peptic ulcer in the elderly
Introduction
Introduction to peptic ulcer in the elderly Peptic ulcer (PUD) mainly refers to chronic ulcers that occur in the stomach and duodenal bulbs. The formation of ulcers is related to the digestion of gastric acid and pepsin, hence the name. Ulcer refers to the mucosal defect than the mucosal muscle layer, so it is different from erosion, generally refers to gastric ulcer (GU) and duodenal ulcer (duodenalulcer, DU). The condition of peptic ulcer in the elderly is more serious than that of young people, but the clinical symptoms are often atypical and prone to complications. Traditional treatments are less effective, and invasive treatment is limited by concomitant diseases. Despite the progress in the diagnosis and treatment of peptic ulcer in recent years, the mortality rate of peptic ulcer in the elderly has increased, so it should be given enough attention. basic knowledge The proportion of illness: 10% Susceptible people: the elderly Mode of infection: non-infectious Complications: pyloric obstruction, gastric ulcer
Cause
The cause of peptic ulcer in the elderly
Helicobacter pylori (HP) infection (30%):
In 1994, the National Institutes of Health (NIH) organized experts to demonstrate the role of HP infection in the pathogenesis of peptic ulcer, and reached a consensus that HP infection plays an important role in the pathogenesis of peptic ulcer. 1996 and Europe in 1997 The region also organized experts to hold a consensus meeting on HP. On the issue of the relationship between HP infection and peptic ulcer, the same views as the US NIH consensus report were obtained, and there was a certain expansion. It is currently believed that Helicobacter pylori infection is digestive. The leading cause of ulcers, the hand may be a key factor in the spread of Helicobacter pylori, a study of 242 Guatemalans in an isolated village showed 58% of Helicobacter pylori-positive, 87% of them around the teeth or tongue There is a Helicobacter pylori in the gap, and it can be seen that there is a significant positive correlation between tongue infection and fingernails (J Clin Microbiol 1999; 37: 2456-60).
Non-steroidal anti-inflammatory drugs (NSAID) (20%):
With the application of different NSAIDs, the frequency of gastrointestinal (GI) complications such as hemorrhage, perforation, obstruction or symptomatic ulceration also changes, and the frequency of complications is increased by about 40%. By inhibiting prostaglandin synthesis, it has a negative impact on several factors of mucosal defense. Many NSAIDs have local stimulating effects on the epithelium, which may play a particularly important role in intestinal injury, although the presence of gastric acid in the gastric cavity is not the NSAID-induced gastrointestinal The main factor of the disease, but in the acidic environment, anti-inflammatory drugs such as aspirin can not be ionized and dissolved in the stomach acid. The original aspirin is fat-soluble, so it can penetrate the epithelial cells to destroy the mucosal barrier, and the absorbed aspirin can Inhibition of cyclooxygenase activity interferes with prostaglandin synthesis in the gastroduodenal mucosa, causing mucosal cells to lose normal prostaglandin protection, and ulceration occurs under the action of other substances that damage the mucosa (such as bile). NSAID can damage the repair process, hinder hemostasis, and inactivate several growth factors involved in mucosal defense and repair. A variety of factors can cause chronic mucosal injury and bleeding.
Excessive gastric acid secretion (15%):
Hydrochloric acid is the main component of gastric juice. It is secreted by parietal cells and regulated by nerves and body fluids. It is known that the parietal cell membrane contains three kinds of receptors, namely histamine receptors, cholinergic receptors and gastric secretion. Gastrin receptors, which are activated by histamine, acetylcholine and gastrin, respectively, increase gastric acid secretion in patients with duodenal ulcer, mainly related to the following factors: (1) increased number of parietal cells: average stomach of normal people There are about 1 billion parietal cells in the mucosa, and the number of parietal cells in patients with duodenal ulcer is 1.9 billion, which is 1 times higher than that of normal people. The increase in the number of parietal cells may be due to genetic factors and/or gastric acid secretion. The result of long-term effects of irritants such as gastrin. (2) Increased sensitivity of parietal cells to stimulating substances: patients with duodenal ulcer respond more to gastric acid secretion after stimulation with food or pentagastrin gastrin than normal people, which may be gastrin receptors on the parietal cells of patients. An increase in affinity or a decrease in the body's inhibitory effect on gastrin-stimulated gastric acid secretion (such as somatostatin). (3) The normal feedback inhibition mechanism of gastric acid secretion is defective: under normal circumstances, gastric acid secretion has its own regulatory effect, but some patients with duodenal ulcer have hypertrophic G cell function in gastric antrum, and its gastric acid feedback inhibition effect is also defective. HP infection can cause hypergastrinemia, and feedback inhibition of G cell secretion of gastrin is one of the reasons. (4) Increased vagal tone: The vagus nerve releases acetylcholine, which indirectly stimulates the secretion of hydrochloric acid by the parietal cells and stimulates the secretion of gastrin by G cells. The ratio of partial basal secretion (BAO) to nocturnal secretion (MAO) is increased by BAO/MAO. Patients with duodenal ulcer disease did not respond to gastric acid secretion due to eating, suggesting that these patients are already under maximum vagal tension. The basis of gastric ulcer patients and the gastric acid excretion after stimulation are mostly normal or even lower than normal. The gastric acid excretion of patients with gastric ulcer only in patients with anterior pyloric or patients with duodenal ulcer can be higher than normal, so The change in the amount of gastric acid secretion does not appear to be significant in the occurrence of gastric ulcer.
Genetic factors (10%):
Genetic factors on the incidence of peptic ulcer in duodenal ulcers are more obvious than gastric ulcers, ulcer disease sometimes shows a trend of family multiple, indicating that it is related to heredity. In recent years, studies have found that the incidence of O-type ulcer disease is higher than other The blood type is 1.5 to 2 times, because the gastric mucosal cells are susceptible to bacteria. In vitro experiments have shown that HP causing ulcers easily attacks cells with O-type blood antigens on the surface, and bacteria enter the cells after contact with the antigen. Infection and chronic inflammation with ulceration (Thomas Boren, 1993).
Psychological factors (10%):
Acute stress can cause acute peptic ulcer. It is currently believed that psychological fluctuations can affect the physiological function of the stomach. In patients with peptic ulcer, the symptoms may recur or increase in anxiety and sorrow.
Smoking (10%):
Both epidemiology and clinical observations are closely related to smoking and peptic ulcer. The incidence of this disease in long-term smokers is higher than that of non-smokers. Nicotine in tobacco leaves can slightly damage gastric mucosa and can exacerbate ethanol or NSAID. Damage to the gastric mucosa; can also reduce the content of prostaglandin E (PGE) in the mucosa, long-term smoking can make wall cells proliferate and gastric acid secretion too much, nicotine reduces the pyloric sphincter tension, so that bile can easily flow back into the stomach, and can inhibit The gland secretes HC03-, thereby weakening the neutralizing ability of gastric acid in the duodenal cavity.
Pathogenesis
The pathogenesis of peptic ulcer is very complicated, but it can be summarized as the counterbalance between the two forces. One is the invasiveness of the mucous membrane, the other is the defense of the mucous membrane itself, the invasiveness is too strong, the defense power is too low or the invasiveness When it exceeds the defense force, it will produce ulcers.
The invasiveness of the injured mucosa is mainly gastric acid, pepsin digestion, especially gastric acid, mucosal defense factors including mucosal shielding, mucus-HCO3-barrier, prostaglandin cell protection, cell renewal, epidermal growth factor and mucosal blood flow, etc. , can promote the repair of damaged mucosa.
1. Attack of gastric acid/pepsin gastric acid-pepsin digestion: no acid and no ulcer, this famous saying still plays an important role in ulcer development, drug development, treatment, etc., also on the stomach, duodenum Mucosal invasive factors, many years of research to prove that the formation of ulcers is the result of gastric wall or duodenal wall tissue digestion by gastric acid and pepsin, this self-digestion process is the direct cause of ulcer formation, jejunum and ileum In an alkaline environment, this ulcer rarely occurs. Under normal circumstances, the gastric mucosa is not digested by gastric juice. This is because the mucosa has a defensive barrier function: mucus secreted by the gastric mucosa, forming a mucous membrane on the surface of the gastric mucosa, covering The mucosal surface can avoid or reduce the direct contact of gastric acid with the mucosa, and the mucus has a neutralizing effect on gastric acid. When the barrier function of the mucous membrane is damaged, the hydrogen ions in the gastric acid secreted into the gastric cavity can be diffused into the gastric mucosa ( Reverse diffusion), in addition, bile can change the characteristics of the mucous layer on the surface of the gastric mucosa, thereby impairing the gastric mucosal barrier function, duodenum When sores, caused by excessive stomach acid into the duodenum bulb, is not well and normal physiological function, such duodenum excessive load is an important condition caused by duodenal ulcer.
2. Mucosal defense force weakens
(1) Mucus-HCO3-barrier destruction: Mucus is a sticky glycoprotein gel secreted by gastric epithelial cells and gastric gland mucous cells. Mucosal epithelial cells also secrete HCO3- ions, and HCO3- and mucus layer together form mucus. The HCO3-barrier forms part of the mucosal defense mechanism. In addition to lubricating the food, the mucus-HCO3-barrier can prevent the harmful effects of harmful substances in the stomach on the mucosa. In addition, it can regulate gastric motility and control bacterial growth. It has also been revealed that phospholipid-rich mucin glycoprotein is one of the important factors in the body's stomach to resist HP colonization. Therefore, factors affecting the metabolism of epithelial and glandular cells can affect the maintenance and regeneration of mucus-HCO3-barrier. Intestinal ulcer patients often have gastric antrum epithelial metaplasia, which creates a suitable environment for HP colonization, causes duodenal inflammation, weakens mucosal resistance, and the ability of gastric antrum mucus to secrete mucus is far less than duodenum. In the strong, and the mucosal inflammation of the metaplasia, the ability to manufacture HCO3- is also weakened. Therefore, it can be seen that the mucinous mucosa of the ball has a mucus-HCO3-barrier destruction and is easily attacked by gastric acid.
(2) The decrease of prostaglandin level: gastric mucosa itself can synthesize a variety of prostaglandins, among which prostaglandin I and E levels are high, prostaglandins have cytoprotective effect, can protect mucous membrane from harmful substances, reduce Mucosal damage, prostaglandins can enhance mucus-HCO3- barrier by increasing mucus mucus and bicarbonate secretion; counteract vasoconstrictor substances such as thromboxane A2, increase mucosal blood flow; promote release of surface active phospholipids Free radical scavenging; maintain mucosal sodium pump function; inhibit mast cell degranulation, reduce the release of inflammatory mediators, in addition, some cerebral gut peptides with cytoprotective effects, such as somatostatin, neurotensin, enkephalin, etc. Its mucosal protective effect may eventually be achieved by stimulating the production of prostaglandins.
The decrease of endogenous prostaglandins is one of the important mechanisms of mucosal damage in peptic ulcer. With the occurrence of cell damage, accompanied by decreased endogenous prostaglandin synthesis, non-steroidal anti-inflammatory drugs (NSAID) pass through the inhibition ring. The activity of cyclooxygenase (COX), which reduces the production of prostaglandins, can lead to mucosal damage, and the protection of exogenous prostaglandins is protective and therapeutic.
(3) changes in blood circulation: normal blood supply is one of the foundations for maintaining the normal defense function of the organs. The good blood circulation of the mucosa has many functions. Firstly, it provides abundant nutrients and provides the basis for the regeneration of mucosal epithelial cells. The latter is an important part of the mucosal defense mechanism, followed by the removal of local harmful metabolites. Normal mucosal blood flow also helps maintain the local acid-base balance of the mucosa, and participates in cell protection. Generally, the blood vessels supplying the mucosa are composed of muscles. The blood vessels in the layer penetrate into the submucosal layer and cross-link to form a vascular network, and then branch to the mucosal layer, in addition to the small curvature of the stomach and the duodenum (mainly within 2.5 cm of the starting end) The arteries directly penetrate the muscular layer and the mucosal muscle layer to reach the mucosal layer, and do not form a cross-linked vascular network in the submucosa. However, the blood flow of the gastric mucosa in the elderly reduces the thickening of the blood vessel wall, and the lumen is narrow, which makes the gastric mucosal blood flow significantly lower. Young people, poor mucosal barrier function is one of the reasons for the high incidence of ulcers in the elderly. On the other hand, due to the small cross-linking between blood vessels, the mucosa is When the blood is squeezed or embolized, the blood supply is not easy to compensate for the decrease of blood supply to the tissue, and the mucosal tissue is damaged.
(4) Gastroduodenal motor dysfunction: Partial gastric ulcer patients with pyloric sphincter relaxation, pyloric insufficiency, easy to cause duodenal juice to flow back into the stomach cavity, bile in the reflux fluid, pancreatic juice, etc., can dissolve mucosal epithelial cells The lipoprotein membrane destroys the gastric mucosal barrier, allowing hydrogen ions to diffuse into the mucosa, stimulating mast cells to release histamine, and forming ulcers under the action of gastric acid and pepsin.
Gastric acid secretion in the gastric ulcer is in the normal range, and often low, the lack of mucosal defense, apparently plays a major role in the formation of gastric ulcer, which directly destroys the submucosal blood vessels.
In conclusion, gastric acid-pepsin plays a decisive role in the formation of peptic ulcer, the increase of PCM, the increase of gastric acid and pepsin secretion caused by neuroendocrine dysfunction, and the rapid emptying of the stomach, the formation of duodenal ulcer. The basis; the destruction of the gastric mucosal barrier, the weakening of the gastric pyloric function, and the reflux of the duodenal juice is the condition for the formation of gastric ulcer.
3. HP infection
(1) The pathogenesis of HP-induced duodenal ulcer is not completely clear. One theory is that HP can cause mucosal damage and lead to duodenal ulcer formation by colonizing the gastric epithelium in the duodenum. A process is similar to the pathogenesis of HP-associated gastritis. Gastroduodenal metaplasia in the duodenum is a prerequisite for HP colonization and ulceration. It is believed that the gastric epithelial metaplasia in the duodenum and the stomach caused by stomach acid Mucosal injury is related, abnormal gastric acid secretion may be related to HP infection, and may be related to the patient's innate acid-promoting function. Most patients have disorder of gastric acid metabolism, which is characterized by accelerated gastric emptying, or increased gastric acid secretion at night, or sensitive to gastrin. Enhancement, while the duodenum is subjected to high acid load, HP colonizes the gastric metaplasia, HP releases toxins, destructive enzymes and stimulated immune responses lead to duodenal inflammation, due to inflammation of the mucosa The attack tolerance of other ulcerating factors is reduced, leading to ulceration, or severe inflammation itself leading to ulceration.
(2) The pathogenesis of HP in the development of gastric ulcer is not yet clear. HP is known to be an important cause of chronic gastritis. Peptic ulcer and chronic gastritis are almost always combined, and must be preceded by peptic ulcer. Chronic gastritis, if HP persists, can cause intestinal metaplasia, gland atrophy and dysplasia, HP's pathogenic factors including urease, protease, phospholipase, peroxidase and HP toxin can activate neutral Granulocytes and eosinophils, which release free radicals from neutrophils and cause inflammatory reactions, have shown that one of HP's most important pathogenicities is the production of a cytotoxin that is harmful to epithelial cells, called vacuolating toxins ( VacA) can destroy the formation of vacuolar cells in the epithelial cells. Another protein-associated antigen (CagA) is encoded by the CagA gene. The expression of the CagA gene is often associated with the expression of VacA, from the gastric mucosa of patients with duodenal ulcer. The HP isolated from the CagA gene is a highly virulent strain producing vacuolating toxin. The mucosal damage caused by HP is caused by the combination of gastric acid and pepsin. Induced gastric ulcer formation, addition, HP itself can stimulate the secretion of gastric acid, high acid and has prompted the formation of ulcers.
4. Lesions: Most of the gastric ulcers are located in the small curvature of the stomach. The more common the pylorus is, the more common it is in the antrum of the stomach. It is very rare in the fundus and the large curved side. The ulcer is usually only one, round or oval, and the diameter. More than 2.5cm, the edge of the ulcer is neat, like a knife cut, the bottom usually passes through the submucosa, deep into the muscle layer or even the serosa layer, the submucosa to the muscle layer of the ulcer can be completely destroyed by erosion, replaced by granulation tissue and scar organization.
The form of duodenal ulcer is similar to that of gastric ulcer. The site of the duodenal ulcer is mostly at the beginning of the duodenum (ball part). It is most common in the anterior or posterior wall of the pyloric ring. The ulcer is generally smaller than the gastric ulcer. Shallow, the diameter is more than 1cm.
Concurrent lesions: further development of the ulcer, can penetrate the serosa layer and cause perforation, the perforation of the anterior wall causes acute peritonitis; the posterior wall perforation often adheres to adjacent organs such as liver, pancreas, transverse colon, etc., and is called penetrating ulcer, when ulcer When the blood vessels of the base, especially the arteries, are eroded, it will cause massive hemorrhage. The ulcer healing usually takes 4-8 weeks, or even longer. Many recurrences or destructions may occur. After healing, scars may remain. Scar contraction may become a local malformation of ulcer lesions. And the cause of pyloric obstruction.
Histopathological changes of ulcers During the active period of ulcers, at the bottom of the ulcer, the surface is divided into four layers from the surface to the deep: 1 The first layer is acute inflammatory exudate, which is composed of necrotic cells, tissue fragments and fibrin-like substances. 2, the second layer is composed of non-specific cellular infiltration with neutrophils; 3 the third layer is granulation tissue layer, containing proliferating capillaries, various components of inflammatory cells and connective tissue; The fibrous or scar tissue layer is fan-shaped and can be extended to the muscular layer and even to the serosa layer.
Prevention
Elderly peptic ulcer prevention
Dietary wine, coffee, strong tea, Coca-Cola and other beverages can stimulate the increase of gastric acid secretion, easy to induce ulcer disease, quit bad habits, reduce the stimulation of tobacco, alcohol, spicy, strong tea, coffee and certain drugs, the healing of ulcers and Prevention of recurrence is important. At the same time, maintaining a good mood is also very effective in preventing peptic ulcer.
Complication
Elderly peptic ulcer complications Complications pyloric obstruction gastric ulcer
Peptic ulcer is prone to complications in the elderly. About half of patients with peptic ulcer over 70 years old have complications. Some patients have complications as the first performance. Using NSAID is one of the causes of complications. Peptic ulcer in the elderly The mortality rate of complications is as high as 30%, and the prognosis depends on the age of the patient, especially the presence or absence of the disease.
1. Bleeding: Bleeding is the most common complication of peptic ulcer in the elderly. It is characterized by the largest bleeding, easy to repeat bleeding, and high mortality. Studies have shown that the mortality rate of peptic ulcer bleeding in the elderly is 4-10 for young patients. Times, up to 25%, some scholars believe that gastric ulcers are more likely to bleed than duodenal ulcers, but whether the mortality rate is higher, there are different opinions.
2. Perforation: Perforation accounts for the second complication of peptic ulcer in the elderly. There is no typical clinical manifestation of peptic ulcer complicated with perforation in the elderly. According to statistics, about half of the patients have medical treatment for more than 24 hours, and 25% to 33% of patients With sudden failure as the first performance, 30% to 65% of patients have no symptoms of peptic ulcer before perforation. These factors delay the diagnosis of peptic ulcer perforation in the elderly. It should be pointed out that it cannot be excluded because there is no underarm free gas. The diagnosis of ulcer perforation is due to the absence of 25% to 28% of patients.
3. Pyloric obstruction: The incidence of obstruction of gastric output caused by peptic ulcer is significantly reduced in Western countries, but it is still not common in developing countries. Obstruction of the output is duodenal deformation caused by duodenal ulcer. Caused by gastric ulcer is less common, all patients with peptic ulcer combined with output obstruction have a history of long-term ulcers, patients often have weight loss, weight loss and metabolic disorders.
Symptom
Peptic ulcer symptoms in the elderly Common symptoms Peptic ulcer fatigue abdominal pain ulcer pain upper abdominal discomfort upper abdominal pain abdominal discomfort bloating dull pain black stool
1. Symptoms of typical peptic ulcer pain:
(1) Long-term: Long-term recurrent episodes of upper abdominal pain, the entire course of disease is 6 to 7 years on average, and some can last up to 20 years or even longer.
(2) Periodicity: The upper abdominal pain is repeated and periodic, which is one of the characteristics of ulcers, especially duodenal ulcer.
(3) Rhythm: The relationship between ulcer pain and diet has obvious correlation and rhythm.
(4) Pain area: The pain of the duodenum is mostly located in the middle and upper abdomen, or placed on the umbilicus, or on the right side of the umbilicus; the location of gastric ulcer pain is also in the upper abdomen, but slightly higher, Or under the xiphoid process and to the left of the xiphoid process, the pain range is about a few centimeters in diameter.
(5) The nature of pain: mostly dull pain, burning pain or hunger-like pain, generally light and tolerable, persistent severe pain suggests ulcer penetration or perforation.
(6) Influencing factors: Pain is often induced or aggravated by mental stimulation, excessive fatigue, inadvertent diet, drug influence, climate change, etc.; can be caused by rest, eating, taking acid medicine, hand pressing pain parts, vomiting, etc. Reduce or alleviate.
The above manifestations are more common among young people and the symptoms of adolescent peptic ulcer patients are more atypical. Analysis of domestic and foreign statistics, 40% to 50% asymptomatic or atypical symptoms, which may be related to the decline of gastric acid secretion in the elderly.
1 asymptomatic type: some patients with peptic ulcer may have no clinical manifestations, but may be found by gastroscopy or X-ray barium meal examination for other diseases; or when complications such as bleeding or perforation occur, even when the autopsy is performed It has been found that such peptic ulcers can be seen at any age, but are more common in the elderly.
2 subclinical type: Sometimes the patient only has stomach discomfort, loss of appetite, and it is not easy to relieve after eating and taking the medicine. Even if there is pain, the normal rhythm is lost. Because the location of the stomach ulcer is high in the elderly, the pain can be radiated to the chest or Behind the sternum, it is easy to be misdiagnosed as angina pectoris, irregularity than the vague upper abdominal pain and discomfort, abdominal fullness, loss of appetite, weight loss, anemia, and occult blood positive symptoms are more common in elderly ulcer disease.
With the development of the disease, symptoms may change due to the occurrence of complications. If the pain is intensified and the site is fixed, it is radiated to the back and cannot be relieved by the antacid. It often indicates chronic perforation of the posterior wall; sudden severe abdominal pain is rapidly prolonged. Acute perforation should be considered in the whole abdomen; sudden vertigo indicates possible and blood is emitted, and the complications of senile peptic ulcer disease also increase with age. Hemorrhage is the most common complication, and the amount of bleeding is often more, bleeding The amount is inconsistent with clinical manifestations. Some patients, especially those associated with non-steroidal anti-inflammatory drugs (NSAIDs), can suddenly develop bleeding without symptoms. When chronic bleeding and black stools are not noticed by patients, it is easy to delay diagnosis. The second complication of peptic ulcer in the elderly, elderly patients often have only unclear abdominal pain, so strict clinical observation and abdominal fluoroscopy are very important for the confirmation of suspicious cases. Older ulcers are often located at the proximal end of the stomach, so obstruction in the elderly Peptic ulcer is rare, such as the occurrence of pyloric obstruction should first consider the possibility of gastric cancer.
Gastric cancer has become a controversial issue. It is generally estimated that the incidence of gastric ulceration is only 2% to 3%, but duodenal ulcer does not cause cancer. In the case of gastric ulcer, there are actually some cases. It may be ulcerative gastric cancer at first, not ulcerative cancer, but you should be alert to the possibility of cancerous cancer when the following conditions occur:
1 Strict medical treatment for 4 to 6 weeks, no symptoms improved.
2 without complications but still painful and rhythmic disappearance, loss of appetite, weight loss significantly.
3 fecal occult blood test continued to be positive and anemia occurred.
4 gastroscopy or X-ray examination can not rule out malignant changes should be reviewed regularly.
Because the symptoms of stomach problems in the elderly are often atypical, it is sometimes difficult to distinguish between chronic gastritis, ulcer disease, and stomach cancer by clinical symptoms. Therefore, in addition to regular physical examination, the elderly should have abnormalities such as upper abdominal discomfort, hernia, abdominal distension, and vomiting. Symptoms should be done by gastrointestinal X-ray barium meal examination and fiber gastroscopy to avoid delay in diagnosis and treatment.
2. Signs
There is a fixed and limited tenderness point under the xiphoid process at the time of attack, which can be accompanied by intentional muscle defense. There is no obvious signs when it is relieved.
Several special types of peptic ulcer in the elderly:
(1) Non-steroidal anti-inflammatory drugs (NSAID)-induced ulcers: Aspirin and other non-steroidal anti-inflammatory drugs (NSMD) have damage to the gastric mucosa, and mucosal damage caused by such drugs passes through the mucosal muscle layer. Known as NSAID ulcers, comorbidities often appear suddenly, 10% to 25% of comorbidities are upper gastrointestinal hemorrhage, 50% have hemorrhagic gastritis, and the elderly are more likely to use heart, cerebrovascular disease and joint lesions than young people. Carcass anti-inflammatory drugs, and their tolerance is worse than young people, so the risk of NSAID ulcers in the elderly will inevitably increase, the domestic group 1 data show that 24% of the 24 elderly peptic ulcer patients take non- A history of steroidal anti-inflammatory drugs, a prospective study in a foreign country for patients taking NSAIDs showed that about 25% of them will develop ulcers within 12 weeks. Currently, oral enteric-coated aspirin is widely used clinically, but there is no sufficient evidence. Can reduce the risk of ulcers.
(2) giant stomach and duodenal ulcer: diameter of gastric ulcer > 3cm or diameter of duodenal ulcer > 2cm, called giant ulcer, huge gastric ulcer more men than female, male incidence peak age For the 60 to 70 years old, the female is 70 to 80 years old, 10% of the patients have no abdominal pain, and the clinical manifestations are mostly bleeding as the first symptom. Previously, there was no symptoms of abdominal pain, and the elderly showed more obvious performance.
Giant duodenal ulcers often occur in men aged 60 to 70 years. The main symptoms are unbearable upper abdominal pain, which often spreads to the back. Ulcers often occur in the posterior wall of the ball, which is prone to stenosis and obstruction. When X-ray barium meal is examined, Ulcers are often misdiagnosed as duodenal bulbs or diverticulum, and gastroscopy can help diagnose.
(3) pyloric tube ulcer: occurs in the 50 to 60 years old, rare, clinical features are: pain soon after meals, not easy to use antacid control, early vomiting, easy pyloric obstruction, bleeding and perforation, internal medicine The treatment is poor and often requires surgery.
(4) esophageal ulcer: its occurrence is the result of contact between esophagus and acidic gastric juice. Ulcers often occur in the lower esophagus, mostly single, about 10% are multiple, ulcers vary in size, the disease mostly occurs in reflux esophagitis And patients with slidable esophageal hiatus with gastric-esophageal reflux.
Esophageal ulcers occur mostly between 30 and 70 years old. About 2/3 of the patients are over 50 years old. The main symptoms are pain in the lower back of the sternum or high upper abdominal pain. It often occurs when eating or drinking water, and it is aggravated when lying down. Pain It can be radiated to the interscapular region, the left chest, or upward to the shoulders and neck. The difficulty in swallowing is also common. It is the result of esophageal stricture caused by secondary esophageal fistula or fibrosis. Other symptoms that can occur are Nausea, vomiting, belching and weight loss, the main complications are obstruction, bleeding and perforation, the diagnosis mainly depends on X-ray examination and endoscopy.
(5) Stress ulcer: Stress ulcer refers to severe burns, craniocerebral trauma, brain tumors, intracranial neurosurgery and other central nervous system diseases, severe trauma and major surgery, severe acute or chronic medical diseases (such as sepsis, pulmonary insufficiency) and other stress conditions, acute ulcers in the stomach and duodenum, due to the widespread presence of arteriosclerosis in the elderly, the incidence of acute heart and cerebrovascular events is obvious Higher than other populations, and the decline of randomized immunity in the elderly can lead to severe infections, and the chances of clinically complicated stress ulcers in the elderly are also significantly increased. The pathogenesis is still unclear for two reasons:
1 Excessive secretion of gastric juice occurs during stress, which leads to the self-digestion of mucous membranes to form stress ulcers.
2 The strong sympathetic stimulation caused by severe and persistent stress and the increase of circulating catecholamine levels can open the arteriovenous short circuit of the submucosal layer of the stomach and duodenum. Therefore, it normally flows through the capillary bed of the gastroduodenal mucosa. The blood is shunted to the submucosal arteriovenous short circuit and no longer flows through the gastric duodenal mucosa. Thus, during severe stress, the mucosa can develop ischemia, which can last for hours or even days, eventually causing serious damage. Stress ulcers form when necrosis occurs in the ischemic area of the mucosa. At this time, the digestion of hydrochloric acid and pepsin can accelerate the formation of stress ulcers, and another possible cause of ischemic injury of the gastroduodenal mucosa is Acute thrombosis in the blood vessels of the gastric mucosa caused by disseminated intravascular coagulation. Disseminated intravascular coagulation is often a complication of sepsis and burns.
Examine
Examination of peptic ulcer in the elderly
1. Analysis of gastric juice: gastric acid secretion in patients with gastric ulcer is normal or slightly lower than normal; patients with duodenal ulcer often have high gastric acid secretion, but only in 1/4 to 1/3 cases, with basal secretion (BAO) and Nighttime secretion (MAO) is obvious, and has reference value in the following cases:
1 to help distinguish between gastric ulcer is benign or malignant, if the maximum acid displacement MAO proves that gastric acid is absent, it should be highly suspected that the ulcer is cancerous.
2 Exclude or affirm gastrinoma, if BAO>15mmol/h, MAO>60mmol/h, BAO/MAO ratio>60%, suggesting the possibility of gastrinoma, serum gastrin should be determined.
3 The results of the comparison were compared before and after gastric surgery to evaluate whether the vagus nerve was completely cut.
2. Determination of serum gastrin: The diagnosis of peptic ulcer is of little significance, but if gastrinoma is suspected, this test should be made. The serum gastrin value is generally inversely proportional to gastric acid secretion, that is, low gastric acid, stomach secretion. Su Gao; high stomach acid, low gastrin; gastrin tumors are elevated at the same time.
3. Fecal occult blood test: active duodenal ulcer or gastric ulcer often has a small amount of oozing blood, so that the fecal occult blood test is positive, but generally short-lived, after 1 to 2 weeks of treatment, if the patient continues to be positive, Suspected of having cancer.
4. Helicobacter pylori examination: The diagnostic criteria for HP infection are in principle reliable and simple, so as to facilitate implementation and promotion. There are many diagnostic methods for HP infection. The diagnosis method should be selected according to different diagnostic purposes and unit conditions. Sensitive and specific reagents and methods are tested. According to the characteristics of each test method, the following scientific and clinical diagnostic criteria are established.
(1) Scientific diagnostic criteria for HP infection: HP culture positive or 2 of the following 4 items are positive for HP:
1HP morphology (smear, histological staining or immunohistochemical staining).
2 urease-dependent test [rapid urease test (RUT), 13C or 14C-urea breath test (UBT)].
3 serological test (ELISA or immunoblot test, etc.).
4 specific PCR test, HP epidemiological investigation can be based on the research purpose and conditions, select one or two in the above test.
(2) Clinical diagnostic criteria for HP infection: Any one of the following 2 cases is diagnosed as HP-positive: 1HP morphology (smear or histological staining); 2 urease-dependent test (RUT, 19C or 14C- UBT).
5. X-ray barium meal examination: is a direct sign of X-ray barium meal diagnosis of ulcers, due to inflammation around the ulcer, edema, there may be a translucent band around the shadow, the shadow of gastric ulcer is more common in the stomach, and often The sputum of the duodenal ulcer is common in the bulb, which is usually smaller than the shadow of the stomach. Less than 2%, if the nature is unknown (both benign and malignant), it is 9.5%, if it is accompanied by duodenal ulcer, about 1%, indirect signs include local tenderness, and the large curved side of the stomach , duodenal bulb irritation and ball deformity, etc., indirect signs only suggest but can not be diagnosed with ulcers.
6. Gastroscopy and mucosal biopsy: gastroscopy has a diagnostic value for peptic ulcer. The ulcers under gastroscope are mostly round or elliptical. Microscopic examination can also find gastritis and duodenitis with ulcers. Compared with gastroscope, it is more reliable to find the posterior wall ulcer and the duodenal ulcer. When performing gastroscopy, multiple biopsy should be performed on the edge of the ulcer and adjacent mucosa. This can not only distinguish between good and malignant ulcers, but also check the pylorus. Helicobacter has a guiding significance for treatment. Because of the atypical symptoms of the elderly, it is recommended to expand the scope of gastroscopy and barium meal examination in places where conditions permit.
Most of the ulcers under the gastroscope are round or elliptical, a few are linear ulcers, and yellow and white moss are attached to the bottom. According to the ulcer and surrounding mucosa, the ulcer can be divided into three phases:
(1) Activity period (A period):
The A1 stage ulcer center is attached with thick moss, and the surrounding mucosa is hyperemia and edema.
The A2 stage has thick moss and redness around the ulcer.
(2) Healing period (H period):
In the H1 stage, the moss is thin, and the base is still invisible. There is redness around the ulcer and the mucous membrane is concentrated.
The H2 ulcer becomes shallow, and the red ulcer base is seen.
(3) Scar stage (S period):
S1 ulcerated moss completely disappeared, forming a bright red scar.
The local color of the S2 ulcer is similar to or whitish to the surrounding mucosa.
Diagnosis
Diagnosis and diagnosis of peptic ulcer in the elderly
Diagnostic criteria
The main manifestation of stress ulcers is massive hemorrhage, which occurs on the 2nd to 15th day of the disease and is often difficult to control. This is because the stress ulcers are sharp, and the blood vessels under the gastric ulcer fail to form a blood clot. In addition, Perforation can occur, sometimes with only upper abdominal pain.
The diagnosis of stress ulcer mainly relies on emergency endoscopy. It is characterized by ulcers occurring in the high corpus, forming multiple superficial irregular ulcers with a diameter of 0.5-1.0 cm or even larger. No scars left.
1. Diagnosis of gastric ulcer:
(1) Upper abdominal discomfort during empty stomach, which can be relieved by eating, antacid or vomiting, but relapse early after meal and often lose weight.
(2) upper abdominal tenderness and random muscle defense.
(3) Anemia, there will be occult blood.
(4) X-ray or gastroscopic examination showed ulcers.
(5) Analysis of gastric juice is acid.
2. Diagnosis of duodenal ulcer
(1) 45 to 60 minutes after a meal, abdominal discomfort or nighttime pain, can be relieved by eating, antacid or vomiting, tenderness and muscle protection in the upper abdomen.
(2) Chronic periodic symptoms.
(3) All cases have stomach acid, and some are secreted.
(4) X-ray or oral endoscopic examination of the duodenal bulb visible deformity or ulcer "shadow" ("crater").
Because the symptoms of peptic ulcer in the elderly are often atypical, the diagnosis depends on endoscopy and X-ray and barium meal examination. Endoscopy can determine the location, shape, size and number of ulcers. Combined with biopsy pathology, benign and malignant ulcers can be identified. X-ray examination found that tick or shadow is the only basis for diagnosis, other signs as a reference, gastric juice analysis is helpful for diagnosis.
Differential diagnosis
1. Gastric cancer: The identification of the two is sometimes difficult. The following situations should be given special attention:
1 middle-aged and elderly people have mid-upper abdominal pain, bleeding or anemia in the near future.
2 The clinical manifestations of patients with gastric ulcer have changed significantly or the anti-ulcer drug treatment is ineffective.
3 gastric ulcer biopsy pathology of intestinal metaplasia or dysplasia, clinically, patients with gastric ulcer should be actively treated under internal medicine, regular follow-up endoscopy until ulcer healing.
2. Functional dyspepsia (or non-ulcerative dyspepsia): These patients often have upper abdominal pain, acid reflux, belching, heartburn, upper abdominal fullness, nausea, vomiting, loss of appetite and other dyspeptic symptoms, some patients can There are typical symptoms of peptic ulcer, but there is no ulcer lesion in endoscopy. The differential diagnosis depends mainly on endoscopy.
3. Chronic cholecystitis and cholelithiasis: pain is related to eating greasy, located in the right upper abdomen, and radiated to the back, typical cases with fever, jaundice, not difficult to identify, for patients with atypical symptoms, identification needs to rely on abdominal ultrasound or internal Retrograde cholangiography.
4. Gastrinoma: This disease is also known as Zollinger-Ellison syndrome. It has refractory multiple ulcers or ectopic ulcers. It is easy to relapse after subtotal gastrectomy. It is often accompanied by diarrhea and obvious weight loss. Non--cell tumor or gastric antral G cell hyperplasia, serum gastrin levels increased, gastric juice and gastric acid secretion increased significantly.
