Pancreatitis Flashcards
exocrine pancreas
secretes:
- digestive enzymes
- bicarbonate ions
- intrinsic factor
- bactericidal peptides
pancreas - dog specific
- IF produced in both pancreas + stomach
- CBD and pancreatic duct enter duodenum at major duodenal papilla SEPARATELY
- accessory pancreatic duct opens at minor duodenal papilla
pancreas - cat specific
- IF produced only in pancreas
- CBD and pancreatic duct MERGE before entering the duodenum at the major duodenal papilla
- accessory pancreatic duct only present in 20% of cats
acinar cells
produce, store, and release digestive enzymes as inactive zymogens
ductular cells
produce bicarbonate and water (flushes enzymes into duodenum)
protective mechanisms of the pancreas
- enzymes produced and stored as inactive zymogens
- enzymes are activated by enterokinase in the duodenum
- intracytoplasmic membranes separate lysosomal proteases from zymogens (prevents activation)
- SPINK1 gene/protein binds and inactivates any prematurely activated zymogens
acute pancreatitis characteristics
fully reversible
neutrophilic inflammation
edema & necrosis
chronic pancreatitis characteristics
irreversible
lymphoplasmacytic inflammation
fibrosis
often a complication of acute pancreatitis
- can be subclinical with periodic flare ups
pathogenesis of pancreatitis
almost always STERILE
failure of protective mechanisms resulting in activated enzymes; caused by:
1. auto-activation of cationic trypsinogen
2. anesthesia induced: toxemia, ischemia, hypoxia triggers zymogen activation via thrombin
3. apical block of zymogen granule secretion –> causes co-localization of lysosomal proteases and zymogens –> activation
4. biliary pancreatic reflux - enterokinase enters pancreas and activates enzymes
how does the disease progress
inflammation perpetuates disease severity due to:
- increased vascular permeability
- influx of neutrophils –> release of destructive granules –> additional pancreatic damage
- loss of apical paracellular barriers
acute pancreatitis pathogenesis
- zymogen activation
- cell injury
- local inflammation (pancreatitis)
- pain
- systemic inflammation from enzyme leakage
- SIRS, MODS
- shock, poor perfusion, hypoxia
- additional zymogen activation, etc. (repeat cycle)
chronic pancreatitis pathogenesis
occurs after acute insult OR develops independently
if acute insult: stimulates CCK and oxidative stress –> chronic low grade inflammation –> activation of pancreatic stellate cells –> fibrosis
can get primary inflammation of abdominal organs –> increased inflammatory mediators and receptors –> inflammation of pancreas
what are canine pancreatitis risk factors
- breed
- hypertriglyceridemia + obesity
- diet
- endocrinopathies
- concurrent disease
- drugs
what canine breeds are at risk of pancreatitis
yorkies, schnauzers, CKCS, boxers, collies
is hypertriglyceridemia a direct cause of clinical pancreatitis
NO - patients with TG > 862 mg/dL are 4.5x more likely to have an increased PLI
increased PLI does NOT mean clinical pancreatitis - not diagnostic unless combined with fitting clinical signs
