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Flashcards in Haemostasis Deck (49):
1

What is haemostasis?

Arrest of bleeding and maintenance of vascular patency

2

What is the lifespan of platelets?

7-10 days

3

When is Von Willebrand Factor released?

When there is vessel endothelial damage which exposes collagen.

4

What is the screening test for primary haemostats?

Platelet count
(can measure von Willebrand factor if history indicates it)

5

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

tissue plasminogen activator (tPA)
To break down clots e.g. acute stroke

6

What are D-dimers?

Cross-linked Fibrin Degradation Products (FDPs)

7

What 2 factors convert prothrombin to thrombin?

Factor V and Xa

8

What factors are affected in prolonged PT?

Tissue factor
Factor VIIa

9

What factors are affected in prolonged APTT?

Factor VIII
Factor IXa

10

What condition can cause isolated prolonged APTT?

Haemophilia

11

What is thrombophilia?

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

12

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

Protein S and Protein C

13

What is primary haemostats?

Formation of platelet plug

14

What is secondary haemostats?

Formation of fibrin clot

15

What are the causes pf platelet functional defects?

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

16

Where are all the clotting factors produced?

Liver

17

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

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.

18

What are the multiple clotting factor deficiencies?

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

19

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

Both prolonged

20

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

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

Why do you get end organ failure in DIC

Microvascular thrombus formation

22

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

Multiple clotting factors problem

23

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

Increase, due to excess fibrinolysis

24

What are the PT and APTT in haemophilia?

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

25

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

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

What are the complications of PE?

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

27

What are the risk factors of VTE?

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

28

Which naturally occurring anticoagulant binds to thrombin?

Anti-Thrombin III

29

What is the commonest hereditary thrombophilia?

Factor V Leiden (Impairs protein C/S)

30

When would you consider hereditary thrombophilia screening?

Venous thrombosis

31

How is hereditary thrombophilia managed?

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

What is acquired thrombophilia?

Antiphospholipid antibody syndrome

33

What happens to ATPP in Antiphospholipid syndrome?

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

How is anti-phospholipid syndrome treated and why?

aspirin and warfarin
(anti-platelet and anti-coagulant because there is activation of primary and secondary haemostasis)

35

What are the immune causes of thrombocytopenia?

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

36

What drugs are used to prevent strokes?

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

37

What do you monitor in patients on Warfarin?

PT (INR)

38

What do you monitor in patients on unfractionated Heparin?

APTT

39

Give an example of a coumarin anticoagulant

Warfarin

40

What is a complication of long term heparin therapy?

Osteoporosis

41

What is the target INR for most patients in warfarin?
What might make you aim for higher?

2 - 3
Further event despite warfarin treatment - aim for a max of about 3.5 - 4

42

What are the bleeding complications of warfarin therapy?

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

43

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

6 hours

44

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

Administer clotting factors (FFP or factor concentrates)

45

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

Oral direct thrombin inhibitors e.g. Dabigatran
Oral Factor Xa inhibitors e.g. Rivaroxaban, Apixaban

46

What is the risk of giving Dabigabtran to elderly patients?

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

47

What do platelets do in arterial thrombosis?

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

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?

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

49

What does an isolated prolonged APTT suggest?

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