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Romesh Path Fellah > Haematology 3: Haemostasis And Bleeding Disorders > Flashcards

Haematology 3: Haemostasis And Bleeding Disorders Flashcards

1
Q

List 4 Pro-coagulant factors in the body?

A

Platelets
vWF
Endothelium
Coagulation cascade

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2
Q

List 4 Anti-coagulant factors in the body ?

A

AT (antithrombin)
Protein S + Protein C
TFPI (Tissue factor pathway inhibitor)
Fibrinolysis

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3
Q

List 2 thrombopoietic factors ?

A

Thrombopoietin
IL-6
IL-12

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4
Q

Which Surface glycoprotein do platelets use to bind to vWF ?

A

GpIb

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5
Q

Which glycoprotein do platelets use to bind directly to collagen ?

A

GpIa

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6
Q

Which glycoproteins do platelets use to bind to other platelets when aggregating ?

A

GpIIb/IIIa

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7
Q

Which 2 mediators do platelets release when they bind to subendothelial structures (vWF or collagen) to cause platelet aggregation ?

A

ADP

Thromboxane A2

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8
Q

How does Aspirin inhibit platelet aggregation?

A

aspiring irreversibly Inhibits Cyclo-oxygenase (COX)
This prevents Arachidonic acid being converted to endoperoxides
This prevents formation of thromboxane A2
Less Thromboxane A2 means less platelet aggregation

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9
Q

List 2 drug targets for inhibiting platelet aggregation ?

A

Thromboxane A2 production - Aspirin

ADP receptors - Clopidogrel

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10
Q

Which pathway is more important for coagulation in the human body ?

A) Intrinsic pathway
B) Extrinsic pathway
C) Contact activation pathway

A

B) extrinsic pathway

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11
Q

Describe the sequence of events in the Initiation phase of the Clotting cascade ?

A

1) Damage to endothelium causes TF to be exposed
2) Factor VII binds to TF and becomes activated to FVIIa
3) FVIIa/TF complex activate FIX and FX to FIXa and FXa
4) FXa binds to FVa

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12
Q

Describe the sequence of events in the activation phase of the clotting cascade ?

A

1) FXa/FVa complex converts prothrombin to thrombin
2) Thrombin activates FVIII, FXI and recruits more FVa
3) FXIa activates FIX to FIXa
4) Activated platelet binds FVa, FVIIIa and FIXa

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13
Q

Describe the sequence of events in the propagation phase of the clotting cascade ?

A

1) FVIIIa/ FIXa complex on platelets activates FXa on the surface of the platelet.
2) FXa and FVa cause a “thrombin burst” where loads of Prothrombin is converted to Thrombin
3) Thrombin converts fibrinogen to fibrin
4) Fibrin is cross linked to form a stable fibrin clot

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14
Q

Which 4 clotting factors are vitamin K dependent ?

A

10
9
7
2

Think 1972

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15
Q

What is the role of tPA (tissue plasminogen activator) ?

A
  • Converts plasminogen to plasmin
  • Plasmin cleaves The fibrin clot

tPA is produced by the endothelium

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16
Q

Which of these molecules does not promote Plasminogen conversion to Plasmin ?

A) tPA
B) Urokinase 
C) FXIIa
D) FXIa 
E) PAI 1
A

E) PAI1

Plasminogen activator inhibitor inhibits Plasminogen conversion to Plasmin by inhibiting Urokinase and tPA

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17
Q

What does TAFI do ?

A

TAFI (thrombin Activated Fibrinolysis inhibitor) is a Thrombin dependent inhibitor of Fibrin breakdown

18
Q

Deficiency of which component is the most Thrombogenic ?

A) TAFI
B) FVIIIa
C) AT3
D) vWF 
E) Protein S
A

C) AT3

Deficiency of Antithrombin (AT) is very rare but is the most thrombogenic

19
Q

What is the role of Protein C and protein S ?

A

Inhibit FVIIIa and FVa

20
Q

What is the role of Thrombomodulin ?

A

Thrombomodulin is an endothelial receptor for Protein C
It first needs to be activated by Thrombin.
EPCR is another receptor which helps Thrombomodulin bind to protein C

When Thrombomodulin binds to Thrombin and Protein C the complex is called APC (activated protein C)

21
Q

What is the role of APC (activated protein C) ?

A

APC inactivates FVa and FVIIIa

Requires protein S as cofactor

22
Q

What is different in the interaction between APC and FVa in people with Factor V Leiden ?

A

People with Factor V Leiden have APC resistance.

This means activated factor V is not inactivated by APC.

23
Q

What is the physiological role of TFPI as an anticoagulant ?

A

TFPI neutralises the TF/FVIIa complex.

TFPI is produced as a result of TF/FVIIa complex formation in order to stop activation by the extrinsic pathway. (TF/FVIIa is only required for a very short time to activate FX and FIX)

24
Q

What disease is associated with large platelets ?

A

grey platelet syndrome

25
Q

What is ITP (immune thrombocytopenia purpura) ?

A

Autoantibodies against platelets

This causes the platelets to b e removed and destroyed by the immune system

26
Q

List 2 common inherited disorders of coagulation (bleeding disorders) ?

A

Haemophilia A / B

Von willibrand disease

27
Q

Which coagulation factors are deficient in:

Haemophilia A
Haemophilia B

A

Haemophilia A - Factor 8

Haemophilia B - Factor 9

28
Q

What is the inheritance pattern of haemophilia A /B ?

A

X-linked

29
Q

What happens to APTT and PT in Haemophilia A/B ?

A

APTT - INCREASED
PT- normal

APTT Is a measure of the intrinsic pathway

30
Q

List 3 clinical features of haemophilia A/B ?

A

Haemarthroses (bleeding into joints)
Prolonged bleeding after surgery
Ecchymoses

31
Q

How is vWD inherited ?

A

Autosomal dominant

32
Q

What are the differences in type1, type 2 and type 3 vWD ?

A

Type 1- partial quantitative defficiency in vWF
Type 2- Partial Qualitative decency in vWF
Type 3- Complete quantitative deficiency in vWF

33
Q

How does most of vWF circulate in the blood ?

A

Most of it is bound to factor 8

34
Q

What happens to APTT, PT, TT and fibrinogen in DIC ?

A

APTT- prolonged
PT- prolonged
TT- prolonged
Fibrinogen- decreased

35
Q

What are 3 treatments of Vitamin K deficiency ?

A

I.V Vitamin K
FFP
PCC (Prothrombin complex concentrate) Vit K dependent coagulation factors

36
Q

List 3 differences in clinical presentation of Coagulation and platelet disorders ?

A

Platelet disorders

  • Superficial bleeding (petechia)
  • mucous membrane bleeding
  • bleeding immediately after surgery

Coagulation disorders

  • Deep bleeding into Joints (haemarthroses)/muscles
  • delayed bleeding after surgery/trauma
  • no prolonged bleeding after cuts
37
Q

List 2 congenital causes of Vascular defects of coagulation ?

A

Older-Weber-rendu syndrome

Ehler’s danlos syndrome

38
Q

List 3 acquired vascular defects of coagulation ?

A

Dengue haemorrhagic fever
Scurvy
Meningococcal infection

39
Q

What is the treatment of Haemophilia A / B ?

A

Factor 8 / 9 concentrates replacement therapy

40
Q

Which drug is used in the treatment of Haemophilia A ?

A

Desmopressin (causers increased vWF release from the endothelium. vWF is a factor VIII carrier)

41
Q

Name 1 carrier protein of Factor VIII ?

A

vWF

42
Q

Describe how you can used Ristocetin to test for vWD ?

A

Add Ristocetin to the patients vWF and platelets in a test tube. Ristocetin normally causes vWF to find to Gp1b on platelets causing platelet aggregation. If there is no platelet aggregation then this means there is a qualitative defect in vWF or Gp1b (Bernard soulier syndrome).

Romesh Path Fellah (96 decks)

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