Antiplatelet/Anticoagulant/Thrombolytics Flashcards
Anticoagulants
disrupt coagulation cascade → suppress production of fibrin
Antiplatelets
inhibit platelet aggregation
Thrombolytics
promotes lysis of fibrin → dissolution of thrombi
MoA of Heparin
- binds antithrombin → leading to thrombin inactivation (and other factors) → end result is suppression of fibrin formation
- occurs w/in minutes of IV admin
AEs of Heparin
- Hemorrhage
- HIT if used > 4 days
- hypersensitivity
Antidote for Heparin
Protamine sulfate
What to monitor while on heparin
- H/H
- platelets
- aPTT (60-80 seconds while on hep)
Uses for Heparin
- Treat/prevent VTE
- Adjunct in acute coronary disease/STEMI
- Low dose, surgical prophylaxis
- Line flush (10 or 100 units/mL)
MoA of LMWH
- Subq/IV
- binds antithrombin → inactivates and suppresses formation of fibrin (same as heparin, just a smaller molecules so less of an effect)
AEs of LMWH
- bleeding
- thrombocytopenia
- hyperkalemia
antidote for LMWH
- Protamine sulfate
Uses for LMWH
- Non-emergency situations
- treat/prevent DVT after surgery
- Management of acute coronary syndrome
LMWH drugs
- Enoxaparin (1st choice)
- dalteparin
Fondaparinux (route/MoA/AEs/Uses)
- Subq
- MoA: selectively inhibits Xa by binding antithrombin
- AEs: bleeding
- Uses: treatment/prevention of DVT
Argatroban (route/MoA/AEs/Uses)
- IV/Subq
- MoA: directly inhibits thrombin
- AEs: bleeding
- Uses: treatment and prophylaxis of HIT and coronary artery thrombosis
MoA of Warfarin
- PO
- Vitamin K antagonist → blocks synthesis of vitamin K dependent clotting factors; long half life, effect takes several days
AEs of Warfarin
- bleeding
- teratogenic (avoid during pregnancy)
monitoring for warfarin
- PT and INR
- INR should be between 2-3 range
Uses of Warfarin
Prevention of:
- DVT
- Systemic arterial embolism
- MI and stroke
- Atrial fibrillation
- & if patient has prosthetic heart valve
Warfarin drug interactions
- w/ foods rich in vitamin K (decreases med effects)
- Additive effects if used in combo with other bleeding risk meds (ex. aspirin)
- Inhibitor drugs (ex. CCBs, -azole antifungals) will cause warfarin to remain longer in system → promote excess bleeding
- Inducer drugs (ex. Carbamazepine, smoking) cause warfarin to be excreted faster → decreased desired effects
Antidote for warfarin
vitamin K
RivaroXAban/ApiXAban
- oral anticoags
- MoA: direct Xa factor inhibitor
- AEs: bleeding; premature d/s increases risk of thrombotic events
- Uses: Post-op thromboembolism prophylaxis (esp. If knee surgery),
VTE tx,
A-fib,
Systemic embolism prophylaxis
DabigaTran
- PO
- MoA: Direct thrombin inhibitor
- AEs: bleeding/abdominal pain; premature d/s increases risk of thrombotic events
- Uses: DVT/PE prophylaxis & following parenteral therapy;
Decrease risk of CVA/systemic embolism in pts with AFib
Aspirin (route/MoA/Uses)
- PO
- MoA: irreversibly inhibits platelet aggregation by blocking cyclo-oxygenase (responsible for synthesizing protein that promotes platelet aggregation)
- Uses: Primary and secondary prevention of MI
ADP-Induced aggregation inhibitor drugs
- clopidogrel (prodrug)
- prasugrel
- both PO!
Clopidogrel/Prasugrel MoA/Uses
- MoA: inhibits binding of ADP to ADP receptors on platelets → which then inhibits GPIIb/IIIa complex → leads to inhibition of platelet aggregation
- Uses:
MI
Secondary prevention after acute STEMI, NSTEMI, unstable angina, PCI
if ASA intolerance
GPIIb/IIIa receptor blocker drugs
- Eptifibatide
- Tirofiban
- both IV!
Eptifibatide & Tirofiban MoA/Uses
- MoA: GP IIb/IIIa receptor inhibition → no platelet aggregation
- Uses: For acute/emergency situations (prevent ischemia for those with acute coronary syndrome; unstable angina, non-STEMI/STEMI)
- Adjunct to ASA or LMWH to reduce complication in PCI
Clopidogrel & CYP2C19
- People who are poor CYP2C19 metabolizers (determined by genetics) experience decreased anti-platelet effects due to poor conversion of clopidogrel into its active metabolite
- increase risk of CV events
Atleplase (class/MoA)
- thrombolytic agent
- IV
- MoA: convert plasminogen to plasmin → increase in digestion of fibrin clots
Alteplase (Uses & time considerations)
- Acute MI: Time from hospital arrival to IV admin < 30 minutes for best outcomes
- Acute ischemic stroke: Within 3 hours from onset of s/sx for best outcomes
- PE/VTE
Ferrous sulfate
20% of elemental iron
Ferrous fumarate
33% of elemental iron
Iron dextran
for those patients unable to tolerate/absorb oral iron or in cases of extensive chronic blood loss
what vitamin increases absorption of iron
Ascorbic acid aka Vit C
Oral iron AEs
- GI disturbances
- Staining of teeth
- Poisoning in children
IV irons AEs
- BBW: fatal anaphylactic reactions (test dose required)
Vitamin B12
- essential for DNA synthesis
- absorption requires intrinsic factor
- PO or
- IV/IM for patients with impaired B12 absorption
VB12 Deficiency
- megaloblastic anemia
- neurologic damage (if severe, may be irreversible)
- GI disturbances
Folic Acid
- essential factor for DNA synthesis
- combined with B12 to treat B12 deficiency
Epoetin (route/MoA/BBW)
- Sub q 3xs/week
- MoA: stimulates production of RBCs
- BBW: HTN; increase risk of death, MI, stroke and other CVD events if HgB >/= 11
Filgastrin aka Neupogen (route/MoA/Use)
- Subq/IV
- MoA: increases WBC production via receptors on progenitors
- Use: Bone marrow transplant;
Following chemotherapy to reduce febrile neutropenia;
HIV;
Aplastic anemia (investigational)
