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POM 2 G: HAEMATOLOGY > 2.7 Haemostasis And Thrombosis > Flashcards

2.7 Haemostasis And Thrombosis Flashcards

1
Q

What is Haemostasis

A

Halting of blood following trauma to blood vessels

A state of equilibrium

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2
Q

Functions of Haemostasis

A

Prevention of blood loss from intact vessels
Arrest of bleeding from injured vessels

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3
Q

Balance model

A

Fibrinolytic factors, anticoagulant proteins vs. Coagulation factors, platelets

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4
Q

Why is the balance important

A

Coagulation, thrombosis, fibrinolysis

Allows stimulation of blood clotting processes following injury
Limits extent of response to prevent excessive or generalised blood clotting
Starts the process leading to the breakdown of the clot as part of the healing process

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5
Q

First stage o Haemostasis

A

Vessel constriction

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6
Q

Stage 2 of Haemostasis

A

Primary Haemostasis
Formation of unstable platelet plug

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7
Q

Stage 3 of Haemostasis

A

Secondary Haemostasis
Stabilisation of the plug with fibrin

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8
Q

4th stage of Haemostasis

A

Fibrinolysis

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9
Q

Brief vessel constriction

A

Vascular smooth muscle cells contract locally
Limits blood flow to injured vessel

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10
Q

Brief formation of unstable platelet plug

A

Platelet adhesion
Platelet aggregation

Limits blood loss and provides surface for coagulation

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11
Q

Brief stabilisation of the plug with fibrin

A

Blood coagulation
Stops blood loss

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12
Q

Brief vessel repair and dissolution of clot (fibrinolysis)

A

Cell migration/ proliferation and fibrinolysis
Restores vessel integrity

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13
Q

Why is it important to understand Haemostatic mechanisms

A

Diagnose and treat bleeding disorders
Control bleeding
Identify and treat thrombotic disorders
Monitor drugs used in treatment

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14
Q

What are platelets differentiated from

A

Megakaryocytes

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15
Q

How long do platelets circulate

A

10 days

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16
Q

Haemostatic 0latelet plug formation overview

A

Vessel constriction

Primary Haemostasis (formation of unstable platelet plug)

Secondary Haemostasis (stabilisation of plug with fibrin)

Fibrinolysis (dissolution of clot and vessel repair)

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17
Q

Platelet adhesion

A

Primary

Vwf forms a bridge for platelet to bind to via Glp1b

Or platelets bind directly to exposed collagen by Glp1a

Changes shape from discoid to rounded with spicules for platelet platelet interactions

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18
Q

What’s released following platelet adhesion

A

ADP and prostaglandins

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19
Q

Which components are used in binding sites between platelets in platelet aggregation

A

Fibrinogen and Ca2+

Glp2b/3a

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20
Q

How is the prostaglandins thromboxane a2 produced

A

From arachidonic acid in the cell membrane

Catalysed by cyclo oxygenate (cox) to cyclic endoperoxides

Thromboxane synthesise in platelets then produces TXA2

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21
Q

Arachidonic acid in endothelial cells

A

Catalysed by cox to cyclic endoperoxides

Prostacyclin synthetase then catalyses to prostacyclin PGI2 in endothelial cells

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22
Q

Prostacyclin function

A

Inhibits platelet aggregation

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23
Q

Aspirin and clopidogrel are

A

Antiplatelet drugs

Irreversibly bind to. Cox

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24
Q

Clopidogrel function

A

Irreversibly blocks ADP receptor p2y12 on platelets

Last 7-10 days due to platelet life span

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25
Q

Why can endothelial cells still produce prostacyclins even with aspirin

A

Can synthesise it’s own cox

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26
Q

Where are clotting factors produced

A

Mostly in the liver

Vwf in endothelial cells and platelets

Factor 5 in platelets

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27
Q

Which factors are reliant on vit k

A

1972 - 10, 9, 7 and 2 (prothrombin)

28
Q

Initiation stage

A

Tissue factor binds to factor 7a

Triggers activation of 9 and 10 to a

Results in generation of small amount of thrombin (2a) from prothrombin (2)

29
Q

Amplification propagation phase

A

Thrombin activates factor 11 and cofactors 5 and 8 to a and platelets to their activated form

11a amplifies factor 9 to 9a

Factors 9a and 8a cause amplification of conversion of 10 to 10a

10a causes a rapid burst in the generation of thrombin 2a which cleaves the soluble fibrinogen to insoluble fibrin clot

30
Q

What is calcium needed for in coagulation

A

Binding clotting factors to the platelet surface

31
Q

Direct coagulation inhibition

A

Antithrombin - inhibitor of thrombin and other clotting proteinases

32
Q

Indirect coagulation inhibition

A

Inhibition of thrombin generation by pathways (e.g. protein c and s antiocoagulant oathways)

33
Q

What does antithrombin bind to

A

Heparin

34
Q

What are protein c and protein s involved in

A

Thrombin generation

35
Q

What does antithrombin have its affect on

A

10a and thrombin (2a)

36
Q

What does protein c have its affect on

A

8a

37
Q

What does protein s have its affect on

A

5a

38
Q

Therapeutic anti coagulation approaches

A

Reduce procoagulant factors (vit k antagonist)

Inhibit procoagulant factors (direct oral anticoagulant)

Enhance natural anticoagulant pathways (heparins and derivatives)

39
Q

Anticoagulant drugs

A

Heparin

Warfarin

DOACs (direct oral antiocoagulant drugs)

40
Q

Heparin works by

A

Indirectly by potentiating acting of antithrombin causing inactivation of factors 10a and 2a (thrombin)

Long chains of heparin wrap around both antithrombin and thrombin

41
Q

How is heparin administered

A

Intravenously or subcutaneous injection

42
Q

What is heparin derived from

A

Mixture of glycosaminylglycan chains extracted from porcine mucosa

43
Q

What is warfarin derived from

A

Coumarin

44
Q

How does warfarin work

A

Vit k antagonist which works by interfering with protein carboxylation (factors 1972)

Competes with vit k to stop its recycling

45
Q

How is warfarin administered

A

Oral tablet

46
Q

Why does warfarin take several days to take effect

A

Because it reduces synthesis of coagulation factors rather than inhibiting existing factor molecules

47
Q

DOACs

A

Orally available drugs which directly inhibit 10a or 2a (thrombin) without antithrombin

Don’t need monitoring predictable

48
Q

Why is there usually no fibrinolytic reaction

A

Plasminogen and tPA need to be brought together

49
Q

Fibrinolysis

A

Plasminogen binds to the lysine residues of fibrin, activated by tissue plasminogen activator to plasminogen causing degradation of the clot

50
Q

Plasmin breaks down

A

Fibrin (1a)

5a and 8a

51
Q

What inhibits plasmin

A

Antiplasmin

Alpha 2 macroglobulin

52
Q

Tranexamic acid in fibrinolysis

A

Competitive inhibitor of of plasminogen to lysine residues of fibrin

Used to treat bleeding in trauma patients surgical patients and those with inherited bleeding disorders

53
Q

Haemophilia

A

Failure to generate fibrin to stabilise platelet plug

54
Q

What is a prolonged aptt without prolonged pt seen in

A

Haemophilia A (factor 8 deficiency)

Haemophilia b (facto r9 deficiency)

Factor 12 deficiency(no bleeding)

55
Q

What is a prolonged aptt seen in

A

Reduction in single or multiple clotting factors

If multiple may also be prolonged pt

56
Q

Aptt

A

Activated partial thromboplastin time
Measure Intrinsic (and common) pathways

Performed by the contact activation of factor 12 by glass silica or kaolin
Added with phospholipid to citrated plasma followed by calcium
Time taken for mixture to clot is measured

57
Q

Prothrombin time

A

Measures integrity of extrinsic (and common pathway)

Blood added to sodium citrate which doesn’t contain calcium to prevent clotting
Spun to produce platelet poor plasma
TF and phospholipid added to citrated plasma sample with calcium to start the reaction

Time taken for mixture to clot is recorded

58
Q

What does pt estimate

A

Activity of factors 7,10,5 and 2 and fibrinogen

59
Q

What is often used as a source of TF and phospholipid in pt

A

Thromboplastin

60
Q

What are results of pt expressed as in the control of vit k antagonist anticoagulant therapy

A

INR international normalises ratio

61
Q

What could loss of Haemostatic equilibrium balance result in

A

Bleeding

62
Q

What can cause bleeding in regards to the Haemostatic balance

A

Reduction in platelet number or function (primary Haemostasis)

Reduction in coagulation factors (secondary haemostasis)

Increased fibrinolysis

63
Q

Thrombocytopenia

A

Reduction in platelet number

64
Q

Thrombosis describes

A

Formation of blood clot where you don’t need it - within an intact vessel

65
Q

Virchow’s triad

A

Three contributory factors to pathological clotting (thrombosis)

Blood
Blood flow
Vessel wall

66
Q

Changes in blood constituents is important in regard to which thrombosis

A

Venous thrombosis

POM 2 G: HAEMATOLOGY (8 decks)

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