Erythromycin:

Questions 52

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Chapter 12 principles of pharmacology Questions

Question 1 of 5

Erythromycin:

Correct Answer: B

Rationale: Erythromycin has a shorter half-life than azithromycin (B), approximately 1-2 hours versus 68 hours, requiring more frequent dosing. It's well absorbed orally (A is incorrect), though food can reduce bioavailability, and IV forms are used for severe infections. The most common adverse effect is gastrointestinal upset (nausea, diarrhea), not headache (C). It inhibits CYP450 enzymes (D), notably CYP3A4, causing drug interactions (e.g., with statins). It can be prescribed with amoxicillin (original E is incorrect) if clinically indicated. Erythromycin's macrolide action targets protein synthesis in Gram-positive and atypical bacteria, but its shorter half-life and GI side effects often make newer macrolides like azithromycin preferable in outpatient settings.

Question 2 of 5

Aciclovir:

Correct Answer: A

Rationale: Aciclovir inhibits viral DNA polymerase (A), a key mechanism in treating herpes simplex virus (HSV) and varicella-zoster virus (VZV) infections, activated by viral thymidine kinase to halt replication. It's indicated in herpetic keratitis (B), effectively treating ocular HSV. It's safe in pregnancy (C is incorrect), with no clear teratogenic risk, often used for severe HSV/VZV. It's indicated in herpetic meningoencephalitis (D), critical for HSV encephalitis. It's effective in chickenpox (original E is incorrect), reducing severity. Aciclovir's specificity for virally infected cells minimizes host toxicity, making it a cornerstone antiviral, though resistance in immunocompromised patients is a challenge.

Question 3 of 5

Properties of HIV protease inhibitors include:

Correct Answer: A

Rationale: HIV protease inhibitors cause hypertriglyceridemia and truncal fat redistribution (A), part of lipodystrophy syndrome, linked to metabolic changes (e.g., with lopinavir/ritonavir), affecting patient adherence. They're not the most effective at reducing HIV RNA (B); integrase inhibitors often achieve faster suppression. Oral bioavailability varies, not consistently >95% (C), often boosted by ritonavir. They cause many drug-drug interactions via CYP3A inhibition (D), critical for co-administered drugs. Cross-resistance within the class (original E) occurs but isn't universal. Their role in blocking viral maturation ensures potent virologic control, though metabolic side effects require lipid and glucose monitoring.

Question 4 of 5

During cancer chemotherapy:

Correct Answer: A

Rationale: Infection is the commonest life-threatening complication during cancer chemotherapy (A), due to myelosuppression reducing neutrophils, increasing sepsis risk from opportunistic pathogens. It's often from the patient's gut flora (B), like E. coli, translocating during mucositis. Pyrexia is usually present (C is incorrect), a key sign of febrile neutropenia. Conception must be avoided (D), due to teratogenic risks. Second malignancies (original E) are a long-term risk, not immediate. Chemotherapy's immunosuppression, especially with alkylating agents or antimetabolites, disrupts immune barriers, necessitating prompt antibiotic therapy and G-CSF in high-risk cases.

Question 5 of 5

Filgrastim (human granulocyte colony-stimulating factor):

Correct Answer: D

Rationale: Filgrastim stimulates proliferation and differentiation of myeloid progenitor cells (D), a G-CSF boosting neutrophil production, used post-chemotherapy to reduce neutropenia duration and infection risk. It's given subcutaneously (A), the standard route. It causes a transient neutrophil increase, not neutropenia (B is incorrect). It's not used in myeloid leukemia (C) treatment; it supports recovery. It causes bone pain (original E), from marrow expansion. Filgrastim's role in accelerating granulopoiesis is critical in oncology, shortening neutropenic periods, though leukocytosis and rare splenic rupture are concerns.

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