Brainscape's Knowledge GenomeTM

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


See full index

Haematology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

When will blood contain coagulation factors/platelets etc. for clot formation?

A

All the time

But these things are not active until damage to BV occurs

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

What is the main job of the endothelium lining the BV walls?

A

Encourage flow

Prevent things sticking to the BV wall

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

How does the endothelium prevent things sticking to it?

A

Produces: heparans, TFPI, thrombomodulin, nitric oxide, prostacyclin

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

What occurs when you cut yourself?

A

Bleeding which stops after 2-3 mins and then forms a clot (thanks to platelets, vWF, coagulation factors), clot remains confined to area of damage (thanks to natural anticoagulants) and after 1 week clot disappears (thanks to fibrinolytic system)

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

How does damage to the BVs lead to the activation of clotting factors and platelets?

A

Signals -
Abnormal surface of damaged BV
Physiological activators of coagulation which are present at the site

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

Why do platelets adhere to the site of vessel damage?

A

As subendothelial collagen is exposed which is sticky so platelets stick and become activated

vWF has binding sites for collagen and platelets so sticks everything together too

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

What surface proteins are present on the surface of a platelet?

A 
Glycoproteins:
2b/3a - binds fibrinogen 
1b-9-5 - binds vWF 
1a/2b - binds collagen 
6 - binds collagen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What structures are present inside platelets?

A

Sources of energy
Granules containing chemicals involved in coagulation, e.g. alpha or dense granules
Granules are next to open canalicular systems that allow for their expulsion

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

What are the three steps that platelets take in haemostasis?

A

Adhere
Activate
Aggregate

and also provide a surface phospholipid layer for coagulation proteins to be activated on

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

What is involved in adhering of a platelet?

A

GP1a binds collagen
GP1b binds vWF
This holds the platelet in place where the tissue damage is

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

What is involved in activation and aggregating of the platelets?

A

Activation is via the ADP pathway (via ADP/P2Y12 receptor) –> activates platelets through cyclooxygenase pathway
Where arachidonic acid is converted into thromboxane A2 via COX enzyme
Thromboxane A2 allows the platelets to aggregate (stick together)

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

How does the platelet produce a surface for coagulation factor activation to take place on?

A

Scramblase enzyme allows phospholipids to be externalised to outside of cell

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

What is the role of vWF?

A

Big sticky protein that sticks to many things, including factor 8
Also adheres sticks clot to collagen and allows platelets to stick to each other

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

What is the primary haemostatic (platelet) plug?

A

Straight after BV damage, platelets adhere and become activated
This clot is too weak and needs reinforcement by fibrin

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

What is the definitive haemostasis?

A

Fibrin clot forms on top of platelet clot

Coagulation cascade activated to eventually cleave fibrinogen to form fibrin

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

How does the coagulation cascade work?

A

Physiological activator activates first factor, which activates the next one and so on (like dominoes)

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

If one coagulation factor is missing what happens to the clotting cascade?

A

Might not work at all/will be reduced`

I.e. will be unable to make proper fibrin clot –> bleeding diathesis

18
Q

How do anticoagulants work?

A

They remove a clotting factor and hence halt the clotting cascade

19
Q

Describe the events that occur in the clotting cascade?

A

Tissue factor is produced by damaged tissues
TF binds to factor 7 and activates it (–> 7a)
7a activates 10
10a along with 5a turns prothrombin –> thrombin
Thrombin cleaves fibrinogen –> fibrin

Thrombin activates 11, then 8 and 9 leading to even more activation of prothrombin –> thrombin leading to even more fibrin

Forms a strong clot

20
Q

What are the three main natural anticoagulant pathways?

A

TFPI - tissue factor pathway inhibitor
Protein C and S
Antithrombin

21
Q

How does TFPI work?

A

Binds to 7a and 10a and switches them off and prevents them becoming activated –> reduced thrombin –> stops clot forming

22
Q

How does protein C and S work?

A

Targets activated factor 5 and 8 –> reduced thrombin –> reduced clot

23
Q

How does antithrombin work?

A

Activates lots of proteases (mainly 10a) and directly inactivates thrombin

24
Q

What is fibrinolysis?

A

Breaking down of the clot

25
Q

How is fibrinolysis carried out?

A

Endothelial cells produce activators of plasminogen (tPA and uPA)
Plasminogen is a zymogen in the blood
tPA cleaves plasminogen –> plasmin –> breaks down

26
Q

What substances result from clot breakdown?

A

Fibrin degradation products, including D-dimer

27
Q

To ensure there is not excessive fibrinolysis, what mechanisms are in place?

A

Inhibitors of plasminogen - PA1-1 and PA1-2

Inhibitors of plasmin - alpha2-antiplasmin, alpha2-macroglobulin

28
Q

Why might someone need antithrombotic drugs?

A

Vascular disease (esp. old age, diabetes, HTN)

29
Q

What are common presentations of abnormal clotting in hospital?

A

DVT, stroke, MI, PE

30
Q

How does aspirin work?

A

Inhibits cyclooxygenase

Arachidonic acid comes from platelet wall and COX catalyses it into thromboxane A2 –> platelet aggregation but aspirin blocks COX

31
Q

How do clopidogrel, ticagrelor, and prasugrel work?

A

P2Y12 inhibitors (ADP receptor) which is important for activation of platelets

32
Q

How do abciximab/tirofiban/eptifibatide work?

A

GP2b/3a inhibitors - prevents platelet aggregation/binding to fibrin

33
Q

In which patients would you use clopidogrel etc?

A

Tends to be stented patients

34
Q

How does warfarin work?

A

Vitamin K antagonist –> reduced vitamin K dependent clotting factors (2, 4, 7, 9)

35
Q

If someone is on warfarin and are bleeding uncontrollable what can you give them?

A

Vitamin K

If really acute - IV prothrombin

36
Q

Why might you give warfarin?

A

If patient has prosthetic heart valve

37
Q

What are examples of DOACs?

A

Rivaroxaban, edoxaban, apixaban

38
Q

How do Rivaroxaban, edoxaban and apixaban work?

A

Target activated factor 10

39
Q

What are the DOACs used for?

A

Prevention of stroke/systemic embolism in AF, prevention and treatment of DVT/PE

40
Q

How do Dabaigataran/bivalirudin/argatroban work?

A

Act directly on thrombin to deactive it

Haematology (14 decks)

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