L27 BW (HIV) Flashcards

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

A

education

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
Q

what are the AIDS defining conditions

A

kaposi’s sarcoma

MAC infection

PCP

CMV

candidiasis

cryptosporidiosis

26
Q

how do you decide if a new tx regimen is needed

A

follow viral load count trends

27
Q

typical HIV dx through screening:

A

2 step system: (1) EIA screen to reveal anti-HIV antibodies in serum and (2) western blot for confirmation

28
Q

HIV tx

A

combo antiviral agents (HAART)

29
Q

times of highest risk of HIV transmission

A

early disease periods when virus load is high but pt may be unaware they have it

30
Q

how many types of HIV

A

2 distinct types (HIV-1 and HIV-2) and many subtypes

31
Q
A
32
Q

NNRTI MOA

A

bind to reverse transcriptase and inhibit enzyme activity

33
Q

all HIV pts are considered to be

A

lifelong carriers and continuously infectious

34
Q

HIV ___ is less transmissable, slower progression to AIDS, and resistant to NNRTIs

A

2

35
Q

what is HAND

A

HIV Associated Neurocognitive Disorder

** can impact ability to adhere to tx regimen**

36
Q

how do insects transmit HIV

A

THEY DON’T