Hemostasis Testing Modalities

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Vocabulary practice flashcards covering veterinary diagnostic hemostasis testing, pre-analytic considerations, coagulation factor pathways, viscoelastic testing parameters, fibrinolysis assays, and endogenous anticoagulants based on Dr. Amir Kol's lecture notes.

26 Terms

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Syringe Citrate Anticoagulation Ratio

The required ratio of sodium citrate anticoagulant to blood (1:91:9) when drawing samples with a syringe for plasma-based coagulation testing.

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Intrinsic Coagulation Pathway

The contact-activated branch of secondary hemostasis comprising coagulation factors 1212, 1111, 99, and 88, clinically assessed by ACT and aPTT.

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Extrinsic Coagulation Pathway

The coagulation cascade pathway initiated by tissue factor (TF) complexing with factor 77, clinically evaluated by Prothrombin Time (PT).

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Common Coagulation Pathway

The converging segment of the coagulation cascade where the intrinsic and extrinsic pathways unite, comprising factors 1010, 55, 22 (prothrombin), and 11 (fibrinogen).

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<p>Activated Coagulation Time (ACT)</p>

Activated Coagulation Time (ACT)

A point-of-care test performed on un-anticoagulated whole blood in specialized activator tubes incubated at 37∘C37^\circ\text{C}, measuring the time to visual clot formation (55–80 sec55\text{--}80\,\text{sec} in dogs, 55–85 sec55\text{--}85\,\text{sec} in cats).

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ACT Factor Sensitivity Threshold

The detection limit of the Activated Coagulation Time assay; it is an insensitive test that only becomes prolonged when a single intrinsic or common pathway factor drops below <10%<10\% of normal activity.

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Activated Partial Thromboplastin Time (aPTT / PTT)

A coagulation assay performed on citrated plasma with added procoagulant phospholipids, calcium, and contact activators (kaolin, silicates) that detects intrinsic and common pathway factor deficiencies (<30%<30\% activity of a single factor) and is unaffected by thrombocytopenia.

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Prothrombin Time (PT)

A coagulation assay performed on citrated plasma with added phospholipids, calcium, and tissue factor reagent that detects extrinsic and common pathway deficiencies; it is unaffected by thrombocytopenia and contains a heparin inactivator.

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International Normalized Ratio (INR)

A unitless mathematical ratio used to standardize Prothrombin Time (PT) results across different laboratories and reagents, calculated as INR=Patient PTReference PT\text{INR} = \frac{\text{Patient PT}}{\text{Reference PT}}.

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PIVKA (Proteins Induced by Vitamin K Antagonism or Absence)

Inactive, non-carboxylated precursor forms of coagulation factors 22, 77, 99, and 1010 that accumulate when Vitamin K is absent or antagonized.

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Veterinary PIVKA Test (Thrombotest PT)

A modified PT assay with factor 55 and fibrinogen added to the reagent that detects decreased functional activities of factors 22, 77, and 1010, although it is not specific for PIVKA.

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Thrombin Clotting Time (TT / TCT)

An assay performed on citrated plasma where exogenous thrombin is added to cleave fibrinogen into fibrin, measuring functional fibrinogen concentration and detecting dysfibrinogenemia or fibrin polymerization inhibitors.

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Clauss Fibrinogen Assay (TTclauss)

A modified thrombin time assay commonly utilized by diagnostic laboratories to quantitatively measure functional plasma fibrinogen concentration.

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Russell Viper Venom Test (RVVT)

A coagulation assay using venom from Daboia species to directly activate factors 1010 and 55 in the presence of added phospholipids, primarily used to detect anti-phospholipid antibodies (lupus anticoagulant).

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<p>Viscoelastic Testing</p>

Viscoelastic Testing

A methodology providing kinetic recording of global hemostasis in whole blood (or plasma/PRP) without endothelial cells, assessing clot formation, platelet-fibrin interactions, and clot lysis via platforms such as TEG, ROTEM, and Sonoclot.

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Reaction Time (R) / Clot Time (CT)

The viscoelastic testing parameter (TEG RR, ROTEM CTCT, in minutes) defining the time until the initial onset of fibrin polymerization; shortened times reflect hypercoagulability, while prolonged times reflect hypocoagulability.

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K and Alpha (α) Angle

Viscoelastic kinetics parameters in TEG (analogous to ROTEM Clot Formation Time, CFTCFT) reflecting the rate of fibrin polymerization; a shortened KK and increased α\alpha angle indicate hypercoagulability.

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Maximum Amplitude (MA) / Maximum Clot Firmness (MCF)

Viscoelastic parameters (TEG MAMA in mm\text{mm} and GG in dyn/sec2\text{dyn/sec}^2; ROTEM MCFMCF in mm\text{mm}) measuring maximal clot strength dependent on platelet count, platelet function, and fibrinogen.

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<p>LY30 and LY60</p>

LY30 and LY60

Viscoelastic parameters measuring percentage clot lysis 3030 and 60 minutes60\,\text{minutes} after maximal clot strength (analogous to ROTEM CLI30CLI30 and CLI60CLI60), where elevated values indicate hyperfibrinolysis.

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Fibrin/ogen Degradation Products (FDPs)

Breakdown products resulting from plasmin cleavage of fibrinogen and soluble fibrin, measured in μg/ml\mu\text{g/ml} by latex agglutination immunoassays; increased with hyperfibrinolysis, hyperfibrinogenolysis, or decreased hepatic clearance.

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<p>D-dimers</p>

D-dimers

Specific neoantigen cleavage fragments generated exclusively by plasmin degradation of factor 13a13\text{a}-cross-linked fibrin, measured in ng/ml\text{ng/ml} via latex agglutination immunoassays.

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Tissue Plasminogen Activator (tPA)

An endothelial enzyme that converts plasminogen to active plasmin to trigger fibrinolysis; it is physiologically inhibited by plasminogen activator inhibitors (PAIs).

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Thrombin-Activatable Fibrinolysis Inhibitor (TAFI)

An enzyme activated by thrombin that suppresses fibrinolysis by directly inhibiting plasmin-mediated breakdown of fibrin clots.

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Alpha-2-Antiplasmin (α2-antiplasmin)

A primary circulating endogenous inhibitor (along with α2\alpha_2-macroglobulin) that rapidly inactivates free plasmin in plasma.

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Antithrombin (AT / ATIII)

An endogenous anticoagulant serine protease inhibitor measured by functional chromogenic assays; only decreased activity is clinically significant (resulting from decreased hepatic production, protein-losing nephropathy/enteropathy, or consumptive coagulopathies).

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Protein C

An endogenous anticoagulant protein evaluated via chromogenic assays; decreased levels occur from liver dysfunction, congenital deficiency, or Vitamin K antagonism, while increased activation is seen in Trauma-Induced Coagulopathy.