L2 Upper Gastrointestinal Motility.pdf

L2: Upper Gastrointestinal Motility Learning Outcomes By the end of the lecture, the students will be able to: 1. To describe the electrical activity of GIT wall. 2. To recognize the mechanism of chewing. 3. To outline the different stages of swallowing and its abnormalities. 4. To describe the mec...

L2: Upper Gastrointestinal Motility Learning Outcomes By the end of the lecture, the students will be able to: 1. To describe the electrical activity of GIT wall. 2. To recognize the mechanism of chewing. 3. To outline the different stages of swallowing and its abnormalities. 4. To describe the mechanism and function of different types of gastric motility. 5. To enumerate the factors controlling gastric emptying. 6. To recognize the mechanism of vomiting. References Guyton & Hall textbook of Medical Physiology. Elsevier, 14th Edition 2021. USMLE STEP I Lecture notes 2017 Physiology. KAPLAN Medical LO1: Electrical Activity of Gastrointestinal Smooth Muscle Slow Waves and Spike Potential Slow waves are spontaneous oscillating membrane potentials (electrical current) of smooth muscles of the GI tract. They are not action potentials (don't cause contraction), but when reach to firing level they cause action potentials and cause muscle contraction. Originate in the interstitial cells of Cajal, which serve as the pacemaker for GI smooth muscle. These interstitial cells are present between the smooth muscle layers. Frequency of slow waves The number of slow waves per minute varies in different parts of the GI tract, but is constant and characteristic for each part. The basic rate can not be changed by nervous or hormonal stimulation. In contrast, the height (strength) of the slow waves and the frequency of the action potentials that occur on top can be modified by neural and hormonal stimulations. The rate is lowest in the stomach (3/min) and highest in the duodenum (12/min). Lo2: Chewing lubricates food by mixing it with saliva. decreases the size of food particles to facilitate swallowing and to begin the digestive process. Chewing reflex: The presence of a bolus of food in the mouth at first initiates reflex inhibition of the muscles of mastication, which allows the lower jaw to drop. The drop in turn initiates a stretch reflex of the jaw muscles that leads to rebound contraction. This automatically raises the jaw to cause closure of the teeth, but it also compresses the bolus again against the linings of the mouth, which inhibits the jaw muscles once again, allowing the jaw to drop and rebound another time; this is repeated again and again. LO3: Swallowing The swallowing reflex is coordinated in the medulla. Afferent fibers are the vagus and glossopharyngeal (IX) (X) nerves. Efferent fibers are trigeminal (V), glossopharyngeal (IX), vagus (X) and hypoglossal (XII) nerves Swallowing has three phases: Oral phase (voluntary), Pharyngeal phase: and Esophageal phase (Involuntary). 1. Oral Phase (voluntary phase): After the end of chewing, the tongue moves upward and backward to push the bolus of food into the pharynx. 2. Pharyngeal phase The following sequence of events occurs during this phase: a. The nasopharynx closes by upward movement of soft palate and, b. At the same time, breathing is inhibited. c. The vocal cords of the larynx are strongly approximated. d. The larynx is pulled upward and anteriorly by the neck muscles. e. The epiglottis swings backward to close the opening of the larynx. f. Peristalsis begins in the pharynx to propel the food bolus toward the esophagus. Simultaneously, the upper esophageal sphincter relaxes to permit the food bolus to enter the esophagus. SWALLOWING 3. Esophageal Phase The esophagus propels the swallowed food into the stomach. The upper esophageal sphincter prevents air from entering the upper esophagus and the lower esophageal sphincter prevents gastric acid from entering the lower esophagus. A) primary peristaltic contraction; Begins behind the food bolus as a continuation of pharyngeal peristalsis. The peristaltic contraction moves down the esophagus and propels the food bolus along. Gravity accelerates the movement. B) Secondary peristaltic contraction results from distention of the esophagus itself by the retained food; clears the esophagus of any remaining food. C) As the food bolus approaches the lower end of the esophagus, the lower esophageal sphincter relaxes. This relaxation is vagally mediated, and the neurotransmitter is VIP (vaso-active intestinal peptide). D) The wall of the fundus of the stomach relaxes “receptive relaxation” to allow the food bolus to enter the stomach.  Abnormalities in lower esophageal sphincter a. Gastroesophageal reflux (heartburn) may occur if the tone of the lower esophageal sphincter is decreased and gastric contents reflux into the esophagus. b. Achalasia may occur if the lower esophageal sphincter does not relax during swallowing and food accumulates in the esophagus. These are the common risk factors for acid reflux disease: Eating large meals or lying down right after a meal Being overweight or obese Eating a heavy meal and lying on your back. Snacking close to bedtime Eating certain foods, such as citrus, tomato, chocolate, mint, garlic, onions, or spicy or fatty foods Drinking carbonated drinks, coffee, or tea Smoking Pregnantcy Taking aspirin, ibuprofen, certain muscle relaxers, or blood pressure medications. Stress.  Lo4: Gastric motility The stomach has three anatomic divisions—the fundus, body, and antrum. Functionally, it is divided into two regions The proximal region which includes the fundus and the proximal body. This region is responsible for receiving the ingested food. The distal region includes the antrum and the distal body.This region is responsible mixing food with gastric juice for digestion and propelling it into the duodenum. 1. “Receptive relaxation” It is a vagovagal reflex that is initiated by distention of the stomach by incoming food. It reduces the tone in the muscular wall of the body of the stomach so that it accommodates greater and greater quantities of food up to a limit of 0.8 to 1.5 liters. The pressure in the stomach remains low until this limit is approached. 2. Mixing and digestion The distal region of the stomach contracts to mix the food with gastric secretions and begins the process of digestion. Gastric contractions are increased by vagal stimulation and decreased by sympathetic stimulation.. Motilin is the mediator of these contractions. Lo5: Stomach emptying (pyloric pump and pyloric resistance) Stomach emptying occurs by peristaltic contractions in the stomach antrum (pyloric pump) and is opposed by the resistance of pylorus. The degree of constriction of the pylorus is increased or decreased by nervous and humoral signals from the stomach and duodenum. Gastric Factors that Promote Emptying 1-Stretching of the stomach by food causes local reflex that increases gastric contractions and inhibits the pylorus. 2. Gastrin hormone: increases the rate of stomach emptying.  Duodenal Factors That Inhibit Stomach Emptying A. Enterogastric Nervous Reflexes from the Duodenum When food enters the duodenum, multiple nervous reflexes are initiated from the duodenal wall and pass to the stomach to slow or even stop stomach emptying. These factors include: 1. Distention of the duodenum. 2. Irritation of the duodenal mucosa. 3. Acidity of the duodenal chime. 4. Osmolality of the chime (hypo or hyper osmolarity). 5. The presence of proteins and, to a lesser extent, of fats. B. CCK and secretin hormones. Lo6: Vomiting A wave of reverse peristalsis begins in the small intestine, moving the GI contents in the orad direction. The gastric wall relaxes and the gastric contents are pushed into the esophagus. If the pressure in the esophagus becomes high enough to open the upper esophageal sphincter, vomiting occurs. The vomiting center in the medulla is stimulated by tickling the back of the throat, gastric distention, and vestibular stimulation (motion sickness). The chemoreceptor trigger zone in the fourth ventricle is activated by emetics, radiation, and vestibular stimulation.