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IHO Week 6 > HIV Drugs > Flashcards

HIV Drugs Flashcards

1
Q

Nucleoside Reverse Transcriptase Inhibitors (NRTIs)

A

Zidovudine (Azidothymidine or AZT)
Lamivudine
Abacavir
Emtricitabine

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2
Q

Nucleotide Reverse Transcriptase Inhibitors (NRTI)

A

Tenofovir

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3
Q

Non-nucleoside reverse transcriptase inhibitors (NNRTIs)

A

Etravirine
Efavirenz
Rilpivirine

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4
Q

Protease Inhibitors

A

Atazanavir +/- ritonavir (ritonavir boosting)

Darunavir + rionavir (ritonavir boosting)

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5
Q

Integrase Inhibitors

A

Raltegravir

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6
Q

Fusion Inhibitors

A

Enfuvirtide (T-20)

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7
Q

CCR5 agonist

A

Maraviroc

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8
Q

Goal of HIV treatment

A

Fully undetectable levels of virus

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9
Q

The lower the viral RNA is driven.. the lower the rate of ___

A

drug resistance

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10
Q

Less resistance =

A

longer therapeutic effect

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11
Q

To achieve maximal and durable suppression of viral RNA, _____ and ____ are required

A

Drug combinations

Compliance

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12
Q

What two things should you monitor in HIV treatment

A

CD4+ counts

HIV RNA levels (viral load)

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13
Q

Typical treatment regime

A

(NNRTI, Protease Inhibitor, integrase inhibitor) + Dual NRTI

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14
Q

Nucleoside RTI mechanism

A
  • Competitively inhibits reverse transcriptase and can be incorporated into the viral DNA chain - cause termination
  • Requires phosphorylation by cellular enzymes to triphosphate form to be activated
  • Resistance to one may result in resistance to another in the class
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15
Q

AE of Nucleoside RTI

A
  • Lactic acidosis with hepatic steatosis probably due to mt toxicity (No ETC on mt means pyruvate to lactic acid)
  • fat redistribution and hyperlipidemia
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16
Q

Zidovudine (Azidothymidine or AZT) AE

A

NRTI
granulocytopenia and anemia
CNS disturbances - severe headache, nausea, insomnia, malaise

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17
Q

Didanosine

A

NRTI

more toxic than AZT

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18
Q

Lamivudine and Emtricitabine

A

NRTI
Best tolerated NRTIs (nucleoside)
Active against Hepatitis B

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19
Q

Abacavir

A

NRTI
Hypersensitivity
MUST test for HLA-B*5701

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20
Q

HLA-B*5701

A

Hypersensitivity to to Abacavir

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21
Q

Tenofovir class

A

Nucleotide Reverse Transcriptase Inhibitor

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22
Q

Tenofovir mechanism

A

competitive inhibition of reverse transcriptase.

Encorporated into viral DNA chain and causes termination

23
Q

AE of Tenofovir

A

nausea, vomiting, diarrhea, RENAL FAILURE

Lactic acidosis with hepatic steatosis (mt toxicity)

24
Q

Do not give Tenofovir to patients with low _____

A

baseline GFR (indicating reduced kidney function)

25
Q

What should you think of when thinking of NNRTIs?

A

Drug interactions

26
Q

NNRTI mechanism

A
  • bind directly to the reverse transcriptase at a site distinct from that of the NRTI. The site cannot then produce viral DNA
  • Does not require phosphorylation for activity and are primarily effective against HIV1
27
Q

No cross resistance with NNRTIs and NRTIs and ___

A

protease inhibitors

28
Q

Do NNRTIs require phosphorylation?

A

No - acts at a distinct site from NRTIs

29
Q

General AE of NNRTIs

A

Varying levels of GI intolerance and skin rash

Metabolized by and can affect hepatic CYP450 drug interactions (induce, inhibit or mixed)

30
Q

Efavirenz

A

NNRTI
Once a day
CNS effects (vivid dreams, nightmares, hallucinations)

31
Q

Etravirine

A

NNRTI

Rash, Nausea, Peripheral neuropathy

32
Q

Rilpivirine

A

NNRTI

Do not use in a patient with pretreatment viral loads >100,000 copies/ml

33
Q

MOA of protease inhibitors?

A
  • Prevent protease action. As virus buds, proteolytic cleavage occurs. Without, virus in not infectious.
  • Protease is required for cleavage of polypeptide precursors for structural proteins
34
Q

Protease inhibitors prevent the post translational cleavage of the ____ polyprotein

A

gag-pol

prevent the processing of viral proteins into functional conformations

35
Q

With protease inhibitors, new viral particles cannot

A

mature (therefore, cannot become infectious)

36
Q

Inhibiting HIV protease activity presents HIV replication

A

in vitro

37
Q

Protease inhibitors are active against HIV strains that are resistant to

A

reverse transcriptase inhibitors (NRTIs/ NNRTIs)

38
Q

General AE of protease inhibitors

A

GI disturbances, hepatotoxicity, hyperglycemia/insulin resistance, dyslipidemia, cardiac conduction abnormalities, Peripheral lipoatrophy and central fat accumulation

39
Q

Protease inhibitors are metabolized by

A

CYP3A4, therefore can inhibit as well

40
Q

Ritonavir boosting

A
  • High doses of protease inhibitor ritonavir is poorly tolerated.
  • Used at lower doses to increase serum concentration of other protease inhibitors and decrease frequency of other PI
41
Q

Why does Ritonavir boosting work?

A

Potent inhibitor of CYP3A4 (which metabolizes several PIs)

42
Q

Cobicistat

A

Inhibits CYP3A4 and intestinal proteins - booster for PIs.

By itself is not a protease inhibitor

43
Q

Enfuvirtide (T-20)

A

Fusion inhibitor
After HIV binds to host, conformation change occurs in gp41 and virus enters. Enfuviritide is a 36 aa synthetic peptide that binds to gp41 and prevents conformational change

44
Q

Enfuvirtide administration

A

Subcutaneous 2x daily
high incidence of local reactions with pain, erythema, induration, nodules and cysts
rare systemic hypersensitivity
Higher incidence of bacterial pneumonia?

45
Q

Enfuviritide is active against HIV classes that are…

A

resistant to other drug classes

46
Q

Raltegravir

A

Integrase Inhibitor
Integrase is a viral enzyme essential to the rep of HIV1 and HIV2. Binding integrase inhibits strand transfer - the final step of provirus integration

47
Q

CCR5 Antagonist MOA

A

CCR5 and CXCR4 are two major co recpetors used by HIV1 to gain entry into the host cell with the R5 strains predominating during early stages of infection and 50-60% of the late stage disease.

BINDS TO host CCR5 SELECTIVELY

48
Q

CCR5 Antagonist Name

A

Maravironic

49
Q

Integrase inhibitor name

A

Raltegravir

50
Q

Why is Raltegravir beneficial?

A

Fewer drug interactions than NRTIs or PIs

51
Q

Maraviroc AE

A

Pyrexia, rash, postural dizziness

52
Q

HAART

A
  • Highly active antiretroviral therapy

- Therapy with RTI and PI

53
Q

HHART AE

A

lipodystrophy

other secondary effects

54
Q

Lipodystrophy and HHART

A

25-50% of patients
Wasting of subcutaneous fat
Central adiposity
Hyperlipidemia, insulin resistance and diabetes m.
Usually NRTI and PI together, sometimes just NRTI

IHO Week 6 (7 decks)

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