DERM: Pustules, Vesicles & Bullae I & II Flashcards by Kara Rieth

acne

pathogenesis
presentation
treatment

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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candidiasis

pathogenesis
demographics
presentation
diagnosis
treatment

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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candidias

+ germ tube test

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impetigo contanegeousa

pathogenesis
demographics
presentation
complications

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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how is bullous impetigo different than impentigo contagiousum

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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what is the major complication of impetigo?

what is the role of early tx in this risk?

post-streptococcal glomerulonephritis

early tx does NOT reduce risk of developing this PSGN

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ecthyma

pathogenesis
demographics
presentation
comlications

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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folliculitis

pathogenesis
presentation
diagnosis
comlications

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

what will it show?

psuedomonas: green
malassezia:blueish-white

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kerion

pathogenesis
presentation
diagnosis
therapy

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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identify pictures & explain significance

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

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hidradenitis suppurativa

pathogenesis
demographics
presentation
complications

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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curtaneous myiasis

pathogenesis
presentation
treatment

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

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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hand, foot & mouth disease

pathogenesis
demographics
presentation
complications

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

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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herpes simplex virus

pathogenesis
presentation
diagnosis
complication:
treatment:

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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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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tzanck test: 3 syncitita with cowdry bodies

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

chickenpox (varicella)

pathogenesis
demographics
presentation
diagnosis
complications
prevention

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

what is reye’s syndrome?

what is its cause?

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

herpes zoster

pathogenesis
presentation
complications
prevention

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 dermatom_e
- 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 V1)
- __indicated by hutchinson’s nose (refer to opthalmologist)
prevention: Shingrex vaccine - recommended for individuals > 50

gonoccocemia

pathogenesis
demographics
presentation
diagnosis
treatment

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

disseminated vibrio vulnificus infection

pathogenesis
presentation
diagnosis
complications

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

ricksettsiapox * pathogenesis * demographics * presentation * treatment

* 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

molluscum contagiosum * pathogenesis * presentation * diagnosis

* 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

orf * pathogenesis * demographics * presentation

= 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

monkeypox * pathogenesis * demographics * presentation * prevention

* 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

ecthyma (s. pyogenes) ulcers that are - punched out with erythematous borders that form thick, brown black crusts

folliculitis - *s. aureus, p. aeruginosa, malassezia*

kerion (dermatophytes) furuncle that is - painful, rounded, boggy, suppurative

hidradenitis suppurativa sinus tracts that are - tender, purulent, malodorous

hand, foot & mouth disease (cocksackie A)

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

gonococcemia ## Footnote **thayer martin agar showing gram - diplococci**

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

vibrio fulnificus TCBS agar is green - showing growth, but not fermentation

varciella / chickenpox (HHV-3) vesicles surrounded by red halo ("dew drops on rose petal") - pruritic, centrifigual distribution: trunk -\> extremiies

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

ovoid dsDNA molluscipoxvirus molluscum contagiosum, orf, monkeypox

molluscum contiogsum **henderson-patterson bodies:** virus filled keratinocytes ("mollusck shaped"

orf / echtyma contagiosum evolving pustule (here, "target nodule" - red-white-red) on hand, from direct contact with goats / sheep

milkers nodule presents just like orf: but from contact with _cows_ udders / muzzles

molluscum contagiosum (ovoid dsDNA molluscipoxvirus) lesion that is - flesh colored, dome shaped, umbilitcated, NOT on palms & soles - can express cheese-like material with pressure