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34 Cards in this Set
- Front
- Back
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What does it mean that the heart is very important for systemic health? |
If the heart fails so do many other organs |
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What do endothelial cells do |
Act as a physical barrier to blood cells( without blood cells would be activated and clot(thrombus)) Release bioactive substances to prevent inadvertent thrombus formation Release mediators that inhibit platelet activation Cause relaxation/contraction of underlying smooth muscle |
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What was atherosclerosis previously thought to be and what is it nie |
Previously though- disease of lipid/cholesterol storage Now considered inflammatory condition |
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What is the earliest stage of atherosclerosis developement |
Development of a fatty streak (Fatty streak happens because something has damaged the epithelium) |
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What happens in stage 1 atherosclerosis |
Insult to vascular endothelium(smoking, infection, stress) Increased adhesion and migration of leucocytes Increased permeability to lipids (LDL-bad cholesterol) Build up of fatty streak and focus of inflammation |
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How does foam cells occur |
Monocyte and ldl move into the endothelial layer Macrophages give off oxidative species so oxidise LDL macrophages then phagocytose the lipids and allow them to become foam cells |
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Explain the LDL uptake and monocyte migration |
LDL uptake occurs via transcytosis Rate limiting factor is plasma cholesterol conc Monocytes migrate in response to high LDL and mature into macrophages LDL is oxidised via release of superoxide from macrophages-OxLDL taken up by macrophages to form lipid-laden foam cells |
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What happens in stage 2 of atherosclerosis development |
Platelet adhesion and release of PDGFs leads to migration of smooth muscle cells to form a fibrous cap over the foam cell layer |
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What happens in stage 2 of atherosclerosis development |
Platelet adhesion and release of PDGFs leads to migration of smooth muscle cells to form a fibrous cap over the foam cell layer |
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What happens in stage III atherosclerosis development |
Lesions become stiff, bulky and calcified Plaques become very brittle and may rupture Plaque rupture exposes underlying tissue and leads to thrombus formation. If large enough can cut off blood supply in coronary artery (M.I) |
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What characteristics would an atherosclerotic human coronary artery have |
Severe stenosis Calcification Recent thrombosis Cholesterol crystals |
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Effects of atherosclerosis |
Reduced vessel lumen diameter Impaired relaxant function of smooth muscle Impaired thrombotic function of endothelium |
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Effects of atherosclerosis |
Reduced vessel lumen diameter Impaired relaxant function of smooth muscle Impaired thrombotic function of endothelium |
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effect of atherosclerosis, explain: decreased vessel lumen diameter |
Decreased blood flow at rest |
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effect of atherosclerosis, explain: impaired relaxant function of smooth muscle |
Inability to increase the flow in response to demand (angina) |
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effect of atherosclerosis, explain: impaired relaxant function of smooth muscle |
Inability to increase the flow in response to demand (angina) |
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effect of atherosclerosis, explain: impaired anti thrombotic function of endothelium |
Propensity to thrombosis(myocardial infarction) |
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Risk factors for plaque formation |
Hypertension Hugh plasma cholestrol LDL WITH LOW HDL Smoking Disease Lifestyle factors Infections? |
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How does angina occur |
Due to ishchaemia/coronary artery disease |
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What are the types of angina |
Angina of effort(stable angina) Variant (prinzmetals) angina Unstable angina |
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Explain angina of effort(stable angina) |
Predictable chest pain brought on by exercise Cause by permanent narrowing of coronary by atheroma Attacks short lived 2-3 min |
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Explain variant (prinzmetals) angina |
Uncommon Occurs at rest Caused by coronary artery spasm |
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Explain unstable angina |
Sudden alteration in pattern of angina pain May imply impending acute coronary occlusion Dangerous with high mortality |
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Symptoms of angina |
Pain Breathlessness Elevated left ventricular end-diastolic pressure Reduced coronary blood flow Metabolic changes Changes in electrocardiogram |
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Whats oxygen supply you need to consider |
Cardiac output Haemoglobin levels Respiratory function fitness of muscle |
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Whats oxygen supply you need to consider |
Cardiac output Haemoglobin levels Respiratory function fitness of muscle |
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What’s oxygen demand you need to consider |
Work of the heart - contractility -heart rate Hypertrophy of heart |
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What happens in myocardial ischemia |
Myocardium becomes ischemic within 10 seconds if coronary occlusion Working cells remain viable for up to 20 minutes |
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What is the pathway for acyte coronary syndrome, what can it lead to |
Atherosclerotic plaque- unstable plaque- acute coronary syndrome Either Transient ischaemia/unstable angina to sustained ischemia myocardial infarction then necrosis Or Sustained ischemia myocardial infarction then necrosis |
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What drugs can treat stable angina |
Nitrates Beta blockers Calcium channel blockers |
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Whats the surgery for stable angina |
Bypass PCI( PTCA, Stent) |
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What is nitroglycerines vasodilating actions |
Primarily on veins and large arteries Uptake by VSM cells and converts to Active from NO |
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Nitroglycerines therapeutic uses :stable angina |
Decreases pre load so decreases contraction and oxygen demand Does not dilate coronary arteries |
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What are some lipid lowering drugs |
Statins Fibrates Inhibitors of cholesterol absorption fish oil derivatives |
