Acute Coronary Syndrome Flashcards

1
Q

How does ACS develop?

A

plaque building up (atherosclerosis) in the coronary arteries of the heart. Plaque can break off an reduce blood flow (ischemia)

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2
Q

Risk factors of ACS

A

Age: men > 45 years, women > 55 years
Family history
Smoking
HTN
Known CAD
DLD
Diabetes
Chronic Stable Angina (SIHD)
Lack of exercise
Excessive Alcohol

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3
Q

A patient comes in with chest pain radiating down the arms and back. ECG found ST segment elevation and troponin levels were 10. What would be this patient’s diagnosis and treatment?

A

STEMI (full blockage)
**patient NEEDS a PCI if it can be done within 90 minutes of arrival to the hospital or 120 minutes of ambulance

Morphine
Oxygen
Nitrate
Aspirin

GP 11b/ IIIa antagonist
Anticoagulants
P2Y12 inhibitors

Beta blockers
ACE inhibitors

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4
Q

Mechanism of nitrates for ACS

A

Antianginal
dilate the coronary artiers and improve collateral blood flow

  • decrease preload
    and reduce chest pain
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5
Q

Mechanism of beta blockers for ACS

A

Antianginal
decrease BP and HR
Negative inotropic (decrease contractility)

increase long-term survival!

***beta -1 selective is preferred

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6
Q

Mechanism of ACE inhibitors for ACS

A

prevent cardiac remodeling
decrease preload and afterload

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7
Q

What medications should you avoid in an acute setting of ACS?

A

NSAIDs
IR Nifedipine

***have an increase risk of mortality!

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8
Q

Aspirin MOA

A

irreversibly inhibits COX-1 and 2 to decrease the production of thromboxane A2 (an inducer of platelet aggregation)

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9
Q

Effient MOA

A

Prasugrel
P2Y12 inhibitor prevents ADP mediated activated of GPIIb/IIIa receptor complex for platelet aggregation

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10
Q

Brillinta MOA

A

Ticagrelor
P2Y12 inhibitor prevents ADP mediated activated of GPIIb/IIIa receptor complex for platelet aggregation

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11
Q

What enzymes are involved in Plavix metabolism and activation?

A

ACTIVATION by CYP2C19

inhibitors = decrease efficacy
—– test for poor metabolizers

***do not use with esomeprazole or omeprazole!!!!

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12
Q

Plavix SE

A

CI: serious internal bleeding
Warning: bleeding risk (stop 5 days before surgery), do NOT use with esomeprazole or omeprazole, Thrombotic Thrombocytopenix Purpura

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13
Q

Effient SE

A

***dispense in the original container to protect from moisture

BW: fatal bleeding, patients >/= 75 years old

CI: serious bleed, history of TIA or stroke, CABG

**stop 7 days before surgery

SE: thrombotic thrombocytopenic purpura

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14
Q

Brillinta SE

A

Ticagrelor
BW: fatal bleeding

Warning: serious bleed, history of ICH, avoid in CABG

SE: thrombotic thrombocytopenic purpura

**stop 5 days before surgery

***DO NOT exceed ASA dose of 100 mg === decreases effectiveness of ticagrelor

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15
Q

What time frame is appropriate for ACS treatment with fibrinolytic?

A

within 30 minutes of hospital arrival

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16
Q

ReoPro MOA

A

Abciximab
Glycoprotein IIb/IIIa receptor antagonist to block platelet aggregation

17
Q

Integrillin

A

Eptifibatide
Glycoprotein IIb/IIIa receptor antagonist to block platelet aggregation

18
Q

Vorapaxar (Zontivity) MOA

A

Protease Activated Receptor Antagonist (PAR), a thrombin receptor to signal for platelet aggregation

*** avoid use with strong CYP indicers and inhibitors

19
Q

Activase MOA

A

Alteplase
recombinant tissue plasminogen activator (tPA)
Fibrinolytic that breaks down the clot by binding to fibrin and converting plasminogen to plasmin

***ONLY used for STEMI if necessary

20
Q

TNKase MOA

A

Tenecteplase
Fibrinolytic that breaks down the clot by binding to fibrin and converting plasminogen to plasmin

***ONLY used for STEMI if necessary

21
Q

Activase SE

A

CI: internal bleeding, history of stroke, prior ICH, severe uncontrolled HTN

SE: bleeding

***dosing different than ischemic stroke!

22
Q

How long should a ACS patient remain on a beta blocker if no history of heart failure or HTN?

A

3 years

23
Q

A patient with ACS needs DAPT for how long?

A

At least 12 months