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 Screenshot 2023-03-23 at 9.18.46 am

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