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IDIS > DERM: Intro to Maculopapular Rash I & II > Flashcards

DERM: Intro to Maculopapular Rash I & II Flashcards

1
Q

define “viral exanthem”

A

widspread maculopapular rashes that are accompanied by systemic sx of inflammation

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2
Q

what are the childood infections that cause viral exanthems?

A
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3
Q

which enteroviruses cause exthanthems?

A
  • Cocksackie A
  • echovirus
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4
Q

which childhood viral infection causes nonspecific exanthems?

what does this mean?

A
  • echovirus 9
  • echovirus 16

(enteroviruses)

= means there are no vesicles

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5
Q

enterovirus exanthem - pathogenesis

A

start in the GI tract -> progress to rest of body

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6
Q

enterovirus exanthem - presentation

A

cocksackie A, echovirus

  • systemic
    • prodrome
    • major: GI sx PRECEDES development of rash
    • possible respiratory tract sx
  • skin: rash that is
    • follows GI sx
    • mild macular / maculopapular
    • non-pruritic
    • 1-3 days (fleeting)
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7
Q

enterovirus exanthem - epidemiology

  • demographics
  • transmissions
  • means of spread
  • other
A
  • mostly young infants
  • transmitted by saliva & feces (fecal oral)
  • spread: _multiple family member_s may be infected concurrently
  • most common childhood rash in the summer / fall
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8
Q

enterovirus exanthem - complications

A

rarely, to meningitis / encephalitis (HA)

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9
Q

parvovirus B12 exanthem - pathogenesis

A

(erythema infectiosum

virus infects erythroid progenitor cells -> leading to anemia

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10
Q

parvorirus B19 exanthem - presentation

A

erythema infectiosum

differ in child vs adult:

  • child:
    • systemic: nonspecific
    • skin: “slapped check rash”
      • ​starts on cheek - typically as child is feeling better
      • +/- pruritis
      • lasts 1-3 weeks
      • often waxes / wanes (relapses)
  • adult
    • ​systemic: ​acute polyarthritic sx common
    • skin: rash rare
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11
Q

parvovirus B12 exanthem - epidemiology

  • demographics
  • transmission
  • infectivity
  • other
A

erythema infectiosum

  • m/c in school age children
  • transmitted via nasal/salivary droplets
  • can cross placenta & rarely cause anemia (TORCH dz)
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12
Q

parvovirus B12 exanthem - complications

A
  • acute asplastic crisis (adults) severe aplastic anemia that can laed to CHF, bone marrow necrosis, ect.
  • neonatal erythema infectiosum (neonates only)
    • asplastic anemia
    • hydrops fetalis
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13
Q

rubella exanthem - pathogenesis

A

german / 3 day measles

virus replicates in the URT/cerivcal lymph nodes then disseminates -> creates virus-Ab complexes in skin

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14
Q

rubella exanthem - presentation

A

german measles, 3 day rash

  • ​systemic
    • prodrome ONLY in adults, precedes rash
    • polyarthritis in 50% of women
    • forcheimer spots: petechial hemorrhage on soft palate
  • rash
    • non-confluent - widely spaced, discrete lesions
    • starts on face -> descends (& fades on face)
    • lasts up to 3 days
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15
Q

rubella exanthem - epidemiology

  • demographics
  • transmission
  • infectivity
  • other
A
  • all ages affected
  • transmitted by droplet inhalation
  • can cross placenta (TORCH dz)
  • rare in US d/t vaccine
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16
Q

rubella - complications

A

= congenital rubella syndrome (CRS)

  • classic triad: deafness + eye issues + CDH
    • deafness
    • eye abnormalities - cataracts, glaucoma, retinopathy
    • congenital heart disease (“blue baby)
  • blueberry muffin rash (purpura)
  • growth restriction - low birth weight / microcephaly
  • CNS abnormalities - retardation, behavioral disorders
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17
Q

describe the presentation of CRS

A
  • classic triad: deafness + eye issues + CDH
  • blueberry muffin rash (purpura)
  • growth restriction - low birth weight / microcephaly / radiolucent bone dz
  • CNS abnormalities - retardation, behavioral disorders
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18
Q

measles exanthem - pathogenesis

A

rubeola

paramyxovirus infects leukocytes/lymphatic tissue -> producing multinucleated giant cells (warthin-finkeldey cells) in lymph nodes

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19
Q

identify

A

warthin-finkeldey cells

mutli-nucleated giant cells resulting from paramyxovirus-infected leukocytes / lymphatic tissue

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20
Q

measles exanthem - presentation

A
  • systemic: prodrome =
    • photophobia
    • koplik’s spots: white lesions of buccal mucosa opp. molars
    • C-triad: cough + coryza + conjuncitivits
    • HA
    • otitis media (infants)
  • skin: rash​
    • ​onset follows fever but overlaps with it
    • starts at hairline & descends slowly
    • mildly pruritic
    • petichial lesions on mucosa
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21
Q

measles exanthem - epidemiology

  • demographics
  • transmisision
  • infectivity
  • other
A
  • n/a
  • direct contact / droplets / fomites
  • highly contagious
  • generally rare in US due to vaccine
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22
Q

what are these and what exanthem are they indicative of?

A

koplik’s spots

measles (rubeola)

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23
Q

measles exanthem - complications

A

several - pneumonia is key (m/c cause of death d/t measles)

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24
Q

measles

  • prognosis
  • therapy
  • prevention
A
  • prognosis - inc mortality d/t complications (pneumonia m/c). complications indicator = inc risk of complications w/ fever persistence after the 4th day of the rash \
  • therapy
    • vitamin A
    • ribavirin
  • prevention - MMR vaccine
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25
Q

rosaela infantum exanthem - pathology

A

HHV-6 results in antibody-antigen complex formation -> rash

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26
Q

roseola infantum exanthom - pathologenesis

A

HHV-6B (sometimes HHV-7) causes antibody-antigen complex formation -> rash

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27
Q

roseola infantum - presentation

A
  • systemic: sudden high fever then rapid defervescence followed by a surprise rash
    • in infants: cause cause febrile seizures
  • skin:
    • a “surprise rash” that
      • follows rapid defervescence (decline in fever with no overlap)
      • is maculopapular
    • along with Nagayama spots: small, erythematous papules on the soft palate (uvula)
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28
Q

roseola infantum exanthem - epidemiology

  • demographics
  • transmission
  • infectivity
  • other
A
  • kids 6 mos - 2 years (infants)
  • transmission via:
    • saliva
    • genetic: integration of HHV-6 intoparent chromosome (congenital “roseola”)
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29
Q

roseola infantum exthanthem

  • diagnosis
  • prognosis
  • therapy
A
  • diagnosis: presentation usually sufficient
  • prognosis: typically self limiting, febrile seizures in infants can inc morbidity
  • therapy: avoidance, no vax
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30
Q

scarlet fever exanthem - pathology

A

streptococcus pyogenes express pyrogenic (fever causing) exotoxins A, B and C -> induces a type IV hypersensitivity reaction

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31
Q

scarlett fever exanthem - presentation

A

s. pyrogenes

  • systemic prodrome
    • abrupt onset of sore throat + fever
      • sore throat = pharyngitis / tonsillitis
      • but, no other upper respiratory signs
    • tongue: either
      • STRAWBERRY TONGUE - bright red
      • WHITE STRAWBERRY TONGUE - yellowish white coating
  • skin: sandpaper rash + pastia’s lines + circumoral pallor + superfiial desquamation
    1. sandpaper rash - confluent, punctate papules that
      • blanch under pressure
      • are concentrated in
        • ​neck
        • axilla
        • groin
    2. pastia’s lines - peteiae in creases
    3. circumoral pallor (red cheeks + pale around mouth)
    4. ​​superficial desquamation of palms & soles
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32
Q

scarlet fever exanthem - complications

A

= s. pyogenes

  • rheumatic fever (type II hypersensitivity)
  • glomerulonephritis (type III hypersensitivity)
33
Q

tx of scarlett fever?

A

penicillin G

34
Q

identify this feature & explain its significance

A

pastia’s lines: petichiae in creases

seen in scarlett fever exanthem (s. pyogenes)

35
Q

what childhood viral exanthem do these signs indicate?

A

scarlett fever

  • strawberry & white strawberry tongue = systemic
  • desquamation of palms = skin
36
Q

which childhood viral exanthems are nationally notifiable disease?

A
  • rubella (rubella virus)
  • measles (paramyxovirus)
37
Q

which childhood viral exanthems are TORCH disease?

A
  • erythema infectiosum (parvovirus B19)
  • rubella
38
Q

differentiate the key differences between the skin presentations of each childhood viral exanthem

A
  • erythema infectiosum (parvovirus B19)
    • slapped cheeks
    • reticulate (lacy) body rash
  • enterovirus rash: descenending from face down
  • rubella (german / 3-days measles): descending from face down
  • measles:
    • kopliks spots
    • descending rash from harline down
    • goes from blanching -> non-blanching
  • roseola infantum
    • ​”surprise rash” (on trunk) following rapid defervescence
  • scarlett fever
    • sand-paper rash (punctate, confluent papules) on neck + axilla + groin
    • circumforal pallor
    • pastias lines
    • post-rash desquamation on palms & soles
39
Q

which childhood viral exanthem can cause postauricular lymph node enlargement?

40
Q

which childhood viral exanthem is the most common infection of summer / fall?

A

enteroviruses (cocksackie A and B)

41
Q

which childhood viral exanthems involve no / short prodrome ?

A
  • erythema infectiosum (parvovirus B12)
  • enteroviruses
  • rubella

EER - extra extra rapid

43
Q

tinea versicolor - pathogenesis

A

= pityriasis versicolor (cutaneous malsseziasis)

  • malassezia sp (a dimorphic fungi) metabolize lipids to generate acids that can damage melanocytes causing -> hyperpigmented or hypopigmented lesions
44
Q

tinea versicolor presentation

A

malasseziasis sp

  • skin: lesions on upper trunk that are
    • HYPOPIGEMENTED (white-ish) or HYPERPIGMENTED (brown)
    • “branny” - scaly, non-blanching
45
Q

tinea versicolor - diagnosis

A
  • 10% KOH treated scin scraping: “spaghetti & meatball appearance”
  • wood’s lamp: shows yellow/orange luminescence
46
Q

tinea versicolor - summary

  • pathogenesis
  • demographics
  • presentation
  • treatment
A
  • pathogenesis malassezia sp (a dimorphic fungi) metabolize lipids to generate acids that can damage melanocytes
  • demographics
    • m/c in tropical environments
    • repeated overgrowth in - oily skin or I/C
  • presentation: HYPOPIGEMENTED (white-ish) or HYPERPIGMENTED (brown) lesions that are scaly & non-blanching
  • treatment: anti-fungals
47
Q

identify

A

spaghetti & meatbals appearance from KOH stain

dx of tinea versicolor (malasezzia sp fungi)

48
Q

tinea versicolor - demographics

A
  • m/c in tropical environments
  • repeated overgrowth is m/c in people with
    • oil skin
    • weak immune system
49
Q

tinea versicolor - tx

A

topical anti-fungals

50
Q

toxic shock syndrome (TSS) - pathogenesis

A
  • infection w/ s. aureus > strep pyogenes, which release pyogenic superantigens that act as T-cell mitogens -> cytokine strom -> high fever
    • s. aureus: TSST-1 & enterotoxins (enterotoxin = also cause GI sx)
    • s. pyogenes: exotoxins & poss M-protein
51
Q

toxic shock syndrome (TSS) - demographics

A

s. aureus > s. pyogenes

  • generally very rare in US
    • though - is m/c in individuals that are negative for anti-TSST-1 antibodies & are unable to make any after being exposed
52
Q

toxic shock syndrome - presentation

A

s. aureus > s. pyogenes

  • systemic:
    • sudden, rapidly progressing fever that can progress to SHOCK: HYPOTENSION + tachycardia / tachypenea
      • GI sx if s. aureus
  • skin :erythyematous, macular rash + elements resembling scarlett fever, esp if s. pyo
    • desquamation of palms & soles
    • strawberry tongue
    • if so pyo: sandpaper rash
53
Q

toxic shock syndrome (TSS) - dx

A

s. aureus > s. pyro

  • must meet the following criteria to fit CDC definition:
    1. fever of 102 F or greater
    2. rash that is: macular & erythematous OR scarlittiniform (sandpaper)
    3. HYPOtsn: SBP < 90 or orthostatic drop in SBP > 15 mmHg
    4. at least 3 major organs involved
54
Q

toxic shock syndrome (TSS) - treament

A
  • abx: nacillin or oxicillin
  • TREAT SHOCK
55
Q

TSS - summary

  • pathogenesis
  • demographics
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: infection w/ s. aureus > strep pyogenes, which release pyogenic superantigens that act as T-cell mitogens -> cytokine strom -> high fever
    • s. aureus: TSST-1 & enterotoxins (enterotoxin = also cause GI sx)
    • s. pyogenes: exotoxins & poss M-protein
  • demographics: generally very rare in US, but m/c in indiivduals negative for anti-TSST-1 Abx
  • presentation:
    • systemic:
      • sudden, rapidly progressing fever that can progress to SHOCK: HYPOTENSION + tachycardia / tachypenea
        • GI sx if s. aureus
    • skin :erythyematous, macular rash + elements resembling scarlett fever, esp if s. pyo
      • desquamation of palms & soles
      • strawberry tongue
      • if so pyo: sandpaper rash
  • diagnosis: must meet the following criteria to fit CDC definition: 4
    1. fever of 102 F or greater
    2. rash that is: macular & erythematous OR scarlittiniform (sandpaper)
    3. HYPOtsn: SBP < 90 or orthostatic drop in SBP > 15 mmHg
    4. at least 3 major organs involved
  • treatment: nafcillin / oxicillin + TX shock
56
Q

meningococcemia - pathogenesis

A

neisseria meningitidis (gram - diplococci) releases lipooligosacharide (LOS) endotoxin, leading to -> vasculitis / localized thrombohemorrhaghic lesions

57
Q

meningococcemia - demographics

A
  • infants
  • teens
  • complement deficient: C5, C6, C7 or C8
58
Q

leptospirosis

  • pathogenesis
  • trasmission
  • presentation
  • prognosis
  • treatment
A

= aka weil’s syndrome:

  • pathogenesis: leptospirosis (spirochete with hooked ends) reside in kidneys & lead to vasculitis
  • transmission: exposure to urine / urine contaminated water from infected mammals
  • presentation:
    • macular rash -> purpura
    • weil’s triad: JAUNDICE + ACUTE KIDNEY INJURY + HEMORRHAGE
      • hemorrhage:
        • pulmonary hemorrhage
        • subconjunctival hemorrhage
        • epistaxis
        • purpura
  • prognosis:
    • self limiting except in unborn fetus (> 50% mortality)
    • better if there is NO juandice
  • treatment: Abx (prevention with doxycyline)
59
Q

identify & explain significance

A

= leptospirosis:

  • spirochete with hooked ends
  • contracted via contact w/ urine from infected mammals
  • causes:
    • weil’s triad: jaundice + acute kidney injury + hemorrhage
      • hemorrhage =
        • purpura
        • subconjunctival hemorrhage
        • pulmonary hemorrhage
  • prognosis better when there is NO jaundice
60
Q

meningococcemia - presentation

A
  • systemic: nonspecific prodrome
  • skin: non-blanchng macules & petichiae that
    • begin on trunk & legs then spreading to areas where pressure is applied
    • can progress
      • purpura
      • ecchymosis with central necrosis (confluent purpura)
61
Q

meningococcemia - complications

A
  • septic shock
  • meingitis
  • disseminated itravascular coagulation (DIC)
  • waterhouse-friedrichsen syndrome
62
Q

meningococemia - treatment

A
  • penicillin G / ceftriaxone: NECESSARY, OR IS FATAL
  • prevention with menACYW vaccine: meningococcal conjugated polysaccharide vaccine
    • note: booster & menB serotype given during epidemics
63
Q

rat-bite fever

  • pathogenesis
  • presentation
  • treatment
A
  • d/t one of two gram negative bacteria that cause hematogenous dissemination:
    • streptobacillary:- d/t streptobacilus monoformis:
      • microaerophillic
      • pleomorphic
      • filamentous rod
    • spirillary: d/t spirillum minus:
      • ​aerobic
      • bipolar-flagellated spiral
  • presentation:
    • systemic:
      • polyarthralgia
      • relapsing fever at irregular intervals
    • skin: purpuric maculopapular rash -> small pustules on palms & soles
  • treatment: penicillin G
64
Q

what are the two etiologic agents of rat-bite fever and

  • how are they different?
  • which one causes RBF in the US?
A
  • streptobacillary (streptobacilus monoformis) - only form seen in the US
    • microaerophillic
    • pleomorphic
    • filamentous rod
  • spirillary (spirillum minus)
    • ​aerobic
    • bipolar-flagellated
    • spiral
65
Q

secondary syphyllis

  • pathogenesis
  • transmission
  • presentation
  • diagnosis
  • prognosis
  • treatment
A
  • pathogenesis: treponema pallidum (spirochete) causes a chancre at innoculation site
  • transmission:
    • sexually
    • congenital (TORCH dz)
  • presentation:
    • rash:
      • maculopapular lesions ​on the palms & soles are non-pruritic
      • mucutaneous lesions ton oral, genital, anal
    • condyomata latum: wart like, moist
    • alopecia
  • diagnosis:
    • VDLR/RPR, then FTA-ABS
    • darkfield microscopy - shows spirochete
  • treatment: penicillin G
66
Q

erlichiosis

  • pathogenesis
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: one of two obligate intracellular pathogens is transmitted via lone star tick bite
    • erlichiae chaffeensis: infects monocytes - human form
    • erlichiae ewingii: infects granulocytes
  • presentation: same as anaplasmosis
    • rash: often NOT even seen* - pinpoint maculopapular (“lacy”) rash
    • systemic:
      • prodrome - fever, chills
      • thrombocytopenia
      • elevated liver enzymes
  • diagnosis: morulae - microbe within cytosplasmic vacules in phagocytic cells
  • treatment: doxycycline
67
Q

what are the two etiological agents for ehrlichiosis and how do they differ?

A

both obligate intracellular parasites carried by lone star tick

  • erlichiae chaffeensis: infects monocytes - human form
  • erlichiae ewingii: infects granulocytes
68
Q

which form of erlichiosis invades humans?

A

erlichiae chaffeensis: infects monocytes - human form

69
Q
A

morulae

cytplasmic inclusions of erlichiosis / amaplasmosis in a phagocyte

(in this case, anaplasma in a granulocyte)

70
Q
A

morulae

cytplasmic inclusions of erlichiosis / amaplasmosis in a phagocyte

(in this case, erlichiosis in a monocyte)

71
Q

anaplasmosis

  • pathogenesis
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: anaplasma phagocytophilum - an obligate intracellular pathogen - is transmitted via ixodes tick
  • presentation: same as anaplasmosis
    • rash: often NOT even seen* - pinpoint maculopapular (“lacy”) rash
    • systemic:
      • prodrome - fever, chills
      • thrombocytopenia
      • elevated liver enzymes
  • diagnosis: morulae - microbe within cytosplasmic vacules in granulocytes
  • treatment: doxycycline
72
Q

rocky mountain spotted fever

  • pathogenesis
  • presentation
  • diagnosis
  • treatment
A
  • pathogenesis: rickesttiae rickettsiae - a obligate intracellular pathogen transmitted by ixodid tick - infects vascular endothelial cells
  • presentation:
    • skin: ascending rash that starts from the wrists & ankles and the moves centripitally (outward -> inward) within hours. is
      • ​non-pruritic
      • involving the soles & palms
    • systemic: significant involvement
      • muscle degeneration
      • edema - periorbital* & peripheral (pulmonary, cerebral)
      • conjunctival suffusion*
      • thrombocytopenia (like anaplasma, erclichiosis)
  • treatment: doxycyline
73
Q

what presentations can rock mountain spotted fever have with respect to the eye?

A
  • periorbital edema
  • conjunctival suffusion
74
Q

contrast the rashes caused by rickettsia (rocky mounted spotted fever & rickettsiapox) and erlichiosis / anaplasma ?

A
  • RMSF (rickettsia, ixodids tick): ascending / centripital rash starting at wrists & ankles
  • rickettialpox (rickettsia, mice): initial eschar + subsequent crop of vesiculopapules
  • erlichiosis / anaplasma (lone star tick, ixodids tick): often undetectible, punctate rash
75
Q

endemic typhus

  • pathogenesis
  • presentation
  • diagnosis
A
  • pathogenesis: infection via obligate intracellular pathogen by carried by lice from a flying squirrel vector
  • presentation:
    • systemic: prolonged high fever (104 F for ~2 weeks)
    • rash: begins in axilla & trunk -> spreads centrifugally and out to extremities
  • diagnosis: weil-felix test
76
Q

flea-borne murine typhus

  • pathogenesis
  • demographics
  • presentation
A
  • pathogenesis: contraction of ricksettia typhi - an obligate intracellular coccobacillus - via fleas (from several animal reservoirs)
  • demographics: contact with animals - cats, mice, opposum
  • presentation:
    • rash: begins on the trunk - spreads centrigually to extremities (like endemic typhus)
    • systemic: classic prodrome
77
Q

cutaneous tuberculosis

  • pathogenesis
  • presentation
  • diagnosis
A
  • pathogenesis. m tuberulosis (acid-fast aerobic bacillus) forms caseating (necrotic) granulomas
    • ​can be triggered by BCG vaccination
  • presentation: depends on if infection of primary or secondary:
    • primary: enters skin via trauma sites
      • no prior exposure to TB - > papule / nodule (“innoculation chancre”
      • rrior exposure to TB -> warty lesions (“verrucosa cutis”)
    • secondary: patient with TB In lung that dissseminates
      • tuburculoid granulomas
        • red-brown
        • painless
        • on the head or the neck
  • diagnosis:
    • Mantoux test / IGRA test (no false + from vax)
    • lesions beomes yellow-brown “apple jelly” upon application of pressure
78
Q

leprosy / hansen’s disease

  • pathogenesis
  • presentation
  • diagnosis
    *
79
Q

compare and contrast the etiological agents of

  • cutaneous tuberulosis
  • leprosy / hansen’s disease
A
  • both are acid fast aerobic bacillus
    • m. tuberulosis:
      • NOT an obligate intracellular pathogen
      • growth NOT restricted at 37 C
    • m. leprae is
      • obligate intracellulate
      • growoth restricted at 37 C

IDIS (12 decks)

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