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68 Cards in this Set
- Front
- Back
Leakage enzymes are released as a result of membrane damage. List some reasons for this damage.
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-hypoxia
-lipid accumulation -glycogen accumulation -toxin exposure -trauma |
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What are 3 common hepatocellular leakage enzymes?
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AST, ALT (small animals), SDH (lg animals)
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What is AST specific for?
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muscle, liver, RBC
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What are the 2 induced hepatic enzymes?
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ALP and GGT
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What is ALP specific for?
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liver, steroids (dogs only), bone
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What are differentials for elevation is ALT?
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D - degenerative
A - anomalous M - metabolic N - neoplastic/non-infectious/nutritional I - inflammation T - toxix/trauma |
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What does it mean when AST is elevated, but CK is not?
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greater decree of liver damage
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Which type of hepatocytes have first contact with blood and therefore oxygen, nutrients and toxins?
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periportal
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Where are the centrilobular hepatocytes?
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in the center around the central vein - most affected by anemia, dehydration and shock
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What 4 structures are at the portal area?
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-portal vein
-hepatic artery -lymphatic vessel -bile duct |
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What is the flow of blood flow in the liver?
Which way does lymph and bile flow? |
-from portal vein into sinusoids, thru sinusoids, to central vein
-hepatosites line these sinusoids and remove toxins from the blood -lymph flows in the opposite direction |
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What is bilirubin conjugated to?
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glucuronic acid
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Is unconjugated bilirubin water soluble?
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No
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What is the rate limiting step for bile?
What does this mean? |
secretion into the SI
-overwhelmed hepatocytes can regurgitate bilirubin back into the circulation where it is eliminated byt the kidneys |
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Why is pee yellow?
Why is poop brown? |
urobilinogen + O2
stercobilinogen stays in feces because it is water insoluble |
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What does poop look like if the common bile duct is completely blocked?
urine? |
grey feces (bc no urobilinogen or stercobiligion can be produced in the SI)
-urine is brown bc of massive regurgitation of conjugated bilirubin and its passage into the urine (bilirubinuria) |
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What is a cause of pre-hepatic hyperbilirubinemia?
hepatic? Post-hepatic? |
(1) accelerated RBC destruction - lysis
(2) diffuse blockage of bile ducts or canaliculi (liver injury, necrosis, fibrosis, swelling) (3) common bile duct obstruction --> grey poop |
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What supports intra and post hepatic causes of hyperbilirubinemia (cholestasis)?
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-elevation of ALP and GGT
-elevation in leakage enzymes with liver damage |
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What comes first hyperbillirubin - uria or nemia?
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hyperbilirubinuria comes first
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What will be elevated in horses with anorexia?
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unconjugated bilirubin - no elevation in liver enzymes
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Is bilirubin a specific indicator of hepatic disease in the ruminant?
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no
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What are bile acids made from in the hepatocytes?
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cholesterol
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What do bile acids do?
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released with bile after a meal to aid pancreatic enzymes with lipolysis
-then 90% are reabsorbed in terminal ileum -5% absorbed in colon 5% lost in poop (replaced by hepatic synthesis) |
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What is more difficult - to replace lost bile acids or recycle them?
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recycle
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Why is it not necessary to evaluate the bile acids of a hyperbilirubinemic patient?
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bile acids will regurgitate into systemic circulation with intra or post hepatic biliary obstruction
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What happens to bile acid levels when > 80% of hepatocellular mass is lost?
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increase in bile acids because hepatocytes can't take up the bile acids from circulation
-this is also true in a PSS |
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What happens to ammonia after it is made from proteins in the gut?
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absorbed into portal circulation from GI
-removed by hepatocytes and converted to urea -urea released into circulation and cleared b kidneys and helps maintain the concentration gradient |
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What are some common causes of hyperammonemia?
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-decreased functional hepatic mass
-decreased presentation of ammonia to the liver (PSS) -urea toxicosis -severe GI disease in horses |
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Why might isothenuria occur with liver disease?
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decreased conversion of ammonia to BUN therefore reduced concentrating ability
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What might happen to cholesterol with cholestsis?
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increase
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Are vitamin K def. possible with cholestasis? Why?
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yes - fat digestion and absorption is negatively affected (K is fat slouble)
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Why might FDPS be increased with liver failure?
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the liver clears FDPs
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What are 2 causes of hypcholesterolemia?
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1 - PSS
2 - PLE |
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How is glucose derived?
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-intestinal absorption
-hepatic production --> gluconeogenesis (non CHO sources) and glycogenolysis (from stored gylcogen) |
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In what 3 ways are blood glucose concentrations regulated?
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(1) time since last meal
(2) hormonal influences (3) peripheral utilization of glucose |
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What do the following hormones do for blood glucose levels?
-insulin -glucocorticoids -glucagon -catecholamine -growth hormone |
-insulin --> decrease
-glucocorticoids --> increase (promote gluconeogenesis) -glucagon --> increase -catecholamine --> increase (promote glycogenolysis) -growth hormone --> increase |
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What are the 5 top reasons for hyperglycemia?
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(1) post-prandial
(2) corticosteroids-mediated stress (3) catecholamine release (4) DM (5) hyperadrenocortism (Cushings) |
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What are causes of hypoglucemia?
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-starvation/malabsorption
-increased insulin production -decreased glucocorticoid production (addisons) -liver failure -sepsis -neoplasia -ketosis in cattle pregnancy toxemia in sheep |
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What does an amended insulin: glucose ratio greater than 30 suggest?
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hyperinsulinism
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What does PTH target and what does it do?
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bone, intestine, kidney
-increases Ca (intestinal and renal absorption) -decrease P (renal excretion) -mobilization of both from the bone -increase formation of active vitamin D |
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Where does vitamin D3 come from?
-which animal lacks the kidney enzyme so that they are less dependent on the renal function for activation of vitamin D3 |
diet
-conversion of cholesterol by UV light to cholecalciferol (vitamin D3) -D2 (ergocalciferol from plants) --horses |
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What does vitamin D3 do?
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-increases Ca and P
-action on GI, bone and kidney -when Ca is low, PTH in increased and enhances formation of active vitamin D |
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Where is calcitonin made and what does it do?
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parafollicular cells of thyroid (C-cells)
-decreases Ca and P |
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What are the major fractions of Ca?
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- free or ionized (50%) --> regulated by hormones and contributes to pathologic states
-anion-bound Ca (40-50%) --> bound to albumin -bound to non-protein ions |
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What are the 6 determinants of serum Ca?
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1 - Age (higher in older, not kittens or foals)
2 - albumin concentration 3 - GI absorption 4 - resorption from or deposition of calcium in the bone 5 - kidneys 6 - Calcium and P interaction (if product is greater than 70, mineralization can occur) |
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What are causes of hypercalcemia?
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Granulomatous (increase Ca and P)
Osteolytic Spurious Hyperparathyroidism D- Vitamin D (indirectly with granulomatous) Addison's disease (lack aldosterone, Na decreases) R - ARF in horses and rabbits Neoplasm (secretion of PTHrp) |
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What are causes of hypocalcemia?
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-hypoalbuminemia
-decreased PTH (hypomagnesemia - grass tetany) -decreased vitamin D -EPI -lactational causes -furosemide treatment |
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What 5 factors determine serum phosphorous concentrations?
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1 - renal function and hydration status
2 - IC and EC shifts 3 - GI absorption 4 - bone resorption 5 - age (young will have increased levels) |
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What are causes of hyperphosphatemia?
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- decreased GFR
-increased GI absorption - ICF - ECF (acute renal failure, exertional rhabdomyolysis, cholechalciferol intoxication) |
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What are causes of hypophosphatemia?
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-increased GFR
-decreased intestinal absorption - ECF - ICF shift - defective mobilization of P from bone (hyperparathyroid, administration of insulin --> ECF - ICF) |
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Cortiocosteroid administration can result in a 5 fold increase in what?
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lipase
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What type of increase in amylase and lipase is seen in animals with pancretis?
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3 fold increase
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What is TLI and is it specific?
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trypsin-like immunoreactivity
-yes |
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What does an elevate TLI mean?
decreased? |
- pancreatis or decreased GFR
- EPI |
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What animal is cPLI used in?
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dogs - improved sensitivity to TLI in cases of pancreatis
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What is the test of choice for diagnosis pancreatis?
-EPI? |
PLI
-TLI |
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What are the 3 main diseases of the exocrine pancreas that can be detected by lab eval?
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-pancreatisi
-pancreatic neoplasia -EPI |
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What is seen with pancreatis?
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-inflammation
-azotemia -increased liver enzymes -increase in amylase, lipase, TLI and PLI -hyperglycemia -hypocalcemia |
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Increased serum folate could mean what?
decreased? |
-EPI or bacterial overgrowth
-severe intestinal disease |
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Will cobalamin be increased or decreased with EPI?
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decreased
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Hyperadrenocorticism includes 3 types, what are they?
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1 - pituitary dependent
2 - adrenal dependent 3 - iatrogenic |
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In hyperadrenocortisim, what does primary disease at the adrenal gland produce?
what does secondary disease at the pituitary gland produce? |
-adrenal --> excess glucocorticoids
-pituitary --> excess ACTH |
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What is more common - primary or secondary Cushings?
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secondary - 85% at pituitary
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What type of hypoadrenocortism is more common?
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-adrenal gland failure - most common -- immune mediated destruction
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What test would you use to take advantage of the normal negative feedback mechanism in the HPA axis?
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Low-dose dexamethasone suppression test
-used to SCREEN animals for PDH or ADH |
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What is the high-dose dexamethasone test used for?
-which lesion should suppress? |
to distinguish between PDH and ADH
-PDH should suppress adrenal tumor will not suppress -this test is not really used |
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What test helps determine:
hypoaderenocortism iatrogenic hyperadrenocorticism SCREENING test for hyperadrenocorticism |
ACTH stim test
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What is the best test to differentiate PDH from adrenal tumors?
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Endogenous ACTH
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