Clinical Medicine and Surgery I · Exam 1 — Study Guide

Also tested

• Sensitivity. It is related to fewer false-negatives and does not address false-positives.
• Highly sensitive test. A negative result is most useful for ruling the disease out in that patient (SnNout: high Sensitivity and a Negative result help rule out a disease).
• False-positives in human immunodeficiency virus (HIV) screening. A few are acceptable because they can be corrected by later confirmatory testing, whereas a missed case may unknowingly infect others.

Also tested

• Posttest probability. Posttest probability is the likelihood after the result is known, the pretest likelihood revised by the test's sensitivity and specificity; with identical tests, different pretest probabilities give different posttest probabilities.
• Pretest versus posttest probability. Pretest probability is estimated from signs, symptoms, history and frequency; posttest probability additionally reflects the test result.

Also tested

• VINDICATE mnemonic. A category-based differential framework: vascular, infectious, neoplastic, degenerative, iatrogenic, congenital, autoimmune, trauma, and endocrine or metabolic.
• Common things occur commonly. Bet on uncommon manifestations of common conditions rather than common manifestations of uncommon conditions: when you hear hoof beats, think horses, not zebras. An unusual presentation of a common condition is more probable than a textbook presentation of a rare one.
• Clinical guideline. A clinical guideline following an if-then rule, for example: if a patient is febrile and neutropenic, then use broad-spectrum antibiotics.
• Three questions a clinician must answer. What disease is present, should testing be done, and should this patient be treated. Which clinician should take over the patient's care is not among them.
• Clinical decision making. Setting the sensitivity and specificity of the tests available is not part of it; these are fixed properties of a test, not decisions a clinician makes at the bedside.
• Clinical guideline caution. Guidelines are straightforward and easy to use but should be applied to patients with similar characteristics to those studied.
• Clinical reasoning first steps. Gather initial patient information, then organize and interpret it, then synthesize it into a problem representation, before hypotheses are generated and tested.
• Good clinical decision-making. Remember you are often wrong, and consider the immediate implications; also slow down, weigh base rates, consider what data is truly relevant, and seek alternatives.

Also tested

• Naturalistic (event-driven) approach. It is characterized by treating signs and symptoms before a definitive diagnosis is reached.
• Naturalistic approach. It suits unstable patients and atypical presentations, along with ruling out the worst-case scenario and following responses to interventions.

Also tested

• Treating despite diagnostic uncertainty. The value of treatment versus no treatment is a linear function of the probability of disease, together with the likelihood of success and the ability to tolerate treatment, weighed as risk against benefit.

Also tested

• Tzanck smear. It gives rapid evaluation of vesicular lesions for herpesvirus cytologic changes. Polymerase chain reaction is preferred for confirmation: the smear is fast, the polymerase chain reaction is definitive.
• Barriers to treatment and medication adherence. Cost and affordability of medications or services, low health literacy or lack of understanding, and cultural or religious considerations.
• Barriers to treatment and medication adherence. Mental health challenges or cognitive impairment are listed among the barriers, alongside cost, low health literacy, cultural or religious beliefs, fear of side effects, transportation and poor follow-up.
• FRAMES elements. Responsibility of the patient is the element that places the decision to change with the patient; FRAMES also includes feedback, advice, a menu of options, an empathetic style and promoting self-efficacy.

Also tested

• Resistant dermatophytosis. Suspect it when disease is widespread, intensely inflammatory, epidemiologically linked, or refractory to an adequate terbinafine course; obtain species identification and susceptibility testing when available.
• Severe or extensive allergic contact dermatitis. Treat with high-dose oral corticosteroids tapered over two to three weeks, because early discontinuation causes high rates of rebound; limited eruptions can be managed with high-potency topical steroids.
• Urushiol lesions. They are intensely pruritic vesicular lesions in linear distributions, erupting within 4 to 96 hours and persisting up to 3 weeks; the linear pattern comes from grazing the plant in passing.
• Seborrheic dermatitis treatment. The mainstay is topical antifungals such as ketoconazole, with steroids used early to reduce inflammation; scalp disease uses ketoconazole or selenium sulfide shampoo, and facial disease uses ketoconazole cream or lotion.
• Stasis dermatitis priorities. The two primary clinical priorities are distinguishing it from cellulitis, and determining whether compression therapy can be used safely.
• Irritant versus candidal diaper rash. Fold involvement separates them: irritant disease affects convex surfaces and generally spares the inguinal folds, while candidal disease gives beefy erythema in the folds with satellite papules and pustules.
• Tinea corporis versus nummular eczema. Both are red or pink itchy circular patches. Tinea corporis is a fungal infection that is annular and clears centrally; nummular eczema is non-infectious and coin-shaped without central clearing.
• Stasis dermatitis red flag. Acute unilateral swelling or pain should raise concern for deep venous thrombosis, particularly when it is a new unilateral change on chronic bilateral changes.
• Atopic dermatitis diagnosis. Diagnosis is usually clinical, supported by family history, personal history of atopy and recurrent rash. Immunoglobulin E may be elevated but is not routinely tested, and routine laboratory testing is not required.
• Irritant reaction timing. Mild irritants such as soaps may cause subacute symptoms progressing over weeks; alkalis and acids may present minutes after exposure or delayed up to 24 hours or more. Concentrated agents can cause chemical burns and necrosis.
• Perioral dermatitis versus acne vulgaris. Open or closed comedones point to acne vulgaris; perioral dermatitis produces grouped monomorphic papules, papulovesicles or papulopustules without comedones.
• Emollient use in atopic dermatitis. Apply emollient to the skin after rinsing, avoid irritants, and keep skin care fragrance-free. Clinicians should also demonstrate medication quantity and correct application.
• Toxicodendron (urushiol) dermatitis. Urushiol sap produces intensely pruritic vesicular lesions in linear distributions. Lesions erupt within 4 to 96 hours and may appear in multiple stages.
• Contact dermatitis pattern. It is often distinguishable from other dermatologic conditions by its clearly demarcated, unnatural patterns, tracing the shape of whatever touched the skin rather than a biological distribution.
• Contact dermatitis versus cellulitis. Contact dermatitis is itchy with vesicles and no fever, whereas cellulitis is tender and warm rather than itchy.
• Atopic dermatitis epidemiology. About 20% of children worldwide are affected, and it is more common in males. It often begins in infancy or childhood; adult-onset disease occurs but is rare.
• Allergic contact dermatitis cause. The most common cause is urushiol sap from Toxicodendron species, and approximately 50 to 75% of people in the United States react to it, which explains why not everyone who contacts poison ivy, sumac or oak reacts.
• Xerosis. It reflects impaired stratum-corneum hydration, promoted by aging, low humidity, hot water, detergents, atopy and systemic disease. It commonly affects older adults, especially in winter, causing tightness, pruritus, rough scale, fissuring or eczema.
• Nummular eczema plaques. They are intensely pruritic, round coin-shaped, light pink, scaly, thin plaques 1 to 10 cm, uniform without central clearing, most commonly on the extremities though they can occur on the trunk.
• Atopic dermatitis education. Apply emollient after rinsing, avoid irritants, use fragrance-free skincare, demonstrate quantity and application, and give a written flare and infection action plan. Corticosteroid concerns are addressed directly rather than avoided.
• Extensive allergic contact dermatitis. When the eruption is extensive rather than limited, high-dose oral corticosteroids replace the high-potency topical steroid used for limited disease. Soothing measures such as oatmeal baths and cool compresses are used throughout.
• Atopic dermatitis prognosis. The disease is chronic and relapsing, but many patients improve with age; it may improve, persist or recur.
• Irritant contact dermatitis timing. Mild irritants such as soaps may progress over weeks, while alkalis and acids may present within minutes or be delayed up to 24 hours or more. The agent determines the tempo.
• Counseling for atopic dermatitis steroid worries. Address the concern directly, review the side effects, demonstrate how much to apply, and provide a written flare and infection action plan.
• Chronic hand dermatitis from detergent exposure. Avoid the exposure and repair the barrier with emollients, sleeping in cotton gloves after applying a heavy emollient such as petroleum jelly, with antihistamines such as hydroxyzine or diphenhydramine for itch.
• Stasis dermatitis with acute leg swelling. Acute unilateral swelling or pain should raise concern for deep venous thrombosis, so order venous duplex ultrasonography to evaluate for it.
• Childhood atopic dermatitis treatment. A flexural distribution (antecubital and popliteal fossae) with family atopy history is classic. Initial treatment is topical hydrocortisone with regular emollient use: a low-potency steroid plus barrier repair is first line.
• Allergic contact dermatitis to adhesives. A rash that reproduces the shape of the object is the hallmark. A rectangular rash sparing a central area reflects a reaction to the adhesive in the dressing, with the spared center corresponding to the cotton pad.
• Nickel allergy. Nickel is the most common metal allergen, and eruptions reproduce the shape of the item worn, such as under a necklace or beneath a jeans button.
• Greasy scaling of the scalp and face. Initial treatment is ketoconazole shampoo and topical ketoconazole cream. Topical antifungals are the mainstay because Malassezia overgrowth drives the condition; steroids may be added early to reduce inflammation.
• Recurrent greasy scaling of the scalp and nasolabial folds. The condition is chronic and relapsing, so repeated and long-term use of medication is often required.
• Culture in atopic dermatitis. Bacterial culture is indicated for purulent, pustular or significantly crusted lesions, such as weeping, thickly crusted plaques with pustules, to rule out infection.
• Infantile atopic dermatitis. Weeping inflammatory patches and crusted plaques on the cheeks, scalp, and extensor surfaces; rubbing commonly replaces scratching at this age. Roughly 80 percent of patients have a personal or family history of atopy.
• Allergic contact dermatitis. It is an immunologic cell-mediated, delayed, type IV hypersensitivity reaction, most often to urushiol, the sap of Toxicodendron species (poison ivy, sumac, oak); roughly 50 to 75 percent of people in the United States are allergic.
• Patch testing. It is the diagnostic test for atypical, adult-onset or treatment-resistant eczema, and eyelid and hand involvement raises contact allergy.
• Irritant contact dermatitis. The eyelids and face are among the commonest sites, from makeup and masks, with a glazed, well-demarcated appearance.

Also tested

• Prodromal bullous pemphigoid. Weeks of intense itching with pruritic urticarial or edematous lesions and no blisters may be the prodromal phase, which may precede bullae by weeks to months.
• Bullous pemphigoid diagnosis. Biopsy the lesion for histopathology and perilesional tissue for direct immunofluorescence. Serum indirect immunofluorescence or enzyme-linked immunosorbent assay can identify anti-basement membrane zone antibodies.
• Pemphigus mechanism. Autoantibodies to adhesion molecules cause loss of keratinocyte-to-keratinocyte adhesion, called acantholysis, producing intraepithelial blisters in a life-threatening blistering disorder of skin and mucous membranes.
• Light microscopy in bullous pemphigoid. Neutrophils are aligned in a straight narrow row at the dermal-epidermal junction. Biopsy a lesion for histopathology and perilesional tissue for direct immunofluorescence.
• Confirming bullous pemphigoid. Biopsy of perilesional tissue for direct immunofluorescence confirms the diagnosis. Lesional tissue goes for histopathology, with serum studies or ELISA identifying anti-basement membrane zone antibodies.
• Acantholysis. On biopsy of flaccid skin bullae with painful oral erosions, it is the defining histological feature: loss of keratinocyte-to-keratinocyte adhesion. Immunofluorescence and serum ELISA are confirmatory.
• Pemphigus treatment. Pemphigus is life-threatening, so treatment is urgent: rituximab or high-dose oral prednisone. A steroid-sparing agent is usually added so steroids can be tapered.
• Nikolsky sign. A positive sign is when the top layers of skin slip away or slough off from the lower layers when rubbed; it is positive in pemphigus and negative in bullous pemphigoid.

Also tested

• Psoriatic arthritis radiograph. The expected finding is a pencil-in-a-cup deformity; psoriatic arthritis is associated with HLA-B27 and affects the distal and proximal interphalangeal joints while sparing the metacarpophalangeals.
• Pityriasis rosea course. It is self-limited and typically fades over 4 to 6 weeks, though darker skin may show post-inflammatory hyperpigmentation for several months; reassurance is the mainstay, with antihistamines or topical steroids used cautiously for itch.
• Von Zumbusch pustular psoriasis. A rare, severe, abrupt and life-threatening form associated with other forms of psoriasis; it may follow systemic steroid withdrawal, begins with several days of fever, and is commonly mistaken for bacterial or viral infection.
• Impetigo herpetiformis. The psoriasis of pregnancy, typically in the third trimester, with erythematous patches whose margins are studded with subcorneal pustules. Onset brings fever, chills, malaise, diarrhea, nausea and arthralgia.
• Psoriasis heredity. About 8 percent of children are affected when one parent has psoriasis and 41 percent when both do, reflecting a genetic predisposition in which PSORS1 is the major susceptibility locus.
• Pityriasis rosea management. It is self-limited, so reassurance is the mainstay, with oral antihistamines or topical steroids used cautiously for pruritus. Ultraviolet B phototherapy or sunlight helps if begun in the first week; severe cases may be treated with acyclovir.
• Lichen planus histology. Biopsy shows a band-like lymphocytic infiltrate in the dermis, plus hyperkeratosis without parakeratosis, basal layer vacuolisation, Civatte bodies in the lower epidermis and saw-tooth shaped rete ridges.
• Guttate psoriasis. It presents as raindrop-shaped erythematous papules and plaques in children, typically 2 to 3 weeks after a streptococcal infection or upper respiratory infection. It often needs no treatment, though phototherapy and topical steroids may be used.
• Lichen planus histology. A biopsy shows a band-like infiltration of lymphocytes in the dermis, a classic descriptive phrase worth recognizing on sight.
• Herald patch. It is a single 2 to 5 cm round or oval, sharply demarcated pink or salmon plaque on the chest, neck or back, occurring in 50 to 90% of cases. It precedes the general eruption by one to two weeks.
• Lichenoid drug reactions. Nonsteroidal anti-inflammatory drugs, sulfonamides, tetracyclines, hydrochlorothiazide, quinidine and some beta blockers can produce them. Ask about these, since the eruption can mimic idiopathic lichen planus.
• Von Zumbusch pustular psoriasis. Onset is abrupt and life-threatening: several days of fever, then generalized 2 to 3 mm pustules over trunk and extremities, including nail beds, palms and soles, that may form lakes of pus. It may follow systemic steroid withdrawal.
• Lichen planus biopsy. The confirming finding is a band-like infiltration of lymphocytes in the dermis, with hyperkeratosis without parakeratosis, basal vacuolization, Civatte bodies and a saw-tooth rete ridge.
• Lichen planus counseling. Genital and erosive oral disease carry an increased risk of squamous cell carcinoma, so ongoing surveillance is needed. This is why mucosal involvement must be identified and followed.
• Lichenoid eruption after a new medication. Review the medication list, since several drugs produce lichenoid reactions: nonsteroidal anti-inflammatory drugs, sulfonamides, tetracyclines, hydrochlorothiazide, quinidine and some beta blockers.
• Oval scaly plaque followed by smaller oval lesions down the trunk. Diagnosis is clinical, based on the herald patch and the typical pattern. The herald patch and cleavage-line distribution are enough.
• Guttate psoriasis. No specific treatment is required, though phototherapy or topical steroids may be used. It often needs no treatment.
• Diagnosing psoriasis. It is generally a clinical diagnosis, though skin biopsy may be needed for definitive diagnosis, for example when the picture is not clear-cut and treatment has failed.
• Four Ps of lichen planus. Pruritic, purple, polygonal, papules or plaques: flat-topped, pink to violaceous and shiny, coalescing into larger plaques.

Also tested

• Male-pattern hair loss. Dihydrotestosterone is the androgen chiefly responsible; it is an androgen-dependent trait with a strong paternal influence on risk.
• Minoxidil. It is primarily effective in the crown region of the scalp; it prevents further loss and may produce regrowth, working best with finasteride.
• Scalp biopsy in alopecia. It is performed when scarring alopecia, diffuse atypical loss or persistent diagnostic uncertainty remains after clinical and dermoscopic assessment.
• Finasteride. It is an oral 5-alpha-reductase type 2 inhibitor; about 2% of men report reduced libido and erectile function, reversible on stopping. It works best combined with minoxidil, is not indicated in women and is contraindicated in pregnancy.
• Supportive care in alopecia areata. Psychological support, with support groups offered, is one of the most important considerations.
• Female-pattern hair loss treatment. Options are limited; oral antiandrogens such as combined oral contraceptives may be considered, and finasteride is not indicated in women.
• Female-pattern hair loss. It produces diffuse thinning of the central and parietal scalp without significant change to the frontal hairline, with increased frequency of balding among first-degree male relatives.
• Alopecia areata dermoscopy. Yellow dots, black dots, broken hairs, tapered hairs and short regrowth support the diagnosis. The diagnosis is clinical and dermoscopy strengthens it.
• Alopecia areata extent. Alopecia totalis describes loss of all scalp hair, and alopecia universalis describes loss of all body hair.
• Alopecia areata counseling. Psychological support is one of the most important considerations in managing this condition, and support groups may be offered.
• Non-scarring patchy hair loss with exclamation point hairs and nail pitting, in children. Topical corticosteroids are first line in children 10 years old and younger, avoiding the discomfort of intralesional injection in a young child.
• First-line treatment of alopecia areata by age. Topical steroids are first line in children ten and under; intralesional steroids are first line in adolescents and adults, since injections are avoided in young children.
• Alopecia areata treatment. Intralesional corticosteroids are first line in adolescents and adults; topical steroids are first line for children aged ten and under.

Also tested

• Biopsy of lichen simplex chronicus. Biopsy a plaque that is atypical, unilateral, nodular, ulcerated or treatment-resistant, to exclude neoplasia or another inflammatory disorder.
• Psoriasis comorbidities. Patients are at increased risk of cardiovascular events, type 2 diabetes mellitus, metabolic syndrome and lymphoma; psoriasis is a systemic inflammatory disease, not only a skin condition.
• Refractory bullous pemphigoid. When prednisone and doxycycline fail, immunosuppressives such as methotrexate and azathioprine are used, with biologics and intravenous immunoglobulin also used. Low-dose methotrexate is described as safe and effective in the elderly, with folic acid.
• Compression for stasis dermatitis. Consider an ankle-brachial index or toe pressure before starting substantial compression. Arterial status has to be clarified first, because compression on an ischemic limb causes harm.
• Dyshidrotic eczema hand care. Use lukewarm water and soap-free cleansers, dry thoroughly, then apply emollient immediately and as often as possible. Also avoid detergents, solvents, hair lotions or dyes, and acidic foods.
• Lichen simplex chronicus recurrence. Recurrence depends on whether the initiating itch is controlled; it is common if the itch is not controlled. Sleep, anxiety, neuropathic symptoms and the primary dermatosis all need addressing.
• Extensive or persistent perioral dermatitis. When it persists despite stopping the topical corticosteroid and simplifying the routine, treat with oral tetracycline or doxycycline.
• Reducing flares of recurrent palmar vesicles. Avoid irritants such as detergents, solvents and hair dyes, wash with lukewarm water and soap-free cleanser, dry hands thoroughly, and apply emollients immediately afterwards.
• Perioral dermatitis after stopping corticosteroid. The eruption may temporarily worsen after corticosteroid withdrawal before it improves. Telling the patient in advance stops her restarting the steroid.
• Topical retinoid counseling. Start gradually and expect irritation; the important considerations are irritation, dryness and photosensitivity, and pregnancy precautions apply.
• Before compression therapy. Perform an ankle-brachial index (or toe pressure) when peripheral arterial disease is suspected, such as with diminished pulses; compression is the cornerstone only once adequate arterial circulation is established.
• Papules and pustules around the mouth with topical corticosteroid use. Initial management is to discontinue the corticosteroid and simplify the skin-care routine. Topical corticosteroid exposure is the most important modifiable association, and continued use perpetuates the condition.
• Choosing a vehicle for barrier preparations. Ointments are more occlusive than creams (or lotions). Emollients and barrier preparations are foundational for many inflammatory conditions, including xerosis, eczema, irritant dermatitis and diaper dermatitis.

Also tested

• Highest-mortality epidermolysis bullosa subtype. Junctional epidermolysis bullosa, especially the Herlitz subtype, carries the highest mortality, so early palliative care integration is appropriate in severe Herlitz disease.
• Hyperhidrosis counseling. It is not about poor hygiene or anxiety; suggest moisture-wicking clothing, which reduces impairment, and set realistic expectations, including botulinum toxin retreatment every three to six months.
• Primary hyperhidrosis. It is a medical condition rather than a problem of hygiene or anxiety, with quality-of-life impairment comparable to severe psoriasis.
• Acanthosis nigricans counseling. It is a metabolic warning sign of insulin resistance rather than a hygiene problem, and losing even 5 to 10% of body weight improves the findings.
• Most common acanthosis nigricans. Hyperinsulinemia stimulates keratinocyte and fibroblast proliferation through insulin-like growth factor 1 receptor cross-activation; this insulin-resistant or benign form is the commonest, and malignant, drug-induced and endocrine forms make up the rest.
• Epidermolysis bullosa referrals. Referral is needed to essentially every specialty, given the multisystem burden; palliative care, genetics and family support are all involved.
• Fixed drug eruption versus erythema multiforme. Fixed drug eruption recurs at the same site, leaves residual hyperpigmentation, and has few lesions without three concentric zones; the three-zone target defines an erythema multiforme lesion.
• Granuloma annulare counseling. It is benign and self-limiting, with about half resolving within two years and no malignant potential, so treatment is for cosmesis or discomfort.
• Pyoderma gangrenosum. Despite its name, it is a neutrophilic dermatosis that is not infectious; dysregulated innate immune activation with neutrophil recruitment causes the tissue destruction.
• Pyoderma gangrenosum in inflammatory bowel disease. Infliximab at 5 mg/kg intravenously is the biologic of choice and is approved for pyoderma gangrenosum in inflammatory bowel disease.
• Ocular rosacea. Ocular rosacea with keratitis, visual symptoms or corneal involvement needs urgent ophthalmology referral for slit-lamp examination, since untreated disease risks corneal scarring.
• Rapidly expanding ulcer before treating as pyoderma gangrenosum. Malignancy and infection must be excluded because the diagnosis is one of exclusion and the immunosuppression used would worsen an infection.
• Granuloma annulare variants. The generalized or disseminated variant carries the strongest systemic associations: diabetes, thyroid disease, dyslipidemia and lymphoma. It is more common in adults over forty.
• Endoscopic thoracic sympathectomy risk. The principal risk is compensatory sweating elsewhere, occurring in over 30%. The procedure is permanent, so the trade-off must be discussed thoroughly beforehand.
• Urticaria mechanism. Mast cell degranulation releases histamine, prostaglandins and leukotrienes, causing transient dermal edema. Immunoglobulin E mediated immunologic triggers include shellfish, nuts, eggs, penicillin and insect stings.
• Velvety hyperpigmented plaques of the neck and axillae. Primary management is treating the underlying cause through weight loss and glycemic control, discontinuing any offending drug. Metformin reduces insulin resistance and may improve the skin findings.
• Ocular rosacea. Keratitis, visual symptoms or corneal involvement warrants urgent ophthalmology referral; visual symptoms and photophobia raise exactly those concerns.
• Epidermolysis bullosa and cancer. Dystrophic epidermolysis bullosa causes severe scarring and carries the greatest long-term squamous cell carcinoma risk, so its multidisciplinary team includes hematology and oncology for surveillance. Scarring subtypes carry the malignancy risk.
• Localized granuloma annulare. The localized variant (about 75 percent of cases) is asymptomatic, with flesh-colored to erythematous papules in an annular ring on the dorsal hands, feet and ankles. It is a benign, self-limiting granulomatous dermatosis.
• Rosacea triggers. Sun exposure is the most universal trigger, alongside heat, alcohol, spicy foods and stress. Chronic ultraviolet exposure is also a listed risk factor.
• Acne vulgaris epidemiology. It is the most common skin disease in the United States, affecting about 80% of Americans in their lifetime, and usually begins with the onset of puberty.
• Beremagene geperpavec. It is a topical gene therapy gel approved in 2023 for dystrophic epidermolysis bullosa, accessible through dermatology referral centers and gene therapy trials.
• Referrals in generalized granuloma annulare in older adults. Refer to oncology if lymphoma is suspected, alongside dermatology for phototherapy or systemic therapy and endocrine workup for diabetes or thyroid disease.
• Erythema nodosum. Histologically it is a septal panniculitis without vasculitis; it is the most common form of panniculitis, a delayed hypersensitivity reaction in subcutaneous fat.
• Localized granuloma annulare course. Half of cases resolve spontaneously within two years, so watchful waiting is reasonable. Treatment is primarily for cosmesis or discomfort, and there is no malignant potential.
• Most common epidermolysis bullosa. Epidermolysis bullosa simplex accounts for about 70% of cases, with intraepidermal cleavage, keratin 5 and 14 mutations, and autosomal dominant inheritance.
• Genetics of dermatitis herpetiformis. HLA-DQ2 and HLA-DQ8 are strongly associated, the same haplotypes that underlie celiac disease.
• Key diagnostic feature of urticaria. Individual lesions last less than twenty-four hours; lesions persisting beyond that suggest urticarial vasculitis.
• Erythema multiforme minor. It shows three-zone target lesions (dusky center, pale swollen ring, outer red halo) on acral surfaces after herpes simplex, with skin involvement only and no mucosal involvement.
• Botulinum toxin for axillary hyperhidrosis. It is effective for three to six months, so retreatment will be needed; setting that expectation is named in the patient education.
• Rosacea counseling. It is a chronic condition that therapy controls rather than eliminates, so long-term management and daily sun protection are expected, alongside a trigger diary and gentle non-irritating skincare.
• Severe Herlitz junctional epidermolysis bullosa. Early palliative care integration is appropriate, alongside genetics counseling and family support resources; goals-of-care discussion, pain optimization and psychosocial support are all indicated.
• Primary axillary hyperhidrosis not helped by aluminum chloride. Use glycopyrronium 2.4% cloth applied once daily, which is approved for axillary disease, or an oral anticholinergic as second line.
• Trigger testing for target lesions with oral erosions after cough and fever. Order Mycoplasma pneumoniae immunoglobulin M serology or polymerase chain reaction; elevated Mycoplasma immunoglobulin M is characteristic in children and atypical presentations.
• Biopsy in erythema multiforme. Negative direct immunofluorescence with interface dermatitis on histology supports the diagnosis; negativity distinguishes it from pemphigoid and pemphigus.
• Course of chronic urticaria. About half resolves spontaneously within a year, and over half of cases have no identifiable trigger, so the search for a cause often finds none.
• Angioedema without wheals. It should raise hereditary angioedema, and initial testing is complement C4 with C1-esterase inhibitor level and function.
• Episodic sweating with headache, palpitations and hypertension. This points to pheochromocytoma, and initial testing is twenty-four hour urine metanephrines and catecholamines.
• Pyoderma gangrenosum and debridement. The ulcer worsens with trauma, a phenomenon called pathergy, so debridement makes it larger; this is the single most consequential management point in the condition.
• Velvety, darkened, thickened skin at the neck and axillae. It is a visible marker of insulin resistance and warrants metabolic assessment: fasting glucose, hemoglobin A1c, fasting insulin and a lipid panel.
• Recessive dystrophic epidermolysis bullosa. Annual squamous cell carcinoma surveillance starts after the age of ten, because the severe scarring of dystrophic disease carries a substantial carcinoma risk.
• Malignant acanthosis nigricans. Rapid onset, extensive velvety hyperpigmentation, mucosal change and tripe palms without obesity call for urgent evaluation for an underlying malignancy, particularly of the gastrointestinal tract.
• Erythema nodosum infectious triggers. The most common is Group A Streptococcus, alongside Yersinia, tuberculosis, coccidioidomycosis, histoplasmosis and hepatitis B and C.
• Dapsone for dermatitis herpetiformis. Check glucose-6-phosphate dehydrogenase status before the first dose, then monitor the blood count for hemolytic anemia and methemoglobinemia.
• Secondary versus primary hyperhidrosis. Generalized sweating, nocturnal sweating, or an asymmetric distribution should raise suspicion of secondary disease. Primary disease is bilateral, focal and absent during sleep.
• Generalized granuloma annulare in an adult over fifty. Screen for diabetes, thyroid disease and dyslipidemia, with age-appropriate malignancy screening. These associations include lymphoma.
• Urticaria versus erythema multiforme. Urticarial wheals are pruritic, migratory and blanch fully, with no fixed target lesions; wheals migrate and last under 24 hours. Fixity over days identifies erythema multiforme.
• Drugs causing acanthosis nigricans. Niacin, corticosteroids, oral contraceptives and protease inhibitors; drug-induced disease sits alongside the insulin-resistant and malignant forms.
• Erythematotelangiectatic rosacea. The most common subtype: persistent central facial erythema, flushing, and telangiectasias with sensitive, stinging skin, and specifically no papules or pustules.
• Generalized granuloma annulare screening. Fasting glucose and hemoglobin A1c screen for diabetes, alongside a lipid panel and thyroid studies for associated systemic disease.
• Epidermolysis bullosa diagnosis. Skin biopsy with transmission electron microscopy is the gold standard for the level of cleavage. Immunofluorescence antigen mapping localizes missing or reduced proteins; genetic testing is confirmatory and guides prognosis and family counseling.

Also tested

• Dermatitis herpetiformis distribution. The eruption is symmetric on the knees, elbows, buttocks and back, with intensely pruritic papules and vesicles that group in a herpetiform pattern.
• Löfgren syndrome. Erythema nodosum, bilateral hilar lymphadenopathy, fever and arthralgia form its recognized presentation, and it is referred to pulmonology or rheumatology.

Also tested

• Staphylococcal scalded skin syndrome. It spares the mucosa and is toxin-mediated, which separates it from Stevens-Johnson syndrome on the differential.
• Stevens-Johnson syndrome versus toxic epidermal necrolysis. They lie on one spectrum separated by body surface area involved: Stevens-Johnson syndrome has less than 10 percent detachment, toxic epidermal necrolysis more than 30 percent.
• Stevens-Johnson syndrome first step. Immediate withdrawal of the causative drug is the first step; earlier withdrawal is strongly associated with improved survival, and each day of delay worsens prognosis. Allopurinol is the most common trigger worldwide.
• Systemic complications of toxic epidermal necrolysis. Sepsis, acute respiratory distress syndrome, acute kidney injury, electrolyte imbalance, hypovolemia and gastrointestinal hemorrhage; survivors also face sicca syndrome, lung disease and psychological trauma.
• Level of care in Stevens-Johnson syndrome. Patients should be under intensive care or a burn unit, with dermatology involved. Nasogastric feeding is often needed because mucosal involvement prevents eating.
• First action in Stevens-Johnson syndrome. Discontinue the suspected drug and every other non-essential medication; earlier withdrawal is strongly associated with improved survival, and each day of delay worsens it.
• Pathognomonic test for Stevens-Johnson syndrome. Punch biopsy showing full-thickness epidermal necrosis with junctional separation is the pathognomonic finding.
• SCORTEN of 5 in toxic epidermal necrolysis. A score of five or above carries a predicted mortality near 90%, and palliative care is referred for an early goals-of-care discussion.
• SCORTEN in toxic epidermal necrolysis. Age, malignancy, heart rate, detachment, urea and bicarbonate each score; a SCORTEN of 6 indicates a predicted mortality of about 90%.
• Toxic epidermal necrolysis mortality. Mortality is up to 30 to 35%, predicted by the SCORTEN score calculated within 24 hours and repeated on day three.

Also tested

• Polymorphous light eruption presentation. Papules appear thirty minutes to hours after exposure on the décolletage, forearms and dorsal hands, sparing chronically exposed skin, resolving in seven to ten days without scarring and recurring each spring.
• Hardening in polymorphous light eruption. This is improvement through the summer as tolerance develops after repeated exposure; prophylactic narrowband ultraviolet B in spring is the most effective preventive strategy.
• Sunburn management. Do not pop blisters, because intact blisters are protective; use cool rather than cold water.
• Polymorphous light eruption workup. An antinuclear antibody panel including anti-Ro and anti-La is described as mandatory before the diagnosis is accepted, because lupus can present identically and must be excluded.
• Demodex-associated papulopustular rosacea. Ivermectin 1 percent cream is described as superior to metronidazole, reflecting the contribution of Demodex folliculorum mite overgrowth to the pathogenesis.
• Tender pretibial nodules. A deep incisional biopsy, needed because the pathology lies in subcutaneous fat, shows septal panniculitis without vasculitis and Miescher's granulomas.
• Sunscreen use. Broad-spectrum sun protection factor 30 or above is advised for daily use and 50 or above for prolonged outdoor exposure, applied 15 minutes before sun exposure and reapplied every 2 hours.
• Blisters in second-degree sunburn. Do not pop them, because intact blisters are protective. Use cool compresses and early nonsteroidal anti-inflammatory drugs for pain.
• Antinuclear antibody in unclear facial erythema. It helps rule autoimmune disease out; a positive result only means more testing is needed, because many things make it positive and it cannot rule a condition in.
• Tanning beds. They are not safer at all than natural sun and are classified as Group 1 carcinogens; there is no safe level of tanning.
• Chronic urticaria escalation. If symptoms persist on a standard dose of a non-sedating antihistamine, increase up to four times the standard dose and consider adding an H2 blocker; omalizumab and ciclosporin follow if that fails.
• Photodermatitis versus seborrheic dermatitis. Photodermatitis spares the nasolabial folds, which seborrheic dermatitis involves, because shadowed areas are protected from light.
• Fitzpatrick types IV to VI. These patients are not immune to ultraviolet damage or skin cancer, and melanoma is frequently diagnosed at advanced stages; delayed diagnosis is common because of a lower index of suspicion.
• Sunscreen in photoaging. Daily broad-spectrum sunscreen of SPF 30 or higher, applied as the last skincare step, is the single most evidence-supported intervention; use about one teaspoon for face and neck.
• Severe blistering sunburn. Severe blistering above 20% of the body surface with systemic symptoms warrants hospitalization, with intravenous fluids and wound care given the systemic toxicity.
• Post-phytophotodermatitis pigmentation. It fades over months, and daily sunscreen prevents it darkening further. Reassurance is first line, with hydroquinone or azelaic acid if it persists.
• Initial workup of erythema nodosum without bowel or respiratory symptoms or drug exposure. Order antistreptolysin O titer, throat culture, chest radiograph and inflammatory markers, with tuberculin or interferon gamma testing and a pregnancy test where relevant.
• Drug therapy in toxic epidermal necrolysis. Cyclosporine at 3 to 5 mg/kg daily, started early, has the strongest current evidence of the available options; early initiation is preferred.
• Photoaging. Tretinoin is the only approved topical agent; expect initial irritation (retinoid dermatitis) over 6 to 12 months. It stimulates collagen synthesis, inhibits matrix metalloproteinase activity, and reduces fine lines and dyspigmentation.
• Photoallergy diagnosis. Photopatch testing with duplicate sets, one of which is irradiated, is the gold standard; a reaction only on the irradiated set confirms it.
• Photopatch test. The suspected photohaptens are applied in duplicate and one set is irradiated with ultraviolet A. A reaction only on the irradiated patch indicates photoallergy; a reaction on both indicates contact allergy.
• Löfgren syndrome. Erythema nodosum, bilateral ankle arthritis and hilar lymphadenopathy on chest radiograph indicate sarcoidosis presenting as Löfgren syndrome, which has the best prognosis of all sarcoidosis presentations, with over 90% spontaneous remission.
• Biologic for refractory chronic urticaria. Omalizumab, an anti-immunoglobulin E antibody given every four weeks, is approved for refractory chronic urticaria.
• Toxic epidermal necrolysis disposition. Admission to a burn unit or intensive care unit is mandatory for all cases, together with immediate discontinuation of all suspect drugs, fluid resuscitation estimated as for major burns, and non-adhesive biological dressings.
• Topical azelaic acid in rosacea. At 15 to 20%, it is anti-inflammatory and anti-keratinizing, and is effective for both papulopustular and erythematotelangiectatic rosacea.
• Classic causes of phototoxicity. Tetracyclines, fluoroquinolones, amiodarone and thiazides, alongside furosemide, voriconazole, some nonsteroidal anti-inflammatory drugs and psoralens.

Also tested

• Acne pointing to polycystic ovarian syndrome. In a woman with persistent acne, hirsutism together with irregular or absent menses points toward polycystic ovarian syndrome, indicating androgen hypersecretion.
• Acne mechanica. Pressure on the skin occludes the pilosebaceous follicle; shoulder pads, orthopedic casts and helmets are the named examples.
• Acne vulgaris hallmark. The comedone, either open (blackhead) or closed (whitehead), defines acne, although acne is polymorphic.
• Acne scarring out of proportion. Suspect patient manipulation of the lesions through picking or squeezing; patients and families are educated about that risk.
• Tretinoin with benzoyl peroxide. Separate the two by at least three hours, because applying them together irritates the skin.
• Acne with inadequate response. After six to eight weeks of inadequate response, add an oral tetracycline, keeping benzoyl peroxide to limit resistance.
• Isotretinoin requirements. iPledge enrollment of the prescriber is required, with a one-month supply at a time; a pregnancy test is not needed for a man.
• Acne response time. Improvement takes four to six weeks, and the back and chest may take three to four months; clinical improvement is judged by new lesion count at six to eight weeks.
• First-line topical acne therapy. Topical retinoids (adapalene, tazarotene, tretinoin) are typical first line for comedonal and inflammatory acne; they are comedolytic, normalize hyperkeratinization and are generally the most effective for mild disease.
• Combination acne products against antibiotic resistance. BenzaClin (clindamycin with benzoyl peroxide) and Benzamycin (erythromycin with benzoyl peroxide); both pair a topical antibiotic with benzoyl peroxide.

Also tested

• Preventing hot tub folliculitis. Maintain continuous water filtration, monitor disinfectant levels and change the water often; showering after contact does not prevent the infection.
• Hot tub folliculitis course. It is usually self-limiting, clearing in two to ten days; ciprofloxacin is reserved for widespread or resistant cases.
• Hot tub folliculitis management. Reassure, since most cases clear in two to ten days, and use dilute acetic acid compresses: 3 tablespoons of 5% vinegar in a pint of water, for 20 minutes, two to four times daily.
• Recurrent folliculitis. Recurrent or recalcitrant folliculitis raises the Staphylococcus aureus carrier state, treated with mupirocin ointment to the nares. Nasal swabs of the patient and family members evaluate carriage.
• Pseudomonas folliculitis. It is usually self-limiting, and most cases resolve without specific treatment in 2 to 10 days. A wet dressing of 5 percent acetic acid for 20 minutes, 2 to 4 times daily, may relieve symptoms.
• Erythrasma sites. Most common on the inner thighs, crural region, scrotum, and between the fourth and fifth toes; less common in the axilla, under the breasts and intergluteal folds. It is usually asymptomatic and may be pruritic.
• Wood's lamp. A handheld diagnostic device emitting long-wave ultraviolet light to highlight subtle changes in skin, scalp and hair; it evaluates pigment changes in selected fungal or bacterial infections.
• Folliculitis sites. Small papules or pustules pierced by a central hair, commonly on the scalp, thighs, trunk, axilla and inguinal area.
• Hot tub folliculitis timing and distribution. Onset is eight hours to five days after exposure, on the trunk, extremities and buttocks, usually sparing the face, neck, soles and palms.
• Pseudofolliculitis barbae. This foreign-body reaction to hair in shaved areas is most common in Black males with tightly curled hair and keratin gene variations, and in anyone who shaves and has curlier hair.
• Carbuncle versus furuncle. A carbuncle is extremely painful and more often produces systemic symptoms: malaise, chills and fever.
• Hidradenitis suppurativa diagnosis. No test is required: it is a clinical diagnosis resting on lesions, distribution and recurrence. Biopsy is not usually required, though it shows follicular occlusion and apocrine gland destruction.
• Hidradenitis suppurativa steroids. Intralesional triamcinolone acetonide decreases the size of draining sinuses. Oral prednisone reduces inflammation and prevents future lesions.
• Endocarditis prophylaxis. Endocarditis prophylaxis before the procedure is named for at-risk patients in both furuncle and carbuncle management.
• Extensive hidradenitis suppurativa. When medical therapy has failed, wide excision of the affected areas gives the best chance of permanent cure. Large fluctuant cysts are meanwhile incised and drained.
• Recurrent folliculitis. Swab the nose for Staphylococcus aureus carriage and treat with mupirocin if positive; nasal mupirocin twice daily for five days addresses the carrier state.
• Spironolactone in hidradenitis suppurativa. It is an aldosterone antagonist that lowers androgens by inhibiting ovarian and adrenal androgen production; combination birth control pills are used similarly.
• Carbuncle. A deeper infection made of interconnecting furuncles in several follicles, with several loculated abscesses, superficial pustules, necrotic plugs and sieve-like draining openings.
• Hot tub folliculitis. Caused by Pseudomonas aeruginosa, a Gram-negative organism, from inadequately chlorinated water; named sources are whirlpools, hot tubs, water slides and physiotherapy pools.
• Folliculitis. Defined by inflammatory cells within the wall and ostia of the hair follicle, forming a follicular pustule; causes include infection, physical injury and chemical irritation.
• Furuncle. A deep-seated abscess of a hair follicle and the adjacent subcutaneous tissue; Staphylococcus aureus is the commonest organism.

Also tested

• Cultures in impetigo. Obtain cultures when the patient is at high risk for methicillin-resistant Staphylococcus aureus (for example a health-care worker or teacher) or when post-streptococcal glomerulonephritis is present.
• Erysipelas work-up. In a classic presentation it is a clinical diagnosis. Leukocytosis and raised erythrocyte sedimentation rate and C-reactive protein are common, but blood and tissue cultures are not cost effective (extremely low yield) and imaging is not indicated.
• Cellulitis examination. All four cardinal signs of inflammation are present, most often on one lower leg, with borders neither raised nor demarcated. Bilateral disease almost never occurs.
• Non-bullous impetigo. A macule evolves into a vesicle or pustule that ruptures, leaving a honey-colored adherent crust, typically on the face and extremities, with regional lymphadenopathy common.
• Cellulitis portals of entry. Named portals are tinea pedis, open lesion, trauma, surgical wound, insect bite, fissure and radiation therapy. These are distinct from the risk factors, which include diabetes and lymphedema.
• Erysipelas laboratory findings. Leukocytosis with raised erythrocyte sedimentation rate and C-reactive protein are common but not diagnostic; the diagnosis remains clinical in a classic presentation.
• Tinea pedis and erysipelas. Tinea pedis is a named risk factor for erysipelas, serving as the portal of entry and predicting recurrence, so treat it.
• Cellulitis treatment failure. Fever persisting beyond forty-eight hours of antibiotics is the stated trigger to change the antimicrobial therapy, guided by the culture results.
• Abscess versus furuncle. An abscess arises from traumatic inoculation of bacteria into the skin, whereas a furuncle arises from an infected hair follicle.
• Erysipelas risk factor. Impaired lymphatic drainage, such as after axillary node clearance, is the first risk factor named for erysipelas and explains recurrence.
• Cellulitis. It involves the deeper dermis and subcutaneous tissue, from Group A streptococci or Staphylococcus aureus; it may be purulent or non-purulent, which changes the antibiotic choice.
• Non-purulent cellulitis on oral antibiotics. Fever that persists beyond 48 hours should prompt a change in antimicrobial therapy guided by culture results; with antibiotics fever usually resolves in 24 hours.
• Culture in impetigo. Obtain a culture rather than relying on appearance alone if the patient is at high risk for methicillin-resistant Staphylococcus aureus infection, such as a healthcare worker or teacher, or if acute post-streptococcal glomerulonephritis is present.
• Devitalized tissue in cellulitis. Tense, cyanotic, necrotic, bronzed, blanched tissue is devitalized and will not be perfused, so antibiotics cannot reach it; surgical debridement is required.
• Cellulitis course on antibiotics. It may look worse on day one, fever usually resolves within twenty-four hours, and inflammation clears over one to two weeks; fever beyond forty-eight hours prompts a change guided by culture.
• Cellulitis. Warm, tender erythema whose border fades out rather than stopping; the infection is deeper.

Also tested

• Laboratory studies in necrotizing fasciitis. Send complete blood count with differential, chemistry, arterial blood gas, urinalysis, and blood and tissue cultures, but they must not delay surgical intervention, because it is a surgical emergency with high mortality.
• Testing in acute paronychia. It is usually a clinical diagnosis, so testing is directed rather than routine: Gram stain and culture for the bacterial cause, potassium hydroxide for candida, and Tzanck smear for herpetic whitlow.
• Testing in classic erysipelas. No laboratory or imaging studies are routine; the diagnosis is clinical and blood and tissue cultures have very low yield. Leukocytosis and raised inflammatory markers are common but not diagnostic.
• Necrotizing fasciitis microbiology. It is polymicrobial, with aerobic, anaerobic or mixed flora, and group A streptococci (Streptococcus pyogenes) are common.
• Nail fold vesicles. A Tzanck smear rules out herpetic whitlow. Potassium hydroxide rules out candida and Gram stain identifies bacteria.
• Necrotizing fasciitis admission. Admit to a surgical intensive care unit, ideally a burn or trauma center; a team approach with consultations is required, not optional.
• Chronic paronychia. An inflammatory reaction of the proximal nail fold to irritants and allergens, with Candida albicans commonest; at risk are diabetics, laundry workers, cleaners, cooks, bartenders, dishwashers and swimmers.
• Chronic paronychia treatment. Keep the hands dry and use a broad-spectrum topical antifungal, with oral fluconazole in severe cases, treating the underlying inflammation and infection together.
• Necrotizing fasciitis care. Requires aggressive surgical debridement, broad antibiotic cover of aerobic Gram-positive and Gram-negative organisms and anaerobes, and surgical intensive care admission with a team approach.
• Acute paronychia. A red, swollen, acutely tender nail fold, with the nail plate itself still normal.

Also tested

• Preventing erythrasma recurrence. Keep the area clean and dry, avoid excessive heat and moisture, and maintain a healthy body weight, alongside good general hygiene.
• Specimens in serious cellulitis. Take blood cultures and a skin punch biopsy, alongside a complete blood count and creatine phosphokinase, with imaging considered for underlying fasciitis or osteomyelitis.
• Cellulitis without diagnostic workup. It can be managed this way when involvement is limited, pain is minimal, there are no systemic signs and no risk factor for serious illness; serious infections warrant blood cultures, punch biopsy, blood count and creatine phosphokinase.
• Cellulitis work-up. Cellulitis is usually a clinical diagnosis; no work-up is needed with a limited area of involvement, minimal pain, no systemic signs, and no risk factor for serious illness such as extremes of age or immunocompromise.
• Erysipelas organism and drug. Group A streptococcus (Streptococcus pyogenes) is the most common organism, involving the upper dermis and superficial lymphatics. Penicillin V is the drug, with clindamycin if penicillin allergic; tinea pedis is a risk factor.
• Topical therapy for impetigo. For a single or limited number of non-bullous lesions, mupirocin ointment is adequate for most cases and as effective as oral therapy with fewer side effects. Remove crusts before applying it.
• Resistant folliculitis testing. A potassium hydroxide wet mount of a plucked hair rules out fungal (dermatophyte) folliculitis. Culture and Gram stain from an unroofed pustule are also performed.
• Bullous impetigo differential. It includes thermal burn, allergic contact dermatitis, and herpes simplex or zoster; non-bullous impetigo has a different differential list.
• Impetigo portal of entry. The primary portal is minor superficial breaks in the skin such as cuts and bug bites, though no predisposing lesion is identified in most patients.
• Impetigo isolation. A child may return once treatment has been underway for twenty-four to forty-eight hours. Towels, clothing, bath water, washcloths and razors must not be shared.
• Folliculitis not clearing on topical treatment. This is now a resistant case: unroof a pustule for Gram stain and culture. Culture, potassium hydroxide mount, nasal swab and biopsy are all available.
• Excluding fungal folliculitis. A potassium hydroxide wet mount using a plucked hair is the specific test named for dermatophyte folliculitis.
• Topical tretinoin in pseudofolliculitis barbae. It relieves the hyperkeratosis, removing the epidermis the emerging hair embeds in. Mild corticosteroids reduce inflammation and topical antibiotics reduce colonization.
• Impetigo in high-risk occupations. Teachers and health-care workers are at high risk for methicillin-resistant Staphylococcus aureus, so their impetigo is cultured rather than diagnosed on appearance alone.
• Diagnosis of classic erysipelas. No routine testing is needed, since blood and tissue cultures have extremely low yield. Leukocytosis and raised inflammatory markers are common but not diagnostic.
• Early acute paronychia. With erythema and tenderness but no fluctuance, treat with warm water soaks for twenty minutes three times daily; incision and drainage is reserved for severe cases with purulent collection.
• Oral agents for methicillin-resistant Staphylococcus aureus skin infection. Trimethoprim-sulfamethoxazole, clindamycin and doxycycline recur as the core options, with linezolid added in particular settings; fluoroquinolones such as ciprofloxacin are not reliable against it.
• Shaving with pseudofolliculitis barbae. Avoid lift-and-cut razors and use a single blade (at most double) at a mild angle, because lift-and-cut systems cut the hair below the skin surface where it can re-enter the follicular wall.
• Spontaneously draining abscess. Give warm soaks and broad-spectrum antibiotic cover that considers methicillin-resistant Staphylococcus aureus, then adjust to the culture result.
• Acute paronychia treatment. Warm soaks for twenty minutes three times daily in mild cases; incision and drainage in severe cases, with oral antibiotics and cultures to rule out resistant organisms where appropriate.
• Pseudofolliculitis barbae shaving advice. Use a single or double blade at a mild angle, avoid lift-and-cut systems, and keep razors clean; chemical depilatories and laser hair removal are alternatives.
• Secondary bacterial infection. A secondary bacterial infection can develop within skin already affected by acne, arising in skin damaged by an existing condition.
• Impetigo. A superficial epidermal infection, most often Staphylococcus aureus or Streptococcus pyogenes; it is very contagious and autoinoculable, and common in infants and children.

Also tested

• Counseling during scabies treatment. Excessive washing with harsh soap can worsen skin irritation and should be stopped; the permethrin course itself is what treats the infestation.
• Facility-associated scabies. It is a particular concern because residents are elderly and immunosuppressed, and a hospital epidemic can follow their admission; it is difficult to eradicate once healthcare workers are infested.
• Body louse risk settings. Homelessness, displacement by war or disaster, and crowded conditions with poor hygiene predispose to infestation; the inability to wash or change clothes allows it to persist.
• Scabies in pregnancy. Pregnant patients are treated only where the diagnosis is documented; otherwise all infested persons in a family or group are treated.
• Cutaneous larva migrans, procedures to avoid. Surgical excision and cryotherapy are specifically not recommended. Topical therapy is also described as less effective than oral.
• Hookworm folliculitis. It may need repeated treatments, so repeat the course if pustules persist; the folliculitic form is specifically noted to be more resistant.
• Persistent post-scabietic papules. They are a recognized complication and are treated with a mid to high potency topical corticosteroid, or intralesional triamcinolone acetonide.
• Scabies contacts in pregnancy. Pregnant patients are treated only where scabies is documented, so an asymptomatic pregnant contact with no lesions has treatment withheld.
• Recurrent head lice. Use a multimodal approach combining physical methods with adjuvant chemical therapy, because of increasing resistance.
• Head lice and school. After treatment a child can return to school now; a no-nit policy is not recommended because of the school absence it causes, a position from the American Academy of Pediatrics.
• Body louse infestation. Typically found in homeless people, refugees, war victims and those in crowded conditions, persisting via unwashed clothing; transmission is through contaminated clothing and bedding.
• Scabies recovery. Most patients feel relief in about three days, though rash and itch may last up to four weeks; triamcinolone can be used for the residual itch.
• Pubic lice. Screen for concurrent sexually transmitted infection, since pubic lice often coexist with one. Slate-gray to bluish macules are maculae caerulae, representing hemorrhage at feeding sites.
• Head lice. Most affect children between three and twelve years, spread primarily by direct head-to-head contact; indirect spread through combs, brushes, bedding and headgear is less common.
• Multimodal head lice treatment. It is warranted because resistance is rising; the World Health Organization recommends that pediculicidal testing be read 24 hours after application.
• Nits versus dandruff. Nits cannot be removed from the hair shaft. Live lice indicate active infestation while nits indicate past or present infestation; viable eggs are tan to brown and hatched remains are clear, white or light.
• Physical methods for head lice. Head shaving, or combing nits out after two minutes of hair moisturizer every few days; effective but slow and painful. They need adjuvant therapy alongside them.
• Multimodal approach to pediculosis. Recommended because of increasing resistance. Pediculicidal effect is read twenty-four hours after application, the World Health Organization recommendation.
• Differential of scabies. Atopic dermatitis, body and pubic lice, other arthropod bites, dermatitis herpetiformis, fungal infection and psoriasis; all can produce an intensely itchy eruption.
• Lice causing pediculosis. Pediculus humanus capitis affects the scalp, Pediculus humanus humanus the trunk, and Phthirus pubis pubic skin; the body louse is about 30% larger than the head louse.
• Scabies transmission and itch timing. Transmission is by close contact for 15 to 20 minutes, and also from the bedding or underclothing of an infested individual; itch appears 4 to 6 weeks after infestation, and many patients have no symptoms for up to 3 months.
• Burrow ink test for scabies. When scraping is difficult, blue or black ink is applied to a suspected lesion, looking for a zigzag line running across and away from the lesion.
• Scabies not cleared by individual therapy. The regimen is ivermectin every two weeks for two to three doses, with topical permethrin every three days to weekly, the same regimen used for hyperkeratotic or immunosuppressed disease.

Also tested

• Bedbug bites. The usual reaction is wheals and papules with a hemorrhagic punctum; a bullous reaction occurs particularly in sensitized patients.
• Hymenoptera sting anaphylaxis. Treat with subcutaneous or intramuscular epinephrine, emergency department transfer and supportive measures.
• Removing a honeybee sting. Scrape it off as fast as possible with a card edge or dull knife held parallel to the skin, because the barbed ovipositor stays impaled and continues to pump venom.
• Fire ants. The venom induces mast cell degranulation, and the ants usually attack in groups. Flushing, pruritus, hives, abdominal pain, nausea, vomiting and diarrhea can follow.
• Caterpillar skin disease. Mechanisms are mechanical irritation by pointed hairs, toxin injection through hollow hairs, and hypersensitivity to hairs; the aggregate of these effects is called lepidopterism.
• Bedbug infestation. Diagnosis is by physical examination. Management is symptomatic, with a professional exterminator required: topical antiseptic or antibiotic for secondary infection, and steroids or antihistamines for itch.
• Tungiasis complication. A severe local complication is autoamputation of toes, alongside pain and pruritus at the affected sites.
• How bedbugs spread. They spread in the clothing and baggage of travelers and visitors, and in second-hand mattresses and laundry; infestation is not a marker of poor hygiene.
• Anaphylactic reaction to a sting. Give epinephrine intramuscularly or subcutaneously, with emergency transfer and supportive measures; this is an anaphylactic reaction rather than a severe local one.
• Avoiding tungiasis. Do not walk barefoot or in sandals on beaches, and do not sit directly on the sand. Nigeria, the Caribbean, India and Brazil are the named endemic settings.
• Severe asp caterpillar sting pain. Options are oral or parenteral narcotic analgesia, with antivenom for certain categories, alongside antihistamines, menthol or camphor, and corticosteroids.
• After sting-induced anaphylaxis. Carry an epinephrine auto-injector, and be referred for desensitization therapy where the skin test is positive; immunotherapy is specified for fire ant hypersensitivity.
• Tungiasis management. Surgical excision or cryotherapy and topical agents, with tetanus prophylaxis and systemic antibiotics; prevention centers on avoiding walking barefoot in endemic areas.
• Most poisonous caterpillar. The asp or puss caterpillar produces an intensely painful sting and train-track purpura. The gypsy moth caterpillar causes erucism and processionary caterpillars cause anaphylaxis.
• Bedbugs. A professional exterminator is necessary; treatment of the bites themselves is symptomatic. Use topical antiseptic or antibiotic for secondary infection, and steroids or antihistamines for itch.
• Mild local reaction to a bee sting. Treat with cleaning, ice, and possibly injection of local anesthetic for pain control; management is graded to the severity of the reaction.

Also tested

• Cercarial dermatitis systemic features. Headaches, fever and lymphangitis can accompany it; pain and swelling peak at forty-eight to seventy-two hours.
• Cercarial dermatitis treatment. Treat symptomatically with antihistamines, oatmeal baths, antipruritic lotions, aspirin for pain and topical or oral glucocorticoids; proper washing and hygiene are also advised.
• Pathology of cutaneous larva migrans. Larvae are 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.
• Diagnosing cutaneous larva migrans. It is diagnosed clinically on the presence of the serpentine rash; if biopsy is done, histology shows larvae with an eosinophilic infiltrate.
• Testing uncertain larva migrans. When the diagnosis is uncertain and follicular pustules are present, light microscopy with mineral oil shows live and dead larvae in folliculitis; the serpentine rash alone is enough for a clinical diagnosis.
• Preventing swimmer's itch. Wash and dry the skin properly after leaving the water. When the eruption occurs, treatment is symptomatic.
• Cercarial dermatitis epidemiology. Particularly affects the Great Lakes region, and paddy workers and rice farmers of the Far East; all share exposure to cercaria-infested water.
• Cercarial dermatitis. Also called swimmer's itch or clam digger's itch, it results from skin penetration by cercarial forms of parasitic flatworms; snails complete the cycle after eggs passed by host animals such as waterfowl and muskrats hatch and infect them.
• Cutaneous larva migrans lesion. An erythematous, raised, vesicular, linear or serpentine trail advancing 2 to 3 cm each day. It is intensely pruritic and painful, lasting two to eight weeks, with rare systemic symptoms.

Also tested

• Tarantula hair in the eye. It needs urgent ophthalmology referral, since embedded hairs can cause corneal granuloma; topical corticosteroid addresses only the cutaneous reaction.
• Black widow bite. The very old, the very young and those with cardiovascular disease are at increased risk and are hospitalized. Treat with calcium gluconate, narcotic analgesia, muscle relaxants and benzodiazepines; tetanus vaccination must be up to date.
• Tarantula disease. Shed hairs embed in skin or eyes, causing pruritus, granulomas or conjunctivitis. Symptoms are generally mild and local; treat with topical steroid and refer eye involvement to ophthalmology.
• Hobo spider bite. Headaches may persist for about a week and symptoms are managed supportively; death from severe systemic effects, including aplastic anemia, is rare.
• Hobo spider bite prognosis. Wounds heal within several weeks and headaches may last a week; treatment is supportive. Death from severe systemic effects, including aplastic anemia, is rare.
• Black widow bite, first thirty minutes. Localized erythema, piloerection and sweating around the bite, then crampy abdominal pain and muscle spasm. Headache, paresthesia, nausea, vomiting, hypertension and seizures may follow.
• Brown recluse spider. Identified by a dark fiddle or violin marking on the cephalothorax; abundant in the American Midwest and Southeast. It is non-aggressive and shelters in closets, attics and stored bedding.
• Hobo spider bite presentation. A painless bite with induration and paresthesia within thirty minutes, a large red area, and vesicles within thirty-six hours. Eschar may follow; systemic symptoms include headache, nausea and memory impairment.
• Brown recluse bite timeline. Systemic symptoms develop one to two days after the bite and necrosis at two to three days. Eschar forms between days five and seven, then deep ulcers.
• Southern black widow spider. It is identified by a red hourglass on the underside of the abdomen, and its venom contains the neurotoxin alpha-latrotoxin. Latrodectus mactans is found in all but the most northern part of the country.
• Hobo spider. It is found in the Pacific Northwest, where it is the predominant cause of necrotic arachnidism and is mistaken for the brown recluse; it is brown with a gray herringbone pattern and bites from July to September.
• Hobo spider. Also called the aggressive house spider, it is the predominant cause of necrotic arachnidism in the Pacific Northwest. The bite is painless, with induration and paresthesia within 30 minutes, a large erythematous area, and vesicles during the first 36 hours.

Also tested

• Rocky Mountain spotted fever. Rickettsia rickettsii, carried by dog ticks, wood ticks and rodents, causes it; risk is higher in males, adults 40 to 64, children under 10 and rural dwellers. It is prevalent in southeastern and south central states in spring and early summer.
• Rocky Mountain spotted fever laboratory findings. Thrombocytopenia with a normal white count is characteristic, and indirect immunofluorescence assay is the gold standard test. Cerebrospinal fluid may show leukocytosis, moderately elevated protein and normal glucose.
• Erythema migrans. Stage 1, early localized infection: a lesion greater than 5 cm that expands with central clearing and often a darker punctate center (bull's-eye). Diagnose and treat on that basis; testing helps most in non-endemic regions with non-diagnostic symptoms.
• Rocky Mountain spotted fever triad. Fever above 39.5 degrees Celsius, headache and rash, present in only about 60 percent of patients. Fever presents in the first 3 days, with rash following 2 to 4 days after fever onset.
• Stage 2, early disseminated Lyme disease. It occurs days to weeks later and involves skin, central nervous system, heart, musculoskeletal system and eyes, with cranial nerve palsies, meningitis, radiculopathies, arthralgias and stiff neck.
• Serologic testing for Lyme disease. It is most useful in patients who do not live in an endemic region and present with signs possibly consistent with it; a patient with erythema migrans is diagnosed and treated clinically.
• Laboratory findings in Rocky Mountain spotted fever. Cerebrospinal fluid shows leukocytosis with moderately raised protein and normal glucose; blood shows thrombocytopenia, anemia, mild hyponatremia and mild transaminitis with a normal white count and increased bands.
• Tick bite and Rocky Mountain spotted fever prevention. Prophylactic antibiotic therapy is not recommended; prevention rests on avoidance, clothing, tick checks and DEET. Patients should return if fever or headache develop.
• Rocky Mountain spotted fever in children. Treat with doxycycline at 2.2 mg per kilogram by mouth twice daily for five to ten days. It is used in children and pregnancy, with desensitization where contraindicated.
• Doxycycline for Rocky Mountain spotted fever in young children. It is still used, with a desensitization protocol available where it is contraindicated, because the risk of untreated disease outweighs the concern about tooth staining.
• Erythema migrans. A patient with the classic lesion is diagnosed and treated on clinical grounds without waiting for serology; testing is most useful outside endemic regions.
• Lyme testing outside endemic regions. Testing is most helpful in patients outside an endemic region with possibly consistent symptoms: enzyme-linked immunosorbent assay first, with Western blot more specific.
• Rocky Mountain spotted fever treatment. Doxycycline is used for adults, pregnant patients and children, with desensitization where it is contraindicated.
• Suspected Rocky Mountain spotted fever. Start doxycycline now without waiting for serology, since treatment should begin by day 5 and the indirect immunofluorescence assay is rarely diagnostic before day 7.
• Rocky Mountain spotted fever rash. It starts on the ankles and wrists and spreads centripetally over six to eighteen hours, involving palms and soles but sparing the face. Blanching macules or papules may become petechial and purpuric.
• Intravenous antibiotics in Lyme disease. Used for some cutaneous manifestations, acrodermatitis chronica atrophicans and arthritis. Ceftriaxone, cefotaxime or penicillin G are the agents named.
• Stage 3 (late persistent) Lyme disease. The classic manifestation is monoarticular or oligoarticular arthritis affecting the knee or weight-bearing joints. Subacute encephalopathy and acrodermatitis chronica atrophicans also occur.
• Oral antibiotics for Lyme disease. Doxycycline is first line, with amoxicillin as the alternative first line for early erythema migrans; macrolides such as azithromycin are second line.
• Attached tick. Remove the tick immediately, then watch for the rash and constitutional symptoms; antibiotics are indicated once the disease is diagnosed, at all stages.
• Rocky Mountain spotted fever without rash. It can present without a rash in about 20% of patients; the full triad is present in only about 60%, and the rash follows the fever.
• Preventing tick-borne illness. Avoid tick habitat, use DEET, PMD or picaridin reapplied about every two hours, and treat clothing with pyrethrins; there is no human vaccine, though one exists for dogs.

Also tested

• Ulceration versus erosion. Ulceration is full-thickness loss extending to the dermis or deeper, whereas an erosion loses only the epidermis; depth is the discriminator and determines whether the lesion can scar.
• Scaling. It is accumulation of loose or adherent cornified fragments of the epidermis, typically gray or white; lichenification is thickening and hardening of the skin.
• Household measures after head lice. Put clothing and bedding from the past week in the dryer or bag it for two weeks, wash combs and vacuum; fumigation is specifically not recommended.
• Ulceration versus erosion. Ulceration is full-thickness skin loss extending to the dermis or deeper, whereas erosion is partial loss of only the epidermis. Depth is the entire distinction.
• Bedbug behavior. Warmth and carbon dioxide draw them out to feed; by day they hide in cracks and crevices of headboards and picture frames, behind loose wallpaper and in other dark places.

Also tested

• Negative potassium hydroxide preparation. High clinical suspicion of tinea corporis with a negative preparation is an indication for fungal culture, as are refractory cases.
• Scaly patch of alopecia. Before a prolonged systemic antifungal course, confirm with potassium hydroxide microscopy and fungal culture when feasible.
• Testing round, scaly plaques. The initial test is a potassium hydroxide preparation, because tinea corporis is the main differential and is excluded by it; absent central clearing already argues against tinea corporis.
• Diaper rash with fold involvement. Fold involvement and satellite lesions suggest Candida; the test is a potassium hydroxide preparation, where budding yeast or pseudohyphae supports it.

Also tested

• Imidazole antifungals. They block ergosterol synthesis, as clotrimazole and ketoconazole do; ergosterol is a vital component of the fungal cell membrane, so blocking it halts growth and replication.
• Pustular beard eruption with firmly anchored hairs. Bacterial culture helps separate it from tinea barbae by ruling out bacterial folliculitis.
• Safety steps before systemic antifungals for tinea capitis. Review drug interactions and hepatic disease, and obtain baseline liver tests when indicated by the agent, its labeling, and patient risk; baseline testing is indication-driven, not automatic.
• Allylamine antifungals. They destroy the fungal cell membrane, which prevents growth and ultimately kills the fungus. Names end in -fine, such as terbinafine and naftifine.
• Tinea capitis and school. School exclusion is generally unnecessary once effective treatment has started. Avoid sharing personal hair items and clean clippers, combs, brushes, bedding and hats; household contacts may use a sporicidal shampoo.
• Allylamine class. Terbinafine is an allylamine, a class that destroys fungal cell membranes; members end in -fine (terbinafine, naftifine). Imidazoles instead block synthesis of ergosterol, a vital component of the fungal cell membrane.
• Tinea cruris. Commonly called jock itch, it is more common in men and often coexists with tinea pedis, which is why the coexisting foot infection must be treated too.
• Topical antifungal in tinea corporis. Localized disease is treated with topical terbinafine, butenafine or an azole applied to the lesion and 1 to 2 centimeters beyond its border, which covers the advancing edge.
• Vesiculobullous tinea pedis. It presents as a moist, acute, pruritic and painful vesicular or bullous eruption on underlying erythema, and is caused by Trichophyton species like the other two forms.
• Tinea pedis patient education. Drying between the toes after bathing is essential. Also advise antifungal foot powder for shoes, open-toed sandals when possible, sandals in community showers, and changing socks frequently.
• Tinea capitis and shared items. Fungal particles remain viable for months, so hair-care items must not be shared and should be cleaned.
• Tinea barbae management. Use oral antifungal therapy with griseofulvin or terbinafine, plus shaving or hair removal and warm compresses to remove crusts, because topicals do not penetrate the follicle.
• Tinea capitis treatment. It requires oral therapy, because topical agents alone do not penetrate the infected hair shaft; antifungal shampoo reduces viable spore shedding but does not replace oral treatment.
• Tinea corporis (ringworm). Progressive central clearing produces the annular outline. The lesion is a circular, sharply circumscribed, slightly erythematous, dry scaly patch or plaque.
• Recurrent tinea pedis with thickened discolored toenails. Consider oral therapy, treat the coexisting onychomycosis, and reinforce moisture control. An untreated nail reservoir drives recurrence.
• Tinea of the hand with foot scaling. A thickened, dry, scaly palm with interdigital foot scaling is two feet–one hand syndrome, in which the hand used to scratch the foot becomes affected. Patients often blame dry skin or manual labor.
• Tinea manuum. On the dorsum of the hand it shows an annular plaque like tinea corporis; the palm is hyperkeratotic like tinea pedis (thickened, dry and scaly), and palms and soles can be infected at once.
• Variations of tinea pedis. Interdigital, hyperkeratotic and vesiculobullous; all three are caused by Trichophyton species, and the interdigital form is the most common.

Also tested

• Confirming thickened discolored toenails. Use potassium hydroxide microscopy, periodic acid-Schiff stain of clippings, culture, or amplification testing; sample subungual debris after trimming the onycholytic nail, from the most proximal accessible diseased nail bed.
• Id reaction criteria. A dermatophyte infection is present elsewhere, none is found at the id site, and the eruption resolves. The primary site is potassium hydroxide positive, the id site negative, and onset is 1 to 2 weeks after the primary infection.
• Essential tinea pedis self-care. Dry between the toes after bathing.
• Onychomycosis. Trichophyton rubrum causes most cases (dermatophytes cause most, though yeasts and molds also occur); distal lateral disease produces debris, onycholysis, thickening and crumbling, with discoloration.

Also tested

• Cutaneous candidiasis appearance. It is beefy red in the depth of the fold, with satellite papules scattered beyond the edge.
• Recurrent candidal intertrigo. Recurrent or extensive disease prompts evaluation for diabetes and immunosuppression.
• Vitiligo versus pityriasis versicolor. Vitiligo is completely white (depigmented) and autoimmune, whereas pityriasis versicolor is hypopigmented rather than depigmented, and it scales.
• Candidal intertrigo. It produces well-demarcated erythematous patches in warm moist folds, with satellite papules and pustules beyond the main area; pruritus with burning pain is typical.
• Pityriasis versicolor distribution and appearance. Lesions favor the trunk, neck and proximal arms as finely scaling macules and patches that are hypopigmented, hyperpigmented or pink and velvety, from 4 to 5 millimeters up to large confluent areas.
• Risk factors for intertrigo and cutaneous candidiasis. Obesity, diabetes, incontinence, occlusion, immobility, antibiotics and immunosuppression. Common sites are inframammary, axillary, abdominal, inguinal, perineal and interdigital folds.
• First step in candidal intertrigo. Correct the environment first: gently dry the folds, reduce friction and occlusion, use moisture-wicking fabric or absorbent material, and address incontinence or hyperhidrosis.
• Sites to inspect for candidal skin disease. The inframammary, axillary, abdominal, inguinal, perineal and interdigital folds are the six named common sites.
• Pityriasis versicolor pallor. Pigment recovery lags months behind clearance, because hypopigmentation reflects altered melanocyte function and reduced tanning; persistent pallor does not indicate treatment failure.
• Extensive or recurrent pityriasis versicolor. Oral terbinafine is not appropriate because adequate drug levels are not achieved in sweat, although topical terbinafine can be effective. The route matters for this organism.
• Candidal intertrigo treatment. Well-demarcated erythematous patches with satellite papules and pustules are treated with a topical azole, which covers both Candida and dermatophytes, whereas topical nystatin treats Candida only.

Also tested

• Herpes zoster scarring. It scars when deeper epidermal or dermal layers are compromised by excoriation or secondary infection; otherwise it typically heals without visible sequelae.
• Polymerase chain reaction in herpes zoster. Use it for atypical, disseminated, vaccine-modified or immunocompromised presentations, on vesicle fluid, scab, or cells from the lesion base; typical unilateral dermatomal vesicles are diagnosed clinically.
• Antiviral timing. For a dermatomal vesicular eruption, start antivirals as soon as possible, ideally within 72 hours of rash onset. Treatment is still given after 72 hours when new lesions are forming or there is ophthalmic involvement.
• Varicella complication risk. Adults, pregnancy, newborn age and immunocompromise carry an increased risk of complications.
• Varicella and prompt consultation. Pregnancy, neonatal exposure, immunocompromise or severe complications are the four situations that warrant prompt consultation.
• Testing atypical or immunocompromised varicella-type eruptions. Polymerase chain reaction is preferred, using vesicle fluid, a scab, or cells from the lesion base.
• Hutchinson sign. Herpes zoster lesions on the tip or side of the nose increase ocular risk, but its absence does not exclude eye involvement; systemic antiviral therapy should be started immediately.
• Herpes simplex virus type and site. Either type causes either site: either virus type can cause oral or genital infection, lesion location does not reliably determine type, and typing requires a type-specific test.
• Primary varicella-zoster infection. Its most characteristic feature is lesions in multiple stages of healing appearing simultaneously: macules progress to papules, vesicles, and crusts.
• Herpes zoster pre-eruptive phase. Dysesthesia or pain within the affected dermatome, with lesions appearing by 48 to 72 hours. Malaise, myalgia, headache and photophobia may occur, and rarely fever.
• Zoster over the forehead, upper eyelid and nose tip with eye pain and photophobia. Start systemic antiviral therapy immediately and arrange same-day ophthalmology evaluation. Do not delay the antiviral while awaiting the eye review.
• Severe disseminated zoster with visceral involvement. Manage with intravenous acyclovir with specialist or hospital management, as also for central nervous system or sight-threatening disease.
• Cause of herpes zoster. It results from reactivation of latent varicella-zoster virus, which stays latent in cranial-nerve or dorsal-root ganglia; risk rises with age and impaired cell-mediated immunity.
• Phases of a dermatomal grouped-vesicle eruption. Pre-eruptive (dysesthesia or pain in the dermatome, lesions by 48 to 72 hours), acute eruptive (grouped herpetiform vesicles on erythematous base, new lesions over 3 to 5 days), and postherpetic neuralgia (chronic).
• Varicella contagious period. The child is contagious from 1 to 2 days before the rash until all lesions have crusted; contagiousness begins before the rash is visible.

Also tested

• Dermatitis herpetiformis immunology. Immunoglobulin A antibodies against epidermal transglutaminase form complexes that deposit in the dermal papillae; complement and neutrophils are then activated, producing subepidermal blisters.
• Herpes simplex virus. It is a double-stranded DNA virus of the Herpesviridae family that produces latent but lifelong infection; latency for life is its defining feature.
• Genetics of dermatitis herpetiformis. HLA-DQ2 and HLA-DQ8 are strongly associated, and nearly all patients have underlying gluten-sensitive enteropathy even when gastrointestinally asymptomatic.
• Recurrent herpes-associated erythema multiforme. Chronic suppressive antiviral therapy, such as aciclovir 400 mg twice daily, is appropriate, because preventing the herpes recurrence prevents the eruption.
• Recurrent erythema multiforme after oral herpes. Recurrent disease is strongly associated with recurrent herpes simplex, and long-term suppression is suppressive acyclovir 400 mg twice daily or valacyclovir 500 mg daily.
• Low-positive herpes simplex type 2 serology. Confirm it with a second method when one is available, because low-positive results may be false positives.
• Herpetic whitlow. Do not incise; cover it and give antivirals. Incision and drainage does not treat herpes simplex virus and can delay healing; early oral acyclovir, valacyclovir, or famciclovir may shorten the episode.
• Herpes simplex virus. A tight group of vesicles and erosion at the vermilion border, recurring in the same place.
• Herpes simplex virus infection. A first episode gives painful grouped vesicles on an erythematous base, for example on the vulva, that become shallow painful ulcers, with a systemic prodrome of fever, headache and tender inguinal nodes.

Also tested

• Treating cutaneous warts. No therapy eradicates human papillomavirus with certainty, and recurrence can occur. Choose treatment by location, symptoms, age, pregnancy status, immune status, and risk of scarring or dyspigmentation, avoiding excessive freezing or destruction.
• Plantar warts. They occur on weight-bearing surfaces, and clustered together they form a mosaic wart.
• Red or black dots in a wart. Tiny dots are thrombosed capillaries, made more prominent by trimming the surface, and distinguish a wart from a callus, which lacks them.
• Molluscum contagiosum natural history. In immunocompetent patients most clear spontaneously, although resolution may take months to several years. Clearance is spontaneous but often slow.
• Warts. Caused by human papillomavirus, which infects keratinocytes and remains confined to the epidermis, producing a benign proliferation.
• Variations of verruca. Five variants are recognized: verruca vulgaris, verruca plana, verruca plantaris, mosaic warts, and genital warts.
• Verruca vulgaris. It occurs most often between 5 and 20 years, with spontaneous resolution; common warts usually resolve on their own.

Also tested

• Tinea pedis prevention. Drying between the toes after bathing is essential, alongside antifungal foot powder for shoes, open-toed sandals when possible, sandals in community showers, and frequent sock changes.

Also tested

• Calluses. They typically develop on the palms of the hands or the balls of the feet; if the process is acute and severe, a blister forms.
• Preventing callus recurrence. Well-fitting shoes and socks and pads inside the shoe remove the friction so the lesion stops re-forming; tight shoes, high heels and wearing shoes without socks are named as causes.
• Corn and callus management. Use padding and avoid poorly fitting footwear, with over-the-counter keratolytic products: remove the pressure first, then thin the keratin.
• Clavus (corn). Mechanical trauma such as ill-fitting shoes causes hyperkeratosis with a cone-shaped central core of hard keratin pointing into the skin; the central core separates a corn from a callus.
• Painful corn with diabetes mellitus. A diabetic foot lesion goes to podiatry: refer the patient to podiatry.
• Wart versus corn or callus. A wart interrupts the skin lines, has a blackened center, and is not confined to pressure areas; corns and calluses both let the skin lines run through.

Also tested

• Post-surgical advice for keloid-prone patients. Avoid stretching the immature scar, avoid hot baths, keep the wound clean, and avoid body piercings; stretching provokes scar inflammation and overgrowth, and hot baths can aggravate surgery-induced inflammation.
• Radiation for keloids. It may be used during the first two weeks after the keloid has been excised, as an adjunct to surgery rather than a primary treatment.
• Compression therapy for keloids. The regimen is 25 millimeters of mercury, round the clock, for six to twelve months; the mechanism is not understood but possibly induces tissue hypoxia with fibroblast degeneration and subsequent collagen degradation.
• Surgical excision of a keloid alone. Recurrence is fifty to one hundred percent and the recurrent lesion is often larger than the original, so excision is never done alone and steroid injection follows; combination therapy has the best success rates.
• Raised scar confined to the incision. A raised, firm, red scar that stops exactly at the edges of the original incision should stay stable and then flatten with time, which is why observation is reasonable.
• Keloid management. Prevention is the most important treatment. High-risk patients should avoid cosmetic procedures such as ear piercing; post-surgical education includes avoiding stretching of an immature scar and avoiding hot baths.
• Silicone sheets for keloid. They are worn twelve to twenty-four hours a day for up to a year, theorized to raise scar temperature and increase collagenase activity.
• Silicone gel sheets for scars. The theory is that occlusive dressings warm the scar, raising collagenase activity; they are worn 12 to 24 hours a day for up to a year.
• Keloid treated with laser. The best result comes from combining the laser with intralesional steroids; laser works by shrinking collagen or inducing microvascular thrombosis.
• Hypertrophic scar versus keloid timing. Hypertrophic scars develop soon after surgery and usually improve with time; keloids may develop months after the trauma and rarely improve.
• Keloid. Scar tissue that has grown beyond the boundaries of the original wound.

Also tested

• Cutaneous horn management. It depends on the underlying etiology, with excision to the standard for the tumor type and location if malignant; treat what is at the base, not the horn.
• Cutaneous horn epidemiology. It is seen in Caucasians over fifty, on the head, neck and upper extremities, such as a lesion on the ear.
• Cutaneous horn. It arises from the surface of another lesion, benign or malignant (actinic keratosis, warts, squamous cell carcinoma). There is often no clinical feature to distinguish them, so the lesion at the base must be diagnosed.
• Skin tags. Increased in females and obese patients, in areas of friction such as the neck, axilla and groin; very common, present in sixty percent of people by age seventy.

Also tested

• Pilonidal disease education. Maintain good hygiene, and seek care if an abscess occurs; recurrence is common, so this is ongoing advice.
• Pilonidal disease testing. No diagnostic testing is usually needed; the diagnosis is clinical.
• Pilonidal disease presentation. Acutely, sudden pain and swelling in or along the gluteal cleft; chronically, recurrent drainage and pain from one or more sinus tracts. A hair may occasionally be seen protruding from a sinus opening.
• Pilonidal disease risk factors. Obesity, sedentary life and dense cleft hair; the male to female ratio is 3 to 1.

Also tested

• Epidermoid cyst testing. Laboratory testing is usually not required, because the diagnosis is clinical.
• Epidermoid cyst contents. It is often called a sebaceous cyst because the material looks like sebum, but the contents are keratin, not sebum.
• Squamous cell carcinoma risk factors. Besides sun exposure and immunosuppression: chronic wounds, scars or prior radiation fields; certain genetic diseases; and mucosal or genital disease.
• Keratoacanthoma risk factors. Age over forty, sun exposure, very fair skin that always burns and never tans, male sex, tattoos with red ink, skin trauma such as lasers, surgery or cryotherapy, and human papillomavirus infection.
• Dermatofibroma symptoms. Usually asymptomatic, sometimes with a history of insect bite; when symptomatic it may cause slight pruritus or pain, and it is described as the commonest painful skin tumor.
• Epidermoid cyst. Enclosed epithelium filled with keratin within the dermis; it is often called a sebaceous cyst because it appears to contain sebum, which makes that term a misnomer.
• Differential of dermatofibroma. Basal cell carcinoma, hypertrophic scar, cutaneous melanoma and keratoacanthoma; two of the four are malignancies.

Also tested

• Cherry angiomas. Patients should be told that new lesions will likely develop and there is no way to prevent them; treatment is not necessary unless they bother the patient.
• History in spider angiomas. Cover pregnancies, hormone use, alcohol history, and medications that carry a risk of liver damage, because the lesion can be a marker of estrogen excess or liver disease.
• Nevus flammeus over time. Early, it is a flat blanchable patch, well-circumscribed, pink to red to purple, usually unilateral with fairly sharp midline cutoffs; later the vasculature dilates and it may become a raised, thickened plaque of deeper color.
• Natural course of a raised red plaque in an infant. Most involute on their own over several years: complete involution in fifty percent by age five, seventy percent by seven and ninety percent by nine, so serial observation is often all that is needed.
• History in spider angiomas. Take alcohol use, liver-damaging medication and hormone use, and ask about pregnancies too; spider angiomas track estrogen excess and cirrhosis or liver failure.
• Excision of a bleeding red papule. Surgical excision has the lowest recurrence rate and also provides histopathologic analysis, at the cost of the highest rate of scarring.
• Infantile hemangioma growth. Rapid proliferation is followed by slower involution, with rapid growth in the neonatal period and most growth in the first 4 to 6 months. The earliest sign is blanching, then fine telangiectasias, then a red macule.
• Nevus araneus. A central arteriole with radiating capillaries, caused by dilation of pre-existing vessels with no vascular proliferation. Estrogen excess may be the cause; ask about pregnancies, hormone use, alcohol and medications high-risk for liver damage.
• Pyogenic granuloma education. It is benign and often resolves over months to years; treatment is available if wanted, for cosmetic reasons or to prevent bleeding. If it recurs, early follow-up is appropriate because small lesions are easier to treat than large ones.
• Infantile hemangioma types. Superficial, mixed, and deep, classified by depth of vessel involvement; superficial is commonest, presenting as a bright red papule, plaque, or nodule, and the deep type is the least common.
• Cherry angioma. A benign capillary proliferation (capillary or venule proliferation), very common and increasing with age; treatment is unnecessary unless it bothers the patient, and new lesions will likely develop with no way to prevent them.
• Telangiectasia. A dilated capillary under 1 mm that blanches; these are acquired vascular lesions of permanently dilated capillaries, single or grouped with a central punctum, primary or secondary.
• Pyogenic granuloma. This acquired vascular lesion is a misnomer, being neither infectious nor granulomatous. It is a benign vascular tumor common in children, young adults, and pregnancy, arising in response to injury or hormonal factors, most often on the head, neck, and fingers.
• Differential of pyogenic granuloma. Cherry angioma, malignant melanoma and squamous cell carcinoma; two of these are malignancies.
• Flat blanchable pink-purple patch present since birth. No treatment is required; options are tinted waterproof makeup, or pulsed dye laser, which selectively destroys the superficial target vessels.
• Nevus simplex. Most common on the head and neck and more noticeable with crying; it appears as pink to erythematous blanchable macules or patches, single or multiple.
• Hemangioma complications. Hemangiomas may cause compression of vital structures, block vision, interfere with feeding or respiration, obstruct the external auditory canal, and occur at extracutaneous sites.

Also tested

• Uncertain basal cell carcinoma. The next step is dermoscopy, with biopsy if concern remains.
• Xanthelasma. A collection of lipid-laden macrophages forming soft yellow cholesterol plaques, most commonly on the medial eyelids; it is asymptomatic.
• New lesion in a sun-exposed area. It is an opening to counsel on sunscreen, sun avoidance at peak hours and skin checks, as general skin-cancer education.
• Lipoma. Soft, painless, rubbery subcutaneous nodules, usually under five centimeters, that can occur anywhere on the body; asymptomatic unless adjoining structures are invaded.
• New benign lesion in a sun-exposed area. Use the opportunity for counseling on sunscreen and self-examination, including avoiding direct sun during peak hours and performing periodic skin self-examinations.
• Infantile hemangioma first-line treatment. Beta-blockers (propranolol by mouth or timolol topically) and corticosteroids (topical, intralesional or oral, to slow growth and shrink the lesion) are both named first line.
• Xanthelasma. Soft, flat yellow plaques near the inner canthus, prompting a lipid profile.

Also tested

• Solar lentigo versus lentigo maligna. Solar lentigo has uniform pigmentation, whereas lentigo maligna is asymmetric with irregular border and color; dermoscopy is essential, and solar lentigo shows finger-like projections and a moth-eaten border.
• Solar lentigines. The lesions themselves are benign, but they mark cumulative sun damage that is also associated with actinic keratosis, squamous cell carcinoma, basal cell carcinoma and melanoma.
• Lentigines. They are well-circumscribed round to oval uniformly black or brown macules under 5 mm, on skin, conjunctiva and mucocutaneous surfaces, occurring on both sun-exposed and sun-protected areas.
• Lentigo maligna. Melanoma in situ that is asymmetric with irregular border and color and darker areas; dermoscopy is essential. A solar lentigo that has diverged from its uniform neighbors requires that evaluation.
• Biopsy of a pigmented facial macule. Atypical or uncertain morphology on dermoscopy is the stated indication for biopsy; an asymmetric macule with an irregular border and two darker areas is biopsied to exclude lentigo maligna.
• Solar lentigo risk factors. They are older age, sun damage, a history of ephelides, tanning, and birth control use. Solar lentigines are common: 90% of people have them by the age of fifty.
• Numerous solar lentigines. Advise daily broad-spectrum sunscreen of SPF 30 or higher, with an annual full-body skin examination. Dermoscopic surveillance is added for atypical lesions.
• Asymptomatic, unchanged flat brown patches on the backs of the hands. No treatment is necessary; cosmetic removal by cryotherapy or quality-switched laser is offered only if the patient wishes. Treatment is elective, not indicated.
• Forms of lentigines. Lentigo simplex, acral lentigo, agminated lentigo and generalized lentigo; they follow a bimodal age distribution.
• Ephelides. Inherited autosomal dominant, most commonly in fair-skinned people with blonde or red hair and possibly Celtic ancestry. Males and females are equally affected.
• Solar lentigines over time. They can progress into lichenoid keratoses. They may also enlarge, darken, stay stable or regress.
• Solar lentigines. Well-defined with irregular borders, coalescing 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.
• Ephelides. They are small light brown symmetric macules 3 to 5 mm across, with lentigines as the main differential; they are asymptomatic and the diagnosis is clinical.
• Solar lentigines. Arise from basal melanocyte proliferation with more melanin production. They are strongly associated with older age (about 90 percent by age 50), sun damage, tanning, a history of ephelides, and birth control use.
• Agminated lentigines. A grouping of small light brown macules, one of the named lentigo types.

Also tested

• Seborrheic keratosis features. Dermoscopy shows comedone-like openings, with a stuck-on appearance clinically. Solar lentigo shows finger-like projections and a moth-eaten border instead.
• Biopsy in dermatosis papulosa nigrans. Biopsy is indicated when the diagnosis is uncertain; the diagnosis is otherwise clinical.
• Dermatosis papulosa nigrans counseling. The lesions are benign and best left untreated, with removal available for cosmetic reasons. Options are excision, curettage or laser, avoiding cryotherapy.
• Cryotherapy in dermatosis papulosa nigrans. Cryotherapy is avoided in this condition because of post-inflammatory hyperpigmentation. Excision, curettage or laser can be used where treatment is wanted.
• Multiple dark warty growths in older adults. They are benign and common in older adults, and the diagnosis is clinical without any need for biopsy. Cryotherapy helps if a lesion becomes itchy or inflamed, though it may recur.
• Symptomatic seborrheic keratosis. An itchy, inflamed lesion can be treated with cryotherapy, though the lesion may recur afterwards; asymptomatic lesions need no treatment at all.
• Seborrheic keratoses. Benign beige to brown to black papules and plaques 2 to 20 mm across, velvety or warty, looking stuck onto the skin, common in older adults. They are easily mistaken for neoplasms.
• Seborrheic keratosis diagnosis and management. They are benign, diagnosed clinically, and management is supportive. They are common in older adults and easily mistaken for neoplasms.

Also tested

• Segmental versus non-segmental vitiligo. Distinguishing them matters because the two differ in their diagnostic tools and in their treatment. Segmental disease is unilateral, does not cross the midline, and follows block-like patterns.
• Psychosocial impact of vitiligo. The psychological and social impact is real, and psychological intervention is part of management. Low self-esteem and poor body image are named explicitly.
• Vitiligo treatment. Phototherapy with narrow band ultraviolet B, ideally combined with topical therapy, is preferred over PUVA, which carries adverse effects including increased skin cancer risk.
• Vitiligo above five percent of body surface. Narrow-band ultraviolet B phototherapy is first line, ideally combined with topical therapy.
• Non-pharmacologic vitiligo management. Psychological intervention, cosmetic therapies and non-traditional approaches; the psychological and social impact is emphasized.
• Surgery for vitiligo. Tissue or cellular grafting is an option, since surgery is reserved for highly stable disease.
• First-line vitiligo treatment. Topical therapy suits under five percent involvement, ideally combined with phototherapy; calcineurin inhibitors are useful where steroids cannot be applied, such as face and neck.

Also tested

• Macule. It is a flat lesion less than one centimeter, without elevation or depression; a patch is the same lesion larger than one centimeter.
• Purulent wound testing. Order bacterial culture and sensitivity: the culture names the organism and the sensitivity directs the antibiotic.
• Bulla. A fluid-filled lesion greater than one centimeter is called a bulla; a vesicle is the same lesion up to one centimeter.
• Common acquired melanocytic nevi. They are usually under 6 mm, homogeneous in surface and color, round to oval with sharp demarcation. A very dark brown or black lesion on a light-skinned individual is suspicious and warrants evaluation.
• Purpura. Non-blanching blood deposits of 4 mm or more are purpura, a medical emergency until proven otherwise; with fever in a child it demands immediate evaluation.
• Potassium hydroxide wet preparation. It detects fungal elements in skin, hair or nail samples and is the appropriate bedside confirmation before treating a suspected dermatophyte infection.
• Poorly demarcated. A poorly demarcated lesion has an irregular or blotchy appearance without well-defined borders, in contrast to a well-demarcated lesion, which has clearly defined borders.
• Dermatoscope. It is used for magnified examination of a lesion's surface and pigment pattern, and is the first-line tool for evaluating a pigmented lesion.
• Plaque versus patch. A plaque is elevated and plateau-like, while a patch is flat with no elevation; both exceed one centimeter, so elevation is the discriminator.
• Wheal. A wheal is a firm edematous plaque produced by infiltration of fluid into the dermis. The fluid is in the tissue rather than in a cavity, which separates it from a vesicle.
• Describing a skin finding. Six features translate a dermatological finding into words: primary morphology, secondary morphology, demarcation, color, size and distribution. Including all six lets another provider picture the lesion without seeing it.
• Lichenification. It is thickening and hardening of the skin, and it develops from chronic rubbing or scratching.
• Transillumination. This bedside technique shows whether a soft subcutaneous nodule is fluid-filled: a fluid-filled lesion glows when a light is placed against it.
• Common acquired melanocytic naevi natural history. They develop slowly after birth, enlarge symmetrically, stabilize and regress, peaking in number in the thirties and then declining. Melanoma risk rises with the number of lesions.
• Common acquired melanocytic naevi risk factors. They include ultraviolet radiation exposure, male sex, and a genetic component, with more lesions in light skin tones that sunburn. The number of lesions peaks in the thirties.
• Naevus spilus. It is thought to arise from a somatic mutation and appears at birth or in the first years of life. It is a variant of congenital naevus.
• Congenital melanocytic naevi. Neurofibromatosis type I is a named associated risk factor. Congenital naevi also carry a high risk of developing into melanoma.
• Large congenital naevus with neurological symptoms. Seizures and vomiting with a large naevus over the head and neck indicate neurocutaneous melanosis, and the prognosis is poor once neurological symptoms appear. Symptoms usually appear within the first few years of life.
• Large congenital naevus workup. Head, neck or posterior midline lesions raise neurocutaneous melanosis, so magnetic resonance imaging of the brain, with or without total spine, is required, matched to where the naevus sits.
• Numerous dysplastic naevi counseling. Between visits, use sun protection and report any lesion that changes or is newly developing. Management is observation, biopsy of changing lesions and excision where melanoma is a concern.
• Removing a melanocytic naevus. Removal for symptomatic or cosmetic reasons is reasonable, alongside sun protection counseling. The diagnosis is clinical and management is otherwise observation.
• Neurocutaneous melanosis. A related condition in patients with naevi on the head, neck or posterior midline, causing seizures, hydrocephalus, neurological deficits and vomiting; prognosis is poor once neurological symptoms appear, usually in the first few years of life.
• Pigmented spindle cell naevus (Reed naevus). A sharply circumscribed darkly pigmented papule usually under 7 mm, jet-black with shades of blue, gray or brown, on the extremities and mainly the thigh. Commonest in the thirties, females more than males; benign.
• Melanoma risk and common acquired melanocytic naevi. Risk increases as the number of naevi increases. Naevus numbers peak in the thirties and then decline.
• Blue naevi location. Most commonly on the dorsal hands and feet, scalp, buttocks or sacral region. The lesions are blue, blue-gray or blue-black.
• Spitz naevus. A solitary asymptomatic pink or red hairless firm dome-shaped lesion on face, neck, trunk or extremities, sparing palms, soles and mucous membranes. It has a growth phase, fast or slow, followed by a stable period.
• Pigmented spindle cell naevus management. Confirmed by biopsy, with excision and negative margins as management. The lesion is benign despite its jet-black appearance.
• Common versus cellular blue naevi. Common blue naevi are deeply pigmented lesions under 1 cm arising in adolescence; cellular blue naevi are larger plaques or nodules over 1 cm arising before age forty. Both occur on dorsal hands and feet, scalp, buttocks or sacral region.
• Changing lesion in dysplastic naevi. Biopsy the lesion, since all changing or developing lesions are biopsied. Excision follows where there is concern for melanoma.
• Dysplastic naevi. They are common on sun-exposed skin surfaces. They are at least 5 mm with irregular indistinct borders and variable pigmentation.
• Cellular blue naevus diagnosis. Diagnosis is clinical for small lesions but by biopsy for larger ones. Observation follows, with biopsy or excision if changes are noted.
• Excisional biopsy. An excisional biopsy removes the whole lesion, taking all deep and wide margins, and always needs stitches to close the wound.
• Dysplastic nevus syndrome and melanoma. The higher the number of nevi, the higher the risk of melanoma; over one hundred nevi by adolescence defines the syndrome.
• Diagnosing a dysplastic melanocytic nevus. Biopsy establishes the diagnosis, because the lesion is diagnosed histologically.
• Management of nevus spilus. Observation with periodic clinical evaluation, plus sun protection counseling, because it rarely progresses to melanoma.
• Common acquired nevus color. It is skin colored, brown or pink, with a homogenous surface and color, whereas a dark brown or black nevus on light skin is suspicious; it is usually under 6 mm, round to oval, and sharply demarcated.
• Dysplastic melanocytic nevus. Diagnosis is by biopsy; management is observation, biopsy of all changing or developing lesions, excision where melanoma is a concern, and sun protection. Melanoma risk rises with the number of nevi present.

Also tested

• Treating freckles. Start with sun protection and counseling, then topical depigmenting agents, with intense pulsed light or laser if needed; the topical options are hydroquinone, retinoids, alpha-hydroxy acids and botanicals.
• Light or laser treatment of freckles. Patients should expect that lesions can relapse, so treatment is not necessarily permanent.
• Freckles management. Manage with sun protection, patient education and topical depigmenting agents; cryotherapy is not used because of the size of the lesions. Laser or intense pulsed light is preferred, but the lesions can relapse.
• Ephelides. Topical depigmenting agents named are hydroquinone, retinoids, alpha-hydroxy acids and botanicals, though sun protection and counseling remain the priority.
• Treating solar lentigines. Treatment is cosmetic; reducing skin cancer risk depends on sun protection and surveillance for other lesions. The lesions mark sun damage rather than causing the cancers associated with it.
• Very large congenital naevus. Counseling and support groups for families and patients with large naevi are appropriate support, named alongside the surgical and observational decision.
• Cryotherapy of seborrheic keratosis. Tell the patient beforehand that the lesion can come back after freezing, so she is not surprised or disappointed later.
• Removing seborrheic keratoses. Treatment is not necessary; removal is elective, for cosmetic or symptomatic reasons, using retinoids, cryotherapy or quality-switched laser.
• Congenital melanocytic naevus management. It depends on melanoma risk together with cosmetic and functional considerations, removing as much as possible while preserving function; observation may be better where there is little skin for a graft site.
• Very large congenital naevus. Point families to counseling and support groups; management balances melanoma risk, cosmetic outcome and preserved function. The goal is removing as much as possible while preserving function and improving appearance.
• Small congenital melanocytic nevus. Observation, since management balances melanoma risk with cosmetic and functional considerations; smaller lesions carry lower melanoma risk than larger ones.
• Cosmetic removal of solar lentigines. Retinoids, cryotherapy or quality-switched laser; treatment is not necessary as the lesions are benign.

Also tested

• Describe before naming. Evaluate any premalignant or malignant lesion by first characterizing it: primary lesion type, color, surface texture, border definition, size, distribution, palpability, ulceration and bleeding, before assigning a diagnosis.
• Examining a suspected malignant skin lesion. Use good lighting, dermoscopy when trained, and a total-body skin survey when indicated; examine palms, soles and nails, the oral mucosa when Kaposi sarcoma is possible, and regional nodes for invasive or high-risk disease.

Also tested

• Concerning actinic keratosis. Induration, tenderness and bleeding are the concerning features named for progression; biopsy the lesion to exclude invasive squamous cell carcinoma.
• Actinic keratosis versus early squamous cell carcinoma. Squamous cell carcinoma must be excluded when a lesion is thick, indurated, ulcerated, enlarging, painful, bleeding, persistent or recurrent.
• Thickened, indurated, bleeding actinic keratosis. Order a shave or punch biopsy, because induration and bleeding raise concern for squamous cell carcinoma and are not part of a typical actinic keratosis.
• Actinic keratosis pathogenesis. Actinic keratoses are intraepidermal keratinocytic dysplasias induced by cumulative ultraviolet B exposure; ultraviolet-induced TP53 mutation is the critical molecular event. They represent a field cancerization process.
• Field cancerization. Clinically normal skin around the lesions harbors subclinical mutations, so multiple or confluent lesions need field-directed therapy: 5-fluorouracil, imiquimod, tirbanibulin or diclofenac treat the field rather than single lesions.
• Transplant recipients. Immunosuppression raises the risk of actinic keratosis and skin cancer about sixty-fold, so they need aggressive photoprotection and biannual skin surveillance.
• Actinic keratosis biopsy. Morphology or behavior raising concern for squamous cell carcinoma, or persistence or recurrence after therapy, prompts biopsy. A shave or punch biopsy is used.
• Fate of an actinic keratosis. An individual lesion may persist, involute, recur, or progress, so individual lesion behavior is unpredictable.
• Actinic keratosis field therapy. Warn patients to expect erythema and crusting, and stress adherence to the full treatment duration. Patients who are not warned stop the course early.
• Actinic keratosis recurring after therapy. Persistence or recurrence after therapy is a biopsy trigger, so take a shave or punch biopsy. Recurrence plus induration is exactly what should prompt sampling.
• Squamous cell carcinoma. A firm nodule with heaped keratin or ulceration, on chronically sun-damaged skin.

Also tested

• Squamous cell carcinoma pathology report. It should identify differentiation grade, depth or thickness, perineural or perivascular invasion, margin status, and aggressive subtype. Each feeds the decision about Mohs and about follow-up.
• Regional assessment in squamous cell carcinoma. Alongside biopsy, palpate the draining lymph-node basins, considering imaging or nodal evaluation for high-risk tumors. The nodes are examined at diagnosis, not only at follow-up.
• Squamous cell carcinoma prevention in transplant recipients. Nicotinamide five hundred milligrams twice daily reduces new squamous cell carcinoma by about thirty percent in high-risk patients.
• Squamous cell carcinoma biopsy requirement. The sample must allow the pathologist to determine whether the disease is in situ or invasive, along with the histologic risk features. Sufficient depth makes that distinction possible.

Also tested

• Mohs surgery for basal cell carcinoma. Indicated for high-risk anatomic sites, recurrent tumors, aggressive histology, or where tissue sparing is needed. The goal is complete eradication with minimal cosmetic and functional deformity.
• Sampling basal cell carcinoma. A suspected lesion is sampled with a shave or punch biopsy to confirm the diagnosis. Pathology then determines the histologic subtype, which dictates treatment.
• Basal cell carcinoma in immunosuppression. It is more common and more likely to recur after non-Hodgkin lymphoma, solid-organ transplant, or allogeneic stem cell transplant.
• Imaging in basal cell carcinoma. Routine imaging is not needed in typical localized disease; it is reserved for advanced, deeply invasive or metastatic disease. That specialist-directed workup is the exception rather than the rule.
• Topical therapy for basal cell carcinoma. Patients must understand that local inflammation is expected, and that clearance has to be confirmed afterwards. Inflammation is not a reason to stop, and clearing visibly is not the same as being clear.

Also tested

• Stage IV melanoma. It is defined by any T, any N, with M1, meaning distant metastasis is present whatever the primary or nodal status; M1 alone determines it.
• Melanoma with nodal spread. Nodal spread, such as a positive sentinel node, is an explicit referral trigger to an expert center for coordinated dermatology and surgical oncology care. Nodal or other-site spread crosses the threshold regardless of thickness.
• Suspicious pigmented lesion. The initial diagnostic test is biopsy or excision to confirm the diagnosis. Tissue is required before staging decisions.
• Small suspicious pigmented lesions. An asymmetric lesion with an irregular border that is darkening should be biopsied or excised, because smaller lesions can still be melanoma; the 6 mm figure is a prompt, not a rule-out.
• Melanoma self-examination. Perform it monthly using the recognition mnemonic and ugly-duckling principles, including the scalp, back, palms, soles and nails, since acral and scalp sites are easy to miss.
• Malignant melanoma appearance. The lesion is asymmetric, irregularly bordered and unevenly colored; a lesion on the sole demands more suspicion.
• Re-excision margin for melanoma in situ. The margin is 0.5 to 1 cm; margins widen with Breslow thickness from there.
• Melanoma levels of invasion (Clark level). I is confined to the epidermis; II into the papillary dermis; III filling the papillary dermis; IV into the reticular dermis; V into the subcutaneous tissue. It is an anatomic layer, unlike Breslow thickness, a measurement.
• Melanoma re-excision margins by thickness. Definitive local margins are 0.5 to 1 cm in situ, 1 cm under 1 mm, and 1 to 2 cm over 1 mm; expert-center referral applies to melanoma deeper than 1 mm or with lymph node involvement.
• Melanoma stages 0 to II. Stage 0 is melanoma confined to the epidermal region of the skin; stage I is localized disease, only in skin and very thin; stage II is localized disease thicker than stage I. All three are still local.
• Melanoma subtype with delayed diagnosis. Acral lentiginous melanoma is frequently delayed in diagnosis, so early reporting is critical: patients report new pigment, widening bands or periungual pigment promptly.
• Melanoma deeper than 1 mm. A thickness over 1 mm calls for a 1 to 2 cm re-excision margin and referral to an expert center; the same threshold governs both.
• Melanoma re-excision margin. A melanoma under 1 mm Breslow thickness with no adverse features takes a 1 cm margin.

Also tested

• Confirming Kaposi sarcoma. Biopsy a representative lesion; human herpesvirus 8-associated findings on histology support the diagnosis.
• Kaposi sarcoma immune reconstitution inflammatory syndrome. It is especially dangerous in patients with visceral disease; endemic or visceral disease with this syndrome can be aggressive and rapidly fatal.
• Cutaneous T-cell lymphoma prognosis. Tumors, erythroderma and lymphadenopathy worsen prognosis; survival is not reduced in limited patch-stage disease.
• Mycosis fungoides. It may resemble psoriasis, eczema or tinea; the discriminators are chronicity, treatment resistance, and large or oddly distributed lesions. Early patches or scaly plaques are usually on the trunk, frequently greater than 5 cm.
• Cutaneous T-cell lymphoma versus psoriasis, eczema and tinea. Discriminators are chronicity, treatment resistance, large or oddly distributed patches, severe pruritus, follicular hair loss, tumors or erythroderma, nodes, and histology over time. No single one settles it, so longitudinal reassessment is stressed.
• Procedures in Kaposi sarcoma. Bronchoscopy is for suspected pulmonary disease, and endoscopy is driven by symptoms or management rather than done routinely in asymptomatic patients. A chest radiograph is used when pulmonary involvement is possible.
• Antiretroviral therapy in Kaposi sarcoma. Patients must be told the lesions may worsen early, as immune reconstitution inflammatory syndrome. Warning them beforehand stops early worsening being read as treatment failure.
• Biopsy site in suspected cutaneous T-cell lymphoma. Select an active, representative, untreated lesion, coordinating with dermatopathology. Treating a lesion first can obscure the histology being read.
• Establishing cutaneous T-cell lymphoma. Patients should be told the diagnosis may require repeated biopsies and the disease is usually chronic. Setting that expectation early matters, because the diagnosis is often slow to confirm.
• Regression of Kaposi sarcoma. Iatrogenic disease may regress when immunosuppression is reduced, which is why the transplant team is consulted before any reduction.
• Kaposi sarcoma versus lookalikes. It is told apart from bacillary angiomatosis, hemangioma and other violaceous lesions by immune status, distribution, oral lesions, edema, visceral symptoms and biopsy, not color alone.
• Immune context in suspected Kaposi sarcoma. Test for human immunodeficiency virus if status is unknown; if known, assess CD4 count, viral load, antiretroviral history and adherence. Knowing the status is not enough; the degree of immune suppression matters.
• Blood tests in advanced cutaneous T-cell lymphoma. They are complete blood count with differential, eosinophilia, circulating Sezary cells, T-cell gene-rearrangement testing and specialist flow cytometry. These belong to advanced disease rather than the initial skin diagnosis.
• Nondiagnostic biopsy in suspected cutaneous T-cell lymphoma. A single nondiagnostic biopsy does not exclude the disease; correlate clinically and reassess over time. Numerous biopsies may be needed.
• Enlarged nodes in cutaneous T-cell lymphoma. They may be benign dermatopathic change or lymphoma involvement, and require directed biopsy or imaging to distinguish. Enlargement alone does not establish spread.
• Kaposi sarcoma in a transplant recipient. Reduce immunosuppressive medication doses where clinically feasible, coordinating with the transplant team before making any change.
• Classic Kaposi sarcoma. The classic form affects older men, has a chronic indolent course, is rarely fatal, and is related to age-associated immune senescence.

Also tested

• Biopsy of a suspicious nail lesion. It requires prompt referral to a dermatologist experienced in nail-unit biopsy, with the biopsy sampling the correct site.

Also tested

• Diagnosing squamous cell carcinoma. Use shave, punch or excisional biopsy sampling sufficient depth to separate in situ from invasive disease, because they carry different treatment, margins and risk.
• Single persistent nail abnormality. Avoid repeated empiric antifungal, antibiotic or wart treatment when the abnormality persists despite treatment. Repeating empiric therapy on a solitary persistent nail lesion is how diagnostic delay happens.
• Follow-up after squamous cell carcinoma. Examine skin and lymph nodes at least annually, with closer intervals if the patient is high-risk or immunosuppressed. The interval tightens rather than the examination changing.
• Photographing a concerning pigmented band. Do not let photographing it delay referral. Documentation is for tracking change, not for postponing the specialist.
• Neurologic symptoms after squamous cell carcinoma. New numbness and tingling in the distribution of the scar are an urgent referral trigger, since they raise concern for perineural invasion.
• Mohs micrographic surgery. Indicated for invasive squamous cell carcinoma on a high-risk site such as the temple, and for a lesion exceeding 1 cm on the face; either is a separate indication.
• Nail unit squamous cell carcinoma. Incomplete excision, immunosuppression, delayed diagnosis and bone invasion increase recurrence and functional morbidity. It is often curable with complete surgery.
• Early-stage cutaneous T-cell lymphoma. Early aggressive treatment has not been proven to cure the disease or prevent progression, and may itself cause harm. A stage-directed, skin-first approach suits most early disease.
• Mohs micrographic surgery for squamous cell carcinoma. Refer when the site is high-risk, the tumor is over one centimeter on the face, or histology is aggressive such as perineural invasion; each independently qualifies.
• Spread of actinically induced squamous cell carcinoma. An estimated 3 to 7%, raised substantially by high-risk sites or features, immunosuppression, multiple tumors, recurrence, or nodal involvement. The baseline is modest but modifiable.