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Block 4: Pharm > Calcium-Channel Blockers (CCBs) > Flashcards

Calcium-Channel Blockers (CCBs) Flashcards

1
Q

what are the 2 main group of calcium channel blockers?

A

DHP and non DHP

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2
Q

dihydropyridine calcium channel blockers have what ending in their drug name?

A

Dipine

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3
Q

Thiazedes, ACES,ARBS, and calcium channel blockers are used for treating ___.

A

HTN

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4
Q

advantage of Amlodipine dosing

A

Once-daily dosing

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5
Q

what Dihydropyridines Calcium channel blocker can only be administered via IVand is used for HTN

A

Clevidipine

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6
Q

what Dihydropyridines Calcium channel blockers has PO formulation for treatment of subarachnoid hemorrhage

A

Nimodipine

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7
Q

What are the 4 main calcium channel blockers used?

A

Amlodipine Nifedipine Diltiazem Verapamil

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8
Q

what are the two non-dihydropyridines Calcium channel blockers

A

Diltiazem Verapamil

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9
Q

CCBs: MOA There are as many as 5 types of voltage-gated Ca++ channels that Differ in voltage sensitivity and conductivity, L, N, and T types are best characterized. There is only 1 type that is sensitive to CCBs, what is it?

A

Only L-type is sensitive to CCBs

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10
Q

CCBs work more specifically on the heart because that is where ___ calcium channels dominate.

A

L calcium channels

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11
Q

L-type Ca++ channels are made up of 5 subunits. CCBs bind to ___-subunit (main pore-forming subunit). Each class of CCB binds to different sites in α1-subunit. this Provides a basis for differences in the pharmacology of these drugs (cardiac vs vascular effects)

A

α1-subunit

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12
Q

CCBs: MOA Summary CCBs Bind/block L-type Ca++ channel –> closed channel –> ↓Ca++ entry during depolarization. this causes what three things to occur?

A

o Decrease cardiac contractility (negative inotropy) o Dilate coronary arteries & ↑ O2 supply to heart o Dilate peripheral vessels (↓ Total Peripheral Resistance)

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13
Q

Dihydropyridines have little-to-no rate effect, so they don’t work on the contractility or the nerve impulses to the heart. They work mostly on _____. That’s why we use them mainly for HTN.

A

blood vessels

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14
Q

Dihydropyridines mainly treat what two things?

A

HTN, angina

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15
Q

Non-DHPs: ↓ heart rate (↓SA & AV node) and contractility, they work somewhat on blood vessels but mostly are used in ____ .

A

SVT

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16
Q

Non-DHPs have what effect in HR and contractility?

A

↓ heart rate (↓SA & AV node) and contractility

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17
Q

what three things do Non-DHPs mainly treat?

A

HTN, angina, supraventricular arrhythmias

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18
Q

CCBs lower blood pressure by relaxing arteriolar smooth muscle and decreasing _____.

A

total peripheral resistance

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19
Q

CCBs Block L-type voltage-gated Ca++ channels on cell membrane, this Inhibits Ca++ entry into cells which is necessary for _____.

A

contraction

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20
Q

what type of CCBs have the greatest effect on vasodilation?

A

Dihydropyridines >>> diltiazem > verapamil

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21
Q

________ reflex causes reflex tachycardia and ↑CO with dihydropyridines, but less so with verapamil and diltiazem

A

Baroreceptor

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22
Q

What type of CCBs have the greatest effect on lowering contractility and conduction?

A

Verapamil > diltiazem >>>> dihydropyridines (verapamil does the best job decreasing HR and force of contraction, so remember DHP blood vessel dilation and verapamil cardiac contractility and rate)

23
Q

are CCBs a good drug to use in Heart Failure?

A

no CCBs are not good options in heart failure (unless very mild), including left ventricular hypertrophy; in post-MI patients; or in patients with SA or AV node conduction defects

24
Q

CCBs are Most effective in_____ hypertension

A

low-renin

25
Q

Most effective in low-renin hypertension, this is most often seen in what types of patients?

A

elderly and black patients

26
Q

for patients with low-renin hypertension, which CCBs should be used for treatment?

A

Dihydropyridines *For HTN we want DHPs

27
Q

Decreased Ca++ entry into Vascular smooth muscle cells causes relaxation and arteriolar _____; has little effect on venous beds. This is most evident with dihydropyridines

A

vasodilation

28
Q

Cardiac myocytes decreases contractility of heart muscle (negative inotropic effect) and ↓CO. this is seen most evident with what CCBs?

A

verapamil and diltiazem

29
Q

SA and AV node pacemaker cells leads to slowed conduction and decreased HR (negative ____ effect) This is Most evident with verapamil and diltiazem

A

chronotropic

30
Q

All CCBs increase coronary blood flow by coronary _____.

A

vasodilation remember: Dihydropyridines >>> verapamil > diltiazem

31
Q

All CCBs are well absorbed, but bioavailability is reduced by first-pass ____metabolism

A

hepatic

32
Q

All CCBs are highly bound to _____ (70-98%)

A

plasma proteins

33
Q

CCBs Dosages may need to be reduced in what type of patients?

A

elderly and those with impaired hepatic function (cirrhosis)

34
Q

Verapamil blocks the what drug transporter?

A

P-glycoprotein drug transporter

35
Q

Verapamil blocks the P-glycoprotein drug transporter. Why might this be important with Heart Failure patients?

A

This Decreases clearance of digoxin and other P-glycoprotein substrates. Heart Failure patients may be on digoxin so this could reduce the effects of digoxin.

36
Q

Verapamil is a ______ substrate

A

Verapamil is a CYP3A4 substrate

37
Q

Should you prescribe to DHPs together?

A

no, never.

38
Q

When is it acceptable to combine Dihydropyridine + diltiazem?

A

hard-to-control HTN cases

39
Q

Hypotensive effects are most prominent with which group of CCBs?

A

dihydropyridines

40
Q

ADRs that are more common with dihydropyridines

A

Hypotensive effects are most prominent with dihydropyridines o Dizziness, headache, flushing, nausea o Edema(up to 30% incidence at higher doses of dihydropyridines) o Myocardial ischemia with dihydropyridines (short-acting, SL nifedipine)

41
Q

Myocardial ischemia with dihydropyridines is most evident with what formulations?

A

Most evident with immediate-release formulations

42
Q

Patient may have Myocardial ischemia with dihydropyridines (short-acting, SL nifedipine) due to what 3 things??

A

♣ Excessive hypotension → ↓ coronary perfusion ♣ Vasodilation of coronary arteries that are not already dilated (coronary “steal”) ♣ Increased O2 demand from tachycardia

43
Q

Gastroesophageal reflux is common due to relaxation of_______ (mainly with verapamil)

A

esophageal sphincter

44
Q

ADRs of CCBs that are mainly associated with verapamil

A

Gingival hyperplasia Gastroesophageal reflux constipation bradycardia Elevation of liver function tests (rarely)–> associated with verapamil and diltiazem

45
Q

ADRs of CCBs

A
  • Coughing, wheezing, pulmonary edema - Rash - Gingival hyperplasia ( mainly verapamil) - Gastroesophageal reflux ( mainly verapamil) - constipation ( mainly verapamil) - bradycardia ( mainly verapamil) - Elevation of liver function tests (rarely)(associated with verapamil and diltiazem) - Myocardial ischemia (mainly with dihydropyridines) - Edema (mainly with dihydropyridines) - Hypotensive effects: Dizziness, headache, flushing, nausea (mainly with dihydropyridines)
46
Q

Bradycardia ADR is Most likely with verapamil, especially intravenous. It will be potentiated in presence of what other drug class?

A

β-blockers

47
Q

Bradycardia ADR is Most likely with verapamil, especially intravenous. It Can be dangerous in patients with ______. (SA, AV node defects)

A

conduction defects

48
Q

Bradycardia ADR is Most likely with verapamil, especially intravenous. It Can increase ______ and cause cardiac arrest, so if someone has a underlying cardiac issue or bradycardia issue then don’t use verapamil and diltiazem.

A

QT interval

49
Q

If a patient has bradycardia or underlying cardiac issue, which CCBs can you not prescribe?

A

verapamil and diltiazem

50
Q

What are the approved calcium channel blockers for HTN

A
51
Q

What are the approved calcium channel blockers for angina?

A
52
Q

What are the approved calcium channel blockers for SVT?

A
53
Q

what calcium channel blockers are safe to use in patients with moderate HF?

A
54
Q

What calcium channel blockers are safe to use with beta blockers?

A

Block 4: Pharm (7 decks)

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