Symptomatic gastroduodenal ulcers

Symptomatic duodenal ulcers include:

• medicinal ulcers;
• "Stressful" ulcers;
• ulcers with Zollinger-Ellison syndrome;
• ulcers with hyperparathyroidism;
• ulcers in other diseases of internal organs.

[1], [2], [3], [4], [5]

Medicinal gastroduodenal ulcers

Gastroduodenal ulcers can be caused by various drugs: NSAIDs (most often when treated with acetylsalicylic acid, indomethacin, butadiene); preparations of rauwolfia (reserpine, combined antihypertensive agents containing reserpine-adelfan, adelfan-ezidrex, cristepin-adelfan, etc.); glucocorticoids; preparations containing caffeine. Ulcerogenic effect can also have anticoagulants, potassium chloride, hypoglycemizing oral agents - sulfanylurea derivatives, digitalis preparations, nitrofuran compounds. The mechanism of the ulcerogenic effect of various drugs is different and diverse. The main pathogenetic factors of drug ulcerogenesis are:

• oppression of the gastric mucosa by the gastroprotective prostaglandins and protective mucus (aspirin and other NSAIDs);
• direct damaging effect on the superficial epithelium of the stomach with increasing its permeability for hydrogen ions (other non-steroidal anti-inflammatory drugs, potassium chloride, sulfonamide preparations, etc.);
• stimulation of secretion of hydrochloric acid by the covering cells and increase of aggressive properties of gastric juice (reserpine, caffeine, glucocorticoid preparations);
• hyperplasia gastrinprodutsiruyuschih cells of the gastric mucosa and increased secretion of gastrin, which in turn stimulates the secretion of gastrin and pepsin (glucocorticoid drugs);
• release of a number of biologically active compounds (histamine, serotonin, etc.), which contribute to an increase in the secretion of hydrochloric acid (reserpine, etc.).

Drug gastroduodenal ulcers are acute, as a rule, they occur more often in the stomach than in the duodenum, they can be multiple, often combined with erosions of the gastroduodenal region. The danger of medicinal gastroduodenal ulcers is that they are often complicated or first manifest by gastrointestinal bleeding, sometimes perforation. Medicinal ulcers of the stomach can be asymptomatic (this is typical primarily for glucocorticoid ulcers). The most important feature of medicinal ulcers is their rapid healing after the elimination of the drug ulcerogenic drug.

Ulcerogenic drugs can cause an aggravation of peptic ulcer.

"Stressful" ulcers

"Stress" ulcers - this gastro duodenal ulceration, which occurs in severe pathological processes that cause the development of stress in the human body. It is customary to refer to "stressful" ulcers:

• Cushing's ulcers in patients with severe CNS pathology;
• ulcers of Kurling with extensive and deep burns;
• ulcers that develop after severe, traumatic surgeries;
• ulcers with myocardial infarction, various types of shock.

Cushing's ulcers, erosion of the gastroduodenal region are especially often observed in severe craniocerebral trauma.

Kurling's ulcers develop with very extensive and deep burns within the first 2 weeks of the burn. Usually, they occur on a small curvature of the stomach and in the bulb of the duodenum and are often manifested by bleeding (latent or obvious), accompanied by paresis of the stomach and intestines; Possible perforation in the free abdominal cavity or covered perforation.

In a number of cases, "stressful" ulcers develop after severe and traumatic surgical interventions, and often they go unnoticed and are cured independently. Gastroduodenal ulcers in patients with acute myocardial infarction, with decompensated heart defects are also described. They can also occur latent or immediately manifest as complications, most often gastrointestinal bleeding, which is generally characteristic of "stressful" ulcers.

The main mechanisms for the development of "stressful" gastroduodenal ulcers are:

• activation of the hypothalamic-pituitary-adrenal system, increased secretion of glucocorticoids that stimulate gastric secretion, reduce the production of protective mucus, reduce the regeneration of the gastric mucosa, increase the formation of histamine from histidine by activating the histidine-decarboxylase enzyme (which in turn leads to hyperproduction of hydrochloric acid );
• increased secretion of catecholamines, which contributes to the violation of microcirculation in the gastric mucosa and the development of ischemia in it;
• violations of the motor function of the stomach, the development of duodenogastric reflux, throwing duodenal contents into the stomach and damage to the gastric mucosa;
• an increase in the tone of the vagus nerve and an increase in the activity of the acid-peptic ulcerogenesis factor.

Zollinger-Ellison Syndrome

Described by Zollinger and Ellison in 1955. It has now been established that this syndrome is caused by a gastrin-producing tumor. In 85-90% of cases, it is located in the head or tail of the pancreas, originates from the cells of the islets of Langerhans, but not from the a-cells that produce glucagon, and not from the beta cells that produce insulin, but from the cells that produce gastrin. In 10-15% of cases the tumor is localized in the stomach, 12 duodenum, liver, adrenal glands. There is a point of view that gastrinomas of extra-pancreatic localization are found even more often than pancreatic. Sometimes, Zollinger-Ellison syndrome is a manifestation of multiple endocrine adenomatosis (multiple endocrine neoplasia) of type I.

In 60-90% of gastrinomas are malignant tumors with slow growth rates.

The leading feature of the Zollinger-Ellison syndrome is the formation of peptic ulcers resistant to treatment caused by hyperproduction of gastrin and, accordingly, hyperproduction of hydrochloric acid and pepsin.

In the vast majority of patients, the ulcer is localized in the duodenum, less often in the stomach, and also in the jejunum. Quite often, multiple ulcers of the stomach, 12-finger and jejunum are observed.

Clinical manifestations of the disease:

• pains of vegabastria have the same patterns in relation to food intake as in the usual ulcer of the duodenum and stomach, but unlike them, they are very persistent, intense and resistant to antiulcer therapy;
• extremely stubborn heartburn and belching sour;
• an important sign of the disease are diarrhea caused by the intake of a large amount of hydrochloric acid in the small intestine and the consequent increase in the motility of the small intestine and the slowing of absorption; stool is plentiful, watery, with a lot of fat;
• a significant reduction in body weight is possible, which is most typical for malignant gastrinomas;
• stomach ulcers and 12 duodenal ulcer with Zollinger-Ellison syndrome can not be healed even with prolonged adequate therapy;
• in many patients marked manifestations of esophagitis, sometimes even with the formation of ulcers and strictures of the esophagus;
• when palpation of the abdomen is determined by severe tenderness in the epigastrium or pyloroduodenal zone, it can be a positive symptom of Mendel (local palpation pain in the projection of the ulcer), there is a local protective muscular tension;
• in cases of malignant nature, metastasis to the liver and, correspondingly, a significant increase thereof;
• X-ray and endoscopic examination of the stomach and duodenum reveals an ulcer, the symptoms of which do not differ from those described above with the usual peptic ulcer of the stomach and duodenum.

[6], [7], [8]

Laboratory criteria of Tsodlinger-Ellison syndrome

Relatively reliable laboratory signs of the Zollinger-Ellison syndrome are the following:

• hypergastrinemia (gastrin content in the blood up to 1000 pg / ml and more, while in peptic ulcer it does not exceed the upper limit of the norm of 100 pg / ml);
• the test with secretin - the patient is administered intravenously secretin in a dose of 1-2 ED per 1 kg of body weight. With Zollinger-Ellison syndrome, the content of gastrin in the blood increases significantly in comparison with the baseline level, while gastric secretion also increases. With peptic ulcer, the content of gastrin in the blood after the application of secretin, on the contrary, decreases, and gastric secretion is inhibited;
• test with calcium gluconate - intravenously, calcium gluconate is administered at a dose of 4-5 mg per 1 kg of body weight. With Zollinger-Ellison syndrome, the level of gastrin in the blood is increased by more than 50% compared to the baseline (to almost 500 pg / ml and above), while in peptic ulcer the increase in gastrinemia is much less pronounced;
• indices of gastric secretion (AA Fisher, 1980):
  • basal acid production above 15 and especially 20 mmol / h;
  • ratio of basal acid production to a maximum of 0.6 or more;
  • volume of basal secretion over 350 ml / h;
  • acidity of basal secretion (basal secretion rate) more than 100 mmol / h;
  • the maximum acid production is over 60 mmol / h.

Instrumental methods of gastrinoma detection

The detection of the tumor itself (gastrinoma) is performed using ultrasound, computed tomography, selective abdominal angiography.

Pancreatic ultrasound and computed tomography detect tumors only in 50-60% of patients due to small tumor size.

The most informative method is the method of selective abdominal angiography with the taking of blood from pancreatic veins and the definition of gastrin in it. Using this method, a correct diagnosis is established in 80% of patients.

Computed tomography usually does not detect a tumor less than 1 cm in diameter.

Ulcers in hyperparathyroidism

Hyperparathyroidism is a disease caused by parathyroid pathological hyperproduction of the parathyroid glands.

Gastroduodenal ulcers with hyperparathyroidism occur with a frequency of 8-11.5%. The mechanism of ulceration is as follows:

• excess parathyroid hormone has a damaging effect on the mucosa of the gastroduodenal zone and stimulates gastric secretion and the formation of hydrochloric acid;
• hypercalcemia stimulates the secretion of hydrochloric acid and gastrin;
• when hyperparathyroidism is sharply reduced trophism of the mucosa of the gastroduodenal zone.

Clinical features of the course of gastroduodenal ulcers in hyperparathyroidism:

• ulcers are most often localized in the duodenum;
• ulcers for a long time atypical;
• clinically manifested forms are characterized by severe pain syndrome, persistence of the course, resistance to antiulcer therapy, propensity to complications (bleeding, perforation);
• is characterized by frequent recurrence of ulcers.

With FEGDS and fluoroscopy of the stomach, an ulcer is detected, characterized by the same endoscopic and radiographic manifestations as the usual peptic ulcer.

The clinical picture and diagnosis of hyperparathyroidism is outlined in the corresponding chapter of the manual "Diagnosis of internal diseases".

Gastroduodenal ulcers with other diseases of internal organs

Gastroduodenal ulcers in atherosclerosis of the abdominal aorta and arteries of the abdominal cavity

With severe atherosclerosis of the abdominal aorta, the frequency of gastroduodenal ulcers is 20-30%. In the origin of such ulcers, the main significance is the deterioration of the blood supply of the stomach and a sharp decrease in the trophism of the mucosa of the gastroduodenal zone.

The clinical features of gastroduodenal ulcers developing as a result of atherosclerosis of the abdominal aorta are the following:

• ulcers develop not only in asthenics (which is more typical of peptic ulcer sui generis), but also in hypersthenics;
• quite often ulcers are multiple;
• characterized by a tendency to complications, most often there are bleeds that have a tendency to relapse;
• scarring of ulcers occurs very slowly;
• the course of ulcers is often latent;
• often there is a mediogastral localization of ulcers;
• in patients the clinical and biochemical symptoms of atherosclerosis are revealed.

Ulcers with cirrhosis of the liver

Ulcers of the gastroduodenal region are observed in 10-18% of patients with cirrhosis of the liver. The mechanism of ulceration is as follows:

• decrease inactivation of histamine Igastrin in the liver, increase in their content in the blood, which leads to hyperproduction of hydrochloric acid;
• violation of blood flow in the portal system and development of hypoxia and ischemia of the gastroduodenal mucosa;
• reduction of secretion of protective gastric mucus;

Clinical features of ulcers in cirrhosis are:

• preferential localization in the stomach;
• a rather often erased clinical picture;
• a frequent complication with ulceration of the duodenal bleeding;
• low effectiveness of antiulcer therapy.

Ulcers in chronic pancreatitis

Pancreatogenic ulcers develop in 10-20% of patients with chronic pancreatitis. In their pathogenesis, the decrease in the secretion of hydrocarbonates by the pancreas, alcohol abuse, duodenogastric reflux, increased production of kinins are important.

Pancreatogenic ulcers have the following features:

• more often localized in the duodenum;
• have a persistent current;
• rarely occur sharply compared with other symptomatic ulcers;
• rarely complicated by bleeding.

Gastroduodenal ulcers in chronic nonspecific lung diseases

In chronic nonspecific lung diseases, gastroduodenal ulcers develop in 10-30% of patients. The main cause of their development is hypoxemia and a decrease in the resistance of the gastroduodenal mucosa to aggressive gastric juice factors.

The clinical features of these ulcers are:

• predominantly gastric localization;
• low severity of pain syndrome; lack of a clear link between pain and food intake;
• moderate dyspeptic disorders;
• tendency to bleeding.

Gastroduodenal ulcers in chronic renal failure

In chronic renal failure gastroduodenal ulcers are observed in 11% of patients. Especially characteristic is the development of ulcers in patients on programmed hemodialysis. In the pathogenesis of these ulcers it is important to reduce the destruction in the kidneys of gastrin and the damaging effect on the gastric mucosa of uremic toxic substances.

Ulcers with chronic renal failure are more often localized in the duodenum and are prone to severe bleeding.

Gastroduodenal ulcers in diabetes mellitus

In the origin of gastroduodenal ulcers in diabetes mellitus, the most important role is played by the defeat of the vessels of the submucosal layer ("diabetic microangiopathy"). These ulcers are usually localized in the stomach, flow with an erased symptomatology, often complicated by gastroduodenal bleeding.