Motility of GI Tract Flashcards
Major activity in GI tract
Motility
What is motility?
- contraction and relaxation of walls and sphincters
What are the four functional layers of the GI tract?
Mucosal layer
Submucosa
Muscularis externa
Serosa
What is part of the mucosal layer?
- epithelium
- lamina propria
- muscularis mucosae
What is the muscularis mucosae?
function?
SMOOTH MUSCLE
- its contraction will change the shape and surface area of epithelium
What is function of the muscle layers ( muscularis propria)?
SMOOTH MUSCLE
- inner circular muscle
- outer longitudinal muscle
provide motility to GI tract
What is function of circular muscle?
contraction will decrease DIAMETER of segment
What is function of longitudinal muscle?
contraction will decrease LENGTH of segment
- shortening the length of bowel contraction
Are slow waves the same as Action potential?
NO!
What are slow waves?
depolarization and repolarization of the membrane potential
What modulates AP and strength of contraction?
neural activity and hormonal activty
What happens after slow waves?
slow waves are followed by contraction (tension) of muscle
Phasic contractions
- examples
periodic contactions followed by relaxation
- esophagus, stomach (antrum) , small intestine, tissues for mixing and propulsion
Tonic Contractions
- examples
- maintains CONSTANT level of contraction without regular periods of relaxation
- stomach (orad), lower esophageal, ileocecal, and internal anal sphincters
Relationship between slow waves, APs, contractions in smooth muscle
The greater the # of APs on top of the slow, the larger the contraction
What will increase the amplitude of slow waves? effects?
1) stretch
2) Acetylcholine
3) Parasympathetics
increase contraction
What will decrease the amplitude of slow waves? effects?
1) Norepinephrine
2) Sympathetics
decrease contraction
What mainly controls GI movements?
MYENTERIC PLEXUS
What is part of the enteric nervous system/
1) Submucosal plexus
2) Myenteric plexus (Auerbach’s)
Describe submucosal plexus
- location
- function
in the submucosa
- mainly controls GI secretion and local blood flow
Describe Myenteric plexus
- location
- function
aka Auerbach’s
- btw longitudinal and circular layers
- mainly control GI movements
Role of Pacemaker region in plexuses
Pacemaker regions in myenteric and submucosal plexuses generate spontaneous slow wave activity
What cells are the pacemaker of GI smooth muscle?
Interstitial Cells of Cajal (ICC)
Describe Interstitial Cells of Cajal (ICC)
- function
- cell type
- generate and propagate slow waves
- slow waves occur SPONTANEOUSLY in ICC and spread rapidly to smooth muscle via GAP JUNCTIONS
- drives frequency of contraction
Describe Mastication
- innervation
- controlled by what
- function
- innervated by motor ranch of fifth cranial nerve
- both voluntary and involuntary
- controlled by nuclei in brain stem
- chewing reflex
Phases of Swallowing (3)
- describe in detail
- involuntary/ voluntary
1) Oral Phase ( voluntary)
- initiate swallowing process
2) Pharyngeal phase (involuntary)
soft palate is pulled forward-> epiglottis moves -> UES relaxes-> peristaltic wave of contractions is initiated in pharynx-> food is propelled through open UES
3) Esophageal phase (involuntary)
- control by the swallowing reflex and ENS
-Primary peristaltic wave
- Secondary peristaltic wave
What is the involuntary swallowing reflex controlled by?
- pathway
Medulla
Food in pharynx-> afferent sensory input via vagus/glossopharyngeal N.-> swallowing center (medulla)-> brainstem nuclei-> efferent input to pharynx
Two Types of peristaltic waves
1) Primary peristaltic wave
2) Secondary peristaltic wave
Primary peristaltic wave
- continuation of pharyngeal peristalsis
- controlled by the medulla
- can NOT occur after vagotomy
Secondary peristaltic wave
- occurs if primary wave fails to empty the esophagus or if gastric contents reflux into esophagus
- Medulla & ENS are involved
- can occur in absences of oral & pharyngeal phass
- occurs EVEN after vagotomy
How does pressure change during swallowing as food bolus passes?
as food goes down, pressure increases in the region where the food bolus is down the esophagus
Problems with intrathoracic location of esophagus (2)
- how are these problems solved
1) keeping air out of esophagus at upper end
2) keeping acidic gastric contents out of the lower end
Solution
- UES and LES are closed, except when food bolus is passing from pharynx to esophagus or from esophagus to stomach
Achalasia
- description (3)
- causes (2)
- symptoms
- impaired peristalsis
- incomplete LES relaxation during swallowing
- elevation of LES resting pressure
Causes
- lack of VIP or ENS
- damage to nerves in esophagus, prevent it from squeezing food into stomach
- backflow of food in throat (regurgitation), difficulty in swallowing to both liquids and solids (dysphagia), chest pain
GERD
- causes
- symptoms
- changes in barrier between esophagus and stomach
- motor abnormalities that result in low pressures in LES
- persistent reflux and inflammation
- backwash of acid, pepsin, bile into esphagus
- heartburn and acid regurgitation
- irritation/scar of esophageal lining
- Barrett’s esophagus
Anatomical division of stomach
Fundus
body
Antrum
Regions of stomach
1) Orad Region
- Fundus
- Upper half of body
2) Caudad Region
- lower half of body
- antrum
3 muscle layers of stomach
circular
longitudinal
oblique
Extrinsic innervation of stomach
parasympathetics and sympathetics
Intrinsic innervation of stomach
myenteric and submucosal plexus ( ENS)
Receptive Relaxation
- location
- describe
- reflex
- hormone
Orad region
- decrease pressure and increase volume
- vagovagal reflex
- minimal contractile activity
- little mixing or ingested food occurs there
CCK decrease contractions and increase gastric distensibility
Mixing and Digestion
- location
- describe
- peristaltic contraction (mid stomach-> pylorus)
- contractions increase in force and velocity as they approach the pylorus
- frequency is 3-5 waves/min
Retropulsion: contents propelled back into stomach for further mixing and REDUCTION of particle size
Sequence of gastric motility
1) food comes in stomach-> initial peristaltic wave
2) Pylorus is opened
3) Mixing in lower stomach
4) Retropulsion
5) Propulsion into duodenum
- takes a few hours
Regulation of gastric contraction
- what will increase/ decrease contractions
Increase contraction (increase AP):
1) Parasympathetic stimulation
2) Gastrin
3) Motilin
Decrease contraction (decrease AP):
1) sympathetic stimulation
2) secretin
3) GIP
How can you increase gastric emptying? (4)
1) decrease distensibility of orad
- distensibility= ability to become stretched, dilated, enlarged
2) increase force of peristaltic contractions of caudad stomach
3) decrease tone of pylorus
4) increase diameter and inhibition of segmenting contractions of proximal duodenum
What inhibits gastric emptying? (4)
1) Relaxation of Orad (increase in distensibility)
2) decrease force of peristaltic contractions
3) increase tone of pyloric sphincter
4) segmentation contractions in intestine
Entero-gastric reflex
- how?
negative feedback from duodenum that will slow down rate of gastric emptying
acid in duodenum-> stimulate secretin release-> inhibit stomach motility via gastrin inhibition
fats in duodenum-> stimulate CCK and GIP-> inhibit stomach motility
hypertonicity in duodenum-> unknown hormone-> inhibit gastric emptying
Disorders of gastric motility
- symptoms
- causes
- treatment
Symptoms: fullness, loss of appetite, nausea, vomit
Causes: gastric ulcer (scar tissue), cancer (physical obstruction), eating disorders, vagotomy
Treatment: pyloroplasty, balloon dilation
Gastroparesis
- slow emptying of stomach/paralysis in absence of mechanical obstruction
- DM most common
- injury to vagus nerve
symptoms: nausea, vomit, fullness when eating, weight loss
Migrating Myoelectric Complex
- periodic, bursting peristaltic contractions
- occur at 90 mins intervals, during fasting
- Motilin play role
- inhibited during feeing
- large particle of undigested residue
Small Intestine motility
- mix chyme and digestive enzyme and pancreatic secretion
- expose nutrients to intestinal mucosa for absorption
- propel unabsorbed chyme along the small intestine to large intestine
Segmentation Contractions
- generates back and forth movement
- produce no forward, propulsive movement along the small intestine
Peristaltic contractions
- circular and longitudinal muscles works in opposition to complement each other’s actions
- reciprocally innervated
Electrical activity in small intestine
slow wave frequency
- Duodenum: 12 cycles/ min
- Jejunum: 10 cycles/ min
- Ileum- 8 cycles/ min
Serotonin in peristaltic reflex
released by enterochromaffin cells and bind to receptos in IPANS
Myenteric plexus regulation in SI
relaxation and contraction of intestinal wall
Submucosal (meissner) plexus regulation in SI
senses lumen environment
Neural input in SI contractions
- peristaltic reflex mediated by ENS
- PNS stimulates and SNS inhibits contractions
Hormonal control in SI contraction
— Serotonin stimulates contractions
— Certain prostaglandins can stimulate contractions
— E, released from adrenal glands, inhibits contractions
- gastrin, CCK, motilin, and insulin tend to stimulate contractions
- secretin and glucagon tend to inhibit contractions
Vomiting Reflex
- controlled by
- nerves
- pathway
- coordinated by medulla
- nerve impulses are transmitted by vagus and sympathetic afferents to multiple brain stem nuclei
- reverse peristalsis in SI-> stomach and pylorus relaxation-> forced inspiration to increase abdominal pressure-> movement of larynx -> LES relaxation-> glottis closes-> forceful expulsion of gastric contents
Ileocecal Junction
sphincter that control contents coming from SI into LI
- distention of ileum-> relaxation of sphincter
- distention of colon -> contraction of sphincter
Anatomical features of LI
- muscle layers
- sphincters
- haustra
Muscle layer
- longitudinal
- taeniae coli: 3 flat bands of longitudinal fibers that run from cecum to rectum
- Circular
- continuous from the cecum to anal canal
Sphincter:
- internal anal sphincter (smooth muscle)
- external anal sphincter (striated muscle)
Haustra: small pouches that give LI a segmented appearance
- no fixed
Innervations of LI
- ENS
- PNS
- SNS
- Somatic pudendal nerves
- ENS
- concentrated beneath teneae
- innervate muscle layers
- PNS
- vagus nerve: cecum, ascneding and transverse colon
- pelvic nerves: sacral portion of spinal cord (S2-S4), descending and sigmoid colon, rectum
- SNS
- superior mesenteric ganglion: proximal regions
- inferior mesenteric ganglion: distal regions
- hypogastric plexus: distal rectum & anal canal
- Somatic pudendal nerves; external anal sphincter
Motility in LI
• Occur in the colon, over large distances • 1 - 3 times/day • Stimulate defecation reflex • A final mass movement propels the fecal content into the rectum
Poor Motility in LI
- effects
greater absorption
- hard feces in transverse colon -> constipation
Excess Motility in LI
- effects
less absorption
- diarrhea
- loose feces
Motility of rectum and anal canal
• Rectum fills intermittently - Mass movements - Segmentation contractions • As it fills with feces, SM wall of the rectum contracts & INTERNAL anal sphincter RELAXES (rectosphincteric reflex) • The EXTERNAL anal sphincter is tonically CLOSED (under voluntary control)
Rectosphincteric reflex & defecation
- under what control
- mediated by
• Under neural control
— Controlled partially by ENS
— Reflex is reinforced by
cortex activity of neurons within the spinal cord
-Sensation of rectal distention & voluntary control of the external anal sphincter are mediated by pathways within the spinal cord that lead to the cerebral cortex
- destruction will cause loss of voluntary control od defecation
Hirschsprung Disease
- cause
- result
- symptoms
- treatment
cause: ganglion cells absent from colon segment
Result:
- VIP level low
- SM constriction
- loss of coordinated movement
- colon contents accumulate
- difficulty of passing stool
Symptoms: poor feeding, jaundice, vomiting, constipation, swollen belly, malnutrition
Treatment: surgical resection of colon segment lacking ganglia
Vago-vagal reflex
long reflex
- generally stimulatory (increase motility, secretomotor, vasodilatory activities)
afferent (75)
efferent (25)
Intestino-intestinal reflex
depends on extrinsic
connections; inhibitory
if an area of the bowel
distended, contractile activity in the rest of the
inhibited
Enterogastric Reflex
Negative feedback from d
will slow down the rate of gastric emptying
Gastroileal reflec (gastroenteric)
gastric distentionsrelaxes ileocecal sphincter
Gastro- & duodeno-colic reflexes
distention of
stomach/duodenum initiates mass movements
- Transmitted by way of the ANS
Defecation reflex (rectosphincteric)
rectal distention initiates defecation
Gastrin
secreted G cells of antrum & duodenum
stimulates motility
CCK
secreted from I cells of duodenum and jejenum
stimulates motility
Insulin
secreted from pancreatic beta cells
stimulates motility
Motilin
secreted from duodenum & jejunum
stimulates motility
Serotonin
neurotransmitter
stimulates motility
Secretin
secreted by S cells of duodenum
inhibits motility
Glucagon
secreted from pancreatic alpha cells
inhibits motility
