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PHRM 844 > Calcium channel blockers > Flashcards

Calcium channel blockers Flashcards

1
Q

what are ion channels

A

proteins that form pores in the plasma membrane
these pores allow ions to go through

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2
Q

what determines direction of ion flow?

A

conc gradient
electrical gradient

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3
Q

what is membrane potential of K

A

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

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4
Q

what is membrane potential of Na

A

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

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5
Q

what is membrane potential of Ca

A

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

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6
Q

contribution of specific ions to action potentials

A
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7
Q

structure of voltage gated channels

A

Closed form - helices are crossed, ions can’t get through
open form - inner helices bend away after ion binding happens to open channel

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8
Q

Cav1.1 type, location, function

A

L-type
skeletal muscle
voltage sensor in E/C coupling

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9
Q

Cav1.2 type, location, function

A

L-type
cardiac, smooth muscle
Ca2+ entry triggers contraction

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10
Q

Cav1.3 type, location, function

A

L-type
neurons, endocrine cells
trigger for hormone secretion

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11
Q

Cav2.1 type, location, function

A

P/Q-type
neurons
triggers neurotransmitter release at synapse

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12
Q

Cav2.2 type, location, function

A

N-type
neurons
triggers neurotransmitter release at synapse

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13
Q

Cav2.3 type, location, function

A

R-type
neurons
functions unknown

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14
Q

block of channels in VSM effect

A

vasodilation
decrease in BP
relief of angina pectoris

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15
Q

block of channels in cardiac muscle and SA/AV node effect

A

antiarrhythmic

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16
Q

vsm contraction moa

A

Ca2+ influx via Cav1.2 induces release of Ca from intracellular stores via RYR2 in SR
extracellular Ca is required for contraction of cardiac and smooth muscle

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17
Q

Beta adrenergic modulation of Ca2 channels

A

PKA phosphorylation of Cav1.2 increases Ca2 influx
increases contractility/force of contraction
increases AV nodal action potential conduction rate

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18
Q

what is required for contraction of cardiac and vsm but not for skeletal muscle

A

extracellular ca2

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19
Q

how does cardiac muscle contraction occur

A

Ca2+ ions released from sarcoplasmic reticulum binds to troponin C
Ca2 binding by troponin C causes displacement of tropomysin
displacement of tropomyosin allows myosin to bind actin –> leads to contraction

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20
Q

how does skeletal muscle contraction happen

A

mechanical coupling between Cav1.1 and RYR1

21
Q

what are the clinical applications of CCBs

A

angina pectoris, arrhythmias, htn

22
Q

what are the 3 distinct chemical classes of CCBs

A

Dihydropyridines
phenylalkylamines
benzothiazepines

23
Q

Dihydropyridines structure activity

A

dihydropyridine ring
aryl group
chiral center
ester linked side chains

24
Q

members of the dihydropyridines

A
25
Q

what is clevidipine (cleviprex)

A

short acting DHP

26
Q

what is clevidipine (cleviprex) half life

A

1 min (85-90%)
15 min (10-15%)

27
Q

how is clevidipine given

A

IV to tx htn when PO admin of drugs not possible/desirable

28
Q

what is clevidipine formulated from

A

lipids from soy and egg

29
Q

what is the metabolism of clevidipine

A

cleaved by esterases

30
Q

what does a + enantiomers DHP do

A

blocks current
aka interferes with opening of CBB

31
Q

what does a - enantiomer DHP do

A

potentiates current
aka interferes with closing

32
Q

what tissue is DHP more selective for

A

more selective and potent in relaxing smooth muscle (esp. coronary artery)

33
Q

what is DHP tissue selectivity result of

A

aa differences in channel splice variants
differences in membrane potential properties

34
Q

what is characteristic of DHP block

A

voltage dependence
binds to closed channels and prevent opening - tonic block
no frequency dependence
marked tonic block

35
Q

what are clinical considerations for DHPs

A

vascular selectivity - marked decrease in peripheral resistance, decreased afterload, little effect on HR or force of contraction
DHPs reduce heart oxygen demand (efficacy for angina)
DHPs (except nifedipine) don’t depress cardiac function
DHPs may inhibit atherosclerosis

36
Q

which DHPs are vasoselective

A

nisoldipine, felodipine, nicardipine, isradipine, amlodipine, nifedipine

37
Q

which DHP exhibits selectivity for cerebral arteries

A

nimodipine - used in sub-arachnoid hemorrhage to prevent neuropathy

38
Q

DHPs pk factors

A

all dhps are highly bound to serum proteins
all dhps undergo extensive first pass metabolism in liver
amlodipine has slow onset and long DOA

39
Q

nifedipine risks

A

increased risk of subsequent MI
fast release nifedipine may increase risk of subsequent heart attack

40
Q

verapamil (calan, isoptin) drug class

A

phenylalkylamine

41
Q

verapamil clinical considerations

A

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

42
Q

where does verapamil bind

A

in the pore and blocks Ca2 influx

43
Q

characteristics of verapamil block

A

channel has to be open for drug to enter pore - frequency dependent block…
…so marked freqency dependence
very little tonic block

44
Q

diltiazem (cardizem) drug class

A

benzothiazepine

45
Q

diltiazem clinical considerations

A

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

46
Q

diltiazem potency

A

inhibits heart less than verapamil, but more than DHPs

47
Q

diltiazem block characteristics

A

some frequency dependent block of Ca2 channels
some tonic block

48
Q

summary of cv effects

A
49
Q

CCBs side effect profile

A

all classes have 5-10% of ankle edema
verapamil has >10% of constipation
DHPs have 10-20% of facial flushing
DHPs have 5-10% of tachycardia

PHRM 844 (13 decks)

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