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Haematology > Coagulation > Flashcards

Coagulation Flashcards

1
Q

Recall 4 endogenous anti-coagulants and where they act

A

TFPI: inhibits initiation of coagulation (factor TF-f7)

Anti-thrombin: inhibits propagation of coagulation (F2 and F10)
Protein C/Protein S: inhibits propagation of coagulation (

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2
Q

Recalll 3 procoagulant factors and 1 anticoagulant factor that are synthesised in vascular endothelium

A

PGI2
vWF

Plasminogen activators
Thrombomodulin

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3
Q

Recall the 2 possible mechanisms of platelet activation

A
  1. vWF binds to Gp1b which binds to platelets to activate them
  2. Endothelial Gp1a binds directly to the platelet to activate

i.e. one pathway requires vWF, the other one does not

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4
Q

Via which receptors to platelets adhere to each other, and what is needed for this to happen?

A

GpIIb/IIIa using fibrinogen and calcium

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5
Q

Recall one inducer and one inhibitor of platelet aggregation, and the enzyme required for the synthesis of both

A

Thromboxane A2 increases aggregation
PGI2 inhibits platelet aggregation

COX enzyme

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6
Q

Why does aspirin have an anticoagulant effect?

A

Inhibits COX enzyme which is necessary for thromboxane A2 production

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7
Q

What is the rate-limiting step in fibrin formation?

A

Factor Xa

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8
Q

Which clotting factors are vitamin K dependent?

A

II, VII, IX and X

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9
Q

How does vitamin K activate clotting factors?

A

Via gamma decarboxylation

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10
Q

Recall 4 factors that promote fibrinolysis

A

Factor IXa, Xa, TPA and urokinase
These all increase plasmin production which cleaves fibrin

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11
Q

What is the role of plasmin?

A

Breaks down fibrin in fibriolysis

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12
Q

What is the mechanism of action of heparin?

A

Augments anti-thrombin effect

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13
Q

What is the role of proteins C and S?

A

Inactivate Factors 5 and 8

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14
Q

What are the roles of tissue factor and TFPI

A

Tissue factor activates factor Xa
TFPI neutralises tissue factor

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15
Q

How can platelet and coagulation factor disorders be distinguisghed clinically?

A

Platelet problems –> immediate superficial bleeding
Coagulation factor deficiencies –> delayed, deep bleeding and haemarthroses

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16
Q

Recall 4 possible causes of ITP

A

Vancomycin
SLE

Sarcoidosis
Lymphoproliferative disease

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17
Q

Why does DIC cause thrombocytopaenia?

A

Increased utilisation

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18
Q

How does the presentation of auto-immune thrombocytopaenia differ between children and adults?

A

In children it tends to be acute whereas it is chronic in adults

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19
Q

How should autoimmune ITP be treated?

A 
Steroids 
IV Ig (to compete with auto-antibody)
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20
Q

What is the expected APTT and PT results in haemophilia

A

APTT prolonged
Normal PT

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21
Q

What is the inheritance pattern of von willebrand disease?

A

Autosomal dominant

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22
Q

vWD

**what are some key differentials??**

A

Types

  1. Type 1: quant deficiency (AD)
  2. Type 2: qual defieincy (AD)
  3. Type 3: quant and qual deficiency (AR)

Key features

  • mucocutaneous bleeding
  • low platelet count
  • prolonged bleeding time
  • prolonged APTT (as vWF stabilises factor 8)
  • normal PT

Management

  • desmopressin
  • vwF and factor 8 concentrates

**key differentials:

  • bernard soulder disease: BIG platelets
  • glanzman’s thromasthenia (normal ristocetin)
23
Q

Recall some causes of DIC

A

Sepsis
Trauma

Cancer
Obstetric complications
Vascular disorders
Reaction to a toxin

**rmb it can happen in an underlying malignancy**

24
Q

What is DIC?

A

Activation of both coagulation and fibrinolysis causing both thrombosis and bleeding

25
Q

What is the antidote to heparin?

A

Protamine sulphate

26
Q

Examples of disorders of primary haemostasis

A
  1. Qualitative: vWD,
  2. Quantitative: ITP, HIT
27
Q

Examples of disorders of secondary haemostasis

A
  1. Inherited: haemophilia A/B,
  2. Acquired: Liver disease, vitamin K deficiency
28
Q

what are the 3 stages of primary haemostasis?

A
  1. platelet aggregation
  2. platelet binding
  3. platelet activation

___

  1. vWF binds to extracellular matrix, collagen and tissue factor
  2. platelets now adhere to the ECM
  3. platelets are then activated
29
Q

what are the 3 stages of secondary haemostasis?

A
  1. initiation- initial thrombin production
  2. propagation - positive feedback loop from thrombin
  3. clot stabilisation - fibrinogen to fibrin
30
Q

describe the initiation phase of secondary haemostasis

A
  • vessel wall injury leads to tissue factor being exposed to the blood
  • tissue factor binds to factor 7a - tissue factor/factor 7a complex
  • TF/7a complex activates 8–>8a and 9–>9a
  • 10ase complex: TF/7a, 8a and 9a
  • the 10ase complex then activates 10–>10a
  • 10a binds to 5a, forming the thrombinase complex
  • thrombinase complex (10a/5a) converts prothrombin–>thrombin
31
Q

describe the propagation phase of secondary haemostasis

A

thrombin acts via positive feedback. feeds into:

  1. 8–>8a
  2. 5–>5a
32
Q

Describe the clot stabilisation phase of secondary haemostasis

A

thrombin causes conversion of fibrinogen to fibrin

33
Q

Haemophilia A

A
34
Q

Haemophlia B

A
35
Q

Vitamin K deficiency

A

- factor 7 depleted first- becaiuse this has the shortest half life (often tested in exams)

  • factor 2 depleted last
  • most common cause- warfarin therapy

*7 is lucky number..but in this case not so lucky*

36
Q

ITP

A
37
Q

Factor 5 leiden

A
38
Q

Antithrombin defieincy

A
39
Q

Protein C/S deficiency

A
40
Q

What are the common anticoagulant drugs and how can we categorise them?

A
  1. Immediate acting
    a) Heparin - unfractionated and LMWH
    b) DOACs
  2. Long acting

Warfarin

41
Q

Heparins: MOA, side effects, types and differences

A

MOA: potentiate antithrombin, immediate action.

SE: injection site reactions, long term risk of osteoporosis, variable renal dependence

Types:

  1. Unfractionated: LARGE molecule. Factor 2>Factor 10. Given IV. Monitoring needed (via APTT or anti-Xa assay)
  2. LMWH: SMALL molecule. Factor 10>factor 2. Given SC. Monitoring not needed (unless in renal failure- anti-Xa assay)
42
Q

DOACs

A
  1. Anti 2a (anti-thrombin): dabigatran
  2. Anti 10a: rivaroxaban, apixiban, edoxaban (have x in the name)

DON’T NEED TO MONITOR!!

43
Q

Warfarin

A
  • given orally
  • vitamin K antagonist. indirect effects.
  • fall in levels of factor 2, 7, 9, 10 AND protein C/S
  • need to do bridging heparin therapy as initially protein C/S are inhibited more.
  • remember the thing about warfarin induced necrosis with protein C/S deficiency

USES;

  • metallic heart valves
  • atrial fibrillation (based on trust guidelines)
44
Q

What INR do we aim for with Warfarin?

A

2-3

45
Q

Principles of warfarin reversal

A

higher INR- less clotting, more bleeding

46
Q

Compare the different types of anticoagulant drugs

A
47
Q

What is the most common inherited thrombophilia?

A

factor V leiden

aka: hereditary acttivated protein C deficiency

48
Q

What is post thrombotic syndrome?

A

A complication of DVT

It is increasingly recognised that patients may develop complications following a DVT. Venous outflow obstruction and venous insufficiency result in chronic venous hypertension. The resulting clinical syndrome is known as post-thrombotic syndrome. The following features maybe seen:

painful, heavy calves

pruritus

swelling

varicose veins

venous ulceration

49
Q

What is the target INR usually?

A

2-3

50
Q

WHat is the target INR in someone with atrial fibrillation?

A

Same as normal- 2-3

51
Q

Target INR in someone with first episode DVT or PE

A

2-3 (2.5)

52
Q

Target INR for recurrent DVT?

A

2.5-3.5

*slightly higher due to increased clotting tendency*

53
Q

Target INR for someone with prosthetic valve

A

2.5-3.5 - as this increases clotting tendency as well

54
Q

best choice anticoagulant for cancer patient

A

DOACs not LMWH!!

Haematology (16 decks)

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