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Cardio > Anticoagulant, Antiplatelet and Thrombolytic Drugs > Flashcards

Anticoagulant, Antiplatelet and Thrombolytic Drugs Flashcards

1
Q

spectrum of thromboembolic disease

A
  • myocardial infarction
  • stroke
  • transient cerebral ischemic attack
  • acute coronary syndrome
  • atrial fibrillation
  • deep venous thrombosis
  • pulmonary embolism
  • peripheral arterial disease

*DVT and PE are collectively referred to as venous thromboembolism (VTE)

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2
Q

venous thrombosis

A
  • most likely in primary hypercoagulable states (defects in coagulation proteins or the fibrinolytic system)
  • or secondary hypercoagulable states, where there is vessel injury or blood flow abnormalities
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3
Q

arterial thrombosis

A
  • associated with the involvement of vessel wall pathology and platelets
  • for example: erosion or rupture of an atherosclerotic plaque in a mildly stenosed coronary artery can result in thrombus formation followed by an acute coronary syndrome
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4
Q

three factors that predispose to thrombus

A
  1. endothelial injury
  2. abnormal blood flow (stasis)
    •hypercoagulable states (inherited or acquired)
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5
Q

antiplatelets drugs

A
  • aspirin
  • clopidogrel
  • abciximab
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6
Q

aspirin

A
  • antiplatelet
  • COX 1/2 inhibitor, preventing platelet aggregation
  • analgesic, antipyretic, antiplatelet, prophylaxis following MI, transient ischemic attacks and stroke
  • bleeding. allergic reaction, overdose, respiratory alkalosis and metabolic acidosis
  • irreversible block of prostaglandin (thromboxane A2 - platelet aggregation and local vasoconstriction) synthesis
  • primary (less well established) and secondary MI prevention/bleeding (well established)
  • side effects: dyspepsia, GI bleeding, allergic reactions, overdose: respiratory alkalosis and metabolic acidosis
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7
Q

clopidogrel

A
  • antiplatelet
  • irreversible inhibition of AP-mediated platelet aggregation
  • prevention of ischemic events, dual antiplatelet therapy with ASA for PCI/stents
  • bleeding, thrombotic thrombocytopenic purpura

•blocks ADP receptor, P2Y12
-irreversibly blocks one of the platelet ADP receptors (P2Y12 ) responsible for activation of the Gp IIb/IIIa receptor. Recall that fibrinogen binds the Gp IIb/IIa receptors on platelet surfaces to promote platelet aggregation
•for people who can’t take aspirin, or in dual therapy with aspirin in ACS bleeding, TTP, stents
•side effects: bleeding, thrombotic thrombocytopenic purpura (TTP)

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8
Q

abciximab

A
  • antiplatelet
  • binds and inactivates platelet glycoprotein IIb/IIIa receptors for fibrinogen
  • antiplatelet, antithrombotic
  • bleeding, thrombocytopenia

•monoclonal aty blocks GP iiB/IIIa to block platelet aggregation, mouse/ human
-Gp IIb/IIIa receptor antibody that inhibits the final step of platelet activation: the cross- linking of platelets by fibrinogen binding to Gp IIb/IIIa receptors
•for PCI anticoagulation/bleeding
•side effects: bleeding, thrombocytopenia

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9
Q

anticoagulant drugs

A
  • unfractionated heparin
  • low molecular weight heparin
  • fondaparinux
  • bivalirudin
  • argatroban

*the onset of pain during anticoagulant therapy signifies the occurrence of bleeding until proven otherwise!

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10
Q

heparin (UFH)

A
  • indirect anticoagulant
  • binds and activates antithrombin III, leading to inactivation of Factor Xa and thrombin
  • parenteral anticoagulant, reversed by protamine sulfate
  • bleeding, thrombocytopenia “HIT”
  • monitor with aPTT
  • facilitates interaction of AT with clotting factors Xa and IIa
  • for prevention and treatment of VTE and PE bleeding, HIT
  • neutralize with protamine
  • does not cross placenta
  • side effects: bleeding, thrombocytopenia (HIT)
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11
Q

low molecular weight heparin

A
  • enoxaparin
  • indirect anticoagulant, monitoring not required
  • less effect on thrombin
  • binds and activates antithrombin III, leading to inactivation of Factor Xa and thrombin
  • parenteral anticoagulant, reversed by protamine sulfate
  • bleeding, thrombocytopenia “HIT” (less risk)

•facilitates interaction of AT with Xa
for prevention and treatment of VTE and PE bleeding, HIT
•response in unpredicatable in renal insufficiency
•protamine does not completely neutralize
•side effects: bleeding, less risk of thrombocytopenia (HIT)

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12
Q

fondaparinux

A
  • indirect anticoagulant, monitoring not required
  • binds and activates antithrombin III and inactivates Factor Xa
  • parenteral anticoagulant, reversed by protamine sulfate
  • bleeding
  • pentasaccharide portion of heparin, binds to AT to inhibit Xa
  • for prevention and treatment of VTE and PE bleeding, HIT
  • cannot be used in the presence of renal insufficiency
  • side effect: bleeding
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13
Q

bivalirudin

A
  • anticoagulant
  • direct thrombin inhibitor
  • for PCI/bleeding
  • side effects: bleeding
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14
Q

argatroban

A
  • anticoagulant
  • direct thrombin inhibitor - reversible
  • for management HIT
  • side effects: bleeding
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15
Q

oral anticoagulants

A
  • Vitamin K antagonists

* warfarin

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16
Q

warfarin

A
  • direct acting anticoagulant
  • VKA - blocks synthesis of factors VII, IX, X and II, monitor with PT (INR), Vitamin K to reverse
  • prevention of VTE and PE/bleeding, teratogenic (crosses placenta), drug and food may alter the response
  • side effects: bleeding, increased risk for thrombosis in early treatment due to decrease in protein C (warfarin skin necrosis)
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17
Q

non Vitamin K antagonist oral anticoagulants

A
  • dabigatran
  • rivaroxaban
  • apixaban
  • idarucizumab (dabigatran reversal)
18
Q

dabigatran

A
  • oral, non Vitamin K anticoagulant
  • direct thrombin inhibitor, monitoring not required
  • stroke prevention in AF/bleeding, VTE prophylaxis
  • side effects: bleeding
19
Q

rivaroxaban

A 
•oral, non Vitamin K anticoagulant
-apixaban
-edoxaban
•Xa antagonist
•stroke prevention in AF/bleeding, no antidote, VTE prevention
•side effects: bleeding
20
Q

idarucizumab

A
  • monoclonal antibody to dabigatran and its active metabolite
  • used for dabigatran reversal
21
Q

limited use anticoagulants

A
  • bivalirudin

* argatroban

22
Q

bivalirudin

A
  • limited use anticoagulant
  • direct thrombin inhibitor
  • for PCI/bleeding
  • side effects: bleeding
23
Q

argatroban

A
  • limited use anticoagulant
  • direct thrombin inhibitor - reversible
  • for management of HIT
  • side effects: bleeding
24
Q

thrombolytic drugs

A

•tissue plasminogen activator (tPA)

25
Q

tissue plasminogen activator (tPA)

A
  • thrombolytic, fibrinolytic
  • action forms plasmin from plasminogen to lyse thrombi
  • ACS (STEMi) when PCI not possible (12 hr window) ischemic stroke (3 hour window), clot dissolution and in selected cases of DVT/bleeding, recent surgery
  • side effects: bleeding
26
Q

drug interactions with warfarin

A

•any substance or condition is potentially dangerous when used with warfarin if it alters:

  • the uptake or metabolism of warfarin or Vitamin K
  • the synthesis, function or clearance of any clotting factor or cell involved in hemostasis or fibrinolysis
  • the integrity of any epithelial surface
  • rifampin
  • antimicrobials
  • alcohol
  • metronidazole
  • amiodarone
  • aspirin and other NSAIDs
27
Q

rifampin - drug interactions with warfarin

A
  • CYP2C9 induction

- loss of anticoagulant action

28
Q

antimicrobials - drug interactions with warfarin

A
  • decrease gut flora that synthesize Vitamin K or CYP inhibition
  • increases anticoagulant action
29
Q

alcohol - drug interactions with warfarin

A

-CYP2E1 inhibition with acute use of alcohol, induction with chronic use of alcohol
-increased anticoagulant effect, decrease of anticoagulant effect after cessation of alcohol use
•metronidazole (antimicrobial)
-decreased metabolic clearance of S isomer of warfarin with increased anticoagulant effect

30
Q

metronidazole - drug interactions with warfarin

A
  • antimicrobial

- decreased metabolic clearance of s isomer of warfarin with increased anticoagulant effect

31
Q

amiodarone - drug interactions with warfarin

A
  • decreased metabolic clearance of R and S isomers of warfarin
  • marked potentiation of anticoagulant effects
32
Q

aspirin and other NSAIDs - drug interactions with warfarin

A
  • antiplatelet action

- risk of bleeding is increased >5X

33
Q

APIXABAN & RIVAROXABAN - INHIBITORS OF CYP3A4 OR P-gp INCREASED DRUG EFFECT

A
  • KETOCONAZOLE
  • RITONAVIR
  • CLARITHROMYCIN
  • ERYTHROMYCIN
  • FLUCONAZOLE

SAFEST NOT TO USE THESE XA INHIBITORS WHEN THE ABOVE DRUGS ARE
IN USE

34
Q

APIXABAN & RIVAROXABAN - INDUCERS OF CYP-3A4 OR P-gp DECREASED DRUG EFFECT

A
  • RIFAMPICIN
  • PHENYTOIN

SAFEST NOT TO USE THESE XA INHIBITORS WHEN THE ABOVE DRUGS ARE
IN USE

35
Q

Andexanet

A

•reversal of Factor Xa inhibitors
•Given its mechanism of action, andexanet is expected to reduce the anti-factor Xa activity of all
direct (apixaban, betrixaban, edoxaban, and rivaroxaban) and indirect (enoxaparin and
fondaparinux) factor Xa inhibitors.
•Presently andexanet is only approved for reversal of apixaban and rivaroxaban. Other use is
considered off-label. The drug is given intravenously as a bolus injection followed by an
infusion.
•side effects:
Arterial and venous thromboembolic events
• Ischemic events, including myocardial infarction and ischemic stroke
• Cardiac arrest
• Sudden deaths

36
Q

risk/ benefit decisions regarding anticoagulants

A

• The hazards of thromboembolism
• The lack of distinct therapeutic endpoints (the drugs are used in prophylaxis)
• That hemorrhage may occur even when there is careful control of pharmacologic effect
of the anticoagulant
• The great variation in patient response especially to warfarin
• Patient adherence is variable
• In warfarin therapy with “tight control” the INR is therapeutic only about 50% of the time

37
Q

initial therapy of VTE

A

In most patients, anticoagulation should be started immediately (initial anticoagulation) as a
delay in therapy increases the risk of potentially life-threatening embolization. Parenteral
anticoagulation is administered over the first 5 to 10 days to provide immediate protection from
recurrent thrombosis in this period of highest risk.
Long term oral anticoagulation (3 months) is recommended over no therapy. Therapy with
dabigatran, rivaroxaban, or apixaban is recommended over VKA therapy. Heparin is given for
several days before dabigatran but not with apixaban or rivaroxaban.
For patients with proximal DVT or PE and no cancer who are not treated with the drugs
described in the preceding paragraph VKA therapy is recommended over LMWH. VKA therapy
is overlapped with parenteral heparin therapy until the target INR of 2.5 is achieved.

38
Q

thromboprophylaxis in medical/surgical patients

A

Low dose UFH (LDUFH), LMWH and fondaparinux are used in thromboprophylaxis in selected
surgical and medical patients who are immobilized even for short times. The UFH doses used
are lower than in therapy of venous thromboembolism hence the term LDUFH Therapy is for the
duration of the hospitalization. APTT monitoring is not required.

39
Q

stroke prevention in AF

A

Patients with atrial fibrillation (AF) have a 5-fold increased risk of ischemic stroke and 20% to
30% of all strokes are generally attributed to AF. Oral anticoagulation (OAC) therapy with either
vitamin K antagonists or non–vitamin K antagonist oral anticoagulants reduces this risk by more
than 60% and is recommended as both primary and secondary stroke prophylaxis in patients
with AF.
AF is the most commonly encountered arrhythmia requiring therapy. With AF the atria are in a
constant state of fibrillation. Atrial transport function is impaired causing stasis, especially in the
left atrial appendage. Stasis predisposes to thrombus formation in the atrial appendage.
Embolization from the atria is a major cause of cardioembolic ischemic stroke. Anticoagulant
therapy is used for stroke prevention in persons with non-valvular atrial fibrillation. It is
customary to initiate therapy with i.v.full dose UFH along with warfarin. This dual therapy is
continued until the INR is 2.5.
With the advent of the recent approval of the NOACs anticoagulant therapy for the prevention of
stroke and systemic embolism in patients with non-valvular atrial fibrillation has changed remarkably. Recent data indicates that there is about an even use of warfarin vs. the NOACs.
The clinical trial data suggest that the NOACs are more effective than warfarin and that their use
is associated with less bleeding. With the NOACs PT monitoring is not required as with warfarin.

40
Q

vitamin K

A
  • needed for synthesis of Factors VII, IX, X and II
  • reversal of warfarin
  • anaphylaxis with rapid IV infusion

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