A patient presents with anxiety, increased heart rate, and fear. The nurse suspects the activation of which neurotransmitter?

Histamine

Acetylcholine

GABA

Norepinephrine

Answer and Explanation

The Correct Answer is D

Choice A reason: Histamine regulates wakefulness and allergic responses, not anxiety or fear. Its receptors in the brain promote alertness, but excessive histamine does not drive sympathetic activation like increased heart rate. This makes histamine an incorrect choice for the symptoms described, which align with autonomic arousal.

Choice B reason: Acetylcholine mediates parasympathetic responses, like slowing heart rate, not the sympathetic activation seen in anxiety. While it plays a role in attention, it does not primarily cause fear or tachycardia, making it an unsuitable choice compared to norepinephrine’s role in stress responses.

Choice C reason: GABA inhibits neural activity, reducing anxiety via GABA-A receptor activation. Low GABA levels may contribute to anxiety, but the symptoms described (tachycardia, fear) result from sympathetic activation, not GABA excess. This makes GABA incorrect for the neurotransmitter driving these symptoms.

Choice D reason: Norepinephrine, released during stress, activates the sympathetic nervous system, increasing heart rate and inducing fear via locus coeruleus activation. It heightens arousal in the amygdala, contributing to anxiety symptoms. This aligns with the fight-or-flight response, making norepinephrine the correct neurotransmitter for these symptoms.

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Correct Answer is C

Explanation

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.

A. The client should not stop this medication abruptly to avoid discontinuation syndrome B. The client may experience frequent constipation and should increase their intake of dietary fiber C. This medication takes 4-6 months to be effective, the client should be told to be patient D. This medication can cause addiction, so the client should not take more than prescribed

Correct Answer is A

Explanation

Choice A reason: Abruptly stopping fluoxetine, an SSRI, disrupts serotonin levels, causing discontinuation syndrome with symptoms like dizziness and irritability due to rapid neurotransmitter imbalance in the brain. Gradual tapering stabilizes serotonin, preventing withdrawal, making this critical teaching for safe medication management in anxiety treatment.

Choice B reason: Constipation is not a common side effect of fluoxetine, which primarily causes nausea or diarrhea via serotonin modulation. Anticholinergic drugs, not SSRIs, typically cause constipation. This teaching is inaccurate, as fluoxetine’s side effect profile does not emphasize gastrointestinal slowing, making it incorrect.

Choice C reason: Fluoxetine takes 4-8 weeks, not months, to reach efficacy by increasing serotonin in the prefrontal cortex and amygdala. Overstating the timeline discourages adherence, as patients expect faster relief from anxiety symptoms, making this teaching point scientifically inaccurate and misleading.

Choice D reason: Fluoxetine is not addictive, as it lacks the reinforcing GABA effects of benzodiazepines. It modulates serotonin for anxiety without dependence risk. This teaching is incorrect, as it misrepresents fluoxetine’s pharmacological profile, potentially causing unnecessary fear about its safe use in treatment.

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A patient presents with anxiety, increased heart rate, and fear. The nurse suspects the activation of which neurotransmitter?

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Naxlex Comprehensive Predictor Exams

On the basis of current knowledge of neurotransmitter effects, a nurse anticipates that the treatment plan for a patient with memory difficulties may include medications designed to do what?

Correct Answer is C

Explanation

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Correct Answer is A

Explanation

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