Chronic gastric ulcer microslide description. Chronic gastric ulcer during exacerbation. Causes of pain
Hematoxylin and eosin staining. In the area of the gastric wall defect there is fibrinous-purulent exudate (a), with an underlying large area of fibrinoid necrosis (b), the presence of granulation tissue (c) and the proliferation of coarse fibrous connective tissue penetrating to varying depths muscle layer (d). The serous membrane of the stomach wall is preserved (e).
2. Chronic atrophic gastritis. Heme staining
toxilin and eosin. In the gastric mucosa there is atrophy of the integumentary epithelium (a) and the epithelium of the glands with restructuring
which glands are of intestinal type - “intestinal metaplasia” (b), in the lamina propria of the mucous membrane of the sclerosis field
(c) and lymphoplasmacytic infiltration with the formation of lymphoid follicles (d).
3. Adenocarcinoma. Hematoxylin and eosin staining. All layers of the stomach wall are infiltrated with tumor tissue with signs of cellular atypia (a). Multiple pathological mitoses are visible in hyperchromic (b) and polymorphic tumor cells (c).
4. Mucosal cancer of the stomach. Hematoxylin staining and
eosin. The tumor tissue is represented by an abundance of large atypical “ring-shaped” cells (a) with the formation of a large amount of mucus (b). The infiltrative nature of tumor growth is visible (c). Demonstration.
5. Scirrhus of the stomach. Hematoxylin and eosin staining. In the wall of the stomach there are groups of atypical cells with large hyperchromatic nuclei (a), in the stroma of the tumor there is a proliferation of fibrous connective tissue (b). Demonstration.
MACRO-PREPARATIONS.
1. Acute catarrhal gastritis: in the preparation the stomach, the mucous membrane is thickened, with high hyperemic folds, covered with thick viscous mucus, with petechial hemorrhages. Causes: poor quality food, consumption of alcohol substitutes, anti-tumor 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. Erosion and acute gastric ulcers: in the preparation the stomach,
the mucous membrane is swollen, on the surface there are multiple pinpoint hemorrhages and conical defects of various sizes, their bottom and edges are black. Erosions are localized within the mucous membrane, and ulcers penetrate
They reach different depths of the mucous membrane, some reach the muscular layer.
Causes: endocrine diseases (Solinger-Ellison syndrome, hyperparathyroidism), acute and chronic circulatory disorders, intoxication, allergies, chronic infections (tuberculosis, syphilis), postoperative, steroid and stress ulcers.
Complications: perforation, peritonitis.
Exodus: erosions are epithelialized, the ulcerative defect is replaced by scar tissue.
3. Chronic gastric ulcer during remission: in the preparation of the stomach, on the lesser curvature there is a pathological focus in the form of a depression in the mucous membrane, round in shape, measuring 3 cm in diameter. The folds of the mucous membrane converge radially towards the defect, the edges of which are dense, raised in a roller-like manner, and calloused (calecal ulcer). On the cut, the entrance hole is a crater, smaller than the inside of the ulcer. The edge facing the cardia is undermined, the mucous membrane hangs over it. The edge facing the gatekeeper is gentle - terrace-like. The thickness of the ulcer is represented by connective tissue, gray-white, 2.5 cm. At the bottom of the ulcer, the vessels are sclerotic, their lumen gapes.
Causes: genetic predisposition, Helicobacter pylori, inflammatory and dysregenerative changes in the mucous membrane, leading to exposure to factors of peptic aggression (hydrochloric acid and pepsinogen).
Complications: perigastritis, bleeding, perforation, penetration, cicatricial deformation of the stomach with the development of stenosis of the inlet or outlet. Against the background of a chronic ulcer, a second disease can develop - stomach cancer.
4. Stomach polyps (adenomas): in the antrum
stomach there are two tumor-like formations the size of pigeon eggs, on thin stalks, irregular oval shape with a villous surface, soft consistency.
On the section, pathological neoplasms are abundantly vascularized and localized exclusively on the surface of the mucous membrane, without growing into the underlying tissue.
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, of an irregular round shape measuring 5 cm in diameter, on a wide base in the form of a mushroom cap, with a retraction in the center. The section shows that the tumor grows throughout the entire wall of the stomach.
b) Diffuse gastric cancer: the organ is reduced in size, the wall is thickened throughout its entire length to 1 cm, has a dense “woody” consistency, and is represented by gray-pinkish tissue in the section. The mucous membrane is uneven, its folds are of varying thickness, the serous membrane is thickened, dense, and lumpy. The lumen of the stomach is narrowed.
c) Saucer-shaped stomach cancer: on the lesser curvature there is a pathological focus in the form of a formation rising above the surface of the mucous membrane with dense roll-like edges and a sinking bottom, measuring 3.5 cm by 2.0 cm. The bottom is covered with gray-brown disintegrating masses. On the section, the tumor tissue infiltrates the entire thickness of the organ wall.
Causes: nutrition (smoked meats, canned food, pickled vegetables, peppers), biliary reflux (after gastric surgery, especially 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 lymphogenic metastases to the left supraclavicular lymph node - Virchow's metastasis, to the ovaries - Krukenberg's
cancer, perirectal tissue - Schnitzler metastases, 3. Hematogenous metastases to the liver, lungs, brain, bones, kidneys, and less often to the adrenal glands and pancreas. 4. Implantation- carcinomatosis of the pleura, pericardium, diaphragm, peritoneum, omentum.
TEST CONTROL
Select one or more correct answers
1. SIGNS OF ACUTE CATARHAL GASTRITIS
1) thickening of the mucosa
2) atrophy of the glands
3) multiple erosions
4) sclerosis of the mucosa
5) neutrophilic infiltration of the mucosa
6) lymphoid infiltration of the mucosa
2. MORPHOLOGICAL FORMS OF ACUTE GASTRITIS
1) fibrinous
2) atrophic
3) hypertrophic
4) catarrhal
5) corrosive (necrotic)
3. CHANGES IN THE EPITHELIUM IN CHRONIC GASTRITIS
1) atrophy
2) intestinal metaplasia
3) hyperplasia
4) dysplasia
5) appearance of Mallory bodies in the cytoplasm
4. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS A
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
5. PATHOGENESIS OF PERNICIOUS ANEMIA IN AUTOIMMUNE GASTRITIS
1) stopping the production of HCl
2) production of antibodies to Helicobacter pylori
3) production of antibodies to parental cells
4) production of antibodies to intrinsic factor
5) destruction of glands and atrophy of the mucous membrane
6. CHARACTERISTIC FEATURES OF CHRONIC GASTRITIS
1) predominant localization - antrum
2) autoantibodies in the blood
to parietal cells
3) Helicobacter pylori -
main etiological factor
4) accompanied by G-cell hyperplasia, gastrinemia
5) often 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,
does not affect the muscle plate
3) atrophy of the mucous membrane
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 ACHIEVEMENT
1) often occurs in patients with alcoholism
2) the mucous membrane is not changed
3) diffuse lymphoid-plasmacytic infiltration with a significant admixture of PMNs
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 duodenum
3) acute stomach ulcer
and duodenum
4) chronic recurrent ulcer of the stomach and duodenum
5) inflammation of the duodenal mucosa
10. Sclerotic deformity of the stomach IS an outcome
1) catarrhal gastritis
2) diphtheritic gastritis
3) corrosive gastritis
4) phlegmonous gastritis
11. SIGNS of chronic atrophic gastritis, as a precancerous disease
1) lymphoplasmacytic infiltration
2) sclerotic processes
3) structural restructuring of the epithelium
(intestinal metaplasia)
4) all answers are correct
5) all answers are incorrect
12. ULCEROGENIC PROMOTERS
1) corticosteroids
3) aspirin
4) smoking
5) increased tone of the vagus nerve
13. Gastric ulcers include
1) endocrine gastric ulcers
2) allergic ulcers
3) peptic ulcers
4) postoperative ulcers
5) tuberculous ulcers
14. local factors in the development of gastric ulcer
1) increased aggressiveness of gastric juice
2) campillobacteria
3) presence of chronic gastritis
4) circulatory disorders
5) all answers are correct
6) all answers are incorrect
15. REASONS FOR THE DEVELOPMENT OF ACUTE STOMACH ULCER
1) corticosteroids
3) aspirin
4) smoking
5) increased tone
vagus nerve
16. MORPHOLOGICAL SIGNS of acute gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
on a cross section
3) soft jagged edges
4) dense calloused edges
7) multiple ulcers
17. MORPHOLOGICAL SIGNS of chronic gastric ulcer
1) funnel shape
2) the shape of a truncated pyramid
on a cross section
3) soft jagged edges
4) dense calloused edges
5) the bottom of the ulcer is painted black with hydrochloric acid hematin as it is cleansed
6) the edge of the ulcer, facing the pylorus, has the appearance of a terrace, the cardiac edge is undermined
18. SIGNS OF CHRONIC STOMACH ULCER
DURING REMISSION
1) the presence of exudate on the surface
2) scar tissue interrupts the muscle sheath to varying depths
3) endovasculitis
4) fibrinoid changes in the fundus and vessels
5) epithelization of the surface
19. SIGNS OF CHRONIC STOMACH ULCER
DURING THE PERIOD OF EXCERNSATION
1) the presence of fibrinous-purulent exudate
on the surface 2) scar tissue interrupts muscle
shell at different depths
3) endovasculitis
4) fibrinoid changes in the walls of blood vessels and in the bottom of the ulcer
12. MECHANISM OF Bleeding in peptic ulcer disease
arrosive
diapedetic
as a result of a ruptured vessel
as a result of purulent melting
21. Chlorohydropenic uremia – result
1) bleeding from an ulcer
2) chronic nephritis
3) penetration of ulcers
4) cicatricial pyloric stenosis
5) all answers are correct
6) all answers are incorrect
22. Peritonitis complicating a chronic ulcer is the result
1) penetration
2) perforation
3) gastritis
4) duodenitis
5) cicatricial pyloric stenosis
23. COMPLICATIONS OF CHRONIC ULCERS
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) Ménétrier'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 pitted epithelium
4) hyperplasia of the glandular epithelium
5) severe sclerosis
26. MORPHOLOGICAL SIGNS OF INFLAMMATORY POLYP
1) inflammatory infiltrate in the stroma
2) atypical cells
3) without clear differentiation into pedicle and body
4) dysplasia of the glandular epithelium
5) erosion on the surface
27. BENIGN TUMORS OF THE STOMACH
1) angiosarcoma
2) adenoma
3) leiomyoma
4) adenocarcinoma
5) hyperplasiogenic polyp
28. BACKGROUND FOR THE DEVELOPMENT OF GASTRIC ADENOMA
1) chronic superficial gastritis
2) acute erosive-hemorrhagic gastritis
3) acute fibrinous gastritis
4) chronic gastritis with enterolization
29. ADENOMA IS
1) benign tumor
from glandular epithelium
2) malignant tumor of the glandular epithelium
3) epidermal cancer
4) malignant tumor from transitional cell epithelium 5) benign tumor from squamous epithelium
30. DISEASES WITH A RISK OF CANCER
1) superficial gastritis
2) chronic gastric ulcer
3) acute erosive gastritis
4) chronic atrophic gastritis
5) adenomatous polyps
31. HISTOLOGICAL VARIANTS OF STOMACH CANCER
1) adenocarcinoma
2) sarcoma
3) signet ring cell
4) undifferentiated
32. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF INTESTINAL TYPE 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) affects men 2 times more often
5) develops from metaplastic epithelial cells
33. CLINICAL AND MORPHOLOGICAL CHARACTERISTICS OF DIFFUSE TYPE STOMACH CANCER
1) develops from epithelial cells
2) occurs at a relatively young age
3) histologically signet ring cell
4) occurs against the background of chronic gastritis
5) has a low degree of differentiation
34. PROGNOSTIC SIGN FOR STOMACH CANCER
1) histological variant
2) macroscopic shape
3) depth of invasion
4) mucus formation
5) secondary changes
35. HISTOLOGICAL SIGNS OF POLYPOID STOMACH CANCER
1) atypical glandular structures of bizarre shape
2) signet ring 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 FEATURES OF SIGNET CELL CANCER OF THE STOMACH
1) characterized by extensive hemorrhages
2) the nuclei of atypical cells are displaced
to the cell membrane
3) poorly differentiated cells with very large hyperchromatic nuclei of irregular shape
4) atypical glandular structures
5) massive sclerosis and hyalinosis in the wall
37. MICROSCOPIC CHARACTERISTICS OF SCIRROUS GASTROCANCER
1) atypical cells with large
the 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. KRUCKENBERG AND SCHNITZLER METASTASES OF STOMACH CANCER
1) hematogenous
2) implantation
3) lymphogenous orthograde
4) lymphogenous retrograde
39. COMPLICATIONS OF STOMACH CANCER
1) hemoptysis
2) pyloric dilatation
3) perforation
4) exhaustion
5) stomach bleeding
40. SIGNS THAT CHARACTERIZE VIRCHOWSKI METASTASIS
1) hematogenous metastasis
2) retrograde lymphogenous metastasis
3) peritoneal carcinomatosis
4) damage to the left supraclavicular lymph node
5) ovarian damage
Standard answers for test tasks
9. Toxic liver dystrophy.This macrodrug is the liver. The shape is preserved, the weight and dimensions are reduced. The liver is yellow.
These pathological changes could develop as a result of intoxication, allergic or viral damage to the liver. Fatty (yellow) degeneration develops in the organ, the morphogenetic mechanism of which is decompensation. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic destruction of hepatocytes in the central sections. Fat-protein detritus is phagocytosed, and the reticular stroma with dilated vessels is exposed (red degeneration). Due to necrosis of hepatocytes, the liver shrinks and decreases in size.
1) favorable: transition to a chronic form.
2) unfavorable:
a) death from liver or kidney failure;
b) post-necrotic cirrhosis of the liver;
c) damage to other organs (kidneys, pancreas, myocardium, central nervous system) as a result of intoxication.
Conclusion: these morphological changes indicate fatty degeneration of hepatocytes and their progressive necrosis.
Diagnosis: Toxic liver dystrophy. Stage of yellow dystrophy.
^ 10. Stomach cancer.
This macropreparation is the stomach. The shape and size of the organ are changed due to the growth of whitish-yellow tissue, which has grown into the wall of the stomach and significantly thickens it (up to 10 cm or more). Reliefs of the mucous membrane are not pronounced. In the central part of the growth, depressions, loosening and hanging areas are visible - ulcerations.
Description of pathological changes:
These pathological changes could develop as a result of precancerous conditions and precancerous changes (intestinal metaplasia and severe dysplasia).
In areas of epithelial change, cell malignancy and tumor development occur (or cancer develops de novo). Based on the macroscopic picture, we can say that this is a cancer with predominantly endophytic infiltrating growth - infiltrative-ulcerative cancer (this is evidenced by tumor ulcerations). Histologically, it can be either adenocarcinoma or undifferentiated cancer. Progression, the tumor grows into the wall of the stomach and significantly thickens it.
1) favorable:
a) slow growth of cancer;
b) well-differentiated adenocarcinoma;
c) late metastasis;
2) unfavorable: death from exhaustion, intoxication, metastasis; spread of cancer beyond the stomach and germination into other organs and tissues, secondary necrotic changes and disintegration of carcinoma; dysfunction of the stomach.
Conclusion: these morphological changes indicate mutational transformation of epithelial cells with their malignancy and subsequent tumor progression, which, with infiltrating growth, led to germination of the stomach wall with ulcerations, which may represent secondary necrotic changes and tumor disintegration.
Diagnosis: Infiltrative-ulcerative stomach cancer.
^ 11. Erosion and acute stomach ulcers.
This macropreparation is the stomach. The shape and size of the organ are preserved, the mass is not changed. The organ is whitish in color. The mucous membrane is strewn with black formations of dense consistency. Among the numerous small ones, the diameter is 1-5 mm. There are also larger ones with a diameter of 7 mm, as well as conglomerates 8x1 cm, 3x0.5 cm, consisting of fused formations with a diameter of 5 mm. Near one of them we see a triangular-shaped formation, the boundaries of which are markedly different from the gastric mucosa, since they are formed by connective tissue.
These morphological changes could develop as a result of exogenous and endogenous influences: malnutrition, bad habits and harmful agents, as well as autoinfections, chronic autointoxication, reflux, neuroendocrine, vascular allergic lesions. Since the lesions are localized in the fundus, we can talk about an autoimmune process with damage to parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, impaired regeneration and atrophy. Probably in this case, chronic atrophic gastritis developed with atrophy of the mucous membrane and its glands. Defects in the mucosa lead to erosion, which forms after hemorrhage and rejection of dead tissue. The black pigment at the bottom of the erosion is hydrochloric acid hematin. These changes are accompanied by restructuring of the epithelium. A formation whose border is formed by the mucosa and represents the healing of an acute gastric ulcer by scarring and epithelization.
1) favorable:
a) healing of an acute ulcer by scarring or epithelization;
b) inactive chronic gastritis (remission);
c) mild or moderate changes;
d) epithelization of erosions;
2) unfavorable:
a) development of chronic peptic ulcer disease;
b) malignancy of epithelial cells;
c) pronounced changes;
d) active severe gastritis.
Conclusion: these morphological changes indicate long-term dystrophic and necrobiotic changes in the epithelium of the mucous membrane with disruption of its regeneration and structural restructuring of the mucous membrane.
Diagnosis: chronic atrophic gastritis, erosion and acute gastric ulcer.
^ 12. Chronic gastric ulcer.
This macropreparation is the stomach. The mass and size of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is highly developed. On the lesser curvature of the stomach in the pyloric region, a significant depression of 2x3.5 cm is localized in the wall of the stomach. Its limiting surface of the organ is devoid of characteristic folding. The folds converge towards the boundaries of the formation. In the area of the pathological process there are no mucous, submucosal and muscular layers of the stomach wall. The bottom is smooth, filled with a serous membrane. The edges are raised like a roller, dense, and have a different configuration: the edge facing the pylorus is flat (due to gastric peristalsis).
Description of pathological changes:
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; medications; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased motility, increased number of gastrin-producing cells; and a general disorder: excitation of the subcortical centers and the hypothalamic-pituitary region, increased tone of the vagus nerve, increased and subsequent depletion of the production of ACTH and glucocarticoids). By affecting the gastric mucosa, these disorders lead to the formation of a defect in the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic influences, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer may be covered with a thin layer of epithelium, overlying the scar tissue. But during the period of exacerbation, “healing” is leveled out as a result of fibrinoid necrosis (which leads to damage not only directly, but also through fibrinoid changes in the walls of blood vessels and disruption of trophic tissue of the ulcer).
1) favorable: remission, healing of the ulcer through scarring followed by epithelization.
2) unfavorable:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative-scarring processes.
Conclusion: these morphological changes indicate a destructive process in the wall of the stomach, which leads to the formation of a defect in the mucous, submucosal and muscular membrane - an ulcer.
Diagnosis: Chronic gastric ulcer.
^ 13. Hyalinosis of the spleen capsule. Glazed spleen.
This macroscopic specimen is the spleen. The mass and size of the organ are not increased, the shape is preserved. The color of the capsule is white, it is coarsely tuberous, and the tuberosity is more pronounced in the front. The recesses are more or less large. There is a noticeable area with a diameter of 0.5 cm on the front surface of the organ that is yellow. At the back and on the side, sections of yellowish tissue are fused to the capsule.
Descriptions of pathological changes.
These pathological changes could develop as a result of destruction of fibrous structures and increased tissue-vascular permeability (plasmorrhagia) in connection with angioedema, metabolic and immunopathological processes. Plasmorrhages - impregnation of tissue with plasma proteins, their absorption on fibrous structures, precipitation and formation of hyaline. Hyalinosis can develop as a result of plasma impregnation, fibronoid swelling, inflammation, necrosis, sclerosis. In the splenic capsule, hyalinosis develops as an outcome of sclerosis. The connective tissue swells, loses fibrillation, its bundles merge into a homogeneous dense, cartilaginous mass, the cells are compressed and atrophy. The fabric becomes dense, whitish, translucent. Along with hyalinosis of connective tissue in the spleen, local hyalinosis of arterioles may be present as a physiological phenomenon. In this case, simple hyaline is formed (due to sweating of unchanged or slightly changed components of the blood plasma).
1) favorable:
a) was possible only as a stage of the process during its stabilization and resorption of hyaline masses;
b) unfavorable - the most common: dysfunction of an organ, limitation of its functionality.
Conclusion: the data of morphological changes indicate dystrophic processes in the spleen capsule, which led to its hyalinosis.
Diagnosis: Hyalinosis of the spleen capsule.
^ 14. Dysenteric colitis.
This macropreparation is the large intestine. The shape of the organ is preserved, the weight and size are increased due to the thickening of the wall. The mucous membrane is dirty-gray in color, at the top of the folds and between them, filmy deposits of brown-green color covering the mucous mass are necrotic, ulcerated, and in many places hang freely into the intestinal lumen (which is narrowed).
Description of pathological changes:
These pathological changes could develop as a result of an acute intestinal disease with a predominant lesion of the colon, the cause of which was the penetration, development and reproduction of Shigella bacteria and their species in the epithelium of the mucous membrane. This group of bacteria has a cytoplasmic effect on these cells, which is accompanied by destruction and desquamation of the latter, the development of desquamative catarrh. Enterotoxin from bacteria has a vasoneuroparalytic effect, which is associated with paralysis of blood vessels > increased exudation as well as damage to the intramural nerve ganglia, which leads to the progression of processes and the development of fibrinoid inflammation (as a result of increased leakage of fibrinogen from dilated vessels). If in the first stage we find only superficial necrosis and hemorrhage, then in the second stage a fibrinoid film appears at the apex and between the folds. Necrotic masses of the mucous membrane are permeated with fibrin. Dystrophic and necrotic changes in the nerve plexuses are combined with infiltration of the mucous and submucosal mucosa by leukocytes, swelling, and hemorrhages. With the further development of the disease, due to the rejection of fibrin films and necrotic masses, ulcers are formed, which at 3-4 weeks of the disease are filled with granulation tissue, which matures and leads to the regeneration of ulcers.
1) favorable:
a) complete regeneration for minor defects;
b) abortive form;
2) unfavorable:
a) incomplete regeneration with scar formation > narrowing of the intestinal lumen;
b) chronic dysentery;
c) lymphadenitis;
d) follicular, polycular ulcerative colitis;
e) severe general changes (necrosis of epithaleal tubules of the kidneys, fatty degeneration of the heart and liver, impaired mineral metabolism). Complications:
a) perforation of an ulcer: peritonitis; paraproctitis;
b) phlegmon;
c) intraintestinal bleeding.
Extraintestinal complications - bronchopneumonia, pilonephritis, serous arthritis, liver abscesses, ameloidosis, intoxication, exhaustion.
Conclusion: these morphological changes indicate diphtheria colitis of the colon associated with the toxic effects of Shigella.
Diagnosis: Dysentery and colitis. Stage of diphtheria colitis.
^ 15. Typhoid fever.
This macropreparation is the ileum. The shape of the organ is preserved, the weight and size are normal. The intestine is whitish in color, the folding of the mucous membrane is pronounced, on which formations of 4x2.5 cm and 1x1.5 cm are visible, which protrude above the surface of the mucous membrane. There are visible grooves and convolutions on them, the surface itself is uneven and loosened. These formations are dirty gray in color. A noticeable formation is 0.5 cm in diameter, with loss of characteristic folding, whitish in color, slightly indented and compacted.
Description of pathological changes:
These pathological changes could develop as a result of infection (parenteral) with typhoid bacillus and their reproduction in the lower part of the small intestine (with the release of endotoxin). Along the lymphatic tract -> into Peyer's patches -> saline follicles -> regional lymph nodes -> blood -> bacteremia and bacteriocholia
-> into the intestinal lumen -> hyperergic reaction in the follicles, which leads to enlargement and swelling of the follicles, and tortuosity of their surface. This occurs as a result of the proliferation of monocytes, histiocytes, and reticulocytes, which extend beyond the follicles into the underlying layers. Monocytes turn into macrophages (typhoid cells) and form clusters - typhoid granulomas. These changes are accompanied by catarrhal enteritis. With further progression of the process, typhoid granulomas become necrotic and surrounded by a zone of demarcation inflammation; sequestration and rejection of necrotic masses leads to the formation of “dirty ulcers” (as a result of impregnation with bile), which change their appearance over time: they are cleared of necrotic masses, the edges are rounded. The proliferation of granulation tissue and its maturation leads to the formation of delicate scars in their place. Lymphoid tissue is restored. Exodus:
1. favorable:
Complete regeneration of lymphoid tissue and healing of ulcers;
2. unfavorable:
Death as a result of intestinal (bleeding, perforation of ulcers, peritonitis) and extraintestinal complications (pneumonia, osteomyelitis, intramuscular abscesses, sepsis, waxy necrosis of the rectus abdominis muscles);
dystrophic changes in parenchymal organs, the formation of typhoid granulomas in them.
Conclusion: these morphological changes indicate an acute infectious disease with local changes in the small intestine - ileolitis.
Diagnosis: Ileolith.
^ 16. Gangrene of the small intestine.
This macropreparation is a section of the small intestine. Its dimensions and weight have not been changed. The intestinal loops are enlarged, the consistency of one part is loose, the second is not changed. The surface is smooth. The serous membrane is dull and matte. Between the loops is a sticky, viscous, stretchy liquid in the form of threads. On a section of the intestine, the walls are enlarged, the lumen is narrowed.
Possible causes: impaired blood supply as a result of strongometic necrochodaemonia of the mesenteric arteries.
Morphogenesis: ischemia, dystrophy, atrophy, necrosis of an organ in contact with the external environment - gangrene.
1) unfavorable - putrefactive melting, will distill.
Conclusion: indirect vascular necrosis.
Diagnosis: Wet gangrene of the small intestine.
9. What is the average total duration of the first three stages of development of lobar pneumonia?
10. Indicate the ways of spread of inflammation in lobar pneumonia.
11. List the pulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.
12. Characterize the composition of the exudate in lobar pneumonia in the flushing stage.
13. Characterize the composition of the exudate in lobar pneumonia in the stage of red hepatization.
14. Characterize the composition of exudate in lobar pneumonia in the stage of gray hepatization.
15. Specify extrapulmonary complications of lobar pneumonia caused by Streptococcus pneumoniae.
16. Give macroscopic characteristics of changes in the lungs during bronchopneumonia.
17. Give microscopic characteristics of changes in the lungs during 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 a complication of lobar pneumonia that develops with insufficient activity of neutrophils and the development of the organization of fibrinous exudate.
21. Name the reasons for the formation of a lung abscess.
22. List the reasons for the formation of a lung abscess.
23. Define the term atelectasis.
24. What develops when the airway lumen is completely closed?
25. What develops when the pleural cavity is partially filled with liquid exudate?
26. What develops during respiratory distress syndrome due to the destruction of surfactant?
27. Specify the cause of hemodynamic pulmonary edema.
28. A 25-year-old patient fell ill suddenly after hypothermia while intoxicated. Complains of a rise in body temperature to 390C, chills, stabbing pain in the right side and severe weakness for 7 days. Objectively: a dull sound is heard over the lower lobe of the right lung during percussion; during auscultation, breathing is not carried out; a pleural friction noise is heard. X-ray shows darkening of the lower lobe of the right lung, a cavity in the area of the 8th segment, thickening of the pleura. Your conclusion.
29. In a patient with a stroke and left-sided hemiparesis, on the 14th day the body temperature increased to 380C, which was accompanied by the appearance of cough and fine wheezing in the lower parts of the left lung. Your conclusion.
30. A 67-year-old man undergoing hospital treatment for phlegmon of the scalp developed shortness of breath, cough, and body temperature increased to 38.50C. 4 weeks after massive antibiotic therapy, body temperature decreased, shortness of breath decreased, and moderate leukocytosis remained. During an X-ray examination, a ring-shaped shadow with a fluid level appeared in the second segment of the right lung. Your diagnosis.
Lesson II
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 diseases. 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 diseases. Classification, clinical and morphological characteristics, pathogenesis. Alveolitis. Morphological characteristics, pathogenesis. Pneumoconiosis (anthracosis, silicosis, asbestosis, berylliosis). Pathogenesis and morphogenesis, clinical manifestations, complications, causes of death. Sarcoidosis. Clinical and morphological characteristics, morphology of extrapulmonary lesions.
6. Idiopathic pulmonary fibrosis. Classification, etiology, pathogenesis and morphogenesis, stages and variants, clinical and morphological characteristics, prognosis.
7. Pneumonitis(desquamative interstitial pneumonitis, hypersensitivity pneumonitis): patho- and morphogenesis, clinical and morphological characteristics, causes of death. Eosinophilic infiltrate of the lung. Classification, causes, clinical and morphological characteristics.
8. Tumors of the bronchi and lungs. Epidemiology, principles of classification. Benign tumors. Malignant tumors. Lung cancer. Bronchogenic cancer. Epidemiology, etiology. Biomolecular markers of lung cancer. Precancerous changes in the bronchi and lung. The concept of “cancer in the scar.” 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: pp.415-433, 446-480.
vol.2, part I: pp.293-307, 317-344.
4. Guide to practical classes in pathological anatomy (2002) p. 547-567.
5. Atlas of pathological anatomy (2003) p. 213-217.
TRAINING CARD
GOAL SETTING OF THE LESSON: study the morphology of the main forms of chronic lung diseases using macropreparations, microspecimens and electronograms and make clinical and anatomical comparisons.
CHRONIC NON-SPECIFIC
LUNG DISEASES
View macropreparations, the main clinical and anatomical forms of chronic nonspecific lung diseases. Describe CHRONIC LUNG ABSCESS, CHRONIC BRONCHITIS WITH BRONCHIECTASIS, PULMONARY EMPHYSEMA.
Microslide No. 12 CHRONIC DEFORMING BRONCHITIS (hematoxylin and eosin staining). Note the components of chronic bronchial inflammation: peribronchial sclerosis, vascular pericalibration, inflammatory infiltration in the bronchial wall and peribronchial tissue, metaplasia of the bronchial epithelium.
Electron diffraction pattern 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-hematic barrier.
PNEUMOCONIOSIS
Macropreparation ANTHRACO-SILICOSIS OF THE LUNG. Pay attention to the change in volume and decrease in airiness of the lung tissue. Characterize sclerotic areas in the lung: their shape, size, color, distribution.
Microslide No. 000 ANTHRACO-SILICOSIS OF THE LUNG (hematoxylin and eosin staining). Outline the structure of a silicotic nodule, concentrically located collagen fibers around sclerotic vessels. Pay attention to a significant amount of coal dust contained both in the cytoplasm of macrophages (coniophages) and freely lying in the interalveolar septa.
LUNG CANCER
By set of macropreparations determine the growth patterns and localization of cancerous tumors in the lungs.
Microslide No. 33 SQUAMOUS CELL LUNG CANCER (hematoxylin and eosin staining). Pay attention to the degree of atypia of tumor cells and signs of infiltrating growth.
Microslide No. 34 UNDIFFERENTIATED (anaplastic) LUNG CANCER (hematoxylin and eosin staining). Assess the degree of anaplasia of cancer cells (shape, size, layout). Pay attention to the invasive nature of tumor growth.
KEY VOCABULARY FOR THE CLASS
Bronchiectasis– chronic pathological dilatation of the bronchi.
Obstructive pulmonary diseases– a group of diseases characterized by obstruction of the airways.
Restrictive lung diseases– a group of diseases characterized by the predominance of restrictive (limiting) changes, usually in the interstitial tissue.
Pneumoconiosis– a general name for occupational lung diseases caused by exposure to industrial dust.
Epidermoid cancer– squamous cell carcinoma.
Hamman-Rich syndrome– idiopathic pulmonary fibrosis, diffuse fibrosing alveolitis, chronic interstitial pneumonitis.
Emphysema– excessive and sustained expansion of the airways and respiratory structures located distal to the terminal bronchioles.
Emphysema bullous– emphysema, characterized by the formation of large subpleural blisters (bullas).
Emphysema vicarious (compensatory)– emphysema, which develops when a significant part of the lung is lost (for example, during pneumonectomy, lobectomy).
Emphysema interstitial (intermediate)– emphysema, localized in the interstitium (stroma) of the lung.
Emphysema irregular- emphysema, which affects the acini unevenly, which is almost always associated with cicatricial changes in the lung tissue.
Emphysema obstructive– emphysema caused by incomplete blockage (obstruction) of the airways with the formation of a valve mechanism.
Emphysema panacinar (panlobular)– emphysema, involving the acini from the respiratory bronchioles to the terminal alveoli.
Emphysema paraseptal- emphysema, characterized by changes in the distal part of the acinus, while the proximal part remains normal.
Emphysema centriacinar (centrilobular)– emphysema affecting the central or proximal parts of the acinus, leaving the distal alveoli intact.
List of questions for the lesson,
1. Specify the changes in the myocardium that underlie the development of cor pulmonale in COPD.
2. Select obstructive pulmonary diseases.
3. What is the name for excessive and persistent expansion of the 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 a predisposition to chronic obstructive pulmonary emphysema?
6. Select the most important factors in the development of chronic bronchitis.
7. Name the pathogenetic variants of chronic bronchitis.
8. Name the possible complications of chronic obstructive bronchitis.
9. What disease causes increased reactivity of the mucous membrane of the airways?
10. Specify the pathogenetic variant of bronchial asthma.
11. Name the molecule that binds to 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 pulmonary parenchyma?
16. Name the etiological factors for the development of silicosis.
17. Name the etiological factors in the development of asbestosis.
18. Name the etiological factors for the development of anthracosis.
19. Select the components of 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 for 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 for lung cancer that develops from the epithelial lining of the main, lobar and proximal third of the segmental bronchi?
26. Specify precancerous conditions in the lungs.
27. Name the complications of bronchial cancer.
28. A 53-year-old patient has been smoking 2 packs of cigarettes a day for 30 years. He went to the clinic with complaints of a constant productive cough, worsening in the morning after waking up, and progressive shortness of breath. X-ray images show an increase in the airiness of the lung tissue and an intensification of the pulmonary pattern. Your conclusion.
29. A 30-year-old patient was admitted to the clinic with complaints of shortness of breath, general cyanosis, and weakness. From the anamnesis it is known that the woman has been working on a poultry farm for a long time. During the examination: the level of immunoglobulins in the blood is increased, immune complexes are determined. X-ray examination shows a picture of a “honeycomb lung”. Please indicate the most likely diagnosis.
30. A 67-year-old patient who had suffered for a long time from chronic diffuse bronchitis died with increasing symptoms of pulmonary heart failure. During the pathological examination, the lungs were highly airy and there were many different-sized bubbles in the peripheral sections. Indicate changes in internal organs found at autopsy.
DISEASES OF THE DIGESTIVE ORGANS
(section is studied in two laboratory classes)
Learning goals
The student must know :
1. The cause and main nosological forms of diseases of the digestive system.
2. Classification, morphological manifestations of diseases of the digestive system, their complications and causes of death.
The student must be able to :
1. Describe the morphological changes in the studied macropreparations and micropreparations.
2. Based on the descriptions, compare the structural manifestations of heart and vascular diseases at various levels of the structure of organs, tissues and cells.
The student must understand :
Mechanisms of formation of structural changes that occur in organs during diseases of the digestive system.
Iclass
DISEASES OF THE STOMACH AND INTESTINES
1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, principles of classification. Forms identified based on 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 locations. Epidemiology, etiology, patho- and morphogenesis, its features in pyloro-duodenal and medio-gastric ulcers. Morphological characteristics of chronic ulcers during exacerbation and remission. Complications, outcomes. Acute gastric ulcers: etiology, pathogenesis, morphological characteristics, outcomes.
3. Stomach tumors. Classification. Hyperplastic polyps. Gastric adenoma. Morphological characteristics. Malignant tumors of the stomach. Stomach cancer. Epidemiology, etiology, principles of classification. Features of metastasis. Macroscopic and histological forms.
4. Idiopathic inflammatory bowel diseases. Nonspecific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, prognosis. Criteria for differential diagnosis of chronic colitis.
5. Epithelial tumors of the intestine. Benign tumors. Adenomas: epidemiology, classification, clinical and morphological characteristics, prognosis. Familial adenomatous polyposis. Adenoma and cancer: the concept of multistage carcinogenesis in the colon. Colon cancer. Epidemiology, etiology, classification, macro- and microscopic morphological characteristics, clinical manifestations, prognosis.
6. Diseases 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: pp.384-405, 416-422, 425-441.
4. Guide to practical classes in pathological anatomy (2002) pp. 580-585, 601-612.
5. Atlas of pathological anatomy (2003) p. 256-265.
TRAINING CARD
GOAL SETTING OF THE LESSON: study the morphology of individual nosological forms of diseases of the gastrointestinal tract using macropreparations and micropreparations and make clinical and anatomical comparisons.
STOMACH DISEASES
Macropreparation MULTIPLE EROSIONS OF THE STOMACH. Pay attention to the gastric mucosa with multiple surface defects, note the color of the bottom of the erosions.
Macropreparation CHRONIC GASTRITIS. Pay attention to the relief of the mucous membrane in various parts (body, pyloric canal), the presence of erosion.
Microslide No. 000 Helicobacter pylori in the parietal mucus in the gastric pits (gastrobiopsy, Giemsa stain). View and note the ability of bacteria to adhere to an epithelial cell.
Microslide No. 000 CHRONIC ACTIVE GASTRITIS OF THE ANTRUM WITH GLAND ATROPHY AND COMPLETE INTESTINAL METAPLASY (gastrobioptat, Alcian blue and hematoxylin staining). Describe and evaluate semi-quantitatively the morphological signs of chronic gastritis: activity (presence of neutrophilic leukocytes) and severity of inflammation (density of mononuclear infiltrate), degree of atrophy of the glands of the lamina propria, prevalence of intestinal metaplasia of the integumentary pitted epithelium.
Macropreparation CHRONIC STOMACH ULCER (caleptic). Pay attention to the localization of the ulcer, its shape, edges, depth, and the nature of the bottom. Determine which edge faces the esophagus and which one faces the pylorus.
Microslide No. 000 CHRONIC STOMACH ULCER (with exacerbation) (staining with hematoxylin and eosin). Identify the layers at 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 set of macropreparations, illustrating the complications of a chronic ulcer: PERFORMED STOMACH ULCER, PENETRATING STOMACH ULCER, ARROSION OF A VESSEL AT THE BOTTOM OF THE ULCER, ULCER-CANCER OF THE STOMACH, SCAR DEFORMITY OF THE STOMACH. Pay attention to the localization of ulcers, shape, nature of the edges, changes in the bottom and edges of the ulcer.
Macropreparations different forms of STOMACH CANCER. Determine the macroscopic forms of the tumor. Describe one of the forms.
Microslide No. 000 HIGHLY DIFFERENTIATED GASTRIC ADENOCARCINOMA (intestinal type) (hematoxylin and eosin staining). Identify the signs of tissue and cellular atypia, the invasive nature of tumor growth.
Microslide No. 000 UNDIFFERENTIATED CANCER - signet ring cell (stained with hematoxylin and eosin and alcian blue). Pay attention to tumor cells with alcianophilic cytoplasm located in “lakes” of mucus. Note the shape of the cell - signet ring, the nucleus is pushed to the periphery, the cytoplasm is filled with mucus.
GOW DISEASES
Macropreparation Phlegmonous appendicitis. Pay attention to the size of the appendix, the condition of the serous membrane (appearance, degree of blood supply), wall thickness, and the nature of the contents in the lumen.
Microslide No. 000 PHLEGMONOUS APPENDICITIS (hematoxylin and eosin staining). Describe. Note the degree of preservation of the mucous membrane, the nature of the exudate, its distribution in the layers of the wall and the mesentery (mesenteriolitis).
Macropreparation CHRONIC APPENDICITIS. Pay attention to the size of the process, the condition of the serous membrane, the thickness and appearance of its wall on the section.
Microslide No. 000 CHRONIC APPENDICITIS (hematoxylin and eosin staining). Describe. Note sclerotic changes in the wall and obliteration of the lumen of the process. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.
Macropreparation LIVER ABSCESSES (pylephlebitic), as a complication of appendicitis. View.
View set of macropreparations intestinal tumors.
KEY VOCABULARY FOR THE CLASS
Acute gastritis– diseases manifested by inflammation of the gastric mucosa.
Chronic gastritis– active inflammatory-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 area of the esophagogastric junction.
Penetration– penetration of the defect into neighboring organs (“covered” perforation).
Perforation– perforation.
Pylorospasm– sustained contraction of the pyloric sphincter of the stomach, leading to disruption of the evacuation function.
Polyp- any exophytic node rising above the surface of the mucous membrane.
Enteritis– a group of inflammatory diseases of the small intestine.
Erosion- a defect that does not extend beyond the mucous membrane.
Ulcer- a defect extending beyond the mucous membrane.
Stricture– stenosis, narrowing.
List of questions for the lesson,
which are the basis of the control test
1. Define Barrett's esophagus.
2. Specify the features of Zenker's diverticulum.
3. Indicate the provisions characteristic of Mallory-Weiss syndrome.
4. Specify the factors that ensure the cytoprotective function of the gastric mucosa.
5. Specify the most common cause (etiological factor) of chronic gastritis.
6. Specify methods for detecting H. pylori in a biopsy specimen.
7. Indicate the conditions characteristic of a chronic gastric ulcer.
8. List the factors that significantly reduce the synthesis of prostaglandins and have an ulcerogenic effect.
9. Specify the microscopic features of an acute gastric ulcer.
10. Describe perforation of a gastric ulcer.
11. Check the statements that are characteristic of Zollinger-Ellisson syndrome.
12. Indicate the primary location of gastric ulcers.
13. Select the positions characteristic of cambial cells of the intestinal epithelium.
15. Predisposing factors to the development of hemorrhoids are:
16. Select extraintestinal manifestations of Crohn's disease.
17. Specify the complications of Crohn's disease.
18. Indicate a disease that is characterized by a combination of the following microscopic characteristics - crypt abscesses, granulomas with the presence of giant Pirogov-Langhans cells.
19. Specify microscopic signs of exacerbation of Crohn's disease.
20. Select statements characteristic of volvulus.
21. Specify the pathogenetic factors of colon diverticulosis.
22. Characterize pseudopolyps in ulcerative colitis.
23. What disease is characterized by a macroscopic “cobblestone” type appearance of the colon mucosa?
24. What disease can be suspected if the following signs are present: skin hyperpigmentation, lymphadenopathy and the presence of a large number of macrophages with swollen cytoplasm and PAS-positive granules in an intestinal biopsy?
25. Indicate the characteristic features of celiac disease.
26. Under what conditions does malabsorption syndrome occur?
27. A 64-year-old patient with diabetes developed sharp pain in the epigastric region, which after a few hours moved to the right iliac region, fever up to 39° C, and single vomiting. 12 hours after the onset of the disease, the patient was hospitalized. Upon examination by the emergency room doctor, confusion, fever of 39.6 ° C are noted, and symptoms of peritoneal irritation are positive. Specify the presumptive diagnosis.
28. A 28-year-old patient has been experiencing weight loss for several years, pain in the epigastric region, in the last month he has noticed pallor of the skin, black stool, girdle pain at the epigastric level, yellowness of the skin and visible mucous membranes. FGDS revealed a callous ulcer of the posterior wall of the stomach with undermined edges, the bottom is located deep, filled with dirty gray contents. What complication of an ulcer are we talking about in this case?
29. In a gastrobiopsy of a 43-year-old patient, the presence of lymphoplasmacytic infiltrate in the lamina propria of the mucous membrane is determined; there are clusters of lymphocytes with light centers. Histobacterioscopically, with Giemsa staining, S-shaped rods are detected in the layer of superficial mucus. Specify a 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 fatty liver. Alcoholic hepatitis. Alcoholic cirrhosis of the liver. Epidemiology, pathogenesis and morphogenesis, clinical manifestations, complications and causes of death, outcomes, prognosis.
3. Cirrhosis of the liver. Concept. Pathomorphological signs and classification of cirrhosis according to 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). Changes in the liver in hemochromatosis, Wilson-Konovalov disease, alpha-1-antitrypsin deficiency. Pathogenesis, clinical and morphological characteristics.
4. Liver tumors. Classification, epidemiology. Benign neoplasms. Hepatocellular adenoma. Adenoma of the intrahepatic bile ducts. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification depending on macro - and microscopic features. Complications. Patterns of metastasis. Levels of hepatocellular adenocarcinoma prevalence according to the TNM system. Cholangiocellular carcinoma.
5. Diseases of the gallbladder and bile ducts. Gallstone disease (cholelithiasis). Etiology, pathogenesis, types of stones. Cholecystitis, definition. Acute and chronic cholecystitis: etiology, pathogenesis, clinical and morphological characteristics, complications, causes of death.
6. Diseases of the exocrine pancreas. 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 classes in pathological anatomy (2002) p.634-654, 585-589.
5. Atlas of pathological anatomy (2003) p. 282-288.
TRAINING CARD
GOAL SETTING OF THE LESSON: study the morphology of individual nosological forms of liver diseases using macropreparations, microspecimens and electronograms and make clinical and anatomical comparisons.
LIVER DISEASES
Macropreparation TOXIC LIVER DYSTROPHY (fatty hepatosis). Pay attention to the size of the liver, its color, consistency, and condition of the capsule.
Microslide No. 4 MASSIVE LIVER NECROSIS - subacute form (hematoxylin and eosin staining). Note discomplexation of the beams, signs of fatty degeneration and necrosis of liver cells. Compare the state of hepatocytes in the center and periphery of the lobules. Pay attention to the beginning of stromal fibrosis and infiltration of the portal tracts with lymphoid-macrophage elements.
Microslide No. 5 CHRONIC HEPATITIS OF WEAK ACTIVITY, STAGE I (hematoxylin and eosin staining). Note the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, “spreading” of lymphocytes along the sinusoids, dystrophic changes in hepatocytes, lymphohistiocytic infiltration of the portal tracts. Note the signs of chronic inflammation (hepatitis stage): fibrosis of the portal tracts, fibrous septa growing into lobules. Pay attention to cholestasis: dilation of bile capillaries, imbibition of hepatocytes by bile pigments.
Electron diffraction pattern HYDROPIC DYSTROPHY OF HEPATOCYTE 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.
Macropreparations LIVER CIRRHOSIS. Note the size, color, consistency, appearance of the liver from the surface and in the section. Assess the size of regenerated nodes and determine the macroscopic form of cirrhosis based on this feature.
Microslide No. 48 CHRONIC HEPATITIS OF MODERATE ACTIVITY WITH TRANSITION TO LIVER CIRRHOSIS (staining with hematoxylin and eosin and picrofuchsin). Pay attention to the presence of moderate signs of inflammatory activity (lymphoid infiltration of the stroma, spreading to the parenchyma, fatty degeneration of hepatocytes), dominance of fibrosis (porto-portal, porto-central septa, formation of false lobules) and regeneration of hepatocytes (loss of beam structure, presence of cells with large kernels).
Macropreparations: PRIMARY LIVER CANCER, LIVER METASTASES OF TUMORS OF OTHER PRIMARY LOCALIZATION.
KEY VOCABULARY FOR THE CLASS
Budd-Chiari syndrome– obstruction of the main hepatic veins as a result of thrombosis.
Hepatitis– any diffuse inflammatory disease of the liver.
Hepatoses– a group of liver diseases characterized by the dominance of dystrophic changes and necrosis of hepatocytes.
Jellyfish head– dilation 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.
Councilman's Taurus– eosinophilic round formations in the perisinusoidal space.
Mallory corpuscles– alcoholic hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.
Massive liver necrosis (confluent)– extensive widespread necrosis of most of the liver parenchyma.
Bridging necrosis of the liver (necrosis-bridge)– confluent necrosis of a large number of hepatocytes with the formation of “bridges” between adjacent lobules.
Liver necrosis stepwise (periportal)– destruction of hepatocytes along the border of the parenchyma and stroma, i.e. in the peripheral parts of the lobule.
Liver necrosis focal (spotty)– death of individual small groups of hepatocytes in different parts of the acinus.
Pancreatitis– an inflammatory disease of the pancreas, often accompanied by necrosis.
Goose liver– macroscopic view of the organ with fatty degeneration.
Hepatolienal syndrome– enlargement of the spleen in liver diseases, accompanied by hypersplenism.
Wilson's disease (Wilson-Konovalov disease)– hepatolenticular degeneration, hepatocerebral dystrophy.
Cholangitis– inflammatory disease of the bile ducts.
Cholelithiasis- cholelithiasis.
Cholestasis– insufficiency of bile flow.
Cholecystitis– inflammatory disease of the gallbladder.
Cirrhosis– excessive growth of connective tissue in an organ against the background of dystrophic and regenerative processes, accompanied by a change in the shape of the organ.
List of questions for the lesson,
which are the basis of the control test
1. Indicate the variants of the structure of the liver.
2. List the options for necrosis of the liver parenchyma.
3. What results in the formation of Councilman's bodies?
4. List the forms of acute hepatitis.
5. Indicate the route of transmission of the virus in acute hepatitis A.
6. Indicate the routes of transmission of the virus in acute hepatitis B.
7. Name the indirect markers of viral damage to hepatocytes.
8. Indicate the predominant localization of HBcAg in hepatocytes.
9. What appearance does the accumulation of HBsAg in the hepatocyte give to the cytoplasm?
10. List the etiological variants of chronic hepatitis.
11. Specify the microscopic signs of chronic hepatitis.
12. List the morphological forms of chronic hepatitis.
13. Specify the characteristic signs of alcoholic liver damage.
14. List the options for alcoholic liver damage.
15. Name the cells responsible for collagen formation in alcoholic liver damage.
16. Characterize 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. Specify the signs of portal hypertension.
22. List the causes of death in patients with liver cirrhosis.
23. Characterize primary sclerosing cholangitis.
24. Characterize primary biliary cirrhosis of the liver.
25. Give a description of Wilson-Konovalov 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 suffered from chronic alcoholism for 30 years. Upon examination, the liver is dense, the surface is lumpy. The veins on the anterior abdominal wall are dilated, the spleen is palpable. Indicate possible histological manifestations in the biopsy material.
29. A 50-year-old woman has been bothered by fatigue and skin itching for 8 months. Laboratory testing revealed a minimal increase in the level of transaminases, a significant increase in the level of alkaline phosphatase, and high titers of antimitochondrial antibodies. A biopsy examination revealed granulomatous inflammation in the cholangioles and a decrease in the number of bile ducts with pronounced lymphomacrophage infiltration along the portal tracts with symptoms of sclerosis. Your conclusion.
30. A 63-year-old sick man, who had long suffered from chronic viral hepatitis B, was admitted to the clinic with complaints of heaviness in the right hypochondrium and yellowness of the skin. Upon examination, the liver is dense, its edge is tuberous, an enlargement of the spleen and dilation of the veins of the anterior abdominal wall are noted. Note possible histological findings in the biopsy material.
GASTRITIS (gastritis; Greek, gaster stomach + -itis) - damage to the gastric mucosa with predominantly inflammatory changes during the acute development of the process and phenomena of dysregeneration, structural restructuring with its progressive atrophy during chronic periods, accompanied by dysfunction of the stomach and other body systems.
Ideas about G. changed depending on the level of development of honey. Sciences. Mentions of 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 gastric disorders is associated with the name of the French. doctor F. B. Rousset (1803), who considered glandular disease the most common disease and associated the development of diseases of the heart, brain, and lungs with it. Since the introduction into the wedge, the practice of the gastric probing method [Kussmaul (A. Kussmaul), 1867] G. was considered as a functional disease. However, this point of view was revised in the 2nd half of the 19th century. - early 20th century based on new data patol, anatomy, abdominal surgery, rentgenol. method, research by I.P. Pavlov and his school in the field of physiology of the digestive tract.
Introduction to the wedge, the practice of gastroscopy methods and especially aspiration gastrobiopsy led to an expansion of ideas about gastrointestinal tract. Soviet scientists Yu. M. Lazovsky, N. I. Leporsky, O. L. Gordon, I. P. made a great contribution to the development of the doctrine of gastroscopy Razenkov, S. M. Ryss.
There are acute and chronic. G.
Acute gastritis
There are the following forms of acute gastrointestinal tract: simple (banal, catarrhal), corrosive, fibrinous, phlegmonous.
Pathogenesis of acute gastritis
The pathogenesis of acute gastritis comes down to the development of an inflammatory process of varying severity - from superficial changes to deep inflammatory-necrotic ones. The pathogenesis of the wedge signs is determined, on the one hand, by a violation of the secretory and motor function of the stomach (vomiting, cramping pain, etc.), the depth and severity of inflammatory changes in the stomach (leukocytosis, accelerated ROE, elevated body temperature, pain as a result of irritation of the nerve endings in wall of the stomach), on the other hand, involvement in the patol 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. There are catarrhal, corrosive, phlegmonous and fibrinous G.
Fig. 10. The mucous membrane of the stomach with phlegmonous gastritis (sharp thickening of the folds); On the cut there is purulent infiltration.
At catarrhal G. the mucous membrane is infiltrated with leukocytes (tsvetn, table Fig. 1-3), which are also located between the epithelial cells, inflammatory hyperemia, dystrophic and necrobiotic changes in the epithelium are noted.
At corrosive G. necrotic-inflammatory changes are observed in the wall of the stomach (color. Fig. 9).
At phlegmonous G. (tsvetn. fig. 10) diffuse leukocyte infiltration of all layers of the stomach wall is observed, but Ch. arr. submucosa. Phlegmonous G. is accompanied by perigastritis (see) and can result in peritonitis.
Fibrinous G. is characterized by diphtheritic inflammation of the mucous membrane.
Simple gastritis
Simple gastritis (banal, 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 toxic infections (see. Food toxic infections). The irritating effect of some drugs is known (salicylates, butadione, bromides, iodine, digitalis, antibiotics, sulfonamides, etc.). G.'s development from taking small amounts of medications and under the influence of certain types of food (eggs, strawberries, crabs, etc.) may indicate an allergic mechanism of damage to the gastric mucosa.
Klin, painting of a simple G.(caused by the most common reasons - dietary errors and foodborne toxic infections) 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 covered with a grayish-white coating. On palpation of the abdominal wall - pain in the epigastric region. The pulse is usually frequent, blood pressure is slightly reduced. Possible increase in body temperature, in the peripheral blood - neutrophilic leukocytosis. The urine may contain albuminuria, oliguria, cylindruria, i.e. changes characteristic of toxic kidney damage. There is a lot of mucus in the gastric contents; secretory and acid-forming functions can be suppressed or enhanced. Motor disorders are manifested by pylorospasm (see), hypotension and even gastric atony (see). The duration of the acute period of the disease with timely treatment is 2-3 days.
Complications with simple G. are rare. General intoxication and disorders in the cardiovascular system may develop.
Diagnosis simple G. is based on a wedge, a picture. With an increase in temperature and intestinal dysfunction, gastroenterocolitis can be assumed (see); it is also necessary to differentiate G. from salmonellosis (see). Decisive importance is attached to bacterial, and serol, research.
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, atropine (0.5-1 ml of 0.1% solution subcutaneously), platiphylline (1 ml of 0.2% solution subcutaneously), papaverine (1 ml of 2% solution subcutaneously) is administered. If dehydration develops, fiziol solution, 5% glucose solution is administered subcutaneously. For acute cardiovascular failure - caffeine, mesatone, norepinephrine. It is necessary to prescribe treatment. nutrition. For the first 1 - 2 days you 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 pureed 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 prescribed table No. 1 (see Medical nutrition), and after 6-8 days - normal nutrition.
Forecast with simple G., if treatment is started in a timely manner, it is favorable. If the effect of etiol factors is repeated, then acute G. may become chronic.
Prevention simple G. comes down to rational nutrition, observance of sanitary hygiene. events in everyday life and at public catering establishments, health education, work.
Corrosive gastritis
Corrosive gastritis develops due to the ingestion of substances such as strong acids, alkalis, salts of heavy metals, and highly concentrated alcohol into the stomach.
Wedge, picture of corrosive G. depends on the degree of damage to the mucous membrane of the mouth, esophagus and stomach, the nature and resorptive effect of the substances that caused corrosive G. Patients usually complain of pain in the mouth, behind the sternum and in the epigastric region, repeated painful vomiting; in the vomit - blood, mucus, and sometimes tissue fragments. There are traces of burns on the lips, mucous membrane of the mouth, pharynx and larynx - swelling, hyperemia, ulceration. Sometimes, by the nature of the changes in the mucous membranes, it is possible to determine the cause of the burn: grayish-white spots appear from sulfuric and salt acids, yellow and greenish-yellow scabs from nitrogen, brownish-red scabs from chrome, bright white plaque from carbolic acid, resembling lime, from vinegar - superficial whitish-gray burns. In severe cases, collapse may develop (see). The abdomen is usually swollen, painful on palpation in the epigastric region, and sometimes signs of peritoneal irritation are detected. In some patients, in the first hours after poisoning, acute perforation of the stomach wall occurs, signs of toxic damage to the kidneys are noted (protein, casts in the urine) 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, a 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, wedge, signs (including the nature of changes in the mucous membrane of the mouth, pharynx and larynx).
Treatment You should start by rinsing the stomach with plenty of water through a tube lubricated with vegetable oil. Contraindications to the insertion of a probe are collapse and, obviously, severe destruction of the esophagus.
In case of poisoning, add milk, lime water or burnt magnesia to the water; in case of damage by alkalis - diluted lemon and acetic acid, antidotes are administered. For severe pain, morphine, promedol, fentanyl, droperidol are administered; for collapse, in addition, caffeine, cordiamine, mesaton, norepinephrine, strophanthin (subcutaneously or intravenously with blood substitute fluids, glucose, physiol. solution, etc.). During the first days, fasting, parenteral administration of fiziol, solution and 5% glucose solution are necessary. If it is impossible to feed by mouth for several days, parenteral administration of plasma and protein hydrolysates. In case of gastric perforation, urgent surgical treatment is indicated.
Forecast corrosive G. depends on the severity of inflammatory-destructive changes and therapeutic tactics in the first hours and days of the disease; death may occur from shock, hemorrhage or peritonitis. The outcome of corrosive gastritis is usually cicatricial changes in the stomach, often in the pyloric and cardiac regions.
Fibrinous gastritis
Fibrinous gastritis is rare and develops in severe infectious diseases (smallpox, scarlet fever, sepsis, etc.), as well as poisoning with sublimate, acids, etc., which determines the wedge, picture, treatment and prognosis.
Phlegmonous gastritis
Phlegmonous gastritis occurs, as a rule, primarily as a result of infection entering directly into the wall of the stomach. 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 secondary to certain infections - sepsis, typhoid fever, etc.
Wedge, picture of phlegmonous G. characterized by an acute onset, increased body temperature, chills, severe adynamia and pain in the upper abdomen, usually aggravated by palpation, nausea and vomiting. The general condition is deteriorating sharply. Patients refuse to eat and drink; exhaustion sets in quickly. In peripheral blood - neutrophilic leukocytosis, toxigenic granularity in granulocytes, accelerated erythrocyte sedimentation, changes 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 of large vessels (see Thrombophlebitis), liver abscess (see), etc. .
Diagnosis phlegmonous G. is very rarely diagnosed before surgery.
It is often recognized on the operating table or at autopsy.
Treatment phlegmonous G. consists mainly of parenteral administration of broad-spectrum antibiotics in large doses. If conservative treatment is ineffective, surgical intervention is indicated.
Forecast phlegmonous G. is serious. After treatment, persistent organic changes in the stomach may remain.
Chronic gastritis
Chron. G. makes up the majority of stomach diseases. It is often combined with other diseases of the digestive system.
Chron. G. is the concept of wedge-morphol., it is manifested by a wedge, signs, functional and morphol, changes in various combinations and can occur with various secretion disorders, but more typical is a decrease in gastric juice secretion. Function of acid formation during chronic G. is disrupted 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 etiology
1. Exogenous gastritis: long-term violations of the diet - qualitative and quantitative composition of food; alcohol and nicotine abuse; action of thermal, chemical, fur. and other agents; the influence of occupational hazards - systematically tasting raw meat seasoned with spices (canning industry), ingesting alkaline vapors and fatty substances (soap factories, margarine and candle factories), inhaling cotton, coal, metal dust, working in hot shops, etc.
2. Endogenous gastritis: neuro-reflex (patol, reflex effect from other affected organs - intestines, gall bladder, pancreas); G., associated with violations in the. n. With. and endocrine organs; hematogenous G. (chron, infections, metabolic disorders); hypoxemic G. (chron, circulatory failure, pneumosclerosis, emphysema, cor pulmonale); allergic G. (allergic diseases).
II. According to morphological characteristics
1. Superficial.
2. Gastritis with damage to the glands without atrophy.
3. Atrophic: a) moderate; b) expressed; c) with phenomena of epithelial restructuring; d) atrophic-hyperplastic; other rare forms of atrophy (phenomena of fatty degeneration, absence of submucosa, 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 hydrochloric acid on an empty stomach (or a decrease in its concentration after a test stimulus below 20 titer, units); decrease in pepsin concentration after the test stimulus to 1 g%, mucoprotein concentration below 23%, positive reaction to histamine administration, normal uropepsinogen content.
3. With pronounced secretory insufficiency: lack of free hydrochloric acid in all portions of gastric juice, decreased pepsin concentration (or its complete absence), absence (or traces) of mucoprotein, histamine-refractory reaction; decrease in uropepsinogen content.
IV. According to the clinical course
1. Compensated (or remission phase): absence of wedge, symptoms, normal secretory function or moderate secretory insufficiency.
2. Decompensated (or acute phase): the presence of distinct wedges. symptoms (with a tendency to progress), persistent, difficult to treat, pronounced secretory insufficiency.
V. Special forms of chronic gastritis
1. Rigid.
2. Giant hypertrophic (Menetrier's disease).
3. Polypous.
VI. Chronic gastritis accompanying other diseases
1. For Addison-Biermer anemia.
2. For stomach ulcers.
3. For cancer.
Chron, gastritis, is a polyetiological disease that is the result of untimely and insufficient treatment of acute gastrointestinal tract, as well as prolonged malnutrition, eating foods that irritate the gastric mucosa (spices, onions, garlic, pepper), addiction to hot food and drink, poor chewing food, eating dry food, frequent consumption of alcoholic beverages, poor nutrition, especially with a lack of protein, vitamins and iron. The reason may be long-term use of certain medications (quinine, atophan, digitalis, salicylates, butadione, prednisolone, sulfonamide drugs, potassium chloride, antibiotics, etc.), the influence of factors such as inhalation of cotton, metal, coal dust, alkali vapors, etc. T. Disturbances in the endocrine system (diabetes, gout) can cause the development of structural changes in the gastric mucosa. The release of metabolic products such as acetone, indole, skatole through the gastric mucosa, 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 the development of hron. G. Often chronic. G. develops in diseases that cause tissue hypoxia (chron, circulatory failure, pneumosclerosis, anemia).
From the blood serum of patients hron. G. isolated antibodies with the help of which a model of autoimmune damage to the stomach was reproduced. However, the pathogenetic nature of circulating gastric antibodies has not yet been clarified. There is evidence about the role of genetic factors in the occurrence of hron. G. In patients with a severe form of atrophic G., first-degree relatives are predisposed to this disease, which is manifested by the early (at a young age) onset of G. and its rapid transformation into a severe form.
The pathogenesis is complex and not the same in different forms of hron. G. With chronic G., which develops from acute, there is a progression of primary inflammatory changes in the stroma and the development of secondary dystrophic-regenerative changes in the glandular apparatus (atrophy, hyperplasia, metaplasia, etc.). The mechanism of development of individual forms hron. G., etiologically associated with various nutritional disorders and neuroreflex effects on the stomach, comes down to functional secretory motor disorders of the stomach (see) with subsequent structural changes in its glandular apparatus and the development of the inflammatory process in the stroma. Changes in the secretory activity of the 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.
According to the morphological characteristics, superficial G. and various stages of mucosal atrophy are distinguished. Ts. G. Masevich (1967) distinguishes G. with damage to the bay glands, atrophy of the mucous membrane and G. atrophic. Schindler (R. Schindler, 1968) and Elster (K. Elster, 1970) distinguish hypertrophic G.
The results of histochemistry and electron microscopic examination of biopsy material suggest that the forms hron. G. are phases of disturbance of 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 damage to the glands, and then into atrophic. Surala et al. (1968) estimate 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 secretion accumulation phase: there are no neutral mucopolysaccharides in the apical part of the cells, and a large amount of mucus on the cell surface. The presence of PAS-positive granules above the nuclei indicates increased mucus synthesis (see PAS reaction). Sometimes the epithelium lining the gastric fields and pits appears flattened, with a narrow strip of mucoid, sparse supranuclear granules and high RNA content. Granular and vacuolar dystrophy of the epithelium, infiltration of the ridges' own membrane with lymphoid and plasma cells is revealed (tsvetn, table, Fig. 4). Accessory cells, normally located in the isthmus of the gastric glands, often extend to their middle third.
For chronic gastritis with damage to the glands the surface epithelium of the mucous membrane is flattened, deepening of the gastric dimples is noted, and accessory glandulocytes are hyperplastic.
In the main glandulocytes, vacuoles are detected (Fig. 1), containing neutral mucopolysaccharides (tsvetn, 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 expanded cisterns is revealed (Fig. 2). Thus, in these cells elements of both main (zymogen, RNA, ergastoplasma) and accessory glandulocytes (neutral mucopolysaccharides, well-developed lamellar complex) are found. These cells are, apparently, immature main glandulocytes of the isthmus of the gastric glands. As a result of the slowdown in 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 not usually observed.
Chronic atrophic gastritis is characterized by a decrease (sometimes significant) in the number of main and accessory glandulocytes, deepening of the gastric dimples (tsvetn. fig. 7 and tsvetn, table fig. 6 and 7), which often have a corkscrew appearance (fig. 3), hyperplasia of accessory glandulocytes. The epithelium covering the gastric fields and pits is often flattened, contains a lot of RNA and little neutral mucopolysaccharides, and is in places replaced by intestinal epithelium (color table, Fig. 8) with typical enterocytes, goblet cells and Paneth cells (intestinal metaplasia). The gastric glands are often replaced by mucous glands (pyloric metaplasia). The remaining main glandulocytes are vacuolated; in the parietal glandulocytes, a rarefaction of the cytoplasm is detected in the perinuclear zone and around the intracellular tubules, as well as a decrease in the number of microvilli and tubulovesicles; There is a reduction in the cristae of mitochondria of parietal glandulocytes.
Wolf (G. Wolf, 1968) distinguishes three stages of atrophy of the gastric mucosa: beginning atrophy, when the glands are not yet shortened, but look as if compressed; partial atrophy (glands), in which groups of glands containing main and parietal (lining) glandulocytes are preserved; 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 table 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, found at the edges of the ulcers; for proliferative - proliferation of the surface epithelium, deepening of dimples, glandular apparatus without changes; in the glandular form, the mucous membrane is thickened 2-7 times due to hyperplasia of the glands; this form is chronic. G. occurs with duodenal ulcer (see Peptic ulcer), Zollinger-Ellison syndrome (see Zollinger-Ellison syndrome) and as an independent disease. Some authors attribute hron to the glandular form. G. and Ménétrier’s disease, designating it as gastritis hypertrophica gigantea, although Ménétrier 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 Ménétrier’s disease with G., considering it as an anomaly of the development of the gastric mucosa.
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 diet, consumption of alcoholic beverages, including table wines and beer. Patients complain of heartburn, sour belching, a feeling of pressure, burning and distension in the epigastric region, constipation (sometimes diarrhea), and rarely vomiting. The pain is usually dull, aching, without any specific irradiation, localized in the epigastric region, and its occurrence is usually associated with food intake. But the pain can be “hungry” and “night”, and subside after eating.
Early complications are motor disorders of the intestines and biliary tract (hyper- and hypomotor dyskinesias). Subsequently, 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 - concept wedge; morphol, its picture may be different. Bleeding in G. is most often associated with the development of erosions, but sometimes the mechanism of bleeding remains unclear even after histol, examination of the resected part of the stomach. The acidity of gastric juice plays a certain role in the occurrence of gastric bleeding (the higher the acidity, the more frequent the bleeding). Heavy gastric bleeding usually develops in patients with minor wedge manifestations, who are believed to have increased permeability of the blood vessels of the stomach. The development of massive gastric bleeding can also be caused by allergic reactions (see Gastrointestinal bleeding).
Special wedge-morphol. chronic form. G. with normal and increased secretion is gastroduodenitis (syn.: pyloroduodenitis, hypertrophic glandular gastropathy, hypertrophic hypersecretory gastropathy), which occurs mainly at a young age. It is similar in wedge, manifestations to duodenal ulcer, although not identical to it. I.M. Flekel (1958) considered gastroduodenitis a prestage of peptic ulcer disease or a form of “peptic ulcer without ulcer.” The frequency of the disease (during the day and year) is less pronounced than with peptic ulcer disease. The most characteristic of the wedge symptoms is pain (“painful gastritis”), 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” pain.
The secretory and acid-forming functions of the stomach are usually enhanced, but less than with a duodenal ulcer: the value of basal secretion is up to 10 meq/hour, and the maximum secretion is 35 meq/hour (Yu. I. Fishzon-Ryss, 1972). Often there is abundant gastric secretion at night.
Chronic gastritis with secretory insufficiency more common in mature and elderly people. Patients usually experience weight loss, adynamia, and symptoms of multivitamin deficiency - dry skin, loose and bleeding gums, changes in the tongue (thickening, redness, smoothness of the papillae, the presence of teeth marks), cracks on the lips, particularly in the corners of the mouth. Gastric symptoms include loss of appetite and the desire to eat hot and spicy foods outside the period of exacerbation. Some patients cannot take solid food without liquid, which they drink before and during meals. Patients note an unpleasant taste in the mouth, especially in the morning, nausea, a feeling of fullness and distension in the epigastric region, and belching of air. The stool is unstable with a tendency to diarrhea. Dyspeptic symptoms usually occur soon after eating; patients tolerate milk especially poorly. In some cases, nausea and drooling are persistent and painful for patients, and they seek to alleviate their condition with frequent meals. Pain in the epigastric region is sometimes noted.
Complications - hypermotor dysmnesia of the intestine or involvement in the patol, process of the pancreas and gall bladder. Stomach bleeding is rare. Some patients have allergic reactions to certain food and medicinal substances.
Sometimes (more often in women) iron deficiency anemia develops (see). Changes in the intestines are often observed, the exocrine function of the pancreas decreases, and dysbiosis develops (see), manifested by fermentative or putrefactive dyspepsia.
Special forms hron. G. (rigid, polypous and giant hypertrophic) are distinguished by the originality of the wedge, manifestations and morphology, features. Some researchers attribute these forms to complications of 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. study and based on gastroscopy data. The outlet section of the stomach is predominantly affected, which, due to hypertrophic changes, edema and spastic contraction of the muscles, is deformed, turning into a narrow tube-like canal with dense, rigid walls.
Polypous gastritis(tsvetn. fig. 8) usually develops against the background of atrophic G. with histamine-refractory achlorhydria, it can be considered as a further progression of hron. G. (disregenerative hyperplasia of the mucous membrane).
Giant hypertrophic gastritis, or more precisely, excessive development of the mucous membrane, described by Menetrier (P. Menetrier, 1886), is a relatively rare disease manifested by metabolic disorders (usually protein) and very rarely the development of iron deficiency anemia. Changes in the acid-forming function of the stomach vary (see also table).
The diagnosis is based on an analysis of the wedge, manifestations of the disease, the results of a study of gastric secretion (see Stomach, research methods), rentgenol, studies, gastroscopy data (see) and gastrobiopsy.
In assessing morphol, pictures of the gastric mucosa, preference should be given to gastrobiopsy data. Exfoliative cytodiagnosis, 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 (see).
With functional disorders of the stomach, there are usually no sharp morphological changes. In addition, they have a relatively short-term (up to 1 year) course, less dependence of the occurrence of pain on food intake, and greater variability wedge. manifestations, which is associated with neuropsychic influences, atypical localization of pain on palpation of the abdomen and, finally, a sharp fluctuation in acidity during individual studies.
X-ray diagnosis is based on a thorough x-ray examination of the stomach. In this case, changes in the relief of the gastric mucosa and other x-ray functional and morphological symptoms are determined. These include: excessive secretion on an empty stomach, a rapid increase in secretory fluid, changes in tone, persistent deformation of the pyloric part of the stomach, impaired peristalsis, etc. The most constant symptom of increased secretion on an empty stomach, sometimes manifested by a horizontal level of fluid against the background of the gastric bladder before taking a barium suspension. The first one or two sips of barium suspension confirms the presence of excess fluid. By the nature of the mixing of barium with the 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 (mucus phenomenon) are pinpoint clearings in the layer of barium suspension - tiny droplets of mucus suspended in a barium suspension. The phenomenon of mucus is indistinguishable during transillumination and can only be ascertained on compression images. Chron. G. is often accompanied by a decrease in gastric tone. The increase in tone is often local; with antral gastritis, this is manifested by spastic conditions or motor excitation of the outlet part of the stomach. Violation of peristaltic function is not always detected. In approximately half of the cases hron. G. superficial and rare peristalsis is observed. Severe 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 in normal times, although occasionally it may be delayed.
Chron forms. G. radiographically differ hl. arr. by the nature of the relief of the mucous membrane. According to the Schindler-Gutzeit classification, there are: hypertrophic G., atrophic G., mixed G., superficial chronic, mucous catarrh. In turn, hypertrophic G. has subtypes: 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 hypertrophy and atrophy of the mucous membrane; in addition, with chronic 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.
X-ray, data chronicle. G. can be taken into account only with an appropriate wedge, picture, history, etc. Numerous facts are known when pronounced rentgenol, G.’s symptoms were not confirmed by biopsy data and, conversely, morphologically proven G. did not manifest itself radiographically.
At hron, universal G. the area of the reconstructed 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 some places, the folds form polyp-like thickenings and have a distinct appearance (Fig. 6). Along the greater curvature, oblique and transverse bridges between the folds thicken, so the contour of the greater curvature, Ch. arr. the lower half of the body of the stomach and sinus becomes jagged and fringed. With severe swelling, the mucous membrane loses its plasticity, which is accompanied by a symptom of relief rigidity. Inflammatory restructuring of the relief of the mucous membrane during chronic G. is sometimes so disorderly and chaotic that it is difficult to distinguish it from the atypical relief in stomach cancer. Only a series of targeted photographs of the relief of the mucous membrane help to establish the remaining 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 to G. Similar pictures can occur with allergic swelling of the mucous membrane, with systemic diseases, etc. An important aid in the X-ray diagnosis of chronic, universal G. is the symptom of hypersecretion, as well as signs of the presence of mucus in the gastric contents on an empty stomach.
Hron, antral G. are among the most common varieties of hron. D. It has a bright, diverse, and most importantly, the most convincing x-ray semiotics. X-ray, the picture is characterized by signs of hypersecretion, the phenomenon of mucus, patol, restructuring of the relief of the mucous membrane. In addition, deformation of the antrum and disturbance of its peristalsis are detected. The relief pattern varies: more often there are sharply swollen, expanded folds, but retaining the usual longitudinal direction, their number is reduced. With severe swelling, they form shapeless, pillow-shaped relief defects, the grooves between the folds disappear, and the relief is smoothed out. A classic example of relief during hron. G. of the antrum are quite persistently preserved thickened transverse folds of the mucous membrane (Fig. 7), along the greater curvature of the stomach there is an uneven contour in the form of uniform serration. With long-term chronic G. with secretory insufficiency, the relief is disordered and consists of shapeless bulges (defects) and spots and strips of barium randomly located between them. In some cases, relief atypia occurs due to increased mobility of the swollen mucous membrane relative to the loose, inflammatory altered submucosa. With a wide pyloric canal, partial prolapse of the mucous membrane into the duodenal bulb is possible. With normal lumen of the pylorus, the gastric mucosa does not prolapse. However, the periodically “sliding” mucous membrane, accumulating in front of the pylorus, forms a kind of defect here, reminiscent of a tumor lesion (Fig. 8). This “crawling phenomenon” of the mucous membrane was first explained and described by Yu. N. Sokolov and V. K. 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 deformation with infiltrating cancer, in which 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 permanent. As a result of inflammatory submucosal sclerosis (the so-called sclerosing G.), peristalsis disappears and rigid antral G. appears, which is undoubtedly a late stage of hron, antral G. with secretory insufficiency. In these patients, on the basis of the wedge, gastric cancer is often suspected, which is often difficult to refute with radiographs, research. The deformation of the antrum is very pronounced and persistent. Noteworthy is the circular narrowing of the pyloric part of the stomach, while its simultaneous shortening often goes unnoticed (Fig. 9). On palpation, a sensation of a dense and painful tumor is created. The presence of cancer is indicated by a symptom of the aperistaltic zone, which usually covers the entire antrum. The observation against cancer is evidenced by the observation of at least short-term peristalsis, which can also be induced with the help of morphine.
With polypous (warty) G. patol, changes are often localized in the antrum. They are multiple, homogeneous in size, round, blurred defects in diameter. 3-5 mm, sometimes in the form of elevations on the crests of folds, but more often forming a random or honeycomb pattern (Fig. 10). With true polyps, even multiple ones, the relief of the gastric mucosa is usually not changed. With polypous G., as a rule, other rentgenol symptoms are found. With smaller growths, G. is called warty, or verrucous; minor defects are usually recognized only on targeted compression images.
Granular gastritis is recognized by the symptom of “graininess” of the relief (Fig. 11). This symptom was studied by W. Frik using relief photographs of a high-focus X-ray tube at short shutter speeds (no more than 0.1 sec.). This creates the impression of a granular surface of the mucous membrane with tiny elevations - the so-called. gastric fields. A comparison of the “fine relief” study data with the results of gastrobiopsy revealed a parallelism between the picture of 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 chronic. G. gastric fields become more convex - “granular” type, and in advanced cases - larger (diameter 3 mm or more), uneven, resembling a warty surface. Along with this symptom, it is necessary to detect the other above-described rentgenol, signs of G.
Erosive G. is rarely recognized radiologically, since the possibilities of detecting erosions rentgenol, by the research method are very limited.
So-called accompanying (concomitant) G. is constantly detected radiographically in peptic ulcers (the exception is the so-called senile gastric ulcers) and less often in gastric cancer.
Pronounced patterns of accompanying G. are observed in cases of duodenal ulcer, after gastroenterostomy surgery. When accompanied by G., the outlet part of the stomach is more often affected. All of the above described rentgenol are also observed. symptoms G. A rough pattern of relief of the mucous membrane, disorder and swelling of the folds are often noted. Dynamic klin.-rentgenol, observations of the course of accompanying G. with peptic ulcer disease 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.
When rentgenol, research, recognition of polyposis G., which should be differentiated from true polyps of the stomach, can present certain difficulties. When diagnosing chronic antral G., it is also necessary to keep in mind pernicious anemia, in which 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 gastritis with a sharp restructuring of the relief of the mucous membrane, which is sometimes indistinguishable from the atypical relief in cancer. In this sense, the “phenomenon of crawling of the mucous membrane” described above is of particular importance. If there are difficulties, a series of photographs or x-ray cinematography, fiberoscopy and gastrobiopsy are used. With the so-called In systemic diseases, only a thorough analysis of the entire wedge picture allows us to arrive at the correct diagnosis.
See also Stomach, X-ray diagnostics.
Treatment complex and differentiated. Treatment is usually carried out on an outpatient basis; patients are hospitalized during exacerbations, especially those occurring with complications and severe general disorders.
Medical nutrition in complex therapy G. is of leading importance. During the period of exacerbation hron. G., regardless of the nature of secretory disorders, adhere to the principle of sparing the gastric mucosa and its functions. Food should be well cooked and chopped. Products and dishes that have a strong juice effect, as well as those that cause mechanical, thermal and chemical damage, are excluded from the diet. irritation of the gastric mucosa. Diet 1A is prescribed (see Medical nutrition). Small meals, 5-6 times a day. As the exacerbation subsides, diet therapy is carried out in accordance with secretory disorders.
In case of secretory gastric insufficiency (outside of exacerbations), the diet should be complete with a sufficient amount of proteins (110-115 g), fats (80-90 g), carbohydrates, vitamins; it must correspond in terms of caloric intake to work activity and the patient’s lifestyle. Diet No. 2 is prescribed. Food must be taken 4-5 times a day. The diet includes a normal amount of table salt and extractives. In case of stable remission, extended nutrition can be prescribed. Fresh bread and other fresh dough products, fried (including breaded) 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 move to table 1B, and after the next 7-10 days - to diet No. 1. The diet should be complete, but with a limitation of table salt, carbohydrates and extractives, especially with high acidity. At night, milk laxatives (fresh kefir, yogurt) are recommended. Cabbage soup, borscht, fatty meat, fried fish, pickles, smoked foods, marinades, and raw vegetables are prohibited. Alcohol, beer, sparkling water, and fruit water are strictly contraindicated.
Drug treatment of patients chronically. G. provides an impact on the pathogenetic links of the patol process. To normalize the functional state of the higher parts of the c. n. With. They recommend valerian preparations, minor tranquilizers, and sleeping pills.
In case of increased secretory and motor-evacuation functions of the stomach, anticholinergic drugs (atropine, platiphylline, antispasmodic, benzohexonium) should be prescribed in combination with antacids (vicalin, almagel, etc.) and agents that stimulate regenerative processes (methyluracil, pentoxyl, licorice preparations, etc. ).
In case of secretory insufficiency, anticholinergic drugs are prescribed, like quaterone and ganglerone, 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 by using 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, replacement therapy is used - gastric juice, abomin, betacid, pancreatin, etc.
Physical methods of treatment are also included in the complex to treat. activities: heating pads, mud therapy, diathermy, electro- and hydrotherapy.
Sanatorium-resort treatment of patients with chronic gastritis is carried out without exacerbation of the disease. Resorts with mineral waters for drinking treatment are shown: Arzni, Arshan, Berezovsky mineral waters, Borjomi, Izhevsk, Jalal-Abad, Jermuk, Druskininkai, Essentuki, Zheleznovodsk, Pyatigorsk, Sairme, Feodosia, Shira, etc. Mineral waters can also be used outside the resort conditions: in case of secretory insufficiency, it is preferable to drink chloride, chloride-bicarbonate waters within 15-20 minutes. before meals, and with normal and increased secretory function - bicarbonate water 1 hour before meals.
Treatment chronic. G. is also possible in local sanatoriums, as well as under normal conditions, subject to diet.
The prognosis for life is favorable. Under the influence of treatment, the well-being of patients improves relatively quickly. But the main morphol, changes characteristic of hron. G., as well as the secretory function of the stomach, are not normalized under the influence of treatment. With massive bleeding in patients chronic. 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 system (chron, pancreatitis, chronic, cholecystitis, etc.). With special forms hron. G. (rigid, polypous, giant hypertrophic) there is a danger of malignancy.
Prevention of chronic G. consists of a balanced diet and compliance with food hygiene rules, as well as in the fight against the consumption of alcoholic beverages and smoking. It is necessary to monitor the condition of the oral cavity, promptly treat diseases of other abdominal organs, eliminate occupational hazards and helminthic-protozoal infestations. Clinical examination of patients with G. is of great importance.
Gastritis in children
Acute gastritis in children occurs as a result of infection, consumption of infected, difficult to digest food, overeating and as a manifestation of allergies. Its etiology, clinical picture and treatment methods are similar to acute gastritis in adults.
Chronic gastritis occurs mainly in children of preschool and school age; Its prevalence is higher in school-age children.
The reasons for the occurrence of 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 impaired synthesis of hydrochloric acid, which is confirmed by the presence of persistent achylia (in practically healthy and sick G. children), to This cannot be explained either by past illnesses or by nutritional defects.
In children with long-term diseases and disorders, gout. tract chronic. G. as an independent disease is rarely observed. At the same time, the study of the gastric mucosa by gastrobiopsy has changed ideas about the prevalence of G. in children: wedge, G.’s diagnosis is confirmed only in half of the cases. In children of high school age and adolescents, chronic. G. is becoming a fairly common disease.
Morphologically, superficial gastritis and gastritis with damage to the glands without atrophy predominate in children; atrophic gastritis is less common (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 - a low-symptomatic form and a form with severe symptoms, often similar to peptic ulcer disease. The asymptomatic course of G. has also been described.
Low-symptomatic form of chronic. G. is less common than the form with severe symptoms; often occurs in younger children: the pain usually appears after eating, is low-intensity, localized in the epigastrium or diffuse. Some children have no dyspeptic symptoms. The acid-forming function of the stomach is reduced or histamine-reflex achylia is determined.
With chronic G. with severe symptoms, the pain symptom is intense and can occur immediately after eating, after 1 - 2 hours or at night. Dyspeptic symptoms are constant. The acid-forming function in most sick children is increased during long-term observation. Some children later develop peptic ulcer disease, in which case G. is essentially a pre-ulcerative condition.
G.'s diagnosis is established on the basis of a combination of data from the anamnesis, wedge, manifestations and laboratory tests.
Differential diagnosis hron. G. in children is carried out with peptic ulcer (see), diseases of the liver (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 the milder course of the chronic disease than in adults. G., there are no sufficient grounds for the widespread use of gastrobiopsy for diagnostic purposes in pediatric practice. It is used only according to strict indications and always in a specialized clinic to eliminate possible complications.
Treatment of gastritis in children is basically the same as in adults (taking into account age and form of the disease).
For G., clinically similar to a peptic ulcer, treatment is carried out according to the antiulcer type, including seasonal preventive courses.
Prevention of chronic G. in children has the same principles as in adults.
Constitutionally weakened children with signs of dysfunction of the gastrointestinal tract require special attention. tract (increased acid-forming function, achylia, etc.), with residual effects after diseases of the digestive and other systems.
Sick chronic. D. children are subject to observation by a pediatrician in order to prevent exacerbations of the disease, carry out preventive anti-relapse courses of treatment and recreational activities.
Gastritis in old and senile age
Features of the course of G. are due to age-related changes in the 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 mild, and a decrease in appetite is rarely observed. The digestive ability of gastric juice and the content of gastromucoproteins in it is reduced as well as the acid-forming function of the stomach. The electropherogram of gastric juice proteins, compared to the electropherogram of young patients, has a more “compressed” appearance, the flow rate of the protein component is lower in both fractions of gastric mucus, and the carbohydrate component is increased in insoluble mucus. A glassy basal secretion 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 occur in patients with chronic. G. at the age of over 60 years is 2-3 times more common than in 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 high prevalence of atrophic G. in old age is apparently associated with the frequent development at this age of hron, diseases of the liver, pancreas, and intestines, which contribute to the development of hron. G.
Treatment and prevention are based on concomitant chronic conditions, diseases and the characteristics of the elderly body’s reaction to the administration of medicinal substances. When determining the prognosis, one should keep in mind the possibility of cancer occurring against the background of chronic, atrophic G.
Experimental gastritis
In order to study the patterns of activity and mechanisms of regulation of the digestive system under pathological conditions, as well as to develop issues of G.’s therapy, the G. model is reproduced in animals.
There are two groups of experimental G. models, which are used depending on the objectives of the study: a) G. caused by the local effect 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 mucous membrane of the stomach of animals, hot and cold water, as well as chemicals, are used. substances (1 - 10% solutions of silver nitrate, 1% acetic and 10% hydrochloric acid, alcohol solutions, infusion of mustard, red pepper, etc.), which are introduced once or repeatedly into the stomach cavity. With such exposure to a damaging agent, it cannot be excluded that it will enter the initial part of the duodenum, which complicates the picture of functional and morphological disorders and cannot always be taken into account. There are techniques for limited damage to the gastric mucosa that reproduce focal G., usually acute. With repeated injuries, experimental acute G. can pass into a chronic form. Of practical interest in the models of this group is experimental gastritis, caused by the introduction of various volumes of alcohol of different concentrations into the stomach.
I. P. Pavlov created models of experimental gastrointestinal tract by directly damaging the stomach and observing the work of an isolated ventricle. He established the compensatory ability of the preserved mucous membrane and analyzed in detail the complex complex of intrasystemic and extrasystemic reactions in the body in response to damage to the stomach. I.P. Pavlov initiated the classification of types of gastric secretion disorders, which is used in the clinic.
Model of G., caused by the creation of non-fiziol. conditions of contact of normal secretion products of the gastric glands (acidopeptic factors) with the mucous membrane are achieved by prolonged repeated imaginary feeding (gastric juice remains in the stomach cavity), by adding salt or gastric juice in excess to food. Experimental disturbance of physiol. The relationship 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 changing the spectrum of proteolytic enzymes or by administering histamine or pilocarpine. This model of G. develops gradually against the background of microcirculation disorders and trophic processes in the mucous membrane, and has a chronic course.
Clinical and diagnostic characteristics of some clinical forms of chronic gastritis
|
chronic gastritis |
Main clinical signs |
Data from gastric secretion studies |
X-ray research |
Gastroscopy data |
Biopsy data |
|
Antral |
Pain in the epigastric region is hungry, nocturnal, sometimes subsiding after eating; heartburn, sour belching, often vomiting at the height of pain. Tendency to constipation |
Promoted |
The relief of the mucous membrane in the antrum is changed: thickening of the longitudinal folds, patol. restructuring, granular formations, the presence of mucus phenomenon. Increased tone and weakened peristalsis of the antrum. Signs of hypersecretion. Often deformation of the antrum |
In the pyloric part of the stomach, redness of the mucous membrane, swelling of folds, erosion and hemorrhages in the submucosal layer are detected. The tone of the pyloric part is increased, and sometimes prolonged pylorospasm is observed. Signs of hypersecretion |
Gistol, the picture of the mucous membrane is normal or has signs of hron, gastritis of varying severity. In the antrum there are signs of hyperplasia, often a rare location of the pyloric glands, pronounced cellular infiltration of the own layer, areas of intestinal metaplasia |
|
Giant hypertrophic gastritis (Menetrier's disease) |
Weight loss, signs of hypoproteinemia, iron deficiency anemia. Persistent gastric dyspepsia. Patients note a feeling of spasm and pressure in the epigastric region. The pain sometimes resembles the pain of a peptic ulcer; vomiting may be bloody |
Decreased, normal or increased |
Pronounced changes in the relief of the mucous membrane along the greater curvature (in the area of the sinus and the lower half or third of the body of the stomach) in the form of redundantly located, elastic thickened folds hanging into the lumen of the stomach, and sometimes into the duodenum |
The mucous membrane is swollen, with wide tortuous 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 condition does not change. Pain in the epigastric region occurs immediately after eating, combined with a feeling of heaviness and fullness. The pain is diffuse, dull, aching, usually moderate, less often intense, lasting 1 - 11/2 hours. Heartburn, often belching air, intermittent vomiting |
Basal secretion increases to 10 mEq/hour, maximum histamine secretion increases to 35 mEq/hour. Often there is abundant gastric secretion at night |
Widespread restructuring of the relief of the mucous membrane with thickening of the folds (sometimes their cushion-like bulging) until the disappearance of the grooves; smoothness of the relief in the antrum. Violation of tone and peristalsis. Signs of hypersecretion |
Redness, hypertrophy of folds, swelling, the presence of mucus, isolated erosions and hemorrhages in the submucosa, signs of hypersecretion. With pronounced hypertrophy, the mucous membrane has a velvety appearance without the usual shine |
Flattening of the mucous membrane due to hyperplasia of the surface epithelium, less often interstitial tissue. The epithelium is often flattened, with a basal arrangement of nuclei of different sizes; hypersecretion of flour yes, signs of granular and vacuolar degeneration; abundant cellular infiltration of the own layer |
|
Polyposis |
Reminds the clinic of chronic gastritis with secretory insufficiency; may also be asymptomatic. The prolapse of polyps into the duodenum and their strangulation is clinically manifested by severe pain syndrome. Bleeding may occur |
Often reduced |
Characteristic changes are most often localized in the antrum - typical small, uniform, round filling defects, sometimes on the crests of the folds, but usually they form a random or honeycomb pattern. With true polyps, even multiple ones, the relief of the mucous membrane is usually not changed |
Multiple polyps are found, identical or different in shape and size, which are often located in the pyloric part. The mucous membrane is pale, thinned, its folds are smoothed, blood vessels are visible (atrophic gastritis) |
Outside the localization of the polyp, the picture of atrophic gastritis |
|
Rigid |
Long-term 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 |
Deformation, rigidity and narrowing of the pyloric part of the stomach, swelling of the mucous membrane |
In the outlet section there is a picture of atrophic-hyperplastic hron, gastritis. In other parts there is atrophy of the glandular apparatus of varying degrees of severity |
|
Gastritis with secretory insufficiency |
Weight loss and loss of appetite, a feeling of heaviness and pressure in the epigastric region after eating. The pain is moderate and intermittent, nausea, rarely vomiting. Tendency to diarrhea, flatulence; poor tolerance to milk, 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, 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. Sometimes erosions and pinpoint hemorrhages are observed |
Various degrees of gland atrophy (reduction of main and parietal glandulocytes), flattening of the mucosal epithelium, deepening of the pits, intestinal and pyloric metaplasia |
|
Erosive gastritis (hemorrhagic) |
Pain in the epigastric region: early, on an empty stomach and late; sour heartburn, sometimes vomiting with blood (from traces to clots). The higher the acidity, the more often the bleeding Tendency to constipation |
Normal or increased |
The relief of the mucous membrane is changed more often in the pyloric part of the stomach. The ability to detect erosions is very limited |
Multiple erosions of a round or stellate shape are detected, 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 often similar to the picture of hron, gastritis with increased secretion. Erosions are more often detected during targeted biopsy |
Bibliography: Aruin L.I. Morphological study of biopsies of the gastric mucosa, Arch. pathol., t. 31, no. 3, p. I, 1969; AruinL. I. and Sh and -r about in V. G. On the question of the morphogenesis of chronic gastritis, in the same place, t. 33, No. 10, p. 21, 1971; Belousov A. S. Essays on the functional diagnosis of diseases of the esophagus and stomach, M., 1969, bibliogr.; Gordon O. L. 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 for diagnosing diseases of the stomach, L., 1964; Lazovsky Yu. M. Functional morphology of the stomach in normal and pathological conditions, M., 1947; Levin G. L. Essays on gastric pathology, M., 1968; L i s o h k i n B. G., Ultrast structure of the gastric glands and its changes in conditions of chronic gastritis, Arkh. pathol., t. 34, no. 10, p. 11, 1972; Masevich T. G. Aspiration biopsy of the mucous membranes of the stomach, duodenum and small intestine, L., 1967; o n e, Precancerous diseases of the stomach, L., 1969, bibliogr.; Menshikov F.K. Diet therapy, M., 1972, bibliogr.; Pavlov I.P. Complete works, vol. 2, book. 2, M.-L., 1951; PeleschukA. P. Diseases of the digestive system and organs, in the book: Fundamentals of Gerontology, ed. D. F. Chebotareva et al., p. 322, M., 1969; Rachvelishvi-l and B. X. Gastrobiopsy in clinical practice, Tbilisi, 1969; P s with S. M. Diseases of the digestive organs, L., 1966; Tugolukov V.N. 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 with Yu. I. Modern methods of research of gastric secretion, L., 1972, bibliogr.; about n e, Gastritis, L., 1974, bibliogr.; V o s k u s H. Gastroenterology, u. 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 Patienten mil umunischer Gastritis im hoheren 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 A.N. and Sokolov Yu.N. Rigid antral gastritis as a precancerous disease of the stomach, Surgery, No. 4, p. 34, 1947; Saghatelyan G. M. X-ray diagnosis of diseases of the esophagus, stomach and gastroscopy, Yerevan, 1966, bibliogr.; Smirnova N.V. Diagnosis of gastritis of the distal stomach, Klin, med., t. 49, No. 1, p. 69, 1971; With about to about l about in Yu. N. and In l and with about in P. V. Relief of the gastric mucosa in normal conditions and pathologies, M., 1968, bibliogr.; Sokolov Yu. N. and Gasmaev V. K. About the phenomenon of “crawling” of the gastric mucosa, Vestn, rentgenol, i radiol., No. 2, p. 66, 1969; Sokolov Yu. N. id r. Our experience in studying the fine relief of the stomach in chronic gastritis, ibid., No. 5, p. 3, 19 73, bibliogr.; Tikhonov K. B. and Pruchansky V. S. Microrelief of the gastric mucosa and its significance in the diagnosis of chronic gastritis, ibid., No. 2, p. 82, 1970, bibliogr.; F a n a r d-sh i n V. A. X-ray diagnosis of diseases of the digestive tract, vol. 1, Yerevan, 1961; Sh l and f e r 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 s r i s h M. Rontgendiagnostik des Magen-Darmka-nals, Stuttgart, 1959, Bibliogr.
G. in children- Balashova T. F. Enzyme-forming function of the stomach in chronic gastritis in children, Pediatrics, No. 5, p. 14, 1971; G and al about in S. M. et al. Endocrine cells of the gastric mucosa in children, in the same place, No. 3, p. 12, 1975, bibliogr.; Koroleva R.I. and Bialik V.L. On the diagnostic value of aspiration biopsy of the gastric mucosa in chronic gastritis in children, ibid., JNft 12, p. 22, 1966; CossuratM. B. Stomach diseases in children, M., 1968, bibliogr.; Lukyanova E. M., Korole-z v a R. I. and Sh l y k o v I. A. Endoscopic studies of the stomach in chronic gastritis in children, Pediatrics, No. 3, p. 17, 1975; Multi-volume guide to pediatrics, ed. Yu. F. Dombrovskaya, vol. 4, p. 191 and others, M., 1963; O s t r o p o-let S. S. et al. Morphological condition of small gastritis with normal secretory function of the scutum in children, Ped1at., Obstetrics. i gshek., No. 4, p. 3, 1975; Samarina G. Ya. Clinical features of antral gastritis in children, Vopr. ocher mat. and children, vol. 18, no. 6, p. 23, 1973; Smirnov N. 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, Gastroen-terologia (Basel), v. 107, p. 251, 1967.
F. I. Komarov; L. I. Aruin (path. an.), M. B. Kossyura (ped.), N. N. Lebedev (path. physic.), A. P. Peleshchuk (geront.), Yu. N. Sokolov ( rent.), compiler of the table F.I. Komarov.
lung tissue
lobar pneumonia
hematoxylin and eosin staining
stomach wall
chronic stomach ulcer
hematoxylin and eosin staining
metastasis of mucous cancer in lymph nodes
with tumor progression
coloring Sudan Sh
Congo red coloring
kidney tissue
kidney amyloidosis
hematoxylin and eosin staining
LN tissue section
tuberculosis
hematoxylin and eosin staining
septic myocarditis
causes – sepsis
hematoxylin and eosin staining
cause - damage
brain tissue
local hemosiderosis
hematoxylin and eosin staining
skin section
the reasons are polyetiological
hematoxylin and eosin staining
gastric mucosa
gastric adenocarcinoma
the reasons are polyetiological
hematoxylin and eosin staining
aortic section
the wall of the aorta, in its middle shell, where the vasavasorum are located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.
syphilitic mesaortitis
hematoxylin and eosin staining
myocardial hypertrophy
hematoxylin and eosin staining
brain tissue
purulent leptomeningitis
meningococcal infection
picrofuchsin staining according to Van Gieson
fibroids
the reasons are polyetiological
MICROPREPARATION No. 58. Fibromyoma ()
hematoxylin and eosin staining
kidney tissue
ischemic renal infarction
hematoxylin and eosin staining
lung tissue
hemorrhagic pulmonary infarction
thrombosis, embolism
MICROPREPARATION No. 62.
hematoxylin and eosin staining
brain tissue
cerebral hemorrhage
coloring Sudan Sh
lung tissue
fat embolism of the lung
Glandular hyperplasia of the endometrium
MICROPREPARATION No. 80.
hematoxylin and eosin staining
LU for lymphogranulomatosis
the reasons are polyetiological
hematoxylin and eosin staining
papillary thyroid cancer
the reasons are polyetiological
MICROPREPARATION No. 87.
hematoxylin and eosin staining
ovary slice
actinomycosis
picrofuchsin staining according to Van Gieson
cardiosclerosis
hematoxylin and eosin staining
kidney tissue
the reasons are polyetiological
hematoxylin and eosin staining
acute myocardial infarction
Perls reaction
lung tissue
brown induration of the lung
picrofuchsin staining according to Van Gieson
liver tissue
hematoxylin and eosin staining
liver tissue section
nutmeg liver
hematoxylin and eosin staining
lung tissue
focal influenza pneumonia
hematoxylin and eosin staining
cross section of a vessel
hematoxylin and eosin staining
lung tissue
miliary pulmonary tuberculosis
hematoxylin and eosin staining
thyroid tissue
hematoxylin and eosin staining
section of tumor tissue (skin)
skin melanoma
hematoxylin and eosin staining
lung tissue
bronchopneumonia
hematoxylin and eosin staining
lung tissue
emphysema
hematoxylin and eosin staining
lung tissue, pleura
pleural hyalinosis
hematoxylin and eosin staining
lung tissue
healed tubercular affect
hematoxylin and eosin staining
leather tissue
skin papilloma
the reasons are polyetiological
hematoxylin and eosin staining
uterine tissue
hydatidiform mole
the reasons are polyetiological
coloring Sudan Sh
cross section of an artery
artery atherosclerosis
hematoxylin and eosin staining
fallopian tube section
tubal pregnancy
hematoxylin and eosin staining
breast tissue
the reasons are polyetiological
hematoxylin and eosin staining
liver tissue
cavernous hemangioma of the liver
the reasons are polyetiological
hematoxylin and eosin staining
small intestine section
reasons - salmonellosis
hematoxylin and eosin staining
uterine tumor tissue
chorionepithelioma
the reasons are polyetiological
hematoxylin and eosin staining
subarachnoid hemorrhage
MICROPREPARATION No. 185.
hematoxylin and eosin staining
pancreatic tissue
pancreatic atrophy in diabetes
reasons – diabetes
hematoxylin and eosin staining
tracheal tissue
MICROPREPARATION No. 187.
hematoxylin and eosin staining
cross section of the appendix
hematoxylin and eosin staining
kidney tissue
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MICROPREPARATIONS (treat)
MICROPREPARATION No. 2. Croupous pneumonia
hematoxylin and eosin staining
lung tissue
Almost all alveoli are filled with fibrinous exudate, the septa are thickened, and the vessels are full of blood. In the lumen of the alveoli there is pink exudate. It contains fibrin filaments (homogeneous in the form of a network or grains) and polymorphonuclear leukocytes. A characteristic pathognomonic symptom is the presence of Kohn bridges (fibrin threads from one alveoli pass to another). The capillaries of the interalveolar septa are empty, different from the
lobar pneumonia
infectious agents - pneumococci, streptococci, staphylococci
MICROPREPARATION No. 8. Chronic gastric ulcer
hematoxylin and eosin staining
stomach wall
There is an ulcerative defect in the wall of the stomach. The bottom of the ulcer is filled with necrotic masses. The defect extends to the mucous and muscular membranes. Muscle fibers in the bottom of the ulcer are not identified. In the bottom, 4 layers can be distinguished: fibrinous-purulent exudate, fibrinoid necrosis, granulation and scar tissue
chronic stomach ulcer
The reasons are polyetiological: stress, nutritional factors, bad habits, helicobacter pylori
MICROPREPARATION No. 9. Metastasis of mucous cancer in lymph nodes
hematoxylin and eosin staining
on the preparation, the pattern of the lymph nodes is erased due to the proliferation of atypical cells containing a large amount of mucus. Among the tumor cells there are signet ring-shaped (the nucleus is pushed to the periphery by the mucous mass)
metastasis of mucous cancer in lymph nodes
with tumor progression
MICROPREPARATION No. 14. Fatty liver (Sudan III staining)
coloring Sudan Sh
liver tissue (peripheral cells)
on the preparation in the cytoplasm of hepatocytes there are accumulations of large droplets of fat, colored yellow-orange. Larger fat droplets are contained in the cytoplasm of hepatocytes of the peripheral (periportal) sections of the hepatic lobules, smaller ones - in the cells of the central zone of the lobule
large fatty liver degeneration
causes – chronic alcoholism, intoxication, protein starvation, vitamin deficiencies, anemia, transfusion of incompatible blood
MICROPREPARATION No. 15. Kidney amyloidosis (Congo red staining)
Congo red coloring
kidney tissue
in the capillary loops of the renal glomeruli, in the walls of the arterioles and under the basement membrane of the renal tubules there are red deposits of amyloid. Amyloid deposited along the reticular fibers
kidney amyloidosis
causes - chronic infections (tuberculosis), purulent-destructive processes, malignant neoplasms, rheumatoid diseases
MICROPREPARATION No. 16. Caseous necrosis of lymph nodes in tuberculosis
hematoxylin and eosin staining
LN tissue section
focus - homogeneous substance, in healthy tissue - lymphocytes, at the border - macrophage productive reaction
caseous necrosis of lymph nodes in tuberculosis
tuberculosis
MICROPREPARATION No. 18. Septic myocarditis
hematoxylin and eosin staining
in the myocardium there are foci of purulent fusion of tissue, in the center of which bacterial emboli are visible among polymorphonuclear leukocytes
septic myocarditis
causes – sepsis
MICROPREPARATION No. 20. Granulation tissue
hematoxylin and eosin staining
section of skin (granulation tissue)
superficial leukocyte-necrotic layer; superficial layer of vascular loops; layer of vertical vessels; maturing layer (collagen fibers, fewer vessels); horizontal layer of fibroblasts (black elongated cells); fibrous layer
regeneration through the formation of granulation tissue (the outcome is scar formation)
cause - damage
MICROPREPARATION No. 23. Hemosiderin at the site of hemorrhage (Perls reaction)
Perls reaction (Prussian blue)
brain tissue
in the macrophages located in the cyst wall, bluish-green granules of the Prussian blue dye are visible, deposited in places where hemosiderin granules accumulate. The formation of Prussian blue is due to the presence of iron cation in hemosiderin. There is a focus of hemorrhage in the brain tissue: hematoidin (light brown) is formed in the center under anaerobic conditions, hemosiderin (turquoise) is formed at the periphery
local hemosiderosis
atherosclerosis, cerebral form of hypertension, cerebral aneurysm, stroke, trauma
MICROPREPARATION No. 25. Squamous cell keratinizing carcinoma
hematoxylin and eosin staining
skin section
the tumor consists of strands and layers of atypical squamous epithelium that grow into the underlying dermis. At high magnification, signs of polymorphic cells with hyperchromic nuclei of different sizes, containing 2 or more nucleoli, are visible. Figures of pathological mitoses are detected. In the center of the tumor cells, formed bulbous structures of keratinized cells are visible - cancer pearls
squamous cell keratinizing skin cancer
the reasons are polyetiological
MICROPREPARATION No. 27. Adenocarcinoma of the stomach
hematoxylin and eosin staining
gastric mucosa
growths of atypical glands are visible in all layers of the stomach wall. Cells forming glands of various sizes and shapes with hyperchromatic nuclei, with figures of pathological mitoses
gastric adenocarcinoma
the reasons are polyetiological
MICROPREPARATION No. 36. Syphilitic mesaortitis
hematoxylin and eosin staining
aortic section
the wall of the aorta, in its middle shell, where the vasa vasorum is located, there is an inflammatory infiltrate consisting of lymphocytes, plasma cells, fibroblasts and single giant cells of the Pirogov-Langhans type. There are also small foci of necrosis.
syphilitic mesaortitis
Causes: syphilis (pale spirochete)
MICROPREPARATION No. 38. Myocardial hypertrophy
hematoxylin and eosin staining
muscle cells are thickened and increased in size. The nuclei are large, hyperchromic. There are many blood vessels in the enlarged myocardial stroma
myocardial hypertrophy
MICROPREPARATION No. 39. Purulent leptomeningitis
hematoxylin and eosin staining
brain tissue
the pia mater is sharply thickened and diffusely infiltrated with polymorphonuclear leukocytes. The vessels of the membranes are dilated and full of blood. Perivascular and pericellular edema is expressed in the brain substance
purulent leptomeningitis
meningococcal infection
picrofuchsin staining according to Van Gieson
muscle and connective tissue
smooth muscle fibers alternate with bundles of collagen fibers of varying thickness. Muscle and collagen fibers are arranged randomly (tissue atypia). Muscle fibers are colored yellow-green, connective tissue is pink. The nuclei are black, randomly arranged
fibroids
the reasons are polyetiological
MICROPREPARATION No. 61. Ischemic renal infarction
hematoxylin and eosin staining
kidney tissue
against the background of unchanged components of the kidney, a triangular-shaped lesion is visible, in which only the contours of the glomeruli and tubules are preserved. In the cells of these structures there are no nuclei (karyolysis), in some places the cytoplasm is in a state of lysis, and there are pink areas lacking organization (necrotic detritus). This is the zone of necrosis. It is separated from the unchanged tissue by a demarcation zone 9 in which there are full-blooded vessels and an accumulation of leukocytes)
ischemic renal infarction
thrombosis, embolism, prolonged spasm, atherosclerosis of the renal arteries
hematoxylin and eosin staining
lung tissue
the focus of necrosis is red. The septal cells and alveolar epithelium lack nuclei. Some alveolar septa are torn. The area of necrosis is infiltrated with red blood cells. Around the necrosis there is congestion of blood vessels, an accumulation of leukocytes, and in the lumen of the alveoli there is protein fluid. Many branches of the pulmonary artery are thrombosed.
hemorrhagic pulmonary infarction
thrombosis, embolism
MICROPREPARATION No. 71. Hemorrhage in the brain
hematoxylin and eosin staining
brain tissue
brain tissue is swollen. The focus of hemorrhage is represented by an accumulation of red blood cells in the brain tissue, located in the form of a lake around anatomically intact vessels (diapedetic hemorrhage). In the area of the hemorrhage, arterioles with thickened walls and signs of plasmorrhagia are visible
cerebral hemorrhage
atherosclerosis, cerebral aneurysm, trauma, hypertension
MICROPREPARATION No. 75. Fat embolism of the lung (Sudan Sh staining)
coloring Sudan Sh
lung tissue
interalveolar septa are practically invisible. The lumen of the vessel is obstructed by bright orange fat emboli
fat embolism of the lung
fractures of tubular bones, crushing of subcutaneous fat, use of oil preparations in the form of intravenous injections
Hematoxylin and eosin staining
section of uterine tissue (endometrial scraping)
The endometrium is thickened, has many elongated glands with a convoluted course. In some places, the lumen of the glands is expanded and looks like cysts. The epithelium of the glands proliferates, the endometrial stroma is rich in cellular elements.
Glandular hyperplasia of the endometrium
Causes: ovarian dysfunction, ovarian cyst
MICROPREPARATION No. 81. Lymphogranulomatosis
hematoxylin and eosin staining
in the lymph nodes there are conglomerates of remaining cells (lymphatic), some of the tissue is necrotic (a focus without cellular infiltrates), areas of fibrosis (bundles of collagen fibers with fibroblasts). In the lymph node there are cells that are not typical for it: reticular (irregularly shaped, large, purple cells with one nucleus), plasmacytes (oval cells with a rounded nucleus, displaced to the periphery), eosinophils (the nucleus is pushed to the periphery, the cytoplasm is orange). Uncharacteristic cells - Berezovsky-Stenberg-Reed cells (large, similar to a reticulocyte, but multinucleated - 2 large nuclei next to each other owl's eye syndrome)
LU for lymphogranulomatosis
the reasons are polyetiological
hematoxylin and eosin staining
section of a thyroid tumor
the tumor consists of cavities of varying sizes, filled with villi - papillary papillae, emanating from the walls of the cavities, covered with atypical epithelium. In some places, the tumor papillae grow into the wall of the cavities and the tumor capsule. There are practically no follicles.
papillary thyroid cancer
the reasons are polyetiological
MICROPREPARATION No. 88. Actinomycosis
hematoxylin and eosin staining
ovary slice
Irregularly shaped fungal drusen are observed in the ovarian tissue. The surrounding tissue is infiltrated with polymorphonuclear leukocytes. Around the growth of connective tissue - capsule
actinomycosis
radiant fungus (actinomycetes)
MICROPREPARATION No. 89. Cardiosclerosis (picrofuchsin staining according to Van Gieson)
picrofuchsin staining according to Van Gieson
among the normal myocardium, extensive fields of scar tissue are visible (colorless with dots - fibroblast cells), surrounded by hypertrophied cardiomyocytes (green with nuclei)
cardiosclerosis
productive inflammation, myocardial infarction, ischemic heart disease
MICROPREPARATION No. 90. Kidney for myeloblastic leukemia
hematoxylin and eosin staining
kidney tissue
the tissue is diffusely infiltrated with tumor cells such as myeloblasts. Areas of hemorrhage and necrosis are noted. In the lumens of blood vessels there are leukemic thrombi
kidney in myeloblastic leukemia
the reasons are polyetiological
MICROPREPARATION No. 94. Myocardial infarction
hematoxylin and eosin staining
3 zones are visible on the preparation: 1) a zone of necrosis with characteristic changes in cardiomyocytes, lysis of nuclei, coagulation and clumpy disintegration of myoplasm, disappearance of transverse striations and cell boundaries; 2) demarcation zone - dilation and congestion of blood vessels, hemorrhages and infiltration of polymorphonuclear leukocytes; 3) zone of healthy myocardium along the periphery
acute myocardial infarction
spasm of the coronary arteries, thrombosis, embolism, atherosclerosis of the coronary arteries, functional overstrain of the myocardium with insufficient blood supply
MICROPREPARATION No. 97. Brown induration of the lung (Perls reaction)
Perls reaction
lung tissue
the interalveolar septa are thickened due to the expansion and overflow of blood vessels. Some of the alveoli are filled with edematous fluid, in others there are accumulations of siderophages with hemosiderin - a bluish-green color. Part of the interalveolar septa is thickened and sclerotic. Overgrowth of connective tissue around the bronchi
brown induration of the lung
general and chronic venous congestion, heart defects, vascular atherosclerosis, congestion and hypertension in the ICC
MICROPREPARATION No. 100. Liver cirrhosis (picrofuchsin staining according to Van Gieson)
picrofuchsin staining according to Van Gieson
liver tissue
The liver parenchyma is represented by false lobules of various sizes. In each pseudolobule, fragments of several pre-existing normal liver lobules can be seen (multiglobular cirrhosis). The hepatic beams are indistinguishable. The central lobular vein is absent or displaced to the periphery of the false lobule. Hepatocytes of false lobules are in a state of protein degeneration and necrosis. There are large hepatocytes with 2 or more nuclei. Areas of hepatic parenchyma are separated by wide fields of connective tissue stained magenta pink. Among the fields of connective tissue, close hepatic triads are visible, which are infiltrated with lymphocytes and histiocytes
multiglobular cirrhosis of the liver
hepatitis, hepatosis of various etiologies
MICROPREPARATION No. 103. Nutmeg liver
hematoxylin and eosin staining
liver tissue section
in the liver, the veins and sinusoids in the central zone of the lobules are dilated and full of blood. Foci of diapedetic hemorrhages in the form of “lakes”, discomplexation of the hepatic beams, necrosis and atrophy of hepatocytes are also visible. In the peripheral, periportal zone of the lobules, the blood supply to the capillaries and venules is normal, the structure of the hepatic beams is preserved. Hepatocytes are in a state of fatty degeneration (variegation of color)
nutmeg liver
chronic cardiovascular failure, heart defects, hepatic vein thrombosis
MICROPREPARATION No. 109. Focal influenza pneumonia
hematoxylin and eosin staining
lung tissue
against the background of airy lung tissue, airless areas are visible. The alveoli are filled with serous-hemorrhagic exudate. In places, accumulations of polymorphonuclear leukocytes forming microabscesses are visible. The bronchial epithelium is desquamated and rejected; there is exudate in the bronchial lumen
focal influenza pneumonia
influenza virus, bacterial infection
MICROPREPARATION No. 110. Mixed thrombus
hematoxylin and eosin staining
cross section of a vessel
the lumen of the vessel is completely obstructed by a thrombus, which consists of platelets, fibrin threads, hemolyzed erythrocytes and leukocytes. In a mixed thrombus, the quantitative composition of formed elements is proportional to their number in the blood. A significant part of the thrombotic masses has grown with connective tissue, which grows from the intimal side of the vessel. Thrombotic masses have gaps lined with endothelium
damage to the vessel wall, disruption of the interaction between the coagulation and anticoagulation systems of the blood, increased blood viscosity, slowing of blood flow as a result of cardiovascular failure, decreased muscle tone of the veins
MICROPREPARATION No. 113. Miliary pulmonary tuberculosis
hematoxylin and eosin staining
lung tissue
Numerous tuberculous granulomas are visible in the preparation. In the center of the granulomas there is caseous necrosis, around it there are epithelioid, individual multinucleated giant Pirogov-Langhans macrophages, lymphocytes and individual plasmacytes. There are no vessels in the granuloma
miliary pulmonary tuberculosis
Mycobacterium tuberculosis, hematogenous generalization of primary tuberculosis
MICROPREPARATION No. 117. Colloid goiter
hematoxylin and eosin staining
thyroid tissue
The follicles of the thyroid gland are round in shape and dilated. Their wall is thinned, its ruptures and fusion of fluids with each other are visible with the formation of cysts of various sizes. The epithelium lining the follicles is flattened. The lumen of follicles and cysts is filled with a thick mucus-like mass (colloid). Full-blooded vessels and hemorrhages are visible (brownish contents in the follicles)
mucous (colloid) dystrophy (colloid goiter)
iodine deficiency, impaired thyroid hormone synthesis, goitrogens, immunopathology
MICROPREPARATION No. 126. Skin melanoma
hematoxylin and eosin staining
section of tumor tissue (skin)
a tumor node is located in the skin - it has an intense brown color due to accumulations of mealnin in tumor cells located along the periphery of the tumor node. Tumor cells vary in size and shape.
skin melanoma
reasons are polyetiological (with tumor progression)
MICROPREPARATION No. 127. Bronchopneumonia
hematoxylin and eosin staining
lung tissue
the wall of the bronchus is diffusely infiltrated with polymorphonuclear leukocytes (panbronchitis), in the lumen of the bronchi there is serous-leukocyte exudate with an admixture of desquamated epithelial cells. Perifocally, sharply dilated, air-filled alveoli are visible (perifocal emphysema)
bronchopneumonia
The reasons are polyetiological: inflammation in the respiratory tract, pneumococci, viruses
MICROPREPARATION No. 133. Emphysema of the lung
hematoxylin and eosin staining
lung tissue
in dilated acini - complete smoothing of the walls, the walls of the alveoli become thinner and straighten. The capillaries of the interalveolar septa become empty. The alveoli are increased in volume. Black inclusion – tobacco
emphysema
chronic bronchitis, age-related changes in lung tissue, vicarious in pathology of another lung
MICROPREPARATION No. 135. Hyalinosis of the pleura
hematoxylin and eosin staining
lung tissue, pleura
the visceral pleura is thickened, its fibrous structures are difficult to distinguish. The mesothelium covering the pleura is atrophic. The thickening of the pleura occurred due to the coarsening of bundles of collagen fibers, which turned into translucent glassy formations. Around the pleural vessels there is a pronounced proliferation of connective tissue
pleural hyalinosis
Causes: metabolic disorders in connective tissue, formation of hyaline. The result of progression of fibrinoid swelling, inflammation, necrosis, sclerosis
MICROPREPARATION No. 136. Healed tuberculous affect in the lung
hematoxylin and eosin staining
lung tissue
purple areas are visible in the lung tissue, representing lime deposits. They are surrounded by a connective tissue capsule - this is a healed tuberculous affect. In the field of view, a focus of necrosis surrounded by connective tissue, as well as an island of nascent bone tissue (pseudobone). Along the periphery in the zone of necrosis - deposition of calcium salts
healed tubercular affect
causes – primary tuberculosis
MICROPREPARATION No. 141. Skin papilloma
hematoxylin and eosin staining
leather tissue
numerous outgrowths of stratified squamous keratinizing epithelium that make up the tumor parenchyma. The tumor has a well-defined stroma, represented by outgrowths of the dermis, which, like the fingers of a glove, are covered with multilayered squamous epithelium. Tissue atypia is characteristic (increase in epithelial layers, hyperkeratosis). This is a papillary formation covered with stratified squamous epithelium with underlying stroma and blood vessels
skin papilloma
the reasons are polyetiological
MICROPREPARATION No. 150. Hydatidiform mole
hematoxylin and eosin staining
uterine tissue
the chorionic villi are cystically changed, their stroma is swollen, the central vessel is absent, the trophoblast has a two-row structure, and is atrophic in places
hydatidiform mole
the reasons are polyetiological
MICROPREPARATION No. 153. Atherosclerosis of the artery (Sudan III staining)
coloring Sudan Sh
cross section of an artery
yellow spots, stripes (lipid deposits) and whitish-gray plaques protruding into the lumen are visible on the intima. Some of the plaques are ulcerated. Around the growth of connective tissue
artery atherosclerosis
unbalanced diet, physical inactivity, genetic defect of cholesterol receptors (hypercholesterolemia)
MICROPREPARATION No. 159. Tubal pregnancy
hematoxylin and eosin staining
fallopian tube section
a decidual reaction is observed in the CO of the pipe. In the lumen of the tube, chorion villi are visible, penetrating into the thickness of the muscular membrane
tubal pregnancy
reasons – disruption of the passage of the fetus through the tube (inflammation, tumor, defective tube development, etc.)
MICROPREPARATION No. 163. Fibroadenoma of the mammary gland
hematoxylin and eosin staining
breast tissue
The ducts are visible in the form of oddly shaped slits. Connective tissue grows into them. The color is yellow. Pink connective tissue visible
intracanalicular fibroadenoma
the reasons are polyetiological
MICROPREPARATION No. 178. Cavernous hemangioma of the liver
hematoxylin and eosin staining
liver tissue
the tumor is well demarcated from the surrounding liver tissue by a pronounced fibrous capsule. The tumor consists of large cavernous vascular thin-walled cavities (cavities), lined with endothelium and filled with liquid or clotted blood
cavernous hemangioma of the liver
the reasons are polyetiological
MICROPREPARATION No. 182. Ulcerative enteritis due to salmonellosis
hematoxylin and eosin staining
small intestine section
There is an ulcerative defect in the wall of the small intestine. The bottom of the ulcer is filled with necrotic masses. The mucous and submucous membranes around the ulcer are infiltrated with polymorphonuclear leukocytes
ulcerative enteritis due to salmonellosis
reasons - salmonellosis
MICROPREPARATION No. 183. Chorionepithelioma
hematoxylin and eosin staining
uterine tumor tissue
the tumor is composed of two types of tumor cells: monomorphic light epithelial cells (Langhans cells) and giant dividing cells with hyperchromic polymorphic nuclei (syncytiotrophoblasts). There is no stroma in the tumor. Instead of vessels, cavities filled with red blood cells are visible. The walls of the cavities are lined with tumor cells instead of endothelium
chorionepithelioma
the reasons are polyetiological
hematoxylin and eosin staining
brain tissue, subarachnoid space
the artery wall is thickened, erythrocyte diapedesis, signs of plasmorrhagia
subarachnoid hemorrhage
closed craniocerebral injury, cerebral atherosclerosis
hematoxylin and eosin staining
pancreatic tissue
some lobules are atrophied, others are compensatory hypertrophied. Atrophy of the islets of Langerhans. They are reduced in size. The preparation shows the proliferation of connective tissue (sclerosis), fat deposition (lipomatosis - transparent cells). Hyalinosis, fibrosis and lymphoid infiltration of microvessels are observed. Sclerosis and lipomatosis, both intralobular and interlobular
pancreatic atrophy in diabetes
reasons – diabetes
MICROPREPARATION No. 196. Croupous tracheitis
hematoxylin and eosin staining
tracheal tissue
on the surface of the tracheal mucosa there is fibrinous exudate infiltrated with polymorphonuclear leukocytes. In the underlying tissues, capillaries and venules are sharply expanded and full of blood
purulent-nercotic tracheitis with influenza
Causes: influenza virus and bacterial infection
MICROPREPARATION No. 198. Phlegmonous-ulcerative appendicitis
hematoxylin and eosin staining
cross section of the appendix
the wall of the process is thickened, all its layers are diffusely infiltrated with polymorphonuclear leukocytes. On the serous surface there are deposits of fibrinous exudate, intensely stained with eosin. Lymphatic follicles are enlarged.
phlegmonous-ulcerative appendicitis
reasons are polyetiological, autoinfection
MICROPREPARATION No. 203. Serous extracapillary glomerulonephritis
hematoxylin and eosin staining
kidney tissue
there is a sharp congestion of the capillaries, the lumen of the Shumlyansky-Bowman capsule is enlarged and filled with serous exudate. As a result of proliferation of the capsule epithelium, podocytes and macrophages, crescent formations (crescents) appear. The capillary loops undergo necrosis, and there are fibrin thrombi in their lumen
serous (productive) extracapillary glomerulonephritis
causes - infectious and allergic diseases
MICROPREPARATION No. 205. Septic warty endocarditis
hematoxylin and eosin staining
in the area of necrosis of the valve leaflet, massive thrombotic deposits and colonies of bacteria appear. Growing granulation tissue, when mature, deforms the valve leaflets. Histiolymphocytic infiltrates and granulomas are found in the interstitial myocardial tissue
septic verrucous endocarditis
causes: rheumatism, sepsis
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Methodological developments
practical classes for students
Diseases of the digestive organs and liver
Peptic ulcer of the stomach and duodenum
| Study macroscopic specimens: stomach ulcer, ulcer duodenum, hemorrhagic erosions of the stomach. |
|
| Acute stomach ulcers | |
| Describe the macroscopic specimen Hemorrhagic erosions of the stomach
№88 Hemorrhagic erosion of the stomach
| Pay attention to the extent of the lesion; determine the shape, color of defects, as well as the type and consistency of the edges of defects. Note the superficial nature of the defect in the stomach wall and find brownish-brown masses of hydrochloric acid hematin. |
| Describe the macroscopic specimen Chronic stomach ulcer
| Pay attention to the extent of the lesion, determine the shape, type and consistency of the edges of the defects, the condition and surface of their bottom. |
| Sketch and describe microscopic specimen Stomach ulcer Helicobacter pylori (1) in the lumen of the glands (Romanovsky Giemsa stain)
Overhanging edge of a stomach ulcer Undermined edge of a stomach ulcer
The bottom of a stomach ulcer during an exacerbation
| Find a defect in the stomach wall and determine its depth. Characterize changes in the area of the bottom of the ulcer and the edges of the defect. Describe changes in the deeper layers of the stomach wall and determine the nature of the ulcerative process. |
Appendicitis. Peritonitis.
| Study macroscopic specimens: phlegmonous appendicitis, gangrenous appendicitis, appendicular empyema, chronic appendicitis. Describe one of the macroscopic preparations. |
|
| Describe the macroscopic specimen Phlegmonous appendicitis
Gangrenous appendicitis
| Pay attention to the size, wall thickness, and condition of the serous membrane of the appendix. |
| Draw and describe the microslide No. 90 Phlegmonous appendicitis
| Characterize the condition of the mucous membrane of the appendix and its lumen. Determine the nature and prevalence of exudate, the degree of blood filling of the vessels. |
| Sketch and describe microscopic specimen Obliteration of the appendix
| Determine the topography of the growth of connective tissue, note the presence of islands of adipose tissue, atrophy of the layers of the appendage wall. |
| Examine a microscopic specimen Fibrinous purulent peritonitis | Characterize the state of the peritoneal mesothelium, blood vessels, and exudate. Note changes in the underlying fiber and muscle tissue. |
Hepatitis. Toxic liver dystrophy. Cirrhosis of the liver.
| 1. Study macroscopic preparations: toxic liver dystrophy, cirrhosis of the liver, varicose veins of the esophagus. 2. Describe one of the macroscopic preparations. |
|
| Describe the macroscopic specimen Toxic liver dystrophy
| Pay attention to size, consistency; mark the color on the cut surface; determine the stage of the disease. |
| Examine a microscopic specimen No. 93a Toxic liver dystrophy. (Sudan III staining) | Note the violation of the liver structure, obesity and necrobiosis of liver cells in the center of the lobule. |
| Sketch and describe microscopic specimen No. 93 Toxic liver dystrophy
| Note the violation of liver architecture, find foci of necrosis. Describe changes in the stroma of the organ. Determine the stage of the process. |
| Describe the macroscopic specimen Postnecrotic cirrhosis of the liver
Portal cirrhosis of the liver
| Pay attention to the configuration, size, consistency, color of the organ; note the sizes of the nodes. Pay attention to the size, consistency, color of the organ; note the sizes of the nodes. |
| Sketch and describe microscopic specimen No. 94 Portal cirrhosis of the liver (picrofuchsin staining)
| Determine the topography of the newly formed connective tissue, the degree of its maturity, and identify the morphological features of the “false lobules.” Note changes in liver cells (phenomena of fatty degeneration and perverted regeneration), bile ducts. Pay attention to the distinctive features of various forms of cirrhosis. |
Adjacent files in item [UNSORT]
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Pathological anatomy of peptic ulcer
Pathological anatomy. Initial ulcers do not penetrate deeper than the mucous membrane. A chronic ulcer can spread to the muscular and serous membranes. An ulcer with hard, raised edges is called a callous ulcer. An ulcer that involves all layers of the gastric wall can cause perforation. An ulcer that penetrates into neighboring organs, most often the pancreas, is called penetrating. After the ulcer heals, scars appear, sometimes deforming the stomach (“hourglass”, snail-shaped stomach) or causing narrowing (stenosis) of the pylorus of the stomach. Inflammation of the serous membrane at the location of the ulcer leads to perigastritis or periduodenitis and the formation of adhesions with nearby organs.
Acute ulcers are usually round or oval in shape. The edges of the ulcers are clear, the bottom is usually clean, without overlaps. Acute ulcers can cause perforation of the stomach wall and fatal gastric bleeding.
A chronic ulcer, according to most researchers, is the outcome of an acute one and differs from it by the significant development of fibrous tissue in the bottom and edges. A chronic ulcer is usually round or oval in shape, less often it has an irregular outline. The cardial edge of the ulcer seems to be undermined, the pyloric edge is flat. The bottom is covered with dirty gray deposits; the organ into which penetration occurred is visible in the bottom of the penetrating ulcers. A stomach ulcer is usually larger than a duodenal ulcer. The size of the niche determined by x-ray examination does not always correspond to the size of the ulcer. Due to swelling of the edges, filling of the ulcer crater with mucus, exudate or food masses, the ulcerative defect may not be completely filled with barium. Most gastric ulcers are located on the lesser curvature and in the pylorus. Duodenal ulcers are usually localized 1-2 cm from the pylorus, equally often on the anterior and posterior walls of the intestine. Postbulbar ulcers are less common. Chronic ulcers are usually single, but multiple lesions also occur. During gastroscopy, near a large ulcer, several small ones are sometimes found that are not detectable x-ray. In patients with gastric ulcers, duodenal ulcers are sometimes simultaneously detected. Multiple duodenal ulcers are often located on opposite walls of the intestine (“kissing” ulcers). The most rare locations of ulcers in the stomach are the cardia, fundus and greater curvature.
Upon microscopic examination, four layers are distinguished at the bottom of the ulcer. On the inside, fibrinous-necrotic deposits, desquamated epithelium, leukocytes, erythrocytes and hydrochloric acid hematin are visible, coloring the bottom of the ulcer gray or dark brown. Under this layer is a layer of fibrinoid necrosis, formed by disorganized and necrotic collagen fibers. In rapidly and rapidly progressing ulcers, this layer can reach several millimeters in width. The granulation tissue lies deeper. Often it is not detected, since it is completely involved in the destructive process. Granulation tissue passes into the next, most developed layer - scar tissue, which is formed by loose and dense fibrous connective tissue. There are small lymphoid follicles with pronounced reactive centers. When the ulcer recurs, many mast cells with signs of increased secretory activity can be seen in the scars. Scar tissue grows into the muscle layers, submucosal layer, its volume significantly exceeds the size of the ulcer itself.
With an exacerbation of peptic ulcer disease, necrosis of granulation tissue and collagen fibers, an inflammatory reaction in the surrounding tissues, rejection of areas of necrosis and, as a result, an increase in the ulcerative defect usually occur. Yu. M. Lazovsky believes that the progressive proliferation of fibrous tissue at the bottom of the ulcer is not associated with the transformation of granulation tissue into a scar, but with the direct formation of collagen fibers from the ground substance.
In the area of the ulcer, changes in the blood vessels are usually observed with the development of inflammatory-necrotic processes in them, areas of fibrinoid necrosis of the arterial walls, thrombosis of the arteries and veins and their subsequent recalibration. These secondary vascular lesions disrupt tissue trophism and serve as one of the reasons preventing the healing of chronic ulcers. At the bottom of the ulcer there are nerve trunks immured in scar tissue and growths of nerve fibers such as amputation neuromas. In the ganglion cells of the intramural nerve nodes, dystrophic changes and irritation phenomena are observed (S. S. Weil, P. V. Sipovsky).
With a peptic ulcer, changes occur in the entire mucous membrane of the stomach and duodenum. At the edges of a gastric ulcer, proliferation of epithelium is observed, which can grow deep into the mucosa and along its surface, taking the form of polyps. The pyloric glands undergo hynerplasia and show signs of increased mucoid secretion. Acid mucopolysaccharides, which are normally absent, appear in the secretion. With the long-term existence of an ulcer, atrophic changes in the glands occur, and their secretion weakens. In the fundic glands, patterns of atrophy and intestinal metaplasia are observed; the so-called pseudopyloric glands of Stern, containing mucoid secretion, are formed. In the stroma one can see diffuse lymphoplasmacytic infiltrates, large lymphoid follicles, and growths of smooth muscle fibers. With a duodenal ulcer, the number of parietal cells increases significantly, which are found even in the pyloric region.
Healing of chronic ulcers occurs through the formation of a scar. Before healing begins, swelling and inflammatory infiltration of the edges of the ulcer occur. The edges smooth out, approach the bottom, and the necrotic masses covering the bottom are torn away. Granulations appear in the bottom and edges, which gradually fill the ulcer crater. The surface epithelium, saturated with RNA, grows onto the granulation tissue and lines it. The muscular layer of the mucous membrane, gastric and duodenal glands do not regenerate. The accumulation of acidic mucopolysaccharides is of great importance in the healing of ulcers. It takes about 5-7 weeks for an ulcer with mild fibrosis of the bottom and edges to heal. Sometimes complete healing occurs within 10 days, sometimes it takes several months. As a result of healing of deep, especially penetrating ulcers, gastric deformities may occur. Scar healing of pyloric ulcers can lead to pyloric stenosis. Diverticula (ulcus diverticulum) may develop between a healed duodenal ulcer and the pylorus.
Complications. V. M. Samsonov identifies five groups of complications of peptic ulcer disease. 1. Complications of ulcerative-destructive origin: perforation, arrosive bleeding and penetration. Perforation of an ulcer is one of the most dangerous complications. Most often, perforation occurs in the second half of the day. The diameter of the perforation hole is about 0.5 cm. Histological examination reveals a picture of exacerbation of peptic ulcer disease, necrosis and leukocyte infiltration of the edges and bottom of the ulcer, and fibrin overlay on the serous cover.
Arrosive bleeding occurs from large vessels at the bottom of the ulcer. M.K. Dahl et al. found that vessel arrosion may be preceded by limited necrosis of the wall with the formation of an aneurysm and its subsequent rupture. Bleeding from chronic ulcers, the vessels of which are fixed by scar tissue that prevents the contraction of the arteries, is especially dangerous. Ulcers of the lesser curvature of the stomach usually penetrate into the lesser omentum, and duodenal ulcers into the pancreas.
When ulcers penetrate into hollow organs, gastric fistulas occur (gastrocolic, gastrointestinal, gastrointestinal). Ulcers of the cardial and subcardial sections can penetrate into the diaphragm. In the future, such an ulcer may break through into the pleural cavity, into the pericardial cavity. 2. Complications of an inflammatory nature: gastritis, duodenitis, perigastritis, periduodenitis, gastric phlegmon, hepatocholangitis. 3. Complications of ulcerative-scar origin: stenosis of the cardiac part of the stomach, pylorus, duodenum, shortening of the lesser curvature, hourglass deformation of the stomach, diverticula of the stomach and duodenum. 4. Malignancy of a stomach ulcer, according to A.I. Abrikosov, occurs in 8-10% of cases. The lack of consensus on the frequency of ulcer malignancy is associated with the difficulties of differential diagnosis of malignant ulcers and primary ulcerative cancer. Malignancy of duodenal ulcers is extremely rare.
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