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Anesthesia Pharm II > CCB ppt > Flashcards

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
Q

can someone be on a BB and DHP CCB

A

sure the DHP CCB don’t effect HR

26
Q 
********************************
out of the drugs
Verapamil Non-DHP (phenylalkylamine)
Diltiazem Non-DHP (benzothiazepine)
Nifidipine DHP
Nicardipine DHP
which ones in order cause coronary vasodilation
A

Verapamil- moderate
Diltiazem - mod
Nifidipine - marked
Nicardipine ** greatest

27
Q 
*********************
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
A

Verapamil-moderate
Diltiazem -mod
Nifidipine - mod
Nicardipine -0/slight

28
Q 
******************
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
A

Verapamil -mod
Diltiazem - slight
Nifidipine - none
Nicardipine - none

29
Q 
************
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
A

Verapamil - marked
Diltiazem - mod
Nifidipine - none
Nicardipine - none

30
Q

ex of DHP CCB

A 
Nicardipine
nifedipine
nimodipine
clevidipine
amlodipine
(-pine)
(remember Ca++le graze in the -pine)
31
Q

pharmacology of Non-DHP

A

Neg inotropic
Neg- chronotropic
Neg-dromotropic
positive- Lusitropic (myocardial relaxation)

32
Q

what do ALL CCB do pharmacology wise

A
  • decrease coronary vascular resistance and increase coronary blood flow
  • Decrease PVR via vasodilation of arterioles
  • minimal venous tone effects
33
Q

which CCB is best for variant angia
eg vasospastic or prinzmetal’s angina

A

Narcardapine

34
Q

which CCB is good for subarachnoid hemorrhage (posthemoragic cerebrovascular spasm

A

Nimodipine

35
Q

which CCB’s are good for Hypertrophic cardiomyopathy

A

Nifidipine

verapamil

36
Q

Common SE of CCB

A

-orthrostatic hypotension
-bradycardiam(DHP increase HR)
- periphreal edema
- dizziness
headaches
flushing
N/V

37
Q

Verapamil can increase the levels of what drug

A

Digoxin

38
Q

which CCB is commonly used in the OR Can be given bolus or infusion and what class

A

Nicardapine

DHP

39
Q

Which CCB is very fast onset off set, faster than nicardapine, prepared in a lipid emulsion, only given in bolus no infusion?

A

Clevidipine

40
Q

Contraindications to Verapimil

A

WPW
Sicksinus syndrome
Av block
Heart rate

41
Q

how do CCB decrease contraction

A

decrease influx of Ca++ causes decrease in contraction

42
Q

**** basic way Non-DHP work

A

slow cardiac conduction

decrease HR via SA and AV nodes

43
Q

basic way DHP work

A

no effect on conduction
vasodilate
increase HR

44
Q

what CCB is the greatest coronary vasodilator and can cause coronary steal?

A

Nicardapine

45
Q

Why are DHP and BB ok to use in combination

A

DHP incease HR and BB decrease HR

46
Q

why do Non-DHP slow HR

A

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
Q

If HR is 45 and B/P is 210/105 what drug would you give

A

DHP like nicardapine or any

if has no effect on HR and will decrease BP

Anesthesia Pharm II (19 decks)

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