Medications for Thromboembolic Disorders, Angina and ACS

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Pharmacologic Approaches for thromboembolic Disorders

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Pharmacologic Approaches for thromboembolic Disorders

antiplatelet, anticlotting, thombolytics

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Drugs that interfere with platelet aggregation =

antiplatelet medications

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Drugs that interfering with the clotting cascade =

anticlotting medications, aka anticoagulants

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Drugs that lyse thrombi =

thombolytics

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Antiplatelet Agents / Anticoagulants:

Suppress thrombosis (thrombus formation). Do NOT "dissolve" clots

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Antiplatelet Agents Are used to prevent or manage conditions such as:

DVT, Atrial fibrillation sequelae, Hypercoagulable states, Supplement post-thrombolytic therapy or stent plcement

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Thrombolytics:

Lyse an existing thrombus

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Thrombolytics Are used to treat conditions such as:

STEMI, ischemic stroke, PE

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The P2Y12 receptor is the predominant __ receptor involved in the ADP-stimulated activation of the __ IIb/IIIa receptor

ADP, glycoprotein

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ASPIRIN blocks

COX-1

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CLOPIDOGREL blocks

P2Y12 receptor

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Aspirin Mechanism

Irreversible inhibitor of COX-1 function for the life of the platelet

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Platelets do not have a __ so they cannot make new COX -1

nucleus

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For the __ of the platelet (7-10 days) COX-1 cannot function

life

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No COX-1 --> no TxA2 produced via __ Cascade

AA

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Aspirin blocks production of __

TxA2

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Platelets have __ for pro-clotting signals

receptors

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Platelets secrete __-clotting substances - many of which they also have __ for

pro, receptors

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Aspirin class

Antiplatelet, NSAID

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Aspirin indication

Secondary prevention of MI and ischemic stroke. Acute MI

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Aspirin mechanism

antiplatelet; irreversibly inhibits COX (COX-1 > COX-2)

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Inhibition of prostacyclin (PGI2) occurs when __ is blocked

COX-2

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PGI2 inhibits platelets and __

vasodilates

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Inhibiting PGI2 would partially __ the benefits of aspirin therapy

offset

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if we keep the aspirin __-dose, we minimize the inhibition of __ , while still inhibiting TxA2

low, PGI2

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Aspirin adverse effects

bleeding

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Aspirin interactions

any combination of antiplatelet, anticoagulant and thrombolytic medications

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Aspirin In Acute MI: 325 mg of non-enteric coated aspirin should be

chewed if an MI is strongly suspected

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Avoid aspirin if __ is suspected, as it could be a __ stroke, and not ischemic

stroke, hemorrhagic

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Why 325 mg?

loading dose, minimize the size of the clot

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Clopidogrel Mechanism

blocks ADP receptor on platelets

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Clopidogrel (Plavix®) class

Antiplatelet; ADP receptor antagonist

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Clopidogrel (Plavix®) indication

ACS, prevent stroke, MI and death in patients with recent MI/stroke/PAD

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Clopidogrel (Plavix®) mechanism

antiplatelet; irreversible ADP receptor antagonist

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Clopidogrel (Plavix®) is what kind of drug

prodrug

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What converts the prodrug to its active form?

CYP2C19

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Clopidogrel (Plavix®) adverse effects

bleeding, dyspepsia, abdominal pain, diarrhea, rash

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Clopidogrel (Plavix®) interactions

PPIs that inhibit CYP2C19, Cannabis also inhibits CYP2C19

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Poor metabolizers will get __ or __ benefit from clopidogrel

little, no

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Ultra-rapid metabolizers may experience more __ effects, including bleeding, from Clopidogrel

adverse

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Anticoagulants are __ Alert Medications

High

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In high-alert meds, the consequences of an error are clearly more __ to patients

devastating

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warfarin prevents regeneration of active Vitamin __

K

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active Vitamin K, necessary to make these 4 factors __ and __

activated, functional

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Warfarin (Coumadin®) class

Anticoagulant; Vitamin K Antagonist

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Warfarin (Coumadin®) indication

prevention of thrombosis associated with DVT/PE, prosthetic valves, atrial fibrillation. Tx of DVT/PE

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Warfarin (Coumadin®) mechanism

anticoagulant; prevents active Vitamin K regeneration which reduces levels and functionality of activated vitamin-K-dependent clotting factors

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Warfarin (Coumadin®) is how protein bound?

99%

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How long does Warfarin (Coumadin®) take to become effective?

several days

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What is the specific enzyme that Warfarin (Coumadin®) inhibits?

VKORC1

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The Warfarin (Coumadin®) process occurs in what organ?

liver, in hepatocytes

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Warfarin (Coumadin®) 2 genes that may affect metabolism

VKORC1 or CYP2C9

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Warfarin (Coumadin ®) adverse effects

bleeding

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Warfarin (Coumadin ®) contraindicated in

pregnancy

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Warfarin (Coumadin ®) interactions

antiplatelet, anticoagulants, vitamin K, ANTIBIOTICS

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Warfarin (Coumadin ®) antidote

Vitamin K, 4F-PCC

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Warfarin Patient & Family Teaching: INR

get checked at frequency recommended by provider

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Warfarin Patient & Family Teaching: avoid other drugs that

increase bleeding risk

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Warfarin Patient & Family Teaching: tell other providers (including dentist)

that you are taking warfarin

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Warfarin Patient & Family Teaching: safety precautions to avoid

falls, cuts, bruises

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Warfarin Patient & Family Teaching: Food that contain vitamin K

maintain a consistent intake

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Warfarin Patient & Family Teaching: wear a

medical alert bracelet

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Heparin and enoxaparin increase activity of

antithrombin, which inhibits thrombin (Factor IIa) and Factor Xa

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Enoxaparin preferentially inactivates

Factor Xa

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Heparin (aka Unfractionated Heparin) class

Anticoagulant; unfractionated heparin (UFH)

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Heparin (aka Unfractionated Heparin) indication

treatment/prevention of thrombosis, prevention of postop venous thrombosis, extracorporeal circulation, dialysis

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Heparin (aka Unfractionated Heparin) mechanism

anticoagulant; increases antithrombin activity 1000x

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Heparin binds antithrombin which then binds and inactivates

Factor Xa

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Does Factor Xa come into direct physical contact with heparin molecule?

no

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Antithrombin also binds and inactivates __/thrombin but IIa must also come into direct __ contact with heparin to be inactivated

IIa, physical

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Heparin adverse effects

bleeding, heparin‐induced thrombocytopenia (HIT)

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Heparin interactions

antiplatelet, anticoagulant medications

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Heparin monitor

aPTT

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Heparin antidote

Protamine sulfate

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Heparin-induced thrombocytopenia (HIT)

Prothrombotic disorder caused by formation of antibodies to complexes of platelet factor 4 and heparin

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In HIT: The antibodies bind to the PF4-heparin complexes on quiescent platelet surface and induce

platelet activation

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In HIT: The activated platelets increase the __ and surface expression of __

release, PF4

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In HIT: this creates

a positive feedback loop in which further release of PF4 promotes further platelet activation

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In HIT: Platelet activation causes

release of procoagulant platelet microparticles, thrombosis, platelet consumption, and eventual thrombocytopenia

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In HIT: Greatly increased generation of __, activation of inflammatory cells, and endothelial __ and activation follow

thrombin, injury

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HIT: can cause both

venous and arterial thromboses, with devastating results

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Enoxaparin (Lovenox®) (Low Molecular Weight Heparin) class

Anticoagulant; low molecular weight heparin (LMWH)

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Enoxaparin (Lovenox®) indication

treatment and prevention of DVT, ischemic complications of acute MI, post-thrombolysis

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Enoxaparin (Lovenox®) mechanism

anticoagulant; low-molecular weight heparin - increases anti-thrombin activity. Preferentially inactivates Factor Xa

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