Anti-Anginal/STEMI meds

Question 1

Organic Nitrates indications (short vs long acting)

Answer 1

If short: acute treatment for symptomatic relief of angina pectoris

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

Question 2

Nitrate (short acting) meds/route/use

Answer 2

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

Question 3

Nitrate (long acting) meds/route/use

Answer 3

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

Question 4

Nitroglycerin MoA

Answer 4

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

Question 5

Nitroglycerin pharmacodynamic effects

Answer 5

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

Question 6

Nitrates adverse effects

Answer 6

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

Question 7

Nitrates D-D interactions

Answer 7

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

Question 8

Beta-blocker indication/outcome

Answer 8

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

Question 9

Beta-blocker meds/selectivity

Answer 9

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

Question 10

Beta-blockers MoA/effects

Answer 10

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

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

Question 11

Beta-blocker AEs

Answer 11

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

Question 12

BB contraindications

Answer 12

• asthma
• severe bradycardia
• AV block
• severe LV failure

Question 13

BB D-D interactions

Answer 13

• 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

Question 14

Calcium channel blockers indication/outcomes

Answer 14

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

Question 15

CCBs meds/type

Answer 15

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

Question 16

CCBs MoA

Answer 16

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

Question 17

CCBs AEs

Answer 17

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

Question 18

calcium channel blockers D-D interactions

Answer 18

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

Question 19

Sodium channel blocker indication/outcomes

Answer 19

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

Question 20

Sodium channel blocker med

Answer 20

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

Question 21

sodium channel blocker MoA

Answer 21

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

Question 22

Ranolazine D-D interactions

Answer 22

• 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!

Question 23

Ranolazine AEs

Answer 23

• prolonged QT interval
• N/V, constipation
• headache/dizziness

Question 24

Morphine MoA/Pharm effect

Answer 24

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

Question 25

Morphine AEs

Answer 25

- respiratory depression - hypotension - bradycardia - pruritis - hypersensitivity

Question 26

Morphine D-D interactions

Answer 26

- PDE-5 inhibitors combo and other antihypertensive meds use leads to hypotension

Question 27

Oxygen outcomes

Answer 27

- theoretically increases O2 delivery - no mortality reduction - caution in COPD

Question 28

Aspirin outcomes in STEMI

Answer 28

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

Question 29

Aspirin AEs

Answer 29

- dyspepsia, N/V - bleeding - increased liver enzymes - increased SCr

Question 30

Aspirin D-D interactions

Answer 30

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

Question 31

P2Y12 (ADP) inhibitors in STEMI

Answer 31

- clopidoGREL & prasuGREL - used with aspirin - reduce platelet aggregation

Question 32

IV antiplatelet therapy in STEMI (GII/IIIb inhibtors)

Answer 32

- eptifibatide & tirofiban - inhibits platelet aggregation - alternative to oral anti-platelet therapy

Question 33

STEMI drugs used to inactivate thrombin

Answer 33

- Bivalirudin --> direct thrombin inhibitor - LMWH aka enoxaparin - unfractioned heparin

Question 34

thrombolytic therapy meds in STEMI

Answer 34

- alteplASE & tenecteplASE - lyse coronary artery thrombi - activate plasminogen to plasmin (initiates fibrinolysis)

Question 35

ACE inhibitors in STEMI

Answer 35

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