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17 Cards in this Set

  • Front
  • Back
Where are the L type calcium channels located in the body?
Vascular SM
Cardiac myocytes
Cardiac nodal tissues
How do calcium channel blockers work?
Vasodilation
Decreased contractility
Decreased HR
Decreased conduction velocity
What are the indications for calcium channel blockers?
Hypertension
Angina
Anti-arrythmia
What is an important class of CCB used to treat hypertension? What do they end with?
dihydropyridines
-pines (e.g. amlodipine, felodipine)
What are the non-dihydropyridine two classes of CCB?
Verapamil
Ditiazem (benzothiazepine)
What are the three classes of CCBs?
Dihydropyridines
Verapramil
Benzothiazepines
What is the indication for dihydropyridines and why?
Indicated for hypertension. Selective for vascular SM.
What is the indication for verapramil?
Angina and arrythmias.
More selective for myocardium.
Works by reducing myocardial oxygen demand and reversing coronary vasospasm.
What is the indication for benzothiazepine?
Have both cardiac depressant and vasodilator effects. Effect not as marked as the other two classes. Can reduce arterial pressure without the reflex cardiac stimulatory effect produced by dihydropryridines.
SEs of dihydropyridine CCB
flushing
headache
hypotension
edema
reflex tachycardia
SEs of verapramil
excessive bradycardia
heart block
depressed contractility
Absolute CIs for CCBs
Patients with:
- bradycardia
- heart block
- heart failure
- treated with beta blockers
What are MOAs of beta blockers?
Inhibits sympathetic effects by binding to beta 1 and 2 adrenoreceptors (thus blocking epinephrine and norepinephrine)
What are the cardiac and vascular effects of beta blockers?
Cardiac effect:
- Decreased contractility
- Decreased HR
- Decreased relaxation rate
- Decreased conduction velocity

Vascular effect:
- Smooth muscle constriction (mild vasoconstriction)
Where are beta 1 and 2 receptors located?
Heart - beta 1 and 2
Blood vessels - beta 2
What are indications for beta blockers?
Heart failure
Myocardial infarction
Angina
Arrythmias
Hypertension
MOA of ACE inhibitor
Blocks formation of angiotensin II --> decrease in aldosterone --> decreased sodium and water reabsorption

Also inhibits metabolism of bradykinin (which has vasoconstrictory action)