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Summer-Pharm II--PA

What are the two types of Thrombi? Arterial- mainly platelets in a white clot sits on atherosclerotic plaque and Venous- Mainly fibrin and RBCs occurs when procoagulant stimuli overwhelm the natural protective mechs
What are the 3 components of Virchow's Triad? 1) Venous stasis (i.e. bed-rest) 2) Hypercoagulable state (i.e. pregnancy) 3) Endothelial damage (i.e. HTN)
What do Arterial Thrombi tend to cause? MI, limb gangrene, CVA
What do Venous Thrombi tend to cause? DVT, PE, Postphlebitic syndrome
What are some medical mpatient groups at especially high risk for DVT? Gen surgery, GYN surgery, Urol. surgery, neuro surgery, stroke, Hip fractures, Hip or knee athroplasty, major trauma, spinal injury, critical care pts
What are classes of antithrombic agents? Which is the most indicated? Most indicated: Anticoagulants Antiplatelet drugs Thromboltic drugs
The intrinsic pathway of the clotting cascade involves_____ damage, while the extrinsic pathway involves____damage surface, tissue
Prothrombin Time (PT)is defined as: Time for blood to clot in presence of thromboplastin and CaCl measures: factors X IX VII II (1972)
What does INR do? Standizes the PT (especially between hospitals) and should not normally be >1.1-1.2 INR = [Patient's measured PT (norm: 10-13s)] _____________________________________\ mean normal PT
What is an aPTT? activated Partial Thromboplastin Time -used to monitor heparin -measures factors XI IX VIII VII of the intrinsic pathway and II V and X of the extrinsic
What effects aPTT other than heparin? Warfarin, Thrombin inhibitors, Liver disease, or factor deficiency
What is D-dimer? -a breakdown product of fibrin -marker of: -fibrinolysis -active inflammation -prothrombotic states (DVT, PE, DIC)
What is the normal range for D-dimer? <0.5μg/mL or <200ng/mL
What are the two MC used LMWH? Enoxaparin & Deltaparin
What are differences between UFH and LMWH? ratio of Xa to IIa equal in hep; 3-4:1 in LMWH Hep less predictable dosing (30-70% bioavailable; LMWH 80-99%) clearence hepatic and renal in heparin, only renal in LMWH
What is the MOA of UFH? Binds ATIII causing confirmational change to make ATIII 1000-100000x more potent to inhibit clotting factors IIa and Xa
How many 1/2 lives must go by before a drug is totally eliminated? 5 1/2
When is IV heparin given? When is SQ given? to treat a clot; to prevent a clot
What is the target aPTT for UFH? 60-85s for PE, venous thrombus 50-70s for acute coronary
What adjustment should be made to LMWH if Cr Clearence <30? renal adjustment to dose; usu cut in 1/2
What levels are used to monitor a Patient on a LMWH? -SCr -Anti Xa -platelets
What adverse drug reactions occur in only UFH? in both UFH and LMWH? UFH only: alopecia and osteoporosis UFH and LMWH: Bleeding, HIT, pain at injection site
What agent reverses UFH and LMWH? HOW? Protamine-binds to (-) charged sulfa groups and cleaves at random Xa- 100% neutralized IIa- 32-44% neutralized (reverses up to 60% of LMWH effects)
What is Fondaparinux? A pentassacharide anticoagulant medication that selectively binds Xa with reversible binding
What are indications for Fondaparinux? -hepatic failure -patient compliance (1/2 life = 17-21 hours) -no reports of HIT -favored in orthopedics
What are CI of Fondaparinux? -up-coming surgery -not ideal for renal failure (renal clearence)
Why might Fondaparinux be dangerous versus UFH/ LMWH? Although NovoSeven may have potential at reversal, there is no recognized reversal agent
What agent is used as a "bridging therapy", usually after a heparin? Warfarin
What are the Vitamin K-dependent factors? 1972: X IX VII II
How is Vit K involved in clotting? Reduced Vit K and a Prothrombin precursor interact to form oxidized Vit K and Prothrombin
Why does it take about 17 days to get patients to a steady state on Warfarin? The 1/2 lives of the clotting factors are long (up to 100 hours)
What is the target INR for PE? valve replacement? Afib? Afib and PE: 2-3, Valve replacement: 2.5-3.5
How is Warfarin administered? metabolized? admin: PO metab:CYP2C9 and CYP1A2
Factors that increase bleeding risk -intensity of anticoag -concommitant conditions -concommitant meds -quality of management
Risk factors for bleeding include? age >75, treated HTN, ASA/ NSAIDs, Heart disease, female, severe anemia, malignancy, DDI, Risk of falling, Carrier of CYP2C9*3 gene, Hx of stroke, alcoholism or liver disease, DM, anemia
How should INR be adjusted if it is <5.0 (no bleeding) lower &/or omit a dose or no change
How should INR be adjusted if it is 5.0-9.0 (no bleeding)? Vit K hold Warfarin until therapeutic INR
How should INR be adjusted if it is >9.0? hold Warfarin, IV Vit K with fresh plasma or prothrombin complex or recombinant factor VIIa
Why shouldn't Vitamin K be given liberally? Administration of a large dose of Vit K may result in warfarin resistance for up to a week or more
What is HIT? -type I and type II - an immune-mediated adverse reaction to UFH or LMWH
How is HIT diagnosed? -antiP4/ heparin Antibodies -90% have thrombocytopenia
Why is HIT still an issue in the absence of thrombocytopenia? Pts will still have endothelial damage that will predispose them to clots
How is thrombocytopenia defined? Platelets <150,000/mm3 or reduced by 50% from baseline
How long are the antibodies present? How long does it take for platelet recovery? 85-100 days for Antibody circulation 4-14 days for platelet recovery
What is rapid-onset HIT? HIT that occurs d/t a second exposure to heparin/ LMWH within 100 days
Why do the thromboembolic complications of HIT contribute to high morb/mortality? Without appropriate treatment ~1/2 patients will develop a new thrombosis
The risk of HIT left untreated, even when platelet counts return to normal is: Thrombosis
The clinical presentation of HIT includes: -DVT/PE -CVA MI -skin lesions at injection sites -Warfarin-induced venous limb gangrene -acute limb ischemia -acute systemic reactions following IV bolus
Diagnostic Tests for HIT include: Why are 100% specific methods not always used? SRA (C-Serotonin-release assay) -100% specific--time consuming HIPAA (Heparin-induced platelet activation assay)-100% specific--Time consuming ELIZA (enzyme-linked immunosorbancy assay) -80% effective--faster results
What non-pharmacological patient care should be implimented? -Update allergy profile -Stop all Heparin products -Stop all platelet infusions (as they amplify the building of clot complexes)
What Direct Thrombin Inhibitors are FDA approved? Which is not, but may be used in treatment? FDA approved: Argatroban and Lepirudin Non-FDA: Bivalrudin
What pentasaccharide may be used in treatment of HIT? What is it indicated for? CI? Fondaparinux- approved for tx/prophylaxis of thromboembolism (DVT, PE) -often used in orthopedic surgery -Heparin allergy CI-Afib and valve replacement--d/t lack of supportive data
What are requirements for the prescription of Warfarin? -not a monotherapy (or initial therapy) - platelets must recover (to baseline) -aPTT therapeutic (must have 2 therapeutic readings)
What are indications for Agatroban? CI? -prophilaxis/ tx thrombosis in patients with HIT CI: hepatic failure -undergoing PCI (percutaneous coronary intervention/ cath)
What are indications for Lepirudin? -in pts w/ HIT and associated thromboembolic disease to prevent further complications
What are indications for Bivilrudin? Patients at risk of or w/ HIT or HITTS or undergoing PCI (cath)
Agatroban: what is it? MOA Onset Agatroban: what is it? synthetic thrombin inhibitor MOA: Reversible binding to thrombin catalytic site Onset: 1-3 hrs
Argatroban: Metabolism & Elimination 1/2 life aPTT indication Metabolism/ Elimination: CYP450 3A4 metab/ Hepatobiliary elimination 1/2 life-24-50 min aPTT indication- aPTT q 2 hrs, 60-85s, have two therapeutic readings
Argatroban: Advantages -No interaction with Heparin-dependent Ab -Short 1/2 life -Easily monitored -No dosage adjustment in renal failure
Argatroban: Disadvantages -Falsely prolongs INR (scares docs) -needs dosage adjustment in hepatic failure -lack of data for SQ administration (only IV)
Lepirudin: What is it? MOA Onset Lepirudin: What is it? A polypeptide direct thrombin inhibitor MOA: Irreversibly binding to catalytic sites of fibrin and thrombin Onset: 3-4 hrs
Lepirudin: 1/2 life elimination aPTT indications Lepirudin: 1/2 life: 40-120 min elimination:renal aPTT indications-aPTT q 4hrs -titrate 20% -2 therapeutic readings
Lepirudin: Advantages -no interactions with Heparin-dependent Ab -Short 1/2 life -Easily monitored -no dosage adjustment in hepatic failure -may be administered SQ
Lepirudin: Disadvantages -Antihirudin Ab form in patients treated for >5 days (increase anticoagulants) -renally cleared -expensive
Bivalrudin: Approved for MOA Clearence 1/2 life Bivalrudin: Approved for: treatment of HIT patients undergoing PCI MOA: bivalent direct thrombin inhibitor -reversible inhibition -proteolytically cleaved by thrombin Clearence: independent of organ function 1/2 life: 25 minutes
Summary of FDA approval: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of FDA approval: Fondaparinux-no Lepirudin-yes Argatroban-yes Bivilrudin-no
Summary of direct antithrombin inhibition: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of direct antithrombin inhibition Fondaparinux-no Lepirudin-yes Argatroban-yes Bivilrudin-yes
Summary of route of elimination: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of route of elimination Fondaparinux-renal Lepirudin-renal Argatroban-hepatic Bivilrudin-enzyme cleavage
Summary of 1/2 life: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of 1/2 life Fondaparinux-17-21 hr Lepirudin-1.3 hr Argatroban-39-51 min Bivilrudin-10-24 min
Summary of Antidote Available: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of Antidote Available: all = no
Summary of Monitoring: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of Monitoring: Fondaparinux-anti-Xa Lepirudin-aPTT/ ECT Argatroban-aPTT/ ACT Bivilrudin-aPTT/ ACT
Summary of {regnancy Category: Fondaparinux Lepirudin Argatroban Bivilrudin Summary of Pregnancy category: all B
Created by: tgodin4