Pancreas Flashcards
Draw and Label the Pancreas
- Left Lobe of the Pancreas (Orange)
- Body of Pancreas (Red)
- Right Lobe of Pancreas (Blue)
- Common Bile Duct (Green)
What are som causes of Exocrine Pancreatic Insufficiency?
- Primary
- Juvenilepancreatic atrophy
- Secondary
- Pancreatic duct obstruction
- Extensive pancreatic necrosis
- Chronic pancreatitis
- Pancreatic Hypoplasia
- Occasionally observed in calves
- Pancreatic agenesis
Compare the Gross and Histo appearance of Acute and Chronic Pancreatitis
-
Chronic pancreatitis
- Pancreas is distorted, shrunken and irregular with pallor and enhanced lobulation
- +/- fibrous adhesions
- Histopath: Fibrosis and chronic inflammation
-
Acute Pancreatitis
- Variable distrubution often multifocal
- Foci of fat necrosis
- Swollen (oedematous) and nottles pancreas
- Red-black (haemorrhage) and gray-white (necrosis)
- May see peritonitis with fibrinous adhesions
What is acute pancreatic autolysis, and what can it lead to?
- Consequence of premature release of activated pancreatic enzymes (Trypsin) into the parenchyma which digests the pancreatic tissue.
- this can lead to Acute pancreatic necrosis/pancreatitis
What is the difference between the Bile ducts of a cat v’s a dog?
This is a cat pancreas, what is wrong here?
Nothing, these are Pacinian Corpuscles and are completely normal in cats.
What tests can you use to confirm Pancreatitis?
- Pancreas specific lipase (cPL/fPL)
- Detects pancreatic lipase, cf total lipase activity
- Least affected by GIT, renal disease, corticosteroids
- Requires 12hour fasted sample (lipaemia)
- Other less utilised markers
- Trypsin activation peptide (TAP) in urine/serum
- C-reactive protein (CRP) in serum
- Trypsin like immunoreactivity TLI in serum
Discuss why acute pancreatitis can cause extrahepatic cholestasis and secondary bile inducedhepatocellular injury
- Pancreatitis is an inflammatory process which can obstruct the bile ducts causing cholestasis
How are Fats and Protiens in the Duodenal Lumen Digested, and what hormone triggers this?
Describe the two parts of the pictured pancreas
- Left side is the Exocrine section, containing Pancreatic acinar cells (apical zymogen granules)
- Right side the Islets of Langerhans
What are some Pancreatic defence mechanisms?
- Continuous flow prevents reflux
- Enzymes sequestered in zymogen granules
- Most enzymes (except amylase and lipase) secreted as inactive proenzymes
- Local secretion of protective trypsin inhibitors
- Acinar cells have innate resistance to several enzymes
- Degradation of prematurely active enzymes
- Lysosomal enzymes can degrade zymogen granules
What does EPI lead to?
What are some clinical signs?
- EPI leads to
- Maldigestion and Malabsorption
- +/- diabetes mellitus
- Clinical Signs
- Diarrhoaea and weight loss normal to increased appetite +/- poor haircoat, pica
- Fatulence and marked borborygmus common
- Pale, soft voluminour, greasy and malodourous faeces (steatorrhoea)
- Concurrent SIBO
- What are the endocrine portion of the Pancreas?
- In a Histo slide how do you reconise these?
- Islets of Langerhan
- Histologically its the sections with lots of dots
What are the 3 major mechanisms of Acute pancreatic necrosis/pancreatitis?
- Obstructiom of the duct(s)
- eg. Calculi, Parasites
- Direct Injury to acinar cells
- Cassia occidentalis and T-2 mycotoxin toxicosis
- Zinc toxicosis of dogs, veal calves and sheep
- Ischaemia
- Certain drugs eg. sulfonamides
- Infectious agents eg. Bacteria, Viruses, Parasites
- Disturbances of enzyme trafficking within cytoplasm of acinar cells
- What are the Pro Pancreatic Enzymes?
- Which ones are released in Active form and what are their cofactors?
- What is required to activate the other pro enzymes?
- Pro-Pancreatic Enzymes
- Pancreatic Amylase (Calcium as CoFactor)
- Pancreatic Lipase (Calcium, Colipase and Bile Salts as cofactors_
- Trypsinogen
- Chymotrypsinogen
- Procarboxypeptidase
- Pancreatic Amylase and Pancreatic Lipase
- Trypsin Activates the others