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Pharm 225A > Anti-Anginal/STEMI meds > Flashcards

Anti-Anginal/STEMI meds Flashcards

1
Q

Organic Nitrates indications (short vs long acting)

A

If short: acute treatment for symptomatic relief of angina pectoris

if long: prevents recurrent anginal episodes; NOT for acute episode

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2
Q

Nitrate (short acting) meds/route/use

A
  • Nitroglycerin (NTG)
  • route: sublingual (SL) tablet/spray/powder
  • use: short onset/duration; PRN
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3
Q

Nitrate (long acting) meds/route/use

A
  • Isosorbide DInitrate or MONOnitrate
  • route: PO
  • use: slow onset/long duration; preventative
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4
Q

Nitroglycerin MoA

A
  • Nitrates converted to nitric oxide (NO) –> vessel relaxation/vasodilation
  • less work, less O2 demand/afterload
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5
Q

Nitroglycerin pharmacodynamic effects

A
  • reduced left ventricular volume/tension (preload)
  • reduced vascular resistance (afterload)
  • reduces spasms and improves O2 delivery
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6
Q

Nitrates adverse effects

A
  • headache
  • hypotension, flushing, orthostasis
  • reflex tachycardia
  • dizziness
  • tolerance/tachyphylaxis (reversible)
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7
Q

Nitrates D-D interactions

A

avoid combo with:
- PDE-5 inhibitors
- HTN/pulmonary HTN drugs
(all lead to major drop in BP)

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8
Q

Beta-blocker indication/outcome

A
  • long-term treatment of stable angina pectoris
  • reduced risk of death
  • will suppress reflex tachycardia (happens with nitrate use)
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9
Q

Beta-blocker meds/selectivity

A
  • metoprolol & atenolol (beta-1 cardioselective)
  • nadolol & propranolol (beta-1/beta-2 non selective)
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10
Q

Beta-blockers MoA/effects

A

block B1 receptors
- decreases cAMP
- no Ca2+ influx
- reduced HR/contractility/oxygen demand

  • also B2 receptors –> broncho/vaso-dilation (increase in oxygen delivery)
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11
Q

Beta-blocker AEs

A
  • Common: bradyarrhythmia, hypotension, bronchospasm
  • Less: N/V/D
  • Sig: heart block
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12
Q

BB contraindications

A
  • asthma
  • severe bradycardia
  • AV block
  • severe LV failure
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13
Q

BB D-D interactions

A
  • with other drugs of similar affects (ex. CCBs): bradycardia, hypotension, AV block
  • antagonistic effects: albuterol/catecholamine
  • CYP2D6 inhibitors ex. some SSRIs
  • CYP2D6 inducers ex. rifampin
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14
Q

Calcium channel blockers indication/outcomes

A
  • Treatment of angina at rest (chronic, vasospastic, unstable)
  • no proven mortality benefit
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15
Q

CCBs meds/type

A
  • Nifedipine XL (dihydropyridine aka in arterioles)
  • verapamil & diltiazem (non-dihydropyridine aka in cardiac cells)
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16
Q

CCBs MoA

A
  • Ca2+ channels get blocked –> vascular relaxation
  • reduce O2 demand (decrease HR/contractility) & increased O2 delivery
17
Q

CCBs AEs

A
  • Dihydropyridine: peripheral edema as arterioles get dilated
  • Non-Dihydros: AV-block, bradycardia, cardiac failure, constipation
18
Q

calcium channel blockers D-D interactions

A
  • additive effects (increased hypotension)
  • hepatic metabolism interactions (CYP inducers/inhibitors)
19
Q

Sodium channel blocker indication/outcomes

A
  • treatment of chronic angina
  • leads to decreased frequency of anginal episodes and increased exercise tolerance
20
Q

Sodium channel blocker med

A
  • ranolazine
    **contraindicated in hepatic cirrhosis, pre-existing prolonged QT interval
21
Q

sodium channel blocker MoA

A
  • blocks sodium influx into cell
  • less contractility, vasoconstriction, SA pacemaker rate/AV conduction velocity
  • overall decreased O2 demand
22
Q

Ranolazine D-D interactions

A
  • CYP3A4 inducers/inhibitors (ex. rifampin, ketocanazole)
  • interaction w/ p-glycoprotein inhibitors/some -statins/SSRIs/antibiotics
  • all either increase ranolazine concentration in body or lead to QT prolongation –> cardiac dysrhythmia, death!
23
Q

Ranolazine AEs

A
  • prolonged QT interval
  • N/V, constipation
  • headache/dizziness
24
Q

Morphine MoA/Pharm effect

A
  • bind opioid receptors to inhibit pain pathways
  • reduced response to pain –> decreases O2 demand, afterload, and preload
  • no mortality reduction
25
Q

Morphine AEs

A
  • respiratory depression
  • hypotension
  • bradycardia
  • pruritis
  • hypersensitivity
26
Q

Morphine D-D interactions

A
  • PDE-5 inhibitors combo and other antihypertensive meds use leads to hypotension
27
Q

Oxygen outcomes

A
  • theoretically increases O2 delivery
  • no mortality reduction
  • caution in COPD
28
Q

Aspirin outcomes in STEMI

A
  • inhibit platelet aggregation/clot forming
  • mortality reduction when in combo with fibronlytics
  • reduced risk of re-infarction, death, and stroke
29
Q

Aspirin AEs

A
  • dyspepsia, N/V
  • bleeding
  • increased liver enzymes
  • increased SCr
30
Q

Aspirin D-D interactions

A
  • high bleed risk when in combo with other anti-coags
  • increased nephrotoxicity w/ ACE-Is
  • decreased cardioprotective effect with NSAIDS**
31
Q

P2Y12 (ADP) inhibitors in STEMI

A
  • clopidoGREL & prasuGREL
  • used with aspirin
  • reduce platelet aggregation
32
Q

IV antiplatelet therapy in STEMI (GII/IIIb inhibtors)

A
  • eptifibatide & tirofiban
  • inhibits platelet aggregation
  • alternative to oral anti-platelet therapy
33
Q

STEMI drugs used to inactivate thrombin

A
  • Bivalirudin –> direct thrombin inhibitor
  • LMWH aka enoxaparin
  • unfractioned heparin
34
Q

thrombolytic therapy meds in STEMI

A
  • alteplASE & tenecteplASE
  • lyse coronary artery thrombi
  • activate plasminogen to plasmin (initiates fibrinolysis)
35
Q

ACE inhibitors in STEMI

A
  • lisinopril & ramipril
  • admin w/in first 24 hours
  • reduce major CV events and prevent LV remodeling

Pharm 225A (7 decks)

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