Deep vein thrombosis and thromboembolism Flashcards

(34 cards)

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
Treatment of DVT
LMW Heparin | other anticoagulation also possible e.g. Oral warfarin
26
Give example of a LMW Heparin
SC Enoxaparin
27
Prevention of DVT
* Early mobilisation after operation * Compression stockings * Thrombophylaxis for both low risk and high risk
28
WHat can be used to score risk factors of DVT
WELLS score
29
Risk factors e.g. in WELLS score
Active cancer, bed ridden, calf swelling,
30
NOAC (DOAC same thing) VS Warfarin
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
Example of Vitamin K supplement
Beriplex (used to reverse effects of excess bleeding)
32
Examples of anticoagulants
Heparin Warfarin NOACs
33
Examples of NOACs and what they inhibit
Factor Xa inhibitors: Rivaroxaban, Apixaban Thrombin inhibitor: Dabigatran
34
How does warfarin work
Inhibits reductase enzyme responsible for regenerating active form of vitamin K - leads to analogous vitamin K deficiency