A patient prescribed a muscarinic-receptor blocker will require assessment for what side effect?

Choice A reason: Histamine blockade, as in antipsychotics like olanzapine, promotes sedation, not weight loss. Weight gain is common due to histamine’s role in appetite regulation via hypothalamic signaling. Weight loss is not a typical side effect, making this response inaccurate for histamine-blocking medications.

Choice B reason: Histamine receptor blockade, common in medications like quetiapine, reduces wakefulness by inhibiting histamine’s alerting effects in the cortex. This causes drowsiness, a frequent side effect in psychiatric treatments, aligning with the pharmacological mechanism and making this the correct response.

Choice C reason: Insomnia is not typical with histamine blockade, which promotes sedation. Histamine enhances alertness; blocking it, as in antihistaminic antipsychotics, induces sleepiness, not wakefulness. This response contradicts the neuropharmacological effect, making it incorrect for expected side effects.

Choice D reason: Blood pressure increase is unrelated to histamine blockade. Histamine affects wakefulness and appetite, not vascular tone directly. Antihistaminic drugs may cause orthostatic hypotension via other receptors, not hypertension, making this response inaccurate for histamine-blocking medication effects.

Choice A reason: Decreasing dopamine is used for disorders like schizophrenia, where excess mesolimbic dopamine causes hallucinations. Memory difficulties, often linked to Alzheimer’s, involve cholinergic deficits, not dopamine excess. Reducing dopamine could worsen cognition by disrupting reward and attention pathways, making this approach scientifically inappropriate for memory issues.

Choice B reason: Inhibiting GABA production is irrelevant for memory. GABA regulates neural inhibition, and its reduction could increase excitability, worsening conditions like seizures. Memory deficits, particularly in dementia, stem from reduced acetylcholine in the hippocampus, not GABA, making this option misaligned with the neurobiology of memory impairment.

Choice C reason: Preventing acetylcholine destruction, via cholinesterase inhibitors, enhances cholinergic activity in the hippocampus and cortex, critical for memory in conditions like Alzheimer’s. Low acetylcholine levels impair neural signaling, causing memory deficits. This approach directly addresses the neurochemical basis of memory difficulties, making it scientifically appropriate for treatment.

Choice D reason: Increasing dopamine sensitivity is relevant for disorders like Parkinson’s, not memory deficits. Dopamine affects motivation and movement, not memory, which relies on acetylcholine in the hippocampus. Enhancing dopamine could disrupt cognitive balance, worsening memory without addressing the cholinergic deficits central to memory impairment.