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Infectious Disease 2 > Pharm - HIV > Flashcards

Pharm - HIV Flashcards

1
Q

drugs in the NRTI class

A
  • abacavir
  • tenofovir disoproxil fumarate
  • tenovir alafenamide
  • lamivudine
  • emtricitabine
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2
Q

Drugs in NNRTI class

A
  • etravirine
  • efavirenz
  • rilpivirine
  • nevirapine
  • doravirine
  • delavirine
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3
Q

drugs in PI class

A
  • darunavir

- atazanavir

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4
Q

Drugs in INSTI class

A
  • dolutegravir

- raltegravir

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5
Q

what drug is the fusion inhibitor?

A

enfuvirtide

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6
Q

what drug is the CCR5 antagonist?

A

maraviroc

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7
Q

what drug is the CD4 post attachment inhibitor?

A

ibalizumab

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8
Q

MoA of the NRTIs

A
  • NRTIs undergo phosphorylation mediated by several intracellular enzymes
  • The active form inhibits viral replication through competitive bidding to the viral enzyme, reverse transcriptase.
  • DNA chain elongation is terminated after the NRTI triphosphate is incorporated
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9
Q

overall ADRs of NRTIs

A
  • The hallmark toxicity of the NRTI class is mitochondrial toxicity, which may manifest as:
  • Peripheral neuropathy
  • Pancreatitis, lipoatrophy, and/or hepatic steatosis
  • Black box warning: possibility of lactic acidosis syndrome
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10
Q

place in therapy for NRTIs

A

for HIV-1 and HIV-2

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11
Q

CI for abacavir (NRTI)

A
  • CI: in persons who test positive for HLA-B*57:01 d/t high risk of developing an abacavir hypersensitivity reaction
  • Also avoid in pts w/ CAD and multiple risk factors for CAD
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12
Q

ADRs of tenofovir disoproxil fumarate (NRTI)

A

kidney injury and bone loss

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13
Q

ADR of lamivudine (NRTI)

A

pancreatitis

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14
Q

ADR of emtricitabine (NRTI)

A

hyperpigmentation on the palms and/or sole of feet

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15
Q

MoA of NNRTIs

A
  • NNRTIs prevent HIV-1 reverse transcriptase from adding new nucleotides to the growing DNA chain.
  • NNRTIs block viral cDNA elongation at a site that is separate from the active site targeted by the NRTI class.
  • They decrease viral replication.
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16
Q

place in therapy for NNRTIs

A
  • active against HIV-1 but NOT HIV-2

* Usually administered with a dual NRTI combo

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17
Q

Overall ADRs of NNRTIs

A
  • Teratogenic – avoid in women likely to become pregnant or are in first 8 weeks of pregnancy
  • CNS toxicity manifested as vivid dreams, confusion, dizziness, and hung over feeling
  • Psych: increased risk of anxiety, mood changes, depression, irritability, and increased suicide risk
  • Rash, hyperlipidemia, elevated liver transaminases
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18
Q

ADRs of etravirine (NNRTI)

A

mild rash but severe rash can occur (Steven-Johnson syndrome)

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19
Q

ADRs of rilpivirine (NNRTI)

A
  • Caution in pts w/ prolonged QT
  • ADR: severe skin rash, depression, mood changes, liver problems
  • Do not take w/ PPI
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20
Q

MoA of PIs

A

PIs competitively inhibit the cleavage of the Gag-Pol polyproteins in HIV-infected cells, which is a crucial step in the viral maturation process, thereby resulting in the production of immature virions that are not infectious

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21
Q

place in therapy of PIs

A

avtive against HIV-1 and HIV-2

22
Q

overall ADRs of PIs

A

insulin resistance, hyperglycemia, DM, hyperlipidemia, lipodystrophy, hepatotoxicity, bleeding in pts w/ hemophilia, PR interval prolongation

23
Q

ADRs of the PI darunavir

A
  • nausea, diarrhea, increased transaminases, HA, rash

* Severe: Stevens-Johnson syndrome, TEN

24
Q

CI of PI darunavir

A

severe liver disease

25
Q

ADRs of the PI atazanavir

A
  • Not associated w/ insulin resistance**
  • Better GI tolerance
  • ADR: increase in indirect serum bilirubin, jaundice, renal stones, kidney injury
26
Q

MoA of the INSTIs

A
  • HIV integrase is one of three enzymes (reverse transcriptase, protease, and integrase) that are encoded by the virus and are essential for HIV replication.
  • After entry into CD4+ T cells, viral RNA is reverse transcribed into DNA by HIV reverse transcriptase.
  • The integrase enzyme catalyzes the process by which viral DNA is integrated into the genome of the host cell. This process is essential for maintenance of the viral genome and viral gene expression
  • The integrase inhibitors target the strand transfer step of viral DNA integration and are sometimes referred to as an “INSTI.”
  • These drugs prevent or inhibit the binding of the preintegration complex (PIC) to host cell DNA, thus terminating the integration step of HIV replication
27
Q

place in therapy of INSTIs

A
  • active against HIV-1 and HIV-2

* Preferred third agent for treatment-naïve when used in combo w/ 2 nucleoside analogues

28
Q

ADRs of dolutegravir (INSTI)

A
  • ADR: insomnia and dizziness

* Increased risk of NTDs in infants so not recommended for those who are pregnant and w/I 12 weeks post conception

29
Q

ADRs of raltegravir (INSTI)

A

well tolerated but can cause nausea, dizziness, and HA

30
Q

MoA of fusion inhibitors

A

Block HIV from getting into and infecting CD4 cells. Fusion inhibitors act by binding to an envelope protein and blocking the structural changes necessary for the virus to fuse with the host CD4 cell. This prevents HIV from multiplying and can reduce the amount of HIV in the body.

31
Q

place in therapy of infusion inhibitors

A
  • For tx of HIV infection in adults and children 6 yo and older
  • For those whose HIV infection is not well controlled byongoing tx w/ other meds
  • Always used in combo w/ other HIV meds
32
Q

ADRs of fusion inhibitors

A

injection site reactions and pneumonia

33
Q

MoA of CCR5 antagonists

A
  • CCR5 antagonists block HIV from getting into and infecting certain cells of the immune system. This prevents HIV from multiplying and can reduce the amount of HIV in the body.
  • It works by attaching to a protein on the surface of the immune cells. The protein is called the CCR5 coreceptor. When maraviroc attaches to the CCR5 coreceptor, certain strains of HIV—called R5 tropic virus—cannot attach to, enter, or infect the cell.
34
Q

place in therapy for CCR5 antagonists

A
  • For the tx of HIV infection in people 2 years or older weighing at least 22 pounds (10 kg)
  • Always used in combo with other meds
  • Should be used only in people whose strain of HIV uses the CCR5 coreceptor
35
Q

ADRs of CCR5 antagonists

A

life-threatening reactions can affect the liver, heart (orthostatic hypotension), skin, and allergic reactions

36
Q

MoA of CD4 post attachment inhibitor

A

works by attaching to a protein on the surface of the immune cells. The protein is called the CD4 receptor. When ibalizumab attaches to the CD4 receptor, HIV cannot attach to, enter, or infect the cell

37
Q

place in therapy for CD4 post attachment inhibitor

A

To treat HIV infection in adults:
• Who have taken several HIV meds in the past, AND
• Have a strain of HIV that is resistant to many HIV medicines, AND
• Whose HIV infection is not well controlled by ongoing tx w/ other HIV meds

38
Q

ADRs of CD4 post attachment inhibitors

A

nausea and occasional dizziness, diarrhea and rash

• Serious: changes in immune system (immune reconstitution inflammatory syndrome)

39
Q

Explain the reasons to use pharmacologic boosting agents

A
  • Most PIs are administered in combo w/ boosting agents to increase trough plasma drug concentrations, increase drug half lifes, and increase maximum plasma concentrations
  • Boosters improve the potency of the antiviral agent and enables lower and less frequent dosing of the parent drug, thereby decreasing pill burden
40
Q

Identify which anti-retrovirals require a boosting agent

A
  • Ritonavir boosting is required for darunavir and preferred for atazanavir
  • Colbicistat is also used to boost the integrase inhibitor, elvitegravir and the PIs atazanavir and darunavir
41
Q

Identify methods to improve patient adherence.

A
  • Patients should understand the link b/w adherence and drug resistance
  • Assess at each visit and assume non adherence
  • Consider depression and substance abuse
  • Use pharmacy records to track compliance when refills are obtained from a single pharmacy source
42
Q

Identify the lab monitoring for patients taking anti-retrovirals.

A
  • virologic response
  • CD4 counts
  • CBC w/ diff
  • basic chem - BUN and Cr
  • UA
  • ALT AST and bili
  • Cardio - BP
  • Dyslipidemia
  • Glucose tolerance and DM
43
Q

virologic response monitoring

A

Plasma HIV RNA should be measured in all pts at baseline and regularly during therapy (it’s the most reliable indicator of response to tx)

44
Q

CD4 count monitoring frequency

A

3 mos after initiating tx; then every 3-6 mos

45
Q

UA monitoring frequency

A

q 12 mos

46
Q

ALT AST and bilirubin monitoring frequency

A

2-8 weeks after initiation of tx and q 3-6 mos

47
Q

dyslipidemia monitoring

A

o Very common in HIV infected pts!
o Same indications for tx
o When using statin, MUST check drug interactions

48
Q

glucose tolerance and DM monitoring frequency

A
  • A1c and fasting blood glucose at baseline
  • w/1 1-3 mos after starting a new regimen
  • q 3-6 mos while on tx
49
Q

State the indication for using PrEP in high risk patients.

A
  • For sexually active adult MSM at substantial risk of HIV acquisition
  • For adult heterosexually active men and women who are at substantial risk of HIV acquisition
  • For adult persons who inject drugs
  • Should be discussed w/ heterosexually active women and men whose partners are known to have HIV
50
Q

describe IRIS

A

some who start ART get health problems even though HIV is under control. It could be a previous infection returning or development of a new disease. It’s linked to improvement in the pts immune system. The problems usu occur in the first 2 mos after starting HIV therapy.

51
Q

Diseases and condition that a pt could experience w/ IRIS

A 
o	CMV
o	Cognitive (memory and thinking) problems
o	Cryptococcal meningitis 
o	Hep B and C 
o	Herpes zoster and simplex
o	MAC
o	PML (viral brain infection) 
o	Swollen lymph nodes
o	Tb

Infectious Disease 2 (13 decks)

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