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Pharmacy CPS Flashcards > HIV Treatment > Flashcards

HIV Treatment Flashcards

1
Q

NNRTIs avaliable for HIV

A 
Efavirenz (EFV)
Etravirine (ETR)
Nevirapine (NVP)
Rilpivirine (RPV)
Doravirine
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2
Q

NRTI meaning and target?

A

Nucleoside reverse transcriptase inhibitor

Blocks the reverse transcription of RNA into DNA

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3
Q

NRTIs avaliable for HIV

A 
Abacavir (ABC)
Emtricitabine (FTC)
Lamivudine (3TC)
Tenofovir (TDF & TAF)
Zidovudine (AZT, ZDV)
Islatravir (under investigation)
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4
Q

PIs avaliable for HIV

A

Atazanavir (ATV)
Darunavir (DRV)
Lopinavir (LPV)

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5
Q

Pharmacokinetic Boosters for HIV

A

Cobicistat (c)

Ritonavir (r)

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6
Q

Integrase inhibitors for HIV

A

Raltegravir (RAL)
Elvitegravir (EVG)
Dolutegravir (DTG)
Bictegravir (BIC)

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7
Q

CCR5 Antagonists avaliable for HIV

A

Maraviroc (MVC)

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8
Q

NNRTI meaning and target?

A

Non-nucleoside reverse transcriptase inhibitors

Same general target as NRTIs (halting reverse transcription) but specifically isnt a nucleoside itself

Binds HIV-1s reverse transcriptase to prevent RNA -> DNA conversion

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9
Q

PI meaning and target?

A

Protease inhibitor

Prevents protease from cleaving immature proteins and completing viral assembly

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10
Q

What do integrase inhibitors do and how does this work against HIV

A

Stops insertion of viral genome (once its converted to DNA) into the host genome (thus stopping replication)

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11
Q

CCR5 mechanism of action

A

Blocks CCR5 receptor by binding the chemokine coreceptor and inducing a conformational change

This change blocks HIV entry into host cells (specifically CD4 T-cells)

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12
Q

General HIV treatment combination?

A

three ACTIVE drugs (not including boosters) from two different classes

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13
Q

What happens to NRTIs once within a cell?

A

undergo phosphorylation via kinases and phosphotransferases

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14
Q

What do activated NRTIs do?

A

when in triphosphate form they competatively bind viral reverse transcriptases

They get incorporated within the growing DNA transcription and terminate it

NRTIs are all analogues of nucleosides and nuclotides

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15
Q

What agents are the “backbone” of HIV treatment?

A

NRTIs

Generally used in pairs w/ a third agent of another class

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16
Q

Traditional NRTI pairs?

A

TDF/FTC
TAF/FTC
ABC/3TC
3TC/AZT

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17
Q

NRTI adverse effects

A

Mitochondrial toxicity (results in neuropathy, lipoatrophy, pancreatitis, hepatic steatosis)

Lactic acidosis (rarer)

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18
Q

Which patient catagory would you be more selective with NRTI drugs

A

Patients that concurrently have HBV as lamivudine, emtricitabine and tenofovir have anti-HBV activity

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19
Q

Primary method of excretion for TDF (tenofovir disoproxil fumarate)

A

Mostly via urination as unchanged drug

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20
Q

Do you adjust TDF tenofovir disoproxil fumate dosage in renal or hepatic impairment?

A

Renal-> yes, adjustments w/ 30-49mL/min no use <30

Hepatic -> no

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21
Q

TDF (Tenofovir disoproxil fumarate) adverse effects

A

Fanconi syndrome (reabsorption issue in the renal proximal tubule)

renal failure

bone mineral density decreases via phosphate wasting

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22
Q

TDF (tenofovir disoproxil fumarate) drug interactions of note

A

NSAIDS (renal dysfunction from both drugs)

Nephrotoxic medications (methotrexate, cisplatin etc)

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23
Q

Why might you choose TDF over other NRTIs

A

Resistance mutations affecting most NRTIs tend to not cause cross resistance to TDF

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24
Q

Difference between tenofovir disoproxil fumerate (TDF) and tenofovir alafenamide (TAF)?

A

TAF is a prodrug of tenofovir diphospate requires activation

TAF has higher bioavaliability and intracellular t1/2

TAF dose is 25mg daily vs 300mg for TDF

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25
Q

Benefits of using TAF over TDF

A

Less affects on kidneys and bone mineral density

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26
Q

Renal adjustments for TAF

A

> 30mL/min - no adjustments are necessary

<30mL/min - DO NOT USE

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27
Q

Abacavir (ABC) excretion mechanism

A

Renal mostly, as a metabolite (1.2% unchanged)

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28
Q

Abacavir (ABC) renal and hepatic adjustments

A

Renal = no changes needed
Hepatic = Child-Pugh A = 200mg BID (300mg BID is normal)
Child-Pugh B or C = DO NOT USE

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29
Q

What test is required before ABC use?

A

HLA-B*5701 testing prior to use

Presence of this can increase hypersensitivity reaction incidence

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30
Q

Why are FTC (emtricitabine) and 3TC (lamivudine) associated with each other?

A

both cytosine analogues they are “relatively” interchangable

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31
Q

Can you use FTC and 3TC together?

A

NO!

they are competative inhibitors of each other

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32
Q

Excretion of 3TC and FTC mechanism

A

largely unchanged through the urine

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33
Q

Adjustments for FTC and 3TC during hepatic or renal dysfuction

A

Renal = requires dosages for ESRD

No hepatic dose adjustments

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34
Q

Between FTC and 3TC which agent is known to cause more hyperpigmentation

A

FTC

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35
Q

Difference between NNRTI and NRTIs

A

NNRTIs bind to the actual reverse transcriptase protein and interupt its action via sterochemical changes at the enzymatic site

NRTIs get incorporated within the growing DNA strand an prematurely end reverse transcription

36
Q

Known class effect of NNRTIs

A

Neuropsychiatric effects are fairly common

37
Q

Elimination mechanism of rilpivirine (RPV)

A

mostly via metabolism from 3A4 and excreted via feces as the metabolite

38
Q

Whats known to decrease rilpivirine (RPV) absorption?

A

Protein shakes

39
Q

Does Rilpivirine (RPV) need food?

A

Yes! normal meal that contains fat

40
Q

pH requirements for rilpivirine (RPV) absorption

A

acidic pH

41
Q

Any adjustments needed for rilpivirine (RPV) in hepatic or renal dysfunction?

A

None recommended, but not studied in ESRD or hepatic impairment

42
Q

Rilpivirine drug interactions of note

A

Anything that changes stomach acid (so watch for PPIs, H2RAs, PPIs etc)

Enzyme inducers (3A4 metabolized) -> phenytoin, ketoconazol, st johns

QTc prolonging drugs -> escitalopram

43
Q

Rilpivirine (RPV) adverse effects of note?

A

Severe rash, depression and mood changes, liver damage (so be careful with some combinations that require hepatic changes)

44
Q

Can you use rilpivirine (RPV) in a naive patient?

A

No! must have a viral load <100,000 c/mL as higher counts increase treatment failure risk

Might be due to low genetic resistance barrier

45
Q

Efavirenz (EFV) mechanism of excretion

A

Mostly in feces as unchanged (61%)

Some metabolites (34%) found in urine via 3A4 and 2B6 metabolism

46
Q

Dose adjustments needed for Efavirenz (EFV)

A

Renal = no changes even in ESRD

Hepatic -> child-pugh B/C is CI

47
Q

Efavirenz drug interactions of note

A

this is an inducer of 3A4, and 2B6
inhibitor of 2c19, 2c9, 2c8
Do not combine with PIs and INSTIs

48
Q

Efavirenz (EFV) adverse effects to note

A

CNS effects such as dizziness, depression, vivid dreams, insomnia, fatigue so youll be tired but unable to sleep :(

Increase in lipids, and hepatic dysfunction

Diarrhea, nausea (can we name like any drugs that dont cause these two) , abdominal pain

Rash and SJS -> SJS more important to remember

49
Q

Which patient population can doravirine (DOR) be used in?

A

Treatment naive patients only

50
Q

NNRTI common name motif

A

Most end in some virenz, virine, vira

look for vir BUT NOT AT THE END like other antivirals

51
Q

Is doravirine (DOR) studied in any dysfunctional patients?

A

No neither hepatic or ESRD have been studied

52
Q

Adverse effects of doravirine (DOR) to know

A

nausea, dizziness, headache, fatigue, diarrhea, abdoinal pain, abnormal dreams

53
Q

difference between efavirenze and doravirine in regards to enzyme activity

A

Doravirine does not inhibit or induce CYPs

54
Q

Where are PI medications best used?

A

Patients that have suboptimal adherence and they cannot be monitored

High genetic barrier to resistance

55
Q

Why are PIs commonly prescribed with a booster?

A

short t1/2, need something to slow down their breakdown to allow for less frequent dosing

56
Q

Adverse effects associated with PI use?

A

effects on sugar -> insulin resistance, hyperglycemia, and increased risk of diabetes mellitus

effects on lipids -> hyperlipidemia, lipodystrophy, hepatic toxicity

Bleeding risk in hemophiliacs

57
Q

Excretion of ritonavir

A

Mostly via feces and as a metabolite

3A4 and 2D6

58
Q

Adjustments for ritonavir (RTV)

A

Renal = no worries

hepatic = Child C = not reccomended

59
Q

drug interactions w/ ritonavir

A

known inducer of 1A2

known inhibitor of 3A4, 2C8, 2D6, and P-glycoprotein

60
Q

Major adverse effects known to be caused by ritonavir

A 
Dyslipidemia
glucose intolerance and diabetes
lipodystrophy and lipoatrophy
increased bleeding w/ hemophilia
diarrhea, vomiting, abdom pain, dyspepsia
61
Q

What is cobicistat?

A

inhibitor of 3A4 used to prolong 3A4 metabolized drugs

understandably be worried with 3A4 drugs

62
Q

cobicistat requires adjustment in combination with which drug

A

TDF -> cannot be used if CrCl <70mL/min

63
Q

Whats known to happen when you start cobicistat?

A

CrCl “decrease” just lab value, not an actual decrease in renal function

64
Q

what PI has the highest genetic resistance

A

dorunavir

65
Q

Darunavir (DRV) elimination

A

3A4 metabolism and fecal exretion

66
Q

darunavir food effect

A

40% increase

67
Q

darunavir adverse effects of note

A

similar metabolic effects as other PIs
rash (rare cross sensitivity with sulfa allergy patients)
Diarrhea and GI upset

68
Q

Does atazanavir need food during dosing?

A

Yes! must be given with food for increased absorption

69
Q

atazanavir metabolism

A

3a4 mostly

70
Q

Atazanavir dose adjustments

A

no use in ESRD

not recd in severe hepatic impairment

71
Q

Does atazanavir require a specific environment for absoption

A

needs an acid environment

72
Q

atazanavir adverse effects of note

A

Benign asymptmatic hyperbilrubinemia

-> leads to jaundice, scleral icterus -> sclera goes yellow

73
Q

INSTIs drug interactions

A

chelation w/ polyvalent cations (anything with more then 1+

74
Q

drug interactions of raltegravir (RAL)

A

polyvalent cations

rifabutin and rifampin can decrease concentration of RAL

75
Q

Adverse effects of raltegravir (RAL)

A

increased ALT, insomnia, headache, dizziness, fatigue

76
Q

Elvitegravir (EVG) dosing with respect to meals?

A

Absorption increased with food and should be taken with meals

77
Q

does EVG intereact with medications?

A

Yes! antacids, fibabutin and rifampin (can increase [])

caution with other ARVs - dose adjustments may be needed

78
Q

Adverse effects of EVG

A

Diarrhea, nausea, vomitting, dyspepsia, abdominal pain, insomnia, headache, depression, fatigue, sucidial ideation, increase in SCr from cobicistat

79
Q

Dolutegravir meal adjustments needed?

A

No dosing with respect to meals

80
Q

DTG interesting drug interactions

A

Can increase concentrations of metformin (max dose 1000mg daily)
phenobarb, phenytoin, carbamazepine, oxcarazepine, and rifampin decrease []

81
Q

what medication is bictegravir more known as?

A

Biktarvy as its only avaliable as a single tablet regiement w/ FTC/TAF

82
Q

Bictegravir (BIC) dosage?

A

50mg po daily without respect to meals

83
Q

Bictegravir (BIC) drug interactions

A

Inhibition of organic ion transporter 2 (OCT2) and multidrug and toxin extrusion transporter 1 w/ no clinical impact on metformin

Atazanvir increases BIC

84
Q

What 2 drug regiements have indicated efficacy in certain populations

A

Dovato (Dolutegravir + lamivudine) for treatment of naive patients w/ initial viral load <500,000 c/mL

Juluca (Dolutegravir + rilpivirine) indicated only for switch in those who are already virally suppressed

85
Q

What are our goals of therapy for a patient with HIV starting ARV therapy?

A

Want to reach an undetectable viral load -> <20 copies/mL

CD4+ cell count above 500 cells/mL (return immune function)

86
Q

How long till patients become virally supressed?

A

6-12 weeks (so 1.5months - 3 months)

87
Q

When should patients hold ARV therapy?

A

> 10 days since last dose
~60% of fills are inconsistant
no monitoring for the last 6-12 months
“socially chaotic”?

Pharmacy CPS Flashcards (27 decks)

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