Infiltration of the intestine - All about diseases of the gastrointestinal tract. Morphological changes in the intestinal mucosa in various diseases
Infiltrate - what is it? Doctors distinguish several of its types - inflammatory, lymphoid, post-injection and others. The causes of infiltration are different, but all its types are characterized by the presence of unusual cellular elements in the tissue (or organ), its increased density, and increased volume.
Post-injection infiltrate
1. The rules of antiseptic treatment were not followed.
2. Short or blunt syringe needle.
3. Rapid drug administration.
4. The injection site was chosen incorrectly.
5. Multiple administration of the drug in the same place.
The appearance of a post-injection infiltrate also depends on the individual characteristics of the human body. In some people, it occurs extremely rarely, while in other patients it occurs after almost every injection.
Treatment of post-injection infiltrate
There is no infection in the infiltrated tissue, but the danger of this pathology after the injection is that there is a risk of an abscess. In this case, treatment can only take place under the supervision of a surgeon.
If there are no complications, then the infiltrate after injections is treated with physiotherapeutic methods. It is also recommended to apply an iodine mesh to the place of tissue compaction several times a day, use Vishnevsky's ointment.
Traditional medicine also offers several effective methods for getting rid of the “bumps” that appeared after injections. Honey, burdock leaf or cabbage, aloe, cranberries, cottage cheese, rice can have a healing effect when a similar problem occurs. For example, burdock or cabbage leaves should be taken fresh for treatment, applying them for a long time to a sore spot. Previously, the “bump” can be greased with honey. Cottage cheese compress also helps to get rid of old "bumps".
No matter how good this or that method of treating this problem is, the decisive word should belong to the doctor, since it is he who will determine how to treat it and whether it should be done.
Inflammatory infiltrate
This group of pathologies is divided into several types. Inflammatory infiltrate - what is it? Everything is explained by the medical encyclopedia, which talks about the ways in which the focus of inflammation occurs and indicates the causes of the appearance of pathological tissue reactions.
Medicine distinguishes a large number of varieties of infiltrates of the subgroup under consideration. Their presence may indicate problems with the immune system, congenital diseases, the presence of acute inflammation, a chronic infectious disease, and allergic reactions in the body.
The most common type of this pathological process is an inflammatory infiltrate. What it is helps to understand the description of the characteristic features of this phenomenon. So, what should you pay attention to? Thickening of tissues in the area of inflammation. When pressed, pain occurs. With stronger pressure, a hole remains on the body, which levels out slowly, since the displaced cells of the infiltrate return to their original place only after a certain period of time.
Lymphoid infiltrate
One of the types of tissue pathology is lymphoid infiltrate. What it is, allows you to understand the Big Medical Dictionary. It says that such a pathology occurs in some chronic infectious diseases. The infiltrate contains lymphocytes. They can accumulate in different tissues of the body.
The presence of lymphoid infiltration indicates a malfunction of the immune system.
Postoperative infiltrate
For what reason can a postoperative infiltrate form? What it is? Does it need to be treated? How to do it? These questions are of concern to people who had to face this problem.
The development of postoperative infiltrate occurs gradually. Usually its detection occurs 4-6 or even 10-15 days after surgery. The patient's body temperature rises, there are aching pains in the abdominal cavity, stool retention. The presence of painful compaction is determined.
In some cases, it can be difficult to determine where the infiltrate is located - in the abdominal cavity or in its thickness. To do this, the doctor uses special diagnostic methods.
The causes of infiltration after surgery are not always possible to accurately determine, but its therapy in most cases ends successfully. Antibiotics and various types of physiotherapy give positive results.
Very often there is an infiltrate of the postoperative scar. Sometimes it can appear several years after the surgical procedure. One of the reasons for its occurrence is the suture material used. Perhaps the infiltrate will resolve on its own. Although this rarely happens. Most often, the phenomenon is complicated by an abscess, which must be opened by the surgeon.
Infiltrate in the lungs
This is a dangerous pathology that requires immediate treatment. With the help of X-ray and biopsy data, doctors can detect a lung infiltrate in a patient. What it is? Pulmonary infiltration must be distinguished from pulmonary edema. With such a pathology, the patient experiences penetration and accumulation of fluids, chemicals, cellular elements in the tissues of the internal organ.
Lung infiltration is most often of inflammatory origin. It can be complicated by the processes of suppuration, which leads to loss of organ function.
Moderate enlargement of the lung, compaction of its tissue are characteristic signs of infiltration. X-ray examination helps to recognize them, in which darkening of the tissues of the internal organ is visible. What does it give? By the nature of the blackout, the doctor can determine the type of pathology under consideration and the degree of the disease.
Tumor infiltrate
Tumor infiltrate is one of the most common pathologies. What it is? It is most often composed of atypical tumor cells of a different nature (cancer, sarcoma). Affected tissues change color, become dense, sometimes painful. Manifested in tumor growth.
Reasons for the appearance
The likelihood of infiltration is equally present in people of any age.
The results of the study showed that various kinds of injuries, diseases of an infectious nature can become the cause of the disease. They can be transmitted by contact, have a lymphogenous type of distribution.
In the tissues of the maxillary region, an infiltrate often develops. What it is? How can it be distinguished from other diseases? Only an experienced doctor can assess the patient's condition and give an accurate answer to the questions posed. The causative agents of inflammation are staphylococci, streptococci and other representatives of the microflora of the oral cavity.
A complicated condition of acute appendicitis can also cause the development of an infiltrate. It occurs with untimely surgical intervention.
Symptoms of infiltration
With the development of the disease, the patient may experience a slightly elevated temperature. It stays at a certain level for several days. Sometimes this indicator remains normal. The spread of the infiltrate occurs on one or more parts of the body. This is expressed in swelling and compaction of tissues with a clearly defined contour. All tissues are affected at the same time - mucous membranes, skin, subcutaneous fat and muscle membranes.
The infiltrate, which develops against the background of complications of appendicitis, is characterized by persistent pain in the lower abdomen, fever up to 39 degrees, chills. In this case, the recovery of the patient is possible only with timely surgical intervention. The presence of this type of infiltrate is established upon examination by a doctor (does not require special diagnostic methods).
In other cases, only a differential approach allows you to accurately establish the diagnosis and prescribe the right treatment. Sometimes, to establish a diagnosis, data from the results of a puncture from the site of inflammation are taken into account.
Specialists conduct a study of materials taken from the inflamed area. The different nature of the cells constituting the infiltrate was established. It is this circumstance that allows physicians to classify the disease. As a rule, a large accumulation of yeast and filamentous fungi is found in the infiltrate. This indicates the presence of such a condition as dysbacteriosis.
The main goal of the treatment of infiltrate is the elimination of inflammatory foci. This is achieved by conservative methods of treatment, which include physiotherapy. The patient should not self-medicate and delay a visit to a specialist.
Thanks to physiotherapy, they achieve resorption of the infiltrate by increasing blood flow. At this time, the elimination of stagnation occurs. It also reduces swelling and relieves pain. Most often, electrophoresis of antibiotics, calcium is prescribed.
Physiotherapy is contraindicated if purulent forms of the disease are present. Intensive impact on the affected area will only provoke the rapid development of the infiltrate and the further spread of the focus.
Stomach lymphoma
Stomach lymphoma
Lymphoma of the stomach is a malignant non-leukemic neoplasm originating from lymphoid cells in the wall of the organ. Usually characterized by a relatively favorable course, slow growth and rare metastasis, but the degree of malignancy of the tumor may vary. Most often located in the distal part of the stomach. It is not associated with damage to peripheral lymph nodes and bone marrow. Lymphomas of the stomach make up from 1 to 5% of the total number of neoplasias of this organ. They usually develop over the age of 50. Men are affected more often than women. In the initial stages, the prognosis is favorable. The average five-year survival rate for gastric lymphomas of all stages ranges from 34 to 50%. The treatment is carried out by specialists in the field of oncology, gastroenterology and abdominal surgery.
Causes of stomach lymphoma
The precursor of this neoplasm is lymphoid tissue, located in the mucous membrane in the form of individual lymphocytes and clusters of cells. Under certain conditions (for example, in chronic gastritis caused by infection with Helicobacter pylori), such accumulations form lymphoid follicles, in which areas of atypia may occur. Taking into account the fact that 95% of patients with gastric lymphoma are found to have various strains of Helicobacter pylori during the examination, this infection is considered as one of the main causes of this pathology.
Along with Helicobacter pylori, the development of various types of gastric lymphomas can be triggered by other factors, including contact with carcinogenic substances, prolonged stay in areas with high levels of radiation, previous radiation therapy, taking certain medications, excess ultraviolet radiation, non-specific decrease in immunity, immune disorders in AIDS, autoimmune diseases and artificial suppression of immunity after organ transplant operations.
Classification of gastric lymphomas
Taking into account the origin and characteristics of the clinical course, the following types of gastric lymphomas are distinguished:
Taking into account the characteristics of growth, the following types of gastric lymphomas are distinguished:
Taking into account the depth of the lesion, determined during endoscopic ultrasound, the following stages of gastric lymphomas are distinguished:
Along with the above classification, a standard four-stage classification of oncological diseases is used to determine the prevalence of gastric lymphoma.
Symptoms of stomach lymphoma
There are no specific signs; in its clinical manifestations, gastric lymphoma may resemble gastric cancer. less often - gastric ulcer or chronic gastritis. The most common symptom is epigastric pain, often aggravated after eating. Many patients with gastric lymphoma report a feeling of premature satiety. Some patients develop an aversion to certain types of food. Characterized by weight loss, due to a feeling of fullness in the stomach and a decrease in appetite. Perhaps a critical decrease in body weight up to cachexia.
In gastric lymphoma, nausea and vomiting are common, especially when eating too much food, which further contributes to the reduction of portions, refusal to eat and subsequent weight loss. With the spread of the oncological process, stenosis of the stomach can develop. In some cases, patients with gastric lymphoma experience bleeding of varying severity (including small ones, with an admixture of blood in the vomit). There is a risk of developing severe complications - perforation of the stomach wall when it grows into a tumor and profuse bleeding when the stomach lymphoma is located near a large vessel. Along with the listed symptoms, there is an increase in body temperature and profuse sweating, especially at night.
The diagnosis is established taking into account complaints, medical history, external examination, abdominal palpation, laboratory and instrumental studies. Due to the non-specificity of symptoms, late detection of gastric lymphoma is possible; cases are described in the literature when the time period between the appearance of pain in the epigastrium and the diagnosis was about 3 years. The main method of instrumental diagnostics is gastroscopy. to determine the location and type of tumor growth. On endoscopy, gastric lymphoma can be difficult to differentiate from cancer, gastritis, and non-malignant ulcers.
To clarify the diagnosis, the endoscopist takes material for subsequent histological and cytological examination. A distinctive feature of taking an endoscopic biopsy for gastric lymphomas is the need to take tissue from several sites (multiple or loop biopsy). To determine the prevalence of the oncological process, endoscopic ultrasound and CT of the abdominal cavity are performed. To detect metastases, chest MRI and abdominal MRI are prescribed. Despite diagnostic difficulties, due to slow growth, most gastric lymphomas are detected at the first or second stage, which increases the likelihood of a successful outcome in this pathology.
Treatment of stomach lymphoma
With localized, favorably flowing MALT-lymphomas, eradication anti-Helicobacter therapy is carried out. It is acceptable to use any treatment regimen with proven effectiveness. If there is no result after applying one of the standard regimens, patients with gastric lymphoma are prescribed a complicated three-component or four-component therapy, which includes the administration of proton pump inhibitors and several antibacterial agents (metronidazole, tetracycline, amoxicillin, clarithromycin, etc.). With the ineffectiveness of complicated schemes, depending on the stage of gastric lymphoma, chemotherapy or systemic therapy is performed.
In other forms of gastric lymphoma and MALT lymphomas that extend beyond the submucosal layer, surgical intervention is indicated. Depending on the prevalence of the process, gastric resection or gastrectomy is performed. In the postoperative period, all patients with gastric lymphoma are prescribed chemotherapy drugs. In advanced cases, chemotherapy or radiation therapy is used. Chemotherapy can provoke ulceration and perforation of the stomach wall (including asymptomatic), therefore, when using this technique, CT is performed regularly to detect free fluid and gas in the abdominal cavity. In the later stages of gastric lymphoma, there is a risk of developing gastric stenosis, gastric perforation, or gastric bleeding. therefore, operations are recommended even for stage III and IV tumors.
Due to slow growth, late invasion into the deep layers of the stomach wall, and rather rare metastasis, the prognosis for gastric lymphomas is relatively favorable. The use of eradication therapy in the early stages of MALT-lymphomas provides complete remission in 81% of patients and partial remission in 9% of patients. Radical surgery is possible in 75% of cases. The median five-year survival rate for stage I gastric lymphoma is 95%. At stage II, this figure decreases to 78%, at stage IV - up to 25%.
What is lymphoid gastritis?
Medicine has several types of gastritis, among which lymphoid gastritis, according to the international classification, belongs to special types of diseases. It occurs infrequently, according to statistics, no more than 1% of the number of patients have it. It is characterized by the fact that the mucous membrane is damaged not quite usually. In its wall, in place of diseased areas, lymphocytes appear in large numbers - special cells. They form follicles (vesicles).
Lymphoid gastritis is a special type of gastritis.
This disease mainly begins to develop against the background of chronic gastritis. According to doctors, Helicobacter pylori bacteria are to blame for the appearance of such an unusual illness. These microorganisms colonize the gastric mucosa, gradually causing its inflammation. The resulting lymphocytes act in two ways. On the one hand, they have a healing effect, neutralizing the pathogenic effect of bacteria. On the other hand, follicles prevent unaffected cells from producing gastric juice.
Due to the formation of follicles, the disease has another name - follicular gastritis.
Lymphoid gastritis does not cause very severe suffering to patients, such as ulcerative gastritis. Patients complain of the following symptoms:
The signs are not very obvious, so diagnosing lymphoid gastritis is very problematic. To make a diagnosis, doctors try to use instrumental methods.
Lymphoid gastritis is quite difficult to diagnose. Even experienced gastroenterologists make mistakes. The patient is prescribed a special endoscopic examination without fail: using an optical flexible device, the mucous membrane is examined. And the doctor on the display sees what is happening inside the stomach. As a result, the whole picture of the disease emerges. In addition, the device helps to obtain mucosal tissue for microscopic examination. A biopsy is being performed. As a result, the patient is given an accurate diagnosis.
Back to index
Treatment of lymphoid gastritis
If the Helicobacter pylori bacterium is detected in the patient's stomach, then antibiotic therapy is mandatory. Antibiotics are taken for two weeks. If the disease is accompanied by heartburn, then drugs are prescribed that help reduce acidity. Symptomatic treatment is recommended.
Due to the fact that the bacterium is transmitted by contact, there is a high risk of infection with this form of gastritis through cutlery, dishes and other common items.
Of the drugs, the doctor prescribes:
Treatment of lymphoid gastritis will not give a positive result without following a special diet. The patient should exclude from his diet all foods that irritate the stomach. Strong broths, spicy foods, salinity, smoked meats, canned food and spices cannot be present in food. Boiled fish and meat, crumbly cereals, mashed vegetables, jelly, cottage cheese casseroles - this is exactly the food that is shown to patients.
Meals should be frequent, but in small portions. Meals - at least four times a day, and preferably six. It is advisable to eliminate alcohol completely. And mineral water is welcome. Which one - the doctor will advise.
Good results in the treatment of gastritis gives the combined use of traditional methods and treatment with folk remedies.
On the advice of traditional healers, it is necessary to take plantain juice. It relieves the inflammatory process, relieves pain, has a healing effect. Propolis and fresh garlic are used as antimicrobials.
Traditional treatment courses are long. This leads to a good healing result and the exclusion of the possibility of recurrence of the disease.
Disease prevention is also important. Since this disease is caused by bacteria and transmitted by contact, it is desirable to provide a patient with obvious manifestations of infection with complete isolation. But this is practically impossible. Therefore, in order to prevent the spread of the disease, it is better to treat all family members at once. This will reduce the risk of gastritis growth.
Enlarged lymph nodes of the stomach
Lymphoma of the stomach is a rare disease. Its distinguishing feature is the defeat of nearby lymph nodes. Of the entire list of cancers, 1-2% are lymphoma.
The essence of pathology
At risk are men over 50 years of age. Since lymphoma affects the lymphoid nodes, oncology in the stomach develops on the basis of metastasis. Therefore, primary tumors are less common than secondary ones. Another name for the pathology is malt lymphoma of the stomach. Features of the pathology:
There are several forms of pathology with different symptoms. In each case, lymphoid tissue is affected along with the gastric mucosa. The increase in the incidence of lymphoma is due to environmental degradation, the use of harmful, chemically contaminated food, and an increase in the load on the immune system. Antibodies begin to form in lymphocytes, neutralizing and destroying pathogenic irritants and pathogenic agents. This leads to malfunctions of the immune system, characterized by a decrease in the secretion of antibodies. This encourages them to destroy the cells of their own body.
Mechanism
Lymphocytes are active cells of the immune system. In case of malfunctions in its work, excessive or insufficient production of these cells occurs, which leads to an increase in their aggression relative to their own body. Histological analysis of stomach tissues affected by lymphoma reveals an abnormal accumulation of lymphoid cells in the mucous and submucosal layers of the organ. At the same time, the lymphoid follicle infiltrates the gastric glands, which leads to digestive dysfunction. If the lymphoma is initially formed in the stomach, there are no metastases in the bone marrow and peripheral lymph nodes in most cases.
In the bulk, the pathological process initially affects the lymph node in the neck or groin. The stomach undergoes metastasis with a decrease in local immunity against the background of the development and progression of gastritis in a chronic form, which appeared as a result of Helicobacter pylori infection.
Varieties and causes
Distinguish:
95% of all gastric malt-lymphomas are accompanied by intoxication with HP infection. With this form, the lymph node is always enlarged. Other predisposing factors:
Symptoms
The clinical picture of lymphoid neoplasms is similar to the external and symptomatic manifestations of cancerous lesions and other pathologies of the gastrointestinal tract. The first sign of stomach lymphoma is an enlarged lymph node in the neck or groin. Symptoms:
Often, lymphoma infiltration of the stomach is accompanied by serious complications, such as:
These complications require emergency surgery. Of particular difficulty in diagnosing is characteristic of follicular lymphoma, which occurs with virtually no symptoms. However, pathological follicles can be treated even in advanced form.
Kinds
Malignant lymphoma tumors of the follicles in the stomach have a different cellular structure, features of growth with spread. There are 5 types of neoplasms that are localized in different layers of gastric tissues. The following parameters were taken for classification:
- polypoid or exophytic tumor growing into the lumen of the organ;
- primary nodular, formed in the mucous layer of the stomach;
- infiltrative ulcerative - the most aggressive.
- Histological sign:
- malignant;
- benign.
Diagnosis of stomach lymphoma
Based on the data obtained, a treatment technique is selected.
Treatment
Lymphoma is treated under the supervision of an oncologist, who selects a technique in accordance with the type, prevalence and rate of progression of the pathology.
I stage
Early lymphoma can be cured with chemo-radiotherapy or surgery. An integrated approach is preferable, as it has a low risk of relapse. To do this, the tumor is completely excised with part of the stomach. The organ may be removed completely. During the operation, nearby lymph nodes of the stomach and organs are carefully examined. After the operation, a course of chemistry and radiation is carried out in order to remove possible distant metastases.
II stage
X-ray and chemotherapy are always used with such powerful antitumor drugs as Prednisolone, Vincristine, Doxorubicin. The treatment regimen is prescribed in accordance with the specific nature of the course of the pathology. If non-Hodgkin's neoplasms are enlarged to large sizes, they are first reduced and then removed.
III and IV stages
Treatment is prescribed complex phased:
If a non-Hodgkin's tumor affects the blood vessels or enlarged lymphoid follicles are found, such pathologies are inoperable. In this case, palliative therapy is prescribed. The goals of treatment are to take medications that reduce pain, improve the condition, which will prolong the life of the patient.
Course against helicobacteria
B-cell or Helicobacter bacterial lymphoma of the digestive organ undergoes a special treatment technique. For this, special medicines are used that stop inflammation, suppress vital activity and destroy Helicobacter pylori.
To date, there is no consensus on the preferred method of treating this type of lymphoma, so an individual approach is used.
In the absence of the effect of drug treatment, a course of radiation and chemistry is carried out. The operation is prescribed in extreme cases. After it, a repeated antitumor course is shown.
Rehabilitation
In the postoperative period, it is important to establish proper nutrition. The nutritionist prepares the menu and the required amount of food. The complexity of the situation lies in the patient's loss of appetite due to abdominal pain. The patient must follow all the recommendations of the doctor, undergo regular examinations, take alternative recipes as a preventive measure.
Folk remedies
The use of any prescription requires consultation with a doctor. Recipes:
Forecast
Gastric lymphoma is characterized by a favorable prognosis when detected in the early stages. Grades III and IV are curable, but 5-year survival depends on the severity of the infiltration, the size of the tumor, and its prevalence. Survival rate with I degree is 95%, with II - 75%, with III and IV - 25%. A complete cure is possible in most cases with the right treatment tactics. The outcome depends on the rate of spread of the lymphoma and the possibility of metastasis.
Nutrition and diet
The effectiveness of lymphoma treatment depends on proper nutrition and diet. The patient must receive enough calories and building protein to restore the body, regenerate tissues and maintain weight. Good nutrition will soon return to normal health. But certain foods can cause problems.
Often patients refuse to eat due to pain, lack of taste during treatment. Therefore, a specific diet is being developed with a limited amount of animal protein, fatty foods. The content of vegetable protein, fiber, dairy and sour-milk products in the menu is increasing.
Products should be well boiled in water or steamed. Meals should be prepared in liquid or semi-liquid form. It is not recommended to eat cold or hot food. Diet:
sample menu
Despite the strict restriction in products, a nutritionist can create a menu that is acceptable in terms of variety and nutrition for gastric lymphoma.
Table #1
- first: meatballs from lean meat and rice, weak green tea;
- second: crushed to puree apple.
- Lunch: mashed vegetable soup, boiled chicken, freshly squeezed fruit juice.
- Afternoon snack: fresh homemade yogurt.
- Dinner: freshly cooked macaroni and cheese.
- A glass of goat's milk before bed.
- Two meals for breakfast:
- first: steamed omelette (can be replaced with soft-boiled egg), tea;
- second: shredded cottage cheese.
- Lunch: mashed soup with vegetables, boiled low-fat fish.
- Afternoon snack: freshly squeezed juice from vegetables or fruits.
- Dinner: heavily boiled cereal porridge with boiled chicken.
Table number 2
Prevention
Ways to prevent lymphoma do not completely protect against the possibility of its development due to the ambiguity of the true causes of the appearance. But the following rules contribute to the reduction of risk factors:
According to this information, it becomes clear that leukocyte infiltration of the cervix is a condition that develops in the presence of an inflammatory process in the tissues. It is most common in cervicitis and vaginitis.
The diagnosis of leukocyte infiltration is made by women who have taken a smear at a gynecological examination. The resulting material is sent to a laboratory for examination under a microscope. A smear is obtained using a Volkmann spoon, after inserting a gynecological speculum into the vagina.
Where do they get the material for research? The doctor takes tissue from those places where he sees pathological changes. The resulting material is applied to a glass slide and dried, only then the smear is checked in the laboratory.
Training
Only a comprehensive examination will make it possible to detect the cause of leukocyte infiltration and cure the ongoing changes in the cervix. An increased number of leukocytes is treated with antiseptic and antibiotic drugs, as well as lacto- and bifidobacteria.
Treatment of leukocyte infiltration also depends on the cause itself. Having got rid of the disease, the level of leukocytes in the epithelium of the cervix will be restored. It is possible to have sex in this condition if additional tests have not detected a specific infection.
Lymphocytic gastritis is a rare variety of common chronic gastritis of unknown origin. The disease is characterized by nonspecific clinical manifestations and endoscopic signs. It affects most often the elderly after 60-65 years, but sometimes infants up to 1 year of age. Adult women get sick 3 times more often than men.
The disease manifests itself in severe infiltration of the epithelium of the stomach. In this condition, there are small lymphocytes (or T-lymphocytes) in the gastric pits on the surface of the mucosa and there is an infiltration of the membrane by plasma cells. Lymphocytic gastritis in the absence of treatment in most cases leads to serious complications.
Causes of lymphocytic gastritis
The causes of this type of gastritis have not yet been fully elucidated by medical scientists to this day.
But the most plausible are such assumptions:
- The onset of the disease is given by the development of celiac disease (gluten disease). It is characterized by intolerance to gluten, a protein found in most grains, especially rye, barley, wheat, and oats. For the body of people with celiac disease, gluten is foreign, so immune cells begin to block it already in the stomach. But along with this protein, they also injure healthy cells of the surface layer of the mucosa.
- The development of this form of gastritis leads to infection of the mucous membrane of the stomach and duodenum with pathogenic microorganisms Helicobacter pylori. The proof of this theory is the specific changes in the tissues of the mucous membrane, typical for the bacterial form of the disease.
In addition, people whose menu is dominated by smoked, pickled, spicy, fried, fatty and salty foods, as well as those who are overly fond of alcoholic beverages and smoking, are at increased risk.
There are no special signs that testify specifically to lymphocytic gastritis. The disease can be completely asymptomatic, in other cases it manifests itself with signs similar to those of bacterial gastritis caused by Helicobacter pylori microorganisms. The main manifestation of the disease is epigastric pain, which appears in the morning on an empty stomach or 1 hour after eating.
Moreover, pain can be of a different nature.:
- pulling;
- aching;
- cramping:
- cutting;
- baker.
Moreover, most often the pain intensifies after eating coarse and hard food, which can quickly irritate the damaged mucosa. With gastritis with increased production of acid, pain is accompanied by nausea, heartburn and belching. A dense whitish coating forms on the tongue.
With lymphocytic gastritis with reduced acid secretion, patients are disturbed by a feeling of fullness in the stomach, rumbling and a feeling of transfusion in it, belching with a pungent heavy odor, flatulence, diarrhea or constipation. The tongue in this case is dry. If the condition of the patients worsens, they begin to vomit sour masses mixed with blood. If the disease lasts a long time, patients lose weight, but their appetite does not decrease.
Since the disease has no specific symptoms, it can only be confirmed in a person with the help of diagnostics.
For this, the following diagnostic procedures are prescribed:
- General blood analysis. It allows you to identify inflammation in the tissues by reducing the number of red blood cells and hemoglobin protein and increasing the ESR. They indicate the development of anemia as a result of the chronic course of the inflammatory process.
- An extended blood test. It makes it possible to more accurately detect deviations of metabolic processes from the norm.
- Fecal analysis to determine occult blood.
- Fibrogastroduodenoscopy. This is a method of visual examination of the esophagus, stomach and duodenum using a flexible optical probe. It allows you to examine the walls of the affected organs, and take a tissue sample for microbiological study.
- Histological examination. This method makes it possible to determine the degree of damage to the cells of inflamed tissues.
Fibrogastroduodenoscopy is the main and most informative method for diagnosing lymphocytic gastritis, therefore, it is on the basis of its results that conclusions are drawn about the presence or absence of the disease.
Features of tissue damage in lymphocytic gastritis
During an endoscopic examination, granular accumulations characteristic of this type of gastritis, which resemble papillae or small nodules, are found on the surface of the stomach affected by inflammation. Another typical sign of this disease is damage to the epithelium in the form of small erosions with necrotic tissues of their upper part.
The gastric mucosa in lymphocytic gastritis is pale, thickened and edematous, there is a large amount of mucus on the surface of the membrane. The gastric pits are elongated and dilated, pinpoint hemorrhages (small hemorrhages) and cysts (cavities with thin walls and semi-liquid contents) can form on the mucosal epithelium.
Treatment of lymphocytic gastritis
Therapy of the disease is carried out with the help of the following medicines:
- Histamine receptor blockers (Famotidine and Ranitidine).
- proton pump inhibitors (omeprazole, parieta).
- Antacids (Almagel, Gastala, Maalox).
- Means that have a protective effect on the mucous surface of the diseased organ (De-nol).
- Antibiotics, if Helicobacter pylori (Amoxicillin, Amoxiclav, Azithromycin and Clarithromycin) are found in the stomach cavity.
- Regulators of motility of the digestive system (Lactiol, Linaclotide, Motilium, Itomed).
- Enzyme drugs (Mezima, Festal, Panzinorm, Enzistal, Abomin).
- Combined drugs that combine antacid, antispasmodic, laxative and astringent effects (Rothera, Vikalina).
- Antiemetics (Cisapride, Cerucal, Domperidone).
The effectiveness of the treatment of lymphocytic gastritis depends on the degree of neglect of the disease, therefore, at the first suspicious symptoms, you should contact a gastroenterologist for an immediate examination and appropriate treatment.
Diet for lymphocytic gastritis
During the treatment of this type of gastritis, patients must follow a strict diet in order to reduce the activity of inflammation of the tissues of the stomach and accelerate the healing of erosions on its mucosa.
From the diet they need to exclude all foods containing a large amount of fiber, as well as too:
- sour;
- sharp;
- spicy;
- fried;
- salty
dishes, rich meat and fish broths, pastries. Do not drink carbonated drinks, fresh milk and coffee, alcohol of any strength. You need to eat cooked food in a warm form, not cold, but not hot. Meals should be fractional (up to 6 times during the day).
With lymphocytic gastritis, food should be boiled, baked, stewed or steamed and eaten grated, in a mushy or semi-solid form. You should also quit smoking, move more, and be outdoors more often.
Diseases of the gastrointestinal tract are of great variety. Some of them are primary independent diseases and constitute the content of a large section of medicine - gastroenterology, others develop secondarily in various diseases of an infectious and non-infectious, acquired and hereditary nature.
Changes in the gastrointestinal tract can be of an inflammatory, dystrophic, dysregenerative, hyperplastic and tumor nature. To understand the essence of these changes, the mechanism of their development and diagnosis, morphological study is of great importance. biopsy specimens the esophagus, stomach, intestines, obtained by biopsy, since in this case it becomes possible to use subtle research methods, such as histochemical, electron microscopic, radioautographic.
In this section, the most important diseases of the pharynx and pharynx, salivary glands, esophagus, stomach and intestines will be considered. Diseases of the dentoalveolar system and organs of the oral cavity are described separately (see.
Diseases of the throat and throat
Among diseases of the pharynx and pharynx, the most important is angina (from lat. angere- choke), or tonsillitis, - an infectious disease with pronounced inflammatory changes in the lymphadenoid tissue of the pharynx and palatine tonsils. This disease is widespread among the population and is especially common in the cold season.
Angina is divided into acute and chronic. Acute angina is of the greatest importance.
Etiology and pathogenesis. The occurrence of angina is associated with exposure to a variety of pathogens, among which staphylococcus aureus, streptococcus, adenoviruses, microbial associations are of primary importance.
In the mechanism of development of angina are involved as exogenous, so endogenous factors. Of paramount importance is an infection penetrating transepithelially or hematogenously, but more often it is an autoinfection provoked by general or local hypothermia, trauma. Of the endogenous factors, age-related features are of primary importance.
of the lymphadenoid apparatus of the pharynx and the reactivity of the body, which can explain the frequent occurrence of angina in older children and adults up to 35-40 years old, as well as rare cases of its development in young children and the elderly. plays an important role in the development of chronic tonsillitis. allergic factor.
Pathological anatomy. There are the following clinical and morphological forms acute angina: catarrhal, fibrinous, purulent, lacunar, follicular, necrotic and gangrenous.
At catarrhal angina the mucous membrane of the palatine tonsils and palatine arches is sharply plethoric or cyanotic, dull, covered with mucus. The exudate is serous or muco-leukocytic. Sometimes it lifts the epithelium and forms small vesicles with cloudy contents. Fibrinous angina manifested by the appearance of fibrinous white-yellow films on the surface of the mucous membrane of the tonsils. More often it diphtheria angina, which is usually observed in diphtheria. For purulent tonsillitis characterized by an increase in the size of the tonsils due to their swelling and infiltration by neutrophils. Purulent inflammation often has a diffuse character (quinsy), less often it is limited to a small area (abscess of the tonsil). Possible transition of the purulent process to adjacent tissues and dissemination of infection. Lacunar angina characterized by accumulation in the depths of lacunae of serous, mucous or purulent exudate with an admixture of desquamated epithelium. As exudate accumulates in the lacunae, it appears on the surface of the enlarged tonsil in the form of whitish-yellow films that are easily removed. At follicular angina the tonsils are large, full-blooded, the follicles are significantly enlarged in size, in the center of them areas of purulent fusion are determined. In the lymphoid tissue between the follicles, hyperplasia of the lymphoid elements and accumulations of neutrophils are noted. At necrotizing sore throat there is superficial or deep necrosis of the mucous membrane with the formation of defects with jagged edges (necrotic-ulcerative angina). In this regard, hemorrhages in the mucous membrane of the pharynx and tonsils are not uncommon. With gangrenous decay of the tonsil tissue, they speak of gangrenous angina. Necrotic and gangrenous tonsillitis are observed most often in scarlet fever, acute leukemia.
A special variety is ulcerative membranous angina of Simonovsky-Plaut-Vinsen, which is caused by a symbiosis of a spindle-shaped bacterium with ordinary spirochetes of the oral cavity. This angina is epidemic. The so-called septic angina, or angina with alimentary-toxic aleukia, arising after eating products from overwintered grain in the field. Special forms of angina include those that have unusual location: angina of the lingual, tubal or nasopharyngeal tonsils, tonsillitis of the lateral ridges, etc.
At chronic sore throat (chronic tonsillitis), which develops as a result of multiple relapses (recurrent tonsillitis), hyperplasia and sclerosis of the lymphoid tissue of the tonsils, sclerosis
capsules, expansion of lacunae, ulceration of the epithelium. Sometimes there is a sharp hyperplasia of the entire lymphoid apparatus of the pharynx and pharynx.
Changes in the pharynx and tonsils in both acute and chronic angina are accompanied by hyperplasia of the tissue of the lymph nodes of the neck.
Complications angina can be both local and general. Complications of a local nature are associated with the transition of the inflammatory process to the surrounding tissues and the development paratonsillar, or pharyngeal, abscess, phlegmonous inflammation of the tissue of the pharynx, thrombophlebitis. Among the complications of angina of a general nature, one should name sepsis. Angina is also involved in the development rheumatism, glomerulonephritis and other infectious-allergic diseases.
Diseases of the salivary glands
Most often, inflammatory processes are found in the salivary glands. Inflammation of the salivary glands is called sialadenitis, and the parotid glands mumps. Sialoadenitis and parotitis can be serous and purulent. They usually occur secondary to infection by the hematogenous, lymphogenous or intraductal route.
A special type of sialadenitis with destruction of the glands by cellular lymphomacrophage infiltrate is characteristic of dry syndrome (disease or Sjögren's syndrome).
Dry syndrome is a syndrome of insufficiency of exocrine glands, combined with polyarthritis. Among the etiological factors, the role of viral infection and genetic predisposition is most likely. The basis of pathogenesis is autoimmunization, and dry syndrome is combined with many autoimmune (rheumatoid arthritis, struma Hashimoto) and viral (viral chronic active hepatitis) diseases. Some authors classify Sjögren's dry syndrome as a rheumatic disease.
Independent diseases of the salivary glands are parotitis, caused by myxovirus cytomegaly, the causative agent of which is the cytomegaly virus, as well as tumors(see also Diseases of the dentoalveolar system and organs of the oral cavity).
Diseases of the esophagus
Diseases of the esophagus few. The most common are diverticula, inflammation (esophagitis), and tumors (cancer).
Esophageal diverticulum- this is a limited blind protrusion of its wall, which can consist of all layers of the esophagus (true diverticulum) or only the mucous and submucosal layers, protruding through the gaps of the muscle layer (muscular diverticulum). Depending on the localization and topography distinguish between pharyngoesophageal, bifurcation, epinephric and multiple diverticula, and from origin features - Adhesive diverticula resulting from
inflammatory processes in the mediastinum, and relaxation, which are based on local relaxation of the esophageal wall. Diverticulum of the esophagus can be complicated by inflammation of its mucous membrane - diverticulitis.
Causes of diverticulum formation can be congenital (inferiority of connective and muscular tissues of the wall of the esophagus, pharynx) and acquired (inflammation, sclerosis, cicatricial narrowing, increased pressure inside the esophagus).
Esophagitis- inflammation of the mucous membrane of the esophagus - usually develops secondary to many diseases, rarely - primary. It is either acute or chronic.
acute esophagitis, observed when exposed to chemical, thermal and mechanical factors, with a number of infectious diseases (diphtheria, scarlet fever, typhoid), allergic reactions, may be catarrhal, fibrinous, phlegmonous, ulcerative, gangrenous. A special form of acute esophagitis is membranous, when there is a rejection of the cast of the mucous membrane of the esophagus. After deep membranous esophagitis, which develops with chemical burns, cicatricial stenosis of the esophagus.
At chronic esophagitis, the development of which is associated with chronic irritation of the esophagus (the effect of alcohol, smoking, hot food) or circulatory disorders in its wall (venous congestion in cardiac decompensation, portal hypertension), the mucous membrane is hyperemic and edematous, with areas of epithelial destruction, leukoplakia and sclerosis. For specific chronic esophagitis, found in tuberculosis and syphilis, the morphological picture of the corresponding inflammation is characteristic.
In a special form allocate reflux esophagitis, in which inflammation, erosion and ulcers are found (erosive, ulcerative esophagitis) in the mucous membrane of the lower esophagus due to regurgitation of gastric contents into it (regurgitation, peptic esophagitis).
Esophageal carcinoma most often occurs at the border of the middle and lower thirds of it, which corresponds to the level of tracheal bifurcation. Much less often, it occurs in the initial part of the esophagus and at the entrance to the stomach. Esophageal cancer accounts for 2-5% of all malignant neoplasms.
Etiology. Predispose to the development of cancer of the esophagus chronic irritation of its mucous membrane (hot coarse food, alcohol, smoking), cicatricial changes after burns, chronic gastrointestinal infections, anatomical disorders (diverticula, ectopia of the columnar epithelium and gastric glands, etc.). Among precancerous changes, leukoplakia and severe dysplasia of the mucosal epithelium are of the greatest importance.
Pathological anatomy. There are the following macroscopic forms of cancer of the esophagus: annular dense, papillary and ulcerated. Annular solid cancer is a tumor
ion, which circularly covers the wall of the esophagus in a certain area. The lumen of the esophagus is narrowed. With the collapse and ulceration of the tumor, the patency of the esophagus is restored. papillary cancer the esophagus is similar to mushroom-shaped stomach cancer. It easily breaks down, resulting in ulcers that penetrate into neighboring organs and tissues. ulcerated cancer is a cancerous ulcer that is oval in shape and extends along the esophagus.
Among microscopic types of esophageal cancer carcinoma in situ, squamous cell carcinoma, adenocarcinoma, squamous cell carcinoma, glandular cystic, mucoepidermal and undifferentiated cancer.
Metastasis esophageal cancer is predominantly lymphogenous.
Complications are associated with germination in neighboring organs - the trachea, stomach, mediastinum, pleura. Esophageal-tracheal fistulas are formed, aspiration pneumonia, abscess and gangrene of the lung, pleural empyema, purulent mediastinitis develop. In cancer of the esophagus, cachexia appears early.
Diseases of the stomach
Among diseases of the stomach, gastritis, peptic ulcer and cancer are of the greatest importance.
Gastritis
Gastritis(from Greek. gaster- stomach) - an inflammatory disease of the gastric mucosa. There are acute and chronic gastritis.
Acute gastritis
Etiology and pathogenesis. In the development of acute gastritis, the role of irritation of the mucous membrane with abundant, indigestible, spicy, cold or hot food, alcoholic beverages, drugs (salicylates, sulfonamides, corticosteroids, biomycin, digitalis, etc.), chemicals (occupational hazards) is important. Microbes (staphylococcus, salmonella) and toxins, products of disturbed metabolism also play a significant role. In some cases, for example, in case of alcohol poisoning, poor-quality food products, pathogenic factors directly affect the gastric mucosa - exogenous gastritis, in others, this action is indirect and is carried out with the help of vascular, nervous, humoral and immune mechanisms - endogenous gastritis, which include infectious hematogenous gastritis, eliminative gastritis with uremia, allergic, congestive gastritis, etc.
Pathological anatomy. Inflammation of the mucous membrane can cover the entire stomach (diffuse gastritis) or certain departments (focal gastritis). In this regard, distinguish fundic, antral, pyloroanthral and pyloroduodenal gastritis.
Depending on the features morphological changes gastric mucosa distinguish the following forms of acute gastritis: 1) catarrhal (simple); 2) fibrinous; 3) purulent (phlegmous); 4) necrotic (corrosive).
At catarrhal (simple) gastritis the mucous membrane of the stomach is thickened, edematous, hyperemic, its surface is abundantly covered with mucous masses, multiple small hemorrhages and erosions are visible. Microscopic examination reveals dystrophy, necrobiosis and desquamation of the surface epithelium, the cells of which are characterized by increased mucus formation. Desquamation of cells leads to erosion. In cases where there are multiple erosions, they talk about erosive gastritis. The glands change slightly, but their secretory activity is suppressed. The mucous membrane is permeated with serous, serous-mucous or serous-leukocyte exudate. Its own layer is plethoric and edematous, infiltrated with neutrophils, diapedetic hemorrhages occur.
At fibrinous gastritis a fibrinous film of gray or yellow-brown color is formed on the surface of the thickened mucous membrane. The depth of necrosis of the mucous membrane in this case can be different, and therefore they are isolated croupous(superficial necrosis) and diphtheric(deep necrosis) options fibrinous gastritis.
At purulent, or phlegmonous, gastritis, the wall of the stomach becomes sharply thickened, especially due to the mucous membrane and submucosal layer. The folds of the mucous membrane are rough, with hemorrhages, fibrinous-purulent overlays. A yellow-green purulent liquid flows from the surface of the incision. Leukocyte infiltrate, containing a large number of microbes, diffusely covers the mucous membrane, submucosal and muscular layers of the stomach and the peritoneum covering it. Therefore, often with phlegmonous gastritis develop perigastritis and peritonitis. Phlegmon of the stomach sometimes complicates its injury, it also develops in chronic ulcers and ulcerated stomach cancer.
Necrotizing gastritis usually occurs when chemicals (alkalis, acids, etc.) enter the stomach, cauterizing and destroying the mucous membrane (corrosive gastritis). Necrosis can cover the superficial or deep sections of the mucous membrane, be coagulative or coagulative. Necrotic changes usually end with the formation of erosions and acute ulcers, which can lead to the development of phlegmon and gastric perforation.
Exodus acute gastritis depends on the depth of the lesion of the mucous membrane (wall) of the stomach. Catarrhal gastritis can result in complete restoration of the mucous membrane. With frequent relapses, it can lead to the development of chronic gastritis. After significant destructive changes characteristic of phlegmonous and necrotic gastritis, atrophy of the mucous membrane and sclerotic deformation of the stomach wall - cirrhosis of the stomach develops.
Chronic gastritis
In some cases, it is associated with acute gastritis, its relapses, but more often this connection is absent.
Classification of chronic gastritis, adopted by the IX International Congress of Gastroenterologists (1990), takes into account the etiology, pathogenesis, topography of the process, morphological types of gastritis, signs of its activity, severity.
Etiology. Chronic gastritis develops under the action on the gastric mucosa primarily exogenous factors: violation of the diet and rhythm of nutrition, alcohol abuse, the action of chemical, thermal and mechanical agents, the impact of occupational hazards, etc. great role and endogenous factors - autoinfections (Campylobacter piloridis), chronic autointoxication, neuroendocrine disorders, chronic cardiovascular insufficiency, allergic reactions, regurgitation of duodenal contents into the stomach (reflux). An important condition for the development of chronic gastritis is prolonged exposure pathogenic factors of exogenous or endogenous nature, capable of "breaking" the usual regenerative mechanisms of constant renewal of the epithelium of the gastric mucosa. It is often possible to prove the long-term influence of not one, but several pathogenic factors.
Pathogenesis. Chronic gastritis can be autoimmune (type A gastritis) or non-immune (type B gastritis).
autoimmune gastritis characterized by the presence of antibodies to parietal cells, and therefore the defeat of the fundus of the stomach, where there are many parietal cells (fundic gastritis). The mucous membrane of the antrum is intact. There is a high level of gastrinemia. In connection with the defeat of the parietal cells, the secretion of hydrochloric (hydrochloric) acid is reduced.
At non-immune gastritis antibodies to parietal cells are not detected, so the fundus of the stomach is relatively preserved. The main changes are localized in the antrum (antral gastritis). Gastrinemia is absent, secretion of hydrochloric acid is reduced only moderately. Type B gastritis is distinguished reflux gastritis(gastritis type C). Type B gastritis is 4 times more common than type A gastritis.
Guided process topography stomach, secrete chronic gastritis - antral, fundic and pangastritis.
Morphological types. Chronic gastritis is characterized by long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane, as a result of which there is a violation of its regeneration and structural restructuring of the mucous membrane, culminating in its atrophy and sclerosis; cellular reactions of the mucous membrane reflect the activity of the process. There are two morphological types of chronic gastritis - superficial and atrophic.
Chronic superficial gastritis characterized by dystrophic changes in the surface (pit) epithelium. In some areas, it flattens, approaches the cubic and is characterized by reduced secretion, in others it is high prismatic with increased secretion. There is a translocation of additional cells from the isthmus to the middle third of the glands, the histamine-stimulated secretion of hydrochloric acid by parietal cells and pepsinogen by the main cells decreases. Own layer (lamina) of the mucous membrane is edematous, infiltrated with lymphocytes, plasma cells, single neutrophils (Fig. 197).
At chronic atrophic gastritis a new and basic quality appears - atrophy of the mucous membrane, its glands, which determines the development of sclerosis. The mucous membrane becomes thinner, the number of glands decreases. Connective tissue grows in place of the atrophied glands. The surviving glands are located in groups, the ducts of the glands are dilated, certain types of cells in the glands are poorly differentiated. In connection with the mucoidization of the glands, the secretion of pepsin and hydrochloric acid is disturbed. The mucous membrane is infiltrated with lymphocytes, plasma cells, single neutrophils. Added to these changes remodeling of the epithelium moreover, both superficial and glandular epithelium undergoes metaplasia (see Fig. 197). The gastric folds resemble intestinal villi, they are lined with bordered epithelial cells, goblet cells and Paneth cells appear (intestinal metaplasia of the epithelium, "enterolization" of the mucous membrane). The main, additional (mucous cells of the glands) and parietal cells of the glands disappear, cubic cells appear, characteristic of the pyloric glands; so-called pseudopyloric glands are formed. It joins the metaplasia of the epithelium dysplasia, the degree of which may vary. Mucosal changes may be mild (moderate atrophic gastritis) or pronounced (pronounced atrophic gastritis).
The so-called giant hypertrophic gastritis, or sickness Menetrie, in which there is an extremely sharp thickening of the mucous membrane, which takes on the appearance of a cobblestone pavement. Morphologically, proliferation of cells of the glandular epithelium and hyperplasia of the glands, as well as infiltration of the mucous membrane with lymphocytes, epithelioid, plasma and giant cells are found. Depending on the predominance of changes in the glands or interstitium, the severity of proliferative changes is isolated glandular, interstitial and proliferative variants this disease.
Signs of activity of chronic gastritis allow to allocate active (exacerbation) and inactive (remission) chronic gastritis. Exacerbation of chronic gastritis is characterized by edema of the stroma, plethora of blood vessels, but cell infiltration is especially pronounced with the presence of a large number of neutrophils in the infiltrate; sometimes crypt abscesses and erosions appear. In remission, these signs are absent.
Rice. 197. Chronic gastritis (gastrobiopsy):
a - chronic superficial gastritis; b - chronic atrophic gastritis
Severity chronic gastritis can be mild, moderate or severe.
Thus, chronic gastritis is based on both inflammatory and adaptive-reparative processes of the gastric mucosa with imperfect regeneration of the epithelium and metaplastic restructuring of its "profile".
The perversion of the regeneration of the epithelium of the mucous membrane in chronic gastritis is confirmed by the data of an electron microscopic study on the material of gastrobiopsies. It has been established that undifferentiated cells, which normally occupy the deep sections of the gastric pits and the neck of the glands, appear on the gastric folds, in the area of the body and bottom of the glands in chronic gastritis. Immature cells show signs of premature involution. This indicates a deep violation of the coordination of the phases of proliferation and differentiation of the epithelium of the glands during the regeneration of the gastric mucosa, which leads to cellular atypia, the development of dysplastic processes.
Due to the fact that in chronic gastritis, violations of the processes of regeneration and structure formation are pronounced, leading to cellular atypia (dysplasia), it often becomes the background against which it develops. stomach cancer.
Meaning chronic gastritis is extremely high. It ranks second in the structure of gastroenterological diseases. It is also important to note that chronic atrophic gastritis with severe epithelial dysplasia is precancerous disease stomach.
peptic ulcer
peptic ulcer- a chronic, cyclically current disease, the main clinical and morphological expression of which is a recurrent gastric or duodenal ulcer. Depending on the localization of the ulcer and the characteristics of the pathogenesis of the disease, peptic ulcer is distinguished with localization of the ulcer in pyloroduodenal zone or body of the stomach although there are also combined forms.
In addition to ulcers as manifestations of gastric and duodenal ulcers, there are so-called symptomatic ulcers, those. ulceration of the stomach and duodenum, occurring in various diseases. These are the ulcers observed in endocrine diseases. (endocrine ulcers with parathyroidism, thyrotoxicosis, Ellison-Zollinger syndrome), with acute and chronic circulatory disorders (dyscirculatory-hypoxic ulcers), with exogenous and endogenous intoxications (toxic ulcers) allergies (allergic ulcers), specific inflammation (tuberculous, syphilitic ulcers), after operations on the stomach and intestines (postoperative peptic ulcers), as a result of medical treatment (drug ulcers, for example, in the treatment of corticosteroids, acetylsalicylic acid).
Peptic ulcer is a widespread disease that occurs more often in the urban population, especially in men. In the pyloroduodenal zone, an ulcer occurs more often than in the body of the stomach. Peptic ulcer is a purely human suffering, in the development of which stressful situations play the main role, which explains the increase in the incidence of peptic ulcer in the 20th century in all countries of the world.
Etiology. In the development of peptic ulcer are of primary importance stressful situations, psycho-emotional overstrain, leading to the disintegration of those functions of the cerebral cortex that regulate the secretion and motility of the gastroduodenal system (cortico-visceral disorders). The same processes of disintegration can develop in the cerebral cortex when pathological impulses are received from organs in which pathological changes appear (viscero-cortical disorders). neurogenic theory peptic ulcer can be considered sufficiently substantiated, but it does not allow to explain the occurrence of the disease in all cases. plays an important role in the development of peptic ulcer nutritional factors(violation of the mode and nature of nutrition), bad habits(smoking, and alcohol abuse), exposure to a number of medicines(acetylsalicylic acid, indomethacin, corticosteroids, etc.). Of unconditional importance are hereditary-constitutional (genetic) factors, among them O (I) blood type, positive Rh factor, “non-secretory status” (lack of histocompatibility antigens responsible for the production of gastric mucus glycoproteins), etc. Recently, the occurrence of peptic ulcer has been associated with infectious agent- campylobacter piloridis, which is detected in duodenal ulcers in 90%, and stomach ulcers in 70-80% of cases.
Pathogenesis. It is complex and closely related to etiological factors. Not all aspects of it can be considered sufficiently studied. Among pathogenetic factors peptic ulcers are divided into general and local. The general ones are represented by disorders of the nervous and hormonal regulation of the activity of the stomach and duodenum, and local - disorders of the acid-peptic factor, mucosal barrier, motility and morphological changes in the mucous membrane of the stomach and duodenum.
Meaning neurogenic factors huge. As already mentioned, under the influence of external (stress) or internal (visceral pathology) causes, change in the coordinating function of the cerebral cortex in relation to subcortical formations (midbrain, hypothalamus). This leads in some cases (ulcer of the pyloroduodenal zone) to excitation of the hypothalamic-pituitary region, vagus nerve centers and increased tone of the nerve itself, increased activity of the acid-peptic factor and increased gastric motility. In other cases (an ulcer of the body of the stomach), on the contrary, there is a suppression of the function of the hypothalamic-pituitary region by the cortex, a decrease in the tone of the vagus nerve and inhibition of motility; while the activity of the acid-peptic factor is normal or reduced.
Among hormonal factors in the pathogenesis of peptic ulcer, the main role is played by disorders in the hypothalamic-pituitary-adrenal system in the form of an increase, and in the subsequent depletion of the production of ACTH and glucocorticoids, which increase the activity of the vagus nerve and acid-peptic factor.
These violations of hormonal regulation are clearly expressed only in peptic ulcer of the pyloroduodenal zone. With peptic ulcer of the body of the stomach, the production of ACTH and glucocorticoids is reduced, therefore, the role of local factors increases.
Local factors to a large extent, they realize the transformation of an acute ulcer into a chronic one and determine exacerbations, relapses of the disease. With an ulcer of the pyloroduodenal zone, an increase in activity is of great importance. acid-peptic factor, which is associated with an increase in the number of gastrin-producing cells, increased secretion of gastrin and histamine. In these cases, aggression factors (acid-peptic activity) prevail over mucosal defense factors (mucosal barrier), which determines the development or exacerbation of peptic ulcer. With an ulcer of the body of the stomach with normal or reduced activity of the acid-peptic factor and depressed motility, the mucous barrier suffers as a result of diffusion into the gastric wall of hydrogen ions (theory of back diffusion of hydrogen ions), which determines the release of histamine by mast cells, dyscirculatory disorders (blood shunting) and violations of tissue trophism. Morphological changes in the mucous membrane of the stomach and duodenum are presented, respectively, by the picture chronic gastritis and chronic duodenitis. Mucosal damage is also likely to be involved Campylobacter piloridis.
Thus, the significance of various factors in the pathogenesis of peptic ulcer with different localization of the ulcer (pyloroduodenal zone, body of the stomach) is not the same (Table 12). In peptic ulcer of the pyloroduodenal zone, the role of vagal-gastrin influences and an increase in the activity of the acid-peptic factor is great. In peptic ulcer of the body of the stomach, when the vagal-gastrinic influences, as well as the activation of the acid-peptic factor, are less pronounced, circulatory disorders and trophic disorders in the gastric wall become the most important, which creates conditions for the formation of a peptic ulcer.
Pathological anatomy. The morphological substrate of peptic ulcer is chronic recurrent ulcer. In the course of formation, it goes through the stages erosion and acute ulcer, which allows us to consider erosion, acute and chronic ulcers as stages morphogenesis peptic ulcer. These stages are especially well observed in gastric ulcer.
erosion called mucosal defects that do not penetrate the muscularis mucosa. Erosion is usually sharp, in rare cases - chronic. Acute erosions are usually superficial and are formed as a result of necrosis of an area of the mucous membrane, followed by hemorrhage and rejection of dead tissue. Hydrochloric acid hematin is found in the bottom of such erosion, and leukocyte infiltrate is found in its edges.
Table 12 Pathogenetic features of peptic ulcer depending on the localization of the ulcer
AT stomach multiple erosions may occur, which are usually easily epithelialized. However, in cases of peptic ulcer development, some erosions do not heal; not only the mucous membrane is subject to necrosis, but also the deeper layers of the stomach wall, develop acute peptic ulcers. They have an irregular round or oval shape. As the necrotic masses are cleared, the bottom of an acute ulcer is revealed, which is formed by a muscular layer, sometimes a serous membrane. Often the bottom is painted dirty gray or black due to the admixture of hematin hydrochloride. Deep defects of the mucous membrane often acquire a funnel-shaped shape, with the base of the funnel facing the mucous membrane, and the top - to the serous cover.
Acute stomach ulcers usually appear on the lesser curvature, in the antrum and pyloric sections, which is explained by the structural and functional features of these sections. It is known that the lesser curvature is a “food path” and therefore is easily injured, the glands of its mucous membrane secrete the most active gastric juice, the wall is richest in receptor devices and the most reactive, but the folds are rigid and when the muscle layer is reduced, they are not able to close the defect. These features are also associated with poor healing of an acute ulcer of this localization and its transition to a chronic one. Therefore, a chronic stomach ulcer is more often localized in the same place as an acute one, i.e. on the lesser curvature, in the antrum and pyloric regions; cardiac and subcardial ulcers are rare.
Chronic stomach ulcer is usually single, multiple ulcers are rare. The ulcer is oval or round (ulcus rotundum) and sizes from a few millimeters to 5-6 cm. It penetrates the stomach wall to various depths, sometimes reaching the serous layer. The bottom of the ulcer is smooth, sometimes rough; callus- corn; rice. 198). The edge of the ulcer facing the esophagus is undermined, and the mucous membrane hangs over the defect. The edge facing the pylorus is gentle (see Fig. 198), sometimes it looks like a terrace, the steps of which are formed by layers of the wall - the mucous membrane, submucosal and muscle layers. This type of edges is explained by the displacement of the layers during the peristalsis of the stomach. On a transverse section, a chronic ulcer has the shape of a truncated pyramid,
Rice. 198. Chronic stomach ulcer:
a - General view of a chronic ulcer penetrating into the head of the pancreas; b - callous ulcer of the stomach (histotopographic section); the bottom and edges of the ulcer are represented by fibrous tissue, the cardiac edge of the ulcer is undermined, and the pyloric edge is gently sloping
the narrow end of which faces the esophagus. The serous membrane in the area of the ulcer is thickened, often soldered to adjacent organs - the liver, pancreas, omentum, transverse colon.
Microscopic picture chronic gastric ulcer in different periods of the course of peptic ulcer disease is different. AT remission period scar tissue is found in the edges of the ulcer. The mucous membrane along the edges is thickened, hyperplastic. In the bottom area, the destroyed muscle layer and the scar tissue replacing it are visible, and the bottom of the ulcer can be covered with a thin layer of epithelium. Here, in the scar tissue, there are many vessels (arteries, veins) with thickened walls. In many vessels, the lumen is narrowed or obliterated due to proliferation of intimal cells (endovasculitis) or proliferation of connective tissue. Nerve fibers and ganglion cells undergo dystrophic changes and decay. Sometimes in the bottom of the ulcer among the scar tissue there is an overgrowth of nerve fibers by the type of amputation neuromas.
AT period of exacerbation peptic ulcer in the area of the bottom and edges of the ulcer appears a wide area fibrinoid necrosis. On the surface of necrotic masses is located fibrinous-purulent or purulent exudate. The area of necrosis is delimited granulation tissue with a large number of thin-walled vessels and cells, among which there are many eosinophils. Deeper after the granulation tissue is located coarse fibrous scar tissue. The exacerbation of the ulcer is evidenced not only by exudative-necrotic changes, but also fibrinoid changes in the walls of blood vessels, often with blood clots in their gaps, as well as mucoid and fibrinoid swelling of scar tissue at the bottom of the ulcer. In connection with these changes, the size of the ulcer increases, it becomes possible to destroy the entire wall of the stomach, which can lead to serious complications. In cases where exacerbation is followed by remission (healing ulcer) inflammatory changes subside, the necrosis zone grows into granulation tissue, which matures into coarse fibrous scar tissue; epithelialization of the ulcer is often observed. As a result of fibrinoid changes in blood vessels and endarteritis, sclerosis of the wall and obliteration of the lumen of the vessels develop. Thus, exacerbation of peptic ulcer, even in cases of a favorable outcome, leads to increased cicatricial changes in the stomach and exacerbates the violation of the trophism of its tissues, including the newly formed scar tissue, which is easily destroyed during the next exacerbation of peptic ulcer.
Morphogenesis and pathological anatomy of a chronic ulcer duodenum do not fundamentally differ from those in chronic gastric ulcers.
Chronic duodenal ulcer in the vast majority of cases is formed on the anterior or posterior wall of the bulb (bulbar ulcer); only in 10% of cases it is localized below the bulb (postbulbar ulcer). Multiple ulcers are common
duodenum, they are located opposite each other along the anterior and posterior walls of the bulb (kissing ulcers).
Complications. Among the complications of chronic ulcers in peptic ulcer disease, there are (Samsonov V.A., 1975): 1) ulcerative-destructive (bleeding, perforation, penetration); 2) inflammatory (gastritis, duodenitis, perigastritis, periduodenitis); 3) ulcerative-cicatricial (narrowing of the inlet and outlet sections of the stomach, deformation of the stomach, narrowing of the lumen of the duodenum, deformation of its bulb); 4) malignancy of the ulcer (development of cancer from the ulcer); 5) combined complications.
Bleeding- one of the frequent and dangerous complications of peptic ulcer. There is no relationship between the frequency of bleeding and the localization of the ulcer in the stomach; when the ulcer is localized in the duodenum, bleeding is more often caused by ulcers located in the back wall of the bulb. Bleeding occurs due to erosion of the walls of blood vessels - arrosive bleeding, therefore, it occurs, as a rule, during an exacerbation of peptic ulcer.
perforation(perforation) is also usually observed during an exacerbation of peptic ulcer. Pyloric ulcers of the stomach or ulcers of the anterior wall of the duodenal bulb are more often perforated. Perforation of the ulcer leads to peritonitis. Initially, inflammation in the form of fibrinous overlays on the peritoneum appears only in the region of the perforation, then it spreads and becomes not fibrinous, but fibrinous-purulent. In the presence of adhesions, perforation may only lead to limited peritonitis. Chronic peritonitis is rare. Then the masses of gastric contents are encapsulated, on the peritoneum and in the omentum are formed foreign body granulomas. In rare cases, when the perforation is covered by the liver, omentum, pancreas, or rapidly appearing fibrin overlays, one speaks of covered perforation.
penetration ulcers are called its penetration beyond the wall of the stomach or duodenum into neighboring organs. Ulcers of the posterior wall of the stomach and the posterior wall of the duodenal bulb usually penetrate, and more often into the lesser omentum, head and body of the pancreas (see Fig. 198), into the hepatoduodenal ligament, less often into the liver, transverse colon, gallbladder. Penetration of a stomach ulcer in some cases leads to the digestion of an organ, such as the pancreas.
Complications of an inflammatory nature include periulcerous gastritis and duodenitis, perigastritis and periduodenitis, resulting in the formation of adhesions with neighboring organs. Rarely, gastric ulcer worsens phlegmon.
Severe ulcer complications are due to cicatricial stenosis gatekeeper. The stomach expands, food masses are retained in it, vomiting often occurs. This can lead to dehydration of the body, depletion of chlorides and the development chlorohydropenic uremia(gastric
tania). Sometimes the scar constricts the stomach in the middle part and divides it into two halves, giving the stomach an hourglass shape. In the duodenum, only ulcers of the posterior wall of the bulb lead to cicatricial stenosis and deformation.
Malignization(malignancy) of chronic gastric ulcer occurs in 3-5% of cases; the transition of a chronic duodenal ulcer to cancer is an extremely rare occurrence. Among combined complications the most common are perforation and bleeding, bleeding and penetration.
Stomach cancer
Stomach cancer in terms of morbidity and mortality, since 1981, it has ranked second among cancerous tumors. Over the past 50 years in many countries of the world there has been a decrease in the incidence of stomach cancer. The same trend was observed in the USSR: for 1970-1980. the incidence of stomach cancer decreased in men by 3.9%, in women - by 6.9%. Stomach cancer is more common in men between the ages of 40 and 70. It accounts for about 25% of cancer deaths.
Etiology. In the experiment, with the help of various carcinogenic substances (benzpyrene, methylcholanthrene, cholesterol, etc.), it was possible to obtain stomach cancer. It is shown that as a result of exposure exogenous carcinogens there is usually cancer of the stomach "intestinal" type. The development of cancer of the "diffuse" type is largely associated with the individual genetic characteristics of the organism. important role in the development of stomach cancer precancerous conditions(diseases in which the risk of developing cancer is increased) and precancerous changes(histological "abnormality" of the gastric mucosa). Precancerous conditions of the stomach include chronic atrophic gastritis, pernicious anemia(with it constantly developing atrophic gastritis), chronic stomach ulcer, adenomas (adenomatous polyps) of the stomach, stomach stump(consequences of resection of the stomach and gastroenterostomy), Menetrier's disease. The "malignant potential" of each of the precancerous conditions is different, but in sum, they increase the likelihood of gastric cancer by 90-100% compared with the general population. Precancerous changes in the gastric mucosa include intestinal metaplasia and severe dysplasia.
Morphogenesis and histogenesis gastric cancer are not well understood. The restructuring of the gastric mucosa, observed in precancerous conditions, is of unconditional importance for the development of a tumor. This restructuring is also preserved in cancer, which allows us to speak of the so-called background, or profile, cancerous stomach.
The morphogenesis of gastric cancer finds a definite explanation in dysplasia and intestinal metaplasia of the epithelium of the gastric mucosa.
Dysplasia of the epithelium called the replacement of a part of the epithelial layer with proliferating undifferentiated cells with varying degrees of atypism. There are several degrees of mucosal dysplasia
membranes of the stomach, with a severe degree of dysplasia close to non-invasive cancer (cancer in situ). It is believed that depending on the predominance of dysplastic processes in the integumentary pit epithelium or in the epithelium of the gland necks, cancer of a different histological structure and different differentiation occurs.
intestinal metaplasia The epithelium of the gastric mucosa is considered as one of the main risk factors for gastric cancer, the importance of incomplete intestinal metaplasia with the secretion of sulfomucins by cells, which are capable of absorbing mutant carcinogens, is especially high. In the foci of intestinal metaplasia, dysplastic changes appear, the antigenic properties of cells change (a cancer embryonic antigen appears), which indicates a decrease in the level of cell differentiation.
Thus, in the morphogenesis of gastric cancer, an important role is played by dysplasia as non-metaplastic(pit, cervical), and metaplastic epithelium(intestinal type). However, the possibility of developing gastric cancer de novo, those. without previous dysplastic and metaplastic changes.
Histogenesis different histological types of gastric cancer, probably common. The tumor originates from single source - cambial elements and progenitor cells in the foci of dysplasia and outside them.
Classification. Clinical and anatomical classification of gastric cancer takes into account the localization of the tumor, the nature of its growth, the macroscopic form of cancer and the histological type.
Depending on the localization Cancer in a particular part of the stomach is divided into 6 types: pyloric(50%), less curvature of the body with the transition to the walls(27%), cardiac(15%), greater curvature(3%), fundamental(2%) and total(3%). Multicentric gastric cancer is rare. As can be seen, in 3/4 of cases, cancer is localized in the pyloric region and on the lesser curvature of the stomach, which is of undoubted diagnostic value.
Depending on the growth patterns allocate the following clinical and anatomical forms of stomach cancer (Serov VV, 1970).
1. Cancer with predominantly exophytic expansive growth: 1) plaque-like cancer; 2) polyposis cancer (including those developed from an adenomatous polyp of the stomach); 3) fungous (mushroom) cancer; 4) ulcerated cancer (malignant ulcers); a) primary ulcerative gastric cancer; b) saucer-shaped cancer (cancer-ulcer); c) cancer from a chronic ulcer (ulcer-cancer).
2. Cancer with predominantly endophytic infiltrating growth: 1) infiltrative-ulcerative cancer; 2) diffuse cancer (with limited or total damage to the stomach).
3. Cancer with exoendophytic, mixed, growth patterns: transitional forms.
According to this classification, the forms of gastric cancer are simultaneously phases of cancer development, which makes it possible to identify certain
options for the development of gastric cancer with a change in forms - phases in time, depending on the predominance of exophytic or endophytic character.
Guided by the features of the microscopic structure, the following histological types of gastric cancer are distinguished: adenocarcinoma(tubular, papillary, mucinous), undifferentiated(solid, scirrhous, cricoid), squamous, glandular squamous(adenocancroid) and unclassified cancer.
Pathological anatomy. Plaque-like cancer (flattened, superficial, creeping) occurs in 1-5% of cases of gastric cancer and is the rarest form. The tumor is found more often in the pyloric region, on the lesser or greater curvature in the form of a small, 2-3 cm long, plaque-like thickening of the mucous membrane (Fig. 199). The mobility of the folds of the mucous membrane in this place is somewhat limited, although the tumor rarely grows into the submucosal layer. Histologically, plaque-like cancer usually has the structure of adenocarcinoma, less often - undifferentiated cancer.
Polyposis cancer accounts for 5% of cases of gastric carcinoma. It has the appearance of a node with a villous surface 2-3 cm in diameter, which is located on the leg (see Fig. 199). Tumor tissue is grey-pinkish or
Rice. 199. Forms of stomach cancer:
a - plaque-like; b - polyposis; c - mushroom-shaped; g - diffuse
gray-red, rich in blood vessels. Sometimes polyposis cancer develops from an adenomatous polyp of the stomach, but more often it represents the next phase of exophytic growth of plaque-like cancer. Microscopic examination often reveals adenocarcinoma, sometimes undifferentiated cancer.
Fungous (mushroom) cancer occurs in 10% of cases. Like polyposis cancer, it looks like a nodular, tuberous (less often with a smooth surface) formation, sitting on a short, wide base (see Fig. 199). Erosions, hemorrhages, or fibrinous-purulent overlays are often found on the surface of the tumor node. The tumor is soft, gray-pink or gray-red, well demarcated. Fungal cancer can be considered as a phase of exophytic growth of polyposis cancer, therefore, in histological examination, it is represented by the same types of carcinoma as polyposis.
ulcerated cancer occurs very often (more than 50% of cases of gastric cancer). It combines malignant gastric ulcers of various genesis, which include primary ulcerative cancer, saucer-shaped cancer (cancer-ulcer) and cancer from a chronic ulcer (cancer-cancer).
Primary ulcerative cancer stomach (Fig. 200) is little studied. It is rarely found. This form includes exophytic cancer with ulceration in
at the very beginning of its development (plaque-like cancer), the formation of an acute and then a chronic cancerous ulcer, which is difficult to distinguish from a cancerous ulcer. Microscopic examination often reveals undifferentiated cancer.
Saucer-shaped cancer(cancer-ulcer) - one of the most common forms of stomach cancer (see Fig. 200). Occurs with ulceration of an exophytically growing tumor (polypous or fungal cancer) and is a rounded formation, sometimes reaching large sizes, with roller-like whitish edges and ulceration in the center. The bottom of the ulcer may be adjacent organs into which the tumor grows. Histologically, it is more often represented by adenocarcinoma, less often by undifferentiated cancer.
Cancer ulcer develops from a chronic stomach ulcer (see Fig. 200), so it occurs where a chronic ulcer is usually localized, i.e. on a small curvature. Signs of a chronic ulcer distinguish cancer ulcer from saucer-shaped cancer: extensive proliferation of scar tissue, sclerosis and thrombosis of blood vessels, destruction of the muscle layer in the cicatricial bottom of the ulcer, and, finally, thickening of the mucous membrane around the ulcer. These signs remain with the malignancy of a chronic ulcer. Of particular importance is the fact that in case of saucer-shaped cancer, the muscle layer is preserved, although it is infiltrated by tumor cells, and in case of ulcer cancer, it is destroyed by scar tissue. The tumor grows predominantly exophytically in one of the edges of the ulcer or along its entire circumference. More often it has the histological structure of adenocarcinoma, less often - undifferentiated cancer.
Infiltrative-ulcerative cancer found in the stomach quite often. This form is characterized by pronounced cancrotic infiltration of the wall and ulceration of the tumor, which can compete in time sequence: in some cases it is late ulceration of massive endophytic carcinomas, in others it is endophytic growth of the tumor from the edges of the malignant ulcer. Therefore, the morphology of infiltrative-ulcerative cancer is unusually diverse - these are small ulcers of various depths with extensive infiltration of the wall or huge ulcerations with a bumpy bottom and flat edges. Histological examination reveals both adenocarcinoma and undifferentiated cancer.
diffuse cancer(see Fig. 199) is observed in 20-25% of cases. The tumor grows endophytically in the mucous, submucosal and muscular layers along the connective tissue layers. The wall of the stomach becomes thickened, dense, whitish and immobile. The mucous membrane loses its usual relief: its surface is uneven, folds of uneven thickness, often with small erosions. Gastric injury may be limited (in this case, the tumor is most often found in the pyloric region) or total (the tumor covers the wall of the stomach throughout). As the tumor grows, the wall of the stomach sometimes shrinks, its size decreases, and the lumen narrows.
Diffuse cancer is usually represented by variants of undifferentiated carcinoma.
Transitional forms of cancer make up approximately 10-15% of all gastric cancers. These are either exophytic carcinomas, which acquired a pronounced infiltrating growth at a certain stage of development, or endophytic, but limited to a small area, cancer with a tendency to intragastric growth, or, finally, two (sometimes more) cancerous tumors of different clinical and anatomical forms in one and the same volume. same stomach.
In recent years, the so-called early stomach cancer which has up to 3 cm in diameter and grows no deeper than the submucosal layer. Diagnosis of early gastric cancer has become possible due to the introduction of targeted gastrobiopsy. Isolation of this form of cancer is of great practical importance: up to 100% of such patients live after surgery for more than 5 years, only 5% of them have metastases.
Gastric cancer is characteristic Spread outside the organ itself germination to neighboring organs and tissues. Cancer, located on the lesser curvature with the transition to the anterior and posterior walls and in the pyloric region, grows into the pancreas, the portal of the liver, the portal vein, the bile ducts and the gallbladder, the lesser omentum, the root of the mesentery and the inferior vena cava. Cardiac cancer of the stomach passes to the esophagus, fundic - grows into the hilum of the spleen, the diaphragm. Total cancer, like cancer of the greater curvature of the stomach, grows into the transverse colon, the greater omentum, which shrinks, shortens.
Histological types gastric cancer reflect the structural and functional features of the tumor. adenocarcinoma, which occurs very often with exophytic tumor growth, may be tubular, papillary and mucinous(Fig. 201), and each of the varieties of adenocarcinoma - differentiated, moderately differentiated and undifferentiated. characteristic of endophytic tumor growth undifferentiated cancer represented by several options - solid, scirrhous(Fig. 202), cricoid cell. Rarely found squamous, glandular-squamous(adenocancroid) and unclassifiable types of stomach cancer.
In addition to the International Histological Classification, gastric cancer is divided according to the nature of the structure into intestinal and diffuse types (Lauren, 1965). The intestinal type of gastric cancer is represented by glandular epithelium, similar to the columnar epithelium of the intestine with mucous secretion. The diffuse type of cancer is characterized by diffuse infiltration of the stomach wall with small cells containing and not containing mucus and forming glandular structures in some places.
Metastases are very characteristic of gastric cancer, they occur in 3/4-2/3 cases. Metastasizes gastric cancer in various ways - lymphogenous, hematogenous and implantation (contact).
Lymphogenic pathway
metastasis plays a major role in tumor spread and is clinically the most important (Fig. 203). Of particular importance are metastases to regional lymph nodes located along the lesser and greater curvature of the stomach. They occur in more than half of cases of gastric cancer, appear first and largely determine the volume and nature of the surgical intervention. In distant lymph nodes, metastases appear as orthograde
(according to the lymph flow), and retrograde
(against the flow of lymph) by. Retrograde lymphogenous metastases, which are of great diagnostic value in gastric cancer, include metastases to the supraclavicular lymph nodes, usually the left ones ("Virchow's metastases", or "Virchow's gland"), to the lymph nodes of pararectal tissue ("Schnitzler's metastases"). A classic example of lymphogenous retrograde metastases of gastric cancer is the so-called Krukenberg ovarian cancer.
Rice. 203. Spread of cancer through the lymphatic pathways of the peritoneum and mesentery (white stripes). Cancer metastases in the mesenteric lymph nodes
As a rule, a metastatic lesion affects both ovaries, which increase sharply, become dense, whitish. Lymphogenic metastases appear in the lungs, pleura, peritoneum.
Peritoneal carcinomatosis- a frequent companion of stomach cancer; at the same time, the lymphogenous spread of cancer along the peritoneum is supplemented by implantation(see fig. 203). The peritoneum becomes dotted with tumor nodes of various sizes, merging into conglomerates, among which intestinal loops are immured. Often, in this case, a serous or fibrinous-hemorrhagic effusion appears in the abdominal cavity (the so-called cancrotic peritonitis).
hematogenous metastases, spreading through the portal vein system, affecting primarily liver (Fig. 204), where they are found in 1/3-1/2 cases of gastric cancer. These are single or multiple nodes of various sizes, which in some cases almost completely replace the liver tissue. Such a liver with multiple cancer metastases sometimes reaches a huge size and weighs 8-10 kg. Metastatic nodes undergo necrosis and fusion, sometimes being a source of bleeding into the abdominal cavity or peritonitis. Hematogenous metastases occur in the lungs, pancreas, bones, kidneys, and adrenal glands. As a result of hematogenous metastasis of gastric cancer, miliary lung carcinomatosis and pleura.
Complications. There are two groups of complications of gastric cancer: the first are associated with secondary necrotic and inflammatory changes.
tumors, the second - with the germination of gastric cancer in neighboring organs and tissues and metastases.
As a result secondary necrotic changes breakdown of carcinoma occur wall perforation, bleeding, peritumorous (periulcerous) inflammation, up to development phlegmon of the stomach.
Growth of stomach cancer into the gates of the liver or the head of the pancreas with compression or obliteration of the bile ducts and portal vein leads to the development jaundice, portal hypertension, ascites. Tumor ingrowth into the transverse colon or the root of the mesentery of the small intestine leads to its wrinkling, accompanied by intestinal obstruction. When cardiac cancer grows into
The esophagus often narrows
its lumen. In pyloric cancer, as in gastric ulcer, it is also possible pyloric stenosis with a sharp expansion of the stomach and characteristic clinical manifestations, up to "gastric tetany". Germination of cancer in the diaphragm can often be accompanied by seeding of the pleura, development hemorrhagic or fibrinous-hemorrhagic pleurisy. The breakthrough of the tumor through the left dome of the diaphragm leads to pleural empyema.
A common complication of stomach cancer is exhaustion, the genesis of which is complex and is determined by intoxication, peptic disorders and alimentary insufficiency.
Bowel disease
The pathology of the intestine, which has the greatest clinical significance, includes malformations (megacolon, megasigma, diverticula, stenosis and atresia), inflammatory diseases (enteritis, appendicitis, colitis, enterocolitis) and dystrophic (enteropathy) nature, tumors (polyps, carcinoid, colon cancer intestines).
Developmental defects. A peculiar malformation is the congenital expansion of the entire colon (megacolon- megacolon congenitum) or just the sigmoid colon (megasigma- megasigmoideum) with a sharp hypertrophy of the muscular layer of its wall. Congenital diseases are intestinal diverticula- limited protrusions of the entire wall (true diverticula) or only the mucous membrane and submucosal layer through defects in the muscular layer (false diverticula). Diverticula are observed in all parts of the intestine. Diverticula of the small intestine are more common at the site of the umbilical-intestinal tract - Meckel's diverticulum and diverticula of the sigmoid colon. In cases where multiple diverticula develop in the intestine, they speak of diverticulosis. In diverticula, especially of the large intestine, the intestinal contents stagnate, fecal stones form, inflammation joins (diverticulitis), which can lead to perforation of the intestinal wall and peritonitis. Congenital stenosis and atresia intestines are also found in different parts of the intestine, but more often at the junction of the duodenum into the jejunum and the end of the ileum into the blind. Stenosis and atresia of the intestine lead to its obstruction (see. diseases of childhood).
Inflammation of the intestine can take place predominantly in the thin (enteritis) or large intestine (colitis) or spread more or less evenly throughout the intestines (enterocolitis).
Enteritis
With enteritis, inflammation does not always cover the small intestine throughout. In this regard, inflammation of the duodenum is distinguished - duodenitis, jejunum - eunite and iliac ileitis. Enteritis can be acute and chronic.
Acute enteritis
Acute enteritis- acute inflammation of the small intestine.
Etiology. It often occurs with many infectious diseases (cholera, typhoid fever, colibacillary, staphylococcal and viral infections, sepsis, giardiasis, opisthorchiasis, etc.), especially with food poisoning (salmonellosis, botulism), poisoning (chemical poisons, poisonous mushrooms, etc.) .). Acute enteritis of alimentary (overeating, eating coarse food, spices, strong alcoholic drinks, etc.) and allergic (idiosyncrasy to food, drugs) origin is known.
Pathological anatomy. Acute enteritis can be catarrhal, fibrinous, purulent, necrotic-ulcerative.
At catarrhal enteritis, which occurs most often, the full-blooded and edematous intestinal mucosa is abundantly covered with serous, serous-mucous or serous-purulent exudate. Edema and inflammatory infiltration cover not only the mucous membrane, but also the submucosal layer. Degeneration and desquamation of the epithelium are noted, especially at the tops of the villi (catarrhal desquamative enteritis), hyperplasia of goblet cells ("goblet transformation"), small erosions and hemorrhages.
At fibrinous enteritis, more often ileite, the intestinal mucosa is necrotic and permeated with fibrinous exudate, as a result of which gray or gray-brown membranous overlays appear on its surface. Depending on the depth of necrosis, inflammation may be croupy or diphtheria, in which, after rejection of fibrinous films, deep ulcers form.
Purulent enteritis characterized by diffuse impregnation of the intestinal wall with pus (phlegmonous enteritis) or pustular formation, especially at the site of lymphoid follicles (apostematous enteritis).
At necrotizing ulcerative enteritis destructive processes can mainly concern the group and solitary lymphatic follicles of the intestine, as is observed in typhoid fever, or cover the mucous membrane out of touch with the lymphatic apparatus of the intestine. In this case, necrosis and ulceration are widespread (influenza, sepsis) or focal in nature (allergic vasculitis, periarteritis nodosa).
Regardless of the nature of inflammatory changes in the mucous membrane, acute enteritis develops hyperplasia and reticulomacrophage transformation of the lymphatic apparatus of the intestine. Sometimes it is expressed extremely sharply (for example, the so-called brain-like swelling of group and solitary follicles in typhoid fever) and causes subsequent destructive changes in the intestinal wall.
in the mesenteric lymph nodes reactive processes are observed in the form of hyperplasia of lymphoid elements, their plasmacytic and reticulomacrophage transformation, and often inflammation.
Complications acute enteritis include bleeding, perforation of the intestinal wall with the development of peritonitis (for example, with typhoid fever), and
also dehydration and demineralization (for example, in cholera). In some cases, acute enteritis can become chronic.
Chronic enteritis
Chronic enteritis- Chronic inflammation of the small intestine. It can be an independent disease or a manifestation of other chronic diseases (hepatitis, liver cirrhosis, rheumatic diseases, etc.).
Etiology. Chronic enteritis can be caused by numerous exogenous and endogenous factors that, with prolonged exposure and damage to enterocytes, can disrupt the physiological regeneration of the small intestine mucosa. exogenous factors are infections (staphylococcus, salmonella, viruses), intoxication, exposure to certain drugs (salicylates, antibiotics, cytostatic agents), long-term alimentary errors (abuse of spicy, hot, poorly cooked food), excessive consumption of coarse vegetable fiber, carbohydrates, fats, insufficient intake of proteins and vitamins. Endogenous factors may be autointoxication (for example, with uremia), metabolic disorders (with chronic pancreatitis, cirrhosis of the liver), hereditary deficiency of small intestine enzymes.
Morphogenesis. The basis of chronic enteritis is not only inflammation, but also a violation of the physiological regeneration of the mucous membrane of the small intestine: proliferation of the epithelium of the crypts, differentiation of cells, their “advancement” along the villus and rejection into the intestinal lumen. At first, these disorders consist in increased proliferation of the crypt epithelium, which seeks to replenish the rapidly shedding damaged villi enterocytes, but the differentiation of this epithelium into functionally complete enterocytes is delayed. As a result, most of the villi are lined with undifferentiated, functionally incompetent enterocytes, which quickly die. The shape of the villi adapts to the reduced number of epithelial cells: they become shorter and atrophy. Over time, the crypts (cambial zone) are unable to provide a pool of enterocytes, undergo cystic transformation and sclerosis. These changes are the final stage of disturbed physiological regeneration mucous membrane, develop it atrophy and structural adjustment.
Pathological anatomy. Changes in chronic enteritis have recently been well studied on the material of enterobiopsies.
There are two forms of chronic enteritis - without atrophy of the mucous membrane and atrophic enteritis.
For chronic enteritis without mucosal atrophy very characteristic is the uneven thickness of the villi and the appearance of club-shaped thickenings of their distal sections, where destruction of the basal membranes of the epithelial lining is noted. The cytoplasm of the enterocytes lining the villi is vacuolated (Fig. 205). Activity of redox and hydrolytic (alkaline phosphatase) enzymes
the cytoplasm of such enterocytes is reduced, which indicates a violation of their absorption capacity. Adhesions, "arcades" appear between the enterocytes of the apical parts of the nearby villi, which is apparently associated with the formation of surface erosions; the stroma of the villi is infiltrated with plasma cells, lymphocytes, and eosinophils. The cellular infiltrate descends into crypts, which may be cystically dilated. The infiltrate pushes the crypts apart and reaches the muscular layer of the mucous membrane. If the changes described above concern only the villi, they speak of surface version this form of chronic enteritis, if they capture the entire thickness of the mucous membrane - about diffuse version.
Chronic atrophic enteritis characterized primarily by the shortening of the villi, their deformation, the appearance of a large number of fused villi (see Fig. 205). In shortened villi, argyrophilic fibers collapse. Enterocytes are vacuolated, the activity of alkaline phosphatase in their brush border is reduced. A large number of goblet cells appear.
Crypts are atrophied or cystically enlarged, their infiltration with lymphohistiocytic elements and replacement with growths of collagen and muscle fibers are noted. If atrophy concerns only the villi of the mucous membrane, and the crypts are little changed, they speak of hyper-regenerative variant this form of chronic enteritis, if
Rice. 205. Chronic enteritis (enterobiopsy) (according to L.I. Aruin):
a - chronic enteritis without atrophy; uneven thickness of the villi, club-shaped thickening of their distal sections, enterocyte dystrophy, polymorphic cell infiltration of the stroma; b - chronic atrophic enteritis; shortening of the villi, their deformation and fusion; pronounced lymphohistiocytic infiltration of the stroma
villi and crypts are atrophic, the number of which is sharply reduced, - about the hyporegenerative variant.
With prolonged, severe chronic enteritis, anemia, cachexia, hypoproteinemic edema, osteoporosis, endocrine disorders, vitamin deficiency, and malabsorption syndrome may develop.
enteropathy
Enteropathies called chronic diseases of the small intestine, which are based on hereditary or acquired enzymatic disorders of enterocytes (intestinal fermentopathy). A decrease in the activity or loss of certain enzymes leads to insufficient absorption of those substances that these enzymes normally break down. As a result, a syndrome develops malabsorption certain nutrients (malabsorption syndrome).
Among enteropathies, there are: 1) disaccharidase deficiency (for example, alactasia); 2) hypercatabolic hypoproteinemic enteropathy (intestinal lymphangiectasia); 3) celiac disease (non-tropical sprue, celiac disease).
Pathological anatomy. Changes in various enteropathies are more or less the same and are reduced to varying degrees of severity of dystrophic and atrophic changes in the mucous membrane of the small intestine. Particularly characteristic are shortening and thickening of the villi, vacuolization and a decrease in the number of enterocytes with the loss of microvilli (brush border), deepening of the crypts and thickening of the basement membrane, infiltration of the mucous membrane by plasma cells, lymphocytes, macrophages. In the later stages, there is an almost complete absence of villi and a sharp sclerosis of the mucous membrane.
At hypercatabolic hypoproteinemic enteropathy the described changes are combined with a sharp expansion of the lymphatic capillaries and vessels of the intestinal wall (intestinal lymphangiectasia). Histoenzymatic study of biopsy samples of the intestinal mucosa allows you to determine the enzyme disorders characteristic of a certain type of enteropathy, for example, a lack of enzymes that break down lactose and sucrose, with disaccharidase enteropathy. At celiac disease the diagnosis is made on the basis of the study of two enterobiopsies taken before and after the gluten-free diet.
Enteropathy is characterized by the same consequences as for severe chronic enteritis. They lead, in addition to the syndrome of impaired absorption, to hypoproteinemia, anemia, endocrine disorders, beriberi, edematous syndrome.
Whipple disease
Whipple disease(intestinal lipodystrophy) is a rare chronic disease of the small intestine, which is characterized by malabsorption syndrome, hypoprotein- and hypolipidemia, progressive weakness and weight loss.
Etiology. Many researchers, in connection with the detection of bacilli-shaped bodies in macrophages of the mucous membrane, attach importance to the infectious factor. The infectious nature of the disease is also supported by the fact that these bodies disappear from the mucous membrane during antibiotic treatment and reappear when the disease is exacerbated.
Pathological anatomy. As a rule, thickening of the wall of the small intestine and its mesentery is noted, as well as an increase in the mesenteric lymph nodes, which is associated with the deposition of lipids and fatty acids in them and a sharp lymphostasis. Characteristic changes are found on microscopic examination. They are manifested by a pronounced infiltration of the lamina propria of the intestinal mucosa by macrophages, the cytoplasm of which is stained with Schiff's reagent (PIC-positive macrophages). In addition to the mucous membrane, the same type of macrophages appear in the mesenteric lymph nodes (fig. 206), liver, synovial fluid. In macrophages and epithelial cells of the mucous membrane, electron microscopic examination reveals bacillus-like bodies (see fig. 206). In the intestine, lymph nodes and mesentery, in areas of fat accumulation, lipogranulomas are found.
Colitis
In colitis, the inflammatory process mainly covers the blind (typhlitis), transverse colon (transverse), sigmoid (sigmoiditis) or direct (proctitis) intestine, and in some cases extends to the entire intestine (pancolitis). Inflammation can be either acute or chronic.
Acute colitis
Acute colitis- acute inflammation of the colon.
Etiology. There are infectious, toxic and toxic-allergic colitis. To infectious include dysentery, typhoid, colibacillary, staphylococcal, fungal, protozoal, septic, tuberculous, syphilitic colitis, to toxic - uremic, sublimate, medicinal, and to toxic-allergic - alimentary and coprostatic colitis.
Pathological anatomy. The following forms of acute colitis are distinguished: catarrhal, fibrinous, purulent, hemorrhagic, necrotic, gangrenous, ulcerative.
At catarrhal colitis the mucous membrane of the intestine is hyperemic, edematous, accumulations of exudate are visible on its surface, which may have a serous, mucous or purulent character (serous, mucous or purulent catarrh). The inflammatory infiltrate penetrates not only the thickness of the mucous membrane, but also the submucosal layer, in which hemorrhages are visible. Degeneration and necrobiosis of the epithelium are combined with desquamation of the surface epithelium and hypersecretion of the glands.
fibrinous colitis depending on the depth of necrosis of the mucous membrane and the penetration of fibrinous exudate, they are divided into croupous
and diphtheritic
(cm. Dysentery). Purulent colitis usually characterized by phlegmonous inflammation - phlegmonous colitis, phlegmon of the large intestine. In cases where multiple hemorrhages occur in the intestinal wall during colitis, areas of hemorrhagic impregnation appear, they speak of hemorrhagic colitis. At necrotizing colitis necrosis is often subjected not only to the mucous membrane, but also to the submucosal layer. gangrenous colitis- a variant of necrotic. Spicy ulcerative colitis usually completes diphtheritic or necrotic changes in the intestinal wall. In some cases, for example, with amebiasis, ulcers in the colon appear at the very beginning of the disease.
Complications acute colitis: bleeding, perforation and peritonitis, paraproctitis with pararectal fistulas. In some cases, acute colitis takes a chronic course.
chronic colitis
chronic colitis- chronic inflammation of the colon - occurs primarily or secondarily. In some cases, it is genetically associated with acute colitis, in other cases this relationship is not traced.
Etiology. The factors causing chronic colitis are essentially the same as for acute colitis, ie. infectious, toxic and toxic-allergic. Of great importance is the duration of these factors in conditions of increased local (intestinal) reactivity.
Pathological anatomy. Changes in chronic colitis, studied on biopsy material, differ little from those in chronic enteritis, although they are more pronounced in colitis. inflammatory events, which are combined with dysregenerative and lead to atrophy and sclerosis mucous membrane. Guided by this, chronic colitis without mucosal atrophy and chronic atrophic colitis are distinguished.
At chronic colitis without mucosal atrophy the latter is edematous, dull, granular, gray-red or red, often with multiple hemorrhages and erosions. Flattening and desquamation of the prismatic epithelium, an increase in the number of goblet cells in the crypts are noted. The crypts themselves are shortened, their lumen is widened, sometimes they resemble cysts. (cystic colitis). The lamina propria, in which hemorrhages occur, is infiltrated by lymphocytes, plasma cells, eosinophils, and the cellular infiltrate often penetrates into its muscular layer. The degree of cellular infiltration can be different - from very moderate focal to pronounced diffuse with the formation of individual abscesses in the crypts. (crypt abscesses) and foci of ulceration.
For chronic atrophic colitis flattening of the prismatic epithelium, a decrease in the number of crypts, and hyperplasia of smooth muscle elements are characteristic. The mucosa is dominated by histioli-
focytic infiltration and proliferation of connective tissue; in some cases, epithelializing and scarring ulcers occur.
Among the forms of chronic colitis, the so-called collagen colitis, which is characterized by the accumulation around the crypts of the mucous membrane of collagen, amorphous protein and immunoglobulins ("pericryptal fibroblast disease"). The development of this form of colitis is associated with a perversion of collagen synthesis or with autoimmunization.
Complications. Parasigmoiditis and paraproctitis, in some cases hypovitaminosis.
Nonspecific ulcerative colitis(synonyms: idiopathic ulcerative colitis, ulcerative proctocolitis) is a chronic relapsing disease, which is based on inflammation of the colon with suppuration, ulceration, hemorrhages and outcome in sclerotic deformation of the wall. This is a fairly common disease that occurs more often in young women.
Etiology and pathogenesis. In the occurrence of this disease, of course, the importance of local allergies, which is apparently caused by the intestinal microflora. In favor of the allergic nature of colitis, its combination with urticaria, eczema, bronchial asthma, rheumatic diseases, Hashimoto's goiter testifies. In the pathogenesis of the disease, autoimmunization is of great importance. This is confirmed by the detection of autoantibodies in ulcerative colitis, which are fixed in the epithelium of the intestinal mucosa, the nature of the mucosal cellular infiltrate, which reflects a delayed-type hypersensitivity reaction. The chronic course of the disease and the imperfection of reparative processes are apparently associated not only with autoaggression, but also with trophic disorders due to severe destruction of the intramural nervous apparatus of the intestine.
Pathological anatomy. The process usually begins in the rectum and gradually spreads to the blind. Therefore, there are both relatively isolated lesions of the rectum and sigmoid or rectum, sigmoid and transverse colon, and a total lesion of the entire large intestine (Fig. 207).
Morphological changes depend on the nature of the course of the disease - acute or chronic (Kogoy T.F., 1963).
acute form corresponds to an acute progressive course and exacerbation of chronic forms. In these cases, the wall of the large intestine is edematous, hyperemic, with multiple erosions and irregularly shaped superficial ulcers that merge and form large areas of ulceration. The islands of the mucous membrane preserved in these areas resemble polyps. (fringed pseudopolyps). Ulcers can penetrate into the submucosal and muscle layers, where fibrino-
Rice. 207. Nonspecific ulcerative colitis (drug Zh.M. Yukhvidova)
id necrosis of collagen fibers, foci of myomalacia and karyorrhexis, extensive intramural hemorrhages. At the bottom of the ulcer, both in the zone of necrosis and along their periphery, vessels with fibrinoid necrosis and erosion of the walls are visible. Often there is perforation of the intestinal wall in the area of the ulcer and intestinal bleeding. Such deep ulcers form pockets with necrotic masses that are rejected, the intestinal wall becomes thinner, and the lumen becomes very wide. (toxic dilatation). Individual ulcers undergo granulation, and the granulation tissue grows in excess in the area of the ulcer and forms polypoid outgrowths - granulomatous pseudopolyps. The intestinal wall, especially the mucous membrane, is abundantly infiltrated with lymphocytes, plasma cells, and eosinophils. During the period of exacerbation, neutrophils predominate in the infiltrate, which accumulate in crypts, where crypt abscesses(Fig. 208).
For chronic form characterized by a sharp deformation of the intestine, which becomes much shorter; there is a sharp thickening and compaction of the intestinal wall, as well as diffuse or segmental narrowing of its lumen. Reparative-sclerotic processes prevail over inflammatory-necrotic ones. Granulation and scarring of ulcers occur, but their epithelialization is usually incomplete, which is associated with the formation of extensive scar fields and chronic inflammation.
Rice. 208. Nonspecific ulcerative colitis (drug Zh.M. Yukhvidova):
a - accumulation of leukocytes in the crypt (crypt abscess); b - pseudopolyp
A manifestation of perverted reparation are multiple pseudopolyps(see Fig. 208) and not only as a result of excessive growth of granulation tissue (granulomatous pseudopolyps), but also reparative regeneration of the epithelium around areas of sclerosis (adenomatous pseudopolyps). In the vessels, productive endovasculitis, sclerosis of the walls, obliteration of the lumen are noted; fibrinoid necrosis of the vessels is rare. Inflammation is predominantly productive and is expressed in the infiltration of the intestinal wall with lymphocytes, histiocytes, and plasma cells. Productive inflammation is combined with crypt abscesses.
Complicationsnonspecific ulcerative colitis can be local and general. To local include intestinal bleeding, perforation of the wall and peritonitis, stenosis of the lumen and intestinal polyposis, the development of cancer, to general - anemia, amyloidosis, exhaustion, sepsis.
Crohn's disease
Crohn's disease- a chronic relapsing disease of the gastrointestinal tract, characterized by nonspecific granulomatosis and necrosis.
Crohn's disease previously meant a nonspecific granulomatous lesion of only the final section of the small intestine and therefore called it terminal (regional) ileitis. Later it was shown that the changes characteristic of this disease can occur in any part of the gastrointestinal tract. Descriptions of Crohn's disease of the stomach, colon, appendix, etc. have appeared.
Etiology and pathogenesis.The cause of Crohn's disease is not known. There are suggestions about the role of infection, genetic factors, hereditary predisposition of the intestine to the response to various
exposure to a stereotypical granulomatous reaction, autoimmunization. Among the pathogenetic theories, in addition to autoimmune, the so-called lymphatic one is widespread, according to which primary changes develop in the lymph nodes of the mesentery and lymphoid follicles of the intestinal wall and lead to "lymphatic edema" of the submucosal layer, culminating in destruction and granulomatosis of the intestinal wall.
Pathological anatomy. Most often, changes are found in the terminal ileum, in the rectum (especially in the anal part) and appendix; other localizations are rare. Amazed the entire thickness of the intestinal wall, which becomes sharply thickened and edematous. The mucous membrane is tuberous, reminiscent of a "cobblestone pavement" (Fig. 209), which is associated with the alternation of long, narrow and deep ulcers, which are arranged in parallel rows along the length of the intestine, with areas of normal mucous membrane. There are also deep slit ulcers, located not along the length, but along the diameter of the intestine. The serous membrane is often covered with adhesions and multiple whitish nodules that look like tuberculosis. The lumen of the intestine is narrowed, fistulous passages are formed in the thickness of the wall. The mesentery is thickened, sclerosed. Regional lymph nodes are hyperplastic, white-pink in section.
The most characteristic microscopic sign is nonspecific granulomatosis, which covers all layers of the intestinal wall. Granulomas have a sarcoid-like structure and consist of epithelioid and giant cells of the Pirogov-Langhans type (see Fig. 209). Edema and diffuse infiltration by lymphocytes, histiocytes, and plasma cells are also considered characteristic. submucosal layer, hyperplasia of its lymphoid elements, formation of slit-like ulcers (see fig. 209). Abscesses in the thickness of the wall, sclerosis and hyalinosis as a result of the evolution of diffuse infiltrate cells and granulomas often join these changes. With a long course, a sharp cicatricial deformation of the wall occurs.
Complication in Crohn's disease, there is a perforation of the intestinal wall with the formation of fistulous passages, in connection with which purulent or fecal peritonitis develops. Stenosis of various parts of the intestine is not uncommon, but more often the ileum, with symptoms of intestinal obstruction. Crohn's disease is considered a pre-cancer of the intestine.
Appendicitis
Appendicitis- inflammation of the appendix of the caecum, giving a characteristic clinical syndrome. From this it follows that in clinical and anatomical terms, not every inflammation of the appendix (for example, with tuberculosis, dysentery) is appendicitis. Appendicitis is a widespread disease that often requires surgery.
Rice. 209. Crohn's disease with damage to the colon:
a - macropreparation (according to Zh.M. Yukhvidova); b - epithelioid cell granuloma with giant cells of the Pirogov-Langhans type (according to L.L. Kapuller); c - slit-like ulcer (according to L.L. Kapuller)
Etiology and pathogenesis. Appendicitis is an enterogenic autoinfection. The flora vegetating in the intestine becomes pathogenic, the most important are Escherichia coli, Enterococcus. The study of possible conditions contributing to the invasion of microbes into the wall of the process and the manifestation of the virulent properties of the intestinal flora showed the importance of various factors, which served as the basis for the creation of pathogenetic theories of appendicitis.
Angioedema theory pathogenesis of appendicitis is widespread. Built on a physiological basis (violations of the process kinetics as the starting point of the disease), it easily explains the initial manifestations of the disease (simple, superficial appendicitis) and those clinical cases when there are no morphological changes in the removed process. At the same time, from the standpoint of the neurovascular theory, it is difficult to explain the dynamics of the development of destructive forms of appendicitis, which is easily explained by L. Ashoff's concept of the progression of the primary affect.
Pathological anatomy. There are two clinical and anatomical forms of appendicitis: acute and chronic. Each of them has a certain morphological characteristic.
Acute appendicitis. There are the following morphological forms of acute appendicitis: 1) simple, 2) superficial, 3) destructive (phlegmonous, apostematous, phlegmonous-ulcerative, gangrenous). These forms are a morphological reflection of the phases of acute inflammation of the appendix, ending in destruction and necrosis. It usually lasts 2-4 days.
Changes specific to acute simple appendicitis, develop within the first hours from the onset of an attack. They consist in a disorder of blood and lymph circulation in the form of stasis in capillaries and venules, edema, hemorrhages, accumulation of siderophages, as well as marginal standing of leukocytes and leukodiapedesis. These changes are expressed mainly in the distal appendix. Disorders of blood and lymph circulation are combined with degenerative changes in the intramural nervous system of the process.
In the following hours, against the background of dyscirculatory changes in the distal appendix, foci of exudative purulent inflammation of the mucous membrane appear, called primary affect. At the top of such a cone-shaped focus, facing the lumen of the process, superficial defects of the epithelium are noted. These microscopic changes characterize acute superficial appendicitis, in which the process becomes swollen, and its serous membrane becomes full-blooded and dull. Changes characteristic of simple or superficial appendicitis are reversible, but if they progress, it develops acute destructive appendicitis.
By the end of the first day, the leukocyte infiltrate spreads to the entire thickness of the process wall - it develops phlegmonous appendicitis(Fig. 210). The dimensions of the process increase, its serous membrane becomes dull and full-blooded, a fibrinous coating appears on its surface (Fig. 211, see on color incl.); the wall on the incision is thickened, pus is released from the lumen. The mesentery is edematous, hyperemic. If multiple small pustules (abscesses) appear against the background of diffuse purulent inflammation of the process, they speak of apostematous appendicitis, if ulceration of the mucous membrane joins phlegmonous appendicitis - o phlegmonous-ulcerative appendicitis. Completes purulent-destructive changes in the process gangrenous appendicitis, which is called secondary, since it occurs as a result of the transition of the purulent process to the surrounding tissues (periappendicitis, see fig. 211), including on the mesentery of the process (mesenteriolite), which leads to thrombosis of the appendicular artery.
Secondary gangrenous appendicitis must be distinguished from gangrene of the appendix developing with primary thrombosis or thromboembolism of his artery. Obviously, therefore, gangrene of the appendix is not quite aptly called primary gangrenous appendicitis.
Rice. 210. Phlegmonous appendicitis. Swelling of the wall and stratification of its purulent exudate
The appearance of the appendix in gangrenous appendicitis is very characteristic. The process is thickened, its serous membrane is covered with dirty green fibrinous-purulent overlays. The wall is also thickened, gray-dirty in color, pus is released from the lumen. Microscopic examination reveals extensive foci of necrosis with colonies of bacteria, hemorrhages, blood clots in the vessels. The mucous membrane is ulcerated almost throughout.
Complications. In acute appendicitis, complications are associated with the destruction of the process and the spread of pus. Often occurs with phlegmonous-ulcerative appendicitis perforation walls leads to the development of limited and diffuse peritonitis, which also appears during self-amputation of a gangrenous appendix. If, with phlegmonous appendicitis, the proximal process is closed, then the lumen of the distal part is stretched and develops. process empyema. The spread of the purulent process to the tissues surrounding the process and the caecum (periapendicitis, perityphlitis) accompanied by the formation of encysted abscesses, the transition of inflammation to the retroperitoneal tissue. Very dangerous development purulent thrombophlebitis of the vessels of the mesentery with its spread to the branches of the portal vein and the occurrence pylephlebitis(from Greek. pile- gates, flebos- vein). In such cases, thrombobacterial embolism of the portal vein branches in the liver and the formation of pylephlebitic abscesses.
Chronic appendicitis. It develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against which inflammatory and destructive changes may appear. Usually, inflammation and destruction are replaced by the growth of granulation tissue in the wall and lumen of the process. Granulation tissue matures, turns into scar tissue. There is a sharp sclerosis and atrophy of all layers of the wall, obliteration of the lumen process, adhesions appear between the appendix and surrounding tissues. These changes can be combined with granulating and acute ulcers, histiolimphocytic and leukocyte infiltration of the appendix wall.
Sometimes, with cicatricial obliteration of the proximal process, serous fluid accumulates in its lumen and the process turns into a cyst - it develops edema of the process. If the contents of the cyst becomes the secret of the glands - mucus, then they talk about mucocele. Rarely, mucus due to the peristalsis of the process is collected in spherical formations (myxoglobules), which leads to myxoglobulosis process. When a cyst ruptures and the mucus and cells that form it enter the abdominal cavity, these cells can be implanted on the peritoneum, which leads to its changes, resembling a tumor - myxoma. In such cases, one speaks of pseudomyxome peritoneum.
About false appendicitis they say in cases where the clinical signs of an attack of appendicitis are not due to an inflammatory process, but dyskinetic disorders. In cases of hyperkinesis, the process
as its muscle layer is reduced, the follicles are enlarged, the lumen is sharply narrowed. With atony, the lumen is sharply expanded, filled with feces (coprostasis), the wall of the process is thinned, the mucous membrane is atrophic.
Intestinal tumors
Among intestinal tumors, epithelial - benign and malignant - are of the greatest importance.
From benign epithelial tumors are the most common adenomas(as adenomatous polyps). They are usually localized in the rectum, then in frequency - in the sigmoid, transverse colon, blind and thin. Among intestinal adenomas, there are tubular, tubulo-villous and villous. Villous adenoma, which is a soft pink-red tissue with a villous surface (villous tumor) has a glandular-papillary structure. She can become malignant. With multiple adenomatous polyps, they talk about intestinal polyposis, which is familial.
Cancer occurs in both the small and large intestines. small intestine cancer rare, usually duodenum, in the area of her large (vater's) nipple. The tumor does not reach a large size, very rarely causes difficulty in the outflow of bile, which is the cause of subhepatic jaundice, and is complicated by inflammation of the biliary tract.
colon cancer tends to increase, mortality from it increases. Of the various parts of the colon, cancer is more common in rectum, less often in the sigmoid, blind, hepatic and splenic angles of the transverse colon.
rectal cancer usually preceded by chronic ulcerative colitis, polyposis, villous tumor or chronic rectal fistulas (precancerous lesions).
Depending on the growth patterns There are exophytic, endophytic and transitional forms of cancer.
To exophytic crayfish include plaque-like, polypous and large-tuberous, to endophytic- ulcerative and diffuse-infiltrative, usually narrowing the intestinal lumen (Fig. 212), to transitional- saucer-shaped cancer.
Among histological types bowel cancer isolated adenocarcinoma, mucinous adenocarcinoma, cricoid, squamous cell, squamous glandular, undifferentiated, unclassifiable cancer. Exophytic forms of cancer usually have the structure of adenocarcinoma, endophytic forms - the structure of cricoid or undifferentiated cancer.
Separately allocate anal cancers: squamous, cloacogenic, mucoepidermal, adenocarcinoma.
Metastasizes rectal cancer to regional lymph nodes and liver.
Rice. 212. Diffuse infiltrative rectal cancer
Peritonitis
Peritonitis, or inflammation of the peritoneum, often complicating diseases of the digestive system: perforation of a stomach or duodenal ulcer, intestinal ulcers in typhoid fever, ulcerative colitis, dysentery; it occurs as a complication of appendicitis, liver disease, cholecystitis, acute pancreatitis, etc.
Peritonitis can be limited to one or another part of the abdominal cavity - limited peritonitis or be common - diffuse peritonitis. More often it acute exudative peritonitis(serous, fibrinous, purulent), sometimes it can be feces, bile. At the same time, the visceral and parietal peritoneum is sharply hyperemic, with areas of hemorrhage, accumulations of exudate are visible between the intestinal loops, which, as it were, sticks together the loops. The exudate is located not only on the surface of the organs and walls of the abdominal cavity, but also accumulates in the underlying sections (lateral canals, pelvic cavity). The intestinal wall is flabby, easily torn, there is a lot of liquid content and gases in the lumen.
With diffuse peritonitis, the organization of purulent exudate is accompanied by the formation of encysted interintestinal accumulations of pus - "abscesses"; with limited peritonitis, a subdiaphragmatic "abscess" appears in the area of the diaphragm. In the outcome of fibrinous peritonitis, adhesions are formed in the abdominal cavity, in some cases it develops chronic adhesive peritonitis(adhesive disease), which leads to intestinal obstruction.
Sometimes chronic peritonitis emerges "originally". It is usually limited perigastritis with gastric ulcer, perimetritis and perisalpingitis after childbirth or with a long-term infection (gonorrhea), pericholecystitis with calculosis of the gallbladder, periappendicitis without clinical manifestations of appendicitis in history. In such cases, sclerosis usually appears in a limited area of the peritoneum, adhesions are formed, often disrupting the function of the abdominal organs.
Infiltrate - what is it? Doctors distinguish several of its types - inflammatory, lymphoid, post-injection and others. The causes of infiltration are different, but all its types are characterized by the presence of unusual cellular elements in the tissue (or organ), its increased density, and increased volume.
Post-injection infiltrate
This type of pathological changes appears after injections as a result of the penetration of the drug into the tissues. There are several reasons why a post-injection infiltrate occurs:
1. The rules of antiseptic treatment were not followed.
2. Short or blunt syringe needle.
3. Rapid drug administration.
4. The injection site was chosen incorrectly.
5. Multiple administration of the drug in the same place.
The appearance of a post-injection infiltrate also depends on the individual characteristics of the human body. In some people, it occurs extremely rarely, while in other patients it occurs after almost every injection.
Treatment of post-injection infiltrate
There is no infection in the infiltrated tissue, but the danger of this pathology after the injection is that there is a risk of an abscess. In this case, treatment can only take place under the supervision of a surgeon.
If there are no complications, then the infiltrate after injections is treated with physiotherapeutic methods. It is also recommended to apply an iodine mesh to the place of tissue compaction several times a day, use Vishnevsky's ointment.
Traditional medicine also offers several effective methods for getting rid of the “bumps” that appeared after injections. Honey, burdock leaf or cabbage, aloe, cranberries, cottage cheese, rice can have a healing effect when a similar problem occurs. For example, burdock or cabbage leaves should be taken fresh for treatment, applying them for a long time to a sore spot. Previously, the “bump” can be greased with honey. Cottage cheese compress also helps to get rid of old "bumps".
No matter how good this or that method of treating this problem is, the decisive word should belong to the doctor, since it is he who will determine how to treat it and whether it should be done.
Inflammatory infiltrate
This group of pathologies is divided into several types. Inflammatory infiltrate - what is it? Everything is explained by the medical encyclopedia, which talks about the ways in which the focus of inflammation occurs and indicates the causes of the appearance of pathological tissue reactions.
Medicine distinguishes a large number of varieties of infiltrates of the subgroup under consideration. Their presence may indicate problems with the immune system, congenital diseases, the presence of acute inflammation, a chronic infectious disease, and allergic reactions in the body.
The most common type of this pathological process is an inflammatory infiltrate. What it is helps to understand the description of the characteristic features of this phenomenon. So, what should you pay attention to? Thickening of tissues in the area of inflammation. When pressed, pain occurs. With stronger pressure, a hole remains on the body, which levels out slowly, since the displaced cells of the infiltrate return to their original place only after a certain period of time.
Lymphoid infiltrate
One of the types of tissue pathology is lymphoid infiltrate. What it is, allows you to understand the Big Medical Dictionary. It says that such a pathology occurs in some chronic infectious diseases. The infiltrate contains lymphocytes. They can accumulate in different tissues of the body.
The presence of lymphoid infiltration indicates a malfunction of the immune system.
Postoperative infiltrate
For what reason can a postoperative infiltrate form? What it is? Does it need to be treated? How to do it? These questions are of concern to people who had to face this problem.
The development of postoperative infiltrate occurs gradually. Usually its detection occurs 4-6 or even 10-15 days after surgery. The patient's body temperature rises, there are aching pains in the abdominal cavity, stool retention. The presence of painful compaction is determined.
In some cases, it can be difficult to determine where the infiltrate is located - in the abdominal cavity or in its thickness. To do this, the doctor uses special diagnostic methods.
The causes of infiltration after surgery are not always possible to accurately determine, but its therapy in most cases ends successfully. Antibiotics and various types of physiotherapy give positive results.
Very often there is an infiltrate of the postoperative scar. Sometimes it can appear several years after the surgical procedure. One of the reasons for its occurrence is the suture material used. Perhaps the infiltrate will resolve on its own. Although this rarely happens. Most often, the phenomenon is complicated by an abscess, which must be opened by the surgeon.
This is a dangerous pathology that requires immediate treatment. With the help of X-ray and biopsy data, doctors can detect a lung infiltrate in a patient. What it is? Pulmonary infiltration must be distinguished from pulmonary edema. With such a pathology, the patient experiences penetration and accumulation of fluids, chemicals, cellular elements in the tissues of the internal organ.
Lung infiltration is most often of inflammatory origin. It can be complicated by the processes of suppuration, which leads to loss of organ function.
Moderate enlargement of the lung, compaction of its tissue are characteristic signs of infiltration. X-ray examination helps to recognize them, in which darkening of the tissues of the internal organ is visible. What does it give? By the nature of the blackout, the doctor can determine the type of pathology under consideration and the degree of the disease.
Tumor infiltrate
Tumor infiltrate is one of the most common pathologies. What it is? It is most often composed of atypical tumor cells of a different nature (cancer, sarcoma). Affected tissues change color, become dense, sometimes painful. Manifested in tumor growth.
The likelihood of infiltration is equally present in people of any age.
The results of the study showed that various kinds of injuries, diseases of an infectious nature can become the cause of the disease. They can be transmitted by contact, have a lymphogenous type of distribution.
In the tissues of the maxillary region, an infiltrate often develops. What it is? How can it be distinguished from other diseases? Only an experienced doctor can assess the patient's condition and give an accurate answer to the questions posed. The causative agents of inflammation are staphylococci, streptococci and other representatives of the microflora of the oral cavity.
A complicated condition of acute appendicitis can also cause the development of an infiltrate. It occurs with untimely surgical intervention.
Symptoms of infiltration
With the development of the disease, the patient may experience a slightly elevated temperature. It stays at a certain level for several days. Sometimes this indicator remains normal. The spread of the infiltrate occurs on one or more parts of the body. This is expressed in swelling and compaction of tissues with a clearly defined contour. All tissues are affected at the same time - mucous membranes, skin, subcutaneous fat and muscle membranes.
The infiltrate, which develops against the background of complications of appendicitis, is characterized by persistent pain in the lower abdomen, fever up to 39 degrees, chills. In this case, the recovery of the patient is possible only with timely surgical intervention. The presence of this type of infiltrate is established upon examination by a doctor (does not require special diagnostic methods).
In other cases, only a differential approach allows you to accurately establish the diagnosis and prescribe the right treatment. Sometimes, to establish a diagnosis, data from the results of a puncture from the site of inflammation are taken into account.
Specialists conduct a study of materials taken from the inflamed area. The different nature of the cells constituting the infiltrate was established. It is this circumstance that allows physicians to classify the disease. As a rule, a large accumulation of yeast and filamentous fungi is found in the infiltrate. This indicates the presence of such a condition as dysbacteriosis.
The main goal of the treatment of infiltrate is the elimination of inflammatory foci. This is achieved by conservative methods of treatment, which include physiotherapy. The patient should not self-medicate and delay a visit to a specialist.
Thanks to physiotherapy, they achieve resorption of the infiltrate by increasing blood flow. At this time, the elimination of stagnation occurs. It also reduces swelling and relieves pain. Most often, electrophoresis of antibiotics, calcium is prescribed.
Physiotherapy is contraindicated if purulent forms of the disease are present. Intensive impact on the affected area will only provoke the rapid development of the infiltrate and the further spread of the focus.
Choice of method of treatment of patients with rectal cancer
After completion of the clinical examination, both the nature and extent of the surgical intervention and the choice of the optimal method of treatment are determined. The decisive factor in the choice of the nature of the surgical intervention is the observance of two fundamental provisions - ensuring the maximum radicalism of the surgical intervention, i.e. removal of the tumor together with the zones of regional metastasis in a single fascia-case capsule (block) and the desire to ensure the maximum physiology of the operations performed. These two provisions constitute the main strategic direction in choosing the volume and nature of the surgical intervention.
Among the numerous factors that determine the nature and extent of surgical interventions, and primarily organ-preserving ones, the degree of local spread of the tumor process (stage of the disease) and the level of tumor localization in the rectum play a fundamental role.
AT Department of Oncoproctology, N.N. Blokhin Russian Cancer Research Center of the Russian Academy of Medical Sciences adopted the following classification of the rectum
1) 4.1 -7.0 cm - lower ampulla
2) 7.1 - 10.0 cm - middle ampoule section
3) 10.1 - 13.0 cm - upper ampulla
4) 13.1-16.0 cm - rectosigmoid department
According to this classification, in almost half of the patients (47.7%) the tumor was localized in the lower ampullar rectum, in 29.5% in the middle ampullar and in 22.8% in the upper ampullar and rectosigmoid rectum.
Among the less significant factors influencing the choice of indications for various types of surgical intervention, a certain role is given to the age of the patient, the degree and severity of concomitant pathology, and the presence of complications from the tumor process.
Taking into account these factors, the entire range of surgical interventions on the rectum can be conditionally divided into two categories - with and without preservation of the sphincter apparatus of the rectum. Moreover, in recent years, everywhere in large oncoproctological clinics, there has been a clear trend towards an increase in the number of organ-preserving operations. A similar pattern is noted in the RONTS them. N.N. Blokhin, where in recent years the percentage of sphincter-preserving operations has increased to 70.1% (diagram)
Of course, the expansion of indications for organ-preserving operations should go hand in hand with the development of clear criteria for their implementation based on a comparative analysis of long-term results of treatment, the development and implementation of stapling devices, the rationale for indications for the use of combined and complex treatment programs that increase the ablasticity of surgical interventions.
Cancer of the upper ampulla and rectosigmoid rectum
In cancer of the upper ampullar and rectosigmoid rectum, according to the vast majority of oncoproctologists, the method of choice is transabdominal (anterior) resection of the rectum. So, this operation is performed in more than 85%. Other types of surgical interventions (abdomino-perineal extirpation of the rectum, Hartmann's operation, abdomino-anal resection) with this localization of the tumor account for only 14-15% of operated patients. Moreover, these surgical interventions were performed, as a rule, with a complicated tumor process or severe concomitant somatic pathology of patients, when the formation of an interintestinal anastomosis is associated with a high risk of developing insufficiency of the anastomosis sutures.
With an uncomplicated course of the tumor process, the implementation of surgical interventions for cancer of the rectosigmoid and upper ampullar rectum does not present technical difficulties, and the possibility of conducting a full-fledged intraoperative visualization of the degree of local and lymphogenous spread of the tumor process allows you to fully comply with the principles of oncological radicalism (preliminary ligation of arteriovenous trunks, isolation tumors only in an acute way, minimal contact with the tumor, i.e. compliance with the “no touch operation” principle, etc.).
When the tumor is localized at the level of the pelvic peritoneum, the latter is opened with a lyre-shaped incision in the presacral region and the rectum with pararectal fiber is mobilized in a single fascial-case capsule 5-6 cm below the tumor. At this level, the fascial capsule of the rectum is dissected and the intestinal wall is freed from pararectal fiber . In this case, pararectal tissue is displaced to the tumor and removed in a single block. It is important to emphasize that only complete and adequate mobilization of pararectal tissue distal to the tumor at least 5-6 cm and removal of the latter is the most important factor for the prevention of extraintestinal relapses (from pararectal lymph nodes).
Another important factor in the prevention of locoregional relapses is the implementation of a full-fledged lymph node dissection, taking into account the main ways of lymph outflow. Taking into account that the main path of lymphatic drainage from tumors of this section of the rectum is along the course of the upper rectal vessels, the latter should be tied off at the place where they originate from the inferior mesenteric artery (or from the sigmoid artery) and removed together with the tumor in a single block. If enlarged lymph nodes are found along the course of the inferior mesenteric artery, the latter is ligated at the place where it originates from the aorta.
After removal of a part of the intestine with a tumor, in most cases, the continuity of the colon is restored - an inter-intestinal anastomosis is formed. Interintestinal anastomosis during transabdominal (anterior) resection is formed either using stapling devices (domestic device AKA-2 for applying compression anastomoses, imported devices ETICON or JOHNSON & JOHNSON) or manually. The choice of the method of forming an interintestinal anastomosis (manual or hardware) largely depends on the experience of using staplers, the qualifications of the operating surgeons, the setting of the clinic, etc.
Analyzing the results of surgical treatment of cancer of the upper ampullar rectum, it should be noted that local recurrences occur in 11.2%, the overall 5-year survival rate is 79.9%, the 5-year relapse-free survival rate is 69.4% (data from the Russian Cancer Research Center)
This clinical situation prompts an urgent search for ways to increase the ablasticity of surgical interventions, using the possibilities of a combined method with the inclusion of preoperative large-fraction radiation therapy in the treatment program.
Using a combined method of treatment in a total focal dose of 25 Gy. in patients with tumors larger than 5 cm, it was possible to reduce the frequency of locoregional recurrences to 6.2% (with surgical treatment 11.2%), due to their reduction in patients with regional lymph node metastases (from 15.1% to 5.8%).
The obtained data give grounds to believe that the most reasonable method of treating cancer of the upper ampulla and rectosigmoid rectum with tumors not exceeding 5 cm and in the absence of metastatic lesions of regional lymph nodes is surgical, and the combined method should be used in cases of suspected metastatic lesions of regional lymph nodes. and (or) in patients where the size of the tumor process exceeds 5 cm.
Cancer of the middle ampulla of the rectum
Surgery for cancer of the middle ampulla of the rectum has a number of specific features due to the localization of the tumor process in the small pelvis - under the pelvic peritoneum. Under these conditions, the mobilization of the rectum with a tumor after dissection of the pelvic peritoneum occurs in the depths of the small pelvis in conditions of a surgical field limited by bone structures, creating certain difficulties for observing the basic principles of surgical ablation. So in cancer of the middle ampulla, if the preliminary ligation of the upper rectal vessels does not present technical difficulties, then the ligation, and even more so separate, of the middle rectal vessels passing in the depths of the small pelvis is impossible without preliminary mobilization of almost the entire rectum. Certain difficulties arise when trying to comply with the “no touch operation” principle, i.e. using the technique of “non-contact” with the tumor during the operation.
The desire to increase the radicalism of surgical interventions and at the same time preserve the sphincter apparatus in cancer of the middle ampulla of the rectum prompts the authors to use a wide variety of types of surgical interventions. The most performed surgical interventions for this localization of the tumor process are transabdominal (anterior) resection, abdomino-anal resection with colon relegation, Hartmann operation, supranal resection, modification of the Duhamel operation, and abdominoperineal extirpation of the rectum.
For a long time, the issue of the possibility of performing sphincter-preserving operations in the presence of such a prognostically unfavorable sign of the local spread of the tumor process as germination of the intestinal wall by the tumor was not unambiguously resolved. This applies especially to circular tumors, with infiltration of pararectal tissue and possible damage to adjacent structures (posterior wall of the vagina, prostate, seminal vesicles), as well as tumors of non-epithelial origin.
In these clinical situations, a number of authors strongly recommend performing abdominoperineal extirpation of the rectum. However, as subsequent clinical observations have shown, such characteristics of the tumor process as the circular nature of growth with invasion into the pararectal tissue, in some cases and into neighboring organs, should not serve as absolute contraindications to performing sphincter-preserving operations.
Contraindications to such interventions are complicated forms of rectal cancer (perifocal inflammation, pararectal fistulas), and also if the neoplasm is of a connective tissue nature. This approach made it possible to increase the proportion of combined and extended sphincter-preserving operations from 44.7% to 53.8%. without compromising the long-term results of treatment compared with abdominoperineal extirpation of the rectum.
As in the case of abdomino-perineal extirpation of the rectum, and during abdomino-anal resection, the rectum with the tumor is mobilized in its own facto-case capsule to the pelvic floor muscles with their subsequent removal in a single block. Such a volume of mobilization makes it possible to perform total mesorectumectomy, which is a key moment in the prevention of extraintestinal cancer recurrence and allows you to retreat below the tumor by at least 2-3 cm and thereby prevent the possibility of submucosal spread of tumor cells.
The differences between these two operations relate only to the preservation of the levators and sphincter during abdominal-anal resection, the removal of which is not justified oncologically, due to the lack of their involvement in the tumor process. Thus, oncologically justified and justified is the desire to both perform and expand the indications for performing sphincter-preserving abdomino-anal resection of the rectum when the tumor is located in the middle ampullar section of the rectum, even with the involvement of adjacent organs in the tumor process.
All of the above makes it possible to recommend in clinical practice the performance of organ-preserving operations for cancer of the middle ampulla of the rectum only if two of the most important oncological requirements are met - this is the removal of the mesorectum (i.e., performing a total mesorectumectomy) and resection of the intestine at least 2-3 cm below the distal border of the tumor.
Another aspect when choosing indications for performing various types of sphincter-preserving operations (trans-abdominal or abdominal-anal resection) for cancer of the middle ampulla of the rectum is the possibility of performing a full-fledged (adequate) lymph node dissection, especially for the removal of lymph nodes along the middle intestinal arteries.
Based on the experience of treating cancer of the middle ampulla of the rectum, accumulated in the Department of Oncoproctology of the N.N.
At the same time, despite the observance of a differentiated approach to the choice of indications for performing sphincter-preserving operations, the recurrence rate remains quite high. This gave grounds to believe that the surgical method in the treatment, in particular, of cancer of the distal rectum, has reached its limit and further improvement in the technique of surgical intervention is unlikely to lead to further improvement in long-term results of treatment. In this regard, further progress in this direction is associated with the need to create a comprehensive program for the prevention of locoregional cancer recurrence.
Based on radiobiological data on increasing the effectiveness of radiation exposure to the tumor with large fractions, the oncoproctology department of the N.N. with daily fractionation in single doses of 5 Gy.
The combined method of treatment made it possible to significantly reduce the recurrence rate from 22.1% to 10.1% and increase the 5-year relapse-free survival by 15.1%.
Thus, the results of the study give grounds to assert that the combined method of treating cancer of the middle ampulla of the rectum should be considered the method of choice, especially when it is planned to perform sphincter-preserving operations. The use of one surgical method for the treatment of tumors of this localization, due to the high incidence of locoregional cancer recurrences, should be of limited use and used only in cases of a complicated course of the tumor process, when preoperative radiation therapy cannot be applied.
Cancer of the lower ampulla of the rectum
In case of localization of cancer in the lower ampullar part of the rectum for a long time, the performance of abdominoperineal extirpation of the rectum was the only reasonable operation from the standpoint of compliance with the principles of oncological radicalism. However, the long-term results of the surgical method of treating cancer of this localization when performing seemingly such an extensive surgical intervention remain disappointing. The frequency of locoregional cancer recurrence ranges from 20 to 40% of operated patients, and relapse-free survival in case of regional lymph node metastases does not exceed 26.3%.
Earlier (in the treatment of cancer of the middle ampulla of the rectum), radiobiological data were presented to substantiate the program of preoperative large-fraction gamma therapy and the treatment method was given. The more neglected the tumor process, namely in cancer of the lower ampulla of the rectum (the advanced stages include stages classified as T3N0 and T2-3N1), the less significant is the role of preoperative radiation therapy in improving long-term results of treatment.
At the present stage of development of oncology, further progress in the development of radiation therapy, and hence the combined method of treatment, is associated with the development of a selective effect on the radiosensitivity of tumor and normal tissues. Among the factors that selectively increase the sensitivity of a tumor to the action of ionizing radiation, one should first of all include the use of local hyperthermia, which has been increasingly used in recent years. However, only recently this technique has received sufficient scientific justification. The use of hyperthermia is based on the fact that due to the large heating of the tumor compared to normal surrounding tissues, due to the peculiarities of the blood supply in them, there is an increased thermal susceptibility of tumor cells. It was found that thermal radiation directly destroys, first of all, cells that are in the DNA synthesis phase (S) and in a state of hypoxia. Overheating causes a pronounced disturbance, up to the cessation of microcirculation, and a decrease in the supply of cells with oxygen and other necessary metabolites. This effect cannot be achieved by any of the methods alternative to hyperthermia.
All of the above, as well as the negative results of the combined method of treating cancer of the lower ampulla of the rectum using one preoperative gamma therapy, served as the basis for the creation, together with the Department of Radiation Therapy of the N.N. component of radiation therapy.
Intracavitary hyperthermia is carried out in the microwave mode of radio waves on domestic devices Yalik, Yahta-3, Yahta-4 with a frequency of electromagnetic oscillations of 915 and 460 MHz. For this, special emitter antennas were used, which are inserted into the intestinal lumen. The temperature in the tumor was maintained in the tumor at 42.5-43 degrees for 60 minutes. In case of pronounced tumor stenosis (clearance less than 1 cm), large tumor sizes (more than 10 cm), heating through the sacrum is applied on the devices Screen-2, Yagel, Yahta-2, operating in the radio wave mode with an electromagnetic oscillation frequency of 40 MHz. Local microwave hyperthermia is carried out starting from the third session of preoperative radiation therapy over the next three days. Surgery is performed over the next three days.
The use of local microwave hyperthermia is a powerful radiosensitizing agent of radiation therapy, significantly (more than 4 times) reducing the frequency of locoregional relapses for the entire group, compared with one surgical method of treatment. Moreover, this pattern is observed in the treatment of locally advanced (operable) tumor lesions of the rectum and especially in metastatic lesions of regional lymph nodes, where the frequency of cancer recurrence decreases by more than five times (22.7% with surgical and 4.4% with thermal radiation treatment) . The consequence of this was a significant increase in 5-year relapse-free survival in combined treatment with a thermal radiation component in patients with regional lymph node metastases, compared with radiation and one surgical method of treatment.
Thus, the fundamental possibility of increasing the efficiency of the radiation component of the combined method of treating cancer of the lower ampulla of the rectum using a radiomodifier of sensitivity tissues, local microwave hyperthermia, has been shown.
CModern strategy for choosing a treatment method for patients with rectal cancer (algorithm for choosing a treatment method)
Based on the results of treatment of more than 900 patients with rectal cancer, we can formulate the following indications for choosing the optimal treatment method, taking into account the main prognostic factors (localization and degree of local spread of the tumor process):
1) Cancer of the rectosigmoid and upper ampulla of the rectum:
2) Cancer of the middle ampulla of the rectum:
The method of choice for any degree of local spread of the tumor process is combined treatment with preoperative radiation therapy. The use of a combined method of treatment is especially indicated when planning sphincter-preserving operations.
3) Cancer of the lower ampulla:
at any degree of local spread of the tumor process, the use of preoperative thermoradiation therapy in terms of combined treatment is indicated. The surgical method of treatment should have limited application and be performed only in case of a complicated tumor process.
Prognostic factors in rectal cancer
The criterion for evaluating the effectiveness of a method of treating oncological diseases is considered to be a 5-year survival rate. This figure for the surgical treatment of rectal cancer has not changed over the past decades and is 50-63%. Assessment of long-term results of treatment should be carried out taking into account the size of the tumor, its localization, the depth of tumor invasion into the intestinal wall, the presence or absence of metastatic lesions of regional lymph nodes, the degree of differentiation of tumor cells, and a number of other factors. Only such a comprehensive analysis, characterizing the degree of spread of the tumor process, is necessary for objectivity and allows one to judge the prognosis in each specific group of patients with a certain set of prognostic signs.
Factors such as the sex of patients, the duration of the history, the amount of blood transfusion during surgery, according to most authors, do not have an important prognostic value. The young age of the patient is a factor that aggravates the prognosis. However, it has been established that in young patients the frequency of metastatic lesions of regional lymph nodes is significantly higher than in patients of other age groups, and therefore a more unfavorable prognosis in patients of this category is due to this circumstance, and the patient's age itself is a secondary prognostic factor.
One of the most negative prognostic factors is the large size of the tumor. Based on the study of the prognostic value of the extent of the tumor, which most often occupies more than half of the circumference of the intestinal tube, it is clearly established that this factor almost always correlates with the depth of invasion of the intestinal wall and therefore rarely has an independent prognostic value.
A thorough analysis of clinical and morphological observations shows that the most important are the data of the pathomorphological study of removed preparations: the depth of germination of the intestinal wall, the presence or absence of regional metastases, the histological structure of the tumor.
It is known that the deeper the invasion of the intestinal wall, the worse the prognosis: 88.4% of patients in whom the tumor infiltration has not gone beyond the muco-submucosal layer live more than 5 years, 67% - with the spread of the tumor to the muscle layer, 49.6 % - with invasion of adrectal tissue. However, it should be noted that the degree of spread of the neoplasm deep into the intestinal wall has an independent prognostic value only in the absence of regional metastases; if they do occur, then the depth of invasion has practically no effect on the 5-year survival rate.
In fact, the only prognostic factor in rectal cancer, the role of which is not discussed in the literature, but is unanimously recognized, is metastatic involvement of regional lymph nodes. At the same time, the difference in life expectancy of patients with metastases to regional lymph nodes increases every 5 years of observation.
The analysis of the prognostic value of the histological structure of rectal cancer is based on the International Classification of Bowel Tumors (Morson et al., 1976), which distinguishes the following forms:
well-differentiated, moderately differentiated, poorly differentiated, mucoid adenocarcinoma and signet cell carcinoma. A relatively more favorable clinical form with relatively satisfactory long-term results is characteristic of highly and moderately differentiated adenocarcinoma, while poorly differentiated, mucosal and cricoid cell carcinoma, characterized by severe structural and cellular anaplasia, is characterized by a more aggressive course and a worse prognosis.
It can be assumed that the variability of the results of treatment of rectal cancer to a certain extent by varying the degree of differentiation of neoplasm cells, which is associated with growth rates, and therefore the depth of wall invasion, and the tendency to metastasize. Namely, these factors determine the prognosis. Thus, regional metastases in low-grade forms of rectal cancer are detected 3 times more often than in highly differentiated ones.
One of the manifestations of the body's ability to respond to the development of a neoplastic process with protective reactions is the immunological activity of regional lymph nodes. VI Ulyanov (1985), who studied in detail the significance of these factors, believes that they can explain the discrepancy between unfavorable clinical tests and a favorable outcome of treatment. A five-year period is experienced by 72.8% of patients with hyperplasia of the lymphoid tissue of regional lymph nodes and 58.2% of those in whom it was not expressed.
Very important in prognostic terms is the question of the level of resection of the rectum, i.e. distance from the line of intersection of the intestinal wall to the distal border of the neoplasm. Among patients in whom this distance was less than 2 cm, 55% survived the 5-year period, and when it was large - 70%; Moreover, according to such cardinal indicators as the frequency of regional metastases and the depth of invasion, both groups were identical. It can be assumed that in the case when the resection line is close to the edge of the tumor, the worst results are due not only to tumor infiltration of the intestinal wall, but also to the insufficiently radical removal of fiber from the lymph nodes.
Of undoubted interest are data on long-term results, depending on the type of operation, which is mainly due to the localization of the tumor. The highest 5-year survival rate (69.6%) was noted among patients who underwent transabdominal resection of the rectum, usually performed when the tumor is localized in the upper ampullar and rectosigmoid sections of the intestine.
It should be noted that none of these factors can explain why, even with similar clinical and morphological signs, as well as the volume and nature of the surgical intervention, the effectiveness of treatment is different: some patients live for 5 years or more, while others die in the early stages. after treatment for disease progression. An attempt to explain this fact prompted the study of the finer structure of tumor cells and its relationship with the prognosis of the disease.
The works of N.T. Raikhlin, N.A. Kraevsky, A.G. Perevoshchikov showed that human cancer cells retain ultrastructural features characteristic of the original, homologous for a given tumor, cells.
For the epithelium of the mucous membrane of the colon, these are several types of cells, which can only be differentiated using an electron microscope:
1) bordered enterocytes that perform the function of absorption;
2) goblet enterocytes that produce mucus;
3) endocrine cells that carry the function of humoral regulation,
4) oncocytes, the role of which has not been established;
5) squamous epithelial cells, which are apparently the result of metaplasia.
All these cells originate from the general population of intestinal crypt stem cells. Depending on the detection of the indicated ultrastructural signs of specific differentiation in cancer cells, it became possible to divide the cell population of colon cancer into 2 groups: the so-called differentiated tumor cells - the 5 types listed above (group 1), which retained the ultrastructural signs of a certain prototype of normal mucosal epithelium colon, and undifferentiated - without ultrastructural signs of organ specificity (Group 2).
The ultrastructural classification of colon tumors contains the concept of a tumor variant depending on the ratio of the ultrastructure of differentiated and undifferentiated cells: variant I - more than 50% differentiated, variant II - an equal number of them, variant III - more than 50% undifferentiated, IV variant - only undifferentiated cells.
It should be emphasized that the criterion for the degree of differentiation at the light-optical level is the similarity of the microscopic structure of the tumor with the normal epithelium of the colon mucosa, and at the ultrastructural level it is the ratio of ultrastructurally differentiated and undifferentiated elements of the tumor, defined as one of four variants of the structure. Therefore, regardless of the light-optical differentiation of adenocarcinoma, both ultrastructurally differentiated and undifferentiated cells could predominate in its cellular composition. This fact allows, to a certain extent, to explain the reason for the different prognosis for the same histological form of neoplasms.
Lymphocytic (microscopic) colitis is an inflammatory disease of the colon, accompanied by lymphocytic infiltration of the mucosa. This type of colitis is characterized by recurrent diarrhea with a long course.
Collagen colitis differs from lymphocytic colitis and is characterized by hypertrophy of collagen tissue in the subepithelial layer of the colon.
Causes of lymphocytic colitis
Collagenous and lymphocytic colitis are rare forms of pathology. The causes of the disease are not known.
The occurrence of the disease is associated with immunological disorders in the colon mucosa.
It is known that these types of colitis are observed, as a rule, in patients with Sjögren's syndrome, rheumatoid arthritis and celiac disease, i.e., diseases associated with HLA A1 and HLA AZ antigens. A pathogenic effect on the differentiation and formation of fibroblasts of the microbial flora of the intestine is also suspected.
The function of colonocytes is significantly impaired due to the presence of a large amount of connective tissue. As a result, the absorption of electrolytes and water in the colon is disrupted, which leads to chronic predominantly secretory diarrhea. The depth of the haustra and the height of the semilunar folds decrease, and the motor-evacuation function of the intestine also decreases. The colon takes the form of a tube with smooth walls in collagen colitis.
Stage I of the disease (lymphocytic or microscopic colitis) is characterized by a nonspecific inflammatory reaction, which can manifest itself as a pronounced infiltration of the intestinal wall with lymphoid cells.
Stage II of the disease (collagen colitis) differs from the previous one in that a collagen layer is found under the basement membrane of epitheliocytes.
Symptoms of lymphocytic colitis
- diarrhea (4-6 times a day), which has an intermittent, periodic character with periods of remission
- cramping abdominal pain
- weight loss (anemia rarely develops)
Treatment of lymphocytic colitis
For the treatment of mild forms of lymphocytic colitis, antidiarrheal, anti-inflammatory, antibacterial drugs are prescribed for up to 2 months (smecta, bismuth, tannalbin).
The main treatment is budesonide (budenofalk). The drug is not systemic, therefore it is maximally concentrated in the focus of inflammation and has a small number of side effects.
From non-drug means, various herbal teas with a high content of tannins are used.
A decoction of the rhizome of the burnet rhizome and the root of willow-tea is used 1 tablespoon 5-6 times a day, a decoction of the cinquefoil rhizome - 1 tablespoon 3 times a day, a decoction of bird cherry fruits - half a cup 2-3 times a day, infusion of seedlings alder (1:20) - 1 tablespoon 3-4 times a day, decoction of oak bark or blueberries - 2 tablespoons 3 times a day.
Nutrition for lymphocytic colitis
During the period of severe diarrhea, diet No. 4a is prescribed with fractional meals up to 6 times a day. Diet No. 4b is prescribed after the cessation of profuse diarrhea. During the period of remission of the disease, with the normalization of the stool - diet No. 4.
Dishes that increase fermentation are also excluded. Food is consumed in boiled and baked form. Fruits - only in baked form. You can use milk, and if it is intolerant - low-fat kefir, cottage cheese, mild cheeses.
Foods that enhance intestinal motility are excluded: chocolate, strong coffee, alcohol, rich foods, fresh fruits and vegetables, fatty fish and meat, cakes, carbonated drinks, concentrated juices, cereals (millet, pearl barley, barley), milk, fatty sour cream.
Diagnosis of abdominal infiltrate - what is it?
When a doctor diagnoses an abdominal infiltrate, what it is is of interest to any patient. This is the name of the condition when biological fluids (blood, lymph) or tissue cells accumulate in the organs of the cavity or in it itself, due to which a pathological seal is formed. It is important to eliminate the infiltrate in a timely manner so that it does not cause the formation of an abscess, fistula, or bleeding. With adequate treatment, the effusion resolves completely, leaving no traces.
Most often, this is a consequence of many different diseases, primarily inflammatory. The accumulation of biological fluids - effusion (exudate) - a sign of such processes or excess blood, lymph in the internal organs. These fluids may contain blood elements, proteins, minerals, dead cells, as well as pathogens, which, in fact, cause inflammation. Depending on the composition, hemorrhagic (bloody), serous (from blood serum), fibrinous (mainly from leukocytes with localization in some organ), putrefactive, purulent effusions are diagnosed. It is necessary to distinguish exudate from transudate, when water accumulates in the cavities during edema.
According to medical statistics, an inflammatory infiltrate develops with effusion from blood vessels in 23% of cases as a result of various infections (staphylococci, streptococci, candida, etc.), and in 37% due to injuries. It happens that with appendicitis a tumor forms with an inflamed process inside, if the latter is not removed in a timely manner. Sometimes, during surgical interventions, a postoperative infiltrate of the abdominal organs is detected after a few weeks. The causes of seals in them are anesthetics, antibiotics, alcohol, foreign bodies. Due to poor-quality surgical threads, a scar infiltrate can form, even several years after the operation. If it causes the development of an abscess (strong suppuration of tissues with their decay), it must be surgically eliminated.
When malignant cells multiply, tissues proliferate, increase in volume, forming a tumor infiltrate that causes pain. Lymphoid seals of the abdominal organs with a predominance of lymphocytes appear in chronic infectious diseases, weakened immunity.
Often, post-injection infiltrates are formed if the injections are made unsuccessfully or in violation of the rules of medical manipulations.
Manifestations of pathology
Its main symptoms are:
- weak aching pain in the abdominal cavity;
- more distinct pain and denting when pressed;
- redness, swelling of the peritoneum, a visually distinguishable seal under the skin;
- normal body temperature or a slight increase (with appendicitis significant, up to 39 ° C);
- digestive disorders - constipation, diarrhea, flatulence.
Additionally, the hallmarks of the infiltrate may be such mild manifestations as slight redness or a shiny appearance of the skin. The symptomatology that occurs when there is air in the abdominal cavity is important for the diagnosis of acute peritonitis - a total inflammation that is life-threatening. When purulent foci, delimited by muscles, are detected, an increase in the signs of inflammation is essential for the prognosis of the development of the disease. For this purpose, they are monitored and repeated palpation of the abdominal organs.
To determine the composition of the exudate, the biopsy method is used - the selection of a fluid sample from the peritoneum with a special needle. The latter is subjected to histological analysis, which allows you to make a final diagnosis. If an inflammatory infiltrate is suspected, differential diagnosis is necessary, taking into account the cause of the pathology, its duration and the conditions under which it arose.
It is possible to reveal the structure of the infiltrate, the presence of an abscess or cystic neoplasms in which water accumulates, using echography. To determine the localization and exact dimensions of the seal, an ultrasound of the abdominal organs is performed. In difficult cases, a CT scan is required.
The main goal is the elimination of infiltration. Often this is achieved by methods of only conservative treatment. The general principles of therapy for this pathology are as follows:
- bed rest;
- local hypothermia;
- taking antibiotics;
- physiotherapy.
Local hypothermia - cold on the peritoneal area - constricts blood vessels, inhibits metabolic processes, reduces the production of enzymes and thus helps to stabilize the inflammatory process, preventing its further spread. A course of antibiotic treatment is usually prescribed for a period of 5-7 days. The most commonly used antibiotics are Amoxicillin, Ampicillin, Ceftriaxone, Metronidazole, etc. They are taken simultaneously with drugs that restore beneficial intestinal microflora, such as Linex or Bifiform.
Sanitation of the abdominal cavity is very effective in the absence of suppuration and tumors by means of physiotherapy. Thanks to electrophoresis with antibiotics, calcium chloride, sessions of laser, electromagnetic or ultraviolet irradiation, pain disappears, swelling subsides, local blood circulation improves and the seal gradually resolves. However, when conservative treatment fails, abscess formation, or signs of peritonitis, surgical intervention is required. The abscess is removed using laparoscopic surgery under ultrasound control, during which the purulent focus is drained. With peritonitis, you can not do without extensive abdominal surgery.
After removal of the purulent focus, the abdominal cavity is sanitized with antiseptic solutions of sodium hypochlorite, chlorhexidine. One of the most important conditions for successful treatment is drainage of the abdominal cavity. To do this, several tubes are installed in the latter, through which the outflow of exudate is carried out (an average of 100-300 ml per day). Drainages reduce the degree of intoxication of the body, provide early diagnosis of possible postoperative complications: divergence of surgical sutures, perforation of organs, bleeding.
Timely drainage of the abdominal cavity, medical and physiotherapeutic treatment of infiltrate, used in combination, lead to rapid resorption of the formation and provide a favorable prognosis for the patient.
What do we know about hemorrhoids?
In a special section of our website you will learn a lot of necessary and useful information about the disease "hemorrhoids". The widespread belief that "everyone" suffers from hemorrhoids is wrong, however, hemorrhoids are the most common proctological disease. Hemorrhoids are most susceptible to people aged 45 to 65 years. Hemorrhoids are equally common in both men and women. Many patients prefer to self-treat, or do not treat hemorrhoids at all. As a result, neglected cases of hemorrhoids are, unfortunately, quite common. Specialists of the "Treatment and Diagnostic Center of Coloproctology" strongly do not recommend postponing the treatment of hemorrhoids, because hemorrhoids cannot go away on their own. Also, we recommend you products from hemorrhoids on the website vitamins.com.ua. Always up-to-date prices, original goods and fast delivery throughout Ukraine. For all questions, please contact the Contacts section on the website vitamins.com.ua.
Medical and Diagnostic Center of Coloproctology LIDIKO
The main activities of the medical center
Symptoms of proctological diseases
Here are the symptoms of hemorrhoids and other diseases of the colon: pain in the anus, rectal bleeding, discharge of mucus and pus from the anus, constipation, obstruction of the colon, bloating, diarrhea.
Diseases of the colon and anal canal
Diagnostic methods used in proctology
You will be calmer and more comfortable at the appointment with a proctologist if you know and understand the features and objectives of the examinations conducted or prescribed by him to diagnose hemorrhoids and other diseases.
Articles and publications about the problems of coloproctology
Various articles and publications on the problems of coloproctology are divided into topics: "General coloproctology" (including the problems of treating hemorrhoids), "Tumors of the colon", "Non-tumor diseases of the colon", "Colitis". The section is periodically updated with new materials.
NEW IN UKRAINE: Painless treatment of hemorrhoids.
Transanal dearerialization of hemorrhoids. THD technique. Presentation of the methodology. Video.
REMOVAL OF INFILTRATE IN THE RECTUM
Appointment for a consultation: 8-926-294-50-03;
The address of the Clinic is Moscow, Troitskaya st., 5 (Tsvetnoy Boulevard metro station)
CREATE A NEW MESSAGE.
The next problem worries - there are hemorrhoids and a fissure. Often only the crack gets worse. I want to clarify - I have a constant thrush / vaginal candidiasis. I get treated and it gets better, but if I get nervous or another bad factor, vaginal candidiasis reappears. I understand how immunity weakens and thrush is right there. Why am I writing about this, I think maybe my vagina self-infected the anal canal and the skin is unhealthy, as it were, and does not allow the crack to heal. dear doctors, tell me is it possible? So candida anal dermatitis is invisible to my eye?
To rate answers and comment, go to this question's page »»»
