Stomach Anatomy PDF

Anatomy of Stomach Dr. Mohamed Elfiky PROFESSOR OF Anatomy and embryology  Left Hypochondrium Epigastrium Umbilical Region Mohamed el fiky Stear Horn Stomach J- Shaped Stomach...

Anatomy of Stomach Dr. Mohamed Elfiky PROFESSOR OF Anatomy and embryology  Left Hypochondrium Epigastrium Umbilical Region Mohamed el fiky Stear Horn Stomach J- Shaped Stomach Mohamed el fiky  Lesser curvature Cardiac orifice Greater curvature Cardiac orifice Mohamed el fiky  Stomach Position: It lies in the epigastrium, Lt. hypochondrium and umbilical regions. Shape : a. J- shape (common). b. Steer-horn (less common). Orifices of the stomach : 1- Cardiac orifice or end : - Lies at the junction with oesophagus in the upper part of epigastrium in contact with Lt. lobe of the liver. - It is the more fixed end. - N.B. The cardiac end has no anatomical sphincter but has physiological sphincter: a. The lower end of the oesophagus pierces the right crus of the diaphragm. b. The oesophagus joins the stomach in an acute angle. c. The mucosal folds act as valves. Mohamed el fiky  Stomach 2- Pyloric orifice or end : It is lies at the junction with the duodenum and in contact with the qaudate lobe of the liver. Surface anatomy of pyloric orifice: 1/2 inch to the Rt. of median plane in the transpyloric plane (L1). It is more mobile than the cardiac end. It has a true anatomical sphincter (thickening of circular muscle layer). The position of the pyloric sphincter is indicated by : a. Anterior groove. b. Feeling of the thickness of the pyloric sphincter. c. The pre-pyloric vein of Mayo (connecting Rt. gastric and Rt. Gastro-epiploic veins together). Mohamed el fiky  Borders of the stomach (curvatures) 1- The lesser curvature (Rt. border): ▪ Gives attachment to the lesser omentum. ▪ Along it runs Rt. and Lt. gastric vessels. ▪ Its lower part presents a notch called angular notch or incisura angularis. 2- The greater curvature ( Lt. border): ▪ Gives attachment to the following ligaments from above downwards: a. Gastro-splenic ligament. b. Greater omentum. c. Along it runs Rt. and Lt. gastro-epiploic vessels. Mohamed el fiky  Parts of the stomach I- Fundus: - It is the dome shaped part above the horizontal line joining the cardiac orifice to the greater curvature. II- Body : - It is present between: a. The horizontal line that limits the fundus. b. A vertical line passing from the angular notch to the greater curvature. III. Pylorus : - It is the part to the right of the previous vertical line. -It is subdivided into: a. Pyloric antrum: It is the dilated part next to the body. b. Pyloric canal : the distal narrow part. c. Pyloric sphincter : the end of the pylorus. Mohamed el fiky  Relations of the stomach The antero-superior surface (anterior relations): a. Left lobe of liver: related to a narrow area adjoining the lesser curvature. b. Diaphragm: related to the upper and left area of anterior surface, separating it from the left pleura and lung. c. Left costal margin. d. Anterior abdominal wall related to the lower and right part of the anterior surface. Mohamed el fiky  3-The postero-inferior surface( stomach bed ) 1- Transverse colon. 2- Transverse mesocolon. 3- Body of pancreas. 4- Splenic artery along upper border of pancreas. 5- Left kidney. 6- Left suprarenal gland. 7- Left crus of diaphragm. 8- Spleen. N.B. The stomach is separated from the previous structures by the lesser sac except spleen by greater sac Mohamed el fiky  Ligaments of the stomach (Omenta) 1- Greater omentum.. 2- Lesser omentum. 3- Gastro-splenic ligament. 4- Gastro-phrenic ligament. Mohamed el fiky  Arterial supply of the stomach Blood supply of the stomach is derived from the coeliac trunk & its branches). 1- left gastric artery: - Arises from the coeliac trunk. - Runs along the upper part of the lesser omentum. - It is the largest artery of stomach. 2- Right gastric aretry : - Arises from the hepatic artery. - Runs along the lower part of lesser curvature and anastomoses with left gastric aretry. 3- Left gastro-epiploic artery: - Arises from the splenic artery. - Runs along the upper part of greater curvature. 4- Right gastro-epiploic artery: - Arises from the gastro-duodenal artery (branch of hepatic artery). - Runs along the right part of greater curvature. - Anastomoses with left gastroepiploic artery. 5- Short gastric arteries : - Arise from splenic artery and pass to the fundus. Mohamed el fiky  Venous drainage of the stomach The venous blood of the stomach drains into portal circulation as follows: 1- Lt. gastric vein : end portal vein 2- Rt. gastric vein : end portal vein 3- Lt gastroepiploic : end splenic vein 4- short gastric veins : end splenic vein 5- Rt. gastro epiploic vein : ends in the sup. mesentric vein. Mohamed el fiky  Lymphatic drainage Lymphatics of the stomach pass to the following lymph nodes: 1- Paracardiac L.N.s (around cardiac end) 2- Lt. gastric L.N.s (along Lt. gastric vessels) 3- Pyloric L.N.s (around the pyloric end) 4- Pancreatico splenic L.N.s (accompany splenic a.) 5- Rt. gastro epiploic L.N.s (along Rt. gastroepiploic vessels) N.B. All the above mentioned L..N.s drain into the coeliac L.N.s around coeliac trunk. Some lymphatics pass to the hepatic L.N.s in porta hepatis. Mohamed el fiky  Nerve supply: (autonomic fibers ) 1- Sympathetic fibres: arise from the coeliac ganglion around coeliac trunk. The preganglionic arise from the thoracic ganglion 5,6,7 &8 2- Parasympathetic Fibres: Derived from the ant. &post. Gastric nerves which are the continuation of left and right vagus respectively. Mohamed el fiky Case Scenario A 68-year-old man with atrial fibrillation comes to the emergency department with acute-onset severe upper abdominal pain. He takes no medications. He is severely hypotensive. Despite maximal resuscitation efforts, he dies. Autopsy shows necrosis of the proximal portion of the greater curvature of the stomach caused by an embolic occlusion of an artery. The embolus most likely passed through which of the following vessels? A. Superior mesenteric artery * B. Splenic artery C. Inferior mesenteric artery D. Gastroduodenal artery Muscles of Shoulder By Dr. Hassan Rezk November 12, 2023 16 References 1- Gray's anatomy for students, 3rd edition. ISBN: 978-0-7020-5131-9 Copyright© 2015, 2010, 2005 by Churchill Livingstone, an imprint of Elsevier Inc. 2- Gray’s Anatomy 40th edition. ISBN: 978-0-443-06684-9 International Edition ISBN: 978-0-8089-2371-8 3. CLINICAL ANATOMY BY REGIONS Richard ร. Snell. ISBN 978-1-60913-446-4 Muscles of Shoulder By Dr. Hassan Rezk November 12, 2023 17  The physiology of gastrointestinal smooth muscle fibers Dr. Sherin Magdi M.B.B.Ch , M.Sc , MD in Physiology Assistant professor Physiology department-Medicine program 1 The learning Objectives Describe the followings: The types of smooth muscle fibers. Mechanism of smooth muscles contraction. Properties of smooth muscles contraction. Control of visceral smooth muscle contraction Basal electrical activity of GIT smooth muscle fibers with its clinical correlation. 2 Smooth muscle cells The smooth muscle fibers are spindle-shaped , non-striated cells. ❑ They are present in : The walls of viscera , blood vessels ,some glands (the prostate and seminal vesicles), as well as in the skin(erector pili muscles), eye (ciliary and pupillary muscles) and subcutaneous tissue (in the scrotum). ❑ Although they do not move the body, but they regulate most of internal activities of the body. 3 Types of smooth muscle cells Multiunit smooth muscle Single unit (visceral) smooth muscle Made up of discrete (separate) smooth They made up of large sheets of muscle fibers without interconnecting smooth muscle fibers that have low bridges in between(each fiber can resistance bridges in between forming a contract independent to others) functional syncytium Does not obey all or none law. It obeys all or none law They are mainly under control of Mainly under Chemical autonomic nervous system control(hormones) EX: ciliary muscle, erector pili muscles EX: smooth muscle cells in the walls of hollow viscera (the intestine, uterus and ureter..,) and many blood vessels. 4 5 Mechanism of smooth muscles contraction In contrast to skeletal muscles, the contraction of smooth muscles is involuntary. The mechanism of smooth muscles contraction is almost like that of skeletal muscles, since they contain parallel filaments of actin and myosin which slide over each other during contraction. They also contain tropomyosin and calmodulin (but no troponin). The source of Ca++ is mainly from The ECF as the sarcoplasmic reticulum is rudimentary. Ca++ –Calmodulin activates the myosin light chain kinase (MLCK) which phosphorylates light chains of myosin heads and increases the activity of myosin ATPase. Phosphorylation (Activation) of the Myosin Head Tilting of myosin sliding over actin contraction. Relaxation can happen by decreasing Ca++ level which cause: 1-Inhibition of calmodulin 2-Activation of myosin phosphatase which cause dephosphorylation of myosin head. 6 7 8 9 PROPERTIES OF SMOOTH MUSCLES (1)It is sensitive to changes in pH, osmotic pressure, temperature ,drugs , chemicals and hormones (because it is continuously exposed to the changes that occur in the internal environment of the body). (2)Slow Cycling of the Myosin Cross-Bridges leads to slowness of onset of Contraction and Relaxation. (3)Its O2 consumption is about 1/4 that of skeletal muscles, so it is not rapidly fatigued.(Low Energy Requirement to sustain Contraction).(Latch effect) (4)The maximum force of contraction is greater in smooth muscle than in Skeletal Muscle. (5)The percentage of shortening in smooth muscle fibers during contraction is more than the same percentage in skeletal muscle. 10 (6)The sarcoplasmic reticulum, which provides virtually all the calcium ions for skeletal muscle contraction, is only slightly developed in most smooth muscle. Instead, most of the calcium ions that cause contraction enter the smooth muscle cell from the extracellular fluid at the time of the action potential or other stimulus. (7)Plasticity (length adaptation) (Stress-relaxation) If a piece of visceral muscle is slowly stretched, the developed tension is high at first, but if the stretch is maintained (the muscle is held at the greater length) ,the tension gradually decreases. This is called the property of plasticity. It allows the hollow viscera to accommodate large amounts of contents without much increase in pressure. 11 Length adaptation 12 Control of visceral smooth muscle contraction The visceral smooth muscle fibers is controlled by : A-Nervous control : Autonomic nervous system Enteric nervous system Gastrointestinal nerve reflexes B- Hormonal control: GIT hormones 13  Autonomic control Sympathetic noradrenergic nerves It pass in the splanchnic nerves It decreases the smooth muscle activity in the visceral wall and contract the sphincters. Parasympathetic cholinergic nerves It pass in both Vagi & pelvic nerves It increases the smooth muscle activity in the visceral wall and relax the sphincters. The function of these nerves is not to initiate smooth muscle contraction but only to modify its activity which is produced by intrinsic myogenic activity. 14 15  Enteric nervous control The gastrointestinal tract has Its own nervous system which is called the enteric nervous system. The enteric nervous system is composed mainly of two plexuses: (1) Myenteric plexus or Auerbach’s plexus: An outer plexus lying between the longitudinal and circular muscle layers. It controls mainly the gastrointestinal movements (2)Submucosal plexus or Meissner’s plexus: An inner plexus lying in the submucosa. It controls mainly gastrointestinal secretion and local blood flow. 16  The extrinsic sympathetic and parasympathetic fibers connect to both the myenteric and submucosal plexuses and control their function. Parasympathetic Stimulation Increases activity of the Enteric Nervous System. Sympathetic Stimulation Usually decreases activity of the Enteric Nervous System. 17 18  Gastrointestinal nerve reflexes They are group of nerve reflexes that regulate the function of the gut. They can be stimulated by : (1)Chemical Irritation of the gut mucosa. (2) Mechanical distention of the gut lumen. 1. Local reflexes which integrated within the enteric nervous system. These reflexes include those that control the gastrointestinal secretion , peristalsis, mixing contractions or local inhibitory effects. 2. Ganglionic Reflexes which arise from the gut to the paravertebral sympathetic ganglia and then back to the gastrointestinal tract. These reflexes transmit signals long distances to other areas of the gastrointestinal tract, such as: The enterogastric reflex : It starts from small intestine to inhibit stomach motility and secretion The colo-ileal reflex: It starts from the colon to inhibit emptying of ileal contents into the colon. 19 3. Central Reflexes They start from the gut to the spinal cord or brain stem and then back to the gastrointestinal tract. (1)Vagal reflexes that travel from the stomach and duodenum to the brain stem and back to the stomach—by way of the vagus nerves—to control gastric motor and secretory activity. (2) Defecation reflex that travel from the colon and rectum to the spinal cord and back again to produce the powerful colonic, rectal, and abdominal contractions required for defecation. 20 21 Electrical Activity of GIT Smooth Muscle Two basic types of electrical waves: (1) Slow waves (2) Spikes Potentials 1-Slow Waves They are not action potentials. Instead, they are slow, undulating changes in the resting membrane potential. Their intensity usually varies between 5 and 15 millivolts Their frequency depends on the section of the digestive tube - in the small intestine, they occur 10 to 20 times per minute and in the stomach and large intestine 3 to 8 times per minute. Slow wave activity appears to be a property intrinsic to smooth muscle and not dependent on nervous stimuli. They appear to be caused by complex interactions among the smooth muscle cells and specialized cells, called the interstitial cells of Cajal, which are believed to act as electrical pacemakers for smooth muscle cells. The slow waves usually do not cause muscle contraction by themselves. Instead, they mainly excite the appearance of intermittent spike potentials, and the spike potentials in turn excite the muscle contraction. 22 2-Spike Potentials. The spike potentials are true action potentials. They occur automatically when the resting membrane potential of the gastrointestinal smooth muscle becomes more positive than about −40 millivolts. (The normal resting membrane potential in the smooth muscle fibres of the gut is between −50 and −60 millivolts). They allow especially large numbers of calcium ions to enter along with smaller numbers of sodium ions and therefore are called calcium-sodium channels. These channels are much slow to open and close which accounts for the long duration of the action potentials` 23  Factors that depolarize the membrane (Its potential becomes more positive) ( More excitability) (1) Stretching of the muscle. (2) Acetyl choline (3) Parasympathetic stimulation. (4) Excitatory gastrointestinal hormones. Factors that hyperpolarize the membrane (Its potential becomes more negative) ( Less excitability) (1) Norepinephrine or epinephrine (2) Sympathetic stimulation (3) Inhibitory gastrointestinal hormones. Dopamine It is secreted from enteric neurons, immune cells, intestinal flora and gastrointestinal epithelium. It stimulates exocrine secretions, inhibits gut motility, modulates sodium absorption and mucosal blood flow, and is protective against gastroduodenal ulcer disease 24 25  Irritable bowel syndrome (IBS) It is a common chronic condition that affects the digestive system in which the patients present with : *Abdominal pain : Which is typically related to defecation *Altered bowel habits: Diarrhea and/or Constipation *Other gastrointestinal symptoms o Nausea, reflux, early satiety o Passing of mucus, abdominal bloating It is thought to be caused by : *Altered gastrointestinal motility *Visceral hypersensitivity *Altered permeability of the gastrointestinal mucosa. *Psychosocial aspects Treatment *First-line treatment includes lifestyle modifications (physical activity, stress management), dietary adjustments ( adequate hydration, high-fiber foods and avoidance of trigger foods) *Psycho behavioral therapies. *Pharmacological therapies such as Laxatives Antidiarrheals Antispasmodics 26  Diabetic gastroparesis Definition: It is a complication of long-term diabetes characterized by delayed gastric emptying that is not associated with mechanical obstruction. Risk factors: Inadequate diabetic control and obesity. Pathophysiology: Hyperglycemia → neuronal damage → impaired neural motor control of gastric function → delayed gastric emptying Symptoms typically include nausea, vomiting, abdominal discomfort, and early satiety Treatment: Conservative management with glycemic control, dietary modifications, and avoidance of medications and substances that delay gastric emptying. First line pharmacotherapy is : metoclopramide It is a dopamine-2 receptor antagonist. Commonly used to promote gastrointestinal motility in patients with gastroparesis. 27 Case scenario A 72-year-old man with a 1-year history of constipation comes to the physician for a follow-up examination. He has bowel movements 1–2 times a week. Defecation is painful and preceded by a sense of bowel obstruction. He starts to take a medication which increases the excitability of the gastrointestinal smooth muscle fibres. What is the normal resting membrane potential of the gastrointestinal smooth muscle fibres (In millivolts)? A. From –5 to -10 B. From –15 to -20 C. From –30 to -40 D. From –50 to -60 28 References Guyton and Hall Textbook of Medical Physiology,13th edition ,Unit II ,Chapter 8 page 97-101 Guyton and Hall Textbook of Medical Physiology,13th edition ,Unit XII (Gastrointestinal Physiology). Chapter 63 page 797- 801 29 Thank You 30  Gastric motility and secretion Dr. Sherin Magdi M.B.B.Ch , M.Sc , MD in Physiology Assistant professor Physiology department-Medicine program 1 The learning Objectives Describe the gastric motor function. Describe the gastric secretory function. Explain the pathophysiology of peptic ulcer disease. 2 3 The gastric motor function The motor functions of the stomach are : (1)Storage of large quantities of food until the food can be processed in the stomach, duodenum, and lower intestinal tract. (2)Mixing of this food with gastric secretions until it forms a semifluid mixture called chyme. (3)Slow emptying of the chyme from the stomach into the small intestine at a rate suitable for proper digestion and absorption by the small intestine. 4  1-Storage function It is the ability to accommodate extra quantities of food coming from the oesophagus It occurs mainly in the fundus and upper 2/3 of the stomach body. It can be explained by a vago-vagal reflex : Stimulus : Esophageal distention Afferent : Sensory vagal afferent fibers Center : Vagal nucleus in the medulla Efferent : Motor vagal efferent fibers. Response : 1-Stimuation of smooth muscle fibers In the wall of the esophagus (Secondary peristalsis). 2-Receptive relaxation of the Lower Esophageal Sphincter and Stomach which allows easy propulsion of the swallowed food into the stomach. 5  2-Mixing &propulsion function Presence of food in the stomach is associated with slow peristaltic waves ,called mixing waves. They can happen 3-4/min. They begin in the lower 1/3 of stomach body and move toward the antrum. As the mixing waves progress from the body of the stomach into the antrum, they become more intense that provide powerful peristaltic action which force the antral contents toward the pylorus. Due to pyloric contraction most of the antral contents are squeezed upstream towards the body of the stomach (upstream squeezing action) which is called “retropulsion,”. 6  3-Emptying function Stomach emptying is promoted by intense peristaltic contractions in the stomach antrum. At the same time, emptying is opposed by varying degrees of resistance to passage of chyme at the pylorus (Pyloric Pump). 7  Stimulatory Factors for gastric emptying 1-Effect of Gastric Food Volume (Nervous control) Increased food volume in the stomach promotes increased emptying from the stomach by stretching of the stomach wall that elicit local myenteric reflexes in the wall that greatly increase the activity of the pyloric pump and increase gastric emptying. 2-Effect of Gastrin hormone (Hormonal control) The stretching of the stomach wall elicit release of the gastrin hormone from the G cells of the antral mucosa which seems to enhance the activity of the pyloric pump and increase gastric emptying. 8  Duodenal inhibitory factors for gastric emptying 1-Enterogastric reflexes:(Nervous control) Stimulus: 1. Distension of the duodenum 2. Irritation of the duodenal mucosa 3. High acidity of the duodenal chyme 4.The presence of proteins breakdown products(or fat breakdown products for less extent) Types of initiated reflexes: 1. Local reflexes that mediated by enteric nervous system. 2. Ganglionic sympathetic reflexes from the duodenum to the paravertebral sympathetic ganglia and then back to the stomach. 3. Vagal reflexes from the duodenum to the vagal nucleus in the brain stem then inhibitory vagal pathway back to the stomach. Response: Slowing or even stoppage of stomach emptying 9 2- Hormonal control: Cholecystokinin (CCK). Secretin. Gastric inhibitory peptide (GIP). All these hormones are secreted from the upper small intestine mucosal cells, and they can inhibit the gastric emptying. 10  Other factors can affect the gastric emptying 1-Food factors: Consistency of food: Liquids are easy to be evacuated than solids. Type of food: They arranged from fastest to slowest evacuation as follow, carbohydrate, proteins then lipids. 2-Autonomic factors: Sympathetic stimulation can decrease the gastric emptying. Parasympathetic stimulation can stimulate gastric emptying. 3-Chemical factors: Adrenergic medications inhibit gastric emptying. Cholinergic medications stimulate gastric emptying. 11 The gastric secretory function The gastric glands secrete about 1.5 liters of gastric juice daily Gastric juice is a mixture of: Mucus, hydrochloric acid, and digestive enzymes (pepsinogen and gastric lipase). Pepsinogen is the precursor molecule of the very potent protein- digesting enzyme pepsin. The main source of gastric acid secretion is: The oxyntic cells (The parietal cells ) Are located on the inside surfaces of the body and fundus of the stomach The pH of gastric acid is about 1.5 to 3.5 in the human stomach lumen. 12 13 FUNCTIONS OF HCI secretion: ( I) It activates pepsinogens into pepsins (which start protein digestion) (2) It sterilizes the stomach by killing most ingested bacteria. (3) It helps absorption of iron and calcium (4) It regulates gastric emptying ❑ The mucus gel layer together with the HC03 secreted by the surface mucosal cells constitute a mucosal barrier that protects the gastric mucosa against damage by gastric HCL. 14 Basic Mechanism of Hydrochloric Acid Secretion 1-Water inside the parietal cell becomes dissociated into H+ and hydroxide (OH−) in the cell cytoplasm. 2-The H+ is then actively secreted into the lumen in exchange for K+, an active exchange process that is catalysed by H+-K+ ATPase. 3- By the sodium Na+-K+ ATPase pump on the basolateral (extracellular) side of the membrane: A) K+ ions increased inside the cell and tend to leak into the lumen, but it is recycled back to inside the cell by H+-K+ ATPase. B) Na+ ions decreased inside the cell that allow more Na+ reabsorption from the lumen. 15 4-With more H+ ion secretion to the lumen ,there is more OH- accumulation inside the cell. Carbonic anhydrase enzyme 5- OH- +CO2 HCO3- 6-The HCO3− is then transported across the basolateral membrane into the extracellular fluid in exchange for chloride ions, which enter the cell and are secreted through chloride channels into the lumen. 7-More Cl- accumulated inside the cell that become easy to secreted through chloride channels into the lumen. From 2 and 7 steps we have strong solution of hydrochloric acid in the lumen. 8-Water passes into the lumen by osmosis because of extra ions secreted into the lumen. 16  Postprandial alkaline tide : When gastric secretion increases after a meal. excess HC03- is added to the blood by the parietal cells, so the pH of the blood is increased and becomes alkaline. 17 18  Factors affecting gastric acid secretion Factors That Stimulate Gastric Acid Secretion: Increased parasympathetic discharge (Acetylcholine) Histamine. Gastrin hormone. Sever emotional stress Hypoglycemia (through stimulating the feeding center in the hypothalamus which in turn stimulates the vagus nucleus). Factors That Inhibit Gastric Acid Secretion : Marked drop in PH of gastric juice (high acidity) that cause direct inhibition of parietal cells Decreased gastrin hormone secretion. Entero-gastric reflex. Secretin hormone , Cholecystokinin(CCK) and somatostatin. Prostaglandins have anti-histaminic effect (Inhibit Gastric Acid Secretion ) So prolonged use of anti - prostaglandins can increase the HCL secretion and increase the risk for peptic ulcer. 19 Phases of Gastric Secretion 20 1-Cephalic Phase: Stimulation of acid secretion ,when you see ,smell, think or taste food.(Conditioned reflex). Presence of food in the mouth will stimulate acid secretion. (Unconditioned reflex). The Neurogenic signals that cause the cephalic phase of gastric secretion originate in the cerebral cortex then they are transmitted by the vagus nerve to the stomach. This phase of secretion accounts for about 20% of the HCL secretion. 21  2-Gastric Phase: Once food enters the stomach, it stimulates Acid secretion due to: (1) local enteric reflexes. (2) long excitatory vagal reflexes from the stomach to the brain and back to the stomach. (3) The secretion of gastrin hormone. The gastric phase of secretion accounts for about 70 % of the total gastric secretion. 22 3-Intestinal Phase: After stomach emptying small amount of HCL still secreted by the effect of gastrin hormone but this effect is limited by inhibitory enterogastric reflex. It accounts for about 10% of acid secretion. 23 Peptic ulcer disease (PUD) It is an erosion in the mucosa of the stomach and the upper part of small intestine. It occurs due to imbalance between the rate of gastric secretion and the degree of mucosal protection. 24 (A) Causes of excessive gastric secretion: (I) Hereditary factors (2) Prolonged stress or anxiety (3) Stress ulcers are ulcers associated with increased level of glucocorticoids (4) Increased gastrin secretion Zollinger-Ellison syndrome is a rare condition in which there are tumors, called gastrinomas, secrete large amounts of the hormone gastrin, which causes the stomach to produce too much acid. (B) Causes of mucosal barrier breakdown : (1) Decreased mucus secretion (or secretion of an abnormal mucus). (2) Excessive intake of gastric irritants (smoking ,alcohol, vinegar and spices). 25 (3)NSAID-induced ulcers: due to excessive intake of NSAID which irritates the gastric mucosa and inhibits the formation of prostaglandins which normally decrease HCI secretion. (4) Infection of the gastric mucosa with certain types of bacteria (specially helicobacter pylori). It is the strongest predisposing factor for this patient's PUD (5) Curling ulcer: severe burns → decreased plasma volume → decreased gastric blood flow → hypoxic tissue injury of stomach surface epithelium → weakening of the normal mucosal barrier. (6) Cushing ulcer: brain injury → increased vagal stimulation → increased production of stomach acid. 26 Complications of PUD Upper gastrointestinal bleeding: Which may cause black or bloody stool and may lead to anemia. Common risk Gastric wall perforation : Which may cause peritonitis. Greatest risk Gastric outlet obstruction: Which may cause Bloating ,repeated vomiting and weight loss. Gastric cancer: People infected with H. pylori have an increased risk of gastric cancer 27 Treatment of peptic ulcer : Reduce or avoid triggers Sedatives (which help to relieve anxiety and stress). H. pylori eradication therapy with antibiotics. H + - K+ ATPase blockers (Proton pump inhibitors) Anti-histamine medications ( H2 antagonists ) Antacid medications (Contain alkaline ions that chemically neutralize stomach gastric acid)(ex: Calcium carbonate) 28 Case scenario A healthy 47-year-old man comes to the physician for the evaluation of an 8-week history of intermittent burning epigastric pain. By investigations he was diagnosed as a case of peptic ulcer disease. Which of the following can be a cause for increasing pain in this case? A. Histamine B. Prostaglandin C. Noradrenaline D. Somatostatin 29 References Guyton and Hall Textbook of Medical Physiology,13th edition ,Unit XII (Gastrointestinal Physiology). Chapter 64 page 809- 812 Guyton and Hall Textbook of Medical Physiology,13th edition ,Unit XII (Gastrointestinal Physiology). Chapter 65 page 821- 825 30 Thank You 31  Histology of Stomach By: Dr. Moustafa Al Sawy Dr. Shaimaa Mohamed Amer MBBCH, M.SC. M.D HISTOLOGY MBBCH, M.SC. M.D HISTOLOGY Associate Professor of Histology & Cell Biology Associate Professor of Histology & Cell Biology Certified Medical Educator  Learning objectives Knowledge & Cognition : Learning Objectives At the end of the lecture , each student will be able to: 1.Describe the histological features of the gastric mucosa and list points of differences between the cardiac, fundic and pyloric mucosae. 2.List cell types of the gastric epithelium and mention characteristic features and functions of each of them. 3.Differentiate between the esophagus and various parts of the stomach with L.M. General Structure Of GIT Tubes  Stomach Anatomically: stomach is subdivided into four regions: The cardia, fundus , body and pylorus. Histologically : stomach is subdivided into three regions: Cardiac region, fundic region, pyloric region. Gastric glands possess: Isthmus: connects the gland to bottom of a gastric pit. Neck: is the middle part. Base: is the deep part. Gastric glands are lined by: Parietal (Oxyntic), Chief (Zymogenic),Mucous neck, Stem (Regenerative) & APUD. Both cardiac & pyloric glands are similar.  Fundus of Stomach *It is made of mucosa (epithelium, corium & muscularis mucosa), submucosa, musculosa and outer serosa. 1-Mucosa: *It is thick, highly thrown into longitudinal folds (rugae) which disappear when the stomach is distended. The mucosa is made of: A-Epithelium: *It is a simple columnar epithelium. They secrete a thick, insoluble and alkaline mucus that protects the stomach from auto digestion. Their apical surfaces have microvilli covered with glycocalyx layer Their apical cytoplasm contain mucous granules. Their lateral cell membranes form junctional complex (zonulae occlumency and zonulae adherence).  Fundus of Stomach B- Lamina propria (Corium) : It is formed of dense areolar C.T. and nerve fibers. It contains the fundic glands having these characters; *Simple branched tubular glands. * Very crowded with minimal connective tissue. * Occupy the whole thickness of the mucosa. * Arranged perpendicular to the surface. *Open into the lumen by short narrow gastric pits (1/5 mucosa) lined with mucous, peptic, oxyntic, argentaffin & stem cells.  1. Mucous neck cells *Site: they are located in the neck of the glands. *LM: They are low columnar cells with pale cytoplasm & they have round nuclei and apical secretory granules.. *Function: secretion of soluble and less alkaline mucous that lubricate the secretion of the gastric contents.  2.Peptic (Chief or Central) cells: * Site: They are most numerous located in the lower part of the glands. *LM: They are pyramidal cells with basal rounded nuclei. The cytoplasm shows basal basophilia and apical acidophilia. So, it is called polar cell. *E/M: they show basal RER & a supranuclear Golgi apparatus, & apical secretory (zymogen) granules. * Function: They secrete pepsinogen, lipase & renin.  3.Oxyntic (Parietal) cells: *Site; They are less numerous located in the lower part of the glands & do not reach lumen of the gland. LM: They are rounded cells, with acidophilic cytoplasm and central rounded nuclei. *E/M: they show few RER and ribosomes, as well as well developed SER for manufacture of HCl, many intracellular canaliculi with numerous long microvilli & numerous mitochondria. * Function: They secrete HCL and intrinsic anti pernicious anemia factor that helps the absorption of Vit.B12. Parietal cells Synthesis of Hcl by Parietal cells  Medical Application In cases of atrophic gastritis, both parietal and chief cells are much less numerous, and the gastric juice has little or no acid or pepsin activity. *In humans, parietal cells are the site of production of intrinsic factor, a glycoprotein that binds to vitamin B12. *The complex of vitamin B12 with intrinsic factor is absorbed by pinocytosis into the cells in the ileum; this explains why a lack of intrinsic factor can lead to vitamin B12 deficiency. *This condition results in a disorder of the erythrocyte-forming mechanism known as pernicious anemia, usually caused by atrophic gastritis. *In a certain percentage of cases, pernicious anemia seems to be an autoimmune disease, because antibodies against parietal cell proteins are often detected in the blood of patients with the disease.  4.APUD 4- APUD ( Amine Precursor Uptake and Decarboxylation) Enteroendocrine, Enterochromaffin or Argentaffin: *Site; They are present in base of gastric glands. *LM: They are pyramidal with darkly stained round nucleus. They can be stained black with silver, and brown with dichromate salts. *E/M: They show scattered mitochondria, RER and Golgi apparatus is not prominent & numerous basal neurosecretory granules. * Function: They secrete Serotonin, Somatostatin, Endorphin &gastric hormones like Gastrin and Glucagon-like substance.  4.APUD There are at least 13 different APUD cell types. The most important types that present in gastric gland are: 1.G-cells that secrete gastrin which stimulate gastric motility. 2. D- cells that secrete somatostatin which inhibits the release of other DNES cells hormone. 3. A- cells that secrete enteroglucagon which is similar to glucagon hormone secreted by pancrease. 4. EC-cells that secrete serotonin which influence the gastric motility. 5. ECL-cells that secrete histamine which stimulate gastric secretion. EM of Enteroendocrine Cells  Medical Application *Tumors called carcinoids, which arise from the enterochromaffin cells, are responsible for the clinical symptoms caused by overproduction of serotonin. *Serotonin increases gut motility, but high levels of this hormone/neurotransmitter have been related to mucosal vasoconstriction and damage.  5.Stem Cells *They are located mostly in the neck, isthmus or gastric pits. *They are small cells with oval basal nucleus. *They can replace all gastric gland cells (pluripotent).  Fundus of Stomach C-Muscularis mucosa: formed of smooth muscles fibers arranged in inner circular and outer longitudinal layers. 2-Submucosa: Loose CT containing blood vessels, lymphatics & nerve fibers (Meissner's plexus). 3-Musculosa: It consists of Smooth muscle fibers arranged in 3 layers (inner oblique, middle circular & outer longitudinal) and Auerbach's plexus.. 4-Serosa: Loose CT containing blood vessels, nerves & lymphatics covered with mesothelium.  Pylorus of Stomach 1-Mucosa is lightly stained & less folded. 2- Lamina propria (Corium) contains the pyloric glands. 3- Pyloric glands A-They are less crowded with abundant CT in between. B-Glands are coiled tubular with many branches. C-Their gastric pits are deep and wide (1/2 mucosa). D-Glands are lined mainly by mucus cells with few APUD & oxyntic cells 4- Musculosa is made of thick inner circular (pyloric sphincter) & outer longitudinal layers Layers Fundus Pylorus Darkly stained & highly Lightly stained & less folded. folded. Fundic glands Pyloric glands *Glands are simple branched *Less crowded with tubular occupying corium. abundant CT. Mucosa *Gastric pits are shorter & *Glands are coiled tubular narrow (1/5 mucosa). with many branches occupying whole corium. *Glands are lined with mucous, peptic, oxyntic, argentaffin & *Gastric pits deep & wide stem cells. (1/2 mucosa). *Glands are lined mainly by mucous cells with few argentaffin & oxyntic cells.  Loose CT, blood vessels Loose CT, blood vessels & Submucosa & nerves. nerves. 3 layers inner oblique, Thick inner circular Musculosa middle circular and forming pyloric sphincter outer longitudinal. and outer longitudinal. Loose areolar CT Loose CT covered by Serosa covered by mesothelium. mesothelium. Fundus Pylorus  Medical Application *Gastric and duodenal ulcers are painful erosive lesions of the mucosa that may extend to deeper layers. *Such ulcers can occur anywhere between the lower esophagus and the jejunum. Causes : *Bacterial infections with Helicobacter pylori. *Effects of nonsteroidal anti-inflammatory drugs. *Overproduction of HCl or pepsin. *Lowered production or secretion of mucus or bicarbonate.  Medical Application Zollinger-Ellison syndrome Excessive secretion of gastrin by enteroendocrine cells located in the duodenum or in the pancreatic islet leading to excessive secretion of hydrochloric acid (HCl) by parietal cells. The excess acid cannot be adequately neutralized in the duodenum, thereby leading to gastric and duodenal ulcers.  Medical Application Zollinger-Ellison syndrome  Changes at gastro-esophogeal junction *Mucosa: Epithelium: stratified squamous epithelium changes to simple columnar secretory epithelium. CT corium: thick shows fundic glands. Muscularis mucosa: not changed. *Submucosa: Esophageal glands stop gradually at stomach side. *Musculosa: Thickens by the addition of an inner oblique layer (inner oblique, middle circular and outer longitudinal) at stomach side. *Adventitia or serosa: Adventitia covered with mesothelium changes to serosa at stomach side. Gastro-esophogeal junction  Case Scenario A 38-year-old man comes to the physician because of an 8-month history of upper abdominal pain. During this period, he has also had nausea, heartburn, and multiple episodes of diarrhea with no blood or mucus. He has smoked one pack of cigarettes daily for the past 18 years. He does not use alcohol or illicit drugs. Current medications include an antacid. The abdomen is soft and there is tenderness to palpation in the epigastric and umbilical areas. Upper endoscopy shows several ulcers in the duodenum and the upper jejunum as well as thick gastric folds. Gastric pH is < 2. Biopsies from the ulcers show no organisms. Which of the following tests is most likely to confirm the diagnosis? A) 24-hour esophageal pH monitoring B) Fasting serum gastrin level C) Urine metanephrine levels D) Urea breath test E) Serum vasoactive intestinal polypeptide level Any Questions?  References: 1.Basic Histology: Text & Atlas. Editor: Luiz Carlos Junqueira, MD, PhD; Jose Carneiro, MD, PhD. 14th Ed. 2. Wheatear’s functional histology. A text & color atlas.15th Ed. 3.AMBOSS platform. Thank You