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Haemotology > Haemostasis > Flashcards

Haemostasis Flashcards

1
Q

What balance is required in haemostasis

A

Fibrinolytic factors, anticoagulant proteins Coagulation factors, platelets

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2
Q

Why is the balance in haemostasis important

A

Allows the stimulation of blood clotting processes following injury Limit the extent of the response to the area of injury to prevent excessive or generalised blood clotting Start the process of fibrinolysis

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3
Q

What does haemostasis describe

A

Halting of blood following trauma Contraction of blood vessels Formation of unstable platelet plug Formation of stable fibrin clot

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4
Q

How would you describe platelets

A

Discoid, non-nucleated, granule-containing cells Plasma membrane contains glycoproteins

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5
Q

How to platelets stick to damaged endothelium

A

Directly to collagen via the platelet GP1a receptor Indirectly via Von Willebrand Factor which binds to platelet GP1b receptor Activation causes change of disc to rounded form which spicules to encourage interaction

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6
Q

What does adhesion of platelets mean

A

Release contents of their storage granules: a-granules and dense granules by invaginating their platelet membrane Components of the contents include ADP, fibrinogen and VWF

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7
Q

What does thromboxane A2 do (platelets are stimuated to make this)

A

Platelet aggregation Vasoconstrictor From arachidonic acid Tissue injury and inflammation

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8
Q

What do ADP and thromboxane A2 do

A

Positive feedback effects resulting in further platelet recruitment activation and aggression They do this by binding onto P2Y12 and thromboxane A2 receptor

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9
Q

What does platelet activation do in terms of GP2b/3a receptor

A

Conformational change of receptor Fibrinogen binds to it which further activates the platelets Fibrinogen causes the platelet plug However suppressed by PG12 (prostacyclin) which is released from endothelial cells and is a powerful vasodilator and suppresses platelet activation

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10
Q

What are antiplatelet drugs used for

A

Prevention and treatment of cardiovascular and cerebrovascular disease

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11
Q

What does aspirin do

A

Inhibits the production of thromboxane A2 by irreversibly blocking the action of cyclo-oxygenase(COX) COX also inhibits prostacyclin However endothelial cells can synthesise more COX whereas platelets can’t Aspirin last 7 days until the platelets present have been replaced

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12
Q

How does clopidogrel work

A

It irreversibly blocks the ADP receptor (P2Y12)

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13
Q

What is the Von Willebrand factor

A

Glycoprotein Synthesised by endothelial cells and megakaryocytes Circulates the plasma as multimers of different sizes It mediates the adhesion of platelets Promotes platelet-platelet aggregation Specific carrier for factor VIII

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14
Q

Why is secondary haemostasis (coagulation) needed

A

Primary platelet plus is sufficient for small vessel injuries Fibrin formation stabilises the platelet plug

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15
Q

All but two clotting factors are synthesised in the liver

A

Factor VIII and VWF

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16
Q

What factors are dependent on Vitamin K for carboxylation of glutamix acid residues

A

Factor 2, Factor VII, UX X

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17
Q

What does the process of blood coagulation entail

A

Inactive zymogen (proenzyme) into an active clotting factor

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18
Q

Where are many clotting factors believed to work on

A

Exposed phospholipid surface surface of platelets

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19
Q

What do calcium ions play an important role in

A

Binding of activated clotting factors

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20
Q

Diagram of platelet activation

A
21
Q

What is the trigger to initiate coagulation

A

Tissue factor

(located at sites where blood is normally not exposed to)

This means that blood only encounters TF at the site of injury

22
Q

What is the initiation phase of coagulation

A

Tissue factor binds to factor VIIa which activate IX to IXa and X to Xa

Leads to the activation of prothrombin (factor 2)

Generate a small about of thrombine factor 2a

23
Q

What is the amplication phase of coagulation

A

Small amounts of thrombin activates cofactors V and VIII, the zymogen factor XI and platelets

24
Q

What is the propagation phase in coagulation

A

Factor 6 converts more factor IX to factor IXa, which in cocert with factor VIIa, amplifies the conversion of factor X to Xa and there is a rapid burst in thrombin generation which cleaves fibrinogen to form fibrin

25
Q

What are the anticoagulants

A

Thrombin binds to thrombomodulin on endothelial cells leading to acitvation of protein C to activated protein C. APC inactivates factors Va and VIIIa in prescence of of protein S

Thrombin and factor Xa are inactivated by antithrombin by binding of antithrombin do endothelial cell associated heparins

26
Q

What is heparin

A

Mixture of glycosaminylglycan chains

Potentiating the action of antithrombin leading to inactivation of Xa and factor 2a

Inactivation of thrombin requires longer chain of heparin chains which can wrap around antithrombin and thrombin

Intravenously or subcutaneous injection

27
Q

Warfarin

A

Vitamin K antagonist (interferes with protein carboxylation)

Reduces synthesis of 2, VII, IX and X by the liver

Oral tablet

Reduce synthesis so takes a few days

28
Q

What are DOACs

A

Direct oral anticoagulants

Directly inhibit thrombin or factor Xa

Do not require monitoring

29
Q

What is the activation of plasmin mediated by

A

Tissue plasminogen activator (t-PA)

30
Q

Why doesn’t t-PA activate plasminogen

A

Need to be brought together by binding to lysine residues

31
Q

What does the breakdown of fibrin lead to

A

Generation of fibrin-degradation produces

32
Q

What other products can plasmin breakdown

A

It can breakdown fibrin, fibrinogen and clotting factors Va and VIIIa

33
Q

What type of thrombolytic therapy is there

A

Recombinant t-PA work by generating plasmin to lyse clots

Administered intravenously

Time beneficial

High risk of bleeding

34
Q

What are antifibrinolytic drugs

A

Tranexamic acid is derivative of lysin that binds to plasminogen

It prevents plasminogen binding to the lysine residue of fibrin

Competitive inhibition

Used to treat bleeding in trauma and surgical patients

35
Q

Diagram of intrinsic and extrinsic pathway

A

Intrinsic is in the plasma and factor XII, XI, IX, X and co-factors VIII and V

Extrinsic is TF and factor VII, X and co-factor V

36
Q

What does the prothrombin time do

A

Measures the integrity of the extrinsic pathway

37
Q

How is PT measured

A

Blood collected into bottle containign sodium citrate (stops calcium from clotting)

Spun to produce platelet poor plasma

TF and phosphilipid is added together with calcium to start the reaction

Length of time for mixture to clot is recorded

Normally recombinant thromboplastin is used as the source of both TF and phospholipid

When PT is used to mointor bitamin K antagonist results are express as the international normalised ratio to correct different laboratories results

38
Q

How does APTT work

A

Contact activation of factor XII such as silica or kaolin

Phospholipid also added to citrated plasma sample followed by calcium

Time to clot measured

Prolongation of APTT shows there is a reduction in clotting factors

39
Q

An isolated prolonged APTT seend in haemophilia A (VIII) haemophilia B (IX) and factor XI deficiency might not be because of the intrinsic pathway why?

A

Can be caused by factor XII deficiency which is not important for clotting in vivo

40
Q

What might result in bleeding

A

Reduction in the platelet number of function (primary haemostasis - platelet plug)

Reduction in coagulation factors (secondary haemostasis - fibrin clot)

Increased fibrinolysis

41
Q

Why we bleed (reduction in platelet number - thrombocytopenia)

A

Failure of platelet produciong - drugs, viruses, bone marrow infiltration, egaloblastic anaemia, hereditary thrombocytopenia

Shortned platelet survival - immune thrombocytopenia, disseminated intravascular coagulation

Increased splenic pooling

42
Q

Reduction in platelet function

A

Antiplatelet drugs

Inherited causes

43
Q

Reduction in coagulation factors (congenital)

A

Von Willebran Disease (VWD) disorder

Haemophilia A - (Factor VIII deficiency, X linked)

Haemophilia B (Factor IX deficiency, X linked)

1 % of patients have deficiencies in one of the other clotting factors

Replacing clotting factor main treatment

44
Q

What are acquired causes of reduced coagulation factors

A

Liver disease

Anticoagulant drugs

45
Q

Disseminated intravascular coagulation (DIC)

A

Uncontrolled activation of coagulation followed by activation of the fibrinolytic system

Results in the expression of TF within the circulation and leads to generation and dissemination of large amounts of thrombin, activation and consumption of platelets (thrombocytopenia) and formation of thrombin in small blood vessels (microcirculation)

Clotting factors and fibrinogen become deleped

High levels of fibrin degradation products

Thrombi may cause shearing of circulating red blood cells

46
Q

Causes of DIC

A

Bacterial sepsis

Advanced cancer

Obstetric emergencies

47
Q

Inreased fibrinolysis

A

Administration of thrombolytic therapy

48
Q

Contributing factors to thrombosis

A

Blood: dominant in venous thrombosis

Vessel wall: dominant in arterial thrombosis

Blood flow: complex, contributes to both arterial and venous thrombosis

49
Q

Changes in blood that increase the risk of venous thrombosis

A

Reduced levels of anticoagulant proteins (usually genetic e.g. inherited thromobophilia)

Reduced fibrinolytic activity (pregnancy inhibition of plasminogen activation)

Increased levels of clotting factors or platelets (factor VIII increase during pregnancy, factor V leiden makes factor V more resistant to inactivation by protein C)

Platelets increase in myeloproliferative disorders, bone marrow output is increased

Haemotology (9 decks)

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