89 - Venous Thrombosis and Pulmonary Thromboembolism Flashcards

1
Q

Most common preventable cause of death in hospitalised patients

A

Pulmonary thromboembolism

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2
Q

Clot

A

A solid mass composed of blood components which forms after death

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3
Q

Thrombus

A

Solid mass composed of blood components formed in an artery of vein during life

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4
Q

Where do thrombi often form?

A

Deep veins of the lower limbs

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5
Q
Deep veins of lower limb 
1
2
3
4
A

Distal to proximal:

Anterior, posterior tibial veins
Popliteal vein
Femoral vein
Iliac vein (in the pelvis)

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6
Q

Most important venous plexus in lower limb

A

In soleus muscle

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7
Q

Superficial veins of the lower limb

A

Great and small saphenous veins

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8
Q

Location of formation of venous thrombi

A

Form upstream of valve.

Become more occlusive, thicker.

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9
Q

Feature of growth of venous thrombi

A

Can propagate up- and downstream of where thrombus began forming.

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10
Q

Why are venous thrombi red?

A

Form in an environment of low flow.

Have lots of RBCs.

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11
Q

Structure of venous thrombi

A

Lines of Zahn.

Alternating layers of red (RBC) and pink (platelets and fibrin)

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12
Q

Thrombi that are often occlusive

A

Venous thrombi

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13
Q

When are venous thrombi more likely to embolise?

A

When recently-formed.

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14
Q

Examples of changes to vessel wall that can predispose to thrombi

A

Trauma from catheterisation.

Bacterial infection of vessel wall.

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15
Q

Polycythaemia

A

Condition where too many RBCs are produced.
Can’t be cured, only can control symptoms.
Predisposes to thrombosis.

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16
Q
Things that can lead to non-laminar flow, causing thromboses
1
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A
Prolonged immobilisation
Dehydration
Hypotension
Congestive cardiac failure
Polycythaemia
17
Q

What cause most arterial thromboses?

A

Complications of atherosclerosis.

18
Q

Example of a genetic hypercoagulable state

A

Factor V Leiden

19
Q

Factor V Leiden

A

Point mutation in factor V prevents activated protein C (natural anticoagulant) from binding to a cleavage site.

20
Q

Proportion of patients with DVT that have factor V Leiden

A

50%

21
Q

Uncommon genetic predispositions to hypercoagulable state
1
2
3

A

(1) Antithrombin III deficiency
(2) Protein C deficiency
(3) Protein S deficiency

22
Q

Common genetic predispositions to hypercoagulable state
1
2

A

Factor V Leiden

Prothrombin III deficiency

23
Q
Examples of secondary predisposing factors to hypercoagulability
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7
8
A

• Surgery
• Massive trauma and burns
• Malignancy – release of thrombogenic substances from
tumours especially mucinous adenocarcinomas
• Obesity – mechanism unknown
• Smoking – probably
• Hyper-oestrogenic states (pregnancy and the OCP)
• Nephrotic syndrome (both cause and effect of renal
vein thrombosis)
• Anti-phospholipid antibody syndrome

24
Q
Fates of venous thrombi
1
2
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4
A

1) Lysis of thrombus
2) Organisation of thrombus (can form scar tissue, forming a stricture on the vessel wall)
3) Recanalisation (most common fate. New blood vessels form, restoring blood flow around thrombus)
4) Embolism (most dangerous outcome)

25
Q

Embolus

A

An embolus is a mobile mass of material within the

vascular system able to lodge within a vessel, occlude its lumen and obstruct blood flow.

26
Q

Thromboembolus

A

A detached piece of thrombus

27
Q

What do clinical effects of pulmonary thromboemboli depend on?

A

Size of occluded vessel

28
Q

Pulmonary thromboembolus that can cause sudden death

A

‘Saddle embolus’

Thromboembolus lodges at the bifurcation of the pulmonary artery.

29
Q

‘Saddle embolus’

A

Thromboembolus lodges at the bifurcation of the pulmonary artery.

30
Q

Features of a saddle embolus

A

Red, with some pale areas.
Lodged at the bifurcation of the pulmonary artery.
Coiled shape, reflecting vein of origin.
Occlusive.

31
Q

Clinical effects of a saddle embolus

A

Sudden death - Cardiac arrest with electromechanical dissociation.

32
Q

Electromechanical dissociation

A

Electrical activity of heart is continuing in normal fashion, but mechanical activity of heart is prevented from thromboembolus.

33
Q
Clinical effects of a thromboembolus in a right or left pulmonary artery
1
2
3
4
A

Sudden death.
Dyspnoea.
Chest pain.
Circulatory failure mimicking myocardial infarction

34
Q

Thoracic catastrophes presenting with central chest pain, SOB

A

MI.
Pulmonary thromboembolus
Aortic dissection

35
Q
Clinical features of a small pulmonary thromboembolus 
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A
Share features with other solid-organ infarcts
Sharply demarcated infarct
Wedge-shaped infarct
Pleural base.
Red
Occluded artery at apex
36
Q

Clinical features of a small pulmonary thromboembolus
1
2
3

A

Dyspnoea
Haemoptysis
Pleuritic chest pain

37
Q

Why are lung infarcts red and not pale?

A

Dual blood supply (pulmonary circulation and bronchial circulation from descending aorta)

38
Q

Clinical features of a small pulmonary thromboembolus without infarct

A

Unexplained tachycardia in a patient with risk factors for pulmonary thromboembolism

39
Q

What could be occurring if a patient has an unexplained tachycardia, and has risk factors for venous thromboses.

A

Small pulmonary thromboembolism without an infarct