<unk><unk>  failure is a sudden and severe loss of<unk>  function with evidence of encephalopathy and coagulopathy with elevated prothrombin time (PT) and (INR) in a person without a preexisting<unk>  disease. The consequences of<unk><unk>  failure are due to the loss of its metabolic, secretory and regulatory effects. This results in the accumulation of toxic substances and causes deleterious effects. The major<unk> cal mechanisms of morbidity and mortality in patients with<unk><unk>  failure are cerebral edema, hypoperfusion to the<unk> , idiosyncratic drug reactions, depletion of glutathione and viral hepatitis. Cerebral edema in<unk><unk>  failure can be due to vasogenic and cytotoxic effects. In cytotoxic type, there is intracellular swelling but blood-brain barrier is intact. In vasogenic type, the blood-brain barrier breaks down and plasma and water accumulate in the extracellular space. The increased ammonia concentration in<unk>  failure in combination with the glutamine produced by the astrocytes causes excess levels of glutamine with the help of enzyme glutamine synthetase. The excess glutamine is cytotoxic and may influence the osmotic gradient which could result in brain edema. In<unk><unk>  failure, the increased levels of nitric oxide in the circulation can also disrupt the cerebral autoregulation. Acetaminophen is the leading cause of<unk><unk>  failure in the United States. Acetaminophen causes dose-related toxicity. Toxicity is rarely seen at normal therapeutic doses (up to 4 g/day) without underlying<unk>  disease. Viral hepatitis is the leading cause of<unk><unk>  failure in the developing world. Hepatitis A, B, D (associated with B), and E (in endemic countries) are commonly associated with<unk><unk>  failure.
Acute liver failure pathophysiology
Acute kidney injury pathophysiology
Hepatopulmonary syndrome pathophysiology
Hepatorenal syndrome risk factors
Hepatorenal syndrome pathophysiology
Hepatotoxicity pathophysiology
Acute liver failure causes
Ascites pathophysiology