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CASE FILES: BIOCHEMISTRY
A N SW E R S TO C A SE 37: C IR R H O SIS
Summary:
A 45-year-old male presents with cirrhosis, likely secondary to hep-
atitis C, with acute mental status change coinciding with recent onset of
hematemesis. Patient has an elevated serum ammonia level and otherwise neg-
ative workup.
Diagnosis: Hepatic encephalopathy likely secondary to elevated
ammonia levels.
Asterixis: Nonspecific to hepatic encephalopathy. Nonrhythmic
asymmetric tremor with loss of voluntary control of extremities while
in a sustained position. It is also known as “liver flap.”
Precipitating factor: Increased nitrogen load from upper gastrointestinal
bleed.
C L IN IC A L C O R R E L A T IO N
Cirrhosis is a chronic condition of the liver with diffuse parenchymal injury and
regeneration leading to distortion of the liver architecture and increased resist-
ance of blood flow through the liver. The patient usually manifests malaise,
lethargy, palmar erythema, ascites, jaundice, and hepatic encephalopathy in the
late stages. Toxins accumulating in the blood stream affect the patient’s mental
status. The most common etiologies of cirrhosis are toxins such as alcohol, viral
infections such as hepatitis B or C infection, or metabolic diseases in children
(Wilson disease, hemochromatosis, or ^-antitrypsin deficiency). Treatment
depends on the exact etiology, although the common therapy includes avoidance
of liver toxins, salt restriction, and possibly procedures to reduce the portal
pressure.
A PPR O A C H TO A M IN O A C ID M E T A B O L ISM
A N D A M M O N IA
O bjectives
1.
Be familiar with the urea cycle.
2.
Know about amino acid metabolism.
3.
Be aware of the biochemical means of removing excess ammonia.
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