acute gastritis

[ACUTE GASTRITIS]

• Acute gastritis is a sudden inflammation of the lining of the stomach.

• The inflammation may involve the entire stomach (pangastritis) or a region of the stomach (eg, antral gastritis). Acute gastritis can be broken down into 2 categories:

i. erosive (eg, superficial erosions, deep erosions, hemorrhagic erosions) ii. non-erosive (generally caused by Helicobacter pylori).

Pathophysiology:

Acute gastritis has a number of causes:

- certain drugs- alcohol

- bile

- ischemia

- bacterial

- viral

- fungal infections

- acute stress (shock)

- radiation

- allergy and food poisoning

- direct trauma.

The common mechanism of injury is an imbalance between the aggressive and the defensive factors that maintain the integrity of the gastric lining (mucosa).

Acute erosive gastritis can result from the exposure to a variety of agents or factors. This is referred to as reactive gastritis. These agents/factors include:

- nonsteroidal anti-inflammatory medications (NSAIDs)- alcohol

- cocaine

- stress

- radiation

- bile reflux

- ischemia.

• The gastric mucosa exhibits hemorrhages, erosions, and ulcers.

[NSAIDs]

• NSAIDs, such as aspirin, ibuprofen, and naproxen, are the most common agents associated with acute erosive gastritis.

• Because of gravity, the inciting agents lie on the greater curvature of the stomach the development of acute gastritis distally on or near the greater curvature of the stomach in the case of orally administered NSAIDs.

• However, the major mechanism of injury is the reduction in prostaglandin synthesis. PG responsible for maintaining mechanisms that result in the protection of the mucosa from the injurious effects of the gastric acid.

[Bacterial infection]

H pylori is the most common cause of gastritis.

• The infection is usually acquired in childhood.

• Transmission is likely from person to person through the oral-fecal route or through the ingestion of contaminated water or food the prevalence is higher in lower socioeconomic classes and in developing countries.

• H pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time, it may extend to involve the entire gastric mucosa resulting in chronic gastritis.

• The acute gastritis encountered with H pylori is usually asymptomatic. The bacterium imbeds itself in the mucous layer, a protective layer that coats the gastric mucosa. It protects itself from the acidity of the stomach through the production of large amounts of urease catalyzes the breakdown of urea to the alkaline ammonia and carbon dioxide.

• The alkaline ammonia neutralizes the gastric acid in the immediate vicinity of the bacterium conferring protection.

• It produces inflammation via the production of a number of toxins and enzymes.

• The intense inflammation can result in the loss of gastric glands responsible for the production of acid atrophic gastritis. Consequently, gastric acid production drops.

[TB]

• rare cause of gastritis, but an increasing number of cases have developed because of patients who are immunocompromised.

• Gastritis caused by tuberculosis is generally associated with pulmonary or disseminated disease.

[Secondary syphilis of the stomach]

• rare cause of gastritis.

[Phlegmonous gastritis]

• is an uncommon form of gastritis caused by numerous bacterial agents:

- streptococci- staphylococci

- Proteus species

- Clostridium species

- Escherichia coli.

• Phlegmonous gastritis usually occurs in individuals who are debilitated. It is associated with a recent large intake of alcohol, a concomitant upper respiratory tract infection, and AIDS.

• Phlegmonous means a diffuse spreading inflammation of or within connective tissue. In the stomach, it implies infection of the deeper layers of the stomach (submucosa and muscularis). As a result, purulent bacterial infection may lead to gangrene.

• Phlegmonous gastritis is rare.

[Viral infections]

• Cytomegalovirus (CMV) is a common viral cause of gastritis.

• It is usually encountered in individuals who are immunocompromised, including those with cancer, immunosuppression, transplants, and AIDS.

• Gastric involvement can be localized or diffuse.

[Fungal infections]

• eg: Candida albicans and histoplasmosis

• The common predisposing factor is immunosuppression.

• C albicans rarely involves the gastric mucosa

• Disseminated histoplasmosis can involve the stomach. The usual presenting clinical feature is bleeding from gastric ulcers or erosions on giant gastric folds.

[Parasitic infections]

• rare causes of gastritis.

• Anisakidosis is caused by a nematode that embeds itself in the gastric mucosa along the greater curvature.

• Anisakidosis is acquired by eating contaminated sushi and other types of contaminated raw fish.

• It often causes severe abdominal pain that subsides within a few days. This nematode infection is associated with gastric fold swelling, erosions, and ulcers.

Causes:

Drugs

o NSAIDs, such as aspirin, ibuprofen, and naproxen

o Cocaine

Potent alcoholic beverages, such as whisky, vodka, and gin

Bacterial infections

o H pylori (most frequent) o H heilmanii (rare) o Streptococci (rare) o Staphylococci (rare)

o Proteus species (rare) o Clostridium species (rare) o E coli (rare) o Tuberculosis (rare) o Secondary syphilis (rare)

Viral infections (eg, CMV)

Fungal infections most often in AIDS pto Candidiasiso Histoplasmosis

o Phycomycosis Parasitic infection (eg, anisakidosis)

Acute stress (shock)

Radiation

Allergy and food poisoning

Bile: The reflux of bile (an alkaline medium important for the activation of digestive enzymes in the small intestine) from the small intestine to the stomach can induce gastritis.

Ischemia: This term is used to refer to damage induced by decreased blood supply to the stomach. This rare etiology is due to the rich blood supply to the stomach.

Direct trauma

Symptoms:

Abdominal indigestion Loss of appetite Nausea Vomiting Vomiting blood or coffee-ground like material Dark stools Belching Bloating Fever Chills Hiccups

INVESTIGATIONS:

A number of laboratory tests are usually ordered.

o Complete blood count (CBC) to assess for anemia, as acute gastritis can cause gastrointestinal bleeding

o Liver and kidney function tests

o Gallbladder and pancreatic function tests

o Pregnancy test

o Stool for blood

Imaging Studies:

Four radiologic signs of acute gastritis are fairly consistent regardless of the etiology. These signs include thick folds, inflammatory nodules, coarse area gastrica, and erosions.

o Thick folds are defined by a size greater than 5 mm in caliber. These folds are measured on radiographs with the stomach moderately distended. If thick folds are found in a patient who is symptomatic, H pylori is generally involved.

o Nodularity of the gastric mucosa (bumpy appearance) is a second sign of acute or subacute gastritis. Its origin is uncertain. Nodules may represent erosions that have epithelialized (healed) but still have the associated edema. Compared with benign neoplastic polyps, gastritis-related nodules are smaller, and their edges are less well defined. They taper onto the adjacent mucosa, and they are seen most often in the distal

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stomach. Nodules due to gastritis are referred to as inflammatory. They generally line up on the folds of the gastric antrum and are a characteristic appearance of gastritis.

o Enlarged area gastrica are a sign of gastritis that is not strongly associated with a specific cause. They usually are 1-3 mm in size. Enlargement of these areas may reflect inflammatory swelling and is often associated with gastritis. Because of the loss of the mucosal layer, the barium suspension can more completely fill the intervening grooves.

o Gastric erosions are noted to be one of the most specific signs of gastritis. Erosions may be linear or serpiginous. They may be accompanied by edema and may be seen on or near the greater curvature of the stomach. A double-contrast examination usually is required to best reveal gastric erosions.

Tomography scan and plain films of the abdomen can demonstrate thickening of the gastric wall in the case of phlegmonous gastritis.

Double-contrast barium radiography can demonstrate the nematodes that cause anisakidosis.

Other Tests:

A number of H pylori tests are available. They are classified as either nonendoscopy based or endoscopy based.

o Three nonendoscopy-based H pylori tests: The first test is the H pylori stool antigen test (HpSA). This test is based on the

detection of the H pylori antigen in the stool. It has sensitivity and specificity of greater than 90%. It can be used for both the diagnosis of H pylori and the confirmation of eradication after therapy.

The second test is an urea breath test. It uses 13C- or 14C-labeled urea taken orally. H pylori metabolizes the urea and liberates labeled carbon dioxide that is exhaled. This, in turn, can be quantified in breath samples. The sensitivity and specificity of the urea breath test is greater than 90%. This is considered the noninvasive diagnostic method of choice in situations where endoscopy is not indicated. It can also be used to confirm eradication after therapy.

The third test depends on the presence of antibodies to H pylori in the serum . The major drawback to this test is that serologic assays may remain positive for as long as 3 years after eradication of the bacteria. Therefore, serologic assays are often unreliable to document eradication of H pylori. This test can be used for the diagnosis of H pylori, provided that the patient has not received any prior therapy for it.

o Three endoscopy-based H pylori tests: The first test is the rapid urease test (RUT). It is performed by placing a gastric

biopsy specimen, obtained on endoscopy, onto a gel- or membrane-containing urea and a pH-sensitive indicator. If H pylori is present, the bacterial urease

hydrolyzes urea and changes the color of the media. The sensitivity and specificity of this test is greater than 90%.

Another test is a bacterial culture H pylori. It is highly specific but is not widely used because of the degree of expertise required. It is used when antibiotic susceptibilities are necessary.

Histologic detection of H pylori in the biopsy specimen is another endoscopy-based test. Appropriate staining is achieved using such stains as hematoxylin and eosin, Warthin-Starry, Giemsa, or Genta.

Mycobacterium tuberculosis may be diagnosed when acid-fast stain detects the bacilli in a biopsy specimen.

Syphilis may be diagnosed when the organism is found in the gastric mucosa. Endoscopic biopsy, silver impregnation, and fluorescent antibody techniques also can be used.

U Endoscopy may reveal a thickened, edematous, nonpliable wall with erosions and reddened gastric folds. The edema can be severe resulting in gastric outlet obstruction. Ulcers and frank bleeding might be present.

U The nematodes that cause anisakidosis can be seen on endoscopy.

U Endoscopy can be used to help diagnose gastric syphilis and tuberculosis (TB).

Complications:

Bleeding from an erosion or ulcer

Gastric outlet obstruction due to edema limiting the adequate transfer of food from the stomach to the small intestine

Dehydration from vomiting

Renal insufficiency as a result of dehydration

Treatment

Treatment depends on the cause of the gastritis. Antacids or other medications to decrease or neutralize gastric acid in the stomach will usually eliminate the symptoms and promote healing. Medications that cause gastritis should be discontinued. A gastric ulcer may be present, requiring treatment.

Gastritis due to stress is best treated by prevention. Medications to decrease gastric acid production such as proton pump inhibitors should be given to stressed hospital patients.

Medical Care:

Administer medical therapy as needed, depending on the cause and the pathological findings.

No specific therapy exists for acute gastritis, except for cases caused by H pylori.

Administer fluids and electrolytes as required, particularly if the patient is vomiting.

Discontinue the use of drugs known to cause gastritis (eg, NSAIDs, alcohol).


Surgical Care: Surgical intervention is not necessary, except in the case of phlegmonous gastritis. With this entity, surgical intervention with resection of the affected area may be the most effective form of treatment.

Specific treatment is dependent on the etiology of gastritis.

According to the Centers for Disease Control and Prevention (CDC), the treatment of TB consists of a 2-month period of daily isoniazid, rifampin, and pyrazinamide, followed by 4 months of daily isoniazid along with rifampin. See Tuberculosis.

Medical management generally is ineffective in treating phlegmonous gastritis. No effective antiviral therapy exists for the treatment of human cytomegalovirus (HCMV) infection, though 2 agents (ie, ganciclovir, foscarnet) have been shown to be virostatic. See Cytomegalovirus.

The treatment of C albicans includes a variety of agents, including nystatin, oral clotrimazole, itraconazole, fluconazole, amphotericin B, and ketoconazole. See Candidiasis.

The treatment of disseminated histoplasmosis includes a variety of agents, including amphotericin B, itraconazole, and fluconazole. They have all been determined to be effective. See Histoplasmosis.

No drugs are available to treat anisakidosis. Endoscopic removal may be necessary.

Drug Category: Antacids -- Used for general prophylaxis. Antacids containing aluminum and magnesium can help relieve symptoms of gastritis by neutralizing gastric acids. These agents are inexpensive and safe.

Drug Name

Aluminum and magnesium hydroxide, magnesia and alumina oral suspension (Rulox) -- Drug combination that neutralizes gastric acidity and increases pH of the stomach and duodenal bulb. Aluminum ions inhibit smooth-muscle contraction and inhibit gastric emptying. Magnesium/aluminum antacid mixtures are used to avoid bowel function changes.

Adult Dose 5-15 mL PO; 650 mg to 1.3 g tab PO qid

Pediatric Dose 0.5 mL/kg PO qid prior to eating

Contraindications Documented hypersensitivity

Interactions

Decreases effects of allopurinol, amprenavir, chloroquine, corticosteroids, diflunisal, digoxin, ethambutol, iron salts, H2-antagonists, isoniazid, penicillamine, phenothiazines, tetracyclines, thyroid hormones, and ticlopidine; increases effects of benzodiazepines and amphetamine; may cause aluminum toxicity with ascorbic acid; aluminum and magnesium potentiate effects of valproic acid, sulfonylureas, quinidine, and levodopa

PregnancyC - Safety for use during pregnancy has not been established.

Precautions Antacids may mask the symptoms of internal bleeding secondary to NSAIDs; magnesium-containing antacids may cause diarrhea and potentially lead to dehydration;

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caution with aluminum-containing antacids in patients who recently have had a massive upper GI hemorrhage

Drug Category: H2 blockers -- This class includes drugs whose mechanism of action is competitive inhibition of histamine at the histamine 2 (H2) receptor. Histamine plays an important role in gastric acid secretion, thereby making H2 blockers effective suppressors of basal gastric acid output and acid output stimulated by food and the neurological system. When used alone, they are frequently used as antisecretory drugs in H pylori therapy regimens. There are different drugs with different potencies and half-lives (eg, cimetidine, ranitidine, famotidine, nizatidine). Cimetidine will be discussed below as a representative of this class of drugs.

Drug Name

Cimetidine (Tagamet) -- Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

Adult Dose150 mg PO qid; not to exceed 600 mg/d50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d

Pediatric DoseNot establishedSuggested dose is 10-20 mg/kg/d PO/IV divided q6h; not to exceed 40 mg/d


Interactions

Can increase blood levels of theophylline, warfarin, tricyclic antidepressants, triamterene, phenytoin, quinidine, propranolol, metronidazole, procainamide, and lidocaine

Pregnancy B - Usually safe but benefits must outweigh the risks.

Precautions Elderly may experience confusional states; may cause impotence and gynecomastia in young males; may increase levels of many drugs; adjust dose or

discontinue treatment if changes in renal function occur; may increase risk of necrotizing enterocolitis in premature infants

Drug Category: Proton pump inhibitors -- Proton pump inhibitors are potent inhibitors of the proton (acid) pump (ie, the enzyme H+,K+-ATPase), located in the apical secretory membrane of the gastric acid secretory cells (parietal cell). Proton pump inhibitors can completely inhibit acid secretion and have a long duration of action. They are the most effective gastric acid blockers. Omeprazole will be discussed as a representative of this class of drugs.

Drug NameOmeprazole (Prilosec) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.

Adult Dose 20 mg PO bid

Pediatric Dose Not established


InteractionsMay decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin


Precautions Bioavailability may increase in the elderly

Drug Category: Antibiotics -- Bacterial infections also can cause gastritis. The most common causative organism is H pylori. A number of therapeutic regimens are effective against H pylori. Single antimicrobial agents generally are not recommended because of the potential development of resistance.

Dual therapy includes a proton pump inhibitor plus amoxicillin (no longer recommended because eradication rates are 30-80%) or a proton pump inhibitor plus clarithromycin (eradication rate of roughly 71%). Adding a second antimicrobial agent is recommended for successful eradication. Triple regimens are preferred in clinical practice. One drug is a proton pump inhibitor or a bismuth-based drug, the second drug is clarithromycin, and the third drug is amoxicillin or metronidazole. Quadruple therapy regimens (ie, 2 antibiotics, bismuth, antisecretory agent) generally are effective; however, because more drugs are prescribed and taken, increased adverse effects and decreased patient compliance can occur. This regimen is used in the event that triple therapy fails. The decision of which medications to use is based on the following 4 criteria: (1) the different toxicities of the various medications, (2) the relative costs of each medication and regimen, (3) the emergence of antimicrobial-resistant bacteria, and (4) the level of patient compliance.

Drug Name

Amoxicillin (Amoxil, Trimox) -- Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Adult Dose 500 mg PO qid



Interactions Reduces the efficacy of oral contraceptives


Precautions Adjust dose in patients with renal impairment

Drug NameTetracycline (Sumycin) -- Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s).


Pediatric Dose<8 years: Not recommended>8 years: Not established

ContraindicationsDocumented hypersensitivity; severe hepatic dysfunction

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants

Pregnancy D - Unsafe in pregnancy

Precautions

Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in patients with renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines

Drug NameMetronidazole (Flagyl) -- Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.




Interactions

Cimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol


PrecautionsAdjust dose in patients with hepatic disease; monitor for seizures and development of peripheral neuropathy

Drug Name

Clarithromycin (Biaxin) -- Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from ribosomes and causing RNA-dependent protein synthesis to arrest.

Adult Dose 500 mg PO bid/tid


ContraindicationsDocumented hypersensitivity; coadministration of pimozide or cisapride

Interactions

Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; clarithromycin effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; serious cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents


Precautions

Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer one half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Drug Category: Antidiarrheal agents -- Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists to eradicate H pylori.

Drug NameBismuth subsalicylate (Bismatrol, Pepto-Bismol) -- Drug combination that treats active duodenal ulcer associated with H pylori.




Interactions

Coadministration with anticoagulants may increase risk of bleeding; may increase toxicity of aspirin and hypoglycemics; decreases effects of tetracyclines and uricosurics


Precautions May cause temporary and harmless darkening of tongue and/or black stool; alcohol consumption may

cause abdominal cramps, nausea, and vomiting

[CHRONIC GASTRITIS]

Chronic gastritis is an inflammation of the lining of the stomach that occurs gradually and persists for a prolonged time.

Causes, incidence, and risk factors

Chronic gastritis may be caused by prolonged irritation:

- from the use of nonsteroidal anti-inflammatory drugs (NSAIDs)- infection with the bacteria Helicobacter pylori

- pernicious anemia (an autoimmune disorder)

- degeneration of the lining of the stomach from age

- chronic bile reflux.

U Many people with chronic gastritis have no symptoms of the condition.

Pathophysiology:



• The pathophysiology of chronic gastritis complicating a systemic disease, such as hepatic cirrhosis, uremia, or another infection. The pathogenesis of the most common forms of gastritis is described as follows.

H pylori–associated chronic gastritis

• The host response to H pylori and bacterial products is composed of T- and B-cell lymphocytes, denoting chronic gastritis, followed by infiltration of the lamina propria and gastric epithelium by polymorphonuclear leukocytes that eventually phagocytize the bacteria.

• The presence of polymorphonuclear leukocytes in the gastric mucosa is diagnostic of active gastritis.

• The interaction of H pylori with the surface mucosa results in the release of proinflammatory cytokine interleukin (IL)-8, which leads to recruitment of polymorphonuclear cells 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 further cytokine release and more inflammation. High levels of cytokines, particularly tumor necrosis factor- (TNF-) and multiple ILs (eg, IL-6, IL-8, IL-10), are detected in the gastric mucosa of patients with H pylori gastritis.

• Leukotriene levels are also quite elevated, especially leukotriene B4, which is synthesized by host neutrophils and is cytotoxic to gastric epithelium. 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.

• Differences in virulence factors that characterize different strains of H pylori influence the clinical outcome of H pylori infection. Eg:

- 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.

- H pylori pathogenicity island (PAI). The PAI contains the sequence for several genes and encodes the CAGA gene.

- Strains that produce CagA protein (CagA+) greater risk of development of gastric carcinoma and peptic ulcer. However, infection with CagA- strains also predisposes the person to these diseases.

• H pylori–associated chronic gastritis progresses with the following 2 main topographic patterns that have different clinical consequences:

Antral predominant gastritis is characterized by inflammation and is mostly limited to the antrum. Individuals with peptic ulcers usually demonstrate this pattern of gastritis.

Multifocal atrophic gastritis 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 of gastritis.

Infectious granulomatous gastritis

• rare.

• Tuberculosis may affect the stomach and cause caseating granulomas.

• Fungi can also cause caseating granulomas and necrosis, a finding that is usually observed in patients who are immunosuppressed.

Gastritis in patients who are immunosuppressed

• Cytomegalovirus (CMV) infection of the stomach typical intranuclear eosinophilic inclusions and smaller intracytoplasmic inclusions are found

• Herpes simplex causes basophilic intranuclear inclusions in epithelial cells.

• Mycobacterial infections by Mycobacterium avium-intracellulare are characterized by diffuse infiltration of the lamina propria by histiocytes, which rarely form granulomas.

Autoimmune gastritis

• associated with serum antiparietal and anti-intrinsic factor (IF) antibodies.

• The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia.

• Two types of IF antibodies are detected, ie, types I and II. Type I IF antibodies block the IF-cobalamin binding site, thus preventing the uptake of vitamin B-12. Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to epithelial cell destruction and resulting gastric atrophy.

Chronic reactive chemical gastropathy

• is associated with long-term intake of aspirin or NSAIDs.

• It also develops when bile-containing intestinal contents reflux into the stomach.

Chronic noninfectious granulomatous gastritis

Noninfectious diseases are the usual cause of gastric granulomas and include:

i. Crohn diseaseii. Sarcoidosis

iii. isolated granulomatous gastritis

Lymphocytic gastritis

• This is a type of chronic gastritis with dense infiltration of the surface and foveolar epithelium by T lymphocytes and associated chronic infiltrates in the lamina propria.

• High anti–H pylori antibody titers have been found in patients with lymphocytic gastritis, and, in limited studies, the inflammation disappeared after H pylori eradication.

• 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 anisakiasis

• 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

• Small doses of radiation (up to 1500 R) cause reversible mucosal damage, whereas higher radiation 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

• Ischemic gastritis is believed to result from atherosclerotic thrombi arising from the celiac and superior mesenteric arteries.

Symptoms

Upper abdominal pain, possibly aggravated by eating Abdominal indigestion Loss of appetite Nausea Vomiting Vomiting blood or coffee-ground like material Dark stools

Note: there may be no symptoms

Signs and tests

EGD (esophagogastroduodenoscopy) and biopsy showing gastritis








CBC showing anemia A guaiac stool test

Physical examination :

In uncomplicated H pylori–associated atrophic gastritis, clinical findings are few and nonspecific.

o Epigastric tenderness may exist.

o If gastric ulcers coexist, guaiac-positive stool may result from occult blood loss.

Bad breath (ie, halitosis) and abdominal pain or discomfort may occur, with bloating associated with bacterial overgrowth syndrome.

Physical findings may result from the development of pernicious anemia and neurologic complications in patients with autoimmune atrophic gastritis.

With severe cobalamin deficiency, the patient is pale and has slightly icteric skin and eyes. The pulse is rapid, and the heart may be enlarged. Auscultation usually reveals a systolic flow murmur.

Causes:

Infectious gastritis

o Chronic gastritis caused by H pylori infection - This is the most common cause of chronic gastritis.

o Infection by Helicobacter heilmannii

o Granulomatous gastritis associated with gastric infections in mycobacteriosis, syphilis, histoplasmosis, mucormycosis, South American blastomycosis, anisakiasis, or anisakidosis

o Chronic gastritis associated with parasitic infections - Strongyloides species, schistosomiasis, Diphyllobothrium latum

o Viral infections such as CMV and herpes virus infection

Noninfectious gastritis

o Autoimmune gastritis

o Chemical gastropathy, usually related to chronic bile reflux or NSAID and aspirin intake

o Uremic gastropathy

o Chronic noninfectious granulomatous gastritis, associated with the following: Crohn disease 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 Langerhans cell histiocytosis

o Lymphocytic gastritis, including gastritis associated with celiac disease

o Eosinophilic gastritis

o Radiation injury to the stomach

o GVHD

o Ischemic gastritis

o Gastritis secondary to drug therapy

Chronic gastritis of undetermined etiology or gastritis of undetermined type

INVESTIGATIONS

The diagnosis of chronic gastritis can only be ascertained histologically. Therefore, histological assessment of endoscopic biopsies is essential. The identification of the underlying cause of chronic gastritis and the assessment of specific complications can require several laboratory tests.

Atrophic gastritis may be assessed by measuring serum levels of the pepsinogen I–to–pepsinogen II ratio. Pepsinogen I (PGA, PGI) and pepsinogen II (PGC, PGII) are synthesized and secreted by gastric chief cells. After secretion into the gastric lumen, they are converted into proteolytic active pepsins. The level of PGA in the serum decreases as loss of gastric chief cells during gastric atrophy occurs, resulting in a decreased PGI/PGII ratio. Gastric carcinoma occurs, especially the intestinal type, usually in association with severe atrophic gastritis. Measuring the levels of pepsinogen I and II and the pepsinogen I/II ratio in the serum is useful for screening atrophic gastritis and gastric cancer in regions with high incidence of these diseases. Pepsinogen

determination is especially useful in epidemiological studies; however, the sensitivity and specificity of the assay is relatively low, with 84.6% and 73.5% values, respectively, reported in a recent study.

Rapid urease test from gastric biopsy tissue

Bacterial culture of gastric biopsy: This is usually performed in the research setting or to assess antibiotic susceptibility in patients for whom first-line eradication therapy fails.

Diagnosis of autoimmune gastritis

o Antiparietal and anti-IF antibodies in the serum

o Achlorhydria, both basal and stimulated, and hypergastrinemia

o Low serum cobalamin (vitamin B-12) levels (<100 pg/mL)

o Possible abnormal result on Schilling test (can be corrected by IF)

Treatment

The treatment depends on the cause of the gastritis. Antibiotic therapy will treat chronic gastritis caused by infection with Helicobacter pylori.

Antacids or other medications, such as cimetidine (to decrease or neutralize gastric acid in the stomach) or proton pump inhibitors such as Prilosec, will usually eliminate the symptoms and promote healing. Medications known to cause gastritis should be discontinued. Gastritis caused by pernicious anemia is treated with vitamin B12.

Medical Care: Treatment of chronic gastritis can be directed to a specific etiologic agent, when it is known. In other situations in which gastritis represents gastric involvement of a systemic disease, treatment is targeted to the primary disease. The treatment approach for H pylori infection is described in detail in this article and elsewhere. Treatment for other diseases is detailed in specific disease articles.

H pylori infection antibiotics: clarithromycin, amoxicillin, metronidazole, tetracycline, and furazolidone. Monotherapy is associated with the rapid development of antibiotic resistance, especially to metronidazole and clarithromycin.

Five regimens are approved by the FDA for the treatment of H pylori infection. A version of the traditional bismuth, metronidazole, tetracycline (BMT) triple therapy has been approved and is available commercially as Helidac. The regimen combines a histamine 2 (H2) receptor antagonist, bismuth subsalicylate, metronidazole, and tetracycline, which are administered for 14 days.. Three different combinations using clarithromycin have been approved, including 2 dual therapies consisting of 500 mg of clarithromycin 3 times daily plus either omeprazole or ranitidine bismuth citrate ([RBC] Tritec).

Currently, the most widely used efficient therapies to eradicate H pylori are triple therapies, and they are recommended as first-line treatments; quadruple therapies are recommended as second-line treatment when triple therapies fail to eradicate H pylori. In both cases, the best results are achieved by administering therapy for 10-14 days, although some studies have limited the duration of treatment to 7 days. The accepted definition of a cure is that no evidence of H pylori exists for 4 or more weeks after ending the antimicrobial therapy.

Triple therapy with indicated adult dose




o Twice-a-day PPI or RBC triple therapies PPI - Lansoprazole (Prevacid) 30 mg PO bid, omeprazole (Prilosec) 20 mg PO

bid, or RBC (Tritec) 400 mg bid Clarithromycin (Biaxin) 500 mg PO bid Amoxicillin 1000 mg PO bid or metronidazole 500 mg PO bid

o Pack kits containing combination triple therapies are available as combinations of lansoprazole, amoxicillin, and clarithromycin (PrevPac) and bismuth subsalicylate, tetracycline, and metronidazole (Helidac).

o PrevPac contains drug combinations in the dosage recommended as first-line treatment by the Maastricht 2-2000 Consensus Report in Europe. PrevPac components include the following:

Lansoprazole (Prevacid) 30 mg PO bid Clarithromycin (Biaxin) 500 mg PO bid Amoxicillin 1000 mg PO bid

o Helidac triple therapy components include the following: Bismuth subsalicylate 525 mg (two, 262.4-mg chewable tablets) qid Metronidazole 250 mg qid Tetracycline hydrochloride 500 mg qid

Quadruple therapy with indicated adult dose

o A PPI twice a day - Lansoprazole (Prevacid) 30 mg PO bid or omeprazole (Prilosec) 20 mg PO bid

o Tetracycline HCl 500 mg PO qid o Bismuth subsalicylate 120 mg PO qid o Metronidazole 500 mg PO tid

Do not administer antibiotic therapy if the patient does not have a confirmed infection and assess the results of the therapy. Manage cases of subsequent H pylori eradication failure on a case-by-case basis and base antibiotic selection on pretreatment antibiotic sensitivity test results.

Treatment of H pylori infection in children: The optimal treatment for H pylori in childhood is not well established. Treatment has not been studied extensively, and no consensus exists for the optimum regimen. However, the benefits of treating the infection in patients with duodenal ulcer are obvious, whereas treating children who are asymptomatic is controversial. While the literature is replete with contrary recommendations, many authorities now recommend treating all people, adults and children, in whom H pylori infection is demonstrated. Isolated studies have shown eradication efficiencies with triple therapies, ranging from 56-87% of the cases. In children, clarithromycin and metronidazole H pylori resistance are a problem in several countries, resulting in less efficient eradication regimens.

Drug Category: Antibiotics -- Antimicrobial activity against most H pylori strains. Rare resistant strains have been reported.

Drug NameAmoxicillin (Amoxil, Trimox) -- Acid-stable semisynthetic penicillin. The antimicrobial activity of amoxicillin is pH-dependent, with the minimal inhibitory concentration decreasing as the pH increases.




Interactions Reduces the efficacy of oral contraceptives


Precautions

Adjust dose in patients with renal impairment; pseudomembranous colitis has been reported with nearly all antibacterial agents, including amoxicillin, and may range in severity from mild to life threatening (consider diagnosis in patients who present with diarrhea subsequent to administration of antibacterial agents); caution in cephalosporin allergy

Drug Name

Clarithromycin (Biaxin) -- Macrolide that binds to bacterial ribosomes and disrupts protein synthesis, leading to bacterial cell death. Most acid-stable of the macrolides and has lowest minimal inhibitory concentration. Major metabolite also is active against H pylori.



Contraindications Documented hypersensitivity; coadministration of pimozide

Interactions

Toxicity increases with coadministration of fluconazole and pimozide; effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, HMG CoA reductase inhibitors; serious cardiac arrhythmias may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmias and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents; consider monitoring serum theophylline concentrations for patients receiving high doses of theophylline or for patients with baseline concentrations in the upper therapeutic range

Pregnancy C - Safety for use during pregnancy has not been established.

Precautions

Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; administer half dose or increase dosing interval if CrCl <30 mL/min; diarrhea may be sign of pseudomembranous colitis; superinfections may occur with prolonged or repeated antibiotic therapies

Drug Name

Tetracycline (Sumycin) -- Treats infection with gram-positive and gram-negative organisms as well as mycoplasmal, chlamydial, and rickettsial infections. Inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). Potency is affected in solutions of pH <2 and is rapidly destroyed by alkali hydroxide solutions.


Pediatric Dose<8 years: Not recommended>8 years: Not established

Contraindications Documented hypersensitivity; severe hepatic dysfunction

Interactions

Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of oral contraceptives, causing breakthrough bleeding and increased risk of pregnancy; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; concurrent use of methoxyflurane has been reported to result in fatal renal toxicity

Pregnancy D - Unsafe in pregnancy

Precautions Photosensitivity may occur with prolonged exposure to sunlight or tanning

equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; tetracycline use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines; diarrhea may be sign of pseudomembranous colitis

Drug Name

Metronidazole (Flagyl) -- Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents. Activity is pH independent, theoretically making it an ideal drug for the gastric environment.




InteractionsCimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with orally ingested ethanol


Precautions

Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy; caution in patients with blood dyscrasias; mild leukopenia has been observed; however, no persistent hematologic abnormalities were observed; known or previously unrecognized candidiasis may develop more prominent symptoms during therapy, requiring treatment with a candicidal agent

Drug Category: Proton pump inhibitors -- A substituted benzimidazole (a compound that inhibits gastric acid secretion) is the active ingredient. PPIs do not exhibit anticholinergic or H2 antagonistic activities but suppress acid secretion by specific inhibition of the H+/K+-ATPase enzyme system on the secretory surface of parietal cells.

Drug NameOmeprazole (Prilosec) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump.




InteractionsMay decrease effects of itraconazole and ketoconazole; may increase toxicity of warfarin, digoxin, and phenytoin


Precautions Bioavailability may increase in elderly patients

Drug NameLansoprazole (Prevacid) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump.




Interactions

May decrease effects of ketoconazole and itraconazole, ampicillin esters, iron salts, and digoxin; may increase theophylline clearance (dose titration may be indicated when therapy is started or stopped); metabolized through cytochrome P-450 system (CYP3A and CYP2C19 isozymes); does not have clinically significant interactions with other drugs metabolized by the cytochrome P-450 system; absorption delayed and bioavailability reduced with coadministration of sucralfate (separate sucralfate dosing by at least 30 min)


Precautions Consider adjusting dose in patients with liver impairment

Drug NameRabeprazole (Aciphex) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump.




Interactions None reported


PrecautionsSymptomatic response to this product does not exclude possibility of malignancy

Drug NamePantoprazole (Protonix) -- Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATP pump.






Precautions Symptomatic response to this product does not exclude possibility of

malignancy

Drug NameEsomeprazole (Nexium) -- Inhibits gastric acid secretion by inhibiting H+/K+-ATPase enzyme system at secretory surface of gastric parietal cells.

Adult Dose 20-40 mg PO qd for 4-8 wk





Precautions Symptomatic relief with PPIs may mask symptoms of gastric malignancy

Drug Category: Bismuth compounds -- The components of bismuth-containing therapies, including bismuth subsalicylate, metronidazole, clarithromycin, and tetracycline, individually have demonstrated in vitro activity against most susceptible strains of H pylori.

Drug Name Ranitidine bismuth citrate (Tritec) -- Combination of ranitidine (inhibits H2 receptor in gastric parietal cells, which reduces gastric acid secretion, gastric volume, and hydrogen concentrations) and bismuth citrate. Do

not administer as monotherapy. Administer 30 min before sucralfate.

Adult Dose400 mg PO bid; coadministered with clarithromycin (500 mg PO) and amoxicillin (1000 mg PO)


Contraindications Documented hypersensitivity; porphyria

Interactions

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin; coadministration with clarithromycin increases plasma ranitidine concentrations (57%), plasma bismuth trough concentrations (48%), and 14-hydroxy-clarithromycin plasma concentrations (31%)


Precautions

Caution in patients with renal or liver impairment; if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment; not recommended in patients with CrCl <25 mL/min; bismuth may cause temporary and harmless darkening of the tongue and/or stool (not to be confused with melena); caution in women who are breastfeeding

Expectations (prognosis)

Most gastritis improves rapidly with treatment. Prognosis depends on the underlying cause. Most chronic gastritis does not cause symptoms and does not result in significant illness.

Complications

Loss of blood and increased risk of gastric cancer are potential complications.

Prevention

Avoid use of aspirin or NSAIDs if you are prone to gastritis.

ACUTE CHOLECYSTITIS

Acute cholecystitis is a sudden inflammation of the gallbladder that causes severe abdominal pain.

Causes:

• gallstones in the gallbladder (most common cause!)




• severe illness

• alcohol abuse

rarely, tumors of the gallbladder

U Acute cholecystitis causes bile to become trapped in the gallbladder. The build up of bile causes irritation and pressure in the gallbladder. This can lead to bacterial infection (empyema) and perforation of the organ (acute gangrenous cholecystitis which can perforate with generalized peritonitis)

U Gallstones occur more frequently in women than men. Gallstones become more common with age in both sexes. Native Americans have a higher rate of gallstones.

Symptoms

• The main symptom is abdominal pain -- particularly after a fatty meal -- that is located on the upper right quadrant of the abdomen. The pain is assoc with:

- tenderness

- muscle guarding or rigidity

• nausea

• vomiting

• fever

Signs and tests

A doctor's examination of the abdomen by touch (palpation) may reveal tenderness.

Tests that detect the presence of gallstones or inflammation include:

Abdominal ultrasound . Look for:- gallstones w/i the bladder- focal tenderness over the underlying gall bladder- thickening of the gall bladder wall.

Abdominal x-ray . Might see: - radio-opaque stones- calcification of the gall bladder- gas in lumen and wall of gall bladder.

CBC . It shows:- infection by an elevated white blood cell count and ↑ CRP- ↑ levels of serum bilirubin, alkaline phosphatase and aminotransferase Oral cholecystogram Gallbladder radionuclide scan Abdominal CT scan Biliary scintigraphy using technetium derivatives of iminodiacetate.










Treatment

Although cholecystitis may clear up on its own, surgery to remove the gallbladder (cholecystectomy) is usually needed when inflammation continues or recurs.

This operation is done as soon as possible, unless the patient is very ill or if the inflammation is thought to have been present for many days. Emergency surgery may be necessary if gangrene (tissue death), perforation, pancreatitis, or inflammation of the common bile duct occurs.

Occasionally, in very ill patients, a tube may be placed through the skin to drain the gallbladder until the patient gets better and can have surgery.

Nonsurgical treatment includes pain medicines, antibiotics to fight infection, and a low-fat diet (when food can be tolerated). Patients usually need one or more doses of antibiotics.

Expectations (prognosis)

Patients who have cholecystectomy usually do very well.

Complications

Empyema (pus in the gallbladder) Peritonitis (inflammation of the lining of the abdomen) Gangrene (tissue death) of the gallbladder Injury to the bile ducts draining the liver (a rare complication of cholecystectomy)

Prevention

Removal of the gallbladder and gallstones will prevent further attacks. Reduce the fat content in the diet if you are prone to attacks of cholecystitis.

CHRONIC CHOLECYSTITIS

• Chronic cholecystitis is long-standing swelling and irritation of the gallbladder.

Causes:





• repeated mild attacks of acute cholecystitis. This leads to thickening of the walls of the gallbladder. The gallbladder begins to shrink and eventually loses the ability to perform its function: concentrating and storing bile.

• Eating fatty foods may aggravate the symptoms of cholecystitis, because bile is needed to digest such foods.

•The disease occurs more often in women than in men, and the incidence increases after the age of 40. Risk factors include the presence of gallstones and a history of acute cholecystitis.

Symptoms:

Chronic indigestion Vague abdominal pain Nausea Belching

Signs and tests:

Tests that reveal inflammation or gallstones in the gallbladder:

Abdominal CT scan Oral cholecystogram Abdominal ultrasound HIDA scan (gallbladder scan)

Treatment:

• Cholecystectomy (surgical removal of the gallbladder) can be performed as an open or laparoscopic procedure. The open procedure requires a large incision (cut), while laparoscopic surgery requires a cluster of small incisions for the insertion of instruments, including a small camera.

• For patients who are poor candidates for surgery because of other diseases or conditions, methods to dissolve gallstones may be of use. The symptoms of chronic indigestion can be managed by low-fat diet and weight reduction. Acid-suppressing and anticholinergic medications may also be helpful, as may antacids.

Complications:

Gallstones with chronic inflammation of the gallbladder can result in a worsening of the condition, pancreatitis, or (rarely) cancer of the gallbladder.

Prevention: The condition is not always preventable. People who have had an attack of acute cholecystitis but have not had their gallbladder removed may feel better when eating less fatty foods.
















acute gastritis

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