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POM 3: Haematology > 1: Haemostasis > Flashcards

1: Haemostasis Flashcards

1
Q

2 factors necessary for maintaining circulation of blood in fluid state to blood vessels

A

Fibrinolytic anticoagulant proteins
Coagulation factors, platelets

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2
Q

Structure of platelets (3)

A

Discoid
Non-nucleated
Granule-containing

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3
Q

Where and how are platelets formed

A

Bone marrow
Fragmentation of megakaryocytic cytoplasm from myeloid stem cells

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4
Q

Haemostasis is

A

Halting of blood following trauma to blood vessels

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5
Q

2 functions of haemostasis

A

Prevention of blood loss from intact vessels
Arrest of bleeding from injured vessels

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6
Q

Balance in haemostasis is important for (3)

A

Coagulation
Prevents thrombosis
Fibrinolysis - break down of clot as part of healing process

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7
Q

Mechanism of haemostasis

A

1) Response to injury ( vessel constriction)
2) [1°] unstable platelet plug formation (platelet adhesion and aggregation)
3) [2°]stabilisation of platelet plug with fibrin (blood coagulation)
4) [fibrinolysis] dissolution of clot and vessel repair (cell proliferation + fibrinolysis)

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8
Q

Primary haemostasis is

A

Formation of unstable platelet plug
- platelet adhesion
-platelet activation
-platelet aggregation

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9
Q

Platelets are

A

Granule cont. cells
Made from myeloid stem cells
Plasma membrane contains glycoproteins

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10
Q

Lifespan of platelets

A

10 days

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11
Q

Formation of unstable platelet plug

A
  1. Platelet adhesion
  2. Platelet aggregation
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12
Q

Process of Platelet adhesion

A

Collagen exposed on endothelium of damaged vessel wall
Platelets stick to collagen directly via GP1a
Stick to VWF (Von willebrand factor) which binds to GP1b on collagen
Adhesion activates platelets

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13
Q

Process of platelet activation

A

platelets activated after adhesion

releases alpha granules and dense granules (storage)
stored granules also release ADP, VWF, fibrinogen
platelets produce thromboxane A2 from arachidonic acid (plasma membrane)
conformational change in GP2b/3a receptor

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14
Q

process of platelet aggregation

A

Thromboxane A2 and ADP have positive feedback on platelet recruitment, activation and aggregation
ADP binds to P2Y12 receptor and thromboxane A2 binds to thromboxane A2 receptor
GP2b/3a allows binding of fibrinogen and calcium
fibrinogen links platelets to form unstable platelet plug

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15
Q

Arachidonic acid produces ______ which inhibits platelet adhesion and aggregation, how?

A

Prostacyclin (PGI)
- released from endothelial cells
- vasodilator
- supresses platelet activation to avoid inappropriate aggregation

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16
Q

Why is dosage of antiplatelet drugs important

A

platelets have a lifespan of 10 days
dose lasts around 7 days until all platelets are replaced

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17
Q

2 antiplatelet drugs

A

aspirin
clopidogrel

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18
Q

How does aspirin act as an antiplatelet drug

A

Irreversibly blocks COX (enzyme)
inhibits thromboxane A2 production
so platelet activation inhibited
[PGI production also inhibited by blocking COX, but endothelial cells can produce more COX, but platelets can’t)

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19
Q

How does Clopidogrel act as an antiplatelet drug

A

Irreversibly blocks ADP receptor (P2Y12) on platelet cell membrane

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20
Q

Secondary haemostasis is

A

formation of stable fibrin clot

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21
Q

Reason for stabilisation of primary platelet plug

A

sufficient for small vessel injury
in larger vessels it falls apart
fibrin formation stabilises it

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22
Q

Process of primary platelet plug stabilisation

A

Blood coagulation generates thrombin
cleaves fibrinogen to generate fibrin clot, stabilising platelet plug at site of injury

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23
Q

Synthesis of clotting factors

A

most made in liver (12 total)
factor VIII and VWF made by endothelial cells
VWF also made in megakaryocytes and put into platelet granules

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24
Q

How do clotting factors produce fibrin

A

work in a cascade to produce fibrin

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25
Q

What is Vitamin K needed for in secondary haemostasis

A

carboxylation of factors II, VII, IX and X (2,7,9,10)

26
Q

How do clotting factors work

A

bind to exposed phospholipid surfaces of platelets -helps localise and accelerate reaction
Ca2+ important for binding of clotting factors to surfaces
convert inactive zymogen (proenzyme) into active clotting factor
factors V and VIII are co-factors

27
Q

3 Phases of Coagulation (cellular based model)

A

initiation phase
amplification phase
propagation phase

28
Q

In the initiation phase of coagulation

A

Tissue factor (TF) exposed on endothelial cell surface post injury
TF binds to 7a — activates 9— 9a and 10— 10a — activation of prothrombin (factor2)— small amount of thrombin (factor 2a)

29
Q

In the amplification phase of coagulation

A

small amount of thrombin activates cofactors 5 and 8, zymogen factor 9 and platelets

30
Q

In the propagation phase of coagulation

A

activated factor 9 (9 to 9a) with 8a form 10 to 10a - rapid burst in thrombin
thrombin cleaves soluble fibrinogen to form insoluble fibrin clot

31
Q

3 Natural anticoagulants

A

confine coagulation to site of injury only
- protein C, protein S and antithrombin

32
Q

How do protein C, S and antithrombin act as natural anticoagulants

A

-thrombin binds to thrombomodulin on endothelial cell surface
leads to activation of protein C to activated protein C (APC)
APC inactivates factors Va and VIIIa in presence of co-factor protein S
-thrombin and factor Xa inactivated by circulating inhibitor antithrombin

33
Q

3 Anticoagulant drugs

A

Heparin
Warfarin
DOACs (Direct oral anticoagulants)

34
Q

How does Heparin work as an anticoagulant drug

A

Works indirectly by potentiating action of antithrombin leading to inactivation of factors Xa and IIa (thrombin)

administered intravenously or by subcutaneous injection

35
Q

How does Warfarin work as an anticoagulant drug

A

Vit K antagonist : interfere with protein carboxylation
reduces synthesis of functional factors, 2,7,9,10 by liver

Given as an oral tablet, effects monitored by regular blood testing
several days to work

36
Q

How do DOACs work as an anticoagulant drug

A

Orally available drugs that directly inhibit either thrombin or factor Xa
Do not require monitoring

37
Q

Fibrinolysis is

A

Vessel repair and dissolution of clot

38
Q

Main fibrinolytic enzyme

A

plasmin

39
Q

How does plasmin work

A

Plasminogen (inactive zymogen form) circulates in blood
Tissue plasminogen activator (t-PA) and plasminogen bind to lysine residues on fibrin
break down fibrin into fibrin degradation products (FDPs)

40
Q

2 things inhibiting plasmin

A

Antiplasmin (circulating in blood)
alpha 2 macroglobulin

41
Q

Thrombolytic therapy is

A

artificial fibrinolysis

42
Q

Example of thrombolytic therapy

A

Recombinant t-PA generate plasmin to lyse clots, break down fibrin to FDPs
- administered intravenously to patients presenting with ischaemic stroke
- needs to be given ASAP, preferably within 1h to onset of symptoms
- can be administered to patients with pulmonary emboli

43
Q

Function of antifibrinolytic drugs

A
  • stops body breaking fibrin clot
  • keep clots = bleed less
44
Q

Effects of Tranexamic acid as an antifibrinolytic drug

A

Antifibrinolytic drug derived from lysine
binds to plasminogen and prevents it from binding to lysine on fibrin
Competitive inhibitor

  • treats: bleeding in trauma, surgical patients, patients with bleeding disorders
45
Q

Test of coagulation - common pathway

A

Factors V and X form factor II
Which converts Fibrinogen to Fibrin

46
Q

Test of coagulation - Extrinsic pathway

A

PT (prothrombin time)
VII a converts TF into factor X
then follows common pathway

47
Q

Test of coagulation - Intrinsic pathway

A

APTT
PK - XII
converted into XI
converted into VIII and IX
both converted to factor X and follow common pathway

48
Q

INR is

A

standardising method of Prothrombin time for comparison

49
Q

Prothrombin time PT measures

A

integrity of extrinsic pathway

50
Q

How to measure PT

A
  • Blood collected in bottle containing sodium citrate - chelates calcium- preventing clotting in bottle
  • sample spun to produce platelet-poor plasma
    -source of TF, calcium and phospholipid added to start reaction
  • length of time taken for mixture to clot is recorded
51
Q

Activated partial thromboplastin time (APTT) measures

A

integrity of intrinsic pathway

52
Q

Prolonged APPT and normal Pt seen in what 4 conditions

A

Haemophilia A (FVIII deficiency)
Haemophilia B (FIX deficiency)
Factor XI deficiency
Factor XII deficiency - no bleeding

53
Q

How to measure APTT

A

Contact activation of factor XII by glass or using silica or kaolin

contact activator, together with phospholipid, added to citrated plasma sample followed by calcium
time taken for mixture to clot is measured

54
Q

Prolonged PT signifies

A

reduction in FVII, X, V, prothrombin or fibrinogen activity

55
Q

3 Things that increase bleeding

A
  • Reduction in platelet number (thrombocytopenia) or function (primary haemostasis - platelet plug)
  • Reduction in coagulation factors (secondary haemostasis - fibrin clot)
  • Increased fibrinolysis
56
Q

Virchows triad

A

3 most important factors in blood clot formation:
Blood - dominant in venous thrombosis
Vessel wall - dominant in arterial thrombosis
Blood flow - complex and contributes to both

57
Q

Venous thrombosis is

A

Blood clots forming in veins

58
Q

2 main things that occur in venous thrombosis

A

Decrease in fibrinolytic factors and anticoagulant proteins
Increase in coagulation factors and platelets

59
Q

What factors cause a decrease in fibrinolysis and anticoagulant proteins in venous thrombosis

A

pregnancy - inhibition of plasminogen, activation through placental production of inhibitor PAI-2

genetics - inherited antithrombin deficiency

60
Q

what factor increases coagulation factors and platelets leading to venous thrombosis

A

levels of FVIII increase in pregnancy

FV leiden - mutation in FV gene makes it more resistant to inactivation by protein C

Myeloproliferative disorders cause incr. in platelet output by bone marrow

POM 3: Haematology (3 decks)

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