duodenal ulcer

Introduction

Introduction to duodenal ulcer Duodenal ulcer due to a variety of factors caused by duodenal mucosal and muscular layer defects. Although it is similar to gastric ulcer in terms of clinical manifestations and drugs, it has significant differences in terms of incidence, age, sex, and pathogenesis. Refers to chronic ulcers that are only found in the contact area between the gastrointestinal tract and gastric juice, also known as ulcer disease. Traditional Chinese medicine refers to the category of "stomach pain", "heartache", and "stomach pain". Folk treatment of this disease is no shortage of strange medicine, short course of treatment, quick effect, low cost, that is, can eliminate the disease, promote ulcer healing, and can not operate, no longer relapse. basic knowledge The proportion of illness: 0.1% - 0.2% Susceptible people: no special people Mode of infection: non-infectious Complications: peptic ulcer Helicobacter pylori infection abdominal pain

Cause

Cause of duodenal ulcer

Genetics (25%):

Genetic factors play an important role in the susceptibility of the disease, the main basis is: 1 high incidence of patient families; 2 genetic markers (blood type and blood type secretion substances, HLA antigen, high pepsinogen) correlation 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 double The consistency of the zygote twins has also increased.

Duodenal mucosal defense mechanisms are attenuated (20%):

The duodenum passes through a specific pH-sensitive receptor, acidification reaction, feedback delays gastric emptying, maintains the pH in the duodenum close to neutral, and the duodenal mucosa can absorb hydrogen ions in the cavity and are not Bile salt damage, in patients with duodenal ulcer, this feedback delays gastric emptying and inhibits gastric acid, and gastric emptying accelerates, causing an increase in acid load in the duodenal bulb cavity, resulting in mucosa Damage can form ulcers.

Excessive gastric acid secretion (25%):

The pathogenesis of duodenal ulcer is not a single clear process, but a complex, interactive factor; due to damage factors and imbalance between defenses.

Helicobacter pylori infection (15%):

Helicobacter pylori infection is closely related to the pathogenesis of peptic ulcer. Eradication of Hp can significantly reduce the recurrence rate of ulcer. Hp infection is the main cause of antral sinusitis and an important factor causing peptic ulcer.

Other factors (15%):

Epidemiological data suggest that the formation and development of duodenal ulcers are closely related to many lifestyles and environments. Such as the use of analgesics, smoking, stress response, dietary fiber and diet linoleic acid.

Pathogenesis

1. The site of occurrence

Typical duodenal ulcers occur in the first part of the duodenum (95%), most commonly within 3 cm of the pylorus (90%), with ulcers occurring in the anterior wall, accounting for 50%; followed by the posterior wall, accounting for 23%; the lower wall accounts for 22%; the upper wall is the least, accounting for 5%, even in the front and the back, duodenal ulcers generally do not malignant, duodenal ulcer occurs in the first part of the duodenum It is rare and must be considered for atypical duodenal ulcers, including Zollinger-Ellison syndrome, drug ulcers, malignant tumors or Crohn's disease.

2. Pathological process

The formation of duodenal ulcers has experienced the development of erosion, acute ulcers, and chronic ulcers.

(1) erosion: erosion is a shallow depression of the mucosa layer, its depth does not pass through the mucosal muscle layer, the naked eye is red dot-like shallow depression, the diameter is generally less than 0.5cm, erosion can occur in the duodenum, can be divided into acute Erosion and chronic erosion, combined bleeding is hemorrhagic erosion, observed under the microscope, the depth of erosion is different, shallow only to the glandular neck, deep to the mucosal muscle layer, but not through the layer, there is a small amount of necrotic tissue at the bottom of the erosion, There are most neutrophil infiltration at the bottom and edge of the erosion, and generally no scars are left after the erosion is healed.

(2) acute ulcers: acute ulcers refer to ulcers that pass through the muscular layer of the mucosa and deep into the submucosa. They can be developed from erosion, the diameter is generally less than 1cm, the boundary is clear, and the mucosa and mucosal muscle layers have all been destroyed and disappeared under the microscope. A small amount of necrotic tissue adhered to the bottom of the ulcer, a small amount of cellulose on the surface and most neutrophils exuded, which may be accompanied by hemorrhage, mucosal congestion at the edge of the ulcer, and infiltration of neutrophils and lymphocytes.

(3) Chronic ulcer: 15% of duodenal ulcer is multiple, which may be accompanied by gastric ulcer. The bottom of the ulcer is observed by the naked eye. It is relatively clean, with a small amount of exudate and necrotic tissue attached. When the ulcer is bleeding, blood coagulation is visible at the bottom of the ulcer. Block, microscopic observation: the bottom of the ulcer consists of 4 layers of tissue, the inflammatory exudate layer, with neutrophils and cellulose cells; underneath is a layer of unstructured coagulative necrotic tissue, under the necrotic tissue layer is granulation Tissue and scar tissue.

Prevention

Duodenal ulcer prevention

Quit smoking

Smokers have a 2-fold higher incidence of ulcer disease than non-smokers. Smoking affects ulcer healing and promotes ulcer recurrence. Possible mechanisms:

(1) Smoking can promote the secretion of gastric acid and pepsinogen.

(2) Smoking may inhibit the secretion of HCO3-salt from the pancreas, thereby weakening the ability to neutralize acidic fluids in the ball.

(3) Smoking can affect the pyloric sphincter closure function and lead to bile reflux, destroying the gastric mucosal barrier; smoking can delay gastric emptying and affect the gastric and duodenal motor function.

(4) Smoking can affect prostaglandin synthesis in the gastric duodenal mucosa, reduce mucus volume and mucosal blood flow, thereby reducing the defense function of the mucosa.

2. Diet control

Drinks such as alcohol, coffee, strong tea, and Coca-Cola can stimulate the increase of gastric acid secretion and easily induce ulcer disease. Those who eat refined low-fiber foods have higher incidence of ulcers than those who eat high-fiber. Some people think that multi-slag food may promote epidermal growth factor. Or the role of increased prostaglandin release.

3. Mental factors

People with long-term mental stress, anxiety or mood swings are prone to duodenal ulcers. When stressed, people may promote gastric secretion and motor function, increase gastric acid secretion and accelerate gastric emptying, and stimulate sympathetic nerves. The gastro-duodenal vasoconstriction, the mucosal blood flow decreased, and the mucosal defense function was weakened.

4. Drugs

About 10% to 25% of patients with long-term oral non-steroidal anti-inflammatory drugs develop ulcer disease, of which gastric ulcer is more common, except for drugs that directly stimulate the gastric mucosa mucosa, mainly due to such drugs. Inhibition of cyclooxygenase activity in the body reduces the synthesis of prostaglandins in the mucosa and weakens the protective effect on the mucosa. The original aspirin is fat-soluble and can penetrate the epithelial cell membrane to destroy the mucosal barrier.

Complication

Duodenal ulcer complications Complications Peptic ulcer Helicobacter pylori infection abdominal pain

Gastric outlet obstruction

Chronic duodenal ulcer can cause scar formation, which affects the emptying of the stomach. This condition is called gastric outlet obstruction. Patients often complain of upper abdominal fullness after eating, early satiety and vomiting for hours or even days before. Eating food, vomiting can be aggravated at night; the relationship between vomiting and ulcer pain is uncertain, vomit often contains the last meal of indigestion, after the vomiting, upper abdominal discomfort or pain can be temporarily relieved, long-term gastric outlet obstruction often shows Slight pain and vomiting episodes at longer intervals, when the patient's weight loss is obvious, and eventually lead to an apex in an acute episode, accompanied by dehydration and electrolyte imbalance, chronic export obstruction patients may have hypochlorine alkalosis, hand and foot convulsions , weight loss, and sometimes combined with aspiration pneumonia.

2. Duodenal ulcer perforation

Recent data show that the rate of perforation per year for men and women with ulcer disease is 0.8% and 0.3%, respectively. Most of the patients have a large history of smoking. The incidence of such perforation has not been statistically related to the large-scale application of ASA/NSAIDs in the elderly. The incidence of perforation is increasing in some patients. The relative risk of perforation in patients with Helicobacter pylori infection, Helicobacter pylori-negative but with ASA/NSAIDs or both risk factors is unclear.

Ulcer perforation often starts suddenly, accompanied by severe abdominal pain at the beginning, bowel sounds disappeared and obvious abdominal muscle tension (plate-like abdomen), patients do not want to move, there is a sense of sudden death, perforation can be the first performance of ulcers Especially, it is more common in patients who use ASA/NSAIDs or Zhuo-Ai syndrome.

3. Penetrating ulcer

Unlike perforation, ulcer penetration to adjacent organs such as the liver, pancreas or biliary system rarely causes serious consequences, clinical manifestations of increased abdominal pain, loss of rhythm, increased local tenderness, increased drug requirements or other The most common manifestations of disease, such as pancreatitis or cholangitis, are pancreatitis. In most cases, strict medical treatment is effective, and only a few patients require surgical treatment.

4. Bleeding

Peptic ulcer bleeding is the most common cause of upper gastrointestinal bleeding, accounting for 1/3 to 1/2 of them, 10% to 15% of patients with ulcers with bleeding as the first symptom, the total mortality rate is about 10%, but elderly patients The mortality rate of patients with other serious diseases increased significantly. The long-term follow-up observation showed that about 15% of patients with ulcers developed bleeding in 10 to 15 years; in 15 to 25 years, 25% to 40% of ulcer patients occurred. Bleeding, these statistics are derived from earlier studies where ulcer disease treatment was often irregular and inadequate, and recent statistics showed that about 12% of patients developed bleeding within 5 years, or 2.7% of men per year. Patients and 2.5% of female patients developed bleeding. Patients with a history of bleeding had a rebleeding rate of 5%. Patients with duodenal ulcer bleeding had no specific symptoms, and only 30% to 40% of patients with bleeding had pre-existing ulcer symptoms. In addition to duodenal ulcer typical, rhythmic, periodic upper abdominal pain, other symptoms include bloating, anorexia, acid reflux, nausea or vomiting, as well as hematemesis, asymptomatic.

Symptom

Symptoms of duodenal ulcers Common symptoms Abdominal bloating Acute stomach pain Spine tenderness Ridge rib bulging Upper abdominal pain Middle upper abdominal persistent pain Abdominal pain Hunger upper abdominal pain Balloon after ulcer

The main clinical manifestation of duodenal ulcer is upper abdominal pain, which may be dull pain, burning pain, pain or severe pain, or it may manifest as pain and discomfort only when starving. Typical manifestations are persistent pain under mild or moderate xiphoid and can be relieved by antacids or eating. About 2/3 of the pain in the clinic is rhythmic: upper abdominal pain begins to appear 1 to 3 hours after breakfast. If you do not take the medicine or eat it, it will last until after lunch. It hurts 2 to 4 hours after eating, and it is necessary to eat to ease. About half of the patients have midnight pain and the patient can often wake up. Rhythmic pain lasts for a few weeks and can occur repeatedly with relief for several months.

Typical performance

The main symptoms of peptic ulcer are upper abdominal pain or indigestion. The pain is located on the right side of the midline of the upper abdomen, and the location is more limited. Patients often describe pain as "gnawing" or "starving." Pain has obvious rhythm, which can be relieved by eating food or taking antacids, often 1 to 3 hours after a meal (the diet stimulates gastric acid to continue to secrete for 3 to 4 hours, and the food is completely empty from the stomach for about 2 hours). Patients often wake up during sleep between 1:00 and 3:00 in the morning, especially those who eat snacks before going to bed.

Pain can be radiated to the right rib area or right back, and radioactive pain is rare if there is no comorbidity. Sustained back pain often indicates the penetration of posterior wall ulcers. Another major feature of ulcer pain is its periodicity, which is often recurred weeks to months. Abdominal pain often worsens every day and lasts for several weeks until the next recurrence. The incidence is mostly in the late autumn and early spring. Because eating often relieves pain, duodenal patients often like to eat snacks, and their weight is often slightly higher than normal.

Patients with duodenal ulcer, such as abdominal pain, significantly exacerbate and spread to the abdomen, often suggesting that the ulcer has been perforated. Often, there is a rapid disappearance of bowel sounds and a large amount of rebound pain. Similarly, the loss of normal rhythm and the conversion to persistent pain often suggests a possible penetration.

In some patients with chronic duodenal ulcers, "water-brash" can occur, which means that the mouth is suddenly filled with clear, colorless, odorless liquids (such as saliva). This is different from the entrance cavity of the stomach contents caused by gastroesophageal reflux (the stomach contents are colored and bitter) and should not be confused. Gastroesophageal reflux symptoms such as acid reflux and heartburn are not uncommon in patients with ulcer disease, especially those with different degrees of gastric emptying.

However, heartburn is a manifestation of gastroesophageal reflux, not a duodenal ulcer. There is no abnormality in physical examination. In the period of acute ulcer, there may be mild tenderness in the upper abdomen. The tender point is usually 2.5 cm or more in the middle of the upper abdomen. It is necessary to check fecal occult blood. If occult blood is found, it should be further examined and should not be delayed.

2. Atypical performance

Atypical cases in patients with duodenal ulcer are very common. In fact, typical performance is only found in a few cases, not as a measure of scale. Therefore, relying solely on medical history and physical examination to diagnose or identify duodenal ulcers is not reliable. Many patients have no clear abdominal pain, or the pain is blurred. The patient may be completely asymptomatic, or only complain of "dyspepsia" or faint dyspepsia. These symptoms are very unspecific and a large part is not caused by ulcers.

Less than 1% of duodenal ulcers and a slightly higher proportion of post-balloon and jejunal ulcers are associated with potentially high gastric acid secretion status, such as Zollinger-Ellison syndrome, antral sinus syndrome, systemic mast cells Storage disease, granulocyte leukemia, hyperparathyroidism or small bowel resection.

The clinical suggestion that there may be manifestations of this lesion is: diarrhea, weight loss, and the pH in the stomach continues to approach 1.0. When there is a clear high gastric acid performance without other symptoms, it is necessary to determine the fasting serum gastrin and blood calcium for the diagnosis. These tests are rarely used in clinical practice, and it is often difficult to explain if there is no careful study of gastric acid secretion.

Examine

Duodenal ulcer examination

1. Examination of Helicobacter pylori infection

It can be roughly divided into two types of invasive and non-invasive methods. Invasive methods refer to endoscopic biopsy for rapid urease test, Helicobacter pylori culture and histological examination. Non-invasive diagnostic methods include serum anti-pyloric Detection of Helicobacter antibodies, 14C-urea breath test or 13C-urea breath test.

The rapid urease test may be of the utmost value in routine testing methods, which are highly sensitive (85% to 95%) and highly specific (98%), and are inexpensive, easy to handle, and the results are quickly obtained, Giemsa or The specificity and sensitivity of the histological examination method of warthin-starry staining are more than 90%. This method is simple and convenient. The microscope can easily identify the Helicobacter pylori on the smear, which can avoid the false positive or false negative of the urease test, and urea. The combined test of enzyme tests has a complementary effect.

Among all the Helicobacter pylori diagnostic methods, the gastric mucosa is the most reliable for Helicobacter pylori culture. It is regarded as the "gold standard" for the diagnosis of Helicobacter pylori, and its sensitivity is slightly poor (70%-80%) due to the pyloric screw. Bacteria are microaerobic bacteria, require special equipment, and are technically difficult. Sometimes culture is not easy to be successful. Most hospitals do not use Helicobacter pylori culture as a routine test. However, Helicobacter pylori culture is unique in the selection of antibiotics, especially It is for those who fail to treat Helicobacter pylori.

The anti-lgG antibody is detected by enzyme labeling method, which has high sensitivity and specificity (both over 90%). The method is easy to operate, and the patient is more tolerant and relatively inexpensive. If positive, it means that there is a current or past Helicobacter pylori infection, especially suitable for epidemiological investigation, after the Helicobacter pylori infection is cured, the serum anti-Helicobacter pylori IgG antibody titer is gradually decreased, the titer is significantly reduced or the conversion takes about 6 months, so the serological method Can not determine whether Helicobacter pylori infection is cured, using radionuclide 14C or 13C labeled urea for respiratory test, can determine whether the patient has Helicobacter pylori infection in the stomach, 14C or 13C labeled urea after oral administration, the pylorus in the stomach The urease contained in Helicobacter can decompose urea into ammonia and 14C or 13C.

The latter is detected from the respiratory tract, and the radionuclide-labeled urea breath test has high sensitivity and specificity. It can be used for the establishment of Helicobacter pylori infection and as a basis for the cure of Helicobacter pylori infection. The advantage of the 13C urea breath test is that it is non-radioactive. The disadvantage is that the operation is complicated, special equipment is required, and the price is relatively expensive. In contrast, the 14C urea breath test is easy to carry out, but the radioactivity of 14C is insufficient.

In recent years, with the advancement and wide application of molecular biology technology, the method of detecting Helicobacter pylori DNA by molecular biology has been gradually carried out. At present, there are many molecular biological methods for detecting Helicobacter pylori, the main purpose There are two aspects, one is to check the presence of the DNA sequence of Helicobacter pylori, and the other is to perform bacterial typing on Helicobacter pylori, and the urease gene fragment and pylorus of Helicobacter pylori can be detected by polymerase chain reaction (PCR). The Helicobacter specific antigen gene fragment is highly sensitive to the detection of Helicobacter pylori by this method in view of the high sensitivity of the PCR technique.

Studies have shown that PCR can be used to detect Helicobacter pylori urease-related gene fragments with sensitivity of 10 to 100 Helicobacter pylori or 0.01 to 0.1 pg DNA. In addition to detecting gastric mucosa, PCR can also be used for saliva. Detection of plaque, gastric juice and fecal Helicobacter pylori, restriction fragment length polymorphism (RFLP) analysis of Helicobacter pylori, Helicobacter pylori plasmid, Helicobacter pylori ribosome fingerprinting technique to help identify isolated strains Type, any primer amplification polymorphism (RAPD) analysis can also better distinguish subtypes of Helicobacter pylori strains. These methods are clinically judged whether re-infection of Helicobacter pylori after anti-Helicobacter pylori treatment is recurrence or crossover. The infection is very helpful,

2. Determination of gastric acid

In the basic situation, the normal person is 2mmol/h, and the average secretion of duodenal ulcer patients is 4mmol/h. If the basal acid output (BAO) is >10mmol/h, it should be considered as gastric tumor (gastrinoma, Zollinger-Ellison syndrome (ZES), if BAO is close to maximal acid output (MAO), BAO/MAO 0.6, ZES is more likely, although gastric acid determination for preoperative and initial surgery of duodenal ulcer The choice of mode is of little significance, but as a vagus nerve in patients with ulcer disease, gastric acid can be measured before and after surgery. It can be used to evaluate whether vagus nerve cutting is complete or not. After successful vagus nerve cutting, MAO decreases by 70%. Ulcer gastric acid determination BAO 2mmol / h, if > 4mmol / h, almost recurrent ulcers must be confirmed, before the gastric acid determination must stop antacids, withdrawal time, H2 receptor antagonist 48h, omeprazole 5 days.

3. Determination of serum gastrin

Normal fasting serum gastrin <100pg/ml, this basal gastrin tumor screening test must be carried out in every ulcer patient, because the location and symptoms of ulcers in most patients with gastrinoma are similar to those of general ulcer patients. Difficult to distinguish, especially in patients with medical failure, endocrine neoplasia, recurrence of duodenal ulcer, ulcer symptoms after ulcer surgery, fasting serum gastrin >1000pg / ml, should be highly suspected ZES, patient serum stomach The hormone is 100-500pg/ml, and an excitation test is needed to release gastrin. The serum gastrin level of ZES patients is rapidly increased after intravenous injection of secretin, usually increased by >200pg/ml, and the gastric antrum remains. Gastric sinus G cell hyperplasia, pyloric obstruction, etc., serum gastrin levels unchanged, decreased or increased <200pg / ml.

Film degree exam

1. X-ray barium meal inspection

Duodenal ulcers are often used in combination with sputum and air double contrast angiography and conventional barium meal examination. Double contrast angiography in the supine position can detect posterior wall ulcers, but sometimes the inflated antrum can cover the ball, especially When the position of the stomach is higher or in the horizontal position (horn type), the lesion is easily covered. It should be displayed in a semi-erect or standing position. About 50% of the ulcers occur in the anterior wall, and the double-contrast contrast in the supine position is difficult to find the lesion or only The "circular shadow" is easy to be confused with the bulging lesions. The double contrast angiography in the prone position can show the lesions, but it is often poorly displayed due to the overlapping of the gastric antrums. The prone position compression method is helpful for the display of lesions.

(1) shadow: for the direct signs of duodenal bulb ulcer diagnosis, its shadow is generally small, often mung bean or soybean, large diameter less than 1cm, duodenal bulb ulcer It is indicated by the dose of the ball, the position of the ball, etc. Some people counted 597 cases of 12 intestinal ulcers, which can show 101 cases of shadows, accounting for 17%. The shadow of the ball is more common in the base of the ball. It is round, elliptical, polygonal, ring-shaped and dotted. The edges are mostly smooth. The pressure is checked around the shadow. The semicircular shape outside the cavity, the nipple shape and the saw-shaped shadow, the shadow represents the size, shape, and position of the ulcer. The posterior wall ulcer is on the near-surface wall (near the table). Due to the low enthalpy, most of them are round or Elliptical shadow, the anterior wall ulcer is in the far wall (away from the table). Because the sputum in the ulcer cavity is empty, the ulcer surface is coated with a thin layer of tincture, and the X-ray is tangent to the ulcer sidewall, which can show the linear shape. The ring shadow, also known as the "circle sign", at this time the outer edge of the ring shadow is sharp and inside Fuzzy, thus it can be identified with elevated lesion.

The tangential position of the ball ulcer can be seen as a papillary or rectangular shape outside the cavity. The shadow of penetrating ulcer is relatively large and deep, generally more than 0.5cm. Even in the standing position, even the liquid level is visible, and the giant penetrating ulcer is observed. Its shadow can be up to 2~3cm in diameter. Don't mistake it for the ball itself. The huge ulcer is mostly in the posterior wall. It often goes deep into the pancreas and has a wide translucent band around it, but it must be after the barium meal into the duodenal bulb or the lower part. At this time, the whole picture of this translucent band can be displayed, the active period ulcer, due to the surrounding tissue congestion and edema, the X-ray can show the ring-shaped translucent halo, the tangential position sometimes shows the Hampton line and the collar sign, the healing period ulcer, due to fibrous tissue hyperplasia, around the shadow Mucosal folds are radially concentrated, but some shallow ulcers can not be found in the shadows. Therefore, no shadows are found in the barium meal examination, and the presence of ulcers cannot be ruled out.

(2) Changes in mucosal folds: When fresh ulcers occur, there are inflammations and edema around the shadows, and the mucosal folds are thickened, flattened and blurred, and disappear into the transparent area of edema. The repair period is due to fibrous tissue hyperplasia and contraction. The formation of the mucosal folds centered on the shadow of the shadow, that is, the appearance of the "vehicle-like" fold.

(3) Deformation: Deformation of the ball is an important manifestation of duodenal ulcer. The main causes of deformation are functional and organic type 2, edema around the ulcer, and the intestinal wall is localized to the cavity; ring muscle Or longitudinal tendon contraction, a cut on one side of the ball; scar contraction; inflammatory adhesion and traction of the ball in the ball, the shape of the ball is different, mainly: one side of the ball (more common on the side of the big bend) The cut is concave; the ball is two-leaf, three-leaf and petal-shaped; the ball is pseudo-chamber-like deformation. When the ulcer is off the base of the ball, the deformation that can be formed on the large or small curved side is more complicated. Multiple diverticulum deformations are formed; severe scar contraction can cause the ball to be narrow and accompanied by pyloric obstruction.

(4) Other signs: 1 irritating sign, due to ulceration and inflammation in the ball, the expectorant can not stay in the ball, and immediately empty when reaching the ball; 2 pyloric sputum, can not be opened for a long time; , pyloric obstruction; 3 antrum sinus, gastric sinus stenosis; 4 increased gastric secretion to form an empty stomach; 5 local tenderness, the ball has obvious fixed tenderness, can be used as a reference for diagnosis.

2. Endoscopic diagnosis

Endoscopy is the most reliable method for morphological diagnosis of duodenal ulcer. It can make a clear diagnosis of the location, size, depth, shape, number and activity of duodenal ulcer.

Duodenal bulb ulcers are most common in the anterior wall, followed by large bends, and again for the posterior wall, small bends, which are basically the same as gastric ulcers, but have the following characteristics: generally small, about 80% ulcers are less than 1cm; Sexual, linear, frosty and kiss ulcers are more common; often cause pyloric and ball deformation or stenosis; ulcers are generally benign, no routine biopsy is required.

X-ray barium meal and gastroscopy are the most effective methods for the diagnosis of duodenal ulcer. The advantages of X-ray barium meal imaging are: cheap; non-invasive examination, patient suffering; the possibility of aspiration pneumonia and arrhythmia Small, the advantages of gastroscope: more sensitive in the detection of erosion and shallow ulcers; can get biopsy, send pathological examination; in the case of X-ray barium meal observation of ball deformation, the gastroscope can directly observe the presence or absence of ulcers.

3. CT examination

Because the duodenal bulb is relatively narrow relative to the gastric cavity, when the ball is ulcerated, the deformation is often the least obvious sign, and the shadow is often affected by the deformation of the ball. Not easy to display.

The CT deformation of the ball is characterized by the disappearance of the normal triangle, the narrow lumen of the ball, which can be irregular or lobulated. The obvious deformation can cause the ball to be thin and narrow, and the mucosal surface is irregular and can be jagged. And the serosal surface is relatively smooth.

Thickening of the intestinal wall of the duodenal bulb is another sign of duodenal ulcer. It is more common in recurrent old ulcers. At this time, the ball is easy to be affected by thickening of the wall and deformation of the pylorus. Misunderstood as part of the antrum, carefully observe its movement, pay attention to its relationship with the descending segment of the duodenum to help identify.

In the acute phase of the lesion or the onset of chronic bulbar ulcer, the intestinal wall of the bulb is characterized by decreased density due to edema, thickened intestinal wall, blurred outline of the outer edge, and edema may also manifest as stratification of the intestinal wall. After the treatment, the edema subsided and the contour of the intestinal wall was clear. These imaging findings were helpful in explaining the clinical symptoms and evaluating the treatment effect.

In the case of chronic recurrent duodenal ulcer, the common serous surface of the duodenal bulb is not smooth on CT, and the long multiple radial fiber cords around the fat space around the ball can be seen. The thickness of the surrounding adipose tissue can be slightly increased. The long cord can extend to the colonic hepatic flexure and gallbladder area. The reason for these manifestations is that the duodenal wall is not as thick as the stomach wall and ulcer. It is more prone to transmural inflammation, edema, and then caused by scarring changes outside the intestinal wall.

Diagnosis

Diagnosis and diagnosis of duodenal ulcer

diagnosis

Patients with uncomplicated duodenal ulcer have poor signs. Even during the active period, physical examination can be found without positive findings. The common positive signs are upper abdomen, especially the right side of the midline, with limited local tenderness and tenderness. When there is more inflammatory reaction around the ulcer, the range of tenderness may be large, and even abdominal muscle tension may occur, and a tender mass, active stomach and duodenal ulcer disease may be touched on the upper abdomen, especially with There are closed perforation cases in the posterior wall. The tender points (Boas tender points) appear on the left and right sides of the 10, 11 or 12 spinous processes of the thoracic vertebrae. However, Bockus finds that the position of the back tenderness is often higher, often Between 6 and 10 of the thoracic vertebrae, patients with active stomach and duodenal ulcer disease may also have tenderness points on the left and right hips (the buttocks of Onoji hip), and the tender points of similar parts may also appear in the upper abdomen. Other diseases, such as acute attacks of gallbladder disease, are less diagnostic.

Typical rhythm, 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. The pain episode lasts for a few days to weeks or months. Symptoms are prone to recurrence. Duodenal ulcers often have no painful recurrence or complications. The remission period is usually several months or years, almost always longer than seizure pain. Time, however, in some patients the pain is more aggressive, frequent symptoms and persistent episodes or complications, changes in the nature of ulcer pain may be a sign of comorbidities, such as ulcer pain becomes persistent, no longer food Or antacids relieved, or radiated to the back, showing penetration (often penetrated back to the pancreas).

Many active duodenal ulcers have no ulcer symptoms. Endoscopic gastrointestinal examination shows that nearly half of duodenal recurrent ulcers are asymptomatic. Endoscopy also shows a lack of ulcer activity, symptom relief and ulcer healing. Good interrelationship, no ulcer pain and 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 useful in diagnosing gastric tumor. However, the diagnosis of duodenal ulcer is not significant.

Differential diagnosis

1. Functional dyspepsia FD is characterized by upper abdominal pain or fullness discomfort. It can also have acid reflux, hernia and other manifestations. The physical examination can be completely normal or only mild tenderness in the upper abdomen. Gastroscope and X-ray examination can be identified.

2. It is difficult to distinguish between benign ulcer and malignant ulcer in gastric cancer. Cancer ulcer can be temporarily healed after treatment, so it is easy to be misdiagnosed as benign ulcer. The two methods mainly rely on X-ray barium meal and gastroscopy. In general, barium meal examination When the shadow is found in the contour of the stomach cavity, the mucous membrane around the shadow is stiff and stiff, and the mucosal folds that accumulate to the ulcer are interrupted. It is a characteristic of malignant ulcer. Under the gastroscope, the diameter of the ulcer is more than 2.5cm, the shape is irregular, and the bottom is attached. It is characterized by malignant ulcers, which can be diagnosed by pathological histological examination of the marginal mucosa of the ulcer.

3. Gastrinoma, also known as Zollinger-Ellison syndrome, is caused by the secretion of a large amount of gastrin from pancreatic non--cell tumors. It is characterized by abnormal increase of serum gastrin, increased gastric acid secretion, multiple upper digestive tract, and refractory Ulcer with diarrhea, compared with common peptic ulcer, ulcers caused by gastrinoma are multiple, the location is not typical (such as the ball, the jejunum), and difficult to cure, complications are more common, gastric acid secretion and serum stomach The detection of the hormone helps the identification of the two. B-ultrasound, CT, MRI examination can help the diagnosis of the disease if it can be found in the pancreas or other tissues with small tumor tumors.

4. Hookworm disease Duodenal hookworm symptoms can be similar to duodenal ulcer, but gastroscopy such as hookworm body or bleeding point in the duodenal descending, or fecal examination found hookworm eggs It is helpful for diagnosis.

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