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Here are the short flashcard topics from the Antiviral Drugs PDF:

🦠 Antiviral Drugs - Flashcard Topics

Topic 1: Virus Basics

Q: Why are antiviral drugs difficult to develop? A: Viruses are obligate intracellular parasites that use host metabolic machinery - drugs must be selective enough to harm the virus without injuring host cells.
Q: Name the 7 steps of viral replication. A: Attachment & Entry → Penetration → Uncoating → Nucleic Acid Synthesis → Protein Synthesis → Packing & Assembly → Release

Topic 2: Anti-Influenza Drugs

Q: Name the 3 neuraminidase inhibitors and their routes. A: Oseltamivir (oral), Zanamivir (inhalation), Peramivir (IV)
Q: What is the mechanism of neuraminidase inhibitors? A: Inhibit viral neuraminidase → prevent release of new virions from infected host cells → block cell-to-cell spread in the respiratory tract.
Q: Oseltamivir dosing: treatment vs. prophylaxis? A: Treatment: 75 mg twice daily x 5 days (within 48 hrs of symptoms); Prophylaxis: 75 mg once daily (70-90% effective).
Q: What is Peramivir's unique feature? A: Single 600 mg IV dose; renally eliminated; main side effect is diarrhea; can cause Stevens-Johnson syndrome (rare).
Q: How do Adamantanes work and why are they no longer recommended? A: Block M2 proton ion channel → inhibit uncoating of viral RNA. Not recommended in the US due to widespread resistance. Limited to Influenza A only.
Q: What is Baloxavir's mechanism? A: Interferes with viral RNA transcription; acts early in the replication cycle; long half-life of 80 hours.

Topic 3: Ribavirin (RSV & HCV)

Q: What is Ribavirin and its main clinical uses? A: Synthetic guanosine analog; used for severe RSV infections in immunosuppressed infants (aerosol) and chronic Hepatitis C (in combination with DAAs or interferon).
Q: Key adverse effect and contraindication of Ribavirin? A: Dose-dependent transient anemia; contraindicated in pregnancy.

Topic 4: COVID-19 Antivirals

Q: Name 3 drugs used for COVID-19 and their mechanisms. A:
  • Nirmatrelvir/Ritonavir - protease inhibitor (oral)
  • Remdesivir - adenosine triphosphate analog; inhibits RNA-dependent RNA polymerase (IV); approved for SARS-CoV-2 in hospitalized patients ≥12 years
  • Molnupiravir - oral ribonucleoside analog; inhibits SARS-CoV-2 replication; reduced hospitalization/death by ~50% in Phase 3 trial

Topic 5: Hepatitis B Drugs

Q: List the 6 treatments for chronic Hepatitis B. A: Adefovir, Entecavir, Lamivudine, Telbivudine, Tenofovir, Peginterferon-α-2a
Q: What is the MOA of Entecavir? A: Inhibits all 3 functions of HBV DNA polymerase: base priming, reverse transcription of the negative strand, and synthesis of the positive strand.
Q: What makes Lamivudine special in HBV? A: Also inhibits HIV reverse transcriptase; safe in decompensated liver disease; prevents vertical HBV transmission when given in the last 4 weeks of gestation.
Q: What is Tenofovir's key adverse effect? A: Chronic renal insufficiency (proximal tubulopathy), decreased bone mineral density, Fanconi syndrome (in HIV patients).
Q: How does pegylation improve Peginterferon-α-2a? A: Delays absorption, lengthens duration of action, decreases clearance. Dose-limiting toxicities: bone marrow suppression, severe fatigue, neurotoxicity, autoimmune disorders.

Topic 6: Hepatitis C - Direct-Acting Antivirals (DAAs)

Q: What are the 3 HCV replication targets for DAAs? A: NS3/NS4A protease, NS5B polymerase, NS5A replication complex
Q: Name NS3/NS4A protease inhibitors. A: Paritaprevir (needs ritonavir boosting), Grazoprevir, Voxilaprevir, Glecaprevir. Metabolized by CYP3A - significant DDIs.
Q: Name the 2 types of NS5B polymerase inhibitors with examples. A: Nucleoside analogs (Sofosbuvir) - compete at active site; Nonnucleoside analogs (Dasabuvir) - target allosteric sites.
Q: Name NS5A inhibitors. A: Ledipasvir, Ombitasvir, Elbasvir, Velpatasvir, Pibrentasvir, Daclatasvir. (Only Daclatasvir is not coformulated.)

Topic 7: Herpes Virus Drugs

Q: What is Acyclovir's mechanism of action? A: Guanosine analog → phosphorylated by viral thymidine kinase (TK) → converted to triphosphate by host kinases → competes with deoxyguanosine triphosphate → incorporates into viral DNA → chain termination.
Q: Why are virus-infected cells most susceptible to Acyclovir? A: Initial phosphorylation requires viral thymidine kinase, which is only present in infected cells.
Q: What is Valacyclovir's advantage over Acyclovir? A: Prodrug converted to acyclovir in the liver; achieves plasma levels 3-5x higher; longer duration of action.
Q: How does TK-deficiency cause antiviral resistance? A: TK- strains of HSV lack thymidine kinase → cannot phosphorylate acyclovir → cross-resistant to famciclovir, ganciclovir, and valacyclovir.
Q: What is Ganciclovir's advantage over Acyclovir? A: Greater activity against CMV; distributed to CSF. Key adverse effect: severe dose-dependent neutropenia; carcinogenic and teratogenic (boxed warning).
Q: Why can Cidofovir work against TK-deficient strains? A: Its phosphorylation does NOT depend on viral enzymes - it uses cellular enzymes. Active against TK-deficient CMV and HSV.
Q: What is unique about Foscarnet's mechanism? A: NOT a purine/pyrimidine analog; does NOT require phosphorylation. Directly inhibits viral RNA polymerase, DNA polymerase, and HIV reverse transcriptase.
Q: What electrolyte problems does Foscarnet cause? A: Chelates divalent cations → hypocalcemia, hypomagnesemia, hypokalemia; also hypo/hyperphosphatemia, seizures, arrhythmia.
Q: What drugs are used only topically for Herpes Keratitis? A: Trifluridine and Idoxuridine - too toxic for systemic use. Trifluridine is a fluorinated pyrimidine nucleoside that inhibits viral DNA synthesis.

Total: 64 pages covered across 5 major sections - Respiratory Viruses (Influenza, RSV, COVID-19), Hepatitis B, Hepatitis C, and Herpes Viruses.
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