NBME 18 Question about Coagulation Factor II

[Shrugged]

Hello,
Trying to get information about what makes Prothrombin (coag factor II) affect PT. Since there are weird rules about 'reproducing' NBME exam questions I cannot specifically state the question but I will summarize.
A pt is on Heparin, a day later gets Warfarin, the do a blood test and find that his PTT is elevated but PT and INR are normal. The question asks what is the best explaination for normal PT and INR in this patient.

They wanted long half-life of factor II.

I am not understanding:
1) how this answers the question: since the only difference between PT and PTT is the measurement intrinsic vs extrinsic pathways and II is part of the combined pathways (I.E. a deficiency will cause an increase in both)
and
2) how does Factor II half-life play into these measurements?

It almost seems like a typo (best answer is Warfarin didn't have enough time to kill Factor VII) or the usual NBME way of answering a question they didn't actually ask. Any information or insight would be really helpful!
Thanks in advance.

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[Interferon Gamma]

Hello,
Trying to get information about what makes Prothrombin (coag factor II) affect PT. Since there are weird rules about 'reproducing' NBME exam questions I cannot specifically state the question but I will summarize.
A pt is on Heparin, a day later gets Warfarin, the do a blood test and find that his PTT is elevated but PT and INR are normal. The question asks what is the best explaination for normal PT and INR in this patient.

They wanted long half-life of factor II.

I am not understanding:
1) how this answers the question: since the only difference between PT and PTT is the measurement intrinsic vs extrinsic pathways and II is part of the combined pathways (I.E. a deficiency will cause an increase in both)
and
2) how does Factor II half-life play into these measurements?

It almost seems like a typo (best answer is Warfarin didn't have enough time to kill Factor VII) or the usual NBME way of answering a question they didn't actually ask. Any information or insight would be really helpful!
Thanks in advance.

yea I agree... this doesnt make any sense
The reality is if the patient is on Heparin at anticoagulation levels both aPTT and PT would be prolonged as heparin affects the common pathway... We just use aPTT because at prophylactic doses of heparin aPTT would be prolonged...
In my opinion, I think the answer should actually be too low of a heparin dose... It wouldnt be too low of a warfarin dose because it didnt have time to exert its action yet as It was given on the second day... I feel like they tried to test the long half-life concept of factor II but they werent able to deliver a proper question over it...

 

[Necrosis03]

Warfarin inhibits the synthesis of factors 2, 7, 9, and 10. PT lab assays have anti-heparin reagents which prevent the effects of heparin on results. PT time is only a measurement of the time it takes for the cascade to complete following artificial activation of Factor 7 from the extrinsic pathway. But because Factor 2 has a long half life, high levels of circulating Factor 2 (and already activated Factor 2) will continue to complete the cascade at a fast rate and show normal PT times, even with minimal Factor 7 levels. A fire will still spread quickly if there is a lot of brush, even if you reduce the size of the spark. This is in part because activated Factor 2 self sustains by also activating Factors 8 and 11 leading to intrinsic pathway activation as well. PT will only prolong when all of the already synthesized vitamin K dependent factors are degraded, Factor 2 being the most crucial.

Whereas, Heparin activates AT, which directly inhibits the already formed Thrombin (Factor 2) + Factors 12, 11, and 9. Thrombin additionally activates factors 11 and 8. So by increasing AT, you directly inhibit Factors 12, 11, 9 and also reduce the activation of 11, 8; leading to instant and widespread inhibition of multiple intrinsic pathway factors (12, 11, 9, 8), so prolonged PTT will be the first detectable measurement for heparin usage and is evident early because Heparin works immediately via inhibition of multiple intrinsic factors. PT can also become prolonged but will not prior to PTT, because a high enough dose of Heparin needs to be used to significantly inhibit the common pathway, but at which point both PT and PTT will be elevated.

TLDR:

PTT measures cascade completion following intrinsic pathway stimulation. Heparin directly inhibits many of the intrinsic pathway factors, which is why it is the earliest detectable and best measurement for Heparin levels. PT would not be good for measuring heparin levels as it bypasses many of the inhibitory effects stemming from enhanced AT (And it has anti heparin reagents). PT measures cascade completion following extrinsic pathway stimulation. Warfarin reduces the synthesis of Factors 2 and will therefore prolong PT time, making it a good test for measuring Factor 2 serum levels / Warfarin levels. PTT would not be a good measure because even in vitamin K deficient states, PTT may remain normal (possibly due to Factor 2's ability to activate and speed up the intrinsic pathway), making it hard to accurately measure thrombin levels when reduced amounts still have the ability to stimulate the pathway and mimic normal PTT times.