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IDIS DERM > DERM: Pustules, Vesicles & Bullae I & II > Flashcards

DERM: Pustules, Vesicles & Bullae I & II Flashcards

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Dermatology Board Prep flashcards
1
Q

acne

  • pathogenesis
  • presentation
  • treatment
A
  • pathogenesis: cutibacterium acnes hydrolyze fats (sebum) into fatty acids -> greasy plug at follicular orifice made of keratin + sebum + bacteria
  • presentation: on face, upper chest and back
    • open comedo (blackhead)
    • closed comedo (whitehead)
    • pustules, papules
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2
Q

candidiasis

  • pathogenesis
  • demographics
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: candida albicans (gram + yeast) colonizes skin + mucosa + GI, leading to formation of biofilms
  • demographics: I/C - AIDS, DM, steroids, elderly
  • presentation: beefy / dark-red plaques with satellite lesions on areas that are
    • ​moist, occluded (like intertriginous)
    • cutaneous
  • diagnosis:
    • 10% KOH wet mount: pseudohyphae + budding yeast cells (spores)
    • + germ tube test
  • treatment: anti-fungals
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3
Q
A

candidias

+ germ tube test

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4
Q

impetigo contanegeousa

  • pathogenesis
  • demographics
  • presentation
  • complications
A
  • pathogenesis: s. pyogenes / s. aureus
  • demographics: children (2-5 yeares)
  • presentation: non-bullous vesicles that rupture into -> purulent erosions with honey-colored thick crusts
  • complications: post-streptococcal glomerulonephritis
  • diagnosis: rising anti-DNase B-titer / anti-streptolysins (titer)
    • catalase negative = s. pyognees (GAS)
    • catalase positive = s. aureus
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5
Q

how is bullous impetigo different than impentigo contagiousum

A
  • always d/t s. aureus - phase type 71 specifically (impetigo contagiousum d/t s. pyo > staph)
  • is a flacid bullae (impetigo contagiousum arises from non-bullous pustules)
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6
Q

what is the major complication of impetigo?

what is the role of early tx in this risk?

A

post-streptococcal glomerulonephritis

early tx does NOT reduce risk of developing this PSGN

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7
Q

ecthyma

  • pathogenesis
  • demographics
  • presentation
  • comlications
A
  • s. pyogenes > s. aureus causes purulent ulcers
  • demographics: I/C
  • presentation:
    • punched out ulcers that are
      • painful
      • shallow
      • have erythematous border
        • -> form thick, brown black crusts
    • fever
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8
Q

folliculitis

  • pathogenesis
  • presentation
  • diagnosis
  • comlications
A
  • pathogenesis: inflammation of any part of the hair follicle, typically d/t:
    • s. aureus: typical
    • pseudomonas aeruginosa: gram - folliculitis
    • malassezia furfur: fungal folliculitis
  • presentation: pustules at hair follicles, commonly in areasof terminal hair growth
  • diagnosis: clinical picture typically sufficient
    • but might confirm etiology if chronic:​ ​wood’s lamp:
      • psuedomonas folliculitis: flouresce green
      • ​malassezia folliculitis: flourescent blueish-white
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9
Q

wood’s lamp can differentate between what two etiological causes of folliculitis?

what will it show?

A
  • psuedomonas: green
  • ​malassezia:blueish-white
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10
Q

kerion

  • pathogenesis
  • presentation
  • diagnosis
  • therapy
A
  • pathogenesis: dermatophytes (fungus) -> induce type IV sensitivity reaction
  • presentation: furuncle / carbuncle like like lesion that is
    • painful
    • rounded
    • boggy
  • diagnosis: culture demeratophytes sabrouaud dextrose agar (will show growth)
  • therapy: griseofulvin
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11
Q

identify pictures & explain significance

A

shown are the dermatophytes that can cause kerion after application of a 10% KOH exam

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12
Q

hidradenitis suppurativa

  • pathogenesis
  • demographics
  • presentation
  • complications
A
  • demographics: polymicrobial flora (mostly anaerobes) -> occlude follicles in areas with many oil and sweat glands
  • demographics: more common in obese patients
  • presentation: sinus tracts (scars) that
    • drain purulent + malodour fluid
    • are painful
    • are on the axillary / inguinal / peranial skin
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13
Q

curtaneous myiasis

  • pathogenesis
  • presentation
  • treatment
A
  • pathogenesis: infestation by non-contagious fly larvae that burrow into skin leaving wounds. one of the following:
    • human bot fly (dermatobia hominus) - most common
      • stays for 5-10 weeks
    • new world screw worm fly (cochliomyia hominovorax) - most dangerous
      • stays for 5-7 days
    • blowfly larvae (calliphora)
      • stays for 3-9 days
  • presentation: small red papule that becomes a -> painful furuncle with central pore
  • treatment: removing with local anesthetic
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14
Q

what are the causes of cutaneous myiasis and how are they different?

A

all non infectious flies: differ based on how long they stay burrowed in skin

  • human bot fly (dermatobia hominus) - most common: 5-10 weeks*
  • screw worm fly (cochliomyia hominovorax) - most dangerous: 5-7 days*
  • blowfly larvae (calliphora): 3-9 days
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15
Q

hand, foot & mouth disease

  • pathogenesis
  • demographics
  • presentation
  • complications
A
  • pathogenesis: cocksackie A16 > enteroviruse 71 (echoviruses) infiltrates -> keratinocyte apopotosis
  • demographics: children < 10 yrs
  • presentation:
    • painful vesicles on tongue, +
    • macular rash - _of elliptical, gray lesion_s - restricted to hands & feet
  • complications:
    • onchyomadesis: shedding of nails after recovering
    • fatality: rare, but tends to be associated with enterovirus 71
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16
Q

list each member of the herpesvirus family abd which disease it is associated with

A
  • HHV-1: HSV-1 - oral herpes
  • HHV-2: HSV-2 - genital herpes
  • HHV-3: varicella zoster: chickenpox, shingles
  • HHV-4: mononucleosis, gionetii-crost
  • HHV-5: CMV
    HHV-6: roseola
  • HHV-7: pitryiasis rosea
  • HHV-8: kaposi-sarcoma
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17
Q

herpes simplex virus

  • pathogenesis
  • presentation
  • diagnosis
  • complication:
  • treatment:
A
  • pathogenesis: HSV-1 or HSV-2 induce formation of epithelial multinucleated giant cells then -> invade sensory nerve ends to trigminal ganglion to establish latencey
  • presentation: grouped, painful vesicles on an erythematous plaque that rupture to form ulcers with yellow crust
    • ​HSV-1: oral mucosa
    • HSV-2: genitals
    • herpes gladioatorum (HSV-1): face, neck & arms (wrestlers)
    • hepertic whitlow (HSV-1/2): on hand, esp at distal phalanx (healthcare workers + children sucking thumbs)
  • diagnosis: + Tzanck test: Cowdry Type A bodies
  • complications: congtenital transmission (TORCH dz) - most likely during delivery
  • treatment: acycylovir
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18
Q
A

herpetic whitlow (HSV-1 or HSV-2)

vesicles on erythematous plaque - on distal phalanx

commonly in _health-care worker_s or children sucking thumbs

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19
Q
A

tzanck test: 3 syncitita with cowdry bodies

indicative of HSV-1 / HSV-2 of varicella-zoster (HHV-3)

20
Q

chickenpox (varicella)

  • pathogenesis
  • demographics
  • presentation
  • diagnosis
  • complications
  • prevention
A
  • pathogenesis: HHV-3 induces ballooning degernation of epithelial cells (forms clear vesicle) and epithelial multinucleated giant cells (forms erythematous base)
  • demographics: unvaccinated individuals
  • prseentation: vesicles on an erythematous base (“dewdrops on a rash”) that rupture -> form crust
    • painless but pruritic
    • appear in” crops”
    • have centrifugal distribution: go from trunk -> outward to extremities
  • diagnosis: + Tzacnk test - multinucleated giant cells
  • complications:
    • congenital varicella syndrome - transmission to fetus (TORCH dz)
    • reyes syndrome: encephalitis + fatty liver disease
    • herpez zoster: latent reactivation
  • prevention: varivax (live attenuated) - recommended for children & unvaxed, non-pregnant adults
21
Q

what is reye’s syndrome?

what is its cause?

A
  • a complication of varicella / chickenpox (HHV-3)
  • characterized by:
    • encephalitis
    • fatty liver / hepatitis
  • increases risk with ASAS: avoid aspirin
22
Q

herpes zoster

  • pathogenesis
  • presentation
  • complications
  • prevention
A

aka shingles

  • pathogenesis: reactivation of HHV-3 from VZV -> affecting a single sensory dermatome on trunk
  • presentation: vesicles on a red, erythematous base (just like VZV) that rupture -> crust over, that are:
    • on the trunk in single dermatome
    • approach but dont cross midline
    • preceded by paresthesia & disabling pain
      • pain that resembles “rib fracture or myocardial infarction”
  • diagnosis: + Tzank test
  • complications: opthalmic zoster via opthalmic branch of trigeminal nerve (also indicated by hutchinson’s nose - refer to opthalmologist)
  • prevention: Shingrex vaccine - recommended for individuals > 50
23
Q

gonoccocemia

  • pathogenesis
  • demographics
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: neisseria gonorrhoeae (gram - diplococci) releases a host of virulence factors that facilitates skin invasion
    1. IgA protease: mucous membrane colonization
    2. type IV pili: mucous membrane penetrate
    3. ability to replicate within PMNS
  • demographics:
    • ​high # of sexual partners
    • complement deficiency
    • menstration, pregnancy
  • presentation:
    • purpuric pustules (hemorraghic) scattered over distal extremities
    • systemic: classic triad
      • dermatiits
      • migratory polyarthralgia
      • tenosynovitis
  • diagnosis: thayer-martin agar - shows gram - diplococci
  • treatment: ceftriaxone
24
Q

disseminated vibrio vulnificus infection

  • pathogenesis
  • presentation
  • diagnosis
  • complications
A
  • pathogenesis: vibrio vulnificus (a halophillic, flagellated gram - curved rod) is contracted via either
    • seafood ingestion (primary septicemia)
    • exposure of open wound to contamined sea water
  • presentation: systemic symptoms preceed skin presentation
    • systemic:
      • fever / chills / malaise +/- HYPOtn
      • GI - nausea / vomitting / water diarrhea
    • skin: painful lesions -> necrosis, sloughing
  • diagnosis: thiosulfate-citrate-bile-sucrose (TCBS) agar will show growth, but not fermentation: i.e, will stay a GREEN color
  • complications: fatality is must more likely if primary septicemia > wound infection
25
Q

ricksettsialpox

  • pathogenesis
  • demographics
  • presentation
  • treatment
A
  • pathogenesis: ricksettsia - a obligate intracellular pathogen contracted via mite bite from mouse vector
  • demographics: more common in urban areas: MORE MICE (vector) in homes
  • presentation: eschar lesion / fever + papulovescicle crop
    1. tender, papular lesion immediately forms at bite site -> forms eschar
    2. next, a papulovesicular rash crop breaks out anywhere EXCEPT palms or soles
  • treatment: doxycycline
26
Q

molluscum contagiosum

  • pathogenesis
  • presentation
  • diagnosis
A
  • diagnosis: infection by ovoid dsDNA molluscipoxvirus
  • presentation: lesions that are
    • flesh colored
    • dome-shaped
    • umbilicated (central depression)
    • expresses a cheese-like materal with pressure
    • found anywhere EXCEPT palms and soles
  • diagnosis: with henderseon-patterson bodies: virus containing kerationcytes; shown with giemsa stain
27
Q

orf

  • pathogenesis
  • demographics
  • presentation
A

= echthyma contagiosum

  • pathogenesis: orf virus - ovoid dsDNA parapoxvirus - from direct contact with either:
    • SHEEP
    • GOAT
  • demographics: farmers, butchers, veterians
  • presentation: seriss of phases at site of abrasian - m/c, on hand:
    • ​tender papule
    • target nodule: red center - white middle ring - red halo
    • umbilicated pustule
    • weeping nodule - white, gray crust
28
Q

monkeypox

  • pathogenesis
  • demographics
  • presentation
  • prevention
A
  • pathogenesis: orthopoxvirus
  • demographics: endemic to central and west africa
  • presentation: like small-pox + lymphadenopathy
    • umcilicated pustules that
      • start on face / arms then rapidly descend
      • are everywhere INCLUDING palms and soles\
  • prevention: smallpox vaccine
29
Q
A

ecthyma (s. pyogenes)

ulcers that are - punched out with erythematous borders that form thick, brown black crusts

30
Q
A

folliculitis - s. aureus, p. aeruginosa, malassezia

31
Q
A

kerion (dermatophytes)

furuncle that is - painful, rounded, boggy, suppurative

32
Q
A

hidradenitis suppurativa

sinus tracts that are - tender, purulent, malodorous

33
Q
A

hand, foot & mouth disease (cocksackie A)

34
Q
A

tzacnk test

HSV-1/ HSV-2, or VZV (HHV-3), or HZV (HHV-3)

35
Q
A

gonococcemia

thayer martin agar showing gram - diplococci

36
Q
A

vibrio vulnificus

gram - rod that is: halophillic (salt loving), flagellated, and curved

37
Q
A

vibrio fulnificus

TCBS agar is green - showing growth, but not fermentation

38
Q
A

varciella / chickenpox (HHV-3)

vesicles surrounded by red halo (“dew drops on rose petal”) - pruritic, centrifigual distribution: trunk -> extremiies

39
Q
A

HZV (HHV-3)

vesicles on a red base - unilateral (doesn’t cross midline), following 1-2 contiguous dermatome on trunk, often preceded with paresthesia & debilitating pain

40
Q
A

ovoid dsDNA molluscipoxvirus

molluscum contagiosum, orf, monkeypox

41
Q
A

molluscum contiogsum

henderson-patterson bodies: virus filled keratinocytes (“mollusck shaped”

42
Q
A

orf / echtyma contagiosum

evolving pustule (here, “target nodule” - red-white-red) on hand, from direct contact with goats / sheep

43
Q
A

milkers nodule

presents just like orf: but from contact with cows udders / muzzles

44
Q
A

molluscum contagiosum (ovoid dsDNA molluscipoxvirus)

lesion that is - flesh colored, dome shaped, umbilitcated, NOT on palms & soles - can express cheese-like material with pressure

45
Q
A

molluscum contagiosum (ovoid dsDNA molluscipoxvirus)

lesion that is - flesh colored, dome shaped, umbilitcated, NOT on palms & soles - can express cheese-like material with pressure

IDIS DERM (3 decks)

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