Motility Of GI Flashcards
Slow waves
- Not APs
- Depolarization (membrane potential becomes less -)/repolarization (MP becomes more -) of membrane potential
- Frequency of slow waves determines frequency of AP, therefore frequency of contractions
- Originate in interstitial cells of Cajal
Phasic Contractions
Periodic contractions followed by relaxation
Seen in esophagus, antrum of stomach, SI
**Mixing and propulsing
Tonic contractions
Maintain a constant level of contraction without regular relaxation periods
Found in orad of stomach, lower esophageal, IC, int. Anal sphincters
ACh effect on Slow waves
ACh increases amplitude of slow waves and # of APs
Other stimulators of slow waves: stretch/parasympathetics
*Increase membrane potential
NE effect of slow waves
NE decreases amplitude of slow waves
Sympathetics w/ same effect
Creates hyperpolarization
Submucosal Plexus of Meissner
- Found between submucosa and circular muscle layer
- Controls GI secretions and local blood flow
Myenteric plexus of Auerbach
- Found between longitudinal and circular muscle layers
- Controls GI movements
Oral Phase
Voluntary and initiates swallowing process
Pharyngeal phase
Involuntary
- Soft palate pulled upward, epiglottis moves, UES relaxes, peristaltic wave of contractions initiated in pharynx and food is propelled through open UES
Esophageal Phase
Involuntary
Control by the swallowing reflex and ENS
Neural control of digestion
Mastication: 5th CN
Swallowing: 9th/10th CN
Primary Peristaltic Wave
Continuation of pharyngeal peristalsis
*Medulla controlled (cannot occur with vagotomy)
Secondary Peristaltic Wave
Occurs if primary wave fails to empty esophagus or if reflux occurs
*Medulla and ENS control (can occur post-vagotomy)
Issues w/ intrathoracic location of eso
- Keep air out at upper end
2. Keep acid gastric contents out of lower end
Achalasia
- Impaired peristalsis
- Incomplete LES relaxation during swallowing (food backs up)
- LES resting P increases
Causes of Achalasia
Lack of VIP/ENS knocked out
Damage to esophageal nerves, preventing it from squeezing food into stomach
Effects of Achalasia
Backflow of food in throat
Difficulties swallowing
Chest pain
GERD
- Changes in barrier b/w esophagus and stomach
- LES relaxes abnormally/weakens
- Persistent GERD can lead to irritation of esophagus, strictures and Barrett’s esophagus
Causes of GERD
- Motor abnormalities resulting in abnormally low pressures in LES
- When intragastric pressure increases (large meal, pregnancy, heavy lifting)
Receptive Relaxation
- In orad region of stomach
- Decreases pressure and increases volume in orad region
- Vagovagal reflex
- Orad has minimal contractile activity
- CCK decreases contractions and increases gastric distensibility
Caudad region of stomach
- Primary contractile event occurs midstomach-pylorus
- Contractions increase with force and velocity approaching pylorus
- 3-5 waves/minute = maximum
- Retropulsion*
Increased AP and force of contraction
Parasympathetic stimulation
Gastrin
Motility
Decreased AP and force of contractions
Sympathetic Stimulation
Secretion
GIP (increased insulin)
Gastric emptying
Via coordinated contractile activity of stomach, pylorus, and proximal small intestine
Rate of gastric emptying increases with
- Decreased orad distensibility
- Increased force of peristaltic contractions in caudad stomach
- Decreased tone of pylorus
- Increased diameter and inhibition of segmenting contractions in prox. Duodenum
= 3hrs
Factors that inhibit gastric emptying:
- Relaxation of orad (increased distensibility)
- Decreased force of peristaltic contractions
- Increased tone of pyloric sphincter
- Segmentation contractions in intestine
Enterogastric reflex
- Negative feedback from duodenum slows down rate of gastric emptying
- Acid in duodenum stimulates secretin release and inhibits stomach motility via gastrin inhibition
- Fats in duodenum stimulates CCK and GIP which inhibits stomach motility
- Hypertonicity in duodenum inhibits gastric emptying
Slow gastric emptying
- Associated with disorders of gastric motility
- Causes: gastric ulcer, cancer, eating disorders, vagotomy
Gastroparesis
- Slow emptying of stomach w/o mechanical obstruction
- DM common cause
- Vagal injury
Sx: N/V, feeling of fullness, weight loss, abdominal discomfort
Migrating Myoelectric complex
- Periodic, bursting peristaltic contractions
- 90 min intervals
- Motilin mediates complex
Segmental Contractions
Back and forth movements
No forward/propulsive movements along SI
Peristaltic contractions
Circular and longitudinal muscles work in opposition to each other and complement actions
ICC and Smooth muscle in SI
- Slow waves always present
- Slow waves do NOT initiate contractions in SI
- Spike potentials (aka AP) needed for muscle contractions
- Slow wave frequency sets max. Frequency of contractions
Stimulate Contractions
- PNS
- Serotonin
- Prostaglandins
- Gastrin
- CCK
- Motilin
- Insulin
Inhibit Contractions
- Epinephrine
- Secretin
- Glucagon
Vomiting Reflex
Medulla coordinates
- Reverse peristalsis
- Stomach and pylorus relax
- Forced inspiration to increase abdominal pressure
- Mvmt of larynx
- LES relaxation
- Glottis closes
- Forceful expulsion of gastric contents
Flow from SI to LI
Ileum distention causes relaxation of sphincter
Colonic distention causes contraction of sphincter
**Via Ileocecal Valve
Muscle layers of LI
- Longitudinal w/ teniae coli
- Circular run from cecum to anal canal
- Internal anal sphincter (smooth m)
- External anal sphincter (skeletal m)
Haustras
Small pouches that give LI segmented appearance (not fixed)
Parasympathetic Innervation of LI
- Vagus n.: cecum, ascending and transverse colon
- Pelvic nn.: sacral portion of spinal cord (S2-S4): descending and sigmoid colon and rectum
Sympathetic Innervation of LI
- T10-L2
- Superior mesenteric ganglion: proximal regions
- Inferior mesenteric ganglion: distal regions
- Hypogastric plexus: distal rectum and anal canal
Somatic pudendal nn.
External anal sphincter
Key function of LI motility
Water absorption/vitamin absorption
Conversion of digested food into feces
Motility of rectum/anal canal
- Rectum fills intermittently (mass movements and segmental contractions)
- As it fills with feces, SM wall of rectum contracts and Int. Anal Sphincter relaxes (rectosphincteric reflex)
- Ext. Anal sphincter voluntarily relaxes
Rectosphincteric reflex and defecation
- Neural Control (partially by ENS and reinforced with spinal cord neurons)
- Sensation and voluntary control of EAS by pathways leading to cerebral cortex
- Destruction of these pathways causes loss of voluntary control of defecation
Hirschsprung’s Disease
VIP levels low - SM constriction/loss of coordinated mvmt. - colon contents accumulate
Vago-vagal reflex
Long reflex
Generally stimulatory (increases motility, secretomotor, vasodilatory activities)
75% afferent
25% efferent
Intestino-intestinal reflex
Inhibitory if bowel is distended
Contractile if rest of bowel is inhibited
Enterogastric reflex
Negative feedback from duodenum will slow down rate of gastric emptying
Gastroileal reflex (gastroenteric)
Gastric distention relaxes ileocecal sphincter
Gastro and duodeno-colic reflexes
Distention of stomach and duodenum initiates mass mvmts.
Via ANS
Defecation reflex (rectospincteric)
Rectal Distention initiates defecation
