A nurse is preparing an educational training session about collaborating with the provider to prevent medication errors. Which of the following information should the nurse include in the teaching?
"Reading back the provider's prescription is only necessary for high alert medications."
"Providers should cosign all verbal prescriptions."
"Utilize assistive personnel as a witness to verbal provider prescriptions."
"Safe abbreviations should only be used by providers."
The Correct Answer is B
A) "Reading back the provider's prescription is only necessary for high alert medications": Reading back the provider's prescription is a crucial step in preventing medication errors and should be done for all medications, not just high alert ones. Verbal orders are prone to miscommunication, so repeating the order back to the provider helps ensure accuracy and clarity.
B) "Providers should cosign all verbal prescriptions": This is the correct intervention. Verbal prescriptions are considered high risk for medication errors due to misinterpretation or miscommunication. Having the provider cosign verbal prescriptions adds an extra layer of verification and accountability, reducing the likelihood of errors.
C) "Utilize assistive personnel as a witness to verbal provider prescriptions": While involving another healthcare professional as a witness to verbal prescriptions may provide additional verification, it is not a standard practice and may not be feasible in all situations. Relying solely on assistive personnel for this purpose may not ensure accuracy and could introduce potential communication errors.
D) "Safe abbreviations should only be used by providers": Safe abbreviations should be used by all healthcare team members, not just providers, to prevent medication errors. Standardizing abbreviations reduces the risk of misinterpretation and enhances communication among healthcare providers.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A) Hypertension: Amiodarone is not typically associated with hypertension. Instead, it is more commonly associated with hypotension.
B) Bradypnea: Amiodarone is not typically associated with bradypnea. Instead, it is more commonly associated with pulmonary toxicity, which can manifest as cough, dyspnea, and pulmonary fibrosis.
C) Fever: While fever is a possible adverse effect of amiodarone, it is not one of the most commonly observed adverse effects. Other adverse effects, such as thyroid dysfunction, pulmonary toxicity, and hepatic toxicity, are more frequently reported.
D) Bradycardia: This is the correct answer. Amiodarone is known to cause bradycardia as an adverse effect. It has a negative chronotropic effect, meaning it can slow down the heart rate. Bradycardia is one of the most commonly observed adverse effects of amiodarone and can be significant, particularly in individuals with pre-existing sinus node dysfunction or conduction abnormalities.
Correct Answer is D
Explanation
D) Oxycodone causes central nervous system depression: Oxycodone is an opioid analgesic that acts centrally on the central nervous system (CNS) to relieve pain. One of the most significant side effects of opioids like oxycodone is respiratory depression, which occurs due to the suppression of the CNS, particularly in the brainstem respiratory centers. The brainstem regulates respiratory rate and rhythm, and when opioids depress these centers, it can lead to decreased respiratory drive, resulting in a decrease in respiratory rate. A respiratory rate of 8/min is significantly below the normal range, indicating respiratory depression caused by oxycodone.
A) Oxycodone inhibits prostaglandin synthesis: Oxycodone does not directly inhibit prostaglandin synthesis. Prostaglandins are lipid compounds with various physiological effects, including inflammation and pain modulation. Nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, inhibit prostaglandin synthesis by blocking cyclooxygenase enzymes. However, oxycodone primarily acts on opioid receptors in the CNS to relieve pain, rather than through prostaglandin inhibition.
B) Oxycodone promotes vasodilation of cranial arteries: While opioids can cause peripheral vasodilation, particularly in large doses, the primary mechanism of action of oxycodone is not through the promotion of vasodilation of cranial arteries. Vasodilation may occur as a side effect of opioid use, but it is not the primary cause of respiratory depression associated with oxycodone.
C) Oxycodone blocks the sodium channel suspending nerve conduction: This statement describes the mechanism of action of local anesthetics, such as lidocaine, which block sodium channels to inhibit nerve conduction. However, oxycodone is not a sodium channel blocker. Its analgesic effects result from binding to opioid receptors in the CNS, particularly mu-opioid receptors, rather than blocking sodium channels. Therefore, this option is not the pathophysiology for the respiratory rate of 8/min observed in the client receiving oxycodone.
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