16 – Pancreas Flashcards
1
Q
What is the pancreas’ role in digestion?
A
- Produces digestive enzymes
- Produces bicarbonate
2
Q
Pancreatitis
A
- Inflammation of pancreas
- Develops when the digestive enzymes are activated in pancreases causing AUTODIGESTION
- Acute: very ill and many complications
- Chronic: don’t even know it is there
3
Q
What are some mechanisms to prevent autodigestion of pancreas?
A
- Enzymes are synthesized, stored and secreted as INACTIVE zymogens
- Activation of zymogens in intestine
- Enteropeptidases (enterokinase) cleaves activation peptides from trypsinogen to form trypsin
- Trypsin cleaves the activation peptide off of other zymogens
- Digestive enzymes segregated in lumen of rER
- Acinar cells contain trypsin inhibitor that is synthesized, segregated, stored and secreted with digestive enzymes
4
Q
What is the pathophysiology of pancreatitis?
A
- Develops with autodigestion
- Abnormal mixing of lysozomes and zymogen granules in abnormal intracellular vacuoles
- Activation of trypsinogen by lysosomal proteases
- Trypsin activates the other digestive enzymes
- Activated enzymes increases capillary permeability, damage the pancrease and activate vasoactive amine cascade
- Local extension of inflammation
- Vasoactive peptides in circulation
- *will be most severe if protease inhibitors are consumed
o More severe with hypoperfusion
5
Q
What might the vasoactive peptides in circulation (due to pancreatitis) lead to?
A
- ARDS (acute respiratory distress syndrome)
- DIC
- Hypotension
- Myocarditis
- Hepatocellular necrosis
- Renal tubular damage
6
Q
What are some of the proposed etiology’s of pancreatitis?
A
- Nutrition: obesity, fat content
- Hyperlipoproteinemia
- Drugs: azathioprine, diuretics, antibiotics
- Duodenal reflux with vomiting or trauma
- Alcohol ingestion
- Ischemia
- Duct obstruction
- Hypercalcemia
- Infection
- Cushing’s disease
- Zinc
7
Q
What are the risk factors in acute pancreatitis?
A
- Mean age: 8 +/- 3 years
- Breed (Schanauzers, Yorkies, poodles, Siamese cats)
- Obesity
- Prior GI disease, DM, Cushing’s
- NO risk with oral glucocorticoids, anesthesia, trauma
8
Q
Feline risk factors in pancreatitis: Triad disease
A
- Combination of pancreatitis, IBD, and cholangiohepatitis
- *was a statistical association
- *common with other GI problems, but just plain common
- Older=more common
9
Q
What are some complications of pancreatitis?
A
- Cardiac arrhythmias
- DIC
- Dyspnea
- Acutre renal failure
- DM
- Sepsis (more in people)
- Bile duct obstruction (jaundice), abscess, pseudocyst
10
Q
How do you diagnose pancreatitis in dogs?
A
- History and physical exam
- Amylase, lipase
- Ultrasound (severe)
- PLI, cPL, precision PSL
11
Q
How do you diagnose pancreatis in cats?
A
- History and physical exam
- Clinical signs: lethargy, anorexia, vomiting (half), abdominal pain (19-25%)
- Amylase and lipase: NOT useful (need species specific)
- CBC about half will have leukocytosis
- Liver enzymes elevated
- Hyperglycemia
- Hypokalemia
- Low calcium
- Pancreatic specific lipases
- Ultrasound
- *hard to differentiate from gastric enteritis in CATS
12
Q
Ultrasound for pancreatitis diagnosis
A
- No gold standard so hard to know how good it is
- More agreement when pancreatitis was worse
13
Q
How do you treat pancreatitis?
A
- Fluid therapy (should be aggressive)
- Antiemetics
- Early feeding (enteral preferred)
- Analgesia
- *Pan O Quel (US and elsewhere)
14
Q
What is exocrine pancreatic insufficiency (EPI)?
A
- progressive loss of exocrine pancreatic acinar cells
- inadequate digestive enzyme production
- failure to absorb nutrients properly
- large functional reserve
- *signs show when 85-90% of pancreas lost
15
Q
What is the history of an animal with EPI?
A
- Weight loss
- Polyphagia
- Coprophagia
- Pica (eat things that normally should not be eaten)
- Diarrhea, responds to fasting, steatorrhea
- Borborygmus
- Flatulence
16
Q
What is the etiology of EPI?
A
- Pancreatic acinar atrophy (PAA)
- Chronic pancreatitis
- Idiopathic
- Neoplasia
17
Q
What is pancreatic acinar atrophy?
A
- Etiology is unknown
- Post natal atrophy
- High prevalence in G. Shepherd
o Autosomal recessive - Other breeds as well: usually large dogs
18
Q
Chronic pancreatitis and EPI
A
- Common cause in humans
- Uncommon in dogs
- May result in EPI and DM
- *Underlying cause in the majority of feline EPI
19
Q
Pathophysiology of EPI: nutrient malabsorption
A
- Failure of intraluminal digestion
- Abnormalities in SI mucosa function
o Absence of trophic influence
o SI bacterial overgrowth
20
Q
EPI and SIBO (dysbiosis)
A
- SIBO common problem with EPI
- May be lack of antibacterial pancreatic secretions
- May account for SI mucosal changes
o Changes in brush border enzyme activity
o Varying villus atrophy
o Competition for ingested nutrients
o Depends on bacterial species
21
Q
EPI and diarrhea: osmotic
A
- Volume of feces increased in proportion to % oral intake escaping absorption
- CHO osmotically active
22
Q
EPI and diarrhea: secretory
A
- Hydroxy-fatty acid production by bacteria
- Release enterotoxins and deconjugate bile salts’
23
Q
EPI and cats
A
- 70% have diarrhea and weight loss
- *no specific clinical signs
24
Q
EPI diagnosis
A
- TLI (trypsin-like immunoreactivity) is standard at this time
o Dogs: value below 2.5ug/L WITH clinical signs
o It below 2.5ug/L but NO signs: probably subclinical EPI
o Cats: values below 8ug/L
25
Q
How do you treat clinical EPI?
A
- *enzymes
o Uncoated
o Enteric coated
o Raw pancreas - *coated vs. uncoated: no differences with clinical signs but weight gain greater with coated
