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122 Cards in this Set
- Front
- Back
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comedones, papules, pustules, cysts from inc in sebum causing abnl keratinization and bact overgrowth from inc in sebum causing abnl keratinization and bact overgrowth
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Acne vulgaris
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Recurrent boils and abscesses (more severe then nl acne) in axilla, anogenital, under breasts RF: female, obese- chronic, progressive, scarring
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Hidradenitis suppurativa
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Follicular inflammation resulting in scarring so develop patches of alopecia Variant of acne vulgaris; most common in AA men; on spectrum of acne but more severe
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Dissecting cellulitis of the scalp
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Fine papules, micropustules, and scale (may look like a rash b/c papules are so tiny) on mouth, nose, eyes Females 20-45 yoaCauses are hormones, seborrhea overlap, cosmetics, corticosteroid use, multifactorial
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Perioral dermatitis
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Flushing, redness, edema, telangiectasias, papules, pustules, nodules, and plaques (comedones are absent) on central face +/- ocular involvement >30 yoa; caused by sun induced vascular damage, inflammatory response to vascular changes, genetic predisposition, possibly infection (dermodex mite – will do scraping if see pustules)aggravating factors – spicy foods, etoh, heat, emotional stress
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Rosacea
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Acute phase: pruritis, erythema, edemaChronic phase: thickening, lichenification, scaling From hyperirritability of skin
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Eczema
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Erythema, pruritis, dryness and scaling, oozing and weeping, excoriations and fissures, lichenificationInfants – face, scalp, ext surfaces, not on diaper area)Kids: flexures (inside of elbows)Adults: eyelids, hands, extremities (more diffuse)AA: more popular, follicular prominence, post-inflam pigmentation Onset is early in life c + fam h/o atopy (asthma and allergic rhinitis)From exaggerated response to enviro antigens (humoral-mediated immunity) that causes inc IgE, eos, and mast cells (release histamine and cause itching)
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Atopic dermatitis
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Prominent follicular papules on lateral arms, legs, and cheeks Improves c age; common in atopic pt’s
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Keratosis pilaris
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Thick, rough plaque that is lichenified From chronic rubbing that causes skin thickening
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Lichen simplex chronicus
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Temporary loss of pigment on face and extremities In atopic kids and young adults
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Pityriasis alba
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Prurigo nodules
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Excoriated papules
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Dry rectangular scales usually on extremities Inherited disorder of keratinization; usually assoc c atopic hx
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Ichthyosis vulgaris
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Pt loses subcutaneous fat and makes skin really dry
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Asteatotic eczema
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1-5 mm vesicles (clear/white) on palms, lat fingers, and soles H/o atopy, sudden onset and pruritic
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Dyshidrotic eczema
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Acute onset of vesicles, weeping, intense pruritis, and erythema; LINEAR lesions (will follow linear arrangement) Actual immunological response to poison oak, poison ivy, sumac, cashew nutshell, mango rind20% of contact derms
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Allergic contact dermatitis (rhus dermatitis?)
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Insidious onset, chronic, erythema c scale and excoriations; dryness and fissuring; hands most often involved 80% of contact derms; nickel, neomycin, balsum of peru, fragrances, preservatives; from repeated contact causing disruption of skin barrier
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Irritant contact dermatitis
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Hyperpigmentation (tend not to go away), xerosis, fissures, ulcers Assoc c varicosities and edema
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Stasis dermatitis
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All ages; affects skin, nails, joints; cause is inc turn over and rate of prod of skin cells (3 day maturation instead of nl 28 d maturation); + genetic influence; from inapprop T-cell activation (T1 Tcells or CD8 cell driven à cytokine release causes epidermal hyperplasia, neutrophil infiltration, and vascular changes); often in areas of trauma; dilated blood vessels produce redness and bleeding points
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Psoriasis
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Tan/fawn colored 2-10 mm oval lesions c collarette of fine scale (surrounded by v fine scale) in Christmas tree appearance; preceded by Herald Patch (big lesion that comes 1-2 wk before dz); on trunk and proximal extremities Viral infection; inc in spring and fall; 10-35 y/o’s
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Pityriasis Rosea
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Flat top, pruritic, planar, polyangular, pink-purple papules c fine lacey scale (5P’s) usually on distal extremities (wrist/ankles), oral and genital mucosa, nails; white reticular lines on top of plaques (Wickham’s straie) Inflammatory rxn of unknown etiology; more common in women
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Lichen planus
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Greasy adherent scale; Head, neck, axilla, public areas (on scrotom and glans) Infancy through adulthood; ST’s due to pityrosporin ovale colonization (yeast overgrowth); genetic and environ factors; affects areas high in sebaceous glands
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Seborrheic dermatitis
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Hr to days after starting drug; sudden onset of pruritic lesion; mostly on trunk and extremities; +/- fever, conjunctivitis, edema; NO LAD Hypersensitivity; RF for drug rxn: 1. female2. advanced age3. multiple drugs4. HIV5. + fam hx (possibly)Precipitating medications – ABX, anti-inflammatories, antiepileptics
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Drug eruptions
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red lesions <1 cm that can be flat or raised; onset 7-10d; on trunk and extremities; lasts 1-2 wk Most common of the drug eruptions
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Maculopapular drug eruption
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Edema “leaking” into tissue that is causing elevation Aspirin, PCN, and blood products (onset is 4-21 d)
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Urticarial drug eruption
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Mimics lichen planus (Flat top, pruritic, planar, polyangular, pink-purple papules c fine lacey scale); generalized eruption (onset is wks-yrs) Gold and antimalarials
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Lichenoid drug eruption
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V few (2-3) sharply demarcated dusky red plaques that p/w itching and burning initially; fades to brown pigmentation and recurs in the same areas; min-hr after drug admin; common on genitals (esp glans) Aspirin, tetracycline, nsaids
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Fixed drug eruption
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Skin eruption (urticaric) c fever, joint pain, inc liver enzymes; fever, rash, internal organ involvement (liver most common) More immune mediated rnx (possibly); don’t have to have prev exposure; caused by dilantin and tetracycline family
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Drug hypersensitivity
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Target-like lesions on skin and mucous membranes (20% of time); symmetrical acral (palms and soles) distribution; discrete macules progress to edematous papules c periphery of erythema Caused by meds and infections (HSV); mild or no prodrome
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Erythema Multiforme
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Larger, atypical target lesions and blisters; must involve ≥2 MM; febrile prodrome and diffuse distribution Antiepileptic and antibiotics; occurs at all ages
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Stevens-Johnson
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Pain, erythema, and rapid exfoliativ skin loss; >30% of body surface involved More severe then SJS; occurs at all ages; antiepileptics and antibiotics
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Toxic Epidermal necrolysis
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Crops of red-purple papules, nodules, and blisters on LE; +/- fever, malaise, arthralgias; 20% involve other organs; “palpable purpura” Leakage of fluid from vessels; triggers are drugs, infections, connective tissue dz, and malignancies; LE involvement because gravity
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Vasculitis
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Purpuric lesions on legs and buttocks; abd pain, arthralgias, and hematuria Preceded by strep or viral URI; 25% will develop hematuria and need to be followed for glomerular dz; primarily affects males 4-8 yrs
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Henoch-Scholein Purpura
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Brown-red pinpoint macules (“cayenne pepper” spots) - nonpalpable; lower extremities; discoloration will persist Localized capillary dz (not true vasculitis b/c only involves superficial vessels); men more women; no systemic involvement
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Schamberg’s Dz
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From drug eruptions, viral exanthems, insect bites, food allergy (autoimmune response lasting <6 wk)
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Acute urticaria
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Lesions lasts <24 h; reoccurring lesions >6 wks Think about inhalants, ingestants, injections, infections, and internal dz
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Chronic Urticaria
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Erythematous, tender deep nodules on LE Reactivity to infection or drugs1. infections – strep, hep B, fungal2. chronic dz – sarcoid, colitis3. drugs – OCP, sulfa
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Erythema nodosum
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Annular papules and plaques s scale c firm, raised edge; common extremities (tinea corporis will have flat edge); most common on acral sites; may have central clearing Unknown etiology; can be chronic; assoc c DM; affects females more then males
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Granuloma annulare
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Violaceous patches on shin c yellow-brown waxy surface; atrophic plaques; won’t go around to back of leg (stays localized to calf) 50% occur in diabetics
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Necrobiosis lipoidica
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Thickened velvety hyperpigmented skin on body folds (axilla and flexural neck most common); gradual symmetrical onset Usually the result of insulin resistance in overwt individuals; extensive involvement and sudden onset more common c malignant type (type V)
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Acanthosis nigricans
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Tan to brown macules/patches (non palpable); larger then freckles >6 macules > 5mm is suspicious for neurofibromatosis; present at birth and inc in childhood
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Café Au Lait Spots
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Café au lait spots, axillary freckling, and neurofibromas; CNS, eye, renal, and skeletal system involvement Inherited disorder; equally affects males and females; found in birth/early childhood; neurofibromas can be segmental and SQ
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Neurofibromatosis
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Skin findings only if discoid lupus; scalp, face, ears (sun exposed sites) most common; well defined red plaques c scale; follicular plugs are common; will develop atrophy and scarring; can get permanent alopecia; “burned out” lesion will have no scale but perm hypopigmentation Most common cutaneous form; peaks at 30-40 yrs; <10% have systemic involvement; more common in females and AA; exacerbated by UV light
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Cutaneous lupus
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Skin lesions of ears, nose, cheeks, and upper trunk; papules, plaques, nodules around resp tract (around nose, mouth, eyes); scarring look and atrophy may look like lupus; fever, fatigue, wt loss; primarily lung involvement (but may involve any organ) Unknown etiology; systemic granulomatous dz; common in AA, women more then men
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Sarcoidosis
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Vascular and sclerotic changes of skin and internal organs (lungs, heart, and GI) Multisystem disorder of connective tissue; localized and systemic involvement 1. physical therapy2. protection from cold and trauma3. topical steroids and nitroglycerin (vasodilates)4. CCB (nifedipine) – for Raynauds5. corticosteroids and immunosuppressants6. ACEI (captopril) – for renal dysfnx causing a hypertensive crisis
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Scleroderma
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Ivory-pink plaques c violaceous borders usually on trunk that heals c atrophy Localized scleroderma; will not progress to systemic form; Children and adult
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Morphea
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Raynaud’s c pallor, cyanosis, and rubor; nonpitting edema of hands and feet; hard, bound down, waxy, and atrophic skin; flexure contractures, loss of facial skin lines, and digital ulcerations; heart, lungs, GI, kidney can be involved Affects adult women most commonly; ANA always +
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Systemic scleroderma
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Calcinosis cutis; Raynauds, Esophageal dysfnx, Sclerodactyly, Telangiectasia Limited systemic involvement; hardening of skin (scleroderma) limited to face and hands; + ANA
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CREST variant (Limited scleroderma
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Photodistributed skin changes; symmetrical proximal ms weakness; skin findings procede ms sx; flat violaceous papules on dorsal fingers (Gottron’s papules), periorbital red-purple edema (heliotrope), periungual erythema, telangiectases, thrombosed capillary loops Inflammatory dz of skin and ms; 2 peaks – 1 at childhood and 2 at adults (40-65 yoa); women>men, AA > whites
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Dermatomyositis
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Chronic pruritic dermatitis; vesicles on elbows, knees, scalp, and buttock (often won’t see blisters); severe itching and burning; remissions and flares common 20’s-50’s yoa; usually in whites; uncommon; IgA autoantibodies; assoc c gluten-sensitive subclinical enteropathy (Celiac’s dz?)
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Dermatitis herpetiformis
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Skin and MM involvement; Nikolsky’s sign (skin separates s blister being present c little pressure being applied) Autoimmune blistering dz that can be fatal; pt produce intercellular IgG antibodies; causes separation of cells within the epidermis forming blisters
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Pemphigus
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Subepidermal blister on flexures of extremities and lower trunk; tense bullae form, rupture, and heal; initially resembles urticaria; blistering is underneath basement membrane Most common blistering condition; IgG basement membrane autoantibody; affects males/females >60 yoa; may be assoc c malignancy
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Bullous Pemphigoid
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Abnormalities of heme synthesis (rbc synth); involve bone marrow or hepatic heme synth; enzy deficiencies cause accumulation of intermediate metabolites (porphyrins) which prod cutaneous and systemic sx
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Porphyrias
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Skin fragility c blisters; no hypertrichosis or dyspigmentation Usually medication induced (NSAIDS and tetracycline) or tanning beds; porphyrin levels nl
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Psuedoporphyria
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Red-brown plaques c fine scale in warm, moist, intertriginous areas; will shine coral-red c wood’s lamp Corynebacterium
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Erythrasma
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Plantar pits on wet, sweaty, malodorous feet Micrococcus sedentarius and Corynebacterium 1. benzoyl peroxide or Al Cl drying agents2. erythro or clindamycin topical abx3. rarely will need oral abx
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Pitted Keratolysis
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Prodrome followed by eruption of tender vesicles on erythematous base; vesicles may look white/pustular if on thicker skin like palms Triggers – UV exposure, abrasions, chapping, stress; will see multinucleated giant cells c Wright stain on a tzanck smear
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HSV 1 and HSV 2
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Vesicular eruption along a dermatome (usually on face and trunk) Reactivation of varicella virus; affects all ages; RF for reactivation are age, immunosuppression, readiation, stress, and exposure to chicken pox; tzanck smear will confirm
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HZV
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Common – rough, grayish, dry papules often in groups; hands, feet, and acralFlat – thin, flat, flesh-colored papules; face, arms, and legsGenital – lobulated, cauliflower-like papules DVA virus that infects epidermis only; peaks in childhood and early adulthood; enters through defect in skin barrier via direct contact or autoinoculation; RF are young age, sexual activity, and immunosuppression
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Warts
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Smooth, pearly, dome-shaped papules c umbilicated center; multiple lesions In children and sexually active adults; called “water warts”
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Molluscum
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invasion of hair shaft, inc in kids and AA and latinos, occipital LAD commonCruris is in postpubertal males, incidence inc in summer and c sweatingOnychomycosis increases c age and immunosuppressionDXHair – KOH and cx of hair shaftBody – KOHNails – KOH, cx, and PAS stain
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Tinea
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Multiple oval pigmented macules c scale on trunk, neck, upper arms Pityrosporum (Malassezia) – lipophilic yeast that overgrows; affects adolescents and young adults; KOH prep shows spores and hyphae (spaghetti and meatballs)
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Tinea Versicolor
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Red, moist, glistening plagues c satellite lesions Nl flora or mouth, vagina, GI track; overgrowth causes infection; RF of overgrowth are preg, OCP, abx, steroids, DM, skin breakdown, immunosuppression
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Candidiasis
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Extremely pruritic papules and burrows of fingers, wrists, elbows, axilla, and genitalia; head and neck if pt is infant or immunosuppressed Burrows into upper layer of skin and deposits eggs; inc in sexually active young adults; Sx are 4-6 wk after exposure; dx c scabies prep (avoid KOH)
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Scabies
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Capitis – headCorporis – body (hair bearing ares like axilla, pubis, beard, and eye lashes)Phthirus Pubis - pubic Head – typically in kids; girls>boys; highly contagious; 7-10 days for eggs on hair shaft (NITS) to hatch; immature eggs not affect by tx
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Pediculosis
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Cluster of papules on legs; pruritis depends on sensitivity
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Fleas
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Hookworm larvae H/o travel v important clue (Caribbean, S and central America, SE US)
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Cutaneous larva migrans
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Superficial pigmented lesion c stuck-on appearance; fresh-dark brown in color; trunk most common area; usually will have many of these (so less likely to be melanoma or wart) Hereditary influence; common after 50 yoa
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Seborrheic keratosis
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Flesh colored/tan papules on stalk; soft; on flexural sites, inguinal areas, under breasts More common in overwt individuals
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Skin tags
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Firm raised lesion c smooth surface; initially red and gradually whiten; usually on upper chest and back, shoulders, and earlobes Caused by exuberant healing rxn following trauma (surgery, acne, body piercing)
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Scars
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May be darker around edges, dimple sign; most common on extremities From localized area of scar; possibly a rxn to shaving (ingrown hair rxn?)
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Dermatofibroma
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Milia – faceEpidermal – face and trunkPilar – scalpMucoid – fingers and toesMucosal - oral Occluded sebaceous glands that are NOT inflamed
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Cysts
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Multiple white/yellow papules on forehead and cheeks (resembles BCC) Overgrowth of sebaceous gland; common after 30 yoa
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Sebaceous hyperplasia
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Multiple 1-2 mm white/yellow papules (no central depression); symmetrical on lower eyelids; confused c flat warts Sweat gland tumors – benign
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Syringomas
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On eyelids Cholesterol deposits
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Xanthelasma
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1. stork bites – 25-30% of newborns, less pronounced then port wine2. port wine stain - .3% of newborns Caused by extra vessels of low or high flow; will persist
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Vascular malformations
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Vascular tumor; occur c/in 1st yr of life; slowly involute over years; more common in girls and preterm; 1-3% of infants
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Hemangioma of infancy
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Dome-shaped papule; red/purple; easily blanch; can bleed if raised and nicked Common in preg and >30 yoa
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Cherry angioma
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Dome-shaped papule; red/purple; easily blanch; can bleed if raised and nicked Common in preg and >30 yoa
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Cherry angioma
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Central red papule c radiating legs; commonly on face and upper trunk; blanch c pressure Seen in 15% of kids
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Spider angioma
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On sun exposed sites, easy to blanch Dilatation of superficial vessels; inc incidence in preg, etoh abuse, skin ca, connective tissue dz, and rosacea
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Telangiectasia
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Vascular papules on scrotom and vulva Possibly from inc venous press; may inc c pregnancy; appear in midlife
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Angiokeratomas of Fordyce
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Larger then angiokeritinomas; on sun-exposed sites (lips v common) From localized venous dilatation
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Venous lake
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Vascular papule that bleeds easily (very raised papule) Increased vascular response to injury; common kids and young adults
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Pyogenic granuloma
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Melanocytic, pigmented, common, congenital, acquired, giant congenital, becker’s nevus (starts at adolescents), nevus spilus (lots of tiny ones together), spitz nevus, halo, blue, nevus sebaceous (malig potential to BCC) Skin tumors composed of melanocyte-derived cells (does not imply malignancy); def is growth of normally occurring cells or tissues
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Nevi/mole
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On sun exposed sites; may inc in size and darken during puberty and preg; lighten and disappear in elderly Most occur by age 30; changes in moles after 40 yoa are suspicious; most adults have 10-20 moles
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Common mole
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Rim of hypopigmentation around nevus (halo can repigment) Most occur in adolexcence; can occur in vitiligo and melanoma
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Halo nevi
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Larger irreg shaped nevi, variegated color and irregular elevations Can be familial or sporatic; can occur in early childhood; heterogeneity of lesions; inc risk of melanoma
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Atypical nevi
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Damage to epidermal causes atrophy, wrinkling, pigmentary alterations; damage to dermis causes loose skin and yellowing Caused by UVA and UVB; fair skin pt’s are increased risk
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Photoaging
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Localized area of hyperpigmentation; they are freckles in kids and adult lentigines tend to be larger then freckles Common in caucasians
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Lentigo
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Red macule c surface scale; often sx to pt (pt can feel scale and is often tender); most common on sun exposed sites from localized areas of sun damage; 10-15% turn into SCC; inc after 40 yoa
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Actinic keratosis
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Several varieties: nodular, superficial, morpheaform, pigmented (most common below the neck)Usually hits head and neck (central face most commonly) Most common skin caIntrinsic RF: fam hx, gene defects, blonde/red hair, fair complexion, blue eyesExtrinsic RF: accumulated sun exposure, immunosuppressionSolar risk: marked freckling of upper back and shoulders, ≥3 blistering sunburns under 20 yoa, ≥3 yr of outdoor summer jobs as a teen, inhabitant of southern US
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Basal Cell Carcinoma
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Head, neck, arms and lower legs (in females)More common then BCC in immunosuppressed individualsKeratoacanthoma – 1-2 cm dome shaped nodule; sudden onset of rapidly growing lesion Bowen’s dz – in situ lesion; can look like eczemaKeratoacanthoma – low grade SCC; RF’s are the same as BCC2nd most common skin ca
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Squamous cell carcinoma
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Most common sites are back (males) and legs (females) RF: fair skin, presence of atypical nevi or >50 pigmented nevi, personal or fam h/o melanoma, blistering sunburn (esp <21), accumulated sun exposure, outside jobs, reg use of tanning booths (1x/mo)
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Melanoma
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Premature loss of scalp hair; shorter, smaller hairs; males – crown and all but occipital fringe; females – gradual thinning, wide part lines, retain frontal hair line Men=women; genetic and hormonal factorsMen: onset after puberty, bitemporal recession progressing to frontal and vertex loss, + fam hxFemales: after puberty
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Androgenic alopecia
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Temporal losses? More common in AA; women>men; can lead to perm alopecia; from keeping hair pulled back tightly
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Traction alopecia
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Diffuse loss (<50%) Occurs 2-4 mo after insult; causes are physical and emotional stresses (pregnancy) and/or drugs (anticonvulsants)
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Telogen effluvium
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Hair shaft thins and breaks Sudden hair loss from chemo; onset after 1-3 wks
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Anagen Effluvium
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Will have various length hairs and irregular and bizarre patterns Any age pt; OCD
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Trichotillomania
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Sudden loss of hair in defined areas, can affect all body hair (most often scalp, eyelashes, beard); spontaneous regrowth areas in milder forms Autoimmune rejections; peaks 15-29 yoa; assoc c vitiligo and thyroid dz and DM1 (may check free t4 and TSH levels); males = females
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Alopecia areata
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Post inflam: in dark skinned pt’s, trauma induced Drug induced: nonphysio pigment; gray and blue common; Minocycline*Melasma: from UV exposure, genetic or hormonal factorsOther: diet or endocrine
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hyperpigmentation
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Post inflam, pityriasis alba, burns, halo nevus
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Hypopigmentation
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On extremities – “raindrops” of lighter areas Caucasians; women>men; genetics; photo damage; >50yoa
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Guttate hypomelanosis
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Presents as v superficial bact skin infection (intraepidermal) on the face that begins c formation of vesicles/pustules in epidermis; lesion eventually ruptures and releases a honey-colored liquid, which forms a yellow/brown crust S aureus>s pyogenes (GAS); both may be present though (bullous impetigo caused by staph); common in early childhood; v contagious; not assoc c pain or constitutional sx
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Impetigo
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Vesicle that progresses to a punched-out ulcer, surrounded by a violaceus border and covered by an adherent crust; usually on LE S pyogenes; Deeper form of impetigo
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Ecthyma
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Looks like ecthyma Pseudomonas bacteremia and occurs in neutropenic pt
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Ecthyma gangrenosum
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Begins as red spot; imflam spreads and it becomes tender, warm, glistening, red, edematous, and indurated area of skin; fever and leukocytosis common; vesicles or bullae possible; skin desquamation occurs as healing begins; Often on extremities or face, also in areas of lymphatic obstrx S pyogenes; RF are nephrotic syndrome, venous stasis, DM; entry portals are ulcers, local trauma or barasion, psoriatic or eczematous lesions, fungal infection
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Erysipelas
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Erythema, warmth, swelling/induration, local pain/tenderness; commonly have lymphangitis c regional LAD and F/C and malaise (flu-like); systemic toxicity and bacteremia can occur S pyogenes or S aureus; superficial infection that involves epi, dermis, and connective tissue; entry portal is through local trauma or skin lesions (ulcers, furuncles, tinea)
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Cellulitis
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- Post CABG vein harvest leg + ipsilat tinea pedis: unilat cellulitis- Post-pelvic radiation: bilat- Post-mastectomy c LN biopsy: unilat
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Recurrent cellulitis 2º to chronic lymphedema
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Small, tender erythematous papules topped by a central pustule; on face, buttocks, or extensor surface of an extremity S aureus; bact infection that involves ostium of a hair follicle and apocrine glands
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Folliculitis
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Pruritic, +/- tender, papulourticarial lesion (c/in 48 h of exposure) that will turn into pustule formation; lesions limited to area of water exposure (so not under swimsuit?) Pseudomonas; from contaminated swimming pools or hot tubs
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Hot tub folliculitis
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Tender, firm, erythematous nodules that become fluctuant; in moist skin areas that contain hair and are subject to friction (neck, axillae, buttocks) S aureus or GNB if pt is immunocomp; dev from folliculitis that invades SQ tissues; RF are obesity, abnl neutrophil fnx (CGD), immunocomp pt (DM, AIDS, immunosupp meds, hematological dyscrasias)
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Furuncles (boil)
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Collection of furuncles at nape of neck, back, or thighs; fever/other systemic sx are common S aureus; multiple abscesses separated by CT extending into SQ fat in areas covered by thick, inelastic skin
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Carbuncles
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Common on extremitiesEarly: spreads rapidly along fascial planes and through venous/lymph channels (mimics cellulitis); bullae, edema that extends beyond area of erythema, focal cutaneous ecchymosis/ischemia, crepitus, cutaneous anesthesia, no lymphangitis; pain out of proportion to PE findingsLater: cutaneous anesthesia 2º to blood vessel thrombosis and destruction of superficial nerves; compartment syndrome possible; systemic toxicity (hypotension and MODS) Progressively destroys SQ fascia/fat (not ms); common in pt’s c DM, obesity, and PVD
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Necrotizing fasciitis
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Localized area of swelling, erythema, tenderness that causes ulcer (often encircled by gangrenous skin c surrounding violaceus skin) Polymicrobial infection (anaerobic or microaerophilic streph c s aureus or facultative gnb); Variant of necrotizing fasciitis c prominent involvement of skin, SQ tissue, fascia, and muscle
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Meleney’s synergistic gangrene
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Sudden onset of severe local pain, dec BP, systemic toxicity; area becomes edematous, c pale surrounding skin, blood-tinged, serous d/c may be present; surrounding tissue finally becomes dusky (ischemic) c fluid-filled bullae; gas may be palpable in tissues; in contaminated, devitalized tissue c. perfringens; predisposing conditions are traumatic injuries (compound frx, penetrating wounds), surgical wounds after enteric surgery, limp injuries in pt c PVD;
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Clostridial myonecrosis (“gas gangrene”)
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Stage I (d/wk after bite): erythemamigrans (central clearing) +/- F/C, myalgias, arthralgias, fatigueStage II(wk/mo after bite): neuro sx - lymphocytic meningitis (CSF ~100 wbc), CN palsy/Bell’s palsy, painful radiculoneuritis followed by dec sensation, weakness, and absent reflexes; cardiac sx – weakness, fatigue, palpitation, AV block, mild pericarditis or myocarditisStage III: chronic arthritis (monoarticular or asymmetric oligoarticular arthritis of large joints – usually knee) Borrelia burgdorferi (spirochete); may-sept in NE, upper Midwest, N CA;
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Lyme disease
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F/C, HA, myalgias, +/- rash (more so in HME then HGA, on trunk, spares hands/feet, not assoc c site of tick bite); 7-14 d incubation Ehrlichiae – obligate intracell bact that grow c/in leukocytes; HGA is in WI, MN, and CA b/t may-sept and usually in men; HME is SE, south central, mid atlantic US
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Ehrlichiosis
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F/C, HA, ms aches, malaise, rash c/in 1st wk (blanching 1-4 mm macular lesions that turn into petechial – won’t blanch; starts on wrist/ankles and moves to trunk, palms, and soles); 7 d incubation Rickettsia rickettsii (obligate intracellular bacterium s cell wall); mostly in SE atlantic coast states and Midwest (N/S Carolina, OK, Tenn)
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Rocky Mountain Spotted Fever
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Cutaneous – most common, pruritic papules (3-5 d post exposure) à vesicles that dev central area of necrosis and characteristic eschar (d 10) surrounded by edema and purplish vesiclesInhalation – mediastinitis and hemorrhagic lymphadenitis (hilar/mediastinal widening), +/- exudative pleural effusions Bacillus anthracis (GPB, spore-forming); naturally occurring in dirt
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Anthrax
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Prodromal – like flu, c 2-4 d of high fever, frontal HA, vomiting, and severe backacheCutaneous – discrete rash appears on oral mucosa, face, palms and soles, hands/LE and spreads centrally to trunk, 1st wk – lesions change from macules à papules à vesicles; 2nd wk of rash the pustules form eschars à hypopig scars on healing Variola major; transmitted via aerosolized resp secretions, direct contact, or on fabrics/other surfaces; most infection b/t D7-10 of rash; 7-17 d incubation
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Smallpox
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Bubonic – most common, sudden onset F/C, HA, intense pain in areas of LN, tender, fluctuant bubos, +/- N/V/D, and abd painSepticemic – febrile and extremely ill s localizing s/s, hypotension, DIC, MSOF, skin necrosis (from DIC)Pneumonic – 2º to bacteremia in bubonic or septicemic plague Yersinia pestis; fleas feeding of squirrels, rabbits, prarie dogs infested c yersinia; AZ, CA, CO, NM
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Plague
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Periodic chills à impressive fever à v impressive sweats (q other day or 3rd day); +/- HA, myalgia, splenomegaly Plasmodium falciparum (worst type of plasmodium to get); in tropical areas; transmitted by female mosquito
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Malaria
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