THEORITICAL BACKGROUND

GASTRITIS

A. GASTROINTESTINAL SYSTEM CONCEPT

a. Definition of Gastrointestial System
The digestive or gastrointestinal system is a system in charge of converting food into basic
material that serves to build, maintain and repair damaged body cells. The human digestive tract
consists of the mouth, throat, esophagus, stomach, small intestine, colon, rectum and anus. The
digestive system includes organs located outside the gastrointestinal tract, the pancreas, the liver and
the gallbladder. (Nian Afrian Nuari, 2015)
The digestive system has a function :
a. Ingesti
The process of entering the food and drink into the mouth.
b. Digesti
Mechanical and chemical processes by the digestive tract to convert food into
absorptionable nutrients.
c. Secretion
Everyday, cells within the walls of GI tract and gastrointestinal organs remove about 7
liters of water, acids, buffers and enzymes into the digestive lumen.
d. Mixing and propulsion
The process of muscle contraction and relaxation of the gastrointestinal wall to mix food
and pushed food.
e. Absorption
The process carried out by the lumen of the intestinal villi-villi absorb the processing of
carbohydrates, proteins, fats, vitamins and minerals. Substances that have been absorbed
will pass through blood or lymphatic and circulate to the cells of the body.
f. Metabolism
The process of energy formation of absorbed nutrients. The energy can be used by body
cells or stored by body cells.
g. Excretion
The process of spending the remains of digestion that are not digested or used again.
Toxins, non-digestible substances, bacteria, residual absorption, remaining loose epithelial
cells will be removed from the body through the anus. This process is known as defecation.

b. Anatomy and Physiology of the Stomach

The gastric is a muscular sac that located between the esophagus and the small
intestine, to the left of the abdomen, below the diaphragm of the front of the pancreas and
lymph. The gastric is a duct that can expand due to peristalsis, especially in the epigaster

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region. Variations of the stomach form correspond to the amount of food that enters, the
peristaltic waves of other organ pressure, and the posture. The stomach has a normal
capacity in adults about 2 liters. The volume of the stomach will increase at mealtime and
decrease as the kimus enters the small intestine.
1) Parts of the gastric:
a. Fundus : The upper curvature of the gastric.
b. Korpus (body) : A curve at the bottom of the minor curvature, which is the main
part of the gastric.
c. Pyloric antrum : The gastric section is tubular, has a thick muscle forming the
pyloric sphincter. The pyloric antrum is the distal estuary and continues to the
duodenum.
d. Lesser curvature : It is on the right side of the gastric, expanding from the
cardiac osteum to the pylorus. The lesser curvature is connected to the liver by
the minor osteum, a double fold of the peritoneum.
e. Greater curvature : located at the bottom of the gastric.
f. Esophagus Cardiac Junction (ECJ) : It is the esophagus of the abdomen enters
the stomach, there is a pyloric orifice that has no special sphincter, but only a
ring that opens and closes the osteum by contraction and relaxation. Osteum can
be covered by the folds of the mucous membranes and the muscles at the base
of the esophagus.
g. Pylorus : The lower part of the gastric is bordered by the duodenum.
2) Gastric Function
a. Food warehouse, crushing and smoothing food by peristaltic stomach and
gastric sap. Normal stomach capacity allows for long intervals between each
meal and the ability to store large amounts of food until the food can be
accommodated in the bottom part of the duct.
b. Producing kimus, gastric activity resulted in the formation of a kimus
(homogeneous half-liquid mass, high acid content derived from the bolus) and
pushed it into the duodenum.
c. Digestion of protein, the gastric begins digestion of proteins through the
secretion of trypsin and hydrochloric acid.
d. Producing mucus, the resulting mucus of the gland forms a 1 mm thick barrier
to protect the stomach from its own digestive action and secretion.
e. The production of intrinsic factor, namely glycoprotein in parietal cell secretion
and vitamin B12 which can be from digested food in the gastric is bound to
intrinsic factor. The complex intrinsic factor of vitamin B12 is brought to the
ileum, where vitamin B12 is absorbed.

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 f. Absorption, in the gastric there is little nutrient absorption. Some substances in
absorption are some fat-soluble drugs (aspirin) and alcohols in the absorption of
the gastric wall and water-soluble substances in the absorption in an uncertain
amount

IMAGE : GASTRIC ANATOMY

B. GASTRITIS CONCEPT
a. Definition
Gastritis is a localized or spreading inflammation of the gastric mucosa that develops when the
protective mechanism of the mucosa is filled with bacteria or irritant substances. Gastritis is an
acute, chronic, diffuse and local gastric inflammation caused by food, drugs, chemicals, stress and
bacteria.

b. Etiology

Gastritis caused by Helicobacter pylori infection and at the beginning of gastric mucosal
infection indicates acute inflammatory response and if ignored will be chronic (Sudoyo Aru, et al.
2009).

Broadly speaking, gastritis can be divided into 3 types based on pathway and clinical
symptoms:

1) Acute haemorrhagic gastritis erosive

This type of gastritis often causes active ulcers. Categorized as erosive hemorrhagic because of
the risk of massive bleeding and gastric perforation. Erosive hemorrhagic gastritis is caused by:
 Use of NSAIDs
 Ischemia
 Stress

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  Alcohol abuse, corrosive chemicals.
 Trauma
 Radiation trauma
2) Non erosive chronic gastritis
This type of inflammation is common in the antrum region. The main cause of chronic non-
erosive active gastritis is Heliobacter pylori infection. This type of gastritis can lead to gastric
ulcers of gastric cell dysplasia and can lead to gastric cancer. Heliobacter pylori bacteria can
trigger gastric ulcers because these bacteria are able to stimulate increased secretion of gastrin in
the antrum part and increase in HCl on the fundus.
3) Atrophic gastritis
The most common cause of this type is autoantibodies. Immunoglobulin G and B-lymphocytes
do not recognize the stomach cells so it actually destroys them
4) Reactive gastritis
Because of postoperative areas of antrum or pyloric area resulting in enterogastric reflux that
causes pancreatic enzymes and bile salts to attack the gastric mucosa resulting in erosion. In
addition, an alkaline gut can neutralize gastrin, making it particularly suitable for the
development of Heliobacter pylori.
c. Clinical Manifestations

Clinical manifestations that appear different according to the type of gastritis.

1) Acute haemorrhagic gastritis erosive

 Hematemesis
 Epigastric pain
 Nausea and vomiting
 Gastrointestinal bleeding
 D eficiency anemia with unclear aetiology
 Signs and symptoms of real hemodynamic disturbances such as: hypotension, pallor,
cold sweat, tachycardia to impaired consciousness.
2) Non erosive chronic gastritis
 Symptoms vary between one person and another and sometimes not clear.
 Feelings of fullness, anorexia.
 Unexplained epigastric distress.
 Fast satiety.
3) Athropic gastritis
 Epigstric pain.
 Pernicious anemia.
 Nausea and vomiting
4) Reaktive Gastritis
 Excessive vomiting
 Epigastric pain.
 Weakness.

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d. Pathophysiological / pathway

Drugs (NSAIDs, aspirin, H. Phylori Cafein

sulfonamide steroids,
digitalis)
Attached to the stomach Decreased production of
epithelium bicarbonate (HCO3-)
Disrupts the formation of
the gastric mucosal barrier Destroy the gastric mucosal Decreased protective
layer ability to acid

Reduced gastric barrier to Causes back diffusion of

acid and pepsin gastric acid & pepsin

Deficiency of fluid volume

Inflammation Gastric mucosal erosion Bleeding

Epigastric pain
Reduced tone and gastric The gastric mucosa loses
peristaltic tissue integrity

Decreased sensory to eat Reflux of duodenal

contents into the stomach

Anorexia
Nausea Encouragement of the
contents of the stomach
contents into the mouth

Acute pain Nutrition imbalance is Nausea

less than body needs

Kekurangan volume
cairan

Source: NANDA (North American Nursing Diagnostic Association) NIC-NOC

e. Supporting Investigation
1) Blood Examination
This test is used to check for the presence of H. pylori antibodies in the blood.
2) Respiratory Examination
This test can determine a patient is infected by the bacteria H. pylori or not.
3) Stool Examination
This test also aims to examine the H. Pylori bacteria in the stool.
4) Upper gastrointestinal endoscopy.
With this test can be seen abnormalities in the upper gastrointestinal tract that may not be visible
from X-rays.
5) X-ray of upper gastrointestinal tract.
This test will see signs of gastritis or other digestive diseases.

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 f. Management
The main orientation of gastritis treatment is on drugs. Drugs that reduce the amount of acid in
the gastric can reduce the symptoms that may accompany gastritis and promote healing of the layer
of the gastric. These treatments include:
 Antacids containing aluminum and magnesium, and antacids containing calcium and
magnesium carbonates. Antacids are able to relieve mild heartburn or dyspepsia by
neutralizing acid in the stomach. Ion H+ is the main structure of stomach acid. With the
addition of aluminum hydroxide or magnesium hydroxide then the acid atmosphere in
the stomach can be reduced. These drugs can cause side effects such as diarrhea or
constipation because the impact of H+ decrease is a decrease in intestinal peristaltic
stimulation
 Histamin (H2) blocker, such as famotidine and ranitidine. H2 Blocker has the effect of
decreasing acid production by directly affecting the epithelial layer of the gastric by
inhibiting the stimulation of secretion by the autonomic nerves in the vagus nerve.
 Pump Proton Inhibitor (PPI), such as omeprazole, lansoprazole, pantoprazole,
rabeprazole, esomeprazole, and dexlansoprazole. This drug works inhibits acid
production by inhibition of electrons that give rise to action potential on the autonomic
nerves of the vagus. PPI is believed to be more effective in reducing the production of
stomach acid than H2 blockers.
 If gastritis is caused by long-term use of NSAIDs (Nonsteroid Antiinflammatory Drug)
such as aspirin and aspilet, then patients are advised to stop using NSAIDs, reduce
NSAID doses, or switch to another class of drugs for pain.
 If the cause is Heliobacter pylori it is necessary to combine antacids, PPIs and antibiotics
such as amoxicillin and clarithromycin to kill bacteria.
 Giving food that does not stimulate stomach acid. Although not directly affect the
increase in stomach acid but stimulating foods such as spicy and sour can increase the
acidic atmosphere in the stomach so as to increase the risk of inflammation in the
stomach. In addition, it is also advisable to consume foods that do not aggravate the
work of the stomach.
 Patients are also trained for stress management because it can affect gastric acid
secretion through the vagus nerve.
g. Complication
 Upper gastrointestinal bleeding, such as haematemesis and melena.
 Hemorrhagic shock.
 Stomach ulcers.
 Stomach cancer.
 Hypokalemia.
C. THE BASIC CONCEPT OF NURSING CARE
1. Assesment
Some things that become orientation of gastritis patient that is:
a. Main complaint

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 Patients come to the hospital with epigastric pain. The emergence of pain complaints on the
epigastrium due to gastric mucosal irritation that stimulates the pain nociceptors in the
gastric muscle layer in the nerve plexus mienterikus (Auerbach).
b. Health history
Patients with alcoholic history, irregular eating patterns, eating foods that stimulate gastric
acid removal such as spicy, acid, and consumption of medicines such as aspilet, aspirin are
predisposing factors of gastritis. Alcohol, aspirin and aspirin are consumed in the long term
(> 3 months) can erode the gastric mucosa so easily irritated. Foods that are irritating like
spicy and acid in a long time can also erode the gastric mucosa. Eating irregular foods will
lead to increased stomach acid, but no food is digested so that stomach acid actually damages
the mucosal layer of the stomach. Families with habits often consume spicy foods can also
contribute to affect the number of family members who have gastritis. From the age factor,
40% - 50% of gastritis sufferers due to infection have 50 years of age, developing countries
the rate of happiness reaches 90% of the average cases worldwide.
c. Assessment of needs patterns.
Pattern needs are often disturbed is :
1) Needs a sense of security and comfort
Prominent complaints in people with gastritis is epigastric pain. Pain especially during
empty stomach, stress (increased sympathetic stimulation that raises HCI levels).
Epigastric pain-related data is often reported by patients with various types such as
slashed, squashed, or perhaps burning.
The patient's discomfort condition is expressed as well as the tension of facial expression
during an attack. The scale of pain depends on the extent and depth of the ulcer, the
volume of stomach acid. The deeper the threat of irritation can be on the webbing so as
to trigger a fairly strong pain sensation (scale 6-8).
2) Nutritional and fluid needs
Increased stomach acid in patients with gastritis will decrease appetite, because the
product sekretorik stomach will more fill the lumen of the stomach. Decreased appetite
causes a decrease in the amount of nutrients that enter. Lack of intake of major energy
ingredients such as carbohydrates will occur the mechanism of discharge of fat and
protein to be used as energy materials. The formation of muscle mass and body mass
decreases so that the patient gradually loses weight, dry and coarse skin (decreased
production of sebaceous glands from fat), hair loss (decreased amino acids as hair
reinforcement and new cell replacement). Patients may also experience decreased fluid
through vomiting due to excessive gastric contractions. Indications of fluid decrease can
be seen from decreased urine production (<1500 ml / 24 h).
3) Mobilization needs
Energy is obtained from the breakdown of carbohydrates, proteins or fats. The materials
will be converted into ATP that can be used muscle and other body cells to produce heat.
The decreased amount of heat may affect the depolarization phase of the muscles and
innervation so that the muscle becomes decreased in strength. Patients with gastritis
appear weak with a score of muscle strength in each part of the extremity is less than 5.

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 Patients also seem lazy to move, many lie down, in fulfilling daily needs such as eating,
bowel, BAK much assisted by families with scores need more help than 1.
4) The need to maintain body temperature
Noninfectious gastritis may produce clinical symptoms of subhipothermia (temperature
from normal approaching hypothermia) due to decreased body heat production through
nutrient breakdown. In infectious gastritis the body temperature is likely high
(hyperthermate with temperature> 38 ° Celsius). Increased body temperature is caused
by pyrogens derived from toxic microorganisms that activate the hypothalamus to raise
the body temperature threshold followed by increased blood flow, vasodilation of vessels
and increased muscle contraction that can increase the production of body heat. Other
signs that support, among others, face looks reddish, warm skin palpable on large
vascular parts such as face, abdomen but cold on the periphery like toe of the perforated
by perfusion.
5) Oxygenation and respiratory needs
Respiratory gastritis may experience an increase due to increased gastric insistence that
may inhibit lung development. Breathing may be fast, the frequency is between 24 - 30
times per minute. Possibility of small oxygen anacaman except in erosive gastritis
patients with bleeding. Gastritis with bleeding can quickly lower blood volume and
lower the bonds to oxygen. The tissue oxygen has decreased starting from the sign of
cold skin, pale to the heaviest is bluish. The accumulation of CO2 in the vessels can
trigger vasoconstriction of blood vessels thus exacerbating tissue perfusion conditions.
d. Physically Assesment
 General circumtances
Possible weakness due to decreased tissue oxygen, body fluids and nutrients. The
level of consciousness may still be composmentis to apathy if accompanied by
decreased perfusion and electrolytes (potassium, sodium, calcium).
 Physically condition
a) Eyes
Possibly visible concave (due to decreased body fluids), anemis (decreased
tissue oxygen, pernicious anemia, iron deficiency anemia).
b) Mouth
Possible dry mouth mucosa (decreased intracellular mucosal fluid), chapped lips,
bad mouth odor (decreased lip hydration and personal hygiene).
c) Respiratory
Respiratory rate between 20-30 times per minute, may be fast rhythm due to
gaster enlargement that inhibits lung development. Vesicular lung sound.
d) Cardiovascular
The possibility of increased heart rate, weak palpable pulse (hypovolemia
tachycardia and decreased oxygen of the body), peripheral vessel constriction,
capillary refill more than 2 minutes (CO2 accumulation in vascular). In gastritis
erosive with bleeding. If non-erosive gastritis may be found a decrease in pulse
strength due to metabolic decline.

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 e) Genitourinaria
Decreased urine production, less than 500 ml / day as the oligouria category (due
to decreased GFR of the kidney) in erosive gastritis.
f) Extremities
A decrease in muscle mass of upper and lower extremities, muscle arm
circumference, biceps and triceps less than 10 cm. The skin decreases its
elasticity, it looks dry.
2. Nursing Diagnosis
1) Acute pain related to gastric mucosal irritation, mucosal perforation, postoperative soft tissue
damage.
2) Nutrition is less than body needs related to food intake is inadequate.
3) Liquid and electrolyte imbalances related to fluid out due to excessive vomiting.
4) High risk of hypovolemic shock related to decrease in blood volume secondary to excessive
vomiting, less fluid intake.
5) Fulfillment information related to inadequacy of diet management information and irritant trigger
factors in gastric mucosa.
3. Nursing Intervention
1) Nursing diagnoses : Acute pain related to gastric mucosal irritation, mucosal perforation,
postoperative soft tissue damage.
Goal : Within 1 x 24 hours there is a decrease in the scale of pain.
Criteria:
 The scale of pain is reduced.
 The reduced lesion decreases and gradually heals.
 Moist oral mucous membranes.
 No swelling and hyperemia.
 Normal body temperature.

Intervention Rational
Assessment PQRST pain To identify the cause, the spread, the degree of
severity and the timing of the pain.
Assess client's ability to control pain. Many factors of physiology (affective, cognitive
and emotional motivation) affect the perception
of pain
Pain management: Rest can decrease the oxygen requirement
 Rest the patient. required to meet the needs of basal metabolism.
 Teach breathing relaxation techniques Relaxation to increase oxygen intake.
when pain appears. Distraction can decrease pain stimulation.
 Teach distraction techniques when pain
develops.
Encourage clients to multiply the consumption of Vegetables, Vitamin B12, Vitamin C and iron
fruits and vegetables especially vitamin B12 can prevent the sprue and increased nutrients will

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Vitamin C and iron. accelerate the healing process.
Give family explanation of the importance of oral The patient's family knows the importance of oral
hygiene. hygiene so that no stomatitis occurs again.
Collaboration with doctors: Analgesics block the path of pain so that pain is
Giving analgesics. reduced.

2) Nursing diagnoses : Nutrition is less than body needs related to food intake is inadequate.
Goal : Within 3x24 hours the appetite reappears and nutritional status is fulfilled.
Criteria :
 Nutritional status is fulfilled.
 The client's appetite reappears.
 Normal weight.

Intervention Rational
Assess the nutritional status of patients. To know the nutritional status of patients.
Nutrition in soft, small portions but often. Soft foods minimize the work of the mouth in
chewing food.
Monitor body weight every day. Evaluate the weight loss or increase, increased
nutrition will increase body weight.
Collaborate with nutritionists to supply nutrition. The presence of calories (energy sources) will
increase the healing process.
Provide food with a comfortable and quiet Patients can concentrate on eating mechanisms
environment. without external distraction / interference.
Provide information about food substances that By providing information then the client will
are very important for the body's metabolism know how to sufficient the nutritional needs
balance. every day accelerate the healing process.
Collaboration with medical: Use of H2 inhibitors To reduce gastric acid, and reduce the irritation of
(such as cimetidine / ranitidine). the gastric mucosa.

3) Nursing diagnoses : Liquid and electrolyte imbalances related to fluid out due to excessive
vomiting.
Goal : Within 1x24 hours fluid and electrolyte imbalance didn’t occur.
Criteria :
 Patient shows improvement of fluid balance, moist mucous membrane, normal
skin turgor.
 Vital signs normal, CRT> 3 seconds, urine production > 600 ml / day.
 Laboratory: Normal electrolyte value, hematocrit value and serum protein
increased, BUN / creatinine decreased.

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Intervention Rational
Observation of vital signs. Blood pressure checks need to be done because
hypotension can occur hypovolemia.
Monitor fluid status (skin turgor, mucous The amount and liquid replacement determined
membrane, and urine output). the fluid status, decreasing the volume of fluid
resulting in decreased urine production.
Maintain bed rest, to prevent vomiting and intra- Activity / vomiting increases intraabdominal
abdominal pressure during defecation. pressure and may trigger further bleeding.
Elevate the head of the bed during or during Prevents gastric reflux and antacid aspiration,
antacid administration. which can lead to serious pulmonary
complications.
Tindakan kolaborasi : Pertahankan pemberian Jalur yang paten penting untuk pemberian cairan
cairan intravena. cepat dan memudahkan perawat dalam
melakukan control intake dan output cairan.

4) Nursing diagnoses : High risk of hypovolemic shock related to decrease in blood volume
secondary to excessive vomiting, less fluid intake.
Goal : Within 3 × 24 hours there is no hypovolemic shock.
Criteria :
 Patients show improvement of the cardiovascular system.
 Hematemesis and melena is controlled.
 Conjunctiva is not anemic.
 Patients do not complain of dizziness, moist mucous membranes, normal skin turgor, and
warm acral.
 Vital signs normal, CRT> 3 seconds, urine 600 ml / day.
 Laboratory: hemoglobin value, red blood cells, hematrocytes, and BUN / creatinine
within normal limits.

Intervention Rational
Assess the source and response of bleeding from Preliminary detection of how far the level of
melena and hematemesis. intervention will be provided according to
individual needs.
Monitor vital signs  Decline in quality and quantity of heart rate is
an important parameter of early symptoms of
shock.
 Hypotension can occur in hypovolemics, it
provides a manifestation of the involvement of
the cardiovascular system in compensating for
maintaining blood pressure.
 Increased respiratory frequency is a

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 manifestation of respiratory compensation to
take up as much oxygen as a result of a
decrease in hemoglobin secondary from
decrease in blood volume.
Monitor fluid status (skin turgor, mucous The amount and type of blood replacement fluid
membrane, and urine output). is determined from the state of the fluid status. A
decrease in blood volume results in decreased
urine production, strict monitoring of urine
production <500 ml / day is a sign of
hypovolaemic shock.

5) Nursing diagnoses : Fulfillment of information related to inadequate information on diet

management and irritant trigger factors in the mucosal lambug, diagnostic evaluation,
chemotherapy intervention, radio therapy, gastrectomy surgery plan, and home care plan.
Goal : Within 1 × 24 hours health information is fulfilled.
Criteria :
 Patients are able to re-explain the health education provided.
 Patients are motivated to carry out the explanations given.

Intervention Rational
Assess patient's level of knowledge about The level of knowledge is influenced by the
diagnostic procedures, chemotherapy socio-economic condition of the patient. Nurses
interventions, radiation, surgery, gastrectomy, use approaches appropriate to the individual
and home activities plan patient's condition. By knowing the level of
knowledge the nurse can be more focused in
providing education in accordance with the
patient's knowledge effectively and efficiently.
Find sources that can increase the acceptance of The patient's immediate family needs to be
information. involved in fulfilling the information to lower the
risk of misinterpretation of the information
provided. Especially for patients who have
secondary bleeding from gastritis perforation.
Give motivation and moral support Interventions to increase the patient's desire in
performing post-operative gastrectomy function
control procedures.

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 REFERENCES

Afrian Nuari, Nian. 2015. Asuhan Keperawatan pada Gangguan Sistem Gastrointestinal. Jakarta: Trans
Info Media

Amin Huda Nurarif, Hardhi Kusuma S. 2015. Aplikasi Asuhan Keperawatan Berdasarkan Diagnosa
Medis dan Nanda NIC-NOC Edisi Revisi Jilid 2. Jogjakarta : Mediaction

Muttaqin, Arif. 2011. Gangguan Gastrointestinal: Aplikasi Asuhan Keperawatan Medikal Bedah. Jakarta:
Salemba Medika.

Niman, Susanti. 2013. Anatomi dan Fisiologi Sistem Pencernaan. Jakarta: Trans Info Media

Sukarmin. 2013. Keperawatan pada Sistem Pencernaan. Yogyakarta: Pustaka Pelajar

Suratun dan Lusianah. 2010. Asuhan Keperawatan Klien Gangguan Sistem Gastrointestinal.
Jakarta:Perpustakaan Nasional.

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