Thrombosis, Embolism and Infarction 1

Annotations:

• Solid or a semi-solid mass formed from the constituents of blood within the vascular system during life.

1. Differences from haemostassis

   Annotations:

   • Similar to haemostassis but then it is not adaptive like thrombosis but maladaptive.
2. Factors inhibiting thrombosis

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   • Intact endothelial cells to prevent platelet adhesion and it also produces anticoagulant molecules (like heparin-like) It also produces Tissue Factor Pathway Inhibitor (TFPI). Fibrinolysis: Clear fibrin deposits from endothelial surfaces Laminar flow to stop platelets to come in contact with walls and deliver anticoagulant molecules.
3. Virchow's Triad

   Annotations:

   • Factors predisposing thrombosis (this may occur anywhere in the Cardiovascular system)
   1. Changes in vessel walls

      Annotations:

      • Either injury or dysfunction of the endothelium with exposure of sub-endothelial layers (collagen) Might be due to atherosclerosis, inflammation, trauma.
   2. Change in flow

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      • Normal flow is laminar with plasma layer at edges and central column of cells. This like before said, removes clotting factors. Prevent platelets to come in contact with wall. Changes in flow occur mostly at branch points where there are loads of turbulence. At valves, or at aneurysm.
   3. Change in constituents of blood

      Annotations:

      • Hereditary: Factor V mutation like (factor V Leiden) Inherited deficiency of anti-coagulant molecules. Acquired: Increased coagulation factors such as IL-12 or TNF-alpha. Or increased liver synthesis Hyperviscosity: Due to increase in blood cells (polycytaemia) or dehydration (decrease in plasma)

Annotations:

• 3 steps: Reflex vasoconstriction Primary Haemostassis (by which a platelet plug form) Secondary Haemostassis (protein aggregation and activation)

1. Venous

   Annotations:

   • Occur due to low flow Mostly originate in the deep veins of the calf i.e DVT
   1. Predisposing factors

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      • Immobilization, decreased flow Post-surgical, Increased clotting factors and platelets plus the factor above Poor peri-operative care Cancer Pregnancy Heart failure Dehydration.
   2. Type

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      • Starts by attachment to valves or damaged endothelium. Propagates in the direction of flow. Occlusive.
   3. Outcomes

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      • 1. Resolution: Regular degradation, to restore normal function. 2. Organised and incorporated into wall. 3. Organized and recanalized. 4. Embolism in the lungs.
   4. DVT
      1. Clinical

         Annotations:

         • Wells' Criteria: Swollen Tender Predisposing Factors Plus it may have associated warmth and redness....
      2. Investigations

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         • Venous Doppler
      3. Prevention

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         • Graduated compression stockings Heparin intermittent calf pressure Early mobilisation
2. Arterial Thrombus

   Annotations:

   • Forms under high flow. Usually due to injured endothelium especially caused by atheroscelerosis. Usually really really laminated appearance with alternate layers of white fibrin and platelets, increased numbers of red cells.
   1. Outcomes

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      • Occlusion Embolism Coronary circulation Cerebral circulation Femoral arteries
3. Mural

   Annotations:

   • Occurs in heart. Commonly in left ventricle after myocardial infarction due to low flow injured endothelium TNF and IL-12

Annotations:

• Transportation by the blood of the abnormal material and the point 

1. Arterial embolism

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   • Moves with flow of blood, lodges in vessel fo matching size. Cause distal ischaemia
   1. Source

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      • 80% Heart: From mural thrombus in Left ventricle after MI. or Mural thrombus in LA related to atrial fibrillations. From valvular vegetations. 20% Atherosclerosis
   2. Infarction

      Annotations:

      • Circumscribed area of ischaemic necrosis in an organ or tissue resulting from interference of blood flow.
   3. Effects/Outcomes

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      • Leg: Ischaemia/gangrene Brain: Cerebral infarct Kidney/spleen: Wedge shaped infarct. Gut: Infarct.