56 terms

Hematology Coag

Factor I
Fibrinogen; Genetic deficiency; Increase PT, PTT, TT
Decrease Fibrinogen Assay; Cryo is best source of fibrinogen
Factor II
Prothrombin, Rare, Increase PTT, PT; Treat with FFP or prothrombin complex
Factor III
Tissue thromboplastin; no deficiencies; Found in all tissues
Factor IV
Calcium; Low enough to interfere with clotting would be incompatible with live; only non protein factor
Factor V
Labile Factor; Mild systemic bleeding; Increase PT, PTT; treat with FFP
Factor VII
Stable factor; Moderate to severe bleeding; Increase PT, Normal PTT; Treat with FFP
Factor VIII
Antihemophili Factor; Hemophilia A; Normal PT and Bleed time; Increase PTT; Only factor produced by vessel endothelial cells instead of liver
Factor VIII: C
Coagulation; part of the intrinsic system
Factor VIII: VonWillibrand Factor
Cause platelets to adhere to vessel wall; Normal PT; sl. increase PTT, Increase Bleed time
Factor IX
Christmas factor; Hemophilia B; Normal PT; increase PTT
Factor X
Stuart-Prower factor, Rare; Increase PT, PTT; treat with FFP or PCC
Factor XII
Hageman Factor; Thrombosis not bleeding; Normal PT, Increase PTT; Treat with FFP
Factor XIII
Fibrin-Stabilizing factor; Mild bleeding; poor wound heeling;
All tests normal except abnormal urea solubility; treat with Cryo
High Molecular weight Kininogen, Usually no symptoms; Normal PT, Increase PTT
Pre Kallikrein; Kallikrein is best plasminogen activator; No symptoms; Normal PT, Increase PTT; PT corrects when Increase incubation time
Vitamin K Dependant
Inhibited by coumadin, absent in absorbed plasma
Consumed in clot
Not found in serum because are consumed in the clot
Labile factor
V and VIII
Intrinsic Path
Measured by PTT
Extrinsic Path
Measured by PT
Common Path
X, V, II, I
Factor V is a cofactor for Factor X which then converts prothrombin to thrombin
Measured by both PT and PTT
Present in Serum and Aged plasma
All but consumed factors
Factor present in Serum
Serum lacks
Present in absorbed plasma
All but the vitamin K factors
Normal Plasma
Contains all factors
Vitamin K factors: II, VII, IX, X; VII affected first; Mostly extrinsic; Overdose give Vit K or FFP; can't be used on Pregnant women; takes days to affect
Inhibits formation of thromboxane A2 and platelet aggregation; affects plts; oral; GI bleeding; will prolong bleeding time
Combines with AT and rapidly inhibits thrombin (IIa) and Xa, XIIa, XIa and IXa; stops clotting; Overdoses treated with protamine sulfate because it inactivates heparin. Does not work if pt has AT; PTT tests; Increase TT; Pt can be sl. increase;
Breaks up existing clot
Rabbit Thromboplastin and Calcium; NR - 9-12.5 may vary by lab; Factors measured: I, II, V, VII, X; used to monitor coumadin
Plasma mixed with commercial phospholipid substitute and activator of factor XII (actin) plus Ca. NR 20-35. Measures all factors except: VII and XIII
Plasma mixed with thrombin; Less than 20; measures only the conversion of fibrinogen to fibrin
Reptilase Time
Snake venom converts fibrinogen to fibrin w/o thrombin
If the reptilase is normal and TT is increase heparin is present
Latex particles coated with FSP fragments D and E; detectes DIC, Thrombosis, primary fibrinogenolysis
Trypsin inhibitor to prevent invitro fibrinolysis
D Dimer
Crosslinked fibrin and therefor is positive only in secondary fibrinolysis; if D-dimer is neg and FSP is positive, pt has primary fibrinogenlysis; More specific for DIC and Thrombosis
Bleeding time
Reference range 212 minutes; prolonged in disorders of plt function such as vonWillibrand, bernard soulier, Glanzmann disorder, and aspirin ingestion
Mixing studies
If the prolonged PTT correct with the 1:1 mixture, a factor deficiency is suspected and appropriate factor assays should be performed. Aged serum corrects the PTT in factor IX, XI, and XII deficiencies; Absorbed plasma corrects the PTT in factor VIII: C; XI and XII deficiencies
Hemophilia A
Sex linked; Increas PTT, Normal PT; Factor VIII assay; Assay corrects with absorbed plamsa; Normal Bleed time
Normal and platelet function normal; autosomal deficiency;
Sl. Increase PT and normal PT; Increase Bleed time; no plt aggregation with ristocetin; treat with DDVAP or cryoprecipitate
Hemophilia B
Sex linked; Increase PTT, Normal PT; Factor IX assay; Not as severe as Hemo A
Increase PT, PTT, TT, FSP
decrease Fibrinogen, platelet count
+ D Dimer
Schistocytes on blood smear
Liver dz
Acquired; plasma production decrease; Increase PT and PTT
Liver function test; Factor VIII normal or increase; Treat with FFP
Vit K deficiency
Diet or antibiotic; PT eleveated; multiple factors present
Lupus Anticoagulants
Pt develops an autoantibody against phospholipds on plt surfaces. Increase PTT. 50:50 Mix of pt plasma with normal plasma doe snot correct; confirm with Plt Neutraliztion; DRVVT and anti-phospholipd assay
Protein C or S deficiency
Protein C binds to activated factors V and VIII and stops clotting. Act as natural anticoagulants, Both proteins are Vit K dependent so can't assay them til 2 weeks after stopping coumadin; associated with lie long blood clots that can be fatal
Factor V Leiden Mutation
W/O the ability to inhibit activated factors V and VIII, clots form; Most common genetic thrombophilia (excess clotting)
Plasma is mixed with known excess of thrombin or Xa in the presence of heparin. Amount of thrombin left after neutralization inversely proportional to AT
Chronic/ Acute ITP
Chronic: Young women; Autoantibody to plts causes increased destruction by the spleen. Acute: Children after infection; Acquired
Toxic damage to endothelial cell. HUS seen in children after infection; Decrease Plt, schistocytes
Bernard Soulier disorder
Defective glycoprotein 1b; inhibits plt adhesion to vWF; Giant platelets
Glanzmann's thrombasthenia
Defective glycoprotein IIb/IIIa inhibits platelet aggregation; increase bleeding time; clot retraction absent
Plt count is reduced if pt is on methotrexate
Factor VIII level
can distinguish liver dz from DIC; low in DIC
Short draw
Will prolong coag test. Sodium Citrate will be present and not bound to calcium and will use up calcium in test.