Lecture 9: Pancreas (Freeman) Flashcards Preview

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Flashcards in Lecture 9: Pancreas (Freeman) Deck (23):
1

What are zymogen granules?

-capsules within pancreatic glandular cells that enzymes are secreted in
-most enzymes are in an inactive form within the granules
-usually lie at the apex of the cell

2

Most important stimulus of the pancreas*

the intestinal lumen. The brush border responds to a stimulus and releases hormones (CCK or secretin), which target the pancreas through endocrine, paracrine, or neurocrine signalling.

3

protein and fat in intestinal lumen cause release of CCK, which causes pancreas to release:

digestive enzymes

4

hydrogen in intestinal lumen causes release of secretin from duodenum, which causes pancreas to release:

bicarbonate and chlorine

5

What is the most important source of digestive enzymes? *

why, the pancreas of course!

6

Where are the digestive enzymes of the pancreas produced?

In the acinar and duct cells (the exocrine portion of the pancreas)

7

Islets of langerhans for the _____ portion of the pancreas

endocrine

8

3 main fxs of pancreatic secretions

1) enzymes: digest carbs, fat, protein
2) cofactors: colipase that aids in fat digest.
3) HCO3 neutralizes pH in the duodenum, thereby inactivating pepsin, protecting duodenal mucosa, providing functional pH for enzymes, and increasing solubility of bile and fatty acids

9

neural control of pancreatic secretion*

via vagus nerve and Ach from cholinergic neurons. Involved in all 3 phases of stimulation

10

hormonal control of pancreatic secretion*

from duodenum in response to:
1)H+ --> secretin released from duodenum --> HCO3 and water released from pancreas
2) protein, fat --> CCK released from duodenum--> enzymes released from pancreas

11

3 phases of stimulation of the pancreas

cephalic, gastric, intestinal

12

cephalic phase stimulation of pancreas

-vagal activity (via Ach) induced by conditioned responses or taste of food.
-causes enzyme secretion

13

gastric phase stimulation of pancreas

-vagovagal reflex (via Ach) secondary to gastric distension
-gastrin release secondary to stimulants such as enzymes and water/electrolytes

14

intestinal phase stimulation of pancreas

-CCK release secondary to protein and fat in the intestinal lumen --> enzyme release
- secretin release secondary to H+ in intestinal lumen --> bicarb/water release

15

effect of trypsin in the intestinal lumen on secretin and CCK release by the intestine

suppresses the release of secretin and CCK

16

amylase

enzyme secreted into the duodenum in ACTIVE form. Digest starch and glycogen into smaller sugars

17

lipase

enzyme secreted into the duodenum in ACTIVE form. Digests ingested long-chain triglycerides into monoglycerides and fatty acids

18

trypsin **

enzyme secreted into duodenum in INACTIVE form (trypsinogen). activates other enzymes, breaks down proteins, inhibits CCK and secretin release

19

steatorrhea means

loss of fat

20

pancreatic exocrine insufficiency (PEI)

clinical condition in which there is decreased digestion of macronutrients resulting in caloric deficiency, steatorrhea, and diarrhea (maldigestion/malassimilation)

21

4 mechs. of pancreatic protection *

1) enzymes transported in membrane compartments
2) enzymes secreted as inactive zymogens
3) trypsin activated by enteropeptidase and then activates other enzymes (trypsin has to get into lumen where there is enteropeptidase in order to be activated)
4) trypsin inhibitor in acinar cell

*failure of these protective mechs. can cause pancreatitis*

22

What is unique about the equine pancreas? *

-almost CONTINUOUS secretion
-secretion is PROFUSE
-concentration of BICARB. is always LOW (just high enough to protect the mucosa)
-LOW ENZYME activity
-GASTRIN plays a bigger role in water and electrolyte secretion (gastrin, not secretin drives bicarbonate secretion in the horse)

23

Role of pancreatic Cl- in the equine small intestine

There is very little bicarb. that reaches the small intestine, but bicarb. is needed to buffer fermentation in the cecum/colon. High Cl- in the pancreatic and intestinal fluid compensates for this via Cl-/HCO3- exchange in the ileum and distal jejunum.

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