The mechanism of fluoroquinolones’ action is:

Correct Answer: B

Rationale: The correct answer is B: Inhibition of DNA gyrase. Fluoroquinolones target DNA gyrase, an enzyme involved in bacterial DNA replication and repair. By inhibiting DNA gyrase, fluoroquinolones prevent bacterial DNA from unwinding and replicating, ultimately leading to bacterial cell death. Explanation of other choices: A: Inhibition of phospholipase C - This is incorrect as fluoroquinolones do not target phospholipase C. C: Inhibition of bacterial cell synthesis - While fluoroquinolones do affect bacterial cell synthesis indirectly by inhibiting DNA gyrase, this is not the primary mechanism of action. D: Alteration of cell membrane permeability - This is incorrect as fluoroquinolones primarily target DNA gyrase, not cell membrane permeability.

Correct Answer: A

Rationale: The correct answer is A: Isosorbide mononitrate and nifedipine. Isosorbide mononitrate is a vasodilator that reduces the workload on the heart, beneficial for hypertrophic cardiomyopathy. Nifedipine is a calcium channel blocker that helps relax the heart muscle. Nitroglycerin (B and C) and captopril (B) are not commonly used in hypertrophic cardiomyopathy. Verapamil (C) can worsen symptoms in some patients with hypertrophic cardiomyopathy. Metoprolol (D) is a beta-blocker that may be used in some cases but is not as effective as nifedipine for this condition.

Correct Answer: C

Rationale: The correct answer is C: Quinidine. Quinidine is contraindicated due to its potential to prolong the QT interval, leading to serious arrhythmias like Torsades de Pointes. Mexiletine and Lidocaine are sodium channel blockers with lower risk of QT prolongation. Phenytoin is an anti-seizure drug and does not typically impact cardiac conduction. Therefore, Quinidine is the absolute contraindication for this patient.

Correct Answer: B

Rationale: In patients with chronic granulomatous disease (CGD), the correct agent that increases the synthesis of tumor necrosis factor, leading to the activation of phagocytosis is Interferon gamma (Option B). Interferon gamma plays a crucial role in activating macrophages and enhancing their ability to phagocytize pathogens, which can be beneficial in patients with CGD who have impaired phagocytic function due to defective NADPH oxidase. Option A, Aldesleukin, is a recombinant interleukin-2 that primarily stimulates T-cell proliferation and activation, not phagocytosis. Option C, Filgrastim, is a granulocyte colony-stimulating factor that primarily stimulates the production and mobilization of neutrophils, which are not the primary cells involved in phagocytosis in CGD. Option D, Infliximab, is a tumor necrosis factor-alpha inhibitor and would not increase the synthesis of tumor necrosis factor as required in this scenario. In an educational context, understanding the specific mechanisms of action of immunomodulatory agents is crucial for healthcare professionals, especially when managing patients with immunodeficiencies like CGD. Knowing the appropriate agents that can enhance phagocytic activity in these patients is essential for providing effective treatment and improving outcomes.

Correct Answer: A

Rationale: The correct answer to the question is option A) Digoxin. Digoxin is a cardiac glycoside that is commonly used to reduce the frequency of angina pectoris by increasing the strength of the heart muscle contractions, which helps to improve blood flow and reduce the workload of the heart. Additionally, Digoxin can help terminate an acute attack of angina by improving cardiac output and reducing strain on the heart during times of increased demand, such as during an angina attack. Option B) Furosemide is a loop diuretic primarily used to treat conditions such as edema and hypertension by increasing urine production. It is not indicated for reducing the frequency of angina pectoris or for terminating acute angina attacks. Option C) Enalapril is an angiotensin-converting enzyme (ACE) inhibitor used to treat conditions like hypertension and heart failure by relaxing blood vessels and reducing the workload of the heart. While it can be beneficial for certain cardiovascular conditions, it is not typically used to reduce the frequency of angina pectoris or to terminate acute angina attacks. Option D) Amrinone is a phosphodiesterase inhibitor that is used in the treatment of heart failure and some types of arrhythmias by increasing the strength of heart contractions. However, it is not commonly used for reducing the frequency of angina pectoris or for terminating acute angina attacks. In an educational context, understanding the appropriate use of medications for cardiovascular conditions is crucial for healthcare professionals. Knowing which medications are effective for specific conditions, like angina pectoris, can help ensure optimal patient outcomes and prevent medication errors. This knowledge also highlights the importance of accurate drug administration and patient education to manage cardiovascular conditions effectively.