More Drugz Flashcards Preview

Heme Block > More Drugz > Flashcards

Flashcards in More Drugz Deck (12):

Ginko biloba, garlic, and ginger

all show anti-platelet activity, important to remember



• Oral administration
• COX inhibitor
• Reduces platelet aggregation
o Irreversible acetylates COX-1 for platelet lifespan
o Reduces PGI2 production, this is bad initially because it inhibits platelet activation, but the endothelial cells its made in make more COX because they have a nucleus
o Stops TXA2 production, a pro-aggregation product, for the lifespan of the platelet because platelets have no nucleus and can’t recover
• Only used in low doses (COX-1 inhibition)
• High doses can produce adverse effects (COX-1/COX-2 inhibition)
o GI bleeding, dyspepsia, gut perforation, hepatic, renal problems
• Check to see if patient has aspirin-induced bronchospasm
• Ibuprofen is a reversible version of aspirin


Clopidogrel/ Ticlopidine/Pasurgrel

• Oral administration
• ADP-P2Y12 inhibitors
o Blocks ADP binding at the P2Y12 receptor on the platelet
o Normally: P2Y12 receptor binds ADP and inhibits adenylyl cyclase; lower cAMP means less cAMP inhibition of platelet activation; so inhibition of this raises cAMP levels to inhibit platelet aggregation
o P2Y1 receptor also plays a role by inducing a shape change/aggregation, but both are needed for activation so blocking on is sufficient



o Pro-drug that depends on CYP2C19 activity for activation; poor metabolizers at risk for having little to no effect
o Prasugrel is essentially the same thing



o No need for activation
o Extremely toxic metabolites; effects seen in first 3 months
• Agranulocytosis – lack of all granulocytes, immunosuppression
• Neutropenia – low neutrophils, immunosuppression
• Thrombocytopenia – low platelets, bleeding problems
• Thrombolytic thrombocytopenic pupura – anemia+thrombocytopenia, not fun
• Anemia – low RBCs



• Phophodiesterase inhibitor
o Induces cAMP elevations to block arachidonic acid release, thus reduce TXA2 levels
o Releases prostacyclin to induce adenylyl cyclase activity to raise cAMP levels and stop platelet aggregaton
• Well tolerated, adverse effects generally resolve with time


Abciximab/ Eftifibatide/Tirofiban

• IV administration
• GPIIb/GPIIIB inhibitor
o Blocks fibrinogen/vWF binding to the GPIIb/GPIIIB receptor
• This stops crosslinking between platelets to prevent clot formation
• Works best when >80% of GPIIb/GPIIIB receptors are blocked
• Major risk of bleeding (thrombocytopenia) and anaphylactic rxns with all three
• Abciximab irreversibly binds (persistence up to 2 weeks)
• Eftifibatide/Triofiban bind reversibly (persistence is 4 hours)



• Oral administration
• PAR-1 inhibitor
• Reversible but long T1/2 makes it essentially irreversible; persistence of up to 4 weeks
• Major risk of GI bleeding; difficult to reverse


Proamine sulfate

o Derived from fish sperm (don’t give to people with fish allergy)
o Neutralizes heparin (its basic, heparin is acidic) through ternary complex disruption
o Excess is also an anti-coagulant!
o Infusion reactions can happen if infused too quickly
• Flushing, vasomotor collapse, rash, others


Fresh frozen plasma or Vitamin K1 supplementation

warfarin antidotes
o If hemorrhage, give these (usually controls it 3-8 hours after injection)


• Prothrombin complex concentrate

warfarin antidote
o Contains uninhibited clotting factors prepared from plasma
o Extremely rapid onset



• Factor Xa inhibitors
o Enoxaparin is LMWH
o Direct inhibitors – bind to factor Xa to inhibit it
• Apixaban/Rivaroxaban – simply bind to any factor Xa to inhibit it
• Both are metabolized by CYP enzymes
o Indirect inhibitors – bind to ATIII to permanently change its structure increasing its affininty for factor Xa by 300x
• Fondaparinux – simple copy of ATIII binding area of heparin
• Major worry is uncontrolled bleeding w/out reversible agent
o T1/2 is extremely low so its not a major problem