general introduction and oral eosphageal response to a meal Flashcards
General tract from mouth to anus
- mouth and esophagus - 8-10 sec 2. stomach - 1-3 hours 3. small intestine - 7-9 hours 4. large intestine - 25-30 hours 5. rectum and anus - 30-120 hours
Bristol stool scale
7 types of stool assessment of transit time in GI tract
optimal delivery rate, maintaining barrier function the above are mediated by
- extrinsic nerves 2. intrinsic nerves 3. neurocrines 4. paracrines 5. hormones
Extrinsic nerves
autonomic nervous system (ANS) - sympathetic - parasympathetic
intrinsic nerves
enteric nervous system (ENS)
neurocrine
signals released from nerve endings
paracrine
released from specialized mucosal cell some are involved in immune modulation
endocrine hormones
released into systemic circ. - return to exert action
parasympathetic and sympathetic effect on: motility sphincter tone secretion vascular resistance
Para - increase motility - decrease the sphincter tone - increase secretion - no effect on vascular resistance (blood flow to gut) sym - decrease motility - increase sphincter tone - decrease secretion (except salivary glands) - increase vascular resistance (vasocontrict blood flow to gut)
two major nerve plexuses
- myenteric (Auerbach’s) plexus 2. submucosal (Meissner’s) plexus these are collections of neuronal ganglia and their fibers the above is Enteric Nerve System (ENS) and can be viewed as third branch of AUTOMATIC NERVOUS SYSTEM
nuerotransmitters of ENS
- acetylcholine 2. norepinephrine 3. peptides
NANCs
non adrenergic, non cholinergic neurons
parasympathetic and sympathetic nerve innervation of the gut
postganglionic sympathetic fiber - direct projection to smooth muscle of gut wall, b-vessel, and enteric neurons in both plexus parasympathetic fiber - project to enteric neuron, myenteric plexus - indirect (para affect via ENS neurons para and sym modulate each other through ENS
3 types of neurons in ENS
- sensory neurons 2. interneurons 3. motor neurons
sensory neuron
monitor changes, input to interneurons and CNS
interneurons
relay signal - activate or inhibit motor neurons interneurons of both plexuses synapse
motor neurons
simulate or inhibit smooth m. and secretion
program libraries
ENS neuronal circuits operate autonomously
short reflex
peristaltic reflex program library based
long reflex
i.e. Vago-vagal reflex autonomic input modify program libraries to produce long reflex
vago-vagal reflex
sensory input -> vagal afferent fiber -> CNS -> resulting coordinated alteration -> vagal efferent fibers -> affect all regions of the gut
major neurotransmitters of GI
- acetylcholine (ACh) - parasympathetic and enteric 2. substance P - parasympathetic and enteric 3. nitric oxide (NO) - parasympathetic and enteric 4. norepinephrine (NE) - sympathetic 5. neuropeptide Y - sympathetic and enteric 6. vasoactive Intestinal polypeptide (VIP) - enteric
acetylcholine (ACh) (GI nervous sys, and function)
- parasympathetic and enteric - increase motility - increase secretion released from autonomic fibers -> effect activity of enteric neuron -> release different NT
substance P (GI nervous sys, and function)
- parasympathetic and enteric - increase motility
nitric oxide (NO) (GI nerve sys, and function)
- parasympathetic, enteric - muscle relaxation
norepinephrine (NE) (GI nerve sys, and function)
- sympathetic - decrease motility, blood flow and secretion released from autonomic fibers -> effect activity of enteric neuron -> release different NT
neuropeptide Y (GI nerve sys, and function)
- sympathetic, enteric - decrease motility and secretion
vasoactive intestinal polypeptide (VIP)
- enteric - muscle relaxation - increase secretion (include electrolyte)
other (minor) NT of GI
- opiods (Met and Leu enkephalins) 2. 5-HT (5-hydroxythryptamine) (serotonin) - enteric 3. gamma amino butyric acid (GABA) - enteric
serotonin (5-hydroxytryptamine) (func)
- released by luminal stimuli - stimulate intrinsic sensory neuron ->local peristaltic reflex - stimulate extrinsic sensory nerve -> discomfort signal from GI to CNS
GABA (gamma-amino butyric acid)
inhibitory effect on motility and secretion
brain-gut-axis
TBA
GI endocrine hormones (6 of them)
- gastrin 2. CCK 3. secretin 4. GIP 5. Motilin 6. ghrelin
hormone secreting cell distribution through GI tract
- gastrin - from antrum to jejunum 2. CCK - from duodenum to ileum 3. Secretin - from duodenum to ileum 4. GIP - from duodenum to jejunum 5. Motilin - from duodenum to jejunum 6. ghrelin - from fundus to antrum
6 distinct regions for endocrine hormone secretion
- fundus - ghrelin 2. antrum - gastrin 3. duodenum - decreasing gastrin, CCK, Secretin, GIP, Motilin 4. jejunum - CCK, secretin, GIP, motilin 5. Ileium - decreasing CCK, decreasing secretin
control of the hormone release
- protein and amino acid - increase gastrin and CCk, decrease motilin 2. carbohydrates - increase in GIP, decrease in Motilin 3. fatty acid - increase CCK, Secretin, GIP, decrease in motilin 4. luminal acid pH - increase secretin, decrease gastrin (by release of somatostatin - paracrine factor) 5. distension - increase gastrin 6. paraysm nerve activity - increase gastrin, CCK and motilin
cholecystokinin- hormone actions
via CCKa and CCKb receptors increase pancreatic enzyme secretion (CCKa) increase gall bladder contraction (CCKa) decrease sphincter of Oddi tone (indirect) decrease gastric emptying (CCKb) regulation of the entry of bile into the duodenum decreases gastric motility slow down gastric emptying and acid secretion enterogastrone effect
gastrin - hormone actions
via CCKb receptors increase the following: gastric acid secretion - via stimulating gastric parietal cells gastric motility gastric mucosal growth direct and indirect (via histamine release) mechanisms
secretin
increase pancreatic and biliary bicarbonate secretion (biliary duct cells) decrease gastric acid secretion released by luminal acidity of the small intestine enterogastrone - slow the rate of gastric acid secretion
glucose-dependent insulinotropic polypeptide (GIP)
increase pancreatic insulin secretion (incretin effect) example of incretin luminal carbohydrate and fatty acids triggers the release of GIP stimulates pancreatic beta-cells to secret insulin
motilin
increase gastric and intestinal motility (MMC) (non-fed state) released from small intestine, periodic recurring patterns
ghrelin
GH secretion, feeding and weight gain
enterogastrone effect
decrease gastric motility slow down gastric emptying and acid secretion
two families of GI hormones
- Gastrin/CCK family 2. secretin family 3. other - not official?
receptors of all GI peptide hormone
G protein coupled receptor
Gastrin/CCKI family
members - Gastrin, CCK receptors: CCKa and CCKb receptor CCKa receptor - pancreatic acinar cells - for CCK only CCKb receptor - brain and stomach - for gastrin and CCK both CCK receptor activation - increase intracellular calcium in target cells CCK and gastrin - homologous carboxyl terminal Gastrin stronger agonist for CCKb receptor
paracrine signals of GI
- histamine 2. somatostatin 3. prostaglandins 4. serotonin 5, adenosine
histamine - function
increase gastric acid secretion via H2 receptor released from mast cell and enterochromaffin-like cell (ECL cells) stimulate intestinal chloride secretion
somatostatin - function
released from D cell in the pancrease and GI mucosa inhibit release gastrin and secretin and etc inhibit acid secretion from gastric parietal cells directly, motility, other absorptive processes
prostaglandin - function
stimulate bicarbonate secretion by gastric surface epithelial cells -> protect the gastric barrier function
serotonin (5-HT)
released from enteric neurons, enterochromaffin cells activate sensory neurons (transmission of discomfort/pain) initiate peristaltic and secretory reflexes irritable bowel syndrome - drug targeting 5-HT is used
adenosin
released in response to inflammation and etc. via several A-receptor subtypes on neuronal and non-neuronal cells modulate sensory transmission in the gut -> change in blood flow, modulation of motility reflexes and colonic chloride secretion
Mastication
increase surf area for digestive enz contact grind food to fine particle - protect mucosal surface and make smooth food movement through GI Cranial nerve V - voluntary and involuntary control chewing reflex programmed pattern of movement
saliva functions (6 of them)
- maintenance of oral hygiene - lysozyme, peroxidases, etc. 2. maintain mineralization of teeth (pH) 3. lubrication - speaking and swallowing - mucin 4. digestive function - amylase and lipase 5. solvation - enables taste 6. lytic - hypotonic fluid causes cell lysis (can be protective)
major salivary glands
- parotid gland 2. sublingual gland 3. submandibular gland know the locations of these
3 important saliva enzymes
- alpha-amylase (ptyalin) 2. lipase 3. kallikrein
alpha-amylase (function, source, gland)
function - starch digestion source - acinar cells gland - parotid and submandibular gland not essential, but can compensate for pancreatic insuffiency
lipase (function, source, gland)
function - fat digestion source - acniar cells gland - sublingual gland not essential, but can compensate for pancreatic insuffiency
kallikrein (function, source, gland)
function - blood flow regulation source - acinar cells (maybe also ducts) gland - parotid, submandibular, sublingual gland serine protease control the salivary blood flow cleave bradykininogen (alpha-2-globulin) to bradykinin, a strong vasodilator
autonomic regulation of salivary secretion
stimuli - smell, sound, sight, taste, chewing inhibitors - sleep, fatigue, fear stimuli/inhibitor -> higher centers -> medullary salivatory nucleus -> sympathetic/parasympathetic -> salivary glands -> increase blood flow and secretion -> salivary flow GI sensory inputs -> medullary salivatory nucleus -> same as above irritating food, nauseated due to GI abnormality -> reflex from stomach and upper small intestine -> induce salivation sympathetic nerve - from superior cervical ganglia -> travel along the surface of b-vessel to salivary glands
salivary secretion stimuli - taste and tactile stimuli
taste - sour taste increase the saliva secretion tactile - smooth object (pebble) increase the saliva, rough object less salivation
control of salivary secretion paraysympathetic - pathway
acetylcholine (NT) -> muscarinic (M3) (receptor) -> signalling pathway (Ca2+) -> fluid > protein secretion (cellular response) substance P (NT) -> Tachykinin NK-1 (receptor) -> Ca2+ (signalling pathway) -> fluid > protein secretion (cellular response)
control of salivary secretion sympathetic - pathway
norepinephrein (NT) -> alpha-adrenergic (receptor) -> Ca2+ (signalling pathway) -> fluid > protein secretion (cellular response) norepinenphrine (NT) -> beta-adrenergic (receptor) -> cAMP (signalling pathway) -> protein > fluid secretion
stimulation of blood flow to salivary gland
salivary grand -high rate of metabolism and b-flow - proportional to rate of saliva formation things that increase blood flow to salivary glands 1. parasympathetic nerve -> increase b-flow to sal gland. 2. VIP and acetylcholine - vasodilatory 3. increase salivation -> increase kallikrein -> cleave bradykininogen (alpha-2-globulin) to bradykinin -> strong vasodilator, increase capillary permeability 4. sympathetic fiber -> initially reduce the b-vessel, but overridden by other vasodilators
two stages of salivary secretion
- primary secretion - isotonic, ECF-like composition + proteins (enzymes, mucins) 2. secondary ductal modification - low H2O permeability of ducts, absorption of Na+ and Cl- greater than secretion of K+ and HCO3-, hypotonic saliva
permeability of duct cells
low permeability to H2O