Lecture 28- Propulsion and Mixing of the Food in Alimentary Tract PDF

PROPULSION AND MIXING OF THE FOOD IN ALIMENTARY TRACT Dr. Kelly Roballo Learning Objectives 1. Describe the process of mastication and swallowing (Voluntary, pharyngeal, and esophageal stages). 2. Describe the food mixing and propulsion in the stomach (basic electrical rhythm). 3. Describe the mot...

PROPULSION AND MIXING OF THE FOOD IN ALIMENTARY TRACT Dr. Kelly Roballo Learning Objectives 1. Describe the process of mastication and swallowing (Voluntary, pharyngeal, and esophageal stages). 2. Describe the food mixing and propulsion in the stomach (basic electrical rhythm). 3. Describe the motor functions and propulsive movements of individual small intestine segments. 4. Describe the motor functions and movements of l large intestine segment. 5. Describe the GI reflexes and hormones involved in the control of colonic movements. 6. Define the function of the myenteric plexus in peristalsis. 7. Identify the motor functions of the stomach. Motility of the GI Tract: Basics ◦ Role of Motility ◦ ◦ ◦ ◦ Propulsion throughout the GI tract and beyond Mixing with digestive juices Grinding and fragmenting Storage (stomach and colon) ◦ Types of muscle ◦ Skeletal ◦ Smooth ◦ Motility patterns differ from region to region in different phases: ◦ ◦ ◦ ◦ ◦ ◦ Oropharyngeal: swallowing Esophageal: peristalsis (primary and secondary) Gastric: propulsion and retropulsion Small intestinal: peristalsis Large intestinal: mass movements, defection Interdigestive phase: migrating motor complex ◦ There is a “program library” of characteristic patterns initiated by the ENS ◦ Movement is highly regulated and coordinated with other functions ◦ Regulation and coordination of movement has neural and hormonal influences involving complex reflexes Slow waves ◦ Slow waves are not action potentials but rather oscillating depolarization and repolarization of the membrane potential of the smooth muscle cells ◦ 3-12 PER MINUTE ◦ Stomach having the lowest rate (3 slow waves per minute) and the duodenum having the highest rate (12 slow waves per minute) Chewing ◦ 1) It mixes food with saliva, lubricating it to facilitate swallowing; ◦ (2) it reduces the size of food particles ◦ (3) it mixes ingested carbohydrates with salivary amylase to begin carbohydrate digestion Swallowing ◦ The reflex portion is controlled by the swallowing center, which is located in the medulla. ◦ Oral phase ◦ Pharyngeal phase ◦ Esophageal phase Swallowing Sequence Oral Phase (voluntary): 1. Tongue presses up against hard palate and propels food to pharynx 2. Swallowing reflex initiated by sensors in pharynx Pharyngeal Phase (involuntary): 1. Soft palate moves upward and protect nasal cavity 2. Larynx moved forward and up; epiglottis deflected down to protect airway 3. UES (upper esophageal sphincter) relaxes 4. Superior constrictor contracts to propel bolus and initiates peristaltic wave 5. Bolus travels through UES into esophagus During this sequence, respiration is inhibited Esophageal Phase (involuntary): 1. UES constricts 2. Primary peristaltic wave Swallowing Video: http://ww w.youtube .com/watc h?v=xu_YY OAlZEw&t= 18s Why would someone have trouble swallowing? Swallowing: Timing ◦ One swallow takes about 1.2 seconds ◦ Some of the steps overlap ◦ Swallowing center in brainstem is critical for coordinating sequence and timing Clinical correlation: Dysphagia Dysphagia is difficulty swallowing. Mechanisms: Disruption of the innervation, neuromuscular junction, musculature, swallowing center; obstructive processes Differential diagnosis: Peripheral neuropathy, MS, Cerebrovascular accident, brainstem tumor, neuromuscular disease (ALS), muscular dystrophy, obstructive process (tumor, diverticulum) Workup: H+P is critical, swallowing study Berne and Levy Esophageal motility ◦ 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 ◦ 3. The lower esophageal sphincter opens just after the upper esophageal sphincter returns to its resting tone. ◦ Opening of the lower esophageal sphincter is mediated by peptidergic fibers in the vagus nerve that release VIP and nitric oxide (NO) as their neurotransmitters. VIP and NO produce relaxation in the smooth muscle of the lower esophageal sphincter. Clinical Application: Interpreting Manometry Tracings ◦ Evaluate the resting pressures ◦ Look at the time of swallow and identify function of pharynx UES and LES ◦ Look for a normal progression of contraction and relaxation in esophageal body Esophageal Motility Disorders Diffuse esophageal spasm Achalasia Scleroderma Basic physiology of select motility disorders: Scleroderma: Smooth muscle becomes rigid, cannot generate peristaltic waves Achalasia: Impaired ability of LES to relax due to loss of inhibitory enteric neurons in this region Diffuse esophageal spasm: Uncoordinated smooth muscle activity leading to simultaneous contractions rather than peristalsis Pharyngeal paralysis: Skeletal muscle disorder lacking in sufficient pharyngeal constriction and an incompetent UES The Gastric Phase ◦ The gastric phase of digestion serves to sterilize, mix food, begin digestion of protein and store food for timely delivery to duodenum, secretion of intrinsic factor. ◦ Processes: ◦ Secretion: Gastric Juice ◦ Motility: Storage, Mixing and Propulsion ◦ Digestion: Minimal (protein) ◦ Absorption: Minimal (drugs, ETOH) ◦ Endocrine function (Gastrin, Ghrelin) Gastric motility Gastric Motility Basics ◦ Functions of gastric motility: ◦ Receive food bolus ◦ Storage of food ◦ Mix with digestive juices ◦ Grind to smaller pieces ◦ Propulsion (gastric emptying) ◦ Clear food during interdigestive period (migrating motor complex) ◦ Functional Anatomy of the Stomach with respect to motility: ◦ Regions: orad (Proximal Stomach) and caudad (Distal Stomach) ◦ 3 muscle layers, thickest in antrum and pylorus ◦ 2 sphincters: pyloric (part of stomach), LES (part of esophagus) ◦ Three components to gastric emptying: ◦ Proximal stomach motility ◦ Distal stomach motility ◦ Gastric emptying Gastric Motility Video: http://www.youtube.com/watch?v= YH3U_SLp9G0&feature=autoplay&list =PL61894C8350478D12&playnext=2 Note the difference in movement in proximal versus distal stomach Proximal Distal what affect does swallowing have on the stomach? Proximal (orad) Distal (caudad) Gastric Motility: Proximal Stomach ◦ Receptive Relaxation ◦ Vasovagal Reflex ◦ Swallowing and distension of the proximal stomach leads to relaxation to accommodate up to 1.5L of food ◦ VIP (vasointestinal peptide) is the mediator for gastric relaxation Berne and Levy ◦ Tonic Contraction ◦ Also mediated by the vagus nerve ◦ Sustained contraction compresses contents toward antrum to facilitate mixing and gastric emptying ◦ There are no phasic contractions (peristalsis) in the proximal stomach Rhoades and Bell Gastric Motility: Distal Stomach Slow waves: • originate at greater curvature (ICCs in pacemaker region) in the midbody and propagate circumferentially and migrate distally • Rate of 3 per minute (slowest in the GI) • In antrum, action potential spikes occur on top of slow waves resulting in peristaltic contractions Peristalsis: ◦ Peristaltic wave “mixing wave” propagates distally Retropulsion: ◦ Terminal antral contraction spreads to pylorus which contracts ◦ Chyme is “retropulsed” proximally ◦ Allows for mixing and grinding ◦ Chyme (food) particles must be ~1mm3 in order to enter the duodenum Influences on Antral Contractions: • • Neural: • Parasympathetics increase frequency • Sympathetics decrease frequency Hormonal: • Gastrin, Motilin increase frequency • Secretin and GIP decrease frequency Gastric Motility: Gastric emptying mechanisms ◦ Requires proximal and distal regions of the stomach ◦ Can only occur when particles are small enough (1-2mm) Gastric emptying of egg sandwich ◦ Sequence: ◦ Proximal tone increases (Vagus) ◦ Antral contractions become forceful (ACh, Gastrin) ◦ Several milliliters of chyme are propelled through open pylorus ◦ Normal gastric emptying: 1-3 hours ◦ During the interdigestive period, the migrating motor complex clears any residual meal Dog eating mashed potatoes Gastric Motility: Gastric Emptying - Effects of composition Composition and volume affect gastric emptying rate • Nutrient composition ‒ Solid, hypo- and hypertonic, and acidic meals empty slower ‒ Rates for nutrients (fastest to slowest) • Carbohydrates > Protein > Fat • Liquids ‒ Liquid meals empty in ½ time as solids (~ 90 min vs. 3h) ‒ Exponential rate, volume main determinant • Solids ‒ Have a “lag phase” ‒ What do you think causes the lag phase? • Influenced by composition and chewing • Can be up to 60 minutes • Mixed meal ‒ Liquids empty before solids Gastric Emptying: Regulation When a meal enters the duodenum, feedback loops can slow gastric emptying to ensure timely delivery ◦ Neural feedback ◦ Enterogastric reflex: contents of duodenum lead to decreased gastric emptying ◦ Stimulus: contents in the duodenum (H+, osmolality, protein) sensed by chemoreceptors ◦ Local and long reflexes (vagovagal) ◦ Long reflexes lead to ↑sympathetic ↓parasympathetic ◦ Result: ◦ Decrease tone in proximal stomach ◦ Decrease strength of antral contractions ◦ Contraction of pyloric sphincter ◦ Hormonal feedback: ◦ CCK secreted in response to fatty and amino acids leads to ↓ gastric emptying ◦ GIP and secretin lead to ↓ gastric emptying Clinical Correlation: Patient Presentation A 62-year-old patient presents with nausea, a brackish taste in his mouth after he eats, a feeling a fullness after eating small amounts and has experienced a weight loss of 8lbs in past 2 months. His past medical history is significant for Type II diabetes (diagnosed 20 years ago) and hypertension. His diabetes has been controlled with oral hypoglycemics, but his blood sugars have been elevated and his endocrinologist is considering insulin. How can you explain his presentation? Clinical Correlation: Gastric Emptying Disorders Notice that many of the symptoms overlap DELAYED DELAYED GASTRIC EMPTYING Disrupts innervation Disrupts innervation, hormonal input and/or feedback loops Disrupts blood supply Disrupts anatomy Causes: Diabetes Vagotomy Eating Disorders Stress Medications Ischemia Obstruction Idiopathic RAPID RAPID GASTRIC EMPTYING Disrupts anatomy Disrupts hormonal input Causes: “Dumping Syndrome” -Gastric surgery Zollinger-Ellison Syndrome Idiopathic Clinical correlation: Gastrinoma. Our patient presented with epigastric pain, diarrhea and greasy stools. Gastrin increases gastric emptying and chyme and acid overwhelm the duodenum. Clinical Correlation: Vagotomy ◦ History: Vagotomies used to be performed in ulcer patients to control gastric acid secretion. When the vagus nerves to the stomach are cut (truncal vagotomy), acid secretion decreases (proximal stomach) but so does gastric emptying (impaired antral contraction and denervation of pylorus). A pyloric drainage procedure was performed at the same time. Medications have largely replaced this procedure. ◦ Current use: Highly selective vagotomies (HSV) are performed in some cases of ulcer refractory to medication. This procedure involves only ligating the nerves to the upper body and fundus. This reduces acid secretion. It may also somewhat impair receptive relaxation leading to early satiety and rapid emptying of liquids. http://www.yoursurgery.com/Pr ocedureDetails.cfm?BR=1&Pro c=48 Vagal innervation of the stomach Truncal vagotomy Highly selective vagotomy Note: The boards like to ask about vagotomies. What else would you expect if vagus innervation to the abdomen were interrupted? Small intestinal motility ◦ Parasympathetic stimulation increases contraction of intestinal smooth muscle, and sympathetic activity decreases contraction ◦ Segmentation contractions- mix the chyme ◦ Peristaltic contractions-propel the chyme Step-by-step ◦ Peristalsis: ◦ The food bolus in the intestinal lumen is sensed by enterochromaffin-like (ECL) cells of the intestinal mucosa, which release serotonin (5-HT). ◦ The 5-HT binds to receptors on intrinsic primary afferent neurons (IPANs) that, when activated, initiate the peristaltic reflex in that segment of small intestine. ◦ Behind the bolus, excitatory transmitters (e.g., ACh, substance P, neuropeptide Y) are released in circular muscle, while these pathways are simultaneously inhibited in the longitudinal muscle; this segment of small intestine narrows and lengthens. ◦ In front of the bolus, inhibitory pathways (e.g., VIP, NO) are activated in circular muscle, while excitatory pathways are activated in longitudinal muscle; this segment of small intestine widens and shortens. Large intestinal motility ◦ Segmentation contractions ◦ Segmentation contractions occur in the cecum and proximal colon. As in the small intestine, these contractions function to mix the contents of the large intestine. In the large intestine, the contractions are associated with characteristic sacklike segments called haustra. ◦ Mass movements ◦ Mass movements-> colon and function to move the contents of the large intestine over long distances, such as from the transverse colon to the sigmoid colon. Mass movements occur anywhere from 1 to 3 times per day. ◦ Water absorption -> distal colon, making the fecal contents of the large intestine semisolid and increasingly difficult to move. ◦ A final mass movement propels the fecal contents into the rectum, where they are stored until defecation occurs. Large intestinal motility ◦ Defecation ◦ As the rectum fills with feces, the smooth muscle wall of the rectum contracts and the internal anal sphincter relaxes in the rectosphincteric reflex. ◦ Defecation will not occur at this time, however, because the external anal sphincter (composed of striated muscle and under voluntary control) is still tonically contracted. However, once the rectum fills to 25% of its capacity, there is an urge to defecate. ◦ When it is appropriate, the external anal sphincter is relaxed voluntarily, the smooth muscle of the rectum contracts to create pressure, and feces are forced out through the anal canal. Vomiting ◦ vomiting center in the medulla coordinates the vomiting reflex THANK YOU!!!!