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haemostasis Flashcards

1
Q

define haemostasis

A

cessation of bleeding at vascular injury site via the formation of a thrombus

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2
Q

what are the 2 primary components of a thrombus?

A

platelet plug

fibrin clot

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3
Q

what is primary haemostasis?

A

aggregation of platelets

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4
Q

what is secondary haemostasis?

A

fibrin clot formation

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5
Q

what are platelets?

A

not cells

small bags of cytoplasm shed from megakaryocytes

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6
Q

how many platelets can a megakaryocyte produce?

A

over 1000 platelets

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7
Q

what is the normal platelet to red cell ratio?

A

1-2 per 20 red cells

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8
Q

how long do platelets survive for?

A

8.5-10 days

4 day half life

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9
Q

where are platelets destroyed?

A

spleen

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10
Q

what chemical regulates megakaryocytes and platelet production?

A

Thrombopoietin

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11
Q

where is thrombopoietin made?

A

kidneys and liver

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12
Q

what are the normal levels of platelets?

A

150-400x10^9 per litre

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13
Q

what is thrombocytopenia?

A

platelet count less than 150x10^9 per litre

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14
Q

what is thrombocytosis?

A

platelet count of more than 400 x 10^9 per litre

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15
Q

how does normally intact endothelial lining prevent platelet adhesion?

A

continuous release of nitric oxide and prostacyclin

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16
Q

when there’s damaged endothelium, what binds to the exposed collagen?

A

von Willebrand Factor

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17
Q

what type of molecule is von Willebrand factor?

A

glycoprotein

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18
Q

how can platelets bind directly to exposed collagen?

A

directly via Gp1a/Gp6

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19
Q

why do platelets need to bind to VWF? why don’t they bind to the collagen directly?

A
  • platelets adherance to the collagen is weak on its own

- VWF acts as a bridge

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20
Q

once platelets have adhered to the VWF, what receptor do they express?

A

GP2b/3a receptor

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21
Q

what do adherent platelets bind?

A

fibrinogen –> forms a meshwork

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22
Q

what chemicals do adherent platelets release?

A

adenosine diphosphate (ADP), thromboxane A2 (TXA2) and serotonin (5-HT) from granules

also release cytokines

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23
Q

what do ADP and TXA2 fo?

A

attract more platelets to site which aggregates to form platelet plug

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24
Q

what effect does 5-HT have?

A

acts on local smooth muscle to increase local vasoconstriction

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25
Q

what is the bleeding time?

A

time taken to form an effective plug and to stop initial haemorrhage

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26
Q

what is the bleeding time test?

A

make a puncture wound in a superficial area of the skin and monitor the time needed for the bleeding to stop

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27
Q

what is the normal bleeding time in adults?

A

1-9 mins

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28
Q

what is the normal bleeding time in children?

A

1-13 mins

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29
Q

what is endothelin?

A

a powerful vasoconstrictor stored in endothelium, released by damage

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30
Q

what stabilises and strengthens the platelet plug?

A

thrombin formed by the coagulation cascade

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31
Q

when does the extrinsic pathway trigger coagulation?

A

when its exposed to factor 7 and tissue damage

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32
Q

which cells express tissue factor?

A

fibroblasts

smooth muscle cells

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33
Q

explain the extrinsic pathway?

A
  • Factor 7 is exposed to Tissue Factor (7 –> 7a)
  • 7a and calcium convert 10 to 10a
  • Xa converts prothrombin to thrombin
34
Q

what is the tenase complex?

A

the enzymes and calcium which convert factor X to Xa

35
Q

what is the start of the common pathway?

A

conversion of prothrombin to thrombin by Xa

36
Q

what is the function of thrombin?

A

converts soluble fibrinogen to insoluble fibrin

37
Q

what factor does thrombin activate?

A

factor 13

38
Q

what does factor 13a do?

A

stabilises polymerised fibrin

39
Q

explain the positive feedback loop that thrombin is in?

A
  • thrombin converts factors V, VIII and XI (11) into active forms
  • XIa (11a) converts factor IX to IXa (9a)
  • 9a and 8a increase the conversion of 10 –> 10a
  • 5a increases effectiveness of 10a
40
Q

explain the intrinsic pathway

A
  • factors 12 and 7 are activated by exposure to collagen
  • 12a converts 11 to 11a
  • 11a converts 9 to 9a
  • 9a converts 10 to 10a
41
Q

when does the intrinsic pathway activate clotting?

A

when the blood is stagnant e.g. in the atria or in deep vein thrombosis

42
Q

what does prothrombin time assess?

A

assesses extrinsic and common pathway

43
Q

what does the activated partial prothrombin time?

A

assesses intrinsic and common pathways

44
Q

explain the process of finding the bleeding time?

A

Scalpel/lancet makes a shallow 1mm deep incision on the underside of the forearm. Time from incision being made till all the bleeding has stopped = bleeding time

45
Q

what is the INR derived from?

A

prothrombin time

46
Q

what is the normal range for INR?

A

0.8 - 1.2

47
Q

what is INR used for?

A

to assess the coagulability of blood in patients taking warfarin or heparin bc they’re at risk of abnormal clot formation e.g. DVT or pulmonary emboli. In these patients an INR of 2.0-3.0 is aimed for

48
Q

what does a higher INR mean?

A

the longer it takes you to clot

49
Q

what can cause a higher INR?

A

drugs like heparin or warfarin

50
Q

what is the function of factor 13a?

A

Factor XIIIa (from thrombin) increases crosslinking in the fibrin fibrils to form a mechanically stable clot

51
Q

what is haemophilia A?

A

deficiency of factor 8

52
Q

what does a deficiency in factor 8 result in?

A

reduces the effectiveness of the positive feedback loop forming thrombin

53
Q

what is haemophilia B?

A

factor IX deficiency

54
Q

what is antithrombin?

A

a small plasma protein that regulates coagulation system activity
binds and inactivates several enzymes in the coagulation cascade

55
Q

what is a-antithrombin?

A

dominant form of antithrombin found in blood plasma

56
Q

what is plasmin?

A

main enzyme responsible for the removal of clots (fibrinolysis) when the damaged tissue is healed

57
Q

how does plasmin circulate in the blood?

A

in the form of an inactive precursor plasminogen

58
Q

how does plasminogen work?

A

binds to platelet plugs as they form

gets incorportated into the final clot

59
Q

how is plasminogen held in its inactive form?

A

by alpha-2-antiplasmin

circulates in high concentration in the plasma

60
Q

what does tissue plasminogen activator do?

A

catalyses plasminogen –> plasmin

stops a clot extending too far along a blood vessel into healthy tissue

61
Q

where is TPA released from?

A

from normal endothelial cells

62
Q

when is TPA released?

A

when the injury has healed

plasminogen gets converted to plasmin so that the clot can be destroyed

63
Q

what is D-Dimer?

A

a product of fibrin breakdown – protein fragment that circulates in the blood

64
Q

why is d-dimer measured and what does the measurement of it show?

A

an important test performed in patients with suspected thrombotic disorders (e.g. DVT)

low plasma levels of d-dimer are an indication that thrombosis is not present

65
Q

what is vitamin K?

A

Group of vitamins that the body needs for full effectiveness of factors VII, IX and X

66
Q

why is vitamin K important?

A

modifies the factors VII, IX and X and allows them to bind to calcium ions
without it, blood coagulation is impaired and uncontrolled bleeding occurs

67
Q

what are the 2 forms of vitamin K?

A

K1 and K2

68
Q

where is vitamin K1 found in highest amounts?

A

K1 and K2

69
Q

what can convert K1 to K2?

A

animals and bacteria in the gut flora

70
Q

what are risk factors for vitamin K deficiency?

A

liver disease, poor diet (no green vegetables), poor absorption, antibiotics

71
Q

how is vitamin K deficiency seen in blood tests?

A

increased INR

may result in unstable clots

72
Q

what is vitamin K a risk factor for?

A

osteoporosis

73
Q

what is vitamin K a treatment for?

A
  • one of the treatments for bleeding events caused by overdose of the anticoagulant drug warfarin
  • Vitamin K is also used to treat poisoning by rat poisons (coumarin poisoning).
74
Q

what does heaprin do?

A

binds to and increases the activity of anti-thrombin

75
Q

what does activated AT inhibit?

A

thrombin

factor Xa

76
Q

how is heparin given and why?

A

Must be given parenterally (i.v. or subcutaneous) as not absorbed through gut

77
Q

why is heparin given regularly?

A

has a short half life

78
Q

how does warfarin work?

A

Warfarin interferes with the hepatic synthesis of vitamin K–dependent coagulation factors especially Factors VII, IX and X

79
Q

name a direct thrombin inhibitor

A

dabigatran

80
Q

name factor Xa inhibitors

A

rivaroxaban, apixaban and edoxaban

81
Q

how do platelets bind to VWF?

A

Gp1b receptors

c2 (37 decks)

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