102841
Beschreibung
Karteikarten von tanitia.dooley, aktualisiert more than 1 year ago
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Erstellt von tanitia.dooley
vor fast 11 Jahre
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| Frage | Antworten |
| What is secondary dyslipidaemia? | caused by environment diet etc |
| What is the effect of statins? | They are competitive inhibitors for HMG-CoA reductase the rate limiting enzyme in the synthesis of cholesterol. Lowered cholesterol synthesis leads to increased LDL receptor synthesis and LDL is therefore removed |
| What is atorvastatin? | a statin which has long-lasting effects and is used to lower serum cholesterol conc in people with LDL-R mutations |
| What are the clinical uses of statins? | prevent arterial disease in people with high risk and reduce risk of MI & stroke in people with symptomatic atherosclerosis disease |
| Name some other actions of statins | improved endothelial function, reduced platelet aggregation, reduced vascular inflammation, plaque stabilisation, increased fibrinolysis |
| What are fibrates? | agonists for PPARa (when activated stimulate synthesis of lipoprotein lipase) therefore increased TG hydrolysis to form FFA in VLDL and chylomicrons. Also inhibit SMC inflammation by inhibiting NFkB |
| What is the effect of bile acid binding resins? | sequester bile acids in the intestine and reduce cholesterol absorbtion from the exogenous pathway. They increase the metabolism of endogenous cholesterol into bile acids and increase the expression of LDL-receptor to increase LDL clearance |
| What are the side effects of resins? | bloating nausea & diarrhoea |
| What is haemostasis? | the arrest of blood loss from damaged vessels |
| what is thrombosis? | abnormal function of the haemolytic plug in the absence of bleeding |
| What three main factors can lead to thrombosis? | damage to endothelium (atherosclerosis), poor or turbulant blood flow or hypercoagulabiltiy |
| what substances induce platelet activation? | collagen when blood cells lined with endothelial cells are damaged, thrombin which is produced when blood coagulation cascade is activated, activated platelets which produce substances that cause further aggregation |
| What is a thrombi? | organised aggregates of wBC & RBC bound with fibrin- fixed to blood cell wall but may break of an lodge in small blood vessel (embolus) |
| What is the main anticlotting factor? And what is it's co factor? | antithrombin III- heparin |
| What is clot lysis mediated by? | plasmin |
| What causes the clot formation? | conversion of fibrinogen to fibrin using thrombin mediated by cascade of serine proteases that require vitamin K |
| What do anticoagulants treat? | venous thrombosis |
| Describe heparin | it is naturally occurring, administed by IV, reduces blood clotting by activating antithrombin |
| Describe the effects of warfarin | orally given, interferes with vit K synthesis |
| Name some antiplatelet drugs | aspirin, clopidogrel, epoprostenol |
| What is the effect of aspirin? | inhibits formation of thromboxane A2 |
| What is the effect of cloridogrel? | irreversibly blocks effects of ADP on platelets |
| What are the effects of epoprostenol? | synthetic PGIs-promotes vasodilation and inhibits platelet aggregation |
| What do antiplatelet drugs treat? | arterial thrombosis |
| What do thrombolytic drugs treat>? | acute myocardial infarction and stroke |
| Name thrombolytic drugs | streptokinase and tissue plasminogen activator |
| What is the effect of streptokinase? | activates plasminogen |
| What do thrombolytic drugs do? | activate conversion of plasminogen into plasmin to dissolve the clot by degrading fibrin |
| describe tissue plasminogen activator? | present in endothelial cells- made recombinantly for drug use |
| Describe the stages that lead to athersclerosis | 1. endothelial dysfunction (synthesis of NO, PG) 2.endothelial damage leads to monocyte attachment 3. monocytes and Ec's oxidise LDL attached to EC's 4.oxidised LDL is taken up by macrophages forming foam cells. These emerge sub-endothelially to form fatty streaks 5. SMC hyperplasia and matrix deposition= dense fibrous cap overlaying a lipid-rich core 6. ruptures leading to thrombus formation |
| Describe the exogenous lipoprotein transport pathway | 1. chylomicrons transport dietary lipids from gut to capillary beds. 2.TG is hydrolysed to free fatty acids by lipoprotein lipase 3. chylomicron remnants transport cholesterol esters to the liver where they are taken up by endocytosis 4. C is then either stored/ oxidised to bile acids or transported in the endogenous pathway |
| Describe the endogenous pathway for lipid transport | VLDL transport cholesterol from the liver to the tissues where it is taken up leaving LDL with cholesterol esters. The LDL is then taken up by cells by LDL receptors that recognise apolipoprotein. Cholesterol can return to the plasma from the tissues in HDL particles |
| How does LDL promote thrombosis? | Apo(A) inhibits plasmin formation and LDL activates plaelets which drive thrombosis |
| What is dyslipidaemia? | high LDL and low LDL can cause increased risk of cardiovascular disease |
| What is primary dyslipidaemia? Give an example? | Genetic and characterised by 6 phenotypes. Eg type IIa hyper-lipoproteinaemia is caused by LDL receptor defects= increased LDL and dysfunctional thrombosis= increased risk of ischaemic heart disease |
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