Histopath - cardio Flashcards
Describe the pathogenesis of an atherosclerotic plaque
- ENDOTHELIAL injury –> endothelial dysfunction (increased permeability and adhesion)
- LDL enters intima and is oxidised
- MACROPHAGES enter intima + take up ox-LDL –> FOAM CELLS!
- Foam cells die –> necrotic core
- Attracts even more white cells
- VSMCs form fibrous cap
3 main components of a plaque
- Lipid core - necrotic
- Fibrous cap with collagen and ECM
- Cells - VSMCs, foam cells,
Which part of the aorta is more commonly affected by atherosclerosis - thoracic or abdominal?
ABdominal
What kinda flow through vessels is atherogenic? What kinda flow protects against atherogenesis
Atherogenic = Turbulent, oscillatory shear stress Protective = High laminar flow
4 outcomes of atheromatous plaques?
i.e. what can happen to them eventually which has subsequent v bad results
- Obstruction (70% occlusion –> stable angina)
- Rupture (exposes pro-thrombotic contents)
- Erode(exposes pro-thrombotic contents)
- Haemorrhage into plaque
RFs for atherosclerosis ? split them into 2 categories
Non-modifiable: age, gender, family Hx
Modifiable: cholesterol, HTN, obesity, T2DM, smoking
CAUSE OF STABLE ANGINA?
Atheromatous plaque causes 70% occlusion of a vessel, + myocyte demand exceeds supply.
This level of occlusion cannot be reversed by vasodilatation
3 types of angina
stable
unstable
Prinzmetal
Describe the pathogenesis of myocardial infarction
Myocyte necrosis due to acute ischemia as a result of a sudden event - eg plaque rupture + thrombosis or vasospasm
At what point does myocyte schema –> myocyte necrosis
after 20-40 mins of ischemia
How can psychological stress –> MI?
Adrenaline release –> vasoconstriction –> physical stress on atheromatous plaque –> plaque rupture etc etc
Does HF always come after and MI?
No!
Myocardial ischemia for 1 minute leads to reduced myocyte contractility –> HF
However, myocytes don’t die until >20 mins of ischemia
Thus HF can precede myocardial infarction
3 most common complications of Mi
- Contractile dysfunction (–> shock)
- Arrhythmia
- Cardiac rupture of ventricular wall(–> haemopericardium)
A patient develops mitral regurgitation after an MI. How has this happened?
Papillary muscle dysfunction/necrosis/rupture due to LV infarct
Mean time post-MI for ventricular wall rupture?
4-5 days
2 Most commonly affected arteries in MI?
LAD
RCA
Mean time post-MI for arrhythmia
within 24 hours
Mean time post-MI for ventricular aneurysm?
> 4 weeks
Mean time post-MI for pericarditis?
2-4 days
Pt develops chest pain relieved on leaning forward, and fevers, 2 months after admission for MI?
Dresslers syndrome
Histological findings of MI after 4 hours?
Normal histology
Histological findings of MI after 23 hours?
Loss of nuclei, necrotic cell death
Histological findings of MI after 3 days
Infiltration of neutrophils, then macrophages
Histological findings of MI after 10 days
NEW BLOOD VESSELS (angioblasts)
Collagen synthesis
