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Week 3 - haematology > Bleeding and thrombotic disorders > Flashcards

Bleeding and thrombotic disorders Flashcards

1
Q

What is disseminated intravascular coagulation?

A
  • An acquired, consumptive process
  • The coagulation cascade is activated and micro thrombi are laid down (intravascular deposition of fibrin) leading to thrombosis of small and midsize vessels and organ failure
  • Exhaustion of the coagulation cascade resulting in bleeding due to decreased platelets and coagulation factors
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2
Q

What are the causes of disseminated intravascular coagulation?

A
  • Sepsis
  • malignancy
  • massive haemorrhage
  • Severe trauma
  • Pregnancy complications e.g. pre-eclampsia, placental abruption, amniotic fluid embolism
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3
Q

What are the investigations that should be carried out in DIC?

A
  • Coagulation PT, aPTT and fibrinogen
  • D-dimers
  • FBC and film
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4
Q

What is the treatment of DIC?

A
  • Treat underlying cause!!
  • Fresh frozen plasma +/- platelets if bleeding or high risk for bleeding
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5
Q

Why is fibrinogen low in DIC?

A

Because it is being converted into fibrin

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6
Q

Why are d dimers increased in DIC?

A

Because fibrin is being broken down to d dimers

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7
Q

What can you do if a patient who is on warfarin has a high INR?

A
  • Stop warfarin or reduce the dose
  • Give vitamin K (oral or IV)
  • Give coagulation factors (II, VII, IX and X) - prothrombin complex concentrates e.g. beriplex or octaplex
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8
Q

Describe the pathogenesis of coagulopathy in liver disease

A
  • Poor coagulation factor synthesis in the liver
  • Vitamin K deficient (poor diet ± obstructive component to jaundice)
  • Poor clearance of activated coagulation factors
  • DIC
  • Hypersplenism leading to low white blood cells and platelets
  • Reduced thrombopoietin synthesis leading to low platelets
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9
Q

If a patient has prolonged APTT, what test should you do next?

A
  • Mix the patient plasma with normal plasma (1:1 ratio)
  • If there is a full correction of APTT, then there is a factor deficiency
  • If there is a partial correction of APTT, then there is a inhibitor
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10
Q

What is lupus anticoagulant?

A
  • Phospholipid dependent antibody
  • It interferes with phospholipid depended tests such as APTT resulting in a prolonged APTT
  • If persistent then may be associated with a prothrombotic state
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11
Q

What is antiphospholipid syndrome?

A

Persisting lupus anticoagulant and thrombosis (or recurrent foetal loss)

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12
Q

Explain how you can test for lupus anticoagulant

A
  • APTT is often prolonged
  • APTT 50:50 dilution only partially corrects
  • DRVVT (dilute Russel viper venom test) ratio is prolonged but corrects with excess phospholipid
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13
Q

What is acquired thrombophilia?

A 
•Acquired antiphospholipid syndrome 
•Presence of antiphospholipid antibodies 
 - lupus anticoagulant 
 - anti cardiolipin antibodies 
 - beta-2 glycoprotein 1 antibodies
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14
Q

What is the mechanism of acquired thrombophilia?

A

Disruption of annexing V shield exposing excess phospholipid

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15
Q

What is the clinical scenario of acquired thrombophilia?

A
  • Venous/arterial thrombosis with a high risk of thrombosis recurrence
  • Recurrent miscarriage
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16
Q

What is haemophilia A?

A
  • Classical haemophilia
  • Factor VIII deficiency
  • X linked inheritance
  • Results in a prolonged ATPP
17
Q

What is the treatment of coagulation factor deficiency?

A 
•Eduction of patients and doctor 
•Desmopressin - increases VIII 
•Replacement therapy 
 - FFP 
 - plasma derived factor concentrate 
 - recombinant produced factor concentrate 
•Gene therapy
18
Q

What is Von willebrand disease?

A
  • Most common mild bleeding disorder
  • Autosomal dominant but variable penetrance
  • mucosal type bleeding pattern
  • Reduced VWF ± reduced platelet aggregation ± reduced FVIII
19
Q

What are the primary classifications of von willebrand disease?

A
  • Type 1= partial quantitive deficiency of VWF
  • Type 2 = qualitative deficiency
  • Type 3 = virtually complete deficiency of VWF
20
Q

Name 2 severe inherited platelet disorders

A
  • Glansmanns thrombasthenia

* Bernard soulier syndrome

21
Q

What is glansmanns thrombasthenia?

A
  • Absent/defective GP IIb/IIIa

* Normal platelet count

22
Q

What is Bernard soupier syndrome?

A
  • Absent/defective GP Ib/V/IX

* Macrothrombocytopenia

23
Q

What is the treatment of bleeding in those with inherited platelet disorders?

A
  • Pressure to any wound
  • Tranexamic acid/desmopressin
  • HLA matched platelet transfusion
  • rFVIIa
24
Q

What is inherited thrombophilia?

A
  • Deficiencies of natural anticoagulants: antithrombin, protein C or protein S
  • Specific genetic mutations: factor V Leiden (resistance to APC) or prothrombin gene mutation resulting in increased prothrombin

Week 3 - haematology (17 decks)

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