Prevention of stress erosive-ulcerative lesions of the gastroduodenal zone in patients in critical conditions. Macro preparations Gastric cancer micropreparations description

Date of: 19.07.2019

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B. Chronic insufficiency of preganglionic autonomic nerve fibers.
Long-term mechanisms for compensating metabolic acidosis are realized mainly by the kidneys and to a much lesser extent with the participation of buffers of bone tissue, liver and stomach.
Acid and pepsin of the stomach. Chopping and stirring food
Contrast radiography - the emergence of contrasting broadcasts beyond the contour of the stomach.
MACHINE № 16. Chronic aneurysm of the left ventricle of the heart
Acute gastritis is an acute inflammatory disease of the stomach.

This macro product is the stomach. The masses and sizes 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 region, a significant deepening in the stomach wall of 2x3.5 cm is localized. Its bounding surface of the organ is devoid of characteristic folding. Folds converge to the boundaries of the formation. In the area of \u200b\u200bthe pathological process there are no mucous membranes, submucosal and muscle layers of the stomach wall. The bottom is smooth, made by the serous membrane. The edges are roller-shaped, dense, and have a different configuration: the edge facing the pylorus is gentle (due to peristalsis of the stomach).

Description of pathological changes:

These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; drug habits; bad habits that lead to local disorders: glandular hyperplasia, increased activity of the acid-peptic factor, increased motility, increased number of gastrin-producing cells; and a common violation: the excitation of the subcortical centers and the hypothalamic-pituitary region, increased vagus nerve tone, increased and subsequent depletion of ACTH production and glucocarticoids). By acting on the gastric mucosa, these violations lead to the formation of a mucosal defect - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic influences, turns into a chronic ulcer, which goes through periods of exacerbation and remission. During remission, the bottom of the ulcer can be covered with a thin layer of epithelium, which is layered on the 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 by fibrinoid changes in the walls of blood vessels and impaired trophism of ulcer tissues).

1) favorable: remission, ulcer healing by scarring, followed by epithelization.

2) adverse:

a) bleeding;

b) perforation;

c) penetration;

d) malignancy;

e) inflammation and ulcerative-cicatricial processes.

Conclusion: these morphological changes indicate a destructive process in the wall of the stomach, which leads to the formation of a mucosal, submucosal, and muscle membrane defect - ulcers.

Diagnosis: Chronic gastric ulcer.

Time: 2 hours.

Motivational characteristic of the topic: knowledge of the topic is necessary for further study of diseases of the stomach, stomach cancer in the clinical departments of general and private courses of pathological anatomy, in the practical work of the doctor it is necessary for the clinical and anatomical analysis of sectional observations and the comparison of clinical data with the results of a biopsy study.

The general purpose of the training: to study the etiology, pathogenesis and pathological anatomy of esophagitis, gastric and duodenal ulcer, stomach cancer; be able to distinguish between them, guided by a morphological characteristic.

Specific objectives of the lesson:

1. To be able to define gastritis, explain its classification, characterize the morphology of various forms of gastritis;

2. To be able to define peptic ulcer disease, explain its classification;

3. To be able to characterize the morphology of peptic ulcer of the stomach and duodenum, depending on the stage of the course, be able to name its complications;

4. To be able to name the macroscopic forms and histological types of stomach cancer, explain the features of their growth and metastasis;

5. To be able to name the complications and causes of death in stomach cancer. Necessary initial level of knowledge: the student must remember the anatomical and histological structure of the esophagus, stomach, intestines, physiology of their activity, types and morphology of inflammation and regeneration.

Questions for self-study (initial level of knowledge):

1. Etiology, pathogenesis, morphological characteristics of acute and chronic esophagitis and gastritis;

2. Etiology, pathogenesis, morphological characteristics of peptic ulcer disease, its complications and outcomes;

3. Risk factors for developing stomach cancer. Classification of gastric cancer. Morphological characteristics, features of metastasis.

Terminology

Callous (callus - corn) - callous, dense.

Penetration - (penetratio - penetration) - penetration of an ulcer through the wall of the stomach or duodenum into the adjacent organ (e.g., into the pancreas), fused with it due to the organization of fibrinous deposits during perigastritis (periduodenitis). Perforation (perforatio - perforation) - through perforation of the walls of a hollow organ.

Ulceration (ulcus - ulcer) - ulceration.

1. To study gastritis by the example of macro-preparations “Chronic hypertrophic gastritis”, “Chronic atrophic gastritis” and micropreparations “Chronic superficial gastritis”, “Chronic atrophic gastritis with epithelial remodeling”.

2. To study the morphology of the stages and complications of peptic ulcer of the stomach and duodenum by the example of the macro-preparations “Multiple erosions and acute gastric ulcers”, “Chronic gastric ulcer”, “Gastric cancer ulcer” and micropreparations “Chronic gastric ulcer during exacerbation”.

3. To study precancerous processes in the stomach, macroscopic forms and histological types of cancer of the stomach and esophagus by the example of macropreparations "Polyposis of the stomach", "Squamous cell carcinoma of the esophagus", "Mushroom cancer of the stomach", "Saucerous cancer of the stomach", "Ulcer-cancer of the stomach", "Diffuse cancer of the stomach" and micropreparation "Adenocarcinoma of the stomach."

Equipment classes, characteristics of the studied drugs

1. Chronic superficial gastritis (stained with hematoxylin and eosin) - the mucous membrane of normal thickness, integumentary epithelium with moderately pronounced dystrophic changes. In the own plate of the mucous membrane at the level of the rollers, moderate lymphoplasmacytic infiltration is mixed with a small amount of polymorphic-nuclear leukocytes. Fundal glands are not changed.

2. Chronic atrophic gastritis with reorganization of the epithelium (stained with hematoxylin and eosin) - the mucous membrane of the stomach is thinned, lined in places with integumentary epithelium, in some places with limbic and goblet cells. The main parietal and mucous cells in the fundus glands are displaced by large cells with foamy cytoplasm, characteristic of pyloric glands. The number of glands is small, they are replaced by proliferation of connective tissue. In its own plate of the mucous membrane, lymphohistiocytic infiltration is noted.

3. Chronic gastric ulcer (Van Gieson stain) - in the wall of the stomach, the defect captures the mucous and muscle membranes, while the muscle fibers in the bottom of the ulcer are not detected, their break at the edges of the ulcer is visible. One edge of the ulcer is undermined, the other is gentle. At the bottom of the ulcer, 4 layers are distinguishable: fibrinous-purulent exudate, fibrinoid necrosis, granulation tissue and scar tissue. In the last zone, vessels with thickened sclerosed walls (endovasculitis) and destroyed nerve trunks, which have grown as amputation neuromas, are visible.

4. Squamous cell carcinoma of the esophagus (stained with hematoxylin and eosin) - strands and complexes of atypical squamous cells are visible in the wall of the esophagus. In the center of the complexes, excessive formation of horny matter occurs in the form of layered structures called “cancerous pearls”. Tumor stroma is well defined, represented by coarse fibrous connective tissue infiltrated by lymphocytes.

5. Adenocarcinoma of the stomach (stained with hematoxylin and eosin) - in all layers of the wall of the stomach, growths of bizarre, atypical glands are visible. The cells that form these glands of various sizes and shapes, with hyperchromic nuclei and figures of pathological mitoses

Macro preparations

1. Erosion and acute stomach ulcers. In the mucous membrane of the stomach, numerous small (0.2-0.5 cm) defects of a conical shape are visible, the bottom and edges of which are painted with a dark brown color in hematin hydrochloride. Several deeper round-shaped defects with soft edges are visible.

2. Chronic stomach ulcer. On the lesser curvature, a deep defect in the wall of the stomach is visible, capturing the mucous and muscle membranes, oval-rounded in shape with very dense, calloused, roll-shaped raised edges. The edge facing the esophagus is undermined, the edge facing the pyloric department is gentle, has the appearance of a terrace formed by the mucous membrane, submucous membrane and muscle layer of the stomach. The bottom of the ulcer is represented by a dense whitish tissue.

3. Chronic hypertrophic gastritis. The mucous membrane of the stomach is thickened, swollen, with high hypertrophic folds covered with thick viscous mucus, a few small hemorrhages are visible.

4. Chronic atrophic gastritis. The mucous membrane of the stomach is sharply thinned, actually smooth, with single atrophied folds, numerous small-point hemorrhages, erosion are visible.

5. Polyposis of the stomach. On the mucous membrane of the stomach there are many rounded outgrowths on the leg, grayish in color, with an uneven surface. Histologically, the polyp of the stomach often has an adenomatous structure.

6. Mushroom cancer of the stomach. On the lesser curvature of the stomach, a nodular formation resembling a mushroom is seen on a broad base. It is grayish red in color. Along the periphery of the tumor, the mucous membrane is thinned, its folds are smoothed (signs of atrophic gastritis). An ulceration of the mushroom cancer of the stomach leads to its transition into a saucer-shaped form.

7. Saucerous cancer of the stomach. The tumor has the appearance of a rounded formation on a wide base with raised, roll-shaped edges, which gives the tumor some resemblance to a saucer. The bottom of the ulcer is covered with dirty gray decaying masses.

8. An ulcer is a cancer of the stomach. Occurs with malignancy of chronic gastric ulcer. In the wall of the stomach (usually on the lesser curvature) there is a deep rounded defect. The bottom of the ulcer is a dense grayish tissue. One of the edges of the ulcer is roller-like raised, represented by a gray-pink tissue, which sprouts the surrounding mucous membrane. There are histological differences between saucer-like cancer and ulcer cancer. With ulcerated cancer of the stomach, complications such as bleeding, perforation are frequent; perhaps the development of phlegmon of the stomach.

9. Diffuse cancer of the stomach. The wall of the stomach (especially the mucous membrane and submucosal layer) is sharply thickened throughout, along the whitish section. The mucous membrane is uneven, its folds are of various thicknesses; the serous membrane is thickened, dense, tuberous. The lumen of the stomach is narrowed (the stomach type "pistol holster"). With diffuse cancer, complications are often associated with germination in the surrounding organs (intestinal obstruction, jaundice, ascites, etc.).

Gastritis is an inflammatory disease of the gastric mucosa. With the course, acute and chronic gastritis are distinguished.

Acute gastritis develops as a result of irritation of the gastric mucosa by alimentary, toxic and microbial agents. Morphologically acute gastritis is characterized by a combination of alternative, exudative and proliferative processes.

Depending on the morphological changes in the mucous membrane, the following forms of acute gastritis are distinguished: catarrhal (simple), fibrinous, purulent (phlegmonous), necrotic (corrosive).

Chronic gastritis can develop in connection with relapses of acute gastritis or out of touch with it. Chronic gastritis is characterized by long-standing dystrophic and necrobiotic changes in the epithelium, as a result of which its regeneration and structural rearrangement are disturbed. Changes in the mucous membrane in chronic gastritis go through certain stages (phases), well studied by repeated gastrobiopsies.

The appearance of intestinal-type epithelium in the stomach is called enterolization, or intestinal metaplasia, and the presence of pyloric glands in the body of the stomach, called pseudopiloric, is called pyloric type rearrangement. Both of these processes reflect perverse epithelial regeneration.

Peptic ulcer is a chronic, cyclically ongoing disease, the main clinical and morphological expression of which is a recurrent ulcer of the stomach or duodenum. Depending on the localization of the ulcer and the characteristics of the pathogenesis of the disease, peptic ulcer is distinguished with the localization of the ulcer in the pyloroduodenal zone and in the body of the stomach. Among the pathogenetic factors of peptic ulcer, there are general (disorders of the nervous and hormonal regulation of the stomach and duodenum) and local factors (violations of the acid-septic factor, mucous barrier, motility and morphological changes of the gastroduodenal mucosa). The significance of these factors in the pathogenesis of pyloroduodenal and fundal ulcers is not the same.

The morphological substrate of peptic ulcer is a chronic recurrent ulcer, which initially goes through the stages of erosion and acute ulcer. Erosion is a defect in the mucous membrane of the stomach. An acute ulcer is a defect not only in the mucosa, but also in the other membranes of the wall of the stomach. The presence of necrosis in the bottom of the ulcer and fibrinoid changes in the walls of blood vessels indicates an exacerbation of the pathological process. During remission, the bottom of the ulcer is usually scar tissue, ulcer epithelization is sometimes noted.

The period of exacerbation of the ulcer is dangerous due to complications of a ulcer-destructive nature: perforation, bleeding and penetration of the ulcer. In addition, there are complications of a ulcerative scar type: deformation, stenosis of the inlet and outlet of the stomach and inflammatory nature: gastritis, perigastritis, duodenitis, periduodenitis. Possible malignancy of chronic ulcers.

Precancerous processes in the stomach include chronic gastritis, a chronic ulcer and polyposis of the stomach. Clinical and anatomical classification of gastric cancer takes into account the localization of the tumor, the nature of growth, macroscopic forms, histological types, the presence and nature of metastases, complications. Most often, gastric cancer is localized in the pyloric department (up to 50%) and on the lesser curvature (up to 27%), most rarely - in the fundus section (2%). Depending on the nature of growth, the following clinical and anatomical forms are distinguished:

I. Cancer with predominantly exophytic expansive growth: plaque-like; polypous; fungal (mushroom); ulcerated cancer (primary ulcerative, saucer-like, cancer from a chronic ulcer, or ulcer cancer);

II. Cancer with predominantly endophytic infiltrating growth: infiltrative-ulcerative, diffuse (limited and total);

III. Cancer with exoendophytic, mixed growth.

These types of stomach cancer can also be phases of carcinoma.

The following histological types of gastric cancer are distinguished: adenocarcinoma, solid cancer, undifferentiated cancer (mucous, fibrotic, small cell), squamous cancer. Adenocarcinoma, as a more differentiated form of cancer, is more common in forms with predominantly exophytic expansive growth. Fibrous cancer (skyr), as a variety of undifferentiated, is very common in forms with predominantly endophytic infiltrating growth. The first metastases of gastric cancer are found in regional lymph nodes. For hematogenous metastasis, the liver serves as the main target organ.

9. Toxic dystrophy of the liver.

This macro product is the liver. The shape is saved, weight and size are reduced. The liver is yellow.

These pathological changes could develop as a result of intoxication, allergic or viral liver damage. Fatty (yellow) dystrophy develops in the body, the morphogenetic mechanism of which is decompensation. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic decay of hepatocytes of the central departments. Fat-protein detritus is phagocytosed, while the reticular stroma with dilated vessels (red dystrophy) is exposed. Due to hepatocyte necrosis, the liver shrinks and decreases in size.

1) favorable: transition to a chronic form.

2) adverse:

a) death from hepatic or renal 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 yellow dystrophy.

^ 10. Cancer of the stomach.

This macro product is the stomach. The shape and size of the organ is changed due to the growth of whitish-yellow tissue, which has grown over 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 proliferation, indentations, loosening and drooping areas are visible - ulceration.

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). Guided by the macroscopic picture, we can say that this is a cancer with predominantly endophytic infiltrating growth - an infiltrative ulcerative cancer (this is indicated by ulceration of the tumor). Histologically, this can be either an adenocarcinoma or an undifferentiated cancer. Progression, the tumor sprouts the wall of the stomach and significantly thickens it.

1) favorable:

a) the slow growth of cancer;

b) highly differentiated adenocarcinoma;

c) late metastasis;

2) adverse: death from exhaustion, intoxication, matastases; spread of cancer beyond the stomach and germination in other organs and tissues, secondary necrotic changes and decay of carcinoma; violation of the function 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 ulceration, which may represent secondary necrotic changes and tumor decay.

Diagnosis: Infiltrative ulcerative cancer of the stomach.

^ 11. Erosion and acute stomach ulcers.

This macro product is the stomach. The shape and dimensions of the organ are preserved, the mass is not changed. The organ is whitish. The mucous membrane is strewn with black formations of dense consistency. Among the numerous small ones, the diameter is 1-5 mm. there are also larger diameters of 7 mm., as well as conglomerates of 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 borders of which have pronounced differences from the gastric mucosa, since they are formed by connective tissue.

These morphological changes could develop as a result of exogenous and endogenous effects: malnutrition, bad habits and harmful agents, as well as auto-infections, chronic auto-intoxications, reflux, neuro-endocrine, vascular allergic lesions. Since lesions are localized in the fundus, we can talk about an autoimmune process with damage to parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, 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 forms after hemorrhage and rejection of dead tissue. The black pigment at the bottom of erosion is hydrochloric acid hematin. Reorganization of the epithelium joins these changes. The formation, the border of which is formed by the mucosa and represents the healing of an acute stomach ulcer by scarring and epithelization.

1) favorable:

a) healing of an acute ulcer by scarring or epithelization;

b) inactive chronic gastritis (remission);

c) mild or moderate changes;

d) epithelization of erosion;

2) adverse:

a) the development of chronic peptic ulcer disease;

b) malignancy of epithelial cells;

c) expressed changes;

g) active expressed gastritis.

Conclusion: these morphological changes indicate the long-existing dystrophic and necrobiotic changes in the epithelium of the mucous membrane with a violation of its regeneration and structural rearrangement of the mucosa.

Diagnosis: chronic atrophic gastritis, erosion and acute gastric ulcer.

^ 12. Chronic stomach ulcer.

Description of pathological changes:

1) favorable: remission, ulcer healing by scarring, followed by epithelization.

2) adverse:

a) bleeding;

b) perforation;

c) penetration;

d) malignancy;

e) inflammation and ulcerative-cicatricial processes.

Conclusion: these morphological changes indicate a destructive process in the wall of the stomach, which leads to the formation of a mucosal, submucosal, and muscle membrane defect - ulcers.

Diagnosis: Chronic gastric ulcer.

^ 13. Hyalinosis of the capsule of the spleen. Glazed spleen.

This macro product is a spleen. The masses and sizes of the organ are not increased, the shape is preserved. The color of the capsule is white, it is coarse-tuberous, and the tuberosity is more pronounced in front. The recesses are more or less large. A plot with a diameter of 0.5 cm is noticeable. On the front surface of the organ is yellow. Sites of yellowish tissue are soldered behind and on the side of the capsule.

Descriptions of pathological changes.

These pathological changes could develop as a result of the destruction of fibrous structures and an increase in tissue-vascular permeability (plasmorrhagia) in connection with angioneurotic metabolic and immuno-pathological processes. Plasmorrhagia - impregnation of tissue with plasma proteins, their absorption on fibrous structures, precipitation and the formation of hyaline. Hyalinosis can develop in the outcome of plasma soaking, fibronoid swelling, inflammation, necrosis, sclerosis. In the spleen capsule, hyalinosis develops as an outcome of sclerosis. Connective tissue swells, loses fibrillarity, its bundles merge into a homogeneous, dense, cartilaginous mass, cells are compressed, and atrophy. The fabric becomes dense, whitish, translucent. Along with connective tissue hyalinosis in the spleen, local hyalinosis of arterioles may be present as a physiological phenomenon. In this case, simple hyaline is formed (due to sweating of unchanged or unchanged components of blood plasma).

1) favorable:

a) was possible only as a stage of the process during its stabilization and resorption of hyaline masses;

b) unfavorable - the most frequent: violation of the function of the body, limitation of its functional capabilities.

Conclusion: data of morphological changes indicate dystrophic processes in the capsule of the spleen, which led to its hyalinosis.

Diagnosis: Hyalinosis of the spleen capsule.

^ 14. Dysenteric colitis.

This macro product is the colon. The shape of the organ is preserved, the mass and dimensions are increased due to thickening of the wall. The mucous is dirty gray in color, on the top of the folds and between them, film overlays of brown-green color covering the mucous mass are necrotic, ulcerated, in many places freely hang in the intestinal lumen (which is narrowed).

Description of pathological changes:

These pathological changes could develop as a result of acute intestinal disease with a predominant lesion of the colon, the cause of which was the penetration, development and reproduction in the epithelium of the mucous membrane of Shigella bacteria and their species. This group of bacteria has a cytoplasmic effect on these cells, which is accompanied by destruction and desquamation of the latter, the development of desquamative catarrh. The bacterium enterotoxin exerts a vasoneuroparalytic effect, with which blood vessel paralysis is associated\u003e increased exudation and 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 and hemorrhage, then in the second stage a fibrinoid film appears on top and between the folds. Necrotic masses of the mucosa are penetrated by fibrin. Dystrophic and necrotic changes in the nerve plexuses are combined with leukocyte infiltration of the mucosa and submucosa, its edema, and hemorrhages. With the further development of the disease in connection with the rejection of fibrin films and necrotic masses, ulcers form, which are filled with granulation tissue at 3-4 weeks of the disease, which matures and leads to the regeneration of ulcers.

1) favorable:

a) complete regeneration with minor defects;

b) abortive form;

2) adverse:

a) incomplete regeneration with scarring\u003e narrowing of the intestinal lumen;

b) chronic dysentery;

c) lymphadenitis;

d) follicular, polycular-ulcerative colitis;

e) severe general changes (necrosis of the renal tubule, fatty degeneration of the heart and liver, impaired mineral metabolism). Complications:

a) ulcer perforation: peritonitis; paraproctitis;

b) phlegmon;

c) intestinal bleeding.

Extraintestinal complications - bronchopneumonia, pilonephritis, serous arthritis, liver abscesses, ameloidosis, intoxication, exhaustion.

Conclusion: these morphological changes indicate diphtheria colitis of the colon associated with the toxic effects of shigella.

Diagnosis: Dysentery and colitis. Stage diphtheria colitis.

^ 15. Typhoid fever.

This macro product is the ileum. The shape of the organ is preserved, the weight and size are normal. The intestine is whitish in color, the folding of the mucous membrane is expressed, on which the formation 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 off-gray. A noticeable formation is 0.5 cm in diameter, with a loss of characteristic folding, whitish, slightly deepened and densified.

Description of pathological changes:

These pathological changes could develop as a result of infection of the (parenteral) typhoid bacillus and their reproduction in the lower part of the small intestine (with the release of endotoxin). According to the lymphatic paths -\u003e to Peyer's patches -\u003e salitary follicles -\u003e regional lymph nodes -\u003e blood -\u003e 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 go beyond the boundaries of 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 are necrotic and surrounded by a zone of demarcation inflammation, sequestration and rejection of necrotic masses leads to the formation of “dirty ulcers” (as a result of soaking with bile), which change their appearance over time: they are cleaned of necrotic masses and 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. adverse:

Death due to intestinal (bleeding, perforation of ulcers, peritonitis) and extraintestinal complications (pneumonia, osteomyelitis, intramuscular abscesses, sepsis, waxy necrosis of the rectus abdominis muscles);

dystrophic changes in parenchymal organs, the formation of typhoid granulomas in them.

Conclusion: these morphological changes indicate an acute infectious disease with local changes in the small intestine - ileolitis.

Diagnosis: Ileolitis.

^ 16. Gangrene of the small intestine.

This macro product is a section of the small intestine. Its dimensions, weight are not changed. The intestinal loops are enlarged, the consistency of one part is loose, the second is not changed. The surface is smooth. The serous membrane is dull and dull. Between the loops there is a sticky, viscous, stretching fluid in the form of threads. In the section of the intestine, the walls are enlarged, the lumen is narrowed.

Possible causes: impaired blood supply as a result of strong-mesenteric necrohodemonia of the mesenteric arteries.

Morphogenesis: ischemia, dystrophy, atrophy, necrosis of an organ in contact with the external environment - gangrene.

1) unfavorable - putrefactive fusion, distill.

Conclusion: indirect vascular necrosis.

Diagnosis: Wet gangrene of the small intestine.

Name the organ, tissue, establish the nature of the pathological process, date the morphology of the known knowledge, set the diagnosis, enter the nature of the possible acceleration with this pathology.
List of examinations of micropreparations
1. granular dystrophy nirok
2. fat and oil stoves (Sudan-Z)
3. Anthrosis
4. caseous necrosis
5. calcenosis of the heart valve
6. printed legend
7. Muscatna stove
8. hemorrhagic infarction
9. fibrinous pericarditis
10. abscesses
11. milennial tuberculosis legen
12. layering hypoplasia endometrium
13. atrophy shkіri
14. squamous cancer of the orogovinnam
15. Intracanalіkulyurna fibroademona
16. fibroma
17. gigantskoklіtna sarcoma
18. nirka with leukemia
19. lymphogranulomatosis
20. mіloma
21. adenocarcinoma
22. postinfarction cardiosclerosis
23. warty endocarditis
24. large pneumonia
25. hypostatic pneumonia
26. chronic virazka slunku
27. phlegmonous appendicitis
28. cirrhosis of the liver
29. gostra nirkova lack
30. amiloidoz nirki
31. abortion
32. goiter
33. tuberculosis hump.

1. Examination macrodrugs
1. blood in the brain
2. Aortic atherosclerosis
3. nyrka is wrinkled a second time
4. Ishem_ninfarkt nirki
5. cancer metastasis
6. fibrinous pericarditis ("volokhate heart")
7. spherical thrombus of the left atrium
8. guma sertsya (syphilitic)
9. toxic dystrophy of the liver
10. cancer slap
11. Erosii i gostrі virazki slunku
12. Chronic Slice Slunk
13. Hyalinosis capsules of the spleen
14. dysentery colitis
15. Typhoid
16. bowel gangrene
17. Hypertrophy myocardium
18. abscesses stoves
19. Ischemic Infarction of the Spleen
20. mі traralny stenosis of heart
21. cirrhosis of the liver
22. amyloidolipid necrosis
23. metastases of cancer in selezіntsі
24. muscatna stove
25. chronic abscess leg
26. borax atrophy myocardium
27. pristіnkovy thrombosis arteriy
28. uterine fibroids
29. puzirchaty zanis
30. fibrous cavernous tuberculosis leg
The scheme will describe the macrodrug
1. a body
2. Significance of the first look: the color, the rosemary, the view of the surface, the most empty - what won’t take revenge.
3. Identify the nature of the pathological process: localization, familiarity with the signs, practical characteristics, clinical and anatomical characteristics, possible improvement in case of pathology, and diagnosis.
Electronogram Description
Become familiar with the nature of the pathological process when caught up, and find the most characteristic ultrastructural signs of the pathological process.

1.Blood hemorrhage in the brain.
This macro product 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. On the section, small inclusions of brown color with a diameter of 1 mm are visible. Light brown elongated sections (5x7 and 4x11 mm.) Are located in the crust above the section. At the bottom of the sections there is a large spot with a diameter of 7 cm. With unevenly distributed color. Sites of dark brown color with blurry borders alternate with lighter ones. The zone is well delimited from surrounding tissue.
These pathological changes could develop with:
1) break;
2) erosion of the vessel wall, which led to massive bleeding and hemorrhagic impregnation of brain tissue (heterogeneous hemorrhage -\u003e partially retained cellular elements).
Small brown inclusions are pinpoint hemorrhages from veins that occurred during an incision.
Light brown areas are the result of an increase in the permeability of the vessel wall, which developed as a result of angioneurotic disorders, changes in microcirculation, tissue hypoxia. Rupture or corrosion of a vessel could occur as a result of atherosclerosis, necrosis, inflammation, sclerosis, and a malignant tumor.
Exodus:
1) favorable: resorption of blood; cyst formation at the site of hemorrhage, encapsulation or organization.
2) adverse: death as a result of the defeat of 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 brain tissue.
Diagnosis: Hemorrhagic stroke.
2. Atherosclerosis of the aorta.
This macrodrug is an aorta. The shape of the organ is saved. The inner surface of the wall is dark brown, tuberous, intima uneven, whitish, its entire surface consists of tubercles and depressions. On the tubercles, orange patches with white borders are noticeable. Yellow spots with a diameter of 5 mm are visible. On the aortic intima, plaques ulcerate, which leads to delamination of the aortic wall.
Description of pathological changes.
These pathological changes could occur as a result of impaired fat and protein metabolism. Unregulated cell metabolism leads to the appearance of foam cells in the intima of the arteries, which are associated with the formation of atherosclerotic plaques (yellow spots). Such factors also play a role:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- ethnic.
The whitish tubercles are fibrous plaques resulting from the germination of connective tissue in the thickness of the detritus. Orange spots with a white border represent intramural hematomas, due to destruction of the plaque tire or ulceration of it with atheromatosis. White border - plot calcenosis; plaques indicate that atherosclerosis is progressive and a new wave of lipoidosis was layered on the old changes, exfoliation of a part of the endothelial lining of the aorta (the section hanging inside the vessel) indicates stratifying aneurysm.
Exodus:
1) favorable: regression of atherosclerosis with leaching of lipids from plaques by macrophage resorption and dissolution of connective tissue;
2) adverse:
a) thrombosis;
b) thromboembolism;
c) embolism with atheromatous masses or pieces of intima;
-\u003e heart attack and gangrene
d) rupture of the aortic aneurysm ~ "death from acute anemia.
Conclusion: these morphological changes in the aortic wall indicate dystrophic changes in the aortic intima with subsequent wall growth and complications that underlie aortic atherosclerosis.
Diagnosis: Progressive atherosclerosis of the aorta. Exfoliating aneurysm.
3. Secondarily shriveled kidney.
This macro product is the kidneys. The shape of the organs is preserved, the mass and size are reduced. The left kidney is larger than the right. The organs are light gray, the surface is fine-humped. There are no foci of hemorrhage
Description of pathological changes
These pathological changes could develop primarily in connection with sclerosis of the renal vessels - with hypertension, and secondly due to inflammatory and dystrophic changes in the glomeruli, tubules, and stroma. The disease proceeds in 2 stages: nosological and syndromic. Given the small tuberous surface of the kidneys (which happens with hypertension and glomerulonephritis). as well as the absence of foci of hemorrhage or heart attack (in the kidneys - white with a hemorrhagic nimbus - and-white), chronic glomerulonephritis can be considered the cause of this disease. which in stage I leads to glomerulosclerosis, and in stage II - a block of blood flow at the glomerulus level leads to ischemia of the kidney substance -\u003e progression of parenchyma atrophy and kidney sclerosis - "wrinkling of the kidneys (chronic renal failure) Outcome
1) chronic suburemia develops favorable with the use of regular hemodialysis,
2) adverse death as a result of chronic renal failure and its consequences
Conclusion. These morphological changes indicate structural rearrangement of the renal tissue and the replacement of its connective tissue parenchyma.
Diagnosis Secondary shriveled kidney Chronic glomerulonephritis.
4. Heart attack of the kidney.
This macro product is a kidney. The shape of the organ is preserved, the mass and size are not increased. The cortex and medulla are visible in the section. Significant deposits of adipose tissue in the cups and pelvis of the kidney. In the cortical substance, multiple areas of whitish color 1x0.5 cm are visible. The granules of some of them are dark brown. The organ is light brown in color.
These pathological changes could develop as a result of prolonged vasospasm of the organ functional tension in conditions of insufficient blood supply, atherosclerosis, thromboembolism, or renal artery thrombosis. Ischemia of the substance of the kidneys leads to necrosis (ischemia\u003e hypoxia\u003e metabolic disturbance\u003e dystrophy\u003e necrosis), the morphogenetic mechanism of which is decomposition, and the biochemical mechanism is protein denaturation\u003e coagulation necrosis as a result of ischemia\u003e 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 is diapedetic hemorrhage (granules of white areas of brown color).
Outcome: 1) favorable:
a) autolysis and regeneration of necrosis;
b) the organization and formation of the scar; 2) adverse:
a) death as a result of acute renal failure during a heart attack;
b) death as a result of chronic renal failure during 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 cortical substance of the kidneys due to circulatory disorders.
Diagnosis: kidney infarction.
5. Metastasis of cancer in the lungs.
This macro product is the lungs. The shape of the organ is saved. The lung is brown in section with multiple dark point inclusions, inside a whitish color, roundish, diameter 3-5 mm. The lung is heterogeneous: light bronchial 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 genome of the epithelial cell, which could be facilitated by factors such as inhalation of carcinogens (cigarette smoke), especially since there are a lot of small inclusions of dark gray in the lung, which can represent soot, dust and are especially pronounced smokers and miners. In addition to smoking, the prerequisites for a change in the genome of the cell could create chronic inflammatory processes, pulmonary infarction, since hyperplasia, dysplasia and epithelial metaplasia develop on their soil. Conditions for these changes often arise in the scar.
Multiple round spots represent an accumulation of tumor cells, probably peripheral cancer, as evidenced by the diffuse location of the spots. Point inclusions in cancer clusters represent areas of hemorrhage.
Exodus:
1) favorable.
In the initial stage of lung cancer, it was still possible in the case of elimination of cancer cells due to a strong immune response or would cause a slow tumor growth; 2) unfavorable - death.
a) hematogenous and lymphogenous metastases (in 70% of cases).
b) complications associated with tumor necrosis, cavity formation, bleeding, suppuration.
c) cachexia.
Conclusion: these morphological changes indicate a change in the genome of epithelial cells and cancer progression with the growth of altered cells in the lung tissue.
Diagnosis: lung cancer. Tumor progression.
6. Fibrinous pericarditis.
This macro product is a heart enclosed in a pericardial sac.
The shape of the organ is preserved, the size is slightly enlarged. The epicardium is dull gray, grungy, covered with light brown fibrin. There are no foci of hemorrhage and necrosis. Fibrin is more pronounced on the anterior wall of the right ventricle
Descriptions of pathological changes.
These pathological changes can develop with rheumatic diseases with heart damage. In the leaves of the heart shirt, disorganization of the connective tissue, vascular lesions and immunopathological processes develop. The increased vascular permeability in the exudation stage leads to the “sweating” of fibrinogen beyond 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 developed in the pericardial leaves with rheumatism.
Diagnosis: Fibrinous pericarditis (hairy heart).
7. Spherical thrombus of the left atrium.
This macro product is the heart. The shape of the organ is preserved, the mass and size are increased due to the thickened wall of the left ventricle (the 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 and necrosis. The consistency is tightened, 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, with a diameter of 5 cm. A dense consistency that occupies the entire cavity of the left atrium. Valves of the mitral valve are enlarged and thickened, they are fused. On valve endothelium thrombotic overlays.
Description of pathological changes.
These pathological changes develop as a result of:
a) endocarditis of the mitral valve;
b) slowdowns and disturbances in blood flow;
c) violation of the relationship of coagulation, anticoagulation and fibrinolytic systems;
g) a change in rheological properties in the blood.
As a result of inflammation of the valve, desotation of the endothelium occurred, which led to pre-parietal thrombus formation and also to thickening and sclerosis of the mitral valve and their fusion. In this preparation, valve stenosis is combined with its insufficiency, with the latter prevailing. This is due to the fact that during ventricular systole, blood is ejected not only into the aorta, but also, as a result of insufficiency of the mitral valve, into the left atrium. Therefore, 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 - stagnation of blood in the left atrium - the formation of a stagnant mixed thrombus - its separation and grinding in the cavity of the left atrium.
Exodus:
1) relatively favorable: organization with subsequent sewage and vascularization. Connective tissue grows into a blood clot from the endocardium.
2) adverse: death. A blood clot of such a size that 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 impaired blood circulation and the formation of a parietal thrombus and its subsequent separation.
Diagnosis: Mitral combined heart disease. Mitral stenosis with mitral valve insufficiency. Globular thrombus.
8. Gumma of the heart *
This macro product is the heart. The shape of the organ is preserved, weight and size are increased due to the thickened wall of the left ventricle (up to 3 cm). chords thickened, papillary muscles enlarged. Endocardium is yellowish, subepicardial fat is moderately developed. The aortic valve is intact. In the wall of the left ventricle there is a recess of 5x4x3 cm., On the inner surface of which there are spots of yellow, orange and dark gray, as well as gnotted and whitish areas. At the lower edge of the recess, overlapping 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 occurs in three periods - primary, secondary, tertiary (or gummous), which is presented on the drug. The first period occurs against the background of increasing sensitization and manifests itself as a solid chancre on the mucous membrane at the site of the introduction of treponema and involvement of the lymphatic system. The second period is the period of hyperergy and generalization, characterized by the appearance of syphilis and an increase or swelling of the lymphatic follicles. In these places there is inflammation. After 3-6 years, a third period begins in the form of chronic diffuse interstitial inflammation and the formation of gum, which represent a focus of syphilitic productive necrotic inflammation, syphilitic granuloma. In this case, visceral syphilis led to heart damage in the form of gummy myocarditis. The inflammatory process rises deep into the myocardium, necrotic masses are washed out by the blood stream, the zone is limited by demarcation inflammation. There are accumulations of lymphoid, plasma giant Pirogov-Langhans cells, fibroblasts. Specific inflammation leads to scarring and ends with the development of massive cardiosclerosis. Atherosclerosis is superimposed on the area of \u200b\u200bspecific changes, with which yellow, white, orange spots, as well as joined thrombotic overlays are associated.
Outcome: 1) favorable.
a) was possible in the treatment and elimination of the pathogen to serious changes in the organs;
b) the long course of the process with its compensation;
2) unfavorable: cardiosclerosis\u003e development of chronic heart failure, first hypertrophy: tonogenic, and then myogenic, left ventricular delegation\u003e stagnation of blood in the left ventricle\u003e in the left atrium\u003e in the lung.
Death is the result of a pulmonary heart. Conclusion: These morphological changes indicate a specific inflammation of the myocardium with the formation of heart gum.
Diagnosis: visceral syphilis. Gumma of the heart.
9. Toxic dystrophy of the liver.
This macro product is the liver. The shape is saved, weight and size are reduced. The liver is yellow.
Description of "pathological changes.
These pathological changes could develop as a result of intoxication,
allergic or viral liver damage. Fatty (yellow) develops in the organ
dystrophy. Dystrophy spreads from the center to the periphery of the lobules. It is replaced by necrosis and autolytic
decay of hepatocytes of the central departments. Fat-protein detritus is phagocytosed, while
the reticular stroma with dilated vessels (red dystrophy) is exposed. Due to hepatocyte necrosis, the liver shrinks and decreases in size.
Exodus:
1) favorable: transition to a chronic form.
2) unfavorable: "a) death from hepatic or renal 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 yellow dystrophy.
10. Cancer of the stomach.
This macro product is the stomach. The shape and size of the organ is changed due to the growth of whitish-yellow tissue, which has grown over 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 proliferation, indentations, loosening and drooping areas are visible - ulceration.
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 the cells and the development of tumors (or the cancer develops (de novo). Based on the macroscopic picture, we can say that this is a cancer with predominantly endophytic infiltrating growth - infiltrative-ulcerative cancer (this is indicated by ulceration of the tumor). Histologically, this may be both an adenocarcinoma and undifferentiated cancer.Progression, a tumor grows on the wall of the stomach and significantly thickens it.
Outcome: 1) favorable:
a) the slow growth of cancer;
b) highly differentiated adenocarcinoma;
c) late metastasis;
2) adverse: death from exhaustion, intoxication, matastases; spread of cancer beyond the stomach and germination in other organs and tissues, secondary necrotic changes and decay of carcinoma; violation of the function 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 ulceration, which may represent secondary necrotic changes and tumor decay.
Diagnosis: Infiltrative ulcerative cancer of the stomach.
11. Erosion and acute stomach ulcers.
This macro product is the stomach. The shape and dimensions of the organ are preserved, the mass is not changed. The organ is whitish in color. The mucous membrane is strewn with black in formations of dense consistency. Among the numerous small ones, the diameter is 1-5 mm. there are also larger diameters of 7 mm., as well as conglomerates of 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 borders of which have pronounced differences from the gastric mucosa, since they are formed by connective tissue.
Descriptions of pathological changes.
These morphological changes could develop as a result of exogenous and endogenous effects: disruption, nutrition, bad habits and harmful agents, as well as auto-infections, chronic auto-intoxications, reflux, neuro-endocrine, vascular allergic lesions. Since lesions are localized in the fundus, we can talk about an autoimmune process with damage to parietal cells, which led to dystrophic and necrobiotic changes in the epithelium, 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 forms after hemorrhage and rejection of dead tissue. The black pigment at the bottom of erosion is hydrochloric acid hematin. Reorganization of the epithelium joins these changes. The formation, the border of which is formed by the mucosa and represents the healing of an acute stomach ulcer by scarring and epithelization.
Outcome: 1) favorable:
a) healing of an acute ulcer by scarring or epithelization;
b) inactive chronic gastritis (remission);
c) mild or moderate changes;
d) epithelization of erosion; 2) adverse:
a) the development of chronic peptic ulcer disease;
b) malignancy of epithelial cells;
c) expressed changes;
g) active expressed gastritis.
Conclusion: these morphological changes indicate the long-existing dystrophic and necrobiotic changes in the epithelium of the mucous membrane with a violation of its regeneration and structural rearrangement of the mucosa.
Diagnosis: chronic atrophic gastritis, erosion and acute gastric ulcer
12. Chronic stomach ulcer.
This macro product is the stomach. The masses and sizes 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, a significant indentation in the stomach wall of 2 x 3.5 cm is localized in the pyloric section. Its limiting surface of the organ is devoid of characteristic folding. Folds converge to the boundaries of the formation. In the area of \u200b\u200bthe pathological process there are no mucous, submucosal, and muscle layers of the stomach wall. The bottom is smooth, made by the serous membrane. The edges are roller-shaped, dense, and have a different configuration: the edge facing the pylorus is gentle (due to peristalsis of the stomach).
Description of pathological changes.
These pathological changes could develop as a result of general and local factors (general: stressful situations, hormonal disorders; drug habits; bad habits that lead to local disorders: glandular hyperplasia, increased acid-peptic factor activity, increased history, increased number of gastrin-producing cells; and a common violation: excitation of the subcortical centers and the hypothalamic-pituitary region, increased vagus nerve tone, increased and subsequent depletion of ACTH production glkzhokartikoidov.) By acting on the gastric mucosa, these disorders lead to the formation of a mucosal defect - erosion. Against the background of non-healing erosion, an acute peptic ulcer develops, which, with continued pathogenic influences, becomes a chronic ulcer, which goes through periods of exacerbation and remission. may be covered with a thin layer of epithelium, which is layered on the scar tissue, but during the period of exacerbation, the “healing” is leveled as a result of fibrinoid necrosis (which leads to damage elimination not only directly, but also by fibrinoid changes in the walls of blood vessels and impaired trophism of ulcer tissues).
Exodus:
1) favorable: remission, ulcer healing by scarring, followed by epithelization.
2) adverse:
a) bleeding;
b) perforation;
c) penetration;
d) malignancy;
e) inflammation and ulcerative-cicatricial processes.
Conclusion: these morphological changes indicate a destructive process in the wall of the stomach, which leads to the formation of a mucosal, submucosal, and muscle membrane defect - ulcers.
Diagnosis: Chronic gastric ulcer.
14 dysenteric colitis
This macro product is the colon. The shape of the organ is preserved, the mass and dimensions are increased due to thickening of the wall. The mucous is dirty gray in color, on top of the folds and between them, film overlays of brown-green color covering the mucous mass are necrotic, ulcerated, in many places freely hang in the intestinal lumen (which is narrowed).
These pathological changes could develop as a result of acute intestinal disease with a predominant lesion of the colon, the cause of which was the penetration, development and reproduction in the epithelium of the mucous membrane of Shigella bacteria and their species. 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. The enterotoxin of bacteria carries out a vasoneuroparalytic effect, with which blood vessel paralysis is associated, 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 of a hemorrhage, then in the second stage a fibrinoid film appears on top and between the folds. Necrotic masses of the mucosa are penetrated by fibrin. Dystrophic and necrotic changes in the nerve plexuses are combined with leukocyte infiltration of the mucosa and submucosa, its edema, and hemorrhages. With the further development of the disease in connection with the rejection of fibrin films and necrotic masses, ulcers form, which are filled with granulation tissue for 3-4 weeks of the disease, which matures and leads to the regeneration of ulcers.
Exodus
1. favorable
a) complete regeneration with minor defects b) abortive form
2. adverse
a) incomplete regeneration with scar formation 1 ^ narrowing of the intestinal lumen
B) chronic dysentery
c) lymphadenitis
oh!) follicular, follicular and ulcerative colitis
f) severe general changes (necrosis of the epithelial tubules of the kidneys, fatty degeneration of the heart and liver, impaired 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 associated with the toxic effects of shigella
Diagnosis of dysentery and colitis. Stage diphtheria colitis.
15. Typhoid fever.
This macro product is the ileum. The shape of the organ is preserved, the weight and size are normal. The intestine is whitish in color, the folding of the mucous membrane is pronounced, on which the formation 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 off-gray. A noticeable formation is 0.5 cm in diameter, with a loss of characteristic folding, whitish, slightly deepened and densified.
Description of pathological changes.
These pathological changes could develop as a result of infection of the (parenteral) typhoid bacillus and their reproduction in the lower part of the small intestine (with the release of endotoxin). According to the lymphatic paths -\u003e to Peyer's patches -\u003e salitory follicles - "regional lymph nodes -\u003e 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 go beyond the boundaries of the follicles into the underlying layers. Monocytes turn into macrophages (typhoid cells) and form clusters of typhoid granulomas. Catarrhal enteritis joins these changes. With further progression of the process, typhoid granulomas are necrotic and surrounded by a zone of demarcation inflammation, sequestration and rejection of necrotic masses leads to the formation of “dirty ulcers” (as a result of soaking with bile), which change their appearance over time: they are cleaned of necrotic masses and 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. adverse:
- death due to 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 macro product is a section of the small intestine. Its dimensions, weight are not changed. Kishka loops are enlarged, the consistency of one part is loose, the second is not changed. The surface is smooth. The serous membrane is dull and dull. Between the loops there is a sticky, viscous, stretching fluid in the form of threads. In the section of the intestine, the walls are enlarged, the lumen is narrowed.
Possible causes: impaired blood supply as a result of strongomethia netphoemonemia of the mesenteric arteries.
Morphogenesis: ischemia, dystrophy, atrophy, necrosis of an organ in contact with the external environment - gangrene
Outcome: 1) unfavorable - putrefactive fusion, overheat.
Conclusion: indirect vascular necrosis.
Diagnosis: Wet gangrene of the small intestine.
18. Abscess of the liver.
This macro product is the liver. The shape of the organ is preserved, the mass and size are not increased. The color is dark brown. At the bottom of the organ is an oval-shaped depression 5x8 cm deep up to 4 cm, the inner surface of which is lined with connective tissue. Connective tissue is located on the border of the recess and in the immediate vicinity of it.
Description of pathological changes. These pathological changes could develop as a result of an infectious lesion of the liver, which could be primary (an independent disease) and be a manifestation of another disease. Exudative suppurative inflammation develops, in which a granulation tissue shaft is formed around the infection site, delimiting the abscess cavity and supplying tissue protection cells (leukocytes) to the infection site. Granulation tissue is replaced over time with coarse-fiber connective tissue. Capsules are formed and the acute abscess becomes chronic.
Outcome: 1) favorable:
a) the elimination of infectious agents and the organization of the abscess cavity (replacement with granulation tissue);
b) the chronic course of the disease;
c) thickening of pus, turning it into necrotic detritus and petrification; 2) adverse:
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 infection of the liver with the development of exudative inflammation and the formation of an abscess.
Diagnosis: Hepatitis. Abscess of the liver. _
17. Myocardial hypertrophy.
This macro-preparation of the heart is enlarged due to the efferent tract, the bringing path is not changed. The wall of the left ventricle is thickened. There are no traces of necrosis and hemorrhages.
Descriptions of pathological changes.
Visible changes indicate an increase in the sarcoplasm mass of muscle cells, the size of the nucleus, the number of myofilaments, the size and number of mitochondria, i.e. hyperplasia of intracellular ultrastructures. In this case, the volume of muscle fibers increases. At the same time, hyperplasia of the fibrous structures and stroma occurs, which should be considered as strengthening the connective tissue framework of a busy working heart. Elements of the nervous system 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 have led to the provision of the necessary functional level of general circulation. Subsequently, dystrophic changes will occur in hypertrophied cardiomyocytes, the contractile ability 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 valve defects accompanied by stenosis of the atrioventricular openings and ventricular ventricular tracts of the ventricle. In this case, aortic valve defect due to rheumatic process, the development of stenosis and endocardial hyalinosis, which led to ossification and deformation of the valve cusps
20. Combined mitral heart disease.
This macro product is the heart. The shape of the organ is preserved, the mass and dimensions are slightly increased. Subepicardial fat is highly developed. Fat layers are also located in the myocardium. The mitral valve clearance is sharply narrowed. Overlays of thrombotic masses are noticeable on its wings. The organ is light gray. 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 cusps thicken, sclerosis, and grow together, which leads to a narrowing of the lumen. There are disturbances in 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 cavity of the left atrium, as well as dystrophic processes in cardiomyocytes (fatty degeneration). Developing congestion of blood in the left atrium -\u003e venous congestion in the lungs - "pulmonary heart -\u003e death from acute heart failure. Exodus:
1) favorable: compensation;
2) adverse:
- death from acute heart failure;
- the formation of a congestive thrombus in the left atrium;
- heart attacks as a result of ischemia of a hypertrophic myocardium;
- pneumonia due to venous stasis.
Conclusion: these morphological changes indicate inflammatory processes of the mitral valve with the development of stenosis. Diagnosis: Combined mitral heart disease.
19. Ischemic spleen infarction.
This macro product is a spleen. The shape and dimensions are not changed. The color is heterogeneous - in general, it is brownish-red, but from the gate to the periphery of the organ stretch two sections with a width of 1-2 cm. A paler color. The surface is smooth, without tears, hemorrhage, scarring.
Description of pathological changes.
These pathological changes indicate that they were caused by a sharp violation of arterial circulation in large branches of the lienapar arteries, which led to ischemia of a significant portion of the spleen parenchyma and subsequently to a heart attack. Heart attack in the spleen is most often white, less often white with a hemorrhagic corolla, which is due to the peculiarities of angioarchitectonics of the organ. In this case, it is most likely white, since necrotic areas have a characteristic color and are clearly distinguished from intact parts of the organs.
Exodus:
1) favorable:
a) scarring and replacement of necrotic tissue;
2) adverse:
a) rupture of an organ capsule and intra-abdominal bleeding;
b) death from shock;
c) intoxication and autoimmunization with decay products (resorption-necrotic syndrome), which exacerbates the situation.
Conclusion: these morphological changes indicate sharp discirculatory changes in the pool of branches of the splenic artery, leading to the development of a heart attack
Diagnosis: Acute ischemic spleen infarction.
21. Cirrhosis of the liver.
This macro product is the liver. The shape of the organ is preserved, the mass and size are reduced. The capsule is thickened, the surface of the organ is coarse, the color is whitish-red, the right lobe is darker.
Description of pathological changes.
These pathological changes could develop as a result of degeneration and necrosis of hepatocytes. which led to increased regeneration of hepatocytes and the formation of regenerative nodes surrounded on all sides by connective tissue. The death of hepatocytes stimulates the growth of connective tissue (due to hypoxia of cells inside the nodes). Capillary sinusoids of the false lobules occur, and the ensuing hypoxia leads to a new wave of dystrophy and necrosis. Hepatic cell failure is associated with these phenomena. Regenerative nodes undergo diffuse fibrosis (coarse liver), which is associated with necrosis of hepatocytes and hypoxia due to vascular compression by nodes, their sclerosis, capillarization of sinusoids, and the presence of intrahepatic porto-caval shunts. It activates fibroblasts, Kupffer cells and increases the production of connective tissue. Sclerosis of re-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 anastamoses.
Exodus:
1) favorable: compensated cirrhosis;
2) adverse: death from hepatic cell failure, 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 structural restructuring of the body.
Diagnosis: Postnecrotic cirrhosis of the liver.
23. Cancer metastases in the spleen.
This macro product is a spleen (in section). The sizes are not changed, the shape is normal. The surface is smooth with small patches of tuberosity. On a section - multiple white-pink round spots with a diameter of 3-15 mm. Where spots are closer to the surface, they "protrude" it and form the aforementioned tuberosity.
Description of pathological changes.
These pathological changes indicate that in the body there is a growth of a malignant tumor and its metastasis. The most likely metastasis of the adenocarcinoma of the uterus. Breeding cancer cells form these spherical white-pink clusters.
Exodus:
1) favorable: prolongation of the patient's life as a result of complex chemooperative radiation treatment of the tumor and metastases.
2) adverse:
- cachexia;
- intra-abdominal bleeding;
- progression and further metastasis;
Conclusion: these pathological changes indicate tumor progression and tumor metastasis.
Diagnosis: adenocarcinoma. Distant matastases.
24. Nutmeg liver.
This macro product is the liver. Weight and dimensions are reduced, the shape is saved. The color of the organ in the section is mottled, gray-yellow with red specks, and the variegation increases to the periphery. The liver is tuberous, the tuberosity increases to the periphery.
Description of pathological changes.
These pathological changes could develop as a result of increased pressure in the veins of the liver, which is possible with general (chronic right-stomach 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 degeneration and necrosis of adjacent hepatocytes and the expansion of sinusoids. In them, shaped elements are located to the center, and on the periphery there is plasma (due to an increase in pressure at the confluence of the arterial capillary)\u003e plasmorrhagia, diapedetic hemorrhage. Due to stagnation of venous blood\u003e hypoxia\u003e synthesis of connective tissue of Kupffer cells - the formation of the basement membrane and the transformation of the sinosoid into a capillary\u003e hypoxia. In the central sections of the lobules, fatty degeneration (decomposition) develops up to necrosis. Due to complete regeneration in the places where hepatocytes die, connective tissue\u003e sclerosis grows. Venous congestion\u003e hypoxia\u003e 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\u003e hypoxia, dystrophy\u003e hepatocyte necrosis.
Exodus:
1) favorable: chronic course of the disease; elimination of the cause of venous plethora;
2) adverse: death from liver failure, cancer, the formation of sclerosis and portal hypertension, infection, jaundice, etc.
Conclusion: these morphological changes indicate venous congestion of the liver and hypoxia that developed on this soil, which leads to structural restructuring of the organ.
Diagnosis: Muscat cirrhosis.
25. Chronic lung abscess
This macro product is a lung. An organ in the context of a heterogeneous consistency. Color - gray, with dense inclusions of whitish color. The incision is perpendicular to many bronchi of different calibers. Pronounced connective tissue dividing the lobes of the lung. At the top of the organ is a large cavity with a diameter of 5 cm, porous, on the periphery of which there is a whitish tissue. The inner surface of the cavity is also lined with this fabric.
Description of pathological changes.
These pathological changes could develop as a result of inflammatory disease of the lungs or bronchiectasis. which is unlikely, since then we would see multiple cavities. With pneumonia of any ethnology, tissue that has undergone necrosis and then suppuration, turns into a purulent-necrotic mass, which is secreted through the bronchi along with sputum. A cavity of acute abscess has formed. If the cause of suppuration is not eliminated, the granulation tissue formed first around the cavity is replaced with time by coarse-fiber connective tissue, which blocks the abscess from the lung parenchyma. Dense connective tissue whitish inclusions, which are many in the lung tissue, are characteristic of a chronic abscess, when not only the bronchi, but also the lymphatic drains, along which purulent inflammation spreads, are involved in the process.
Exodus:
1) favorable: organization, encapsulation.
2) adverse: fibrosis and deformation of lung tissue, due to the spread of purulent inflammation.
Conclusion: these morphological changes indicate that the inflammatory processes in the lung tissue led to the development of an acute abscess with a transition to chronic.
Diagnosis: Chronic lung abscess. Exudative suppurative inflammation.
27. Parietal thrombus of an artery.
This macro product is the abdominal aorta. The shape of the organ is preserved, the dimensions are not increased. The organ is light gray. On the intimen, formations of a dark gray color with a diameter of 5 mm are visible. with an uneven surface, and next to it, the formation of the same consistency and color 3x1.5 cm. This formation is located at the site of branching of the aorta.
Description of pathological changes.
These morphological changes could develop as a result of impaired fat and protein metabolism, which was facilitated by factors such as:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- ethnic.
Unregulated cell metabolism of cholesterol leads to the formation of foamy cells and the further development of atherosclerotic changes that we see on the aorta intima: fat spots, fibrous plaques, the formation of thrombotic deposits at the site of ulceration of the plaque. In the formation of thrombotic overlays (the formation of a dark gray color of a dense consistency), sites are taken not only for disturbances in the vascular wall, but also with impaired blood circulation, blood composition, vascular wall, dysregulation of the coagulation, anticoagulation and fibrinolytic systems.
A particularly important factor in this case is circulatory disturbance in the form of a swirling blood flow at the site of abdominal aortic bifurcation. This slowdown of blood flow and contributes to the imposition of thrombotic masses on ulcerated intima.
Outcome: 1) favorable:
a) aseptic autolysis of a blood clot;
b) organization; 2) adverse:
a) petrification;
b) thromboembolism;
c) septic melting;
d) obstruction of the lumen of the aorta.
Conclusion: these morphological changes indicate dystrophic changes in the aortic intima, which, together with impaired blood flow, created the prerequisites for thrombosis.
Diagnosis: Aortic thrombosis.
Uterine fibromyoma.
This drug is the uterus. Size and weight significantly increased due to tumor nodes. The color is whitish yellow. Two nodes of the tumor tissue are visible: the first is located inside the myometrium of the uterus (closer to the endometrium), diameter 2.5 cm .; another in the uterine fundus, grows outward of the organ. The dimensions of this knot are 10-12 cm, round shape, dense consistency. Foci of necrosis and hemorrhage are not observed.
Description of the pathological process
This pathological process is polyetiological, but disharmonious disturbances are the most probable cause. An obligatory stage is precancerous changes, among which there are so-called background changes, manifested by dystrophy, atrophy, hyperplasia. Hyperplasia is considered as a pre-tumor process itself. Stage of tumor development: diffuse hyperplasia, focal hyperplasia, benign tumor. The tumor is represented in this drug by smooth muscle cells. Since the stroma of the tumor is well developed, it is called fibromyoma. In the uterus, depending on localization, intramural, subserous and submucosal fibroids are distinguished.
Complications: the development of swollen 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 drift.
This macro product is represented by many cysts resembling clusters of grapes (matte color) and a diameter of 0.5 to 1.5 cm. These spherical vesicles are located (as if growing and hanging over a cluster-like dome) over areas of yellowish tissue of soft consistency - uterine tissue. The cavity of the bubbles is filled with a transparent mucus-like liquid.
Description of pathological changes.
Examining the morphology of this drug, we can assume that this formation could have formed during pregnancy pathology, with cystic drift. That is, if the placenta with hydropic and cystic transformation of chorionic villi, which is accompanied by proliferation of the epithelium and collapse of the villi, a sharp increase in their number and turning into clusters of cystic vesicles (the fetus dies). Sections 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 start up and at the same time there is a strong proliferation of the epithelium of these villi (both rows of villi cells mix randomly and form a thickening on the surface of the villi). The villi can grow deep into the wall of the uterus, destroy blood vessels, causing severe uterine bleeding (such a deep and extensive ingrowth can occur with one of the types of cystic drift - destruction of the cystic drift). Clinically, the disease manifests itself in the fact that the uterus grows much more in volume than corresponds to this period) of pregnancy, while uterine bleeding may appear from 2-4 months of pregnancy, and gonadotropin level increases in a woman’s urine 5 times
The reasons for the occurrence of cystic skidding are "non-significant violations of harmonious homeostasis - carbonic dysfunctions due to a decrease in estrogen production (with cysts of the corpus luteum of the ovary; mutations of the ovum due to viral infection and intoxication are possible).
Exodus:
1) favorable: surgical removal of all chorionic villi from the uterine cavity;
2) adverse:
a) malignancy of cystic skidding in chorionepithelium;
b) the development of severe bleeding (uterine), which leads to the development of chronic anemia -\u003e death.
Conclusion: this macro product is a placenta with the transformation of chorionic villi, which indicates pregnancy pathology; 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: Bubble drift.
30. Fnbro-cavernous pulmonary tuberculosis.
This macro product is a lung. The organ is gray-pink. The porous lung parenchyma is visible, the stroma is represented by connective tissue layers of a whitish color. In the parenchyma, spotted inclusions of black color are visible - the vessels of the lung. Against the background of this picture, multiple rounded formations with a diameter of 0.5 cm are visible. Whitish. The configuration of the slice of the lung is violated by caverns in the amount of 3 pcs. The first is 8 cm long and 7 cm wide .. 4 cm deep. The second is 4x3x1.5. The third 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. During the exudative reaction, an inflammation center 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, characteristic of tuberculous inflammation, Pirogov-Langhans cells, so the inflammation becomes productive. With the weakening of the body's resistant forces as a result of incomplete phagocytosis of mycobacteria, exudation intensifies, which ends with curdled necrosis of the granuloma and the adjacent tissue. A cavern arises 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 of the following layers: internal pyogenic (necrotic), rich in decaying white blood cells; the middle layer of tuberculosis granulation tissue; external - connective tissue, connective tissue grows around the cavity and sections of lung atelectasis are visible between the layers of connective tissue. Caverns 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 of tuberculoma infiltrates in various stages of inflammation (exudative, productive). The process gradually spreads in the apeka-caudal direction, going down from the upper segments to the lower ones, both by contact and along the bronchi, occupying new sections of the lung. Therefore, the oldest changes (large caverns organized) are located higher.
Exodus:
1) favorable (unlikely) - with a significant increase in the body's resistant forces, a way out of the chronic course of the disease and the organization of tissue detritus with complete phagocytosis of mycobacteria are possible. In this case, sclerosis of a segment of the lung affected by the inflammatory process with areas of bronchial atelectasis develops.
2) adverse - associated with caverns -\u003e bleeding arises from the cavity: 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 a wave-like course of the tuberculosis process.
Diagnosis: Fibrinous-cavernous pulmonary tuberculosis.

MACHINE NUMBER 1 FAT DYSTROPHY OF THE LIVER

In the preparation, sections of the liver are visible.

The liver is small, as it is the liver of a child. But still, the size of the liver is increased, because its capsule is tense, and the corners are rounded.

The color of the liver in the section is yellow.

The consistency of the liver is flabby.

When cutting such a liver with a knife, droplets of fat remain on its blade.

This is parenchymal fatty degeneration of the liver, or "goose" liver.

It can develop in people suffering from chronic cardiovascular diseases, chronic lung diseases, blood system diseases, chronic alcoholism.

In the outcome of parenchymal fatty degeneration over time, a portal, small-node cirrhosis of the liver may develop.

MACRO PRODUCT №2 HEMORRHAGE IN THE BRAIN

A horizontal section of brain tissue is visible in the preparation. The cerebellum is visible below and behind the brain.

In the right hemisphere of the brain in the area of \u200b\u200bthe subcortical nuclei there is a focus of dark brown color due to the fact that in the focus of hemorrhage we see clotted blood. This is a center of hemorrhage in the dead brain tissue, with fairly clear boundaries - a hematoma. Hematoidin pigment is formed in the center of the hematoma under anaerobic conditions, and hemosiderin is formed on the periphery, at the border with healthy tissues. Blood from the site of hemorrhage broke into the anterior horn of the right lateral ventricle, into the third ventricle of the diencephalon, Silviev’s aqueduct of the midbrain, and into the fourth ventricle of the rhomboid.

Hematoma is a type of hemorrhagic stroke.

It was clinically accompanied by the development of focal symptoms on the opposite side of the body - left-sided paresthesia, hemiplegia, hemiparesis, paralysis.

If the patient had not died, then at the place of the hemorrhage a cyst would have formed with walls rusty from hemosiderin.

MACRO PRODUCT №3 KEPHALOGEMATOMA

The preparation presents the integumentary bone of the skull of a newborn. On the upper - the lateral surface of the bone, under its periosteum there is clotted blood of a dark brown, almost black color - this is subperiosteal hemorrhage. This is a birth injury to the skull related to the external cephalohematoma.

MACRO PRODUCT №4 "TAMPONADA" HEART

The preparation shows a longitudinal section of the heart from the side of the left ventricle, since the thickness of the ventricular myocardium is more than 1 cm. It is noteworthy that the cavity of the left ventricle is slit-like, that is, the heart is somewhat compressed from the outside. Determined subepicardial layer of fat, epicardium, pericardium. Blood clots of a gray - brown color are visible in the pericardial cavity. Due to their presence in the pericardial cavity, the heart was compressed from all sides, and the cavity of the left ventricle became slit-like. This bleeding into the pericardial cavity is hemopericardium, an example of internal bleeding, figuratively - “tamponade” of the heart. It is also noteworthy that in the region of the posterior - lower wall of the heart, myocardial tissue is stained with hemosiderin in brown color, due to rupture of the heart wall in this place and hemorrhage from the damaged vessel. The rupture of the heart wall occurred due to myomalacia in the area of \u200b\u200btransmural myocardial infarction.

Thus, hemorrhage in the heart shirt was the result of myomalacia and rupture of the heart wall in the area of \u200b\u200btransmural myocardial infarction.

MACRO PRODUCT №5 PURULENT MENINGITIS

In the preparation, the brain is visible from the side of its upper - lateral surfaces. Under the soft meninges, an accumulation of exudate of white - yellow color, consistency of thick sour cream is determined. This is a purulent exudate. The exudate lies on the surface of the convolutions, goes into the furrows, smoothing the relief of the surface of the brain.

Inflammation of the pia mater is meningitis.

Primarily purulent meningitis can occur with meningococcal infection, and secondarily can complicate infectious diseases with generalization of the infection (with sepsis).

MACROPREPARATIONS No. 6 THE BRAIN TUMOR

The preparation presents a horizontal section of the brain. In one of the hemispheres (in the left), in the white matter there is a focus of pathological proliferation of brain tissue with fuzzy contours, fuzzy growth boundaries. The consistency of the pathological growth site of brain tissue approaches the consistency of the brain itself. Color - variegated, since there are hemorrhages and necrosis in the focus. This is a brain tumor. Since the boundaries of tumor growth are fuzzy, a malignant tumor occurs. It can be assumed that this is glioblastoma, the most common malignant tumor of adults.

MACHINE №7 SARCOMA TIBERAIS

The preparation contains bones that form the knee joint. In the area of \u200b\u200bthe upper part of the tibia diaphysis there is a pathological proliferation of tissue that destroys the posterior surface of the bone, which has fuzzy growth boundaries. This is a tumor. It is white, layered, resembles fish meat. Fuzzy growth boundaries indicate the malignant nature of the tumor. A malignant tumor from bone tissue is osteosarcoma. Since the process of bone destruction prevails over the process of bone formation, this is osteolytic osteosarcoma.

MACRO PRODUCT №8 ABCESSES OF THE BRAIN IN SEPTICOPIEMIA

The preparation contains sections of the brain. In each section there are multiple foci of irregular round shape, clearly delimited from the brain tissue by a thick wall. Filled with contents of white - yellowish or white - greenish color, thick sour cream consistency. This is a purulent exudate.

Focal accumulations of pus, delimited from the brain tissue by the wall, are abscesses.

The wall of an acute abscess consists of two layers: 1) the inner layer is a pyogenic membrane and 2) the outer layer is a non-specific granulation tissue.

Three layers are distinguished in the wall of a chronic abscess: 1) inner — pyogenic membrane, 2) middle — nonspecific granulation tissue, and 3) outer — coarse fibrous connective tissue.

Brain abscesses develop with a generalization of purulent inflammation in the lungs, intestines and other organs, that is, with sepsis, septicopyemia.

MACRO PRODUCT №9 MITRAL HOLE STENOSIS (RHEUMATIC HEART DISEASE)

The preparation presents a cross section of the heart, produced above the level of the atrio - ventricular openings, so that the cusps of the bicuspid, mitral and tricuspid valves are clearly visible.

Valves of the mitral valve are deformed. They are sharply thickened, with a rough surface, opaque, rigid due to the proliferation of connective tissue in them. There is a gap between the closed valve flaps, i.e. mitral valve insufficiency has developed.

In addition, there is a narrowing of the left atrio - ventricular foramen.

Thus, in the area of \u200b\u200bthe mitral valve there is a combined heart disease - insufficiency and stenosis of the mitral valve.

Such acquired heart defects are most often formed during rheumatic valve endocarditis.

The described mitral valve changes correspond to the stage of fibroplastic endocarditis.

It can be assumed that the patient died of progressive chronic cardiovascular failure due to decompensated rheumatic heart disease.

MACHINE №10 CHORION-EPITELIOMA UTERUS

The preparation has a longitudinal section of the uterus with appendages.

The size of the uterus is increased (normally the height of the poppies is 6 - 8 cm, width - 3 - 4 cm and thickness - 2 - 3 cm). In the uterine cavity, the growth of tumor tissue is visualized, which grows into the myometrium, that is, there is an invasive tumor growth.

The consistency of the tumor is soft, porous, since the tumor is absolutely free of connective tissue.

The color of the tumor tissue in the preparation is gray with dark brown blotches. In a fresh preparation, it is dark red, mottled, as there are cavities in the tumor, lacunae filled with blood.

Based on the nature of growth, the tumor is malignant. It develops from the epithelium of the chorionic villi (placenta). This is chorionepithelioma.

It is an organ-specific tumor. It is built of two types of cells - large mononuclear cells with a light cytoplasm, or Langhans cells, derivatives of the cytotrophoblast, and large ugly multinuclear cells, derivatives of synthsitrofoblast. The tumor is hormonal. Tumor cells secrete the hormone gonadotropin found in a woman’s urine; thanks to the hormone, the uterus is enlarged.

The tumor developed due to pregnancy. This is a differentiated tumor.

Metastasizes mainly by the hematogenous route to the liver, lungs, and vagina.

In this preparation, in the area of \u200b\u200bthe vaginal portion of the cervix and in the wall of the vagina, rounded foci are visible in appearance similar to the primary tumor. These are tumor metastases.

MACHINE №11 CHRONIC ULCER OF THE STOMACH WITH PENETRATION TO THE Pancreas

The preparation presents a fragment of the wall of the stomach from the mucous membrane and the pancreas located behind the stomach.

In the wall of the stomach there is a peptic ulcer with towering dense, calloused, callous edges and a flat bottom. One edge of the defect, facing the esophagus, proximal - undermined, with an overhanging mucous membrane. The other edge, the opposite, distal is gently sloping or terraced. The difference in the edges is due to the presence of a peristaltic wave.

A defect in the wall of the stomach is a chronic ulcer, since in its edges there was an overgrowth of connective tissue, which caused a change in the edges of the defect.

At the bottom of the ulcer is not determined the tissue of the wall of the stomach, but lobed, white tissue of the pancreas.

Thus, there is an ulcerative - destructive complication of chronic gastric ulcer - penetration into the pancreas.

It can be assumed that the patient died of spilled stains.

MACRO PRODUCT №12 MUSCULAR LIVER

The preparation shows a frontal section of the liver.

The size of the liver is increased.

The color of the liver tissue in the section is variegated: patches of gray - black color (these are patches with clotted blood) interspersed with patches of gray - brown color (the color of hepatocytes).

Sites of gray - black color, and in a fresh preparation - red color, are caused by plethora and expansion of the central veins and central 2/3 sinusoids of the liver lobules flowing into them.

Due to the similarity of the type of the surface of the incision of the liver to the surface of the transverse cut of nutmeg, the drug got its name.

It occurs during the development of chronic venous congestion in the body, which occurs in conditions of chronic cardiovascular failure, which is a complication of chronic diseases of the graft, such as mitral valve disease, myocarditis with outcome in cardiosclerosis, chronic coronary heart disease.

MACROPREPARATION №13 ADENOMA OF THE PROSTATE GLAND WITH UTERETHYDRONEFROSIS

An organocomplex is presented in the preparation, consisting of a longitudinal section of the kidney with the ureter, longitudinal sections of the bladder and prostate gland.

Changes in the structure of the prostate gland entailed compensatory - adaptive changes in the structure of the overlying organs.

The prostate gland is enlarged, due to the growth in one of its shares of the tumor node, round shape, with clear boundaries of growth, delimited from the tissue of the prostate by the connective tissue capsule. This is a benign tumor - prostate adenoma.

Due to the presence of adenoma, the prostatic part of the urethra narrowed sharply, which led to a violation of the outflow of urine.

Working bladder hypertrophy developed in the bladder wall. Along with wall hypertrophy, the bladder cavity expanded, that is, eccentric decompensated bladder hypertrophy developed.

The ureter, pelvis and kidney cups expanded due to impaired outflow of urine - hydroureteronephrosis.

In the kidney parenchyma, a form of local pathological atrophy has developed - atrophy from pressure.

MACRO PRODUCT №14 CENTRAL LUNG CANCER

The trachea with cartilaginous semicircles located on its front surface, the main bronchi, the part of the left lung adjacent to the left main bronchus are visible in the preparation.

The lumen of the left main bronchus is sharply narrowed due to the fact that around the bronchus in the lung tissue there is a pathological proliferation of gray - beige color tissue, of dense consistency, in the form of a node with fuzzy growth boundaries. This is a malignant tumor growing from the epithelium of the main bronchus - lung cancer. Outside of the main node of the tumor, there are multiple foci of irregular round shape - cancer metastases to the lungs.

Since cancer grows from the main bronchus, it is central in location.

Since tumor growth is represented by a node, the macroscopic form of cancer is nodular.

Most often, the central lung cancer in histological form is squamous, the development of which is preceded by metaplasia of the glandular epithelium of the bronchi into a multilayered squamous non-keratinizing epithelium during chronic bronchitis.

In relation to surrounding tissues, cancer grows infiltratively.

In relation to the lumen of the main bronchus - into its wall, that is, endophytic, compressing the lumen of the bronchus.

Due to impaired patency of the bronchus due to compression of the tumor in the lung tissue adjacent to the bronchus, such infusions as atelectasis, abscess, pneumonia, bronchiectasis may develop.

Lung cancer is an epithelial organ-specific tumor.

Metastasizes mainly by the lymphogenous route. The first lymphogenous metastases in this case are found in regional lymph nodes - peribronchial, paratracheal, bifurcation.

MACRO PRODUCT №15POLIC - ULCERIC AORTIC VALVE ENDOCARDITIS

We see a heart preparation in a longitudinal section from the side of the left ventricle, since its myocardium has a thickness of more than 1 cm. The cavity of the left ventricle is dilated. There is an eccentric decompensated working hypertrophy of the myocardium of the left ventricle of the heart and tonogenic dilatation.

The aortic valve half moon is altered, they are thickened, bumpy, rigid, opaque. On two semi-moons of three, a ulcerative defect is clearly visible, on the surface of which thrombotic overlays in the form of polyps formed. Such changes in the semilunar aortic valve are called polypous - ulcerative endocarditis, which is one of the clinical and morphological forms of sepsis.

Microscopically in the thickness of these thrombotic deposits, microbial colonies and deposits of lime salts can be detected.

Thrombobacterial embolism and the formation of aortic heart disease can become complications of this process.

Since polypous - ulcerative endocarditis has developed on the already changed semilunar aortic valve, this is secondary endocarditis.

MACHINE №16 CANCER OF THE STOMACH (DISEASING FORM)

The preparation presents a fragment of the stomach from the mucous membrane. The stomach is cut along a large curvature.

In the region of lesser curvature of the body of the stomach, there is a pathological proliferation of tumor tissue into the lumen of the stomach with loose raised edges and a shallow bottom. The boundaries of tumor growth in places are fuzzy. At the bottom of the tumor growth there are foci of white necrosis.

Fuzzy boundaries of tumor growth and the presence of secondary changes in it in the form of foci of necrosis indicate malignancy of the tumor.

A malignant tumor growing from the epithelium of the stomach is stomach cancer.

By localization, it is a cancer of the body of the stomach.

By the nature of growth, it is an ecophyte-expansive cancer.

By macroscopic appearance, it is saucer-shaped cancer.

Microscopically, it will most often be represented by a differentiated form of cancer - an adenocarcinoma.

Since gastric cancer, according to the international classification of tumors, belongs to the group of epithelial organ-specific tumors, lymphogenous will be the predominant way of its metastasis. The first lymphogenous metastases can appear in regional lymph nodes - four collectors of lymph nodes located along the small and large curvatures of the stomach.

Since the stomach is an unpaired abdominal organ, the first hematogenous metastases are found in the liver.

MACHINE №17ABCEDING PNEUMONIA IN SEPTICOPIEMIA

We see a cross section of the right lung, since it contains three lobes.

In each lobe, against the background of light beige airy fabric, there are multiple foci of round and irregular shape, the size of a match head, sometimes merging with each other, of dense consistency, airless or low-air, with a smooth cut surface, white - gray in color. These are foci of inflammation in the lung tissue - foci of pneumonia.

A white wall forms around some foci, and the contents of the foci become a consistency of thick sour cream. A complication of pneumonia develops - abscess formation.

Abscessing pneumonia can develop with septicopyemia, one of the clinocomorphological forms of sepsis.

MACRO PRODUCT №18 CORNE PNEUMONIA (WITH ABSEDIATION)

The preparation presents a longitudinal section of the right lung, since three lobes are visible.

The lower lobe is completely gray, airless. The surface of its section is fine-grained.

The consistency of the lobe of the lung corresponds to hepatic density.

The interlobar pleura is thickened with filmy overlays of gray - beige color.

This is croupous pneumonia, the stage of hepatitis, a variant of gray hepatitis.

In the lower segments of the lobe, cavities are defined that are delimited from the lung tissue by the wall. These are abscess cavities.

There is one of the pulmonary complications of pneumonia - abscess formation. The reason for it is the attachment of a secondary purulent infection due to a decrease in immunity and increased fibrinolytic activity of neutrophilic leukocytes.

MACRO PRODUCT №19 SMALL-NODE LIVER CIRRHOSIS

The preparation contains a section of the liver.

The liver is reduced in size, as its corners are pointed, and the capsule is wrinkled.

Multiple regenerate nodes are determined on the outer surface of the liver, up to 1 cm in size, making the surface of the liver non-smooth.

On the surface of the incision, the boundaries of the false lobules are clearly visible (whereas normally the boundaries of the hepatic lobules are not visualized) due to the growth of fibrous tissue in the region of the portal tracts.

This is cirrhosis of the liver.

By macroscopic appearance, it is small-knotted. By microscopic appearance, it is monolobular, since the size of the false lobules corresponds to the size of the nodes - regenerates.

According to pathogenesis, this is portal cirrhosis of the liver, in which portal hypertension develops primarily, and secondly, hepatic cell failure.

Such cirrhosis can develop in the outcome of fatty hepatosis, a chronic form of viral hepatitis B and a chronic course of alcoholic hepatitis.

MACRO PRODUCT №20 CANCER OF THE UTERUS BODY

A longitudinal section of the uterus is presented.

The uterus is enlarged. It is seen that in the uterine cavity there is a pathological proliferation of tissue with a nonsmooth, papillary surface, in places with ulcerations, with fuzzy growth boundaries. This is a tumor growth.

The tumor develops from the endometrium, it is clear that it grows into the wall of the uterus. This is a malignant tumor from the epithelium - cancer of the uterus.

Histologically represented by a differentiated form of cancer - adenocarcinoma.

The nature of the tumor growth in relation to the lumen of the uterus is exophytic, in relation to the surrounding tissues - infiltrating.

It can develop in the outcome of atypical glandular endometrial hyperplasia.

It is an epithelial organ-specific tumor. Metastasizes mainly by the lymphogenous route. The first lymphogenous metastases are found in regional lymph nodes.

MACRO PRODUCT №21 PURULENT - FIBRINOUS ENDOMYOMETRIT

A longitudinal section of the uterus with appendages is visible.

The uterus is sharply increased in size, its cavity is sharply expanded, the wall is thickened.

The endometrium is dirty gray, dull, covered with beige overlay, hanging in places in the uterine cavity. In the endometrium there is an inflammatory process - purulent - fibrinous endometritis.

In addition, the inflammation spread to the muscle membrane of the uterus, as the myometrium is dull, dirty - gray in color.

Thus, in the presented preparation there is purulent - fibrinous endomyometritis, which could arise due to criminal abortion and cause uterine sepsis.

MACHINE №22 MULTIPLE UTERINE FIBROMIOMAS

A cross section of the uterus is presented.

In the wall of the uterus, the growth of tumor tissue in the form of nodes, of different sizes, round and oval in shape, with clear growth boundaries, surrounded by a thick-walled capsule, which is a reflection of the expansive growth of the tumor, is visible.

The nodes located inside the uterine wall are intramural, lying under the endometrium - submucous, lying under the serous membrane - subserous.

The nodes are built of two types of fibrous structures - some beige fibers are smooth muscle fibers, others are gray - white fibers - connective tissue fibers. Fibrous structures have different thicknesses and go in different directions, which are manifestations of tissue atypism.

Since the nodes of the tumor contain a large number of connective tissue fibers, their consistency is dense.

Due to the fact that the tumor grows expansively and has only signs of tissue atypism, it is benign. A benign tumor of smooth muscle with an admixture of fibrous tissue is called fibromyoma.

Based on the international classification of tumors, it belongs to mesenchymal tumors.

MACRO PRODUCT №23

The drug is represented by a cluster of clusters of thin-walled vesicles, adhered to each other, and filled with a transparent liquid. This is a bladder drift, a benign organ-specific tumor that develops during and after pregnancy from the epithelium of the chorionic villi.

The development of cystic drift is based on hydropic dystrophy of epithelial cells.

Bubble drift is benign until it begins to grow into the wall of the uterus, into the veins. After that, it becomes malignant, or destroying. Against the background of malignant cystic drift, a malignant organ-specific tumor of chorionepithelioma can develop.

MACRO PRODUCT №24 THROMBOEMBOLISM OF THE STEM OF PULMONARY ARTERY

The drug is represented by an organocomplex: the heart and fragments of both lungs.

The heart is trimmed from the right ventricle, since its myocardium is approximately 0.2 cm thick. A pulmonary trunk emerges from the right ventricle, which is divided into two pulmonary arteries, respectively, of the right and left lungs.

In the lumen of the pulmonary trunk and its bifurcation are massive, heavy, dense, crumbling, with a corrugated surface masses that are not attached to the walls of blood vessels. These are thromboembolism. The source of such massive thromboembolism could most likely be the veins of the lower extremities.

The thromboembolum located in the lumen of the pulmonary artery trunk and its bifurcation irritates the reflexogenic zone receptors located in the intima of the above vessels and causes the development of the pulmono-coronary reflex, which consists in the instant spasm of the small bronchi and bronchioles and coronary arteries of the heart, with the development of acute cardiovascular and vascular insufficiency instant death.

MACRO PRODUCT №25 ATHEROSCLEROSIS OF THE AORTA WITH ATHEROMATOSIS AND PARETHENE THROMBOSIS

The abdominal aorta is shown in longitudinal section and the area of \u200b\u200baortic bifurcation into the common iliac arteries.

Intima aorta changed. It defines multiple roundish - longitudinal spots of white - yellow color, which are lipid deposits and the proliferation of fibrous tissue. These are atherosclerotic plaques. They bulge into the lumen of the aorta, making it narrower. Below the opening of the inferior mesenteric artery, the plaques are ulcerated, atheromatous (necrotic) masses have formed on their surface and hemorrhages have arisen.

The appearance of atherosclerotic plaques in the aortic intima indicates the presence of atherosclerosis disease, the clinical and morphological form of aortic atherosclerosis.

The described changes in plaques correspond to the macroscopic stage of complicated lesions.

Damage to the aortic intima was one of the local prerequisites for thrombosis. In the lumen of the abdominal aorta and in the lumens of the iliac arteries, parietal and even obturating thrombi formed, disrupting the passage of blood through the aorta to the lower extremities.

MACRO PRODUCT №26 SUCTION OF THE THIN GUT WITH ABDOMINAL TYPE

The preparation presents the small intestine in a longitudinal section from the mucous membrane.

On the mucous membrane visible longitudinal oval formations, bulging above the surface of the mucous membrane and having on their surface a kind of grooves and convolutions, as in the brain. These formations are pathognomonic for typhoid fever. They arose as a result of acute productive inflammation in the area of \u200b\u200blymphatic follicles located in the submucosal layer of the intestine. Due to the proliferation of macrophage and histiocytic elements, the follicles increased in volume, size and began to rise above the surface of the mucosa.

Due to the presence of furrows and convolutions on the surface of the follicles, the first stage of typhoid fever is called cerebral swelling.

MACROPREPARATION №27 FIBROSOUS - Cavernous TUBERCULOSIS OF THE LUNGS

The drug is represented by a longitudinal section of the right lung, since it has 3 lobes. In each of the lobes there are cavities, caverns of large sizes with thick, non-falling walls. Since the walls of the cavities do not collapse, these are old, chronic caverns inherent in fibro-cavernous pulmonary tuberculosis, one of the phases of the form of secondary pulmonary tuberculosis.

The wall of the old cavity consists of 3 layers: 1) internal - caseous necrosis; 2) medium - specific granulation tissue; 3) external - fibrous tissue.

The patient develops pulmonary heart disease, chronic pulmonary heart failure, tuberculous intoxication and cachexia, from which he dies.

MACRO PRODUCT №28 LYMPHOGRANULEULOMATOSIS OF PARAORORTAL LYMPHOUS NODES

The drug presents aorta in a longitudinal section.

In the aortic intima, atherosclerotic plaques are determined.

On both sides of the abdominal aorta, above the bifurcation, sharply enlarged and due to this lymph nodes welded together, forming “packets” of the lymph nodes, are determined.

The consistency of the lymph nodes is tightly elastic, the surface is smooth, the color in the section is gray - pink.

Lymph nodes lying on the sides of the aorta are called paraaortic.

The enlargement of paraaortic lymph nodes and their fusion into packets takes place with lymphogranulomatosis, malignant Hodgkin's lymphoma.

MACRO PRODUCT №29 ARTERIOLOSCLEROTIC NEFROSCLEROSIS

Two whole kidneys are visible in the preparation.

Their size and weight are sharply reduced (both kidneys in a person weigh 300-350 g). The surface of the kidneys is wrinkled, fine-grained. The consistency of the kidneys is very dense.

This type has a primary - wrinkled kidney due to the benign course of primary arterial hypertension. Shrinkage is based on hyalinosis and sclerosis of the capillaries of the renal glomeruli - arteriolosclerotic nephrosclerosis.

The second-wrinkled kidney, which develops in the outcome of chronic glomerulonephritis, has the same appearance.

Clinically, against the background of primary and secondary wrinkled kidneys, chronic renal failure develops, accompanied by the development of azotemic uremia, which can be treated with chronic hemodialysis or a kidney transplant.

MACRO №30 MILLAR TUBERCULOSIS OF THE LUNGS

Presents a longitudinal section of the lung, increased in size.

It is clearly seen that the entire surface of the lung tissue is diffusely dotted with small, about the size of a millet grain, dense tubercles, light yellow in color.

This type of lung has miliary tuberculosis, which develops with generalized hematogenous and hematogenous tuberculosis with a primary lung lesion.

Each tubercle has the following structure: in the center there is a focus of caseous necrosis, the severity of which depends on the state of immunity of the patient; it is surrounded by a cell wall of epithelioid cells, lymphocytes, plasmocytes and single multinucleated Pirogov-Langhans cells.

According to the classification of granulomas, tuberculous granulomas are infectious, specific. Specific cells of tuberculous granuloma are epithelioid cells of hematogenous, monocytic origin, which are the most in the granuloma.

MACRO PRODUCT №31 NODE GOITER

The preparation presents the thyroid gland in section.

Its dimensions are sharply increased (normally it weighs 25 g).

The outer surface is hilly.

On the surface of the incision, the lobular structure of the gland is distinguished, and in the lobes - follicles of different sizes filled with a brown colloid.

A persistent increase in the size of the thyroid gland, not associated with inflammation, a tumor, or a violation of blood circulation in it, is called goiter.

In appearance it is a knotty goiter.

According to the internal structure - colloidal goiter.

Most often occurs with endemic goiter, the occurrence of which is associated with exogenous iodine deficiency.

Despite the compensatory increase in the size of the gland, its function is reduced.

MACHINE №32 TUBE PREGNANCY

The fallopian tube is visible in cross section.

The pipe is sharply expanded. The wall is thinned in places, thickened in places. In places of thickening of the wall of the pipe, the tissues have a dark brown color due to hemorrhage. In the center of the tube there is a human embryo, in which the head, trunk, hands with fingers are clearly distinguishable. The embryo is surrounded by fetal membranes.

This is an ectopic tubal pregnancy complicated by incomplete tubal abortion.

The fetal egg separated from the walls of the fallopian tube, as evidenced by hemorrhage, but remained in the tube.

MACRO PRODUCT №33 RENAL - CELLULAR CANCER

It is represented by a section of the kidney, in the upper pole of which the tumor tissue grows in the form of a node with clear growth boundaries, forming a pseudocapsule around itself, which indicates the expansive growth of the tumor.

The tumor node is light yellow in color, since the tumor cells contain a large amount of lipids; motley, since the development of a tumor is characterized by the development of necrosis and hemorrhage; soft consistency, since the tumor contains little fibrous tissue.

Despite the nature of growth, the tumor is malignant, differentiated, epithelial organ-specific, developing from the renal tubule epithelium.

It occurs in adults.

MACHINE №34 DRY GANGREN STOP

The preparation shows the foot of the right lower limb.

In the area of \u200b\u200bthe dorsal metatarsus of the foot, at the base of the fingers, the skin is absent, and the soft tissues are dry, mummified, gray - black.

This is dry gangrene of the foot, one of the clinical and morphological forms of necrosis.

Gangrene is called necrosis of tissues in contact with the external environment.

Soft gangrene tissue is painted in gray - black color with a pigment pseudomelanine, or iron sulfide.

Gangrene of the foot can develop in the outcome of atherosclerotic damage to the vessels of the lower extremities, which occurs primarily or as a result of diabetes mellitus due to the development of macroangiopathy.

MACRO №35 EMBRYONAL KIDNEY CANCER

It is represented by a kidney in a longitudinal section.

In the upper pole of the kidney there is an overgrowth of tumor tissue, large sizes, with clear growth boundaries, forming a pseudocapsule around itself. In the center of the tumor node there is a large cavity due to necrosis of the tumor tissue.

The lower pole of the kidney is small, which indicates that the kidney belongs to a small child.

Despite the nature of tumor growth - expansive and given the presence of secondary changes in the tumor - it is a malignant, undifferentiated tumor that develops from metanephrogenic tissue and affects children from two to six years old.

Expansive growth over time gives way to invasive growth.

A tumor is epithelial organ-specific.

Metastasizes mainly by the hematogenous route to the opposite kidney, lungs, bones, brain.

MACRO PRODUCT №36 BREAST CANCER

The drug is represented by the mammary gland.

In one of the quadrants of the mammary gland, there was a pathological proliferation of tumor tissue, emanating from the epithelium of the ducts of the mammary gland, and sprouted onto the surface of the skin, indicating an invasive tumor growth.

This is a malignant, epithelial organ-specific tumor - breast cancer.

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MACHINERY (lay down)

Chronic heart aneurysm

Brown myocardial atrophy

wet gangrene of the small intestine

causes - syphilis

abdominal aorta
aortic aneurysm with thrombosis

Brain

spleen
ischemic spleen infarction

MACRO PRODUCT No. 53.

Lung fraction
Hemorrhagic pulmonary infarction

apex of the lung
emphysema

congenital heart defect

appendix
phlegmonous appendicitis

Chronic stomach ulcer

Baby's liver

part of the liver
nutmeg liver

Cancer of the body and cervix
Reasons - polyetiologic

part of the fallopian tube
tubal pregnancy

Complications:

Full tube abortion

Incomplete tube abortion

Pipe rupture

Mummification of the fetus

Calcification of the fetus

Bleeding

saucer-like stomach cancer
the reasons are polyetiological

uterus (pregnant)
uterine fibroma and pregnancy
the cause is polyetiological

bladder
Bladder papilloma
the reasons are polyetiological

MACRO PRODUCT No. 172. Lipoma

adipose tissue (tumor tissue)
the reasons are polyetiological

cut femur
the cause is polyetiological

part of the lung
central lung cancer
the reasons are polyetiological

colon fragment
colon cancer
the reason is polyetiological

causes - septicemia

micronodular nephrocirrhosis

subacute glomerulonephritis
unfavorable outcome - renal failure, uremia
causes - infectious and allergic diseases

part of the large intestine
colitis with dysentery

organocomplex

meningococcal infection

spleen

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Patan_MAKROPRYePARAT

MACRO PRODUCT No. 1. Warty mitral valve endocarditis

The heart is slightly enlarged, the papillary muscles and chords are not changed, the mitral valve walls are dull, the chords are thin, along the free edge of the cusps facing the atria, small gray-pink, loose, easily removable thrombotic overlays are visible - warts
Acute warty mitral valve endocarditis
the outcome is unfavorable. thromboembolism in a large circle. Complications: the formation of acquired heart disease, heart attack of the kidneys, gangrene of the intestine
causes - rheumatism, infections, intoxications, infectious and allergic diseases

MACRO PRODUCT No. 6. Polypous ulcerative endocarditis of lunar aortic valves

the organ is enlarged, ulceration and polypous-ulcerative overlays are visible on the lunar aortic valves.
Polypous ulcerative endocarditis of lunar aortic valves
unfavorable outcome - the formation of aortic valve insufficiency and vascular thromboembolism BKK.
causes - infectious and allergic diseases

MACRO PRODUCT No. 9. Mitral valve fibroplastic endocarditis

The heart is sharply enlarged in size and weight, papillary muscles and chords are thickened and sclerotic. The wall of the LV is thickened to 2 cm, the cusps of the mitral valve are sharply thickened, represented by a dense, opaque tissue, sclerotic, narrow the left atrioventricular opening, which has the form of a gap. The cavity of the left atrium is expanded
Fibroplastic endocarditis, mitral stenosis.
The outcome is unfavorable. Complications - chronic heart failure, acquired heart defects
causes - viral and infectious diseases, rheumatism

MACHINE № 16. Chronic aneurysm of the left ventricle of the heart

heart is enlarged. on the preparation - bag-shaped protrusions of the wall of the left ventricle in the apex - aneurysm with a diameter of 7 cm, the wall in its area is thinned to 0.3 cm, represented by connective tissue.
Chronic heart aneurysm
The outcome is unfavorable. Complications - rupture of aneurysm, bleeding, chronic heart failure, parietal thrombosis  thromboembolism
causes - myocardial infarction (postinfarction cardiosclerosis)

MACRO PRODUCT No. 18. Fibrinous pericarditis

the organ is enlarged, exudate of loose consistency is localized on the outer leaf of the pericardium. The pericardium is dull, covered with rough, grayish-yellow overlays in the form of threads and very vaguely resembles a hairline. Overlays are easily removed.
Fibrinous pericarditis (hairy heart)
the outcome is unfavorable. Due to the germination of the deposited fibrin masses by fibroblasts, adhesions are formed between the pericardial sheets, which leads to obliteration of the pericardial cavity. Sometimes sclerotic membranes are petrified with the formation of a shell-like heart, which leads to a violation of contractility.
causes - infectious agents, mercuric chloride poisoning, uremia, inflammatory processes, myocardial infarction

MACRO PRODUCT № 21. Hypertrophy of the heart

heart (cross section through the ventricles)
the size of the organ is almost not increased. The wall of the left ventricle is thickened due to the concentric narrowing of the cavity. Swollen papillary muscles are clearly visible.
Hypertrophy of the heart (compensatory, working (tonogenic), concentric)
favorable outcome (heart function compensated) complications - cell tissue dies, dilated hypertrophy (decompensation) develops - chronic heart failure, hemodynamic disturbances, congestion in BCC, development of a bovine heart
Heart forms of hypertension, aortic valve insufficiency, excessive prolonged and emotional stress

MACRO PRODUCT No. 26. Brown myocardial atrophy

the organ is reduced in size, there is no subepicardial fatty tissue, coronary vessels have a pronounced convoluted course, the color of the heart muscle in the section is yellow-brown
Brown myocardial atrophy
Adverse outcome - chronic heart failure
causes - cachexia, vitamin E deficiency, drug intoxication, increased functional loads, debilitating diseases

MACRO № 28. Gangrene of the small intestine

part of the small intestine with mesentery

the wall is swollen, thickened, dark brown, the intestinal lumen is sharply narrowed. In the lumen of the vessels of the mesentery - thrombotic masses

wet gangrene of the small intestine

the outcome is favorable if a small area of \u200b\u200bthe intestine is damaged  resection. But more often adverse  perforation with peritonitis

causes - mesenteric artery thrombosis and their embolism

MACHINE No. 31. Aneurysm of the aortic arch with syphilis

whitish tuberosity with wrinkles and cicatricial retractions, giving the aorta the appearance of shagreen skin, are visible on the aortic intima. There is an inflammatory process in the aortic wall.

syphilitic aneurysm of the ascending aortic arch

the outcome is unfavorable. Complications - a decrease in the strength of the aortic wall - its rupture; development of syphilitic aortic defect.

causes - syphilis

heart, place of pulmonary bifurcation

In the main trunk of the pulmonary artery, vermiform dryish gray-red masses are visible. They fill the lumen of the vessel, but are not associated with intimacy.

unfavorable outcome; sudden death due to the development of pulmonary cardiac and pulmonary coronary reflex  spasm of the coronary arteries; pulmonary pulmonary reflex  spasm of pulmonary arteries and bronchi  respiratory and heart failure  death

causes - vein thrombosis of the lower extremities, pelvis, hemorrhoid plexus, the formation of a thrombus in the right half of the heart and from the vena cava system

MACRO PRODUCT No. 35. Atherosclerosis with aneurysm and parietal thrombus

abdominal aorta
there is a saccular protrusion of a round-shaped wall with a diameter of 5 -8 cm with the formation of a cavity - a saccular aortic aneurysm. In the cavity of the aneurysm there are ribbed, dark red dryish masses that are tightly soldered to the wall of saccular protrusion in the aorta
aortic aneurysm with thrombosis
the outcome depends on the complications. Favorable - replacement with connective tissue, wall sealing. Adverse - septic melting, blockage of the lumen, impaired blood flow, rupture of the wall of the aneurysm, bleeding, hemorrhage, separation of the thrombus (thromboembolism)
causes - ulceration of atherosclerotic plaques, vascular damage, slow blood flow, hemostasis, thrombosis

MACRO PRODUCT No. 48. Subarachnoid hemorrhage

Brain
in the temporal region of the right hemisphere in the base area, a lamellar hemorrhage of 7 x 5 cm with clear maroon borders. Brains and furrows are smoothed out.
Subarachnoid hemorrhage
relatively unfavorable outcome: the development of edema, compression, dislocation of the brain  hypoxia  death of the cortex
Hypertension, atherosclerosis, leukemia, trauma, aneurysm

MACRO PRODUCT No. 50. Ischemic spleen infarction

spleen
2 foci of a triangular shape (base directed toward the capsule): lower white, upper white with a hemorrhagic nimbus. The spleen is slightly enlarged, the consistency is dense. The area of \u200b\u200bnecrosis bulges out from under the capsule. The surface of the capsule in the area of \u200b\u200ba heart attack is rough with overlays of fibrinoid exudate
ischemic spleen infarction
outcome: favorable - scar formation, ossification, cyst formation, encapsulation, petrification. Adverse - death, purulent fusion, adhesion formation
spleen circulation disorder - thrombosis, embolism

Lung fraction
in lung tissue - a focus of triangular-shaped necrosis, dark red in color, the base of a heart attack (red) is facing the pleura, the apex is toward the root of the lung. On the surface of the pleura corresponding to the base of the heart attack - fibrinous overlays
Hemorrhagic pulmonary infarction
The outcome is favorable - scar formation, ossification, cyst formation, encapsulation, petrification. Adverse - purulent fusion, passing to the pleura; pneumonia, death
causes - thromboembolism of the middle and small branches of the pulmonary artery

MACRO PRODUCT No. 70. Bullous pulmonary emphysema

apex of the lung
in the upper part of the lung, subpleurally there is a thin-walled bubble filled with air with a diameter of about 5 cm (bulla)
emphysema
outcome: unfavorable - respiratory failure, congestion in the ICC, pulmonary heart, pneumothorax with rupture of the bladder is possible
causes - around scars after tuberculosis, age-related changes in lung tissue, with chronic bronchitis, occupational diseases (glass blowers), impaired protein synthesis in surfactant

MACROPREPARATION No. 74. Repeated myocardial infarction

the organ is enlarged, in the back wall of the left ventricle there is a focus of a heart attack with a size of 2 x 3.5 cm in white, it is represented by dense fibrous tissue (primary heart attack). Above it is a secondary lesion of irregular shape, clay-yellow in color, soft consistency of 5 x 6 cm in size (secondary heart attack, later in time)
repeated transmural myocardial infarction
outcome - favorable - organization and scar formation (chronic heart failure); unfavorable - death. Complications - asystole, ventricular fibrillation, acute heart failure, development of aneurysm with rupture of the heart
the reason is thrombosis, spasm, coronary artery thromboembolism, atherosclerosis, functional overstrain in conditions of insufficient blood supply

MACRO PRODUCT No. 84. Complex congenital heart and vascular malformation

organocomplex of a stillborn child
in the upper part of the interventricular septum - a defect of round shape, with a diameter of 0.5 cm (non-closure of the interventricular septum). The general arterial trunk departs from the right heart, giving the branch to the left lung and giving rise to the carotid arteries. 2 common carotid arteries depart. The mouth of the right pulmonary artery is missing. Light bluish, airless, sleeping
congenital heart defect
unfavorable outcome, defect incompatible with life
exposure to adverse factors during 3-11 weeks of fetal development

MACRO PRODUCT No. 90. Hypertrophic gastritis

the stomach is enlarged, the wall is thickened, the presence of thick folds, thickened mucous membrane
hypertrophic gastritis (Minetrie disease)
outcome - digestive disorders, precancerous condition
reasons - the etiology is not clarified; predisposing factors: excess nutrition, heredity, national character

MACRO PRODUCT No. 97. Phlegmonous appendicitis

appendix
the process is enlarged, the serous membrane is dull, full-blooded, fibrinous plaque is noted on its surface. The mesentery is edematous, hyperemic. On a section - 2 full-blooded vessels.
phlegmonous appendicitis
favorable outcome - surgical intervention; unfavorable - perforation of the wall  peritonitis. If there is a closure of the proximal process  extension of the distal  empyema of the process. Periappendicitis, peritiflitis, purulent thrombophlebitis of the mesenteric vessels
causes - autoinfection, E. coli, enterococcus

MACRO PRODUCT No. 98. Chronic gastric ulcer

on the lesser curvature in the pyloric region, a deep defect in the wall of the stomach is visible, extending to the mucous and muscle membranes. The defect has an oval-round shape, with a diameter of about 0.5 cm, high density, calloused, roll-shaped, raised edges. The edge facing the esophagus is overhanging, and the edge facing the pyloric department is terraced, gently sloping (due to peristaltic contractions of the muscular membrane). The bottom of the ulcer is represented by a dense whitish scar tissue
Chronic stomach ulcer
complications: ulcerative and destructive (perforation, bleeding, penetration); inflammatory (gastritis, perigastritis, duodenitis, perideodenitis); ulcerative-cicatricial (stenosis of the inlet and outlet, stomach deformity, stenosis and deformity of the duodenal bulb); ulcer malignancy, combined complications. Favorable outcome - scar scarring
causes - recurrent acute gastritis, Helicobacter pillory, stress, psycho-emotional stress, nutritional factors, bad habits, hereditary predisposition

MACRO PRODUCT No. 104. Fatty degeneration of the liver

Baby's liver
the organ is enlarged, the surface is smooth, clay-yellow in color, the parenchyma has a flabby consistency. The cut has a characteristic oily sheen.
fatty liver (goose liver)
unfavorable prognosis. Complications - necrosis, cirrhosis, chronic liver failure, hepatic coma, death
causes - intoxication, infection, hypoxia, vitamin deficiency, protein starvation, transfusion of an incompatible blood group

MACRO PRODUCT No. 110. Muscat liver

part of the liver
the liver is enlarged. Dense consistency, smooth. The surface, in the section has a motley color, there are foci of gray-yellow with alternating brown-red color. Gray-yellow - peripheral hepatocytes with fatty degeneration. Brown-yellow - venous hyperemia of the central vein
nutmeg liver
unfavorable, because muscular fibrosis develops  cirrhosis  portal hypertension  ascites, intoxication
chronic heart failure, impaired outflow of venous blood, general and chronic venous congestion

MACRO PRODUCT No. 115. Macronodular cirrhosis of the liver

organ is reduced in size, dense texture, reddish-brown. The surface is hilly due to the formation of regenerative knots, between them are dense connective tissue partitions (more than 1 cm is macronodular, less than 1 cm is micronodular)
macronodular cirrhosis
adverse outcome - liver failure, portal hypertension, ascites, heart failure
causes - viral hepatitis, hepatosis, toxic liver dystrophy

MACRO PRODUCT No. 116. Cancer of the uterus

Organocomplex - uterus, ovaries, fallopian tubes
The uterus is enlarged, in the cavity - growing into the cavity and into the wall from the epithelium of the mucous membrane, gray-red color of the formation of an ovoid shape, on the surface - multiple ulcerations. There are no capsules. The wall is thickened, especially in the cervical region
Cancer of the body and cervix
The outcome is unfavorable. Complications - lymphogenous metastases, necrosis, hemorrhages
Reasons - polyetiologic

MACRO PRODUCT No. 118. Varicose veins of the esophagus with rupture of the vessel wall

lower third of the esophagus and cardiac part of the stomach
The ES of the esophagus is thinned, in the submucosal glands of the lower and middle third of the esophagus there are swollen, bluish-colored sinuous varicose veins of the esophagus, which have become a source of bleeding
Esophageal varicose veins with rupture of the vessel wall
Adverse outcome - death from massive bleeding
Cirrhosis of the liver in the stage of decompensation of portal hypertension with the development of porto-caval internal anastomoses. When a vein is damaged by a food lump - bleeding

MACRO PRODUCT No. 125. Tubal pregnancy

part of the fallopian tube
the fallopian tube is dilated, deformed, impregnated with blood, the fimbrial region expanded to 7 cm with a rupture of the wall, in the lumen of the fetus with membranes and placenta. In the expanded area - traces of massive hemorrhages
tubal pregnancy
the outcome is favorable in the event of surgery and stopping the bleeding.

Complications:

Full tube abortion

Incomplete tube abortion

Pipe rupture

Secondary abdominal pregnancy

Mummification of the fetus

Calcification of the fetus

Bleeding

Causes - changes in the fallopian tubes  impaired progress of the fertilized egg (chronic inflammation, congenital malformations, swelling)

MACHINE No. 131. Saucerous carcinoma of the stomach

on the lesser curvature, the formation grows into the lumen and into the wall, with a diameter of about 10 cm. It looks like a saucer of gray-pink color. The edges are raised, in the center a depression
saucer-like stomach cancer
unfavorable outcome: metastases, dyspepsia, intoxication
the reasons are polyetiological

MACRODrug № 154. Uterine fibromyoma, pregnancy

uterus (pregnant)
the uterus is enlarged, in the section, in the thickness of the myometrium there is a tumor node in the capsule, gray, fibrous structure, dense consistency, about 8 cm in diameter. The fibers of the tumor node have a fibrous structure, the fibers are randomly arranged, have vortices
uterine fibroma and pregnancy
outcomes are different. Complications - an obstacle to pregnancy, malignancy
the cause is polyetiological

MACRO PRODUCT No. 165. Papilloma of the bladder

bladder
the formation of a spherical shape, soft, elastic consistency, 3 cm in diameter, growing in the lumen of the bladder is seen on the bladder CO. The wall under it is not thickened. On the surface, the tumor resembles cauliflower.
Bladder papilloma
The outcome is favorable, with surgical intervention. Depends on localization. If it grows at the mouth of the ureter, the urethral opening is unfavorable. In trauma, bleeding. Complication - malignancy, tissue compression, recurrence of operations
the reasons are polyetiological

MACRO PRODUCT No. 172. Lipoma

adipose tissue (tumor tissue)
the tumor node of dense elastic consistency in the capsule, with a diameter of about 10 cm, has a lobed structure, yellow, sebaceous in section
outcomes are different, more often benign. Complications: malignancy, compression of the surrounding tissue
the reasons are polyetiological

MACRO PRODUCT No. 175. Hip osteosarcoma

cut femur
the bone channel was opened: from the bone and around it growth of the tumor node of large sizes without clear boundaries is visible, it does not have a capsule, in the section it is gray in color, resembling fish meat, with a soft consistency. Diameter - 15 x 20 cm
osteoblastic hip osteosarcoma
the outcome is unfavorable. Complication: hematogenous metastasis
the cause is polyetiological

MACRO № 178. Lung cancer

part of the lung
in the root zone of the lung there is a whitish-pink tumor node with uneven contours. WITH lobar bronchus in the tumor area tuberous. No capsule. Grows from the epithelium through the wall of the bronchus
central lung cancer
the outcome is unfavorable. Complications - respiratory failure (respiratory failure, metastases, necrosis, hemorrhage, ulceration)
the reasons are polyetiological

MACRO № 179. Colon cancer

colon fragment
in the central part - tumor growth into the lumen and the wall of the intestine, circulating enveloping the wall of the intestine. The gut clearance is narrowed here. Grows from the epithelium. The surface of the tumor is tuberous. The growth boundary is fuzzy. From the mesentery - an increase in LU. Tumor tissue (metastases) in section
colon cancer
adverse outcome. Complications - metastasis, peritoneal carcinomatosis, lumen obstruction, obstruction
the reason is polyetiological

MACRO PRODUCT No. 191. Embolic purulent nephritis

The organ is enlarged, under the capsule in the thickness of tissues - multiple foci of purulent inflammation of gray-yellow color, prone to fusion, ranging in size from 0.2 to 2 cm.
Embolic purulent interstitial nephritis
Outcome - adverse, acute renal failure, uremia
causes - septicemia

MACRO PRODUCT No. 199. Nephrocyrosis

the organ is sharply reduced in size, gray in color, the surface is finely tuberous. On a cut - all tissue is replaced by a connective. There is no border between the cortical and medulla
micronodular nephrocirrhosis
unfavorable outcome - renal failure, uremia
causes - hypertension, atherosclerosis, amyloidosis, glomerulonephritis

MACRO PRODUCT No. 207. Kidney stones and hydronephrosis.

the organ is enlarged, the surface is coarse. Pressure ulcers are visible on the surface. Under the capsule are foci of black and gray in various shapes. In the cavity of the cups and pelvis - stones of irregular shape with a diameter of about 2 cm of a layered structure of white and light brown color. There are no boundaries between the cortical and medulla. The parenchyma is severely thinned due to atrophy. Visible cavities filled with urine.
urolithiasis, hydronephrosis
the outcome is unfavorable. Complications - pyelonephritis, pyonephrosis, pressure sores of the kidneys, perinephritis, paranephritis.
violation of mineral metabolism, stagnation of secretion, inflammation of the kidneys, compression of the tumor

MACRO PRODUCT No. 208. Hypoplasia and vicar hypertrophy of the kidneys.

the upper kidney is small, gray, tuberous, dense - congenital hypoplasia. The second kidney is sharply increased in size, the surface is smooth - vicar hypertrophy
vicar hypertrophy and renal hypoplasia
the outcome is favorable - the second kidney takes on the function of the first. Complications - acute renal failure
causes - underdevelopment of one of the kidneys - congenital hypoplasia, inflammation, nephrosis, glomerulonephritis, surgical removal of the second kidney. Hypertrophy - Vicar

MACRO PRODUCT No. 223. Subacute glomerulonephritis (large mottled kidney).

kidneys are enlarged in size, flabby consistency. In the section, the cortical layer is expanded, swollen, yellow-gray, dull with red specks. It is clearly demarcated from the dark red medulla.
subacute glomerulonephritis
unfavorable outcome - renal failure, uremia
causes - infectious and allergic diseases

MACRO PRODUCT № 232. Colitis with dysentery.

part of the large intestine
the wall of the colon is sharply thickened, CO is covered with a grayish-yellow film of purulent exudate, consisting of numerous dead enterocytes and polymorphonuclear leukocytes, colonocytes and thickened mucus.
colitis with dysentery
unfavorable outcome - ulceration, perforation, fistulas, transition to adjacent tissues, peritonitis, bleeding
dysentery (Shigella infectious agents)

MACRO PRODUCT No. 236. Cerebral swelling and necrosis of Peyer's patches in typhoid fever.

large intestine fragment (ileum)
WITH the distal ileum thickened, swollen. Lymphatic follicles are enlarged, protrude above the surface of CO. The group of lymphatic follicles is necrotic. The surface resembles the surface of the brain - a cerebral swelling. In the proximal sections - ulceration, exfoliation of necrotic masses
cerebral swelling and necrosis of Peyer's patches in typhoid fever
favorable outcome - scarring, healing. Adverse - the development of complications. Intestinal complications - intestinal bleeding, perforation of an ulcer. Extraintestinal - pneumonia, purulent perichondritis of the larynx, waxy necrosis of the rectus abdominis muscles, osteomyelitis, intramuscular abscesses
ebert-Gaffka's wand (Salm. Typhi)

MACRO PRODUCT No. 237. Ulcerative necrotic tonsillitis.

organocomplex
tonsils enlarged, swollen. At the bottom are visible ulcers 1 x 0.5 cm in size, performed by necrotic masses
ulcerative necrotic tonsillitis
a favorable outcome is recovery. Adverse - pharyngeal abscess, otitis media, temporal bone osteomyelitis, neck phlegmon, brain abscess, meningitis, septicopyemia, severe intoxication, glomerulonephritis, serous arthritis, vasculitis
beta hemolytic streptococcus A virus

MACRODrug № 238. Purulent leptomeningitis.

soft part of the brain
on the outside, the gyrus and furrows are flattened. Overlay of a gray-white exudate is visible under a soft shell. The dilated full-blooded vessels are clearly visible. The soft shell is thickened, dull, saturated with a thick yellowish mass of exudate
purulent leptomeningitis (meningitis of the pia mater)
the outcome is favorable in organizing. Adverse - violation of the outflow of cerebrospinal fluid, edema, dislocation of the brain, the formation of abscesses, encephalitis, sepsis, hydrocephalus
meningococcal infection

MACRO PRODUCT No. 240. Septic spleen.

spleen
the organ is enlarged, the capsule is tense. The spleen pulp is flabby, has a red color, when carried out with a knife, it gives an abundant scraping of the substance.
spleen hyperplasia in sepsis

MACRO PRODUCT No. 242. Primary pulmonary tuberculosis complex with miliary generalization.

in the III segment, under the pleura, a focus of caseous pneumonia with a diameter of about 1.5 cm in yellow-gray color, dense (primary affect) is visible. From affect to the root of the lung, a path is made up of small, millet-grain, yellowish tubercles (lymphangitis). Regional LNs are enlarged; they are rather dry, yellow-gray in color (caseous lymphadenitis). On all fields of lung tissue there are small, about the size of millet grain, yellowish foci.
Primary pulmonary tuberculosis complex with miliary generalization.
3 options are possible for the course: attenuation of primary tuberculosis and healing of the foci of the primary complex; progression of primary tuberculosis with a generalization of the process; chronic course
causes - Mycobacterium tuberculosis

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Determination of the properties of diseases (Acute gastric ulcer. Interstitial pneumonitis. Chronic gastric ulcer. Bronchopneumonia)

O-88 Acute gastric ulcer

1) a mucosal necrochus alternates with preserved sections of the mucous membrane of the pyloric stomach,

2) foci of necrosis reach the muscle plate and submucosal layer,

3) the necrotic mucosa is saturated with hydrochloric acid hematin,

4) leukocyte infiltration of areas of necrosis and submucosal layer.

O-124 Interstitial pneumonitis

1) the condition of the interalveolar septa (thickened, lymphohistiocytic infiltration)

2) the cellular composition of the inflammatory infiltrate (lymphocytes, histiocytes)

3) the contents of the alveoli and bronchioles (protein exudate)

4) primary is inflammation of the walls of alpha

5) complications of interstitial pneumonitis: respiratory failure

Ch-26 Micropreparation Ch / 26-diphtheria colitis

1) necrosis and ulceration of the mucosa,

2) the bottom of the ulcer is represented by the submucosa,

3) the surface of the ulcer is covered with necrotic mucosa with fibrin (fragments of the diphtheria film) and leukocytes,

4) under the film leukocyte infiltration of the entire submucosal layer,

5) vasodilation and plethora (paresis).

Ch-32 Micropreparation Ch / 32 - Idiopathic ulcerative colitis (acute)

1) in the wall of the intestine, an ulcer reaching the muscle layer,

2) at the bottom of the necrotic masses, infiltrated by white blood cells,

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