SA DIGESTIVE FINAL STUDY GUIDE PDF
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Summary
This study guide covers liver function, clinical signs of liver disease, and diagnostics in animals. The guide reviews pre-hepatic, hepatic, and post-hepatic classifications of liver disease. It also examines hematology results and changes in albumin, globulin, cholesterol, BUN, and glucose.
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SA Digestive Final (going to try and include pictures from lecture and highlight important material over the next few days, might have to zoom in on the pictures since there are many of them highlighted in yellow) Liver 1. Where do...
SA Digestive Final (going to try and include pictures from lecture and highlight important material over the next few days, might have to zoom in on the pictures since there are many of them highlighted in yellow) Liver 1. Where do most of the nutrients of the liver come through? a. Portal vein b. 2. What makes up the portal triad? a. Portal vein, bile duct, and hepatic artery 3. What part of the liver has the lowest oxygen concentration? a. Centrilobular (zone 3), closest to central vein b. 4. How does blood move in the liver? a. In the opposite direction as bile 5. What are functions of the liver? a. Amino acid synthesis, glucose to glycogen and vice versa, bile production, deactivate poisons and toxins, RBC decomposition, cholesterol synthesis, regulates blood composition, hormone production and metabolism, vitamin absorption/metabolism/production b. 6. What are clinical signs of liver disease and their pathogenesis? a. Secondary GI disease: vomiting, diarrhea, hypo/anorexia b. Icterus/jaundice c. d. Hepatic encephalopathy (affects the brain): head pressing, seizures, fly biting, blind, star gazing, aggression e. f. PU/PD: decreased urea production i. urea is important because it converts a toxic form of ammonia into a less toxic form which is eliminated in urine……without urea, the dog has to continually urinate and drink fluids to flush those substances out. g. Bleeding: decreased coagulation factors (just know 2,7,9,10 are most affected), fibrinogen defect, thrombocytopenia and platelet activation h. Ascitis: low albumin (decreased production or loss) > decreased colloid oncotic pressure > abdominal effusion AND increased portal P (mostly caused by either a cirrohotic liver which blocks or obstructs flow from the portal vein into liver)) > increased hydrostatic P > abdominal effusion i. j. Bile peritonitis: gall bladder rupture k. Drug sensitivity: less albumin to bind, decreased metabolism l. KIND OF A TREND WITH LIVER DISEASE AND ALBUMIN>>>plays a role in drug metabolism, portal pressure, and making sure the abdomen doesn’t fill with fluid. 7. What are the classifications of liver disease? *might be important to know a. Pre-hepatic: hemolysis b. Hepatic: liver prob c. Post-hepatic: bile obstruction ______________________________________________________________________________ REVIEW FROM CLIN PATH (the things highlighted in this section are for my knowledge and reminder) 8. What causes hepatic encephalopathy? a. Ammonia and other toxins not metabolized by liver or by-pass via shunt 9. What are diagnostics for liver disease? a. CBC b. Pseudo function tests: total bilirubin, glucose, BUN, cholesterol, albumin c. Ammonia, bile acids, imaging, biopsy 10. What can the hematology results tell us? a. Normocytic, normochromic anemia: chronic inflammatory disease, early blood loss b. Macrocytic, hypochromic anemia: blood loss anemia c. Microcytic, hypochromic anemia: iron deficiency anemia, anemia of portosystemic shunts d. Thrombocytopenia with GI blood loss or DIC e. Reactive thrombocytosis with GI blood loss 11. What can changes in albumin tell us? a. Increased: dehydration or GI fluid loss b. Decreased: decreased production from liver dysfunction or GI loss (PLN) 12. What can changes in globulin tell us? a. Increased: chronic inflammation or neoplasia b. Decreased: gut loss (with low albumin = PLE) 13. What can decreased cholesterol tell us? a. Decreased production from liver dysfunction, GI loss or decreased absorption 14. What do changes in BUN (urea nitrogen, the body’s natural waste product) tell us? a. Increased: dehydration, GI blood loss/absorption (normal creatinine) b. Decreased: liver dysfunction 15. What can decreased glucose mean? a. Liver dysfunction (liver and kidneys are gluconeogenesis organs) 16. What does increased bilirubin mean? a. Liver disease b. Bilirubin needs to be converted into bile. If it is not converted into bile, it can over accumulate and cause the patient to have jaundice, seizures, and terminal brain damage. ______________________________________________________________________________ 17. What does increased ALP tell us and why is it more telling in cats? a. indicator of Biliary stasis/cholestatic disease b. Much shorter half life in cats (6 hours) c. can be increased for growing animals, steroid induced, GI, prostate d. 18. What does increased GGT mean? a. Cholestatic disease 19. What does an increased GGT and ALP likely mean? a. Cholestatic disease 20. What does increased ALT mean? a. Liver and muscle damage b. Also short half life in cats (