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Medicine II > HIV infection > Flashcards

HIV infection Flashcards

1
Q

normal CD4 count

A

500

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2
Q

immunosuppressed CD4 count

A

200

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3
Q

HIV transmission

A
  • blood/blood products

- body fluids/ sexual transmission

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4
Q

blood/blood products that transmit HIV

A
  • transfusion (RBC + Clotting factors)
  • IVDU (sharing needles)
  • Lab/ Health care workers/ needle stick
  • vertical transmission
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5
Q

Body fluids/ sexual transmission of HIV

A
  • MSM

- heterosexual

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6
Q

where are the majority of deaths + those with HIV in children?

A

Africa

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7
Q

percent of those HIV infected do not know their status

A

1/3

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8
Q

who should be screened annually?

A

people at high risk

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9
Q

HIV ab testing should be performed routinely in all patients age

A

13-64

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10
Q

clinical manifestatios of acute HIV infections in order of most prominent to least

A 
fever
fatigue
myalgia
skin rash
headache
pharyngitis
cervical adenopathy
arthralgia
night sweat
diarrhea
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11
Q

myalgia

A

pain in a muscle or group of muscles

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12
Q

arthralgia

A

pain in a joint

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13
Q

inquire new partners

A
  • within last 3 mos
  • past testing
  • sexual risk
  • exposure/assault
  • needle sharing
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14
Q

screening test for HIV use 4th generation use

A

immunoassays that combine HIV antigen + HIV antibody

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15
Q

inquire about new partners

A
  • within last 3 mos
  • past testing
  • sexual risk
  • exposure/assault
  • needle sharing
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16
Q

remember the window period

A

earliest positive= 15-20 days

prior to that window, may test negative despite symptoms of acute HIV

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17
Q

diagnosis of acute HIV requires detectable plasma RNA

A

-test RNA early if symptomatic

-

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18
Q

4th generation diagnostic HIV tests= window

A

IgM + IgG antibody and p24 antigen

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19
Q

4th generation HIV test target of detection

A

IgM + IgG antibody and p24 antigen

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20
Q

4th generation window to take positive tset

A

15-20 days

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21
Q

HIV viral load test target of detection

A

RNA

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22
Q

HIV viral load test approximate time to positivity

A

10-15 days

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23
Q

HIV II

A

rare

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24
Q

how many years does it take to develop advanced disease

A

8-12 years

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25
Q

untreated HIV can be

A

very progressive + infectious

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26
Q

What does HIV target that declines infection?

A

CD4 cells

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27
Q

HIV is most common in people with

A

lower CD4 counts

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28
Q

acute antiretroviral infection

A

seroconversion

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29
Q

evolution of untreated HIV leads to

A

acute antiretroviral infection (seroconversion)

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30
Q

acute antiretroviral infection

A
  • viral syndrome in most, but may be mild

- within 2 weeks, develop Mono-like syndrome

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31
Q

established HIV

A

start ART (acute antiretroviral infection) at any CD4 count, even if asymptomatic

  • CD4>350 -500 cells
  • symptomatic
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32
Q

untreated, progressive HIV

A
  • opportunistic infections/malignancies

- risk for OIs depends on exposure

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33
Q

opportunistic infections/malignancies

A

-cell mediated immune deficit
-exposure to opportunistic pathogens
-epidemiology of frequent OIs
(diagnostic methodology + tx)

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34
Q

risk for Opportunistic Infections depends on exposure

A
  • geography/prior exposure
  • practices/habits
  • degree of immunosupression
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35
Q
A

pneumonias, shingles, candida

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36
Q

early opportunistic infectious, CD4 count

A

> 200

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37
Q

Late opportunistic infections : CD4 count

A

> 200

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38
Q

What kind of population do early Opportunistic infections affect?

A

in healthy population, more common in HIV+ before severely immunocompromised

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39
Q

early Opportunistic Infections

A 
TB
Candida/thrush
VZV/shingles
Recurrent Bacterial/Pneumonia
Histoplasmosis
Kaposi's sarcoma
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40
Q

late opportunistic infections

A
  • pneumocystis pneumonia

- chronic diarrhea cryptosporidia

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41
Q

CD4

A
  • toxoplasma (seizures)
  • CMV (visual loss)
  • MAC (actypial mycobac)
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42
Q

AIDS Defining conditions

A
  • recurrent bacterial infections
  • candidal infection of esophagus, trachea, bronchi
  • disseminated coccidiomycosis, histoplasmosis
  • extrapulmonary cryptococcosis
  • chronic cryptosporidiosis or isospora
  • CMV
  • persistent mucocutaneous HSV
  • HIV encephalopathy
  • Kaposi’s sarcoma
  • Primary lymphoma of the brain
  • Non Hodgkin’s B cell lymphoma
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43
Q

women with uncontrolled HIV are more prone to more rapid

A

cervical cancer

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44
Q

AIDS defining conditions, cont: HIV plus

A
  • lymphoid interstitial pneumonitis (LIP) (Pediatric)
  • Cervical cancer (women)
  • Disseminated Mycobacterial infection (not tb)
  • extrapulmonary tb
  • pneumocystis pneumonia
  • progressive multifocal leucoencephalopathy
  • recurrent salmonella infection
  • toxoplasmosis of the brain
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45
Q

primary prevention of opportunistic infections

A

prevents the 1st occurrence

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46
Q

secondary prevention of opportunistic infections

A
  • previously treated for disease

- often a reduced dose to prevent reactivation of serious disease

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47
Q

primary prevention for CD4

A
  • penumocysits- prevent with trimethoprim/sulfa
  • cheap + effective
  • also prevents toxo
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48
Q

percent risk of pneumocystis / year

A

60%

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49
Q

primary prevention for CD4

A

MAC- prevent with azithromycin weekly dose

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50
Q

secondary prevention

A
  • candida
  • cryptococcal meningitis, histo, cocci
  • CMV
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51
Q

ART

A

anti retroviral therapy

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52
Q

ART era= chronic manageable disease

A
  • more testing, early ID, newly identified HIV+ are asymptomatic
  • more sophisticated understanding of viral pathogenesis and more treatment options
  • prefer ART once diagnosed, AND ready yo take pills regularly
  • CD4 recovery and viral plasma RNA undetectable expected in all
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53
Q

complications of long term infection and long term therapy (difficult to separate)

A
  • body shape abnormalities

- metabolic abnormalities (DM, hyperlipidemia, osteoporosis)

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54
Q

not all HIV associated conditions are diminishing in the era of ART

A

even higher CD4 counts, HIV infection is linked to

  • chronic immune activation
  • progressive HCV liver disease, renal disease
  • Cardiovascular disease
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55
Q

even with HIV suppression through ART, HIV is linked to

A
  • chronic immune activation

- increased cancer risk, particularly lymphomas, lung cancer and invasive cervical

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56
Q

traditional indications for antiretrovirals

A

“the cocktail” in combo for acute or chronic HIV, highly active ART

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57
Q

known positive HIV patient takes ART

A

reduces the viral concentration from the source

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58
Q

If giving tablets to HIV neg to prevent them from getting the risk, use

A

selectively

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59
Q

Post-exposure prevention (PEP) indications for antiretrovirals

A

occupational: (needlestick/sharp/blood exposure or mucosal splash)

Non-occupational: mother infant transmission + sexual exposure (high risk, known positive)

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60
Q

pre-exposure prevention (PrEP) indications for antiretrovirals

A

prevention for those with ongoing high risk

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61
Q

goals for anti retroviral therapy

A
  • reduced HIV related illness and death
  • improve quality of life
  • restore and preserve immune function
  • provide potent sustained HIV control
  • prevent HIV transmission
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62
Q

each class of medications have similar

A

targets at diff points

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63
Q

antiretroviral drug classes

A

-nucleoside/nucleotides
reverse transcriptase inhibitors
(NRTIs)
-non-nucleoside reverse transcriptase inhibitors (NNRTIs)
-protease inhibitors (PIs)
-HIV entry inhibitors (fusion inhibitors + CCR5 inhibitors)
-integrase inhibitors

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64
Q

goal of ART

A

HIV RNA below the level of detection

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65
Q

2014 ART first regimen guidelines

A

2 NRTI + integrase inhibitor or with darunavir/rtv

66
Q

most commonly used NRTI

A

truvada

67
Q

most commonly used multi-class drug combos

A

atripia, complena, strolloid?

68
Q

most commonly used protease inhibitors

A

norvir, prozigta, reyataz

69
Q

optimal ART response

A

CD4 counts recovering quickly

-viral load below testing threshold which is 75

70
Q

adverse effects of ART

A
  • gaining weight too fast
  • fatigued
  • had headaches
  • concerned that she was putting poison into her body each time she took ART
  • discontinued ART and was lost to care for 3 years
71
Q

CURRENT ART IS

A

well tolerated, much less likely Gi distress, fat wasting, fat accumulatoin and hyperlipidemias

72
Q

protease inhibitors side effects

A

caused upset stomachs, diarrhea, triclyerol problmes, facial appearance changes with wasting of the temples of the cheek
-arms and legs look very muscular by you lose subcutaneous tissues

73
Q

morphologic complications of ART

A

fat accumulations (lipohypertrophy)

  • buffalo hump
  • arm wasting
  • skin very thin but fat accumulation in musculature
  • wasted hollow cheeks and temples
74
Q

benefit /risk ration

A

greater benefit

  • reduction in mortality
  • risk= short and long term toxicities
75
Q

HIV associated body shape, metabolic and CV risk host factors

A
  • age
  • prior weight + body composition
  • family history
76
Q

HIV associated body shape, metabolic and CV risk viral factors

A
  • severity + duration of disease (chronic inflammation)

- cannot be measured simply by CD4 count + viral load

77
Q

HIV associated body shape, metabolic and CV risk treatment factors

A

individual agents associated with selected metabolic and body shape changes

78
Q

who needs to be psychologically ready for that daily dose

A

newly positive patient

79
Q

evaluation of a newly positive patient

A
  • psychological readiness for tx

- social and economic situation

80
Q

blood tests of a newly positive patient

A

blood count, renal, liver, HIV drug resistance, past and chronic infections, (RPR, Hep A/B/C, toxo)

81
Q

preventives for a newly positive patient

A

bactrim, Azithro, vaccinations

82
Q

ART for newly positive patient

A

if ready, willing, and able

83
Q

HIV therapy 2015

A
  • HIV preventives and ART need to be individualized for each patient, and supported for adherence
  • current agents are potent and durable HIV control with a min of short and long term side effects, but require life long tx
84
Q

if a patient is taking BACTRIM , count is

A
85
Q

pep

A

post exposure prophylaxis

86
Q

bactrim for pneumocystis prevention implies CD4 count is

A

low

87
Q

off ART + low CD4 count implies

A

greater HIV RNA in blood, increases infectivity

88
Q

risk

A

anything that is blood contaminated

89
Q

definitions of occupational exposure

A
  • percutaneous injury
  • contact of mucous membranes or non-intact skin with blood, tissue or infectious fluids
  • not infectious unless they contain visible blood
90
Q

contact of mucous membranes or non-intact skin with blood, tissue or infectious fluids

A 
CSF
snynovial 
plueral
peritoneal
percardial
amniotic 
("internal" body fluids)
91
Q

not infectious unless they contain visible blood

A

(“external” fluids) feces, nasal secretions, saliva, sputum, sweat, tears, urine, vomitus

92
Q

are you at risk if you had a patient who was coughing during a tooth extraction and may have splashed your eyes with some bloody saliva

A

YES

93
Q

Are you at risk if you had a patient who was coughing during a tooth extraction and may have splashed your eyes with some bloody saliva splash onto an ungloved wrist?

A

no

94
Q

Are you at risk if you had a patient who was coughing during a tooth extraction and may have splashed your eyes with some bloody saliva onto yoru recently surgically repaired elbow (less than perfectly intact skin)

A

yes

95
Q

definitions of occupational exposure

A
  • any direct contact (i.e. no barrier protection) to concentrated virus in a laboratory facility
  • human bite
96
Q

human bite occupational exposure

A

both the person bitten and the person who inflicted the bite have potentially been exposed to bloodborne pathogens
(HIV/HBV/HCV transmission very rarely reported by this route

97
Q

most frequent to least frequent needlestick injuries

A 
nurses (37.9%)
residents/fellows (11.4%)
attending physicians (10.7%)
surgery attendings (9.0%)
phlebotomists (5.4%)
nonlaboratory technologists (4.7%)
98
Q

what is associated with a 3-fold increase in the risk of needle stick injuries

A

long work hours + sleep deprivation among medical trainees result in fatigue

99
Q

what increases the risk of transmission more than intact skin or mucous membrane exposures

A

percutaneous

100
Q

estimated risk of transmission from percutaneous exposure to blood through needle punctures or other injuries caused by contaminated sharp objects:

A

HBV: 1%- 30%
HCV: 1.8-3%
HIV .3%

101
Q

percutaneous

A

pertains to any medical proceudre where access to inner organs or other tissue is done via needle puncture of the skin, rahter than by using an “open” approach where inner organs or tissue are exposed (typically with the use of a scalpel)

102
Q

percentage of HIV transmission percutaneously

A

0.3%

103
Q

percentage of HIV transmission mucocutaneous

A

0.09%

104
Q

percentage of HIV transmission non-intact skin exposure

A

?

105
Q

mucocutaneous zone

A

region of the body in which mucosa transitions to skin

106
Q

risk of HIV infection increased with exposure to larger amounts of

A

blood

  • device visibly contaminated with patient’s blood
  • procedure involving direct venous or arterial puncture on the patient
  • deep injury to HCW
  • risk for infection increased if source patient has a high viral load
107
Q

CDC estimates how many needle-stick injuries in US hospitals each year

A

61% of injuries are due to hollow bore needles

108
Q

cases of documented HIV seroconversion after occupational exposure (mostly nurses) predominantly before 1995

A

57 cases

109
Q

no proven HIV transmission from occupational exposure reported since

A

1999

110
Q

cases of PEP failure, complex reasons

A

21

111
Q

after first mucosal exposure, how many days does it take for virus to get taken by dendritic cells , to expand and replicate

A

5-14 days

112
Q

HIV infection + dissemination

A
  • virions trapped by FDCs
  • follicular dendritic cells are in germinal centers of LN
  • fusion of FDC and CD4 cells
  • travel to regional lymph nodes
  • wide spread to brain, spleen, GALT, and other lymph nodes (Day 5-14)
113
Q

when is PEP most effected

A

if implemented ASAP

114
Q

PEP probably not effective when started how many hours after exposure

A

> 36 hrs but interval when there is NO benefit from PEP is unknown

115
Q

100 % of macaques receiving PEP (tenofovir) within 24 hours ater iV SIV infection remained

A

uninfected

116
Q

50% protection if PEP given in

A

48 hours

117
Q

25% protection of PEP given in

A

72 hours

118
Q

consider PEP if

A

> 36 hours

119
Q

optimal duration of PEP

A

28 days

120
Q

if given PEP for 28 days

A

100 % protecition

121
Q

if given PEP for 10 days

A

50% protection

122
Q

if given PEP for 3 days

A

0 protection

123
Q

based on animal studies, larger innocula decreases efficacy of

A

PEP

124
Q

innoculation

A

the action of inoculating or of being inoculated; vaccination

125
Q

PEP efficacy decreased by

A
  • delaying initiation
  • shortening duration or
  • inappropriate choice of ARV drugs
126
Q

CDC’s retrospective case-control study of HCW showed that PEP with AZT alone decreased risk of infection by

A

81%

127
Q

if source patient has a highly resistant virus, patient might need a

A

different med

128
Q

before starting HIV PEP

A

-standard HIV ELISA on exposed person
(-HIV viral load if patient known to be HIV positive
-If thought to be high risk to be in window period)
-consider medication interactions
-

129
Q

get baseline labs before starting HIV PEP

A

those include Lytes, BUN, Cr, LFTs, CBC, beta HCG, baseline HIV Ab

130
Q

decision to treat and choice of meds made on a

A

case by case basis

131
Q

patients should be given first dose of meds in the ED and a 4-5 day starter pack only to geth through their

A

f/u/ appt. not a prescription

132
Q

PEP tx options

A

-current CDC Recs (Tenofovir + Emtricitabine (TDF/FTC) and Raltegravir 100 mg BID)

133
Q

alternatives to raltegravir PEP trx option

A

ritonavir 100 mg qd with either darunavir 800mg qd or with atazaniavir 300mg qd

134
Q

how many days is a PEP tx starter pack and how many days does it take to complete?

A

3-5 days; complete 28 days

135
Q

raltegravir is replacing PI

A

-improved tolerability

136
Q

Duration of PEP is how many weeks?

A

4

137
Q

lab tests at 2 weeks of PEP should include

A

BUN, Cr, LFTs, and CBC

138
Q

repeat HIV Ab at what weeks?

A

4-6 weeks, 12, wks, 24 weks

139
Q

secondary transmission to others extremely remote but

A

important to modify behavior in first 6-12 weeks after exposure when most seroconversions occur

140
Q

source patient

A 
history
past testing
risk factors
testing
useful but not always available
141
Q

HIV/HCV risk

A

hemophilia
injection drug use
hemodialysis
history of STD

142
Q

HBV risk?

A
  • known liver disease
  • past testing
  • vaccination for HBV
143
Q

past vaccination and antibody confirmation of HVsAB for HBV is

A

protective

144
Q

recommendations of hep B PEP depends on

A
  • vaccination status of HCW
  • patient’s serologic status
  • if results from source patient will be known in 48-72 hours, treatment can be deferred until results known
145
Q

hep B transmission

A

if HBSAg not detected in blood from source patient, transmission unlikely

146
Q

HBSAg found in blood as early

A

1-2 weeks post infection

147
Q

symptomatic hepatitis occurs

A

4 weeks after appearance of HBSAg

148
Q

most hep B infection

A

sub-clinical

149
Q

what percentage of hep B progresses to chronic infection

A

5-10%

150
Q

hepatitis B PEP primary immunization

A

very effective

  • unvaccinated adults; 3 doses given at 0, 1, 6 mos
  • primary immunization fails
151
Q

50% of people in whom vaccine fails for Hep B (i.e. nonresponders, serum HB SAb

A

subsequent revaccination

152
Q

in those who do not respond to hep B revaccination, double dose HBV vaccination can be considered

A

20 micrograms at 0,1, 6 mos

153
Q

almost all persons with low antibody levels after a prior documented protective titer have

A

rapid increase after a booster dose of vaccine

154
Q

Hep B evaluation:check HBSAb in exposed person if

A

HBV vaccination or responder status is unknown

-only check other HBV serologies if there is suspicion the exposed person could be HV infected

155
Q

Hep B evaluation:check HBSAb in source person if

A

no indication for other serologies

156
Q

hep B follow up

A

check HB SAb titer 102 mos after last dose of vaccine

-HBS Ab response cannot be ascertained if HBIG was given in the last 3-4 mos

157
Q

rate of HCV transmission after accidental percutaneous exposure is

A

2-3%

158
Q

% of patients with spontaneous resolution of HCV infection

A

15-20% of patient

159
Q

HCV antibody usually positive within 15 weeks post exposure, median incubation how long

A

3 mos

160
Q

HCV transmission and prevention

A
  • no available HCV vaccination
  • HCV antibody /immunoglobulin does not prevent infection
  • high risk exposure can be monitored with antibody and RNA
  • early positive result, warrants empiric tx

Medicine II (8 decks)

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