QUESTIONS

1. In the dog, the mildest form of acute pancreatitis is called _______________ pancreatitis. In this form there is mild neutrophilic exudate.  Acinar & duct structures remain intact.
   
   The severe form of canine pancreatits, which is almost untreatable, is called _______________ pancreatitis. Here there is fat necrosis not only around the pancreas but in the abdomen no where near the pancreas & even outside the abdomen. Coagulation necrosis destroys the parenchyma.
   
   In the cat, the three histologic types of pancreatitis are _______________, _______________, & _______________.
    
2. How does an obstructed pancreatic duct lead to pancreatitis?
    
3. Hypercalcemia is listed as a cause of pancreatitis.  How?
    
4. Typical canine acute pancreatitis patients are (choose one):
   
   young / middle-aged / aged
   
   (choose one):
   
    male / female.
    
5. Therapy for pancreatitis consists of fluid support, NPO for 5-7 days, pain relief, antibiotics (controversial), heparin, insulin (if needed)  and often plasma.
   
   a) Why NPO?
   
   b) Why is morphine a bad choice for pain relief in pancreatitis?
   
   c) Why give heparin?
    
6. Why might a diet high in fat predispose a dog to pancreatitis?
    
7. Trypsinogen activation is critical for the initiation of disease.  How does trypsinogen get activated?
    
8. Amylase is used in the diagnosis of pancreatitis.  Is Amylase also
   involved in the pathogenesis of pancreatitis?
    
9. Alpha 2 macroglobulin & alpha 1 protease are helpful in protecting against pancreatitis. How do they work?
    
10. Trivial pursuit question:  what biotoxin can cause pancreatitis? Hint: Dave Williams lists it as a misc cause in his CVT article.
     
11. Your patient has been getting dexamethasone for a chronic disc problem. Suddenly the owner reports some nausea. Blood work shows a normal amylase and a lipase 4x the normal range. Does this point you toward pancreatitis?
     
12. Why might a pancreatitis case develop pulmonary edema?
     
13. Can TLI be used to diagnose pancreatitis?
     
14. Why do pancreatitis patients sometimes have low serum calciums?
     
15. What breed of cat is over-represented for pancreatitis?
     
16. 64% of cats with pancreatitis have concurrent ______________. What's the connection? (FYI: 68% of cats with pancreatitis have renal pathology. Sure makes it hard to interpret amylase & lipase, don't it.)
     
17. In feline pancreatitis, what infectious organism might be worth ruling out?
    
    
    
    
     

ANSWERS

1. Mild form = edematous pancreatitis
   
   Severe form = hemorrhagic or necrotizing pancreatitis
   
   Cats get acute, chronic-active, & chronic pancreatitis
   
   
   
   
    
2. Obstructed pancreatic duct is pretty uncommon but the idea is that enzyme production & secretion doesn't stop just because the duct is blocked. Enzymes back up all the way & finally the zymogen granules are so full that they mush into & fuse with lysosomes. Voila! Trypsinogen is activated.
   
   
   
   
    
3. Elevated calcium in the serum goes with elevated tissue levels of calcium in the actual pancreas & pancreatic secretions.  Calcium is able to activate trypsinogen & when it's right there, that's just what happens.  Elevated calcium also supposedly induces vasculitis within the pancreas which leads to inflammation which leads to leaking enzymes. Calcium also increases pancreatic secretion.
   
   
   
   
    
4. Classically patients are middle aged & female.
   
   
   
   
    
5. a) Patients are kept NPO because even stomach distention due to water will lead to gastrin secretion which will stimulate the pancreas to secrete. We want to reduce any thing that would stimulate pancreatic secretion.  In cats, things are a little different and often there is a concurrent hepatic lipidosis. For cats, we tend to feed them as long as they don't vomit.
   
   b) Morphine causes spasm of the sphincter of Oddi.  The last thing we want in pancreatitis is cholestasis so its better to use demerol which causes no such spasm.  I do not know what the effect of fentanyl is. Anyone?
   
   c) Heparin is used to prevent DIC ( which stands for "death is coming") . Pancreatitis is the BIGGIE for DIC with all those enzymes running around causing thrombosis wherever they go.  The enzymes also digest clotting factors, too. :(
   
   
   
   
    
6. Diets > 60% fat reduce resistence of acinar cell membranes to trypsin digestion. Fatty diets may also alter the lipid concentrations of cell membranes (which might enhance leaking enzymes) & might alter the enzyme content of acinar cells (promoting autodigestion).
   
   
   
   
    
7. No one is sure how trypsinogen gets activated but we think that it occurs intracellularly when lysosomes fuse with zymogen granules. Remember, for safety reasons (sort cosmic OSHA), we have been designed to make trypsin in a ``pro" form (ie it has to be activated). The zymogens used in this activation are supposed to be stored in granules separate from the trypsinogen containing lysosomes.
   
   
   
   
    
8. Amylase is not involved in the pathogenesis of pancreatitis (unlike lipase which is very involved in fat necrosis).
   
   
   
   
    
9. Alpha1 protease binds trypsin, reversibly inactivating it. Alpha 1 protease then transfers typsin to alpha 2 macroglobulin. While bound to alpha 2 macroglobulin trypsin is active but this doesn't last long as binding induces a change in the macroglobulin which is recognized by the RE system. The whole complex is thus removed from circulation.  The bad news is: Once the RE system has removed all the Alpha 2 macroglobulin, you die from DIC in
   minutes. It takes too long to make new macroglobulin so unless you get a plasma transfusion, you're in deep doo doo.  You still have alpha 1 protease, but that only reversibly inactivates trypsin. Also note that corticosteroids inhibit the removal of alpha 2 macroglobulin & its bound trypsin  (one of the reasons steroids are controversial in pancreatitis).
   
   There's more:  alpha1 protease, being an inhibitor of trypsin, prevents its own digestion & can be measured in feces. If you have a protein losing gastroenteropathy, alpha one protease amounts in feces are elevated as it is lost into the lumen with other serum proteins.  This testing is currently in use for people; an ELISA test for dogs is being developed.
   
   
   
   
    
10. Scorpion venom can cause pancreatitis.
    
    
    
    
     
11. Not very good evidence of pancreatitis.  Dexamethasone has been shown to increase serum lipase levels up to 5x normal without histopathologic evidence of pancreatitis.
    
    
    
    
     
12. Many reasons why pancreatitis can lead to pulmonary edema. For one thing, phospholipase A is digesting surfactants. Other enzymes are digesting the alveolar/capillary membranes.  Also, myocardial depressant factor is being released from the pancreas and there are thrombi in the myocardial vessels.  (Heart failure)
    
    
    
    
     
13. Dave William in CVT hints strongly that TLI can be used in the diagnosis of pancreatitis but doesn't list any values. Amylase & lipase both have extra-pancreatic sources while TLI does not; however, all are influenced/removed by kidneys and are thus affected by renal function.
    
    
    
    
     
14. Lipase leads to saponification of fat (like omasal fat) which releases triglycerides. These bind calcium & bring the serum level down.
    
    
    
    
     
15. In feline pancreatitis, the Siamese cat is over-represented.
    
    
    
    
     
16. 64% of cats with pancreatitis also have cholangiohepatitis.  This is because the bile duct & pancreatic duct empty into the same papilla. The theory is that bile refluxes into the pancreatic duct & causes big time inflammation.  Note, though, in our Thursday session, Pancreas1 says that this connection is not evident in every case.
     
17. Toxoplasma gondii has been implicated in some feline pancreatitis cases (remember 90% of the time feline pancreatitis is idiopathic but that doesn't mean you should assume you wont' be able to find the underlying cause)