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Haematology > Haemostasis and Thrombosis > Flashcards

Haemostasis and Thrombosis Flashcards

1
Q

main mechanism in body to stop bleeding from small vessels?

A

thrombosis.

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2
Q

what is virchow’s triad for thrombosis?

A
  1. damage to vessel wall
  2. stasis or alteration of blood flow
  3. alteration of blood components
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3
Q

what does 1. damage to vessel wall involve?

A
  • atherosclerosis
  • vasculitis
  • myocardial infarction
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4
Q

what is athosclerosis?

A

rupture of a plaque exposing subendothelium, which releases of tissue factor and causes platelets clot formation.

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5
Q

what is vasculitis?

A

immune and non-immune damage to vessels causing platelet microthrombi and occlusion that can trigger inappropriate thrombus

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6
Q

what is myocardial infarction?

A

full thickness infarction of heart muscle, which releases tissue factor and promotes blood clotting that can break and cause and embolism.

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7
Q

what does 2. stasis involve?

A
  • atrial fibrillation - causes stasis in the heart which promotes blood clots
  • immobility - dvt
  • extrinsic compression - upsets (anti)coagulant balance
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8
Q

what does 3. alteration of blood components involve?

A

-alteration in blood components ca cause balance between pro and anti coagulants to shift, causing thrombus formation.

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9
Q

what happens if there is no breach in the vessel?

A

blood is maintained in a fluid state.

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10
Q

what can occur if vessel is damaged?

A
  1. vascular spasm
  2. exposure of subendothelium
  3. dissolution of clot.
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11
Q

what is vascular spasm?

A

muscle in the vessel contracts to reduce blood glow to damaged area (hence reduce blood loss)

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12
Q

what is exposure of the subendothelium do?

A

activated platelets, which aggregate forming a platelet plug.

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13
Q

what is dissolution of the clot?

A

occurs via fibrinolysis and allows healing process to occur.

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14
Q

what is cellular component?

A

platelets.

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15
Q

what is protein component?

A

coagulative proteins.

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16
Q

how id blood maintained in fluid phase?

A

endothelium contains and secretes anti-coagulant proteins such as thrombomodulin and prostacyclin to maintain circulating blood in fluid phase.

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17
Q

how do clots form?

A

once subendothelium is exposed, subendothelium contains collagen and von Willebrand factor (vWF) which enables platelets to bind (ligands for platelets surface receptors)

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18
Q

process of platelet adhesion?

A
  • collagen and vWF binds to the Ib/IX receptor creating a signalling cascade that leads to a shape change.
  • this activates the IIb/IIIa receptor which binds to fibrinogen and allows platelets to bind to each other - this process is called aggregation
  • platelets that have been activated will thens secrete pro-coagulant proteins to further stimulate blood coagulation.
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19
Q

what do blood coagulation proteins circulate as?

A

inactive proteins called zymogens.

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20
Q

when do blood coagulation proteins become active?

A

when particular chemical groups are cleaved at sites of vessel damage and protein adhesion.

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21
Q

what is the main aim of coagulation proteins?

A

to form an insoluble fibrin clot.

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22
Q

what are the phases of forming a clot?

A

initiation
amplification/propagation
clot formation.

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23
Q

what is initiation done by?

A

tissue factor (TF).

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24
Q

what is tissue factor?

A

a protein released from damaged tissue surrounding the injured vessel.

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25
Q

what is the extrinsic pathway?

A

TF enters the circulation through the breach in the endothelium and binds and activates Factor VII

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26
Q

what activates IX and X?

A

TF/VIIa complex.

27
Q

What is deficient in haemophilia A?

A

VIII

28
Q

what is deficient in haemophilia B?

A

IX

29
Q

what does Xa do?

A

converts prothrombin to thrombin

30
Q

what does conversion into thrombin require?

A

Va and calcium

31
Q

what happens in amplification?

A

activation of a small amount of thrombin created a positive feedback network. increases F10, F9, and F5 activity.
basically a lot of thrombin is produced.

32
Q

what happens in clot formation?

A

thrombin cleaves soluble fibrinogen into fibrin monomers which polymerise to form an insoluble clot

33
Q

what is the clot stabilised by?

A

XIIIa

34
Q

What happens to the scar?

A

once healing is complete, fibrinolysis will eventually dissolve the scar.

35
Q

what happens to the thrombin once it is made?

A

it must be regulated to prevent unnecessary clotting.

36
Q

how is thrombin regulated?

A

anticoagulative proteins start being produced to control fibrin formation.

37
Q

what are the anticoagulative proteins produced?

A

antithrombin (catalysed by heparin), thrombomodulin, protein C and protein S

38
Q

what is heparin?

A

a catalyst that helps in the activation of thrombin.

BLOOD THINNER.

39
Q

What does fibrin clot contain?

A

trapped red cells and platelets.

40
Q

what performs dissolution of the clot?

A

plasmin.

41
Q

what does plasmin circulate as?

A

an inactive precursor, plasminogen.

42
Q

features of pt?

A
  • reported as ratio of patient pt/control pt
  • normal is 1-1.2
  • consistent b/w labs
43
Q

what can prolonged pt mean?

A
  • F2, F7, F9, F10 deficiency
  • Warfarin (blood-thinning drug)
  • Liver disease
  • Vitamin K deficiency
44
Q

features of APTT?

A
  • reported as a time in seconds

- normal lab range 24-35seconds

45
Q

what can prolonged APTT mean?

A
  • heparin anticoagulation therapy
  • liver disease
  • vWF disease
  • F8, F9, F11, F12 deficiency
46
Q

what are thromboembolic diseases?

A

-inappropriate or adverse IV clotting.

47
Q

what is thrombosis?

A

inappropriate or adverse intravascular blood clot formation leading to occlusion of the vessel

48
Q

what is embolism?

A

sudden obstruction of an artery by a blood clot which breaks free from the initial site of thrombus formation and travels in the blood to a downstream site.

49
Q

what are congenital coagulation disorders?

A
  • von-willebrands disease

- haemophilia A

50
Q

what are acquired coagulation disorders?

A
  • liver disease
  • vitamin k deficiency
  • desseminated intravascular coagulation (DIC)
51
Q

initiation process reactions?

A
  • tissue factor binds to factor 7.
  • factor 7 will activate factor 9.
  • factor 7, and 9 along with TF will activate factor 10.
  • factor 10 along with factor 5 will generate pro thrombin to thrombin.
52
Q

what activated factor 13?

A

thrombin.

53
Q

how does thrombomodulin regulate thrombin levels?

A

thrombin will bind to thrombomodulin which will cause activation of protein c.

54
Q

what does activation of protein c do?

A

activation of protein c along with protein s will cause inhibition of factor 8 and factor 5.

55
Q

where is thrombomodulin located?

A

surface of endothelial cells.

56
Q

what is second thing protein c does?

A

inhibits TPAI which causes enhanced fibrinolysis.

57
Q

how does antithrombin regulate thrombin levels?

A

thrombin will bind to antithrombin, and heparin will help inactive the thrombin bound to antithrombin.

58
Q

what does normal ATPP refer to?

A

normal intrinsic pathways.

59
Q

normal PT?

A

normal extrinsic pathways

60
Q

what does factor 2, 7, 9, 10 synthesis need?

A

Vitamin K dependant gamma carboxylation.

61
Q

what does it mean if aptt corrects with mixing?

A

factor deficiency.

62
Q

what does it mean if aptt doesn’t correct with mixing?

A

coagulation factor inhibitor.

63
Q

what is thrombocytopenia?

A

decreased platelet count.

64
Q

what are causes of thrombocytopaenia?

A
  1. -increased peripheral platelet destruction/consumption.
    - megakaryocytes in bone marrow are making enough platelets, but they are being destroyed in circulation.
  2. platelets are trapped in splenic sinusoids
  3. decreased platelet production by megakaryocytes in bone marrow.

Haematology (5 decks)

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