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Therapeutics 2 - Exam 5 > calcium channel blockers > Flashcards

calcium channel blockers Flashcards

hockerman

1
Q

what are ion channels?

A

proteins that form pores in the plasma membrane?

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2
Q

what are ion channels are categorized by?

A

gating (opening and closing)
mechanism
ion selectivity
pharmacology

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3
Q

what is a passive ion channel?

A

allows ions to flow down their electrochemical gradient

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4
Q

what gradients are used to determine the direction of ion flow?

A

concentration
electrical

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5
Q

what is the cause of negative inward potential for excitable cells?

A

selective permeability of the resting membrane to K+

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6
Q

what is the difference of free calcium between the inside and outside of the cell?

A

inside –> very low (100 nM)
outside –> high (1.5 mM) 15,000x

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7
Q

can negatively charged ion cross the membrane?

A

no

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8
Q

what is membrane potential set by during rest?

A

K+ permeability

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9
Q

what is the ion that reduces mV?

A

K+

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10
Q

what is the ion that increased mV?

A

Na+

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11
Q

what is the effect of calcium contraction?

A

reduced mV

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12
Q

where do the opening on ion-selective channels drive the membrane potential towards?

A

the equilibrium potential of the permeant ion

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13
Q

what is the Kcsa?

A

H-gated K+ channel from bacteria
(v shaped)

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14
Q

what is the MthK?

A

Ca2+ gated K+ channel from bacteria that is crystallized in the presence of Ca2+
(up and down swiggling lines)

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15
Q

what is KvAP

A

bacterial voltage-gated K+ channel
(crazy squiggling lines)

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16
Q

what are the voltage-gated calcium channels?

A

Cav1.1
Cav1.2
Cav1.3
Cav2.1
Cav2.2
Cav2.3

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17
Q

what is Cav1.1?

A

L-type calcium channel in the skeletal muscle that is a voltage sensor in E/C coupling

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18
Q

what is Cav1.2?

A

L-type calcium channel in the cardiac and smooth muscle that contracts with calcium entry

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19
Q

what is Cav1.3?

A

L-type calcium channel in the neurons and endocrine cells that is triggered for hormone secretion

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20
Q

what is Cav2.1?

A

P/Q-type calcium channel in the neurons that triggers neurotransmitter release at synapse

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21
Q

what is Cav2.2?

A

N-type calcium channel in neurons that triggers neurotransmitter release at synapse

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22
Q

what is Cav2.3?

A

R-type calcium channel in the neurons with an unknown function

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23
Q

what is the effects of blocked calcium channels in vascular smooth muscle?

A

vasodilation
reduced BP
relief of angina pectoris

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24
Q

what are the Effects of blocked calcium channels in cardiac muscle and SA/AV node?

A

antiarrhythmic

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25
what is CICR?
calcium-induced calcium release cause of vascular smooth muscle contraction
26
what is the MOA of CICR?
calcium influx via Cav1.2 induced release of calcium from intracellular stores via RYR2 in the SR
27
what is MOA of vascular smooth muscle contraction?
Calcium channels (L-type) open and release intracellular calcium stores --> increases intracellular calcium concentration --> Calcium binds to calmodulin and activates myosin LC kinase (MLCK) --> MLCK phosphorylates myosin LC, creating myosin LC-PO4 --> Myosin LC-PO4 interacts with actin --> leading to muscle contraction
28
what is required for contraction of cardiac and smooth muscle?
extracellular calcium
29
what are the effects of PKA phosphorylation of Cav1.2?
increased calcium influx --> increases contractility/force of contraction --> increases AV nodal action potential conduction rate
30
what is the MOA of cardiac muscle contraction?
Calcium ions are released from the sarcoplasmic reticulum and bind to troponin C --> displacement of tropomyosin --> myosin to bind actin and induce contraction
31
what is the MOA of skeletal muscle contraction?
Mechanical coupling between activated Cav1.1 and RYR --> releases calcium from the SR to the muscle cytoplasm --> released calcium binds to troponin --> allows actin and myosin to interact and induce contraction (does not require extracellular calcium)
32
what are the clinical applications of calcium channel blockers?
angina pectoris arrhythmia hypertension
33
what are the distinct classes of CCBs?
dihydropyridines phenylalkylamines benzothiazepines
34
what is the structure of dihydropyridines?
dihydropyridine ring aryl group chiral center ester linked side chains
35
what drugs are dihydropyridines?
nifedipine (procardia) isradipine (dynacirc) felodipine (plendil) amlodipine (norvasc) nisoldipine (sular) nimodipine (nimotop) nicardipine (cardene) clevidipine (cleviprex)
36
what is clevidipine?
cleviprex short-acting dihydropyridine give IV to treat HTN when oral administration is not possible/desirable
37
what is the half-life of clevidipine?
1 to 15 minutes
38
what is the metabolism of clevidipine?
esterases
39
what is blockade mechanism of dihydropyridines via pair of enantiomers?
positive --> blocks current and interferes with gate opening negative --> potentiates current and interferes with gate closing
40
what are the tissue selectivity of dihydropyridinees?
most potent in relaxing smooth as a result of amino acid differences in channel splice variants and differences in membrane potential properties
41
when is vascular selectivity of dihydropyridines observed?
in functional/intact cells not binding assays
42
what are the characteristics of dihydropyridine block?
voltage-dependent (affinity of drug the channel is different at different voltages) no frequency dependence marked tonic block
43
what is binding of dihydropyridines?
bind allosterically (outside of pore) to closed channels and preventing opening
44
what is the vascular selectivity of dihydropyridines?
marked decrease in peripheral resistance --> dilation of arterioles/little affect on venules decreased afterload little effect on heart rate or force of contraction
45
what dihydropyridines are vasoselective?
nisoldipine felodipine nicardipine isradipine amlodipine nifedipine
46
what is nimodipine?
dihydropyridine that exhibits selectivity for cerebral arteries used in sub-arachnoid hemorrhage to prevent neuropathy
47
what are the SE of dihydropyridine?
reflex tachycardia secondary to vasodilation (except amlodipine)
48
what is nifedipine?
dihydropyridine that depresses cardiac function risk of subsequent heart attack after administration due to rapid decrease in BP leading to reflex sympathetic response/tachycardia
49
what are the clinical pearls of dihydropyridines?
reduce oxygen demand in the heart (efficacy in angina) may inhibit atherosclerosis
50
what is the pharmacokinetics of dihydropyridines?
highly bound to serum proteins undergo extensive first pass metabolism in the liver
51
what is unique about amlodipine?
has a slow onset and long duration so it does not cause reflex tachycardia
52
what are the clinical pearls of verapamil?
causes vasodilation that is less potent than DHPs slows conduction through SA and AV nodes --> reduces HR and force of contraction blunted reflex tachycardia
53
what is the binding of verapamil?
channel has to open for verapamil to bind in the pore to block calcium influx
54
what is the characteristics of phenylalkylamine (verapamil) block?
marked frequency dependence very little tonic block
55
what are the clinical pearls of dilitiazem?
less potent vasodilation than DHPs slows conduction through SA and AV nodes initial reflex tachycardia directly inhibits the heart less than verapamil but more than DHPs
56
what are the characteristics of a benzothiazepine block (diltiazem)?
some tonic block and some frequency dependence
57
what are CV effects of verapamil?
intermediate reduction of HR intermediate reduction of AV conduction intermediate reduction of myocardial contraction intermediate increase in arteriole vasodilation
58
what are the CV effects of DHPs?
small increase of HR large increase arteriole vasodilation
59
what are the CV effect of diltiazem?
small reduction of HR small reduction in AV conduction small reduction in myocardial contraction small increase in arteriole vasodilation
60
what is the SE of diltiazem?
ankle edema dizziness
61
what are the SE of DHPs?
ankle edema dizziness facial flushing HA tachycardia
62
what are the SE of verapamil?
ankle edema constipation dizziness facial flushing

Therapeutics 2 - Exam 5 (14 decks)

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