A patient with benign prostatic hypertrophy (BPH) has been prescribed prazosin (Minipress) and asks the nurse what this is going to do for him. The nurse’s response will include what action to explain the purpose of taking this medication?

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Introduction to Pharmacology ATI Quizlet Questions

Question 1 of 5

A patient with benign prostatic hypertrophy (BPH) has been prescribed prazosin (Minipress) and asks the nurse what this is going to do for him. The nurse’s response will include what action to explain the purpose of taking this medication?

Correct Answer: C

Rationale: Alpha1-selective adrenergic blocking agents block smooth muscle receptors in the prostate, prostatic capsule, prostatic urethra, and urinary bladder neck, which leads to a relaxation of the bladder and prostate and improved flow of urine in male patients. Although they also block the postsynaptic alpha1-receptor sites, causing a decrease in vascular tone and vasodilation that leads to a fall in blood pressure without the reflex tachycardia that occurs when the presynaptic alpha2-receptor sites are blocked, this is not the purpose for administering the drug to a patient with BPH. They do not reduce the size of the prostate.

Question 2 of 5

Anticipatory nausea and vomiting associated with chemotherapy occurs:

Correct Answer: C

Rationale: Anticipatory nausea and vomiting occur before chemotherapy administration and are a conditioned response to previous chemotherapy experiences. This psychological response is triggered by cues such as the sight or smell of the treatment environment. It is distinct from acute or delayed nausea and vomiting, which occur during or after chemotherapy. Anticipatory nausea and vomiting can be challenging to manage and often require behavioral interventions or anti-anxiety medications.

Question 3 of 5

A pregnant client is receiving magnesium sulfate therapy for the control of preeclampsia. A nurse discovers that the client is encountering toxicity from the medication in which of the following assessments?

Correct Answer: A

Rationale: Magnesium sulfate toxicity can cause respiratory depression, which is indicated by a respiratory rate of 10 breaths per minute or less. This is a life-threatening complication requiring immediate intervention. Deep tendon reflexes are typically absent in severe toxicity, not present. A urine output of 25 ml/hr may indicate renal impairment but is not specific to magnesium toxicity. A serum magnesium level of 7 mEq/L is elevated but does not alone confirm toxicity without clinical symptoms. Therefore, respiratory depression is the key indicator.

Question 4 of 5

A 20-year-old woman who is 15 weeks pregnant is admitted feverish and dehydrated with acute severe asthma associated with a community-acquired pneumonia. She has a history of angioedema following a cephalosporin. Which of the following is not appropriate therapy?

Correct Answer: D

Rationale: Acute asthma and pneumonia in pregnancy require urgent care. IV crystalloids rehydrate, safe and necessary. High FiO2 (40%) supports oxygenation in asthma/pneumonia, appropriate. Nebulized salbutamol, a beta-agonist, relieves bronchospasm, standard and safe. IV hydrocortisone reduces inflammation, suitable. IV gentamicin, an aminoglycoside, treats pneumonia but is inappropriate due to cephalosporin cross-reactivity risk (angioedema history) and fetal ototoxicity concerns, making it unsafe here. Alternative antibiotics (e.g., macrolides) are preferred, prioritizing maternal and fetal safety.

Question 5 of 5

Regarding calcium channel blockers:

Correct Answer: C

Rationale: All calcium channel blockers (CCBs) like verapamil and nifedipine are orally active, so that's false. Half-lives vary (e.g., nifedipine ~2-5 hours, diltiazem longer), not uniformly 8-12 hours, making that false. They block L-type voltage-gated calcium channels, reducing vascular and cardiac contractility, a true statement. They relax bronchiolar smooth muscle, not unaffected, so that's false. Dihydropyridines cause reflex tachycardia, not bradycardia. The L-type blockade is their unifying mechanism, key to antihypertensive and antianginal effects.

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