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Pharmacology Practice

5 MCQs • Practice Free attempt

Practice Test

Pharmacology — 5 Questions

1
Pharmacology

Which of the following is a common adverse effect associated with HIV protease inhibitors?
1). Lipodystrophy and metabolic disturbances
2). Acute renal failure
3). Cardiotoxicity
4). Pancreatic necrosis

📝 Explanation:

Protease inhibitors are commonly associated with metabolic complications including lipodystrophy, insulin resistance, hyperglycemia, hypercholesterolemia, and hypertriglyceridemia. Patients receiving long-term therapy should undergo regular monitoring of blood glucose and lipid profiles to reduce the risk of cardiovascular disease.

2
Pharmacology

How does ganciclovir, an antiviral drug, treat cytomegalovirus (CMV) infections?
1). By inhibiting viral RNA synthesis
2). By blocking the uncoating of viral particles
3). By increasing host cell interferon production
4). By inhibiting viral DNA polymerase

📝 Explanation:

Ganciclovir is a guanosine analog that is phosphorylated by viral kinases in CMV-infected cells. Its active triphosphate form competitively inhibits viral DNA polymerase and terminates viral DNA elongation, thereby suppressing CMV replication. A major adverse effect of ganciclovir is bone marrow suppression, particularly neutropenia.

3
Pharmacology

How do integrase inhibitors, such as raltegravir, function in the treatment of HIV?
1). By preventing the integration of viral DNA into the host genome
2). By disrupting viral protein synthesis
3). By inhibiting viral reverse transcriptase
4). By enhancing the host immune response

📝 Explanation:

Integrase inhibitors such as raltegravir, dolutegravir, and bictegravir inhibit the HIV integrase enzyme, preventing insertion of viral DNA into the host cell genome. Without integration, viral replication cannot proceed effectively, making integrase inhibitors one of the most effective components of modern antiretroviral therapy.

4
Pharmacology

What is the primary function of non-nucleoside reverse transcriptase inhibitors (NNRTIs) in HIV treatment?
1). They bind to the active site of reverse transcriptase to block DNA synthesis
2). They bind to a non-active site on reverse transcriptase, inducing conformational changes that inhibit enzyme activity
3). They inhibit the integration of viral DNA into the host genome
4). They prevent the cleavage of viral polyproteins

📝 Explanation:

NNRTIs such as efavirenz, nevirapine, and etravirine bind allosterically to HIV-1 reverse transcriptase rather than the active site. This induces a conformational change that inhibits enzyme activity, preventing conversion of viral RNA into DNA. Unlike nucleoside reverse transcriptase inhibitors (NRTIs), NNRTIs do not require intracellular phosphorylation for activation.

5
Pharmacology

What is a common mechanism of resistance to neuraminidase inhibitors in influenza viruses?
1). Increased expression of viral RNA polymerase
2). Enhanced viral protease activity
3). Altered viral surface proteins
4). Mutations in the viral neuraminidase gene

📝 Explanation:

Resistance to neuraminidase inhibitors such as oseltamivir most commonly occurs through mutations in the viral neuraminidase gene. These mutations alter the drug-binding site, reducing the affinity of the drug for the enzyme while allowing neuraminidase to remain functional. As a result, newly formed virions continue to be released from infected cells despite antiviral therapy.

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