Gastrointestinal System: Motility
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Swallowing Reflex
Stimulated when a food bolus stimulates pressure receptors in the back of the throat and pharynx Signals to the swallowing centre located in the medulla Swallowing centres triggers nerve impulses Innervates skeletal muscles in the pharynx andupper oesophagus Involuntary contraction in the pharyngeal muscles pushes material into the oesophagus Involves more than 25 pairs of muscles
Swallowing
The passage of a food bolus from the oral cavity to the stomach Involves the co-ordinated activity ofmuscles in the oral cavity, pharynx, larynx and oesophagus Partly under voluntary control and partlyreflexive in nature
Gastric Motility - Stomach
Peristalsis and mixing (churning) Movement depends on viscosity Retropulsionforces solids back Liquids exit faster than solids Production of chyme
Motility in the Small Intestine
Mixed by segmentation Movement by peristalsis Sequential activity in muscle bands Co-ordinated by the enteric nervous system
Intestinal Motility: Role of the Enteric Nervous System (ENS)
Intestinal and colonic motility is controlled primarily by the ENS Two main branching networks: Auerbach’s (myenteric) plexus Meissner’s (submucosal) plexus
Contraction of GI Smooth Muscle
Activated/inhibited by many neurotransmitters Acetylcholine induces contraction through activation of muscarinic receptors Histamine induces contraction through activation of H1 receptors
Control of theENS
Sympathetic nervous system - “fight or flight” - inhibits ENS - decreased peristalsis,blood flow, secretion andabsorption Parasympathetic nervous system - “rest and digest” - stimulates ENS - increased peristalsis,blood flow, secretionandabsorption Hormonal control - increased by cholecystokinin, gastrin, motilin, serotonin and insulin - decreased by secretin and glucagon
The Migrating Motility Complex
Recurring motility pattern Regulated by electrical activity Occurs between feeding Progress from stomach to large intestine Cleansing mechanism
Motility in the Large Intestine– Haustral Shuttling
Faeces stored in haustra Haustra collapse to cause bulk movements Defaecatory reflex triggered by faeces in descending colon/rectum
Defaecation
Eliminate waste Temporarily stored in rectum Process initiated by activation of stretch receptors Involves involuntary and voluntary steps
Vomiting
Vomiting reflex Vomiting centrein medulla oblongata Forcible expulsion of gastric contents through the mouth Gastrointestinal irritation – mechanical or chemical
A Vomiting Timeline
Pre-Ejection Phase: Nausea often occurs Autonomic changes such as tachycardia and increased salivation Food contents move into the stomach due to reverseperistalsis Pyloricsphincter relaxes allowing food content to fill the stomach Ejection Phase: Involuntary reflex called retching Rhythmic contraction of the muscles of the chest wall, diaphragm andabdomen Intense contraction forces the contents of the stomach into the oesophagus Epiglottis closes to prevent food travelling down to the lungs Vomiting occurs Post-Ejection Phase: Feeling of fatigue and muscle weakness Epiglottis remains closed
mobility overview
mouth and esophagus: chewing, swallowing and peristalsis stomach : filling, churning, peristalsis , emptying small intestine: segmental contractions, peristalsis large intestine: haustral shuttling, mass movement, defecation sphincter: regulation of movement
secretion in the stomach
parietal cell: secrete HCl denatures protein pepsinogen to pepsin chief cell: secrete pepsinogen converted to pepsin protein digestion mucous cell: protection lubrication G cell: produce gastrin controls HCl, motility, pepsin, mucous
Gastric Acid Secretion
Hydrochloric acid (~ 2.5 L/day) Stomach pH 2-3 Optimal for activity of pepsin Role of parietal cells, enterochromaffin cells & G-cells Stimulated by histamine, gastrin & acetylcholine
Fat Absorption
Fatty acid and monoglycerides pass through epithelial cell layer Converted to triglycerides Combine with cholesterol, phospholipids and protein to form chylomicron Chylomicron water soluble and enters lacteal Transported from lacteal to bloodstream
Enteric Coating
Prevent formulations from gastric fluid in stomach. Release drug component in intestinal region. Coating prepared from gastric resistant polymers. Polymers insoluble at low pH. Drug release is controlled by pH. Prevent gastric distress or nausea due toirritationfrom drugs. Protect acid-labile drugs. Deliver drugs intended for local action in intestine. Provide delayed release compounds