Atherosclerosis and ischemic heart disease Flashcards
What is coagulative necrosis?
What is the pathogenesis of ischemic heart disease?
What is atherosclerosis?
What underlies it?
Which vessels are mostly affected?
Go through the steps from healthy artery to atheroma formation?
Which layer is the atheroma formed?
What are each of the arrows pointing to?
What is the early stage of atherosclerosis formation?
Fatty streaks
Explain what ‘hardening’ of arteries mean?
how does an aneurysm form?
Hardening of the arteries occurs because the tunica media can become ischemic because the diffusion of the blood cannot reach the muscle. It then becomes fibrous tissue instead. This can weaken the wall and a secular dilation of the wall can occur causing an aneurysm.
The main complications of atherosclerosis?
- Acute plaque change also.
What is this and why does it occur?
AAA: Abdominal aortic aneurysm
Right and left iliac artery bifurcation.
It often occurs here.
There is always a thrombus here because of the endothelial injury, stasis of the blood and hypercoagulability states (thrombogenic substances often).
A ruptured aneurysm often causes hypovolemic shock and death.
What causes an acute plaque change?
What are the consequences?
Stable vs vulnerable plaque
What is this showing?
What is this showing?
What is considered to be a critical stenosis amount?
Chronic vascular occlusion of 70-75% of vessel (one or more of the LAD, RCA, LCX occluded).
What are the 4 main presentations of IHD?
Stable angina, vs unstable angina, vs prinzmetal angina?
What occurs in an MI that doesnt occur in angina?
How does it present differently?
What blood tests can you do for an MI?
What is a STEMI?
Where does necrosis start first?
How can you avoid getting one?
Necrosis starts at the subendocardial area as it is furthest from the blood supply. More time it involved the whole wall of the left ventricle.
Mur means wall in french.
Relieving the obstruction as quickly as possible will save muscle.
STEMI (pronunced stemy): ST elevation of an MI. ST elevation are typical on the ecg of a transmural MI.
Arteris involved and percentage of occurance?
How late is this infarct and how do you know?
How old is this infarct and how do you know?
Hyperemic=large amounts of blood=granulation tissue.
HOw old is this infarct?
What is the problem with it?
Eosinophilia=uptakes more of the eosin stain because of the loss of the rna (which takes up the haemolotoxin). Nucleas dissapears.
How old is this infarct?
Myocytes are devoid of nuclei (cental nucleus normally).
Lack striations. L.
How old is this infarct?
How old is this infarct?
MI complications?
Right side vs left side complications?
- Pericarditis: 1-2 days after transmural infarct.
- Mural (wall) thrombus formation: due to stasis, endothelial damage. This may embolise (anticoagulants given).
- Ventricular aneurysm formation: late scarring and bulging of ventricle wall, can lead to mural thrombus formation.
What are each of these complications?
Explain how IHD can lead to heart failure?
Left sided vs right sided lead to what?
What are these complications of?
Explain each
- Congestion of the liver in certain areas which gives it a mottled appearance: call it nutmeg liver: cut a nutmeg in half.
- Crepitations: listen to the lungs you can hear something like water bubbling. You are hearing air going inside the alveoli which have water in them.
