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122 Cards in this Set

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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
Acne vulgaris
Recurrent boils and abscesses (more severe then nl acne) in axilla, anogenital, under breasts RF: female, obese- chronic, progressive, scarring
Hidradenitis suppurativa
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
Dissecting cellulitis of the scalp
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
Perioral dermatitis
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
Acute phase: pruritis, erythema, edemaChronic phase: thickening, lichenification, scaling From hyperirritability of skin
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)
Atopic dermatitis
Prominent follicular papules on lateral arms, legs, and cheeks Improves c age; common in atopic pt’s
Keratosis pilaris
Thick, rough plaque that is lichenified From chronic rubbing that causes skin thickening
Lichen simplex chronicus
Temporary loss of pigment on face and extremities In atopic kids and young adults
Pityriasis alba
Prurigo nodules
Excoriated papules
Dry rectangular scales usually on extremities Inherited disorder of keratinization; usually assoc c atopic hx
Ichthyosis vulgaris
Pt loses subcutaneous fat and makes skin really dry
Asteatotic eczema
1-5 mm vesicles (clear/white) on palms, lat fingers, and soles H/o atopy, sudden onset and pruritic
Dyshidrotic eczema
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
Allergic contact dermatitis (rhus dermatitis?)
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
Irritant contact dermatitis
Hyperpigmentation (tend not to go away), xerosis, fissures, ulcers Assoc c varicosities and edema
Stasis dermatitis
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
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
Pityriasis Rosea
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
Lichen planus
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
Seborrheic dermatitis
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
Drug eruptions
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
Maculopapular drug eruption
Edema “leaking” into tissue that is causing elevation Aspirin, PCN, and blood products (onset is 4-21 d)
Urticarial drug eruption
Mimics lichen planus (Flat top, pruritic, planar, polyangular, pink-purple papules c fine lacey scale); generalized eruption (onset is wks-yrs) Gold and antimalarials
Lichenoid drug eruption
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
Fixed drug eruption
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
Drug hypersensitivity
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
Erythema Multiforme
Larger, atypical target lesions and blisters; must involve ≥2 MM; febrile prodrome and diffuse distribution Antiepileptic and antibiotics; occurs at all ages
Pain, erythema, and rapid exfoliativ skin loss; >30% of body surface involved More severe then SJS; occurs at all ages; antiepileptics and antibiotics
Toxic Epidermal necrolysis
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
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
Henoch-Scholein Purpura
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
Schamberg’s Dz
From drug eruptions, viral exanthems, insect bites, food allergy (autoimmune response lasting <6 wk)
Acute urticaria
Lesions lasts <24 h; reoccurring lesions >6 wks Think about inhalants, ingestants, injections, infections, and internal dz
Chronic Urticaria
Erythematous, tender deep nodules on LE Reactivity to infection or drugs1. infections – strep, hep B, fungal2. chronic dz – sarcoid, colitis3. drugs – OCP, sulfa
Erythema nodosum
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
Granuloma annulare
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
Necrobiosis lipoidica
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)
Acanthosis nigricans
Tan to brown macules/patches (non palpable); larger then freckles >6 macules > 5mm is suspicious for neurofibromatosis; present at birth and inc in childhood
Café Au Lait Spots
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
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
Cutaneous lupus
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
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
Ivory-pink plaques c violaceous borders usually on trunk that heals c atrophy Localized scleroderma; will not progress to systemic form; Children and adult
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 +
Systemic scleroderma
Calcinosis cutis; Raynauds, Esophageal dysfnx, Sclerodactyly, Telangiectasia Limited systemic involvement; hardening of skin (scleroderma) limited to face and hands; + ANA
CREST variant (Limited scleroderma
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
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?)
Dermatitis herpetiformis
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
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
Bullous Pemphigoid
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
Skin fragility c blisters; no hypertrichosis or dyspigmentation Usually medication induced (NSAIDS and tetracycline) or tanning beds; porphyrin levels nl
Red-brown plaques c fine scale in warm, moist, intertriginous areas; will shine coral-red c wood’s lamp Corynebacterium
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
Pitted Keratolysis
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
HSV 1 and HSV 2
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
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
Smooth, pearly, dome-shaped papules c umbilicated center; multiple lesions In children and sexually active adults; called “water warts”
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
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)
Tinea Versicolor
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
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)
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
Cluster of papules on legs; pruritis depends on sensitivity
Hookworm larvae H/o travel v important clue (Caribbean, S and central America, SE US)
Cutaneous larva migrans
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
Seborrheic keratosis
Flesh colored/tan papules on stalk; soft; on flexural sites, inguinal areas, under breasts More common in overwt individuals
Skin tags
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)
May be darker around edges, dimple sign; most common on extremities From localized area of scar; possibly a rxn to shaving (ingrown hair rxn?)
Milia – faceEpidermal – face and trunkPilar – scalpMucoid – fingers and toesMucosal - oral Occluded sebaceous glands that are NOT inflamed
Multiple white/yellow papules on forehead and cheeks (resembles BCC) Overgrowth of sebaceous gland; common after 30 yoa
Sebaceous hyperplasia
Multiple 1-2 mm white/yellow papules (no central depression); symmetrical on lower eyelids; confused c flat warts Sweat gland tumors – benign
On eyelids Cholesterol deposits
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
Vascular malformations
Vascular tumor; occur c/in 1st yr of life; slowly involute over years; more common in girls and preterm; 1-3% of infants
Hemangioma of infancy
Dome-shaped papule; red/purple; easily blanch; can bleed if raised and nicked Common in preg and >30 yoa
Cherry angioma
Dome-shaped papule; red/purple; easily blanch; can bleed if raised and nicked Common in preg and >30 yoa
Cherry angioma
Central red papule c radiating legs; commonly on face and upper trunk; blanch c pressure Seen in 15% of kids
Spider angioma
On sun exposed sites, easy to blanch Dilatation of superficial vessels; inc incidence in preg, etoh abuse, skin ca, connective tissue dz, and rosacea
Vascular papules on scrotom and vulva Possibly from inc venous press; may inc c pregnancy; appear in midlife
Angiokeratomas of Fordyce
Larger then angiokeritinomas; on sun-exposed sites (lips v common) From localized venous dilatation
Venous lake
Vascular papule that bleeds easily (very raised papule) Increased vascular response to injury; common kids and young adults
Pyogenic granuloma
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
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
Common mole
Rim of hypopigmentation around nevus (halo can repigment) Most occur in adolexcence; can occur in vitiligo and melanoma
Halo nevi
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
Atypical nevi
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
Localized area of hyperpigmentation; they are freckles in kids and adult lentigines tend to be larger then freckles Common in caucasians
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
Actinic keratosis
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
Basal Cell Carcinoma
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
Squamous cell carcinoma
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)
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
Androgenic alopecia
Temporal losses? More common in AA; women>men; can lead to perm alopecia; from keeping hair pulled back tightly
Traction alopecia
Diffuse loss (<50%) Occurs 2-4 mo after insult; causes are physical and emotional stresses (pregnancy) and/or drugs (anticonvulsants)
Telogen effluvium
Hair shaft thins and breaks Sudden hair loss from chemo; onset after 1-3 wks
Anagen Effluvium
Will have various length hairs and irregular and bizarre patterns Any age pt; OCD
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
Alopecia areata
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
Post inflam, pityriasis alba, burns, halo nevus
On extremities – “raindrops” of lighter areas Caucasians; women>men; genetics; photo damage; >50yoa
Guttate hypomelanosis
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
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
Looks like ecthyma Pseudomonas bacteremia and occurs in neutropenic pt
Ecthyma gangrenosum
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
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)
- Post CABG vein harvest leg + ipsilat tinea pedis: unilat cellulitis- Post-pelvic radiation: bilat- Post-mastectomy c LN biopsy: unilat
Recurrent cellulitis 2º to chronic lymphedema
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
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
Hot tub folliculitis
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)
Furuncles (boil)
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
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
Necrotizing fasciitis
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
Meleney’s synergistic gangrene
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;
Clostridial myonecrosis (“gas gangrene”)
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;
Lyme disease
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
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)
Rocky Mountain Spotted Fever
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
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
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
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