Match each clinical presentation following the initiation of antipsychotic therapy (left) with the underlying receptor mechanism or affected neuroanatomical pathway (right).
- A patient experiences a significant reduction in auditory hallucinations and persecutory delusions.Dopamine D2 receptor antagonism in the mesolimbic tract
- A patient develops bilateral breast enlargement and a milky nipple discharge, accompanied by the cessation of menses.Dopamine D2 receptor antagonism in the tuberoinfundibular tract
- A patient develops a sustained, painful contraction of the neck muscles (torticollis) shortly after receiving an intramuscular injection.Dopamine D2 receptor antagonism in the nigrostriatal tract
- A patient experiences sudden dizziness, lightheadedness, and a drop in blood pressure immediately upon standing from a seated position.Alpha-1 adrenergic receptor antagonism
- A patient reports severe dry mouth, new-onset constipation, and blurred vision, with a physical exam showing resting tachycardia.Muscarinic M1 cholinergic receptor antagonism
Cevap
The reduction in hallucinations matches mesolimbic D2 antagonism; galactorrhea/amenorrhea matches tuberoinfundibular D2 antagonism; acute dystonia matches nigrostriatal D2 antagonism; orthostatic hypotension matches alpha-1 adrenergic antagonism; and anticholinergic effects match muscarinic M1 antagonism.
Each clinical presentation is a direct consequence of receptor blockade by antipsychotic medications. Mesolimbic D2 antagonism controls positive symptoms. Tuberoinfundibular D2 antagonism causes hyperprolactinemia. Nigrostriatal D2 antagonism causes acute extrapyramidal symptoms. Alpha-1 antagonism causes orthostatic hypotension. Muscarinic antagonism causes anticholinergic effects.
Adım Adım Çözüm
Anahtar Kavram
Antipsychotic medications exert their primary therapeutic effects and cause distinct adverse side effects through the blockade of various receptors (D2, alpha-1, M1) across different neuroanatomical pathways.