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submucosal plexus lies between submucosa and circular muscle
myenteric plexus is between circular muscle and longitudinal muscle
relax smooth muscle, contract sphincters, increase salivary secretion
from neurons of mucosa and smooth muscle - relax smooth muscle, increase intestinal and pancreatic secretion
peptides released from endocrine cells of GI tract. secreted into portal circulation, pass thru the liver, and enter systemic circulation. systemic circulation then delivers hormone to target cells with receptors for that hormone. The target cells may be located in GI tract itself or elsewhere.
4 GI peptides classified as hormones: Gastrin, CCK, Secretin, and Glucose-dependent insulintropic peptide (gastric inhibitory peptide)
like hormones, are peptides secreted by endocrine cells of GI tract. they act locally within the same tissue that secretes them. reach their target cells by diffusing short distances through intestinal fluid or carried in capillaries.
function: promotes hydrogen ion secretion by gastric parietal cells.
-in response to eating a meal, gastrin is secreted from G cells located in antrum of stomach. Stimuli include products of protein digestion (small peptides and amino acids), distention of the stomach by food, and vagal stimualtion. Local vagal reflexes also simulate gastrin secretion - vagal endings release gastrin-releasing peptide onto G cells.. Gastrin secretion is inhibited by a low pH of gastric contents and by somatostatin
phasic contractions: periodic contractions followed by relaxation. found in the esophagus, gastric antrum, and small intestine - all tissues involved in mixing and propulsions.
Tonic Contractions: maintain constant level of contraction or tone wihtout regular periods of relaxation. They found in upper region of stomach & and in lower esophageal, ileocecal, and internal anal sphincters.
3 functions: 1. mixes food with saliva lubricating it to facilitate swallowing 2. reduces size of food particles facilitating swallowing 3. mixes ingested carbs with salivary amylase to begin carb digestion
chewing has both voluntary and involuntary components: involuntary component involes reflexes by initated byfood in mouth. sensory info is relayed from mechanoreceptors in mouth to the brain stem, which orchestrates a reflex oscillatory pattern of activity to muscles involved in chewing. voluntary chewing can ovveride involuntary or reflex
parasymp stimulation and hormones motilin and gastrin increase freq of APs and force of gastric contractions.
Sympathetic Stimulation: and hormones secretin and GIP decrease the frequency of APs and force of contractions
-usually excitatory on the functions of the GI tract, carried via the vagus and pelvic nerves.
-pre-ganglionic parasympathetic fibers synapse in the myenteric and submucosal plexuses.
-cell bodies in the ganglia of the plexuses then send information to the smooth muscle, secretoy cells, and endocrine cells of the GI tract.
innervates the esophagus, stomach, pancreas, and upper large intestine
-reflexes in which both afferent and efferent pathways aer contained in e vagus nerve are called vagovagal reflexes.
-contains 17 amino acids ("little gastrin"), little gastrin is the form secreted in response to a meal. all of the biologic activity of gastrin resides in 4 C-terminal amino acids.
-"big gastrin" contains 34 amino acids
-actions of gastrin: increases H+ secretion by gastric parietal cells, stimulates growth of gastric mucosa by stimulating synthesis of RNA and new protein. patients with gastrin-secrreting tumors have hypertrophy and hyperplasia of gastric mucosa
gastrin is secreted from G cells of the gastric antrum in response to a meal. Gastrin is secreted in response to: small peptides and amino acids in lumen of stomach (most potent: phenylalanine and trp), distention of stomach, vagal stimulation - mediated by gastrin-releasing peptide
-atropine does not block vagally mediated gastrin secretion because the mediator of the vagal effect is GRP, not ACh
-CCK is released from I cells of the duodenal and jejunal mucosa by:
-small peptides and amino acids
-fatty acids and monoglycerides (TG's dont stimulate release of CCK becuase they acn't cross intestinal cell membranes
coordinated to reduce amount of H+ in lumen of the small intestine
-stimulates pancreatic HCO3- secretion and increases growth of pancreas. Pancreatic HCO3- neutralizes H+ in the intestinal lumen. -stimulates HCO3- and H20 secretion by liver and increases bile production. -inhibits H+ secretion by gastric parietal cells
secretin is released by the S cells of the duodenum in response to:
1. H+ in the lumen of duodenum
2. fatty acids in the lumen of the duodenum
contains 42 aa, homologous to secretin and glucagon. stimulates insulin release (in presence of oral glucose load - inhibits H+ secretion by gastric parietal cells
stimuli: secreted by duodenum, and jejunum, GP is only GI hormone that is releaesd in resposne to fat, protein, and carbohydrate (orally administered glucose)
contains 28 aa and homolgous to secretin, released from neurons in the mucosa, and smooth muscle of GI tract, produces relaxation of GI smooth muscle, including the lower esophageal spinchter
-stimulates pancreatic HCO3- secretion and inhibits gastric H+ secretion (in these actions it represents secretin)
-secreted by pancreatic islet cell tumors and is presumed to mediate pancreatic cholera
Contractile tissue of the GI tract is almost exclusively unitary smooth muscle, with exception of pharynx and upper 1/3 of esophagus and anal external sphincter (striated muscle)
-phasic contractions occur in espohgaus, gastric antrum, and small intestine - contract/relax periodically
-Tonic Contractions: occurs in LES, orad stomach, ileocecal, and internal anal sphincter
oscillating membrane potentials inherent to smooth muscle cells of some parts of GI tract, occur spontaneously, originate in the interstitial cells of cajal, which serve as the pacemaker for GI smooth muscle, they are not action potentials although they determine the pattern of action potentials and therefore pattern of contraction
-depolarization during each slow wave brings membrane potential of smooth muscle cells closer to threshold, and therefore, increases probability that Aps will occur
-varies along the GI tract, but is constant and characteristic for each part of the GI tract, not influenced by neural or hormonla input, in contrast, the frequency of action potentials that occur on top of the slow waves is modified by neural and hormonal influences
-frequency of slow waves sets the max frequency of contraction for each part of GI tract, its lowest in stomach and highest in duodenum
esophagus propels food into stomach, sphincters at either end of esophgaus prevent air from entering upper esopgaus and gastric acid from entering lower esophagus
-because esophagus is located in thorax, intraesophageal pressure equals thoracic, which is low than atmospheric.
stomach has 3 layers of SM: longutidinal, circular, and third oblique layer
-stomach has 3 anatomic divisions - fundus, body, antrum
-orad region of stomach: includes fundus and proximal body, this regions contains oxyntic glands and is responsible for recieving ingestedmeal
as teh rectum fills with fecal material, it contracts and internal sphincter relaxes, oncerectum is filled to about 25% of its capacity, there is urge to defecate, however defecation is prevented because external anal sphincter is toncically contracted, when it is conveniate to defecate, the external anal sphincter is relaxed volunatrily, the smooth muscle of rectum contracts forcing feces out of body.
Intraabdominal pressure is increased by expiring against closed glottis (valsava maneuver
wave of peristalsis begins in small intestine, moving GI contents in orad direction. the gastric contents are eventially pushed into esophagus, if UES remains closed retching occurs, if pressure in esophagus becomes high enough, to open UES - vomting occurs. the vomiting center in medulla is stimulated by ticklying of back oft throat, gastric distension, and vestibular stimulation
-chemoreceptor trigger zone in 4V activated by emetics, radiation, and vestibular stimulation
-high volume, High K+ and HCO3- concentrations, low Na and Cl concentrations, hypotonic, and presence of alpha-amylase, lingual lipase and kallikrein
composition of sliva varies with salivary flow rate
modify inital saliva:
-the ducts reabsorb na and cl- therefore the concentrations of tehse ions are lower than their plasma concentrations
-the ducts secrete K+ and HCO3-, therefore, the concentrations of these ionsare higher
-thus at high flow rates, saliva is most like the initial secretion from the acinus, it has the highest Na and Cl ocncentration and the lowest K+ concentration.
At low flow rates, saliva is least like the initial secretion from the acinus, it has teh lowest Na and Cl concentrations and the highest K concentration. HCO3- secretion is selectively stimulated when saliva secretion is stimulated.
saliva production is controlled by the parasympathetic and sympathetic nervous systems (both increase salivary secretion)
-parasympathetic stimulation (cranial nerves 7 and 9) - increases saliva proudction by increasing transport processes in the acinar and duct cells and and by causing vasodilation. Cholinergic receptors on acinar and ductal cells are muscarinic(IP3 and increased Ca2)
-anticholinergic durgs (atropine) inhbit production of saliva causing dry mouth
parietal cells (located in fundus/body) -secrete HCL and intrinsic factor
-Chief cells (located in fundus body) and secrete pepsinogen
-G cells located in antrum - secrete gastrin
parietal cells secrete HCl into lumen of stomach and concurrently absorb HCO3- into blood stream.
-in parietal cells Co2 and H2o-> H+ and HCO3-, catalized by CA
-H+ is secreted into lumen of stomach by H+-K+ ATPase pump, CL- is secreted along with H+ thus secretion product of parietal cells is HCl
-the drug omezoprole: inhibts, H/K ATPase and blocks H secretion
-HCO3- produced in cells is absorbed into bloodstream in excahnge for Cl-
vagal stimulation: increases H+ secretion by direct and indirect path, in the direct path, the vagus nerve innervates parietal cells and stimulates H+ secretion directly via ACh/M3 receptor on parietal cells and second messenger is IP3 and increased Ca2. In the indirect path, the vagus nerve innervates G cells and stimulates gastrin secretion, which then stimulates H+ secretion by an endocrine action via NTer GRP (not ACh)
-vagotomy eliminates both direct and indirect paths, atropine only direct
released from enterochromaffin cells (ECL) cells in the gastric mucosa and diffuses to the nearby parietal cells. stimulates H+ secretion by activating H2 receptors on the parietal cell membrane (coupled to adenylyl cyclase via Gs protein) (second messenger cAMP)
H2 receptor blocking drugs: cimetidine
inhibited by low pH in stomach (< 3.0)
-inhbit gastrin secretion and thereby inhbit H+secretion, somatostain inhibits gastric H+ secretion by direct and indirect path, in direct path somatostatin binds receptors on parietal cells that are coupled to adsenylyl cyclaes via Gi (thus inhibiting adenylyl cyclase and decreaseing cAMP levels antagonizing action of histamine H+ secretion. In the indirect path, somatostatin inhibits release of histamine and gastrin decreasing H+secretion indirectly
ulcerative lesion of gastric and duodenal mucosa, can occur when there is loss of protective mucous barrier ( of mucus and HCO3-) and/or excessive scretion of H+ and pepsin. protetctive factors are mucus, Hco3-, prostanglandins, mucosal bloood flow, and grwoth factors
-damaging factors are H+, pepsin, H.pylori, NSAIDS, stress, smoking,and alcohol
gastric mucosa is damaged. gastric H+ secretion is decreased becaue secreted H+ leaks back through damaged gastric mucosa. Gastrin levels are increased because decreaed H+ secretion stimulates gastrin secretin. major cause of gastric ulcer is gram negative H. pylori which colonizes teh gastric mucus and releases cytotoxins that damage gastric mucosa
-H pylori contains urease which converts urea to NH3, thus alkalzining the local enviroment and permitting pylori to survive in an other acidic gastric lumen
high volume, virtually same Na and K concentration as plasma, much higher HCO3- concentration than plasma, much lower Cl- concnetration than plasma, Isotonic, pancreatic lipase, amylase and proteases
-at low flow rates: pancreas stimulates isotonic fluid compoesd mainly of Na and Cl
-high flow rates: pancreas secretes isotonic fluid compoesd mainly of Na and HCo3-
produce a small volume of initial pancreatic secretion by secreting Na and Cl
duct cells - modify secretion by secreting HCO3- and abosrbing CL-, because pacnreatic ducts are permeable to water H20 moves into lumen to make pacnreatic secretion isoosmotic
only monosaccarharides are absorbed. carbs must be digested to glucose, galactose, fructose for absorption to proceed. alpha amylases hydrolyze 1,4 glycosidic bonds in starch yielding maltose, maltotriose and alpha-limit dextrins
-maltase, alpha dextrinase, sucrase in intestinal brush border then hydrolyze oligosacccarhides to glucose
-lactase, trehelase and sucarse - degrade disaccharides into monosaccharides
endopeptidases, exopeptidsaes, pepsin (not essential, actiavted to pepsin by gastric H+)
-pancreatic proteases: trypsin, chymotrypsin, elastase, carboxypeptidae A and B
-secreted in inactive forms that are activated in SI, trypsinogen is activated to trypsin by brush border enzyme (enterokinase), trypsin is converts chymotrypsinogen, proelastaes, procarboxypeptidase A and B to their active forms
digestive products of protein can be absorbed as amino acids, dipeptides, and tripeptides
-free amino acids absorbed via Na+-dependent amino acid cotransport, and then into the blood via facilitiated diffusion
-4 separate carriers for neutral ,acidic, basic and imino amino acids
-in stomach, mixing breaks lipids into droplets to increaes the SA for digestion by pancreatic enzymes. lingual lipases digest some of ingested TGs to monoglycerides and FA's, however mots of ingetsted lipids are digested in the intestine via pancreatic lipases. CCK slows gastric empyting.
-SI: bile acids emulsify lipids in SI, increasing SA for digestion, pancreatic lipases hyrdrolyze lipds to FA's, monoglycerides and cholesterol and lysolecithin. (enzymes: pancreatic lipase, choelster eseter hydrolase, and phospholipase A2) hydrophobic products of lipid digestion are solubilized into micelles by bile acids
pancreatic diseaes (pancreatitis, CF) - no enzyme
-hypersecretion of gastrin - duodnenal pH go down and pancreatic lipaes doesn't work in acidic environment
-ileal resection - leads to depeltion of bile acid pool because they dont recircualte in the liver
-bacterial overgrowth: may lead to deconjugated of bile acids and early absorption in the small intestine
-decreased number of intestinal cells for lipid abdorption
-failure to synthesize apoprotein B which leads to inability to form chylomicrons.
Na moves into intestinal cells across the luminal memrbanea nd down its concentration gradient by following mechanisms:
-passive diffusion (through na channels)
-Na+-glucose/Na+ amino acid transport
-Na-Cl co transport
passive diffusion via Na+ channels.stimulated by aldosterone
Cl- absorption accompanies na+ absorption throughout the GI tract by: passive diffusion by paracellular route, Na-Cl cotransport, and Cl-HCO3- exchange
dietary K+ is absorbed in the small intestine vy passive diffusion via paracellular route. K+ is actively secreted in colon (stimulated by aldo),
-in diarrhea - K+ secretion by the colon is increaed because of flow rate -dependent mechanism similar to that in the renal distal tubule. excessive loss of K+ in diarrheal fluid causes hypokalemia
absorption depends on presence of adequate amounts of actie Vitamind D produced in kidney, it induces synthesize of intestinal Ca2+ binding protein, calbindin
-vitamin D deficiency or chronic renal failure: result in inadequate intestina lCa absorption causing rickets in children and osteomalacia in adults
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