treatment. Slides 129, 133

Alopecia areata2 not covered

Name of Condition: Alopecia areata (also: alopecia totalis, alopecia universalis) Slide 137
Definition: Autoimmune, non-permanent hair loss; totalis = all scalp hair lost, universalis = all body hair lost. Slide 137
Etiology (cause): Autoreactive T cells infiltrate the hair follicle. Slide 137
Epidemiology (who): Not covered in the lecture
Risk Factors: Family history, atopy, autoimmune disease; strong association with stress and psychiatric disorders (causality unproven). Slide 137
Pathology: Inflammation shifts follicles from growing to resting phase but spares the stem-cell compartment, so balding is not permanent. Slide 137
Clinical Manifestation: Sudden, round 1–4 cm patches of smooth hair loss on scalp, beard, eyebrows or anywhere; "exclamation point" hairs (thin at root, normal at top) are pathognomonic; nail pitting or ridging in 10–20% of severe cases. Slide 138
Diagnosis: Clinical; dermoscopy supports it (yellow dots, black dots, broken, tapered and short regrowth hairs); scalp biopsy if scarring, diffuse atypical loss or persistent uncertainty. Slide 139
Treatment/Therapy: Intralesional steroids first line in adolescents and adults; topical steroids first line at 10 years and younger; psychological support and support groups. Slide 140
Mortality ★: Not covered in the lecture

Androgenetic alopecia1 not covered

Name of Condition: Androgenetic alopecia (also: male-pattern hair loss, female-pattern hair loss) Slide 144
Definition: Most common type of hair loss: progressive shrinking of hair follicles in a patterned distribution in genetically predisposed men and women. Slide 144
Etiology (cause): Multifactorial. Male pattern: largely genetic (multiple genes) and androgen-dependent, chiefly dihydrotestosterone. Female pattern: cause less known, some genetic role. Slide 145
Epidemiology (who): Men and women; onset any time after puberty, frequency increases with age. Slide 144
Risk Factors: Genetic predisposition; strong paternal influence (men); balding in first-degree male relatives (women). Slide 145
Pathology: Hair follicles progressively get smaller. Slide 144
Clinical Manifestation: Men: frontotemporal recession in a triangular pattern, then crown (vertex) loss. Women: diffuse central and parietal thinning with the frontal hairline preserved. Slide 146
Diagnosis: Clinical (history and exam); further testing can rule out other alopecias. Slide 147
Treatment/Therapy: Men: topical minoxidil (best at the crown) plus oral finasteride (5α-reductase type 2 inhibitor; 2% lose libido or erectile function, reversible; not indicated in women, contraindicated in pregnancy). Women: oral antiandrogens such as oral contraceptive pills. Surgery: hair transplant, scalp reduction/flaps. Slide 148
Mortality ★: Not covered in the lecture

Xerosis3 not covered

Name of Condition: Xerosis (also: xeroderma) Slides 46, 152
Definition: Extremely dry skin. Slides 46, 152
Etiology (cause): Impaired stratum-corneum hydration. Slide 152
Epidemiology (who): Common in older adults, especially in winter. Slide 152
Risk Factors: Aging, low humidity, hot water, detergents, atopy, systemic disease. Slide 152
Pathology: Not covered in the lecture
Clinical Manifestation: Tightness, pruritus, rough scale, fissuring or eczema; excoriation, sleep loss and infection amplify morbidity. Slide 152
Diagnosis: Not covered in the lecture
Treatment/Therapy: Short lukewarm showers, fragrance-free cleanser only where needed, thick ointment or cream within minutes of bathing; petrolatum, ceramides, humectants (urea, lactic acid), though keratolytics may sting fissures; recurrence expected if exposures persist. Slides 40, 153
Mortality ★: Not covered in the lecture

Psoriasis1 not covered

Name of Condition: Psoriasis (also: plaque, guttate and pustular (von Zumbusch) psoriasis) Slide 155
Definition: Chronic immune-mediated skin disease in genetically predisposed people; variants: plaque (most common), guttate, pustular, psoriatic arthritis. Slide 155
Etiology (cause): Genetic: PSORS1 is the major locus; HLA (human leukocyte antigen)-Cw6 in 90% of early-onset and 50% of late-onset cases; HLA-B27 with psoriatic arthritis. Slide 155
Epidemiology (who): One affected parent: 8% of children; both: 41%. Guttate: children. Higher risk of cardiovascular events, type 2 diabetes, metabolic syndrome and lymphoma. Slides 155, 160
Risk Factors: Family history. Guttate follows strep or upper respiratory infection by 2–3 weeks; pustular may follow systemic steroid withdrawal. Slides 155, 160
Pathology: Not covered in the lecture
Clinical Manifestation: Plaque: salmon-pink plaques with silvery scale on extensor elbows/knees, trunk, scalp, umbilicus, sacrum, genitals; Koebner phenomenon (new lesions on injured skin); Auspitz sign (bleeding when scale is removed). Guttate: raindrop papules. Pustular: fever, generalized 2–3 mm pustules. Arthritis: hand joint pain, sausage digits, nail pitting. Slides 159–161
Diagnosis: Generally clinical; biopsy may be needed for definitive diagnosis. Psoriatic arthritis: X-ray shows pencil-in-a-cup deformity. Slides 161–162
Treatment/Therapy: Mild plaque: emollients, topical steroids, calcipotriene (vitamin D analog), UVB (ultraviolet B); then salicylic acid, coal tar. Moderate–severe: methotrexate, acitretin, apremilast, biologics. Guttate: none needed (phototherapy or topical steroids optional). Pustular: acitretin (not in pregnancy), methotrexate; high-potency topical steroid if pregnant. Slides 163–164
Mortality ★: Pustular (von Zumbusch) psoriasis is abrupt and life-threatening, needing fast hospital care. Slide 160

Pityriasis rosea★ Professor emphasized3 not covered

Name of Condition: Pityriasis rosea Slides 168, 171
Definition: Acute, self-limited skin eruption. Slides 168, 171
Etiology (cause): Thought to be viral. Slide 168
Epidemiology (who): Older children and young adults (10–43 years); slightly more common in women. Slide 168
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Herald patch (50–90%): single 2–5 cm salmon-pink oval plaque on chest, neck or back, clearing centrally with a "collarette" of scale; 1–2 weeks later smaller lesions along cleavage lines (Christmas tree pattern), spreading top-down, fading over 4–6 weeks; ★ post-inflammatory hyperpigmentation for months in darker skin. Slide 169
Diagnosis: Clinical: herald patch plus typical pattern. Slide 171
Treatment/Therapy: Reassurance (self-limited); oral antihistamines and/or topical steroids cautiously for itch; UVB (ultraviolet B) or sunlight if begun in the first week; acyclovir for severe cases. Slide 171
Mortality ★: Not covered in the lecture

Lichen planus1 not covered

Name of Condition: Lichen planus Slide 173
Definition: Pruritic, chronic inflammatory disease of the skin and mucous membranes (skin, mouth, genitalia, scalp, nails, esophagus). Slide 173
Etiology (cause): Not well known; drugs can cause lichenoid reactions: NSAIDs (nonsteroidal anti-inflammatory drugs), sulfonamides, tetracyclines, hydrochlorothiazide, quinidine, some beta blockers. Slide 173
Epidemiology (who): Middle-aged adults; more common in females. Slide 173
Risk Factors: Possible increased incidence with hepatitis C (causal link never established); lichenoid-reaction drugs. Slide 173
Pathology: Hyperkeratosis without parakeratosis, basal-layer vacuolization, wedge-shaped hypergranulosis. Slide 177
Clinical Manifestation: Four P's: pruritic, purple, polygonal papules/plaques, flat-topped and shiny; Wickham striae (fine white lines on the surface); Koebner phenomenon; wrists and ankles most common; oral: lacy white buccal lesions or erosions; genital and erosive oral disease raise squamous cell carcinoma risk. Slides 173, 176
Diagnosis: Biopsy: band-like lymphocytic infiltrate in the dermis, Civatte bodies (apoptotic keratinocytes), saw-tooth ridges. Slide 177
Treatment/Therapy: Superpotent topical steroids first line; topical tacrolimus for oral and vaginal disease; oral steroids if severe; PUVA (psoralen plus ultraviolet A)/phototherapy if refractory. Slide 178
Mortality ★: Not covered in the lecture

Lichen simplex chronicus2 not covered

Name of Condition: Lichen simplex chronicus (also: neurodermatitis) Slide 180
Definition: Thick, rough, leathery lichenified skin produced by repeated rubbing and scratching (itch-scratch cycle). Slide 180
Etiology (cause): Repeated rubbing and scratching triggered by itch, stress, neuropathic sensation or another dermatosis. Slide 180
Epidemiology (who): Not covered in the lecture
Risk Factors: Atopy, anxiety, chronic pruritus, occlusion, friction, local irritant or allergic exposure. Slide 180
Pathology: Self-perpetuating itch-scratch cycle; lichenification is chronic repair from scratching. Slides 18, 180
Clinical Manifestation: Intensely pruritic, well-demarcated lichenified plaques with exaggerated skin markings, excoriation, scale, pigment change; often worse with stress or at night. Slide 180
Diagnosis: Clinical; biopsy atypical, unilateral, nodular, ulcerated or resistant plaques to exclude neoplasia; unexplained generalized pruritus prompts a targeted systemic evaluation. Slide 182
Treatment/Therapy: Break the itch-scratch cycle (education, trigger treatment, emollients, behavioral substitution, nail care, occlusion); limited course of potent topical steroid; calcineurin inhibitor for sensitive sites or maintenance; address sleep and anxiety; recurrence common. Slide 183
Mortality ★: Not covered in the lecture

Lecture 3 · Dermatology II

Monique Jaquith, DMSc, PA-C · 18 conditions · source: 3. Dermatology II.pptx

Erythema multiforme1 not covered

Name of Condition: Erythema multiforme Slides 4, 9
Definition: Acute, immune-mediated hypersensitivity reaction triggered mainly by infections and medications, with characteristic target lesions; minor form = skin only, major form = 2 or more mucosal surfaces Slides 4, 9
Etiology (cause): Herpes simplex virus (types 1 and 2) triggers over 50% (most common precipitant); also Mycoplasma pneumoniae, histoplasmosis, Epstein-Barr virus, coxsackievirus; drugs (nonsteroidal anti-inflammatory drugs, sulfonamides, penicillins, anticonvulsants); ~10% idiopathic Slide 8
Epidemiology (who): Incidence 0.01–1% of the general population; peak age 20–40; slightly more common in males; minor form is the majority; recurrent disease strongly tied to recurrent herpes simplex Slide 8
Risk Factors: Recurrent herpes simplex infection; immunosuppression (HIV (human immunodeficiency virus), transplant, malignancy); recent high-risk medications; recent M. pneumoniae respiratory infection; prior episode Slide 9
Pathology: Biopsy: interface dermatitis with vacuolar degeneration of the basal layer, scattered necrotic keratinocytes, lymphocytic infiltrate; direct immunofluorescence negative Slide 11
Clinical Manifestation: Target lesions with three concentric zones (dusky/necrotic center, pale edematous ring, erythematous halo), symmetric on acral surfaces (palms, soles, dorsal hands); prodrome of mild fever, malaise, upper respiratory symptoms; evolves over 1–2 weeks, self-limited Slide 9
Diagnosis: Clinical in most cases; punch biopsy when uncertain (direct immunofluorescence excludes autoimmune blistering); herpes simplex PCR (polymerase chain reaction) or serology and Mycoplasma serology or PCR to confirm the trigger Slides 11, 125
Treatment/Therapy: Stop offending drug; supportive care (analgesics, oral antihistamines, wound care), topical corticosteroids; oral acyclovir/valacyclovir if herpes-triggered; hospitalize major form with poor oral intake; suppressive antivirals for recurrent herpes-associated disease; dapsone or hydroxychloroquine if refractory non-herpes Slide 12
Mortality ★: Not covered in the lecture

Dermatitis herpetiformis★ Professor emphasized1 not covered

Name of Condition: Dermatitis herpetiformis Slide 13
Definition: Chronic, intensely pruritic blistering disorder intrinsically linked to gluten sensitivity and celiac disease, mediated by IgA (immunoglobulin A) immune-complex deposition Slide 13
Etiology (cause): IgA (immunoglobulin A) antibodies against epidermal transglutaminase in genetically susceptible people eating dietary gluten; nearly all have underlying celiac disease, even without gastrointestinal symptoms Slide 16
Epidemiology (who): 11–75 per 100,000 in Western populations; Northern European descent; peak onset 30–40; male:female ~1.5:1; up to 90% have villous atrophy on small bowel biopsy Slide 16
Risk Factors: HLA (human leukocyte antigen)-DQ2 or -DQ8 positivity; personal or family history of celiac disease; Northern European ancestry; high dietary gluten; autoimmune thyroid disease, type 1 diabetes, other autoimmune conditions Slide 17
Pathology: IgA (immunoglobulin A)–epidermal transglutaminase immune complexes deposit in dermal papillae, activating complement and neutrophils → subepidermal blisters Slide 16
Clinical Manifestation: Intensely pruritic papules, vesicles, urticarial plaques; symmetric on elbows, knees, buttocks, back, scalp; herpetiform grouping, often excoriated; burning and stinging precede lesions; gastrointestinal symptoms may be absent; worsens with gluten Slide 17
Diagnosis: ★ Perilesional skin biopsy with direct immunofluorescence is the gold standard (granular IgA (immunoglobulin A) in dermal papillae); serum anti-tissue transglutaminase and anti-endomysial antibodies; anti-epidermal transglutaminase most specific; small bowel biopsy; iron-deficiency anemia Slide 18
Treatment/Therapy: Dapsone for rapid relief — ★ check G6PD (glucose-6-phosphate dehydrogenase) deficiency before dapsone; monitor for hemolytic anemia and methemoglobinemia; ★ strict lifelong gluten-free diet (cornerstone); sulfapyridine if dapsone intolerant; refer gastroenterology and dietitian Slide 19
Mortality ★: Not covered in the lecture

Acanthosis nigricans1 not covered

Name of Condition: Acanthosis nigricans Slide 20
Definition: Velvety, hyperpigmented skin change in body folds; a visible cutaneous marker of insulin resistance, hyperinsulinemia and underlying systemic disease Slide 20
Etiology (cause): Most commonly insulin-resistant (benign) form; also malignant/paraneoplastic (especially gastric adenocarcinoma), drug-induced (niacin, corticosteroids, oral contraceptives, protease inhibitors), endocrine (polycystic ovary syndrome, Cushing, acromegaly, hypothyroidism), rare familial Slide 22
Epidemiology (who): Up to 74% of obese individuals in some populations; high in Hispanic, African American, Native American populations; up to 13% of school-age children with obesity; malignant form <1% of cases; rises with body mass index Slide 22
Risk Factors: Obesity; type 2 diabetes or prediabetes; polycystic ovary syndrome; metabolic syndrome; Cushing, acromegaly, hypothyroidism; internal malignancy (especially gastrointestinal); niacin, systemic corticosteroids, insulin, oral contraceptives Slide 23
Pathology: Hyperinsulinemia stimulates keratinocyte and fibroblast proliferation via insulin-like growth factor 1 receptor cross-activation; biopsy shows papillomatosis and hyperkeratosis Slides 22, 24
Clinical Manifestation: Velvety, hyperpigmented, papillomatous plaques on posterior neck, axillae, groin, inframammary folds, antecubital fossae; usually asymptomatic, pruritus may occur; malignant form: rapid onset, extensive, oral mucosa, palms (tripe palms), knuckles, lips, perioral area Slide 23
Diagnosis: Primarily clinical; fasting glucose, hemoglobin A1c, fasting insulin for insulin resistance; lipid panel; polycystic ovary workup; if malignant form suspected: cancer screening, CT (computed tomography) of chest/abdomen/pelvis, upper endoscopy Slide 24
Treatment/Therapy: Treat the underlying cause (weight loss, glycemic control, stop offending drug); metformin; topical retinoids, salicylic acid, ammonium lactate for cosmesis; laser or dermabrasion if refractory; malignant form: urgent oncology, skin regresses with tumor treatment Slide 25
Mortality ★: Not covered in the lecture

Epidermolysis bullosa★ Professor emphasized1 not covered

Name of Condition: Epidermolysis bullosa Slide 26
Definition: Rare group of inherited mechanobullous disorders: extreme skin fragility and blisters at sites of minor trauma, from structural protein defects at the dermal-epidermal junction Slide 26
Etiology (cause): ★ Mutations in structural proteins that maintain skin integrity: simplex (keratin 5/14, autosomal dominant), junctional (laminin-332 or α6β4 integrin, recessive), dystrophic (type VII collagen, dominant or recessive), Kindler (FERMT1, recessive) Slide 29
Epidemiology (who): 8–19 per million live births in the U.S.; simplex most common (~70%); no racial, geographic or sex predilection; rare acquired form (acquisita) is autoimmune, not genetic Slide 29
Risk Factors: Not covered in the lecture
Pathology: Classified by cleavage level: intraepidermal (simplex), lamina lucida (junctional), sub-lamina densa (dystrophic), mixed planes (Kindler) Slide 29
Clinical Manifestation: Blisters from minimal trauma (diapering, handling, friction); simplex: palms/soles, heals without scarring; junctional: generalized, poor healing, nail and enamel defects; dystrophic: severe scarring, mitten deformity, esophageal strictures, squamous cell carcinoma risk; anemia, failure to thrive Slide 30
Diagnosis: Skin biopsy with transmission electron microscopy — gold standard for cleavage plane; immunofluorescence antigen mapping; genetic testing confirms; nutritional labs; endoscopy for strictures; slit-lamp exam Slide 31
Treatment/Therapy: No cure — supportive and preventive: meticulous wound care with non-adherent dressings, trauma prevention, pain control, nutritional support; annual squamous cell carcinoma surveillance after age 10 (recessive dystrophic); topical gene therapy (beremagene geperpavec) for dystrophic; genetic counseling for all families Slides 31–32
Mortality ★: Junctional type carries the highest mortality, especially the Herlitz subtype; early palliative care for severe Herlitz junctional disease Slides 29, 32

Urticaria★ Professor emphasized1 not covered

Name of Condition: Urticaria (also: hives) Slides 33, 36
Definition: Common mast cell–mediated disorder of transient, pruritic wheals with or without angioedema; acute (<6 weeks) or chronic (>6 weeks) Slides 33, 36
Etiology (cause): IgE (immunoglobulin E)-mediated: foods, drugs (penicillin, nonsteroidal anti-inflammatory drugs), insect stings; non-immunologic mast cell activation (opioids, radiocontrast); autoimmune autoantibodies (chronic); physical (cold, heat, pressure, exercise, sunlight); idiopathic in >50% of chronic Slide 36
Epidemiology (who): Lifetime prevalence 15–25%; acute most common; chronic affects 0.5–1%, female:male ~2:1, peak 20–40; angioedema in ~40%; half of chronic cases resolve within 1 year Slide 36
Risk Factors: Atopy; known food or drug allergies; autoimmune disease (thyroid, lupus, rheumatoid arthritis); chronic infections (H. pylori, hepatitis B/C, parasites); female age 20–40 (chronic); stress; nonsteroidal anti-inflammatory drug or ACE (angiotensin-converting enzyme) inhibitor use Slide 37
Pathology: Mast cell degranulation releases histamine, prostaglandins and leukotrienes → transient dermal edema; angioedema is deeper dermal/subcutaneous swelling Slides 36–37
Clinical Manifestation: Raised, erythematous, pruritic wheals with central pallor that blanch; individual lesions last <24 hours; dermographism (wheal along a line where the skin is stroked) in physical urticaria; angioedema of lips, tongue, periorbital area; anaphylaxis risk (bronchospasm, hypotension, stridor) Slide 37
Diagnosis: Acute with clear trigger: clinical, no labs; chronic: complete blood count with differential, metabolic panel, thyroid-stimulating hormone, anti-thyroid peroxidase; tryptase; C4 and C1-esterase inhibitor if angioedema without wheals; biopsy if lesions persist >24 hours Slide 38
Treatment/Therapy: Second-generation antihistamines first-line (cetirizine, loratadine, fexofenadine); short prednisone course if severe; ★ intramuscular epinephrine for anaphylaxis plus auto-injector; chronic: up to 4× antihistamine dose, add histamine-2 blocker or montelukast, then omalizumab, cyclosporine Slide 39
Mortality ★: Not covered in the lecture

Erythema nodosum★ Professor emphasized2 not covered

Name of Condition: Erythema nodosum Slides 40, 45
Definition: Most common panniculitis: a delayed hypersensitivity reaction in subcutaneous fat causing tender, erythematous lower-extremity nodules; a reaction pattern signaling an underlying condition Slides 40, 45
Etiology (cause): Infections: ★ group A Streptococcus (most common), Yersinia, tuberculosis, coccidioidomycosis, histoplasmosis, hepatitis B/C; sarcoidosis (Löfgren syndrome); inflammatory bowel disease (Crohn > ulcerative colitis); drugs (oral contraceptives, sulfonamides, penicillins); ~50% idiopathic Slide 42
Epidemiology (who): 1–5 per 100,000 per year; female:male 3–6:1; peak age 15–40; rare before puberty Slide 42
Risk Factors: Not covered in the lecture
Pathology: Septal panniculitis without vasculitis; Miescher granulomas on deep biopsy Slides 42, 44
Clinical Manifestation: Bilateral, tender, erythematous ★ nodules 1–5 cm on the anterior shins; may involve thighs, forearms, trunk; do not ulcerate; evolve over 3–6 weeks from bright red to bruise-like; prodrome of fever, arthralgia, malaise 1–3 weeks before Slide 43
Diagnosis: Usually clinical; deep incisional biopsy if atypical; complete blood count, sedimentation rate, C-reactive protein; throat culture and antistreptolysin O titer; chest X-ray (bilateral hilar lymphadenopathy); tuberculosis testing; fungal serology; pregnancy test; colonoscopy if bowel symptoms Slide 44
Treatment/Therapy: Treat the underlying cause; rest, leg elevation, compression stockings, nonsteroidal anti-inflammatory drugs; potassium iodide for idiopathic/recurrent; short systemic corticosteroids if infection excluded; colchicine if recurrent; hydroxychloroquine if sarcoid-associated; stop oral contraceptives if drug-induced Slide 44
Mortality ★: Not covered in the lecture

Granuloma annulare1 not covered

Name of Condition: Granuloma annulare Slide 46
Definition: Benign, self-limiting granulomatous dermatosis with annular plaques, most often on the dorsal hands and feet; localized and generalized variants Slide 46
Etiology (cause): Unknown; thought to be a type IV delayed hypersensitivity reaction; proposed triggers: minor trauma, insect bites, viral infections (Epstein-Barr, HIV (human immunodeficiency virus), hepatitis), sun exposure Slide 49
Epidemiology (who): 0.1–0.4% of dermatology patients; localized form in children and young adults; female:male ~2:1; disseminated form in adults >40; subcutaneous form almost only in children under 6 Slide 49
Risk Factors: Generalized form associated with diabetes, thyroid disease, dyslipidemia, malignancy (lymphoma); suggested genetic susceptibility (HLA-A31 and BW35 human leukocyte antigen haplotypes) Slide 49
Pathology: Palisading granulomas around degenerating collagen (necrobiosis) with mucin deposition Slides 49, 51
Clinical Manifestation: Localized (75%): flesh-colored to erythematous papules in an annular ring on dorsal hands, feet, ankles, asymptomatic; generalized: hundreds of small papules, may itch; subcutaneous: deep firm nodules in children; perforating: umbilicated papules; patch: flat hyperpigmented patches Slide 50
Diagnosis: Usually clinical for localized form; punch biopsy; in generalized form screen fasting glucose/hemoglobin A1c, lipids, thyroid tests; HIV (human immunodeficiency virus) testing if risk factors; malignancy screening in adults >50 Slide 51
Treatment/Therapy: Localized: watchful waiting (50% resolve within 2 years); intralesional triamcinolone, high-potency topical steroids with occlusion, cryotherapy; generalized: doxycycline, hydroxychloroquine, dapsone, isotretinoin or narrowband ultraviolet B phototherapy; treat any systemic condition Slide 51
Mortality ★: Not covered in the lecture

Pyoderma gangrenosum★ Professor emphasized1 not covered

Name of Condition: Pyoderma gangrenosum Slides 53, 57
Definition: Rare, devastating neutrophilic dermatosis (not infectious) with rapidly progressive, painful ulceration and pathergy (worsening with trauma), often with serious systemic disease Slides 53, 57
Etiology (cause): Associated with inflammatory bowel disease (25–50%), rheumatoid and seronegative arthritis, hematologic malignancy (acute myeloid leukemia, myelodysplastic syndrome, myeloma), monoclonal gammopathy of undetermined significance, PAPA syndrome (pyogenic arthritis, pyoderma gangrenosum, acne) Slide 57
Epidemiology (who): 3–10 per million per year; adults 25–55; slight female predominance; peristomal form in up to 15% of patients with intestinal ostomies and inflammatory bowel disease; rare in children (<4%) Slide 57
Risk Factors: Not covered in the lecture
Pathology: Dysregulated innate immune activation → neutrophil recruitment and uncontrolled inflammation → tissue destruction; biopsy shows dense neutrophilic infiltrate Slides 57, 59
Clinical Manifestation: ★ Classic: starts as a pustule or nodule → rapidly expanding, painful ulcer with undermined violaceous border; lower extremities most common; pathergy; bullous (hematologic malignancy), pustular (bowel flares), peristomal variants Slide 58
Diagnosis: Diagnosis of exclusion, no gold standard; biopsy of ulcer edge; wound cultures; serum/urine protein electrophoresis for monoclonal gammopathy; antinuclear and antineutrophil cytoplasmic antibodies; colonoscopy; Paracelsus score or Delphi criteria Slide 59
Treatment/Therapy: Avoid debridement (pathergy); moist dressings; prednisone first-line for rapid progression; cyclosporine (steroid-sparing); dapsone, mycophenolate or azathioprine for maintenance; infliximab is the biologic of choice with inflammatory bowel disease; adalimumab, ustekinumab if refractory Slide 60
Mortality ★: Mortality often attributable to the underlying systemic disease rather than pyoderma gangrenosum itself Slide 57

Acne rosacea★ Professor emphasized1 not covered

Name of Condition: Acne rosacea (also: rosacea) Slide 61
Definition: Chronic, relapsing inflammatory facial dermatosis of mostly fair-skinned adults: central facial erythema, telangiectasias, possible ocular and rhinophyma complications Slide 61
Etiology (cause): Neurovascular dysregulation, innate immune dysfunction and skin microbiome changes; Demodex folliculorum overgrowth (papulopustular); H. pylori in some; ultraviolet, heat and vasomotor triggers; genetic predisposition Slide 65
Epidemiology (who): 5–10% of the global population; Celtic, Nordic, Eastern European ancestry; female:male ~3:1, but males more often get rhinophyma; onset 30–60; underdiagnosed in darker skin Slide 65
Risk Factors: Fitzpatrick types I–III (fair skin, light eyes); family history; female sex; age 30–60; prior acne vulgaris; chronic ultraviolet exposure. Triggers: sun (most universal), heat, hot drinks, spicy foods, alcohol (red wine), stress, topical steroids Slide 67
Pathology: Upregulated toll-like receptor 2 → cathelicidin (LL-37) overproduction → inflammation; biopsy: perivascular lymphocytic infiltrate, Demodex, dilated vessels Slides 65, 68
Clinical Manifestation: Erythematotelangiectatic (most common: flushing, persistent erythema, telangiectasias); papulopustular (papules and pustules, no comedones); phymatous (rhinophyma, mostly males); ocular (blepharitis, conjunctivitis, keratitis; corneal scarring risk) Slide 66
Diagnosis: Clinical, no labs in typical cases; biopsy rarely; antinuclear antibody to exclude lupus if atypical; skin scraping to quantify Demodex; slit-lamp exam for ocular disease; urinary 5-hydroxyindoleacetic acid if flushing with gastrointestinal symptoms Slide 68
Treatment/Therapy: ★ Topical metronidazole first-line for papulopustular; azelaic acid; ivermectin cream (Demodex); brimonidine/oxymetazoline for erythema; sub-antimicrobial doxycycline; isotretinoin if refractory; lasers for telangiectasia; laser or excision for rhinophyma; daily sunscreen 30+ Slide 69
Mortality ★: Not covered in the lecture

Hyperhidrosis1 not covered

Name of Condition: Hyperhidrosis Slides 71–72
Definition: Excessive sweating beyond thermoregulatory need, impairing quality of life; primary (focal) and secondary (generalized) forms Slides 71–72
Etiology (cause): Excess eccrine gland activity. Primary: idiopathic, familial. Secondary: diabetes, hyperthyroidism, pheochromocytoma, lymphoma, menopause, obesity, drugs (selective serotonin reuptake inhibitors, opioids, cholinesterase inhibitors, venlafaxine) Slide 72
Epidemiology (who): 2.8–4.8% of the U.S. population; primary is the majority; onset 14–25 for palmar/plantar and axillary forms; no sex predominance; only ~38% discuss it with a physician Slide 72
Risk Factors: Family history (autosomal dominant, primary); adolescent/young adult onset; obesity and metabolic syndrome; anxiety (exacerbating, not causative); hyperthyroidism, diabetes, menopause; selective serotonin and serotonin-norepinephrine reuptake inhibitors, opioids, cholinesterase inhibitors; lymphoma, pheochromocytoma Slide 73
Pathology: Primary: normal eccrine glands with heightened sympathetic cholinergic neural drive Slide 72
Clinical Manifestation: Primary: bilateral, symmetric sweating of palms, soles, axillae, craniofacial region; at least weekly; absent during sleep; secondary: generalized, asymmetric, may occur at night; pheochromocytoma: episodic sweating with headache, palpitations, hypertension Slide 73
Diagnosis: Primary: clinical criteria (bilateral focal, ≥6 months, Hyperhidrosis Disease Severity Scale ≥2); Minor starch-iodine test maps sweating; gravimetry; secondary workup: thyroid-stimulating hormone, glucose, hemoglobin A1c, complete blood count, 24-hour urine metanephrines Slide 74
Treatment/Therapy: First-line topical aluminum chloride 20% nightly, glycopyrronium cloth/gel; second-line iontophoresis, oral anticholinergics (glycopyrrolate, oxybutynin); third-line botulinum toxin A, microwave thermolysis, endoscopic thoracic sympathectomy (compensatory sweating risk) Slide 75
Mortality ★: Not covered in the lecture

Stevens-Johnson syndrome

Name of Condition: Stevens-Johnson syndrome Slides 78–80
Definition: Life-threatening mucocutaneous emergency: a severe type IV hypersensitivity reaction with epidermal detachment <10% body surface area (10–30% = overlap with toxic epidermal necrolysis) Slides 78–80
Etiology (cause): Mostly medications: aromatic anticonvulsants (carbamazepine, phenytoin, lamotrigine, phenobarbital), sulfonamides (trimethoprim-sulfamethoxazole), allopurinol (most common in Asia), oxicam anti-inflammatories, nevirapine; infections: M. pneumoniae, herpes simplex (children) Slide 79
Epidemiology (who): 1–7 per million per year; higher in immunocompromised — HIV (human immunodeficiency virus) 1,000-fold risk; Asian carriers of HLA (human leukocyte antigen)-B*15:02 at markedly elevated risk with carbamazepine Slide 79
Risk Factors: HIV (human immunodeficiency virus) and other immunodeficiencies; HLA-B*15:02 (carbamazepine), HLA-B*58:01 (allopurinol); prior episode; active malignancy or radiation; slow acetylator phenotype (sulfonamides) Slide 80
Pathology: Biopsy: full-thickness epidermal necrosis with dermal-epidermal junction separation Slide 82
Clinical Manifestation: Prodrome of fever, malaise, upper respiratory symptoms 1–3 days before skin; painful erythematous macules and target lesions starting on the trunk; mucosal erosions (oral, ocular, genital) in >90%; positive Nikolsky sign (lateral pressure induces skin slippage) Slide 80
Diagnosis: Punch biopsy (full-thickness epidermal necrosis is pathognomonic); blood counts, metabolic panel, liver and kidney tests; blood cultures if infection suspected; chest X-ray; ophthalmology slit-lamp exam; SCORTEN (Severity of Illness Score for Toxic Epidermal Necrolysis) for triage and prognosis Slide 82
Treatment/Therapy: Withdraw the causative drug immediately (each day of delay worsens prognosis); burn unit or intensive care, intravenous fluids, non-adhesive dressings, avoid silver sulfadiazine; intravenous immunoglobulin or cyclosporine; steroids controversial; eye and mucosal care; lifelong drug avoidance Slides 83–84
Mortality ★: 1–5% mortality for Stevens-Johnson alone; overlap with toxic epidermal necrolysis increases it substantially; SCORTEN (Severity of Illness Score for Toxic Epidermal Necrolysis) estimates in-hospital mortality Slide 79

Toxic epidermal necrolysis★ Professor emphasized

Name of Condition: Toxic epidermal necrolysis Slides 85, 88
Definition: The most severe end of the Stevens-Johnson–toxic epidermal necrolysis spectrum: a dermatologic emergency with epidermal detachment >30% body surface area Slides 85, 88
Etiology (cause): Same agents as Stevens-Johnson; ★ drug-induced in >80%: allopurinol (most common worldwide), aromatic anticonvulsants (carbamazepine, phenytoin, lamotrigine), sulfonamides, oxicam anti-inflammatories, nevirapine; rarely contrast media, herbal preparations Slide 87
Epidemiology (who): 0.4–1.9 per million per year; all ages, highest risk in elderly and immunocompromised; HIV (human immunodeficiency virus)-positive patients 1,000× more likely; female predominance in some series Slide 87
Risk Factors: HIV (human immunodeficiency virus), bone marrow transplant; HLA (human leukocyte antigen) haplotypes B*15:02, B*58:01; prior Stevens-Johnson/toxic epidermal necrolysis; active (especially hematologic) malignancy; brain irradiation with anticonvulsant use Slide 87
Pathology: Massive CD8+ T-cell–mediated keratinocyte apoptosis, with granulysin a key cytotoxic mediator; full-thickness necrosis with dermal separation Slides 87, 126
Clinical Manifestation: Prodrome of high fever, malaise, stinging eyes, painful swallowing 1–3 days before; painful erythema → flaccid bullae → confluent detachment >30%; positive Nikolsky sign (lateral pressure induces skin slippage); "wet parchment" look; near-universal mucosal erosions; sepsis, acute respiratory distress syndrome, acute kidney injury Slide 88
Diagnosis: SCORTEN (Severity of Illness Score for Toxic Epidermal Necrolysis) within 24 hours of admission and on day 3, 1 point each: age >40, malignancy, heart rate >120, detachment >10%, blood urea nitrogen >28 mg/dL, bicarbonate <20, glucose >252 mg/dL; biopsy: full-thickness necrosis Slides 89, 126
Treatment/Therapy: Burn unit or intensive care mandatory; stop all suspect drugs; burn-style fluid resuscitation; non-adhesive biological dressings; early enteral feeding; cyclosporine (strongest evidence); intravenous immunoglobulin or etanercept adjuncts; no prophylactic antibiotics; daily ophthalmology; palliative care if SCORTEN ≥5 Slide 90
Mortality ★: Up to 30–35%; SCORTEN (Severity of Illness Score for Toxic Epidermal Necrolysis) predicted mortality: 0–1 = 3.2%, 2 = 12%, 3 = 35%, 4 = 58%, ≥5 = 90% Slides 85, 89

Sunburn2 not covered

Name of Condition: Sunburn Slide 91
Definition: Acute ultraviolet B–induced cutaneous inflammation; the most common photobiologic injury in clinical practice Slide 91
Etiology (cause): Mainly ultraviolet B (290–320 nm) causing direct DNA damage (pyrimidine dimers); ultraviolet A (320–400 nm) contributes via oxidative stress and indirect DNA damage Slide 94
Epidemiology (who): ~33% of U.S. adults and 70% of adolescents report at least one episode per year; highest in non-Hispanic white populations, warm climates, outdoor work and recreation Slide 94
Risk Factors: Fitzpatrick types I–II (fair skin that burns easily); high-altitude or equatorial ultraviolet; photosensitizing drugs (tetracyclines, fluoroquinolones, thiazides); reflective snow, sand, water; immunosuppression; childhood and adolescent exposure Slides 94, 122
Pathology: DNA damage → keratinocyte apoptosis ("sunburn cells"), prostaglandin release, vasodilation, inflammation (biopsy: sunburn cells, epidermal spongiosis); onset 3–5 hours after exposure, peaks at 12–24 hours Slides 94, 126
Clinical Manifestation: First degree: erythema, warmth, tenderness, no blisters, resolves in 3–5 days with desquamation; second degree: blistering, intense pain, edema, 1–2 weeks; "sun poisoning": fever, chills, nausea/vomiting, dehydration, headache, tachycardia Slide 95
Diagnosis: Not covered in the lecture
Treatment/Therapy: Cool compresses; early nonsteroidal anti-inflammatory drugs; oral hydration (intravenous if severe); moisturizers such as aloe; do not pop blisters; topical steroids of limited benefit; hospitalize if blistering >20% body surface area, systemic toxicity, elderly/pediatric; sunscreen 30+, avoid 10 AM–4 PM Slide 96
Mortality ★: Not covered in the lecture

Drug-induced photosensitivity3 not covered

Name of Condition: Drug-induced photosensitivity (also: phototoxic and photoallergic reactions) Slides 97–98
Definition: Abnormal skin reaction to ultraviolet or visible light caused by a drug, by two mechanisms: phototoxicity and photoallergy Slides 97–98
Etiology (cause): Phototoxic: tetracyclines (especially doxycycline), fluoroquinolones, amiodarone, thiazides, furosemide, voriconazole, nonsteroidal anti-inflammatory drugs, psoralens, St. John's wort. Photoallergic: sunscreen chemicals (oxybenzone), sulfonamides, topical antihistamines, phenothiazines Slide 98
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Phototoxic: non-immunologic, dose-dependent; the drug absorbs ultraviolet energy → reactive oxygen species → direct cell damage. Photoallergic: type IV delayed, dose-independent; the drug acts as a photohapten and needs prior sensitization Slide 98
Clinical Manifestation: Phototoxic: exaggerated sunburn within hours, on first exposure. Photoallergic: pruritic eczematous eruption on re-exposure, extending beyond sun-exposed skin; may persist after the drug is stopped (persistent light reaction) Slide 98
Diagnosis: Thorough drug history (including over-the-counter and topical products); phototesting (minimal erythema dose); photopatch testing is the gold standard for photoallergy (reaction only on the irradiated patch = photoallergy, both patches = contact allergy); biopsy rarely Slide 99
Treatment/Therapy: Stop or substitute the offending drug; strict photoprotection (sunscreen 50+, zinc oxide, titanium dioxide); phototoxic: cool compresses, nonsteroidal anti-inflammatory drugs, topical steroids; photoallergic: topical or short systemic steroids, antihistamines; persistent light reaction: narrowband ultraviolet B Slide 99
Mortality ★: Not covered in the lecture

Phytophotodermatitis2 not covered

Name of Condition: Phytophotodermatitis (also: lime disease, margarita dermatitis; includes berloque dermatitis) Slide 100
Definition: Photodermatitis in which plant furanocoumarins (psoralens) on the skin plus ultraviolet A cause a phototoxic reaction; berloque dermatitis is the fragrance variant Slide 100
Etiology (cause): Furanocoumarins in limes, celery, parsley, wild parsnip, fig + ultraviolet A; berloque: bergapten (5-methoxypsoralen) in bergamot oil in fragrances/cosmetics + ultraviolet exposure Slide 100
Epidemiology (who): Berloque form now largely historical due to reformulation of cosmetics Slide 100
Risk Factors: Not covered in the lecture
Pathology: Phototoxic (non-immunologic) reaction from light interacting with an exogenous chemical Slides 98, 100
Clinical Manifestation: Painful blistering in the acute phase, then linear/streaked hyperpigmentation (classic: lime juice + sun); berloque: drip-pattern hyperpigmentation on the neck and décolletage Slide 100
Diagnosis: Detailed exposure history (plants, topicals, fragrances, medications); photopatch testing; biopsy if uncertain Slide 101
Treatment/Therapy: Avoid contactant plus ultraviolet together; acute blistering: cool compresses, wound care, mid-potency topical steroids; hyperpigmentation: reassure, fades over months (hydroquinone or azelaic acid if persistent), sunscreen; wash skin right after plant contact Slide 101
Mortality ★: Not covered in the lecture

Chronic actinic dermatitis3 not covered

Name of Condition: Chronic actinic dermatitis (also: includes actinic reticuloid) Slide 100
Definition: Photodermatitis: a persistent eczematous eruption in chronically sun-exposed areas; spectrum includes actinic reticuloid Slide 100
Etiology (cause): Associated with contact and photocontact allergies Slide 100
Epidemiology (who): Older males Slide 100
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Persistent eczematous eruption on chronically sun-exposed skin Slide 100
Diagnosis: Phototesting required to confirm: low minimal erythema dose to ultraviolet B and ultraviolet A; photopatch testing Slides 100–101
Treatment/Therapy: Strict photoprotection; potent topical steroids, tacrolimus, hydroxychloroquine; narrowband ultraviolet B or PUVA (psoralen plus ultraviolet A) for refractory cases; azathioprine if severe Slide 101
Mortality ★: Not covered in the lecture

Polymorphous light eruption★ Professor emphasized2 not covered

Name of Condition: Polymorphous light eruption Slides 102, 104
Definition: ★ The most common idiopathic photodermatosis: an acquired photodermatosis affecting up to 15–20% of the general population Slides 102, 104
Etiology (cause): Idiopathic; delayed-type hypersensitivity to an ultraviolet-induced photoantigen; ultraviolet A is the primary trigger (ultraviolet B and visible light also); strong hereditary component (up to 50% family concordance) Slide 104
Epidemiology (who): 10–20% in temperate climates; ★ young to middle-aged women (female:male ≈ 2–3:1); higher latitudes; spring and early summer; up to 35% in Native American populations; all skin types, relative sparing of darker skin Slide 104
Risk Factors: Not covered in the lecture
Pathology: Delayed-type hypersensitivity to an ultraviolet-induced photoantigen; regulatory T-cell suppression and failure of normal ultraviolet-induced immunosuppression may play central roles; biopsy: perivascular lymphocytic infiltrate with dermal edema Slides 104, 106
Clinical Manifestation: 30 minutes to hours after ultraviolet, first sunny days of spring or travel; papular (2–5 mm, décolletage, forearms, dorsal hands) most common, also vesicular, plaque, urticarial; spares chronically exposed face/hands; resolves in 7–10 days; improves with summer "hardening" Slide 105
Diagnosis: Largely clinical; phototesting reproduces the eruption in ~50–60%; antinuclear antibody panel mandatory to exclude lupus (anti-Ro/La); biopsy supportive, not pathognomonic; porphyrin screen if protoporphyria suspected Slide 106
Treatment/Therapy: Acute: avoid ultraviolet, cool compresses, moderate-potency topical steroids, oral antihistamines, short prednisolone if severe. Prevention: sunscreen 50+; prophylactic narrowband ultraviolet B in spring (most effective); hydroxychloroquine if refractory Slide 106
Mortality ★: Not covered in the lecture

Dermatoheliosis3 not covered

Name of Condition: Dermatoheliosis (also: photoaging) Slides 114, 116
Definition: Cumulative structural and functional skin damage from chronic ultraviolet exposure, distinct from intrinsic chronological aging; the dominant form of skin aging Slides 114, 116
Etiology (cause): Ultraviolet A penetrates the dermis → reactive oxygen species and matrix metalloproteinases (1, 3, 9) that degrade collagen and elastin; ultraviolet B drives TP53 mutation and epidermal atrophy over decades Slide 116
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Solar elastosis (thickened, tangled elastin replacing collagen) is the hallmark; epidermal atrophy with loss of rete ridges; irregular melanocytes; telangiectasia; fewer fibroblasts, less collagen Slide 116
Clinical Manifestation: Coarse, deep wrinkles; leathery skin (cutis rhomboidalis nuchae: leathery, rough posterior neck, marker of severe photoaging); solar lentigines, guttate hypomelanosis, mottled pigment, telangiectasias; actinic keratoses and skin cancers Slide 117
Diagnosis: Clinical: chronic sun exposure history plus distribution; biopsy confirms solar elastosis and excludes malignancy; dermoscopy of individual lesions; DNA repair assay/genetic testing if xeroderma pigmentosum suspected; annual full-body skin exam Slide 118
Treatment/Therapy: Tretinoin (only approved topical for photoaging; 6–12 months for results); vitamin C, niacinamide, hydroquinone; peels, laser resurfacing, intense pulsed light; daily broad-spectrum sunscreen 30+ is the most evidence-supported prevention Slide 119
Mortality ★: Not covered in the lecture

Lecture 4 · Cutaneous Bacterial Infections

Monique Jaquith, DMSc, PA-C · 15 conditions · source: 4. Cutaneous Bacterial Infections.pptx

Acne vulgaris★ Professor emphasized1 not covered

Name of Condition: Acne vulgaris Slide 4
Definition: Common skin eruption of areas with hormonally responsive sebaceous glands (face, neck, chest, upper back, upper arms); not physically disabling but major psychological impact (low self-esteem, depression, anxiety) Slide 4
Etiology (cause): Four factors: follicular hyperkeratinization; increased sebum; Cutibacterium acnes (formerly Propionibacterium acnes; anaerobic Gram-positive rod of normal flora) in the follicle; inflammation from immune response to C. acnes Slide 6
Epidemiology (who): Most common skin disease in US (~80% of Americans in their lives); begins with puberty; adolescent acne more common and severe in males; post-adolescent (over 25 years) more common in women Slide 5
Risk Factors: Puberty (androgens drive sebum); genetics (3-fold risk if first-degree relative); drugs (lithium, systemic steroids, anabolic steroids); acnegenic mineral oils; increased androgens, insulin resistance; stress; acne mechanica (pressure from pads, casts, helmets); possible skim milk link (not chocolate or fatty food) Slides 8–9, 17
Pathology: Excess keratin plugs follicle while sebum feeds C. acnes; progression: normal follicle → open comedo (blackhead) → closed comedo (whitehead) → papule → pustule → nodule/cyst Slides 6–7
Clinical Manifestation: Lesions on face, neck, upper arms, back, chest; pain, tenderness, erythema; systemic symptoms usually absent; premenstrual flares in women; polymorphic: comedones (hallmark) (non-inflammatory) plus papules, pustules, nodules (inflammatory) Slides 10–11, 13
Diagnosis: Clinical; culture if no response to treatment; grade by lesion number/type, severity, sites, scarring, quality of life (mild: under 20 comedones, under 15 inflammatory or under 30 total; severe: over 5 cysts or over 125 total); differential: polycystic ovarian syndrome, rosacea, anabolic steroids, folliculitis Slides 12, 17–18
Treatment/Therapy: ★ Comedonal: topical retinoid (else azelaic/salicylic acid) · mild papulopustular: benzoyl peroxide ± topical antibiotic + retinoid · moderate: retinoid + oral doxycycline/minocycline + benzoyl peroxide · severe: same, or oral isotretinoin (teratogen); ★ don't apply tretinoin and benzoyl peroxide together Slides 20–22, 26–30, 32–33, 35
Mortality ★: Not covered in the lecture

Folliculitis★ Professor emphasized3 not covered

Name of Condition: Folliculitis Slides 38–39
Definition: Inflammation of hair follicle(s): inflammatory cells within the wall and ostia of the follicle, creating a follicular-based pustule Slides 38–39
Etiology (cause): Infection (bacterial, fungal, viral), physical injury (tight clothing), or chemical irritation (waxing, tar); bacterial: ★ S. aureus most common, occasionally Pseudomonas aeruginosa Slide 39
Epidemiology (who): Not covered in the lecture
Risk Factors: Obesity; poor hygiene; occlusive clothing; hot, humid temperatures; immunocompromise (corticosteroids, diabetes mellitus); nasal carriage of S. aureus Slide 40
Pathology: Not covered in the lecture
Clinical Manifestation: Usually abrupt eruption; pustule painless or tender; afebrile, no systemic involvement; small papules/pustules on an erythematous base pierced by a central hair; scalp, thighs, trunk, axilla, ★ inguinal area Slide 41
Diagnosis: Clinical (history and appearance); resistant cases: culture and Gram stain of unroofed pustule, KOH (potassium hydroxide) wet mount of plucked hair to rule out fungal folliculitis, nasal swab of patient/family for S. aureus colonization, biopsy; differential: acne, tinea barbae, molluscum contagiosum, eczema Slides 42–44
Treatment/Therapy: Moist heat, antibacterial soap, loose clothing, glycemic control; don't squeeze · mild: topical mupirocin (Bactroban), clindamycin · carrier: ★ nasal mupirocin ointment twice a day for 5 days · extensive: oral cephalexin, dicloxacillin · MRSA (methicillin-resistant S. aureus): ★ Bactrim, ciprofloxacin, linezolid Slides 45–47
Mortality ★: Not covered in the lecture

Pseudomonas (hot tub) folliculitis3 not covered

Name of Condition: Pseudomonas (hot tub) folliculitis (also: hot tub folliculitis) Slide 48
Definition: Usually self-limiting folliculitis acquired from contaminated water Slide 48
Etiology (cause): Pseudomonas aeruginosa (Gram-negative); from contaminated whirlpools, hot tubs, water slides, physiotherapy pools with inadequate chlorine treatment Slide 48
Epidemiology (who): Not covered in the lecture
Risk Factors: Exposure to inadequately chlorinated whirlpools, hot tubs, water slides, physiotherapy pools Slide 48
Pathology: Not covered in the lecture
Clinical Manifestation: Rash 8 hours to 5 days after exposure; pruritic or tender; follicular papules, vesicles, pustules that can crust; trunk, extremities, buttocks, usually sparing face, neck, soles, palms Slide 49
Diagnosis: Usually clinical; if unclear or treatment-resistant, bacterial culture of a pustule or of the contaminated water Slide 51
Treatment/Therapy: Most resolve without treatment in 2-10 days; diluted acetic acid 5% (vinegar) wet dressings 20 minutes 2-4 times a day; widespread/resistant: ciprofloxacin · prevention: showering after exposure does not prevent it; continuous filtration, frequent chlorine monitoring and water changes Slides 52–53
Mortality ★: Not covered in the lecture

Pseudofolliculitis barbae★ Professor emphasized1 not covered

Name of Condition: Pseudofolliculitis barbae Slide 54
Definition: Foreign body reaction to hair in any shaved area Slide 54
Etiology (cause): Shaving of tightly curled hair; cut hair curves back into the skin Slides 54–55
Epidemiology (who): ★ Commonly Black males (tightly curled facial hair plus keratin gene variations), or anyone who shaves and has curlier facial/body hair Slide 54
Risk Factors: Shaving; curly facial/body hair Slide 54
Pathology: Cut hair curves into the follicular wall and penetrates the skin, re-entering the dermis and provoking an inflammatory response to hair keratin Slide 55
Clinical Manifestation: Erythematous papule with central hair shaft; painful and/or pruritic; secondary infection → pustules, abscess Slide 56
Diagnosis: Clinical Slide 56
Treatment/Therapy: Stop shaving if possible; clean razors, avoid "lift-and-cut" systems, mild angles, single or double blades; chemical depilatories; laser hair removal (permanent) · topical tretinoin, mild corticosteroids, eflornithine (Vaniqa) · topical clindamycin, benzoyl peroxide, erythromycin · oral tetracycline Slides 57–58
Mortality ★: Not covered in the lecture

Furuncle★ Professor emphasized2 not covered

Name of Condition: Furuncle (also: boil) Slide 59
Definition: Deep-seated infection (abscess) of a hair follicle and adjacent subcutaneous tissue; about 1 cm tender red papule or fluctuant nodule Slide 59
Etiology (cause): ★ S. aureus most common Slide 59
Epidemiology (who): Not covered in the lecture
Risk Factors: Immunocompromise (alcoholism, malnutrition, immunosuppression, diabetes); trauma (shaving, insect bite); nasal S. aureus carriage; recurrent furunculosis: obesity, diabetes, nasal carriage Slides 61–62
Pathology: Follicular abscess extending into subcutaneous tissue; favors areas of friction or minor trauma Slides 59, 61
Clinical Manifestation: Painful, firm, tender, fluctuant nodule with a single opening and surrounding erythema; may drain spontaneously; back of neck, face, axillae, buttocks Slides 61–62
Diagnosis: Clinical appearance; organism identified via aspiration or incision and drainage; differential: cystic acne, folliculitis, hidradenitis suppurativa Slide 64
Treatment/Therapy: Warm compresses; no antibiotics if afebrile, single lesion under 5 mm · incise, drain and culture large ones · oral dicloxacillin or cephalexin if over 5 mm, fails drainage, expanding cellulitis, immunocompromised, endocarditis risk · MRSA (methicillin-resistant S. aureus): Bactrim, clindamycin, doxycycline Slides 65–66
Mortality ★: Not covered in the lecture

Carbuncle2 not covered

Name of Condition: Carbuncle Slide 59
Definition: Two or more confluent furuncles with separate heads; several-cm red plaque Slide 59
Etiology (cause): S. aureus most common (as for furuncle) Slide 59
Epidemiology (who): Not covered in the lecture
Risk Factors: Immunocompromise (alcoholism, malnutrition, immunosuppression, diabetes); trauma (shaving, insect bite); nasal S. aureus carriage Slide 61
Pathology: Deeper infection of interconnecting furuncles arising in several hair follicles Slide 63
Clinical Manifestation: Extremely painful; systemic symptoms (malaise, chills, fever) more common than with furuncle; several loculated abscesses, superficial pustules, necrotic plugs, sieve-like openings draining pus; back of neck, face, axillae, buttocks Slides 61, 63
Diagnosis: Clinical appearance; organism via aspiration or incision and drainage; differential: cystic acne, folliculitis, hidradenitis suppurativa Slide 64
Treatment/Therapy: Incision and drainage is the mainstay; endocarditis prophylaxis if at risk · oral dicloxacillin or cephalexin · if MRSA (methicillin-resistant Staphylococcus aureus): Bactrim, doxycycline, clindamycin Slide 67
Mortality ★: Not covered in the lecture

Hidradenitis suppurativa2 not covered

Name of Condition: Hidradenitis suppurativa (also: acne inversa) Slide 68
Definition: Inflammation of cutaneous apocrine (sweat) glands; resembles acne vulgaris Slide 68
Etiology (cause): Keratin plug obstructs the apocrine gland/duct, followed by secondary bacterial infection Slides 68–69
Epidemiology (who): Not covered in the lecture
Risk Factors: Hot weather, excessive perspiration, obesity, apocrine duct obstruction, secondary bacterial infection, cigarette smoking Slide 68
Pathology: Keratin plug blocks apocrine gland → infection → abscess drains → healing with scarring; biopsy: follicular occlusion by keratin, folliculitis, apocrine gland destruction Slides 69, 74
Clinical Manifestation: Recurrent painful/suppurative lesions; axilla (most common), groin, perineum, gluteal, inframammary; nodules, sinus tracts, abscesses, scarring, double comedone (blackhead with 2 or more openings) Slides 68, 70
Diagnosis: Clinical, requiring 3 elements: typical lesions, characteristic distribution (axilla, groin), recurrence more than twice in 6 months; biopsy not usually required; differential: acne vulgaris, folliculitis, carbuncle, furuncle Slides 73–74
Treatment/Therapy: Avoid heat/friction, antibacterial wash, weight loss, smoking cessation essential, laser hair removal · mild topical steroid + topical clindamycin · isotretinoin, intralesional triamcinolone, prednisone, infliximab, spironolactone, oral contraceptives · drain large cysts; wide excision best chance of cure Slides 75–79
Mortality ★: Not covered in the lecture

Erythrasma2 not covered

Name of Condition: Erythrasma Slide 80
Definition: Chronic superficial bacterial infection of intertriginous skin Slide 80
Etiology (cause): Corynebacterium minutissimum Slide 80
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetes; heat and humidity Slide 80
Pathology: Bacteria invade the upper third of the stratum corneum under warm, humid conditions Slide 80
Clinical Manifestation: Usually asymptomatic, may be pruritic; inner thighs, crural region, scrotum, between 4th and 5th toes; less often axilla, under breasts, intergluteal folds Slide 81
Diagnosis: Coral-red fluorescence under Wood's lamp (ultraviolet light); differential: cutaneous candidiasis, contact dermatitis, psoriasis, tinea corporis/cruris/pedis Slides 82–83
Treatment/Therapy: Localized: topical erythromycin or clindamycin first line · widespread: oral erythromycin or clarithromycin · yeast present: add miconazole cream · keep area clean and dry, avoid heat/moisture, healthy weight, hygiene Slide 84
Mortality ★: Not covered in the lecture

Impetigo (non-bullous, bullous, ecthyma)★ Professor emphasized1 not covered

Name of Condition: Impetigo (non-bullous, bullous, ecthyma) Slides 85, 87, 89, 91
Definition: Very contagious, autoinoculable superficial epidermal skin infection; types: non-bullous (more common), bullous, and ecthyma (deeper, ulcerating) Slides 85, 87, 89, 91
Etiology (cause): Most often S. aureus or Streptococcus pyogenes; bullous is exclusively S. aureus; entry via minor skin breaks (cuts, bug bites) Slides 85–86, 89
Epidemiology (who): Common in infants and children; ecthyma not common Slides 85, 91
Risk Factors: Moist environment, poor hygiene, chronic nasopharyngeal staph/strep carriage; ecthyma: preexisting tissue damage (bites), immunocompromise (diabetes), crowding Slides 86, 91
Pathology: Epidermal infection; bullous: epidermolytic toxins cause epidermal splitting; ecthyma deepens into dermal ulceration; may be followed by APSGN (acute post-streptococcal glomerulonephritis), especially ages 3-7; antibiotics do not prevent it (immune response precedes treatment) Slides 85, 89, 91, 97
Clinical Manifestation: Non-bullous: macule → vesicle/pustule → ruptures, leaving honey-colored adherent crust; face, extremities; lymphadenopathy common · bullous: fragile tense bullae, erosions, collarettes; lymphadenopathy uncommon · ecthyma: ulcer with thick gray-yellow crust, lower legs, heals with scar Slides 87–91
Diagnosis: Clinical; culture if high risk for MRSA (methicillin-resistant Staphylococcus aureus) (health-care worker, teacher) or post-streptococcal glomerulonephritis present; differential: varicella, insect bites, herpes simplex, tinea corporis, scabies (non-bullous); burn, contact dermatitis, herpes (bullous) Slides 92–93
Treatment/Therapy: Cover staph/strep · limited non-bullous: ★ mupirocin (Bactroban) ointment (remove crusts first) or retapamulin · oral: dicloxacillin, amoxicillin-clavulanate, cephalexin (drug of choice in children), clindamycin if penicillin allergic · MRSA: clindamycin, Bactrim, doxycycline (over 8 years) · isolate children 24-48 hours into treatment Slides 94–96
Mortality ★: Not covered in the lecture

Erysipelas2 not covered

Name of Condition: Erysipelas (also: superficial cellulitis) Slide 98
Definition: Bacterial infection of the upper dermis extending to superficial cutaneous lymphatics (superficial cellulitis) Slide 98
Etiology (cause): Group A Streptococcus (S. pyogenes) most common Slide 98
Epidemiology (who): Not covered in the lecture
Risk Factors: Impaired lymphatic drainage (mastectomy), immunocompromise, tinea pedis, obesity, trauma, pre-existing skin infection (impetigo); inciting event often not recalled Slide 99
Pathology: Infection of the superficial dermis with lymphatic spread Slides 98, 101
Clinical Manifestation: Sudden onset; malaise, myalgias, chills, high fever (38-40 °C) within 48 hours, nausea, headache; lower extremities (80%) or face; rapidly spreading erythema, edema, warmth; raised plaque with clear line of demarcation; "red streaks" to lymph nodes Slides 98, 100–101
Diagnosis: Clinical; leukocytosis, raised erythrocyte sedimentation rate and C-reactive protein common; blood/tissue cultures and imaging low yield, not indicated; differential: discoid lupus, deep vein thrombosis, cellulitis Slides 102–103
Treatment/Therapy: Prompt treatment (can progress rapidly); symptomatic care, hydration, cold compresses, elevation · penicillin V; clindamycin if penicillin allergic Slide 104
Mortality ★: Not covered in the lecture

Cellulitis2 not covered

Name of Condition: Cellulitis Slide 105
Definition: Acute inflammatory infection of the deeper dermis and subcutaneous tissue; purulent or non-purulent Slide 105
Etiology (cause): Group A beta-hemolytic streptococci (S. pyogenes) or Staphylococcus aureus; portals: tinea pedis, open lesion, trauma, surgical wound, insect bite, fissure, radiation Slides 105–106
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetes mellitus, intravenous drug use, immunocompromise, chronic lymphedema, previous cellulitis Slide 106
Pathology: Deeper infection than erysipelas; devitalized (necrotic) tissue is not perfused so antibiotics cannot reach it Slides 105, 111
Clinical Manifestation: Erythema, warmth, edema, tenderness; ± fever/chills; lower leg, almost never bilateral; borders not elevated or demarcated (unlike erysipelas); severe: lymphadenopathy, tachycardia, septicemia Slides 105, 107
Diagnosis: Usually clinical; serious infection: blood cultures, punch biopsy, complete blood count (leukocytosis), elevated creatine phosphokinase; plain films, computed tomography or magnetic resonance imaging for fasciitis or osteomyelitis; differential: necrotizing fasciitis (no response in 48 hours), deep vein thrombosis, contact dermatitis Slides 108–109
Treatment/Therapy: Oral vs intravenous by presentation · non-purulent: dicloxacillin or cephalexin; clindamycin if penicillin allergic · purulent (consider MRSA (methicillin-resistant S. aureus)): Bactrim, doxycycline, clindamycin, linezolid · necrotic tissue: surgical debridement · fever over 48 hours: change antibiotic per culture Slides 110–112
Mortality ★: Not covered in the lecture

Abscess★ Professor emphasized4 not covered

Name of Condition: Abscess Slide 113
Definition: Collection of purulent material within the dermis and deeper skin tissues Slide 113
Etiology (cause): Often polymicrobial; ★ S. aureus most common; usually traumatic inoculation of bacteria (unlike furuncles, which arise from hair follicles) Slide 113
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Pus collects in a central necrotic area walled by granulation tissue Slides 113–114
Clinical Manifestation: Early erythematous tender nodule; later pus collects centrally, may drain spontaneously; pain, erythema, warmth, edema; axilla, vulva, perianal, head, neck, buttocks, extremities, perineum Slides 113–114
Diagnosis: Not covered in the lecture
Treatment/Therapy: Goal: eradicate and prevent recurrence · drains spontaneously: warm soaks + broad-spectrum antibiotics considering MRSA (methicillin-resistant Staphylococcus aureus), adjusted to culture · does not drain: surgical incision and drainage Slide 115
Mortality ★: Not covered in the lecture

Acute paronychia2 not covered

Name of Condition: Acute paronychia Slide 116
Definition: Infection of the perionychium (soft tissue around the nail); starts as cellulitis and progresses to abscess Slide 116
Etiology (cause): Staphylococcus aureus, Streptococcus pyogenes Slide 116
Epidemiology (who): Not covered in the lecture
Risk Factors: Manicure, ingrown nail, hangnail, nail biting Slide 116
Pathology: Cellulitis of the nail fold progressing to abscess Slide 116
Clinical Manifestation: 2-5 days after trauma; rapid erythema and edema; advanced: pus collects under the nail folds Slide 117
Diagnosis: Usually clinical; Gram stain and culture if needed; KOH (potassium hydroxide) to rule out Candida; Tzanck smear to rule out herpetic whitlow; differential: onychomycosis, felon, herpetic whitlow, pseudomonal nail infection, psoriasis, nail squamous cell cancer Slides 118, 121
Treatment/Therapy: Mild: warm soaks 20 minutes 3 times a day · severe: incision and drainage, culture to rule out MRSA (methicillin-resistant S. aureus), oral amoxicillin-clavulanate or cephalexin; clindamycin if nail biting (oral flora) Slide 119
Mortality ★: Not covered in the lecture

Chronic paronychia1 not covered

Name of Condition: Chronic paronychia Slides 120, 122
Definition: Inflammatory reaction of the proximal nail fold to irritants and allergens; may be eczematous; present at least 6 weeks Slides 120, 122
Etiology (cause): Candida albicans most common Slide 120
Epidemiology (who): Laundry workers, cleaners, cooks, bartenders, dishwashers, swimmers Slide 120
Risk Factors: Diabetes; continuous hand immersion in water or chemical contact Slides 120, 123
Pathology: Cuticles and nail folds separate from the nail plate, creating a space for microorganisms Slide 122
Clinical Manifestation: Edematous, erythematous, tender nail folds without fluctuance; nail plates later thickened and discolored Slide 122
Diagnosis: Clinical, with history of water immersion or chemical contact; differential: psoriasis, onychomycosis, felon, herpetic whitlow, pseudomonal nail infection, squamous cell cancer Slides 121, 123
Treatment/Therapy: Treat inflammation and infection; keep hands dry · topical miconazole; oral fluconazole if severe Slide 123
Mortality ★: Not covered in the lecture

Necrotizing fasciitis

Name of Condition: Necrotizing fasciitis Slide 124
Definition: Bacterial infection of tissue under the skin surrounding muscles, nerves, fat, and vessels, leading to necrosis Slide 124
Etiology (cause): Polymicrobial (aerobic, anaerobic, mixed); group A Streptococcus (S. pyogenes) common; Clostridium perfringens produces gas Slides 124, 129
Epidemiology (who): Male more than female Slide 125
Risk Factors: Trauma, burns, surgery, immunosuppression, renal failure, alcoholism, periodontal infection, intravenous drug abuse Slide 125
Pathology: Tissue necrosis; destruction of superficial nerves makes area non-tender; gas in fascial planes with Clostridium (not group A strep) Slides 124, 127, 129
Clinical Manifestation: Hard to recognize early, progresses rapidly; may be sent home as cellulitis; pain out of proportion to exam; red-purple → blue-gray skin, bullae, gangrene, loss of tenderness (superficial nerves destroyed); compartment syndrome; fever 38.9-40.5 °C, tachycardia, toxicity, hypotension Slides 126–127
Diagnosis: Surgical emergency: tests must not delay surgery; complete blood count with differential, chemistry, arterial blood gas, urinalysis, blood/tissue cultures; ultrasound (air bubbles); computed tomography or magnetic resonance imaging (site, depth, gas) Slides 128–130
Treatment/Therapy: Aggressive surgical debridement; team approach, surgical intensive care unit admission; broad antibiotics covering gram-positive, gram-negative, and anaerobes Slide 131
Mortality ★: High mortality; septic shock, organ failure, and death Slides 126–128

Lecture 5 · Dermatological Infestations

Chand Shah, MPAS, PA-C · 17 conditions · source: CMS I Dermatological Infestations - Shahsv.pptx

Scabies★ Professor emphasized1 not covered

Name of Condition: Scabies Slides 5, 9
Definition: Infestation of the skin by the scabies mite, which tunnels through the stratum corneum Slides 5, 9
Etiology (cause): Sarcoptes scabiei var hominis (mite); spread by close physical contact for 15-20 minutes, or via bedding or underclothing of an infested person Slide 5
Epidemiology (who): Facility-associated scabies is common in long-term care facilities (elderly, immunosuppressed residents); hospital epidemics follow their admission and are hard to eradicate once healthcare workers are infected Slide 5
Risk Factors: Close physical contact with an infested person; shared bedding or underclothing; long-term care facility residence (elderly, immunosuppressed patients) Slide 5
Pathology: Burrow = tunnel made by the mite moving through the stratum corneum; pruritus starts 4-6 weeks after first infestation (up to 3 months), within 2-3 days on reinfestation; carriers stay asymptomatic Slides 6, 9
Clinical Manifestation: Severe nocturnal pruritus (almost always); excoriations and eczematous dermatitis of finger webs, volar wrists, lateral palms, elbows, axillae, genitals, areolae; head and neck spared in healthy adults (not infants, elderly, immunocompromised); crusted nodules in infants; pathognomonic burrow (thin linear or J-shaped, 1-10 mm) Slides 6–7, 9
Diagnosis: Microscopic identification of mite, ova or feces: skin scraping of a ★ non-excoriated burrow or papule (#15 blade, mineral oil); dermoscopy: ★ delta-wing jet (triangular mite head and front legs with body, eggs, burrow); burrow ink test (★ blue-black ink; zigzag line = burrow); confirmed by response to treatment Slides 13–15
Treatment/Therapy: Topical permethrin overnight to the entire skin surface, repeated 1 week later; wash bedding and clothing at 60 °C or bag for 14 days; ★ treat all infected persons in the family or group; pruritus: triamcinolone, hydroxyzine, diphenhydramine; pregnancy: treat only documented scabies Slides 18–20
Mortality ★: Not covered in the lecture

Crusted scabies4 not covered

Name of Condition: Crusted scabies (also: hyperkeratotic scabies) Slides 7, 12
Definition: Severe form of scabies with thick flaking scale caused by a massive mite infestation Slides 7, 12
Etiology (cause): Massive infestation with Sarcoptes scabiei; lesions contain millions of mites Slides 7, 12
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Enormous mite burden makes patients highly infectious; higher risk of Staphylococcus aureus superinfection, which can progress to sepsis if untreated Slide 12
Clinical Manifestation: Thick flaking scale; poorly defined patches; thickened or discolored nails; pruritus usually absent (patients may not itch) Slides 7, 12
Diagnosis: Not covered in the lecture
Treatment/Therapy: Oral ivermectin every 2 weeks for 2-3 doses plus topical permethrin every 3 days to once weekly when single therapy fails (also used in immunosuppressed patients); or permethrin 5% daily for 7 days then twice weekly until cured Slides 19–20
Mortality ★: Not covered in the lecture

Pediculosis capitis1 not covered

Name of Condition: Pediculosis capitis (also: head lice) Slide 23
Definition: Parasitic infestation of the scalp by the head louse Slide 23
Etiology (cause): Pediculus humanus capitis: blood-sucking, wingless, host-specific insect about 2 mm long with 6 claw-like legs Slide 23
Epidemiology (who): Common in children aged 3-12 years Slide 24
Risk Factors: Direct head-to-head contact (primary); less often shared combs, brushes, blow dryers, hair accessories, upholstery, pillows, bedding, helmets, headgear Slide 24
Pathology: Incubation of 4-6 weeks before symptoms; some infested patients remain asymptomatic carriers Slide 25
Clinical Manifestation: Pruritus, low-grade fever, regional lymphadenopathy, irritability; 2 mm erythematous macules or papules with excoriations, erythema, scaling Slide 25
Diagnosis: Seeing nits or live lice · live lice = active infestation, best found by wet combing (water and conditioner) with a nit comb · nits (past or present infestation) cannot be removed from the hair shaft, unlike dandruff; viable eggs tan to brown, hatched eggs clear to white Slide 28
Treatment/Therapy: Multimodal approach (resistance is rising): topical pediculicides (pyrethrins, permethrin 1%, malathion, benzyl alcohol, spinosad, ivermectin) or oral ivermectin; shaving or combing needs adjuvant therapy; wash combs, vacuum; no fumigation; no-nit school policy not recommended Slides 29–30
Mortality ★: Not covered in the lecture

Pediculosis corporis2 not covered

Name of Condition: Pediculosis corporis (also: body lice) Slide 23
Definition: Parasitic infestation of the skin of the trunk by the body louse Slide 23
Etiology (cause): Pediculus humanus humanus (body louse), about 30% larger than the head louse; spread via contaminated clothing and bedding Slides 23–24
Epidemiology (who): Homeless individuals, refugees, victims of war and natural disasters, people in crowded living conditions with poor hygiene Slide 24
Risk Factors: Inability to wash or change clothes (lets the infestation persist); crowded living conditions; poor hygiene Slide 24
Pathology: Not covered in the lecture
Clinical Manifestation: Pruritus; linear excoriations mainly on the back, neck, shoulders and waist; postinflammatory pigmentation in chronic cases Slide 26
Diagnosis: Close examination of the seams of clothing for nits; shaking clothing over white paper (lice move on the paper) Slide 28
Treatment/Therapy: Multimodal approach (resistance is rising): topical pediculicides (pyrethrins, permethrin, malathion, spinosad, ivermectin); effect read 24 hours after application; then clean clothing, and dry (unwashed) or bag for 2 weeks all clothing, bedding and towels from the prior week Slides 29–30
Mortality ★: Not covered in the lecture

Pediculosis pubis1 not covered

Name of Condition: Pediculosis pubis (also: crabs) Slide 23
Definition: Parasitic infestation of the pubic area by the pubic (crab) louse Slide 23
Etiology (cause): Phthirus pubis: 0.8-1.2 mm with a wide, short, crab-like body; spread sexually, also via contaminated clothing, towels, bedding Slides 23–24
Epidemiology (who): Found in all levels of society and ethnic groups; patients often have a concurrent sexually transmitted disease Slide 24
Risk Factors: Sexual contact; shared clothing, towels or bedding Slide 24
Pathology: Maculae caerulae represent hemorrhage; papular urticaria forms at feeding sites Slide 26
Clinical Manifestation: Often asymptomatic or mild-moderate pruritus for months; maculae caerulae (slate-gray to bluish irregular macules about 1 cm); papular urticaria, often periumbilical; eyelash infestation (pediculosis or phthiriasis palpebrarum) Slide 26
Diagnosis: Nits at the base of hairs; confirmed by microscopic examination of a plucked hair Slide 28
Treatment/Therapy: Multimodal approach (resistance is rising): topical pediculicides (pyrethrins, permethrin, malathion, spinosad, ivermectin); effect read 24 hours after application; then clean clothing, and dry (unwashed) or bag for 2 weeks all clothing, bedding and towels from the prior week Slides 29–30
Mortality ★: Not covered in the lecture

Bedbug bites2 not covered

Name of Condition: Bedbug bites Slide 32
Definition: Bites from bedbugs, nocturnal blood-feeding insects that hide by day in cracks and crevices Slide 32
Etiology (cause): Cimex lectularius (common bedbug) and Cimex pilosellus (batbug) Slide 32
Epidemiology (who): Not covered in the lecture
Risk Factors: Clothing and baggage of travelers and visitors; secondhand mattresses; laundry Slide 32
Pathology: Hide in headboards, picture frames, behind loose wallpaper; feed at night, drawn by warmth and carbon dioxide; need a blood meal every 5-10 days but survive up to 1 year; can shed pathogens (hepatitis B) but no convincing evidence they act as vectors Slide 32
Clinical Manifestation: Painless, multiple bites grouped in a line; a row of 3 = breakfast, lunch, and dinner; wheals and papules with a hemorrhagic punctum; bullous in sensitized patients; blood flecks on bed linens Slide 33
Diagnosis: Physical examination Slide 34
Treatment/Therapy: Symptomatic treatment and local wound care; secondary infection: topical antiseptic lotion or antibiotic cream; pruritus: topical corticosteroids or oral antihistamines; professional exterminator needed to eradicate Slide 35
Mortality ★: Not covered in the lecture

Tungiasis and flea bites1 not covered

Name of Condition: Tungiasis and flea bites (also: fleas) Slides 37–38
Definition: Tungiasis: infestation by penetration of the adult female flea (family Tungidae) into human skin to lay eggs; Pulicidae fleas cause papular bite reactions Slides 37–38
Etiology (cause): Wingless blood-sucking fleas that jump up to 18 cm; Tungidae cause tungiasis; rat fleas (Xenopsylla cheopis, Xenopsylla brasiliensis) transmit bubonic plague; cat flea (Ctenocephalides felis) carries bubonic plague and endemic typhus Slide 37
Epidemiology (who): Tungiasis endemic in the West Indies, Central America, Africa, India, Pakistan, South America Slide 37
Risk Factors: Travel to or residence in endemic areas; walking barefoot or in sandals on beaches, sitting in sand (Nigeria, the Caribbean, India, Brazil) Slides 37, 40
Pathology: Flea bite reactions scale with sensitization: urticarial papules (non-sensitized), papular urticaria (sensitized), bullae (hypersensitive) Slide 38
Clinical Manifestation: Tungiasis: papules enlarging over weeks to 4-10 mm, firm yellow translucent nodule, may be painful; plantar feet, subungual/periungual skin, web spaces, legs; pain, pruritus, autoamputation of toes · flea bites: linear or clustered urticarial papules, usually lower legs Slide 38
Diagnosis: Dermoscopy showing ovoid eggs (tungiasis) Slide 40
Treatment/Therapy: Surgical excision, or cryotherapy/topical agents; tetanus prophylaxis; systemic antibiotics; prevention: avoid going barefoot or in sandals on beaches in endemic areas Slide 40
Mortality ★: Not covered in the lecture

Hymenoptera stings3 not covered

Name of Condition: Hymenoptera stings (also: bees, wasps, fire ants) Slide 42
Definition: Stings from bees, wasps and ants, insects with poison glands for defense or hunting Slide 42
Etiology (cause): Stings inflicted by female insects through a modified ovipositor (egg-laying apparatus) when the nest or insect is threatened; fire ants attack in groups Slide 42
Epidemiology (who): Generalized systemic reactions in 0.4-3% Slide 43
Risk Factors: Not covered in the lecture
Pathology: Honeybee barbed stinger stays impaled and keeps pumping venom; fire ant venom triggers mast cell degranulation (flushing, pruritus, hives, abdominal pain, nausea, vomiting, diarrhea) Slide 42
Clinical Manifestation: Typical: immediate burning pain, then intense local erythema, swelling, urticaria · severe local: extensive edema and induration up to 1 week · systemic: anaphylaxis (generalized urticaria, angioedema, bronchospasm) Slide 43
Diagnosis: Not covered in the lecture
Treatment/Therapy: Remove stinger fast by scraping with a credit card edge or dull knife parallel to the skin; mild: cleaning, ice, local anesthetic injection; anaphylaxis: subcutaneous or intramuscular epinephrine, emergency room; hypersensitive patients carry an EpiPen; desensitization, immunotherapy for fire ants Slides 42, 44
Mortality ★: Not covered in the lecture

Caterpillar dermatitis4 not covered

Name of Condition: Caterpillar dermatitis (also: lepidopterism; erucism) Slides 46–47
Definition: Lepidopterism: the aggregate medical effects of caterpillars, moths and butterflies; erucism (caterpillar dermatitis) is the gypsy moth caterpillar form Slides 46–47
Etiology (cause): About 100-150 species; gypsy moth, processionary and asp (puss) caterpillars Slides 46–47
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Mechanical irritation by pointed hairs; toxin injection through hollow hairs; cell-mediated hypersensitivity to hairs Slide 46
Clinical Manifestation: Varies by species: gypsy moth: pruritic erythematous papules in linear streaks · processionary: urticaria, angioedema, anaphylaxis · asp or puss caterpillar (most poisonous): intense painful sting, train-track purpura Slide 47
Diagnosis: Not covered in the lecture
Treatment/Therapy: Remove hairs by stripping with adhesive tape; symptomatic: systemic antihistamines, topical menthol or camphor, moderate-high potency topical corticosteroids, systemic corticosteroids, oral or parenteral narcotic analgesics; antivenom for certain categories Slide 48
Mortality ★: Not covered in the lecture

Cutaneous larva migrans★ Professor emphasized1 not covered

Name of Condition: Cutaneous larva migrans Slide 50
Definition: Syndrome in which larvae of animal nematodes infect humans, who are a dead-end host Slide 50
Etiology (cause): Animal hookworm larvae, mostly from dogs and cats; infection requires contact with sand or soil contaminated with animal feces Slide 50
Epidemiology (who): Tropical and subtropical areas: southeastern United States, Caribbean, Africa, Central and South America, India, Southeast Asia Slide 50
Risk Factors: Skin contact with sand or soil contaminated with animal feces Slide 50
Pathology: Larvae trapped in the follicular canal, stratum corneum or dermis with an inflammatory eosinophilic infiltrate Slide 53
Clinical Manifestation: Classic: erythematous, raised, vesicular, linear or serpentine track advancing 2-3 cm/day; intense pruritus and pain; lasts 2-8 weeks; often feet and buttocks; systemic signs rare · hookworm folliculitis: follicular papules and pustules, usually the buttock Slides 51–52
Diagnosis: ★ Clinical diagnosis when the serpiginous rash is present; light microscopy with mineral oil shows live and dead larvae (in folliculitis) Slide 53
Treatment/Therapy: ★ Albendazole 400 mg by mouth daily for 3 days, or ivermectin for 1-2 days; hookworm folliculitis may need repeated treatment; topical therapy less effective; excision or cryotherapy not recommended Slide 54
Mortality ★: Not covered in the lecture

Black widow spider bite1 not covered

Name of Condition: Black widow spider bite Slide 56
Definition: Envenomation by the black widow spider, marked by a red hourglass on the underside of the abdomen Slide 56
Etiology (cause): Latrodectus mactans (southern black widow); bites follow accidental or deliberate provocation Slide 56
Epidemiology (who): Found in all but the most northern part of the country; webs in corners of doors and windows, woodpiles, garages, sheds, outdoor toilet seats Slide 56
Risk Factors: Higher risk of complications in the very old, very young, or those with cardiovascular disease Slide 58
Pathology: Venom contains the neurotoxin alpha-latrotoxin Slide 56
Clinical Manifestation: Painful bite, mild skin findings; within 30 minutes local erythema, piloerection, sweating; agonizing crampy abdominal pain and muscle spasms; headache, paresthesia, nausea, vomiting, hypertension, lacrimation, salivation, seizures, tremors, acute renal failure, paralysis Slide 57
Diagnosis: Not covered in the lecture
Treatment/Therapy: Local wound care or hospitalization depending on symptoms; envenomation: calcium gluconate 10%, narcotic analgesics, muscle relaxants, benzodiazepines; ensure tetanus vaccine is up to date Slide 58
Mortality ★: Death is uncommon Slide 57

Brown recluse spider bite★ Professor emphasized3 not covered

Name of Condition: Brown recluse spider bite Slides 59–60
Definition: Bite of the brown recluse spider, ranging from mild local reactions to severe ulcerative necrosis Slides 59–60
Etiology (cause): Loxosceles reclusa: non-aggressive spider with a dark brown fiddle/violin marking on the cephalothorax; bites when threatened or provoked Slide 59
Epidemiology (who): Abundant in the American Midwest and Southeast; shelters in undisturbed places (closets, attics, stored bedding and clothing) Slide 59
Risk Factors: Not covered in the lecture
Pathology: In a small percentage, the wound progresses to necrosis (days 2-3), eschar (days 5-7), then deep ulcers Slide 61
Clinical Manifestation: ★ Hallmark: red, white, and blue sign (central violaceous area, rim of blanched skin, surrounding large asymmetric area); systemic symptoms 1-2 days after the bite: nausea, vomiting, headache, fever, chills Slides 60–61
Diagnosis: Not covered in the lecture
Treatment/Therapy: Pain control, warm compresses, avoid strenuous exercise; antibiotics for secondary bacterial infection; slow-healing necrotic wounds may need surgical reconstruction, delayed until the wound is stable Slide 62
Mortality ★: Not covered in the lecture

Hobo spider bite★ Professor emphasized3 not covered

Name of Condition: Hobo spider bite (also: aggressive house spider) Slide 63
Definition: Bite of the hobo spider, the predominant cause of necrotic arachnidism in the Pacific Northwest Slide 63
Etiology (cause): Tegenaria agrestis, the ★ aggressive house spider: brown with a gray herringbone pattern on the abdomen; often mistaken for the brown recluse Slide 63
Epidemiology (who): Pacific Northwest of the United States; bites July to September (mating season); webs in basements, wood piles, bushes Slide 63
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Painless bite; induration and paresthesia within 30 minutes; large erythematous area; vesicles in the first 36 hours; sometimes eschar; systemic: headache, fatigue, nausea, vomiting, diarrhea, paresthesia, memory impairment Slide 64
Diagnosis: Not covered in the lecture
Treatment/Therapy: Supportive measures; wounds heal within several weeks; headaches may last up to 1 week Slide 65
Mortality ★: Rarely fatal from severe systemic effects, including aplastic anemia Slide 64

Tarantula hair reaction4 not covered

Name of Condition: Tarantula hair reaction Slide 66
Definition: Skin and eye reactions to tarantula hairs that land and embed when the tarantula is threatened Slide 66
Etiology (cause): Tarantulas (family Theraphosidae) Slide 66
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Embedded hairs provoke responses from mild local pruritus to granulomatous reactions Slide 66
Clinical Manifestation: Generally mild and local: pruritus to granulomatous skin reactions; eye: conjunctivitis, corneal granuloma Slide 66
Diagnosis: Not covered in the lecture
Treatment/Therapy: Topical corticosteroids for skin reactions; ophthalmology consult for ocular involvement Slide 66
Mortality ★: Not covered in the lecture

Lyme disease1 not covered

Name of Condition: Lyme disease Slides 68, 71
Definition: Tick-borne illness caused by a spirochete, progressing through early localized, early disseminated and late persistent stages Slides 68, 71
Etiology (cause): Borrelia burgdorferi (spirochete), carried by Ixodes ticks (I. scapularis, I. pacificus, I. ricinus, I. persulcatus) Slides 68–69
Epidemiology (who): Northern hemisphere (North America, Europe, Asia); in the United States: Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, Vermont, Wisconsin Slide 68
Risk Factors: Living in or travel to an endemic region Slide 77
Pathology: Ticks feed on animals that maintain the organism, then pass it on by transstadial transmission (from one tick life stage to the next); birds and deer disperse it Slide 68
Clinical Manifestation: Stage 1 (about 1 week): erythema migrans (bull's-eye: over 5 cm, expanding, central clearing, darker punctate center), fever, myalgia, arthralgia · Stage 2 (days-weeks): cranial nerve palsies, meningitis, radiculopathy, arthritis · Stage 3 (months-years): mono/oligoarthritis of knee, encephalopathy, acrodermatitis chronica atrophicans Slides 72, 74–76
Diagnosis: Erythema migrans: diagnose and treat clinically · other presentations: two-tier serology, ELISA (enzyme-linked immunosorbent assay) for IgM (immunoglobulin M) and IgG (immunoglobulin G), the IgG C6 peptide test being more specific, then confirm with Western blot; testing most useful outside endemic regions Slide 77
Treatment/Therapy: Remove tick immediately; antibiotics in all stages: doxycycline first line, amoxicillin for early erythema migrans, azithromycin second line, 10-14 days · intravenous ceftriaxone, cefotaxime or penicillin G if oral not tolerated, early disseminated or late neurologic disease, recurrent arthritis · repellents; no human vaccine Slides 79–80
Mortality ★: Not covered in the lecture

Rocky Mountain spotted fever

Name of Condition: Rocky Mountain spotted fever Slides 81–82
Definition: Tick-borne rickettsial illness with a classic triad of fever, headache and rash Slides 81–82
Etiology (cause): Rickettsia rickettsii; vectors: dog tick, wood tick, rodents; incubation 3-12 days Slide 81
Epidemiology (who): Southeastern and South Central states, in spring and early summer Slide 81
Risk Factors: Male sex; adults 40-64 years; children under 10 years; rural dwelling Slide 81
Pathology: Delayed or inadequate treatment leads to severe cardiac, gastrointestinal, hepatic, neurologic, ophthalmologic, renal and pulmonary manifestations; long-term sequelae in severe-disease survivors Slide 81
Clinical Manifestation: Triad (only about 60%): fever over 39.5 °C, headache, rash; rash 2-4 days after fever, starts at wrists and ankles, spreads centripetally, involves palms and soles, spares face; blanching macules becoming petechiae and purpura; about 20% have no rash; abdominal pain mimics appendicitis in children Slides 82–83, 85
Diagnosis: Labs: thrombocytopenia, anemia, mild hyponatremia, mild transaminase elevation, normal white count with increased bands · IFA (indirect immunofluorescence assay) is the gold standard but rarely positive before day 7, so start treatment while awaiting results Slide 85
Treatment/Therapy: Doxycycline by mouth every 12 hours for 5-10 days in adults, pregnancy and children (weight-based); allergy: doxycycline desensitization; start by day 5; no prophylactic antibiotics; prevention: avoid ticks, protective clothing, tick checks, DEET (diethyltoluamide) Slides 85–86
Mortality ★: Life-threatening if not treated Slide 81

Cercarial dermatitis2 not covered

Name of Condition: Cercarial dermatitis (also: schistosome dermatitis; swimmer's itch; clam digger's itch) Slide 88
Definition: Acute pruritic eruption from skin penetration by cercariae (free-swimming larval stage) of certain parasitic flatworms Slide 88
Etiology (cause): Fluke cercariae: host animal (waterfowl, marsh birds, finches, muskrats, mice, deer) passes eggs into water, which infect a snail within 12 hours; cercariae released after 5 weeks and carried to shore by wind and currents Slides 88–89
Epidemiology (who): Great Lakes region; paddy workers and rice farmers of the Far East Slide 89
Risk Factors: Exposure to cercaria-infested water; paddy and rice farming Slides 89–90
Pathology: Cercariae penetrate the epidermis and dermis, then blood vessels, intrahepatic veins and intestinal walls Slide 89
Clinical Manifestation: Urticaria-like lesions and prickling about 30 minutes after exposure; severe pruritus 10-12 hours later; erythematous papules within 24 hours becoming vesicles then pustules; pain and swelling peak at 48-72 hours; sometimes headache, fever, lymphangitis Slide 90
Diagnosis: Not covered in the lecture
Treatment/Therapy: Symptomatic: antihistamines, oatmeal baths, antipruritic lotions, aspirin for pain, washing and hygiene, topical or oral glucocorticoids Slide 91
Mortality ★: Not covered in the lecture

Lecture 6 · Cutaneous Viral and Fungal Infections

Monique Jaquith, DMSc, PA-C · 22 conditions · source: 6. Fungal and Viral Skin Infections - Jaquith.pptx

Tinea capitis★ Professor emphasized1 not covered

Name of Condition: Tinea capitis (also: ringworm of the scalp; black dot tinea capitis) Slides 7, 9, 15
Definition: Dermatophyte (tinea) infection of the scalp and hair shaft. Slides 7, 9, 15
Etiology (cause): Trichophyton and Microsporum; Trichophyton tonsurans most common in the United States. Spread by infected people, pets, fallen hairs, clothing, combs, hats, furniture; asymptomatic carriers. Slides 9–10
Epidemiology (who): Predominantly preadolescent children; most common fungal infection in children. Slide 9
Risk Factors: Contact with infected persons, pets or shared fomites (combs, brushes, hats, towels); fungal particles stay viable for months. Slides 10, 16
Pathology: Dermatophytes survive only on dead keratin (stratum corneum, hair, nails); after puberty, changed fatty acid content of sebum is believed to inhibit growth. Slides 6, 9
Clinical Manifestation: Pruritus; alopecia common (not in all cases); red papules progressing to grayish ring-formed scaly patches with perifollicular papules; black dot form (hairs broken at the scalp surface); lymphadenopathy often; kerion may develop (may have purulent drainage). Slides 11–12, 14, 17
Diagnosis: KOH (potassium hydroxide) microscopy and fungal culture when feasible, especially before prolonged systemic therapy; Wood lamp may support Microsporum (Trichophyton tonsurans usually does not fluoresce); bacterial culture if a kerion drains pus. Differential: folliculitis, psoriasis, seborrheic dermatitis, alopecia areata. Slides 13–14
Treatment/Therapy: Oral therapy required (topicals do not penetrate the hair shaft): terbinafine for Trichophyton, griseofulvin for Microsporum; ★ obtain baseline liver tests when indicated. Adjunct selenium sulfide or ketoconazole shampoo; no sharing hair items; complete course; treat inflammation promptly to limit scarring alopecia. Slides 15–17
Mortality ★: Not covered in the lecture

Tinea barbae★ Professor emphasized3 not covered

Name of Condition: Tinea barbae (also: ringworm of the beard) Slides 7, 18
Definition: Dermatophyte infection of the beard area. Slides 7, 18
Etiology (cause): Trichophyton species common; inflammatory form usually acquired from animals (zoophilic), noninflammatory form usually from another person (anthropophilic). Slide 19
Epidemiology (who): Rare. Slide 19
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Asymptomatic or mild pruritus. Inflammatory: tender, boggy, pustular, kerion-like plaques, loose easily removed hairs, possible scarring alopecia. Noninflammatory: annular scaly plaques or folliculitis-like eruption; hairs break near the surface. Slide 19
Diagnosis: KOH (potassium hydroxide) microscopy, culture; biopsy for refractory cases. Differential: bacterial folliculitis (hair easily removed in tinea barbae, not in bacterial folliculitis; bacterial culture to rule out), acne, rosacea, seborrheic dermatitis. Slide 21
Treatment/Therapy: Oral antifungal required (topicals do not penetrate the follicle): griseofulvin or terbinafine; ★ baseline liver tests before oral antifungals. Shave or remove hair; warm compresses to remove crusts. Slide 22
Mortality ★: Not covered in the lecture

Tinea corporis2 not covered

Name of Condition: Tinea corporis (also: ringworm of the body) Slides 7, 23
Definition: Dermatophyte infection of the body skin. Slides 7, 23
Etiology (cause): Trichophyton rubrum common pathogen; contact with infected humans or animals. Slide 24
Epidemiology (who): Not covered in the lecture
Risk Factors: Contact with infected humans or animals (ask about cats, dogs, kids); topical steroid or steroid-combination use can mask and worsen it. Slides 24, 27–28
Pathology: Dermatophyte living on dead keratin of the stratum corneum; progressive central clearing produces the annular outline. Slides 6, 24
Clinical Manifestation: Asymptomatic or pruritic; one or more circular, sharply circumscribed, slightly erythematous, dry scaly patches/plaques with central clearing (annular "ringworm"); sharper outer ring than nummular eczema. Slides 24, 27
Diagnosis: KOH (potassium hydroxide) microscopy from the active border; culture if high suspicion with negative KOH or refractory; species and susceptibility testing if resistance suspected. Differential: psoriasis, nummular eczema (KOH negative), discoid lupus, fixed drug eruption. Slides 26–27, 29
Treatment/Therapy: Localized: topical terbinafine, butenafine or an azole to the lesion and 1-2 cm beyond; avoid steroid-antifungal combinations. Oral (terbinafine; itraconazole or fluconazole) for extensive, follicular, immunocompromised, refractory or recurrent disease. Slides 28–29
Mortality ★: Not covered in the lecture

Tinea cruris2 not covered

Name of Condition: Tinea cruris (also: jock itch) Slides 7, 31
Definition: Dermatophyte infection of the inguinal creases (crural fold). Slides 7, 31
Etiology (cause): Most often Trichophyton rubrum and Epidermophyton floccosum. Slide 31
Epidemiology (who): More common in men; often coexists with tinea pedis. Slide 31
Risk Factors: Warm, moist environment; obesity; diabetes; tight-fitting clothes for long periods; sharing clothes. Slide 31
Pathology: Not covered in the lecture
Clinical Manifestation: Pruritic, sharply demarcated plaque on the proximal medial thigh; scrotum typically spared. Slide 33
Diagnosis: KOH (potassium hydroxide) microscopy from the active border in uncertain cases. Differential: candidal intertrigo (involves scrotum, satellite papules/pustules), erythrasma (may fluoresce coral-red). Slide 33
Treatment/Therapy: Topical allylamine (terbinafine) or azole (ketoconazole); oral only for extensive/refractory disease. Treat coexisting tinea pedis, keep folds dry, avoid steroid combination products. Slide 33
Mortality ★: Not covered in the lecture

Tinea pedis2 not covered

Name of Condition: Tinea pedis (also: athlete's foot; interdigital, hyperkeratotic (shoe distribution) and vesiculobullous forms) Slides 7, 35, 37
Definition: Dermatophyte infection of the feet; three variants: interdigital, hyperkeratotic, vesiculobullous (inflammatory). Slides 7, 35, 37
Etiology (cause): Trichophyton rubrum, Trichophyton interdigitale or Epidermophyton floccosum; spread by contact with infected desquamated skin. Slides 35, 39
Epidemiology (who): Most common dermatophyte infection in adults; men more than women. Slide 35
Risk Factors: Warm, moist environment: shoes, locker room floors, sweating; immunocompromise. Slide 35
Pathology: Not covered in the lecture
Clinical Manifestation: Scaling, pruritus, burning or stinging; hands may be infected too. Interdigital (most common): maceration, erosions, scale and fissures between toes, especially 3rd-4th web space. Hyperkeratotic: plantar scale to diffuse thickening in a shoe distribution. Vesiculobullous: painful vesicles/bullae on erythema. Slides 37, 39–41
Diagnosis: Clinical; KOH (potassium hydroxide) microscopy from advancing scale if uncertain; culture for atypical, recurrent, severe or refractory disease; bacterial studies if marked maceration, malodor, drainage or cellulitis. Differential: candidiasis/mixed toe web infection, contact dermatitis, psoriasis. Slides 42–43
Treatment/Therapy: Topical terbinafine/butenafine or an azole; keratolytic (salicylic acid, lactic acid, urea) plus antifungal for hyperkeratotic; oral for extensive, recurrent, refractory or immunocompromised. Treat coexisting onychomycosis; dry between toes, sandals in showers, change socks, antifungal powder. Slides 44–45
Mortality ★: Not covered in the lecture

Onychomycosis★ Professor emphasized3 not covered

Name of Condition: Onychomycosis (also: tinea unguium) Slides 47, 49
Definition: Fungal infection of the nail; forms: distal lateral subungual, superficial white, proximal subungual, endonyx, total dystrophic. Slides 47, 49
Etiology (cause): Dermatophytes, especially Trichophyton rubrum, cause most cases; yeasts and molds also occur. Slide 47
Epidemiology (who): Not covered in the lecture
Risk Factors: Tinea pedis, age, diabetes, trauma, occlusive footwear, psoriasis, vascular disease. Slide 47
Pathology: Not covered in the lecture
Clinical Manifestation: Distal lateral disease: subungual debris, onycholysis, thickening, discoloration, crumbling. Slide 47
Diagnosis: Confirm fungus before oral therapy (many dystrophic nails are not fungal): KOH (potassium hydroxide) microscopy, PAS (periodic acid-Schiff) stain of clippings, fungal culture or PCR (polymerase chain reaction); sample the most proximal diseased nail bed/subungual debris. Slides 50–51
Treatment/Therapy: Oral terbinafine first-line: about 6 weeks fingernails, 12 weeks toenails; ★ baseline liver tests per labeling and risk. Itraconazole alternative (fluconazole off label). Limited disease: topical efinaconazole, tavaborole or ciclopirox (lower cure). Needs nail growth; treat tinea pedis. Slide 52
Mortality ★: Not covered in the lecture

Tinea manuum4 not covered

Name of Condition: Tinea manuum (also: two feet-one hand syndrome) Slides 7, 54
Definition: Dermatophyte infection of the hand. Slides 7, 54
Etiology (cause): Not covered in the lecture
Epidemiology (who): Associated with tinea pedis; palms and soles may be infected at the same time. Slide 54
Risk Factors: Coexisting tinea pedis; the hand used to scratch the feet is affected (two feet-one hand syndrome). Slide 54
Pathology: Not covered in the lecture
Clinical Manifestation: Often unnoticed (blamed on dry skin or labor). Dorsum: annular plaque like tinea corporis. Palm: thickened, dry, scaly (hyperkeratotic) like tinea pedis; high recurrence. Slides 54, 56
Diagnosis: Not covered in the lecture
Treatment/Therapy: Same as tinea pedis: topical terbinafine/butenafine or an azole; keratolytic plus antifungal for hyperkeratotic; oral for extensive, recurrent, refractory or immunocompromised; treat coexisting onychomycosis; moisture control. Slides 56–57
Mortality ★: Not covered in the lecture

Id reaction3 not covered

Name of Condition: Id reaction (also: dermatophytid or identity reaction) Slide 59
Definition: Inflammatory dermatitis at sites distant from a primary dermatophyte infection. Slide 59
Etiology (cause): Occurs with any dermatophyte infection; tinea pedis common. Slide 59
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Unknown; possibly delayed-type hypersensitivity. Slide 59
Clinical Manifestation: 1-2 weeks after primary infection; extremely pruritic papules or papulovesicles, common on fingers; toe webs may show an asymptomatic fissure or maceration (tinea pedis). Slide 60
Diagnosis: KOH (potassium hydroxide) positive at the primary site, negative at the id site. Three criteria: dermatophyte infection elsewhere; no fungal elements at the id site; resolution once the primary infection is treated. Slide 62
Treatment/Therapy: Treat the primary dermatophyte infection; the id reaction then resolves. Slide 62
Mortality ★: Not covered in the lecture

Tinea incognito3 not covered

Name of Condition: Tinea incognito Slide 64
Definition: Tinea with a clinically altered appearance due to inappropriate treatment, usually topical steroids. Slide 64
Etiology (cause): Topical steroids used for anything inflammatory; steroid-antifungal combinations (clotrimazole/betamethasone dipropionate) are a common cause; calcineurin inhibitors also. Slides 28, 64–65
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Steroids mask and worsen dermatophytosis; when stopped the lesion flares, prompting more steroid. Slides 28, 64
Clinical Manifestation: Altered-looking tinea that flares when steroids are stopped; inflammation may rebound after withdrawal. Slides 64–65
Diagnosis: KOH (potassium hydroxide) preparation and/or culture from an active edge. Slide 65
Treatment/Therapy: Stop the corticosteroid or calcineurin inhibitor; topical antifungal for localized disease, systemic for extensive, follicular or refractory infection. Slide 65
Mortality ★: Not covered in the lecture

Cutaneous candidiasis (candidal intertrigo)★ Professor emphasized1 not covered

Name of Condition: Cutaneous candidiasis (candidal intertrigo) (also: intertrigo) Slides 67–68
Definition: Yeast infection of the skin; intertrigo is an inflammatory rash from friction, moisture and heat in body folds that Candida may secondarily infect. Slides 67–68
Etiology (cause): Yeast; Candida albicans most common; opportunistic organism. Slide 67
Epidemiology (who): Males equal females. Slide 67
Risk Factors: Obesity, diabetes, incontinence, occlusion, immobility, recent antibiotics, immunosuppression. Slide 68
Pathology: Yeasts are unicellular fungi that reproduce by budding and live on moist surfaces. Slides 4, 67
Clinical Manifestation: Pruritus, burning pain; well-demarcated erythematous patches of varying sizes with ★ satellite lesions (papules/pustules) (small red bumps just outside the main rash edge); inframammary, axillary, abdominal, inguinal, perineal, interdigital folds; commonly involves the scrotum. Slides 33, 68–69, 71
Diagnosis: Clinical; KOH (potassium hydroxide) preparation; culture. Malodor, erosions or drainage raise concern for bacterial coinfection. Slides 68, 71
Treatment/Therapy: Dry folds, reduce friction/occlusion, manage incontinence. Topical nystatin (Candida only) or azole (Candida and dermatophytes); brief low-potency steroid only with antifungal. Recurrent/extensive: evaluate for diabetes, immunosuppression, resistance, alternative diagnosis. Slide 72
Mortality ★: Not covered in the lecture

Pityriasis versicolor★ Professor emphasized2 not covered

Name of Condition: Pityriasis versicolor (also: tinea versicolor) Slide 74
Definition: Overgrowth of normal skin yeast causing hypopigmented, hyperpigmented or pink finely scaling macules/patches. Slide 74
Etiology (cause): Lipid-dependent Malassezia species that normally inhabit skin; not considered contagious. Slide 74
Epidemiology (who): Not covered in the lecture
Risk Factors: Heat, humidity, oily skin, sweating, immunosuppression, corticosteroid exposure; warm climates. Slide 74
Pathology: Hypopigmentation from altered melanocyte function and reduced tanning; hyperpigmentation/erythema from inflammation and stratum corneum change. Slide 77
Clinical Manifestation: Usually asymptomatic or mild pruritus; velvety tan, pink or white scaling macules 4-5 mm to confluent areas on trunk, neck, upper arms, groin; recurrence common. Slides 74, 78
Diagnosis: Clinical; scrape to reveal fine scale; KOH (potassium hydroxide): short hyphae and yeast clusters, "spaghetti and meatballs"; Wood lamp yellow-gold (limited). Differential: seborrheic dermatitis, pityriasis rosea, vitiligo. Slides 79–80
Treatment/Therapy: Topical first-line: ketoconazole, selenium sulfide, zinc pyrithione, ciclopirox or topical terbinafine. Oral fluconazole/itraconazole if extensive/refractory; oral terbinafine ineffective; ★ never oral ketoconazole (hepatic, adrenal toxicity). Pigment lags scale. Slides 81–82
Mortality ★: Not covered in the lecture

Varicella2 not covered

Name of Condition: Varicella (also: chickenpox) Slide 84
Definition: Primary varicella-zoster virus infection: a generalized pruritic eruption with lesions in multiple stages of healing. Slide 84
Etiology (cause): Primary infection with varicella-zoster virus; exposure to vesicular fluid (or airborne virus from disseminated zoster) in a susceptible person can cause varicella. Slides 84, 91
Epidemiology (who): Not covered in the lecture
Risk Factors: Susceptible people (no evidence of immunity); complication risk rises in adults, pregnancy, newborn age and immunocompromise. Slides 84, 89
Pathology: Contagious from 1–2 days before the rash until all lesions crust (breakthrough disease without crusts: until no new lesions for 24 hours); virus then stays latent in cranial-nerve or dorsal-root ganglia. Slides 89, 96
Clinical Manifestation: Pruritic eruption evolving macules → papules → vesicles → crusts, with several stages present simultaneously; concentrated on the trunk, scalp and face. Slide 84
Diagnosis: Usually clinical; lesion PCR (polymerase chain reaction) preferred when confirmation is needed; a reportable disease (Florida Department of Health). Slides 87–88
Treatment/Therapy: Supportive; avoid aspirin in children, caution with nonsteroidal anti-inflammatory drugs; early oral antivirals if higher risk; intravenous acyclovir if severe/disseminated; prompt consult for pregnancy, neonatal exposure, immunocompromise. Prevention: two-dose vaccine; airborne and contact precautions. Slides 87, 89
Mortality ★: Not covered in the lecture

Herpes zoster★ Professor emphasized2 not covered

Name of Condition: Herpes zoster (also: shingles) Slides 91, 96
Definition: Reactivation of latent varicella-zoster virus causing neuropathic pain and a usually unilateral dermatomal vesicular eruption. Slides 91, 96
Etiology (cause): Varicella-zoster virus latent in cranial-nerve or dorsal-root ganglia reactivates as virus-specific cellular immunity wanes. Slide 96
Epidemiology (who): Not covered in the lecture
Risk Factors: Increasing age; impaired cell-mediated immunity. Slide 91
Pathology: Reactivated virus travels along a sensory nerve to the skin; each spinal nerve supplies one side only. Contagious (about one third as much as varicella) to non-immune contacts, who get varicella, not shingles; infectious until lesions dry. Slides 91, 96, 98, 100
Clinical Manifestation: Prodrome of dermatomal pain/dysesthesia, lesions by 48–72 hours; then grouped herpetiform vesicles on an erythematous base in one or two adjacent dermatomes that ★ does not cross midline; thoracic 55%; crusts; heals in 10–15 days; zoster sine herpete (pain without rash). Slides 97–101
Diagnosis: Typical unilateral dermatomal vesicles: clinical; PCR (polymerase chain reaction) of vesicle fluid, scab or lesion-base cells for atypical, disseminated, vaccine-modified or immunocompromised cases. Differential: herpes simplex, contact dermatitis, impetigo, varicella. Slide 105
Treatment/Therapy: Oral valacyclovir, famciclovir or acyclovir ideally within 72 hours (later if new lesions or complicated); intravenous acyclovir if severe/sight-threatening; analgesics, cool compresses; ★ corticosteroids do not prevent postherpetic neuralgia; Shingrix 2 doses at ≥50 years (≥19 if immunosuppressed). Slides 106–107, 110
Mortality ★: Not covered in the lecture

Postherpetic neuralgia★ Professor emphasized1 not covered

Name of Condition: Postherpetic neuralgia Slide 102
Definition: Zoster pain persisting ≥ 90 days after rash onset. Slide 102
Etiology (cause): Injury of peripheral nerves by herpes zoster. Slide 108
Epidemiology (who): The most common complication of herpes zoster. Slide 108
Risk Factors: Older age, severe acute pain, severe rash, ophthalmic involvement, immunocompromise. Slide 102
Pathology: Neuropathic pain resulting from injury of peripheral nerves. Slide 108
Clinical Manifestation: Burning, aching, stabbing, shooting or electric shock–like pain, or allodynia (pain evoked by light touch); very debilitating; may last months to years, impairing sleep, mood and function. Slides 102, 108
Diagnosis: Pain persisting ≥ 90 days after zoster rash onset (the commonly used definition). Slide 102
Treatment/Therapy: First line: gabapentin/pregabalin, a tricyclic antidepressant, or topical lidocaine; capsaicin patch may help; individualize for kidney function, falls, interactions; avoid routine long-term opioids; refer severe pain. ★ Corticosteroids do not prevent postherpetic neuralgia. Slides 107, 109
Mortality ★: Not covered in the lecture

Herpes zoster ophthalmicus4 not covered

Name of Condition: Herpes zoster ophthalmicus Slide 103
Definition: Herpes zoster involving the ophthalmic division (V1) of cranial nerve V. Slide 103
Etiology (cause): Reactivation of latent varicella-zoster virus (herpes zoster) in the V1 distribution. Slides 96, 103
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Hutchinson sign (lesions on the tip/side of the nose) raises ocular risk, but its absence does not exclude eye involvement; eye pain, visual symptoms, red eye, photophobia, eyelid/ocular lesions; urgent, can cause blindness. Slide 103
Diagnosis: Clinical; evaluate urgently for ophthalmic disease. Slide 105
Treatment/Therapy: Start systemic antiviral therapy immediately; intravenous acyclovir with specialist care for sight-threatening disease; same-day ophthalmology evaluation for eye symptoms, Hutchinson sign or eyelid/ocular involvement. Slides 103, 106
Mortality ★: Not covered in the lecture

Ramsay Hunt syndrome★ Professor emphasized4 not covered

Name of Condition: Ramsay Hunt syndrome (also: herpes zoster oticus) Slide 104
Definition: Herpes zoster of the ear: peripheral facial palsy with painful vesicles of the ear canal/auricle or oropharynx. Slide 104
Etiology (cause): Reactivated varicella-zoster virus (herpes zoster oticus). Slides 96, 104
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Peripheral facial palsy; ★ painful vesicles of the ear canal, auricle or oropharynx; hearing loss, tinnitus or vertigo; can cause eye damage, permanent hearing changes and altered taste. Slide 104
Diagnosis: Clinical; evaluate urgently for otic and neurologic disease. Slide 105
Treatment/Therapy: Antiviral therapy plus a systemic corticosteroid, started early when not contraindicated; urgent ear, nose and throat or neurology evaluation; protect the cornea if eyelid closure is impaired. Slide 104
Mortality ★: Not covered in the lecture

Herpes simplex virus infection2 not covered

Name of Condition: Herpes simplex virus infection (also: HSV-1 and HSV-2) Slides 112, 116–117
Definition: Lifelong latent HSV (herpes simplex virus) infection with episodic reactivation, causing grouped vesicles and ulcers orally, genitally or anywhere on skin. Slides 112, 116–117
Etiology (cause): HSV-1 or HSV-2 (Herpesviridae, double-stranded DNA); either type can cause oral or genital infection; spread by contact with oral/genital secretions or lesions, including asymptomatic shedding. Slides 112, 116
Epidemiology (who): Not covered in the lecture
Risk Factors: Reactivation triggers: stress, illness, menstruation, ultraviolet light exposure. Slide 117
Pathology: Neurovirulent (invades and replicates in the nervous system), with latency and reactivation; HSV-1 genital infection recurs and sheds less often than HSV-2 genital infection. Slides 112, 116
Clinical Manifestation: Prodrome of burning, pain or paresthesias ± tender lymphadenopathy, headache, fever; grouped vesicles on an erythematous base → shallow painful ulcers; dysuria in women with genital lesions; last up to two weeks, heal without scarring; first episode longer and worse than recurrences. Slides 117–119
Diagnosis: Type-specific NAAT (nucleic acid amplification test)/PCR (nucleic acid amplification test/polymerase chain reaction) of a fresh vesicle, ulcer base or crust is preferred; culture less sensitive; a negative swab does not exclude; no HSV IgM (immunoglobulin M); no routine serologic screening. Differential: chancroid, syphilis (usually painless). Slides 121–123
Treatment/Therapy: Treat every first episode with oral acyclovir, valacyclovir or famciclovir; recurrent genital: episodic or daily suppressive therapy; suppressive valacyclovir lowers HSV-2 transmission; condoms reduce risk; avoid contact during prodrome or lesions; topical antivirals give minimal benefit. Slide 124
Mortality ★: Not covered in the lecture

Herpetic whitlow4 not covered

Name of Condition: Herpetic whitlow Slide 126
Definition: Painful HSV (herpes simplex virus) infection of the distal finger or thumb. Slide 126
Etiology (cause): HSV-1 or HSV-2, often inoculated through broken skin; highly contagious through skin contact. Slide 126
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Prodromal burning/tingling, then grouped vesicles on an erythematous, swollen digit near the nailbed; fever or lymphangitis may occur. Slide 126
Diagnosis: Confirm atypical cases with HSV NAAT (nucleic acid amplification test)/PCR (nucleic acid amplification test/polymerase chain reaction) from a fresh vesicle or lesion base; mimics bacterial felon/paronychia, contact dermatitis, blistering dactylitis. Slide 126
Treatment/Therapy: Do not incise and drain (delays healing); early oral acyclovir, valacyclovir or famciclovir; suppression for frequent recurrence; treat bacterial superinfection only if present; cover lesions, hand hygiene. Slide 128
Mortality ★: Not covered in the lecture

Molluscum contagiosum2 not covered

Name of Condition: Molluscum contagiosum Slide 130
Definition: Benign poxvirus skin infection producing smooth, dome-shaped, centrally umbilicated papules. Slide 130
Etiology (cause): Poxvirus spread by direct skin contact, shared contaminated objects and autoinoculation; sexual contact is common in adults with genital lesions. Slide 130
Epidemiology (who): Not covered in the lecture
Risk Factors: Immunosuppression (more numerous, larger or atypical lesions). Slide 130
Pathology: Most immunocompetent patients clear it spontaneously, though resolution may take months to several years. Slide 130
Clinical Manifestation: Asymptomatic, tender or pruritic; discrete, smooth, firm, flesh-colored, dome-shaped pearly papules averaging 3–5 mm; central umbilication is characteristic. Slide 134
Diagnosis: Clinical; biopsy if uncertain. Genital lesions: assess teens/adults for STIs (sexually transmitted infections); in a child, location alone does not prove abuse. Extensive/giant facial lesions: evaluate for immunosuppression including HIV (human immunodeficiency virus). Differential: basal cell carcinoma, sebaceous hyperplasia, condyloma acuminata. Slides 133, 135
Treatment/Therapy: Observation for many; berdazimer 10.3% gel at home (age ≥1 year) or clinician-applied cantharidin 0.7% (age ≥2 years); curettage or cryotherapy; topical retinoids off label; treat associated dermatitis. Slide 136
Mortality ★: Not covered in the lecture

Verruca vulgaris1 not covered

Name of Condition: Verruca vulgaris (also: common warts) Slides 138, 140
Definition: Common wart: benign proliferation of skin caused by HPV (human papillomavirus). Slides 138, 140
Etiology (cause): HPV infection of keratinocytes; spread by skin-to-skin contact, autoinoculation and contaminated surfaces. Slide 138
Epidemiology (who): Frequently ages 5–20 years. Slide 140
Risk Factors: Nail biting (periungual, lip and tongue warts). Slide 140
Pathology: Confined to the epidermis but expands and displaces the dermis, so it appears deeper; no roots (round, smooth underside); spontaneous resolution is the natural history. Slides 138–140
Clinical Manifestation: Usually on the hands (fingers/palms); usually < 1 cm, elevated round papules with a rough, grayish surface; tiny red/black dots (thrombosed dilated capillaries) that trimming makes more prominent. Slides 140, 142
Diagnosis: Clinical; biopsy generally unnecessary, but for immunocompromised patients or uncertain lesions (ruling out squamous cell carcinoma). Differential: squamous cell carcinoma, molluscum contagiosum, seborrheic keratosis. Slide 147
Treatment/Therapy: Observation (many resolve); salicylic acid; cryotherapy every 2–3 weeks (pain, blistering, pigment change); no therapy eradicates HPV (human papillomavirus) with certainty; refer periungual, facial, extensive, recalcitrant or atypical lesions. Slides 148–149
Mortality ★: Not covered in the lecture

Verruca plana2 not covered

Name of Condition: Verruca plana (also: flat warts) Slides 138, 143
Definition: Flat warts: multiple smooth, slightly elevated, flat-topped papules caused by HPV (human papillomavirus). Slides 138, 143
Etiology (cause): HPV infection of keratinocytes; spread by skin contact and autoinoculation. Slide 138
Epidemiology (who): Not covered in the lecture
Risk Factors: Shaving spreads lesions through autoinoculation. Slide 143
Pathology: HPV proliferation confined to the epidermis; spontaneous resolution is common. Slides 138, 143
Clinical Manifestation: Multiple smooth, slightly elevated, flat-topped, skin-colored to light-brown papules on the face, forehead, dorsal hands and shins. Slide 143
Diagnosis: Clinical; biopsy for immunocompromised patients or lesions of uncertain etiology. Slide 147
Treatment/Therapy: Observation is reasonable; carefully selected salicylic acid, topical retinoids or cryotherapy, balanced against dyspigmentation and scarring risk; refer facial or extensive cases. Slides 143, 149
Mortality ★: Not covered in the lecture

Verruca plantaris3 not covered

Name of Condition: Verruca plantaris (also: plantar warts) Slides 138, 145
Definition: HPV (human papillomavirus) wart on the weight-bearing surface of the foot. Slides 138, 145
Etiology (cause): HPV infection of keratinocytes; spread by skin contact, autoinoculation and contaminated surfaces. Slide 138
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Confined to the epidermis with no roots, though it displaces the dermis and looks deeper. Slide 139
Clinical Manifestation: Wart on a weight-bearing surface; may cluster into a mosaic wart (cluster of many warts). Slides 138, 145
Diagnosis: Clinical; biopsy only if uncertain or immunocompromised. Differential: squamous cell carcinoma, molluscum contagiosum, seborrheic keratosis. Slide 147
Treatment/Therapy: No therapy unless painful; salicylic acid 40%; cryotherapy. Slides 145–146
Mortality ★: Not covered in the lecture

Lecture 7 · Benign Skin Lesions

Prof. Hugh E. Griffenkranz, MPAS, PA-C · 24 conditions · source: 7. Benign Skin Lesions Prof Griffenkranz 8-25-2025-2.pptx

Clavus (corn)2 not covered

Name of Condition: Clavus (corn) (also: clavi; hard corn (clavus durum); soft corn (clavus mollum)) Slide 4
Definition: Localized, well-defined hyperkeratotic papule from focal pressure, with a hard central keratin core; hard and soft types Slide 4
Etiology (cause): Mechanical trauma to the skin, e.g. ill-fitting shoes; pressure on a localized area Slide 4
Epidemiology (who): Not covered in the lecture
Risk Factors: Tight or loose shoes, high heels; shoes without socks; walking barefoot; tools (hammer, rake) or sports equipment (tennis racket) rubbing the skin Slide 10
Pathology: Focal pressure causes hyperkeratosis (thickened stratum corneum) with a central cone-shaped core of hard keratin pointing into the skin Slide 4
Clinical Manifestation: Hard corn: dorsal/lateral fifth toe, hyperkeratotic papules; soft corn: 4th-5th toe web space, soft from moisture maceration; well defined, <1.5 cm; pain with direct downward pressure; skin lines run through Slides 4, 7
Diagnosis: Distinguished by central hyperkeratotic core, pain on downward pressure, skin lines run through; vs wart (verruca vulgaris, human papillomavirus): interrupts skin lines, blackened center, pain with side pressure Slides 7–8
Treatment/Therapy: Padding; avoid poorly fitting footwear; over-the-counter keratolytics (salicylic acid pads, liquids, plasters); diabetic patient: refer to podiatry; well-fitting shoes and socks, no barefoot walking, shoe pads Slides 9–10
Mortality ★: Not covered in the lecture

Callus2 not covered

Name of Condition: Callus (also: calluses) Slide 6
Definition: Diffuse hyperkeratotic thickening from broad-area pressure or friction; no central core; larger than a corn Slide 6
Etiology (cause): Broad area of skin pressure/friction Slide 6
Epidemiology (who): Not covered in the lecture
Risk Factors: Tight or loose shoes, high heels; shoes without socks; walking barefoot; tools (hammer, rake) or sports equipment (tennis racket) rubbing the skin Slide 10
Pathology: Pressure/friction leads to hyperkeratosis with diffuse thickening and no central core; acute, severe process forms a blister Slide 6
Clinical Manifestation: Palms of hands or balls of feet; painless; poorly defined, irregular shape; larger than a corn; skin lines run through Slides 6–7
Diagnosis: Larger, irregular, usually painless, skin lines run through; vs corn (central core, pain on downward pressure) and wart (interrupts skin lines, not specific to pressure areas) Slides 7–8
Treatment/Therapy: Padding; avoid poorly fitting footwear; over-the-counter keratolytics (salicylic acid pads, liquids, plasters); diabetic patient: refer to podiatry; well-fitting shoes and socks, no barefoot walking, shoe pads Slides 9–10
Mortality ★: Not covered in the lecture

Keloid1 not covered

Name of Condition: Keloid Slide 12
Definition: Fibroproliferative overgrowth of dense scar tissue extending beyond the original wound site; does not regress and tends to recur Slide 12
Etiology (cause): Abnormal wound healing (loss of the control mechanisms balancing repair) after surgical incisions, traumatic wounds, vaccination sites, burns, chickenpox, acne, or even minor scratches Slides 11–12
Epidemiology (who): Rare incidence; associated with dark skin color; populations at risk: African American, Hispanic, Asian Slides 12, 24
Risk Factors: African American, Hispanic, or Asian ancestry; ear piercing and other cosmetic procedures in high-risk patients; acne (early treatment favors scar-free healing) Slides 12, 15, 20
Pathology: Mechanism unclear; overgrowth of dense fibrous tissue; develops slowly and keeps enlarging for months to years; no regression with time Slide 12
Clinical Manifestation: May appear months after trauma; asymptomatic or pruritic/burning pain; cosmetic concern; firm bulbous nodules or markedly elevated plaques beyond wound margins; ear lobe, shoulders, sternal notch; rarely across joints Slides 12–13, 24
Diagnosis: Clinical; biopsy only if clinical doubt (may induce new scarring); differential: hypertrophic scar, dermatofibroma, foreign-body granuloma Slide 14
Treatment/Therapy: Prevention most important (high-risk: avoid piercings); combination therapy works best: silicone gel sheets, compression, intralesional steroids, cryotherapy, laser, intralesional 5-fluorouracil; excision (50-100% recurrence, often larger; keloids often worsened by surgery) then steroid injections or radiation Slides 15–20
Mortality ★: Not covered in the lecture

Hypertrophic scar1 not covered

Name of Condition: Hypertrophic scar Slides 21, 24
Definition: Raised scar from abnormal wound healing that stays confined to the wound margins and regresses with time Slides 21, 24
Etiology (cause): Abnormal wound healing (loss of the control mechanisms balancing repair) after surgery or injury Slides 11, 21, 24
Epidemiology (who): Frequent incidence; no association with skin color Slide 24
Risk Factors: Scars that cross joints or skin creases at a right angle Slide 24
Pathology: Active proliferative phase of wound healing; develops rapidly within 4 weeks; stable, then regresses (flattens) Slide 21
Clinical Manifestation: Asymptomatic; develops soon after surgery, within 4 weeks of the event; confined to wound site margins; improves with time Slides 21, 24
Diagnosis: Clinical; biopsy only if clinical doubt (may induce new scarring); differential: keloid, dermatofibroma, foreign-body granuloma Slide 22
Treatment/Therapy: Intralesional corticosteroid or 5-fluorouracil; compression therapy and silicone sheeting; surgical excision (improves with appropriate surgery); pulsed dye laser reduces erythema by reducing neovascularization Slides 23–24
Mortality ★: Not covered in the lecture

Cutaneous horn2 not covered

Name of Condition: Cutaneous horn Slide 25
Definition: Hard, conical, outward-growing keratin projection resembling an animal horn, arising from the surface of another lesion Slide 25
Etiology (cause): Arises from benign or malignant lesions: actinic keratosis, warts, seborrheic keratosis, keratoacanthoma, basal or squamous cell carcinoma Slide 25
Epidemiology (who): Males = females; Caucasians over age 50; head, neck, upper extremities; common on sun-exposed areas (face, ears, hands) Slide 26
Risk Factors: Not covered in the lecture
Pathology: Composed of keratin (keratotic papule); the process at the base of the lesion is most important Slide 25
Clinical Manifestation: Possible bleeding and/or pain from trauma; papular or nodular base with firm hornlike protuberance; may be flat, keratotic, nodular, pedunculated, and/or ulcerated Slide 26
Diagnosis: Often no clinical feature separates benign from malignant; deep shave biopsy samples the underlying lesion; differential: wart, actinic keratosis, squamous cell carcinoma Slide 27
Treatment/Therapy: Depends on the underlying etiology; an underlying malignancy frequently needs excision per standard practice for tumor type and location Slide 28
Mortality ★: Not covered in the lecture

Acrochordon (skin tag)2 not covered

Name of Condition: Acrochordon (skin tag) (also: skin tag; fibroepithelial polyp) Slides 29, 31
Definition: Harmless soft, pedunculated growth of normal skin in areas of friction Slides 29, 31
Etiology (cause): Forms where skin rubs together (friction) Slides 29, 31
Epidemiology (who): Very common: present in 60% of people by age 70; increased in females and obese patients Slide 29
Risk Factors: Female sex; obesity/overweight; increasing age; friction areas Slides 29, 31
Pathology: Fibroepithelial pedunculated papilloma (polyp) with a narrow stalk and broad tip Slide 29
Clinical Manifestation: Asymptomatic; soft, pedunculated, skin-colored papules on a thin stalk, about 1-10 mm; neck, axilla, under the breasts, groin Slides 29–31
Diagnosis: Not covered in the lecture
Treatment/Therapy: Usually for cosmesis: scissor excision, cryotherapy, or electrodesiccation; anesthesia not necessary; never cut or pull one off at home (bleeds); new tags may form in the same area Slides 30–31
Mortality ★: Not covered in the lecture

Pressure injury★ Professor emphasized3 not covered

Name of Condition: Pressure injury (also: pressure ulcer; bedsore) Slide 32
Definition: Localized damage to skin and underlying tissue caused by unrelieved pressure Slide 32
Etiology (cause): Soft tissue compressed between a bony prominence and an external surface for a prolonged time; shear and friction (patient moved carelessly or sliding down in bed) Slide 32
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Prolonged unrelieved pressure damages underlying tissue; injury ranges from non-blanchable intact skin to deep ulcers extending to bone Slide 32
Clinical Manifestation: ★ Stages 1-4: 1 non-blanchable erythema of intact skin; 2 partial-thickness loss, exposed dermis; 3 full-thickness loss, fat visible; 4 exposed fascia, muscle, tendon, ligament, cartilage or bone; unstageable (obscured by slough/eschar); deep tissue (persistent non-blanchable deep red/purple) Slides 33–34
Diagnosis: Clinical staging by depth of tissue loss; unstageable when slough or eschar hides the extent; frequent skin assessments Slides 33–35
Treatment/Therapy: Prevention is best: skin and nutrition assessment, clean dry skin, incontinence care, barrier creams, reposition every 2 hours, pain control, specialty (air) mattress; stage-based care, wound care specialist referral, infection control, silicone/hydrocolloid dressings, surgical debridement and closure Slides 35–36
Mortality ★: Not covered in the lecture

Pilonidal cyst1 not covered

Name of Condition: Pilonidal cyst (also: pilonidal disease; pilonidal sinus) Slide 38
Definition: Sac filled with hair and skin debris near the tailbone at the top of the gluteal cleft Slide 38
Etiology (cause): Acquired (once thought congenital): disrupted skin over the coccyx forms a pit that draws in hair and debris Slide 37
Epidemiology (who): Male to female ratio 3:1; recurrence common Slide 37
Risk Factors: Obesity; local trauma/irritation; sedentary lifestyle; increased hair density in the natal cleft; family history Slide 39
Pathology: Pit causes follicular plugging; ingrown hairs block drainage and promote abscess; chronic disease forms sinus tracts (blind tracks) Slides 37, 40, 42
Clinical Manifestation: Asymptomatic, or abscess: sudden pain and swelling in the gluteal cleft, warm, tender, erythematous, fluctuant (wave-like fluid shift on palpation), purulent/bloody drainage; chronic: recurrent draining sinus openings, hair may protrude Slides 40–41
Diagnosis: Diagnostic testing usually not needed Slide 43
Treatment/Therapy: Keep area clean and free of debris; shaving or laser hair therapy; incision and drainage for acute abscess; surgical referral for excision of chronic disease; hygiene education Slide 43
Mortality ★: Not covered in the lecture

Dermatofibroma★ Professor emphasized2 not covered

Name of Condition: Dermatofibroma Slide 44
Definition: Common benign firm dermal nodule (0.5-1 cm) formed by dense clusters of fibroblasts Slide 44
Etiology (cause): Uncertain; may form after trauma, viral infection, or insect bites Slide 44
Epidemiology (who): Male to female 1:2; all races; legs (most common site) and arms; multiple (>15) lesions reported with systemic lupus erythematosus, HIV (human immunodeficiency virus), Down syndrome, Graves disease, leukemia Slide 44
Risk Factors: Not covered in the lecture
Pathology: Dermal fibroblasts form small dense clusters, creating a firm nodule Slide 44
Clinical Manifestation: Usually asymptomatic, often after an insect bite; slight pruritus or pain (most common painful skin tumor); firm nodule, brown halo, pink hue, raised scaly center; ★ dimple sign (retracts beneath skin with lateral compression) Slide 45
Diagnosis: Dermoscopy: peripheral pigment network with central white mass; differential: basal cell carcinoma, hypertrophic scar, melanoma, keratoacanthoma Slide 46
Treatment/Therapy: None unless diagnosis questioned or symptoms warrant; small lesions: shave or punch biopsy (diagnostic and therapeutic); larger lesions: surgical excision Slide 47
Mortality ★: Not covered in the lecture

Keratoacanthoma1 not covered

Name of Condition: Keratoacanthoma Slides 48, 50
Definition: Rapidly growing dome-shaped tumor with a central keratin crater that often regresses spontaneously; histologically similar to squamous cell carcinoma Slides 48, 50
Etiology (cause): Believed to arise from the pilosebaceous unit (hair follicle) Slide 48
Epidemiology (who): Males > females; classically middle-aged, light-skinned people in hair-bearing, sun-exposed areas Slides 48–49
Risk Factors: Age >40; sun exposure; very fair skin (always burns, never tans); male; tattoos (red ink); skin trauma (lasers, surgery, cryotherapy); human papillomavirus infection Slide 49
Pathology: Histopathologically similar to squamous cell carcinoma, with strong arguments for classifying it as a variant of invasive squamous cell carcinoma; may keep growing or rarely metastasize Slide 48
Clinical Manifestation: Triphasic: rapid growth (6-8 weeks), stabilization, regression (after 3-6 months); solitary smooth shiny dome-shaped red papule/nodule with central keratin-filled crater (volcano) Slide 50
Diagnosis: Biopsy: the only reliable method; differential: squamous cell and basal cell carcinoma, amelanotic melanoma, molluscum contagiosum Slide 51
Treatment/Therapy: Excise or destroy (possible malignancy): elliptical excision with 5-mm margins; Mohs surgery for large, recurrent, or cosmetically/functionally sensitive sites; intralesional methotrexate before excision to shrink it Slide 52
Mortality ★: Not covered in the lecture

Epidermoid (epidermal) cyst3 not covered

Name of Condition: Epidermoid (epidermal) cyst (also: epidermal inclusion cyst; improperly called sebaceous cyst) Slide 53
Definition: Most common cutaneous cyst: epithelium enclosed within the dermis and filled with keratin Slide 53
Etiology (cause): Not covered in the lecture
Epidemiology (who): Males > females (2:1); very common; face, scalp, neck, trunk Slide 53
Risk Factors: Not covered in the lecture
Pathology: Cystic enclosure of epithelium in the dermis filled with keratin; looks like sebum but is keratin, so not a sebaceous cyst; fibrous capsule Slides 53, 57
Clinical Manifestation: Asymptomatic or drains foul-smelling material; single firm, moveable, round nodule with central pore (punctum); expresses cream-colored pasty material smelling of rancid cheese Slide 54
Diagnosis: Lab tests usually unnecessary; differential: cystic acne, lipoma, neurofibroma, keratoacanthoma, basal cell carcinoma Slide 55
Treatment/Therapy: Asymptomatic: none; inflamed: postpone excision a few weeks, intralesional triamcinolone, antibiotics if needed; surgical removal of the entire capsule when not inflamed; small (1-3 cm): punch incision and removal of contents Slides 56–57
Mortality ★: Not covered in the lecture

Syringoma3 not covered

Name of Condition: Syringoma Slide 58
Definition: Benign neoplasm of the eccrine (sweat gland) ducts, forming small papules around the eyes Slide 58
Etiology (cause): Not covered in the lecture
Epidemiology (who): Appears at puberty; females > males Slide 58
Risk Factors: Not covered in the lecture
Pathology: Benign neoplastic growth of eccrine sweat ducts Slide 58
Clinical Manifestation: Usually asymptomatic; multiple 1-2 mm skin-colored, pink or brown papules, mostly on the eyelids (periorbital) and upper cheeks Slide 58
Diagnosis: Usually clinical; biopsy if malignancy concern; differential: milia, xanthelasma, basal cell carcinoma Slide 59
Treatment/Therapy: Cosmetic only: oral isotretinoin (higher recurrence risk); curettage and electrodesiccation, laser, cryotherapy, or excision (possible poor cosmetic results) Slide 59
Mortality ★: Not covered in the lecture

Infantile hemangioma1 not covered

Name of Condition: Infantile hemangioma (also: hemangioma of infancy; superficial type formerly called strawberry hemangioma) Slides 61, 66
Definition: Congenital benign vascular neoplasm; most common tumor of infancy, with rapid proliferation then slow involution Slides 61, 66
Etiology (cause): Mutations of genes regulating endothelial cell proliferation Slide 61
Epidemiology (who): Noticed in first days to weeks of life; more common in preterm infants, females (3:1), Caucasians; head and neck 60%, trunk 25%, extremities 15% Slides 61–62
Risk Factors: Prematurity; female sex; Caucasian; history probes low birth weight, multiple gestation, placental abnormalities, family history Slides 62–64
Pathology: Rapid endothelial proliferation; superficial (most common): dilated dermal vessels, bright red papule/plaque/nodule; deep (least common): deep dermis/subcutis, pale, skin-colored or blue nodule Slides 61, 67, 70
Clinical Manifestation: Half present at birth; earliest sign blanching, then fine telangiectasias, then red macule; rapid growth in the neonatal period, most growth in the first 4-6 months, slowing at 6-12 months; involution 50% by age 5, 70% by 7, 90% by 9; may block vision, feeding, breathing, or ear canal Slides 65–66, 71
Diagnosis: Mostly clinical; refer to a vascular anomalies specialist if in doubt; differential: nevus flammeus, pyogenic granuloma; 5 or more skin lesions may be associated with hepatic hemangiomas Slides 62, 72
Treatment/Therapy: Often none (serial observation); treat for cosmetic, functional, ulceration, or infection reasons: beta-blockers first line (oral propranolol, topical timolol); corticosteroids (also listed as first line; topical, intralesional, oral) slow growth and shrink proliferating lesions; pulsed dye laser; surgical excision Slides 73–76
Mortality ★: Not covered in the lecture

Nevus flammeus4 not covered

Name of Condition: Nevus flammeus (also: port-wine stain) Slides 77, 79
Definition: Congenital vascular lesion of dilated dermal capillaries, present at birth and persisting for life Slides 77, 79
Etiology (cause): Not covered in the lecture
Epidemiology (who): More common in Caucasians; male = female; present at birth Slide 78
Risk Factors: Not covered in the lecture
Pathology: Dilated superficial dermal capillaries through the entire depth of the dermis; no endothelial proliferation; grows with the child, no involution Slides 77–78
Clinical Manifestation: Early: flat, well-circumscribed, blanchable pink-to-purple patches, darker with crying, fever, or heat, usually unilateral with sharp midline cutoff; later darker, thickened, raised plaque; psychosocial burden; forehead/upper eyelid stain may mark Sturge-Weber syndrome Slides 78–80
Diagnosis: Not covered in the lecture
Treatment/Therapy: No treatment required; tinted waterproof makeup; pulsed dye laser (selective vessel destruction via intravascular coagulation, later replaced by collagen) Slides 81–82
Mortality ★: Not covered in the lecture

Nevus simplex5 not covered

Name of Condition: Nevus simplex (also: stork bite) Slide 83
Definition: Congenital vascular lesion; a more superficial variant of nevus flammeus Slide 83
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Dermal capillaries, more superficial than nevus flammeus Slide 83
Clinical Manifestation: Present at birth; more noticeable with crying; pink to erythematous, irregular, blanchable macules/patches, single or multiple; most common on head and neck Slide 84
Diagnosis: Not covered in the lecture
Treatment/Therapy: Expectant: fades within 1 year, or may persist for life (neck) Slide 84
Mortality ★: Not covered in the lecture

Cherry angioma★ Professor emphasized2 not covered

Name of Condition: Cherry angioma (also: senile angioma) Slide 85
Definition: Very common acquired vascular papule formed by capillary (venule) proliferation, increasing with age Slide 85
Etiology (cause): Unknown Slide 85
Epidemiology (who): Very common; occurs with increasing age Slide 85
Risk Factors: Increasing age Slide 85
Pathology: Capillary (venule) proliferation Slide 85
Clinical Manifestation: Most common on the trunk; may bleed after trauma; smooth, firm, deep red papules <5 mm that ★ blanch with pressure (may not blanch completely if fibrotic) Slide 86
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not necessary unless bothersome; new lesions will develop and cannot be prevented; laser for superficial lesions; shave excision and electrocautery for large lesions Slide 87
Mortality ★: Not covered in the lecture

Telangiectasia6 not covered

Name of Condition: Telangiectasia Slide 88
Definition: Acquired vascular lesion: a permanently dilated capillary (<1 mm) Slide 88
Etiology (cause): Primary or secondary; associated with numerous diseases Slide 88
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Blanchable; single, in groups, or with a central punctum Slide 88
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Nevus araneus (spider angioma)2 not covered

Name of Condition: Nevus araneus (spider angioma) (also: spider angioma) Slide 89
Definition: Acquired vascular lesion from dilation of preexisting vessels, without vascular proliferation Slide 89
Etiology (cause): Estrogen excess states Slide 89
Epidemiology (who): Hands and fingers in children; face, neck, upper trunk, and arms in adults Slide 89
Risk Factors: Pregnancy; birth control pills; cirrhosis, liver failure; history should cover hormone use, alcohol, liver-toxic medications Slides 89–90
Pathology: No vascular proliferation; dilation of preexisting vessels (arterioles on the body) Slides 89–90
Clinical Manifestation: Asymptomatic; solitary or multiple lesions <10 mm; lesion blanches Slide 90
Diagnosis: Not covered in the lecture
Treatment/Therapy: None may be needed; pregnancy- and pill-related lesions resolve after delivery or stopping; pulsed dye laser resolves most lesions Slides 89–90
Mortality ★: Not covered in the lecture

Pyogenic granuloma1 not covered

Name of Condition: Pyogenic granuloma Slide 91
Definition: Benign, rapidly growing vascular tumor of skin and mucous membranes; misnamed, as it is neither infectious nor granulomatous Slide 91
Etiology (cause): Exact cause unknown; response to irritation, injury/trauma, or hormonal changes Slide 91
Epidemiology (who): Common in children, young adults, and pregnancy Slide 91
Risk Factors: Trauma to the area; pregnancy/hormonal factors Slides 91–92
Pathology: Acquired overgrowth of blood vessels in skin/mucous membranes Slide 91
Clinical Manifestation: Head, neck, fingers; rapid growth, painless, bleeds spontaneously or after irritation; bright red exophytic papule/nodule, moist surface, epithelial collarette base; average 6.5 mm; may erode, ulcerate, crust Slide 92
Diagnosis: Usually clinical; differential: cherry angioma, malignant melanoma, squamous cell carcinoma Slide 95
Treatment/Therapy: May resolve spontaneously (pregnancy-related often after delivery); for cosmesis or bleeding: surgical excision (histology, lowest recurrence, most scarring); shave with curettage and electrodesiccation, laser, cryotherapy; early follow-up if it recurs Slides 94–96
Mortality ★: Not covered in the lecture

Neurofibromatosis type 1★ Professor emphasized3 not covered

Name of Condition: Neurofibromatosis type 1 (also: von Recklinghausen disease) Slide 97
Definition: Common neurocutaneous genetic disorder causing tumors on nerve tissue; also called ★ von Recklinghausen disease Slide 97
Etiology (cause): NF1 (neurofibromatosis type 1) gene on chromosome 17; ★ three types: NF1, NF2 (neurofibromatosis type 2; NF2 gene, chromosome 22), schwannomatosis or NF3 (SMARCB1 and LZTR1 genes, chromosome 22) Slide 97
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Cutaneous neurofibromas: benign nerve sheath tumors from peripheral nerves; plexiform neurofibromas: large tumors in tissue covering nerves, anywhere except brain and spinal cord, may be locally invasive Slides 100–101, 103
Clinical Manifestation: Café-au-lait macules (>5 mm prepubertal, >15 mm postpubertal; often first sign, at birth or first year); cutaneous neurofibromas from puberty, more with age; Crowe sign (grouped axillary/inguinal freckles <5 mm, more prominent with sun); plexiform neurofibromas Slides 98–102
Diagnosis: Six or more café-au-lait spots are diagnostic, but the macules alone do not establish the diagnosis; axillary/inguinal freckling is a criterion (under-breast site is not) Slides 99, 102
Treatment/Therapy: Surveillance: skin exam at each visit for new or progressing neurofibromas; evaluate the extent of plexiform lesions; national and regional support groups Slide 103
Mortality ★: Not covered in the lecture

Xanthelasma3 not covered

Name of Condition: Xanthelasma Slide 104
Definition: Soft, yellow cholesterol plaques, most often on the medial eyelids Slide 104
Etiology (cause): Associated with lipid disorders Slide 104
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Collection of lipid-laden macrophages Slide 104
Clinical Manifestation: Asymptomatic; soft yellow plaques; most common location medial eyelids Slide 104
Diagnosis: Screen for hyperlipidemia; may signify increased risk of cardiac disease Slide 104
Treatment/Therapy: Laser or surgical excision; recurrence common Slide 104
Mortality ★: Not covered in the lecture

Lipoma3 not covered

Name of Condition: Lipoma Slide 105
Definition: Most common soft tissue tumor: benign localized overgrowth of fat cells in subcutaneous tissue Slide 105
Etiology (cause): Not covered in the lecture
Epidemiology (who): Most common soft tissue tumor Slide 105
Risk Factors: Not covered in the lecture
Pathology: Benign localized overgrowth of fat cells in subcutaneous tissue; single or multiple tumors Slide 105
Clinical Manifestation: Asymptomatic unless adjoining structures invaded; anywhere on the body; soft, painless, rubbery subcutaneous nodules, usually <5 cm Slide 105
Diagnosis: Typically clinical; differential: epidermal cyst, dermatofibroma, abscess Slide 106
Treatment/Therapy: Observe asymptomatic tumors; excise cosmetically deforming enlarging masses or those with uncertain diagnosis Slide 106
Mortality ★: Not covered in the lecture

Digital mucous cyst2 not covered

Name of Condition: Digital mucous cyst (also: mucous cyst) Slide 107
Definition: Pseudo-cyst on the distal digit without a true cellular lining, formed by mucin extruded from a joint Slide 107
Etiology (cause): Extrusion of mucinous contents from a local joint space into the surrounding dermis Slide 107
Epidemiology (who): Females > males Slide 107
Risk Factors: Osteoarthritis Slide 107
Pathology: No cellular lining (true capsule); collecting mucin compacts dermal cells at the margin, mimicking a capsule Slide 107
Clinical Manifestation: Asymptomatic unless large; translucent skin-colored cystic papule, typically over the distal interphalangeal joint, over the proximal nail matrix or nail bed; may cause a longitudinal nail groove Slides 107–108
Diagnosis: Not covered in the lecture
Treatment/Therapy: Observe asymptomatic lesions; excise symptomatic cysts or those causing nail dystrophy Slide 108
Mortality ★: Not covered in the lecture

Sebaceous hyperplasia1 not covered

Name of Condition: Sebaceous hyperplasia Slide 109
Definition: Common benign enlargement of sebaceous glands with no known potential for malignant transformation Slide 109
Etiology (cause): Aging slows turnover of sebocytes (sebum-producing cells) Slide 109
Epidemiology (who): Common Slide 109
Risk Factors: Increasing age; immunosuppression (high risk) Slide 109
Pathology: Slowed sebocyte turnover crowds the gland, which enlarges Slide 109
Clinical Manifestation: Asymptomatic, cosmetic or malignancy concern; single or multiple soft whitish-yellow or skin-colored papules 2-9 mm with central umbilication (sebum may be expressed); common on the face Slide 110
Diagnosis: Dermoscopy distinguishes it from basal cell carcinoma; biopsy if malignancy concern; differential: basal cell carcinoma Slide 111
Treatment/Therapy: Treatment not required; lesions tend to recur and treatment risks scarring; light electrocautery Slide 111
Mortality ★: Not covered in the lecture

Lecture 8 · Pigmented Skin Lesions

Chand Shah, MPAS, PA-C · 13 conditions · source: CMS I Pigmented Skin Lesions - Shahsv-2.pptx

Ephelides1 not covered

Name of Condition: Ephelides (also: freckles) Slides 4–5
Definition: Freckles: small, light brown, symmetric macules on (mostly) sun-exposed skin Slides 4–5
Etiology (cause): Autosomal dominant; related to mutation in the MCR-1 gene (the receptor for alpha-melanocyte-stimulating hormone); carriers are at high risk of developing freckles Slide 4
Epidemiology (who): Fair-skinned people, often blonde or red hair, possibly Celtic ancestry; male = female; first appear in young children Slide 4
Risk Factors: Fair skin; MCR-1 gene mutation carriers; ultraviolet exposure darkens them Slide 4
Pathology: Decreased MCR-1 pathway activity (via cyclic adenosine monophosphate) favors pheomelanin (yellow/red, sulfur-containing pigment); biopsy: normal to reduced number of hypertrophic melanocytes with increased melanin in basal epidermis Slides 4–5
Clinical Manifestation: Asymptomatic 3-5 mm light brown macules, may become confluent; darken with sun (spring/summer), fade with cessation of sun exposure (winter); regress later in life Slides 4–6
Diagnosis: Clinical diagnosis; lentigines are the main differential diagnosis Slide 5
Treatment/Therapy: Sun protection with patient education/counseling; topical depigmenting agents (hydroquinone, retinoids, alpha-hydroxy acids, botanicals); intense pulsed light or lasers preferred (may relapse); no cryotherapy (lesions too small) Slide 7
Mortality ★: Not covered in the lecture

Lentigines (lentigo simplex)2 not covered

Name of Condition: Lentigines (lentigo simplex) (also: age spots; simple lentigo) Slides 9–10
Definition: Common benign melanocytic lesion; types: lentigo simplex, acral, agminated, generalized Slides 9–10
Etiology (cause): Not well known; possibly disrupted melanocyte homeostasis from increased melanocyte density; dysregulated melanization Slide 9
Epidemiology (who): Bimodal age distribution: early childhood or later in life Slide 9
Risk Factors: Not covered in the lecture
Pathology: Increased melanocyte density; melanin macroglobules; lentigo simplex lacks the mutations found in solar lentigo, PUVA (psoralen plus ultraviolet A) lentigines and common acquired nevi Slide 9
Clinical Manifestation: Well-circumscribed, round to oval, uniformly black or brown macules <5 mm; skin, conjunctiva, mucocutaneous surfaces; sun-exposed and protected sites; do not fade without sun; agminated = grouped light brown macules; partial/generalized lentigo raises concern for an inherited syndrome Slides 9–11
Diagnosis: Clinical diagnosis Slide 12
Treatment/Therapy: Treatment not necessary; cosmetic removal if preferred: cryotherapy or quality-switched laser Slide 12
Mortality ★: Not covered in the lecture

Solar lentigo1 not covered

Name of Condition: Solar lentigo Slides Lecture 3: 107, 110
Definition: Benign accumulation of pigment-producing cells from cumulative ultraviolet exposure; architecturally distinct from melanocytic nevi Slides Lecture 3: 107, 110
Etiology (cause): Chronic ultraviolet exposure: UVB (ultraviolet B) stimulates melanocyte proliferation; UVA (ultraviolet A) causes oxidative damage to melanin and DNA; PUVA (psoralen plus ultraviolet A) therapy causes a variant Slides 13; Lecture 3: 110
Epidemiology (who): Older age (90% at age 50; >90% of white patients over 70); white skin (Fitzpatrick I-III) and Asians Slides 13; Lecture 3: 110
Risk Factors: Older age, sun damage/cumulative ultraviolet dose, ephelides, tanning (tanning beds), birth control use; PUVA lentigines: number of treatments, male sex, fair skin, older age Slides 13; Lecture 3: 110
Pathology: Proliferation of basal melanocytes with increased melanin production; keratinocytes stimulate melanocytes by paracrine signaling Slides 13; Lecture 3: 110
Clinical Manifestation: Light to dark brown macules, <1 mm to several cm, well defined with irregular borders, may coalesce at severe-sunburn sites; face, dorsal forearms/hands; PUVA type also on buttocks/genitalia; over time enlarge/darken, stay stable, regress or become lichenoid keratoses; associated with actinic keratosis, squamous/basal cell carcinoma, melanoma Slides 13–14; Lecture 3: 110
Diagnosis: Dermoscopy: finger-like projections, "moth-eaten" border; biopsy if atypical or uncertain, especially to exclude lentigo maligna (melanoma in situ) Slides Lecture 3: 111
Treatment/Therapy: Treatment not necessary; cosmetic: retinoids, cryotherapy (first-line office treatment), quality-switched laser, peels; daily broad-spectrum sunscreen SPF (sun protection factor) 30 or more; annual skin exam Slides 15; Lecture 3: 111
Mortality ★: Not covered in the lecture

Seborrheic keratosis4 not covered

Name of Condition: Seborrheic keratosis Slide 17
Definition: Benign beige to brown to black papules and plaques Slide 17
Etiology (cause): Not covered in the lecture
Epidemiology (who): Common in older adults Slide 17
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: 2-20 mm; velvety or warty feel; "stuck on" or pasted-on appearance; easily mistaken for neoplasms Slide 17
Diagnosis: Clinical diagnosis Slide 17
Treatment/Therapy: Supportive; cryotherapy may help if itchy or inflamed (lesions recur after treatment) Slide 17
Mortality ★: Not covered in the lecture

Dermatosis papulosa nigrans2 not covered

Name of Condition: Dermatosis papulosa nigrans Slide 19
Definition: Multiple small black or dark brown papules on the face and neck, identical to small seborrheic keratoses Slide 19
Etiology (cause): Likely genetic Slide 19
Epidemiology (who): Common in African Americans, dark-skinned Asians and Polynesians; female > male Slide 19
Risk Factors: Not covered in the lecture
Pathology: Believed to be a developmental defect of the hair follicle Slide 19
Clinical Manifestation: Multiple smooth, firm, 1-5 mm black or dark brown papules on face and neck Slide 19
Diagnosis: Clinical diagnosis; biopsy if uncertain Slide 19
Treatment/Therapy: Best left untreated; excision, curettage or laser if needed; avoid cryotherapy (post-inflammatory hyperpigmentation) Slide 19
Mortality ★: Not covered in the lecture

Vitiligo2 not covered

Name of Condition: Vitiligo Slides 21, 23
Definition: Common autoimmune skin disease causing depigmentation; nonsegmental and segmental forms Slides 21, 23
Etiology (cause): Autoimmune: T cell-mediated destruction of melanocytes Slide 21
Epidemiology (who): Any age; usually starts before the 30s (half before 20s, one-third before age 12); male = female Slide 21
Risk Factors: Not covered in the lecture
Pathology: T cell-mediated destruction of melanocytes causes depigmentation Slide 21
Clinical Manifestation: Asymptomatic white, non-scaly macules/patches with distinct margins, usually symmetric; face (periorificial), acral, genital sites first; segmental = unilateral, block-like, not crossing midline; unpredictable flares; psychological burden; associated with other conditions Slides 21–23
Diagnosis: Clinical diagnosis; Wood lamp exam in a dark room (lesions fluoresce); labs for associated autoimmune disease: CBC (complete blood count), antinuclear antibody Slides 22–23
Treatment/Therapy: <5% body surface area: topical steroids or calcineurin inhibitors (tacrolimus, pimecrolimus; face/neck/intertriginous/children); >5%: narrowband UVB (ultraviolet B) phototherapy first line; topical + phototherapy ideal; psychological support; grafting only for stable disease Slides 24–25
Mortality ★: Not covered in the lecture

Congenital melanocytic nevus2 not covered

Name of Condition: Congenital melanocytic nevus Slides 27–28
Definition: Pigmented neoplasm of melanocytes evident at birth or shortly after; small, medium or large; high risk of melanoma, rising with lesion size Slides 27–28
Etiology (cause): Somatic mutations Slide 28
Epidemiology (who): Not covered in the lecture
Risk Factors: Associated with neurofibromatosis type 1 Slide 28
Pathology: Arise from neural crest-derived melanocytic precursors that migrate along neurovascular bundles Slide 27
Clinical Manifestation: Flat brown patches or plaques, smooth or slightly uneven borders; pebbly, rugose, verrucous or lobular; trunk/extremities most often; nevi on head, neck, posterior midline: neurocutaneous melanosis (seizures, hydrocephalus, neurological deficits, vomiting; poor prognosis) Slides 28–29
Diagnosis: Clinical diagnosis, sometimes biopsy; cranial or axial lesions: MRI (magnetic resonance imaging) of brain ± total spine for neurocutaneous melanosis Slide 30
Treatment/Therapy: Individualized by melanoma risk, cosmetic and functional concerns; ideally surgical removal of as much nevus as possible; observation if little graft-site skin; counseling/support groups for large nevi Slide 31
Mortality ★: Not covered in the lecture

Nevus spilus4 not covered

Name of Condition: Nevus spilus (also: spotted nevus) Slide 32
Definition: Spotted nevus; a variant of congenital nevus; rarely progresses to melanoma Slide 32
Etiology (cause): Possibly a somatic mutation Slide 32
Epidemiology (who): Present at birth or in the first years of life Slide 32
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Café-au-lait-like tan background (<1 cm to >10 cm) with scattered superimposed darker macules or papules; trunk and extremities; associated with vascular, central nervous system or connective tissue anomalies Slides 32–33
Diagnosis: Not covered in the lecture
Treatment/Therapy: Observation with periodic clinical evaluation; sun protection counseling Slide 34
Mortality ★: Not covered in the lecture

Common acquired melanocytic nevus2 not covered

Name of Condition: Common acquired melanocytic nevus (also: mole) Slides 27, 35
Definition: Mole: benign melanocytic neoplasm arising after birth Slides 27, 35
Etiology (cause): Not covered in the lecture
Epidemiology (who): Develop slowly after birth; number peaks in the 30s then declines; more numerous in light-skinned people who sunburn easily Slide 35
Risk Factors: Ultraviolet radiation exposure, male sex, some genetic component Slide 35
Pathology: Arise from junctional melanocytes; junctional and compound nevi Slides 27, 36
Clinical Manifestation: Usually <6 mm, round to oval, sharply demarcated, homogeneous surface and color (skin-colored, brown, pink); anywhere on body; enlarge symmetrically, stabilize, regress; very dark brown/black in light skin is suspicious Slides 35–36
Diagnosis: Clinical diagnosis Slide 37
Treatment/Therapy: Observation; removal for cosmetic or symptomatic relief; sun protection counseling Slide 37
Mortality ★: Not covered in the lecture

Blue nevus3 not covered

Name of Condition: Blue nevus Slide 38
Definition: Group of lesions of deeply pigmented spindle or epithelioid melanocytes in the dermis: common, cellular, combined and atypical cellular blue nevi Slide 38
Etiology (cause): Not covered in the lecture
Epidemiology (who): Women > men; most common in the 20s; common type arises in adolescence, cellular type before age 40 Slides 38–39
Risk Factors: Not covered in the lecture
Pathology: Deeply pigmented spindle or epithelioid melanocytes located in the dermis Slide 38
Clinical Manifestation: Single blue, blue-gray or blue-black macule/papule; dorsal hands/feet, scalp, buttocks, sacrum; common <1 cm, cellular >1 cm plaques or nodules Slides 38–39
Diagnosis: Clinical for small lesions; biopsy for larger lesions Slide 40
Treatment/Therapy: Observation; biopsy/excision if changes noted Slide 40
Mortality ★: Not covered in the lecture

Pigmented spindle cell nevus★ Professor emphasized4 not covered

Name of Condition: Pigmented spindle cell nevus (also: Reed nevus) Slide 41
Definition: Benign, sharply circumscribed, darkly pigmented papule Slide 41
Etiology (cause): Not covered in the lecture
Epidemiology (who): Commonly in the 30s; female > male Slide 41
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Jet-black papule (may show blue, gray or brown), usually <7 mm; extremities, mainly lower, especially the thigh Slide 41
Diagnosis: Confirm with biopsy Slide 41
Treatment/Therapy: ★ Excision with negative margins Slide 41
Mortality ★: Not covered in the lecture

Spitz nevus★ Professor emphasized5 not covered

Name of Condition: Spitz nevus Slide 42
Definition: Usually benign nevus with a growth phase (fast or slow) followed by a stable period Slide 42
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Solitary, asymptomatic, pink/red, hairless, firm, dome-shaped; ★ sometimes resembles melanoma; mm to cm; face, neck, trunk, extremities, sparing palms/soles/mucous membranes; multiple lesions can signal a familial cancer syndrome Slide 42
Diagnosis: Biopsy vs ★ wide excision Slide 42
Treatment/Therapy: Excision Slide 42
Mortality ★: Not covered in the lecture

Dysplastic melanocytic nevus2 not covered

Name of Condition: Dysplastic melanocytic nevus Slides 27, 43
Definition: Nevus with atypical architectural and cytologic features; may progress to melanoma (more nevi, higher risk) Slides 27, 43
Etiology (cause): Not covered in the lecture
Epidemiology (who): Common in Caucasians Slide 43
Risk Factors: Family history; dysplastic nevus syndrome can give over 100 nevi by adolescence Slide 43
Pathology: Atypical architectural and cytologic features Slide 27
Clinical Manifestation: At least 5 mm with irregular, indistinct borders; variable tan to brown pigment; smooth or "pebbly" surface; sun-exposed skin Slide 43
Diagnosis: Biopsy Slide 44
Treatment/Therapy: Observation; biopsy all changing or developing lesions; excision if concern for melanoma; sun protection Slide 44
Mortality ★: Not covered in the lecture

Lecture 9 · Premalignant and Malignant Cutaneous Lesions

Monique Jaquith, DMSc, PA-C · 15 conditions · source: Premalignant and Malignant Cutaneous Lesions - Jaquith.pptx

Actinic keratosis1 not covered

Name of Condition: Actinic keratosis (also: solar keratosis) Slides 6, 11
Definition: Premalignant rough, scaly patch or bump caused by UV (ultraviolet) damage; lies on a continuum with keratinocyte carcinoma, and some turn into squamous cell carcinoma. Slides 6, 11
Etiology (cause): Chronic cumulative UV (ultraviolet) injury → dysplastic keratinocytes in a field of sun-damaged skin; UV-induced TP53 mutations are the critical molecular event. Slides 11; Lecture 3: 112
Epidemiology (who): Fair-complexioned people, sun-exposed skin; most common precancerous skin lesion worldwide; up to 60% of men over 60 in high-UV (ultraviolet) climates. Slides 11; Lecture 3: 112
Risk Factors: Advanced age; cumulative UV (ultraviolet) exposure, outdoor work or recreation; prior actinic keratosis or keratinocyte carcinoma; male sex/bald scalp; immunosuppression (transplant recipients 65× risk). Slides 11; Lecture 3: 112
Pathology: Intraepidermal keratinocytic dysplasia; field cancerization (surrounding normal-looking skin carries subclinical mutations); ~1 in 1,000 lesions per year progresses to squamous cell carcinoma (Lecture 3 instead gives 0.025–16% per lesion per year), cumulative field risk matters more. Slides 6, 11; Lecture 3: 112
Clinical Manifestation: 0.2–0.6 cm flesh-colored, pink, or slightly hyperpigmented papules with sandpaper texture, often felt more than seen; face, scalp, ears, forearms, dorsal hands; may be tender. Bleeding, induration, ulceration, rapid growth are not typical. Slide 12
Diagnosis: Usually clinical ± dermoscopy; shave or punch biopsy if concerning for squamous cell carcinoma or persists/recurs after therapy; key call: actinic keratosis vs squamous cell carcinoma in situ vs invasive. Differential: early squamous cell carcinoma (most important), superficial basal cell carcinoma, seborrheic keratosis, solar lentigo, verruca. Slide 13
Treatment/Therapy: Few lesions: liquid nitrogen cryotherapy (crusts, clears in 10–14 days). Multiple lesions in one area: field therapy, topical fluorouracil most effective; imiquimod; photodynamic therapy. Daily sun protection; refer for uncertainty, high burden, recurrence, immunosuppression. Slides 14–15
Mortality ★: Not covered in the lecture

Cutaneous squamous cell carcinoma1 not covered

Name of Condition: Cutaneous squamous cell carcinoma (also: SCC in situ = Bowen disease) Slides 16, 23
Definition: Second most common skin cancer, arising in the flat squamous cells of the outer skin layer; in situ form is Bowen disease. Almost always easy to cure when found early. Slides 16, 23
Etiology (cause): Long-term UV (ultraviolet) damage from sun or tanning beds; may arise from an actinic keratosis. Slides 16, 21
Epidemiology (who): Mainly fair-skinned people who burn easily, on exposed sites; common and often aggressive in organ transplant recipients (multiple tumors ~5 years after transplant). Slide 21
Risk Factors: Prolonged cumulative sun exposure; immunosuppression (transplant, CLL (chronic lymphocytic leukemia), HIV (human immunodeficiency virus)/AIDS (acquired immunodeficiency syndrome), iatrogenic); chronic wounds, scars, prior radiation fields; certain genetic diseases. Slide 21
Pathology: Pathology grades differentiation, depth, perineural/perivascular invasion, margins, aggressive subtype. High-risk sites (lip, ear, scalp, temple, nose, genitalia, mucosa) and >10 tumors raise recurrence/metastasis; metastatic rate 3–7% when sun-induced. Slides 22–23, 26
Clinical Manifestation: Small red, conical, hard nodule that may ulcerate; or nonhealing ulcer, warty nodule, pink plaque with hemorrhagic crust. Red flags: rapid growth, pain, bleeding, induration, fixation, palpable nodes. Slide 22
Diagnosis: Shave, punch, or excisional biopsy deep enough to separate in situ from invasive; palpate draining nodes; imaging/nodal evaluation for high-risk tumors. Differential: actinic keratosis, keratoacanthoma, verruca, basal cell carcinoma. Slide 23
Treatment/Therapy: In situ: imiquimod, topical fluorouracil, or curettage and electrodesiccation. Invasive: surgical excision or Mohs surgery (high-risk sites, recurrent, >1 cm face/>2 cm trunk or extremities, immunosuppressed). Advanced: PD-1 (programmed cell death protein 1) blockade, cetuximab. Nicotinamide cuts new tumors ~30% in high-risk patients. Slides 21, 24
Mortality ★: Not covered in the lecture

Basal cell carcinoma1 not covered

Name of Condition: Basal cell carcinoma Slides 27, 38
Definition: The most common form of cancer; slow-growing and highly curable early, but capable of significant local destruction; often a shiny bump or a sore that does not heal. Slides 27, 38
Etiology (cause): UV (ultraviolet) light drives carcinogenesis in sun-exposed skin; sun exposure is the main cause. Slides 27, 33
Epidemiology (who): Most common cancer; fair-skinned people with intense, intermittent sun exposure; a second basal cell carcinoma develops in up to 50%. Slide 33
Risk Factors: Intense intermittent UV (ultraviolet) exposure, fair skin; immunosuppression (non-Hodgkin lymphoma, solid-organ transplant, allogeneic hematopoietic stem cell transplant) raises incidence and recurrence. Slide 33
Pathology: Histologic subtypes: superficial, nodular, micronodular, infiltrative; subtype dictates behavior and treatment. Morpheaform, micronodular, and infiltrative are aggressive. Metastasis rare but serious. Slides 33, 36–38
Clinical Manifestation: Nodular: pearly papule with central erosion and telangiectasias (seen better on stretching). Pigmented: mimics melanoma. Superficial: red, shiny, scaly thin plaques on back/chest. Morpheaform: ivory-white, scar-like, subclinical spread. Slide 35
Diagnosis: Shave or punch biopsy confirms and gives histologic subtype (low vs high risk); no routine imaging for localized disease. Differential: sebaceous hyperplasia, nevus, squamous cell carcinoma. Slide 36
Treatment/Therapy: Curettage and electrodesiccation, excision (≤5% recurrence), or Mohs (~98% cure; eyelids, nasolabial folds, canthi, external ear, temple, recurrent, aggressive histology). Superficial: imiquimod or topical fluorouracil. Advanced: hedgehog pathway inhibitors (vismodegib, sonidegib). Annual full-skin exam. Slides 37–38
Mortality ★: Not covered in the lecture

Malignant melanoma★ Professor emphasized

Name of Condition: Malignant melanoma Slides 2, 39
Definition: Malignant melanocytic skin cancer; the leading cause of death due to skin disease. Slides 2, 39
Etiology (cause): UV (ultraviolet) exposure and sunburn; fewer than 30% arise from an existing mole, most arise de novo; acral lentiginous type is not clearly UV-driven. Slides 40–41
Epidemiology (who): 4th most common cancer in the U.S.; incidence doubled over 30 years; lifetime risk ~2% in white individuals vs 0.1–0.5% in skin of color; 1 in 4 before age 40; men over 70 especially affected. Slide 40
Risk Factors: UV (ultraviolet) exposure/sunburn history, fair phenotype, numerous or atypical nevi, personal or family history, immunosuppression. Slide 40
Pathology: Subtypes: superficial spreading (~2/3; radial then vertical growth), lentigo maligna (older, chronic sun), nodular (rapid, often amelanotic), acral lentiginous (palms, soles, nails), ocular, mucosal. Breslow thickness = most important prognostic factor. Slides 41, 49–50
Clinical Manifestation: ABCDE: Asymmetry, irregular Border, Color variegation, Diameter >6 mm, Evolution (most important). Ugly duckling sign (a lesion unlike the patient's other nevi). Acral: dark irregular palm/sole lesion or new broad nail streak. Slides 46–47
Diagnosis: Excisional biopsy allowing full-thickness depth; report Breslow, ulceration, margins, mitoses. Sentinel lymph node biopsy at ≥1.0 mm (≥0.8 mm with risk features); BRAF testing. Staging: ★ 0 epidermis only, I–II localized, III nodes, IV other organs. Slides 49, 51, 53
Treatment/Therapy: Re-excision margins: in situ 0.5–1 cm; <1 mm 1 cm; >1 mm 1–2 cm. ★ Refer deeper than 1 mm or with spread to an expert center. Advanced: BRAF-targeted therapy, immune checkpoint therapy (anti-PD-1, programmed cell death protein 1). Monthly self-exam (ABCDE), sun protection. Slides 52, 56
Mortality ★: Leading cause of death due to skin disease; ~7,990 U.S. deaths in 2023 (~two-thirds men); mortality declining (earlier detection, immunotherapy); survival drops sharply with Breslow thickness and nodal/distant spread. Slides 39–40, 55

Kaposi sarcoma

Name of Condition: Kaposi sarcoma Slide 57
Definition: Rare cancer of cells lining blood and lymph vessels, causing abnormal patches, spots, or lumps on skin, in the mouth, or in internal organs. Slide 57
Etiology (cause): HHV-8 (human herpesvirus 8) causes all forms, combined with a weakened immune system; host immune status shapes expression. Slides 57, 63
Epidemiology (who): Classic: older men. Endemic: young Black men in equatorial Africa. Iatrogenic: immunosuppressive therapy. Epidemic: HIV (human immunodeficiency virus), falling with antiretroviral therapy. Fifth form: HIV-negative men who have sex with men. Slide 63
Risk Factors: HIV (human immunodeficiency virus) immune deficiency; immunosuppressive therapy (transplant); age-related immune senescence; men who have sex with men. Slide 63
Pathology: Vascular-lining cell tumor; five clinical forms: classic (chronic), endemic (often aggressive), iatrogenic (may improve as immunosuppression is reduced), epidemic, fifth form (indolent). Biopsy shows HHV-8 (human herpesvirus 8)-associated findings. Slides 57, 63, 65
Clinical Manifestation: Red or purple macules, plaques, nodules on skin or mucosa; hard palate lesions common (oral exam essential); marked edema even with few lesions; gastrointestinal (often silent) and pulmonary (dyspnea, cough, hemoptysis); may worsen on starting antiretrovirals (immune reconstitution inflammatory syndrome). Slide 64
Diagnosis: Biopsy a representative lesion; HIV (human immunodeficiency virus) test, CD4 count, viral load; skin, oral, node, edema review; chest radiograph if pulmonary possible, bronchoscopy for suspected lung disease. Differential: bacillary angiomatosis, pyogenic granuloma. Slide 65
Treatment/Therapy: Epidemic: start/optimize antiretroviral therapy first. Iatrogenic: reduce immunosuppression (with transplant team). Classic: palliative intralesional vincristine, vinblastine, bleomycin, or radiation. Advanced: liposomal doxorubicin, paclitaxel. Slides 66–67
Mortality ★: Classic: usually indolent and rarely fatal; endemic, visceral, or immune reconstitution inflammatory syndrome disease can be aggressive and rapidly fatal. Slides 63, 67

Cutaneous T-cell lymphoma1 not covered

Name of Condition: Cutaneous T-cell lymphoma (also: mycosis fungoides) Slides 68–69
Definition: Rare non-Hodgkin lymphoma in which malignant T cells migrate to the skin, causing itchy, scaly patches, plaques, or tumors; may stay skin-confined for years or decades. Slides 68–69
Etiology (cause): No specific causative exposure is well defined. Slide 69
Epidemiology (who): Rare; no established incidence rate; nondescript patches may be present >10 years before histologic confirmation. Slides 68–69
Risk Factors: Not covered in the lecture
Pathology: Malignant T-cell skin infiltrates (localized or generalized) before any systemic spread; may progress to Sézary syndrome (erythroderma with circulating malignant T cells). Slide 69
Clinical Manifestation: Erythematous patches or scaly plaques on the trunk, often >5 cm, mimicking psoriasis, eczema, or tinea; itch out of proportion to inflammation; follicular involvement with hair loss is a clue; advanced: tumors, erythroderma, lymphadenopathy. Slides 68, 70
Diagnosis: Skin biopsy, often repeated (one nondiagnostic biopsy does not exclude it); advanced: CBC (complete blood count) with differential, circulating Sézary cells, T-cell gene rearrangement, flow cytometry; node staging. Slide 74
Treatment/Therapy: Stage-directed, skin-first: topical corticosteroids, topical mechlorethamine, bexarotene gel, UV (ultraviolet) phototherapy. Progressive: PUVA (psoralen plus ultraviolet A), methotrexate, photopheresis, systemic bexarotene, romidepsin/vorinostat, total-skin electron beam. Slide 75
Mortality ★: Survival not reduced in limited patch disease; tumors, erythroderma, nodes, and Sézary syndrome worsen prognosis; overly aggressive therapy may cause premature death. Slides 69, 75–76

Nail unit melanoma2 not covered

Name of Condition: Nail unit melanoma Slide 79
Definition: Rare acral melanoma of the nail unit, arising most often in the matrix. Slide 79
Etiology (cause): Not clearly UV (ultraviolet)-driven. Slide 79
Epidemiology (who): May occur in any skin tone; thumb and great toe are high-yield sites. Slide 79
Risk Factors: Not covered in the lecture
Pathology: Matrix tumors produce longitudinal nail-plate bands (melanonychia); delayed recognition leads to advanced-stage presentation; outcome driven by stage, Breslow thickness, ulceration, spread. Slides 78–79, 95
Clinical Manifestation: New or evolving longitudinal melanonychia in one digit: widening, irregular color/lines, proximal widening or triangular shape, blurred borders, dystrophy; Hutchinson sign (pigment extending onto the proximal nail fold); amelanotic form is red, pink, eroded. Slides 84–85
Diagnosis: Onychoscopy; urgent referral for nail-unit biopsy sampling the site of origin (often the matrix). Differential: subungual hematoma, benign longitudinal melanonychia. Slides 49, 78, 93, 95
Treatment/Therapy: Dermatology, nail surgery, surgical oncology; digit-sparing wide excision or Mohs with immunostaining; amputation only for deep, extensive, or bone-involving disease; staging per Breslow principles. Slide 94
Mortality ★: Not covered in the lecture

Nail unit squamous cell carcinoma1 not covered

Name of Condition: Nail unit squamous cell carcinoma (also: nail unit Bowen disease) Slide 79
Definition: Most common malignant nail tumor, including its in situ form (Bowen disease). Slide 79
Etiology (cause): Associated with high-risk HPV (human papillomavirus); periungual HPV-associated disease may be multifocal. Slide 79
Epidemiology (who): Most common malignant nail tumor; older age. Slide 79
Risk Factors: High-risk HPV (human papillomavirus), immunosuppression, chronic inflammation/trauma, prior radiation, older age. Slide 79
Pathology: May be multifocal; can invade bone of the distal phalanx. Slides 79, 94
Clinical Manifestation: Chronic unilateral verrucous periungual papule or plaque, subungual hyperkeratosis, onycholysis, oozing, bleeding, nail-plate destruction, longitudinal erythronychia, pain; often repeatedly labeled a wart, paronychia, or fungal infection. Slide 86
Diagnosis: Refer for biopsy of the site of origin; KOH (potassium hydroxide), fungal culture, or PAS (periodic acid–Schiff) to rule out onychomycosis (a positive result does not exclude cancer); radiography/MRI (magnetic resonance imaging) for bone extent. Slides 93, 95
Treatment/Therapy: Margin-controlled surgery: Mohs or wide excision (limited destruction recurs more); amputation only for bone invasion or uncleared disease; avoid repeated empiric wart/antifungal treatment. Slides 94–95
Mortality ★: Not covered in the lecture

Nail unit basal cell carcinoma5 not covered

Name of Condition: Nail unit basal cell carcinoma Slides 79, 82
Definition: Basal cell carcinoma of the nail fold or bed. Slides 79, 82
Etiology (cause): Not covered in the lecture
Epidemiology (who): Exceptionally uncommon. Slide 79
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Persistent ulcerated or pearly lesion of the nail fold or bed. Slide 79
Diagnosis: Prompt referral for nail-unit biopsy sampling the site of origin; persistent ulceration or bleeding is an urgent referral trigger. Slides 93, 95
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Glomus tumor3 not covered

Name of Condition: Glomus tumor Slides 86, 89
Definition: Rare benign growth from glomus bodies (tiny structures controlling blood flow and body temperature), most often under the fingernails or in fingertips. Slides 86, 89
Etiology (cause): Not covered in the lecture
Epidemiology (who): Rare; most common under the fingernails or in the fingertips. Slide 89
Risk Factors: Not covered in the lecture
Pathology: Benign nail-unit neoplasm that can mimic malignancy. Slide 79
Clinical Manifestation: Classic triad: severe paroxysmal pain, exquisite point tenderness, cold sensitivity; small red-blue subungual focus; nail may look nearly normal. Slide 86
Diagnosis: Triad strongly suggests it but does not replace imaging: ultrasound or MRI (magnetic resonance imaging) to localize an occult tumor. Slides 86, 93
Treatment/Therapy: Surgical removal when symptomatic; excellent outcome after complete removal. Slides 94–95
Mortality ★: Not covered in the lecture

Onychopapilloma / onychomatricoma6 not covered

Name of Condition: Onychopapilloma / onychomatricoma Slides 79, 87–88
Definition: Benign nail-unit tumors that can mimic malignancy. Slides 79, 87–88
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Single nail with longitudinal erythronychia or leukonychia, distal subungual hyperkeratosis, splinter hemorrhages, thickening, or localized plate abnormality. Slide 86
Diagnosis: Not covered in the lecture
Treatment/Therapy: Surgical removal when symptoms, growth, diagnostic uncertainty, or functional impairment justify it. Slide 94
Mortality ★: Not covered in the lecture

Acquired digital fibrokeratoma7 not covered

Name of Condition: Acquired digital fibrokeratoma Slide 79
Definition: Benign nail-unit neoplasm that can mimic malignancy. Slide 79
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Surgical removal when symptoms, growth, diagnostic uncertainty, or functional impairment justify it. Slide 94
Mortality ★: Not covered in the lecture

Pyogenic granuloma (nail unit)6 not covered

Name of Condition: Pyogenic granuloma (nail unit) Slides 79, 90
Definition: Non-cancerous, fast-growing red bump of abnormal blood vessels around the nail fold or under the nail plate. Slides 79, 90
Etiology (cause): Minor injury, ingrown nail, or irritation. Slide 90
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Rapidly growing, friable, bleeding papule; bleeds very easily. Slides 86, 90
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Digital myxoid cyst7 not covered

Name of Condition: Digital myxoid cyst Slides 79, 86
Definition: Benign nail-unit lesion arising near the DIP (distal interphalangeal) joint. Slides 79, 86
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Arises near the DIP (distal interphalangeal) joint; raised translucent area that can produce a longitudinal groove in the nail plate, sometimes with linear hemorrhages. Slides 86, 91
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Subungual exostosis3 not covered

Name of Condition: Subungual exostosis Slide 92
Definition: Non-cancerous bony growth or spur under the fingernail or toenail, most commonly the big toe. Slide 92
Etiology (cause): Past injury or constant pressure. Slide 92
Epidemiology (who): Most common on the big toe. Slide 92
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Firm, painful mass that elevates the nail plate. Slides 86, 92
Diagnosis: Plain radiography for a firm subungual mass. Slide 93
Treatment/Therapy: Surgical removal when symptoms or function justify it. Slide 94
Mortality ★: Not covered in the lecture