upper abdominal pain when hungry
Introduction
Introduction Upper abdominal pain during starvation is a clinical manifestation of duodenal ulcer. The pain appears in the center of the upper abdomen, just on the umbilicus or just to the right of the midline. Typical duodenal ulcer pain often occurs 2 to 3 hours after a meal (fasting pain) and continues unabated until after eating or taking an acid generator.
Cause
Cause
The pathogenic factors of duodenal ulcer are complicated. In the past 20 years, duodenal ulcer has been considered as a multifactorial disease. Or a variety of harmful damage to the mucous membrane exceeds its ability to withstand damage and repair. Until recently, duodenal ulcers were still considered a lifelong disease. However, the recent belief that multiple biological and environmental factors only have a detrimental effect on susceptible individuals has gradually been replaced by the following recognition.
1. Genetics: Genetic factors play an important role in the susceptibility of the disease, the main basis is:
1 high incidence of patient families;
2 Correlation between genetic markers (blood type and blood type secretory substances, HLA antigen, and high pepsinogen). The incidence of duodenal ulcer in siblings of patients with duodenal ulcer is 2.6 times higher than that of the general population; more notably, the consistency of duodenal ulcer in the incidence of monozygotic twins is 50%, in the dichozygosis The consistency of twin sibs is also increasing.
(1) Relationship between duodenal ulcer and blood type: In 1953, Aird et al found that duodenal ulcer in O-type blood may be about 35% higher than other blood type; O-type blood in duodenal ulcer patients It accounted for 56.5% of the total, accounting for 45.8% of the control population, and those with ulcers and perforation were more common with O-type blood. According to the statistics of duodenal ulcer cases in China, the type O blood is also significantly higher than the control group, which is basically consistent with the foreign reports.
The blood type substance ABH is secreted in saliva and gastric juice. According to foreign data, the risk of duodenal ulcer in the blood-free substance secretion is 1.5 times higher than that of the blood-type substance secretion.
(2) Relationship between peptic ulcer and HLA antigen: HLA is a complex genetic polymorphism system, and the gene locus is on the short arm of the sixth pair of chromosomes. A variety of diseases have been found to be associated with certain HLA antigens to date. HLA-B5, HLA-B12 and HLA-BW35 have been reported to be associated with duodenal ulcer in foreign data, but the results in some literatures are not relevant.
(3) Duodenal ulcer and some genetic syndromes: Some rare genetic syndromes such as multiple endocrine neoplasia type I (islet secretion of gastrin adenoma, parathyroid adenoma, pituitary) Leaf adenomas, systemic mastocytosis and other rare syndromes are associated with duodenal ulcers. In particular, systemic mastocytosis is an autosomal dominant genetic disease, and about 40% of patients suffer from duodenal ulcer at the same time.
Although duodenal ulcer is associated with blood type, blood type secretory substance, and HIL-A antigen, it is not strongly correlated. The results of family surveys of other data cannot confirm that the inheritance of this disease is governed by simple Mendel's law. In view of this, the more common hypothesis is that duodenal ulcer is a group of genetic heterogeneity diseases that are genetically inherited, and may be non-inherited based on this genetic quality. Or external factors lead to the onset of disease.
2. Excessive gastric acid secretion: The pathogenesis of duodenal ulcer is not a single clear process, but the formation of complex and interactive factors; due to damage factors and imbalance between defenses.
(1) Excessive gastric acid secretion: In the pathogenesis of duodenal ulcer, the gastric acid secretion process plays an important role. As early as 1910, Schwartz's view that "no acid is no ulcer" is still correct. Duodenal ulcer does not occur in patients with low gastric acid secretion and maximum gastric acid secretion (MAO) <10mmol/h. Although the maximum gastric acid secretion capacity of patients with normal and duodenal ulcers overlaps, patients with duodenal ulcers can secrete a greater amount of gastric acid (average acid secretion of 20 mmol/h), especially for meal stimulation. Gastric acid secretion. The amount of gastric acid secretion is parallel to the total parietal cell mass (PCM). The average number of duodenal ulcer patients is 180 million wall cells, which is about twice that of normal people. 1.09×109, female is 0.82×109). In addition to the increase in the number of parietal cells in patients with duodenal ulcer, the sensitivity of the parietal cells to gastrin, histamine, and vagal cholinergic pathways is enhanced. The increase in gastric acid secretion is an important factor in the development of duodenal ulcer.
(2) The effect of eating on gastric acid secretion: Food can also stimulate gastric acid secretion, and about 60% of patients with duodenal ulcer are more sensitive to food stimulation. Not only after a meal, but also during the meal, the acid secretion level is high and lasts for a long time. This phenomenon can also be confirmed by pH monitoring. The response to the type of the object is not the same. Foods with high protein content are strong, and foods with high fat content are weak.
3. Duodenal mucosal defense mechanism weakens the duodenum through specific pH-sensitive receptors, acidification reaction, feedback delays gastric emptying, maintains pH in the duodenum close to neutral, and duodenum The mucous membrane can absorb hydrogen ions in the cavity and is not damaged by bile salts. In patients with duodenal ulcer, this feedback delays the effect of gastric emptying and inhibition of gastric acid, and the gastric emptying accelerates, causing the acid load in the duodenal bulb to increase, causing mucosal damage to form ulcers. Prostaglandin E not only has the effect of inhibiting gastric acid, but more importantly, it directly protects the mucosa and promotes ulcer healing. The content of duodenal mucosal prostaglandin E in patients with duodenal ulcer was significantly lower than that in the normal control group, which reduced the protective effect of duodenal mucosa.
Decreased duodenal mucosal bicarbonate secretion in patients with duodenal ulcer can lead to acid digestive damage.
4. Helicobacter pylori infection: Helicobacter pylori (Hp) infection is closely related to the pathogenesis of peptic ulcer. Eradication to Hp treatment can significantly reduce the recurrence rate of ulcers. Hp infection is the main cause of antral sinusitis and an important factor in causing peptic ulcer. Hp is a microaerobic Gram-negative bacillus with a spiral shape. Human gastric mucosal epithelial cells are its natural colonization site. Hp can survive in acidic gastric juice because it has a highly active urease, which decomposes urea to produce ammonia and forms a protective layer around the cells. The most reliable method for detecting Hp in mucosal tissue is combined with bacterial culture and histological staining. A more convenient and rapid method for detecting Hp is endoscopic biopsy tissue urease test with a sensitivity of 88% to 93% and a specificity of 99% to 100%.
Hp is a common bacterial infection in humans and its prevalence is related to age, race, economics and health. Hp can be transmitted by human-to-human or oral-oral-oral route. Virtually all patients with duodenal ulcer have Hp infection. Patients with acute duodenal ulcer and Hp infection responsively secrete more acid and release more gastrin after a meal than a non-infected ulcer patient.
When gastric acid secretion increases, the duodenal bulb is excessively acidified, causing gastric epithelialization in the duodenal bulb, creating conditions for Hp transplantation of the duodenal bulb from the gastric antrum mucosa, and Hp survives in the bulb. Acute duodenitis occurs during reproduction, and ulceration occurs under the induction of other ulcerating factors. However, the mechanism of this duodenal ulcer remains to be confirmed. Although the above factors are related to duodenal ulcer, acid is still the most important, and medical and surgical treatments reduce gastric acid secretion, resulting in ulcer healing. Excessive acid secretion causes ulcer formation. Animal experiments The stimulation of chronic histamine produces hyperacidity which can form duodenal ulcers identical to humans.
5. Other factors: Epidemiological data suggest that the formation and development of duodenal ulcers are closely related to many living habits and the environment.
(1) Analgesic: Non-steroidal anti-inflammatory drugs (NSAID) can cause damage to the gastric mucosa. In recent years, there have been many studies supporting NSAIDs that can cause gastric ulcers, ulcer perforations, bleeding from the stomach and duodenal ulcers, and death from ulcer disease. There is increasing evidence that NSAIDs are closely related to perforation of elderly ulcers. Reports in the United Kingdom and Germany have also found that the mortality rate of duodenal ulcers in the elderly has increased, partly because of the increased use of analgesics. Although the risk of duodenal ulceration is small, the risk of complications due to duodenal ulcer is not less than that of gastric ulcer, suggesting that NSAID may cause complications in existing gastric or duodenal ulcers.
(2) Smoking: If smoking is a causative factor, the dramatic increase in duodenal ulcers may have been associated with it since the early 19th century. Because cigarettes were first made in the United States by James Bonsack in 1880, the Bonsack tobacco manufacturing machine was introduced to the United Kingdom in 1883 and introduced to other European countries in a few years, leading to an increase in smokers in the first half of the 20th century in Europe and the United States. The decline in the sex ratio of peptic ulcers in recent years is also consistent with the increase in female smoking. Similarly, the decline in the incidence of ulcers in Western countries in the past 30 years is also consistent with the general decline in the number of smokers in recent years. Smoking has been reported to cause an increase in basal and maximal gastric acid secretion and can cause duodenal reflux.
(3) Stress: If stress is the causative factor of peptic ulcer, the increase in ulcer incidence at the beginning of industrialization and urbanization in Western countries in the early 20th century may be related to this. At the same time, it can also explain the increase of perforation of duodenal ulcer in some areas such as Hong Kong, and the use of analgesics in these areas is generally less. It can also explain the seasonal differences in the prevalence of duodenal ulcers, the regional and temporal differences in male-to-sex ratios, and the difference in the ratio of duodenal ulcers to gastric ulcers in different regions, as well as in bed rest to cure ulcers.
(4) Dietary fiber: The incidence of duodenal ulcer in southern China and southern India, which is dominated by rice, is higher than that of the northern region where flour is the main food, suggesting that dietary fiber is the causative factor of duodenal ulcer. In Mumbai, India, after the healing of duodenal ulcers continued to eat rice, the 5-year recurrence rate of ulcers was 14%, and the diet was changed to Punjab (containing wheat that was not well processed). The 5-year recurrence rate of ulcers was 81%. It is suggested that the recurrence of duodenal ulcer is also related to dietary fiber content. However, a recent case-control study in the UK found that although vegetable fiber is associated with ulcers, total dietary fiber is not associated with duodenal ulcer.
(5) Dietary linoleic acid: The decline in the incidence of peptic ulcer in some western countries in the past 30 years, Hollander and Tarnawski speculate that this decline may be related to increased intake of linoleic acid, an important prostate in food. The precursor of the prime E. They measured the fatty acid profile of duodenal ulcer and control adipose tissue, showing that linoleic acid in adipose tissue was significantly reduced in patients with ulcer disease. The fatty acid profile of adipose tissue is a good indicator of the amount of linoleic acid in the diet. This finding supports the hypothesis that linoleic acid is associated with peptic ulcer.
Examine
an examination
Related inspection
Gastric examination of gastric basal gastric acid secretion (BAO) gastroscope
Typical rhythmic, periodic upper abdominal pain is an important basis for the diagnosis of ulcer disease, but it should be noted that more than 10% of patients with ulcers can be asymptomatic. In addition, patients with chronic gastritis have symptoms of upper abdominal pain similar to ulcer disease but no ulcers. Pain attacks can last from a few days to weeks or months. Symptoms are prone to recurrence, and duodenal ulcers often have no painful recurrence or complications. The remission cycle is usually months or years, almost always longer than the time of the onset of pain. However, in some patients the pain is more aggressive, with frequent and persistent onset or complications. A change in the nature of ulcer pain may be a sign of a complication. For example, ulcer pain becomes persistent, no longer relieved by food or antacids, or radiated to the back, showing penetration (often penetrating into the pancreas).
Many active duodenal ulcers have no ulcer symptoms. Endoscopic upper gastrointestinal examination showed that nearly half of the duodenal recurrent ulcers were asymptomatic. Endoscopy also showed a lack of good correlation between ulcer activity, symptom relief and ulcer healing. No ulcer pain can not rule out duodenal ulcer. Duodenal ulcer is a potential cause of acute or chronic gastrointestinal bleeding, gastric outlet obstruction or ulcer perforation. X-ray barium meal examination can be used as a basis for the diagnosis of duodenal ulcer. Endoscopy is the most important diagnostic method. Biopsy of gastric antrum mucosa can be used for HP examination. Gastric acid determination is meaningful in diagnosing gastric tumors, but has little diagnostic effect on duodenal ulcers.
Diagnosis
Differential diagnosis
1, right upper abdominal pain: right upper abdominal pain is generally the liver, gallbladder, biliary tract, pancreas, duodenum, right kidney, right segment of the large intestine.
2, left upper abdominal pain: In most cases, there is a corresponding relationship between the abdominal lesions and abdominal pain. Generally, according to the abdominal organ, the abdomen can be centered on the navel, and the painting is divided into four areas: upper right, lower right, upper left, and lower left. According to the site of abdominal pain, it can be divided into left upper abdominal pain, right upper abdominal pain, left lower abdominal pain, right lower abdomen. Pain and abdominal pain in the abdomen. Left upper abdominal pain may be a problem in the stomach, spleen, pancreas, left kidney, and left colon.
3, right lower abdominal pain: abdominal pain is one of the most common clinical symptoms. But because abdominal pain is mostly sporadic, it is often easy for patients to take it lightly. The approximate division of the location of the abdominal organs. Upper right: liver, gallbladder, biliary tract, pancreas, duodenum, right kidney, right segment of the large intestine. Top left: stomach, spleen, pancreas, left kidney, left colon. Bottom right: cecum, appendix, right ovary and fallopian tube, right ureter. Bottom left: sigmoid colon, left ovary and fallopian tube, left ureter. Right lower abdominal pain is a disease of the cecum, appendix, right ovary and fallopian tube, right ureter.
4, lower abdominal pain: lower abdominal pain is a common symptom of women, mostly caused by gynecological diseases. Various gynaecological conditions should be considered based on the nature and characteristics of lower abdominal pain.
5, small abdomen tingling: common symptoms of gynecological diseases in the lower abdomen, which brings great pain to the patient, sometimes it feels painful, and there are many types of abdominal pain, and there are many reasons.
6. Total abdominal pain: Total abdominal pain refers to the lesions of the internal and external organs caused by various reasons, and the pain of the whole abdomen. Total abdominal pain can be divided into acute and chronic. The cause is extremely complex, including inflammation, tumors, bleeding, obstruction, perforation, trauma, and dysfunction.
7, middle and upper abdominal pain: upper abdominal pain is the main symptom, can be dull pain, burning pain, pain or severe pain, but sometimes only hunger-like discomfort. Typical cases have persistent pain under mild or moderate xiphoid and can be relieved by antacids and eating. About 2/3 of the duodenal patients have a rhythmic pain: upper abdominal pain begins to appear 1 to 3 hours after breakfast. If they do not take the medicine or eat, they will continue until lunch. 2 to 4 hours after eating, it is painful. It also needs to be eaten to relieve. About half of them have midnight pain, and patients are often awakened. Regular pain can also occur in gastric ulcers, but it occurs earlier after the meal, about half an hour to one hour after the meal, and disappears until the next meal. Midnight pain is not as common as duodenum.
