Deep vein thrombosis and thromboembolism Flashcards

1
Q

Define Thrombosis

A

A solid mass formed IN the circulation from the constituents of the blood during life
(thrmobus is a clot in a BV essentially that results from a complex series of events involving coagulation factors, platelets, red blood cells and vessel wall)

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2
Q

What are fragments of thrombi called?

A

Emboli

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3
Q

What is the difference between a thrombus in the arterial and venous circulation

A

Arterial circulation = High pressure and platelet rich

Venous circulation = Low pressure and fibrin rich

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4
Q

What can result from an arterial thrombus in the coronary circulation

A

Myocardial ischaemia or infarction

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5
Q

What can result from an arterial thrombus in the cerebral circulation

A

Transient Ischaemic Attack (TIA) or Stroke

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6
Q

What can result from an arterial thrombus in the peripheral vascular circulation

A

Peripheral vascular disease (PVD) - claudication, rest pain and gangrene

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7
Q

Risk factors of arterial thrombosis

A
(Similar to that of atherosclerosis)
Smoking
Hypertension
Diabetes
Hyperlipidemia
Obesity/sedentary lifetsyle
Stress
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8
Q

Pathophysiology of arterial thrombosis

A
  • Result of an atheroma that forms in areas of turbulent blood flow such as the bifurcation of arteries
  • Platelets adhere to the damaged vascular endothelium and aggregate in response to ADP and thromboxane A2
  • Plaque rupture leads to the exposure of blood containing factor VIIa to tissue factor within the plaque which may trigger blood coagulation and lead to thrombus formation
  • This can result in complete occlusion of the vessel or embolisation that produces distal obstruction
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9
Q

Diagnosis of arterial thrombosis

A
Myocardial infarction
History
Cardiac enzymes
Cerebrovascular accident
Peripheral vascular disease
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10
Q

Diagnosis of arterial thrombosis myocardial infarction

A
STEMI ECG
Diagnosed on presentation
ST elevation
Tall T waves
LBBB
T wave inversion and pathological Q waves follow
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11
Q

Diagnosis of arterial thrombosis Cerebrovascular accident

A

History and examination

CT/MRI scan

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12
Q

Diagnosis of arterial thrombosis peripheral vascular disease

A

History and examination

Ultrasound and angiogram

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13
Q

Prevention of arterial thrombosis

A
  • COX inhibitor e.g. ASPIRIN which inhibits platelet aggregation
  • P2Y12 inhibitor e.g. CLOPIDOGREL which inhibits ADP from binding to the P2Y12 receptor
  • DIPYRAMIDOLE inhibits phosphordiesterase-mediated breakdown of cyclic AMP which prevents platelet activation
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14
Q

Prevention (and treatment) of MI from arterial thrombosis

A

• ASPIRIN - inhibits platelet function as COX inhibitor
• Thrombolytic therapy:
- STREPTOKINASE
- TISSUE PLASMINOGEN ACTIVATOR which generates plasmin and degrades fibrin clot

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15
Q

Prevention (and treatment) of stroke from arterial thrombosis

A
  • ASPIRIN or CLOPIDOGREL
  • TISSUE PLASMINOGEN ACTIVATOR (for brain attack, only have a narrow window)
  • Treat risk factors
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16
Q

Clinical presentation of DVT

A

Often progresses to pulmoary embolism before presenting.
Classical features include:
Limb pain and tenderness along the lines of the deep veins, pain/swelling of the calf, increase in skin temperature, pitting oedema.
Resembles cellulitis

17
Q

Aetiology of DVT

A

Thrombotic risk factors
Surgery, immobility, leg fracture, oral contraceptive pill
Genetic or acquired causes

18
Q

What is more concerning:

DVT in calf below the knee or above the knee

A

Above the knee is potentially fatal and occurs in the proximal leg vein.

19
Q

Genetic cause of DVT

A

Factor V Leiden

PT20210A

20
Q

Acquired causes of DVT

A

Anti-phospholipid syndrome
Lupus anticoagulant
Hyperhomocysteinaemia

21
Q

Risk factors of DVT

A
Age (higher)
Pregnancy
Synthetic oestrogen
Trauma
Surgery (especially pelvic or orthopaedic)
Past DVT
Cancer
Obesity
Immobility
22
Q

DVT pathophysiology

A

Formation of the thrombus in the deep vein.

This can embolise and often flows up into the pulmonary circulation as a pulmonary embolism

23
Q

Diagnosis of DVT

A

Ultrasound (compression Ultras = find popliteal vein, if can squash it shut then NO DVT and vice versa)
D-dimers (plasma)
Contrast venography

24
Q

What is D-dimer

A

Type of fibrinogen degradation product that is released into the circulation when a clot begins to dissolve

25
Q

Treatment of DVT

A

LMW Heparin

other anticoagulation also possible e.g. Oral warfarin

26
Q

Give example of a LMW Heparin

A

SC Enoxaparin

27
Q

Prevention of DVT

A
  • Early mobilisation after operation
  • Compression stockings
  • Thrombophylaxis for both low risk and high risk
28
Q

WHat can be used to score risk factors of DVT

A

WELLS score

29
Q

Risk factors e.g. in WELLS score

A

Active cancer, bed ridden, calf swelling,

30
Q

NOAC (DOAC same thing) VS Warfarin

A

NOAC - New oral anticoagulant drugs (INR does not need monitoring); easy to reverse side effects compared to warfarin (vitamin K replacement); shorter half life

Warfarin has more complications

31
Q

Example of Vitamin K supplement

A

Beriplex (used to reverse effects of excess bleeding)

32
Q

Examples of anticoagulants

A

Heparin
Warfarin
NOACs

33
Q

Examples of NOACs and what they inhibit

A

Factor Xa inhibitors: Rivaroxaban, Apixaban
Thrombin inhibitor:
Dabigatran

34
Q

How does warfarin work

A

Inhibits reductase enzyme responsible for regenerating active form of vitamin K - leads to analogous vitamin K deficiency