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Blood Book > Blood coagulation > Flashcards

Blood coagulation Flashcards

1
Q

What is blood coagulation?

A

Forming a tough protein ‘coagulum’ of fibrin

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2
Q

How does vasoconstriction occur?

A

Neural sympathetic input

Myogenic response

Endothelin

Platelet TXA2 + serotonin

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3
Q

What produces endothelin?

A

Damaged endothelium

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4
Q

Which usually keeps blood from coagulating?

A

NO, prostacycline, antithrombin, protein C + S

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5
Q

Which factors does antithrombin inhibit?

A

2, 9 , 10

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6
Q

Which factors does protein C inhibit?

A

5 and 8

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7
Q

What is von willebrand factor?

A

Released from endothelial cells when they are injured

Binds to other platelets

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8
Q

What platelet receptor binds vWF?

A

glycoprotein1b

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9
Q

Which is released with platelet granule release + functions (hint 3)?

A

ADP
TXA2
Serotonin

First two - activate more platelets
Last two - vasoconstrict

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10
Q

How do platelets bind together?

A

Via their GpIIb/IIIa receptors, which are branched by fibrinogen/vWF

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11
Q

What are the five steps of stopping bleeding?

A

1) vascular spasm
2) Platelet plug
3) Coagulation cascade
4) Retraction + repair
5) Fibrinolysis

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12
Q

What does heparin do do?

A

Acts to activate antithrombin, which inhibits factors 2 (thrombin), 9, 10

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13
Q

What does clopidergral do?

A

ADP receptor inhibitor

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14
Q

What does aspirin do?

A

blocks TXA2 production (both activates other platelets + vasoconstrictor)

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15
Q

What does factor 13 do?

A

Crosslinks fibrin via transamidation, creating a fibrin mesh which overlays the platelet plug

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16
Q

How does dabigatrin work?

A

Direct thrombin inhibitor (factor II)

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17
Q

What are the other names for factor 1, 2 ,3

A

1= fibrinogen/fibrin
2 = prothrombin/thrombin
3= tissue factor

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18
Q

Are the extrinsic + intrinsic pathways really seperate?

A

No.. the factors IRL interact lots like 3 helps activate 9… common pathway

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19
Q

What are the steps of clot retraction + repair?

A

1) platelet contraction via myosin + actin
2) Secretion of platelet-derived growth factor (works on smooth muscle + connective tissue)
3) VEGF - helps grow back the endothelium

20
Q

What does plasminogen do?

A

Breaks down fibrin into FDPs (back to fibrinogen, D dimer)

21
Q

Which are the VitK dependent factors

A

2, 7, 9, 10, c + s

22
Q

What does warfarin do?

A

inhibition of vitamin K epoxide reductase, blocks the synthesis of the vitK dependant factors

23
Q

T or F The main physiological process for
activating coagulation requires
activation of FXII & FXI.

A

F, just XI to get to common pathway. 12 is slow asf

24
Q

What happens to clotting tests if vit k is low?

A

Both PT and APTT prolonged

25
Q

What drug can TCT measure?

A

Dabigatrin, a direct thrombin inhibitor

26
Q

What is DIC?

A

pathological process in which tissue factor
is released into blood vessels.

–> platelets, fibrinogen will be used up,
FDPs increases. PT/APTT could increase as factors used up.

27
Q

What is the most common cause of DIC?

A

Gram negative sepsis

(E coli, Pseudomonas aeruginosa, Klebsiella)

28
Q

What is PFA-100?

A

A platelet function test, assesses aggregation. Often not needed, can use bleeding time

29
Q

What are some causes of thrombocytopenia?

A

Reduced production
Reduced survival
Haemodilutation after haemorrhage
Splenic sequestration

30
Q

How do NSAIDs work?

A

COX-1 inhibitors, this enzyme is required for TXA2

31
Q

How is aspirin different to other NSAIDs?

A

Aspirin permanently inhibits COX-1 enzyme, other NSAIDs just do so temporarily.

32
Q

What is haemophilia A?

A

Factor 7 deficiency

33
Q

What is haemophilia B?

A

Factor 9 deficiency

34
Q

What genetic inheritance pattern is vWF disease?

A

Autosomal dominant

35
Q

What are the two types of vWF disease?

A

Type I: reduced production of vwF
Type II: abnormal protein

36
Q

How do you diagnose vWF disease?

A

Normal platelet level but function is reduced

Factor 8 can also be slightly reduced due to vWF carrying VIII in blood.

37
Q

How to prepare a vWF disease patient for surgery?

A

Desmopression (temporarily increases synthesis + release of vWF), fibrinolysis inhibitor (tranexamic acid)

38
Q

How to treat vWF patient with heavy periods?

A

e.g. OCP, Mirena could stop periods

Tranexamic acid can help too

39
Q

How does tranexamic acid work?

A

Binds to plasminogen.

(compare to alteplase, which is tPA which activates plasminogen to plasmin!)

40
Q

Which chromosome is implicated in Haemophilia disorders?

A

X chromosome

41
Q

How does haemophilia lead to increased bleeding?

A

Platelet function is fine but the coagulation pathway is affected –> reduced thrombin burst –> weak fibrin mesh overlaying platelet plug

42
Q

How to treat haemophilia?

A

Can inject the actual factor that is missing.

43
Q

What is ‘acquired haemophilia’? How can it be treated?

A

Autoantibody reacts with the factor, usually factor 8, and therefore injection of the factor will not help - the body will attack it.

Needs intense immunosuppressives!

44
Q

How can we test to differentiate between Inherited Haemophilia A/B(deficiency) vs acquired haemophilia (autoantibody)

A

Inherited/deficiency - when mix with 1/2 normal plasma, the bleeding time will correct

Autoantibody - will not correct!

45
Q

What is the antidote for heparin?

A

Protamine sulphate, very positive histone protein. Binds to form a stable salt.

46
Q

Which test do we use to monitor heparin?

A

APTT (PT lower sensitivity) , remember heparin activates antithrombin which inhibits factor 2,9,10 (FACTOR 9–>APTT)

47
Q

What inheritance pattern does haemophilia follow?

A

Sex-linked (X) recessive

Blood Book (10 decks)

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