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Hematology > secondary hemostasis > Flashcards

secondary hemostasis Flashcards

1
Q

secondary hemostasis events

A

Coagulation cascade
Fibrin clot formation
Healing
Fibrinolysis

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2
Q

TF

A

tissue factor

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3
Q

PL

A

Platelet membrane phospholipid

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4
Q

XIII

A

fibrin stabilizing factor, transglutaminase

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5
Q

VII

A

stable factor, serine protease

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6
Q

IX

A

Christmas factor, serine protease

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7
Q

XI

A

plasma thromboplastin

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8
Q

XII

A

hangman factor, serine protease

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9
Q

factor I

A

fibrinogen

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10
Q

Factor II

A

prothrombin

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11
Q

Factor III

A

Tissue factor/ tissue thromboplastin

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12
Q

factor IV

A

ionized calcium

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13
Q

Factor V

A

labile factor (proaccelerin)

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14
Q

Factor VI

A

not assigned

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15
Q

Factor VII

A

stable factor

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16
Q

Factor VIII

A

anti hemophilic factor, factor VIII:C

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17
Q

Factor X

A

stuart power factor

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18
Q

factor XI

A

plasma thromboplastin antecedent

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19
Q

Factor XII

A

Hageman factor

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20
Q

Factor XIII

A

fibrin stabilizing factor (plasma transglutaminase)

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21
Q

HMWK or HK

A

high molecular weight kininogen (Fitzgerald factor)

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22
Q

PK

A

Prekallikerin factor

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23
Q

Extrinsic pathway activation

A

some substance has to enter the blood stream

injury to endothelium - tissue factor from damaged tissue

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24
Q

Intrinsic pathway activation

A

substances are in the blood stream

certain inactivated factors come in contact with exposed sub endothelium or collagen and are activated

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25
Q

Both extrinsic (TF) and Intrinsic (contact activation)

A

come together to the common pathway by activation of Factor X.

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26
Q

factors of extrinsic pathway

A

VII, TF (III)

First in the coagulation cascade to occur.

injury to vessel causes vessel wall to secrete Tissue Factor (III) (Tissue Thromboplastin)

Tissue Factor activates and complexes with Factor VII (stable factor)

= TF:VIIa

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27
Q

TF:VIIa

A

This serine protease complex of extrinsic pathway acts on factor X (Stuart Power Factor) starting the common pathway.

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28
Q

Extrinsic pathway measured by

A

PT

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29
Q

TF doesn’t originate in

A

the blood

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30
Q

Extrinsic pathway study strategy

3+7 =

A

10 ! Factor X = common pathway

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31
Q

Intrinsic pathway factors

A

XII
XI
IX
VIII

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32
Q

all factors of the intrinsic pathway originate from

A

the blood

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33
Q

surface contact - intrinsic pathway

A

negatively charged

Phospholipids on platelet membrane - or collagen from sub endothelium

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34
Q

Intrinsic pathway measured by

A

APTT

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35
Q

Factor VIII - Intrinsic Pathway

A

Largest protein in coag. cascade.

(anti-hemophilic factor)

activated by thrombin in the common pathway

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36
Q

Factor VIII =

A

vWF + VIII:c + antigenic portion

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37
Q

vWF -

A

von willebrand factor

carrier protein of VIII:c

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38
Q

VIII:c

A

coagulant portion of factor VIII

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39
Q

Order of factors in intrinsic pathway

think TENET

A

XII
XI
IX
VIII
X

40
Q

PF3

A

platelet thromboplastin

41
Q

XIIa –> HMWK

A

PK –> K –> K

42
Q

common pathway starts with

A

Factor X

activated from either intrinsic pathway or the extrinsic pathway

43
Q

both extrinsic and intrinsic pathway requires a “tenase” complex that includes

A

calcium, ca2+

44
Q

tense for intrinsic

A

IXa + Ca2+ PF3 + VIII:c

45
Q

tense for extrinsic

A

TF:VIIa + Ca2+

46
Q

Factors of the common pathway

A

X
V
II
I
XIII

47
Q

common pathway is measured by

A

PT, APTT, TT

48
Q

IIa (II = prothrombin)

A

thrombin

49
Q

Ia (I = fibrinogen)

A

fibrin

50
Q

Common pathway - Prothombinase complex

A

Xa + Va + PF3 + Ca2+

enzymatically converts prothrombin into thrombin

assembles on the surface of activated platelets

Activation of thrombin is slow, but once generated, it further amplifies coagulation

51
Q

Common pathway - thrombin

A

converts fibrinogen (I) into fibrin (Ia)

Activates factor XIII

Activation of cofactors V and VIII

induces platelet aggregation and secretion

52
Q

Thrombin splits

A

fibrinogen into fibrino-peptide A and B from main molecule producing fibrin monomer and fibrin peptides

fibrin monomers line up end to end and side to side to produce fibrin polymers

soluble fibrin polymers become cross linked and stable through the action of FXIIIa and Ca2+

A stable fibrin clot is formed

52
Q

Thrombin splits

A

fibrinogen into fibrino-peptide A and B from main molecule producing fibrin monomer and fibrin peptides

fibrin monomers line up end to end and side to side to produce fibrin polymers

soluble fibrin polymers become cross linked and stable through the action of FXIIIa and Ca2+

A stable fibrin clot is formed

53
Q

substrate

A

I

54
Q

cofactors

A

Proteins that accelerate enzymatic reactions

III
V
VII:c
HMWK

55
Q

serine proteases

A

II
VII
IX
X
XI
XII
PK

56
Q

transaminase

A

XIII

57
Q

Contact proteins

A

XI
XII
PK
HMWK

58
Q

prothrombin proteins

A

II
VII
IX
X

59
Q

fibrinogen groups

A

I
V
VIII
XIII

60
Q

substrate acted on to produce product

A

I - Fibrinogen –> fibrin

61
Q

enzymes

A

catalyze biochemical reactions

serine protease - cleaves peptide bond ( IIa, VIIa, Xa, XIa, XIIa, prekallikrein)

transaminases - transfers amino groups

62
Q

transaminase example

A

transfers amino groups

XIII, crosslink between fibrin monomers to form stable fibrin clot

63
Q

consumed
yes/no

A

yes = all used up
no = found in serum

64
Q

stable
yes/no

A

yes = can be found in stored plasma

no= requires fresh sample

65
Q

vitamin k dependent?

A

yes = affected by Vitamin K deficiency or Warfarin/Coumadin

no = not affected

66
Q

contact proteins - chart

A

Found in initial phase of intrinsic pathway

NOT consumed

Fairly stable - can be present in stored plasma

NOT vitamin K dependent

67
Q

Prothrombin proteins - chart

A

Found in ALL pathways

NOT consumed, except II !!!!

Stable

VITAMIN K DEPENDENT

attracted to surface of activated platelets

68
Q

Only one that is vitamin K dependent

A

Prothrombin proteins

69
Q

Fibrinogen group chart

A

Found in intrinsic and common pathway

ARE consumed - NOT present in serum

V and VIII are least stable/very labile

NOT VITAMIN K DEPENDENT

70
Q

stable groups

A

contact proteins
prothrombin proteins

71
Q

consumed groups

A

fibrinogen group
prothrombin

72
Q

complexes are assembled on

A

anionic (neg-charged) phospholipid surface

Ca2+ Required.

73
Q

Extrinsic tenase

A

Enzyme: VIIa
Cofactor: TF
Substrate: X

74
Q

Intrinsic tenase

A

Enzyme: IXa
Cofactor: VIIIa
Substrate: X

75
Q

Prothrombinase tenase

A

Enzyme: Xa
Cofactor: Va
Substrate: II

76
Q

protein C complex

A

Enzyme: IIa

Cofactor: Thrombomodulin Protein S

Substrate: Protein C

77
Q

Factor decreased reasons

A

Decreased synthesis

Synthesis of dysfunctional factor molecule

Excessive destruction of factors through acquired disorders

Inactivation of factors through circulating inhibitors

78
Q

Consequences of factor decreased

A

Coagulation will not proceed at normal rate

initiation of next subsequent reaction delayed

time required for clot to form prolonged

bleeding from the injured vessel continues for a longer time

79
Q

PT test

A

Reagent contains Thromboplastin (TF)

  • Extrinsic and common
  • Factors: VII, X, V, II, I

detects vitamin K deficiency (II,VII, X)

used to monitor Warfarin (Coumadin) - removes vitamin K

involves INR

80
Q

Normal range PT test

A

11-13 seconds

81
Q

INR

A

varies in TF conc.

  • helps compare between different laboratories

INR = PTpatient/PTcontrol ^ISI

82
Q

Normal range APTT

A

25-38 seconds

83
Q

APTT test

A

reagent contains phospholipids mimicking activated platelets; lacks tissue factor –> partial thromboplastin

Intrinsic and Common Pathway

deficiency in any of these factors will result in a prolonged test
(XII,XI,IX,VIII,X,V,II,I,PK,HMWK)

84
Q

what test is used for monitoring heparin treatment

A

APTT

85
Q

TT test

A

Reagent contains thrombin

measures conversion of fibrinogen into fibrin
- bypasses extrinsic + intrinsic pathway

86
Q

Prolonged TT test

A

Hypofibrinogenemia/Dysfibrinogenemia

Treatment w/ heparin

FDP - circulating degradation products

Pathologic circulating anticoagulants

87
Q

APTT abnormal
PT abnormal
TT normal

A

Vitamin K defect
Liver disease
Inhibitor present
Factor deficiency common pathway

88
Q

APTT abnormal
PT normal

A

Factor deficiency - intrinsic
Lupus anticoagulant
Specific factor inhibitor (ex: VIII)

89
Q

APTT normal
PT abnormal

A

Factor deficiency extrinsic pathway
Specific factor inhibitor

90
Q

APTT abnormal
PT abnormal
TT abnormal

A

Factor deficiency I
Severe liver disease
DIC
Potent inhibitor
Hypofibrinogenemia/dysfibrinogenemia

91
Q

fibrinogen normal range

A

200-400mg/dL

92
Q

High fibrinogen

A

low TT

93
Q

low fibrinogen

A

high TT

94
Q

Factor XIII screening test

A

Measures XIII presence
- only presence in pathways is crosslinkong fibrin monomers to stabilize fibrin clot
- not effectively measured in PT, APTT, TT

95
Q

Factor XIII screening test principle

A

in the absence of XIII fibrin is soluble in 5 M Urea or 1% monocholreacetic acid

dissolution of clot indicates factor deficiency

Hematology (36 decks)

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