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6 Cards in this Set

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6 hours after MI light microscopic changes in mycoardium
contraction band necrosis
the beginning of coagulation necrosis
*The contraction bands are formed at the infarction border upon reperfusion of the damaged tissue.
Creatinine kinase and Lactate dehydrogenase serum [] changes following MI
CPK levels rise within hours and fall to baseline within a few days.
LDH rises later and persists longer.
*SGOT (ALT) levels are also altered, but these are less specific.
Marfan's syndrome effects on heart
leads to dilation of the aortic root and myxoid degeneration of the aortic valve leaflets.
These patients are at risk for aortic dissection as well aortic regurgitation.
In tertiary syphilis affect on heart
inflammation of the aortic wall leads to aneurysmal dilatation of the proximal aorta and the aortic valve ring. The coronary ostia are often involved. There is risk of rupture of the aortic aneurysm.
histological appearacne of mitral prolapse
There is increased mucopolysaccaride material within the stroma of the valve as shown in this alcian blue stain of a resected prolapsed mitral valve.

The histologic appearance of aortic valves in patients with Marfan's syndrome is identical.
increased mucopolysaccaride material within the stroma of the valve

The histologic appearance of aortic valves in patients with Marfan's syndrome is identical.
Factors implicated in the development of infective endocarditis by organisms of low virulence include:
1.) Defective or regurgitant blood flow creating turbulence;
2.) Platelet-fibrin deposits forming in endocardium in areas of turbulence;
3.) Seeding of the thrombotic deposits by organisms circulating in the blood;
4.) Antibody agglutination producing clumps of organisms. Thus, previously damaged or abnormal valves, which distort blood flow, actually aid in the deposition of low virulent organisms onto their surfaces.

*Highly virulent organisms possess adhesion surface proteins that enable the bacteria to agglutinate on normal valve tissue directly. Thus, these organisms may infect otherwise undamaged endocardium and may induce further valvular damage.