In cirrhosis, what happens to serum ammonia and serum BUN levels?

In cirrhosis, the liver's ability to detoxify ammonia is significantly impaired due to the loss of hepatocyte function. The liver converts ammonia, a toxic byproduct of protein metabolism, into urea, which can be safely excreted by the kidneys. In cases of cirrhosis, the damaged liver cannot effectively carry out this conversion, leading to an accumulation of serum ammonia levels, known as hyperammonemia.

Simultaneously, the ability of the liver to synthesize urea is compromised. This reduction in urea synthesis results in lower blood urea nitrogen (BUN) levels. BUN is a measure of the amount of nitrogen in the blood that comes from urea, and since the production of urea is diminished in liver disease, BUN levels decrease.

Therefore, in cirrhosis, we observe increased serum ammonia due to the impaired conversion of ammonia to urea, combined with decreased serum BUN due to reduced synthesis of urea in the liver. This dynamic is critical in understanding the pathophysiology of hepatic encephalopathy, where elevated ammonia levels may contribute to neurological symptoms.