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28 Cards in this Set
- Front
- Back
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1. What are the two major divisions of the pancreas?
What do the cells of each portion secrete? |
1. Acinar portion
**acinar cells secrete enzymes 2. Ductal portion **ductal cells secrete ions mainly HCO3- |
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2. What stimulates duct cells?
What is this hormone released in response to? What does this hormone cause? |
Stimulated by hormone secretin
Secretin is released by duodenal S cells in response to acidic chyme in duodenum (pH < 4) Causes fusion of Na-H ion exchanger to basolateral membrane |
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3. What does the fusion of the Na-H ion exchanger to the basolateral membrane trigger?
(two things) |
1. CO2 from stimulated cell metabolism
*diffuses in 2. Plasma forms H2CO3 *HCO3- plus H from Na-H exchanger |
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4. How can the H be neutralized by just a "small" increase in plasma pH?
What transporters does the apical membrane contain? What transporters does the basolateral membrane contain? |
H is overwhelmed by the HCO3-
**small increase in plasma pH is really quite large Apical: Cl-HCO3 exchanger Basolateral: Na-K ATPase and Na-H exchanger |
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5. What does H2CO3 form in the cell?
Where is HCO3- secreted into? How are Cl and HCO3- exchanged? What is the ratio? |
Forms H+ and HCO3-
HCO3- is secreted into the lumen Exchanger transports HCO3- out and Cl channels open to provide Cl for the exchanger into the lumen There is a 1:1 exchange of Cl for HCO3 |
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6. What happens to the pH as the secretion rate increase?
What is the maximum pH? How is the secretion in relation to the plasma? |
As secretion rate increases, pH increases due to addition of bicarbonate
Max pH can rise to pH of 8.2 Secretion is isosmolar to plasma |
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7. What stimulates acinar cell secretion?
When is this hormone released? What will it stimulate? What else can stimulate acinar cells? |
Stimulated by hormone CCK
CCK is released by duodenal I cells exposed to fat 1. Directly stimulate pancreatic acinar cells at physiologic concentrations 2. Also stimulate vago-vagal reflex Secretin by a separate intracellular pathway **increase cAMP |
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8. In short how can pancreatic acinar cells be stimulated?
(two ways) What are the two intracellular pathways for acinar cell secretion? What stimulates each pathway? |
1. Directly via blood borne CCK
2. Indirectly by CCK activation of a vago-vagal neural circuit 1. Main pathway -stimulated by CCK, GRP, ACh & SP 2. Secondary pathway -stimulated by secretin & VIP **main pathway is more effective pathway |
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9. How does the main pathway work?
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1. Increased IP3 and DAG
2. IP3 stimulates Ca release from SR 3. cGMP (from DAG) increases Ca flux into cell 4. Increased intracellular Ca increases enzyme synthesis and release |
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10. How does the secondary pathway work?
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1. Activates adenylate cyclase (produce cAMP)
2. Increases enzyme synthesis |
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11. What is the optimal pH of acinar cell enzymes?
What food classes do the enzymes secreted by the acinar cells work on? |
pH 6.8 - 7.2 range
All three food classes 1. Carbs - pancreatic amylase 2. Proteins -proteolytic enzymes secreted as zymogens -trypsinogen is activated 3. Lipids -works w/ bile -pro colipase secretion |
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12. Where does the bile duct originate from?
What do hepatic ducts feed into? What do cystic ducts feed into? What do the common bile ducts empty into? |
Originate from the liver
Feed into cystic duct or common bile duct Feed into gall bladder and the common bile duct Empties into duodenum at sphincter of Oddi |
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13. How are most (70%) of bile pigments forms?
What are the two main types of bile pigments? What is the significance of bile pigments? |
Formed by reticulo endothelial cells consequent of catabolism of hemoglobin
1. Biliverdin 2. Bilirubin Mainly diagnostic **plasma bilirubin levels are indices of liver and Hb activity **excess bilirubin leads to jaundice |
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14. How are primary bile acids synthesized?
How are secondary bile acids synthesized? How are bile salts formed? What are two characteristics of bile salts? |
Synthesized by liver from cholesterol to form cholic and chenodeoxycholic acids
Primary bile acids acted on by bacteria to form secondary biles acids deoxycholic and lithocholic acids Primary and secondary bile acids conjugated w/ glycine and taurine to form bile salts 1. More water soluble 2. Amphiphatic |
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15. What does bile salt (acid) dependent fraction include?
What does the bile salt dependent fraction do? |
1. Re-secretion of recovered bile salts (acids) by liver
2. Secretion of De novo bile acids Osmotically draws water and electrolytes into duct |
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16. What is the bile salt (acid) independent fraction?
What stimulates it? What does it function to do? |
Secretion of H20, electrolytes and HCO3-
**bile acid (salt) concentration is low Stimulate by hormone secretin Functions to neutralize intestinal acid |
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17. What happens when bile concentrations reach a critical concentration (1 to 5 mM/L)?
How do these affect lipids? |
Bile salts form cylindrical crystals called micelles
Bile micelles have a detergent like action on lipids **products of fat digestion insert themselves in the micelle **bile micelles transport products of fat digestion to absorptive mucosa |
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18. What do bile salts do?
What do micelle then do? How does lack of bile affect fat absorption? What does this lead to? |
Bile salts emulsify large fat droplets
**allows more efficient action of pancreatic lipase Micelle diffuse to and penetrate unstirred water layer reducing its size and thickness Lack of bile reduces absorption of fat Unabsorbed fate causes special case of diarrhea (steatorrhea) |
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19. Where are bile salts recovered?
How does this occur? What extracts the bile salts (acids) and re-secretes them? How often are bile salts recovered? What is bile salt recovery efficiency? |
Recovered at ileum
Na coupled transporter which takes bile salts into ileal mucosal cells and then into hepatic portal blood to liver Cells of liver sinusoids 2 to 4 times per normal meal 85% to 97% |
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20. When does bile secretion begin?
What hormone is released? What does this cause? |
When fat enters the duodenum
Release of CCK 1. Contraction of gall bladder 2. Relaxation of sphincter of Oddi **concentrated bile flows into duodenum |
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21. What does high plasma bile salt concentrations cause?
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1. Release of preformed bile (positive feedback)
2. Inhibition of de novo bile secretion ***Turn off de novo synthesis of bile and stimulation of increased hepatocyte re-uptake of preformed bile |
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22. When does bile secretion cease?
What happens as a result? Where is the bile directed? How is the bile between meals? |
Bile secretion ceases when stimuli for CCK release are absent
**lipid has been digested and absorbed 1. Gall bladder relaxes 2. Sphincter closes Directed into gall bladder Is concentrated but remains isosmotic |
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23. What does low plasma bile salt concentration do?
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Inhibits secretion of preformed bile but stimulates secretion of de novo bile
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24. What are the three phases of bile and pancreatic secretion?
What is the stimulus for each |
1. Cephalic phase
-anticipation, aroma, taste of food (5% to 10%) 2. Gastric phase -distension of stomach (10% to 20%) 3. Intestinal phase -distension fat, acid, hyperosmolarity in proximal bowel (70% to 85%) |
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25. What stimulates the intestinal phase of bile and pancreatic secretion?
How is the emptying of the gall bladder during this phase? How is the sphincter of Oddi? |
Stimulation by CCK
Strongest emptying of gall bladder Sphincter of Oddi is relaxed |
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26. What do the three phases of GI secretion assume?
What is cholelithiasis (stones) as result of? Where can they occur? |
Assume that the meal will be appetizing
**unappetizing and/or unknown foods do not initiate secretion A phenomenon of supersaturation Can occur in hepatic duct, gall bladder (most common) and/or common bile duct |
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27. What is the primary problem from cholelithiasis?
What happens if the stone also blocks the pancreatic duct? |
Primary problem is impaired fat soluble vitamin absorption
Acute pancreatitis develops w/ attendent malabsorptive syndrome |
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28. Where can stones form in the biliary tract?
Five places |
1. Seed crystals can form in hepatic ducts forming stones
2. Small stones in hepatic duct (rare) 3. Stone blocking cystic duct (gall stones) 4. Stones in common bile duct 5. Stones blocking both common bile duct and pancreatic duct **may lead to pancreatitis |
