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Phys4 GI Lect7
Phys4 GI secretions: Pancreas, liver, Gallbladder
| Question | Answer |
|---|---|
| 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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