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Haematology RCOA > Bleeding & Clotting > Flashcards

Bleeding & Clotting Flashcards

1
Q

What are the 3 processes that stop bleeding?

A
  • Vasoconstriction
    -Platelet plug
  • Coagulation
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2
Q

What happens in the platelet cascade?

A

Conformational change to spike shape
Granules move to surface
Release of ADP & TxA2
Signal other platelets to clot

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3
Q

What is the role of factor 10? Where is it made?

A

Cleaves prothrombin to thrombin (activates fibrin)
Liver

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4
Q

What factors are involved in the intrinsic pathway?

A

8, 9, 11, 12

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5
Q

What factors are involved in the extrinsic pathway?

A

7

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6
Q

Where’s tissue factor found?

A

Injured endothelium
TF bearing fibroblasts & monocytes

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7
Q

Describe the common pathway

A

Factor 10 activated to 10a
Causes prothrombin to become thrombin
Causes fibrinogen to become fibrin

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8
Q

What’s needed to help activate factor 10?

A

Calcium
Lipids
Factor 5

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9
Q

Which factors require vitamin K?

A

2, 7, 9, 10, protein C & S

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10
Q

What’s the role of t-PA?

A

Converts plasminogen to plasmin causing the breakdown of fibrin

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11
Q

Which part of the coag pathway does PT & APTT assess?

A

PT: Extrinsic
APTT: Intrinsic

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12
Q

What prolongs INR?

A

Vit K deficiency
Warfarin
DIC
Liver disease

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13
Q

What can prolong APTT?

A

Heparin treatment
Haemophilia
DIC
Liver disease

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14
Q

What can cause decreased production of platelets?

A
  • Aplastic anaemia
  • Marrow infiltration (myeloma, leukaemia)
  • Marrow suppression (chemo, RT)
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15
Q

What causes increased platelet destruction?

A
  • Immune thrombocytopenia (SLE, CLL, drugs, viruses)
  • Non immune (DIC, HUS)
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16
Q

What are the causes of poor functioning platelets?

A
  • Myeloproliferative disease
  • NSAID
  • Inc urea
17
Q

What are the common coagulation disorders?

A

Congenital: Haemophilia, vWD
Acquired: Therapy, Liver disease, DIC

18
Q

How is Haemophilia A passed?

A

X-linked (to males)

19
Q

Why is von Willebrand factor important?

A

Important in platelet adhesion to collagen & other platelets

20
Q

What are the causes of thrombophilia?

A

Inherited: Factor V Leiden, Protein C&S deficiency, antithrombin 3 deficiency
Acquired: Antiphospholipid syndrome, SLE, COCP, HRT, polycythaemia, malignancy, pregnancy, obesity

21
Q

Which blood groups have a higher clotting rate?

A

A
B
AB

22
Q

What are the 3 steps of the coagulation phase

A
  • INITIATION: Formation of prothrombinase
  • AMPLIFICATION: Activation of platelets by coagulation factors & thrombin
  • PROPAGATION: Massive thrombin burst converting fibrinogen to fibrin
23
Q

How does the cell based coagulation model initiation phase work?

A

1) Partial activation on platelets by TF releases vWF which attaches platelet to subendothelial collagen
2) Externalization of plasma membrane phosphatidylserines provides scaffold for coagulation complexes
3) Circulating factor 7 attaches to TF
4) Factor 7a/TF complex activates factors 9 (on plt surface) & 10 (at TF site)
5) Factor 10a activates factor 5
6) Factor Factor 10/5 complex becomes prothrombinase

24
Q

How does the cell based coagulation model amplification phase work?

A

1) Occurs on surface of plts
2) Prothrombinase converts prothrombin into thrombin
3) Thrombin activates factors 5, 8, 10, 11
4) Factors fully activate platelets

25
Q

How does the cell based coagulation model propagation phase work?

A

1) On surface of activated platelets
2) Activated plts express prothrombinase & tenase
3) Cause thrombin burst
4) Converts fibrinogen into fibrin

26
Q

What is HIT?

A
  • Immune mediated thrombocytopenia where Heparin is recognised as foreign
  • Heparin binds to platelet factor 4 stimulating IgG antibody formation
  • Predisposes to thrombosis
  • Typically plt drop 5-14days after starting Heparin
27
Q

What is an alternative anticoagulant to use in HIT?

A
  • Danaparoid
  • Factor 10a inhibitor
  • Mixture of Heparan, Dermatan, Chondroitin
28
Q

What are the side effects of Danaparoid?

A

Low plt
Exacerbation of asthma

29
Q

What is the process of platelet adhesion & aggregation?

A

-GPIIb/IIIa receptor binds to fibrinogen & leads to plt aggregation
- Thromboxane A2 & ADP activate this receptor
- TXA2 aids haemostasis through vasoC
-ADP binds to adjacent plt receptors & activates receptor

30
Q

How is TXA2 produced?

A

Arachidonic acid pathway inside the platelet

31
Q

How does Aspirin work?

A
  • Inhibits COX enzyme in plt
  • Prevents formation of TXA2 therefore reduced GPIIb/IIIa receptor activation

Haematology RCOA (2 decks)

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