A patient reports becoming “immune” to a medication because it no longer works to alleviate symptoms. The nurse recognizes that this decreased effectiveness is likely caused by:

Synthesis of more receptor sites in response to the medication

Decreased selectivity of receptor sites, resulting in a variety of effects

Desensitization of receptor sites by continual exposure to the drug

Antagonists produced by the body that compete with the drug for receptor sites

Answer and Explanation

The Correct Answer is C

Choice A reason: Synthesis of more receptor sites (upregulation) typically occurs with receptor antagonists, not agonists, as the body compensates for blocked receptors. This would increase drug sensitivity, not decrease effectiveness. For most medications, continuous exposure leads to desensitization, not receptor proliferation, making this choice incorrect for explaining tolerance.

Choice B reason: Decreased receptor selectivity implies a drug binding to unintended receptors, causing varied effects, not reduced efficacy. Tolerance results from receptor desensitization, not altered selectivity. This mechanism doesn’t explain the patient’s “immunity” to the drug’s therapeutic effects, making this choice scientifically inaccurate for the scenario.

Choice C reason: Desensitization occurs when continuous drug exposure reduces receptor responsiveness, leading to tolerance. For example, opioid receptors downregulate or internalize with prolonged agonist exposure, decreasing drug efficacy. This explains the patient’s perception of “immunity” as the drug’s effect diminishes over time, making this the correct choice.

Choice D reason: The body does not produce antagonists to compete with drugs for receptor sites. Tolerance arises from receptor desensitization or metabolic changes (e.g., enzyme induction), not endogenous antagonist production. This mechanism is not a recognized pharmacological process for reduced drug effectiveness, making this choice incorrect.

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Free Nursing Study Resources

Correct Answer is ["A","C","E"]

Explanation

Choice A reason: Enterochromaffin-like (ECL) cells release histamine, which stimulates parietal cells to secrete hydrochloric acid via H2 receptors. This increases gastric acid production, critical for digestion, and is a key component in the acid secretion pathway, making this a correct choice for acid-increasing cells.

Choice B reason: Beta cells, located in the pancreas, secrete insulin to regulate glucose, not gastric acid. They have no role in stomach acid production or regulation, which is controlled by gastric cells like parietal or G cells, making this choice incorrect.

Choice C reason: Parietal cells directly secrete hydrochloric acid into the stomach lumen via the H+/K+-ATPase pump, significantly increasing gastric acidity for digestion. Activated by histamine, gastrin, and acetylcholine, they are central to acid production, making this a correct choice for the question.

Choice D reason: Mucus cells secrete protective mucus to shield the stomach lining from acid and pepsin, not acid itself. They reduce damage from acidity but don’t contribute to its production, making this choice incorrect for cells that increase stomach acid.

Choice E reason: G cells secrete gastrin, a hormone that stimulates parietal cells to produce hydrochloric acid. Gastrin enhances acid secretion indirectly by activating parietal cells and ECL cells, playing a key role in gastric acid regulation, making this a correct choice.

A. Metoprolol [Lopressor] and furosemide [Lasix] B. Furosemide [Lasix] and enalapril [Vasotec] C. Captopril [Capoten] and spironolactone [Aldactone] D. Amlodipine [Norvasc] and propranolol [Inderal]

Correct Answer is C

Explanation

Choice A reason: Metoprolol (beta-blocker) and furosemide (loop diuretic) are commonly used in heart failure. Furosemide may lower potassium, counteracting hyperkalemia (5.5 mEq/L), and metoprolol doesn’t significantly affect potassium. This combination poses less risk for hyperkalemia exacerbation, making it less concerning than potassium-sparing combinations.

Choice B reason: Furosemide promotes potassium excretion, potentially reducing hyperkalemia (5.5 mEq/L), while enalapril (ACE inhibitor) may increase potassium. However, furosemide’s effect often offsets enalapril’s, making this combination less likely to worsen hyperkalemia significantly compared to two potassium-sparing drugs, so this choice is less critical.

Choice C reason: Captopril (ACE inhibitor) and spironolactone (potassium-sparing diuretic) both increase potassium levels by reducing aldosterone activity, exacerbating hyperkalemia (5.5 mEq/L). In heart failure, this combination risks severe hyperkalemia, causing arrhythmias, making it the most concerning interaction requiring close monitoring or adjustment.

Choice D reason: Amlodipine (calcium channel blocker) and propranolol (beta-blocker) primarily affect blood pressure and heart rate, not potassium levels. Their interaction may cause bradycardia or hypotension but doesn’t worsen hyperkalemia (5.5 mEq/L), making this combination less concerning for the patient’s current electrolyte status.

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A patient reports becoming “immune” to a medication because it no longer works to alleviate symptoms. The nurse recognizes that this decreased effectiveness is likely caused by:

Nursing Test Bank

Naxlex Comprehensive Predictor Exams

Which of the following cells increase acid in the stomach? (Select all that apply)

Correct Answer is ["A","C","E"]

Explanation

A nurse is reviewing a patient’s medications before administration. Which drug-to-drug interactions will most concern the nurse in a patient with a history of heart failure and a potassium level of 5.5 mEq/L?

Correct Answer is C

Explanation

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