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Stockham and Scott > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Chediak Higashi syndrome affected species/breeds

A

Persian cats, Hereford, Brangus, Japanese black cattle

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2
Q

cyclic hematopoiesis affected species/breeds

A

grey collie

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3
Q

dense-granule storage pool disease affected species/breeds

A

American cocker spaniels

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4
Q

Glanzmann’s thrombasthenia affected species/breeds

A

great Pyrenees, otterhounds, horses

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5
Q

idiopathic thrombopathia affected species/breeds

A

a thoroughbred

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6
Q

platelet procoagulant defect affected species/breeds

A

German shepherds

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7
Q

thrombasthenic thrombopathia affected species/breeds

A

otterhounds

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8
Q

Type I vWD

A

all vWF multimers are present but at decreased concentrations. Severity varies. Is most common form, occurs in many dog breeds including Dobermans

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9
Q

Type II vWD

A

severe, uncommon. Deficiency of vWF with a disproportionate decrease in large multimers. German shorthair pointers, German wirehaired pointers, reported in horses

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10
Q

Type III vWD

A

severe, involves absence of all vWF multimers. Chesapeake Bay retrievers, Dutch kooikers, Scottish terriers, Shetland sheepdogs

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11
Q

vWD clinical and laboratory signs

A

o Mild to severe mucosal hemorrhage (epistaxis, GI hemorrhage, prolonged estral bleeding), cutaneous bruising, prolonged hemorrhage from nonsurgical or surgical trauma (tail docking, puppy dewclaw removal, tooth extraction), hemarthrosis and hematomas in horses
o Absence of petechiae may help differentiate vWD from platelet disorders
o Prolonged BMBT without thrombocytopenia or prolonged coagulation times

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12
Q

Inhibitor of the TF/extrinsic pathway

A

TFPI

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13
Q

Initiator of the extrinsic pathway

A
  • Initiated by TF expressed on vascular smooth muscle cells, activated monos, other extravascular cells.
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14
Q

Importance of TF/extrinsic pathway

A

Important in initiating thrombin generation

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15
Q

Initiator of the intrinsic pathway

A

initiated when the contact coagulation factors HMWK, PK, and factor XII contact negatively charged surfaces (collagen)

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16
Q

Inhibitor of the surface induced/intrinsic pathway

A

inhibited by AT, protein C, protein S, protein Z

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17
Q

surface induced/intrinsic pathway is also activated secondary to which activation

A

also activated secondary to TF and common pathway activation: TF-VIIa activates factor IX; thrombin activates factors XI and VIII

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18
Q

Importance of surface induced/intrinsic pathway

A

important in propagating and amplifying thrombin generation initiated by the TF pathway

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19
Q

Initiator of common pathway

A

initiated by activation of factor X–>Xa by either surface-induced or TF pathway

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20
Q

Effect of common pathway

A
  • Leads to formation of thrombin from prothrombin by the prothrombinase complex
  • Thrombin acts on fibrinogen to generate fibrin monomers then multimers, which are cross-linked via factor VIIIa
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21
Q

Inhibitor of common pathway

A

inhibited by AT, protein C, protein S, protein Z

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22
Q

amplifier of common pathway

A

Thrombin activation of factor V amplifies the common pathway

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23
Q

transmembrane cellular receptor and cofactor for factors VII and VIIa

A

TF (tissue factor)

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24
Q

Factor I: Name, pathway, and function

A

Fibrinogen, common

Substrate for thrombin–converted to fibrin

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25
Q

Factor II: Name, pathway, and function

A

Prothrombin, common

Proenzyme: IIa (thrombin) cleaves fibrinogen and activates V, VIII, XI, XIII, protein C, platelets

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26
Q

Factor III: Name, pathway, and function

A 
Tissue factor (TF), extrinsic
Cofactor: TF binds and activates VII, and the TF/VIIa complex activates IX and X
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27
Q

Factor IV: Name, pathway, and function

A

Free ionized calcium, all

Cofactor for IIa, VIIa, IXa, Xa, XIIIa

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28
Q

Factor V: Name, pathway, and function

A

Proaccelerin, common

Pro-cofactor for Xa, cofactor after activation to Va

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29
Q

Factor VII: Name, pathway, and function

A

Proconvertin, stable factor, extrinsic

Proenzyme: VIIa activates IX and X

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30
Q

Factor VIII: Name, pathway, and function

A

Antihemophilic factor, intrinsic

Pro-cofactor for IXa, cofactor after activation to VIIIa

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31
Q

Factor IX: Name, pathway, and function

A

Christmas factor, intrinsic

Proenzyme: IXa activates X

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32
Q

Factor X: Name, pathway, and function

A

Stuart/Stuart-Prower factor, common

Proenzyme: Xa activates II

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33
Q

Factor XI: Name, pathway, and function

A

Plasma thromboplastin antecedent, intrinsic

Proenzyme: XIa activates IX

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34
Q

Factor XII: Name, pathway, and function

A

Hageman factor, intrinsic

Proenzyme: XIIa activates XI, PK, HMWK, plasminogen

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35
Q

Factor XIII: Name, pathway, and function

A

Fibrin-stabilizing factor, fibrinase, common

Proenzyme: XIIIa cross-links fibrin and protects it from plasmin degradation

36
Q

Factor HMWK: Name, pathway, and function

A

Fitzgerald factor, intrinsic

cofactor for activation of XII and XI

37
Q

Factor PF3: Name, pathway, and function

A

Platelet factor 3, mostly phosphatidylserine; intrinsic, common
Negatively charged platelet membrane lipoproteins important for in vivo activation of X and II

38
Q

Factor PK: Name, pathway, and function

A

Fletcher factor, intrinsic

Proenzyme: kallikrein activates XII and PK, generates bradykinin from HMWK, leads to plasmin generation

39
Q

major inhibitor of coagulation enzymes

A

antithrombin

40
Q

action of antithrombin

A

 Binds, activates, removes most coagulation enzymes from circulation, most importantly thrombin (IIa), IXa, Xa

41
Q

effect of anemia on coagulation times

A

plasma may be undercitrated because there is more plasma with the same amount of citrate–>may result in falsely shortened coagulation times

42
Q

effect of erythrocytosis on coagulation times

A

plasma may be overcitrated because there is less plasma with the same amount of citrate–>may prolong coagulation times because the excess citrate binds too much of the Ca added to the assay system

43
Q

Factor VII deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A

Dogs
PTT WRI
PT ↑
TT WRI

44
Q

PK deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A

Dogs, horses
PTT ↑
PT WRI
TT WRI

45
Q

Factor XII deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Hageman trait
Dogs, cats
PTT ↑
PT WRI
TT WRI
46
Q

Factor XI deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A

Dogs, cats, cattle
PTT ↑
PT WRI
TT WRI

47
Q

Factor IXa deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Hemophilia B
Dogs, cats
PTT ↑
PT WRI
TT WRI
48
Q

Factor VIIIa deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Hemophilia A
Dogs, cats, cattle, horses
PTT ↑
PT WRI
TT WRI
49
Q

Factor X deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A

Dogs
PTT ↑
PT ↑
TT WRI

50
Q

Factor II deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Hypoprothrombinemia
Dogs
PTT ↑
PT ↑
TT WRI
51
Q

Factor I deficiency
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Hypo-/afibrinogenemia
Dogs, goats
PTT ↑
PT ↑
TT ↑
52
Q

Factor II, VII, IX, X deficiency (hereditary/congenital)
Condition (if named differently)
Species
Expected PTT, PT, TT results

A 
Vitamin K-dependent multifactor deficiency
Cats (devon rex), possibly dogs
PTT ↑
PT ↑
TT WRI
53
Q

Fibrinolytic factor α2-macroglobulin

major function

A

binds, inhibits, and clears plasmin from circulation

54
Q

Fibrinolytic factor fibrin

major function

A

Major protein in a stable thrombus; source of FDPs

55
Q

Fibrinolytic factor Fibrin fragment D-dimer

major function

A

FDP that contain D-dimer moieties generated by factor XIIIa-mediated cross-linking of fibrin; includes HMW and LMW products

56
Q

Fibrinolytic factor fibrin fragments + fibrinogen fragments (FDPs)
major function

A

Fragments of fibrinogen or fibrin produced from enzymatic degradation (fibrinolysis or fibrinogenolysis); inhibit platelets, thrombin, and fibrin polymerization

57
Q

Fibrinolytic factor Fibrinogen (factor I)

major function

A

required fro coagulation to progress to fibrin; converted to fibrin via thrombin (IIa)

58
Q

Fibrinolytic factor plasmin

major function

A

major enzyme that breaks down fibrin; also may degrade fibrinogen and other proteins

59
Q

Fibrinolytic factor plasmin inhibitor (PI, α2-antiplasmin)

major function

A

binds, inhibits, and clears plasmin from circulation

60
Q

Fibrinolytic factor plasminogen

major function

A

inactive plasma protein precursor of plasmin; becomes localized to thrombi by binding to fibrin and fibrinogen

61
Q

Fibrinolytic factor plasminogen activator inhibitor I (PAI-I)
major function

A

inhibitor of fibrinolysis produced by endothelial cells; inactivates t-PA and u-PA

62
Q

Fibrinolytic factor plasminogen activator, tissue type (t-PA)
major function

A

converts plasminogen to plasmin; important in fibrinolysis within the vasculature

63
Q

Fibrinolytic factor plasminogen activator, urokinase type (u-PA)
major function

A

converts plasminogen to plasmin; important in tissue remodeling

64
Q

Fibrinolytic factor thrombin-activatable fibrinolysis inhibitor (TAFI)
major function

A

zymogen activated by thrombin and thrombomodulin; TAFIa cleaves plasminogen-binding sites from fibrin, thus inhibiting fibrinolysis

65
Q

Possible causes of ↑ ACT time

A

Defect in surface-induced and/or common pathways

66
Q

Possible causes of ↓ AT activity

A

Renal or intestinal loss, consumptive coagulation, heparin administration, decreased production

67
Q

Possible causes of ↑ BMBT

A

thrombocytopenia, thrombopathia, vWF deficiency, anemia

68
Q

Possible causes of ↓ clot retraction

A

thrombocytopenia, thrombopathia

69
Q

Possible causes of ↓ coag factor activity

A

hereditary or acquired factor deficiencies (hypocoagulable state)

70
Q

Possible causes of ↑ D-dimers

A

coagulation and fibrinolysis, decreased clearance

71
Q

Possible causes of ↑ FDPs

A

incnreased fibrin(ogen)olysis, decreased clearance

72
Q

Possible causes of ↓ fibrinogen

A

decreased hepatic production, increased consumption (may be hypocoagulable)

73
Q

Possible causes of ↑ fibrinogen

A

inflammation, hypovolemia (dehydration)

74
Q

Possible causes of ↓ protein C activity

A

decreased hepatic production, abnomrla production (vit. K antagonism/absence), loss, consumption (may be hypercoagulable)

75
Q

Possible causes of ↑ PT

A

Defect in TF and/or common pathways

76
Q

Possible causes of ↑ PTT

A

Defect in surface-induced and/or common pathways

77
Q

Possible causes of ↑ RVVT

A

Defect in common pathway

78
Q

Possible causes of ↑ TT

A

hypofibrinogenemia, dysfibrinogenemia, heparinized patient or sample, increased FDPs

79
Q

Possible causes of ↓ vWF:Ag

A

vWD or vWD carrier

80
Q

Possible causes of ↑ vWF:Ag

A

exercise, excitement, pregnancy, vasopressin

81
Q 
Interpret:
PT: ↑
PTT: ↑
FDPs: ↑
Fibrinogen: ↓
Platelets: ↓
BMBT: ↑
A

Fulminant DIC

applies only to the severe, fulminant form

82
Q 
Interpret:
PT: WRI
PTT: WRI
FDPs: WRI
Fibrinogen: WRI
Platelets: WRI
BMBT: ↑
A

Thrombopathia, vWD

83
Q 
Interpret:
PT: WRI
PTT: WRI
FDPs: WRI
Fibrinogen: WRI
Platelets: ↓
BMBT: ↑
A

Thrombocytopenia

84
Q 
Interpret:
PT: WRI
PTT: ↑
FDPs: WRI
Fibrinogen: WRI
Platelets: WRI
BMBT: WRI
A

Intrinsic pathway defect

85
Q 
Interpret:
PT: ↑
PTT: WRI
FDPs: WRI
Fibrinogen: WRI
Platelets: WRI
BMBT: WRI
A

Factor VII defiency (or early stages of hepatic disease or vit K antagonism/absence)

86
Q 
Interpret:
PT: ↑
PTT: ↑
FDPs: WRI
Fibrinogen: WRI
Platelets: WRI
BMBT: WRI
A

Common pathway defect or multiple defects

87
Q 
Interpret:
PT: ↑
PTT: ↑
FDPs: WRI
Fibrinogen: ↓
Platelets: WRI
BMBT: WRI - ↑
A

dys- or afibrinogenemia

Stockham and Scott (9 decks)

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