Antiplatelet/Anticoagulant/Thrombolytics Flashcards

1
Q

Anticoagulants

A

disrupt coagulation cascade → suppress production of fibrin

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2
Q

Antiplatelets

A

inhibit platelet aggregation

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3
Q

Thrombolytics

A

promotes lysis of fibrin → dissolution of thrombi

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4
Q

MoA of Heparin

A
  • binds antithrombin → leading to thrombin inactivation (and other factors) → end result is suppression of fibrin formation
  • occurs w/in minutes of IV admin
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5
Q

AEs of Heparin

A
  • Hemorrhage
  • HIT if used > 4 days
  • hypersensitivity
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6
Q

Antidote for Heparin

A

Protamine sulfate

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7
Q

What to monitor while on heparin

A
  • H/H
  • platelets
  • aPTT (60-80 seconds while on hep)
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8
Q

Uses for Heparin

A
  • Treat/prevent VTE
  • Adjunct in acute coronary disease/STEMI
  • Low dose, surgical prophylaxis
  • Line flush (10 or 100 units/mL)
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9
Q

MoA of LMWH

A
  • Subq/IV
  • binds antithrombin → inactivates and suppresses formation of fibrin (same as heparin, just a smaller molecules so less of an effect)
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10
Q

AEs of LMWH

A
  • bleeding
  • thrombocytopenia
  • hyperkalemia
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11
Q

antidote for LMWH

A
  • Protamine sulfate
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12
Q

Uses for LMWH

A
  • Non-emergency situations
  • treat/prevent DVT after surgery
  • Management of acute coronary syndrome
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13
Q

LMWH drugs

A
  • Enoxaparin (1st choice)
  • dalteparin
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14
Q

Fondaparinux (route/MoA/AEs/Uses)

A
  • Subq
  • MoA: selectively inhibits Xa by binding antithrombin
  • AEs: bleeding
  • Uses: treatment/prevention of DVT
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15
Q

Argatroban (route/MoA/AEs/Uses)

A
  • IV/Subq
  • MoA: directly inhibits thrombin
  • AEs: bleeding
  • Uses: treatment and prophylaxis of HIT and coronary artery thrombosis
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16
Q

MoA of Warfarin

A
  • PO
  • Vitamin K antagonist → blocks synthesis of vitamin K dependent clotting factors; long half life, effect takes several days
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17
Q

AEs of Warfarin

A
  • bleeding
  • teratogenic (avoid during pregnancy)
18
Q

monitoring for warfarin

A
  • PT and INR
  • INR should be between 2-3 range
19
Q

Uses of Warfarin

A

Prevention of:
- DVT
- Systemic arterial embolism
- MI and stroke
- Atrial fibrillation
- & if patient has prosthetic heart valve

20
Q

Warfarin drug interactions

A
  • 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
21
Q

Antidote for warfarin

A

vitamin K

22
Q

RivaroXAban/ApiXAban

A
  • 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
23
Q

DabigaTran

A
  • 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
24
Q

Aspirin (route/MoA/Uses)

A
  • 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
25
Q

ADP-Induced aggregation inhibitor drugs

A
  • clopidogrel (prodrug)
  • prasugrel
  • both PO!
26
Q

Clopidogrel/Prasugrel MoA/Uses

A
  • 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
27
Q

GPIIb/IIIa receptor blocker drugs

A
  • Eptifibatide
  • Tirofiban
  • both IV!
28
Q

Eptifibatide & Tirofiban MoA/Uses

A
  • 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
29
Q

Clopidogrel & CYP2C19

A
  • 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
30
Q

Atleplase (class/MoA)

A
  • thrombolytic agent
  • IV
  • MoA: convert plasminogen to plasmin → increase in digestion of fibrin clots
31
Q

Alteplase (Uses & time considerations)

A
  • 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
32
Q

Ferrous sulfate

A

20% of elemental iron

33
Q

Ferrous fumarate

A

33% of elemental iron

34
Q

Iron dextran

A

for those patients unable to tolerate/absorb oral iron or in cases of extensive chronic blood loss

35
Q

what vitamin increases absorption of iron

A

Ascorbic acid aka Vit C

36
Q

Oral iron AEs

A
  • GI disturbances
  • Staining of teeth
  • Poisoning in children
37
Q

IV irons AEs

A
  • BBW: fatal anaphylactic reactions (test dose required)
38
Q

Vitamin B12

A
  • essential for DNA synthesis
  • absorption requires intrinsic factor
  • PO or
  • IV/IM for patients with impaired B12 absorption
39
Q

VB12 Deficiency

A
  • megaloblastic anemia
  • neurologic damage (if severe, may be irreversible)
  • GI disturbances
40
Q

Folic Acid

A
  • essential factor for DNA synthesis
  • combined with B12 to treat B12 deficiency
41
Q

Epoetin (route/MoA/BBW)

A
  • Sub q 3xs/week
  • MoA: stimulates production of RBCs
  • BBW: HTN; increase risk of death, MI, stroke and other CVD events if HgB >/= 11
42
Q

Filgastrin aka Neupogen (route/MoA/Use)

A
  • Subq/IV
  • MoA: increases WBC production via receptors on progenitors
  • Use: Bone marrow transplant;
    Following chemotherapy to reduce febrile neutropenia;
    HIV;
    Aplastic anemia (investigational)