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Therapeutics II > Calcium Channel Blockers > Flashcards

Calcium Channel Blockers Flashcards

1
Q

ion channels

A

-proteins that form pores in plasma membrane
-gating, ion selectivity, pharamacology categorization
-passive - allows ions to flow down gradient

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2
Q

ion channel flow

A

-determined by concentration gradient or electrical gradient

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3
Q

Membrane potential

A

-excitable cells have neg inward potential across membrane bc selective permeability of resting membrane to K+
-K+ high inside
-Na+ low inside

-free Ca2+ very low inside and very high outside (15,000 fold difference)

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4
Q

membrane potential gradient maintained by

A

-active transport of Na+ out and K+ in
-channels that seletively let K+ out of cell at voltages near resting membrane potential

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5
Q

Nerst equation

A

-membrane potential (Emem)
- -98mV at 37degreesC

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6
Q

Membrane potential at rest

A

-set by K+ permeability
-neg ions do NOT cross membrane
-K+ going in and out in equilibrium, only K channels open
-resting negative potential

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7
Q

Effect of ions on membrane potential

A

-Increases as sodium moves in
-Ca channels maintain membrane potential more positive while Na closes (=plateau = contraction)
-K+ decreases it back to -93mV

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8
Q

structure of voltage gated channels (Kcsa)

A

-selectivity filter outside
-gate inside
-Kcsa is H+ gated K+ channel from bacteria
-closed when helices at gate are crossed

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9
Q

structure of voltage gated channels (MthK)

A

-ca2+ gated K channel
-similar to Kcsa
-selectivity filter and gate
-crystalized in presence of Ca2+
-hinge point

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10
Q

structure of voltage gated channels (KvAP)

A

-4 subunits
-positively charged residues
-senses membrane potential
-if inside neg = inward pull = closed
-if inside less negative = move upward and outward = open

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11
Q

Voltage gated Ca2+ channel family

A

Cav 1.1-1.3
-Cav2.1-2.3

-1.3, 2.1-1.3 neurons
-1.1 skeltal muscle
-1.2 cardiac

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12
Q

Cav1.2

A

-L-type voltage-gated ion channel
-cardiac, smooth muscle
-Ca2+ entry triggers contraction

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13
Q

Block of channels in smooth muscle

A

-vasodilation
-dec blood rpessure
-relieve angina

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14
Q

Block of channels in cardiac muscle and SA/AV node

A

-antiarryhmic

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15
Q

Vasc and smooth muscle contraction

A

-Ca induced Ca release (CICR)
-Ca influx via 1.2 induces Ca release from intracellular stores via RYR2 in the SR (release to cytoplasm, doesnt leave cell)
-extracellular Ca required for contraction

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16
Q

Vasc smooth muscle contraction mech

A

-Ca2+ channels (L-type)
-inc Ca concentration from intracellular stores
-Ca calmodulin inc
-myosin LC kinase
-myosin LC-PO4 + actin
=contraction

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17
Q

Cardiac muscle contraction

A

-Ca ions from SR bindtroponin C
=displacement of tropomyosin
=allows myosin to bind actin
=contraction

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18
Q

Skeletal muscle contraction

A

-mechanical coupling btween Cav1.1 and RYR1
-extracellular Ca not required
-CCBs dont interfere here
-triad in t-tubule physically linked

19
Q

CCB chemical classes

A

-dihydropyridines
-phenylalkylalmines
-benzothiazepines

20
Q

Dihydropine CCBs structure

A

-dihydopyridine ring (2 double bonds and nitrogen and aryl group)

21
Q

Dihydropyridine members CCBs

A

-nifedipine (Procardia) (no chiral center)
-Isradipine (DynaCirc)
-Felodipine (plendil)
-Amlodipine (Norvasc)
-nisoldipine (sular)
-Nimodipine (nimotop) (prevent neuropathies good brain penetration)
-Nicardipine (Cardene)

-Clevidipine (Cleviprex)

22
Q

Amlodipine structure

A

-primary amine off of ether
=longer action

23
Q

Nifedipine structure

A

-no chiral center
-shorter duration
-bind and unbind quickly
-watch reflex tachycardia

24
Q

Clevidipine (Cleviprex

A

-designed to fall apart
-short duration
-1-15min t1/2
-IV infusion to tx HTN when PO admin not favored
-formulated w soy and egg lipids

25
Q

Clevidipine metabolism

A

-esterases
-first cleavage product still blocks channels
-second cleavage product inactive

26
Q

Dihydropyridine mech

A

-guessing from enatiomers
-interference w gating
-(+) blocks current, interferes opening
-(-) potentiates current, interferes closing

27
Q

Tissue selectivity of dihydropyridines

A

-more potent in relaxing smooth muscle (esp coronary artery)
-do not compromise cardiac function
-not antiarrhytmic
-vascular over cardiac

28
Q

vascular tissue selectivity of CCBs is result of

A

-amino acid differences in channel splice variants
-differences in membrane potential properties

29
Q

characteristics of dihydropyridine block

A

-voltage-dependence
-affinity of drug for channel is different at different voltages
-allosteric binding site
-bind closed channels to prevent opening = tonic block
-no frequency dependence
-MARKED tonic block

30
Q

Clinical considerations for DHPs (vascular selectivity)

A

-dec in peripheral resistance
-dilation of artioles
-dec afterload
-little effect of HR or CO
-nisol-, felo-, nicar-, isra-, amlo-, nifedipine all vasoselective
-nimodipine selective in cerebral arteries - use in hemorrhage to prevent neuropathy
-reflex tachycardia secondary to vasodilation except amlodipine

31
Q

DHP considerations

A

-vascular selectivity
-reduce oxygen demand in heart (efficacy in angina)
-nifedipine only one that depresses cardiac function
-may inhibit artherosclerosis

32
Q

DHP PK factors

A

-all DHPs bound to serum proteins
-undergo first pass metbolism in liver
-amlodipine has slow onset and long duration

33
Q

Nifedipine

A

-inc risk of subsequent MI?
-prompt release may inc risk of heart attack
-rapid decrease in BP can lead to reflex tachycardia

34
Q

Phenylalkylamine class drug

A

-Verapamil (Calan, Isoptin)

35
Q

Verapamil

A

-vasodilation but less potent than DHPs
-slows conduction through SA and AV nodes (reduce HR and force of contraction)
-reflex tachycardia is blunted
-works via frequency dependent block

36
Q

Verapamil mech

A

-freq dependent block
=channel has to open for drug to enter pore
-binds IN pore
-very little tonic block

37
Q

Benzothiazepine class drug

A

-Ciltiazen (Cardizem)

38
Q

Diltiazem clinical considerations

A

-causes vasodilation less potent than DHPs
-slows conduction through SA and AV nodes
-initial reflex tachycardia
-directly inhibits heart less than verapamil but more than DHPs
-some freq dependent block of Ca and some tonic block

39
Q

Diltiazem mech

A

-some tonic block
-some frequency block
-bind in pore kind of

40
Q

summary of DHP effects

A

-inc HR
-most vasodilation

41
Q

summary of verapamil effects

A

-DEC HR
-DEC AV and myocard contraction
-inc vasodilation

42
Q

Diltiazem summary

A

-dec HR
-dec AV cond, myocard contract
-inc vasodilation but just a lil

43
Q

CCB side effects

A

-ankle edema
-constipation (verapamil)
-facial flushing (DHPs)
-tachycardia (DHPs)

Therapeutics II (55 decks)

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