Dermatology Comparison Chart
Clinical Medicine and Surgery I · Exam 1 · Class of 2028
146 conditions across Lectures 2, 3, 4, 5, 6, 7, 8 and 9 · 143 images from the lecture slides · 2 sourced elsewhere and credited, for conditions the decks never illustrate
Use the Download as PDF button, top right, to keep this offline — it prints landscape with every row and every photograph intact.
How to use this. Read it left to right for one condition: what it looks like,
what it is called, the words a question will use to hand it to you, how it presents and how a patient
will actually describe it, what you order first and what confirms it, what you give first and what comes
next, and what you tell them. Read it top to bottom down one column to compare across conditions.
The gold “Vignette giveaway” column is the one to scan when a stem is in front of you. Professor Jaquith described this exam as “pretty much all clinical vignettes … make sure that you are able to recognize conditions by the vignette”, and a vignette gives itself away with a handful of words — coin-shaped, glazed appearing, tapioca-like, herald patch, spares the scrotum. Those words are in that column, per condition, so you can read the chart in the direction the question actually arrives: phrase first, diagnosis second. Every phrase there is language the lecture decks themselves use — classic buzzwords that are NOT in your decks are deliberately left out. Every fact here comes from the lecture PowerPoints, and every slide picture cites its deck and slide. Where a deck does not state something, the cell says so rather than being filled in from elsewhere. Two conditions the decks never illustrate — phytophotodermatitis and chronic paronychia — carry an openly licensed photograph from elsewhere, credited under the picture. Postherpetic neuralgia has no picture on purpose: it is pain after the rash has gone, so there is nothing to photograph.
The gold “Labs to order” block in the testing column tells you what blood work to send — and, just as often, that there is none to send. 111 of the 146 conditions here need no blood work at all; dermatology is mostly a clinical diagnosis, and knowing which ones are the exception is the point of reading down that column.
The gold “Vignette giveaway” column is the one to scan when a stem is in front of you. Professor Jaquith described this exam as “pretty much all clinical vignettes … make sure that you are able to recognize conditions by the vignette”, and a vignette gives itself away with a handful of words — coin-shaped, glazed appearing, tapioca-like, herald patch, spares the scrotum. Those words are in that column, per condition, so you can read the chart in the direction the question actually arrives: phrase first, diagnosis second. Every phrase there is language the lecture decks themselves use — classic buzzwords that are NOT in your decks are deliberately left out. Every fact here comes from the lecture PowerPoints, and every slide picture cites its deck and slide. Where a deck does not state something, the cell says so rather than being filled in from elsewhere. Two conditions the decks never illustrate — phytophotodermatitis and chronic paronychia — carry an openly licensed photograph from elsewhere, credited under the picture. Postherpetic neuralgia has no picture on purpose: it is pain after the rash has gone, so there is nothing to photograph.
The gold “Labs to order” block in the testing column tells you what blood work to send — and, just as often, that there is none to send. 111 of the 146 conditions here need no blood work at all; dermatology is mostly a clinical diagnosis, and knowing which ones are the exception is the point of reading down that column.
| Picture | Name | Vignette giveaway the words that hand it to you | Common manifestation and how a patient may describe it |
First test & gold standard | First line → second line treatment | Patient education |
|---|---|---|---|---|---|---|
| Lecture 2 · General Dermatology I — eczema and dermatitis | ||||||
 | Atopic dermatitis | FLEXURES in children and adults; cheeks and extensors in INFANTS · lichenification from chronic scratching · poorly demarcated · personal or family atopy | Chronic relapsing itchy eruption. Infants cheeks and extensors; children and adults the flexures. Poorly demarcated erythematous plaques with excoriation and lichenification. “It itches all the time and it keeps coming back — especially in the creases of my elbows and knees.” | Clinical diagnosis. Supported by family history, personal atopy, recurrent rash and raised immunoglobulin E (not routinely tested). No routine labs. Patch test if atypical, adult-onset or treatment-resistant. Biopsy if atypical or refractory. Culture purulent or crusted lesions; herpes simplex polymerase chain reaction for painful monomorphic erosions. Labs to orderNone routinely. Raised immunoglobulin E supports it but is not routinely tested. Culture purulent, pustular or crusted lesions; herpes simplex polymerase chain reaction for painful monomorphic erosions. | 1st: site-appropriate topical corticosteroid — low potency or non-steroid on the face, low to medium on the body, applied sparingly. Emollients throughout. 2nd: tacrolimus or pimecrolimus for sensitive areas; crisaborole; emollient wet wraps for severe flares; hydroxyzine or another antihistamine for itch. Severe: refer — phototherapy, systemic treatment. | Emollient after rinsing. Avoid irritants; fragrance-free skin care. Demonstrate quantity and correct application. Address steroid concerns directly. Written flare and infection action plan. Refer for uncertain diagnosis, moderate-to-severe disease or recurrent infection. Chronic and relapsing, but many improve with age. |
 | Dyshidrotic eczema | Tapioca-like deep-seated vesicles · palms, soles, sides of fingers | Deep-seated tapioca-like vesicles on the palms, soles and sides of the fingers. “I get these tiny deep blisters on my hands and they itch like mad.” | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | 1st: high-potency topical corticosteroid. 2nd: systemic corticosteroid in severe cases. | Avoid triggers and irritants — detergents, solvents, hair lotions or dyes, acidic foods. Lukewarm water and soap-free cleansers. Dry hands thoroughly. Emollient immediately after drying and as often as possible. |
 | Nummular eczema | COIN-SHAPED discrete plaques — the shape IS the diagnosis · extremities | Discrete coin-shaped plaques, often on the extremities and often in older adults. “I have round itchy patches, almost like coins, on my arms and legs.” | Clinical. Potassium hydroxide preparation if tinea corporis cannot be ruled out. Bacterial culture if lesions look secondarily infected. Patch testing if chronic or recurrent. Labs to orderNo bloods. Potassium hydroxide preparation if tinea cannot be ruled out; bacterial culture if secondarily infected; patch testing if chronic or recurrent. | 1st: medium to high potency topical corticosteroid for active lesions. 2nd: antihistamines for itch (hydroxyzine, diphenhydramine); treat secondary bacterial infection if present. | Emollients restore the barrier and prevent recurrence. |
 | Irritant contact dermatitis | Well demarcated and “GLAZED APPEARING” · shaped like the exposure · hands and forearms · frequent handwashing, gloves · no sensitization needed | The commonest form of contact dermatitis. Sharply demarcated in the shape and distribution of the exposure. “My hands are raw and cracked — I wash them all day at work.” | Clinical, from known irritant exposure with obvious demarcation and distribution. In insidious cases it becomes a diagnosis of exclusion. Labs to orderNone — clinical diagnosis from the exposure. | 1st: avoid the exposure and repair the barrier with emollients. 2nd: antihistamines for itch (hydroxyzine, diphenhydramine). | Sleep in cotton gloves after applying a heavy emollient such as petroleum jelly. |
 | Allergic contact dermatitis | LINEAR vesicles in MULTIPLE STAGES OF HEALING (urushiol / poison ivy) · well-demarcated at the contact site · needs prior sensitization | Well-demarcated rash at the site of contact. With urushiol sap (poison ivy) — linear vesicular lesions in multiple stages of healing with excoriation. “I got these streaks of blisters after I was clearing the yard.” | Clinical diagnosis from the history and the typical appearance. Patch testing identifies the allergen. Labs to orderNo bloods. Patch testing identifies the allergen. | 1st (limited): soothing measures — oatmeal baths, cool wet compresses, topical astringents — plus a high-potency topical steroid. 2nd (extensive): high-dose oral corticosteroid. | Identify and avoid the allergen. Expect lesions in multiple stages of healing at once. |
 | Seborrheic dermatitis | Greasy yellow scale · scalp, eyebrows, nasolabial folds, ears, central chest | Greasy yellow scale on erythema in sebum-rich sites — scalp, eyebrows, nasolabial folds, ears, central chest. “My scalp and the sides of my nose are flaky and greasy and it never fully goes away.” | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | 1st: topical antifungal — ketoconazole is the mainstay. Scalp: ketoconazole or selenium sulfide shampoo. Face: ketoconazole cream or lotion. 2nd: steroids early on to reduce the inflammatory response. | Chronic and relapsing, so repeated and long-term use of medication is often required. |
 | Perioral dermatitis | Papules around the mouth SPARING the vermilion border · after topical steroid on the face · burning | Burning with small erythematous papules around the mouth, sparing the vermilion border. Often follows topical corticosteroid use on the face. “I have a burning rash around my mouth — it started after I used a cream on my face.” | Clinical. Potassium hydroxide if tinea or Candida suspected. Bacterial culture if pustules, crusting or drainage. Patch testing if allergic contact dermatitis suspected. Biopsy if persistent, granulomatous or atypical. Labs to orderNo bloods. Potassium hydroxide if tinea or Candida suspected; bacterial culture if pustules, crusting or drainage; patch testing; biopsy if persistent or atypical. | 1st: stop facial topical corticosteroids — continued exposure perpetuates it. Stop non-essential cosmetics and occlusive moisturizers; simplify the routine. Mild disease: topical metronidazole, erythromycin, pimecrolimus or azelaic acid. 2nd: oral tetracycline or doxycycline for extensive or persistent disease. | Warn that the eruption may temporarily worsen after corticosteroid withdrawal — otherwise the patient restarts the steroid and the cycle continues. |
 | Diaper dermatitis | CONVEX surfaces of the napkin area, sparing the folds · once the FOLDS are involved with satellite lesions, it is candidal | Erythema on the convex surfaces of the napkin area. Fold involvement with satellite lesions suggests candidal overgrowth. “His bottom is red and sore where the nappy sits.” | Clinical. Potassium hydroxide if Candida suspected — budding yeast or pseudohyphae confirm it. Bacterial culture if purulence, bullae, crusting or perianal disease. Labs to orderNo bloods. Potassium hydroxide if Candida suspected; bacterial culture if purulence, bullae, crusting or perianal disease. | 1st: reduce moisture and irritant exposure — frequent changes, gentle cleansing, air exposure, superabsorbent nappies. Thick zinc oxide or petrolatum barrier at every change. 2nd: brief low-potency topical corticosteroid for significant inflammation; topical antifungal if candidal. | The whole previous barrier layer does not need scrubbing away if it is still clean. |
 | Stasis dermatitis | Gaiter region · bilateral · edema and chronic venous change · violaceous/gray/deep brown on darker skin | Pruritic erythematous, violaceous or hyperpigmented patches in the gaiter region, with edema and signs of chronic venous disease. Usually bilateral. “Both my ankles are swollen, itchy and discolored, and it has been going on for months.” On darker skin the erythema reads violaceous, gray or deep brown — palpate for warmth and edema. | Clinical — lower-leg dermatitis with edema and chronic venous disease. Ankle-brachial index or toe pressure before substantial compression, to clarify arterial status. Venous duplex ultrasound if reflux, obstruction or deep vein thrombosis suspected. Labs to orderNo bloods. Ankle-brachial index or toe pressure before compression; venous duplex ultrasound if reflux, obstruction or thrombosis suspected. | 1st: compression therapy is the cornerstone once arterial circulation is established. Leg elevation, walking, calf exercises, weight management, treat the underlying venous disease. Fragrance-free emollients. 2nd: short course of an appropriate topical corticosteroid for active inflammation. | Not cellulitis — bilateral, chronic, itchy and afebrile. Refer to dermatology, vascular surgery or wound care for refractory disease, venous reflux or ulceration. |
| Lecture 2 · Vesiculobullous, papulosquamous, alopecia and xerosis | ||||||
 | Bullous pemphigoid | TENSE bullae that do NOT rupture easily · Nikolsky NEGATIVE — the one of the three that is · elderly · mucosa uncommon | Elderly. Subepidermal split, so tense bullae that do not rupture easily. Nikolsky negative. Mucosal involvement uncommon. May begin with urticarial or edematous lesions before blistering. “I came up in big tight blisters that don't burst easily.” | Light microscopy — neutrophils aligned in a straight narrow row at the dermal-epidermal junction. Gold standard: biopsy lesional tissue for histopathology and perilesional tissue for direct immunofluorescence. Serum indirect immunofluorescence or ELISA identifies anti-basement membrane zone antibodies. Labs to orderSerum indirect immunofluorescence or ELISA for anti-basement membrane zone antibodies, alongside the biopsy and direct immunofluorescence. | 1st (mild): ultrapotent topical steroids. 1st (moderate-severe): oral prednisone or doxycycline. Dapsone is particularly effective with mucous membrane involvement. Low-dose methotrexate is safe and effective in the elderly — with folic acid. 2nd (refractory): methotrexate, azathioprine, biologics, intravenous immunoglobulin. | Better prognosis than pemphigus. |
 | Pemphigus (vulgaris) | FLACCID bullae that rupture, leaving erosions · MUCOSA often the FIRST site · middle-aged · Nikolsky positive — so is toxic epidermal necrolysis, so it does not separate them | Middle-aged. Intraepidermal split, so flaccid bullae that rupture easily leaving erosions. Nikolsky positive. Mucosal involvement common and often the first site. “My mouth is full of sores and the blisters on my skin burst as soon as they form.” | Gold standard: biopsy demonstrating acantholysis. Immunofluorescence studies and serum ELISA for pathogenic antibodies are confirmatory. Labs to orderSerum ELISA for pathogenic antibodies, plus immunofluorescence studies — both confirmatory after the biopsy. | Urgent treatment needed. 1st: rituximab, or high-dose oral prednisone. 2nd: steroid given with azathioprine or mycophenolate so the patient can be transitioned off. Antibiotics as needed. Supportive: cleansing baths, wet dressings, topical or intralesional glucocorticoids, correction of fluid and electrolyte imbalance. | Worse prognosis than bullous pemphigoid; frequently fatal before corticosteroids. |
 | Psoriasis — plaque | Thick SILVERY scale · Auspitz sign when the scale is lifted · EXTENSOR surfaces, scalp, nails · psoriatic arthritis goes with it | Well-demarcated plaques with thick silvery scale; Auspitz sign on removing scale. Extensor surfaces, scalp, nails. Psoriatic arthritis goes hand in hand with it. “Thick scaly patches on my elbows and knees that flake off.” | Generally clinical, though biopsy may be needed for definitive diagnosis. Labs to orderNone for diagnosis. Systemic agents carry their own monitoring — methotrexate always with folic acid. | 1st (mild): emollients, topical steroids, calcipotriene (vitamin D analog — quickest action, caution with nephrotoxicity), ultraviolet B phototherapy for smaller stubborn areas. 2nd: salicylic acid, coal tar. Moderate-severe or after failure: methotrexate (with folic acid), acitretin, apremilast, or a biologic — etanercept, infliximab, adalimumab, ixekizumab. | Chronic. Methotrexate always needs folic acid supplementation. |
 | Psoriasis — guttate | Drop-like small papules · widespread on the trunk | Numerous small drop-like papules, widespread over the trunk. “Hundreds of little scaly spots came up all over my back.” | Clinical, as above. Labs to orderNone — clinical diagnosis. | No treatment needed, though phototherapy and topical steroids may be used. | Distinct from plaque psoriasis in its management — the default is observation. |
 | Psoriasis — pustular | Sterile pustules · palms and soles | Sterile pustules, often on palms and soles. “My palms and soles have come up in little pus-filled spots.” | Clinical, as above. Labs to orderNone for diagnosis. Acitretin is contraindicated in pregnancy, so establish pregnancy status before prescribing. | 1st: acitretin (contraindicated in pregnancy) or methotrexate. If pregnant: high-potency topical steroids. | Pregnancy changes the treatment entirely — ask before prescribing. |
 | Pityriasis rosea | HERALD PATCH alone for a week or two BEFORE the rest · Christmas-tree pattern along skin lines · collarette of SCALE | Herald patch first — one large salmon-colored oval, present a week or two alone — then smaller ovals with a collarette of scale in a Christmas-tree pattern along the skin lines. “I had one big patch, then a week later my whole trunk broke out.” Darker skin: post-inflammatory hyperpigmentation for several months. | Clinical, on the herald patch and the typical pattern. Labs to orderNone — clinical, on the herald patch and the pattern. | 1st: self-limited — reassurance. Oral antihistamines and/or cautious topical steroids for itch. 2nd: ultraviolet B phototherapy or natural sunlight if begun in the first week. Aciclovir for severe cases. | Resolves over about six weeks. The herald patch is what separates it from hives, which appear all at once. |
 | Lichen planus | The six Ps — purple, polygonal, pruritic, planar papules and plaques · Wickham striae · flexor wrists, oral mucosa | The six Ps — purple, polygonal, pruritic, planar papules and plaques, shiny, with Wickham striae. Flexor wrists, ankles, oral mucosa. Genital involvement in both sexes. “Itchy purple flat-topped bumps on my wrists, and my mouth feels raw.” | Biopsy — band-like infiltration of lymphocytes in the dermis. Also hyperkeratosis without parakeratosis, basal vacuolisation, Civatte bodies, saw-tooth rete ridges. Labs to orderNo bloods. Biopsy is the test. | 1st: superpotent topical steroids. 2nd: topical tacrolimus for oral and vaginal disease; oral steroids in severe cases; PUVA or phototherapy in refractory cases. | Certain medications produce lichenoid reactions — take a drug history. |
 | Lichen simplex chronicus | Accentuated skin markings in a thickened plaque · wherever the patient can reach · itch-scratch cycle | Thickened lichenified plaque with accentuated skin markings, wherever the patient can reach to scratch. Sustained by the itch-scratch cycle. “I scratch it without thinking, especially at night, and now the skin has gone thick and leathery.” | Clinical. Biopsy atypical, unilateral, nodular, ulcerated or treatment-resistant plaques to exclude neoplasia. Generalized or unexplained pruritus → targeted systemic evaluation. Labs to orderNone for the plaque itself. Generalized or unexplained pruritus triggers a targeted systemic evaluation guided by history, medications and review of systems. | 1st: break the itch-scratch cycle — education, treat the trigger, emollients, behavioral substitution, nail care, safe physical occlusion. Appropriate potent topical corticosteroid for a limited course. 2nd: calcineurin inhibitor for sensitive sites or maintenance. | Address sleep, anxiety, neuropathic symptoms and the primary dermatosis. Recurrence is common unless the initiating itch is controlled. |
 | Alopecia areata | Exclamation point hairs · discrete smooth round patches · non-scarring | Discrete smooth round patches of complete hair loss, with exclamation point hairs at the edge. Non-scarring. “A round bald patch appeared out of nowhere.” | Clinical, strengthened by dermoscopy — yellow dots, black dots, broken hairs, tapered hairs, short regrowth. Scalp biopsy for scarring alopecia, diffuse atypical loss, or persisting uncertainty. Labs to orderNone — clinical with dermoscopy; scalp biopsy only if scarring, diffuse atypical loss or persisting uncertainty. | 1st (adolescents and adults): intralesional steroids. 1st (children 10 and under): topical steroids. | Psychological support is one of the most important factors. Support groups may be offered. |
 | Androgenetic alopecia | Follicular miniaturisation · temporal recession and vertex in men, widened part in women · non-scarring | Gradual thinning from follicular miniaturisation — temporal recession and vertex in men, widened part in women. Non-scarring. “My hair has been thinning slowly for years.” | Clinical, from history and examination, though additional testing can exclude other causes of alopecia. Labs to orderNone routinely. Additional testing can be done to exclude other causes of alopecia. | Male-pattern: topical minoxidil (mainly effective at the crown); oral finasteride, a 5-alpha-reductase type 2 inhibitor. Works best in combination. Female-pattern: treatments are limited; oral antiandrogens. | About 2% of men on finasteride report reduced libido and erectile function — reversible on stopping. Finasteride is not indicated in women and is contraindicated in pregnancy. |
 | Xeroderma (xerosis) | Dry, rough, cracked · worse in winter · shins and forearms | Dry, rough, cracked skin, worse in winter, typically shins and forearms. “My skin is so dry it cracks and stings.” | Clinical. Labs to orderNone — clinical diagnosis. | 1st: short lukewarm showers, gentle fragrance-free cleanser only where needed, thick ointment or cream within minutes of bathing. 2nd: petrolatum, ceramide-containing products, humectants such as urea or lactic acid. | Keratolytics may sting fissured skin. Most improve with consistent barrier care, but recurrence is expected while environmental exposure, aging or systemic risk persists. |
| Lecture 3 · Dermatology II — reactive and immune-mediated | ||||||
 | Erythema multiforme | Target lesion with THREE concentric zones · acral, starting on the extremities | Target lesions with three concentric zones — central dusky or necrotic area, pale edematous ring, outer erythematous rim. Acral distribution, beginning on the extremities. “I have these bullseye-looking spots on my hands and arms.” | Clinical diagnosis; biopsy if uncertain. Herpes simplex polymerase chain reaction, Mycoplasma serology. If erythema multiforme major or systemic concern: complete blood count, comprehensive metabolic panel, liver function tests. Labs to orderComplete blood count, comprehensive metabolic panel and liver function tests if erythema multiforme major or systemic involvement is a concern. Herpes simplex polymerase chain reaction; Mycoplasma serology / immunoglobulin M. | 1st: supportive — analgesia, antihistamines, wound care. Discontinue the offending drug immediately. Topical corticosteroids for localized lesions. Oral aciclovir or valaciclovir if herpes-triggered. 2nd (recurrent): suppressive antiviral therapy, aciclovir 400 mg twice daily. | Herpes simplex virus triggers over 50% of cases. Hospitalize if erythema multiforme major with poor oral intake or extensive mucosal disease. |
 | Dermatitis herpetiformis | Intensely pruritic · symmetrical knees, elbows, buttocks, back · herpetiform grouping · bloating and diarrhea | Intensely pruritic papules, vesicles and urticarial plaques, symmetrically on knees, elbows, buttocks and back, grouped in a herpetiform pattern. Often bloating and diarrhea. “Unbelievably itchy blisters on my elbows and knees, both sides, and my stomach has been off.” | Gold standard: perilesional direct immunofluorescence — granular immunoglobulin A at the dermal papillae. Also immunoglobulin A anti-tissue transglutaminase, anti-endomysial antibody, small bowel biopsy. She flagged this in class: most of this block is clinical diagnosis, so a disease with a distinctive test is high-yield. Labs to orderImmunoglobulin A anti-tissue transglutaminase and anti-endomysial antibody, plus small bowel biopsy. Screen thyroid function given the association. | 1st: dapsone for rapid symptom control. Cornerstone: a strict lifelong gluten-free diet, which is what allows dapsone to be reduced or stopped over one to two years. | Screen every patient for celiac disease. Also autoimmune thyroid disease and T-cell lymphoma. Rare — 11 to 75 per 100,000, northern European descent, ages 30 to 40. |
 | Acanthosis nigricans | Velvety hyperpigmented thickening · neck, axillae, groin | Velvety hyperpigmented thickening of flexural skin — neck, axillae, groin. “The skin on my neck has gone dark and velvety and it won't wash off.” | Clinical diagnosis. Then hemoglobin A1c, fasting insulin, lipid panel, polycystic ovarian syndrome workup. Labs to orderHemoglobin A1c, fasting insulin and a lipid panel, plus a polycystic ovarian syndrome workup. | 1st: treat the underlying cause — insulin resistance. 5 to 10% weight loss improves it. Metformin. 2nd: topical retinoids for cosmetic improvement. | A metabolic warning sign, not a hygiene problem. Sudden onset in an adult → urgent evaluation for gastrointestinal malignancy, especially gastric adenocarcinoma. |
 | Epidermolysis bullosa | Blistering from minimal trauma · at or shortly after birth · structural protein mutation | Blistering and skin fragility from minimal trauma, evident at or shortly after birth. Caused by a mutation in structural proteins. “His skin blisters and tears wherever he is handled.” | Gold standard: transmission electron microscopy with immunofluorescence antigen mapping. Supported by a genetic panel and nutritional labs. Labs to orderGenetic panel and nutritional labs, alongside the electron microscopy and antigen mapping. | Supportive. Wound care, nutrition, infection control, pain management. | Referral to essentially every specialty given the multisystem burden. Early palliative care integration, genetics counseling and family support in severe forms such as Herlitz junctional disease. |
 | Urticaria | An individual wheal resolves within 24 hours · blanches fully · migrates · ± angioedema | Transient pruritic wheals, with or without angioedema. An individual wheal resolves within 24 hours, blanches fully and migrates. “Itchy welts come up and move around, and each one is gone by the next day.” | Clinical. Biopsy if lesions persist beyond 24 hours — that suggests urticarial vasculitis. Thyroid-stimulating hormone, complement C4, tryptase, specific immunoglobulin E. Labs to orderThyroid-stimulating hormone, complement C4, serum tryptase and specific immunoglobulin E. | 1st: second-generation antihistamine — cetirizine, loratadine, fexofenadine. Short oral prednisone 40–60 mg for 5 days in severe acute disease. Intramuscular epinephrine 0.3 mg immediately for anaphylaxis. 2nd (chronic): scheduled non-sedating antihistamine up to 4× standard dose; add an H2 blocker; then omalizumab 300 mg every 4 weeks; ciclosporin. | Acute versus chronic is defined at six weeks. About half of chronic urticaria resolves within a year, and over half of cases have no identifiable trigger. |
 | Erythema nodosum | Tender nodules, bilateral anterior shins, that do NOT ulcerate · preceded by fever and arthralgia | Tender erythematous nodules, bilateral on the anterior shins, that do not ulcerate. The commonest panniculitis. Often preceded by fever and arthralgia. “Painful red lumps came up on both my shins and I ached all over first.” | Clinical; deep incisional biopsy if atypical (septal panniculitis without vasculitis). Antistreptolysin O titre, chest radiograph, tuberculin or interferon gamma test, inflammatory markers, colonoscopy, pregnancy test where relevant. Labs to orderAntistreptolysin O titre, inflammatory markers, chest radiograph, tuberculin or interferon gamma release assay; colonoscopy; pregnancy test where relevant. | 1st: rest, leg elevation, compression stockings, a nonsteroidal anti-inflammatory drug. 2nd: potassium iodide for idiopathic and recurrent disease; short corticosteroid course once infection is excluded. | It is a reaction pattern, not an isolated disease — identifying and treating the trigger is the point. Löfgren syndrome (with ankle arthritis and hilar nodes) has the best sarcoid prognosis, over 90% remitting. |
 | Granuloma annulare | Annular ring of papules with NO SCALE ANYWHERE — that absence separates it from tinea · dorsal hands and feet · flesh-colored | Annular ring of flesh-colored or erythematous papules, commonly dorsal hands and feet. No scale on the border — which is what separates it from tinea. “A ring of little bumps on the back of my hand. It doesn't itch.” | Clinical; biopsy for confirmation shows palisading granulomas with central necrobiosis and mucin. Labs to orderScreen for diabetes (hemoglobin A1c), thyroid disease and dyslipidemia — and in generalized disease in an adult over fifty, workup for lymphoma. | Localized: benign and self-limiting — treat for cosmesis or discomfort. Intralesional or topical corticosteroid. Generalized: phototherapy or systemic therapy via dermatology. | Localized disease is benign and about half resolve within two years; no malignant potential. Generalized disease in an adult over fifty → screen for diabetes, thyroid disease, dyslipidemia and lymphoma. |
 | Pyoderma gangrenosum | Undermined violaceous border · rapidly expanding painful ulcer from a pustule · pathergy — worsens with trauma | Rapidly expanding painful ulcer with an undermined violaceous border, beginning as a pustule or nodule. Lower extremities most common. Pathergy — it worsens with trauma. “A small spot turned into a big painful ulcer within days, and it got worse after they cleaned it out.” | A diagnosis of exclusion — no gold standard test. Biopsy the ulcer EDGE and take wound cultures to exclude malignancy and infection. Serum protein electrophoresis, antineutrophil cytoplasmic and antinuclear antibodies, colonoscopy. Labs to orderSerum protein electrophoresis, antineutrophil cytoplasmic and antinuclear antibodies, inflammatory markers; colonoscopy. Wound cultures to exclude infection. | Wound care (critical): avoid debridement — pathergy worsens the ulcer. Moist dressings, non-adherent contact layers. Topical tacrolimus or clobetasol to the wound edges for pain. 1st systemic: prednisone 0.5–1 mg/kg/day for acute rapid progression, or ciclosporin 3–5 mg/kg/day. 2nd: infliximab 5 mg/kg — approved with inflammatory bowel disease. | Do not debride. Screen for inflammatory bowel disease (25–50%), hematologic malignancy, monoclonal gammopathy, rheumatoid arthritis. The bullous variant associates with acute myeloid leukemia. |
 | Acne rosacea | Central facial erythema, flushing, telangiectasias · NO COMEDONES — which separates it from acne vulgaris | Persistent central facial erythema with flushing and telangiectasias, and no comedones — which is what separates it from acne vulgaris. Four subtypes: erythematotelangiectatic (commonest), papulopustular, phymatous, ocular. “My face goes red and burns, especially with wine or hot drinks.” | Clinical. Antinuclear antibody if lupus is a consideration — it helps rule out autoimmune disease; a positive result only means more testing is needed. Labs to orderAntinuclear antibody only if lupus is a consideration — it helps rule autoimmune disease OUT; a positive result means more testing, not a diagnosis. | 1st: topical metronidazole. Alternative: azelaic acid — effective but more drying, and these patients already have an impaired barrier. Ivermectin 1% cream is superior where there is a Demodex burden. Brimonidine for erythema. Sub-antimicrobial doxycycline; isotretinoin for refractory disease. | Chronic — therapy controls rather than cures. Trigger diary, gentle non-irritating skincare, daily sun protection. Ocular rosacea with visual symptoms → urgent ophthalmology. |
 | Hyperhidrosis | Absent during sleep & bilateral focal (palms, soles, axillae) = primary · generalized, asymmetric or nocturnal = secondary | Primary focal: bilateral, focal (palms, soles, axillae), adolescent onset, absent during sleep. Secondary: generalized, may be asymmetric, can occur at night. “My hands drip so much I smudge everything I write.” | Clinical + Hyperhidrosis Disease Severity Score. Minor's starch-iodine test maps the distribution; gravimetric measurement quantifies it. Generalized or nocturnal → secondary workup: 24-hour urine metanephrines and catecholamines, thyroid-stimulating hormone. Labs to orderOnly in suspected SECONDARY disease — generalized or nocturnal sweating: 24-hour urine metanephrines and catecholamines, thyroid-stimulating hormone, glucose. | 1st: aluminum chloride topically at night. 2nd: glycopyrronium 2.4% cloth once daily (axillary), or an oral anticholinergic. 3rd: botulinum toxin A; microwave thermolysis. Last resort: endoscopic thoracic sympathectomy for refractory palmar disease. | It is a medical condition, not poor hygiene or anxiety. Quality-of-life impairment is comparable to severe psoriasis. Botulinum toxin lasts 3–6 months and needs repeating; it can be cost-prohibitive. Moisture-wicking clothing; set realistic expectations. |
| Lecture 3 · Severe drug reactions and photodermatology | ||||||
 | Stevens-Johnson syndrome | Prodrome 1–3 days before the skin · mucosal erosions at 2+ sites · painful · <10% body surface | Prodrome of fever, malaise and upper respiratory symptoms 1–3 days before the skin findings. Painful erythematous macules and target lesions starting on the trunk. Mucosal erosions — oral, ocular, genital — in over 90%. Nikolsky positive. Epidermal detachment under 10% body surface. “I had flu symptoms, then my mouth and eyes became raw and my skin started peeling.” | Pathognomonic: punch biopsy showing full-thickness epidermal necrosis with dermal-epidermal junction separation. Complete blood count, metabolic panel, liver function, urea and creatinine. Blood cultures if secondary infection suspected. Chest radiograph. Ophthalmology with slit-lamp. SCORTEN scoring. Labs to orderComplete blood count, comprehensive metabolic panel, liver function tests, urea and creatinine. Blood cultures if secondary infection suspected. Chest radiograph. | 1st and most important: withdraw the causative drug immediately — earlier withdrawal is strongly associated with improved survival. Burn unit or intensive care. Aggressive fluids, temperature control, non-adhesive dressings, nasogastric nutrition, infection surveillance. Avoid silver sulfadiazine (sulfonamide cross-reaction). Antibiotic prophylaxis is NOT recommended. 2nd: intravenous immunoglobulin 1 g/kg/day ×3 or ciclosporin 3–5 mg/kg/day; etanercept emerging. | 1–7 per million per year — uncommon but deadly, so it has to be known. Culprits: aromatic anticonvulsants, sulfonamides, allopurinol, oxicam nonsteroidals, nevirapine. Lifelong avoidance of the drug class, medical alert bracelet, counsel first-degree relatives on shared genetic risk (HLA-B*15:02 with carbamazepine, HLA-B*58:01 with allopurinol). |
 | Toxic epidermal necrolysis | >30% body surface DETACHMENT · “wet parchment” · drug and prodrome 1–3 days before · Nikolsky positive — shared with pemphigus; the body-surface figure is what separates them | The same spectrum, at its severe end. High fever, stinging eyes, painful swallowing 1–3 days before. Painful erythema → flaccid bullae → confluent detachment over 30% body surface, Nikolsky positive, “wet parchment”. Mucosal erosions nearly universal. “My skin is coming off in sheets.” | As for Stevens-Johnson syndrome. SCORTEN within 24 hours of admission and repeated on day 3 — age over 40, malignancy, heart rate over 120, detachment over 10%, urea over 28 mg/dL, bicarbonate under 20 mEq/L, glucose over 252 mg/dL. Score 5+ → 90% predicted mortality. Labs to orderThe same, plus the SCORTEN variables: urea, bicarbonate and glucose, with heart rate and detachment area, within 24 hours and repeated day 3. | Burn unit or intensive care admission is mandatory. Immediate withdrawal of all suspect drugs. Fluid resuscitation as for major burns. Non-adhesive biological dressings. Early enteral feeding. 1st drug: ciclosporin 3–5 mg/kg/day — strongest current evidence, early initiation preferred. 2nd: intravenous immunoglobulin, etanercept. Opioids and gabapentin for pain. | Mortality 30–35%. Antibiotic prophylaxis is NOT recommended — treat infections when confirmed. Palliative care involvement at SCORTEN 5 or more. Survivors face sicca syndrome, lung disease and psychological trauma. |
 | Sunburn | Onset 3–5 hours after exposure, peaking at 12–24 · blistering = second degree | First degree: erythema, warmth, tenderness, no blistering, resolving in 3–5 days with desquamation. Second degree: blistering, intense pain, edema, 1–2 weeks. Onset 3–5 hours after exposure, peaking at 12–24 hours. “Sun poisoning” — fever, chills, nausea, dehydration — with large body surface involvement. | Clinical. Labs to orderNone — clinical diagnosis. | 1st: cool compresses and cool (not cold) water immersion. Nonsteroidal anti-inflammatory drugs started early reduce prostaglandin-mediated pain. Oral hydration; intravenous fluids if severe. 2nd: topical moisturizers — aloe vera, soy — soothing but do not alter healing. Topical steroid has limited evidence, possibly if within 6 hours. | Do not pop blisters — intact blisters are protective. Hospitalize for severe blistering over 20% body surface, systemic toxicity, or extremes of age. Broad-spectrum SPF 30+, reapply every 2 hours; avoid 10 AM–4 PM; tanning beds are Group 1 carcinogens. |
 | Drug-induced photosensitivity | First exposure, dose-dependent, exaggerated sunburn on exposed skin = phototoxic · needs sensitization, eczematous, may spread = photoallergic | Phototoxicity: non-immunologic, dose-dependent, occurs on first exposure, within hours, looks like an exaggerated sunburn confined to exposed skin. Photoallergy: immunologic type IV, dose-independent, needs sensitization, eczematous and pruritic, extends beyond sun-exposed skin, can persist after the drug stops. “I burned badly after barely any sun since starting that antibiotic.” | Thorough drug history including over-the-counter and topical products. Phototesting — minimal erythema dose to ultraviolet A and B before and after drug withdrawal. Gold standard for photoallergy: photopatch testing — duplicate sets, one irradiated with ultraviolet A at 5 J/cm². Reaction on the irradiated patch only = photoallergy; both = contact allergy. Labs to orderNo bloods. Phototesting (minimal erythema dose) and photopatch testing are the investigations. | 1st: identify and discontinue or substitute the offending agent where feasible. Strict photoprotection — SPF 50+ broad-spectrum, physical blockers (zinc oxide, titanium dioxide). 2nd: phototoxicity — supportive care. Photoallergy — topical or short systemic corticosteroid, antihistamine. Persistent light reaction — narrowband ultraviolet B desensitization. | Phototoxic drugs: tetracyclines (especially doxycycline), fluoroquinolones, amiodarone, thiazides, furosemide, voriconazole, nonsteroidals, psoralens, St John's Wort. Photoallergic: sunscreen chemicals (oxybenzone), sulfonamides, topical antihistamines, phenothiazines. Avoid medication during peak sun hours. |
 | Photodermatitis (phytophotodermatitis) | Linear or streaked hyperpigmentation · lime juice and sun — “margarita dermatitis” · celery, parsley, fig | Furanocoumarins from limes, celery, parsley, wild parsnip or fig plus ultraviolet A. Linear or streaked hyperpigmentation after lime juice and sun — “margarita dermatitis”. Painful blistering in the acute phase. Berloque dermatitis: drip-pattern hyperpigmentation on the neck from bergamot oil. Chronic actinic dermatitis: persistent eczematous eruption in chronically exposed skin in older males. | Detailed exposure history — plants, topicals, fragrances, medications. Photopatch testing for photocontact allergy. Antinuclear antibody panel if lupus suspected. Biopsy if uncertain. Photodermatitis spares the nasolabial folds; seborrheic dermatitis involves them. Labs to orderAntinuclear antibody panel if lupus is suspected. Otherwise exposure history and photopatch testing. | 1st: avoid the contactant and ultraviolet exposure concurrently. Acute blistering — cool compresses, wound care, mid-potency topical corticosteroid. 2nd: hyperpigmentation — reassurance, it fades over months; hydroquinone or azelaic acid if persistent. Chronic actinic dermatitis — potent steroids, tacrolimus, hydroxychloroquine, narrowband ultraviolet B or PUVA, azathioprine. | Recognize photosensitising plants, especially in landscaping, gardening and food preparation. Wash skin immediately after plant contact before sun exposure. Year-round sun protection prevents the pigment darkening further. |
 | Polymorphous light eruption | 30 minutes to hours after ultraviolet · first sunny days of spring · décolletage, forearms, dorsal hands | The commonest idiopathic photodermatosis (10–20% of the population). 2–5 mm erythematous papules on décolletage, forearms and dorsal hands, appearing 30 minutes to hours after ultraviolet exposure, in the first sunny days of spring. Spares chronically exposed areas. Resolves in 7–10 days without scarring; “hardening” by late summer. “Every spring the first proper sun brings out an itchy rash, and it settles by July.” | Largely clinical — history and morphology. Antinuclear antibody panel is MANDATORY to exclude lupus, especially anti-Ro/SSA and anti-La/SSB. Phototesting reproduces the eruption in 50–60%. Biopsy shows a perivascular lymphocytic infiltrate with dermal edema — supportive, not pathognomonic. Labs to orderAntinuclear antibody panel is MANDATORY to exclude lupus, especially anti-Ro/SSA and anti-La/SSB. Porphyrin screen (urine, stool, red cell) if erythropoietic protoporphyria is suspected. | 1st (acute): avoid further ultraviolet exposure, cool compresses, moderate-potency topical corticosteroid, oral antihistamine. Short prednisolone 0.5 mg/kg/day ×4–5 days for severe episodes. 1st (preventive): prophylactic narrowband ultraviolet B, 3×/week for 5 weeks in spring — induces tolerance and is the most effective preventive strategy. 2nd: hydroxychloroquine 200 mg twice daily for refractory cases. | Broad-spectrum SPF 50+ including ultraviolet A blockers. Recurs each spring and often improves with summer hardening. Strong hereditary component — up to 50% family concordance. |
 | Solar lentigo also Lecture 8 | Well-defined but irregular borders that coalesce at sites of severe sunburn · 90% of people by 50 | Well-defined light-to-dark brown macules with irregular borders that coalesce at sites of severe sunburn, from under 1 mm to several centimeters, on chronically exposed skin. 90% of people by age 50. “Age spots on the backs of my hands and my shoulders.” | Dermoscopy — finger-like projections and a “moth-eaten” border. Biopsy if atypical or uncertain on dermoscopy, to exclude lentigo maligna (asymmetric, irregular border and color, structureless pigment). Reflectance confocal microscopy where biopsy is deferred. Labs to orderNone — dermoscopy, with biopsy only if atypical. | Treatment is not necessary. Cosmetic removal by preference: 1st: cryotherapy (5–10 second freeze), or quality-switched Nd:YAG, intense pulsed light or fractional laser. 2nd: topical hydroquinone 2–4%, azelaic acid, kojic acid, retinoids, tranexamic acid — slower but less post-procedure pigmentation risk. Chemical peels. | Benign, but monitor for change. Daily SPF 30+ prevents new lesions. Annual full-body skin examination. Associated with actinic keratosis, squamous and basal cell carcinoma, and melanoma — it marks cumulative sun damage. Over time may progress into lichenoid keratoses. |
 | Actinic keratosis | “Sandpaper” texture — felt before it is seen · sun-exposed face, scalp, dorsal hands | Rough, scaly, erythematous papules and plaques on sun-exposed skin — face, scalp, dorsal hands, forearms. Skin-colored to red-brown, “sandpaper” texture on palpation, typically 2–10 mm. “Rough scaly spots I can feel better than I can see.” | Clinical. Biopsy if indurated, ulcerated, tender or bleeding — concerning for invasive squamous cell carcinoma. Labs to orderNone — clinical, with biopsy for concerning features. | 1st (lesion-directed): cryotherapy, 2–3 freeze-thaw cycles — standard of care for isolated lesions. Shave excision or curettage with electrodessication. 1st (field-directed, for multiple or confluent): 5-fluorouracil 5% for 2–4 weeks; imiquimod 3.75% or 5% twice weekly ×16 weeks; photodynamic therapy; tirbanibulin 1%; diclofenac 3% gel for mild disease. | Field cancerization — the clinically normal skin around a lesion already carries mutations, which is why confluent disease gets field therapy. 0.025–16% annual transformation risk per lesion. Organ transplant recipients carry 65× the risk. Hypertrophic lesions have higher malignant potential. |
 | Dermatoheliosis (photoaging) | Cutis rhomboidalis nuchae on the posterior neck · leathery, mottled dyspigmentation · sun-protected skin looks far younger | Coarse deep wrinkles, leathery rough texture, mottled dyspigmentation, telangiectasias, persistent erythema. Cutis rhomboidalis nuchae on the posterior neck is the classic marker of severe photoaging. Sun-protected skin looks far younger. “One side of my face looks a decade older — the side that was by the car window.” | Clinical — chronic sun exposure with the characteristic distribution. Biopsy confirms solar elastosis, the hallmark. Dermoscopy for individual lesions. Ultraviolet photography quantifies subclinical damage. Genetic testing if xeroderma pigmentosum suspected. Annual full-body skin examination. Labs to orderNone routinely. Genetic testing and a DNA repair assay only if xeroderma pigmentosum is suspected. | 1st: tretinoin 0.025–0.1% — the only agent approved by the Food and Drug Administration for photoaging. Start low, titrate; expect initial retinoid dermatitis; minimum 6–12 months for visible results. 2nd: vitamin C 10–20%, niacinamide, hydroquinone 2–4%, azelaic/kojic/tranexamic acid. Chemical peels, ablative or non-ablative laser resurfacing, intense pulsed light, radiofrequency, microneedling. | Broad-spectrum SPF 30+ daily is the single most evidence-supported intervention. Apply as the last skincare step before makeup, 2 mg/cm² (about a teaspoon for face and neck), reapply every 2 hours. Largely preventable; established change can still be meaningfully improved. Tanning is not healthy — a tan is a UV injury response. |
| Lecture 4 · Cutaneous Bacterial Infections | ||||||
 | Acne vulgaris | COMEDONES are the hallmark — open (blackheads) and closed (whiteheads) · systemic symptoms absent | Polymorphic. Comedones are the hallmark — open (blackheads) and closed (whiteheads), non-inflammatory — plus inflammatory papules, pustules and nodules. Face, neck, chest, upper back, upper arms. Systemic symptoms absent. “Spots that keep coming, and they flare before my period.” | Clinical. Culture only if there is no response to treatment. Pre-treatment assessment: type and severity, skin type, scarring, menstrual and hyperandrogenism history, current regimen, psychological impact. Labs to orderNone — clinical. Culture only if there is no response to treatment. Isotretinoin requires pregnancy tests before, monthly during, and 5 weeks after. | Comedonal: topical retinoid (adapalene, tazarotene, tretinoin); azelaic or salicylic acid if not tolerated. Mild papulopustular: topical antimicrobial + retinoid, or benzoyl peroxide + topical antibiotic. Moderate: topical retinoid + oral antibiotic (doxycycline, minocycline; sarecycline; erythromycin if tetracycline contraindicated) + benzoyl peroxide. Severe nodular: the same triple, or oral isotretinoin monotherapy, 16–20 weeks. Hormonal: combined oral contraceptive for hyperandrogenism or unresponsive disease. | Benzoyl peroxide with every antibiotic to cut resistance; oral courses 3–4 months only. Separate tretinoin and benzoyl peroxide by 3+ hours. Wash no more than twice daily, gentle cleanser, warm not hot water. Non-comedogenic products. Improvement takes 4–6 weeks; back and chest 3–4 months. Isotretinoin: pregnancy tests before, monthly, and 5 weeks after; iPledge; one month dispensed at a time; two forms of contraception; no blood donation. |
 | Folliculitis | Each papule or pustule pierced by a central hair · abrupt, afebrile | Small papules or pustules on an erythematous base, each pierced by a central hair. Scalp, thighs, trunk, axilla, inguinal area. Abrupt eruption, afebrile, no systemic involvement. “Little pimples with a hair coming out of the middle.” | History and clinical manifestations. Resistant cases: culture and Gram stain from an unroofed pustule; potassium hydroxide wet mount using a plucked hair to exclude dermatophyte folliculitis; nasal swab of patient and family for Staphylococcus aureus colonization; biopsy. Labs to orderNo bloods. Culture and Gram stain of unroofed pustule material; potassium hydroxide on a plucked hair; nasal swab for staphylococcal carriage. | 1st: moist heat, antibacterial soaps, good glycemic control, good skin hygiene, loose clean clothing. Mild infection — topical mupirocin, clindamycin or erythromycin. Recurrent (carrier state): mupirocin ointment in the nasal vestibule twice daily ×5 days. Extensive: oral cephalexin or dicloxacillin. If MRSA: trimethoprim-sulfamethoxazole, clindamycin, doxycycline or linezolid (the slide also lists ciprofloxacin, but fluoroquinolones are not reliable against MRSA). | Instruct the patient not to squeeze pustules. Superficial pustules rupture and drain spontaneously; deep lesions may be incised and drained. Risk factors: obesity, poor hygiene, occlusive clothing, heat and humidity, immunocompromise, corticosteroids, diabetes, nasal carriage. |
 | Pseudomonas (“hot tub”) folliculitis | 8 hours to 5 days after a hot tub · trunk, extremities, buttocks · spares face, neck, palms, soles | Follicular papules, vesicles and pustules that can crust, primarily on trunk, extremities and buttocks, sparing face, neck, soles and palms. Onset 8 hours to 5 days after exposure. Pruritic or tender. “A day after the hot tub I broke out in an itchy rash everywhere my swimsuit covered.” | Usually clinical. Bacterial culture from a pustule or a sample of the contaminated water if unclear or treatment-resistant. Labs to orderNone usually. Bacterial culture from a pustule or the contaminated water if unclear or resistant. | 1st: most cases resolve without specific treatment, clearing in 2–10 days. Dilute acetic acid 5% wet dressing — 3 tablespoons in a pint of water, 20 minutes, 2–4× daily. 2nd: ciprofloxacin for widespread or resistant cases. | Showering after contact does NOT prevent infection. Continuous water filtration to remove dead skin, frequent monitoring of chlorine levels, frequent changing of the water. Caused by Pseudomonas aeruginosa, a Gram-negative organism, from inadequate chlorination. |
 | Pseudofolliculitis barbae | Foreign-body reaction, NOT infection · cut hair re-penetrates the skin · tender papule with a central hair shaft · tightly curled beard hair | Foreign body reaction, not an infection. The cut hair curves into the follicular wall and re-penetrates the skin, forming a tender red papule with a central hair shaft. Commonly in Black males with tightly curled facial hair, or anyone who shaves curlier hair. “I get sore ingrown bumps every time I shave.” | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | 1st: stop shaving if possible; clean razors; avoid “lift-and-cut” razor systems; mild razor angles, single or at most double blades. Alternatives: chemical depilatories; laser-assisted permanent hair removal. 2nd (topical): tretinoin relieves hyperkeratosis; mild corticosteroid for inflammation; eflornithine cream reduces facial hair; topical clindamycin, benzoyl peroxide or erythromycin to reduce colonization. Oral tetracycline. | The shaving technique itself has to change — treating the papules alone will not resolve it. Secondary infection can produce pustules and abscess. |
 | Furuncle | Single follicular abscess · fluctuant tender nodule with one opening | A painful, fluctuant, erythematous nodule — a deep abscess of a hair follicle and adjacent subcutaneous tissue. Firm tender nodule with a single opening and a surrounding zone of erythema; often fluctuant, may drain spontaneously. Back of neck, face, axillae, buttocks. “A painful boil on the back of my neck.” | Clinical appearance. Organism identified by aspiration or incision and drainage. Labs to orderNo bloods. Culture the material obtained at aspiration or incision and drainage, to identify the organism and check for resistance. | 1st: warm compresses are usually sufficient for small furuncles. No antibiotics if afebrile with a single lesion under 5 mm. Oral antibiotics if: a lesion under 5 mm fails drainage, a single lesion is over 5 mm, expanding cellulitis, immunocompromise, or endocarditis risk. Empiric: dicloxacillin or cephalexin. If MRSA: trimethoprim-sulfamethoxazole, clindamycin or doxycycline. Incise and drain large furuncles and culture the material. | Endocarditis prophylaxis for at-risk patients. Recurrent furunculosis — address obesity, diabetes and nasal Staphylococcus aureus carriage. |
 | Carbuncle | Two or more confluent furuncles with SEPARATE heads · sieve-like openings · systemic symptoms | Two or more confluent furuncles with separate heads. Extremely painful. Several loculated abscesses, superficial pustules, necrotic plugs and sieve-like openings draining purulent material. Systemic symptoms — malaise, chills, fever — are more common than with a furuncle. “A cluster of boils that have joined together, and I feel unwell with it.” | Clinical appearance; organism via aspiration or incision and drainage. Labs to orderNo bloods. Culture from aspiration or incision and drainage. | 1st: incision and drainage is the mainstay of therapy. Endocarditis prophylaxis for at-risk patients. Oral antibiotics: dicloxacillin or cephalexin. If MRSA: trimethoprim-sulfamethoxazole, doxycycline or clindamycin. | Differential: cystic acne, folliculitis, hidradenitis suppurativa. |
 | Hidradenitis suppurativa | Apocrine sites — axilla, groin, breasts, perineum · recurrent more than twice in 6 months · sinus tracts | Also called acne inversa. Inflammation of cutaneous apocrine glands — axilla (most common), groin, breasts, perineum. Recurrent painful or suppurative lesions more than twice in 6 months. Nodules, sinus tracts, abscesses, atrophic or meshlike scarring, and the double comedone (a blackhead with two or more openings). “Painful lumps under my arms that keep coming back and now they leak.” | Primarily clinical. Three key elements: typical lesions + characteristic distribution (axilla and groin) + recurrence more than twice in 6 months. Biopsy is not usually required; it shows follicular occlusion by keratinous material, folliculitis and apocrine gland destruction. Labs to orderNone — clinical, on lesions plus distribution plus recurrence. Biopsy is not usually required. | Prevention: avoid heat, daily antibacterial soap / chlorhexidine / benzoyl peroxide wash, weight loss, avoid constrictive clothing and friction, smoking cessation is essential, laser hair removal. 1st: mild topical steroid with topical antibiotic (clindamycin, erythromycin). 2nd: intralesional triamcinolone for draining sinuses; oral prednisone; oral retinoid; spironolactone; combined oral contraceptive. 3rd: infliximab for disease unresponsive to corticosteroids. Analgesia: codeine, then fentanyl patch for resistant pain. Definitive: incise and drain large fluctuant cysts; wide excision gives the best chance of permanent cure. | Long-term systemic antibiotics have often poor outcomes. Predisposing: hot weather, perspiration, obesity, apocrine duct obstruction, secondary infection, smoking. |
 | Erythrasma | Coral-red fluorescence on Wood lamp · intertriginous, inner thighs · Corynebacterium minutissimum | Chronic superficial infection of intertriginous skin by Corynebacterium minutissimum, invading the upper third of the stratum corneum under heat and humidity. Usually asymptomatic, may be pruritic. Inner thighs, crural region, scrotum, and between the 4th and 5th toes. Diabetics are high risk. “A brownish patch in my groin that doesn't itch much.” | Gold standard: “coral-red” fluorescence under a Wood's lamp (ultraviolet light). Labs to orderNone — Wood's lamp coral-red fluorescence is the test. | 1st (localized): topical erythromycin or clindamycin. Widespread: oral erythromycin or clarithromycin. If yeast also present: add an antifungal cream (miconazole). | Keep the area clean and dry. Avoid excessive heat or moisture. Maintain a healthy body weight and good hygiene. Differential: cutaneous candidiasis, contact dermatitis, psoriasis, tinea. |
 | Impetigo — non-bullous | Honey-colored adherent crust · face and extremities · spreads by self-inoculation from scratching | The more common form. A macule rapidly becomes a vesicle or pustule and ruptures; serous contents dry to a honey-colored adherent crust over an erosion. Face and extremities. Spreads by extension and self-inoculation from scratching. Regional lymphadenopathy common. VERY contagious. “Golden crusty sores around his nose and mouth that keep spreading.” | Clinical appearance. Culture if: high risk for MRSA (health-care worker, teacher), or acute post-streptococcal glomerulonephritis is present. Labs to orderCulture if high risk for methicillin-resistant Staphylococcus aureus (health-care worker, teacher) or if post-streptococcal glomerulonephritis is present. Otherwise none. | 1st (topical, limited non-bullous): mupirocin ointment — adequate for most cases, as effective as oral with fewer side effects. Remove crusts before applying. Retapamulin is licensed but far more expensive. 1st (oral): dicloxacillin, amoxicillin-clavulanate, cephalexin — drug of choice in children, clindamycin if penicillin allergic. If MRSA: clindamycin, trimethoprim-sulfamethoxazole, doxycycline (over 8 years old). | Self-limiting but may last weeks or months. Isolate children until treatment has been underway 24–48 hours. Do not share towels, clothing, bath water, washcloths or razors. Gentle cleansing with antibacterial soap. Acute post-streptococcal glomerulonephritis may follow — especially ages 3–7 — and antibiotics do NOT prevent it. |
 | Impetigo — bullous | Fragile bullae on INTACT skin · exclusively Staphylococcus aureus · epidermolytic toxin | Exclusively Staphylococcus aureus, releasing epidermolytic toxins that split the epidermis. Small or large superficial fragile bullae, tense clear or cloudy, on intact skin or invading pre-existing lesions such as eczema. Rupture leaves shallow moist erosions with remnant collarettes. Lymphadenopathy uncommon. | Clinical appearance, as above. Differential: thermal burn, allergic contact dermatitis, herpes simplex or zoster. Labs to orderAs for non-bullous — culture only on the stated indications. | As for non-bullous impetigo. Coverage must include staphylococci and streptococci. | The bullous form is the one that secondarily invades existing skin disease such as eczema — that is a secondary bacterial infection rather than a primary one. |
 | Ecthyma | Punched-out ulcer through the dermis with a thick gray-yellow crust · lower legs · heals with a scar | Not common. Begins as a vesicle or pustule over inflamed skin and deepens into dermal ulceration with a thicker gray-yellow crust. Usually the lower extremities. Regional lymphadenopathy common; heals slowly and leaves a scar. “A punched-out sore on my shin with a thick crust that isn't healing.” | Clinical appearance, as for impetigo. Labs to orderAs for impetigo — culture on the stated indications. | As for impetigo, covering staphylococci and streptococci. | Predisposed by pre-existing tissue damage (bites) and immunocompromise such as diabetes; crowding and poor hygiene increase risk. The depth is what separates it — it scars, ordinary impetigo does not. |
 | Erysipelas | Sharply demarcated, RAISED border — cellulitis is flat and poorly demarcated · sudden high fever within 48 hours · UPPER dermis | Infection of the upper dermis extending to superficial cutaneous lymphatics — a superficial cellulitis. Group A streptococcus. Sudden onset with malaise, myalgia, chills and high fever (38–40°C) within 48 hours. A plaque raised above the surrounding skin with a CLEAR LINE OF DEMARCATION. Lower extremities in 80%; face is the other common site. “Red streaks” toward lymph nodes. “My face went bright red with a sharp edge to it and I spiked a fever.” | Clinical diagnosis in classic presentation. Leukocytosis, raised erythrocyte sedimentation rate and C-reactive protein are common but not diagnostic. Blood and tissue cultures are not cost effective — extremely low yield. Imaging is low yield and not indicated. Labs to orderLeukocytosis, raised erythrocyte sedimentation rate and C-reactive protein are common but not diagnostic. Blood and tissue cultures are NOT cost effective — extremely low yield. | Prompt treatment matters — progression can be rapid. 1st: penicillin V. If penicillin allergic: clindamycin. Supportive: symptomatic treatment of aches and fever, hydration, cold compresses, elevation of the affected limb. | Risk factors: impaired lymphatic drainage (mastectomy), immunocompromise, athlete's foot, obesity, trauma, pre-existing impetigo. Treat the tinea pedis — it is the portal of entry and predicts recurrence. The inciting event is often not recalled. |
 | Cellulitis | Poorly demarcated and FLAT — erysipelas is sharply demarcated and RAISED · deeper dermis and subcutis · lower leg | Acute inflammation of the deeper dermis and subcutaneous tissue. Group A beta-hemolytic streptococci or Staphylococcus aureus. All four cardinal signs — erythema, warmth, edema, tenderness. Most common site the lower leg, almost never bilateral. Borders are NOT elevated or demarcated — which rules out erysipelas. May be purulent or non-purulent. “My leg is hot, red, swollen and sore, and the edge just fades out.” | Usually clinical. No workup if limited involvement, minimal pain, no systemic signs and no risk factor for serious illness. Serious infection: blood cultures and skin punch biopsy; complete blood count (leukocytosis); creatine phosphokinase if muscle damage. Plain films, computed tomography or magnetic resonance imaging to evaluate for underlying fasciitis or osteomyelitis. Labs to orderNo workup at all in limited disease with no systemic signs and no risk factor. Serious infection: blood cultures, skin punch biopsy, complete blood count (leukocytosis) and creatine phosphokinase for muscle damage. | Non-purulent: dicloxacillin or cephalexin; clindamycin if penicillin allergic. Purulent — consider MRSA: trimethoprim-sulfamethoxazole, doxycycline, clindamycin or linezolid. Oral versus intravenous depends on presentation. Devitalized tissue — tense, cyanotic, necrotic, bronzed or blanched — is not perfused, so antibiotics never reach it. It needs surgical debridement. | May look and feel worse during the first day — sudden destruction of pathogens releases enzymes that increase local inflammation. Fever usually resolves in 24 hours. Fever beyond 48 hours → change the antimicrobial, guided by culture. Inflammation settles over 1–2 weeks. Complications: gangrene and sepsis in the immunocompromised. |
 | Abscess | Collection of pus from traumatic inoculation — unlike a furuncle, which starts in a hair follicle | A collection of purulent material within the dermis and deeper tissues, usually from traumatic inoculation of bacteria — unlike a furuncle, which arises from an infected hair follicle. Early: erythematous tender nodule. Later: purulent material collects centrally and may drain spontaneously. Axilla, vulva, perianal, head, neck, buttocks, extremities, perineum. Often polymicrobial; Staphylococcus aureus commonest. “A painful lump that came up where I injured myself, and now it's got a head on it.” | Clinical. Culture the drained material, with consideration of MRSA. Labs to orderNo bloods. Culture the drained material, considering methicillin-resistant Staphylococcus aureus, then narrow to the result. | If it drains spontaneously: warm soaks; broad-spectrum antibiotics considering MRSA, then narrow to the culture result. If it does not drain: surgical incision and drainage. | The aim is to eradicate infection and prevent recurrence. |
 | Acute paronychia | 2–5 days after trauma · rapid onset · erythematous edematous nail fold · may become fluctuant | Infection of the soft tissue around the fingernail (perionychium), starting as cellulitis and progressing to abscess. Usually 2–5 days after trauma. Rapid onset of an erythematous edematous area; advanced cases collect purulent fluid under the nail folds. Staphylococcus aureus, Streptococcus pyogenes. “My finger went red and throbbing a couple of days after a manicure.” | Usually clinical. Gram stain and culture to identify the bacterial cause; potassium hydroxide to rule out candida; Tzanck smear to rule out herpetic whitlow. Labs to orderNo bloods. Gram stain and culture for the bacterial cause; potassium hydroxide to rule out Candida; Tzanck smear to rule out herpetic whitlow. | 1st (mild): warm water compresses or soaks, 20 minutes 3× daily. Severe: incise and drain; obtain cultures to rule out MRSA. Oral antibiotics — amoxicillin-clavulanate, cephalexin, or clindamycin if exposed to oral flora from nail biting. | Predisposing: manicure, ingrown nail, hangnail, nail biting. Differential: onychomycosis, felon, herpetic whitlow, pseudomonal nail infection, squamous cell cancer of the nail. |
 | Chronic paronychia | Irritant/allergic, not primarily infective · Candida albicans commonest · no fluctuance · thickened nail plates | An inflammatory reaction of the proximal nail fold to irritants and allergens, possibly eczematous. Candida albicans is the commonest organism. Edematous, erythematous, tender nail folds without fluctuance; nail plates thicken and discolor; cuticles separate from the plate. Present at least 6 weeks. “My nail folds have been puffy and sore for months and my nails look ruined.” | Clinical, with a history of continuous hand immersion in water or chemical contact. Labs to orderNone — clinical, on the immersion or chemical exposure history. | 1st: treat the underlying inflammation and infection; keep the hands as dry as possible; broad-spectrum topical antifungal (miconazole). 2nd: oral antifungal in severe cases (fluconazole). | Predisposing: diabetes, laundry workers, cleaners, cooks, bartenders, dishwashers, swimming. The timescale is what separates it from acute paronychia — days versus six weeks. |
 | Necrotizing fasciitis | Unrelenting pain OUT OF PROPORTION to the findings · rapidly progressive · hypotension + white count ≥15,000 + violaceous skin | Bacterial infection of the tissue surrounding muscle, nerve, fat and vessels, leading to necrosis. Polymicrobial; Group A streptococcus common. Difficult to recognize early but rapidly progressive. The clue: unrelenting pain OUT OF PROPORTION to the physical examination. Later: skin changes red-purple to blue-gray, bullae with thick pink or purple fluid, cutaneous gangrene, and the area stops being tender because the superficial nerves have been destroyed. Fever 38.9–40.5°C, tachycardia, hypotension, septic shock. “The pain is far worse than it looks — and now it's gone numb.” | A surgical emergency with high mortality. Laboratory tests and imaging must NOT delay surgical intervention. Complete blood count with differential, chemistry, arterial blood gas, urinalysis, blood and tissue cultures. Ultrasound demonstrates air bubbles in soft tissue; magnetic resonance or computed tomography localizes site and depth. Gas may be present with Clostridium perfringens; it is NOT present with Group A streptococcus. Labs to orderComplete blood count with differential, chemistry, arterial blood gas, urinalysis, and blood and tissue cultures. They must NOT delay surgery. | 1st: aggressive surgical debridement of necrotic tissue. Admit to a surgical intensive care unit (burn or trauma center). Team approach with consultations. Antibiotics: broad-based, covering aerobic Gram-positive and Gram-negative organisms and anaerobes. | Commonly misdiagnosed as cellulitis, sent home, and returns worse. Consider it if there is no response to antibiotics within 48 hours. Risk factors: trauma, burns, surgery, immunosuppression, renal failure, alcoholism, dental infection, injection drug use. Male > female. |
| Lecture 5 · Dermatological Infestations | ||||||
 | Scabies | Intense NOCTURNAL pruritus · interdigital webs, volar wrists, axillae, genitalia · spares the head in adults | Itching almost always, and severe, with intense nocturnal pruritus. Insidious onset. Excoriations and eczematous dermatitis in interdigital webs, sides of fingers, volar wrists, elbows, axillae, scrotum, penis, labia, areolae. Head and neck spared in healthy adults — but involved in infants, the elderly and the immunocompromised, who also get indurated crusted nodules on the trunk. Pathognomonic: a thin, thread-like linear or J-shaped BURROW, 1–10 mm. “The itch is unbearable at night and it's driving me mad.” | Definitive: microscopic identification of the organism, ova or feces. Skin scraping — number 15 blade, unexcoriated burrow or papule, swab with alcohol, apply mineral oil, scrape firmly onto a slide. Dermoscopy — the “delta-wing jet” sign. Burrow ink test — blue/black ink applied; a zigzag line running away from the lesion is positive. Labs to orderNone — microscopic identification of the organism, ova or feces is the diagnosis. | 1st: topical permethrin overnight to the ENTIRE skin surface with attention to creases, and a SECOND APPLICATION ONE WEEK LATER. Non-pharmacologic: wash bedding and clothing at 60°C or bag for 14 days in a warm area; treat all infected persons in the family or group. Hyperkeratotic or immunosuppressed: ivermectin every 2 weeks for 2–3 doses + topical permethrin every 3 days to weekly. Pregnancy: treat only if documented. | Relief in about 3 days, but rash and itch may last up to 4 weeks (triamcinolone if needed). Excessive washing with harsh soap worsens irritation. Pruritus appears 4–6 weeks after a first infestation but 2–3 days after reinfestation. Complications: staphylococcal superinfection (may lead to sepsis), persistent post-scabietic papules, psychological effects. |
 | Crusted (hyperkeratotic) scabies | Thick flaking scale, millions of mites · may NOT itch at all · poorly defined patches | Thick flaking scale containing millions of mites. Nails thickened or discolored, patches poorly defined, and patients may be asymptomatic — not itchy at all. “My skin has gone thick and scaly, but honestly it doesn't itch.” | As for scabies — but the mite burden is massive, so scrapings are strongly positive. Labs to orderNone — as for scabies, but scrapings are strongly positive given the mite burden. | Ivermectin every 2 weeks for 2–3 doses plus topical permethrin every 3 days to weekly. | These patients are HIGHLY INFECTIOUS. Facility-associated scabies is common in long-term care where residents are elderly and immunosuppressed; a hospital epidemic can follow their admission, and it is difficult to eradicate once healthcare workers are infested. |
 | Pediculosis capitis (head lice) | Incubation 4–6 weeks · children · nits on hair shafts · occipital and postauricular | Incubation 4–6 weeks. Pruritus, low-grade fever, regional lymphadenopathy, irritability. 2 mm erythematous macules or papules; excoriations, erythema, scaling. Some patients are asymptomatic carriers. Commonest in children 3–12 years; direct head-to-head contact. “Her head is so itchy and the school sent a note home.” | Visualizing nits or live lice. Live lice mean active infestation — best found by wet combing with water and conditioner using a nit comb. Nits are visible to the naked eye and indicate past or present infestation. Nits cannot be removed from the hair shaft — that is what separates them from dandruff. Viable eggs are tan to brown; hatched remnants are clear, white or light. Labs to orderNone — visualizing nits or live lice. | A multimodal approach is warranted because of increasing resistance. Pediculicidal effect read 24 hours after application (World Health Organization). Physical methods: shaving the head; combing nits after 2 minutes of hair moisturizer, then drying — repeated every few days. These work but are time-consuming, painful and difficult, and need adjuvant therapy. | Wear clean clothing after treatment; dry or bag clothing, bedding and towels from the prior week for 2 weeks; wash combs; vacuum floors, carpets, upholstery, play areas and furniture. Fumigation is NOT recommended. Nits may remain in the hair for months, and a “no nit” policy is NOT recommended by the American Academy of Pediatrics because of school absence. If treatment is not done properly patients turn to essential oils, mayonnaise or mineral oil, which may not be lethal. |
 | Pediculosis corporis (body lice) | Linear excoriations on back, neck, shoulders, waist · lives in clothing seams · homeless, crowded, poor hygiene | Pruritus, with linear excoriations primarily on the back, neck, shoulders and waist; post-inflammatory pigmentation in chronic cases. Found in the homeless, refugees, victims of war and disaster, and crowded living with poor hygiene. “I itch all over my back and I can't get on top of it.” | Close examination of the SEAMS OF CLOTHING for nits. Shaking clothing over white paper — the lice move onto the paper. Labs to orderNone — examine clothing seams; shake clothing over white paper. | As for head lice — multimodal, with attention to clothing. | Transmission is via contaminated clothing and bedding; the inability to wash or change clothes is what allows the infestation to persist. Addressing that is the intervention. |
 | Pediculosis pubis (crabs) | Maculae caerulae — slate-gray/bluish 1 cm macules · periumbilical papular urticaria | Often asymptomatic or mild to moderate pruritus for months. Maculae caerulae — slate-gray to bluish irregular macules about 1 cm, representing hemorrhage. Papular urticaria at feeding sites, commonly periumbilical. Phthiriasis palpebrarum is infestation of the eyelashes. “I've been itching down there for weeks and there are odd bluish marks.” | Locating nits at the base of hairs; confirmed by microscopic examination of a plucked hair. Labs to orderNone for the infestation. Screen for concurrent sexually transmitted infection — patients often have one. | As for the other forms. | Patients often have a concurrent sexually transmitted disease — screen for it. Transmission is sexual, but also via contaminated clothing, towels and bedding. Found across all levels of society and all ethnic groups. |
 | Bedbugs | Painless bites GROUPED IN A LINE · nocturnal · hides in headboards, picture frames, behind wallpaper | Nocturnal feeders hiding by day in cracks and crevices of headboards, picture frames, behind loose wallpaper. Attracted to warmth and carbon dioxide. Bites are painless, multiple, and grouped in a LINEAR fashion — a row of three is “breakfast, lunch and dinner”. Wheals and papules with a hemorrhagic punctum; bullous reactions in sensitized patients. Blood flecks on the bed linen. “I wake up with itchy welts in a line, and there are little blood spots on the sheets.” | Physical examination. Labs to orderNone — physical examination. | Symptomatic treatment and local wound care. Secondary infection: topical antiseptic lotion or antibiotic cream. Pruritus: topical corticosteroids or oral antihistamines. Eradication: a professional exterminator is necessary. | Bedbugs need a blood meal every 5–10 days but can survive up to a year without one — leaving a room empty does not clear them. Spread in clothing and baggage of travelers and visitors, second-hand mattresses, and laundry. Not a marker of poor hygiene. |
 | Tungiasis (fleas) | Yellow, firm, translucent papule with a central black dot · female flea burrowed to lay eggs · feet | Infestation by penetration of an adult female flea into human skin to lay eggs (family Tungidae). Solitary or multiple erythematous papules enlarging over weeks to 4–10 mm; a fully developed yellow, firm, somewhat translucent nodule that may be painful. Over the feet (especially plantar), subungual and periungual skin, web spaces and legs. Pain, pruritus, autoamputation of toes. “I got these sore lumps on my feet after walking barefoot on the beach abroad.” | Dermoscopy to visualize the ovoid eggs. Labs to orderNone — dermoscopy visualizes the ovoid eggs. | 1st: surgical excision, or cryotherapy / topical agents. Plus: tetanus prophylaxis and systemic antibiotics. | Travel or residence in endemic areas — West Indies, Central America, Africa, India, Pakistan, South America. Prevention: avoid walking barefoot or in sandals along beaches, and do not sit in the sand in Nigeria, the Caribbean, India or Brazil. Pulicidae fleas instead cause linear or clustered urticarial papules on the lower legs; rat fleas transmit bubonic plague, cat fleas plague and endemic typhus. |
 | Caterpillars (lepidopterism) | Erucism — pruritic dermatitis from pointed or hollow hairs · gypsy moth | About 100–150 species. Mechanisms: mechanical irritation by pointed hairs, toxin injection through hollow hairs, cell-mediated hypersensitivity to hairs. Gypsy moth: erucism — pruritic dermatitis with multiple erythematous papules in linear streaks. Processionary: urticaria, angioedema, anaphylaxis. Asp or puss caterpillar (most poisonous): intense painful sting with a train-track pattern of purpura. | Clinical, from the exposure history and the pattern. Labs to orderNone — clinical, from the exposure and the pattern. | Symptomatic: systemic antihistamines; topical menthol or camphor; moderate to high potency topical corticosteroids; systemic corticosteroids; oral or parenteral narcotic analgesics for severe pain. Specific: remove the hairs by “stripping” with adhesive tape. Antivenom for certain categories. | The physical removal of hairs with tape is the step that is easy to forget and makes the difference. |
 | Cutaneous larva migrans | SERPIGINOUS raised linear track that MIGRATES · after sand or soil contact · dog and cat hookworm, human a dead-end host | Larvae of animal hookworms — mostly dog and cat — in which the human is a dead-end host. Requires contact with sand or soil contaminated with animal feces. Classic: an erythematous, raised, vesicular, linear or SERPENTINE cutaneous trail that progresses 2–3 cm PER DAY. Intensely pruritic and painful; lasts 2–8 weeks. Systemic signs rare. Hookworm folliculitis: follicular papules and pustules confined to one location, usually the buttock. “There's a winding red track on my foot and it moves every day.” | Clinical diagnosis if the serpiginous rash is present. Pathology: larvae trapped within the follicular canal, stratum corneum or dermis with an eosinophilic infiltrate. Light microscopy with mineral oil shows live and dead larvae in the folliculitic form. Labs to orderNone — clinical if the serpiginous rash is present. Light microscopy with mineral oil shows larvae in the folliculitic form. | 1st: albendazole 400 mg by mouth daily for 3 days, or ivermectin 200 micrograms/kg daily for 1–2 days. Hookworm folliculitis may need repeated treatments. Topical therapy is less effective. Surgical excision and cryotherapy are NOT recommended. | Commonly found in tropical and subtropical areas — southeastern United States, Caribbean, Africa, Central and South America, India, Southeast Asia. |
 | Black widow spider | Red hourglass on the underside · severe pain with MINIMAL skin findings · alpha-latrotoxin · muscle cramps | Latrodectus mactans — characteristic red hourglass on the underside of the abdomen. Venom contains the neurotoxin alpha-latrotoxin. Painful bite with mild dermatologic findings. Within 30 minutes: localized erythema, piloerection and sweating around the bite. Then agonizing crampy abdominal pain and muscle spasms; headache, paresthesia, nausea, vomiting, hypertension, lacrimation, salivation, seizures, tremors, acute renal failure, paralysis. “It bit me and within half an hour my stomach was cramping so badly I thought something had ruptured.” | Clinical, from the exposure and the systemic picture. Labs to orderNone diagnostic. Clinical, from the exposure and the systemic picture. | Local wound care versus hospitalization depending on symptoms. Envenomation: calcium gluconate 10%; narcotic analgesics; muscle relaxants; benzodiazepines. Ensure tetanus vaccination is up to date. | Increased risk of complications in the very old, the very young, and those with cardiovascular disease. Death is uncommon. Webs in corners of doors and windows, under woodpiles, garages, sheds, around outdoor toilet seats. |
 | Brown recluse spider | Dark violin/fiddle on the cephalothorax · closets, attics, stored clothing · Midwest and Southeast | Loxosceles reclusa — non-aggressive, with a dark brown fiddle or violin marking on the cephalothorax. Abundant in the American Midwest and Southeast; shelters in closets, attics and storage areas for bedding and clothing. Ranges from mild local reaction to severe ulcerative necrosis. Hallmark: the RED, WHITE AND BLUE sign — a central violaceous area surrounded by a rim of blanched skin, surrounded by a large asymmetric area. Necrosis 2–3 days after the bite, eschar between days 5 and 7, then deep ulcers. Systemic symptoms 1–2 days after: nausea, vomiting, headache, fever, chills. | Clinical, from the appearance and the exposure history. Labs to orderNone diagnostic. Clinical, from the appearance and the exposure history. | 1st: pain control, warm compresses, avoid strenuous exercise. Antibiotics for secondary bacterial infection. Necrotic wounds heal very slowly and may need surgical intervention or reconstruction to close the defect — surgery is DELAYED until the wound is stable. | Bites occur when the spider feels threatened or provoked. The staged timeline — necrosis at 2–3 days, eschar at 5–7 — is what lets you place a presenting lesion in its course. |
 | Hobo spider | Gray herringbone on the abdomen · Pacific Northwest · mistaken for brown recluse | Tegenaria agrestis, the aggressive house spider — brown with a gray herringbone pattern on the abdomen. Often mistaken for the brown recluse. The predominant cause of necrotic arachnidism in the Pacific Northwest. Bites July to September during mating season; webs in basements, wood piles, bushes. Painless bite; induration and paresthesia within 30 minutes; a large erythematous area; vesicle formation during the first 36 hours; sometimes eschar. Systemic: headaches, fatigue, nausea, vomiting, diarrhea, paresthesia, memory impairment. | Clinical, from geography, season and the appearance. Labs to orderNone diagnostic. Clinical, from geography, season and appearance. | Supportive measures. | Wounds heal within several weeks; headaches may last up to a week. Rare: death from severe systemic effects, including aplastic anemia. |
 | Lyme disease | >5 cm ring EXPANDING over days after a tick, central clearing, darker punctate center · NO scale on the border — unlike tinea | Borrelia burgdorferi, a spirochete. Stage 1 — early localized: erythema migrans — a large (>5 cm) expanding erythematous round or oval lesion with central clearing and often a darker punctate center at the bite site — the “bull's eye”. Occurs 1 week after the bite, with fever, myalgia, arthralgia, fatigue, lymphadenopathy. Stage 2 — early disseminated (days to weeks): skin, central nervous system, cardiac, musculoskeletal, eyes — cranial nerve palsies, meningitis, radiculopathies, arthralgias, headache, stiff neck. Stage 3 — late persistent (months to years): monoarticular or oligoarticular arthritis of the knee or weight-bearing joints; subacute encephalopathy with memory loss, mood change and sleep disturbance; acrodermatitis chronica atrophicans. | If the patient has an erythema migrans lesion, diagnose and treat on CLINICAL signs. Testing is most helpful in patients who do not live in an endemic region and present with possibly consistent signs. ELISA for immunoglobulin M and G; the immunoglobulin G assay (C6 peptide test) has greater specificity; Western blot is more specific still. Labs to orderEnzyme-linked immunosorbent assay for immunoglobulin M and G; the C6 peptide test (immunoglobulin G) is more specific; Western blot more specific still. If erythema migrans is present, diagnose and treat CLINICALLY — do not wait. | Remove the tick immediately. Antibiotics are indicated at all stages. 1st oral: doxycycline. Children and pregnant women: amoxicillin (alternative first line for early erythema migrans). 2nd: macrolides — azithromycin — for those who cannot tolerate other agents. Duration: 10–14 days. Intravenous: ceftriaxone, cefotaxime or penicillin G for some cutaneous manifestations, acrodermatitis chronica atrophicans and arthritis. | Endemic in Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, Vermont, Wisconsin. Prevention: avoid tick habitat; no human vaccine (one exists for dogs); repellents DEET, PMD, picaridin reapplied about every 2 hours; pyrethrins. |
 | Rocky Mountain spotted fever | Fever + headache + rash (all three in only ~60%) · rash from wrists and ankles inward · dog or wood tick | Rickettsia rickettsii. Life-threatening if not treated. Incubation 3–12 days. Vectors: dog tick, wood tick, rodents. Clinical triad: fever (>39.5°C), headache and rash — but present in only about 60%. Fever comes first for 3 days; rash 2–4 days after fever onset. Rash starts on the ankles and wrists and spreads CENTRIPETALLY over 6–18 hours; palms and soles ARE affected; the FACE is spared. Erythematous blanching macules and papules that may evolve to petechiae and purpura. Also chills, malaise, myalgia, nausea, vomiting, anorexia, periorbital edema, abdominal pain (mimics appendicitis, more in children), conjunctival injection, palatal petechiae, dorsal hand edema, calf pain. | Labs: thrombocytopenia, anemia, mild hyponatremia, mild transaminitis, normal white count with increased bands. Cerebrospinal fluid: leukocytosis, moderately elevated protein, normal glucose. Gold standard: indirect immunofluorescence assay — but it is rarely diagnostic before day 7, and treatment should be started by day 5. Start treatment while waiting for results. About 20% present without a rash. Labs to orderComplete blood count (thrombocytopenia, anemia, normal white count with increased bands), chemistry (mild hyponatremia), liver function (mild transaminitis). Cerebrospinal fluid: leukocytosis, moderately raised protein, normal glucose. Gold standard: indirect immunofluorescence assay — rarely diagnostic before day 7, so treat by day 5 while waiting. | Adults: doxycycline 100 mg by mouth every 12 hours for 5–10 days — the same in pregnancy. Children: doxycycline 2.2 mg/kg by mouth every 12 hours for 5–10 days. Second line (allergy or contraindication): doxycycline via desensitization — small initial doses increased every 15–60 minutes until the therapeutic dose is reached — including in pregnancy and children under 8, where teeth staining and hepatotoxicity are the usual contraindications. | Prophylactic antibiotic therapy is NOT recommended. Prevention: avoid tick exposure, protective clothing, tick checks, DEET. Risk factors: male, adults 40–64, children under 10, rural dwelling; southeastern and south central states in spring and early summer. Delayed or inadequate treatment → severe cardiac, gastrointestinal, hepatic, neurologic, ophthalmologic, renal and pulmonary manifestations, with long-term sequelae in survivors. |
 | Cercarial dermatitis (swimmer's itch) | Pruritic eruption after fresh water · snail intermediate host · waterfowl parasite, human a dead-end | Acute pruritic eruption from penetration of the skin by the cercarial forms of parasitic flatworms. Host (waterfowl, marsh bird, finch, muskrat, mouse, deer) passes eggs in feces into water; eggs hatch and infect a snail within 12 hours; in 5 weeks cercariae are released and carried to the shore. Urticaria-like lesions and a prickling sensation lasting about 30 minutes after exposure → severe pruritus at 10–12 hours → erythematous papules within 24 hours → vesicles → pustules. Pain and swelling with pruritus peaking at 48–72 hours. Sometimes headaches, fever, lymphangitis. “After the lake my legs prickled, then that night they itched like fire and came up in spots.” | Clinical, from the freshwater exposure and the characteristic time course. Labs to orderNone — clinical, from the freshwater exposure and the time course. | Symptomatic: antihistamines, oatmeal baths, antipruritic lotions. Aspirin for pain control. Topical or oral glucocorticoids. | Proper washing and hygiene after leaving the water. Affects the Great Lakes region, and paddy workers and rice farmers of the Far East. |
| Lecture 6 · Cutaneous Fungal Infections | ||||||
 | Tinea capitis (scalp) | Preadolescent children — puberty changes sebum fatty acids · Trichophyton tonsurans commonest in the United States | Predominantly preadolescent children — after puberty, changes in the fatty acid content of sebum are believed to inhibit growth. The commonest fungal infection in children; Trichophyton tonsurans is commonest in the United States. Red papules progressing to grayish ring-formed patches with perifollicular papules, scaly patches, and lymphadenopathy is often present. “He has a scaly bald patch on his head and he keeps scratching it.” | Potassium hydroxide microscopy and fungal culture where feasible — especially before prolonged systemic therapy. Wood lamp may rapidly support Microsporum, but T. tonsurans usually does not fluoresce, so a negative lamp excludes nothing. Bacterial culture if a kerion has purulent drainage. Labs to orderNo bloods for the diagnosis. But baseline liver tests when indicated by the selected systemic agent, its labeling and patient risk — oral therapy is mandatory here, so this is where it comes up. Review drug interactions and hepatic disease. | Oral therapy is required — topical agents do not penetrate the infected hair shaft. Terbinafine generally favored for Trichophyton; griseofulvin often favored for Microsporum. Review interactions and hepatic disease; baseline liver tests when indicated by the agent and patient risk. Adjunct: selenium sulfide 1–2.5% or ketoconazole 2% shampoo, 2–3 times weekly — reduces spore shedding but does not replace oral therapy. | Complete the whole oral course even when itching settles early. Do not share combs, brushes, hats, towels or hair accessories; clean tools and washable fomites. Fungal particles stay viable for months. Evaluate symptomatic contacts and consider pets where a zoophilic source is suspected. School exclusion is generally unnecessary once effective therapy has begun; follow local policy. Treat inflammatory disease promptly to reduce scarring alopecia. |
 | Black dot tinea capitis | Hair fractures AT the scalp surface → alopecia patches studded with black dots | The pattern in which the hair fractures at the scalp surface, leaving patches of alopecia studded with visible black dots. “There are little black specks where the hair broke off.” | As for tinea capitis — potassium hydroxide microscopy and culture. Labs to orderNone — the same scalp workup; potassium hydroxide and culture. | As for tinea capitis: oral antifungal therapy. | Distinguish from alopecia areata, where the skin is smooth and shiny without inflammation, and from seborrheic dermatitis, where hair may be lost but is not broken. |
 | Tinea barbae — inflammatory | Boggy pustular kerion-like plaque · hairs loose and easily removed · from ANIMALS | Trichophyton species. Usually acquired from animals. Tender, boggy, pustular kerion-like plaques; infected hairs are loose and easily removed. Scarring alopecia may occur. “My beard is swollen and sore, and the hairs just pull straight out.” | Potassium hydroxide and culture. Bacterial culture to rule out bacterial folliculitis — in tinea barbae the hair is easily removed, unlike folliculitis. Biopsy for refractory cases. Labs to orderNo bloods. Bacterial culture to exclude bacterial folliculitis; biopsy for refractory cases. | Oral antifungal therapy is required — topicals do not penetrate the hair follicle. Griseofulvin or terbinafine. Shave or remove hair; warm compresses to remove crusts and debris. | Differential also includes acne, rosacea and seborrheic dermatitis. The animal source is worth tracing. |
 | Tinea barbae — noninflammatory | Annular scaly plaques or folliculitis-like · from another person · hairs break near the surface | Usually acquired from another person. Annular scaly plaques, or a folliculitis-like eruption; hairs may break near the skin surface. Asymptomatic or mildly pruritic. | Potassium hydroxide and culture; bacterial culture to exclude folliculitis. Labs to orderNo bloods. Potassium hydroxide and culture; bacterial culture to exclude folliculitis. | As for the inflammatory form — oral antifungal therapy. | Person-to-person acquisition, so shared razors and clippers matter. |
 | Tinea corporis (body) — “ringworm” | Annular, with SCALE ON THE ADVANCING BORDER and progressive central clearing · the scale is what separates it from granuloma annulare AND from erythema migrans | Trichophyton rubrum is the common pathogen. One or more circular, sharply circumscribed, slightly erythematous, dry scaly patches or plaques with progressive central clearing producing the annular outline. “It started as a small ring and it's been growing outwards, clearing in the middle.” | Potassium hydroxide from the ACTIVE BORDER — not the cleared center. Culture where clinical suspicion is high and the preparation is negative, and for refractory cases. Labs to orderNone. Potassium hydroxide from the active border; culture when suspicion is high and the preparation is negative. Species identification and susceptibility testing where resistance is suspected. | Localized: topical terbinafine, butenafine or an azole, applied to the lesion and 1–2 cm beyond its border, for the product-specific duration and continued past visible improvement. Systemic: consider oral therapy for extensive, follicular, immunocompromised, refractory or recurrent disease — terbinafine commonly, or itraconazole or fluconazole by organism and interactions. | Avoid corticosteroid–antifungal combination products: steroids mask and worsen dermatophytosis (tinea incognito). Differential is psoriasis, nummular eczema (commonly confused with it), discoid lupus and fixed drug eruption. Suspect resistance when disease is widespread, intensely inflammatory, epidemiologically linked, or fails an adequate terbinafine course — then get species identification and susceptibility testing. |
 | Tinea cruris (groin) — “jock itch” | Sharply demarcated on the proximal medial thigh · THE SCROTUM IS TYPICALLY SPARED · men, with tinea pedis | Involves the crural fold. More common in men; often coexists with tinea pedis. T. rubrum and Epidermophyton floccosum. Pruritic, sharply demarcated plaque on the proximal medial thigh — the SCROTUM IS TYPICALLY SPARED. “The itch is in the crease of my groin, and it's spreading down my inner thigh.” | Potassium hydroxide from the active border for uncertain cases. Labs to orderNone — potassium hydroxide from the active border for uncertain cases. | Localized: topical allylamine (terbinafine) or azole (ketoconazole). Reserve oral therapy for extensive or refractory disease. | Predisposing: warm moist environment, obesity, diabetes, tight clothing worn for long periods, sharing clothes. Scrotal involvement points elsewhere — candidal intertrigo commonly involves the scrotum and throws satellite papules or pustules; erythrasma may fluoresce coral-red. |
 | Tinea pedis — interdigital | Maceration between the toes, especially the 3rd and 4th interspaces · commonest dermatophyte infection in adults | The most common form, and tinea pedis is the most common dermatophyte infection in adults (men more than women). Pruritic. Maceration, erythematous erosions or scaling between the toes, especially the third and fourth interspaces, with associated fissures. “It's raw and peeling between my toes and it itches.” | Clinical. Confirm uncertain cases with potassium hydroxide from the advancing scale. Culture for atypical, recurrent, severe or refractory disease. Add bacterial studies for marked maceration, malodor, erosion, drainage, ulceration or cellulitis. Labs to orderNo bloods. Add bacterial studies for marked maceration, malodor, erosion, drainage, ulceration or cellulitis. | Topical terbinafine or butenafine, or an azole. Consider oral therapy for extensive, recurrent, refractory or immunocompromised disease. Treat coexisting onychomycosis and reinforce moisture control. | Drying between the toes after bathing is essential. Antifungal foot powder in shoes; open-toed sandals where possible; sandals in communal showers; change socks frequently. Spread is by contact with infected desquamated skin — shoes, locker room floors, sweating. |
 | Tinea pedis — hyperkeratotic | “Resembles a SHOE DISTRIBUTION” — soles plus medial and lateral surfaces · diffuse thickening | Trichophyton species. Asymptomatic or pruritic. Plantar erythema with slight scaling through to diffuse thickening, involving the soles and the medial and lateral surfaces — resembling a shoe distribution. “The bottoms of my feet are thick and dry all over.” | As for interdigital disease — potassium hydroxide, culture if atypical or refractory. Labs to orderNone — potassium hydroxide from the advancing scale; culture if atypical or refractory. | Antifungal plus a KERATOLYTIC for the thickening. Oral therapy for extensive, recurrent, refractory or immunocompromised disease. | Often bilateral and long-standing; patients frequently put it down to dry skin. |
 | Tinea pedis — vesiculobullous | The moist, acute form · vesicles or bullae on erythema · pruritic AND painful | Trichophyton species. The moist, acute form — pruritic and painful. Vesicular or bullous eruption on underlying erythema. “Blisters came up on my foot and they hurt.” | Potassium hydroxide; bacterial studies if macerated, malodorous or draining. Labs to orderNone — potassium hydroxide; bacterial studies if macerated or draining. | Topical antifungal; oral therapy for extensive or refractory disease. | Distinguish from contact dermatitis and psoriasis, both of which sit in the tinea pedis differential. |
 | Onychomycosis (tinea unguium) | Distal lateral subungual debris · onycholysis, thickening, crumbling · T. rubrum | Dermatophytes — especially T. rubrum — cause most cases; yeast and molds also occur. Distal lateral disease produces debris, onycholysis, thickening, discoloration and crumbling. “My toenails are thick, yellow and crumbling.” | Confirm fungus BEFORE oral therapy — many dystrophic nails are not fungal. Potassium hydroxide microscopy, periodic acid–Schiff stain of nail clippings, fungal culture, or polymerase chain reaction where available. Sample the most PROXIMAL accessible diseased nail bed or subungual debris, after trimming the onycholytic nail. Labs to orderNo bloods for the diagnosis — but baseline liver tests per labeling and patient risk before oral terbinafine, with a review of hepatic disease and interactions. Confirm fungus first: potassium hydroxide, periodic acid–Schiff of clippings, culture, or polymerase chain reaction. | Oral terbinafine is first-line for most dermatophyte disease: usually 6 weeks for fingernails, 12 weeks for toenails. Review hepatic disease and interactions; baseline liver tests per labeling and risk. Itraconazole is an alternative; fluconazole is off label in the United States. Limited disease: topical efinaconazole, tavaborole or ciclopirox — lower cure rates. | Improvement requires nail growth, so appearance lags well behind treatment. Manage concomitant tinea pedis or it will recur. Risks: tinea pedis, age, diabetes, trauma, occlusive footwear, psoriasis and vascular disease. |
 | Tinea manuum (hand) | TWO FEET–ONE HAND · palm hyperkeratotic like tinea pedis, dorsum annular like tinea corporis | Associated with tinea pedis, with high recurrence. Dorsal hand looks like tinea corporis (annular plaque); palm looks like tinea pedis (hyperkeratotic, thickened, dry, scaly). Two feet–one hand syndrome: the hand used to scratch the foot is the one affected. “My palm has been dry and thick for months — I assumed it was from work.” | Potassium hydroxide and culture, as for the corresponding body site. Labs to orderNone — potassium hydroxide and culture, as for the corresponding site. | Same as tinea pedis — topical for localized disease; oral for extensive, recurrent, refractory or immunocompromised disease. Treat coexisting onychomycosis; reinforce moisture control. | Patients are often unaware they have an infection, believing the change is dry skin or hard physical labor. Check both feet and both palms. |
 | Id (dermatophytid) reaction | Dermatitis at a site DISTANT from the infection · 1–2 weeks after · commonly with tinea pedis | An inflammatory dermatitis at a site DISTANT from the primary dermatophytosis — occurs with any dermatophyte infection, tinea pedis commonly. Mechanism unknown; possibly delayed-type hypersensitivity. Appears 1–2 weeks after the primary infection, extremely pruritic, papules or papulovesicular eruptions, commonly on the fingers. “My hands broke out in itchy little blisters after my foot was treated.” | Potassium hydroxide POSITIVE at the primary site, NEGATIVE at the id site. Three criteria: (1) dermatophyte infection elsewhere on the body, (2) absence of fungal elements at the reaction site, (3) resolution when the primary infection is treated. Labs to orderNone. The diagnosis is made by the pattern of potassium hydroxide results — positive at the primary site, negative at the reaction site. | Treat the primary dermatophyte infection — the id reaction resolves with it. | Examine carefully for an asymptomatic fissure or maceration in the toe webs; the patient may not know the foot is infected. |
 | Tinea incognito | Tinea altered by topical STEROIDS · flares whenever the steroid stops · loses its typical border | Tinea with a clinically altered appearance due to inappropriate treatment, usually topical steroids. Steroids get used on anything that looks inflammatory; when they are stopped the lesion flares, and more steroid follows. “It settles while I use the cream and comes back worse every time I stop.” | Stop the corticosteroid or calcineurin inhibitor, then potassium hydroxide and culture from an active edge. Warn that inflammation may rebound after withdrawal. Labs to orderNone — potassium hydroxide and culture from an active edge, after stopping the corticosteroid. | Topical antifungal for localized disease; systemic for extensive, follicular or refractory infection. | The reason combination steroid–antifungal products are to be avoided in the first place. |
 | Cutaneous candidiasis and intertrigo | SATELLITE lesions beyond the main patch, in body folds · friction, moisture and heat · Candida albicans | Intertrigo is an inflammatory rash from friction, moisture and heat trapped in body folds; Candida may secondarily infect it. Candida albicans is the commonest species, an opportunistic yeast (unicellular fungi reproducing by budding); males equal females. Well-demarcated erythematous patches with SATELLITE papules or pustules. Pruritus and burning pain. “Under my breasts is raw, red and burning.” | Clinical, supported by potassium hydroxide preparation and culture. Satellite papules or pustules support Candida; malodor, erosions or drainage raise concern for bacterial coinfection. Labs to orderNo bloods routinely. But recurrent or extensive disease warrants evaluation for diabetes and immunosuppression. | Correct the environment first: gently dry the folds, reduce friction and occlusion, use moisture-wicking or absorbent material, address incontinence or hyperhidrosis. Topical nystatin treats Candida ONLY; topical azoles treat Candida AND many dermatophytes. Consider a low-potency corticosteroid briefly for marked inflammation, and only alongside adequate antifungal treatment. | Common sites: inframammary, axillary, abdominal, inguinal, perineal and interdigital folds. Risks: obesity, diabetes, incontinence, occlusion, immobility, recent antibiotics, immunosuppression. Recurrent or extensive disease warrants evaluation for diabetes and immunosuppression. |
 | Pityriasis versicolor (tinea versicolor) | “Spaghetti and meatballs” on potassium hydroxide · velvety tan/pink/white finely scaling macules · NOT contagious | Overgrowth of lipid-dependent Malassezia species that normally inhabit the skin — NOT considered contagious. Velvety tan, pink or white finely scaling macules 4–5 mm to large confluent areas on the neck, upper arms, trunk and groin. Usually asymptomatic or mildly pruritic. “I get these pale patches every summer and they won't tan.” | Usually clinical — scrape or stretch the lesion to reveal fine scale. Potassium hydroxide shows short hyphae with clusters of yeast — “spaghetti and meatballs”. Wood lamp may show yellow-gold fluorescence, but sensitivity is limited. Biopsy rarely needed. Labs to orderNone. Potassium hydroxide shows short hyphae with clusters of yeast. Review hepatic risk, pregnancy status and drug interactions before oral fluconazole or itraconazole. | Topical therapy is first-line: ketoconazole shampoo or cream, selenium sulfide, zinc pyrithione, ciclopirox, or topical terbinafine. One common selenium sulfide approach is daily for 7 days with a 10-minute contact time. Systemic for extensive, recurrent or refractory disease: oral fluconazole or itraconazole. Oral terbinafine is INEFFECTIVE — adequate levels are not achieved in sweat (topical terbinafine does work). Do NOT use oral ketoconazole — hepatic and adrenal toxicity outweigh benefit in a superficial infection. | Scale resolves before pigment normalizes, and recovery can lag months. Color change alone does not prove treatment failure — look for scale or confirm with microscopy. Recurrence is common in warm climates; intermittent prophylactic topical therapy may help. Differential: seborrheic dermatitis (yellowish tint, soft greasy scale), pityriasis rosea (herald patch, Christmas-tree distribution), vitiligo (completely depigmented). |
| Lecture 6 · Cutaneous Viral Infections | ||||||
 | Varicella (chickenpox) | SEVERAL STAGES PRESENT SIMULTANEOUSLY — macules, papules, vesicles and crusts together · concentrated on the trunk | Primary varicella-zoster infection. Generalized pruritic eruption in multiple stages of healing: macules → papules → vesicles → crusts, with several stages present SIMULTANEOUSLY. Lesions concentrate on the trunk, scalp and face. “He has spots everywhere — some are blisters and some have already scabbed.” | Usually clinical; lesion polymerase chain reaction is preferred when confirmation is needed. Labs to orderNone routinely — usually clinical; lesion polymerase chain reaction when confirmation is needed. | Supportive care; AVOID ASPIRIN in children and use caution with non-steroidal anti-inflammatories. Consider early oral antivirals for higher-risk patients; intravenous acyclovir for severe or disseminated disease. | Adults, pregnancy, newborn age and immunocompromise increase complication risk. Promptly consult for pregnancy, neonatal exposure, immunocompromise or severe complications. Contagious from 1–2 days before the rash until all lesions crust; in breakthrough disease without crusts, until no new lesions for 24 hours. In healthcare settings use standard, airborne AND contact precautions. Two-dose varicella vaccination is primary prevention. |
 | Herpes zoster (shingles) | Single DERMATOME, does not cross the midline · dysesthesia or pain BEFORE the rash · reactivated varicella-zoster | Reactivation of latent varicella-zoster virus; risk rises with age and impaired cell-mediated immunity. Latent in cranial-nerve or dorsal-root ganglia, traveling along a sensory nerve to the skin. Pre-eruptive: dysesthesia or pain in the dermatome, lesions by 48–72 hours. Acute eruptive: erythematous macules and papules, then grouped herpetiform vesicles on an erythematous base (classic); new lesions over 3–5 days. Blisters confined to one or two adjacent dermatomes and STOP ABRUPTLY AT THE MIDLINE. Thoracic 55%, cranial 20%, lumbar 15%, sacral 5%. “A burning band of blisters across one side of my chest.” | Typical unilateral dermatomal vesicles are diagnosed clinically. Polymerase chain reaction from vesicle fluid, scab, or cells from the lesion base is preferred for atypical, disseminated, vaccine-modified or immunocompromised presentations. Differential: herpes simplex, contact dermatitis, impetigo, folliculitis, insect bites, dermatitis herpetiformis, varicella. Labs to orderNone routinely — typical dermatomal disease is clinical. Polymerase chain reaction from vesicle fluid, scab or lesion base for atypical, disseminated, vaccine-modified or immunocompromised presentations. Adjust antiviral dosing for renal function. | Preferred oral agents: valacyclovir, famciclovir or acyclovir; adjust for renal function. Start as soon as possible — ideally within 72 hours of rash onset. Treat AFTER 72 hours when new lesions are forming, or there is ophthalmic, neurologic, disseminated, severe or immunocompromised disease. Intravenous acyclovir and specialist or hospital management for severe disseminated, visceral, central nervous system or sight-threatening disease. Acetaminophen or a non-steroidal for mild pain; cool compresses, calamine, loose clothing, lesion coverage. | A susceptible contact does not “catch shingles” — exposure to vesicular fluid, or airborne virus from disseminated disease, can cause varicella. Cover lesions, do not scratch, hand hygiene, and avoid susceptible pregnant people, premature infants and immunocompromised people until crusted. Infectious until lesions have dried. Some have pain without eruption (zoster sine herpete). Resolves over 10–15 days; complete healing may take a month, typically without visible sequelae — it scars only when deeper layers are compromised by excoriation or secondary infection. Prevention: two doses of recombinant zoster vaccine (Shingrix) for immunocompetent adults 50 and over, and for adults 19 and over who are or will be immunodeficient or immunosuppressed. Standard interval 2–6 months; for immunocompromised patients the second dose may be given 1–2 months after the first. |
No image, deliberately — this is pain that persists after the rash has healed, so there is nothing to photograph. A picture here would show acute zoster, the wrong phase. | Postherpetic neuralgia | Pain persisting 90 days or more after rash onset · burning, stabbing, allodynia to light touch | The most common complication of herpes zoster, and very debilitating. Pain persisting 90 days or more after rash onset is the commonly used definition. Burning, aching, stabbing, electric shock-like, or evoked by light touch (allodynia) — neuropathic pain from injury of peripheral nerves. May last months to years and impairs sleep, mood and function. “The rash cleared months ago but I still can't bear my shirt touching it.” | Clinical, from the history of a preceding zoster eruption. Labs to orderNone — clinical. Individualize treatment for kidney function, falls risk, anticholinergic burden and interactions. | First line: gabapentin or pregabalin, an appropriate tricyclic antidepressant, or topical lidocaine. A capsaicin patch may help. Individualize for kidney function, falls, anticholinergic burden and interactions. Avoid routine long-term opioids; refer severe, persistent or disabling pain. | Risk rises with age, severe acute pain, severe rash, ophthalmic involvement and immunocompromise. Topical and systemic corticosteroids do NOT prevent it and must never replace antiviral therapy. |
 | Herpes zoster ophthalmicus | Hutchinson sign — lesions on the tip or side of the NOSE · V1 of the trigeminal · its ABSENCE does not exclude eye involvement | Zoster involving the ophthalmic division (V1) of the trigeminal nerve. Hutchinson sign — lesions on the tip or side of the nose — increases ocular risk, but its ABSENCE does NOT exclude eye involvement. “The rash is over my forehead and eyelid, and my eye hurts.” | Clinical. Evaluate urgently for ophthalmic, otic, neurologic, disseminated or visceral disease. Labs to orderNone — clinical; the urgency is the same-day ophthalmology evaluation, not a test. | Start systemic antiviral therapy IMMEDIATELY. Same-day ophthalmology evaluation for eye pain, visual symptoms, red eye, photophobia, Hutchinson sign, or eyelid or ocular involvement. | Do not wait for the ophthalmology review before starting the antiviral. A negative Hutchinson sign is not reassurance. |
 | Ramsay Hunt syndrome (herpes zoster oticus) | Facial palsy + vesicles in the ear canal or auricle · hearing loss, tinnitus or vertigo | Peripheral facial palsy with painful vesicles of the ear canal, auricle or oropharynx; hearing loss, tinnitus or vertigo may occur. “My face has dropped on one side and there are painful blisters in my ear.” | Clinical. Labs to orderNone — clinical; urgent ear, nose and throat or neurology evaluation. | Antiviral therapy PLUS a systemic corticosteroid, started early when not contraindicated — one of the few places a steroid is added. Urgent ear, nose and throat or neurology evaluation. | Protect the cornea if eyelid closure is impaired. |
 | Herpes simplex virus (HSV-1 and HSV-2) | Grouped vesicles on an erythematous base · prodromal tingling · site does NOT reliably determine the type | Either type can cause oral or genital infection — lesion location does NOT reliably determine type. Double-stranded DNA Herpesviridae; neurovirulent, producing latent but lifelong infection with episodic reactivation. First episode is more prominent and longer; recurrences are milder and shorter. Prodrome of tenderness, pain, paresthesias or burning — with localized pain, tender lymphadenopathy, headache, generalized aching and fever characteristic; some have no prodrome. Grouped vesicles on an erythematous base breaking down to a shallow painful ulcer; dysuria in women with genital lesions; last about two weeks, heal without scarring. “It tingled for a day, then painful blisters came up and burst.” | Swab a FRESH vesicle, ulcer base or crust for type-specific nucleic acid amplification — the preferred test. Culture is less sensitive, especially in healing or recurrent lesions; a negative result does not exclude HSV. A negative older-lesion swab does not exclude infection because shedding is intermittent. Do NOT use HSV immunoglobulin M. Confirm low-positive HSV-2 serology with a second method. Routine serologic screening of asymptomatic adults is not recommended. Evaluate genital ulcers for other causes including syphilis, by risk. Labs to orderType-specific serology has selected uses, but low-positive results may be false positive — confirm with a second method. Do NOT use immunoglobulin M. Routine serologic screening of asymptomatic adults is not recommended. The diagnosis is made by lesion amplification testing, not by blood. | Treat EVERY first clinical episode with oral acyclovir, valacyclovir or famciclovir. Recurrent genital HSV: patient-initiated episodic or daily suppressive therapy. Topical antivirals provide minimal benefit for genital herpes. | Suppressive valacyclovir lowers HSV-2 transmission; condoms reduce but do not eliminate risk. Avoid sexual or direct lesion contact during the prodrome or while lesions are active. Reactivation triggers: stress, illness, menstruation, ultraviolet light. Differential: chancroid (painful necrotizing ulcers, Haemophilus ducreyi, inguinal nodes), syphilis (solitary raised papules that erode, usually painless), trauma, candidiasis. |
 | Herpetic whitlow | DISTAL FINGER · grouped vesicles on a swollen digit · inoculation through broken skin | Painful herpes simplex infection of the DISTAL FINGER, often after inoculation through broken skin. Prodromal burning or tingling, then grouped vesicles on an erythematous, swollen digit; fever or lymphangitis may occur. “My fingertip is swollen and throbbing, with little blisters on it.” | Confirm atypical cases with HSV amplification testing from a fresh vesicle or the lesion base. Mimics bacterial felon or paronychia, contact dermatitis, and blistering dactylitis. Labs to orderNone — confirm atypical cases with amplification testing from a fresh vesicle or the lesion base. | DO NOT INCISE AND DRAIN — it does not treat HSV and can delay healing. Early oral acyclovir, valacyclovir or famciclovir may shorten symptoms; consider suppression for frequent recurrence. Treat bacterial superinfection only when it is present. | Cover the lesions, use hand hygiene, and avoid contact with mucosa or broken skin until healed. An occupational risk for anyone whose hands are near other people's mouths. |
 | Molluscum contagiosum | Umbilicated PEARLY FLESH-COLORED dome, 3–5 mm · poxvirus, children · vs sebaceous hyperplasia, which is YELLOW and in older adults | Benign POXVIRUS infection. Discrete, smooth-surfaced, firm, flesh-colored, dome-shaped pearly papules averaging 3–5 mm; CENTRAL UMBILICATION is characteristic. Asymptomatic, or tender or pruritic. “He's got little pearly bumps with a dimple in the middle.” | Clinical diagnosis; biopsy if uncertain. Differential: basal cell carcinoma, sebaceous hyperplasia, condyloma acuminatum. Labs to orderNo bloods routinely. Extensive or giant facial lesions warrant evaluation for immunosuppression, including HIV testing where appropriate. | Observation is appropriate for many patients — procedures may blister, pigment or scar. Berdazimer 10.3% gel (Zelsuvmi), once daily at home, age 1 and over. Cantharidin 0.7% (Ycanth), applied by a clinician, age 2 and over. Others: curettage or cryotherapy; topical retinoids are off label. Treat associated dermatitis. | Spread by direct skin contact, shared contaminated objects, and autoinoculation; sexual contact is common in adults with genital lesions. Most immunocompetent patients clear spontaneously, though it may take months to several years; lesions are more numerous, larger or atypical with immunosuppression. Genital lesions in a child require context-sensitive assessment — location alone does NOT prove abuse. Genital lesions in adolescents or adults may be sexually transmitted; assess for other infections as appropriate. Extensive or giant facial lesions warrant evaluation for immunosuppression, including HIV where appropriate. |
 | Verruca vulgaris (common warts) | Interrupts the skin lines · blackened center (thrombosed capillaries) · NO ROOTS — underside round and smooth · pain on SIDE pressure | Human papillomavirus infecting keratinocytes; confined to the epidermis, though it expands and displaces the dermis, giving a false impression of depth. The underside is round and smooth with NO ROOTS. Frequently ages 5–20; usually on the hands, favoring fingers and palms. Usually under 1 cm, elevated round papules with a rough grayish surface. Tiny red or black dots are thrombosed dilated capillaries — trimming the surface makes them more prominent. Periungual, lip and tongue warts are more common in nail biters. “Rough bumps on my fingers with little black dots in them.” | Clinical diagnosis. Biopsy is generally unnecessary but may suit immunocompromised patients or lesions of uncertain etiology (ruling out squamous cell carcinoma). Differential: squamous cell carcinoma, molluscum contagiosum, seborrheic keratosis. Labs to orderNone — clinical. Biopsy is generally unnecessary but may suit immunocompromised patients or lesions of uncertain etiology. | Observation is reasonable — many resolve spontaneously. Salicylic acid. Cryotherapy every 2–3 weeks — may cause pain, blistering and pigment change. Biopsy or refer atypical, bleeding, ulcerated, growing or refractory lesions. | Transmitted by skin-to-skin contact, autoinoculation and contaminated surfaces. No therapy eradicates the virus with certainty, and recurrence can occur. Choose treatment by location, symptoms, age, pregnancy status, immune status, and risk of scarring or dyspigmentation. Avoid excessive freezing or destructive therapy for benign lesions likely to resolve. Refer periungual, facial, extensive, recalcitrant, diagnostically uncertain or immunocompromised cases. |
 | Verruca plana (flat warts) | FLAT-TOPPED smooth slightly elevated papules · face, forehead, dorsal hands, shins | Multiple smooth, slightly elevated, FLAT-TOPPED, skin-colored to light-brown papules. Common on the face, forehead, dorsal hands and shins. “Lots of small flat bumps across my forehead and shins.” | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | Observation is reasonable because spontaneous resolution is common. Options include carefully selected salicylic acid, topical retinoids, or cryotherapy. | Shaving can spread lesions through autoinoculation. Balance treatment against the risk of dyspigmentation and scarring — particularly on the face. |
 | Verruca plantaris (plantar warts) | Weight-bearing surface · clustering into a MOSAIC wart | On the weight-bearing surface of the foot. May cluster together to form a MOSAIC wart. “It feels like I'm walking on a stone.” | Clinical diagnosis. Distinguish from a callus, which does not interrupt the skin lines and has no capillary dots. Labs to orderNone — clinical diagnosis. | Plantar warts do not require therapy unless they are PAINFUL. Salicylic acid 40% Cryotherapy | Acquired from contaminated surfaces — communal floors and showers. Recurrence is common, and no treatment guarantees eradication. |
| Lecture 9 · Pre-Malignant and Malignant Cutaneous Lesions | ||||||
 | Actinic keratosis | “Sandpaper” texture — felt before it is seen · sun-exposed face, scalp, dorsal hands | Premalignant, on a biologic continuum with keratinocyte carcinoma — not a separate entity. Small 0.2–0.6 cm flesh-colored, pink or slightly hyperpigmented papules with a sandpaper texture; more apparent by touch than by sight. Sun-exposed face, scalp, ears, forearms, dorsal hands. “Rough patches that keep coming back, and I feel them more than I see them.” | Usually clinical; dermoscopy supports it when the clinician is trained. Shave or punch biopsy when morphology or behavior raises concern for squamous cell carcinoma, or the lesion persists or recurs after therapy. Interpretation must separate actinic keratosis vs carcinoma in situ vs invasive carcinoma. Not features of a typical lesion — bleeding, induration, ulceration or rapid enlargement. Labs to orderNone — clinical, with biopsy for concerning features. | Lesion-directed (isolated, clear borders): liquid nitrogen cryotherapy — crusts and disappears over 10–14 days. Field-directed (multiple lesions in one region — field cancerization): topical fluorouracil, imiquimod, photodynamic therapy; fluorouracil plus calcipotriene possibly. | Daily broad-spectrum sun protection and protective clothing. Expect erythema and crusting from field therapy and complete the course. About 1 in 1,000 lesions per year progresses to squamous cell carcinoma, and cumulative FIELD risk matters more than any single lesion. Treatment reduces lesion burden but the field stays at risk — surveillance continues. |
 | Squamous cell carcinoma | CUMULATIVE sun exposure · small red conical HARD nodule that may ulcerate · non-healing ulcer · lip, ear, scalp | The second most common skin cancer. Prolonged CUMULATIVE sun exposure; may arise from an actinic keratosis. Small red, conical, hard nodule that may ulcerate; also a non-healing ulcer, warty nodule, or irregular pink plaque with hemorrhagic crust. “A sore on my lip that just won’t heal.” | Biopsy. Use time course, firmness or induration, ulceration, site, immune status and pathology — not morphology alone. Red flags: rapid growth, pain, bleeding, ulceration, induration, fixation, palpable regional nodes. Differential: actinic keratosis, carcinoma in situ (Bowen), keratoacanthoma, verruca, inflamed seborrheic keratosis, basal cell carcinoma, amelanotic melanoma, chronic ulcer. Labs to orderNo routine bloods. Diagnosis is by biopsy. Investigate the HOST where relevant — transplant, chronic lymphocytic leukemia, or human immunodeficiency virus status all raise risk and aggressiveness, and coordinate transplant, hematology or HIV care. | In situ (no high-risk features): imiquimod, topical fluorouracil, or curettage and electrodesiccation. Invasive: surgical excision or Mohs. Advanced/metastatic: programmed death 1 blockade; cetuximab. Mohs indications: lips, temples, ears, nose, genitalia; recurrent; perineural or perivascular invasion; >1 cm on face or >2 cm on trunk/extremities; immunosuppression; tumors in scars; genetic disease. | High-risk sites: mucosal surfaces, lip, ear, scalp, temple, nose, genitalia. >10 tumors means higher local recurrence and nodal metastasis. Common and often aggressive after transplant, with multiple tumors typically at ~5 years. Nicotinamide 500 mg twice daily cuts new tumors by ~30%. At least annual skin AND node examination. Metastatic rate 3–7%. |
 | Basal cell carcinoma — nodular | PEARLY translucent papule whose telangiectasias STRETCHING THE SKIN accentuates · central erosion · slow growth over years · INTERMITTENT intense sun | The most common form of cancer. INTERMITTENT intense ultraviolet exposure in fair skin. Papule or nodule with central erosion, slow growth over years to 1–2 cm; pearly or translucent with telangiectasias accentuated by STRETCHING the skin. “A shiny bump by my nose that scabs and comes back.” | Shave or punch biopsy. The HISTOLOGIC subtype determines behavior and dictates treatment. Clinical subtypes: superficial, nodular, pigmented, morpheaform. Histologic: superficial, nodular, micronodular, infiltrative. Differential: intradermal naevus, sebaceous hyperplasia, squamous cell carcinoma, actinic keratosis, scar/morphea, pigmented melanoma or seborrheic keratosis. Labs to orderNone. Shave or punch biopsy; the histologic subtype determines behavior and dictates treatment. | Superficial, selected: imiquimod 5 nights weekly for 6–10 weeks, or fluorouracil twice daily up to 12 weeks — confirm clearance afterwards. Surgery: curettage and electrodesiccation, excision, or Mohs by size, site and histologic risk. Excision recurrence ≤5%; Mohs cure ~98%. Advanced/metastatic: hedgehog inhibitors — vismodegib or sonidegib. | A second basal cell carcinoma develops in up to 50% — at least annual full-skin examination is mandatory. Nicotinamide 500 mg twice daily cuts new tumors by ~20% (the squamous figure is 30%). Slow-growing and highly curable early; morbidity comes from local destruction, recurrence and delayed diagnosis. Mohs for eyelids, nasolabial folds, canthi, external ear, temple; recurrence; tissue-sparing need; aggressive histology. |
 | Basal cell carcinoma — superficial | Reddish shiny scaly THIN plaque on the BACK or CHEST · thready pearly border with spotty edge pigment | Reddish, shiny, scaly thin papules or plaques on back or chest, sometimes with a thready pearly border and spotty edge pigmentation. “A dry red patch on my back that never quite clears.” | Shave or punch biopsy, as for any basal cell carcinoma. Distinguish from a superficial inflammatory dermatosis — which is why a “patch of eczema” that fails treatment gets sampled. Labs to orderNone — biopsy as for any basal cell carcinoma. | The subtype most often suitable for topical therapy: imiquimod or fluorouracil, with clearance confirmed. Curettage and electrodesiccation also used. | Warning patterns for basal cell carcinoma generally: a pearly papule, an erythematous patch >6 mm, or a non-healing ulcer — commonly face, trunk or lower legs. |
 | Basal cell carcinoma — pigmented and morpheaform | Scar-like or IVORY-WHITE = morpheaform, extends beyond what you can see · stippled pigment mimicking melanoma = pigmented | Pigmented: stippled or focal pigmentation that may mimic melanocytic disease; the pearly border and slow growth discriminate. Morpheaform/sclerosing: a scar-like or ivory-white lesion whose extension beyond the visible pink segment is clinically subtle. “A scar on my cheek, but I never cut myself there.” | Biopsy. Morpheaform disease carries a higher risk of subclinical spread, which is what makes margin control matter. Labs to orderNone — biopsy, with margin control the issue rather than any laboratory test. | Mohs for aggressive histology — morpheaform, micronodular or infiltrative — and for recurrent tumors or where tissue sparing matters. | A scar with no history of injury deserves a second look. Pigmented disease is the one that gets mistaken for a melanocytic lesion. |
 | Malignant melanoma | ABCDE — asymmetry, border, color variegation, diameter >6 mm, evolution · nodular may be amelanotic and LACK the classic features | 4th most common cancer in the United States and the leading cause of death due to skin disease; incidence doubled over 30 years. 2023: ~97,610 new invasive melanomas, ~7,990 deaths, two-thirds of deaths in men. Lifetime risk ~2% in white individuals; 0.1–0.5% in persons of color. Subtypes: superficial spreading (~2/3, radial then vertical growth); lentigo maligna (chronically sun-exposed skin, older adults); nodular — rapid, often amelanotic, may LACK the classic features; acral lentiginous. “This mole has changed shape and color this year.” | ABCDE: Asymmetry · Border irregular, notched or poorly defined · Color variegation · Diameter >6 mm — though smaller lesions can be melanoma · Evolution. Initial test: biopsy or excision. Sentinel node biopsy offered/discussed at ≥1.0 mm Breslow, or ≥0.8 mm with ulceration, high mitotic rate or lymphovascular invasion. It is a STAGING procedure and may not itself improve overall survival. Level of invasion is the anatomic layer reached (I epidermis → V subcutis) — the deck labels these only “Level I” to “Level V” and never says Clark, which is the conventional name for the same system; Breslow thickness is the dominant prognostic variable. Labs to orderNo blood test makes the diagnosis — it is biopsy or excision, and Breslow thickness from that specimen is the dominant prognostic variable. Sentinel lymph node biopsy is a staging procedure offered at ≥1.0 mm, or ≥0.8 mm with ulceration, high mitotic rate or lymphovascular invasion. | Re-excision margins: in situ 0.5–1 cm; <1 mm → 1 cm; >1 mm → 1–2 cm. Refer to an expert center for melanoma deeper than 1 mm or with nodal/other-site spread. | Monthly self-examination using ABCDE and ugly-duckling principles — including scalp, back, palms, soles and nails. Consistent ultraviolet protection; adhere to the specialist surveillance schedule. Breslow thickness must be measured accurately at the initial biopsy; ulceration and mitotic activity further modify stage-based prognosis. |
 | Nail unit melanoma | Longitudinal melanonychia in ONE digit, widening PROXIMALLY (triangular) · Hutchinson sign onto the proximal nail fold · thumb, great toe | Rare acral melanoma arising most often in the MATRIX. Not clearly ultraviolet-driven; may occur in any skin tone. Thumb and great toe are high-yield sites. Signs: new or evolving longitudinal melanonychia in ONE digit; increasing width; irregular color, thickness or spacing of lines; proximal widening or triangular shape; blurred borders; nail splitting or dystrophy; ulceration or a subungual mass. “A dark stripe in one nail that’s getting wider.” | Hutchinson sign — periungual pigment extending onto the proximal nail fold — is highly concerning and should prompt urgent expert evaluation regardless of other features. Amelanotic nail melanoma may be red, pink, eroded or mass-like with no dark band; absence of pigment does NOT exclude melanoma. Remove polish and inspect every nail, periungual skin, palms, soles and regional nodes. Onychoscopy. Labs to orderNone. Diagnosis is by nail unit biopsy after onychoscopy; staging follows melanoma principles. | Coordinate dermatology, nail surgery and surgical oncology. Digit-sparing wide excision or Mohs with immunostaining for in situ and selected invasive tumors when margins can be reliably assessed. Amputation is NOT automatic — reserved for deep, extensive or bone-involving disease. Sentinel node discussion and systemic therapy follow melanoma stage and Breslow principles. | Delayed recognition contributes to advanced-stage presentation. Check nails during self-examination. Urgent referral: new or changing single-digit melanonychia, proximal widening, Hutchinson sign, nail dystrophy with pigment; unexplained subungual mass or persistent ulceration/bleeding; a chronic “wart” or “infection” failing appropriate therapy. |
 | Nail unit squamous cell carcinoma / Bowen disease | Chronic UNILATERAL verrucous nail lesion repeatedly treated as a wart, paronychia or fungus · longitudinal erythronychia | The most common malignant nail tumor. Chronic unilateral verrucous periungual papule or plaque, subungual hyperkeratosis, onycholysis, oozing, bleeding, ulceration, nail-plate destruction, longitudinal erythronychia, or pain — often repeatedly labeled a wart, paronychia or fungal infection. “They’ve treated this as a wart three times and it’s still there.” | Associations: high-risk human papillomavirus, immunosuppression, chronic inflammation or trauma, prior radiation, older age. Periungual disease may be multifocal. Biopsy any chronic lesion that fails appropriate therapy. Labs to orderNo routine bloods. Biopsy any chronic lesion failing appropriate therapy. Associations worth noting in the history: high-risk human papillomavirus and immunosuppression. | Complete margin-controlled surgery preferred — Mohs or wide surgical excision. Partial or limited destructive treatment carries a higher recurrence risk. Distal phalanx or digital amputation reserved for bone invasion or disease that cannot otherwise be cleared. | The recurring theme of this module is diagnostic delay as a preventable harm. A nail lesion that has been treated as something benign more than once is the one to biopsy. |
 | Glomus tumor and the benign nail tumors | Severe paroxysmal pain + exquisite point tenderness + COLD SENSITIVITY, with a nearly normal-looking nail | Glomus tumor: small red-blue subungual focus with severe paroxysmal pain, exquisite point tenderness and cold sensitivity — the nail may look nearly normal. Onychopapilloma / onychomatricoma: a single nail with longitudinal erythronychia or leukonychia, distal subungual hyperkeratosis, splinter hemorrhages or localized plate abnormality. “It’s agony in cold water and I can point to the exact spot.” | The glomus triad strongly suggests the diagnosis but does not replace imaging or specialist evaluation. Other benign tumors that mimic malignancy: acquired digital fibrokeratoma, melanocytic naevus or lentigo, pyogenic granuloma, digital myxoid cyst, subungual exostosis. Labs to orderNone. The clinical triad suggests it; imaging and specialist evaluation are still required, and the triad does not replace them. | Diagnosis-specific surgical removal when symptoms, growth or diagnostic uncertainty warrant it. | These matter because they mimic malignancy — and because a painful nail with a normal-looking plate is easy to dismiss. |
 | Kaposi sarcoma | Red or purple macules, plaques or nodules — including the HARD PALATE · human herpesvirus 8 + immunosuppression · edema out of proportion to visible lesions | Caused by human herpesvirus 8 combined with a weakened immune system, arising in the cells lining blood and lymph vessels. Red or purple macules, plaques or nodules on skin or mucous membranes. Four forms: classic (older men, chronic, rarely fatal); endemic (young Black men in equatorial Africa, often aggressive); iatrogenic (immunosuppressive therapy); epidemic (acquired immunodeficiency). “Purple patches on my legs, and my mouth is sore.” | ORAL EXAMINATION IS ESSENTIAL when Kaposi sarcoma is suspected — hard palate lesions are common and may be the presenting site. Marked edema may occur with few or no visible skin lesions — do not use edema severity to gauge disease burden. Differential: bacillary angiomatosis, angioma/hemangioma, purpura, venous stasis, pyogenic granuloma, lymphoma, metastatic disease. Labs to orderHuman immunodeficiency virus testing and staging matter here — immune status defines the clinical form and drives treatment. Diagnosis itself is by biopsy. In epidemic disease the first priority is starting or optimizing antiretroviral therapy. | Epidemic (AIDS-associated) — FIRST PRIORITY: begin or optimize antiretroviral therapy. Immune restoration is the cornerstone. Classic/older adult: palliative local therapy — intralesional vincristine, vinblastine or bleomycin, or radiation. Iatrogenic: reduce immunosuppressive doses where feasible — coordinate with the transplant team first. Systemic first-line: liposomal doxorubicin and paclitaxel. Antiretroviral therapy plus chemotherapy beats antiretroviral therapy alone in advanced disease. | Report respiratory or gastrointestinal symptoms — visceral disease. Referral spans dermatology for biopsy, human immunodeficiency virus care, medical oncology, pulmonology or gastroenterology, the transplant team before any dose change, and palliative care. |
 | Cutaneous T-cell lymphoma (mycosis fungoides) | Patches/plaques >5 cm that look like eczema or psoriasis but RESIST treatment for years · itch out of proportion · follicular hair loss | A cutaneous T-cell lymphoma that begins in the skin and may remain confined there for years or decades. Early: localized or generalized erythematous patches or scaly plaques, usually on the trunk, frequently >5 cm. May resemble psoriasis, eczema or tinea, which is why diagnosis is often delayed. “They’ve called it eczema for four years and nothing works.” | Two clues: itch out of proportion to the apparent inflammatory activity, and follicular involvement with hair loss — folliculotropism discriminates from routine eczema or psoriasis. Discriminators: chronicity, treatment resistance, large or oddly distributed plaques, severe pruritus, tumors or erythroderma, nodes, and histology. Enlarged nodes may be benign dermatopathic change OR lymphoma — directed biopsy or imaging is required. Labs to orderHistology is the diagnosis, and it often takes repeated biopsies over time. Blood involvement is assessed when Sézary syndrome or erythroderma is suspected; enlarged nodes need directed biopsy or imaging rather than assumption. | Stage-directed, skin-first. Early aggressive treatment has NOT been proven to cure or prevent progression, and may cause complications and premature death. Initial skin-directed: topical corticosteroids, topical mechlorethamine, bexarotene gel, ultraviolet phototherapy. Progressive: PUVA ± retinoids or interferon; methotrexate; extracorporeal photopheresis; systemic bexarotene; romidepsin or vorinostat; brentuximab or mogamulizumab; total-skin electron-beam treatment. | Diagnosis may take repeated biopsies over time. Referral: dermatology/dermatopathology early for persistent suspicious disease; a cutaneous lymphoma center once blood, node, tumor or erythrodermic involvement is suspected. |
| Lecture 8 · Pigmented Skin Lesions | ||||||
 | Ephelides (freckles) | FADE when the sun goes · 3–5 mm light brown symmetric macules · fair skin, red or blonde hair · MCR1 | Asymptomatic small light brown symmetric macules, 3–5 mm, on sun-exposed skin of fair-skinned people, often with blonde or red hair and possibly Celtic ancestry. Autosomal dominant. More pronounced in spring and summer, fading in winter; first appear in young children and regress later in life. “I've had freckles since I was small — they come out every summer.” | Clinical diagnosis. Histopathology (not needed) shows a normal to reduced number of hypertrophic melanocytes with increased melanin in the basal epidermal layer. Main differential: lentigines. Labs to orderNone — clinical diagnosis. | 1st: sun protection, with proper patient education and counseling — this is the key. 2nd: topical depigmenting agents — hydroquinone, retinoids, alpha-hydroxy acids, botanicals. Preferred procedure: intense pulsed light or laser, though lesions can relapse. NO CRYOTHERAPY — difficult because of the size of the lesions. | Related to a mutation in the MCR-1 gene — the receptor for alpha-melanocyte-stimulating hormone, which activates melanogenesis via cyclic adenosine monophosphate. Decreased pathway activity promotes pheomelanin, the yellow-red sulfur-containing pigment. The distinction from lentigines: freckles fade when the sun goes; lentigines do not. |
 | Lentigines | Do NOT fade without sun — the whole differential against freckles · uniformly black or brown, well circumscribed, <5 mm | Common melanocytic lesion, “age spots”. Benign, well-circumscribed, round to oval, uniformly black or brown macules under 5 mm. On skin, conjunctiva and mucocutaneous surfaces, and on both sun-exposed and sun-protected areas. Bimodal age distribution — early childhood or later life. Do NOT fade with cessation of sun exposure. Types: lentigo simplex, acral, agminated (a grouping of small light brown macules), generalized. | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | Treatment is not necessary. Cosmetic removal if the patient prefers: cryotherapy or quality-switched laser. | Can be associated with isolated or inherited disorders. An inherited disorder should be considered if a partial or generalized lentigo is present — for example LAMB or myxoma syndrome. Lentigo simplex does not carry the mutations found in solar lentigo, PUVA lentigines or common acquired naevi. |
 | Solar lentigo also Lecture 3 | Well defined but irregular borders that COALESCE at severe sunburn sites · chronically exposed skin | Arises from proliferation of basal melanocytes with increased melanin production. Well-defined but with irregular borders, tending to coalesce at sites of severe sunburn; from under 1 mm to several centimeters; light to dark brown. Over time they enlarge, darken, stay stable, regress, or progress into lichenoid keratoses. PUVA lentigines appear on sun-protected sites (buttocks, genitalia) as well as exposed, with brown/black irregular pigmentation. | Dermoscopy — finger-like projections, “moth-eaten” border. Biopsy if atypical or uncertain, especially to exclude lentigo maligna (asymmetric, irregular border and color, darker areas; structureless irregular pigment on dermoscopy). Reflectance confocal microscopy as an adjunct. Labs to orderNone — dermoscopy, with biopsy only if atypical. | Treatment is not necessary. Cosmetic removal: retinoids, cryotherapy, or quality-switched laser. | Strongly associated with older age (90% at 50), sun damage, ephelides, tanning, and birth control use. Also associated with actinic keratosis, squamous cell carcinoma, basal cell carcinoma and melanoma. PUVA lentigines relate to total number of treatments, male sex, fair skin and older age. |
 | Seborrheic keratosis | “STUCK ON” or pasted-on, velvety or warty, beige to black · dermatosis papulosa nigrans is the SAME lesion, small, on the FACE of darker skin | Benign papules and plaques, beige to brown to black, 2–20 mm, feeling velvety or warty and appearing stuck or pasted onto the skin. Common in older adults. “A dark warty growth that looks like it's been stuck on.” | Clinical diagnosis. Dermoscopy shows comedone-like openings. Labs to orderNone — clinical diagnosis. | Management is supportive. If itchy or inflamed: cryotherapy may help — however they do recur after treatment. | Easily mistaken for neoplasms — which is exactly why they matter in an older adult presenting with a new dark growth. |
 | Dermatosis papulosa nigrans | Multiple small dark papules on the FACE and NECK of darker skin · histologically identical to seborrheic keratosis — the site and the skin tone are the clue | Multiple small (1–5 mm), smooth, firm, black or dark brown papules on the face and neck. Identical to small seborrheic keratoses. Common in African Americans, dark-skinned Asians and Polynesians; females more than males. “These little dark bumps on my cheeks — my mother has them too.” | Clinical diagnosis (biopsy if uncertain). Labs to orderNone — clinical, with biopsy only if uncertain. | Best left untreated. If treatment is wanted: excision, curettage or laser. AVOID CRYOTHERAPY — post-inflammatory hyperpigmentation. | Likely genetic, and believed to be a developmental defect of the hair follicle. Benign. |
 | Vitiligo | Depigmented (not hypo-) macules that FLUORESCE under Wood lamp · distinct margins · autoimmune, T-cell destruction of melanocytes | Common autoimmune disease causing depigmentation through T-cell mediated destruction of melanocytes. Can begin at any age but usually starts before the thirties — half before 20, a third before 12. Males and females equally affected. Asymptomatic white, non-scaly macules and patches with distinct margins that FLUORESCE under a Wood's lamp. Usually symmetrical; face, acral and genital areas are often the initial sites. Segmental variant: unilateral, does not cross the midline, block-like patterns, with unpredictable cycles of flare and stabilization. “White patches are spreading and people stare — I've stopped going out.” | Clinical diagnosis. Wood's lamp examination in a DARK ROOM. Labs to correlate with associated autoimmune disease: complete blood count and antinuclear antibody. Distinguishing segmental from non-segmental matters — they differ in diagnostic tools and treatment. Labs to orderComplete blood count and antinuclear antibody, to correlate with the other autoimmune diseases associated with it. | Under 5% body surface (with phototherapy): topical steroids (good efficacy, easy, cheap — watch skin atrophy and intraocular pressure) or topical calcineurin inhibitors — tacrolimus, pimecrolimus — safe and good for face, neck, intertriginous areas and children, but with increased cancer risk. Over 5% body surface: PHOTOTHERAPY is first line — narrowband ultraviolet B, preferred over PUVA (PUVA raises skin cancer risk). Combination of topical + phototherapy is ideal. Surgical (tissue and cellular grafting): only for highly stable disease. | Do not dismiss it as “cosmetic”. It affects patients psychologically and socially through low self-esteem and poor body image. Psychological intervention is part of management, alongside cosmetic and non-traditional therapies. Management is multifactorial — take a thorough medical, social and family history. |
 | Congenital melanocytic naevus | Present at birth · may be pebbly, rugose, verrucous · head, neck or posterior midline → magnetic resonance for neurocutaneous melanosis | Pigmented neoplasms of melanocytes evident at birth or shortly after, from somatic mutations. Flat brown patches or plaques with smooth or slightly uneven borders; may be pebbly, rugose, verrucous or lobular. Small, medium or large. Most commonly trunk and extremities, though scalp and face are affected. The larger the lesion, the higher the risk for melanoma. | Clinical diagnosis; sometimes biopsy. If on the cranium or axial midline, consider NEUROCUTANEOUS MELANOSIS — get MRI brain with or without total spine, concordant with the anatomic location of the naevus. Labs to orderNo bloods. Magnetic resonance imaging of brain, with or without total spine, if cranial or axial — for neurocutaneous melanosis. | Depends on melanoma risk plus cosmetic and functional considerations. The goal is to remove as much as possible while preserving function and improving appearance. Observation versus surgical — ideally surgical, but if there is little skin for a graft site, observation may be the better option. Symptoms are another indication. | Risk: neurofibromatosis type I. Neurocutaneous melanosis affects patients with naevi on head, neck or posterior midline — seizures, hydrocephalus, neurological deficits and vomiting within the first few years of life, and the prognosis is poor once neurological symptoms appear. Counseling and support groups assist families and patients with large naevi. |
 | Naevus spilus | Café-au-lait-like background patch SPECKLED with darker macules · “spotted naevus” | “Spotted naevus” — a variant of congenital naevus, present at birth or in the first years of life. Background pigmentation is circumscribed and similar to a café-au-lait spot in hue, with even light pigmentation, carrying scattered superimposed more darkly pigmented macules or papules. The tan macular background ranges from under 1 cm to over 10 cm. Most commonly trunk and extremities. | Clinical. Labs to orderNone — clinical, with periodic evaluation. | Observation with periodic clinical evaluation. | Rarely progresses to melanoma. Sun protection counseling. Associated with other anomalies of vascular, central nervous system or connective tissue origin. |
 | Common acquired melanocytic naevus (mole) | <6 mm, homogenous, symmetric, sharply demarcated · peaks in the thirties then declines · very dark or black on light skin is suspicious | Develops slowly after birth, enlarges symmetrically, stabilizes and regresses. Numbers peak in the thirties and decline afterwards. Usually under 6 mm, homogenous surface and color (skin colored, brown, pink), round to oval with sharp demarcation. Can be anywhere. Very dark brown or black on a light-skinned individual is suspicious. | Clinical diagnosis. Labs to orderNone — clinical diagnosis. | Observation. Remove for cosmetic reasons or symptomatic relief. | Proper counseling on sun protection. Melanoma risk increases with the number of naevi. Increased numbers in patients with light skin tone and those who tend to sunburn. Risk factors: ultraviolet exposure, male sex, and a genetic component. |
 | Blue naevus | BLUE, blue-gray or blue-black — pigment deep in the DERMIS · women, twenties · dorsal hands and feet, scalp, buttocks | A group of lesions composed of deeply pigmented spindle or epithelioid melanocytes in the DERMIS. Affects women more than men, most commonly in their twenties. Blue, blue-gray or blue-black. On the dorsal hands and feet, scalp, buttocks or sacral region. Common blue: deeply pigmented, under 1 cm, arising in adolescence. Cellular blue: larger plaques or nodules over 1 cm, arising before age 40. | Clinical for small lesions. Biopsy for larger lesions. Labs to orderNone — clinical for small lesions, biopsy for larger ones. | Observation. Biopsy or excision if changes are noted. | Includes common blue, cellular blue, combined blue and atypical cellular blue lesions. |
 | Pigmented spindle cell naevus (Reed) | JET-BLACK sharply circumscribed papule <7 mm on the THIGH · thirties, female · excision with negative margins | Commonly in the thirties; females more than males. Found on the extremities, mainly the lower extremities and especially the thigh. A sharply circumscribed darkly pigmented papule, usually under 7 mm, JET-BLACK but may have shades of blue, gray or brown. Benign. | Confirm with biopsy. Labs to orderNone — biopsy confirms it. | Excision with negative margins. | Benign despite the alarming jet-black appearance — but it is one of the lesions in this lecture that gets a knife rather than a follow-up appointment. |
 | Spitz naevus | Solitary pink or red DOME-SHAPED firm papule that RESEMBLES MELANOMA · spares palms, soles and mucosa · biopsy vs wide excision | Usually benign, with a phase of growth (fast or slow) followed by a stable period. Solitary, asymptomatic, pink or red, hairless, firm and dome-shaped. Several millimeters to centimeters. Located on face, neck, trunk and extremities; SPARES palms, soles and mucous membranes. Sometimes resembles melanoma. | Biopsy versus wide excision. Labs to orderNone — biopsy or wide excision. | Excision. | Multiple lesions can be associated with a familial cancer syndrome. |
 | Dysplastic melanocytic naevus | ≥5 mm with IRREGULAR INDISTINCT borders and variable pigment · “pebbly” surface · sun-exposed skin | Common in Caucasians. At least 5 mm in diameter with irregular, indistinct borders, variable pigmentation (tan to brown) with a smooth or “pebbly” surface. Common on sun-exposed skin. In dysplastic naevus syndrome there can be over 100 naevi by adolescence. May progress to melanoma — the higher the number of naevi, the higher the risk. | Diagnosis is by biopsy. Labs to orderNone — diagnosis is by biopsy. | Observation. Biopsy on ALL changing or developing lesions. Excision where there is concern for melanoma. Sun protection. | Risk factor: family history. The relationship between naevus count and melanoma risk is the point to carry away. |
| Lecture 7 · Benign Skin Lesions | ||||||
 | Clavus (corn) — hard | CENTRAL KERATIN CORE · <1.5 cm, well defined · painful on DIRECT DOWNWARD pressure · skin lines RUN THROUGH · dorsal/lateral 5th toe | Focal mechanical trauma (ill-fitting shoes) → hyperkeratosis with a cone-shaped central core of hard keratin pointing into the skin. Well defined, <1.5 cm, painful on direct downward pressure. Skin lines run through it. Clavus durum favors the dorsal and lateral fifth toe. “It's like walking on a pebble — right on this one spot.” | Clinical diagnosis. No testing needed. Differential: callus (larger, irregular, painless, no core) and verruca vulgaris (interrupts skin lines, blackened center, hurts on side pressure, not confined to pressure areas). Labs to orderNone. Purely clinical. In a diabetic patient the relevant work-up is a foot risk assessment — sensation, pulses, glycemic control — not blood tests for the lesion. | 1st: remove the pressure — padding, and stop wearing poorly fitting footwear. 2nd: over-the-counter keratolytic products. Every one in the deck's table is salicylic acid, 12.6–40%, as a disk, liquid or plaster. Diabetic patient → refer to podiatry. | Caused by shoes too tight or too loose, shoes without socks, going barefoot, and tools or sports equipment rubbing the skin. To heal and prevent: properly fitting shoes and socks, avoid high heels, avoid barefoot, use pads inside the shoe. |
 | Clavus (corn) — soft | 4th-to-5th toe WEB SPACE, macerated by moisture · still has the central core | Same pressure mechanism, but sited in the fourth-to-fifth toe web space, where trapped moisture macerates it — hence clavus mollum, “soft”. Still has the central core. “There's a sore white patch between my little toes.” | Clinical diagnosis. Distinguish from an interdigital fungal infection, which is scaly and itchy rather than cored and tender. Labs to orderNone. Clinical. Potassium hydroxide preparation only if an interdigital fungal infection is the real question. | 1st: as for hard corn — padding and footwear change, plus keeping the web space dry. 2nd: salicylic acid keratolytics. Diabetic → podiatry. | Dry carefully between the toes after washing. Wear socks that wick moisture. The same footwear advice as for any corn. |
 | Callus | NO central core · diffuse, larger, irregular, poorly defined · usually PAINLESS · palms or balls of the feet | Broad-area pressure and friction → diffuse hyperkeratosis with no central core. Larger than a corn, irregular and poorly defined, and usually painless. Typically the palms or the balls of the feet. If the process is acute and severe, a blister forms instead. “The skin on my hands has gone thick and yellow, but it doesn't hurt.” | Clinical diagnosis. The three-way differential is corn (cored, tender, small), callus (diffuse, painless, large) and wart (skin lines interrupted, blackened center). Labs to orderNone — clinical diagnosis. | 1st: padding and better-fitting footwear or gloves. 2nd: over-the-counter salicylic acid keratolytics. Diabetic → podiatry. | Same prevention as corns. A callus is protective as well as symptomatic — the aim is to reduce it, not to remove the protection entirely. |
 | Keloid | EXTENDS BEYOND the original wound · develops slowly, may appear months later, no regression · ear lobe, shoulders, sternal notch · darker skin | A fibroproliferative disorder; pathophysiology remains unclear. Overgrowth of dense fibrous tissue that extends beyond the margins of the original wound, develops slowly and keeps enlarging for months to years, with no regression and a tendency to recur. Firm bulbous nodules or markedly elevated plaques. Predominantly ear lobe, shoulders, sternal notch; rarely across joints. Rare incidence but associated with dark skin color — African American, Hispanic and Asian patients. Triggers: surgical incisions, traumatic wounds, vaccination sites, burns, chickenpox, acne, even minor scratches. “I got my ears pierced and this lump keeps growing — it's way bigger than the hole was.” | Clinical diagnosis. Biopsy only if there is genuine clinical doubt, because it may induce new scarring. Differential: hypertrophic scar, dermatofibroma, foreign-body granuloma. Labs to orderNone. Clinical diagnosis. Biopsy is actively discouraged unless there is real doubt, because it may induce new scarring. | Most important treatment is PREVENTION — advise high-risk patients to avoid cosmetic procedures such as ear piercing. No single modality is best; combination therapy has the best success rates. Occlusive silicone gel sheets 12–24 h/day for up to a year. Compression at 25 mmHg, 24 h/day, 6–12 months. Intralesional steroid (flattens; may cause tissue atrophy). Surgical removal — but 50–100% recurrence, often larger, so always follow with intralesional steroid. Radiation in the first two weeks after excision. Cryotherapy (flattens; causes hypopigmentation). Laser, best combined with intralesional steroid. Intralesional fluorouracil — inhibits fibroblast proliferation. | Post-surgery: avoid stretching the immature scar, avoid hot baths (they aggravate surgery-induced inflammation), keep the wound clean. Avoid body piercings. Adolescents with acne should seek early, appropriate acne treatment — it greatly increases the chance of scar-free healing. |
 | Hypertrophic scar | CONFINED to the wound margins · within four weeks · regresses with time · where scars cross joints at a right angle | The active proliferative phase of wound healing overshooting. Develops rapidly, within four weeks of the event, and stays confined to the wound margins. Remains stable and then regresses (flattens) with time. Asymptomatic. Occurs where scars cross joints or skin creases at a right angle. Frequent incidence, and no association with skin color. “My scar went thick and red about a month after the operation, but it stops right at the edges.” | Clinical diagnosis. Biopsy only if there is clinical doubt, as it may induce new scarring. Differential: keloid, dermatofibroma, foreign-body granuloma. Labs to orderNone. Clinical diagnosis, with the same biopsy caution as keloid. | Intralesional injection — corticosteroid or fluorouracil. Compression therapy and silicone sheeting. Surgical excision — unlike keloid, hypertrophic scars improve with appropriate surgery. Pulsed dye laser — reduces erythema by reducing neovascularization. | Reassure: this is the scar that gets better. It should flatten on its own over months. Distinguish it plainly from keloid, which does not. |
 | Cutaneous horn | Keratin projection ARISING FROM ANOTHER LESION — the base is what matters · deep shave biopsy | A hard conical exophytic projection composed of keratin, with the appearance of an animal horn. It arises from the surface of another lesion — benign or malignant: actinic keratosis, wart, seborrheic keratosis, keratoacanthoma, or basal or squamous cell carcinoma. The process at the base of the lesion is what matters. Caucasians over 50, males = females, on head, neck and upper extremities, commonly sun-exposed face, ears and hands. May bleed or hurt from trauma. “There's a hard little horn growing out of my ear.” | Often NO clinical feature distinguishes benign from malignant. Gold standard: deep shave biopsy to sample the underlying tissue. Differential: wart, actinic keratosis, squamous cell carcinoma. Labs to orderNo bloods, but tissue is essential. Deep shave biopsy to sample the base — the only way to know whether the underlying lesion is benign or malignant. | Depends entirely on the underlying etiology. An underlying malignancy frequently requires excision to the standard practice for that tumor type and location. Removing the horn alone treats nothing. | Explain that the horn itself is only keratin, and the reason for biopsy is what lies beneath it. Counsel on sun protection and periodic skin examination. |
 | Acrochordon (skin tag) | PEDUNCULATED — narrow stalk, broad tip · friction sites: neck, axilla, groin · 60% of people by 70 | A fibroepithelial pedunculated papilloma — a narrow stalk with a broad tip. Soft, skin-colored papules from about 1 mm to 10 mm. Asymptomatic. Increased in females and obese patients, in areas of friction — neck, axilla, groin. Very common: present in 60% of people by age 70. “I've got these little flaps of skin under my arms and they catch on my clothes.” | Clinical diagnosis. No testing needed. Labs to orderNone. Clinical. | Usually for cosmesis only. Scissor excision, cryotherapy, or electrodesiccation. Anesthesia is not necessary. | Harmless growths of normal skin. They form where skin rubs together — armpit, neck, under the breasts, groin — and become more likely with age and with excess weight. Never cut or pull one off yourself: they bleed. A new tag often forms in the same area after removal. |
 | Pressure injury (pressure ulcer) | NON-BLANCHABLE erythema over a BONY PROMINENCE = stage 1 · obscured by slough or eschar = unstageable · the non-blanching is the whole point | Unrelieved pressure damaging underlying tissue, generally soft tissue compressed between a bony prominence and an external surface for a prolonged time. Extent ranges from non-blanchable intact skin to deep ulcers reaching bone. STAGING (from the slide's images): 1 — localized non-blanchable erythema of intact skin. 2 — partial-thickness loss with exposed dermis; bed viable, pink/red, moist, shiny or dry. 3 — full thickness; adipose tissue visible. 4 — full thickness skin AND tissue loss; fascia, muscle, tendon, ligament, cartilage or bone exposed. Unstageable — obscured by slough or eschar, extent cannot be determined. Deep tissue — persistent non-blanchable deep red/purple discoloration; skin intact or not. | Clinical diagnosis and staging. The staging tables illustrate every stage in both lightly and darkly pigmented skin — non-blanchable erythema is harder to see and easier to miss on darker skin. Labs to orderNo test diagnoses or stages it — staging is visual. Bloods support management rather than diagnosis: nutritional markers (albumin, prealbumin) because nutrition assessment is part of prevention, and inflammatory markers plus culture only if infection is suspected. Deep or non-healing wounds over bone may warrant imaging for osteomyelitis. | Best measure is PREVENTION: frequent skin assessment, nutrition assessment, moisture control and skin care (keep clean and dry, manage incontinence, barrier creams), reposition every two hours, manage pain, improve mobility, specialty mattresses. Management depends on stage. Refer to a wound care specialist. Control infection risk. Silicone and hydrocolloid dressings. Surgical referral for debridement — removes necrotic tissue, eschar and slough, which promote infection, delay granulation and impede healing — and for wound closure. | For carers: reposition two-hourly, keep skin clean and dry, manage incontinence promptly, and check the skin over every bony prominence at every opportunity. Report any non-blanching red area at once. |
 | Pilonidal cyst | Pit over the COCCYX drawing in hair and debris · male 3:1 · sinus = blind track; fistula = joins two epithelial surfaces | Disruption of the skin over the coccyx leaves a dimple (pit) that draws in hair and debris → follicular plugging; ingrown hairs prevent drainage and promote abscess formation. Male to female 3:1. Originally thought congenital, now believed acquired. Recurrence is common. Risk factors: obesity, local trauma or irritation, sedentary lifestyle, increased hair density in the natal cleft, family history. Acute abscess: sudden pain and swelling in the gluteal cleft; warm, tender, erythematous, purulent or bloody drainage, may be fluctuant. Chronic: recurrent drainage and pain from one or more sinus tracts; a hair may be seen protruding from a sinus opening. “I get a painful swelling at the top of my bum crack, and sometimes it bursts and drains.” | No diagnostic testing usually needed. Sinus vs fistula (from the slide's diagram): a sinus is a BLIND track; a fistula connects TWO epithelium-lined surfaces. Both usually arise from a preceding abscess. Labs to orderNone usually needed. Clinical diagnosis. Culture of drainage is not routine. | 1st: keep the area clean and free of debris; shaving or laser hair therapy may help. Acute abscess → incision and drainage. Chronic disease → refer to a surgeon for excision. | Maintain good hygiene of the natal cleft, and seek care if an abscess occurs. Recurrence is common, so hair control and hygiene are ongoing rather than one-off. |
 | Dermatofibroma | DIMPLE SIGN — retracts on lateral compression · firm 0.5–1 cm nodule on the LEGS · most common painful skin tumor | Fibroblasts in the dermis forming small dense clusters → a firm 0.5–1 cm nodule. Legs are the commonest site, then arms. Male to female 1:2, all races. Etiology uncertain — may follow trauma, viral infection or insect bites. Usually asymptomatic; if symptomatic, slight pruritus or pain — it is the most common painful skin tumor. Firm nodule with a hyperpigmented brown halo, pink hue, raised center, scaly surface. DIMPLE SIGN: the lesion retracts beneath the skin surface with lateral compression. “There's a hard little brown bump on my shin — I think it started after a bug bite.” | Clinical diagnosis, supported by dermoscopy — often shows a peripheral pigment network with a central white mass. Differential: basal cell carcinoma, hypertrophic scar, cutaneous melanoma, keratoacanthoma. Labs to orderNo bloods. Dermoscopy supports it; shave or punch biopsy is both diagnostic and therapeutic in a small lesion. | Often no treatment unless the diagnosis is questioned or symptoms warrant it. Small lesions: shave or punch biopsy — both diagnostic AND therapeutic. Larger lesions: may require surgical excision. | Benign. The dimple sign is what distinguishes it from the pigmented lesions it can resemble. Return if it changes in size, color or shape. |
 | Keratoacanthoma | Dome with a CENTRAL KERATIN-FILLED CRATER · rapid growth in 6–8 weeks, then regression · red tattoo ink, skin trauma | Believed to arise from the pilosebaceous unit. Rapid, abundant growth then spontaneous resolution — but it may keep growing or rarely metastasize. Histopathologically similar to squamous cell carcinoma; strong arguments support classifying it as a VARIANT of invasive squamous cell carcinoma. Classic in middle-aged, light-skinned people in hair-bearing sun-exposed areas. Males > females. Risk factors: age >40, sun exposure, very fair skin that always burns and never tans, male sex, tattoos (red ink), skin trauma such as lasers, surgery or cryotherapy, human papillomavirus infection. Triphasic: rapid growth in 6–8 weeks, stabilization, regression after 3–6 months. Solitary, smooth, shiny, dome-shaped red papule or nodule with a central keratin-filled crater — resembles a volcano. “This came up out of nowhere in about six weeks and it's got a crusty plug in the middle.” | Biopsy is the ONLY reliable method to make the diagnosis. Differential: squamous cell carcinoma, basal cell carcinoma, amelanotic melanoma, molluscum contagiosum. Labs to orderNo bloods, but BIOPSY IS MANDATORY — it is the only reliable method of diagnosis, because the lesion cannot be separated from squamous cell carcinoma clinically. | Surgical — standard of care is to excise or destroy the tumor, preferred because of possible malignancy. Elliptical excision with 5 mm margins. Mohs surgery for large or recurrent lesions, or lesions in areas with cosmetic or functional considerations. Intralesional methotrexate may be given before excision to reduce the size — it inhibits deoxyribonucleic acid synthesis in actively dividing cells. | Do not wait for it to regress. Even though many do, it cannot be told from a squamous cell carcinoma without histology, so it is treated as one. Counsel on sun protection. |
 | Epidermoid (epidermal) cyst | CENTRAL PORE / punctum · expresses pasty material smelling of rancid cheese · NOT a sebaceous cyst despite the name | Cystic enclosure of epithelium within the dermis, filling with KERATIN. Often called a “sebaceous cyst” because the contents look like sebum — it is not one. Males > females 2:1; very common, on face, scalp, neck and trunk. Usually asymptomatic; may drain foul-smelling material. Single firm papule or nodule, movable, round, protruding, with a central pore or punctum communicating with the skin surface. Expresses cream-colored pasty material with the odor of rancid cheese. “There's a lump on my back with a little hole in the middle, and if I squeeze it something white and awful comes out.” | Clinical diagnosis. Lab tests usually unnecessary. Differential: cystic acne, lipoma, neurofibroma, keratoacanthoma, basal cell carcinoma. Labs to orderLab tests usually unnecessary. Culture only if an inflamed cyst is thought to be secondarily infected. | Asymptomatic: no treatment necessary. If inflamed: POSTPONE excision for a few weeks, reduce inflammation with intralesional triamcinolone, add antibiotics if needed. Standard of care is surgical removal of the ENTIRE capsule, performed when the cyst is not inflamed. A small cyst (1–3 cm) can be treated with a punch incision and removal of the cystic contents. | The lump is keratin, not oil, and it is benign. Squeezing it risks rupture and inflammation. If it becomes red and painful, come in — that is the point at which surgery is delayed rather than brought forward. |
 | Syringoma | ECCRINE duct neoplasms · multiple 1–2 mm papules on the EYELIDS and upper cheeks · appear at puberty, female | Benign neoplasms of ECCRINE ducts (sweat glands). Appear at puberty; females > males. Usually asymptomatic. Multiple 1–2 mm skin-colored, pink or brown papules, most frequently on the eyelids (periorbital region) and upper cheeks. “I've got these tiny bumps under my eyes — they came up in my teens.” | Usually clinical; biopsy if there is concern about malignancy. Differential: milia, xanthelasma, basal cell carcinoma. Labs to orderNone. Usually clinical; biopsy only if malignancy is a concern. | For cosmesis only, and every option has a trade-off. Drugs (e.g. oral isotretinoin) — increased risk of recurrence. Removal procedures (curettage and electrodesiccation, laser therapy, cryotherapy, surgical excision) — possible poor cosmetic results. | Benign and harmless. Any treatment is elective, and the periorbital skin makes cosmetic outcome the main consideration. Recurrence is common with medical treatment. |
 | Infantile hemangioma | INVOLUTES — 50% by 5, 70% by 7, 90% by 9 · preterm, female 3:1 · earliest sign is BLANCHING, then fine telangiectasias, then bright red | Congenital vascular lesion; the most common tumor of infancy, and most are medically insignificant. A benign neoplasm from rapid proliferation of endothelial cells, from mutations in the genes regulating it. Usually noticed in the first days to weeks; usually single; typical maximum size 0.5–5 cm. More common in preterm infants, females 3:1, Caucasians. Head and neck 60%, trunk 25%, extremities 15%. Earliest sign: blanching of the involved skin, then fine telangiectasias, then a red/crimson macule. 50% present at birth. Growth: rapid birth–4 weeks, most growth in the first 4–6 months, slowing 6–12 months. Involution: 50% by age 5, 70% by 7, 90% by 9. Superficial (most common) — dilated vessels in dermis, bright red papule/plaque/nodule, once called “strawberry”. Deep (least common) — deep dermis and subcutis, pale/skin-colored/red/blue nodule. | Most are diagnosed clinically. If the diagnosis is in question, refer to an appropriate and experienced vascular anomalies specialist. Differential: nevus flammeus (present at birth, present for life) and pyogenic granuloma (due to minor trauma). Labs to orderNone for a typical lesion — most are diagnosed clinically. Referral to a vascular anomalies specialist replaces testing when the diagnosis is in question; imaging is that specialist's decision, not a screening test. | No treatment may be needed — serial observation, since most involute. Indications to treat: cosmetic, functional involvement, deep ulceration, infection. First line: BETA-BLOCKERS — oral propranolol or topical timolol (mechanism not well understood). Also first line: corticosteroids — topical, intralesional or oral; slow growth and decrease size. Pulsed dye laser for superficial lesions (depth ~1.2 mm). Surgical excision. | Most disappear on their own over years, and the natural history is the reassurance. Watch for anything that blocks vision, interferes with feeding or breathing, obstructs the ear canal, ulcerates or bleeds — those are the reasons to treat rather than wait. |
 | Nevus flammeus (port-wine stain) | NEVER involutes — dilation with NO endothelial proliferation, which is why · present at birth, DARKENS and THICKENS · sharp midline cutoff | Congenital vascular lesion. Dilated superficial dermal capillaries through the entire depth of the dermis, with NO proliferation of endothelial cells — which is why it never involutes. More common in Caucasians, male = female. Present at birth, grows in proportion with the child, NO involution, becomes darker and thicker. Painless expanding lesion. Early: flat (macular) well-circumscribed blanchable patches, pink to red to purple; color darkens with crying, fever or overheating; usually unilateral with fairly sharp midline cutoffs. Later: vasculature dilates and it may evolve into a raised, thickened plaque of deep red to purple. Psychosocial disability from facial disfigurement can be overwhelming. “He's had this red mark on one side of his face since the day he was born, and it's got darker as he's grown.” | Clinical diagnosis. The critical contrast is with infantile hemangioma: hemangioma proliferates then involutes; nevus flammeus does neither. Labs to orderNone — clinical diagnosis. | No treatment is required. Cosmetics — tinted waterproof makeup. Pulsed dye laser therapy — causes selective destruction of superficial target blood vessels, inducing intravascular coagulation; the vessel is later absorbed and replaced by collagen. | This is permanent and will darken and thicken with time, unlike a hemangioma. Discuss the psychosocial impact openly. Camouflage cosmetics and laser are both legitimate options and neither is compulsory. |
 | Nevus simplex (stork bite) | FADES within a year, or persists on the neck · more noticeable when the baby cries · head and neck | Congenital vascular lesion, a more superficial variant of nevus flammeus involving dermal capillaries. Present at birth; becomes more noticeable when the baby cries. Most common on the head and neck. Pink to erythematous, irregular, blanchable macules and/or patches, single or multiple. “There's a pink patch on the back of her neck that goes bright red when she cries.” | Clinical diagnosis. Distinguish from nevus flammeus, which is usually unilateral with a sharp midline cutoff and does not fade. Labs to orderNone — clinical diagnosis. | No treatment. Fades within one year, or may persist for life on the neck. | Reassure: this is the common birthmark that usually goes away in the first year. The one on the nape may stay, which is why it is nicknamed a stork bite. |
 | Cherry angioma | Deep red dome that INCREASES IN NUMBER WITH AGE · trunk · <5 mm · new ones keep appearing and cannot be prevented | Acquired vascular lesion, formed by capillary (venule) proliferation. Very common, and increases with age — previously known as senile angioma. Cause unknown. Most common on the trunk; may bleed after trauma. <5 mm, smooth, firm, deep red papules that blanch with pressure (a fibrotic one may not blanch completely). “I keep getting these little bright red spots on my chest and back as I get older.” | Clinical diagnosis. Differential includes petechiae (do not blanch, not papular) and pyogenic granuloma (moist, exophytic, grows fast). Labs to orderNone — clinical diagnosis. | Not necessary unless it bothers the patient. Laser therapy for superficial lesions. Shave excision and electrocauterization for large lesions. | Benign, and strongly age-related. New lesions will likely develop and there is no way to prevent them — removing existing ones does not stop new ones forming. |
 | Telangiectasia | A permanently dilated capillary UNDER 1 mm, sometimes with a central punctum · associated with numerous diseases — work up the cause | Acquired vascular lesion. A permanently dilated capillary, <1 mm. Blanchable. Occurs singly, in groups, or with a central punctum. May be primary or secondary, and is associated with numerous diseases. “I've got tiny red lines on my cheeks that don't go away.” | Clinical diagnosis. Because telangiectasias are secondary to many conditions, the work-up follows the suspected cause rather than the lesion. Labs to orderNone for the lesion itself. Because telangiectasias are associated with numerous diseases, any testing follows the suspected underlying condition rather than the skin finding. | Treat the underlying cause where there is one. Cosmetic treatment where wanted follows the same options as other superficial vascular lesions — laser being the mainstay. | Explain that these are dilated existing vessels, not new growths. Their significance is as a possible sign of something else, which is why the history matters more than the lesion. |
 | Nevus araneus (spider angioma) | ESTROGEN EXCESS — pregnancy or the pill (both resolve after), CIRRHOSIS and liver failure · dilation of existing vessels, no proliferation | Acquired vascular lesion. NO vascular proliferation — dilation of preexisting vessels. Estrogen excess states may be the cause: pregnancy or oral contraceptive use (resolve after delivery or after stopping the pill), and cirrhosis or liver failure. Location: hands and fingers in children; face, neck, upper trunk and arms in adults. Asymptomatic. Central arteriole with radiating capillaries; lesion blanches; <10 mm. “There's a little red spot with legs coming off it, like a spider.” | Clinical diagnosis — but the HISTORY is the test. Ask about pregnancies, hormone use, alcohol history, and medications carrying a risk of liver damage. Labs to orderThe history is the test — pregnancy, hormone use, alcohol, hepatotoxic drugs. Where liver disease is suspected on that history, liver function tests are the reasonable follow-on. The lesion itself needs none. | No treatment may be needed — pregnancy- and pill-related lesions resolve on their own. Pulsed dye laser resolves most lesions. | The lesion itself is harmless; its value is as a clue. Several spider angiomas in a non-pregnant adult warrant a conversation about alcohol and liver health. |
 | Pyogenic granuloma | Moist bright red papule that BLEEDS readily, with an EPITHELIAL COLLARETTE at its BASE · pregnancy, fingers · misnamed — neither infectious nor granulomatous | Acquired vascular lesion — MISNAMED: neither infectious nor granulomatous. Exact cause unknown; a response to injury or hormonal factors. Common in children, young adults and pregnancy. A benign vascular tumor of skin and mucous membrane appearing as a rapidly growing vascular papule or nodule, from overgrowth of blood vessels in response to irritation, trauma or hormonal change. Most common on head, neck and fingers. Bright red exophytic papule or nodule with a MOIST surface and an EPITHELIAL COLLARETTE at the base. Bleeding, erosion, ulceration, purulence and crusting all possible. Average 6.5 mm; may reach several centimeters. “It came up really fast after I cut my finger, and it bleeds every time I knock it.” | Usually a clinical diagnosis. Differential: cherry angioma, malignant melanoma, squamous cell carcinoma — two malignancies, which is why many are excised. Labs to orderNone. Usually a clinical diagnosis — though surgical excision has the advantage of providing histopathologic analysis, which matters because melanoma and squamous cell carcinoma are in the differential. | Spontaneous resolution may occur, but patients often opt for treatment for cosmesis or because of bleeding. Surgical excision — provides histopathologic analysis, lowest recurrence rate, highest rate of scarring. Other modalities: shave excision followed by curettage and electrodesiccation, laser, cryotherapy. | These lesions are benign and often resolve spontaneously over months to years. Effective treatments exist if wanted for appearance or to stop bleeding. If it recurs, come back early — small lesions are easier to treat than large ones. |
 | Neurofibromatosis type 1 | Café-au-lait >5 mm prepubertal / >15 mm postpubertal, SIX OR MORE · Crowe sign — axillary and inguinal freckling <5 mm · chromosome 17 | Also von Recklinghausen disease. A common neurocutaneous genetic disorder causing tumors to form on nerve tissue. NF1: NF1 gene, chromosome 17. NF2: NF2 gene, chromosome 22. Schwannomatosis (NF3): SMARCB1 and LZTR1, chromosome 22. NF1 skin manifestations, all four: Café au lait spots — light tan to brown macules, >5 mm prepubertal, >15 mm postpubertal; often the first manifestation; usually present at birth or in the first year; grow in proportion with the child. Six or more are diagnostic — but the macules alone do not establish the diagnosis. Cutaneous neurofibromas — benign nerve sheath tumors from peripheral nerves; well-circumscribed, sessile or pedunculated; protrude just above the skin or lie just under it with a violaceous hue; begin at puberty and increase in number and size with age; a few to hundreds. Plexiform neurofibromas — tumor in the tissue covering nerves; anywhere except brain and spinal cord; large and extensive; may be locally invasive. Intertriginous freckling (Crowe's sign) — freckles <5 mm, smaller than café au lait spots, grouped, more prominent with sun exposure; axillary and inguinal (may be seen under the breasts, but that site is not a diagnostic criterion). | Clinical diagnosis on the recognized criteria. Six or more café au lait macules of the size threshold, plus the other features. Labs to orderNo routine bloods. Diagnosis is clinical on the recognized criteria. Genetic testing exists but is not what this lecture asks for; surveillance is by cutaneous examination at every visit. | Surveillance. A cutaneous examination at every visit, assessing for new neurofibromas or progression of existing lesions. Plexiform neurofibromas may be locally invasive; clinical evaluation should be directed at determining the extent of involvement. | Point patients to national and regional support groups — for continuous updates on treatment advances and for emotional support. This is the education point the lecture names. |
 | Xanthelasma | Soft YELLOW plaques on the MEDIAL EYELIDS · lipid-laden macrophages · check the lipids | Soft, yellow cholesterol plaques — a collection of lipid-laden macrophages. Associated with lipid disorders. Asymptomatic. Most common location: the medial eyelids. “I've got soft yellow patches on my eyelids near my nose.” | Clinical diagnosis. SCREEN FOR HYPERLIPIDEMIA — it may signify an increased risk of cardiac disease. Differential includes syringoma and milia, which share the periorbital site. Labs to orderYES — SCREEN FOR HYPERLIPIDEMIA. A fasting lipid panel. This is the one lesion in the lecture whose blood work is the whole point: it may signify increased risk of cardiac disease. | Laser or surgical excision. Recurrence is common. Treating the lipid disorder is the part that matters medically; removing the plaque is cosmetic. | The plaque itself is harmless, but it can be a marker of a lipid disorder and of cardiac risk — which is why a cholesterol check is part of the visit. Recurrence after removal is common. |
 | Lipoma | Soft, painless, MOBILE subcutaneous mass · the most common soft tissue tumor | The most common soft tissue tumor. A benign localized overgrowth of fat cells in the subcutaneous tissue; single or multiple. Asymptomatic unless adjoining structures are invaded; can occur anywhere on the body. Soft, painless subcutaneous nodules of rubbery consistency, usually <5 cm. “There's a soft squishy lump under my skin — it moves when I push it and doesn't hurt.” | Typically a clinical diagnosis. Differential: epidermal cyst, dermatofibroma, abscess. Labs to orderNone — typically a clinical diagnosis. | Asymptomatic tumors can be observed. Cosmetically deforming enlarged masses, and uncertain diagnosis, can be treated surgically with excision. | Benign and very common. Excision is for appearance, for symptoms from pressure on nearby structures, or to settle a diagnosis — not because the lump is dangerous. |
 | Digital mucous cyst | A PSEUDO-cyst — no cellular lining · mucin extruded from a joint space · may groove the nail | A PSEUDO-cyst — it does not have a cellular lining (a true capsule). Represents an extrusion of mucinous contents from a local joint space into the surrounding dermis; as the mucin collects it compacts the cells at the margin, mimicking a capsule. Females > males. Asymptomatic unless large. Associated with osteoarthritis. Typically located over the distal interphalangeal (DIP) joint — a translucent skin-colored cyst papule on the distal digit, over the proximal nail matrix or the nail bed. May cause a longitudinal groove in the nail from pressure on the matrix. “There's a clear little blister by my fingernail and the nail has a line down it now.” | Clinical diagnosis. The association with osteoarthritis of the distal interphalangeal joint is part of the picture. Labs to orderNone. Clinical. The association is with osteoarthritis of the distal interphalangeal joint. | Asymptomatic lesions may be observed. Symptomatic cysts, or those causing nail dystrophy, can be excised. | The nail groove is caused by the cyst pressing on the nail matrix and usually resolves once the cyst is dealt with. Otherwise no treatment is needed. |
 | Sebaceous hyperplasia | YELLOW umbilicated papule in an OLDER ADULT · face · vs molluscum, which is pearly flesh-colored and in children · no malignant potential | A common benign condition of the sebaceous glands, with NO known potential for malignant transformation. With age, turnover of sebocytes slows, crowding them and enlarging the gland. Immunosuppression is high risk. Asymptomatic; the patient usually presents about appearance or about cancer. Single or multiple whitish-yellow or skin-colored papules, soft, 2–9 mm, with CENTRAL UMBILICATION — a very small globule of sebum can sometimes be expressed. Common on the face. “I've got small yellowish bumps on my forehead with a dip in the middle — is it skin cancer?” | Dermoscopy can distinguish between basal cell carcinoma and sebaceous hyperplasia. Biopsy if concern about malignancy (basal cell carcinoma) remains. Differential: basal cell skin cancer — and that is exactly what the patient is worried about. Labs to orderNo bloods. Dermoscopy distinguishes it from basal cell carcinoma; biopsy only if that concern remains. | Does not require treatment. Lesions tend to recur and treatment carries a risk of scarring. Light electrocautery can be used if treatment is wanted. | Benign, with no potential to become cancerous. The main reason to see a clinician is to have it distinguished from a basal cell carcinoma, which dermoscopy can usually do without a biopsy. |