Thrombosis and Embolism Flashcards

1
Q

Define laminar, stasis and turbulence.

A

L - normal blood flow.
S - stagnation of flow.
T - forceful and unpredictable flow.

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2
Q

What causes defects in blood flow?

A

Thromboembolism - common.
Atheroma, hyperviscosity, spasm, external compression, vasculitis, vascular steal.

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3
Q

What is Virchow’s Triad?

A

Changes in the blood vessel wall.
Changes in blood constituents.
Changes in the pattern of blood flow.

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4
Q

What is thrombosis?

A

A solid mass from the constituents of blood within the vascular system.
Caused by changes in Virchow’s Triad.

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5
Q

What is the pathogenesis of thrombosis?

A

An atheromatous artery causes turbulent blood flow, which causes fibrin deposition and platelet clumping.
The plaque becomes denuded and collagen is exposed, which platelets adhere to.

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6
Q

How do platelets cause thrombus propagation?

A

A fibrin meshwork is laid down and traps RBCs (forms lines of Zahn).
Further turbulence and platelet deposition occur, leading to thrombus propagation and clinical consequences.

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7
Q

What is the relationship between atheroma and thrombosis?

A

Hypercholesterolaemia is a risk factor for atheroma and a part of Virchow’s Triad.
Arterial thrombosis is most commonly superimposed on atheroma.

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8
Q

How is thrombosis linked to Virchow’s Triad?

A

Hyperviscosity or hypercoagulability.
Stasis of blood flow.
Turbulence (plaque, aortic aneurysm).

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9
Q

What are the consequences of thrombosis?

A

Depends on site, extent and collateral circulation. Common clinical scenarios include DVT, ischaemic limbs, and MI.

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10
Q

What is the progression of thrombosis?

A

Resolution.
Organisation and recanalisation.
Death.
Propagation - leads to embolism.

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11
Q

What is embolism?

A

Movement of abnormal material in the blood and its impaction in a vessel, blocking its lumen. A detached intravascular mass. Most emboli are dislodged thrombi (thromboembolism).

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12
Q

What causes systemic thromboembolism?

A

Mural thrombus (associated with MI, or left atrial dilatation and AF).
Aortic aneurysms.
Atheromatous plaques.
Valvular vegetation.
Venous thrombi.

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13
Q

What are the movement and consequences of systemic thromboembolism?

A

Travels to the lower limbs (most common), brain, and other organs.
Consequences depend on the vulnerability of affected tissues to ischaemia; the calibre of occluded vessel; and collateral circulation. Usually infarction occurs.

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14
Q

What is venous thromboembolism?

A

From deep venous thromboses (lower limbs).
Travels to the pulmonary arterial circulation.
May occlude main pulmonary arteries, bifurcations (saddle emboli), or smaller arteries - depends on size. Often multiple.

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15
Q

What are the consequences of venous thromboembolism?

A

Silent, pulmonary haemorrhage/infarction, right heart failure, or sudden death - depends on size.
Multiple pulmonary emboli cause pulmonary hypertension and right ventricular failure.

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16
Q

What are the risk factors for DVT and PTE?

A

Cardiac failure.
Severe trauma and burns.
Post-operation / post-partum.
Nephrotic syndrome.
Disseminated malignancy.
Oral contraceptive.
Age.
Bed rest / immobilisation.
Obesity.
PMH of DVT.

17
Q

What are the different types of embolus?

A

Fat - affects the brain, kidneys and skin.
Gas - N2 forms as bubbles in capillaries.
Air - from head and neck wounds, surgery.
Tumour.
Trophoblast - pregnant women.
Septic material - infective endocarditis.
Amniotic fluid - cause of collapse in childbirth.
Bone marrow - fractures and CPR.
Foreign bodies - cannulae tips, sutures.

18
Q

What is rheumatoid fever?

A

A disease of disordered immunity.
Inflammatory changes in the heart and joints (sometimes neurological symptoms).
Commonly affects 5-15yr olds, M>F.

19
Q

What are the symptoms of rheumatoid fever?

A

Flitting polyarthritis of large joints, skin rashes, fever.
Sore throat (Group A beta-haemolytic streptococcal infection).
Strong antibody reaction to strep, may cross-react with antigens in CT.

20
Q

What are the signs of rheumatoid fever?

A

Pancarditis (inflammation of the -cardium) in the acute phase, heart murmurs.
Damage to heart tissue may be caused by a combination of T Cell mediated and antibody-mediated reactions.

21
Q

What is an Aschoff Body?

A

Seen in the heart in acute rheumatic fever.
Focus of chronic inflammatory cells, necrosis and activated macrophages.

22
Q

What causes valvular heart disease?

A

Valvular stenosis - valve thickening or calcifying.
Valvular incompetence - valve loses normal function.
Vegetations - infective or thrombotic nodules develop on valve leaflets, impairing normal valve mobility. Can embolise.

23
Q

What is rheumatic heart disease?

A

Pancarditis in acute rheumatic fever can progress to chronic rheumatic heart disease, mainly manifesting as valvular abnormalities.

24
Q

How are the valves affected in rheumatic heart disease?

A

Inflammation of the endocardium and left sided valves - fibrinoid necrosis of the valve cusps or chordae tendineae.
Small vegetations form over them.

Characterised by deforming fibrotic valvular disease, involving the mitral valve - leaflet thickening, fusion and thickening of chordae tendineae, commissural fusion/shortening.

25
Q

What specific valves are affected in rheumatic heart disease?

A

Virtually the only cause of mitral stenosis.
Can cause aortic/mitral regurgitation.
Rarely causes aortic stenosis.
Tricuspid valve involvement is infrequent.
Pulmonary valve involvement is rare.