pharm: 10-15 Antianginal drugs Flashcards

1
Q

A: Name the 2 Determinants of Coronary Perfusion

B: Explain how the Sympathetic System causes Net Vasodilation in Coronary Arteries

A
  1. Diastolic Perfusion Pressure (Aortic Diastolic pressure - EDP)
  2. Coronary Vascular Resistance (compression and intrinsic regulation)

B: During INC Myocardial work, Neural Sympathetic Regulation causes some vasoconstriction but also INC Myocardial work more β€”> INC local metabolites β€”> Net VasoDilation Effect

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2
Q

Tx for [Stable Exertional Angina] (6)

A

– Nitrates (also used to tx vasospastic angina)

– Calcium Channel Blockers

– Beta Blockers
– Ranolazine

– Catheter-based techniques (Percutaneous Catheterization Interventions such as balloon angioplasty)

– CABG

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3
Q

A: [T or F] Nitric Oxide mechanism depends on endothelium to be processed

B: 4 Systemic Effects of Organic Nitrates

A

A: FALSE! Relaxation by NO is Endothelium-INDEPENDENT!

B:

  1. DEC VENOUS RETURN by Dilating Venous Capacitance Vessels
  2. DEC LV WALL TENSION
  3. DEC AFTERLOAD (arteriolar vasodilator)
  4. DIRECT CORONARY ARTERY VASODILATATION (Increased Subendocardial Perfusion)
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4
Q

A: Clinical Use of Organic Nitrates (5)

B: Side Effects (5)

A

A:

  1. Angina Pectoris (Exertional,Unstable, Variant)
  2. Hypertensive Emergencies
  3. CHF
  4. Tx and Px of Exercise-induced myocardial ischemia
  5. Coronary Artery Vasospasm

B: SE

a) Orthostatic Hypotension
b) Reflex Tachycardia
c) Headache
d) Nitrate Tolerance (high doses of long acting nitrates)
e) Methemoglobinemia

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5
Q

A:[Ca+ Channel Blockers are potent ______] but have no effect on _______.

B: How do [Ca+ channel blockers] CARDIAC muscle (3)

A

A: [Ca+ Channel Blockers are potent Arteriolar VasoDilators] but have no effect on venous. They do this by affecting Ca+ entry into smooth m.

B: In Cardiac: they are

  1. Negative inotropic agents
  2. Decrease rate of SA node Phase 4 depolarization β€”> [DEC heart rate]
  3. Slow AV nodal conduction velocity
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6
Q

A: Clinical Use of Calcium Channel Blockers (6)

B: Which [Ca+ Channel Blocker] is longg acting? Is it Dihydropyridine or [NON-Dihydropyridine]?

C: List the order from MOST [Negative Inotrope and Negative Chronotrope] to least

D: List order from MOST VasoDilatory to least

A

HARHAM!

  1. Angina (All 3 )
  2. HTN
  3. Arrhythmias
  4. Hypertrophic Cardiomyopathy
  5. Migraine
  6. Raynaud’s Phenomenon (vasospasm of feet and hands when exposed to cold air)

B: Amlodpine = Long Acting Dihydropyridine

C: Verapamil > Diltiazem > nifedipine

D: β€œNever Dilate Vessels”

[Nifedipine > Diltiazem > verapamil]

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7
Q

Adverse Effects of [Dihydropyridine Ca+ Channel Blocker] (3)

A

a) Reflex Tachycardia
b) Peripheral Edema
c) Hypotension

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8
Q

A: Lusitropy

B: What causes this?

C: What is the INC Rate of Conduction referred to as?

A

A; INC Rate of Relaxation by the [Sarcoplasmic Reticulum]

B: cAMP (when activated by Beta 1 sympathetic stimulation in heart)

C: Dromotropy (note: Chronotropy= INC Pacemaker Current)

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9
Q

Beta Blockers

Indications (8)

A

β€œBeta blockers HAMMED my HP”

  1. Exertional Angina
  2. HTN
  3. Arrhythmias
  4. Dissecting Aortic Aneurysm
  5. Mitral Valve Prolapse
  6. Post-MI prophylaxis
  7. Hyperthyroidism
  8. Migraine
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10
Q

Beta Blockers

  • A: Lipid or Water Soluble*
  • B: Which are ONLY eliminated by Renal? (3)*
  • C: Which are ONLY eliminated by Liver? (3)*
A

A: Lipid Soluble

B: RANS - Renal= Atenolol/Nadolol/Sotalol

C: Liver = Propranolol / Carvedilol / Metoprolol β€œPCM”

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11
Q

A: What is Ranolazine and what does it do?

B: How does the heart generate ATP

C: During acute MI, ⬜ rise precipitously, and inhibit β¬œβ€”> glucose oxidation is ______ which is undesirable when O2 supply is limited in MI

D: Net Result of using this drug (3)

E: Indication and Side Effect

A

A: [pFOX inhibitor] inhibits mitochondrial enzymes of beta oxidation which relieves inhibition on pyruvate dehydrogenase.–> allowing heart to use more glucose as a fuel during MI

B: Under normal conditions the heart can use either glucose or fatty acids to generate ATP.

C: During acute MI, fatty acids rise precipitously, and inhibit pyruvate dehydrogenase.β€”>glucose oxidation is depressed which is undesirable when O2 supply is limited in MI

D: The net result is

  • reduced lactic acid accumulation,
  • less intracellular acidosis
  • reduction in severity of MI

E: [1st line - Exertional Angina] (espeically in those w/angina despite other therapy) but causes [Prolonged AP duration]

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12
Q

Name the 3 Drugs that [INC time of Angina onset and [ST segment depression]] in pts with exertional angina

A
  1. Diltiazem (Ca+ channel blockers)
  2. Metoprolol (Beta blockers)
  3. Nitrates
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13
Q

4 CNS Adverse Effects of Beta Blockers

A
  • Insomnia
  • Depression
  • Fatigue
  • Raynaud’s Phenomenon (cold extremities)
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14
Q

Major Adverse Effects of [Nifedipine Non-Dihydropyrdine Ca+ channel Blocker] (3)

A

– Reflex Tachycardia

– Peripheral Edema

– Hypotension

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15
Q

Niseritide

  • A: Indication (2)*
  • B: MOA (2)*
  • C: Effect (2)*
A

A:

  1. [Acute decompensated chronic CHF] in hospitalized patients
  2. HTN

B:

[Human BNP recombinant] tht

  1. Activates [vascular smooth muscle NPR1/2] and [renal BNP receptors]
  2. INC cGMP in [vascular smooth muscle] –> vasoDilation

C:

  1. vasoDilation of arterioles and [renal Afferent arteriole]–> INC GFR
  2. DCT Natriuresis
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16
Q

Niseritide

A: Adverse Effects (2)

B: Contraindications (2)

A

A: Hypotension, ventricular arrhythmias

B:

  • Reduced LV filling pressures
  • systemic hypotension