Gastrointestinal Motility: Comprehensive Notes

Gastrointestinal Motility

GI Motility in Health

  • Coordinated movement of ingested material through the digestive tract is crucial for nutrient absorption and waste expulsion.
  • Intestinal dysmotility can lead to infections, malabsorption, and symptoms like diarrhea and constipation, significantly impacting health and quality of life.

Learning Objectives

  • Basic elements of control
  • The peristaltic reflex
  • Movements of the oesophagus, stomach, & intestine:
    • During hunger
    • After eating
  • Introduction to reflex control & feedback regulation
  • Different movements of the colon

GI Motility Functions

  • Propulsion
  • Propulsion & Retropulsion
  • Accommodation
  • Storage
  • Functional Barrier (sphincter)

GI Motility in Disease

  • Achalasia
  • Reflux
  • Early satiety
  • Nausea
  • Functional Dyspepsia
  • Gastroparesis
  • Vomiting
  • Diarrhoea
  • Constipation
  • Chronic constipation
  • Megacolon
  • Faecal incontinence
  • Impaction
  • Pseudo-obstruction
  • Irritable bowel syndrome

Neuronal Connections Between Gut and Brain

  • The brain is connected to the gut via extrinsic nerves, with the vagal nerve being the most prominent.
  • These connections include both sympathetic and parasympathetic pathways.
  • They connect to the enteric nervous system (ENS), the autonomic neuronal circuitry of the gut.
  • The enteric nervous system interacts with the gut endocrine and immune systems.
  • The gut-brain axis involves various factors:
    • Extrinsic visceral afferents
    • Sympathetic nervous system
    • Vagus nerve
    • Spinal cord
    • Parasympathetic nervous system
    • Enteric nervous system
    • Microbiota

Extrinsic Innervation of the Gut

  • Sympathetic: Generally inhibitory (noradrenergic).
    • Paravertebral ganglia.
    • Greater splanchnic nerve.
    • Lumbar colonic nerve.
    • Hypogastric nerve.
  • Parasympathetic: Generally excitatory (cholinergic).
    • Vagus nerve.
    • Pelvic nerve.

Enteric Nervous System (ENS)

  • Controls GI motility, local blood flow, and transmucosal movement of fluids.
  • Consists of sensory elements, interneurons, and motor neurons.
  • Interacts with gut endocrine and immune systems.
  • Modulated by extrinsic nerves and hormones.
  • Contains around 300 million nerve cells in the gut wall.
  • Operates against a background of spontaneous muscle movements to modulate and initiate GI movements.
  • Can function independently.

Interstitial Cells of Cajal (ICCs)

  • Function somewhere between a muscle cell and a neuron.
  • Found around the myenteric and submucosal plexuses.
  • Create slow waves of muscle contraction activity and help coordinate responses to nerves.
  • Interstitial refers to any cell which lies between other cells.

Cell Types & Functions in GI Movement

  • Interstitial Cells of Cajal (ICC): Spontaneous generation of electrical slow waves.
  • Smooth Muscle Cells: Conduction of slow waves to smooth muscle (gap junctions); depolarization & opening of Ca2+Ca^{2+} channels to cause muscle contraction.
  • Enteric Neurons: Neuronal modulation of muscle contractions (and ICC function).
  • Intrinsic Control of GI Movements

Peristalsis

  • Basic process of propulsion involving contraction and relaxation to move a bolus forward.

Enteric Nervous System and Peristalsis

  • Activation of enteric reflexes:
    • Ascending wave of peristalsis: Excitatory neurotransmission to muscle (mostly by release of acetylcholine).
    • Descending wave of peristalsis: Inhibitory neurotransmission to muscle (mostly by release of the gas nitric oxide).
  • Stimuli:
    • CHEMICAL: From endocrine cells (e.g., 5-HT), nutrients, low pH.
    • MECHANICAL: Mucosal deformation, stretch.

Enteric Sensory Neurons

  • Detect intraluminal stimuli.
  • Initiate peristalsis, plus increased secretion & vascular flow.
  • Respond to chemical (5-HT, nutrients, low pH) and mechanical (mucosal deformation, stretch) stimuli.
  • Potential to make lots of connections.

Peristalsis Summary

  • Enteric sensory nerves, with mechanical and chemosensitive receptors, respond to an intraluminal signal.
  • Information is transmitted, via interneurons, to motor neurons (cholinergic (ACh) and nitrergic (NO)).
  • Initiates the peristaltic reflex and modulates immune, vascular, muscular & epithelial transport systems.

Phases of Food Intake

  • Cephalic Phase:
    • Triggered by thought, sight, smell, taste (learned responses).
    • Prepares GI tract - Saliva, gastric acid, pancreatic secretion, gastrin, ghrelin secretion.
  • Gastric Phase:
    • Satiation, Early Digestion, Gastric emptying.
    • Triggered by mechanical effect.
  • Intestinal Phase:
    • Feedback & Satiation.
    • Triggered mainly by chemoreceptor activation in small bowel.

Migrating Motor Complex (MMC)

  • Occurs during hunger.
  • 3 phases every 90-120 minutes.
  • Culminates in high amplitude propagating contractions.
  • Can originate in the stomach (vagus dependent) or small intestine (vagus independent).
  • Functions:
    • Clear undigested material.
    • Prevent bacterial overgrowth.
    • Hunger sensations.

Hunger and Gastric Phase III MMC Activity

  • Association shown in healthy volunteers after overnight fast.
  • Hunger scored on 100 mm VAS at 5 min intervals. A p-value of P<0.05 was obtained.

Central (Vagal) Control of Peristalsis in Oesophagus

  • Primary peristaltic wave occurs on swallowing when bolus enters the oesophagus (striated muscle; vagus).

Breakdown of Food in Stomach

  • Contraction of mid corpus mixes & breaks down food, together with gastric acid + peptidases.
  • Antrum - powerful contractions (against a closed pylorus) breaks food into particles small enough to be propelled into the duodenum.
  • Three factors regulate the rate of expulsion from the stomach:
    • Physical properties (liquids vs. solids; particle size).
    • Neuronal & hormonal feedback (sense physical properties).
    • Nutritional value.

Gradients of Slow Wave Activity in the Stomach

  • ICCs generate slow waves which propagate from the dominant pacemaker in the corpus (body).
  • Around & down to the pylorus.
  • Slow waves reaching mid-lower corpus form into complete ring wave-fronts.
  • ENS increases the motion.

Sieving Function in the Stomach

  • Antrum:
    • Rapid flow of liquids with suspended small particles.
    • Delayed flow of large particles towards the pylorus.
    • Emptying of liquids with small particles.
    • Large particles retained in bulge of the terminal antrum.
    • Retropulsion of large particles.
    • Clearing of the terminal antrum.

Physical Properties Affect Gastric Emptying

  • Emptying of liquids is exponential.
  • Emptying of large solids is only after sufficient grinding.
  • The viscous chyme is emptied in a mainly linear fashion.
  • Lag Phase: Initial delay before emptying begins.
  • T1/2T_{1/2}: Time taken for half of the stomach contents to empty.

Gastric Emptying based on Time

  • Slow emptying (20-30 minute lag time, to start digesting).
  • Rate of emptying depends on nutrient density.
  • May be slow, to avoid overloading the intestine.
  • Rate of emptying regulated by feedback from intestine and neural/hormonal signals which regulates satiety and insulin secretion.
  • Fast emptying (no solids to grind and liquefy). Large volumes empty faster than small volumes.

Gastroparesis

  • Chronic condition of the stomach.
  • Characterized by delayed gastric emptying.
  • Symptoms include nausea, vomiting, rapid feeling of fullness, reflux, pain, and bloating.
  • Diabetic gastroparesis is caused by neuropathy of vagal endings innervating the stomach.

Relieving Pressure

  • Brief relaxations of the lower esophageal sphincter allows gas to escape. Transient Lower Oesophageal Sphincter Relaxations result in a belch or burp which reduces pressure inside the stomach and avoids early satiety.
  • Gas bubble in the stomach due to swallowing air (eating/drinking).

Feedback Regulation of Gastric Emptying

  • Duodenal, Jejunal, and Ileal Brakes
  • Exposure of the upper gut to nutrients is associated with predominantly GIP and CCK release.
  • Increasing the delivery of nutrients to the distal small intestine and colon is associated with augmented secretion of GLP-1 and PYY.
  • These distal gut hormones appear more potent in mediating postprandial glucose metabolism and suppressing energy intake than those secreted from the proximal gut.
  • The distal gut is becoming an appealing target for the management of T2DM and obesity.

Lower GI Motility

  • The lower GI consists of the colon and the small intestine/ileum.
  • The upper GI consists of the esophagus, stomach, and duodenum.

Colon and Rectum Movements

  • Ascending: Mixing, absorption, fermentation, slow transit.
  • Transverse: Absorption, relatively rapid transit.
  • Descending: Storage, slow, partly voluntary transit.

Movements of the Colon

  • Modified peristalsis.
  • Segmentation.
  • Mass movements.
  • Ascending colon is rich in living bacteria and is the site of fermentation and absorption of water, ions, and nutrients.
  • Formation of haustra increases surface area.
  • Retropulsion/segmentation churns and slows transit.
  • Mass movements in the colon are stronger, less frequent, longer-lasting, and more propulsive than normal peristaltic waves.

Mass Movement

  • Ascending to descending colon.
  • As more barium enters, constrictive ring occurs (giant migrating contraction) and haustra disappear from a portion of the ascending colon.
  • ~20 cm of colon distal to the constrictive ring lose their haustrations & contract as a unit, propelling fecal material into the transverse colon.

Defaecation

  • Reflex relaxation of the IAS and the pelvic floor musculature.
  • Voluntary EAS relaxation.
  • A reduction in the anorectal angle due to sitting or squatting.
  • Dilation of the anal canal.
  • Valsalva manoeuvre.
  • Accompanying propulsive rectal contractions.

Colonic Movements Influenced by Local Environment

  • Luminal content continually modified by:
    • Ingestion of food, drink, and contaminants.
    • Microorganisms.
    • Microbial products.
    • Enzymatic and chemical breakdown of complex molecules.
    • Pharmaceuticals.

Relieving Pressure in the Colon

  • Carbon dioxide, hydrogen, methane, and hydrogen sulfide, as well as a variety of trace gases, are generated by chemical interactions and microbiota within the gut.
  • Intestinal gas composition can influence gut physiology and generate abdominal symptoms in patients with gastrointestinal disorders such as IBS and IBD.
  • Gas bubbles in the colon are a byproduct of microbiome metabolism.

Aetiology of Diarrhoea

  • Osmotic: Increase in intestinal osmotic pressure; transfer of fluids to the intestinal tract.
  • Inflammatory (Exudative): Intestinal mucosal disorders, such as inflammation; increase in intestinal contents due to exudates.
  • Secretory: Enhancement of intestinal secretion by enterotoxins; rapid passage of intestinal contents.
  • Motor: Increased intestinal peristalsis or decrease in intestinal peristalsis.
  • Bacterial: Bacterial growth in the intestine; deconjugation of bile acids or disorder of fat absorption; increased intestinal secretion.

Aetiology of Constipation

  • Behavioural disorders: Autism, ADHD.
  • Psychological disorders: Anxiety, Depression.
  • Lifestyle factors: Diet, Fluid intake, Obesity, Physical activity.
  • Impaired anorectal function.
  • Stress and stressful life events: Abuse, Trauma, Stress.
  • Parental factors: Neuroticism, Depression, Overprotection.
  • Disrupted microbiota.
  • Genetic factors.
  • Colonic dysmotility.

History Taking: Clinical Investigations

  • Stool frequency and consistency (Bristol Scale).
  • Any clear precipitants to onset? abdominal/pelvic surgery; childbirth or emotional trauma.
  • Faecal impaction and faecal soiling: suggest idiopathic megacolon.
  • Comorbid medical history: e.g. thyroid disease, diabetes; renal impairment; neurogenic conditions.
  • Drug history: e.g. opiates.
  • Dietary history: meal frequency and fiber intake.
  • Toilet behavior: sitting properly, routine.

What Controls Movements of the Colon?

  • ENS: Controls reflexes and muscle activity.
    • The myenteric plexus (Auerbach’s plexus) regulates motility.
    • The submucosal plexus (Meissner’s plexus) regulates secretion and blood flow.
    • Works independently but communicates with the central nervous system (CNS).
  • Extrinsic innervation: Controls reflexes and muscle activity.
    • Parasympathetic (stimulates motility): Vagus nerve (CN X). Pelvic nerves (S2-S4).
    • Sympathetic (inhibits motility): Thoracolumbar outflow (T10-L2)
  • Hormones (5-HT, gastrin, motilin, etc.) → Regulate motility. Serotonin (5-HT) – is the key player. produced by Enterochromaffin (EC) cells.
    • Stimulate peristalsis via the ENS.
    • Trigger the gastrocolic reflex (urge to defecate after eating).
  • Muscle contractions (haustral, peristalsis, mass movements) → Physically move contents.