Clotting Disorders and Hypercoagulable Flashcards
Prothrombin Time and INR
time in seconds it takes the plasma to clot after adding calcium and thromboplastin
- Extrinsic pathway
- Monitoring warfarin
Partial Thromboplastin Time (PTT)
time in seconds for plasma to clot after adding phospholipid and calcium
-Intrinsic pathway
What if PT and PTT are decreased?
ignore, not clinically relevant
IF you do a mixing study and adding normal blood doesn’t change the fact that clotting time is prolonged (PTT), what’s the issue?
inhibitor
Ex. heparin, Lupus anticoagulant
IF you are doing mixing studies and adding normal blood normalizes the clotting time (PTT), what’s the issue?
factor deficiency of the intrinsic pathway
Ex. VIII, IX, XI, XII
next step–> get clotting factor assays to determine which is missing
What should you suspect if patient is a young female, no history of bleeding, clot with baseline prolonged PTT and not on anticoagulation?
Lupus anticoagulant
Mixing Study: PT
If it corrects–> deficiency of factors II, VII, X, or fibrinogen
If it doesn’t correct–> inhibitors (ex. warfarin)
Warfarin
- interferes with “1972”
- Pregnancy category X
Most common indications:
- Afib
- VTE
- Mechanical valve (INR 2.5-3.5)*
Unfractionated Heparin (UFH)
- inhibits IIa (thrombin) and Xa
- Not absorbed subcutaneously
Low Molecular Weight Heparin (LMWH)
- inhibit Xa and some IIa
- Lovenox is safe in pregnancy
- Well absorbed subcutaneously
- Doesn’t need to be monitored (unless pt. is very thin or obese)
contraindications: ESRD
Fondaparinux
- inhibits Xa
- binds to antithrombin III
- Use this is pt has pork allergy***
Rivaroxaban (Xeralto), Apixaban (Eliquis)
direct Xa inhibitors
Dabigatran (Pradaxa)
direct thrombin inhibitor
Reversals?
Warfarin–>vitamin K
Heparin, Lovenox–> Protamine
Virchow’s Triad
- Venous stasis
- Venous trauma
- Hypercoagulable state
Deficiency in what molecules causes hypercoagulable state?
- Protein C
- Protein S
- both of these will give 10x more likelihood to form clot - Antithrombin III
- 20x more likelihood to form clot
-usually these help prevent clots, but if they are deficient you will clot more
What are Protein C and S dependent on?
Both are vitamin K dependent
Factor V Leiden Mutation
-mutation with single substitution makes this resistant to inactivation by Protein C so continues to clot
- MC in whites
- Heterozygous 5x risk
- Homozygous 80x risk
Prothrombin Gene G20210A mutation
Causes greater function of prothrombin factor II
Hyperhomocysteinemia
- Increased risk of VTE in arteries
- Deficiency of Vitamin B6, B12, and folic acid
Tx: Vitamin B12 and folate
Antiphospholipid Ab Syndrome
- Recurrent arterial or venous thrombosis
- Loss of fetus
- (+) antiphospholipid antibodies (ex. anticardiolipin antibody)
LAC and Anticardiolipin A
- antibodies (IgG, or IgM) against phospholipids
- More arterial clotting
- Sneddon Syndrome [livedo reticularis + neurologic abnormalities]
Best test for suspected VTE?
Doppler ultrasound**
-more accurate above the knee
Best test for PE?
CT angio
What if you suspect PE but the patient has renal insufficiency, pregnant, or can’t do iodine?
VQ
Why does Warfarin initially increase the likelihood of clot?
initially drops Protein C and S (which prevent clotting normally)
If a patient has had their first VTE how long should you put them on anticoagulation?
3-6 months
First VTE and hypercoagulable state do they need lifelong AC?
No
IF patient has recurrent VTE and is hypercoagulable do you do lifelong AC?
Yes
When should you give Tissue plasminogen activator (tPA) to a PE patient?
significant hemodynamic instability and RV strain
Patient has a superficial clot. What’s the tx?
NSAIDs/ASA + warm compress
When should you consider anti-coagulation in superficial throbophlebitis?
- > 5cm
- Very symptomatic
- If occured while on ASA
