Acute gastric ulcer macropreparation description. Pathological anatomy of peptic ulcer

Name the organ, tissue, establish the nature of the pathological process, give a morphological description of the known changes, make a diagnosis, indicate the nature of possible complications in this pathology.
List of examination micropreparations
1. granular dystrophy nirok
2. fatty liver infection (Sudan-Z)
3. anthrocosis legen
4. caseous necrosis
5. calcification of the heart valve
6. swollen leg
7. nutmeg
8. hemorrhagic infarction
9. fibrinous pericarditis
10. liver abscess
11. miliary tuberculosis legen
12. insular hypoplasia of the endometrium
13. atrophy of the skin
14. flat-sided carcinoma of the cornea
15. intracanalicular fibroademon
16. fibromyoma
17. giant cell sarcoma
18. treatment for leukemia
19. lymphogranulomatosis
20. myeloma
21. adenocarcinoma
22. postinfarction cardiosclerosis
23. verrucous endocarditis
24. lobar pneumonia
25. hypostatic pneumonia
26. chronic wound
27. phlegmonous appendicitis
28. liver cirrhosis
29. gostra nirkova insufficiency
30. Nirca amyloidosis
31. abortion
32. goiter
33. tuberculous hump.

1. Examination macro preparations
1. bloody at the head brain
2. aortic atherosclerosis
3. secondarily wrinkled nirka
4. ischemic heart attack
5. metastasis to cancer of the leg
6. fibrinous pericarditis ("hairy heart")
7. spherical thrombus of the left atrium
8. guma heart (syphilitic)
9. toxic liver dystrophy
10. Cancer slug
11. erozії i gostrі vrazki slunk
12. chronic wound
13. hyalinosis of the splenic capsule
14. dysentery colitis
15. typhus
16. gangrene of the intestine
17. myocardial hypertrophy
18. liver abscess
19. Ischemic infarction of the spleen
20. mitral stenosis of the heart
21. liver cirrhosis
22. amyloid-lipoid necrosis
23. cancer metastases in the spleen
24. nutmeg
25. chronic abscess of the leg
26. borax myocardial atrophy
27. parietal thrombosis of arteries
28. Uterine fibroids
29. bubbly zanis
30. fibrous-cavernous tuberculosis legen
Schematic description of a macropreparation
1. select organ
2. designate the same old look: color, rosemary, surface view, as if it is empty - what is there to avenge.
3. determine the nature of the pathological process: localization, obvious signs, rozpovsudzhenist, clinical and anatomical characteristics, possible aggravation in this pathology, make a diagnosis.
Description of the electron diffraction pattern
Describe the nature of the pathological process in case of illness, indicate the most characteristic ultrastructural signs of the pathological process.

1. Hemorrhage in the brain.
This macropreparation is the brain. The shape of the organ is preserved, the dimensions are not increased. The brain is pale yellow, the boundaries between white and gray matter are pronounced. Small brown inclusions 1 mm in diameter are visible on the section, light brown elongated areas (5x7 and 4x11 mm) are located in the area of ​​the bark on top of the section. At the bottom of the section there is a large spot 7 cm in diameter with an unevenly distributed color. Areas of dark brown color with blurred borders alternate with lighter ones. The area is well demarcated from the surrounding tissue.
These pathological changes could develop with:
1) gap;
2) erosion of the vessel wall, which led to massive bleeding and hemorrhagic impregnation of the brain tissue (hemorrhage site is heterogeneous -> partially cellular elements are preserved).
Small brown inclusions are pinpoint hemorrhages from the veins that occurred during the cut.
Light brown areas are the result of an increase in the permeability of the vessel wall, which has developed as a result of angioedema, changes in microcirculation, and tissue hypoxia. Rupture or corrosion of the vessel could occur as a result of atherosclerosis, necrosis, inflammation, sclerosis, malignant tumor.
Exodus:
1) favorable: blood resorption; cyst formation at the site of hemorrhage, encapsulation or organization.
2) unfavorable: death as a result of damage to vital centers; accession of infection and suppuration.
Conclusion: these morphological changes indicate a rupture or erosion of the vessel wall, which led to hemorrhagic impregnation of the brain tissue.
Diagnosis: Hemorrhagic stroke.
2. Atherosclerosis of the aorta.
This macropreparation is the aorta. The shape of the organ is preserved. Inner surface the walls are dark Brown, tuberous, intima uneven, whitish in color, its entire surface consists of tubercles and depressions. On the tubercles, orange areas with white borders are noticeable. Spots of yellow color with a diameter of 5 mm are visible. On the intima of the aorta, plaques ulcerate, which leads to dissection of the aortic wall.
Description of pathological changes.
These pathological changes could occur as a result of a violation of fat and protein metabolism. Unregulated cell turnover leads to the appearance of foam cells in the intima of the arteries, which are associated with the formation of atherosclerotic plaques (yellow spots). The following factors also play a role:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- ethnic.
Whitish tubercles are fibrous plaques formed as a result of the germination of connective tissue in the thickness of the detritus. Orange spots with a white border represent intramural hematomas, due to the destruction of the plaque cover or its ulceration in atheromatosis. White border - area of ​​calcenosis; plaques indicate that atherosclerosis is progressive and a new wave of lipoidosis was layered on old changes, detachment of a part of the endothelial lining of the aorta (a section hanging inside the vessel) indicates a dissecting aneurism.
Exodus:
1) favorable: regression of atherosclerosis with leaching of lipids from plaques by macrophage resorption and dissolution of connective tissue;
2) unfavorable:
a) thrombosis;
b) thromboembolism;
c) embolism with atheromatous masses or pieces of intima;
-> heart attack and gangrene
d) ruptured aortic aneurysm ~» death from acute anemia.
Conclusion: these morphological changes in the aortic wall indicate degenerative changes in the aortic intima with subsequent growth of the wall and complications that underlie aortic atherosclerosis.
Diagnosis: Progressive atherosclerosis of the aorta. Dissecting aneurysm.
3. Secondarily wrinkled kidney.
This macropreparation is the kidneys The shape of the organs is preserved, the weight and size are reduced Left kidney larger than the right Organs are light gray in color, the surface is finely tuberous No foci of hemorrhages
Description of pathological changes
These pathological changes could develop primarily due to sclerosis of the renal vessels - with hypertension, and secondarily on the basis of inflammatory and degenerative changes in the glomeruli, tubules, stroma. The disease proceeds in 2 stages: nosological and syndromic. Given the finely tuberous surface of the kidneys (which happens with hypertension and glomerulonephritis). as well as the absence of foci of hemorrhage or infarction (in the kidneys - white with a hemorrhagic corolla - and - white), chronic glomerulonephritis can be considered the cause of this disease. which in stage I leads to glomerulosclerosis, and in stage II - blockage of blood flow at the level of the glomeruli leads to ischemia of the substance of the kidneys -> progression of atrophy of the parenchyma and sclerosis of the kidneys - "shrinkage of the kidneys (chronic renal failure) Outcome
1) favorable with the use of regular hemodialysis, chronic suburemia develops,
2) unfavorable death due to chronic renal failure and its consequences
Conclusion These morphological changes indicate a structural reorganization of the renal tissue and the replacement of its parenchyma with connective tissue.
Diagnosis Secondary wrinkled kidney Chronic glomerulonephritis.
4. Kidney infarction.
This macropreparation is a kidney. The shape of the organ is preserved, the mass and dimensions are not increased. The cut shows the cortex and medulla. Significant deposits of adipose tissue in the cups and pelvis of the kidney. In the cortical substance, multiple whitish areas 1x0.5 cm are visible. The granules of some of them are dark brown. Light brown organ.
These pathological changes could develop as a result of prolonged spasm of the vessels of the functional tension of the organ in conditions of insufficient blood supply, atherosclerosis, thromboembolism or thrombosis of the renal arteries. Ischemia of the kidney substance leads to necrosis (ischemia > hypoxia > metabolic disorders > dystrophy > necrosis), the morphogenetic mechanism of which is decomposition, and the biochemical mechanism is protein denaturation > coagulation necrosis as a result of ischemia > ischemic infarction (white areas). A hemorrhagic corolla is formed around the necrosis zone as a result of a sharp expansion of spasmodic vessels. The vessels are full, there are diapedetic hemorrhages (granules of white areas of brown color).
Outcome: 1) favorable:
a) autolysis and regeneration of necrosis;
b) organization and formation of the scar; 2) unfavorable:
a) death as a result of acute renal failure in a heart attack;
b) death as a result of chronic renal failure in the organization of heart attacks, scarring or the development of nephrosclerosis.
c) purulent fusion.
Conclusion: these morphological changes indicate dystrophic and necrotic processes in the renal cortex due to impaired blood supply.
Diagnosis: kidney infarction.
5. Metastasis of cancer in the lungs.
This macropreparation is light. The shape of the organ is preserved. The lung is brown in color with multiple dark dot inclusions, whitish inside, rounded, 3-5 mm in diameter. The lung is heterogeneous: light gray bronchi and black inclusions with a diameter of 0.5-3 mm are visible, which do not have a clear localization. These pathological changes could develop as a result of damage to the epithelial cell genome, which could be facilitated by factors such as inhalation of carcinogens (cigarette smoke), especially since there are many small dark gray inclusions in the lung that can represent soot, dust and are especially pronounced smokers and miners. In addition to smoking, the prerequisites for changing the cell genome could create chronic inflammatory processes, pulmonary infarction, since hyperplasia, dysplasia and metaplasia of the epithelium develop on their soil. The conditions for these changes often occur in the rumen.
Multiple rounded spots represent an accumulation of tumor cells, probably a peripheral cancer, as evidenced by the diffuse location of the spots. Pinpoint inclusions in cancer clusters represent areas of hemorrhage.
Exodus:
1) favorable.
In the initial stage of lung cancer, it was still possible if cancer cells were eliminated due to a strong immune response or would cause slow tumor growth; 2) unfavorable - death.
a) hematogenous and lymphogenous metastases (in 70% of cases).
b) complications associated with tumor necrosis, formation of cavities, bleeding, suppuration.
c) cachexia.
Conclusion: these morphological changes indicate a change in the genome epithelial cells and cancer progression with the growth of altered cells in the lung tissue.
Diagnosis: Lung cancer. tumor progression.
6. Fibrinous pericarditis.
This macropreparation is a heart enclosed in a pericardial sac.
The shape of the organ is preserved, the dimensions are somewhat enlarged. The epicardium is dull gray, rough, covered with light brown fibrin. There are no foci of hemorrhage or necrosis. Fibrin is more pronounced on the anterior wall of the right ventricle
Descriptions of pathological changes.
These pathological changes can develop in rheumatic diseases with heart damage. Disorganization of the connective tissue, vascular lesions and immunopathological processes develop in the sheets of the heart shirt. Increased vascular permeability in the stage of exudation leads to "wetting" of fibrinogen behind their walls and the formation of a "hairy" heart.
Exodus:
1) favorable:
a) resorption of fibrin;
2) unfavorable: obliteration of the cavity of the heart shirt and calcification of the connective tissue formed in it (armored heart).
Conclusion: these morphological changes indicate that dystrophy and exudative fibrinous inflammation have developed in the sheets of the pericardium with rheumatism.
Diagnosis: Fibrinous pericarditis (hairy heart).
7. Spherical thrombus of the left atrium.
This macropreparation is the heart. The shape of the organ is preserved, the mass and dimensions are increased due to the thickened wall of the left ventricle (thickness at the base is up to 2.5 cm). The organ is light gray in color, subepicardial fat is moderately developed. There are no foci of hemorrhage or necrosis. The consistency is compacted, the chords are shortened, the papillary muscles and trobeculae are enlarged. In the cavity of the left atrium there are formations of a round shape, dark gray in color, 5 cm in diameter, of a dense consistency, which occupies the entire cavity of the left atrium. The leaflets of the mitral valve are enlarged and thickened, they are fused. Thrombotic overlays on the endothelium of the valve.
Description of pathological changes.
These pathological changes develop as a result of:
a) mitral valve endocarditis;
b) slowing down and disturbance of blood flow;
c) violation of the relationship of the coagulation, anticoagulation and fibrinolytic systems;
d) change rheological properties in blood.
As a result of valve inflammation, desquamation of the endothelium occurred, which led to prewall thrombus formation, as well as thickening and sclerosis of the mitral valve and their fusion. In this preparation, valve stenosis is combined with valve insufficiency, with the latter predominating. This is due to the fact that during ventricular systole, blood is ejected not only into the aorta, but also, due to mitral valve insufficiency, into the left atrium. Consequently, during diastole, an increased amount of blood enters the ventricle, which first causes its hypertrophy and tocogenic expansion of the heart in the left ventricle - blood stasis in the left atrium - the formation of a congestive mixed thrombus - its separation and polishing in the cavity of the left atrium.
Exodus:
1) relatively favorable: organization with subsequent canalization and vascularization. The connective tissue grows into the thrombus from the side of the endocardium.
2) unfavorable: death. The clot is so large that it blocks the flow of blood into the left ventricle.
Conclusion: these morphological changes indicate the development of an inflammatory sclerotic process in the mitral valve, accompanied by circulatory disorders and the formation of a prewall thrombus and its subsequent separation.
Diagnosis: Mitral combined heart disease. Mitral stenosis with mitral valve insufficiency. Globular thrombus.
8. Heart Gunma*
This macropreparation is the heart. The shape of the organ is preserved, the mass and dimensions are increased due to the thickened wall of the left ventricle (up to 3 cm). the chords are thickened, the papillary muscles are enlarged. The endocardium is yellowish in color, subepicardial fat is moderately developed. The aortic valve is intact. In the wall of the left ventricle there is a recess 5x4x3 cm, on the inner surface of which there are spots of yellow, orange and dark gray, as well as whitish and whitish areas. At the lower edge of the recess, overlays of thrombotic masses are noticeable.
Description of pathological changes.
These pathological changes could develop as a result of sexual or non-sexual infection with pale treponema, the causative agent of syphilis. Acquired syphilis passes in three periods - primary, secondary, tertiary (or gummy), which is presented on the preparation. The first period occurs against the background of increasing sensitization and is manifested by a hard chancre on the mucous membrane at the site of the introduction of treponema and involvement in the process. lymphatic system. The second period - the period of hyperergy and generalization, is characterized by the appearance of syphilis and an increase or swelling of the lymphatic follicles. These places are inflamed. After 3-6 years, the third period begins in the form of chronic diffuse interstitial inflammation and the formation of gums, which represent the focus of syphilitic productive necrotic inflammation, syphilitic granuloma. In this case, visceral syphilis led to heart damage in the form of gummous myocarditis. The inflammatory process goes deep into the myocardium, the necrotic masses are washed out by the blood flow, the zone is limited to demarcation inflammation. There are accumulations of lymphoid, plasmatic Pirogov-Langhans giant cells, fibroblasts. Specific inflammation leads to scarring and ends with the development of massive cardiosclerosis. Atherosclerosis is superimposed on the area of ​​specific changes, which is associated with yellow, white, orange spots, as well as associated thrombotic overlays.
Outcome: 1) favorable.
a) was possible in the treatment and elimination of the pathogen before serious changes in the organs;
b) the long course of the process with its compensation;
2) unfavorable: cardiosclerosis > development of chronic heart failure, first hypertrophy: tonogenic, and then myogenic, delegation of the left ventricle > blood stasis in the left ventricle > into the left atrium > in the lung.
Death is the result of cor pulmonale. Conclusion: These morphological changes indicate a specific inflammation of the myocardium with the formation of gumma of the heart.
Diagnosis: visceral syphilis. Heart gumma.
9. Toxic dystrophy of the liver.
This macropreparation is the liver. The shape is preserved, the weight and dimensions are reduced. Yellow liver.
Description" of pathological changes.
These pathological changes could develop as a result of intoxication,
allergic or viral infection liver. Fat (yellow) develops in the organ
dystrophy. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic
disintegration of hepatocytes of the central departments. Fat-protein detritus is phagocytosed, while
the reticular stroma with dilated vessels is exposed (red dystrophy). Due to necrosis of hepatocytes, the liver shrinks and decreases in size.
Exodus:
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 dystrophy of the liver. Stage of yellow dystrophy.
10. Cancer of the stomach.
This macropreparation is the stomach. The shape and dimensions of the organ are changed due to the growth of a whitish-yellow tissue that has grown through the wall of the stomach and significantly thickens it (up to 10 cm or more). Reliefs of the mucosa are not expressed. In the central part of the growth, depressions, loosening and hanging areas - ulcerations are visible.
Description of pathological changes.
These pathological changes could develop as a result of precancerous conditions and precancerous changes (intestinal metaplasia and severe dysplasia).
In the foci of changes in the epithelium, malignancy of cells and the development of tumors occur (or cancer develops (de novo). Based on the macroscopic picture, we can say that this is cancer with predominantly endophytic infiltrating growth - infiltrative-ulcerative cancer (this is evidenced by tumor ulceration). Histologically, this may be both adenocarcinoma and undifferentiated cancer.Progression, the tumor grows into the wall of the stomach and significantly thickens it.
Outcome: 1) favorable:
a) slow growth of cancer;
b) highly differentiated adenocarcinoma;
c) late metastasis;
2) unfavorable: death from exhaustion, intoxication, matastases; the spread of cancer outside the stomach and germination in other organs and tissues, secondary necrotic changes and the breakdown of carcinoma; dysfunction of the stomach.
Conclusion: these morphological changes indicate a mutational transformation of epithelial cells with their malignancy and subsequent tumor progression, which, with infiltrating growth, led to the germination of the stomach wall with ulcers, which may represent secondary necrotic changes and tumor decay.
Diagnosis: Infiltrative-ulcerative cancer of the stomach.
11. Erosions and acute stomach ulcers.
This macropreparation is the stomach. The shape and dimensions of the organ are preserved, the mass is not changed. The organ is whitish in color. The mucosa is strewn with black formations of a dense consistency. Among numerous small diameter 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 merged formations with a diameter of 5 mm. Near one of them we see the formation of a triangular shape, the boundaries of which have pronounced differences from the gastric mucosa, since they are formed connective tissue.
Descriptions of pathological changes.
These morphological changes could develop as a result of exogenous and endogenous influences: violation, nutrition, bad habits and harmful agents, as well as autoinfections, chronic autointoxication, reflux, neuro-endocrine, vascular allergic lesions. Since the lesions are localized in the fundus, we can talk about an autoimmune process with damage to the parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, a violation of its regeneration and atrophy. Probably, in this case, chronic atrophic gastritis developed with atrophy of the mucosa and its glands. Mucosal defects lead to erosion, which is formed after hemorrhage and rejection of dead tissue. The black pigment in the bottom of the erosion is hydrochloric acid hematin. The restructuring of the epithelium joins these changes. Education, the border of which is formed by the mucosa and is the healing of an acute gastric ulcer by scarring and epithelialization.
Outcome: 1) favorable:
a) healing of an acute ulcer by scarring or epithelialization;
b) inactive chronic gastritis (remission);
c) mild or moderate changes;
d) epithelialization of erosions; 2) unfavorable:
a) development of chronic peptic ulcer;
b) malignancy of epithelial cells;
c) pronounced changes;
d) active expressed gastritis.
Conclusion: these morphological changes indicate long-term dystrophic and necrobiotic changes in the mucosal epithelium with impaired regeneration and structural restructuring of the mucosa.
Diagnosis: chronic atrophic gastritis, erosion and acute stomach ulcer
12. Chronic stomach ulcer.
This macropreparation is the stomach. The masses and dimensions of the organ are normal, the shape is preserved. The organ is light gray in color, the relief is intensely developed. On the lesser curvature of the stomach in the pyloric section, there is a significant depression in the wall of the stomach 2x3.5 cm. Its limiting surface of the organ is devoid of characteristic folding. The folds converge towards the borders 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, made by a serous membrane. The edges are raised like a roll, dense, have a different configuration: the edge facing the pylorus is gentle (due to gastric peristalsis).
Description of pathological changes.
These pathological changes could develop in response to general and local factors (general: stressful situations, hormonal disorders; medicinal; bad habits that lead to local disorders: hyperplasia of the glandular apparatus, increased activity of the acid-peptic factor, increased history, increased number of gastrin-producing cells; and general violation: 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 glkzhokartikoid). Influencing the gastric mucosa, these disorders lead to the formation of a mucosal defect - erosion. Against the background of non-healing erosion, acute peptic erosion develops. an ulcer that, with continued pathogenic influences, turns into a chronic ulcer that goes through periods of exacerbation and remission. During the period of remission, the bottom of the ulcer can be covered with a thin layer of epithelium, superimposed on scar tissue. But during the period of exacerbation, “healing” is leveled 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 the trophism of the ulcer tissues).
Exodus:
1) favorable: remission, ulcer healing by scarring followed by epithelialization.
2) unfavorable:
a) bleeding
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcer-cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect in the mucous, submucosal and muscular membranes - ulcers.
Diagnosis: Chronic peptic ulcer of the stomach.
14 Dysentery colitis
This macropreparation is the large intestine. The shape of the organ is preserved, the mass and dimensions are increased due to the thickening of the wall. The mucosa is dirty-gray, at the top of the folds and between them, the film overlays of brown-green color covering the mucous mass are necrotic, ulcerated, in many places hang freely into the lumen of the intestine (which is narrowed).
These pathological changes could develop as a result of an acute intestinal disease with a predominant lesion of the large intestine, which was caused by 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 recitation of the latter, the development of desquamative catarrh. Bacterial enterotoxin exerts a vasoneuroparalytic action, which is associated with paralysis 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 sweating of fibrinogen from dilated vessels). If in the first stage we find only superficial necrosis - hemorrhage, then in the second stage a fibrinoid film appears at the top and between the folds. Necrotic masses of the mucosa are permeated with fibrin. Dystrophic and necrotic changes in the nerve plexuses are combined with infiltration of mucosal and submucosal leukocytes, its edema, and hemorrhages. With the further development of the disease, due to the rejection of fibrin films and necrotic masses, ulcers are formed, which for 3-4 weeks of the disease are filled with granulation tissue, which matures and leads to the regeneration of ulcers.
Exodus
1. favorable
a) complete regeneration with minor defects b) abortive form
2. unfavorable
a) incomplete regeneration with the formation of scars1^ narrowing of the intestinal lumen
b) chronic dysentery
c) lymphadenitis
o!) follicular, follicular-ulcerative colitis
f) severe general changes (necrosis of the epithelial tubules of the kidneys, fatty degeneration of the heart and liver, disorders mineral metabolism)
Complications
A. ulcer perforation: peritonitis, paraproctitis,
B. phlegmon
C. intestinal bleeding
Extraintestinal complications - bronchopneumonia, pyelonephritis, serous arthritis, liver abscesses, amyloidosis, 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 dimensions 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. Furrows and convolutions are noticeable on them, the surface itself is uneven, loosened. These formations are dirty gray in color. A formation with a diameter of 0.5 cm is noticeable, with a loss of characteristic folding, a whitish color, slightly deepened and compacted.
Description of pathological changes.
These pathological changes could develop as a result of infection (parenteral) with typhoid bacillus and their multiplication in the lower part of the small intestine (with the release of endotoxin). Along the lymphatic pathways -> into Peyer's patches -> salitary follicles -> regional lymph nodes -> blood -> bacteremia and bacteriocholia
-\u003e into the intestinal lumen -\u003e hyperergic reaction in the follicles, which leads to an increase and swelling of the follicles, tortuosity of their surface. This occurs as a result of the proliferation of monocytes, histiocytes, reticulocytes, which extend beyond the follicles into the underlying layers. Monocytes turn into macrophages (typhoid cells) and form clusters - typhoid granulomas. Catarrhal enteritis joins these changes. With further progression of the process, typhoid granulomas become necrotic and are surrounded by a zone of demarcation inflammation; sequestration and rejection of necrotic masses leads to the formation of "dirty ulcers" (as a result of soaking with bile), which change their appearance over time: they are cleared of necrotic masses, the edges are rounded. The growth of granulation tissue and its maturation leads to the formation of tender 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.
Conclusion: these morphological changes indicate an acute infectious disease with local changes in the small intestine - ileolitis.
Diagnosis: Ileolitis.
Gangrene of the small intestine.
This macropreparation is a section of the small intestine. Its dimensions and weight have not been changed. The loops of the intestine are enlarged, the consistency of one part is loose, the second part is not changed. The surface is smooth. The serous membrane is dull and dull. Between the loops is a sticky, viscous, stretching liquid in the form of threads. On the section of the intestine, the walls are enlarged, the lumen is narrowed.
Possible causes: impaired blood supply as a result of strongomecian netphochodemonia of the mesenteric arteries.
Morphogenesis: ischemia, dystrophy, atrophy, necrosis of the organ in contact with external environment- gangrene
Outcome: 1) unfavorable - putrefactive melting, melting.
Conclusion: indirect vascular necrosis.
Diagnosis: Wet gangrene of the small intestine.
18. Liver abscess.
This macropreparation is the liver. The shape of the organ is preserved, the mass and dimensions are not increased. The coloration is dark brown. At the bottom of the organ there is an oval-shaped depression 5x8 cm, up to 4 cm deep, the inner surface of which is lined with connective tissue. The connective tissue is located along the border of the depression and in close proximity to it.
Description of pathological changes. These pathological changes could develop as a result of an infectious lesion of the liver, which could be primary ( independent disease) and be a manifestation of another disease. Exudative develops purulent inflammation, in which a shaft of granulation tissue is formed around the focus of infection, delimiting the abscess cavity and supplying tissue defense cells (leukocytes) to the infectious focus. Granulation tissue is eventually replaced by coarse fibrous connective tissue. Capsules are formed and an acute abscess becomes chronic.
Outcome: 1) favorable:
a) elimination of infectious agents and organization of the abscess cavity (replacement with granulation tissue);
b) chronic course of the disease;
c) thickening of pus, turning it into necrotic detritus and petrification; 2) unfavorable:
a) generalization of inflammation;
b) a breakthrough of the contents of the abscess into the abdominal cavity with the formation of peritonitis or into the lungs;
c) lymphogenous and hematogenous distribution - septiconemia.
Conclusion: these morphological changes indicate an infectious lesion of the liver with the development of exudative inflammation and the formation of an abscess.
Diagnosis: Hepatitis. Liver abscess. _
17. Myocardial hypertrophy.
This heart macropreparation is enlarged due to the outflow tract, the inflow tract is not changed. The wall of the left ventricle is thickened. There are no signs of necrosis or hemorrhage.
Descriptions of pathological changes.
Visible changes indicate an increase in the mass of the sarcoplasm of muscle cells, the size of the nucleus, the number of myofilaments, the size and number of mitochondria, i.e. hyperplasia of intracellular ultrastructures. At the same time, the volume of muscle fibers increases. At the same time, hyperplasia of fibrous structures, stroma, occurs, which should be considered as a strengthening of the connective tissue skeleton of a stressed working heart. Elements of the nervous apparatus of the heart are hypertrophied.
The development of these changes is facilitated by mechanical factors that impede blood flow, as well as neurohumoral influence. These processes led to the provision of the necessary functional level of general circulation. In the future, dystrophic changes will occur in hypertrophied cardiomyocytes, the contractility of the myocardium gradually weakens, which will lead to the development of cardiac decompensation.
Diagnosis: Myocardial hypertrophy
The described phenomena reach a small degree with acquired valvular defects, accompanied by stenosis of the atrioventricular orifices and efferent vascular tracts of the ventricle. In this case, there is a defect in the aortic valve due to a rheumatic process, the development of stenosis and hyalinosis of the endocardium, which led to compliance and deformation of the valve leaflets.
20. Combined mitral defect hearts.
This macropreparation is the heart. The shape of the organ is preserved, the mass and dimensions are slightly increased. Subepicardial fat is strongly developed. Fat layers are also located in the myocardium. The lumen of the mitral valve is sharply narrowed. On its valves imposition of thrombotic masses is noticeable. The organ is light grey. Description of pathological changes.
These pathological changes could develop as a result of inflammatory processes of the mitral valve - endocarditis, which could be caused by rheumatic, septic or atherosclerotic diseases. In the proliferation stage, the valve leaflets thicken, sclerosis, and coalesce, which leads to a narrowing of the lumen. There are violations of the blood flow and the formation of thrombotic masses on the altered valves. Compensatory devices are aimed at ensuring blood flow, which is manifested by hypertrophy and *** expansion of the left atrium. Increased loads, aggressors and other factors, as well as progressive stenosis, lead to decompensation, which is manifested by myogenic expansion of the left atrial cavity, as well as dystrophic processes in cardiomyocytes (fatty degeneration). Developing stagnation of blood in the left atrium -> venous congestion in the lungs -» cor pulmonale -> death from acute heart failure. Exodus:
1) favorable: compensation;
2) unfavorable:
- death from acute heart failure;
- formation of congestive thrombus in the left atrium;
- heart attacks as a result of ischemia of hypertrophied myocardium;
- inflammation of the lungs due to venous congestion.
Conclusion: these morphological changes indicate inflammation of the mitral valve with the development of stenosis. Diagnosis: Combined mitral heart disease.
19. Ischemic infarction of the spleen.
This macropreparation is the spleen. The shape and dimensions are not changed. The color is heterogeneous - in general it is brown-red, but two sections 1-2 cm wide stretch from the gate to the periphery of the organ, of a paler color. The surface is smooth, without breaks, hemorrhages, scars.
Description of pathological changes.
These pathological changes indicate that they were caused by a sharp violation of arterial circulation in the large branches of the liena arteries, which led to ischemia of a significant area of ​​the spleen parenchyma and, subsequently, to a heart attack. An infarction in the spleen is most often white, less often white with a hemorrhagic corolla, which is due to the peculiarities of the angioarchitectonics of the organ. In this case, it is most likely white, since the necrotic areas have a characteristic color and are clearly delimited from the intact areas of the organs.
Exodus:
1) favorable:
a) scarring and replacement of necrotic tissues;
2) unfavorable:
a) rupture of the organ capsule and intra-abdominal bleeding;
b) death from shock;
c) intoxication and autoimmunization with decay products (resorption-necrotic syndrome), which aggravates the situation.
Conclusion: these morphological changes indicate sharp dyscirculatory changes in the basin of the branches of the splenic artery, leading to the development of a heart attack
Diagnosis: Acute ischemic infarction of the spleen.
21. Cirrhosis of the liver.
This macropreparation is the liver. The shape of the organ is preserved, the weight and dimensions are reduced. The capsule is thickened, the surface of the organ is large-hilly, the color is whitish-red, the right lobe is darker.
Description of pathological changes.
These pathological changes could develop as a result of dystrophy and necrosis of hepatocytes. which led to increased regeneration of hepatocytes and the formation of regenerated nodes surrounded on all sides by connective tissue. The death of hepatocytes stimulates the growth of connective tissue (due to cell hypoxia inside the nodes). Capillarization of the sinusoids of the false lobules occurs, and the subsequent hypoxia leads to a new wave of dystrophy and necrosis. These phenomena are associated with hepatocellular insufficiency. Regenerated nodes undergo diffuse fibrosis (coarsely lumpy liver), which is associated with necrosis of hepatocytes and hypoxia as a result of compression of vessels by nodes, their sclerosis, capillarization of sinusoids, and the presence of intrahepatic porto-caval shunts. This activates fibroblasts, Kupffer cells and increases the production of connective tissue. Sclerosis of the portal fields and hepatic veins leads to portal hypertension. as a result, the portal vein is unloaded not only through intrahepatic, but also through extrahepatic anastomoses.
Exodus:
1) favorable: compensated cirrhosis;
2) unfavorable: death from hepatocellular insufficiency, complications due to portal vein hypertension: ascites, varicose veins and bleeding from the veins of the esophagus, stomach, hemorrhoidal veins, peritonitis, sclerosis, cirrhosis, thrombosis. Jaundice, hemolytic syndrome, splenomegaly. hepatorinal syndrome, cancer.
Conclusion: these morphological changes indicate a post-necrotic mesenchymal-cellular reaction of the liver with the development of a vicious circle: a block between blood and hepatocytes, which leads to a structural restructuring of the body.
Diagnosis: Postnecrotic cirrhosis of the liver.
23. Cancer metastases in the spleen.
This macropreparation is the spleen (in section). Dimensions are not changed, the shape is normal. The surface is smooth with small areas of tuberosity. On the section, there are multiple white-pink round spots with a diameter of 3-15 mm. Where the spots are closer to the surface, they "bulge" it and form the aforementioned tuberosity.
Description of pathological changes.
These pathological changes indicate that a malignant tumor grows and metastasizes in the body. The most likely metastasis is adenocarceno.my of the uterus. Cancer cells multiply and form these spherical white-pink clusters.
Exodus:
1) favorable: prolongation of the patient's life as a result of complex chemooperative radiation treatment of tumors and metastases.
2) unfavorable:
- cachexia;
- intra-abdominal bleeding;
- progression and further metastasis;
Conclusion: these pathological changes indicate tumor progression and tumor metastasis.
Diagnosis: Adenocarcinoma. Distant metastases.
24. Nutmeg liver.
This macropreparation is the liver. The weight and dimensions are reduced, the shape is preserved. The color of the organ on the cut is variegated, gray-yellow with red specks, and the variegation increases towards the periphery. The liver is tuberous, tuberosity increases towards the periphery.
Description of pathological changes.
These pathological changes could develop as a result of an increase in pressure in the liver veins, which is possible with general (chronic right gastric failure) or local venous congestion (inflammation of the hepatic veins, thrombosis of their lumens). At the same time, the central veins expand, which leads to dystrophy and necrosis of adjacent hepatocytes and expansion of the sinusoids. In them, formed elements are located to the center, and on the periphery - plasma (due to increased pressure at the confluence of the arterial capillary) > plasmorrhagia, diapedetic hemorrhage. As a result of stagnation venous blood> hypoxia > synthesis of the connective tissue of Kupffer cells - the formation of a basement membrane and the transformation of the sinusoid into a capillary > hypoxia. In the central sections of the lobules, fatty degeneration (decomposition) develops up to necrosis. Due to complete regeneration in the places of death of hepatocytes, connective tissue grows > sclerosis. Venous stasis > hypoxia > thickening of the connective tissue of the liver (interlobular and along the triads). The remaining peripheral hepatocytes, surrounded by connective tissue, begin to multiply. A false lobule is formed, the blood supply of which is extremely poor > hypoxia, dystrophy > necrosis of hepatocytes.
Exodus:
1) favorable: chronic course of the disease; elimination of the cause of venous plethora;
2) unfavorable: death from liver failure, cancer, formation of sclerosis and portal hypertension, infection, jaundice, etc.
Conclusion: these morphological changes indicate venous plethora of the liver and hypoxia that has developed on this soil, which leads to a structural reorganization of the organ.
Diagnosis: Muscat cirrhosis of the liver.
25. Chronic lung abscess
This macropreparation is light. An organ on a section of a heterogeneous consistency. Color - gray, with dense inclusions of a whitish color. The incision runs perpendicular to many bronchi of different calibers. The connective tissue separating the lobes of the lung is expressed. At the top of the organ there is a large cavity 5 cm in diameter, porous, along the periphery of which there is a whitish tissue. The inner surface of the cavity is also lined with this tissue.
Description of pathological changes.
These pathological changes could develop as a result of inflammatory lung disease or bronchiectasis. which is unlikely, since then we would see multiple cavities. With inflammation of the lungs of any ethnology, the tissue, which first underwent necrosis and then suppuration, turns into a purulent-necrotic mass, which is excreted through the bronchi along with sputum. An acute abscess cavity has formed. If the cause of suppuration is not eliminated, the granulation tissue that first formed around the cavity is eventually replaced by coarse fibrous connective tissue, which separates the abscess from the lung parenchyma. Dense connective tissue whitish inclusions, of which there are many in the lung tissue, are characteristic of a chronic abscess, when not only bronchi are involved in the process, but also lymphatic drainages, through which purulent inflammation spreads.
Exodus:
1) favorable: organization, encapsulation.
2) unfavorable: fibrosis and deformation of lung tissue due to the spread of purulent inflammation.
Conclusion: these morphological changes indicate that inflammatory processes in the lung tissue led to the development of an acute abscess with a transition to a chronic one.
Diagnosis: Chronic lung abscess. Exudative purulent inflammation.
27. Parietal thrombus of the artery.
This macropreparation is the abdominal aorta. The shape of the organ is preserved, the dimensions are not increased. The organ is light grey. Dark gray formations with a diameter of 5 mm are visible on the intimae. with an uneven surface, and next to it, a formation of the same consistency and color 3x1.5 cm. This formation is located at the site of aortic bifurcation.
Description of pathological changes.
These morphological changes could develop in rezaltata violations of fat and protein metabolism, which was facilitated by factors such as:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- ethnic.
Unregulated cellular metabolism of cholesterol leads to the formation of foam cells and the further development of atherosclerotic changes that we see on the intima of the aorta: fatty spots, fibrous plaques, formation of thrombotic overlays at the site of plaque ulceration. In the formation of thrombotic overlays (formations of a dark gray color of a dense consistency), areas not only of violations of the vascular wall, but also with impaired blood circulation, blood composition, vascular wall, dysregulation of the coagulation, anticoagulation and fibrinolytic systems take place.
A particularly important factor in this case is a violation of blood circulation in the form of a vortex of blood flow at the site of the bifurcation of the abdominal aorta. This slowing of the blood flow and contributes to the imposition of thrombotic masses on the ulcerated intima.
Outcome: 1) favorable:
a) aseptic autolysis of a thrombus;
b) organization; 2) unfavorable:
a) petrification;
b) thromboembolism;
c) septic melting;
d) obturation of the aortic lumen.
Conclusion: these morphological changes indicate dystrophic changes in the aortic intima, which, together with impaired blood flow, created the preconditions for thrombosis.
Diagnosis: Thrombosis of the aorta.
Fibromyoma of the uterus.
This drug is the uterus. The size and weight are significantly increased due to tumor nodes. Color whitish yellow. Two knots of tumor tissue are visible: the first is located inside the myometrium of the body of the uterus (closer to the endometrium), diameter 2.5 cm; the other in the fundus of the uterus, grows out of the organ. The size of this node is 10-12 cm, rounded, dense consistency. No foci of necrosis or hemorrhage were observed.
Description of the pathological process
This pathological process is polyetiological, but disharmonic disorders are the most likely cause. An obligatory stage is pre-tumor changes, among which the so-called background changes are distinguished, manifested by dystrophy, atrophy, hyperplasia. Hyperplasia is considered as a proper precancerous process. Stage of tumor development: diffuse hyperplasia, focal hyperplasia a benign tumor. The tumor is represented in this preparation by smooth muscle cells. Since the stroma of the tumor is well developed, it is called fibromyoma. In the uterus, depending on the localization, intramural, subserous and submucosal fibroids are distinguished.
Complications: the development of swelling under the endometrium often causes small uterine bleeding, which, even if they themselves are not life-threatening, after a while lead to the development of anemia (iron deficiency with corresponding consequences). Malignancy.
Conclusion: these morphological changes indicate the development of disharmonious elements in the uterus.
Diagnosis: Uterine fibromyoma.
29. Bubble skid.
This macropreparation is represented by many cysts resembling bunches of grapes (opaque color) and with a diameter of 0.5 to 1.5 cm. These spherical vesicles are located (as if they grow and hang in a cluster-shaped dome) over areas of yellowish tissue of soft consistency - uterine tissue. The cavity of the vesicles is filled with a clear mucus-like liquid.
Description of pathological changes.
Examining the morphology of this preparation, it can be assumed that this formation could have formed during the pathology of pregnancy, with hydatidiform mole. That is, if the placenta with hydropic and cystic transformation of the chorionic villi, which is accompanied by the proliferation of the epithelium and the collapse of the villi, a sharp increase in their number and transformation into clusters of cystic vesicles (the fetus dies). Areas of yellow tissue of soft consistency - the uterus (covered with racemose vesicles). Under the microscope (pat. changes) we can see that the vessels of the villi become empty and at the same time there is a strong proliferation of the epithelium of these villi (both rows of cells of the villi mix randomly and form a thickening on the surface of the villi). The villi can grow deep into the wall of the uterus, destroy the vessels, causing severe uterine bleeding (such deep and extensive ingrowth can occur with one of the types of hydatidiform drift - destructive hydatidiform drift). Clinically, the disease is manifested by the fact that the uterus increases much more in volume than it corresponds to this period) "pregnancy, while uterine bleeding may appear from 2-4 months of pregnancy, and the level of gonadotropin in the woman's urine increases 5 times
Causes of cystic drift" non-uterine disturbances of hormonal homeostasis - carbonic dysfunctions due to a decrease in estrogen production (with ovarian corpus luteum cysts; mutations of the fetal egg caused by a viral infection, intoxication are possible).
Exodus:
1) favorable: surgical removal of all chorionic villi from the uterine cavity;
2) unfavorable:
a) malignancy of cystic drift into chorionepithelioma;
b) the development of severe bleeding (uterine), which leads to the development of chronic anemia -> death.
Conclusion: this macropreparation - the placenta with the transformation of chorionic villi, indicates the pathology of pregnancy; the occurrence of unlimited growth of pathologically altered elements of the placenta (due to cell mutation or hormonal disorders in the mother's body).
Diagnosis: Cystic skid.
30. Cavernous pulmonary tuberculosis.
This macropreparation is light. Organ grey-pink. The porous parenchyma of the lung is visible, the stroma is represented by connective tissue layers of a whitish color. In the parenchyma, dotted black blotches are visible - the vessels of the lung. Against the background of this picture, multiple formations of a rounded shape with a diameter of 0.5 cm are visible. Whitish in color. The configuration of the cut of the lung is violated by caverns in the amount of 3 pcs. The first one measures 8 cm long, 7 cm wide, 4 cm deep. The second one is 4x3x1.5. The third one is 6x5x3. Caverns are located next to each other in a checkerboard pattern.
Description of pathological changes.
These pathological changes are a manifestation of a specific inflammation of the lung tissue caused by Mycobacterium tuberculosis. In the course of an exudative reaction, a focus of inflammation is formed in the lung tissue, which undergoes cheesy necrosis. Subsequently, a granuloma is formed around the focus of necrosis, consisting of epithelioid cells, macrophages, lymphocytes, plasma cells and Pirogov-Langhans cells characteristic of tuberculous inflammation, thus the inflammation becomes productive. With the weakening of the body's resistance forces as a result of incomplete phagocytosis of mycobacteria, exudation intensifies, which ends with cheesy necrosis of the granuloma and adjacent tissue. A cavity appears as a result of purulent fusion and liquefaction of caseous masses, inflammation takes the form of acute cavernous tuberculosis. In the future, this process takes a chronic course. The wall of the cavity becomes dense, built from the following layers: internal pyogenic (necrotic), rich in decaying leukocytes; middle - a layer of tuberculous granulation tissue; external - connective tissue, connective tissue grows around the cavity and between the layers of connective tissue, areas of atelectasis of the lung are visible. The cavities communicate with the bronchi. The inner surface of the cavity is uneven, with beams crossing it - obliterating the bronchus or thrombosing the vessel. In the presented picture of a lung section, whitish rounded formations are foci-infiltrates of tuberculoma, in various stages of inflammation (exudative, productive). The process gradually spreads in the apeco-caudal direction, descending from the upper segments to the lower ones, both by contact and through the bronchi, occupying new areas of the lung. Therefore, the oldest changes (caverns large sizes organizing) are located above.
Exodus:
1) favorable (unlikely) - with a significant increase in the body's resistance forces, it is possible to get out of the chronic course of the disease and organize tissue detritus with complete phagocytosis of mycobacteria. At the same time, sclerosis of the segment of the lung, affected by the inflammatory process with areas of bronchial atelectasis, develops.
2) unfavorable - associated with caverns -\u003e bleeding occurs from the cavity: a breakthrough of the contents of the cavity into the pleural cavity -\u003e pneumothorax and purulent pleurisy. The lung tissue itself undergoes amyloidosis.
Conclusion: the described morphological changes indicate an undulating course of the tuberculous process.
Diagnosis: Fibrinous-cavernous pulmonary tuberculosis.

• 1 Causes of pain
• 2Gastritis
• 3 Peptic ulcer
• 5Food poisoning
• 6Duodenitis and pancreatitis
• 7Diagnosis and treatment

1 Causes of pain

If you feel severe discomfort, you should consult a specialist. An important aspect of diagnosis is to clarify the nature of the pathology. Pain in the stomach is most often concentrated in the projection of the organ on the abdominal wall. This region is called the epigastric region. Pain in the stomach can be localized, diffuse, radiating, acute, dull, paroxysmal, burning and cutting.

To establish the cause of its occurrence, it is necessary to identify the intensity of the syndrome. In this case, the main characteristics of pain are determined:

• character;
• appearance time;
• duration;
• localization;
• connection with food intake;
• weakening or strengthening during movement, after defecation or when changing posture;
• combination with other symptoms (nausea, loss of appetite, vomiting, bloating).

The sensation of pain in the stomach in most cases is associated with damage to the organ. The most common reasons are:

• acute and chronic gastritis;
• stomach ulcer;
• the presence of polyps;
• damage to the mucous membrane of an organ during food poisoning (intoxication or toxic infection);
• damage due to abdominal trauma;
• severe stress;
• intolerance to certain products;
• injury to the mucosa by accidentally swallowed objects.

Pain in the stomach area can be due to other reasons. These include pancreatitis, peptic ulcer of the 12th intestine, colitis, enterocolitis, cholecystitis, dyskinesia biliary tract, irritable bowel syndrome, appendicitis, heart disease.

2Gastritis

The most common causes of stomach pain are acute or chronic gastritis. These forms of the disease are characterized by inflammation of the mucous layer of the organ against the background of exposure to irritating factors. Quite often, gastritis has an infectious nature. In this case, Helicobacter pylori bacteria act as a starting point. The disease occurs in children, young and old people. When it hurts in the stomach, in this case there is an acute gastritis, which is divided into simple, catarrhal, erosive, fibrinous and phlegmonous. If the disease becomes chronic, organ atrophy often develops. The main provoking factors for the occurrence of gastritis are:

• abuse of spicy, fried, hot or cold foods;
• alcohol consumption;
• smoking;
• infection with Helicobacter bacteria;
• accidental or intentional use of acids or alkalis;
• uncontrolled intake of medications (drugs of the NSAID group).

The symptoms of gastritis are varied. In children and adults, discomfort in the stomach is the main symptom of the disease. The most common is dull pain. Sharp manifestations are typical for acute inflammation of the mucosa. With gastritis, the pain syndrome can be paroxysmal or constant. There is a clear connection with food intake (spasm appears after eating and when a person is hungry). Additional symptoms of the disease may include belching, nausea, loose stools, bloating, and a feeling of acid in the mouth. Not pronounced aching pain is characteristic of chronic gastritis with normal acidity.

3 Peptic ulcer

Acute pain in the stomach associated with eating may indicate the presence of a peptic ulcer. It proceeds in a chronic form. The pain syndrome is most pronounced during the period of exacerbation. Ulcers are formed on the background of stress, gastritis, the use of certain drugs, endocrine diseases. The pathogenesis of the formation of this defect is associated with the suppression of protective mechanisms (impaired synthesis of mucus covering the stomach), as well as with an increase in the acidity of gastric juice. The symptoms of stomach ulcers are similar to those of gastritis. The main signs of the disease include:

• severe pain in the epigastric region;
• nausea and vomiting after eating;
• weight loss;
• loss of appetite.

With ulcerative lesions, the stomach hurts after eating. This is the main difference from the pathology of the 12th intestine. Pain syndrome occurs almost immediately after eating (within one and a half hours). There is a certain connection of exacerbation with the time of year. Most often, a person suffers from attacks of pain in the fall and spring. In the case of complications (perforation, bleeding), symptoms can increase dramatically. This condition requires urgent care. The processes occurring in the stomach, the causes of which may be different, are often reversible.

4Cancer

If the stomach hurts, the cause may lie in oncology. This is one of the most common malignant pathologies. Nearly a million people worldwide die from stomach cancer every year. For a long time, the disease may not manifest itself. Quite often, cancer is detected already at stage 3 or 4, when treatment is ineffective. Men suffer from this disease more often than women. Cancer is dangerous because the tumor in the later stages is capable of metastasizing to other organs, which is why patients die. The exact cause of the disease is still unknown. Possible etiological factors are: the presence of atrophic gastritis, infection of the organ with Helicobacter bacteria, exposure to toxic and carcinogenic substances, poor nutrition, intake medicines, alcoholism, aggravated heredity, Menetrier's disease.

Cancer symptoms on early stages presented by decreased appetite, aversion to meat, nausea, bloating, weight loss, malaise, weakness, swallowing disorders. In the later stages, patients may be disturbed by aching pain. In most cases, it is due to the germination of the tumor in neighboring organs. Persistent shingles pains appear when the neoplasm is introduced into the pancreas. Operative treatment should be started as soon as possible. Acute pain, resembling an angina attack, is characteristic of a tumor that has grown into the diaphragm. If the pain syndrome is combined with a transfusion in the abdomen, a violation of the stool by the type of constipation, this may indicate the involvement of the transverse colon in the process.

5Food poisoning

Sharp pain in the stomach can be a sign of food poisoning. This is a disease that develops when eating poor-quality food containing pathogenic microorganisms, their decay products, or various toxic compounds. All food poisonings are divided into the following forms:

• microbial;
• non-microbial etiology;
• mixed.

The first group includes food toxic infections and intoxications. In this situation, the pathogens are bacteria (clostridia, E. coli, Proteus, streptococci), fungi, toxins. Poisoning is also possible with poisonous plants, mushrooms, berries, fish caviar, seafood, salts of heavy metals, pesticides, pesticides. Symptoms in this pathology are caused by inflammation of the stomach against the background of exposure to toxins.

In most cases, there are signs of gastroenteritis. These include constant pain in the muscles, head, nausea, vomiting, fever, weakness, frequent stools. Often there are symptoms of dehydration. Diagnostic signs of food poisoning are:

• acute, sudden onset;
• connection of pain with food intake;
• simultaneous onset of symptoms in a group of individuals;
• the speed of the disease.

6Duodenitis and pancreatitis

Pain in the epigastric region may be a symptom of duodenitis (inflammation of the mucous membrane of the 12th intestine). It can occur in acute and chronic form. This is the most common pathology of this organ. Quite often, this disease is combined with enteritis and gastritis. The main causes of inflammation of the 12th intestine are:

• nutritional errors;
• the use of alcoholic beverages;
• bacterial infection;
• the presence of an ulcer or gastritis;
• violation of blood supply;
• chronic pathology of the liver and pancreas.

The main symptoms of the disease depend on its form. Duodenitis, which arose against the background of an ulcer or infectious gastritis, is characterized by pain on an empty stomach, at night and a few hours after eating. Strong manifestations are characteristic of the acute type of pathology. When combined with inflammation of other parts of the small intestine, symptoms may include malabsorption syndrome, dyspeptic disorders. In case of stagnation of the secret of the 12th intestine, there are paroxysmal pains, belching, nausea, vomiting, bloating, rumbling. With duodenitis, the outflow of bile can be disturbed. In this situation, pain appears in the epigastric region. The clinical picture resembles biliary dyskinesia.

If something hurts in the stomach, the cause may be pancreatitis, the symptoms of which, as a rule, are quite pronounced. The pain syndrome is most pronounced in acute inflammation of the pancreas. The latter is located next to the stomach. This pathology is characterized by the appearance of pain in the upper abdomen. It can last from several minutes to several days. The pain is intense, constant and disturbs the patient. It can give to the left or right half of the body, depending on which part of the organ is affected (head, body or tail). The pain syndrome intensifies during meals and requires treatment. Often it takes on a shingling character. Additional signs of the disease include nausea, vomiting, bloating, tenderness on palpation, and an increase in general body temperature.

7Diagnosis and treatment

If the stomach is sick, then you should not put off a visit to the doctor on the back burner, because the consequences can be dangerous. Treatment is carried out only after establishing the cause of the pain syndrome. Diagnostics includes:

• a detailed survey of the patient;
• physical examination (palpation of the abdomen, auscultation of the lungs and heart);
• general and biochemical blood test;
• conducting FGDS;
• determination of the acidity of gastric juice;
• a blood test for the presence of Helicobacter pylori;
• Ultrasound of the abdominal organs;
• laparoscopy;
• study of feces;
• contrast radiography;
• CT or MRI;
• duodenal sounding;
• Analysis of urine.

Colonoscopy may be done if colitis is suspected. A biopsy is done to rule out stomach cancer. How to get rid of stomach pain? Therapy should be aimed at eliminating the underlying cause. If the stomach is inflamed, what to do in this situation? Treatment of gastritis involves adherence to a strict diet, the use of drugs (antacids, proton pump blockers, gastroprotectors). The use of Almagel, Phosphalugel and Omez is indicated for the form of the disease with high acidity. If Helicobacter bacterium is detected, antibiotics and Metronidazole are used.

Therapy acute pancreatitis includes temporary fasting, application of cold on the stomach, the use of antispasmodics, omeprazole, diuretics, infusion therapy.

With purulent pancreatitis, treatment necessarily includes antibiotics. If vomiting is present, antiemetics (metoclopramide) are used. With the development of peritonitis and necrosis of the organ, an operation is indicated. The chronic form of pancreatitis involves dieting, taking enzyme preparations (Panzinorma, Pancreatin, Mezima). In case of gastric cancer, surgical treatment (resection of the organ or its removal). Thus, the causes of abdominal pain can be very different. If any, you should consult your doctor.

What to do in case of exacerbation of peptic ulcer of the stomach?

If the patient has an acute critical condition associated with perforation of a stomach ulcer, then emergency treatment is necessary, since peritonitis in this case is rapidly progressing. The symptoms of perforation are:

• the appearance of a sharp pain, rapidly spreading throughout the abdomen;
• muscle tension of the walls of the peritoneum;
• phenomena preceding fainting (dizziness, ringing in the ears, weakness);
• chills;
• nausea;
• dry mouth.

Traditional Therapies

Therapeutic care in the phase of exacerbation of gastric ulcer is determined based on the patient's condition, his age, the nature of clinical symptoms. However, the treatment of uncomplicated forms is almost always based on the use of bactericidal agents, for example, Amoxicillin, Metranidazole, Clarithromycin. Due to these drugs and some others, also belonging to the group of antibiotics, it becomes possible to cure the pathology of the gastric mucosa, since they eliminate the main cause - pathogen Helicobacter pylori.

In addition to antibacterial drugs in the treatment of acute ulcers, the following can be used:

1. means that normalize the level of acidity of the digestive juice (Omeprazole, Ranitidine);

2. drugs with a gastroprotective (protective) property (De-nol and other bismuth-containing medicines);

3. dopamine central receptor blockers (Primperan, Reglan, Cerucal);

4. drugs with a psychotropic effect, if the patient suffers from irritability, insomnia, a feeling of constant anxiety (Tazepam, Elenium);

5. adrenergic agents that have antisecretory and suppressive gastrin release action (Obzidan, Inderal).

In the treatment of exacerbation of gastric ulcer, certain physiotherapeutic methods have also proven themselves: ozocerite and paraffin applications, magnetic and hydrotherapy, sessions of modulated sinusoidal currents.

Carrying out all activities in combination with a diet in 80-90% of cases allows you to achieve a stable remission of the pathology. However, conservative treatment does not always help, and then the patient is shown surgical intervention in various ways depending on the circumstances (selective proximal vagotomy, resection, endoscopy).

Indications for gastric surgery:

• perforation ulceration;
• an ulcer complicated by bleeding of a profuse nature (bleeding leading to hypovolemia);
• pyloric stenosis;
• defect penetration.

Folk recipes for treatment

Experts do not recommend using folk methods to cure an ulcer because of the risk of aggravating the situation. Such treatment is especially prohibited in complicated acute forms. But in order to prevent exacerbation, doctors allow, for example, a remedy to use some non-traditional recipes:

1. from birch leaves (1 teaspoon of crushed fresh leaves of this tree is poured with a glass of boiling water, infused for 1-2 hours);

2. from coltsfoot (the infusion is prepared similarly to the previous method with one difference that not only the leaves of the plant, but also the flowers themselves can be used); besides, this folk recipe helps to treat both the stomach and the bronchi;

3. from the medicinal marshmallow (1 large spoonful of its ground rhizome is poured with 250 ml of boiling water, everything languishes over low heat for 30 seconds, and then infused for about half an hour).

All of the listed traditional medicine should be drunk before meals 3 times a day.

Diet for ulcers

Compliance with dietary nutrition is equally important during exacerbation of the inflammatory process, and in the stage of its remission, and in case of complications with stenosis, bleeding and other life-threatening factors. Therefore, the doctor prescribes a personal diet to the patient, based on:

• sparing of the gastroduodenal mucosa with the elimination of all chemical, thermal and mechanical stimuli;
• fractional nutrition (the patient is recommended to eat and drink in small portions, but every 3-4 hours);
• correction of fats in the direction of increase;
• increasing the protein quota;
• reducing the proportion of carbohydrates in the daily diet.

Diet in the treatment of stomach ulcers should be observed for at least 6-9 months. When the disease recedes, going into a remission phase, and food does not cause discomfort to the stomach, you can gradually return to the usual type of dishes (not pureed and not very boiled), but you still have to completely abandon coarse and harmful industrial products.

In addition to diet, an important role in the prevention and treatment of acute ulcers is played by the exclusion of alcohol and energy drinks because they cause bleeding and the growth of erosive inflammation.

Ulcer of the duodenal bulb

One of the most common types of erosive formations of the gastrointestinal tract is the ulcer of the duodenal bulb. The disease is common. According to official data, up to 10% of the world's population is ill. Deformation develops due to a failure in chemical treatment food. The anatomy of erosive formations is different, but more often they form on a bulb that has the shape of a ball. The bulb of the duodenum is located at the very beginning of the intestine, at the exit from the stomach. Treatment is long and difficult.

It can be deformed on the anterior and posterior wall (kissing ulcers). The duodenal ulcer also has a special location - at the end or at the beginning (mirror). Mirror erosions are treated like other forms. Negative factors, affecting the work of the stomach and intestines, provoke the appearance of ulcers of various shapes. The risk group includes middle-aged people and those who are forced to work the night shift.

If there is a failure in the processing of food by the stomach, an ulcer of the duodenal bulb may occur.

Causes of duodenal ulcer

Most often, inflammation of the duodenum occurs due to the aggressive action of acid. In the absence of therapy, the development of perforated ulcers and bleeding is possible. There can be a number of reasons:

• disturbed diet (a lot of fatty, spicy, diet abuse, carbonated drinks);
• bacterium Helicobacter - the cause of ulcerative formations in most cases;
• smoking, alcohol;
• severe stress or systematic stay in a state of emotional stress;
• hereditary predisposition;
• long-term use of certain anti-inflammatory drugs;
• incorrectly prescribed treatment at the initial stage of the disease.

Kissing ulcers in the intestines may appear due to concomitant causes: HIV infection, liver cancer, hypercalcemia, renal failure, Crohn's disease, etc.

Symptoms

Symptoms of a duodenal ulcer are also characteristic of other types of gastrointestinal ulcers, and they appear depending on the stage of the disease:

• heartburn;
• nausea in the morning or after eating;
• pain in the epigastric region;
• pain in the stomach at night;
• flatulence;
• the appearance of a feeling of hunger after a short period of time after eating;
• if the disease is in advanced form, bleeding may open;
• vomit;
• pain localized in the lumbar region, or retrosternal part.

The inflammatory lymphofollicular form of the duodenum has a different nature of pain: stabbing pain, sharp or aching. Sometimes it goes away after the person has eaten. Hunger pains usually occur at night, and to eliminate discomfort, it is recommended to drink a glass of milk or eat a little. Night pain is caused by a sharp increase in acidity.

stages

The intestinal healing process is divided into 4 main stages:

• Stage 1 - initial healing, the creeping of layers of the epithelium is characteristic;
• stage 2 - proliferative healing, in which protrusions in the form of papillomas appear on the surface; these formations are covered with regenerating epithelium;
• Stage 3 - the appearance of a polysade scar - an ulcer on the mucous membrane is no longer visible; a more detailed study shows many new capillaries;
• Stage 4 - scar formation - the bottom of the ulcer is completely covered with new epithelium.

Erosive kissing formations on the duodenum 12 heal after therapy. Many ulcers in a small area of ​​the intestine leads to the formation of several scars. The result of such healing is cicatricial and ulcerative deformity of the duodenal bulb. The appearance of fresh scars leads to a narrowing of the lumen of the bulbous sector. Inflammatory cicatricial deformity duodenal bulb has negative consequences, for example, stagnation of food and malfunctions of the entire gastrointestinal tract.

There is also a distribution by stage: exacerbation, scarring, remission.

One of the forms of intestinal ulcers is lymphoid hyperplasia of the duodenal bulb, which is characterized by inflammation due to a violation in the outflow of lymph. The causes of occurrence are exactly the same as those of a duodenal ulcer. There are also similar symptoms. Lymphofollicular dysplasia is a pathology in the mucous membrane of the intestine or stomach. It is characterized by the appearance of rounded formations on a wide base. Lymphofollicular dysplasia is deformed and has a dense texture and punctate dimensions. The lymphofollicular mucosa is infiltrated. Development stages:

1. acute;
2. chronic.

Diagnosis of the disease

The FGDS method (fibrogastroduodenoscopy) will help to accurately diagnose the presence of a duodenal ulcer. Using a special probe with a camera, the surface of the intestine is examined. It is this diagnostic method that will determine the location of the ulcer, its size and stage of the disease. Inflammation is usually observed, or the surface is hyperemic, covered with dotted erosions of a dark red color. The area of ​​the intestine is inflamed in the region of the mouth, and the mucosa is hyperemic.

Be sure to appoint tests to determine the bacterium Helicobacter. As a material for testing, not only blood and feces are used, but also vomit, material after a biopsy. Auxiliary diagnostic methods include x-ray, palpation in the stomach area, general analysis blood.

Treatment

After the diagnosis of "inflammation of the duodenal bulb" is made, treatment should be started immediately, since serious complications may develop. Kissing ulcers are treated mainly with medication. During an exacerbation, hospitalization is necessary.

The doctor selects drugs and physiotherapy individually for each patient, taking into account the characteristics of the body and stage. For example, the chronic or lymphofollicular stage is treated differently than during an exacerbation. This scheme usually includes such medicines:

• bismuth-based drugs, in case of detection of Helicobacter bacteria; such drugs have a depressing effect on pathogenic microflora;
• drugs that reduce the amount of gastric juice produced: blockers, inhibitors, anticholinergics;
• prokinetics - improve intestinal motility;
• unpleasant pain is eliminated with the help of antacids;
• antibiotics are prescribed to combat the bacterial cause of the appearance of a lymphofollicular ulcer;
• gastroprotectors will help prevent the negative effects of hydrochloric acid on the affected area;
• inflammation is relieved by analgesics and antispasmodics.

The combination of medication and physiotherapy contributes to a faster recovery of the body. These techniques include: electrophoresis, ultrasound, the use of microwaves, modulated current therapy to relieve pain. Special physiotherapy exercises will help normalize the motility of the stomach. Gymnastics is a good prophylactic against stagnation in the intestines and stomach.

In addition to the generally accepted methods of healing intestinal ulcers, traditional medicine has long proven its effectiveness. In first place at ulcerative lesions worth freshly squeezed potato juice. It must be drunk three times a day, and only freshly squeezed. Pre-peel the potatoes, rub on a grater, and squeeze through gauze. The first few days, the dosage is one tablespoon. Gradually, it can be increased to half a glass. It is necessary to drink before eating.

Other equally effective remedies include honey, healing herbs(calendula, St. John's wort, plantain), olive and sea buckthorn oils.

During the period acute form obligatory observance of a bed rest. After the aggravation has passed, you can take short walks. Heavy physical activity and exercise are prohibited. The army is contraindicated for those who have an ulcer. In order not to provoke new attacks, it is important to avoid stress and protect the nervous system.

Compliance with the diet is one of the important factors on the way to recovery and reduction of inflammatory processes. General recommendations for diet food the following:

• small portions;
• chew each piece thoroughly;
• temporarily exclude foods that provoke the active production of gastric juice (vegetable soups, fish and meat broths);
• in order not to additionally irritate the mucous membrane, the food should be frayed;
• fruit juices should be diluted with water;
• consume milk more often;
• do not use spices in dishes;
• cook grated cereals;
• eat food at the optimum temperature, not too hot and not too cold;
• fractional meals, up to 5 times a day.

Cooking food should be steamed or in the oven. The diet must include non-acidic fruits, kefir, milk, cottage cheese, boiled or steamed vegetables. It is necessary to stop drinking alcohol and smoking, as this can lead to the development of serious complications.

Forecast

A favorable prognosis for recovery can be if the treatment was carried out on time and the correct diet was observed. In case of untimely access to a doctor or incorrectly prescribed drugs, serious complications may develop: lymphofollicular ulcer, bleeding (vomiting blood), perforation of the ulcer ( sharp pain under the sternum) and penetration (due to adhesions, intestinal contents enter neighboring organs). In each of these cases, the only option is surgery.

Duodenal stenosis is a complication. After healing, there are cicatricial changes, which later can cause swelling and spasm. Stenosis usually manifests itself during the acute form or after therapy. There is stenosis in those patients in whom the ulcer does not heal for a long time. Stenosis is accompanied by impaired motility of the intestines and stomach.

Toxic dystrophy of the liver

Toxic dystrophy of the liver or progressive massive liver necrosis is an acute or chronic disease characterized by massive tissue necrosis and the development of liver failure. Toxic dystrophy develops as a result of the action of exogenous (mushrooms, foods with toxins, etc.) and endogenous (pregnancy toxicosis, thyrotoxicosis) toxins. These substances have a hepatotoxic effect and damage hepatocytes.
pathological anatomy. Toxic dystrophy of the liver It has various manifestations that depend on the prescription of damage to liver cells. In the first few days, the organ enlarges, it becomes dense, yellow in color. Further, there is a progressive decrease in liver tissue and wrinkling of the capsule. On the cut, the liver is clay-colored or gray. Under the microscope, fatty degeneration of hepatocytes is first found in the center of the lobules, these changes are quickly replaced by necrosis and autolysis of the hepatic tissue. The progression of necrosis leads to complete necrosis of the lobule by the end of the second week, and only a narrow strip of fatty degeneration remains along the periphery. All this is a stage of yellow dystrophy. On the 3rd week there is a further reduction in the liver and it becomes red. These are manifestations of phagacytosis and resorption of necrotic detritus. In this case, the stroma of the organ with dilated blood vessels is exposed. Changes on the 3rd week are a manifestation of the stage of red liver dystrophy.
With progressive necrosis, patients die from acute hepatic-renal failure. Survivors have liver changes characteristic of postnecrotic cirrhosis.

24. Toxic dystrophy of the liver.

The liver is enlarged, flabby, with a wrinkled capsule. On the section, the structure is erased, variegated color

305. Portal cirrhosis of the liver.

The liver is deformed, compacted, reduced in size, the surface is granular. The section shows large and small nodules of hepatic tissue of various sizes, surrounded by a ring of connective tissue - the so-called "false lobules".

553. Cirrhosis of the liver.

The liver is of a dense consistency, tuberous, on the cut with yellow foci and false lobules.

325. Fatty degeneration of the liver of the "goose" type. Chronic fatty hepatosis.

The liver is enlarged, yellow.

279. Cancer of the liver on the background of cirrhosis.

Against the background of cirrhosis of the liver, a focus of tumor tissue of a variegated appearance is visible.

198. Thrombosis of the hepatic vein.

Part of the liver with the hepatic vein, in the lumen of which a thrombus is visible.

127. Icteric necrotic nephrosis.

The kidney on the cut is yellow-green, the border of the cortical and medulla stale bark dull, wide.

462. Splenomegaly. Hyalinosis capsule.

The spleen is enlarged, on the capsule there are matte translucent foci

37. Hemorrhoids. Brown varicose veins in the distal colon.

Model 35. Varicose veins of the esophagus in liver cirrhosis.

Sharp plethora and dilatation of the veins of the esophagus with erosion of the vessel wall.

To study micropreparations:

38. Acute viral hepatitis.

Hepatocytes in a state of hydropic (balloon) dystrophy and coagulation necrosis. In the perisinusoidal lumens, hyaline-like bodies of Kaunsilman are found. Cholestasis and lymphohistiocytic infiltration of the portal tracts are pronounced.

Indicate in the picture:

1 - balloon dystrophy of hepatocytes.

2 - Councilmen's bodies.

3 - cholestasis

4 - histiolimphocytic infiltration of the portal tracts

171. Subacute toxic dystrophy of the liver(acute hepatosis, stage of red dystrophy).

The structure of the hepatic lobules is broken. Hepatocytes in a state of cell necrosis are homogeneous, eosinophilic, without nuclei. Many necrotic hepatocytes have undergone phagocytosis and resorption. In these areas, a bare (free) reticular stroma with dilated sinusoids and bile capillaries is visible.

Indicate in the picture:

1 - necrotic hepatocytes.

2 - free stroma.

3 - dilated sinusoids and bile capillaries.

99. Portal cirrhosis.

Growth of the connective tissue along the portal tracts in the form of rings with the formation of the so-called "false lobules", in which the architectonics of the vessels is disturbed. hepatocytes in a state of fatty degeneration (cells in the form of vacuoles) and regeneration (large cells with large or double nuclei)

Indicate in the picture:

1 - connective tissue

2 - false segments

3 - hepatocytes in a state of fatty degeneration

4 - young liver cells

44. Billiary cirrhosis.

Growth of connective tissue along the periphery of the lobules. Cholestasis is pronounced, the bile ducts are dilated, filled with yellow or dark green bile.

76. Postnecrotic cirrhosis (Masson stain).

The structure of the liver is sharply disturbed, extensive areas of blue connective tissue in place of necrotic hepatic tissue. The preserved liver cells in a state of necrosis are homogeneous, pink-violet, without nuclei. Regeneration is not expressed.

397. The basis of toxic dystrophy of the liver is:

inflammation

proteinaceous dystrophy

1. fatty degeneration

398. Outcomes of toxic dystrophy are:

hepatic-renal insufficiency

cirrhosis of the liver

399. The cause of toxic liver dystrophy is:

infection

alcohol poisoning

poisoning with mushrooms and poisons

toxicosis of pregnancy

400. "Goose" liver develops when:

acute hepatosis

chronic hepatosis

401. The mechanism of alteration of hepatocytes in serum hepatitis is:

direct effect of viruses

immune cytolysis

402. AIDS is accompanied by hepatitis:

whey

epidemic

403. Degeneration of hepatocytes in serum hepatitis:

1. granular

   vacuolar

404. The etiological factors of hepatitis include:

1. medicines

allergy

dystrophy

405. Morphological form of chronic hepatitis is:

phlegmonous

persistent

fibrinous

fatty hepatosis

406. Hepatitis is considered chronic:

after 1 month

after 3 months

after 6 months

after 1 year

407. Indications for biopsy in case of clinical diagnosis"hepatitis" are:

diagnosis verification

establishing the form and severity of hepatitis

evaluation of treatment outcomes

408. The safest type of biopsy for diffuse liver damage is:

puncture

transvenous

marginal liver resection

pinched at laparoscopy

409. The main histological signs of chronic active hepatitis are:

stepwise necrosis

emperiopolesis

bridging necrosis

410. The main histological sign of persistent hepatitis is:

1- clear boundary of the boundary plate

2- sclerosis of the periportal tracts

3- granulomatous inflammation in the centrilobular zones

4- pericellular fibrosis

411. One of the main histological signs of viral hepatitis is:

1- Councilmen's bodies

2- giant mitochondria

3- granulomatous inflammation

4- pericellular fibrosis

5- sclerosing

412. Histological signs of liver tissue regeneration include:

1- binuclear hepatocytes

2- giant multinucleated hepatocytes, such as simplasts

3- “rosette-like” structures

413. The most common cause of toxic liver dystrophy is:

414. The following stages of toxic liver dystrophy are distinguished:

1- active

2- red dystrophy

3- moderate

4- persistent

415. Signs of the 1st stage of toxic liver dystrophy include:

bright yellow liver

the liver is reduced in size

the liver is dense, sclerotic

diffuse hemorrhages in the liver tissue

416. Histological signs of stage II of toxic liver dystrophy include:

necrosis of hepatocytes in the centrilobular regions

carbohydrate dystrophy

macrofocal sclerosis

mallory bodies

417. Macroscopic sign of the liver in cirrhosis is:

soft-elastic liver

the liver is enlarged

hard liver

nutmeg liver

418. Acute viral hepatitis is characterized by:

extralobular cholestasis

bile lakes

fatty degeneration of hepatocytes

Councilmen's bodies

419. Councilman's bodies are related to hepatitis:

serum

alcoholic

none of the above

420. What changes do hepatocytes undergo during the formation of Kaunsilmen's bodies:

hyalinosis

colliquative necrosis

coagulative necrosis

421. Necrosis spreading between the center of the liver lobules and the branches of the crow's vein are called:

massive

stepped

bridging

422. The inflammatory infiltrates in acute serum hepatitis are dominated by:

neutrophils

macrophages

lymphocytes

423. Inflammatory infiltrates in alcoholic hepatitis necessarily contain:

lymphocytes

neutrophils

macrophages

424. Reddish (light) color of the liver in cirrhosis depends on:

dystrophy

obstruction of blood flow through the inferior vena cava

obstruction of blood flow through the portal vein

425. "Lobular liver" refers to cirrhosis:

1- circulatory

3- infectious

4- exchange.

Theme VI. Diseases of the gastrointestinal tract.

Gastritis is an inflammatory disease of the gastric mucosa. There are acute and chronic gastritis.

Acute gastritis is characterized by:

Macroscopically - thickening of the mucous membrane due to edema, redness, erosion.

FORMS OF ACUTE GASTRITIS:

1. Catarrhal (simple)

2. Fibrinous

3. Purulent

4. Necrotic

Chronic gastritis is a chronic inflammation of the gastric mucosa, accompanied by violations of the clonal renewal of the epithelium.

Morphological forms of chronic gastritis:

surface

atrophic

hypertrophic

combined atrophic-hyperplastic.

Modern international classification of chronic gastritis:

autoimmune (type A)

bacterial (type B)

mixed (type A and B)

chemical-toxic due (type C)

lymphocytic

special forms (Menetrier's disease)

acute ulcer - an ulcer that captures the thickness of the mucous membrane, which does not have sclerotic changes in the bottom and at the edges; is usually secondary.

symptomatic ulcers are observed when:

stressful conditions

endocrine diseases

acute and chronic circulatory disorders

after taking medication

chronic ulcer - an ulcer that penetrates beyond the mucosa into the thickness of the stomach wall, has gross fibrous changes in the bottom and ridge-like raised edges; the proximal edge of the ulcer is undermined.

LAYERS OF CHRONIC GASTRIC ULCER:

1. zone of exudation or necrosis

2. zone of fibrinoid swelling

3. zone of granulation tissue

4. zone of sclerosis.

MAIN COMPLICATIONS OF ULCER:

penetration

perforation

malignancy

pyloric stenosis

bleeding

perigastrid, periduodenitis

diverticulum - protrusion of the wall of the gastrointestinal tract.

Appendicitis - inflammation appendix caecum, giving a characteristic clinical syndrome.

Acute appendicitis is:

1. simple

2. superficial

3. destructive (phlegmanous, phlegmanous-ulcerative, apostematous, gangrenous)

chronic appendicitis develops after acute appendicitis and is characterized by sclerotic and atrophic processes, against which inflammatory and destructive changes may appear.

forms of CHOLECYSTITIS:

1. Catarrhal

2. Purulent (phlegmonous)

3. Diphtheritic

4. Chronic

Crohn's disease - a chronic relapsing disease of the gastrointestinal tract, characterized by nonspecific granulomatosis, necrosis, scarring of the intestinal wall.

Explore macros:

79. Phlegmanous appendicitis.

The appendix is ​​thickened, the serous membrane is dull, with fibrinous overlays, the vessels are plethoric. The enlarged lumen is filled with pus (process epiema),

570. Normal gallbladder.

The wall of the gallbladder is thin, the mucous membrane is velvety.

49. Calculous cholecystitis.

The wall of the gallbladder is thickened, sclerosed, there are many stones in the lumen.

50, 180. Cholecystitis.

The wall of the gallbladder is unevenly thickened, the mucous membrane is swollen, dark red

348. Erosion of the gastric mucosa.

On the gastric mucosa, there are multiple superficial mucosal defects with smooth edges, the bottom is black (hematin hydrochloric pigment).

376. Acute stomach ulcers.

On the gastric mucosa, superficial defects with smooth edges of dark red color from 1.5 to 3 cm in diameter are visible

183. Acute duodenal ulcer with perforation.

386. Chronic stomach ulcer.

On the lesser curvature of the stomach, an ulcerative defect of a steep shape up to 1 cm in diameter is visible, the bottom and edges are dense, roll-like.

108. Chronic ulcers of the stomach and duodenum.

On the mucous membrane of the stomach and duodenum, 3 ulcerative defects are visible. In the stomach, an elongated ulcer with undermined dense edges and a dense bottom. In the 12 duodenum there are 2 rounded ulcers located opposite each other ("kissing ulcers"), in one of them there is a perforated hole

128. Melena (bleeding into the lumen of the gastrointestinal tract).

The mucous membrane of the intestine is black (pigment hematin hydrochloride, methemoglobin, iron sulfide)

149, 184. Saucer-shaped stomach cancer. Scirrhus of the stomach.

178. Cancer of the stomach.

Exo- and endophytic growth.

146. Nonspecific ulcerative colitis.

On the mucous membrane of the large intestine, multiple ulcerative defects

various shapes and sizes.

75. Polypoid cancer.

Myoma of the stomach.

To study micropreparations:

62a. Chronic gastric ulcer..

In the bottom of a chronic ulcer, 4 layers are distinguished:

1) on the surface of the ulcerative defect there is a zone of necrosis with leukocytes, 2) under it is a fibrinous exudate, 3) a zone of granulation tissue is visible below, followed by 4) a zone of deep sclerosis with lymphoid infiltrates and sclerosed vessels.

Indicate in the picture:

1 - I zone - necrosis.

2 - II zone - fibrinoid

3 - III zone - granulation tissue.

4 - IV zone - sclerosis.

90. Acute purulent appendicitis (phlegmanous-ulcerative).

(see preparation 151 at the same time. Normal appendix)

All layers of the process are infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosa, plethoric vessels and hemorrhages

Indicate in the picture:

1 - mucous membrane with ulcerations

2 - submucosa

3 - muscular membrane.

4 - serous membrane

5 - leukocyte infiltration of all layers of the appendix wall.

177. Chronic appendicitis with regeneration of the mucous membrane.

The wall of the process is thickened due to the growth of fibrous connective tissue in all layers. Newly formed low cubic epithelial cells creep onto the ulcerative defect.

140. Cholecystitis.

The wall of the gallbladder is thickened due to the growth of connective tissue. Against the background of sclerosis, there are infiltrates consisting of leukocytes. The mucous membrane is atrophied

74. Solid cancer of the stomach.

The parenchyma and stroma in the tumor are evenly developed. The parenchyma is represented by atypical cells forming cells. The anaplastic epithelium proliferates, in some places it grows beyond the mucosa - infiltrating growth

Tests: choose the correct answers.

426. The causes of acute gastritis are:

1- alcoholism

2- infection

3- ingestion of traumatic substances

427. The following changes are characteristic of atrophic gastritis:

1 - mucous pink, with well-defined folds

2- pale mucous

3- there is a lot of mucus in the stomach

4- focal regeneration of the epithelium

428. The main severe complication of gastric ulcer is:

1- lymphadenitis of regional nodes

2- perforation

3- perigastritis

4- "inflammatory" polyps around the ulcer

429. The most characteristic changes in blood vessels in the bottom of a chronic ulcer are:

1- inflammation and sclerosis of the wall

2- plethora

3- anemia

4- large thin-walled sinusoidal vessels

430. The local factor that is important in the pathogenesis of gastric and duodenal ulcers includes:

1- infectious

2- violation of trophism

3- toxic

4- decrease in the secretion of gastrin and histamine

5- exogenous

431. Layers of the bottom of a chronic stomach ulcer are:

1- exudate

3- granulation tissue

4- sclerosis

432. An autopsy of the deceased revealed a lot of erosions of the stomach from a burn, covered with hematin hydrochloric acid. Erosion formed:

1- before the burn

2- during a burn

433. Coffee-like liquid on the gastric mucosa. When cleared of it, pinpoint hemorrhages and defects the size of a pinhead are visible. Specify the name of the process:

1- petechiae

3- acute ulcers

434. At autopsy, two round ulcers were found in the stomach, located on the lesser curvature, the edges are even, the bottom is thin. Ulcers are:

1- sharp

2- chronic

435. Signs of a chronic ulcer are:

1 - recurrent bleeding

2- dense sclerosed bottom

3- multiplicity of ulcers

4- one, two ulcers

436. The most common localization of stomach cancer is:

2- big curvature

3- lesser curvature

437. Cancer tumor diffusely sprouts all layers of the stomach wall, dense, the stomach cavity is reduced. Cancer refers to:

1- differentiated adenocarcinoma

2- mucous cancer

438. A woman has clinically determined solid ovarian tumors on both sides. It is necessary to investigate the presence of metastases first of all:

1- in the lungs

2- in the stomach

439. Acute gastritis usually manifests itself in the form of:

1- atrophic

2- hypertrophic

3- purulent

4- surface

5- with restructuring of the epithelium

440. Chronic atrophic gastritis is characterized by:

1- ulceration

2- hemorrhages

3- fibrinous inflammation

4- enterolization of the mucous membrane

5- plethora and diffuse infiltration by leukocytes of the own layer of the mucous membrane

441. Exacerbation of gastric ulcer is characterized by:

1- hyalinosis

2- enterolization

3- regeneration

4- lymphoplasmacytic infiltrate

5- necrotic changes

442. A characteristic symptom of Menetrier's disease is:

1- enterolization of the gastric mucosa

2- chlorhydrolenic uremia (gastric tetany)

3- Virchow metastases

4- giant hypertrophic folds of the gastric mucosa

5- nonspecific intestinal granulomatosis

443. Ischemic colitis can be detected:

1- with atherosclerosis

2- with scleroderma

3- in diabetes

4- for rheumatoid arthritis

444. Rectal changes are characteristic:

1- for ulcerative colitis

2- for Crohn's disease

3- for Hirschsprung disease

445. When ulcerative colitis is malignant, the intestinal mucosa is:

1- smooth

2- polypoid (granular)

3- atrophic

446. Malignancy of adenomatous polyps is more often detected:

1- in the basal sections

2- in superficial departments

3- in the middle departments

447. Familial multiple colon polyposis is found more often:

1- from birth

4- at the end of the first year of life

5- after 3 years

448. Characteristic histological signs of Whipple's disease are revealed:

1- in the lungs

2- in the myocardium

3- in the liver

4- in the kidneys

449. The most characteristic histological sign of Whipple's disease:

1- hemorrhage

3- macrophage infiltrate

4- leukocytosis

450. Cancer is suspected in an emaciated patient. An enlarged, indurated lymph node is palpated above the left clavicle. It is necessary to examine first of all:

2- stomach

3- esophagus

451. The appendix is ​​thickened in the distal part, the serous cover is dull, hyperemic, there are feces and purulent exudate in the lumen. Microscopically - diffuse infiltration of the process wall with neutrophils, no ulcers. Appendicitis refers to:

1- to simple

2- to destructive

452. The appendix is ​​thickened in the middle segment, the serous cover is covered with fibrinous films. Histologically, against the background of diffuse infiltration of the entire thickness of the ulcer wall.

Appendicitis refers to:

1- to phlegmonous-ulcerative

2- to gangrenous

3- to simple

453. The appendix is ​​thickened, the serous cut is covered with fibrin, the wall is black throughout, dull. Appendicitis refers to:

1- to catarrhal

2- to gangrenous

3- to phlegmonous

454. Abortive appendicitis is characterized by:

1- inflammation is mild

2- primary changes resolved

3- area of ​​inflammation is extremely small

455. Thickening of mucus in the lumen of a sclerosed appendix is ​​called:

1- cystic fibrosis

2- mucocele

3- melanosis

456. Characteristic features acute appendicitis are:

2- serous exudate in the mucosa and muscle membrane

3- hyperemia

4- sclerosis of the process wall

5- destruction of muscle fibers

457. Characteristic signs of chronic appendicitis are:

1- sclerosis of the walls of blood vessels

2- sclerosis of the process wall

3- purulent bodies

4- lymphoplasmacytic infiltration

5- granulomas

458. Morphological forms of appendicitis are:

1- acute purulent

2- acute superficial

3- acute destructive

4- chronic

5- croupous

459. Complications of appendicitis are:

1- perforation

2- peritonitis

3- liver abscesses

460. Most often cause subhepatic jaundice:

1- Cancer of Vater's nipple

2- pancreatic head cancer

3- liver cancer

461. Cancer of the head of the pancreas causes jaundice:

1- parenchymal

2- hemolytic

3- mechanical

462. Crohn's disease in the destructive phase is characterized by:

1- mucosa in the form of "cobblestone pavement"

2- deep slit-like longitudinal ulceration of the mucosa

3- superficial ulceration

4- granulomas in the intestinal wall

463. The mucosa of the ileum is divided by deep ulcers in the form of cracks and resembles a cobblestone pavement. Name the disease:

3- typhoid fever

464. Nonspecific ulcerative colitis of allergic origin is characterized by:

1- fibrinous inflammation

2- multiple ulcers

3 - polypoid protrusions of excessively regenerating epithelium

4- fibrinous necrosis of individual sections of the intestine.

Theme VII. Introduction to infections. Typhus: abdominal, typhus, recurrent.

Infectious diseases are diseases caused by infectious agents: viruses, bacteria, fungi.

Invasive - called diseases when protozoa and helminths are introduced into the body.

Typhoid fever is an acute and long-term infectious disease caused by salmonella (Salmonella typhi), in the first week of the disease it is characterized by symptoms of general intoxication (fever, chills) associated with bacteremia; wide involvement of the reticuloendothelial system, accompanied by a rash, abdominal pain and severe weakness in the second week of the disease; ulceration in Peyer's patches with bleeding from the small intestine and the development of shock in the third week of the disease.

stages of CHANGES IN GROUP LYMPHATIC FOLLICLES OF THE SMALL INTESTINE IN ABDOMINATE TYPHUS:

1. Cerebral swelling

4. Clean ulcers

5. Regeneration

cellular composition of typhoid granuloma - macrophages, the so-called typhoid and lymphoid cells.

ATYPICAL FORMS OF TYPHUS:

1. Kolotief

2. Laryngotif

3. Pneumotyphoid

4. Cholecystothyphus

THE MOST COMMON AND DANGEROUS COMPLICATIONS OF TYPHUS:

1. Intestinal bleeding

2. Perforation of ulcers with subsequent peritonitis

Epithemic typhus. European typhus (lousy typhus) -

an acute infectious disease caused by rickettsia, characterized by damage to the nervous system and blood vessels. It is manifested by general toxic effects, fever, roseolo-petechial rash and disruption of the activity of internal organs, especially the circulatory system.

Macroscopic characteristics are most often poorly expressed - skin rash in the form of red or brown roseola, petechiae, small-point hemorrhages of the conjunctiva of the eyeball (Chiari symptom). In advanced cases, foci of skin necrosis with areas of gangrene are possible.

Microscopic changes in the capillaries develop - destructive-proliferative-endo-thrombo-vyskulitis.

TYPES OF GRANULOMAS IN TYPHUS:

1. mesenchymal - Davydovsky

microglial - Popova.

Recurrent disease is very rare - this is Brill-Zinser disease. (Repeated sporadic typhus).

Explore macros:

Description of preparations for Pathological Anatomy in Lesson No. 28

ACTIVITY #28diseases of the liver and biliary system.

macropreparation "Massive progressive necrosis liver - stage yellow dystrophy" .

The liver is sharply reduced in size, its capsule is wrinkled, the consistency is flabby, on the section, the liver tissue is of a clayey appearance.

micropreparation № "Massive progressive necrosis liver - stage yellow dystrophy.

In the central sections of the lobules, hepatocytes are in a state of necrosis. Among the necrotic masses, individual PMNs are found. In the peripheral sections of the lobules, hepatocytes are in a state of fatty degeneration: when stained with Sudan III, fatty detritus is visible in the hepatocytes of the peripheral sections of the lobules - drops of fat.

macropreparation "Adipose dystrophy liver ( fatty hepatosis ) »

The liver is enlarged in size, the surface is smooth, the edge is rounded, the consistency is flabby, on the cut it is ocher-yellow.

micropreparation № "Spicy viral hepatitis ».

Hepatocytes in a state of hydropic and balloon dystrophy, which is an expression of focal colliquat necrosis. Some hepatocytes are in a state of apoptosis: reduced in size, with eosinophilic cytoplasm and a pycnotic nucleus, or have the appearance of a hyaline-like body that is pushed into the lumen of the sinusoid (Kownsilman's body). Bile capillaries are dilated, filled with bile. Portal tracts are dilated, infiltrated with lymphohistiocytic elements, accumulations of which are visible inside the lobules in the sinusoids, as well as in areas where groups of hepatocytes are in a state of necrosis. In the peripheral parts of the lobules, binuclear and large hepatocytes (regenerative forms) are often found.

electronogram "Balloon dystrophy hepatocyte at acute viral hepatitis" - demonstration .

micropreparation № "Chronic viral hepatitis AT moderate activity" .

The portal tracts are thickened, sclerosed, abundantly infiltrated with lymphocytes, macrophages (histiocytes), plasma cells with an admixture of PMNs. The infiltrate goes through the border plate into the parenchyma and destroys hepatocytes. Foci of necrotic hepatocytes are surrounded by lymphocytes and macrophages (stepwise necrosis). Foci of infiltration are visible inside the lobules. Outside the areas of necrosis, hepatic cells are in a state of hydropic dystrophy.

electronogram "Hepatocyte destruction by killer lymphocyte in chronic active hepatitis".

At the site of contact of the lymphocyte with the hepatocyte, destruction of its cytoplasmic membrane is visible.

macropreparation "Viral SKD ( postnecrotic ) cirrhosis liver"

The liver is reduced in size, dense, the surface is coarse-nodular: nodes of uneven size, more than 1 cm, separated by wide fields of connective tissue.

micropreparation № "Viral multilobular ( postnecrotic ) cirrhosis liver" - picture . The liver parenchyma is represented by false lobules (regenerate nodes) of various sizes. In each node, fragments of several lobules can be seen (multilobular cirrhosis), hepatic beams are not distinguishable, the central vein is absent or displaced to the periphery. Protein dystrophy and hepatocyte necrosis. There are large hepatocytes, with two or more nuclei. Parenchymal areas are separated by wide fields of connective tissue stained red with picrofuchsin. Contiguous triads, sinusoid-type vessels, proliferating cholangiols, and lymphohistiocytic infiltrates are visible in the connective tissue fields.

macropreparation "Alcoholic small-knot ( portal ) cirrhosis liver"

The liver is enlarged (in the final - reduced) in size, yellow, dense, with a uniform small-hilly (small-nodular) surface; nodes no more than 1 cm in diameter, separated by uniform narrow layers of connective tissue.

micropreparation № "Alcoholic monolobular ( portal ) cirrhosis liver" - picture . The parenchyma is represented by false lobules, uniform in size, built on fragments of one lobule (monolobular cirrhosis). The nodes are separated by narrow strands of connective tissue (septa), hepatocytes with symptoms of fatty degeneration. In the connective tissue septa, lymphohistiocytic infiltration with an admixture of PMN proliferation is visible. bile ducts.

macropreparation "Liver at mechanical jaundice" - demonstration .

Description of preparations for Pathological Anatomy in Lesson No. 26

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

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

micropreparation № 37 "acute catarrhal gastritis" - description .

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

micropreparation № 112 "chronic superficial gastritis" - demo .

micropreparation № 229 "chronic atrophic gastritis" - description .

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

macropreparation "Acute erosions and stomach ulcers" - description .

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

macropreparation "chronic stomach ulcer" - description .

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

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

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

macropreparation "stomach polyp" - description .

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

macropreparation "saucer-shaped stomach cancer" - description .

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

macropreparation "diffuse gastric cancer" - description .

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

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

micropreparation № 79 "cricoid cell carcinoma" - demo .

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

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

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

1. lung tissue

   lobar pneumonia

1. stained with hematoxylin and eosin

   stomach wall

   chronic stomach ulcer

1. stained with hematoxylin and eosin

2. metastasis of mucosal cancer in the LU

   with tumor progression

1. coloring Sudan Sh

1. coloring Congo red

   kidney tissue

   kidney amyloidosis

1. stained with hematoxylin and eosin

   section of LU tissue

   tuberculosis

1. stained with hematoxylin and eosin

2. septic myocarditis

   causes - sepsis

1. stained with hematoxylin and eosin

   cause is damage

1. brain tissue

   local hemosiderosis

1. stained with hematoxylin and eosin

   cut of skin

   causes are polyetiological

1. stained with hematoxylin and eosin

   gastric mucosa

   gastric adenocarcinoma

   causes are polyetiological

1. stained with hematoxylin and eosin

   aortic section

   In the wall of the aorta, in its middle shell, where the vasavasorum 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

1. stained with hematoxylin and eosin

2. myocardial hypertrophy

1. stained with hematoxylin and eosin

   brain tissue

   purulent leptomeningitis

   meningococcal infection

MICROPRODUCTION No. 58. Fibromyoma ()

1. stained with picrofuchsin according to Van Gieson

   fibromyoma

   causes are polyetiological

1. stained with hematoxylin and eosin

   kidney tissue

   ischemic infarction of the kidney

MICRO PREPARATION No. 62.

1. stained with hematoxylin and eosin

   lung tissue

   hemorrhagic pulmonary infarction

   thrombosis, embolism

1. stained with hematoxylin and eosin

   brain tissue

   hemorrhage in the brain

1. coloring Sudan Sh

   lung tissue

   pulmonary fat embolism

MICRO PREPARATION No. 80.

1. Glandular hyperplasia of the endometrium

1. stained with hematoxylin and eosin

   LU in lymphogranulomatosis

   causes are polyetiological

MICRO PREPARATION No. 87.

1. stained with hematoxylin and eosin

   papillary thyroid cancer

   causes are polyetiological

1. stained with hematoxylin and eosin

   section of the ovary

   actinomycosis

1. stained with picrofuchsin according to Van Gieson

2. cardiosclerosis

1. stained with hematoxylin and eosin

   kidney tissue

   causes are polyetiological

1. stained with hematoxylin and eosin

2. acute myocardial infarction

1. Perls reaction

   lung tissue

   brown induration of the lung

1. stained with picrofuchsin according to Van Gieson

   liver tissue

1. stained with hematoxylin and eosin

   slice of liver tissue

   nutmeg liver

1. stained with hematoxylin and eosin

   lung tissue

   focal influenza pneumonia

1. stained with hematoxylin and eosin

   cross section of a vessel

1. stained with hematoxylin and eosin

   lung tissue

   miliary pulmonary tuberculosis

1. stained with hematoxylin and eosin

   thyroid tissue

1. stained with hematoxylin and eosin

   section of tumor tissue (skin)

   skin melanoma

1. stained with hematoxylin and eosin

   lung tissue

   bronchopneumonia

1. stained with hematoxylin and eosin

   lung tissue

   emphysema

1. stained with hematoxylin and eosin

   lung tissue, pleura

   hyalinosis of the pleura

1. stained with hematoxylin and eosin

   lung tissue

   healed tuberculosis affect

1. stained with hematoxylin and eosin

   skin tissue

   skin papilloma

   causes are polyetiological

1. stained with hematoxylin and eosin

   uterine tissue

   hydatidiform mole

   causes are polyetiological

1. coloring Sudan Sh

   cross section of an artery

   artery atherosclerosis

1. stained with hematoxylin and eosin

   fallopian tube cut

   tubal pregnancy

1. stained with hematoxylin and eosin

   breast tissue

   causes are polyetiological

1. stained with hematoxylin and eosin

   liver tissue

   cavernous hemangioma of the liver

   causes are polyetiological

1. stained with hematoxylin and eosin

   section of the small intestine

   causes - salmonellosis

1. stained with hematoxylin and eosin

   uterine tumor tissue

   chorionepithelioma

   causes are polyetiological

MICRO PREPARATION No. 185.

1. stained with hematoxylin and eosin

   subarachnoid hemorrhage

MICRO PREPARATION No. 187.

1. stained with hematoxylin and eosin

   pancreatic tissue

   pancreatic atrophy in diabetes

   causes - SD

1. stained with hematoxylin and eosin

   tracheal tissue

1. stained with hematoxylin and eosin

   transverse section of the appendix

1. stained with hematoxylin and eosin

   kidney tissue

studfiles.net

MICRO PREPARATIONS (to lay down)

MICROPROGRAM No. 2. Croupous pneumonia

stained with hematoxylin and eosin

lung tissue

almost all alveoli are filled with fibrinous exudate, septa are thickened, full-blooded vessels. Pink exudate in the lumen of the alveoli. It contains fibrin threads (homogeneous in the form of a network or grains) and polymorphonuclear leukocytes. A characteristic pathognomonic symptom is the presence of Kohn's bridges (fibrin strands from one alveolus pass into another). The capillaries of the interalveolar septa are empty, differ from the

lobar pneumonia

infectious agents - pneumococci, streptococci, staphylococci

MICROPRODUCTION No. 8. Chronic gastric ulcer

stained with hematoxylin and eosin

stomach wall

ulcerative defect in the wall of the stomach. The bottom of the ulcer is filled with necrotic masses. The defect extends to the mucosa and muscular membrane. Muscle fibers in the bottom of the ulcer are not defined. In the bottom, 4 layers can be distinguished: fibrinous-purulent exudate, fibrinoid necrosis, granulation and scar tissue

chronic stomach ulcer

causes are polyetiological: stress, nutritional factors, bad habits, helicobacter pylori

MICROPREP No. 9. Metastasis of mucosal cancer in the LU

stained with hematoxylin and eosin

on the preparation, the LU pattern is erased due to the growth of atypical cells containing a large number of mucus. Among the tumor cells there are cricoid (the nucleus is pushed to the periphery by the mucous mass)

metastasis of mucosal cancer in the LU

with tumor progression

MICROSLOPE No. 14. Fatty degeneration of the liver (staining Sudan III)

coloring Sudan Sh

liver tissue (peripheral cells)

on the preparation in the cytoplasm of hepatocytes there are accumulations of large drops of fat, painted in yellow-orange color. 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 droplet fatty degeneration of the liver

causes - chronic alcoholism, intoxication, protein starvation, beriberi, anemia, transfusion of incompatible blood

MICROSLOPE No. 15. Kidney amyloidosis (Congo red stain)

coloring Congo red

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 amyloid deposits. 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

stained with hematoxylin and eosin

section of LU tissue

the focus is a homogeneous substance, in a healthy tissue - lymphocytes, at the border - a macrophage productive reaction

caseous necrosis of lymph nodes in tuberculosis

tuberculosis

MICROPRODUCTION No. 18. Septic myocarditis

stained with hematoxylin and eosin

in the myocardium, foci of purulent fusion of tissue, in the center of which bacterial emboli are visible among polymorphonuclear leukocytes

septic myocarditis

causes - sepsis

MICROSLOPE No. 20. Granulation tissue

stained with hematoxylin and eosin

skin section (granulation tissue)

superficial leukocyte-necrotic layer; superficial layer of vascular loops; a layer of vertical vessels; maturing layer (collagen fibers, fewer vessels); a layer of horizontal fibroblasts (black elongated cells); fibrous layer

regeneration through the formation of granulation tissue (outcome - scar formation)

cause is damage

Micropreparation No. 23. Hemosiderin in the focus of hemorrhage (Perls reaction)

Perls reaction (prussian blue)

brain tissue

in the macrophages located in the wall of the cyst, bluish-green granules of the Prussian blue dye are visible, which have settled in the places of accumulation of hemosiderin granules. The formation of Prussian blue is due to the presence of an iron cation in hemosiderin. In the brain tissue, a focus of hemorrhage: in the center under anaerobic conditions, hematoidin (light brown) is formed, on the periphery - hemosiderin (turquoise)

local hemosiderosis

atherosclerosis, cerebral form of hypertension, cerebral aneurysm, stroke, trauma

MICROPRODUCTION No. 25. Squamous cell keratinizing cancer

stained with hematoxylin and eosin

cut of skin

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 various sizes containing 2 or more nucleoli are visible. Figures of pathological mitoses are found. In the center of the tumor cells, formed bulbous structures from keratinized cells are visible - cancer pearls.

squamous cell keratinizing skin cancer

causes are polyetiological

MICROpreparation No. 27. Adenocarcinoma of the stomach

stained with hematoxylin and eosin

gastric mucosa

in all layers of the wall of the stomach, growths of atypical glands are visible. Gland-forming cells of various sizes and shapes with hyperchromic nuclei, with figures of pathological mitoses

gastric adenocarcinoma

causes are polyetiological

MICRO PREPARATION No. 36. Syphilitic mesaortitis

stained with hematoxylin and eosin

aortic section

In 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)

MICROPRODUCTION No. 38. Myocardial hypertrophy

stained with hematoxylin and eosin

muscle cells are thickened, increased in size. The nuclei are large, hyperchromic. There are many blood vessels in the enlarged myocardial stroma

myocardial hypertrophy

MICRO PREPARATION No. 39. Purulent leptomeningitis

stained with hematoxylin and eosin

brain tissue

the pia mater is sharply thickened and diffusely infiltrated with polymorphonuclear leukocytes. Vessels of the shells are dilated, full-blooded. Perivascular and pericellular edema is expressed in the substance of the brain

purulent leptomeningitis

meningococcal infection

stained with picrofuchsin according to Van Gieson

muscle and connective tissue

smooth muscle fibers alternate with bundles of collagen fibers of different thicknesses. Muscle and collagen fibers are arranged randomly (tissue atypism). Muscle fibers are colored yellow-green, connective tissue is pink. The nuclei are black, randomly arranged

fibromyoma

causes are polyetiological

Micropreparation No. 61. Ischemic infarction of the kidney

stained with hematoxylin and eosin

kidney tissue

against the background of unchanged components of the kidney, a triangular focus 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, there are areas of pink color, devoid of organization (necrotic detritus). This is the zone of necrosis. It is separated from unaltered tissue by a demarcation zone 9 in which there are full-blooded vessels and an accumulation of leukocytes)

ischemic infarction of the kidney

thrombosis, embolism, prolonged spasm, renal artery atherosclerosis

stained with hematoxylin and eosin

lung tissue

red necrosis. There are no nuclei in the septal cells and epithelium of the alveoli. Some alveolar septa are torn. The area of ​​necrosis is infiltrated with erythrocytes. Around the necrosis - the plethora of blood vessels, the accumulation of leukocytes, and in the lumen of the alveoli - protein liquid. Many branches of the pulmonary artery are thrombosed.

hemorrhagic pulmonary infarction

thrombosis, embolism

MICROSLOPE No. 71. Hemorrhage in the brain

stained with hematoxylin and eosin

brain tissue

brain tissue is edematous. The focus of hemorrhage is represented by an accumulation of erythrocytes in the brain tissue, located in the form of a lake around anatomically intact vessels (diapedetic hemorrhage). In the area of ​​the focus of hemorrhage, arterioles with thickened walls and signs of plasmorrhagia are visible.

hemorrhage in the brain

atherosclerosis, cerebral aneurysm, trauma, GB

MICROSLOPE No. 75. Fatty embolism of the lung (staining Sudan III)

coloring Sudan Sh

lung tissue

interalveolar septa are practically invisible. The lumen of the vessel is obturated with fatty emboli of bright orange color.

pulmonary fat embolism

fractures of tubular bones, crushing of subcutaneous fat, the use of oil preparations in the form of intravenous injections

Stained with hematoxylin and eosin

slice of uterine tissue (endometrial scraping)

the endometrium is thickened, has many elongated glands with a tortuous course. In some places, the lumen of the glands is enlarged and looks like cysts. The epithelium of the glands proliferates, the stroma of the endometrium is rich in cellular elements.

Glandular hyperplasia of the endometrium

causes - ovarian dysfunction, ovarian cyst

MICROPRODUCTION No. 81. Lymphogranulomatosis

stained with hematoxylin and eosin

in the lymph nodes, conglomerates of the remaining cells (lymphatic), some of the tissues are necrotic (a focus without cell infiltrates), areas of fibrosis (bundles of collagen fibers with fibroblasts). In the LU cells that are not characteristic of it: reticular (cells irregular shape large purple with one nucleus), plasmocytes (oval cells with a rounded nucleus, shifted to the periphery), eosinophils (the nucleus is pushed to the periphery, the cytoplasm is orange). Uncharacteristic cells - Berezovsky-Shtenberg-Reed cells (large, reticulocyte-like, but multinucleated - 2 large nuclei next to each other  owlet eye syndrome)

LU in lymphogranulomatosis

causes are polyetiological

stained with hematoxylin and eosin

section of a thyroid tumor

The tumor consists of cavities of various sizes filled with villi - papillary papillae emanating from the walls of the cavities covered with atypical epithelium. In places, tumor papillae grow into the wall of the cavities and the tumor capsule. Virtually no follicles.

papillary thyroid cancer

causes are polyetiological

MICRO PREPARATION No. 88. Actinomycosis

stained with hematoxylin and eosin

section of the ovary

irregularly shaped drusen of fungi are observed in the ovarian tissue. Around the tissue are infiltrated with polymorphonuclear leukocytes. Around the proliferation of connective tissue - capsule

actinomycosis

radiant fungus (actinomycetes)

MICROSLOPE No. 89. Cardiosclerosis (staining with picrofuchsin according to Van Gieson)

stained with picrofuchsin 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, coronary artery disease

MICRO PREPARATION No. 90. Kidney with myeloid leukemia

stained with hematoxylin and eosin

kidney tissue

the tissue is diffusely infiltrated with tumor cells such as myeloblasts. There are areas of hemorrhage, necrosis. In the lumen of blood vessels - leukemic thrombi

kidney in myeloid leukemia

causes are polyetiological

MICROSTREP No. 94. Myocardial infarction

stained with hematoxylin and eosin

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 striation and cell boundaries; 2) demarcation zone - expansion and plethora of blood vessels, hemorrhages and infiltration by polymorphonuclear leukocytes; 3) a zone of healthy myocardium along the periphery

acute myocardial infarction

spasm coronary arteries, thrombosis, embolism, atherosclerosis of the coronary arteries, functional myocardial overstrain with insufficient blood supply

Micropreparation No. 97. Brown induration of the lung (Pearls reaction)

Perls reaction

lung tissue

interalveolar septa are thickened due to the expansion and overflow of blood vessels. Some of the alveoli are filled with edematous fluid, in others - accumulations of siderophages with hemosiderin - bluish-green staining. Part of the interalveolar septa is thickened and sclerosed. Growth of connective tissue around the bronchi

brown induration of the lung

general and chronic venous plethora, heart defects, vascular atherosclerosis, congestion and hypertension in the ICC

MICROSLOPE No. 100. Cirrhosis of the liver (stained with picrofuchsin according to Van Gieson)

stained with picrofuchsin according to Van Gieson

liver tissue

the liver parenchyma is represented by false lobules of various sizes. Fragments of several pre-existing normal hepatic lobules can be seen in each pseudolobule (multiglobular cirrhosis). 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 the hepatic parenchyma are separated by wide fields of connective tissue stained magenta pink. Contiguous hepatic triads are visible among the connective tissue fields, which are infiltrated by lymphocytes and histiocytes.

multiglobular cirrhosis of the liver

hepatitis, hepatosis of various etiologies

MICROPRODUCTION No. 103. Nutmeg liver

stained with hematoxylin and eosin

slice of liver tissue

in the liver, the veins and sinusoids in the central zone of the lobules are dilated and full-blooded. Also visible are foci of diapedetic hemorrhages in the form of "lakes", discomplexation of the hepatic beams, necrosis and atrophy of hepatocytes. 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 insufficiency, heart defects, hepatic vein thrombosis

MICROpreparation No. 109. Focal influenzal pneumonia

stained with hematoxylin and eosin

lung tissue

airless areas are visible against the background of airy lung tissue. The alveoli are filled with serous-hemorrhagic exudate. In places, accumulations of polymorphonuclear leukocytes forming microabscesses are visible. The epithelium of the bronchi is desquamated and rejected, exudate in the lumen of the bronchi

focal influenza pneumonia

influenza virus, bacterial infection

MICROPRODUCTION No. 110. Mixed thrombus

stained with hematoxylin and eosin

cross section of a vessel

The lumen of the vessel is completely obturated by a thrombus, which consists of platelets, fibrin filaments, 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 sprouted connective tissue, which grows from the side of the intima 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, an increase in blood viscosity, a slowdown in blood flow as a result of cardiovascular insufficiency, a decrease muscle tone veins

MICRO PREPARATION No. 113. Miliary tuberculosis lung

stained with hematoxylin and eosin

lung tissue

numerous tuberculous granulomas are visible in the preparation. In the center of the granulomas there is caseous necrosis, around it are epithelioid, separate multinuclear giant Pirogov-Langhans macrophages, lymphocytes and individual plasmocytes. There are no vessels in the granuloma

miliary pulmonary tuberculosis

Mycobacterium tuberculosis, hematogenous generalization of primary tuberculosis

MICROpreparation No. 117. Colloidal goiter

stained with hematoxylin and eosin

thyroid tissue

thyroid follicles are rounded, dilated. Their wall is thinned, its ruptures and merges of fv among themselves with formation of cysts of various size are visible. The epithelium lining the follicles is flattened. The lumen of the follicles and cysts is filled with a thick mucus-like mass (colloidal). Full-blooded vessels and hemorrhages are visible (brownish contents in the follicles)

mucous (colloid) dystrophy (colloidal goiter)

iodine deficiency, impaired synthesis of thyroid hormone, goitrogenic substances, immunopathology

MICROpreparation No. 126. Skin melanoma

stained with hematoxylin and eosin

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

causes are polyetiological (with tumor progression)

MICROpreparation No. 127. Bronchopneumonia

stained with hematoxylin and eosin

lung tissue

the wall of the bronchus is diffusely infiltrated with polymorphonuclear leukocytes (panbronchitis), in the lumen of the bronchi there is serous-leukocytic exudate with an admixture of desquamated epithelial cells. Perifocally, sharply dilated, air-filled alveoli are seen (perifocal emphysema)

bronchopneumonia

causes are polyetiological: inflammation in the respiratory tract, pneumococci, viruses

MICROPRODUCTION No. 133. Emphysema of the lung

stained with hematoxylin and eosin

lung tissue

in dilated acini - complete smoothing of the walls, the walls of the alveoli become thinner, straighten. The capillaries of the interalveolar septa become empty. Alveoli are enlarged. Black inclusion - tobacco

emphysema

chronic bronchitis, age-related changes in the lung tissue, vicarious in the pathology of another lung

MICRO PREPARATION No. 135. Hyalinosis of the pleura

stained with hematoxylin and eosin

lung tissue, pleura

the visceral pleura is thickened, its fibrous structures are hardly distinguished. 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 vitreous formations. Around the vessels of the pleura - a pronounced proliferation of connective tissue

hyalinosis of the pleura

causes - metabolic disorders in the connective tissue, the formation of hyaline. The result of the progression of fibrinoid swelling, inflammation, necrosis, sclerosis

Micropreparation No. 136. Healed tuberculous affect in the lung

stained with hematoxylin and eosin

lung tissue

in the lung tissue, purple areas are visible, which are 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 (pseudo-bone). On the periphery in the zone of necrosis - the deposition of calcium salts

healed tuberculosis affect

causes - primary tuberculosis

MICROpreparation No. 141. Skin papilloma

stained with hematoxylin and eosin

skin tissue

numerous outgrowths of stratified squamous keratinized 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 stratified squamous epithelium. Tissue atypia is characteristic (an increase in the layers of the epithelium, hyperkeratosis). It is a papillary formation covered with stratified squamous epithelium with underlying stroma and vessels.

skin papilloma

causes are polyetiological

MICROPRODUCTION No. 150. Cystic skid

stained with hematoxylin and eosin

uterine tissue

chorionic villi are cystically changed, their stroma is edematous, the central vessel is absent, the trophoblast has a two-row structure, is atrophic in places

hydatidiform mole

causes are polyetiological

MICROSLOPE No. 153. Atherosclerosis of the artery (staining Sudan III)

coloring Sudan Sh

cross section of an artery

yellow spots, stripes (deposits of lipids) and whitish-gray plaques protruding into the lumen are visible on the intima. Some of the plaques are ulcerated. Around the proliferation of connective tissue

artery atherosclerosis

unbalanced diet, hypodynamia, genetic defect of cholesterol receptors (hypercholesterolemia)

MICROPREPARATION No. 159. Tubal pregnancy

stained with hematoxylin and eosin

fallopian tube cut

a decidual reaction is noted in the CO tube. In the lumen of the tube, chorionic villi are visible, penetrating into the thickness of the muscular membrane

tubal pregnancy

causes - violation of the passage of the fetus through the tube (inflammation, swelling, underdevelopment of the tubes, etc.)

MICRO PREPARATION № 163. Fibroadenoma of the mammary gland

stained with hematoxylin and eosin

breast tissue

ducts are visible in the form of cracks of a bizarre shape. Connective tissue grows into them. The coloring is yellow. Visible pink connective tissue

intracanalicular fibroadenoma

causes are polyetiological

Micropreparation No. 178. Cavernous hemangioma of the liver

stained with hematoxylin and eosin

liver tissue

the tumor is well delimited from the surrounding liver tissue by a pronounced fibrous capsule. The tumor consists of large cavernous thin-walled vascular cavities (cavities) lined with endothelium and filled with liquid or clotted blood.

cavernous hemangioma of the liver

causes are polyetiological

MICRO PREPARATION No. 182. Ulcerative enteritis with salmonellosis

stained with hematoxylin and eosin

section of the small intestine

ulcerative defect in the wall of the small intestine. The bottom of the ulcer is filled with necrotic masses. The mucous and submucosal membranes around the ulcer are infiltrated with polymorphonuclear leukocytes.

ulcerative enteritis with salmonellosis

causes - salmonellosis

Micropreparation No. 183. Chorionepithelioma

stained with hematoxylin and eosin

uterine tumor tissue

The tumor is built from tumor cells of two types: monomorphic light epithelial (Langhans) and giant dividing cells with hyperchromic polymorphic nuclei (syncytiotrophoblasts). There is no stroma in the tumor. Instead of vessels, cavities filled with erythrocytes are visible. Cavity walls lined with tumor cells instead of endothelium

chorionepithelioma

causes are polyetiological

stained with hematoxylin and eosin

brain tissue, subarachnoid space

thickened artery wall, erythrocyte diapedesis, signs of plasmorrhagia

subarachnoid hemorrhage

closed craniocerebral injury, cerebral atherosclerosis

stained with hematoxylin and eosin

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). There is hyalinosis, fibrosis and lymphoid infiltration of microvessels. Sclerosis and lipomatosis, both intralobular and interlobular

pancreatic atrophy in diabetes

causes - SD

Micropreparation No. 196. Croupous tracheitis

stained with hematoxylin and eosin

tracheal tissue

on the surface of the tracheal mucosa there is a fibrinous exudate infiltrated with polymorphonuclear leukocytes. In the underlying tissues, capillaries and venules are sharply expanded and full-blooded.

purulent-nercotic tracheitis with influenza

causes - influenza virus and bacterial infection

Micropreparation No. 198. Phlegmonous-ulcerative appendicitis

stained with hematoxylin and eosin

transverse section of the appendix

the wall of the process is thickened, all its layers are diffusely infiltrated with polymorphonuclear leukocytes. On the serous surface, deposits of fibrinous exudate intensely stained with eosin are noted. Lymph follicles are enlarged.

phlegmonous-ulcerative appendicitis

causes are polyetiological, autoinfection

Micropreparation No. 203. Serous extracapillary glomerulonephritis

stained with hematoxylin and eosin

kidney tissue

there is a sharp plethora of capillaries, the lumen of the Shumlyansky-Bowman capsule is enlarged, filled with serous exudate. As a result of the proliferation of the epithelium of the capsule, podocytes and macrophages, crescent formations (crescents) appear. Capillary loops undergo necrosis, in their lumen there are fibrin thrombi

serous (productive) extracapillary glomerulonephritis

causes - infectious-allergic diseases

MICROpreparation No. 205. Septic verrucous endocarditis

stained with hematoxylin and eosin

massive thrombotic deposits and bacterial colonies appear in the area of ​​necrosis of the valve leaflet. Growing granulation tissue during maturation deforms the valve leaflets. In the interstitial tissue of the myocardium, histiolimphocytic infiltrates and granulomas are found.

septic verrucous endocarditis

causes - rheumatism, sepsis

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Methodological developments

practical classes for students

Diseases of the digestive system and liver

Peptic ulcer of the stomach and duodenum

Examine macroscopic preparations: gastric ulcer, ulcer duodenum, hemorrhagic erosion of the stomach.
Acute stomach ulcers
Describe macroscopic specimen Hemorrhagic erosions of the stomach №88 Hemorrhagic erosion of the stomach	Pay attention to the prevalence 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 hematin hydrochloride.
Describe macroscopic specimen Chronic stomach ulcer	Pay attention to the prevalence of the lesion, determine the shape, type and consistency of the edges of the defects, the condition and surface of their bottom.
Draw and describe microscopic specimen stomach ulcer Helicobacter pylori (1) in the lumen of the glands (coloring according to Romanovsky Giemsa) Overhanging edge of gastric ulcer Undermined edge of gastric ulcer The bottom of a stomach ulcer during an exacerbation	Find the defect in the stomach wall and determine its depth. To characterize the changes in the bottom of the ulcer and the edges of the defect. Describe the changes in the deeper layers of the stomach wall and determine the nature of the course of the ulcerative process.

Appendicitis. Peritonitis.

To study macroscopic preparations: phlegmonous appendicitis, gangrenous appendicitis, process empyema, chronic appendicitis. Describe one of the macroscopic preparations.
Describe macroscopic specimen Phlegmonous appendicitis Gangrenous appendicitis	Pay attention to the size, wall thickness, condition of the serous membrane of the appendix.
Draw and describe a micropreparation №90 Phlegmonous appendicitis	To characterize the state of the mucous membrane of the process and its lumen. Determine the nature and prevalence of exudate, the degree of blood filling of the vessels.
Draw and describe microscopic specimen Obliteration of the appendix	Determine the topography of connective tissue growth, note the presence of adipose tissue islands, atrophy of the layers of the process wall.
Examine the microscopic preparation Fibrinous-purulent peritonitis	To characterize the state of the peritoneal mesothelium, vessels, exudate. Note changes in underlying fiber and muscle tissue.

Hepatitis. Toxic dystrophy of the liver. Cirrhosis of the liver.

1. To study macroscopic preparations: toxic liver dystrophy, cirrhosis of the liver, varicose veins of the esophagus. 2. Describe one of the macroscopic preparations.
Describe macroscopic specimen Toxic dystrophy of the liver	Pay attention to the size, consistency; mark the color on the cut surface; determine the stage of the disease.
Examine the microscopic preparation No. 93a Toxic dystrophy of the liver. (Stained with Sudan III)	Note the violation of the structure of the liver, obesity and necrobiosis of liver cells in the center of the lobule.
Draw and describe microscopic specimen №93 Toxic liver dystrophy	Note the violation of the architectonics of the liver, find foci of necrosis. Describe changes in the stroma of the organ. Determine the stage of the process.
Describe 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 size of the nodes. Pay attention to the size, texture, color of the organ; note the size of the nodes.
Draw and describe microscopic specimen №94 Portal cirrhosis of the liver (stained with picrofuchsin)	To determine the topography of the newly formed connective tissue, the degree of its maturity, to 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.

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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. A callous ulcer is called an ulcer with hard raised edges. An ulcer that involves all layers of the gastric wall can cause it to perforate. An ulcer penetrating into neighboring organs, most often into the pancreas, is called penetrating. After the ulcer heals, scars appear, sometimes deforming the stomach (“hourglass”, stomach in the form of a snail) or causing narrowing (stenosis) of the pylorus. 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 overlays. Acute ulcers can cause perforation of the stomach wall and fatal stomach bleeding.

A chronic ulcer, according to most researchers, is the outcome of an acute one and differs from it by a significant development of fibrous tissue in the bottom and edges. A chronic ulcer is usually round or oval in shape, less often it has irregular outlines. The cardial edge of the ulcer is, as it were, undermined, the pyloric edge is gently sloping. The bottom is covered with dirty gray overlays, in the bottom of the penetrating ulcers, the organ into which the penetration has occurred is visible. 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 ulcerative 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 pyloric region. Duodenal ulcers are usually localized 1-2 cm from the pylorus, equally often on the anterior and posterior walls of the intestine. Rarely observed postbulbar ulcers. Chronic ulcers are usually solitary, but multiple lesions also occur. During gastroscopy, sometimes several small ones are found near a large ulcer, which are not detected radiologically. In patients with gastric ulcers, duodenal ulcers are sometimes simultaneously detected. Multiple ulcers duodenal ulcers are often located on opposite walls of the intestine ("kissing" ulcers). The most rare localization of ulcers in the stomach are the cardia, fundus and greater curvature.



On microscopic examination, four layers are distinguished in the bottom of the ulcer. With inside fibrinous-necrotic overlays, desquamated epithelium, leukocytes, erythrocytes and hydrochloric hematin are visible, staining the bottom of the ulcer in gray or dark brown. Beneath 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. Deeper is the granulation tissue. Often it is not detected, as 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 in the scars, you can see a lot of mast cells with signs of increased secretory activity. The scar tissue grows into the muscle layers, the submucosal layer, its volume significantly exceeds the size of the ulcer itself.

With an exacerbation of peptic ulcer, necrosis of the granulation tissue and collagen fibers usually occurs, an inflammatory reaction in the surrounding tissues, rejection of areas of necrosis and, due to this, an increase in the ulcer. Yu. M. Lazovsky believes that the progressive growth of fibrous tissue in 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 blood vessels are usually observed with the development of inflammatory-necrotic processes in them, areas of fibrinoid necrosis of the walls of the arteries, 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 ganglions, dystrophic changes and irritation phenomena are observed (S. S. Vail, P. V. Sipovsky).



With peptic ulcer, changes occur throughout the mucous membrane of the stomach and duodenum. At the edges of the stomach ulcer, proliferation of the epithelium is observed, which can grow deep into the mucosa and along its surface, taking the form of polyps. The pyloric glands hyperplasia, showing signs of increased mucoid secretion. In a secret, acidic mucopolysaccharides that are not normally present appear. With prolonged existence of an ulcer, atrophic changes in the glands occur, their secretion weakens. In the fundic glands, there are pictures of atrophy, intestinal metaplasia, the so-called pseudopyloric glands of Stern are formed, containing a mucoid secret. In the stroma, one can see diffuse lymphoplasmacytic infiltrates, large lymphoid follicles, growths of smooth muscle fibers. With a duodenal ulcer, the number of parietal cells significantly increases, which are found even in the pyloric region.

Healing of chronic ulcers occurs by scar formation. Before healing begins, edema and inflammatory infiltration of the edges of the ulcer occur. The edges are smoothed out, approaching the bottom, the necrotic masses covering the bottom are rejected. Granulations appear in the bottom and edges, which gradually fill the ulcer crater. The surface epithelium, saturated with RNA, grows on the granulation tissue and lines it. The muscular layer of the mucous membrane, gastric and duodenal glands do not regenerate. In the healing of ulcers, the accumulation of acid mucopolysaccharides is of great importance. An ulcer with mild fibrosis of the bottom and edges takes about 5-7 weeks to heal. Sometimes complete healing occurs after 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 distinguishes five groups of complications of peptic ulcer. 1. Complications of ulcerative-destructive origin: perforation, arrosive bleeding and penetration. Ulcer perforation is one of the most formidable complications. Most often, perforation occurs in the second half of the day. The diameter of the perforation is about 0.5 cm. Histological examination reveals a pattern of exacerbation of peptic ulcer, necrosis and leukocyte infiltration the edges and bottom of the ulcer, the imposition of fibrin on the serous cover.

Arrosive bleedings arise from large vessels of a bottom of an ulcer. M. K. Dal et al. found that vessel erosion may be preceded by limited necrosis of the wall with the formation of an aneurysm and its subsequent rupture. Especially dangerous is bleeding from chronic ulcers, the vessels of which are fixed by scar tissue, which prevents the contraction of the arteries. Ulcers of the lesser curvature of the stomach usually penetrate into the lesser omentum, duodenal ulcers into the pancreas.

When ulcers penetrate into hollow organs, gastric fistulas occur (gastrocolic, gastrointestinal, gastro-gall bladder). Ulcers of the cardiac and subcardiac regions may penetrate 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, stomach phlegmon, hepatocholangitis. 3. Complications of ulcerative cicatricial origin: stenosis of the cardial part of the stomach, pylorus, duodenum, shortening of the lesser curvature, deformity of the stomach in the form of an "hourglass", diverticula of the stomach and duodenum. 4. Malignancy of gastric ulcer, according to AI 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 a malignant ulcer and primary ulcerative cancer. Malignancy of duodenal ulcers is extremely rare.