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."

Answer and Explanation

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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Correct Answer is B

Explanation

B) Sepsis: Propofol is an intravenous sedative-hypnotic agent commonly used for sedation in mechanically ventilated patients. While propofol itself does not directly cause sepsis, its use can increase the risk of sepsis-related complications, such as infection. Propofol is typically administered intravenously, and improper handling or contamination of equipment, including intravenous lines and medication vials, can introduce pathogens into the bloodstream, leading to bloodstream infections (sepsis). Additionally, prolonged use of propofol may suppress immune function, further increasing the susceptibility to infection. Therefore, the nurse should monitor the client for signs and symptoms of sepsis, such as fever, chills, hypotension, tachycardia, and altered mental status, as a potential complication of propofol administration.

A) Hypokalemia: Hypokalemia, or low potassium levels, is not a common complication directly associated with propofol administration. While electrolyte imbalances may occur in critically ill patients, especially those receiving mechanical ventilation, hypokalemia is more likely to result from other factors such as diuretic therapy, gastrointestinal losses, or inadequate potassium intake.

C) Urinary retention: Urinary retention is not a typical complication of propofol administration. While sedative medications like propofol can affect bladder function, causing urinary retention in some cases, it is not a commonly reported complication of propofol use in mechanically ventilated patients.

D) Hypoglycemia: Hypoglycemia, or low blood sugar levels, is a potential complication of propofol administration, particularly in critically ill patients who may have altered glucose metabolism. However, hypoglycemia is not as commonly associated with propofol use as sepsis-related complications. Close monitoring of blood glucose levels is essential when administering propofol, especially if the client has preexisting diabetes mellitus or other risk factors for hypoglycemia. However, sepsis is a more direct and significant complication associated with propofol administration in mechanically ventilated patients.

A. Oxycodone inhibits prostaglandin synthesis. B. Oxycodone promotes vasodilation of cranial arteries. C. Oxycodone blocks the sodium channel suspending nerve conduction. D. Oxycodone causes central nervous system depression.

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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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?

Nursing Test Bank

Naxlex Comprehensive Predictor Exams

A nurse is caring for a client who is mechanically ventilated and receiving propofol intravenously. Which of the following manifestations should the nurse identify as a complication of administration?

Correct Answer is B

Explanation

A nurse is assessing a client who has received oxycodone. The nurse notes that the client's respiratory rate is 8/min. The nurse should identify that which of the following is the pathophysiology for the client's respiratory rate?

Correct Answer is D

Explanation

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