Gross Anatomy: The specimen in Figure 1 shows a Chronic Gastric Ulcer ( CGU ) – otherwise known as peptic ulcer disease. The image shows the tummy of a 66 twelvemonth old male in which portion of the posterior wall is hollowed out. This has occurred where the ulcer has broken through the mucosal liner of the tummy and affected the implicit in pancreas. In the hollow part it is possible to see an scoured arteria which has besides been affected by the ulcer.
Microscopic Anatomy: The tummy is microscopically made of four beds: mucous membrane, submucosa, muscularis externa and serous membrane. An expected alteration as a consequence of CGU is hurt of the stomachic mucosal liner. This can ensue from extra hydrochloric acid secernment, impaired mucose secernment, Helibactor pylori infection, or usage of nonsteroidal anti-inflammatory drugs ( NSAIDs ) . This consequences in ulceration. In transverse sectional scrutiny of this specimen you would see devastation to all four beds of the intestine tubing. Inflammotory response will be activated and the figure of white blood cells would be increased. During active stage of the inflammatory response, the base of the ulcer can be microscopically seen in four beds. These beds are inflammatory exudation, fibrinoid mortification, granulation tissue ( can be seen in figure 2 ) , and mature hempen connective tissue
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Figure 2- Diagram demoing the microscopic anatomy of inflammatory response to a peptic ulcer
The cardinal cause of Chronic Gastric Ulcer is harm to the stomachic mucous membrane. This can be caused by inordinate hydrochloric acid in the tummy or deficiency of mucose secernment from the surface epithelial cells. This allows incursion and a hollow ulcer signifiers which is composed of chronic inflammatory and hempen cells. On the borders of the ulcer, cell proliferation is seen ( Warrell, 2003 ) .
Helibactor pylori ( H. pylori ) is a major causative factor of CGU. H. pylori is a bacterium that through version can boom in acidic conditions. It colonizes the tummy antrum where it promotes gastrin production. This consequences from damage in somatostatin release ( Ramakrishnan & A ; Salinas, 2007 ) . Gastric infection can do stomachic wasting every bit good as a lessening in acid production which may be due to an addition in Interluken production. Interluken is a cytokine that increases the cistron look of mending advancing factors. Hence Interluken plays an of import function in stomachic ulcer healing ( Takahasi, Fujita, & A ; Yammamoto, 2001 ) .
H. pylori produces ammonia which allows it to last the acidic environment in the tummy. H. pylori secretes enzymes which play a function in damaging the stomachs mucosal liner. This causes ulceration.
The usage of nonsteroidal anti-inflammatory drugs ( NSAIDs ) can ensue in CGU. The epithelial tissue of the tummy mucous membrane secretes an indissoluble mucose which protects it from stomachic acid. Prostaglandins initiate epithelial cells to let go of mucose. NSAIDs block prostaglandins ensuing in a deficiency of epithelial cell mucose secernment doing the tummy more susceptible to ulceration ( Ramakrishnan & A ; Salinas, 2007 ) ( Warrell, 2003 ) .
Research has shown ulceration tendencies happening in households. It shows that first grade relations have a twice the hazard of acquiring stomachic ulcer. This is due to H. pylori infection. All patients infected with H. pylori develop stomachic harm of which 17 % develop a peptic ulcer. H. pylori can be transmitted orally through infected spit by nutrient and contaminated H2O and as a consequence it is normally seen developing in households ( Malaty, Graham, Isaksson, Engstrand, & A ; Pedersen, 2000 ) .
Physiologically, emphasis is a causative factor in CGU formation. However it is no longer considered the primary cause. Peoples under emotional and phyisical emphasis frequently have an increased hazard of developing ulcers. Examples of physical emphasis advancing ulcer formation are Burnss or surgey. ( Warrell, 2003 ) ( Ramakrishnan & A ; Salinas, 2007 ) .
Symptoms: The major symptom of CGU is abdominal hurting. Pain normally occurs when the tummy is empty. Other symptoms of CGU include hapless appetency, and weight loss ( Ramakrishnan & A ; Salinas, 2007 ) .
There are besides alarm symptoms for instances such as my specimen where the peptic ulcer has expanded to the point of spliting doing hematemesis ( Gralnek, Barkun, & A ; Bardou, 2008 ) . The symptoms are acute tummy hurting, bloody stools or puke. This consequences when a peptic ulcer erodes a blood vas ( as can be seen in this specimen in figure 1 ) .
Methods of Probe: The method of probe varies with symptoms presented and age. If a individual over the age of 55 nowadayss with dismay symptoms of CGU such as anaemia, haematemesis, melaena, or purging it is advised they undergo endoscopy. Endoscopy is specific to peptic ulcers and allows biopsy of lesions and a good position of the affected country ( Ramakrishnan & A ; Salinas, 2007 ) .
If the patient is under 55, H. pylori is normally tested for first. This can be done utilizing one of three trials ; a blood trial ( proving for H. pylori antibodies ) , a urea breath trial ( proving for C in breath, bespeaking presence of H. pylori ) , or a stool antigen trial ( proving for H. pylori ) . If H. pylori is found endoscopy is normally carried out every bit good as disposal of drugs that kill H pylori ( Ramakrishnan & A ; Salinas, 2007 ) .
Treatment: If the disease is caused by H. pylori, A ternary combination of drugs is needed to cut down the sourness in the tummy, protect the mucosal liner in tummy and kill the bacterium. Examples of these drugs include proton pump inhibitors, clarithomycin and Bi subsalicylate is used. Bismuth subsalicylate coats ulcers protecting them from stomachic acerb incursion. ( Gralnek, Barkun, & A ; Bardou, 2008 ) .
Features bearing on forecast: Ulcers tend to develop when people reach the age of 40 and beyond. Gastric ulcers are non normally life threatening and sometimes harmless. However in this specimen the peptic ulcer has got big, perforating more than merely the mucous membrane. As a consequence it has caused an arteria to be eroded and has integrated the tummy with the pancreas. In this scenario it is of import to acquire to the infirmary every bit shortly as possible ( Gralnek, Barkun, & A ; Bardou, 2008 ) .