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Cardiovascular System > DVT & Pulmonary Embolism > Flashcards

DVT & Pulmonary Embolism Flashcards

1
Q

What is a thrombus?

A
  • blood Clotting in the wrong place

- haemostasis

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2
Q

What are the components of a thrombus?

3

A
  • fibrin (end product of clotting cascade)
  • platelets
  • RBCs
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3
Q

What factors make up Virchow’s Triad?

3

A
  • stasis
  • endothelial damage
  • hypercoagubility
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4
Q

What is meant by the stasis of blood?

A
  • pooling of blood

- when blood flow is reduces (haemostasis) - it becomes stagnant and thrombosis sets in

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5
Q

What is meant by endothelial damage?

A
  • it can mean several things
  • complex atheroma plaques can rupture which leads to platelet aggregation (hypercoagubility) where thrombosis sets in.
  • a complication to this could be a thromboembolism which could lead to PE (in venous thrombosis)
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6
Q

What is the difference between arterial and venous thrombosis, in terms of mechanism of action?

A

Arterial: atheroma/plaque rupture (platelet aggregation)

Venous: haemostasis/hypercoagubility

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7
Q

What is the difference between arterial and venous thrombosis, in terms of location of origin?

A

Arterial: arteries (esp. at bifurcations), coronary arteries, left heart chambers, carotid arteries

Venous: veins, venous valves, sinusoids

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8
Q

What is the difference between arterial and venous thrombosis, in terms of what they result in (not specifically the disease)?

A

Arterial: ischaemia/infarction

Venous: back pressure

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9
Q

What is the difference between arterial and venous thrombosis, in terms of diseases caused?

A

Arterial: ACS, MI, stroke, HF

Venous: DVT, PE

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10
Q

What is the difference between arterial and venous thrombosis, in terms of their composition?

A

Arterial: cream (platelets and fibrin)

Venous: red (RBCs and fibrin)

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11
Q

Give examples of causes of endothelial dysfunction (not damage).

(3)

A
  • hypertension
  • smoking (increased platelet aggregation)
  • hyperlipidaemia (atheroma)
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12
Q

Give examples of causes of endothelial damage.

3

A
  • catheters (thrombosis around catheter)
  • trauma
  • surgery
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13
Q

Give examples of causes of hypercoagubility.

3

A
  • pregnancy (increased oestrogen, sticky platelets)
  • cancer (e.g. adenocarcinoma)
  • sepsis
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14
Q

What is an embolism?

Give examples.

A

Intravascular material that migrates from its original location to a distal vessel

E.g: blood clot, fat, air, tumour

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15
Q

Who is at higher risk of venous thromboembolism at a young age?

Why?

A

females - female sex hormones make their platelets more sticky.

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16
Q

What are some risk factors to VTE?

5

A
  • surgery (e.g. C-section)
  • varicose veins
  • hypertension
  • oral contraceptive
  • obesity
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17
Q

How is VTE prevented in hospitals?

What are the specific actions taken?

A

thromboprophylaxis: mechanical and pharmacological
mechanical: anti-embolism stockings
pharmacological: anticoagulation therapy

18
Q

What are the signs and symptoms of DVT?

5

A
  • asymptomatic
  • unilateral oedema
  • pain
  • warmth
  • erythema
  • prominent collateral veins
19
Q

What would be the first line of investigations into DVT?

A
  • history and examination

- Wells score (pretest probability score)

20
Q

If the Wells score was low what would be the next line of investigation?

A

d-dimer blood test

21
Q

If the d-dimer blood test was negative, what would this tell us?

A

unlikely DVT

22
Q

If the d-dimer blood test was positive, what would the next line of investigation be?

A

compression ultrasound

23
Q

Outline the investigations carried out to assess for possible DVT.

A
  • Hx/examination
  • Wells score
  • d-dimer blood test
  • compression ultrasound
24
Q

What would be the next line of investigation if the Wells score indicated high probability of DVT?

What would be the next line of investigation if the test came back normal?

A

compression ultrasound

d-dimer blood test, then repeated ultrasound in a week if findings were positive.

25
Q

What is d-dimer?

How would you describe this blood test, in relation to DVT?

A
  • breakdown product of cross-linked fibrin
  • produced during fibrinolysis
  • sensitive but not specific - it can be used to rule out DVT i.e. there can be other causes of d-dimer if test is positive.
26
Q

What are some other causes of increased d-dimer in blood?

4

A
  • recent surgery
  • bleeding
  • sepsis
  • cancer
27
Q

Plasmin breaks down fibrinogen into what?

A
  • fibrin degradation products (FDPs)

- d-dimer

28
Q

What are the clinical signs and symptoms of pulmonary embolism (PE)?

(5)

A
  • pleuritic chest pain
  • dyspnoea
  • haemoptysis
  • tachycardia
  • pleural rub (infarction)
29
Q

What signs and symptoms would be an indication of a massive, severe pulmonary embolism?

(5)

A
  • central cyanosis
  • dyspnoea of sudden onset
  • collapse
  • hypotension
  • raised JVP
30
Q

When investigating for PE, what would be the next line of investigation following a Wells’s score probability pretest? (2)

What are the imaging modalities used? (2)

A

If score is low:

  • d-dimer blood test
  • then, CTPA if positive

If score is high:
- CTPA

Imaging:

  • isotope ventilation-perfusion scan
  • CT pulmonary angiogram
31
Q

What questions should be asked to patients with diagnoses VTE?

A
  • was there a clear cause/precipitant? (e.g. surgery, hospitalisation)
  • any signs/symptoms to suggest underlying cause? (e.g. cancer)
32
Q

Outline the main treatment in treating PE?

A

anticoagulation

33
Q

What would be the drug therapy regime for treating PE?

2

A
  • LMWH preferred

- secondary management drug

34
Q

Give an example of a common LMWH used to treat PE?

What are the contraindications to LMWH?

A

dalteparin

renal failure

35
Q

If a patient has severe renal failure, what could be administered as an alternative to LMWH?

A

unfractioned heparin (UFH)

36
Q

Which secondary measurement therapy is administered to most patients in treating VTE?

Give an example of common drugs used for this therapy?

A

DOAC’s

e.g.
rivaroxaban
dabigatran

37
Q

What are the contraindications to direct thrombin inhibitors (e.g. dabigatran)?

What would be a suitable alternative?

A

obesity, renal impairment

warfarin

38
Q

What is warfarin mechanism of action?

A

vitamin K inhibitor

39
Q

What other treatment options are available for treating massive DVT/PE?

(2)

A
  • vascular surgery interventions

- thrombolysis

40
Q

What thrombolytic agents would be used to break down a PE?

A

alteplase
tenecteplase
streptokinase (not as common)

41
Q

What are potential long-term consequence of DVT?

5

A
  • oedema/lymphoedema
  • pain
  • pigmentation
  • ulceration
  • venous insufficiency
42
Q

What are the aims of treatment of VTE?

3

A

Prevent clot extension
Prevent clot embolisation
Prevent recurrent clot

Cardiovascular System (37 decks)

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