4) Biochemistry of factors Flashcards

1
Q

3 biochemical categories of coag proteins based on function

A

substrate
cofactor
enzyme

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2
Q

each zymogen is first a ———– (proenzyme)

A

substrate

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3
Q

2 biochemical changes that activate a zymogen

A

proteolytic cleavage
conformational change

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4
Q

only substrate acted on which does not become an enzyme

A

fibrinogen

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5
Q

enhance function of factors they interact with

A

cofactors

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6
Q

tissue factor is cofactor for…

A

VII

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7
Q

V is cofactor for…

A

X

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8
Q

VIII is cofactor for…

A

IX

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9
Q

HMWK is cofactor for…

A

prekallikrein

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10
Q

XIIIa is not a serine protease but rather a…

A

transglutaminase

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11
Q

why does ↓ XII lead to clotting?

A

↓ kallikrein, ↓ double chain u-PA
↓ fibrinolysis

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12
Q

PIVKAs

A

(dysfunctional) proteins induced by vitamin K absence

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13
Q

3 groups of factors based on physical properties

A

contact factors
prothrombin proteins
fibrinogen factors

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14
Q
  • activation of intrinsic system in vitro
  • activated by negatively charged surfaces
  • no essential role in vivo in activating cascade
A

contact factors

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15
Q

contact factors

A
  • XII
  • XI
  • prekallikrein
  • HMWK
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16
Q
  • vitamin K dependent
  • low MW
A

prothrombin proteins

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17
Q

prothrombin proteins

A
  • II (prothrombin)
  • VII
  • IX
  • X
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18
Q

why is vitamin K needed for the prothrombin proteins?

A
  • contain glutamic acid
  • undergoes gamma-carboxylation to become gamma-carboxyglutamic acid
  • becomes Ca-binding receptor
  • without K, carboxylation is disturbed
  • no Ca binding
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19
Q

action of warfarin

A

inhibits vitamin K dependent factors

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20
Q
  • not found in serum, consumed in clotting
  • high MW
A

fibrinogen factors

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21
Q

fibrinogen factors

A
  • I (fibrinogen)
  • V
  • VIII
  • XIII
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22
Q

fibrinogen factors are acted on by ——- during coagulation

A

thrombin

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23
Q

Hageman

A

XII

24
Q

plasma thromboplastin antecedent

A

XI

25
Q

Fletcher

A

prekallikrein

26
Q

Fitzgerald

A

HMWK

27
Q

stable factor

A

VII

28
Q

Christmas

A

IX

29
Q

Stuart-Prower

A

X

30
Q

labile factor

A

V

31
Q

anti-hemophilic factor

A

VIII

32
Q

fibrin stabilizing factor

A

XIII

33
Q

2 forms of VIII found in body

A
  • VIII:vWF —inactive form carried by vWF (stabilized)
  • VIII:c —active form that breaks away when activated by thrombin
34
Q

function of vWF in secondary hemostasis

A

carrier protein for VIII

35
Q

extrinsic tenase

A

TF-Ca-VIIa

36
Q

“extrinsic”

A

TF is not normally found in blood

37
Q

“intrinsic”

A

factors are already present in blood

38
Q

intrinsic tenase

A

PF3-IXa-Ca-VIII

39
Q

2 ways to activate intrinsic pathway in vivo

A
  • by the extrinsic pathway at factor IX
  • by thrombin at factor XI
40
Q

prothrombinase

A

PL-Xa-Ca-V

41
Q

thrombin stimulates endothelials to…

A

release vWF
express TF

42
Q

3 steps of formation of insoluble fibrin clot from fibrinogen

A
  1. hydrolytic cleavage of A & B peptides
  2. spontaneous polymerization of fibrin monomers
  3. stabilization by XIIIa (D crosslinking)
43
Q

increases resistance to proteolytic digestion by plasmin

A

D crosslinking

44
Q

steps of fibrinolysis and FDPs

A
  1. small fragments cleaved, forming fragment X
  2. D cleaved, forming fragment D + fragment Y
  3. Y cleaved, forming D and E fragments
45
Q

marker for pathologic clotting, especially DVT

A

D-dimers

46
Q

D-dimer test has —— negative predictive value and ——- positive predictive value

A

good
poor

47
Q

test systems cannot detect ——–

A

XIII

48
Q

inhibitor of thrombin, Xa, IXa, XIa, and XIIa

A

antithrombin II

49
Q

heparin greatly enhances effect of —— on thrombin and Xa

A

antithrombin II

50
Q

thrombin activates protein C when…

A

in high concentration and bound to thrombomodulin

51
Q

important in inflammation, vascular permeability, and chemotaxis

A

kinin system

52
Q

pathologic condition of developing Ab to factors

A

protease inhibitors

53
Q

bridge from extrinsic to intrinsic (2)

A
  • extrinsic tenase activates IX
  • thrombin activates XI
54
Q

no enzyme activity (cofactors)
most labile

A

V
VIII

55
Q

effect of vW disease on secondary hemostasis

A

VIII deficiency