2nd lecture clinical cases of cell death Flashcards
Renal infraction (anemic, coagulative necrosis) description
Thrombosis: in one of the vessels = triangular necrosis in cortex and medulla. Related to atherosclerotic plaque, superimposed with the coagulative blood
Embolus: fragments of blood clots. The source of the emboli 90% come from the heart; atrium and ventricle.
what causes the embolus to come from the atria of the heart?
In atria due to: arrhythmia absoluta, the oscillating of atria (not contracting) the stasis of the blood predisposes it to coagulation.
what causes the embolus to come from the ventricle of heart?
after myocardial infraction. It can also come from an atherosclerotic plaque from large vessels such as the aorta. 90% from heart, 10% from the aorta.
The process of healing in the kidney after Renal infraction?
1st day = pale area of in the shape of wedge
LATER = hyperemic rim around the tissue due to the ingrow of vessels and fibroblasts to heal tissue, macrophages eat up tissue to replace it with fibrotic tissue which contracts and make depression in the organ, as they pull the 2 sides of the organ together.
MOSTLY clinically silent: no problems as long as its not too big of an infraction.
Spleen infraction (coagulative anemic)
Very similar to Renal infraction but 100% related to emboli. Scar tissue healing and depression is seen. Silent clinical effects.
Acute myocardial infraction description?
related to ischemia of tissue (disruption of supply and demand of cells)
- coronary disease due to atherosclerosis (narrowing of lumen) the atherosclerosis plaque development take 10-20 years to develop, but the infraction is very sudden.
what is the Fixed coronary?
fixed coronary = arteriosclerosis narrowing of lumen of coronary vessel in heart.
critical stenosis?
Lumen is occluded more then 70-75%, at any moment the patient may have myocardial infraction.
what is needed in a fixed coronary atherosclerotic artery.
it needs dynamic changes such as: 2 methods.
- vasospasm (emotional stress event), the atherosclerotic plaque ruptures, which releases cell debris causing activation of clotting in artery
- plaque lipid core extends and grows into the vasa-vasorum rupturing them causing blood to go into the plaque and increasing its size as a result rupture occurs.
Myocardial infraction results in 3 types of changes, name them?
biochemical = drop in O2 supply = acidity of myocardium do to lactic acid.
functional = loss of contraction ability
morphological changes = wave front theory
what is the WAVE front theory?
the infraction starts in the subendocardial layer to progress to transmural. withing 30 minutes the subendocardium is effected, it takes 3-6 hours
why does the infraction start in the subendocardium 1st?
- The pressure is higher in the subendocardium area, the high pressure may compress the arteries.
- The heart contraction occurs in a more of a spiral. Thus the subenocardium works harder and is more sensitive to O2 deprivation. (hypoxia, ischemia)
what is the therapeutic window?
the window of times that you have to re-establish blood flow in an occluded coronary artery to save as much tissue as possible as the wave front progresses.
3-6 hours is the therapeutic window.
occlusion of Left coronary interventicular descending blood?
myocardial infarction of anterior wall and the 1st part of septum and apex.
occlusion of left coronary circumflex?
Marginal myocardial infraction.
obstruction of right coronary?
posterior wall and posterior 2/3 septum
morphological alteration of myocardial infraction at less then 30 minutes?
less then 30 minutes: reversible damage, no micro/macroscopic changes.
Electron microscopy changes: small dilated mitochondria, more relaxed myocardium. (stunned myocardium)
what is “stunned myocardium”
non-functional myocardium but still alive. (dilated mitochondria, relaxed myocardium.