Staining with hematoxylin and eosin. In the area of the defect of the stomach wall, there is a fibrinous-purulent exudate (a), with an underlying extensive zone of fibrinoid necrosis (b), the presence of granulation tissue (c) and the growth of coarse-lined connective tissue penetrating to different depths muscle layer (d). The serous membrane of the stomach wall is preserved (e).
2. Chronic atrophic gastritis. Heme staining
toxylin and eosin. In the gastric mucosa, atrophy of the integumentary epithelium (a) and epithelium of the glands with restructuring
coy glands of 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. Staining with hematoxylin and eosin. All layers of the stomach wall are infiltrated by tumor tissue with signs of cellular atypism (a). Multiple pathological mitoses are seen in hyperchromic (b) and polymorphic tumor cells (c).
4. Mucous cancer stomach. Hematoxylin staining and
eosin. 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 nature of tumor growth is visible (c). Demonstration.
5. Skirr of the stomach. Staining with hematoxylin and eosin. The lining of the stomach is a group of atypical cells with large hyperchromic nuclei (a), in the stroma of the tumor is the growth of fibrous connective tissue (b). Demonstration.
MACROPREPARATIONS.
1. Sharp catarrhal gastritis: v preparation stomach, 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 substitutes, anticancer chemotherapy drugs, burns with acids and alkalis, uremia, salmonellosis, shock, severe stress.
Complications: acute ulcers, transition to chronic gastritis. Exodus: restoration of the mucous membrane.
2. Erosions and acute stomach ulcers: in the preparation stomach,
the mucous membrane is edematous, on the surface there are multiple punctate hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucous membrane, and ulcers penetrate
cabins to 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: erosion is epithelized, the ulcerative defect is replaced by scar tissue.
3. Chronic stomach ulcer in remission: in the preparation 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 folds of the mucous membrane converge radially to the defect, the edges of which are dense, roller-like raised, callous (callosal ulcer). In the section, the inlet is a crater, smaller than the inner part of the ulcer. The edge facing the cardia is undermined, a 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 sclerosed, their lumen gapes.
Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to the effects of peptic aggression factors (hydrochloric acid and pepsinogen).
Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformity stomach with the development of steno-for the inlet or outlet. Against the background of a chronic ulcer, a second disease, stomach cancer, can develop.
4. Polyps of the stomach (adenomas): in the antrum
There are two tumor-like formations the size of pigeon eggs, on thin legs, irregular oval shape with a villous surface, soft consistency.
On the cut, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without invading the underlying tissues.
Complications: bleeding, torsion of the leg, obstruction of the outlet 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, irregularly rounded, 5 cm in diameter, on a broad base in the form of a mushroom cap, with a retraction in the center. The section shows that the tumor invades the entire wall of the stomach.
b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened to 1 cm throughout its length, with a dense “woody” consistency, and is represented by a gray-pinkish tissue on the cut. The mucous membrane is uneven, its folds are of varying thickness, the serous membrane is thickened, dense, and bumpy. 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 towering above the surface of the mucous membrane with dense cushion-shaped edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown decaying masses. On the cut, the tumor tissue infiltrates the entire thickness of the organ wall.
Causes: food (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after stomach surgery, especially according to Billroth II), Helicobacter pylori(promotes the development of mucosal atrophy, intestinal metaplasia, epithelial dysplasia). Metastasis: 1. Orthograde lymphogenous metastases to regional nodes on the lesser and greater curvature, retrograde lymphogenous metastases in the left supraclavicular lymph node - Virchow's metastasis, in the ovaries - Krukenberg's
cancer, perrectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, less often to the adrenal glands and pancreas. 4. Implant- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.
TEST CONTROL
Choose one or more correct answers
1. SIGNS OF Acute catarrhal gastritis
1) thickening of the mucosa
2) atrophy of the glands
4) mucosal sclerosis
5) neutrophilic mucosal infiltration
6) lymphoid mucosal infiltration
2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS
1) fibrinous
2) atrophic
3) hypertrophic
4) catarrhal
5) corrosive (necrotic)
3. CHANGES IN EPITHELIUM IN CHRONIC GASTRITIS
1) atrophy
2) intestinal metaplasia
3) hyperplasia
4) dysplasia
5) the appearance in the cytoplasm of Mallory's bodies
4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
5. PATHOGENESIS OF PERNICIAL ANEMIA IN AUTOIMMUNE GASTRITIS
1) stopping the production of HCl
2) production of antibodies to Helicobacter pylori
3) production of antibodies to parient cells
4) production of antibodies to intrinsic factor
5) destruction of glands and mucosal atrophy
6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS IN
1) predominant localization - antrum
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
basic etiological factor
4) is accompanied by G-cell hyperplasia, gastrinemia
5) often combined with pernicious anemia
6) localized in the fundus
7) reflux of duodenal contents into the stomach - the basis of pathogenesis
ACUTE EROSION OF THE STOMACH IS
inflammation of the mucous membrane
necrosis of the mucous membrane,
not affecting the muscle plate
3) mucosal atrophy
4) sclerosis of the mucous membrane
5) necrosis involving the muscle layer
8. CLINICAL AND MORPHOLOGICAL SIGNS OF CHRONIC ATROPHIC GASTRITIS
IN THE STAGE OF EXCERVATION
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 DISEASE
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 ulcers
5) inflammation of the duodenal mucosa
10. Sclerotic deformity of the stomach IS an outcome
1) catarrhal gastritis
2) diphtheria 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 reconstruction of the epithelium
(intestinal metaplasia)
4) all answers are correct
5) all answers are wrong
12. ULTSIROGENIC PROMOTORS
1) corticosteroids
3) aspirin
4) smoking
5) increasing the tone of the vagus nerve
13. Stomach ulcers include
1) endocrine stomach ulcers
2) allergic ulcers
3) peptic ulcers
4) postoperative ulcers
5) tuberculous ulcers
14.Local factors in the development of gastric ulcer
1) increasing the aggressiveness of gastric juice
2) campylobacter
3) the presence of chronic gastritis
4) circulatory disorders
5) all answers are correct
6) all answers are wrong
15. REASONS OF DEVELOPMENT OF ACUTE STOMACH ULTRA
1) corticosteroids
3) aspirin
4) smoking
5) increased tone
vagus nerve
16. MORPHOLOGICAL SIGNS OF Acute gastric ulcer
1) funnel-shaped
2) the shape of the truncated pyramid
cross-section
3) soft jagged edges
4) dense calcified edges
7) multiple ulcers
17. MORPHOLOGICAL SIGNS of chronic gastric ulcer
1) funnel-shaped
2) the shape of the truncated pyramid
cross-section
3) soft jagged edges
4) dense calcified edges
5) the bottom of the ulcer is colored black with hydrochloric acid hematin
6) the edge of the ulcer, facing the gatekeeper, looks like a terrace, the cardiac edge is undermined
18. SIGNS OF CHRONIC STOMACH ULTRA
IN THE PERIOD OF REMISSION
1) the presence of exudate on the surface
2) scar tissue interrupts the muscular layer to different depths
3) endovasculitis
4) fibrinoid changes in the bottom and blood vessels
5) epithelialization of the surface
19. SIGNS OF CHRONIC STOMACH ULTRA
IN THE PERIOD OF EXCERVATION
1) the presence of fibrinous-purulent exudate
on the surface 2), the scar tissue interrupts the muscle
shell at different depths
3) endovasculitis
4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer
12. MECHANISM of bleeding in peptic ulcer disease
arrosive
diapedetic
as a result of vessel rupture
as a result of purulent fusion
21. Chlorohydropenic 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 - the result
1) penetration
2) perforation
3) gastritis
4) duodenitis
5) cicatricial pyloric stenosis
23. COMPLICATIONS OF CHRONIC Ulcer
1) penetration
2) perforation
3) empyema
4) hypercalcemia
5) cicatricial stenosis
and wall deformation
6) bleeding
24. TYPES OF GASTROPATHIES
1) Meniere's disease
2) Menetrie'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 fossa epithelium
4) hyperplasia of the glandular epithelium
5) severe sclerosis
26. MORPHOLOGICAL SIGNS OF INFLAMMATORY POLYPS
1) inflammatory infiltrate in the stroma
2) atypical cells
3) without clear differentiation on the leg and body
4) dysplasia of the glandular epithelium
5) surface erosion
27. BENEFITS 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
1) benign tumor
from glandular epithelium
2) a malignant tumor from the glandular epithelium
3) epidermal cancer
4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium
30. DISEASES WITH RISK OF CANCER
1) superficial gastritis
2) chronic stomach ulcer
3) acute erosive gastritis
4) chronic atrophic gastritis
5) adenomatous polyps
31. HISTOLOGICAL OPTIONS OF STOMACH CANCER
1) adenocarcinoma
2) sarcoma
3) cricoid
4) undifferentiated
32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL STOMACH CANCER
1) occurs more often before the age of 30
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 epithelial cells
33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUS TYPE STOMACH CANCER
1) develops from epithelial cells
2) occurs at a relatively young age
3) histologically cricoid-cellular
4) occurs against the background of chronic gastritis
5) has a low degree of differentiation
34. PREDICTIVE SIGN IN STOMACH CANCER
1) histological variant
2) macroscopic shape
3) depth of invasion
4) mucus formation
5) secondary changes
35. HISTOLOGICAL SIGNS OF POLYPOSE 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 PERSONOID CELL GASTRIC CANCER
1) are characterized by extensive hemorrhages
2) the nuclei of atypical cells are displaced
to the cell membrane
3) poorly differentiated cells with very large hyperchromic nuclei of irregular shape
4) atypical glandular structures
5) massive sclerosis and hyalinosis in the wall
37. MICROSCOPIC CHARACTERISTICS OF 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 METASTASIS OF GASTRIC CANCER
1) hematogenous
2) implantation
3) lymphogenous orthograde
4) lymphogenous retrograde
39. COMPLICATIONS OF GASTRIC CANCER
1) hemoptysis
2) dilatation of the gatekeeper
3) perforation
4) exhaustion
5) stomach bleeding
40. SIGNS WHICH VIRKHOVSKY METASTASIS IS CHARACTERIZED
1) hematogenous metastasis
2) retrograde lymphogenous metastasis
3) peritoneal carcinomatosis
4) defeat of the left supraclavicular lymph node
5) ovarian damage
Standards of answers To test tasks
Description of drugs in Pathological Anatomy in Lesson No. 26
(This is an indicative description, not a cathedral, some drugs may be missing, since the description of past years)
LESSON No. 26 stomach diseases: gastritis, peptic ulcer, stomach tumors
Micropreparation No. 37 "acute catarrhal gastritis" - description.
The mucous membrane of the stomach is covered with purulent exudate, which penetrates into all layers of the stomach wall. The openings of the glands are widened. The cytoplasm of the epithelium is vacuumed. Own layer of the mucous membrane with congested vessels, in places with diapedesic hemorrhages, polymorphonuclear leukocytes (PMN).
Micropreparation № 112 "chronic superficial gastritis" - demo.
Micropreparation No. 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 growing connective tissue are visible. The fossa epithelium with symptoms of hyperplasia. Epithelium of the glands with signs of intestinal metaplasia. The entire wall of the stomach is diffusely infiltrated by histolymphocytic elements with an admixture of polymorphonuclear leukocytes.
Macrodrug "acute erosions and stomach ulcers" - description.
The mucous membrane of the stomach with smooth folds and numerous defects of the mucous membrane of a round and oval shape, the bottom of which is painted black.
Macrodrug "chronic stomach ulcer" - description.
On the lesser curvature of the stomach, a deep defect of the mucous membrane is determined, affecting the muscular layer, of a rounded shape with dense, raised, amosolized edges. The edge of the defect facing the esophagus is undermined, to the gatekeeper it is shallow.
Micropreparation № 121 "chronic stomach ulcer in the acute stage" - description.
A defect in the wall of the stomach is determined, capturing the mucous and muscular layer, with an undermined edge facing the esophagus, and shallow, facing the gatekeeper. At the bottom of the defect, 4 layers are determined. The first is 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, strips of muscle fibers, amputation neuroma are visible. Vessels of the cicatricial zone with sclerosed thickened walls. The mucous membrane at the edges of the defect with symptoms of hyperplasia.
Macrodrug "stomach polyp" - description.
On the gastric mucosa, a tumor formation on a broad base (pedicle) is determined.
Macrodrug "saucer-shaped stomach cancer" - description.
The tumor looks like a rounded flat formation on a wide base. The central part of the tumor sinks, the edges are somewhat raised.
Macrodrug "diffuse stomach cancer" - description.
The wall of the stomach (mucous and submucous layers) is sharply thickened, represented by a uniform grayish-white dense tissue. The mucous membrane over the tumor with symptoms of atrophy with smoothed folding.
Micropreparation No. 77 "adenocarcinoma of the stomach" - description.
Micropreparation № 79 "cricoid cell carcinoma" - demo.
The tumor is built of atypical glandular complexes formed by cells with pronounced cellular polymorphism. The stroma is not developed.
Micropreparation № 70 "metastasis of adenocarcinoma in the lymph node" - description.
The pattern of the lymph node is erased, the growth of tumor tissue is represented by atypical glandular cosplexes.
studfiles.net
Types of chronic gastritis
| Etiology | Pathogenetic mechanism | Histological changes | |
| Autoimmune | Pernicious anemia |
||
| Peptic Ulcers Stomach Cancer |
|||
| Peptic Ulcers Stomach Cancer |
Other forms of gastritis
lymphocytic;
eosinophilic;
granulomatous.
Acute ulcers
Chronic ulcers
Helicobacter pylori infection.
Chronic distress syndrome.
Fibrinoid necrosis;
Granulation tissue;
Fibrous tissue.
Peptic ulcer pathomorphosis.
studfiles.net
Training card of the lesson (for independent work)
1. To diagnose catarrhal serous gastritis according to the macroscopic picture. Study and write down the name of the macro-preparation "Catarrhal serous gastritis". Pay attention to the thickening of the folds of the mucous membrane, its hyperemia, a large amount of turbid viscous exudate on its surface (see "Textbook", p. 344).
2. To diagnose acute catarrhal gastritis by a microscopic picture. To study the micropreparation "Acute catarrhal gastritis" (staining with hematoxylin and eosin). Write down the name of the drug. The mucous membrane of the stomach is covered with serous-mucous exudate mixed with polymorphonuclear leukocytes. Desquamation of the integumentary epithelium is observed. The cytoplasm of the epithelium of the glands is vacuolated. The own layer of the mucous membrane is full-blooded with focal accumulations of predominantly neutrophilic leukocytes (see "Textbook" p. 344; "Atlas", p. 100, Fig. 101). Solve a problem similar to problem No. 1.
3. To diagnose chronic superficial gastritis by a microscopic picture. To study the micropreparation "Chronic superficial gastritis" (staining with hematoxylin and eosin). Write down the name of the drug. The superficial epithelium is flattened in places, desquamated, the glands are not changed. The own layer of the mucous membrane is swollen, infiltrated with lymphoid, plasma cells, polymorphonuclear leukocytes (see "Textbook", p. 346, Fig. 267, a).
4. To diagnose chronic atrophic gastritis with restructuring according to the microscopic picture. To study and describe the micropreparation "Chronic atrophic gastritis with restructuring" (staining with hematoxylin and eosin). At low magnification of the microscope, note the thickness of the gastric mucosa, a decrease in the number of glands. At high magnification, pay attention to the nature of the changes in the glands: the absence of the main, accessory, parietal (parietal) cells, the appearance of light cubic cells characteristic of the pyloric glands, and intestinal epithelium, goblet cells (see "Textbook", pp. 346-347; "Atlas", p. 278, fig. 290).
5. To diagnose erosion and acute gastric ulcers according to the macroscopic picture. To study the macro-preparation "Multiple erosions and acute gastric ulcers". Write down the name of the drug. The mucous membrane of the stomach with multiple superficial defects, mainly on the lesser curvature, in the antrum and pyloric regions. In the same sections, there are deeper wall defects - acute ulcers. They have a round or oval shape, their bottom is formed by the muscle layer. The bottom of erosions and ulcers is colored dirty gray or black due to the formation of hydrochloric acid hematin (see "Textbook", p. 349).
6. To diagnose chronic gastric ulcer according to the macroscopic picture. To study and describe the macro-preparation "Chronic gastric ulcer". Pay attention to the localization of the ulcer, its shape, edges, depth, wall density, the nature of the bottom. Determine and describe which edge is facing the esophagus, which one - to the gatekeeper (see "Textbook", pp. 350-351, Fig. 268; "Atlas", p. 281, Fig. 293).
7. Diagnose chronic gastric ulcer by microscopic picture. To study the micropreparation "Chronic gastric ulcer with exacerbation" (staining with hematoxylin and eosin) and sketch it. Find the cardiac and pyloric edges and the bottom of the ulcer at low magnification of the microscope. Determine the depth of the defect. At high magnification, note the layer-by-layer changes in the bottom of the ulcer, characterizing the chronic course and exacerbation of the process (see "Textbook", p. 351; "Atlas", p. 282, Fig. 294). Solve a problem similar to problem number 2.
8. To diagnose an ulcer, stomach cancer according to the macroscopic picture. To study and write down the name of the macro-preparation "Ulcer-stomach cancer". Pay attention to the proliferation of dense whitish-gray tumor tissue at the edges of the ulcer (see "Textbook", p. 356, Fig. 271).
9.To diagnose phlegmonous appendicitis according to the macroscopic picture. To study and describe the macropreparation "Phlegmonous appendicitis". Pay attention to the size of the appendix, the state of the serous membrane ( appearance, the degree of blood filling), the thickness and type of its wall in section, the nature of the contents in the lumen ("see" Textbook ", p. 372).
10. To diagnose phlegmonous-ulcerative appendicitis by a microscopic picture. To study and describe the micropreparation "Phlegmonous-ulcerative appendicitis" (staining with hematoxylin and eosin). Pay attention to the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall (see "Textbook", p. 372, Fig. 281; "Atlas", p. 289, Fig. 300). Solve a problem similar to problem No. 3.
www.studfiles.ru
Types of chronic gastritis
| Etiology | Pathogenetic mechanism | Histological changes | Associated clinical changes |
| Autoimmune | Antibodies against parietal cells and receptors for external factor Kastl. Sensitized T-lymphocytes. | Atrophy of the glands in the body of the stomach. Intestinal metaplasia. | Pernicious anemia |
| Bacterial infection (H. pilori) | Cytotoxins. Mucolytic enzymes. Synthesis of ammonium ions by bacterial urease. Tissue damage during immune response. | Active chronic inflammation. Multifocal atrophy, more in the antrum. Intestinal metaplasia. | Peptic Ulcers Stomach Cancer |
| Chemical damage Nonsteroidal anti-inflammatory drugs Bile reflux Alcohol | Direct damage. Damage to the mucous layer. Mast cell degranulation. | Hyperplasia of the pit epithelium. Edema. Vasodilation. A small number of inflammatory cells. | Peptic Ulcers Stomach Cancer |
Other forms of gastritis
The following types of chronic gastritis are distinguished separately:
lymphocytic;
eosinophilic;
granulomatous.
With lymphocytic gastritis, the main histological manifestation is the presence of numerous mature lymphocytes in the surface layers of the epithelium. This form is sometimes found in patients with specific erosions along the enlarged folds of the mucous membrane. The etiology and relationship with Helicobacter-associated gastritis has not been established.
Eosinophilic gastritis is characterized by mucosal edema and the presence of numerous eosinophils in the inflammatory infiltrate. It is assumed that eosinophilic gastritis is an allergic response to a food antigen to which the patient is sensitized.
Granulomatous gastritis is a rare form of gastritis in which epithelioid cell granulomas form. These granulomas can be a manifestation of Crohn's disease or sarcoidosis, but in rare cases it is cryptogenic.
Microdrug "Chronic atrophic gastritis with epithelial restructuring" (staining with hematoxylin and eosin). The mucous membrane of the stomach is thinned, lined in places with integumentary epithelium, in places with limb and goblet cells. The main, parietal and mucous cells in the fundic glands are displaced by large cells with foamy cytoplasm characteristic of pyloric glands... The number of glands is small, they are replaced by growths of connective tissue. In the lamina propria of the mucous membrane, lymphohistiocytic infiltration is noted.
Peptic ulcer and duodenal ulcer
Peptic ulceration is a violation of the integrity of the epithelial cover and underlying tissues digestive tract as a result of damage to them by acid and pepsin. According to the clinical course, ulcers are divided into acute and chronic.
Acute ulcers
Acute ulcers can be caused by:
Severe acute gastritis. The deep spread of erosions in acute gastritis usually occurs with the use of non-steroidal anti-inflammatory drugs or alcohol, with corticosteroid treatment, which leads to the appearance of deep ulcers.
Severe stress. Acute ulcers can result from a variety of stressful factors, such as extensive burns or trauma to the brain. In this case, ulcers form as a result of ischemia of the mucous membrane, which leads to a decrease in its resistance to acid.
A pronounced increase in acidity. Increased acidity, for example, in patients with gastrin-secreting tumors (Zollinger-Ellison syndrome), leads to the formation of multiple ulcers in the antrum, duodenum, and even the jejunum.
Chronic ulcers
Chronic ulcers can be caused by:
Helicobacter pylori infection.
Chemical influences, including steroid drugs and non-steroidal anti-inflammatory drugs.
Chronic distress syndrome.
Chronic peptic ulcers most often form at the junction of various types of mucous membranes. So, for example, in the stomach, ulcers are observed at the place of transition of the body to the antrum, in the duodenum - in the proximal area on the border with the pylorus, in the esophagus - in the stratified epithelium in front of the esophageal-gastric junction, postoperative ulcers are localized in the stoma (in the anastomosis ). That is, ulcers appear in places where acid and pepsin come into contact with the unprotected mucous membrane.
Pathogenesis. For many years, it was believed that the cause of peptic ulcer disease is hyperacidity. However, in many cases, patients were observed to have normal and even reduced acidity of gastric juice. Conversely, ulcers were rarely observed in patients with high acidity. In addition, during treatment with antacids (drugs that reduce acidity), relapses were observed in many cases. This prompted the idea that the main role in the development of ulcers is played not by acidity, but by the ratio of factors of aggression and factors of mucous protection. It is believed that in the genesis of duodenal ulcer the main role an increase in factors of aggression plays, and in the development of gastric ulcer, a decrease in defense factors is in the first place. With a decrease in the latter, ulcers may develop even with low acidity.
Stomach ulcer. Gastric juice is a highly acidic medium (pH
The superficial epithelium forms the second line of defense; To ensure this function, proper functioning of both the apical membrane, which prevents the transport of ions, and the synthetic apparatus, which produces bicarbonates, is necessary. Both of these functions depend on the blood supply to the mucous membrane.
Ulceration occurs as a result of either a violation and destruction of the mucous barrier, or a violation of the integrity of the epithelium. As a result of bile reflux, the mucous barrier is easily destroyed by its components. Acid and bile together destroy the surface epithelium, increasing the permeability and vulnerability of the mucous membrane. This leads to congestion and swelling in the lamina propria, which is seen in reflux gastritis.
The epithelial barrier can also be disrupted by the use of NSAIDs. they disrupt the synthesis of prostaglandins, which normally protect the epithelium. Also, in the destruction of the epithelium, an infection with Helicobacter pylori plays a significant role, in which both cytotoxins and ammonium ions and an inflammatory reaction have a destructive effect.
Duodenal ulcer. High acidity plays a major role in the development of duodenal ulcers. In half of the patients, acid hypersecretion is observed, however, even with normal stomach acidity, the daily cycle of secretion may be disrupted: there is no decrease in secretion at night. It is also known that when stimulated with gastrin in patients infected with Helicobacter pylori, acid synthesis is 2-6 times higher than in uninfected ones.
Factors damaging the anti-acid protection in the stomach usually do not affect the duodenum: Helicobacter pylori does not colonize the duodenal mucosa, the mucosa is resistant to the action of bile and alkaline ions of pancreatic juice, drugs are significantly diluted and absorbed before entering the intestine. However, Helicobacter pylori affects ulceration, because infection promotes gastric hypersecretion, which causes the development of gastric metaplasia in the duodenum, and then colonization of the metaplastic epithelium of Helicobacter pylori occurs, which leads to the development chronic inflammation, which also provokes ulceration.
Morphological changes. Macroscopically, chronic ulcers are usually round or oval in shape. Their sizes, as a rule, do not exceed 2 cm in diameter, however, cases have been described when ulcers reached 10 cm in diameter or more. The depth of the ulcer is different, sometimes it reaches the serous membrane. The edges of the ulcer are clear, dense and rise above the normal surface.
In the stage of exacerbation in the bottom of the ulcer, 4 layers are clearly distinguishable:
Fibrinous-purulent exudate;
Fibrinoid necrosis;
Granulation tissue;
Fibrous tissue.
Vascular sclerosis is noted, in the walls of some of them - fibrinoid necrosis.
Macrodrug "Chronic stomach ulcer". On the lesser curvature, a deep defect of the stomach wall is visible, capturing the mucous and muscular membranes, oval-round in shape with very dense, calcified, roller-like raised edges. The edge facing the esophagus is undermined; the edge facing the pylorus is flat and looks like a terrace formed by the mucous membrane, the submucosa and the muscular membrane of the stomach wall. The bottom of the ulcer is represented by a dense whitish tissue.
Microdrug "Chronic gastric ulcer during an exacerbation" (staining with hematoxylin and eosin). A defect in the wall of the stomach captures the mucous membrane and muscle membranes, while the muscle fibers in the bottom of the ulcer are not detected, their break is visible at the edges of the ulcer. One edge of the ulcer is undermined, the other is shallow. At the bottom of the ulcer, 4 layers are distinguishable: fibrinous-purulent exudate, fibrinoid necrosis, granulation tissue and scar tissue. In the last zone, vessels with thickened sclerosed walls and manifestations of fibrinoid necrosis are visible.
During the period of remission, scar tissue is found at the edges of the ulcer. The mucous membrane is thickened at the edges, hyperplastic.
Complications. Ulcer healing occurs by regeneration of the epithelium and fibrosis of the underlying tissues. In this case, as a result of the reduction and compaction of scars, a narrowing of the lumen of the organ can develop: stenosis of the pylorus or central narrowing of the stomach (stomach in the form of an hourglass). Perforation of the wall of the stomach or duodenum is also possible, while the contents of the digestive tract are poured into the abdominal cavity, which leads to the development of peritonitis. During penetration, the ulcer is perforated into the closer lying organs, for example, the pancreas or liver. Erosion of blood vessels can cause bleeding, which can be fatal. With prolonged existence, stomach ulcers can become malignant, duodenal ulcers are very rarely malignant.
Peptic ulcer pathomorphosis.
1. Rejuvenation of peptic ulcer disease.
2. An increase in the number of combined ulcers of the stomach and duodenum.
3. Reducing the number of ulcers malignancy.
4. Increase in the number of acute ulcers.
5. An increase in the number of ulcers of medicinal origin.
MACROPREPARATION No. 1 FATTY LIVER DYSTROPHY
Liver incisions are visible in the specimen.
The liver is small, as it is the liver of a child. But nevertheless, the size of the liver is increased, since its capsule is tense, and the corners are rounded.
The color of the liver is yellow on the cut.
The consistency of the liver is flabby.
When such a liver is cut with a knife, droplets of fat remain on its blade.
This is parenchymal fatty degeneration of the liver, or "goose" liver.
May develop in people with chronic cardiovascular disease - vascular diseases, chronic lung diseases, diseases of the blood system, chronic alcoholism.
As a result of parenchymal fatty degeneration, portal, small-nodular cirrhosis of the liver may develop over time.
MACROPREPARATION No. 2 BLEEDING IN THE BRAIN
A horizontal section of the brain tissue is visible in the specimen. The cerebellum is visible below and behind the brain.
In the right hemisphere of the brain, in the region of the subcortical nuclei, there is a focus of dark brown color due to the fact that in the focus of hemorrhage we see caked blood. This is a focus of hemorrhage in the necrotic tissue of the brain, with fairly clear boundaries - a hematoma. In the center of the hematoma under anaerobic conditions, the pigment hematoidin is formed, and along the periphery, on the border with healthy tissues, hemosiderin. Blood from the focus of hemorrhage broke into the anterior horn of the right lateral ventricle, into the third ventricle of the diencephalon, the Silvian aqueduct of the midbrain and into the fourth ventricle of the rhomboid brain.
Hematoma is a type of hemorrhagic stroke.
Clinically it was accompanied by the development of focal symptoms on the opposite side of the body - left-sided paresthesia, hemiplegia, hemiparesis, paralysis.
If the patient had not died, then a cyst with walls rusty from hemosiderin would have formed at the site of the hemorrhage.
MACROPREPARATION No. 3 KEPHALOGEMATOMA
The preparation contains the integumentary bone of the newborn's skull. On the upper - lateral surface of the bone, under its periosteum there is caked blood of a dark brown, almost black color - this is a subperiosteal hemorrhage. This is a birth injury to the skull related to external cephalohematoma.
MACROPREPARATION No. 4"TAMPONADA" OF THE HEART
The preparation shows a longitudinal section of the heart from the side of the left ventricle, since the thickness of the ventricular myocardium is more than 1 cm. It is noteworthy that the cavity of the left ventricle is slit-like, that is, the heart is compressed by something from the outside. The subepicardial fat layer, epicardium, pericardium are determined. In the pericardial cavity, gray-brown blood clots are visible. It is due to their presence in the pericardial cavity that the heart was compressed from all sides, and the cavity of the left ventricle became slit-like. This is bleeding into the pericardial cavity - hemopericardium, an example of internal bleeding, figuratively - "tamponade" of the heart. Attention is also drawn to the fact that in the region of the posterior - lower wall of the heart, the myocardial tissue is stained with hemosiderin in a brown color, due to the rupture of the heart wall in this place and hemorrhage from the damaged vessel. The rupture of the heart wall occurred due to myomalacia in the area of transmural myocardial infarction.
Thus, the hemorrhage in the cardiac shirt was a consequence of myomalacia and rupture of the heart wall in the area of transmural myocardial infarction.
MACROPREPARATION No. 5 Purulent Meningitis
In the preparation, the brain is visible from the side of its upper - lateral surfaces. Under the pia mater, an accumulation of exudate of white-yellow color, the consistency of thick sour cream, is determined. This is a purulent exudate. The exudate lies on the surface of the convolutions, enters the grooves, smoothing the relief of the surface of the brain.
Inflammation of the pia mater is meningitis.
Primarily purulent meningitis can occur with meningococcal infection, and secondarily, it can complicate infectious diseases with generalization of the infection (with sepsis).
MACROPREPARAI No. 6 A BRAIN TUMOR
The preparation shows a horizontal section of the brain. In one of the hemispheres (in the left), in the white matter, there is a focus of pathological proliferation of brain tissue with indistinct contours, indistinct growth boundaries. The consistency of the node of pathological growth of brain tissue approaches the consistency of the brain itself. The color is variegated, since there are hemorrhages and necrosis in the focus. This is a brain tumor. Since the boundaries of tumor growth are indistinct, a malignant tumor occurs. It can be assumed that this is glioblastoma, the most common malignant tumor in adults.
MACROPREPARATION No. 7 Tibial sarcoma
The preparation contains the bones that form the knee joint. In the area of the upper part of the diaphysis of the tibia, there is a pathological proliferation of tissue that destroys the posterior surface of the bone, which has indistinct growth boundaries. This is a tumor. It is white, layered, reminiscent of fish meat. The indistinctness of the growth boundaries indicates the malignant nature of the tumor. Malignant tumor from bone tissue - osteosarcoma. Since the process of bone destruction prevails over the process of bone formation, this is osteolytic osteosarcoma.
MACROPREPARATE No. 8 BRAIN ABSCESSES IN SEPTICOPYEMIA
The preparation contains sections of the brain. In each section, there are multiple foci of irregular rounded shape, clearly delimited from the brain tissue by a thick wall. Filled with contents of white - yellowish or white - greenish color, consistency of thick sour cream. This is a purulent exudate.
Focal accumulations of pus, separated from the brain tissue by a wall, are abscesses.
The wall of an acute abscess consists of two layers: 1) an inner layer - a pyogenic membrane and 2) an outer layer - a nonspecific granulation tissue.
In the wall of a chronic abscess, three layers are distinguished: 1) inner - pyogenic membrane, 2) middle - nonspecific granulation tissue and 3) outer - coarse fibrous connective tissue.
Brain abscesses develop with the generalization of purulent inflammation in the lungs, intestines and other organs, that is, with sepsis, septicopyemia.
MACROPREPARATE No. 9 Stenosis of the mitral orifice (rheumatic heart disease)
The specimen presents a cross-section of the heart, produced above the level of the atrio-ventricular foramen, so that the cusps of the bicuspid, mitral and tricuspid valves are clearly visible.
Sash mitral valve deformed. They are sharply thickened, with a tuberous surface, opaque, rigid due to the proliferation of connective tissue in them. There is a gap between the closed valve leaflets, that is, mitral valve insufficiency has developed.
In addition, there is a narrowing of the left atrio-ventricular opening.
Thus, in the area of the mitral valve there is a combined heart defect - insufficiency and stenosis of the mitral valve.
Such acquired heart defects most often form in the course of rheumatic valvular endocarditis.
The described changes in the mitral valve correspond to the stage of fibroplastic endocarditis.
It can be assumed that the patient died of progressive chronic cardiovascular failure due to decompensated rheumatic heart disease.
MACROPREPARATE No. 10 UTERINE CHORIONEPITELIOMA
The preparation contains a longitudinal section of the uterus with appendages.
The size of the uterus is increased (normally the height of the poppy is 6 - 8 cm, the width is 3 - 4 cm and the thickness is 2 - 3 cm). In the uterine cavity, the growth of tumor tissue is visualized, which grows into the myometrium, that is, invasive tumor growth takes place.
The consistency of the tumor is soft, porous, since the tumor contains absolutely no connective tissue.
The color of the tumor tissue in the preparation is gray with dark brown blotches. In a fresh preparation, it is dark red, variegated, since the tumor has cavities, lacunae filled with blood.
Based on the nature of the growth, the tumor is malignant. It develops from the epithelium of the chorionic villi (placenta). This is chorionepithelioma.
It is an organ-specific tumor. It is built of two types of cells - large mononuclear cells with light cytoplasm, or Langhans cells, derived from cytotrophoblast, and large ugly multinucleated cells, derived from synticyotrophoblast. The tumor is hormonally active. Tumor cells secrete the hormone gonadotropin found in a woman's urine; thanks to the hormone, the uterus is enlarged.
The tumor developed in connection with pregnancy. This is a differentiated tumor.
Metastasizes mainly by hematogenous route to the liver, lungs, vagina.
In the present preparation, in the area of the vaginal portion of the cervix and in the wall of the vagina, rounded foci similar in appearance to the primary tumor are visible. These are tumor metastases.
MACROPREPARATE No. 11 CHRONIC STOMACH ULTRA WITH PENETRATION INTO THE PANCREAS
The preparation shows a fragment of the stomach wall from the side of the mucous membrane and the pancreas located behind the stomach.
In the wall of the stomach there is an ulcerative defect with raised dense, callous, callous edges and a shallow bottom. One edge of the defect facing the esophagus, the proximal one is subdued, with an overhanging mucous membrane. The other edge, opposite, distal, is gently sloping or terraced. The difference in edges is due to the presence of a peristaltic wave.
A defect in the wall of the stomach is a chronic ulcer, since at the edges of it there was an overgrowth of connective tissue, which caused a change in the edges of the defect.
At the bottom of the ulcer, it is not the tissue of the stomach wall that is determined, but the lobular, white tissue of the pancreas.
Thus, there is an ulcerative - destructive complication of chronic gastric ulcer - penetration into the pancreas.
It can be assumed that the patient died from a spilled den.
MACROPREPARATE No. 12 MUSKATIC LIVER
A frontal section of the liver is visible in the specimen.
The liver is enlarged.
The color of the liver tissue on the cut is variegated: areas of gray - black color (these are areas with clotted blood) interspersed with areas of gray - brown color (color of hepatocytes).
Areas of gray-black color, and in a fresh preparation - red, are caused by plethora and expansion of the central veins and the central 2/3 of the sinusoids of the liver lobules flowing into them.
Due to the similarity of the surface of the liver incision to the surface of the cross section of nutmeg, the drug got its name.
It occurs with the development of chronic venous plethora in the body, which occurs in conditions of chronic cardiovascular insufficiency, which is a complication of chronic diseases of the heart, such as mitral valve disease, myocarditis with an outcome in cardiosclerosis, chronic ischemic heart disease.
MACROPREPARATION No. 13 Adenoma of the prostate gland with ureterohydronephrosis
The preparation contains an organocomplex consisting of a longitudinal section of the kidney with the ureter, longitudinal sections of the bladder and prostate gland.
Changes in the structure of the prostate gland entailed compensatory - adaptive changes in the structure of the overlying organs.
The prostate gland is enlarged, due to the proliferation of a tumor node in one of its lobes, rounded, with clear boundaries of growth, delimited from the prostate tissue by a connective tissue capsule. This is a benign tumor - prostate adenoma.
Due to the presence of an adenoma, the prostatic part of the urethra narrowed sharply, which led to a violation of the outflow of urine.
Working hypertrophy developed in the bladder wall. Along with wall hypertrophy, the bladder cavity expanded, that is, eccentric decompensated bladder hypertrophy developed.
The ureter, pelvis and cups of the kidney have dilated due to impaired outflow of urine - hydroureteronephrosis.
In the parenchyma of the kidney, a type of local pathological atrophy has developed - atrophy from pressure.
MACROPREPARATE No. 14 CENTRAL LUNG CANCER
The trachea with cartilaginous half-rings located on its front surface, the main bronchi, a part of the left lung adjacent to the left main bronchus are visible in the preparation.
The lumen of the left main bronchus is sharply narrowed due to the fact that around the bronchus in the lung tissue there is a pathological proliferation of gray - beige tissue, dense consistency, in the form of a node with indistinct growth boundaries. This is a malignant tumor growing from the epithelium of the main bronchus - lung cancer. Outside the main node of the tumor, there are multiple foci, irregularly rounded, - cancer metastases to the lungs.
Since cancer grows from the main bronchus, it is central in localization.
Since tumor growth is represented by a nodule, the macroscopic form of cancer is nodular.
Most often, the histological form of central lung cancer is squamous, the development of which is preceded by metaplasia of the glandular epithelium of the bronchi into stratified squamous non-keratinizing epithelium in the course of chronic bronchitis.
In relation to the surrounding tissues, cancer grows infiltratively.
In relation to the lumen of the main bronchus - into its wall, that is, endophytic, compressing the lumen of the bronchus.
Due to a violation of the patency of the bronchus due to its compression by a tumor in the lung tissue adjacent to the bronchus, such diseases as atelectasis, abscess, pneumonia, bronchiectasis can develop.
Lung cancer is an organ-specific epithelial tumor.
Metastasizes mainly by the lymphogenous pathway. The first lymphogenous metastases are found in the regional lymph nodes - peribronchial, paratracheal, bifurcation.
MACROPREPARATION No. 15 POLIPOSO - ULCER AORTIC VALVE ENDOCARDITIS
We see the heart preparation in a longitudinal section from the side of the left ventricle, since its myocardium has a thickness of more than 1 cm. The cavity of the left ventricle is expanded. There is eccentric decompensated working hypertrophy of the left ventricular myocardium and tonogenic dilation.
The crescent moon of the aortic valve is changed, they are thickened, tuberous, rigid, opaque. On two of the three half-moon, an ulcerative defect is clearly visible, on the surface of which thrombotic overlays in the form of polyps have formed. Such changes I in the aortic valve crescent are called polypoid - ulcerative endocarditis, which is one of the clinical and morphological forms of sepsis.
Microscopically, microbial colonies and lime scale deposits can be detected in the thickness of these thrombotic deposits.
Complications of this process can be thrombobacterial embolism and the formation of aortic heart disease.
Since polypoid - ulcerative endocarditis has developed on the already changed aortic valve crescents, this is secondary endocarditis.
MACROPREPARATE No. 16 STOMACH CANCER (Saucer-shaped)
The preparation contains a fragment of the stomach from the side of the mucous membrane. The stomach is cut along the greater curvature.
In the area of the lesser curvature of the body of the stomach, there is a pathological proliferation of tumor tissue into the lumen of the stomach with loose raised edges and a shallow bottom. The boundaries of tumor growth are indistinct in places. At the bottom of the tumor growth, there are foci of white necrosis.
The indistinct boundaries of tumor growth and the presence of secondary changes in it in the form of foci of necrosis indicate the malignancy of the tumor.
A malignant tumor growing from the epithelium of the stomach is stomach cancer.
By localization, it is a cancer of the body of the stomach.
By the nature of its growth, it is an ecophytic - expansive cancer.
On a macroscopic basis, it is a saucer-shaped cancer.
Microscopically, it will most often be represented by a differentiated form of cancer - adenocarcinoma.
Since stomach cancer, according to the international classification of tumors, belongs to the group of organ-specific epithelial tumors, the predominant route of its metastasis will be lymphogenous. The first lymphogenous metastases can appear in the regional lymph nodes - four collectors of lymph nodes located along the lesser and greater curvatures of the stomach.
Since the stomach is an unpaired abdominal organ, the first hematogenous metastases are found in the liver.
MACROPREPARATION No. 17 ABSCEDING PNEUMONIA IN SEPTICOPYEMIA
We see a cross section of the right lung, as it contains three lobes.
In each lobe, against the background of an airy tissue of a light beige color, there are multiple foci of a round and irregular shape, the size of a match head, in places merging with each other, dense consistency, airless or low-air, with a smooth cut surface, white-gray. These are foci of inflammation in the lung tissue - foci of pneumonia.
A white wall is formed around some foci, and the contents of the foci become the consistency of thick sour cream. A complication of pneumonia, abscess formation, develops.
Absolute pneumonia can develop with septicopyemia, one of the clinico-morphological forms of sepsis.
MACROPREPARATE No. 18 LARGE PNEUMONIA (WITH ABSCEDING)
The preparation shows a longitudinal section of the right lung, as three lobes are visible.
The lower lobe is entirely gray, airless. The surface of its section is fine-grained.
The consistency of the lung lobe corresponds to the hepatic density.
The interlobar pleura is thickened with gray-beige filmy overlays.
This is croupous pneumonia, hepatization stage, a variant of gray hepatization.
In the lower segments of the lobe, cavities are determined, delimited from the lung tissue by the wall. These are abscess cavities.
There is one of the pulmonary complications of pneumonia - abscess formation. Its cause is the addition of a secondary purulent infection due to decreased immunity and increased fibrinolytic activity of neutrophilic leukocytes.
MACROPREPARATE No. 19 SMALL-NODED LIVER CIRROSIS
A section of the liver is presented in the preparation.
The liver is reduced in size, since its corners are pointed, and the capsule is wrinkled.
On the outer surface of the liver, multiple nodes of regenerates are determined, up to 1 cm in size, making the surface of the liver non-smooth.
On the surface of the incision, the boundaries of the false lobules are clearly visible (whereas in the norm the boundaries of the hepatic lobules are not visualized) due to the proliferation of fibrous tissue in the area of the portal tracts.
This is cirrhosis of the liver.
In macroscopic form, it is small-knot. In microscopic form, it is monolobular, since the size of the false lobules corresponds to the size of the nodes - regenerates.
According to its pathogenesis, it is portal cirrhosis of the liver, in which portal hypertension develops primarily, and hepatocellular failure secondarily.
Such cirrhosis can develop as a result of fatty hepatosis, chronic form viral hepatitis B and chronic course of alcoholic hepatitis.
MACROPREPARATE No. 20 UTERINE BODY CANCER
A longitudinal section of the uterus is shown.
The uterus is enlarged. It can be seen that in the uterine cavity there is a pathological proliferation of tissue with a non-smooth, papillary surface, in places with ulceration, with indistinct growth boundaries. This is a tumor growth.
The tumor develops from the endometrium, it can be seen that it grows into the wall of the uterus. This is a malignant tumor from the epithelium - cancer of the body of the uterus.
Histologically, it is represented by a differentiated form of cancer - adenocarcinoma.
The nature of tumor growth in relation to the lumen of the uterus is exophytic, in relation to the surrounding tissues - infiltrating.
It can develop as a result of atypical glandular hyperplasia of the endometrium.
It is an organ-specific epithelial tumor. Metastasizes mainly by the lymphogenous pathway. The first lymphogenous metastases are found in the regional lymph nodes.
MACROPREPARATION No. 21 PURULENT - FIBRINOUS ENDOMYOMETRITIS
A longitudinal section of the uterus with appendages is visible.
The uterus is sharply increased in size, its cavity is sharply expanded, the wall is thickened.
The endometrium is dirty gray in color, dull, covered with filmy beige overlays, hanging in places into the uterine cavity. In the endometrium there is an inflammatory process - purulent - fibrinous endometritis.
In addition, the inflammation has spread to the muscular membrane of the uterus, since the myometrium is dull, dirty gray in color.
Thus, in the presented preparation there is purulent - fibrinous endomyometritis, which could arise as a result of a criminal abortion and cause uterine sepsis.
MACROPREPARATE No. 22 MULTIPLE UTERINE FIBROMIOMAS
A cross section of the uterus is shown.
In the wall of the uterus, the growth of tumor tissue in the form of nodes, of various sizes, round and oval, with clear growth boundaries, surrounded by a thick-walled capsule, is visible, which is a reflection of the expansive growth of the tumor.
The nodes located inside the wall of the uterus - intramural, lying under the endometrium - submucous, lying under the serous membrane - subserous.
The nodes are built of two types of fibrous structures - some beige fibers are smooth muscle fibers, the other gray-white fibers are connective tissue fibers. Fibrous structures have different thicknesses and go in different directions, which are manifestations of tissue atypism.
Since the tumor nodes contain a large number of connective tissue fibers, their consistency is dense.
Due to the fact that the tumor grows expansively and has only signs of tissue atypism, it is benign. A benign tumor of smooth muscle with an admixture of fibrous tissue is called fibroids.
Based on the international classification of tumors, it belongs to mesenchymal tumors.
MACROPREPARATE No. 23 BUBBLE FAN
The drug is represented by an uviform cluster of thin-walled vesicles adhered to each other and filled with a transparent liquid. This is a cystic mole, a benign organ-specific tumor that develops during and after pregnancy from the epithelium of the chorionic villi.
The development of cystic drift is based on hydropic degeneration of epithelial cells.
A vesicular mole is benign until it begins to grow into the wall of the uterus, into the veins. After that, it becomes malignant, or destructive. Against the background of a malignant cystic drift, a malignant organ-specific tumor of chorionepithelioma may develop.
MACROPREPARATE No. 24 THROMBOEMBOLIA OF THE PULMONARY ARTERY
The drug is represented by an organocomplex: the heart and fragments of both lungs.
The heart is clipped from the side of the right ventricle, since the thickness of its myocardium is approximately 0.2 cm. The pulmonary trunk emerges from the right ventricle, which is divided into two pulmonary arteries, respectively, to the right and left lungs.
In the lumen of the pulmonary trunk and its bifurcation there are massive, heavy, dense, crumbling masses with a corrugated surface that are not attached to the walls of blood vessels. These are thromboemboli. The source of such massive thromboemboli could most likely be the veins of the lower extremities.
The thromboembolus located in the lumen of the pulmonary artery trunk and its bifurcation irritates the reflexogenic zone receptors located in the intima of the above vessels and causes the development of the pulmo - coronary reflex, which consists in an instant spasm of small bronchi and bronchioles and coronary arteries heart, with the development of acute cardiovascular failure and the onset of instant death.
MACROPREPARATION No. 25 AORTIC ATHEROSCLEROSIS WITH ATHEROMATOSIS AND PARALLEL THROMBOSIS
The abdominal aorta in a longitudinal section and the area of bifurcation of the aorta to the common iliac arteries are presented.
The intima of the aorta is changed. It defines multiple round-longitudinal spots of white-yellow color, which are lipid deposits and proliferation of fibrous tissue. These are atherosclerotic plaques. They bulge into the lumen of the aorta, making it narrower. Below the opening of the inferior mesenteric artery, the plaques are ulcerated, atheromatous (necrotic) masses have formed on their surface, and hemorrhages have occurred.
The appearance of atherosclerotic plaques in the intima of the aorta indicates the presence of a disease of atherosclerosis, a clinical and morphological form of atherosclerosis of the aorta.
The described plaque changes correspond to the macroscopic stage of complicated lesions.
Damage to the aortic intima was one of the local prerequisites for thrombus formation. In the lumen of the abdominal aorta and in the lumen of the iliac arteries, parietal and even obstructing blood clots formed, disrupting the passage of blood through the aorta to the lower extremities.
MACROPREPARATE No. 26 Lesion of the small intestine with abdominal typhus
The specimen presents the small intestine in a longitudinal section from the side of the mucous membrane.
On the mucous membrane, longitudinal oval-shaped formations are visible, protruding above the surface of the mucous membrane and having on their surface a kind of grooves and convolutions, as in the brain. These formations are pathognomonic for typhoid fever. They arose as a result of acute productive inflammation in the area of lymphatic follicles located in the submucosa of the intestine. Due to the proliferation of macrophage and histiocytic elements, the follicles increased in volume, size and began to rise above the mucosal surface.
Due to the presence of grooves and convolutions on the surface of the follicles, the first stage of typhoid fever is called cerebral swelling.
MACROPREPARATE No. 27 FIBROZOUS - CAvernous pulmonary tuberculosis
The specimen is represented by a longitudinal section of the right lung, since it has 3 lobes. Each of the lobes has cavities, large cavities with thick, non-collapsing walls. Since the walls of the cavities do not collapse, these are old, chronic cavities inherent in fibrous-cavernous pulmonary tuberculosis, one of the phases of forms of secondary pulmonary tuberculosis.
The wall of the old cavity consists of 3 layers: 1) internal - caseous necrosis; 2) medium - specific granulation tissue; 3) external - fibrous tissue.
The patient develops cor pulmonale, chronic pulmonary heart failure, tuberculous intoxication and cachexia, from which he dies.
MACROPREPARATE No. 28 PARA-AORTIC LYMPHONULOMATOSIS
The specimen shows the aorta in longitudinal section.
In the intima of the aorta, atherosclerotic plaques are determined.
On both sides of the abdominal aorta, above the bifurcation, sharply enlarged and because of this lymph nodes welded to each other are determined, forming "packets" of lymph nodes.
The consistency of the lymph nodes is densely elastic, the surface is smooth, the color on the cut is gray-pink.
The lymph nodes that lie on the sides of the aorta are called paraaortic.
Enlargement of the paraaortic lymph nodes and their fusion into packets occurs in lymphogranulomatosis, malignant Hodgkin's lymphoma.
MACROPREPARATE No. 29 ARTERIOLOSCLEROTIC NEPHROSCLEROSIS
Two whole kidneys are visible in the preparation.
Their size and weight are sharply reduced (both kidneys in humans weigh 300 - 350 g). The surface of the kidneys is wrinkled, fine-grained. The consistency of the kidneys is very dense.
This is primarily a wrinkled kidney due to the benign course of the primary arterial hypertension... At the heart of wrinkling is hyalinosis and sclerosis of the capillaries of the renal glomeruli - arteriolosclerotic nephrosclerosis.
The same appearance is secondary - a wrinkled kidney, which develops as a result of chronic glomerulonephritis.
Clinically, against the background of primary and secondary contracted kidneys, chronic renal failure develops, accompanied by the development of azotemic uremia, which can be treated with chronic hemodialysis or kidney transplantation.
MACROPREPARATE No. 30 MILIARY TUBERCULOSIS OF PULMONARY
An enlarged longitudinal section of the lung is presented.
It is clearly seen that the entire surface of the lung tissue is diffusely dotted with small, millet-sized grain, dense tubercles, light yellow in color.
The lung has this type in miliary tuberculosis, which develops in hematogenous generalized and hematogenous tuberculosis with a predominant lesion of the lungs.
Each tubercle has the following structure: in the center there is a focus of caseous necrosis, the severity of which depends on the state of the patient's immunity; it is surrounded by a cell wall of epithelioid cells, lymphocytes, plasma cells and single multinucleated cells of Pirogov-Langhans.
According to the classification of granulomas, tuberculous granulomas are infectious, specific. Specific cells of a tuberculous granuloma are epithelioid cells of hematogenous, monocytic origin, which are the most in the granuloma.
MACROPREPARATION No. 31 NODULAR GOITER
The cutaway of the thyroid gland is presented in the preparation.
Its dimensions are dramatically increased (normally weighs 25 g).
The outer surface is bumpy.
On the surface of the incision, the lobular structure of the gland is distinguished, and in the lobules there are follicles of different sizes filled with a brown colloid.
Persistent increase in size thyroid gland not associated with inflammation, swelling or poor circulation in it is called goiter.
In appearance, it is a nodular goiter.
Internal structure - colloid goiter.
Most often occurs with endemic goiter, the occurrence of which is associated with a deficiency of exogenous iodine.
Despite the compensatory increase in the size of the gland, its function is reduced.
MACROPREPARATE No. 32 TUBULAR PREGNANCY
The fallopian tube is visible in cross section.
The pipe is sharply expanded. Its wall is thinned in places, thickened in places. In places of thickening of the pipe wall, the fabrics have a dark Brown color the consequence of hemorrhage. In the center of the tube is a human embryo, in which the head, torso, hands and fingers are clearly distinguishable. The embryo is surrounded by membranes.
This is an ectopic, tubal pregnancy, complicated by an incomplete tubal abortion.
The fertilized egg has separated from the walls fallopian tube, as evidenced by hemorrhage, but remained in the tube.
MACROPREPARATE No. 33 RENAL - CELLULAR CANCER
It is represented by a section of the kidney, in the upper pole of which tumor tissue grows in the form of a node with clear growth boundaries, forming a pseudocapsule around itself, which indicates the expansive growth of the tumor.
The tumor node is light yellow in color, since the tumor cells contain a large amount of lipids; motley, since the tumor is characterized by the development of necrosis and hemorrhage; soft consistency, since the tumor contains little fibrous tissue.
Despite the nature of growth, the tumor is malignant, differentiated, organ-specific epithelial, developing from the epithelium of the kidney tubules.
It occurs in adults.
MACROPREPARATE No. 34 DRY GANGRENA FOOT
The foot of the right lower limb is visible in the specimen.
In the area of back surface the metatarsus, at the base of the toes, the skin is absent, and the soft tissues are dry, mummified, gray-black.
This is dry gangrene of the foot, one of the clinical and morphological forms of necrosis.
Gangrene is called necrosis of tissues in contact with the external environment.
With gangrene, soft tissues are stained in a gray-black color with a pigment pseudomelanin, or iron sulfide.
Gangrene of the foot can develop as a result of atherosclerotic damage to the vessels of the lower extremities, which occurs primarily or as a result of diabetes mellitus due to the development of macroangiopathy.
MACROPREPARATION No. 35 EMBRYONIC KIDNEY CANCER
It is represented by a kidney in longitudinal section.
In the upper pole of the kidney there is an overgrowth of tumor tissue, large in size, with clear boundaries of growth, forming a pseudocapsule around itself. In the center of the tumor node there is a large cavity due to necrosis of the tumor tissue.
The lower pole of the kidney is small, which indicates that the kidney belongs to a small child.
Despite the nature of tumor growth - expansive and given the presence of secondary changes in the tumor - this is a malignant, undifferentiated tumor that develops from metanephrogenic tissue and affects children from two to six years old.
Expansive growth gives way to invasive growth over time.
The tumor is organ-specific epithelial.
Metastasizes mainly by hematogenous route to the opposite kidney, lungs, bones, brain.
MACROPREPARATE No. 36 MAMMARY CANCER
The drug is represented by the mammary gland.
In one of the quadrants of the mammary gland, a pathological proliferation of tumor tissue occurred, emanating from the epithelium of the mammary gland ducts, and grown to the surface of the skin, which indicates an invasive tumor growth.
This is a malignant, epithelial organ-specific tumor - breast cancer.
GASTRITIS (gastritis; Greek, gaster stomach + -itis) - damage to the gastric mucosa with predominantly inflammatory changes in the acute development of the process and the phenomena of dysregeneration, structural restructuring with progressive atrophy during hron, course, accompanied by dysfunction of the stomach and other body systems.
Representations about G. changed depending on the level of development of honey. Sciences. References to functional and organic disorders of the stomach can be found in the works of Hippocrates, Galen, Razi, Ibn-Sina, and others. The beginning of the study of G. is associated with the name of French. doctor F. Brouss (1803), who considered G. the most common disease and associated with it the development of diseases of the heart, brain, and lungs. Since introduction into a wedge, practice of a method of sounding of a stomach [A. Kussmaul, 1867] G. was considered as a functional disease. However, this point of view was revised in the second half of the 19th century. - the beginning of the 20th century. on the basis of new data patol, anatomy, surgery of the abdominal cavity, rentgenol. method, research by I.P. Pavlov and his school in the field of physiology of the digestive tract.
Introduction into a wedge, practice of methods of gastroscopy and especially aspiration gastrobiopsy led to the expansion of ideas about G. A great contribution to the development of the doctrine of G. was made by Soviet scientists Yu. M. Lazovsky, N. I. Leporsky, O. L. Gordon, I. P Razenkov, S. M. Ryss.
Distinguish between acute and hron. G.
Acute gastritis
There are the following forms of acute G.: simple (banal, catarrhal), corrosive, fibrinous, phlegmonous.
Pathogenesis of acute gastritis
The pathogenesis of acute gastritis is reduced to the development of an inflammatory process of varying severity - from superficial changes to deep inflammatory-necrotic. The pathogenesis of a wedge, signs is caused, on the one hand, by a violation of the secretory and motor function of the stomach (vomiting, spastic pain, etc.), by the depth and severity inflammatory changes in the stomach (leukocytosis, accelerated ROE, elevated temperature body, pain as a result of irritation of the nerve endings in the wall of the stomach), on the other - the involvement in patol, the process of other organs, body systems and some aspects of metabolism (collapse, dehydration of the body, blood thickening, etc.).
Pathological anatomy of acute gastritis
The pathological anatomy of acute gastritis is characterized by inflammatory changes in the gastric mucosa. Distinguish between catarrhal, corrosive, phlegmonous and fibrinous G.
Fig. 10. The mucous membrane of the stomach with phlegmonous gastritis (pronounced sharp thickening of the folds); on the cut - purulent infiltration.
At catarrhal G. the mucous membrane is infiltrated with leukocytes (color, table. Fig. 1-3), which are also located between the cells of the epithelium, there is inflammatory hyperemia, dystrophic and necrobiotic changes in the epithelium.
At corrosive G. there are necrotic-inflammatory changes in the wall of the stomach (printing. Fig. 9).
At phlegmonous G. (tsvetn. Fig. 10) diffuse leukocytic infiltration of all layers of the stomach wall is observed, but hl. arr. submucosa. Phlegmonous G. is accompanied by perigastritis (see) and can end with peritonitis.
Fibrinous G. is characterized by diphtheria inflammation of the mucous membrane.
Simple gastritis
Simple gastritis (commonplace, catarrhal)- the most common form. Occurs at all ages and regardless of gender. A common cause of simple G. is errors in nutrition, infections, especially foodborne toxicoinfections (see. Food toxicoinfections). The irritating effect of some drugs is known (salicylates, butadion, bromides, iodine, digitalis, antibiotics, sulfonamides, etc.). G.'s development from taking small amounts of drugs and under the influence of certain types of food (eggs, strawberries, crabs, etc.) may indicate an allergic mechanism of damage to the gastric mucosa.
Wedge, picture of a simple G.(caused by the most common causes - errors in nutrition and foodborne diseases) usually develops after 4-8 hours. after exposure to etiol, factor. Patients note pain, a feeling of heaviness and fullness in the epigastric region, nausea, weakness, dizziness, vomiting, sometimes diarrhea, salivation, or, conversely, severe dry mouth. The tongue is coated with a grayish-white bloom. On palpation of the abdominal wall - pain in the epigastric region. The pulse is usually fast, the blood pressure is slightly reduced. An increase in body temperature is possible, in the peripheral blood - neutrophilic leukocytosis. In the urine there may be albuminuria, oliguria, cylindruria, i.e., changes characteristic of toxic renal damage. There is a lot of mucus in the stomach contents; secretory and acid-forming functions can be suppressed or enhanced. Motor disorders are manifested by pylorospasm (see), hypotension and even atony of the stomach (see). Duration acute period diseases with timely treatment started - 2-3 days.
Complications at simple G. are rare. General intoxication, disorders in the cardiovascular system may develop.
Diagnosis simple G. is based on a wedge, a picture. With an increase in temperature and a disorder of intestinal activity, it is possible to assume gastroenterocolitis (see), it is also necessary to differentiate G. with salmonellosis (see). In this case, bacteriol, and serol, research is of decisive importance.
Treatment simple G. must begin with cleansing the stomach and intestines and prescribing antibacterial drugs (enteroseptol 0.25-0.5 g 3 times a day, chloramphenicol up to 2 g per day, etc.) and absorbent substances (activated carbon, clay, etc. .). In case of severe pain syndrome, atropine (0.5-1 ml of 0.1% solution subcutaneously), platifillin (1 ml of 0.2% solution subcutaneously), papaverine (1 ml of 2% solution subcutaneously) are injected. With the development of dehydration, physiol, solution, 5% glucose solution is injected subcutaneously. In acute cardiovascular failure - caffeine, mezaton, norepinephrine. It is necessary to prescribe to lay down. nutrition. The first 1 - 2 days should refrain from eating, drinking is allowed in small portions (strong tea, borzhom). On the 2-3rd day - low-fat broth, slimy soup, semolina and mashed rice porridge, jelly. On the 4th day - meat and fish broth, boiled chicken, fish, steamed cutlets, mashed potatoes, crackers, dried white bread. Then the patient is assigned a table number 1 (see. Therapeutic nutrition), and after 6-8 days - the usual food.
Forecast at simple G. in case of timely started treatment is favorable. If the action of etiol, factors is repeated, then acute G. can go to hron.
Prophylaxis simple G. is reduced to rational nutrition, observance a dignity. - gigabyte. events in everyday life and at catering establishments, dignity. - skylight, work.
Corrosive gastritis
Corrosive gastritis develops as a result of the ingestion of substances such as strong to-you, alkalis, salts of heavy metals, highly concentrated alcohol into the stomach.
Wedge, painting by the corrosive G. depends on the degree of damage to the mucous membrane of the mouth, esophagus and stomach, the nature and resorptive action of the substances that caused the corrosive G, Patients usually complain of pain in the mouth, behind the sternum and in the epigastric region, repeated excruciating vomiting; in vomit - blood, mucus, sometimes tissue fragments. On the lips, mucous membrane of the mouth, pharynx and larynx there are traces of burns - edema, hyperemia, ulceration. Sometimes, by the nature of the changes in the mucous membranes, it is possible to establish the cause of the burn: from sulfuric and saline to-t appear grayish-white spots, from nitrogen - yellow and greenish-yellow scabs, from chrome - brownish-red scabs, from carbolic - bright white bloom, resembling lime, from vinegar - superficial whitish-gray burns. In severe cases, a collapse may develop (see). The abdomen is usually swollen, painful on palpation in the epigastric region, sometimes there are signs of irritation of the peritoneum. In some patients, in the first hours after poisoning, acute perforation of the stomach wall occurs, signs of toxic damage to the kidneys (in the urine - protein, cylinders) are noted up to the development of acute renal failure.
Complication with corrosive G., it can occur in the first hours from the moment of exposure to etiol, factor and is manifested by perforation of the stomach wall with the development of peritonitis (see) and penetration into neighboring organs.
Diagnosis corrosive G. is based on anamnesis data, a wedge, signs (including the nature of changes in the mucous membrane of the mouth, pharynx and larynx).
Treatment should start with gastric lavage large quantity water through a probe, lubricated with vegetable oil. Contraindications to the introduction of the probe are collapse and, obviously, severe destruction of the esophagus.
In case of poisoning with to-tami add milk, lime water or burnt magnesia to the water; in case of damage with alkalis - diluted lemon and acetic to - you, antidotes are introduced. For severe pain, morphine, promedol, fentanyl, droperidol are administered; in case of collapse, in addition, caffeine, cordiamine, mezaton, norepinephrine, strophanthin (subcutaneously or intravenously with blood substitute fluids, glucose, physiological solution, etc.). During the first days, fasting, parenteral administration of fiziol, solution and 5% of glucose solution are necessary. If it is impossible to feed by mouth for several days - parenteral administration of plasma and protein hydrolysates. With perforation of the stomach, urgent surgical treatment is indicated.
Forecast corrosive G. depends on the severity of inflammatory and destructive changes and therapeutic tactics in the first hours and days of the disease; death can result from shock, bleeding, or peritonitis. Corrosive G.'s outcome is usually cicatricial changes in the stomach, more often in the pyloric and cardiac departments.
Fibrinous gastritis
Fibrinous gastritis is rare, develops in severe infectious diseases (smallpox, scarlet fever, sepsis, etc.), as well as poisoning with mercuric chloride, acids, etc., which determines the wedge, picture, treatment and prognosis.
Phlegmonous gastritis
Phlegmonous gastritis occurs, as a rule, primarily as a result of infection directly into the stomach wall. It is caused by streptococcus, often hemolytic, often in combination with Escherichia coli, less often staphylococcus, pneumococcus, Proteus, etc. Sometimes it develops as a complication of an ulcer or disintegrating stomach cancer, with abdominal trauma due to damage to the gastric mucosa. Phlegmonous G. can develop a second time with some infections - sepsis, typhoid fever, etc.
Wedge, picture of phlegmonous G. characterized by an acute onset, fever, chills, severe adynamia and pain in the upper abdomen, usually aggravated by palpation, nausea and vomiting. General state deteriorates sharply. Patients refuse to eat and drink; exhaustion quickly sets in. In peripheral blood - neutrophilic leukocytosis, toxigenic granularity in granulocytes, accelerated erythrocyte sedimentation, change in the ratio of protein fractions and other reactions.
Complications with phlegmonous G.: purulent diseases of the chest - mediastinitis (see), purulent pleurisy (see) and abdominal cavity - subphrenic abscess (see), thrombophlebitis large vessels(see Thrombophlebitis), liver abscess (see), etc.
Diagnosis phlegmonous G. before operation is placed very rarely.
It is often recognized on the operating table or at autopsy.
Treatment phlegmonous G. consists mainly in parenteral administration of broad-spectrum antibiotics in large doses. If conservative treatment is ineffective, surgical intervention is indicated.
Forecast phlegmonous G. is serious. After healing, persistent organic changes may remain in the stomach.
Chronic gastritis
Chron. G. makes up most of the diseases of the stomach. It is often combined with other diseases of the digestive system.
Chron. G. - the concept of wedge. - morfol., It is shown by a wedge, signs, functional and morfol, changes in various combinations and can proceed with various disorders of secretion, but a decrease in gastric juice secretion is more characteristic. Function of acid formation at hron. G. is disturbed earlier and more often than enzyme-forming and excretory.
There are many different classifications hron. D. The classification according to Ryss (1966) is given.
I. By etiological basis
1. Exogenous gastritis: long-term violations of the diet - the qualitative and quantitative composition of food; alcohol and nicotine abuse; action of thermal, chemical, fur. and other agents; the influence of occupational health - the systematic tasting of seasoned spices raw meat(canning industry), ingestion of alkaline vapors and fatty acids (soap, margarine and candle factories), inhalation of cotton, coal, metal dust, work in hot shops, etc.
2. Endogenous gastritis: neuro-reflex (patol, reflex action from other affected organs - intestines, gall bladder, pancreas); G., associated with violations in Article. n. With. and endocrine organs; hematogenous G. (hron, infections, metabolic disorders); hypoxemic G. (hron, circulatory failure, pneumosclerosis, pulmonary emphysema, pulmonary heart); allergic G. (allergic diseases).
II. By morphological characteristics
1. Superficial.
2. Gastritis with glandular involvement without atrophy.
3. Atrophic: a) moderate; b) pronounced; c) with the phenomena of restructuring of the epithelium; d) atrophic-hyperplastic; other rare forms of atrophic (the phenomenon of fatty degeneration, the absence of a submucosa, the formation of cysts).
4. Hypertrophic.
5. Antral.
6. Erosive.
III. Functionally
1.With normal secretory function.
2. With moderately expressed secretory insufficiency: absence of free salt to - you on an empty stomach (or a decrease in its concentration after a test stimulus below 20 titers, units); a decrease in the concentration of pepsin after a test stimulus to 1 g%, the concentration of mucoprotein is below 23%, positive reaction for the introduction of histamine, the normal content of uropepsinogen.
3. With a pronounced secretory insufficiency: the absence of free hydrochloric acid in all portions of gastric juice, a decrease in the concentration of pepsin (or its complete absence), the absence (or traces) of mucoprotein, a histamine refractory reaction; decrease in the content of uropepsinogen.
IV. According to the clinical course
1. Compensated (or remission phase): absence of a wedge, symptoms, normal secretory function or moderately expressed secretory insufficiency.
2. Decompensated (or exacerbation phase): the presence of a distinct wedge. symptoms (with a tendency to progression), persistent, difficult to treat, pronounced secretory insufficiency.
V. Special forms of chronic gastritis
1. Rigid.
2. Giant hypertrophic (Menetrie's disease).
3. Polyposis.
Vi. Chronic gastritis concomitant with other diseases
1. With Addison-Birmer anemia.
2. With stomach ulcers.
3. With cancer.
Chron, gastritis is a polyetiologic disease, is a consequence of untimely and insufficient treatment of acute G., as well as prolonged malnutrition, eating foods that irritate the gastric mucosa (spices, onions, garlic, pepper), addiction to hot food and drink, bad chewing food, eating dry food, frequent consumption of alcoholic beverages, malnutrition, especially with a lack of protein, vitamins and iron. The reason may be long-term intake some medicines (quinine, atophan, digitalis, salicylates, butadion, prednisolone, sulfa drugs, potassium chloride, antibiotics, etc.), the influence of factors such as inhalation of cotton, metal, coal dust, alkali vapors, etc. Disorders in the endocrine system (diabetes, gout) can cause the development of structural changes in the gastric mucosa. The release through the gastric mucosa of metabolic products such as acetone, indole, skatole, like toxins in infectious diseases and local foci of infection, causes the development of the so-called. elimination G. Chron, diseases of the digestive system (appendicitis, cholecystitis, colitis, etc.) are especially important in development hron. G. Often hron. G. develops in diseases causing tissue hypoxia (hron, circulatory failure, pneumosclerosis, anemia).
From the blood serum of sick hron. G. isolated antibodies, with the help of which the model of autoimmune lesions of the stomach is reproduced. However, the pathogenetic nature of circulating gastric antibodies has not yet been clarified. There is evidence of the role of genetic factors in the emergence of hron. D. In patients with a severe form of atrophic G., relatives of the first degree of kinship are predisposed to this disease, which is manifested by the early (at a young age) G.'s emergence and its rapid transformation into a severe form.
The pathogenesis is complex and not the same at various forms hron. G. At hron. G., which developed from acute, progresses primary inflammatory changes in the stroma and the development of secondary degenerative-regenerative changes in the glandular apparatus (atrophy, hyperplasia, metaplasia, etc.). Development mechanism individual forms hron. G., etiologically associated with various nutritional disorders and neuroreflex effects on the stomach, is reduced to functional secretory motor disorders of the stomach (see) with subsequent structural changes in its glandular apparatus and the development of an inflammatory process in the stroma. The change secretory activities stomach and neuroreflex influences from the affected organ are, in turn, the cause of disruption of the activity of other organs of the digestive system.
By morfol, signs distinguish superficial G., different stages mucosal atrophy. Ts. G. Masevich (1967) allocates G. with defeat of the glands of the bey of atrophy of the mucous membrane and G. is atrophic. Schindler (R. Schindler, 1968) and Elster (K. Elster, 1970) distinguish hypertrophic G.
The results of histochemical, and electron microscopic research of biopsy material allow us to consider that the forms hron. G. are phases of violation fiziol, regeneration of the gastric mucosa. According to M. Siurala et al. (1963, 1966), Ts. G. Masevich (1967) and others, superficial G. passes into G. with defeat of the glands, and then into atrophic. Syurala et al. (1968) believe that this process takes approx. 17 years.
Chronic superficial gastritis characterized by a picture of mucus hypersecretion, sometimes with a predominance of the excretion phase over the phase of secretion accumulation: there are no neutral mucopolysaccharides in the apical section of the cells, and a large amount of mucus on the cell surface. The presence of CHIK positive granules over the nuclei indicates increased mucus synthesis (see CHIC response). Sometimes the epithelium lining the gastric fields and dimples looks flattened, with a narrow strip of mucoid, rare supranuclear granules, and a high content of RNA. Revealed granular and vacuolar degeneration of the epithelium, the infiltration of lymphoid and plasma cells of the own shell of the rollers (color, table., Fig. 4). Accessory cells, normally located in the isthmus of the gastric glands, often spread to their middle third.
For chronic gastritis with glandular involvement the surface epithelium of the mucous membrane is flattened, there is a deepening of the gastric pits, additional glandulocytes are hyperplastic.
In the main glandulocytes, vacuoles are detected (Fig. 1) containing neutral mucopolysaccharides (color, table. Fig. 5). In the cytoplasm of these cells, among the zymogen granules, shapeless masses are found, in places surrounded by a membrane. These masses are similar to "immature" or "mature" mucoid. In the supranuclear zone, a developed lamellar complex (Golgi) with dilated cisterns is revealed (Fig. 2). Thus, these cells contain elements of both the main (zymogen, RNA, ergastoplasm) and additional glandulocytes (neutral mucopolysaccharides, a well-developed lamellar complex). These cells are, apparently, the immature main glandulocytes of the isthmus of the gastric glands. As a result of slowing down their differentiation, they occupy the territory of mature main glandulocytes. Accessory glandulocytes are also "immature", with a developed lamellar complex and ergastoplasm; they are found in those parts of the glands where they are usually not observed.
Chronic atrophic gastritis characterized by a decrease (sometimes significant) in the number of main and accessory glandulocytes, deepening of the gastric dimples (color. Fig. 7 and color, table. Fig. 6 and 7), which often have a corkscrew-like appearance (Fig. 3), hyperplasia of accessory glandulocytes. The epithelium covering the gastric fields and dimples is often flattened, contains a lot of RNA and little neutral mucopolysaccharides, in places it is replaced by intestinal epithelium (color table. Fig. 8) with typical enterocytes, goblet cells and Paneth cells (intestinal metaplasia). The stomach glands are often replaced by mucous membranes (pyloric metaplasia). The remaining main glandulocytes are vacuolated; in the obstructive glandulocytes, a rarefaction of the cytoplasm in the perinuclear zone and around the intracellular tubules is revealed, as well as a decrease in the number of microvilli and tubulovesicles; there is a reduction in the mitochondrial cristae of the parietal glandulocytes.
Wolf (G. Wolf, 1968) distinguishes three stages of atrophy of the gastric mucosa: incipient atrophy, with a cut the glands are not yet shortened, but look as if squeezed; partial atrophy(glands), with a cut preserved groups of glands containing the main and parietal (lining) glandulocytes; total atrophy of the glands (atrophy of the mucous membrane), when the main and parietal (parietal) glandulocytes are not detected, the glands are lined only with mucus-forming epithelium.
Chronic hypertrophic gastritis- thickening of the mucous membrane and increased proliferation of the epithelium (color. Fig. 6, color. Table Fig. 9 and Fig. 7).
There are three forms of hron, hypertrophic G.: interstitial, proliferative, glandular. The interstitial form is characterized by abundant lymphoplasmacytic infiltration, which occurs at the edges of ulcers; for proliferative - the growth of the superficial epithelium, deepening of the dimples, the glandular apparatus unchanged; with a glandular form, the mucous membrane is thickened 2-7 times due to glandular hyperplasia; this form is hron. G. meets with duodenal ulcer (see. Peptic ulcer), Zollinger-Ellison syndrome (see Zollinger-Ellison syndrome) and as an independent disease. Some authors refer hron to the glandular form. G. and Menetrie's disease, designating it as gastritis hypertrophica gigantea, although Menetrie himself considered this condition of the mucous membrane not as hypertrophic G., but as a "creeping adenoma." Most authors (Yu. N. Sokolov, P. V. Vlasov, etc.) deny the connection of Menetrie's disease with G., considering it as an anomaly in the development of the gastric mucosa.
The clinical picture. Depending on the state of the secretory function of the stomach, hron is distinguished. G. with normal and increased secretion and hron. G. with secretory insufficiency.
Chronic gastritis with normal and increased secretion usually occurs at a young age, more often in men. The main symptoms are dyspeptic disorders and pain, which usually appear during an exacerbation of the disease, after errors in the diet, the use of alcoholic beverages, including table wines and beer. Patients complain of heartburn, sour belching, a feeling of pressure, burning and distention in the epigastric region, constipation (sometimes diarrhea), rarely vomiting. The pains are usually dull, aching, without a certain irradiation, localized in the epigastric region, their occurrence, as a rule, is associated with food intake. But the pains can be "hungry" and "night", and subside after eating.
Early complications are movement disorders of the intestines and biliary tract (hyper- and hypomotor dyskinesias). In the future, functional disorders are replaced by organic changes, and then hron, cholecystitis (see), hron develop. pancreatitis (see), hron, enterocolitis with metabolic disorders - hypovitaminosis, iron deficiency anemia, etc. (see. Enteritis, enterocolitis).
Massive bleeding from the gastric mucosa is possible, which on average accounts for half of non-ulcer bleeding. In this case, they talk about the so-called. hemorrhagic gastritis. Hemorrhagic gastritis - the concept of a wedge; morfol, its picture may be different. Bleeding at G. is most often associated with the development of erosions, but sometimes the mechanism of bleeding remains unclear even after gistol, research of the resected part of the stomach. A certain value in the occurrence of gastric bleeding is attributed to the acidity of gastric juice (the higher the acidity, the more often bleeding). Abundant gastric bleeding usually develops in patients with minor wedge, manifestations, in which, as it is believed, increased permeability of the blood vessels of the stomach. Allergic reactions can also be the cause of the development of massive gastric bleeding (see Gastrointestinal bleeding).
Special wedge-morfol. form hron. G. with normal and increased secretion is gastroduodenitis (synonym: pyloroduodenitis, hypertrophic glandular G., hypertrophic hypersecretory gastropathy), which occurs mainly at a young age. It is similar in wedge, manifestations with duodenal ulcer, although not identical to it. IM Fleckel (1958) considered gastroduodenitis to be the pre-stage of peptic ulcer disease or a form of "peptic ulcer disease without an ulcer." The frequency of the disease (during the day and year) is less pronounced than with peptic ulcer disease. Of the wedge, the most characteristic symptoms are pain ("painful gastritis"), which are usually localized under the xiphoid process or to the right of it. Often there is a combination of pain immediately after eating with "hungry" and "night" pains.
The secretory and acid-forming functions of the stomach are usually enhanced, but less than with a duodenal ulcer: the amount of basal secretion is up to 10 meq / hour, and the maximum is 35 meq / hour (Yu. I. Fishzon-Ryss, 1972). Abundant gastric secretion is often observed at night.
Chronic gastritis with secretory insufficiency more common in people of mature and old age. In patients, weight usually decreases, weakness appears, symptoms of multivitamin deficiency are revealed - dry skin, loosening and bleeding of the gums, changes in the tongue (thickening, redness, flattened papillae, the presence of dental prints), cracks on the lips, in particular in the corners of the mouth. Of the gastric symptoms, a violation of appetite and a desire to eat spicy and spicy food outside the period of exacerbation are noted. Some patients cannot take solid food without liquid, which they drink before and during the meal. Patients note an unpleasant taste in the mouth, especially in the morning, nausea, a feeling of fullness and distention in the epigastric region, belching with air. The stool is unstable, with a tendency to diarrhea. Dyspeptic symptoms usually occur soon after eating, especially poorly patients tolerate milk. In some cases, nausea and salivation are persistent and painful for patients, and they seek to alleviate their condition with frequent meals. Sometimes there is pain in the epigastric region.
Complications - hypermotor dysmnesia of the intestine or involvement in patol, the process of the pancreas and gallbladder. Gastric bleeding is rare. Some patients show allergic reactions to certain food and medicinal substances.
Sometimes (more often in women) iron deficiency anemia develops (see). Changes in the intestines are often noted, the exocrine function of the pancreas decreases, dysbiosis develops (see), manifested by fermentation or putrefactive dyspepsia.
Special forms hron. G. (rigid, polypous and giant hypertrophic) differ in originality a wedge, manifestations and morfol, features. Some researchers attribute these forms to complications hron. G.
Rigid gastritis first described by A. N. Ryzhikh and Yu. N. Sokolov (1947). It is manifested by persistent dyspepsia (see) and achlorhydria (see). The diagnosis is established with rentgenol. research and based on gastroscopy data. The outlet section of the stomach is mainly affected, which, due to hypertrophic changes, edema and spastic contraction of the muscles, is deformed, turning into a narrow tubular canal with dense rigid walls.
Polypoid gastritis(tsvetn. fig. 8) usually develops against the background of atrophic G. with histamine refractory achlorhydria, it can be considered as further progression hron. G. (dysregenerative hyperplasia of the mucous membrane).
Giant hypertrophic gastritis, or rather excessive development of the mucous membrane, described by P. Menetrier (1886), is a relatively rare disease, manifested by metabolic disorders (usually protein) and very rarely by the development of iron deficiency anemia. The change in the acid-forming function of the stomach is different (see also table).
The diagnosis is based on the analysis of a wedge, manifestations of the disease, the results of a study of gastric secretion (see. Stomach, research methods), rentgenol, research, gastroscopy data (see) and gastrobiopsy.
In the assessment of morfol, the picture of the gastric mucosa, gastrobiopsy data should be preferred. Exfoliative cytodiagnostics, determination of the absorption and excretory functions of the stomach are of secondary importance.
Certain difficulties arise in differential diagnosis with functional disorders of the stomach, stomach cancer (see. Stomach, tumors) and peptic ulcer disease (see).
With functional disorders of the stomach, there are usually no sharp morfol, changes. In addition, they have a relatively short-term (up to 1 year) course, less dependence of the occurrence of pain on food intake, greater variability of the wedge. manifestations, which is associated with neuropsychic influences, atypical localization of pain on palpation of the abdomen and, finally, a sharp fluctuation in acidity in individual studies.
X-ray diagnostics is based on a thorough rentgenol, examination of the stomach. At the same time, changes in the relief of the gastric mucosa and other X-ray functional and morfol, symptoms are determined. These include: excessive fasting secretion, rapid growth of secretory fluid, changes in tone, persistent deformation of the pyloric part of the stomach, impaired peristalsis, etc. The most constant symptom of increased fasting secretion, sometimes manifested by a horizontal fluid level against the background of the gastric bladder before taking barium suspension. The first one or two sips of barium suspension confirm the presence of excess liquid. By the nature of the mixing of barium with a liquid, one can, to a certain extent, judge the amount of mucus contained in it: slow mixing with the formation of shapeless flakes indicates the presence of mucus. Another symptom of the presence of mucus (the phenomenon of mucus) is small-point enlightenment in the layer of barium suspension - the smallest droplets of mucus suspended in a suspension of barium. The mucus phenomenon is indistinguishable when translucent and can only be ascertained on images with compression. Chron. G. is often accompanied by a decrease in stomach tone. The increase in tone is often local in nature; at antral G. it is manifested by spastic conditions or motor excitation of the output part of the stomach. Violation of the peristaltic function is not always detected. In about half of the cases hron. G. superficial and rare peristalsis is observed. Pronounced disorders of peristalsis up to the appearance of the aperistaltic zone are observed with the so-called. rigid antral G. Evacuation of barium from the stomach usually occurs within normal periods, although occasionally it can be slowed down.
Forms hron. G. radiographically differ hl. arr. by the nature of the relief of the mucous membrane. According to Schindler's classification - Gutzeit, there are: hypertrophic G., atrophic G., mixed G., superficial hron, mucous catarrh. In turn, hypertrophic G. has subspecies: polypous, warty, ulcerative, or erosive. However, this classification is outdated and needs to be revised, since the inaccuracy of rentgenol has been proven. criteria for mucosal hypertrophy and atrophy; besides, at hron. G., as a rule, atrophic processes progress.
Based on the capabilities of rentgenol. the method is distinguished: hron, universal G., hron, antral G. and its wedge, and rentgenol, varieties (including rigid antral G.); hron, polypous (warty) G .; hron, granular G .; erosive G .; so called. accompanying gastritis (concomitant), for example, with peptic ulcer.
Rentgenol, data cron. G. can be taken into account only at the corresponding wedge, picture, anamnesis, etc. Numerous facts are known when expressed rentgenol, G.'s symptomatology was not confirmed by biopsy data and, conversely, morphologically proven G. did not appear radiologically.
At hron, universal G. the area of the rebuilt relief is usually very extensive (the body of the stomach is also captured). As a result of edema, hyperemia and inflammatory cell infiltration, mainly of the submucosal layer and connective tissue stroma, the folds of the mucous membrane swell unevenly (Fig. 4 and 5), sometimes so significantly that their number decreases. In places, the folds form polyp-like thickenings and have a distinct appearance (Fig. 6). Along the greater curvature, the oblique and transversely located bridges between the folds thicken, therefore the contour of the large curvature, Ch. arr. the lower half of the body of the stomach and sinus, becomes serrated and fringed. With severe edema, the mucous membrane loses its plasticity, which is accompanied by a symptom of relief rigidity. Inflammatory restructuring of the relief of the mucous membrane at hron. G. is sometimes so disordered and chaotic that it is difficult to distinguish it from the atypical relief in stomach cancer. Only a series of sighting images of the relief of the mucous membrane help to establish the still preserved variability of its pattern. In difficult cases, it is useful to resort to pharmacol, stimulation of peristalsis (morphine).
The described changes in the relief of the mucous membrane are not specific for G. Similar pictures can occur with allergic edema of the mucous membrane, with systemic diseases, etc.
Chron, antral G. refers to the most often found varieties hron. D. It has a bright, diverse, and most importantly the most convincing roentgenosemiotics. Rentgenol, the picture is characterized by signs of hypersecretion, the phenomenon of mucus, patol, restructuring of the relief of the mucous membrane. In addition, a deformation of the antrum and a violation of its peristalsis are found. The relief pattern varies: more often sharply swollen, widened folds, but retaining the usual longitudinal direction, their number is reduced. With pronounced edema, they form shapeless, pillow-like defects in the relief, the grooves between the folds disappear, the relief is smoothed out. A classic example of a relief at hron. G. of the antrum are rather persistently persistent thickened transverse folds of the mucous membrane (Fig. 7), along the greater curvature of the stomach - an irregularity of the contour in the form of uniform serration. With a long flowing hron. G. with secretory insufficiency, the relief is disordered and consists of shapeless bulges (defects) and spots and strips of barium chaotically located between them. In some cases, atypism of the relief occurs due to the increased mobility of the swollen mucous membrane of a relatively loose, inflammatory altered submucosa. With a wide pyloric canal, partial prolapse of the mucous membrane into the duodenal bulb is possible. With a normal lumen of the pylorus, the gastric mucosa does not fall out. However, periodically "sliding" mucous membrane, accumulating in front of the gatekeeper, here forms a kind of defect, reminiscent of a tumor lesion (Fig. 8). This "phenomenon of crawling" of the mucous membrane was first explained and described by Yu. N. Sokolov and VK Gasmaeva (1969).
Due to the thickening of the circular and longitudinal muscles, the antrum of the stomach is deformed: it narrows and shortens, in contrast to the deformity in infiltrating cancer, when the lumen of the pyloric part of the stomach only narrows, but does not shorten. As the process progresses, the walls of the antrum become thicker, lose elasticity, and the deformation becomes persistent. As a result of inflammatory submucosal sclerosis (the so-called sclerosing G.) peristalsis disappears and rigid antral G. arises, which, undoubtedly, is a late stage hron, antral G. with secretory insufficiency. At these patients quite often on the basis of a wedge, data suspect stomach cancer, which is often difficult to refute at rentgenol, research. The deformation of the antrum is very pronounced and persistent. Attention is drawn to the circular narrowing of the pyloric part of the stomach, while its simultaneous shortening often remains unnoticed (Fig. 9). On palpation, a feeling of a dense and painful tumor is created. The presence of cancer is indicated by a symptom of the aperistaltic zone, usually covering the entire antrum. The observation of at least short-term peristalsis testifies against cancer, edges can also be caused with the help of morphine.
At polypous (warty) G. patol, changes are often localized in the antrum. They represent multiple, uniform in size, rounded, blurred defects to dia. 3-5 mm, sometimes in the form of elevations on the crests of the folds, but more often forming a disorderly or honeycomb pattern (Fig. 10). With true polyps, even multiple ones, the relief of the gastric mucosa is usually not changed. At polypous G., as a rule, other rentgenol, symptoms are also found. At smaller growths G. is called warty, or verrucous; small defects are usually recognized only on sighting images with compression.
Granular gastritis is recognized by the symptom of "granularity" of the relief (Fig. 11). This symptom was studied by W. Frik using images of the relief of a sharp-focus X-ray tube at short exposures(no more than 0.1 sec.). This creates the impression of a granular surface of the mucous membrane with the smallest elevations - the so-called. gastric fields. Comparison of the data of the study of "fine relief" with the results of gastrobiopsy revealed a parallelism between the picture of the gastric fields and the presence of inflammatory changes in the mucous membrane. If under normal conditions the diameters of the fields are 0.5-1.5 mm, then with chron. G. gastric fields become more convex - "granular" type, and in advanced cases - and larger (dia. 3 mm and more), uneven, reminiscent of a warty surface. Along with this symptom, it is necessary to detect other rentgenol described above, G.'s signs.
Erosive G. is rarely recognized roentgenologically, since the possibilities of identifying erosions rentgenol are very limited by the research method.
The so-called. accompanying (accompanying) G. is radiologically constantly found in case of peptic ulcer disease (the exception is the so-called senile stomach ulcers) and less often in case of stomach cancer.
The expressed pictures of accompanying G. are observed with duodenal ulcer, after gastroenterostomy operation. At accompanying G. the outlet part of the stomach is more often amazed. All of the above-described rentgenol are also observed. G.'s symptoms. Often there is a rough drawing of the relief of the mucous membrane, disorder and swelling of the folds. Dynamic wedge. - rentgenol, observations of accompanying G.'s course at peptic ulcer show that if under the influence of conservative treatment the ulcer "niche" disappears, and other rentgenol, G.'s symptoms remain unchanged, then, as a rule, patients do not notice improvement.
At rentgenol, research, the recognition of polyposis G., which should be differentiated with true polyps of the stomach, can present known difficulties. When diagnosing hron. antral G. it is necessary to keep in mind also pernicious anemia, at a cut polymorphic changes in the relief of the mucous membrane of the pyloric part of the stomach can be observed.
In addition to rigid antral gastritis, it is necessary to take into account other types of antral G. with a sharp restructuring of the relief of the mucous membrane, which is sometimes indistinguishable from the atypical relief in cancer. Of particular importance in this sense is the "mucosal crawling phenomenon" described above. In case of difficulties, a series of images or X-ray cinematography, fibroscopy and gastrobiopsy are used. With the so-called. systemic diseases only a thorough analysis of the entire wedge, pictures allows you to come to the correct diagnosis.
See also Stomach, X-ray diagnostics.
Treatment complex and differentiated. Usually, treatment is carried out on an outpatient basis; patients are hospitalized with exacerbations, especially those occurring with complications and severe general disorders.
Health food in G.'s complex therapy is of leading importance. During an exacerbation hron. G., regardless of the nature of secretory disorders, observe the principle of sparing the gastric mucosa and its functions. Food should be well cooked and chopped. Products and dishes that have a strong sokogonny effect, as well as causing mechanical, thermal and chemical, are excluded from the diet. irritation of the gastric mucosa. Prescribe a diet 1A (see Nutritional Medicine). Food is fractional, 5-6 times a day. As the exacerbation subsides, diet therapy is carried out in accordance with secretory disorders.
In case of secretory insufficiency of the stomach (outside exacerbations), the diet should be complete with a sufficient amount of proteins (110-115 g), fats (80-90 g), carbohydrates, vitamins; it should correspond to the calorie content of work and the patient's lifestyle. Prescribe diet number 2. Food must be taken 4-5 times a day. The diet includes normal amount table salt and extractives. With persistent remission, extended nutrition can be prescribed. Fresh bread and other fresh dough products, fried (including boneless in breadcrumbs) meat and fish, fatty meats and fish, spicy, salty dishes, canned fish, cold drinks, ice cream are prohibited.
With normal and increased secretion, they begin with the appointment of table 1A, after 7-10 days they switch to table 1B, and after the next 7-10 days - to diet No. 1. The diet should be complete, but with restriction of table salt, carbohydrates and extractives, especially with increased acidity. Dairy laxatives (fresh kefir, yogurt) are recommended at night. Cabbage soup, borscht, fatty meat are prohibited, Fried fish, salted, smoked, pickled vegetables, not grated. Alcohol, beer, carbonated water, fruit water are strictly contraindicated.
Medical treatment of sick hron. G. provides for the impact on pathogenetic links patol, process. To normalize the functional state of the higher sections of the c. n. With. recommend valerian preparations, small tranquilizers, sleeping pills.
With an increased secretory and motor-evacuation function of the stomach, anticholinergic drugs (atropine, platifillin, spasmolitin, benzohexonium) in combination with antacids (vicalin, almagel, etc.) and agents that stimulate regenerative processes (methyluracil, pentoxil, licorice preparations, etc.) should be prescribed. ).
With secretory insufficiency, anticholinergic drugs are prescribed, similar to quateron and gangleron, which cause a pronounced antispasmodic effect, but have relatively little effect on the secretory function of the stomach. A good wedge, the effect is achieved with the use of Caucasian dioscorea, plantain juice, plantaglucide, which cause a slight increase in secretion, enhance the motor function of the stomach and have anti-inflammatory and antispasmodic effects. In order to influence the secretory function of the stomach, vitamins PP, C, B 6 and B 12 are also prescribed.
Outside the period of exacerbation, substitution therapy is used - gastric juice, abomin, betacid, pancreatin, etc.
Physical methods of treatment are also included in the complex to lay down. activities: heating pads, mud therapy, diathermy, electro- and hydrotherapy.
Sanatorium treatment of patients with chronic gastritis is carried out without exacerbation of the disease. Shown are the resorts with mineral waters for drinking treatment: Arzni, Arshan, Berezovskie mineral water, Borjomi, Izhevsk, Jalal-Abad, Jermuk, Druskininkai, Essentuki, Zheleznovodsk, Pyatigorsk, Sairme, Feodosiya, Shira, etc. Mineral waters can also be used in out-of-resort conditions: in case of secretory insufficiency, it is preferable to use chloride, chloride-bicarbonate waters for 15 20 minutes. before meals, and with normal and increased secretory function - bicarbonate waters 1 hour before meals.
Treatment hron. G. is possible in local sanatoriums, as well as in the usual regime, subject to dietary conditions.
The prognosis for life is favorable. Under the influence of treatment, the well-being of patients relatively quickly improves. But the main morfol, changes characteristic of hron. G., like the secretory function of the stomach, does not normalize under the influence of treatment. At massive bleeding in patients hron. G. with normal and increased secretion, the prognosis is more serious, as well as in patients with insufficient secretory function when they develop anemia, gastritis enterocolitis with impaired absorption processes and involvement in patol, the process of other organs of the digestive apparatus (hron, pancreatitis, hron, cholecystitis, etc.). With special forms hron. G. (rigid, polypous, giant hypertrophic) there is a danger of malignancy.
Prevention hron. G. consists in rational nutrition and observance of food hygiene rules, as well as in the fight against the consumption of alcoholic beverages and smoking. It is necessary to monitor the state of the oral cavity, timely treat diseases of other organs of the abdominal cavity, eliminate occupational hazards and helminthic-protozoal invasions. Great importance has a clinical examination of patients G.
Gastritis in children
Acute gastritis in children occurs as a result of infection, the consumption of infected, difficult to digest food, overeating and as a manifestation of allergies. Its etiology, clinic and treatment methods are similar to acute gastritis in adults.
Chronic gastritis occurs mainly in preschool and school age; its prevalence in school-age children is higher.
The causes of occurrence hron. G. are irrational nutrition and regimen, various diseases of the digestive and other systems, infection, allergies, as well as congenital features of the neuro-endocrine system and a violation of the synthesis of hydrochloric acid, which is confirmed by the presence of persistent achilia (in practically healthy and sick children of G.), to -It can not be explained by any illness or nutritional deficiencies.
At children with long-term diseases and disorders went. - kish. path hron. G. as an independent disease is rarely observed. At the same time, the study of the gastric mucosa by the gastrobiopsy method changed the idea of G.'s prevalence in children: a wedge, G.'s diagnosis is confirmed only in half of the cases. Children of senior school age and adolescents have hron. G. becomes a fairly frequent disease.
Morphologically, superficial G. and gastritis with defeat of glands without atrophy prevails in children, atrophic G. is less often observed (some authors do not find it in children).
The disease usually occurs gradually, has relatively little effect on the development of the child, has a milder course than in adults, and is easier to treat; sometimes there is a persistent course.
There are two forms of hron. G. in children - malosymptomatic and a form with severe symptoms, often similar to peptic ulcer disease. The asymptomatic course of G.
Malosymptomatic form hron. G. is less common than a form with severe symptoms; often occurs in children with more early age: pain usually appears after eating, low intensity, localized in the epigastrium or diffuse. Dyspeptic symptoms are absent in some children. The acid-forming function of the stomach is reduced or histamine reflex achilia is determined.
With hron. G. with severe symptoms, the pain symptom is intense, can occur immediately after a meal, after 1 - 2 hours or at night. Dyspeptic symptoms are persistent. Acid-forming function in most sick children is increased during long-term follow-up. In some children, peptic ulcer disease comes to light in the future, in this case G. is essentially a pre-ulcer state.
G.'s diagnosis is established on the basis of anamnesis data set, a wedge, manifestations and laboratory tests.
Differential diagnosis hron. G. at children is carried out with a peptic ulcer (see), liver diseases (see), bile ducts (see Bile ducts) and diseases of the nervous system. Taking into account the exceptional rarity of malignant neoplasms of the stomach in children and an easier course of hron than in adults. G., there are no sufficient grounds for widespread use in pediatric practice of the gastrobiopsy method for diagnostic purposes. It is used only for strict indications and necessarily in a specialized clinic in order to exclude possible complications.
Treatment of gastritis in children is basically the same as in adults (taking into account the age and form of the disease).
At G., similar in clinic to peptic ulcer, treatment is carried out as antiulcer, including seasonal preventive courses.
Prevention hron. G. in children has the same principles as in adults.
Constitutionally weakened children with signs of dysfunction demanded special attention went. - kish. tract (increased acid-forming function, achilia, etc.), with residual effects after diseases of the digestive and other systems.
Sick hron. D. children are subject to supervision by a pediatrician in order to prevent exacerbations of the disease, to carry out prophylactic anti-relapse courses of treatment and recreational activities.
Gastritis in old and old age
Features of G.'s course are due to age-related changes digestive organs and a decrease in general reactivity. Wedge, G.'s manifestations in elderly and senile patients are less pronounced than in young ones. Dyspeptic symptoms and pain are relatively little expressed, and a decrease in appetite is rarely observed. The digestive ability of gastric juice and the content of gastromucoproteins in it are reduced, as is the acid-forming function of the stomach. The electrophoretogram of gastric juice proteins, in comparison with the electropherogram of young patients, has a more "compressed" appearance, the debit of the protein component is lower in both fractions of gastric mucus, and the carbohydrate component is increased in insoluble mucus. A vitreous basal secret is often found - a jelly-like mass with a large number of desquamated cells of the mucous membrane. Atrophic changes in the gastric mucosa (according to aspiration biopsy) and secretory insufficiency are found in patients hron. G. over the age of 60 is 2-3 times more often than among 30-40-year-olds. After 60 years, atrophic G. is more often observed in women, while at a younger age - more often in men. The great prevalence of atrophic G. in old age is connected, apparently, with the frequent development at this age hron, diseases of the liver, pancreas, intestines, promoting development hron. G.
Treatment and prevention are based on the accompanying hron, diseases and characteristics of the reaction of the elderly organism to the introduction of medicinal substances. When determining the forecast, one should bear in mind the possibility of cancer on the background of hron, atrophic G.
Experimental gastritis
In order to study the patterns of activity and mechanisms of regulation of the digestive system in conditions of pathology, as well as to develop issues of therapy, G. on animals reproduce G.
There are two groups of models of experimental G., which are used depending on the objectives of the study: a) G. caused by local action of various damaging agents on the gastric mucosa; b) G. caused by unusual conditions of contact of normal acidopeptic factors with the gastric mucosa.
To damage the gastric mucosa of animals, use hot and cold water, as well as chem. substances (1 - 10% silver nitrate solution, 1% acetic acid and 10% hydrochloric acid, alcohol solutions, infusion of mustard, red pepper, etc.), which are injected once or repeatedly into the stomach cavity. With such an effect of a damaging agent, it cannot be ruled out that it gets into the initial section of the duodenum, which complicates the picture of functional and morfol, disorders and cannot always be taken into account. There are techniques of limited damage to the gastric mucosa, which reproduce focal G., usually acute. At repeated damages, experimental acute G. can pass into hron, form. Of practical interest in the models of this group is experimental gastritis caused by the introduction into the stomach of various volumes of alcohol of different concentrations.
IP Pavlov created models of experimental G., directly damaging the stomach and observing the work of an isolated ventricle. He established the compensatory ability of the preserved mucous membrane, analyzed in detail the complex complex of intrasystemic and extrasystemic reactions in the body in response to damage to the stomach. IP Pavlov initiated the classification of types of gastric secretion disorders, which is used in the clinic.
G.'s model caused by the creation of nephysiol. the conditions of contact of normal secretion products of the gastric glands (acidopeptic factors) with the mucous membrane, is achieved by prolonged repeated imaginary feeding (gastric juice remains in the stomach cavity), by adding salt to food or gastric juice in excess. Experimental violation fiziol. the ratio between free and bound hydrochloric acid in the stomach also has a damaging effect on the mucous membrane.
Experimental G. can also be caused by a change in the spectrum of proteolytic enzymes or the introduction of histamine or pilocarpine. This G.'s model develops gradually against the background of microcirculation disturbances and trophic processes in the mucous membrane, has hron, current.
Clinical and diagnostic characteristics of some clinical forms of chronic gastritis
|
chronic gastritis |
Main clinical signs |
Gastric secretion study data |
radiological research |
Gastroscopy data |
Biopsy data |
|
Antral |
Pains in the epigastric region are hungry, nocturnal, sometimes subsiding after eating; heartburn, sour belching, often vomiting at the height of pain. Constipation tendency |
Increased |
The relief of the mucous membrane in the antrum is changed: thickening of the longitudinal folds, patol. restructuring, granular formations, the presence of the phenomenon of mucus. Increased tone and weakening of the peristalsis of the antrum. Signs of hypersecretion. Often, deformity of the antrum |
In the pyloric part of the stomach, redness of the mucous membrane, swelling of the folds, erosion and hemorrhage in the submucous layer are found. The tone of the pyloric part is enhanced, sometimes there is a prolonged pyloric spasm. Signs of hypersecretion |
Gistol, the picture of the mucous membrane is normal or has signs of hron, gastritis of varying severity. In the antrum - signs of hyperplasia, often a rare location of the pyloric glands, pronounced cellular infiltration of its own layer, areas of intestinal metaplasia |
|
Giant hypertrophic gastritis (Menetrie's disease) |
Weight loss, signs of hypoproteinemia, iron deficiency anemia. Obstinate gastric dyspepsia. Patients report a feeling of spasm and pressure in the epigastric region. The pains sometimes resemble those of a peptic ulcer; vomiting may be mixed with blood |
Decreased, normal or increased |
Pronounced changes in the relief of the mucous membrane along the greater curvature (in the sinus and the lower half or third of the body of the stomach) in the form of overly spaced, elastic thickened folds hanging down into the lumen of the stomach, and sometimes into the duodenum |
The mucous membrane is swollen, with wide winding folds covered with mucus, sometimes with warty, polypoid growths |
Hyperplasia of all elements of the mucous membrane |
|
Gastritis with normal and increased secretory function |
The general state does not change. Pain in the epigastric region occurs immediately after eating, combined with a feeling of heaviness, overflow. The pains are diffuse, dull, aching, usually moderate, less often intense, last 1 - 11/2 hours. Heartburn, often belching with air, intermittent vomiting |
Basal secretion increases to 10 meq / hour, maximum histamine secretion - up to 35 meq / hour. Abundant gastric secretion is often observed at night |
Widespread restructuring of the relief of the mucous membrane with thickening of the folds (sometimes their pillow-like bulging) until the grooves disappear; smoothness of the relief in the antrum. Violation of tone and peristalsis. Signs of hypersecretion |
Redness, hypertrophy of folds, edema, the presence of mucus, single erosion and hemorrhage in the submucosa, signs of hypersecretion. With severe hypertrophy, the mucous membrane has a velvety appearance without the usual shine |
Flattening of the mucous membrane due to hyperplasia of the superficial epithelium, less often interstitial tissue. The epithelium is often flattened, with a basal arrangement of nuclei of various sizes; hypersecretion with flour yes, signs of granular and vacuolar degeneration; abundant cellular infiltration of its own layer |
|
Polypoid |
Reminds clinic hron, gastritis with secretory insufficiency; can be asymptomatic. The prolapse of polyps into the duodenum and their infringement is clinically manifested by a pronounced pain syndrome. Bleeding may occur |
More often reduced |
Typical changes are more often localized in the antrum - typical small uniform rounded filling defects, sometimes on the crests of the folds, but usually they form a disorderly or honeycomb pattern. With true polyps, even multiple ones, the relief of the mucous membrane is usually not changed. |
Found multiple polyps, the same or different in shape and size, which are often located in the pylorus. The mucous membrane is pale, thinned, its folds are smoothed, translucent blood vessels(atrophic gastritis) |
Outside the localization of the polyp, the picture of atrophic gastritis |
|
Rigid |
Prolonged persistent dyspepsia. In the epigastric region, patients note diffuse moderate pain, often a feeling of heaviness and pressure. There is a tendency to diarrhea and the development of anemia |
Sharply reduced |
Deformation (narrowing, shortening) of the antrum, restructuring of its internal relief; weakening or disappearance of peristalsis |
Deformity, rigidity and narrowing of the pyloric stomach, edema of the mucous membrane |
In the output section, there is a picture of atrophic and hyperplastic hron, gastritis. In other departments, atrophy of the glandular apparatus of varying severity |
|
Gastritis with secretory insufficiency |
Weight loss and decreased appetite, feeling of heaviness and pressure in the epigastric region after eating. Moderate and intermittent pain, nausea, rarely vomiting. Tendency to diarrhea, flatulence; poor milk tolerance, without exacerbation - addiction to sour and salty foods. Often anemia |
Basal secretion approx. 0.8 meq / hour, maximum histamine secretion up to 10 meq / hour |
The relief of the mucous membrane is smoothed, tone and peristalsis are often weakened, the evacuation of stomach contents is accelerated |
Diffuse or focal thinning of the mucous membrane, its color is pale, dilated blood vessels of the submucosa are clearly visible. The folds of the mucous membrane are small, in places covered with mucus, when the stomach is inflated with air, the folds are easily smoothed out. Erosions and punctate hemorrhages are sometimes observed |
Various degrees of glandular atrophy (decrease in the main and parietal glandulocytes), flattening of the epithelium of the mucous membrane, deepening of the fossae, intestinal and pyloric metaplasia |
|
Erosive gastritis (hemorrhagic) |
Pain in the epigastric region: early, fasting and late; acidic heartburn, sometimes vomiting mixed with blood (from traces to clots). The higher the acidity, the more often bleeding Tendency to constipation |
Normal or elevated |
The relief of the mucous membrane is changed more often in the pylorus of the stomach. Erosion detection capabilities are very limited |
Multiple erosions of a round or stellate shape are determined, mainly in the outlet of the stomach, against the background of the phenomena of superficial gastritis - edema, infiltration, hyperemia of the mucous membrane |
Gistol, the picture of the mucous membrane is more often similar to the picture of hron, gastritis with increased secretion. Erosions are more often detected with targeted biopsy |
Bibliography: Aruin LI Morphological study of biopsies of the gastric mucosa, Arkh. patol., t. 31, No. 3, p. And, 1969; Aruin L. I. and Sh and -r about in V.G. To the question of the morphogenesis of chronic gastritis, in the same place, t. 33, No. 10, p. 21, 1971; Belousov AS Essays on functional diagnostics of diseases of the esophagus and stomach, M., 1969, bibliogr .; Gordon OL Chronic gastritis and so-called functional diseases of the stomach, M., 1959, bibliogr .; Gubar V. L. Physiology and experimental pathology of the stomach and duodenum, M., 1970; Kanishchev P. A. Methods of diagnosis of diseases of the stomach, L., 1964; Lazovsky Yu. M. Functional morphology of the stomach in norm and pathology, M., 1947; Levin GL Sketches of gastric pathology, M., 1968; L and with about h to and B. G. N., Ultrast ^ structure of the glands of the stomach and its change in conditions of chronic gastritis, Arkh. patol., t. 34, No. 10, p. 11, 1972; Masevich Ts. G. Aspiration biopsy of the mucous membranes of the stomach, duodenum and small intestine, L., 1967; about N e, Pre-tumor diseases of the stomach, L., 1969, bibliogr .; Menshikov FK Diet therapy, M., 1972, bibliogr .; Pavlov I.P. Complete Works, vol. 2, book. 2, M.-L., 1951; Peleschuk A. P. Diseases of the system and digestive organs, in the book: Fundamentals of gerontol., Ed. D.F. Chebotareva and others, p. 322, M., 1969; Rachvelishvi-l and B. X. Gastrobiopsy in clinical practice, Tbilisi, 1969; P y with with SM Diseases of the digestive system, L., 1966; Tugolukov VN Modern methods of functional diagnostics of the state of the gastric mucosa and their clinical significance, L., 1965; F and sh-z about N-P y with Yu. I. Modern methods of research of gastric secretion, L., 1972, bibliogr .; about N e, Gastritis, L., 1974, bibliogr .; In about with k u s H. Gastroenterology, at. 1-3, Philadelphia-L. * 1963-1965; Gastritis, hrsg. v. G. Clemenson, Basel, 1973; HafterE. Praktische Gastroenterologie, Stuttgart, 1962, Bibliogr .; M o r s o n B. C. a. Davson I. M. P. Gastrointestinal pathology, p. 80, Oxford, 1972, bibliogr .; Peleschtschuk A. P. u. a. Funktionelle und morphologische Veranderungen des Magens bei Pa-tienten mil umunischer Gastritis im hohe-ren Lebensalter, Z. Alternsforsch., Bd 25, S. 271, 1972; Schindler R. Gastritis, N. Y., 1947, bibliogr .; Spiro H. M. Clinical gastroenterology, p. 155, L., 1970; Wolff G. Chronische Gastritis, Lpz., 197 4.
X-ray diagnostics G.- Ryzhikh AN and Sokolov Yu. H. Rigid antral gastritis as a precancerous disease of the stomach, Surgery, No. 4, p. 34, 1947; Saghatelyan G. M. X-ray diagnostics of diseases of the esophagus, stomach and gastroscopy, Yerevan, 1966, bibliogr .; Smirnova NV Diagnostics of gastritis of the distal stomach, Wedge, medical, t. 49, No. 1, p. 69, 1971; With about to about l about in Yu. N. and V l and with about in P. V. Relief of the mucous membrane of the stomach is normal and pathological, M., 1968, bibliogr .; Sokolov Yu. N. and Gasmaev VK About the phenomenon of "crawling" of the gastric mucosa, Vestn, rentgenol, and radiol., No. 2, p. 66, 1969; Sokolov Yu.N. id r. Our experience in the study of the fine relief of the stomach in chronic gastritis, ibid., No. 5, p. 3, 19 73, bibliogr .; Tikhonov KB and Pruchansky VS Microrelief of the gastric mucosa and its significance in the diagnosis of chronic gastritis, ibid., No. 2, p. 82, 1970, bibliogr .; F and N and r d-sh I V. A. N. Radiodiagnosis of diseases of the digestive tract, t. 1, Yerevan, 1961; Sh l and f er I. G. Relief of the mucous membrane of the stomach and duodenum, Gastritis, ulcer, carcinoma, b. m., 1935, bibliogr .; Cummack D.H. Gastrointestinal X-ray diagnosis, Edinburgh - L., 1969; Pr £ v6t R. u. L a s r i c h M. Rontgendiagnostik des Magen-Darmka-nals, Stuttgart, 1959, Bibliogr.
G. in children- Balashova TF Enzyme-forming function of the stomach in chronic gastritis in children, Pediatrics, No. 5, p. 14, 1971; And in scarlet about in SM, etc. Endocrine cells of the gastric mucosa in children, in the same place, No. 3, p. 12, 1975, bibliogr .; Queen R. I. and Bialik V. L. O diagnostic value aspiration biopsy of the gastric mucosa in chronic gastritis in children, ibid., JNft 12, p. 22, 1966; Cossure M. B. Diseases of the stomach in children, M., 1968, bibliogr .; Lukyanova EM, Korole-z in and RI and Shly to about in IA Endoscopic studies of the stomach in chronic gastritis in children, Pediatrics, No. 3, p. 17, 1975; Multivolume Guide to Pediatrics, ed. Yu. F. Dombrovskaya, vol. 4, p. 191 and others, M., 1963; About s tr about polo-lets S. S. and others. Morphological day-n1st of small gastritis with normal i shdvshtsenoy secretory function of the shlun-ka at d1tey, Ped1at., Obstetrician. i gshek., no. 4, p. 3, 1975; Samarina G. Ya. Clinical features of antral gastritis in children, Vopr. okhr. mat. and children., v. 18, no. 6, p. 23, 1973; Smirnov H. M. Chronic gastritis in children, Minsk, 1967, bibliogr .; Sandberg D. N. Hypertrophic gastropathy (Menetrier's disease) in childhood, J. Pediat., V. 78, p. 866, 1971; Sedl & ckov & M. a. Bedn £ r B. Chronic gastritis in childhood, Gastroenterologia (Basel), v. 107, p. 251, 1967.
F. I. Komarov; L. I. Aruin (pat.an.), M. B. Cossyura (ped.), H. N. Lebedev (pat. Phys.), A. P. Peleschuk (geront.), Yu. N. Sokolov ( rent.), the compiler of the table F.I.Komarov.
9. What is, on average, the total duration of the first three stages of development of lobar pneumonia?
10. Specify the ways of spreading inflammation in lobar 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 tidal 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 lobar pneumonia in the stage of gray hepatization.
15. Specify the extrapulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.
16. Give the macroscopic characteristics of changes in the lungs with bronchopneumonia.
17. Give a microscopic characterization of changes in the lungs with focal pneumonia.
18. Name the features of the causative agents of nosocomial pneumonia.
19. Name the 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. Give a definition of the term atelectasis.
24. What develops when the airway 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 the 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 to 390C, chills, dagger pain in the right side and severe weakness for 7 days. Objectively: a dull sound is heard above the lower lobe of the right lung during percussion, during auscultation, breathing is not performed, a pleural friction noise is heard. Radiographically - darkening of the lower lobe of the right lung, in the region of the 8th segment there is a 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 small bubbling rales in the lower parts of the left lung. Your conclusion.
30. A 67-year-old man who is inpatient treatment for phlegmon of the scalp developed shortness of breath, coughing, and his body temperature rose to 38.50C. 4 weeks after the massive antibiotic therapy, the body temperature dropped, dyspnea decreased, and moderate leukocytosis persisted. During an X-ray examination, an annular shadow with a fluid level appeared in the second segment of the right lung. Your diagnosis.
II lesson
CHRONIC NON-SPECIFIC LUNG DISEASES. INTERSTITIAL LUNG DISEASES. PNEUMOCONIOSIS. 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 characteristics.
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, beryllium). 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 lung infiltrate. 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.
vol. 2, part I: p. 415-433, 446-480.
vol. 2, part I: pp. 293-307, 317-344.
4. Guide to practical training in pathological anatomy (2002) p. 547-567.
5. Atlas on pathological anatomy (2003) p. 213-217.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of the main forms of chronic lung diseases using macrospecimens, microspecimens and electronograms and conduct 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 BRONCHEECTASES, LUNG EMFYZEMA.
Micropreparation No. 12 CHRONIC DEFORMAL BRONCHITIS (staining with hematoxylin and eosin). To note the components of chronic inflammation of the bronchi: peribronchial sclerosis, vascular pericalibration, inflammatory infiltration in the wall of the bronchi 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
Macrodrug ANTHRAKO-LUNG SILICOSIS. Pay attention to the change in volume and decrease in the airiness of the lung tissue. To characterize the sclerotic areas in the lung: their shape, size, color, prevalence.
Micropreparation No. 000 LUNG ANTHRAKO-SILICOSIS (staining with hematoxylin and eosin). Outline the structure of the silicotic nodule, concentrically located collagen fibers around the sclerosed vessels. Pay attention to the 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 macro-preparations determine the forms of growth and localization cancerous tumors in the lungs.
Micropreparation No. 33 SQUAT CELL LUNG CANCER (staining 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 Lesson
Bronchiectasis- chronic pathological expansion of the bronchi.
Obstructive pulmonary disease- a group of diseases characterized by obstruction of the airways.
Restrictive lung diseases- a group of diseases characterized by the predominance of restrictive (restrictive) changes, usually in the intermediate tissue.
Pneumoconiosis- the general name for occupational lung diseases caused by exposure to industrial dust.
Epidermoid cancer- squamous cell carcinoma.
Hammen-Rich syndrome- idiopathic pulmonary fibrosis, diffuse fibrosing alveolitis, chronic interstitial pneumonitis.
Emphysema- excessive and stable expansion of the airways and respiratory structures located distal to the terminal bronchioles.
Bullous emphysema- emphysema, characterized by the formation of large subpleural bubbles (bullae).
Emphysema vicar (compensatory)- emphysema, which develops with the loss of a significant part of the lung (for example, with pulmonectomy, lobectomy).
Interstitial emphysema (interstitial)- emphysema, localized in the interstitium (stroma) of the lung.
Irregular emphysema- emphysema affecting the acini unevenly, which is almost always associated with scarring changes in the lung tissue.
Obstructive emphysema- emphysema caused by incomplete blockage (obstruction) of the airways with the formation of a valve mechanism.
Panacinar emphysema (panlobular)- emphysema, capturing acini from respiratory bronchioles to terminal alveoli.
Emphysema paraseptal- emphysema, characterized by changes in the distal part of the acin, while the proximal part remains normal.
Emphysema centriacinar (centrilobular)- emphysema, affecting the central or proximal part of the acinus, leaving the distal alveoli intact.
The list of questions for the lesson,
1. Specify the change in the myocardium underlying the development of cor pulmonale in COPD.
2. Select obstructive pulmonary disease.
3. What is the name of the excessive and persistent expansion of air 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 the 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. In what disease does the increased reactivity of the mucous membrane of the airways occur?
10. Specify the pathogenetic variant of bronchial asthma.
11. Specify a molecule that fixes on mast cells in atopic bronchial asthma.
12. Name the changes in the bronchial wall during bronchiectasis.
13. Name the macroscopic types of bronchiectasis.
14. Name the complications of bronchiectasis.
15. What is the name of an occupational disease 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 the sarcoid granuloma.
20. In what disease are asteroid inclusions found in the cytoplasm of multinucleated cells?
21. Name the types of lung cancer classified by location.
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 that develops 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. Indicate precancerous conditions in the lungs.
27. What are the complications of bronchial cancer?
28. A 53-year-old patient has been smoking 2 packs of cigarettes a day for 30 years. I went to the clinic with complaints of persistent productive cough, worsening 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 pulmonary pattern are determined. Your conclusion.
29. A 30-year-old patient was admitted to the clinic with complaints of shortness of breath, general cyanosis, weakness. It is known from the anamnesis that the woman has been working on a poultry farm for a long time. In the study: the level of immunoglobulins in the blood is increased, immune complexes are determined. X-ray examination shows a picture of a "cellular lung". Indicate the most likely diagnosis.
30. A 67-year-old patient, suffering from chronic diffuse bronchitis for a long time, died with increasing symptoms of pulmonary heart disease. At postmortem examination of the lungs of increased airiness, in the peripheral regions there are many different-sized bubbles. Indicate the changes in the internal organs found at the autopsy.
DISEASES OF THE DIGESTIVE ORGANS
(the section is studied in two laboratory sessions)
Learning objectives
The student must know :
1. The cause 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 of the studied macro-preparations and micro-preparations.
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 the formation of structural changes that occur in organs in diseases of the digestive system.
Iclass
DISEASES OF THE STOMACH AND INTESTINAL
1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, classification principles. Forms identified on the basis of the study of gastrobiopsies, and their morphological characteristics. Complications, outcomes, prognosis. Chronic gastritis as a precancerous condition.
2. Peptic ulcer disease. Definition. General characteristics of peptic (chronic) ulcers of different localizations. Epidemiology, etiology, patho - and morphogenesis, its features in pyloric-duodenal and medio-gastric ulcers. Morphological characteristics of chronic ulcers during exacerbation and remission. Complications, outcomes. Acute stomach ulcers: etiology, pathogenesis, morphological characteristics, outcomes.
3. Tumors of the stomach. Classification. Hyperplastic polyps. Adenoma of the stomach. Morphological characteristics. Malignant tumors of the stomach. Stomach cancer. Epidemiology, etiology, classification principles. Features of metastasis. Macroscopic and histological forms.
4. Idiopathic inflammatory bowel disease. Nonspecific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, prognosis. Criteria for the differential diagnosis of chronic colitis.
5. Intestinal epithelial tumors. Benign tumors. Adenomas: epidemiology, classification, clinical and morphological characteristics, prognosis. Familial adenomatous polyposis. Adenoma and cancer: a concept of multistage colon carcinogenesis. Colon cancer. Epidemiology, etiology, classification, macro- and microscopic morphological characteristics, clinical manifestations, prognosis.
6. Diseases of the appendix of the cecum. 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) vol. 2, part I: pp. 537-562, 586-593, 597-618.
3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: p. 384-405, 416-422, 425-441.
4. Guide to practical training in pathological anatomy (, 2002) p.580-585, 601-612.
5. Atlas on pathological anatomy (2003) p. 256-265.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of certain nosological forms of diseases of the gastrointestinal tract using macros and microsamples and to conduct clinical and anatomical comparisons.
DISEASES OF THE STOMACH
Macrodrug MULTIPLE STOMACH EROSION. Pay attention to the gastric mucosa with multiple superficial defects, note the color of the bottom of the erosion.
Macrodrug CHRONIC GASTRITIS. Pay attention to the relief of the mucous membrane in various parts (body, pyloric canal), the presence of erosion.
Micropreparation No. 000 Helicobacter pylori in parietal mucus in gastric fossa (gastrobiopsy, Giemsa stain). View, note the ability of bacteria to adhere to the epithelial cell.
Micropreparation No. 000 CHRONIC ACTIVE GASTRITIS OF ANTHRUM WITH IRON ATROPHIA AND COMPLETE INTESTINAL METAPLASIA (gastrobiopsy, staining with alcian blue and hematoxylin). To describe and evaluate semi-quantitatively morphological signs of chronic gastritis: activity (presence of neutrophilic leukocytes) and severity of inflammation (density of mononuclear infiltrate), degree of atrophy of the lamina propria glands, prevalence of intestinal metaplasia of the integumentary epithelium.
Macrodrug CHRONIC STOMACH Ulcer (kalezny). Pay attention to the localization of the ulcer, its shape, edges, depth, the nature of the bottom. Determine which edge is facing the esophagus and which is the gatekeeper.
Micropreparation No. 000 CHRONIC STOMACH Ulcer (with exacerbation) (staining with hematoxylin and eosin). Designate the layers in the bottom of the ulcer that characterize the chronic course of the disease. Note fibrinoid necrosis and leukocyte infiltration, indicating an exacerbation of the process.
View a set of macro-preparations, illustrating the complications of chronic ulcers: PROTECTING GASTRIC ULTRA, PENETRATING GASTRIC ULTRA, ARROSION OF THE VASCULAR IN THE BOTTOM OF THE ULTRA, ULTRA-CANCER OF THE STOMACH, CURRIC DEFORMATION OF THE STOMACH. Pay attention to the localization of ulcers, the shape, nature of the edges, changes in the bottom and edges of the ulcer.
Macro preparations different forms CANCER OF THE STOMACH. 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). Identify the signs of tissue and cellular atypism, the invasive nature of tumor growth.
Micropreparation No. 000 UNDIFFERENTIATED CANCER - signet ring (staining with hematoxylin and eosin and alcian blue). Pay attention to tumor cells with alcyanophilic cytoplasm, located in the "pools" of mucus. Mark the shape of the cell - cricoid, the nucleus is pushed back to the periphery, the cytoplasm is filled with mucus.
INTESTINAL DISEASES
Macrodrug PHLEGMONOUS APPENDICITIS. Pay attention to the size of the appendix, the state of the serous membrane (appearance, degree of blood filling), wall thickness, the nature of the contents in the lumen.
Micropreparation No. 000 PHLEGMONOUS APPENDI-CITY (staining with hematoxylin and eosin). Describe. To 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 (mesenteriolitis).
Macrodrug CHRONIC APPENDICITIS. Pay attention to the size of the appendix, the state of the serous membrane, the thickness and the appearance of its wall in section.
Micropreparation No. 000 CHRONIC APPENDICITIS (staining with hematoxylin and eosin). Describe. Mark sclerotic changes in the wall and obliteration of the lumen of the appendix. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.
Macrodrug Liver abscesses (pylephlebitic), as a complication of appendicitis. View.
View set of macro-preparations intestinal tumors.
BASIC Vocabulary for Lesson
Acute gastritis- diseases manifested by inflammation of the gastric mucosa.
Chronic gastritis- Dative inflammation-dysregenerative diseases of the gastric mucosa.
Hematomesis- bloody vomiting.
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 region of the esophageal-gastric junction.
Penetration- penetration of the defect into adjacent organs ("covered" perforation).
Perforation- perforation.
Pylorospasm- a steady contraction of the pyloric sphincter of the 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 go beyond the mucous membrane.
Ulcer- a defect extending beyond the mucous membrane.
Stricture- stenosis, narrowing.
The list of questions for the lesson,
which are the basis of the control test
1. Give the definition of Barrett's esophagus.
2. Specify the features of Zenker's diverticulum.
3. Indicate the positions characteristic of Mallory-Weiss syndrome.
4. Indicate the factors providing the cytoprotective function of the gastric mucosa.
5. Indicate the most common reason(etiological factor) chronic gastritis.
6. Specify the methods for detecting H. pylori in biopsy.
7. Indicate the positions typical for chronic stomach ulcers.
8. List the factors that significantly reduce the synthesis of prostaglandins and have an ulcerogenic effect.
9. Indicate microscopic features acute ulcers stomach.
10. Describe the perforation of the gastric ulcer.
11. Note statements specific to Zollinger-Ellisson syndrome.
12. Specify the preferred localization of stomach ulcers.
13. Select the positions characteristic of the cambial cells of the intestinal epithelium.
15. The predisposing factors for the development of hemorrhoids are.
16. Select the extraintestinal manifestations of Crohn's disease.
17. Specify the complications of Crohn's disease.
18. Specify a disease characterized by a combination of the following microscopic characteristics - crypt-abscesses, granulomas with the presence of giant cells of Pirogov-Langhans.
19. Specify microscopic signs of exacerbation of Crohn's disease.
20. Select statements specific to volvulus.
21. Specify the pathogenetic factors of colon diverticulosis.
22. Describe the pseudopolyps in ulcerative colitis.
23. What disease is characterized by a macroscopic appearance of the mucous membrane of the large intestine of the "cobblestone" type?
24. What disease can be suspected in the presence of 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 characteristics celiac disease.
26. In what conditions does malabsorption syndrome occur?
27. A 64-year-old patient with diabetes mellitus developed 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. On examination by the doctor of the emergency room, confusion, fever of 39.6 ° C, symptoms of peritoneal irritation are positive. Indicate the presumptive diagnosis.
28. A 28-year-old patient has been losing weight, pain in the epigastric region for several years, in the last month, pallor of the skin, black feces, girdle pain at the epigastric level, yellowness of the skin and visible mucous membranes have appeared. With FGDS, a callous ulcer of the posterior wall of the stomach with undermined edges was found, the bottom is deep, filled with dirty gray contents. What complication of the ulcer are we talking about in this case?
29. In the gastrobiopsy of a 43-year-old patient, the presence of lymphoplasmacytic infiltrate in the lamina propria of the mucous membrane is determined, there are accumulations of lymphocytes with light centers. Histobacterioscopically, when staining according to Giemsa, S-shaped sticks are determined in the layer of superficial mucus. What is the presumptive diagnosis?
IIclass
DISEASES OF THE LIVER, GALL BLADDER
AND PANCREAS
1. Hepatitis: definition, classification. Acute viral hepatitis. Epidemiology, etiology, transmission routes, patho - and morphogenesis, clinical and 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 obesity of the 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. Pathomorphological 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. Liver tumors. Classification, epidemiology. Benign neoplasms. Hepatocellular adenoma. Intrahepatic bile duct adenoma. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification according to macro - and microscopic features. Complications. Regularities of metastasis. Levels of spread of hepatocellular adenocarcinoma according to the TNM system. Cholangiocellular carcinoma.
5. Diseases of the gallbladder and bile ducts. Cholelithiasis(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. Acute pancreatitis (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) vol. 2, part I: pp. 637-669, 672-682, 687-709.
3. Textbook on pathological anatomy (, Anichkov N. M, 2005) vol. 2, part I: pp. 452-477, 479-487, 489-501.
4. Guide to practical training in pathological anatomy (, 2002) p.634-654, 585-589.
5. Atlas on pathological anatomy (2003) p. 282-288.
LEARNING CARD
PURPOSE INSTALLATION OF THE LESSON: to study the morphology of individual nosological forms of liver diseases using macropreparations, microspecimens and electron diffraction patterns and conduct clinical and anatomical comparisons.
LIVER DISEASES
Macrodrug TOXIC LIVER DYSTROPHY (fatty hepatosis). Pay attention to the size of the liver, its color, consistency, the state of the capsule.
Micropreparation No. 4 MASSIVE LIVER NECROSIS - subacute form (staining with hematoxylin and eosin). To note the discomplexation of the beams, signs of fatty degeneration and necrosis of hepatic cells. Compare the state of hepatocytes in the center and periphery of the lobules. Pay attention to the incipient stromal fibrosis 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). To note signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" of lymphocytes along sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of portal tracts. Note the signs of chronic inflammation (stage of hepatitis): fibrosis of the portal portal tracts, fibrous septa growing into the lobules. Pay attention to cholestasis: expansion of bile capillaries, imbibition of hepatocytes with 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.
Macro preparations LIVER CIRROSIS. Mark the size, color, consistency, surface and section view of the liver. Estimate the size of the regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.
Micropreparation No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRROSIS (staining with hematoxylin and eosin and picrofuchsin). Pay attention to the presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of the stroma, extending to the parenchyma, fatty degeneration of hepatocytes), dominance of fibrosis (port-portal, port-central septa, formation of false lobules) and regeneration of hepatocytes (loss of the beam structure, presence of cells with large nuclei).
Macro preparations: PRIMARY LIVER CANCER, LIVER METASTASES, TUMORS OF ANOTHER PRIMARY LOCALIZATION.
BASIC Vocabulary for 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 the dominance of degenerative changes and necrosis of hepatocytes.
Jellyfish 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 pigment rings in the cornea of the eyes in Wilson's disease.
Kaunsilmana Taurus- eosinophilic rounded formations in the perisinusoidal space.
Mallory Taurus- alcoholic hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.
Massive liver necrosis (confluent)- extensive widespread necrosis of most of the hepatic parenchyma.
Liver necrosis bridged (bridge necrosis)- confluent necrosis of a large number of hepatocytes with the formation of "bridges" between adjacent lobules.
Graded liver necrosis (periportal)- destruction of hepatocytes along the border of the parenchyma and stroma, i.e. in the peripheral parts of the lobule.
Focal liver necrosis (macular)- 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- a macroscopic view of an organ with 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 proliferation of connective tissue in the organ against the background of degenerative and regenerative processes, accompanied by a change in the shape of the organ.
The list of questions for the lesson,
which are the basis of the control test
1. Specify the options for the structure of the liver.
2. List the variants of liver parenchyma necrosis.
3. What results in the formation of Kaunsilman's little bodies?
4. List the forms of acute hepatitis.
5. Specify the route of transmission of the virus when acute hepatitis A.
6. Specify the routes of transmission of the virus in acute hepatitis B.
7. What are the indirect markers of viral damage to hepatocytes.
8. Specify the predominant localization of HBcAg in hepatocytes.
9. What kind does the accumulation of HBsAg in the hepatocyte impart 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 options for 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 the hereditary forms of liver cirrhosis.
21. Indicate the signs of portal hypertension.
22. List the causes of death of patients with liver cirrhosis.
23. Give the characteristics of primary sclerosing cholangitis.
24. Give a characteristic of primary biliary cirrhosis of the liver.
25. Give a characteristic of 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 suffered 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. Indicate the possible histological manifestations in the biopsy material.
29. A 50-year-old woman has suffered from fatigue and itching for 8 months. In a laboratory study, a minimal increase in the level of transaminases, a significant increase in the level of alkaline phosphatase, and high titers of antimitochondrial antibodies were found. A biopsy study revealed a granulomatous nature of inflammation in the cholangioli and a decrease in the number of bile ducts with pronounced lymphoma-macrophage infiltration along the portal tracts with symptoms of sclerosis. Your conclusion.
30. A 63-year-old male patient, suffering from chronic viral hepatitis B for a long time, was admitted to the clinic with complaints of heaviness in the right hypochondrium, yellowness of the skin. On examination, the liver is dense, its edge is bumpy, there is an increase in the spleen and expansion of the veins of the anterior abdominal wall. Note possible histological manifestations in the biopsy material.
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