DVT & PE Flashcards

1
Q

What are the three main components to the haemostasis system?

A

Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel.

  1. Vasoconstriction
  2. Platelet plug formation
  3. Blood clotting-leads to formation of fibrin
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2
Q

What systems prevent blood clotting?

A

Healthy endothelium
1. Anti-thrombins-prevent thrombin formation
2. Protein C and S inactivate clotting factors
3. Fibrinolysis-Plasmin breaks down fibrin - breakdown product of this is D-dimer-used in diagnosis

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3
Q

Provide a brief overview of how a platelet plug is formed.

A

Platelets stick to ruptured surface – produce A2 (inhibited by aspirin) and ADP – driving the sticking of more platelets – emergency quick response

Coagulation cascade activated to form fibrin mesh – solid/long-term clot

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4
Q

Overview of the coagulation cascade.

A
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5
Q

Outline how a suspected DVT is investigated.

A

Use Well’s score to calculate liklihood of DVT

D-Dimer is a thrmbus breakdown product - elevated levels indicates high levels of clotting

Doppler Ultrasound - allows for visualisation of clot

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6
Q

How are DVTs treated

A

Most patients treated with

Factor Xa inhibitors e.g. apixaban - Often called Direct oral anticoagulants (DOAC)

or

Low molecular weight heparin (LMWH)

Warfarin – difficult to work with – low therapeutic window - inhibits the production of vitamin K dependent clotting factors

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7
Q

What is Virchow’s triad?

A

Outlines three factors that contribute to venous thrombosis formation.

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8
Q

Do tumours increase DVT risk?

A

Yes!

Tumours release tissue-factor like molecules-HYPERCOAGULABILITY (Virchows Triad)

Tumours produce molecules that damage endothelium- VESSEL WALL INJURY (Virchows Triad)

Unprovoked DVT – suspicion of cancer

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9
Q

How does a pulmonary embolus typically present?

A
  1. Breathlessness (most common)/Tachypnoea-rapid breathing
  2. Tachycardia, including AF – look out for this – typically in a hospital environment
  3. Cough
  4. Calf or leg swelling
  5. Crackles or reduced breath sounds in around 1/5th
  6. Elevated JVP – jugular venous pressure

Less common
1. Haemoptysis
2. Syncope
3. Pleuritic chest pain

Need high degree of clinical suspicion to spot

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10
Q

What is the treatment for PE?

A

Oral factor Xa inhibitor e.g. apixaban, rivaroxaban - This is option for majority

or

Low molecular weight heparin e.g. dalteparin followed by either thrombin inhibitor e.g. dabigatran or vitamin K antagonist e.g. warfarin

Treatment normally given for three months after a “provoked” PE or DVT

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11
Q

Why is venothromboembolism risk increased in hospital patients?

A
  1. Immobility
  2. Age – likely due to a lack of mobility
  3. Underlying conditions like heart failure
  4. Cancer
  5. Surgery-activates clotting system
  6. Inflammation-release of tissue factor
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12
Q

What measures can reduce the risk of venothromboembolism in hospitals?

A
  1. Mobilisation
  2. Adequate hydration
  3. Compression stockings or pneumatic compression devices - Sufficient in low risk patients
  4. Prophylactic dose low molecular weight heparin e.g. dalteparin - Treatment based on risk assessment
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13
Q

How is a pulmonary embolism diagnosed?

A

CT pulmonary angiogram

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