| Question |
Answer |
| Does osmolality increase or decrease with an increase in flow rate | increase |
| With a low flow rate do you have more or less time to modify slaiva | more |
| Which flow rate would give you the highest pH, high rate or low rate | high rate |
| Are both parasympathetic and sympathetic nervous systems used in the salivary secretion | Yes |
| What does aldosterone do to Na reabsorbtion and K secretion | increases both |
| What does ADH do to Na reabsorbtion | increases it |
| If you increase cell activity, what else will you accomplish | increaseing vasodilator metabolites |
| In the salivary duct, which ions or compounds are being absorbed into the duct | HCO3- and K+ |
| In the salivary duct, which ions are being reabsorbed into the interstitium | Na, H20 and Cl- |
| What nuerotransmitter does the sympathetic nervous system use to create salivary secretions | NE |
| What enzyme is released by ductal cells that eventually causes increased capillary permiability and vasodilation | Kallikrein |
| What is the main contributer to H+ concentration in the lumen of the stomach | Proton Pump |
| Does the proton pump require ATP | Yes |
| What is the ion exchanged with H+ in the proton pump | K (potassium) |
| The Cl that is excreted aling with the H+ originally comes from where | Interstitial Space |
| What is the mechanism that bring Cl into the parietal cell to be able to be excreted into the lumen | Cl/HCO3- exchanger |
| What is the shift of HCO3- from the partieal cell into the interstial space refered to as | Alkaline tide |
| Where does the H+ in the parietal cell come from | dissociation from H20 or H2CO3 |
| High secretory rate yeilds high or low amounts of K+ and Na+ | LOW |
| Which molecules act to stimulate the parietal cell in the direct pathway | ACh, gastrin, abd histimine |
| What molecules work to stimulate the parietal cell in the indirect pathway | ACh, gastrin, and histimine, but keep in mind the ECL cell is also stimulated so that it secretes histimine to activate the parietal cell |
| What are PPI's | Proton pump inhibitors. Work to limit acid sectretion in the stomach |
| What mechanisms/treatments are avaiable for hyperacidity | vagoitmy, antacids, PPI's, H2 blockers (zantec and tagament, |
| What is the main nerve in the cephalic phase | VAGUS VAGUS VAGUS |
| Name the four physiological events of cephalic phase | 1. Vagus stimulates parietal cell (ACh)2. Vagus stimulates G-cell (GRP) (stimulates ECL and parietal)3. Stimulates ECL cell (ACh)4. Stimulates D-Cell (ACh, inhibits somatostatin) |
| On what cell is there an inhibiting of an inhibitor | D-cell |
| What causes excretion of H+ by the parietal cell in the gastric phase | distention of food in the stomach, local and long relflexes, and finally stimulation of parietal cells |
| What percent of acid secretion does the gastric phase account for | 50-60% |
| What stimulates the release of H+ from parietal cells in the intestinal cell | Protein digestion prducts, entero-oxyntin, absorbed amino acids and gastrin |
| What percent of H+ secretion does the intestinal phase make up | 5-10% |
| What does somatostatin inhibit | G-cells and parietal cells |
| What stimulates secretin | acid |
| Fatty acids cause the release of what protein that acts to inhibit g-cells and parietal cells | GIP |
| How else do fatty acids work to inhibit the parietal cell | through local relexes |
| Name two other minor inhibitors of parietal cell | CCK and PGE2 |
| What causes pesinogen to be converted to pepsin | H+ or acid |
| High levels of what can inhibit Gastrin | Acid |
| What is PUD | peptic ulcer disease, defined as a break in the mucosal surface >5mm |
| What are the two functions of the mucosal layer in the stomach | 1. Diffusion barrier for H+2. Traps HCO3- |
| An inflammatory response in the stomach may be caused by what | H+ leaking through the mucosal layer and cause the release of histimine |
| How does H. Pylori produce an inflammation in the stomach | Inhibits somatostatin and makes excess NH4 |
| Intrinsic factor is essential for the uptake of what vitamin | B12 |
| What is the only essential secretion of the stomach | IF (intrinsic factor) |
| Acinar cells secrete what | pancreatic enzymes |
| What are the four general types of enzymes | Amylases, lipases, proteases, nucleases |
| What do ductal and centroacinar cells secrete | Na+ and HCO3- |
| In the pancreatic ductal cell, what is the main exchanger used to move HCO3- into the lumen | HCO3-/Cl- exchanger |
| Where is 90% of the HCO3- in the pancreatic juice coming from | plasma |
| How is cAMP linked to secretin | Secretin activates adenylate cyclase, which releaes cAMP. This causes PKA to phosphorylate CFTR channels and release Cl- into the lumen |
| In the pancreas, H+ is moved from the ductal cell to the blood by what mechanism | Na+/H+ exchanger |
| In the pancreas, the flood of H+ into the blood is called what? | Acid tide |
| What pulls Na+ through tight junctions in the pancreatic ductal cells | negative lumen |
| What does the rate of HCO3- depend on | The availability of luminal Cl- |
| What follows as Na+ moves down its gradient | H20 |
| The faliure of the CFTR channel to function results in what occuring | The lack of Na+ being pulled into the lumen and thus a lack of H20. This causes thick secretiosn which become stuck in the lungs and unabel to be moved out |
| Pancreatic secretion has an osmolality similar to what | plasma |
| What are the three controllers fo pancreatic secretion | CCK, secretin, and vagovagal reflexes |
| What effect does the sympathetic nervous system have on pancreatic secretion | None or inhibitory |
| What neurotranmitter is used to cause secretions from the ductal and acinar cells | ACh |
| In what phase does distention cause vagovagal reflexes to occur | Gastric |
| What are the three main "actors" in the intestinal phase | CCK, Vagus, and secretin |
| What action does CCK have in the intestinal phase | causes secretions from the ductal and acinar cells |
| which two cell types will secretin inhibit | G-cells and Parietal cells |
| During the intestinal phase, the products from protein and lipid breakdown do what | stimulate a vagovagal relfex to trigger acinar cells to secrete |
| An absence of Cl- exchanger channels on the apical side of the ductal cell will result in a loss of secretion of what | HCO3- |
| Where are primary bile acids made | Liver |
| What process takes place to change primary bile acids to secondary bile acids | dehydroxylation (makes bile acids more soluable) |
| synthesis of bile acids help to rid what compound from the body | cholesterol |
| At the pH of the intestines, are conjugated bile acids water or fat soluable | water |
| What structures do bile acids form around fats | micelles |
| if you have a large return of bile acids to the liver, does the rate of synthesis increase, decrease or stay the same | decreases |
| Deconjugated/dehydroxylated bile salts are absorbed actively or passively | passivley |
| Which type of bile acid is absorbed actively | conjugated or more hydrophilic ones |
| What percentage of bile salts are returned to the liver | 90% |
| If you increase the rate of return of bile salts to the liver, does the rate of release of secretin increase, decrease or stay the same | increase |
| While HCO3- is being secreted, which ions/electrolytes are being absorbed and secreted | Na+, Cl- and H20 |
| Does billirubin become conugated or uncojugated in the liver | conjugated |
| Is conugated billirubin direct or indirect | direct |
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