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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

25
Most effective in low-renin hypertension, this is most often seen in what types of patients?
elderly and black patients
26
for patients with low-renin hypertension, which CCBs should be used for treatment?
Dihydropyridines \*For HTN we want DHPs
27
Decreased Ca++ entry into Vascular smooth muscle cells causes relaxation and arteriolar \_\_\_\_\_; has little effect on venous beds. This is most evident with dihydropyridines
vasodilation
28
Cardiac myocytes decreases contractility of heart muscle (negative inotropic effect) and ↓CO. this is seen most evident with what CCBs?
verapamil and diltiazem
29
SA and AV node pacemaker cells leads to slowed conduction and decreased HR (negative ____ effect) This is Most evident with verapamil and diltiazem
chronotropic
30
All CCBs increase coronary blood flow by coronary \_\_\_\_\_.
vasodilation remember: Dihydropyridines \>\>\> verapamil \> diltiazem
31
All CCBs are well absorbed, but bioavailability is reduced by first-pass \_\_\_\_metabolism
hepatic
32
All CCBs are highly bound to _____ (70-98%)
plasma proteins
33
CCBs Dosages may need to be reduced in what type of patients?
elderly and those with impaired hepatic function (cirrhosis)
34
Verapamil blocks the what drug transporter?
P-glycoprotein drug transporter
35
Verapamil blocks the P-glycoprotein drug transporter. Why might this be important with Heart Failure patients?
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
Verapamil is a ______ substrate
Verapamil is a CYP3A4 substrate
37
Should you prescribe to DHPs together?
no, never.
38
When is it acceptable to combine Dihydropyridine + diltiazem?
hard-to-control HTN cases
39
Hypotensive effects are most prominent with which group of CCBs?
dihydropyridines
40
ADRs that are more common with dihydropyridines
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
Myocardial ischemia with dihydropyridines is most evident with what formulations?
Most evident with immediate-release formulations
42
Patient may have Myocardial ischemia with dihydropyridines (short-acting, SL nifedipine) due to what 3 things??
♣ Excessive hypotension → ↓ coronary perfusion ♣ Vasodilation of coronary arteries that are not already dilated (coronary “steal”) ♣ Increased O2 demand from tachycardia
43
Gastroesophageal reflux is common due to relaxation of\_\_\_\_\_\_\_ (mainly with verapamil)
esophageal sphincter
44
ADRs of CCBs that are mainly associated with verapamil
Gingival hyperplasia Gastroesophageal reflux constipation bradycardia Elevation of liver function tests (rarely)--\> associated with verapamil and diltiazem
45
ADRs of CCBs
- 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
Bradycardia ADR is Most likely with verapamil, especially intravenous. It will be potentiated in presence of what other drug class?
β-blockers
47
Bradycardia ADR is Most likely with verapamil, especially intravenous. It Can be dangerous in patients with \_\_\_\_\_\_. (SA, AV node defects)
conduction defects
48
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.
QT interval
49
If a patient has bradycardia or underlying cardiac issue, which CCBs can you not prescribe?
verapamil and diltiazem
50
What are the approved calcium channel blockers for HTN
51
What are the approved calcium channel blockers for angina?
52
What are the approved calcium channel blockers for SVT?
53
what calcium channel blockers are safe to use in patients with moderate HF?
54
What calcium channel blockers are safe to use with beta blockers?

Block 4: Pharm (7 decks)

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