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14 Cards in this Set

  • Front
  • Back
Zymogens released from acinar cells
release zymogens and trypsinogen, trypsinogen activated via enteropeptidase (on brush border). Trypsin activates other zymogens EXCEPT amylase and lipase (released in active form)
Mechanisms to prevent autodigestion
1. Storage in vessicles
2. Proenzymes
3. Pancreas secretes trypsin inhibitors
Regulation of exocrine pancreas
1. CCK- released when food is in the duodenum, stimulates the pancreas to release zymogens, lipase and amylase.
2. Secretin- released when food is in the duodenum, pancreas stimulated to release NaCl, water, bicarb
Exocrine vs. endocrine pancreas
Exocrine- from acinar cells; secretes enzymes
Endocrine- from islet cells; secretes insulin
Systemic effects of pancreatic necrosis/peritonitis
DIC, inflammation, shock, cardiopulmonary dys, peritonitis, hypocalcemia
Etiology of pancreatic necrosis
idiopathic, nutrition, drug, ischemia, obstruction (neoplasia, inflammation, stones, parasites)
qualities of acute pancreatitis
inflammation and necrosis of fat (bright white spots)
can be fibrinous (heals by fibrosis)
qualities of chronic pancreatitis
fibrosis, will not see neutrophils
fat necrosis
diagnosis of pancreatic necrosis
clinical sings
CBC/chem
TLI, Spec cPL
imaging
laparotomy
biopsy
painful on palpation
exocrine pancreatic insufficiency (EPI) etiology
occurs after singificant portions of the pancreas are destroyed, results in maldigestion because of a lack of enzymes
clinical signs of EPI
very skinny, history of chronic diarrhea
hypoglycemic
hypoproteinemic
hypocholesterolemic
Diagnosing EPI
TLI- trypsin like immunoreactivity
will be DECREASED in EPI because it is a pancreatic enzyme and pancreas is not functioning normally
pancreatic disorders of growth
nodular hyperplasia- common in cats, not pathogenic
carcinomas- not common, will destroy mechanisms preventing autodigestion
PLI as diagnostic for inflammation
pancreatic lipase immunoreactivity
species specific for dogs and cats- VERY sensitive and specific