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PDA2 > Pharmacology of Calcium Channel Blockers > Flashcards

Pharmacology of Calcium Channel Blockers Flashcards

1
Q

Describe the role of Calcium (Ca2+) in cardiac pacemaker cells:

A

-sinoatrial (SA) node is the pacemaker of the heart
-Ca2+ enters through calcium channels in the SA node allowing for the development of action potential (AP)
-Ca2+ influx in conduction tissues (including AV node) -> propagates electrical impulses -> excitation linked with myocyte contraction

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2
Q

Describe the role of Calcium (Ca2+) in cardiac muscle cells (myocytes):

A

-during phase II action potential (AP), Ca2+ enters through voltage gated L-type calcium channels
-release of Ca2+ from sarcoplasmic reticulum through the ryanodine receptor (RyR) complexes
-Ca2+ binds to troponin C
-CONTRACTION (force of contraction is dependent on the total amount of calcium

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3
Q

Describe the role of Calcium (Ca2+) in vascular smooth muscle:

A

-Ca2+ enters the cell through L-type calcium channels
-vascular smooth muscle contraction
clinical hypertension due to enhanced peripheral vasoconstriction

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4
Q

What chemical drives the actin-myosin contraction?

A

calcium (Ca2+)

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5
Q

Where do all Calcium Channel Blockers bind on L-type receptors?

A

alpha1 subunit (helps form the transmembrane channel)

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6
Q

What is the cause of hypertension?

A

changes in calcium channel function and/or increased calcium channel density

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7
Q

Describe : Timothy Syndrome 1 (TS1)

A

gain of function mutation in Ca 1.2 alpha subunit of the voltage-dependent L-type cardiac calcium channel that results in prolonged channel opening

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8
Q

What are the general effects of blocking Ca2+ by calcium channel blockers (CCBs)?

A

-vasodilation
-negative inotropy (decreased force of contraction)
-negative chronotropy (decreased HR)
-negative dromotropy (decreased conduction velocity in the heart and AV)

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9
Q

Where is the binding site of Nifedipine?

A

N-site

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10
Q

Where is the binding site of Verapamil?

A

V-site

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11
Q

Where is the binding site of Diltiazem?

A

D-site

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12
Q

What are the general approved used of calcium channel blockers (CCBs)?

A

-hypertension
-angina and coronary vasospasms
-supraventricular arrhythmias (rapid HR)

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13
Q

What drugs are 1,4-Dihydropyridines?

A

-nifedipine (1st gen)
-nicardipine (2nd gen)
-amlodipine (3rd gen)
many others

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14
Q

What is the MOA of 1,4-Dihydropyridines?

A

in general, provides dose-dependent voltage gated L-type calcium channel block with greater selectivity in vascular smooth muscle by binding inactive calcium channels. THEY ARE PREDOMINANTLY PERIPHERAL ARTERIAL VASODILATORS. they will also work on coronary arteries by vasodilating (decrease in arterial BP), reducing resistance, increasing blood flow.

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15
Q

What is the main use of 1,4-Dihydropyridines?

A

hypertension, but also angina

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15
Q

Which calcium channel blockers (CCB) have the lowest selectivity for vascular smooth muscle?

A

-verapamil
-diltiazem

16
Q

Which calcium channel blockers (CCB) have the highest selectivity for vascular smooth muscle?

A

-felodipine
-nimodipine
-nicardipine

17
Q

1,4-Dihydropyridines have little impact on cardiovascular tissue- WHY?

A

best binding of Ca2+ channels found in vascular smooth muscle

18
Q

What are the adverse effects of 1,4-Dihydropyridines?

A

-peripheral edema
-headache, flushing
-hypotension
-reflex tachycardia

19
Q

Why does reflex tachycardia occur with 1,4-Dihydropyridines?

A

nifedipine is the worst offender
drastic decrease in arterial BP and vasodilation can lead to excessive hypotension and elicits the sympathetic reflex to cause tachycardia

20
Q

What are the effects of Nifedipine (2nd gen DHP)?

A

-coronary vasodilation
-arterial vasodilator
-intermediate vascular selectivity

21
Q

What are the clinical uses of Nifedipine (2nd gen DHP)?

A

-hypertension (extended release only)
-chronic stable and Prinzmental’s variant angina pectoris

22
Q

What are the adverse effects of Nifedipine (2nd gen DHP)?

A

reflex tachycardia

23
Q

What are the unique characteristics of Felodipine (2nd gen DHP)?

A

-reversible competes with other 1,4DHP for the same binding site
-NO NEGATIVE INOTROPIC (force of contraction) EFFECTS AT THERAPEUTIC DOSES
-only approved indication is HTN
-includes the adverse effect of gingival hyperplasia

24
Q

What are the unique characteristics of Clevidipine (3rd gen DHP)?

A

-ultra short-acting and IV formulation
-indicated for acute hypertensive emergencies when oral therapy is not feasible (hospital use only)
-adverse effects include Afib and AKI

25
Q

What are the unique characteristics of Isradipine (2nd gen DHP)?

A

-potent
-high affinity, high selectivity for arterial smooth muscle
-INHIBITORY EFFECTS ON SA NODE= NO REFLEX TACHYCARDIA

26
Q

What are the unique characteristics of Amlodipine (3rd gen DHP)?

A

-potent arterial vasodilator
-peripheral arterial vasodilation and coronary dilation
-indicated for angina, HTN, and safest CCB for pt with systolic HF (no neg inotropic effects and less incidence of reflex tachycardia)

27
Q

What are the unique characteristics of Nimodipine (atypical DHP)?

A

-highly selective for cerebral arteries
-indicated for SUBARACHNOID HEMORRHAGE (not used for HTN!)
-only can be taken by mouth

28
Q

What is the MOA of Verapamil?

A

binds V site on L-type calcium channels in the open conformation (frequency dependent receptor binding) and delays recovery of Ca2+ channel to pre-activated state.
-negative chronotropic effect (SA node)= decreased HR
-slows AV conduction
-negative inotropic effects= decreased force of contraction

29
Q

What is the MOA of Diltiazem?

A

binds D site on L-type calcium channels in the open conformation (frequency dependent receptor binding).
-negative chronotropic effect (SA node) = decreased HR
-reduced AV conduction
-less negative inotropic effect (decreased force of contraction) than verapamil

30
Q

What are the indications for Diltiazem and Verapamil?

A

-angina
-HTN
-atrial fibrillation/flutter (due to frequency dependent receptor binding of blocking open Ca2+ channels)
-paroxysmal supraventricular tachycardia

31
Q

What are the adverse effects of Diltiazem and Verapamil?

A

-AV heart block
-bradycardia
-negative inotropic effect
-myocardial infarction
-constipation (verapamil at high doses)

32
Q

What is the cause for the differences in the effects of calcium channel blockers (CCBs)?

A

-different binding sites
-different chemical structures
-different affinities

PDA2 (13 decks)

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