A client is prescribed a serotonin-norepinephrine reuptake inhibitor. The nurse would identify that which of the following will be prescribed?

Choice A reason: Blocking norepinephrine at alpha-1 receptors inhibits vasoconstriction, reducing vascular tone. This disrupts baroreceptor-mediated blood pressure regulation, causing orthostatic hypotension when standing. The autonomic nervous system fails to compensate for positional changes, leading to dizziness and fainting, a common side effect of alpha-1 blockers like prazosin.

Choice B reason: Increased psychotic symptoms are linked to dopamine dysregulation, not alpha-1 receptor blockade. Norepinephrine blockade affects autonomic functions, not psychosis, which involves mesolimbic dopamine hyperactivity. This side effect is unrelated to alpha-1 receptors, making this option scientifically inaccurate for the described mechanism.

Choice C reason: Appetite disturbance is typically associated with serotonin or histamine receptor effects, not alpha-1 norepinephrine blockade. Norepinephrine at alpha-1 receptors regulates vascular tone, not appetite control, which involves hypothalamic signaling. This side effect is not a direct consequence of alpha-1 blockade, rendering this option incorrect.

Choice D reason: Hypertensive crisis results from excessive norepinephrine activity, often due to monoamine oxidase inhibitors, not alpha-1 receptor blockade. Blocking alpha-1 receptors causes vasodilation, lowering blood pressure, not raising it. This makes hypertensive crisis an unlikely side effect, contrary to the pharmacological mechanism of alpha-1 blockers.

Choice A reason: Arising slowly addresses orthostatic hypotension, a side effect of alpha-1 receptor blockade, not dopamine effects. First-generation antipsychotics primarily block D2 receptors, affecting motor and cognitive pathways, not vascular tone. Hypotension is unrelated to dopaminergic effects, making this teaching point scientifically inaccurate.

Choice B reason: Dopamine D2 receptor blockade in the nigrostriatal pathway causes extrapyramidal symptoms, like muscle stiffness, in first-generation antipsychotics. This mimics Parkinson’s disease due to reduced dopamine signaling, impairing motor control. Teaching patients to report stiffness ensures early detection and management, aligning with the neuropharmacological impact of these drugs.

Choice C reason: Chewing sugarless gum addresses dry mouth, an anticholinergic side effect, not dopaminergic. First-generation antipsychotics block muscarinic receptors, not dopamine, causing reduced salivation. While common, this is unrelated to dopaminergic effects, making this teaching point irrelevant for the specified drug mechanism.

Choice D reason: Increasing dietary fiber addresses constipation, another anticholinergic effect, not dopaminergic. Dopamine blockade affects motor and reward systems, not gastrointestinal motility, which is regulated by muscarinic receptors. This teaching point does not correspond to the dopaminergic effects of first-generation antipsychotics, rendering it incorrect.