CCB ppt Flashcards

1
Q

what is the role of intracellular Ca++

A

regulates contraction

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2
Q

how can you tell a myocyte cell from the rest?

A

it has troponin c

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3
Q

how does Ca++ work in cardiac muscle

A

Ca++ binds to troponinC releives troponin I inhibition of actin-myocin interaction

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4
Q

how does Ca++ work in smooth muscle

A

binds to calmodulin causing actin and myosin interaction

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5
Q

where is most Ca++ at intracellular or extracellular?

A

extracellular

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6
Q

where is most of the Ca++ at intracellularly

A

the SR

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7
Q

Ca++ bound to SR is what

A

inactive

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8
Q

Free Ca++ inctracellular concentration is markedly increased when?

A

during contraction b/c SR releases Ca++ and the Ca++ channel is open allowing Ca++ in

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9
Q

what are the 6 types of Ca++ channels

A
L
N
P
Q
R
T
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10
Q

What are the Ca++ channels we deal with ?

A

L
and
T

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11
Q

what type of channels are Ca++ channels

A

voltage gate

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12
Q

what is a voltage gated channel

A

when they reach a voltage then the open

a ligand gated is a drug or hormone binding

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13
Q

what is the L-type channel

A

sustained conductance, slow inactivation

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14
Q

What is T-type channels

A

similar to L but rapid inactivation’have minimal sensitivity to CCB

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15
Q

with CCB what type of channel are me using the most

A

L-type

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16
Q

5 subunits of L-type (slow) Ca++ channels

A
alpha 1
alpha 2
beta
gamma
delta
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17
Q

3 main types of CCB then what are the real way to differentiate them into 2 goups?

A

Non-dihydropyridines
-Phenylalkylamines-
-Benzothiazepines-
1,4- dihydropyridines (DHPs)

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18
Q

so basically all CCB are DHP except for what 2 drugs?

A

verapamil
and
diltiazem

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19
Q

what is an example of a NonDHP phenylaklylamine and benzothiazepines

A

phenylaklylamine- verapamil
benzothiazepines- diltiazem
a way to try and remember
(benz=lorazepam sounds like diltazem)

20
Q

what is the main difference b/t NonDHP and DHP?

A

Non-DHP-affect nodes (both verap and diltaz)

DHP-do not effect Nodes

21
Q

how do phenylalkylamines work?

A

Verapamil

binds to intracellular portion of alpha subunit 1

22
Q

how do benzothiazepines work

A

diltiazem

MOA not understood

23
Q

how do DHP work

A

modulate the L-type channel

vascular smooth muscle

24
Q

should someone be on cardizen and a BB?

A

no b/c they both affects nodes

25
***************************** | can someone be on a BB and DHP CCB
sure the DHP CCB don't effect HR
26
``` ******************************** out of the drugs Verapamil Non-DHP (phenylalkylamine) Diltiazem Non-DHP (benzothiazepine) Nifidipine DHP Nicardipine DHP which ones in order cause coronary vasodilation ```
Verapamil- moderate Diltiazem - mod Nifidipine - marked Nicardipine **** greatest
27
``` ********************* out of the drugs Verapamil Non-DHP (phenylalkylamine) Diltiazem Non-DHP (benzothiazepine) Nifidipine DHP Nicardipine DHP whcih ones in order cause supression of cardiac contractility ```
Verapamil-moderate Diltiazem -mod Nifidipine - mod Nicardipine -0/slight
28
``` ****************** out of the drugs Verapamil Non-DHP (phenylalkylamine) Diltiazem Non-DHP (benzothiazepine) Nifidipine DHP Nicardipine DHP which ones in order cause supression of SA node ```
Verapamil -mod Diltiazem - slight Nifidipine - none Nicardipine - none
29
``` ************ out of the drugs Verapamil Non-DHP (phenylalkylamine) Diltiazem Non-DHP (benzothiazepine) Nifidipine DHP Nicardipine DHP which ones in order cause supression of AV node ```
Verapamil - marked Diltiazem - mod Nifidipine - none Nicardipine - none
30
*********** | ex of DHP CCB
``` Nicardipine nifedipine nimodipine clevidipine amlodipine (-pine) (remember Ca++le graze in the -pine) ```
31
pharmacology of Non-DHP
Neg inotropic Neg- chronotropic Neg-dromotropic positive- Lusitropic (myocardial relaxation)
32
*********** | what do ALL CCB do pharmacology wise
- decrease coronary vascular resistance and increase coronary blood flow - Decrease PVR via vasodilation of arterioles - minimal venous tone effects
33
************** which CCB is best for variant angia eg vasospastic or prinzmetal's angina
Narcardapine
34
************ | which CCB is good for subarachnoid hemorrhage (posthemoragic cerebrovascular spasm
Nimodipine
35
************* | which CCB's are good for Hypertrophic cardiomyopathy
Nifidipine | verapamil
36
Common SE of CCB
-orthrostatic hypotension -bradycardiam(DHP increase HR) - periphreal edema - dizziness headaches flushing N/V
37
Verapamil can increase the levels of what drug
Digoxin
38
which CCB is commonly used in the OR Can be given bolus or infusion and what class
Nicardapine | DHP
39
Which CCB is very fast onset off set, faster than nicardapine, prepared in a lipid emulsion, only given in bolus no infusion?
Clevidipine
40
Contraindications to Verapimil
WPW Sicksinus syndrome Av block Heart rate
41
**************** | how do CCB decrease contraction
decrease influx of Ca++ causes decrease in contraction
42
************** basic way Non-DHP work
slow cardiac conduction | decrease HR via SA and AV nodes
43
************** | basic way DHP work
no effect on conduction vasodilate increase HR
44
*********** | what CCB is the greatest coronary vasodilator and can cause coronary steal?
Nicardapine
45
Why are DHP and BB ok to use in combination
DHP incease HR and BB decrease HR
46
************** | why do Non-DHP slow HR
closes the Ca++ channels in phase 4 thus decreasing hr | so it basically blocks the conduction and prolongs the time it takes to reah the threshold
47
If HR is 45 and B/P is 210/105 what drug would you give
DHP like nicardapine or any | if has no effect on HR and will decrease BP