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SBL Exam 2 > HIV Pharm > Flashcards

HIV Pharm Flashcards

1
Q 
interferes with thymidine incorporation 
first ART drug 
inhibit HIV 1 & 2, HTLV 1 & 2 
toxicities: bone marrow suppression 
skeletal m. myopathy when inhibiting mitochondrial DNA polymerase inhibition 
hepatic steatosis
A

zidovudine

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2
Q

interfere with thymidine incorporation
inhibit HIV 1 & 2
excreted in urine unchanged

most common serious toxicity: peripheral neuropathy
NRTI associated most strongly with lipodystrophy/fat wasting
Lactic acidoses & hepatic steatosis

A

stavudine (d4T)

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3
Q 
interferes with cytosine 
treat with HIV 1 & 2
active against HBV 
low barrier to resistance if on its own
co-formulated with tenofovir, superior combination 
long intracellular half-life 
excreted unchanged in urine

one of the least toxic antiretroviral drugs
prolonged use leads to hyperpigmentation esp. in palms & soles
more common in AA

A

emtricitabine (FTC)

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4
Q

interfere with cytidine incorporation
use in HIV 1 & 2 & HBV
low resistance on its own, co-formulated with tenofovir
lamivudine + doltegravir used for naive treatments with low HIV numbers
long half-life
excreted primarily unchanged in urine

one of the least toxic antiretroviral drugs

A

lamivudine

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5
Q

only guanosine analog
don’t give to HLAB5701 genotype due to fatal hypersensitivity syndrome
half-life of 21 hrs
not effective against HBV
not a CYP substrate and will be conjugated w/glucuronide for renal elimination
generally avoided in patients w/CAD

A

abacavir (ABC)

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6
Q

nucleotide reverse transcriptase inhibitor
approved for HBV
co-formulated with emtricitabine
resistance due to single substitution (K65R)
intracellular half-life 10-50 hours 1x/day dosing
excreted primarily unchanged in urine
generally well tolerated with few adverse effects
can see nephrotoxicity w/ acute tubular necrosis –> Fanconi syndrome
decreased bone mineral density

A

tenofovir disproxil fumarate (TDF)

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7
Q

nucleotide reverse transcriptase inhibitor adenosine analong
broad spectrum against viral DNA polymerases approved for HBV
resistance due to single substituion
very similar to TDF
TAF transported differently than TDF –> lower doses administered –> lower plasma concentration but –> higher intracellular concentration of tenofovir-diphosphate
less renal & bone toxicity than TDF

A

tenofovir alafenamide (TAF)

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8
Q

block strand transfer
retains its activity against viruses resistant to other drug classes
terminal elimination: 9 hrs
eliminated in urine & feces unchanged & undergoes glucuronidation
generally well tolerated:
can see immune reconstitiution syndrome
some incidence of myopathy/rhadomyolysis
excellent target since human DNA is not known to undergo excision/reintegration

A

raltegravir

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9
Q

block chromosomal integration of viral DNA
resistance can develop but has high genetic barrier to resistance
primarily metabolized by UGR1A1 glucuronidation before renal excretion
available in combinations w/ abacavir & lamivudine & rilpvirine
Toxicities similar to raltegravir
avoid in pregnancy

A

doultegravir

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10
Q

part of 1X/day fixed dose combinations of elivitegtavir, cobicistat, emtricitabine & either TAF/TDF
metabolized by CYP3A4 and needs to be boosted

A

elvitegravir

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11
Q

blocks chromosomal integration of viral DNA
resistance can develop but high genetic barrier to resistance
termination elimination half-time is 16-23 hrs
more soluble/readily absorbed than other INSTI
glucuronidated by UGT1A1 & metabolized by CYP3A4 and only affected with dual inhibitors or strong CYP3A4 inducers
only available as a fixed-dose single tablet regimen
generally well tolerated

A

bictegravir

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12
Q 
1st protease inhibitor 
inhibit both HIV-1 &2 
no longer used to huge pill burden due to its short half-life 
Toxicitiy: GI distress
long-term --> lipodystrophy
A

saquinavir

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13
Q

often works after failure of other PI-containing regimens
Toxicities: GI distress, nausea, vomiting diarrhea
increase TAGs & cholesterol

A

lopinavir

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14
Q

non-peptic but peptide-like
treatment naive & experienced (with guidance)
doubled half-life when boosted
metabolized by CYP3A4
first choice when boosted w/ritonavir or cobicistat
Toxicities: elevated bilirubin, unconjugated hyperbilirubinemia not associated with hepatitis
fat redistribution, immune reconstitution & increased serum cholesterol

A

atazanavir

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15
Q

non-peptidic protease inhibitor
inhibt HIV 1 & 2 indicated for HIV-1
used off-label for post-exposure prophylaxis
current 1st choice PI when boosted w/ ritonavir
Toxicities: increased TAGs & cholesterol, fat redistribution/ immune reconstitution syndrome
sulfa drug hypersenstivity

A

darunavir

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16
Q

early one

Toxicities crystaluria/renal stones

A

indinavir

17
Q

only used to block CYP3A4
boots levels of other more potent protease inhibitors
Toxicities: flushing, rash, GI upset & misc

A

ritonavir

18
Q

not a protease inhibitor

used to boost atazanavir and darunavir

A

cobistat

19
Q

co-formulated with tenofovir
1st NNRTI approved for once daily dosing
induce CYP3A4
Toxicities: most significant CNS toxicity/psychiatirc side effects
Was considered teratogenic
rash also common

A

efavirenz

20
Q

still works after mutations that disrupt activity of other NNRTI
induce CYP3A4
treatment-experience HIV-1 patients
Toxicities: fat redistribution, immune reconstitution syndrome, rash common

A

etravirine

21
Q

treatment naive w/ HIV-1
not susceptible to common mut. that renders efavirenz & nevirapine ineffective
metabolized by CYP3A4
Toxicities: more common in children & adolescents, CNS & endo issues

A

rilpivirine

22
Q

treatment naive HIV-1 patients swtiching to stable regimens
works when resistance to efavirenz or rilpiviridine
metabolized by CYP3A4
co-formulated with lamivudine & tenofovir
decreased incidence of side effects

A

doraviridine

23
Q

approved for HIV-1 in adults & children
long half-life
decreased level of contraceptives
induced by CYP3A4
Toxicities: rash/itching –> most common side effects

A

nevirapine

24
Q

36 aa peptide derived from viral gp41 part that fuses w/ cell mem.
inhibit formation of 6-helix bundle critical for membrane fusion
inhibit CD4+ infection
inhibit cell to cell transmission in vitro
retains its activity against viruses resistant to other drug classes
must be administered paraenterally
Toxicity: injection site reaction

A

enfuvirtide

25
Q

block binding of GP120 to CCR5 co-receptor
approved for use i ART combinations for HIV caused by CCR5 trophic virus
essential phenotypic test required
orally active
a CYP3A4 substrate need to be wary of other CYP3A4
generally well tolerated
not recommended as initial therapy, rare systemic allergic rxn followed by hepatic toxicity

A

maraviroc

SBL Exam 2 (2 decks)

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