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Gross Anatomy: The specimen in Figure 1 shows a Chronic Gastric Ulcer (CGU) - otherwise known as peptic ulcer disease. The picture shows the stomach of a 66 year old male in which part of the posterior wall is hollowed out. This has occurred where the ulcer has broken through the mucosal lining of the stomach and affected the underlying pancreas. In the hollow region it is possible to see an eroded artery which has also been affected by the ulcer.
Microscopic Anatomy: The stomach is microscopically made of four layers: mucosa, submucosa, muscularis externa and serosa. An expected change as a result of CGU is injury of the gastric mucosal lining. This can result from excess hydrochloric acid secretion, impaired mucous secretion, Helibactor pylori infection, or use of nonsteroidal anti-inflammatory drugs (NSAIDs). This results in ulceration. In cross sectional examination of this specimen you would see destruction to all four layers of the gut tube. Inflammotory response will be activated and the number of white blood cells would be increased. During active phase of the inflammatory response, the base of the ulcer can be microscopically seen in four layers. These layers are inflammatory exudate, fibrinoid necrosis, granulation tissue (can be seen in figure 2),and mature fibrous connective tissue
Figure 2- Diagram showing the microscopic anatomy of inflammatory response to a peptic ulcer
The fundamental cause of Chronic Gastric Ulcer is damage to the gastric mucosa. This can be caused by excessive hydrochloric acid in the stomach or lack of mucous secretion from the surface epithelial cells. This allows penetration and a hollow ulcer forms which is composed of chronic inflammatory and fibrous cells. On the margins of the ulcer, cell proliferation is seen (Warrell, 2003).
Helibactor pylori (H. pylori) is a major causative factor of CGU. H. pylori is a bacteria that through adaptation can thrive in acidic conditions. It colonizes the stomach antrum where it promotes gastrin production. This results from impairment in somatostatin release (Ramakrishnan & Salinas, 2007). Gastric infection can cause gastric atrophy as well as a decrease in acid production which may be due to an increase in Interluken production. Interluken is a cytokine that increases the gene expression of healing promoting factors. Hence Interluken plays an important role in gastric ulcer healing (Takahasi, Fujita, & Yammamoto, 2001).
H. pylori produces ammonia which allows it to survive the acidic environment in the stomach . H. pylori secretes enzymes which play a role in damaging the stomachs mucosal lining. This causes ulceration.
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) can result in CGU. The epithelium of the stomach mucosa secretes an insoluble mucous which protects it from gastric acid. Prostaglandins initiate epithelial cells to release mucous. NSAIDs block prostaglandins resulting in a lack of epithelial cell mucous secretion making the stomach more susceptible to ulceration (Ramakrishnan & Salinas, 2007) (Warrell, 2003).
Research has shown ulceration trends occurring in families. It shows that first degree relatives have a twice the risk of getting gastric ulcer. This is due to H. pylori infection. All patients infected with H. pylori develop gastric damage of which 17% develop a peptic ulcer. H. pylori can be transmitted orally through infected saliva by food and contaminated water and as a result it is commonly seen developing in families (Malaty, Graham, Isaksson, Engstrand, & Pedersen, 2000).
Physiologically, stress is a causative factor in CGU formation. However it is no longer considered the primary cause. People under emotional and phyisical stress often have an increased risk of developing ulcers. Examples of physical stress promoting ulcer formation are burns or surgey. (Warrell, 2003) (Ramakrishnan & Salinas, 2007).
Symptoms: The major symptom of CGU is abdominal pain. Pain commonly occurs when the stomach is empty. Other symptoms of CGU include poor appetite, and weight loss (Ramakrishnan & Salinas, 2007).
There are also alarm symptoms for cases such as my specimen where the peptic ulcer has expanded to the point of bursting causing haematemesis (Gralnek, Barkun, & Bardou, 2008). The symptoms are acute stomach pain, bloody stools or vomit. This results when a peptic ulcer erodes a blood vessel (as can be seen in this specimen in figure 1).
Methods of Investigation: The method of investigation varies with symptoms presented and age. If a person over the age of 55 presents with alarm symptoms of CGU such as anemia, hematemesis, melena, or vomiting it is advised they undergo endoscopy. Endoscopy is specific to peptic ulcers and allows biopsy of lesions and a good view of the affected area (Ramakrishnan & Salinas, 2007).
If the patient is under 55, H. pylori is usually tested for first. This can be done using one of three tests; a blood test (testing for H. pylori antibodies), a urea breath test (testing for carbon in breath, indicating presence of H. pylori), or a stool antigen test (testing for H. pylori). If H. pylori is found endoscopy is usually carried out as well as administration of drugs that kill H pylori (Ramakrishnan & Salinas, 2007).
Treatment: If the disease is caused by H. pylori, A triple combination of drugs is needed to reduce the acidity in the stomach, protect the mucosal lining in stomach and kill the bacteria. Examples of these drugs include proton pump inhibitors, clarithomycin and bismuth subsalicylate is used. Bismuth subsalicylate coats ulcers protecting them from gastric acid penetration. (Gralnek, Barkun, & Bardou, 2008).
Features bearing on prognosis: Ulcers tend to develop when people reach the age of 40 and beyond. Gastric ulcers are not usually life threatening and sometimes harmless. However in this specimen the peptic ulcer has got large, penetrating more than just the mucosa. As a result it has caused an artery to be eroded and has integrated the stomach with the pancreas. In this scenario it is important to get to the hospital as soon as possible (Gralnek, Barkun, & Bardou, 2008).