Case 10 Diseases of the cardio-vascular system

 

 

1. Recurrent-warty  endocarditis.

2. The Lerish’s  syndrome.

3. Stenosing  atherosclerosis of coronal arteries of heart.

4. Septic endocarditis.

6. Concentric hypertrophia  of myocuardium (compensating, tonogenic).

7. Artificial valve of heart.

8. Primary-wrinkled kidney.

9. Unspecific aortoarteritis (the Tacayasu illness).

10. Warty endocarditis with hypertrophia of myocardium.

11. Lipidosis of aorta.

12. Atherosclerotic cardiosklerosis.

13. Hypertrophia  of left ventricle with cardiosklerosis.

14. Concentric hypertrophia of myocardium

      (compensating ).

15. Hemorrhage in a cerebrum. 

16. Hemorrhage in lateral ventricles.

17. Thrombosis of aorta.

18. Artificial valve of heart.

19. Hemorrhage in a cerebrum. 

20. Poliposis-ulcerous endocarditis.

23. Perforation of ulcer at a polipous-ulcerous   endocarditis.     

24. Heart attack of myocardium with parietal  blood clots.

25. Heart postinfarctis cardiosclerosis.

26. Vast heart attack of myocardium.

28. Aterosclerosis aortas.

29. Complication of atherosclerosis of aorta.

30. Heart attack of myocardium and tamponade pericardium.

31. Separation  aneurism of aorta.

32. Artificial valve of heart and nutmeg liver.

33. Polipous-ulcerous endocarditis.

34. Atherosclerosis of aorta, atherosclerotic-wrinkled kidney.     

 

 

1. Recurrent-warty  endocarditis. Cuspids of mitrale valve are represented on preparation, they are thickened due the excrescence of connecting tissue, that points on the carried more early inflammation and dystrophic changes in connecting tissue of valve and chords. On the extremities of valve the bulges which are the result of depositing of trombocytic  masses on the damaged cuspids are visible. Consequently combination of sclerotic changes with the fresh destructive changes of valves takes place , that confirms chronical motion of disease. The acquired defect, and also thromboembolic complications, in the vein part of blood circulation is often formed in such case.

 

2. The Lerish’s  syndrome. Pathology of aorta in the place of its bifurcation  with a next injuring of arteriae iliacae communis of atherosclerotic genesis. There are of obturatorical blood clots  in the place of bifurcation of aorta. Such changes develop in the stage of complications of atherosclerosis. The consequens of thromb`s formations of iliac arteries is ischimia of lower extremities that will cause the gangrene.

 

3. Stenosing  atherosclerosis of coronal arteries of heart. On preparation there are convoluted and thickened coronal arteries of heart. The bulge is caused by depositing of atherosclerotic plaque, that’s why the arterial space narrows on 25-75%, that determines decreasing  blood supply of myocardium. As a result one can see a myocardial ischemia, dystrophic changes  and even circulatory ischemic necrosis (heart attack). Finaly, as a result of these changes one can see forming of cardiosclerosis – replasing of myocardium by connecting tissue. It can have diffuse and large focal postinfarct cardiosclerosis of grey color are exposed in the apical region there.

 

4. Septic endocarditis. On preparation we can see the injuring of cuspids of aortic valves. Cuspids are thickened with the signs of destructive changes which appears as a result of septic injuring by the staphilococcus. There are valve’s condyles and ulcers on preparation, that  is polypous-ulcerous endocarditis. The complication development of septic (bacterial) emboli  in the large circle of  blood  circulation.

 

5. Concentric hypertrophia  of myocuardium (compensating, tonogenic). There is the cut of heart’s camera of right and left ventricles. The wall of left ventricle is hypertrophied to 2 sm. Hypertrophy develops in a heart during hypertension illness, and heart defects  (stenosis of aortic valves at a septic endocarditis).  The initial stages of disease  is characterized by development of compensating hypertrophy not only of muscular fibres but also stromal (vessels, nervous fibres, connectivetissular framework). Hypertrophia of muscular fibres  courses due to hyperplasy of organelles.

 

7. Artificial valve of heart. There is an artificial valve in the mitralis valve, it is put in connection of the acquired defect of mitralis  valve, which developed after its rheumatic injuring.

 

8. Primary-wrinkled kidney. The kidney is diminished in sizes. On the surface it is small tubercular, with solid consistency. Such changes in kidney develop during hypertensive illness when in glomerulas artery appears the phenomenon of hialinosis and sclerosis, that worsen blood supplement of kidney’s parenchyma and cause the sclerotic changes in it. Macroscopically it looks like invagination on the surface of kidney with the near building, which are the result of compensating hypertrophy processes in well-kept glomerules.

 

9. Unspecific aortoarteritis (the Tacayasu illness). In the wall of aorta and large arteries we can see development of inflammatory processes. Productive character of inflammation takes place, granulomas can appear. Aorta wall deformation, aneurism can develops. For liquidation of destructive changes they provide operative interference with the change of aorta damage by artificial material, that we can see on preparation.

 

10. Warty endocarditis with hypertrophia of myocardium.

Example of rheumatic injuring of mitralis valve. As a result of mucoud, fibrunoid edema damage of endocardis on the cuspids of valve appear warty stratifications of trombotic  masses with next destructive changes. Such changes in the wall of valve coused defects with hipertrophia of myocardium or to tromboembolicus complications.

 

11. Lipidosis of aorta. There are yellov-grey strips on intima of aorta, which are hardly visible. That’s the first stage of development of atherosclerosis, when lipids such as a cholesterol and his ethers are deposited in intima.

 

12. Atherosclerotic cardiosklerosis. Cut of cardiac muscle with the presence of grey stripes of diffuse character. It is the areas of changing of cardiac muscle with connecting tissue. Atherosclerotic eccentric testifies stenosis coronal arteries point on the atherosclerotic origin of these changes.

 

13. Hypertrophia  of left ventricle with cardiosklerosis. On preparation  we can see the cut of cardiac muscle with the signs of hypertrophia of left ventricle by 2см with simultaneous hypertrophia of nipples muscle. Among myocardium we can see grey areas of diffuse character, that is a result of injuring of cardiac muscle at hypertensive illness.

 

14. Concentric hypertrophia of myocardium

      (compensating ). There is the cut of chambers of right and left ventricles of heart. The wall of left ventricle is hypertrophied by 2см, hipertrophia in a heart develops at hypertensive illness, at the defects of heart (stenosis aortic valves at a septic endocarditis). On the initial stages it characterized by development of hypertrophia not only muscular fibres but also stromalis (vessels, nervous fibres, connectivetissular framework). Hypertrophia of muscular fibres  passes due to hyperplasia of organel.

 

15. Hemorrhage in a cerebrum.  On the cut of cerebrum tissue the hemorrhage  of small sizes is visible in the area of grey matter. Such complication can develop at hypertensive illness, that is observed in the third stage of its motion (stage of organ changes) or in other stage in the case of development of hypertensive crisis. Consequences is formation of hemosiderin, which damages parenhyma of brain and it results in excrescence of connecting tissue and gliosis.

 

16. Hemorrhage in lateral ventricles. On the preparation of cerebrum we can see a hemorrhage in a lateral ventricle and distribution of haematoma on the neighbouring areas of matter of cerebrum and his destruction. Such changes arise up at  hypertensive illness or at the break  of cerebral arteries. It is mortal complication which  not compatible with life.

 

17. Thrombosis of aorta. On preparation there is aorta in the fourth stage of its injuring by atherosclerosis, when ulceration, hemorrhage and calcificatia develop in the wall of aorta. Formation of blood clot will be consequences of changes in an aorta, that takes place in this preparation. It results in worsening of blood sapplement of internal organs and lethal consequences.

 

18. Artificial valve of heart. In place of mitralis valve there is an artificial valve which put in the case of origin of the acquired defect of mitralis valve, which develops after rheumatic injuring.

 

19. Hemorrhage in a cerebrum.  On preparation there is the hemorrhage in a cerebrum, wich develop at hypertensive illness – the third stage and characterized by destruction of tissue of cerebrum.

Consequences: 1) deats; 2) forming of cyst in connection with development of coliquation necrosis. The walls of cyst have a ferruginous color in communication with depositing of hemosiderin.

 

20. Poliposis-ulcerous endocarditis. The injuring of cuspids of aortic valves is on the preparation. Cuspids are thickened with the signs of destructive changes which appears as a result of septic injuring of staphylococcus. Condilars and ulcers are on a valve is called polipous-ulcerat endocarditis. Complication is development of septic (bacterial) embolis in the large circle of of blood circulation

 

23. Perforation of ulcer at a polipous-ulcerous   endocarditis.  The injuring of cuspids of aortic valves is on the preparation. Cuspids are thickened with the signs of destructive changes which appears as a result of septic injuring of staphylococcus. Condilars and ulcers are on a valve is called polipous-ulcerat endocarditis. Complication is development of septic (bacterial) embolis in the large circle of of blood circulation. We see predominance of destructive changes in the wall of valve, that characterised by a septic endocarditis.

 

24. Heart attack of myocardium with parietal  blood clots.

On the cut of wall of left ventricle the change of colouring of cardiac is visible to the muscle with the areas of hemorrhage, necrosis. The injuring of wall has total character with fascination in the process of all layers. Depositing of trombosis  the masses is visible in the cavity of heart, that is observed as a result of injuring of internal wall, when the mechanism of trombogeniciti  is activated.

 

25. Heart postinfarctis cardiosclerosis. On preparation the cut of chamber of left ventricle is visible with his dilatation and presence of large focal areas of grey color in a intraventrycularis membrane in place of the carried heart attack of myocardium.

 

26. Vast heart attack of myocardium. On the preparation we can see the cut of chamber of left ventricle with the local injuring of wall of dark color, which occupies mainly internal and middle layers. The such massive injuring of cardiac to the muscle at the heart attack of myocardium is closed by miomallation or by forming of sharp aneurism of heart.

 

28. Aterosclerosis aortas. There is the injuring of aorta with the presence of all macroscopic stages:

1) the stage of fatty spots and bars is the areas of yellow;

2) stage of phibrunosis plaque – above a surface the phibrunosis thrusting out;

3) stage of ulceration – most expressly shown in the area of departure  large vessels from an aorta;

4) stage of calcinosis.

 

29. Complication of atherosclerosis of aorta. The last stages of motion of atherosclerosis are represented on the preparation. The areas of ulceration,  hemorrhage, formation of parietal  blood clots are visible.

 

30. Heart attack of myocardium and tamponade pericardium. The cut of heart with the areas of dark color is heart attack. In the cavity of cardiac shirt is accumulation of blood as a result of break of cardiac to the muscle and output of blood in a pericardium. Blood accumulation in the cardiac shirt  squeezes a heart and leads to death.

 

31. Separation  aneurism of aorta. Wall of aorta with the atherosclerotic injurings in the stage of complications and formation of aneurism which appears as a result of tear and removing of  the layer of intima and blood penetration in the walls of aorta and formation of thrusting out 7х10см. Consequences – dug up death.

32. Artificial valve of heart and nutmeg liver. Tere is morphogenesis of violation of blood circulation, which arises up at the rheumatic defect of heart. The defect of heart was corrected by a surgical method, substituting the valve damaged by a rheumatic process by artificial one. In a liver the signs of violation of blood circulation as vein stagnation and next morphological changes which develop in nutmeg liver.

 

33. Polipous-ulcerous endocarditis. On preparation we can see the injuring of cuspids of aortic valves. Cuspids are thickened with the signs of destructive changes which appears as a result of septic injuring of staphilococcus. There is a  condylar on a valve and ulcers  is polipous-ulcerous endocarditis. Complication: septic (bacterial) embol in the large circle of circulation of blood.

 

34. Atherosclerosis of aorta, atherosclerotic-wrinkled kidney.  On preparation there are variants of injuring of aorta and kidneys at atherosclerosis. In both cases kidneys are diminished in sizes, one kidney is deformed due to the presence of deep invagination  in place of the carried heart attacks and areas of hypertrophia. Such changes develop  as a result of atherosclerotic injurings of vessels of kidney or as a result of tearing off of atherosclerotic name-plate from an aorta,  hit from aorta in the vessels of kidneys and a next development of heart attacks of kidney.