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Phys4 GI Lect7

Phys4 GI secretions: Pancreas, liver, Gallbladder

What cell is responsible for secreting all the digestive enzymes from the pancreas? Acinar cells.
What do Pancreatic ductal and centroacinar cells secrete 1.Na+. 2.HCO3- (neutralizes the lumen and optimizes digestion)
What are the 4 main types of digestive enzymes the pancreatic acinar cell releases? 1.Amylase. 2.Lipase. 3.Proteases. 4.Nucleases.
Secretory process from acinar cells 1.uptake of aa's. 2.Rough ER. 3.Golgi (segregated by lysosomal enzymes). 4.Golgi vesicles (lowest pH). 5.Condensing Vacuoles. 6.Secretory/zymogen granules. 7.wait at apical mem for stimulus. 8.Exocytosis in response to signal**
What is the only step of the acinar cell secretion that requires a stimulus? Secretion of secretory/zymogen granules from the apical membrane of the acinar cells.
Final destination of HCO3- and H+ produced by CA in Pancreatic ductal cell? 1.HCO3: Lumen. 2.H+: Blood.
How is HCO3- secreted from the pancreatic ductal cell? Cl-/HCO3- exchanger on the apical membrane. **Not enough Cl- can create digestive problems b/c HCO3- wont be readily secreted into the pancreatic duct.
How does Cl- get back across the apical membrane to continue to drive the Cl-/HCO3- exchanger? CFTR channels on the apical membrane. **ACh and Secretin activate these channels.
How does HCO3- enter the ductal cell so it can be secreted via Cl-/HCO3- exchanger? Na/HCO3 Symporter on basolateral membrane. **Activated by Secretin. Over 90% of HCO3- in pancreatic juice is derived from the plasma
Acidic Tide Created by the active pancreatic ductal cells when they secrete a lot of HCO3-, a lot of H+ is reabsorbed back across basolateral mem into BL via: 1.Na/H+ exchanger. 2.H+ channels
What is HCOs- secretion from the ductal cells dependent on? lumenal Cl-. **The Cl/HCO exch creates a neg cell which pulls Na (via Na/HCO symport & Na/H exch) and water into the cell.
What channel is mutated in Cystic Fibrosis? What does this cause? CFTR channel causes: 1.Dec HCO and water secretion. 2.Thickened secretions. 3.Obstructed lumen. 4.ducts fill with fibrotic tissue. 5.Tissue is destroyed. **children used to die from malnutrition.
3 primary controllers of Pancreatic secretions 1.Vagovagal reflex. 2.Secretin. 3.CCk.
Cephalic phase of pancreatic secretion Vagus N secrets ACh onto pancreatic acinar and ductal cells: 1.Enzyme secretion from acinar cells. 2.HCO3- AND secretin secretion from ductal cells.
Gastric phase of pancreatic secretion Distention triggers: 1.vago-vagal reflex (via fat & protein) causes ductal & acinar secretion, 2.CCK (via Fat & Protein) cuases ductal & acinar secretion, 3.Secretin (via H+) causes ductal secretion.
In the pancreas, does CCK work directly through a CCK receptor on the ductal and acinar cells? NO, instead it works by eliciting a vago-vagal reflex
Potential agents working to turn off pancreatic secretions 1.Pancreatic polypeptide. 2.Peptide YY. 3.Somatostatin. 4.Glucagon. 5.Secretions dec several hours after max stimulation.
Clinical complications of absence of pancreatic digestive enzymes? 1.Problem with digestion (although you can lose up to 90% of pancreas and still be healthy). 2.Lipases most susceptable to insult (will see fat in stool: Stiatorrhea)
Clinical complications of absence of Cl- channels in ductal cells? 1.Not proper HCO3- secretions. 2.Denatured enzymes due to acidic environment.
Clinical complications of autodigestion (acute pancreatitis) Inflammation & autodigestion caused by alcohol, toxins, trauma, viral, gall stones. **leads to premature activation of proteolytic enzymes
7 Important functions of the liver 1.Digestive function: produce bile. 2.Carb, lipid, aa metabolism. 3.synthesis of non-essential aa's. 4.synthesis of plasma proteins. 5.Degradation of drugs/toxins. 6.Excretion of Bilirubin. 7.Storage of iron, vitB12, vitA, vitD
Contents within Bile 1.Bile salts (primary & secondary). 2.Phospholipids. 3.Cholesterol. 4.HCO3- and H2O. 5.Bile pigments (bilirubin). 6.Inorganics
Enterohepatic recirculation 80% of bile acids are reabsorbed from the intestine. **Recirculate 5-20X per day.
Synthesis of Primary Bile acids Synthesized in the liver from cholesterol and conjugated with: 1.Glycine. 2.Taurine. **Conjugation makes them ionized at intestinal pH which makes them more WATER soluble.
Syntheis of Secondary Bile acids Primary bile acids get dehydroxylated in the intestine by bacteria which creates secondary acids. They can also be conjugated with glycine or taurine. **dehydroxylation makes them more LIPID soluble.
What is a major pathway of cholesterol ELIMINATION in the body? Bile salt production in the liver.
Difference b/w a Simple Vs Mixed Micelle? 1.Simple: amphiphatic bile salts aggregated into micelle with no inside contents. 2.Mixed: amphiphatic bile salts aggregated into micelle with cargo in the center (fat, digestive products).
Function of Micelles Tuck lipid digestion products into their interior and deliver them across the water layer at the epithelial cell so they can be absorbed.
Critical Miceller Concentration The concentration of lumenal bile salts required for the bile salts aggregate into micelles. **Conjugated salts have lower CMC than unconjugated salts.
What type of bile acids are passively reabsorbed all along intestine? DEconjugated and DEhydroxylated bile acids (ie secondary unconjugated). **Bacteria dehydroxylates and deconjugates.
What type of bile acids are ACTIVELY reabsorbed and where? Conjugated, hydrophilic bile acids in the Terminal Ileum. **these primary and secondary bile acids are reconjugated and resecreted in the liver along with those passively absrobed.
Can Increased bacteria in Jejunum affect lipid digestion? YES, excess bacteria will cause more dehydroxylation and deconjugation of bile acids which will then be passively reabsorbed instead of facilitating lipid digestion.
How is the rate of synthesis of NEW bile acids related to the return of bile acids from the portal circulation? INVERSELY RELATED.
how is the rate of bile acid secretion related to the return of bile acids by the portal circulation? DIRECTLY RELATED. **similar to positive feedback
____% of bile acids are returned to the liver via the portal circulation 90%
Clinical consequence of Ileal resection (in terms of bile acids)? Inc dumping of bile acids into colon (dec cholesterol levels)
What happens to HCO3, Na, Cl, H2O in the common bile duct? HCO3 is SECRETED. Na, Cl, and H2O can be secreted or absrobed. **Net Secretion
what is the main stimulatory hormone of the ductal secretion/reabsorption process in the bile duct SECRETIN. **VIP and glucagons are also stimulatory, Somatostatin is Inh.
What happens to bile in the gallbladder? How? CONCENTRATION. The Isotonic reabsorption of H2O and HCO3- causes concentration of bile within the GB.
Causes of Increased Unconjugated/indirect bilirubin? 1.Impaired uptake by the liver. 2.Impaired conjugation. 3.Overproduction (RBC breakdown, lipolysis).
Causes of Increased conjugated/direct bilirubin? DEC excretion from the liver due to: 1.Bile duct obstruction. 2.Gall stones. 3.Tumors & scaring. 4.Inflammation.
Created by: WeeG



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