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R9 > Chapter 36 - Normal coagulation > Flashcards

Chapter 36 - Normal coagulation Flashcards

1
Q

Overview of hemostasis

A

FIGURE 36.1

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2
Q

Vitamin K dependent proteins

A

Factor 7, 9, 10, 2 (prothrombin) Anticoagulant protein C, S, Z except for S and Z, the rest are serine proteases

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3
Q

Procoagulant proteins overview

A

TABLE 36.1

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4
Q

Anticoagulant protein, inhibitor and receptors overview

A

TABLE 36.2

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5
Q

Action of vitamin K

A

Reduces glutamate into gamma-carboxyglutamate allows protein to interact with Ca2+

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6
Q

Cofactor proteins in hemostasis

A

1) Factor V 2) Factor VIII 3) TF (tissue factor) 4) TM (thrombomodulin)

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7
Q

Molecular change of factor V leiden

A

arg506Gln mutation Slow to inactivate factor Va Leiden = prothrombotic

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8
Q

Factor VIII activation

A

1) by thrombin cleavage at 3 sites –> heterotrimeric cofactor VIIIa (lacks vWF binding site) 2) downregulated by spontaneous dissociation or by APC

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9
Q

Tissue factor keypoints

A

1) cell bound 2) non-enzymatic cofactor with Factor VIIa that activates factor 9 and 10

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10
Q

Thrombomodulin key points

A

1) cofactor for activation of protein C 2) cell bound 3) thrombin binds TM –> thrombin activity neutralized and inactivated 4) thrombin-TM complex activates protein C

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11
Q

Action of protein C-ase

A

1) inactivate cofactor Va and Factor VIIIa 2) suppress thrombin formation 3) activate thrombin-activatable fibrinolysis inhibitor (antifibrinolytic role)

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12
Q

4 vitamin-k-dependent enzyme complexes

A

FIGURE 36.4 1) extrinsic tenase complex: factor 7a, TF 2) intrinsic tenase complex: factor 9a, 8a 3) prothrombinase complex: factor 10a, 5a 4) anticoagulant protein case complex: thrombin, TM

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13
Q

Deficiency in hemophilia C

A

Factor 11

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14
Q

Factor 11 key points

A

1) catalyzed by thrombin to form 11a 2) function in propagation phase of thrombin generation

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15
Q

Proteins necessary for activation of intrinsic pathway

A

1) factor 12 2) prekallikrein 3) HMWK (high molecular weight kininogen)

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16
Q

Intrinsic pathway

A

1) factor 12 autoactivate to factor 12a when foreign surface 2) activated kallikrein and factor 11a kallikrein positively cleave HMWK more Factor 11a negatively regulates HMWK cleavage

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17
Q

Part of the three elements of the HMWK complex in intrinsic pathway

A

HMWK prekallikrein factor 11

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18
Q

Inhibitors of clot formation

A

1) antithrombin 2) tissue factor pathway inhibitor 3) heparin cofactor 2 4) protein C inhibitor

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19
Q

Incidence of congenital AT deficiency

A

1 in 2000-5000

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20
Q

Antithrombin key points

A

1) broad-spectrum anticoagulant 2) interacts with thrombin, factor 10a, 9a, 7a-TF, 11a, 12a, kallikrein, HMWK 3) potentiated by heparin and heparan sulfates (10000x)

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21
Q

Tissue factor pathway inhibitor key points

A

1) associated with lipoprotein 90% 2) cleared by liver, short half life 3) inhibits extrinsic tenase complex (7a-TF) 4) binds 10a and some forms of 5a

22
Q

Texas bleeding disorder pathology

A

binding of TFPI and Va tightly due to factor V splice variant

23
Q

Heparin cofactor 2 key points

A

1) inhibits thrombin ONLY 2) potentiated by heparin 1000x 3) increase in pregnancy, decrease in preeclampsia

24
Q

Scott’s syndrome

A

improper presentation of platelet binding sites = pathologic hemorrhage

25
Q

Granules in platelets

A

1) alpha granules = procoagulant, adhesive, fibrinolytic, antifribrinolytic 2) lysosomes 3) dense granules

26
Q

Most potent activator of platelets

A

thrombin

27
Q

Primary proteins of clot

A

1) fibrin 2) transglutaminase factor 13a

28
Q

Interaction of clot proteins

A

1) fibrinogen bridges platelet aggregation 2) fibrin becomes insoluble 3) factor 13a stabilizes fibrin clot

29
Q

Fibrinolytic proteins, inhibitors and receptors overview

A

TABLE 36.3

30
Q

Hereditary plasminogen deficiency types

A

TYPE 1 = deficiency of plasminogen antigen and activity TYPE 2 = normal antigen level but reduced activity (dysplasminogenemia)

31
Q

Plasminogen activation primarily inhibited by

A

PAI-1 PAI -1 reduces lifetime of plasminogen activators

32
Q

Lysine analogues that block plaminogen activity

A

aminocaproic acid and tranexamic acid bind to protein lysyl residues prevent binding to plasminogen

33
Q

Role of alpha-2 antiplasmin in vivo

A

Prevent plasmin activity beyond locale of fibrin deposition plasmin activity slower with alpha 2 antiplasmin than when free in solution

34
Q

tPA binding

A

binds fibrin –> aligns binding to plasminogen

35
Q

uPA function

A

1) promote degredation of extracellular matrix 2) triggers plasminogen activation and matrix metalloproteinase

36
Q

half life of alpha 2 antiplasmin

A

2.6 days

37
Q

Thrombin-activatable fibrinolysis inhibitor (TAFI) key points

A

1) plasma procarboxypeptidase B synthesized in liver 2) circulate in blood in complex with plasminogen 3) activated by thrombin-TM complex 4) removal of lysine residues in fibrin degradation prevents plasminogen binding site and activation

38
Q

Initiation phase of coagulation

A

1) exposure of subendothelial TF binds circulating 7a 2) Factor 7a-10a complex (regulated by TFPI) 3) enough interaction to overcome TFPI 4) thrombin generation 5) activate platelets, factor 5, 8, 11 6) thrombin activates factor 13a –> fibrin formation

39
Q

Propagation phase of coagulation

A

1) factor 8a combine with 9a on platelet –> intrinsic tenase complex 2) activate 10a and not under control of TFPI 3) combines with factor 5a –> prothrombinase complex 4) AT prevents inhibition of factor 10a and 9a

40
Q

Termination phase of coagulation

A

1) thrombin bound to TM –> converts to anticoagulant enzyme = protein C-ase complex 2) cleaves factors 8a and 5a 3) TAFI activation prolongs clot lysis

41
Q

Elimination phase (fibrinolysis) of coagulation

A

1) tPA generates plasmin at fibrin surface –> fibrin homeostasis 2) uPA binds to cellular uPA receptor to generate pericellular plasmin (matrix metalloproteinase) –> tissue remodelling and cellular migration

42
Q

Prothrombin time uses

A

1) evaluate warfarin therapy 2) assess liver function 3) screen for deficiences in extrinsic and common pathway

43
Q

prothrombin time steps

A

1) infusion of Ca2+ and exogenous TF-lipid preparation to citrated plasma 2) intrinsic pathway contribution negligible because of large amounts of TF-lipid use 3) standardize by INR 4) most sensitive to factors 2, 5, 7, 10 and fibrinogen

44
Q

Activated partial thromboplastin time steps

A

1) phospholipid, Ca2+ and foreign surface to citrated plasma 2) absence of TF

45
Q

Factors evaluated in aPTT

A

1) intrinsic pathway catalyst: factor 12, prekallikrein, HMWK, factor 11, 8, 9 2) common pathway: fibrinogen, prothrombin, factor 5, 10 3) test for hemophilia A (F8), B (F9), monitor heparin therapy, detect lupus anticoagulant

46
Q

Thrombin time (TT)

A

1) detects direct inhibitors of thrombin or fibrin polymerization 2) distinguish between problem in thrombin generation or thrombin inhibition

47
Q

Thrombin generation assay

A

1) thrombin once produced, hydrolyzes specific substrate to give fluorescent signal 2) continuously recorded to give evaluation of the phases of thrombin generation

48
Q

Platelet function tests

A

1) platelet aggregometry 2) platelet function analyzer 3) flow cytometry 4) molecular biology techniques

49
Q

Platelet aggregometry uses

A

test how agonists affect platelets in the milieu of plasma/whole blood

50
Q

Activated clotting time

A

Adjusted aPTT for samples of citrated whole blood

51
Q

Thromboelastography

A

1) measure increasing velocity of blood during coagulation process producing time-based record 2) Rotational thromboelastography or thromboelastometry

R9 (200 decks)

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