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HAART Flashcards

1
Q

When is Highly Active Antiretroviral Therapy (HAART) usage most indicated?

A

-CD4+ below 500cells/mm3-high viral load

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2
Q

HAART is a 3-drug regimen consisting of:

A

-2 NRTIs and 1 of the following:NNRTI or protease inhibitor or integrase inhibitor

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3
Q

What should be done following HIV diagnosis (via multiple positive ELISA and Western blot test)?

A

Perform viral load and resistance and begin a preferred ARV regimen

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4
Q

What is the appropriate action if a viral load is detectable after 12-24 weeks of treatment OR if a viral rebound is seen after suppression?

A

-make sure the patient is adhering to treatment-If they are, perform resistance testing and change to a different, non-resistant regimen of 3 drugs

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5
Q

What are the NRTIs?

A

-Abacavir-Lamivudine-tenofovir-zidovudine-Emtricitabine-didanosine-stavudine

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6
Q

What are the NNRTIs?

A

EfavirenzNevirapineDelavirdine

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7
Q

What are the HIV-1 protease inhibitors?

A

atazanavir, ritonavir, indinavir, lopinavir, saquinavir (others)

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8
Q

What are the HIV inhibitors?

A

-enfuviritude-maravaroc

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9
Q

What are the integrase inhibitors?

A

Raltegravir

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10
Q

How are NRTIs given?

A

PO 1x-2x daily (NNRTIs same)

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11
Q

CYP interactions of NRTIs?

A

Nope

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12
Q

Other interactions of NRTIs?

A

substrates for glucuronide

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13
Q

Elimination of NRTIs?

A

urine as drug + metabolites

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14
Q

CYP interactions of Delvirdine (NNRTI)?

A

-inhibits 3A4, 2D6, 2C9, and 2C10

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15
Q

CYP interactions of nevirapine and efavirenz (NNRTI)?

A

induce 3A4 and 2B6

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16
Q

Elimination of NNRTs?

A

urine as metabolites

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17
Q

How are HIV protease inhibitors given?

A

PO 1x-2x daily

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18
Q

Interactions of Atazanavir?

A

inhibits 3A4 and UGT-3A4 substrate

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19
Q

Interactions of Ritonavir?

A

inhibits 3A4, UGT, P-gp, and 2D6

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20
Q

Interactions of Saquinavir?

A

inhibits 3A4 and UGT

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21
Q

Interactions of Lopinavir?

A

3A4 substrate (Darunavir is same)

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22
Q

Interactions of Indinavir?

A

3A4 and P-gp substrate and 3A4 inhibitor

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23
Q

How are HIV protease inhibitors eliminated?

A

stool as metabolites

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24
Q

How is Enfuvirtide given?

A

S.C.

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25
Q

Metabolism of Enfuvirtide?

A

catbolized to AAs

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26
Q

How is Maraviroc given?

A

PO 1-2x daily

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27
Q

Interactions of Maraviroc?

A

3A4, P-gp substrate

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28
Q

Elimination of Maraviroc?

A

stool/urine as drug + metals

29
Q

How is Raltegravir given?

A

PO 1-2x daily

30
Q

Interactions of Raltegravir?

A

glucuronide metabolite

31
Q

Elimination of Raltegravir?

A

stool/urine as drug + metals

32
Q

What is Cobicistat?

A

An orally active CYP3A4 inhibitor used as a pharmacokinetic enhancer to increase the serum concentration of CYP3A substrates, such as theprotease inhibitors atazanavir and darunavirHas no antiviral activity

33
Q

What is ATRIPLA?

A

a once daily pill consisting of tenofovir, entricitabine and efavirenz- a complete regimen

34
Q

Side effects of Abacavir?

A

hypersensitivityhepatic disease

35
Q

Which NRTIs have a BBW for hepatic disease?

A

-all but Abacavirespecially in obese patients and with prolonged exposure, especially in women

36
Q

Which NRTIs have a BBW for lactic acidosis?

A

allespecially in obese patients and with prolonged exposure, especially in women

37
Q

What are the BBWs for Zidovudine?

A

-anemia (only one)-hepatic disease-lactic acidosis-myopathy-neutropenia

38
Q

Which NRTIs have a BBW for pancreatitis?

A

Didanosine and stavudine

39
Q

Which NRTI have the most intense neuropathy impact?

A

Stavudine (but all but Abacavir do to some extent)

40
Q

What are some contraindications of Nevirapine?

A

-female-hepatic disease-hepatitis-nevirapine hypersensitivity-serious rash

41
Q

Which side effects of Nevirapine are common to all NNRTIs?

A

hepatic disease and serious rash

42
Q

Side effects of Efavirenz?

A

vivid dreamsCNS symptoms

43
Q

Which NNRTIs are contraindicated in pregnancy?

A

Delavirdine and Efavirenz

44
Q

Side effects of PIs?

A

-GI pain, N/V-Lipodystrophy-Hyperglycemia/Diabetes mellitus-Dyslipidemia-Nephrolithiasis -Severe rash including SJS

45
Q

How do PIs cause hyperglycemia/diabetes?

A

PIs acutely inhibit GLUT4

46
Q

The Nephrolithiasis seen in PIs is most common in which one?

47
Q

T or F. Peripheral neuropathy is a common consequence of HIV

A

T. Mainly attributed to myelinated fiber involvementIt is also exacerbated by HAART (mainly NNRTI, NRTIs, and some PIs)

48
Q

Whats the recommended ART in pregnancy (assuming a NRTI, NNRTI, and PI combo regimen)?

A

-NRTIs- lamivudine, zidovudine-NNRTIs- nevirapine-PI- lopinavir/ritonavir

49
Q

Infection is an obvious consequence of HIV progression. What is the recommended treatment for a Pneumocystis jiroveci infection?

A

trimethoprim-sulfamethoxazole (QT prolongation common)

50
Q

Infection is an obvious consequence of HIV progression. What is the recommended treatment for a M. tuberculosis infection?

A

isoniazid + Pyridoxine

51
Q

Infection is an obvious consequence of HIV progression. What is the recommended treatment for a Toxoplasmosis infection?

A

trimethoprim-sulfamethoxazole

52
Q

Infection is an obvious consequence of HIV progression. What is the recommended treatment for a CMV infection?

A

ganciclovir (foscarnet and cidofovir can be useful with retinitis treatment)

53
Q

Infection is an obvious consequence of HIV progression. What is the recommended treatment for a Cryptococcosis, candidiasis, endemic fungal infections?

A

Fluconazole (QT prolongation common and 3A4/2D6 inhibitor)

54
Q

T or F. CMV infections occur primarily in the setting of advanced immunosuppression and are typically due to reactivationof latent infection

55
Q

What is the end-game of unrelated CMV?

A

-retinitis-colitis-esophagitis-CNS disease-pneumonitis

56
Q

Several drugs are available for CMV treatment. What is the ROA for them?

A

valganciclovir- PO (can be used for CMV retinitis treatment and prophylaxis for transplant patients)ganciclovir, foscarnet, cidofovir- IV (all approved for CMV retains treatment only)

57
Q

Side effects of valganciclovir?

A

-leukopenia-neutropenia-thrombocytopenia-renal toxicity (metabolized via GF and active RTS)

58
Q

What is Foscarnet?

A

A viral DNA polymerase inhibitor that binds pyrophosphate binding site and does NOT need viralactivation

59
Q

How can resistance arise against Foscarnet?

A

mutated viral DNA polymerase

60
Q

How is foscarnet given?

A

It is a very insoluble drug so you saline hydrate the patient and give by infusion pump

61
Q

What are the toxicities of foscarnet?

A

– genital ulcerations due to high levels of ionized drug in urine-Nephrotoxicity – electrolyte imbalances– hyper- and hypo- calcemia, phosphatemia, hypokalemia andhypomagnesemia can lead to seizures

62
Q

What is Vidarabine?

A

A nucleoside analog used for EBV treatment that requires phosphorylation for activity– ara-ATP is a substrate & inhibitor of viral DNA polymerase– Viral DNA polymerase mutation gives resistance

63
Q

How is vidarabine given?

A

Very poor oral bioavailability – applied to eye as ointment

64
Q

Side effects of vidarabine?

A

Risk of systemic side effects is low because of the drugs insolubility and low ocular penetration

65
Q

What drugs are used to treat Kaposi’s sarcoma-associated herpesvirus?

A

Antiviral drugs, such as ganciclovir, valganciclovir and cidofovir• Cidofovir, IV is the main

66
Q

Does Cidofovir need to be activated? How does it work?

A

Yes, Intracellular conversion to active diphosphate form– Competes with deoxycytosine triphospate (dCTP) for incorporation into viral DNA– Selective for viral DNA polymerase versus host

67
Q

How is Cidofovir cleared?

A

renal with active RTS

68
Q

Side effects of Cidofovir?

A

-Dose-dependent nephrotoxicity (proximal tubular cells)– monitor serum creatinine & urinary protein• Adverse effects include, but are not limited to,neutropenia, ocular hypotonia, GI toxicity & rash/alopecia

STEP Pharm I (36 decks)

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