My Ssec Capstone Project Anatomy The stomach can be found in the part of the abdomen between the esophagus and small intestine

Anatomy The stomach can be found in the part of the abdomen between the esophagus and small intestine

The stomach can be found in the part of the abdomen between the esophagus and small intestine (duodenum). 1
Position and parts of the stomach
There are a wide variety of positions the stomach can accommodate depending on its volume (which can constantly change), whether a person is supine or erect, degree in which the diaphragm is causing its displacement and bodily variations. In the normal, supine person the stomach can be found in the left hypochondrium, epigastric region, umbilical region and left flank. 1
The stomach can be classified as having a fundus, body, pyloric antrum, pyloric canal and pylorus. A region known as the cardial orifice (posterior to the 6th left costal cartilage) indicates the position where the esophagus can be found opening into the stomach. The fundus (posterior to the 6th rib, in line with the midclavicular line) will be found towards its left, above the horizontal line connecting the superior part of the greater curvature and the cardiac notch. At the inferior part of the lesser curvature the incisura angularis can be found and a line drawn from this point towards the opposite greater curvature indicates the inferior border of the body. It is important to note that the patient’s gastric ulcer was found at the incisura of the lesser curvature. The superior part of the stomach’s body is found at the horizontal line indicating the beginning of the fundus. Below the body of the stomach, the pyloric antrum is found which narrows to become the pyloric canal and finally pylorus. 1, 2
The stomach contains two curvatures: a concave, lesser curvature (found at the right border) which provides attachment for the lesser omentum and the inferiorly located greater curvature which provides attachment for the greater omentum. 3
Interior anatomy of stomach
During contraction the interior of the stomach has longitudinal ridges known as gastric rugae. These folds are most prominent along the greater curvature and pyloric part of the stomach. The pyloric part of the stomach is pinkish in color while the rest of the stomach appears reddish-brown. When a patient person swallows, a groove (gastric canal) is temporarily created in between longitudinal folds along the lesser curvature of the stomach. This canal provides a pathway for ingested food and fluids to follow when the stomach is primarily unfilled. 1
Structures in relation to the stomach
The left lobe of the liver, diaphragm and anterior abdominal wall can be found anterior to the stomach. Inferiorly you will find the transverse colon. The omental bursa and pancreas can be found on the posterior side. 1
Arterial supply of the stomach
The celiac trunk, which branches off from the abdominal aorta, supplies the gastric tissue with blood. The stomach’s blood supply originates from anastomoses by the left and right gastro-omental arteries running along the greater curvature and the left and right gastric arteries along the lesser curvature. Posterior and short gastric arteries provide a blood supply to the upper body and fundus of the stomach. Due to the presence of rich anastomoses (due to a high physiological requirement), the stomach is not extremely susceptible to ischemia and infarction. 1, 2

Venous supply of the stomach
The venous system of the stomach runs along its arterial supply. The right gastro-omental vein is found to drain into the superior mesenteric vein. It’s counterpart, the left gastro-omental vein, together with the short gastric veins empty into the splenic vein. The splenic vein then joins the superior mesenteric vein to form the hepatic portal vein. Furthermore, the left and right gastric veins open directly into the common hepatic vein. There is also surgically relevant vein, the prepyloric vein, which links with the right gastric vein. 1
Lymphatic drainage of the stomach
Similarly to the veins, lymphatic vessels run parallel to the arteries of the stomach. Lymph is drained from the surfaces of the stomach towards the gastro-omental and gastric lymph nodes. Thereafter, lymph runs toward the celiac lymph nodes. 1
Innervation of the stomach
The nerve supply from the T6 to T9 spinal cord segments are responsible for the sympathetic gastric innervation. These nerves run from the greater splanchnic nerve towards the celiac plexus and are then spread across the plexuses surrounding arteries such as the gastro-omental and gastric arteries. 1
The vagus nerve is responsible for the parasympathetic innervation of the stomach and this is made possible by the posterior and anterior vagal trunks. The anterior vagal trunk (originating primarily from the left vagus nerve) runs on the anterior surface of the esophagus and moves in the direction of the lesser curvature of the stomach where it forms branches towards the liver and duodenum. The hepatoduodenal ligament serves as an exit for these branches. Further on the anterior trunk gives off anterior gastric branches while moving parallel to the lesser curvature. A posterior vagal trunk (larger and originating primarily from the right vagus nerve) runs towards the stomach’s lesser curvature. It is important to note that this nerve innervates the anterior and posterior parts of the stomach. The posterior trunk lets off a celiac branch that moves toward the celiac plexus. Furthermore, the trunk gives off posterior gastric branches as it runs parallel to the lesser curvature. Parasympathetic nerve supply of the stomach is important for controlling mucosal secretions and motoric control of muscles. 1,2

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The stomach’s interior epithelium contains gastric pits which house glands that secrete gastrin, somatostatin, gastric acid, intrinsic factor, histamine, pepsinogen, gastric lipase, mucus and bicarbonate. 4
Gastrin, a hormone that increases gastric acid release, is secreted by G cells in the pyloric antrum. Secretion of this hormone can be stimulated by the stomach distending, or peptides and amino acids being present within it. Another way to stimulate the release of gastrin is through gastrin-releasing peptide (GRP) which is controlled by the enteric nervous system (ENS) – this route of stimulation is known as short reflexes. With cephalic reflexes, the vagus nerve (parasympathetic) stimulates G cells to release gastrin. By indirectly increasing the secretion of histamine and directly influencing parietal cells, gastrin increases the secretion of gastric acid. 4,5
Enterochromaffin-like cells (ECL cells) secrete histamine (paracrine secretion). Stimulation by acetylcholine or gastrin secretion causes the ECL cells to secrete histamine, and this paracrine secretion binds to the parietal cell’s H2-receptor which stimulates gastric release. 4,5
Gastric acid
Within the body of the stomach there are parietal cells – which are responsible for gastric acid (hydrochloric acid) secretion. Gastric acid fulfills many roles: It is responsible for the secretion and activation of pepsin (digests protein) within the stomach. Furthermore, it denatures proteins and thereby causes their peptide bonds to be better exposed in order to be digested by pepsin. The acid also inhibits the digestion of carbohydrates, makes amylase in saliva inactive and destroys microorganisms. 4
Pepsin and Gastric Lipase
Chief cells (in the body of the stomach) secrete pepsinogen (inactive) into the stomach lumen. The lowering of the stomach’s pH by gastric acids leads to the conversion of inactive pepsinogen to active pepsin, which is responsible for protein digestion. Vagul stimulation is the primary source which initiates pepsinogen secretion. Another enzyme, gastric lipase is secreted together with pepsinogen and they are responsible for the breaking down of triglycerides. 4,5
Somatostatin and Intrinsic factor
Somatostatin (secreted by D cells) decreases gastric acid secretion through inhibiting the secretion of histamine and gastrin. At the same time it also results in less pepsinogen being secreted. Intrinsic factor plays a vital role in the absorption of Vitamin B12 and is also secreted by the gastric parietal cells. 4
Mucus and Bicarbonate
Mucus (secreted by glandular cells) and bicarbonate (secreted by the stomach’s) epithelial cells are responsible for protecting the gastric mucosa against damage from gastric acid and pepsin. It does this by forming a physical barrier between the gastric mucosa and stomach contents. Within this barrier there is bicarbonate present and this protects the mucosa by neutralizing or inactivating any gastric acid or pepsin that should penetrate the mucus.

Additionally, prostaglandin E2 plays an important role in keeping the gastric mucosal cells healthy and by also aiding in the secretion of bicarbonate. Taking non-steroidal anti-inflammatory drugs, such as aspirin in the case of the presenting patient, causes less prostaglandin to be produced and thus leads to impaired host defenses against gastric acid. 5,6
Gastric ulcers form whenever there is an excess of gastric acid secretion or damage to the mucosal defenses which can be caused by gastric acid and pepsin .5


Anatomical pathology of peptic ulcers
Peptic ulcer disease can be subdivided into gastric and duodenal ulcers. They represent a pathological defect in the gastric mucosa which is caused by two gastric secretions – gastric acid and pepsin. 6 In the presenting case, the patient was diagnosed with a gastric ulcer – the following information regarding anatomical pathology will thus mainly focus on gastric ulceration.
Epidemiology and etiology
Gastric ulcers are known to be less common than duodenal ulcers, generally occur in individuals from a lower socio-economic class and its incidence increases with age. People who have a type A blood group are also known to be more susceptible to gastric ulcers, as opposed to having a type O blood group. 6
The most important etiological factors of peptic ulcer disease include Helicobacter pylori gastritis, the usage of non-steroidal anti-inflammatory drugs, excessive gastric acid secretion and duodeno-gastric reflux. Genetic factors also play a role. Smoking and tobacco use will also increase the risk of developing gastric ulcers. 6,7
According to the Modified Johnson Classification, the patient has a type 1 gastric ulcer. This means that it can be found, as stated before, on the lesser curvature of the stomach. It is, however, important to note that with a type 1 gastric ulcer there is not acid hypersecretion present and the main causative organism is Helicobacter pylori. Type 1 are the most common of the gastric ulcers and constitutes approximately 60% of the cases. 8
In order to diagnose H. pylori as the causative factor, one should do a urea breath test or serological test that looks for circulating antibodies. 9 Since no information was given about any of these two tests being done and a history of NSAID use by the patient it is safe to deduct that the gastric ulcer was caused by the use of NSAID’s.
Acute vs Chronic ulcers
Acute peptic ulcers usually develop as a result of acute gastritis, excessive gastric acid secretion (eg. Zollinger-Ellison syndrome) and mucosal ischemia. Chronic peptic ulcers occur mostly at sites where different types of mucosa meet. In the stomach this can be found at the incisura on the lesser curvature where the pyloric antrum meets the body. 6
Mucosal damage leads to ulcer formation. The mucosa can become damaged when the stomach’s defense mechanisms are impaired by the use of non-steroidal anti-inflammatory drugs. Using NSAID’s impairs prostaglandin secretion and result in less mucosal maintenance and bicarbonate secretion. This can then eventually lead to gastric acid and pepsin damaging the mucosa. The other important cause of peptic ulcers is the reflux of pancreatic and bile juice into the stomach. 5,6
Aspirin is the most serious NSAID when it comes to drugs that destroy the mucus barrier which is protecting the stomach lining. 10 Since the patient has been using aspirin as pain relief, it reinforces the probability that the gastric ulcer was caused by NSAID’s.

Morphology of an ulcer
Peptic ulcers can have a diameter of 20mm to well over 100 mm. An ulcer contains edges and a base. Within the base one will find exudate from polymorphs and necrotic tissue. Beneath this, granulation tissue and fibrous tissue can be found. Ulcers are known to cause stenosis of the pylorus or cause the stomach diameter to decrease in the central part.
The arteries found within the base of the ulcer often undergo luminal narrowing which can also be known as endarteritis obliterans. 6
An acute complication is when gastric contents leak out into the peritoneal cavity after the peptic ulcer becomes perforated. Bleeding can also ensue due to the erosion of a blood vessel. The patient’s blood results indicate that his hemoglobin levels are lower than the normal reference range, whereas his blood urea levels have been found to be just less than double the upper normal limit. Both these factors indicate that there was gastrointestinal bleeding due to the peptic ulcer. The lower hemoglobin is a good measure of the severity, whereas an increase in urea indicates that bleeding is present. It is also possible for the ulcer to erode into structures lying near it. For more information regarding complications, see the Medicine and Surgery section. 6,11

There are various pharmacological treatment options available for peptic ulcer disease. They include antimicrobial drugs, proton pump inhibitors, H^2-histamine receptor antagonists, prostaglandins, anti-muscarinic agents and mucosal protective agents. 7
Eradication of the Helicobacter pylori organism is known to play an integral role in the healing of a peptic ulcer and decreases the risk of relapse. The treatment regimen lasts between 7 and 14 days. 12, 13 Pharmacological treatment of the H. pylori bacteria has a 90% success rate. 13 Drugs used in combination:
(1) Azithromycin, Metronidazole and proton pump inhibitor
(2) Amoxicillin, Metronidazole and proton pump inhibitor
(3) Clarithromycin, Metronidazole and proton pump inhibitor 7
It is important to note that oral metronidazole has a worse side-effect profile and together with clarithromycin, they are also prone to developing resistance. 13
Proton pump inhibitors
It has been found that proton pump inhibitors are better in the treatment of peptic ulcer disease, in comparison with histamine receptor antagonists. 12 The mechanism of action of PPI’s is that their activated form of the drug binds irreversibly (through a covalent bond) to H^+,K^+-ATP ase. Resulting from this covalent bond is the halting of the secretion of gastric acid into the lumen by parietal cells. Their plasma is about two hours but they have a long inhibitory effect due to their covalent bonds and they have an optimal effect if taken before eating a meal. Drugs included in this class are: omeprazole, rabeprazole, lansoprazole, pantoprazole, esomeprazole and dexlansoprazole. 7, 12
Adverse effects of proton pump inhibitors include low Magnesium levels, polyps, risk of infections within the stomach, pneumonia and osteoporosis. Furthermore, PPI use also increases a person’s risk of Vitamin B12 deficiency, diarrhea and C. difficile colitis. Omeprazole, specifically, has an inhibitory effect on CYP450 enzymes and is thus prone to having drug interactions. An important drug interaction takes place between omeprazole and the drugs: cyclosporine, phenytoin, warfarin and diazepam. The PPI inhibits their metabolism which will lead to higher concentrations of these drugs to be present within the blood. Furthermore, omeprazole is also known for decreasing the pharmacological effect of clopidogrel. 7, 12
H^2-histamine receptor antagonists (H2RAs)
H2RA drugs decrease gastric acid within the stomach by competitively inhibiting acid secretion (by parietal cells) which is mediated by the presence of histamine (they effectively block the receptor to which the histamine is supposed to bind). Drugs from this class include nizatidine, ranitidine, cimetidine and famotidine. These drugs are relatively safe and their absorption is not affected by eating after taking an oral dose. Unfortunately, after a while, the body develops resistance against the inhibitory effect of this drug. 7,12