A client is newly prescribed a medication that will block the effects of histamine for the treatment of a mental health disorder. The client asks, “What side effects should I anticipate with this new medication?” Which response by the nurse is accurate?

Choice A reason: Serotonin modulates mood and anxiety but is not primarily linked to schizophrenia’s core symptoms. While serotonin imbalances contribute to depression, schizophrenia’s hallucinations and delusions stem from dopamine hyperactivity in the mesolimbic pathway, making serotonin an incorrect choice for this disorder’s pathophysiology.

Choice B reason: GABA inhibits neural activity, and its dysfunction is linked to anxiety or seizures, not schizophrenia’s positive symptoms. Schizophrenia involves dopamine excess in the mesolimbic pathway, not GABA deficits. GABA’s role is secondary, making it an inaccurate choice for explaining hallucinations and delusions.

Choice C reason: Dopamine hyperactivity in the mesolimbic pathway causes hallucinations, delusions, and bizarre behavior in schizophrenia. Excess dopamine signaling disrupts cognitive and perceptual processes, leading to positive symptoms. Antipsychotics target D2 receptors to reduce these effects, confirming dopamine’s central role in schizophrenia’s pathophysiology.

Choice D reason: Acetylcholine is involved in memory and attention, not schizophrenia’s core symptoms. While cholinergic deficits occur in dementia, schizophrenia’s hallucinations and delusions are driven by dopamine dysregulation, not acetylcholine. This makes acetylcholine an incorrect choice for the neurotransmitter associated with these symptoms.

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.