Haematology > Coagulation > Flashcards

Coagulation Flashcards

(54 cards)

Study These 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 (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

PGI2
vWF

Plasminogen activators
Thrombomodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does aspirin have an anticoagulant effect?

A

Inhibits COX enzyme which is necessary for thromboxane A2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the rate-limiting step in fibrin formation?

A

Factor Xa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which clotting factors are vitamin K dependent?

A

II, VII, IX and X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does vitamin K activate clotting factors?

A

Via gamma decarboxylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Recall 4 factors that promote fibrinolysis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the role of plasmin?

A

Breaks down fibrin in fibriolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of action of heparin?

A

Augments anti-thrombin effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of proteins C and S?

A

Inactivate Factors 5 and 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the roles of tissue factor and TFPI

A

Tissue factor activates factor Xa
TFPI neutralises tissue factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Recall 4 possible causes of ITP

A

Vancomycin
SLE

Sarcoidosis
Lymphoproliferative disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Why does DIC cause thrombocytopaenia?

A

Increased utilisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How should autoimmune ITP be treated?

A 
Steroids 
IV Ig (to compete with auto-antibody)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the expected APTT and PT results in haemophilia

A

APTT prolonged
Normal PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the inheritance pattern of von willebrand disease?

A

Autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

vWD

**what are some key differentials??**

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
A

Activation of both coagulation and fibrinolysis causing both thrombosis and bleeding

25
What is the antidote to heparin?
Protamine sulphate
26
Examples of disorders of primary haemostasis
1. Qualitative: vWD, 2. Quantitative: ITP, HIT
27
Examples of disorders of secondary haemostasis
1. Inherited: haemophilia A/B, 2. Acquired: Liver disease, vitamin K deficiency
28
what are the 3 stages of primary haemostasis?
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
what are the 3 stages of secondary haemostasis?
1. initiation- initial thrombin production 2. propagation - positive feedback loop from thrombin 3. clot stabilisation - fibrinogen to fibrin
30
describe the initiation phase of secondary haemostasis
- 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
describe the propagation phase of secondary haemostasis
thrombin acts via positive feedback. feeds into: 1. 8--\>8a 2. 5--\>5a
32
Describe the clot stabilisation phase of secondary haemostasis
thrombin causes conversion of fibrinogen to fibrin
33
Haemophilia A
34
Haemophlia B
35
Vitamin K deficiency
**- 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
ITP
37
Factor 5 leiden
38
Antithrombin defieincy
39
Protein C/S deficiency
40
What are the common anticoagulant drugs and how can we categorise them?
1. Immediate acting a) Heparin - unfractionated and LMWH b) DOACs 2. Long acting Warfarin
41
Heparins: MOA, side effects, types and differences
_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
DOACs
1. Anti 2a (anti-thrombin): dabigatran 2. Anti 10a: rivaroxaban, apixiban, edoxaban (have x in the name) DON'T NEED TO MONITOR!!
43
Warfarin
- 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
What INR do we aim for with Warfarin?
2-3
45
Principles of warfarin reversal
higher INR- less clotting, more bleeding
46
Compare the different types of anticoagulant drugs
47
What is the most common inherited thrombophilia?
factor V leiden ## Footnote **aka: hereditary acttivated protein C deficiency**
48
What is post thrombotic syndrome?
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
What is the target INR usually?
2-3
50
WHat is the target INR in someone with atrial fibrillation?
Same as normal- 2-3
51
Target INR in someone with first episode DVT or PE
2-3 (2.5)
52
Target INR for recurrent DVT?
2.5-3.5 \*slightly higher due to increased clotting tendency\*
53
Target INR for someone with prosthetic valve
2.5-3.5 - as this increases clotting tendency as well
54
best choice anticoagulant for cancer patient
DOACs not LMWH!!
Haematology
flashcards
Decks in class (16)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions