1. Chronic gastritis involves swelling or inflammation of the stomach lining.

If you have this condition, you might feel

full after eating just a few bites. Chronic gastritis might be painless or cause you dull, persistent stomach pain. It
occurs slowly over time, as opposed to acute gastritis, which comes on suddenly.
In some cases, chronic gastritis is associated with ulcers and may increase your risk for stomach cancer. In most
people, however, the condition gets better quickly with treatment and has few lasting effects.

A variety of medications and conditions can irritate the lining of your stomach, leading to -- chronic gastritis. Examples:
 long-term use of certain medications (aspirin and ibuprofen)
 excessive alcohol consumption
 bacteria that cause stomach ulcers (H. pylori)
 certain illnesses (kidney failure)
 a viral infection in a weakened immune system
 persistent, intense stress
 bile flowing into the stomach (called bile reflux)

You are at greater risk for chronic gastritis if your lifestyle and dietary habits increase the acidic content of your
stomach. If you frequently eat large amounts of fats, oils, and citrus fruits and drink lots of coffee, you are at greater
risk for the condition. Similarly, drinking large amounts of alcohol long-term can lead to chronic gastritis.
A stressful lifestyle or traumatic experiences that increase anger and hostility can also increase the amount of acid in
your stomach. If you have a weakened immune system or certain illnesses, like Crohn’s disease, you are also more at
risk for chronic gastritis.

Symptoms : upper abdominal pain, indigestion or bloating, nausea &vomiting, belching, loss appetite or weight loss.
In more extreme cases, you may experience stomach bleeding and/or black stools. Seek treatment immediately if you
have black stools, vomit blood, or have a persistent stomach ache.

Diagnosis -> medical history and symptoms. A series of tests may also be necessary, including:
 a stomach ulcer bacteria test
 a stool test to look for stomach bleeding
 a blood count and an anemia test
 an endoscopy (a stomach exam using a camera attached to a long tube that is inserted into your mouth and
down into your digestive tract)

Treatments
Medications : Your doctor may prescribe medication to reduce your stomach acid. The most common medicines to
reduce gastric acid are antacids (Alka-Seltzer and Tums), H2 antagonists (Zantac), and proton-pump inhibitors
(Prilosec) available both over-the-counter and by prescription. Reducing or eliminating aspirin and similar medicines is
also recommended in order to decrease stomach irritation.

Bland diet to reduce stomach irritation. Foods to avoid include: fried foods, French fries or other vegetables fried in
oil, citrus juices, coffee, alcohol.
Recommended foods generally include foods with little oil, fat, caffeine, or citrus: all vegetables and fruits, except
citrus fruits, low-fat dairy products, lean meats, pasta and rice prepared with little or no fat

Abstrak
The term "gastritis" was first used in 1728 by the German Physician, Georg Ernst Stahl to describe the inflammation of
the inner lining of the stomach- now known to be secondary to mucosal injury (ie, cell damage and regeneration). In
the past many considered gastritis a useful histological finding, but not a disease. This all changed with the discovery
of Helicobacter pylori by Robin Warren and Barry Marshall in 1982 leading to the identification, description and
classification of a multitude of different gastritides. This article focuses on the pathophysiology, etiology, epidemiology
and prognosis of chronic gastritis.

The chronic gastritides are classified on the basis of their underlying cause (eg, H pylori, bile reflux, nonsteroidal anti-
inflammatory drugs [NSAIDs], autoimmunity or allergic response) and histopathologic pattern, which may suggest the
cause and the likely clinical course (eg, H pylori –associated multifocal atrophic gastritis). Other classifications are
based on the endoscopic appearance of the gastric mucosa (eg, varioliform gastritis).
It is important to distinguish between gastritis and gastropathy (in which there is cell damage and regeneration, but
minimal inflammation); these entities are discussed in this article because they are frequently included in the
differential diagnosis of chronic gastritis.
Chemical or reactive gastritis is caused by injury to the gastric mucosa resulting from reflux of bile and pancreatic
secretions into the stomach, but it can also be caused by exogenous substances, including NSAIDs, acetylsalicylic
acid, chemotherapeutic agents, and alcohol.[3] These chemicals cause epithelial damage, erosions, and ulcers that are
followed by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to capillaries, with mucosal
edema, hemorrhage, and increased smooth muscle in the lamina propria with minimal or no inflammation.
Because there is minimal or no inflammation in these chemical-caused lesions, gastropathy or chemical gastropathy is
a more appropriate description than chemical or reactive gastritis, as proposed by the updated Sydney classification of
gastritis. It is important to keep in mind that mixed forms of gastropathy and other types of gastritis, especially H
pylori gastritis, may coexist.
There is no universally accepted classification system (including the Sydney system and Olga staging system) that
provides an entirely satisfactory description of all of the gastritides & gastropathies. However, an etiologic classification
at least provides a direct target toward which therapy can be directed,& for this reason, such a classification is used in
this article. In many instances, chronic gastritis is a relatively minor manifestation of diseases that predominantly
manifest in other organs or manifest systemically (eg, gastritis in individuals who are immunosuppressed).
H pylori gastritis is a primary infection of the stomach and is the most frequent cause of chronic gastritis, infecting 50%
of the global population. Cases of histologically documented chronic gastritis are diagnosed as chronic gastritis of
undetermined etiology or gastritis of undetermined type when none of the findings reflect any of the described patterns
of gastritis and a specific cause cannot be identified.
For patient education resources, see the Esophagus, Stomach, and Intestine Center, as well as Gastritis.

Pathophysiology
The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or another
infection, is described in the articles specifically dealing with these diseases. The pathogenesis of the most common
forms of gastritis is described below.

H pylori–associated chronic gastritis

Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma and primary
gastric lymphoma. First described by Marshall and Warren in 1983, H pylori is a spiral gram-negative rod that has the
ability to colonize the stomach and infect the stomach. The bacteria survive within the mucous layer that covers the
gastric surface epithelium and the upper portions of the gastric foveolae. The infection is usually acquired during
childhood. Once present in the stomach, the bacteria passes through the mucous layer and becomes established at
the luminal surface of the stomach causing an intense inflammatory response of the underlying tissue.

The presence of H pylori is associated with tissue damage and the histologic finding of both an active and a chronic
gastritis. The host response to H pylori and bacterial products is composed of T and B lymphocytes, denoting chronic
gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes (PMNs)
that eventually phagocytize the bacteria. The presence of PMNs in the gastric mucosa is diagnostic of active gastritis.
Interaction of H pylori with the surface mucosa results in the release of interleukin (IL)-8, which leads to recruitment of
PMNs and may begin the entire inflammatory process. Gastric epithelial cells express class II molecules, which may
increase the inflammatory response by presenting H pylori antigens, leading to the activation of numerous
transcription factors, including NF-kB, AP-1 and CREB-1. This in turn leads to further cytokine release and more
inflammation. High levels of cytokines, particularly tumor necrosis factor-α (TNF-α)[12] and multiple interleukins (eg, IL-
1β, IL-6, IL-8, IL-10, IL-12, IL-17 and IL-18), are detected in the gastric mucosa of patients with H pylori gastritis.[10, 11]
Leukotriene levels are also quite elevated, especially the level of leukotriene B4, which is synthesized by host
neutrophils and is cytotoxic to gastric epithelium.[13] This inflammatory response leads to functional changes in the
stomach, depending on the areas of the stomach involved. When inflammation affects the gastric corpus, parietal cells
are inhibited, leading to reduced acid secretion. Continued inflammation results in loss of parietal cells, and the
reduction in acid secretion becomes permanent.

Antral inflammation alters the interplay between gastrin and somatostatin secretion, affecting G cells (gastrin-secreting
cells) and D cells (somatostatin-secreting cells), respectively. Specifically, gastrin secretion is abnormal in individuals
who are infected with H pylori, with an exaggerated meal-stimulated release of gastrin being the most prominent
abnormality.
 When infection is cured, neutrophil infiltration of tissue quickly resolves, with slower resolution of chronic inflammatory
cells. Paralleling the slow resolution of the monocytic infiltrates, meal-stimulated gastrin secretion returns to normal.

Various strains of H pylori exhibit differences in virulence factors, and these differences influence the clinical outcome
of H pylori infection. People infected with H pylori strains that secrete the vacuolating toxin A (vacA) are more likely to
develop peptic ulcers than people infected with strains that do not secrete this toxin.
Another set of virulence factors is encoded by the H pylori pathogenicity island (PAI). The PAI contains the sequence
for several genes and encodes the CAGAgene. Strains that produce CagA protein (CagA+) are associated with a
greater risk of development of gastric carcinoma and peptic ulcers. However, infection with CagA- strains also
predisposes the person to these diseases.

H pylori- associated chronic gastritis progresses according to the following 2 main topographic patterns, which have
different clinical consequences:
 Antral predominant gastritis – This is characterized by inflammation and is mostly limited to the antrum; individuals
with peptic ulcers usually demonstrate this pattern
 Multifocal atrophic gastritis – This is characterized by involvement of the corpus and gastric antrum with progressive
development of gastric atrophy (loss of the gastric glands) and partial replacement of gastric glands by an intestinal-
type epithelium (intestinal metaplasia); individuals who develop gastric carcinoma and gastric ulcers usually
demonstrate this pattern.
As previously mentioned, 50% of the world's population is infected with H Pylori.The overwhelming majority of those
infected do not develop significant clinical complications and remain carriers with asymptomatic chronic gastritis.
Some individuals who carry additional risk factors may develop peptic ulcers, gastric mucosa–associated lymphoid
tissue (MALT) lymphomas, or gastric adenocarcinomas.
An increased duodenal acid load may precipitate and wash out bile salts, which normally inhibit the growth of H
pylori. Progressive damage to the duodenum promotes gastric foveolar metaplasia, resulting in sites for H
pylori growth and more inflammation. This cycle renders the duodenal bulb increasingly unable to neutralize acid
entering from the stomach until changes in bulb structure and function are sufficient for an ulcer to develop. H
pylori can survive in areas of gastric metaplasia in the duodenum, contributing to the development of peptic ulcers. [8]
MALT lymphomas may develop in association with chronic gastritis secondary to H pylori infection. The stomach
usually lacks organized lymphoid tissue, but after infection with H pylori, lymphoid tissue is universally present.
Acquisition of gastric lymphoid tissue is thought to be due to persistent antigen stimulation from byproducts of chronic
infection with H pylori.
The continuous presence of H pylori results in the persistence of MALT in the gastric mucosa, which eventually may
progress to form low- and high-grade MALT lymphomas. MALT lymphomas are monoclonal proliferations of neoplastic
B cells that have the ability to infiltrate gastric glands. Gastric MALT lymphomas typically are low-grade T-cell–
dependent B-cell lymphomas, and the antigenic stimulus of gastric MALT lymphomas is thought to be H pylori.
Another complication of H pylori gastritis is the development of gastric carcinomas, especially in individuals who
develop extensive atrophy and intestinal metaplasia of the gastric mucosa. It is well accepted that a multistep process
initiating from H pylori related chronic inflammation of gastric mucosa progresses to chronic atrophic gastritis, intestinal
metaplasia, dysplasia, & finally leading to the development adenocarcinoma. Although the relationship between H
pylori and gastritis is constant, only a small proportion of individuals infected with H pyloridevelop gastric cancer. The
incidence of gastric cancer usually parallels incidence of H pylori infection in countries with a high incidence of gastric
cancer and is consistent with H pylori being the cause of precursor lesion, chronic atrophic gastritis.

Persistence of the organisms and associated inflammation during long-standing infection is likely to permit the
accumulation of mutations in the gastric epithelial cells’ genome, leading to an increased risk of malignant
transformation and progression to adenocarcinoma. Studies have provided evidence of the accumulation of mutations
in the gastric epithelium secondary to oxidative DNA damage associated with chronic inflammatory byproducts and
secondary to deficiency of DNA repair induced by chronic bacterial infection.
Although the role of H pylori in peptic ulcer disease is well established, the clinical role of the infection in non-ulcer or
functional dyspepsia remains highly controversial. A recent meta-analysis demonstrates that H. pylori eradication
therapy is associated with improvement of dyspeptic symptoms in patients with functional dyspepsia in Asian,
European, and American populations.[23] Although this study illustrates that H. pylori eradication may be beneficial for
symptom relief in some populations, routine H pylori testing and treatment in nonulcer dyspepsia are not currently
widely accepted. Therefore, H pylori eradication strategies in patients with nonulcer dyspepsia must be considered on
a patient-by-patient basis.
Infectious granulomatous gastritis
Granulomatous gastritis is a rare entity. Tuberculosis may affect the stomach and cause caseating granulomas. Fungi,
including cryptococcus, can also cause caseating granulomas and necrosis, a finding that is usually observed in
patients who are immunosuppressed. Granulomatous gastritis has also been associated with H. Pylori. infection.

Gastritis in patients who are immunosuppressed

Cytomegalovirus (CMV) infection of the stomach is observed in patients with underlying immunosuppression.
Histologically, a patchy, mild inflammatory infiltrate is observed in the lamina propria. Typical intranuclear eosinophilic
inclusions and, occasionally, smaller intracytoplasmic inclusions are present in gastric epithelial cells and in
endothelial or mesenchymal cells in the lamina propria. Severe necrosis may result in ulceration.
Other infectious causes of chronic gastritis in immunosuppressed patients, include the Herpes simplex virus (HSV),
which causes basophilic intranuclear inclusions in epithelial cells. Mycobacterial infections involving Mycobacterium
avium-intracellulare are characterize by difuse infiltration lamina propria by histiocytes, which rarely form granulomas.

Autoimmune atrophic gastritis

Autoimmune atrophic gastritis is associated with serum anti-parietal and anti–intrinsic factor (IF) antibodies. The
gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.
The development of chronic atrophic gastritis (sometimes called type A gastritis) limited to corpus-fundus mucosa and
marked diffuse atrophy of parietal and chief cells characterizes autoimmune atrophic gastritis. In addition to
hypochlorhydria, autoimmune gastritis is associated with serum anti-parietal and anti-IF antibodies that cause IF
deficiency, which, in turn, causes decreased availability of cobalamin, eventually leading to pernicious anemia in some
patients. Hypochlorhydria induces G-Cell (Gastrin producing) hyperplasia, leading to hypergastrinemia. Gastrin exerts
a trophic effect on enterochromaffin-like (ECL) cells and is hypothesized to be one of the mechanism leading to the
development of gastric carcinoid tumors (ECL tumors).
In autoimmune gastritis, autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-
canalicular), and plasma membrane antigens. There are two types of IF antibodies, types I and II. Type 1 antibody
prevents the attachment of B12 to IF and Type II antibody prevents attachment of the vitamin B12-intrinsic factor
complex to ileal receptors.Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the
gastric mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy.

Chronic reactive chemical gastropathy

Chronic reactive chemical gastritis is associated with long-term intake of aspirin or NSAIDs. It also develops when bile-
containing intestinal contents reflux into the stomach. Although bile reflux may occur in the intact stomach, most of the
features associated with bile reflux are typically found in patients with partial gastrectomy, in whom the lesions develop
near the surgical stoma.
The mechanisms through which bile alters the gastric epithelium involve the effects of several bile constituents. Both
lysolecithin and bile acids can disrupt the gastric mucous barrier, allowing the back diffusion of positive hydrogen ions
and resulting in cellular injury. Pancreatic juice enhances epithelial injury in addition to bile acids. In contrast to other
chronic gastropathies, minimal inflammation of the gastric mucosa typically occurs in chemical gastropathy.

Chronic noninfectious granulomatous gastritis

Noninfectious diseases are the usual cause of gastric granulomas; they include Crohn disease, sarcoidosis, and
isolated granulomatous gastritis. Crohn disease demonstrates gastric involvement in approximately 33% of the cases.
Granulomas have also been described in association with gastric malignancies, including carcinoma and malignant
lymphoma. Sarcoidlike granulomas may be observed in people who use cocaine, and foreign material is occasionally
observed in the granuloma. An underlying cause of chronic granulomatous gastritis can not be identified in up to 25%
of cases. These patients are considered to have idiopathic granulomatous gastritis (IGG).

Lymphocytic gastritis
Lymphocytic gastritis is a type of chronic gastritis characterized by dense infiltration of the surface and foveolar
epithelium by T lymphocytes and associated chronic infiltrates in the lamina propria. Because its histopathology is
similar to that of celiac disease, lymphocytic gastritis has been proposed to result from intraluminal antigens.
High anti– H pylori antibody titers have been found in patients with lymphocytic gastritis, and in limited studies, the
inflammation disappeared after H pylori was eradicated.[35] However, many patients with lymphocytic gastritis are
serologically negative for H pylori. A number of cases may develop secondary to intolerance to gluten and drugs such
as ticlopidine.
 Eosinophilic gastritis
Large numbers of eosinophils may be observed with parasitic infections such as those caused by Eustoma
rotundatum and Anisakis marina. Eosinophilic gastritis can be part of the spectrum of eosinophilic gastroenteritis.
Although the gastric antrum is commonly affected and can cause gastric outlet obstruction, this condition can affect
any segment of the GI tract and can be segmental.[37] Patients frequently have peripheral blood eosinophilia.
In some cases, especially in children, eosinophilic gastroenteritis can result from food allergy, usually to milk or soy
protein. Eosinophilic gastroenteritis can also be found in some patients with connective tissue disorders, including
scleroderma, polymyositis, and dermatomyositis.

Radiation gastritis
Radiation Gastritis usually occurs 2-9 mo after initial radiotherapy. The dose at which 5 percent of patients develop
complications at five years, when the entire stomach is irradiated, is estimated to be 50 Gy. Small doses of radiation
(up to 15 Gy) cause reversible mucosal damage, whereas higher doses cause irreversible damage with atrophy and
ischemic-related ulceration. Reversible changes consist of degenerative changes in epithelial cells and nonspecific
chronic inflammatory infiltrate in the lamina propria. Higher amounts of radiation cause permanent mucosal damage,
with atrophy of fundic glands, mucosal erosions, and capillary hemorrhage. Associated submucosal endarteritis results
in mucosal ischemia and secondary ulcer development.

Ischemic gastritis is believed to result from atherosclerotic thrombi arising from celiac & superior mesenteric artery.
Etiology : Chronic gastritis caused by either infectious or noninfectious conditions. Infectious forms of gastritis include:
 Chronic gastritis caused by H pylori infection – This is the most common cause of chronic gastritis.
 Gastritis caused by Helicobacter heilmannii infection
 Granulomatous gastritis associated with gastric infections in mycobacteriosis, syphilis, histoplasmosis,
mucormycosis, South American blastomycosis, anisakiasis, or anisakidosis
 Chronic gastritis associate with parasitic infections - Strongyloides species, schistosomiasis,/ Diphyllobothrium latum
 Gastritis caused by viral (eg, CMV or herpesvirus) infection

Noninfectious forms of gastritis include the following:

 Autoimmune gastritis
 Chemical gastropathy- usually related to chronic bile reflux, NSAID and aspirin intake
 Uremic gastropathy
 Chronic noninfectious granulomatous gastritis – may associated w/ Crohn dz, sarcoidosis, Wegener granulomatosis,
foreign bodies, cocaine use, isolated granulomatous gastritis, chronic granulomatous disease of childhood,
eosinophilic granuloma, allergic granulomatosis and vasculitis, plasma cell granulomas, rheumatoid nodules, tumoral
amyloidosis and granulomas associated with gastric carcinoma, gastric lymphoma, or Langerhans cell histiocytosis
 Lymphocytic gastritis, including gastritis associated with celiac disease (also called collagenous gastritis)
 Eosinophilic gastritis
 Radiation injury to the stomach
 Graft-versus-host disease (GVHD)
 Ischemic gastritis
 Gastritis secondary to drug therapy (NSAIDs and aspirin)
Some patients have chronic gastritis of undetermined etiology or gastritis of undetermined type (eg, autistic gastritis ).

2. Differential Diagnosis
A.Atrophic Gastritis is a histopathologic entity characterized by chronic inflammation of the gastric mucosa with loss
of gastric glandular cells and replacement by intestinal-type epithelium, pyloric-type glands, and fibrous tissue. Atrophy
of the gastric mucosa is the endpoint of chronic processes, such as chronic gastritis associated with Helicobacter
pylori infection, other unidentified environmental factors, and autoimmunity directed against gastric glandular cells.

The 2 main causes of atrophic gastritis result in distinct topographic types of gastritis, which can be distinguished
histologically. H pylori- associated atrophic gastritis is usually a multifocal process that involves both the antrum and
oxyntic mucosa of the gastric corpus and fundus, whereas autoimmune gastritis essentially is restricted to the gastric
corpus and fundus. Individuals with autoimmune gastritis may develop pernicious anemia because of extensive loss of
parietal cell mass and anti-intrinsic factor antibodies.H pylori- associated atrophic gastritis is frequently asymptomatic,
but individuals with this disease are at increased risk of developing gastric carcinoma, which may decrease following H
pylori eradication. Patients with chronic atrophic gastritis develop low gastric acid output and hypergastrinemia, which
may lead to enterochromaffin-like (ECL) cell hyperplasia and carcinoid tumors
B.Crohn Disease is an idiopathic, chronic inflammatory process that can affect any part of the gastrointestinal tract
from the mouth to anus. Individuals with this condition often experience periods of symptomatic relapse & remission.

Essential update: Risk stratification model may significantly reduce CT use in Crohn disease patients
A risk-stratification model based on C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), which are
significantly associated with complications of Crohn disease, could reduce the use of computed tomography (CT)
scans in patients reporting to the emergency room by 43%, while missing only 0.8% of emergencies, according to a
recent retrospective analysis of 613 adult patients. Researchers used logistic regression to model associations
between these laboratory values and perforation, abscess, or other serious complications. Further validation studies of
the models need to be performed.

Signs and symptoms in Crohn disease is abdominal pain and diarrhea, which may be complicated by intestinal
fistulization or obstruction. Unpredictable flares and remissions characterize the long-term course.
Other signs and symptoms of Crohn disease may include the following: Rectal bleeding, Fever, Weight loss, anorexia,
Nausea, vomiting, Malnutrition, vitamin deficiencies, Generalized fatigability, Bone loss, Psychosocial issues (eg,
depression, anxiety, and coping difficulty); pediatric patients may also experience psychological issues regarding
quality of life & body image, Growth failure in pediatric patients: May precede gastrointestinal symptoms by years

Diagnosis : Examination for Crohn disease includes the following:

 Vital signs: Normal, but possible presence of tachycardia in anemic or dehydrated patients; possible chronic
intermittent fever
 Gastrointestinal: May vary from normal to those of an acute abdomen; assess for rectal sphincter tone, gross rectal
mucosal abnormalities, presence of hematochezia
 Genitourinary: May include presence of skin tags, fistulae, ulcers, abscesses, and scarring in the perianal region;
nephrolithiasis, hydronephrosis, and enterovesical fistulae
 Musculoskeletal: Possible arthritis and arthralgia, particularly of the large joints [7]
 Dermatologic: May show pallor or jaundice, mucocutaneous or aphthous ulcers, erythema nodosum, and pyoderma
gangrenosum
 Ophthalmologic: May reveal episcleritis; possible uveitis
 Growth delay: Decreased growth velocity (eg, height), pubertal delay
 Hematologic: Hypercoagulable state

Laboratory Tests
Although laboratory results for Crohn disease are nonspecific and are of value principally for facilitating disease
management, they may also be used as surrogate markers for inflammation and nutritional status and to screen for
deficiencies of vitamins and minerals. Routine laboratory studies include the following: CBC count, Chemistry
panel,Liver function tests, Inflammatory markers, Stool studies, Serologic tests.

Imaging studies
Imaging modalities used for Crohn disease include the following: Plain abdominal radiography, Barium contrast
studies (eg, small bowel follow-through, barium enema, enteroclysis), CT scanning of the abdomen, CT enterography
or magnetic resonance enterography: Replacing small bowel follow-through studies, MRI of the pelvis, Abdominal
and/or endoscopic ultrasonography, Nuclear imaging

The following procedures may help in the evaluation of Crohn disease: Endoscopic visualization and biopsy,
Colonoscopy, ileocolonoscopy, Small bowel enteroscopy, Interventional radiology: For percutaneous drainages of
abscesses

Management  Pharmacotherapy :
 5-Aminosalicylic acid derivative agents (eg, mesalamine rectal, mesalamine, sulfasalazine, balsalazide)
 Corticosteroids (eg, prednisone, methylprednisolone, budesonide, hydrocortisone, prednisolone)
 Immunosuppressive agents (eg, mercaptopurine, methotrexate, tacrolimus)
 Monoclonal antibodies (eg, infliximab, adalimumab, certolizumab pegol, natalizumab, vedolizumab)
 Antibiotics (eg, metronidazole, ciprofloxacin)
 Antidiarrheal agents (eg, loperamide, diphenoxylate-atropine)
 Bile acid sequestrants (eg, cholestyramine, colestipol)
 Anticholinergic agents (eg, dicyclomine, hyoscyamine, propantheline)
 Surgery : Unlike ulcerative colitis, Crohn disease has no surgical cure. Most patients with Crohn disease require
surgical intervention during their lifetime.
Surgical management of the terminal ileum, ileocolon, and/or upper gastrointestinal tract may include the following :
 Resection of the affected bowel
 Ileocolostomy or proximal loop ileostomy
 Drainage of any septic foci with later definitive resection
 Strictureplasty
 Bypass
 Endoscopic dilatation of symptomatic, accessible strictures

Surgical management of the colon may include the following :

 Subtotal or total colectomy with end ileostomy (laparoscopic or open approach)
 Segmental or total colectomy with or without primary anastomosis
 Total proctocolectomy or proctectomy with stoma creation

C.Gastroesophageal Reflux Disease

Gastroesophageal reflux disease occurs when the amount of gastric juice that refluxes into the esophagus exceeds
the normal limit, causing symptoms with or without associated esophageal mucosal injury

Signs and symptoms : Heartburn, Regurgitation, Dysphagia

Abnormal reflux can cause atypical (extraesophageal) symptoms, such as the following:
 Coughing and/or wheezing
 Hoarseness, sore throat
 Otitis media
 Noncardiac chest pain
 Enamel erosion or other dental manifestations
A history of nausea, vomiting, or regurgitation should alert the physician to evaluate for delayed gastric emptying.

Diagnosis
Testing
The following studies are used to evaluate patients with suspected gastroesophageal reflux disease:
 Upper gastrointestinal endoscopy/esophagogastroduodenoscopy: Mandatory
 Esophageal manometry: Mandatory
 Ambulatory 24-hr pH monitoring: Criterion standard in establishing a diagnosis of gastroesophageal reflux disease

Imaging studies
Upper gastrointestinal contrast-enhanced studies are the initial radiologic procedure of choice in the workup
gastroesophageal reflux disease. Plain chest radiographic findings are not useful in evaluating of this condition, but
they are helpful in assessing pulmonary status and basic anatomy. Chest images may also demonstrate a large hiatal
hernia, but small hernias can be easily missed.
Currently, no role exists for computed tomography scanning, magnetic resonance imaging, or ultrasonography in the
routine evaluation of patients with reflux disease.

Management
Treatment of gastroesophageal reflux disease involves a stepwise approach. The goals are to control symptoms, to
heal esophagitis, and to prevent recurrent esophagitis or other complications. The treatment is based on lifestyle
modification and control of gastric acid secretion through medical therapy with antacids or proton pump inhibitors or
surgical treatment with corrective antireflux surgery.

Nonpharmacotherapy
Lifestyle modifications used in the management of gastroesophageal reflux disease include the following:
 Losing weight (if overweight)
 Avoiding alcohol, chocolate, citrus juice, and tomato-based products
 Avoiding peppermint, coffee, and possibly the onion family [7]
 Eating small, frequent meals rather than large meals
 Waiting 3 hours after a meal to lie down
 Refraining from ingesting food (except liquids) within 3 hours of bedtime
 Elevating the head of the bed 8 inches
 Avoiding bending or stooping positions

Pharmacotherapy
The following medications are used in the management of gastroesophageal reflux disease:
 H2 receptor antagonists (eg, ranitidine, cimetidine, famotidine, nizatidine)
 Proton pump inhibitors (eg, omeprazole, lansoprazole, rabeprazole, esomeprazole, pantoprazole)
 Prokinetic agents (eg, aluminum hydroxide)
 Antacids (eg, aluminum hydroxide, magnesium hydroxide)

Surgical option
Transthoracic and transabdominal fundoplications are performed for gastroesophageal reflux disease, including partial
(anterior or posterior) and circumferential wraps. Open and laparoscopic techniques may be used.
Placement of a device to augment the lower esophageal sphincter is another surgical option.

Indications for fundoplication include the following:

 Patients with symptoms that are not completely controlled by proton pump inhibitors
 Patients with well-controlled reflux disease who desire definitive, one-time treatment
 The presence of Barrett esophagus
 The presence of extraesophageal manifestations
 Young patients
 Poor patient compliance with regard to medications
 Postmenopausal women with osteoporosis
 Patients with cardiac conduction defects
 Cost of medical therapy

3. Helicobacter pylori-associated gastritis is characterized by an abundant inflammatory response and gastric epithelial
cell injury. Adherence of H. pylori to gastric epithelial cells seems to be required for bacterial colonization of the gastric
mucosa. Attachment of the bacterium to polarized gastric epithelial cells causes damage to microvilli and stimulates
actin polymerization, which is associated with adherence pedestal formation. Studies suggest that H. pylori directly
contributes to the injury of gastric epithelial cells by the elaboration of cytotoxic factors. The first toxin identified from H.
pylori strains, known as vacuolating cytotoxin, induces vacuole formation in eukaryotic cells. Elaborated enzymes by
H. pylori may also contribute directly to epithelial cell injury. Ammonia produced through urease activity may be toxic to
gastric epithelial cells. H. pylori protease and lipase degrade gastric mucus and disrupt the phospholipid-rich layer at
the apical epithelial cell surface, allowing for cell injury from back diffusion of gastric acid. This cell injury may lead to
cell death, believed to result from induction of apoptosis. There are sufficient data to suggest that H. pylori, through
direct pathogenic mechanisms, contributes significantly to the gastric mucosal injury associated with this infection, and
may enhance the susceptibility of gastric epithelial cells to carcinogenic conversion.

4. Long-Term Monitoring
If a patient was treated for H pylori infection, confirm that the organism has been eradicated. Evaluate eradication at
least 4 weeks after the beginning of treatment. Eradication may be assessed by means of noninvasive methods such
as the urea breath test or the stool antigen test.
Follow-up may be individualized, depending on findings during endoscopy. For example, if dysplasia is found with
endoscopy, increased surveillance is necessary. For patients with atrophic gastritis or dysplasia, follow-up endoscopy
is recommended after 6 months.