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Pharmacology Test #3 > Calcium Channel Blockers > Flashcards

Calcium Channel Blockers Flashcards

1
Q

What determines the direction of flow for ions?

A

concentration gradient and electrical gradient

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2
Q

What kind of potential do excitable cells have?

A

negative inward potential across the membrane due to the selective permeability of the resting membrane to K+

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3
Q

Describe the concentration gradient of K+ across an excitable cell membrane

A

K+ is high inside (155 mM) and low outside the cell (4 mM)

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4
Q

Describe the concentration gradient of Na+ across an excitable cell membrane

A

Na+ is low inside (12 mM) and high outside the cell (145 mM)

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5
Q

The membrane potential gradient across a cell membrane is maintained by what?

A

maintained by active transport of Na+ out of the cell and K+ into the cells, and by channels that selectively permit K+ to run out of the cell at voltages near the resting membrane potential

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6
Q

Nerst Equation

A

Emem = (RT/F) ln ([K+out]/[K+in])

at 37 degrees C, Emem = -98 mV

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7
Q

Calcium distribution across the cell membrane

A

Ca2+ is very low inside (100 nM) and high outside the cell (1.5 mM)

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8
Q

Location/Function of L-type Cav1.2 voltage gated channel

A

cardiac, smooth muscle / Ca2+ entry triggers contraction

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9
Q

Location/Function of L-type Cav1.3 voltage gated calcium channels

A

neurons, endocrine cells / trigger for hormone secretion

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10
Q

What is the result of blocking calcium channels in vascular smooth muscle?

A

Vasodilation, decrease in blood pressure, and relief of angina pectoris

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11
Q

What is the result of blocking calcium channels in cardiac muscle and SA/AV node?

A

antiarrhythmic

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12
Q

Describe Ca2+-inducedd Ca2+ release (CICR)

A

Ca2+ influx via Cav1.2 induces release of Ca2+ from intracellular stores via RYR2 (ryanodine receptor 2) in the SR

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13
Q

What is required for the contraction of cardiac and smooth muscle?

A

Extracellular Ca2+

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14
Q

Describe cardiac muscle contraction

A

Ca2+ ions released from the SR binds to troponin C; Ca2+ binding by troponin C causes displacement of tropomyosin; displacement of tropomyosin allows myosin to bind actin; contraction

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15
Q

In skeletal muscle contraction, mechanical couple occurs between what?

A

mechanical coupling between Cav1.1 and RYR1

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16
Q

Clinical applications of calcium channel blockers

A

angina pectoris, arrhythmia, and hypertension

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17
Q

Three distinct classes of calcium channel blockers

A

Dihydropyridines, Phenylalkylamines, and Benzothiazepines

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18
Q

Structure activity of dihydropyridines

A

dihydropyridine ring, aryl group, chiral center, ester linked side chains

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19
Q

What does the (+) enantiomer of dihydropyridines do?

A

blocks current; interferes with opening

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20
Q

What does the (-) enantiomer of dihydropyridines do?

A

potentiates current; interferes with gate closing

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21
Q

Mechanism of Dihydropyrdines involves

A

involves interference with gating

22
Q

Members of the dihydropyridine class

A

Nifedipine (Procardia)

Isradipine (DynaCirc)

Felodipine (Plendil)

Amlodipine (Norvasc)

Nisoldipine (Sular)

Nimodipine (Nimotop)

Nicardipine (Cardene)

Clevidipine

23
Q

What is Clevidipine metabolized by?

A

esterases

24
Q

What is significant about Amlodipine (Norvasc)

A

slow-onset of action; less likely to produce reflex tachycardia

25
Q

Describe Clevidipine (Cleviprex)

A

short acting DHP; formulated with lipids derived from soy and egg (watch for allergies)

26
Q

How is Clevidipine used?

A

given I.V. to treat hypertension when PO administration of drugs is not possible/desirable

27
Q

Tissue selectivity of Dihydropyridines

A

more potent in relaxing smooth muscle - esp. coronary artery

do not compromise cardiac function

not antiarrhythmic

28
Q

Tissue selectivity of DHPs is due to

A

amino acid differences in channel splice variants

differences in membrane potential properties

29
Q

characteristics of dihydropyridine block

A

voltage dependent - the affinity of drug for the channel is different at different voltages

No frequency dependence

Marked tonic block

30
Q

clinical consideration for the vascular selectivity of DHPs

A

marked decrease in peripheral resistance (dilation of arterioles, little affect on venules); decreased afterload; little effect on HR or force of contraction

31
Q

Only DHP where reflex tachycardia is NOT secondary to vasodilation

A

amlodipine

32
Q

Used in sub-arachnoid hemorrhage to prevent neuropathy

A

Nimodipine (exhibits selectivity for cerebral arteries)

33
Q

DHP with the lowest vascular specificity

A

Nifedipine

34
Q

General clinical considerations for DHPs

A

DHPs reduce oxygen demand in the heart - efficacy in angina; do not depress cardiac function (except nifedipine); and may inhibit atherosclerosis

35
Q

Pharmacokinetic Factors for DHPs

A

All DHPs are highly bound to serum proteins; All DHPs undergo extensive first pass metabolism in the liver; Amlodipine has slow onset and long duration of action

36
Q

DHP with a slow onset and a long duration of action

A

Amlodipine

37
Q

Phenylalkylamine calcium channel blocker

A

Verapamil (Calan, Isoptin)

38
Q

Clinical considerations for Verapamil

A

Causes vasodilation, but less potent than DHPs; slows conduction through the SA and AV nodes; reflex tachycardia is blunted

39
Q

Verapamil’s inhibitor effect on the heart is due to

A

Frequency dependent block

40
Q

Characteristics of phenylalkylamine block

A

Marked frequency dependence; very little tonic block

41
Q

Benzothiazepine calcium channel blocker

A

Diltiazem (Cardizem)

42
Q

Clinical considerations for Benzothiazepine

A

causes vasodilation; less potent than DHPs; slows conduction through SA/AV nodes; initial reflex tachycardia

43
Q

Compare Diltiazem to Verapamil (affects on heart)

A

Diltiazem directly inhibits the heart less than verapamil, but more than DHPs

44
Q

Diltiazem exhibits what kind of block of Ca2+ channels

A

exhibits frequency dependent block of Ca2+ channels

45
Q

Characteristics of benzothiazepine block

A

Some tonic block; some frequency dependence

46
Q

Side effects of DHPs

A

facial flushing; ankle edema, tachycardia, headaches

47
Q

Side effects of Diltiazem

A

ankle edema, dizziness

48
Q

Side effects of Verapamil

A

constipation; ankle edema; facial flushing, dizziness

49
Q

Negative effects of Nifedipine

A

prompt release nifedipine formulations may increase the risk of subsequent heart attacks

50
Q
A

Pharmacology Test #3 (13 decks)

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