Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

2.2 Haematology > Haemostasis 2 > Flashcards

Haemostasis 2 Flashcards

1
Q

What is another name for procoagulant?

A

Thrombogenic

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

What is another name for anticoagulant?

A

Antithrombogenic

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

Which factors are referred to by their common name?

A

Factors 1 to 4
Fibrinogen
Prothrombin
Tissue factor
Calcium

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

Which factor no longer exists

A

Factor 6 -> it was named incorrectly

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

Which factors have not yet been assigned Roman numerals?
(2)

A

Prekallikrein

Kininogen

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

Which factors have more than one factor

A

Factors V and VIII are also referred to as the labile factors

This is because their coagulant activity is not durable in stored blood

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

What are the vitamin K dependent factors

A

II
VII
IX
X

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

Why are factors II, VII. IX and X referred to as vitamin K Dependent Factor?
(2)

A

During their biosynthesis in the liver, a series of post translational enzymatic reaction include a step that required vitamin K to function as a cofactor to a carboxylase enzyme

Vitamin K serves as an essential cofactor for a carboxylase that catalyses carboxylation of glutamic acid (Gla) residues on vitamin K-dependent proteins

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

What is haemophilia C?

A

Complete lack of factor XI

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

What are the symptoms of haemophilia C

A

exhibit mild haemorrhagic disorder

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

What happens if a patient has trace quantities of factor XI?

A

They can have withstand major trauma without unusual bleeding

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

What is Haemophilia A

A

Complete lack of factor 8

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

What is Haemophilia B

A

Complete lack of factor 9

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

What is the main pitfall of the the coagulation cascade theory of the intrinsic and extrinsic pathways?
(4)

A

Doesn’t explain why Haemophilia A or B results in an inability to clot blood

Loss of factor 8 or 9 are from the intrinsic pathway

Therefore clotting should form from the extrinsic pathway

This means the theory may only provide a reasonable model of in vitro coagulation test e.g. aPTT and PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Current evidence proposes what theory
(2)

A

The intrinsic pathways is not a parallel pathway to the extrinsic

Instead the intrinsic pathway augments thrombin generated primarily by the extrinsic pathway

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

What factors are involved in the extrinsic pathway
(4)

A

Tissue factor
VII
X
Calcium

17
Q

Where is tissue factor produced

A

Released by damaged endothelial cells

18
Q

What is the role of tissue factor?
(2)

A

It is a co-factor with factor VII

It helps convert X to Xa

19
Q

What factors are involved in the intrinsic pathway?
(9)

A

XII
XI
IX
VIII
X
Prekallikrein (PK)
Kininogens (HK)
Calcium
Platelet phospholipids

20
Q

How is PK converted to kallikrein

A

Activated platelets present a negatively charged surface which activates PK to kallikrein

21
Q

What does kallikrein do?

A

This protease activates Factors XII to XIIa

22
Q

What does factor XIIa do?

A

Converts XI to XIa which converts IX to IXa which converts X to Xa = cascade

This needs Ca++ as a co-factor

23
Q

What is calcium needed for?

A

It mediates the binding of the coagulation factors to the negatively-charged phospholipids surfaces expressed by platelets via the negatively charged residues on Factor Xa and Factor IXa

It is also required at other points in the coagulation cascade

24
Q

Where are negatively-charged phospholipids found

A

Found on the surface of activate platelets

25
Q

Who proposed the cell based model of coagulation

A

D. Monroe
M. Hoffman

26
Q

What is notable about the cell based model of coagulation?

A

The cascade is a biochemical model
Not a true reflection of what happens in the body

27
Q

What are the three differences between the cascade and cell based model of coagulation?
Give three characteristics of the cascade

A

Cascade
- extrinsic and intrinsic pathways work independently, meet at common end-point
- Both can generate large amount of thrombin to form clot
- Coag factors control the rate of coagulation, cells are only phospho-lipid surface

28
Q

What are the differences between the coagulation cascade and the cell based model?
(Give five characteristics of the cell based model)

A

Cell Based
- Extrinsic pathway initiates the process
- Generates small amount of the Thrombin Spark
- Followed by Intrinsic Pathway, works on platelets to produce the Thrombin Burst
- No role of factor XII
- Cells (platelets and endothelium) control the coagulation

29
Q

What are the five steps to the cell based model of coagulation?

A

Initiation (TF Cell)

Amplification (platelet)

Propagation (active platelet)

Stabilisation of clot

Inhibition of further coagulation

30
Q

How is the cell based model initiated?
(5)

A

It occurs by expression of Tissue Factor

Tissue binds factor VIIa to activate factor IX and factor X

This activation of factor IX by TF-VIIa complex serves as the bridge between classical extrinsic and intrinsic pathways.

Factor Xa then binds to factor II to form thrombin (factor IIa)

Thrombin generation through the reaction is not robust and can be effectively terminated by TF pathway inhibitor.

31
Q

How is the cell based model amplified (amplification step)?
(2)

A

Since the amount of thrombin generated is not sufficient, therefore numerous positive feedback loops are present that bind thrombin with platelets

Thrombin that is generated in the initiation phase further activates factor V and factor VIII, which serves as a cofactor in prothrombinase complex and accelerates the activation of FII by FXa by FIXa, respectively

32
Q

What is the propagation step in the cell based model?
(2)

A

The accumulated enzyme complexes (tenase complex and prothrombinase complex) on platelet surface support robust amount of thrombin generation and platelet activation

This ensures continuous generation of thrombin and subsequently fibrin to form a sufficiently large clot

33
Q

What is the stabilisation step of the cell based model?
(2)

A

Thrombin generation leads to activation of factor XIII (fibrin stabilising factor) which covalently links fibrin polymers and provides strength and stability to fibrin incorporated in platelet plug

In addition, thrombin activates thrombin activatable fibrinolysis activatable fibrinolysis inhibitor (TAF) that protects the clot from fibrinolysis

34
Q

What is anticoagulation

A

The inactivation of the pro-coagulant pathway

2.2 Haematology (38 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions