DERM: Pustules, Vesicles & Bullae I & II

Question 1

acne

• pathogenesis
• presentation
• treatment

Answer 1

• 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

Question 2

candidiasis

• pathogenesis
• demographics
• presentation
• diagnosis
• treatment

Answer 2

• 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

Question 3

Answer 3

candidias

+ germ tube test

Question 4

impetigo contanegeousa

• pathogenesis
• demographics
• presentation
• complications

Answer 4

• 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

Question 5

how is bullous impetigo different than impentigo contagiousum

Answer 5

• 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)

Question 6

what is the major complication of impetigo?

what is the role of early tx in this risk?

Answer 6

post-streptococcal glomerulonephritis

early tx does NOT reduce risk of developing this PSGN

Question 7

ecthyma

• pathogenesis
• demographics
• presentation
• comlications

Answer 7

• 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

Question 8

folliculitis

• pathogenesis
• presentation
• diagnosis
• comlications

Answer 8

• 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

Question 9

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

what will it show?

Answer 9

• psuedomonas: green
• ​malassezia:blueish-white

Question 10

kerion

• pathogenesis
• presentation
• diagnosis
• therapy

Answer 10

• 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

Question 11

identify pictures & explain significance

Answer 11

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

Question 12

hidradenitis suppurativa

• pathogenesis
• demographics
• presentation
• complications

Answer 12

• 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

Question 13

curtaneous myiasis

• pathogenesis
• presentation
• treatment

Answer 13

• 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

Question 14

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

Answer 14

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

Question 15

hand, foot & mouth disease

• pathogenesis
• demographics
• presentation
• complications

Answer 15

• 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

Question 16

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

Answer 16

• 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

Question 17

herpes simplex virus

• pathogenesis
• presentation
• diagnosis
• complication:
• treatment:

Answer 17

• 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

Question 18

Answer 18

herpetic whitlow (HSV-1 or HSV-2)

vesicles on erythematous plaque - on distal phalanx

commonly in _health-care worker_s or children sucking thumbs

Question 19

Answer 19

tzanck test: 3 syncitita with cowdry bodies

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

Question 20

chickenpox (varicella)

• pathogenesis
• demographics
• presentation
• diagnosis
• complications
• prevention

Answer 20

• 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

Question 21

what is reye’s syndrome?

what is its cause?

Answer 21

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

Question 22

herpes zoster

• pathogenesis
• presentation
• complications
• prevention

Answer 22

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

Question 23

gonoccocemia

• pathogenesis
• demographics
• presentation
• diagnosis
• treatment

Answer 23

• 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

Question 24

disseminated vibrio vulnificus infection

• pathogenesis
• presentation
• diagnosis
• complications

Answer 24

• 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

Question 25

ricksettsiapox

• pathogenesis
• demographics
• presentation
• treatment

Answer 25

• 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

Question 26

molluscum contagiosum

• pathogenesis
• presentation
• diagnosis

Answer 26

• 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

Question 27

orf

• pathogenesis
• demographics
• presentation

Answer 27

= 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

Question 28

monkeypox

• pathogenesis
• demographics
• presentation
• prevention

Answer 28

• 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

Question 29

Answer 29

ecthyma (s. pyogenes)

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

Question 30

Answer 30

folliculitis - s. aureus, p. aeruginosa, malassezia

Question 31

Answer 31

kerion (dermatophytes)

furuncle that is - painful, rounded, boggy, suppurative

Question 32

Answer 32

hidradenitis suppurativa

sinus tracts that are - tender, purulent, malodorous

Question 33

Answer 33

hand, foot & mouth disease (cocksackie A)

Question 34

Answer 34

tzacnk test

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

Question 35

Answer 35

gonococcemia

thayer martin agar showing gram - diplococci

Question 36

Answer 36

vibrio vulnificus

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

Question 37

Answer 37

vibrio fulnificus

TCBS agar is green - showing growth, but not fermentation

Question 38

Answer 38

varciella / chickenpox (HHV-3)

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

Question 39

Answer 39

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

Question 40

Answer 40

ovoid dsDNA molluscipoxvirus

molluscum contagiosum, orf, monkeypox

Question 41

Answer 41

molluscum contiogsum

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

Question 42

Answer 42

orf / echtyma contagiosum

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

Question 43

Answer 43

milkers nodule

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

Question 44

Answer 44

molluscum contagiosum (ovoid dsDNA molluscipoxvirus)

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

Question 45

Answer 45

molluscum contagiosum (ovoid dsDNA molluscipoxvirus)

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