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Quizzes > Quizzes for Business > Healthcare

Antiviral Medication Knowledge Quiz Challenge

Test Your Skills on Viral Drug Therapy

Difficulty: Moderate
Questions: 20
Learning OutcomesStudy Material
Colorful paper art representing a quiz on Antiviral Medication Knowledge.

Ready for a deep dive into antiviral drug therapy? This antiviral medication quiz offers 15 targeted questions to challenge your understanding of drug classes, mechanisms, dosing, and resistance. Ideal for pharmacy students and healthcare professionals seeking to strengthen viral treatment knowledge, it's fully editable in our intuitive quiz quizzes editor. For broader medication expertise, try the Medication Safety Knowledge Quiz or the Medication Management Knowledge Test. Customize the questions freely to fit any learning objective.

Which antiviral drug is a guanosine analog that selectively inhibits viral DNA polymerase after phosphorylation by viral thymidine kinase?
Acyclovir
Zidovudine
Famciclovir
Oseltamivir
Acyclovir is a guanosine analog activated by viral thymidine kinase and then host kinases. It inhibits viral DNA polymerase by chain termination.
Oseltamivir prevents the release of new influenza virions by inhibiting which viral enzyme?
M2 ion channel
Protease
Reverse transcriptase
Neuraminidase
Oseltamivir is a neuraminidase inhibitor that blocks cleavage of sialic acid residues, preventing release of progeny influenza virions.
Which of the following is a neuraminidase inhibitor used to treat influenza A and B?
Amantadine
Ribavirin
Acyclovir
Oseltamivir
Oseltamivir is a neuraminidase inhibitor active against both influenza A and B. Amantadine targets the M2 ion channel, not neuraminidase.
What is the mechanism of action of zidovudine in HIV therapy?
CCR5 antagonist that blocks viral entry
Protease inhibitor that blocks viral maturation
Nucleoside reverse transcriptase inhibitor that causes chain termination
Integrase inhibitor that prevents proviral integration
Zidovudine is a thymidine analog NRTI that is incorporated into viral DNA and causes chain termination by inhibiting reverse transcriptase.
Raltegravir is classified as which type of antiviral agent?
Integrase inhibitor
Protease inhibitor
Non-nucleoside reverse transcriptase inhibitor
Fusion inhibitor
Raltegravir specifically inhibits HIV integrase, preventing the integration of viral DNA into the host genome.
Which common adverse effect is most associated with ganciclovir therapy?
Neutropenia
Retinopathy
Ototoxicity
Nephrotoxicity
Ganciclovir commonly causes bone marrow suppression, especially neutropenia. Nephrotoxicity is more characteristic of cidofovir.
Ribavirin is contraindicated in which of the following patient populations?
Cardiac disease patients
Pregnant women
Patients with renal failure
Children under 5 years old
Ribavirin is teratogenic and contraindicated in pregnancy. It carries a high risk of birth defects and requires strict avoidance in pregnant patients.
Rifampin reduces plasma levels of HIV protease inhibitors primarily by inducing which enzyme?
UGT1A1
CYP3A4
CYP2D6
CYP1A2
Rifampin is a potent inducer of CYP3A4, which accelerates the metabolism of many protease inhibitors, lowering their plasma concentrations.
HSV strains with deficient viral thymidine kinase are resistant to which drug?
Foscarnet
Ganciclovir
Oseltamivir
Acyclovir
Acyclovir requires phosphorylation by viral thymidine kinase. Strains lacking thymidine kinase cannot activate acyclovir and thus are resistant.
Compared to intravenous acyclovir, oral valacyclovir offers which pharmacokinetic advantage?
Higher oral bioavailability
Shorter half-life
No phosphorylation required
No renal excretion
Valacyclovir is a prodrug of acyclovir with significantly higher oral bioavailability, improving systemic drug levels when taken orally.
Which antiviral requires phosphorylation by both viral and host kinases to become active?
Foscarnet
Ritonavir
Acyclovir
Cidofovir
Acyclovir is first phosphorylated by viral thymidine kinase and then by host kinases to its active triphosphate form. Foscarnet and cidofovir do not require viral kinase activation.
Which antiviral agent has the longest plasma half-life?
Ribavirin
Valacyclovir
Oseltamivir
Acyclovir
Ribavirin has a prolonged half-life (up to several days due to extensive erythrocyte uptake), whereas acyclovir and oseltamivir have much shorter half-lives.
In a patient with creatinine clearance below 30 mL/min, oseltamivir dosing should be:
Reduced by half of the normal dose
Stopped completely
Doubled to maintain efficacy
Unchanged from standard dosing
Oseltamivir is renally excreted and requires dose reduction in severe renal impairment to avoid accumulation and toxicity.
A cytomegalovirus strain with a UL97 kinase mutation will be resistant to which agent?
Foscarnet
Ganciclovir
Acyclovir
Cidofovir
UL97 kinase is required to phosphorylate ganciclovir. Mutations in UL97 prevent activation of ganciclovir, causing resistance, while foscarnet does not require phosphorylation.
Which HIV protease inhibitor is most commonly co-administered with low-dose ritonavir as a pharmacokinetic booster?
Saquinavir
Amprenavir
Lopinavir
Indinavir
Lopinavir is formulated with low-dose ritonavir to inhibit CYP3A4 and boost lopinavir plasma levels, improving efficacy.
Foscarnet inhibits viral DNA polymerase by binding to which site on the enzyme?
Protease substrate channel
Active-site magnesium ion
Allosteric RNase H site
Pyrophosphate-binding site
Foscarnet mimics pyrophosphate and binds directly to the pyrophosphate-binding site of viral DNA polymerase, blocking nucleotide addition.
The M184V mutation in HIV reverse transcriptase confers high-level resistance to which antiretroviral drug?
Efavirenz
Zidovudine
Lamivudine
Tenofovir
The M184V mutation alters the binding site for lamivudine, significantly reducing its incorporation and conferring high-level resistance.
Co-administration of tenofovir and didanosine is associated with which pharmacokinetic interaction?
Decreased tenofovir levels
Increased didanosine concentrations
Reduced didanosine toxicity
No significant interaction
Tenofovir inhibits didanosine clearance, leading to higher didanosine plasma levels and increased risk of toxicity.
Sofosbuvir targets which enzyme in the hepatitis C virus replication cycle?
NS5A replication complex
NS3/4A protease
NS5B RNA-dependent RNA polymerase
Viral envelope glycoprotein
Sofosbuvir is a nucleotide analog inhibitor of the HCV NS5B RNA-dependent RNA polymerase, halting viral RNA synthesis.
Cidofovir differs from acyclovir primarily because it:
Does not require initial phosphorylation by viral kinase
Is a protease inhibitor
Binds to the M2 ion channel
Has high oral bioavailability
Cidofovir only requires host cell kinases for activation and bypasses the need for viral kinase phosphorylation, unlike acyclovir.
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Learning Outcomes

  1. Identify antiviral drug classes and their mechanisms of action.
  2. Evaluate common adverse effects and contraindications of antiviral agents.
  3. Analyse resistance mechanisms in antiviral therapy scenarios.
  4. Apply appropriate dosing regimens for viral infections.
  5. Compare pharmacokinetic profiles of key antiviral medications.
  6. Demonstrate knowledge of potential antiviral drug interactions.

Cheat Sheet

  1. Major antiviral drug classes - From nucleoside analogs to protease and neuraminidase inhibitors, these medications block viruses at key stages of their lifecycle. For instance, aciclovir hijacks viral thymidine kinase to become ACV-TP, which then stops viral DNA polymerase in its tracks, forcing chain termination and halting replication. Think of it as a molecular Trojan horse! Aciclovir
  2. Common adverse effects - No drug is a magic bullet, and antivirals often come with sidekicks like diarrhea, nausea, or dizziness. In clinical trials, molnupiravir showed mild diarrhea (2%), occasional nausea (1%), and a dash of dizziness (1%), reminding us that patient comfort matters. Always weigh benefits versus tummy troubles! Molnupiravir
  3. Key contraindications - Knowing who should avoid certain antivirals is as vital as knowing how they work. Nirmatrelvir/ritonavir is a no-go for patients allergic to its components or those with severe kidney or liver impairment, making a thorough medical history check your best defense. Safety first! Nirmatrelvir/ritonavir
  4. Resistance mechanisms - Viruses can be sneaky, mutating to evade drugs. Resistance to aciclovir often arises from changes in viral thymidine kinase or DNA polymerase, cutting the drug's effectiveness by altering its target. Staying ahead means understanding how these microscopic shape-shifters dodge therapy. Aciclovir
  5. Optimal dosing schedules - Timing can be as important as dose. Nirmatrelvir/ritonavir's design calls for twice-daily dosing (every 12 hours) due to its roughly 6-hour half-life, so you keep drug levels steady and viruses on the run. Stick to the clock for best results! Nirmatrelvir/ritonavir
  6. Pharmacokinetic profiles - How drugs travel and exit your body shapes their power. Nirmatrelvir (with ritonavir) is excreted about 35% in feces and 50% in urine, whereas ritonavir alone shows 86% fecal and 11% urinary excretion, giving clues for dose adjustments. These numbers guide safe and effective therapy. Nirmatrelvir/ritonavir
  7. Potential drug interactions - Ritonavir acts like a bouncer at the liver's CYP3A club - blocking many drugs from entering, which can lead to serious interactions. When nirmatrelvir/ritonavir is on board, always vet concurrent medications to avoid unwanted party crashers in your patient's system. Knowledge is your best defense! Nirmatrelvir/ritonavir
  8. Next-gen mechanisms of action - Molnupiravir plays a wild card by inducing rampant mutations during viral RNA replication, leading to an "error catastrophe" that the virus can't recover from. This unique approach turns the virus's own machinery into a self-destruct button. Talk about turning the tables! Molnupiravir
  9. Viral enzymes in activation - Some antivirals need a kickstart from viral enzymes to become active medicines. Aciclovir relies on viral thymidine kinase to add the first phosphate, unlocking its power to inhibit DNA polymerase and wreck viral replication. It's like getting a VIP pass straight to the action! Aciclovir
  10. Resistance development over time - Resistance isn't just a buzzword; it's a real hurdle, especially in immunocompromised patients where aciclovir resistance can spike up to 10%. Healthy immune systems keep resistance rare, but vigilance is key to staying one step ahead. Keep those microscopes ready! Aciclovir
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