Digestion
chemical alteration of food into absorbable things
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| Term | Definition |
|---|---|
| Digestion | chemical alteration of food into absorbable things |
| Absorption | movement of digested food from intestine to blood or lymphatic system |
| From what point of the GIT does the composition become similar | mid-esophagus to anus |
| What is the mucosa made of | Epithelium, lamina propria, muscularis mucosa |
| Structures of the GIT | mucosa, submucosa, muscularis externa, serosa |
| T/F: epithelial layer is not polarized | False, it is (diff at one surface than the other) |
| What arrangements are the mucosa | basolateral and apical |
| How do transport proteins bind to membrane | tight junctions |
| T/F: epithelial layer is selective | True |
| Paracellular pathway | limited by tight junctions water/small ions diffuse |
| Transcellular pathway | two step process requires transport protein on apical/basolateral side of cell |
| Components of Lamina Propria | connective tissue lymphatic vessels immunity cells small vessels |
| Components of Muscularis mucosa | thin, smooth muscle - NOT involved in contraction controls villi movement |
| Purpose of submucosa | - nerve cell bodies - relay info to/away from mucosa |
| Purpose of muscularis externa | thick inner layer (fibers cause narrowing of lumen) of circular muscle - myenteric nerve plexus thinner outer layer of longitudinal muscle (fibers shorten tube) |
| Purpose of serosa | thin layer of connective tissue |
| How does blood travel in the GIT | perfuses intestine then flows to liver via portal vein |
| How does the portal vein circulate blood | drains blood from digestive tract and empties into liver - circulation of nutrient-rich blood between gut and liver = PORTAL CIRCULATION |
| Purpose of portal circulation | remove harmful substances process nutrients |
| T/F: the liver receives blood from only venous (portal circulation) | False, it receives blood from venous and arterial circulation |
| Is venous supply series or parallel | in series |
| What does "in parallel" mean | most circulation to organs is in parallel |
| What does the enteric nervous system control | activity of secretomotor neurons (motility and secretory function) |
| Can enteric nervous system function independently of the CNS | Yes, its critical for involuntary functions |
| What are the two nerve networks of the enteric nervous system | - myenteric plexus and submucosal plexus |
| What does the myenteric plexus control | influences smooth muscle |
| What does the submucosal plexus control | influences secretion |
| Extrinsic neuronal regulation of GI process | - regulates through ANS (parasympathetic/sympathetic) |
| Chemical messengers: endocrine | messenger passes from cell -> produces it into blood and carried by blood to target |
| Chemical messengers: neurocrine | messenger released from nerve cell, travels across synapse |
| Chemical messengers: paracrine | messenger diffuses through interstitial fluid to near cells |
| Chemical messengers: autocrine | messenger acts on cells which produced it |
| Where are endocrine cells located | through epithelium of stomach and SI |
| How do hormones function in GI (endocrine cells) | one surface of each endocrine cell is exposed to GI lumen - chemicals in lumen stimulate release across surface of cell into blood vessels in lamina propria |
| 4 GI hormones | - secretin - CCK - gastrin - GIP (glucose dependent insulinotropic peptide) - all peptides too |
| What is the feedback system of CCK | - fatty acids/amino acids in SI trigger CCK from SI cells into blood - CCK stimulates pancreas to increase digestive enzymes AND gallbladder to contract (releases bile acids to breakdown fat) - fats/AA absorbs and stimulation of CCK stops |
| Steps of peristalsis | - circular muscle contracts on a bolus of food (longitudinal layer relaxed) - circular contracting = towards anus, then longitudinal muscle contracts = smooth passage of bolus |
| What is segmentation | contraction/relaxation of intestine with no movement toward LI - essentially mixing |
| How does the GIT acquire a basic electrical rhythm | GIT has pacemaker cells throughout smooth muscle cells - causes spontaneous depol/repol = slow waves propagate through circular and longitudinal muscle layer through gap junctions |
| T/F: force of contraction does not affect neuronal/hormonal input | False |
| Cephalic (head) phase of GI control | receptors in head stimulated by the senses - parasympathetic fibers activate neurons in GI plexuses |
| Gastric phase of GI control | receptors in stomach stimulated by digestion, pH, AA, peptides - gastrin/acetylcholine |
| Intestinal phase of GI control | receptors in intestine stimulated by distension, osmolarity - CCK/GIP |
| What happens when there is lesions on the hypothalamus | animals become anorectic and lose weight - activation of hypo causes hunger |
| What makes you feel full | activation of satiating center |
| What happens when theres lesions on the satiating center | animals become obese |
| Purpose of orexigenic factors | increase intake |
| Types of orexigenic factors | - Neuropeptide Y: stimulates hunger - Ghrelin: made and released from endocrine cells in stomach during fasting - stimulates release of NPY in hypo feeding center |
| Purpose on anorexic factors | decrease intake |
| Types of anorexic factors | - Leptin (from adipose tissue) - insulin (from pancreas) - Peptide YY (from intestines) - Melanocortin (from hypothalamus) |
| What causes an increase in thirst | - increase plasma osmolarity - decreased plasma volume - dry mouth |
| What antidiuretic hormone is released when thirsty | vasopressin conserves water at kidney |
| How does plasma volume decrease | baroreceptors in kidney aff arteries activate renin-angiotensin system - produces angiotensin II = increases thirst |
| Types and purposes of salivary glands | - parotid (watery secretion) - submandibular (serous/mucous secretion) - sublingual (muscous) |
| Composition of saliva | - water, electrolytes, digestive enzymes, glycoproteins |
| What electrolytes is saliva poor in | poor in Na and Cl |
| What cell secretes the initial saliva | acinar cells |
| T/F: initial secretion is isotonic | true |
| What cells modify initial saliva | ductal cells, modify to hypotonic, alkaline state - loss of Na and CL - addn of K and HCO3 - impermeable to water |
| How is starch digestion initiated in the mouth? | amylase (ptyalin) |
| How is starch digestion inhibited? | acidic pH in stomach |
| T/F: lingual lipase is active in stomach | True |
| Solution to dry mouth | water and flouride |
| How is swallowing initiated? | by pressure receptors in walls of pharynx |
| Mechanism of swallowing | 1. tongue pushes bolus to back of pharynx 2. soft palate elevates to block nasal passage 3. epiglottis covers glottis to block trachea 4. food into esophagus |
| When are the esophagus sphincters open | swallowing, vomiting, burping |
| Upper esophageal sphincter | ring of skeletal muscle below pharynx |
| Lower esophageal sphincter | ring of smooth muscle at stomach - comes after upper sphincter |
| What organ secretes pepsinogen, HCl, and IF | The stomach |
| What does a vitamin B12 deficiency cause? | pernicious anemia, Need a lack of IF too |
| What is the purpose of the fundus (stomach) | - thin layer of smooth muscle - secretes: pepsinogen, HCl |
| What is the purpose of the antrum (stomach) | - thick smooth muscle layer - secretes: pepsinogen, gastrin |
| Exocrine | chemical messengers secreted into ducts then onto spithe |
| What are the major exocrines? | - mucus: protective coating to avoid self-digestion - HCl: hydrolysis of proteins - Pepsinogen: digests proteins |
| What are the minor exocrines? | - IF: for b12 absorption |
| Purposes of Gastrin and Histamine? Are they endo or exocrines? | - Gastrin: stimulates HCl production and moves stomach, endocrine - Histamine: stimulates HCl, paracrine |
| Purpose of somatostatin? | paracrine, inhibits HCl production |
| Chief cells | - gastric glands in all regions - secrete pepsinogen |
| Enteroendocrine cell | - gastric glands in antrum - secrete gastrin |
| ECL cells | - gastric glands in all regions - secrete histamine |
| D-cells | - gastric glands in all regions - Secrete somatostatin |
| Parietal cell purpose | - secrete HCl and IF - acid secretion requires energy (lots of mitochondria) - aka an oxyntic cell |
| Canaliculi | increase SA and maximize secretion into stomach lumen |
| T/F: the lumen has a higher pH then the cytosol | False |
| How does the H/K ATPase acidify the stomach lumen | - pumps H into lumen in exchange for K into cell - Active transport - electroneutral |
| Carbonic anhydrase | catalyzes formation of H2CO3, which dissociates into H and HCO3 |
| How does the Cl/HCO3 exchanger acidify the stomach | OH is effluxed from cell as HCO3 in exchange for Cl |
| How do K channels acidify stomach | K is recycled back into stomach - Diffusion - loss of pos charge |
| How do Cl channels acidify stomach | Cl leaks back into stomach lumen - diffusion - compensate for loss of pos charge |
| What 4 chemical messengers regulate acid secretion | - gastrin, ACh, histamine, somatostatin |
| What is happening to the plasma membrane to create acid secretion | chemical messengers regulate insertion of H/K ATPase into plasma membrane |
| T/F: pepsin is only active at low pH | true |
| Describe 3 phases of gastric secretion | 1. Cephalic phase: excitatory, via vagus nerve 2. Gastric phase: excitatory, via gastrin 3. Intestinal phase: inhibitory (bc of acid/fat/digestion products and hypertonic soln in duodenum) |
| How can ACh increase acid secretion by parietal cell? | - stim release of gastrin from G-cells - stim release of histamine from ECL cells - inhibit somatostatin from d-cells - stim histamine release |
| What happens to parasympathetic input when acid secretion is at a high rate | reduces (cephalic phase) |
| What happens to gastrin production once acid secretion is high | acid inhibits release |
| What happens in body when vomiting | - glottis closes of trachea - lower esophageal sphincter and esophagus relax - diaphragm and abdominal muscles contract - reverse peristalsis moves upper intestinal contents into stomach - stomach moves it through esophagus and out through mouth |
| What is a peptic ulcer | - damaged area of GIT mucosa (in acidic regions) |
| What causes an ulcer | - imbalance between aggressive and protective factors - bacterial infection: helicobacter pylori - non-bacterial factors: NSAIDS - decrease prostaglandin |
| How to treat ulcers | antibiotics, H/K inhibitor ATPase inhibitor, histamine antagonist, prostaglandin drugs |
| What does the exocrine pancreas do | - produce secretions for going into gut - source for digestion enzymes - secreting HCO3 into duodenum for neutralization |
| What does the endocrine pancreas do | produce hormones that regulate entire body |
| What type of cells to pancreatic ducts include | acinar cells: produce and secrete digestive enzymes - also secrete H20 and HCO3 |
| What electrolytes are in pancreatic juices | - High HCO3, low Cl - Na/K - HCO3 and H2O (duct cells) |
| Describe the sequence of events for ductular cell secretion of HCO3 | - Chloride channel opens (allows diffusion of Cl into lumen) - Cl exchanged for HCO3 - H2O and Na follow in response to electric gradient across eipthelium - neutral pH maintained by H exchange for Na - resulting watery secretion neutralizes gastric acid and washes enzymes through |
| What is alkaline tide | large amount of HCO3 pumped across basolateral surface into bloodstream - from large meal (parietal cells producing lots of acid) |
| What is acid tide | large amount of H pumped across basolateral surface into bloodstream - duct cells producing and secreting HCO3 |
| What do acinar cells do to pro-enzymes? | synthesize and package them into zymogen granules to store at apical pole of the cell |
| How do zymogen cells enter the lumen of the duct | exocytosis due to neurohormonal input |
| Enterokinase | enzyme in luminal membrane of duodenum - cleaves trypsinogen to trypsin (protease) |
| How does the body prevent autodigestion under normal conditions | - releasing trypsin inhibitors to stop any activated trypsin from acting |
| What channel is mutated in cystic fibrosis | the Cl- channel involved in HCO3 secretion in pancreas |
| What are the symptoms of CF patients "pancreatic insufficiency" | - still produce all digestive enzymes - HCO3 and H2O secretion is minimal and enzymes don't reach intestine - retained proteolytic enzymes = autodigestion - need supplements of digestive enzymes/antacids |
| Describe the hexagonal structure of the hepatic | - central vein through center - portal triads at each corner |
| What is a portal triad composed of? | - hepatic artery, portal vein, bile duct |
| Major functions of the liver | - exocrine gland (form/secretion of bile) - metabolism/storage of nutrients (ie. glucose) - detoxification - produce circulating proteins (coag factors) |
| Components of bile | - bile acids (made in hepatocyte from cholesterol) - cholesterol - salts - phospholipids - bile pigments - trace metals |
| Role of bile in fat digestion | - emulsification - formation of micelles |
| Purpose of micelles | - keep fats in small globules - holding stations for small, non soluble lipids |
| T/F: heptocytes secrete bile acids through diffusion | false, always secrete through active transport pathways |
| Purpose of gallbladder | stores bile between meals then expels into duodenum after |
| How does the recycling of bile acids happen | enterohepatic circulation |
| Why is enterohepatic circulation good | secretion rate is higher than synthesis rate |
| Steps of bile acid recycling | 1. bile acids released by liver/gallbladder in duodenum for fat digestion 2. bile acids reabsorbed across SI (ileum) into portal circulation 3. bile acids transported into hepatocytes |
| What does dietary fibre do to bile acids | prevents them from cycling back to liver and resulting in their loss in feces - lowers plasma cholesterol |
| What happens when more bile salts are absorbed by the ileum during hepatobilary secretion | - more salts secreted into bile - salt synthesis reduced when enterohepatic circulation is working well |
| What happens when secretin is released by s-cells during hepatobiliary secretion | - increases HCO3 secretin in bile ducts and pancreas - secretin release stimulated by acid is duodenum |
| What happens when CCK is produced by I-cells during hepatobiliary secretion | - increases contraction of gallbladder and relaxes sphincter of Oddi - bile released CCK released stimulated by digested fats/protein in SI |
| How is cholesterol kept in bile? | through formation of micelles with bile acids and phospholipids |
| What is required when conc of cholesterol becomes too high | nucleating agent to precipitate it out |
| What causes pigment stones | excessive hemolysis, which increases bile pigment conc, and precipitates w/ Ca |
| Function of duodenum | - mixing of pancreatic digestive enzymes and bile w/ food - absorption of nutrients - release of endocrine hormones |
| Function of jejunum/ileum | - digestion and absorption |
| Function of brush border enzyme | enzyme anchored to catalytic activity in lumen - breaks down carbs and peptides into sugars/amino acids prior to enterocyte transfer |
| Describe the steps of fat digestion | 1. lipid droplets are emulsified and allow pancreatic lipase to release FA and monoglycerides 2. products of lipase are incorporated into micelles 3. micelles break down and release FA and monoglycerides to diffuse across SI 4. enterocyte FA and monoglycerides processed in ER into triglycerides 5. ER triglycerides aggregate into lipid droplets coated w/ amphipathic proteins 6. lipid droplets packaged in golgi and secreted via exocytosis |
| Name for extracellular fat droplets | chylomicrons |
| Components of chylomicrons | triglycerides, phospholipids, fat soluble, vitamins, cholesterol |
| What system do chylomicrons enter? | lymphatic |
| How do lymphatics enter into systemic circulation | thoracic duct |
| How does the protein iron complex form | Iron is actively transported into enterocyte and incorporated into ferritin (protein) - storage form |
| What happens to iron that is not stored | released on blood side of enterocyte and transported through blood attached to transferrin (plamsa protein) |
| How is iron remaining in enterocyte excreted from body | iron bound to ferritin excreted with enterocytes slough off villi tips |
| What happens when iron stores are ample | too much ferritin = reduced absorption of iron |
| What happens when iron stores are depleted | production of intestinal ferritin decreased = increased absorption |
| What does iron accumulation do | toxicity (skin pigmentation) and heart failure |
| Where does water absorb and secrete from | absorbs: villi secretes: crypts |
| How does water flow? what causes it? | Intestinal epithelium establishes osmotic gradient and water follows through tight junctions |
| Which electrolytes are important for water transport | Na, Cl, HCO3 |
| What electrolyte is crucial for water absorption | Na gradients generated during secondary active nutrient uptake - glucose and AA |
| What electrolyte is crucial for water secretion | Cl gradients during secondary active Na/K/2Cl transporter - NKCCl |
| What is segmentation | continuous division of intestinal contents - mechanical breakdown - mixing food with digestive enzymes |
| What are the frequencies of contraction for the duodenum and ileum | duodenum: 12 contractions/min ileum: 9 contractions/min |
| How is contraction force set | neurohormonal input |
| Migrating myoelectric complex | - in lower portion of stomach - overlapping wave starts in SI then repeats - pushes any undigested material from SI to LI - prevents bacteria from remaining in SI |
| What regulates MMC | motilin |
| When does MMC stop | when next meal is consumed |
| What enzyme is lactose digested by | lactase (brush border enzyme) breaks it into monosaccharides glucose and galactose |
| Cannot completely digest lactose symptoms | - decreased water absorption - lactose containing fluid passes onto LI = gas |
| How do you get cholera | - occurs after eating food or drinking water w/ Vibrio cholerae bacteria |
| What does Vibrio cholerae toxin do | increase production cAMP in crypt epithelium of SI - results in activation of Cl and secretion of Cl in gut, lumen, water follows |
| Ileocecal valve | - sphincter between cecum and ileum |