GI Motility Physiology PDF
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Marmara University
Dr. Alper YILDIRIM
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Summary
This document discusses the physiology of gastrointestinal motility, covering various aspects, including electrical activity, motility patterns in different segments (mouth, esophagus, stomach, small intestine, colon, rectum), and mechanisms like peristalsis and segmentation. It also explores how factors like food intake and hormonal regulation influence motility.
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Physiology of Gastrointestinal Motility Dr. Alper YILDIRIM [email protected] Objectives List the major forms of motility in the gastrointestinal tract and their roles in digestion and excretion. Distinguish betwee...
Physiology of Gastrointestinal Motility Dr. Alper YILDIRIM [email protected] Objectives List the major forms of motility in the gastrointestinal tract and their roles in digestion and excretion. Distinguish between peristalsis and segmentation. Explain the electrical basis of gastrointestinal contractions and the role of basic electrical activity in governing motility patterns. Describe how gastrointestinal motility changes during fasting. Understand how food is swallowed and transferred to the stomach. Define the factors that govern gastric emptying and the abnormal response of vomiting. Define how the motility patterns of the colon subserve its function to desiccate and evacuate the stool. Gastrointestinal Physiology: Motility Electrical Activity of GI Smooth Muscles Slow wave or Basic electrical rhythm (BER) Depolarization influx of Ca+ Repolarization eflux of K+ Done by interstitial cells of cajal Intrinsic system 1. Submocosal Plexus Secretion 2. Myenteric plexsus Peristalsis Electrophysiology of Gastrointestinal Smooth Muscle (tension) General Patterns of Motility Peristalsis elicited by distension, propels the food bolus. Distension of gut wall by bolus → sensory Short reflex nerves → ENS → activation of 1) excitatory neurons (proximal to bolus) 2) inhibitory neurons (distal to bolus) efferent Distal Neurotransmitters – VIP & NO afferent Distension Proximal Neurotransmitters – Ach & Substance P General Patterns of Motility Segmentation & Mixing promotes the mixing of food with digestive secretions. initiated by presence of chyme in lumen coordinated by ENS independent of ANS This mixing pattern persists for as long as nutrients remain in the lumen to be absorbed. Some propulsion of bolus because BER in duodenum ≈ 12/min → ileum ≈ 8/min General Patterns of Motility Tonic contraction Sphincters promote compartmentation in GI tract. Parasympathetics ↑ peristalsis ↓ sphincter tone Sympathetics ↓ peristalsis ↑ sphincter tone Migration Motor Complex Motilin Secreted by: M-cells in duodenum & jejunum (atropine-sensitive) Stimuli for release: neural input, fat, acid Actions: Stimulates gastric & intestinal The migrating motor complex (MMC) is a series of contractions that begin in the motility in inter-digestive period. empty stomach and end in the large intestine. every 90 min – “housekeeper” Segment – Specific Patterns – Mouth & Esophagus Function of chewing: – particle size 1. Prevent scratching of GI tract 2. Increase emptying of the stomach – surface area of ingested food for digestive enzymes activity Mixes food particles with saliva Mucus coats particles Forms cohesive bolus Chewing muscles are controlled by nuclei in brain stem. Breathing continues Chewing reflex: Food against lining of mouth Reflex inhibition Lower jaw raises of chewing muscles Rebound contraction Lower jaw drops Stretch reflex Segment – Specific Patterns – Mouth & Esophagus Esophageal pressures during swallowing. The swallowing center in the medulla that initiates deglutition. Segment – Specific Patterns - Stomach Proximal (orad) stomach Slow tonic contraction High distensibility Gastric reservoir Duodenum Distal (caudad) stomach Peristaltic contractions Low distensibility Grinding of solids Segment – Specific Patterns - Stomach Determinants of gastric emptying. Liquids > digested solids ( undigested solids (>2 mm3) Isotonic saline > hypotonic saline or hypertonic saline Normal mixed meal (1500 ml) empties into duodenum in ~ 3 hrs Emptying rates: Carbohydrates > Proteins >> Fats Segment – Specific Patterns - Stomach Hormonal Control Stomach Pancreas & Hormone Source Stimulus motility & gallbladder secretions S cells Pancreatics Secretin Acid Inhibits (duedonum) (HCO3-) 1. Pancreatic I cells secretion CCK Fat &AA Inhibits (duedonum) 2. Gallbladders contraction 1. Stomach G cells distension Gastrin Inhibits motility (stomach) 2. GRP 3. Proteins K cells GIP Fat, CHO, AA Inhibits Insulin (duedonum) Segment – Specific Patterns - Vomiting central regulation of gut motility Protective mechanism – removes irritants Segment – Specific Patterns – Small intestine Duodenum Ileum BER = 12/min BER = 8/min gradient Segment – Specific Patterns - COLON Ileocecal junction: Sphincter/valve system regulating the movement of chyme into cecum. Chyme enters colon Ileal distension relaxes 1) During digestion of meal sphincter chyme → ileum & distends 2) After digestion of a meal Cecal distension some residual chyme remains in contracts ileum sphincter 3) Next meal → gastro-ileal reflex Valve prevents empties ileum reflux of cecal material Chyme remains in ileum Both ENS & extrinsic nerves play a role in these reflexes Segment – Specific Patterns - Colon Haustral shuttling: segmental contractions (Erratic and slow movement of contents between haustra) Mush Semi-solid Fluid Solid Segment – Specific Patterns - Rectum Defecation – an intrinsic (short) reflex Intrinsic reflex - as stool distends rectum (sufficiently) 1) rectum contracts (stretch receptors) 2) internal sphincter relaxes (myenteric reflex) 3) external sphincter contracts Pressures Accommodation Distension Opposing urge to defecate by voluntary contraction of external sphincter stretch receptor adaptation internal sphincter regains tone (accommodation) Segment – Specific Patterns - Rectum Defecation – an extrinsic (long) reflex Enhances the intrinsic defecation reflex Extrinsic reflex mediated via parasympathetics - afferent signals from rectum - efferent signals to descending & sigmoid colon & rectum Intensifies peristaltic waves & relaxes internal anal sphincter You are responsible Guyton & Hall Textbook of Medical Physiology 13th Edition Chapter 64 Key Concepts Motility patterns in the small and large intestines serve not only to propel intestinal contents, but also to mix them with enzymes and other digestive juices, and to retain them in a given segment long enough for optimal absorption to occur. Patterns of motility in both the small intestine and colon result primarily from the programmed activity of the enteric nervous system, which responds to the physicochemical characteristics of luminal contents to generate appropriate motility patterns for a given set of physiologic conditions. Progress of intestinal contents along the small and large intestines is regulated in part by sphincters. The ileocecal valve appears to be important primarily to prevent the reflux of colonic contents into the ileum, thus maintaining the relative sterility of the small intestine. Movement of colonic contents out of the body is controlled by the internal and external anal sphincters, under involuntary and voluntary control, respectively. In the fed state, the small intestine engages primarily in segmentation and mixing motility patterns, with propulsion occurring both orally and aborally. After the meal has left the small intestine, the migrating motor complex (MMC) cycles to sweep the intestine clear of undigested residues. Phase III, the propulsive component of the MMC, is stimulated by the hormone motilin. Motility patterns can be modulated by humoral input, or by extrinsic neural activity. Motility and transit times are proportional to the caloric content of the meal. The colon serves predominantly a salvage and reservoir function, with slow transit of contents along its length and marked dehydration of luminal contents. Periodically, large propulsive contractions sweep through the colon and precede the urge to defecate. Induced or developmental abnormalities of the enteric nervous system, or traumatic injury to muscle layers, can lead to pathophysiologic effects on the ability to handle intestinal contents appropriately.