Lecture 1 — Clinical Reasoning and Problem Solving. The reasoning every later block exam tests through cases.
| Term | What you need to know |
|---|---|
| ★★ HOW THE EXAM IS BUILT | Her words, opening Lecture 9: “there's gonna be like clinical vignettes or PRETTY MUCH ALL CLINICAL VIGNETTES… make sure that you are able to RECOGNIZE CONDITIONS BY THE VIGNETTE.” 65 QUESTIONS. “Way more non-pictures than pictures, but there's a couple.” |
| ★★ Where the marks are | “There might be SOME question, what's the most likely diagnosis, but A LOT OF THEM are — what's the NEXT MANAGEMENT PLAN? What's your FIRST LINE TREATMENT plan?… what's the proper PATIENT EDUCATION?” NAMING THE DISEASE IS THE EASY HALF. Do the vignette sets, not just the recall quizzes. |
| ★★ HOW FAR INTO TNM TO GO | She capped this herself: “I want you to kind of know this… but I DON'T NECESSARILY WANT YOU TO MEMORIZE IT.” And on the sub-rows: “that's why I didn't put all that, YOU GUYS DON'T NEED TO KNOW THAT. I just want you to know this exists.” WHAT SHE DOES WANT: T = tumor, N = nodes, M = metastasis; and the five stages plainly — 0 epidermal region, I localized and very thin, II localized but thicker, III lymph nodes, IV other organs. “That's the general of what I do want you to know.” |
| Survival figures said ALOUD only (on no slide) | Under 1 mm Breslow → “over 95-ish percent survival”. Distant metastases → “about a 15 Percent survival”. NOT ON ANY SLIDE — the deck only says survival drops sharply with thickness and spread. No quiz question is built on them. Her point: that gap is why you catch it early. |
| Referral, verbatim | Anything deeper than 1 mm goes to a specialist. “I AM NOT TREATING FAMILY MEDICINE MELANOMA. NEITHER SHOULD YOU. IT'S TOO DANGEROUS.” |
| ★ The question she said she'd write | Three separate times: “how do you diagnose this?” → BIOPSY. But NEVER a bare biopsy — SCC needs DEPTH ENOUGH TO SEPARATE IN SITU FROM INVASIVE; BCC is SHAVE OR PUNCH; KAPOSI needs a REPRESENTATIVE lesion with HHV-8 findings; CTCL needs an ACTIVE, REPRESENTATIVE, UNTREATED lesion, possibly several, and ONE NEGATIVE BIOPSY DOES NOT EXCLUDE IT. |
| Term | What you need to know |
|---|---|
| Sensitivity | Probability the test shows a person HAS the condition when they do have it. How well a test DETECTS disease. Related to fewer false-negatives; says nothing about false-positives. |
| Specificity | Probability the test shows a person DOES NOT have the condition when they do not. How well a test EXCLUDES disease. Related to fewer false-positives; says nothing about false-negatives. |
| SnNout | High Sensitivity + Negative result = rules the disease OUT. “With sensitivity, a negative is a negative.” |
| SpPin | High Specificity + Positive result = rules the disease IN. “With specificity, a positive is a positive.” |
| The two questions | Sensitivity: how good is the test at FINDING disease? Specificity: how good is it at EXCLUDING people without disease? |
| Human immunodeficiency virus (HIV) example | Screening is highly sensitive so few infected people are missed; confirmatory (supplemental) testing is highly specific to minimize false-positive diagnoses. |
| When a false-positive is catastrophic | Acceptable in HIV screening because confirmation corrects it. NOT acceptable for serious, non-curable disease — e.g. a cancer diagnosis. |
| Conditional probability | Probability of disease or event IF another event, test result, or condition is present. |
| Term | What you need to know |
|---|---|
| Pretest probability | Likelihood of the condition BEFORE the result is known. |
| Built from | Signs and symptoms · history and risk factors · how common the condition is in the population. |
| Posttest probability | Likelihood of the condition AFTER the result is known. Depends on sensitivity and specificity. |
| Why it matters | The same result means different things for two patients who started at different pretest probabilities. |
| Term | What you need to know |
|---|---|
| Screening testing | Identifies the likelihood of OCCULT disease. |
| Diagnostic testing | Complements the history and physical; reduces uncertainty about diagnosis and/or prognosis; helps decide management. |
| Which property, which job | Highly SENSITIVE test = best for SCREENING. Highly SPECIFIC test = best for CONFIRMING a diagnosis. |
| Term | What you need to know |
|---|---|
| Six-step process | 1 Gather initial information → 2 Organize and interpret → 3 Synthesize / problem representation → 4 Generate hypotheses → 5 Test hypotheses, working diagnosis → 6 Plan diagnostic and treatment strategy. |
| The three questions | What disease does the patient have? Should testing be done? Should this patient be treated? |
| VINDICATE | Vascular, Infectious, Neoplastic, Degenerative, Iatrogenic, Congenital, Autoimmune, Trauma, Endocrine (metabolic). |
| Hypothetico-deductive method | Propose hypotheses, test whether the observed data is consistent. Cues → generation → evaluation (confirm/exclude) → refinement (add new) → verification (confirm fit) → management (monitor response). |
| Pattern recognition | LOWEST level of decision making. Easy to use, but errs because other possibilities are never considered. |
| Analytic methods (complex cases) | Evidence-based medicine, clinical guidelines, quantitative techniques. |
| Evidence-based medicine | Formulate question → gather evidence → evaluate quality/validity → decide how to use it. Limits: time consuming; many questions have no relevant studies. |
| Clinical guidelines | Often “if–then” (febrile + neutropenic → broad-spectrum antibiotics). Cost-effective, the “standard of care” — but apply only to patients with similar characteristics. |
| Diagnostic principles | Common things occur commonly. Hear hoof beats, think horses not zebras. Bet on UNCOMMON manifestations of COMMON conditions. |
| Treatment principles | Working → keep doing it. Not working → stop doing it. Don't know what to do → do nothing. |
| Good decision-making | Slow down; know the base rate; consider what data is truly relevant; seek alternatives; ask questions to DISPROVE your hypothesis; remember you are often wrong. |
| Term | What you need to know |
|---|---|
| Definition | Event-driven: treat signs and symptoms BEFORE a definitive diagnosis. |
| Where | Mostly emergency medicine. |
| When | Unstable patients · atypical presentations · rule out the worst-case scenario · follow responses to interventions. |
| Term | What you need to know |
|---|---|
| Value of treatment | A LINEAR function of the probability of disease. |
| Also weighed | Likelihood of success · the patient's ability to tolerate treatment. |
| Risk vs benefit | Balance the benefit of treating a sick person against the risk of erroneously treating a well person, or one with a different disorder. |
| What that encompasses | Both financial AND medical consequences — accounting for the likelihood of disease and the magnitude of benefit and risk. |
| Term | What you need to know |
|---|---|
| Five As | Ask · Advise · Assess · Assist · Arrange. |
| FRAMES | Feedback about personal risk · Responsibility of the patient · Advice to change · Menu of options · Empathetic style · promote Self-efficacy. |
| Behavior change | Identify where the patient sits on the continuum; tailor to their readiness and self-efficacy. Behavioral counseling is one of the most important skills. |
| Barriers to adherence | Cost/affordability · low health literacy · cultural or religious beliefs · fear of side effects or mistrust · transportation or time · mental health or cognitive impairment · poor communication or follow-up. |
| Specific guidelines | Bates' Chapter 7 — unhealthy alcohol use, tobacco smoking cessation, sexually transmitted infections. |
| Term | What you need to know |
|---|---|
| Epidermis | Keratinocytes in five strata, melanocytes, Langerhans, Merkel. Avascular. Loss of this layer alone = no scar. |
| Dermis | Collagen, elastin, vessels, nerves, follicles, glands. Damage here scars. |
| Subcutaneous | Fat, larger vessels, base of follicles. |
| Depth ladder (memorize) | Impetigo = epidermis. Erysipelas = upper dermis + lymphatics. Cellulitis = deeper dermis + subcutaneous. Necrotizing fasciitis = below all of it. |
| Skin functions | Barrier · thermoregulation · sensation · vitamin D synthesis under ultraviolet B · immune surveillance. |
| Term | What you need to know |
|---|---|
| STEROID POTENCY — she said she'd ask this | Mild: HYDROCORTISONE, all strengths (0.1/0.5/1/2.5%). Moderate: betamethasone valerate 0.025%. Medium-high: triamcinolone acetonide 0.1%, betamethasone valerate 0.1%, betamethasone dipropionate 0.05%. High: clobetasol propionate 0.05%. |
| Her exact words | “If my slide says treatment would be a low dose corticosteroid, you might have these answer choices — you need to know that it's gonna be your hydrocortisone.” |
| Sensitive sites | Face or genitals → hydrocortisone or another LOW potency agent. Thin skin atrophies. |
| The betamethasone trap | TWO salts. Valerate 0.025% = moderate; valerate 0.1% AND dipropionate 0.05% = medium-high. Concentration alone does not tell you the tier. |
| Steroid course | Twice a day for two weeks. Prolonged use → atrophy, striae, telangiectasia, hypopigmentation. |
| Retinoids | Adapalene, tretinoin, tazarotene, trifarotene. Tazarotene also treats psoriasis. Start low, build to nightly. AVOID eyes, nose, mouth. Pregnancy precautions. |
| NOT ON THE EXAM | The NAAT / RT-PCR / qPCR / multiplex taxonomy (slides 30–31). Her words: “this is not going to be on your exam.” Know only that viral PCR detects viral genetic material. |
| Also not asked | Drug DOSES — names only. (An image-interpretation exclusion was also heard, but two transcriptions disagree on the negation, so treat images as fair game.) |
| IN scope though obsolete | TZANCK SMEAR (vesicular lesions → multinucleated giant cells; PCR preferred to confirm) and MINERAL OIL PREP (scabies mite, eggs, fecal pellets). “Could be on your board, so you need to know about it.” |
| Cultures | Fungal culture identifies the fungal organism. Bacterial culture AND SENSITIVITY identifies the bacterium and tells you which antibiotic works. |
| Transillumination | Fluid-filled vs solid nodule — fluid glows. |
| Direct immunofluorescence | Autoimmune blistering disease — where the antibody sits. Separates bullous pemphigoid from pemphigus. |
| SKIN TYPE — she spent real time here | “What you're gonna be tested on is gonna describe the rash on Caucasian skin… it is really important that you know how to identify all of these on every single skin type.” |
| Atopic dermatitis by skin tone | Lighter skin: angry, inflamed. Darker skin: can look almost SILVERY. |
| Stasis dermatitis by skin tone | Darker skin: erythema reads VIOLACEOUS, GRAY or DEEP BROWN. PALPATE for warmth and edema — do not rely on color. |
| Pityriasis rosea by skin tone | Darker skin: post-inflammatory HYPERPIGMENTATION lasting several months. Still no scarring. |
| Fitzpatrick scale | How skin type is classified by response to ultraviolet light. |
| Atopic triad | Atopic dermatitis + asthma + allergic rhinitis. |
| Methotrexate | ALWAYS with folic acid supplementation. |
| Lichen planus biopsy | Buzzword: BAND-LIKE INFILTRATION OF LYMPHOCYTES in the dermis. |
| Read the headers | “When you go over the PowerPoints, read headers — that's really important, because I'm separating here.” |
| Term | What you need to know |
|---|---|
| Atopic dermatitis | Infants cheeks/extensors; children and adults flexures. Personal or family atopy. |
| Contact dermatitis | Sharp margins in the shape of the exposure. Patch testing. |
| Seborrheic dermatitis | Greasy yellow scale on erythema: scalp, brows, nasolabial folds, ears, central chest. |
| Dyshidrotic eczema | Deep tapioca-like vesicles on palms, soles, sides of fingers. |
| Stasis vs cellulitis | Stasis = BILATERAL, chronic, itchy, afebrile. Cellulitis = unilateral, acute, tender, often febrile. “Bilateral cellulitis” is almost always stasis. |
| Bullous pemphigoid | Elderly · SUBepidermal split · TENSE bullae · Nikolsky NEGATIVE · mucosa uncommon · better prognosis. |
| Pemphigus vulgaris | Middle-aged · INTRAepidermal split · FLACCID bullae · Nikolsky POSITIVE · mucosa common and often first. |
| Psoriasis | Well-demarcated plaques, thick silvery scale, Auspitz sign. Extensors, scalp, nails. |
| Pityriasis rosea | Herald patch, then collarette-scaled ovals in a Christmas-tree pattern. Self-limiting 6–8 weeks. |
| Lichen planus | Six Ps: purple, polygonal, pruritic, planar papules and plaques. Wickham striae. |
| Alopecia areata vs androgenetic | Areata = discrete smooth patches, exclamation point hairs, autoimmune. Androgenetic = gradual miniaturisation, temporal/vertex in men. |
| Term | What you need to know |
|---|---|
| Erythema multiforme | Target lesions, acral. Herpes simplex virus triggers OVER 50%. |
| Urticaria | Individual wheal resolves within 24 h. Persisting past 24 h → BIOPSY for urticarial vasculitis. |
| Erythema nodosum | Tender BILATERAL anterior shin nodules that do NOT ulcerate. Löfgren = EN + ankle arthritis + hilar nodes. |
| Granuloma annulare | Annular papules with NO SCALE — that is what separates it from tinea. |
| Pyoderma gangrenosum | Undermined violaceous border. PATHERGY — debridement makes it worse. Do not debride. |
| Acne rosacea | Central facial erythema, flushing, telangiectasias, NO comedones. Ivermectin cream if Demodex. |
| Hyperhidrosis | Primary = bilateral, focal, adolescent onset, ABSENT IN SLEEP. Generalized or nocturnal → secondary cause. |
| Dermatitis herpetiformis | Perilesional direct immunofluorescence: GRANULAR immunoglobulin A. Dapsone + lifelong gluten-free diet. Screen all for celiac. |
| Acanthosis nigricans | Screen HbA1c, lipids. Sudden onset in an adult → gastrointestinal malignancy. |
| Epidermolysis bullosa | Transmission electron microscopy + immunofluorescence antigen mapping. |
| Term | What you need to know |
|---|---|
| The percentages | SJS under 10% detachment · overlap 10–30% · TEN over 30%. Mortality 1–5% vs 30–35%. |
| Drugs | Aromatic anticonvulsants (carbamazepine, phenytoin, lamotrigine, phenobarbital) · sulfonamides · ALLOPURINOL (the slide says commonest IN ASIA) · oxicam NSAIDs · nevirapine. |
| HLA | B*15:02 with carbamazepine · B*58:01 with allopurinol. |
| SCORTEN (1 point each) | Age over 40 · malignancy · heart rate over 120 · detachment over 10% · urea over 28 mg/dL · bicarbonate under 20 · glucose over 252. Score 5+ → 90% mortality. |
| The single action | STOP THE DRUG. Earlier withdrawal = better survival; each day of delay worsens it. |
| Also | Burn unit/ICU · cyclosporine 3–5 mg/kg has the strongest evidence in TEN · AVOID silver sulfadiazine · antibiotic prophylaxis NOT recommended · daily ophthalmology. |
| Phototoxic vs photoallergic | Phototoxic = non-immunologic, dose-dependent, FIRST exposure, within hours, exaggerated sunburn. Photoallergic = type IV, needs sensitization, eczematous, extends BEYOND exposed skin. |
| Photopatch reading | Irradiated patch ONLY = photoallergy. BOTH patches = contact allergy. |
| Polymorphous light eruption | Commonest idiopathic photodermatosis. Spring onset, spares chronically exposed skin, hardens by late summer. Antinuclear antibody is MANDATORY to exclude lupus. Prophylactic narrow band ultraviolet B in spring is the most effective prevention. |
| Actinic keratosis | Sandpaper texture · TP53 · field cancerization → field therapy (5-fluorouracil, imiquimod, photodynamic therapy) for confluent disease. |
| Dermatoheliosis | Solar elastosis is the histological hallmark. TRETINOIN is the only agent approved for photoaging. |
| Millimeters | CMS uses 1 cm for macule/patch and papule/plaque. Clinical Pathophysiology uses 5 mm. Answer with the course in front of you. |
| Term | What you need to know |
|---|---|
| HER RULE FOR WHAT IS TESTABLE | “If you think it's DIFFERENT from any other disease, what's the likelihood it's going to be on the test? PROBABLY PRETTY HIGH.” Said while pointing at dermatitis herpetiformis — because almost everything else in this lecture is a CLINICAL diagnosis, and the few that are not stand out. |
| EXPLICITLY NOT ON THE EXAM | The LUPUS-versus-ROSACEA distinction. “Don't worry, that's not going to be on the test. I won't do that to you. I'm not testing for lupus right now.” Worth knowing clinically — lupus butterfly rash SPARES the nasolabial folds, rosacea involves them; ANA can rule OUT but a positive only means MORE TESTING — and worth not revising. |
| Dermatitis herpetiformis — the full package | GOLD STANDARD = SKIN BIOPSY (one of the very few here that is not purely clinical). ACUTE: DAPSONE — but CHECK FOR G6PD DEFICIENCY FIRST, it is a contraindication. CHRONIC: STRICT GLUTEN-FREE DIET. REFER to GASTROENTEROLOGY for COLONOSCOPY (high chance of celiac disease) and to a REGISTERED DIETITIAN. |
| Rosacea first line — her words | TOPICAL METRONIDAZOLE, “by far the first line treatment”. AZELAIC ACID is an alternative but is DRYING, and these patients already have an IMPAIRED SKIN BARRIER. If really bad: LOW-DOSE DOXYCYCLINE, started twice daily and stepped down to once. |
| Pyoderma gangrenosum — “the one I want you to really know” | Begins as a small PUSTULE or NODULE → RAPIDLY EXPANDING PAINFUL ULCER with a WELL-UNDERMINED BORDER. LOWER EXTREMITY is the most common site. |
| Toxic epidermal necrolysis | DRUG INDUCED IN MORE THAN 80% OF CASES (slide 87). She said allopurinol is the commonest cause WORLDWIDE — the SLIDE says commonest IN ASIA, one of several leading culprits alongside aromatic anticonvulsants, sulfonamides, oxicam NSAIDs and nevirapine. GO WITH THE SLIDE. |
| Epidermolysis bullosa — flagged despite being rare | “I've never seen it, but YOU NEED TO KNOW IT.” What she wants is the MECHANISM: a MUTATION IN STRUCTURAL PROTEINS. |
| Erythema nodosum numbers | 1–5 CM nodules on the ANTERIOR SHINS / tibial surface. STREPTOCOCCAL PHARYNGITIS is the most common trigger. |
| Polymorphous light eruption | The MOST COMMON IDIOPATHIC PHOTODERMATOSIS. Particularly YOUNG TO MIDDLE-AGED WOMEN. Associated with HIGHER ALTITUDES. |
| Urticaria / angioedema take-home | EPINEPHRINE — EpiPen is the brand name. She named this the take-home of the section. |
| Term | What you need to know |
|---|---|
| Four factors | Follicular hyperkeratinization · increased sebum · Cutibacterium acnes (anaerobic Gram-positive rod) · inflammation. |
| Hallmark | The COMEDONE. Its absence rules acne out and rosacea in. |
| Guideline ladder | Comedonal → topical retinoid. Mild papulopustular → topical antimicrobial + retinoid. Moderate → retinoid + oral antibiotic + benzoyl peroxide. Severe nodular → same, or isotretinoin monotherapy. |
| Benzoyl peroxide | Add to EVERY antibiotic, topical or oral, to cut resistance. Oral tetracyclines 3–4 months only. |
| Isotretinoin safety | Pregnancy tests before, MONTHLY during, and 5 WEEKS AFTER. iPledge. One month dispensed at a time. Two forms of contraception. NO blood donation. |
| Acne education | Separate tretinoin and benzoyl peroxide by 3+ hours. Wash twice daily max. Improvement 4–6 weeks; back and chest 3–4 months. |
| Folliculitis | Pustule pierced by a CENTRAL HAIR. Staphylococcus aureus. Recurrent → nasal mupirocin twice daily for 5 days. |
| Hot tub folliculitis | Pseudomonas aeruginosa. 8 hours to 5 days after exposure. Spares face, neck, palms, soles. Clears in 2–10 days; dilute acetic acid compresses. |
| Pseudofolliculitis barbae | FOREIGN BODY reaction, not infection. Single/double blade, mild angle, no lift-and-cut. Tretinoin, mild steroid, eflornithine, laser. |
| Furuncle vs carbuncle | Furuncle = one follicle, single opening. Carbuncle = confluent furuncles, sieve-like openings, systemic symptoms, incision and drainage is the mainstay. |
| Furuncle antibiotics | None if afebrile with ONE lesion under 5 mm. Give if over 5 mm, failed drainage, expanding cellulitis, immunocompromise, or endocarditis risk. |
| Hidradenitis suppurativa | Three criteria: typical lesions + axilla/groin + recurrence over twice in 6 months. Smoking cessation essential. WIDE EXCISION for best chance of cure. |
| Erythrasma | Corynebacterium minutissimum. CORAL-RED under Wood's lamp. Topical erythromycin/clindamycin; oral if widespread. |
| Term | What you need to know |
|---|---|
| Impetigo | Superficial EPIDERMAL. Staphylococcus aureus or Streptococcus pyogenes. Mupirocin topically; CEPHALEXIN is the drug of choice in children. |
| Three types | Non-bullous = honey crust, lymphadenopathy common. Bullous = EXCLUSIVELY staph, epidermolytic toxins, collarettes, nodes uncommon. Ecthyma = ulcerates into dermis, gray-yellow crust, scars. |
| Post-streptococcal glomerulonephritis | Follows impetigo, esp. 3–7 year olds. ANTIBIOTICS DO NOT PREVENT IT. Edema, tea-colored urine, proteinuria, hypertension. |
| Erysipelas | Upper dermis + superficial lymphatics. Group A strep. RAISED, SHARPLY DEMARCATED plaque. Penicillin V; clindamycin if allergic. No routine cultures — yield is extremely low. |
| Cellulitis | Deeper dermis + subcutaneous. Borders NOT raised, NOT demarcated. Almost never bilateral. Dicloxacillin/cephalexin; cover MRSA if PURULENT. |
| Cellulitis course | Worse on day 1 is expected. Fever gone by 24 h. Inflammation settles over 1–2 weeks. Fever past 48 h → change antibiotic. |
| The cellulitis pitfall | Tense, cyanotic, bronzed, blanched = devitalized, NOT PERFUSED, antibiotics never reach it. Needs surgical debridement. |
| Abscess vs furuncle | Abscess = traumatic inoculation. Furuncle = infected follicle. Abscess that won't drain → incision and drainage. |
| Acute paronychia | 2–5 days after manicure/hangnail/nail biting. Warm soaks; incision and drainage if purulent. CLINDAMYCIN if nail biting (oral flora). |
| Chronic paronychia | At least 6 weeks. Irritant/allergen reaction, CANDIDA commonest. Keep hands dry + topical antifungal; fluconazole if severe. |
| Necrotizing fasciitis | UNRELENTING PAIN OUT OF PROPORTION. No response at 48 h. Area later goes NUMB (nerves destroyed) — that is progression. Tests must NOT delay debridement. |
| Gas on imaging | Clostridium perfringens produces gas; Group A strep does NOT. |
| MRSA orals | Trimethoprim-sulfamethoxazole · clindamycin · doxycycline (+ linezolid; the slide’s ciprofloxacin is not reliable for MRSA). Sensitive = dicloxacillin, cephalexin. |
| Primary vs secondary | Primary = previously normal skin (impetigo through a cut). Secondary = skin already damaged (impetigo invading eczema). |
| Term | What you need to know |
|---|---|
| HER EXAM HEURISTIC | “You don't know the answer, GUESS STAPH AUREUS.” Her words. Staph aureus is the recurring organism across folliculitis, furuncle, carbuncle, abscess, impetigo and cellulitis. Know the EXCEPTIONS properly — erysipelas and ecthyma lean STREPTOCOCCAL, hot tub folliculitis is PSEUDOMONAS — and default to staph everywhere else. |
| Slides she named out loud | “These are really important slides right here. 32 and 33, MAKE SURE YOU KNOW THIS.” The ACNE TREATMENT LADDER. Mild comedonal → topical retinoid (azelaic acid if not tolerated). Mild mixed/pustular → benzoyl peroxide + topical retinoid, OR benzoyl peroxide + topical antibiotic. Moderate → topical retinoid + ORAL antibiotic + benzoyl peroxide. Severe → same three, or ORAL ISOTRETINOIN. |
| Bactroban: OINTMENT, not cream | Mupirocin — the prescription version of over-the-counter triple antibiotic. WRITE THE OINTMENT: the cream is roughly a hundred times the price and is NEVER COVERED; the ointment is. Not on any slide. |
| Her default oral antibiotics | CEPHALEXIN (Keflex) is the most common agent. IF MRSA IS SUSPECTED, ADD TRIMETHOPRIM-SULFAMETHOXAZOLE DOUBLE STRENGTH — the combination is broad enough to cover before susceptibilities return, and susceptibility testing then confirms. |
| Decolonizing a staph carrier | For RECURRENT folliculitis: check whether they carry staph aureus, then NASAL MUPIROCIN TWICE A DAY FOR FIVE DAYS. The pre-filled swabs were discontinued, so it is applied manually. |
| The cellulitis safety net | Non-purulent cellulitis, small surface area → outpatient oral antibiotics. BUT “I ask them to come back 24 TO 48 HOURS and make sure it's effective, BECAUSE THIS SPREADS SO FAST.” That interval is the answer to a follow-up question. |
| Necrotizing fasciitis in one line | “Flesh-eating bacteria.” POLYMICROBIAL — aerobic or anaerobic from mixed flora — or GROUP A STREPTOCOCCUS. |
| Acne education, none of it on a slide | DON'T apply tretinoin and benzoyl peroxide TOGETHER (irritation): RETINOID AT NIGHT, BENZOYL PEROXIDE BY DAY. Don't wash the face more than TWICE a day. Gentle cleanser, WARM NOT HOT water (hot strips the barrier). Avoid oil-based make-up. FOUR TO SIX WEEKS to improve. DON'T PICK — picking is what scars. |
| Pseudofolliculitis barbae — who | Most commonly BLACK AND BROWN MALES, or anyone with CURLIER facial or body hair. Hair curvature, not hygiene. “Very, very common.” |
| Term | What you need to know |
|---|---|
| Scabies organism | Sarcoptes scabiei var. hominis. Close contact 15–20 minutes, or bedding/underclothing. |
| Pathognomonic lesion | Thread-like linear or J-shaped BURROW, 1–10 mm, interdigital webs and wrists. |
| Itch timing | First infestation 4–6 weeks (some 3 months). REINFESTATION 2–3 DAYS. |
| Distribution | Webs, finger sides, volar wrists, elbows, axillae, genitals, areolae. HEAD AND NECK SPARED in healthy adults — involved in infants, elderly, immunocompromised. |
| Crusted scabies | Thick scale, MILLIONS of mites, thickened nails, OFTEN NO ITCH, highly infectious. The long-term care outbreak risk. |
| Diagnosis | Skin scraping (number 15 blade + mineral oil, unexcoriated burrow) · dermoscopy DELTA-WING JET · burrow ink test = zigzag line. |
| Treatment | Permethrin overnight to the ENTIRE skin surface + SECOND APPLICATION AT ONE WEEK. Wash at 60°C or bag 14 days. Treat all contacts. Ivermectin for crusted/immunosuppressed. Itch may last 4 weeks after cure. |
| Nits vs dandruff | Nits CANNOT be removed from the hair shaft. Live lice = active; nits = past or present. |
| Lice sites | Head = children 3–12, head-to-head. Body = homeless/crowded, clothing seams. Pubic = MACULAE CAERULAE, often a concurrent sexually transmitted infection. |
| School policy | A NO-NIT POLICY IS NOT RECOMMENDED (American Academy of Pediatrics) — nits persist for months. Fumigation not recommended. |
| Bedbugs | PAINLESS bites in a linear ROW OF THREE (breakfast, lunch, dinner). Blood flecks on linen. Survive a year without a meal. PROFESSIONAL EXTERMINATOR required. |
| Tungiasis | Female flea burrows into the skin. Feet/web spaces after barefoot beach exposure. Dermoscopy shows ovoid eggs. Excision or cryotherapy + tetanus + antibiotics. |
| Hymenoptera | SCRAPE the honeybee stinger off with a card edge. Systemic reaction in 0.4–3%. Severe LOCAL = edema and induration up to a week. Auto-injector + desensitization after anaphylaxis. |
| Caterpillars | Gypsy moth → papules in linear streaks. Asp/puss (most poisonous) → intense pain, TRAIN-TRACK PURPURA. Strip hairs with ADHESIVE TAPE. |
| Term | What you need to know |
|---|---|
| Black widow | Red HOURGLASS. Alpha-latrotoxin. Painful bite; sweating and piloerection in 30 min, then CRAMPING ABDOMINAL PAIN and spasm. Calcium gluconate, narcotics, muscle relaxants, benzodiazepines, tetanus. |
| Brown recluse | Dark FIDDLE on cephalothorax. Midwest and Southeast. RED, WHITE AND BLUE SIGN. Necrosis 2–3 days, eschar 5–7 days. DELAY SURGERY until the wound is stable. |
| Hobo spider | Gray HERRINGBONE. Pacific Northwest, July–September. PAINLESS bite, induration and paresthesia in 30 min, vesicles by 36 h. Supportive; heals over weeks. |
| Tarantula | Shed hairs embed in skin and EYES. Topical steroid; OPHTHALMOLOGY for the eye. |
| Cutaneous larva migrans | Animal hookworm from sand/soil with dog or cat feces. Serpentine trail advancing 2–3 cm A DAY. Albendazole 400 mg × 3 days or ivermectin. NO excision, NO cryotherapy. |
| Cercarial dermatitis | Swimmer's itch. Flatworm cercariae via snails. Prickling 30 min → itch 10–12 h → papules 24 h → peak 48–72 h. Symptomatic only. |
| Lyme disease | Borrelia burgdorferi. ERYTHEMA MIGRANS over 5 cm with central clearing, about 1 week after the bite. Diagnose and TREAT CLINICALLY if the lesion is present. |
| Lyme stages | 1 early localized (erythema migrans) · 2 early disseminated days-to-weeks (cranial nerve palsy, meningitis, radiculopathy) · 3 late persistent months-to-years (MONOARTICULAR ARTHRITIS of a weight-bearing joint, encephalopathy, acrodermatitis chronica atrophicans). |
| Lyme treatment | DOXYCYCLINE first line; AMOXICILLIN in children and pregnancy; macrolide second line; 10–14 days. Intravenous ceftriaxone for arthritis and acrodermatitis. NO human vaccine (one for dogs). |
| Rocky Mountain spotted fever | Rickettsia rickettsii. Triad fever/headache/rash in only ~60%. Rash starts ANKLES AND WRISTS, spreads CENTRIPETALLY over 6–18 h, involves PALMS AND SOLES, SPARES THE FACE. |
| RMSF labs & treatment | Thrombocytopenia, anemia, mild hyponatremia, transaminitis, normal white count with bands. Indirect immunofluorescence is the gold standard but rarely diagnostic before day 7 — TREAT BY DAY 5. DOXYCYCLINE FOR EVERYONE including children and pregnancy. Prophylaxis after a bite NOT recommended. |
| Primary vs secondary lesions | Primary = epidermis and superficial dermis. Secondary = infiltrated into dermis or subcutaneous. Crust or scale means the EPIDERMIS is affected. |
| Term | What you need to know |
|---|---|
| HER CLEAREST EXAM FLAG | On cutaneous larva migrans: “you CAN'T ask that history question. THAT'LL BE SOMETHING YOU SEE ON YOUR EXAM.” On paper you get the PICTURE, not the travel history — so recognize the SERPIGINOUS ADVANCING TRACK with scratch marks that FLAKE BUT DO NOT BREAK THE SKIN. |
| Cutaneous larva migrans — diagnosis and treatment | CLINICAL diagnosis; she deprecates going further once the serpiginous track is visible. ALBENDAZOLE 400 mg PO daily × 3 DAYS (she said the name three times), or IVERMECTIN 200 mcg/kg daily × 1–2 days — but ivermectin needs FOLLOW-UP AND LIVER LABS, which is what makes albendazole the easier choice. |
| Scabies dermoscopy | “DELTA-WING JET” — the classic finding, a dense area of mite head, body, eggs and burrow. You will practice with a dermatoscope in PD lab. |
| Burrow ink test — the condition that makes it work | Apply BLUE-BLACK INK to a NON-EXCORIATED lesion. A scratched lesion takes up ink everywhere and tells you nothing. The three routes: SKIN SCRAPING, DERMOSCOPY, BURROW INK TEST. |
| Why 'treatment failure' usually isn't | “They need to know these steps… otherwise they'll come back with the same symptoms EVEN IF THEY'RE USING THE MEDICATIONS, because they're going to get RE-INFECTED. WHOEVER THEY'RE LIVING WITH, YOU SHOULD TREAT THEM ALL.” Slide 18: bedding and clothing at 60°C, or bagged in a warm place for 14 DAYS, and treat every infected person in the family or group. |
| Brown recluse — and the words for it | HALLMARK: RED, WHITE AND BLUE. BLUE center (ischemia), WHITE ring (vasoconstriction), RED outer (inflammation). “YOU HAVE TO BE THE ONE DESCRIBING IT, so make sure you're aware of what the words are.” Progression: NECROSIS → ESCHAR → ULCERATION; systemic symptoms (nausea, vomiting) mean escalate. |
| Which spider is the aggressive one | THE HOBO. Tegenaria agrestis, “aka aggressive house spider”. The other two — black widow and brown recluse — are NOT aggressive. Often mistaken for a brown recluse; predominant cause of necrotic arachnidism in the PACIFIC NORTHWEST. Bites JULY TO SEPTEMBER during mating; webs in BASEMENTS, WOOD PILES, BUSHES. |
| If the patient brings the spider in | That is USEFUL, not alarming — identification guides treatment instead of leaving you to guess from the wound. “We fix our face and then we take care of our patient.” |
| Head lice — a clinical addition, not a slide fact | She said “NECK IS THE MOST COMMON PLACE” to look. The DECK gives the method rather than the site: nits found by NIT COMBING and WET COMBING, distinguished from dandruff because NITS CANNOT BE REMOVED FROM THE HAIR SHAFT; viable eggs TAN TO BROWN, hatched remains CLEAR/WHITE. |
| Term | What you need to know |
|---|---|
| BRAND ↔ GENERIC (she said generics are what's keyed) | Learn the GENERIC; the exam may show both. Brands the deck actually names: LAMISIL = terbinafine. GRIS-PEG = griseofulvin. ZELSUVMI = berdazimer 10.3% gel (molluscum, at home, age 1+). YCANTH = cantharidin 0.7% (molluscum, clinician-applied, age 2+). ZEOSORB AF = antifungal foot powder (tinea pedis education). |
| What KOH does | DISSOLVES KERATIN, leaves FUNGUS behind. DERMATOPHYTE = branching HYPHAE. MALASSEZIA = short hyphae + clusters of yeast, 'SPAGHETTI AND MEATBALLS'. CANDIDA = BUDDING YEAST + PSEUDOHYPHAE. |
| WHERE to sample — 3 rules | TINEA: the ACTIVE BORDER, never the cleared center. NAIL: the MOST PROXIMAL accessible diseased nail bed / subungual debris, after trimming the onycholytic nail. ID REACTION: BOTH sites — the diagnosis is the PATTERN (positive primary, NEGATIVE at the reaction). |
| Wood lamp — both limits | TINEA CAPITIS: may rapidly support MICROSPORUM, but T. TONSURANS (commonest in the US) USUALLY DOES NOT FLUORESCE — a negative lamp excludes NOTHING. PITYRIASIS VERSICOLOR: may show YELLOW-GOLD, but SENSITIVITY IS LIMITED. |
| Antifungal classes | ALLYLAMINE ends in '-fine' (TERBINAFINE, NAFTIFINE) — DESTROYS THE CELL MEMBRANE. IMIDAZOLE ends in '-azole' (CLOTRIMAZOLE, KETOCONAZOLE) — BLOCKS ERGOSTEROL SYNTHESIS. |
| Dermatophytes: the defining fact | Infect and survive ONLY ON DEAD KERATIN — stratum corneum, hair, nails. CANNOT SURVIVE ON MUCOUS MEMBRANES (this is what separates them from Candida). Three genera: MICROSPORUM, TRICHOPHYTON, EPIDERMOPHYTON. Classified BY BODY LOCATION. |
| Tinea capitis | PREADOLESCENT CHILDREN — after puberty SEBUM FATTY ACID changes inhibit growth. Commonest fungal infection in children; T. TONSURANS commonest in the US. Gray ring patches, BLACK DOTS (hair fractured at the surface), LYMPHADENOPATHY OFTEN PRESENT. Fungal particles VIABLE FOR MONTHS. ORAL THERAPY REQUIRED — topicals DO NOT PENETRATE THE HAIR SHAFT. |
| Capitis drug pairing | TERBINAFINE for TRICHOPHYTON. GRISEOFULVIN for MICROSPORUM. Baseline LIVER tests when indicated by agent/label/risk. Adjunct shampoo (selenium sulfide 1–2.5% or ketoconazole 2%) 2–3x weekly REDUCES SPORE SHEDDING but NEVER REPLACES ORAL THERAPY. School exclusion GENERALLY UNNECESSARY once effective therapy has begun. |
| Capitis differential | FOLLICULITIS (perifollicular pustules). PSORIASIS (well demarcated, white/silver scale). SEBORRHEIC DERMATITIS (fine dry or greasy scale; hair LOST BUT NOT BROKEN). ALOPECIA AREATA (skin SMOOTH AND SHINY, no inflammation). |
| Tinea barbae | TRICHOPHYTON. INFLAMMATORY form = from ANIMALS, boggy pustular kerion-like, SCARRING ALOPECIA may occur. NONINFLAMMATORY = from ANOTHER PERSON, annular scaly or folliculitis-like. KEY SIGN: HAIRS ARE LOOSE AND EASILY REMOVED (unlike bacterial folliculitis). ORAL THERAPY REQUIRED — griseofulvin or terbinafine; shave/remove hair; warm compresses. |
| Tinea corporis | T. RUBRUM. Circular, sharply circumscribed, dry scaly plaque with PROGRESSIVE CENTRAL CLEARING = 'RINGWORM'. KOH FROM THE ACTIVE BORDER. Culture if suspicion high and KOH negative. TOPICAL terbinafine/butenafine/azole applied TO THE LESION AND 1–2 cm BEYOND THE BORDER. Differential: PSORIASIS, NUMMULAR ECZEMA (commonly confused), DISCOID LUPUS, FIXED DRUG ERUPTION. |
| NEVER: combination steroid-antifungal | Steroids MASK AND WORSEN dermatophytosis → TINEA INCOGNITO. Reconsider the diagnosis or test if atypical or failing appropriate therapy. |
| Resistant dermatophytosis | SUSPECT when disease is WIDESPREAD, INTENSELY INFLAMMATORY, EPIDEMIOLOGICALLY LINKED, or FAILS AN ADEQUATE TERBINAFINE COURSE → get SPECIES IDENTIFICATION AND SUSCEPTIBILITY TESTING. |
| Tinea cruris | 'JOCK ITCH', CRURAL FOLD. MORE COMMON IN MEN; often coexists with TINEA PEDIS. T. RUBRUM and E. FLOCCOSUM. THE SCROTUM IS TYPICALLY SPARED. Risks: warm moist environment, OBESITY, DIABETES, TIGHT CLOTHING, SHARING CLOTHES. SCROTAL INVOLVEMENT → think CANDIDAL INTERTRIGO (satellite papules/pustules); ERYTHRASMA may fluoresce CORAL-RED. |
| Tinea pedis — 3 variants | MOST COMMON DERMATOPHYTE INFECTION IN ADULTS, men>women. INTERDIGITAL (most common): maceration/erosion, 3rd & 4th INTERSPACES, fissures. HYPERKERATOTIC: plantar thickening in a SHOE DISTRIBUTION → ADD A KERATOLYTIC. VESICULOBULLOUS: the MOIST ACUTE form, pruritic AND PAINFUL, vesicles/bullae on erythema. |
| Tinea pedis: testing & education | Add BACTERIAL STUDIES for marked maceration, malodor, erosion, drainage, ulceration or cellulitis. DRYING BETWEEN THE TOES AFTER BATHING IS ESSENTIAL. Antifungal foot powder in shoes; sandals in communal showers; change socks frequently. TREAT COEXISTING ONYCHOMYCOSIS. |
| Tinea manuum | Associated with TINEA PEDIS, HIGH RECURRENCE. DORSAL hand = like tinea corporis (annular). PALM = like tinea pedis (hyperkeratotic). TWO FEET–ONE HAND SYNDROME: the hand used to SCRATCH the foot. Patients often think it is DRY SKIN OR HARD LABOR. Treat AS FOR TINEA PEDIS. |
| Term | What you need to know |
|---|---|
| Onychomycosis — the first rule | CONFIRM FUNGUS BEFORE ORAL THERAPY — MANY DYSTROPHIC NAILS ARE NOT FUNGAL. Tests: KOH, PAS STAIN OF CLIPPINGS, culture, or PCR. |
| Onychomycosis facts | DERMATOPHYTES, especially T. RUBRUM, cause most; yeast and molds also occur. Distal lateral disease → debris, ONYCHOLYSIS, thickening, discoloration, crumbling. Risks: TINEA PEDIS, AGE, DIABETES, TRAUMA, OCCLUSIVE FOOTWEAR, PSORIASIS, VASCULAR DISEASE. |
| Onychomycosis treatment + the numbers | ORAL TERBINAFINE FIRST-LINE: usually 6 WEEKS FINGERNAILS, 12 WEEKS TOENAILS. Baseline LIVER tests per labeling/risk. ITRACONAZOLE is the alternative; FLUCONAZOLE IS OFF LABEL IN THE US. Limited disease: topical EFINACONAZOLE, TAVABOROLE, CICLOPIROX — LOWER CURE RATES. IMPROVEMENT REQUIRES NAIL GROWTH. Manage concomitant tinea pedis. |
| ID (dermatophytid) reaction | Inflammatory dermatitis at a site DISTANT from the primary dermatophytosis, TINEA PEDIS common. Mechanism UNKNOWN, possibly DELAYED-TYPE HYPERSENSITIVITY. Occurs 1–2 WEEKS after the primary infection, EXTREMELY PRURITIC, papules/papulovesicles, COMMON ON THE FINGERS. |
| Id reaction — the 3 criteria | (1) DERMATOPHYTE INFECTION ON ANOTHER PART OF THE BODY. (2) ABSENCE OF FUNGAL ELEMENTS FROM THE ID REACTION SITE. (3) RESOLUTION WHEN THE PRIMARY INFECTION IS TREATED. KOH: (+) primary, (–) id site. TREATMENT = TREAT THE PRIMARY INFECTION. Look for an ASYMPTOMATIC FISSURE OR MACERATION in the toe webs. |
| Tinea incognito | Tinea with an ALTERED APPEARANCE due to INAPPROPRIATE TREATMENT, usually TOPICAL STEROIDS. Cycle: steroid settles it → stopping flares it → more steroid. STOP the corticosteroid/calcineurin inhibitor; KOH+culture FROM AN ACTIVE EDGE; WARN INFLAMMATION MAY REBOUND AFTER WITHDRAWAL. Topical for localized; SYSTEMIC for extensive, follicular or refractory. |
| Intertrigo — the ordering matters | INTERTRIGO IS NOT PRIMARILY AN INFECTION: inflammatory rash from FRICTION, MOISTURE AND HEAT trapped in body folds — CANDIDA MAY SECONDARILY INFECT IT. So CORRECT THE ENVIRONMENT FIRST: dry folds gently, reduce friction/occlusion, moisture-wicking or absorbent material, address incontinence/hyperhidrosis. |
| Candida facts + sites + risks | CANDIDA ALBICANS most common, OPPORTUNISTIC, MALES = FEMALES. YEASTS are UNICELLULAR fungi reproducing BY BUDDING. Sites: INFRAMAMMARY, AXILLARY, ABDOMINAL, INGUINAL, PERINEAL, INTERDIGITAL folds. Risks: obesity, diabetes, incontinence, occlusion, immobility, RECENT ANTIBIOTICS, immunosuppression. |
| Reading a fold rash | SATELLITE PAPULES/PUSTULES SUPPORT CANDIDA. MALODOR, EROSIONS OR DRAINAGE → BACTERIAL COINFECTION. Well-demarcated erythematous patches; pruritus and burning pain. |
| NYSTATIN vs AZOLE — know the spectrum | TOPICAL NYSTATIN TREATS CANDIDA ONLY. TOPICAL AZOLES TREAT CANDIDA AND MANY DERMATOPHYTES. Low-potency corticosteroid ONLY BRIEFLY for marked inflammation and ONLY with adequate antifungal. RECURRENT/EXTENSIVE → evaluate for DIABETES and IMMUNOSUPPRESSION. |
| Pityriasis versicolor | OVERGROWTH of LIPID-DEPENDENT MALASSEZIA that NORMALLY INHABITS THE SKIN → NOT CONSIDERED CONTAGIOUS. More common with HEAT, HUMIDITY, OILY SKIN, SWEATING, IMMUNOSUPPRESSION, CORTICOSTEROID EXPOSURE. Velvety tan/pink/white finely scaling macules 4–5 mm to confluent; NECK, UPPER ARMS, TRUNK, GROIN. RECURRENCE COMMON in warm climates. |
| Versicolor: the pigment counseling point | HYPOPIGMENTATION reflects ALTERED MELANOCYTE FUNCTION and reduced tanning; RECOVERY CAN LAG MONTHS after the yeast is cleared. COLOR CHANGE ALONE DOES NOT PROVE TREATMENT FAILURE — look for SCALE or confirm with KOH. |
| Versicolor differential | SEBORRHEIC DERMATITIS: erythematous YELLOWISH tint, SOFT GREASY scales. PITYRIASIS ROSEA: HERALD PATCH then CHRISTMAS-TREE distribution. VITILIGO: COMPLETELY WHITE (DEPIGMENTED), autoimmune. |
| Versicolor treatment + 2 drug traps | TOPICAL IS FIRST-LINE: ketoconazole, selenium sulfide, zinc pyrithione, ciclopirox, topical terbinafine. Common selenium sulfide approach: DAILY FOR 7 DAYS, 10-MINUTE CONTACT TIME. ORAL TERBINAFINE IS INEFFECTIVE — inadequate levels IN SWEAT (topical works). DO NOT USE ORAL KETOCONAZOLE — HEPATIC AND ADRENAL TOXICITY outweigh benefit in superficial infection. |
| Term | What you need to know |
|---|---|
| Varicella — the defining feature | LESIONS IN MULTIPLE STAGES AT ONCE: macules → papules → vesicles → crusts, SEVERAL STAGES SIMULTANEOUSLY. Concentrate on TRUNK, SCALP, FACE. ADULTS, PREGNANCY, NEWBORN AGE, IMMUNOCOMPROMISE increase complication risk. |
| Varicella management | Usually CLINICAL; LESION PCR preferred when confirmation needed. SUPPORTIVE CARE; AVOID ASPIRIN IN CHILDREN, caution with NSAIDs. Early oral antivirals for HIGHER-RISK patients; IV ACYCLOVIR for SEVERE/DISSEMINATED. Prompt consult for PREGNANCY, NEONATAL EXPOSURE, IMMUNOCOMPROMISE, SEVERE COMPLICATIONS. |
| Varicella contagion + precautions | CONTAGIOUS FROM 1–2 DAYS BEFORE THE RASH UNTIL ALL LESIONS CRUST. Breakthrough disease without crusts: until NO NEW LESIONS FOR 24 HOURS. Healthcare: STANDARD + AIRBORNE + CONTACT precautions. Primary prevention = TWO-DOSE VARICELLA VACCINATION. |
| Zoster pathophysiology | REACTIVATION of latent VZV. Latent in CRANIAL-NERVE OR DORSAL-ROOT GANGLIA; travels ALONG A SENSORY NERVE to the skin as cell-mediated immunity wanes. Risk rises with AGE and IMPAIRED CELL-MEDIATED IMMUNITY. |
| Zoster — 3 phases | PRE-ERUPTIVE: DYSESTHESIA OR PAIN IN THE DERMATOME, lesions by 48–72 HOURS. ACUTE ERUPTIVE: macules/papules → GROUPED HERPETIFORM VESICLES ON AN ERYTHEMATOUS BASE (classic); new lesions over 3–5 DAYS; INFECTIOUS UNTIL LESIONS HAVE DRIED; resolves over 10–15 DAYS. CHRONIC: postherpetic neuralgia. |
| Zoster distribution — the numbers | One or TWO ADJACENT dermatomes; STOPS ABRUPTLY AT THE MIDLINE — DOES NOT CROSS IT. THORACIC 55%, CRANIAL 20%, LUMBAR 15%, SACRAL 5%. ZOSTER SINE HERPETE = pain WITHOUT vesicular eruption. Scars only when DEEPER LAYERS are compromised by EXCORIATION OR SECONDARY INFECTION. |
| Can a contact catch shingles? NO | A susceptible contact DOES NOT 'CATCH SHINGLES'. Exposure to VESICULAR FLUID, or AIRBORNE VIRUS FROM DISSEMINATED DISEASE, CAN CAUSE VARICELLA. Cover lesions, no scratching, hand hygiene, avoid SUSCEPTIBLE PREGNANT PEOPLE, PREMATURE INFANTS and IMMUNOCOMPROMISED PEOPLE UNTIL CRUSTED. |
| Zoster antivirals + the 72-hour rule | VALACYCLOVIR, FAMCICLOVIR or ACYCLOVIR; adjust for RENAL function. START AS SOON AS POSSIBLE, IDEALLY WITHIN 72 HOURS. TREAT AFTER 72 HOURS WHEN: NEW LESIONS ARE FORMING, or OPHTHALMIC, NEUROLOGIC, DISSEMINATED, SEVERE or IMMUNOCOMPROMISED disease. IV ACYCLOVIR + specialist for severe disseminated, visceral, CNS or SIGHT-THREATENING disease. |
| Zoster testing | Typical unilateral dermatomal vesicles = CLINICAL. PCR FROM VESICLE FLUID, SCAB, OR CELLS FROM THE LESION BASE preferred for ATYPICAL, DISSEMINATED, VACCINE-MODIFIED or IMMUNOCOMPROMISED presentations. Differential: HSV, contact dermatitis, impetigo, folliculitis, insect bites, dermatitis herpetiformis, varicella. |
| POSTHERPETIC NEURALGIA | THE MOST COMMON COMPLICATION. PAIN PERSISTING 90 DAYS OR MORE AFTER RASH ONSET. Burning, aching, stabbing, ELECTRIC SHOCK-LIKE, or EVOKED BY LIGHT TOUCH (ALLODYNIA). Lasts MONTHS TO YEARS. Risk: AGE, SEVERE ACUTE PAIN, SEVERE RASH, OPHTHALMIC INVOLVEMENT, IMMUNOCOMPROMISE. |
| PHN treatment | FIRST LINE: GABAPENTIN/PREGABALIN, an appropriate TRICYCLIC ANTIDEPRESSANT, or TOPICAL LIDOCAINE. CAPSAICIN PATCH may help. Individualize for KIDNEY FUNCTION, FALLS, ANTICHOLINERGIC BURDEN, INTERACTIONS. AVOID ROUTINE LONG-TERM OPIOIDS; refer severe/persistent/disabling pain. |
| STEROIDS AND PHN — say it as a sentence | TOPICAL OR SYSTEMIC CORTICOSTEROIDS DO NOT PREVENT PHN AND SHOULD NEVER REPLACE ANTIVIRAL THERAPY. Systemic steroids require individualized risk–benefit assessment. |
| Herpes zoster ophthalmicus | OPHTHALMIC DIVISION (V1) of CN V. HUTCHINSON SIGN = lesions on the TIP/SIDE OF THE NOSE, increases ocular risk — BUT ITS ABSENCE DOES NOT EXCLUDE EYE INVOLVEMENT. START SYSTEMIC ANTIVIRAL IMMEDIATELY. SAME-DAY OPHTHALMOLOGY for eye pain, visual symptoms, red eye, photophobia, Hutchinson sign, or eyelid/ocular involvement. |
| RAMSAY HUNT (herpes zoster oticus) | PERIPHERAL FACIAL PALSY with PAINFUL VESICLES OF THE EAR CANAL/AURICLE OR OROPHARYNX; hearing loss, tinnitus or vertigo may occur. ANTIVIRAL PLUS SYSTEMIC CORTICOSTEROID EARLY when not contraindicated. Urgent ENT/NEUROLOGY. PROTECT THE CORNEA if eyelid closure is impaired. |
| SHINGRIX | TWO DOSES for IMMUNOCOMPETENT ADULTS 50 AND OVER. TWO DOSES for ADULTS 19 AND OVER who ARE OR WILL BE immunodeficient/immunosuppressed. STANDARD INTERVAL 2–6 MONTHS; for IMMUNOCOMPROMISED the second dose may be given 1–2 MONTHS after the first when faster completion is beneficial. |
| Term | What you need to know |
|---|---|
| HSV — the assumption to drop | EITHER TYPE CAN CAUSE ORAL OR GENITAL INFECTION — LESION LOCATION DOES NOT RELIABLY DETERMINE TYPE. HSV-1 GENITAL infection generally RECURS AND SHEDS LESS OFTEN than HSV-2 genital infection. |
| HSV transmission & virology | Contact with infected ORAL/GENITAL SECRETIONS OR LESIONS — AND CAN OCCUR DURING ASYMPTOMATIC SHEDDING. DOUBLE-STRANDED DNA, HERPESVIRIDAE. NEUROVIRULENT — invades and replicates in the nervous system. LATENT BUT LIFELONG. |
| HSV presentation | FIRST EPISODE more prominent and LONGER; RECURRENCES milder and shorter. Prodrome: tenderness, pain, paresthesias or burning — SOME HAVE NO PRODROME. Characteristic prodromal symptoms: LOCALIZED PAIN, TENDER LYMPHADENOPATHY, HEADACHE, GENERALIZED ACHING, FEVER. PE: GROUPED VESICLES ON AN ERYTHEMATOUS BASE breaking down to a SHALLOW PAINFUL ULCER; DYSURIA in women; last ~2 WEEKS; HEAL WITHOUT SCARRING. Triggers: STRESS, ILLNESS, MENSTRUATION, UV LIGHT. |
| HSV testing — 2 do's, 2 don'ts | DO swab a FRESH vesicle, ulcer base or crust for TYPE-SPECIFIC NAAT/PCR — the PREFERRED test. KNOW culture is LESS SENSITIVE (especially healing/recurrent) and a NEGATIVE DOES NOT EXCLUDE; a negative OLDER-lesion swab does not exclude either because SHEDDING IS INTERMITTENT. DON'T use HSV IgM. DON'T routinely screen asymptomatic adults serologically. Confirm LOW-POSITIVE HSV-2 serology with a SECOND METHOD. |
| HSV differential | CHANCROID: bacterial, HAEMOPHILUS DUCREYI, PAINFUL NECROTIZING ULCERS, INGUINAL LYMPHADENOPATHY. SYPHILIS: solitary raised papules that erode, USUALLY PAINLESS. Also TRAUMA and CANDIDIASIS. Evaluate genital ulcers for OTHER CAUSES INCLUDING SYPHILIS, based on risk. |
| HSV treatment & counseling | TREAT EVERY FIRST CLINICAL EPISODE with oral ACYCLOVIR, VALACYCLOVIR or FAMCICLOVIR. Recurrent genital: PATIENT-INITIATED EPISODIC or DAILY SUPPRESSIVE. SUPPRESSIVE VALACYCLOVIR LOWERS HSV-2 TRANSMISSION; CONDOMS REDUCE BUT DO NOT ELIMINATE RISK. Avoid sexual/direct lesion contact DURING THE PRODROME OR ACTIVE LESIONS. TOPICAL ANTIVIRALS = MINIMAL BENEFIT for genital herpes. |
| HERPETIC WHITLOW | PAINFUL HSV OF THE DISTAL FINGER, often INOCULATED THROUGH BROKEN SKIN. Prodromal burning/tingling → GROUPED VESICLES on an ERYTHEMATOUS SWOLLEN DIGIT; fever or lymphangitis may occur. Mimics BACTERIAL FELON/PARONYCHIA, CONTACT DERMATITIS, BLISTERING DACTYLITIS. Confirm atypical cases with NAAT/PCR from a fresh vesicle or lesion base. |
| WHITLOW: the one instruction | DO NOT INCISE AND DRAIN — it DOES NOT TREAT HSV and CAN DELAY HEALING. Cover lesions, hand hygiene, avoid contact with MUCOSA/BROKEN SKIN UNTIL HEALED. Early oral antiviral may shorten symptoms; consider SUPPRESSION for frequent recurrence. Treat bacterial superinfection ONLY WHEN PRESENT. |
| Molluscum contagiosum | BENIGN POXVIRUS. Discrete, smooth, firm, FLESH-COLORED DOME-SHAPED PEARLY PAPULES, 3–5 mm average; CENTRAL UMBILICATION IS CHARACTERISTIC. Spread by DIRECT SKIN CONTACT, SHARED CONTAMINATED OBJECTS, AUTOINOCULATION; sexual contact common in adults with genital lesions. MOST CLEAR SPONTANEOUSLY but may take MONTHS TO SEVERAL YEARS. Differential: BASAL CELL CARCINOMA, SEBACEOUS HYPERPLASIA, CONDYLOMA ACUMINATUM. Clinical diagnosis; BIOPSY IF UNCERTAIN. |
| Molluscum treatment — the ages | OBSERVATION APPROPRIATE FOR MANY — 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. Also CURETTAGE or CRYOTHERAPY; TOPICAL RETINOIDS ARE OFF LABEL. |
| Molluscum: 3 higher-risk presentations | GENITAL in ADOLESCENTS/ADULTS may be SEXUALLY TRANSMITTED — assess for STIs. GENITAL IN A CHILD requires CONTEXT-SENSITIVE ASSESSMENT — LOCATION ALONE DOES NOT PROVE ABUSE. EXTENSIVE OR GIANT FACIAL lesions → EVALUATE FOR IMMUNOSUPPRESSION, INCLUDING HIV when appropriate. |
| Warts — the anatomy point | HUMAN PAPILLOMAVIRUS infecting KERATINOCYTES. CONFINED TO THE EPIDERMIS, but EXPANDS AND DISPLACES THE DERMIS, giving the impression it extends deeper. Underside is ROUND AND SMOOTH — NO ROOTS. Transmitted: SKIN-TO-SKIN, AUTOINOCULATION, CONTAMINATED SURFACES. |
| Verruca vulgaris | Frequently AGES 5–20. Usually HANDS, favoring FINGERS/PALMS. PERIUNGUAL, LIPS & TONGUE more common in NAIL BITERS. Usually <1 cm, elevated round papules, ROUGH GRAYISH surface. TINY RED/BLACK DOTS = THROMBOSED DILATED CAPILLARIES; TRIMMING THE SURFACE MAKES THEM MORE PROMINENT. Natural history: SPONTANEOUS RESOLUTION. |
| Verruca plana & plantaris | PLANA (flat): multiple SMOOTH, slightly elevated, FLAT-TOPPED, skin-colored to light-brown papules; FACE, FOREHEAD, DORSAL HANDS, SHINS; SHAVING SPREADS THEM BY AUTOINOCULATION; balance treatment against DYSPIGMENTATION AND SCARRING. PLANTARIS: WEIGHT-BEARING SURFACE; DO NOT REQUIRE THERAPY UNLESS PAINFUL; cluster into a MOSAIC WART; SALICYLIC ACID 40% or CRYOTHERAPY. |
| Wart diagnosis & referral | CLINICAL. BIOPSY GENERALLY UNNECESSARY but may be appropriate for IMMUNOCOMPROMISED patients or LESIONS OF UNCERTAIN ETIOLOGY (ruling out SCC). Differential: SQUAMOUS CELL CARCINOMA, MOLLUSCUM CONTAGIOSUM, SEBORRHEIC KERATOSIS. BIOPSY/REFER ATYPICAL, BLEEDING, ULCERATED, GROWING or REFRACTORY lesions. |
| Wart treatment principles | NO THERAPY ERADICATES HPV WITH CERTAINTY; RECURRENCE CAN OCCUR. Choose by LOCATION, SYMPTOMS, AGE, PREGNANCY STATUS, IMMUNE STATUS, RISK OF SCARRING/DYSPIGMENTATION. CRYOTHERAPY EVERY 2–3 WEEKS may cause PAIN, BLISTERING, PIGMENT CHANGE. AVOID EXCESSIVE FREEZING/DESTRUCTIVE THERAPY for benign lesions likely to resolve. REFER PERIUNGUAL, FACIAL, EXTENSIVE, RECALCITRANT, DIAGNOSTICALLY UNCERTAIN or IMMUNOCOMPROMISED cases. |
| Term | What you need to know |
|---|---|
| Corn vs callus vs wart | CORN: focal pressure, CENTRAL KERATIN CORE, <1.5 cm, well defined, hurts on DIRECT DOWNWARD pressure, skin lines RUN THROUGH. CALLUS: broad pressure, diffuse, NO core, larger and irregular, PAINLESS, skin lines run through. WART: human papillomavirus, cauliflower with BLACKENED CENTER, INTERRUPTS skin lines, hurts on SIDE pressure, not confined to pressure areas. |
| Hard vs soft corn | HARD (clavus durum) = dorsal/lateral FIFTH TOE. SOFT (clavus mollum) = 4th-to-5th WEB SPACE, soft because moisture MACERATES it. |
| Corn/callus treatment | 1st REMOVE THE PRESSURE — padding, better footwear. 2nd over-the-counter keratolytics: every product in the deck's table is SALICYLIC ACID, 12.6–40%. DIABETIC → REFER TO PODIATRY. |
| Wound healing phases | HEMOSTASIS → INFLAMMATION → PROLIFERATION → REMODELING. Tensile strength comes from PROGRESSIVE CROSS-LINKING OF COLLAGEN FIBERS. |
| KELOID vs HYPERTROPHIC SCAR — the one to know | KELOID: develops SLOWLY, may appear MONTHS after trauma; EXTENDS BEYOND the wound; enlarges for months–years, NO regression, recurs; EAR LOBE / SHOULDERS / STERNAL NOTCH, rarely across joints; RARE; ASSOCIATED WITH DARK SKIN; often WORSENED by surgery. HYPERTROPHIC: within FOUR WEEKS, soon after surgery; CONFINED to the wound; stable then REGRESSES; where scars cross joints/creases at a RIGHT ANGLE; FREQUENT; NO skin-color association; IMPROVES with appropriate surgery. |
| Keloid treatment numbers | Silicone sheets 12–24 h/day up to a YEAR. Compression 25 mmHg, 24 h/day, 6–12 MONTHS. Surgical excision alone = 50–100% RECURRENCE, often LARGER → always follow with intralesional steroid. Radiation only in the FIRST TWO WEEKS after excision. Cryotherapy → HYPOPIGMENTATION. Intralesional steroid → TISSUE ATROPHY. Laser best COMBINED with intralesional steroid. Fluorouracil INHIBITS FIBROBLAST PROLIFERATION. |
| Both scars: diagnosis | CLINICAL. BIOPSY ONLY IF GENUINE DOUBT — it may INDUCE NEW SCARRING. Differential for each: the other one, dermatofibroma, foreign-body granuloma. |
| Keloid prevention | THE MOST IMPORTANT TREATMENT. Avoid cosmetic procedures such as ear piercing. Treat adolescent acne EARLY — greatly increases the chance of scar-free healing. Post-op: no stretching, no hot baths, keep clean. |
| Term | What you need to know |
|---|---|
| Cutaneous horn — the whole point | It is NOT a diagnosis. Keratin projection ARISING FROM ANOTHER LESION: actinic keratosis, wart, seborrheic keratosis, keratoacanthoma, basal or squamous cell carcinoma. THE PROCESS AT THE BASE IS WHAT MATTERS. Often NO clinical feature separates benign from malignant → DEEP SHAVE BIOPSY. Caucasians >50, head/neck/upper extremities. |
| Acrochordon (skin tag) | Fibroepithelial PEDUNCULATED PAPILLOMA — narrow stalk, broad tip, 1–10 mm. Females and obese; FRICTION SITES (neck, axilla, groin). 60% OF PEOPLE BY AGE 70. Scissor excision, cryotherapy or electrodesiccation — ANESTHESIA NOT NECESSARY. NEVER cut or pull one off at home: they bleed. |
| PRESSURE INJURY STAGING (slides 33–34 are IMAGES) | 1 = NON-BLANCHABLE ERYTHEMA of INTACT skin. 2 = PARTIAL thickness, EXPOSED DERMIS, viable pink/red bed. 3 = FULL thickness, ADIPOSE TISSUE VISIBLE. 4 = full thickness skin AND tissue loss, EXPOSED FASCIA/MUSCLE/TENDON/LIGAMENT/CARTILAGE/BONE. UNSTAGEABLE = obscured by SLOUGH or ESCHAR. DEEP TISSUE = persistent non-blanchable DEEP RED/PURPLE, skin intact or not. |
| Pressure injury prevention | THE BEST MEASURE. Frequent skin assessment · nutrition assessment · moisture control and skin care · REPOSITION EVERY TWO HOURS · manage pain · improve mobility · specialty mattresses. Note the staging tables show every stage in LIGHTLY AND DARKLY pigmented skin — stage 1 erythema is hardest to see on darker skin. |
| Pressure injury management | Depends on STAGE. REFER TO A WOUND CARE SPECIALIST. Control infection. 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. |
| Pilonidal cyst | Pit over the coccyx draws in HAIR AND DEBRIS → follicular plugging → abscess. MALE:FEMALE 3:1. Now believed ACQUIRED, not congenital. Recurrence common. Risks: obesity, local trauma, sedentary, INCREASED HAIR DENSITY IN THE NATAL CLEFT, family history. |
| Pilonidal: acute vs chronic | ACUTE ABSCESS: sudden pain and swelling, warm/tender/erythematous, may be FLUCTUANT (wave-like fluid shift on palpation) → INCISION AND DRAINAGE. CHRONIC: recurrent drainage from SINUS TRACTS, hair may protrude → REFER TO SURGEON for excision. NO diagnostic testing usually needed. |
| SINUS vs FISTULA (slide 42 is an IMAGE) | SINUS = a BLIND track. FISTULA = a track CONNECTING TWO EPITHELIUM-LINED SURFACES. Both usually arise from a preceding abscess. |
| Term | What you need to know |
|---|---|
| Dermatofibroma | Dermal FIBROBLASTS in dense clusters, 0.5–1 cm. LEGS most common, then arms. F:M 2:1. May follow trauma, viral infection or INSECT BITE. DIMPLE SIGN — retracts beneath the skin on LATERAL compression. Brown halo, pink hue, raised scaly center. MOST COMMON PAINFUL SKIN TUMOR. Dermoscopy: PERIPHERAL PIGMENT NETWORK WITH CENTRAL WHITE MASS. Small lesions: shave or punch biopsy is BOTH DIAGNOSTIC AND THERAPEUTIC. Differential includes MELANOMA. |
| Keratoacanthoma | From the PILOSEBACEOUS UNIT. ARGUED TO BE A VARIANT OF INVASIVE SQUAMOUS CELL CARCINOMA. TRIPHASIC: rapid growth in 6–8 WEEKS → stabilization → regression after 3–6 MONTHS. Dome with a CENTRAL KERATIN-FILLED CRATER. Risks: age >40, sun, very fair skin, male, RED TATTOO INK, SKIN TRAUMA (lasers, surgery, cryotherapy), human papillomavirus. BIOPSY IS THE ONLY RELIABLE DIAGNOSIS. EXCISE OR DESTROY — 5 mm MARGINS; MOHS for large, recurrent or cosmetically sensitive. Intralesional METHOTREXATE before excision to shrink it. |
| Epidermoid cyst | Epithelium enclosed in dermis filling with KERATIN. NOT A SEBACEOUS CYST despite the name. M:F 2:1; face, scalp, neck, trunk. CENTRAL PORE/PUNCTUM; expresses cream-colored pasty material smelling of RANCID CHEESE. Lab tests usually unnecessary. IF INFLAMED: POSTPONE excision, intralesional TRIAMCINOLONE, antibiotics if needed. Standard of care = REMOVE THE ENTIRE CAPSULE when NOT inflamed; 1–3 cm can be punched and emptied. |
| Syringoma | Benign neoplasms of ECCRINE DUCTS. Appear at PUBERTY, females > males. Multiple 1–2 mm papules on EYELIDS and UPPER CHEEKS. Cosmesis only: drugs (oral isotretinoin) → INCREASED RECURRENCE; procedures → POSSIBLE POOR COSMETIC RESULT. Differential: MILIA, XANTHELASMA, basal cell carcinoma. |
| Term | What you need to know |
|---|---|
| Sort them this way first | CONGENITAL: infantile hemangioma, nevus flammeus, nevus simplex. ACQUIRED: cherry angioma, telangiectasia, nevus araneus, pyogenic granuloma. Then within congenital, ask: DOES IT INVOLUTE? |
| Infantile hemangioma | MOST COMMON TUMOR OF INFANCY. PROLIFERATION of endothelial cells. Preterm, FEMALE 3:1, Caucasian. Head/neck 60%, trunk 25%, extremities 15%. Earliest sign: BLANCHING → fine telangiectasias → red/crimson macule. Rapid growth birth–4 weeks, most in first 4–6 MONTHS. INVOLUTION 50% BY 5, 70% BY 7, 90% BY 9. Superficial = commonest, bright red (once 'strawberry'); deep = least common, pale/blue. |
| Hemangioma treatment | Serial observation unless: COSMETIC, FUNCTIONAL INVOLVEMENT, DEEP ULCERATION, INFECTION. FIRST LINE = BETA-BLOCKERS (oral propranolol, topical timolol) AND CORTICOSTEROIDS. Pulsed dye laser depth ~1.2 mm. Refer to a VASCULAR ANOMALIES SPECIALIST if the diagnosis is in question. |
| Nevus flammeus (port-wine stain) | DILATION of dermal capillaries through the FULL DEPTH, with NO ENDOTHELIAL PROLIFERATION — which is WHY IT NEVER INVOLUTES. Present at birth, grows with the child, DARKENS AND THICKENS. Blanchable, usually UNILATERAL with SHARP MIDLINE CUTOFF; darkens with crying, fever or overheating. No treatment; tinted waterproof makeup; PULSED DYE LASER. |
| Nevus simplex (stork bite) | More SUPERFICIAL variant of nevus flammeus. Head and neck, more noticeable when crying. FADES WITHIN A YEAR, or persists on the NECK. |
| Cherry angioma | ACQUIRED, capillary/venule PROLIFERATION, cause unknown, INCREASES WITH AGE (once 'senile angioma'). TRUNK, <5 mm, smooth firm deep red, BLANCH. Treat only if it bothers the patient. NEW LESIONS WILL KEEP DEVELOPING AND CANNOT BE PREVENTED. |
| Telangiectasia | Permanently DILATED capillary <1 mm, BLANCHABLE, single/grouped/central punctum. Primary or secondary; ASSOCIATED WITH NUMEROUS DISEASES — the work-up follows the suspected cause. |
| Nevus araneus (spider angioma) | DILATION of preexisting vessels, NO proliferation. ESTROGEN EXCESS: pregnancy or oral contraceptives (RESOLVE after delivery / stopping), CIRRHOSIS and LIVER FAILURE. Hands and fingers in CHILDREN; face, neck, upper trunk, arms in ADULTS. <10 mm, blanches. ASK about pregnancies, hormones, ALCOHOL, hepatotoxic drugs. |
| Pyogenic granuloma | MISNAMED — NEITHER INFECTIOUS NOR GRANULOMATOUS. Response to INJURY or HORMONAL factors; children, young adults, PREGNANCY. Head, neck, FINGERS. Bright red EXOPHYTIC papule, MOIST surface, EPITHELIAL COLLARETTE at base, BLEEDS. Average 6.5 mm. Differential: cherry angioma, MELANOMA, SQUAMOUS CELL CARCINOMA. SURGICAL EXCISION = lowest recurrence, HIGHEST SCARRING, gives histopathology. |
| Term | What you need to know |
|---|---|
| Neurofibromatosis genes | Von Recklinghausen disease. NF1 = NF1 gene, CHROMOSOME 17. NF2 = NF2 gene, CHROMOSOME 22. Schwannomatosis (NF3) = SMARCB1 and LZTR1, CHROMOSOME 22. |
| NF1 — the four skin signs | CAFÉ AU LAIT SPOTS · CUTANEOUS NEUROFIBROMAS · INTERTRIGINOUS FRECKLING · PLEXIFORM NEUROFIBROMAS. |
| Café au lait spots | >5 mm PREPUBERTAL, >15 mm POSTPUBERTAL. Often the FIRST manifestation; 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. |
| Crowe's sign | INTERTRIGINOUS FRECKLING, freckles <5 mm — SMALLER than café au lait spots. Grouped, more prominent with sun. AXILLARY and INGUINAL; under the breasts is NOT a diagnostic site. |
| Neurofibromas | CUTANEOUS: benign NERVE SHEATH tumors from peripheral nerves; BEGIN AT PUBERTY, increase with age; a few to hundreds. PLEXIFORM: tumor in the tissue COVERING nerves, anywhere EXCEPT brain and spinal cord, large and extensive, MAY BE LOCALLY INVASIVE. Management = SURVEILLANCE with a cutaneous exam at EVERY visit. Education = national and regional SUPPORT GROUPS. |
| Xanthelasma | Soft YELLOW CHOLESTEROL PLAQUES — LIPID-LADEN MACROPHAGES — on the MEDIAL EYELIDS. SCREEN FOR HYPERLIPIDEMIA; MAY SIGNIFY INCREASED CARDIAC RISK. Laser or excision; RECURRENCE COMMON. This is the one benign lesion here where blood work is the point. |
| Lipoma | THE MOST COMMON SOFT TISSUE TUMOR. Benign overgrowth of SUBCUTANEOUS FAT. Soft, painless, RUBBERY, usually <5 cm; asymptomatic unless adjoining structures invaded. Observe if asymptomatic; excise if COSMETICALLY DEFORMING or the DIAGNOSIS IS UNCERTAIN. Differential: epidermal cyst, dermatofibroma, abscess. |
| Digital mucous cyst | A PSEUDO-CYST — NO CELLULAR LINING. Mucin extruded from a JOINT SPACE compacts dermal cells into something that only MIMICS a capsule. Females > males; ASSOCIATED WITH OSTEOARTHRITIS; over the DISTAL INTERPHALANGEAL joint; may cause a LONGITUDINAL GROOVE in the nail. Observe, or excise if symptomatic or causing nail dystrophy. |
| Sebaceous hyperplasia | SEBOCYTE TURNOVER SLOWS WITH AGE → crowding → gland enlarges. NO KNOWN POTENTIAL FOR MALIGNANT TRANSFORMATION. IMMUNOSUPPRESSION HIGH RISK. Whitish-yellow soft papules 2–9 mm with CENTRAL UMBILICATION, on the face. Differential = BASAL CELL CARCINOMA, and DERMOSCOPY CAN DISTINGUISH THEM. No treatment needed — recurs, and treatment risks scarring; light electrocautery if wanted. |
| General education, any benign lesion | In a sun-exposed area, use the visit to counsel on SUNSCREEN, avoiding direct sun at PEAK HOURS, and PERIODIC SKIN EXAMINATION. Before cosmetic removal, warn about the RISK OF PIGMENTARY CHANGES and the CHANCE OF RECURRENCE. |
| Term | What you need to know |
|---|---|
| Ephelides vs lentigines | FRECKLES FADE WHEN THE SUN GOES; LENTIGINES DO NOT. That single fact is the whole differential. |
| Ephelides | Autosomal dominant, MCR-1 variant → pheomelanin. 3–5 mm light brown symmetric macules. Sun protection + depigmenting agents + laser. NOT cryotherapy — lesions too small. |
| Lentigo simplex | Uniformly black or brown, well circumscribed, under 5 mm. Sun-exposed AND protected skin. No treatment needed. |
| Solar lentigo | 90% of people by age 50. Irregular borders coalescing at sunburn sites. Associated with actinic keratosis, squamous and basal cell carcinoma, melanoma. Can become lichenoid keratoses. |
| PUVA lentigines | Total treatments, male, fair skin, older age. Appear on BUTTOCKS AND GENITALIA as well as exposed sites. |
| Seborrheic keratosis | Beige-to-black, velvety, look STUCK ON, 2–20 mm, older adults. Easily mistaken for neoplasms. Cryotherapy only if itchy or inflamed — and it recurs. |
| Dermatosis papulosa nigrans | Identical to small seborrheic keratoses. Face and neck, African American / dark-skinned Asian / Polynesian, F > M. Genetic — hair follicle developmental defect. AVOID CRYOTHERAPY (post-inflammatory hyperpigmentation). |
| Vitiligo | T-cell destruction of melanocytes. Usually before 30; half before 20, a third before 12. White non-scaly macules with distinct margins, FLUORESCE under Wood's lamp in a DARK ROOM. |
| Segmental vs non-segmental | Segmental = UNILATERAL, does not cross midline, block-like, unpredictable cycles. Non-segmental = symmetrical, prefers face, genitals, acral. |
| Vitiligo treatment | Under 5% → topical steroid (atrophy, intraocular pressure) or calcineurin inhibitor (face/neck/children; cancer risk). Over 5% → NARROW BAND ULTRAVIOLET B first line, preferred over PUVA. Grafting ONLY for highly stable disease. Psychological intervention is part of management. |
| Congenital melanocytic naevus | LARGER = HIGHER MELANOMA RISK. Head, neck or posterior midline → magnetic resonance imaging for NEUROCUTANEOUS MELANOSIS (seizures, hydrocephalus; poor prognosis). |
| Naevus spilus | Tan café-au-lait-like patch with scattered darker macules. RARELY progresses to melanoma. Observation + sun protection. |
| Common acquired naevus | Under 6 mm, homogenous, sharply demarcated. Peaks in the THIRTIES then declines. VERY DARK BROWN OR BLACK ON LIGHT SKIN IS SUSPICIOUS. |
| Blue naevus | Dermal spindle/epithelioid melanocytes. Women, twenties. Dorsal hands and feet, scalp, buttocks, sacrum. Common blue under 1 cm; cellular blue over 1 cm. Small = clinical, larger = biopsy. |
| Pigmented spindle cell (Reed) | JET-BLACK papule under 7 mm, thirties, females, THIGH. Benign — but biopsy to confirm and EXCISE WITH NEGATIVE MARGINS. |
| Spitz naevus | Solitary PINK/RED hairless dome-shaped. Growth phase then stable. SPARES palms, soles, mucosae. Resembles melanoma → biopsy or wide excision. Multiple → familial cancer syndrome. |
| Dysplastic naevus | At least 5 mm, irregular indistinct borders, variable tan-to-brown, pebbly. Caucasians, family history. Over 100 by adolescence = the syndrome. MORE NAEVI = MORE MELANOMA RISK. Biopsy ALL changing lesions. |
| Term | What you need to know |
|---|---|
| ★ THE PATTERN — and its two exceptions | She teaches nearly every pigmented lesion the same way: DIAGNOSE CLINICALLY → OBSERVE → BIOPSY IF IT CHANGES in size, color or shape. Verbatim: “I hope everyone's still REMEMBERING THE PATTERN here… there's like TWO THINGS THAT IT'S NOT LIKE THAT FOR.” The two are the ones that IMITATE MELANOMA and need tissue out WITH MARGINS: REED NAEVUS (excision with negative margins) and SPITZ (biopsy vs WIDE EXCISION — “not just removing part of the lesion but the ENTIRE AREA SURROUNDING it”). One frame for the whole lecture: WATCH THEM ALL, CUT OUT THE TWO THAT LOOK LIKE MELANOMA. |
| Ephelides vs lentigines, her wording | On lentigines: “THESE DO NOT GO AWAY as sun exposure gets less and less” — “that will be one way that you will be able to DIFFERENTIATE LENTIGINES, SUNSPOTS, FROM EPHELIDES, FRECKLES.” |
| Counseling — cryotherapy recurrence | Warn BEFORE you freeze a seborrheic keratosis that it can come back, “OTHERWISE THEY'LL BE PRETTY UPSET AT YOU.” |
| ⚠ What the recording misses | Starts at about SLIDE 3 OF 47 (only title + objectives lost), stops MID-SENTENCE in the practice cases, and has a TWELVE-MINUTE HOLE between its two segments, 13:44 to 13:56. That hole is exactly where SPITZ was named — which is why neither transcript contains the word. NO emphasis note on a topic does NOT mean she skipped it; the deck content is covered in full regardless. |
| Term | What you need to know |
|---|---|
| Actinic keratosis — what it IS | PREMALIGNANT, and on a BIOLOGIC CONTINUUM with keratinocyte carcinoma — not a separate entity. Chronic ultraviolet injury across a FIELD of sun-damaged skin. |
| Actinic keratosis — appearance | 0.2–0.6 cm flesh-colored, pink or slightly hyperpigmented papules with a SANDPAPER TEXTURE. MAY BE MORE APPARENT BY TOUCH THAN BY SIGHT. Face, scalp, ears, forearms, dorsal hands. |
| Actinic keratosis — the number | ABOUT 1 IN 1,000 LESIONS PER YEAR progresses to squamous cell carcinoma. Cumulative FIELD risk matters more than any one lesion's risk. |
| Lesion-directed vs field-directed | 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 + calcipotriene possible benefit. |
| When an actinic keratosis needs a BIOPSY | BLEEDING · INDURATION · ULCERATION · RAPID ENLARGEMENT. Those are NOT typical. The interpretation must separate actinic keratosis from CARCINOMA IN SITU from INVASIVE squamous cell carcinoma, because invasion changes treatment, margins and risk. Treating lesions does NOT clear the field — surveillance continues. |
| Squamous cell carcinoma — exposure pattern | SECOND most common skin cancer. PROLONGED CUMULATIVE sun exposure — contrast basal cell carcinoma's INTENSE INTERMITTENT exposure. May arise from an actinic keratosis. |
| Squamous cell carcinoma — appearance | Small RED CONICAL HARD NODULE that MAY ULCERATE; also a NON-HEALING ULCER, a warty nodule, or an irregular pink plaque with hemorrhagic crust. |
| Squamous cell carcinoma — risk raisers | HIGH-RISK SITES: mucosal surfaces, LIP, EAR, scalp, temple, nose, genitalia. MORE THAN 10 TUMORS = higher local recurrence and nodal metastasis. Also chronic SCARS, wounds and old RADIATION sites. |
| Squamous cell carcinoma — immunosuppression | Common and often AGGRESSIVE after transplant, with multiple tumors typically at ABOUT 5 YEARS. Chronic lymphocytic leukemia and human immunodeficiency virus also raise risk and aggressiveness. |
| NICOTINAMIDE — the two numbers | 500 mg ORALLY TWICE DAILY both times. Reduces new SQUAMOUS cell carcinoma by ABOUT 30%; reduces BASAL cell carcinoma by ABOUT 20%. If you mix them up, remember the more dangerous cancer gets the bigger number. |
| Squamous cell carcinoma — treatment by stage | IN SITU without high-risk features: imiquimod, topical fluorouracil, or curettage and electrodesiccation. INVASIVE: SURGICAL EXCISION OR MOHS. ADVANCED/METASTATIC: PROGRAMMED DEATH 1 BLOCKADE; CETUXIMAB. |
| MOHS indications | High-risk sites (LIPS, TEMPLES, EARS, NOSE, GENITALIA) · recurrent tumors · aggressive histology with PERINEURAL or PERIVASCULAR invasion · OVER 1 cm ON THE FACE or OVER 2 cm on trunk/extremities · immunosuppression · tumors WITHIN SCARS · genetic disease-associated tumors. |
| Squamous cell carcinoma — follow-up and prognosis | AT LEAST ANNUAL SKIN AND LYMPH-NODE EXAMINATION. Urgent referral for high-risk site/size, recurrence, aggressive histology, immunosuppression, NEUROLOGIC SYMPTOMS or nodal disease. Metastatic rate for actinically induced disease 3–7%. |
| Term | What you need to know |
|---|---|
| The headline | THE MOST COMMON FORM OF CANCER. The HISTOLOGIC subtype determines behavior and dictates treatment — NOT the clinical appearance. |
| Nodular | Papule/nodule with CENTRAL EROSION, slow growth over years to 1–2 cm. PEARLY OR TRANSLUCENT with TELANGIECTASIAS ACCENTUATED BY STRETCHING THE SKIN. |
| Pigmented | Stippled or focal pigmentation that MAY MIMIC MELANOCYTIC DISEASE. The PEARLY BORDER and SLOW GROWTH are what discriminate. |
| Superficial | Reddish, shiny, SCALY THIN papules or plaques on BACK OR CHEST; may have a thready pearly border and spotty edge pigmentation. |
| Morpheaform / sclerosing | SCAR-LIKE OR IVORY-WHITE, with clinically subtle extension BEYOND the visible pink segment — HIGHER RISK OF SUBCLINICAL SPREAD. |
| Warning patterns | A PEARLY PAPULE · an ERYTHEMATOUS PATCH LARGER THAN 6 mm · a NON-HEALING ULCER. Face, trunk, lower legs. |
| The recurrence number | A SECOND basal cell carcinoma develops in UP TO 50% of patients → at least ANNUAL full-skin examination is mandatory. Excision recurrence 5% OR LESS; MOHS CURE ABOUT 98%. |
| Topical option for SELECTED superficial disease | IMIQUIMOD FIVE NIGHTS WEEKLY FOR 6–10 WEEKS, or FLUOROURACIL TWICE DAILY FOR UP TO 12 WEEKS — with CLINICAL CLEARANCE CONFIRMED AFTERWARDS. |
| Advanced or metastatic | HEDGEHOG PATHWAY INHIBITORS — VISMODEGIB or SONIDEGIB. |
| Prognosis | Slow-growing and highly curable when treated early. The morbidity is LOCAL DESTRUCTION, recurrence, delayed diagnosis and anatomically complex sites — NOT spread. |
| Term | What you need to know |
|---|---|
| The headline numbers | 4th MOST COMMON CANCER IN THE UNITED STATES and the LEADING CAUSE OF DEATH DUE TO SKIN DISEASE. Incidence doubled over 30 years; mortality FALLING with earlier detection and immunotherapy. 2023: ~97,610 new invasive melanomas, ~7,990 deaths, ~TWO-THIRDS OF DEATHS IN MEN. |
| Lifetime risk | ABOUT 2% IN WHITE INDIVIDUALS; 0.1–0.5% IN PERSONS OF COLOR. Lower but NOT zero — which is why palms, soles and nails are still examined. |
| Four subtypes | SUPERFICIAL SPREADING ~2/3, intermittently sun-exposed skin, radial before vertical growth. LENTIGO MALIGNA, chronically sun-exposed skin of OLDER adults, slow radial phase. NODULAR, RAPIDLY GROWING, OFTEN AMELANOTIC, MAY LACK THE CLASSIC FEATURES. ACRAL LENTIGINOUS, palms/soles/nail units. |
| ABCDE | ASYMMETRY · BORDER irregular, notched or poorly defined · COLOR variegation (brown, red, white, black, blue in one lesion) · DIAMETER over 6 mm THOUGH SMALLER LESIONS CAN BE MELANOMA · EVOLUTION. |
| LEVEL OF INVASION, i.e. CLARK (slide 50 is an IMAGE, and the deck never says "Clark") | I = confined to the EPIDERMIS. II = into the PAPILLARY dermis. III = FILLING the papillary dermis. IV = into the RETICULAR dermis. V = into the SUBCUTANEOUS TISSUE. |
| Level of invasion vs Breslow | THE LEVEL (Clark) = an anatomic LAYER. BRESLOW = a MEASUREMENT, and BRESLOW IS THE DOMINANT PROGNOSTIC VARIABLE — measure it accurately at the INITIAL BIOPSY. Ulceration and mitotic activity further modify stage-based prognosis. |
| STAGES (slide 53 is an IMAGE) | 0 = confined to the epidermal region of skin. I = localized, only in skin, VERY THIN. II = localized, THICKER than stage I. III = SPREAD TO LYMPH NODES. IV = SPREAD TO OTHER ORGANS. |
| TNM (slide 54 is an IMAGE TABLE) | T = primary tumor THICKNESS. N = NUMBER OF TUMOR-INVOLVED REGIONAL LYMPH NODES. M = NUMBER OF METASTASES AT A DISTANT SITE. Stage 0 = Tis N0 M0 · I = T1–T2a N0 M0 · II = T2b–T4b N0 M0 · III = any N ≥ N1, M0 · IV = ANY T, ANY N, M1. |
| Sentinel lymph node biopsy | Offered or discussed at BRESLOW 1.0 mm OR GREATER, or 0.8 mm OR GREATER WITH ulceration, high mitotic rate or lymphovascular invasion. It is a STAGING PROCEDURE AND MAY NOT ITSELF IMPROVE OVERALL SURVIVAL. |
| Re-excision margins | IN SITU → 0.5–1 cm. LESS THAN 1 mm → 1 cm. MORE THAN 1 mm → 1–2 cm. |
| Referral and education | REFER TO AN EXPERT CENTER for melanoma DEEPER THAN 1 mm, or with lymph-node or other-site spread. Patients do MONTHLY self-examination with ABCDE and ugly-duckling principles — INCLUDING SCALP, BACK, PALMS, SOLES AND NAILS. |
| Term | What you need to know |
|---|---|
| Kaposi sarcoma — cause | HUMAN HERPESVIRUS 8 COMBINED WITH A WEAKENED IMMUNE SYSTEM, 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 → palliative local therapy (intralesional vincristine, vinblastine or bleomycin, or radiation). ENDEMIC: young Black men in equatorial Africa, often aggressive, CAN BE RAPIDLY FATAL. IATROGENIC: with immunosuppressive therapy → REDUCE DOSES WHERE FEASIBLE, COORDINATE WITH THE TRANSPLANT TEAM FIRST. EPIDEMIC: acquired immunodeficiency → BEGIN OR OPTIMIZE ANTIRETROVIRAL THERAPY. |
| The two examination points | ORAL EXAMINATION IS ESSENTIAL — HARD-PALATE lesions are common and MAY BE THE PRESENTING SITE. And MARKED EDEMA MAY OCCUR WITH FEW OR NO VISIBLE SKIN LESIONS — do not gauge disease burden from edema. |
| Kaposi sarcoma — systemic therapy | First line LIPOSOMAL DOXORUBICIN and PACLITAXEL. ANTIRETROVIRAL THERAPY PLUS CHEMOTHERAPY IS MORE EFFECTIVE THAN ANTIRETROVIRAL THERAPY ALONE in advanced disease. |
| Cutaneous T-cell lymphoma — course | Mycosis fungoides. Begins in the skin and MAY REMAIN CONFINED THERE FOR YEARS OR DECADES. |
| Cutaneous T-cell lymphoma — appearance | Localized or generalized erythematous PATCHES or scaly PLAQUES, usually TRUNK, frequently LARGER THAN 5 cm. RESEMBLES PSORIASIS, ECZEMA OR TINEA — which is why it is diagnosed late. |
| The two discriminating clues | ITCH OUT OF PROPORTION to the apparent inflammatory activity, and FOLLICULAR INVOLVEMENT WITH HAIR LOSS. Folliculotropism is what separates it from routine eczema or psoriasis. |
| The management philosophy — this is the exam point | Early AGGRESSIVE treatment HAS NOT BEEN PROVEN TO CURE DISEASE OR PREVENT PROGRESSION, and overly aggressive therapy MAY CAUSE COMPLICATIONS AND PREMATURE DEATH. Stage-directed, SKIN-FIRST: topical corticosteroids, topical mechlorethamine, bexarotene gel, ultraviolet phototherapy. |
| Term | What you need to know |
|---|---|
| The theme | DIAGNOSTIC DELAY IS A RECURRING THEME AND A PREVENTABLE HARM. Every item below is arranged around it. |
| Nail unit melanoma | Rare acral melanoma, most often from the MATRIX. NOT CLEARLY ULTRAVIOLET-DRIVEN; ANY SKIN TONE. THUMB AND GREAT TOE. New or evolving LONGITUDINAL MELANONYCHIA IN ONE DIGIT, increasing width, irregular color/thickness/spacing, PROXIMAL WIDENING OR TRIANGULAR SHAPE, blurred borders, nail splitting, ulceration or subungual mass. |
| HUTCHINSON SIGN | Periungual pigment extending onto the PROXIMAL NAIL FOLD → highly concerning for nail unit melanoma → URGENT EXPERT EVALUATION REGARDLESS OF OTHER FEATURES. (Different sign from the zoster ophthalmicus Hutchinson sign in Lecture 6.) |
| AMELANOTIC nail melanoma | May be red, pink, eroded or mass-like WITH NO DARK BAND AT ALL. THE ABSENCE OF PIGMENT DOES NOT EXCLUDE MELANOMA. Consider biopsy for any unexplained, progressive SINGLE-NAIL lesion. |
| Nail unit squamous cell carcinoma / Bowen | THE MOST COMMON MALIGNANT NAIL TUMOR. Chronic UNILATERAL verrucous periungual papule or plaque, subungual hyperkeratosis, onycholysis, oozing, bleeding, nail-plate destruction, longitudinal ERYTHRONYCHIA — OFTEN REPEATEDLY LABELED A WART, PARONYCHIA OR FUNGAL INFECTION. Associations: high-risk human papillomavirus, immunosuppression, chronic inflammation or trauma, prior radiation, older age. |
| Nail unit basal cell carcinoma | EXCEPTIONALLY UNCOMMON. Consider it in a persistent ULCERATED or PEARLY lesion of the nail fold or bed. |
| Glomus tumor | Small RED-BLUE SUBUNGUAL focus with SEVERE PAROXYSMAL PAIN, EXQUISITE POINT TENDERNESS and COLD SENSITIVITY; THE NAIL MAY LOOK NEARLY NORMAL. The triad SUGGESTS it but DOES NOT REPLACE IMAGING OR SPECIALIST EVALUATION. |
| Onychopapilloma / onychomatricoma | A SINGLE nail with longitudinal ERYTHRONYCHIA or LEUKONYCHIA, distal subungual hyperkeratosis, splinter hemorrhages or localized plate abnormality. |
| Before you inspect | REMOVE THE POLISH. Examine EVERY nail, the periungual skin, PALMS AND SOLES, and the REGIONAL NODES. |
| AMPUTATION IS NOT AUTOMATIC | Contemporary care is DIGIT-SPARING wide excision or MOHS with immunostaining where margins can be reliably assessed. Amputation is reserved for DEEP, EXTENSIVE OR BONE-INVOLVING disease. For nail unit squamous cell carcinoma, COMPLETE MARGIN-CONTROLLED SURGERY IS PREFERRED — partial destructive treatment carries higher recurrence. |
| Term | What you need to know |
|---|---|
| Characterize before you diagnose | PRIMARY LESION TYPE · COLOR · SURFACE TEXTURE · BORDER DEFINITION · SIZE · DISTRIBUTION · PALPABILITY · ULCERATION · BLEEDING · INDURATION · TEMPORAL EVOLUTION. |
| The two examination steps people skip | THE ORAL CAVITY — a hard-palate lesion may be the presenting site of KAPOSI SARCOMA. And CHRONIC SCARS OR OLD RADIATION FIELDS — SQUAMOUS CELL CARCINOMA arises in them. Also palms, soles, NAILS, and regional nodes for invasive or high-risk disease. |
| History that changes the answer | Onset and change · bleeding or non-healing · sunburns, occupational/recreational ultraviolet, TANNING BEDS · PRIOR SKIN CANCER · IMMUNOSUPPRESSION OR TRANSPLANT · human immunodeficiency virus risk · family history · the lesion THE PATIENT has noticed. |
| ADULT | Cumulative AND intermittent ultraviolet exposure both accumulate through working life. IMMUNOSUPPRESSION AND TRANSPLANT STATUS DOMINATE RISK — squamous cell carcinoma common and aggressive, typically MULTIPLE AT ABOUT 5 YEARS, nicotinamide 500 mg twice daily is a real option. Melanoma self-examination monthly and lifelong. Kaposi sarcoma here is usually EPIDEMIC or IATROGENIC — treat the immune state first. |
| ELDERLY | Actinic keratosis burden and FIELD CANCERIZATION rise with cumulative exposure → favor FIELD-DIRECTED therapy. LENTIGO MALIGNA arises on chronically sun-exposed skin of older adults. CLASSIC Kaposi sarcoma is a disease of older men, managed PALLIATIVELY. In cutaneous T-cell lymphoma the PREMATURE DEATH warning weighs most heavily here. Basal cell carcinoma's UP-TO-50% second-primary rate makes annual full-skin examination non-negotiable. |
| The cross-cutting rule | IMMUNOSUPPRESSION MOVES EVERY ANSWER THE SAME WAY: more disease, more aggressive disease, a LOWER THRESHOLD for biopsy and for Mohs, and EARLIER referral. |