143 - Haemostasis + Thrombosis Flashcards

1
Q

If a baby presented with life threatening bleeding, all coagulation tests came back fine, but it had an increased bleeding time, what sort of disorder might it have?

A

Primary dysfunction

- platelet function disrupted

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2
Q

A 30 year old man presents with a swollen left knee. His APTT was prolonged
FVIII levels were <2%

What is condition may he have?

A

Haemophilia A

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3
Q

A 36yr old pregnant women has SOB and chest pain.

She has an increased thrombin time
Her APTT was hugely prolonged
Other tests were normal

What is this due to?

A

On heparin treatment - for a PE?

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4
Q

A 7 year old child presents with petechiae and investigations show a low platelet count, what may be wrong?

A

ITP - Idiopathic Thrombocytoponic purpura

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5
Q

A 2 week old premature baby has an intracranial bleed
The INR was increased
The APTT was increased

What might this be due to?

A

Vit K deficiency

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6
Q

What is another name for INR test?

A

OSPT

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7
Q

What is haemostasis?

A

The process of blood clot formation at the site of an injury

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8
Q

What is purpura? What are the 2 types?

A

Bleeding under the skin
Petichae - little dots of bleed
Echymoses - Bruise - large + continuous

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9
Q

What are the steps of haemostasis?

A

Cut -> vasoconstriction
Primary -> platelet plug forms
Secondary -> fibrin clit/mesh forms (coag cascade)

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10
Q

Describe primary haemostasis

A

Platelets interact with the exposed collagen fibres - cause adhesion (bind to VWF in the subendothelial matrix, adhere to themselves using GP1b receptors)

Platlets are activated and release contents of dense alpha granules - and express active phospholipid and GPIIb/IIa

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11
Q

Describe the coagulation cascade

A

2 pathways (intrinsic and extrinsic) that can be independently activated, that join to form a common pathway which ends in the formation of fibrin from fibrinogen, which can cross link and form a mesh.

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12
Q

What factors are involved in the intrinsic pathway? How is it activated?

A

Direct contact activation - contact with platelet phospholipids, also activated by thrombin formation int he common pathway.

FXII
FXI
FIX

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13
Q

What factors are involved int he extrinsic pathway? What activates it?

A

Tissue factor activation

FVII + Tissue factor

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14
Q

What factors are involved in the common pathway?

A

FVIII
FX
Prothrombin - thrombin
Fibrinogen - Fibrin

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15
Q

What is fibrinolysis?

A

Breakdown of clots
Plasminogen - plasmin
Fibrin -> fibrin degrading products

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16
Q

What activates/helps fibrinolysis?

A

Urokinase - a tPA

17
Q

What coagulation screen tests check the intrinsic pathway?

A

APTT - activated partial thromboplastin time

18
Q

Which coag screen checks the extrinsic pathway?

A

PT - prothrombin time

19
Q

What coag screen checks the common pathway?

A

TCT - Thrombin clotting time

20
Q

What coag screen result is used to calculate the INR?

A

PT

21
Q

What are the characteristics of bleeding due to a disorder of primary haemostasis?

A

Bleeding in skin or muscosa
Bleeding is immediate
Purpura - petichae form

22
Q

What are the characteristics of secondary haemostasis disorder’s bleeding?

A

Bleeding in soft tissues, joints, muscles
Bleeding is delayed + severe, eg. after surgery not minor cuts
Echymoses form

23
Q

Name an example of an inherited primary haemostasis disorder?

A

Connective tissue disorders (vessel can’t constrict well)

Inherited haemorrhagic telangiectasia

24
Q

Name an example of acquired primary haemostasis disorder

A

Henoch-scholein purpura

Infections, drug reactions, steroids, trauma
senile purpura
Scurvy

25
Q

Name some platelet disorders causing primary haemostasis issues

A

Thrombocytopenia - due to bone marrow failure, splenomegaly, DIC (intravascular thrombosis), Autoimmune thrombocytoponia / ITP

26
Q

Name 3 examples of disorders of secondary haemostasis

A

Haemophilia A
Haemophilia B (Christmas disease)
Von Willebrand disease

27
Q

What will you see on a coag screen os someone with haemophilia A ?

A

Prolonged APTT

Low FVIII

28
Q

What deficiency is christmas disease?

A

FIX

29
Q

What will you see in a coag screen of someone with Von willebrand disease?

A

Prolonged APTT

Prolonged bleeding time

30
Q

What are some acquired causes of secondary haemostasis dysfunction?

A

Liver disease
Vit K deficiency
Anticoagulation

31
Q

What is Virchow’s triad of thrombosis?

A

Altered blood flow
Vessel wall damage
Incresed coagulability

32
Q

What are our natural anticoagulants?

A

Antithrombin - a glycoprotein synthesised in the liver which inhibits Fxa and thrombin (heparin makes effect 2000x stronger)

Protein C system - Vit K dependant
Inhibits Va + VIIIa
Acts using thrombomodulin module attached to endothelium wall - Protein C gets activated then Protein S blocks their function

33
Q

What are some inherited disorders of thombosis?

A

Factor V leiden - stops prot C being able to inactive FV - so have weak natural anticoag ability

Antithrombin deficiency
Protein C/S deficiency

34
Q

What is a non-inherited disorder of thrombosis?

A

APS - Antiphospholipid syndrome

  • A vascular thrombosis
  • Increased complications in pregnancy - esp. abortions after 10 weeks
  • Investigation - anticardiolipin antibodies + lupus anticoag
  • Treatment? - Anticoagulants for life
35
Q

How can you treat low platelet count?

A

Steroids - for ITP

Platelet transfusions

36
Q

How do you enhance coagulation?

A

Give coagulant factors - e.g give fresh frozen plasma or using recombinant technology
Vitamin K - needed for lots of the coag factors

37
Q

How does tranexamic acid work?

A

An anti-fibrinolytic

blocks plasminogen-plasmin so helps stabilise clots

38
Q

There are 3 areas of drugs to help with thrombosis risk - what are they?

A

Antiplatlets
Anticoagulants
Fibrinolytic therapy

39
Q

What anticoagulants can we use?

A

Heparin (unfractionated or LMWH)
Warfarin (Vit K antagonist)
Dabigatran (antithrombin)
Rivaroxabam + apixabam (Anti Xa)