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secondary hemostasis Flashcards

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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
Both extrinsic (TF) and Intrinsic (contact activation)
come together to the common pathway by activation of Factor X.
26
factors of extrinsic pathway
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
27
TF:VIIa
This serine protease complex of extrinsic pathway acts on factor X (Stuart Power Factor) starting the common pathway.
28
Extrinsic pathway measured by
PT
29
TF doesn't originate in
the blood
30
Extrinsic pathway study strategy 3+7 =
10 ! Factor X = common pathway
31
Intrinsic pathway factors
XII XI IX VIII
32
all factors of the intrinsic pathway originate from
the blood
33
surface contact - intrinsic pathway
negatively charged Phospholipids on platelet membrane - or collagen from sub endothelium
34
Intrinsic pathway measured by
APTT
35
Factor VIII - Intrinsic Pathway
Largest protein in coag. cascade. (anti-hemophilic factor) activated by thrombin in the common pathway
36
Factor VIII =
vWF + VIII:c + antigenic portion
37
vWF -
von willebrand factor carrier protein of VIII:c
38
VIII:c
coagulant portion of factor VIII
39
Order of factors in intrinsic pathway think TENET
XII XI IX VIII X
40
PF3
platelet thromboplastin
41
XIIa --> HMWK
PK --> K --> K
42
common pathway starts with
Factor X activated from either intrinsic pathway or the extrinsic pathway
43
both extrinsic and intrinsic pathway requires a "tenase" complex that includes
calcium, ca2+
44
tense for intrinsic
IXa + Ca2+ PF3 + VIII:c
45
tense for extrinsic
TF:VIIa + Ca2+
46
Factors of the common pathway
X V II I XIII
47
common pathway is measured by
PT, APTT, TT
48
IIa (II = prothrombin)
thrombin
49
Ia (I = fibrinogen)
fibrin
50
Common pathway - Prothombinase complex
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
Common pathway - thrombin
converts fibrinogen (I) into fibrin (Ia) Activates factor XIII Activation of cofactors V and VIII induces platelet aggregation and secretion
52
Thrombin splits
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
Thrombin splits
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
substrate
I
54
cofactors
Proteins that accelerate enzymatic reactions III V VII:c HMWK
55
serine proteases
II VII IX X XI XII PK
56
transaminase
XIII
57
Contact proteins
XI XII PK HMWK
58
prothrombin proteins
II VII IX X
59
fibrinogen groups
I V VIII XIII
60
substrate acted on to produce product
I - Fibrinogen --> fibrin
61
enzymes
catalyze biochemical reactions serine protease - cleaves peptide bond ( IIa, VIIa, Xa, XIa, XIIa, prekallikrein) transaminases - transfers amino groups
62
transaminase example
transfers amino groups XIII, crosslink between fibrin monomers to form stable fibrin clot
63
consumed yes/no
yes = all used up no = found in serum
64
stable yes/no
yes = can be found in stored plasma no= requires fresh sample
65
vitamin k dependent?
yes = affected by Vitamin K deficiency or Warfarin/Coumadin no = not affected
66
contact proteins - chart
Found in initial phase of intrinsic pathway NOT consumed Fairly stable - can be present in stored plasma NOT vitamin K dependent
67
Prothrombin proteins - chart
Found in ALL pathways NOT consumed, except II !!!! Stable VITAMIN K DEPENDENT attracted to surface of activated platelets
68
Only one that is vitamin K dependent
Prothrombin proteins
69
Fibrinogen group chart
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
stable groups
contact proteins prothrombin proteins
71
consumed groups
fibrinogen group prothrombin
72
complexes are assembled on
anionic (neg-charged) phospholipid surface Ca2+ Required.
73
Extrinsic tenase
Enzyme: VIIa Cofactor: TF Substrate: X
74
Intrinsic tenase
Enzyme: IXa Cofactor: VIIIa Substrate: X
75
Prothrombinase tenase
Enzyme: Xa Cofactor: Va Substrate: II
76
protein C complex
Enzyme: IIa Cofactor: Thrombomodulin Protein S Substrate: Protein C
77
Factor decreased reasons
Decreased synthesis Synthesis of dysfunctional factor molecule Excessive destruction of factors through acquired disorders Inactivation of factors through circulating inhibitors
78
Consequences of factor decreased
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
PT test
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
Normal range PT test
11-13 seconds
81
INR
varies in TF conc. - helps compare between different laboratories INR = PTpatient/PTcontrol ^ISI
82
Normal range APTT
25-38 seconds
83
APTT test
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
what test is used for monitoring heparin treatment
APTT
85
TT test
Reagent contains thrombin measures conversion of fibrinogen into fibrin - bypasses extrinsic + intrinsic pathway
86
Prolonged TT test
Hypofibrinogenemia/Dysfibrinogenemia Treatment w/ heparin FDP - circulating degradation products Pathologic circulating anticoagulants
87
APTT abnormal PT abnormal TT normal
Vitamin K defect Liver disease Inhibitor present Factor deficiency common pathway
88
APTT abnormal PT normal
Factor deficiency - intrinsic Lupus anticoagulant Specific factor inhibitor (ex: VIII)
89
APTT normal PT abnormal
Factor deficiency extrinsic pathway Specific factor inhibitor
90
APTT abnormal PT abnormal TT abnormal
Factor deficiency I Severe liver disease DIC Potent inhibitor Hypofibrinogenemia/dysfibrinogenemia
91
fibrinogen normal range
200-400mg/dL
92
High fibrinogen
low TT
93
low fibrinogen
high TT
94
Factor XIII screening test
Measures XIII presence - only presence in pathways is crosslinkong fibrin monomers to stabilize fibrin clot - not effectively measured in PT, APTT, TT
95
Factor XIII screening test principle
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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