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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
GI motility

Describe the lamina propria
layer of CT which epithelia attach
contain blood vessels, lymph nodes, and some glands
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
GI motility

describe the submucosa
loose CT, blood and lymphatic vessels, major nerve tracts, and some glands
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
GI motility

describe the Serosa
outermost layer consisting of mainly CT
GI motility

Myenteric plexus (Auerbachs)
larger of the 2 plexuses
located b/w muscle layers of the muscularis externa
mainly concerned with motility
GI motility

Submucosal plexus (Meissners)
located in the submucosa of the small and large intestine
control of secretion from glands
GI motility

Simulation of the sympathetic nervous system leads to what?
postganglionic
Inhibits contraction in muscularis externa
Contracts sphincters and muscularis mucosa
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
GI motility

Central reflex arcs
Cell bodies of afferents located in the dorsal root ganglion
GI motility

Local reflex arc
cell bodies of afferents that lie in the nerve plexuses
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
GI motility

resting membrane potential of smooth muscle
less negative than skeletal due to the higher Na resting potential
GI motility

The slow waves/basic electrical rhythm are generated by what cells
pacemaker cells (interstitial) located between muscle layers of muscularis externa
GI motility

Autonomic effect on slow waves
Para: increase amplitude
Sympa: decrease amplitude
GI motility

Slow wave amplitude effect on stomach, small and large intestine
Stomach and small: if sufficient amplitude then contraction
Large: not clear
GI motility

What determines the maximum frequency of contraction in the stomach and small intestine
frequency of the slow waves
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
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
GI motility

contraction time of smooth muscle
~10X slower than skeletal, AP burst generate a smooth increase in tension rather than individual twitches
GI motility

tone of smooth muscle
resting tone due to slightly elevated intracellular Ca level
GI motility

Control of voluntery and muscles of mastication
Mastication center in brain stem
GI motility

Swallowing reflex
Neurons of the swallowing center in medulla and pons
GI motility

Deglutition
Swallowing initially voluntery then under control of swallowing refkex
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
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
GI motility

Primary peristalsis
Begins in pharynx through esophagus taking 10s to reach the stomach
Mainly controlled by vagus
GI motility

Secondary peristalsis
If primary fails to clear food, secondary wave comes from intrinsic nervous system
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
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
GI motility

How is LES relaxed
Vagus from vasoactive intestinal peptide (VIP) and nitric oxide (NO)
GI motility

Achalasia
insufficient relaxation of LES to allow food to enter stomach.
Result of defect in enteric nervous system
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
GI motility

diffuse esophageal spasm
prolonged painful contraction of esophagus instead of normal peristalsis after swallowing
GI motility

Muscle layers of the stomach
Outer-longitudinal
Middle-circular
Inner-oblique
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)
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
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
GI motility

Antrum
Site where most mixing occurs
Vigorous peristaltic contractions and gastric juices break down food
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
GI motility

Retropulsion
Closing of pyloric sphincter forces contents back into proximal Antrum
GI motility

Frequency and duration of peristaltic waves
3/min for about 2-20 sec
GI motility

Duodenal factors delaying gastric emptying
Hypertonic contents
pH<3.5
distention
Fatty acids (mono/diglycerides)
Peptides and AA (tryptophan)
GI motility

Ileal break
Glucose or fats in ileum reduces gastric contraction
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
GI motility

Gastroduodenal Junction (pylorus)
Prevents regurgitation of duodenal contents back into stomach
Stomach damaged by bile
Duodenum damaged by acid
GI motility

Retching
Due to vomiting (emesis) some gastric contents forced into esophagus but does not reach pharynx
GI motility

Major portion of digestion and absorption
Small intestine (small amount of fat, alcohol, aspirin in stomach)
GI motility

What triples the surface area of the small intestine
Circular folds (plicae circularis)
GI motility

Villi
Projects of small intestine into the mucosa increasing surface area 10x
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
GI motility

Brush border
Microvilli across the entire epithelial surface of the small intestine
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
GI motility

Lymphatic capillarie (lacteals) absorption and drainage of small intestine
Lipids draining Into venous circulation ending in the left subclavian
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
GI motility

Factors influencing amplitude of slow waves and therefore force of contraction
Hormones, autonomics through intramural plexuses, ENS
GI motility

Segmentation
Movement of the small intestine. Circular muscle contracts diving the small intestine into segments at a similar frequency of slow waves
GI motility

Parerstalsis of the small intestine in the fed state
Much lower frequency than segmentation. Traveling a short distance
GI motility

Local reflex (law of the intestine)
Contract oral relax aboral. Moves bolus in aboral direction. Mediated by intramural plexuses
GI motility

Intestinointestinal reflex
Distention in one part of the intestine relaxes the rest of the intestine. Requires extrinsic innervation
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.
GI Motility

Ileocecal sphincter
Prevents retrograde flow
Distension of distal ileum and peristalsis causes relaxation
Distention of cecum causes constriction
GI Motility

Colon
Absorbs most of the water and salt
Movement is slow, major of transit time is spent in colon
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
GI Motility

Hirschsprungs disease
Defect in ENS due to congenital or Radiation
Colon becomes constricted where intramural plexus is absent
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
GI Motility

Mass movements of colon
Haustrum relax and are replaced by intense peristalsic waves propelling chyme a long distance
GI Motility

Colonocolonic reflex
Over distention of one part of colon relaxes the rest
Mediated by sympathetic
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
GI Motility

Internal anal sphincter
Thickening of circular smooth muscle
ENS and para
GI Motility

External anal sphincter
Voluntary striated muscle
Somatic nerves from puedendal
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
GI Motility

Osmotic diarrhea
Presence of a poorly absorbable solute draws water into intestine (lactate in a lactose intolerant person)
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
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
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
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)
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
Salivary and gastric glands

Exocrine
Gland cells release secretory products into ducts which open on epithelial surface
Salivary and gastric glands

Endocrine
Hormone released into blood stream acting on a distant target
Salivary and gastric glands

Neurocrine
Hormone synthesized in a neuron released into blood stream acting on a distant target
Salivary and gastric glands

Paracrine
Hormone released traveling a short distance in the interstitial fluid to act on a neighboring cell
Salivary and gastric glands

Neurotransmitter
Substance released into synaptic cleft acting on a nearby cell
Salivary and gastric glands

Secretagogue
Substance that stimulates secretion from a cell
Salivary and gastric glands

Parotid gland
Pure serous, largest salivary gland
Watery secretion of amylase but not mucins
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
Salivary and gastric glands

Mucins
lubricates food for easy swallowing
Salivary and gastric glands

Amylase
begins digestion of starch
Salivary and gastric glands

Lysozyme and SIgA
clean mouth and teeth
Salivary and gastric glands

Proteins released from non-acinar cells
Lysozyme
SigA
Gastric Mucosal growth factor
Vasodilation regulatory peptides
Salivary and gastric glands

Composition of saliva with increased rate of secretion
Decreased K
Increased Na, HCO3, Cl
Increased pH=8
Less hypotonic
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)
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)
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
Salivary and Gastric glands

Histology of gastric mucosa
Simple columnar secreting HCO3 and mucous for protection
Gastric pits secrete gastric juices
Salivary and Gastric glands

HCl
Secreted by parietal cells
Kills bacteria
Activates pepsinogen
Enhances iron absorption
Releases free cobalamins (vit B12) for absorption
Salivary and Gastric glands

Intrinsic factor
Only gastric secretion required to maintain life
Secreted from parietal cells
Bind B12 for absorption in ileum
Salivary and Gastric glands

Pepsinogen
Secreted by chief cells (peptic)
Cleaved into pepsin to begin digestion of proteins
Salivary and Gastric glands

Gastrin
Secreted by G cells
stimulate gastric acid secretion
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)
Salivary and Gastric glands

Glands of Cardiac stomach
Mucus secreting cells
Salivary and Gastric glands

Glands of the Oxyntic stomach (acid secreting)
Parietal (oxyntic) cells
Chief cells
Mucus secreting cells
Salivary and Gastric glands

Glands of the pyloric stomach
Few if any parietal or chief cells
Mostly mucus secreting
G cells
D cells (somatostatin)
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
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
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
Salivary and Gastric glands

Inhibitors of gastric acid secretion
Somatostatin (D cells of body and antrum)
Prostaglandins
Epidermal growth factor
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
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
Salivary and Gastric glands

Intestinal phase
Chyme in duodenum leads to stimulation and then inhibition of acid secretion
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
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
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
Intestine and Pancreas secretions

Rest of small intestine
Goblet cells (mucus)
Epithelial cells (watery secretion, slightly less than rate of fluid absorption)
Intestine and Pancreas secretions

Colon
Goblet cells secrete less volume but more alkaline than small intestine.
Irritation of mucosa and para stimulate secretion
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
Intestine and Pancreas secretions

Structure of pancreas secretion
Acini>lobules>intercalated ducts>larger ducts>main collecting duct>duodenum through sphincter of oddi with CBD
Intestine and Pancreas secretions

Pancreatic innervation
Para: preganglionic vagus stimulates pancreatic juices
Sym: postganglionic (celiac and mesenteric) inhibit
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
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)
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
Intestine and Pancreas secretions

Gastric phase of pancreatic secretion
Gastric distention leads to vago-vago reflex resulting in low volume high enzyme secretion
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
Liver and gallbladder

Functions of the liver
Many digestive function in secretion of bile
Principal source for secretion of cholesterol
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
Liver and gallbladder

Contents of bile
Bile pigments (bilirubin from breakdown of Hg)
Bile acids (from cholesterol)
Cholesterol
Lecithin (phosphatidylcholine)
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
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.
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
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
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
Liver and Gallbladder

Gallbladder emptying during cephalic and gastric phases
Vagus stimulates intermittent contraction of gallbladder squeezing bile through partially relaxed sphincter of oddi
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.
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
Liver and Gallbladder

Secretins effect on cholangiocytes
Stimulates greater release of HCO3 fluid but does not stimulate bile secretion from hepatocytes
Liver and Gallbladder

CCK effect on bile secretion from hepatocytes
CCK does NOT control bile secretion from hepatocytes