Chapter I

Introduction
1.1 Background
Gastrointestinal system is a system that effecting food intestine and nutrition
which are needed by body. The accuracy of choosing food and food hygiene become
important consideration for citizen. In the developing countries like Indonesia, many
citizens who live in dirty and narrow environment have a apathetic character about
food choosing. Selection of the wrong foods will affect the digestive system due to
viruses, bacteria and other resources that will appears some problem that attack the
digestive system. Some diseases such as diarrhea, gastritis, constipation and other
digestive system disorders often arise in society. According to Rosenthal (2005),
Schaffner (2007) and Cindy (2005), gastrointestinal tract infections caused by
microbes are often hit indonesian people. This incident was evidenced by the
prevalence of diarrhea and dysentery are increased. In general, the microbes that
cause gastrointestinal into the human body through via the oral. Thousands of
microbes attached to the human hand and then went into the human body along with
the food into the mouth.
Gastritis or commonly known as the ulcer is a disease that often occurs in the
community, but once the disease is often underestimated and overlooked by the
sufferer. In fact, gastritis cant be underestimated. Gastritis is a digestive disease
caused by excessive gastric acid production. Patients will feel pain in their stomach
and heart burn in the area around the sternum.
In 2004, gastritis ranks 9 out of 50 major things outpatients in hospitals
throughout Indonesia with 218.500 cases. (Health Department of RI) Gastritis disease
incidence increased since the last 5-6 year and attack man more than woman. Other
factors related with gastritis include a family history and lack of overcome or poor
adaptation to stress.
Therefore, as the development of lifestyle into a modern, society needs to know
about the lifestyle and healthy food hygiene to avoid disruption of digestive disease.
1.2 Formulation of Problem
1.2.1 What is definition Gastritis?
1.2.2 What is the classification of gastritis?
1.2.3 What is the etiology of gastritis?
1.2.4 What are the signs and symptoms of gastritis?
1.2.5 How is the patophysiology of gastritis?
1.2.6 What is complication of gastritis?
1

1.2.7 What is the risk factor of gastritis?

1.2.8 How is the nursing care plan of gastritis?
1.3 Purpose
1.3.1 Knowing definition of gastritis
1.3.2 Knowing the classification of gastritis
1.3.3 Knowing the etiology of gastritis
1.3.4 Knowing sign and symptoms of gastritis
1.3.5 Knowing the patophysiology of gastritis
1.3.6 Knowing the complication of gastritis
1.3.7 What is the risk factor of gastritis
1.3.8 Knowing the nursing care plan of gastritis

Chapter II
Literature Review
2.1 Anatomy and Physiology of Gastrointestinal System
The digestive or gastrointestinal system prepares food for use by hundreds
millions of body cells. Food when eaten cannot reach cells because it cannot pass
through the intestinal walls to the bloodstream and, if could not be useful chemical
state. The gut modifies food physically and chemically and disposes of unusable
waste. Physical and chemical modification (digestion) depends on exocrine and
2

endocrne secretions and controlled movement of food through the gastrointestinal

tract. Exocrine secretions prepare food for absorption by diluting it to the osmolality
of plasma (isotonic), altering the pH for hydrolysis, and hydrolyzing complex foods.
The exocrine secretions also protect the mucosa from physical and chemical irritants.
Endocrine secretions play a major role in the control and coordination of secretory
and motor activities involved in the digestion and absorption of food. The
gastrointestinal system consists of the mouth, pharynx, esophagus, stomach,small and
large intestines, rectum and anus. Accessory organs include liver, gallbladder, and
pancreas. The accessory organs found in the mouth are the teeth and salivary glands.

Picture. Gasrointestinal System

2.1.1

Stomach
The stomach is located in the upper portion of the abdomen, to the left in the
midline. The lower esophagus, or cardiac, sphincter divides the esophagus and
stomach, which on contraction, closes the stomach off from the esophagus. The
stomach has a capacity of approximately 1500 ml and has three anatomic
divisions. Three anatomic divisions consist of:
1) The fundus, which lies above and to the left of the cardiac sphincter.
2) The body of central area.
3) The lower area, called the antrum or pyloric region.

Picture: Anatomy of Stomach

The outlet from the distal end of the stomach and the duodenum is called
pyloric sphincter. It permits the flow of chime from the stomach. The stomach has
four layers:
1) Serosa: The serosa outer layer is the visceral peritoneum.
2) Muscularis: The muscular layers (tunica muscularis) produce peristaltic
activity of the stomach as it churns food during digestion.
3) Submucosa: The submucosa (or tela submucosa) connecs the muscular and
mucous layers of the stomach wall and contains the blood, lymph channels,
and nerve plexus.
4) Mucosa: The epithelial lining of the stomach contains many :
a. Cardiac glands secrete muscus.
b. Peptic (chief) cells secrete mucus and pepsinogen. Pepsinogen is converted
to pepsin, a proteolytic enzyme.
c. Parietal (oxyntic) cells secrete hydrochloric acid and water. The parietal
cells are stimulated by gastrin to produce hydrochloric acid, which helps
digestion of protein. These cells also produce the intrinsic factor that
allows vitamin B2 to be absorbed.
d. Neck cells secrete mucus.
e. Pyloric glands secrete gastrin and mucus.

Picture: Layers of Stomach

The function of the stomach include storage, mixing, liquefaction of the
bolus of food into chime, and control of passage of food into duodenum. The first
stage of protein breakdown occurs in the stomach. The major portion of the
mechanical breakdown of food occurs in the antrum. At the distal end of the
stomach, the pyloric sphincter permits the flow of chime from the stomach into
the duodenum.
4

Digestion or starches, which begins in the mouth by the action of ptyalin,

continues in the stomach. Digestion can last for as long as 30 minutes, or until the
mixing function of the stomach allows its acid contents to inactive the ptyalin.
Digestion of fats in the stomach is minimal. Small quantities of water, alcohol,
glucose, and some drugs may be absorbed through the gastric mucosa. Most
organisms are destroyed by the acidic gastric juice.
The stomach secrets 1500 to 3000 ml of gastric juice per day. Its major
secretions are hydrochloric acid, pepsin, and mucus. Gastric juice contains mucin,
intrinsic factor, lipase, pepsinogen, and protein. Gastric acid secretion is directly
stimulated by distention of the stomach and the presence of protein. Gastric acid
secretion is also stimulated by vagal activity, acetylcholine, histamine, and the
hormone gastrin. Gastrin is released when the stomach becomes distended with
food.
Hydrochloric acis and pepsin provide the corrosive power of gastric
secretions. Pepsin is the most active factor in the digestive process of the
stomach, acting to break down proteins to polypeptides, proteases, and peptones.
Peptic activity is greatest at pH levels ;ess than 3.5. Pepsin is stimulated by food,
whereas mucus has a neutralizing effect, which protects the stomach mucosa.
The three phases of gastric secretion are cephalic, gastric, and intestinal:
1) The cephalic (nervous) phase of digestion is dependent on stimulation of
gastric secretions by receptors in the brain that are mediated by the vagus
nerve. This phase is stimulated by hunger and by the odors, sigh, smell,
thought, and discussion of food. The cephalic phase results in secretion of
acid, pepsin, and mucus.
2) The gastric (hormonal) phase of secretion occurs when the bolus of food
reaches the antrum. This phase consists of three mechanisms. When the food
enters the stomach, the long vagovagal reflex, local enteric reflexes, and
gastrin mechanisms are excited. These mechanisms lead to the secretion pf
gastric juice. This phase continues for several hours, until the acidity of the
gastric contents reaches 1.5 or less.
3) The intestinal phase includes both nervous and hormonal mechanisms. This
phase is stimulated by food entering duodenum, resulting in the secretion of a
small amount of gastrin by the intestine. This process, in turn stimulates gastric

secretion of pepsin and mucus. The duodenal pH the decreases, resulting in the
2.1.2

release of secretin, which inhibits gastric secretion and slows gastric emptying.
Small Intestine
Jejenum (8 feet) and ileum (12 feet) continue degenerative process. Surface

area increased by plica circulares (circular folds) carrying villi, cells of villi cary
microvilli. Each villus has a capillary and a lacteal (lymphatic capillary). Absorption
of digested foodstuffs is via these to the rich venous and capillary drainaged of the
gut. Towards the end of the small intestine accumulations of lymphoid tissue (Peyers
patches) more common. Undigested residue of food is rich in bacteria.
2.1.3

Large Intestine
Jejenum terminates at cecum. Cecum is small sac like evagination, important

in some animals as a repository for bacteria/other organism able to digest cellulose. A

blind ending appendix may give trouble (appendictis) if infected. The large intestine
has three longitudinal muscle bands (taenia coli) with bulges in the wall (haustra)
between them. These may evaginate in the elderly to become diverticuli and infected
in diverticulitis. The large intestine resorbs water then eliminates drier residues as
feces. Regions recognized are the ascending colon, from appendix in right groin up to
a flexure at the liver, transverse colon, liver to spleen, descending colon, spleen to left
groin, then sigmoid (S-shaped) colon back to midline and anus. Anus has voluntary
and involuntary sphincter and ability to distinguish whether contents are gas or solid.
No villi in large intestine, but many goblet cells secreting lubricative mucus.
2.1.4

Rectum
The rectum is the final straight organ of the large intestine, terminating in the

anus. The human rectum is about 12 cm long. The rectum intestinum acts as a
temporary storage facility for feces. As the rectal walls expand due to the materials
filling it from within, stretch receptors from the nervous system located in the rectal
walls stimulate the desire to defecate. If the urge is not acted upon, the material in the
rectum is often returned to the colon where more water absorbed. If defecation is
delayed for a prolonged period, it will result constipation and harderned feces. When
the rectum becomes full the increase in intrarectal pressure forces the walls of the
anal canal apart allowing the fecal matter to enter the canal. The rectum shortens as

material is forced in to the anal canal and peristaltic waves propel the feces out of the
rectum. The internal and external sphincter allow the feces to be passed by muscles
pulling the anus up over the exiting feces.
2.1.5

Anus
In anatomy, anus or bottom hole is an opening from rectum to the outside of

body. Opening and closing of anus is arranged by sphincter muscle. Feces is thrown
away from body although defecation process, which is the main function of anus. In
anus, feces is pulled out. This is a final digestive process.
2.1.6

Accessory Digestive Organs

a. Salivary glands
Three pairs, parotid, submandibular, sublingual. Mumps begins as
infective parotitis in the parotid glands in the cheek. The others open into the
floor of the mouth. Saliva is a mixture of mucus and serous fluids, each
produced to various extents in various glands. Also contains salivary amylase,
(start to break down starch) lysozyme (antibacterial) and IgA antibodies.
b. Pancreas
Endocrine and exocrine gland. Exocrine part produces many enzymes
which enter the duodenum via the pancreatic duct. Endocrine part produces
insulin, blood sugar regulator.
c. Liver and Gallbladder
Bile, a watery greenish fluid is produced by the liver and secreted via
the hepatic duct and cystic duct to the gall bladder for storage, and thence on
demand via the common bile duct to an opening near the pancreatic duct in the
duodenum. It contains bile salts, bile pigments (mainly billirubin, essentially
the non-iron part of haemoglobin) cholesterol and phospholipids. Bile salt and
phospholipids emulsify fats, the rest are just being excreted. Gallstones are
usually cholesterol based, may block the hepatic or common bile ducts causing
pain, jaundice.

2.2 Definition Gastritis

Gastritis is an inflammation of the mucosa that can be acute, chronic diffusion,

or local. Acute superficial gastritis and chronic atrophic gastritis are the most types of
gastritis.(Silvia A. Price et al, 1994, page.376).
Gastritis is the inflammation process in mucus and gastric submucosa. Gastritis
is a disorder that most frequently encountered in the clinic because the diagnosis is
only based on clinical symptoms instead of histopathology (Hirlan 2006, page.337).
2.3 Classification Of Gastritis
In

General,

the gastritis is

divided

the clinical manifestations,

into some

the

sort based

image

on
of a

typical hispatologis, Anatomy, distribution and possible pathogenesis of gastritis:

a. Acute Gastritis
Acute gastritis is
and bleeding of
two forms

an inflammation

gastric mucosa due

of

the gastric mucosa that cause erosion

to exposure

of the clinical manifestations

to irritant substances. There

of acute gastritis can

are

be shaped into

a severe illness that is acute gastritis acute gastritis and erosif hemoragik.
1) Acute Gastritis erosive,

Erosif acute gastritis is

the gastric mucosal surface of the acute damage

an inflammation

of

from erosion is not deeper in the

mucous muskularis.
2) Acute Gastritis hemoragik, Hemoragik acute gastritis is an inflammation caused by a
drink of

alcohol

or other

drugs that cause irritation

to mucous gastrik excessive stress gastritis experienced bypatients in the hospital.

Picture: Acute Gastritis

b. Chronic Gastritis

Chronic gastritis is inflammation

time. Chronic gastritis befell to

of

him

the gastric mucosa in long

who

periods

has an incurable disease

of
of

the gastritis. On chronic gastritis have a classification based on histology, namely:

1) Chronic superficial Gastritis
Chronic superficial gastritis Is the change of inflammatory or inflammation of
the mucosal surface is

limited,

which

causes mucous,

edema eritemia with a

small erosion and bleeding.

2) Chronic Gastritis atrofik
The inflammation extends deeper into the mucosa and accompanied by distortion
and destruction of the mucous gland cells are progressive.

Picture: Chronic Gastritis

2.4 Etiology Of Gastritis
The etiology can be distinguished based on the type classifications are:
a. Acute Gastritis
It is the inflammation of the mucosa of the stomach that causes the presence of
gastric mucosal erosion and bleeding due to exposure to irritant substances. Aspirin
and drugs other nonsteroidal annti-inflammatory (NSAID) drug, digitalis, kemotrapik,
steroids, radiation theraphy, acute alcoholism and consume cocaine, food poisoning
caused by Staphylococcus organisms, and HIV/AIDS. Other causes also comes
from foods that are acidic or alkali strong, spicy, and contain gas, which can cause the
mucous become gandren or perforation.
9

b. Chronic Gastritis
An inflammation of the gastric mucosa in the long term. Chronic gastritis befall the
people who have incurable diseases gastritis. Peptic ulcer disease (PUD) or gastric
surgery may lead to chronic gastritis. Another risk factor is equal to acute gastritis.
After resection with gastrojejunostomy may occur bile reflux and bile acids to the rest
of the stomach, causing gastritis. H. pylori infection has been identified as an
independent risk factor for gastric cancer. Because these bacteria can cause chronic
gastritis. Age is also a risk factor for chronic gastritis, usually occurs in older people.
2.5 Pathophysiology of Gastritis
Acute erosive gastritis is a transient secondary inflammation of the gastric
mucosa that, although short-lived, can result a mild or severe bleeding state. It is most
commonly caused by nonsteroidal antiinflammantory drugs (NSAIDs) or aspirin or
excessive ingestion of alcohol, but its also seen in critically ill patients as part of a
stress response to a bacterial infection. If left untreated, it can lead to cgronic gastritis.
NSAIDs such as aspirin, ibuprofen, and naproxen are widely used to treat
musculoskeletal and other chronic pain disorders. They act by suppressing the
synthesis of prostaglandins. One source of prostaglandin production is from the gastric
ephitelial cells, which produce prostaglandins to protect the stomach mucosa from
gastritis acid. Without prostaglandins, the mucosa is susceptible to the effect of the
gastric acid. The condition is often asymptomatic, with complaints, if any, being
anorexia, nausea, vomiting, and epigastric pain. Vomiting of material resembling coffe
grounds or the discovery of blood in a nasogastric tube aspirate is the most common
initial manifestation of problem. On endoscopy, superficial injury to the mucosa is
found, including small hemorrhages, petechiae, and erosion. These lesions can very in
size and number and may be located at a single site or scattered throughout the
stomach. The extent of the injury is not related to the amount of bleeding. Only the
mucosa is affected; the submucosa and muscularis mucosae are not penetrated, as is
the case with peptic ulcer disease. Endoscopy hemostasis techniques are not affective
in treating the gastritis because the bleeding is usually diffuse. (Bernadette, 2008)

10

A stress-induced gastritis usually occurs within the first 198 hours of the onset
of the illness episode. Critically ill patients who experience respiratory failure are put
on mechanical ventilation; those who develop a coagulopathy are at high risk.
Although not causing death, the development of gastritis is associated with a high
mortality rate.
For stress-induced gastritis, treatment is aimed at prevention by administering
sucralfete or H2 receptor antagonist prophylaxis routinely to those patients who fall in
the categories of those likely to suffer from stress-induced gastritis.
Alcoholic gastritis accounts for 20% of all upper gastrointestinal bleeding in
that population. Because alcohol is a gastric irritatant that stimulates gastric acid
secretion, the individual must completely stop drinking alcohol for any kind of
recovery to be possible.
Other causes of gastritis are acute bacterial infections, viral infections with
cytomegalovirus commonly seen in those with human immunodeviciency virus or
after organ transplant. Fungal infections eith Candida seen in immunocompromised
patient, and granulomatous gastritis caused by a variety of systemic diseases such as
Chrons disease, tuberculosis, and sacroidosis. Acute bacterial infections that cause
gastritis can be life threatening, especially in the elderly or immunocompromises. The
causative organisms include streptococci, staphylococci, Escherichia coli, proteus, and
Haemophilus, and may lead to a gastrectomy. (Vanessa, 2008)
2.6 Sign and symptoms of Gastritis
1. Nausea or recurrent upset stomach
2. Abdominal bloating
3. Abdominal pain
4. Vomiting
5. Indigestion
6. Burning or gnawing feeling in the stomach between meals or at night
7. Hiccups
8. Loss of appetite
9. Vomiting blood or coffee ground-like material
10.Black, tarry stools
2.7

Complication Of Gastrits
a. Peptic ulcers. Peptic ulcers are sores involving the lining of the stomach or
duodenum, the first part of the small intestine. NSAID use and H. pylori gastritis
increase the chance of developing peptic ulcers.
11

b. Atrophic gastritis. Atrophic gastritis happens when chronic inflammation of the

stomach lining causes the loss of the stomach lining and glands. Chronic gastritis
can progress to atrophic gastritis.
c. Anemia. Erosive gastritis can cause chronic bleeding in the stomach, and the blood
loss can lead to anemia. Anemia is a condition in which red blood cells are fewer or
smaller than normal, which prevents the body's cells from getting enough oxygen.
Red blood cells contain hemoglobin, an iron-rich protein that gives blood its red
color and enables the red blood cells to transport oxygen from the lungs to the
tissues of the body. Research suggests that H. pylorigastritis and autoimmune
atrophic gastritis can interfere with the body's ability to absorb iron from food,
which may also cause anemia..
d. Vitamin B12 deficiency and pernicious anemia. People with autoimmune atrophic
gastritis do not produce enough intrinsic factor. Intrinsic factor is a protein made in
the stomach and helps the intestines absorb vitamin B12. The body needs vitamin
B12 to make red blood cells and nerve cells. Poor absorption of vitamin B12 may
lead to a type of anemia called pernicious anemia..
e. Growths in the stomach lining. Chronic gastritis increases the chance of developing
benign, or noncancerous, and malignant, or cancerous, growths in the stomach
lining. Chronic H. pylori gastritis increases the chance of developing a type of
cancer called gastric mucosa-associated lymphoid tissue (MALT) lymphoma.
2.8 Risk Factors
Factors that increase your risk of gastritis include:
1. Bacterial infection
Although infection with Helicobacter pylori is among the most common worldwide
human infections, only some infected people develop gastritis or a similar stomach
disorder. Doctors believe vulnerability to the bacterium could be inherited or could be
2.

caused by lifestyle choices, such as smoking and high stress levels.

Regular use of pain relievers
Common pain relievers such as aspirin, ibuprofen (Advil, Motrin IB, others) and
naproxen (Aleve, Anaprox) can cause both acute gastritis and chronic gastritis.
Using these pain relievers regularly or taking too much of these drugs may reduce a
key substance that helps preserve the protective lining of your stomach. Stomach

12

problems are less likely to develop if you take pain relievers only occasionally.
Acetaminophen (Tylenol, others) does not lead to gastritis.
3. Older age
Older adults have an increased risk of gastritis because the stomach lining tends to
thin with age and because older adults are more likely to have H. pylori infection or
4.

autoimmune disorders than younger people are.

Excessive alcohol
Alcohol can irritate your stomach lining, which makes your stomach more likely to be
harmed by digestive juices. Excessive alcohol use is more likely to cause acute

5.

gastritis.
Stress
Severe stress due to major surgery, injury, burns or severe infections can cause acute

gastritis.
6. Your own body attacking cells in your stomach
Called autoimmune gastritis, this type of gastritis occurs when your body attacks the
cells that make up your stomach lining. This produces a reaction by your immune
system that can wear away at your stomach's protective barrier. Autoimmune gastritis
is more common in people with other autoimmune disorders, including Hashimoto's
disease and type 1 diabetes. Autoimmune gastritis can also be associated with vitamin
7.

B-12 deficiency.
Other diseases and conditions. Gastritis may be associated with other medical
conditions, including HIV/AIDS, Crohn's disease and parasitic infections.

2.8 Diagnose Gastritis

To diagnose gastritis, your doctor will review your personal and family medical history,
perform a thorough physical evaluation, and may recommend any of the following tests:
1

Upper endoscopy. An endoscope, a thin tube containing a tiny camera, is inserted through
your mouth and down into your stomach to look at the stomach lining. The doctor will
check for inflammation and may perform a biopsy, a procedure in which a tiny sample of
tissue is removed and then sent to a laboratory for analysis.

Blood tests. The doctor may perform various blood tests, such as checking your red blood
cell count to determine whether you have anemia, which means that you do not have
enough red blood cells. He or she can also screen for H. pylori infection and pernicious
anemia with blood tests.

Fecal occult blood test (stool test). This test checks for the presence of blood in your
stool, a possible sign of gastritis.
13

Biopsy or take a small sample, of the lining of the stomach if they find anything
unusual during the examination.

X-rays of digestive tract after patient swallow a barium solution, which will help
distinguish areas of concern.

2.9 Treatments and Drugs of Gastritis

Treatment of gastritis depends on the specific cause. Acute gastritis caused by
nonsteroidal anti-inflammatory drugs or alcohol may be relieved by stopping use of
those substances. Chronic gastritis caused by H. pylori infection is treated with
antibiotics.
Medications used to treat gastritis include:
a.

Antibiotic medications to kill H. pylori. For H. pylori in digestive tract, recommend

a combination of antibiotics, such as clarithromycin (Biaxin) and amoxicillin or
metronidazole (Flagyl), to kill the bacterium. Be sure to take the full antibiotic
prescription, usually for 10 to 14 days.

b.

Medications that block acid production and promote healing. Proton pump
inhibitors reduce acid by blocking the action of the parts of cells that produce acid.
These drugs include the prescription and over-the-counter medications omeprazole
(Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex), esomeprazole (Nexium),
dexlansoprazole (Dexilant) and pantoprazole (Protonix). Long-term use of proton
pump inhibitors, particularly at high doses, may increase your risk of hip, wrist and
spine fractures. Ask your doctor whether a calcium supplement may reduce this risk.

c.

Medications to reduce acid production. Acid blockers also called histamine (H2) blockers reduce the amount of acid released into your digestive tract, which
relieves gastritis pain and promotes healing. Available by prescription or over-thecounter, acid blockers include ranitidine (Zantac), famotidine (Pepcid), cimetidine
(Tagamet) and nizatidine (Axid).

d.

Antacids that neutralize stomach acid. Antacids neutralize existing stomach acid
and can provide rapid pain relief. Side effects can include constipation or diarrhea,
depending on the main ingredients.
14

2.10

Home care
Lifestyle changes may also help reduce your acute gastritis symptoms. Changes that
could help include:

2.11

1.

avoiding or limiting alcohol consumption

2.

avoiding spicy, fried, and acidic foods

3.

eating frequent, small meals

4.

reducing stress

5.

avoiding drugs that can irritate the stomach lining, such as NSAIDs or aspirin.

Preventing acute gastritis

You can reduce your risk of developing this condition with a few simple steps:
1.

Wash your hands with soap and water regularly and before meals. This can
reduce your risk of becoming infected with H. pylori.

2.

Cook foods thoroughly. This also reduces the risk of infection.

3.

Avoid alcohol or limit your alcohol intake.

4.

Avoid NSAIDs or dont use them frequently. Consume NSAIDs with food and
water to avoid symptoms.

Nursing Care Plan Patient with Gastritis

a. Assesment
1) Patient Identity: Name, age, sex, religion, address, etc
2) Health History
a) Chief Complaint: Pain in the upper and middle abdomen, nausea,
vomiting every feeding
b) Past Nursing Hystory: Client has been treated
3) Observation And Physical Examination
a. General appearance
TTV: TD: 100/80 mmHg, N: 84 x/minute, RR: 20 x/minute, S:36,5 C
Anthropometry: 48 kg
B1: RR 20 x/minute, regular rhythm
B2: Pulse : 84x /minute, regular rhythms ,BP: 110/60 mmHg
B3: GCS: 4, 5, 6. Reflex : normal

15

B4:B5: lost appetite, nausea, abdominal pain in the upper middle (scale: 5)
B6: turgor : elastic

Ancillary Data
1)

Laboratory

Examination
Hb

Results
14 mg/dl

Normal
P: 12-14 gr/dl

Hematokrit

41,2 %

P : 37-43%

Platelets

189.000/ul

P : 115.000-400.000/ul

Leukocytes

7.800/ul

P : 5.000-10.000/ul

SGOT

15

P : < 32

SGPT

13
4) Medical diagnosis : gastritis
5) Data Analysis
No. Data
1
Ds:

P : < 31

Etiology
the pattern of bad nutrition

Clients

complain

of

stomach pain in upper left nutrition

abdomen.

Prablem
impaired sense of
comfort: pain

intake

contains

irritant (pepper, seasoning)

Do:

irritate the gastric mucosa

Clients seem to

grimace
while

and
holding

pain stimulates nerve periper

her

stimulate spending serotinin,

upper left abdomen
Pain scale: 5
bradykinin
The client looked

16

agitated

pains

gastric mucosa Irritation

Ds:

Imbalanced

A client complaining of

nutrition less than

nausea while eating and increased

always throw up

stomach

acidbody requirements

(HCL)

Do:

3.

nausea and vomiting

Havent breakfast
weak
nutritional intake is less
vomit
Laboratory

results: HB: 14 gr/dl

Ds:

Less

knowledge

about

a Anxiety

Families of inquire aboutdisease that inflicted on the

illnesses suffered by theclient
client

Do:

anxious

-Family seemed

actively ask

b. Nursing Diagnosis
1.
Pain related to irritation gastric mucosa
1.
Imbalanced nutrition less than body requirements related to nause and
vomiting
Anxiety related to lack of knowledge about the disease suffered

2.

Intervention
No

Diagnosa

1.

Pain

related

irritation
mucosa

Intervention
to Review the level of pain.

Rational
In order to determine the

gastric Provide information about the level of pain experienced by

different strategies chosen to the

client.
17

reduce

pain. Able to learn methods of pain

Encourage clients to use the reduction

Purpose: Pain is chosen strategy to reduce pain
gone / no pain

(example:

guided

and

Assist

in

imaginary, experienced

Distraction,

can

do

it.

menurunhkan

pain

threshold.

relaxation) In order for clients to find

Encourage clients to avoid foods that stimulate stomach

eating foods that stimulate an acid and does not consume
increase

in

stomach

acid. them.

Collaboration with the medical Reduce the level of pain

team for the administration of experienced by the client.
2.

anti-analgesic.
Describe the client and family

Imbalanced

Clients and families can learn

nutrition less than about the importance of food for the

body requirements the
related to

body.

importance
To

know

the

of
food

is

nausea Monitor the amount of food consumed.

and vomiting

intake.

As the data to perform

Monitor

and

record

the nursing actions and subsequent

number of vomiting, frequency treatment.

Purpose: Nutrition and
balanced.

color To klirn be motivated and

Provide

according

a
to

varied
his

diet

stimulate

diet stimulates

appetite.

to To reduce the feelings and

appetite. needs

food

for

patients.

Provide food in small portions As a therapy for inhibiting /

but

frequently. stimulating

nausea

and

Collaboration with the medical vomiting.

team for the administration of
3.

anti-emetic drugs.
Anxiety related to Assess the client's

anxiety.

As

the

initial

data

to

lack of knowledge Give the client an opportunity determine the client's anxiety
about the disease to
suffered

express

anxiety. level.

Explain to clients that can In order to determine the

challenge
after

Purpose:

his

dijalankankan

diet cause of anxiety is experienced

recovery. as

well

as

reduce

the

No Explain to the client about psychological burden of the

18

Anxiety

medical procedures / treatments client.

will be done and encouraged The client can adhere to diet
cooperative

therein. and

avoid

disease

relapse

Provide motivation to the again.

client

about

his

recovery. Able to understand and accept

all the measures taken to cure
the

disease

process.

Clients and families are

optimistic for the healing of
disease and comply with all
recommended clients are given.

Evaluation
1.

Chapter III
19

Conclusion
3.1 Conclusion
Gastritis is an inflammation of the mucosa that can be acute, chronic diffusion,
or local. Acute superficial gastritis and chronic atrophic gastritis are the most types of
gastritis.(Silvia A. Price et al, 1994, page.376). Gastritis is commonly caused by
NSAIDs. Acute superficial gastritis and chronic atrophic gastritis are the most types
of gastritis. The signs and symptoms are like Nausea or recurrent upset stomach,
abdominal bloating, abdominal pain, and vomiting.

BIBLIOGRAPHY

1. Brunner dan Suddarth. 2001. Keperawatan Medikal Bedah Ed. 8 Vol 2. Buku
Kedokteran EGC. Jakarta.
2. Bulechek, Gloria M, et al. 2013. Nursing Interventions Classification (NIC) Sixth
Edition. Missouri : Elsevier Inc.
3. Campbell, Neil A. 2004. Biologi : Edisi Kelima - Jilid 3. Jakarta : Erlangga
4. Charles, J.Reeves, dkk. 2001. Buku 1 Keperawatan Medikal Bedah Ed. I. Salemba
Medika. Jakarta.
5. Price, Sylvia A dan Lorraine M. Wilson. 1994. Patofisiologi : Konsep Klinis ProsesProses Penyakit. Jakarta : EGC
6. Hirlan. 2006. Gastritis. Ilmu Penyakit Dalam. 4ed. AW Sudoyo , editor. Jakarta: Pusat
Penerbitan Departemen Ilmu Penyakit Dalam FKUI.
7. http://www.healthline.com/health/gastritis#CausesandRiskFactors2 (Gastritis
Written by Carmella Wint and Winnie Yu..Medically Reviewed by Steven Kim,
MD on October 21, 2015)
20

8. http://www.healthline.com/health/gastritis-acute (Acute Gastritis Written by Rose

Kivi,

Ana

Gotter,

and

Elizabeth

Boskey,

PhD

Medically Reviewed by Graham Rogers, MD on August 31, 2016)

9.

Tambhan gmbar dibesarin

Untuk gejla diberikan keterangan
Pengurutan blum urut

21