Pathophysiology

Acute gastritis has a number of causes, including certain drugs; alcohol; bile; ischemia;
bacterial, viral, and fungal infections; acute stress (shock); radiation; allergy and food
poisoning; and 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, and
ischemia. The gastric mucosa exhibits hemorrhages, erosions, and ulcers. NSAIDs, such
as aspirin, ibuprofen, and naproxen, are the most common agents associated with acute
erosive gastritis. This results from oral or systemic administration of these agents either
in therapeutic doses or in supratherapeutic doses.

Because of gravity, the inciting agents lie on the greater curvature of the stomach. This
partly explains 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. Prostaglandins are
chemicals responsible for maintaining mechanisms that result in the protection of the
mucosa from the injurious effects of the gastric acid. Long-term effects of such
ingestions can include fibrosis and stricture.

Bacterial infection is another cause of acute gastritis. The corkscrew-shaped bacterium

called H pylori is the most common cause of gastritis. Complications result from a
chronic infection rather than from an acute infection. The prevalence of H pylori in
otherwise healthy individuals varies depending on age, socioeconomic class, and country
of origin. The infection is usually acquired in childhood. In the Western world, the
number of people infected with H pylori increases with age. Evidence of H pylori
infection can be found in 20% of individuals younger than 40 years and in 50% of
individuals older than 60 years. How the bacterium is transmitted is not entirely clear.
Transmission is likely from person to person through the oral-fecal route or through the
ingestion of contaminated water or food. This is why the prevalence is higher in lower
socioeconomic classes and in developing countries. H pylori is associated with 60% of
gastric ulcersand80%ofduodenal ulcers.

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, an enzyme that 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.

H pylori also has flagella that enable it to move and help it to penetrate the mucous layer
so that it comes into contact with gastric epithelial cells. It also has several adhesions that
help it to adhere to these cells. It produces inflammation by activating a number of toxins
and enzymes that activate IL-8, which eventually attracts polymorphs and monocytes that
cause acute gastritis.

Antigen-presenting cells activate lymphocytes and other mononuclear cells that lead to
chronic superficial gastritis. The infection is established within a few weeks after the
primary exposure to H pylori. 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. This is referred to as atrophic gastritis.
Consequently, gastric acid production drops. The virulence genotype of the microbe is an
important determinant for the severity of the gastritis and the formation of intestinal
metaplasia, the transformation of gastric epithelium. This transformation can lead to
gastric cancer.Reactive gastropathy is the second most common diagnosis made on
gastric biopsy specimens after H pylori gastritis. This entity is believed to be secondary
to bile reflux and was originally reported after partial gastrectomy (Billroth I or II). It is
now considered to represent a nonspecific response to a variety of other gastric irritants.

Helicobacter heilmanii is a gram-negative, tightly spiraled, helical-shaped organism with

5-7 turns. The prevalence of H heilmanii is extremely low (0.25-1.5%). The source of H
heilmanii infection is unclear, but animal contact is thought to be the means of
transmission.

Tuberculosis is a 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 is a rare cause of gastritis.

Phlegmonous gastritis is an uncommon form of gastritis caused by numerous bacterial

agents, including streptococci, staphylococci, Proteus species, Clostridium species, and
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. The clinical diagnosis is usually established in
the operating room, as these patients present with an acute abdominal emergency
requiring immediate surgical exploration. Without appropriate therapy, it progresses to
peritonitis and death.

Viral infections can cause gastritis. 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 that cause gastritis include Candida albicans and histoplasmosis.
Gastric phycomycosis is another rare lethal fungal infection. The common predisposing
factor is immunosuppressant. C albicans rarely involves the gastric mucosa. When
isolated in the stomach, the most common locations tend to be within a gastric ulcer or an
erosion bed. It is generally of little consequence. Disseminated histoplasmosis can
involve the stomach. The usual presenting clinical feature is bleeding from gastric ulcers
or erosions on giant gastric folds.

Parasitic infections are 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.

Ulcero-hemorrhagic gastritis is most commonly seen in patients who are critically ill.
Ulcero-hemorrhagic gastritis is believed to be secondary to ischemia related to
hypotension and shock or to the release of vasoconstrictive substances, but the etiology is
often unknown. The gastric mucosa reveals multiple petechiae, mostly in the fundus and
body, or exhibits a diffusely hemorrhagic pattern. The gross pathology may resemble that
of NSAID- or other ingestion-induced gastritis, except that the location of injury is
different. This form of gastritis can be life-threatening if the patient experiences
hemorrhaging and may even require emergency gastrectomy.

Microscopic evidence of acute gastritis can be seen in patients with Crohn disease,
though clinical manifestations are rare (occurring in only about 2-7% of patients with
Crohn disease). Focally enhancing gastritis is now recognized as a condition seen in both
Crohn disease and ulcerative colitis.

Eosinophilic gastritis is often seen in conjunction with eosinophilic gastroenteritis but can
be associated with various disorders, including food allergies (eg, cow milk, soy protein),
collagen vascular diseases, parasitic infections, gastric cancer, lymphoma, Crohn disease,
vasculitis, drug allergies, and H pylori infections. An eosinophilic infiltrate is seen
involving the gastric wall or epithelium

Mortality/Morbidity
The mortality/morbidity is dependent on the etiology of the gastritis. Generally, most
cases of gastritis are treatable once the etiology is determined. The exception to this is
phlegmonous gastritis, which has a mortality rate of 65%, even with treatment.

Sex

No sexual predilection exists.

Age

Gastritis affects all age groups. The incidence of H pylori infection increases with age.

Physical

The physical examination findings are often normal with occasional mild epigastric
tenderness. The examination tends to exhibit more abnormalities as the patient develops
complications in relation to gastritis.

Causes

Acute gastritis has a number of causes, including certain drugs; alcohol; bacterial, viral,
and fungal infections; acute stress (shock); radiation; allergy and food poisoning; bile;
ischemia; and direct trauma.

* Drugs

o NSAIDs, such as aspirin, ibuprofen, and naproxen

o Cocaine

o Iron

o Colchicine, when at toxic levels, as in patients with failing renal or hepatic

function

o Kayexalate
 o Chemotherapeutic agents, such as mitomycin C, 5-fluoro-2-deoxyuridine, and
floxuridine

* 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

o Candidiasis

o 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

Laboratory Studies

* A number of laboratory tests are usually ordered.

o CBC count 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
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 are available.

 + 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 are available.

+ 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.

Procedures

* Endoscopy

o 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.

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

o Endoscopy can be used to help diagnose gastric syphilis and tuberculosis.

Histologic Findings

Histologic examination of a biopsy specimen can help in establishing the etiologic agent
of gastritis.

H heilmanii is better diagnosed on smears using Giemsa or Warthin-Starry silver stains

than by gastric biopsy specimens via observation of distinct morphology. A culture of H
heilmanii has not been established yet, and the diagnosis of this bacterial infection is
based on morphological identification by histologic examination and tissue smear
cytology.

As mentioned earlier, H pylori can be found by histologic staining of a gastric mucosal

biopsy specimen. It has a sensitivity and specificity of greater than 90%.
The main histologic feature of CMV infection is cytomegalic cells with intranuclear
inclusions. Viral cultures, immunocytochemistry, and in situ hybridization can further aid
in establishing the diagnosis.

The main histologic feature of C albicans infection is yeast forms in a biopsy specimen.

The main histologic feature of tuberculosis is necrotizing granulomas.

The main histologic feature of histoplasmosis is nonnecrotizing granulomas containing

the organisms. The diagnosis of histoplasmosis requires a positive culture result from a
gastric mucosal biopsy specimen.

In ulcero-hemorrhagic gastritis, the epithelium appears eroded with edema and

hemorrhage with typically little inflammation. In severe cases, the lumen of the stomach
may be coated with fibropurulent exudates and the lamina propria may be replaced by
eosinophilic hyaline material.

In iron-induced gastritis, erosions, foveolar hyperplasia, or even hyperplastic-type polyps

can be detected. Iron has been associated with infarctlike necrosis given its corrosive
properties. Iron stains can highlight the golden brown pigments in tissue samples, but
these are often easily visible. Of note, such findings should be differentiated from
glandular siderosis seen in systemic iron overload or hemochromatosis.

Histologic features of chemotherapy-induced gastritis may include atypical epithelial

cells with bizarre features at the base of the glands, limited mitoses, and pleomorphic
nuclei. These characteristics may make it difficult to differentiate from an
adenocarcinoma.

The histology of radiation-induced gastritis include nuclear karyorrhexis and cytoplasmic

eosinophilia of the gastric pit epithelium in the first 10 days following treatment,
followed by mucosal edema, congestion, submucosal collagen bundle swelling, fibrin
deposition, and telangiectasia. If extensive, hemorrhage and ulceration may be evident.In
eosinophilic gastritis, a prominent eosinophilic infiltrate is present in the gastric wall or
epithelium. Distribution can be patchy, so multiple biopsy specimens should be obtained
during endoscopy.

Medications

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.

Consultations

Consult a gastroenterologist in complicated cases.

Medication

Specific treatment is dependent on the etiology of gastritis.

According to the Centers for Disease Control and Prevention (CDC), the treatment of
tuberculosis 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.

Prevention of Gastritis:

Methods of prevention of Gastritis mentioned in various sources includes those listed

below. This prevention information is gathered from various sources, and may be
inaccurate or incomplete. None of these methods guarantee prevention of Gastritis.

* Prevention measures depend on the cause of gastritis

* Eat moderately

* Drink moderately

* Avoid spicy foods

* Avoid foods that trigger attacks

* Avoid hot foods

* Reduce alcohol usage

* Quit smoking

* Avoid aspirin
 * Avoid ibuprofen

Risk Factors:

* Infection with H. pylori

* Crowded, unsanitary conditions -- this may increase risk of contracting H. pylori

* Acquired immunodeficiency syndrome (AIDS)

* Any condition that requires relief from persistent pain using NSAIDS, such as
chronic low back pain, fibromyalgia, or arthritis

* Alcoholism

* Cigarette smoking

* Older age

* Genetic abnormalities

Drugs Study

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.

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.
Dosage:

Adult

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

Pediatric

0.5 mL/kg PO qid prior to eating

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

ContraIndications:

Documented hypersensitivity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus

Precautions

Precaution:

Antacids may mask the symptoms of internal bleeding secondary to NSAIDs;

magnesium-containing antacids may cause diarrhea and potentially lead to dehydration;
caution with aluminum-containing antacids in patients who recently have had a massive
upper GI hemorrhage

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.

Cimetidine (Tagamet)

Inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced

gastric acid secretion, gastric volume, and hydrogen concentrations.

Dosage:

Adult

150 mg PO qid; not to exceed 600 mg/d

50 mg/dose IV/IM q6-8h; not to exceed 400 mg/d

Pediatric

Not established

Suggested 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

ContraIndications;

Documented hypersensitivity

Precaution:

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

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

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.

Omeprazole (Prilosec)

Decreases gastric acid secretion by inhibiting the parietal cell H+/K+-ATPase pump.

Dosage:
Adult

20 mg PO bid

Pediatric

Not established

Interactions:

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

ContraIndications;

Documented hypersensitivity

Precautions

Bioavailability may increase in the elderly

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus

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.

Amoxicillin (Amoxil, Trimox)

Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting
in bactericidal activity against susceptible bacteria.

Dosage:

Adult

500 mg PO qid

Pediatric

Not established

Interactions:

Reduces the efficacy of oral contraceptives

CI: Documented hypersensitivity

Precaution:

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions

Adjust dose in patients with renal impairment

Tetracycline (Sumycin)

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

Dosage:

Adult

500 mg PO qid

Pediatric

<8 years: Not recommended

>8 years: Not established

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

ContraIndications:
Documented hypersensitivity; severe hepatic dysfunction

Precautions:

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

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

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.

Dosage:

Adult

250 mg PO qid

Pediatric

Not established

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

Documented hypersensitivity\
Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in
animals

Precautions

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

Clarithromycin (Biaxin)

Inhibits bacterial growth, possibly by blocking dissociation of peptidyl t-RNA from

ribosomes and causing RNA-dependent protein synthesis to arrest.

Adult

500 mg PO bid/tid

Pediatric

Not established

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
Contraindications:

Documented hypersensitivity; coadministration of pimozide or cisapride

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus

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

Antidiarrheal agents

Used in combination with antibiotics and proton pump inhibitors/H2 receptor antagonists
to eradicate H pylori.

Bismuth subsalicylate (Bismatrol, Pepto-Bismol)

Drug combination that treats active duodenal ulcer associated with H pylori.

Dosage:

Adult

525 mg PO qid

Pediatric

Not established

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

Contraindications:

Documented hypersensitivity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans;
may use if benefits outweigh risk to fetus

Precautions

May cause temporary and harmless darkening of tongue and/or black stool;
alcohol consumption may cause abdominal cramps, nausea, and
vomiting

Nursing Care Plan