Quiz 4: Liver Flashcards
(19 cards)
Synthesized Liver Products
Proteins, Coag factors, ammonia, carbohydrates, fat, ketones, Vit A, enzymes, ect
Bilirubin
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
