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PHRM 844 Therapeutics > Exam 5 - Calcium Channel Blockers Hockerman > Flashcards

Exam 5 - Calcium Channel Blockers Hockerman Flashcards

1
Q

K+ is _____ inside and _____ outside the cell

a. low; high
b. low; low
c. high; low
d. high; high

A

c. high; low

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2
Q

Na+ is _____ inside and _____ outside the cell

a. low; high
b. low; low
c. high; low
d. high; high

A

a. low; high

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3
Q

is calcium low or high INSIDE the cell?

A

very low (100 nM compared to 1.5 mM outside)

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4
Q

is calcium low or high OUTSIDE the cell?

A

high (1.5 mM compared to 100 nM inside)

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5
Q

location of CaV 1.2 receptor (2 locations)

A

cardiac and smooth muscle

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6
Q

function of CaV1.2 receptor

A

Ca2+ entry triggers contraction

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7
Q

membrane potential is set by _____ permeability at rest

a. Ca2+
b. K+
c. Na+

A

b. K+

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8
Q

what structural feature of potassium channels is responsible for the selective and rapid conduction of K+?

A

selectivity filter

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9
Q

blocking of channels in vascular smooth muscle leads to __________

A

vasodilation

(dec in BP; relief of angina)

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10
Q

blocking on channels in cardiac muscle & SA/AV node leads to an __________ effect

A

antiarrhythmic

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11
Q

Ca2+-induced Ca2+ release (CICR):

_____ influx via _____ induces release of _____ from intracellular stores via _____ in the SR

(second and fourth blanks are receptors)

A

Ca2+
CaV1.2
Ca2+
RYR2 (ryanodine receptor 2)

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12
Q

what is required for contraction of cardiac and smooth muscle?

A

extracellular Ca2+

(not required for skeletal muscle)

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13
Q

beta adrenergic modulation of Ca2+ channels: _____ phosphorylation of CaV1.2 inc Ca2+ influx

(the blank is an enzyme)

A

PKA (protein kinase A)

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14
Q

in vascular smooth muscle, what are the two end products that lead to contraction?

A

myosin LC-PO4 (phosphorylated myosin light chain) + actin

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15
Q

cardiac muscle contraction: Ca2+ ions released from the SR binds to _______

A

troponin C

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16
Q

cardiac muscle contraction: Ca2+ binding by troponin C causes displacement of __________

A

tropomyosin

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17
Q

what causes contraction in cardiac muscle contraction?

A

displacement of tropomyosin allows myosin to bind actin -> contraction

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18
Q

skeletal muscle contraction requires mechanical coupling of what two receptors?

A

CaV1.1 and RYR1

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19
Q

what drug is given for subarachnoid hemorrhage (bleeding in space around brain)?

A

nimodipine

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20
Q

3 clinical applications for calcium channel blockers

A

angina, arrhythmia, HTN

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21
Q

which is not one of the 3 distinct chemical classes of calcium channel blockers?

a. dihydropyridines
b. phenylalkylamines
c. organic nitrates
d. benzothiazepines

A

c. organic nitrates

(these are vasodilators)

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22
Q

what do dihydropyridine CCB drugs end in?

A

“-dipine”

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23
Q

what structural element gives nifedipine, amlodipine, isradipine, and other “-dipines” their name?

A

dihydropyridine ring

24
Q

which drug is a short acting DHP formulated with lipids derived from soy and egg, and is given IV to treat hypertension when PO admin of drugs is not possible/desirable?

a. amlodipine
b. nifedipine
c. nicardipine
d. isradipine
e. clevidipine
f. felodipine

A

e. clevidipine

25
Q

clevidipine’s active form is cleaved by what enzymes?

A

esterases

26
Q

blockade mechanism of dihydropyridines: the (+) enantiomer of Bay K 8644 __________ current, and interferes with __________

a. blocks; opening
b. blocks; closing
c. potentiates; opening
d. potentiates; closing

A

a. blocks; opening

27
Q

blockade mechanism of dihydropyridines: the (-) enantiomer of Bay K 8644 __________ current, and interferes with __________

a. blocks; opening
b. blocks; closing
c. potentiates; opening
d. potentiates; closing

A

d. potentiates; closing

28
Q

dihydropyridines are more potent in relaxing _____ muscle, especially which artery?

A

smooth; coronary artery

(DHPs do not compromise cardiac function)

29
Q

tissue selectivity of CCBs are the result of what 2 things?

A

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

30
Q

vascular selectivity of DHPs is observed in _____ assays but not _____ assays

a. functional; binding
b. binding; functional

A

a. functional; binding

(Idk what this means though)

31
Q

what does voltage-dependence block mean?

A

affinity of drug for the channel is diff at diff voltages

32
Q

what is it called when DHP drugs bind to closed channels (at allosteric site) and prevent opening?

A

tonic block

33
Q

clinical considerations for DHPs: reflex tachycardia secondary to vasodilation occurs in all drugs except _________

A

amlodipine (due to slow onset of action)

34
Q

why is nimodipine used for subarachnoid hemorrhage?

A

it’s selective for cerebral arteries

(it can relax arteries in brain that have been contracted due to a brain bleed)

35
Q

clinical considerations for DHPs: DHPs reduce oxygen demand in heart, may inhibit atherosclerosis, and all (except ________) do not depress cardiac function

A

nifedipine

36
Q

true or false: all DHPs are not highly bound to serum proteins and undergo extensive first pass metabolism in liver

A

false

(they are all highly bound)

37
Q

amlodipine has _____ onset and _____ duration of action

A

slow; long

38
Q

rapid release __________ may inc risk of subsequent heart attack due to tachycardia

a. amlodipine
b. nifedipine
c. clevidipine
d. nisoldipine

A

b. nifedipine

39
Q

only drug in phenylalkylamine CCB class

A

verapamil

40
Q

verapamil inhibitory effect on heart is due to what type of block?

A

frequency dependent block

41
Q

which is the most potent for vasodilation, DHPs, verapamil, or diltiazem?

A

DHPs

42
Q

verapamil and diltiazem _____ conduction through the SA and AV nodes, reducing heart rate and force of contraction

A

slows

43
Q

why is reflex tachycardia blunted for verapamil?

A

bc it is also inhibiting channels in the heart

44
Q

where does verapamil bind in calcium channels?

a. allosteric site
b. pore

A

b. pore

(blocks Ca2+ influx through pore)

45
Q

true or false: verapamil has marked tonic block and very little freq dependent block

A

false (marked freq dependece, very little tonic block)

46
Q

what is the only drug in benzothiazepine class (that we talked about)?

A

diltiazem

47
Q

diltiazem directly inhibits the heart _____ than verapamil, but _____ than DHPs

a. less; more
b. more; less

A

a. less; more

48
Q

characteristics of benzothiazepine (diltiazem) block: is it tonic, frequncy dependent, or both?

A

both (some tonic block, some freq dependence)

49
Q

most common side effect of DHPs (slide 39)

A

flushing (they are good vasodilators)

50
Q

which is considered a clinically significant side effect of all 3 drugs: diltiazem, DHPs, and verapamil?

a. constipation
b. ankle edema
c. rash
d. facial flushing
e. dizziness

A

b. ankle edema

51
Q

what are the 3 clinically significant side effects of DHPs?

a. ankle edema
b. constipation
c. dizziness
d. facial flushing
e. headaches
f. ischemia
g. rash
h. tachycardia

A

a, d, h

52
Q

what are the two clinically significant side effects of verapamil?

a. ankle edema
b. constipation
c. dizziness
d. facial flushing
e. headaches
f. ischemia
g. rash
h. tachycardia

A

a. ankle edema
b. constipation

53
Q

diltiazem’s clinically significant side effect (1)

A

ankle edema

54
Q

potential for drugs selective for CaV1.3: treatment of ______ ______ (studies with _____)

(Last blank is a drug)

A

drug addiction; isradipine

55
Q

potential for drugs selective for CaV2.1: treatment of ______ ______ ______, some types of ______

A

familial hemiplegic migraine; ataxia

56
Q

potential for drugs selective for CaV2.2: treatment of refractory chronic pain due to what toxin? What drug can treat this?

A

Conus magus;

omega-Conotoxin MVIIA (Ziconotide, Prialt)

PHRM 844 Therapeutics (28 decks)

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