L27 BW (HIV) Flashcards

(36 cards)

1
Q

how long dose the development of AIDS lag behind HIV

A

a decade

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2
Q

NRTI MOA

A

competitive inhibitors that inhibit the production of DNA by premature chain termination

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3
Q

HIV ___ is more prevalent worldwide,

whereas HIV ___ is more prevalent in W. Africa

A

HIV 1 is more prevalent worldwide,

whereas HIV 2 is more prevalent in W. Africa

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4
Q

how is donated blood screened for HIV

A

(1) the presence of HIV antigens (p24) or (2) RNA NAT

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5
Q

what complicates tx and necessitates the use of combo chemo to suppress infections

A

the fast mutation rate

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6
Q

how do we break HIV transmission

A

education about U=U

undetectable = untransmissable

+ PrEP

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7
Q

AIDS defining conditions emerge when

A

as immune system fails due to opportunistic infections, CA and other conditions

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8
Q

U = U

A

Undetectable = Un-transmissible

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9
Q

reverse transcriptase inhibitors include

A

nucleoside/tide analogs and non-nucleoside reverse transcriptase inhibitors

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10
Q

why is simultaneous tx with multiple agents required in HIV

A

HIV has such a high mutation rate

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11
Q

what makes us hope that more HIV infections will be recognized sooner

A

that HIV antibody detecting rapid tests are in use

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12
Q

what population in the US is currently showing the greatest rates of increase

A

heterosexuals

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13
Q

what reduces emergence of opportunistic infections, threat from AIDS associated CA, and reduced risk of transmission

A

starting HAART early

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14
Q

what does the future of HIV tx?

A

maturation inhibitors and integrase inhibitors

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15
Q

How do you determine tx for HIV pts

A

watch viral loads trends. If they dip, adjust meds

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16
Q

downsides of the typical infection screening approach

A

does not ID pts with recent infections who have not yet developed an antibody response

17
Q

best method of HIV prevention

18
Q

combination of which 2 drug groups has made a huge difference in clinical condition of HIV pts and sinks the virus to undetectable levels

A

protease inhibitors

and

nucleotide analogs

19
Q

is donated blood safe from HIV

A

yes- the 2 techniques it uses do not rely on patient antibodies (which can take a while to develop in an infected person)

20
Q

HIV tx is ___ but ____

A

HIV tx is difficult but compliance is essential to avoid drug resistance

21
Q

HIV virus load pattern

A

rise, dip, return

22
Q

fusion penetration inhibitors

A

interfere with HIV entry into host

23
Q

what test ID’s HIV even if the pt has not yet developed antibodies

A

Nucleic Acid Tests (NAT)

24
Q

protease inhibitors

A

stop maturation/ viral assembly

25
what are the AIDS defining conditions
kaposi's sarcoma MAC infection PCP CMV candidiasis cryptosporidiosis
26
how do you decide if a new tx regimen is needed
follow viral load count trends
27
typical HIV dx through screening:
2 step system: (1) EIA screen to reveal anti-HIV antibodies in serum and (2) western blot for confirmation
28
HIV tx
combo antiviral agents (HAART)
29
times of highest risk of HIV transmission
early disease periods when virus load is high but pt may be unaware they have it
30
how many types of HIV
2 distinct types (HIV-1 and HIV-2) and many subtypes
31
32
NNRTI MOA
bind to reverse transcriptase and inhibit enzyme activity
33
all HIV pts are considered to be
lifelong carriers and continuously infectious
34
HIV ___ is less transmissable, slower progression to AIDS, and resistant to NNRTIs
2
35
what is HAND
HIV Associated Neurocognitive Disorder \*\* can impact ability to adhere to tx regimen\*\*
36
how do insects transmit HIV
THEY DON'T