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
what endocrinopathies increase the risk of pancreatitis
cushing’s
hypothyroidism
diabetes mellitus
what are the clinical signs of pancreatitis
non-specific
- lethargy
- hyporexia
- vomiting
- diarrhea (large +/- hemorrhage)
- weight loss
- dyspnea
PE:
- dehydration
- hypo or hyperthermia
- abdominal pain
- icterus
- abdominal organomegaly
is abdominal pain highly sensitive for pancreatitis
NO - not all animals will sho signs of pain
what is the test of choice for diagnosing pancreatitis
spec PLI
cats: > 5.4 mg/dL
dogs: >400 mg/dL
ONLY test animals with consistent clinical signs
- poor specificity - not a good screening test
what should you do if a patient tests in the grey zone on spec PLI
retest in 2-3 weeks
cats: 3.6-5.3 mg/dL
dogs: 201-399 mg/dL
abdominal ultrasound - pancreatitis
abdominal ultrasound
- acute: large, hypoechoic pancreas with hyperechoic mesentery +/- abdominal effusion, cysts, abscesses
- chronic: large, hyperechoic to mixed echogenicity pancreas with dilated CBD, irregular margins, and pancreatic nodular hyperplasia
what lab values can be altered with pancreatitis
CBC: NNN anemia, dehydration
Chem: hepatocellular hepatopathy, hyperbilirubinemia (EHBDO), hypercholesterolemia, hypertriglyceridemia, hypocalcemia (from saponification)
treatment of acute pancreatitis
- fluids
- analgesia - opioids
- antiemetics - ondansetron, maropitant
- nutrition - enteral feeding, appetite stimulants
treatment of chronic pancreatitis
- treat underlying conditions
- hypertriglyceridemia - low fat diet
- chronic enteropathy - B12, folate supplementation - analgesia
- antiemetics
- nutrition PRN
what treatments are contraindicated for pancreatitis
- antimicrobials
- steroids
- NSAIDs
- acid suppressants (unless signs of ulcers)
- plasma transfusion (unless DIC)
- surgical intervention (unless abscesses present)
what type of pancreatitis is most common in cats
chronic
acute on chronic
what is the most common etiology of feline pancreatitis
comorbidities
- chronic enteropathies
- cholangiohepatitis
(triaditis)
what are the common complications of feline pancreatitis
- hepatic lipidosis
- EPI
- diabetes mellitus
treatment for feline pancreatitis
- fluids
- analgesia
- antiemetics
- enteral nutrition + mirataz
- treat comorbidities
- chronic enteropathy - B12, folate
what type of pancreatitis is most common in dogs
acute
acute on chronic
what is the most common etiology of canine pancreatitis
predisposing factors
- breed
- diet
- hypertriglyceridemia + obesity
- anesthesia
- endocrinopathies
what are common complications of canine pancreatitis
- diabetes mellitus
- EPI
treatment for acute canine pancreatitis
hospitalization
1. IV fluids
2. opioids
3. antiemetics
4. enteral nutrition + appetite stimulants
treat predisposing factors (ex. hypertriglyceridemia - start a low fat diet)
treatment for acute episode of chronic pancreatitis
- gabapentin
- antiemetics
- enteral nutrition + appetite stimulants
- low fat diet
