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Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What is haemostasis?

A

Arrest of bleeding and maintenance of vascular patency

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2
Q

What is the lifespan of platelets?

A

7-10 days

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3
Q

When is Von Willebrand Factor released?

A

When there is vessel endothelial damage which exposes collagen.

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4
Q

What is the screening test for primary haemostats?

A

Platelet count

can measure von Willebrand factor if history indicates it

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5
Q

What converts plasminogen to plasmin? When can it be used as a treatment?

A

tissue plasminogen activator (tPA)

To break down clots e.g. acute stroke

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6
Q

What are D-dimers?

A

Cross-linked Fibrin Degradation Products (FDPs)

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7
Q

What 2 factors convert prothrombin to thrombin?

A

Factor V and Xa

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8
Q

What factors are affected in prolonged PT?

A

Tissue factor

Factor VIIa

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9
Q

What factors are affected in prolonged APTT?

A

Factor VIII

Factor IXa

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10
Q

What condition can cause isolated prolonged APTT?

A

Haemophilia

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11
Q

What is thrombophilia?

A

Deficiency of naturally occurring anticoagulants (may be hereditary). Therefore, increased tendency to develop venous thrombosis.

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12
Q

What proteins are involved in natural anticoagulation by switching off factor V and VII?

A

Protein S and Protein C

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13
Q

What is primary haemostats?

A

Formation of platelet plug

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14
Q

What is secondary haemostats?

A

Formation of fibrin clot

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15
Q

What are the causes pf platelet functional defects?

A

Hereditary (rare)
Acquired:
- drugs (aspirin, NSAIDs etc)
- renal failure

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16
Q

Where are all the clotting factors produced?

A

Liver

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17
Q

What is the significance of low albumin in the context of abnormal bleeding?

A

Liver produces both albumin and clotting factors, so if there is low albumin due to liver disease, suggests the liver won’t be producing enough clotting factors either.

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18
Q

What are the multiple clotting factor deficiencies?

A

Liver failure
Vitmain K deficiency/Warfarin therapy
Complex coagulopathy: DIC

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19
Q

What is the effect of multiple clotting factor deficiencies on PT and APTT?

A

Both prolonged

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20
Q

What causes Haemorrhagic disease of the newborn and how is it prevented?

A

Babies don’t have dietary intake of vitamin K or any gut flora to make vit K so they have clotting deficiency. Newborns get IM vitamin K to prevent this

21
Q

Why do you get end organ failure in DIC

A

Microvascular thrombus formation

22
Q

If both PT and APTT are prolonged, what does this suggest?

A

Multiple clotting factors problem

23
Q

What happens to D-dimer levels in DIC and why?

A

Increase, due to excess fibrinolysis

24
Q

What are the PT and APTT in haemophilia?

A

PT: normal
APTT: very prolonged (because the problem is with Factor VIII or IX)

25
Q

What is the main component of arterial thrombus vs venous thrombus and what are the targeted treatments in each case?

A

arterial: platelet-rich clot - treat with anti-platelets
Venous: fibrin-rich clot - treat with fibrinolytics and drugs that interfere with fibrin clots (heparin, warfarin etc)

26
Q

What are the complications of PE?

A 
pulmonary infarction
pleuritic chest pain
cardiovascular collapse/sudden death
hypoxia
right heart strain
27
Q

What are the risk factors of VTE?

A 
age
marked obesity
pregnancy
puerperium
oestrogen therapy
previous DVT/PE
trauma/surgery
malignancy
paralysis
infection
thrombophilia
28
Q

Which naturally occurring anticoagulant binds to thrombin?

A

Anti-Thrombin III

29
Q

What is the commonest hereditary thrombophilia?

A

Factor V Leiden (Impairs protein C/S)

30
Q

When would you consider hereditary thrombophilia screening?

A

Venous thrombosis

31
Q

How is hereditary thrombophilia managed?

A

Advice on avoiding risk
Short term prophylaxis - to prevent thrombotic events during periods on known risk (e.g. pregnancy)
Short term anticoagulation - to treat thrombotic events
Long term anticoagulation - if recurrent thrombotic events

32
Q

What is acquired thrombophilia?

A

Antiphospholipid antibody syndrome

33
Q

What happens to ATPP in Antiphospholipid syndrome?

A

It is prolonged
- paradoxical as you would expect this make pt prone to bleeding but the clotting factors are unaffected and pts are actually prone to thrombosis

34
Q

How is anti-phospholipid syndrome treated and why?

A

aspirin and warfarin

anti-platelet and anti-coagulant because there is activation of primary and secondary haemostasis

35
Q

What are the immune causes of thrombocytopenia?

A

ITP
Drugs (penicillin, thiazides, oral hypoglycaemics, heparin, blood transfusion)
SLE
HIV

36
Q

What drugs are used to prevent strokes?

A

Atherosclerosis - anti-platelets

AF (fibrin-rich clot in LA) - anti-coagulants

37
Q

What do you monitor in patients on Warfarin?

A

PT (INR)

38
Q

What do you monitor in patients on unfractionated Heparin?

A

APTT

39
Q

Give an example of a coumarin anticoagulant

A

Warfarin

40
Q

What is a complication of long term heparin therapy?

A

Osteoporosis

41
Q

What is the target INR for most patients in warfarin?

What might make you aim for higher?

A

2 - 3

Further event despite warfarin treatment - aim for a max of about 3.5 - 4

42
Q

What are the bleeding complications of warfarin therapy?

A 
Mild:
- skin bruising
- epistaxis
- haematuria
Severe:
- GI bleeds
- intracranial bleeds (risk is about 1 in 200)
- significant drop in Hb
43
Q

How long does it take for vitamin K to reverse the effects of warfarin therapy?

A

6 hours

44
Q

What can you given for immediate reversal of warfarin therapy in a life-threatening situation?

A

Administer clotting factors (FFP or factor concentrates)

45
Q

What are the 2 groups of new anticoagulants? Give an example of each

A

Oral direct thrombin inhibitors e.g. Dabigatran

Oral Factor Xa inhibitors e.g. Rivaroxaban, Apixaban

46
Q

What is the risk of giving Dabigabtran to elderly patients?

A

Dabigatran is renally excreted so patients with renal impairment are at risk of build-up of the drug - risk of bleeding.

47
Q

What do platelets do in arterial thrombosis?

A

Plaque rupture due to high pressure environment of arteries
Platelets adhere to exposed endothelium and there is release of vWF
Platelets become activated - release granules that activate coagulation and recruit other platelets to developing platelet plug
platelet aggregation via membrane glycoproteins

48
Q

A 21 year old girl has a history of heavy periods and investigations indicate a defect in primary haemostasis. Her blood count is normal. What is the most likely diagnosis?

A

Von Willebrand’s Disease (primary haemostats failure but normal platelet count)

49
Q

What does an isolated prolonged APTT suggest?

A

Deficiency of factors involved in the ‘intrinsic’ pathway of coagulation (Factor VIII, IX, vWF [as it binds Factor VIII]) or the presence of an anti-phospholipid antibody (lupus anticoagulant) that is not associated with a bleeding phenotype

Haematology (5 decks)

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