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HSHD Block 4 > Acute Ischemic Heart DiseaseTherapeutics > Flashcards

Acute Ischemic Heart DiseaseTherapeutics Flashcards

1
Q

MONA

A

Morphine

O2

Nitro

ASA

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2
Q

ABCs drugs (5 As)

A
  • Anti-thrombotic/ anti-coagulant
  • ASA
  • (Another) Anti-platelet
  • Anti-anginal
  • (ACE-i)
  • BB
  • “Cholesterol” (Statin)
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3
Q

Examples of anitplatelets

A

–Aspirin (ASA)

–P2Y12 receptor blockers

–GPIIb/IIIa receptor blockers

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4
Q

Examples of antithrombotics

A

–Unfractionated heparin

–Low molecular weight heparin (LMWH)

–Direct thrombin inhibitors

–Factor Xa inhibitors

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5
Q

Aspirin MOA

A

Irreversibly inhibits cyclooxygenase-1 and 2 (COX-1 and 2) enzymes

Aspirin inhibits the production of thromboxane A2, thereby inhibiting platelet aggregation.

By the selective and irreversible acetylation of a single serine residue within prostaglandin G/H synthase, aspirin causes the inactivation of cyclooxygenase activity.

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6
Q

Aspirin side effects

A

Upper gastrointestinal (UGI) events (eg, symptomatic or complicated ulcers): Low-dose aspirin for cardioprotectiveeffects is associated with a two- to fourfold increase in UGI events.

GI intolerance such as nausea and dyspepsia, rare

  • Bleeding outside GI tract
  • Salicylate sensitivity
  • Tinnitus
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7
Q

What is aspirin resistance

A
  • Resistance = Measurable, persistent platelet activation that occurs in patients prescribed a therapeutic dose of aspirin.
  • Clinical aspirin resistance, the recurrence of some vascular event despite a regular therapeutic dose of aspirin, is considered aspirin treatment failure.
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8
Q

Mechanism of aspirin resistance

A

Mechanisms

–poor adherence or absorption

–drug interactions

–COX-2 activity, COX-1 polymorphism

–platelet alloantigen 2 polymorphism of platelet glycoprotein IIIa

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9
Q

Thienopyridines MOA

A

Block the adenosine diphosphate (ADP) receptor P2Y12 on platelets

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10
Q

Thienopyridine Side Effects

A

•Bleeding is major side effect and contraindicated in patients with active bleeding

  • Rare TTP (thrombotic thrombocytopenic purpura) reported
  • Rare allergies to thienopyridines – cross reactivity reported
  • Ticagrelor – 10% of patients report dyspnea
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11
Q

Examples of thienopyridines

A

Clopidogrel, prasugrel, ticagrelor

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12
Q

How long does clopidogrel last? Price?

A

Still commonly used, most clinical data, oldest agent, off patent (cheap)

Platelets blocked by clopidogrel are affected for the remainder of their lifespan (~7-10 days).

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13
Q

Clopidogrel metabolism and drug interaction

A
  • Prodrug that requires in vivo biotransformation (oxidation) by the cytochrome P450 (CYP-450) system, principally CYP2C19.
  • The active metabolite irreversibly blocks the P2Y12 component of ADP receptors on the platelet surface, which prevents activation of the GPIIb/IIIa receptor complex, thereby reducing platelet aggregation.
  • Poor metabolizers have higher cardiovascular event rates than patients with normal CYP2C19 function (2-14% of population)
  • Proton Pump Inhibitors reduce antiplatelet effect
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14
Q

Why were newer thienopyridines developed?

A

•Clopidogrel has delayed onset of action, large variability in platelet response, and irreversible

  • Led to development of prasugrel and ticagrelor, cangrelor (IV)
  • Each induces more intense platelet inhibition and associated with higher rates of bleeding
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15
Q

Prasugrel use

A
  • More rapid onset, higher levels of platelet inhibition
  • *Acts at same site on P2Y12 receptor as clopidogrel

•Contraindicated in patients with active bleeding, history of stroke or TIA

•High efficacy in diabetic patients

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16
Q

What is unique about ticagrelor

A

•*Binds reversibly to P2Y12 receptor (only one!)

•*Acts at different site than clopidogrel/prasugrel

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17
Q

Glycoprotein IIb/IIIainhibitors MOA

A

When platelets are activated, this receptor undergoes a change in conformation that increases its affinity for binding to fibrinogen.

The platelet GP IIb/IIIa receptor antagonistssterically inhibit fibrinogen from binding,preventing platelet aggregation.

18
Q

Glycoprotein IIb/IIIainhibitors side effects and contraindications

A

Major side effect is bleeding

Contraindicated in recent stroke, severe hypertension, recent major surgery

Rarely used outside of procedures, due to high bleeding risk outweighs therapeutic benefit

19
Q

Glycoprotein IIb/IIIa inhibitor examples and clearance

A

Eptifibatide (Integrillin): Renal clearance, max effect in 1hr, platelet returns to normal 4-8hr after d/c

Abciximab (ReoPro): Safe in renal disease, max effect 10 min, platelet takes 72hr to return to normal after d/c

20
Q

Antiplatelet Therapeutic Strategy

A
  • All UA/NSTEMI/STEMI patients without a contraindication should receive chewable aspirin
  • Most should receive P2Y12 inhibitor unless active bleeding or high risk of needing CABG
  • In selected patients, IIb/IIIa inhibitors can be added at the time of angiography
21
Q

Targets for antithrombotics

A
22
Q

Use of heparin in UA/NSTEMI

A

In UA/NSTEMI, addition of heparin to aspirin likely

lowers risk of death or MI

23
Q

Unfractioned Heparin MOA

A

•Potentiates the action of antithrombin III (by binding to it) and thereby inactivates thrombin (and weakly Xa). Cannot bind or inactivate thrombin already bound within a clot (this requires lysis)

•Prevents the conversion of fibrinogen to fibrin

•Stimulates release of lipoprotein lipase (lipoprotein lipase hydrolyzes triglycerides to glycerol and free fatty acids)

24
Q

Monitoring of UFH

A

Monitor aPTT for therapeutic range, every 4-6hr

25
Q

LMHW Mechanism

A

Low molecular weight heparins have a small effect on the activated partial thromboplastin time (aPTT) and strongly inhibit factor Xa.

Half-life elimination, plasma: 2 to 4 times longer than standard heparin, independent of dose; based on anti-Xa activity: 4.5 to 7 hours

26
Q

Example of LMWH

A

Enoxaparin - Given as subcutaneous injection

27
Q

Direct thrombin inhibitors MOA

A
  • Bind to the catalytic site of both circulating and clot-bound thrombin.
  • Prevents thrombin-mediated cleavage of fibrinogen to fibrin monomers, and activation of factors V, VIII, and XIII.
  • Specific and reversible, immediate onset and labs return to normal an hour after stopping
28
Q

Direct Thrombin Inhibitors example

A

Bivalirudin

29
Q

What is Heparin Induced Thrombocytopenia (HIT)

A

•Marked by a progressive fall in platelet counts and, in some cases, thromboembolic complications

–skin necrosis, pulmonary embolism, gangrene of the extremities, stroke, or MI

Immunologically mediated

30
Q

Use of ACE inhibitors

A

–MUST if EF <35%

–If hypertensive, most other patients with ACS benefit

31
Q

Aldosterone receptor blocker examples and use

A

eplerenone/spironolactone

–Must monitor for hyperkalemia!

–All patients with LVEF <35% and NYHA II symptoms

32
Q

When should Renin-Angiotensin-Aldosterone Agents not be used

A

•Should not be started in acute setting if systolic blood pressure < 100 mmHg

33
Q

Use of Beta Blockers

A

Much larger benefit of beta blockers seen in the post-discharge setting

34
Q

Contraidications of beta blockers

A
  • Any sign of heart failure (based on COMMIT): S3 gallop, rales/crackles, elevated JVP, pulmonary edema
  • Heart Block
  • Asthma
  • Evidence of low output state
  • Hypotension (SBP < 90 mmHg)
  • Significant sinus bradycardia (<50 bpm)
35
Q

Effect of nitroglycerin

A

•Reduces myocardial oxygen demand while enhancing myocardial oxygen delivery. It has both peripheral and coronary vascular effects.

36
Q

Contraindication for nitroglycerin

A

Severe aortic stenosis (USE YOUR STETHOSCOPE!), RV infarct, concurrent use of PD#5 inhibitors (Sildenafil/Viagra), Hypotension

37
Q

Morphine use

A

•Morphine should only be administered after nitroglycerin and other anti-ischemic therapies have failed to render the patient symptoms free (so almost never)

impairs absorption of thienopyridines

38
Q

When should oxygen be administered

A
  • Inhaled oxygen should be administered IF the arterial oxygen saturation (SaO2)declines to less than 90%.
  • Routine use in non-hypoxic patients may worsen outcomes, as hyperoxia leads to ROS formation and oxidative damage
39
Q

Different in treatment for STEMI and NSTEMI

A

–UA/NSTEMI: medical management with Percutaneous Coronary Intervention (PCI) in select patients

–STEMI: emergent reperfusion!

40
Q

Time for reperfussion

A

–Thrombolytics Door to Needle <30min

–PCI Door to Balloon <90 min

41
Q

Major contraidications for thrombolytics

A
42
Q

PCI vs lytics

A

HSHD Block 4 (8 decks)

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