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This study guide provides comprehensive questions and answers related to gastrointestinal (gi) physiology, focusing on gastric function, acid secretion, and digestive processes. It covers topics such as gastrin's role, somatostatin's mechanism, atropine's effects, and the factors influencing gastric emptying. The guide also addresses saliva composition, mmc patterns, esophageal peristalsis, and various reflexes like the gastroileal reflex. Additionally, it explains absorption mechanisms for glucose and fructose, the function of m cells in peyer's patches, and the role of peptide yy in regulating intestinal motility. Designed to help students understand the complex interactions within the gi system and prepare for exams. (415 characters)
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What gastrin does besides acid secretion -- Answer โโ Besides acid secretion, gastrin relaxes the ileocecal sphincter, increases pyloric sphincter tone, and reduces gastric emptying by lowering stomach motility. Somatostatin function, mechanism of action (GPCR), difference between SST from antral D cells vs. from corpus D cells -- Answer โโ Somatostatin is secreted from D cells in response to antral acidification, and it inhibits further acid and gastrin release. To do this, it binds to an inhibitory GPCR on the basolateral membrane of the parietal cell and inhibits adenylyl cyclase to functionally antagonize histamine's stimulatory effect and lead to a decrease in acid secretion. SST in corpus D cells adjacent to parietal and ECL cells has paracrine action on these parietal and ECL cells to decrease acid secretion and histamine release. SST in antral D cells has endocrine action on corpus parietal cells to inhibit acid secretion and paracrine action on neighboring G cells to inhibit gastrin secretion. How atropine affects gastric acid secretion -- Answer โโ Atropine blocks the M muscarinic AChR on parietal cells, and can reduce acid secretion that is done in this manner. Atropine does not affect G cell secretion of gastrin or ECL cell secretion of histamine, so these mechanisms can still function to secrete gastrin and acid. Events that increase acid secretion due to vagal stimulation -- Answer โโ Vagal postganglionic nerves in the corpus release ACh, which acts on mAChRs and directly stimulates secretion of acid. ACh also triggers histamine release from ECL cells to stimulate acid secretion. Peptidergic postganglionic vagal neurons and other enteric neurons release GRP, which stimulates gastrin release and will ultimately result in acid
secretion. The vagus nerve also inhibits SST release from D cells to reduce any background inhibition of gastrin release in the corpus or antrum. Why the stomach pH needs to drop after a meal -- Answer โโ When a meal is ingested, the stomach pH must drop because pepsinogens are only activated when the pH falls below 3. The pH drop activates pepsin and also ensures that any bacteria that may have been consumed are not able to survive in the stomach. How H2 blockers work -- Answer โโ H2 blockers attenuate the secretory responses to both ACh and gastrin by blocking the H2 receptor on the basolateral membrane of the parietal cell. This reduces acid secretion by this mechanism, but does not have a specific effect on the direct activity of gastrin or ACh on acid secretion. What the salivary ductal cells absorb and secrete -- Answer โโ The salivary ductal cells actively absorb Na+, passively absorb Cl-, actively secrete K+, and also secrete HCO3-. Hypergastrinemia from long-term acid suppression -- Answer โโ Hypergastrinemia can result from long-term suppression of acid secretion. Gastrin is normally inhibited by the presence of acid in the antrum, so when acid secretion is continually suppressed, serum gastrin will be chronically high to continue trying to stimulate acid secretion. The negative feedback mechanism is not working properly in this situation to stop gastrin secretion. Function of calocrine -- Answer โโ Calocrine is secreted from salivary glands, and it produces bradykinin, which is a vasodilator that increases salivary secretion rates. How saliva tonicity and K+ concentration compares to plasma -- Answer โโ Saliva is always hypotonic to plasma and salivary K+ concentration is always greater than plasma K+ concentration. MMC definition and function -- Answer โโ MMCs are rhythmic changes in motor and electrical activity of the SI that occur during the interdigestive phase. Their function is to sweep undigested contents toward the colon for excretion, with the goal of decreasing bacteria in the small intestine.
pressure at the LES is also low to prepare for arrival of the food bolus and movement into the stomach. Pressure in the esophagus between swallows -- Answer โโ In between swallows, UES pressure is high to contract the sphincter and prevent air from entering the esophagus. LES pressure is also high to prevent reflux of stomach contents. Muscle contraction pattern during swallowing -- Answer โโ During swallowing, the soft palate is pulled upwards to cover the nares and make sure no food gets into the nasal cavities. The larynx is also pulled upwards to move the epiglottis so food can get into the esophagus and does not get into the trachea. The UES relaxes and the pharyngeal muscles contract to move the food to the proximal esophagus from the mouth. Dumping syndrome -- Answer โโ Dumping syndrome is a rapid gastric emptying disorder that occurs when ingested substances (i.e. refined sugars) enter the intestine too quickly to be properly digested and absorbed. The nutrients will remain in the intestine and water will follow, leading to diarrhea. Intrinsic defecation reflex -- Answer โโ The intrinsic defecation reflex promotes contraction in the descending and sigmoid colon to push stool toward the anus. When stool distends the rectum, rectal smooth muscle contracts and IAS relaxes. If the EAS has been voluntarily relaxed, defecation will occur. This reflex is mediated by the enteric NS, specifically the myenteric plexus, except for the voluntary EAS relaxation. CCK secretion and gastric emptying -- Answer โโ CCK secretion will increase gastric distensibility (storage function) and decrease gastric emptying. Gastroileal reflex -- Answer โโ The gastroileal reflex promotes distal intestine motility to clear the distal intestine as a new meal is being ingested and is stretching the stomach. The ileocecal sphincter relaxes and ileal peristalsis increases to get the intestine cleared and ready for the incoming meal. SGLT1 mechanism, what would happen to glucose absorption if the Na+/K+ pump was inhibited, requirements for binding to SGLT1, and why SGLT1 cannot absorb fructose -- Answer โโ In SGLT1, Na+ moves down its electrochemical gradient into the cell, and
glucose is pulled into the cell with the Na+ against its gradient. The energy to move glucose against its gradient comes from the Na+/K+ pump. If the Na+/K+ pump was inhibited, there would be decreased glucose absorption because the loss of pump activity means loss of power to fuel glucose movement against its gradient. To bind to SGLT1, the hexose sugar must be in the D-conformation, and it must be a 6-membered pyranose ring. SGLT1 cannot absorb fructose because fructose has a 5-membered ring. Hormones secreted in response to luminal fat -- Answer โโ When there is fat present in the intestinal lumen, CCK is secreted from the duodenum and peptide YY is secreted from the ileum and proximal colon. Mechanism of fructose absorption -- Answer โโ Fructose is absorbed through facilitated diffusion via GLUT-5. M cells in Peyer's patches -- Answer โโ M cells in Peyer's patches of the lymphoid follicles in the lamina propria of the submucosa work to package whole proteins in clathrin-coated vesicles. The vesicles are secreted across the basolateral membrane into the lamina propria, where immunocompetent cells can process the protein antigens to initiate immune responses in the body. Peptide YY function (ileal brake) -- Answer โโ When there are fats in the intestinal lumen, peptide YY secretion exerts a feedback mechanism to slow gastric emptying, reduce food intake, and slow intestinal motility, which allows more time for fatty acids to be digested and absorbed, so there are not excess amounts being excreted in the stool. This is the ileal brake phenomenon. Lipid assimilation if there is a deficiency of pancreatic enzymes -- Answer โโ If there is a deficiency of pancreatic enzymes (i.e. lipase), then gastric lipase will continue to be active once the chyme has reached the duodenum, which will partially alleviate the malabsorption of fat due to the lack of pancreatic lipase. Endopeptidases and the residues they cleave -- Answer โโ Trypsin cleaves basic amino acid residues. Chymotrypsin cleaves aromatic amino acid residues. Elastase cleaves neutral amino acid residues.
transepithelial voltage of the enterocyte due to loss of the Na+ (cations) from the lumen of the enterocyte. Function of Paneth cells -- Answer โโ Paneth cells sense the presence of bacteria in the SI and trigger an antimicrobial response that limits the ability of the bacteria to penetrate the SI mucosa and enter the body. Ions that the SI has net absorption and secretion of -- Answer โโ The SI has net absorption of Na+, Cl-, K+, and water, and a net secretion of HCO3-. GPCR mechanism of action for cholera toxin -- Answer โโ The cholera toxin interferes with the G-alpha-s subunit's ability to hydrolyze GTP and inactivate itself, so you end up with chronically high adenylyl cyclase activity and high intracellular cAMP levels. Enzyme that B12 is a cofactor for -- Answer โโ B12 is a cofactor for the homocysteine:methionine methyltransferase, which takes a methyl group from tetrahydrofolate and transfers it to homocysteine to create methionine. How Na+ is extruded across the enterocyte basolateral membrane into the blood -- Answer โโ Na+ is extruded across the basolateral membrane of the enterocyte and into the blood via the Na+/K+ pump. Tonicity of chyme as it leaves the duodenum and what would happen if it was different -
How rotavirus causes diarrhea (secretory and osmotic) -- Answer โโ Rotavirus stimulates the enteric NS and triggers an increase in intracellular Ca2+, which activates Cl- channels to secrete Cl- into the gut lumen, and water will follow the Cl-. This is secretory diarrhea. Rotavirus damages the enterocytes, which disrupts SGLT1 and disaccharidase enzyme function, so nutrient absorption is decreased and the presence of the nutrients in the gut lumen draws water into the lumen as well. This is osmotic diarrhea. How electrogenic Na+ absorption occurs in the distal colon -- Answer โโ Electrogenic Na+ absorption in the distal colon occurs via epithelial Na+ channels. Effect of chronically high cAMP in cholera -- Answer โโ In cholera, the chronically elevated levels of cAMP acts on the apical CTFR Cl- channel to increase secretion of Cl- into the gut lumen. Secretion and paracellular movement of Na+ and water will follow Cl- into the gut lumen, and this will overwhelm any absorptive mechanisms in the gut, leading to secretory diarrhea. How K+ is secreted in the colon -- Answer โโ K+ is secreted in the colon in two possible ways. There can be passive paracellular K+ movement across tight junctions, and this is driven by negative luminal voltage. There can also be active secretion of K+ when aldosterone or cAMP are present. How K+ is absorbed in the colon -- Answer โโ In the colon, K+ is actively absorbed when there is depleted dietary K+, and this is mediated by the colonic H+/K+ pump. K+ will be taken up across the enterocyte apical membrane and then leave on the basolateral side to go into the blood. Difference between monophasic and biphasic secretion. -- Answer โโ Monophasic secretion reaches a maximum point and does not decrease from there, so any increases in secretagogue concentration does not affect the hormone secretion once the maximum has been reached. Amylase is secreted in this manner. Biphasic secretion can reach a maximum point, and then will taper off after that, even if secretagogue concentration is increased. CCK is secreted in this manner.
How ACh potentiates the actions of secretin -- Answer โโ ACh potentiates the actions of secretin by increasing intracellular Ca2+, which activates kinases that directly activate the Cl-/HCO3- exchanger to increase bicarbonate secretion into the gut lumen. How bilirubin is excreted -- Answer โโ In the intestine, half of the conjugated bilirubin is converted to soluble urobilinogen. Most urobilinogen that is re-absorbed in the intestine is recycled to the liver and then re-excreted back into the gut. Urobilinogen can be oxidized to urobilin, which is excreted in the urine. Urobilinogen can also be oxidized to stercobilin, which is excreted in the stool. Difference between the CCK-A and CCK-B receptors -- Answer โโ The CCK-A receptor has a higher affinity for CCK than gastrin. The CCK-B receptor has an equal affinity for CCK and gastrin. How CCK receptors and mAChRs mediate acinar secretions -- Answer โโ CCK receptors and mAChRs mediate pancreatic acinar secretions via a G-alpha-q cascade, which uses phospholipase C to increase intracellular Ca2+ and trigger enzyme secretion. How VIP secretion affects pancreatic secretions -- Answer โโ When VIP and CCK are secreted together, the overall rate of pancreatic secretion will be greater compared to when only CCK is secreted. How salivary flow rate affects ionic composition and HCO3- concentration -- Answer โโ As salivary flow rate increases, the ions in the saliva will approach their plasma values, meaning that the osmolarity of the saliva will increase. Increased salivary flow rate will also increase the concentration of HCO3- in the saliva, and this alkalinizes the saliva to help neutralize gastric acid that would normally reflux into the esophagus. Different GPCR responses between gastrin/ACh and histamine -- Answer โโ When gastrin and ACh bind their receptors on parietal cells, they initiate a GPCR response through a G-alpha-q cascade, resulting in elevated intracellular Ca2+ and activation of kinases to stimulate acid secretion.
When histamine binds its receptor on parietal cells, it initiates a GPCR response through a G-alpha-s cascade, which activates adenylyl cyclase to increase intracellular cAMP, which stimulates PKA to phosphorylate the H+/K+ pump to cause acid secretion. Transport of K+, H+, HCO3-, and Cl- in parietal cells -- Answer โโ When H+ and HCO3- are produced from H2O and CO2 via carbonic anhydrase, the H+ goes to the canalicular lumen of the parietal cell in exchange for K+ leaving to the interstitial fluid using the H+/K+ pump. HCO3- leaves the parietal cell and goes to the interstitial fluid in exchange for Cl-, which is secreted into the canalicular lumen of the parietal cell. This results in net accumulation of HCl within the parietal cell, decreasing the pH.