Thrombosis and Embolism Flashcards
Define thrombosis
Formation of a solid mass of blood within the circulatory system during life
State Virchow’s triad
Abnormalities of the vessel wall (endothelial injury)
Abnormalities of blood flow (stasis of blood flow)
Abnormalities of blood components (hypercoagulability)
Explain how abnormalities of vessel wall can lead to thrombosis
Occur in situations of MI, atheroma, inflammation, stress of hypertension, scarred heart valves, trauma, surface of atherosclerotic plaques when they break
Platelets adhere to von Willebrand factor on damaged wall
When blood flow is quick, generally no platelet thrombi, however forms with blood stasis
Explain how abnormalities of blood flow can lead to thrombosis
Stagnation and turbulence
Abnormal blood flow gives platelets a better chance to stick to the endothelium and clotting factors a chance to accumulate
Thrombosis more common in veins as slower flow and can be trapped in valves
Explain how abnormalities of blood components can lead to thrombosis
Blood becomes hypercoagulable (sticky) after surgery, post partum and in smokers
Can be inherited in disorders that decrease coagulation
Explain how a thrombus forms
Platelets are the smallest component of blood and thus flow near the vessel wall
They can catch onto a valve and further likely if Virchow’s triad
Further platelets will aggregate
As in haemostasis, fibrinogen binds platelets together and the fibrin traps red blood cells to form a red layer of RBC on top of white platelet layer
Red layer is thrombogenic and platelets stick to exposed fibrin to form a second platelet layer which further continues (lines of Zahn)
Describe the difference in appearance between an arterial and venous thrombi
Arterial - pale, granular, lines of Zahn (layered appearance depending on number of red cells), lower cell content so paler
Venous - soft, gelatinous, deep red, higher cell content
What are the outcomes of thrombosis
Lysis - complete dissolution of thrombus and blood flow re-established
Fibrinolytic system active
Most likely when thrombi are small
Propagation - progressive enlargement of thrombosis in direction of blood flow
Turbulence and stagnation propagate thrombosis
Organisation - fibroblasts and capillaries grow (similar to granulation tissue) - replacement by scar tissue
Reparative process
Flow is not restored
Recanalisation - blood flow re-established but usually incompletely
One or more new channels formed through occluding
Turbulent flow
Embolism - when part of thrombus breaks off, travels through blood stream and lodges at distant site
What are some clinical effects of thrombosis
Occlusion of an artery at the site of thrombus causing ischaemia and infarction
Embolisation of part of the thrombus resulting in occlusion of an artery distant to the site of the thrombus
Congestion and oedema in the venous bed resulting in pain and sometimes skin ulceration
Repeated miscarriages due to thrombosis of the uteroplacental vasculature which is often seen in inherited thrombophilias
Define embolism
Blockage of a blood vessel by solid, liquid or gas at a site distant from its origin
State where the common thrombo-emoboli locations are
If the thrombus occurs in the systemic vein, it can only become pulmonary embolism
From the heart pass via the aorta to renal, mesenteric and other arteries (anywhere in body)
From atheromatous carotid arteries (towards neck and head), move to the brain to cause stroke
From atheromatous abdominal aortic pass to arteries of the legs
Why are thrombi commonly found in the left side of heart
Infarcts mainly occur on the left ventricle, thrombi can form on damaged walls
Atrial fibrillation results in decrease atrial contraction, dilatation of the left atrium, stagnation of blood in the left atrium and hence thrombus formation
Vegetation (thrombi forming in cardiac valves) are more common in the left side of heart
What are paradoxical emboli
Thrombus form in systemic veins but bypass lungs and enter systemic arteries
Small emboli can pass through small gaps in the pulmonary circulation
Larger emboli can pass through interventricular septum defects or a patent foramen ovale
Myocardial infarction role of thrombus, laboratory diagnosis, complications
Obstruction of coronary artery by thrombosis causes ischaemia and infarction
Troponin I and troponin T are elevated in MI, creatine kinase less commonly measured nowadays
Leak out through damaged membranes of myocardial cells
Complications - heart failure, arrhythmia, pericarditis
Deep vein thrombosis pathophysiology, predisposing factors
Thrombus forms in legs, veins become larger closer to the heart and so embolism stops in pulmonary circulation
Many patients asymptomatic unless embolism because of collateral blood circulation within legs
Predisposing factors -
Immobility/bed rest
Post operative, pregnancy, post partum - increase coagulability of blood
Oral contraceptives
Severe burns
Cardiac failure
Disseminated cancer
