CCBs

Question 1

Nifedipine

Answer 1

• MOA: protoypical dihydropyridine CCB that inhibits calcium from entering the slow channels or select voltage-sensitive arease of vasc sm m and myocardium during depol
• Effects: releaxtion of coronary sm m -> coronary vasodilation; ↑ myocardial oxygen delivery in pts w/ vasospastic angina; negative inotrope; ↓ PVR –> ↓ arterial BP; frequency-independent, no cardioactive
• CAs: Chronic stable or vasospastic angine, HTN (sustained release only); JNC8 recommends CCBs as 1st-line trx for HTN –> non-black population w/o CKD, black population w/o CKD (instead of ACEI or ARB); off-label: hypertensive emergency in pregnancy, preterm labor, Raynaud’s, distal ureteral stone, high altitude pulm edema, pulm HTN
• PKs: Immediate & ER; extensive hepatic metabolism via CYP3A4; half life 2-5 hrs, ↑ by cirrhosis; excreted as metabs in urine and feces
• Toxicities: flushing, peripheral edema, dizzy, lightheaded, giddiness, HA, neasuea heartburn; uncommon –> palps, dose-related hypotension, CHF, nervousness/mood changes, shakiness, sleep disturbances, dermatitis, pruritis, urticaria, gingival hyperplasia, blurred vision, cough/wheezing, nasal congestion/sore throat, chest congestion, diaphoresis

Question 2

Amlodipine

Answer 2

Hihydropyridine CCB w/ use limited to CAD & HTN, but very widely used in part d/t long half life of 30-50 hrs

Question 3

Verapamil

Answer 3

• MOA: non-dihydropyridine CCB; inhibits calcium from entering the slow channels or select voltage-sensitive areas of vasc sm m and myocardium during depol
• Effx: relaxation of coronary vasc sm m & coronary vasodilation; ↑ myocardial oxygen delivery in pts w/ vasospastic angina; slows automaticity and conduction of AV node; ↓ myocardial contractility (negative inotrope); frequency-dependent (cardioactive)
• CAs: IV –> SVT-arrhythmias; PO –> primary HTN, angina pectoris, SVT-arrhythmias
• PKs: tablets ER & IR; extensive hepatic metab by multiple CYPS; metabs excreted in urine; half life = 3-7 hrs (↑ w/ hepatic impairment)
• Toxicity: Common –> HA, gingival hyperplasia, constipation; rare –> periph edema, CHF/pulm edema, hypotension, fatigue, dizzy, lethargy, AV block, brady, flushing, rash, dyspepsia, flu-like syndrome

Question 4

Diltiazem

Answer 4

• MOA: non-DHP CCB; inhibits calcium from entering the slow channels or select voltage-sensitive areas of vasc sm m and myocardium during depol
• Effx: relaxation of coronary vasc sm m & coronary vasodilation; ↑ myocardial oxygen delivery in pts w/ vasospastic angina; slows automaticity and conduction of AV node; ↓ myocardial contractility (negative inotrope); frequency-dependent (cardioactive)
• CAs: IV –> control of RVR in Afib or flutter; conversion of paroxysmal SVT; oral –> primary HTN, chronic stable angina or angina from coronary artery spasm; off-label –> Afib, anal fissures, stable narrow-complex tachy uncontrolled or unconverted by adenosine or vagal maneuvers; hypertrophic cardiomyopathy; Raynauds; peds HTN
• PKs: tablets ER & IR; extensive hepatic metab by multiple CYPS; metabs excreted in urine; half life = 3-7 hrs (↑ w/ hepatic impairment)
• Toxicity: common –> edema, HA; uncommon –> AV block, brady, hypotension ,extrasystoles, flushing, palps, dizzy, nervousness, pain, skin rash, gout, dyspepsia, consitpation, NVD, injxn site rxn, weakness, myalgias, rhinitis, pharyngitis, dyspnea bronchitis, cough