Secondary Hemostasis Flashcards

(89 cards)

1
Q

Requirements of ACT coagulation test

A

Whole Blood

Contact Activator

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2
Q

Significance of prolonged Thrombin Time

A

Quantitative or qualitative abnormalities of fibrinogen

Inhibitors of fibrin formation

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3
Q

_______________ is required for the initation of secondary hemostasis when initiated by wounds

A

Tissue Factor

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4
Q

Result of Disseminated Intravascular Coagulation (DIC)

A

Thrombosis of the microvasculature

Depletion of coagulation factors and platelets → bleeding

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5
Q

Significance of prolonged PT

A

Factor VII deficiency

Deficiency or inhibition of common pathway factor

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6
Q

Inhibitor Consumption Tests

A

Antithrombin (AT)

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7
Q

Requirements for PT coagulation test

A

Citrated plasma

Tissue factor

Calcium

Platelet substitute

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8
Q

Cause of Disseminated Intravascular Coagulation (DIC)

A

Continued activation of coagulation and fibrinolysis

Induction or exposure of tissue factor or other activators of coagulation

Endothelial damage exposing collagen

Proteolytic enzymes

Stagnant blood flow

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9
Q

Increased concentration of D-Dimers occurs wtih

A

Increased fibrinolysis

Severe internal hemorrhage with fibrinolysis

Decreased clearance of FDP by liver

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10
Q

Coagulation test for the common pathway

A

Fibrinogen

TT

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11
Q

Tissue Factor Pathway Inhibitor inhibits

A

Generation of Xa

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12
Q

Loads of thrombin generated on the platelet surface drives the formation of

A

Fibrin

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13
Q

Thromibin time measures

A

Time for fibrin clot formation in citrated plasma + thrombin

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14
Q

Inhibitors of coagulation

A

Antithrombin

Activated Protein C (APC)

Tissue Factor Pathway Inhibitor (TFPI)

Alpha-2 Macroglobulin

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15
Q

Significance of fibrinogen concentration increase

A

Inflammation

Relative increase with dehydration

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16
Q

Two phases of DIC

A

Hypercoagulabile Phase

Consumptive Phase

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17
Q

Steps of the Common Pathway of the Coagulation Cascade

A
  1. X → Xa
  2. Prothrombin → Thrombin by Xa
  3. Fibrinogen → Fibrin by Thrombin
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18
Q

Vitamin K dependent Factors?

A

II, VII, IX, X

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19
Q

Categories of coagulation tests

A

Procoagulant Tests

Anticoagulat Tests

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20
Q

PIVKA would be increased in

A

Vitamin k antagonism/deficiency

Human hepatocellular carcinomas

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21
Q

Hypercoagulable Phase of DIC

A

Thrombosis

Ischemic necrosis and organ dysfunction

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22
Q

Prothrombin Time (PT) measures

A

Time for fibrin clot formation in citrated plasma + tissue factor + calcium + platelet phospholipid substitute

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23
Q

Clinical signs of DIC

A

Associated with the signs of primary disease

Signs of organ dysfunction secondary to thrombosis

Bleeding

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24
Q

Requirements of aPTT coagulation test

A

Citrated Plasma

Contact activator

Calcium

Platelet substitute

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25
Plasmin degrades fibrin into
Fibrin Degradation Products D- Dimers
26
Pathogenesis of the hypercoagulable phase of DIC leading to organ dysfuction
Thrombus formation → blockage of the microvasculature → Ischemic necosis → Organ dysfunction
27
Hemophilia B
Factor IX deficiency Dogs and Cats Signs and inheritance patterns similar to Hemophilia A
28
Requirements for Thrombin Time coagulation test
Citrated plasma Thrombin
29
Mechanism of action of Antithrombin
1. Heparin binds to antithrombin 2. Heparin causes conformational change and exposes the thrombin binding site 3. Thrombin binds to AT = TAT complex and heparin floats away 4. Tat Comples is cleared by the phagocytic system
30
Secondary Hemostasis
Stabilization of the platelet plug via fibrin meshwork - used in large defects
31
Laboratory findings in Warfarin Toxicity
PT - prolonged aPTT, ACT - prolonged PIVKA - positive Platelet count - normal
32
Three phases of the cell-based model
Initiation Amplification Propagation
33
Why does vitamin k antagonism work?
Vitamin K dependent factors los their negative charge and are not recruited to sites of injury
34
Hageman's Disease
Factor XII deficiency Cats and Killer Whales Deficiency not associated with bleeding - prolonged PTT
35
Secondary hemostasis occurs on
Platelet surface
36
Fibrin Degradation Products inhibit
Platelet function and fibrin polymerization
37
Which of the intrinsic pathway coagulation tests is more sensitive?
aPTT
38
Laboratory findings of hemophilia A
Platelet Count - Normal Bleeding Time - Normal aPTT and ACT - Prolonged PT- normal Factor activity - reduced
39
Pathophysiology of Warfarin Toxicity
Coumarins block enzymes required to reduce vitamin K Negative charge not transferred to coagulation factors Platelet surface charge remains positive Factors X and II unable to bind to platelet
40
Coagulation factors are synthesized in the
Liver
41
Treatment of warfarin toxicosis
Decontamination Supplement vitamin K Plasma and/or blood transfusions
42
Fibrinolytic Activity Tests
Fibrin Degradation Products D-Dimer
43
How is citrated plasma different than blood?
No RBC, WBC or Platelets Decreased Calcium
44
Key factor that promotes amplification of secondary hemostasis
Thrombin
45
For collection of blood for coagulation tests, what tube should be used?
Blue Top - Citrate Tube
46
Factors involved in the Intrinisc Pathway
XII, XI, IX, VIII
47
X is converted to Xa by what in the Intrinisc Pathway?
IXa
48
Activated Protein C inhibits
Va, VIIa
49
Coagulation test for the intrinsic pathway
aPTT ACT
50
aPTT and ACT tests measure
Time for fibrin clot formation
51
Factors involved in the Extrinsic Pathway
Tissue Factor III VII
52
Pathways that make up the coagulation cascade
Intrinsic pathway - Contact Activation Extrinsic pathway - Tissue Activation Common Pathway
53
Clinical features of Warfarin Toxicosis
**Bleeding** - Anemia, weakness, pallor, hypovolemia, shock, dyspnea, lameness, neurologic signs ## Footnote **Death**
54
What is the cardinal bloodwork finding for a patient in consuptive phase of DIC?
Thrombocytopenia
55
Significance in fibrinogen concentration decrease
Consumption due to hypercoagulation - excessive conversion of fibrinogen to fibrin Decreased production by the liver
56
Pathogenesis of hypercoagulable phase of DIC leading to bleeding
Thrombus formation → fibrinolysis → increased FDPs → decreased platelet function → bleeding
57
Significance of prolonged aPTT and ACT time
Deficiency or inhibition of any intrinsic or common pathway factor Heparin therapy
58
IX is converted to IXa in the Intrinsic Pathway by
VIIa
59
Coagulopathy and Liver disease
Decreased synthesis of coagulation factors Production of dysfunctional factors
60
X is converted to Xa by what in the Extrinisic Pathway
VIIa
61
Treatment for DIC
Identify and eliminate underlying disorder Fluid therapy Transfusion therapy
62
Hemophilia A
Factor VIII deficiency X linked recessive inheritance Causes mild, moderate or severe bleeding
63
Non-Enzymatic factors of the coagulation cascade
Tissue Factor (Factor III, Thromboplastin) Factor VIIIa Factor Va Calcium Platelets
64
Factors affected by amplification
XI VII VIIIa Va
65
Coagulation Tests
Activated Partial Thromboplastin Time (aPTT, PTT) Prothrombin Time (PT) Thrombin Time (TT), Fibrinogen PIVKA Special Factor Assay
66
PIVKA
Proteins induced by vitamin K antagonism Indirectly measures abnormal forms of vitamin K dependent factors
67
Increased concentration of fibrin degradation products occus when
Increased fibrinolysis Severe internal hemorrhage with fibrinolysis Decreased clearance of FDP by liver
68
Antithrombin inhibits
Thrombin, IXa, Xa
69
VII is converted to VIIa in the extrinsic pathway by
Xa
70
Fibrinogen is an indicator of what in large animals
Inflammation
71
Laboratory findings of DIC
Thrombocytopenia PT, aPTT - Prolonged Fibrinogen - decreased FDP and D-Dimers - increased Antithrombin - decreased Hemorrhagic anemia Schistocytes
72
aPTT requires \_\_\_\_\_\_% deficiency before prolongation is detected
70%
73
ACT requires \_\_\_\_\_\_% deficiency of factor before prolongation is detected
95%
74
Serum biochemistries for DIC depend on
Primary Disease Location of microthrombosis
75
PT requires \_\_\_\_\_\_% deficiency of factor before prolongation is detected
70%
76
Alpha-2 Macroglobulin inhibits
Thrombin Plasmin Kallikrein
77
Prothrombin is converted to Thrombin by
Xa
78
Enzymatic Factors of the Coagulation Cascade
XII, XI, IX, VII, X Prothrombin Thrombin Fibrinogen Fibrin
79
Pathogenesis of consumptive phase of DIC
Depletion of coagulation factors and platelets → bleeding
80
Fibrinogen is converted to Fibrin by
Thrombin
81
Activated Clotting Time ACT measures
Time for fibrin clot formation in non-anticoagulated whole blood
82
Coagulation test for the extrinsic pathway
PT
83
Plasminogen is converted to Plasmin by
Tissue Plasminogen Activator (TPA)
84
Inherited Factor Deficiencies
Hemophilia A - VIII Hemophilia B - IX Hagemans Disease - XII
85
Factors involved in the common pathway
X, V Prothrombin Fibrinogen Fibrin
86
Cell Based Model
Focuses on the roll of cells involved with coagulation
87
Why is PT a good choice in test for screening for Vitamin K deficiency?
Because Factor VII has the shortest half life
88
Causes of Warfarin Toxicosis
Poisoning with coumarin derivatives Fat malabsorption Dietary deficiency Antibiotics that cause decreased absorption or utilization by liver
89
It is good practice to supplement a patient with prolonged aPTT with what before surgery?
Plasma