Activities In The Stomach PDF

Activities in the Stomach Two Types of Activities in the Stomach 1. Gastric secretion. 2. Gastric motility. Anatomic consideration Sac-like structure Divided anatomically into three regions: fundus, body, antrum, with different secretory & motility functions. Its wall consist of the same b...

Activities in the Stomach Two Types of Activities in the Stomach 1. Gastric secretion. 2. Gastric motility. Anatomic consideration Sac-like structure Divided anatomically into three regions: fundus, body, antrum, with different secretory & motility functions. Its wall consist of the same basic layers. Mucosa thrown into folds (rugae), contain pits (openings of gastric glands). Mucosa contain several cell types that secrete various components of gastric juice including parietal cells secrete HCl & IF, Chief cells secrete pepsinogen, G cells secrete gastrin, mucus neck cells secrete mucus+HCO3. Regions of the Stomach Functions of the Stomach 1. Storage function & control of emptying into duodenum (most important, stomach not essential for life) 2. Digestive function: three main food stuff by enzymes, HCl & motility 3. Secretory function: HCl, Pepsinogen, IF, Gastric lipase, Mucus & Bicarbonate 4. Absorptive function: absorption of water, alcohol, some drugs 5. Protective function: HCl, Protection of gastric mucosa by bicarbonate mucus barrier & by secretion of pepsinogen in inactive form Gastric Secretion Gastric juice composition: 1. Hydrochloric acid 2. Pepsinogen & gastric lipase 3. Mucus 4. Bicarbonate 5. Intrinsic factor Rate of secretion 2-3 L/d, Highly acidic (pH=1-4) Need protective mechanisms for the mucosa  Glands & Cell Types in Gastric Mucosa Anatomical Region Gland Type Cell Type Secretions Body Parietal glands 1. Oxyntic cells 1. HCl, IF 2. Chief cells 2. Pepsinogen 3. Mucus neck cells 3. Bicarbonate & Mucus Antrum Pyloric glands 1. Mucus neck cells 1. Bicarbonate & Mucus 2. G cells 2. Gastrin 1. Gastric Hydrochloric Acid Secretion From parietal cells in the oxyntic glands in the body of the stomach Functions: not essential for life, acidify the contents (pH=1 up to 4), activation of pepsinogen to pepsin, liquefaction of food, sterilization of food, absorption of iron & calcium Mechanisms for Secretion of HCl Cellular Mechanisms of HCl Secretion: Regulation of Gastric Acid Secretion According to the site of the stimulus is divided into three phases: 1. Cephalic phase: - Responsible for about 30% of the volume of gastric acid secreted. - Occur by conditioned & non conditioned reflexes. - In the non conditioned reflexes, presence of food in the mouth will stimulate gastric acid secretion through the taste receptors & other receptors, afferent impulses reach the vagus nucleus in the medulla & efferent impulses reach the stomach in the vagus nerve to cause secretion. - In the conditioned reflexes, psychic stimuli seeing, hearing, smelling & thinking of food will stimulate secretion mediating their effect through higher centers & efferent impulses reach the stomach the vagus nerve to cause secretion. - Vagus nerve stimulate secretion directly through acetylcholine & indirectly through stimulation of secretion of gastrin through non cholinergic mechanism involving gastrin releasing peptide (GRP). - The cephalic phase of gastric secretion is affect by emotional factors, so chronic stress stmulate secretions, while acute stress reduce secretion. Cont. 2. Gastric phase: - Represent about 60% of gastric acid secretion. - Is mediated by nervous & hormonal mechanisms. - Distension of the stomach by food stimulate secretion through long vagovagal reflexes & short local reflexes. - These reflexes mediate their effect through acetylcholine & gastrin. 2. Intestinal phase: - Represent only about 10% of gastric acid secretion. - Distension & protein digestion products in the upper intestine results in gastric acid secretion during this phase. - Secretion during this phase is partially mediated by gastrin release by food in the upper small intestine. Regulation of Gastric Acid Secretion Peptic Ulcer Ulcerative lesion of the gastric or duodenal mucosa caused by the erosive & the digestive action of HCL & pepsin on the mucosa. Can be caused by: 1. Loss of protective mucus barrier - Mucus & bicarbonate barrier - Prostaglandins - Mucosal blood flow - Growth factors 2. Damaging factors: HCl, Pepsin, H pylori infection, NSAID, Smoking, Stress, Alcohol Cont. Peptic ulcer is divided into: 1. Gastric ulcer: - Ulceration of the mucosa of the stomach. - Caused mainly by H pylori. - Acid secretion is low. - Gastrin secretion is high. 2. Duodenal ulcer: - Ulceration of the mucosa of the duodenum. - More common than the gastric ulcer. - Caused by increased HCl secretion. - H pylori may have a direct & indirect role. - Zollinger-Ellison syndrome (gastrinoma) is gastrin secreting tumors that play important role in duodenal ulcer. Cont. Treatment of peptic ulcer: 1. Antacids. 2. Omeprazole. 3. Cimetidine & ranitidine. 4. Vagotomy & muscarinic blockers. 2. Secretion of pepsinogens, gastric lipase, Intrinsic factor, Mucus & Bicarbonate, Gastrin Pepsinogens: - Inactive precursors of pepsins. - At least seven types of pepsinogens are secreted. - Pepsinogens are activated by hydrochloric acid & also by active pepsin (Autocatalysis). - Optimum pH for pepsin is 1.8—3.5. - Pepsins hydrolyse proteins into short chain peptides. Cont. Gastric lipase: This enzyme hydrolyses triacylglycerols (mainly act on triacylglycerol with short chain fatty acids e.g. Butric acid found in butter) It is much less important than pancreatic lipase It has a PH of 4—7 (therefore act while food inside bolus) Cont. Intrinsic Factor: - Secreted by parietal cells. - It is a glycoprotein that combines with vitamin B12 to protect it through its passage in the small intestine & it also helps absorption of the vitamin at the distal part of the ileum. - Deficiency of vitamin B12 causes megaloblastic anemia. - This occurs in atrophy of parietal cells or removal of a large portion of the stomach. - In these cases the vitamin should be given in an injectable form. Cont. Mucus & bicarbonate: - Secreted by mucus neck cells & surface epithelial cells. - Protective function by forming the mechanical & chemical barrier.  Cont. Gastrin: - Secreted by G cells in the antrum mainly & upper small intestine into the blood. - It is a peptide that exists in many forms. - Its secretion is stimulated by distension of the stomach & by the presence of digestion products proteins, alcohol& caffeine also stimulate secretion, the vagus stimulates secretion through the three phases. - Has got so many actions some of them are physiological & others are pharmacological. - These include: a. Physiological functions: 1. Gastric acid secretion. 2. Pancreatic secretion. 3. Trophic effect on gastric mucosa. 4. Contraction of lower esophageal sphincter. b. Pharmacological functions:1. Pepsin secretion. 2. Secretion of intrinsic factor. 3. Pancreatic secretion of enzyme & bicarbonate. 4. Biliary secretion of water & bicarbonate. 5.Stimulates gastric motility but slows gastric emptying. 6. Stimulate the intestinal motility & relaxes ileocecal sphincter. - Secretion of gastrin can be inhibited by many factor including the effect of emotions & presence of high acidity in the stomach. Gastric Motility According to motility functions that occur during the fed state the stomach is divided into: 1. Orad region: - Fundus & proximal one third of the body of the stomach. - Thin walled. - Receptive relaxation. - Accommodate food. 2. Caudal region: - Distal body & antrum. - Thick walled. - Peristaltic contractions. - Mix, grind & propel food The electrical basis of gastric motility is slow wave activities (Basal Electrical Rhythm BER) superimposed on it spikes, originate from a base maker in the grater curvature of the stomach at rate of 3/minute & become stronger as it moves distally. Slow wave activity (Basal Electrical Rhythm) Cont. Three components of gastric motility occurring during the fed state are: 1. Receptive relaxation. 2. Peristaltic contractions. 3. Gastric emptying. Cont. 1. Receptive relaxation: - Relaxation of the proximal part. - Accommodate food. - Orad region (fundus & proximal body). - Continuation of esophageal motility. - Mediated through vagovagal reflex & the transmitter is VIP. - Also slow sustained contractions occur in the proximal part of the stomach to slowly push the contents towards the distal region of the stomach & duodenum providing the pressure for emptying of liquefied chyme. Cont. 2. Peristaltic contractions: - The main motility function in the distal part of the stomach. - Begin in the middle of the body of the stomach & move distally. - Propulsion & retropulsion. - Grinding & mixing of food. - Play a role in gastric emptying. - Initiated by distension & mediated by vagovagal reflexes. - The pylorus is an atypical sphincter in that it open most of the time & close only when a peristaltic contraction approach it, this is important for retropulsion & grinding of food & also it plays a role in control of gastric emptying.  Cont. 3. Gastric emptying: - After a meal the stomach contains about 1-5 L of contents composed of solids, liquids & gastric secretion. - The maximum normal emptying time for the healthy intact stomach is 6 hours. - Gastric emptying is regulated to control delivery of partially digested food into duodenum. - Gastric emptying occur through coordinated motility activities in the antrum, pylorus & duodenal bulb, these being called the gastroduodenal pump which control gastric emptying. - As the gastric contents are propelled into the distal stomach, the antrum, pylorus & proximal duodenum are relaxed & the part of the chyme which has been liquefied or already in liquid form passes readily into the duodenum being pushed by the tonic contraction which occur in the proximal part of the stomach. - The terminal antrum then contracts, further aiding the propulsion of chyme, this is followed by contraction of pylorus which closes it off. - The proximal duodenum contract to push the contents into the rest of the small intestine. - Then the antrum, pylorus & duodenal bulb relax & the sequence is repeated. Cont. Regulation of gastric emptying: The rate of emptying depend on the state of stomach, pyloric sphincter & duodenum (the gastroduodenal pump). Regulation of gastric emptying depend on signals from stomach & duodenum. Gastric emptying depends in turn depend on the characteristics of food in the stomach (physical & chemical nature of food) & in the duodenum. Factor affect gastric emptying can be divided into: 1. Factors enhance gastric emptying: Gastrin, large volume of food. 2. Factors slow gastric emptying: Presence of H+ & fat in the duodenum (duodenal reflexes), mediated by CCK or local neural reflexes, Cont. These three types of gastric motility functions occur during the fed state are going to be replaced by peristaltic contractions that pass along the stomach & known as Migrating Myoelectric Complexes (MMC) during fasting (in empty stomach during the interdigestive period). MMC move along the whole length of the stomach & small intestine to reach the ileocecal sphincter after 1.5 to 2 hrs. Occur at 90 minute intervals, mediated by motilin, clean the stomach, terminated when food is ingested. Vomiting (Emesis) Forceful expulsion of stomach & intestinal contents through the mouth. Centrally regulated by vomiting center locate bilaterally in the medulla & the center receive inputs from so may area including widespread part of the gastrointestinal tract through the two divisions of the autonomic nervous system, in addition it receive inputs from different areas of the brain. Is a protective mechanism by which the stomach remove harmful substances. Stimulated by irritant substances in the stomach or duodenum, or by over distension of them. Substances produce vomiting are known as emetics. Vomiting may also accompany motion sickness or disgusting sights or smells. Cont. Vomiting (Emesis) Mechanism of vomiting: - Involve a number of steps, which are: 1. Usually preceded by with salivation, retching & the sensation of nausea. 2. A deep breath is taken, the glottis is closed & the soft palate rises to close the nasopharynx, the cricopharyngeal sphincter the relaxes. 3. The breath is held in mid inspiration. 4. This is immediately followed by strong contractions of the diaphragm & abdominal muscles, increase in the intragastric pressure & squeeze of the stomach between the diaphragm & the abdominal wall is considered to be the most important factor in propulsion of contents. 5. In the mean time the body & the fundus of the stomach relaxes & reverse peristalsis starts & propel contents up orally, some times the peristaltic contractions starts in the lower small intestine to push contents into the stomach. 6. The lower esophageal sphincter & the esophagus relax & the gastric contents are expelled through the mouth. Cont. Vomiting (Emesis) 7. Accompanied by autonomic changes including increased heart rate, increase breathing rate & in fact respiration becomes irregular (wretched breathing), sweating, salivation & dilatation of the pupil. 8. Emetics can produce vomiting either by act: 1. Peripherally by irritation of the gastrointestinal tract mucosa. 2. Centrally by stimulation of vestibular nuclei, limbic system or chemoreceptor trigger zone. Cont. Vomiting (Emesis) Control of vomiting: - In the medulla there are two centers concerned with control of vomiting. - The main center is the vomiting center, which is connected to the other center known as chemosensitive trigger zone. - Sensory impulses from the different parts of the gastrointestinal tract resulting from distension or chemical irritation reach the vomiting center through both sympathetic and parasympathetic nerves. - Impulses from the internal ear (labyrinth) are transmitted via the vestibular nerve to the cerebellum, which in turn conveys them to the chemosensitive trigger zone. - Drugs like morphine causes vomiting because of its effects on the chemosensitive trigger zone which is connected to the vomiting center.