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CVS > CVS 10 - Haemostasis & Thrombosis > Flashcards

CVS 10 - Haemostasis & Thrombosis Flashcards

1
Q

What are the two main mechanisms involved in haemostasis?

A

Platelets and Clotting Cascade

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2
Q

What happens in primary and secondary haemostasis?

A

Primary - platelet activation and aggregation - formation of an unstable platelet plug
Secondary - stabilisation of the plug with fibrin

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3
Q

Define coagulation.

A

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

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4
Q

What cells secrete Von Willebrand Factor?

A

Endothelial cells and platelets

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5
Q

What is exposed when the endothelial layer is damaged?

A

Subendothelial layer - collagen

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6
Q

How can the subendothelial layer be recognised?

A

The Von Willebrand factors bind to the collagen and the GlpIb receptors on the platelet binds to VWF (high sheer conditions)

OR

GlpIa receptors on the platelets can bind directly to the collagen (less sheer stress)

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7
Q

When the platelets bind to collagen/VWF what do they release?

A

ADP and prostaglandins (thromboxane) which will cause the second process - platelet aggregation - release activates other platelet

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8
Q

What receptors become available on the platelets to allow fibrinogen to bind?

A

GlpIIa and GlpIIIb - receptors change conformation as a response to ADP and thromboxane

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9
Q

Describe the effect of thrombin on the formation of the primary platelet plug.

A

Thrombin stimulates the activation of platelets so that they aggregate.

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10
Q

Describe the changes in the morphology of the platelets that take place when they are activated.

A

The platelets become more spiculated and their membrane changes composition. Phospholipids that were on the inside of the membrane move to the outside, which is important because they bind to coagulation factors. The platelets express GlpIIa and GlpIIIb receptors that can bind to fibrinogen.

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11
Q

Where are clotting factors, fibrinolytic factors and inhibitors synthesised?

A

Mainly in the LIVER
Von Willebrand Factor is produced in high concentration by the endothelial cells
Factor V is produced by megakaryocytes (platelets)

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12
Q

Which factors are cofactors?

A

Factor 8 and Factor 5

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13
Q

Describe the extrinsic pathway.

A

The extrinsic pathway is activation of factor 10 to 10a by Tissue factor bound to Factor 7 and calcium. This is the normal physiological activation of the clotting cascade.

Activation of FXII to FXIIa is mainly an in vitro reaction (intrinsic pathway).

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14
Q

What are factor 1 and factor 2 more commonly called?

A

Factor 1 = Fibrinogen —> Fibrin

Factor 2 = Prothrombin —> Thrombin

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15
Q

What protein breaks down fibrin clots and what is its precursor? How is it activated?

A

Plasmin - the precursor is plasminogen.
Plasminogen is converted to plasmin by the action of Tissue Plasminogen Activator (tPA).
tPA (in tissue) doesn’t usually come into contact with plasminogen (in plasma) but when a fibrin clot forms, it assembles tPA and plasminogen on its surface so they come into contact and plasminogen is converted to plasmin.
Plasmin breaks down fibrin clot to give FDP.

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16
Q

What products can be given in therapeutic thrombolysis of myocardial infarction?

A

tPA (tissue plasminogen activator) and bacterial activator (streptokinase)
(Clot busters)

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17
Q

What are the two main coagulation inhibitory mechanisms?

A

DIRECT inhibition - eg. antithrombin

INDIRECT inhibition - Protein C inhibition pathway (target co factors 5 and 8)

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18
Q

What factors are inhibited by antithrombin?

A 
Factor 2a (=thrombin), 9a, 10a and 11a 
It is a broad scale clotting factor inhibitor
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19
Q

Describe the effect of heparin.

A

Heparin accelerates the action of antithrombin

20
Q

What are factor 8 and factor 5 activated by?

A

Trace amounts of thrombin

21
Q

Describe the protein C inhibitory pathway.

A

Thrombin, once produced is usually involved in clot formation, activating platelets and activating factor 8 and factor 5.
Thrombin can binds to thrombomodulin when more thrombin has been activated (a protein on the surface of the endothelium) which changes its specification.
It then activates Protein C and Protein S, which then inactivate Factor 8 and Factor 5. This is the second anticoagulant mechanism.
SO thrombin has 2 opposing roles.

22
Q

What are the consequences of Factor V Leiden?

A

Factor V Leiden is a common polymorphism in the population (4%). Factor V Leiden can’t be inactivated as well as wild type Factor V. If protein C can’t inactivate the factor V leiden as well, there is increased risk of thrombosis.

23
Q

State four failures of coagulation inhibitory mechanisms that cause increased risk of thrombosis.

A

Antithrombin deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden

24
Q

What constitutes the unstable platelet plug?

A

Exposed collagen - von Willebrand factor - platelets

25
Q

A disease of primary haemostasis could be due to the affectation of what components of the unstable platelet plug?

A

Collagen/vessel wall -> ageing and steroids can damage the endothelium
Von Willebrand factor -> VWF disease means that you have no VWF
Platelets -> warfarin and other drugs affect platelets. Thrombocytopenia.

26
Q

Describe the pattern of bleeding of a defect in primary haemostasis.

A

IMMEDIATE - prolonged nose bleeds, easy bruising, menorrhagia, prolonged gum bleeding

27
Q

What is a characteristic feature of thrombocytopenia?

A

Petechiae

28
Q

What is the main role of secondary haemostasis?

A

To produce fibrin from fibrinogen and stabilise the platelet plug by forming an insoluble mesh around it.

29
Q

Why is there a lag between the administration of a tissue factor trigger and the thrombin burst?

A

This is when cofactors and clotting factors are synthesised.

30
Q

State some other causes of problems with secondary haemostasis.

A

Liver disease (failure to produce clotting factors), drugs, consumption of clotting factors

31
Q

What is DIC?

A

Disseminated intravascular coagulation - widespread activation of the coagulation cascade. Associated with sepsis, major tissue damage, inflammation.
Leads to consumption of the clotting factors and platelets - that’s why it’s also called consumptive coagulopathy.
Activation of fibrinolysis depletes fibrinogen.
Consequences: organ failure due to deposition of fibrin in vessels; widesprad bleeding.

32
Q

What is haemophilia defined as?

A

Failure to generate enough fibrin to stabilise the platelet plug because of factor VIII or FIX deficiency.
Primary haemostasis remains ok, secondary no.

33
Q

Describe the pattern of bleeding of defects in secondary haemostasis.

A

DELAYED - people with defects in secondary haemostasis are generally fine with small cuts. They bleed deeper into joints and muscles. Do NOT tend to bleed excessively from small cuts (because the primary haemostasis is fine)

34
Q

What is the hallmark of haemophilia?

A

Haemarthrosis - bleeding into joints

35
Q

State some defects of clot stability.

A 
Excess fibrinolytic (tPA)
Deficient antifibrinolytic (eg. antiplasmin deficiency)
36
Q

What are the consequences of thromboembolism?

A

Thrombophlebitic syndrome

Pulmonary hypertension

37
Q

How does risk of thrombosis change with age? What is thromboembolism’s prevalence?

A

Increases

Overall 1 in 1000 - 10 000 per annum

38
Q

What are the three components of Virchow’s triad?

A

Hypercoagulability
Vessel wall injury
Stasis

39
Q

Why is pregnancy associated with an increase in the risk of thrombosis?

A

Pregnancy involved reduced mobility and reduced flow and a decrease in protein S meaning that blood becomes procoagulant

40
Q

What is the only circumstance in which thrombolytic therapy is given? Why is it not given more often?

A

STROKE

Because giving thrombolytic therapy increases the risk of bleeding.

41
Q

What happens in haemophilia?

A

Deficiency of factor 8 or factor 9. Massively slows down the production of thrombin and so there is no real thrombin burst. Not much fibrin mesh is formed and so the clot is not stabilised.

42
Q

What are the two functions of haemostasis?

A
  1. Prevention of blood loss from intact vessels

2. Arrest of bleeding from injured vessels

43
Q

Describe the overview of a haemostatic plug formation

A

Response to injury:
Vessel constriction

Then primary haemostasis:
Formation of an unstable platelet plug (platelet adhesion, platelet aggregation)

Then secondary haemostasis:
Stabilisation of the plug with fibrin (blood coagulation)

Then dissolution of clot and vessel repair (fibrinolysis)

44
Q

Describe the intrinsic pathway of blood coagulation

A

Ends up with factor Xa. Process takes place on activated platelets.
Starts with factor XII which activates XI which will activate X with the help of co factor 8 and PI (platelet membrane phospholipid)

45
Q

Describe the common pathway of blood coagulation

A

Factor X activates (with the help of co factor V and PI) prothrombin to give thrombin. Then thrombin activates Fibrinogen to Fibrin. Thrombin crosslinks fibrin by activating XII.

46
Q

What are the 2 things that need to be in equilibrium for normal haemostasis?

A

Fibrinolytic factors, anticoagulant proteins
and
coagulation factors, platelets

CVS (18 decks)

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