Note the organ, fabric, stand up the character of the pathogue process, the date of morphologists is described by the inference of ZMIN, delivering Dіignnosis, praise the character of Mozlivih accelerated at Dania Patologia.
List of Ecameniyiy Mіkropreparatіv
1. Granist dystroof
2. Zhirov Infіltratzіya Pechinka (Sudan-s)
3. Antrocosis of Long
4. Casominia necrosis
5. Calcenosis of the age valve
6. Nabeer Len
7. Muscat Pechinka
8. Hemoragіchnya Іnfark Light
9. Figrinition pericarditis
10. Abscess Pechinka
11. Мілірний tuberculosis
12. Zarosista Gіpoplasia Endometer
13. Atrophia Shkiri.
14. Flat Cancer Cancer Z Orogin
15. Intrakanal_kulurna Fіbroademon
16. Fіbromіom.
17. Gigantskoclіtinna Sarkoma
18. Nirque at leukemia
19. L_mfognulmatosis
20. Mієєloma
21. Adenokarcinoma
22. Postinfarc Card_osclerosis
23. Bearding Judocarditis
24. Krucious pneumonіya
25. Gpostatichna Pneumonia
26. Chronichna diversulus Slunk
27. FLEGMONOSNY APENDISIT
28. Cyros Pechinka
29. Sleeping Nirkova lack of
30. Amіloїdoz Nirka
31. Abortion
32. Kolojezhy goiter
33. Tuberculous Gorbiton.

1. Ecamena Namіinі Macropreparati
1. Warving in brass head
2. Atherosclerosis Aorta
3. Rimschen nirque
4. Ishіchnya Іnfart Nirki
5. Metastasis Cancer Less
6. FIRRININE PERIKITARD ("Wolokhant Hell")
7. Fracking Trombus L_VOV resorting
8. GUMA SERZA (SIFІLITICHN)
9. Toxic Peat Distrophy
10. Cancer Slunku.
11. Erozії І GRUPIA Sluncu
12. Chronichna Vibrant Slunk
13. Galіnos Capsules Selezinki
14. Diecenier Kolіt.
15. Cheress Tiff
16. Gangrena Kishka
17. G_PERTROFIY MIOKARDU
18. Abscess Pechinka
19. Ishіchnya Іnfart Selezinki
20. MI TRANSIONS STEZEN MOTSA
21. Tsiros Pechinka
22. AmіlojdnolіPyptic necrosis
23. Metastasi cancer in Selezіntz
24. Muscat Pechinka
25. Chronіchni Abscess Light
26. Bura Atrophia Mіokard
27. PriTynkoviy thrombosis arteriy
28. Fіbromіomom Mattik
29. Puchisters Zanis
30. F_Bronzno-Cavernous Tuberculosis Light
Scheme Description Macropreparation
1. Apply the Organ
2. Visnochiti yogo sovnіshniy Visigands: Coliri, Rosemiri, view of the surface, Yakschko, Yakovnina - Shaust.
3. Visnochiti the nature of the pathologic process: Lockalizatsiya, Zovnіshnі Means, Rippovyujnіst, Klіniko-Anatomіchnі characteristics, Mozdalі Acceptance at Dani Patologia, Put the Diagnosis.
Described to ELECTRONOrovograms
Visitati the character of the pathogue process with Zakhvorniyi, Applicat Nab_lsh is characteristic of the ultrastructural process, meaning a pathogue process.

1.Crevel to the brain.
This macropreparation is the brain. The form of the organ is preserved, dimensions are not increased. Brain pale yellow color, the boundaries between white and gray substance. On the cut, the small inclusions of the brown color with a diameter of 1 mm are visible., Light brown elongated areas (5x7 and 4x11 mm) are located in the area of \u200b\u200bthe cortex of the cut. At the bottom of the cuts are a large spot with a diameter of 7 cm. With unevenly distributed coloring. Sections of dark brown color with blurred boundaries alternate with lighter. The zone is well deliberate from the surrounding fabric.
These pathological changes could develop with:
1) break;
2) corrosion of the vessel wall, which led to massive bleeding and hemorrhagic impregnation of the brain tissue (hemorrhage section of heterogeneous -\u003e partially cell elements are stored).
Small inclusions of brown color are point hemorrhages from the veins that occurred when cutting.
Light brown areas - the result of increasing the permeability of the wall of the vessel, developed as a result of angioedema disorders, changes in microcirculation, tissue hypoxia. Deal or corrosive vessels could occur as a result of atherosclerosis, necrosis, inflammation, sclerosis, malignant tumor.
Exodus:
1) favorable: blood dissipation; The formation of cysts at the site of hemorrhage, encapsulation or organization.
2) unfavorable: death as a result of the defeat of vital centers; Attachment infection and suppuration.
Conclusion: These morphological changes indicate a break or separating the vessel wall, which led to hemorrhagic imgusting of the brain tissue.
Diagnosis: Hemorrhagic stroke.
2. Atherosclerosis aorta.
This macropreparate is aorta. The form of the organ is preserved. The inner surface of the wall is dark brown color, buggy, intima is uneven, whitish color, its entire surface consists of tubercles and recesses. Plots of orange color with white borders are noticeable on the tubercles. Winged yellow spots with a diameter of 5 mm. On the intima, the aorta of plaques are ulcerated, which leads to the bundle of the aorta wall.
Description of pathological changes.
These pathological changes could occur as a result of a violation of fat and protein metabolism. An unregulated cellular exchange leads to the appearance of foam cells in the intima arteries, with which the formation of atherosclerotic plaques (yellow spots) is associated with the role and factors are played:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- Ethnic.
Bigcarca colors are fibrous plaques resulting as a result of germination of connective tissue in the thickness of the Derita. The spots of orange color with white border represent intramural hematomas, due to the destruction of the plaque tires or the ulceration of it during atheromatosis. White border - a plot of calcplerose; The plaques indicate that atherosclerosis progressive and the new lipoid wave launched on old changes, detachments of the part of the endothelial liner of the aorta (hanging the plot inside the vessel) speaks of separating aneurism.
Exodus:
1) favorable: regression of atherosclerosis with the flushing of lipids from plaques macrophagum resorption and dissolution of the connective tissue;
2) unfavorable:
a) thrombosis;
b) thromboembolia;
c) embolism atheromatous masses or slices of sex;
-\u003e heart attack and gangrene
d) the aortic aortic aneurysm ~ "death from acute anemia.
Conclusion: The data of morphological changes of the aortic wall indicate dystrophic changes in the intima aorta, followed by the growth of the wall and complications that underlie atherosclerosis of the aorta.
Diagnosis: progressive atherosclerosis of aorta. Stratifying aneurysm.
3. Secondary-shredded kidney.
This macropreparation - the kidney form of organs is preserved, mass and dimensions reduced the left kidney more than the right organ of light gray color, the surface of the fine blood hemorrhage
Description of pathological changes
These pathological changes could develop primarily due to sclerosis of the renal vessels - with hypertension, and secondly on the soil of inflammatory and dystrophic changes in glomes, tubes, stromas. The disease occurs in 2 stages: nozological and syndromic. Considering the small-tracting surface of the kidneys (which happens with hypertension and-glomerulonephritis). As well as the lack of hemorrhage or heart attack (in. kidneys - white with hemorrhagic wenchant and white), the cause of this disease is chronic glomerulonephritis. Which in the I stage leads to glomerosclerosis, and in stage II - the blood flow unit at the level of glomers leads to ischemia of the kidney substance -\u003e progression of parenchyma and sclerosis of the kidneys - »Kidney wrinkling (chronic renal failure)
1) Chronic submodymia is conducive to the use of regular hemodialysis,
2) adverse death as a result of chronic renal failure and its consequences
Conclusion These morphological changes indicate a structural restructuring of the renal tissue and the substitution of its parenchyma of the connective tissue
Diagnosis of the secondary-wrinkled kidney chronic glomerulonephritis.
4. Infarction kidney.
This macropreater is a kidney. The form of the organ is preserved, mass and dimensions are not increased. The cut is visible with a cortical and brainstant. Significant sediments of adipose tissue in cups and lobby kidneys. In the cortical substance, multiple sections of whipped color 1x0.5 cm. The granules of some of them are dark brown. Organ of light brown color.
These pathological changes could develop as a result of a long spasm of the vessels of the functional tension of the organ under conditions of insufficient blood supply, atherosclerosis, thromboembolism or renal arterial thrombosis. The kidney substance ischemia leads to necrosis (ischemia\u003e Hypoxia\u003e Violation of metabolism\u003e Dystrophy\u003e Necrosis), the morphogenetic mechanism of which is a decomposition, and biochemical - protein denaturation\u003e necrosis coagulative as a result of ischemias\u003e Ischemic infarction (white sites). A hemorrhagic whisk is formed around the necrosis zone, as a result of a sharp expansion of spasped vessels. The vessels are overflowing, there are diapelline hemorrhages (granules of white plots of brown color).
Exodus: 1) favorable:
a) autolysis and necrosis regeneration;
b) the organization and education of the scar; 2) unfavorable:
a) death as a result of acute renal failure in a heart attack;
b) death as a result of chronic renal failure in the organization of infarction, the formation of scars or the development of nephrosclerosis.
c) purulent melting.
Conclusion: These morphological changes indicate dystrophic and necrotic processes in the cortical substance of the kidneys due to a violation of blood supply.
Diagnosis: kidney infarction.
5. Cancer metastasis in the lungs.
This macropreparation is light. The form of the organ is preserved. Easy to cut brown with multiple dark point inclusions, inside the whorescent color, rounded shape, diameter 3-5 mm. Light inhomogeneously: bronets of light gray 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 genes of the epithelial cell, which could contribute to such factors as inhalation of carcinogenic substances (cigarette smoke), especially since in a light small inclusions of dark gray color, which can represent soot, dust and are especially pronounced In smokers and miners. In addition to smoking, the prerequisites for changes in the cell genome can create chronic inflammatory processes, a light infarction, as hyperplasia, dysplasia and epithelia metaplasia develop on their basis. Conditions for these changes often occur in the scar.
The multiple stains of the rounded form represent the accumulation of tumor cells, it is likely to be peripheral cancer, as evidenced by the diffuse location of the spots. Point inclusions in cancer bugs represent areas of hemorrhages.
Exodus:
1) favorable.
In the initial stage of the lung cancer, it was still possible in the case of elimination of cancer cells due to a strong immune response or determined the slow growth of the tumor; 2) Adverse - death.
a) Hematogenic and lymphogenic metastases (in 70% of cases).
b) Complications associated with necrosis of the tumor, the formation of cavities, 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 on the pulmonary fabric.
Diagnosis: lung cancer. Tumor progression.
6. Fibrinous pericarditis.
This macro-preparation is a heart enclosed in a window-shaped bag.
The form of the organ is preserved, dimensions. Domestically increased. Epicard dwarf gray, grungy, covered with fibrin light brown. Hemorrhage and necrosis. Fibrin is more pronounced on the front wall of the right ventricle
Descriptions of pathological changes.
These pathological changes may develop with rheumatic diseases with heart damage. In cardiac leaflets, the disorganization of connective tissue, vessel damage and immunopathological processes is developing. The increased permeability of the vessels in the exudation stage leads to the "rugbery" of fibrinogen for their walls and the formation of the "hairy" heart.
Exodus:
1) favorable:
a) dissolving fibrin;
2) Adverse: obliteration of the cavity of the heartfelt and the occurrence of the connective tissue formed in it (shell heart).
CONCLUSION: These morphological changes indicate that dystrophy and exudative fibrinous inflammation have evisted in rheumatism.
Diagnosis: fibrinous pericarditis (hairy heart).
7. Ball-shaped thrombus of the left atrium.
This macropreater is a heart. The form of the organ is preserved, the mass and dimensions are increased due to the thickened wall of the left ventricle (the thickness of the yield is up to 2.5 cm.). The organ of light gray, the subepicarudual fat is moderately developed. There are no hemorrhage and necrosis. The consistency is compacted, chords are shortened, the nobble muscles and the tracules are increased in volume. In the left atrium cavity, the formation of a round shape, dark gray, diameters of 5 cm. Dense consistency, which occupies the entire cavity of the left atrium. Sash mitral valve Enlarged and thickened, they have grown. On the endothelium valve thrombotic overlay.
Description of pathological changes.
These pathological changes are developing as a result:
a) endocarditis of the mitral valve;
b) deceleration and blood flow disorders;
c) violation of the relationship of coagulation, antoslude and fibrinolytic systems;
d) change of rheological properties in the blood.
As a result of the inflammation of the valve, the endothelium desquamation occurred, which led to pre-trombosis as well as to thickening and sclerosing the mitral valve and their battle. In this drug, the stenosis of the valve is combined with its insufficiency, with which the latter prevails. This is due to the fact that during the systole of the ventricles, blood is thrown not only in the aorta, but, as a consequence of the deficiency of the mitral valve, in left atrium. Consequently, during the diastole in the ventricle, an increased amount of blood flows, which determines its hypertrophy and tokogenic expansion of the heart in the left ventricle - blood stagnation in the left atrium - the formation of a stagnant mixed thrombus-separation of it and the collar in the left atrium cavity.
Exodus:
1) Relatively favorable: Organization with subsequent sewage and reconciliation. The connecting tissue is growing into a thrombus from an endocardium.
2) unfavorable: death. Thrombus of such sizes, which overlaps blood flow into the left ventricle.
Conclusion: These morphological changes indicate the development of an inflammatory sclerotic process in a mitral valve, accompanied by a circulatory impairment and the formation of a pre-tromba and its subsequent separation.
Diagnosis: Mitral combined heart disease. Stenosis mitral hole With deficiency of the mitral valve. Frame thrombus.
8. Gumma Hearts *
This macropreater is a heart. The form of the organ is preserved, the mass and dimensions are increased due to the thickened wall of the left ventricle (up to 3 cm.). These chords are thickened, the puffy muscles are increased. Endocardian yellowish color, piccardial fat moderately developed. Valve Aorta Intacten. In the wall of the left ventricle, there is a 5x4x3 cm deepening, on the inner surface of which there are spots of yellow, orange and dark gray, as well as gential and whitewastered areas. At the lower edge of the deepening, the imposition of thrombotic masses is noticeable.
Description of pathological changes.
These pathological changes could develop as a result of infection with sex or incomplete pathway, the causative agent of syphilis. The acquired syphilis passes in three periods - primary, secondary, tertiary (or gummime), which is presented on the preparation. The first period arises against the background of increasing sensitization and is manifested by a solid chancro on the mucous membrane at the site of the introduction of the treponama and involvement in the process of the lymphatic system. The second period is a period of hyperairgia and generalization, characterized by the appearance of syphilizes and an increase in or ecreation of lymphatic follicles. In these places there is inflammation. After 3-6 years, the third period occurs in the form of chronic diffuse interstitial inflammation and the formation of GUMM, which represent the focus of syphilitic productive necrotic inflammation, syphilitic granuloma. In this case, the visceral syphilis led to the impact of the heart in the form of a gummime myocarditis. The inflammatory process is asked to deep into the myocardium, necrotized masses are washed out of blood flow, the zone is limited to demarcation inflammation. There are clusters of lymphoid, plasma giant Pyrogov-Langhans cells, fibroblasts. Specific inflammation leads to scarring and ends with the development of massive cardiosclerosis. Atherosclerosis is enjoyed on the area of \u200b\u200bspecific changes, with which yellow, white, orange spots are connected, as well as the joined thrombotic overlaps.
Exodus: 1) favorable.
a) was possible in the treatment and elimination of the pathogen to major changes in the bodies;
b) a long course of the process when it compensation;
2) Adverse: Cardiosclerosis\u003e Development of chronic heart failure, first hypertrophy: tall, and then miogenic, delegation of left ventricle\u003e Blood stagnation in the left ventricle\u003e In the left atrium\u003e in lung.
Death - as a result of a pulmonary heart. Conclusion: These morphological changes indicate a specific inflammation of myocardium to form a gum of the heart.
Diagnosis: syphilis visceral. Gumma hearts.
9. Toxic liver dystrophy.
This macropreparation is a liver. The form is preserved, mass and dimensions are reduced. Yellow liver.
Description "Pathological changes.
These pathological changes could develop as a result of intoxication,
Allergic or viral lesion of the liver. In the body develops fat (yellow)
dystrophy. Dystrophy spreads from the center to the periphery of the Polek. It is replaced by necrosis and autolytic
The collapse of hepatocytes of the central departments. Zimbelkova dedrita phagocytestation, while
The reticular stromter is taken with extended vessels (red dystrophy). Due to the necrosis of hepatocytes, the liver is wrinkled and decreases in size.
Exodus:
1) Favorable: transition to chronic form.
2) unfavorable: "a) death from hepatic or. Renal failure;
b) post-necrotic cirrhosis of the liver;
c) defeat other organs (kidneys, pancreas, myocardium, central nervous system) as a result of intoxication.
Conclusion: These morphological changes indicate fatty dystrophy of hepatocytes and their progressive necrosis.
Diagnosis: liver toxic dystrophy. Stage of yellow dystrophy.
10. Cancer stomach.
This macropreparation is a stomach. The form and sizes of the body are changed due to the growth of whiteish yellow tissue, which sprouted the wall of the stomach and significantly thickens it (up to 10 cm or more). Reliefs of the mucosa is not expressed. In the central part of the growing, the deepening, bursting and testing sites - ulceration are visible.
Description of pathological changes.
These pathological changes could develop as a result of precancerous states and precancerous changes (intestinal metaplasia and heavy dysplasia).
In the foci of changing the epithelium, the cells of the cells and the development of tumors (or cancer develops (DE NOVO). Guided by a macroscopic picture, it can be said that this is a cancer with mainly endophic infiltrating growth - infiltrative-ulcerative cancer (tumor ulcerations). Histologically To be like adenokartomoma and undifferentiated cancer. Progression, the tumor germinates the wall of the stomach and thickens it significantly.
Exodus: 1) favorable:
a) the slow growth of cancer;
b) high-efficient adenocarcera;
c) later metastasis;
2) unfavorable: death from exhaustion, intoxication, matastases; the spread of cancer beyond the limits of the stomach and germination to other organs and fabrics, secondary necrotic changes and the decay of kartscents; Violation of the function of the stomach.
Conclusion: These morphological changes indicate a mutational transformation of epithelium cells with their malignation and subsequent tumor progress, which in infiltrating growth led to germination of the stomach wall with ulcenes, which can represent secondary necrotic changes and the disintegration of the tumor.
Diagnosis: Infiltratively ulcerative gastric cancer.
11. Erozia I. sharp ulcers stomach.
This macropreparation is a stomach. The form and sizes of the body are preserved, the mass has not changed the organ of whisen color mucosa of the black color of the formations of a dense consistency. Among the numerous small diameter of 1-5 mm. There are also larger diameter of 7 mm., As well as 8x1 cm., 3x0.5 cm. Consisting of a spilled formation with a diameter of 5 mm. About one of them we see the formation of a triangular shape, the boundaries of which have pronounced differences from the gastric mucosa, so they are formed by a connective tissue.
Descriptions of pathological changes.
These morphological changes could develop as a result of exogenous and endogenous impacts: violation, nutrition, harmful habits and harmful agents, as well as autoinfection, chronic autoinoxication, reflux, neuro-endocrine, vascular allergic lesions. Since lesions are localized in the foundal department, we can talk about an autoimine process with lesions of the shepherd cells, which led to dystrophic and necrobiotic changes in the epithelium, violation of its regeneration and atrophy. Probably, in this case, chronic atrophic gastritis with atrophy of the mucous and its glands developed. Defects of mucosa lead to erosion, which is formed after hemorrhage and rejection of dead fabric. Black pigment in the day of erosion is a salt-sour hematin. To these changes join the restructuring of the epithelium. Education, the boundary of which is formed by the mucous membrane and is healing the acute stomach ulcers by scarring and epithelization.
Exodus: 1) favorable:
a) healing of acute ulcers by scarring or epithelization;
b) inactive chronic gastritis (remission);
c) easily or moderately pronounced changes;
d) epithelization of erosions; 2) unfavorable:
a) the development of chronic ulcerative disease;
b) Malignization of epithelium cells;
c) pronounced changes;
d) active pronounced gastritis.
Conclusion: These morphological changes indicate long-lasting dystrophic and necrobiotic changes in the epithelium of the mucous membrane with a violation of its regeneration and the structural adjustment of the mucous membrane.
Diagnosis: chronic atrophic gastritis, erosion and acute stomach ulcer
12. Chronic stomach ulcer.
This macropreparation is a stomach. The masses and size of the organ normal, the form is preserved. Light gray organ, relief is strongly developed. At the low curvature of the stomach in the pyloric department, a significant recess in the wall of the stomach 2x3.5 cm. Its limiting the surface of the organ is deprived of the characteristic folding. The folds are converted to the borders of education. In the area of \u200b\u200bthe pathological process, there is no mucous, submembricted and muscle layers of the stomach wall. Bottom smooth, performed serous sheath. The edges roluit are raised, dense, have a different configuration: the edge addressed to the gatekeeper, gentle (due to the peristalsis of the stomach).
Description of pathological changes.
These pathological changes could develop in the rescue "Ltate common and local factors (general: stressful situations, hormonal violations; medicinal; Harmful habits that lead to local disorders: the hyperplasia of the ferrous apparatus, an increase in the activity of the acid-peptic factor, an increase in historical, an increase in the number of gastrosis cells; and general impairment: the excitation of subcortex centers and the hypothalamic-pituitary area, increasing the tone wandering nerve, enhancement and subsequent exhaustion of the production of ACTH and GLCCARTICIDS). Driving on the gastric mucosa, these violations lead to the formation of the defect of the mucous membrane - erosion. Against the background of non-healing erosion develops acute peptic. A ulcer, which, with continued pathogenic effects, goes into a chronic ulcer, which takes place periods of exacerbation and remission. During the period of remission, the bottom of the ulcers can be p / outdoor with a thin layer of the epithelium, layering on a scar cloth. But during the exacerbation of "healing" is leveled as a result of fibrinoid necrosis (which causes damage not only directly, a and by fibrinoid changes in the walls of the vessels and violation of tissue trophics).
Exodus:
1) Favorable: remission, healing of ulcers by scarring with subsequent epithelization.
2) unfavorable:
a) bleeding;
b) running;
c) penetration;
d) malignancy;
e) inflammation and ulcer-scar processes.
Conclusion: These morphological changes indicate a destructive process in the stomach wall, which leads to the formation of a defect of the mucous, submucosal and muscle shell - ulcers.
Diagnosis: chronic stomach peptic disease.
14 Dysenteric colitis
This macropreparation is a fat intestine. The form of the organ is preserved, the mass and dimensions are increased by thickening the wall. The mucous-gray mucosa, on top of the folds and between them, the film imposition of brown-green color covering the mucous mass is necrotic, ulcerated, in many places freely hang in the intestinal lumen (which is narrowed).
These pathological changes could develop as a result of an acute intestinal disease with a preferably lesion of the colon, the cause of which was penetration, development and reproduction in the epithelium of the mucous membrane of Bacteria Shigell and their species. This group of bacteria has a cytoplasmic effect on these cells, which is accompanied by the destruction and declaration of the latter, the development of the deskvatamative cathar. Enterotoxin bacteria performs a vaselyroparalic effect with which paralysis is associated with blood vessels Strengthening exudation, as well as damage to intramural nerve ganglia, which leads to the progression of processes and the development of fibrinoid inflammation (as a result of increasing the pebornation of fibrinogen from extended vessels). If in the first stage we find only surface necrosis of hemorrhage, then a fibrinoid film appears on the top of the top and between the folds. The necrotic masses of the mucosa are permeated with fibrin. Dystrophic and necrotic changes in nerve plexuses are combined with infiltration by leukocytes of mucous membranes and submucosal, its edema, hemorrhages. With the further development of the disease in connection with the rejection of fibrin films and necrotic masses, ulcers are formed, which for 3-4 weeks of the disease are filled with a granular tissue, which matures and leads to the regeneration of the ulcers.
Exodus
1. Favorable
a) complete regeneration with minor defects b) abortive form
2. Adverse
a) incomplete regeneration with the formation of scars1 ^ narrowing of the intestine
B) chronic dysentery
c) Lymphadenit
Oh!) Follicular, Folicular-ulcerative colitis
(e) Heavy general changes (necrosis of the epitlyan channels of the kidneys, health dystrophy and liver, disorders mineral exchange)
Complications
A. Perforation of ulcers: peritonitis, paraproctitis,
V. Flegmon
S. Intraniful bleeding
Extra case complications - bronchopneumonia, pyelonephritis, serous arthritis, liver abscesses, amyloidosis, intoxication, exhaustion
Conclusion: These morphological changes indicate a division of the colon associated with toxic exposure Shigell
Diagnosis of dysentery and colitis. Difteric colitis stage.
15. Abdominal tit.
This macropreparation is the ileum. The form of the organ is preserved, the mass and dimensions are normal. The intestine of whiskers, expressed folding of the mucous membrane, on which 4x2.5 cm formations are noticeable. And 1x1.5 cm., Which protrude above the surface of the mucous membrane. They are noticeable to the grooves and gyrus, the surface itself is uneven, loosened. These formation of dirty gray. Noticeably formation with a diameter of 0.5 cm., With a loss of characteristic folding, whitish color, slightly in-depth and compacted.
Description of pathological changes.
These pathological changes could develop as a result of infection (parhengteral) abdominal chopstick and reproduction of them in the lower division of the small intestine (with the release of endotoxin). On lymphatic paths -\u003e in Peyer plaque -\u003e Salitarian follicles - »Regional lymph nodes -\u003e Blood -» Bacteriamia and bacteriochalia
-\u003e In the intestinal lumen -\u003e hyperairgic reaction in follicles, which leads to the increase and swelling of follicles, the spike of their surface. This occurs as a result of proliferation of monocytes, histiocytes, reticulocytes, which go beyond the follicles to the subject layers. Monocytes are converted to macrophages (abdominal cells) and form accumulations - cut-off-nepophotic granulomas. Catarial enteritis joins these changes. With the further progression of the process, the abdominal granulomas is necrotized and the zone of demarcation inflammation sequestration and the rejection of necrotic masses leads to the formation of "dirty ulcers" (as a result of the impregnation of bile), which over time change their form: the edges are cleared of necrotic masses. The growth of granulation tissue and its ripening leads to formation in their place of gentle logs. Lymphoid tissue is restored. Exodus:
1. Favorable:
- complete regeneration of lymphoid tissue and healing of ulcers;
2. Adverse:
- death as a result of intestinal (bleeding, sprinkling ulcers, peritonitis) and extra integne
Complications (pneumonia, osteomyelitis, intramuscular abscesses, sepsis, wax
Necrosis of straight abdominal muscles):
Dystrophic changes in parenchymal organs, the formation of abdominctophosic
Granuloma.
Conclusion: These morphological changes indicate an acute infectious disease with local changes in the small intestine - Ileolite.
Diagnosis: Ileolite.
Gangrena small intestine.
This macropreparation is a plot of small intestine. Its dimensions, weight is not changed. The loops of the guts are increased, the consistency of one part is loose, the second - the surface is not changed smooth. Serous shell - dull and matte. Between loops sticky, viscous, stretching fluid in the form of threads. On the cut section of the walls are increased, the lumen is narrowed.
Possible causes: violation of blood supply as a result of the strong-comer non-contacting of the mesenteric arteries.
Morphogenesis: Ischemia, Dystrophy, Atrophy, Nursing the organ of contact with the external environment - Gangrena
Exodus: 1) Adverse - rotten melting, will respond.
Conclusion: Indirect vascular necrosis.
Diagnosis: Wet gangrene fine intestine.
18. Liver abscess.
This macropreparation is a liver. The form of the organ is preserved, mass and dimensions are not increased. Coloring dark brown. At the bottom of the organ there is a deepening of oval shape 5x8 cm, a depth of 4 cm, the inner surface of which is lined with a connective tissue. The connecting tissue is located along the border of the deepening and in close proximity to it.
Description of pathological changes. These pathological changes could develop as a result of the infectious lesion of the liver, which could be primary (independent disease) and be a manifestation of another disease. Developing excomettive purulent inflammationwhere the granulation tissue shaft is formed around the focus of the infection, the lifting cavity of the abscess and supplying tissue protection (leukocytes) to the infectious focus. Granulation fabric over time is replaced by a rough fiber connecting tissue. Capsules and acute abscess proceeds to chronic form.
Exodus: 1) favorable:
a) the elimination of infectious agents and the organization of the abscess cavity (replacement of granulation tissue);
b) chronic course of illness;
c) thickening in pus, turning it into necrotic child and petrification; 2) unfavorable:
a) generalization of inflammation;
b) breakthrough of the contents of the abscess into the abdominal cavity with the formation of a failure or into the lungs;
c) lymphogenic and hematogenous distribution - septiconium.
Conclusion: These morphological changes indicate infectious liver damage to the development of exdivalent inflammation and the formation of an abscess.
Diagnosis: hepatitis. Liver abscess. _
17. Myocardial hypertrophy.
This macropreap-headed hearts is increased due to the ending path, bringing the tract is not changed. The wall of the left ventricle is thickened. There are no traces of necrosis and hemorrhage.
Descriptions of pathological changes.
Visible changes indicate an increase in the mass of sarcoplasm of muscle cells, the size of the nucleus, the number of myofilms, the size and number of mitochondria, i.e. Intracellular ultrastructures hyperplasia. In this case, the volume of muscle fibers increases. At the same time, hyperplasia of fibrous structures, stroma, which should be considered as the strengthening of the connective mounted frame of the intense working heart hypertrophy elements of the nervous heart of the heart
The development of these changes contributes to mechanical factors that prevent the stream of blood, the attack of the neurohumoral influence. These processes led to providing the necessary functional level of general blood circulation. In the future, dystrophic changes will arise in hypertrophy cardiomyocytes, the contractile ability of myocardium gradually weakens, which will lead to the development of cardiac decompensation.
Diagnosis: myocardial hypertrophy
The described phenomena reaches a small extent when the valve shutdowns accompanied by stenosis of atrioventricular holes and the ventricular vascular tracts in this case, the aortic valve is observed due to the rheumatic process, the development of stenosis and the endocardium hyalinosis, which led to the treasure and deformation of the valve sesters
20. Combined mitral heart disease.
This macropreater is a heart. The form of the organ is preserved, the mass and dimensions are slightly increased. Subpiccardial fat are strongly developed. Fat layers are located in myocardium. The lumen of the mitral valve is sharply narrowed. The imposition of thrombotic masses are noticeable on its sash. Light gray organ. Description of pathological changes.
These pathological changes could develop as a result of inflammatory processes of the mitral valve - endocardits, the cause of which could be rheumatic, septic or atherosclerotic diseases. In the proliferation stage of the valve sash thicken, the sclerosyports and grow together, which leads to a narrowing of the lumen. The blood current and the formation of thrombotic masses on the modified valves arise. Compensatory devices are aimed at providing blood current, 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 a myogenic expansion of the leftopean cavity, as well as dystrophic processes in cardiomyocytes (fatty dystrophy). Developing blood stagnation in the left atrium -\u003e venous stagnation in the lungs - "The pulmonary heart -\u003e death from acute heart failure. Exodus:
1) favorable: compensation;
2) unfavorable:
- death from acute heart failure;
- formation of a stagnant thrombus in the left atrium;
- infarction as a result of hypertrophied myocardial ischemia;
- Inflammation of the lungs due to venous stagnation.
Conclusion: These morphological changes indicate inflammatory processes of the mitral valve with the development of stenosis diagnosis: combined mitral heart disease.
19. Ischemic infarction spleen.
This macropreparation is a spleen form and dimensions are not changed. The color is non-uniform - in general, it is a brown-red, but from the gate to the periphery of the organ, two parts of 1 -2 cm wide are stretched. More pale color. The surface is smooth, without breaks, hemorrhage, scars.
Description of pathological changes.
These pathological changes indicate that their reason was a sharp impaired blood circulation in the large branches of the lionenpy arteries, which led to ischemia a significant portion of the parenchyma spleen and later to the heart attack. The heart attack in the spleen is most often white, less often - white with a hemorrhagic wedge, which is due to the peculiarities of the angioarchitectonics of the body in this case, it is most likely white, since necrotic sites are characteristic and clearly excluded from intact sections of organs.
Exodus:
1) favorable:
a) scarring and replacement of necrotic tissues;
2) unfavorable:
a) the gap of the capsule of the organ and intra-abdominal bleeding;
b) death from shock;
c) intoxication and agogammunization of decay products (resorption-necrotic syndrome), which aggravates the position.
CONCLUSION: These morphological changes indicate sharp discirculatory changes in the Branch of the spleen artery branches leading to the development of heart attack
Diagnosis: acute ischemic spleen infarction.
21. Cirrhosis of the liver.
This macropreparation is a liver. The form of the organ is preserved, the mass and dimensions are reduced. The capsule is thickened, the surface of the organ is large bore, the color of the whores-redhead, the right share is darker.
Description of pathological changes.
These pathological changes could develop as a result of dystrophy and necrosis of hepatocytes. What led to an increase in the regeneration of hepatocytes and the formation of regenerate nodes surrounded by a connecting tissue from all sides. The death of hepatocytes stimulate the growth of connective tissue (due to cell hypoxia inside the nodes). The capillary of sinusoids of false poles occurs, and Hypoxia coming after this leads to a new wave of dystrophy and necrosis. Loading cellular insufficiency is connected with these phenomena. Regenerate nodes are subjected to diffuse fibrosis (large-born liver), which is associated with necrosis of hepatocytes and hypoxia, as a result of blood vessels, their sclerosis, the capillary of sinusoids, the presence of intrahepatic port-caval shunts. This activates fibroblasts, kraper cells and increases the products of the connective tissue. Sclerosis of the convertible fields and hepatic veins leads to portal hypertension. As a result, the portal vein is unloaded not only through intrahepatic, but through extrahepatic anastasms.
Exodus:
1) favorable: compensated cirrhosis;
2) unfavorable: death from hepatic cellular insufficiency, complications in the consequence of portal veins hypertension: ascites, varicose extensions and bleeding from the veins of the esophagus, stomach, hemorrhoids, peritonitis, sclerosis, cirrhosis, thrombosis. Jaundice, hemolytic syndrome, splenomegaly. Hepatoric syndrome, cancer.
CONCLUSION: These morphological changes indicate a post-crude mesenchymal-cell liver reaction with the development of a vicious circle: a block between blood and hepatocytes, which leads to the structural restructuring of the body.
Diagnosis: postnurotic cirrhosis of the liver.
23. Cancer metastasis in the spleen.
This macropreparation is a spleen (on the cut). Dimensions are not changed, the form is normal. The surface is smooth with small areas of the pests. On the section - multiple white-pink round spots with a diameter of 3-15 mm. Where stains closer to the surface, they "protruding" it and form the aforementioned bugness.
Description of pathological changes.
These pathological changes indicate that a malignant tumor increases in the body and its metastasis. The most likely metastasis of adenocarcene. We are the uterus. Cancer cells multiply form indicated spherical white-pink clusters.
Exodus:
1) Favorable: extension of the life of the patient as a result of complex chemophole-beam treatment of tumor and metastases.
2) unfavorable:
- cachexia;
- impregnoric bleeding;
- progression and further metastasis;
Conclusion: These pathological changes indicate tumor progression and tumor metastasis.
Diagnosis: adenocarcinoma. Remote Matastases.
24. Muscat liver.
This macropreparation is a liver. Mass and sizes are reduced, the form is saved. The color of the organ on the section is motley, gray-yellow with a red grip, and the re-arrangement increases to the periphery. The liver is littering, the bugness increases to the periphery.
Description of pathological changes.
These pathological changes could develop as a result of an increase in pressure in the veins of the liver, which is possible with general (chronic right-minded failure) or local venous stitch (inflammation of hepatic veins, thrombosis of their lumen). At the same time, the central veins are expanding, which leads to dystrophy and necrosis of adjacent hepatocytes and the expansion of sinusoids. They contain uniform elements to the center, and on the periphery-gloss (due to an increase in pressure at the arterial capillary placement site)\u003e Plasmorragia, diapered hemorrhage. As a result of stagnation venous blood \u003e Hypoxia\u003e Synthesis of the connecting tissue of the Krafera cells - the formation of the basal membrane and the transformation of the Sinooid in capillary\u003e hypoxia. In the central departments of rally, fatty dystrophy (decomposition) is developing up to necrosis. Because of the complete regeneration in the field of hepatocytes, connective tissue is grouped\u003e Sclerosis. Venenous stagnation\u003e Hypoxia\u003e Thickening of the connective tissue of the liver (interdolkaya and in the course of triad). The remaining peripheral hepatocytes surrounded by the connective tissue, begin to multiply. False slices are formed, the blood supply is extremely poor\u003e hypoxia, dystrophy\u003e necrosis of hepatocytes.
Exodus:
1) favorable: chronic course of the disease; elimination of the causes of venous full-board;
2) Adverse: death from hepatic insufficiency, cancer, formation of sclerosis and portal hypertension, attachment of infection, jaundice and t.
CONCLUSION: These morphological changes indicate the venous physique of the liver and developed on this soil of hypoxia, which leads to a structural restructuring of the body.
Diagnosis: Muscade liver cirrhosis.
25. Chronic lung abscess
This macropreparation is easy. The organ at the cut of inhomogeneous consistency. The color is, with dense inclusions of the whorescent color, the incision passes perpendicular to many bronchmas of different caliber. The connecting tissue is expressed, separating the lungs 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 is a whorescent fabric. The inner surface of the cavity is also lined with this cloth.
Description of pathological changes.
These pathological changes could develop as a result of inflammatory diseases of the lungs or bronchiectasis. What is unlikely, since then we would see multiple cavities. With inflammation of the lungs of any ethnology, the fabric, which was subjected to necrosis, and then suppuration, turns into a purulent-necrotic mass, which is released through bronchi with the wet. The cavity of the acute abscess was formed if the cause of the suppuration is not eliminated, the granulation tissue first formed around the cavity is replaced by a rough fiber connecting tissue, which shrinks the abscess from the lung parenchyma. Dense connective tissue whipped inclusions that are many in the pulmonary tissue are characteristic of chronic abscess, when not only bronons are involved in the process, but also lymphatic drains, which are propagated by purulent inflammation.
Exodus:
1) Favorable: Organization, encapsulation.
2) unfavorable: fibrosis and deformation of the lung tissue, due to the spread of purulent inflammation.
Conclusion: These morphological changes indicate that inflammatory processes in the pulmonary tissue led to the development of acute abscess with the transition to chronic.
Diagnosis: chronic lung abscess. Exudative purulent inflammation.
27. Priest blood thrombus artery.
This macropreparation is the abdominal aorta. The form of the organ is preserved, dimensions are not increased. Light gray organ. The intimiment shows the formation of a dark gray color with a diameter of 5 mm. With an uneven surface, and next to it, the formation of the same consistency and colors is 3x1.5 cm. This formation is located at the place of branching aorta.
Description of pathological changes.
These morphological changes could develop in the rescue "Ltate disorders of fat and protein exchange, which contributed such factors as:
- alimentary;
- hormonal;
- nervous;
- hemodynamic;
- vascular;
- hereditary;
- Ethnic.
The unregulated cellular exchange of cholesterol leads to the formation of foam cells and the further development of atherosclerotic changes that we see on the intima aorta: fat stains, fibrous plaques, the formation of thrombotic overlaps on the site of the plaques ulceration. In the formation of thrombotic impositions (the formation of dark gray color of dense consistency), sections are taken not only of violations of the vascular wall, but also with a circulatory impairment, blood composition, vascular wall, a violation of the regulation of coagulation, antoslude and fibrinolytic systems.
A particularly important factor in this case is a violation of blood circulation in the form of a blood flow of blood at the bifurcation site of the abdominal aorta. This is a slowdown in blood current and contributes to the imposition of thrombotic masses on an ulcerated sex.
Exodus: 1) favorable:
a) aseptic autolysis thromba;
b) organization; 2) unfavorable:
a) petrification;
b) thromboembolia;
c) septic melting;
d) Obbitation of the aorta lumen.
Conclusion: These morphological changes indicate dystrophic changes in the intima aorta, which, together with a blood flow, created prerequisites for thrombosis.
Diagnosis: thrombosis aorta.
Fibromomomomomoma of the uterus.
This preparation is a uterus. Dimensions and weight are significantly increased due to tumor nodes. Blessed color yellow. Two nodes of the tumor tissue are visible: the first is located inside the myometrium of the body of the uterus (closer to the endometry), the diameter of 2.5 cm; Another in the bottom of the uterus, germinates the outside of the organ. The dimensions of this node 10-12 cm., Rounded shape, dense consistency. Foci of necrosis and hemorrhage is not observed.
Description of the pathological process
This pathological process is polyethological, but the most probable reason are disharmonal disorders. Supply stages are prepubropeous changes, among which there are so-called background changes that are manifested by dystrophy, atrophy, hyperplasia. Hyperplasia is considered as a prematurity process. The stage of development of the tumor: diffuse hyperplasia, a focal hyperplasia, a benign tumor. The tumor is presented in this preparation by smooth muscle cells. Since the sturge of the tumor is well developed - it is called a fibromy. In the uterus, depending on the localization, intramural, subseasonous and submembratus misa differ.
Complications: Developed Used under the endometry often cause small uterine bleeding, which even after themselves, not dangerous for life after a while lead to the development of anemia (iron deficiency with relevant consequences). Malignation.
Conclusion: These morphological changes indicate the development in the disharmonary elements in the uterus.
Diagnosis: fibromyoma of the uterus.
29. Bubble skid.
This macropreater is represented by a set of cyst resembling grapes (matte color) and a diameter of 0.5 to 1.5 cm. These spherical bubbles are located (as if they grow and hang in a clouded dome) above the sections of the yellowish fabric soft consistency - the uterus tissue. The bubble cavity is filled with transparent mucus fluid.
Description of pathological changes.
Investigating the morphology of this drug it can be assumed that this education could form in the pathology of pregnancy, with bubble drift. That is, if the placenta with the hydropic and cystic transformation of the chorion Vorsin, which is accompanied by the proliferation of the epithelium and the falling of the vigor, a sharp increase in their number and the transformation into a cluster of cyst-shaped bubbles (the fetus dies). Plots of yellow fabric soft consistency - uterus (creeps-shaped bubbles). Under the microscope (Pat. Changes), we can see that the vessels of the Village are engaged and the strong proliferation of the epithelium of these vapors occurs (both rows of pork cells are mixed randomly and form a thickening on the surface of the Vorsin). Pork can germinate deep into the wall of the uterus, destroy the vessels, causing strong uterine bleeding (Such deep and extensive rusts can occur with one of the types of bubble drift -tresting bubble drift). The clinically disease is manifested by the fact that the uterus increases much more in volume than this period corresponds to this period) "pregnancy, and uterine bleeding may appear from 2-4 months of pregnancy, and in the urine women rises 5 times the level of gonadotropin
Causes of bubble drift "Maverny disorders of harmonious homeostasis - carbonal dysfunctions due to lowering estrogen production (with the cysts of the yellow bodies of the ovary; Mutations are possible fruit eggcaused by viral infection, intoxication).
Exodus:
1) favorable: removal of all chorion vane from the uterine cavity surgically;
2) unfavorable:
a) the observation of bubble drift in chorionepithels;
b) the development of strong bleeding (uterine), which leads to the development of chronic anemia -\u003e death.
CONCLUSION: This macropreparation is a placenta with the transformation of the village of Chorion, testifies to the pathology of pregnancy; The emergence of an unlimited growth of pathologically changed elements of the placenta (due to cell mutation or with hormonal disorders in the mother's body).
Diagnosis: bubble skid.
30. FNBROSNO-Cavernous tuberculosis of the lung.
This macropreparation is easy. Serious pink organ. A porous parenchyma of the lung is visible, the stroma is represented by the connective tissue layers of whitish color. In the parenchyma, dotted black spots are visible - lung vessels. Against the background of this pattern, multiple formations of a rounded shape with a diameter of 0.5 cm are visible. Blessed color. The configuration of the slice of the lung violate the cavity in the amount of 3 pcs. The first has dimensions in length 8 cm., Width - 7 cm. Depth - 4 cm. The second is 4x3x1.5. Third - 6x5x3. Kaverns are located next to each other in a chess order.
Description of pathological changes.
These pathological changes are a manifestation of specific inflammation of the tissue of the lung caused by mycobacterium tuberculosis. In the course of an exudative reaction in lung tissue, the focus of inflammation is formed exposed to curly necrosis. Subsequently, granuloma, consisting of epithelioid cells, macrophages, lymphocytes, is formed around the necromosis. plasma cells and, characteristic of tuberculosis inflammation, Pirogov-Langhans cells, thus inflammation becomes productive. With the weakening of the resistant forces of the body as a result of an unfinished phagocytosis of mycobacteria, an exudation is enhanced, which is completed with the granuloma curls and adjacent to it fabric. There is a cavity as a result of purulent melting and the ignition of caseose. Mass, inflammation takes the form of acute cavernous tuberculosis. In the future, this process takes a chronic course. The wall of the cavity becomes dense, constructed from the following layers: internal pyrogen (necrotic), rich in disintegrating leukocytes; medium - layer of tuberculosis granulation tissue; Outdoor - connective ones, the connecting tissue grows around the cavity and between the interlayers of the connective tissue are visible sections of the lung atelectasis. Caverns communicate with bronchi. The inner surface of the cavity is uneven, with crossing it beams - transmitting bronchus or thrombizing vessel. At the presented picture of the slice of light, whimsized formations of a rounded form are foci-infiltrates of tuberculle, in a variety of stages of inflammation (exudative, productive). The process is gradually distributed in the APO-Caudal direction, descending from the upper segments to the lower, both contact path, and through the bronchum, occupying new parts of the lung. Therefore, the oldest changes (larger cavities, organized) are located above.
Exodus:
1) Favorable (unlikely) - with a significant strengthening of the resistant forces of the body, it is possible to exit a chronic course of the disease and the organization of tissue detritus with the completed phagocytosis of mycobacteria. This develops the sclerosis of the light segment, affected inflammatory process With the portions of the atelectasis of bronchi.
2) Adverse - connected with Kavernins -\u003e From the cavity of bleeding: breakthrough the contents of the cavity into the pleural cavity -\u003e pneumothorax and purulent pleurisy. The pulmonary fabric itself is subjected to amyloidosis.
Conclusion: The morphological changes described indicate the wave-like flow of the tuberculosis process.
Diagnosis: fibrin-cavernous tuberculosis of the lung.

9. What is the average for the total duration of the first three stages of the development of equity pneumonia?

10. Specify ways of spreading inflammation with a bruboral pneumonia.

11. List pulmonary complications Pneumonia caused by Streptococcus Pneumoniae.

12. Describe the composition of the exudate during shared pneumonia in the tide stage.

13. Describe the composition of the exudate during shared pneumonia in the red-compelling stage.

14. Describe the composition of the exudate during shared pneumonia in the gray legged stage.

15. Specify the extravalous complications of the equity pneumonia caused by Streptococcus Pneumoniae.

16. Give the macroscopic characteristic of lung changes at bronchopneumonia.

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

18. Name the features of pathogens of nosocomial pneumonia.

19. Name the complication of equity pneumonia, developing with excessive activity of neutrophils with massive destruction of lung tissue.

20. Indicate the complication of equity pneumonia, developing with insufficient activity of neutrophils and the development of the organization of fibrinous exudate.

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

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

23. Give the definition of the term atelectasis.

24. What is developing with the full closure of the breathing paths?

25. What is developing with a partial filling of the pleural cavity with liquid exudate?

26. What is developing in respiratory distress syndrome, due to the destruction of the surfactant?

27. Indicate the cause of the hemodynamic edema of the lungs.

28. Patient 25 years fell ill after supercooling in a state of alcoholic intoxication. It makes complaints on the rise of body temperature up to 390s, chills, dwarf pain in the right side and sharp weakness for 7 days. Objectively: over the lower share of the right lung at percussion is heard a stupid sound, with auscultation - breathing is not carried out, the noise of friction of the pleura is listened. X-ray - blackout the lower share of the right lung, in the region of the 8th segment, the cavity, the thickening of the pleura. Your conclusion.

29. In a patient with a stroke and left-sided hemiparesis for 14 days, the body temperature rose to 380s, which was accompanied by the appearance of cough and fine-grained wheezes in the lower left-handed departments. Your conclusion.

30. The man has 67 years old, which is in stationary treatment about the phlegmon of the scalp, appeared shortness of breath, cough, the body temperature up to 38.50s increased. 4 weeks after massive antibiotic therapy, the body temperature decreased, the shortness of breath decreased, a moderate leukocytosis remained. When conducting an x-ray study in the second segment of the right lung, an annular shadow appeared with the presence of a liquid level. Your diagnosis.

Event II

Chronic nonspecific lung diseases. Interstitial lung diseases. Pneumoconiosis. LUNG CANCER.

1. Diffuse chronic lung lesions: Defining concept and classification. Chronic obstructive lung diseases. General characteristics.

2. Chronic obstructive lung emphysema - definition, classification, epidemiology, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Other types of emphysema (compensatory, senile, vicar, intermediate): Clinical and morphological characteristics.

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

4. Bronchiectase and bronchiectatic disease. Concept, classification, etiology, pathogenesis, morphological characteristics, clinical manifestations, complications, outcomes, causes of death. Cartageer syndrome. Clinical and morphological characteristics.

5. Diffuse interstitial lung diseases. Classification, clinical and morphological characteristics, pathogenesis. Alveolit. Morphological characteristics, pathogenesis. Pneumoconiosis (antrake, silicosis, asbestosis, beryllium). Pathogenesis and morphogenesis, clinical manifestations, complications, causes of death. Sarcoidosis. Clinico-morphological characteristic, morphology of extrapilence lesions.

6. Idiopathic pulmonary fibrosis. Classification, etiology, pathogenesis and morphogenesis, stages and options, clinical and morphological characteristics, forecast.

7. Pneumonites(Deskvamative interstitial pneumonitis, pneumonite hypersensitivity): Pato - and morphogenesis, clinical and morphological characteristics, causes of death. Eosinophilic lung infiltration. Classification, causes, clinical and morphological characteristics.

8. Tumors of bronchi and lungs. Epidemiology, classification principles. Benign tumors. Malignant tumors. Lung cancer. Bronchogenic cancer. Epidemiology, etiology. Biomolecular lung cancer markers. Prejudice changes of the bronchi and lung. The concept of "cancer in the scar". Clinical manifestations. Diagnostic methods, morphological characteristics, macroscopic variants, histological types (flat-belling, adenocarcinoma, fine-cell, large cell). BronchiologyAlveolar Cancer: Clinical and morphological characteristics.

1. Lecture material.

t.2, h. I: C.415-433, 446-480.

t.2, h. I: C.293-307, 317-344.

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

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

Training Map

Target setting: Examine on macropreparations, micro-processing and electron diffraction diffraction of the major forms of chronic lung diseases and conduct clinical and anatomical comparisons.

Chronic nonspecific

Light diseases

View macroprerats, the main clinical and anatomy forms of chronic nonspecific lung diseases. Describe the chronic abscess of light, chronic cue bronchitis with bronchiectases, emphiza lungs.

MicroPreparation number 12. Chronic deforming bronchitis (hematoxylin and eosin coloring). Mark the components of chronic inflammation of the bronchi: peribronchial sclerosis, pericalibration of vessels, inflammatory infiltration in the wall of the bronchi and peribroscial tissue, metaplacia of the bronchial epithelium.

Electron diffraction Intrakapillar sclerosis in the emphysema of the lungs (atlas, Fig. 11.13). Mark the formation of the capillary with a sclerized wall and destruction of the aerohematic barrier.

Pneumoconiosis

Macropreparat.Anthrako-silicosis of the lung. Pay attention to the change in the volume and reduced airiness of the pulmonary fabric. Describe sclerotic areas in lung: their shape, sizes, color, prevalence.

MicroPreparation number 000 Anthrako-silicosis of the lung (hematoxylin and eosin color). Designation of the structure of the silicothic nodule, concentrically located collagen fibers around the sclerosic vessels. Pay attention to a significant amount of coal dust contained both in the cytoplasm of macrophages (coniophages) and freely lying in the inter-vololar partitions.

LUNG CANCER

By set Macroprerats Determine the form of growth and localization of cancer tumors in the lungs.

MicroPreparation number 33. Flat-cell lung cancer (hematoxylin and eosine coloring). Pay attention to the degree of atypics of tumor cells, signs of infiltrating growth.

MicroPreparation number 34. Untifferentiated (anaplastic) lung cancer (hematoxylin and eosin painting). Assess the degree of cancer cell aptlasia (shape, dimensions, layout). Pay attention to the invasive nature of tumor growth.

Basic vocabulary

Bronchiectaz - Chronic pathological expansion of bronchi.

Lung disease obstructive - A group of diseases that differ in the obstruction of the air pathways.

Lung disease restrictive - A group of diseases, distinguished by the predominance of restrictive (restrictive) changes, as a rule, adjustable tissue.

Pneumoconiosis- The general name of professional diseases of the lungs caused by the impact of production dust.

Epidermoid cancer - flat-belling cancer.

Hamman Rich Syndrome - idiopathic pulmonary fibrosis, diffuse fibrosis alveolitis, chronic interstitial pneumonite.

Emphysema- excess and sustainable expansion of air-capable and respiratory structures located distal than terminal bronchioles.

Emphysema Bullosis - Emphysema, characterized by the formation of large subleumal bubbles (Bull).

Emphysema Vicarine (compensatory) - Emphysema developing with a significant part of the lung (for example, with pulmonectomy, lobectomy).

Emphysema interstitial (intermediate) - Emphysema, which is localized in an interface (stroma) of the lung.

Emphysema irregular - Emphysema, affecting the acins unevenly, which is almost always connected with the scarsing changes in the pulmonary fabric.

Emphysema obstructive - Emphysema caused by incomplete blockage (obstruction) of airway paths with the formation of the valve mechanism.

Panacinarian emphysema (panlobular) - Emphysema, exciting acins from respiratory bronchioles to terminal alveoli.

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

Centrcenar Emphysema (Centrobular) - Emphysema, striking the central or proximal part of the acinus, leaving distal alveios intact.

List of questions to the lesson,

1. Indicate the change in myocardium underlying the development of a pulmonary heart with a CHNZL.

2. Choose obstructive lung diseases.

3. What do they call an excess and persistent expansion of air and respiratory structures (or spaces) located distal than respiratory bronchioles, with the destruction of the walls of these structures without subsequent fibrosis?

4. Name the types of emphysema of the lungs.

5. What determines the predisposition to the chronic obstructive emphysema of the lungs?

6. Choose the most important factors for the development of chronic bronchitis.

7. Name the pathogenetic options for chronic bronchitis.

8. Name the possible complications of chronic obstructive bronchitis.

9. With what disease occurs increased reactivity of the mucous membrane of the air paths?

10. Indicate the pathogenetic version of bronchial asthma.

11. Specify the molecule locking on fat cells in atopic bronchial asthma.

12. Call changes in the bronchop wall at bronchiectase.

13. Name macroscopic types of bronchiectasis.

14. Name complications of bronchiectatic disease.

15. What is the name of a professional disease associated with the impact of production dust and characterized by the gradual development of sclerotic changes of the pulmonary parenchyma?

16. Name the etiological factors for the development of silicose.

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

18. Name the etiological factors for the development of anthratracosis.

19. Select Sarcoid Granuloma Components.

20. With what disease are asteroid inclusions in the cytoplasm of multi-core cells detect?

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

22. Name the most frequent historical type of central lung cancer.

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

24. What are the lung cancer, developing from the epithelial liner of the distal third of segmentary bronchi, bronchiole or alveolar epithelium?

25. What are the lung cancer, developing from the epithelial chipping of the main, equity and proximal third of segmental bronchi?

26. Indicate the prejudice states in the lungs.

27. Call the complications of bronchus cancer.

28. Sick 53 years for 30 years smokes 2 packs of cigarettes per day. He appealed to the clinic with complaints on a permanent productive cough, amplifying in the morning after awakening, and progressive shortness of breath. Radiographic images determine the increased airiness of the pulmonary fabric and the gain of the pulmonary pattern. Your conclusion.

29. Patient for 30 years entered the clinic with complaints of shortness of breath, common cyanosis, weakness. From the anamnesis it is known that a woman works for a long time on a poultry farm. In the study: the level of immunoglobulins is elevated in the blood, immune complexes are determined. With a x-ray study - a picture of "Cellular Lung". Specify the most likely diagnosis.

30. Patient 67 years, long-term suffering from chronic diffuse bronchitis, died with increasing phenomena of pulmonary heart failure. With a pathological analytical study, light heightened airiness, in the peripheral departments, many different-caliber bubbles. Specify changes in the internal organs detected at the autopsy.

Diseases of digestive organs

(The section is studied at two laboratory classes)

Training goals

The student must know :

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

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

The student must be able to :

1. Describe the morphological changes in the studied macropreats and micro.

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

The student must understand :

Mechanisms for the formation of structural changes arising in organs for diseases of the digestive system.

I. occupation

Diseases of the stomach and intestines

1. Gastritis. Definition. Acute gastritis: etiology, pathogenesis, clinical and morphological characteristics. Chronic gastritis, concept, etiology, pathogenesis, principles of classification. Forms allocated on the basis of the study of gastrobills and their morphological characteristics. Complications, outcomes, forecast. Chronic gastritis as a precancerous state.

2. Peptic disease. Definition. The overall characteristics of peptic (chronic) ulcers of different location. Epidemiology, etiology, Pato - and morphogenesis, its features for pyloro-duodenal and medio-gastral ulcers. The morphological characteristics of chronic ulcers during the period of exacerbation and remission. Complications, outcomes. Acute stomach ulcers: etiology, pathogenesis, morphological characteristics, outcomes.

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

4. Idiopathic inflammatory bowel diseases. Nonspecific ulcerative colitis. Crohn's disease. Epidemiology, etiology, pathogenesis and morphogenesis, clinical manifestations, complications, outcomes, forecast. Differential diagnosis criteria for chronic colitis.

5. Epithelial bowel tumors. Benign tumors. Adenoma: epidemiology, classification, clinical and morphological characteristics, forecast. Family adenomatous polyposis. Adenoma and Cancer: The concept of multistage carcinogenesis in the colon. Colon cancer. Epidemiology, etiology, classification, macro - and microscopic morphological characteristics, clinical manifestations, forecast.

6. Diseases of a worm-like transformation of a blind intestine. Appendicitis. Classification, epidemiology, etiology, pathogenesis. Morphological characteristics and clinical manifestations of acute and chronic appendicitis. Complications.

1. Lecture material.

2. Tutorial on pathological anatomy (, Anichkov N. M, 2000) t.2, h. I: S.537-562, 586-593, 597-618.

3. Tutorial on pathological anatomy (, Anichkov N. M, 2005) t.2, h. I: p.384-405, 416-422, 425-441.

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

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

Training Map

Target setting: To study the morphology of individual nosological forms of diseases of the gastrointestinal tract organs and to carry out clinical and anatomical comparisons.

Diseases of the stomach

Macropreparat.Multiple stomach erosion. Pay attention to the mucous membrane of the stomach with multiple surface defects, mark the color of the erosion.

Macropreparat.Chronic gastritis. Pay attention to the relief of the mucous membrane in various departments (body, pyloric channel), the presence of erosion.

MicroPreparation number 000 Helicobacter pylori in the trim mucus in gastric pits (gastrobyopotate, painting by gymzema). View, note the ability of bacteria to adhesion on the epithelial cell.

MicroPreparation number 000 Chronic Active Gastritis Antrum with atrophy of the glands and full intestinal metaplasia (gastrobatto, color of alzian-blue and hematoxylin). Describe and evaluate semi-grapped morphological signs of chronic gastritis: activity (the presence of neutrophilic leukocytes) and the severity of inflammation (the density of mononuclear infiltrate), the degree of atrophy of the glands of its own plate, the prevalence of intestinal metaplasia of the coupling epithelium.

Macropreparat.Chronic stomach ulcer (coal). Pay attention to the localization of ulcers, its shape, edge, depth, the nature of the bottom. Determine which edge is facing the esophagus and what to the gatekeeper.

MicroPreparation number 000 Chronic stomach ulcer (with exacerbation) (hematoxylin and eosin color). Denote the layers in the bottom of the ulcers, characterizing the chronic course of the disease. Mark fibrinoid necrosis and leukocyte infiltrationindicating the exacerbation of the process.

View set of macro products Illustrating complications of chronic ulcers: the penetrating ulcer of the stomach, penetrating ulcer of the stomach, arrosion of the vessel in the day of the ulcers, ulcer-cancer of the stomach, the scar deformation of the stomach. Pay attention to the localization of ulcers, shape, nature of the edges, changes in the bottom and edges of ulcers.

Macroprerats Different forms of gastric cancer. Determine the macroscopic forms of the tumor. Describe one of the forms.

MicroPreparation number 000 Highly differentiated stomach adenocarcinoma (intestinal type) (gematoxylin and eosin color). Designate the signs of tissue and cellular atypism, the invasive nature of the tumor growth.

MicroPreparation number 000 Untifferentiated cancer - pisner-cell cell (painting by hematoxylin and eosin and alziano blue). Pay attention to the tumor cells with alcianophilic cytoplasm, located in the "Lakes" of the mucus. Mark the shape of the cell is pistened, the core is pushed back to the periphery, the cytoplasm is filled with mucus.

Intestinal diseases

Macropreparat. Phlegmous appendicitis. Pay attention to the dimensions of the process, the condition of the serous shell (appearance, degree of blood flow), the thickness of the wall, the nature of the content in the lumen.

MicroPreparation number 000 Phlegmosic appendi cyt (hematoxylin and eosin coloring). Describe. Mark the degree of preservation of the mucous membrane, the nature of the exudate, its propagation in the layers of the wall and the mesenter (mesenteriolite).

Macropreparat.Chronic appendicitis. Pay attention to the size of the process, the condition of the serous shell, the thickness, and the appearance of its wall on the cut.

MicroPreparation number 000 Chronic appendicitis (gematoxylin and eosin coloring). Describe. Mark sclerotic changes in the wall and obliteration of the enlightenment of the process. Pay attention to lipomatosis and diffuse chronic inflammatory infiltration.

Macropreparat.Liver abscesses (pylephlebitic), as complication of appendicitis. View.

View set of macropreparats Intestine tumors.

Basic vocabulary

Gastritis sharp - Diseases manifested by inflammation of the gastric mucosa.

Chronic gastritis Living inflammatory-disperseration diseases of the stomach mucosa.

Gematomisis- Bloody vomiting.

Colitis - A group of inflammatory diseases of the colon.

Crown disease - Terminal Ileit, Regional Ileit.

Mulldari Weis Syndrome - longitudinal breaks of the mucous membrane in the area of \u200b\u200bthe esophageal and gastric compound.

Penetration- penetration of defect in neighboring organs ("covered" perforation).

Perforation - Split.

Pylorospasm - Sustainable reduction in the pyloric sphincter of the stomach, leading to a disruption of the evacuation function.

Polyp - Any exophytic node rising above the surface of the mucous membrane.

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

Erosion - Defect that does not go beyond the mucous membrane.

Ulcer - Defect leaving the limits of the mucous membrane.

Stricture - Stenosis, narrowing.

List of questions to the lesson,

being the basis of the control test

1. Give the esophageal of Barrett.

2. Specify the features of the codcker diverticula.

3. Specify the provisions characteristic of Mulldari Wece syndrome.

4. Specify the factors providing the cytoprotective function of the stomach mucosa.

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

6. Specify the methods of detection of H. pylori in bioptate.

7. Enter the provisions characteristic of chronic stomach ulcers.

8. List the factors that significantly reduce the synthesis of prostaglandins and possess a ulcerogenic effect.

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

10. Describe the perforation of the stomach ulcers.

11. Note the assertions characteristic of the Zolinger-Ellisson syndrome.

12. Indicate the predominant localization of the stomach ulcers.

13. Select the positions characteristic of the cambial cell epithelial cells.

15. The predisposing factors for the development of hemorrhoids are.

16. Choose extraordinary manifestations of crown disease.

17. Specify the complications of Crohn's disease.

18. Indicate the disease for which the combination of the following microscopic characteristics is characterized by crypt-abscesses, granulomas with the presence of giant Pirogov-Langhance cells.

19. Specify microscopic signs of aggravation of Crohn's disease.

20. Select the approvals characteristic of the ward of the intestine.

21. Indicate the pathogenetic factors of the colon diverticulosis.

22. Describe pseudopolys with ulcerative colitis.

23. For what disease is the macroscopic view of the gum mucosa of the colon in the type of "cobblestone"?

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

25. Specify characteristics celiac disease.

26. Under what conditions does Malabsorption syndrome meet?

27. In a patient, 64 years ago, harsh pains in the epigastric area appeared in diabetes, which in a few hours moved to the right iliac area, fever up to 39 ° C, one-time vomiting. After 12 hours of the beginning of the disease, the patient was hospitalized. When examining a doctor of the receiving rest, a consciousness confusion is noted, fever 39.6 ° C, the symptoms of the peritonean irritation are positive. Specify the estimated diagnosis.

28. Patient 28 years old for several years missing, pain in the epigastric region, notes the pallor of the skin, feces of black, appeared with epigastria, the joy of skin and visible mucous membranes. When FGDS found a cellular ulcer back wall The stomach with impressed edges, the bottom is deeply located, filled with dirty content of gray. What complication of ulcers are we talking in this case?

29. In the patient's gastrobotte, 43 years old is determined by the presence of a lymphoplasemic infiltrate mucous membrane in its own plate, there are clusters of lymphocytes with light centers. Histobacterioscopically, the S-shaped sticks are determined by the gymse in the surface mucus layer. Indicate the estimated diagnosis?

II. occupation

Diseases of the liver, gallbladder

And pancreas

1. Hepatitis: Definition, classification. Acute viral hepatitis. Epidemiology, etiology, paths of transmission of infection, Pato - and morphogenesis, clinical and morphological forms, viral markers, outcomes. Chronic hepatitis: concept, etiology, clinical and morphological characteristics and classification, signs of activity, outcomes, forecast.

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

3. Cirrhosis of the liver. Concept. Patomorphological signs and classification of cirrhosis on etiology, pathogenesis, macro-, microscopic changes, etc. Clinical and morphological characteristics of the most important types of cirrhosis. Alcoholic cirrhosis. Cirrhosis after viral hepatitis. Bilyary cirrhosis (primary, secondary). Changes in liver during hemochromatosis, Wilson-Konovalov disease, insufficiency of alpha-1-antitripsein. Pathogenesis, clinical and morphological characteristics.

4. Liver tumors. Classification, epidemiology. Benign neoplasms. Hepatocellular adenoma. Adenoma of intrahepatic bile ducts. Malignant neoplasms. Classification. Hepatocellular adenocarcinoma. Epidemiology, etiology. Classification depending on macro and microscopic signs. Complications. Patterns of metastasis. The levels of propagation of hepatocellular adenocarcinoma over the TNM system. Cholangiocellular cancer.

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

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

1. Lecture material.

2. Tutorial on pathological anatomy (, Anichkov N. M, 2000) t.2, h. I: p.637-669, 672-682, 687-709.

3. Tutorial on pathological anatomy (, Anichkov N. M, 2005) t.2, h. I: p.452-477, 479-487, 489-501.

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

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

Training Map

Target setting: Examine on macro production, micro-processing and electronograms of morphology of individual nosological forms of liver diseases and carry out clinical and anatomical comparisons.

Diseases of the liver

Macropreparat.Toxic liver dystrophy (fat hepatosis). Pay attention to the size of the liver, its color, consistency, condition of the capsule.

MicroPreparation number 4. Massive liver necrosis is a subacted form (hematoxylin and eosin color). Mark discoversion of beams, signs of fatty dystrophy and necrosis of hepatic cells. Compare the state of hepatocytes of the center and periphery of the Polek. Pay attention to the starting fibrosis of stroma and infiltration of portal paths with lymphoid-macrophaghal elements.

MicroPreparation number 5. Chronic hepatitis of weak activity, stage I (gematoxylin and eosin color). Mark the signs of hepatitis activity: intralobular lobular lymphoid infiltrates, "spreading" lymphocytes in sinusoids, dystrophic changes in hepatocytes, lymphogistocitary infiltration of portal paths. Mark the signs of chronicness of inflammation (hepatitis stage): fibroids of portal portal paths, fibrous septa, growing into slices. Pay attention to cholestases: the expansion of bile capillaries, the immigination of hepatocytes with bile pigments.

Electron diffraction Hydropic hepatocyte dystrophy with viral hepatitis (atlas, Fig. 14.5). Pay attention to the expansion of the hepatocyte endoplasmic network and the sharp swelling of mitochondria.

MacropreratsLiver cirrhosis. Note the size, color, consistency, view of the liver from the surface and on the context. Assess the size of regenerate nodes and determine the macroscopic form of the cirrhosis on this basis.

MicroPreparation number 48.Chronic hepatitis of moderate activity with the transition to liver cirrhosis (hematoxylin and eosin and picrofoxin coloring). Pay attention to the presence of moderately pronounced signs of inflammation activity (lymphoid infiltration of stroma, propagating in the parenchyma, hepatocyte fatty dystrophy), the dominance of fibrosis (portal portal, port-central septa, formation of false poles) and the regeneration of hepatocytes (the loss of the beam structure, the presence of cells with large nuclei).

Macrobrerats: Primary liver cancer, metastases in the liver of tumors of different primary localization.

Basic vocabulary

Badda Kiari Syndrome - obstruction of the main hepatic veins as a result of thrombosis.

Hepatitis - Any diffuse inflammatory liver disease.

Hepatozia - A group of liver diseases characterized by dominance of dystrophic changes and necrosis of hepatocytes.

Head of Medusa - expansion of the veins of the anterior abdominal wall with portal hypertension.

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

Kaiser-Fleischer Rings - Greenish brown or yellowish green pigment rings in the cornea of \u200b\u200bthe eyes during Wilson's disease.

Kowsilman Tales - Eosinophilic rounded formations in the perisinusoidal space.

Mulletri Tales - Alcohol hyaline, homogeneous eosinophilic inclusions in the cytoplasm of hepatocytes.

Massive liver necrosis (drain) - Extensive common necrosis most of the hepatic parenchyma.

Liver necrosis bridge (necrosis jumper) - Drain necrosis of a large number of hepatocytes with the formation of "jumpers" between adjacent slices.

Loading necrosis (periportal) - Destruction of hepatocytes along the border of parenchyma and stroma, i.e. in the peripheral divisions of the slices.

Focal liver necrosis (spotted) - The death of individual small groups of hepatocytes in different departments of the acinus.

Pancreatitis- Inflammatory disease of the pancreas, often accompanied by her necrosis.

Gusina liver - macroscopic appearance of the organ at fatty dystrophy.

Hepatolyenal syndrome - an increase in the spleen in the diseases of the liver, accompanied by hyperplanism.

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

Cholangit - Inflammatory disease of bile ducts.

Hollyatiasis- cholelithiasis.

Cholesteas - Insufficiency of the tower of bile.

Cholecystitis - Inflammatory gallbladder disease.

Cirrhosis- Excessive growth of connective tissue in the body against the background of dystrophic and regenerative processes, accompanied by a change in the form of the organ.

List of questions to the lesson,

being the basis of the control test

1. Specify the layer structure options.

2. List the liver parenchyma necrosis options.

3. As a result, the Cauncilman's Taurus is formed?

4. List the shapes of sharp hepatitis.

5. Specify the path of transmitting the virus when acute hepatitis BUT.

6. Specify the transmission paths of the virus in acute hepatitis V.

7. Name the indirect markers of viral lesion of hepatocytes.

8. Indicate the predominant Localization of the NVSAG in hepatocytes.

9. What species gives the cytoplasm the accumulation of NVSAG in hepatocyte?

10. List the etiological options for chronic hepatitis.

11. Specify microscopic signs of chronic hepatitis.

12. List the morphological forms of chronic hepatitis.

13. Indicate the characteristic signs of alcoholic liver damage.

14. List the variants of alcohol liver damage.

15. Name the cells responsible for collagenization during alcohol liver damage.

16. Describe macroscopic liver changes with alcoholic steatosis.

17. List the microscopic signs of the false lobby in the liver cirrhosis.

18. Name the morphological forms of liver cirrhosis.

19. List the acquired liver cirrhosis forms.

20. List hereditary liver cirrhosis forms.

21. Specify the signs of portal hypertension.

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

23. Give the characteristic of the primary sclerosing cholangitis.

24. Give the characteristic of the primary biliary liver cirrhosis.

25. Give the characteristic of Wilson-Konovalov disease.

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

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

28. Patient 60 years for 30 years suffered from chronic alcoholism. During the examination, the liver is dense, the surface is buggy. On the front abdominal wall of the veins are extended, the spleen is palpable. Specify possible histological manifestations in the biopsy material.

29. Woman 50 years old for 8 months worried fast fatigue and skin itching. With a laboratory study, a minimal increase in TRNSAMINAZ levels is established, a significant increase in the level of alkaline phosphatase, high titers of antimicochondrial antibodies. In a biopsy study, the granulomatous nature of inflammation in cholangiols was found and the decrease in the number of bile ducts with pronounced lymphomacrophah infiltration in the course of portal paths with sclerosis phenomena. Your conclusion.

30. The sick man is 63 years old, a long-suffering chronic viral hepatitis In, entered the clinic with complaints about the severity in the right hypochondrium, the yellowness of the skin. During the examination, the liver is dense, the edge of it is buggy, there is an increase in the spleen and the expansion of the veins of the anterior abdominal wall. Note possible histological manifestations in biopsy material.

Catad_TEMA Ulcerative Disease - Articles

Catad_TEMA Anesthesiology Resuscitation - Articles

Prevention of stressful erosive-ulcerative lesions of the gastroduodenal zone in patients in critical states

D.M. MA Evseev
MMA named I.M. Sechenov

The occurrence of acute erosive-ulcerative damage to the mucous membrane of the gastroodenal zone in patients in critical states, including in the postoperative period, is, on the one hand, an extremely unfavorable, but natural consequence of the available multisystem disorders and, on the other hand, a factor, a fundamentally deteriorating forecast of life patient. According to M. Fennerty (2002), B. Raynard (1999), sharp erosion and ulcers in the gastroduodenal zone are revealed already in the first hours of patient's stay in the separation of intensive therapy in 75% of cases. According to V.A. Kubyushkin and K.V. Shishishin (2005), in the postoperative period, sharp ulceration of gastroduodenal mucous membrane, having clinical manifestations of no more than 1% of patients, are detected at openings in 24% observations, and with non-recreational esophagastrodenoscopy - in 50-100% operated on. 75% of acute ulcers are complicated by bleeding, while on esophagogastroscopy, signs of continuing bleeding are noted in 20-25% of patients. Acute ulceration of the mucous membrane of the stomach and duodenum develops over the next 3-5 days under the influence of provoking factors (operation, shock, sepsis, extensive burns, etc.). General mortality in the operated patients with the development of acute erosive-yazine damage to the stomach, complicated by bleeding, reaches 80%. The same authors main reason The relevance of the problem discussed is seen in the almost complete absence of clinical symptoms of erosive-ulcer damage and the last manifestation of the latter only by their complications, in the overwhelming majority of cases - gastroduodenal bleeding. At the same time, ulcerative bleeding even low intensity deteriorate sharply the general condition of the patients, which is primarily manifested by the disorders of central hemodynamics. Significantly later, local symptoms appear in the form of vomiting with blood or melan, which is observed only in 36-37% of patients.

A.A. Kurygin, O.N. Scriabin, Yu.M. Stall (2004) reported that with the help of systematic fibrogastroduodenoscopy, acute ulcenes were discovered in 64% of the operated patients who had increased risk of ulcerative formation. Even 6% of patients, this complication either appeared to an unexpected find in autopsy, or was detected by clinical signs. Gastrointestinal bleeding served as the main manifestation of sharp ulcers in the postoperative period in 60% of patients, of which in 33% it was massive, and at the same time only 13% of patients presented complaints about increased pain in the opposite region, nausea, sharp weakness, dizziness. In four cases, a faint condition is noted. More than half of all sharp ulcers (56%) is formed in the first three days and the more difficult than the harder preceding surgery and related diseases. Acute ulceration of the gastric mucosa in more late time It is usually associated with complications of operation in the form of cardiovascular, renal and respiratory failure, as well as with purulent processes.

For the first time, the occurrence of acute erosive-ulcer lesion in the postoperative period was described by TH. BILLROTH in 1867, suggesting the existence of a causal relationship between operating injury and damage to the gastroduodenal zone. In 1936, G. Selye proposed the term "stress-ulcer" to designate the relationship between psychosomatic disease and a gastroduodenal ulcer. Currently near the authors (B.R. Gel Fand, A.N. Martynov, V.A. Guryanov et al., 2004) proposed the term "syndrome of acute damage to the stomach", which implies damage to the mucous membrane of the stomach and duodenal intestine Violation of the mechanisms of its protection in patients in critical states, and includes swelling and disruption of the integrity of the mucous membrane, as well as a violation of the engine-evacuator function of the stomach.

It should be borne in mind that the morphology and pathogenesis of acute erosive-ulcer damage to the stomach and duodenum differ in many ways from chronic gastroduodenal erosions and ulcers (L.I. Aruin, V.A. Isakov, 1998) (Fig. 1). Erosions Called defects of the mucous membrane, which do not penetrate the muscle plate of the mucous membrane. The most often erosion arising under the influence of stress factors is localized in the Foundal Stomach Department. Acute erosion can be superficial and deep. Surface erosions are characterized by necrosis and rejection of the epithelium, localized on the vertices of gastric rollers and are usually multiple. Deep erosion destroy their own plate mucous membrane, not capturing the muscular plate. The microscopic pattern of sharp erosions is not characteristic of damage to the mucosa with an acidic peptic factor of the gastric juice, but is a consequence of trophic disorders. It has been established that the development of erosions is preceded by significant disturbances of microcirculation, which gives the basis to most morphologists to consider sharp erosion as ischemic infarction of the mucous membrane.

. A) Macropreparation: multiple acute stomach ulcers with bleeding; B) Microdrug of acute stomach ulcers, complicated by bleeding: necrotic masses of the bottom of the ulcer, unchanged muscular sheath, salt-oxidic hemathine

Acute ulcers Called defects (necrosis) of the mucous-submembered layer, propagating deep into the wall of the organ on the muscular shell and associated with the influence of a pronounced stress factor. You are dividing "postoperative" acute ulcers, "Yazv Kushing", "Jazv Koronga" has extremely historical interest, since morphological differences do not have these ulcers, and their treatment and prevention are universal. The sharp ulcers are usually multiple, localized predominantly in a small crision stomach, the diameter of the sharp ulcers usually does not exceed 1 cm. Microscopically, areas of granulation tissue in the depth of the gastric or duodenal wall, full-blooded, stakes, edema, thrombosis, hemorrhage, are detected. What testifies to vascular or, rather, the ischemic genesis of acute ulcerations.

Currently, most authors are supported by the concept of ischemic damage in the occurrence of stressful ulcerations in the gastroduodenal zone, arguing that the main cause of stress-ulcers is the inadequate blood supply to the wall of the stomach and duodenum. Improving the acidity of gastric juice becomes important only when the protective barrier is damaged earlier than local ischemia occurs. A.L. Kostyuchenko et al. (2000), N.A. Maystrenko et al. (1998) indicate that the result of the assisted effects of the resistant spasm of the vascular zone with a violation of both arterial perfusion and venous outflows is indicated. At the same time, the latter leads to stagnation of blood in the mucous-subliftedness of the layer of the stomach and duodenum, an increase in capillary pressure, intragrogenous loss of plasma, local hemokoncentration, followed by the appearance of microtrombosis. Synchronically discloses the preterminal arterio-venous shunts, which further aggravates the ischemia of the mucous membrane.

B.R. Gelfand et al. (2004) It is believed that the most pronounced microcirculation disorders in patients in critical states occur precisely in the proximal sections of the digestive tube due to the greatest content in their arteries of α-adrenoreceptors. In this connection, the main causes of the occurrence of gastroduodenal stress-ulcers are local ischemia, activation of free-radical oxidation in the insufficiency of antioxidant protection systems, reducing the content of prostaglandin E1, which are implemented by the occurrence of foci of typical ischemic necrosis. The restoration of the regional blood circulation after long-term hypoperfusion leads to a non-pilus impaired of the splashing blood flow, which, leading to the reperfusion syndrome, further aggravates damage to the gastroduodenal zone.

On the other hand, a number of authors adhere to a somewhat different point of view on the pathogenesis of stressful erosions and an ulcers of the gastroduodenal zone. So, V.A. Cuba Kin and K.V. Shishin (2005) It is believed that the main pathogenetic mechanism for the formation of erosive-ulcer damage is to strengthen the factors of intragastric aggression in relation to protection factors. The complex assessment of the acid-forming function of the stomach with the help of several methods (titration, intragastric and aiming ph-metry) showed that in the first 10 days after the operation, the maximum stimulation of the acid-forming function of the stomach occurs, and its "peak" falls on 3-5 days, that is, For the period of the most likely ulcerative formation. At the same time, the greatest increase in proteolytic activity is recorded in the field of the bottom - the places most frequently susceptible to the erosive-ulcer process. The study of night secretion, which is a particular case of basal secretion and reflecting, mainly the vagus phase, made it possible to establish the maximum increase in the acidity of the gastric juice in the first 4 h. It is interesting that the increase in free hydrochloric acid products is observed even in cases where akhlorhydria is registered on the eve of the operation. The authors argue that the indicated reaction of the digestive system on surgical stress underlies the formation of early true stressful ulcers, which account for about 80% of all ulcerations of the mucous membrane of the upper sections of the tract, resulting in the postoperative period. In the remaining 20% \u200b\u200bof cases of ulcers occur in the phase of dystrophy of the mucous membrane in a more long time after surgery, with a complicated monthly period of the postoperative period in the form of cardiovascular, renal and respiratory failure, as well as purulent and septic complications, leading to the development of polyorgan deficiency, one of the manifestations Which are just ulcers. The occurrence of sharp ulcerations of the mucous membrane of the stomach on a background no longer depends on the acid-peptic aggression.

It would be quite logical to doubt in the possibility of gastric hypersecretion in the conditions of stress activation of the sympathy-adrenal system in the oppression of vagal influences. But, as often happens, the pathogenesis mechanisms turn out to be at first not so obvious to us, and the evidence subsequently increases directly proportional to our awareness of the subject. Thus, in the context of this report, it should be noted that an indirect morphological confirmation of the eligibility of the point of view on the determining role of the acid-peptic factor is the fact of the presence in the bottom of the sharp ulcers (not always) areas of fibrinoid necrosis, which indicates the participation in ulcergenesis of acute oral-peptic ulcers factor a. Back in 1957, N. nechels and M. Kirsten in the experiment showed that acid production is in direct connection with the level of hypercapinia and the severity of metabolic acidosis, that is, it is compensatory in relation to disorders of acid-alkaline equilibrium by the mechanism.

It should be noted that the concept of the priority of the ischemic or acid-peptic factor in the pathogenesis of stress-ulcers are not mutually exclusive (Fig. 2). A provision seems to be quite logical according to which the ischemic damage to the mucous membrane of the gastroduodenal zone is a predisposing factor, and hydrochloric acid and pepsin - a factor producing. As indicated by A.L. Kostyuchenko et al. (2000), under the conditions of ischemia of the mucous membrane, the natural neutralization of hydrochloric acid becomes insufficient, and even at the usual level of acidic products, acidosis of the mucous membrane develops, which is easily subjected to a digestive action of pepsin. These changes are exacerbated under the influence of bile acid salts (duodenogastral reflux during violations of the stomach motility), to which the urban mucosa is particularly sensitive in the 4dal stomach department. Ischemia joins the activation of intraprometal and intricumenate proteolysis, which limits the possibility of forming full-fledged thrombus in arrine vessels of the bottom of the ulcer.

. Pathogenesis of gastroduodenal stress-ulcers

Thus, a number of circumstances become obvious. First, given the high frequency of erosive-ulcerative lesion of the gastroduodenal zone in patients in critical condition, the fatal effects of bleeding from stress-ulcers and almost complete absence of clinical symptoms of sharp ulcers, the only method of solving the problem is the prevention of erosive-ulcer lesion. Every surgeon and resuscitator is known not one sad clinical caseWhen on the background of the background of the patient's status achieved to stabilize the status of a patient who has suffered not one relaparotomy, "suddenly" is developing difficult to actually corrected hypotension, a slightly later than a nastastric probe begins to do " coffee grounds"With unchanged blood, the endoscopists are bred by their hands (" crying "the whole mucous, reliable endogamostasis is unlikely), and it is impossible to operate the patient due to the severity of the state. Secondly, taking into account the significance of the acid-panic factor for the occurrence of acute erosive-ulcerative damage to the gastroduodenal mucosa, pathogenetically reasonable will be preventive use in patients in the critical states of antisecretory drugs. Third, the pathogenetically reasonable method for the prevention of stressful damage to the gastroduodenal mucosa will be the use of drugs that improve hemoperfusion, which contribute to an increase in the delivery of oxygen, as well as the activation of free radical oxidation in the mucosa of the digestive tube.

The question is natural from the point of view of a practical doctor: to whom and when preventive use of antisecretory preparations is shown? That is what is the objective criteria for the risk of stress-ulcers in the postoperative period and in patients in critical condition? Agree that retrospective data that "acute ulceration of mucosa is detected in 20-50% of those who died after various abdominal operations," are small help in solving daily clinical issues.

Today, the following risk factors for the occurrence of acute erosive-ulcer damage to gastroduodenal mucosa in patients in critical states are proven: Long artificial ventilation of the lungs, long hypotension various origin, sepsis, hemokoagulation disorders (hypercoagulant and waf syndromes), liver and renal failure, as well as elderly and old age, malignant tumors, acute pancreatitis, Hypovolemia, peritonitis, cardiovascular failure, exhaustion. The frequency of the occurrence of bleeding from sharp ulcers increases many times during extensive traumatic interventions, reaching, according to some authors, 60%. MB Yarustovsky et al. (2004) Indicates that the use of artificial blood circulation during operational interventions on the heart and mainstream vessels increases the frequency of bleeding from acute stress-ulcers in the postoperative period by more than 6 times compared with operations performed without artificial blood circulation. Nevertheless, the overwhelming majority of postoperative bleeding from the upper digestive tract sections develops in patients who have undergone extensive surgical interventions severe diseases organs of the hepatopancarmatobiliary zone (tumor and scar strictures of bile ducts, primary and metastatic liver tumors, pancreatic tumors, pseudotumorous pancreatitis, gall-eyed disease, complicated by jaundice, cholangitis and choledocholithiasis, pancreathenecosis, etc.). Yu.I. Pathetko and A.G. Kotelnikov (2007) indicate that bleeding from sharp erosions and ulcers complicate the flow rate of the postoperative period in each tenth patient who has undergone gastropancratopodogenic resection. In this regard, the appropriateness is apparent to the allocation of specific risk factors for the development of acute gastroduodenal stress-ulcers. For this purpose, N. Stollman, D. Metz (2004) conducted a meta-analysis of several prospective studies: D. Cook et al. (1994) - 2200 patients in the postoperative period; P. Hastings et al. (1998) and R. Fiddian-Green (1993) - 100 and 564 patients in the separation of intensive therapy, respectively. Based on the analysis carried out by the authors, the following risk factors for the development of erosive-ulcer affects of the stomach in critical states are presented in descending order of importance:

• Respiratory failure C IVL lasting more than 48 hours
• Coagulopathy
• Long hypotension or shock
• Sepsis
• Liver failure
• Renal failure
• Operational interventions
• Burn disease
• Heavy injuries
• Acute coronary syndrome
• CNS damage
• Polyorgan deficiency.

B.R. Gelfand, A.N. Martynov, V.A. Guryanov, A.S. Bazarov (2004) cause more specific criteria for the occurrence of erosive-ulcerative stress-lesion of the stomach:

• IVL more than 48 hours
• Coagulopathy
• Acute hepatic insufficiency
• Pronounced arterial hypotension and shock
• Sepsis
• Chronic renal failure
• Alcoholism
• Treatment of glucocorticoids
• Long nasogastric intubation
• Heavy brain injury
• Burns are more than 30% of the body area.

It is obvious that the patient corresponding to one or more risk criteria for the occurrence of a gastroduodenal zone stress-ulcer needs a complex of preventive measures. At the same time, it is quite difficult to distinguish between these events for "specific" and "non-specific". Patients in critical condition are shown:

• correction of hypoperfusion and local ischemia of the gastroduodenal zone;
• an increase in the protective properties of the gastroduodenal zone mucosa and stimulation of its reparative potential;
• inhibition gastric secretion.

Correction of hypoperfusion and local ischemia of the gastroduodenal zone are carried out using infusions of rheological solutions (solutions of hydroxyethyl stroke, refooliglucin, gelatinoly, emulsion of perfluorocarbons), oxygen-visiting media (perfluorocarbon emulsion, erythrocyte mass - in the presence of a proven hemic component of hypoxia), drugs, increasing mining, preparations, drugs, providing a compensatory effect on oxidative stress (calcium oxibutirate, Mafusol, ascorbic acid, tocopherol, piracetam).

Speaking about increasing the protective properties of the mucous membrane of the gastroduodenal zone, first of all, they mean the use of drugs with antacid and gastroprotective effects. Antacid preparations (magnesium hydroxide, aluminum hydroxide, calcium carbonate, magnesium trisilicate, sodium bicarbonate) implement its effect by neutralizing already available hydrochloric acid. However, the practical application of these drugs in patients in critical states revealed a number of significant drawbacks. First of all, the oral use of drugs in the patient in a critical condition (artificial ventilation of the lungs, the state after operations in the gastroduodenal zone, the paresis of the gastrointestinal tract) is technically very problematic, since it is necessary for an hourly administration of drugs. In addition, the separation of carbon dioxide in the process of the interaction of hydrochloric acid and carbonates can lead to stretching the stomach and regurgitation of gastric content in the trachea and bronchi (Mendelssohn syndrome, aspiration pneumonia). With systematic use of antacids, systemic alkalosis is possible.

The sukralfat gastroprotector does not have an acid-meal effect and has its own protective effect by forming a film on the gastric mucosa and duodenum. It should be noted that the formation of a polymer film from sublofate occurs only at pH below 4, which far from always occurs, and, in addition, the frequency of bleeding from stress-ulcers with the prophylactic use of sublofate, according to D. Cook (1998), was Twice above compared to that when using antisecretory preparations. However, Sukral Fat is still better than nothing.

Today, generally accepted the fact that the leading component of the prevention and pharmacotherapy of acute erosive-ulcerative lesions of the stomach is modern antisecretory drugs.

In the 70-90s of the twentieth century, H 2-blocks were quite widely used for the prevention of stress damage to the gastroduodenal zone. Based on the analysis of a large sample of patients in critical states in 1992, D. Cook concluded that the preventive use of H 2-blocks prevents sharp erosive-ulcerative lesions of the gastroduodenal zone much more efficiently of antacids and sucralfat. However, many authors indicate that achieving reliable control over the state of the gastroduodenal mucosa during prophylactic use of H 2-blocks is sufficiently problematic. So, B. Erstadt et al. (1999), M. Feldman (1990) lead data on a short antisecretoric effect of H 2-blocks, due to a short period of semi-liquefaction of these drugs. The same authors noted the instability of the antisecretory effect, manifested by a decrease in intragastric pH less than 3.5-4, both in the Bolus and with continuous mode of administration of drugs, including when a dose increases. P. Netzer (1999) explains this fact that the effect of "fatigue H 2 -receptors" is already on the first day of the start of therapy.

We want to draw the attention of readers for another feature of pharmacodynamics H 2-blocks, which is questionable by the expediency of their use for the prevention of stress-ulcers, namely, exacerbation of the ischemia of the gastric or duodenal wall due to the blocking of H 2 receptors of the arteries of the submembratus and muscular layers and, as Corollary, vasoconstrictions with a decrease in the volumetric rate of blood flow. Thus, n 2-blocks in patients in critical states, on the one hand, reduce the intensity of acid-peptic aggression, but on the other, the local ischemia is enhanced, which is the main pathogenetic factor in stressful ultercerenesis.

In addition, the use of H 2-blocks, especially in large doses, is extremely negatively affected by the disinfectivation function of the liver (the inhibition of the cytochrome R450 system), leads to the aggravation of already existing encephalopathy, which can be concerned, disorientation, delirium and hallucinoses. It should be remembered for the possibility of negative chron and inotropic effects, extrasystoles and an atrio-ventricular blockade due to the action of H 2-blocks.

Obviously, the appearance in the wide clinical practice of inhibitors proton pump (IPS), which are the most powerful antisecretory drugs and possessing a favorable security profile, immediately attracted the attention of researchers the possibility of prophylactic use of these drugs in patients in critical states. Initially, an IPP was tested in the clinic with an oral administration - the suspension of the drug was injected with patients through a nasogastric probe. However, due to the small number of observations, the effectiveness of oral ipp for the prevention of stress-ulcers was not formally proven. In turn, I would like to emphasize once again that attempts to oral administration of antisecretory drugs, including through a nasogastric probe in the form of suspensions, in patients in critical states (sharp blood loss, sepsis, sharp heart or respiratory failure) In our opinion, it is initially deprived of any meaning. This is due to a number of circumstances. First, the proton pump inhibitors are acid-resistant compounds inactivating in contact with hydrochloric acid, which determines the need to conclude an active substance of oral molds of the IPP in a capsule or gelatin shell. The introduction of unprotected active form The IPP in the form of a suspension into the lumen of the stomach naturally leads to its inactivation. Secondly, since the absorption of IPP occurs in a small intestine, reduced due to blood loss, peritonitis or polyorganic insufficiency The motor activity of the digestive tube determines the pronounced decrease in the bioavailability of IPS. A. Dunn et al. (1999), D. Heyland et al. (1995) indicate that the IPP injected in the form of suspension may have unstable bioavailability and require patient adequate absorbative activity, which changes in critical states. Thirdly, to ensure the informativeness of dynamic endoscopic control, it is necessary to maintain the lumen of the stomach and duodenum "clean". In this regard, it should be recognized that only the parenteral administration of proton pump inhibitors is considered the only acceptable embodiment of antisecretory prevention of stressful erosive-ulcerative damage to the gastroduodenal zone.

The real possibility of the prophylactic use of IPP in patients in critical states has appeared with the introduction into the clinical practice of omeprazole for parenteral administration. Currently, another representative of IPP with the possibility of parenteral administration is available for clinical use - Pantoprazole (controls).

Pantoprazole is a highly efficient inhibitor H + / K + -ATF-Ase. The drug reduces the level of basal and stimulated (regardless of the type of irritant) secretion of hydrochloric acid in the stomach. As is known, the duration of the validity of the IPP depends on the rate of regeneration of new proton pumps, and not on the duration of finding the drug in the body. The average half-life of pantoprazole after its single intravenous administration at a dose of 40 mg is about one hour. Nevertheless, the suppression of the secretion of hydrochloric acid is preserved for about three days. This is due to the achievement of a certain balance between the number of newly synthesized proton pump molecules and the number of already inhibited molecules. The unit / in Pantoprazole dose provides fast (for 1 hour) dose-dependent inhibition of acidic products: with the introduction of 40 mg - acidic products decreases by 86%, 60 mg - by 98%, 80 mg - by 99%, and not only acidic acid decreases Products, but also the volume of gastric secretion. After intravenous administration of a standard dose of pantoprazole in 80 mg after 12 hours, the degree of acidity decrease is 95%, and after 24 hours - 79%. In a person, a half-period of the oppression of the secretion of acid after taking Lansoprazole is ~ 13 hours, omeprazole - ~ 28 hours and pantoprazole - ~ 46 hours. Consequently, Pantoprazole is caused by the longest oppression of the secretion of acid compared to the listed IPSs. This is due to the specific binding of it with a cysteine \u200b\u200blocated in 822, which is immersed in the transport domain of the gastric acid pump. Binding precisely with this amino acid determines the longest effect of pantoprazole compared to other IPPs (Fig. 3). This is an important factor, since the restoration of acid products is completely dependent on self-renewal of proteins of the proton pump.

. Advantages of controllers in patients with gastrointestinal bleeding (HCR)

Controls has a permanent linear predictable pharmacokinetic. Just doubling the dose of IPPs having nonlinear pharmacokinetics, their serum concentration will be either lower or higher than expected, i.e. She is unpredictable. This can lead to inadequate monitoring of acid secretion or affect the safety of the use of the drug.

A distinctive feature of the controller is its lowest potential of drug interaction. Pantoprazole's ability to interact with other simultaneously injected drugs is very small due to its low affinity to the metabolizing isoenzyme of cytochrome P-450 and passing in the II phase of the conjugation reaction. Pantoprazole is not included in the known metabolic pathways of interaction with other drugs, which is of fundamental importance for patients of intensive therapy offices receiving a large amount of drugs at the same time.

Metz D. et al. (2001) A study was conducted in the effectiveness of the use of pantoprazole for the prevention of repeated bleeding from peptic ulcers. Used two doses of pantoprazole - 40 mg 1 / day. For 3 days (low dose) and 40 mg, followed by continuous administration (8 mg / h) for 3 days (large dose). 168 patients with bleeding ulcers (forrest IA, IB and IIA) after endoscopic hemostasis by the introduction of adrenaline on a randomized principle was administered a large or low dose of pantoprazole. The frequency of recycling of bleeding for 72 hours in both groups was the same - 12% in the group that received a small dose, and 13% is a large dose. The need for blood transfusions was also the same with both types of treatment. The authors concluded that "both continuous B / in pouring pantoprazole after the injection of the initiating dose and the repeated introduction is equally effective for the prevention of re-ulcer bleeding." For the prevention of re-IDC after its primary stop, it is necessary to maintain ahhorhydria, which requires repeated injections or constant slow pantoprazole infusion. To this end, it is recommended to be permanent in / under the main dose of 8 mg / h.

The positive role of intravenously administered pantoprazole for the prevention of stress-ulcers in the departments of intensive therapy was also demonstrated in the study of ARIS R. et al. (2001), which is a retrospective analysis of the clinical use of an intravenous IPN form for a six-month period. Of 97% of patients who had a high risk of developing stressful ulcers, preventive effect Against the background of intravenous administration of 40 mg pantoprazole, once a day was achieved in almost 90% of cases. Only in 7% of cases it took treatment for ulcerative bleeding. Very important result this study There was no indication of adverse effects and significant interactions of intravenously administered pantoprazole with drugs traditionally used with intensive care departments in urgent situations.

A number of researchers (based on more of theoretical conclusions) is a fear that increasing the intragastric pH can enhance the bacterial colonization in the rotoglot and appear by the risk factor for the development of nosocomial pneumonia. However, the works of W. Geus (2000), D. Cook and SowA. (1991, 1996, 1998) and M. Tryba et al. (1991) It is proved that the colonization of bacteria in the stomach rarely leads to the pathological colonization of bacteria in the rotoglot, and the risk of developing nosocomial pneumonia when using proton pump inhibitors does not increase.

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

Table 1. Significance of risk factors for the development of gastroduodenal stress-ulcers in patients in critical states

At the same time, if the sum of RR in a particular patient is equal to or exceeds the value 2, then the use of IPP V / V according to the scheme is shown: 40 mg twice a day Bolus or continuous infusion of the drug at a rate of 4 mg / h. If the sum of RR in a particular patient is less than the value 2, the use of IPP V / V according to the scheme: 40 mg once a day Bolus or continuous infusion of the drug at a speed of 2 mg / h.

In conclusion, we will focus on another aspect of the prevention of stress damage to gastroduodenalzones, namely, on the pharmacoeconomic significance of prevention. Domestic studies in this issue So far has not been conducted. On the contrary, foreign colleagues, for whom, the concept of adequacy of treatment is invariably included its value, demonstrated that in the absence of full-fledged prevention in patients with risk groups under stress ulcers, "the miser is forced to pay twice." So, S. CONRAD ET AL. (2002) indicate that when bleeding from stress-ulcer, the patient in the separation of intensive therapy is required, additional 7 hematological studies are required, 11 units of erythrocyte mass, at least two endoscopic studies. D. Heyland et al. (1995) under similar circumstances noted an increase in the period of finding a patient in the separation of intensive therapy to 11.4 days, and the required period of use of anti-rich agents - up to 23.6 days. B. ERSTAD (1997) noted that the average cost of treating one patient from the risk group on the occurrence of stress-ulcers without preventing stressful damage is $ 19850, and using antisecretory prophylaxis - $ 15812. Moreover, if the cost of prophylactic parenteral use H 2-blocks amounted to $ 2275, then the cost of using proton pump inhibitors is only $ 1417.

Thus, the high frequency of stressful erosive-ulcerative lesions of the gastroduodenal zone and the enormous figures of mortality during bleeding from stressful ulcers require bonded adequate prophylactic measures in patients in critical states. The main component of this prevention is preventive administration of risk group patients on the occurrence of stress-ulcers of parenteral forms of proton pump inhibitors.

Literature

1. Aruine L.I., Kapuleler L.L., Isakov V.A. Morphological diagnosis of stomach and intestines. M., 1998, p. 165-222.
2. Gelfand B.R. et al. Prevention of stress-ulcers in patients in critical states. Guidelines Races. 2004.
3. Gutsheev V.K., Evseev M.A. Antisecretory therapy as a component of a conservative hemostasis in acute gastroduodenal ulcerative bleeding. Surgery, No. 8, 2005, p. 52-57.
4. Gutsheev V.K., Evseev M.A. Gastroduoden bleeding of ulcerative etiology. Guide for doctors. M., 2008, 380 p.
5. Evseev MA Nonteroidal anti-inflammatory drugs and digestive tract. M., 2008, 194 p.
6. Efimenko N.A., Lysenko M.V., Astashov V.L. Bleeding from chronic gastroduodenal ulcers: modern views and treatment perspectives. Surgery, 2004, № 3, p. 56 - 59.
7. Isakov V.A. Proton pump inhibitors: their properties and use in gastroenterology. M., "Academkniga", 2001, 304 p.
8. Kostyuchenko A.L., Gurevich K.Ya., Lykin M.I. Intensive therapy postoperative complications. SPb., 2000, 575 p.
9. Kubashkin V.A., Shishin K.V. Erosive-ulcer lesion of the upper departments of the gastrointestinal tract in the early postoperative period. Consilium Medicum, 2004, №1, p. 29-32.
10. Tipman N., Metz D.S. Pathophysiology and prevention of stressful ulcers in postoperative patients. RMW, 2005, Volume 13, No. 25, p. 1668-1674. Ahmed T. Update On Treatment of Stress-Related Bleeding In Critically Ill Patients. Resident Reporter, 2000; 5: 71-75.
11. ARIS R., Karlstadt R., Paoletti V. et al. Intermittent Intravenous Pantoprazole Achieves a Similar Onset Time to Ph\u003e 4.0 in ICU Patients As Continuous Infusion H2-Receptor Antagonist, without Tolerance. Abstr. Am. J. Gastroenterol., 2001; 96: S48.
12. Cook D.J., Fuller H.D., Guyatt G.h. et al.: Risk Factors for Gastrointestinal Bleeding In Critically Ill Patients. N ENGL J MED 1994; 330: 377-381.
13. Cook D.J., Reeve B.k. , Guyatt G.h. ET AL: STRESS ULCER PROPHYLAXIS IN CRITCALLY ILL PATIENTS: RESOLVING Discordant Meta-Analyses. Jama 1996; 275: 308-314.
14. Fennerty M.B.: Pathophysiology of the Upper Gastrointestinal Tract in the Critically Ill Patient. Rationale for Therapeutic Benefits of Acid Suppression. CRIT CARE MED 2002; 30: S351-S355.
15. Kauffman GL, Conter RL. Stress Ulcer and Gastric Ulcer. In: Greenfield LJ, Mulholland MW, Oldham Kt, Zelenock GB, Lillemoe Kd, Editors. Surgery: Scientific Principles and Practice. 2nd ed. Philadelphia: Lippincott-Raven; 1997. p. 773-88.
16. Metz D. C. et al. Am. J. Gastroenterol. 2000; 95, 3: 626-633.
17. Morgan D.G., Jain A., Bednarowski C. Utilization of Iv Ranitidine and IV Pantoprazole in the Intensive Care Unit of a University TEACHING CENTRE. Abstr. Gastroenterology 2001; 120: A1309.
18. Schonekas H. et al. Gastroenterology 1999; 116, 4 (Part 2): A305.
19. Sharma v.k., Howden C.W. High Dose IV PPI IS LESS COSTLY THAN STANDARD MEDICAL MANAGEMENT FIR PREVENTING ACUTE RECURRENCE OF PEPTIC ULCER HEMORRHAGE A COST-MINIMIZATION ANALYSIS. Gastroenterology 2001; 120: A251.
20. Sharma V.K., Leontiadis G.I., Howden C.W. Intravenous Proton Pump Inhibitors for Peptic Ulcer Hemorrhage: Meta-Analysis of Randomised Controlled Triaals Allowing Endoscopic Treatment. Gastroenterology 2001; 120: A248.
21. Somberg L., Karlstadt R., Gallager K. et al: Intravenous Pantoprazole Rapidly Achieves PH\u003e 4.0 in Icu Patients without the Development of Tolerance. Abstr. Gastroenterology 2001; 120: A838
22. Zhonglin Y. et al. J. Gastroenterol. Hepatol. 2002; 17 (Suppl): A257.

Read: B. Chronic insufficiency of pregglicionary vegetative nerve fibers. Long-term mechanisms for compensation for metabolic acidosis are implemented mainly by the kidneys and is substantially at least with the participation of buffers of bone tissue, liver and stomach. Acid and pepsin stomach. Grinding and mixing food Contrast radiography - the discovery of a contrasting substance beyond the contour of the stomach. Macrobreparation number 16. Chronic aneurysm left ventricular heart Acute gastritis acute inflammatory disease of the stomach.

This macropreparation is a stomach. The masses and size of the organ normal, the form is preserved. Light gray organ, relief is strongly developed. At the small curvature of the stomach in the pyloric department, a significant recess in the wall of the stomach 2x3.5 cm is localized. Its limiting the surface of the organ is deprived of the characteristic folding. The folds are converted to the borders of education. In the area of \u200b\u200bthe pathological process, there are no mucous membranes, submembricted and muscle layers of the stomach wall. The bottom is smooth, made by a serous shell. The edges roluit are raised, dense, have a different configuration: the edge addressed to the gatekeeper, gentle (due to the 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; drugs; the harmful habits that lead to local disorders: the hyperplasia of the ferrous apparatus, an increase in the activity of the acid-peptic factor, an increase in motorbish, an increase in the number of gastrosis cells; and a general impairment: the excitation of the centers and the hypothalamic-pituitary area, an increase in the tone of the wandering nerve, an increase and subsequent depletion of the production of ACTH and glucocartycoids). Driving on the gastric mucosa, these violations lead to the formation of the defect of the mucous membrane - erosion. Against the background of non-healing erosion, an acute peptic ulcer is developing, which, with continued pathogenic effects, goes into a chronic ulcer, which takes place periods of exacerbation and remission. During the remission period, the bottom of the ulcers can be powered by a thin layer of the epithelium, layering on a scar cloth. But during the exacerbation of "healing" is leveled as a result of fibrinoid necrosis (which causes damage not only directly, a and by fibrinoid changes in the walls of the vessels and violation of tissue trophics).

1) Favorable: remission, healing of ulcers by scarring with subsequent epithelization.

2) unfavorable:

a) bleeding;

b) running;

c) penetration;

d) malignancy;

e) inflammation and ulcer-scar processes.

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

Diagnosis: chronic stomach peptic disease.

386. Chronic stomach ulcer.

On the small curvature of the stomach, the ulcerative defect is visible to 1 cm in diameter, bottom and edges dense, rolic-shaped.

108. Chronic stomach and 12-rosisse ulcers.

On the mucous membrane of the stomach and the 12-repulitory intestine, 3 ulcerative defects in the stomach of the ulveneous shape with imputed dense edges and a dense bottom are visible. In a 12-risen intestine of 2 ulcers of a rounded form, located against each other ("kissing ulcers"), in one of them perforated hole

128. Melena (bleeding in the gastrointestinal clearance).

Black gloss mucosa (pigment salty hemathine, methemoglobin, sulfur iron)

149. Swifts of stomach cancer. 184. SKIRR stomach.

Stomach cancer.

Ex-and endophyte growth.

146. Non-specific ulcerative colitis.

On the mucous membrane of the colon multiple ulcerative defects

various shapes and sizes.

A. Polypoid cancer.

75b. Myoma stomach.

Examine microspections:

62a. Chronic stomach ulcer (aggravation stage).

In the bottom of chronic ulcers, 4 layers are distinguished:

1) On the surface of the ulcerative defect there is a necrosis area with leukocytes, 2) under it - fibrinoid necrosis, 3) below the zone of granulation tissue is visible, followed by 4) the sclerosis zone with lymphoid infiltrates and sclerized vessels.

90. Acute purulent appendicitis (phlegmozno-ulceal).

(see simultaneously drug 151. Normal appendix)

All layers of the process infiltrated with leukocytes, the mucous membrane is ulcerated. In the submucosal shell, full-blooded vessels and hemorrhage

177. Chronic appendicitis with the regeneration of the mucous membrane.

The wall of the process is thickened due to the growth in all layers of fibrous connective tissue, the newly formed low cubic cells of the epithelium are enclosed on a pepper

140. Cholecystitis.

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

74. Solid stomach cancer.

Parenchima and stromium in tumors are uniformly developed. Parenchima is represented by atypical cells forming cells. Anaplazated epithelium proliferates, it germs outside the mucous membrane - infiltrating growth

And t (drawings):

T e s t s: Select the right answers.

433. The causes of acute gastritis are:

1- alcoholism

2 - infection

3- Swallowing of traumatic substances

434. The following changes are characteristic of atrophic gastritis:

1- mucous pink, with well-pronounced folds

2- mucous pale

3- in the stomach a lot of mucus

4- focal regeneration of the epithelium

435. The main heavy complication of the stomach ulcers is:

1- lymphadenitis of regional nodes

2- perforation

3-perigastrites

4- "inflammatory" polyps around ulcers

436. The most characteristic changes in vessels in the bottom of chronic ulcers are:

1- Inflammation and sclerosis of the wall

2- full-range

3- Malokrovia

4- large thin-walled sinusoidal vessels

437. To the local factor having a value in the pathogenesis of ulcerative disease of the stomach and duodenum, refers:

1- infectious

2- trophic violation

3- Toxic

4- Reducing the secretion of gastrin and histamine

5-exogenous

438. Layers of the bottom of chronic stomach ulcers are:

1- Exusudate

3- granulation fabric

4- sclerosis

439. Many stomach erosions from the burn coated with salty hematine detected at the opening of the deceased. Erosion formed:

1- to burn

2- During burn

440. On the gastric mucosa, the liquid of the coffee form. When cleaning from it, dotted hemorrhages and defects with a magnitude with a pin head are visible. Specify the name of the process:

1 - Petechia

3-sharp ulcers

441. At opening in the stomach, two round ulcers were found, located on a small curvature, the edges are smooth, the bottom is thin. Ulcers are:

1-sharp

2-chronic

442. Signs of chronic ulcers are:

1- Repeated bleeding

2- dense sclerosed bottom

3- multiplicity of ulcers

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