GASTRITIS

INTRODUCTION

A person’s nutritional status depends not only on the type and

amount of intake but also on the functioning of the gastric and intestinal portions
of the gastric and intestinal system. Gastritis is a common medical problem, with
up to 10% of people who come to hospital emergency department.

DEFINITIONS

1.”Gastritis, an inflammation or irritation of the lining of the stomach, is not a

single disease. Rather, gastritis is a condition that has many causes.’’

JERRY.R.BALENTINE.

2.”Gastritis is an inflammation,irritation,or erosion of the lining of the stomach. It

can occur suddenly (acute)or gradually(chronic).”

KIMBALL JOHNSON.

3.”Gastritis, an inflammation of the gastric mucosa.”

JOYCE.M.BLACK.

INCIDENCE

The incidence of gastritis is highest in the fifth and sixth decades of

life,men are more frequently affected than women.

The incidence in India is approximately 3 in 869.

The incidence of gastritis is greater in clients who are heavy smokers and drinkers

CLASSIFICATIION

Its mainly divided into :

 Acute
 Chronic
ACUTE GASTRITIS

Acute Gastritis is the term covering a broad spectrum of entities that

induce inflammatory changes in the gastric mucosa.

Types

Depending on the anatomical site :

1.Type A(Fundic gland)

2.Type B(Antral)

3.Type AB(Pan gastritis)-whole stomach gets inflammed.

Categories

1.Erosive(superficial or deep erosions)

2.Non-erosive(generally caused by Helico bacter Pylori)

ACUTE HEMORRHAGIC EROSIVE
Hemorrhagic and erosive lesions occur shortly after exposure of the
gastric mucosa to various injurious substances or a substantial reduction in
mucosal blood flow.

Etiology

 Drugs :NSAIDS, such as aspirin,ibruprofen,and naproxen.

Chemotherapeutic agents such as Mitomycin C,5-Fluro-2-deoxy
uridine ,and floxuridine.
 Potent alcoholic beverages
 Bacterial infections:H.Pylori(most frequent)streptococci,staphylo cocci,
proteus species,E.coli(rare)
 Viral:CMV
 Fungal:Candidiasis,histoplasmosis.
 Parasitic infections:(eg: anisakidosis)
 Bile:reflux of bile as seen in GERD.
 Ishchemia
 Food substances:spicy,hot,corrosive,tea and foods with rough texture.
 Gastric and duodenal ulcero inflammatory ulcers occurring during severe
damage to the central nervous system (Cushing’s ulcers)are often considered
in this group.

Disorders linked with acute gastritis

 Uremia,shock,
 CNS Lesions,
 hepatic cirrhosis,
 portal HTN,and
 Prolonged emotion tension.
Pathophysiology:

Due to any etiological factor

decreased prostaglandins synthesis

injury to the mucosa

barrier is penetrated

HCl comes into contact with mucosa

injury to small vessels occur with edema

hemorrhrage and possible ulcer formation.

Clinical manifestations

 Epigastric discomfort
  Abdominal tenderness
 Cramping
 Belching
 Reflux
 Severe nausea and vomiting
 Sometimes hematemesis
 G.I. bleeding
 Diarrhea within 5hrs of ingestion of the offending substances
 Loss of appetite.

Assessment and diagnostic findings

 Upper GI X-ray
 Endoscopy
 Biopsy
 Detection of H.pylori.
Medical management
 Initially, foods and fluids are withheld until nausea and vomiting
subside. Once the client tolerates food, the diet includes decaffeinated
tea, gelatin ,toast and simple bland foods. The clients should avoid
spicy foods, caffeine and large heavy meals.
 Vomiting frequently responds to Phenothiazine group
 Pain responds to Ant acids or Histamine(H2) Receptor
Antagonists(Rantidine ,Cimetidine, Famotidin)
 If ingestion of NSAIDS is a problem,a prostaglandin E1(PGE1)analog
may be prescribed to protect the stomach
 HELICO BACTER PYLORI

Helico bacter pylori is a spiral micro aerophilic, gram negative bacterium, which
measures about 3.0microns in length and 0.5 microns width.

H.Pylori attaches to gastric epithelial tissues by means of specific receptor

mediated adhesion.The route by which infection occurs remains unknown.Person
to person transmission of H.Pylori through feco-oral or oral oral exposure seems
most likely.

Humans appear to be the major reservoir of infection, however, bacteria have been
isolated from primates in and from domestic cats and in milk and gastric tissue of
sheep.

Patients with a history of uncomplicated or complicated peptic ulcers should be

tested for H.Pylori prior to beginning a NSAIDS or low dose aspirin. If present,
H.pylori should be treated with appropriate therapy, even if it is believed that the
prior ulcer was due to NSAIDS.

CHRONIC GASTRITIS

This condition appears in three different forms:

 Superficial gastritis:causes a reddened edematous mucosa with small

erosions and hemorrhages.
 Atropic gastritis:occurs in all layers of stomach ,develops frequently in
association with gastric ulcer,and is invariably present in pernicious
anemia;it is characterized by a decreased number of parietal and chief cells.
 Hypertropic gastritis:produces a dull and nodular mucosa with
irregular,thickened or nodular rugae,hemorrhages occur frequently.
METAPLASTIC ATROPHIC GASTRITIS

Metaplasia is highly relevant to the pathogenesis of atrophic gastritis and its

complications(pernicious anemia, gastric ulcer,gastric cancer)

AUTO IMMUNE METAPLASTIC ATROPHIC GASTRITIS(AMAG):

It is an inherited form that is associated with an immuneresponse in the oxyntic
mucosa (mucosa of body and fundus)directed against parietal cells and intrinsic
factor. AMAG is inherited as an autosomal dominant disorder .

Synonyms of AMAG

Type A gastritis

Auto immune gastritis

Diffuse corporal gastritis.

 The loss of parietal cell mass leads to profound hypochlorhydria,while the

inadequate production of intrinsic factor leads to vitamin B12 malabsorption
and pernicious anemia.
 Patients with AMAG are at increased risk for the development of gastric
carcinoid tumors and adenocarcinoma.
 Patients with AMAG are likely to be infected by H.Pylori

ENVIRONMENTAL METAPLASTIC ATROPHIC GASTRITIS(EMAG):

It is due to environmental factors such as diet and H.Pylori infection, on the gastric
mucosa.

There is an increased risk for gastric ulcer than AMAG.

ETIOLOGY:

 H.Pylori,gastric surgery
 Gastrojejunostomy

Other risk factors are similar to those of acute gastritis.

PATHOPHYSIOLOGY

Due to any etiological factors

Injury to the mucosa

 HCl comes in contact with the mucosa

Injury to small vessels

Edema hemorrhage

Stomach lining becomes thickened and erythematous

Lining becomes thin and atropic

Continued deterioration and atrophy lead to loss of function of the parietal cells

Decreased acid secretion

Inability to absorb VitB12

Development of pernicious anaemia.

CLINICAL MANIFESTATIONS;

Manifestations are vague and may be absent:

 Anorexia,dyspepsia,belching
 Feeling of fullness
 Vague epigastric pain
 Nausea
  Vomiting
 Intolerance of spicy or fatty foods.

DIAGNOSIS

Blood tests

 Blood cell count

 Presence of H.Pylori
 Pregnancy
 Liver,kidney,gall bladder,or pancreas function.
 Urinalysis
 Stool sample(blood in stools)
 X-rays
 ECGs
 Endoscopy
 Stomach biopsy

COMPLICATIONS

 Bleeding
 Pernicious anaemia

MANAGEMENT

Medical management:

 Bland diet
 Small frequent meals
 Ant acids
 H2 receptors antagonists
 Proton pump inhibitors
 If H.Pylori is present Antibiotics are to be given
 If pernicious anemia develops Intra muscular injections of Vit B12 may be
administered months for the remainder of the clients life.

Surgical management
If conservative measures have not controlled bleeding,surgery may be
necessary.Subtotal gastrectomy,pyloroplasty,vagotomy,or total gastrectomy may
be indicated with severe erosive gastritis.

Nursing management

 Assessment

History collection

Assess for the signs and symptoms of gastritis like heart burn ,nausea,Wt.loss/loss.

Physical examination

 Nursing diagnosis
1.Acute pain related to irritation of stomach mucosa
-Assess level of pain using pain scale
-provide comfortable position to the patient
-Provide bland diet to patient
-Avoid using spicy, hot and corrosive food items.
-Administer prescribed medications to the patient

2.Anxiety related to treatment

-Establish good rapport with the patient
-Encourage the patient to verbalize his/her doubts
-Educate the patient regarding the disease conditions,its manifestations and
its prognosis
-Provide psychological support to the patient

3.Imbalanced nutrition ,less than body requirement related to insufficient

fluid and excessive fluid loss subsequent to vomiting
- Assess the nutritional status of the patient
-Provide IV fluids if necessary
-Provide small and frequent diet to the patient
-Provide bland diet to the patient
-Administer the anti emetics as prescribed
4.Deficient knowledge about dietary management and disease process.
-Assess the knowledge level of the patient
-Encourage the patients to clarify his/ her doubts
-Educate the patient regarding the disease condition,its treatment and
complications