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40 Cards in this Set
- Front
- Back
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What is ischemia and what is reperfusion injuries?
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Ischemia is reduced blood flow or lack of blood flow to a tissue
Reperfusion injury is due to reintroduction |
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What are the stages of ischemia/levels of myocardial injury including timing?
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1-5 minutes: myocardial arrhythmias and no death really quick recovery
5-20 minutes: you get myocardial stunning where you can see a decrease in ventricular functions for up to 24 hours 20+ minutes: you get cell death with infarction |
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What happens in ischemia in terms of things that are released?
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increased reactive oxygen species with extra free radicals or electrons, increase in calcium levels, caplain (calcium activated proteases) increase which will destroy stuff, increase in H+, decreased ATP
Decreased ATP will slow down cell signalling and mess with ATP dependent channels for repolarization/depolarization (i can't remember heart physio right now which is pretty bad) |
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What happens in reperfusion in terms of things that are released?
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Increased Calcium, still increased reactive oxygen species such as free electrons or free radicals, increased calpain still, and an increase in CASPASE-3 which is responsible for cell death via apooptosis
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What type of injury does ischemia and reperfusion injury cause on the cell?
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Cardiac cell death due to necrosis and apoptosis
We also get heavy mitochondrial injury due to lack of ATP and the like with all those weird ass chemicalss |
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What type of ischemia or how long of ischemia do you need for a myocardial infarction?
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You need a prolonged ischemia...usually longer than 20 minutes
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What is a myocardial infarction??
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Damage or death of heart muscle
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What are the main causes of ischemia leading to MI?
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Atherosclerosis- causing stenosis or thrombi ******* main one
Blood clots from other areas |
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How are CABG categorized?
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They're categorized by the number of Coronary Arteries needed to be bypassed
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How do you detect MI on lab work?
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Blood test for damaged cardiomyocytes: seeing similar results when you damage normal muscle cells: Cardiac troponins, creatine kinase, myoglobin, troponin I, troponin T levels increasing
This is seen via ELISA |
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What do you see on ECG indicative of ischemia?
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T wave inversion at first before anything else
Then you will see STelevation or Depression STele or STdepress will occur in prolonged ischemia |
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What is a j point?
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Point at which the potential in the heart is zero meaning that the entire heart is depolarized. This is true zero
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Where does the vector point and why?
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it points away from the current of injury because it only points to the positive way which is not going to be at the injury site
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Where do you find the J point?
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right at the beginning of the st segment or the end of the QRS segment: this is at the same spot duh dummy
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What happens Post MI?
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VFIB, Myocardial Cell death, Hypertrophy, Dilation, Heart failure
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How does VFib/Arrhythmias occur pre/post MI?
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If you don't have blood you don't have oxygen to an area, if you don't have oxygen you don't have ATP in that area, if you don't have ATP in that area you're not operating pumps properly which means it will be the perfect time for arrhythmia
ALSO if you have one part of the heart depolarized but another not because of conduction defects due to dead cells, you got problems |
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What is one thing to survive in MI which will show a good prognosis?
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Surviving any Arrhythmias
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What occurs due to myocardial cell death?
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If you have death in some part of the heart, you must overcome that to compensate for activity loss of that part of death. This will cause hypertrophy in other parts of the heart which is good at first to provide compensation but in the long term is it pathological and weaken the heart.
You also get dilation because of pressure overload in the RV because of everything backing up and causing increased PRELOAD: volume overload; also because of weakening of ventricular wall due to myocardial cell death causing wall expansion outward Both of these will lead to Heart Failure |
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How do you get Heart Failure Post MI?
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Pathological dilation or Hypertrophy because you can't pump enough blood in the LV. The blood will back up in the lungs and then you get pulm edema and can't oxygenate blood which will cause the heart to want to work harder because of lack of oxygen but it won't be able to so it will get weaker and will decrease pumping ability all over again. CIRCLED ****, you need to slow down the pathology to treat this
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What helps provide protection against MI?
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exercise.
this will increase SODimutase to get rid of superoxides, it will increase NO for dilation, and also help the mitochondria withstand changes |
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What is the coronary chemoreflex and how does it work?
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It is a parasympathetic reflex which acts to lower the heart rate in theory.
Inflammatory factors released during an infarct will stimulate vagal afferent nerves going into the medulla oblongata which cause vagal efferent nerves to act on the heart lowering HR Advantages of this is reducing oxygen demand by heart to protect it |
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What are general causes of MI?
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MAIN IS ATHEROSCLEROSIS!!!!!
development of plaques which will harden. oxLDL will deposit in coronary arteries There will be an immune response to attack LDLs which are disturbing endothelial layers which causes fibrosis, calcification, and plaques and recruits MACS |
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What is the issue with plaques?
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They cause occlusion and reduce flow with stenosis
They can cause thrombis thereby causing ischemia |
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How does a plaque cause ischemia?
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It can rupture and lodge somewhere
It can also rupture and expose collagen at the site of rupture. This will cause platelets to bind there to the already stenosed area, and cause a thrombus formation due to the exposed collagen |
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What determines resistance to blood flow?
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Poiseuile's Law: R = 8nl/pier^4
Flow = pietimesdeltaPxr^4/8nl Higher the radius the lower the resistance the higher the flow |
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What prostaglandins affect blood clotting and how do they work?
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PGI2 and TxA2
PGI2 causes inhibition of platelet aggregation, and vasodilation while TxA2 causes platelet aggregation and vasoconstriction |
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What COX makes TxA2 and PGI2?
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ONLY COX1 makes TxA2 while PGI2 is made by both COX2 and COX1
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What do you need to make Prostaglandins?
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PGE synthase, PGI synthase, TXA synthase and also COX 1 or 2 which requires a precursor of arachnidonic acid
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Which prostas are required for protection of the stomach?
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PGI2 and PGE2
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Which COX is constitutive?
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COX1
COX 2 is activated by inflammatory response in endothelium which also has pgi2synthase as well as pain stimulation |
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What do pge2 and pgi2 do for the stomach?
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enchanced mucus and bicarbonate secretion while inhibiting acid secretion
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What does aspirin do?
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aspirin selectively inhibits cox 1
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What is the problem with aspirin?
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it will cause the always active COX1 in the stomach to be inactive and therefore inhibit PGI and PGE release disrupting the gut
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What is the selectivity of aspirin?
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it is way more selective for cox 1
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what is the selectivity for naproxen, acetominiphen, ibuprof and the like?
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They are just about equal in cox 1 and 2 inhibition
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Which drugs are selectively cox 2 inhibitors?
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celecoxib which is celebrex
rofecoxib which is vioxx |
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What is the upside with VIOXX made by merck?
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It decreases GI incidences and is significantly better on the stomach
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What are the issues with VIOXX?
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They didn't do a control study, the drug increases chance for a heart attack after 18 months (and maybe before this as well)
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What is the theory behind why vioxx is an issue?
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There will be too much TxA2 in relation to PGI2. Therefore, there will be nothing to balance out the platelet aggregation and vasocontriction caused by it
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Is aspirin really a good thing? What are annual risks?
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It prevents more than just blood clots, it can reduce arrhythmias and heart disease. It might also help with prostrate cancer prevention
Annual risk of GI problems is 0.2 to 1.9% 28% of pop has elevated TxA2 reeceptor activation despite aspirin treatment and chronic aspirin may upregulate TxA2 receptor!!!!!!!!!!!!!!!!!!!!!!!! |
