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45 Cards in this Set
- Front
- Back
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Functions of Liver |
1. excretory 2. storage 3. synthetic/metabolic 4. Protective barrier |
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Function: Storage |
1. lipids 2. carbs 3. iron
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Function: excretory |
*Formation of Bile *excretes toxic substances (cytochrome P450 is the site of drug detox) *exo/endogenous compounds from sinusoidal blood go to the liver where they are transformed and go into bile or urine *hepatocytic microsomes help turn products into less toxic and more soluble forms |
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Bile Formation |
* Main way to get solutes out (conjugated bile acids, phospholipids, cholesterol, bile pigments, hormones, etc) *concentrated in gall bladder and move to GI Tract when contracted *helps with the digestion and absorption of lipids and fat soluble vitamins |
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Function: Synthetic/Metabolic |
*rids body of harmful ammonia by converting it to urea *Carbohydrates *Amino Acids and proteins *lipids and lipoproteins |
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Liver and Carbs |
1. major processor of dietary and endogenous carbs 2. Plays a central role in glucose homeostasis |
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Liver and Amino acids and Proteins |
1. Primary synthetic site for plasma proteins (albumin, a/b globulins, coag factors, transferrin, haptoglobin, ceruloplasmin, fibrinogen, APR |
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Analytes |
*fecal and urine has urobilinogen *albumin, bilirubin, prothrobin time, lipds, plasma, ammonia, bile acids *albumin is used to evaluate chronic disease *protimes used to assess bleeding risk *lipoprotein x used for cholestasis *ammonia elevated in Reye's syndrom and advanced liver disease *bile acids can be measure but offer little addition of info |
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Bilirubin Metabolism |
1. RBC break down in RE which iron and heme is recycled 2. prophyrin ring is enzymatically converted to bilirubin 3. Bilirubin binds to albumin and is transported to the liver as unconjugated bilirubin 4. In the liver, u-bili is transported into the heptocytes 5. u-bili is converted to c-bili by UDP glucuronyl transferase 6. c-bili leaves liver through biliary system and enters intestines at sphincter of oddi 7. in intestine anearobic bacteria convert c-bili to urobili 8. 20-50% is recycled through the liver via the portal vein 9. Urobilinogen is oxidized to urobilin is excreted in feces. Urobili also goes in the urine |
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Elrich |
associated w/ urobilinogen coupled w/ diazotized sulfanilic acid to form a color |
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diazo reaction |
*looks at bilirubin *bilirubin + diazo reagent=azobilirubin *serum bilirubin is coupled with an accelertor (alcohol or caffeine) to get total bilirubin
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Enzyme levels: cellular acute |
*ALT/AST: markedly increase *ALP/GGT: slight increase |
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Enzyme levels: cellular chronic |
*ALT/AST: somewhat increased *ALP/GGT: Little increase in ALP and none in GGT |
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Enzyme levels: Cholestatic acute |
*ALT/AST: little increase *ALP/GGT: markedly increase |
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Enzyme Levels: cholestatic chronic |
*ALT/AST: somewhat increased *ALP/GGT: somewhat increased |
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jaundice |
*disorders of bilirubin mechanism *Prehapatic *Hepatic *Post hepatic |
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Prehaptic |
*increase in u-bili *normal or slight increase in c-bili *urine and fecal urobili will increase
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Hepatic |
*Disorders of enzyme conjugation, transport and excretion, and actual hepatocyte damage *bili depends on cause though you have about 50/50 increase (levels will be similar)--u can't get it into liver to be converted, or it goes to liver but can't be converted, or its converted but leaks out *Increase in total bili, u/c-bili, and urobilinogen |
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post hepatic |
*liver functions correctly but c-bili can't leave through sphincter of oddi to GI Tract *this will cause a back up and no production of urobilinogen (won't show up as decrease in urine since the dipstick test can't show neg) *Increase in c-bili in urine since it is absorbed by blood after conversion in liver and travels to kidney to be excreted *decrease in urobili |
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Unconjugated Hyperbilirubinemia |
1. Gilbert's Disease 2. Crigler-Najjar Syndrome 3. Dubin-Johnson |
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Crigler-Najjar Syndrome |
*has issues with converting u to c-bili due to absence or lack of UDP-glucornyl transferase *increase in unconjugated |
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Gilbert's |
*has issues going into hepatocytes to get converted *has decreased UDPGT *leads to increase in unconjugated (can't get in) |
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Dubin-Johnson |
*it is conjugated but can't get out of cells *leads to increase c-bili in serum |
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a sensitive indicator enzyme for acute ethanol intake |
GGT increases |
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ammonia metabolism |
*product from AA and protein break down *needs to be removed from system since toxic and can issues with CNS *It is synthesized in liver and converted to urea
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ALT |
*alanine aminotransferase *more liver specific |
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AST |
*aspartate aminotransferase *found in all tissues |
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ALP |
*alkaline phosphatase *used to detect liver disease and bone disorders |
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Lipase |
Increases hours after acute pancreatitis and stays elevated and goes back to normal 8-14 days |
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amylase |
increases after 6 hours after acute pancreatitis stays elevated and goes back to normal after 5-7 days |
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portal vein |
collect venous blood from intestinal region and supplies this nutrient rich blood to the liver for processing and metabolizing |
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hepatic artery |
delivers oxygenated blood |
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hepatic veins |
lead directly to the inferior vena cava, draining blood from the liver |
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inverior vena cava (IVC) |
collects blood from hepatic vein and enters heart |
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reyes syndrome |
ALT/AST are greatly elevated plasma ammonia is increased |
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delta bilirubin |
c-bili + albumin= no longer soluble seen in obstructions |
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alpha cells |
secrete glucagon that increases plasma glucose conc. |
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beta cells |
secrete insulin that is the bodies only hypoglycemic agent |
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delta cells |
somatostatin that inhibits insulin and gastrin, inhibits secretion of the pancreatic enzymes and decreases the flow of bile |
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f cells |
pancreatic polypeptides stimulate gastric and intestinal enzyme secretion and inhibit intestinal motility |
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exocrine function |
three major sources of energy: lipids, proteins, carbs |
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cystic fibrosis |
*mtations in the chloride transporter gene that leads to a missing or nofunctional cell membrane protein *sweat chloride
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pancreatic carcinoma |
arise from theductal epithelial cells |
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gastrinomas |
zollinger-ellison syndrome has greatly elevate gastrin levels |
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insulinoma |
hypoglycemia. small, benign tumor |
