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BSMS 103 > Theme 3 - Haemostasis > Flashcards

Theme 3 - Haemostasis Flashcards

1
Q

what are the three main functions of endothelial cells?

A

increase surface area, control blood vessel size, prevent clots

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2
Q

what is extravasation?

A

when cells leave the blood and enter the tissue (injury)

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3
Q

what is haemostasis?

A

a process that causes bleeding to stop by allowing clots to form

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4
Q

what is the response of endothelial cells when there is injury?

A

basement membrane is exposed and endo cells stop secreting factors that promote haemostasis and instead secrete von willebrand factor which promotes clotting

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5
Q

what does von willebrand factor do?

A

promotes clotting

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6
Q

what are the three platelet based ways to repair blood vessels?

A

1) haemostatic plug - plats adhere, activate and aggregate
2) co-agulation - mesh work of protein fibre which acts as a barrier and also traps platelets (an enzyme cascade that requires part of the platelet membrane)
3) vasoconstriction (blood moves slower) - plats secrete vasoconstrictor and pro thrombotic molecules eg 5HT, ADP and thromboxane A2

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7
Q

what is virchows triad?

A

platelet plug, co-agulation and vasoconstriction

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8
Q

which common lineage are platelets derived from?

A

common myeloid lineage (megakaryocytes)

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9
Q

how many platelets can a megakaryocyte make in its lifetime?

A

4000

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10
Q

how does plat count compare to RBC count?

A

40x less

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11
Q

what are the three steps in which plats are activated for haemostasis?

A

exocytosis of dense granules, change in shape (to irregular shape) and increased respiratory rate

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12
Q

what the endothelium is breached what signals to the rest of the body that there has been an injury?

A

the exposed collagen

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13
Q

what do platelets adhere to in injury?

A

the exposed collagens via proteins such as GPIs

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14
Q

what do plats start to exocytose when preparing to activate?

A

dense granules filled with 5HT, ADP and calcium

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15
Q

once platelets active they stick together - what molecule stimulates this?

A

ADP

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16
Q

which two drugs block ADP and therefore plat aggregation and coagulation?

A

prasugrel and popitugrel (P2Y inhibitors)

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17
Q

what facilitates aggregation of plats?

A

fibrinogen and ADP

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18
Q

what is the mechanism of action of ADP?

A
  • usually inside the cell so when its outside the cell its a signalling molecule
  • platelets detect it via a P2Y receptor
  • this leads to flow of cations across the membrane
  • cation flow leads to exocytosis of dense granules and release of thomboxane A2
  • ADP activates dense granule release which also contain ADP - positive feedback loop
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19
Q

what are the three steps to a haemostatic plug formation?

A

1) plats adhere to exposed collagen
2) plats activate then exocytose dense granules with ADP, 5HT and Calcium
3) plats aggregate due to ADP and fibrinogen

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20
Q

which clotting factors aren’t enzymes?

A

factor 5 and factor 8 (they are co-enzymes needed for enzymes to function)

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21
Q

where does tissue factor normally sit?

A

in the basement membrane of the capillary so there is usually an endothelial cell between it and the clotting enzymes in the blood

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22
Q

what causes conversion of fibrinogen to fibrin?

A

thrombin

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23
Q

what factor is fibrin cross linked with to make the cross linked clot?

A

factor XIII (13)

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24
Q

what are two anti coagulation factors used in the lab?

A

heparin and citrate

25
Q

what heart condition can lead to clot formation?

A

atrial fibrillation - atria dont contract so blood sits around and clots then clots spread to body - stroke

26
Q

what factors does serum lack?

A

fibrinogen, factor I, II V and VIII

27
Q

what is factor 1?

A

fibrin (active form of fibrinogen which is made in the liver)

28
Q

which pathway needs tissue factor as its initiator?

A

extrinsic pathway

29
Q

which two factors are needed to activate thrombin?

A

Xa and V

30
Q

what makes up intrinsic Xase?

A

factor 9a and 8a

31
Q

what do factors Xa and Va make?

A

thrombinase which causes prothrombin to thrombin

32
Q

summarise the common coagulation pathway

A

Xa and Va (thrombinase) cause prothrombin to thrombin (2a) which causes fibrinogen to fibrin (Ia)
- fibrin joins with factor XIII to make the fibrin clot

33
Q

what factors are in the thrombin group?

A

I, V and VIII

34
Q

what three things increase the factors in the prothrombin group?

A

inflammation, pregnancy and the oral contraceptive pill

35
Q

what factors are in the pro-thrombin group?

A

II, VII, IX, X

36
Q

what do the pro-thrombin factors require for synthesis and activation?

A

vitamin K for synthesis and calcium for activation

37
Q

what does vitamin K do for the pro thrombin factors?

A

post translational modification of gamma carboxylation

38
Q

what is the main role of plasmin?

A

lyses fibrin therefore destroys clots (fibrinolytic)

39
Q

what is the precursor of plasmin and where is it made?

A

plasminogen made in the liver

40
Q

what is required for plasminogen to plasmin

A

tissue plasminogen activator (TPA) which is on the surface of endothelial cells when in tact

41
Q

what is the function of protein C?

A

inhibits clot formation - by inactivating factor 5a and 8a

- also works with protein S (inhibits 5a)

42
Q

what does anti thrombin III work with?

A

heparin

43
Q

what does anti-thrombin III inhibit?

A

thrombin, factor Xa and factor IXa.

44
Q

what does anti-thrombin deficiency result in and what can be used to treat it?

A

results in lots of clots and recombinant forms can be used to treat it

45
Q

what does vitamin K deficiency result in?

A

clotting insuffiency

46
Q

what are two causes of vitamin K deficiency?

A

GI disease (lack of absorption) or liver disease (lack of bile salts)

47
Q

what drug inhibits vitamin K recycling and what can it be used for?

A

warfarin prevents recycling (not immediately) and can be used in patients that clot too much

48
Q

what is the cause of haemophilia A?

A

congenital lack of factor VIII

49
Q

how is haemophilia A characterised and how is it treated?

A
  • X linked recessive
  • bleed a lot - into joints and muscles
  • usually only males are symptomatic
  • treat with purified factor 8
50
Q

what factor is implicated in haemophilia B?

A

factor 9

51
Q

what is the main function of anti-plat drugs and when are they used

A

block clot formation in arteries (anticoagulants have limited use here)
- used in acute coronary syndromes

52
Q

name two classes of anti-platelet drugs and how they work

A
  • Aspirin - inhibits COX which blocks the formation of thromboxane A2 formation in plats
  • ADP inhibitors (prasugrel and clopidogrel) - P2Y receptor antagonist
53
Q

what is the affect of aspirin on bleeding time and co-agulation time?

A

increases bleeding time but doesn’t increase coagulation time (used for MI prophylaxis)

54
Q

what do anti-coagulants do?

A

prevent clots in veins and the low pressure pulmonary circulation therefore prevent DVT and PE

55
Q

what are three types of anticoagulants?

A

heparin, NOACS and warfarin

56
Q

how does heparin work

A

inhibit coagulation with anti-thrombin III by inhibiting factor X

57
Q

name two NOACs

A

dabigatran (inhibits thrombin) and rivoroxaban (inhibits factor X)

58
Q

what do fibrinolytic drugs do and when are they used?

A

CLOT BUSTERS - break clots apart in arteries

- used in acute coronary syndromes and acute MI

59
Q

name three fibrinolytic drugs

A

recombinant TPA (increases plasminogen to plasmin which lyses fibrin therefore breaks up clot), streptokinase and urokianasae

BSMS 103 (23 decks)

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