ACD – Dermatology – Flashcards
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What dermatologic conditions might be seen in Diabetes? What about insulin resistance? What other things can cause Acanthosis Nigrans?
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Injection site adipose hypertrophy Granuloma annulare Necrobiosis lipoidica (rare but classic - 70% Sp) -begins w red papules/nodules, progresses to yellow-brown telengectasia, then skin atrophy + ulcers -classically lower leg, but can be anywhere Eruptive xanthomas (due to triglycerides if DM poorly controlled - diagnosed by classic biopsy findings. Numerous yellow-red papules, usually on buttocks) Acanthosis nigrans (also obesity, drugs, malignancy) -caused by effects of insulin-like growth factor receptors on keratinocytes -if malignancy related, usually widespread and rapid, with mucosal involvement, and often without other risks (e.g. obesity, DM)
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What dermatologic features might be associated with thyroid disease?
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Pretibial myxedema (Hyperthyroid - diffuse or nodular swelling of front of shins) Hyperthyroid: -facial flushing, sweating, palmar erythema, pruritis, diffuse hair loss Hypothyroid: -Dry/yellowish skin, diffuse hair loss, pruritis, puffiness (feet, face, hands), loss of outer 1/3rd eyebrow, body hair loss, brittle nails, bruising/purpura, cold sensitivity
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What are the cutaneous manifestations of hyperlipidaemia?
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Xanthelysma - most common, fairly refractive to Tx. Neither Sn nor Sp Tuberous xanthoma/Xanthemata - (severe hyperlipidaemia), attached to tendons and ligaments, esp achilles Eruptive xanthomas (as in DM)
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What are the dermatologic effects of Cushing's Syndrome?
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Face - roundness, redness Striae (permanent) Fragile skin (easy tearing), bruising Acne Excess facial/body hair Telengectasia If ACTH up, may see hyperpigmentation (incl oral)
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What are the cutaneous effects of Adrenal Insufficiency?
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If elevated ACTH (i.e. primary adrenal insufficiency), hyperpigmentation (incl oral) - normally resolves once disease treated -may affect nails also Loss of body hair and vitiligo (15%)
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What are the five main presentations of Lupus Erythematosus?
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Discoid (may occur inside mouth. 5% progress to SLE) Sub-acute cutaneous (papulosquamous or annular, photosensitive, no atrophy or scarring like in discoid, 20% still have some discoid lesions) SLE (usually "butterfly" rash, photosensitive. Discoid lesions in 20%) Drug-induced (esp thiazides, CCBs, terbinafine) Neonatal (occurs in mothers with sub-acute disease w circulating abnormalities. Assoc with congenital heart block, haeme and hepatic abnormalities)
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What is Dermatomyositis? What are the typical skin signs?
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Muscle inflammation (weakness) preceded by characteristic skin eruption (may be only manifestation - amyopathic dermatomyositis) -associated with underlying malignancy in 20% Periorbital red-purple erythema Scaly, reddish papules over dorsum of the interphalangeal joints, elbows, and knees (can resemble psoriasis) Ragged cuticles and nail-fold telengectasia Poikiloderma Photosensitivity
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What is scleroderma? What are the 3 main types? What skin manifestations might you see in scleroderma?
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Thickening + hardening of skin -can be isolated or part of autoimmune diseases like systemic sclerosis, SLE, dermatomyositis Morphoea - localised sclerosis CREST - Calcinosis, Raynaud's, Esophageal dysmotility, Scleroderma, Telengectasias Systemic Sclerosis - widespread and associated with GIT, lung, and kidney disease Thick skin plaques, may have red/purple rim Linear lesions, possibly causing contractures Oedema, swelling, and eventually contractures and atrophy of fingers + toes Tightness of facial skin, impaired mouth opening Ragged nail folds with telengectasia Hyperpigmentation Calcifications +/- ulcerations
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What is vitiligo? What is the cause?
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Sharp, well-demarcatted, patchy loss of skin color, sunburns easy -if it affects scalp, hair turns white Autoimmune - associated with other autoimmune disorders (diabetes, thyroid, pernicious anaemia)
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What is the commonest cause of pruritis? What derm conditions can have pruritis without other skin signs? What systemic diseases can create pruritis? What should you investigate for in unexplained pruritis?
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Asteatosis (dry skin) Scabies, urticaria, dermographism - especially if recently treated Malignancies - particularly haematologic Bile salts - renal failure, cholestasis Drug AEs Thyroid and parathyroid disease HIV, parasitic, or other infections Malignancies
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What is "Sweet's Syndrome"? How does it present? What conditions is it associated with? How is it treated?
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Febrile, neutrophilic dermatosis Painful, oedematous, red-to-blue plaques on face, neck, and limbs +/- fever, neutrophilic leukocytosis -plaques may be vascular or pustular Strep throat infection (most common), haeme malignancies, some solid tumors Responds well to systemic corticosteroids
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What is Erythroderma? What diseases is it most often a result of?
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Term for any rash involving >90% BSA -most often a result of psoriasis or eczema -more rarely caused by cutaneous lymphoma or underlying malignancy May be considered a dermatologic emergency
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What are the derm manifestations of Infective Endocarditis?
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Splinter haemorrhages (vasculitic) Osler nodes (autoimmune) - tender red papules on pads of fingers/toes Janeway lesions (embolic) - macular erythema of palms Septic emboli (pustular/pruritic lesions in legs) Roth spots - haemorrhages of conjunctiva
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What is the pathogenesis of varicose veins? What are the skin signs?
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Venous HTN due to incompetence between communications of major veins, leading to tortuousity Venous stasis eczema (chronic dermatitis) - has normal signs (scaling, itch, erythema) + dryness and brown pigmentation due to hemosiderin deposition from extravasation of capillary RBCs. This eczema is more prone to cellulitis Dilated surface capillaries (due to backflow) Lipodermosclerosus - progressive induration due to fibrosis, chronic inflammation, and pigmentation Atrophie blanche Venous ulceration - often after minor trauma
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How are varicose veins managed?
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Elevation + compression - reduces oedema + venous HTN Good skin care re: eczema Tx superinfections Rule out malignancy if appears indurated, rule out contact allergy if stasis eczema resists treatment Use moist wound healing techniques for ulcers Treat general health - obesity, smoking, HTN, lipids, anaemia
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What are the derm signs of hemochromatosis? What about liver cirrhosis?
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Hyperpigmentation (grey-brown, around face and exposed skin), hair loss, koilonychia, dry skin Can cause porphyria cutanea tarda (when iron levels inhibit uroporphyrinogen decarboxylase) -often initiated by liver damage: need to invx cause of this Pruritis, jaundice, Palmar + facial erythema, spider naevi, telengetasias, gynecomastia, striated/white nails, bruising, hair loss, nutritional problems
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What is the main derm sign of gluten insensitivity? How is it confirmed? How is it managed?
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Dermatitis herpetiformis - itchy vesicles, papules, and bullae on elbows, knees, and lumbosacral region Histopathology - classic granular dermal deposition of IgA Gluten-free diet (takes time to have effect) Dapsone (use in interim to control blistering lesions)
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What are the main cutaneous manifestations of inflammatory bowel disease?
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Pyoderma gangrenosum (esp w/ UC) - painful, ulcerative disease -begins as pustule, which breaks down into ulcer or ulcers -needs high dose prednisone or cyclosporin A -also assoc with SLE, RA, or haeme malignancies Erythema nodosum (inflammation of subcutaenous fat) -red, painful, indurated plaque/nodules in lower legs +/- fever, arthralgia -normally lasts 1-2wks, although if assoc with UC, can last months -has classic histopathology - biopsy is diagnostic -also seen in sarcoid, Strep, TB, Yersinia, drugs (OCP, sulfonamides), or paraneoplastic syndromes
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What is Alopecia Areata? What is the pathogenesis? What is the best indicator of severity?
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Discrete, often circular, hair loss that can occur anywhere on the body, with relapses and remissions -can cover whole scalp (alopecia totalis) or body (alopecia univeralis) -33% chance of spontaneous regrowth within 6 months; 50% within a year (hence watch and wait best initial approach). ~1/3 experience ongoing disease Inflammation of anagen hair bulbs, thought to be autoimmune and familial Severity at outset (only in adults though; children tend to worsen with time)
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What is androgenetic alopecia? When does it usually occur? What conditions might accelerate it? What can slow it?
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Change in hair growth with age - 95% of males, 55% of females. Usually genetic Highly variable, but usually after 30s. If happens earlier, tends to be more severe Anything assoc with androgen excess (e.g. PCOS) Anti-androgenic drugs (e.g. finasteride) - however, if these are ceased, all of the patients hair will fall out
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What is Trichotillomania? What is Telogen effluvium? What is anagen effluvium?
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Condition where pts compulsively pull out their hair (either due to psych disturbance, or similar to nail-biting) Where hair diffusely sheds from scalp - can be ID'd by white bulb -Acute - following childbirth, major surgery or illness, severe dieting, or ceasing OCP. Resolves after 3mts -Chronic - primary, idiopathic, or secondary to thyroid disease, malnutrition, cancer, TB, drugs, or iron-def anaemia. Lasts at least 6 months, can be permanent Hair loss during the Anagen phase, often rapid and severe -usually caused by chemo or X-rays/imaging -usually good recovery after insult ceased
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What are the two types of hair? What is hirsutism? Cause? Treatment? What do you need to distinguish it from?
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Terminal (coarse, more pigmented) and Vellus (fine, soft) Terminal hair in women is distributed in a male pattern -dependent on androgens -most commonly PCOS, but can be physiologic (as in menopause around the face) Anti-androgenic drugs Hypertrichosis - widespread growth of non-androgen dependent hair (e.g. from cyclosporin, phenytoin). Sometimes seen normally in pre-puberty; resolves with adolescence
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What are the clinical features of acne? Distinguish between the levels of severity What causes acne? In what 3 settings does it happen pre-pubertally?
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Mixture of pustules, papules, and comedomes (essential for Dx) Mild - as above Moderate - inflammatory with incorporation of deeper lesions, large pustules Severe - deep nodules, large pustules/cysts, significant scarring (which can be hypertrophic or atrophic) Genetics, androgens, blockage -> bacterial superinfection Infantile acne - 1st yr of life, usually resolves by 2yrs, almost exclusively male Pre-adrenarche (5-7yo) - due to adrenal androgens, which have a lesser impact on the sebacious glands Prepubertal (adrenarchal) - genetic predisposition, may signal more severe acne later on
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What conditions must you consider in someone with acne? How might you distinguish each?
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Acne rosacea - usually middle age, no comedones +/- flushing, telengectasias Folliculitis, boils - no comedones, sudden onset, not confined to face Peri-orofacial dermatitis - steroid induced rosacea, no comedones, normally around mouth + sides of nose Ketatosis pilaris - cheeks of young children, keratin plugs Tinea - occasionally pustular/nodular Tuberous sclerosis - firm fixed papules, no comedones or pustules
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Outline the treatment algorithm for acne Which lifestyle factors could exacerbate acne?
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1 Assess severity and impact on pt (incl psych) + investigate causes 2 Modify lifestyle risk factors - do they apply anything to their face, drugs, working environment, sports 3 Topical antiinflammatories, Abx, and keratolytics 4 Oral Abx 5 Hormonal treatments for females 6 Isotrenitoin (if severe nodulistic) 7 Specialist referral Lifestyle - anything greasy applied to face (makeup, sunscreen), working environment, humidity, picking lesions -Drugs - steroids, contraceptives, Li, Phenytoin -Dairy products, high sugar intake
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What should you investigate in acne? What are your 1st, 2nd, and 3rd line drug treatments for Acne? What are some sideeffects you might see?
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Not usually needed, but possibly investigate fungal causes, monitoring for systemic treatment, or androgen excess (e.g. serum testosterone in PCOS) 1 - Topical retinoid (e.g. trenitoin, isotrenitoin) -if papulopustular, add: Topical antiseptic, Antibiotic (clindamycin, erythromycin), OR Keratolytic (salicylic acid) 2 - Oral abx (tetracycline, erythromycin, minomycin [most effective]) +/- hormonal therapy (OCP, spironolactone) 3 - Isotrenitoin + Derm referral if 3 months of no response to 2nd line Topicals - irritation, itching, dryness, redness Doxycycline - photosensitivity, GI upset (esp if taken before bed), vaginal candidiasis (Use erythro if these AEs develop) Hormonal Tx - gastric upset, mood lability, weight gain, raised BP, breast tenderness, metrorrhagia
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How long should Isotrenitoin be given? What is the remission rate for people given the correct dose? What are the main AEs? In whom should Isotrenitoin not be given and why? What is the prognosis of Acne?
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9mts 85% Skin, mucosal, eye dryness Photosensitivity Epistaxis Myalgias, arthralgias, sport intolerance, headaches Increased serum lipids Teratogenic Lethargy, Depression (v rare though) Pregnant women - teratogenic People taking doxycycline - benign intracranial HTN Usually self-limiting and excellent response to medication (assuming pt willing to take Isotrenitoin)
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In whom is Rosacea most common? What are the clinical features? What are some associated conditions in Rosacea?
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People 30-40, familial, fair skinned. Happens in both sexes, rare in children Erythema, telengectasias, pustules, papules. NO comedones -first sign is easy flushing, often with burning/stinging/itching -may be photosensitive or exacerbated by creams -chronic condition - may last years ~50% develop blepharoconjunctivitis Children tend to develop recurrent chalazia Facial oedema can develop Rhinophyma - bulbous enlargement of nose - can occur
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What should you include in your differential of Rosacea? What are the aggravating factors for Rosacea?
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Sun damage - usually only has telengectasia Acne - has conedomes Lupus erythematosus - butterfly distribution, no pustules/papules Vasomotor flushing (menopause) Seborrheic dermatitis - scaly, erythematous, but not usually with telengectasias or pustules Heat, steam (e.g. showers), spicy food Alcohol Emotional stress Sun exposure Many skin care products (incl topical steroids, which induce a worse, rebound rosacea once withdrawn) -steroid induced can happen to people without Rosacea, although the distribution is slightly different
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How does Rosacea present in children? What drug should be used to treat children under 8?
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Teenagers - same as adults Pre-pubertal - one of: -Persistent redness + telengectasia of cheeks -Persistent papular rash around mouth, chin, and under eyes. Indistinguishable from peri-orofacial dermatitis Recurrent chalazia instead of blepharoconjunctivitis Oral erythromycin instead of tetracyclines
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How is Rosacea treated?
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Reduce aggravating factors Topical therapy - Metronidazole, Clindamycin, Erythromycin, Azaleic acid -BD until response, then Mane/Nocte. Response in 6-12wks Systemic therapy: 1st Doxycycline 2nd Erythromycin 3rd Low-dose Isotrenitoin (but refer to Dermatologist) Surgical - Laser or cold steel surgery (req Derm referral though)
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What portion of Aussies suffer from Atopy? What proportion experience childhood eczema? What causes atopic eczema?
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10-30% ~10% (most common reason for paed derm referral) Family history Immune dysregulation Abnormal epidermal barrier - 50% have defective filaggrin protein. Defensin abnormalities also common (predisposes to S aureus infx, S pyogenes in indigenous, pacifics) Environmental irritants Allergies
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What are the clinical features of Atopic Eczema?
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Itching, may be severe enough to wake patient multiple times/night Patchy, red, poorly defined rash in popliteal and cubital fossae and face Dry skin, Excoriation (from itching, scratching) Lichenification (thick skin + attentuated white lines) Crusting + Weeping due to infx Micropapular variant possible in babies - can create transient hypo or hyperpigmentation Distribution varies by age of child -face in babies, moves to arms + legs when they crawl (characteristically flexor surfaces). Can be discoid
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How is Atopic Dermatitis treated non-pharmacologically? What advice do you have for taking baths in eczema? What about moisturiser use?
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Explain chronicity -Disease non-curable; treatment similar to asthma -Establish a daily routine -Inform that disease should reduce in severity as time progresses: many no longer symptomatic by school Lifestyle modification - avoid: -Wool blankets, synthetic fabrics (e.g. lycra) -Soap, shampoo, bubble baths, hot baths -Sand -Cold, dry (mid-winter) type weather Wet dressings - for acute flareups Avoid hot or soapy baths, but otherwise fine (esp if dispersible oil is added) Use 1-3x daily (depending on skin dryness). Ensure greasy enough for adequate moisturisation, non-perfumed, and does not sting
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When should you investigate eczema further? What things might help chronic superimposed infections? Will allergy testing help pts with atopic eczema? In any case, how do you test for allergies? What counselling should be given related to this?
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Crusting or weeping - swab for S aureus (or Group A S epidermis in ATSI/Pacifics) Antiseptic bath oils (triclosan) or chlorine bleach Only in-so-far as they learn and avoid their allergies: it won't help their eczema. This is because patients mistakenly blame their allergies for eczema, when in reality impaired skin defences make patients more susceptible to allergies. Antihistamines are an option for severe allergies RAST or Skin testing (indirect measure of IgE by measuring histamine: -important not to take antihistamines within 1 wk of this testing) -important to counsel patient that allergy reduction won't affect eczema
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How is atopic eczema treated pharmacologically? What is the role of antihistamines? What about oral steroids? What are the indications for Derm Referral?
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Topical anti-inflammatories (typically steroids) -Topical immunomodulators also effective; main benefit is that they have the same effects as steroids, but do not produce cutaneous atrophy Limited in atopic dermatitis, but great for hypersensitivity reactions/allergies (e.g. urticaria, angio-oedema) -can be sedative in some patients, although can also create hyperreactivity in children and are not recommended if <12 No role. If refractory to above, refer to Dermatologist who will look at alternative systemic immunosuppressants Non-compliance (often due to fear or topical steroids), chronic infections, allergies, severe
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What are the AEs of topical steroids? What proportion of a topical steroid is absorbed systemically? What is your maximum potent topical steroid? 2nd most? What are some good first line options (mild potency) Good second line options?
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Minimal - but if they occur: -Irritation/stinging (caused by alcohol in the cream), atrophy causing striae/bruising/visible veins, redness, telengectasia, peri-orifacial dermatitis, masking of infections (esp tinea), glaucoma/cateracts if applied to eyelids -all except striae are reversible About 10% - rises if inflamed or thin skin -Clobetasol -Betamethasone dipriopionate 0.05% optimised vehicle cream -Betamethasone 0.02% cream, Triamcinlone 0.02% -Methylprednisone, Betamethasone creams
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How do you select a good topical corticosteroid? Outline when you would use a Superpotent, Highly potent, moderately potent, and mildly potent topical steroid
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Consider skin being treated - is it inflamed, thin Consider severity of the disease Withdraw medication during remissions, even if they are brief Superpotent - lichenification, nodules (v thick skin) -additionally, use in severe disease for up to 2 weeks to reduce severity, then reduce to less potent version Highly potent - Palms, soles, elbows, knees (thick skin) Moderately potent - Trunk, limbs Mildly potent - genitals, face, flexures (thin skin)
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What are the two forms of Seborrheic Dermatitis? What is the treatment for each?
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Infantile -presents within 3 mts, non itchy but covered in greasy scale -can become superinfected -1/3 self-resolve within weeks. Tx same as atopic derm + add antifungals if needed Adult -chronic, not seen before adolescence. Relapsing-remitting pattern -distribution usually involves central face, brows, eyelids, chest, flexures, and genital area -more severe during stress, HIV, or with neuro conditions -Tx same as atopic + antifungals. Weak tar cream can help
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What is Asteatitic Dermatitis? What things can aggrivate it? What is stasis dermatitis? How is each managed?
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Itchiness from dry skin, often in legs but can generalise in elderly. Not actually inflamed, unless superinfection -drugs e.g. (statins, diuretics), hypothyroid -avoid soap, moisturise 2x/day Dermatitis due to varicose veins - presents as dryness, scale, brown hyperpigmentation (hemosiderin deposition?) + exacerbations of cellulitis, superinfection, oedema, and swelling -fix les veins, treat cellulitis (elevate, compress), wet compress if wounds/ulcers
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What is Nummular (discoid) Dermatitis? What ages affected? Why does lichenification happen fast in this dermatitis? How is it managed?
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V itchy, round, well-defined plaques almost always w superinfection (if acute and untreated) Any, including young children. In adults, may be during times of stress V itchy, so heaps of scratching Same as atopic eczema, however potent steroid usually needed intially (even injected hydrocortisone, given the severity of lichenification). Wet dressings and Abx for superinfection may be handy
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What is Pompholyx? How is it managed?
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Dyshidrotic eczema - vescicular or bullous dermatitis affecting palms, sides of fingers and feet, with unknown etiology (although worse during stress) -tends to occur in acute flare-ups Same as atopic dermatitis -potent steroids needed initially +/- Abx, wet dressings -Rest often needed given locations of lesions -may require oral prednisone if severe - refer dermatologist
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What is pityriasis alba? How is it managed?
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Common paediatric cause of facial dermatitis causing hypopigmentation - asymptomatic white, poorly-defined patches on the face, usually most evident when skin is darker (i.e. summer) -resolves spontaneously by puberty Often confused for vitiligo or pityriasis versicolor Same as mild facial atopic dermatitis -once treated, sun exposure will return the pigment
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What is Impetigo? What things make someone/skin prone to Impetigo? How might the presentation of S Aureus and S Pyogenes differ? How is it treated? What is Ecthyma
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"School sores" (although can be any age) - highly infectious skin infx Skin - Insect bites, superficial injuries, eczema General - Moisture, close contact, poor hygiene S aureus - most common, yellow, crusty lesions, irritative (although not painful). Bullous impetigo exclusively S aureus S pyogenes - more common in ATSI/Islanders. Ulcerative lesions exclusively S Pyogenes. May cause Glomerulonephritis within 8 weeks Treat for Staph Aureus unless culture suggests otherwise - topical Abx (Mupirocin good. Non-multiresistant MRSA may need TMP-SMX or clindamycin) Deeper infection caused by Impetigo
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How is the spread of Impetigo reduced? What is the cause of recurrent/resistant impetigo?
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Cover affected areas + keep children away from school until crusts dry Use separate bath towels + launder daily in hot water Moist compresses 10min 3x/day + removal of excess crust Nomally chronic carriage of Staph aureus - confirm with nasal or perianal swab (depending on lesion locations) -if (+) treat whole family + close contacts for 7days w 2% intranasal Mupirocin Nasal Ointment 2x/day PLUS antiseptic wash for 1mt -Clothes, towels, sheets need hot water washing during this period -2nd line: Rifampacin + flucloxacillin
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What is folliculitis? What causes it? What are the other differentials? What are some initiating factors? How would you treat?
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Inflammation of the hair follicle - the clue is that pustule/papule tends to occur on a hair follicle (may not be obvious) -bacterial, physical. Also fungal (e.g. dermaphytes, Pityrosporum) Malaria rubra (heat rash), insect bites - don't centre on a hair follicle Shaving, waxing Swabs can guide Abx therapy, addressing initiating factors is worthwhile S aureus nasal contamination may require treatment
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What is a boil? What conditions might resemble boils? How is it treated? What is a carbuncle? What are some complications of boils? How are fluctuant pointing lesions treated?
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Deeper form of folliculitis - termed Furuncle Ruptured epidermoid cysts, cystic acne, hidradentis suppurativa (if axilla/groin involved) Same as folliculitis if staphylococcal, but need to exclude other organisms with swabs (incl nasal) If pseudomonal, find source (e.g hot water tank, toys) and cease contact until treated May req drainage or systemic Abx Multiple furuncles which coalesce. More assoc with sinus tracts, and can lead to signs of systemic inflammation -uncommon in childhood Abscesses, fistulae, bacteraemia, rupture, depressed scar, secondary spread -drainage under local anaesthetic
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What is Paronychia? What are the two types? What is the treatment?
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Infx of Paronychium (nail bed) Acute - usually S aureus Chronic - rarely infective (more chronic irritant, although sometimes this irritant is C albicans) Drainage + topical mupirocin
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What is cellulitis? How does it differ to Erysipelas? What are the main underlying causes which precipitate the above conditions? What are the most common locations of cellulitis?
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Infx of subcutaneous fat + dermis - characterised by swelling, pain, heat with spreading, macular, tender erythema Erysipelas is more superficial, well demaracted (main distinguishing feature), with lymphadenopathy, and more prominent streaking -may be preceded by high fever + skin changes Lymphedema, inflammation (eczema, tinea, HSV), wounds, poor circulation, chronic sinus infection Lower leg Periorbital (esp in children)
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What organisms most commonly cause cellulitis? How is it treated?
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Group A Strep Pyogenes (if spontaneous) Staph Aureus (if from a wound) Culture can confirm, some rarer organisms are implicated -blood cultures can even be (+) if high fever Oral Abx usually adequate IV Abx may be needed if severe/spreading B-lactams generally used, may need to add Flucloxacillin to a penecillin if wound infx present -Give special consideration to animal bites, post-surgical cases, burns, and immunosuppressed patients -Consider low-dose prophyactic Abx in people with lymphoedema and recurrent cellulitis
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What is the most common organism implicated in pre-pubertal genital infection? How does strep perianal dermatitis present? How do you treat genital infx?
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GAS (often from throat) Persistent perianal eruption - itchy, tender, may be complicated by painful fissuring. Usually well defined erythema, with scaling or weeping, that may extend a few mm from anal verge. May bleed or discharge Swab to get sensitivities Oral Abx - full 10 day course must be adhered to, or recurrence common +/- topical mupirocin Residual dermatitis is common and can be treated with steroids - do swab before initiating 2nd course Abx
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What is the cause of warts? How quickly do warts spontaneously resolve in children? What are you thinking if a child has genital warts? What are your differentials when you see warts? How are warts treated?
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HPV - hence why warts are infectious, and can cause other warts in the same area -Note: incubation period ~2yrs Usually about 2yrs, regresses as immune system recognises causative virus and eradicates it Consider sexual abuse, but usually caused by transmission during delivery Bowen's disease, SCC, seborrheic keratitis, corns, calluses Pearly penile papules (female equivalent - papillomatosis) Depends on wart, patient factors. Treat when distressing pt -Topical immunotherapies good, esp for genital -Cryo, cautery, laser can work -Topical trenitoin Warts often recur, regardless of how treated
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What causes Molluscum Contangiosum? Where do lesions occur? What do the lesions look like? What are the two age peaks? What might Poxvirus cause in immunocompromised pts?
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DNA Poxvirus - fairly contageous (usually acquired from family members with whom they swim/bath) Anywhere on the body Typical - pearly papule with central umbilication w core which can be expressed by applying firm pressure either side -if there is surrounding inflammation, indicative of host immunity and thus impending resolution 3-9yrs and 16-24yrs -location varies, because of normal cause -children - lesions on body, under armpits -adolescents/adults - lesions on genitals (STI) Giant molluscum contangeosum
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Is biopsy/histopath warranted in Molluscum Contangiosum? How might you distinguish this condition from Verucae and Herpes? How is molluscum treated?
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Only if immunocompromised - to exclude cryptococcosis + histoplasmosis Verucae - lack central umbilication HSV - rapider onset, tender, only transiently umbilicated Usually spontaneous resolution within 2 yrs. May cause atrophic scarring, or be complicated by dermatitis or bacterial infx Showering may reduce spread, as it is waterbourne Imiquimod only topical therapy with much efficacy - only really used if significant interference with life
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What are the most common viral exanthems? How do viral exanthems appear generally? What are some exceptions?
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Coxsackie or Echovirus (ententeroviridae) - due to immunisation against Rubella, Measles, VZV Usually bilaterally symmetrical with facial confluence Peripheral papular eruptions are mainly on arms + legs +/- mild fever, diarrhoea, -Parvovirus - Slapped cheek rash + on limbs -Hand-foot-and-mouth - vesicles on hands + feet + oral ulcers -Roseola - transient rash, appearing as a fever breaks + lymphadenopathy -Pityriasis rosea - single, scaly herald patch followed by multiple ovoid red macules w peripheral scale on trunk
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For Hand-Foot-and-Mouth Disease (Coxsackie A16): -Age? -Incubation Period? -Presenting features? What are some differentials? What is the treatment?
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<5yrs usually 4-6days Px - small, uncomfortable mouth lesions followed by red macules 5-7mm on hands and feet (occasionally extra-acral). Lesions resolve within 10 days without crusting or scarring Consider - Enterovirus 71 (can be serologically tested), Herpetic stomatitis, Aphthous ulceration, Herpangina, E multiforme, and scabies No specific Tx, although isolation for days 3-7 recommended (this is the contageous period) Symptomatic treatment may be warranted - paracetamol, hydration. Acyclovir if severe
