Coagulation Flashcards
Coagulation Factors:
- Firbrinogen
- Prothrombin
- Tissue Factor
- Calcium
- Proaccelerin, Labile factor
- Proconvertin, stable factor
- Antihemophilia Factor A
- Antihemopheliac Factor B, christmas factor
- Stuart factor
- Plasma thromboplastin Antecedent
- Hageman Factor
- Fibrin stabilizing factor
- Fitzgerald, williams flaujeac factor
The goal is to activate thrombin
NO thrombin
NO coagulation
Why do we need thrombin?
Activation of platelets
Conversion of firbrinogen to fibrin
Sustainment of coagulation by activating V, VII, and XI
Activation of XIII leading to clot stability
Coagulation Mechanism Overview
Proteins work in series of complexes that consist of enzymes, protein and ion cofactors and target substrates.
Target substrates become the enzyme for the ensuing complex
Factor Half Lives
Controlling the clot
Once initiated, coagulation must be restricted to the site of injury
Antithrombotic and fibrinolytic system
Plasmin is Key to fibrinolysis
Endothelial cells synthasize tPA and urokinase which convert plasminogen to plasmin
Antithrombotic Properties
- Anticoagulant Effects
- Thrombomodulin
- Antithrombin
- Protein C
- Protein S
- Heparin-like molecules
- Tissue Factor Pathway inhibitor
Importance of Vitamin K:
Vitamin K factors
2, 7, 9, 10
Importance of Vitamin K
Vitamin K proteins
Antithrombotic Proteins C & S
Sample Collectionf or Coagulation Testing:
NOT ACT
Minimal excitement
Clean venimpuncture
Centrifuge and remove plasma within 30 minutes
Test within 4 hours or freeze plasma
3.8% trisodium citrate at ratio of 1:9
Activated Clotting Time
Screens intrinsic and common pathways
Perform at 37C for consistent results
Requires patient platelets to support reaction
Point of care test
Activated Partial Thromboplastin Time
- Requires citrated plasma
- Screens intrinsic and common pathways
- Prolonged if factor activities <30%
- Not affected by thrombocytopenia
Prothrombin Time (PT)
- Requires citrated plasma
- Screens for extrinsic and common pathways
- Prolonged if factor activites
- Not affected by thrombocytopenia
- Sensitive indicator of Warfarin Toxicity
Fibrin / Fibrinogen Degradation Products - FDP
Detects circulating FDPs
FDPs are produced continously in health – rapidly cleared by liver so circulating values low
Measured to detect increased fibrinolysis associated iwth excessive coagulation
Increased production: DIC hemorrhage, thrombosis
Decreased Clearance: liver disease
Fibrin/fibrinogen Degradation Products -FDP
Requires citrated plasma
Antisera to fibrinogen fragments - bound to latex beads
2 dilutions - 3 possible results
D-dimer
Fibrinogen that has been converted to fibrin and cross linked by factor 13 gives rise to specific degradation products when cleaved by plasmin
Plasminolytic cleaveage products of cross linked fibrin are known as D-dimers
The presence of D-dimer fragments in circulation indicates that fibrin has been cleaved
Antithrombin (AT or AT3)
~70% of anticoagulant activity in plasma
In the presence of heparin binds 1:1 ratio with thrombin
Low molecular weight and lost with glomerular dz
Low AT results in increased coagulability and thrombosis
Disorders of Coagulation:
Coagulopathy type bleed
Delayed deep tissue hemorrhage, hematomas, hemorrhage into body cavities
Hemorrhage may be life-threatening within a few hours if not curtailed, especially if hemorrhage is occurring within a body cavitiy such as the abdoment
Prekallikrein Deficiency
Autosomal Recessive
Not usually associated with clinical bleeding
Identified in dogs and horses
Factor 12 deficiency
Hageman’s disease
No clinical Bleeding
Autosomal Inheritiance
Factor 7 Deficiency
Mild to no clinical bleeding
Autosomal inheritance
Factor 8 deficiency
Hemophilia A
Mild to Severe Bleeding
x-linked inheritance
Factor 9 Deficiency
Hemophilia B
Mild to severe Bleeding
x-linked inheritance
Acquired Defects in Coagulation proteins:
Vitamin K deficiency
Dietary inadequancy
Biliary obstruction
Malabsorption / Maldigestion
Liver disease
Drugs
Acquired Defects in Coagulation proteins:
Vitamin K antagonism
Coumarin
Warfarin, Indanedione, Sweet Clover Hay
Disseminated Intravascular Coagulation
Overwhelming activation and consumption of platelets and coagulation, antithrombotic, and fibrinolytic protiens
Occurs secondary to disorders that cause extensive tissue damage
TREATMENT:
Always attempt to identify and treat or remove the underlying cause
Supportive care is vital to maintain fluid volume and tissue perfusion
Congenital
History of prior bleeding?
Specificalyy asked questions about:
tail docking
dew claw removal
Teething
Ear cropping
Other surgical procedures or trauma
Do the parents or siblings have a history of bleeding problems
Acquired
Has the animal come in contact with toxins
Is the animal free roaming
Have ticks been removed recently
is there liver disease
Neoplasia
Medications
