Venous and arterial thrombosis can occur due to slow blood flow, injury to blood vessels, and hypercoagulable states. Venous thrombosis includes deep vein thrombosis (DVTs) and pulmonary embolisms (PEs) which are caused by blood clots in the deep veins or lungs. Arterial thrombosis is caused by atherosclerosis and risk factors like smoking and diabetes, leading to blood clots in arteries like coronary or carotid arteries causing heart attacks or strokes. Both are treated with anticoagulants like heparin or vitamin K antagonists to reduce clotting, while fibrinolytics may break up existing clots.
Venous and arterial thrombosis can occur due to slow blood flow, injury to blood vessels, and hypercoagulable states. Venous thrombosis includes deep vein thrombosis (DVTs) and pulmonary embolisms (PEs) which are caused by blood clots in the deep veins or lungs. Arterial thrombosis is caused by atherosclerosis and risk factors like smoking and diabetes, leading to blood clots in arteries like coronary or carotid arteries causing heart attacks or strokes. Both are treated with anticoagulants like heparin or vitamin K antagonists to reduce clotting, while fibrinolytics may break up existing clots.
Venous and arterial thrombosis can occur due to slow blood flow, injury to blood vessels, and hypercoagulable states. Venous thrombosis includes deep vein thrombosis (DVTs) and pulmonary embolisms (PEs) which are caused by blood clots in the deep veins or lungs. Arterial thrombosis is caused by atherosclerosis and risk factors like smoking and diabetes, leading to blood clots in arteries like coronary or carotid arteries causing heart attacks or strokes. Both are treated with anticoagulants like heparin or vitamin K antagonists to reduce clotting, while fibrinolytics may break up existing clots.
Venous and arterial thrombosis can occur due to slow blood flow, injury to blood vessels, and hypercoagulable states. Venous thrombosis includes deep vein thrombosis (DVTs) and pulmonary embolisms (PEs) which are caused by blood clots in the deep veins or lungs. Arterial thrombosis is caused by atherosclerosis and risk factors like smoking and diabetes, leading to blood clots in arteries like coronary or carotid arteries causing heart attacks or strokes. Both are treated with anticoagulants like heparin or vitamin K antagonists to reduce clotting, while fibrinolytics may break up existing clots.
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Thrombosis - formation of blood clot in vessel Risk Factors Divided into 3 Main Categories
Causes ischaemia (low blood flow to (Virchows Triad)
organ) 1. Circulatory Stasis - slow blood flow 2. Endothelial Injury (injury to Thrombotic Disorders: endothelium) 1. Venous Thrombosis 3. Hypercoagulable State - tendency to DVT - in legs form excess clots PE - blocked supply to lungs 2. Arterial Thrombosis Note - THROMBOPHILIA = excess abnormal Myocardial infarction clot formation Atrial fibrillation Peripheral vascular disease Thrombosis - caused by procoagulant and Stroke anti-fibrinolytic mechanisms Bleeding - caused by anticoagulant + profibrinolytic mechanisms
VTE (venous thromboembolism) - includes Note - Myocardial infarction (heart attack) = DVT and PE blocked coronary arteries 1. DVT - can lead to Pulmonary Embolism (PE) Natural Coagulation Inhibitors in Blood: Blood clot around valves in DEEP 1. Antithrombin (AT) VEINS (around legs/arms) Inhibits thrombin, 9a and 10a Blood clot made of thrombus (fibrin 3. Tissue factor pathway inhibitor (TFPI) and erythrocyte rich) Direct inhibitor of 7a/TF and 10a 4. Activated Protein C (aPC) 2. Pulmonary embolism (PE) - part of Proteolytically cleaves 5a and 8a for DVT thrombus called embolus breaks deactivation off and travels to heart then lungs and 5. Protein S (PS) blocks the arteries in the lungs = Cofactor of aPC - helps inactivate 5a causes low blood supply to tissues and 8a
PE always caused by DVT Deficiency in Coagulation Inhibitors: Broken off DVT = embolus Idiopathy - no clear triggering factor D-Dimer - chemical released from 50% of idiopathic patients with fibrin clots (high in PE patients) thrombosis have APC resistance (like FVL) Risk Factors for VTE: Surgery and cancer can cause high TF Factor 5 Leiden (FVL) - mutation in F5 gene = more clotting (ARGININE 506 to GLUTAMINE 506) Immobilisation Common cause of venous thrombosis Genetic risk factors - Factor 5 Leiden Mutation + Coagulation inhibitor Normally Activated Protein C (APC) cleaves 3 deficiency peptide bonds in F5 = INACTIVATION = low coagulation Factor 5 Leiden mutation = mutation in factor mutation in FVL gene = F5 resistance 5 to APC cleavage = more coagulation)
Treatment of Venous Thrombosis: (like DVT Atherosclerosis causes narrowing of and PE) coronary arteries Heparin (ANTITHROMBIN and ANTI 10) - Unfractionated Heparin or Low Carotid artery - supplies blood to brain, neck Molecular Weight Heparin and face (LMWH/Timaparin) - low molecular weight heparin cleaves ONLY FACTOR Effects of arterial thrombosis: 10 Coronary artery thrombosis = VKA (vitamin K antagonist) - inhibits myocardial infarction vitamin K (vitamin K dependent Carotid artery = stroke factors don’t work) NOACs (non-vitamin K anticoagulants) Drugs used to treat arterial thrombosis: - antithrombin 1. Anti-platelets Aspirin - inhibits COX-1 and Arterial Thrombosis: (caused by thromboxane production atherosclerosis) Anti A2B3 receptor (fibrinogen and Inflammation of vessel wall VWF binding) (macrophages become FOAM CELLS + Anti P2Y receptor (for ADP induced LDL fat) creates an atherosclerotic platelet aggregation) plaque around tunica intima which 2. Fibrinolytics - TPA (TISSUE narrows artery) PLASMINOGEN ACTIVATOR) and UPA Plaque rupture causes myocardial infarction or ischaemic stroke Anti A2B3: Note - thrombus (blood clot) are platelet rich ABCIXIMAB TIROFIBAN Arterial Thrombosis Risk Factors: Smoking Anti P2Y Diabetes CLOPIDOGREL Hypertension TICAGRELOR High cholesterol PRASUGREL
Fibrinolysis - break down of fibrin clot PREVENTION of Stroke in atrial fibrillation:
VKA (vitamin K antagonists) Plaque rupture causes clot to develop which NOACS (either inhibit thrombin or causes myocardial infarction or ischaemic factor 10a) - named with either XA in stroke word for anti 10 or 'TRAN' at the end for anti thrombin Plaques are made of lots of TF and Collagen and LPA TRAN - ANTI THROMBIN + Argatroban Big plaques rupture causes TF and Collagen leak which activates clotting Heparin - helps NOACs inhibit thrombin and factors which causes a thrombus 10a blockage (ARTERIAL THROMBOSIS) + ischaemia Problem with anticoagulant drugs: Heparin can be impure - can cause Collagen - activates platelets via GP6 receptor thrombocytopenia TF expressed by FOAM CELLS - binds factor 7 - Warfarin - needs close monitoring activates coagulation Too much anticoagulant = bleeding Lysophosphatidic Acid (LPA) activates platelets via P2Y receptor