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STEP > ID 13 > Flashcards

ID 13 Flashcards

1
Q

HBV transmission mnemonic

A

Parenteral (blood)
sexual (baby-making)
perinatal (birthing)

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2
Q

HDV transmission

A

same as HBV

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3
Q

most common HEV source

A

waterborne

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4
Q 
incubation
HAV -
HBV -
HCV -
HDV - 
HEV -
A 
HAV - short (weeks)
HBV - long (months)
HCV - long
HDV - superinfection - short, confection = long
HEV - short
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5
Q

HDV superinfection

A

HDV after HBV

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6
Q

HDV coinfection

A

HDV with HBV

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7
Q

HAV clinical course

A

Asymptomatic (usually)

Acute

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8
Q

HV clinical course

A

Initially like serum sickness (fever, arthralgia, rash); may progress to carcinoma.

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9
Q

HDV clinical course?

A

similar to HBV

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10
Q

HEV clinical course

A

fulminant hepatitis in pregnant women

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11
Q

HBV prognosis

A

Most adults have full resolution; minority have chronic infection.

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12
Q

HDV prognosis?

A

Superinfection –> worse prognosis

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13
Q

HCV prognosis?

A

majority develop stable, Chronic hep C

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14
Q

HAV liver biopsy

A

1) hepatocyte swelling
2) monocyte infiltration
3) councilman bodies

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15
Q

HBV liver biopsy

A

granular eosinophilic “ground glass” appearance.

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16
Q

HCV liver biopsy

A

lymphoid aggregates with focal areas of macro vesicular steatosis

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17
Q

HDV liver biopsy

A

similar to HBV

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18
Q

HEV liver biopsy

A

patchy necrosis

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19
Q

carrier state with hepatitis?

A

only seen with HBV and HCV

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20
Q

anti-HAV (IgG) significane

A

IgG antibody indicates prior HAV infection and/or prior vaccination.
*protects against reinfection.

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21
Q

HBsAg indicates…

A

infection

22
Q

Anti-HBs indicates…

A

immunity

23
Q

Significance of Anti-HBc

A

If IgM = acute/recent infection.

If IgG = prior exposure or chronic infection

24
Q

marker of infection during window period?

A

1) Anti-HBe

2) IgM anti-HBc (may be sole positive marker of infection during window period).

25
Q

What is HBeAg

A

Secreted by infected hepatocyte into circulation. Not part of mature HBV virion.

26
Q

Significance of Anti-HBe

A

low transmissibility

27
Q

Marker during incubation period?

A

HBsAg

28
Q

Other marker of alcohol use?

A

ethyl glucuronide

29
Q

Markers of prodrome, acute disease

A

HBsAg
IgM anti-HBc
HBeAg

30
Q

Markers of Chronic high infectivity HBV?

A

HBsAg
HBeAg
IgG anti-HBc

31
Q

Markers of Chronic low infectivity HBV?

A

HBsAg
Anti-HBe
Anti-HBc IgG

32
Q

markers during recovery?

A

Anti-HBs
Anti-HBe
Anti-HBc IgG

33
Q

markers of immunity?

A

anti-HBs

34
Q

HIV envelope proteins?

A

gp120

gp41

35
Q

gp120?

A

docking glycoprotein. attaches to host CD4+ cell

36
Q

gp41?

A

transmembrane glycoprotein. fusion and entry

37
Q

p17?

A

HIV matrix protein

38
Q

p24?

A

HIV capsid protein

39
Q

origin of gp120 and gp41?

A

Formed from cleavage of gp160 to form envelope glycoproteins.

40
Q

what is gag?

A

codes for p24 + p17

41
Q

what is pol?

A

gene that codes for reverse transcriptase + aspartate protease + integrase

42
Q

virus binding mechanism

A

Binds CD4 + coreceptor (either CCR5 on macrophages in early infection or CXCR4 on T cells in late infection).

43
Q

heterozygous CCR5 mutation?

A

slower course

44
Q

homozygous CCR5 mutation?

A

immunity

45
Q

ELISA characteristics

A

sensitive, high false positive rate and low threshold. RULE OUT.

46
Q

Western blot characteristics for HIV

A

Specific, low false positive rate and high threshold. RULE IN.

47
Q

AIDS diagnosis

A

1) CD4 below 200
2) HIV positive with AIDS-defining condition
30 CD4+ percentage lower than 14%

48
Q

problem with ELISA/Western blot

A

Often falsely negative in first 1-2 months of HIV infection and falsely positive initially in babies born to infected mothers (anti-gp120 crosses placenta).

49
Q

What is the window period?

A

Time between acute infection and recovery.

50
Q

How can you tell AIDS stage based on surface proteins?

A

as patients enter the symptomatic period and as immune function declines, peoples’ ability to produce any isotype of antibody declines and thus antibodies to capsid antigen (p24) will decline (can’t class switch due to TH deficiency). Once patients develop AIDS in the final stages of the disease, they’re so deficient in T cells that they can’t undergo class switching. IgM can be made in the absence of TH cells, however, and production of IgM continues against envelope glycoproteins (gp120 and gp41) since those antigens are constantly being altered by the process of random mutation (genetic drift).

51
Q

AIDS virus type

A

lentivirus (long latent period)

52
Q

What is reverse transcriptase?

A

An RNA-dependent DNA polymerase because it synthesizes cDNA from an RNA template.

STEP (85 decks)

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