A nurse receives a verbal order for a client for digoxin. Which of the following entries should the nurse document in the client's medical record?

Hydroxyzine is a first-generation antihistaminethat crosses the blood-brain barrier, leading to significant anticholinergicand sedative effects. In contrast, hydralazine is a peripheral vasodilatorused for hypertension. This look-alike, sound-alike error involves switching a sedative for an antihypertensive, requiring close neurological and cardiovascular monitoring.

Rationale:

A.Sedation is a primary adverse effect of hydroxyzine due to its ability to block H1 receptors in the central nervous system. Because the client received this instead of a blood pressure medication, the nurse must monitor for extreme drowsiness, dizziness, and a possible risk for falls. Sedation is the most immediate and expected neurological consequence of this specific medication error.

B.Drooling is not associated with hydroxyzine; rather, this medication has anticholinergic properties that typically cause dry mouth (xerostomia). Hydroxyzine reduces secretions and blocks parasympathetic activity, making drooling an unlikely finding. If the client experiences drooling, the nurse should investigate other causes, such as neurological impairment or the effect of different pharmacological agents.

C.Diarrhea is not a common side effect of hydroxyzine administration. Antihistamines with anticholinergic effects are more likely to cause constipation due to slowed gastrointestinal motility. The nurse should monitor for decreased bowel sounds rather than increased frequency of stools. Diarrhea would be an atypical response to the mistaken administration of an antihistamine.

D.While hydralazine (the intended drug) treats hypertension, the nurse should monitor for high blood pressure because the client missedtheir antihypertensive dose. However, the prompt asks for the adverse effect of the medication actually given. Hydroxyzine itself does not cause hypertension; instead, the primary risk of the drug actually administered is central nervous system depression and potential hypotension.

Diabetic peripheral neuropathyresults from chronic hyperglycemia-induced nerve fiber damage and microvascular impairment. The resulting pain is neuropathicrather than nociceptive, requiring medications that modulate neurotransmitter release or stabilize neuronal membranes. Standard analgesics are often ineffective for the characteristic parasthesiaand burning sensations associated with this condition.

Rationale:

A.Gabapentin is an anticonvulsant medication frequently used as a first-line treatment for neuropathic pain. It works by binding to the alpha-2-delta subunit of voltage-gated calcium channels in the central nervous system, reducing the release of excitatory neurotransmitters. This stabilization of overactive neurons effectively alleviates the burning and tingling sensations typical of diabetic nerve damage.

B.Acetylcysteine is a mucolytic agent used primarily to thin respiratory secretions or as an antidote for acetaminophen toxicity. It does not possess analgesic properties and has no role in managing nerve-related pain. Administering this medication would not address the underlying pathophysiology of the client's peripheral neuropathy or provide any relief for their sensory symptoms in the feet.

C.Fentanyl is a potent opioid agonist used for severe, acute, or chronic nociceptive pain. While opioids can mask pain, they are generally not recommended as first-line therapy for diabetic neuropathy due to the high risk of dependence and limited efficacy for neuropathic burning. Treatment guidelines prioritize non-opioid neuromodulators like gabapentin or antidepressants over potent narcotics for this condition.

D.Hydromorphone is a strong opioid analgesic indicated for moderate to severe pain that is unresponsive to other treatments. Like fentanyl, it is not the preferred choice for managing the chronic, lancinating pain of diabetic neuropathy. Long-term use of hydromorphone carries a significant risk of tolerance and hyperalgesia without addressing the specific neuronal hyperexcitability that causes the tingling sensations.