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PDA Block 2 > Ca Channel Blockers > Flashcards

Ca Channel Blockers Flashcards

1
Q

How is Ca involved in cardiac muscle cells

A
  • Action Potentials cause Ca channels to open causing Ca to rush in
  • Cardiac muscle contraction is dependent on Ca entering the cell
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2
Q

What drug(s) are in the Phenylalkylamines class

A

Verapamil

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3
Q

What drug(s) are in the Benzothiazepines class

A

diltiazem

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4
Q

What drug(s) are in the 1,4-Dihydropyridines class?

A
  • Nifedipine

- Amlodipine

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5
Q

Compare the chemical structures of the different drug classes

A

They are all so different! But they all work on L-type Ca channels

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6
Q

Widespread use of CBCs

A 
Angina pectoris
Hypertension 
treatment of supraventricular arrhythmias
*Atrial flutter
*atrial fibrillation 
*Paroxysmal SVT
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7
Q

What do the Calcium Channel Blockers (CCBs) target

A

L-type Ca channels in vascular smooth muscle and cardiac muscle

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8
Q

Describe the L-type Calcium chanenl

A

It is a channel made up of four subunits that forms a pore

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9
Q

Describe the binding of the Benzothiazepines and phenylalkylamines

A

Use dependent binding
-They bind when the Calcium channel is in the open state. the binding pocket is inside the pore so the pore has to be open in order for them to bind

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10
Q

Describe the binding of 1,4-dihydropyrimidines

A

Voltage dependent binding

  • depends on membrane potential. When the membrane is more depolarized (more positive) there is more binding!
  • Vascular smooth muscle is more positive so there is more binding of these drugs there, as opposed to in the heart
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11
Q

Describe the three conformation states of the Calcium channel and what that means for drug binding

A
  • When Calcium rushes in the drug is in the open state: All drugs can bind! Especially think about the usage dependent binding of the Benzothiazepines and phenylalkylamines
  • Inactivated State: Only the 1,4 dihydropyrimidines can bind because this is when the cell is quire depolarized but closed
  • closed state: no binding
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12
Q

Describe the results of the Washington University paper

A

There are different binding sites for the use dependent vs voltage dependent drugs but there is some aa overlap so some binding overlap

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13
Q

Describe why two classes of Ca Channel Blockers are not given togetehr

A

They have allosteric interactions, both up-regulating and down-regulating binding of each other. Therefore it makes interactions and effects unpredictable so we don’t give them together.

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14
Q

Mechanism of Action of CCBs

A
  • increase the time that Ca channels are non-conducting
  • relaxation of the arterial smooth muscle, but not much effect on the venous smooth muscle (so decrease afterload but not preload)
  • significant reduction in afterload but not preload (bc no effect on veins and pre-load is related to the veous return)
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15
Q

Why dont CCBs work on neurons

A

Neurons have N-type ad P-type Ca channels to mediate neurotransmitter release.

CCBs work on L-type Ca Channels

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16
Q

Why don’t CCBs work on skeletal muscle

A

Skeletal muscle relies on intracellular Ca for contraction, but this Ca is only to act as a voltage sensor.

SO really you can think that it is voltage dependent and not dependent on Ca entry

Ca entry across the t -tubule membrane is NOT required for skeletal muscle contraction.

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17
Q

Why do CCBs work on cardiac cells

A

cardiac cells rely on L-type Ca channels for contraction (fast response cells) and for the upstroke of the action potential in slow response cells.

Cardiac cells are dependent on Ca entering for contraction

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18
Q

Why do CCBs work on vascular smooth muscle

A

Vascular smooth muscle relies on Ca influx through L-type Ca channels for contraction

-Ca entry is required to maintain th epulsating tone of vascular smooth muscle

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19
Q

Why does the different binding sites of CCBs result in differing pharmacological effects

A
  • use-dependent binding works on cardiac cells

- voltage dependent binding works on smooth muscle

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20
Q

Explain why Dihydropyridines are selective vasodilators and the side effect related to this

A
  • they dilate blood vessels through the voltage dependent Ca channels
  • This causes Reflex tachycardia: a potential reflex increase in HR, myocardial contractility and oxygen demand due to the decreased resistance casued by dilation
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21
Q

Explain how the Non-dihydropyridines are more potent for cardiac tissues vs vasculature and the effects this causes

A
  • -effects th eheart via the use dependent Ca channels
  • helps to slow the heart rate by blocking the channels. The heart can’t contract as much if the Ca channel which allows contraction is blocked!
  • On that note it also decreases contractility
  • Heart rate moderating, reduced inotropism, peripheral and coroanry vasodialtion
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22
Q

Common uses of CCBs

A

Angina
Arrhythmias
HTN

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23
Q

Explain the CCB use for angina

A
  • Diltiazem, Verapamil: reduces workload, lowers heart rate, reduces cardiac afterload, increases coronary blood flow
  • Nifedipine: reduces myocardial oxygen demand, reduces arterial pressure
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24
Q

Explain the CCBs uses for Arrythmias (atrial fibrillation/flutter; supraventricular tachycardia)

A

-Diltiazem, Verapamil: reduces firing rate of the SA node, reduce conduction through the AV node (1,4 Dihydropyridines are not classified as anti-arrhythmic drugs)

(bc they block the AV node if someone is suffering from an AV block CCB use is contraindicated)

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25
Q

Explain the CCB use for Hypertension

A

1,4-Dihydropyridines (nifedipine): potent vasodilator action

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26
Q

Explain the effects of Verapamil on Peripheral vasoldialtion

A

increase

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27
Q

Explain the effects of Verapamil on coronary vasodilation

A

super increase

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28
Q

Explain the effects of Verapamil on preload

A

none

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29
Q

Explain the effects of Verapamil on afterload

A

decrease

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30
Q

Explain the effects of Verapamil on contractility

A

super decrease

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31
Q

Explain the effects of Verapamil on heart rate

A

super decrease

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32
Q

Explain the effects of Verapamil on AV conduction

A

super decrease

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33
Q

Explain the effects of Diltiazem on Peripheral vasodilation

A

increase

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34
Q

Explain the effects of Diltiazem on coronary vasodilation

A

increase

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35
Q

Explain the effects of Diltiazem on preload

A

none

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36
Q

Explain the effects of Diltiazem on afterload

A

decrease

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37
Q

Explain the effects of Diltiazem on contractility

A

decrease

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38
Q

Explain the effects of Diltiazem on heart rate

A

decrease

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39
Q

Explain the effects of Diltiazem on AV conduction

A

decrease

40
Q

Explain the effects of Nifedipine, Amlodipine on Peripheral vasodialtion

A

super increase

41
Q

Explain the effects of Nifedipine, Amlodipine on coronary vasodilation

A

super increase

42
Q

Explain the effects of Nifedipine, Amlodipine on preload

A

none

43
Q

Explain the effects of Nifedipine, Amlodipine on afterload

A

super decrease

44
Q

Explain the effects of Explain the effects of Nifedipine, Amlodipine on contractility

A

increase bc of the reflex tachycardia, but if they are taken with . a B blocker the contractility will decrease

45
Q

Verapamil oral absorption

A

over 90

46
Q

Verapamil bioavailability

A

10-35% very large first pass effect

47
Q

Verapamil Protein Bound %

A

83-92

48
Q

Verapamil Elimination half life

A

2.8-6.3

49
Q

Diltiazem oral absorption

A

over 90

50
Q

Diltiazem bioavialability

A

41-67

51
Q

Diltiazem Protein bound %

A

77-80

52
Q

Diltiazem Elimination Half-life

A

3.5-7

53
Q

Nifedipine oral absorption

A

over 90

54
Q

Nifedipine bioavailability

A

45-86

55
Q

Nifedipine protein bound %

A

92-98

56
Q

Nifedipine Elimination Half-life (h)

A

1.9-5.8

57
Q

Amlodipine oral absorption

A

over 90

58
Q

Amlodipine

bioavialabilty

A

64-90

59
Q

Amlodipine

Protein bound %

A

97-99

60
Q

Amlodipine

Elimination Half-life

A

30-50 hours. This is great bc you only have to take it once a day, but if there are any negative effects from he drug it is hard to intervene bc the half-life is so long

61
Q

What percent comparatively does Diltiazem cause adverse effects

A

0-3%

62
Q

Does Diltiazem cause the adverse effect of Hypotension

A

yes!

63
Q

Does Diltiazem cause the adverse effect of headaches

A

no

64
Q

Does Diltiazem cause the adverse effect of Peripheral edema

A

yes!

65
Q

Does Diltiazem cause the adverse effect of constipation

A

no

66
Q

Does Diltiazem cause the adverse effect of CHF (worsening)

A

yes

67
Q

Does Diltiazem cause the adverse effect of AV block

A

yes

68
Q

Does Diltiazem cause the adverse effect of needing to be cautious bc B blockers

A

yes

69
Q

To what extent comparatively does Verapamil cause adverse effects

A

10-14%

70
Q

Does Verapamil cause the adverse effect of hypotension

A

yes!

71
Q

Does Verapamil cause the adverse effect ofheadaches

A

yes

72
Q

Does Verapamil cause the adverse effect of peripheral edema

A

yes

73
Q

Does Verapamil cause the adverse effect ofconstipation

A

yes

74
Q

Does Verapamil cause the adverse effect of worsening CHF

A

yes a lot

75
Q

Does Verapamil cause the adverse effect of AV block

A

yes a lot

76
Q

Does Verapamil cause the adverse effect of needing to use caution w beta blockers

A

yes a lot!

77
Q

To what extent comparatively do the Dihydropyridines cause adverse effects

A

9-39%

78
Q

Do the Dihydropyridines cause the adverse effect of hypotension

A

yes a lot!!! Bc they directly influence the vasculature

79
Q

Do the Dihydropyridines cause the adverse effect of headaches

A

yes a lot bc increase blood flow to brain

80
Q

Do the Dihydropyridines cause the adverse effect of peripheral edema

A

yes a lot bc they dilate arteries and do nothing on veins, so this means a pressure increase at the capillaries

81
Q

Do the Dihydropyridines cause the adverse effect of constipation

A

no

82
Q

Do the Dihydropyridines cause the adverse effect of worsening CHF

A

no

83
Q

Do the Dihydropyridines cause the adverse effect of AV block

A

no

84
Q

Do the Dihydropyridines cause the adverse effect of needing caution with beta blockers

A

no

85
Q

What do you need to monitor when someone is on a CCB how do you monitor the drugs effectiveness

A
  • heart rate
  • blood pressure
  • anginal symptoms
  • signs of CHF
  • adverse effects
86
Q

Is Diltiazem contraindicated for hypotension

A

yes

87
Q

Is Diltiazem contraindicated for sinus bradycardia

A

yes

88
Q

Is Diltiazem contraindicated for AV conduction defects

A

yes!

89
Q

Is Diltiazem contraindicated for Severe cardiac failure

A

yes

90
Q

Is Verapamil contraindicated for hypotension

A

yes

91
Q

Is Verapamil contraindicated for sinus bradycardia

A

yes

92
Q

Is Verapamil contraindicated for AV conduction defects

A

yes

93
Q

Is Verapamil contraindicated for Severe cardiac failure

A

yes! A lot

94
Q

Are Nifedipine & Amlodipine contraindicated for hypotension

A

yes

95
Q

Are Nifedipine & Amlodipine contraindicated forsinus bradycardia

A

no

96
Q

Are Nifedipine & Amlodipine contraindicated for AV conduction defects

A

no

97
Q

Are Nifedipine & Amlodipine contraindicated for severse cardia failure

A

yes

PDA Block 2 (13 decks)

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