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
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.
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
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
Deficiency 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.
d. Pathophysiological / pathway
4 Drugs (NSAIDs, aspirin,
sulfonamide steroids, digitalis)
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.
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 complaintPatients 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 historyPatients 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. 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.
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 the patient.
Teach breathing relaxation techniques when pain appears.
Teach distraction techniques when pain develops.
Rest can decrease the oxygen requirement required to meet the needs of basal metabolism. Relaxation to increase oxygen intake.
Distraction can decrease pain stimulation.
Encourage clients to multiply the consumption of Vegetables, Vitamin B12, Vitamin C and iron
fruits and vegetables especially vitamin B12 Vitamin C and iron.
can prevent the sprue and increased nutrients will accelerate the healing process.
Give family explanation of the importance of oral hygiene.
The patient's family knows the importance of oral hygiene so that no stomatitis occurs again. Collaboration with doctors:
Giving analgesics.
Analgesics block the path of pain so that pain is 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 environment.
Patients can concentrate on eating mechanisms without external distraction / interference. Provide information about food substances that
are very important for the body's metabolism balance.
By providing information then the client will know how to sufficient the nutritional needs every day accelerate the healing process.
Collaboration with medical: Use of H2 inhibitors (such as cimetidine / ranitidine).
To reduce gastric acid, and reduce the irritation of 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.
Intervention
Rational
Observation of vital signs. Blood pressure checks need to be done because
hypotension can occur hypovolemia. Monitor fluid status (skin turgor, mucous
membrane, and urine output).
The amount and liquid replacement determined the fluid status, decreasing the volume of fluid resulting in decreased urine production.
Maintain bed rest, to prevent vomiting and intra-abdominal pressure during defecation.
Activity / vomiting increases intraabdominal pressure and may trigger further bleeding. Elevate the head of the bed during or during
Jalur yang paten penting untuk pemberian cairan cepat dan memudahkan perawat dalam melakukan control intake dan output cairan.
4) Nursing diagnoses :
High risk of hypovolemic shock related to decrease in blood volumesecondary 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 melena and hematemesis.
Preliminary detection of how far the level of 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 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 diagnostic procedures, chemotherapy interventions, radiation, surgery, gastrectomy, and home activities plan
The level of knowledge is influenced by the socio-economic condition of the patient. Nurses use approaches appropriate to the individual 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
information.
The patient's immediate family needs to be 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.
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
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