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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
Factor II: Name, pathway, and function
Prothrombin, common | Proenzyme: IIa (thrombin) cleaves fibrinogen and activates V, VIII, XI, XIII, protein C, platelets
26
Factor III: Name, pathway, and function
``` Tissue factor (TF), extrinsic Cofactor: TF binds and activates VII, and the TF/VIIa complex activates IX and X ```
27
Factor IV: Name, pathway, and function
Free ionized calcium, all | Cofactor for IIa, VIIa, IXa, Xa, XIIIa
28
Factor V: Name, pathway, and function
Proaccelerin, common | Pro-cofactor for Xa, cofactor after activation to Va
29
Factor VII: Name, pathway, and function
Proconvertin, stable factor, extrinsic | Proenzyme: VIIa activates IX and X
30
Factor VIII: Name, pathway, and function
Antihemophilic factor, intrinsic | Pro-cofactor for IXa, cofactor after activation to VIIIa
31
Factor IX: Name, pathway, and function
Christmas factor, intrinsic | Proenzyme: IXa activates X
32
Factor X: Name, pathway, and function
Stuart/Stuart-Prower factor, common | Proenzyme: Xa activates II
33
Factor XI: Name, pathway, and function
Plasma thromboplastin antecedent, intrinsic | Proenzyme: XIa activates IX
34
Factor XII: Name, pathway, and function
Hageman factor, intrinsic | Proenzyme: XIIa activates XI, PK, HMWK, plasminogen
35
Factor XIII: Name, pathway, and function
Fibrin-stabilizing factor, fibrinase, common | Proenzyme: XIIIa cross-links fibrin and protects it from plasmin degradation
36
Factor HMWK: Name, pathway, and function
Fitzgerald factor, intrinsic | cofactor for activation of XII and XI
37
Factor PF3: Name, pathway, and function
Platelet factor 3, mostly phosphatidylserine; intrinsic, common Negatively charged platelet membrane lipoproteins important for in vivo activation of X and II
38
Factor PK: Name, pathway, and function
Fletcher factor, intrinsic | Proenzyme: kallikrein activates XII and PK, generates bradykinin from HMWK, leads to plasmin generation
39
major inhibitor of coagulation enzymes
antithrombin
40
action of antithrombin
 Binds, activates, removes most coagulation enzymes from circulation, most importantly thrombin (IIa), IXa, Xa
41
effect of anemia on coagulation times
plasma may be undercitrated because there is more plasma with the same amount of citrate-->may result in falsely shortened coagulation times
42
effect of erythrocytosis on coagulation times
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
Factor VII deficiency Condition (if named differently) Species Expected PTT, PT, TT results
Dogs PTT WRI PT ↑ TT WRI
44
PK deficiency Condition (if named differently) Species Expected PTT, PT, TT results
Dogs, horses PTT ↑ PT WRI TT WRI
45
Factor XII deficiency Condition (if named differently) Species Expected PTT, PT, TT results
``` Hageman trait Dogs, cats PTT ↑ PT WRI TT WRI ```
46
Factor XI deficiency Condition (if named differently) Species Expected PTT, PT, TT results
Dogs, cats, cattle PTT ↑ PT WRI TT WRI
47
Factor IXa deficiency Condition (if named differently) Species Expected PTT, PT, TT results
``` Hemophilia B Dogs, cats PTT ↑ PT WRI TT WRI ```
48
Factor VIIIa deficiency Condition (if named differently) Species Expected PTT, PT, TT results
``` Hemophilia A Dogs, cats, cattle, horses PTT ↑ PT WRI TT WRI ```
49
Factor X deficiency Condition (if named differently) Species Expected PTT, PT, TT results
Dogs PTT ↑ PT ↑ TT WRI
50
Factor II deficiency Condition (if named differently) Species Expected PTT, PT, TT results
``` Hypoprothrombinemia Dogs PTT ↑ PT ↑ TT WRI ```
51
Factor I deficiency Condition (if named differently) Species Expected PTT, PT, TT results
``` Hypo-/afibrinogenemia Dogs, goats PTT ↑ PT ↑ TT ↑ ```
52
Factor II, VII, IX, X deficiency (hereditary/congenital) Condition (if named differently) Species Expected PTT, PT, TT results
``` Vitamin K-dependent multifactor deficiency Cats (devon rex), possibly dogs PTT ↑ PT ↑ TT WRI ```
53
Fibrinolytic factor α2-macroglobulin | major function
binds, inhibits, and clears plasmin from circulation
54
Fibrinolytic factor fibrin | major function
Major protein in a stable thrombus; source of FDPs
55
Fibrinolytic factor Fibrin fragment D-dimer | major function
FDP that contain D-dimer moieties generated by factor XIIIa-mediated cross-linking of fibrin; includes HMW and LMW products
56
Fibrinolytic factor fibrin fragments + fibrinogen fragments (FDPs) major function
Fragments of fibrinogen or fibrin produced from enzymatic degradation (fibrinolysis or fibrinogenolysis); inhibit platelets, thrombin, and fibrin polymerization
57
Fibrinolytic factor Fibrinogen (factor I) | major function
required fro coagulation to progress to fibrin; converted to fibrin via thrombin (IIa)
58
Fibrinolytic factor plasmin | major function
major enzyme that breaks down fibrin; also may degrade fibrinogen and other proteins
59
Fibrinolytic factor plasmin inhibitor (PI, α2-antiplasmin) | major function
binds, inhibits, and clears plasmin from circulation
60
Fibrinolytic factor plasminogen | major function
inactive plasma protein precursor of plasmin; becomes localized to thrombi by binding to fibrin and fibrinogen
61
Fibrinolytic factor plasminogen activator inhibitor I (PAI-I) major function
inhibitor of fibrinolysis produced by endothelial cells; inactivates t-PA and u-PA
62
Fibrinolytic factor plasminogen activator, tissue type (t-PA) major function
converts plasminogen to plasmin; important in fibrinolysis within the vasculature
63
Fibrinolytic factor plasminogen activator, urokinase type (u-PA) major function
converts plasminogen to plasmin; important in tissue remodeling
64
Fibrinolytic factor thrombin-activatable fibrinolysis inhibitor (TAFI) major function
zymogen activated by thrombin and thrombomodulin; TAFIa cleaves plasminogen-binding sites from fibrin, thus inhibiting fibrinolysis
65
Possible causes of ↑ ACT time
Defect in surface-induced and/or common pathways
66
Possible causes of ↓ AT activity
Renal or intestinal loss, consumptive coagulation, heparin administration, decreased production
67
Possible causes of ↑ BMBT
thrombocytopenia, thrombopathia, vWF deficiency, anemia
68
Possible causes of ↓ clot retraction
thrombocytopenia, thrombopathia
69
Possible causes of ↓ coag factor activity
hereditary or acquired factor deficiencies (hypocoagulable state)
70
Possible causes of ↑ D-dimers
coagulation and fibrinolysis, decreased clearance
71
Possible causes of ↑ FDPs
incnreased fibrin(ogen)olysis, decreased clearance
72
Possible causes of ↓ fibrinogen
decreased hepatic production, increased consumption (may be hypocoagulable)
73
Possible causes of ↑ fibrinogen
inflammation, hypovolemia (dehydration)
74
Possible causes of ↓ protein C activity
decreased hepatic production, abnomrla production (vit. K antagonism/absence), loss, consumption (may be hypercoagulable)
75
Possible causes of ↑ PT
Defect in TF and/or common pathways
76
Possible causes of ↑ PTT
Defect in surface-induced and/or common pathways
77
Possible causes of ↑ RVVT
Defect in common pathway
78
Possible causes of ↑ TT
hypofibrinogenemia, dysfibrinogenemia, heparinized patient or sample, increased FDPs
79
Possible causes of ↓ vWF:Ag
vWD or vWD carrier
80
Possible causes of ↑ vWF:Ag
exercise, excitement, pregnancy, vasopressin
81
``` Interpret: PT: ↑ PTT: ↑ FDPs: ↑ Fibrinogen: ↓ Platelets: ↓ BMBT: ↑ ```
Fulminant DIC | applies only to the severe, fulminant form
82
``` Interpret: PT: WRI PTT: WRI FDPs: WRI Fibrinogen: WRI Platelets: WRI BMBT: ↑ ```
Thrombopathia, vWD
83
``` Interpret: PT: WRI PTT: WRI FDPs: WRI Fibrinogen: WRI Platelets: ↓ BMBT: ↑ ```
Thrombocytopenia
84
``` Interpret: PT: WRI PTT: ↑ FDPs: WRI Fibrinogen: WRI Platelets: WRI BMBT: WRI ```
Intrinsic pathway defect
85
``` Interpret: PT: ↑ PTT: WRI FDPs: WRI Fibrinogen: WRI Platelets: WRI BMBT: WRI ```
Factor VII defiency (or early stages of hepatic disease or vit K antagonism/absence)
86
``` Interpret: PT: ↑ PTT: ↑ FDPs: WRI Fibrinogen: WRI Platelets: WRI BMBT: WRI ```
Common pathway defect or multiple defects
87
``` Interpret: PT: ↑ PTT: ↑ FDPs: WRI Fibrinogen: ↓ Platelets: WRI BMBT: WRI - ↑ ```
dys- or afibrinogenemia

Stockham and Scott (9 decks)

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