What are the most common types of side effects from SSRIs?

Choice A reason: Previous psychiatric history increases PTSD risk, as pre-existing conditions like depression or anxiety indicate heightened amygdala sensitivity and dysregulated stress responses. These predispose individuals to exaggerated fear responses post-trauma, as the brain’s stress circuitry is already compromised, amplifying the impact of traumatic events on neural pathways.

Choice B reason: PTSD is not associated only with personal characteristics; it requires exposure to a traumatic event, as defined by DSM-5 criteria. Trauma triggers neurobiological changes, including amygdala hyperactivity and hippocampal volume reduction, causing symptoms like flashbacks. Personal characteristics modulate risk, but event exposure is essential, making this statement false.

Choice C reason: A causative trauma is required for PTSD, per DSM-5, involving exposure to actual or threatened death, serious injury, or sexual violence. This triggers neurobiological changes, such as elevated cortisol and amygdala activation, leading to intrusive memories and hyperarousal. This criterion is fundamental to the disorder’s pathophysiology and diagnosis.

Choice D reason: Lack of social support increases PTSD risk, as it exacerbates stress responses by reducing oxytocin-mediated emotional regulation and prefrontal cortex modulation. Social isolation heightens amygdala activity, prolonging trauma-related symptoms. Support systems buffer stress responses, making this a scientifically valid factor in the etiology of PTSD.

Choice A reason: Echinacea is used for immune support and has no significant interaction with paroxetine, an SSRI that increases serotonin by inhibiting reuptake. Echinacea’s effects on cytokine production do not alter serotonin metabolism or CYP450 enzymes, which paroxetine relies on for clearance, making it a safe supplement in this context.

Choice B reason: Ginkgo enhances cerebral blood flow but has minimal interaction with paroxetine. It may affect platelet aggregation, but paroxetine’s serotonin reuptake inhibition is primarily metabolized via CYP2D6, unaffected by ginkgo’s mechanisms. No significant pharmacodynamic or pharmacokinetic interactions occur, making this supplement safe for concurrent use with paroxetine.

Choice C reason: St. John’s Wort induces CYP3A4 and P-glycoprotein, accelerating paroxetine metabolism, an SSRI reliant on CYP2D6. This reduces paroxetine’s efficacy, lowering serotonin levels and risking treatment failure for depression. It also increases serotonin syndrome risk due to additive serotonergic effects, making it a critical interaction to avoid.

Choice D reason: Saw palmetto, used for prostate health, has no significant interaction with paroxetine. It primarily affects androgen pathways, not serotonin metabolism or CYP2D6, which paroxetine uses for clearance. No pharmacodynamic or pharmacokinetic conflicts arise, making saw palmetto a safe supplement for clients taking paroxetine for depression.