Treatment for HIV

Question 1

NRTIs

Answer 1

Nucleoside Reverse Transcriptase Inhibitor

Ex: “bine”, “dine”
Didanosine
Zindovudine
Lamivudine
Abacavir
Tenofovir
Emtricitabine

MOA: competitively inhibit nucleotide binding to reverse transcriptase –> terminate DNA chain

Class AE:
*mitochondrial toxicity
(MOA: inhibit RNA dependent DNA polymerase
-high affinity for DNA polymerase gamma
(mitochondrial polymerase))
-Significant: (starvidine), didanosine, zidovudine
-minimal: (LATE) Lamivudine, Abacavir, Tenoforvir, Emtricitabine
*PLAN
-Pancreatitis
-Lactic acidosis
-Anemia
-Neuropathy (peripheral)

Class Interactions: fewer compared to other HIV drug classes (no CYP interactions)

Question 2

NNRTIs

Answer 2

Non-Nucleoside Reverse Transcriptase Inhibitor

Ex: Efavirenz, Nevirapine, Etravirapine, Rilpivirine “VIR in middle of name”

MOA: Binds to RT, causes a conformational change and disrupt the catalytic center of the RT

Class AE: rash, hepatotoxic (increase LFT)

Class Interactions: CYP interactions (inducers/inhibitors)
-exception: rilpivirine

Question 3

INSTIs

Answer 3

Integrase Strand Transfer Inhibitors

Ex: Raltegravir, Elvitegravir, Dolutegravir, Bictegravir (“tegra”)

MOA: interfere with the integration of viral DNA into host DNA

Class AE: very well tolerated; GI AEs

*Elvitegravir = metabolized via 3A4 –> use with “boosters”

Question 4

PIs

Answer 4

Protease Inhibitors

Ex: Atazanavir, Darunavir, Ritonavir, Nelfinavir, Indinavir
(only used a booster)

MOA: Block Proteolytic cleavage of protein precursors that are necessary for the production of infectious particles

Class AE:
*Metabolic abnormalities (not atazanavir)
“Protease Pouch”: Hyperlipidemia, hyperglycemia, fat redistribution
*Hepatotoxicity (increased LFTs)

Class Interactions: CYP interactions (CYP inhibitors)

Special AE: Atazanavir: Hyperbilirubinemia

Other Characteristics:
Generally boosted with ritonavir or cobicistat; nelfinavir only PI that doesn’t require boosting