Gastritis Theoritical Background

Definition

According to Ash Dheery Putheron (2011: 32) gastritis or mag disease is an inflammation of the gastric mucus. The disease is caused by irritation of the stomach, usually strong acids.

Mansjoer Arief (2008: 492) in his book said that gastritis is inflammation of the gastric mucosa. Clinical features that are found in the form of dyspepsia or indigestion. Based on endoscopic examination found mucosa erythema while the photographs show mucosa irregularity.

Gastric Ulcer Inside The Stomach

Hislan (2010: 246) stated that simply gastritis is an inflammatory process in the gastric mucosa and sub-mucosa. Based on the opinion of experts concluded that gastritis is an inflammation that occurs in the gastric organs.

According to Mansjoer Arief (2008: 492) in his book Kapita Selekta Kedokteran, gastritis can be divided in 2 phase, those are:

Acute Gastritis

Gastritis acute usually is not too long time about< 3 months. It is a clear acute clinical abnormalities caused by special signs and symptoms. It is usually found acute inflammatory cells and neutrofi.

Chronic Gastritis

It is more than 3 months long. There are chronic inflammation that will cause mucosa atrophy and metaplasia epithelial.

 

Etiology

Based on the disease phase, the etiology of gastritis are:

Acute Gastritis

1. The etiology of this phase are:
2. Drugs : aspirin, NSAD.
3. Alcohol
4. Microcirculation disorder of stomach mucosa; trauma, burn, or sepsis.

In microscopy, there is erosive lesion of mucosa in different location.  If it is found in the corpus and funds, it is usually caused by stress. If it is caused because of NSAID, mainly found in the antrum region, but can also all of the region. While microscopically, there is erosion of epithelial regeneration, and found that minimal neutrophil inflammatory cell reaction.

 

Chronic Gastritis

The cause of this phase is unknown; it is usually multifactor with varying clinical course. This disorder is closely related to H. pylory infection.

Phatophysiology

According to Arif Muttaqin (2011: 384) there are some factors that can cause damage to the gastric mucosa, include: (1) damage mucosa barrier, which causes back diffusion of H⁺ ions increases, (2) perfusion mucosa stomach is disturbed, (3) the amount of acid high stomach.

These factors usually do not stand-alone, for example, the physical stress will cause gastric mucosa perfusion disturbed area causing small infarcts; besides it also accelerated gastric acid secretion. Mucosa barrier in physical stress patients are usually not disturbed. This is what distinguishes it from erosive gastritis because they chemicals or drugs. At reflux gastritis, gastritis that is caused by chemicals and drugs makes mucosa barrier is damaged so that back diffusion of H⁺ ions rises. Acidic conditions contained in the lumen of the stomach will accelerate the deterioration of the mucosa barrier by intestinal fluid.

On condition where patients consume alcohol along with aspirin, the effect will be more damaging than the effects of each agent separately. Diffuse hemorrhagic gastritis usually occurs in heavy alcohol drinkers and use of aspirin, these conditions can lead to the need for gastric resection. This serious illness will be considered as ulcers due to stress, because they both have a lot similarity.

Acute erosive gastritis (also called reactive gastritis) because they may occur exposure factors or agents including NSAIDs, Cocaine, and reflux of bile salts, ischemia, radiation resulting hemorrhage conditions, erosive, and ulcers. Under the influence of gravity, these agents will be on the stomach biggest curvature and give the manifestation of gastritis in the distal or closest to the accumulation agent area. The main mechanism of injury is decreased prostaglandin synthesis that responsible for producing stomach acid. Long Influence will cause fibrosis and stricture at the distal area.

Bacterial infection is another cause that can increase inflammation in the gastric mucosa. Helicobacter pylori is a bacterium that is most commonly cause acute gastritis. The prevalence of infection by Helicobacter pylori in individuals depending on age, socioeconomic, and racial. In some studies in the United States, obtained in children by 20% at age 40 years by 40%, and in the elderly by 60%. This illustrates that the increasing age, the more it will also increase the ratio of infection. The process of how the transmission of these bacteria in humans is still not known with certainty, but in some studies it is believed that the transmission of bacteria between individual to another can occur through oral-fecal route, in addition, because they can also consume water or food contaminated. This condition is considered in patients with a low socioeconomic, due to poor sanitation, and poor hygiene nutritional status.

Acute gastritis caused by H. pylori infection is usually asymptomatic. Bacteria that enter will protect itself with a layer of mucus. This layer of protection will cover and protect the gastric mucosa from gastric acid. Penetration of bacteria into the mucosa layer causes contact with gastric epithelial cell adhesion and occur-resulting in an inflammatory response through activation of the enzyme to activate IL-8. This causes gastric barrier function disrupted and there was acute gastritis.

Gastritis in tuberculosis associated with a decrease in immune function and general result of respiratory system disorder. Virus infection of cytomegalovirus or fungal infections occur in some patients with reduced immunity such as cancer, after organ transplantation, and AIDS. The condition causes the risk of chronic gastritis.

These conditions resulted in local inflammatory response, in which mucosa reddening, edema, and covered by mucus that is attached, small erosion, and bleeding. Highly variable degrees of inflammation and cause various nursing problems on patients.

Phatophysiology of chronic gastritis is still not clearly known, but there are several theories related to the level of damage in the chronic gastric mucosa surface, the gastric barrier and penetration in gastritis and gastric atrophy.

Stomach barrier and its penetration in gastritis. Absorption in stomach, usually very low.  Absorption in the stomach, normally very low. A low degree of absorption is mainly caused by two specific features of the gastric mucosa, among others: (1) ikeg dukaousu gastric mucosa cells highly resistant which secrete mucus which is very thick and sticky, and (2) the gastric mucosa have a connection to the very meeting between adjacent epithelial cells.

These two things together then added with gastric absorption barriers are another called gastric barrier. Normally, this barrier is so resistant to diffusion, even the hydrogen ion concentration of gastric fluid has a high about 100,000 times the concentration of hydrogen ions in the plasma, other than that, this barrier also seldom diffuse even through the thinnest layer of the epithelium in the gastric epithelium itself.

In gastritis, the barrier permeability is so high. Hydrogen ion diffusion into stomach epithelial caused addition damage and makes evil circle, progressive atrophy of stomach mucosa. This event also makes stomach mucosa tendency infarct peptide digestion and makes ulcus.

Gastric atrophy. In many people with autoimmune gastritis, mucosa atrophy until gradually became little or no remaining activity of gastric glands. There are also some people have the opinion that autoimmunity against the gastric mucosa, it is also ultimately lead to gastric atrophy. Loss of gastric secretion in gastric atrophy causes achlorhidra and sometimes anemia pernicious.  Achlorhidria means fail to secrete hydrochloric acid in the stomach and it was diagnosed when the pH of gastric secretion fails to fall below 6.5 after maximal stimulation. Hypochlorhidria means reduced acid secretion, usually when the acid is not secreted; it is also not secreted pepsin. Even if there is, the loss of acid will inhibit the function of pepsin is also not secreted. Even if it happened, the absences will inhibit the pepsin function because pepsin needs medium acid to work. Although achorhidria associated with a reduction or even lack of digestion by gastric capacity, the overall digestion of food in the gastrointestinal tract remains almost all normal. It actually happened because the trypsin and other enzymes that is secreted by the pancreas is still able to digest most of the proteins in the food.

Anemia pernicious often accompanies achlorhidria and gastric atrophy. Normal gastric secretion contains a glycoprotein called intrinsic factor secreted by parietal cells that secrete the old with hydrochloric acid; intrinsic factor vitamin B12 join and then protect it from destruction during digestion and pass through the gastrointestinal tract. Then, when vitamin B12 intrinsic factor complex reaches the terminal ileum, intrinsic factor binds to the receptor on the surface of the ileal epithelium. This, in turn makes vitamin B12 can be absorbed. In the absence of intrinsic factor, only about one over fifth of vitamin B12 is absorbed. Because of that, the amount of vitamin B12 is not obtained adequate food so that there is a failure of maturation in the bone marrow caused anemia pernicious.

Helicobacter pylori is a gram negative bacteria that form mucus layer and cover the surface of the gastric epithelium. The presence of these bacteria will cause tissue damage. The body's response to bacteria is producing cells infiltrating lymphocytes and lamina propria and gastric epithelium by leukocytes polymononuclear that phagocyte bacteria. Polymononuclear accumulation of leukocytes in the gastric mucosa causes active inflammation of the gastric mucosa. Interaction of H. pylori to mocuse results in the release of pro-inflammatory cytokines IL-8, which will increase the recruitment of polymorphonuclear cells that will initiate the inflammatory process as a whole.

An increase in acid precipitation duodenum will also be spending bile salts that normally would inhibit the growth of H. pylori. Progressive damage also occurs in the duodenum and presents metaplasia in the stomach. With the process is repeated, and then there will be interference structure in the duodenum and stomach, resulting in the formation of networks of peptic ulcer and gastric cancer cause.Tuberculosis and fungi will influence granular for mation in the gaster. This condition progressively will make necrosis and gastritis granuloma.

Lymphocyte gastritis is a type of chronic inflammation of the gastric mucosa with thickening and foveolt surface epithelium by T lymphocytes and is accompanied by infiltrate in the lamina propria. The existence of a high response to anti Helicobacter pylori increases the production of lymphocytes to perform phagocytes of bacteria, then this in turn results in an accumulation on the surface of the mucosa and cause inflammation.

Eosinophilic Gastritis caused by selective infiltration of eosinophils in the gastric mucosa. Although these conditions still are idiopathic, but in some studies mentioned the role of pro-inflammatory cytokines as an important factor of the occurrence of gastritis eosinophils.

Small doses of radiation can cause reversible mucosa damage, whereas the high dose of radiation will cause irreversible damage and related conditions as well as atrophy and ischemic ulcers. Radiation effects such as permanent mucosa damage, tissue atrophy funds, mucosa erosion and bleeding capillaries progressive will develop the radiation gastritis.

Ischemia gastritis is believed as a condition caused by thrombus which block the artery seliac and mesenteric superior. This condition will decrease blood flow in many stomach area and it will cause ischemic reaction in that area by inflammation around it. Chronic gastritis will rise manifestation, especially nursing problem in patient.

 

Sign and Symptoms

Acute Gastritis

Dyspepsia syndromes such as epigastric pain, nausea, bloating, vomiting. Gastrointestinal bleeding was found also in the form of haematemesis and melaena, followed by signs of anemia after bleeding. Usually, if it is done over the history, there is a history of the use of drugs or certain chemicals.

Chronic Gastritis

Most clients do not have any complaints. Only a small portion complained of heartburn, nausea, anorexia, and on physical examination did not reveal any abnormalities.

Diagnostic Examination

Arif Mansjoer (2008: 492) stated that the diagnostic examination that we can do are:

Endoscopy and radiology mucosa to find a picture of acute lesions in the gastric mucosa in the form of erosion or shallow ulcer with a flat edge.

Single-contrast or double contrast, to know or see the surface of the superficial lesions

Gastric mucosa biopsy to determine the presence of bacteria in gastritis, as the most important bacterial cause of gastritis is Helicobacter pylori.

Treatment

Arif Mansjoer (2008:493) in his book, Kapita Selekta Kedokteran, explained that treatment for gastritis: 

Acute Phase

1. Handling the etiology
2. Gastric diet with small portion but often.
3. H₂Antagonist receptor.
4. Anticholenergic, if excessive acid production.
5. Antaside before meal.

Chronic Phase

1. Handling and avoiding acute gastritis etiology.
2. Antsida, H₂ antagonist caused by pro-kinetic drugs.
3. Eradication Helicobacter pylori that has relation with infection of that bacteria.

Complication

1. Bleeding in upper intestine.
2. Ulcer.
3. Perforation
4. Anemia pernicious

Prognosis

Patient generally heal from acute gastritis within a few days. The incidence of gastric ulcer and gastric cancer increased in chronic gastritis type A. Gastritis can cause gastrointestinal bleeding complications and recurrent clinical symptoms.