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QUESTIONS
- There are two components to pancreatic juice: the enzyme component and the _______________. The major anion of this second component is _______________.
- Zymogen granules are evident in the _______________ cells whereas bicarbonate is produced in the _______________ cells and in cells lining the extralobular ducts. The enzyme which controls production of bicarbonate in these areas is _______________.
- Ingesta in the duodenum stimulates the _______________ cells to release _______________, which leads to an increase in the flow of the enzyme component of the pancreatic juice. These same cells also release ___________ which leads to an overall increase in pancreatic juice flow as well as an increase in bicarbonate content.
- Trypsinogen is activated by _______________ or by trypsin already present.
Chymotrypsinogen is activated by _______________. - How does the pancreas keep from digesting itself?
- Approximately how much pancreatic destruction is necessary before one gets EPI?
- The #1 cause of EPI in the dog is a spontaneous condition called
_______________. - The #1 breed for EPI is _______________.
The mode of inheretance is _______________. - The TLI test tests for trypsinogen as well as _______________. Do you fast an animal prior to running this test? Do you need to withhold viokase prior to the test?
- The PABA:Bentiromide test tests for the presence of what enzyme? What type of EPI could be detected by this test but not by TLI?
- Plasma turbidity test: Explain the rationale for its use in the diagnosis of EPI?
- Same question for x-ray film digestion test.
- Testing for fecal fat content involves the use of what dye?
- Replacement pancreatic enzymes are extracts of pig or cow pancreas. Dose = 2 tsp/20kg (Ettinger) and it is best served mixed in food. Why isn't it digested in the stomach like any other protein?
- How quick do you see a response when an EPI patient begins treatment with replacement enzymes?
- How does the breath hydrogen test work?
ANSWERS
- Alkaline fluid is the other part of pancreatic juice and the major anion is bicarb. The idea is to neutralize all that stomach acid once the ingesta starts to come into the duodenum.
- Digestive enzymes come from the acinar cells, bicarb comes from the centroacinar cells. Carbonic anhydrase is the enzyme that makes all that bicarb for us.
- The GEP cells release cholecystokinin and Secretin (the respective
answers). [By the way, is "GEP" an acronym or something?]
- Trypsinogen is activated by enterokinase & then by trypsin as there is more & more trypsin available. Chymotrypsinogen is activated by trypsin.
- The pancreas probably has many tricks to keep from digesting itself. Secreting enzymes inactive is one. It also seems to have a trypsin inhibiting factor which inactivates trypsin that might get prematurely activated while it sits around in the pancreas. This factor is available in only small amounts though and is easily overwhelmed in pancreatitis. What are some other protective mechanisms in the pancreas?
- 90% destruction is needed .
- In the dog the #1 cause of EPI is pancreatic acinar atrophy. In the human, the #1 cause is chronic pancreatitis. Other causes are neoplasia, obstruction of the duct. Congenetal causes apparently are quite unusual.
- The #1 breed is the German Shepherd dog. The mode of inheretance is autosomal recessive.
- TLI tests for both trypsinogen & trypsin. Yes, you should fast the patient first. (How long?) And, according to Ettinger's book, you do not need to withold viokase.
- Chymotrypsin is needed to split BT from PABA. PABA is then either serially tested in serum or urine. The TLI test may not pick up EPI due to obstruction of the duct. BT:PABA will pick this up.
- After a fatty meal, serum will be turbid unless the patient has EPI.
After viokase or other enzyme supplement, the normal turbidity is supposed to return. This is an extremely poor test since up to 80% of fat may be digested & absorbed even in severe EPI.
- The x-ray film digestion test -- er -- I wrote this question without
knowing the answer & then I couldn't find the answer in any notes. Could some one else please explain about this test? :)
- Sudan III is that funky orange stuff.
- Trick question. It is digested like other proteins. 90% of lipase & 80% of trypsin are destroyed before seeing the jejunum. The good news is that it doesn't seem to matter & the response is good anyway. People have tried enteric coating & preincubation of food but it doesn't really help & may hurt(at least enteric coating many people feel doesn't really work). Tagamet or other H2 blocker may help but it is expensive & most patient respond well without it.
- Most dogs respond to viokase-type stuff in 4-5 days & can be expected to gain 1-2 lbs per week.
- Carbohydrates which not digested or absorbed in the Small intestine get fermented by colon flora. If the amount of CHO reaching the colon is in excess of what the colon can ferment & absorb (EPI or SID) then the fermentation products act as osmotic agents, drawing fluid into the lumen & causing diarrhea. Breath hydrogen tests the fermentation capicity of the colon as some of the hydrogen gas produced in the colon gets absorbed systemically & gets exhaled by the lungs.
Normal dogs fed a defined diet with a highly digestible CHO source have very little breath hydrogen. Dogs with a malabsorption have lots of breath hydrogen. Dogs with SIBO have an early peak in breath hydrogen because the CHO gets fermented before it has time to get to the colon. Breath hydrogen can also be used to determine orocecal transit time.
Problems with the test are: enemas & antibiotics will alter results, motility problems may alter results, we can't get a good alveolar breath sample necessarily, gas chromatography isn't exactly handily come by.
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