Brainscape's Knowledge GenomeTM

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


See full index

My LSS- CVS > CVS 9: Haemostasis > Flashcards

CVS 9: Haemostasis Flashcards

1
Q

What are the two functions of haemostasis?

A
  1. Prevent blood loss from intact vessels

2. Arrest bleeding from injured vessels

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

What is the first response to vessel wall injury?

A

Vessel constriction- the smaller blood vessels constrict to stop blood loss

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

What happens during the primary haemostasis phase?

A

Formation of an unstable platelet plug

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

What happens during the secondary haemostasis phase?

A

Stabilisation of the platelet plug

  • blood coagulation
  • activation of fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is coagulation?

A

The process by which blood is converted from a liquid to a solid state

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

What is Von Willebrand factor?

A

It’s a plasma proteins secreted by endothelial cells and platelets

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

What triggers haemostasis?

A
  • damage to the endothelial lining

- exposure of sub endothelial layer especially the collagen

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

What are the two ways in which the collagen is recognised?

A
  1. Von Willebrand factor binds to collagen and platelets bind to Glp1b receptor on the VWF
  2. Glp1a on platelets directly binds to the collagen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why are there two different mechanisms? And under which circumstances will each of the mechanisms be favoured?

A

Circumstances within the vessels will vary- stressors in blood are different
- Von Willebrand factor= in small blood vessels with high shear stress

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

What happens once the platelets are activated?

A

They release ADP and Prostaglandins (Thromboxane in particular)

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

What is the function of the prostaglandins?

A

To activate other platelets so the platelets aggregate- Glp2b and Glp3a become available for fibrinogen to bind to

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

What molecule is generated during the blood coagulation cascade and what is its function?

A

Thrombin

  • directly activates platelets so that they can aggregate
  • platelets have specific receptors for thrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What happens to activated platelets?

A
  1. Changes shape
  2. Changes membrane composition:
    • Phospholipids usually inside the platelet come to the outside
    • These phospholipids bind to the coagulation factors
    • Platelets present Glp2b and 3a on its surface= can react with fibrinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the life span of platelets?

A

8 days

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

Where are clotting factors, fibrinolytic factors and inhibitors synthesised?

A
  1. The liver- most of these made in the liver
  2. Endothelial cells- Von Willebrand factor is made in high concs
  3. Megakaryocytes==> Platelets - Factor V is synthesised
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two different clotting cascade pathways and what starts of each of the pathways?

A
  1. Intrinsic pathway: Factor 12 => Factor 12a

2. Extrinsic pathway: When vessel is damaged, blood comes into contact with TISSUE FACTOR and involves factor 7a

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

What do the extrinsic pathway and intrinsic pathway merge at?

A

The common pathway

18
Q

What is the main driver of coagulation?

A

Tissue factor > Factor 12

19
Q

What happens to the haemostat platelet plug once it has been stabilised?

A

It is fibrinolysed

20
Q

What is plasminogen converted to and which enzymes does this?

A

Plasminogen==> plasmin

by Tissue plasminogen Activator (tPA)

21
Q

The reaction between tPA and Plasminogen does not usually happen, how does it occur then?

A

The fibrin clot brings the tPA and plasminogen close together on its surface which triggers the cleavage reaction

22
Q

What is the role of plasmin?

A

Plasmin is a powerful proteolytic enzyme that can break down the fibrin clot

23
Q

What are the breakdown products of the fibrin clot? and when might it be measured for diagnostic therapy?

A

Fibrin Degradation Products (FDP).

Measured when we are giving thrombolytic therapy

24
Q

What is tPA used to manage in the pharmaceutical industry? Which other enzyme might be used?

A

tPA and streptokinase (a bacterial activator) used in therapeutic thrombosis for MI

25
Q

Where is tPA formed?

A

Made locally in the endothelial cells right next to where the clot forms

26
Q

What prevents blood from clotting completely when clotting is initiated?

A

Coagulation Inhibitory Mechanisms

27
Q

What are the two different Coagulation Inhibitory Mechanisms?

A

Direct Inhibition

Indirect Inhibition

28
Q

What does direct inhibition involve?

A
  • Direct inhibition of activated coagulation factors
  • inhibitor circulates in blood in high cons
  • ANTITHROMBIN (III)
  • inhibits most coagulation proteinases
29
Q

What does indirect inhibition involve?

A
  • SLOWS DOWN the amount of thrombin that is generated

- activation of protein C in the protein C Anticoagulant pathway

30
Q

What is the function of Heparin?

A
  • Immediate anticoagulation in venous thrombosis and pulmonary embolism.
  • accelerates the action of antithrombin
31
Q

How does antithrombin work?

A
  • Excess of coagulation factors
  • antithrombins inhibits them by forming a complex with these factors
  • complexes cleared from circulation
32
Q

What does an reduction in antithrombin lead to?

A

Thrombosis

33
Q

Trace amounts of thrombin activates which factors? What do these factors form once they have been activated?

A

Factor 8 and Factor 5

Become cofactors

34
Q

What are the functions of cofactors?

A
  • bind to the surface of platelets and make coagulation occur faster
  • Platelet localisation process makes the reaction occur faster
35
Q

What is the function of Protein C?

A
  • down regulates thrombin generation

- inactivates cofactors 8a and 5a

36
Q

How is Protein C activated?

A
  • Factor 5 and 8 accelerate thrombin generation
  • thrombin binds to THROMBOMODULIN on endothelial surface
  • thrombin changes shape
  • new thrombin, instead of forming a clot, activating platelets and activating factor 5/8, activates protein C==> ACTIVATED protein C and protein S
37
Q

What is Factor 5 Leiden?

A
  • Common polymorphism

- Amino acid change in F5 called F5 Leiden

38
Q

What does Factor 5 Leiden cause and how?

A
  • Factor 5 Leiden can’t be inactivated as well as the wild type
  • Protein C anticoagulant pathway can’t inactivate F5 Leiden
  • higher risk of thrombosis
39
Q

Name four coagulation inhibitory mechanism failures that lead to an increased risk of thrombosis

A
  • Antithrombin deficiency
  • Protein C deficiency
  • Protein S deficiency
  • Factor V Leiden
40
Q

Which two things need to be balanced for haemostasis?

A

Fibrinolytic factors (anticoagulant proteins) vs Coagulation factors (platelets)

My LSS- CVS (21 decks)

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