Clotting disorders Flashcards
How do platelets and clotting factors usually circulate
In inactive form
Vascular injury leads to
vascular spasm
Plt adhesion mediated by vWF
coagulation cascade
What are PT/INR measure
integrity of extrinsic (factor VII) and common pathway
Used for Warfarin check
What does PT represent
time in seconds for plasma to clot after you have added calcium and thromboplastin (activates the extrinsic pathway)
What causes a prolonged PT
Deficiencies or inhibitors of clotting factors within the extrinsic or common pathways
Why was INR created
to assess patient’s PT in comparison to a geometric mean of 20+ healthy males and females at THAT specific lab
What does aPTT measure
Integrity of intrinsic (VIII, IX, XI, XII)and common pathways of the coag cascade
What is PTT (partial thromboplastin time)
time in seconds it takes for patients plasma to clot after adding Calcium (phospholipid that activates the intrinsic pathway)
What is the clotting factor where intrinsic and extrinsic all come together
Factor Xa! It activates thrombin and causes a clot to form
What type of patient would we worry about if they have a deficient PT
Young, healthy patient; suspect something autoimmune, (liver disease, DIC)
Those are the patients you should prob preform a mixing study on
-Elderly with deficient PT you think, ok this might just be age related, or they could be on warfarin
What are the outcomes of a mixing study with aPTT
- if PTT corrects when you add “normal blood”: Pt has a factor deficiency* present in intrinsic path (8, 9, 11, 12). Essentially, when you add normal blood, the deficiency corrects bc you add those deficient factors in!
- If PTT stays prolonged: it must be something that is destroying any blood that comes in (drugs like heparin; AI hemophilia A; Lupus anticoagulant)
If PTT corrects and you determine it is 2/2 an intrinsic path factor deficiency, what should you do
Get a clotting factor assay to determine which factor is involved, and determine whether it is acquired or congenital
What is Lupus anticoagulant (LAC)
Prolonged PTT
MC in young females- do NOT have to have SLE!
Suspect if pt: No bleeding Hx or has a clot and baseline prolonged PTT before you started the anticoag
-AutoAbs are directed at phospholipid binding proteins, causes Ab mediated thrombosis
What are the outcomes of a mixing study with PT
PT corrects: deficiency in extrinsic path (factor 2, 7, 10, fibrinogen), liver disease
PT stays prolonged w/ prolonged PTT: inhibitor of extrinsic path, factor V inhibitor
Deficiencies in clotting factors found by PT or aPTT mixing studies are MCC by
Supratherapeutic warfarin (rat poison)
Etiologies that cause inhibition of all pathways found in PT/PTT mixing studies include (what causes to “stay prolonged”)
LAC
nonspecific factor inhibitors w/ lymphoproliferative d/o
monoclonal protein disorder (cause autoimmunity)
What is warfarin
Inhibits vitamin K dependent clotting factors (7, 9, 10, protein C&S)
Pregnancy category X
What can a supratherapeutic INR 2/2 warfarin lead to
elevated PTT
- for every 1.0 increase in PT, 16-17 sec. increase in PTT
- If pt comes in w/ an INR of 8 and they aren’t bleeding, hold dose then decrease
- if pt comes in w/ INR 4, hold dose 1-2 days then continue at same dose
- if pt comes in vomiting and can’t take warfarin, PR/INR will be high
2 MC reasons to use warfarin are
- AFIB (goal INR 2-3)
- VTE (goal INR 2-3)
- Mechanical valve replacement (goal INR 2.5-3.5)
What is UFH
Thrombin (factor IIa) and Xa inhibitor
Large molecule NOT well absorbed subQ, and can cause HIT
What is LMWH
Stronger Xa inhibit, only mild IIa (thrombin) inhibition w/ longer half life
Derived from UFH but defractionated to make a smaller molecule more well absorbed subQ
*SAFE for pregnancy= LOVENOX
(lovenox is dosed by weight)
-generally not good for those that are obese or w/ CKD/ESRD
Do you need to get labs or monitor LMWH
No! no need
But if you want to monitor your pt, you can check efficacy with anti-Xa levels 3-4 hours after Lovenox
-The only people you may need to monitor are obese or very thin patients
What is Fondaparinux
synthetic factor Xa inhibitor that causes ATIII to change in coag cascade. 17 hr half life
NO REVERSAL AGENT*
What are DOAC’s
Rivaroxiban/Epixaban: direct anti-Xa
Dabigatran: oral direct thrombin inhibitor used for AFib and VTE