Lecture 5: Motility of the GI tract Flashcards
Layers of the GI tract (luminal to deep)
(Lumen) Epithelium Lamina propia Muscularis mucosae Submucosa Submucosal plexus Circular muscle Myenteric plexus Longitudinal muscle Serosa (Blood)
What is the significance of the muscularis mucosae?
Whatis the significance of the muscularis propia?
- in the mucosa layer, smooth muscle contractions here directly influence epithelium
- has the circular and longitudinal smooth muscles
Circular muscle vs. Longitudinal muscle
C: decreases diameter of contracting segment
L: decreases length of contracting segment
What are slow waves and how are they different from APs?
shows depolarization and re-polarization of the membrane
- slow waves are simply oscillations of voltage > changes are enough to generate tension/contraction the SM in the GI tract, which usually follows the slow wave
Phasic vs Tonic
P: periodic contractions followed by relaxation (waves)
T: constant contraction with no relaxation (plateau)
What is the relationship of AP to slow waves?
The more AP generated the stronger the contraction in the GI tract
What elements stimulate GI motility (more slow waves)?
Stretch
Ach
Parasympathetics
What elements inhibit GI motility (less slow waves)?
NE
Sympathetics
What is the significance of the Enteric Nervous system?
-have pacemaker regions that control slow wave activity without needing nervous system input
as parts of the ENS, what is the role of the submucosal plexus and the myenteric (auerbach’s) \plexus?
S: controls GI secretions and blood flow
M: controls GI movements
Explain how slow waves are spontaneously generated
Interstitial cells of Cajal (ICC) serves as pacemaker that regulate electrical activity > spreads impuse via gap junctions > smooth muscle cells respond by opening Ca2+ voltage channels > more contraction
What controls mastication?
- CN V
- chewing is essentially a reflex caused by presence of food in mouth = triggers digestion process as well
Describe the physiology of swallowing
Oral phase
Pharyngeal phase
Esophageal phase
Oral phase: voluntary initiation of swallowing
Pharyngeal phase: soft palate ascends > epiglottis moves/vocal cords block trachea > upper esophageal sphincter relaxes > peristalsis in the pharyngeal constrictors pushing food down into esophagus
Esophageal phase: peristaltic waves controlled by the ENS and the swallowing reflex (backup plan 2ndary wave that pushes food down if not successful)
How does the swallowing reflex work?
Food in pharynx > CN IX/X detection > swallowing center in medulla > brainstem nuclei > efferent input to pharynx
Primary vs. Secondary peristaltic wave
Primary: esophageal constriction controlled by the medulla > goal is to bring food into gastric organs
-cannot happen after vagotomy
Secondary: triggered if esophagus failed to bring food into gastric organ controlled by ENS and medulla
-can happen after vagotomy
What does a manometry study show?
- changes in pressure in thorax/abdomen at different parts of the esophageal tract
- contraction means blocking, relaxation means allowing food to come in = results in “wave” down the GI tract = peristalsis
How does the GI tract prevent backflow?
UES (pharynx to esophagus) and LES (esophagus to stomach) - closed and contracted except when food has to pass through
Achalasia
Causes
Clinical
- myenteric plexus ganglion cells reduced, esophageal nerve damage
- more elevated LES resting pressure compared to normal = reduced relaxation of LES during swallowing = impaired peristalsis leading to regurgitation, dysphagia, heartburn and chest pain
GERD
Cause
Clinical
- abnormally low pressure in the LES making it prone to relaxing instead of contracting, reflux of acid, pepsin and bile into esophagus
- heartburn, regurgitation , GI bleeding, esophagitis, Barrett’s esophagus
What controls motility in the stomach?
-Extrinsic innervations: sympathetic and parasympathetic
Intrinsic innervations: ENS (Myenteric and submucosal plexus)
What happens at the LES/Orad junction when there is food present?
What hormone acts on this region and what does it do?
vagovagal reflex causing receptive relaxation (low pressure/high volume)
-Cholecystokinin (CKK) from SI decreases contractions and increases gastric distensibility
What happens at the Caudad region of the stomach?
-contractions increase (n force and velocity in this area > has to be strong enough to actually push food down and open the pyloric sphincter
What happens at the antrum region?
- Contraction at the pyloric sphincter only allows small amount of food through into the duodenum, retropulsion of food occurs and backflows into stomach
- (process is gradual, repetitive peristalsis to push food through not all at once; most of the food pushed out 3-4 hours later)
What are the parasympathetic effectors of gastric contraction?
Sympathetic?
P: gastrin and motilin (increase AP and contraction force)
S: secretin and GIP (decrease AP and contraction force)
What factors increase gastric emptying?
- decreased distensibility in orad, pyloric tone and segmenting contractions in proximal duodenum
- increased peristaltic force in caudad and diameter of proximal duodenum
(triggered after a meal)
What factors decrease gastric emptying?
- increase in segmentation contractions in duodenum and pyloric tone
- decrease peristaltic force and distensibility (contraction) of orad
- Enterogastric reflex (negative feedback from duodenum)
How does the entero-gastric reflex work via acid, fat and hypertonicity?
- Acid in duodenum > secretin release > inhibit gastrin > inhibit motility in stomach
- Fats in duodenum > CKK and GIP > inhibit stomach motility
- Hypertonicity also inhibits, hormone unk
Gastroparesis
Causes
Clinical
- DM 2, vagus n. injury
- n,v, bloating, weight loss, fullness
Common causes of gastric motility issues
Common treatments
- scarring (ulcer), obstruction (cancer), eating disorders, vagotomy
- pyloroplasty, balloon dilation
What is the MMC?
What mediates it?
- Migrating myoelectric complex
- periodic, bursting contractions during fasting that empties undigested residue from stomach
- Motilin
SIBO
What role does MMC play in preventing this?
Small intestinal bacterial overgrowth - overabundance of colonic bacteria in SI which disturbs small bowel movements > nausea, anorexia, bloating
MMC performs cleansing mechanisms in the small intestine
How does the small intestine maximize nutrient absorption?
- mixing chyme with digestive enzyme and pancreatic secretions that exposes as much of the nutrients to the mucosa that will absorb it
- also pushes unabsorbed chyme to the large intestine
What is the difference between segmentation contractions and peristaltic contractions?
- SI contractions that separates the bolus to mix it as much as possible (same action)
- done by circular and longitudinal muscles propel food forward (opposite actions, contraction behind the bolus, relaxation in front of the bolus)
How is the generation of contractions different in the SI compared to stomach?
Stomach does not need spike potential AP to initiate contraction
-slow waves not enough to initiate it, but sets the maximum frequency of SI contractions (decreases the further food goes down the SI)
Describe the pathway of the regulation of the peristalsis in the SI (include role of myenteric and Meissner plexus)
Meissner plexus are the sensory neurons: 5HT (serotonin) released by smooth muscle on IPAN > interneuron > excitatory motor neuron in Myenteric plexus > effector substances released to contract smooth muscle
What neural effectors contract/excite the small intestine?
What neural effectors relax/inhibit the small intestine?
- Ach, Substance P
- VIP, NO
What hormones stimulate SI contractions?
What hormones inhibit SI contractions?
- serotonin, prostaglandins, gastrin, CKK, motilin, insulin
- epinephrine, secretin, glucagon
How does the vomiting reflex work?
Vagus/sympathetic afferents > medulla (vomiting center)
efferents induce: reverse peristalsis in SI > pyloric relaxation > forced inspiration to increase abd. pressure > LES relaxes/glottis closes > gastric expulsion of food = vomiti
How is the bolus propelled into the colon from the SI?
bolus accumulation > distension of the ileum > causing relaxation of the ileocecal sphincter > bolus flows into colon
*distension of the colon causes the sphincter to close to block more bolus from entering
What innervates the two types of anal sphincters?
Internal: Pelvic splanchnic ns. (involuntary)
External: pudendal n. (somatic/voluntary)
What parts of the colon does ….. innervate ?
ENS (myenteric plexus)
PNS
SNS
Pudendal ns. (somatic)
-muscle layers of the colon
-cecum, ascending and transverse colon (via CN X)
descending, sigmoid and rectum (Pelvic splanchnic Ns.)
-Proximal regions (via superior mesenteric ganglion)
Distal regions (via inferior mesenteric ganglion)
Distal rectum and anal canal (via hypogastric plexus)
-external anal sphincter
What characterizes bolus motility in the colon?
-mass movements = large distances to stimulate the defecation reflex and absorption of the water and electrolytes back into blood
How does colon motility result in constipation and diarrhea?
Constipation: poor motility = slower passage = too much time for absorption = dry poop
Diarrhea: high motility = faster passage = too little time for absorption = loose poop
What characterizes motility in the rectum and anal canal?
-colon’s mass movements propel feces into rectum > distension stimulates the rectosphincteric reflex
How does the rectosphincteric reflex work?
What can lead to fecal incontinence?
feces fills the rectum > rectal distension > smooth muscle wall contracts and internal anal sphincter relaxes
external anal sphincter closed unless opened voluntarily
-inability to sense rectal distension or loss of voluntary control of the External anal sphincter
What happens to GI motility control in Hirschsprung disease?
lack of ganglion cells in some segment of the colon > low VIP levels > no relaxation/SM constriction > colon contents accumulate
