Barkley 3P Assessment Practice Exam 2025 – Your All-in-One Guide to Mastering Pathophysiology, Pharmacology, and Physical Assessment!

The risk of death in a patient with hepatic encephalopathy is primarily associated with the toxicity of ammonia to the central nervous system. In hepatic insufficiency, the liver is unable to adequately convert ammonia, a byproduct of protein metabolism, into urea, leading to elevated ammonia levels in the blood. When ammonia accumulates, it can cross the blood-brain barrier and result in neurotoxic effects, causing altered mental status, confusion, and potentially progressing to coma or death. The direct impact of ammonia on brain function is a critical concern in hepatic encephalopathy, making it the most significant risk factor associated with the condition.

The other options do not adequately reflect the primary danger in this scenario. The synthesis of ammonia by brain cells is not a pertinent factor, as it is mainly hepatic dysfunction that causes elevated ammonia. Renal toxicity due to ammonia accumulation in the kidneys is less relevant here, as the central nervous system's response to ammonia is the primary concern. Although esophageal varices can be a complication in liver disease and may lead to dangerous bleeding, this is related to portal hypertension rather than the direct effect of ammonia toxicity. Therefore, the toxicity of ammonia to the central nervous system is the foremost risk leading to mortality in patients with hepatic ence