atherosclerosis and IHD

Question 1

what is the first step in the pathogenesis of atherosclerosis

Answer 1

endothelial injiury and dysfunction causes increased permeability and adhesion

Question 2

what is the second step in the pathogenesis of atherosclerosis

Answer 2

witht eh increased permeability LDL lipoproteins seep into the vessel wall

Question 3

what is the third step in the pathogenesis of atherosclerosis

Answer 3

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

Question 4

what is the fourth step in the pathogenesis of atherosclerosis

Answer 4

further cytokine and growth factor release from endothelial cells and macrophages leads to smooth muscle cell recruitment

Question 5

what is the fifth step in the pathogenesis of atherosclerosis

Answer 5

smooth muscle cells then proliferate and deposit ECM these can also engulf LDL to become a foam cell

Question 6

what is the sixth step in the pathogenesis of atherosclerosis

Answer 6

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.

Question 7

where is there neovascularisation in the atherosclerotic plaque

Answer 7

in the fibrous cap of the plaque there is neovascularisation

Question 8

what is entailed in the term acute plaque change

Answer 8

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

Question 9

how does an abdominal aortic aneurysm form

Answer 9

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

Question 10

where does the angina pain commonly radiate and where to

Answer 10

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

Question 11

a myocardial infarction is caused by what

Answer 11

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.

Question 12

whats the key biomarker when looking at a case of myocardial infarction

Answer 12

the troponin t levels, this is a very cardio specific enzyme

Question 13

what are the gross changes we see in cardiac tissue from 0-12 hours post MI and 12-24

Answer 13

0-12 no change
12-24 dark mottling due to tissue stagnation of blood

Question 14

what are the gross changes we see in cardiac tissue 1-3 days post MI and 3-7 days

Answer 14

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

Question 15

what are the gross changes we see in cardiac tissue 10-14 days and 2-8 weeks post MI

Answer 15

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.

Question 16

what do we see microscopically 4-12 hours and 12-24 hours post MI

Answer 16

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

Question 17

what microscopic changes do we see in the heart 1-3 days and 3-7 days post MI

Answer 17

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

Question 18

what microscopic changes do we see in the heart 10-14 days and 2-8 weeks post MI

Answer 18

10-14 days we get a well established granulation tissue
2-8 weeks there is collagenous scarring

Question 19

whats the difference between STEMI and NSTEMI

Answer 19

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