this unit reviewed some basic concepts about fat digestion and went into some more depth about the anatomy and physiology of the liver and gall bladder. the liver is located in the upper right quadrant of the abdomen, deep to the 5-10th ribs. it is suspended by the lesser omentum ligament, which attaches it to the intestine and the stomach, and the falciform ligament, which attaches it to the anterior of the abdominal wall. it has four lobes- left, right, quadrate, and caudate. the ligamentum teres (round ligament) is the vestigial remains of the umbilical vein that brought blood from the placenta. finally, the porta hepatis is the "hilum" or root of the liver (similar to the hilum of the lung) and contains the bile duct, hepatic portal vein and hepatic artery.
the liver receives nutrient rich and oxygen poor blood from the GI tract- specifically the gastric, splenic, and mesenteric arteries, which comes into the liver via the hepatic portal vein. it receives nutrient poor, oxygenated blood from the hepatic artery which branches off of the celiac artery. the liver cells, hepatocytes, are in hexagonal arrangements which have portal "triads" in each corner which contain bile ducts, hepatic portal veins, and hepatic arteries. in the center of the hexagons is the central vein, which leads to the hepatic vein, which leads to the inferior vena cava back to the heart. running from the edges of the hexagonal "lobule" are the sinuosoids where most of the functional activity of the liver takes place. the liver acinus theory describes the functional unit of the liver as the triangle between two portal triad corners and a central vein-- which is divided into three zones: zone 1 is closest to the central vein and although has lowest oxygen / nutrient content, is the site of most detoxification and chemical activity.
portal hypertension can occur from blockages in liver blood flow, resulting in a backpressure in portal circulation. this can cause a number of pathologies such as caput medusa, esophageal varicosities, and hemorrhoids. additionally, excess lymph can be drained from the liver (lymph drains into the space of disse, the tiny canals between the hepatocytes and sinusoids) and can collect in the peritoneal cavity, resulting in ascites. in this condition, the loss of fluid in the circulatory system must be compensated by renal devices which increase fluid retention such as aldosterone and renin secretion.
bile is secreted by hepatocytes and flows to the periphery of the hexogonal lobule, draining into the bile ducts, which drain into the right and left hepatic ducts. these combine to form the common hepatic duct, which combines with the bile duct from the gall bladder, called the cystic duct, to form the common bile duct. the common bile duct intersects with the main pancreatic duct at the hepatopancreatic ampulla and exits into the duodenum at the major duodenal papilla. the tissue around this point forms a sphincter called the sphincter of odie which contracts between meals or during fasting, which causes bile to stored in the gall bladder instead of being released into the duodenum.
bile stored in the gall bladder is made of bile salts, cholesterol, phospholipids, water, and can be concentrated over time via water reabsorption, or secretion of bile salts and cholesterol. if the bile becomes too concentrated in the gall bladder, over long periods of time with no contraction, then gall stones can precipitate out. in normal function, CCK and secretin are released from duodenal I and S cells, respectively, in response to protein, fat, or acid in the intestine (see "intestinal phase" in last lecture), causing an increase in pancreatic secretion, decrease in gastric secretion/motility, and bile release from gall bladder via contraction of the gall bladder and relaxation of the sphincter of odie. vagal stimulation can have the same effect. once in the intestine, bile surrounds fat molecules and aids in their absorption. the chapter in biochem covers this in much greater detail than what was presented in this lecture.
questions
location and anatomy...
1. where is the liver located?
2. what are the two ligaments that suspend the liver and where are they?
3. what are the lobes of the liver?
4. what is the ligamentum teres of the liver?
5. what is the porta hepatis?
physiology...
6. what are some of the functions of the liver?
7. how much blood does the liver receive (in terms of percentage of cardiac output)?
8. how does the liver get its oxygenated blood?
9. what does the portal vein bring to the liver? where does it bring it from?
10. what are sinusoids lined with?
11. what do the hepatic veins do?
lobules...
12. what is the classical lobule model of the liver?
13. what are the portal triads and what do they contain?
14. what is in the middle of the classical lobule?
15. what is the liver acinus model of the liver?
16. what are the three zones in the liver acinus model?
17. which zone is most susceptible to hypoxia and toxic damage?
hypertension and other pathologies...
18. where are the spaces of disse? what flows in them?
19. what is meant by "portal hypertension"?
20. what are some pathologies that portal hypertension can contribute to?
21. what is ascites?
22. how does ascites affect blood pressure?
bile secretion...
23. describe bile secretion by hepatocytes.
24. what are bile secretions made of?
25. what do the right and left hepatic ducts do?
26. ...common hepatic duct?
27. ...cystic duct
28. ...common bile duct
29. ...hepatopancreatic ampulla
30. ...main pancreatic duct
31. ...major duodenal papilla
gall bladder...
32. what are the three parts to the gall bladder?
33. what are three functions of the gall bladder?
34. how does the sphincter of oddi help store bile in the gall bladder?
35. describe two ways in which bile can be released by the gall bladder.
36. besides gall bladder emptying, what else does CCK mediate?
37. what effect does secretin have on the gall bladder and pancreas?
38. how are gallstones created?
39. what are two functions of bile?
micelles...
40. what is the general scheme for fat digestion?
41. about how big are micelles?
42. what pH is optimal for the action of pancreatic lipase?
43. which enzyme hydrolyzes cholesterol?
44. what are micelles made of?
45. how are bile salts formed?
46. what happens to the micelle contents at the enterocyte?
47. where does most of the reabsorption of bile acids and salts occur in the intestine?
chylomicrons and lipoproteins...
48. what are chylomicrons composed of?
49. 80-90% of chylomicrons are transported into...
50. how is the processing of short and medium chain fatty acids different?
51. what are the roles of: chylomicrons, VLDL, LDL, and HDL?
52. what makes feces brown and urine yellow?
53. jaundice is caused by...
answers
1. upper right abdomen between ribs 5-10.
2. lesser omentum between liver and stomach/intestine, falciform ligament between liver and anterior abdominal wall.
3. left, right, quadrate, caudate.
4. the round ligament, which is a vestigal remains of the umbilical vein carrying blood from the placenta to the fetus.
5. the "hilum" of the liver that contains bile ducts, hepatic arteries, and portal vein.
6. glycogen storage, gluconeogenesis, synthesis of TG's, cholesterol, phospholipids, fatty acid oxidation, protein synthesis, urea cycle, storage of vitamins and iron, detoxification, bile secretion.
7. 29%
8. via the celiac artery which branches off of the aorta
9. nutrient filled, deoxygenated blood from the gastric, splenic, and mesenteric veins.
10. hepatocytes
11. bring blood out of the superior aspect of the liver into the inferior vena cava.
12. divides hepatocytes into hexagonal "lobule" arrangements.
13. the corners of the hexagon in the classical lobule which contain the bile duct, hepatic artery and portal vein.
14. the central vein, which leads to the hepatic vein.
15. a model which has a functional "acinus" unit which is the triangle between two portal triads and a central vein.
16. zone 1 is closest to the portal triads and has the highest concentration of oxygen and nutrients. zone 2 is in the middle, zone 3 is closest to central vein and receives least nutrients but is primary site of alcohol and drug detoxification.
17. zone 3.
18. between hepatocytes and endothelium of sinusoids. lymph flows from sinusoids into space of disse, and sent to thoracic duct or inferior vena cava.
19. when a blockage of blood flow in the liver leads to backpressure in the portal circulation.
20. hemorrhoids, caput medusae, esophageal varicosities.
21. when portal hypertension causes excess lymph to flow in the space of disse, causing buildup of fluid in the peritoneal cavity.
22. since blood volume is lost to the lymph fluid that is trapped in the peritoneal cavity, blood pressure drops and the kidneys compensate by increasing salt and fluid retention until pressure is restored.
23. bile is secreted by hepatocytes and flows to the periphery of the portal lobules.
24. bile acids, phospholipids, cholesterol, along with bicarbonate and bile pigments (bilirubin)
25. bile outflow from the liver
26. junction between right and left hepatic ducts.
27. outflow from gall bladder.
28. outflow of bile from both gall bladder and liver.
29. junction of bile and pancreatic ducts.
30. outflow from pancreas.
31. bile and pancreatic secretion into duodenum.
32. body, neck, fundus.
33. store bile, concentrate bile, release bile into duodenum.
34. by contracting between meals, it allows backflow of bile from common bile duct into cystic duct into gall bladder.
35. CCK release triggered by fat or protein reach chyme entering the duodenum causes the sphincter of oddi to relax and the gall bladder to contract. vagus nerve stimulation has the same effect.
36. inhibits gastric mixing and secretion, stimulates intestinal mixing, stimulates pancreatic secretion.
37. increased water and bicarbonate secretion from duct cells.
38. either too much absorption of water (can be due to inflammation of epithelium), or high cholesterol content in stored bile (from too much absorption of bile salts, or too much secretion of cholesterol into bile)
39. to aid in fat digestion, and also elimination of various endogenous and exogenous substances such as cholesterol, bilirubin, drugs, heavy metals.
40. pancreatic lipase hydrolyzes triacylglycerides into free fatty acids, which are packaged into micelles via bile droplets. fatty acids are absorbed into enterocytes and bile is reabsorbed. fatty acids are reconverted to triacylglycerides, packaged into chylomicrons and transported in the blood.
41. ~1um
42. pH 8.
43. cholesterol esterase.
44. bile acids, phospholipids, cholesterol, and the fat that is trapped in the lipophilic core
45. bile acids are conjugated in the liver to form bile salts.
46. fatty acids are repackaged into triacylglycerol and cholesterol is esterified in the enterocyte, then packaged into a chylomicron in the ER.
47. the ileum.
48. cholesterol and triglycerides in a phospholipid shell with apoproteins.
49. lacteals and thoracic duct.
50. they are not packaged into chylomicrons and instead are transported directly into the venous system and stored in the liver and adipose.
51. chylomicrons transport fat from intestine into the blood. VLDL's transport triacylglycerides from the liver into the blood. LDL's are produced in plasma and trasnport cholesterol esters from liver to organs and tissues. HDL's are produced in plasma and transport cholesterol from peripheral tissues to the liver.
52. bilirubin is converted by colonic bacteria into urobilinogen, which can be excreted in the urine or converted to stercobilin and excreted in feces.
53. excess bilirubin
Showing posts with label digestion. Show all posts
Showing posts with label digestion. Show all posts
Thursday, March 5, 2009
Monday, March 2, 2009
organ systems: salivary and gastric secretion
this lecture covered the salivary and gastric enzymes; what they are, where they come from, what triggers and inhibits them. salivary glands and ducts have acinar cells and duct cells- acinar cells basically produce saliva, which contains a mixture of water, mucus, protective substances, and digestive enzymes. among the digestive enzymse are salivary alpha amylase (recall from carbohydrate digestion that this is the endoglucosidase that starts carbohydrate digestion), lingual lipase, mucins, and antimicrobial elements (such as lysozyme). duct cells regulate the electrolytic content of saliva, generally reabsorbing Na+ and Cl+ and secreting K+ and bicarbonate. the overall pH of saliva that is produced is 7.0, but can range from 6.5 to 8.0.
when these glands are innervated parasympathetically, they produce a watery saliva by three mechanisms: contraction of myoepithelial cells around acinar cells, vasodilation to increase blood supply, and augmentation of cell activity/division. the route for parasympethic innervation of the parotid gland begins at the inferior salivatory nucleus, then the glossopharyngeal nerve (CN IX), synapses at the otic ganglion, then follows the auriculotemporal nerve (recall from the face unit that this is part of the mandibular division of the trigeminal nerve) to the parotid. the sublingual and submandibular innervation starts at the superior salivatory nucleus, follows the facial nerve (CN XII), synapses at the submandibular ganglion, and follows the lingual nerve to the glands. sympathetic stimulation of the glands produce a more concentrated saliva- the sympathetic innervation begins at the nerves exiting the T1 level, which synapses at the superior cervical ganglion, and follows the arterial system to the salivary glands.
the gastric glands can be divided into two categories: oxyntic glands are in the fundus and body of the stomach and contain the H+ secreting parietal cells, histamine secreting enteroendocrine cells, pepsinogen secreting chief cells, and mucus cells (see more detailed descriptions at the histology lecture from last semester). pyloric glands are in the pylorus of the stomach and contain mucus cells and gastrin secreting G cells. parietal cells are the pivotal cells which secrete the H+ which lowers the pH of the stomach. the mechanism for H+ secretion is by production of carbonic acid via carbonic anhydrase, followed by dissociation into bicarbonate and H+, which is pumped into the duct lumen by a H+/K+ ATPase pump. parietal cell secretion of H+ can be stimulated by: acetylcholine/vagal nerve stimulation, gastrin, and histamine. it can also be inhibited by GIP, and factors that decrease gastrin secretion by G cells- namely, somatostatin and secretin.
the process of gastric secretion can be divided into three phases: cephalic, gastric, intestinal. cephalic is initiated by thoughts or sensation of food and causes the limbic system to activate the vagal nerve, which stimulates acid production by parietal cells and gastrin production by G cells. the gastric phase is initiated by gastric distention, or presence of amino acids, caffiene, or calcium, and also causes acid / gastrin secretion. the intestinal phase is triggered by amino acids in the duodenum, triggering gastrin release from duodenal G cells and thereby stimulating acid production.
questions
salivary glands and secretions...
1. what are the 4 types of salivary glands in the mouth?
2. where does the submandibular gland open up into?
3. what do acinar cells secrete?
4. what are the digestive enzymes that are secreted by the acinar cells?
5. how do duct cells affect salivary composition?
6. which ions are reabsorbed vs. secreted by the duct cells?
7. what is the range of salivary pH? what is the average pH?
innervation...
8. describe the parasympathetic route of innervation of the parotid gland.
9. describe the parasympathetic route of innervation of the submandibular and sublingual glands.
10. what are the three effects of parasympathetic stimulation of salivary glands?
11. what is the overall product of parasympathetic stimulation?
12. describe the sympathetic route of innervation of the salivary glands.
13. what is the product of sympathetic stimulation of the salivary glands?
14. what are some factors that increase salivation?
15. what are some factors that decrease salivation?
gastric glands and secretions...
16. what are the two types of glands / ducts in the stomach and where are they located?
17. what are the secretory cells in oxyntic glands and what do they secrete?
18. what are the secretory cells in the pyloric glands and what do they secrete?
19. describe the mechanism of parietal cell's secretion of H+.
20. what are some factors that stimulate parietal cell secretion of H+?
21. what is cimetidine and what cells does it affect?
three phases...
22. what happens in the cephalic phase and what is it initated by?
23. ...gastric phase?
24. ...intestinal phase?
other enzymes...
25. describe the activation and actions of pepsin.
26. what is the purpose of mucus and what is its secretion stimulated by?
27. what are three hormones that inhibit the release of H+ from gastric ducts?
28. describe the secretion and actions of somatostatin.
29. describe the secretion and actions of secretin.
30. describe the secretion and actions of GIP.
31. what are two examples of "positive feedback" of acid secretion?
32. what are two examples of "negative feedback" of acid secretion?
33. peptic ulcers are due to...
34. what happens when gastric acid enters the mucosal lining?
35. what is the role of Intrinsic Factor in digestion?
answers
1. parotid, submandibular, sublingual, palatine.
2. the sublingual papillae.
3. water, mucus, protective substances, digestive enzymes.
4. alpha-amylase, lingual lipase, mucins, lysozyme, calcium/phosphate/flouride (for teeth)
5. they regulate the electrolyte content of saliva.
6. sodium and chloride are reabsorbed and potassium and bicarbonate are secreted.
7. salivary is generally pH 7.0 but can range from 6.5 to 8.0.
8. begins in the inferior salivatory nucleus, glossopharyngeal nerve (CN IX), synapses at otic ganglion, auriculotemporal nerve to parotid.
9. begins in the superior salivatory nucleus, facial nerve (CN VII), synapses at submandibular ganglion, lingual nerve to submandibular and sublingual glands.
10. constriction of myoepithelial cells around acinar cells produces more saliva, vasodilation of nearby blood vessels increases blood supply, and augmentation of cell activity promotes growth and division.
11. produces a copious, watery saliva.
12. begins at the T1 level, synapses at the superior cervical ganglion, follows the arterial system to the salivary glands.
13. produces a enzyme rich saliva that is not very watery.
14. sensations or thoughts about food, and nausea to some extent (to neutralize upcoming vomit)
15. dehydration, negative emotions, sleep, fatigue.
16. oxyntic ducts are in the fundus and body of the stomach and pyloric ducts are in the pylorus of the stomach.
17. parietal cells secrete H+, chief cells secrete pepsinogen, enteroendocrine cells secrete histamine, mucus cells secrete mucus.
18. G cells secrete gastrin and mucus cells secrete mucus.
19. carbonic acid is created from intracellular CO2 via carbonic anhydrase, and dissociates into bicarbonate (which reenters the bloodstream) and H+, which is pumped out into the lumen of the gland by a H+ / K+ ATPase pump.
20. gastrin, acetylcholine (from vagal nerve stimulation), histamine.
21. a histamine blocker which blocks only the histamine receptors on parietal cells, not enterochromaffin like cells (a type of enteroendocrine cell that secretes histamine)
22. it is initated by thoughts or sensation of food (see question 14): the limbic system activates the vagal nerve, which stimulates the parietal cells to secrete more H+ and the G cells to secrete more gastrin.
23. gastric distention, presence of amino acids/peptides, caffiene, or calcium triggers the gastric phase- which also produces more H+ by parietal cells and gastrin by G cells.
24. amino acids/peptides in the duodenum triggers gastrin release from duodenal G cells.
25. pepsin is released from chief cells in the inactivate form, pepsinogen, which is auto cleaved at the low stomach pH. it cleaves proteins into smaller polypeptides.
26. to protect the gastric lining from digestion by acids, stimulated by vagus nerve, chemical stimulants (such as alcohol), and roughage.
27. somatostatin, secretin, GIP.
28. somatostatin is released from somatostatin cells in response to high acid levels in the stomach. somatostatin inhibits gastrin release from G cells, thereby reducing H+ levels.
29. secretin is released from duodenal secretin cells in resposne to high acid and fat levels in the stomach. secretin inhibits G cells gastrin release.
30. GIP is released from duodenal G cells in response to high acid and fat levels in the stomach. GIP directly inhibits parietal cells H+ release.
31. amino acids/peptides stimulating gastrin release, which stimulates acid secretion. vagus nerve stimulates acid secretion while inhibiting somatostatin release.
32. somatostatin inhibits gastrin release (see question 28), acid stimulates somatostatin release.
33. imbalance between aggressive digestive enzymes and protective factors such as mucus and bicarbonate.
34. inflammatory effects such as histamine release, edema, hemorrhage, leakage, etc.
35. it aids in vitamin B12 digestion: vitamin B12 is initially bound to dietary or gastric R proteins, then dissociated by pepsin and bound to intrinsic factor, which allows for its absorption into the ileum.
when these glands are innervated parasympathetically, they produce a watery saliva by three mechanisms: contraction of myoepithelial cells around acinar cells, vasodilation to increase blood supply, and augmentation of cell activity/division. the route for parasympethic innervation of the parotid gland begins at the inferior salivatory nucleus, then the glossopharyngeal nerve (CN IX), synapses at the otic ganglion, then follows the auriculotemporal nerve (recall from the face unit that this is part of the mandibular division of the trigeminal nerve) to the parotid. the sublingual and submandibular innervation starts at the superior salivatory nucleus, follows the facial nerve (CN XII), synapses at the submandibular ganglion, and follows the lingual nerve to the glands. sympathetic stimulation of the glands produce a more concentrated saliva- the sympathetic innervation begins at the nerves exiting the T1 level, which synapses at the superior cervical ganglion, and follows the arterial system to the salivary glands.
the gastric glands can be divided into two categories: oxyntic glands are in the fundus and body of the stomach and contain the H+ secreting parietal cells, histamine secreting enteroendocrine cells, pepsinogen secreting chief cells, and mucus cells (see more detailed descriptions at the histology lecture from last semester). pyloric glands are in the pylorus of the stomach and contain mucus cells and gastrin secreting G cells. parietal cells are the pivotal cells which secrete the H+ which lowers the pH of the stomach. the mechanism for H+ secretion is by production of carbonic acid via carbonic anhydrase, followed by dissociation into bicarbonate and H+, which is pumped into the duct lumen by a H+/K+ ATPase pump. parietal cell secretion of H+ can be stimulated by: acetylcholine/vagal nerve stimulation, gastrin, and histamine. it can also be inhibited by GIP, and factors that decrease gastrin secretion by G cells- namely, somatostatin and secretin.
the process of gastric secretion can be divided into three phases: cephalic, gastric, intestinal. cephalic is initiated by thoughts or sensation of food and causes the limbic system to activate the vagal nerve, which stimulates acid production by parietal cells and gastrin production by G cells. the gastric phase is initiated by gastric distention, or presence of amino acids, caffiene, or calcium, and also causes acid / gastrin secretion. the intestinal phase is triggered by amino acids in the duodenum, triggering gastrin release from duodenal G cells and thereby stimulating acid production.
questions
salivary glands and secretions...
1. what are the 4 types of salivary glands in the mouth?
2. where does the submandibular gland open up into?
3. what do acinar cells secrete?
4. what are the digestive enzymes that are secreted by the acinar cells?
5. how do duct cells affect salivary composition?
6. which ions are reabsorbed vs. secreted by the duct cells?
7. what is the range of salivary pH? what is the average pH?
innervation...
8. describe the parasympathetic route of innervation of the parotid gland.
9. describe the parasympathetic route of innervation of the submandibular and sublingual glands.
10. what are the three effects of parasympathetic stimulation of salivary glands?
11. what is the overall product of parasympathetic stimulation?
12. describe the sympathetic route of innervation of the salivary glands.
13. what is the product of sympathetic stimulation of the salivary glands?
14. what are some factors that increase salivation?
15. what are some factors that decrease salivation?
gastric glands and secretions...
16. what are the two types of glands / ducts in the stomach and where are they located?
17. what are the secretory cells in oxyntic glands and what do they secrete?
18. what are the secretory cells in the pyloric glands and what do they secrete?
19. describe the mechanism of parietal cell's secretion of H+.
20. what are some factors that stimulate parietal cell secretion of H+?
21. what is cimetidine and what cells does it affect?
three phases...
22. what happens in the cephalic phase and what is it initated by?
23. ...gastric phase?
24. ...intestinal phase?
other enzymes...
25. describe the activation and actions of pepsin.
26. what is the purpose of mucus and what is its secretion stimulated by?
27. what are three hormones that inhibit the release of H+ from gastric ducts?
28. describe the secretion and actions of somatostatin.
29. describe the secretion and actions of secretin.
30. describe the secretion and actions of GIP.
31. what are two examples of "positive feedback" of acid secretion?
32. what are two examples of "negative feedback" of acid secretion?
33. peptic ulcers are due to...
34. what happens when gastric acid enters the mucosal lining?
35. what is the role of Intrinsic Factor in digestion?
answers
1. parotid, submandibular, sublingual, palatine.
2. the sublingual papillae.
3. water, mucus, protective substances, digestive enzymes.
4. alpha-amylase, lingual lipase, mucins, lysozyme, calcium/phosphate/flouride (for teeth)
5. they regulate the electrolyte content of saliva.
6. sodium and chloride are reabsorbed and potassium and bicarbonate are secreted.
7. salivary is generally pH 7.0 but can range from 6.5 to 8.0.
8. begins in the inferior salivatory nucleus, glossopharyngeal nerve (CN IX), synapses at otic ganglion, auriculotemporal nerve to parotid.
9. begins in the superior salivatory nucleus, facial nerve (CN VII), synapses at submandibular ganglion, lingual nerve to submandibular and sublingual glands.
10. constriction of myoepithelial cells around acinar cells produces more saliva, vasodilation of nearby blood vessels increases blood supply, and augmentation of cell activity promotes growth and division.
11. produces a copious, watery saliva.
12. begins at the T1 level, synapses at the superior cervical ganglion, follows the arterial system to the salivary glands.
13. produces a enzyme rich saliva that is not very watery.
14. sensations or thoughts about food, and nausea to some extent (to neutralize upcoming vomit)
15. dehydration, negative emotions, sleep, fatigue.
16. oxyntic ducts are in the fundus and body of the stomach and pyloric ducts are in the pylorus of the stomach.
17. parietal cells secrete H+, chief cells secrete pepsinogen, enteroendocrine cells secrete histamine, mucus cells secrete mucus.
18. G cells secrete gastrin and mucus cells secrete mucus.
19. carbonic acid is created from intracellular CO2 via carbonic anhydrase, and dissociates into bicarbonate (which reenters the bloodstream) and H+, which is pumped out into the lumen of the gland by a H+ / K+ ATPase pump.
20. gastrin, acetylcholine (from vagal nerve stimulation), histamine.
21. a histamine blocker which blocks only the histamine receptors on parietal cells, not enterochromaffin like cells (a type of enteroendocrine cell that secretes histamine)
22. it is initated by thoughts or sensation of food (see question 14): the limbic system activates the vagal nerve, which stimulates the parietal cells to secrete more H+ and the G cells to secrete more gastrin.
23. gastric distention, presence of amino acids/peptides, caffiene, or calcium triggers the gastric phase- which also produces more H+ by parietal cells and gastrin by G cells.
24. amino acids/peptides in the duodenum triggers gastrin release from duodenal G cells.
25. pepsin is released from chief cells in the inactivate form, pepsinogen, which is auto cleaved at the low stomach pH. it cleaves proteins into smaller polypeptides.
26. to protect the gastric lining from digestion by acids, stimulated by vagus nerve, chemical stimulants (such as alcohol), and roughage.
27. somatostatin, secretin, GIP.
28. somatostatin is released from somatostatin cells in response to high acid levels in the stomach. somatostatin inhibits gastrin release from G cells, thereby reducing H+ levels.
29. secretin is released from duodenal secretin cells in resposne to high acid and fat levels in the stomach. secretin inhibits G cells gastrin release.
30. GIP is released from duodenal G cells in response to high acid and fat levels in the stomach. GIP directly inhibits parietal cells H+ release.
31. amino acids/peptides stimulating gastrin release, which stimulates acid secretion. vagus nerve stimulates acid secretion while inhibiting somatostatin release.
32. somatostatin inhibits gastrin release (see question 28), acid stimulates somatostatin release.
33. imbalance between aggressive digestive enzymes and protective factors such as mucus and bicarbonate.
34. inflammatory effects such as histamine release, edema, hemorrhage, leakage, etc.
35. it aids in vitamin B12 digestion: vitamin B12 is initially bound to dietary or gastric R proteins, then dissociated by pepsin and bound to intrinsic factor, which allows for its absorption into the ileum.
Wednesday, February 25, 2009
organ systems: GI physiology lecture II
the second lecture by Dr. SSL focused on small and large intestine "motility". in general, the intestines move the chyme (the half digested bolus) in two different ways; segmental, for mixing and absorption, and peristalstic, for moving the chyme along the digestive tract. the submucosal plexus is the nerve cluster in the submucosa of the intestines that are associated with the former, and the myenteric plexus is in between the muscularis mucosa layers and are associated with the latter.
once the bolus enters the small intestine, it takes 3-5 hours to move down to the ileum, where it reaches the ileocecal valve, a thickening of the tissue that prevents chyme from leaking into the cecum of the large intestine. as with all valves in the digestive tract, it is normally closed- when the valve loses tone, it can cause diarrhea, malabsorption, and a backflow of bacteria from the comparatively bacteria rich large intestine. the gastroileac reflex is when gastric or duodenal distention causes the relaxation of the valve. gastric distention can also induce peristalsis in the intestine (also controlled by the current mix of hormones in the lumen), called the gastroenteric reflex. the migrating motor complex is a peristaltic movement from the stomach to the ileum that occurs between meals, at approximately 90 minute intervals.
the large intestine's mixing function is accomplished by "haustration", which is a segmental mixing which aids in the absorption of water and further mixes the chyme. "mass movements" expel the colon's contents, and occur 1-3 times a day: each episode is 10-30 minutes long, with 30 second long contractions occuring every 2-3 minutes. a few reflexes that can induce mass movements: gastrocolic reflex is a mass movement in response to gastric distention or irritation, duodenalcolic is in response to duodenal distention or irritation, and orthocolic is in response to waking up or movement in the morning.
defecation can be induced intrinsically, meaning the distention of the rectum directly causes peristalsis in the descending and sigmoid colon, relaxes the internal and constricts the external anal sphincter. it can also be induced by the parasympathetic nervous system, by pelvic parasympathetic neurons stimulating relaxation of the internal and constriction of the external anal sphincters. in contrast, the sympathetic nervous system inhibits passage of rectal contents, and constricts the internal anal sphincter. lastly, stress causes loss of contractility in stomach and duodenum, as well as expelling fecal matter from large intestine, and chronic stress can ultimately lead to alternating bouts of constipation and diarrhea.
questions
introductory ideas...
1. describe the difference in blood appearance in stool depending on where the bleeding starts in the GI tract. 2. how far can a colonoscope reach?
3. what are the two nerve plexuses in the SI?
4. what is the submucosal plexus mainly involved with?
5. what is the myenteric plexus mainly involved with?
6. what gets absorbed in the duodenum and upper jejunum?
7. what are the upper and lower digestive system separated by?
small intestine motility...
8. what are the two types of contraction in the SI?
9. describe segmental contraction.
10. how long does it take for the bolus to move from the pylorus to ileocecal valve?
11. what is the gastroenteric reflex?
12. what is the gastroileac reflex?
13. what is the ileocecal valve?
14. what happens when the ileocecal valve loses tone?
15. how is appendicitis related to constipation?
16. what is the migrating motor complex?
17. how is the migrating motor complex activated?
large intestine / colon motility...
18. what is the function of the colon?
19. what is "haustration" of the colon?
20. describe the mass movements of the colon.
20b. describe the contractions during each mass movement.
21. what is the gastrocolic reflex?
22. what is the duodenalcolic reflex?
23. what is the orthocolic reflex?
24. how does nicotine affect the contraction of the colon?
reflexes and external influences...
25. describe the intrinsic reflex of defecation.
26. describe the parasympathetic reflex of defecation.
27. how is the external sphincter controlled?
28. what effect does the sympathetic nervous system have on bowel movements?
29. what effect does stress have on digestion?
30. what effect does chronic stress have on digestion?
answers
1. if the bleeding starts in upper GI tract, blood will have coagulated- darker stool. if bleeding in lower GI tract- reddish stool.
2. the terminal ileum.
3. myenteric, submucosal
4. secretion, absorption
5. motility
6. sugars, folic acid, calcium, iron.
7. ligament of treitz.
8. segmental contraction, peristalsis
9. more for mixing and mucosal contact.
10. 3-5 hours.
11. gastric and duodenal distention stimulates the myenteric plexus which stimulates peristalsis. hormones both stimulate and inhibit peristalsis.
12. food entering stomach stimulates relaxation of ileocecal valve.
13. last bit of ileum which delays entrance of chyme into cecum.
14. malabsorption, diahrrea, and backflow of bacteria from long bowel to small bowel.
15. appendicitis irritates the cecum around the ileocecal valve, which can cause it to remain closed.
16. a peristaltic wave that goes from the stomach to the ileum between meals, every 90 minutes.
17. the enteric nervous system, motilin.
18. absorb water and electrolytes, store and expel fecal matter.
19. a segmentation mixing of the large intestine that allows for mixing of chyme and greater absorption of water.
20. propulsive contractions of 20cm portions of the large intestine that occur 1-3 times per day.
21. each mass movement lasts 10-30 minutes, with contractions occuring every 2-3 minutes- with each contraction lasting 30 seconds.
21. when distention or irritation in the stomach triggers mass movement in intestines.
22. distention or irritation of duodenum triggers mass movement in intestines.
23. waking up / movement in the morning triggers mass movement in colon.
24. slows it down.
25. distention of rectum triggers peristalsis in descending and sigmoid colon, followed by relaxation of internal sphincter and contraction of external sphincter.
26. afferent neurons stimulate pelvic parasympathetic nerves to relax the internal sphincter and contract the external sphincter; happens from the splenic flexure to the anus.
27. voluntarily by the pudendal nerve.
28. inhibits passage in rectum, tightens internal spincter.
29. stomach and small intestine lose contraction ability, large intestine expels fecal matter.
30. alternative bouts of constipation and diarrhea.
once the bolus enters the small intestine, it takes 3-5 hours to move down to the ileum, where it reaches the ileocecal valve, a thickening of the tissue that prevents chyme from leaking into the cecum of the large intestine. as with all valves in the digestive tract, it is normally closed- when the valve loses tone, it can cause diarrhea, malabsorption, and a backflow of bacteria from the comparatively bacteria rich large intestine. the gastroileac reflex is when gastric or duodenal distention causes the relaxation of the valve. gastric distention can also induce peristalsis in the intestine (also controlled by the current mix of hormones in the lumen), called the gastroenteric reflex. the migrating motor complex is a peristaltic movement from the stomach to the ileum that occurs between meals, at approximately 90 minute intervals.
the large intestine's mixing function is accomplished by "haustration", which is a segmental mixing which aids in the absorption of water and further mixes the chyme. "mass movements" expel the colon's contents, and occur 1-3 times a day: each episode is 10-30 minutes long, with 30 second long contractions occuring every 2-3 minutes. a few reflexes that can induce mass movements: gastrocolic reflex is a mass movement in response to gastric distention or irritation, duodenalcolic is in response to duodenal distention or irritation, and orthocolic is in response to waking up or movement in the morning.
defecation can be induced intrinsically, meaning the distention of the rectum directly causes peristalsis in the descending and sigmoid colon, relaxes the internal and constricts the external anal sphincter. it can also be induced by the parasympathetic nervous system, by pelvic parasympathetic neurons stimulating relaxation of the internal and constriction of the external anal sphincters. in contrast, the sympathetic nervous system inhibits passage of rectal contents, and constricts the internal anal sphincter. lastly, stress causes loss of contractility in stomach and duodenum, as well as expelling fecal matter from large intestine, and chronic stress can ultimately lead to alternating bouts of constipation and diarrhea.
questions
introductory ideas...
1. describe the difference in blood appearance in stool depending on where the bleeding starts in the GI tract. 2. how far can a colonoscope reach?
3. what are the two nerve plexuses in the SI?
4. what is the submucosal plexus mainly involved with?
5. what is the myenteric plexus mainly involved with?
6. what gets absorbed in the duodenum and upper jejunum?
7. what are the upper and lower digestive system separated by?
small intestine motility...
8. what are the two types of contraction in the SI?
9. describe segmental contraction.
10. how long does it take for the bolus to move from the pylorus to ileocecal valve?
11. what is the gastroenteric reflex?
12. what is the gastroileac reflex?
13. what is the ileocecal valve?
14. what happens when the ileocecal valve loses tone?
15. how is appendicitis related to constipation?
16. what is the migrating motor complex?
17. how is the migrating motor complex activated?
large intestine / colon motility...
18. what is the function of the colon?
19. what is "haustration" of the colon?
20. describe the mass movements of the colon.
20b. describe the contractions during each mass movement.
21. what is the gastrocolic reflex?
22. what is the duodenalcolic reflex?
23. what is the orthocolic reflex?
24. how does nicotine affect the contraction of the colon?
reflexes and external influences...
25. describe the intrinsic reflex of defecation.
26. describe the parasympathetic reflex of defecation.
27. how is the external sphincter controlled?
28. what effect does the sympathetic nervous system have on bowel movements?
29. what effect does stress have on digestion?
30. what effect does chronic stress have on digestion?
answers
1. if the bleeding starts in upper GI tract, blood will have coagulated- darker stool. if bleeding in lower GI tract- reddish stool.
2. the terminal ileum.
3. myenteric, submucosal
4. secretion, absorption
5. motility
6. sugars, folic acid, calcium, iron.
7. ligament of treitz.
8. segmental contraction, peristalsis
9. more for mixing and mucosal contact.
10. 3-5 hours.
11. gastric and duodenal distention stimulates the myenteric plexus which stimulates peristalsis. hormones both stimulate and inhibit peristalsis.
12. food entering stomach stimulates relaxation of ileocecal valve.
13. last bit of ileum which delays entrance of chyme into cecum.
14. malabsorption, diahrrea, and backflow of bacteria from long bowel to small bowel.
15. appendicitis irritates the cecum around the ileocecal valve, which can cause it to remain closed.
16. a peristaltic wave that goes from the stomach to the ileum between meals, every 90 minutes.
17. the enteric nervous system, motilin.
18. absorb water and electrolytes, store and expel fecal matter.
19. a segmentation mixing of the large intestine that allows for mixing of chyme and greater absorption of water.
20. propulsive contractions of 20cm portions of the large intestine that occur 1-3 times per day.
21. each mass movement lasts 10-30 minutes, with contractions occuring every 2-3 minutes- with each contraction lasting 30 seconds.
21. when distention or irritation in the stomach triggers mass movement in intestines.
22. distention or irritation of duodenum triggers mass movement in intestines.
23. waking up / movement in the morning triggers mass movement in colon.
24. slows it down.
25. distention of rectum triggers peristalsis in descending and sigmoid colon, followed by relaxation of internal sphincter and contraction of external sphincter.
26. afferent neurons stimulate pelvic parasympathetic nerves to relax the internal sphincter and contract the external sphincter; happens from the splenic flexure to the anus.
27. voluntarily by the pudendal nerve.
28. inhibits passage in rectum, tightens internal spincter.
29. stomach and small intestine lose contraction ability, large intestine expels fecal matter.
30. alternative bouts of constipation and diarrhea.
Sunday, February 22, 2009
organ systems: GI physiology lecture 1
this is the first lecture in the series of GI physiology by Dr. Steven Sandburg Lewis. we covered a few introductory concepts: basal electric rhythms, some basic anatomy of the mouth and esophagus, gastric motility, and vomiting.
basal electrical rhythms are slow depolarizations that are initiated in GI tissue by the interstitial cells between the two layers of the muscularis mucosa. they generally occur on the frequency of 3-12 per minute, and if they reach the threshold frequency, an action potential will be induced and contraction of the muscle will occur. distention of the lumen in the GI tract, as well as parasympathetic and hormonal stimulation can depolarize the basal rhythm, bringing it closer to the threshold potential and therefore increasing the AP frequency. sympathetic activity and norepinephrine can have the opposite effect, hyperpolarizing the BER and lowering AP frequency.
the act of swallowing is an event in the pharanx is very much a coordinated event: the uvula is tissue in the back of the pharynx that prevents food (the bolus) from entering the nasal canal. the epiglottis is a flap of tissue that opens the esophagus and closes off the trachea. the bolus must pass through the upper esophageal sphincter (UES) which is normally closed to prevent air from entering the stomach. the bolus is then transported down by peristaltic motion to the lower esophageal sphincter (LES), which is normally closed to prevent gastric reflux.
three types of peristalsis are described: primary peristalsis occurs as a direct reaction to swallowing food. secondary peristalsis occurs even without swallowing- it is initiated when there is already a bolus stuck in the esophagus. tertiary peristalsis occurs in response to stress or loud noise, and contracts the entire length of the esophagus simultaneously- which in effect prevents peristalsis.
when the bolus passes through the LES and into the stomach, it induces "receptive relaxation" and peristalsis in the stomach muscularis layers as well. the stomach generally mixes on the frequency of 3 "constrictor waves" per minute, and includes an action called "retropulsion"- a backwards movement of the gastric contents to aid in mixing. (note: the fundus and body of the stomach can accomodate up to 1.5 L of food)
the last topic in this lecture was vomiting. there are three stages to vomiting: nausea, retching, and vomiting. nausea can be induced by a variety of events such as distention of organs, altered body chemistry, extreme fear or stress, etc. in the GI tract, this is manifested as antiperistaltic motion in the jejunum, relaxing of gastric muscle tone, and eventual reflux of duodenal contents into the stomach. in the next phase, wretching, the stomach contracts and pushes upwards into the thorax, against the closed LES. finally, vomiting occurs when the food gets ejected through the UES.
questions
BER's..
1. what are BER's? what are they generated by?
2. how is an action potential produced from a BER?
3. how is the maximum rate of muscle contraction set?
4. how does depolarization relate to action potential production? what causes depolarization of BER?
5. how does hyperpolarization relate to action potential production? what causes hyperpolarization of BER?
the mouth and esophagus...
6. dysphagia is...
7. what does the uvula do?
8. what does the UES do?
9. what does the LES do?
10. what is the difference between the three types of peristalsis in the esophagus?
11. when is tertiary peristalsis painful?
12. what is the relaxation of LES mediated by?
13. what foods relax LES tone?
gastric motility and emptying...
14. what is the first response of the stomach to the entering bolus?
15. fundus and body can accommodate up to...
16. what is the frequency of gastric mixing?
17. how does stress affect gastric contraction?
18. what is retropulsion?
19. how does fat content relate to gastric contraction
20. how many episodes of gastric reflux does the average person have per meal?
vomiting...
21. three phases of vomiting...
22. what occurs during nausea?
23. what occurs during retching?
24. what might happen due to excessive wretching?
25. what occurs during vomiting?
26. what is the vomiting center in the brain affected by?
27. what is an emetic? what are some examples?
answers
1. basal electrical rhythm, generated by interstitial cells between the circular and longitudinal muscularis mucosa.
2. when the BER reaches the threshold potential, an action potential is initiated.
3. by the slow wave frequency.
4. increases the AP frequency, cased by distention of lumen, parasympathetic and hormonal stimulation.
5. decreases AP frequency, caused by sympathetic activity, NE
6. difficulty swallowing.
7. prevents efflux of food into the nasal pharynx.
8. prevents air from getting into the stomach.
9. prevents gastric secretions from entering esophagus.
10. primary is in response to swallowing food. secondary is peristalsis without swallowing- when something is stuck in the esophagus. tertiary has no known function- can be stimulated by loud noises or stress and contracts the whole esophagus.
11. it can cause chest pain in individuals with esophageal motility problems.
12. vagus nerve, VIP, nitric oxide
13. alcohol, antacids, proton pump inhibitors, mint, chocolate, viagra (by way of NO), opiates, drugs to treat angina, bronchodilators. progesterone.
14. "receptive relaxation"
15. 1.5 L
16. 3 constrictor waves / minute.
17. it can cause contraction of the entire stomach (similar to tertiary esophageal contraction) which blanches blood to the brain/muscles and eventually can cause ulcers.
18. the backward motion of contents (to aid in mixing)
19. causes the gastric contents to mix longer. fats float on top and are emptied last.
20. about 3.
21. nausea, retching, vomiting.
22. relaxing of gastric tone, antiperistalsis begins in the jejunum, and eventual reflux of duodenal contents into stomach.
23. upward contraction of stomach, with LES closed.
24. a hiatal hernia.
25. food gets ejected through UES.
26. distention or irritation of viscera, cerebral events, or altered body chemistry. could be stimulated from GI or kidneys.
27. a substance which induces vomiting, such as ipecacuanha.
basal electrical rhythms are slow depolarizations that are initiated in GI tissue by the interstitial cells between the two layers of the muscularis mucosa. they generally occur on the frequency of 3-12 per minute, and if they reach the threshold frequency, an action potential will be induced and contraction of the muscle will occur. distention of the lumen in the GI tract, as well as parasympathetic and hormonal stimulation can depolarize the basal rhythm, bringing it closer to the threshold potential and therefore increasing the AP frequency. sympathetic activity and norepinephrine can have the opposite effect, hyperpolarizing the BER and lowering AP frequency.
the act of swallowing is an event in the pharanx is very much a coordinated event: the uvula is tissue in the back of the pharynx that prevents food (the bolus) from entering the nasal canal. the epiglottis is a flap of tissue that opens the esophagus and closes off the trachea. the bolus must pass through the upper esophageal sphincter (UES) which is normally closed to prevent air from entering the stomach. the bolus is then transported down by peristaltic motion to the lower esophageal sphincter (LES), which is normally closed to prevent gastric reflux.
three types of peristalsis are described: primary peristalsis occurs as a direct reaction to swallowing food. secondary peristalsis occurs even without swallowing- it is initiated when there is already a bolus stuck in the esophagus. tertiary peristalsis occurs in response to stress or loud noise, and contracts the entire length of the esophagus simultaneously- which in effect prevents peristalsis.
when the bolus passes through the LES and into the stomach, it induces "receptive relaxation" and peristalsis in the stomach muscularis layers as well. the stomach generally mixes on the frequency of 3 "constrictor waves" per minute, and includes an action called "retropulsion"- a backwards movement of the gastric contents to aid in mixing. (note: the fundus and body of the stomach can accomodate up to 1.5 L of food)
the last topic in this lecture was vomiting. there are three stages to vomiting: nausea, retching, and vomiting. nausea can be induced by a variety of events such as distention of organs, altered body chemistry, extreme fear or stress, etc. in the GI tract, this is manifested as antiperistaltic motion in the jejunum, relaxing of gastric muscle tone, and eventual reflux of duodenal contents into the stomach. in the next phase, wretching, the stomach contracts and pushes upwards into the thorax, against the closed LES. finally, vomiting occurs when the food gets ejected through the UES.
questions
BER's..
1. what are BER's? what are they generated by?
2. how is an action potential produced from a BER?
3. how is the maximum rate of muscle contraction set?
4. how does depolarization relate to action potential production? what causes depolarization of BER?
5. how does hyperpolarization relate to action potential production? what causes hyperpolarization of BER?
the mouth and esophagus...
6. dysphagia is...
7. what does the uvula do?
8. what does the UES do?
9. what does the LES do?
10. what is the difference between the three types of peristalsis in the esophagus?
11. when is tertiary peristalsis painful?
12. what is the relaxation of LES mediated by?
13. what foods relax LES tone?
gastric motility and emptying...
14. what is the first response of the stomach to the entering bolus?
15. fundus and body can accommodate up to...
16. what is the frequency of gastric mixing?
17. how does stress affect gastric contraction?
18. what is retropulsion?
19. how does fat content relate to gastric contraction
20. how many episodes of gastric reflux does the average person have per meal?
vomiting...
21. three phases of vomiting...
22. what occurs during nausea?
23. what occurs during retching?
24. what might happen due to excessive wretching?
25. what occurs during vomiting?
26. what is the vomiting center in the brain affected by?
27. what is an emetic? what are some examples?
answers
1. basal electrical rhythm, generated by interstitial cells between the circular and longitudinal muscularis mucosa.
2. when the BER reaches the threshold potential, an action potential is initiated.
3. by the slow wave frequency.
4. increases the AP frequency, cased by distention of lumen, parasympathetic and hormonal stimulation.
5. decreases AP frequency, caused by sympathetic activity, NE
6. difficulty swallowing.
7. prevents efflux of food into the nasal pharynx.
8. prevents air from getting into the stomach.
9. prevents gastric secretions from entering esophagus.
10. primary is in response to swallowing food. secondary is peristalsis without swallowing- when something is stuck in the esophagus. tertiary has no known function- can be stimulated by loud noises or stress and contracts the whole esophagus.
11. it can cause chest pain in individuals with esophageal motility problems.
12. vagus nerve, VIP, nitric oxide
13. alcohol, antacids, proton pump inhibitors, mint, chocolate, viagra (by way of NO), opiates, drugs to treat angina, bronchodilators. progesterone.
14. "receptive relaxation"
15. 1.5 L
16. 3 constrictor waves / minute.
17. it can cause contraction of the entire stomach (similar to tertiary esophageal contraction) which blanches blood to the brain/muscles and eventually can cause ulcers.
18. the backward motion of contents (to aid in mixing)
19. causes the gastric contents to mix longer. fats float on top and are emptied last.
20. about 3.
21. nausea, retching, vomiting.
22. relaxing of gastric tone, antiperistalsis begins in the jejunum, and eventual reflux of duodenal contents into stomach.
23. upward contraction of stomach, with LES closed.
24. a hiatal hernia.
25. food gets ejected through UES.
26. distention or irritation of viscera, cerebral events, or altered body chemistry. could be stimulated from GI or kidneys.
27. a substance which induces vomiting, such as ipecacuanha.
Tuesday, December 9, 2008
biochem: mark's medical biochem chapter 27: digestion and transport of carbohydrates
this chapter covers several aspects of carbohydrate digestion. first it goes over some basics about carbohydrates and digestion in general, then talks about the specific enzymes at work in the brush border of the small intestine, then a brief section about lactose intolerance, and finally, a section about the transport of glucose from the intestine into the blood.
the normal american diet is made of 40-50% carbohydrates, and of this, 50-60% is made of the starch molecules (10,000 to 1 million glucosyl units long) amylose and amylopectin. amylose consists of glucose molecules bonded with alpha 1-4 bonds, while amylopectin is the same, but with alpha 1-6 bonds (and therefore branches) as well. digestion of these starches begins in the mouth with alpha amylase, which is an example of an endoglucosidase-- an enzyme which cleaves alpha 1-4 bonds at random intervals. this initial digestion leaves chunks of polysaccharides called alpha-dextrins. stomach acid deactivates the amylase, and carbohydrate digestion continues in the small intestine.
in the small intestine, carbohydrate digestion takes place mainly on the "brush border" of the intestinal mucosa, which have enzymes that are embedded in the intestinal membrane that poke into the intestinal lumen. the four major "glucosidases" are glucoamylase, trehalase, beta-glucosidase, and sucrase-isomaltase. each of these enzymes has a specific structure and catalytic sites that are specific to certain types of carbohydrates. glucoamylase breaks down alpha 1-4 bonds from the non reducing end ("tail end") of the sugar, until isomaltase remains-- isomaltase is basically just two sugar units branched together in an alpha 1-6 bond. the action of glucoamylase on polysaccharides seems similar to the action of glycogen phosphorylase in the breakdown of glycogen in that both are removing glucose residues one at a time from the tail end, and both can not remove the last glucose unit (or in glucose phosphorylase's case, the last 4).
sucrase-isomaltase is another brush border glucosidase with two catalytic sites. one is specific to isomaltose and maltose (and thus can break down the isomaltose from glucoamylase's activity) and one is specific to sucrose and maltose. beta glucosidase also has two catalytic sites. one is specific to breaking the beta 1-4 bond between glucose and galactose in lactose, and the other is specific to cleaving beta 1-4 bonds in glycolipids. the last glucosidase in the brush border is trehalase, which has only one catalytic site which is specific to trehalose, a sugar found only in some insects, mushrooms, and algae. these four enzymes work in tandem to break down the different types of carbohydrates that are dumped into the duodenum. the relative concentration of these enzymes change depending on the location in the gut. for example, pancreatic alpha amylase is secreted mainly in the duodenum, sucrase-maltase and beta-glucosidase is mainly in the jejunum, and glucoamylases is most common in the ileum.
a couple other notes about carbohydrate digestion. lactose intolerance occurs with either a lactase deficiency or intestinal damage. most adults only have 10% of the lactase activity that they had as children. lactose intolerance can ultimately lead to malabsorption of nutrients: lactose is undigested in the gut, and is instead metabolized by the bacterial flora in the colon, producing gases and lactic acid. the lactic acid can increase the intestinal lumen's osmolarity and cause water to distend the abdomen, which increases peristalsis and potentially causes diarrhea and malabsorption of other nutrients.
the last section of the chapter focused on the membrane channels that transport glucose across the intestinal lining into the blood. there are two types of such transport proteins, regular facilitated glucose channels and Na+ facilitated channels. Na+ facilitated channels use an ATPase Na+/K+ pump to establish a low concentration of Na+ inside the intestinal cell. the concentration gradient that is formed from the higher Na+ concentration in the intestinal lumen is then coupled with glucose transport in these membrane proteins. facilitative glucose transporters (also called "GLUT" transporters) do not require ATP and simply allow glucose to flow down its concentration gradient from the intestinal lumen, into the epithelium, and out into the serosa side ("blood side").
a few interesting notes relating to these glucose transporting membrane proteins. the liver's GLUT transporters have a higher than usual Km (the concentration at which the substrate is half-saturated with enzyme-- generally representing the enzyme's affinity for substrate and in this case the GLUT for glucose) for glucose, because it will only accept glucose into its cells (to be converted into glycogen for storage) when the blood glucose concentration is very high, like after a high carb meal. also, in muscle and fat cells, insulin stimulates glucose absorption by means of recruiting intracellular vesicles of glucose transport proteins to the cell membrane, where they can facilitate glucose transport into the cell.
questions
1. what percentage of a normal american diet consists of carbohydrates?
2. what percentage of the carbohydrate calories consists of amylose and amylopectin?
3. how many glucosyl units do amylose and amylopectin have?
4. what types of bonds do amylose and amylopectin have?
5. what are the major natural sweeteners found in fruit, honey, and vegetables?
6. what is the major dietary carb found from animal sources?
7. how much liquid do the salivary glands secrete per day?
8. what is an "endoglucosidase" and what is an example of one?
9. what is salivary amylase inactivated by?
10. how much digestive enzyme is secreted by the pancreas per day?
11. what are in the pancreatic secretions?
12. what are oligosaccharides?
13. what are the glucosidases found in the brush border of the small intestine?
14. describe the digestion of lactose and sucrose in the small intestine.
15. describe the structure and activity of glucoamylase?
16. what are alpha-dextrins vs. limit-dextrins?
17. describe the structure and activity of the sucrase-isomaltase complex.
18. what percentage of maltase activity can be attributed to the sucrose-isomaltose complex?
19. describe the structure and activity of trehalase.
20. describe the structure and activity of the beta-glucosidase complex
21. pancreatic alpha-amylase activity is highest in...
22. sucrase-isomaltase activity is highest in...
23. beta-glucosidase activity is highest in...
24. glucoamylase activity is highest in...
25. what type of carbohydrates enter the colon?
26. what are the fatty acids that result from bacterial starch digestion in the colon?
27. what are the gases that result from bacterial starch digestion in the colon?
28. lactose intolerance can be caused by...
29. what are normal lactase levels of an adult as compared to a child?
30. what happens when lactose is ingested by a lactose intolerant person?
31. what does the glycemic index represent?
32. which sugars have the highest glycemic index?
33. what are the two types of glucose transport proteins?
34. describe the mechanism of the Na+ dependent glucose transporter.
35. what are facilitative glucose transporters?
36. compare the digestion of glucose with that of galactose and fructose.
37. in body tissues, why is glucose transport across membranes not the rate limiting step of glucose metabolism?
38. how does the high Km of glucose transport proteins in the liver relate to the liver's blood glucose regulation?
39. how is insulin related to glucose transport proteins in the liver?
answers
1. 40-45%
2. 50-60%
3. 10,000 to 1 million
4. amylose has alpha 1-4 bonds between glucosyl residues. amylopectin has alpha 1-4 bonds between glucosyl units as well as alpha 1-6 bonds between branches.
5. fructose, sucrose, glucose.
6. lactose, which is made of glucose and galactose.
7. ~1 liter a day
8. an enzyme that breaks internal alpha 1-4 bonds in a polysaccharide at random intervals, such as amylase.
9. acidity of the stomach
10. ~1.5 liters a day
11. trypsinogen, chymotrypsinogen, carboxypeptidase (for digestion of proteins), alpha-amylase (for carbohydrates), lipase (fat), and bicarbonate (neutralizing gastric acidity)
12. 4-9 glucosyl units long, contain one or more alpha-1,6 branches.
13. beta-glucoamylase, sucrase-isomaltase, beta-glycosidase, trehalase.
14. converted to monosaccharides by glucosidases attached to the brush border lining.
15. it has two domains that have different substrate specificity, and acts as an exoglucosidase by breaking alpha 1-4 bonds on the non reducing ("tail end") of the saccharides, releasing glucose units until only isomaltose remains.
16. alpha dextrins are the pieces of polysaccharides that result from salivary alpha-amylase's endoglucosidase activity. limit dextrins are oligosaccharides that have been formed from the further breakdown of polysaccharides by pancreatic alpha-amylase.
17. made of two subunits: sucrose-maltose subunit cleaves alpha 1-4 bonds in sucrose, maltose. isomaltose-maltose unit cleaves alpha 1-6 bonds in isomaltose, and also breaks down maltose.
18. 80%
19. trehalose is a smaller dissaccharidase that only has one catalytic site with specificity for trehalose, which is a relatively rare source of carbohydrate found in some insects, algae, and mushrooms.
20. has two catalytic sites: glucosyl-ceramidase site, which cleaves beta bonds in glycolipids, and lactase site, which breaks beta 1-4 bonds between glucose and galactose in lactose.
21. duodenum
22. jejunum
23. jejunum
24. ileum
25. any undigested starches: starches high in amylose, poorly hydrated starches (like in dried beans), dietary fiber.
26. acetic acid, propionic acid, butyric acid. 2,3,4 carbon.
27. hydrogen gas, CO2, methane
28. low lactase levels or intestinal injury
29. 10% of the level of a child
30. lactose is undigested by the lactase in the small intestine and is therefore metabolized by the colonic bacteria, which produces lactic acid, methane, and H2. the increased lactic acid increases osmolarity of the intestinal lumen, causing more water to be dumped into the lumen, causing excess peristalsis, causing malabsorption of other nutrients.
31. how quickly blood glucose levels rise after consumption of a food.
32. glucose and maltose.
33. sodium dependent glucose transporters and facilitative glucose transporters
34. a Na+ / K+ ATPase pump pumps Na+ out of the intestinal epithelium cells so that there is a low Na+ concentration within. the Na+ dependent transporter channels then use the resulting Na+ concentration gradient to power movement of glucose within the cell.
35. these are glucose channels that exist on both the luminal and serosal side of the intestinal epithelium that allow glucose to move down its concentration gradient without expenditure of energy.
36. galactose passes through the intestinal membrane in a similar way to glucose- via both Na+ facilitated channels and facilitative glucose transporters. fructose passes through by facilitated diffusion only.
37. because the transport proteins have a high affinity for glucose (a low Km) or are present in high numbers.
38. the liver will only transport glucose into its cells (and therefore convert glucose to glycogen for storage) when the blood glucose level is high, such as right after a high carb meal.
39. binding of insulin recruits GLUT proteins from intracellular vescicles onto the membrane.
the normal american diet is made of 40-50% carbohydrates, and of this, 50-60% is made of the starch molecules (10,000 to 1 million glucosyl units long) amylose and amylopectin. amylose consists of glucose molecules bonded with alpha 1-4 bonds, while amylopectin is the same, but with alpha 1-6 bonds (and therefore branches) as well. digestion of these starches begins in the mouth with alpha amylase, which is an example of an endoglucosidase-- an enzyme which cleaves alpha 1-4 bonds at random intervals. this initial digestion leaves chunks of polysaccharides called alpha-dextrins. stomach acid deactivates the amylase, and carbohydrate digestion continues in the small intestine.
in the small intestine, carbohydrate digestion takes place mainly on the "brush border" of the intestinal mucosa, which have enzymes that are embedded in the intestinal membrane that poke into the intestinal lumen. the four major "glucosidases" are glucoamylase, trehalase, beta-glucosidase, and sucrase-isomaltase. each of these enzymes has a specific structure and catalytic sites that are specific to certain types of carbohydrates. glucoamylase breaks down alpha 1-4 bonds from the non reducing end ("tail end") of the sugar, until isomaltase remains-- isomaltase is basically just two sugar units branched together in an alpha 1-6 bond. the action of glucoamylase on polysaccharides seems similar to the action of glycogen phosphorylase in the breakdown of glycogen in that both are removing glucose residues one at a time from the tail end, and both can not remove the last glucose unit (or in glucose phosphorylase's case, the last 4).
sucrase-isomaltase is another brush border glucosidase with two catalytic sites. one is specific to isomaltose and maltose (and thus can break down the isomaltose from glucoamylase's activity) and one is specific to sucrose and maltose. beta glucosidase also has two catalytic sites. one is specific to breaking the beta 1-4 bond between glucose and galactose in lactose, and the other is specific to cleaving beta 1-4 bonds in glycolipids. the last glucosidase in the brush border is trehalase, which has only one catalytic site which is specific to trehalose, a sugar found only in some insects, mushrooms, and algae. these four enzymes work in tandem to break down the different types of carbohydrates that are dumped into the duodenum. the relative concentration of these enzymes change depending on the location in the gut. for example, pancreatic alpha amylase is secreted mainly in the duodenum, sucrase-maltase and beta-glucosidase is mainly in the jejunum, and glucoamylases is most common in the ileum.
a couple other notes about carbohydrate digestion. lactose intolerance occurs with either a lactase deficiency or intestinal damage. most adults only have 10% of the lactase activity that they had as children. lactose intolerance can ultimately lead to malabsorption of nutrients: lactose is undigested in the gut, and is instead metabolized by the bacterial flora in the colon, producing gases and lactic acid. the lactic acid can increase the intestinal lumen's osmolarity and cause water to distend the abdomen, which increases peristalsis and potentially causes diarrhea and malabsorption of other nutrients.
the last section of the chapter focused on the membrane channels that transport glucose across the intestinal lining into the blood. there are two types of such transport proteins, regular facilitated glucose channels and Na+ facilitated channels. Na+ facilitated channels use an ATPase Na+/K+ pump to establish a low concentration of Na+ inside the intestinal cell. the concentration gradient that is formed from the higher Na+ concentration in the intestinal lumen is then coupled with glucose transport in these membrane proteins. facilitative glucose transporters (also called "GLUT" transporters) do not require ATP and simply allow glucose to flow down its concentration gradient from the intestinal lumen, into the epithelium, and out into the serosa side ("blood side").
a few interesting notes relating to these glucose transporting membrane proteins. the liver's GLUT transporters have a higher than usual Km (the concentration at which the substrate is half-saturated with enzyme-- generally representing the enzyme's affinity for substrate and in this case the GLUT for glucose) for glucose, because it will only accept glucose into its cells (to be converted into glycogen for storage) when the blood glucose concentration is very high, like after a high carb meal. also, in muscle and fat cells, insulin stimulates glucose absorption by means of recruiting intracellular vesicles of glucose transport proteins to the cell membrane, where they can facilitate glucose transport into the cell.
questions
1. what percentage of a normal american diet consists of carbohydrates?
2. what percentage of the carbohydrate calories consists of amylose and amylopectin?
3. how many glucosyl units do amylose and amylopectin have?
4. what types of bonds do amylose and amylopectin have?
5. what are the major natural sweeteners found in fruit, honey, and vegetables?
6. what is the major dietary carb found from animal sources?
7. how much liquid do the salivary glands secrete per day?
8. what is an "endoglucosidase" and what is an example of one?
9. what is salivary amylase inactivated by?
10. how much digestive enzyme is secreted by the pancreas per day?
11. what are in the pancreatic secretions?
12. what are oligosaccharides?
13. what are the glucosidases found in the brush border of the small intestine?
14. describe the digestion of lactose and sucrose in the small intestine.
15. describe the structure and activity of glucoamylase?
16. what are alpha-dextrins vs. limit-dextrins?
17. describe the structure and activity of the sucrase-isomaltase complex.
18. what percentage of maltase activity can be attributed to the sucrose-isomaltose complex?
19. describe the structure and activity of trehalase.
20. describe the structure and activity of the beta-glucosidase complex
21. pancreatic alpha-amylase activity is highest in...
22. sucrase-isomaltase activity is highest in...
23. beta-glucosidase activity is highest in...
24. glucoamylase activity is highest in...
25. what type of carbohydrates enter the colon?
26. what are the fatty acids that result from bacterial starch digestion in the colon?
27. what are the gases that result from bacterial starch digestion in the colon?
28. lactose intolerance can be caused by...
29. what are normal lactase levels of an adult as compared to a child?
30. what happens when lactose is ingested by a lactose intolerant person?
31. what does the glycemic index represent?
32. which sugars have the highest glycemic index?
33. what are the two types of glucose transport proteins?
34. describe the mechanism of the Na+ dependent glucose transporter.
35. what are facilitative glucose transporters?
36. compare the digestion of glucose with that of galactose and fructose.
37. in body tissues, why is glucose transport across membranes not the rate limiting step of glucose metabolism?
38. how does the high Km of glucose transport proteins in the liver relate to the liver's blood glucose regulation?
39. how is insulin related to glucose transport proteins in the liver?
answers
1. 40-45%
2. 50-60%
3. 10,000 to 1 million
4. amylose has alpha 1-4 bonds between glucosyl residues. amylopectin has alpha 1-4 bonds between glucosyl units as well as alpha 1-6 bonds between branches.
5. fructose, sucrose, glucose.
6. lactose, which is made of glucose and galactose.
7. ~1 liter a day
8. an enzyme that breaks internal alpha 1-4 bonds in a polysaccharide at random intervals, such as amylase.
9. acidity of the stomach
10. ~1.5 liters a day
11. trypsinogen, chymotrypsinogen, carboxypeptidase (for digestion of proteins), alpha-amylase (for carbohydrates), lipase (fat), and bicarbonate (neutralizing gastric acidity)
12. 4-9 glucosyl units long, contain one or more alpha-1,6 branches.
13. beta-glucoamylase, sucrase-isomaltase, beta-glycosidase, trehalase.
14. converted to monosaccharides by glucosidases attached to the brush border lining.
15. it has two domains that have different substrate specificity, and acts as an exoglucosidase by breaking alpha 1-4 bonds on the non reducing ("tail end") of the saccharides, releasing glucose units until only isomaltose remains.
16. alpha dextrins are the pieces of polysaccharides that result from salivary alpha-amylase's endoglucosidase activity. limit dextrins are oligosaccharides that have been formed from the further breakdown of polysaccharides by pancreatic alpha-amylase.
17. made of two subunits: sucrose-maltose subunit cleaves alpha 1-4 bonds in sucrose, maltose. isomaltose-maltose unit cleaves alpha 1-6 bonds in isomaltose, and also breaks down maltose.
18. 80%
19. trehalose is a smaller dissaccharidase that only has one catalytic site with specificity for trehalose, which is a relatively rare source of carbohydrate found in some insects, algae, and mushrooms.
20. has two catalytic sites: glucosyl-ceramidase site, which cleaves beta bonds in glycolipids, and lactase site, which breaks beta 1-4 bonds between glucose and galactose in lactose.
21. duodenum
22. jejunum
23. jejunum
24. ileum
25. any undigested starches: starches high in amylose, poorly hydrated starches (like in dried beans), dietary fiber.
26. acetic acid, propionic acid, butyric acid. 2,3,4 carbon.
27. hydrogen gas, CO2, methane
28. low lactase levels or intestinal injury
29. 10% of the level of a child
30. lactose is undigested by the lactase in the small intestine and is therefore metabolized by the colonic bacteria, which produces lactic acid, methane, and H2. the increased lactic acid increases osmolarity of the intestinal lumen, causing more water to be dumped into the lumen, causing excess peristalsis, causing malabsorption of other nutrients.
31. how quickly blood glucose levels rise after consumption of a food.
32. glucose and maltose.
33. sodium dependent glucose transporters and facilitative glucose transporters
34. a Na+ / K+ ATPase pump pumps Na+ out of the intestinal epithelium cells so that there is a low Na+ concentration within. the Na+ dependent transporter channels then use the resulting Na+ concentration gradient to power movement of glucose within the cell.
35. these are glucose channels that exist on both the luminal and serosal side of the intestinal epithelium that allow glucose to move down its concentration gradient without expenditure of energy.
36. galactose passes through the intestinal membrane in a similar way to glucose- via both Na+ facilitated channels and facilitative glucose transporters. fructose passes through by facilitated diffusion only.
37. because the transport proteins have a high affinity for glucose (a low Km) or are present in high numbers.
38. the liver will only transport glucose into its cells (and therefore convert glucose to glycogen for storage) when the blood glucose level is high, such as right after a high carb meal.
39. binding of insulin recruits GLUT proteins from intracellular vescicles onto the membrane.
Saturday, November 29, 2008
histology: digestive system
this lecture provided a histological perspective on the different sections of the digestive system, focusing on tissue and cell types. the digestive system is introduced as one long tube which starts in the pharynx, becomes the esophagus, stomach, small intestine, large intestine, then rectum. within all of these sections, there are generally four different layers: the mucosa is the innermost layer and contains the epithelium (either stratified squamous or simple columnar), a loose or reticular CT lamina propria, and a layer of muscle named the muscularis mucosa. beneath this is the submucosa, which contains blood vessels and nerves (and in the small intestine, the meissner's plexus). beneath this is the muscularis externa, which is generally composed of an inner circular layer, middle plexus of ganglia ("myenteric" plexus), and outer longitudinal layer. finally, on the outside of the tube is the serosa (or adventitia in some places, such as the esophagus above the diaphragm), which is made up of connective tissue and mesothelium. all of the sections of the digestive system are made up of variants of these four layers depending on location and function.
the first section, the esophagus, is unique in that its epithelia is made up of non-keratinized stratified squamous (presumably to deal with the abrasion of food coming in, and non-keratinized because waterproofing isn't an issue), which is thrown into esophageal glands that begin the lubricating process. the muscularis layer is also unique in that the top part of the esophagus is mainly skeletal muscle, gradually blends with smooth muscle in the middle, and by the bottom is mainly smooth muscle. the esophagus ends in the esophageal-cardiac junction, where the epithelial layer transitions from the non-keratinized stratified of the esophagus to the simple columnar of the stomach.
the stomach has four sections, from top to bottom: the cardiac, fundic, body, pyloric regions. the mucosa of the stomach is thrown into gastric glands, which contain specialized secretory cells which aid in digestion: surface mucous cells and mucous neck cells secrete mucous near the tops and bottoms of the glands, respectively. parietal cells secrete HCl near the tops of the glands, and chief cells secrete pepsinogen near the base of the glands. the muscularis of the stomach is also unique in that it has an inner oblique layer, middle circular, and outer longitudinal layer. the fundus is the most representative region of the stomach, and the other three regions are variations on this region. for example, the epithelia in both the cardiac and pyloric regions contain only mucous cells, and the muscularis layers are tightened into the cardiac and pyloric sphincters on either end.
after the stomach comes the small intestine, which is divided into three regions, the duodenum, jejunum (the most representative region), and ileum. the intestinal mucosa is unique in that it is folded into large intestinal glands called "Krypts of Lieberkuhn", covered with columnar absorptive/secretory cells called enterocytes, with goblet cells scattered throughout. also present in the epithelium are enteroendocrine cells, which secrete hormone like substances, as well as Paneth cells, which secrete lysozymes to regulate the bacterial flora in the gut. the lamina propria of the intestine is well vascularized with type 2 fenestrated capillaries, with occasional lymph nodes called Peyer's Patches. additionally, there is often a "central lacteal" inside the villi, which is a large lymph vessel that aids in absorption of larger molecules. the muscularis of the small intestine generally contains an inner circular layer, followed by a nerve "net" called the myenteric plexus, followed by an outer longitudinal muscle layer.
the large intestine is similar to the small intestine, the main differences being: more goblet cells, lymph rich, but no microvilli, paneth cells, or enteroendocrine cells. it has two main sections, the colon and the rectum, and at the "end of the line", the rectal-anal junction, there are four notable changes: the transition from the simple columnar absorptive cells of the small intestine to the non-keratinized stratified squamous of the rectum, the patchy muscularis mucosa, the huge blood vessels in the submucosa, and the presence of skeletal muscle in the muscularis externa. (notice how this is similar to the esophagus)
the role of the pancreas and liver in digestion is then looked at: the pancreas is a mostly exocrine gland which secretes from compound acinar glands a variety of enzymes-- carboxypeptidase, chymotrypsinogen, trypsinogen for digestion of proteins, amylase for digestion of carbohydrates, lipase for digestion of lipids, and bicarbonate to neutralize the acidity from gastric digestion. it also functions as an endocrine gland with its "Islets of Langerhans", which contain alpha, beta, and delta cells which release glucagon, insulin, and somatostatin, respectively. the liver also functions as both an endocrine / exocrine gland which aids in digestion by releasing bile for digestion of fats (exocrine) and filtering and adding to blood (endocrine). the liver has many functions, such as processing of glycogen, fetal blood cell production, production of blood clotting factors, and detoxification of the blood.
the basic cell type of the liver is called the hepatocyte, and they are arranged in roughly hexagonally shaped functional units called "lobules". on the borders of the lobules, on roughly every other corner of the hexagon, are "portal triads" which contain hepatic portal veins (which supply oxygen poor, nutrient rich blood to the liver from the intestine), hepatic arteries (supplying fresh blood to the liver), and bile ducts. in the center of the lobules are "central veins" which carry away deoxygenated blood. the last aspect of the liver that's looked at is the liver acinus theory, which states that blood flows from the portal triad laterally to the adjacent central veins, forming a diamond shaped functional unit overlayed on two lobules.
questions
1. what are the four primary layers in the entire digestive system?
2. what is the mucosa composed of?
3. what is in the submucosa?
4. what is the muscularis composed of?
5. what is the serosa composed of?
esophagus
6. describe the mucosa of the esophagus.
7. describe the muscularis of the esophagus.
8. describe the outer wall of the esophagus.
9. what is the esophageal-cardiac junction?
stomach- surface mucosa, mucosa neck, chief, parietal,
10. what are the four parts to the stomach?
11. describe the mucosa of the stomach.
12. what are some other cells that function in the mucosa of the stomach?
13. describe the muscularis externa of the stomach.
14. how does the cardiac region of the stomach differ from the body region?
15. how does the pyloric region of the stomach differ from the body region?
small intestine- lieberkuhn, enterocytes, paneth, meissner's, peyer's patch, brunner's
16. what are the three parts to the small intestine?
17. describe the mucosa of the small intestine.
18. what is unique about the surface of the mucosa of the small intestine?
19. what are the crypts of Lieberkuhn?
20. which digestive enzymes are secreted by the pancreas to aid in digestion in the small intestine?
21. what is secreted from the liver to help in digestion in the small intestine?
22. what are some of the cells in the mucosal epithelium of the small intestine?
23. describe the lamina propria of the small intestine.
24. describe the submucosa of the small intestine.
25. describe the myenteric plexus and what role it plays.
26. the serosa of the small intestine is the...
27. what are brunner's glands and what do they do? where are they found?
28. what are some distinguishing characteristics of the ileum?
large intestine-
29. describe the mucosa of the large intestine.
30. what are the four characteristics of the rectal-anal junction?
accessory glands- salivary glands, pancreas, liver,
31. what are the three types of salivary glands and what do they secrete?
32. describe the exocrine function of the pancreas.
33. describe the endocrine function of the pancreas.
34. name five major functions of the liver.
35. describe how the liver operates both as an exocrine and endocrine gland.
36. what is the hepatic portal vein?
37. what is the hepatic artery?
38. what type of capillaries are in the liver?
39. what is the basic cell type in the liver and what are they assembled into?
40. describe the architecture of the lobule.
41. what is the liver acinus theory? why is it the most likely scheme of blood flow in the liver?
answers
1. mucosa, submucosa, muscularis, serosa
2. epithelium (mostly simple columnar), lamina propria, muscularis mucosa
3. connective tissue with blood vessels and nerves, sometimes a submucosal plexus (meissner's)
4. inner circular layer of smooth muscle, middle plexus of ganglia (myenteric/auerbach's), outer longitudinal smooth muscle
5. CT, mesothelium
6. non-keratinzed stratified squamous epithelium, has esophageal glands for lubrication.
7. upper 1/3 made of skeletal muscle, middle 1/3 mix of skeletal and smooth muscle, lower 1/3 smooth muscle.
8. has adventitia, serosa seen only after tube penetrates diaphragm.
9. the end of the esophagus, an abrupt change from stratified squamous to simple columnar epithelium.
10. cardiac, fundus, body, pylorus
11. simple columnar epithelium with gastric glands for digestion, lamina propria which is richly vascularized, loose / reticular CT.
12. surface mucous cells, mucous neck cells secrete mucous on surface and at base of gastric pits. parietal cells secrete HCl at top of gland proper. chief cells secrete pepsinogen near base of gland.
13. inner oblique, middle circular, outer longitudinal. thickened at either end of stomach to form cardiac and pyloric sphincter.
14. cardiac region glands only have mucous cells, and there is an abrupt change from the esophagus.
15. pyloric region glands only have mucous cells. glands branch more and have deeper pits.
16. duodenum, jejunum, ileum.
17. simple columnar epithelium thrown into glandular tubes called intestinal glands (crypts of Lieberkuhn) and projections called villi.
18. they have a striated border formed from microvilli.
19. intestinal glands that both secrete and absorb.
20. trypsinogen, chymotrypsinogen, carboxypeptidase (for protein), amylase (for carbohydrates), lipase (for lipids)
21. bile salts (for lipids)
22. primarily composed of enterocytes which are columnar absorptive cells with microvilli, with mucous secreting goblet cells throughout, as well as enteroendocrine cells which are at the base of the glands and secrete hormone like substances, and paneth cells which secretes lysozyme to control bacterial flora.
23. well vascularized, type II capillaries, may have a central lacteal for absorption of larger molecules, may have lymph nodules called Peyer's patches.
24. may have a meissner's plexus, which assists in regulating secretion and blood flow.
25. a nerve net in the muscularis layer which helps coordinate peristaltic contractions of muscularis externa.
26. visceral peritoneum.
27. in the submucosa of the duodenum, secretes alkaline-mucoid material and urogastrone.
28. greatest amount of "GALT", Peyer's patches, fewer villi and more goblet cells.
29. simple columnar epithelia with intestinal glands but no villi. abundant goblet cells and lymph rich lamina propria, but no entero-endocrine or paneth cells.
30. epithelial transition from simple columnar to non-keratinized stratified squamous, patchy muscularis mucosa, huge blood vessels in submucosa, skeletal muscle in muscularis externa. transition, patchy, blood, skeletal.
31. parotid secretes mainly serous, submandibular secretes a mixture of mucous and serous, and sublingual secretes mostly mucous.
32. the pancreas' function is mainly to serve as an exocrine gland which secrete digestive enzymes (see question 20), composed of compound acinar glands. it also secretes alkaline bicarbonate in order to neutralize the acidity from gastric digestion.
33. 2% of the pancreas is used for endocrine function, in the form of "islets of langerhans" which are clumped glands which consist of alpha, beta, and delta cells which secrete glucagon, insulin, and somatostatin, respectively.
34. fetal hematopoesis (before shifting to bone marrow), glucagon processing, plasma protein production (such as clotting factors), bile production, and detoxification. blood, glucagon, clotting, bile, detox. detox clotting blood into a bile of glucagon.
35. exocrine because it dumps bile into the intestine, endocrine because it filters blood and adds to it.
36. the vein that brings oxygen poor but potentially nutrient rich blood into the liver from the GI tract.
37. the artery that brings fresh blood to the liver itself.
38. type three discontinuous.
39. basic cell type is the hepatocyte and they are arranged into lobules.
40. hexagonal shaped cell with a large central vein in the middle and a trio of vessels at every other corner of the border of the cell, called the portal area: containing hepatic portal vein (question 36), hepatic artery (question 37), and bile duct.
41. the liver acinus theory of blood flow says that blood flows laterally from the portal areas to the adjacent central vein (creating a diamond shaped functional unit overlayed on top of two lobules). this theory is backed up by the patterns of degradation during liver poisoning.
the first section, the esophagus, is unique in that its epithelia is made up of non-keratinized stratified squamous (presumably to deal with the abrasion of food coming in, and non-keratinized because waterproofing isn't an issue), which is thrown into esophageal glands that begin the lubricating process. the muscularis layer is also unique in that the top part of the esophagus is mainly skeletal muscle, gradually blends with smooth muscle in the middle, and by the bottom is mainly smooth muscle. the esophagus ends in the esophageal-cardiac junction, where the epithelial layer transitions from the non-keratinized stratified of the esophagus to the simple columnar of the stomach.
the stomach has four sections, from top to bottom: the cardiac, fundic, body, pyloric regions. the mucosa of the stomach is thrown into gastric glands, which contain specialized secretory cells which aid in digestion: surface mucous cells and mucous neck cells secrete mucous near the tops and bottoms of the glands, respectively. parietal cells secrete HCl near the tops of the glands, and chief cells secrete pepsinogen near the base of the glands. the muscularis of the stomach is also unique in that it has an inner oblique layer, middle circular, and outer longitudinal layer. the fundus is the most representative region of the stomach, and the other three regions are variations on this region. for example, the epithelia in both the cardiac and pyloric regions contain only mucous cells, and the muscularis layers are tightened into the cardiac and pyloric sphincters on either end.
after the stomach comes the small intestine, which is divided into three regions, the duodenum, jejunum (the most representative region), and ileum. the intestinal mucosa is unique in that it is folded into large intestinal glands called "Krypts of Lieberkuhn", covered with columnar absorptive/secretory cells called enterocytes, with goblet cells scattered throughout. also present in the epithelium are enteroendocrine cells, which secrete hormone like substances, as well as Paneth cells, which secrete lysozymes to regulate the bacterial flora in the gut. the lamina propria of the intestine is well vascularized with type 2 fenestrated capillaries, with occasional lymph nodes called Peyer's Patches. additionally, there is often a "central lacteal" inside the villi, which is a large lymph vessel that aids in absorption of larger molecules. the muscularis of the small intestine generally contains an inner circular layer, followed by a nerve "net" called the myenteric plexus, followed by an outer longitudinal muscle layer.
the large intestine is similar to the small intestine, the main differences being: more goblet cells, lymph rich, but no microvilli, paneth cells, or enteroendocrine cells. it has two main sections, the colon and the rectum, and at the "end of the line", the rectal-anal junction, there are four notable changes: the transition from the simple columnar absorptive cells of the small intestine to the non-keratinized stratified squamous of the rectum, the patchy muscularis mucosa, the huge blood vessels in the submucosa, and the presence of skeletal muscle in the muscularis externa. (notice how this is similar to the esophagus)
the role of the pancreas and liver in digestion is then looked at: the pancreas is a mostly exocrine gland which secretes from compound acinar glands a variety of enzymes-- carboxypeptidase, chymotrypsinogen, trypsinogen for digestion of proteins, amylase for digestion of carbohydrates, lipase for digestion of lipids, and bicarbonate to neutralize the acidity from gastric digestion. it also functions as an endocrine gland with its "Islets of Langerhans", which contain alpha, beta, and delta cells which release glucagon, insulin, and somatostatin, respectively. the liver also functions as both an endocrine / exocrine gland which aids in digestion by releasing bile for digestion of fats (exocrine) and filtering and adding to blood (endocrine). the liver has many functions, such as processing of glycogen, fetal blood cell production, production of blood clotting factors, and detoxification of the blood.
the basic cell type of the liver is called the hepatocyte, and they are arranged in roughly hexagonally shaped functional units called "lobules". on the borders of the lobules, on roughly every other corner of the hexagon, are "portal triads" which contain hepatic portal veins (which supply oxygen poor, nutrient rich blood to the liver from the intestine), hepatic arteries (supplying fresh blood to the liver), and bile ducts. in the center of the lobules are "central veins" which carry away deoxygenated blood. the last aspect of the liver that's looked at is the liver acinus theory, which states that blood flows from the portal triad laterally to the adjacent central veins, forming a diamond shaped functional unit overlayed on two lobules.
questions
1. what are the four primary layers in the entire digestive system?
2. what is the mucosa composed of?
3. what is in the submucosa?
4. what is the muscularis composed of?
5. what is the serosa composed of?
esophagus
6. describe the mucosa of the esophagus.
7. describe the muscularis of the esophagus.
8. describe the outer wall of the esophagus.
9. what is the esophageal-cardiac junction?
stomach- surface mucosa, mucosa neck, chief, parietal,
10. what are the four parts to the stomach?
11. describe the mucosa of the stomach.
12. what are some other cells that function in the mucosa of the stomach?
13. describe the muscularis externa of the stomach.
14. how does the cardiac region of the stomach differ from the body region?
15. how does the pyloric region of the stomach differ from the body region?
small intestine- lieberkuhn, enterocytes, paneth, meissner's, peyer's patch, brunner's
16. what are the three parts to the small intestine?
17. describe the mucosa of the small intestine.
18. what is unique about the surface of the mucosa of the small intestine?
19. what are the crypts of Lieberkuhn?
20. which digestive enzymes are secreted by the pancreas to aid in digestion in the small intestine?
21. what is secreted from the liver to help in digestion in the small intestine?
22. what are some of the cells in the mucosal epithelium of the small intestine?
23. describe the lamina propria of the small intestine.
24. describe the submucosa of the small intestine.
25. describe the myenteric plexus and what role it plays.
26. the serosa of the small intestine is the...
27. what are brunner's glands and what do they do? where are they found?
28. what are some distinguishing characteristics of the ileum?
large intestine-
29. describe the mucosa of the large intestine.
30. what are the four characteristics of the rectal-anal junction?
accessory glands- salivary glands, pancreas, liver,
31. what are the three types of salivary glands and what do they secrete?
32. describe the exocrine function of the pancreas.
33. describe the endocrine function of the pancreas.
34. name five major functions of the liver.
35. describe how the liver operates both as an exocrine and endocrine gland.
36. what is the hepatic portal vein?
37. what is the hepatic artery?
38. what type of capillaries are in the liver?
39. what is the basic cell type in the liver and what are they assembled into?
40. describe the architecture of the lobule.
41. what is the liver acinus theory? why is it the most likely scheme of blood flow in the liver?
answers
1. mucosa, submucosa, muscularis, serosa
2. epithelium (mostly simple columnar), lamina propria, muscularis mucosa
3. connective tissue with blood vessels and nerves, sometimes a submucosal plexus (meissner's)
4. inner circular layer of smooth muscle, middle plexus of ganglia (myenteric/auerbach's), outer longitudinal smooth muscle
5. CT, mesothelium
6. non-keratinzed stratified squamous epithelium, has esophageal glands for lubrication.
7. upper 1/3 made of skeletal muscle, middle 1/3 mix of skeletal and smooth muscle, lower 1/3 smooth muscle.
8. has adventitia, serosa seen only after tube penetrates diaphragm.
9. the end of the esophagus, an abrupt change from stratified squamous to simple columnar epithelium.
10. cardiac, fundus, body, pylorus
11. simple columnar epithelium with gastric glands for digestion, lamina propria which is richly vascularized, loose / reticular CT.
12. surface mucous cells, mucous neck cells secrete mucous on surface and at base of gastric pits. parietal cells secrete HCl at top of gland proper. chief cells secrete pepsinogen near base of gland.
13. inner oblique, middle circular, outer longitudinal. thickened at either end of stomach to form cardiac and pyloric sphincter.
14. cardiac region glands only have mucous cells, and there is an abrupt change from the esophagus.
15. pyloric region glands only have mucous cells. glands branch more and have deeper pits.
16. duodenum, jejunum, ileum.
17. simple columnar epithelium thrown into glandular tubes called intestinal glands (crypts of Lieberkuhn) and projections called villi.
18. they have a striated border formed from microvilli.
19. intestinal glands that both secrete and absorb.
20. trypsinogen, chymotrypsinogen, carboxypeptidase (for protein), amylase (for carbohydrates), lipase (for lipids)
21. bile salts (for lipids)
22. primarily composed of enterocytes which are columnar absorptive cells with microvilli, with mucous secreting goblet cells throughout, as well as enteroendocrine cells which are at the base of the glands and secrete hormone like substances, and paneth cells which secretes lysozyme to control bacterial flora.
23. well vascularized, type II capillaries, may have a central lacteal for absorption of larger molecules, may have lymph nodules called Peyer's patches.
24. may have a meissner's plexus, which assists in regulating secretion and blood flow.
25. a nerve net in the muscularis layer which helps coordinate peristaltic contractions of muscularis externa.
26. visceral peritoneum.
27. in the submucosa of the duodenum, secretes alkaline-mucoid material and urogastrone.
28. greatest amount of "GALT", Peyer's patches, fewer villi and more goblet cells.
29. simple columnar epithelia with intestinal glands but no villi. abundant goblet cells and lymph rich lamina propria, but no entero-endocrine or paneth cells.
30. epithelial transition from simple columnar to non-keratinized stratified squamous, patchy muscularis mucosa, huge blood vessels in submucosa, skeletal muscle in muscularis externa. transition, patchy, blood, skeletal.
31. parotid secretes mainly serous, submandibular secretes a mixture of mucous and serous, and sublingual secretes mostly mucous.
32. the pancreas' function is mainly to serve as an exocrine gland which secrete digestive enzymes (see question 20), composed of compound acinar glands. it also secretes alkaline bicarbonate in order to neutralize the acidity from gastric digestion.
33. 2% of the pancreas is used for endocrine function, in the form of "islets of langerhans" which are clumped glands which consist of alpha, beta, and delta cells which secrete glucagon, insulin, and somatostatin, respectively.
34. fetal hematopoesis (before shifting to bone marrow), glucagon processing, plasma protein production (such as clotting factors), bile production, and detoxification. blood, glucagon, clotting, bile, detox. detox clotting blood into a bile of glucagon.
35. exocrine because it dumps bile into the intestine, endocrine because it filters blood and adds to it.
36. the vein that brings oxygen poor but potentially nutrient rich blood into the liver from the GI tract.
37. the artery that brings fresh blood to the liver itself.
38. type three discontinuous.
39. basic cell type is the hepatocyte and they are arranged into lobules.
40. hexagonal shaped cell with a large central vein in the middle and a trio of vessels at every other corner of the border of the cell, called the portal area: containing hepatic portal vein (question 36), hepatic artery (question 37), and bile duct.
41. the liver acinus theory of blood flow says that blood flows laterally from the portal areas to the adjacent central vein (creating a diamond shaped functional unit overlayed on top of two lobules). this theory is backed up by the patterns of degradation during liver poisoning.
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