Gastrointestinal Motility Notes PDF

Gastrointestinal Motility: Dr. Komnenov Page 1 of 16 Gastrointestinal Motility Learning Objectives: 1. Review the organization of smooth muscle in the alimentary canal. 2. Describe the role of slow waves in the alimentary...

Gastrointestinal Motility: Dr. Komnenov Page 1 of 16 Gastrointestinal Motility Learning Objectives: 1. Review the organization of smooth muscle in the alimentary canal. 2. Describe the role of slow waves in the alimentary canal. a. Describe the mechanism of slow wave production. b. Describe the frequency of slow waves. 3. Describe the processes of chewing, swallowing and esophageal peristalsis. 4. Describe the process of gastric motility. a. Distinguish between the two functional divisions of the stomach. b. Describe the two types of motor activity in the proximal, orad region of the stomach. c. Describe the two types of motor activity in the distal, caudad region of the stomach. d. Describe the process of gastric emptying. 5. Describe the process of small intestinal motility. a. Describe the nature and function of segmentation contractions. b. Describe the nature and function of peristaltic contractions. c. Describe the gastroileal reflex. 6. Describe the process of large intestinal motility. a. Describe the nature and function of contractions that occur in the cecum and proximal colon. b. Describe the nature and function of contractions that occur in the distal colon. c. Describe the nature and function of contractions that occur in the rectum and anal canal and relate them to the process of defecation. d. Describe the gastrocolic reflex. e. Describe the following disorders of large intestinal motility: irritable bowel syndrome and Hirschsprung’s disease. 7. Describe the process of vomiting. Gastrointestinal Motility: Dr. Komnenov Page 2 of 16 Outline: (1) Smooth muscle in the alimentary canal – A review (2) Slow waves (a) Mechanism of slow wave production (b) Frequency of slow waves (3) Chewing, swallowing and esophageal peristalsis (a) Chewing (b) Swallowing (c) Esophageal motility (4) Gastric motility (a) Orad region (b) Caudad region (c) Gastric emptying (5) Small intestinal motility (a) Segmentation contractions (b) Peristaltic contractions (c) Gastroileal reflex (6) Large intestinal motility (a) Cecum and proximal colon (b) Distal colon (c) Rectum, anal canal, and defecation (d) Gastrocolic reflex (e) Disorders of large intestinal motility (7) Vomiting Gastroin ntestinal Mo otility: Dr. Komnenov K Page 3 of 16 Gastrointtestinal M Motility (1) Cell C types fou und in the GI tract (aa) Epitheliall cells- Invollved in secreetion and abssorption in ddifferent partts of the GI ttract (b b) Muscularis mucosa-co ontractile prroperties cauuse a change in the surfacce area for secretion and absorptiion (cc) Circular muscle- m resp ponsible for decrease in i the diameeter of the lumen of the GI tract (d d) Longitudiinal muscle-responsible for shorteening of a secction of the GI tract (ee) Submucosal plexus (M Meissner plexus) an nd myentericc plexus - together comprise c thee enteric Fig. 1 - Structuree of the GI trract nervous system s of thee GI tract. Major role in integrattion and coordination of the motility, m secreetory and en docrine funcctions of the GI tract. Clinical C signnificance: AAchalasia. C Characterizedd by impairedd peristalsis in the distall two-thirds oof the esophhagus and failu ure of the low wer esophaggeal sphincteer to relax duuring swallow wing. Clinical C sign nificance: G GERD. Occuurs when low wer esophag geal sphincteer loses its toone and fails to prevent movemeent of acid coontent into tthe lower esoophagus. Fig. 2- Essophageal sttricture (A) showing obstruction o of o food boluss Clinical C sign nificance: Paralytic Ileu us. Paralysiis of with correesponding barium the intestine, which iis a commonn side effect of certain tyypes swallow (B) ( of surgerries. Contractioons of the GI G muscle con motility. Conntractile tissuue of the GI tract nstitute GI m is almost exclusively unitary smo ooth musclee, except forr the pharynxx, upper one- he esophaguss, and extern third of th nal anal sphiincter, all of which are sttriated musscle. GI smooth h muscle cellls are conneected via gapp junctions, aallowing com mmunicationn among theem through ion channelss. This enablles a large nunumber of cells to be activated simultaneou usly, contracting as a sinngle unit. Gastrointestinal Motility: Dr. Komnenov Page 4 of 16 Depolarization of circular muscle leads to contraction of a ring of smooth muscle and a decrease in diameter of that segment of the GI tract. Depolarization of longitudinal muscle leads to contraction in the longitudinal direction and a decrease in length as well as increase in diameter of that segment of the GI tract. (2) Slow waves Occur spontaneously and are inherent to the smooth muscle cells of some parts of the GI tract Originate in the interstitial cells of Cajal, which serve as the pacemaker for GI smooth muscle They are not action potentials, although they determine the pattern of action potentials and thus the pattern of contraction (a) Mechanism of slow wave production Consists of cyclic opening of Ca2+ channels (depolarization) followed by opening of K+ channels (repolarization) Depolarization during each slow wave brings the membrane potential of smooth muscle cells closer to threshold and, therefore, increases the probability that action potentials will occur Action potentials, produced on top of the background of slow waves, then initiate phasic contractions of the smooth muscle cells (Fig. 3) Fig. 3- GI slow waves superimposed by action potentials. Action potentials produce subsequent contraction. Gastroin ntestinal Mo otility: Dr. Komnenov K Page 5 of 16 (b b) Frequency y of slow waaves Variess along the GI G tract, but are constantt and charactteristic for each part of tthe GI traact Is nott influenced by neural orr hormonal innput. Ratherr, the frequenncy of the acction potenttials that occcur on top off the slow waaves is modiified by neurral and horm monal influences Sets th he maximum m frequency of contractioons for eachh part of the G GI tract. Frequuency is loweest in the sto omach (3 slow w waves/miin) and higheest in the duodeenum (12 sloow waves/miin) (3) Chewing, C swaallowing and d esophageal peristalsis (aa) Chewing-- lubricates food f to faciliitate swallowin ng and to beg gin the digesstive process (b b) Swallowin ng Swallowing is inittiated volunttarily in the mo outh, but theereafter it is under involuuntary or refflex control The reeflex portion n is controlleed by the swalloowing centerr, which is lo ocated in the medulla m Senso ory informatiion (e.g., foo od in the mouth h) is detected d by somatossensory recepttors located near n the phaarynx. Fig. 4- Struucture of the upper GI trract This sensory, s or afferent, a info ormation is carrried to the medullary m swwallowing cennter via the vvagus and gllossopharynngeal nervess. The medu ulla coordinaates the sensoory informattion and direects the motoor, or efferent, output to o the striated d muscle of thhe pharynx aand upper essophagus Three phases are involved i in swallowing: s oral, pharyyngeal, and esophageall. The oral phase is voluntary, v and the pharyyngeal and eesophageal pphases are controolled by refleexes. o Oral phase. The T oral phasse is initiatedd when the ttongue forcees a bolus off food baack toward th he pharynx, which contaains a high ddensity of som matosensoryy receptors. Acttivation of th hese receptorrs then initiaates the involuntary sw wallowing reeflex in the medulla. m Gastroin ntestinal Mo otility: Dr. Komnenov K Page 6 of 16 o Phharyngeal phase. p The purpose p of thhe pharyngeaal phase is too propel the ffood bo olus from thee mouth thro ough the phaarynx to the eesophagus inn the followiing steeps: (1) The soft paalate is pulleed upward, ccreating a naarrow passagge for food too move into the pharynx x so that foodd cannot refl flux into the nasopharynxx. (2) The epigloottis moves to cover the oopening to thhe larynx, annd the larynxx moves upw ward againstt the epiglotttis to prevennt food from entering thee trachea. (3) The upper esophageal sphincter reelaxes, allow wing food to ppass from thhe pharynx to o the esophag gus. (4) A peristalttic wave of contraction c iss initiated inn the pharynxx and propells food throu ugh the open n sphincter. B Breathing is inhibited duuring the pharyngeaal phase of sw wallowing. Fig. 5- 5 Pressure in i esophaguss during swaallowing o Essophageal phase. p The esophageal phhase of swalllowing is coontrolled in ppart byy the swallow wing reflex and a in part bby the entericc nervous syystem. In thee esophageal ph hase, food is propelled thhrough the essophagus to the stomachh. On nce the bolu us has passed d through thee upper esopphageal sphinncter in the phharyngeal ph hase, the swaallowing refllex closes thhe sphincter sso that food caannot reflux into the pharrynx. A prim mary peristalltic wave, alsso coordinatted byy the swallow wing reflex, travels downn the esophaagus (see disscussion of peeristalsis), prropelling thee food along.. If the primaary peristaltiic wave doess not cleear the esoph hagus of foo od, a secondaary peristaltiic wave is innitiated by thhe co ontinued disttention of thee esophagus. The seconddary wave, w which is mediated by th he enteric neervous systemm, begins att the site of ddistention annd traavels downw ward. Gastrointestinal Motility: Dr. Komnenov Page 7 of 16 (c) Esophageal motility The esophagus propels the swallowed food into the stomach. Sphincters are located at either end (upper esophageal sphincter and lower esophageal sphincter), preventing air from entering the upper esophagus and gastric acid from entering the lower esophagus, respectively. Since the esophagus is located in the thorax, intraesophageal pressure equals thoracic pressure, which is lower than the atmospheric pressure. Therefore, a balloon catheter placed in the esophagus can be used to measure intrathoracic pressure. This is particularly pertinent for cases of hiatal hernia, where the lower esophageal sphincter slides into the thoracic cavity. Because it is surrounded by negative pressures, it becomes subject to regurgitation. Sequence of events as food moves into and down the esophagus: 1. The upper esophageal sphincter opens, mediated by the swallowing reflex, allowing the bolus to move from the pharynx to the esophagus. Once the bolus enters the esophagus, the upper esophageal sphincter closes, which prevents reflux into the pharynx. 2. A primary peristaltic contraction, also mediated by the swallowing reflex, involves a series of coordinated sequential contractions (Fig.5). As each segment of esophagus contracts, it creates an area of high pressure just behind the bolus, pushing it down the esophagus. Each sequential contraction pushes the bolus further along. If the person is sitting or standing, this action is accelerated by gravity. 3. As the peristaltic wave and the food bolus approach the lower esophageal sphincter, the sphincter opens. Opening of the lower esophageal sphincter is mediated by peptidergic fibers in the vagus nerve that release VIP as their neurotransmitter. VIP produces relaxation in the smooth muscle of the lower esophageal sphincter. At the same time that the lower esophageal sphincter relaxes, the orad region of the stomach also relaxes, a phenomenon called receptive relaxation. Receptive relaxation decreases pressure in the orad stomach and facilitates movement of the bolus into the stomach. As soon as the bolus enters the orad stomach, the lower esophageal sphincter contracts, returning to its high resting tone. At this resting tone, the pressure at the sphincter is higher than the pressure in the esophagus or in the orad stomach.  Gastroin ntestinal Mo otility: Dr. Komnenov K Page 8 of 16 4. If the primary peristaltic contraction c ddoes not cleaar the esophaagus of foodd, a secondary s peristaltic p co ontraction, mediated byy the enteric nervous sysstem, cleears the esop phagus of anny remainingg food. The ssecondary peeristaltic co ontraction beegins at the point p of disteention and trravels downwward. 5. Ass the food bo olus approacches the loweer end of thee esophagus,, the lower esophageal sp phincter relaxes. This reelaxation is vagally meddiated, and thhe neeurotransmittter is VIP an nd/or nitric ooxide (NO). 6. Thhe orad regiion of the sttomach relaxxes (“recepttive relaxatiion”) to allow the food boluss to enter thee stomach. Lower esoophageal sph hincter (LES in Fig. 6) - has a high toone for two reasons: 1. Myogeenic mechan nisms (intrinssic ability off musculaturre of the sphinccter to resist distension) 2. Excitattory vagal to one Lower esophag geal sphincteer relaxes byy 2 mechanissms: Reduction in n excitatory vagal tone Activation of o inhibitoryy enteric (myyenteric plexxus) nervous system Fig. 6- Exccitatory and inhibitory pa athways to open o and cloose lower esoophageal sphhincter, resppectively (LES-lowerr esophageal sphincter; ENS-entericc nervous sysstem) Gastroin ntestinal Mo otility: Dr. Komnenov K Page 9 of 16 Cliniical significa ance: Achallasia. Characcterized by iimpaired perristalsis in thhe distal two- thirdss of the esop phagus and failure fa of the lower esophhageal sphinncter to relaxx during swalllowing. Wheen lower esophageal sph hincter is commpletely dennervated (succh as occurs in advannced achalassia), it remaiins contracteed due to its m myogenic prroperty. Cliniical significaance: GERD D. Occurs when w lower essophageal spphincter losees its tone annd fails to t prevent movement m off acid conten nt into the low wer esophaggus. Can be a consequennce of hiatall hernia. Alsso diagnosed d radiographiically. (4) Gastric G motiliity The stomaach has threee layers of smooth s muscle: 1. Longiitudinal 2. Circullar 3. Obliqu ue layer The stomaach has threee anatomic divisions: 1. Funduus 2. Body 3. Antru um The stomaach has two functional divisions: Figg. 7- Schemaatic drawingg showing thrree major diivisions of thee stomach: fuundus, body and antrum 1. The proximal, ora ad regionn of the stom mach includees the funduss and the prooximal bodyy. This regionn contaiins oxyntic (fundic ( or gaastric) glandss and is respponsible for rreceiving thee ingestted meal. 2. The distal, d caudad d region of the stomachh includes the antrum andd the distal bbody. This region r is resp ponsible for the contracttions that miix food and ppropel it intoo the duodeenum. (aa) Orad region The prroximal, ora ad region has two types oof motor acttivity 1. Reelaxation 2. Toonic contracttions but no slow wave activity (1) Relax xation Reeceptive relaxation refeers to the oraad stomach bbeing able too accommoddate larrge increases in volume with only smmall increasees in intra-gaastric pressuure. Gastrointestinal Motility: Dr. Komnenov Page 10 of 16 Receptive relaxation is a vagovagal reflex that is initiated by distension of the stomach and is abolished by vagotomy. CCK also participates in receptive relaxation by increasing the distensibility of the orad stomach. The neurotransmitter involved in the vagal path is non-cholinergic and non- adrenergic, and NO and VIP have been implicated. (2) Adaptive relaxation Mechanoreceptors in stomach are stimulated as stomach fills with food. This elicits another vagovagal reflex. The release of CCK also activates a vagovagal reflex. Contractile activity of the proximal stomach also consists of low amplitude tonic contractions which “gently” propel chyme toward the distal stomach. Slow waves do not mediate low amplitude tonic contractions. (b) Caudad region The distal, caudad region has two types of motor activity: 1. Peristaltic Contractions 2. Migrating motor complex AND slow wave activity (1) Peristaltic contractions for mixing and digestion The caudad region of the stomach contracts to mix the food with gastric secretions and begins the process of digestion. Slow waves in the caudad stomach occur at a frequency of 3-5 waves/min. They depolarize the smooth muscle cells. If threshold is reached during the slow waves, action potentials are fired, followed by contraction. Thus, the frequency of slow waves sets the maximal frequency of contraction. A wave of contraction closes the distal antrum. Gastrointestinal Motility: Dr. Komnenov Page 11 of 16 Thus, as the caudad stomach contracts, food is propelled back into the stomach to be mixed (retropulsion). Gastric contractions are increased by vagal stimulation and decreased by sympathetic stimulation. (2) The migrating motor complex In fasting humans, a different pattern of antral contractions occurs. Migrating motor complex is a wave of intense propulsive motor activity that sweeps the length of the gut, from stomach to ileo-cecal junction, at about 90- minute intervals during the inter-digestive (fasting) phase of GI activity. It serves a housekeeping function by sweeping the stomach and intestine clean of residual contents and returning to the colon bacteria that may have migrated across the ileo-cecal junction. Likely mediated by the candidate hormone motilin. (c) Gastric emptying The physical state of the gastric contents is a major determinant of the rate at which the stomach empties. Controlled by negative-feedback mechanisms (neural and hormonal). Liquids empty faster than solids and their rate of emptying is related to the volume ingested. Solids empty more slowly and must first be reduced to small particle size by the retropulsive mechanism in the distal stomach. The rate of emptying also depends on the chemical composition of the gastric contents. The rate of gastric emptying is fastest when the stomach contents are isotonic. If the stomach contents are hypertonic or hypotonic, gastric emptying is slowed. Fat inhibits gastric emptying (i.e., increases gastric emptying time) by stimulating the release of CCK. H+ in the duodenum inhibits gastric emptying via direct neural reflexes as well as via secretin. H+ receptors in the duodenum relay information to the gastric smooth muscle via interneurons in the GI plexuses. Gastroin ntestinal Mo otility: Dr. Komnenov K Page 12 of 16 (5) Small intestin nal motility The smalll intestine fu unctions in th he digestion and absorpttion of nutrieents. Mixes nutrients with w digestiv ve enzymes, exposes thee digested nuutrients to thhe absorptivee mucosa, anda then prop pels any nonn-absorbed mmaterial to thhe large intestine. Slow wav ves set the baasic electricaal rhythm, w which occurs at a frequenncy of 12 waves/min. Action pootentials occu ur on top off the slow waaves and leadd to contracttions. Parasympathetic stimmulation increases intesstinal smooth th muscle contraction; sympatheetic stimulation decreasses it. a) Segmenta (a ation contracctions (Fig. 8 A) Mix th he intestinal contents Consiist of a sectioon of the small intestiine contractiing, sending the intestiinal contentss (chyme) in n both orad and a caudad directions. d This section of small inntestine then n relaxees, and the coontents move back into i the segm ment. This back-and-for b rth movemennt produ uced by segm mentation contraactions causees mixing withouut any net fo orward movem ment of chym me. (b b) Peristalticc contraction ns (Fig. 8 B)) Fig. 8- Comparisonn of segmenttation contraaction Highly y coordinateed, main (A) to tthe peristaltiic contractioon (B) functiion to propell chyme througgh the small intestine tow ward the largge intestine. Ideally, peristalsis occuurs after digestion d andd absorption n have taken place. Contractions behind the boluss and, simulttaneously, reelaxation in ffront of the bbolus cause the chyme to t be propellled caudally.. Gastrointestinal Motility: Dr. Komnenov Page 13 of 16 The peristaltic reflex is coordinated by the enteric nervous system: (i) Food in the intestinal lumen is sensed by enterochromaffin cells, which release serotonin (5-hydroxytriptamine (5-HT)). (ii) 5-HT binds to receptors on intrinsic primary afferent neurons (IPANs), which initiate the peristaltic reflex. (iii) Behind the food bolus, excitatory transmitters cause contraction of circular muscle and inhibitory transmitters cause relaxation of longitudinal muscle. In front of the bolus, inhibitory transmitters cause relaxation of circular muscle and excitatory transmitters cause contraction of longitudinal muscle. (c) Gastroileal reflex Mediated by extrinsic autonomic nervous system and possibly gastrin The presence of food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal sphincter. As a result, the intestinal contents are delivered to the large intestine. (6) Large intestinal motility The large intestine absorbs water and electrolytes from the chyme and stores fecal matter until it is expelled. The colonic movements are slow and sluggish, but segmentation and propulsive movements are nevertheless evident. Haustra, or sac-like segments, appear after contractions of the large intestine (Fig. 9). (a) Cecum and proximal colon When the proximal colon is distended with fecal material, the ileocecal sphincter contracts to prevent reflux into the ileum. Fig. 9- Structure of colon 2 types of contractions occur in the colon: 1) Segmentation contractions in the proximal colon mix the contents and are responsible for the appearance of haustra. Gastrointestinal Motility: Dr. Komnenov Page 14 of 16 2) Mass movements occur 1 to 3 times/day and cause the colonic contents to move distally for long distances (i.e. from the transverse colon to the sigmoid colon). (b) Distal colon Since most of the colonic water absorption occurs in the proximal colon, fecal material in the distal colon becomes semisolid and moves slowly. Mass movements propel it into the rectum. Fig. 10 - Microscopic view of the colon (c) Rectum, anal canal, and defecation (i) As the fecal material populates the rectum, it contracts and the internal anal sphincter relaxes (rectosphincteric reflex). (ii) Once the rectum is filled about 25% of its capacity, there is an urge to defecate. However, defecation is prevented because the external anal sphincter is tonically contracted. (iii) When it is convenient to defecate, the external anal sphincter is relaxed voluntarily. Contraction of the smooth muscle in the rectum forces the feces out of the body. The defecation reflex can be augmented by contraction of the abdominal muscles to force fecal contents from the sigmoid colon into the rectum Gastrointestinal Motility: Dr. Komnenov Page 15 of 16 Intra-abdominal pressure is increased by expiring against a closed glottis (Valsalva maneuver) (d) Gastrocolic reflex The presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements. The gastrocolic reflex has a rapid parasympathetic component that is initiated when the stomach is stretched by the food. A slower, hormonal component is mediated by CCK and gastrin. (e) Disorders of large intestinal motility Extrinsic ANS has a strong influence on large intestinal motility. Irritable bowel syndrome (IBS) may occur during periods of stress and may result in constipation (increased segmentation contractions) or diarrhea (decreased segmentation contractions). Hirschprung diseases (as discussed earlier). (7) Vomiting Vomiting is a reflex controlled by a center in the medulla that receives afferent input from the: 1. GI tract 2. The labyrinth receptors of the inner ear 3. Gag receptors in the throat 4. Pain receptors It also receives afferents from a medullary chemoreceptor trigger zone that responds to certain circulating chemicals, such as apomorphine The most common stimulus for vomiting is irritation of the upper GI tract, but it can also be induced by motion sickness, olfactory, visual, and painful stimuli. The act of vomiting is usually preceded by the sensation of nausea. Initially there is a diffuse sympathetic discharge with tachycardia, tachypnea, sweating, and inhibited gastric motility. Gastrointestinal Motility: Dr. Komnenov Page 16 of 16 This is followed by parasympathetic activation with relaxation of upper and lower esophageal sphincters (although not always simultaneously), increased salivation, and a transient increase in gastric motility. Parasympathetic stimulation also causes reverse peristalsis. A deep inspiration that follows moves the stomach and diaphragm down into the abdomen. The anterior abdominal muscles then contract forcefully, compressing the flaccid stomach (along with reverse peristalsis) and expelling the gastric contents into the esophagus. If the upper esophageal sphincter is not relaxed, secondary peristalsis returns the contents to the stomach. This phase of the process is termed retching and may be repeated many times. If the upper esophageal sphincter is relaxed, the act of vomiting is completed with the expulsion of the gastric contents through the mouth. The consequences of vomiting relate to the composition of gastric juice, which is characteristically acidic, high in chloride, and relatively high in potassium. The major effects of vomiting are dehydration (due to volume loss), hypokalemia (due to potassium loss), and hypochloremic metabolic alkalosis due to loss of hydrogen ion and chloride.