Vascular Disturbances
Thrombosis
Pathology
Arterial thrombi
Venous thrombi
Fate of Thrombi
Clinical effects
Arterial thrombosis
Venous thrombosis
Loss of distal pulses, cold, pale, painful
Area swollen, reddened and tender
Propagation
Embolisation
Dissolution
Pathogenesis - Virchow's triad
Endothelial injury
Alterations in normal blood flow
Changes in blood constituents
Embolism
Pulmonary emboli
Systemic emboli
Infarction
Most result from thrombosis or embolism
Pathology
Wedge shaped, red or white/pale
Initially poorly defined
Coagulative necrosis
Inflammatory response
Travel through arterial circulation
Most arise from intracardial mural thrombi, others from thrombi on atherosclerotic plaques or aortic aneurysms or a valvular vegetation
Fate of pulmonary emboli
95% arise from deep venous thrombosis (DVT)
Site of endothelial injury or turbulence
Sites of stasis
Extend in direction of blood flow
Ischaemia
Result of impaired vascular perfusion depriving tissue of vital nutrients
Effects may be reversible, dependent on speed of onset, duration, severity, location (tissue/organ vulnerability)
Organisation and recanalisation
Cause of obstruction of veins and arteries
Digestion
Organisation
Can cause thrombosis by itself
Particularly heart & arterial system
Caused by haemodynamic stresses e.g. hypertension, turbulent blood flow or bacterial toxins
Turbulence & stasis
Disrupt normal laminar flow, platelets in contact with endothelium
Dilution of activated clotting factors prevented by fresh flowing blood
Inflow of clotting factor inhibitors retarded
Primary hypercoagulability e.g. factor V mutations
Secondary hypercoagulability e.g. oral contraceptives & prenancy, advancing age, disseminated cancer, smoking & obesity
Resemble coagulated blood
Clinical
Most are clinically silent
Sudden death, right heart failure or cardiovascular collapse occur when > 60% occlusion
Medium sized vessel obstruction may result in haemorrhage
Multiple emboli may over time --> pulmonary hypertension
Results due to mechanical plugging, major sites - legs, brain, intestine, kidney and spleen
Exposure of subendothelial collagen --> adherence of platelets, release of tissue factor
Grow in retrograde direction from site of attachment
Lines of Zahn - alternating pale layers of platelets & fibrin & dark layers of RBCs
Most common in veins and legs
Vegetations
Thrombi may form on heart valves
Sterile vegetations - non-bacterial thrombotic endocarditis
Tissue death & gangrene
Possible sources of emboli
Thrombus: Formation of solid or semi solid mass from the blood constituents within the vascular system
Symptoms
Cough
Chest pain
Dyspnoea
Types
Generalised
Localised
Hypovolaemia (e.g. from blood loss or dehydration), poor cardiac output/low mean arterial pressure
Obstruction to blood flow by intralumenal vascular obstruction, vascular constriction/intramural thickening or extramural vascular compression
Ischaemia: Decreased vascular perfusion
Infarction: Localised tissue death (necrosis) from interrupted blood supply