pharm exam 2

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jakeg
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pharm exam 2
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2012-10-19 23:01:01
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  1. A1 Agonist
    BP
  2. B1
    HR
  3. B2
    HTN
  4. Hemostasis
    the physiologic process (coagulation cascade) by which bleeding is stopped
  5. Thrombosis
    the physiologic process by which a thrombus is formed.  Indicates abnormal hemostasis
  6. Thrombus
    • clot in a blood vessel or the heart
    • *Embolism= more dangerous
  7. Anticoagulants
    • Parenteral
    • -Heparin and heparin-related drugs
    • -Direct Thrombin Inhibitors
    • Oral
    • -Warfarin (Coumadin®)
  8. Heparin mech of action, admin, important issues
    • Mechanism of action: inactivates thrombin and other clotting factors indirectly by increasing activity of antithrombin à decreases clot formation especially in veins
    • Administration: parenteral (IV, SC) only.  Too large to cross membranes
    • Some important uses:Prevent postoperative venous thrombosis, Treat various embolic diseases (PE, stroke, DVT), Decrease clotting in heart-lung machines and dialysis units
    • -line patency
    • -during pregnancy (instead of Coumadin)
  9. Heparin part 2 sources, adrs, contradictions
    • Sources: beef lung and pig intestine
    • Important ADR’s:
    • Hemorrhage (the most common complication)  (platelet ct 150-400k)
    • Thrombocytopenia
    • Hypersensitivity reactions (from animal source)
    • Contraindications:
    • Active bleeding (<BP, >HR, <RBC, <HgB, ss of anemia, cold, SOB)
    • Thrombocytopenia
    • Certain surgeries/procedures (brain, spinal cord, eye)
    • Important drug interactions: drugs that also increase risk of bleeding (NSAIDs)
  10. Protamine sulfate
    Heparin overdose (binds to heparin to neutralize)
  11. aPTT
    • Monitor for Heparin
    • -Normal aPTT: 40 sec.
    • -Goal for anticoagulation: 1.5-2 x normal (60-80 sec.) (takes longer to clot)
    • -If aPTT too high, decrease dose
    • -If aPTT too low, increase dose
    • -Remember, to treat clots, the aPTT must be higher than normal without causing bleeding -Monitor aPTT q4-6 hrs. initially (then 1x/d)
  12. HIT
    • heparin induced thrombocytopenia
    • IGG mediated immune response to heparin
    • platelet count drops by 50+%
    • NEVER give heparin again
  13. Low Molecular Weight Heparin
    • enoxaparin (Lovenox)
    • -heparin preparations that are composed of smaller molecules than standard preparations. 
    • Differences from standard heparin:
    • -Does not inactivate thrombin like heparin, but does inactivate other clotting factors
    • -Is usually given SC only; rarely given IV
    • -Can be administered at home because…
    • -can be given on a fixed-dose schedule
    • -no need to monitor aPTT
    • -Less likely to cause thrombocytopenia
    • -Cheaper!  Because given at home
    • -if creatine clearance <30 only admin 1x/d(<dose)
  14. Factor XA Inhibitor
    • Example of heparin-like drug:
    • **Fondaparinux (Arixtra®)
    • -Smaller than LMWH
    • -Use to prevent and treat DVT/PE
    • ADR: Bleeding
    • -Do not use in patients with creatinine clearance below 30ml/min or weigh less than 50 kg
    • HIT not an issue
  15. Direct Thrombin Inhibitors
  16. oMechanism: inhibit thrombin directly whereas the heparin and heparin-like drugs inhibit indirectly
    • oExamples:
    • Bivalirudin (Angiomax®)- IV only; used with ASA to prevent clots in patients with USA undergoing coronary angioplasty
    • Lepirudin (Refludan®)- IV only; used for prophylaxis and treatment for thrombosis in patients with HIT
  17. Warfarin (Coumadin®) mech of action, admin, main use, ADR, contradiction
    • Mechanism of action: blocks the synthesis of 4 clotting factors (VII, IX, X, and prothrombin; which are vitamin K-dependent) à decreases clotting
    • Administration: oral
    • Main use is long-term prophylaxis for:
    • -venous thrombosis and DVT
    • -prosthetic heart valves
    • -atrial fibrillation
    • ADR: hemorrhage
    • Contraindications: pregnancy
  18. Wafarin Tx, drug interaction
    • Treatment in overdose: Vitamin K which is phytonadione (Mephyton/Aquamephyton)
    • Drug interactions: MANY!  Probably has the most drug interactions of any drug!
    • -Drugs that also cause increased bleeding/ or decreased clotting (Heparin, ASA)
    • (heparin used in conjunction until INR=2-3)
    • -Drugs that increase effects of warfarin (sulfonamide antibiotics)
    • -Drugs that decrease effects of warfarin- Example: anti-seizure drugs; rifampin, phenytoin, phenobarbitol, carbamazapine, dilantin
    • -Food-Green leafy veg
  19. INR
    • Monitoring for Warfarin
    • Lab test: INR (international normalized ratio)
    • INR is based on the prothrombin time (PT) and a correction factor.
    • -Normal prothrombin time (PT): 12 sec
    • -Anticoagulation goal (INR) for most patients: 2-3
    • *If INR too high, decrease dose
    • *If INR too low, increase dose
    • -Monitoring must be very frequent initially (daily) à monthly.
  20. Differences Between Heparin and Warfarin:
    • -Heparin must be given parenterally, warfarin is oral.
    • -Different mechanisms of action
    • -Heparin acts quickly, effects are brief. Warfarin acts more slowly, effects are prolonged. (3 d before full effects)
    • -Monitored differently (aPTT vs. INR)
    • -Antidotes for overdose are different
  21. Antiplatelet Drugs Three Main Groups
    • Aspirin (will cover more with pain module)
    • Adenosine Diphosphate Receptor Antagonists
    • *Clopidogrel (Plavix®)
    • *Ticlopidine (Ticlid®)*
    • Glycoprotein IIb/IIIa Receptor Antagonists
    • *Abciximab (ReoPro®)
    • *Eptifibatide (Integrilin®)*
    • *Tirofiban (Aggrastat®)*
  22. Aspirin (Bayer/Ecotrin)
    • Anti-platelets
    • -Inhibits platelet aggregation irreversibly
    • **Duration for the life of the platelets (7d)
    • -Used for prevention and treatment of MI, strokes, USA and occlusion of stents
    • ADR: bleeding, dyspepsia
  23. Clopidogrel (Plavix®)
    • Mechanism of action: causes irreversible blockade of ADP receptors on platelets à prevents ADP-stimulated platelet aggregation
    • Use: reduce risk of MI, stroke, cardiovascular death in those with CHD
    • Effectiveness: slightly better than aspirin
    • Cost: MUCH more than aspirin
    • ADR’s: generally well-tolerated, similar to aspirin such as dyspepsia
    • -May also cause TTP
    • Administration: PO
  24. Abciximab (ReoPro®)
    • Mechanism of action: causes reversible blockade of GP IIb/IIIa receptors on platelets à inhibits final step of platelet aggregation à decreases clotting
    • Effectiveness: member of most effective antiplatelet class available; AKA “super aspirins”.
    • Short-term uses:
    • -Acute coronary syndrome (unstable angina and evolving MI)
    • -Reduce reocclusion after angioplasty
    • **drug of choice for st segment elevation
    • Administration: IV
    • ADR’s: hemorrhage
  25. Thrombolytic Drugs Mech of action, Main use, Admin
    • "Clot Buster" breaks down new & existing clots (dangerous)
    • Mechanism of action: causes formation of plasmin, an enzyme that digests fibrin in clots that have already formed
    • Main uses:
    • -Acute MI
    • **best if begun ASAP within 4-6 hrs of symptom onset
    • -DVT
    • -Massive PE
    • Administration: IV
  26. Thrombolytics ADR, Absolute contradictions, Therapeutic uses w/ extreme caution, drug example
    • Main ADR:
    • -Hemorrhage
    • Absolute contraindications:
    • -Active bleeding
    • -Brain tumors
    • -Intracranial bleeding
    • -Suspected aortic dissection
    • Therapeutic uses with extreme caution:
    • -Ischemic stroke- must rule out intracranial hemorrhage with CT.  (“tPA” has been approved for this use)
    • ***Alteplase (Activase®)- “tPA”

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