Gastric motility Flashcards
Gastrointestinal motility
GI motility is the movements of the digestive system and how its contents transit within it.
GI motility involves coordinated contractions and relaxations of the GIT that moves content from the mouth to the anus.
There are 3 main patterns of motility: peristalsis, segmentation, and tonic contraction.
Muscles in the gastrointestinal tract
There are two types of muscles in the GIT-smooth (involuntary) and skeletal (voluntary) muscles.
Smooth muscles are found throughout most of the GIT. There are usually 2 layers: inner layer (circular) and outer layer (longitudinal).
Skeletal muscles can be found in pharynx, top third of oesophagus, external anal sphincter.
Smooth muscle motility
phasic - rapid contractions - body of oesophagus , stomach antrum , small and large intestines
tonic - sustained contractions - sphincters , upper stomach
Enteric nervous system
Enteric nervous system is made up of myenteric plexus and submucosal plexus.
Activation of the myenteric plexus:
increases tonic contraction
increases intensity of rhythmic contractions
rate of rhythmic contractions increases velocity of conduction
Activation of the submucosal plexus:
increase secretory activity
Modulates intestinal absorption
organisation - sensory neuron –> interneuron –> motor neuron
Gastric motility - food storage
This has to do with the contractions or relaxations of the smooth muscles in the stomach wall.
Empty stomach - volume approx 50ml. When a meal is swallowed, smooth muscles in the fundus relax before the food arrives in the stomach.
Stomach volume increases to 1.5 L with little increase in pressure.
Relaxation in the fundus is regulated by the vago-vagal reflex termed ‘receptive relaxation’ If vagal innervation is interrupted then intra-gastric pressure increases.
Highly folded -> Upon filling the folds flatten out -> Therefore wall tension and intraluminal pressure change only very slightly.
Vagotomy: a medical intervention that interrupts signals by the vagus nerve i.e., the folds of the fundus does not relax.
Intrinsic and vago-vagal reflexes mediate receptive relaxation
Gastric motility - propulsion
Liquids and small particles leave the stomach more rapidly than large particles. This discrimination is called sieving function
Movement of solid particles toward the antrum is accomplished by the interaction of propulsive gastric contractions and occlusion of the pylorus, a process termed propulsion.
These contractions propel the luminal contents toward the pylorus, which is partially closed by contraction of the pyloric musculature before delivery of the bolus.
phase of propulsion - rapid flow of liquids with suspended small particles and delayed flow of large particles towards pylorus
gastric motility - grinding
Once a bolus of material is trapped near the antrum it is churned to help reduce the size of the particles, a process termed grinding.
Only a small portion of gastric material-(that contains particles smaller than 2 mm)-is propelled through the pylorus to the duodenum.
antrum has thicker layer of smooth muscle - more forceful contractions
phase of grinding - emptying of liquids with small particles whereas large particles are retained in the buldge of the terminal antrum and subject to grinding
gastric motility - retropulsion
Most of the gastric contents are returned to the body of the stomach for pulverization and shearing of solid particles, a process known as retropulsion
These processes of propulsion, grinding, and retropulsion repeat multiple times until the gastric contents are emptied.
phase of retropulsion - retropulsion of large particles and clearing of the terminal antrum
The pyloric sphincter limits the flow of chyme into the duodenum to allow slow and efficient absorption in the duodenum
gastric emptying
Gastric emptying is the process by which the contents of the stomach are discharged into the duodenum.
Gastric emptying is primarily regulated by the autonomic nervous system (vagus nerve) and gastrointestinal hormones.
The pyrolic sphincter allow carefully regulated emptying of gastric contents and prevents regurgitation of duodenal contents into stomach
- innervated by vagus (relaxation) and sympathetics (constriction)
control of gastric emptying
cephalic phase - approach of food or food in mouth
gastric phase - food in stomach
intestinal phase - food in duodenum, ileum or colon
Cephalic phase
An inhibitory phase - Inhibitory nerve fibres in the vagus nerve
Results in relaxation of stomach enabling it to store large volumes
Gastric phase
An excitatory phase in which the stomach empties at rate proportional to the volume in it.
Due to:
Myogenic reflex: stretching smooth muscle causes reflex contraction
Activation of pressure receptors which send impulses in local nerve plexi and in the vagus nerve
Gastrin released in response to peptides etc
Gastric: bolus in stomach = distention = stretch in stomach walls
Intestinal phase
An inhibitory phase, through which the duodenum adapts the “work-load” as a function of the state of the digestive process.
This phase is mainly controlled through hormonal and paracrine mechanisms, activated by duodenal chemoreception. The general scheme would be:
- Low pH –> activates secretion of Secretin
High fats/lipids –> increase secretion of CCK
High levels of amino acids –> increase secretion of Gastrin
High levels of carbohydrates –> increased secretion of GIP
There are also some motor reflexes: e.g., the ileogastric reflex –> Chyme entering the ileum activates pressure receptors which delays gastric emptying - via nerves in plexi
Significance allows more time for digestion
Motility of the stomach
The motility of the stomach is regulated by neural and hormonal factors
Motility influences gastric emptying (movement of contents into the duodenum)
Increased gastric emptying results from ↑food volume, pressure, peristaltic waves, hypoglycaemia
Decreased gastric emptying results from solids, fats, non-isotonic solution and hyperglycaemia
Gastroparesis
A disorder that is due to a delay in the gastric emptying in the absence of mechanical obstruction of the stomach. Its pathogenesis is unclear.
Diabetes is the most frequently identified disease linked to gastroparesis
Underdiagnosed due to similar presentation as GORD
Symptoms: postprandial fullness, nausea, vomiting, bloating, and upper abdominal pain
Treatment/management: dietary changes (several small meals/day), pro-motility agents
