Coagulant drugs and hypercoagulation
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What are the 4 classes of anti-coagulants?
- Heparin (UH, LMWH)
- Selective Factor Xa inhibitors
- Direct Thrombin Inhibitors (Dabigatran, etc.)
Of all the classes of the anti-coagulants, which are LEAST selective?
What is a warfarin? (what does it do?)
Vitamin K anagonist
What factors need Vit K??
Vit K is needed for synthesis of factors 2,7,9,10
What labs would you follow for the patient on warfarin and the patient on heparin?
The selective Factor Xa inhibitors are more difficult to monitor, how do we do this and how could we reverse these drugs?
- In general both PT and PTT are elevated but not as helpful as guidelines for monitoring therapeutic levels.
- There’s no reversal and even giving FFP won’t reverse the anticoagulation
What do the direct thrombin inhibitors do and how do we monitor/reverse them??
- They’ll bind directly to thrombin and inhibitor secondary hemostasis.
- There seems to be interest in some that are bivalent and some are univalent thrombin inhibitors.
- These drugs are monitored occasionally w/the PTT and not sure how reliable that is.
- They don’t require the same close monitoring that as patient w/warfarin.
- The downside is no reversal and FFP may not reverse the anticoagulation
What are the anti-platelet medications?
- Cyclooxygenase Inhibitors (ASA)
- Phosphodiesterase Inhibitors (Dipyridamole)
- Glycoprotein IIb/IIIa Inhibitors (Eptifibatide)
- ADP Receptor Pathway Inhibitors (Ticlopidine)
What do the Cyclooxygenase Inhibitors (ASA) do?
- Will block thromboxane A2 generation.
- And so they inhibitor platelet granule release and platelet aggregation.
Decrease platelet aggregation and remember they are used as prophylaxis against thromboembolic events and as an alternative to exercise in thallium myocardial imaging.
What do the GP2b3A inhibitors do??
- these will bind to that particular receptor to prevent the binding of fibrinogen.
- Used for ACS and as adjuncts in PCI
What do the ADP receptor pathway inhibitors do??
- Prevent receptor signaling and will irreversibly inhibit the ADP platelet activation pathway.
- As we know, they are also used in ACS and secondary prevention in thrombotic CVA in patient that can’t take ASA or in combo w/ASA in patient w/stent in place to prevent thrombus of the stent.
What are the Inhibitors of Anticoagulation & Fibrinolysis??
- Lysine analogues (Aminocaproic Acid & Tranexamic)
What does Protamine do??
- chemical analog of Heparin.
- It forms a complex w/heparin itself.
- It’s most active against unfractionated heparin but can also partially reverse the effects of low molecular weight heparin.
- Again it doesn’t work on the other classes of drugs (10A inhibitors and direct thrombin inhibitors)
What does Aprotonin do?
- Inhibit fibrinolysis.
- Promotes clot stability.
- Research has shown decrease in peri-op bleeding and PRBC administered in patient who get this but may increase post op renal failure so limited usefulness.
- Higher 30day mortality associated w/it’s use than Amicar.
What do the Lysine analogues (Aminocaproic Acid & Tranexamic) do??
- will bind and inhibitor plasminogen and plasmin.
- Decreased peri-op bleeding but doesn’t decrease post-op renal failure.
What are the three factors in Virchow's triad?
- Endothelial injury
- Abnormal blood flow
What are the types of hypercoagulable disorders??
- Inherited (thrombophilia)
- -----↓ Antithrombotic proteins
- -----↑ Prothrombotic proteins
- -----Myeloproliferative disorders
- -----Nephrotic syndrome
- -----Lupus anti-coagulant
What are the anesthetic implications for hypercoaguable disorders?
- Early ambulation, elastic stockings, and venous inflation devices.
- Patient will come to us for IVC filter and we’ll be sometimes part of that w/MAC anesthetic.
- Patient with hypercoagulable is at risk for thrombus formation.
- Surgery causes tissue trauma and puts patient at risk.
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