PEPTICUM ULCUUS PAPER COMPLETE
Kamis, 12 Januari 2023
Tulis Komentar
Based on research that 5%-15% of the population in the United States have peptic ulcers, but only about half are known, this incidence has decreased by 50% over the last 20 years. Peptic ulcer is still an important health problem. Peptic ulcer incidence is high in the United States, with 4 million people diagnosed each year. Approximately 20-30% of the prevalence of these ulcers occurs due to the use of non-steroidal anti-inflammatory drugs (NSAIDs), especially non-selective ones. NSAIDs are used chronically in diseases based on chronic inflammation such as osteoarthritis. This chronic use further increases the risk of developing peptic ulcer.
In a normal stomach, there are two defense mechanismserja and affect the condition of the stomach, namely the defense factor ( defence ) of the stomach and the damaging factor ( aggressive ) of the stomach. These two factors, in a healthy stomach, work in balance, so that the stomach is not damaged or injured. Stomach damaging factors include (1) endogenous damaging factors or originating from within the stomach itself, including HCL, pepsin and bile salts; (2) exogenous damaging factors, for example (drugs, alcohol and bacteria). Gastric defense factors are available to counteract or offset the work of the factors mentioned above.
Factors or defense systems in the stomach, including layers (1) pre-epithelium; (2) epithelium; (3) post epithelium.
If there is an imbalance between the two factors above, whether the defense factor is weakened or the damaging factor is getting stronger, it can cause damage to stomach cells, which will eventually form gastric/peptic ulcers. Giving excessive exogenous exposure such as corticosteroids, NSAIDs and caffeine can trigger stomach ulcers. The stomach has its own ulcer healing mechanism. This mechanism is a complex process involving cell migration, proliferation, re-epithelialization, angiogenesis and matrix deposition which will then form scar tissue. Pain in the pit of the stomach is a characteristic sign of this disease and this symptom is definitely often heard.
The stomach as a food reservoir/barn functions to receive food/drink, grind, mix and empty food into the duodenum. Because it is often associated with all kinds of food, drink and drugs, the stomach will experience chronic irritation and become ulcers or ulcers. By definition, peptic ulcer is damage or loss of mucosal tissue up to the lamina propria (extending downwards) in the various digestive tracts of food exposed to gastric acid, namely the oesophagus, stomach, duodenum, and after gastroenterostomy also the jejunum. However, the disease occurs mainly in the duodenum and stomach.
From the data above, making nurses as health workers, must be able to provide an explanation of matters related to peptic ulcer disease about how to understand peptic ulcer, anatomy and physiology, etiology of peptic ulcer, pathophysiology of peptic ulcer, signs and symptoms, clinical manifestations, diagnostic examination (laboratory), management and nursing care of peptic ulcer. That's why we created this book entitled Nursing Care for Patients with Digestive System Disorders Due to Peptic Ulcers.
CHAPTER II
A. Anatomy and Physiology
The stomach is located on the left side of the abdomen. If it's empty it's a J-shaped tube and if it's full it's like a giant avocado. The normal capacity of the stomach is 1-2 L. The main part of the stomach consists of:
1. The fundus is the middle part, the shape is rounded.
2. Gastric body
3. Pylorus is the lower part, the area associated with the 12 finger intestine or often called the duodenum .
The stomach wall is composed of four layers, namely:
1. Mucosa.
Mucosa is the layer where cells secrete various types of fluids, such as enzymes, stomach acid, and hormones. In the mucosal lining there are 3 types of cells that function in digestion, namely:
a. Goblet cells function to produce mucus or mucus to protect the outer layer of cells from being damaged by pepsin enzymes and stomach acid.
b. Parietal cells function to produce gastric acid [ Hydrochloric acid ] which is useful in activating the pepsin enzyme. It is estimated that the parietal cells produce 1.5 mol dm -3 of gastric acid which makes the acidity level in the stomach reach a pH of 2.
c. Chief cells function to produce pepsinogen , which is the enzyme pepsin in an inactive form. Chief cells produce it in an inactive form so that the enzyme does not digest the protein that the cell has which can cause death in the cell.
2. Submucosa
The submucosa is the layer where arteries and veins can be found to deliver nutrients and oxygen to the cells of the stomach as well as to carry absorbed nutrients, urea and carbon dioxide from the cells.
3. Muscularis
Muscularis is a layer of muscles that helps the stomach in mechanical digestion. This layer is divided into 3 muscle layers, namely circular, longitudinal, and oblique muscles. Contraction of the three types of muscle layers causes peristalsis (waving motion).
Peristalsis causes food in the stomach to be stirred. The outermost layer, the serosa , serves as a protective layer for the stomach. The cells in this layer secrete a kind of fluid to reduce the frictional forces that occur between the stomach and the rest of the body.
4. Serosa
In the inner wall of the stomach there are glands that produce gastric juice. Aroma, shape, color, and taste for food will reflexively cause gastric juice secretion. Gastric juice contains gastric acid (HCI), pepsin, mucin and renin . Stomach acid acts as a killer of microorganisms and activates the pepsinogen enzyme to become pepsin.
3. Renin is a special enzyme that is only found in mammals, acts as a caseinogen to casein. Casein is coagulated by Ca 2+ from milk so it can be digested by pepsin. Without the presence of liquid milk rheme, it will just pass through the stomach and intestines without having time to digest it.
The action of enzymes and crushing by the stomach muscles turns food into soft mush, called chyme (kim) or food gruel. The pyloric muscle of the stomach regulates the gradual release of chyme into the duodenum. The trick, the pyloric muscle that leads to the stomach will relax (slacken) if it is touched by acidic chyme. Conversely, the pyloric muscle that leads to the duodenum will contract (contract) if touched by chyme. So, for example, chyme which is acidic arrives at the front pylorus, the pylorus will open, so that food passes. Because acidic food hits the back pylorus, the pylorus closes. The food is digested so that its acidity decreases.
Alkaline food behind the pylorus will stimulate the pylorus to open. As a result, acidic food from the stomach enters the duodenum. And so on. Thus, food passes through the pylorus into the duodenum one piece at a time so that it can be effectively digested. After 2 to 5 hours, the stomach is empty again.
In the stomach there are oxyntic glands ( English : oxyntic gland ) which produce the GHS hormone . Other hormones secreted include GHIH .
Motor Function | Digestive Function | ||
Reservoir function | Storage of food s/d is little by little digested and moves to the digestive tract | Protein digestion | Digestion of protein by pepsin and HCL begins at this time, whereas KH and fat in the stomach are very small |
Mix function | Breaks down food into small particles which are mixed with gastric juice/HCL through contractions of the muscles that surround the stomach | Synthesis and release of gastrin | Synthesis and release of gastrin are influenced by ingested protein, stretching and vagal stimulation |
Gastric emptying function | Regulated by the pyloric sphincter surface which is influenced by viscosity, acidity, volume and regulated by nerves and hormones | Intrinsic F secretion | Allows absorption of vitamin B2 from the distal small intestine |
Mucus secretion | Forms a covering that protects the stomach and acts as a lubricant so that food is easily transported | ||
The stomach produces chyme which is a material consisting of: sticky liquid, strong acids and food digestive components. There are 3 phases of gastric action which are affected by chyme secretion:
1. The cephalic phase prepares the stomach for the arrival of food, very short duration (in minutes), mechanism: neural through the preganglionic fibers of the vagus nerve and synapses in the submucosal plexus, action: increases gastric volume, stimulation of mucus, enzymes, production acid and release of gastrin by G cells.
2. Gastric phase : begins the release of secretions from the chyme beginning of protein digestion by pepsin. Duration: 3-4 hours, there is release of gastrin by G cells and release of histamine by mast cells as protection against antigen-antibody reactions from certain foods. Increasing the production of acid and pepsinogen increases the motility and breakdown of materials.
3. Intestinal phase : controls the release of chyme into the duodenum. Duration: long ( hours. Stimulation of CCK, GIP, feedback in inhibiting gastric acid, pepsinogen and reduction of gastric motility.
B. Basic Concepts of Disease
Peptic ulcer is a gastric mucosal discontinuity that extends below the epithelium (mucous tissue, submucosa and muscle layer of the upper digestive tract, can occur in the esophagus, stomach, duodenum and jejunum caused by stomach acid and pepsin. (Price, 2006). Ulcers are categorized if there is a tear in the gastric mucosa with a diameter of ≥ 5 mm down to the submucosal layer. Mucosal tear < 55 mm and necrosis that occurs deeper than the muscularis mucosa is categorized as an ulcer. The gastric mucosal layer in peptic ulcer is not intact so that the tissue is exposed. This comes in contact with stomach acid so that the client experiences burning pain in the pit of the stomach, nausea and vomiting.Complaints most often occur when the stomach is empty.
Peptic ulcer is an excavation (area of the stomach) that forms in the mucosal wall of the stomach, pylorus, duodenum, or esophagus. Peptic ulcers are often referred to as gastric, duodenal or esophageal ulcers, depending on their location. These ulcers are caused by erosion of a limited area of mucous membrane. These erosions may extend deep into the muscle or throughout the muscle in the peritoneum. Peptic ulcers are more likely to occur in the duodenum than the stomach.
Usually, it occurs singly, but can occur in multiples. Chronic peptic ulcers tend to occur on the lesser curvature of the stomach, near the pylorus. Zollinger-Ellison syndrome is often considered a type of peptic ulcer. Stress ulcers, which differ clinically from peptic ulcers, are ulcerations of the mucosa that can occur in the gastroduodenal area. Both of these conditions will lead to peptic ulcer (Brunner and Suddarth's, 2002).
Peptic ulcer is a break in the continuity of the gastric mucosa that extends beneath the epithelium. Damage to the mucosa that does not extend below the epithelium is referred to as an erosion, although it is often referred to as an 'ulcer' (eg stress ulcer). By definition, peptic ulcers can be located in any part of the digestive tract that is exposed to gastric acid sap, namely the esophagus, stomach, duodenum, and after gastroenterostomy, also the jejunum. (Sylvia A. Price, 2006).
C. Peptic ulcer etiology
The gram-negative bacterium H. Pylori has been strongly believed to be a causative factor. It is known that peptic ulcer occurs only in areas of the GI tract exposed to hydrochloric acid and pepsin. According to some opinions, the predisposing factor is stress or anger that is not expressed as a predisposing factor.
Ulcers appear to occur in people who are emotionally inclined, but whether this is a contributing factor to the condition is uncertain. Familial tendencies also appear to be a significant predisposing factor. Further hereditary relationships were found in individuals with blood groups who were more susceptible than individuals with blood groups A, B, or AB. Other predisposing factors associated with peptic ulcer include chronic use of non-steroidal anti-inflammatory drugs (NSAIDs). Drinking alcohol and smoking excessively. Recent studies have shown that gastric ulcers may be associated with bacterial infection with agents such as H. pylori. The presence of these bacteria increases with age. Ulcers due to excessive amounts of the hormone gastrin, produced by tumors (gastrinomas- Zolinger-Ellison syndrome) are rare. Stress ulcers may occur in patients exposed to stressful conditions. (Brunner and Suddart, 2001)
The cause of peptic ulcer is not clear, but there are many theories that explain the occurrence of peptic ulcer, including:
1. Mucosal resistance to acid gastric juice. Chronic ulcers occur due to excessive gastric acid secretion.
2. Damage to the central nervous system such as neoplasms and malignant hypertension causes chuging, acute erosions and ulcers of the stomach, esophagus, and duodenum.
3. A person's psychological condition influences the appearance of stomach ulcers. Some people who are ambitious and have a high stress and irregular life are at risk of suffering from peptic ulcers.
4. Acute stress in a threatened situation or emergency surgery and choronic stress can worsen the condition of peptic ulcer sufferers.
5. nfark on the stomach wall due to stomach acid. The infarct becomes a thrombus and leaves an ulcer on the stomach wall.
6. Hormonal factors have an effect on causing gastric ulcers such as in Addison's disease, patients taking cortisone for maintenance doses increase the incidence of gastric ulcers which are accompanied by complications. This is because corticosteroid tablets irritate the gastric mucosa. The presence of an adenoma or hyperplasia of the pancreatic endocrine cells gives rise to severe and often multiple gastric ulcers called Zollinger Ellison Syndrome. The increase in the hormone gastrin will stimulate gastric HCL secretion in the antrum.
7. Drugs that cause stomach ulcers. NSAIDS class of drugs such as aspirin, ibupropen, naproxken and diclofenac often cause gastric mucosal abnormalities. Phenylbutazone also causes stomach ulcers because reserpine stimulates gastric acid secretion.
Gastric ulcers are caused by damage to the gastric mucosal barrier. Mucous cells are the first barrier in protecting the stomach surface against various irritants. The gastric mucosa is composed of three types of defense systems:
1. Preepithelial layer, produces mucus containing bicarbonate. This bicarbonate has a high pH content so that it is able to neutralize the gastric lumen surface to 6-7. Bicarbonate secretion is stimulated by calcium, prostaglandins, cholinergic and luminal acidification.
2. The epithelial lining, which is the second line of defense after the preepithelium by producing mucus which maintains intracellular pH and bicarbonate production, and tight junction intracells.
3. The subepithelial layer forms the microvascular system. The rich circulation of the mucosal lining supplies bicarbonate to neutralize hydrochloric acid to the parietal cells of the stomach and supplies adequate nutrients and oxygen.
Acetyl silicic acid (aspirin), alcohol and indomethacin (indocin) damage the gastric mucosal defenses. Damaged mucosal defenses will cause hydrochloric acid and pepsin to damage the epithelial layer. The epithelial layer is unable to produce protaglandins which stimulate bicarbonate secretion so that bicarbonate is reduced and the atmosphere in the stomach becomes very acidic. The decrease in the number of prostaglandins is also thought to be due to the presence of Helicobacter pylori. Gastric mucosal injury by H.pylori causes an imbalance between the production of acid or pepsin with the production of mucus, biocarbonate, and blood flow. H.pylori is a gram-negative bacilli, colonizing the mucous gel layer even though it is this layer that protects the mucosa from various damages. Helicobacter pylori penetrates into the mucous lining of the antrum and adheres firmly to the epithelial surface. The location of this bacterium will protect it from the body's immune system and acidity. Then it secretes the enzyme urease which produces ammonia and increases the pH around the microorganism. D cells in the gastric antrum are destroyed by these bacteria and somatostatin decreases.
then G cells are stimulated by the hypergastrinemia and cause gastric parietal cells to increase HCl secretion. Damage to the mucosa also causes impaired blood flow, the pyloric sphincter does not function normally or does not respond to secretin or cholecystokinin, a substrate that increases gastric pressure and prevents reflux. In the absence of excess bile and chloride in the stomach, it causes back-diffusion of hydrogen ions, leading to inflammation of the mucosa and ulcer formation. Excessive production of HCL, will irritate the lining of the intestinal epithelium in the duodenum so that it can be irritated and trigger metaplasia, a change from intestinal epithelium to gastric epithelium. H. pylori can colonize the duodenum and trigger further damage and ulceration.
E. Signs and Symptoms of Peptic Ulcer
1. Pain:
Relating to food
Periodic nature: occurs some time after eating and sleeping at midnight
Characteristics : sore, like being pricked
Localization : in the epigastrium
· The theory of the onset of pain: motility theory, acid theory, inflammatory theory
2. Decreased appetite
3. Burning taste
3. The subepithelial layer forms the microvascular system. The rich circulation of the mucosal lining supplies bicarbonate to neutralize hydrochloric acid to the parietal cells of the stomach and supplies adequate nutrients and oxygen.
Acetyl silicic acid (aspirin), alcohol and indomethacin (indocin) damage the gastric mucosal defenses. Damaged mucosal defenses will cause hydrochloric acid and pepsin to damage the epithelial layer. The epithelial layer is unable to produce protaglandins which stimulate bicarbonate secretion so that bicarbonate is reduced and the atmosphere in the stomach becomes very acidic. The decrease in the number of prostaglandins is also thought to be due to the presence of Helicobacter pylori. Gastric mucosal injury by H. pylori causes an imbalance between acid or pepsin production and mucus production, biocarbonate, and blood flow. H.pylori is a gram-negative bacilli, colonizing the mucous gel layer even though it is this layer that protects the mucosa from various damages. Helicobacter pylori penetrates into the mucous lining of the antrum and adheres firmly to the epithelial surface. The location of this bacterium will protect it from the body's immune system and acidity. Then it secretes the enzyme urease which produces ammonia and increases the pH around the microorganism. D cells in the gastric antrum are destroyed by these bacteria and somatostatin decreases.
then G cells are stimulated by the hypergastrinemia and cause gastric parietal cells to increase HCl secretion. Damage to the mucosa also causes impaired blood flow, the pyloric sphincter does not function normally or does not respond to secretin or cholecystokinin, a substrate that increases gastric pressure and prevents reflux. In the absence of excess bile and chloride in the stomach, it causes back-diffusion of hydrogen ions, leading to inflammation of the mucosa and ulcer formation. Excessive production of HCL, will irritate the lining of the intestinal epithelium in the duodenum so that it can be irritated and trigger metaplasia, a change from intestinal epithelium to gastric epithelium. H. pylori can colonize the duodenum and trigger further damage and ulceration.
1. Pain:
Relating to food
Periodic nature: occurs some time after eating and sleeping at midnight
Characteristics : sore, like being pricked
Localization : in the epigastrium
· The theory of the onset of pain: motility theory, acid theory, inflammatory theory
2. Decreased appetite
3. Burning taste
4. Acid regurgitation
5. Nausea and vomiting :
- Occurs when severe pain
- Can occur after eating
- Due to pylorospasm or pyloryc stenosis
6. Colonic symptom :
- Complains of constipation
- Pain in the area of acute colic
- Pain during defecation
F. Clinical Manifestations of Peptic Ulcers
1. Changes in appetite and weight changes. Gastric ulcer clients tend to lose weight because they are afraid to eat, whereas duodenal ulcer clients may gain weight because they eat to relieve pain. Nausea, vomiting and anorexia are common in gastric ulcers (Braunwald et al, 2001)
2. Stomach pain is very great. Epigastric pain in duodenal ulcers occurs 1-2 hours after eating, usually relieved by taking antacids or eating. The nighttime pain is typical for duodenal ulcers causing the patient to wake in the middle of the night and at 3am. Pain occurs to the right of the midline, in 20% of patients.
3. Vomiting that is bloody and bloody or black stools, if there is damage to the capillaries in the stomach.
4. Tachycardia indicates dehydration due to vomiting and gastrointestinal bleeding.
5. Belching, chest pain.
G. Diagnostic Examination (Laboratory)
To establish the diagnosis of peptic ulcer are:
1. Helicobacter pylori test, performed on stool, blood and breath testing. In the breath test, the patient is given liquid to swallow and it will be broken down by H. pylori into gas. The gas contained in the patient's breath is tested using a tool. If gas is detected in the exhaled air, it indicates that Helicobacter pylori is present in the stomach.
2. Endoscope, gastroscope inserted through the mouth into the stomach. This endoscope visualizes the mucosal crest and a tissue sample or biopsy is taken. Then the tissue will be analyzed under a microscope and immediately tested for H. pylori.
3. Barium enemas. The patient is asked to swallow a drink containing barium (the substance can be seen on the X-Ray).
4. Gastric analysis.
5. X-ray of the abdomen.
H. Management
1. Administration of H 2 blockers; Ranitidine and Cimetidine.
a. If the ulcer is caused by H. pylori, with two kinds of antibiotics and proton pump inhibitors for example: Omeprazole 2 mg 2x/day + Metronidazole 400 mg 2x/day + calrithromycin 250 mg 2x/day, or Omeprazole 2 mg 2x/day + metronidazole 400 mg/day + 1 g amoxicillin 2x/day.
b. If the cause is NSAIDs or other causes other than H. pylori, the recommended treatment is omeprazole or lansoprazole or pantoprazole H 2 receptor antagonists such as cimetidine, ranitidine and famotidine.
2. Diet management and diet modification.
3. Stress management.
4. Surgery
· Only indicated for failure of medical therapy and complications.
· Elective surgery for duodenal ulcers: highly selective vagotomy; currently used rarely: Elective surgery for gastric ulcers: Billroth I gastrectomy.
· Perforated duodenal/gastric ulcer: simple closure of perforation and biopsy.
· Bleeding: endoscopic control with sclerotherapy, sewing damaged blood vessels.
Pyloric stenosis: gastroenterostomy.
I. Peptic Ulcer Complications
Bleeding with signs: vomiting blood (usually red), blood in the stool (usually dark red), anemia. Perforations cause severe pain and require surgery.
J. Classification of peptic ulcer
Classification of peptic ulcer according to its occurrence, namely:
1. Acute Peptic Ulcer. Arises suddenly and occurs due to causes such as severe burns and severe surgery due to drugs. The location of this peptic ulcer is often found in the duodenum and stomach.
The characteristics of this acute peptic ulcer include multiple and shallow, 1-1.5 cm in diameter, sometimes there is bleeding, heal quickly and can leave scars.
2. Chronic peptic ulcer. Chronic symptoms, the patient has a history of heartburn, pain for more than 2 months that arises related to food or drink, takes a long time to heal and is 2.5-4 cm in diameter.
Based on Ulcer Location
Ulcers that are located in the esophagus are called esophageal ulcers, in the stomach they are called gastric ulcers, in the duodenum they are called duodenal ulcers, and in the jejunum they are called ulcers yeyuni. Esophageal and jejunal ulcers are usually very rare and this chapter will only consider gastric and duodenal ulcers.
1. Stomach ulcer. Most in the angulus, antrum, and prepylorus. Rarely located in the body and fundus. Usually suffered at the age of more than 65 years.
2. Duodenal ulcer / duodenal ulcer. It is most located on the anterior and posterior wall of the bulb and postbulber or pars descending duodeni proximal to the papilla vaterii. Rarely found on the distal papilla vaterii, usually affects 45-65 years. Ulcer depth ranged from 1 mm to 1 cm.
4. Gastric analysis.
5. X-ray of the abdomen.
1. Administration of H 2 blockers; Ranitidine and Cimetidine.
a. If the ulcer is caused by H. pylori, with two kinds of antibiotics and proton pump inhibitors for example: Omeprazole 2 mg 2x/day + Metronidazole 400 mg 2x/day + calrithromycin 250 mg 2x/day, or Omeprazole 2 mg 2x/day + metronidazole 400 mg/day + 1 g amoxicillin 2x/day.
b. If the cause is NSAIDs or other causes other than H. pylori, the recommended treatment is omeprazole or lansoprazole or pantoprazole H 2 receptor antagonists such as cimetidine, ranitidine and famotidine.
2. Diet management and diet modification.
3. Stress management.
4. Surgery
· Only indicated for failure of medical therapy and complications.
· Elective surgery for duodenal ulcers: highly selective vagotomy; currently used rarely: Elective surgery for gastric ulcers: Billroth I gastrectomy.
· Perforated duodenal/gastric ulcer: simple closure of perforation and biopsy.
· Bleeding: endoscopic control with sclerotherapy, sewing damaged blood vessels.
Pyloric stenosis: gastroenterostomy.
I. Peptic Ulcer Complications
Bleeding with signs: vomiting blood (usually red), blood in the stool (usually dark red), anemia. Perforations cause severe pain and require surgery.
J. Classification of peptic ulcer
Classification of peptic ulcer according to its occurrence, namely:
1. Acute Peptic Ulcer. Arises suddenly and occurs due to causes such as severe burns and severe surgery due to drugs. The location of this peptic ulcer is often found in the duodenum and stomach.
The characteristics of this acute peptic ulcer include multiple and shallow, 1-1.5 cm in diameter, sometimes there is bleeding, heal quickly and can leave scars.
2. Chronic peptic ulcer. Chronic symptoms, the patient has a history of heartburn, pain for more than 2 months that arises related to food or drink, takes a long time to heal and is 2.5-4 cm in diameter.
Based on Ulcer Location
Ulcers that are located in the esophagus are called esophageal ulcers, in the stomach they are called gastric ulcers, in the duodenum they are called duodenal ulcers, and in the jejunum they are called ulcers yeyuni. Esophageal and jejunal ulcers are usually very rare and this chapter will only consider gastric and duodenal ulcers.
1. Stomach ulcer. Most in the angulus, antrum, and prepylorus. Rarely located in the body and fundus. Usually suffered at the age of more than 65 years.
2. Duodenal ulcer / duodenal ulcer. It is most located on the anterior and posterior wall of the bulb and postbulber or pars descending duodeni proximal to the papilla vaterii. Rarely found on the distal papilla vaterii, usually affects 45-65 years. Ulcer depth ranged from 1 mm to 1 cm.
The classification based on the depth is as follows:
1. Ulcer degree I: Ulceration only on the mucosa, and is called erosion.
2. Ulcer degree II: Ulceration to the mucosa.
3. Ulcer degree III: Ulceration extends to a deeper part, namely in part of the muscularis layer.
4. Ulcer degree IV: The ulcer penetrates deeper, especially some of the muscularis layer and becomes inflamed up to the serous layer.
CHAPTER III
CASE REVIEW
A. Assessment
1. Anamnesis
Ulcer symptoms may go away for days, weeks, or months and may even disappear only to appear again, often with no identifiable cause. Many individuals develop symptomatic ulcers, and 20-30% have perforations or hemorrhages without any prior manifestations. Subjective data focuses on complaints felt by patients such as:
a. Pain: Usually patients with ulcers complain of a dull, stabbing or burning sensation in the mid epigastrium or back. It is believed that pain occurs when the acid content of the stomach and duodenum increases, causing erosion and stimulating the exposed nerve endings. Another theory suggests that contact of a lesion with acid stimulates a local reflex mechanism that initiates contraction of the surrounding smooth muscle.
Pain is usually relieved by eating, because eating neutralizes acid or by using alkali, but when the stomach is empty or alkali is not used the pain returns. Sharp local tenderness can be relieved by applying gentle pressure to the epigastrium or slightly to the right of the midline. Some symptoms are reduced by applying local pressure to the epigastrium.
2. Pyrosis (heartburn): some patients experience a burning sensation in the esophagus and stomach, which rises to the mouth, sometimes accompanied by acid eructation. Eructation or belching is common when the patient's stomach is empty.
3. Vomiting: although rare in uncomplicated duodenal ulcers, vomiting can be a symptom of peptic ulcer. It is associated with the formation of scar tissue or acute swelling of the inflamed mucous membrane around the acute ulcer. Vomiting may or may not be preceded by nausea, usually after severe pain which is relieved by ejection of gastric acid.
4. Constipation and bleeding : constipation can occur in ulcer patients, possibly as a result of diet and drugs.
Patients may also come with gastrointestinal bleeding, a small proportion of patients who have experienced acute ulcers before experiencing no complaints, but they show symptoms afterward.
4. Anorexia.
5. Diet and diet.
6. The habit of consuming coffee and alcohol.
7. Use of drugs.
8. Individual and family stressors.
9. Work and lifestyle.
10. Usual coping patterns and problem solving.
The assessment includes:
Patient identity
2. Main complaint: pain in the abdomen (stomach)
3. History of current illness:
a. Abdominal pain (stomach) after eating or before eating
b. Feeling nauseous and vomiting after eating
c. Vomiting blood
d. Feeling of heat in the abdomen
4. Past medical history
5. There is a history of gastritis
7. Family history of disease
2. Physical Examination
1. General Condition :
GCS :
- Body characteristics: skin, hair, body posture.
- Vital signs: pulse, body temperature, blood pressure, and respiration.
2. Head to toe
a. Head
- Inspection: head shape, distribution, color, scalp.
- Palpation: tenderness in the head.
b. Face
- Inspection: face shape, facial skin.
- Palpation: tenderness in the face.
c. Eye
- Inspection: shape of the eye, sclera, conjunctiva, pupil.
- Palpation: tenderness in the eyeball, the color of the conjunctival mucosa, the color of the sclera mucosa.
d. Nose
- Inspection: nose shape, nostril breathing, secretions.
- Palpation: tenderness in the nose.
e. Mouth
- Inspection: shape of mouth, shape of mouth, shape of teeth.
- Palpation: tenderness of the tongue, gums, teeth.
f. Neck
- Inspection: shape of the neck, skin color on the neck.
- Palpation: tenderness in the neck.
g. Chest
- Inspection: shape of the chest, chest expansion, respiratory rate.
- Palpation: expansion of the lungs on inspiration and expiration, focal fremitus, tenderness.
- Percussion: heart border, lung limit, there is / no accumulation of secretions.
- Auscultation: lung sounds and breath sounds.
h. Breasts and armpits
- Inspection: shape, lump.
- Palpation: there is / no tenderness, lumps
i. Abdomen
- Inspection: shape of the abdomen, color of the skin of the abdomen.
- Auscultation: bowel sounds, venous sounds, hepatic and spleen friction.
- Percussion: liver limit, kidney limit, spleen limit, presence/absence of fluid accumulation in the stomach
J. Genitalia
- Inspection: genital shape, genital hair distribution, genital hair color, lumps
- Palpation: tenderness in the genitals.
k. Integument
- Inspection: skin color, lumps.
- Palpation: tenderness on the skin.
l. Upper Extremity
- Inspection: skin color, shape of the hand.
- Palpation: tenderness.
m. Lower Extremity
- Inspection: skin color, shape of the feet.
- Palpation: tenderness, muscle strength.
3. Diagnostic Or Support Examination
1. Physical examination may reveal pain, epigastric tenderness or abdominal distention.
2. Bowel sounds may be absent.
3. Barium examination of the upper GI tract may reveal ulcers, but endoscopy is the diagnostic procedure of choice.
4. Upper GI endoscopy is used to identify inflammatory changes, ulcers and lesions. Through endoscopy the mucosa can be directly seen and a biopsy is obtained. Endoscopy has been known to detect some lesions that are not visible on X-ray examination because of their size or location.
5. Stool can be taken every day until the laboratory report is negative for occult blood.
6. Gastric secretory examination is of decisive value in diagnosing achlorhydria (absence of hydrochloric acid in gastric juice) and Zollinger-Ellison syndrome. Pain that is relieved by food or antacids, and no pain relief also identifies an ulcer.
7. The presence of H. pylori can be determined by biopsy and histology by culture, although this is a specific laboratory test as well as a serological test for antibodies to the H. pylori antigen.
B. Data Analysis
No | Problem | Etiology | Symptom |
1. | Painful | Mucosal weakness/damage stomach ¯ Acid concentration and action increased pepsin ¯ Erosion of mucous membranes stomach ¯ cerebral cortex ¯ Pain is perceived | DS : Clients often wince in pain DO : - Pulse pressure 96 beats/minute - grimacing facial expression - Pain on a scale of 3 |
2. | Nutrition less than body requirements | Mucosal weakness/damage stomach ¯ Acid concentration and action pepsin increases ¯ Erosion of mucous membranes stomach ¯ gastric dysfunction ¯ Anorexia ¯ Nutrition mall | DS : The client says his appetite is reduced DO : - Meal portions are not spent - BB decreased |
3 . | anxiety | Don't know the source information ¯ Lack of interpretation information ¯ Lack of knowledge about the disease | DS : The client said that he had never experienced this this disease before DO : Clients complain about the disease |
Issue Priority
1) Pain
2) Changes in nutrition less than body requirements
3) Anxiety
C. Nursing Diagnosis
1. Pain associated with weakness/damage to the gastric mucosa characterized by:
DS: The client says he often winces in pain
DO :
Pulse pressure 96 beats/minute
Grimace facial expression
Pain on a scale of 3
2. Changes in nutrition less than body requirements related to the concentration and action of pepsin acid characterized by:
DS: The client says his appetite is reduced
DO :
· Food portions are not spent
Decreased BB
3. Anxiety related to not knowing the source of information, characterized by:
DS: The client says that the client has never experienced this disease before.
DO: The client complains about his illness
D. Planning (Purpose, Intervention and Rationale)
1. Pain related to tissue trauma and reflex muscle spasm secondary to intestinal visceral disorders.
Objective : after nursing care has been carried out for … x 24 jan it is hoped that the pain in the patient can be reduced or lost.
Outcome criteria : taking medication as prescribed, experiencing pain relief, substituting aspirin for aetaminophen (Tylenol), avoiding over-the-counter drugs, adhering to recommended restrictions, identifying foods and drinks to avoid, adhering to regular meal and snack schedules, and quitting smoke.
Action or Intervention | Rational |
1. Give drug therapy according to the program: a. Histamine antibiotics b. Antibiotic salt / bismuth c. Cytoprotective agent d. Proton pump inhibitors e. antacids | Pharmacotherapy helps reduce: a. histamine antibiotics affect stomach acid b. antibiotics given together with bismuth lethal H.pylori cytoprotective agents c. protect the gastric mucosa d. proton pump inhibitors decrease stomach acid e. Antacids neutralize the acidity of gastric secretions |
2. Advise to avoid over-the-counter drugs | Inhibits the release of stomach acid |
3. Instruct patient to use meals and snacks at regular intervals | Foods and drinks that contain caffeine stimulate the secretion of hydrochloric acid |
4. Advise the patient to stop smoking | Smoking stimulates the possibilities ulcer recurrence |
2. Activity intolerance related to anemia characterized by muscle weakness.
Purpose : after nursing care is carried out, it is hoped that the patient will have a little energy to move.
Outcome criteria : normal vital signs and the patient is not. Changes in nutrition less than body requirements related to anorexia, nausea and vomiting.
Action or Intervention | Rational |
1. Encourage light activity and get plenty of rest | With mild activity and adequate rest can restore the patient's condition. |
2. Assess the factors that cause fatigue | By overcoming the problem of fatigue |
3. Increase tolerance for self-reliance, help if fatigue occurs | Increase independence in activities tolerated self-care, help if fatigue occurs |
3. Changes in nutrition less than body requirements related to anorexia, nausea and vomiting.
Objective : after being given nursing care, it is expected that the patient will get an optimal level of nutrition.
Outcome criteria : avoid irritating foods and drinks, eat and snack at regularly scheduled intervals, and choose a relaxing environment for meals.
Action or Intervention | Rational |
1. Suggest non-irritating foods and drinks | Non-irritating foods reduce epigastric pain |
2. Encourage meals to be eaten on a regular schedule, avoiding snacks before bedtime | Regular meals help neutralize gastric secretions, a snack before bedtime increases gastric acid secretion |
3. Encourage food in a relaxed environment | A relaxed environment causes less anxiety. Reducing anxiety helps reduce the secretion of hydrochloric acid |
4. Lack of knowledge regarding prevention of symptoms and management of conditions associated with inadequate information.
Goal : patient gets knowledge about prevention and management.
Outcome criteria : express interest in learning how to cope with illness, participate in counseling sessions, ask questions, and express a desire to take responsibility for self-care.
Action or Intervention | Rational |
1. Assess the patient's level of knowledge and readiness to learn | The desire to learn depends on the patient's physical condition, level of anxiety and mental readiness |
2. Teach the necessary information: Use words appropriate to the patient's level of knowledge. Limit counseling sessions to 30 minutes or less. | Individualization of the extension plan enhances learning |
3. Reassure the patient that the disease can be overcome | Provide a positive influence on behavior change |
E. Evaluation
Diagnosis | Evaluation |
1. Pain related to tissue trauma and reflex muscle spasm secondary to intestinal visceral disorders. | S: The patient says that the pain has decreased O: Tissue and reflex trauma patients muscle spasms A: Goal achieved, problem solved Q: Maintain conditions |
2. Activity intolerance related to anemia characterized by muscle weakness. | S : The patient says that he can do his own activities O : TTV is normal, the patient doesn't look worried again A : Goal achieved, problem solved Q: Maintain conditions |
3. Changes in nutrition less than body requirements related to anorexia, nausea and vomiting | S : The patient says that he has energy O : Stable weight A : Goal achieved, problem solved Q: Maintain conditions |
4. Lack of knowledge regarding prevention of symptoms and management of conditions associated with inadequate information. | S : The patient said that he understood the explanation given and did not feel anxious anymore O : The patient seems to nod at the moment explained and when asked patient can answer A : Goal achieved, problem solved Q: Maintain conditions |
CHAPTER IV
CLOSING
A. Conclusion
Peptic ulcer is a gastric mucosal discontinuity that extends below the epithelium (mucous tissue, submucosa and muscle layer of the upper digestive tract, can occur in the esophagus, stomach, duodenum and jejunum caused by gastric acid and pepsin. (Price, 2006). The etiology of Peptic ulcer is the resistance of the mucosa to acid gastric juice, damage to the central nervous system such as malignant neoplasms and hypertension causing cussing, acute erosions and ulcers of the stomach, esophagus, and duodenum, a person's psychological condition influences the appearance of gastric ulcers, in some people who are ambitious and burdensome high stress and irregular life are at risk of suffering from peptic ulcers, infarction of the stomach wall due to stomach acid,acute stress in a threatened situation or emergency surgery and choronic stress can exacerbate the condition of peptic ulcer sufferers, factors
Hormonal influences cause stomach ulcers such as in Addison's disease, patients taking cortisone for maintenance doses increase the occurrence of stomach ulcers accompanied by complications, drugs that cause stomach ulcers. The management is non-pharmacological, namely stress reduction and rest, smoking cessation, diet modification, surgical intervention and pharmaco, namely drugs.
B. Suggestion
For students to correctly understand the basic concept of peptic ulcer and understand nursing care for peptic ulcer, namely being able to make assessments, nursing diagnoses, planning (intervention), implementation and evaluation. So to achieve nursing care in caring for clients, the approach in the nursing process must be carried out systematically. Nurses should always establish good cooperative relationships or good collaboration with colleagues, doctors or other medical professionals in the implementation of nursing care and in terms of treatment for clients so that the expected goals can be achieved.
saya hanya seorang individu yang sedang memahami arti dari sebuah kehidupan, belajar akan manis dan pahitnya dunia dan merasakan arti dari sebuah keluarga dan sahabat tentunya seorang kekasih yang kelak akan jadi ibu dari anak-anak saya.
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