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GASTRITIS
169
OVERVIEW OF THE DISEASE
Gastritis is a disorder characterized by irritation or inflammation of the stomach lining
(mucosa). The condition often causes abdominal pain and tenderness, nausea, and
vomiting. Gastritis is not a single disease, and there are a number of different types. The
disorder can be classified according to whether inflammation develops suddenly (acute
gastritis) or whether it develops slowly over time, is long lasting, or comes and goes
(chronic gastritis).Gastritis also can be classified according to the cause (e.g., bacteria,
virus, parasite, fungus) or the location of the stomach lining affected (e.g., upper part
[cardiac], middle part [body], lower part [pylorus]). Acute gastritis, also sometimes
called stress gastritis, often occurs as a result of the following: Alcohol use, Certain
medications (e.g., non steroidal anti-inflammatory drugs [NSAIDs]), Consuming a
corrosive substance (e.g., poison), Extreme stress, Infection, Injury (e.g., during surgery)
Patients who have liver, kidney, or respiratory failure are at increased risk for developing
acute gastritis. If left untreated, acute gastritis caused by stress, alcohol use, or
medications can develop into chronic gastritis (also called erosive gastritis). Chronic
GASTRITIS
170
gastritis is characterized by inflammation and the wearing away of the stomach lining.
Acute gastritis is more common than chronic gastritis. There are three forms of chronic
gastritis. Type A develops primarily in the body of the stomach and is often related to an
autoimmune system disorder, such as pernicious anemia (vitamin B12 deficiency). Type
B chronic gastritis, which is the most common, develops primarily in the lower part of
the stomach (called the pylorus). It usually is related to Helicobacter pylori (H. pylori)
infection. Type AB gastritis is a combination of these two forms and develops both in the
body of the stomach and the pylorus. This type also may be related to H. pylori infection.
Gastritis is a common medical problem. The condition is diagnosed in as many as 10% of
patients seeking emergency medical care for abdominal pain. In the United States, some
ethnic groups are at increased risk for certain types of gastritis. For example, African
Americans, Hispanics, and Native Americans have higher rates of gastritis due to H.
pylori infection, and autoimmune gastritis is more common in African Americans and
people of Northern European descent. Due to an increased risk for H. pylori infection and
thinning of stomach lining, which are associated with aging, gastritis is more common in
adults over the age of 60.
GASTRITIS
171
ASSESSMENT
Abdominal discomfort
Nausea
Vomiting
Anorexia
Due to increase in gastric secretion there is irritation
in the mucosal lining that cause abdominal
disomfort
Nausea is the unpleasant sensation that precedes
vomiting. Vomiting, or emesis, is the forceful
retrograde expulsion of gastric contents from the
body. Nausea and vomiting usually occur due to
increase intra-abdominal pressure and promotes
and gastroesophageal reflux by simultaneous
contraction of the muscles of inspiration, the
abdominal wall muscles, and the diaphragm.
Vomiting usually occurs at end inspiration when
intra-abdominal pressure is highest due to increase
in gastric secretion
Anorexia is an eating disorder there is an intense
fear to eat due to unpleasant sensation that
GASTRITIS
172
Heartburn
Belching
VitaminB12 deficiency
precedes vomiting
Due to increae gastric secretion there is increase
in intra-abdominal pressure and the normal tone
of the fundus and body of the stomach is lost, and
pyloric sphincter pressure decreases that cause
back flow of gastric acid into the esophagus
Belching is the expulsion of swallowed gastric air
due to increase gastric secretion
For the body to use vitamin B-12, it must be broken
down from foods and properly absorbed by cells in
the stomach. Intrinsic factor is a protein that is made
by cells in the lining of the stomach. Without it, the
body would be unable to absorb B-12 into cells. In
conditions, such as chronic gastritis, the lining of the
stomach is damaged, resulting in less intrinsic factor
production. This leads to impaired B-12 absorption
and deficiency
GASTRITIS
173
PATHOPHYSIOLOGY
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 both oral and 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 pyloriincreases 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
GASTRITIS
174
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 ulcers and 80% of duodenal 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.with H pylori is . 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 adhesion molecules 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.
GASTRITIS
175
MEDICAL MANAGEMENT
Endoscopy With the procedure known as gastrointestinalendoscopy, a doctor is able to
see the inside lining of the digestive tract. This examination is performed using an
endoscope-a flexible fiberoptic tube with a tiny TV camera at the end. The camera is
connected to either an eyepiece for direct viewing or a video screen that displays the
images on a color TV. The endoscope not only allows diagnosis of gastrointestinal (GI)
disease but treatment as well.
Biopsy with histologic examination are performed. A biopsy is a procedure to remove a
piece of tissue or a sample of cells from your body so that it can be analyzed in a
laboratory. The gold standard for diagnosis of Helicobacter pylori disease is gastric
biopsy and evaluation for the presence of spirochetes by gram, silver, giemsa, or acridine
orange stains. Alternatively, biopsied tissue can be examined by immunofluorescence or
immunoperoxidase methods, rapid urease testing and/or culture.
Exposure to Helicobacter pylori can be determined by detection of IgA, IgG, or IgM-
class serum antibodies to the organism. Screening patients for the presence of antibody
to Helicobacter pylori is a convenient, noninvasive means for assessing whether a patient
has been exposed to Helicobacter pylori and whether gastrointestinal symptoms may be
related to Helicobacter pylori infection.
GASTRITIS
176
MEDICATION
DRUG ACTION NURSING
RESPONSIBILITY
Antibiotics:
Amoxicillin (Amoxil)
Tetracyclin
Antidiarrheal
Bisuth subsalicylate
H2 Receptor
Antagonist:
Cimetidine (Tagamet),
A bactericidal that assist
with eradicating H.pylori
bacteria in the gastric
mucosa
Exert Bacteriostatic effect
to eradicate H. pylori
bacteria in gastric mucosa
Suppresses H. pylori
Bacteria in the gastric
mucasa
Decreases amount of HCL
produced by stomach by
blocking action of
histamine on histamine
receptors of parietal cells in
the stomach
May cause diarrhea
Should not be used in
patient allergic to penicillin
May cause GI upset
Use caution in patient with
renal or hepatic impairment
Should be taken on empty
stomach
May cause confusion
agitation or coma
Long term use may cause
diarrhea, gynecomastesia
GASTRITIS
177
Famotidine (pepcid)
Ranitidine (Zantac)
Proton Pump Inhibitor:
Omeprazole (Prilosec)
Lansoprazole
(Prevacid
Same as for cimetidine
Same as for cimetidine
Decrease acid secretion by
slowing the H, K, ATPAse
pump on the surface of the
parietal cell of the stomach
Decrease acid secretion by
slowing the H, K, ATPAse
pump on the surface of the
parietal cell of the stomach
Short term relief of GERD
May cause headache,
dizziness, constipation,
nausea and vomiting or
abdominal discomfort
A delayed- release capsule
that is to be swallowed
whole and taken before
meals
May cause diarrhea,
nausea, constipation,
abdominalpain, headache
A delayed- release capsule
that is to be swallowed
whole and taken before
meals
GASTRITIS
178
NURSING DIAGNOSIS
1. Acute / Chronic Pain associated with inflammation or irritation of the gastric
mucosa due to increased gastric acid.
2. Imbalanced Nutrition Less Than Body Requirements related to anorexia, vomiting
3. Knowledge deficit and information related to the conditions and lack of coping
skills
INTERVENTION
Avoids food and fluid by mouth for hours or days until symptom subside. Offer ice chips
and clear liquid when symptom subside. Encourage patient to report any symptom
suggesting a repeat episode of gastritis as food is introduced. Discourage caffeinated
beverages, alcohol and cigarette smoking. Monitor daily input and output for
dehydration. Infuse IV if prescribed assess electrolyte values for 24 hours for fluid
imbalance. Be alert for indication of emorrhagic gastritis (hematemesis tachycardia
hypotension) notify the physician. Instruct patient to avoid food and beverages that may
be irritating to gastric mucosa. Reinforce the importance of completing the medication
regimen as prescribed to eradicate H. pylori infection

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Gastritis NCM 103

  • 1. GASTRITIS 169 OVERVIEW OF THE DISEASE Gastritis is a disorder characterized by irritation or inflammation of the stomach lining (mucosa). The condition often causes abdominal pain and tenderness, nausea, and vomiting. Gastritis is not a single disease, and there are a number of different types. The disorder can be classified according to whether inflammation develops suddenly (acute gastritis) or whether it develops slowly over time, is long lasting, or comes and goes (chronic gastritis).Gastritis also can be classified according to the cause (e.g., bacteria, virus, parasite, fungus) or the location of the stomach lining affected (e.g., upper part [cardiac], middle part [body], lower part [pylorus]). Acute gastritis, also sometimes called stress gastritis, often occurs as a result of the following: Alcohol use, Certain medications (e.g., non steroidal anti-inflammatory drugs [NSAIDs]), Consuming a corrosive substance (e.g., poison), Extreme stress, Infection, Injury (e.g., during surgery) Patients who have liver, kidney, or respiratory failure are at increased risk for developing acute gastritis. If left untreated, acute gastritis caused by stress, alcohol use, or medications can develop into chronic gastritis (also called erosive gastritis). Chronic
  • 2. GASTRITIS 170 gastritis is characterized by inflammation and the wearing away of the stomach lining. Acute gastritis is more common than chronic gastritis. There are three forms of chronic gastritis. Type A develops primarily in the body of the stomach and is often related to an autoimmune system disorder, such as pernicious anemia (vitamin B12 deficiency). Type B chronic gastritis, which is the most common, develops primarily in the lower part of the stomach (called the pylorus). It usually is related to Helicobacter pylori (H. pylori) infection. Type AB gastritis is a combination of these two forms and develops both in the body of the stomach and the pylorus. This type also may be related to H. pylori infection. Gastritis is a common medical problem. The condition is diagnosed in as many as 10% of patients seeking emergency medical care for abdominal pain. In the United States, some ethnic groups are at increased risk for certain types of gastritis. For example, African Americans, Hispanics, and Native Americans have higher rates of gastritis due to H. pylori infection, and autoimmune gastritis is more common in African Americans and people of Northern European descent. Due to an increased risk for H. pylori infection and thinning of stomach lining, which are associated with aging, gastritis is more common in adults over the age of 60.
  • 3. GASTRITIS 171 ASSESSMENT Abdominal discomfort Nausea Vomiting Anorexia Due to increase in gastric secretion there is irritation in the mucosal lining that cause abdominal disomfort Nausea is the unpleasant sensation that precedes vomiting. Vomiting, or emesis, is the forceful retrograde expulsion of gastric contents from the body. Nausea and vomiting usually occur due to increase intra-abdominal pressure and promotes and gastroesophageal reflux by simultaneous contraction of the muscles of inspiration, the abdominal wall muscles, and the diaphragm. Vomiting usually occurs at end inspiration when intra-abdominal pressure is highest due to increase in gastric secretion Anorexia is an eating disorder there is an intense fear to eat due to unpleasant sensation that
  • 4. GASTRITIS 172 Heartburn Belching VitaminB12 deficiency precedes vomiting Due to increae gastric secretion there is increase in intra-abdominal pressure and the normal tone of the fundus and body of the stomach is lost, and pyloric sphincter pressure decreases that cause back flow of gastric acid into the esophagus Belching is the expulsion of swallowed gastric air due to increase gastric secretion For the body to use vitamin B-12, it must be broken down from foods and properly absorbed by cells in the stomach. Intrinsic factor is a protein that is made by cells in the lining of the stomach. Without it, the body would be unable to absorb B-12 into cells. In conditions, such as chronic gastritis, the lining of the stomach is damaged, resulting in less intrinsic factor production. This leads to impaired B-12 absorption and deficiency
  • 5. GASTRITIS 173 PATHOPHYSIOLOGY 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 both oral and 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 pyloriincreases 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
  • 6. GASTRITIS 174 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 ulcers and 80% of duodenal 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.with H pylori is . 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 adhesion molecules 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.
  • 7. GASTRITIS 175 MEDICAL MANAGEMENT Endoscopy With the procedure known as gastrointestinalendoscopy, a doctor is able to see the inside lining of the digestive tract. This examination is performed using an endoscope-a flexible fiberoptic tube with a tiny TV camera at the end. The camera is connected to either an eyepiece for direct viewing or a video screen that displays the images on a color TV. The endoscope not only allows diagnosis of gastrointestinal (GI) disease but treatment as well. Biopsy with histologic examination are performed. A biopsy is a procedure to remove a piece of tissue or a sample of cells from your body so that it can be analyzed in a laboratory. The gold standard for diagnosis of Helicobacter pylori disease is gastric biopsy and evaluation for the presence of spirochetes by gram, silver, giemsa, or acridine orange stains. Alternatively, biopsied tissue can be examined by immunofluorescence or immunoperoxidase methods, rapid urease testing and/or culture. Exposure to Helicobacter pylori can be determined by detection of IgA, IgG, or IgM- class serum antibodies to the organism. Screening patients for the presence of antibody to Helicobacter pylori is a convenient, noninvasive means for assessing whether a patient has been exposed to Helicobacter pylori and whether gastrointestinal symptoms may be related to Helicobacter pylori infection.
  • 8. GASTRITIS 176 MEDICATION DRUG ACTION NURSING RESPONSIBILITY Antibiotics: Amoxicillin (Amoxil) Tetracyclin Antidiarrheal Bisuth subsalicylate H2 Receptor Antagonist: Cimetidine (Tagamet), A bactericidal that assist with eradicating H.pylori bacteria in the gastric mucosa Exert Bacteriostatic effect to eradicate H. pylori bacteria in gastric mucosa Suppresses H. pylori Bacteria in the gastric mucasa Decreases amount of HCL produced by stomach by blocking action of histamine on histamine receptors of parietal cells in the stomach May cause diarrhea Should not be used in patient allergic to penicillin May cause GI upset Use caution in patient with renal or hepatic impairment Should be taken on empty stomach May cause confusion agitation or coma Long term use may cause diarrhea, gynecomastesia
  • 9. GASTRITIS 177 Famotidine (pepcid) Ranitidine (Zantac) Proton Pump Inhibitor: Omeprazole (Prilosec) Lansoprazole (Prevacid Same as for cimetidine Same as for cimetidine Decrease acid secretion by slowing the H, K, ATPAse pump on the surface of the parietal cell of the stomach Decrease acid secretion by slowing the H, K, ATPAse pump on the surface of the parietal cell of the stomach Short term relief of GERD May cause headache, dizziness, constipation, nausea and vomiting or abdominal discomfort A delayed- release capsule that is to be swallowed whole and taken before meals May cause diarrhea, nausea, constipation, abdominalpain, headache A delayed- release capsule that is to be swallowed whole and taken before meals
  • 10. GASTRITIS 178 NURSING DIAGNOSIS 1. Acute / Chronic Pain associated with inflammation or irritation of the gastric mucosa due to increased gastric acid. 2. Imbalanced Nutrition Less Than Body Requirements related to anorexia, vomiting 3. Knowledge deficit and information related to the conditions and lack of coping skills INTERVENTION Avoids food and fluid by mouth for hours or days until symptom subside. Offer ice chips and clear liquid when symptom subside. Encourage patient to report any symptom suggesting a repeat episode of gastritis as food is introduced. Discourage caffeinated beverages, alcohol and cigarette smoking. Monitor daily input and output for dehydration. Infuse IV if prescribed assess electrolyte values for 24 hours for fluid imbalance. Be alert for indication of emorrhagic gastritis (hematemesis tachycardia hypotension) notify the physician. Instruct patient to avoid food and beverages that may be irritating to gastric mucosa. Reinforce the importance of completing the medication regimen as prescribed to eradicate H. pylori infection