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Pancreatitis

Pancreatitis. Dr. S. Eddlestone Diplomate ACVIM (Internal Medicine) Assistant Professor. Pancreatic Anatomy. Major and Minor Papilla in the Dog. Pancreatic Physiology. amylase and lipase secreted into the duodenum in an active form amylase hydrolyzes starch lipase

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Pancreatitis

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  1. Pancreatitis Dr. S. Eddlestone Diplomate ACVIM (Internal Medicine) Assistant Professor

  2. Pancreatic Anatomy

  3. Major and Minor Papilla in the Dog

  4. Pancreatic Physiology • amylase and lipase • secreted into the duodenum • in an active form • amylase • hydrolyzes starch • lipase • in presence of coenzyme colipase, hydrolyzes fats

  5. Pancreatic Physiology • proteolytic enzymes secreted as biologically inactive zymogens: • trypsinogens • chymotrypsinogens • procarboxypeptidases • proelastases • prophospholipase A2

  6. Pancreatic Physiology • trypsin activated by enteropeptidase from enterocytes lining duodenal mucosa • trypsin in turn activates chymotrypsinogen and procarboxypeptidase, etc. • cascade effect

  7. Pancreatic Physiology • Defenses against Autodigestion • enzymes synthesized, stored & secreted as inactive zymogens “pro”- or -”ogen” • enzymes segregated into rough endoplasmic reticulum (RER) • acinar cells contain specific pancreaticsecretorytrypsininhibitor • PSTI

  8. Pancreatic Acinar Cell

  9. Pancreatic Physiology • amylase, lipase, zymogens of pancreatic proteases and phospholipase A2 • present in low concentrations in plasma • leak into the blood stream from gland • cleared by glomerular filtration

  10. Pancreatitis • acute or chronic • clinical signs are variable • diagnostics lack sensitivity • chronic pancreatitis is often a subjective diagnosis or necropsy finding

  11. Pancreatitis • develops upon activation of digestive enzymes within the gland • zymogen granules fuse with protease -containing lysosomes ---> activating trypsinogen • multiple etiologies proposed • experimental and clinical reports • definitive cause is seldom evident • i.e. most are idiopathic

  12. Pancreatic Acinar CellAbnormal Enzyme Activation

  13. Pancreatitis • activation of digestive enzymes • initially trypsinogen ---> trypsin • increase in capillary permeability • initiation of vasoactive amine cascade • hepatocellular necrosis • pulmonary edema • renal tublular degeneration • hypotension • cardiomyopathy, DIC

  14. Pancreatitis • inflammation & free radicals • extends locally: • stomach • duodenum • colon

  15. Pancreatitis • Plasma Protease Inhibitors • vital to protect against proteolytic enzymes in vascular space • prevent protease activation of kinin, coagulation, fibrinolytic, & complement cascades • alpha-macroglobulins • alpha-proteaseinhibitor (1-antitrypsin)

  16. Alpha-macroglobulin

  17. Pancreatitis • Etiology • unknown or idiopathic • inciting or exacerbating factors • nutrition / hyperlipoproteinemia • high fat diets, obese • drugs / toxins • thiazides, furosemide, azathioprine, L-asparginase, sulfonamides, tetracycline, +/- steroids • hyperadrenocorticism (Cushing’s disease) • infection- toxoplasmosis in cats • neoplasia

  18. Pancreatitis • factors (continued) • duct obstruction • duodenal reflux • ischemia & trauma • shock, hypotension • miscellaneous • hypercalcemia • uremia

  19. Pancreatic Necrosis - Dog

  20. Acute Pancreatic Necrosis

  21. Interstitial Pancreatitis - Dog

  22. Pancreatitis • acute • mild or severe • recurrent • chronic • mild or severe • continuing

  23. Pancreatitis • Acute pancreatitis • Edematous • mild, self-limiting • no systemic complications • responds to routine supportive care • Hemorrhagic • severe, progressive inflammation and autodigestion • vascular and multisystemic compromise • intensive therapy indicated • guarded prognosis

  24. Pancreatitis • Chronic pancreatitis • intermittent signs (“flare-ups”) • can be progressive and result in irreversible fibrosis and destruction of parenchyma • may lead to diabetes mellitus or exocrine pancreatic insufficiency

  25. Feline Pancreatitis • Chronic pancreatitis • usually low-grade and may be subclinical • mononuclear cell infiltration and fibrosis • causes vague, nonspecific signs • weight loss, depressed appetite, vomiting • Acute suppurative or necrotizing pancreatitis • rare in cats, can be fatal

  26. Pancreatitis History • middle-age or older • obese • recent fatty meal

  27. Pancreatitis Clinical Signs • depression • anorexia • vomiting • +/- diarrhea • abdominal pain • +/- shock & collapse

  28. Pancreatitis Complete Blood Count • leukocytosis • stress leukogram • hemoconcentration

  29. Pancreatitis Biochemical Profile • azotemia: prerenal or renal • elevated liver enzymes • elevated bilirubin • +/- hyperglycemia • hypercholesterolemia, lipemia • amylase, lipase • hypocalcemia • hypoalbuminemia

  30. Pancreatitis Biochemical Profile • trypsin-likeimmunoreactivity (TLI) • cats • pancreatic lipase immunoreactivity (PLI) • dogs

  31. Pancreatitis Radiography • not pathognomonic • suggestive signs: • ground-glass appearance in right cranial abdomen • static gas pattern in duodenum "fixed" duodenal loop (sentinel loop sign)

  32. Pancreatitis Radiography • suggestive signs (continued): • mass effect: • displace duodenum to right • widen pyloroduodenal angle • delay gastric emptying • reverse “7”

  33. Pancreatitis Radiography • ultrasound • size • shape • homogeneity

  34. Pancreatitis • Abdominocentesis • modified transudate, exudate • lipase level • Coagulation Profile • DIC • increased PT, PTT, FDP’s, d-Dimer’s • low AT III, platelets, fibrinogen • EKG • cardiac arrhythmias • ventricular premature contractions (VPC’s) • ventricular tachycardia

  35. Pancreatitis Treatment • supportive: • maintenance of fluid and electrolyte balance • place the pancreas at physiologic “rest" • nothing per os (NPO) • potential etiologic factors eliminated

  36. Pancreatitis • mild cases: • self-limiting • may improve without therapy

  37. Pancreatitis • severe cases: • NPO with IV fluids for 3-4 days • monitor electrolytes (K+) • analgesics • anti-emetics • plasma or whole blood • protease inhibitors, albumin • +/- antibiotics • +/- shock therapy (corticosteroids)

  38. Pancreatitis Treatment • 1-2 days after vomiting ceases • small amount of water offered • if no recurrence of clinical signs: • food reintroduced • high carbohydrate • gradual low fat diet • if signs recur: • food discontinued • severe: TPN, jejunostomy tube

  39. Pancreatitis Prognosis • unpredictable • varying severity • isolated severe episode: fully recover • acute fulminating: fatal • chronic • recurrent: may lead to euthanasia • weight loss and low fat diet in future!!

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