Ischemic Disease Pt2 Dr. Stewart Flashcards

Dr. Stewart EXAM VI

1
Q

How does an ischemic injury manifest in an ECG?

A

-ST-segment elevation (distance between the S and T wave)
-ST-segment depression
-T-wave inversion
-may cause no ECG changes

-may indicate a severe ischemic injury or an ongoing infarction

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2
Q

Difference between STEMI and NSTE-ACS?

A

-STEMI: ST-elevation MI
ischemic injury with an ST-elevation
-total occlusion -> causing infarction (tissue death)
chest pain at rest -> needs to go to the ER

-NSTE-ACS: no ST-elevation still an urgent event,
no infarction, no necrotic tissue
partial occlusion
chest pain at exertion
PCP referral

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3
Q

Types of blood clot

A

-Red clot: DVT or PE –> anticoagualnt

-White clots: arteriosclerosis causing MI, stroke, PAD -> use antiplatelets

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4
Q

What are the drugs used for early treatment in ACS?

A

early: MONA
Morphine: with severe pain (also it will relax the patient -> relaxes the parasympathetic NS (and the heart) -> less oxygen needed for the heart

Oxygen: (only if they actually need it >90%, infusing it too rapidly can cause oxidative damage)

Nitroglycerin: paste on the chest or continuous infusion

Aspirin: can be given right away (pharmacy), 1x full dose (325 mg) + in the ER they would also get heparin

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5
Q

What are the drugs used for late treatment (home meds) in ACS?

A

SAAB

Statin (new studies: give it earlier)
ACEi: after the patient has stabilized, within 24 hr
Aspirin or DAPT
BB

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6
Q

What is the dose for Morp

A

-2 mg every 15 min PRN for chest pain

-only as much as needed -> could affect the absorption of antiplatelets or other drugs
-can decrease gut motility, cause N/V and impact absorption

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7
Q

What are possible ADRs when given O2?

A

-only given when O2 <90% (when patients really need it)

when given with O2 >90%
-Increases arterial resistance (coronary and SVR)
-Reduces CO
-Reactive oxygen species (free radicals)

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8
Q

MOA of Nitroglycerin

A

-more venodilator -> reduces preload (volume at the end of diastole - the heart is filling after contraction)

-nitric oxide causing vasodilation of smooth muscles of arteries and veins (more veins)

-when blood vessels spasm or constrict -> help to reduce O2 demand through vasodilation

-titrate to chest pain relief

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9
Q

What are the ADRs of nitroglycerin?

A

-Hypotension
-Headache (caused by vasodilation)
-lightheadedness/dizziness
-Nausea
-reflex tachycardia

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10
Q

Which drug is contraindicated with nitroglycerin?

EXAM

A

-PDE-5 inhibitor (sildenafil, tadalafil -> erectile dysfunction)

-artery is blocked and the myocardia doesn’t get enough blood
-2 vasodilator will further decrease the BP and perfusion -> heart attack

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11
Q

What are the doses (chronic and acute) for Aspirin in ACS?

A

Acute: 325 mg

Chronic: 81 mg preferred (75-100 mg) for lifetime

MOA: Inhibits platelet aggregation via TXA2 pathway

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12
Q

What are the types of ACS?

A

-STEMI treatment:
*primary PCI vs fibrinolytic therapy (if PCI is not available)

-NSTE-ACS treatment
aggressive or conservative
*medical therapy
*PCI
*CABG

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13
Q

PCI drugs

A

-Aspirin (already administered in the ER)

-Anticoagulants (d/c after PCI)
*UFH + GP IIb/IIIa (Eptifibatide, Abciximab - potent antiplatelet) -> preferred
*LMWH + GP IIb/IIIa
*Bivalirudin (direct thrombin inhibitor, fe dabigatran can be given w/o GP IIa/IIIb)

-Antiplatelets
GP IIb/IIIa (see above)
*P2Y12i: loading dose after known anatomy

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14
Q

Which drug is released by a drug-eluting stent?

A

-PCI: insertion of a balloon opening the vessel, and inserting the drug-eluting stent

-Immunosuppressant release for about 6 months
-the metal causes an immune reaction and it can cause scaring of the blood vessel

-after time the tissue should nicely overgrowth the stent -> so it doesn’t cause a reaction later (if that doesn’t occur and they stop their DAPT it can cause ACS)

-reduces the risk of thrombosis occurring in the stents

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15
Q

Risk reduction with drug-eluting stents

A

-reduced risk of in-stent thrombosis
-increased risk of late stent thrombosis

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16
Q

Why is the artery anatomy being checked before loading the patient with P2Y12 inhibitors?

A

-bc a loading dose blocks antiplatelet activity for 3-5 days
-they would not be able to undergo surgery -> so their arteries have to be checked (anatomy) before loading them to see if they need a surgery

17
Q

P2Y12 inhibitor - Clopidogrel dosing in PCI therapy

A

Clopidogrel
– Loading dose: 300-600 mg
– Maintenance dose: 75 mg daily

18
Q

P2Y12 inhibitor - Ticagrelor dosing in PCI

A

Ticagrelor (Brilinta)
– Loading dose: 180 mg
– Maintenance dose: 90 mg twice daily

19
Q

P2Y12 inhibitor - Prasugrel dosing in PCI

A

Prasugrel (Effient)
– Loading dose: 60 mg
– Maintenance dose: 10 mg daily

20
Q

Which of the antiplatelets are reversible P2Y12 agents?

A

-Clopidogrel
-Prasugel

longer half-life, but the effect is related to the lifetime of the platelets
-> since it is irreversible the platelet recovery (effect of the drug) is longer compared to ticagrelor

21
Q

Which of the P2Y12 agents are metabolized through CYP2C19?

A

Clopidogrel (Plavix) and Prasugrel (Effient)
-both irreversible, given once a day

22
Q

Why is Ticagrelor (Brilianta) given twice a day?

A

-bc it is reversible and the platelet recovery time is shorter

-benefit: patients on ticagrelor undergo surgery (if they need one, fe bypass) faster than patients on Prasugrel, bc the platelet recovery time is shorter

FYI: there is an assay that helps determine the levels of platelets to tell if the patient is ready to undergo surgery

23
Q

Which of the P2Y12 inhibitors are contraindicated for stroke?

A

Prasugrel (Effient)
-potent antiplatelet
-it didnt show to have any benefit for stroke prevention, but it increases the risk for bleeding

24
Q

Which if the P2Y12 antiplatelets are the most potent ones?

A

-new agents are more potent
-Prasugrel (Effient), Ticagrelor (Brilianta)

25
Q

When are the newer P2Y12 agents used?

A

-post PCI

-Prasugrel and Ticagrelor

26
Q

Which antiplatelets are used for maintenance therapy?

A

-Aspirin
-if ASA allergy -> Clopidogrel

27
Q

What role do GP IIb/IIIa inhibitors have?

A

-reduces risk of acute restenosis/thrombosis in PCI patients

-Abciximab (Reopro) (monoclonal Ab): preferred in STEMI
-eptifibatide
-Tirofiban

28
Q

ADR of Abciximab

A

-delayed Thrombocytopenia (weeks after having a stent)
-hypersensitivity -> leading to Thrombocytopenia?
-higher risk for hypersensitivity and thrombocytopenia with the second dose

29
Q

How is eptifibatide different from Abciximab?

A

needs dose adjustment
if CrCl <50: reduce from 2 to 1 mcg/kg/min

30
Q

What are the preferred anticoagulants for PCI treatment?

A

-UFH “normal heparin”
-Bivalirudin (for STEMI and NSTE-ACS with early invasive strategy)

-do not use with GP IIa/IIIb

31
Q

What are the discharge meds?

SELECT ALL THAT APPLY Q
Check what is indicated and what is contraindicated!!

A

SAAB
Statin -> given earlier: plaque-stabilizing and anti-inflammatory properties during acute reaction
ASA (+P2Y12 if PCI = DAPT - reevaluate P2Y12 after 1 year)
ACEi/ARB: reduces the risk of a 2nd event
BB: reevaluate after 1 year

+ Nitroglycerin SL prn
Eplerenone (technically Spironolactone is acceptable) (if LVEF <40%) - has to be started in the first 7 days for the benefit

32
Q

Which drugs should patients be on for their lifetime?

A

-Aspirin
-ACEi/ARB: if they have a cardiovascular disease and had an event

-BB: reevaluate after 1 year, keep it they have another indication: like heart failure
-reevaluate P2Y12i after 1 year

33
Q

Duration of DAPT therapy post-MI

A

-most commonly 12 months (often no benefit after a year) -> when they need a PCI

-patients with stable ischemic disease getting a stent -> at least 6 months unless there is no bleeding risk (should stop at 6 months if bleeding risk ); they often end up being on DAPT for a year

-in patients with bleed and high bleeding risk: consider stopping after 3 months