What are the two primary ducts in the exocrine pancreas?
1. Accessory pancreatic duct • enters at minor duodenal papillae • Major duct in dogs • Only duct in small ruminant and most cats • Major duct in horses •Lesser duct or absent in dogs • Only duct in pig and ox • Not in small ruminants nor most cats • Lesser duct in horses
2. Pancreatic duct •enters at major duodenal papillae OR into the bile duct (cats, horses, humans) •Only duct in small ruminant and most cats •Major duct in horses •Lesser duct or absent in dogs
what controls the exocrine pancreatic secretion?
Hormonal (mucosal endocrine cells in duodenum)
1. Acidic change (gastric acid, FAs) Secretin released HCO3 and electrolytes from duct epithelium
2. Lipid and protein peptides Cholecystokinin released rapid zymogen release (& gallbladder contraction) Neural (not fully understood) •Parasympathetic
(3. Vagal innervation) •Sympathetic •Intrinsic nerves
If left unchecked, the enzymes that are produced by the pancreas can autodigest the pancreas and cause severe damage, what are some of the protective mechanisms against this and accidental enzyme activation?
a. Synthesized as inactive form (zymogens = enzyme precursors) - must be activated to function b. Intracellular compartmentalization of enzymes - stored in zymogen granules, separated from lysosomal enzymes c. Enzyme inhibitors - local inhibitor synthesized, stored, and released acinar cells - circulating inhibitors (ie. 1-antitrypsin) d. Muscular sphincters in ducts prevent reflux of activated enzymes
what are the common clinical signs for pancreatitis? and what test might you do to confirm your suspicions?
Vomiting Abdominal pain Anorexia Depression Dehydration *DIARRHEA* cPl test
what is the key event preceding pancreatitis?
premature or inappropriate intracellular activation of small amounts of trypsin.
even though rare? what are some possible sequelae of pancreatitis. And why might it be rare?
Hypovolemic shock DIC Pulmonary edema Pancreatic Abscess Peritonitis Hypocalcemia Cardiomyopathy EPI Remember: exocrine pancreas is a labile organ with LARGE FUNCTIONAL RESERVE Need >85-90% loss of parenchyma for insufficiency to occur
what are the causes of pancreatitis?
Common 1.IDIOPATHIC 2.NUTRITION 3.DRUG-INDUCED 4.OBSTRUCTION (duct) less common 5.Ischemia (probably not primary) 6.Neoplasia (primary, metastatic or local invasion) 7.Reflux a)Bile (maybe cats, likely not in dogs) b)Digesta (not likely, high duct pressure)
what is the gold standard for diagnosis of pancreatitis?
• Immunoreaction specific for the lipase isoenzyme produced only by pancreatic tissue • Species specific! cPLI: canine pancreatic lipase immunoreactivity – canine pancreas-specific lipase – Spec cPL™ (IDEXX) »Quantitative measurement (outside lab) – SNAP cPL™ (IDEXX) »Semi -quantitative measurement (in house test) fPLI: feline pancreatic lipase immunoreactivity – Very reliable for diagnosing pancreatitis in cats – Feline pancreatic specific lipase – Spec fPL –SNAP fPL™ (IDEXX)
what is Feline Triaditis?
a combination of intestinal inflammation (IBD) and CCHS
why might it be important to remember that in cats the pancreatic duct opens into the common bile duct?
Therefore….. Biliary tree inflammation and fibrosis can lead to → pancreatic duct obstruction → pancreatitis → pancreatic atrophy
T or F Pancreatitis is generally Acute in cats, and chronic in dogs.
FALSE it is just the opposite Cats are generally very hard to diagnosis as it is chronic in nature and doesn't present with many signs. Dogs is usually acute and presents with vomiting diarrhea and painful abdomen
what is the etiology for EPI?
1.Pancreatic acinar atrophy (PAA) – #1 cause of canine EPI – “pancreatic hypoplasia" (unsupported belief) 2.Chronic pancreatitis (#1 cause in cats) 3.Recurring bouts of acute pancreatic necrosis (uncommon) 4.Neoplasia, other mechanical blockage of duct 5.Atrophy due to starvation, protein deficiency, chronic wasting syndromes (uremia, tumor cachexia) Reversible atrophy (if primary cause Pancreas has a large functional reserve. Clinical signs only after 85%-90% loss.
what are the clinical signs with EPI with PAA?
Chronic small bowel diarrhea weight loss despite ravenous appetitie poor hair coat coprophagy emaciation
T or F because of the atrophy and autodigestion that is associated with EPI, Diabetes mellitus should be an addressed concern in your treatment protocol.
False EPI will only effect the exocrine pancreas so Diabetes is not a concern.
what is the gold standard test for diagnosis of EPI?
Trypsin-like immunoreactivity (TLI; cTLI and fTLI) Good sensitivity and specificity Circulating trypsinogen and trypsin Send serum to Texas A&M
T or F once diagnosis and treatment starts for EPI, given time the patient should be able to regenerate the pancreas and stop treatment.
False Digestive enzyme replacement in diet (lifelong treatment with amazing results)