CHAPTER I
PRELIMINARY
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
THEORETICAL REVIEW
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.
1. Pepsin is an enzyme that can convert proteins into smaller molecules.
2. Mucin is a mucosal protein that lubricates food.
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.
4. HCl ( Hydrochloric Acid) is an enzyme that is useful for killing germs and bacteria in food.
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
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.
D. Pathophysiology of Peptic Ulcer
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 h
