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Flashcards in Motility 1 and 2 Blatter Deck (54):

3 main functions of GI motility

1. Propulsion- transport chyme to appropriate site
2. Mixing- decrease in particle sizeof ingested food for optimal contact with digestive enzymes
3. Reservoir- sections like the stomach and the colon are reservoirs and allow for digestive and absorptive tasks sufficient time


Steps of contraction of GI smooth muscle

1. Requires elevation of cytosolic Ca2+
2. Ca2+ binds to calmodulin
3. Ca/calmodulin complex binds and activates enzyme MLCK
3. MLCK uses ATP to phosphorylate myosin
4. Phosphorylated myosin cross bridges with actin ahd produces force and contraction


Mechanism to increase cytosolic Ca2+

Hormones and NT can depolarize the smooth muscle activating voltage gated Ca2+ channels in sarcolemma

Initial influx of Ca2+ can initiate contraction of RyR on the SR resulting in greater cytosolic increase

Hormones and NT activate Phospholipase C without the presence of change in membrane potential.. phospholipase C produces InsP3 activating channel in the SR


Electromechanical vs pharmacomechanical coupling

Electro- trigger by membrane depol. and AP that travels through gap junction

Pharmacomechanical- contraction in the absence of AP- like in response to NT or hormone


Slow waves
2. Frequency
3. Generation

1. Synonym- basic electrical rhythm
2. 3/min in the stomach and 11-13 min in the duodenum
3. Generation of slow waves is autonomous


Pacemaker cells
What do they generate and how does it spread?

Interstitial cells of Cajal- Between the circular and longitudinal muscularis externa layers and they generate slow waves that spread to neighboring smooth muscles through gap junctions


Modulation of slow waves by enteric

Excitatory motoneurons (AcH and substance P) increase the amplitude and frequency and duration of plateau phase


What happens when slow waves reach electrical

AP! that enhances contraction last 10-20ms


When does contraction begin in GI smooth muscle?

When depol reaches mechanical threshold. This determines the muscle tone and contraction in the absence of AP.


Types of contraction

Tonic- contracile maintained for long period of time (sphincter)

Phasic contraction- twitchlike evoked by slow wave and action potentials


What triggers increase in strength of contraction?

Strength- triggering of AP
Grade/ duration determined by frequency and number of APs


What orgrans structures have tonic contractions? (6)

upper and lower esophageal sphincters
Pyloric valve
Sphincter of Oddi
Iliocecal valve
Internal anal sphincter


What orgrans use propulsive peristalsis?

Lower 2/3 of stomach


What structures use reverse peristalsis

Proximal colon

Prolongs the time that the lumen content is in that content allowing more time for absorption and is important because alot of reabsoprtion of fluid happens here and minimizes the loss of fluid in the GI tract


Mass movemetn structures?

Ascending, transverse, descending colon


Structure of segmentation



Structure of Haustraton



where does migrating myoelectric complex happen?

In SI during fasting or when empty


Explain the structural aspects of the esophagus

Upper third- circular and longitudinal layers of striation

Middle third- skeletal and smooth

Lower third- smooth muscle


Innervation of the esophagus

Afferent- is feedback to the swallowing center

Efferent- mainly vagus
Top 1/3- vagal somactic to striated
Middle 1/3- vagal visceral to enteric system
Bottom 1/3- myenteric plexus to smooth muscle


Purpose of the upper and lower esophageal sphincters

Upper- prevents entry of air
Lower- prevents reflux of corrosive acidic stomach content


Contraction of UES and LES


at the sphincter the cholingeric are nicotinic so atropine would only work at the esophagus no at the sphincter

Relaxation- primary pertalsis causes inhibibitory of vagal nerve and decrease in firing rate of excititory and input from inhibitory fibers by NT such as VIP and NO


Purpose of mastication

Lubrication of food
Digestion- starch containing food mixed with amalyse
Mechanical break down of food for better mixing in stomach


Intially swallowing is____ but is under____

Reflex control


3 phases in swallowing reflex

1. Oral/voluntary- bolus moved to pharynx by tongue (swallowing center in medulla and pons initiates motor impulse of pharynx)
2. Pharyngeal (1 sec)-- soft palate up blocking nose and epiglottis down blocking larynx/airways (THIS INITIATES PERISTALTIC WAVE AND BREATHING IS REFLEXIVELY INHIBITED)
3. Esophageal phase- mainly controlled by swallowing center. Primary peristaltic wave 3-5cm/sec and reaches stomach in 5-10 secs

** this is all a long range reflex)


What happens during distention of the esophageal wall

There is secondary peristaltic wave that is mediated by the intrinsic nerve system and this is short range reflex

This happens when the bolus is stuck there are stretch receptors in the esophageal lining forcing it down into the stomach


What can cause a secondary peristaltic wave?

Bolus so sensory input because of mechanical stretch or chemical stimuli are integrated in myenteric ganglia and efferent fibers and epithelial cells are activated


Explain the law of intestine ????? Revisit

Bolus in GI is transported in the aboral direction.

When stretching of the GI is sensed excitatory to proximal and inhibitory to distal


PArts of the stomach (4)

1 Fundus
2 body (oxyntic glandular mucosa and pacemaker)
3 Antrum (pyloric glandular mucosa)
4 Pylorus( Pyloric sphincter, gastroduodenal junction)


Function of stomach motility

Controlls emptying of gastric contents into the duodenum


Explain electrical slow wave of stomach

Initiated in the greater curvature of the gastric body.
3 phases- rapid depol, plateau and repol


What happens in the antrum and pylorus with APs

They are superimposed on the slow wave and that increases the force of contraction


Explain electrical activity in each part of the stomach

Fundus has little contraction because it's a reservoir

Mid orad corpus- weak contraction

Terminal antrum and pylorus- AP spikes


Why is volume increase not parallel to increase in tension?

Plasticity- stomach can be stretched within limits without tension increase

Receptive relaxation- filling causes reflective relaxation of fundus and body mediated by vagus (NO and VIP)


What main steps happen in gastric mixing

1. Pacemakers initiate autonomous slow waves with increasing velocity towards the antrum/pylorus
2. Strong pertastic contractions causes mixing and formation of chyme
3. Peristaltic waves squirt small portion of antral content to the duodenum but because the sphincter is closes early the contractile waves pushes content back to the antrum (retropulsion)


What regulates gastric emptying?

Neural and hormonal mechanisms in stomach and duodenum/jejunum , but the driving force is the antral peristaltic contraction


Control of pyloric tone

Relaxation- inhibitory vagal fibers (VIP and NO)
Constriction- excitation cholinergic vagal fibers, sympathetic fibers and hormones CCK, gastrin, GIP and secretin


Factors that influence gastric emptying

1. Volume- increase distention of stoamch increases motility and increase distention of SI inhibits gastric emptying
2. Increase fluidity allows increase emptying
3. Fatty acid in Duo and Jej stimulate CCK and GIP so inhibit emptying
4. Hypertonicity
5/ Peptides/AArelease gastrin in duodenum- increase constriction of pyloric ring and decrease emptying


Gastrin main functions

Stimulates secretion by HCL and trophic to stomach
Enhances gastric motility
Constricts pyloric



What happens when duodenal pH<3.5

Decrease in gastric emptying and increase in duodenal motility. Acid in duodenum triggers releases of secretin which constricts the pyloric and inhbits antral contraction and stimulates bicarbonate rich secretion from the liver and pancreas (for neutralization)


Consequences of controlled emptying

1. Fat isn't emptied faster than bile can emulsify
2. Acid is not transported faster than is can be neautralized
3. Other compenents don't enter the SI fastr than they can be processed


Why do we vomit?

Protective mechanism from over distension and/or irritation of the stomach and intestines


Causes of Vomit

Tactile-stimulate back of throat
Irritation/distension of stomach
Elevated intracranial pressure
Rotation/acceleration of head
Intense pain
Chemical agents work in the upper GI tract or on specialized chemoreceptors in the brain
Emotional factors


Vomiting center and vomiting act

Center- medulla oblongata integrates sensory inputs and coordinate vomiting act

Act- reverse peristalsis of SI, relax pyloric sphincter and stomach. Forced inspiration decreases intrathoracic pressure and increases intrabdominal pressure


What prevents aspiration into respiratory tract during vomiting? (3)

Approximation of vocal cords, closure of the glottis and inhibition of respiration


Define retching

Abdominal/gastric content reaches closed UES but doesn't enter the pharynx. This often precedes vomiting


Types of motility in the SI

Digestive motility- segmentation and peristalsis

Interdigestive- migrating myoelectric complex


Segmentation vs Peristalsis


Define segmentation?

Mixing vs. Propulsion

Segmentation is most frequent and is closely spaced contraction in circular muscular layer, dividing SI into small neighboring segments.


What modulates segmentation and short peristalsis waves?

Intramural plexuses but long range reflexes are by extrinsic innervation


Explain the Migrating myoelectric complex

Occurs in fasted organisms where there are burst of electrical/contractile activity that sweep the content of the SI into the cecum which prevents content from the migration from the LI into the bacteria sterile SI



Function of contractile activity of the muscularis mucosa

Changes the topography of the SI and increases contact between the mucosa and content so facilitates absoprtion.


Explain the short range reflex

Bolus causes proximal contraction and aboral relaxation so food moves in the orthograde/aboral direction "law of intestine"


3 long range reflexes

Intestino-intestinal reflex- overdistention of one part relaxes other parts of the GI tract

Ileo-gastro reflex- distention of ileum decreases gastric motility

Gastro-ileal reflex- increased secretory and motor activity of the stomach increases ileal motility and movement through the IC sphincter


Emptying of the ileum

OC sphincter opening by distention of the ileum and short range peristalsis in terminal ileum

1. Through the IC sphincter which is normally closed but relaxed by hormone gastrin
2. Gastro-ileal reflex enhances ileal emptying
3. Distention of cecum contracts IC sphincter