VTE Flashcards
what is the most common causitive factor for VTE?
hospitalisation by a long way
cancer is probably second
what has the strongest evidence for extended DVT prophylaxis?
hip arthroplasty is probably the most rigorous evidence
how does the condition “activated protein C resistance” work?
how much does it increase the risk of VTE?
activated protein C inhibits activated procoagulant factors Va and VIIIa
a single point mutation in factor V interferes with this inhibition
this mutated factor V (position 506: Arg to Gly) is called factor V Leiden
the increase is about 7 fold
how does prothrombin 20210A mutation work?
this is a point mutation in the prothrombin gene
it increases prothrombin activity
it increases risk, although the amount is unclear
how does homocysteine modify clotting risk?
hyperhomocysteinaemia is apparently a risk for VTE, but no one really knows how that works
the increase is only about 2.5x increase
how does the clotting of nephrotic syndrome work?
there is a significant loss of antithrombin III
this can also occur in liver disease
it is the lack of this agent, which is an ANTI-THROMBIN, therefore can cause clot
it is pretty high risk
someone has anti-phospholipid antibody syndrome and has a venous event, what range?
APS and arterial event, what range?
for a venous event, aim 2-3. patient has to be on it for life
for an arterial event, aim 3-4 and also use aspirin
should be thinking about statins and plaquenil too
how would you anticoag in APS in pregnancy?
aspirin and UFH/LMWH
what vein demarcates the above and below knee nature of a DVT?
involvement of the popliteal vein is the major guiding factor.
If there is involvement of the popliteal vein, it is an above knee
what type of bleeding has a higher risk with dabigatran?
this can be associated with increased gastrointestinal bleeding.
that has been common across all the trials
this is balanced out against any major bleeds and any significant bleeds (which were less with the NOACs)
what are the 4 tumour types that are associated with high risk of intracranial bleed?
renal cell
thyroid
melanoma
choriocarcinoma
what is the usual treatment of superficial thrombophlebitis?
are there any times when this is altered?
usually this can be managed with warm compress and NSAIDs
however, when there is extensive superficial thrombophlebitis near the sapheno-femoral junction, this is actually close to the deep venous system
this should be managed as for DVT - with anti-coagulation
how do you manage some one with INR 7 with no bleeding present?
with hold warfarin and remeasure INR
how do you manage someone with INR 7 with no bleeding, but high risk for bleeding (such as known peptic ulcer)
cease warfarin, give 1mg oral or IV
how do you manage someone with INR 11 without bleeding?
cease warfarin, give 5mg oral or 1mg IV vitamin K
