BRS Gastrointestinal Phys

secretion or absorption

contraction changes surface area

contraction causes decrease in diameter of lumen of GI tract

contraction causes segmental shortening of GI tract

- comprises the enteric nervous system of GI tract
- integrates and coordinates the motility, secretory, and endocrine functions of the GI tract

sensory info from chemoreceptors and mechanoreceptors in GI tract to brain stem and spinal cord

- excitatory
- carried via vagus and pelvic nerves
- preganglionic parasympathetic fibers synapse in the myenteric and submucosal plexuses
-

- esophagus, stomach, pancreas, upper large intestine

lower large intestine, rectum, anus

- inhibitory on functions of GI tract
- fibers originate T8-L2

prevertebral ganglia

-myenteric and submucosal plexuses
- direct postganglionic adrenergic innervation of blood vessels and some smooth muscle cells also occurs

- coordinates and relays information from parasympathetic and sympathetic nervous systems to the GI tract
- uses local reflexes to relay information within GI tract
- controls most functions of the GI tract, especially motility and secretion, even in absence of extrinsic innervation

- controls motility of GI smooth muscle

- controls secretion and blood flow
- receives sensory information from chemoreceptors and mecahnoreceptors in GI tract

- released from endocrine cells in the GI mucosa into the portal circulation, enter general circulation- affect target cells

- gastrin
- CCK
- secretin
- glucose-dependent insulinotropic peptide (GIP)

- secreted in response to a meal

within four C-terminal amino acids

1.) increases H+ secretion from parietal cells
2.) stimulates growth of gastric mucosa by stimulating synthesis of RNA and new protein

- hypertrophy and hyperplasia of gastric mucosa

- from the G cells of the antrum in response to a meal
- distention of stomach
- vagal stimulation- mediated by GRP

- atropine does not block vagally mediated gastrin secretion because the mediator of the vagal effect is GRP not ACh

- H+ in the lumen of the stomach
- somatostain

- gastrin is secreted by non-B-cell tumors of the pancreas

- 33 AAs
- homologous to gastrin
- five C-terminal AAs are the same in the two

- C-terminal heptapeptide
- contains sequence that is homologous to gastrin and has gastrin activity as well as CCK activity

1.) contraction of the gallbladder; relaxation of the sphincter of Oddi for secretion of bile
2.) pancreatic enzyme secretion
3.) potentiates secretin-induced stimulation of HCO3- secretion
4.) stimulates growth of exocrine pancreas
5.) inhibits gastric emptying

fatty meals; slows gastric emptying to allow more time for intestinal digestion and absorption

- from the I cells of the duodenal and jejunal mucosa

- small peptides and AAs
- fatty acids and monoglycerides

- triglycerides because they cannot cross intestinal membranes

glucagon

1.) stimulate pancreatic HCO3- secretion and increases growth of exocrine pancrease
2.) stimulates HCO3- and H20 secretion by the liver, and increases bile production
3.) inhibits H+ secretion by gastric parietal cells

S cells in the duodenum

1.) H+ in the duodenal lumen
2.) fatty acids in the duodenal lumen

- secretin and glucagon

1.) stimulates insulin release
2.) inhibits H+ secretion by gastric parietal cells

- secreted by duodenum and jejunum
- only GI hormone that is released in response to fat, protein, and carbohydrate
- stimulated by fatty acids, AAs, and orally administered glucose

oral because of GIP

- released from endocrine cells in GI mucosa
- diffuse short distances to act on target cells in GI tract
- somatostatin and histamine

throughout the GI tract in response to H+ in the lumen

vagal hormones

inhibits release of all GI hormones; also inhibits gastric H+ secretion

- secreted by mast cells of gastric mucosa

increases gastric H+ secretion directly and by potentiating effects of gastrin and vagal stimulation

- made in neurons of the GI tract, moved by axonal transport down the axon; released by action potentials

diffuse across synpatic cleft of the vesicle

vasoactive intestinal peptide, GRP (bombesin), and enkephalins

secretin

- produces relaxation of GI smooth muscle including lower esophageal sphincter
- stimulates pancreatic HCO3- secretion and inhibits gastric H+ secretion
- secreted by pancreatic islet cell tumors

- pancreatic cholera

- from vagus nerves that innervate G cells
- stimulates gastrin release from H cells

nerves int he mucosa and smooth muscle of GI tract

- stimulate contraction of GI smooth muscle (especially lower esophageal, pyloric, and ileocecal sphincters)
- inhibit intestinal secretion of fluid and electrolytes; usefulness of opiates in treatment of diarrhea

- almost exclusively unitary smooth muscle

pharynx, upper 1/3 of the esophagus, external anal sphincter (all striated muscle)

depolarization of circular muscle

depolarization of longitudinal muscle

esophagus, gastric antrum, small intestine (contract and relax periodically)

lower esophageal sphincter, orad stomach, ileocecal and internal anal sphincters

- oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GI tract
- occur spontaneously
- originate in interstitial cells of Cajal which serve as the pacemaker for GI smooth muscle
- NOT action potentials but determine pattern of action potentials

- cyclic opening of Ca channels (depolarization) followed by opening of K+ channels (repolarization)

each one brings the potential of smooth muscle cells closer to threshold and increases likelihood that an AP will occur

- varies along GI tract; constant and characteristic for each part
- not influenced by neural or hormonal input; frequency of the APs that occur on top of slow waves is modified by neural and hormonal influences

- sets the maximum frequency of contractions for each part of the GI tract

- lowest in the stomach: 3 waves/min
- highest in the duodenum: 12 waves/min

-coordinated by the medulla; fibers in vagus and glossopharyngeal nerves

- nasopharynx closes, breathing is inhibited
- laryngeal muscles contract to close the glottis and elevate the pharynx
- peristalsis begins in pharynx to propel food bolus toward esophagus while upper esophageal sphincter relaxes

equal to thoracic pressure so lower than atmospheric pressure

vagally mediated; VIP

if lower esophageal sphincter does not relax during swallowing and foot accumulates in the esophagus

- longitudinal and circular
- oblique

- fundus and proximal body
- contains oxyntic glands and is responsible for receiving the ingested meal

- antrum and distal body
- responsible for contractions that mix food and push it into duodenum

- vasovagal reflex

initiation: distention
abolition: vagotomy

closes the distal antrum; as caudad stomach contracts, food is propelled back into the stomach to be mixed (retropulsion)

increased: vagal stimulation
decreased: sympathetic stimulation

- contractions that occur at 90 minute intervals to clear the stomach of residual food

lower esophageal sphincter, orad stomach, ileocecal and internal anal sphincters

- oscillating membrane potentials inherent to the smooth muscle cells of some parts of the GI tract
- occur spontaneously
- originate in interstitial cells of Cajal which serve as the pacemaker for GI smooth muscle
- NOT action potentials but determine pattern of action potentials

- cyclic opening of Ca channels (depolarization) followed by opening of K+ channels (repolarization)

each one brings the potential of smooth muscle cells closer to threshold and increases likelihood that an AP will occur

- varies along GI tract; constant and characteristic for each part
- not influenced by neural or hormonal input; frequency of the APs that occur on top of slow waves is modified by neural and hormonal influences

- sets the maximum frequency of contractions for each part of the GI tract

- lowest in the stomach: 3 waves/min
- highest in the duodenum: 12 waves/min

-coordinated by the medulla; fibers in vagus and glossopharyngeal nerves

- nasopharynx closes, breathing is inhibited
- laryngeal muscles contract to close the glottis and elevate the pharynx
- peristalsis begins in pharynx to propel food bolus toward esophagus while upper esophageal sphincter relaxes

equal to thoracic pressure so lower than atmospheric pressure