Here are short flashcard topics from the Anti-HIV Treatment presentation:

Card 1 - Classes of Antiretroviral Drugs Q: What are the 5 classes of antiretroviral drugs? A: NRTIs, NNRTIs, Protease Inhibitors (PIs), Entry Inhibitors, Integrase Inhibitors. Plus 2 pharmacokinetic enhancers (boosters): Ritonavir and Cobicistat.

Card 2 - Initial HIV Therapy Regimen Q: What is the standard initial antiretroviral regimen? A: 2 NRTIs + (1 integrase inhibitor OR 1 NNRTI OR 1 boosted PI)

Card 3 - Goals of HIV Therapy Q: What are the goals of antiretroviral therapy? A: Maximally suppress HIV RNA replication, restore/preserve immune function, reduce HIV-related morbidity/mortality, improve quality of life.

Card 4 - NRTI Mechanism of Action Q: How do NRTIs work? A: They are nucleoside/nucleotide analogs that get phosphorylated into triphosphate forms, which are incorporated into viral DNA by reverse transcriptase, terminating DNA chain elongation.

Card 5 - NRTI Pharmacokinetics Q: Key pharmacokinetic feature of NRTIs? A: Orally administered (Zidovudine also IV); primarily renally excreted; all need dose adjustment in renal insufficiency except Abacavir (metabolized by alcohol dehydrogenase and glucuronyl transferase).

Card 6 - NRTI Adverse Effects Q: What are the major adverse effects of NRTIs? A: Dideoxynucleosides (didanosine, stavudine) cause peripheral neuropathy, pancreatitis, lipoatrophy. All NRTIs risk lactic acidosis + hepatomegaly with steatosis.

Card 7 - Abacavir Hypersensitivity Q: How is hypersensitivity to Abacavir screened? A: Genetic test for HLA-B*5701 allele before starting Abacavir.

Card 8 - NNRTI Mechanism of Action Q: How do NNRTIs differ from NRTIs in mechanism? A: NNRTIs bind an allosteric (non-active) hydrophobic site on HIV RT, causing a conformational change and enzyme inhibition. They do NOT require phosphorylation/activation.

Card 9 - NNRTI Key Drug: Efavirenz Q: Why is Efavirenz preferred in TB co-infection? A: It has lower potential for drug interactions with rifamycins compared to other NNRTIs.

Card 10 - NNRTI: Etravirine Q: What makes Etravirine special among NNRTIs? A: It is a 2nd-generation NNRTI active against many HIV strains resistant to 1st-generation NNRTIs (e.g., efavirenz, nevirapine).

Card 11 - PI Mechanism of Action Q: How do Protease Inhibitors (PIs) work? A: They reversibly inhibit HIV aspartyl protease (retropepsin), preventing cleavage of viral polyproteins, resulting in noninfectious virions (immature, non-functional virus).

Card 12 - PI Pharmacokinetics Q: Key PK features of PIs? A: High plasma protein binding; extensively metabolized via CYP3A4; food affects absorption variably (high-fat increases nelfinavir/saquinavir bioavailability but decreases indinavir's).

Card 13 - PI Drug Interactions Q: Name dangerous drug interactions with PIs. A: Simvastatin/lovastatin (rhabdomyolysis), midazolam/triazolam (excess sedation), fentanyl (respiratory depression). Rifampin and St. John's Wort are contraindicated (CYP450 inducers lower PI levels).

Card 14 - Ritonavir as Booster Q: What is Ritonavir's current primary role? A: A pharmacokinetic booster - inhibits CYP3A to increase bioavailability of co-administered PIs, allowing longer dosing intervals. No longer used as a standalone PI.

Card 15 - Cobicistat Q: What does Cobicistat do and what unique adverse effect does it have? A: Booster that inhibits CYP3A, CYP2D6, and P-gp to enhance atazanavir, darunavir, and elvitegravir. Can falsely elevate serum creatinine by inhibiting tubular creatinine secretion.

Card 16 - HIV Life Cycle (Steps 1-4) Q: What are the first 4 steps of the HIV life cycle? A: 1) Fusion to host cell, 2) Release of viral RNA, 3) Transcription of viral RNA to viral DNA (by reverse transcriptase), 4) Integration of viral DNA into host DNA.

Card 17 - HIV Life Cycle (Steps 5-8) Q: What are the last 4 steps of the HIV life cycle? A: 5) Transcription of viral DNA to RNA and polyproteins, 6) Virion budding + protease activation, 7) Cleavage of polyproteins, 8) Assembly into mature virion.

These 17 flashcard topics cover all key concepts from the presentation - drug classes, mechanisms, pharmacokinetics, adverse effects, and the HIV life cycle.