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67 Cards in this Set
- Front
- Back
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what causes angina? |
mismatch between coronary perfusion, oxygen supply and cardiac work, oxygen demand |
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Therapy of stable angina? |
GTN - Beta blockers - vasodilators |
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What is the cause of unstable angina? |
unstable atheromatous narrowing, plaque rupture and thrombosis and vasoconstriction |
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what is the treatment of unstable angina? |
vasodilators, B-AR blockers, aspirin and herarin |
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main treatment for prinzmetal's angina |
calcium entry blockers |
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Uses of B1- antagonists in angina |
-reduce heart rate and force - increase time in diastole |
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Uses of calcium entry blockers in angina? |
-vasodilation hence reduce TPR/ afterload - prevent coronary vasospasm |
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What are the uses of organic nitrates in angina? |
-Venodilation / reduce preload - improve perfusion of ischemic zones - prevent vasospasm - prevent platelet aggregation |
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What is abnormal automaticity? |
- SAN overridden by pacemaker in the the myocardium
- ischaemia - hypokalaemia - catecholamine activity |
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What is triggered automaticity? |
- extra depolarisation events during myocyte action potential - End of phase 2/ start 3 =EAD - Phase 4 =DAD |
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what causes triggered automaticity? |
excessive calcium entry or accumulation |
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what are the degrees of heart block? |
1- slow impulse 2- fraction of the impuse 3- no impulse |
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What phase do class 1 affect? |
- Depress phase 0 - can interupt re-entry circuits and reduce both abnormal and triggered automaticity |
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- What phase doe class II agents affect? |
- depress slope in phase 4 of nodal - Extend phase 2 of non-nodal - prevent sinus tachycardia + both automaticity |
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What phase doe class III agents affect? |
- delay phase 3 - extend phase 2 - might reduce re-entry circuits |
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what phase do class IV agents affect? |
- Depress phase 0 of nodal - Shorten phase 2 in non-nodal - reduces triggered automaticity |
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what is heart failure? |
Inadequate cardiac output for tissue perfusion |
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What are the four types of heart failure? |
- systolic dysfunction - diastolic dysfunction - excessive haemodynamic burden - inrealistic peripheral demands for tissue perfusion |
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What is systolic dysfunction?and what causes it? |
- failure of contractility
- cardiomyopathy (diabetes, infection, MI) - drug toxicity - arrthymias |
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What is diastolic dysfunction? and what causes it? |
- failure to fill ventricles - caused by stiffness (senile fibrosis, cardiac hypertrophy) |
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what is excessive haemodynamic burden? and what causes it? |
relative failure of contractillity - valvular disease - cogenital heart defects - ^ TPR (left heart failure) - ^ pulmonary resistance (cor pulmonale) RHF |
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What causes unrealistic peripheral demand for cardiac output? and what is it |
- Relative failure of contractillity - decrease O2 capacity, severe anaemia - excessive metabolic demand, thyrotoxicosis - maintenace of blood pressure in sepsis, shock |
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What is the aim of Heart failure therapeutics? |
- support cardiac output - remove compensation - reduce workload - reduce oxygen demand - +ve iontropy |
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what are the compensatory mechanisms in CHF? |
- Venocontriction (raise preload) - Vasoconstriction (raise afterload) - increase heart rate and force of contraction |
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What is the sypathetic nervous system role is compensation of CHF? |
- Vasoconstriction + venoconstriction (a AR) - tachycardia and +ve inotropy (b AR) |
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What is the role of RAAS in CHF compensation? |
- Vaso and Venoconstriction (AT1 and V1) - salt and fluid retention (V2 and MC Type 1 receptors) |
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How is compensation removed in heart failure? |
- RAAS inhibitors - Diuretics - Vasodilators |
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how is +ve ionotropy produced in heart failure? |
- cardiac glycosides - B1-AR agonists - PDE III inhibitors |
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What is primary hypertension? and what causes it? |
Chronic, progressive elevation in arterial pressure - Neurogenic (sympathetic stimulation) - renal salt balance (too much intake) |
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what can cause sustained ^ TPR? |
- vasoconstriction (loss of NO, PGI2) - arteriosclerosis (hypertrophy) - rarefaction (loss of vessels) |
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What are the peripheral theraputics for hypertension? |
- RAAS inhibitors - Thiazide diuretics - B1 AR antagonists - calcium entry blockers - vasodilators - a1 AR antagonists |
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What are the centrally acting theraputics for hypertension? |
- a2 AR agonists
- imidazoline |
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what is the use of calcium channel blockers in hypertension? |
- reduce TPR - amlodipine |
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what is the use of RAAS inhibition in hypertension? |
Reduce cardiac output and total peripheral resistance |
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name a fatty acid? |
steric acid - palmitic acid - oleic - arachodonic |
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what is a wax? |
esters of fatty acids with long chain moonohydric alcohols |
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name some uses for lipids? |
-plasma membrane - lipoproteins for cholesterol transport - thromboplastin - myelin sheath - cholesterol |
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what are the roles og cholesterol? |
- membrane stability - synthesis of bile acids and salts - synthesis of steroid hormones - synthesis of vitamin D |
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What hormones influence lipolysis? |
-adrenalin - NA - glucocorticoids |
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where is hormone sensitive lipase found? what does it do and what hormones activate it? |
adipose tissue, - controls release of fatty acids into the blood - adrenaline and glucagon |
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what is the function of all of the lipoproteins? |
- Chylomicrons (dietary) - VLDL's (endogenous store) - LDL's (deliver to cells throughout the body) - HDL's (remove excess cholesterol) |
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what is the percentage of protein by; - C -V -L H |
-2% -10% -25% -40% |
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What apo protein solubolises highly hydrophobic lipids? |
Apo B |
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what are the roles of apolipoproteins ? |
- regulate lipid metabolising enzymes - facilitate lipid transfer between lipoproteins and cells - permit receptor mediated endocytosis |
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How is density related to TG content? |
Proportional |
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what is special about apolipoprotein B |
it is integral where as others are peripheral |
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whare is ApoB100 found? |
LDL |
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Name the origins of the following lipoproteins? - chylomicrons - VLDL - IDL - LDL -HDL |
- Gut - Liver - liver - liver - tissues |
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what are the roles of the following; - chylomicrons - VLDL -IDL - LDL -HDL |
- Transport dietary TG to tissue - Transport endougenous TG - Transport cholesterol - Transport cholesterol - Reverse cholesterol transport |
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What breaks down TG? and converts VLDL into IDL? |
Lipoprotein lipase |
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what are the components and diameter of LDL? |
- 1500 cholesteryl ester - 800 phospholipid - 500 unesterified cholesterol - 1 apoB-100 - 22nm |
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how is LDL uptaken? |
-ApoB-100 binds - endocytosis - lysosome digestion by cell - LDL receptor reused |
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what does the endocytosis in eukaryotic cell require to take place? |
Caveolin and GTPase |
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what makes the cholesteryl ester store? |
ACAT (acyl-CoA cholesterol acyl transferase) |
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what occurs when there is too much cholesterol? |
- Activation of ACAT - Suppression of HMGCoA reductase expression - Down regulation LDL receptor |
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what effect dose insulin and glucagon have on HMG-CoA reductase? |
I- positive G- negative intracellular cholesterol block more extracellular cholesterol and also HMG-CoA |
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What are the roles of HDL? |
- reverse transport - LCAT converts free C to CE |
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what can be the causes of hyperlipidaemia? |
obesity - excess alcohol - DM - nephrotic syndrome - renal failure - cholestasis |
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how does hyperlipidaemia cause plaques? |
- accumalation ion the arty wall - oxidation - macrophage entry - Foam cells - plaque grows - rupture |
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what are the symptoms of hyperlipidaemia? |
- CHD - stroke - nodules of cholesterol |
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high levels of what other than LDL can cause CHD? |
Lipoprotein A |
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name the drugs that mostly reduce LDL and total cholesterol? |
statins - cholesterol absorption inhibitors - bile acid binding resisns |
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name drugs that reduce LDL and TG? |
Niacin |
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name drugs that mainly reduce TG? |
Fibrates - omega 3 fatty acids |
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what drug is most effective at lowering LDL and what drug is most effective at raising HDL? |
- statins - niacin |
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mechanism of statins? |
HMG-CoA reductase inhibitors - increase LDL-R expression - pleiotropic (inprove endothelial function, reduce inflammation) |
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side effects of statins? |
-myopathy - myositis - Rhabdomyolysis |
