A client with bipolar disorder has advanced lithium toxicity with a lithium level of 1.7 mEq/L. Which symptom would the nurse expect to assess?
Clonic movements.
Muscle hyperirritability.
Polyuria.
Fine tremor.
The Correct Answer is C
Choice A reason: Clonic movements are not typical of advanced lithium toxicity (levels >1.5 mEq/L). Lithium affects sodium-potassium ATPase, disrupting neuronal signaling, leading to renal and neurological symptoms, but clonic movements are more associated with seizures from other causes, not lithium’s mechanism.
Choice B reason: Muscle hyperirritability is not a hallmark of advanced lithium toxicity. Lithium’s disruption of renal tubular function and neuronal signaling causes symptoms like polyuria and confusion. Muscle-related symptoms are less prominent compared to renal or neurological effects at toxic levels.
Choice C reason: Polyuria is a common symptom of advanced lithium toxicity due to impaired renal concentrating ability from disrupted aquaporin-2 expression in the collecting ducts. Lithium’s interference with sodium-potassium ATPase also contributes, leading to excessive urine output, a key clinical sign at toxic levels.
Choice D reason: Fine tremor occurs in therapeutic lithium levels (0.6-1.2 mEq/L) due to mild neuronal excitability. In advanced toxicity (>1.5 mEq/L), symptoms escalate to severe neurological and renal effects like confusion and polyuria, making fine tremor less prominent.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Choice A reason: Neuroleptic malignant syndrome is associated with antipsychotics, not SSRIs like paroxetine, causing muscle rigidity and hyperthermia via dopamine blockade. The client’s symptoms, including hyperreflexia and diarrhea, align with serotonin excess, not dopamine-related issues, making this condition unlikely.
Choice B reason: Agranulocytosis, a severe reduction in white blood cells, is unrelated to paroxetine’s mechanism. SSRIs increase serotonin, not affecting hematopoiesis. The client’s symptoms like hyperpyrexia and hyperreflexia indicate serotonin toxicity, not an immunological or bone marrow disorder.
Choice C reason: Acute dystonic reactions involve muscle spasms from antipsychotics’ dopamine antagonism, not SSRIs. Paroxetine’s serotonin increase causes hyperreflexia and hyperpyrexia, consistent with serotonin syndrome, not extrapyramidal symptoms, making this diagnosis inappropriate for the described clinical presentation.
Choice D reason: Serotonin syndrome results from excessive serotonin due to paroxetine, an SSRI, overstimulating 5-HT receptors, causing hyperreflexia, hyperpyrexia, and autonomic instability. These symptoms reflect serotonin-driven neural excitation, particularly in the brainstem and spinal cord, matching the client’s clinical presentation accurately.
Correct Answer is A
Explanation
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.
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