Liver disease

Published on 01/03/2015 by admin

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Last modified 01/03/2015

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Liver disease

Acute liver disease

Acute liver damage occurs for one of three reasons:

inadequate perfusion.

Investigation

Biochemical markers of liver disease such as AST and ALT will indicate hepatocyte damage. Elevated serum bilirubin and alkaline phosphatase levels show the presence of cholestasis. Disease progression or recovery can be followed by serial measurements of LFTs.

Poisoning

The best-documented poisons that affect the liver are paracetamol and carbon tetrachloride. These are metabolized by the intact liver in small amounts, but when present at high concentrations they give rise to toxic metabolites, leading to destruction of hepatocytes with massive release of enzymes. The capacity of the liver to withstand an insult is reduced if there is underlying liver damage due to alcohol, malnutrition or other chronic disease.

Some plant and fungal toxins can also cause catastrophic and fatal liver damage within 48 hours (Fig 30.1).

Fig 30.1 Pattern of LFTs following Amanita phalloides (a highly poisonous species of mushroom) ingestion.

A third group of toxins are those that give rise to acute hepatocellular failure only in certain individuals who are susceptible. Important examples include sodium valproate, an anticonvulsant drug that causes toxicity in some children, and halothane, an anaesthetic agent.

Liver infection

Both bacteria and viruses can give rise to infective hepatitis, which causes many deaths worldwide. Hepatitis A, hepatitis B and hepatitis C are the most common.

Outcome

Acute liver damage can progress in three ways:

It may resolve, as indeed it does in the majority of cases.

It may progress to acute hepatic failure.

It may lead to chronic hepatic damage.

Hepatic failure

Acute hepatic failure is a major medical emergency, since the failure of the complex metabolic functions of the liver cannot be compensated for by any other organ. In severe cases, much of the biochemical picture is disrupted. Electrolyte imbalance occurs, and sodium and calcium concentrations may both fall. There may be severe metabolic acid–base disturbances and hypoglycaemia.

Hepatic failure may give rise to renal failure due to exposure of the glomeruli to toxins usually metabolized by the liver. There may be an increase in blood ammonia as a result of the failure to detoxify this to urea. The pattern of abnormalities found in hepatic failure is shown in Figure 30.2.

Fig 30.2 Laboratory findings in hepatic failure.

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