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HAEMATOLOGY > Haemostasis > Flashcards

Haemostasis Flashcards

(53 cards)

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1
Q

Four components of a normal haeomostatic system?

A
  1. Platelet Plug (primary)
  2. Fibrin clot formation (secondary)
  3. Fibrinolysis
  4. Anticoagulant defences
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2
Q

Platelets budd off from which bone marrow cells?

A

Megakaryocytes

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3
Q

Why is important to stop anti-platelets 7 days before an operation?

A

Stopped to reduce the risk of serious intra-op bleeding.

Stopped at least seven days before as the life span of a platelet is seven days.

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4
Q

What are the two steps to platelet plug formation following endothelial damage?

A

1) platelet adhesion

2) platelet aggregation

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5
Q

How to platelets bind to the damaged vessel wall? (adhesion)

A

Endothelial damage exposes collagen and releases BLOOD CLOTTING PROTEINS (e.g. VWF) which attach to receptors on platelets and hold them down

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6
Q

Platelets secrete certain chemicals to clump together (aggregation) what are these?

A

ADP and TXA2

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7
Q

Platelets bind via which protein?

A

Glycoprotein 2B3A

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8
Q

What are the three main causes of failure of platelet plug formation?

A 
Vascular disease (vasculitis)
Platelet problems (thrombocytopenia or imparied function)
VWF deficiency
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9
Q

Why would VWF deficiency result in failed platelet plug?

A

VWF is an important blood clotting protein released from the damaged endothelium that helps adhere platelets to vessel wall.

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10
Q

Signs of failed platelet plug?

A

Easy brusing and purpura

Bleed from mucous membranes

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11
Q

Platelet count tests which component of haemostasis?

A

Primary haemostasis

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12
Q

Three stages of fibrin clot formation?

A

Initiation

Amplification and propagation

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13
Q

Platelets are full of phospholipids which are -ve/+ve charge?

A

NEGATIVE

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14
Q

Blood clotting factors also have a negative charge, how are they attracted to platelets of the platelet plug?

A

Calcium (POSITIVE) is attracted to the platelets and the new positive layer of Ca formed over the platelets attracts blood clotting factors.

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15
Q

Which factor is released from the damaged endothelium and a) inititates platelet plug formation
B) initiates fibrin clot formation?

A

A) VWF

B) Tissue factor which combines with factor 7 to initiate coagulation.

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16
Q

How does initiation via TF/VII result in the formation of thrombin?

A

Initiation results in factor 5 and 10 being released which activates the conversion of prothrombin to thrombin.

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17
Q

Which conversion does thrombin activate?

A

Fibronogen to fibrin.

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18
Q

How is this this coagulation cascade amplified?

A

Thrombin (aswell as converting fibrinogen to fibrin) activates factor 8/9 which causes the release of factor 5 and 10.

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19
Q

What is fibrinolysis?

A

The enzymatic breakdown of fibrin in blood clots.

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20
Q

In Fribrinolysis what is the function of these enzymes?
A) tPA
B) Plasmin

A

A) tissue plasminogen activator converts plasminogen to plasmin
B) Plasmin catalyses breakdown of fibrin

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21
Q

Which medical condition is characterised by massive activation of fibrinolysis?

A

Disseminated intravascular coagulation (DIC).
Excessive haemostsis results in widespread clotting and ischaemia. Clotting factors become exhausted and fibrinolysis occurs to break them down.

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22
Q

Signs of DIC?

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A

Easy bruising, purpura and severe generalised bleeding.

23
Q

Cause of failure to form fibrin clot?

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A

Single or multiple clotting factor deficiencies.

24
Q

Bleeding into muscles or joints suggests which haemostasis has failed?

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A

Secondary - failure of fibrin clot to form.

25
Sign that both primary and secondary haemostasis is impaired?
General excessive bleeding (everywhere)
26
Which coagulation tests screen for fibrin clot formation?
PT and APTT
27
Prothrombin Time assesses functionality of which component of secondary haemostasis?
Initiation: Tests Factors 5, 7, 10 Activating tissues added to blood sample to initiate factor 7 binding to tissue factor which sets of the cascade. Time taken to form solid clot is measured.
28
APTT assess which component of secondary haemostasis?
Amplification => tests factors 8 and 9. Process: Thromboplastin added to blood sample which aids conversion of prothrombin to thrombin. Time taken to form clot is measured.
29
Why is vitamin K deficiency referred to as a multiple clotting factor deficiency?
Vitamin K activates (carboxylates) factors 2,7,9,10. | Carboxylation makes them negatively charged so they attract to positive surface of platelet plug
30
If the PT is normal, failure to form a fibrin plug is likely because of an issue with which factors?
8&9. | PT assesses initiation including TF, Factor 5,7,10 and prothrombin and thrombin.
31
Natural anitcoagulation occurs through which proteins?
Anti-thrombin and thrombin
32
How does THROMBIN function as a A) procoagulant B) an anticoagulant ?
A) Once converted from prothrombin (by f5&10) it converts fibrinogen to fibrin which incombination with platelet plug, forms a clot B) Once homeostasis is ahcieved it binds to thrombomodulin to activate protein C and S, which switches off clotting factors.
33
Protein C and S are activated by __________ and promote/block coagulation?
THROMBOMODULIN (which is activated by thrombin which has recognised homeostasis has been achieved) BLOCK
34
Numerical names for A) prothrombin and B) thrombin?
A) Factor II | B) factor IIa
35
Which Anti-coagulant potentiates antithrombin for a RAPID effect?
Heparin
36
What are the two forms of heparin and their ROA?
LMWH (-parin) - S/C | Unfractionated - IV
37
LMWH is the preferred form of heparin for anticoagulation, why is unfractionated preferred in situations where someone has blood clots but also needs an urgent operation?
In that scenario the anticoagulation effects are required but MUST be able to be stopped quickly for the surgery. The SHORT HALF-LIFE of unfractionated IV heparin infusion means that anti-coagulation effects can occur before the surgery be stopped during and resume immediately after.
38
Heparin is reversed by?
Protamine
39
Which anticoagulant works through Vit K inibition?
Warfarin
40
Why should warfarin be stopped 5 days before an operation ?
Warfarin has a half-life of 40 hours => 200 hours to be removed from the body.
41
Why shouldn't heparin be used long term (like warfarin)?
Risk of osteoporosis
42
Warfarin must be closely monitored by what and why?
By INR and PT. | Has a very NARROW THERAPEUTIC WINDOW
43
How would you alter warfarin dose after a high INR reading?
Lower dosage as high INR means reduced coaguability and increased bleeding risk. Normal INR = normal coaguability.
44
Which anti-platelet inihbits the COX enzyme?
Aspirin
45
Which NOAC works by directly inhibiting A) activated factor 10? B) thrombin?
A) Rivoroxaban | B) Dabigatran
46
ADP and TXA2 are chemicals that induce what process?
Platelet aggregation
47
Which antiplatelet targets TXA2 and how?
Aspirin. Inhibits COX enzyme => inhibits formation of TXA2 => stops platelet aggregation
48
Clopidigral inhibits the binding of which chemical platelet aggregator does to its receptor, what are the consequences?
ADP. | ADP-mediated activation of platelet glue GPIIb/IIIa cannot occur => platelet aggregation stopped.
49
NOACs are contradicted in which patients and why?
Those with poor renal function as 85% is excreted renally.
50
IV Streptokinase belongs to which class of drug?
Fibrinolytic
51
MOA and ROA of fibrinolytics?
MOA: Initiate clot lysis through activating plasminogen which converts to plasmin which breaks down fibrin. ROA: IV
52
Which drug opposes fibrinolysis and can be used to control haemorrhage?
TRanexamixc acid.
53
What are the three functions of thrombin?
1) FIBRIN FORMATION - converts fibrinogen to fibrin 2) AMPLIFICATION - activates factor 8 and 9 to re-activate factor 5 and 10 to initiate coagulation 3) ANTI-COAGUALTION - when haemostasis has been achieved it activates protein C and S to switch of clotting factors

HAEMATOLOGY (3 decks)

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