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CHAPTER I

PRELIMINARY

A. Background

Cases with gastritis is one of the most common types of cases suffered by
adolescents, especially the disease is increasing among students. caused by a variety of
factors such as irregular eating patterns, wrong lifestyle and increased activity (lecture
duties) so that the student did not have time to set his diet and lazy to eat (Fahrur,
2009).

The causes of gastritis by Herlan in 2001 were excessive alcohol intake (20%),
smoking (5%), spiced food (15%), drugs (18%) and radiation therapy (2%), whereas
according to Hasna and Hurih year 2009 gastritis can also be caused by, bacterial
infections, stress, autoimmune disease, radiation and Chron's Disease.

One cause of gastritis is an infection of the bacterium Helicobacter pylori ( H. pylori)


and is the only bacterium living in the stomach. These bacteria can infect the stomach
since children and cause chronic stomach disease. Even more than 50% of the world's
population is infected with this bacterium since childhood. If left unchecked, it will cause
lifelong problems (Soemoharjo, 2007). According to the Indonesian Society of
Gastroenterology (PGI) and the Helicobacter Pylori Indonesia Study Group (KSHPI) in
2001, it was estimated that 20% of the Indonesian population had been infected by H.
Pylori (Daldiyono, 2004). The discovery of Helicobacter pylori infection this may have
an impact on the high incidence of gastritis, in some areas in Indonesia shows a high
incidence of gastritis.

Common symptoms in people with gastritis are abdominal discomfort, abdominal


bloating, headache and nausea that can interfere with daily activities, discomfort in the
epigastrium, nausea, vomiting, stinging or burning pain in the upper abdomen that can
getting better or worse when eating, missing appetite, belching, and bloating. Can also
be accompanied by fever, chills (chills), hiccups ( hiccups )

If this gastritis disease continues to be left, will result in more severe and ultimately
stomach acid will create injuries (ulcers), known as gastric ulcers. It can even be
accompanied by blood vomiting (Arifianto, 2009). According to research Surya and
Marshall in 2007 to 2008 say gastritis that is not handled properly will lead to
complications that lead to severity. Namely cancer of the stomach and peptic ulcer.

B. Problem Formulation

1. What is gastritis?

2. What is the cause of gastritis?

3. What are the symptoms of gastritis?

4. How is the pathophysiology of acute gastritis and chronic gastritis ?

5. What treatment is done for gastritis disease ?

6. What prevention can be done as a preventive measure ?

C. Writing purpose

1. To know the definition of gastritis

2. To determine the cause of gastric inflammation (gastritis)

3. To know the symptoms of gastritis

4. To know the pathophysiology of acute gastritis and chronic gastritis

5. To know the treatment that can be done for people with gastritis

6. To know the preventive action of the gastritis.


CHAPTER II

LITERATURE REVIEW

A. Anatomy of Physiology

Understanding

The stomach is part of the channel that can inflate mostly in the epigaster region, the
stomach consists of the top of the uterine fundus associated with the esophagus
through the pyloric orifice, located below the diagfragma in front of the pancreas and
the spleen, attached to the left of the uterine fundus (Anatomy of physiology for nursing
students 3.EGC edition: 171).

Anatomy and Physiology

Part of the stomach:

a. The ventricular fundus, the protruding part upwards to the left of the cardiac
osteoum and usually full of gas.

b. The ventricular corpus, as high as the cardiac osteoum, an indentation on the lower
part of the minor curvatura.

c. Antrum pylorus, tubular hull section has thick muscle forming spingter pylorus.

d. The minor curvatura, right side of the stomach, extends from the cardiac osteoum to
the pylorus.

e. The major curvatures, longer than the minor curvature, extend from the left side of
the cardiac ostoeum through the ventricular fundus to the right up to the inferior
pylorus. The ligamnetum of the gastrolinealis extends from the top of the major
curvature to the spleen.

f. Cardio oesteoum, is where the esophagus of the abdomen into the stomach. In this
section there is a pyloric orififum.
Gastric Function

a. Accommodates food, destroys and smooths food by peristaltic stomach and gastric
juice.

b. Gastrointestinal digestion produced:

1. Pepsin functions, breaking egg white into amino acids (albumin and peptone).

2. Salt acid (HCL) function, acidify food, as an antiseptic and disinfectant, and create an
acid atmosphere on pepsinogen to become pepsin.

3. Renin its function, as yeast freeze milk and form casein from kasinogen (kasinogen on
milk protein).

4. Stomach lining : the amounts of a little break down fat into fatty acids that stimulate
gastric secretion.

( Anatomy of Physiology for Nurse Students , Issue 2, EGC 1997: 77-78).

B. Definitions

Gastritis or better known as ulcer is derived from the Greek gastro , which means
stomach / stomach and itis which means inflammation / inflammation. Gastritis is not a
single disease, but is formed from several conditions that all result in inflammation of
the stomach. Usually, the inflammation is the result of infection by the same bacteria
with bacteria that can cause ulcers in the stomach of Helicobacter pylori . But other
factors such as physical trauma and continuous use of some painkillers may also cause
gastritis .

Histologically provable by inflammation of inflammatory cells in the area based on


clinical manifestations can be divided into acute and chronic (Hirlan, 2001: 127).

In some cases, gastritis can lead to ulcers ( ulcers ) and may increase the risk of
gastric cancer. However, for many people, gastritis is not a serious illness and may soon
improve with treatment.

Gastritis is a common disorder with the presence of anorexia, fullness, and


discomfort in the epigastrium, nausea, vomiting.

In general, the definition of gastritis is inflammation of the stomach wall, especially


in the mucosa and submukosa stomach. Gastritis is the most common disorder of the
clinic because its diagnosis is based only on clinical symptoms.
C. Classification
Gastritis by type is divided into 2, namely (David Ovedorf 2002 ):

1. Acute Gastritis

Caused by digesting strong acids or alkalis that can cause the mucosa to become
gangrene or perforation. Acute gastritis is divided into two major lines :

Acute exogenous gastritis (usually caused by external factors, such as kimnamical


material: lisol, alcohol, smoking, pepper caffeine, steroids, mechanical bacterial
irritation, analgesic drugs, anti-inflammatory especially aspirin (low-dose aspirin already
can cause gastric mucosal erosion )).

Acute endogenous gastritis (is a gastritis caused by a body disorder ) .

2. Chronic Gastritis

Prolonged gastric inflammation may be caused by benign or benign or benign


ulcers, or by Helicobacter pylory ( H. Pylory) bacteria. Chronic gastritis is regrouped in 2
types of type A and type B. It is said to be a chronic gastritis of type A if it is capable of
producing its own immune. This type is associated with atrophy of the gland and
mucosal decline. The decrease in gastric secretion affects the production of antibodies.
Pernicious anemia develops in this process. B type chronic gastritis is more prevalent.
This type is associated with a helicobacter pylori infection that causes ulcers in the
stomach wall.

D. Etiology

1. Bacterial infection .

Most of the world's population is infected by H. Pylori bacteria that live on the
inside of the mucous layer lining the stomach wall. Although it is not fully understood
how the bacteria can be transmitted, it is thought to occur through oral route or by
eating food or drink contaminated by this bacteria. H. pylori infection is common in
childhood and can last a lifetime if not treated. H. pylori infection is now known to be
the main cause of peptic ulcer and the most common cause of gastritis. Long-term
infection will cause inflammation to spread which then results in changes in the
protective layer of the stomach wall. One such change is atrophic gastritis, a condition
in which the acid-producing glands are slowly damaged. Researchers concluded that low
levels of stomach acid can result in toxins produced by cancer not to be destroyed or
excreted completely from the stomach, increasing the risk of stomach cancer. But most
people with chronic H. pylori infection have no cancer and no symptoms of gastritis,
indicating that there are other causes that make some people vulnerable to these
bacteria while others are not.

2. Continuous use of painkillers .

Analgesic anti-inflammatory drug (NSAID) such as aspirin, ibuprofen and naproxen


can cause inflammation of the stomach by way of reducing prostaglandin in charge of
protecting the stomach wall. If the use of these drugs only occasionally then the
possibility of stomach problems will be small. But if the use is done continuously or
excessive use can lead to gastritis and peptic ulcer.

3. Excessive use of alcohol .

Alcohol can irritate and erode the mucosa in the gastric wall and make the stomach
wall more susceptible to stomach acid even under normal conditions.

4. Cocaine use .

Cocaine can damage the stomach and cause bleeding and gastritis.

5. Physical stress .

Physical stress due to major surgery, traumatic injury, burns or severe infections can
cause gastritis and ulcers and bleeding in the stomach.

6. Autoimmune disorder .

Autoimmune atrophic gastritis occurs when the immune system attacks healthy cells
that are in the wall of the stomach. This results in inflammation and gradually dilutes the
stomach wall, destroys the gastric acid producing glands and disrupts the production of
intrinsic factors (ie a substance that helps the body absorb vitamin B-12). Lack of B-12, in
the end, can lead to pernicious anemia, a serious con- sumption that if not treated can
affect the entire system in the body. Autoimmune atrophic gastritis occurs mainly in the
elderly.

7. Crohn's disease .

Although the disease usually causes chronic inflammation of the gastrointestinal wall,
it can sometimes also cause inflammation of the gastric wall. When the stomach is
affected, the symptoms of Crohn's disease (ie stomach pain and diarrhea in fluid form)
appear more prominently than symptoms of gastritis.

8. Radiation and chemotherapy .

Treatment of cancer such as chemotherapy and radiation can cause inflammation of


the stomach wall which can further develop into gastritis and peptic ulcer. When the
body is exposed to a small amount of radiation, the damage is usually temporary, but in
large doses will cause the damage becomes permanent and can erode the stomach wall
and damage the gastric acid producing glands.

9. Bile reflux disease .

Bile (bile) is a fluid that helps digest fats in the body. This liquid is produced by the
liver. When released, the bile will pass through a series of small channels and headed to
the small intestine. Under normal circumstances, a ring-like sphincter muscle (pyloric
valve) will prevent bile from flowing back into the stomach. But if this valve does not
work properly, then the bile will enter the stomach and cause inflammation and
gastritis.
10. Other factors .

Gastritis is often also associated with other health concepts such as HIV / AIDS,
parasitic infections, and liver or kidney failure.

E. Pathophysiology

Acute Gastritis

The influence of the side effects of NSAIDs or Non-Steroidal Anti-inflammatory Drug


like aspirin can also cause gastritis.Obat analgesic anti-inflammatory drugs (NSAIDs) such
as aspirin, ibuprofen and naproxen can cause inflammation of the stomach by way of
reducing prostaglandin in charge of protecting the stomach wall. If the use of these
drugs only occasionally then the possibility of stomach problems will be small. But if the
use is done continuously or excessive use can lead to gastritis and peptic ulcer. Giving
aspirin can also decrease the secretion of bicarbonate and mucus by the stomach, so the
ability of defensive factors is disrupted.

Excess alcohol, eating too many foods that contain nitrates (preservatives) or too
acid (vinegar), caffeine as in tea and coffee and smoking can trigger the occurrence of
gastritis. Because these materials when too often in contact with the wall of the
stomach will trigger excessive gastric acid secretion that can erode the gastric mucosal
layer.

Then the old psychological and physiological stress can cause gastritis. Stress such
as shock, sepsis, and trauma cause gastric mucosal ischemia. Gastric mucosal ischemia
results in increased mucosal permeability resulting in H diffusion into the mucosa. The
+

mucosa can no longer withstand excess acid causing edema and then damaged.

Chronic Gastritis

Chronic gastritis may be classified as type A or type B. Type A (often referred to as


autoimmune gastritis) results from parietal cell changes, leading to atrophy and cell
infiltration. It is associated with autoimmune diseases, such as pernicious anemia and
occurs in the fundus or corpus of the stomach.

Type B (sometimes referred to as H. pylory gastritis) This is associated with H.


pylory bacteria, dietary factors such as hot or spicy drinking, drug and alcohol use,
smoking or reflux of intestinal contents into the stomach. H. Pylori includes bacteria that
are not acid resistant, but this type of bacteria can secure itself in the mucosal layer of
the stomach. The presence of these bacteria in the gastric mucosa causes the stomach
lining weakened and brittle so that stomach acid can penetrate the layer . Thus both
gastric acid and bacteria cause injury or ulcers. The immune system will respond to the
H. Pylori bacterial infection by sending leucocyte grains, T-killer cells , and other
infection fighters. However, they are not able to resist the H. pylori infection because
they can not penetrate the stomach lining. But it also can not be removed so that the
immune response continues to increase and grow. Polymorph dies and removes
superoxide radical destructive compounds in the gastric lining cells. Extra nutrients are
sent to strengthen leukocyte cells, but they are also a source of nutrition for H. Pylori.
Finally, the gastric epithelial state is further damaged to form superficial ulceration and
may cause hemorrhage (bleeding). In a few days gastritis and even a gastric ulcer will
form.
F. Pathway

Analogics
Chemical material
Alcohol
Physical stress

Excessive secretion of gastric acid


Damage of the gastric mucosal barrier

Decreased ability to protect the gastric mucosa

Gastric mucosal irritation

pain Intolerance activity Taste Nausea and Vomitus

.
G. Clinical manifestations

a. Acute Gastritis

Dyspepsia syndrome of epigastrum pain, nausea, bloating, vomiting, is one of the most
common complaints. Also found gastrointestinal bleeding in the form of hematemesis
and melena, if done a deep lebig history, there is a history of use of drugs or certain
chemicals . ( capita selekta medical vol 1 1st edition FKUI matters: 492)
b.Gastritis Chronicles

Most patients have no complaints. Only a small fraction complained of heartburn,


anorexia, nausea, and physical examination was not found abnormalities. . ( capita
selekta medicine volume 3rd edition FKUI matters: 493)

H. Complications

1. Acute Gastritis

Upper gastrointestinal haemorrhage (SCBA) in the form of hematemesis and


melena, may end up as hemorrhagic shock. Especially for SCBA bleeding, need to be
distinguished from peptic ulcers. The clinical features shown are almost identical .
However, in peptic ulcers the main cause is helicobactery pylori infection, 100% in
duodenal ulcer and 60-90% in gastric ulcers. The diagnosis can be confirmed by
endoscopy ( 3rd edition medical caption caption: 492-493)

2. Chronic Gastritis

Upper GI bleeding, perforation ulcer, and anemia due to absorption of vitamin B ₁₂ . (


3rd edition of medical selecta caption: 493)

I. Management

Treatment of gastritis includes:

1. Overcoming the medical emergencies that occur.

2. Overcoming or avoiding causes if they can be found.

3. Provision of antacid drugs or other gastric ulcer drugs (Soeparman , 1999 )

Acute Gastritis

The main factor is eliminating its etiology. Gastric diet, with small portions and often.
Drugs intended to regulate gastric acid secretion, such as H receptor antagonist ₂ ,
proton pump inhibitors, anticholinergics, and antacid. Also referred to as cytoprotectors,
sucralfat and prostaglandin. . ( capita selekta medicine volume 3rd edition FKUI matters:
493)
Chronic gastritis

In health care centers where endoscopy can not be performed, management is


administered as in patients with dyspepsia syndrome, especially if the serology test is a
neagtif. First of all was to overcome and avoid the causes of the acute gastritis, then
given empirical treatment in the form of an antacid, an antagonist of H ₂ / proton pump
inhibitors and prokinetic drugs. If endoscopy can be performed, eradication therapy is
performed unless CLO, culture and PA trials are negative or negative serological results.
Eradication therapy is also given to the special selection of patients suffering from other
diseases.

Eradication therapy is given for 1-2 weeks with regard to cost efficiency. The
treatment regimen divided by 3, triple, kuadrel, and dual, but Yag commonly used triple
and kuadrel. If therapy fails, use terapikuadrel. Patients are considered cured, only if
after 4 weeks of therapy is completed CLO and PA negative examination results, in
addition therapy is considered failed. Complete regimen and dose of eradication
therapy. . ( capita selekta medicine volume 3rd edition FKUI matters: 493-494)

In gastritis, its management can be done with (medical and non medical), as follows:

a. Acute Gastritis

1. Instruct patients to avoid alcohol.

2. If the patient is able to eat by mouth, recommend a diet containing nutrients.

3. If the symptoms persist, the fluid should be administered parenterally.

4. If bleeding occurs, do management for hemorrhage of the gastrofestinal tract.

5. To neutralize acid use common antacids.

6. To neutralize alkhali use dilute lemon juice or watery vinegar.

7. Emergency surgery may be needed to remove gangrene or perforation.

8. If gastritis occurs due to ingestion of a strong base, use a watery orange juice or dilute
vinegar.
9. Stomach reactions are needed to overcome the obstruction of polirus.

b. Chronic Gastritis

1. Can be solved by modifying the patient's diet, the soft eating diet is given little
but more often.

2. Reduce stress

3. H. pylori is treated with antibiotics (such as tetracycline ¼, amoxillin) and gram


bismuth (pepto-bismol).

J. Investigations

a. Blood examination

This test is used to check whether there is H. pylori in the blood. A positive test results
showed that the patient had contact with bacteria at some time in his life but that did
not indicate that the patient had an infection. Blood tests can also be performed to
check for anemia that occurs due to gastric bleeding due to gastritis.

b. The urea breath test

A diagnostic method based on the principle that urea is altered by H. pylori urease in
the stomach into ammonia and carbon dioxide (CO ). CO rapidly absorbed through the
2 2 is

stomach wall and can be detected in expiratory air.

c. Stool examination

This test checks whether there is H. pylori bacteria in the feces or not. Positive
results may indicate the occurrence of infection. Examination is also done on the
presence of blood in the feces. This shows the presence of bleeding in the stomach.

d. Upper gastrointestinal endoscopy


With this test can be seen abnormalities in the upper gastrointestinal tract that may
not be visible from x-rays. This test is done by inserting a small flexible tube (
endoscope) through the mouth and into the esophagus, stomach and upper intestine.
The throat will first be anesthetized before the endoscope is inserted to ensure the
patient is comfortable undergoing this test. If any tissue in the gastrointestinal tract
looks suspicious, the doctor will take a small sample ( biopsy) from the tissue. The
sample will then be taken to the laboratory for examination. This test takes
approximately 20 to 30 minutes. Patients are usually not immediately sent home when
the test is completed, but must wait until the effects of anesthesia disappear for an hour
or two. Almost no resioko due to this test. A common complication is the discomfort in
the throat from swallowing the endoscope.

e. X-ray of upper gastrointestinal tract

This test will see signs of gastritis or other digestive diseases. Usually will be required
to swallow the barium liquid first before X-rays. This liquid will coat the gastrointestinal
tract and will be seen more clearly when the x-rays.

f . Gastric Analysis

This test is to determine the secretion of acid and is an important technique to


make the diagnosis of gastric disease. A nasogastric tube is inserted into the stomach
and aspiration of fasting gastric contents is to be analyzed. Basal analysis measures BAO
( basal acid output) without stimulation. This test is useful for establishing the diagnosis
of Zolinger- Elison syndrome ( a pancreatic tumor secreting large amounts of gastrin
which in turn causes real acidity).

g. Stimulation analysis

Can be done by measuring the maximum acid expenditure (MAO, maximum acid
output) after administration of drugs that stimulate the secretion of acids such as
histamine or pentagastrin. This test is to determine whether it is aclorhidria or not.
GASTRITIS NURSING ASSISTANCE

ASSESSMENT.

Anamnese include:

1. Name : Ny. M

2. Age : 58 thn

3. Sex : Female

4. Type of work : house wife

5. Address : Silih wangi RT/RW 002/001

6. Tribe / nation : Sunda

7. Religion : Islam

8. Level of education : for people with low / low education levels gaining knowledge
about gastritis, it will underestimate this disease, even just consider gastritis as an
ordinary stomachache and will eat foods that can cause and aggravate this disease.

9. History of illness and health

a) Main complaints : Pain in the pit of the liver and lower right abdomen.

b) when the medical history is : Covering the course of the disease, the beginning of
your symptoms client, complaints arise suddenly or gradually perceived, can trigger an
effort to resolve the issue.

c) Past medical history : Includes diseases related to current illness, hospital history , and
history of drug use.

Physical examination, the Review of system (ROS)

General circumstances : the appearance of pain in physical examination there is


tenderness in the epigastric quadrant.

1. B1 ( breath) : takhipnea
2. B2 (blood) : tachycardia, hypotension , dysrhythmias , weak peripheral
pulse, slow peripheral fill, pale skin color.

3. B3 (brain) : headaches, weakness, awareness level can be disturbed,


disorientation, pain epigastrum.

4. B4 (bladder) : oliguria, fluid balance disorder.

5. B5 (bowel) : anemia, anorexia, nausea, vomiting, heartburn, intolerance to


spicy foods.

6. B6 (bone) : fatigue, weakness

3.1.3 Focus of Assessment

1. Activity / Rest

Symptoms : weakness, fatigue

Signs : tachycardia, tachypnea / hyperventilation (response to activity)

2. Circulation

Symptoms : weakness, sweating

Sign :- hypotension (including postural)

- tachycardia , dysrhythmias (hypovolemia / hypoxemia)

- weak peripheral pulse

- filling capillary slow / slow (vasoconstriction)

- color pale skin, cyanosis (depending on the amount of blood loss)

- skin / mucous membrane weakness , sweating (indicating shock status, acute pain,
psychological response)
3. Integrity of the ego

Symptoms : acute or chronic stress factors (financial, employment relationship), feelings


of helplessness.

Signs : anxiety signs, eg anxiety, pallor, sweating, narrowed attention, trembling,


trembling sounds.

4. Elimination

Symptoms : previous hospital care history due to gastroenteritis (GE) bleeding or GE-
related problems, eg peptic or gastric wounds , gastritis, gastric surgery, gastric area
irradiation. Changes in the pattern of defecation / faecal characteristics.

Sign :- abdominal tenderness, distension

- intestinal sound : often hyperactivity during bleeding, hypoactivity after bleeding.

- faecal characteristics : diarrhea, dark blood, brownish or sometimes bright red,


foaming, stench (steatorea), constipation may occur (dietary changes, antacid use).

- urine output : decreased, dense.

5. Food / Liquid

Symptoms :- anorexia, nausea, vomiting (elongated vomiting suspected external


pyloric obstruction with respect to duodenal lesions).

- swallowing problem : hiccups

- heartburn, acid sores , nausea or vomiting

Signs : vomiting with dark or bright red coffee, with or without blood clots, dry mucous
membranes, decreased mucosal production, poor skin turgor (chronic hemorrhage).
6. Neurosensi

Symptoms : throbbing, dizziness / headache due to light, weakness.

Signs : the level of consciousness can be disturbed, range from rather likely to sleep,
disorientation / confusion, to fainting and coma (depending on the volume of circulation
/ oxygenation).

7. Pain / Comfort

Symptoms :- pain, described as sharp, shallow, burning, sore, sudden pain can be
accompanied by perforation. Sense of discomfort / distress vaguely after eating a lot
and lost by eating (acute gastritis).

- left / middle epigastric pain / or spread to the back occurring 1-2 hours after
eating and lost with antacids (gastric ulcers).

- left epigastric pain up to / or spread to the back occurs approximately 4 hours


after meals when the stomach is empty and disappears with food or antacids (duodenal
ulcers).

- there is no pain (varicose esofegeal or gastritis).

- trigger factors : food, cigarettes, alcohol, use of certain drugs (salicylate, reserpine,
antibiotics, ibuprofen), psychological stressors.

Signs : face wrinkled, careful on the areas of pain, pale, sweaty, attention narrowed.

8. Security
Symptoms : allergy to drugs / sensitive eg: ASA

Signs : temperature increase, angioma spider, palmar erythema (indicates cirrhosis /


portal hypertension)
9. Counseling / Learning

Symptoms : the use of prescription drugs / sold free containing ASA, alcohol, steroids.
NSAIDs cause GI bleeding. The present complaint may be acceptable due to ( eg:
anemia) or unrelated diagnosis (eg head trauma), intestinal flu, or severe vomiting
episodes. Old health problems such as cirrhosis, alcoholism, hepatitis, eating disorders
(Doengoes, 1999, p. 455).

NURSING DIAGNOSES

1. Pain (acute) b / d gastric mucosal inflammation .

2. The volume of fluid is less than the body's needs associated with inadequate intake
and excessive liquid output (nausea and vomiting)

3 . Nutrition is less than the body needs b / d anorexia

4. Intolerance activity b / d physical weakness

5. Anxiety b / d lack of knowledge about disease


Nursing Intervention

No. Diagnosis Intervention Rational

1. Pain (acute) is 1. Get rid of the patient in 1. Reduces inflammation of


associated with gastric the first 6 hours, the gastric mucosa,
mucosal inflammation.

2. Give soft foods little by 2. Gastric dilatation can


Aim: little and give hot drinks, occur when fasting after
fasting,
After the nursing action
is done for 1 x 24
hours 3. The right position and feel
3. Set a comfortable position
comfortable by the client can
for the client.
- Pain of client is reduce the client's risk of
reduced or lost. pain.

- Pain scale 0.
- Client can relax. 4. Teach distraction and 4. Can make clients better
- The general state of recluse techniques. and forget about pain.
the client is good.

5. Analgesics can block pain


5. Collaboration in giving
receptors in the central
analgesics.
nervous system.
2. The volume of fluid is 1. Meet individual needs. 1. Adequate fluid intake
less than the body's Encourage clients to drink ( will reduce the risk of
needs associated with adults: 40-60 cc / kg / hour). dehydration of the patient
inadequate intake and
excessive liquid output
(nausea and vomiting) 2. Keep an eye on vital signs, 2. indicates dehydration
evaluation of skin turgor, status or possible increased
- Aim :
capillary refill and mucous fluid replacement
After a 1x24hour membrane requirement.
nursing action , the
3. Maintain bed rest, prevent 3. Activity / vomiting
patient's fluid volume
vomiting and stress on increases intra-abdominal
deficiency problem can
defecation pressure and may trigger
be resolved.
advanced bleeding.

4. Replace lost fluid loss and


4. Give IV line therapy as
improve fluid immediately.
indicated
Outcome Criteria : 5. Cimetidine and ranitidine
5. Collaboration of
Maintain adequate fluid serve to inhibit gastric acid
cimetidine and ranitidine
volume as evidenced by secretion
moist lips mucosa, good
skin turgor, pink
capillary fill, balanced
input and output.
3. Nutrition is less than 1. Instruct patient to eat 1. Keep the nutrition fulfilled
the body needs b / d slightly demisedikit with and prevent continuing
anorexia small portions but often. nausea and vomiting.

Aim : 2. To facilitate the patient in


2. Provide soft foods and
chewing food.
After 3x24 hours of foods in the likes of patients
nursing action the / in gemari.
patient's nutritional
3. oral hygiene will stimulate
needs can be met 3. do oral higyne 2x a day
the patient's appetite.

Results criteria: 4. weigh BB patient every 4. Knowing the nutritional

- General situation is day and monitor skin turgor, status of patients.


sufficient lip mucosa etc.

- Good skin turgor

- BB increases
5. Consult with a team of 5. Accelerate the fulfillment
- The difficulty of nutritionists in the menu. of nutritional needs with the
swallowing is reduced right target menu.

4. Activity intolerance b / 1. Observe the extent to 1. Know the activities that


d physical weakness which clients can perform the client can do.
activities.
Destination: Client can
move.
2. Provide a quiet 2. Enhance client breaks.
environment.
Results criteria:

- Client can move 3. Helping if necessary, self-


3. Provide assistance in
without help, esteem is enhanced when
activities.
- Activity scale 0-1 the client does something on
his own.
4. Explain the importance of 4. The client knows the
activity for the client. importance of the move.

5. Increase bed rest or sit 5.The bed lie can increase


and give medication
according to indication the stamina of the patient so
patients can reactivate.

5. Anxiety b / d changes in 1. Keep an eye on 1. Can be an indicator of


health status , threats of physiological responses such the degree of fear
death and pain. as tachypnea, palpitations, experienced by the patient,
dizziness, headaches, tingling but may also be related to
sensations. the physical condition or
Aim : status of shock.

After a 1x24jam patient 2. Creating a therapeutic


2. Encourage the statement
action relationship
of fear and anxiety, give
feedback.

Results criteria: 3. Provide accurate 3. Involve the patient in the


information. care plan and reduce the
- Expressing her feelings
unnecessary anxiety about
and thoughts openly
ignorance.
-M reported less anxiety
and fear
4. Give a quiet environment
4. Moving patients away
-M engungkapkan to rest.
from external stressors,
understand peoses
increasing relaxation, can
disease
improve coping skills.
-M engemukakan aware
5. Helps lower fear through a
of what he wants is to 5. Encourage the nearest
frightening experience of
adjust to the physical person to stay with the
being alone.
changes patient.

6. Show relaxation 6. Learning how to relax can


techniques. help lower fear and anxiety
CHAPTER III

COVER

A. CONCLUSION

Gastritis is an inflammatory process in the mucosal layer and gastric submucosa


and hispatology can be proven by infiltration of inflammatory cells in the area .

Gastritis is not a single disease, but is formed from several conditions that all result
in inflammation of the stomach. Usually, the inflammation is the result of infection by
the same bacteria with bacteria that can cause ulcers in the stomach of Helicobacter
pylori. But other factors such as physical trauma and the continued use of some
painkillers may also cause gastritis. Although many conditions can cause gastritis, the
symptoms and signs of the disease are similar to each other.

B. CRITICISTS AND SUGGESTIONS In order to refine this paper , I really expect criticism
and suggestion from Supervisor and other group's friends.
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Nuzulul. 2011. Askep Gastritis . http://nuzulul-fkp09.web.unair.ac.id/artikel_ detail-


35839-Kep-Digestive-Askep-Gastritis.html . Retrieved on 11th November 2013 at 09.30
WIB