GI notes

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Author:
allisond
ID:
28592
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GI notes
Updated:
2010-08-01 10:32:13
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Physio
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GI system
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  1. goblet cells
    • mucus producing cells,
    • a solution of varying concentrations in different areas of the GI tract
  2. exocrine cells
    produce digestive enzymes and juices released directly into the lumen
  3. endocrine cells
    • produce hormones that enter the underlying vasculature
    • some act locally, have paracrine effects and others can act systemically
  4. inner layer of muscularis externa
    • inner circular layer: fibers arranged around the circumference of GI tract
    • when they contract, the diameter of the tube decreases
  5. outer layer of muscularis externa
    • longitudinal layer: fibers arranged lengthwise along tube
    • when they contract, the tube shortens
  6. Mesentery
    • double fused layer that connects parietal with the visceral
    • connects tube to the cavity wall and organs to tube
    • also a conduit for blood and lymph vessels and nerves
  7. segmentation contraction
    • movement of motility, contraction of inner muscles that narrows diameter and helps to mix food in that area
    • happens in seemingly random sections along GI tract
  8. Peristalsis
    • primary propulsive movements designed to move food along GI tract
    • involves contraction of both inner and outer muscle groups
    • where bolus of food is: behind bolus will have inner muscles contract to move bolus and outer muscles in front of bolus will contract at same time to help move food forward
  9. digestion of carbs
    • start as poly or di- saccharides usually in the form of starch of glycogens
    • long chains of monosaccharides ( glucose, galactose, fructose)
    • need to be monosaccharides for us to digest
  10. digestion of fats
    • start in form of triglycerides, 3 fatty acid chains held together in glycerol backbone
    • broken down by lipase into free fatty acids
  11. secretions in the mouth
    • amylase, mucus, lysozyme: all begin to breakdown cell walls or carbs in the mouth
    • can break down some sublingual drugs
  12. receptive relaxation
    • happens in the stomach
    • capacity of the stomach to hold food
  13. secretions in stomach
    digestive juices: HCL, pepsin, mucus, intrinsic factor ( necessary for us to absorb B12)
  14. non-digestive functions of GI tract
    • excretion
    • fluid and electrolyte balance- small intestine reabsorbs 9-11 liters/day
    • immunity: Kupffer cells in the liver
  15. Enteric Nervous system
    • has intrinsic control of gut function
    • branch of ANS, can still have GI function with a serious spinal injury
    • uses post-ganglionic fibers of the Para NS
  16. Myenteric Plexus
    • governs and regulates all motility
    • between inner and outer layer of muscles,
    • can regulate muscle movement itself, or with outside stimulation
    • sensory component can sense distention or stretch and result in muscle contraction
  17. Sub-Mucosal Plexus
    • direct control of secretion and indirect control of absorption and motility
    • regulating secretion regulates how fast digestion and absorption occur
    • can stimulate myenteric plexus to affect motility
    • sensory neurons can sense osmolarity, nutrient levels, toxins, distension, pH
  18. upper or pharyngoesophageal sphincter
    limits air trapped in GI tract, relaxes only when it needs to
  19. lower or gastroesophageal sphincter
    protects esophagus from acidic juices of the stomach
  20. fundus
    portion of stomach above the level of the lower gastroesophageal sphincter
  21. antrum
    • bottom portion of stomach
    • where muscle is the thickest, responsible for mixing food
  22. pyloric gland area
    refers to mucosal lining, segment of mucus membrane found in antrum of stomach
  23. rugae
    • deep folds of stomach
    • allow for increased capacity of stomach during receptive relaxation, rugae flatten
    • can expand up to 20 times its resting size of 50 ml
  24. pace setter cells
    • in fundus of stomach
    • rhythmically depolarizing cells, waves are sub-threshold with we are at rest
    • when we anticipate food, waves begin to exceed threshold and they become peristalsis that moves down stomach wall to mix food into chyme
    • happens at regular interval
  25. oxyntic mucosa
    • cells of gastric secretion, within gastric pit
    • contain numerous cells types that secrete gastric juices
  26. goblet cells in oxyntic mucosa
    secrete thick alkaline mucus designed to create barrier to buffer walls from pH of stomach
  27. chief cells of oxyntic mucosa
    • create pepsinogen, which is converted to pepsin when it hits acid in stomach
    • pepsin breaks down proteins
    • produced in inactive form to save chief cells from autodigestion by acidic juices
  28. parietal cells in oxyntic mucosa
    release HCL and intrinsic factor
  29. Enterochromaffin-like cells in oxyntic mucosa
    release small amounts of histamine which enhances release of HCL and pepsinogen in the stomach
  30. G cells of pyloric gland area
    • release gastrin which stimulates release of pepsinogen and HCL,
    • enhances gastric motility throughout rest of GI tract
    • "on" switch for gastric secretion
  31. D cells in pyloric gland area
    • release somatostatin
    • beginning of "off" switch for gastric secretion
  32. interdigestive phase of gastric secretion
    • what happens btw periods of digestion
    • governed by circadian rhythms- lowest in morning, highest at night
  33. cephalic phase of gastric secretion
    • cues that are all anticipatory of food entering the stomach
    • stimulates gastric secretion and motility so that as soon as food arrives it can begin to be digested
  34. extrinsic influence of cephalic phase
    • vagal enervation to enteric NS, will affect sub-mucosal plexus
    • this causes secretion stimulation and indirectly affects myenteric plexus
    • increased levels of pepsinogen, HCL, gastrin and histamine ( redundancy)
  35. gastric phase of gastric secretion
    • governed by cues surrounding presence of food in the stomach
    • once food hits stomach, motility and secretion are stimulated
  36. intestinal phase of gastric secretion
    • when we start to ramp down secretion and motility
    • governed by food withdrawal from stomach and entry of food into duodenum
    • cues are withdrawal of protein from stomach, increased acidity of stomach stimulates secretion of somatostatin which inhibits parietal, G and ECL cells
  37. signals of food entering duodenum
    • presence of fat
    • presence of acidity: intestine needs pancreatic secretions to protect itself from HCL
    • hypertonicity: one big substance is becoming 20 smaller substances
    • distention
    • duodenal mucosal cells sense changes and can affect gastric fxn through ENS, reduction in hormone release ( G cells)
  38. CCK
    • released in duodenum, inhibits gastric emptying
    • increases pancreatic and bile secretion
    • acts on acinar cells in response to fat and protein
    • release is shut off when proteins and fats are digested
  39. Secretin
    • released in duodenum, inhibits gastric emptying,
    • decreases HCL secretion, increases pancreatic secretion of Na bicarb to help neutralize acid
    • acts on duct cells
  40. acinar cells
    • exocrine cells of the pancreas
    • digestive enzymes are all packaged and released together, no matter the content of your meal
    • stimulated by CCK
  41. duct cells
    • release sodium bicarbonate to neutralize stomach acid in the intestine
    • stimulated by secretin
    • mixes with bile before it enters duodenum
  42. Pancreatic enzymes
    • all releases in inactive forms
    • trypsinogen: trypsin, actives the next two
    • chymotrypsinogen: chymotrypsin
    • Procarboxypeptidase: carboxypeptidase
    • pancreatic amylase and lipase
  43. sphincter of Oddi
    • between bile duct and duodenum
    • shut when we arent actively digesting fat
    • relaxation is stimulated by CCK to allow bile to enter duodenum
  44. micelle
    • absorbable unit of fat in the body, what lipase works on
    • droplet of fat that is surrounded by bile salts- has been emulsified
    • increases surface area
  45. control of bile secretion
    • absence of fat in the duodenum means there is no longer stimulation for CCK
    • CCK levels drop, Sphincter of Oddi constricts and no more bile gets into the duodenum
  46. cues that increase segmentation in jejunum and ileum
    distention, presence of gastrin, extrinsic nerve activity- vagal input
  47. membrane bound enzymes in small intestine
    • bound to brush border
    • enterokinases: aid in protein digestion
    • disaccharidases: break di into mono
    • aminopeptidases: aid in protein digestion
  48. Intestinal Villi
    • increase surface area by 600 times
    • each is lined with cells that contain microvilli
  49. crypts of Lieberkuhn
    • valleys between villi,
    • contain constantly dividing stem cells that move up the villi to ensure we have the optimal absorptive cells on the top of the villi
    • cells are constantly shedding
  50. central lacteal
    lymph vessel inside the villi where fat enters the systemic circulation
  51. haustral contractions
    • haustra: tiny pouches in the colon
    • similar to peristaltic wave, enhance water and electrolyte reabsorption
    • mass movements that happen 3-4 times/day
    • stimulated by release of gastrin, can drive feces the entire length of the colon
  52. defecation reflex
    • when propulsive movement push feces into the rectum, distention stretch receptors sense stretch and causes receptive relaxation of the internal anal sphincter
    • you voluntary relax the external sphincter when you are ready and this allows you to have a bowel movement
    • lose reflex if you dont have a BM

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