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CV II Exam II > Anticoagulant, Antiplatelet, Thrombolytic drugs > Flashcards

Anticoagulant, Antiplatelet, Thrombolytic drugs Flashcards

1
Q

Unfractionated heparin (UFH)

A

rapid parenteral anticoag

MOA
with antithrombin III binds and inactivates clotting factors IIa, Xa, IXa, XIa, XIIa, Kallikrein
Intrinsic and common pathways

IV
SQ

IV – minutes onset, duration 1-3 hours
SQ 20-30 min onset, 12-24 duration
Urinary excretion

aPTT
thrombin time
high dose PT

side effect - bleeding, thrombocytopenia

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2
Q

indications for UFH

A

UA/NSTEMI, acute MI (STEMI), PCI, VTE prevention and treatment

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3
Q

LOW MW heparin

A

parenteral prophylaxis and treatment of MI, DVT and PE

MOA: binds antithrombin III and inhibits Xa

SQ route of admin

SQ- onset 20 min
t1/2 4.5 hr
urinary excretion

Testing not usually necessary (monitoring )

SE- bleeding

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4
Q

indications for Low MW Heparin

A 
UA/NSTEMI
Acute MI (STEMI) 
PCI
VTE (venous thromboembolisM) 
Prevention and treatment
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5
Q

Warfarin (Coumadin)

A

slow, sustained, oral anticoagulation

MOA: inhibits vit K dependent modification of clotting factors prothrombin, VII, IX, X , protein C and S ***
extrinsic and common pathways
A certain Enzyme reduces active Vit K so it can be recycled. Warfarin blocks enzyme that reduces the active Vitamin K so its less available to help with the reaction that adds carboxyl groups to factors (so Ca can’t bind)

ROA: oral only***–> completely absorbed by GI tract, highly fat soluble and 99% bound to albumin

onset : prolonged 36-72 hours ***DELAYED
prolonged 2-5 days (t 1/2 = 40 hrs)
liver and kidney metabolism

PT test converted to INR
INR 2.5-3.5 (or 2.0-3.0 for less intense therapy)

SE: bleeding
Drug-drug interaction** look over list in notes- (what if warfarin levels were higher or lower than i thought?)

*** contraindicated in pregnant patients

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6
Q

indications for warfarin

A

Overlap with heparin therapy to avoid long delay in onset of action ***

Deep venous thrombosis
Pulmonary embolism
Atrial fibrillation
Rheumatic heart disease
Mechanical and prosthetic heart valves
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7
Q

Enoxaparin (Lovenox)

A

LMWH -

Smaller, active pieces of regular heparin

Greater anti-Xa activity, less anti-platelet activity

Used (SQ injection) for prophylaxis of DVT associated with hip, knee, and abdominal surgery

Longer duration, simpler kinetics, clotting tests not usually required

replacing UF heparin ***

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8
Q

Dalteparin (FRagmin)

A

LMWH

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9
Q

Tinzaparin

A

LMWH

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10
Q

Fondaparinux

A

Factor Xa inhibitor

injected SQ
t 1/2 –> 17-21 hrs

does not effect PT time, aPTT time, bleeding time or platelet function

indicated for treatment of UA/NSTEMI (unstable angina) and acute MI (STEMI)
prevention of DVT and treatment of PE

increases factor Xa inhibition without neutralizing thrombin

does not bind to factor 4

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11
Q

Rivaroxaban

A

direct factor Xa inhibitor ***

oral***

prevention of DVT in pt’s undergoing knee and hip replacement surgery

prevention of stroke and DVT in pt’s with nonvalvular a-fib

peak 2-4 hrs
t 1/2 5-9 hrs
liver CYP3A4
urinary excretion

monitoring not required ***

bleeding > enoxaparin (no antidote)

very expensive

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12
Q

Apixaban

A

direct factor Xa inhibitor

oral

prevention of stroke and systemic emoblism in pt’s with non-valvular atrial fib

binds directly to and inhibits factor Xa

monitoring not required
peak 3-4 hours
t1/2 12 hours

Liver CYP3A4

urinary excretion (feces)

bleeding < warfarin

very expensive

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13
Q

newer anticoagulants

A 
do not require INR testing
have no dietary restrictions
fewer interactions with other drugs 
no method for determining extent of anticoag
no specific antidote

cause less bleeding than warfarin

Dabigatran, Rivaroxaban, Apixaban

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14
Q

Dabigatran

A

oral anticoagulant
used to prevent stroke in non-vavluvar a-fib.
prevent stroke in knee and hip replacement

MOA:
binds to thrombin*** selective
inhibits clot-bound and circulating thrombin
decreases thrombin stimulated platelet aggregation

ORAL***

peak:  1 hour-fasting ***Rapid onset
3 hours (after fatty meal)
t1/2 12-17 hr's 
urinary excretion 
allows 2x day dosing

Monitoring not required***

bleeding < warfarin

SE:
dyspepsia, gastritis, GI bleed

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15
Q

Aspirin

A

MOA
antiplatelet
inhibits formation of TXA2 by platelets and inhibits aggregation

indications:
prophylaxis and treatment of MI ***-should be administered routinely!!

and stroke, PAD, prevention of cardiovascular disease

at low doses–> irreversibly inhibits Cyclooxygenase (COX-1 and COX2) (1/2 baby aspirin per day)

Since platelets cannot synthesize new enzyme, aspirin inhibits TXA2 formation and platelet aggregation for the life of the platelet (7-10 days).
Only low doses are required to inhibit cyclooxygenase. Higher doses inhibit the enzyme in endothelial cells and prevent the formation of prostacyclin (PGI2), a compound that inhibits platelet secretion and stimulates vasodilation.

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16
Q

Clopidogrel (Plavix)

A

antiplatelet
blocks platelet aggregation by blocking P2Y12 ADP receptor

Indications
prophylaxis of stroke , MI , PAD, and acute coronary syndrome

Clopidogrel (Plavix) is approved for the prophylaxis of stroke, MI, peripheral arterial disease, and acute coronary syndrome.

Irreversibly inhibits the platelet adenosine diphosphate (ADP) receptor and thus blocks the subsequent ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. This inhibits fibrinogen binding and platelet aggregation.

Clopidogrel also inhibits platelet aggregation induced by agonists other than ADP by blocking the amplification of platelet activation by released ADP.
Since clopidogrel irreversibly inhibits the ADP receptor, platelets exposed to clopidogrel are affected for the remainder of their lifespan

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17
Q

Prasugrel

A

new drug antiplatelet

prodrug binds to P2Y12 ADP receptor

irreversibly inhibits platelet aggregation

Indications:
prophylaxis of thrombotic CV events in pt’s with ACS being managed with PCI

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18
Q

Dipyridamole

A

antiplatelet
blocks platelet agg
inhibits adenosine uptake and is a cAMP phosphodiesterase inhibitor

indications:
prophylaxis of arterial thromboembolism

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19
Q

Ticlopidine

A

antiplatelet
blocks platelet agg by blocking P2Y 12 ADP receptor

indications
prophylaxis or recurrent stroke, prophylaxis of thrombosis during stent placement

adverse SE–> so limit use. CLopidogrel preferred

20
Q

Cilostazol

A

antiplatelet
blocks platelet agg
causes vasodilation

I:
intermittent claudication and PAD

21
Q

Pentoxifylline

A

antiplatelet
hemorheologic agent
improves blood flow

Indications:
intermittent claudication of the limbs, peripheral vascular disease - efficacy questionable

22
Q

Abciximab

A

GPIIb/IIIa inhibitor

monoclonal antibody vs glycoprotein IIb/IIIa complex

indications: acute coronary syndromes
during percutaneous coronary intervention (PCI) / angioplasty

23
Q

Eptifibatide

A

GPIIb/IIIa inhibitor

blocks fibrinogen binding to IIb/IIIa complex

acute coronary syndromes
during percutaneous coronary intervention (PCI) / angioplasty

24
Q

Tirofiban

A

GPIIb/IIIa inhibitor

blocks fibrinogen binding to IIb/IIIa complex

acute coronary syndromes
during percutaneous coronary intervention (PCI) / angioplasty

25
Q

Lepirudin

A

MOA
direct binding to thrombin

I:
Tx of heparin induced thrombocytopenia

26
Q

bivalirudin

A

direct binding to thrombin
inhibition of platelet activation

I:
percutaneous coronary angioplasty

27
Q

Argatroban

A

direct binding to thrombin

I:
HIT (Heparin induced thrombocytopenia)
coronary agnioplasty in patients wtih HIT

28
Q

Alteplase (rt-PA)

A

thrombolytic
activator of plasminogen

I:
acute MI, PE
arterial thrombosis, non-hemorrhagic ischemic stroke , DVT
NOT FDA approved

29
Q

Reteplase

A

Activator of plasmingen

Acute MI, coronary artery thrombosis

30
Q

Tenecteplase

A

thrombolytic

activator of plasminogen

I: acute MI

31
Q

Streptokinase

A

Thrombolytic
nonenzymatic activator of plasminogen – >stimulates dissolution of fibrin clots

I:
acute MI, PE, DVT, arterial thrombosis

32
Q

monitoring therapy for heparin

A

aPTT 1.5-2.0 times control

test prior to starting therapy and during

33
Q

Heparin induced thrombocytopenia

A

evolves days after initiation of therapy

due to formation of antibodies directed against the heparin-platelet factor 4 complexes

antigen-antibody complexes bind to Fc receptors on adjacent platelets causing aggregation, platelet activation and paradoxical thrombis

34
Q

treatment of heparin overdose

A

protamine sulfate

adminster IV

strongly basic protein that bind s and inactivates heparin b/c of strong positive charge

protamine may cause transient hypotension if given to rapidly

use cautiously to avoid thrombotic complications

anaphylactic rxns can occur

infusion of fresh frozen plasma

NOT an antidote for warfarin

35
Q

low molecular weight heparin

A

DOES NOT suppress factor IIa

does suppress factor Xa

decrease bleeding episodes while still retaining anticoag activity

greater bioavailability after SQ administration, longer duration of anti-factor Xa activity that allows for frequent dosing intervals

possibly fewer side effects (Less HIT) x

36
Q

hirudin

A

irreversible thrombin inhibitor

37
Q

treatment of overdose of warfarin

A

withdraw drug
administer Vitamin K1

infusion of fresh-frozen plasma or plasma concentrates rich in II, VII, X

38
Q

HIT type I

A

transient, reversible clumping of platelets
platelet count >100,000
Usually occurs within first few days of therapy
Usually asymptomatic and recover OK even if heparin continued.

39
Q

HIT Type II

A 
delayed onset (5-14 days) 
severe thrombocytopenia (platelet counts< 100,000).

This is an immune-mediated reaction, a heparin-antibody complex caused significant platelet aggregation.

Recovery can be delayed and consequences of peripheral thrombosis can be severe, including stroke, acute MI, skin necrosis.

Amputation is necessary in up to 25% of patients with Type II HIT and mortality approaches 25%.
Incidence of Type II HIT is about 3% of all treated

much more serious than type I

40
Q

heparin contraindications

A

Any site of active or potential bleeding
Severe hypertension or known vascular aneurysm
Recent head, eye, or spinal cord surgery
Head trauma
Lumbar puncture or regional anesthetic block
Tuberculosis, visceral carcinoma, GI ulcers

41
Q

UFH vs LMWH

A

LMWH –> similar to UFH but they only have high affinity for factor Xa. much more predictable kinetics.
don’t have to do aPTT test
not so much protein binding
no dose-dependent clearance
elimination half life is 2-5 times longer

UFH- high affinity for thrombin AND factor Xa.

42
Q

INR>

A

for warfarin therapy–>adjust according to PT time adjusted to an INR (International Normalized Ratio)

The usual target INR = 2.0 – 3.0
or 3.5 - 4.0 for ongoing PE (aggressive)

Warfarin is often administered concurrently with heparin until target INR is achieved and then patient is maintained on warfarin. This protocol will likely change with acceptance of the new oral anticoagulants.

start them on warfarin right away b/c it takes 5-7 days to start***

43
Q

patient variability and Warfarin ?

A

Individual patient variation is very high
Due to differences in absorption, elimination, liver function, and drug-drug interactions.
Noncompliant and unreliable patients are not good candidates for warfarin therapy
Potential drug-drug interactions are numerous

44
Q

warfarin and drug/drug interactions?

A

Warfarin is a classic example for many types of drug-drug interaction
Inhibition or acceleration of warfarin metabolism
Displacement from plasma protein binding sites
Interference with mechanism of action
Interference with absorption
See appendices at the end of the notes package.

know general mechansims of drug/drug interactions

45
Q

direct thrombin inhibitors

A

These agents all bind directly to thrombin, are highly selectively for thrombin, do not required other proteins such as antithrombin III for activity, and are expensive.

These agents are approved for use in patients with thrombosis related to heparin-induced thrombocytopenia (HIT) and during coronary angioplasty.

Hirudin & lepirudin
an irreversible thrombin inhibitor produced by medicinal leeches now available as the recombinant protein, lepirudin
Bivalirudin
short-acting, synthetic thrombin inhibitor
Argatroban
short-acting, synthetic thrombin inhibitor

46
Q

antiplatelet drugs

A

Platelets form initial hemostatic plug
Platelets are associated with atherosclerotic plague deposits and pathological thrombi
A key activator of platelet aggregation is Thromboxane A2 (TXA2)
TXA2 is a product of the arachidonic acid pathway that involves formation of prostaglandins by the enzyme cyclooxygenase

CV II Exam II (5 decks)

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