GTT2. GIT motility & control

• GIT motility involves:

  • muscle in wall (smooth but skeletal at critical points)
  • nervous system (enteric, some extrinsic control by ANS)
  • endocrine influences from food presence
  • sphincters and valves at critical points to ensure correct timing and delays and one-way traffic. E.g. upper and lower oesophageal sphincters, pyloric, ileo-caecal and internal and external anal sphincters. Found between adjacent segments of GIT
• The muscle in GIT wall is muscularis propria, with both longitudinal and circular muscle around the lumen. It is innervated by:

  • myenteric plexus (auerbach’s plexus) for coordinating muscle contraction, influenced by autonomic supply. Found between muscle layers
  • submucosal plexus (meissner’s plexus) for sensory functions and local responses to stimulation of sensory nerve endings in mucosa e.g. stretch and pH. found closer to lumen
• The enteric nervous system consists of:

  • motor neurones : to smooth muscle, vasomotors to intrinsic arterioles, secretomotors to cells regulating acid secretion by the stomach, and to epithelium i.e. enteroendocrine cells
  • interneurons : coordination of reflexes
  • sensory neurones : can be chemosensitive (for H+) or mechanoreceptors (for distension)

  overall regulation occurs through ANS, contribution from somatic motor neurones to specific regions e.g. upper oesophagus
• The first stage of digestion is mastication from large to small chunks of food, and swallowing:

  • oral - tongue pushes bolus against palate and back of mouth, triggers swallowing reflex
  • pharyngeal - upper oesophageal sphincter relaxes, epiglottis closes to protect airway
  • oesophageal - bolus moves downwards into oesophagus, propelled by peristalsis and gravity
• The upper third of the oesophagus is striated muscle, axons of somatic motoneurons deliver pacemaker pattern from brainstem. The lower two thirds are controlled by enteric nervous system through the vagus nerve, with overarching control from ANS.

  Peristalsis is driven by contraction behind bolus in a rhythmic wave, pushing the food down
• Lower oesophageal sphincter is formed by tonic contraction of circular smooth muscle in the wall of the abdominal oesophagus which only relaxes during swallowing and vomiting. Offset angle means intragastric pressure closes the end by squashing a wall. The surrounding diaphragm restricts orifice diameter, contracts during inspiration or when intra-abdominal pressure rises
• Passage through stomach is from abdominal oesophagus to fundus, body, pyloric antrum, pyloric canal and then to duodenum. When food arrives capacity increases by internal rughae flattening, muscle wall relaxing by receptive relaxation and contraction of wall mixing contents and propelling to pyloric region.

  Pacemaker sets off contractile waves, stronger towards pyloric zone, and raising pressure squirts chyme through sphincter. This is narrow, and incomplete occlusion of pyloric antrum lumen by contraction means larger lumps regurgitated back to wider part of antrum for more mixing
• Control of gastric emptying:

  chyme in duodenum detected by increased acidity, fats, aa, salt and distension which stimulates neural receptors. short neuronal reflexes via enteric neurones to stomach decrease gastric emptying, long neuronal reflexes to CNS decrease PNS and increase SNS efferents. Detection also stimulates secretion of enterogastrones so increased plasma enterogastrones decrease gastric emptying of the stomach.

  this ensures co-ordinated delivery so stomach not overwhelmed
• Small intestine motility is through segmentation for mixing, simultaneous contractions of different segments so slow transit rate. Less peristalsis allows more time, and small pressure gradient to distal end helps forward movement of chyme

  Small to large intestine passage is through ileo-caecal valve and sphincter, which constricts in response to downstream pressure and SNS stimulation

  Large intestine motility is through haustrations for mixing (short segments) and mass movement (long segment contraction) every 30mins. Progressive H2O reabsorption changes consistency.
• Defecation involves coordination of:

  • parasympathetic control - rectal circular and longitudinal smooth muscle, internal anal sphincter
  • voluntary control - levator ani, external anal sphincter

  When rectum filling is detected by afferents, rectal circular muscle contracts and internal anal sphincter relaxes. Then volunterally, external anal sphincter relaxes and levator ani contract. Rectal smooth muscle also contracts
• Gut motility regulated by ANS neurally, and also hormonally:

  • motilin regulates background motility in fasting periods, migrating contractile activity from stomach to SI
  • in post-prandial period, initially gastrin increases gastric motility then later CCK and GIP and GL1-P decrease it

  Motility affected by diet composition (influences water retention for stool consistency, and microbiota, affecting local ENS neurones), medication and age by ENS neurone degeneration
• Problems from abnormal gut motility include:

  • vomiting resulting in erosion of teeth and damage to oesophagus and larynx. May be caused by diaphragmatic hernia, obesity, bulimia, stroke, medication side effects
  • malabsorption including vitamins and minerals
  • bacterial overgrowth in intestine, change in gut microbiota
  • diarrhoea, leading to dehydration and acid-base problems
  • constipation, discomfort and dangerous straining e.g. valsalva manoeuvre which increases intrathoracic pressure, heart rate and blood pressure which can trigger a heart attack.