A 28-year-old woman with schizophrenia develops amenorrhea, galactorrhea, and decreased libido after starting risperidone. The MECHANISM underlying these adverse effects is:
- A Direct stimulation of pituitary lactotroph cells by risperidone
- B Estrogenic effect of risperidone on breast tissue
- C Hypothyroidism induced by risperidone
- D Blockade of tuberoinfundibular dopamine pathway, removing dopamine's inhibitory control over prolactin secretion ✓
Explanation
The tuberoinfundibular dopamine pathway projects from the hypothalamic arcuate nucleus to the pituitary portal system. Dopamine normally inhibits prolactin release from anterior pituitary lactotrophs by binding to D2 receptors. Antipsychotics that block D2 receptors (especially high-affinity D2 blockers like risperidone, amisulpride, haloperidol) remove this inhibitory tone, causing hyperprolactinemia—manifesting as galactorrhea, amenorrhea, sexual dysfunction, and osteoporosis with prolonged exposure. Clozapine and quetiapine have low D2 affinity and minimal effect on prolactin. Aripiprazole (D2 partial agonist) may actually lower elevated prolactin levels.
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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