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Cardio Drugs > Anti-platelet and anti-coagulant drugs > Flashcards

Anti-platelet and anti-coagulant drugs Flashcards

1
Q

What is Heparin’s Mechanism of action?

A

Catalyzes the anti-thrombin-protease “suicide substrate” reaction

  • Inactivation of factor IIa is mediated by the formation of ternary complex heparin, ATIII, thrombin **unfractionated heparin
  • LMWH-> inadequate to form ternary complex-> little antithrombin activity
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2
Q

How do we administer heparin?

A
  • not oral
  • Does not cross the placenta or accumulate in brest milk
  • ** IV-> pts w/ active thrombosis or PE
  • ** Activated partial thromboplastin time (aPTT) should be measured before next admin. of heparin to adjust the dose
  • SubQ-> pts requiring low dose prophylaxis
  • Antidote for excess heparin: Protamine sulfate
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3
Q

Adverse effects of heparin?

A
  • Major bleeding-> incre. risk w/ aPTT > 2.5x norm
  • Osteoporosis, vertebral fractures
  • Heparin resistance* -> elevated factor VIII, antithrombin def, increased clearance, monitor w/ antiXa assay
  • Heparin-induced thrombocytopenia (HIT)
    a. ) immune-onset after 5-10 days, Abs present, thrombosis
    b. ) non-immune, immediate onset, Abs present; no thromb
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4
Q

Describe the characteristics of Enoxaparin

A
  • LMWH
  • inhibit factor Xa
  • longer half life (-4.5h)
  • Less frequent dosing
  • Increased bioavial when admin subQ-> no blood tests
  • Less HIT-> but don’t give to ppl with HIT
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5
Q

When do we use Enoxaparin?

A
  • Prevention of deep venous thrombosis in postop

- Tx of acute venous thromboembolic disease & acute coronary syndromes

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6
Q

Describe the characteristics of Fondaparinux

A
  • LMWH
  • Synthetic analog of the pentasaccharide binding sequence of heparin
  • Pharmacokinetics: long 1/2 life: 17-21H
  • Renal clearance
  • SubQ
  • No HIT
  • No blood test
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7
Q

What are the adverse effects of LMWH?

A

-Severe uncontrolled HTN and bleeding

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8
Q

What are the Direct thrombin inhibitors?

A

Desirudin, Bivalirudin, Argatroban

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9
Q

What are the characteristics of Desirudin?

A
  • Recombinant form of hirudin
  • Independent of antithrombin III
  • Reach and inactivate fibrin-bound thrombin to thrombi
  • Does not cause thrombocytopenia
  • t1/2-2 hours following subQ admin
  • Renal clearance
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10
Q

When do we use Desirudin?

A

-DVT post elective hip replacement

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11
Q

Describe Bivalirudin

A
  • synthetic peptide congener of hirudin
  • short 1/2 life- 25 minutes
  • renal and metabolic clerance
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12
Q

When do we use Bivalirduin?

A

-Coronary angioplasty, Patients w/ HIT

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13
Q

Describe Argatroban

A
  • synth. deriv. of arginine
  • blocks catalytic site of soluble and clot-bound thrombin
  • admin. IV
  • Used in pts w/ heparin-induced thrombocytopenia (HIT)
  • 1/2 life: 40-50 minutes
  • monitored by aPTT
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14
Q

Adverse effects of argatroban

A
  • Hemorrhage
  • Allergic reactions
  • Prolongs PT-when used with Warfarin
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15
Q

What are the Oral anitcoagulants?

A

-Warfarin

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16
Q

Describe warfarin

A
  • Binds vit. K reductase -> blocks 2,7,9,10 Vit. K dependent coag factors(procagulant factors) and (protein C and S-anticoagulant)
  • Peaks 2-8 hours after an oral dose
  • 1/2 life 25-60 hours
17
Q

What VIt. K dependent coagulation factor is affected first by Warfarin and what effects can it have?

A
  • Earliest inhibition in anticoagulant protein C (anticoagulant factor) -> moves into procoagulant state-> pro clotting (not what we want)
  • Narrow therapeutic window-> monitor with INR/prothrombin time
18
Q

What are the adverse effects of warfarin??

A
  • Bleeding-> INR >4,
  • Treat with vit K (delayed response)
  • Birth defects + abortion (use heparin)
  • Skin necrosis
19
Q

What are the new direct oral anticoagulants?

A

Dabigatran (thrombin inhibitor)

-Xa inhibitors (Rivaroxaban, Apixaban, Edoxaban)

20
Q

Dabigatran

A

Direct thrombin inhibitor

21
Q

Rivaroxaban, Apixaban, Edoxaban

A

Thrombin inhibitor

22
Q

What are the fibrinolytic drugs?

A

Ateplase (activase)

23
Q

What is the MOA of ateplase?

A

Physiologically t-PA activates plasminogen to plasmin that is bound to fibrin of thrombus -> dissolution of the clot

24
Q

Characteristics of Ateplase?

A
  • recombinant tissue plasminogen activity
  • 1/2 life 5 minutes in plasma
  • IV bolus then infusion
  • contraindications for pregnant women, uncontrolled HTN
25
Q

When do we use Ateplase?

A
  • acute MI
  • Acute ischemic stroke
  • PE
  • central venous catheter occlusion
26
Q

What are the anti-platelet agents?

A

-Aspirin, Clopidogrel, Prasgrel, Abciximab, Tirofiban, Eptifibatide

27
Q

What is the MOA of aspirin?

A
  • Cyclooxygenase (COX) inhibitor -> prevents the TXA2 from forming
  • Platelets have no nucleus and cannot regenerate COX-> effects lasts the life of the platelet (7-10 days)
  • Endothelial cells-> regenerate COX -> PGI2-> restoring anti-thrombtic effect
  • Low dose -> selectively inhibit platelet COX, sparing endothelial COX
28
Q

What do we use aspirin for?

A
  • primary prophylaxis for MI

- 2ndary prevent for vascular events following heart disease

29
Q

What are the adverse effects of aspirin?

A

-Bleeding, increase risk of peptic ulcer disease

30
Q

What are the ADP receptor antagonists?

A

-Clopidogrel, Prasugrel, Ticarelor

31
Q

Describe the MOA for the ADP receptor antagonists that end in -grel

A

-Irreversibly inhibits the binding of ADP to its receptor on platelets, inhibits platelet aggregation

32
Q

Describe the MOA for Ticarelor

A

-Reversibly inhibits the binding of ADP to its receptor on platelets, inhibits platelet aggregation

33
Q

Adverse effects for ADP receptor antagonists

A
  • Bleeding
  • Dual anti-platelet therapy: ADP inhibitor + aspirin
  • Triple therapy: Oral anticoagulant + ADP inhibitor + aspirin
34
Q

What are the platelet GP IIb/IIIa receptor blockers

A

-Abciximab, Tirofiban, Eptifibatide

35
Q

Describe Abciximab and what it’s used for

A
  • monoclonal ab directed against GPIIb/IIIa complex

- Used for coronary angioplasty and acute coronary syndrome

36
Q

Describe Tirofiban and what it’s used for

A

-non-peptide analog main recognition seq of GPIIb/IIIa receptors -> occupies receptor inhibits binding

37
Q

Eptifibatide

A

-Analog of the sequence -> mediates the binding of fibrinogen to the receptor -> occupies receptor inhibits binding

38
Q

adverse effects of GP IIb/IIIa receptor blockers

A

Bleeding

Cardio Drugs (5 decks)

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