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TT
Thrombin Time
Measures the ability of thrombin to convert fibrinogen to fibrin and is useful in the evaluation of circulating antioagulants (pathologic inhibitors)
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TT is prolonged in what siutations
- Hypo & Dys fibrinogenemia
- Patients on heparin therapy
- Circulating FDP's
- Pathologic circulating inhibitors
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Mixing Studies
Patient plasma is mixed with normal plasma in varying concentrations, then incubated for 2 hours.
Corrected = Deficiency
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Reptilase Time
- Similar to TT, except it uses reptilase instead of thrombin.
- Not affected by heparin
Prolonged with: A & Dys fibrinogenemia
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Russell's Viper Venom
Test is based on the premise that LA/aPL activity is enhanced in the presence of reduced phospholipids. The reagent contains dilute RVV, CaCl, & phospholipids. The reagent is added to PPP. RVV activates FX resulting in a clot formation.
If Las/aPLs are present, the patients dRVVT is longer than that of the normal control
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List inherited coag disorders
- vWD
- TTP
- FV Leiden
- Hemophilia
- Bernard-Soulier
- Glanazmanns Thrombasthenia
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List acquired coag disorders
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Coumadin affect which coag factors
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Heparin inactivates which coag factors
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What is the purpose of mixing studies
To identify a factor deficiency
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What coag factors are missing in aged serum
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What is 5M Urea test useful for
It can qualitatively if a patient is deficient in FXIII by obersving dissolution of a clot after 24 hours of incubation
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What factor deficiency is present given a PT of 15 seconds, a PTT of 60 seconds, a mixing study using aged serum and absorbed plasma that corrected both in the case of the former but corrected neither in the case of the latter?
F 10 is likely deficient: F10 is present in aged serum and is in the common pathway so that both the PT and the PTT should be affected. F10 is not present in adsorbed plasma
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Extrinsic Pathway Coag Factor
Factor 7
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Intrinsic Pathway factors are:
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Common Pathway Factors are:
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What is the normal range for: PT
11-13 seconds
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What is the normal range for: aPTT
22-32 seconds
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List congenital disorders that affect the NUMBER of platelets
- Bernard-Soulier
- May-Hegglin anomaly
- TAR syndrome
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Increased destruction of platelets may be caused by:
- ITP (post viral illness in children, spontaneous in adults)
- Posttransfusion purpura (1week post, antibodies against P1A1 are produced) - Treat with plasmaphoresis without exchange and gamma globulin
- Isoimmune Neonatal Tfhrombocytopenia (antibodies against baby's plateelts)
- Drug induced ITP (Quinine or Heparin)
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vWd Type 1 lab results
Decreased: vWF Ag, RIPA, & F8
PTT might be prolonged
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vWD Type 2a lab results:
Decreased RIPA
Normal Factor 8 and PTT
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vWD Tfype 2B lab results:
- Increased RIPA
- Decreased Platelets
Normal Factor 8 & PTT
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vWF Type 2N lab results
Decreased Factor 8
Normal; vWf: Ag, R:Co
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vWD Type 3 lab results
- Increased PTT & PFA
- Decreased: vWF Ag
- Absent: RIPA
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Glanzmann's Thrombasthenia lab results
- Decreased: GPIIb/IIIa
- Increased: BT & PFA
- Abnormal: ADP aggregation, thrombin, collagen, & epinephrine
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Bernard-Soulier lab results
- Decreased: Plts, GPIb
- Increased: BT & PFA
- Abnormal: thrombin aggregation
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ITP Lab Results
Severe Thrombocytopenia: <20K
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Afibrinogenemia lab results
Increased: BT, PT, PTT, TT, RT
Absent: Fibrinogen
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Dysfibrinogenemia lab results
Increased: TT, RT,
Normal: Fibrinogen
*may have prolonged PT & PTT
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Hypofibrinogenemia lab results
- Increased: TT
- Decreased: Fibrinogen
Normal: PT & aPTT
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PT Measures what pathway and is prolonged with what deficiencies
Extrinsic Pathway
1,2,5,7,9,& 10
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PTT measures what pathway and is prolonged with what deficiencies
Intrinsic Pathway
2,5,8,9,10,11,12 & fibrinogen (1).
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