Clin Med: Dermatology 5 – Flashcards

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Pathophys of abscess
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localized infection of the dermis, may come from punctures and trauma, large cellular inflammatory response created (primarily neutrophils), aggregate of inflammatory cells replace necrotic dermis- creating pus, sterile abscess if possible hidradenitis suppurativa- apocrine duct obstruction with bact infxn, sinus tracts form and may drain purulent material furuncles- bacteria enter through the hair follicle
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types of abscesses
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furuncle- localized at one hair follicle carbuncle- conglomeerate of multiple hair follicles hidradenitis suppuratica- apocrine gland pilonidal disease- gluteal cleft
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prevalance and cause of abscess
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prevalence: common demo: hidradenitis- puberty, menopause pathologic cause: staph aureus most common, MRSA becoming more common
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comorbidities, family and social history of abscess
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comor: hidradenitis- acne, obesity; diabetes, immunocompromised family hx: common with hidradenitis social: IV drug use (dirty needles)
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PE of abscess
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lesion- adematous, erythematous, tender, fluctuant (indicates pus), indurated (early phlegmon) common locations: axilla, buttocks, perirectal, head and neck Hidradenitis: axilla--> scars and tracts pilonidal cyst: gluteal cleft
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diagnostic studies for abscess
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clinical wound culture (if complicated or chronic)- oftern multipl epathogens, MRSSA more common now
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complications of abscess
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fibrosis, scarring, progressive infeciton
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Plan/Tx for abscess
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patient education: hot soaks or warm compresses for 20 minutes- QID procedure- incision and drainage is STANDARD for care- needs to be fluctuant with pus if complicated with fever or cellulitis- use ATB
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essentials of diagnosis and pearls for abscess
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edamatous, tender, fluctuant, incision and drainage, abx if complication Pearls: staph aurerus is the most common pathogen
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pathophys of cellulitis
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bacteria enters dermis ( external or hematogenous acute spreading inflammation of the dermis and subcutaneous tissue most common are Gram + staph, strep, haemophilus
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Hx of cellulitis
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possible trauma history, pailful, erythematous if complicated: fever, chills, sweats
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PE of cellulitis
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leasion- spreading indurated area of skin, erythematous warm, tender, if complicated: lymphadenopahty, phlebitis, fever erysipelas- sharply demarcated boarder, orangle peel surface
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what are the four cardinal signs of inflammation
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calor- warmth rubor- redness tumor- edema dolor- pain
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diagnostic studies and criteria of cellulitis
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diagnosis is clinical may perform- blood culture- if bacteremia, skin culture- often no yield, CBC- leukocytosis criteria: erythematous, warm, tender
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complications of cellulitis
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phlebitis, bacteremia, gas gangrene, necrotizing fasciitis
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plan/ Tx for cellulitis
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patient education: mark the skin at the cellulitis periphery to determine spreading Oral Abx: 1) first gen cephalosporins (Ceohalexin 500 mg QID 7d) 2) macrolides (Erythromycin 7d) 3) PCNase resistance PCN (Dicloxcillin) If not responding to oral abx: IV cephalosprorins if complicated by has gangrene or nerotizing fasciitis: surgical debridement
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epidemiology of folliculitis
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prevalence commo demo: yound adults pathologic cause: staph aureus most common, psudomonas hot tub exposure social: hot tub
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types of folliculitis
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pseudofolliculitis- infrown hairs of the beard area
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differential diagnosis of folliculitis
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acne vulgaris, pseudofolliculitis barbae
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diagnostic studies of folliculitis diagnostic criteria
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clinical diagnosis, Criteria: erythematous papule or pustules, hair follicle seen at pustule
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epidemiology of impetigo
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prevalence: common demo: children pathologic cause: staph aureus comorbidites: atopic dermatitis more likely social hx: contagious, watch other family members
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diagnostic studies and criteria of impetigo
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diagnosis is clinical criteria: honey colored crutst, psutules that have ruptures, erythematous glistening base, most common found perioral
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differential diagnosis of impetigo
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acne vulgaris, folliculitis, ecthyma, herpes simplex
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essential of diagnosis and pearls of impetigo
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honey colored crust, pustules that have ruptures, erythematous glistening base, most common found perioral, topical abx pearls: staph aureus most common bacteria
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epidemiology of anthrax
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prevalence rare- social hx: farmers and vets at higher risk risk of bioterrorism
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essentials of diagnosis for anthrax
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exposure, eschar, gram stain + rods encapsulated chains, cultures, PCR confirmation, fluoroquinolone abx
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epidemiology of cat-scratch disease
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demo: adults and children affected pathologic cause: cats and bartonella
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Hx and PE of cat-scratch disease
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Hx: bump at site, fever, malaise, anorexia PE: painless papule, painful lymphadenopathy most common in axilla
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differential diagnosis of cat-scratch disease
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skin cancer, pyogenic lymphadenitits, mycobacterial infection, syphilis, tularemia, plague, toxophasmosis
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essentials of diagnosis and pearls for cat-scratch disease
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essentials: exposure to car, painless papules/nodules, painful regiaonal lymphadenopathy, PCr +, Bx- lymphoid hyperplasia Pears: Bartonella
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Prognosis and complications of cat-scratch disease
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prognosis- usually benign complications: retinitis
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epidemiology of gas gangrene
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prevalence- rare pathologic cause: clostridium perfringens most common pathogen
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Hx of gas gangrene
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possible skin injury, fever, tachycardia, painful skin
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PE of gas gangrene
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fever (sight), tachycardia skin: wound becomes swollen, surrounding skin is pale ---> pale --->dusky ---> deeply discolored with coalescent red fluid filled vesicles fould smelling browl blood tinged serous discharge skin crepitus
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prognosis and complications of gas gangrene
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prognosis: high risk mortality complications: severe prostration, stuporm delirium, and coma
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comorbidities and social hx of necrotizing fasciitis
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comor: biabetes more common (20-30% of all cases) social: IV drug users more common
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Hx of necrotizing fasciitis
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sweling, heat, erythema, and pain spread proximally and sitally skin darkens, blisters and bullae with clear yellow fluid form development of gangrene and necrosis is associated with mental staus changes and delirium
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prognosis of necrotizing fasciitis
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high mortality (25-75%)
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plan/ tx for necrotizing fasciitis
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emergency! surgical debridement broad spectrum ATB TV supportive therapy- IV fluids
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Diagnostic criteria for necrotizing fasciitis
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fever, tachycardia, hyptension, progressive tender skin darkening and bullae, possible crepitus, imaging may confirm
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pathophys of alopecia areata
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unknown pathogenesis believed to be autoimmune process hair matricies become arrested-loss can be patchy "swarm of bees"
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prevalence, demo, and pathologic cause of alopecia areata
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1.7% of americans over 50 demo: equal pathologic cause: may be from drugs: thallium , vit A, retinoids, antimitoric agents, anticoagulants, oral contraceptives
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Hx and PE of alopecia areata
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Hx: hair loss, acute onset PE: hair loss, oval patches, exclamation point hairs at edge, no scarring, skin may slightly depress, may have diffuse hair loss
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differential diagnosis of alopecia areata
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tinea, syphilis
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prognosis of alopecia areata
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5% may spontaeously resolve resolution unlikely if: if not in 1 year and the larger the area
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prevalence, demo, and genetics of androgenic alopecia
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prevanence: very common demo: 100% of male caucasions ahve some degree, 40% of femailes over 40 family hx +
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differential diagnosis of androgenic alopecia
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hypothyroidism
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Essentials of diagnosis for androgenic alopecia
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Thinning of hair, gradual dark terminal hair replaced with minatureized hairs topical minoxidil OR 5a reducatse inhibitors
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prognosis of androgenic alopecia
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majority of process occurs 30-50 yo variable
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dx of androgenic alopecia
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diagnosis is clinical
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Paronychia pathophysiology
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inflammation of the nail fold- may extend into proximal nail fold and eponychium
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prevalence and social hx of Paronychia
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prev: common Social hx: nail biting, manicures, thumb sucking, occupational
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differential diagnosis of Paronychia
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herpetic witlow onychomycosis
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diagnostic studies of Paronychia
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clinical dx needle "slow motion" to drain consider: KOH and culture
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essentials of diagnosis for Paronychia
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edema of nail fold tender I/D gram + abx
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pathophys of Felon
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infection of distal finger subcutaneous pulp staph aureus most common often from injury or paronychia
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prevalence, pathologic cause and comorbidities of Felon
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prevalence- not as common pathologic cause- staph aureus comorbidities: paronychia
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Hx and PE of Felon
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hx: pain and swelling of finger PE: edema of distal finger at volar aspect, tender
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differential diagnosis of Felon
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paronychia osteromyelitis flexor tenosynovitis
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diagnostic studies of Felon
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consider: X ray- evaluate for soteromyelitis- raised periosteium
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complications of Felon
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osteomyelitis
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plan/tx of Felon
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procedures: incision and drainage Pharm: Initial: oral abx-->cephalosporin If severe: IV antibotics
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essentials of diagnosis and pearls of Felon
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Essentials of diagnosis: edema of distal finger at colar aspect, tender Pearls: small lincision of area of most fluctuance
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Hx of abscess
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pain, swelling, may develop at injection sites
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differential diagnosis of abscess
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acne vulargis epithelial inclusion cyst
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Plan for abscess: patient education and procedure
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Ed: hot soaks or warm compresses for 20 minutes QID Procedure: I/D is standard of care- needs to be fluctuant with pus
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plan for abscess if complicated with fever or cellulitis
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Antibiotics --> MRSA coverage: sulfonamides (TMP-SXM, BID 7-10 days), clindamycin (300 mg QID 7d) tetracyclines (Doxycycline 100 mg BID 7d) ---> MSSA coverage: cephalosporins (Cephalexin 500 mg QID 7d), macrolides (erythromycin 250 mg QID 7d)
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plan for abscess if associated with Hidradenitis and Pilonidal cyst
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Hidradenitis: excision of sinus tract after elimination of infection ---- may add intralesional steroids (triamcinolone) ---- OR oral steroids (prednisone taper 2 week) pilonidal cysts: marsupialization- avoids future infxn ---- I/D ---- sew edges of fibrous tract to wound edge creating a pouch
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referrals for abscess
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general surgeon if complicated --- Pilonidal --- Hidradedenitis
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Prevalence, comorbidities and types of cellulitis
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prevalence: common comorbidities: diabetes and immunocompromise Types: erysipelas- streptococcus
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Differential diagnosis for cellulitis
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contact dermatitis stasis dermatitis superficial thrombophlebitis erythema infectiosum
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essentials of diagnosis for cellulitis
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erythematous, warm tender oral abx
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pathyphys of folliculitis
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inflammation of hair follicles --occusion, perspiration or tight clothing may irritate the follicles --bacteria enter follicle orifice: commonly caused by staphy aureus , create subcorneal pustule at opening of hair follicle --Pseudodomal folliculitis common in hot tubs --non-infectious folliculities may occur in hot oily environments (ships)
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Hx and PE of folliculitis
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Hx: lesions at hairs that may burn, may be chronic or recurrent PE: erythematous papules or pustules, hair follicle seen at pustule most common locations: thigh, buttocks, scalp, beard
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complications of folliculitis
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sycosis- deep seated folliculitis that frequently recurs abscesses may form
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Plan/Tx for folliculitis: Patient education and mild folliculitis
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Ed: avoid offending environments warm compresses gentle cleansing mild: antiseptic cleansers daily of every other day for several weeks --- proidone-iodine (Betadine) --- chlorhexidine (hibiclens) --- benzoyla peroxide used Topical abx --- clindamycin --- macrolides (erythromycin) --- mupirocin
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Plan for severe or hot tub folliculitis
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Severe: oral abx: cephalosporins, clindamycin, macrolides hot tub folliculitis: oral fluoroquinolones (Ciprofloxacin)
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Essentials of Diagnosis and pearls of folliculitis
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Essentials: erythematous papules or pustules hair follical seen at pustule antiseptic cleansers or topical abx Pearls: most common--> staphy aureus Hot tub--> pseudomonas aeruginosa
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Pathophys of Impetigo
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gram + skin infection bacteria infiltrate skin (minor trauma) staph aureus most common creates subcorneal pustules (below statum corneum) --inflammatory cells primarily neutrophils response and pus created --pustules easily burst--> crusts --with dermal inflammation
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Hx and PE of impetigo
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Hx: start with single lesion, multiple other lesions develop, may itch or burn PE: lesions- honey colored crutst, pustules--> ruptured, erythematous glistening base, perioral--> most common
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Plan/ Tx for Impetigo
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Patient education: change washcloth daily, resolves in 2 weeks Pharm: Initial: antibacterial soap, topical abx (mupirocin (Bactroban) 7-10d) Extensive lesions: oral abx: cephalosporins (Keflex) 7-10d
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pathophys for anthrax
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Bacillus anthracis: gram + spore, rods in chains found in cheep, cattle, horses, coats, swine transmitted via broken skin, mucous membrance or inhalation warfare organism creates derm, pulm, and GI manifestiations derm: after 2 weeks creates necrotic tissue that sloughs off, spread hematogenously pulm: pneumonia or mediastinitis GI: bowel irritation, GI tract ulcers
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Hx of anthrax
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possible exposure cutaneous: painless skin lesion Inhaled: viral symptoms: fever, malaise, headache, cough, congestions GI: fever, abdominal pain, vomiting, GI bleeding progress severely to sepsis or meningitis
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PE of anthrax
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curaneous: erythematous papule initially, then vesiculates and creates necrosis, develops into black eschar, +lymph nodes Inhalation: wheezing crackles, fever GI: Diffuse abdominal tenderness, +/- rebound tenderness
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diagnostic studies of anthrax
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skin gram + encapsulated box, rods in chains cultures or area + B. anthracis ---sputum, blood, CSF, Skin CXR: mediastinal widening from hemorrhagic lymphadenitis PCR to confirm
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Prognosis for anthrax
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cutaneous prognosis good inhalational and GI anthrax mortality 85%
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complications of anthrax
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sepsis, hemorrahic meningitis, hemorrhagic lymphadenitis, pneumonia, bowel perforation
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Plan/Tx for anthrax
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patient educaiton: vaccination available, but only for indivudals with high risk Pharm: ATB- fluoroquinolone(ciprofloxacin), tetracycline (doxycycline)
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cat-scratch disease pathophys
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bartonella henselae Gram - bacteria inoculation from cat teeth or claws cats transmit infection through flea feces- higher # fleas= higher likelihood of passing to other cate
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Diagnostic studies for car-scratch disease
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Bx: lymphoid hyperplasia- later stellate granulomata with necrosis, coalescing micro abscessed and occational multinucleated giant cells serolgic testing (immunofluorescence or enzyme immunoassay)--most common with variable sensitivity and specificity, may take a few weeks other tests are of close sensitivity ( culture, Warthin-Starry sliver staining)
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Plan for cat scratch disease
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if abscess-- I/D Pharm: 1st line: Macrolide abx (azithromycin x 5d) alternative (or if eye involement): tetracycline (doxycycline)
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Gas gangrene pathophys
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AKA clostridial myonecrosis produced by any one of several clostridia- clostridium perfrigens, ramosum, biermentans, histolyticum, novyi cause: trauma, injection use toxins produces into devitalized tissues--> anaerobic--> shock, hemolysis, myonecrosis
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Diagnostic studies for gas gangrene
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clinical dx, start treatment! radiography- show gas in soft tissue smear- absence of neutrophils, presence of gram+ rods anaerobic culture- confirms dx
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Plan for gas gangrene
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initial: 1) IV ATB--> PCN G q3 hr, Clindamycin q8hr (decreased production of bacterial toxin) 2) surgical debridement Optional: hyperbaric oxygen
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essentials of diagnosis and pearls for gas gangrene
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sudden onset of pain and adema in the area of owund contamination prostration and systemic toxicity brown to blood tinged watery exudate with skin discoloration of surrounding areagas in tissue by palpation or radiograph gram + rods in culutre or smear of exudate Pearls: clostridium infeciton typically
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pathophys of necrotizing fasciitis
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flesh eating bacteria infnx often polymicrobial common pathogens--> group A strep, clostridium, Vibrio sp (saltwater) deep subcut infnx that results in destruction of fascia and fat
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PE of necrotizing fasciitis
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skin: edema, heat, erythema, tenderness, spread proximally to distally, skin darkens and blisters w/ bullae with clear yellow fluid, tissue crepitus possible high fever as it progresses: sepsis- tachycardia, hypotension, altered mental status
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Diagnostic studies of necrotizing fasciitis
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triad: CBC--> WBC high >14k BUN- high >15 Sodium low <135 should prompt a heighted index of suspicion imaging may confirm: CT, MRI
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Comorbidities and genetics of alopecia areata
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comor: thyroiditis, pernicious anemia, addison's disease, celiac disease, RA, diabetes genetic: 25% have positive family history
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types of alopecia
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alopecia totalis- only the scalp alopecial universalis- entire body
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Diagnostic studies for alopecia areata
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Bx: dystrophic hair, lymphoctic infiltrate surround early anagen hair bulb--> swarm of bees
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Plan for alopecia areata
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pharm: may respond to oral steroids patient education: relapse common
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Essentials of diagnosis for alopecia areata
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hair loos oval patches exclamation point hairs at edge no scarring Bx: dytrophic hair with lymphocyte swarm of bees steroids may help
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Androgenic alopecia pathophys
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genetic loss of hair androgen dependent lower levels of 5a-reductase actually increases dihyrotestosterone which shorens hair cycle and minaturizes hair unpredictibale and variable
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Hx and PE for androgenic alopecia
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Hx: thinning of hair, beginning after puberty and noticable 20-30 yo, gradual, family history PE: thinning of hair, gradual, dark teminal hair replaces with miniaturized hairs (yellus) --> # of follicles stays the same patterns: men--> typically bitemportal women--> top of scalp
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Plan for androgenetic alopecia
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pharm: type 2 alpha reductase inhibitor (Finateride) --90% maintain hair, 66% have regrowth, typically for males only, teratogenic topical minoxidil--> more effective with recent onset (20-40% effective), may be better choice for younger females
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Hx and PE for paronychia
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Hx: pain and swelling at nail, may have recent manicure or admits to bitting nails PE: edematous at nail fold- pus may be seen, tender
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Plan for paronychia
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patient education: avoid wet enviro, stap habits like nail biting or thumb sucking procedure: I/D (if flucutant) pharm: acute: cephalexin, erythomycin, dicloxacillin Chronic: avoid trauma, water, and irritants, Lotrisons (note: did not include dosages)
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