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Biochemistry > Revision lecture B31 > Flashcards

Revision lecture B31 Flashcards

1
Q

What are the 3 major steps of Haemostasis

A

1) vascular spasm
2) formation of platelet plug
3) blood coagulation (clotting)

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2
Q

Why must Haemostasis be appropriately controlled

A

To avoid inappropriate clot formation
Clots must be eventually degraded
Clots are temporarily solution

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3
Q

What si the vascular spasm

A

Vasoconstriction
Muscle cell contracts reducing blood flow nd limit blood loss
Opposing endothelial cell surfaces are pressed together and adhere

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4
Q

What si the vascular spasm mediated by

A

Platelet derived products - serotonin and thromboxane A2

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5
Q

What does normal endothelium produce

A

Vasodilators - nitric oxide

And inhibitors of aggregation - prostaglandin

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6
Q

What are platelets also known as

A

Thrombocytes

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7
Q

Where are platelets derived form

A

Megakaryocytes in the bone marrow

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8
Q

What doe platelets contain

A

No nuclei but other organelles for energy production

Contain high concentrations of actin and myosin therefore can contract

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9
Q

What are some factors involved in platelet activation

A

ADP - released by platelets, erythrocytes and endothelial cells

Thrombin - made by enzyme cleavage of prothrombin

Collagen - in the connective tissue, exposed by vessel damage

PAF - platelet activating factor (phospholipid) form the vessel wall and other cells

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10
Q

What are the effects of platelet activation

A

Change shape form disc to sphere with extended pseudopodia which facilitate aggregation and coagulant activity

Release compounds involved in Haemostasis
Aggregate
Adhere to vessel wall
Synthesis thromboxane A2 a potent labile mediator of platelet activation and vasoconstriction

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11
Q

What si the general formation of the platelet plug

A

Platelets aggregate to form primary plug

To prevent being washed away by blood flow platelets release Chems which enhance blood coagulation, incomrp fibrin

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12
Q

What is vWF

A

Von Willebrand Factor

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13
Q

What sit he role of vWF

A

Binding platelets together

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14
Q

What are Gplb and Gpllb/llla

A

Glycoproteins and receptors

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15
Q

What si the most common defect with platelets

A

Von Willebrand disease which is a group of autosomal dieases affecting vWF

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16
Q

What are less common disorders affecting platelets

A

Affect the receptors found in the platelet membrane involved in platelet adhesion and aggregation

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17
Q

Wat are anti platelet drugs used to treat

A

Arterial thrombosis blood clot in a vessel

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18
Q

How do anti ppateelt durgs work

A

They decrease platelet aggregation and inhibit thrombus formation

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19
Q

What are some examples of anti platelet drugs

A

Aspirin (reduces thromboxane A2)
Platelet receptor antagonists (target Gpllb which binds vWF)
Platelet ADP receptor antagonist

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20
Q

What do blood coagulation factors interact to form

A

The secondary fibrin rich, Haemostatic plug in small vessels and the secondary fibrin thrombus In arteries and veins

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21
Q

What si the intrinsic pathway for blood coagulation

A

Activated by exposure of flowing blood to subendothelial collagen exposed by damaged vessel

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22
Q

What is the extrinsic pathway of blood coagulation

A

Activated by tissue damage which exposes flowing blood to a protein called tissue factor

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23
Q

What does the intrinsic and extrinsic pathways of blood coagulation lead to

A

A final common pathway resulting in conversion of fibrinogen to fibrin

24
Q

What is the clot formation

A

Fibrin clot from red by interaction of intrinsic, extrinsic and final common pathways

A clot on top of platelet plug strengthens the lug reinforces the seal

25
Q

What is fibrin

A

Insoluble, threadlike molecule
Forms a loose, mesh that trans blood cells
Generated form fibrinogen which is a large soluble plasm protein syn by the liver

26
Q

What si the key role of thrombin

A

Catalyses conversion of fibrinogen to fibrin

Activated factor 13

27
Q

Where do cross links form

A

Between adjacent fibrin strands
Strengthens and stabilises clot
Catalysed by factor 13

28
Q

What si the blood clotting cascade in intrinsic pathway

A

Initiates clotting in a damaged vessel
Activated by factor 12 comes into contact with collagen or foreign stance

Aggregated platelets secrete platelet factor (PF3) which is essential for the cascade and platelet aggregation

Activation of factor 10 a protease can digest prothrombin to thrombin

29
Q

What si the blood clotting cascade for the extrinsic pathway

A

Requires contact with tissue factors to blood

Traumatised tissue = release tissue factor which with factor 7 activates factor 10

30
Q

What si fibrinogen

A

Soluble plasma protein

6 polypeptide chains

31
Q

What does thrombin do

A

Converts fibrinogen to fibrin

Cleaves four peptide bonds in fibrinogen relapsing fibrinopeptides and fibrin monomers

32
Q

What do the fibrin monomers do

A

Spontaneously assemble into ordered fibrous arrays called fibrin whci is insoluble

33
Q

What factor causes the cross linking of fibrin

A

Factor 13

34
Q

What si thrombins dual action

A

Catalyses formation of fibrin but also initaties the deactivation of the clotting cascade

35
Q

As well as thrombin in terminating clotting what else is essential

A

Specific inhibitors

36
Q

Clotting factors are labile and short lived due to …

A

Dilution by blood flow
Removal by liver
Degradation by proteases

37
Q

What si the complete list of the roles of thrombin

A

1) converts fibrinogen to fibrin
2) activates factor 13 to stabilise the fibrin meshwork by cross linking
3) stimulates its own activation by positive feedback
4) enhances platelet aggregation

38
Q

What si vitamin k essential for

A

Synthesis of prothrombin and other clotting factors (8, 9 and 10)

39
Q

What does prothrombin have in its N terminus

A

Glutamate residues

40
Q

What is vitamin k enzymatic ally converted to, where and how

A

Conv to - gamma- carboxyglutamate in the liver

41
Q

What does the gamma carboxyglutamate do

A

Binds calcium which facial takes conversion to thrombin

42
Q

What si the role of calcium

A

Binding of calcium anchors prothrombin to the platelet mem surfaces after injury

Brings prothrombin knot proximity of clotting factors required for its activation to thrombin

Activation frees thrombin

43
Q

What are some examples of vitamin k antagonists

A

Discoumarol

Warfarin - anti coagulant sun prothrombin without gamma carboxyglutamate

44
Q

What sit he substance which prevents inappropriate clotting

A

Anti- thrombin
Heparin
Protein C
Tissue factor pathway inhibitor

45
Q

Where is anti thrombin produced

A

In the liver

46
Q

What does anti thrombin do

A

Inactivates thrombin

47
Q

Where is heparin syn and what does it do

A

Syn in mast cell

Activates anti thrombin and used as an anti coag

48
Q

Where is protein c and its cofactors syn and what do they do

A

Syn in the liver

Degrade clotting factors

49
Q

What does the tissue factor pathway inhibitor do

A

Inhibit the tissue factor VIIa complex blocking activation of factor 10

50
Q

What is fibrinolysis

A

Dissolving the clot

51
Q

What happens in fibrinolysis

A

Circulating plasminogen binds to fibrin

Factor 12 activates conversion to plasmin

Plasmin slowly degrades fibrin (phagocytes remove debris)

Tissue plasminogen activator also activates plasmin to do this

52
Q

What is plasminogen

A

A serum protein which is produced int he liver

53
Q

Excessive bleeding may result from

A

congenital or acquired disease of any of the stages of Haemostasis

54
Q

What does congenital mean

A

Present form birth

55
Q

What are some congenital reasons for excessive bleeding

A 
Disorder collagen syn - vessel wall
VWF deficiency (or receps) - platelets 
Coag factors deficiency (factors) - coagulation 
Anti plasmin deficiency - fibrinolysis
56
Q

What are some acquired disorders for excessive bleeding

A

Vit c deficiency - vessel wall
Anti platelet drugs - platelets
Vit k def - coagulation
Fibrinolytic drugs - fibrinolysis

57
Q

What is Haemostasis

A

The arrest of bleeding

Biochemistry (13 decks)

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