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Antibiotics > Antiretroviral Questions > Flashcards

Antiretroviral Questions Flashcards

1
Q

What was the first antiretroviral available in the mid-1980s?

A

Zidovudine

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2
Q

What are challenges with complex antiretroviral drug regimens?

A
  • adherence
  • resistance
  • toxicities
  • interactions
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3
Q

What are NRTIs?

A

Nucleoside reverse transcriptase inhibitors

  • oldest class of antiretrovirals
  • a combination of two of these typically forms the backbone of most anti-HIV regimens
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4
Q

What is Tenofovir disoproxil fumarate / Tenofovir alafenamide?

A

NRTI

  • TDF
  • TAF
  • technically a nucleotide but grouped with these agents
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5
Q

What is Emtricitabine?

A

NRTI

-FTC

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6
Q

What is Lamivudine?

A

NRTI

-3TC

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7
Q

What is Abacavir?

A

NRTI

-ABC

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8
Q

What is zidovudine?

A

NRTI

-ZDV, AZT

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9
Q

What is stavudine?

A

NRTI

-d4T

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10
Q

What is didanosine?

A

NRTI

-ddI

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11
Q

What is in Truvada?

A
  • Emtricitabine

- TDF

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12
Q

What is in Epzicom?

A
  • Abacavir

- Lamivudine

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13
Q

What is in descovy?

A
  • emtricitabine

- TAF

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14
Q

What is in combivir?

A
  • lamivudine

- zidovudine

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15
Q

What is in trizivir?

A
  • abacavir
  • lamivudine
  • zidovudine
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16
Q

What is the MOA of NRTIs?

A

Inhibit the action of the virally encoded protein reverse transcriptase

  • take the place of nucleotides in the elongating strand of viral DNA
  • leads to early termination of the viral DNA strain
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17
Q

Which NRTIs have clinically useful activity against hepatitis B virus?

A
  • tenofovir
  • emtricitabine
  • lamivudine
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18
Q

Which NRTIs that are most problematic from a toxicity perspective are uncommonly used now?

A
  • didanosine
  • stavudine
  • zidovudine
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19
Q

What are the categories of adverse effects of NRTIs?

A
  • extremities
  • GI
  • hematologic
  • hypersensitivity
  • metabolic
  • renal
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20
Q

Describe NRTI extremity adverse effects.

A

Peripheral neuropathy

  • delayed, slowly progressive adverse effect
  • didanosine
  • stavudine
  • especially in combination
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21
Q

Describe NRTI GI adverse effects.

A

Less GI toxicity than many antiretrovirals

  • nausea
  • vomiting
  • diarrhea
  • zidovudine
  • didanosine
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22
Q

Describe NRTI hematologic adverse effects.

A

Bone marrow suppression

  • anemia
  • neutropenia
  • zidovudine (frequently)
  • rarely with other NRTIs
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23
Q

Which NRTI is associated with a hypersensitivity reaction in a minority of patients?

A

Abacavir

  • fever
  • rash
  • flu-like symptoms
  • days to weeks after starting therapy
  • continuation or rechallenge can be fatal
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24
Q

Presence of which allele is predictive of abacavir hypersensitivity toxicity in a genotype screening?

A

HLA-B*:5701 allele

  • routine screening recommended before starting therapy
  • if positive test: do not offer abacavir
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25
Q

Describe NRTI metabolic adverse effects.

A

Complex of toxicities suspected to be of mitochondrial origin

  • lactic acidosis
  • hepatic steatosis
  • pancreatitis
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26
Q

When do NRTI metabolic effects show up?

A
  • symptoms typically delayed (for months) in onset
  • may be nonspecific in initial presentation
  • mortality can be high if symptoms not recognized early
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27
Q

Which NRTIs have a higher propensity for metabolic effects?

A
  • stavudine
  • didanosine
  • zidovudine
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28
Q

What other metabolic effects may didanosine and zidovudine contribute to?

A
  • hyperlipidemia
  • insulin resistance
  • lipoatrophy
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29
Q

Describe lipoatrophy.

A

Loss of fat causing changes in appearance, primarily in the:

  • face
  • buttocks
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30
Q

Which NRTI is associated with nephrotoxicity?

A

Tenofovir

  • increased serum creatinine
  • renal electrolyte and protein wasting
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31
Q

Which formulation of tenofovir appears to confer less risk of nephrotoxicity?

A

TAF

  • new formulation
  • less commonly used alone or in combination pills compared to TDF
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32
Q

What adverse effects does didanosine cause?

A
  • extremities
  • GI
  • metabolic
  • other metabolic
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33
Q

What adverse effects does stavudine cause?

A
  • extremities

- metabolic

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34
Q

What adverse effects does zidovudine cause?

A
  • GI
  • hematologic
  • metabolic
  • other metabolic
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35
Q

Do NRTIs require dose adjustment in renal dysfunction?

A

Yes, most do

-may need to avoid the fixed dose combinations

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36
Q

How do NRTI drug interactions compare with other antiretroviral classes?

A

Fewer metabolic drug interactions

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37
Q

What two NRTIs should not be coadministered together?

A
  • tenofovir with didanosine

- tenofovir with atazanavir (may require dosage adjustment of atazanavir)

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38
Q

Describe NRTI resistance.

A

Various patterns of cross-resistance occur

  • expert interpretation of susceptibility required
  • NRTIs may confer a therapeutic benefit even for resistant viruses in some cases
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39
Q

How do the two formulations of tenofovir differ in dosing?

A

Newer TAF has much lower dose than TDF

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40
Q

What does typical treatment for treatment-naïve HIV patients involve?

A

-two NRTIs

+

-drug from another class

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41
Q

What does typical treatment for treatment-experienced HIV patients involve?

A

3 or more NRTIs as part of a salvage regimen

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42
Q

What should one look for when reviewing an HIV regimen?

A

Patient should be on two NRTIs or something is weird

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43
Q

What are the NNRTIs?

A

Non-nucleoside reverse transcriptase inhibitors

  • inhibit the same enzyme as NRTIs but:
  • work through a different mechanism
  • have greatly different pharmacologic properties
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44
Q

What is Efavirenz?

A
  • EFV

- NNRTI

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45
Q

What is etravirine?

A
  • ETR

- NNRTI

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46
Q

What is rilpivirine?

A
  • RPV

- NNRTI

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47
Q

What is nevirapine?

A
  • NVP

- NNRTI

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48
Q

What is in Atripla?

A
  • efavirenz
  • tenofovir
  • emtricitabine
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49
Q

What is in complera?

A
  • rilpivirine
  • tenofovir
  • emtricitabine
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50
Q

What is the MOA of NNRTIs?

A

Bind to a different part of the reverse transcriptase enzyme compared to NRTIs (do not pretend to be regular nucleosides)

  • causes a change in the conformation of the enzyme
  • interferes with its ability to form the viral DNA chain
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51
Q

Are NNRTIs used for any other viral infections besides HIV?

A

No

-only HIV

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52
Q

What are the categories of adverse effects of NNRTIs?

A
  • CNS
  • dermatologic
  • hepatotoxicity
  • hypersensitivity
  • metabolic
  • pregnancy/lactation
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53
Q

Which NNRTI can cause a broad spectrum of adverse effects?

A

Efavirenz

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54
Q

What are common efavirenz CNS effects?

A
  • dizziness
  • drowsiness (or sometimes insomnia)
  • abnormal (especially vivid) dreams
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55
Q

What are LESS common efavirenz CNS effects?

A
  • depression
  • psychosis
  • suicidal ideation
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56
Q

What is the time frame of efavirenz CNS effects?

A
  • onset usually very rapid (with first few doses)

- often subsides after several weeks of therapy

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57
Q

How can efavirenz CNS effects be minimized?

A

Taking the drug:

  • on an empty stomach
  • at bedtime or 2-3 hours before
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58
Q

What is a relative contraindication to the use of efavirenz?

A

History of:

  • mental illness
  • depression
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59
Q

Describe NNRTI dermatologic effects.

A

Rashes

-mild forms can be treated with antihistamines

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60
Q

What NNRTI dermatologic effect represents an absolute contraindication to rechallenge?

A

Lesions involving mucous membranes SJS or similar eruptions

-must be managed urgently

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61
Q

Which NNRTI appears to have the highest likelihood of causing a dermatologic reaction?

A

Nevirapine

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62
Q

Describe NNRTI hepatotoxicity.

A

Spectrum of hepatotoxicity

  • asymptomatic transaminase elevations
  • clinical hepatitis
  • fulminant hepatic failure
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63
Q

What needs to be monitored for to watch for NNRTI hepatotoxicity?

A
  • signs/symptoms of hepatitis

- liver enzymes

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64
Q

What NNRTI may cause hepatotoxicity in the context of a hypersensitivity reaction?

A

Nevirapine

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65
Q

Describe nevirapine-induced hypersensitivity reactions.

A
  • flu-like symptoms
  • fever
  • jaundice
  • abdominal pain
  • with or without a rash
66
Q

What are the most feared manifestations of nevirapine hypersensitivity reactions?

A
  • fulminant hepatic failure

- severe rash (ex: toxic epidermal necrolysis)

67
Q

In what patients is nevirapine hypersensitivity syndrome more frequent when starting therapy?

A

Patients who are less immunocompromised

-have higher CD4 counts

68
Q

How can the risk of nevirapine hypersensitivity syndrome be reduced?

A

Use reverse taper upon initiation

  • start with lower dose
  • escalate to full dose over 2 weeks (when risk is highest)
69
Q

Describe NNRTI metabolic effects.

A

Lipohypertrophy

  • gradual accumulation of fat in the:
  • abdomen
  • chest
  • neck (buffalo hump)
70
Q

What metabolic effects are efavirenz and nevirapine associated with?

A

Hyperlipidemia

71
Q

With regards to metabolic effects, how does rilpivirine compare to efavirenz?

A

Rilpivirine showed less of an effect on lipid profiles

72
Q

What pregnancy category is efavirenz?

A

Category D

-should not be offered to pregnant women

or

-those trying to conceive

or

-not using effective birth control

73
Q

What pregnancy category is rilpivirine?

A

Category B

74
Q

What pregnancy category are other NNRTIs besides efavirenz and rilpivirine?

A

Category C

75
Q

What adverse effects is efavirenz specifically associated with?

A
  • CNS
  • hyperlipidemia
  • category D
76
Q

What is a key limitation of NNRTIs?

A

Low genetic barrier to resistance

  • single point mutation can lead to high level resistance to the entire class
  • even stricter adherence is necessary
77
Q

What are the advanced generation NNRTIs?

A
  • etravirine
  • rilpivirine
  • possess activity against viruses with some NNRTI mutations
  • may have roles for patients who have failed either efavirenz or nevirapine
78
Q

How does the drug interaction profile of NNRTIs compare to NRTIs?

A
  • much broader profile

- concentrations of NNRTIs can themselves be affected by inhibitors or inducers of drug metabolizing enzymes

79
Q

What is the drug interaction profile of nevirapine?

A

Inducer

80
Q

What is the drug interaction profile of efavirenz and etravirine?

A

Mixed inducing and inhibitory properties

81
Q

What is the drug interaction profile of rilpivirine?

A

-does not yet appear to have significant effects on metabolism of other drugs

82
Q

What is a recommended alternative regimen for initial treatment of treatment-naïve patients with HIV?

A

Atripla

  • efavirenz
  • tenofovir
  • emtricitabine
  • first one pill, once daily HIV regimen
83
Q

Why WAS Atripla a preferred initial regimen?

A

New integrase strand transfer agents also offer this option now

  • lesser degree of toxicity
  • possibly lower genetic barrier to resistance
84
Q

What are other NNRTIs (besides efavirenz) used for?

A

2nd line therapy in treatment-experienced patients

85
Q

What must patients be counseled on when starting an NNRTI?

A
  • adverse effects (skin reactions; symptoms of hepatotoxicity)
  • strict adherence to prevent resistance
  • dose titration schedule for nevirapine
  • CNS effects of efavirenz
86
Q

What are PIs?

A

Protease inhibitors

  • now entering 3rd generation
  • more potent agents with fewer acute toxicities
  • long term toxicities are arising
87
Q

What is HAART?

A

Highly active antiretroviral therapy

  • began with combination regimens that included PIs
  • have had a major impact on prolonging lifespan among HIV patients
88
Q

What is boosting?

A

Using potent inhibition of ritonavir or the PK booster cobicistat to increase serum concentrations and half lives of other PIs

-now routine for essentially all PIs

89
Q

How does boosting work?

A

-take an additional pill of a low dose of ritonavir with their PI (/r)

or

-co-formulation with cobicistat (/c) or ritonavir (/r)

90
Q

What is Atazanavir?

A

PI

-ATV

91
Q

What is Darunavir?

A

PI

-DRV

92
Q

What is Ritonavir (boosting dose)?

A

PI

-/r

93
Q

What is fosamprenavir?

A

PI

-FPV

94
Q

What is saquinavir?

A

PI

-SQV

95
Q

What is indinavir?

A

PI

-IDV

96
Q

What is nelfinavir?

A

PI

-NFV

97
Q

What is tipranavir?

A

PI

-TPV

98
Q

What is ritonavir (full dose)?

A

PI

-RTV

99
Q

What is in Prezcobix?

A
  • darunavir
  • cobicistat
  • DRV/c
100
Q

What is in Evotaz?

A
  • atazanavir
  • cobicistat
  • ATV/c
101
Q

What is in kaletra?

A
  • lopinavir
  • ritonavir
  • LPV/r
102
Q

What does the viral enzyme HIV protease do?

A

Hijacked HIV infected cell uses the cell’s ribosomes to synthesize its own proteins

  • some are created in long chains that need to be cut up into their component parts to work correctly
  • protease enzymes are like a pair of scissors that cut out prefabricated shapes from a piece of cardboard paper
103
Q

What is the MOA of PIs?

A

Selectively inhibit HIV protease

104
Q

Are PIs active against HIV also active against Hepatitis C virus?

A

No; those PIs are different drugs

105
Q

What are the categories of adverse effects of PIs?

A
  • cardiovascular
  • GI
  • hepatotoxicity
  • metabolic
  • nephrotoxicity
106
Q

Describe PI cardiovascular effects.

A

Interact with conventional CV risks factors to increase risk for MI and stroke beyond that expected from just prolonging lifespan

107
Q

How are PI CV risks managed?

A

With all the mainstays of CV risk prevention

  • diet
  • exercise
  • drugs
108
Q

Which PIs may confer somewhat LOWER CV risk compared with other PIs?

A
  • atazanavir

- darunavir

109
Q

Describe PI GI effects.

A

Pretty hard on the GI tract

  • nausea
  • vomiting
  • diarrhea
110
Q

How can PI GI effects be reduced?

A
  • taking with food may reduce symptoms somewhat

- many find the effects more tolerable with time

111
Q

How are severe cases of PI GI effects managed?

A

Administration with

  • antiemetics
  • antidiarrheals
112
Q

Describe PI hepatotoxicity.

A

Ranges from

-asymptomatic transaminase elevations

to

-clinical hepatitis

113
Q

Which PI may have the highest risk of hepatotoxicity?

A

Boosted tipranavir

114
Q

Describe PI metabolic effects.

A
  • adverse effects on the lipid profile (one way in which CV risk is increased)
  • lipodystrophy: fat accumulation in
  • abdomen
  • breasts
  • neck
115
Q

Describe PI nephrotoxicity.

A

Certain PIs cause precipitation in the kidneys or ureters

116
Q

Which PI most commonly associated with nephrotoxicity?

A

Indinavir

-now infrequently used

117
Q

Which PIs is nephrotoxicity rarely reported with?

A
  • atazanavir

- fosamprenavir

118
Q

What strategy is recommended to prevent PI nephrotoxicity?

A

Adequate fluid intake

119
Q

How are PIs against resistance compared to NNRTIs and INSTIs?

A

More robust

  • several mutations in the target enzyme required to confer high level resistance
  • PI based regimens may be slightly more forgiving of less than perfect adherence
120
Q

What is the drug interaction profile of PIs?

A

-all are susbtrates of the common drug metabolizing enzymes

121
Q

What drugs can PI regimens boosted with ritonavir or cobicistat affect?

A

Drugs that are P450 substrates

  • statins
  • macrolides
  • benzodiazepines
  • calcium channel blockers
  • etc
  • can lead to increased levels
  • also more unpredictable effects can occur (result of shunting to alternative pathways or mixed inhibition/induction): voriconazole-ritonavir interaction can lead to reduction of voriconazole
122
Q

How is ritonavir now usually always used?

A

As a PK booster

-much lower dose than originally approved

123
Q

What is ritonavir’s originally approved dose?

A

400mg BID

  • not well tolerated at this dose
  • majority of prescriptions for it are in error
124
Q

Which PI-based regimen is preferred for treatment of initial HIV infection?

A

Darunavir-based combinations

125
Q

Which PI-based regimens are alternatives for treatment of initial HIV infection?

A

Regimens with

-atazanavir

or

-lopinavir

126
Q

Which PI is the only one that can be used unboosted?

A

Only atazanavir (only for selected patients)

-other regimens should have at least some ritonavir or cobicistat

127
Q

What factors need to be taken into consideration when prescribing a PI?

A

Balance the

-durable viral suppression

against

  • long term toxicities (particularly CV effects)
  • patients should be prepared to make appropriate lifestyle changes
128
Q

What are the INSTIs?

A

Integrase inhibitors (integrase strand transfer inhibitors)

-are the anchor of most of the preferred regimens for initial therapy

129
Q

What are the benefits of INSTIs?

A
  • excellent tolerability
  • fewer drug interactions (except elvitegravir)
  • one pill once daily convenience (except raltegravir)
  • novel MOA provides new option for treatment experienced patients
130
Q

What is Dolutegravir?

A

INSTI

-DTG

131
Q

What is Raltegravir?

A

INSTI

-RAL

132
Q

What is in stribild?

A
  • elvitegravir
  • cobicistat
  • emtricitabine
  • TDF
133
Q

What is in genvoya?

A
  • elvitegravir
  • cobicistat
  • emtricitabine
  • TAF
134
Q

What is in triumeq?

A
  • dolutegravir
  • abacavir
  • lamivudine
135
Q

What does the viral protein integrase do?

A

HIV reverse transcriptase creates a strand of viral DNA

-integrase facilitates the transfer of the HIV DNA into the host cell’s genome

136
Q

What is the MOA of INSTIs?

A

Inhibit integrase

  • prevents the viral DNA from becoming a part of the host cell genome
  • this is an important step in HIV replication
137
Q

Are INSTIs used for any other viral infection besides HIV?

A

No

-only HIV

138
Q

Which INSTI has been associated with musculoskeletal adverse effects?

A

Raltegravir

  • increases in creatine phosphokinase
  • most cases have been asymptomatic
  • clinically evident myositis or rhabdomyolysis is rare
139
Q

What kind of renal dysfunction does cobicistat cause?

A

Fake

  • inhibits renal secretion of creatinine
  • leads to increased levels of serum creatinine without a decline in GFR
  • must differentiate between true renal dysfunction caused by tenofovir
140
Q

Is cobicistat an antiviral?

A

No

  • is a PK enhancer
  • used to boost concentrations of other drugs
141
Q

Is elvitegravir available alone?

A

No, only with

-cobicistat

and

-tenofovir

and

-emtricitabine

Has concerns for drug interactions (similar to ritonavir boosted regimens)

142
Q

What is the drug interaction profile of raltegravir?

A

Few documented drug interactions

143
Q

What is the drug interaction profile of dolutegravir?

A

More on the raltegravir end of the spectrum

-should still check for interactions (as with all antiretrovirals)

144
Q

What OTC interaction do INSTIs have?

A

Reduced absorption when given with divalent and trivalent cations (as with FQ and tetracyclines)

  • give at least 2 hours before or 6 hours after oral administration of products containing
  • aluminum
  • magnesium
  • calcium
  • iron
  • zinc
145
Q

Describe the genetic barrier of resistance to INSTIs.

A
  • relatively low barrier

- less forgiving of imperfect adherence than a PI based regimen

146
Q

Which form of tenofovir is elvitegravir available with?

A

Both TDF and TAF

147
Q

What is an important factor to monitor when giving an INSTI?

A

Interactions

-a drug that decreases its concentration can put it at risk for development of resistance due to low level of resistance

148
Q

Which class of antiretrovirals has rocketed to the top of the preferred list of antiretrovirals?

A

INSTIs

-have many favorable characteristics

149
Q

What is Maraviroc?

A

Entry inhibitor

-MVC

150
Q

What is enfuviritide?

A

Fusion inhibitor

-T20

151
Q

How are entry and fusion inhibitors different from other classes of antiretrovirals?

A
  • other classes affect the HIV life cycle after infection of the cell
  • these classes attempt to block HIV from infecting the cell
152
Q

What does the process of HIV binding to and entering a cell involve?

A

A handshake between viral proteins and proteins on the host cell target

153
Q

What does the MOA of maraviroc involve?

A

Targets a human protein that serves as a coreceptor for the virus

154
Q

What human protein does maraviroc target?

A

CCR5

155
Q

What does the MOA of enfuviritide involve?

A

Binds to a viral protein involved in fusion

156
Q

Are the entry and fusion inhibitors active against any viral infections besides HIV?

A

No

-only HIV

157
Q

What are the dermatologic effects of enfuviritide?

A

Is a subcutaneous injection; causes injection site reactions

  • occur in essentially all patients
  • pain
  • erythema
  • pruritis
  • nodule formation
158
Q

What does maraviroc have a black box warning for?

A

Hepatotoxicity

  • based on case reports from healthy subjects who received the drug in early clinical trials
  • seems to be rare in patients treated with maraviroc
159
Q

For what infections is enfuviritide reserved for?

A

Most difficult to treat, multidrug resistant strains

-administered as SC injection associated with substantial injection site reactions

160
Q

What test must be used before starting maraviroc?

A

Tropism test

  • to see whether the virus prefers CCR5 (maraviroc-yes) or CXCR4 (maraviroc-no)
  • there are two coreceptors for HIV viral entry
161
Q

Is maraviroc affected by CYP enzymes?

A

Yes

  • is a substrate for P450 drug metabolizing enzymes
  • different dosage recommendations depending on which other potentially interacting drugs patient is taking
162
Q

When are entry and fusion inhibitors mainly used?

A

In treatment experienced patients

Antibiotics (63 decks)

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