Quiz 4: Liver Flashcards Preview

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Flashcards in Quiz 4: Liver Deck (19)
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Synthesized Liver Products

Proteins, Coag factors, ammonia, carbohydrates, fat, ketones, Vit A, enzymes, ect



Complexes with albumin for transport to liver, is then conjugated to make bilirubin diglucuronide (water-soluble), then excreted in the bile (secreted by liver and stored in Gallbladder) and broken down into urobilinogen


Pre-hepatic jaundice

Caused by excessive erythrocyte destruction, the rate of hemolysis exceeds the liver's ability to take up bilirubin for conjugation shown by an increased level of unconjugated bilirubin in the serum


Gilberts syndrome

Hepatic jaundice, a defect in the ability of hepatocytes to take up bilirubin due to a transport problem with the bilirubin, shown by mild increase in the serum level of unconjugated bilirubin


Crigler-Najjar disease

Partial or complete deficiency of UDP-glycuronyltransferase, no conjugated bilirubin is formed causing an increase in serum levels of unconjugated bilirubin


Dubin-Johnson syndrome

Defective liver cell excretion of bilirubin due to impaired transport in the hepatocytes of conjugated bilirubin, this is shown by increased serum level of conjugated bilirubin


Neonatal physiological jaundice

Low UDP-glycuronyltransferase at birth, it takes several days for the liver to synthesize an adequate amount of the enzyme to catalyze bilirubin conjugation causing increased serum levels of unconjugated bilirubin


Intrahepatic cholestasis

May be caused by hepatocyte injury such as cirrhosis bile duct injury or neoplasms


Posthepatic jaundice

Occurs when an obstruction blocks the flow of bile to the intestines can be caused by gallstones neoplasms or inflammation, it is characterized by a significantly increased level of conjugated bilirubin in serum, an increased level of unconjugated bilirubin in serum, an increased conjugated bilirubin in the urine, decreased urine and fecal urobilinogen, and stool that is pale


Reye syndrome

Unknown cause of the symptoms include encephalopathy, neurologic abnormalities like seizures or coma, and abnormal liver function tests due to hepatic destruction. Occurs mainly in children usually after a viral infection or aspirin therapy


Serum enzymes marking hepatocellular necrosis

ALT: specific for hepatocyte injury
AST: less specific than ALT significant presence in other tissues
LD: least specific, significant presence in other tissues


Serum enzymes marking cholestasis

Alkaline phosphatase
Gamma-glutamyl transferase


Other serum enzymes to assess liver disorders

Total bilirubin, direct bilirubin (conjugated), indirect bilirubin (Unconjugated), albumin, ammonia, AFP


Jendrassik-Grof total bilirubin test

Bilirubin + sodium acetate + caffeine sodium benzoate + diazotized sulfanilic acid gives purple azobilirubin + alkaline tartrate gives green-blue azobilirubin (600 nm)


Jendrassik-Grof total bilirubin test error sources/ranges

Hemolysis, lipemia, avoid exposure to sunlight and fluorescent lighting
Infants: Total: 2-6 mg/dL
Adults: total: 0.2-1.0 mg/dL
Indirect: 0.2-0.8 mg/dL
Direct: 0-0.2 mg/dL


Urobilinogen Test Methodology

Urinary urobilinogen combines with aminobenzaldehyde to give a colored complex
Increase: Hemolytic disease, hepatocellular disease
Decrease: Posthepatic obstruction, impairing excretion of bilirubin to the intestines


Porphyrin Formation

Requires enzymes uroporphyrinogen, coproporphyrinogen, and protoporphyrinogen
If any of these are deficient, it causes an EXCESS FORMATION of the corresponding porphyrin which can build up in BM and Liver


Porphyrin Testing

From a 24hr urine sample, needs light protection (brown plastic) and additives to keep pH around 7


Watson-Schwartz Test

Uses p-dimethylaminobenzaldehyde to form a red product with porphobilinogen