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Hematology 2 Lec > Nomenclature And Intro To Coag Cascade > Flashcards

Nomenclature And Intro To Coag Cascade Flashcards

1
Q

Complex molecule in the plasma

A

VIlI/vWF

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2
Q

: coagulation

A

VIII: C

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3
Q

: platelet adhesion

A

VIII:vWF

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4
Q

Produced as a big complex

A

VIlI/vWF

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5
Q

Platelet adhesion

A

VIlI:vWF

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6
Q

tested by BT

A

VIlI:vWF

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7
Q

acts as an adhesive to the endothelium

A

VIlI:vWF

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8
Q

can be tested by bleeding time when deficient

A

VIlI:vWF

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9
Q

prolonged bleeding time may be caused by VWF due to defect in plt adhesion

A

VIlI:vWF

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10
Q

Starts to separate when matures in the endothelium ([?] moves to the circulation; [?] remains in the endothelium)

A

FVIII

VWF

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11
Q

cofactor (FIX+Ca)

A
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12
Q

tested by PTT

A

VIII:C

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13
Q

VIII:C APTT:

A

Intrinsic

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14
Q

VIII:C PT:

A

extrinsic

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15
Q

individual factor

A

VIII:C

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16
Q

seen in the coagulation cascade

A

VIII:C

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17
Q

“C” for

A

cofactor or coagulant portion of factor VIII

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18
Q

Serves as a cofactor to Factor IX and Calcium (needed to activate FX in the common pathway)

A

VIII:C

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19
Q
  • part of “intrinsic prothrombinase”
A

VIII:C

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20
Q

Antigenic property of VIII:C

A

VIIIC:Ag

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21
Q

Tested by monoclonal antibody (antisera)

A

VIIIC:Ag

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22
Q

FVIII may have an inhibitor and attacks FVIII

A

VIIIC:Ag

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23
Q

Antigenic property of vWF

A

VIIIR:Ag

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24
Q

tested by Laurell rocket

A

VIIIR:Ag

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25
Q

low VWF FVIII Ag : low VWF = prolonged bleeding

A

VIIIR:Ag

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26
Q

Ristocetin cofactor

A

VIIIR:RCo

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27
Q

required for plt aggregation

A

VIIIR:RCo

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28
Q

tested during in vitro aggregation

A

VIIIR:RCo

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29
Q

different factors seen in the circulation

A

Coagulation Factors

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30
Q

Coagulation Factors Synthesis:

A

LIVER

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31
Q

A. Zymogens → serine proteases Factors:

A

II, VII, IX, X, XI, XII, and PK

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32
Q

A. Zymogens → serine proteases Exemption:

A

FXIII, FVIII:C

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33
Q

B. Zymogens → cofactors Factors:

A

V, VIII, TF, HMWK + Thrombospondin & Protein C and Protein S

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34
Q

C. Factor deficiency → abnormal hemostasis Factors:

A

All factors except: FXII,PK,HK

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35
Q

Labile factors Factors:

A

I, V, VIII,VII, IX, X

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36
Q

: produced from the sinusoids of endothelium/lining of blood of the liver, along w/ FVIII:VWF)

A

FVIII:C

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37
Q

: blood island-like in the endothelium, which are tissues that produced VWF (specifically) with FVIII complex

A

Weibel Palade bodies

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38
Q

: transaminase from monocyte, macrophage, reticuloendothelial cell (eliminates foreign bodies)

A

FXIII

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39
Q

: cofactor for plt function

A

Thrombospondin

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40
Q

helps fibrinolytic factors and act as cofactors for plasmin in fibrinolysis

A

Protein C and Protein S

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41
Q

can control activation of factor V, II, IX

A

Protein C and Protein S

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42
Q

inhibits coag factors to enhance fibrinolysis

A

Protein C and Protein S

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43
Q

cofactors for fibrinolysis

A

Protein C and Protein S

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44
Q

in vivo

A

FXII,PK,HK

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45
Q

can still activate FX

A

FVII (extrinsic factor)

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46
Q

Ex. deficiency in [?] will not cause prolonged APTT

A

Contact factor (XII)

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47
Q

Disappears in the body in the presence of other substances

A

I, V, VIII,VII, IX, X

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48
Q

Ex. [?] disappears in the presence of couamarin/heparin (can only use FXII)

A

FVII

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49
Q

Ex. [?] are labile factors outside the body and disappears upon exposure to low temperature

A

FV, FVIII, FIX, FI, FX

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50
Q

Other cells that produces coagulation factors aside from the liver:

A

Monocyte, Macrophage, Reticuloendothelial cell + Megakaryocyte + Tissue factor (FIII)

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51
Q

cells that participate in coagulation except for plt

A

Monocyte, Macrophage, Reticuloendothelial cell + Megakaryocyte

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52
Q

produces FXIII

A

Monocyte, Macrophage, Reticuloendothelial cell + Megakaryocyte

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53
Q

slightly procoagulant: induces coagulation (during bleeding, they increase in number and participate in clotting)

A

Monocyte, Macrophage, Reticuloendothelial cell + Megakaryocyte

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54
Q
  • originates from the bm
A

megakaryocyte

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55
Q
  • does not exist for long due to short lifespan
A

megakaryocyte

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56
Q
  • will release some cag factors if not shedded into platelet
A

megakaryocyte

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57
Q

Activates FVII to become FVIIa

A

Tissue factor (FIII)

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58
Q

originated from fibroblasts and smooth muscles

A

Tissue factor (FIII)

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59
Q

13 coagulation factors are divided to

A

three groups

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60
Q

FIBRINOGEN Heat labile: [?] (disappears when heated above 37C)

A

I,V,VIII

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61
Q

FIBRINOGEN Storage labile:

A

V,VIII

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62
Q

PROTHROMBIN
Heat labile: [?] (disappears when heated above 37C) (Except [?] – consumed)

A

VII,IX,X

FII

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63
Q

PROTHROMBIN Storage:

A

well preserved (most stable)

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64
Q

CONTACT Storage:

A

fairly stable

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65
Q

Vit K Dependent

A

PROTHROMBIN

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66
Q

Not Vit K Dependent

A

FIBRINOGEN
CONTACT

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67
Q

Adsorbed by Ba04 and Al(OH)3

A

PROTHROMBIN

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68
Q

Adsorbed by Ba04 and Al(OH)3

A

FIBRINOGEN
CONTACT

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69
Q

Consumed in coagulation

A

FIBRINOGEN

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70
Q

Not Consumed in coagulation

A

Prothrombin (Except FII)

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71
Q

Partially Consumed in coagulation

A

CONTACT

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72
Q

Site FIBRINOGEN

A

Plasma

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73
Q

Site PROTHROMBIN

A

Plasma/Serum (Except FII)

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74
Q

Site CONTACT

A

Plasma/Serum

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75
Q

Destroyed by Plasmin/High thrombin level

A

FIBRINOGEN

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76
Q

Also destroyed by high/deactivated level of thrombin

A

FIBRINOGEN

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77
Q

Found in plt

A

FIBRINOGEN
I, V, VIIIR:Ag
Cytoplasm: XIII

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78
Q

Acute Phase Reactant (participates in inflammation)

A

FIBRINOGEN

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79
Q

Reduced by oral anticoag (heparin, warfarin, Coumarin)

A

PROTHROMBIN

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80
Q

FIBRINOGEN GROUP:

A

Factors I, V, VIII, XIII

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81
Q

PROTHROMBN GROUP (VITAMIN K- DEPENDENT GROUP):

A

Factors II, VII, IX, X

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82
Q

CONTACT GROUP:

A

Factors XI, XII, Prekallikrein, HMWK

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83
Q

Large molecules

A

FIBRINOGEN GROUP

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84
Q

Substrate for plasmin

A

FIBRINOGEN GROUP

85
Q

consumed during coagulation

A

FIBRINOGEN GROUP

86
Q

most labile

A

FIBRINOGEN GROUP

87
Q

FIBRINOGEN GROUP increased in:

A
  1. Inflammation
  2. Pregnancy
  3. Use of contraceptive pills
88
Q

Not dependent on Vit K

A

FIBRINOGEN GROUP

CONTACT GROUP

89
Q

Vitamin K dependent factors (group)

A

PROTHROMBN GROUP

90
Q

not consumed during coagulation

A

PROTHROMBN GROUP

CONTACT GROUP

91
Q

stable (stored plasma)

A

PROTHROMBN GROUP

92
Q

requires Ca++ as a cofactor in binding to plt phospholipid

A

PROTHROMBN GROUP

93
Q

PROTHROMBN GROUP Decreased in:

A
  1. Oral anticoagulants (function)
  2. GIT absorption problems
94
Q

CONTACT GROUP

A

CONTACT GROUP

95
Q

Fairly stable

A

CONTACT GROUP

96
Q

activation: negatively charged

A

CONTACT GROUP

97
Q

related to fibrinolytic kinin and complement system

A

CONTACT GROUP

98
Q

targeted by plasmin during fibrinolysis

A

Factors I, V, VIII, XIII

99
Q

has the most cf in the clot – attack these 4 to dissolve the
clot

A

Factors I, V, VIII, XIII

100
Q

is converted to fibrin, forming the fibrin clot

A

FI (fibrinogen)

101
Q

is a cofactor in common pathway

A

FV

102
Q

is a cofactor in intrinsic pathway

A

FVIII

103
Q

is a stabilizing factor

A

FXIII

104
Q

Target the cofactors, largest substrate, and stabilizing
factor to stop the coagulation and make the clot very soft

A

Factors I, V, VIII, XIII

105
Q

are affected by temperature

A

FV and VIII

106
Q

affected by temperature Except for [?] (does not activate and disappears in the presence of anticoagulant)

A

FXIII

107
Q

Congenital hemmorhage (Vit K deficiency)

A

Factors II, VII, IX, X

108
Q

Remains as zymogens w/o Vit K

A

Factors II, VII, IX, X

109
Q

: only activates fibrinogen and fibrin (not particularly present in the clot; only activators)

A

FII (thrombin)

110
Q

: only activates FX (not particularly present in the clot; only activators; alr consumed during the coagulation cascade and not in the clot itself)

A

FVII and FIX

111
Q

: substrate inactivated needed to activate FI

A

FX

112
Q

These can go back to the circulation and be reactivated again

A

Factors II, VII, IX, X

113
Q

These can go back to the circulation and be reactivated again Except [?]

A

FII

114
Q

not included in the cf because it only activates the fibrin clot

A

FII

115
Q

also functions in platelets by strengthening plt function

A

FII

116
Q

plays a role in plt plug formation, thus consumed

A

FII

117
Q

: requires Ca and plt phospholipid (PPL)

A

FII, FVII, IX, X

118
Q

FVIII, FIX + Ca + PPL

A
119
Q

: not a coagulation factor, but only a plt

A

PPL

120
Q

Steps in coagulation with participation of platelet

A

FVIII, FIX + Ca + PPL

121
Q

: used to control thrombosis in the body (DVT)

A

Coumarin, Heparin

122
Q

: can cause obstruction of blood vessel, leading to rupture of vein and increased blood pressure, affecting the heart; blood will not clot

A

deep vein thrombosis or DVT

123
Q

: caused by anticoagulant called warfarin

A

PIVKA (Protein in Vitamin K Antagonism)

124
Q

proteins become antagonistic to Vit K

A

PIVKA (Protein in Vitamin K Antagonism)

125
Q

Effect: loss of Vit K and coag factors & Ca (cofactor) cannot bind w/ coag factors

A

PIVKA (Protein in Vitamin K Antagonism)

126
Q

inactivation of Factors II, VII, IX, X + Ca

A

PIVKA (Protein in Vitamin K Antagonism)

127
Q

Ulcerations, pernicious anemia (inability to absorb and breakdown due to stomach acid)

A

Factors II, VII, IX, X

128
Q

Vit K will not be absorbed if there is an absorption problem (ex. Carrot will only pass thru the body)

A

Factors II, VII, IX, X

129
Q

they are just contact factors (first to feel if clot is needed)

A
130
Q

It will take time to disappear after storage

A

XI, XII, PK, HK

131
Q

Not as stable as Prothrombin group

A

CONTACT GROUP

132
Q

injury to endothelium: [?] is exposed to Collagen

A

FXII

133
Q

Collagen: from injured endothelium that gives off negatively charged surface, which will activate

A

FXII to FXIIa and FI to FIa

134
Q

: no role in coagulation but can amplify the action of FXII and FXI

A

PK and HK

135
Q

related to fibrinolytic kinin and complement system specifically

A

PK and HK

136
Q

When isolating a coagulation factor present in a clot, these two are used to extract and elute the coag factors

A

BaSO4 (Barium Sulfate) or Al(OH)3 (Aluminium Hydroxide)

137
Q

: cannot be adsorbed by BaSO4 or Al(OH)3

A

Fibrinogen group and Contact group

138
Q

: can be adsorbed by BaSO4 or Al(OH)3

A

Prothrombin group

139
Q

Clot in BaSO4:
: prothrombin group and other coag factors
: fibrinogen group and contact group (very adhesive to the glass surface)

A
  • extracted/eluted
  • left in the clot/system
140
Q

inhibits coagulation factors

A

Regulatory proteins

141
Q

enhances fibrinolysis

A

Regulatory proteins

142
Q

Regulatory proteins:

A

Protein C, Protein S
Protein Z

143
Q

: inihibits FV and FVIII

A

Protein C, Protein S

144
Q

3 THEORIES ON COAGULATION

A
  1. Morawitz/Classical Theory (1905)
  2. Howell’s theory (1910)
  3. Modern theories: “Waterfall” & “Cascade” (1964)
145
Q

: generate fibrin clot to stop bleeding

A

COAGULATION

146
Q

system addressed to arrest bleeding by fibrin formation

A

COAGULATION

147
Q

: step by step formation of proteins to generate thrombin and fibrin

A

CASCADE

148
Q

Morawitz/Classical Theory (1905)
• believes that there are 2 stages coagulation:

A
  1. thrombin formation
  2. fibrin formation
149
Q

thrombin formation: by the combination of

A

prothrombin (inactive form) + calcium ions + tissue thrombokinase (tissue factor) = generation of thrombin

150
Q

: activators

A

Ca and Thrombokinase

151
Q

known activator:

A

TF (from damaged endothelium) and Ca+

152
Q

fibrin formation: the formed [?] acts on the [?] in
the plasma

A

thrombin

fibrinogen

153
Q

Prothrombin + thrombokinase ——-(Ca)——->

A

thrombin

154
Q

Thrombin + Fibrinoen ———>

A

Fibrin

155
Q

Howell’s theory (1910)
• This theory believed that there are 5 coagulation factors involved:

A

(Fibrinogen, Calcium, Prothrombin, Anti-prothrombin, Thromboplastin)

156
Q

: most common therapeutic circulating antiprothrobin

A

heparin

157
Q

Anti-prothrombin 2 steps: to target

A

1) thrombin (inactivation back to prothrombin)
2) prothrombin (not allowed to be activated to thrombin)

158
Q

Address the circulating anticoagulant to allow thrombin to activate fibrin

A

Anti-prothrombin

159
Q

Thrombin activates fibrinogen to become fibrin

A

Anti-prothrombin

160
Q

Anti-prothrombin • Sequence of reactions:

a. [?] is inactivated by antiprothrombin/heparin
b. [?] neutralizes antiprothrombin and releases prothrombin

A

Prothrombin

Thromboplastin (thrombokinase or TF)

161
Q

Activation of factor X via the intrinsic or extrinsic pathway

A

Modern theories: “Waterfall” & “Cascade” (1964)

162
Q

Conversion of prothrombin to thrombin

A

Modern theories: “Waterfall” & “Cascade” (1964)

163
Q

• Conversion of fibrinogen to fibrin

A

Modern theories: “Waterfall” & “Cascade” (1964)

164
Q

• Advocated the phases of coagulation

A

Modern theories: “Waterfall” & “Cascade” (1964)

165
Q

PHASES of Coagulation

A
  1. Contact Phase
  2. Activation of Factor X
  3. Conversion of Prothrombin to Thrombin
  4. Formation of fibrin
166
Q
  • Starts with the activation XII, then activation of prekallikrein and factor XI.
A
  1. Contact Phase
167
Q

via Intrinsic Pathway or via Extrinsic Pathway

A
  1. Activation of Factor X
168
Q

THE COAGULATION CASCADE

A
  1. INTRINSIC System
  2. EXTRINSIC System / TISSUE FACTOR Pathway
  3. COMMON Pathway
169
Q

All components are found in the [?]. To be activated, the blood must have [?] with a foreign object such as a [?].

A

circulating blood

direct contact

damaged blood vessel or glass

170
Q

This results to absorption of [?] to the [?] exposed by vessel wall damage.

A

XII

negatively- charged collagen

171
Q
  1. INTRINSIC System
    • Sequence of reactions:
  2. Factor [?] is activated by the foreign material into [?]
  3. [?] reacts weakly with [?], thus converting them into their forms
  4. [?] in the presence of Ca++ activates [?]
  5. [?] in the presence of Ca++, platelet phospholipids, and Villa activates [?].
A

XII; XIIa

XIIa; XI, prekallikrein (also by XIIf), and plasminogen

Xla; Ca++; IX

IXa; X

172
Q

Formed [?] feeds back to [?] and causes enzymatic cleavage producing more [?].

A

kallikrein

XIl

Xlla

173
Q

Note: [?] can also be activated by [?]: (CURRENT CONCEPT OF COAGULATION)

A

IX

VIIa-Ca++-TF complex

174
Q

is necessary for the activation of EXTRINSIC system

A

TISSUE FACTOR

175
Q

All cells with the possible exception of those in the blood, contain [?].

A

tissue factor

176
Q

When injury occurs, the [?] is released and acts as a cofactor in initiating coagulation.

A

tissue factor

177
Q

The released tissue factor binds to [?] and activates it to [?].

A

VII

VIla

178
Q

Then VIla, together with calcium, activates [?] to [?] of the common pathway.

A

X

Xa

179
Q

COMMON Pathway

Begins with activation of [?] via the Intrinsic Pathway (?) or via the Extrinsic Pathway (?) to form [?].

A

factor X

IXaVIlla-Ca++-PL

VIla-Ill-Ca++

Prothrombinase/Xa-Va-Ca++-PPL

180
Q

This [?] complex converts [?] to [?] which then cleaves [?] into [?].

A

prothrombinase

prothrombin

thrombin

fibrinogen

fibrin

181
Q

Conversion of Fibrinogen to Fibrin STEPS:
1. [?] cleaves the a and B chains only (releasing fibrinopeptides A and B) forming soluble fibrin monomer/unstable gel.
2. [?] aggregate spontaneously end to end, side to side to form (?) thus vulnerable to enzyme plasmin (also soluble in 5M urea).
3. [?] crosslinks adjacent fibrin monomers by forming COVALENT bonds to form (?)

A

Thrombin

Fibrin monomers; soluble fibrin polymers

Factor XIII: XIlla + Ca++; stable and insoluble clot

182
Q

What activates factor XIII to XIIIa?

A

Thrombin, Collagen

183
Q

The key initiating step is the exposure of TF to the circulation and reaction of [?] with [?].

A

TF

factor VII

184
Q

The [?] complex can enzymatically activate factors [?] and [?].

A

TF-factor/VIla

X

IX

185
Q

The initial activation of (?) may be important in getting the coagulation cascade started, however, (?) rapidly inactivates the (?).

A

factor X to Xa

tissue factor pathway inhibitor (TFP)

TF-VIla-Xa complex

186
Q

The major action of the (?) in vivo is the activation of factor IX to IXa, which then activates factor X to Xa.

A

TFVIla complex

187
Q

Consequently, (?) is converted to thrombin, then (?) is converted to fibrin.

A

prothrombin

fibrinogen

188
Q

Factors (?) have positive feedback activity on earlier steps of the cascade

A

Xa and IIa

189
Q

Thrombin Feedback Mechanism

A

Activation of Coagulation

Inhibitor to Coagulation

190
Q

• It is autocatalytic or self-perpetuating

A

Activation of Coagulation

191
Q

• Low level of thrombin activates

A

Activation of Coagulation

V and VIII

192
Q

• Activates XIlI and XI

A

Activation of Coagulation

193
Q

• Induces platelet aggregation

A

Activation of Coagulation

194
Q

• Controls excessive coagulation

A

Inhibitor to Coagulation

195
Q

• Increase concentration of thrombin

A

Inhibitor to Coagulation

196
Q

destroys V and VIII

A

Inhibitor to Coagulation

197
Q

activates Protein C

A

Inhibitor to Coagulation

198
Q

Protein C and S increase plasminogen activation

A

Inhibitor to Coagulation

199
Q

Promote plasmin generation (fibrinolysis)

A

Inhibitor to Coagulation

200
Q

: activates VIII to VIIIa

A

Factor II, X, residual thrombin (low level)

201
Q

: activates FV

A

Thrombin, residual thrombin (low level)

202
Q

: inhibits FV and VIII

A

residual thrombin (high level)

203
Q
  • regulatory mechanism to stop the cascade
A

residual thrombin (high level): inhibits FV and VIII

204
Q
  • continuous activation slows down the cascade
A

residual thrombin (high level): inhibits FV and VIII

205
Q
  • Thrombin is a very powerful protein that can activate many factor (FIX, FVII, FXIII)
A

residual thrombin (high level): inhibits FV and VIII

206
Q
  • to stop intrinsic pathway from accessing FX; FX will not be able to activate another thrombin/prothrombin to become thrombin
A

residual thrombin (high level): inhibits FV and VIII

207
Q
  • forms soluble fibrin to insoluble fibrin
A

Fibrin XIIIa

208
Q
  • stabilizes the clot
A

Fibrin XIIIa

209
Q
  • soluble clot only forms fibrin meshwork (does not activate)
A

Fibrin XIIIa

Hematology 2 Lec (29 decks)

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