THROMBOSIS 1 BRIAN ANGUS PATHOLOGY UNIVERSITY OF NEWCASTLE UPON TYNE Coronary artery thrombosis Return to Cardiovascular Pathology Index Page.

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2 THROMBOSIS 1 BRIAN ANGUS PATHOLOGY UNIVERSITY OF NEWCASTLE UPON TYNE Coronary artery thrombosis Return to Cardiovascular Pathology Index Page

3 THROMBOSIS 2 CONTENTS DEFINITIONS COMPOSITION PREDISPOSING FACTORS TYPES OUTCOME ARTERIAL THROMBOSIS CARDIAC (Valves and chambers) VENOUS THROMBOSIS Coronary artery thrombosis

4 THROMBOSIS 3 DEFINITION OF THROMBOSIS Solid mass of blood constituents Formed within the vascular system In life Coronary artery thrombosis

5 THROMBOSIS 4 THROMBOSIS IS DIFFERENT FROM CLOT Clotting means coagulation which can occur within or outside the vascular system in life or post mortem. Coronary artery thrombosis

6 THROMBOSIS 5 COMMONEST CLINICAL SYNDROMES Coronary thrombosis causing MI Deep leg vein thrombosis resulting in PE Myocardial infarction

7 THROMBOSIS 6 MYOCARDIAL INFARCTION

8 THROMBOSIS 7 THROMBUS: COMPOSITION 1.FIBRIN: Polymer, shown top. 2.PLATELETS: tiny, shown lower compared to red blood cell. 3.Entrapped RBCs and serum.

9 THROMBOSIS 8 PRODUCTION OF FIBRIN Contact with damaged endothelium or atheromatous plaque contents (etc) triggers the coagulation cascade which converts fibrinogen monomer to the jelly like fibrin polymer.

10 THROMBOSIS 9 PLATELETS Platelets are small compared to RBCs Derived from megakaryocytes in bone marrow No nucleus Containalpha granules (adhesion substances) dense granules (aggregation substances)

11 THROMBOSIS 10 PLATELETS On contact with fibrin or collagen platelets release granules which promote aggregation of adjacent platelets to form a mass which covers, for example, an endothelial defect.

12 THROMBOSIS 11 PLATELETS Platelet aggregation in this way is a normal phenomenon, and occurs continuously in the body to repair minor endothelial injury. In excess, a mass is formed in a vessel: THROMBOSIS

13 THROMBOSIS 12 PREDISPOSING FACTORS FOR THROMBOSIS Factors which promote thrombosis can be found in the blood vessel wall, or be concerned with the flow of blood or its constituents. This group of three factors is known as Virchow’s triad.

14 THROMBOSIS 13 TYPES OF THROMBI Thrombi can occlude a vessel which may result in necrosis of the part served (infarction). Mural thrombus can release fragments (emboli) which can travel in the bloodstream to block distal vessels. Thrombus on heart valves due to infection can also embolise.

15 THROMBOSIS 14 OUTCOMES OF THROMBOSIS 1 THROMBOLYSIS Thrombosis can be cleared by the fibrinolytic system. Plasminogen activator released from endothelial cells converts plasminogen to plasmin which dissolves fibrin.

16 THROMBOSIS 15 OUTCOMES OF THROMBOSIS 2 RECANALISATION Thrombosis can undergo recanalisation. Endothelial cells grow out from the vessel wall and create new channels through the thrombus:

17 THROMBOSIS 16 OUTCOMES OF THROMBOSIS 3 EMBOLISM Thrombosis can throw off emboli which can occlude distal vessels

18 THROMBOSIS 17 OUTCOMES OF THROMBOSIS 4 FIBROSIS: ORGANISATION Thrombosis can simply be organised i.e undergo fibrous tissue replacement

19 THROMBOSIS 18 CONTENTS DEFINITIONS COMPOSITION PREDISPOSING FACTORS TYPES OUTCOME ARTERIAL THROMBOSIS CARDIAC (Valves and chambers) VENOUS THROMBOSIS Coronary artery thrombosis

20 THROMBOSIS 19 ARTERIAL THROMBOSIS: AETIOLOGY Factors predisposing to arterial thrombosis can be considered under Virchow’s triad. Factors in the wall include atheroma and vasculitis. Flow can be affected by atheroma. Cigarette smoking makes platelets sticky.

21 THROMBOSIS 20 ARTERIAL THROMBOSIS: MORPHOLOGY 1 Thrombosis commences with adherence and aggregation of platelets. A mass of fibrin, platelets and blood constituents is then laid down.

22 THROMBOSIS 21 ARTERIAL THROMBOSIS: CLINICAL Thrombosis can lead to vascular occlusion resulting in, for example myocardial infarction if a coronary artery is occluded. Other possible clinical outcomes are gangrene of the leg and cerebral infarct.

23 THROMBOSIS 22 CARDIAC THROMBOSIS: AETIOLOGY 1 We are here concerned with thrombosis of cardiac valves and chambers, and not with coronary artery thrombosis Considering Virchow’s triad, factors in the wall include myocardial infarction and infection (infective endocarditis). A factor affecting flow is atrial fibrillation, a dysrhythmia which results in atrial blood stagnation.

24 THROMBOSIS 23 CARDIAC THROMBOSIS : AETIOLOGY 2 Considering Virchow’s triad, factors in the wall include myocardial infarction and infection (bacterial endocarditis). A factor affecting flow is atrial fibrillation, a dysrhythmia which results in atrial blood stagnation. Identify these factors on the diagram.

25 THROMBOSIS 24 CARDIAC CHAMBER THROMBOSIS

26 THROMBOSIS 25 CARDIAC THROMBOSIS: CLINICAL Thrombosis in each situation can result in systemic embolism. This can result in infarction anywhere, for example, a cerebral infarct.

27 THROMBOSIS 26 VENOUS THROMBOSIS: AETIOLOGY 1 Causes of venous thrombosis can be considred under Virchow’s triad. The most important site of venous thrombosis is in the deep veins of the leg. Careless patient transfer in the operating theatre has been shown to result in an increased incidence of deep venous thrombosis triggerd by damage to endothelium in calf veins.

28 THROMBOSIS 27 VENOUS THROMBOSIS: AETIOLOGY 2 Causes of venous thrombosis can be considred under Virchow’s triad. After operations, injury or severe illness of many kinds fibrinogen and other coagulation factors in the blood are increased due to increased hepatic synthesis. This leads to an increased risk of deep vein thombosis. In the case of surgery, heparin is often given to reduce the incidence of this potentially fatal complication

29 THROMBOSIS 28 VENOUS THROMBOSIS: AETIOLOGY 2 Causes of venous thrombosis can be considred under Virchow’s triad. Slow blood flow promoted by immobility due to chronic illness, or bedrest post-operatively can promote venous thrombosis.

30 THROMBOSIS 29 VENOUS THROMBOSIS: AETIOLOGY 3 PREDISPOSING FACTORS FOR DEEP VENOUS THROMBOSIS Immobility, bed rest Post op coagulability changes Pregnancy OC pill Severe burns and trauma Cardiac failure Disseminated malignancy ?Economy class syndrome

31 THROMBOSIS 30 VENOUS THROMBOSIS: MORPHOLOGY 1 Deep vein thrombi sometimes show alternating pale and dark (red) zones.

32 THROMBOSIS 31 VENOUS THROMBOSIS: MORPHOLOGY 1 Deep vein thrombi sometimes show alternating pale and dark (red) zones. This occurs because as soon as a gradually developing platelet rich (pale) thrombus occludes entry of a branch, immediate stagnation and thrombosis (red, platelet poor) occurs in the segment leading to the next branch. The diagram attempts to illustrate this. This is of no consequence other than to illustrate the contribution of platelets (the initiator) and fibrin to thrombosis.

33 THROMBOSIS 32 DEEP VEIN THROMBOSIS: CLINICAL The patient may be asymptomatic. Often there is pain and swelling of the leg. In the event of pulmonary embolism. A potentially fatal outcome, there nay be chest pain and perhaps haemoptysis due to pulmonary infarction.. MS Clipart

34 THROMBOSIS 33 DEEP VEIN THROMBOSIS: CLINICAL 2 Deep vein thrombosis develops in calf or ileofemoral veins.

35 THROMBOSIS 34 DEEP VEIN THROMBOSIS: CLINICAL 3 The thrombus may embolise to lungs.

36 THROMBOSIS 35 DEEP VEIN THROMBOSIS: CLINICAL 3 In this animation thrombus forms in the deep veins of the calf, a small embolus breaks off and passes up the vena cava. The embolus then passes through the right side of the heart to the pulmonary artery. The embolus lodges in a branch of the pulmonary artery resulting in infarction of a wedge shaped area of lung.

37 THROMBOSIS 36 DEEP VEIN THROMBOSIS: CLINICAL 4 A rarer source of pulmonary thromboemboli is the right atrium, which can develop mural thrombus in atrial fibrillation.

38 THROMBOSIS 37 DEEP VEIN THROMBOSIS: CLINICAL 4 This photograph shows an embolus from deep vein thrombosis in a pulmonary artery. Death has resulted. Prevention of DVT is discussed in the next presentation..

39 THROMBOSIS 38 PULMONARY EMBOLISM

40 THROMBOSIS 39 END OF PRESENTATION Return to Cardiovascular Pathology Index Page