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DEFINITION:
 Gastritis is an inflammation of the gastric mucosa, is
classified as either acute or chronic.
INCIDENCE:
 The incidence of gastritis is highest in the fifth and
sixth decades of life; men are more frequently affected
than women. The incidence is greater in clients who
are heavy drinkers and smokers.
ETIOLOGY AND RISK FACTORS:
 It usually stems from ingestion of a corrosive, erosive, or
infectious substance.
 Aspirin and other non-steroidal anti-inflammatory drugs
(NSAIDs), digitalis, chemotherapeutic drugs, steroids,
acute alcoholism and food poisoning (typically caused by
Staphylococcus organisms) are common causes.
 Food substances including excessive amounts of tea,
paprika, clove and pepper can precipitate acute gastritis.
 Foods with a rough texture or those eaten at an extremely
high temperature can also damage the stomach mucosa.
 Acute gastritis is usually of short duration unless the
gastric mucosa has suffered extensive damage.
 The mucosal lining of the stomach normally protects it
from the action of gastric acid. This mucosal barrier is
composed of prostaglandins.
Due to any cause
↓
This barrier is penetrated
↓
Hydrochloric acid comes into contact with the mucosa
↓
Injury to small vessels
↓
Edema, hemorrhage, and possible ulcer formation
 Epigastric discomfort
 Abdominal tenderness
 Cramping
 Belching
 Reflux
 Severe nausea and vomiting
 Hematemesis
 Sometimes GI bleeding is the only manifestation
 When contaminated food is the cause of gastritis,
diarrhea usually develops within 5 hours of ingestion
Diagnosis is based on a detailed history of
food intake, medications taken, and any
disorder related to gastritis.
The physician may also perform a
gastroscopic examination with endoscopy.
Histological examination by biopsy of a
sample.
 Anti – emetic drugs like Inj. Perinorm or Tab.
Domperidone are frequently effective in
vomiting.
 Antacids like cimetidine, Ranitidine, or
Famotidine are effective to reduce the pain.
 If ingestion of NSAIDs is a problem, a
prostaglandin E1 (PGE1) analog may be
prescribed to protect the stomach mucosa and
inhibit gastric acid secretion.
 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 client should avoid spicy foods, caffeine and
large, heavy meals.
 In the continued absence of nausea, vomiting and
bloating, the client can slowly return to a normal
diet.
 Chronic gastritis occurs in 3 different forms
1) Superficial gastritis, which causes a reddened,
edematous mucosa with small erosions and
hemorrhages.
2) Atrophic gastritis, which occurs in all layers of the
stomach, develops frequently in association with gastric
ulcer and gastric cancer, and is invariably present in
pernicious anemia; it is characterized by a decreased
number of parietal and chief cells.
3) Hypertrophic gastritis, which produces a dull and
nodular mucosa with irregular, thickened, or nodular
rugae; hemorrhages occur frequently.
Peptic Ulcer Disease (PUD), infection with
Halicobacter pylori bacteria or gastric surgery
may lead to chronic gastritis.
After gastric resection with a gastro-
jejunostomy, bile and bile acids may reflux
into the remaining stomach, causing gastritis.
H.Pylori infection can lead to chronic atrophic
gastritis.
Age is also a risk factor; chronic gastritis is
more common in older adults.
The stomach lining first becomes thickened and
erythematous and then becomes thin and atrophic.
↓
Continued deterioration and atrophy
↓
Loss of function of the parietal cells
↓
Acid secretion decreases
↓
Inability to absorb vitamin B12
↓
Development of pernicious anemia
Manifestations are vague and may be absent because
the problem does not cause an increase in hydrochloric
acid.
Assessment may reveal
 Anorexia
 Feeling of fullness
 Dyspepsia
 Belching
 Vague epigastric pain
 Nausea
 Vomiting
 Intolerance of spicy and fatty foods
Bleeding
Pernicious anemia
Gastric cancer
 Discomfort may lessen with a bland diet, small frequent
meals, antacids, H2 receptor antagonists, proton pump
inhibitors, and avoidance of food that cause
manifestations.
 If H.pylori bacteria are present, anti-biotics and other
medications are administered to eliminate the bacteria.
 If 1 week of this regimen does not succeed in eliminating
the bacteria, the regimen may be repeated for an
additional week.
 If pernicious anemia develops, intramuscular injections
of vitamin B12 may be administered monthly for the
remainder of the client’s life.
Nursing Diagnosis:
1) Acute pain related to irritated stomach mucosa.
2) Imbalanced nutrition, less than body requirement,
related to inadequate intake of nutrition.
3) Risk for imbalanced fluid volume related to
insufficient fluid intake and excessive fluid loss
subsequent to vomiting.
4) Anxiety related to treatment.
5) Deficient knowledge about dietary management
and disease process.
Gastritis

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Gastritis

  • 1.
  • 2. DEFINITION:  Gastritis is an inflammation of the gastric mucosa, is classified as either acute or chronic. INCIDENCE:  The incidence of gastritis is highest in the fifth and sixth decades of life; men are more frequently affected than women. The incidence is greater in clients who are heavy drinkers and smokers.
  • 3. ETIOLOGY AND RISK FACTORS:  It usually stems from ingestion of a corrosive, erosive, or infectious substance.  Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs), digitalis, chemotherapeutic drugs, steroids, acute alcoholism and food poisoning (typically caused by Staphylococcus organisms) are common causes.  Food substances including excessive amounts of tea, paprika, clove and pepper can precipitate acute gastritis.  Foods with a rough texture or those eaten at an extremely high temperature can also damage the stomach mucosa.  Acute gastritis is usually of short duration unless the gastric mucosa has suffered extensive damage.
  • 4.  The mucosal lining of the stomach normally protects it from the action of gastric acid. This mucosal barrier is composed of prostaglandins. Due to any cause ↓ This barrier is penetrated ↓ Hydrochloric acid comes into contact with the mucosa ↓ Injury to small vessels ↓ Edema, hemorrhage, and possible ulcer formation
  • 5.  Epigastric discomfort  Abdominal tenderness  Cramping  Belching  Reflux  Severe nausea and vomiting  Hematemesis  Sometimes GI bleeding is the only manifestation  When contaminated food is the cause of gastritis, diarrhea usually develops within 5 hours of ingestion
  • 6. Diagnosis is based on a detailed history of food intake, medications taken, and any disorder related to gastritis. The physician may also perform a gastroscopic examination with endoscopy. Histological examination by biopsy of a sample.
  • 7.  Anti – emetic drugs like Inj. Perinorm or Tab. Domperidone are frequently effective in vomiting.  Antacids like cimetidine, Ranitidine, or Famotidine are effective to reduce the pain.  If ingestion of NSAIDs is a problem, a prostaglandin E1 (PGE1) analog may be prescribed to protect the stomach mucosa and inhibit gastric acid secretion.
  • 8.  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 client should avoid spicy foods, caffeine and large, heavy meals.  In the continued absence of nausea, vomiting and bloating, the client can slowly return to a normal diet.
  • 9.  Chronic gastritis occurs in 3 different forms 1) Superficial gastritis, which causes a reddened, edematous mucosa with small erosions and hemorrhages. 2) Atrophic gastritis, which occurs in all layers of the stomach, develops frequently in association with gastric ulcer and gastric cancer, and is invariably present in pernicious anemia; it is characterized by a decreased number of parietal and chief cells. 3) Hypertrophic gastritis, which produces a dull and nodular mucosa with irregular, thickened, or nodular rugae; hemorrhages occur frequently.
  • 10. Peptic Ulcer Disease (PUD), infection with Halicobacter pylori bacteria or gastric surgery may lead to chronic gastritis. After gastric resection with a gastro- jejunostomy, bile and bile acids may reflux into the remaining stomach, causing gastritis. H.Pylori infection can lead to chronic atrophic gastritis. Age is also a risk factor; chronic gastritis is more common in older adults.
  • 11. The stomach lining first becomes thickened and erythematous and then becomes thin and atrophic. ↓ Continued deterioration and atrophy ↓ Loss of function of the parietal cells ↓ Acid secretion decreases ↓ Inability to absorb vitamin B12 ↓ Development of pernicious anemia
  • 12. Manifestations are vague and may be absent because the problem does not cause an increase in hydrochloric acid. Assessment may reveal  Anorexia  Feeling of fullness  Dyspepsia  Belching  Vague epigastric pain  Nausea  Vomiting  Intolerance of spicy and fatty foods
  • 14.  Discomfort may lessen with a bland diet, small frequent meals, antacids, H2 receptor antagonists, proton pump inhibitors, and avoidance of food that cause manifestations.  If H.pylori bacteria are present, anti-biotics and other medications are administered to eliminate the bacteria.  If 1 week of this regimen does not succeed in eliminating the bacteria, the regimen may be repeated for an additional week.  If pernicious anemia develops, intramuscular injections of vitamin B12 may be administered monthly for the remainder of the client’s life.
  • 15. Nursing Diagnosis: 1) Acute pain related to irritated stomach mucosa. 2) Imbalanced nutrition, less than body requirement, related to inadequate intake of nutrition. 3) Risk for imbalanced fluid volume related to insufficient fluid intake and excessive fluid loss subsequent to vomiting. 4) Anxiety related to treatment. 5) Deficient knowledge about dietary management and disease process.