ATI RN
ATI RN Pharmacology Proctored Exam 2023 Questions
Question 1 of 5
Regarding diazepam:
Correct Answer: B
Rationale: Diazepam, a benzodiazepine, has active metabolites (e.g., desmethyldiazepam) with longer half-lives, contributing to its effects, so that's false. Activated charcoal is effective in overdose by adsorbing diazepam, reducing absorption, a true statement and standard intervention. It undergoes minimal, not extensive, enterohepatic recirculation, making that false. It's a GABA agonist, enhancing chloride influx via benzodiazepine receptors, not an antagonist, so that's incorrect. It also inhibits spinal reflexes, aiding muscle relaxation. The overdose utility of charcoal highlights its role in emergency management, binding unabsorbed drug in the gut, a key pharmacokinetic intervention distinct from flumazenil reversal.
Question 2 of 5
It is rational and advised therapeutic practice to commence treatment with the following drug using a loading dose if a rapid onset of action is required:
Correct Answer: C
Rationale: A loading dose achieves therapeutic levels quickly for drugs with long half-lives or urgent needs. Clozapine's slow titration avoids agranulocytosis, not rapid loading. Zolmitriptan, for acute migraine, acts fast without loading due to short half-life. Amiodarone, with a half-life of weeks, uses loading doses (e.g., 800-1600 mg/day) to rapidly control arrhythmias, rational for urgent onset. Levodopa's short half-life and titration in Parkinson's don't require loading. Doxazosin, for hypertension, starts low to avoid first-dose hypotension. Amiodarone's pharmacokinetics and arrhythmia urgency make loading advised, balancing efficacy and toxicity risks.
Question 3 of 5
The pharmacological property of aspirin comes from its ability to inhibit the synthesis of :
Correct Answer: A
Rationale: Aspirin exerts its pharmacological effects by inhibiting the synthesis of eicosanoids. Eicosanoids are signaling molecules that play a key role in inflammation, pain, and fever. Specifically, aspirin inhibits the enzyme cyclooxygenase (COX), which is crucial for the production of prostaglandins from arachidonic acid. By blocking COX, aspirin reduces the formation of pro-inflammatory prostaglandins, ultimately leading to its anti-inflammatory, analgesic, and antipyretic effects. This mechanism also accounts for aspirin's ability to inhibit platelet aggregation, which is why it is commonly used as an antithrombotic agent.
Question 4 of 5
A patient is receiving heparin therapy as part of the treatment for a pulmonary embolism. The nurse monitors the results of which laboratory test to check the drug™s effectiveness?
Correct Answer: B
Rationale: The nurse monitors the aPTT to check the effectiveness of heparin therapy in preventing and treating blood clots. Heparin acts by inhibiting the clotting cascade, specifically by enhancing the activity of antithrombin III, which inactivates clotting factors such as thrombin and factor Xa. The aPTT measures the intrinsic pathway of the clotting cascade, which is affected by heparin therapy. By monitoring the patient's aPTT levels, the nurse can ensure that the patient is within the therapeutic range for heparin therapy to be effective in preventing further clot formation. Monitoring bleeding times, PT/INR, or vitamin K levels is not typically done to assess heparin therapy effectiveness.
Question 5 of 5
Regarding diazepam:
Correct Answer: B
Rationale: Diazepam, a benzodiazepine, has active metabolites (e.g., desmethyldiazepam) with longer half-lives, contributing to its effects, so that's false. Activated charcoal is effective in overdose by adsorbing diazepam, reducing absorption, a true statement and standard intervention. It undergoes minimal, not extensive, enterohepatic recirculation, making that false. It's a GABA agonist, enhancing chloride influx via benzodiazepine receptors, not an antagonist, so that's incorrect. It also inhibits spinal reflexes, aiding muscle relaxation. The overdose utility of charcoal highlights its role in emergency management, binding unabsorbed drug in the gut, a key pharmacokinetic intervention distinct from flumazenil reversal.