A patient is taking a first-generation antipsychotic medication. What should the nurse teach about the drug’s strong dopaminergic effect?

Choice A reason: Histamine regulates wakefulness and allergic responses, not anxiety or fear. Its receptors in the brain promote alertness, but excessive histamine does not drive sympathetic activation like increased heart rate. This makes histamine an incorrect choice for the symptoms described, which align with autonomic arousal.

Choice B reason: Acetylcholine mediates parasympathetic responses, like slowing heart rate, not the sympathetic activation seen in anxiety. While it plays a role in attention, it does not primarily cause fear or tachycardia, making it an unsuitable choice compared to norepinephrine’s role in stress responses.

Choice C reason: GABA inhibits neural activity, reducing anxiety via GABA-A receptor activation. Low GABA levels may contribute to anxiety, but the symptoms described (tachycardia, fear) result from sympathetic activation, not GABA excess. This makes GABA incorrect for the neurotransmitter driving these symptoms.

Choice D reason: Norepinephrine, released during stress, activates the sympathetic nervous system, increasing heart rate and inducing fear via locus coeruleus activation. It heightens arousal in the amygdala, contributing to anxiety symptoms. This aligns with the fight-or-flight response, making norepinephrine the correct neurotransmitter for these symptoms.

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.