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21 Cards in this Set
- Front
- Back
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Myasthenia Gravis |
- autoimmune disease - neuromuscular junction nACh is blocked with antibodies so ACh cannot bind onto the receptor site |
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Hypertension |
- high blood pressure - caused from renal disease, endocrine disorders, catecholamine-secreting tumour - if not treated, can lead to coronary thrombosis, stroke, kidney faliure |
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Cardiac dysrhythmias |
- disorder of heart rate and rhythm (alteration in beat/ rhythm), resulting in failure in conducting system of heart |
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Types of dysrhythmias |
1) Tachycardia (increased heart beat) - atria: (Supraventricular), flutter, fibrillation - ventricles: fibrillation, torsades de pointes 2) Bradycardia (decreased heart beat) - heart block occurs: damage to AV node or conducting tissue therefore ventricles beat slower and at irregular rate |
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Causes of dysrhythmias |
1) Abnormal pacemaker activity 2) Early or delayed after depolarisation 3) Re-entry |
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Heart Faliure |
- condition where cardiac output is insufficient to meet the metabolic demands of the body - can result from any structural or functional cardiac disorders that impairs the ability of the heart to function to pump blood (circulation) around the body |
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Causes of heart faliure |
ischaemic heart disease, hypertension, heart muscle disorder, valvular heart disease |
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Angina |
- failure in coronary arteries supply blood to the heart muscle - severe chest pain associated with myocardial ischaemia due to reduced coronary flow - (normal) blood flow only occurs during diastole and is affected by metabolites, adenosine (mainly), sympathetic nerves, catecholamines |
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Types of angina |
1) Stable angina: occurring on exertion but relieved by rest (due to fixed narrowing of coronary vessels by atheroma) 2) unstable angina: cannot be treated with drugs, requires stunt for surgery; angina attack occurs from rupture/dissection of an atheromatous plaque causing thrombus without complete occlusion of the vessel 3) Variant angina: prinzmetal angina, occurs at rest and is caused by coronay artery spasm |
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Pathophysiology of coronary circulation |
- ATHEROSCLEROSIS - atheromatous plaques forms within the arteries, narrowing the pathway and decrease perfusion of myocardium 1) platelets, macrophages, LDL adhere to damaged endothelial cells 2) macrophages release free radicals, causing lipid peroxidation of LDL, which macrophages ingest 3) macrophages release inflammatory cytokines and growth factors which cause proliferation of smooth muscle and fibroblasts (develops plaque) |
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Kidney functions |
- excretion of waste products - regulation of salt and water content in body - acid/base balance |
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Atheromatous disease |
- plaque formation in arteries - formed when local damages to the endothelium is followed by deposition of lipoprotein (mainly LDL) - macrophages are adhered and activated, which generates oxygen radicals that cause lipid peroxidation of the LDL - macrophages also produce growth factors that stimulate smooth muscle proliferation and deposition to extracellular matrix - thrombi can develop plaques which narrows artery and blocks - risks: ischaemic heart disease (myocardial infarction etc.) |
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Haemostasis |
arrest of blood loss from damaged blood vessels - haemostatic plug is formed from adhesion and activation of platelets; activation of clotting factors leading to blood coagulation (fibrin formation) |
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Thrombosis/embolus |
- thrombosis: formation of plug associated with arterial diseases - embolus: portion of thrombosis that breaks away into circulation - venous thrombus: can lodge lungs - left heart thrombus: lodge in brain and other organs |
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Aims of drugs to heart faliure |
improve symptoms and reduce mortality (increase cardiac output, decrease venous pressure) - increase force of contraction without increasing oxygen consumption - reduce AV conduction and increase AV node refractory period (increase force of contraction, increase cardiac output) |
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Therapeutic aims for anti-anginal drugs |
- reduce cardiac work and thus metabolic demand - increase perfusion of heart muscle (dilation of coronary collaterals) - prevent myocardial infarction/heart attack (prevent atherosclerosis/plaque development) |
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Therapeutic aims of diuretics |
- drugs that increase salt/water excretion by direct act on kidney - can be done by decreasing absorption of salt from filtrate thus increase in water/salt loss |
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Therapeutic aims of lipid-lowering drugs |
- decrease plasma LDL-cholesterol - used in conjunction with dietary management and correction of other cardiovascular risk factors |
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Normal insulin secretion procedure |
- glucose enters the pancreatic islet of langerhans - it increases ATP and decreases ADP via glucokinase (glucose metabolism) - increase in ATP leads to closure of Katp channels - closure in channel leads to depolarisation thus opens calcium channel (L-type) and allows Ca2+ influx - increase in intracellular [calcium] causes insulin secretion - this is amplified by second messenger DAG and arachidonic acid metabolites |
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Type I diabetes |
- Insulin dependent diabetes - juvenile-onset - insulin therapy is necessary, otherwise rapid progression to ketosis and coma may occur - beta cells have been completely destroyed by autoimmune process |
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Type II diabetes |
- insulin independent diabetes - maturity onset (adult type) - may respond to dietic control alone or together with oral hypoglycaemic drugs - individuals are insulin resistant and fails to secrete sufficient hormone |
