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137 Cards in this Set
- Front
- Back
GI motility
Describe the epithelium? |
Single layer of specialized cells varying in precise composition from part to another
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GI motility
Describe the lamina propria |
layer of CT which epithelia attach
contain blood vessels, lymph nodes, and some glands |
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GI motility
Describe the muscularis mucosa |
thin layer of smooth muscle, contraction creates fold in mucosa helping the mix luminal contents also exposing different surfaces to the luminal contents
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GI motility
describe the submucosa |
loose CT, blood and lymphatic vessels, major nerve tracts, and some glands
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GI motility
describe the muscularis mucosa |
inner circular layer and outer longitudinal layer of muscle
helps to mix and moves contents along the GI tract |
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GI motility
describe the Serosa |
outermost layer consisting of mainly CT
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GI motility
Myenteric plexus (Auerbachs) |
larger of the 2 plexuses
located b/w muscle layers of the muscularis externa mainly concerned with motility |
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GI motility
Submucosal plexus (Meissners) |
located in the submucosa of the small and large intestine
control of secretion from glands |
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GI motility
Simulation of the sympathetic nervous system leads to what? |
postganglionic
Inhibits contraction in muscularis externa Contracts sphincters and muscularis mucosa |
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GI motility
Stimulation of the parasympathetic system leads to what? |
preganglionics from vagus (up to transverse colon) and pelvic (descending colon to rectum) terminate on ganglion cells of the of the 2 nerve plexuses
postganglionics of the plexuses increase contraction and secretion |
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GI motility
Central reflex arcs |
Cell bodies of afferents located in the dorsal root ganglion
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GI motility
Local reflex arc |
cell bodies of afferents that lie in the nerve plexuses
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GI motility
Why is the smooth muscle of the GI tract considered single unit type? |
connected by gap junctions
electric activity spreads easily from cell to cell |
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GI motility
resting membrane potential of smooth muscle |
less negative than skeletal due to the higher Na resting potential
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GI motility
The slow waves/basic electrical rhythm are generated by what cells |
pacemaker cells (interstitial) located between muscle layers of muscularis externa
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GI motility
Autonomic effect on slow waves |
Para: increase amplitude
Sympa: decrease amplitude |
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GI motility
Slow wave amplitude effect on stomach, small and large intestine |
Stomach and small: if sufficient amplitude then contraction
Large: not clear |
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GI motility
What determines the maximum frequency of contraction in the stomach and small intestine |
frequency of the slow waves
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GI motility
NMJ, difference b/w smooth vs skeletal, circular vs longitudinal |
No postjunctional specializations such as Motor end plate in skeletal
Circular extensive innervation and nerve terminals form a close association with muscle cells |
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GI motility
Length tension curve compared to skeletal muscle |
smooth muscle has a much broader curve meaning it can develop force effectively over a wider range of muscle length
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GI motility
contraction time of smooth muscle |
~10X slower than skeletal, AP burst generate a smooth increase in tension rather than individual twitches
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GI motility
tone of smooth muscle |
resting tone due to slightly elevated intracellular Ca level
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GI motility
Control of voluntery and muscles of mastication |
Mastication center in brain stem
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GI motility
Swallowing reflex |
Neurons of the swallowing center in medulla and pons
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GI motility
Deglutition |
Swallowing initially voluntery then under control of swallowing refkex
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GI motility
Voluntary (oral phase) of deglutition |
Tongue moves bolus upward and backward forcing it against the pharynx which then stimulates mechanoreceptors to initiate swallowing reflex
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GI motility
Involuntary (pharyngeal phase) of deglutition |
Soft Patel moves upward blocking nasopharynx->respiration inhibited as vocal cords close->epiglottis closes larynx->upper esophageal sphincter closes->peristaltic wave of contraction begins at superior constrictor muscles
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GI motility
Primary peristalsis |
Begins in pharynx through esophagus taking 10s to reach the stomach
Mainly controlled by vagus |
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GI motility
Secondary peristalsis |
If primary fails to clear food, secondary wave comes from intrinsic nervous system
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GI motility
Peristalsis related to swallowing |
If a second swallow occurs within 5s of the first peristalsis of the first is inhibited until the second catches up moving in tandem with the first
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GI motility
LES tone during quiescent periods |
Tone is high but rest of esophagus is relaxed. Resting tone can be increased by neural (Ach) and hormonal (gastrin) influence
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GI motility
How is LES relaxed |
Vagus from vasoactive intestinal peptide (VIP) and nitric oxide (NO)
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GI motility
Achalasia |
insufficient relaxation of LES to allow food to enter stomach.
Result of defect in enteric nervous system |
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GI motility
Gastroesophageal reflux disease |
abnormally prolonged or more frequent relaxation of LES sphincter allowing reflux of gastric contents into esophagus (acid and pepsin), this can lead to ulcers
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GI motility
diffuse esophageal spasm |
prolonged painful contraction of esophagus instead of normal peristalsis after swallowing
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GI motility
Muscle layers of the stomach |
Outer-longitudinal
Middle-circular Inner-oblique |
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GI motility
Receptive relaxation (response to gastric filling) |
Relaxation of fundus and body Initiated as part of peristalsis or
Initiated as part of filling stomach with gas or liquid (vagovago reflex) |
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GI motility
Mixing of food in body and fundus |
Little mixing occurs due to weak contraction of thin muscle layers.
Contents separated into layers based on densities. Fats form an upper oily layer and are therefore emptied last |
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GI motility
Rate of gastric emptying |
Inert isotonic sln (glucose)-rapid
Nutrients (AA)-slower related to calorie density, feedback from small intestine Solids-slowest 1-2hr preceded by 1 hr lag time, larger the swallowed piece of food longer the lag time |
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GI motility
Antrum |
Site where most mixing occurs
Vigorous peristaltic contractions and gastric juices break down food |
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GI motility
Pyloric pump |
Slow wave originating in middle of the body moves toward pylorus increasing in force and velocity. Small chyme is pushed into duodenum
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GI motility
Retropulsion |
Closing of pyloric sphincter forces contents back into proximal Antrum
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GI motility
Frequency and duration of peristaltic waves |
3/min for about 2-20 sec
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GI motility
Duodenal factors delaying gastric emptying |
Hypertonic contents
pH<3.5 distention Fatty acids (mono/diglycerides) Peptides and AA (tryptophan) |
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GI motility
Ileal break |
Glucose or fats in ileum reduces gastric contraction
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GI motility
Migrating myoelectric complex (MMC) |
During fasting, Quiescent Antrum for 1-2hr followed intense electrical and motor activity lasting 10-20 min causing strong contractions of Antrum with relaxed pylorus. Allows emptying of large undigested material from stomach. Triggered by release of motilin from enteroemdocrine cells
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GI motility
Gastroduodenal Junction (pylorus) |
Prevents regurgitation of duodenal contents back into stomach
Stomach damaged by bile Duodenum damaged by acid |
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GI motility
Retching |
Due to vomiting (emesis) some gastric contents forced into esophagus but does not reach pharynx
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GI motility
Major portion of digestion and absorption |
Small intestine (small amount of fat, alcohol, aspirin in stomach)
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GI motility
What triples the surface area of the small intestine |
Circular folds (plicae circularis)
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GI motility
Villi |
Projects of small intestine into the mucosa increasing surface area 10x
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GI motility
Microvilli |
Apical portions of the absorptive cells of the small intestine containing enzymes that further hydrolyze carbs and peptides increasing surface area 20x
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GI motility
Brush border |
Microvilli across the entire epithelial surface of the small intestine
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GI motility
Absorption and drainage of blood capillaries in the small intestine |
AA and simple sugars and drain into veins that drain into the portal vein gong to the liver
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GI motility
Lymphatic capillarie (lacteals) absorption and drainage of small intestine |
Lipids draining Into venous circulation ending in the left subclavian
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GI motility
Slow waves in the small intestine |
Frequency decreases moving from duodenum to ileum. This is known as the basic electrical Ruth, and is independent of extrinsic innervation
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GI motility
Factors influencing amplitude of slow waves and therefore force of contraction |
Hormones, autonomics through intramural plexuses, ENS
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GI motility
Segmentation |
Movement of the small intestine. Circular muscle contracts diving the small intestine into segments at a similar frequency of slow waves
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GI motility
Parerstalsis of the small intestine in the fed state |
Much lower frequency than segmentation. Traveling a short distance
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GI motility
Local reflex (law of the intestine) |
Contract oral relax aboral. Moves bolus in aboral direction. Mediated by intramural plexuses
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GI motility
Intestinointestinal reflex |
Distention in one part of the intestine relaxes the rest of the intestine. Requires extrinsic innervation
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GI motility
Migrating myoelectric complex (MMC) of the small intestine |
Occurs several hours after a meal (fasting state). Requires ENS and motilin but does not require extrinsic innervation. Usually propagated from Antrum but can originate anywhere in small intestine. Intence electrical activity followed by longer quiescent periods empties small intestine and inhibits colonic bacteria entering ileum. This can be disrupted by phyeiologic stress.
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GI Motility
Ileocecal sphincter |
Prevents retrograde flow
Distension of distal ileum and peristalsis causes relaxation Distention of cecum causes constriction |
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GI Motility
Colon |
Absorbs most of the water and salt
Movement is slow, major of transit time is spent in colon |
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GI Motility
Extrinsic innervation of colon |
Para: promotes motility, (Vagus Cecum->Transverse) (Pelvic sacral (descending->anal canal)
Sym: Inhibits motility, Postganglionics from Mesenteric and hypogastric ganglia |
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GI Motility
Hirschsprungs disease |
Defect in ENS due to congenital or Radiation
Colon becomes constricted where intramural plexus is absent |
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GI Motility
Haustral contractions (Haustral shuffling) |
Bag like sacs constrict and relax moving chyme back and forth very slowly results in a net orthograde direction
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GI Motility
Mass movements of colon |
Haustrum relax and are replaced by intense peristalsic waves propelling chyme a long distance
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GI Motility
Colonocolonic reflex |
Over distention of one part of colon relaxes the rest
Mediated by sympathetic |
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GI Motility
Gastrocolic reflex |
Distention of the stomach increases mass movements of the proximal and distal colin
Mediated by extrinsic and intrinsic innervation as well as CCK or gastrin |
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GI Motility
Internal anal sphincter |
Thickening of circular smooth muscle
ENS and para |
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GI Motility
External anal sphincter |
Voluntary striated muscle
Somatic nerves from puedendal |
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GI Motility
Defecation events |
Mass movement forces feces into rectum>Distension of rectum>Initiate intrinsic and extrinsic (para) urge to defecate>peristalsic waves in descending, sigmoid, and rectum forces feces into anal canal as internal anal sphincter relaxes>Reflex or voluntary relaxation of ext anal sphincter
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GI Motility
Osmotic diarrhea |
Presence of a poorly absorbable solute draws water into intestine (lactate in a lactose intolerant person)
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GI Motility
Bacterial enterotoxins leading to secretory diarrhea |
Cholera or E coli can cause excessive secretion of water and electrolytes from intestinal wall by activation of second messengers (cAMP, cGMP)
Secretion is 2x the amount the colin can absorb which results in high volume watery diarrhea and death |
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GI Motility
Secretory diarrhea from enteritis (non toxin producing bacteria, virus...) |
Infection irritates mucosa leading to inflammation and dysfunction in motility and secretion
Produces low volume of bloody diarrhea |
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GI Motility
Secretory diarrhea from ulcerative colitis |
Unknown cause results in inflamed and ulcerated colon
Causes increased secretion, mass movement and decreased absorption Results in low volume bloody diarrhea |
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GI Motility
Constipation |
Feces remain in rectum for prolonged period usually do to decreased motility
Voluntary suppression, initiation or stimulant laxatives (weakens defecation reflex) Opiods (act on ENS decreasing peristaltic and increasing sphincter tone) |
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GI Motility
Aspirin absorption |
Stomach at optimum pH 2-4
Food raises pH and slows absorption Can also be absorbed from proximal small Intestine faster than stomach Enteric coating reduces gastric bleeding by slowing absorption of aspirin decreasing its effect of inhibiting platelet aggregation |
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Salivary and gastric glands
Exocrine |
Gland cells release secretory products into ducts which open on epithelial surface
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Salivary and gastric glands
Endocrine |
Hormone released into blood stream acting on a distant target
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Salivary and gastric glands
Neurocrine |
Hormone synthesized in a neuron released into blood stream acting on a distant target
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Salivary and gastric glands
Paracrine |
Hormone released traveling a short distance in the interstitial fluid to act on a neighboring cell
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Salivary and gastric glands
Neurotransmitter |
Substance released into synaptic cleft acting on a nearby cell
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Salivary and gastric glands
Secretagogue |
Substance that stimulates secretion from a cell
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Salivary and gastric glands
Parotid gland |
Pure serous, largest salivary gland
Watery secretion of amylase but not mucins |
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Salivary and gastric glands
Submandibular and sublingual |
Mixed serous and mucous
More viscous saliva (amylase and mucins) Acinar cells>Intercalated ducts>Striated ducts>Excretory ducts>Single duct>mouth |
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Salivary and gastric glands
Mucins |
lubricates food for easy swallowing
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Salivary and gastric glands
Amylase |
begins digestion of starch
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Salivary and gastric glands
Lysozyme and SIgA |
clean mouth and teeth
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Salivary and gastric glands
Proteins released from non-acinar cells |
Lysozyme
SigA Gastric Mucosal growth factor Vasodilation regulatory peptides |
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Salivary and gastric glands
Composition of saliva with increased rate of secretion |
Decreased K
Increased Na, HCO3, Cl Increased pH=8 Less hypotonic |
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Salivary and gastric glands
Two stage model of salivary secretion |
Primary secretion in end pieces is isotonic
Excretory ducts modify saliva making it more hypotonic (more Na, Cl removed than K, HCO3 added and decreased H2O permeability) |
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Salivary and gastric glands
innervation of salivary secretion |
Mainly para: slow copious watery amylase saliva (preganglionics from CN 7, 9 synapse on submandibular or otic ganglion)
Sym: short low volume viscous amylase saliva (postganglionics from superior cervical ganglion) |
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Salivary and gastric glands
Cellular mechanisms for saliva secretion |
Activation of B1 recpetors>Inc cAMP>low volume amylase rich
Activation of M2 receptors by Ach>large volume rich in protein and electrolyte |
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Salivary and Gastric glands
Histology of gastric mucosa |
Simple columnar secreting HCO3 and mucous for protection
Gastric pits secrete gastric juices |
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Salivary and Gastric glands
HCl |
Secreted by parietal cells
Kills bacteria Activates pepsinogen Enhances iron absorption Releases free cobalamins (vit B12) for absorption |
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Salivary and Gastric glands
Intrinsic factor |
Only gastric secretion required to maintain life
Secreted from parietal cells Bind B12 for absorption in ileum |
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Salivary and Gastric glands
Pepsinogen |
Secreted by chief cells (peptic)
Cleaved into pepsin to begin digestion of proteins |
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Salivary and Gastric glands
Gastrin |
Secreted by G cells
stimulate gastric acid secretion |
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Salivary and Gastric glands
Gastric secretions of salt and H2O |
Low (basal levels): Na>H
All levels: K>plasma K, vomiting leads to hypokalcemia High levels: HCl approaches isotonic levels, alkaline tide (venous blood from stomach becomes alkaline) |
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Salivary and Gastric glands
Glands of Cardiac stomach |
Mucus secreting cells
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Salivary and Gastric glands
Glands of the Oxyntic stomach (acid secreting) |
Parietal (oxyntic) cells
Chief cells Mucus secreting cells |
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Salivary and Gastric glands
Glands of the pyloric stomach |
Few if any parietal or chief cells
Mostly mucus secreting G cells D cells (somatostatin) |
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Salivary and Gastric glands
Secretagogues neurotransmitter of gastric acid secretion |
Ach from para or ENS
Act on M3 receptor Inc gastric secretion Inhibited by atropine |
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Salivary and Gastric glands
Secretagogues paracrine regulator of gastric secretion |
Histamine released from enterochromaffin-like cells (ECL) near parietal cells, act on H2 receptor Inc acid secretion
Blocked by cimetidine |
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Salivary and Gastric glands
Secretagogue hormonal regulator of gastric acid secretion |
Gastrin released from G cells of the antrum and duodenum, act indirectly on ECL cells to release histamine Inc acid secretion
Also play a role in growth and maintenance mucosa of oxyntic region of the stomach, small and large Intestine |
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Salivary and Gastric glands
Inhibitors of gastric acid secretion |
Somatostatin (D cells of body and antrum)
Prostaglandins Epidermal growth factor |
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Salivary and Gastric glands
Cephalic phase response to food |
Respond to sight, smell, taste
Ach from vagus acts directly on parietal cells and indirectly on G and ECL cells. When pH becomes <3 somatostain inhibits acid secertion by acting as a hormone on parietal cells and paracrine on G and ECL cells |
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Salivary and Gastric glands
Gastric phase of acid secretion |
Greatest amount of secretion in this phase (Cl and H secreted, HCO3 pumped into blood stream-alkaline tide)
Food in stomach leads to distention and activation of ENS and vagus. Act directly on parietal and indirectly on G and ECL cells. AA in stomach (tryptophan, phenylalinine) stimulate G cells. Ca, caffeine, coffee, alcohol also stimulate secretion |
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Salivary and Gastric glands
Intestinal phase |
Chyme in duodenum leads to stimulation and then inhibition of acid secretion
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Salivary and Gastric glands
Pepsinogen secretion |
Mainly due to low pH stimulating vagus input to chief cells
Secretin and gastrin may also stimulate chief cells but effect is not as great |
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Salivary and Gastric glands
Zollinger-Allison syndrome (gastroinoma) |
Tumor in duodenum or non-beta pancreas leads to high levels of circulating gastrin.
This causes large numbers of parietal and ECL cells and constant stimulation of gastric acid |
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Intestine and Pancreas secretions
Duodenum |
Submucosa contains brunners gland rich in alkaline secretion protecting the duodenum from acid.
Ducts empty into Crypts of Lieberkuhn which are found throughout the small and large intestine |
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Intestine and Pancreas secretions
Rest of small intestine |
Goblet cells (mucus)
Epithelial cells (watery secretion, slightly less than rate of fluid absorption) |
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Intestine and Pancreas secretions
Colon |
Goblet cells secrete less volume but more alkaline than small intestine.
Irritation of mucosa and para stimulate secretion |
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Intestine and Pancreas secretions
Exocrine secretion of pancreas |
Hydrolysis or protein, digest starch, b breakdown lipids into monoglycerides and ffa.
Neutralization of gastric acid in stomach Maintain proper pH for digestion |
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Intestine and Pancreas secretions
Structure of pancreas secretion |
Acini>lobules>intercalated ducts>larger ducts>main collecting duct>duodenum through sphincter of oddi with CBD
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Intestine and Pancreas secretions
Pancreatic innervation |
Para: preganglionic vagus stimulates pancreatic juices
Sym: postganglionic (celiac and mesenteric) inhibit |
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Intestine and Pancreas secretions
Aqueous components of pancreatic juice |
HCO3, CL (concentrations vary inversely with each other), Na, K (plasma levels)
At rest: intercalated and intralobular ducts With stimulation (secretin): larger ducts, Inc volume and HCO3 secretion |
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Intestine and Pancreas secretions
Enzymatic components of pancreatic juice |
Secreted from acinar cells
Necessary to prevent malabsorption of proteins, carbs, and fats (proteases, amylase, lipases-secreted as inactive proenzymes activated by hydrolysis in lumen. Trypsin can activate trypsinogen, chymotrypsinogen, procarboxypeptidase Nucleases (DNAase, RNAase) |
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Intestine and Pancreas secretions
Cephalic phase (sham feeding) of pancreatic secretion |
Vagus releases Ach on ductal and Acinar cells.
Results in low volume high enzyme secretion because Ach has greater effect on enzyme than fluid secretion |
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Intestine and Pancreas secretions
Gastric phase of pancreatic secretion |
Gastric distention leads to vago-vago reflex resulting in low volume high enzyme secretion
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Intestine and Pancreas secretions
Intestinal phase of pancreatic secretion |
Caused by presence of acids, peptides, and fats in duodenum
Acids: secretin released from S cells of duodenum Inc HCO3, low enzyme secretion FA, AA (phenylalanine, valine, methionine): CCK from I cells of small intestine lead to enzyme rich secretion |
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Liver and gallbladder
Functions of the liver |
Many digestive function in secretion of bile
Principal source for secretion of cholesterol |
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Liver and gallbladder
Primary function of bile |
Required for fat digestion and absorption
Sole excretory route for some substances not excreted by the kidney In humans the most important route for elimination of cholesterol is its conversion to bile acids and excretion in the feces |
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Liver and gallbladder
Contents of bile |
Bile pigments (bilirubin from breakdown of Hg)
Bile acids (from cholesterol) Cholesterol Lecithin (phosphatidylcholine) |
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Liver and gallbladder
biles role in lipid digestion |
bile acids emulsify lipids allowing greater access of lipases which then form Micelles and absorbed in intestinal epithelium
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Liver and gallbladder
Bile secretion pathway |
Bile acids, cholesterol, phosphitidylcholine, and bilirubin are actively secreted into bile caniliculi, this creates an osmotic gradietn for water and plasma cations. Glucose and AA also enter the caniliculi passively.
Bile then moves to the smallest bile ductules which are lined with simple columnar cells (cholangiocytes). The tight junctions b/w cholangiocytes are permeable to water allowing bile to become isotonic. These cells also secrete HCO3 Inc bile volume and pH but Dec salt concentration. Also actively reabsorb glucose, AA and fluids that leaked into bile. |
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Liver and Gallbladder
Bile secretion regulation |
Secretin, VIP, Glucagon: stimulate release secretion of bile through 2nd messengers (Inc cAMP activation CFTR and Cl-HCO3 exchanger, also insert aquaporins in apical membrane)
Somatostain decreases secretion by lowering cAMP levels |
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Liver and Gallbladder
Storage of bile during interdigestive period |
Constriction of sphincter of oddi forces bile into gall bladder which concentrated bile by absorbing Na, Cl, HCO3
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Liver and Gallbladder
Retrieval of bile through enterohepatic circulation |
Some bile acids are passively absorbed in small intestine and colon.
Majority of bile acid absorption is through Na driven 2ndary active transport in terminal ileum taken up in hepatic portal system and secreted back into bile caniliculi. Bile acids that are not absorbed are secreted in feces |
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Liver and Gallbladder
Gallbladder emptying during cephalic and gastric phases |
Vagus stimulates intermittent contraction of gallbladder squeezing bile through partially relaxed sphincter of oddi
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Liver and Gallbladder
Gallbladder emptying during intestinal phase |
Highest rate of gall bladder emptying, CCK is strongest stimulant
CCK release from duodenal I cells enters circulation acting to constrict gallbladder myoepithelium and relax sphincter of oddi. |
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Liver and Gallbladder
Choleretic effect |
Concentration of bile acids in hepatic portal blood in the major factor influencing synthesis and secretion.
Presence of bile acids stimulates secretion and inhibits synthesis. Low concentration increases synthesis and inhibits secretion |
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Liver and Gallbladder
Secretins effect on cholangiocytes |
Stimulates greater release of HCO3 fluid but does not stimulate bile secretion from hepatocytes
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Liver and Gallbladder
CCK effect on bile secretion from hepatocytes |
CCK does NOT control bile secretion from hepatocytes
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