atherosclerosis and IHD Flashcards
what is the first step in the pathogenesis of atherosclerosis
endothelial injiury and dysfunction causes increased permeability and adhesion
what is the second step in the pathogenesis of atherosclerosis
witht eh increased permeability LDL lipoproteins seep into the vessel wall
what is the third step in the pathogenesis of atherosclerosis
cytokine release from activated EC attracts monocytes which then travel into the intima of the vessel and turn into activated macrophages and englulf the LDL to become the foam cells
what is the fourth step in the pathogenesis of atherosclerosis
further cytokine and growth factor release from endothelial cells and macrophages leads to smooth muscle cell recruitment
what is the fifth step in the pathogenesis of atherosclerosis
smooth muscle cells then proliferate and deposit ECM these can also engulf LDL to become a foam cell
what is the sixth step in the pathogenesis of atherosclerosis
an atherosclerotic plaque forms within the intima and physically closes in on the lumen. neovascularization can occur in the fibrous tissue within these plaques. the core of it is a centre of necrosis with the lipids as they are all dead in the centre.
where is there neovascularisation in the atherosclerotic plaque
in the fibrous cap of the plaque there is neovascularisation
what is entailed in the term acute plaque change
haemorrhage occurring into the plaque, leading to plaque expansion or rupture. or plaque ulceration, erosion or rupture leading to thrombosis and partial or complete vessel occlusion
how does an abdominal aortic aneurysm form
there is the inflammatory process leading to the development of the atherosclerotic plaque which then sees increased intimal thickness and degeneration of the media, resulting in vessel dilation. the vessel can also then just kinda rupture
where does the angina pain commonly radiate and where to
will commonly radiate to left shoulder and the left jaw and neck. this is because the cardiac nerves go into the spinal cord at the same level as the neurons for these dermatomes. all the neurons then synapse on the same interneuros causing afferent pain signalling to be mixed and the brain perceives it from being from different places
a myocardial infarction is caused by what
this is ishcemia of the heart that is severe enough to cause myocardial death, it is mostly due to acute plaque change of atherosclerotic vessels combined with arterial thrombosis that occludes.
whats the key biomarker when looking at a case of myocardial infarction
the troponin t levels, this is a very cardio specific enzyme
what are the gross changes we see in cardiac tissue from 0-12 hours post MI and 12-24
0-12 no change
12-24 dark mottling due to tissue stagnation of blood
what are the gross changes we see in cardiac tissue 1-3 days post MI and 3-7 days
1-3 the same mottling but with a yellow coagulative center due to necrosis with neutrophil infiltrate
3-7 pale yellow tan infarct with hyperemic boarder
what are the gross changes we see in cardiac tissue 10-14 days and 2-8 weeks post MI
10-14 days Reddish depressed hyperemic border (rim of highly vascularized granulation tissue)
2-8 weeks: grey to white scarring due to collagen deposition and scarring.
what do we see microscopically 4-12 hours and 12-24 hours post MI
4-12, oedema, haemmorhage and early coagulative necrosis
12-24 early infiltrate by neutrophils, nuclei of myocytes and dark and small. evidence of acute inflammation as necrosis to muscle elicits acute inflammation
what microscopic changes do we see in the heart 1-3 days and 3-7 days post MI
1-3 days myocytes lose their nuclei and cross striations, there is now marked infiltration into the interstium by neutrophils
3-7 days: infiltration by macrophages to clear the necrotic debris
what microscopic changes do we see in the heart 10-14 days and 2-8 weeks post MI
10-14 days we get a well established granulation tissue
2-8 weeks there is collagenous scarring
whats the difference between STEMI and NSTEMI
STEMI is a full transmural infarct in a person. so it causes significant ST elevation as the full thickness of the cardiac wall has died in the ischemic event
