Stained with hematoxylin and eosin. There is a fibrinous-purulent exudate in the area of ​​the defect in the stomach wall (a), with an underlying extensive area of ​​fibrinoid necrosis (b), the presence of granulation tissue (c) and the growth of coarse fibrous connective tissue, penetrating to different depths of the muscle layer (g). The serous membrane of the stomach wall is preserved (e).

2. Chronic atrophic gastritis. Heme coloring

toxin and eosin. In the gastric mucosa, atrophy of the integumentary epithelium (a) and epithelium of the glands with restructuring

which glands according to the intestinal type - "intestinal metaplasia" (b), in the lamina propria of the mucous membrane of the field of sclerosis

(c) and lymphoplasmacytic infiltration with the formation of lymphoid follicles (d).

3. Adenocarcinoma. Stained with hematoxylin and eosin. All layers of the stomach wall are infiltrated with tumor tissue with signs of cellular atypism (a). Multiple pathological mitoses are seen in hyperchromic (b) and polymorphic tumor cells (c).

4. Mucous cancer of the stomach. Stained with hematoxylin and

eosin. The tumor tissue is represented by an abundance of large atypical "cricoid" cells (a) with the formation of a large amount of mucus (b). The infiltrative character of tumor growth is visible (c). Demonstration.

5. Scirrhus of the stomach. Stained with hematoxylin and eosin. In the wall of the stomach, a group of atypical cells with large hyperchromic nuclei (a), in the stroma of the tumor, the growth of fibrous connective tissue (b). Demonstration.

MACRO PREPARATIONS.

1. Acute catarrhal gastritis: in stomach preparation The mucous membrane is thickened, with high hyperemic folds, covered with thick viscous mucus, with petechial hemorrhages. Causes: poor-quality food, the use of alcohol surrogates, antitumor chemotherapy drugs, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.

Complications: acute ulcers, transition to chronic gastritis. Exodus: mucosal restoration.

2. Erosions and acute stomach ulcers: in the preparation of the stomach,

the mucous membrane is edematous, on the surface there are multiple petechial hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucosa, and ulcers penetrate

cabins at different depths of the mucous membrane, some reach the muscular membrane.

Causes: endocrine diseases (Zolinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, steroid and stress ulcers.

Complications: perforation, peritonitis.

Exodus: erosions are epithelialized, the ulcerative defect is replaced by scar tissue.

3. Chronic stomach ulcer in remission: in the preparation of the stomach, on the lesser curvature, there is a pathological focus in the form of a deepening of the mucous membrane, rounded, 3 cm in diameter. The mucosal folds radially converge to the defect, the edges of which are dense, raised in a roller-like manner, callused (calculous ulcer). On the cut, the inlet is a crater, smaller than the inner part of the ulcer. The edge facing the cardia is undermined, the mucous membrane hangs over it. The edge facing the gatekeeper is flat - terraced. The thickness of the ulcer is represented by connective tissue, gray-white, 2.5 cm. At the bottom of the ulcer, the vessels are sclerotic, their lumen is gaping.

Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to exposure to peptic aggression factors (hydrochloric acid and pepsinogen).

Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformity of the stomach with the development of stenosis behind the inlet or outlet. Against the background of a chronic ulcer, a second disease can develop - stomach cancer.

4. Polyps of the stomach (adenomas): in the antrum

In the stomach there are two tumor-like formations the size of pigeon eggs, on thin legs, irregular oval shape with a villous surface, soft consistency.

In the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without sprouting the underlying tissues.

Complications: bleeding, torsion of the leg, obturation of the exit or inlet.

Exodus: malignancy.

5. Various forms of stomach cancer.a) Fungal cancer:

on the surface of the mucous membrane there is a tumor-like formation growing into the lumen of the stomach, of an irregular round shape, 5 cm in diameter, on a wide base in the form of a mushroom cap, with a retraction in the center. The cut shows that the tumor sprouts the entire wall of the stomach.

b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened up to 1 cm along its entire length, of a dense "woody" consistency, on the section it is represented by a gray-pinkish tissue. The mucous membrane is uneven, its folds of various thicknesses, the serous membrane is thickened, dense, tuberous. The lumen of the stomach is narrowed.

c) Saucer-shaped stomach cancer: on the lesser curvature there is a pathological focus in the form of a formation rising above the surface of the mucous membrane with dense roller-like edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown decaying masses. On section, the tumor tissue infiltrates the entire thickness of the organ wall.

Causes: nutrition (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after stomach operations, especially according to Billroth II), Helicobacter pylori (contributes to the development of mucosal atrophy, intestinal metaplasia, epithelial dysplasia). Metastasis: 1. Orthograde lymphogenous metastases to regional nodes on the lesser and greater curvature, retrograde lymphogenic metastases in the left supraclavicular lymph node - Virchow's metastasis, in the ovaries - Krukenbergovsky

cancer, pararectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, less often to the adrenal glands and pancreas. 4. Implantation- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.

TEST CONTROL

Choose one or more correct answers

1. SIGNS OF ACUTE CATHARAL GASTRITIS

1) thickening of the mucosa

2) glandular atrophy

3) multiple erosions

4) mucosal sclerosis

5) neutrophilic infiltration of the mucosa

6) lymphoid infiltration of the mucosa

2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS

1) fibrinous

2) atrophic

3) hypertrophic

4) catarrhal

5) corrosive (necrotic)

3. CHANGES IN THE EPITHELIUM IN CHRONIC GASTRITIS

1) atrophy

2) intestinal metaplasia

3) hyperplasia

4) dysplasia

5) the appearance of Mallory bodies in the cytoplasm

4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A

2) autoantibodies in the blood

to parietal cells

3) Helicobacter pylori -

5. PATHOGENESIS OF PERNICIOUS ANEMIA IN AUTOIMMUNE GASTRITIS

1) cessation of HCl production

2) production of antibodies to Helicobacter pylori

3) production of antibodies to parental cells

4) production of antibodies to intrinsic factor

5) destruction of the glands and atrophy of the mucous membrane

6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS IN

1) predominant localization - antrum

2) autoantibodies in the blood

to parietal cells

3) Helicobacter pylori -

main etiological factor

4) accompanied by G-cell hyperplasia, gastrinemia

5) often associated with pernicious anemia

6) is localized in the fundus

7) reflux of duodenal contents into the stomach - the basis of pathogenesis

ACUTE EROSION OF THE STOMACH IS

mucosal inflammation

mucosal necrosis,

nonmuscular

3) atrophy of the mucous membrane

4) mucosal sclerosis

5) necrosis involving the muscle layer

8. CLINICAL AND MORPHOLOGICAL SIGNS OF CHRONIC ATROPHIC GASTRITIS

IN THE STAGE OF EXAMINATION

1) often occurs in patients with alcoholism

2) the mucous membrane is not changed

3) diffuse lymphoid-plasmacytic infiltration with a significant admixture of PMN

4) foci of pyloric and intestinal metaplasia

5) increased acidity of gastric juice

9. MORPHOLOGICAL SUBSTRATE OF ULCER

1) inflammation of the gastric mucosa

2) erosion of the gastric mucosa

and 12 duodenal ulcer

3) acute stomach ulcer

and duodenum

4) chronic recurrent gastric and duodenal ulcer

5) inflammation of the mucous membrane of the duodenum

10. Sclerotic deformity of the stomach IS THE OUTCOME

1) catarrhal gastritis

2) diphtheritic gastritis

3) corrosive gastritis

4) phlegmonous gastritis

11. SIGNS of chronic atrophic gastritis as a precancerous disease

1) lymphoplasmacytic infiltration

2) sclerotic processes

3) structural restructuring of the epithelium

(intestinal metaplasia)

4) all answers are correct

5) all answers are wrong

12. ULCEROGENIC PROMOTORS

1) corticosteroids

3) aspirin

4) smoking

5) increased tone of the vagus nerve

13. Stomach ulcers include

1) endocrine ulcers of the stomach

2) allergic ulcers

3) peptic ulcers

4) postoperative ulcers

5) tuberculous ulcers

14. LOCAL FACTORS IN THE DEVELOPMENT OF Peptic Ulcer

1) increased aggressiveness of gastric juice

2) campillobacteria

3) the presence of chronic gastritis

4) circulatory disorders

5) all answers are correct

6) all answers are wrong

15. REASONS FOR THE DEVELOPMENT OF ACUTE GASTRIC ULCER

1) corticosteroids

3) aspirin

4) smoking

5) increase in tone

vagus nerve

16. MORPHOLOGICAL SIGNS OF ACUTE gastric ulcer

1) funnel shape

2) the shape of a truncated pyramid

in cross section

3) soft jagged edges

4) dense callused edges

7) multiple ulcers

17. MORPHOLOGICAL SIGNS of chronic gastric ulcer

1) funnel shape

2) the shape of a truncated pyramid

in cross section

3) soft jagged edges

4) dense callused edges

5) the bottom of the ulcer, as it is cleansed, is stained black with hematin hydrochloride

6) the edge of the ulcer, facing the pylorus, looks like a terrace, the cardial edge is undermined

18. SIGNS OF CHRONIC GASTRIC ULCER

DURING REMISSION

1) the presence of exudate on the surface

2) scar tissue interrupts the muscle membrane to different depths

3) endovasculitis

4) fibrinoid changes in the bottom and vessels

5) surface epithelialization

19. SIGNS OF CHRONIC GASTRIC ULCER

IN THE PERIOD OF EXAGENCE

1) the presence of fibrinous-purulent exudate

on the surface 2) scar tissue interrupts muscle

shell at different depths

3) endovasculitis

4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer

12. Bleeding mechanism in peptic ulcer

arrosive

diapedetic

due to rupture of a blood vessel

as a result of purulent fusion

21. Chlorhydropenic uremia - the result

1) bleeding from an ulcer

2) chronic nephritis

3) ulcer penetration

4) cicatricial pyloric stenosis

5) all answers are correct

6) all answers are wrong

22. Peritonitis complicating a chronic ulcer is the result of

1) penetration

2) perforations

3) gastritis

4) duodenitis

5) cicatricial stenosis of the pylorus

23. COMPLICATIONS OF CHRONIC ULCER

1) penetration

2) perforations

3) empyema

4) hypercalcemia

5) cicatricial stenosis

and wall deformation

6) bleeding

24. TYPES OF GASTROPATHIES

1) Meniere's disease

2) Menetrier's disease

3) Wernicke's syndrome

4) Zollinger-Ellison syndrome

5) hypertrophic hypersecretory gastropathy

25. HISTOLOGICAL SIGNS OF GASTROPATHIES

1) hypertrophy of the gastric mucosa

2) atrophy of the gastric mucosa

3) hyperplasia of the integumentary pit epithelium

4) hyperplasia of the glandular epithelium

5) severe sclerosis

26. MORPHOLOGICAL SIGNS OF THE INFLAMMATORY POLYP

1) inflammatory infiltrate in the stroma

2) atypical cells

3) without a clear differentiation into the leg and body

4) dysplasia of the glandular epithelium

5) surface erosion

27. BENIGN TUMORS OF THE STOMACH

1) angiosarcoma

2) adenoma

3) leiomyoma

4) adenocarcinoma

5) hyperplasiogenic polyp

28. BACKGROUND FOR THE DEVELOPMENT OF GASTRIC ADENOMA

1) chronic superficial gastritis

2) acute erosive-hemorrhagic gastritis

3) acute fibrinous gastritis

4) chronic gastritis with enterolization

29. ADENOMA IS THIS

1) benign tumor

from glandular epithelium

2) a malignant tumor of the glandular epithelium

3) epidermal cancer

4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium

30. DISEASES WITH A RISK OF CANCER

1) superficial gastritis

2) chronic stomach ulcer

3) acute erosive gastritis

4) chronic atrophic gastritis

5) adenomatous polyps

31. HISTOLOGICAL VARIANTS OF GASTRIC CANCER

1) adenocarcinoma

2) sarcoma

3) cricoid

4) undifferentiated

32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL TYPE GASTRIC CANCER

1) occurs more often before the age of 30 years

2) has a high degree of differentiation

3) develops against the background of chronic gastritis

4) 2 times more likely to affect men

5) develops from metaplastic epitheliocytes

33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUSE TYPE GASTRIC CANCER

1) develops from epitheliocytes

2) occurs at a relatively young age

3) histologically cricoid-cell

4) occurs against the background of chronic gastritis

5) has a low degree of differentiation

34. PROGNOSTIC SIGN IN GASTRIC CANCER

1) histological variant

2) macroscopic form

3) depth of invasion

4) mucus formation

5) secondary changes

35. HISTOLOGICAL SIGNS OF POLYPOID STOMACH CANCER

1) atypical glandular structures of a bizarre shape

2) cricoid cells

3) an abundance of mucus in the lumen of the glands

4) atypical polymorphic cells with large hyperchromic nuclei

5) atypical cells characterized by monomorphism

36. HISTOLOGICAL SIGNS OF CRIC CELL GASTRIC CANCER

1) extensive hemorrhages are characteristic

2) the nuclei of atypical cells are displaced

to the cell membrane

3) poorly differentiated cells with very large irregularly shaped hyperchromic nuclei

4) atypical glandular structures

5) massive sclerosis and hyalinosis in the wall

37. MICROSCOPIC CHARACTERISTICS OF SCIRRHOUS GASTRIC CANCER

1) atypical cells with large

nuclei are arranged in groups

2) atypical cells form glands

3) massive growths of connective tissue

4) an abundance of mucus in the lumen of the glands

5) atypical cells do not form glands

38. KRUKENBERG AND SCHNITZLER METASTASES OF GASTRIC CANCER

1) hematogenous

2) implantation

3) lymphogenous orthograde

4) lymphogenous retrograde

39. COMPLICATIONS OF GASTRIC CANCER

1) hemoptysis

2) dilatation of the pylorus

3) perforation

4) exhaustion

5) stomach bleeding

40. SIGNS OF VIRCHOV METASTASIS

1) hematogenous metastasis

2) retrograde lymphogenous metastasis

3) peritoneal carcinomatosis

4) damage to the left supraclavicular lymph node

5) ovarian damage

Sample answers To test tasks

9. What is the average duration of the first three stages of development of lobar pneumonia?

10. Specify the ways of spreading inflammation in croupous pneumonia.

11. List the pulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.

12. Describe the composition of the exudate in case of lobar pneumonia in the tide stage.

13. Describe the composition of the exudate in case of lobar pneumonia in the stage of red hepatization.

14. Describe the composition of the exudate in case of lobar pneumonia in the stage of gray hepatization.

15. Specify extrapulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.

16. Give a macroscopic description of lung changes in bronchopneumonia.

17. Give a microscopic description of changes in the lungs in focal pneumonia.

18. Name the features of nosocomial pneumonia pathogens.

19. Name a complication of lobar pneumonia that develops with excessive activity of neutrophils with massive destruction of lung tissue.

20. Specify the complication of lobar pneumonia that develops with insufficient activity of neutrophils and the development of the organization of fibrinous exudate.

21. Name the reasons for the formation of a lung abscess.

22. List the reasons for the formation of a lung abscess.

23. Define the term atelectasis.

24. What develops when the airway lumen is completely closed?

25. What develops with partial filling pleural cavity liquid exudate?

26. What develops in respiratory distress syndrome due to the destruction of surfactant?

27. Specify the cause of hemodynamic pulmonary edema.

28. A 25-year-old patient fell ill suddenly after hypothermia while intoxicated. Complains of a rise in body temperature up to 390C, chills, dagger pain in the right side and severe weakness for 7 days. Objectively: a dull sound is heard over the lower lobe of the right lung during percussion, during auscultation - breathing is not carried out, a pleural rub is heard. X-ray - darkening of the lower lobe of the right lung, in the area of ​​the 8th segment of the cavity, thickening of the pleura. Your conclusion.

29. In a patient with a stroke and left-sided hemiparesis on the 14th day, the body temperature increased to 380C, which was accompanied by the appearance of cough and fine bubbling rales in the lower sections of the left lung. Your conclusion.

30. A 67-year-old man undergoing inpatient treatment for phlegmon of the scalp developed shortness of breath, cough, body temperature increased to 38.50C. 4 weeks after massive antibiotic therapy, body temperature decreased, shortness of breath decreased, moderate leukocytosis persisted. An annular shadow with a liquid level appeared in the second segment of the right lung during an X-ray examination. your diagnosis.

II lesson

CHRONIC NON-SPECIFIC LUNG DISEASES. INTERSTITIAL LUNG DISEASES. PNEUMOKONIOSIS. LUNG CANCER.

1. Diffuse chronic lung lesions: definition of the concept and classification. Chronic obstructive pulmonary disease. General characteristics.

2. Chronic obstructive pulmonary emphysema– definition, classification, epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Other types of emphysema (compensatory, senile, vicarious, interstitial): clinical and morphological characteristic.

3. Chronic obstructive bronchitis: definition, classification, etiology, epidemiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes.

4. Bronchiectasis and bronchiectasis. Concept, classification, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Kartagener's syndrome. Clinical and morphological characteristics.

5. Diffuse interstitial lung disease. Classification, clinical and morphological characteristics, pathogenesis. Alveolitis. Morphological characteristics, pathogenesis. Pneumoconiosis (anthracosis, silicosis, asbestosis, berylliosis). Pathogenesis and morphogenesis, clinical manifestations, complications, causes of death. Sarcoidosis. Clinical and morphological characteristics, morphology of extrapulmonary lesions.

6. idiopathic pulmonary fibrosis. Classification, etiology, pathogenesis and morphogenesis, stages and variants, clinical and morphological characteristics, prognosis.

7. Pneumonitis(desquamative interstitial pneumonitis, hypersensitivity pneumonitis): patho- and morphogenesis, clinical and morphological characteristics, causes of death. Eosinophilic infiltrate of the lung. Classification, causes, clinical and morphological characteristics.

8. Tumors of the bronchi and lungs. Epidemiology, principles of classification. benign tumors. Malignant tumors. Lung cancer. Bronchogenic cancer. Epidemiology, etiology. Biomolecular markers of lung cancer. Precancerous changes in the bronchi and lung. The concept of "cancer in the rumen". Clinical manifestations. Diagnostic methods, morphological characteristics, macroscopic variants, histological types (squamous cell, adenocarcinoma, small cell, large cell). Bronchioloalveolar cancer: clinical and morphological characteristics.

1. Lecture material.

v.2, part I: pp. 415-433, 446-480.

v.2, part I: pp. 293-307, 317-344.

4. Guide to practical exercises in pathological anatomy (, 2002) p. 547-567.

5. Atlas of pathological anatomy (, 2003) p. 213-217.

EDUCATIONAL CARD

OBJECTIVE SETTING OF THE LESSON: study the morphology of the main forms of chronic lung diseases using macropreparations, micropreparations and electron diffraction patterns and make clinical and anatomical comparisons.

CHRONIC NON-SPECIFIC

LUNG DISEASES

View macropreparations, the main clinical and anatomical forms of chronic nonspecific lung diseases. Describe CHRONIC LUNG ABSCESS, CHRONIC BRONCHITIS WITH BRONCHECTASIS, PULMONARY EMPHYSEMA.

Micropreparation No. 12 CHRONIC DEFORMING BRONCHITIS (staining with hematoxylin and eosin). Note the components of chronic bronchial inflammation: peribronchial sclerosis, vascular percalibration, inflammatory infiltration in the bronchial wall and peribronchial tissue, metaplasia of the bronchial epithelium.

electronogram INTRACAPILLARY SCLEROSIS IN PULMONARY EMPHYSEMA (atlas, Fig. 11.13). Note the formation of a capillary with a sclerosed wall and the destruction of the air-blood barrier.

PNEUMOCONIOSIS

macropreparation ANTRACO-SILICOSIS OF THE LUNG. Pay attention to the change in volume and decrease in the airiness of the lung tissue. Characterize sclerotic areas in the lung: their shape, size, color, prevalence.

Micropreparation No. 000 ANTRACO-SILICOSIS OF THE LUNG (stained with hematoxylin and eosin). Designate the structure of the silicotic nodule, the collagen fibers arranged concentrically around the sclerotic vessels. Pay attention to a significant amount of coal dust contained both in the cytoplasm of macrophages (coniophages) and freely lying in the interalveolar septa.

LUNG CANCER

By a set of macropreparations determine the forms of growth and localization of cancerous tumors in the lungs.

Micropreparation No. 33 SQUAMOUS CELL LUNG CANCER (stained with hematoxylin and eosin). Pay attention to the degree of atypia of tumor cells, signs of infiltrating growth.

Micropreparation No. 34 UNDIFFERENTIATED (anaplastic) LUNG CANCER (stained with hematoxylin and eosin). Assess the degree of anaplasia of cancer cells (shape, size, layout). Pay attention to the invasive nature of tumor growth.

BASIC VOCABULARY FOR THE LESSON

bronchiectasis- chronic pathological dilatation of the bronchi.

Obstructive lung diseases- a group of diseases characterized by obstruction of the airways.

Restrictive lung diseases- a group of diseases characterized by a predominance of restrictive (restrictive) changes, usually in the interstitial tissue.

Pneumoconiosis- the general name of occupational lung diseases caused by exposure to industrial dust.

Epidermoid cancer- squamous cell carcinoma.

Hamman-Rich syndrome- idiopathic pulmonary fibrosis, diffuse fibrosing alveolitis, chronic interstitial pneumonitis.

Emphysema- excessive and persistent expansion of the air and respiratory structures located distal to the terminal bronchioles.

Emphysema bullous- emphysema, characterized by the formation of large subpleural blisters (bull).

Emphysema vicarious (compensatory)- emphysema, which develops with the loss of a significant part of the lung (for example, with pulmonectomy, lobectomy).

Emphysema interstitial (interstitial)- emphysema, localized in the interstitium (stroma) of the lung.

Emphysema irregular- emphysema, which affects the acini unevenly, which is almost always associated with cicatricial changes in the lung tissue.

Emphysema obstructive- emphysema caused by incomplete blockage (obstruction) of the airways with the formation of a valve mechanism.

Emphysema panacinar (panlobular)- emphysema, capturing acini from respiratory bronchioles to terminal alveoli.

Emphysema paraseptal- emphysema, characterized by changes in the distal part of the acinus, while the proximal part remains normal.

Emphysema centriacinar (centrilobular)- emphysema affecting the central or proximal parts of the acinus, leaving the distal alveoli intact.

List of questions for the lesson

1. Specify myocardial changes underlying the development of cor pulmonale in COPD.

2. Select obstructive lung disease.

3. What is the term for excessive and persistent expansion of the air-bearing and respiratory structures (or spaces) located distal to the respiratory bronchioles, with destruction of the walls of these structures without subsequent fibrosis?

4. Name the types of pulmonary emphysema.

5. What causes predisposition to chronic obstructive pulmonary emphysema?

6. Select the most important factors in the development of chronic bronchitis.

7. Name the pathogenetic variants of chronic bronchitis.

8. Name the possible complications of chronic obstructive bronchitis.

9. What disease causes increased reactivity of the mucous membrane of the airways?

10. Specify the pathogenetic variant of bronchial asthma.

11. Specify the molecule fixed on mast cells in atopic bronchial asthma.

12. Name the changes in the bronchial wall in case of bronchiectasis.

13. Name the macroscopic types of bronchiectasis.

14. Name the complications of bronchiectasis.

15. What is the name Occupational Illness associated with exposure to industrial dust and characterized by the gradual development of sclerotic changes in the lung parenchyma?

16. Name the etiological factors in the development of silicosis.

17. Name the etiological factors in the development of asbestosis.

18. Name the etiological factors in the development of anthracosis.

19. Select the components of a sarcoid granuloma.

20. In what disease are asteroid inclusions found in the cytoplasm of multinuclear cells?

21. Name the types of lung cancer classified by localization.

22. Name the most common histological type of central lung cancer.

23. Name the most common histological type of peripheral lung cancer.

24. What is the name of lung cancer developing from the epithelial lining of the distal third of the segmental bronchi, bronchioles or alveolar epithelium?

25. What is the name of lung cancer that develops from the epithelial lining of the main, lobar and proximal third of the segmental bronchi?

26. Specify precancerous conditions in the lungs.

27. Name the complications of bronchial cancer.

28. A 53-year-old patient has been smoking 2 packs of cigarettes a day for 30 years. He went to the clinic with complaints of a persistent productive cough, worse in the morning after waking up, and progressive shortness of breath. On x-ray images, an increase in the airiness of the lung tissue and an increase in the lung pattern are determined. Your conclusion.

29. A 30-year-old patient was admitted to the clinic with complaints of shortness of breath, general cyanosis, and weakness. From the anamnesis it is known that the woman long time works on a poultry farm. During the study: the level of immunoglobulins in the blood is increased, immune complexes are determined. X-ray examination shows a "honeycomb lung" picture. Specify the most likely diagnosis.

30. A 67-year-old patient, who had been suffering from chronic diffuse bronchitis for a long time, died with increasing symptoms of pulmonary heart failure. Pathological anatomical examination of the lungs increased airiness, in the peripheral sections of a lot of blisters of various sizes. Specify Changes internal organs found at autopsy.

DISEASES OF THE DIGESTIVE organ

(the section is studied in two laboratory sessions)

learning goals

The student must know :

1. The cause of occurrence and the main nosological forms of diseases of the digestive system.

2. Classification, morphological manifestations of diseases of the digestive system, their complications and causes of death.

The student must be able to :

1. Describe the morphological changes in the studied macropreparations and micropreparations.

2. Based on the descriptions, compare the structural manifestations of diseases of the heart and blood vessels at various levels of the structure of organs, tissues and cells.

The student must understand :

Mechanisms of formation of structural changes that occur in organs in diseases of the digestive system.

Ioccupation

DISEASES OF THE STOMACH AND INTESTINE

1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, principles of classification. Forms distinguished on the basis of the study of gastrobiopsies and their morphological characteristics. Complications, outcomes, prognosis. Chronic gastritis as a precancerous condition.

2. Ulcer disease. Definition. General characteristics of peptic (chronic) ulcers of different localizations. Epidemiology, etiology, patho- and morphogenesis, its features in pyloro-duodenal and medio-gastric ulcers. Morphological characteristics of chronic ulcers during exacerbation and remission. Complications, outcomes. Acute gastric ulcers: etiology, pathogenesis, morphological characteristics, outcomes.

3. Tumors of the stomach. Classification. hyperplastic polyps. Adenoma of the stomach. Morphological characteristic. Malignant tumors of the stomach. Stomach cancer. Epidemiology, etiology, principles of classification. Features of metastasis. Macroscopic and histological forms.

4. Idiopathic inflammatory bowel disease. non-specific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, prognosis. Criteria for the differential diagnosis of chronic colitis.

5. Epithelial tumors of the intestine. benign tumors. Adenomas: epidemiology, classification, clinical and morphological characteristics, prognosis. Familial adenomatous polyposis. Adenoma and cancer: the concept of multistage carcinogenesis in the colon. Colon cancer. Epidemiology, etiology, classification, macro- and microscopic morphological characteristics, clinical manifestations, prognosis.

6. Diseases appendix blind gut. Appendicitis. Classification, epidemiology, etiology, pathogenesis. Morphological characteristics and clinical manifestations of acute and chronic appendicitis. Complications.

1. Lecture material.

2. Textbook on pathological anatomy (, Anichkov N. M, 2000) v.2, part I: pp. 537-562, 586-593, 597-618.

3. Textbook on pathological anatomy (, Anichkov N. M, 2005) v.2, part I: pp. 384-405, 416-422, 425-441.

4. Guide to practical exercises in pathological anatomy (, 2002) pp. 580-585, 601-612.

5. Atlas of pathological anatomy (, 2003) p. 256-265.

EDUCATIONAL CARD

OBJECTIVE SETTING OF THE LESSON: study the morphology of individual nosological forms of organ diseases using macropreparations and micropreparations gastrointestinal tract and conduct clinical and anatomical comparisons.

DISEASES OF THE STOMACH

macropreparation MULTIPLE GASTRIC EROSIONS. Pay attention to the gastric mucosa with multiple superficial defects, note the color of the erosion bottom.

macropreparation CHRONIC GASTRITIS. Pay attention to the relief of the mucous membrane in various departments (body, pyloric canal), the presence of erosion.

Micropreparation No. 000 Helicobacter pylori in parietal mucus in gastric pits (gastrobiopsy, Giemsa stain). View, note the ability of bacteria to adhere to the epithelial cell.

Micropreparation No. 000 CHRONIC ACTIVE ANTRUM GASTRITIS WITH GLANDS ATROPHY AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, stained with alcian blue and hematoxylin). To describe and evaluate semi-quantitatively the morphological signs of chronic gastritis: activity (presence of neutrophilic leukocytes) and severity of inflammation (density of mononuclear infiltrate), degree of atrophy of the glands of the lamina propria, prevalence of intestinal metaplasia of the pit-covering epithelium.

macropreparation CHRONIC GASTRIC ULCER (calcic). Pay attention to the localization of the ulcer, its shape, edges, depth, nature of the bottom. Determine which edge is facing the esophagus and which is facing the pylorus.

Micropreparation No. 000 CHRONIC GASTRIC ULCER (with exacerbation) (staining with hematoxylin and eosin). Designate the layers in the bottom of the ulcer, characterizing the chronic course of the disease. Note fibrinoid necrosis and leukocyte infiltration, indicating an exacerbation of the process.

View set of macropreparations, illustrating the complications of chronic ulcers: PUNCHING GASTRIC ULCER, PENETRATING GASTRIC ULCER, ARROSION OF THE VESSEL IN THE BOTTOM OF THE ULCER, GASTRIC ULCER-CANCER, GASTRIC Cicatricial Deformation. Pay attention to the localization of ulcers, the shape, nature of the edges, changes in the bottom and edges of the ulcer.

Gross preparations different forms of stomach cancer. Determine the macroscopic forms of the tumor. Describe one of the forms.

Micropreparation No. 000 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (stained with hematoxylin and eosin). Describe the signs of tissue and cellular atypism, the invasive nature of tumor growth.

Micropreparation No. 000 UNDIFFERENTIATED CANCER - cricoid (stained with hematoxylin and eosin and alcian blue). Pay attention to the tumor cells with alcianophilic cytoplasm located in the "lakes" of mucus. Note the shape of the cell - cricoid, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.

DISEASES OF THE INTESTINE

macropreparation PHEGMONOUS APPENDICITIS. Pay attention to the size of the process, the condition of the serous membrane (appearance, degree of blood filling), wall thickness, the nature of the contents in the lumen.

Micropreparation No. 000 PHEGMONOUS APPENDICYT (stained with hematoxylin and eosin). Describe. Note the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall and the mesentery (mesenteriolit).

macropreparation CHRONIC APPENDICITIS. Pay attention to the size of the process, the condition of the serous membrane, the thickness and appearance of its wall in the section.

Micropreparation No. 000 CHRONIC APPENDICITIS (staining with hematoxylin and eosin). Describe. Note sclerotic changes in the wall and obliteration of the process lumen. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.

macropreparation LIVER ABSCESSES (pylephlebitic), as a complication of appendicitis. View.

View a set of macropreparations intestinal tumors.

BASIC VOCABULARY FOR THE LESSON

Acute gastritis- diseases manifested by inflammation of the gastric mucosa.

Gastritis chronic- Digestive inflammatory-dysregenerative diseases of the gastric mucosa.

Hematomesis- hematemesis.

Colitis- a group of inflammatory diseases of the colon.

Crohn's disease- terminal ileitis, regional ileitis.

Mallory-Weiss syndrome- longitudinal ruptures of the mucous membrane in the area of ​​the esophageal-gastric junction.

penetration– penetration of the defect into neighboring organs (“covered” perforation).

Perforation- perforation.

Pylorospasm- sustained reduction pyloric sphincter stomach, leading to a violation of the evacuation function.

Polyp- any exophytic node that rises above the surface of the mucous membrane.

Enteritis- a group of inflammatory diseases of the small intestine.

Erosion- a defect that does not extend beyond the mucous membrane.

Ulcer- a defect that extends beyond the mucous membrane.

Stricture- stenosis, narrowing.

List of questions for the lesson

which are the basis of the control test

1. Define Barrett's esophagus.

2. Specify the features of Zenker's diverticulum.

3. Specify the provisions characteristic of the Mallory-Weiss syndrome.

4. Specify the factors that ensure the cytoprotective function of the gastric mucosa.

5. Specify the most common cause (etiological factor) of chronic gastritis.

6. Specify the methods for detecting H. pylori in the biopsy.

7. Specify the positions characteristic of chronic stomach ulcers.

8. List the factors that significantly reduce the synthesis of prostaglandins and have an ulcerogenic effect.

9. Specify the microscopic features of an acute stomach ulcer.

10. Describe the perforation of the stomach ulcer.

11. Check the statements that are characteristic of the Zollinger-Ellisson syndrome.

12. Specify the predominant localization of stomach ulcers.

13. Select the positions characteristic of the cambial cells of the intestinal epithelium.

15. Predisposing factors for the development of hemorrhoids are.

16. Select extraintestinal manifestations of Crohn's disease.

17. Specify the complications of Crohn's disease.

18. Specify the disease, which is characterized by a combination of the following microscopic characteristics - crypt abscesses, granulomas with the presence of Pirogov-Langhans giant cells.

19. Specify the microscopic signs of an exacerbation of Crohn's disease.

20. Select statements that are characteristic of volvulus.

21. Specify the pathogenetic factors of diverticulosis of the large intestine.

22. Describe pseudopolyps in ulcerative colitis.

23. What disease is characterized by a macroscopic appearance of the large intestine mucosa according to the type of “cobblestone pavement”?

24. What disease can be suspected in the presence of the following signs: skin hyperpigmentation, lymphadenopathy and the presence of a large number of macrophages with swollen cytoplasm and PAS-positive granules in the intestinal biopsy?

25. Specify the characteristic features of celiac disease.

26. Under what conditions does malabsorption syndrome occur?

27. A 64-year-old patient developed on the background of diabetes mellitus sharp pains in the epigastric region, which after a few hours moved to the right iliac region, fever up to 39 ° C, single vomiting. The patient was hospitalized 12 hours after the onset of the disease. When examining a doctor in the emergency room, confusion is noted, fever is 39.6 ° C, symptoms of peritoneal irritation are positive. Specify the presumptive diagnosis.

28. A 28-year-old patient has been experiencing weight loss for several years, pain in the epigastric region, in the last month he has noted pallor of the skin, black feces, girdle pain at the level of the epigastrium, yellowness of the skin and visible mucous membranes. FGDS revealed a callous ulcer of the posterior wall of the stomach with undermined edges, the bottom is deep, filled with dirty gray contents. What complication of ulcer is in question in this case?

29. In the gastrobiopsy of a 43-year-old patient, the presence of a lymphoplasmacytic infiltrate in the lamina propria of the mucous membrane is determined, there are accumulations of lymphocytes with light centers. Histobacterioscopically, when stained according to Giemsa, S-shaped sticks are determined in the layer of superficial mucus. What is the probable diagnosis?

IIoccupation

DISEASES OF THE LIVER, GALL BLADDER

AND PANCREAS

1. Hepatitis: definition, classification. Acute viral hepatitis. Epidemiology, etiology, ways of infection transmission, patho- and morphogenesis, clinical morphological forms, viral markers, outcomes. Chronic hepatitis: concept, etiology, clinical and morphological characteristics and classification, signs of activity, outcomes, prognosis.

2. Alcoholic liver damage. Alcoholic fatty liver. Alcoholic hepatitis. Alcoholic cirrhosis of the liver. Epidemiology, pathogenesis and morphogenesis, clinical manifestations, complications and causes of death, outcomes, prognosis.

3. Cirrhosis of the liver. Concept. Pathological signs and classification of cirrhosis by etiology, pathogenesis, macro-, microscopic changes, etc. Clinical and morphological characteristics of the most important types of cirrhosis. Alcoholic cirrhosis. Cirrhosis after viral hepatitis. Biliary cirrhosis (primary, secondary). Liver changes in hemochromatosis, Wilson-Konovalov disease, alpha-1 antitrypsin deficiency. Pathogenesis, clinical and morphological characteristics.

4. Tumors of the liver. Classification, epidemiology. Benign neoplasms. Hepatocellular adenoma. Adenoma of the intrahepatic bile ducts. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification depending on macro - and microscopic signs. Complications. Patterns of metastasis. Levels of distribution of hepatocellular adenocarcinoma according to the TNM system. Cholangiocellular carcinoma.

5. Diseases of the gallbladder and bile ducts. Gallstone disease (cholelithiasis). Etiology, pathogenesis, types of stones. Cholecystitis definition. Acute and chronic cholecystitis: etiology, pathogenesis, clinical and morphological characteristics, complications, causes of death.

6. Diseases of the exocrine pancreas. Pancreatitis acute (pancreatic necrosis) and chronic. Epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications and causes of death. Tumors of the exocrine pancreas. Cystadenoma. Pancreas cancer. Epidemiology, classification, morphological characteristics, prognosis.

1. Lecture material.

2. Textbook on pathological anatomy (, Anichkov N. M, 2000) v.2, part I: pp. 637-669, 672-682, 687-709.

3. Textbook on pathological anatomy (, Anichkov N. M, 2005) v.2, part I: pp. 452-477, 479-487, 489-501.

4. Guide to practical exercises in pathological anatomy (, 2002) pp. 634-654, 585-589.

5. Atlas of pathological anatomy (, 2003) p. 282-288.

EDUCATIONAL CARD

OBJECTIVE SETTING OF THE LESSON: study the morphology of individual nosological forms of liver diseases using macropreparations, micropreparations and electron diffraction patterns and conduct clinical and anatomical comparisons.

LIVER DISEASES

macropreparation TOXIC DYSTROPHY OF THE LIVER (fatty hepatosis). Pay attention to the size of the liver, its color, texture, condition of the capsule.

Micropreparation No. 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). Note the discomplexation of the beams, signs of fatty degeneration and necrosis of the liver cells. Compare the state of hepatocytes in the center and periphery of the lobules. Pay attention to the beginning fibrosis of the stroma and infiltration of the portal tracts with lymphoid-macrophage elements.

Micropreparation No. 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (staining with hematoxylin and eosin). Note the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along the sinusoids, degenerative changes in hepatocytes, lymphohistiocytic infiltration of the portal tracts. Note the signs of chronic inflammation (hepatitis stage): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes by bile pigments.

electronogram HYDROPIC HEPATOCYTE DYSTROPHY IN VIRAL HEPATITIS (atlas, Fig. 14.5). Pay attention to the expansion of the endoplasmic reticulum of the hepatocyte and the sharp swelling of mitochondria.

Gross preparations LIVER CIRRHOSE. Mark the size, color, consistency, appearance of the liver from the surface and in section. Assess the size of regenerated nodes and determine the macroscopic form of cirrhosis by this feature.

Micropreparation No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRRHOSIS (staining with hematoxylin and eosin and picrofuchsin). Note the presence of moderate signs of inflammatory activity (lymphoid infiltration of the stroma extending to the parenchyma, fatty degeneration of hepatocytes), fibrosis dominance (porto-portal, porto-central septa, formation of false lobules) and regeneration of hepatocytes (loss of the bar structure, the presence of cells with large nuclei).

Gross preparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF ANOTHER PRIMARY LOCATION.

BASIC VOCABULARY FOR THE LESSON

Budd-Chiari syndrome- obstruction of the main hepatic veins as a result of thrombosis.

Hepatitis any diffuse inflammatory liver disease.

Hepatosis- a group of liver diseases characterized by dominance dystrophic changes and hepatocyte necrosis.

medusa head- expansion of the veins of the anterior abdominal wall with portal hypertension.

portal hypertension- increased hydrodynamic pressure in the portal vein system.

Kaiser-Fleischer rings- greenish-brown or yellowish-green pigmented rings in the cornea of ​​​​the eyes in Wilson's disease.

Councilman calf- eosinophilic rounded formations in the perisinusoidal space.

mallory calf- alcoholic hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.

Liver necrosis massive (confluent)- extensive widespread necrosis of most of the hepatic parenchyma.

Bridge necrosis of the liver (bridge necrosis)- confluent necrosis of a large number of hepatocytes with the formation of "bridges" between adjacent lobules.

Liver necrosis stepwise (periportal)- destruction of hepatocytes along the border of the parenchyma and stroma, i.e., in the peripheral parts of the lobule.

Liver necrosis focal (spotted)- the death of individual small groups of hepatocytes in different parts of the acinus.

Pancreatitis- an inflammatory disease of the pancreas, often accompanied by its necrosis.

goose liver- macroscopic view of the organ in fatty degeneration.

Hepatolienal syndrome- enlargement of the spleen in liver diseases, accompanied by hypersplenism.

Wilson's disease (Wilson-Konovalov's disease)- hepatolenticular degeneration, hepatocerebral dystrophy.

Cholangitis- Inflammatory disease of the bile ducts.

Cholelithiasis- cholelithiasis.

cholestasis- insufficiency of bile flow.

Cholecystitis- Inflammatory disease of the gallbladder.

cirrhosis- excessive growth of connective tissue in the organ against the background of dystrophic and regenerative processes, accompanied by a change in the shape of the organ.

List of questions for the lesson

which are the basis of the control test

1. Specify variants of the structure of the liver.

2. List the variants of necrosis of the liver parenchyma.

3. What results in the formation of Councilman's bodies?

4. List the forms of acute hepatitis.

5. Specify the route of transmission of the virus when acute hepatitis BUT.

6. Specify the ways of virus transmission in acute hepatitis B.

7. Name indirect markers viral infection hepatocytes.

8. Specify the predominant localization of HBcAg in hepatocytes.

9. What type does the accumulation of HBsAg in the hepatocyte give to the cytoplasm?

10. List the etiological variants of chronic hepatitis.

11. Specify the microscopic signs of chronic hepatitis.

12. List the morphological forms of chronic hepatitis.

13. Specify the characteristic signs of alcoholic liver damage.

14. List the variants of alcoholic liver damage.

15. Name the cells responsible for collagen formation in alcoholic liver damage.

16. Describe the macroscopic changes in the liver in alcoholic steatosis.

17. List the microscopic signs of a false lobule in liver cirrhosis.

18. Name the morphological forms of liver cirrhosis.

19. List the acquired forms of liver cirrhosis.

20. List hereditary forms of liver cirrhosis.

21. Specify the signs of portal hypertension.

22. List the causes of death in patients with liver cirrhosis.

23. Describe primary sclerosing cholangitis.

24. Describe primary biliary cirrhosis of the liver.

25. Describe Wilson-Konovalov's disease.

26. Changes in the wall of the gallbladder in acute cholecystitis.

27. Changes in the wall of the gallbladder in chronic cholecystitis.

28. A 60-year-old patient has been suffering from chronic alcoholism for 30 years. On examination, the liver is dense, the surface is bumpy. On the anterior abdominal wall, the veins are dilated, the spleen is palpable. Specify the possible histological manifestations in the biopsy material.

29. A 50-year-old woman has been suffering from fatigue and skin itching for 8 months. A laboratory study revealed a minimal increase in the level of transaminases, a significant increase in the level of alkaline phosphatase, and high titers of antimitochondrial antibodies. A biopsy study revealed a granulomatous nature of inflammation in the cholangioli and a decrease in the number of bile ducts with severe lymphomacrophage infiltration along the portal tracts with sclerosis. Your conclusion.

30. A 63-year-old male patient, who had been suffering from chronic viral hepatitis B for a long time, was admitted to the clinic with complaints of heaviness in the right hypochondrium, jaundice of the skin. During the examination, the liver is dense, its edge is bumpy, there is an increase in the spleen and dilation of the veins of the anterior abdominal wall. Note the possible histological manifestations in the biopsy material.

FIGURE 7-1 Normal esophagus and stomach, macroscopic

Normally, the color of the mucosa of the esophagus (left) varies from white to yellowish brown.

In the region of the gastroesophageal junction (in the center and on the left) is the lower esophageal sphincter (NSP), whose function is to maintain muscle tone. The stomach was opened along the greater curvature (top and right). In the bottom area, a small curvature of the stomach is visible. Behind the antrum is the pylorus, which passes into the initial section of the duodenum (bottom right). In the wall of the pylorus there is a thick annular layer of smooth muscles. Normally, the folding of the gastric mucosa is clearly expressed.

FIGURE 7-2 Normal esophagus, endoscopy

Endoscopic picture of the gastroesophageal junction (A). The color of the mucous membrane of the esophagus, lined with stratified squamous non-keratinizing epithelium, has shades from pale pink to yellowish-brown. The mucous membrane of the stomach, lined with glandular epithelium, is dark pink in color. NSP maintains smooth muscle tone. The lower part of the esophagus expands during the passage of food due to relaxation of the NSP and receptive relaxation of the proximal stomach under the influence of vasoactive intestinal peptide produced by postganglionic peptidergic vagal nerve fibers. With a decrease in the tone of the NSP, there is a reflux of acidic gastric contents into the lower esophagus, which is accompanied by burning painful sensations (heartburn) behind and under the sternum. Dysfunction of the esophageal sphincters can also cause difficulty swallowing (dysphagia). Damage to the mucous membrane of the esophagus is accompanied by pain when swallowing (odynophagia). Congenital or acquired disorders of the innervation of the esophagus lead to difficulty in the relaxation of the ESP, achalasia, progressive dysphagia, and expansion of the esophagus above the ESP.

FIGURE 7-3 Normal esophagus, slide

The mucous membrane (left) is lined with stratified squamous nonkeratinized epithelium, the submucosa contains small mucous glands and an excretory duct surrounded by lymphoid tissue. On the right is the muscular layer. In the upper esophagus, where the process of swallowing food begins, voluntary striated muscles predominate. They are located together with smooth muscle cells, the proportion of which in the underlying areas gradually increases, and skeletal muscle tissue is displaced. In the lower part of the esophagus, the muscular membrane is represented by involuntary smooth muscle tissue, which ensures the peristaltic movement of food and liquid into the stomach. The smooth muscles of the NSP are also located here, the muscle tone of which is an effective barrier against regurgitation of gastric contents. In the region of the gastroesophageal junction, the stratified squamous epithelium alternates with the glandular epithelium of the stomach.

FIGURE 74 Tracheoesophageal fistula, gross preparations

Congenital anomalies of the esophagus include atresia and tracheoesophageal fistula. In embryogenesis, the development of the esophagus and lung as derivatives of the endoderm is interconnected with their subsequent budding from each other. The right figure shows atresia of the esophagus (A) in the middle third. On the left figure, below the carina of the trachea, there is a tracheoesophageal fistula (♦). Depending on the location of the atresia or fistula, the newborn may develop vomiting or aspiration. Often other congenital anomalies develop simultaneously. Agenesis (complete absence) of the esophagus is very rare.

FIGURES 7-5, 745 Esophageal stricture and Schatzki ring, barium radiographs

The two images on the left show strictures (♦) (cicatricial stenosis) of the lower third of the esophagus. Esophageal strictures occur with reflux esophagitis, scleroderma, radiation injuries, chemical burns. On the right side of the image in the lower part of the esophagus, the so-called ring of Schatzky (A) is visible, located directly above the diaphragm. In this place there are folds of the muscular membrane. In this condition, progressive dysphagia is observed, which is more pronounced when taking solid food compared to liquid food.

FIGURE 7-7 Hiatal hernia (hiatal hernia), CT

HaKT chest visible hiatal hernia (*). The site of the fundus of the stomach is dilated and moved into the chest cavity through the dilated esophageal opening of the diaphragm. This kind of movement or slippage of part of the stomach is observed in about 95% of hiatal hernias. Approximately 9% of patients with diaphragmatic hernias have symptoms of gastroesophageal reflux disease (GERD). On the other hand, some cases of GERD development are associated with diaphragmatic hernia. The expansion of the esophageal opening of the diaphragm prevents the normal functioning of the ESP. Due to the reflux of gastric contents into the lower esophagus, the patient develops symptoms of heartburn, cardialgia with burning pain behind the sternum, especially pronounced after eating and aggravated in the supine position.

FIGURE 7-8 Periesophageal hernia, CT

Ha CT without contrast enhancement in the left side of the chest, next to the heart, most of the stomach is visible (*). This movement of the stomach was due to a complication of a periesophageal ("rolling") hiatal hernia, a rare but serious form of diaphragmatic hernia. During the movement of the stomach into the chest cavity through a small opening, the blood supply to the stomach may be disturbed with the development of ischemia and infarction.

FIGURE 7-9 Esophageal diverticulum, radiographs

Two serial radiographs of the upper esophagus show a protrusion of the wall, or diverticulum (♦). The contrast agent fills the cavity of the protrusion. A diverticulum is a site of expansion and protrusion of the wall of the esophagus through weak points in the muscular membrane. Typically, diverticula bulge between the constrictor muscles in the upper esophagus or through the muscle lining of the lower esophagus just above the diaphragm. This pathology is known as Zenker's diverticulum. When passing through the esophagus, food can accumulate in the diverticulum and decompose, which leads to the appearance of a fetid odor from the patient's mouth.

4 FIGURE 7-10 Mallory-Weiss syndrome, KT

With severe and prolonged vomiting, longitudinal tears of the esophageal wall and subsequent bleeding can occur. This contrast-enhanced CT shows signs of Boerhaave's syndrome. This syndrome, in turn, is a variation of the Mallory-Weiss syndrome. In the mediastinum, an area of ​​enlightenment (♦) is visible, indicating the presence of air that has penetrated through a spontaneous rupture of the esophagus. The rupture is localized in the lower part of the esophagus, above the gastroesophageal junction. The entry of the contents of the esophagus into the mediastinum leads to inflammation, which quickly spreads to other parts of the chest.

FIGURE 7-11 Esophageal varices, macroscopic

Varicose veins, which were the source of bleeding and hematemesis (bloody vomiting), are located in the area of ​​the gastroesophageal junction. Varicose veins of the submucosa of the esophagus develop with portal hypertension, which usually complicates the course of alcoholic small-nodular cirrhosis of the liver. The esophageal venous plexus is one of the main collateral pathways for the venous outflow of blood. Despite the fact that the esophageal venous plexus also receives blood from the upper parts of the stomach, it is called the esophageal plexus, and bleeding from this localization is also called esophageal bleeding.

FIGURE 7-12 Esophageal varices, endoscopy

The dilated veins of the esophageal plexus located in the submucosa bulge into the lumen of the lower esophagus. Such varicose veins are most often a complication of portal hypertension in cirrhosis of the liver. It has been established that esophageal varicose veins develop in approximately 60-70% of patients with cirrhosis of the liver. Erosions and ruptures of thinned venous walls lead to sudden onset and extremely life-threatening massive hematemesis. For the treatment and prevention of bleeding, methods such as ligation of varicose veins, injection of sclerosing agents (sclerotherapy) and balloon tamponade of the esophagus are used.

FIGURE 7-13 Esophagitis, slide

Reflux esophagitis in GERD occurs due to deficiency of the LES, leading to regurgitation of the acidic contents of the stomach into the lower esophagus. With moderately pronounced reflux esophagitis, microscopic signs are revealed in the wall of the esophagus: epithelial hyperplasia with predominant hyperplasia of the basal layer and the formation of elongated epithelial papillae (acanthosis), inflammatory infiltration with neutrophilic and eosinophilic granulocytes and lymphocytes. The presence of eosinophils (giemsa pink in the figure) is a specific and sensitive sign of reflux esophagitis, especially in children. The causes of reflux esophagitis are diaphragmatic hernia, neurological disorders, scleroderma, impaired esophageal clearance and gastric evacuation function. A severe course of reflux esophagitis can be complicated by ulceration and subsequent formation of cicatricial strictures of the esophagus.

FIGURE 7-14 Barrett's esophagus, macroscopic

Damage to the esophageal mucosa in chronic GERD can lead to metaplasia of the esophageal stratified squamous epithelium into gastric columnar epithelium with the presence of goblet cells of the intestinal type, which is called Barrett's esophagus. It occurs in about 10% of patients with chronic reflux gastritis. In the lower part of the esophagus above the gastroesophageal junction, against the background of a preserved whitish stratified squamous epithelium, reddish areas of mucosal metaplasia are visible. Mucosal ulceration is accompanied by bleeding and pain. As a result of inflammation, strictures of the esophagus occur. Diagnosis requires endoscopy with biopsy.

FIGURE 7-15 Barrett's esophagus, endoscopy

On endoscopic images of the lower esophagus, the reddish areas of esophageal mucosal metaplasia characteristic of Barrett's esophagus are set against a background of pale whitish islets of normal mucosal stratified squamous epithelium. If the length of the lesion in Barrett's esophagus is not more than 2 cm from the point of contact of the glandular and stratified squamous epithelium, such a pathology is called a short segment of Barrett's esophagus.

FIGURE 7-16 Barrett's esophagus, slide

On the left is the glandular epithelium, and on the right is the stratified squamous epithelium. On the left, "typical" Barrett's mucosa is shown, since there are also signs of intestinal metaplasia (goblet cells are visible among the cylindrical cells of the glandular epithelium). A predisposing factor for the development of metaplasia is chronic reflux of gastric contents into the lower esophagus. In most cases, Barrett's esophagus is diagnosed in patients aged 40 to 60 years. The risk of developing adenocarcinoma of the esophagus increases 30-40 times if the length of Barrett's esophagus exceeds 3 cm.

FIGURE 7-1 7 Barrett's esophagus with dysplasia, slide

The preserved stratified squamous epithelium of the esophagus (on the right) is adjacent to the metaplastic glandular epithelium, in which foci of severe dysplasia are identified. Note the densely spaced hyperchromic nuclei of the glandular epithelium, the small number of preserved goblet cells on the mucosal surface (upper left), and tissue atypia of the glands. The basal orientation of the nuclei of glandular cells is a sign of mild dysplasia, the apical orientation is a sign of severe dysplasia and a high likelihood of developing adenocarcinoma. If left untreated, dysplasia can develop several years after the onset of Barrett's esophagus.

FIGURE 7-18 Herpetic esophagitis, gross

In the lower part of the esophagus, against the background of the usual whitish stratified squamous epithelium, clearly demarcated elongated brownish ulcerations are visible. The cause of such ulcerations, which look like "holes", is the defeat of the virus herpes simplex(HSV). Opportunistic infections caused by HSV, Candida, and cytomegalovirus are most commonly seen in immunosuppressive states. A typical symptom is odynophagia. Herpetic esophagitis is usually localized and is rarely complicated by bleeding or esophageal obstruction. Process dissemination is not typical.

FIGURE 7-19 Candida esophagitis, gross specimen

Against the background of hyperemia of the mucous membrane in the lower third of the esophagus, brownish-yellow plaques are visible. The same lesions are present in the upper fundus of the stomach (upper right). Candida infection involving the oral cavity (“thrush of the mouth”) and the upper gastrointestinal tract is usually superficial, but under conditions of immunosuppression, invasion and dissemination of the process is possible. Some members of the genus Candida are part of normal microflora oral cavity. Candidiasis lesions rarely cause hemorrhage or esophageal obstruction, but may coalesce to form pseudomembranous lesions.

FIGURE 7-20 Squamous cell carcinoma of the esophagus (epidermal), gross specimen

On the mucous membrane in the middle part of the esophagus there is an ulcerated exophytic tumor of a reddish color. Distensibility of the esophagus reduces and obscures the early manifestations of the mass effect. By the time of diagnosis, as a rule, there are already signs of cancer spreading into the mediastinum, and the disease may be inoperable. This explains the poor prognosis for a patient with esophageal cancer. Risk factors for esophageal cancer in the United States include smoking and alcohol abuse. In other countries, risk factors such as high levels of nitrates and nitrosamines in food, zinc or molybdenum deficiency in food, and human papillomavirus infection are indicated.

FIGURE 7-21 Squamous cell carcinoma, endoscopy

In the middle part of the esophagus is an ulcerated squamous cell carcinoma, which caused stenosis of the lumen. Pain and dysphagia are characteristic symptoms that present a serious problem for patients. Violation of the passage of food leads to weight loss and cachexia.

FIGURE 7-22 Squamous cell carcinoma, slide

Only at the bottom right there is a small area of ​​remnants of normal stratified squamous epithelium, which is replaced by a thick layer of squamous cell carcinoma structures. Solid nests of tumor cells infiltrate the submucosa and underlying wall layers (left). The tumor often grows into the surrounding tissues, making it difficult to surgically remove it. Tumor cells in squamous cell carcinoma have pink cytoplasm and clear boundaries. In tumor cells, a mutation of the p53 tumor suppressor gene is noted with a frequency of 50%. In some cases, there is a mutation in the pl6/CDKN2A suppressor gene; in others, amplification of the CYCLIN Dl gene. Such mutations can occur during chronic inflammation, which enhances the proliferation of epithelial cells.

FIGURE 7-23 Adenocarcinoma, gross specimen

On the left, the normal yellowish-brown mucosa of the upper esophagus is visible. In the distal esophagus, the appearance of the mucosa with dark erythematous areas is characteristic of Barrett's esophagus. In the distal part of the esophagus, near the gastroesophageal junction, there is a large ulcerated adenocarcinoma node that grows into the wall of the stomach in the region of its upper sections. Most often, adenocarcinoma develops in Barrett's esophagus with a p53 tumor suppressor gene mutation, p-catenin nuclear translocation, and c-ERB B2 amplification. In the early stages of adenocarcinoma, as in squamous cell carcinoma, there are often no clinical manifestations of the disease, which leads to a poor prognosis.

FIGURE 7-24 Adenocarcinoma, CT

HaKT abdominal cavity with contrast enhancement in the lower part of the esophagus, a tumor (♦) is visible, which spreads to the adjacent parts of the stomach and annularly narrows the lumen of the esophagus. In this observation, adenocarcinoma arose in Barrett's esophagus, which, in turn, formed against the background of chronic GERD. The presence of epithelial dysplasia in Barrett's esophagus increases the risk of developing adenocarcinoma. Esophageal adenocarcinoma develops in patients over the age of 40 who have suffered from GERD, usually for many years. Strengthening the processes of cell renewal and an increase in the proliferative activity of the epithelium in the mucosa in Barrett's esophagus is the background for mutations leading to a loss of control of the cell cycle.

FIGURE 7-25 Adenocarcinoma, endoscopy

In the lower esophagus, dark red, loose mucosal patches are visible, related to Barrett's esophagus. A polypoid tumor, biopsied with a pathohistological diagnosis of moderately differentiated adenocarcinoma, grows into the lumen of the esophagus. The patient had suffered from GERD for 30 years and received inadequate treatment. Clinical manifestations of esophageal adenocarcinoma include hematemesis, dysphagia, chest pain, and weight loss.

FIGURE 7-26 Normal gastric mucosa, slide

In the gastric mucosa in the bottom area there are shallow gastric pits (♦), under which the glands extending into the depths (■) are located. The parietal or parietal cells (A) of the gastric fundus glands secrete hydrochloric acid and intrinsic factor. The secretion of hydrochloric acid by parietal glandulocytes is carried out with the help of H * / K * -ATPase (proton pump) under the influence of acetylcholine produced by vagal nerve fibers and acting on muscarinic receptors, as well as mast cell histamine acting on H 2 receptors, and gastrin . The gastric fundus glands also contain chief cells that secrete the proteolytic enzyme pepsinogen. In the region of the neck of the glands there are cubic mucous cells, or mucocytes, which produce mucus that protects the gastric mucosa from the action of acid and pepsin.

FIGURE 7-27 Normal gastric mucosa, slide

In the mucous membrane of the antrum of the stomach, the pits (♦) are deeper, and the glands (■) are shorter than in the wall of the fundus of the stomach. Cylindrical mucous cells (mucocytes) are located in the pits and glands of the antral and pyloric sections of the stomach. The mucosal cells secrete prostaglandins, which promote the production of mucins and bicarbonate and increase mucosal blood flow. These factors play a protective role, protecting the mucous membrane from the action of the acidic contents of the stomach. Thanks to the peristaltic movements of the stomach, the chyme is mixed. The rate of gastric emptying depends on the concentration of hydrogen ions and the amount of fat that has entered the duodenum. Under the influence of fat in the duodenum, the secretion of cholecystokinin, which inhibits gastric emptying, increases.

FIGURES 7-28, 7-29 Normal upper gastrointestinal tract, endoscopy

The left figure shows the endoscopic picture of the fundus of the stomach in the norm, the right picture shows the initial part of the duodenum.

FIGURE 7-30 Congenital diaphragmatic hernia, appearance, section

The left dome of the diaphragm is absent, as a result, the contents of the abdominal cavity of the fetus are located in the chest. A metal probe is inserted behind the left lung, which is located in the right half of the chest, since the left half of it is occupied by the stomach that has moved here. Below the stomach, a dark-colored spleen is visible, lying above the left lobe of the liver, displaced upward. In the fetus, the transfer of the contents of the abdominal cavity to the chest leads to lung hypoplasia. Diaphragmatic hernia as a single congenital anomaly may be potentially treatable. However, more often it is combined with multiple malformations, as well as with chromosomal disorders such as trisomy 18.

FIGURE 7-31 Pyloric stenosis, gross

In the wall of the outlet section of the stomach there is a pronounced hypertrophy of the muscular membrane (A). Pyloric stenosis is rare, but it is the cause of gushing vomiting in infants between the ages of 3 and 6 weeks. Muscle hypertrophy can be expressed to such an extent that it can be determined by palpation. Pyloric stenosis as a multifactorial disease is a manifestation of the genetic phenomenon of the “threshold of predisposition”, beyond which, with an increase in the level of genetic risks, symptoms of the disease appear. Stenosis occurs in 81 cases per 300-900 newborns, more often in boys, since girls have a lower level of risk factors.

FIGURE 7-32 Gastropathy, macroscopic

In the mucous membrane of the stomach, hemorrhages of various sizes and shapes are visible. In these areas there are superficial lesions of the mucous membrane, called erosions. Erosive lesions of the gastric mucosa are the morphological substrate of the collective concept of "gastropathy". Gastropathy is characterized by focal lesions of the gastric mucosa and hemorrhages that have developed as a result of damage to epitheliocytes or endotheliocytes, but without signs of severe inflammation. The causes of gastropathy are similar to those of acute gastritis and include medications such as non-steroidal anti-inflammatory drugs, alcohol, stress, bile reflux, uremia, portal hypertension, ionizing radiation, and chemotherapy. The changes shown in the figure correspond to the picture of acute erosive gastropathy.

The mucous membrane of the fundus of the stomach is diffusely hyperemic, with multiple petechiae, but there are no erosions and ulcerations. Acute gastritis (hemorrhagic gastritis, acute erosive gastritis) may develop as a result of ischemia (shock, burns, trauma) or under the influence of toxic substances such as alcohol, salicylates, non-steroidal anti-inflammatory drugs. Damage to the mucosal barrier promotes back diffusion into the wall of gastric acid. The course of acute gastritis can be either asymptomatic or complicated by massive bleeding. The progression of damage leads to erosions and acute ulcers. Under stress, hypersecretion of hydrochloric acid occurs, which leads to the formation of acute lesions of the gastric mucosa: Curling ulcers (CurIing) with burn injury and Cushing ulcers (Cushing) with trauma to the central nervous system.

FIGURE 7-34 Acute gastritis, slide

Microscopic signs of acute gastritis include hemorrhage, edema, and varying degrees of neutrophilic infiltration as an indicator of acute inflammation. Ha drawing - infiltration by neutrophilic granulocytes of the glands and the lamina propria of the gastric mucosa. Typical clinical symptoms are moderate or severe epigastric pain, nausea, and vomiting. In severe cases of acute hemorrhagic gastritis, hematemesis may develop. This is especially often observed in patients who abuse alcohol for a long time. Exposure to gastric acid precedes ulceration, but its amount is not a determining factor in the development of most gastric ulcers.

FIGURE 7-35 Chronic gastritis, microslide

Chronic nonspecific (antral) gastritis usually develops as a result of Helicobacter pylori infection. Other causes are bile reflux and medications (salicylates) and alcohol. The inflammatory infiltrate consists mainly of lymphocytes, plasma cells; sometimes reveal a small number of neutrophilic granulocytes. Subsequently, mucosal atrophy and intestinal metaplasia develop, which may be the "first step" towards the emergence of gastric adenocarcinoma. Autoimmune gastritis develops under the influence of autoantibodies to parietal cells of the gastric glands and the internal factor of the stomach, which leads to atrophic gastritis and pernicious anemia. The level of gastrin in the blood serum is inversely proportional to the production of gastric acid, therefore, a high concentration of gastrin contributes to the development of atrophic gastritis.

FIGURE 7-36 Helicobaaer pylori, slide

Helicobacter pylori is a small, S-shaped, rod-shaped, Gram-negative bacterium that lives under microaerobic conditions in a neutral environment under mucus on the surface of the gastric mucosa, next to cylindrical mucous cells (mucocytes). When stained with hematoxylin and eosin, the bacteria look like pale pink rods (A). Opportunistically pathogenic strains of Helicobacter pylori have the potential to cause more pronounced lesions in gastritis, increase the risk of developing peptic ulcers and gastric cancer. These microorganisms do not invade and directly damage the mucosa, but rather alter the microenvironment in the stomach, which contributes to mucosal damage. Helicobacter pylori contain urease and produce ammonia, cloud-like accumulations of which surround microorganisms and protect them from the action of gastric acid. In the clinic, a urea breath test is used to detect Helieobacter pylori.

FIGURE 7-37 Helicobacter pylori, slide

Helicobaeter pylori (▲) stimulate the production epithelial cells cytokines that activate immune and inflammatory cells in the underlying lamina propria. It is believed that infection occurs in childhood, but inflammatory changes progress with age. In the US, 20% of residents are infected with Helicobacter pylori, and only a small proportion of patients develop complications such as chronic gastritis, gastric and duodenal ulcers, lymphoma from lymphoid tissue associated with the gastric mucosa (maltoma), and adenocarcinoma. In most patients with active gastritis, Helieobacter pylori is detected in the mucus on the surface of the epithelium. Ha this preparation Helicobacter pylori detected by staining with a solution of methylene blue.

FIGURE 7-38 Acute gastric ulcer, gross

An ulcer is a full-thickness mucosal defect, while erosion is a superficial or partial mucosal defect. Ulcers can be complicated by bleeding, penetration into an adjacent organ, perforation into the peritoneal cavity, cicatricial strictures. In the area of ​​the fundus of the stomach, a shallow delimited ulcer 1 cm in size, surrounded by a zone of hyperemia, is visible. It can be assumed that this ulcer is benign. However, all gastric ulcers should be biopsied to rule out malignancy. Isolated gastric ulcers are observed in chronic atrophic gastritis. They are usually localized in the antrum on the lesser curvature or in the region of transition of the body of the stomach into the antrum. Helicobaeterpylori is the most common cause, followed by non-steroidal anti-inflammatory drugs. The level of acidity of gastric contents in patients is usually normal or low.

FIGURES 7-39, 7^0 Acute gastric ulcers, endoscopy

On the left figure, a small ulcer in the prepyloric region is visible, on the right - a large ulcer in the antrum. All gastric ulcers are biopsied, since visual examination does not allow to establish malignancy. Small stomach ulcers that have a clear outline are most likely benign.

FIGURE 7-41 Acute gastric ulcer, slide

In the area of ​​ulceration, the epithelium is destroyed, the wall defect covers the mucous membrane and extends to the muscle layers. The ulcer is sharply demarcated from the normal mucosa (left), which hangs down to the bottom of the ulcer, represented by inflammatory and necrotic detritus. Small arterial branches at the bottom of the ulcer are damaged, leading to bleeding. The penetration of the ulcer into the deeper layers occurs in the absence of healing and the preservation of the activity of the process, which is accompanied by pain. The destruction of the muscular and serous membranes by an ulcer leads to peritonitis with a clinical picture of an acute abdomen. This type of ulcer is called a perforated ulcer. At perforation on the roentgenogram, signs of the presence of free gas in the peritoneal cavity can be determined.

FIGURE 7^2 Perforated gastric ulcer, x-ray

On an anteroposterior chest x-ray taken with a portable unit in a vertical position of the patient's body, free gas is visible under the right dome of the diaphragm in the abdominal cavity (A). The patient was diagnosed with a peptic ulcer of the duodenum with perforation. When a hollow organ is perforated, the gases contained in it enter the abdominal cavity and are detected mainly under the diaphragm in a vertical radiographic examination. Patients develop a picture of an acute abdomen with pain and sepsis. In the pathogenesis of peptic ulcers of the duodenum, an important role belongs to the increased acidity of gastric juice. They occur in the proximal duodenum on the background of peptic duodenitis. Almost always, with a duodenal ulcer, Helicobacter pylori infection of the stomach is diagnosed.

FIGURE 7^3 Adenocarcinoma, gross specimen

In the wall of the stomach there is a small gastric ulcer 2 to 4 cm in size. A biopsy study found that this ulcer is a malignant neoplasm, so the stomach was resected. In the United States, most cases of gastric cancer are diagnosed at an advanced stage, when there are already signs of invasion or metastasis. All gastric ulcers and all neoplasms in it must be biopsied without fail, since it is impossible to establish the malignant nature of the lesion with a visual macroscopic examination. In contrast to gastric ulcers, almost all peptic duodenal ulcers are benign. Gastric cancer is the second most common in the world. In recent decades, the incidence of stomach cancer in the United States has declined slightly.

FIGURE 7^4 Adenocarcinoma, CT

Contrast-enhanced CT scan of the abdominal cavity has the appearance of an exophytic mass (A), which deforms the stomach cavity. Histopathological examination of the tumor revealed adenocarcinoma. For many years the patient suffered chronic gastritis with Helicobacter pylori infection. However, it is known that gastric cancer develops in a small number of patients infected with Helicobacter pylori. Eating pickled, smoked and salty foods, as well as the formation of nitrosamines in the stomach from dietary nitrites, are risk factors for developing intestinal-type stomach cancer. Normalization of the diet leads to a significant reduction in the incidence of this form of cancer. Less certain are the risk factors for developing stomach cancer. diffuse type. Clinical manifestations of gastric adenocarcinoma include nausea, vomiting, abdominal pain, hematemesis, weight loss, intestinal discomfort, and dysphagia. Early gastric cancer, limited to mucosal lesions, is usually asymptomatic; it is detected by endoscopic examination.

FIGURE 7^5 Adenocarcinoma, slide

Adenocarcinoma of the stomach of the intestinal type is built from newly formed glands that infiltrate the submucosa. Mitoses are seen in some tumor cells (A). Tumor cells are characterized by an increased nuclear-cytoplasmic ratio and nuclear hyperchromatosis. A desmoplastic reaction develops in the stroma, associated with the germination of cancerous glands. Genetic disorders in the intestinal type of gastric cancer include mutation of the p53 gene, atypical expression of E-cadherin, and instability of the TGFfi and BAX genes.

FIGURE 7-46 Adenocarcinoma, gross specimen

With diffuse infiltrating growth of adenocarcinoma, a special form of gastric cancer develops - plastic linitis (Linitis plastica). The appearance of the stomach resembles a wrinkled leather bag or waterskin. The stomach wall is significantly thickened, multiple erosions and ulcerations are determined in the mucous membrane. The prognosis for this type of stomach cancer is extremely unfavorable. On the lesser curvature of the stomach, more limited forms of ulcerative gastric cancer occur. For the intestinal type of gastric cancer, its occurrence is more common against the background of previous changes associated with Helicobacter pylori infection. The decrease in the proportion of intestinal-type gastric cancer in the US appears to be associated with a decrease in the incidence of Helicobacter pylori infection. At the same time, the incidence of diffuse gastric cancer remains constant, a sample of which is shown in this figure.

FIGURE 7^7 Adenocarcinoma, endoscopy

In endoscopic examination of the stomach, diffuse-type adenocarcinoma has the appearance of plastic linitis (Linitis plastica) with pronounced mucosal erosions.

FIGURE 7^8 Adenocarcinoma, slide

The diffuse type of adenocarcinoma of the stomach is characterized by such a low differentiation that it is not possible to identify glandular structures. Instead of glands, chains of tumor cells with pronounced polymorphism and infiltrating growth are formed. In the cytoplasm of many tumor cells there are light vacuoles (A) containing mucus and pushing the nucleus to the cell periphery. Such cells are called cricoid cells. They are a typical feature of diffuse-type adenocarcinoma, which is characterized by rapid infiltrating growth and an extremely unfavorable prognosis.

FIGURE 7~49 Gastrointestinal stromal tumor, CT

Gastrointestinal stromal tumor (CIST) is a large neoplasm (♦) that is localized in the lower esophagus and upper fundus of the stomach. The formation is characterized by a lower signal intensity, as well as its variability due to the presence of foci of necrosis and cysts. The boundaries of the tumor are discrete. Previously, such tumors were classified as smooth muscle neoplasms. However, 8 it is now believed that they originate from the interstitial cells of Cajal, which are an integral part of the nerve plexuses of the muscular layer of the intestine, which regulate peristalsis in the gastrointestinal tract.

FIGURE 7-50 Gastrointestinal stromal tumor, gross specimen

Gastrointestinal stromal tumor originates from the muscular membrane of the stomach, grows exophytically into the lumen, is covered with a mucous membrane, except for the area of ​​ulceration in the center of the tumor. Gastrointestinal stromal tumor may be solitary or multiple.

FIGURE 7-51 Gastrointestinal stromal tumor, slide

Gastrointestinal stromal tumors are subdivided into spindle cell, epithelioid, and mixed types. This tumor is built from characteristic bundles of spindle-shaped cells. Immunohistochemical reaction for c-KIT(CDI 17) is positive in 95% of cases, for CD34 - in 70%. In addition to c-KIT mutations, mutations in platelet-derived growth factor A-chain (PDCFA) receptors are detected in 35% of cases. Evaluation of the biological potential of these tumors presents certain difficulties. The most important indicators are the mitotic index, the size of the tumor and its cellularity. A recently developed tyrosine kinase inhibitor drug (STI57I) has been used to treat these tumors with good effect.

FIGURE 7-52 Normal small intestine and mesentery, appearance

A loop of intestine with an adjacent mesentery. Attention should be paid to the pronounced venous drainage, due to which the blood through the system portal vein takes care of the liver. Here, in the mesentery, there are arcades of arteries that supply blood to the segments of the intestine. The blood supply to the intestine is carried out by the main and collateral branches of the celiac trunk, superior and inferior mesenteric arteries. The presence of a pronounced collateral network protects the intestine from a heart attack. The peritoneum covering the intestine is smooth and shiny.

FIGURE 7-53 Normal small intestine, gross specimens

Terminal ileum with ileocecal (bauginian) valve (upper figure on the right). Several darker, oval-shaped Peyer's patches are visible in the mucosa. The bottom figure also shows Peyer's patch, which is a compactly located lymphoid tissue. In the duodenum, in the thin lamina propria and submucosa, there is a greater amount of lymphoid tissue compared to other parts of the gastrointestinal tract. In the ileum - more pronounced submucosal lymphoid tissue, which is presented in the form of small single nodules or elongated ovoid-shaped Peyer's patches. Gastrointestinal tract-associated lymphoid tissue (CALT) is seen all the way from the root of the tongue to the rectum; in general, it is the largest human lymphoid organ.

FIGURE 7-54 Normal small intestine, slide

On the surface of the mucous membrane of the small intestine there are villi lined with prismatic cells (♦), among which goblet cells are scattered (A). In the region of the lamina propria of the mucous membrane, the villi end, here intestinal glands are formed, known as Lieberkün crypts (■). Thanks to the villi, the suction surface area is significantly increased. In the jejunum, in addition, there are more pronounced mucosal folds, which also increase the absorption surface. In each intestinal villus there is a blindly terminating lymphatic capillary known as the lacteal vessel. Immunoglobulin A, the so-called secretory IgA, is the main immunoglobulin produced by the plasma cells of the gastrointestinal (and respiratory) tract. It binds the protein on the glycocalyx covering the microvilli, which contributes to the neutralization of pathogens, including microorganisms.

FIGURE 7-55 Normal transverse colon, endoscopy

The large intestine is characterized by haustral mucosal folds. The function of the large intestine is primarily to absorb residual water and electrolytes from the small intestine. Intestinal contents are concentrated, so a person loses only about 100 ml of water per day with feces. Approximately 7-10 liters of gases pass through the large intestine daily. They are formed mainly as a result of the growth of normal bacterial flora. In the lumen of the intestine accumulates only about 0.5 liters of gases. The contents of the gases are swallowed air (nitrogen and oxygen), methane and hydrogen formed as a result of digestion and bacterial growth. Irritable bowel syndrome does not have any specific macroscopic or microscopic features. It develops under stress as a result of a pathological increase in the sensitivity of the intestinal wall to physiological stimuli of gas in the lumen. The use of anticholinergic drugs may lead to temporary improvement.

FIGURE 7-56 Normal colon, micropreparation

The mucous membrane of the large intestine is represented by long tubular intestinal glands (Lieberkühn crypts) lined with prismatic mucous cells. A large number of goblet cells provide lubrication of stool. Lymph nodules are localized in the lamina propria and in the submucosa. The outer longitudinal muscular layer is assembled into three long ribbons known as taenia coli. In the region of the anorectal junction, there is a transition of the glandular epithelium to the stratified squamous one. Above and below this junction B, the lumen protrudes from the submucosal veins (internal and external rectal veins). With their expansion, hemorrhoids are formed, which may be accompanied by itching and bleeding. The control of the volume of the contents of the intestine is carried out by the sphincter in the anus, formed by a layer of skeletal muscle.

FIGURE 7-57 Normal endocrine cells of the small intestine, microslide

In the crypts of the mucous membrane of the small intestine, dotted black enteroendocrine, or neuroendocrine, cells (Kulchitsky cells) are found. These cells are scattered in the glands, and their number increases in the distal small intestine. In the intestinal mucosa, various types of enteroendocrine cells are detected depending on the products they secrete. When the contents of the stomach pass into the small intestine, individual enteroendocrine cells produce cholecystokinin (CCK), which slows down gastric emptying, causes contraction of the gallbladder and secretion of bile, which promotes the digestion of fats. CCK also promotes the release of various enzymes from pancreatic acinar cells.

FIGURE 7-58 Omphalocele, appearance

A newborn girl in the middle sections of the abdominal wall has a defect that captures the area of ​​the umbilical cord; this defect is called an omphalocele (embryonic umbilical hernia, or embryonic eventration). The contents of the abdominal cavity, including intestinal loops and the liver, are covered with a thin film. Because in the embryonic period the intestinal loops predominantly developed outside the abdominal cavity, they malrotated, or incomplete rotation, and the abdominal cavity did not form properly and remained too small. Obviously, surgical treatment of such a defect is necessary. Sporadic occurrence of omphalocele is possible. However, there is usually an association with other malformations, and omphalocele may be the result of genetic abnormalities such as trisomy 18.

FIGURE 7-59 Gastroschisis, appearance

A large defect in the lateral wall of the abdominal cavity that does not involve the umbilical cord and is not covered by a membrane. Most of the intestines, stomach and liver developed outside the abdominal cavity. With this variant of gastroschisis, a single complex of limbs and trunk was formed, which is sometimes associated with the syndrome of amniotic cords, however, such fibrous adhesions of the amnion are observed only in 50% of cases. Early amnion damage occurs sporadically in the embryonic period and is not a manifestation of genetic disorders. In this observation, along with a single complex of limbs and torso, there is a decrease in the size of the limbs, especially the left upper limb, and scoliosis. At the same time, there are no craniofacial clefts and defects that occur with such a malformation.

FIGURE 7^>0 Bowel atresia, appearance

The intestine is filled with meconium and ends in a blind sac (A). Such changes are a manifestation of complete obstruction or atresia of the intestine. Partial or incomplete blockage of the intestinal lumen is called stenosis. Bowel atresia, like many anomalies, is often combined with other malformations. In utero, intestinal atresia develops against the background of polyhydramnios (polyhydramnios), since the fetus has impaired ingestion and absorption of amniotic fluid. Atresia is rare, but one localization should be noted: duodenal atresia, 50% of which are due to Down syndrome, but only a few cases of Down syndrome reveal duodenal atresia. Ultrasound examination in the dilated duodenum above the site of atresia and the stomach located next to it determines the sign of a “double-level of gas or liquid” (double-bubble).

FIGURE 74>1 Meckel's diverticulum, gross specimen

Congenital anomalies of the intestine are represented mainly by diverticula and atresia, which are often combined with other congenital malformations. Meckel's diverticulum (*) is the most common malformation of the gastrointestinal tract. Approximately 2% of people have Meckel's diverticulum, which is usually located 60 cm from the ileocecal valve. In the wall of Meckel's diverticulum, there are all three membranes of the intestinal wall, so it is referred to as a true diverticulum, which in adults is usually detected by chance. An exception is surgically removed Meckel's diverticula, complicated by bleeding or ulceration. In the wall of the diverticulum, heterotopias of the gastric mucosa can be observed, undergoing ulceration with subsequent abdominal pain and the possible development of iron deficiency anemia. Heterotopic pancreatic tissue in the wall of the diverticulum is usually of minor consequence.

At large sizes, heterotopias are predisposed to invagination.

FIGURE 7-62 Hirschsprung disease, macroslide

Congenital enlargement of the large intestine (megacolon), which is caused by a violation of the migration of neuroblasts involved in the formation of neuromuscular plexuses in the wall of the distal intestines. The dilated colon (*) is localized proximally to the affected, aganglionic area of ​​the sigmoid colon (G). In newborns, due to the lack of peristalsis in the aganglionic zone, the passage of feces slows down, intestinal obstruction develops, and the lumen of the proximal part of the intestine expands significantly. The incidence of the disease is 1 case per 5000 newborns; the disease affects mainly boys. The cause of Hirschsprung's disease can be various genetic defects, but about 50% of familial and 15-20% of sporadic cases have a mutation in the RET gene. Complications are mucosal damage and secondary infection.

FIGURE 7-63 Meconium ileus (meconium ileus), slide

This form of bowel obstruction is most commonly seen in neonates with cystic fibrosis, but is very rare in normal infants. In cystic fibrosis, impaired pancreatic secretion leads to thickening of the meconium and intestinal obstruction. The figure shows a dilated ileum filled with meconium (*). Macroscopically, meconium is dark green in color and has a tarry or sandy consistency. During childbirth, meconium either does not pass through the rectum at all, or is excreted from it in small quantities. A possible complication is meconium peritonitis due to intestinal rupture. On radiographic examination, meconium plugs may show petrification areas. Another complication of meconium ileus is volvulus.

The surface of the hyperemic mucous membrane of the large intestine is partially covered with yellowish-green exudate, with superficial lesions, HO without erosion. Such changes may be the cause of acute or chronic diarrhea, which may develop with long-term antibiotic treatment. a wide range actions (such as clindamycin) or immunosuppressive drugs. This is due to the predominant and overgrowth of the intestinal bacterial and fungal flora (Oostridium difficile, Staphylococcus aureus or Candida type fungi), which are usually suppressed under normal conditions. Exotoxins of microorganisms damage the mucous membrane, inducing the production of cytokines that cause cell apoptosis.

FIGURE 7-65 Pseudomembranous colitis, CT

Abdominal CT shows the transverse colon and splenic flexure of the colon (A) in antibiotic-associated pseudomembranous colitis. The intestinal lumen is narrowed, the wall is thickened, edematous. Similar changes can also be observed in ischemic colitis and neutropenic colitis (typhlitis). With typhlitis, the caecum is affected, in the wall of which the blood supply is most reduced in patients with weakened immunity and neutropenia.

FIGURE 7-66 Pseudomembranous colitis, endoscopy

On the surface of the mucous membrane of the large intestine there is an exudate of a yellowish-brown and greenish color. Similar changes can be observed in ischemia or severe acute infectious colitis. Patients experience abdominal pain, severe diarrhea develops. Disease progression can lead to sepsis and shock. There may be indications for resection of the affected intestine.

FIGURE 7-67 Giardiasis (giardiasis), smear

FIGURE 7-68 Amoebiasis, slide

FIGURE 7-69 Cryptosporidiosis, slide

Perforation of the wall of the cecum (left *) was a complication of typhlitis. Due to the rupture of the intestinal wall and the release of fecal contents into the peritoneal cavity, peritonitis developed. On the serous membrane (right *) a greenish-brown exudate is visible. Typhlitis is rare, but it can develop in immunocompromised patients, including malignant neutropenia and leukemia. The term "neutropenic enterocolitis" is used in cases of extensive intestinal damage. The combination of weakening of cellular immune responses and circulatory disorders in the intestinal mucosa contributes to the occurrence of the inflammatory process.

FIGURE 7-71 Tuberculous enteritis, gross specimen

Circular ulcers (one small, one large) are characteristic of Mycobacterium bovis infection. Nowadays they are rare due to the use of pasteurized milk in food. Such changes can sometimes be caused by ingestion of sputum infected with M. tuberculosis by patients with pulmonary tuberculosis. In the outcome of the healing of tuberculous ulcers, strictures may form, leading to obstruction of the intestinal lumen.

FIGURE 7-72 ​​Celiac disease (sprue), slides

On the left figure - the normal structure of the mucous membrane of the small intestine. The right figure shows pronounced changes in celiac disease (sprue). In the course of the disease, first there is a thickening and shortening of the villi, and then their complete disappearance. The inner surface of the mucous membrane, devoid of villi, is smoothed out. The brush border of enterocytes gradually disappears, mitotic activity increases, the crypts first hyperplasia and deepen, and then gradually disappear. The lamina propria is infiltrated with CO4 cells and gliadin-sensitive plasma cells. In the population of the white race, celiac disease occurs with a frequency of 1: 2000. Very rarely, this disease affects representatives of other races. More than 95% of patients have leukocyte antigens (HLA DQ2 or DQ8), which confirms the role of genetic disorders in the pathogenesis of the disease. There is an abnormal sensitivity to gluten, which is found in wheat, oats, barley and rye. The exclusion of these cereals from the diet leads to an improvement in the condition of patients.

FIGURE 7-73 Crohn's disease, macroslide

The scrotum of the terminal ileum is thickened (middle of the figure), there is no folding of the mucous membrane, deep cracks or longitudinal ulcers are located here. On the serous membrane there is a compacted adipose tissue of a reddish color, "creeping" over the surface. Inflammation in the form of limited areas strikes various departments intestines (the so-called "jumping" damage, separated from each other at a great distance). In Crohn's disease, any part of the gastrointestinal tract can be affected, but the small intestine is more commonly affected, especially the terminal ileum. The disease is most common in the United States and Western Europe, with women more likely to be affected than men. There is a genetic predisposition for the occurrence of the disease, which may be associated with the presence of certain types of HLA and mutations in the NOD2 gene. Triggering the production of the transcription factor NF-κΒ leads to the release of pro-inflammatory cytokines.

FIGURE 7-74 Crohn's disease, microscope slide

In Crohn's disease, transmural inflammation develops in the intestinal wall. Inflammatory infiltrates (in the figure they look like bluish clusters) diffusely spread from the ulcerated mucous membrane, affect the submucosa, muscular membrane and pass to the serous membrane, on the surface of which they form nodular accumulations in the form of granulomas. Due to transmural inflammation with damage to the serous membrane, there are prerequisites for the formation of adhesions and fistulas with adjacent abdominal organs. Interintestinal and pararectal fistulas are characteristic complications of Crohn's disease. Damage to the mucous membrane of the terminal section of the DOLE gut leads to disruption of absorption processes, including vitamin B 12 . In addition, impaired bile acid recirculation leads to steatorrhea.

FIGURE 7-75 Crohn's disease, slide

In Crohn's disease, the granulomatous nature of the inflammation is characterized by nodular accumulations of epithelioid cells, giant cells, and a large number of lymphocytes. Microorganisms are not detected with special stains. In most patients, relapses of the disease occur decades after the initial lesion, while in others, the disease can be either asymptomatic for a long time or a continuous active course from the very beginning of the disease. Antibodies to Saccharomyces cerevisiae (ASCA) are highly specific and sensitive for Crohn's disease and do not occur in ulcerative colitis (UC). Antineutrophil cytoplasmic autoantibodies with perinuclear staining (pANCA) can be detected in 75% of patients with Crohn's disease and only 11% in UC.

FIGURES 7-76, 7-77 Crohn's disease, radiograph and CT

On the left image of the upper gastrointestinal tract with bright barium contrast filling the intestinal lumen, an extended area of ​​narrowing (A) is visible, covering almost the entire terminal ileum - a "favorite" lesion site in Crohn's disease. The jejunum and colon are normal, although they too may be affected in Crohn's disease. The stomach is rarely involved. On the right figure, CT scan of the abdominal cavity shows an interintestinal fistula with contrast. As a result of adhesions caused by transmural inflammation, there was a convergence (▲) of the loops of the small intestine.

FIGURES 7-78, 7-79 Non-specific ulcerative colitis radiographs

On the left figure (after the administration of a barium suspension using an enema), fine granularity (♦) of the mucous membrane is visible, which starts from the rectum and continues to the transverse colon, which is characteristic of early changes in ulcerative colitis. Like Crohn's disease, UC is classified as an idiopathic inflammatory bowel disease. On the right figure (after a barium enema), a close-up shows coarse granularity (♦) of the mucosa in severe UC. UC is characterized by a diffuse lesion of the colonic mucosa throughout its entire length, which starts from the rectum and extends to various lengths in the proximal direction.

FIGURES 7-80, 7-81 Ulcerative colitis, gross slides

The left figure shows the resected colon with a severe UC lesion that begins in the rectum and completely affects all departments up to the ileocecal valve (A). Diffuse inflammation of the mucous membrane, areas of ulceration, pronounced plethora and coarse granularity of the surface are noted. With the progression of the disease, erosion of the mucous membrane merges into linear ulcers and penetrates under intact areas. Islets of preserved mucosa are called pseudopolyps. The right figure shows pseudopolyps in severe UC. The preserved mucosa is not ulcerated, there is only hyperemia of the submucosa and muscularis.

FIGURES 7-82, 7-83 Ulcerative colitis, endoscopy

Colonoscopy (left figure) revealed loose erythematous mucosa and reduction of haustral folds, indicating the absence of severe UC. On the right figure - a picture of active UC, but without pronounced ulceration and pseudopolyps. Idiopathic disease occurs most frequently in the US and Europe compared to other regions. The course of the disease is usually chronic, with the development of relapses in most patients, which can be single or repeated continuously. The first signs of the disease are small bloody diarrhea with mucus, cramping abdominal pain, tenesmus and fever. Extraintestinal manifestations in UC develop as inflammation progresses in the colon and include sclerosing cholangitis, migratory polyarthritis, sacroiliitis, uveitis, and acanthosis nigricans. In addition, there is a risk of developing colon adenocarcinoma. Extraintestinal manifestations also occur in Crohn's disease, but the risk of developing adenocarcinoma is not as high as in UC.

Inflammation in NUC is localized mainly in the mucous membrane of the colon. The figure shows an ulceration of the mucous membrane, resembling the neck of a bottle. Inflammation spreads under the adjacent mucous membrane, the edges of which become "undermined", which causes a peculiar form of an ulcer. There is exudate in the lumen and on the surface. Cellular composition infiltrates are represented by cells of acute and chronic inflammation. The stool is usually small in volume with blood and mucus. The most typical (in 60% of cases) is a moderate course of the disease with the development of relapses and remissions. However, in some patients, the disease may manifest as a single episode or, conversely, have a continuous course. Some patients (30%) due to the complicated course of colitis, not amenable to treatment within 3 years from the onset of the disease, undergo a colectomy. A formidable complication is toxic megacolon, in which the lumen of the large intestine expands sharply, the wall becomes thinner and there is a threat of its rupture.

FIGURE 7-85 Non-specific ulcerative colitis, slide

With active UC, crypt abscesses, or accumulations of neutrophilic granulocytes (*) in the lumen of inflamed crypts or Lieberkühn glands, are observed. In the submucosa, pronounced inflammation is detected. Involvement of intestinal glands in the inflammatory process leads to disruption of their architectonics, loss of goblet cells, nuclear hyperchromatosis, and inflammatory cell atypia. Histologic findings of crypt abscesses are more common in UC than in Crohn's disease. However, there may be partial coincidences of morphological patterns in these two forms of idiopathic inflammation of the intestine, which does not allow us to classify such observations in full.

FIGURE 7 86 Non-specific ulcerative colitis, slide

In the figure on the left, the colonic glands have a normal structure, contain goblet cells, on the right - irregularly shaped crypts, with signs of dysplasia, which is the first indicator of the development of neoplasia in chronic UC. In dysplasia, there is DNA damage with microsatellite instability. The risk of developing adenocarcinoma with a duration of pancolitis for 10-20 years is so great that total colectomy may be indicated. To identify signs of the development of dysplasia, patients with UC undergo screening colonoscopy.

FIGURE 7-87 Ischemic bowel disease, gross specimen

Early changes in ischemic enteritis are characterized by severe hyperemia of the tops of the villi of the mucous membrane of the small intestine. Most often, intestinal ischemia develops with arterial hypotension (shock) caused by heart failure, massive blood loss, and also due to impaired blood supply during mechanical obstruction (strangulation of the intestine in the hernial opening, volvulus, intussusception). less often to acute ischemia intestine leads to thrombosis or embolism of one or more branches of the mesenteric arteries. Sometimes the reason may be venous thrombosis with the syndrome of increased blood clotting. If the blood supply is not quickly restored, a bowel infarction may develop.

FIGURE 7-88 Ischemic enteritis, appearance

Small bowel infarction. The dark red to gray area of ​​the infarction contrasts with the pale pink color of the normal intestine (lower part of the figure). The affected intestine was localized in the hernial sac, formed as a result of adhesive disease after the previous operation. Similar changes could also develop as a result of infringement of the intestine during inguinal hernia. The mesenteric blood supply in this case was impaired due to infringement in the narrow hernial orifice into which the Kelly surgical forceps were inserted. Ischemia of the intestine due to its stretching is often accompanied by acute pain in the abdomen. The absence of intestinal peristalsis, determined by the absence of intestinal noise, indicates the development of ileus.

FIGURE 7-89 Ischemic enteritis, slide

The intestinal mucosa is necrotic. The plethora of mucosal vessels extends to the submucosa and muscularis, which remain relatively intact. More pronounced ischemia and necrosis of the mucous membrane are accompanied by hemorrhages and acute inflammation. Progression of ischemia can lead to transmural necrosis of the intestinal wall. Patients experience abdominal pain, vomiting, bloody stools, or melena. With ischemic necrosis, the intestinal microflora penetrates into the blood vessels, which leads to the development of septicemia, or into the peritoneal cavity, which leads to peritonitis and septic shock.

Endoscopy of the upper gastrointestinal tract revealed an area of ​​angiodysplasia (A). More often it is detected in adults when determining the cause of gastrointestinal bleeding, which occurs periodically and is rarely massive. Lesions are usually localized in the large intestine, but may be in other places. In the mucous membrane and submucosa there are one or more foci in which unevenly dilated, tortuous, thin-walled veins or capillary-type vessels are determined. Lesions are usually small - less than 0.5 cm, which makes them difficult to find. For diagnosis, colonoscopy and mesenteric angiography are used, and the affected areas of the intestine can be resected. Sometimes bowel angiodysplasia is associated with a rare systemic disorder known as hereditary hemorrhagic telangiectasia, or Osler-Weber-Rendu syndrome. A similar picture has the so-called lesions of Dieulafoy (Dieulafoy), which are most often localized in the wall of the stomach and lead to the development of bleeding. They are focal arterial or arteriovenous malformations of the submucosa of the stomach or intestines, leading to damage in this place of the mucous membrane.

FIGURE 7-91 Hemorrhoids, appearance

In the region of the anus and perianally, true (internal) hemorrhoidal nodes are located, represented by dilated veins (cavernous bodies) of the submucosa that have fallen out of the distal ampulla of the rectum. Hemorrhoids are prone to thrombosis and rupture of the wall with the formation of a hematoma and the development of bleeding. External hemorrhoids are formed above the intersphincteric groove, as a result of which acute hemorrhoids occur with localization along the edge of the anal ring. A prolonged increase in venous pressure leads to varicose veins. Hemorrhoids are characterized by anal itching and bleeding during or immediately after a bowel movement. The blood in the stool is usually bright red, scarlet. Another complication is rectal prolapse. Hemorrhoids may ulcerate. As a result of the healing processes, the organization of thrombosed hemorrhoids occurs and a fibrous polyp can form in the anus.

FIGURE 7-92 Hemorrhoids, endoscopy

In the region of the anorectal junction, there are hemorrhoids that look like polyps (A). Vessels are wrinkled and have signs of thrombosis, at least partial. The outer surface of the walls of the vessels that make up the nodes is whitish in color. Prerequisites for the development of hemorrhoids are chronic constipation, a low fiber diet, chronic diarrhea, pregnancy, and portal hypertension. Hemorrhoids are relatively rare in people under 30 years of age.

FIGURE 7-93 Diverticular disease, appearance, section

In the wall of the sigmoid colon (right side of the figure), whitish ribbons of longitudinal muscles (♦) are visible, so it looks lighter compared to the adjacent small intestine. Multiple rounded bluish-gray protrusions (A) or diverticula of the sigmoid colon wall are visible. The sizes of diverticula range from 0.5 to 1 cm and are most often found in the large intestine compared to the small intestine, affecting mainly its left sections. Diverticula are more commonly diagnosed in people from developed countries due to a diet low in fiber, resulting in reduced peristalsis and increased intra-intestinal pressure. The frequency of the disease increases with age.

FIGURE 7-94 Diverticular disease, gross specimen

The large intestine is opened longitudinally. Diverticula have a narrow isthmus that opens into the intestinal lumen. Colon diverticula rarely exceed 1 cm in diameter. They are not true diverticula because their wall consists only of mucosa and submucosa. Diverticula have the form of hernial protrusions, which are formed in places of acquired weakening of the muscular membrane of the intestinal wall. During peristalsis, the diverticula are not freed from the feces that fill their lumen. Severe failure of the structures of the intestinal wall and increased pressure in the intestinal lumen contribute to the formation of multiple diverticula, or diverticulosis. Colon diverticula rarely develop in people younger than 30 years of age.

FIGURE 7-95 Diverticular disease, CT

Abdominal CT at the pelvic level with contrast enhancement revealed diverticulosis (♦), most pronounced in the sigmoid colon. Small rounded protrusions dark color, because they are filled with feces and air, and not with a contrast agent. Most diverticula are asymptomatic. Complications develop in about 20% of cases of diverticulosis and are manifested by abdominal pain, constipation, periodic bleeding, inflammation (diverticulitis) with possible perforation, and peritonitis.

Colonoscopy shows two diverticula in the sigmoid colon, which were discovered by accident. A complication of diverticulosis is inflammation, which usually begins in a narrow region of the isthmus of the diverticulum, leading to mucosal erosion and pain. Further development of inflammation leads to diverticulitis. Possible manifestations of diverticular disease are cramping pain in the lower abdomen, constipation (less often - diarrhea), rare periodic bleeding. Diverticulosis and diverticulitis can cause iron deficiency anemia. Severe inflammation can sometimes develop, involving the wall of the diverticulum and leading to perforation and peritonitis.

FIGURE 7-97 Hernia, appearance, section

External hernias are protrusions of the peritoneum through defects or weak areas of the abdominal wall. This happens most often in inguinal region. An umbilical hernia, shown in this figure, can also develop in a similar way. Internal hernias in the abdominal cavity are formed during adhesive disease as a result of the formation of abnormal holes between the adhesions. Such openings may be so large that portions of the omentum and intestinal loops pass through them. When opening the anterior abdominal wall, a small hernial sac (*) was revealed, in which the adipose tissue of the greater omentum is located. The bowel loop in a reducible hernia may be sliding, passing through hernial orifice both inside the hernial sac and outside. With an irreducible or strangulated hernia, strangulation of the intestine can occur, followed by a decrease in blood supply and the development of intestinal ischemia.

FIGURE 7-98 Spikes, appearance, section

Between the loops of the small intestine formed adhesions that look like fibrous cords. Most often, adhesions are formed after operations on the abdominal organs. Multiple adhesions also occur after peritonitis. Adhesions can lead to obstruction of intestinal loops when they are localized in intraperitoneal pockets, which are formed as a result of the adhesive process. In patients undergoing abdominal surgery for acute appendicitis, adhesions in the peritoneal cavity are the most common cause of intestinal obstruction. The presence of scarring on the abdominal wall in patients with an acute abdomen, symptoms of intestinal lumen enlargement and intestinal obstruction suggest adhesive disease.

FIGURE 7-99 Intussusception, gross preparations

Intussusception is a rare form of intestinal obstruction in which the proximal segment of the intestine is introduced into the distal lumen. Violation of the blood supply in this area of ​​​​the intestine leads to a heart attack. On the left figure - the opened resected area of ​​the infarcted intestine of dark red color, inside which the invaginated segment of the intestine is located. The right figure shows a cross section of an intussusceptum, which has a peculiar appearance of the intestine in the intestine. In children, this condition is usually idiopathic. In adult patients, increased peristalsis in polyps or diverticula can lead to intussusception.

FIGURE 7-100 Intussusception, CT

Abdominal CT scan shows a target-like thickened part of the small intestine (▲) due to intussusception when one part of the intestine is located in the lumen of another. An x-ray of the abdominal cavity reveals dilated loops of the small intestine, air-liquid bowls, which are signs of intestinal obstruction. Patients present with abdominal pain, anterior abdominal wall tension, constipation, and decreased or abnormal bowel sounds on physical examination.

FIGURE 7-101 Volvulus, appearance, section

When the intestine is twisted, the blood supply to the intestine is disturbed, leading to its ischemia and infarction. Violation of the venous outflow leads to stagnation of blood. B case early diagnosis the intestine can be untwisted with the normalization of blood supply, but this happens infrequently. The figure shows a volvulus (*) of the mesentery of the small intestine, as a result, the latter in the area from the jejunum to the ileum has undergone ischemia and has a dark red color due to a developed infarction. Volvulus is a rare disease, more common in adults, and affects both the small intestine (around the axis of the mesentery) and the large intestine (the sigmoid or caecum, which are more mobile) with equal frequency. In young children, volvulus almost always affects the small intestine.

A small adenomatous polyp is seen in the left colon. A polyp is a formation that protrudes above the surrounding mucosa. It can be on a leg or be located on a wide base. The polyp has the structure of a tubular adenoma and is built from rounded newly formed glands. The outer surface of the polyps is smooth, the boundaries of the neoplasm are clear. Usually polyps occur in adult patients. Adenoma is a benign precursor of adenocarcinoma. Small adenomas are almost always benign, with sizes over 2 cm the risk of malignancy increases significantly. In such adenomas, mutations in the APC 1 SMAD4, K-RAS 1 p53 genes and age-related impairments in DNA gene repair accumulated over the years are detected.

FIGURE 7-103 Adenoma, endoscopy

Colonoscopy revealed polyps of the rectum, which have the structure of tubular adenomas. On the left figure, the polyp looks like a rounded formation on a small stalk with a smooth outer surface. In the right figure, the adenoma has a larger size, an abundance of vessels is determined on the surface, which explains the presence of latent blood in the patient's feces.

FIGURE 7-104 Adenoma, slide

Colon adenoma is a benign tumor built from newly formed glands and villi lined and covered with dysplastic epithelium. This small, short-stalked polyp is a tubular variant of the adenoma. It is characterized by a collection of disorganized, rounded glandular structures that differ from the glands in the surrounding intact colonic mucosa in shape and in fewer goblet cells. The cells lining the glands are densely packed, their nuclei are hyperchromic. At the same time, this small benign neoplasm is highly differentiated and limited; there is no tumor invasion into the polyp pedicle. The accumulation of additional mutations during the ongoing growth of the polyp increases the risk of malignancy.

FIGURE 7-105 Hyperplastic polyp, colonoscopy

Both figures show small, no more than 0.5 cm in diameter, flat polyps of the mucosa. They are tumor-like formations built from enlarged crypts of the mucous membrane. Most often they are observed in the rectum. The number of polyps increases with age, with more than 50% of people having at least one such polyp. Hyperplastic polyps are not true neoplasias and there is no risk of malignancy. It is unlikely that they can be the cause of the appearance of latent blood in the feces. However, most often polyps develop in patients with tubular adenomas and may gradually increase in size. Hyperplastic polyps are usually incidental findings during colonoscopy.

FIGURE 7-106 Peutz-Jeghers polyp, endoscopy

Peutz-Jeghers syndrome involves a combination of focal hyperpigmentation of the skin and mucous membranes with hamartoma polyps in the gastrointestinal tract. Polyps can occur in all parts of the gastrointestinal tract, but mostly in the small intestine. The figure shows small duodenal polyps detected during endoscopy, which were diagnosed as hamartomas during biopsy. This rare autosomal dominant disorder may be associated with polyps elsewhere in the gastrointestinal tract. Patients with this syndrome have an increased risk of developing malignant neoplasms in various organs, in particular in the mammary gland, ovaries. testicles, pancreas, but the polyps themselves are not malignant. Lentiginous pigmentation of the freckle type is observed mainly on the mucous membrane of the mouth and cheeks, in the genital area, hands and feet. Polyps can grow large enough to cause bowel obstruction or intussusception.

FIGURE 7-107 Villous (villous) adenoma, gross specimens

The left picture shows a villous adenoma that looks like a cauliflower, the right picture shows a tumor in a cross section of the intestinal wall. The villous adenoma has a broad attachment base rather than a stalk and is larger than tubular adenoma (adenomatous polyp). The average diameter of villous adenomas is a few centimeters, but can reach up to 10 cm. Larger villous adenomas have an increased risk of developing adenocarcinoma. Polyps built from tubular and villous structures are called tubulovillous (tubulovillous) adenomas.

FIGURE 7-108 Villous (villous) adenoma, slides

The left figure shows the edge of the villous adenoma, the right one shows the area above the basement membrane. The cauliflower-like appearance is due to the presence of elongated glandular structures covered with dysplastic epithelium. Villous adenomas are less common than adenomatous polyps and are more likely (about 40%) to harbor invasive carcinoma.

FIGURE 7-109 Hereditary non-polyposis colon carcinoma, macroscopic

Hereditary non-polyposis colon carcinoma (HNPCC), or Lynch syndrome 1, is genetic in nature and develops in the right colon in young patients. NNPCT is associated with extraintestinal malignant neoplasms (endometrium, urinary tract) and is associated with gene mutations leading to abnormal levels of expression of hMLHl and hMSH2 proteins. In tumors associated with NNPCT, microsatellite instability is detected (in sporadic cases, it is 10-15%). These onycholy are characterized by significantly fewer polyps compared to familial adenomatous polyposis associated with APC mutations, but polyps have a more aggressive course. The figure shows multiple polyps of the caecum (on the right is the terminal ileum).

FIGURES 7-110, 7-111 Familial adenomatous polyposis, gross specimens

In familial adenomatous polyposis, mutation of the APC genes leads to the accumulation of β-catenin with its translocation to the nucleus and activation of transcription of genes such as MYC and cyclin Dl. It is an autosomal dominant disorder resulting in the development of more than 100 colonic mucosal polyps during adolescence (right figure). Nearly all patients develop adenocarcinoma, except for cases of total colectomy. The milder form (left figure) is less common, characterized by greater variability in the number of polyps and the development of colon cancer at an older age. Gardner's syndrome also has a mutation in the APC gene, but in this syndrome, polyposis is accompanied by osteomas, periampullary adenocarcinomas, and cancer. thyroid gland, fibromatosis, dental anomalies and epidermal cysts.

The figure on the right shows an adenocarcinoma that developed from a villous (villous) adenoma. The surface of the tumor is polypoid, reddish-pink. Bleeding from the superficial vessels of the tumor is detected using a positive guaiac test for blood hidden in the feces. This tumor is usually localized in the sigmoid colon, which does not allow it to be detected by digital examination. However, it is relatively easy to recognize with sigmoidoscopy. Mutations, including APC/S-catenin carcinogenesis, loss of SMAD and p53, telomerase activation, microsatellite instability, precede rvlіobroeiys temetmcheekme mutations.

FIGURE 7-113 Adenocarcinoma, macroscopic

Due to exophytic growth of the tumor, obstruction (usually partial) of the colonic lumen can occur, which is one of the complications of adenocarcinoma. Disorders of the stool and digestion can also be caused by a tumor.

FIGURES 7-114, 7-115 Adenocarcinoma, endoscopy

Adenocarcinomas of the large intestine revealed during colonoscopy. There is ulceration and hemorrhage in the center of the formation on the left figure. The presence of these changes explains the need to study feces for occult blood in this pathology. In the right figure, a large tumor-like formation led to partial obstruction of the intestinal lumen.

FIGURES 7-116, 7-117 Adenocarcinoma, barium enema, and CT

The technique of conducting a barium enema consists in introducing dropwise a radiopaque barium suspension into the large intestine, as a result, the intestinal wall and any of its neoplasms are determined. On the left figure in the transverse and descending colon, two annular formations (*) are shown, which have the morphological structure of adenocarcinoma and led to a narrowing of the intestinal lumen. Contrast-enhanced abdominal CT scan of the distended cecum shows a large neoplasm (♦) that is an adenocarcinoma in the distended caecum. Cancer of the caecum often reaches large sizes. Its first manifestation may be iron deficiency anemia due to blood loss.

FIGURES 7-118, 7-119 Adenocarcinoma, slides

On the left figure - adenocarcinoma. Tumor glands of an elongated branching shape resemble fern leaves and are similar to the structures of villous (villous) adenoma, but much more disorganized. The nature of growth is predominantly exophytic (into the intestinal lumen), invasion is not visible in the figure. Determination of the degree of malignancy and stage of the tumor occurs in the study of many histological sections. At high magnification (right figure), the nuclei of tumor cells are hyperchromic and polymorphic. Normal goblet cells are absent. The development of colon cancer may be preceded by a number of genetic mutations. There may be a mutation in the APC gene, as well as mutations in K-Ras, SMAD4 and p53. It has been established that epidermal growth factor receptor (EGFR) can be detected in various solid malignant neoplasms, including colon adenocarcinoma. Anti-EGFR monoclonal antibodies can be used to treat colonic adenocarcinomas expressing EGFR.

FIGURES 7-120, 7-121 Carcinoid, gross and micropreparation

Tumors of the small intestine are rare neoplasms. Benign tumors of the small intestine include leiomyomas, fibromas, neurofibromas, and lipomas. In the left figure, in the region of the ileocecal valve, there is a carcinoid tumor of light yellow color. Majority benign tumors are submucosal masses that are detected incidentally, although sometimes they can be large enough to lead to obstruction of the intestinal lumen. On the right figure, at high magnification, a microscopic picture of a carcinoid is shown, which is built from nested clusters of rounded endocrine cells of small size, having small rounded nuclei and pinkish or pale blue cytoplasm. Sometimes malignant carcinoid is large. In case of carcinoid with liver metastases, the so-called carcinoid syndrome may occur.

FIGURES 7-122, 7-123 Lipoma and non-Hodgkin's lymphoma, gross slides

On the left figure there is a small yellowish subserous formation - a lipoma of the small intestine, discovered by chance during autopsy. It is built from mature adipose tissue cells. Benign neoplasms are built from cells similar in structure to the cells of the maternal tissue, are characterized by clear boundaries and slow growth. On the right figure, in the mucous membrane of the small intestine, multiple uneven formations of reddish-brown and brown color are visible - non-Hodgkin's lymphoma that developed in a patient with AIDS. Lymphomas in AIDS are highly differentiated. On the other hand, the pathology of mucosal-associated lymphoid tissue is sporadic; in the stomach, it may be associated with chronic infection with Helicobacter pylori. More than 95% of gastrointestinal lymphomas originate from B cells. The wall of the affected intestine thickens, peristalsis is disturbed. Large lymphomas may ulcerate or obstruct the intestinal lumen.

FIGURE 7-124 Acute appendicitis, CT

An enlarged appendix is ​​seen (A) with a fecal calculus that is brightened due to partial calcification. The caecum (left) is partially filled with bright contrast. The appendix, located distal to the fecal stone, has a dark lumen due to the presence of air. The presence of brighter areas is noted, corresponding to areas of inflammation that capture the surrounding fatty tissue. In patients with acute appendicitis characteristic symptoms are a sudden onset with acute pain localized in the right lower quadrant of the abdomen, and a sharp pain on palpation of the anterior abdominal wall. Leukocytosis is often noted in the blood. This patient has an increased operative risk due to obesity (note thickened dark subcutaneous adipose tissue).

FIGURE 7-125 Acute appendicitis, gross

The resected appendix after laparoscopic surgery is presented. A brownish-yellow exudate is present in the serous membrane, but the first main signs of acute appendicitis are edema and hyperemia. This patient had an increase in temperature and an increase in the number of leukocytes in the blood with a shift in the formula to the left (an increase in the number of segmented neutrophils). In addition, the patient had mild abdominal pain and severe flank pain due to the retrocecal location of the process.

FIGURE 7-126 Acute appendicitis, slide

Acute appendicitis is characterized by severe inflammation and necrosis of the mucous membrane. The figure shows an abundance of neutrophilic granulocytes that infiltrate the entire thickness of the appendix wall. In peripheral blood, there is often an increase in the number of neutrophils with a shift in the formula to the left. Surgical removal of the inflamed appendix must be performed before the development of potential complications in the form of perforation of the appendix and sepsis. When inflammation is localized only in the serous membrane (periappendicitis), the primary focus of inflammation is apparently located in another part of the abdominal cavity, and process B in this case is not involved in inflammation.

FIGURE 7-127 Appendix mucocele, macroscopic

The lumen of the appendix is ​​sharply expanded and filled with transparent viscous mucus. A persistent mucocele is possibly a true tumour, most commonly a mucinous cystadenoma, and not simply a process obstruction. When the wall ruptures, the mucus enters the peritoneal cavity, which is accompanied by symptoms of tension in the abdominal wall. Similar changes, called pseudomyxomas of the peritoneum, can also occur with mucinous cystadenocarcinomas of the appendix, colon, or ovaries, but they differ in the presence of cancer cells in the mucus.

FIGURE 7-128 Free air perforation, KT

A freely located gas bubble (♦) is visible in the abdominal cavity as a result of perforation of a hollow organ. Inflammation with ulceration of the intestine, stomach, or gallbladder may be complicated by perforation. The presence of free air is a sign of rupture of a hollow organ or its perforation. The figure also shows ascitic fluid to the right of the liver, forming an air-liquid level (A). Perngommt can develop all and Oca perfiration (spontaneous bacterial peritonitis). It usually develops against the background of ascites, which is more common with nephrotic syndrome in children or with chronic liver disease in adults.

FIGURE 7-129 Peritonitis, appearance, section

Perforation in any part of the gastrointestinal tract (from the lower esophagus to the large intestine inclusive) can lead to peritonitis. An autopsy revealed exudate in the form of thick yellowish purulent deposits on the surface of the peritoneum. Contamination of the abdominal cavity can be caused by various microorganisms, including enterobacteria, streptococci, clostridia. Ovarian cancer caused obstruction of the sigmoid colon and its perforation. Sigmoid colon gray-black color is noticeably expanded and localized in the pelvic cavity. Peritonitis can cause the development of functional intestinal obstruction due to paralytic ileus, which is revealed on radiographic examination as dilated intestinal loops with air-liquid levels.

Catad_tema Peptic ulcer disease - articles

Catad_tema Anesthesiology-reanimatology - articles

Prevention of stress erosive and ulcerative lesions of the gastroduodenal zone in critically ill patients

MD M.A. Evseev
MMA named after I.M. Sechenov

The occurrence of acute erosive and ulcerative lesions of the gastroduodenal mucosa in patients in critical conditions, including in the postoperative period, is, on the one hand, an extremely unfavorable, but natural consequence of existing multisystem disorders and, on the other hand, a factor that fundamentally worsens the prognosis of life patient. According to M. Fennerty (2002), B. Raynard (1999), acute erosions and ulcers in the gastroduodenal zone are detected already in the first hours of patients' stay in the intensive care unit in 75% of cases. According to V.A. Kubyshkin and K.V. Shishina (2005), in the postoperative period, acute ulcerations of the gastroduodenal mucosa, having clinical manifestations in no more than 1% of patients, are found at autopsy in 24% of cases, and with nonselective esophagogastroduodenoscopy - in 50–100% of those operated. 75% of acute ulcers are complicated by bleeding, while esophagogastroscopy shows signs of ongoing bleeding in 20–25% of patients. Acute ulceration of the mucous membrane of the stomach and duodenum develop over the next 3-5 days under the influence of provoking factors (surgery, shock, sepsis, extensive burns, etc.). The overall mortality in operated patients with the development of acute erosive and ulcerative damage to the stomach, complicated by bleeding, reaches 80%. The same authors see the main reason for the relevance of the problem under discussion in the almost complete absence of clinical symptoms of erosive and ulcerative lesions and the manifestation of the latter only by its complications, in the vast majority of cases - gastroduodenal bleeding. At the same time, ulcer bleeding, even of low intensity, sharply worsens the general condition of patients, which is manifested primarily by disorders of central hemodynamics. Significantly later, local symptoms appear in the form of vomiting of blood or melena, which is observed only in 36–37% of patients.

A.A. Kurygin, O.N. Scriabin, Yu.M. Stoyko (2004) reported that with the help of systematic fibrogastroduodenoscopy, acute ulcerations were detected in 64% of operated patients who had an increased risk of ulcer formation. In another 6% of patients, this complication was either an unexpected finding at autopsy, or was identified by clinical signs. Gastrointestinal bleeding was the main manifestation of acute ulcers in the postoperative period in 60% of patients, of which 33% of them were massive, and only 13% of patients complained of increased pain in the epigastric region, nausea, severe weakness, dizziness. In four cases, fainting was noted. More than half of all acute ulcers (56%) are formed in the first three days and the more often, the more severe the previous surgical intervention and concomitant diseases. Acute ulceration of the gastric mucosa late dates usually associated with complications of the operation in the form of cardiovascular, renal and respiratory failure, as well as with purulent processes.

For the first time, the occurrence of acute erosive-ulcerative lesions in the postoperative period was described by Th. Billroth in 1867, suggesting the existence of a causal relationship between surgical trauma and damage to the gastroduodenal mucosa. In 1936, G. Selye proposed the term "stress ulcer" to refer to the relationship between psychosomatic illness and gastroduodenal ulcer. Currently, a number of authors (B.R. Gelfand, A.N. Martynov, V.A. Guryanov et al., 2004) have proposed the term "syndrome of acute gastric injury", which implies damage to the mucous membrane of the stomach and duodenum that occurs when violation of the mechanisms of its protection in patients in critical conditions, and includes swelling and violation of the integrity of the mucous membrane, as well as a violation of the motor-evacuation function of the stomach.

It should be borne in mind that the morphology and pathogenesis of acute erosive and ulcerative lesions of the stomach and duodenum differ in many respects from chronic gastroduodenal erosions and ulcers (LI Aruin, VA Isakov, 1998) (Fig. 1). erosion called defects of the mucous membrane, not penetrating beyond the muscular plate of the mucous membrane. Most often, erosions that occur under the influence of stress factors are localized in the fundus of the stomach. Acute erosion can be superficial and deep. Surface erosion are characterized by necrosis and rejection of the epithelium, are localized at the tops of the gastric ridges and are usually multiple. Deep erosions destroy the lamina propria of the mucous membrane, without capturing the muscular lamina. The microscopic picture of acute erosions is not typical for damage to the mucosa by the acid-peptic factor of gastric juice, but is a consequence of trophic disorders. It has been established that the development of erosions is preceded by significant microcirculation disorders, which gives reason to most morphologists to consider acute erosions as an ischemic infarction of the mucous membrane.

. A) Macropreparation: multiple acute gastric ulcers with bleeding; B) A micropreparation of an acute gastric ulcer complicated by bleeding: necrotic masses of the bottom of the ulcer, unchanged muscle membrane, hematin hydrochloride

Acute ulcers called defects (necrosis) of the muco-submucosal layer, extending deep into the wall of the organ to the muscular membrane and associated with the influence of a pronounced stress factor. The division of "postoperative" acute ulcers, "Cushing's ulcers", "Curling's ulcers" is of exclusively historical interest, since these ulcers do not have morphological differences, and their treatment and prevention are universal. Acute ulcers are usually multiple, localized mainly along the lesser curvature of the stomach, the diameter of acute ulcers usually does not exceed 1 cm. Microscopically, in the immediate vicinity of the ulcer, areas of granulation tissue are detected in the depth of the gastric or duodenal wall, plethora, stasis, edema, thrombosis, hemorrhage, which indicates a vascular or, rather, ischemic genesis of acute ulcerations.

Currently, most authors support the concept of ischemic damage in the event of stress ulceration in the gastroduodenal zone, stating that the main cause of stress ulcers is inadequate blood supply to the wall of the stomach and duodenum. An increase in gastric acidity becomes important only when the protective barrier is damaged before local ischemia occurs. A.L. Kostyuchenko et al. (2000), N.A. Maistrenko et al. (1998) indicate that the result of stessor effects is the occurrence of a persistent spasm of the vessels of the celiac zone with a violation of both arterial perfusion and venous outflow. In this case, the latter leads to stagnation of blood in the mucosubmucosal layer of the stomach and duodenum, increased capillary pressure, intraorganic plasma loss, local hemoconcentration, followed by the occurrence of microthrombosis. Synchronously, there is a disclosure of preterminal arteriovenous shunts, which further exacerbates the ischemia of the mucous membrane.

B.R. Gelfand et al. (2004) believe that the most pronounced microcirculation disorders in critically ill patients occur precisely in the proximal parts of the digestive tube due to the highest content of α-adrenergic receptors in their arteries. In this regard, the main causes of gastroduodenal stress ulcers are local ischemia, activation of free radical oxidation in the absence of antioxidant defense systems, a decrease in the content of prostaglandin E1, which are realized by the occurrence of foci of typical ischemic necrosis. Restoration of regional blood circulation after prolonged hypoperfusion leads to non-occlusive disruption of splanchnic blood flow, which, leading to reperfusion syndrome, further exacerbates damage to the gastroduodenal mucosa.

On the other hand, a number of authors adhere to a slightly different point of view on the pathogenesis of stress erosions and ulcers of the gastroduodenal zone. So, V.A. Cubes kin and K.V. Shishin (2005) believe that the main pathogenetic mechanism for the formation of erosive and ulcerative lesions is the strengthening of intragastric aggression factors in relation to protection factors. A comprehensive assessment of the acid-forming function of the stomach using several methods (titration, intragastric and targeted pH-metry) showed that in the first 10 days after the operation, the maximum stimulation of the acid-forming function of the stomach occurs, while its “peak” falls on days 3-5, that is for the period of the most probable ulcer formation. In this case, the greatest increase in proteolytic activity is recorded in the area of ​​the bottom - the place most often subject to erosive-ulcerative process. The study of nocturnal secretion, which is a special case of basal secretion and reflects mainly the vagal phase, made it possible to establish the maximum increase in the acidity of gastric juice in the first 4 hours of the night. An interesting fact is that an increase in the production of free hydrochloric acid is observed even in cases where achlorhydria is recorded on the eve of the operation. The authors argue that this reaction of the digestive system to surgical stress underlies the formation of early true stress ulcers, which account for approximately 80% of all ulcerations of the upper gastrointestinal mucosa that form in the postoperative period. In the remaining 20% ​​of cases, ulcers occur in the phase of mucosal degeneration in a longer period after surgery with a complicated course of the postoperative period in the form of cardiovascular, renal and respiratory failure, as well as purulent and septic complications leading to the development of multiple organ failure, one of the manifestations which just are ulcers. The occurrence of acute ulceration of the gastric mucosa against such a background is no longer dependent on acid-peptic aggression.

It would be quite logical to doubt the very possibility of gastric hypersecretion under conditions of stress activation of the sympathetic-adrenal system during the suppression of vagal influences. But, as often happens, the mechanisms of pathogenesis turn out to be by no means so obvious to us at first, and the obviousness subsequently increases in direct proportion to our awareness of the subject of study. So, in the context of this report, it should be noted that an indirect morphological confirmation of the legitimacy of the point of view about the determining role of the acid-peptic factor is the presence of areas of fibrinoid necrosis in the bottom of acute ulcers (by no means always), which indicates the participation in ulcerogenesis of acute ulcers of the acid-peptic factor. factor a. Back in 1957, N. Nechels and M. Kirsten showed in an experiment that acid production is directly related to the level of hypercapnia and the severity of metabolic acidosis, that is, it is a compensatory mechanism for acid-base balance disorders.

It should be noted that the concept of priority ischemic or acid-peptic factors in the pathogenesis of stress ulcers are not mutually exclusive (Fig. 2). It seems quite logical that ischemic damage to the gastroduodenal mucosa is a predisposing factor, and hydrochloric acid and pepsin are a producing factor. As pointed out by A.L. Kostyuchenko et al. (2000), under conditions of mucosal ischemia, the natural neutralization of hydrochloric acid becomes insufficient, and even at the usual level of acid production, mucosal acidosis develops, which is easily subjected to the digestive action of pepsin. These changes are aggravated under the influence of bile salts (duodenogastric reflux in gastric motility disorders), to which the ischemic mucosa is especially sensitive in the fundus of the stomach. Ischemia is accompanied by activation of intraparietal and intraluminal proteolysis, which limits the possibility of the formation of full-fledged blood clots in arrosed vessels of the bottom of the ulcer.

. Pathogenesis of gastroduodenal stress ulcers

Thus, a number of circumstances become apparent. First, given the high incidence of erosive and ulcerative lesions of the gastroduodenal zone in critically ill patients, the fatal consequences of bleeding from stress ulcers and the almost complete absence of clinical symptoms of acute ulcers, the only way to solve the problem is the prevention of erosive and ulcerative lesions. Each surgeon and resuscitator knows far from one sad clinical case, when, against the background of stabilization of the condition of a patient who has undergone more than one relaparotomy, which has been achieved with such difficulty, difficult-to-correct hypotension “suddenly” develops, somewhat later, the nasogastric tube begins to flow “ coffee grounds” with unchanged blood, endoscopists shrug their hands (“weeping” the entire mucous membrane, reliable endohemostasis is unlikely), and it is impossible to operate on the patient due to the severity of the condition. Secondly, taking into account the importance of the acid-pepic factor for the occurrence of acute erosive and ulcerative damage to the gastroduodenal mucosa, the preventive use of antisecretory drugs in critically ill patients will be pathogenetically justified. Thirdly, a pathogenetically substantiated method of preventing stress damage to the gastroduodenal mucosa will be the use of drugs that improve hemoperfusion, increase oxygen delivery, and also level the activation of free radical oxidation in the mucosa of the digestive tube.

From the point of view of a practical doctor, the question is logical: to whom and when is the prophylactic use of antisecretory drugs indicated? That is, what are the objective criteria for the risk of stress ulcers in the postoperative period and in critically ill patients? Agree that retrospective data that "acute ulceration of the mucosa are detected in 20-50% of the dead after various abdominal operations" are of little help in solving daily clinical issues.

To date, the following risk factors for acute erosive and ulcerative damage to the gastroduodenal mucosa in critically ill patients are proven: artificial ventilation lungs, prolonged hypotension of various origins, sepsis, hemocoagulation disorders (hypercoagulation and DIC syndromes), liver and kidney failure, as well as elderly and senile age, malignant tumors, acute pancreatitis, hypovolemia, peritonitis, cardiovascular insufficiency, exhaustion. The incidence of bleeding from acute ulcers increases many times during extensive traumatic interventions, reaching, according to some authors, 60%. M.B. Yarustovsky et al. (2004) indicate that the use of cardiopulmonary bypass during surgical interventions on the heart and main vessels increases the incidence of bleeding from acute stress ulcers in the postoperative period by more than 6 times compared with operations performed without cardiopulmonary bypass. Nevertheless, the vast majority of postoperative bleeding from the upper digestive tract develops in patients who have undergone extensive surgical interventions for severe diseases of the hepatopancreatobiliary zone (tumors and cicatricial strictures of the bile ducts, primary and metastatic liver tumors, pancreatic tumors, pseudotumorous pancreatitis, cholelithiasis). complicated by jaundice, cholangitis and choledocholithiasis, pancreatic necrosis, etc.). Yu.I. Patyutko and A.G. Kotelnikov (2007) indicate that bleeding from acute erosions and ulcers complicates the course of the postoperative period in every tenth patient who underwent gastropancreatoduodenal resection. In this regard, the expediency of isolating specific risk factors for the development of acute gastroduodenal stress ulcers is obvious. For this purpose, N. Stollman, D. Metz (2004) conducted a meta-analysis of several prospective studies: D. Cook et al. (1994) - 2200 patients in the postoperative period; P. Hastings et al. (1998) and R. Fiddian-Green (1993) - 100 and 564 patients in the intensive care unit, respectively. Based on the analysis, the authors presented, in descending order of importance, the following risk factors for the development of erosive and ulcerative lesions of the stomach in critical conditions:

• Respiratory failure with mechanical ventilation for more than 48 hours
• coagulopathy
• Prolonged hypotension or shock
• Sepsis
• Liver failure
• kidney failure
• Operational interventions
• burn disease
• Severe injuries
• Acute coronary syndrome
• CNS damage
• Multiple organ failure.

B.R. Gelfand, A.N. Martynov, V.A. Guryanov, A.S. Bazarov (2004) give more specific criteria for the likely occurrence of erosive and ulcerative stress lesions of the stomach:

• IVL more than 48 hours
• coagulopathy
• Acute liver failure
• Severe arterial hypotension and shock
• Sepsis
• Chronic renal failure
• Alcoholism
• Treatment with glucocorticoids
• Prolonged nasogastric intubation
• Severe traumatic brain injury
• Burns over 30% of body area.

Obviously, a patient who meets one or more risk criteria for stress ulcers in the gastroduodenal zone needs a set of preventive measures. At the same time, it is quite difficult to distinguish between these events into “specific” and “non-specific”. Patients in critical condition are shown:

• correction of hypoperfusion and local ischemia of the gastroduodenal zone;
• increasing the protective properties of the mucous membrane of the gastroduodenal zone and stimulating its reparative potential;
• inhibition of gastric secretion.

Correction of hypoperfusion and local ischemia of the gastroduodenal zone is carried out using infusions of rheologically active solutions (hydroxyethyl starch solutions, rheopolyglucin, gelatinol, perfluorocarbon emulsion), oxygen transport media (perfluorocarbon emulsion, erythrocyte mass - in the presence of a proven hemic component of hypoxia), drugs that increase cardiac output, drugs, that have a compensatory effect on oxidative stress (calcium oxybutyrate, mafusol, vitamin C, tocopherol, piracetam).

Speaking about the increase in the protective properties of the mucous membrane of the gastroduodenal zone, first of all, they mean the use of drugs with antacid and gastroprotective effects. Antacids (magnesium hydroxide, aluminum hydroxide, calcium carbonate, magnesium trisilicate, sodium bicarbonate) realize their action by neutralizing the already existing hydrochloric acid. However, the practical use of these drugs in critically ill patients has revealed a number of significant drawbacks. First of all, the oral use of drugs in a patient in critical condition (artificial ventilation of the lungs, condition after operations on the gastroduodenal zone, paresis of the gastrointestinal tract) is technically very problematic, since hourly administration of drugs is necessary. In addition, the release of carbon dioxide during the interaction of hydrochloric acid and carbonates can lead to distension of the stomach and regurgitation of gastric contents into the trachea and bronchi (Mendelssohn's syndrome, aspiration pneumonia). With the systematic use of antacids, the development of systemic alkalosis is possible.

The gastroprotector sucralfate does not have an acid-neutralizing effect and exerts its protective effect by forming a film on the gastric and duodenal mucosa. It should be noted that the formation of a polymer film from sucralfate occurs only at pH below 4, which is not always the case, and, in addition, the frequency of bleeding from stress ulcers during the prophylactic use of sucralfate, according to D. Cook (1998), was in two times higher than that when using antisecretory drugs. However, sucralfate is still better than nothing.

To date, it is generally recognized that the leading component of the prevention and pharmacotherapy of acute erosive and ulcerative lesions of the stomach are modern antisecretory drugs.

In the 70–90s of the twentieth century, H 2 blockers were widely used to prevent stress damage to the gastroduodenal zone. Based on the analysis of a large sample of critically ill patients in 1992, D. Cook concluded that the prophylactic use of H 2 blockers prevents acute erosive and ulcerative lesions of the gastroduodenal zone much more effectively than antacids and sucralfate. However, many authors point out that it is rather problematic to achieve reliable control over the state of the gastroduodenal mucosa with the prophylactic use of H2-blockers. So, B. Erstadt et al. (1999), M. Feldman (1990) provide data on the short antisecretory effect of H 2 blockers due to the short half-life of these drugs. The same authors noted the instability of the antisecretory effect, manifested by a decrease in intragastric pH less than 3.5–4, both with bolus and continuous drug administration, including with increasing doses. P. Netzer (1999) explains this fact by the occurrence of the effect of "fatigue of H 2 receptors" already on the first day from the start of therapy.

We would like to draw the attention of readers to one more feature of the pharmacodynamics of H 2 blockers, which casts doubt on the feasibility of their use for the prevention of stress ulcers, namely, the aggravation of ischemia of the gastric or duodenal wall by blocking H 2 receptors of arteries of the submucosal and muscle layers and, as consequently, vasoconstriction with a decrease in the volumetric blood flow velocity. Thus, H 2 blockers in critically ill patients, on the one hand, reduce the intensity of acid-peptic aggression, but on the other hand, increase local ischemia, which is the main pathogenetic factor in stress ulcerogenesis.

In addition, the use of H2-blockers, especially in high doses, has an extremely negative effect on the detoxification function of the liver (inhibition of the cytochrome P450 system), leads to an aggravation of the already existing encephalopathy, which can be manifested by anxiety, disorientation, delirium and hallucinosis. It should be remembered about the possibility of negative chrono- and inotropic effects, extrasystole and atrioventricular blockade, due to the action of H2-blockers.

It is obvious that the appearance in wide clinical practice of proton pump inhibitors (PPIs), which are the most powerful antisecretory drugs and have a favorable safety profile, immediately attracted the attention of researchers by the possibility of prophylactic use of these drugs in critically ill patients. Initially, PPIs with oral administration were tested in the clinic - the suspension of the drug was administered to patients through a nasogastric tube. However, due to the small number of observations, the effectiveness of oral PPIs for the prevention of stress ulcers has not been formally proven. In turn, I would like to emphasize once again that attempts at oral administration of antisecretory drugs, including through a nasogastric tube in the form of suspensions, in patients in critical conditions (acute blood loss, sepsis, acute heart or respiratory failure), in our opinion, initially devoid of any meaning. This is due to a number of circumstances. First, proton pump inhibitors are acid-labile compounds that are inactivated upon contact with hydrochloric acid, which determines the need to encapsulate the active substance of oral forms of PPIs in a capsule or gelatin shell. The introduction of an unprotected active form of PPI in the form of a suspension into the lumen of the stomach naturally leads to its inactivation. Secondly, since PPI absorption occurs in the small intestine, reduced motor activity of the digestive tube due to blood loss, peritonitis, or multiple organ failure causes a pronounced decrease in PPI bioavailability. A. Dunn et al. (1999), D. Heyland et al. (1995) indicate that PPIs administered as a suspension may have unstable bioavailability and require adequate absorptive activity from the patient, which often changes in critical conditions. Thirdly, to ensure the information content of dynamic endoscopic control, it is necessary to maintain the lumen of the stomach and duodenum “clean”. In this regard, it should be recognized that the only acceptable option for antisecretory prevention of stressful erosive and ulcerative damage to the gastroduodenal zone is only parenteral administration of proton pump inhibitors.

A real opportunity for the prophylactic use of PPIs in critically ill patients appeared with the introduction of omeprazole into clinical practice for parenteral administration. Currently, another representative PPI with the possibility of parenteral administration has become available for clinical use - pantoprazole (Controloc).

Pantoprazole is a highly effective H+/K+-ATP-ase inhibitor. The drug reduces the level of basal and stimulated (regardless of the type of stimulus) secretion of hydrochloric acid in the stomach. As is known, the duration of PPI action depends on the rate of regeneration of new proton pumps, and not on the duration of the drug in the body. The mean half-life of pantoprazole after a single intravenous dose of 40 mg is about one hour. Nevertheless, the suppression of hydrochloric acid secretion persists for about three days. This is due to the achievement of a certain balance between the number of newly synthesized proton pump molecules and the number of already inhibited molecules. A single intravenous dose of pantoprazole provides a rapid (within 1 hour) dose-dependent inhibition of acid production: with the introduction of 40 mg - acid production is reduced by 86%, 60 mg - by 98%, 80 mg - by 99%, and not only acid production is reduced products, but also the volume of gastric secretion. After intravenous administration of a standard dose of pantoprazole 80 mg after 12 hours, the degree of acid reduction is 95%, and after 24 hours - 79%. In humans, the half-life of inhibition of acid secretion after administration of lansoprazole is ~13 hours, omeprazole ~28 hours, and pantoprazole ~46 hours. Therefore, pantoprazole causes the longest inhibition of acid secretion compared to the listed PPIs. This is due to its specific binding to the cysteine ​​located at position 822, which is immersed in the transport domain of the gastric acid pump. Binding to this amino acid determines the longest action of pantoprazole compared to other PPIs (Fig. 3). This is an important factor, since the recovery of acid production depends entirely on the self-renewal of proton pump proteins.

. Benefits of Controloc in Patients with Gastrointestinal Bleeding (GIB)

Controloc has a constant linear predictable pharmacokinetics. When doubling the dose of PPIs with non-linear pharmacokinetics, their serum concentration will be either lower or higher than expected, i.e. she is unpredictable. This may lead to inadequate control of acid secretion or affect the safety of the drug.

A distinctive feature of Controloc is its lowest drug interaction potential. The ability of pantoprazole to interact with other simultaneously administered drugs is very low due to its low affinity for the metabolizing isoenzyme of cytochrome P-450 and the conjugation reaction taking place in phase II. Pantoprazole is not included in the known metabolic pathways of interaction with other drugs, which is of fundamental importance for patients in intensive care units receiving a large number of drugs at the same time.

Metz D. et al. (2001) conducted a study on the effectiveness of the use of pantoprazole for the prevention of rebleeding from peptic ulcers. Used two doses of pantoprazole - 40 mg 1/day. for 3 days (small dose) and 40 mg followed by continuous administration (8 mg/h) for 3 days (large dose). 168 patients with bleeding ulcers (Forrest Ia, Ib and IIa) after endoscopic hemostasis with the introduction of adrenaline were randomized to receive high or low doses of pantoprazole. The rebleeding rate at 72 hours was similar in both groups, 12% in the low dose group and 13% in the high dose group. The need for blood transfusions was also similar for both treatments. The authors concluded that "both continuous intravenous infusion of pantoprazole after injection of the initiating dose and repeated administration of pantoprazole are equally effective in preventing recurrent ulcer bleeding." To prevent re-HDC after its initial arrest, it is necessary to maintain achohydria, which requires repeated injections or a continuous slow infusion of pantoprazole. For this purpose, it is recommended to continuously administer it in / in an average dose of 8 mg / h.

The positive role of intravenously administered pantoprazole for the prevention of stress ulcers in intensive care units was also demonstrated in the study by Aris R. et al. (2001), which is a retrospective analysis of the clinical use of the intravenous form of PPI over a six-month period. Of the 97% of patients who had a high risk of developing stress ulcers, preventive effect against the background of intravenous administration of 40 mg pantoprazole once a day was achieved in almost 90% of cases. Only 7% of cases required treatment for ulcerative bleeding. A very important result of this study was the absence of indications of adverse effects and significant interactions of intravenously administered pantoprazole with drugs traditionally used in intensive care units in emergency situations.

A number of researchers (based more on theoretical conclusions) fear that an increase in intragastric pH may enhance bacterial colonization in the oropharynx and be a risk factor for the development of nosocomial pneumonia. However, the works of W. Geus (2000), D. Cook et al. (1991, 1996, 1998) and M. Tryba et al. (1991) proved that colonization of bacteria in the stomach rarely leads to pathological colonization of bacteria in the oropharynx, and the risk of developing nosocomial pneumonia does not increase with the use of proton pump inhibitors.

To determine the mode of prophylactic administration of proton pump inhibitors, it is advisable to use the prognostic criteria for the risk of developing gastroduodenal stress ulcers, proposed by D. Cook back in 1994 (Table 1).

Table 1. Significance of risk factors for the development of gastroduodenal stress ulcers in critically ill patients

In this case, if the sum of RR in a particular patient is equal to or exceeds the value of 2, then the use of an intravenous PPI is indicated according to the scheme: 40 mg twice a day as a bolus or continuous infusion of the drug at a rate of 4 mg/h. If the sum of RR in a particular patient is less than 2, then the use of PPIs in / in the scheme is indicated: 40 mg once a day as a bolus or continuous infusion of the drug at a rate of 2 mg / h.

In conclusion, let us dwell on another aspect of the prevention of stress-damage to the gastroduodenal zone, namely, on the pharmacoeconomic significance of prevention. So far, no domestic research has been conducted on this issue. On the contrary, foreign colleagues, for whom the concept of the adequacy of treatment invariably included its cost, demonstrated that in the absence of full-fledged prevention in patients at risk for stress ulcers, “the miser has to pay twice.” So, S. Conrad et al. (2002) indicate that in the event of bleeding from a stress ulcer, a patient in the intensive care unit needs an additional 7 hematological studies, 11 units of erythrocyte mass, at least two endoscopic studies. D. Heyland et al. (1995) under similar circumstances noted an increase in the duration of the patient's stay in the intensive care unit up to 11.4 days, and the required period of use of antiulcer drugs - up to 23.6 days. B. Erstad (1997) noted that the average cost of treating one patient at risk for stress ulcers without prevention of stress damage is $19850, and with the use of antisecretory prophylaxis - $15812. Moreover, if the cost of prophylactic parenteral use of H 2 blockers was $2275, then the cost of the use of proton pump inhibitors was only $1417.

Thus, the high frequency of stress erosive and ulcerative lesions of the gastroduodenal zone and the colossal mortality rates for bleeding from stress ulcers require obligatory adequate preventive measures in critically ill patients. The main component of this prevention is the preventive administration of parenteral forms of proton pump inhibitors to patients at risk for stress ulcers.

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Description of preparations for Pathological Anatomy in Lesson No. 26

(This is an indicative description, not a cathedral one, some preparations may be missing, as a description of past years)

ACTIVITY #26stomach diseases: gastritis, peptic ulcer, stomach tumors

micropreparation № 37 "acute catarrhal gastritis" - description .

The mucous membrane of the stomach is covered with purulent exudate, penetrating into all layers of the stomach wall. The lumen of the glands is dilated. The cytoplasm of the epithelium is vacuolated. Own layer of the mucous membrane with full-blooded vessels, in places with diapedetic hemorrhages, polymorphonuclear leukocytes (PMNs).

micropreparation № 112 "chronic superficial gastritis" - demo .

micropreparation № 229 "chronic atrophic gastritis" - description .

The mucous membrane of the stomach is sharply thinned, the number of glands is reduced, in place of the glands, fields of expanding connective tissue are visible. Integumentary pit epithelium with hyperplasia. Epithelium of glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated with histolymphocytic elements with an admixture of polymorphonuclear leukocytes.

macropreparation "Acute erosions and stomach ulcers" - description .

The mucous membrane of the stomach with smooth folding and numerous defects of the mucous membrane of round and oval shape, the bottom of which is colored black.

macropreparation "chronic stomach ulcer" - description .

On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting the muscle layer, rounded in shape with dense, raised, callused edges. The edge of the defect, facing the esophagus, is undermined, towards the pylorus - gently sloping.

micropreparation № 121 "Chronic gastric ulcer in the acute stage" - description .

A defect in the wall of the stomach is determined, capturing the mucous and muscle layer, with an undermined edge facing the esophagus, and a flat one facing the pylorus. At the bottom of the defect, 4 layers are determined. The first external - fibrinous-purulent exudate. The second is fibrinoid necrosis. The third is granulation tissue. The fourth is scar tissue. At the edges of the defect, fragments of muscle fibers, an amputation neuroma, are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with hyperplasia.

macropreparation "stomach polyp" - description .

On the gastric mucosa, a tumor formation is determined on a wide base (pedicle).

macropreparation "saucer-shaped stomach cancer" - description .

The tumor has the appearance of a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.

macropreparation "diffuse gastric cancer" - description .

The wall of the stomach (mucosal and submucosal layers) is sharply thickened, represented by a homogeneous grayish-white dense tissue. The mucous membrane over the tumor with symptoms of atrophy with smoothed folding.

micropreparation № 77 "adenocarcinoma of the stomach" - description .

micropreparation № 79 "cricoid cell carcinoma" - demo .

The tumor is built from atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.

micropreparation № 70 metastasis of adenocarcinoma to the lymph node - description .

The drawing of the lymph node is erased, the growth of the tumor tissue is represented by atypical glandular cosplexes.