Flashcards in Coagulation Factors Deck (33):
What factor is associated w/ the extrinsic pathway?
What are your enzymatic factors? Non enzymatic
Xa,XIa,XIIa, IXa, VIIa, I,IIa, II (prothrombin),
• III(tissue factor, factor III, thromboplastin), Va, VIIIa, calcium
(factor IV, platelets
what are you vit K dependent cofactors?
2, 7, 9, 10 (they are neg. charged)
what is needed for efficient coagulation?
Ca2+, platelet membrane, and factor V.
What activates the hemostastis cascade?
Tissue factor activates the 2ndary hemostasis cascade
what acts on plasminogen to create plasmin?
Tissue plasminogen activator.
When can you see a significant increase in fibrinogen concentration? decrease?
Inflammation, increase in dehydration.
• Decrease! consumption due to hypercoagluation, decrease
production by liver.
what does antithrombin act on?
Xa, Thrombin, IXa " inhibits the conversion of prothrombin to
thrombin, inhibits conversion of fibrinogen to fibrin by thrombin
What does thrombin feed back on
IX, VII, VIIIA, Va,
How are antithromin and heparin relate?
Heparin binds to antithrombin causing a conformational change and exposes the thrombin binding site. Thrombin binds to antithrombin and heparin floats away. The thrombin antithrombin complex is cleared by the phagocytic system.
expression of which cofactor initiates coagulation?
tissue factor III
which factor drives amplification? and which 4 does it affect?
thrombin promotes amplification of 2ndary hemostasis and it acts on factor VII, factor XI, factor VIIIA, and factor Va.
what are the four vitamin K dependent factors?
II, VII, IX, X (2,7,9,10)
what 3 components contribute to coagulation efficiency?
Platelet membrane, Ca2+ and factor V
what cofactor required for antithrombin to inactivate thrombin?
what are 2 major end producs of fibrinolysis?
FDPs and D Dimers
To collect a sample of blood for coag test- what tube do you put blood into?
avoid collection w/ a heparinized catheter, and place in sodium
What is aPTT and ACT (test the intrinsic pathway)?
to clot formation. if prolonged" deficiency or inhibition of any intrinsic or common pathway factor, or heparin therapy " citrated plasma + contact activator + Ca2+ + PLT phospholipid substitute- requires 70% deficiency of factor before prolongation is detected!! more sensitive that ACT
• ACT- activate clotting time- measures time for fibrin clot formation in non anticoagulated whole blood + contact activator. requires 95% deficiency of factor before prolongation is detect
what is PT? (extrinsic pathway)
prothrombin time, measures time for fibrin clot formation in
citrated plasma + tissue factor + Ca2+ PLT phospholipid substitute:
o sig. of prolonged time= factor VII deficiency (good screen test for vitK b/c shorted 1⁄2 life of all factors) and also
deficiency /inhibition of common pathway factor. requires 70% deficiency of factor before prolongation
what is TT test?
Thrombin time- measures time for fibrin clot formation in citrated
plasma + thrombin
• significance if prolonged- abnormality of fibrinogen;
inhibitors of fibrin formation (heparin, FDPS)
o fibrinogen decrease w/ consumption due to hypercoagulation (excessive conversion of fibrinogen to fibrin) or w/ decreased production by the liver
what are PIVKA proteins?
proteins induced by vitamin K antagonism- increased in vit K
what can an increase in FDPs demonstrate?
(w/ fibrinogen and soluble fibrin) increased fibrinolysis, severe
internal hemorrhage w/ fibrinolysis, and decreased clearance of
FDPs by liver.
when FDPs are pathologically increased, what do they do to platelet function?
inhibit platelet function and fibrin polymerization (not when normal though)
what causes increase in D-Dimers?
degredation of crosslink fibrin; increase fibrinolysis, severe internal
hemorrhage w/ fibrinolysis, decreased clearance of FDP by liver
how does citrated plasma differ from blood?
No RBC, WBC, platelets. Decreased calcium (chelated by citrate
what can happen to antithrombin in hypercoaguable state?
decreased in consumption- as with DIC and pulmonary thromboembolism or w/ loss- PLE, PLN.
• remember w/out Antithrombin III heparin is useless in its action (heparin activates antithrimbin III resulting in inhibition of thrombin and activated coagulation factors IXa, Xa, Xia, and XIIa in liver
what are the patterns of hemorrhage?
major hemorrhages often in multiple sites- SQ, IM hematomas, large areas of echymosis.;
• bleeding into cavities(thorax and abdomen), joints blood in stool, vomit, urine.
major cause of Vitamin K deficiency? clinical signs?
warfarin toxicity- inhibits vitamin K epoxide reductase- reduction in
factors II, VII, IX, and X.
• anemia, weakness, pallor, hypovolemia, shock, dyspnea, lameness,
neuro signs- signs often from bleeding into respective cavities,
what are lab findings w/ warfarin toxicosis?
regenerative anemia, variable leukogram PLT count normal (not platelet issue), prolonged PT, apt, ACT (why- b/c II, VII, IX, and X are involved in both pathways) PIVKA positive .
What is DIC? causes
syndrome from continued activation of coagulation and fibrinolysis-
results in thrombosis of microvasculature, depletion of coagulation
factors and PLTS leading to bleeding.
• causes- induction or exposure of tissue factor or other activators of
of coagulation" sepsis, tissue necrosis, neoplasia; endothelial damage exposing collagen’ proteolytic enzymes (snake venom, trypsin released during pancreatitis); stagnant blood flow
what are the 2 phases of DIC?
Hypercoaguable state (phase 1)- thrombosis and ischemic necrosis
and organ dysfunction
• Consumptive phase (phase 2)- consumption of PLT, coag factors
and Antithrombin III leading to bleeding.
o increased fibrinolysis w/ increased bleeding.
what are lab changes seen in DIC?
consumptive phase- thrombocytopenia (mild/moderate), prolonged
PT, aPTT, decreased fibrinogen concentration, increased FDP and D dimers, decreased Antithrombin, hemorrhagic anemia, schistocytes (from fibrin formation)