Week 3 Flashcards
What does purple mean on a histology slide of a vessel? Time frame
- calcification
- happens over time which means that pathology has been there for a while
What happens if a patient has endothelial dysfunction?
- there will be increased tone because there is nothing to counter the sympathetics -> Sympathetics cause vasoconstriction → patient can’t compensate and there is an imbalance between supply and demand → will have symptoms at rest
Presentation of patient with 100% occlusion
- unconcious on the floor if major vessel or acute and sudden onset of chest pain, usually radiating to left arm and jaw
1
What happening to this patient?
- sxs?
-cause?
- vasospasms
- chest pain that comes and goes, can be sporadic, not necessarily associated with activity
- cocaine, acute inflammation, infection/other toxins
2
What is this?
patient with 100% occlusion
3
What is this?
- presentation
- less than 60% occluded
- asymptomatic or exertional angina
- biggest risk would be plaque rupture and superimposed vasospasm
Labs for MI?
- when do they show up?
- troponin and CK-MB
- around 2-4 hours
- increased LDH takes hours to show up
What is troponin?
- how does it get into blood?
- allows myosin heads to bind to actin
- Myocyte necrosis occurs within 20 minutes and intracellular components leak out into interstitium, but it still has to get to blood which can take some time.
What would you expect to find on EKG of patient with MI
- ST elevations from V1 to V4 if it was transmural
- Subendocardial would cause ST depression
Cellular changes that occur during ischemia?
- ATP
- Calcium
- sarcomeres and membrane
- Ischemia will cause myocyte to undergo anaerobic respiration which will result in low ATP levels which affects the K+/Na+ ATPase and the Ca2+ ATPase → causes there to be more sodium and calcium on the inside and more potassium on the outside → keeping sodium on the inside of the cell causes an osmotic gradient that causes the cell to swell.
- Increase in calcium also causes an increase in mitochondrial permeability. This causes water to flow into the mitochondria and causes the structure of the electron transport chain to break down. At this point you could still introduce more oxygen to achieve some recovery but if lack of oxygen continued, enzymes would break down the cell membrane and also the sarcomeres.
- Breakdown of sarcomeres causes release of troponin.
- Breakdown of the cell membrane causes cell membrane to lyse. Proteases will start to affect other cells and this causes necrosis.
How can extracellular potassium trigger an arrhythmia?
- Membrane potential is positive so fast action potentials will now be slower
- This causes automaticity to increase
- You alter resting membrane potential of the fast action potentials and now you have slow wave which causes a spontaneous beat which leads to the arrhythmia.
What is the most critical step in management of an MI?
- How?
• We need revascularization in order to lead to reperfusion.
• Catheterization is used to take care of the thrombus
and an Angioplasty and stent are used
• Cabbage if there are multiple vessels involved
What is magic amount of time for revascularization?
- when does irreversible process start?
- reestablishment of blood flow within 90 minutes because this is a critical window beyond which there doesn’t tend to be an increase in outcomes.
- 20 minutes
What happens to contractile property of the infarct cells?
They decrease
Why is re-vascularization important?
- It prevents more muscle from being damaged by re-establishing blood flow
