Which patient meets the criteria for hospice services?

Choice A reason: In PTSD, glutamate drives excitatory signaling in the amygdala, enhancing fear memory consolidation, while norepinephrine heightens arousal via locus coeruleus activation, strengthening traumatic memory encoding. This hyperactive glutamatergic-noradrenergic interaction sustains fear responses, contributing to PTSD’s persistent hyperarousal and intrusive memories.

Choice B reason: GABA inhibits neural activity, counteracting excitation, but its role in PTSD is secondary, modulating rather than driving fear memory formation. Glutamate is critical for memory consolidation in the amygdala, but pairing with GABA does not fully explain PTSD’s hyperarousal and fear encoding mechanisms.

Choice C reason: Histamine regulates wakefulness and arousal but is not directly involved in PTSD’s fear memory encoding. GABA modulates inhibition but does not drive the excitatory processes in the amygdala critical for trauma-related memory consolidation, making this pair irrelevant to PTSD’s core neurochemistry.

Choice D reason: Acetylcholine modulates attention and memory but is not a primary driver of PTSD’s fear responses. Serotonin influences mood but plays a secondary role in trauma memory encoding compared to glutamate and norepinephrine, which directly mediate amygdala hyperactivity in PTSD.

Choice A reason: Lamotrigine does not require monthly blood tests, as it has minimal hematologic or hepatic toxicity. It stabilizes mood via sodium channel inhibition, with skin rash (e.g., Stevens-Johnson syndrome) being the primary concern, not routine blood monitoring.

Choice B reason: Lamotrigine rarely affects liver function, unlike valproic acid. Its primary risk is cutaneous reactions due to immune-mediated hypersensitivity, not hepatotoxicity. Monitoring focuses on skin, not liver enzymes, as it modulates neuronal excitability without significant hepatic metabolism.

Choice C reason: Lamotrigine carries a risk of serious skin rashes, like Stevens-Johnson syndrome, due to immune-mediated hypersensitivity affecting epidermal cells. Notifying the provider about rashes is critical, as this reflects understanding of the drug’s most significant adverse effect, ensuring timely intervention.

Choice D reason: Salt intake is relevant for lithium, not lamotrigine, which stabilizes mood via sodium channel inhibition without affecting renal sodium handling. Dietary salt monitoring is unnecessary, as lamotrigine’s primary risk is dermatologic, not electrolyte-related, making this statement incorrect.