Antiretroviral Agents Flashcards

1
Q

If you get stuck with a needle that has been injected in a patient positive for HIV, what is the chance that you will undergo seroconversion?

A

3/1,000 or 0.33%

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2
Q

What is considered the “backbone” of HIV antiretroviral therapy?

A

Two NRTIs and either (1) a protease inhibitor, (2) an NNRTI, or (3) an integrase inhibitor

Integrase inhibitors are the preferred first-line because they have few side effects and no documented resistance thus far.

Note: fusion inhibitors (enfurvitide) and CCR5 inhibitors are not recommended as first-line agents.

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3
Q

What is the only fusion inhibitor?

A

Enfuvirtide (which inhibits gp41)

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4
Q

Which class of HAART drugs is also active against HBV?

A

NRTIs (tenofovir)

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5
Q

Efavirenz has a declining use due to its psychiatric and teratogenic effects, but it is useful in what patient population?

A

Those being treated with rifampin for TB because efavirenz does not induce CYP as much as nevirapine.

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6
Q

Tenofovir should be avoided in which patients?

A

Those with osteoporosis or chronic kidney disease

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7
Q

What are INSTIs?

A

Integrase strand inhibitors

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8
Q

How is enfuvirtide administered?

A

Subcutaneous injection

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9
Q

Which regimens are least likely to induce resistance?

A

2 NRTIs + either boosted PI or INSTIs

Note: the best is 2 NRTIs and an INSTIs

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10
Q

The most absorbed form of tenofovir is __________.

A

TAF (tenofovir alafenamide or brand name Descovy)

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11
Q

Why are NRTIs toxic against mitochondrial?

A

They inhibit mitochondrial DNA polymerase.

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12
Q

Which class of HIV drugs is inhibited by PPIs?

A

NNRTIs (like rilpivirine or etravirine)

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13
Q

What mechanism allows resistance to maraviroc?

A

If an HIV strain develops X4 tropism –in which it uses predominantly CXCR4 rather than CCR5.

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14
Q

Why is maraviroc not in any combinations?

A

It is dosed twice daily, whereas most other antiretroviral drugs are once daily.

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15
Q

HIV never enters a state of true ______________.

A

latency

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16
Q

Resistance testing is recommended when ________________.

A

the patient is first seen and if their CD4 counts start to drop while on treatment

17
Q

How do NRTIs work?

A

They mimic nucleotides but lack the 3’ hydroxyl group necessary for elongation of the genome (like Sanger sequencing).

18
Q

How are the NRTIs administered?

A

Orally (most have good bioavailability)

19
Q

NRTIs are excreted renally with the exception of ______________.

A

abacavir (hepatic through glucuronidation) and zidovudine

20
Q

The NNRTIs work by _________________.

A

inhibiting reverse transcriptase at a different, non-active site

21
Q

Which class of antiretroviral drugs is usually the most resistant to mutations that confer resistance?

A

Protease inhibitors

22
Q

What are some side effects of protease inhibitors?

A

Hyperlipidemia, hyperglycemia, and central adiposity (remember Guinevere with the raised candy and butter next to the fat horse with skinny legs)

Also, hepatotoxicity

23
Q

Describe how HIV tropism changes with disease progression.

A

HIV typically starts out with R5 tropism –meaning it targets cells with CCR5 –then progresses to X4 tropism.

24
Q

Tenofovir is contraindicated in patients with ______________.

A

osteoporosis and chronic kidney disease

25
Q

What is “boosting”?

A

Adding ritonavir to combinations to increase the serum concentration (because ritonavir is a potent inhibitor of CYP)

26
Q

Which of the entry-inhibiting drugs is hepatically metabolized?

A

Maraviroc

Enfuvirtide is metabolized by proteolysis so DDI with CYP is not a concern.

27
Q

what drugs make up PrEP

A

tenofovir-emtricitabine