An increase of which laboratory value is associated with hepatic encephalopathy?
Uric acid
Urea
Bilirubin
Ammonia
The Correct Answer is D
A. Uric acid: Uric acid is primarily associated with purine metabolism and is elevated in conditions like gout or renal impairment. It does not play a direct role in the development of hepatic encephalopathy, so increased levels are not a typical finding in this condition.
B. Urea: Urea is the end product of nitrogen metabolism produced by the liver. In liver dysfunction, urea production may actually decrease, and accumulation of nitrogenous waste contributes to complications, but elevated urea is not the hallmark laboratory abnormality in hepatic encephalopathy.
C. Bilirubin: Bilirubin levels rise in liver dysfunction and cholestasis, leading to jaundice. While elevated bilirubin indicates hepatic impairment, it is not directly responsible for the neurocognitive changes seen in hepatic encephalopathy.
D. Ammonia: Ammonia is a neurotoxic byproduct of protein metabolism that is normally converted to urea by the liver. In hepatic failure, ammonia accumulates in the blood and crosses the blood-brain barrier, contributing to cerebral edema, altered mental status, and the neuropsychiatric manifestations characteristic of hepatic encephalopathy.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
A. Dopamine:Dopamine primarily functions as a neurotransmitter in the central nervous system, influencing mood, behavior, and motor control. It also plays a role in renal perfusion, but it is not a primary mediator of inflammation, temperature regulation, or water balance.
B. Serotonin:Serotonin regulates mood, sleep, appetite, and gastrointestinal motility. Although it can contribute to vasoconstriction and platelet aggregation, it is not centrally involved in inflammatory responses or the regulation of body temperature and water balance.
C. Acetylcholine:Acetylcholine is a neurotransmitter of the parasympathetic nervous system, controlling muscle contraction, heart rate, and glandular secretions. It does not directly mediate inflammation, body temperature, or fluid balance.
D. Histamine:Histamine is a chemical mediator released by mast cells and basophils during inflammation. It increases vascular permeability, contributing to the inflammatory response, and acts on the hypothalamus to influence body temperature. Histamine also affects renal and vascular function, indirectly influencing water balance through its effects on capillary permeability and fluid distribution.
Correct Answer is C
Explanation
A. Rapid breathing:Tachypnea is a respiratory manifestation that can occur with hypoxia or heart failure, but it is not a primary neurologic sign. Neurologic changes result from cerebral perfusion deficits rather than respiratory rate changes.
B. Dyspnea:Shortness of breath reflects cardiopulmonary compromise and decreased oxygen delivery, but it is not a neurologic manifestation. It indicates the cardiovascular system is affected rather than the nervous system directly.
C. Dizziness:Dizziness is a neurologic manifestation caused by reduced cerebral perfusion due to cardiac dysrhythmias. When the heart beats irregularly or inefficiently, blood flow to the brain may decrease, leading to lightheadedness, syncope, or imbalance.
D. Chest pain:Chest pain is a cardiovascular symptom associated with myocardial ischemia or strain but does not reflect neurologic dysfunction. It indicates cardiac tissue distress rather than cerebral involvement.
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