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Anesthesia Pharm 1-Josh > Muscle relaxant drugs (11) > Flashcards

Muscle relaxant drugs (11) Flashcards

To perform anesthesia as a perfectionist, with nothing less than pure anesthesia badassary!!!!!!

1
Q

Acetylcholine contains a positively charged quaternary ammonium group that attaches to the _________ charged _________ receptors

A
  • negatively

- cholinergic

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2
Q

how is acetylcholine synthesized?

acetyl-Coa + choline —-????—-> acetylcholine (basiaclly what is the enzyme that helps is convert)

A

choline acetyl transferase

see slide #4 (Muscle relaxant drugs)for the chemical structures it may help

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3
Q

how is acetylcholine metabolised

acetylcholine ——-??????—–> choline + acetic acid (basically what is the enzyme that breaks acetylcholine down?)

A

cholinesterase

see slide #4 (Muscle relaxant drugs)for the chemical structures it may help

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4
Q

So acetylcholine is rapidy metabolized by acetylcholinesterase into _______ and _____

A

Acetate and Choline

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5
Q

acetylcholinesterase is also called _________ ___________ or _____ _________

A 
specific cholinesterase or
true cholinesterase
 (just incase he tries to throw a curve ball)
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6
Q

how does acetylcholine work in the neuro muscular junction (NMJ)

A

1st- Ach is released presynaptically and bindsto the postsynaptic nicotinic receptor
-NEXT- there are 2 alpha subunits on the nicotinic receptor
-LAST(LY)- Na+ channels open when both subunits are occupied by Ach
((((side note this will show why and where the NMBD work and why they block the Na+ channels)))))

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7
Q

(5) main structures of Muscle relaxants

A
  • -ALL are quaternary ammonium compounds ( 4 carbon atoms attached to 1 Nitrogen atom)
  • ALLcontain at least 1 ammonium group
  • ALL MIMIC ACh to exert relaxant properties
  • the POSITIVELY charged quaternary ammonium group is electrostatically attracted to the negatively charged cholinergic receptor
  • SCh (a small slender molecule) binds to (both alpha units) and activated ACh receptor
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8
Q

Look at slide 11 in the Muscle relaxant drugs ppt

A

to see the chemical makeup of vec and pan

mono vs bisquaternary

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9
Q

2main categories of muscle relaxants (don’t over think it)

A

Depolarizers

non-depolarizers

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10
Q

2 examples of depolarizers (only that we really use I am not even sure if the other is still in use)

A
  • Succinylcholine

- Decamethonium

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11
Q

6 main non-depolarizers ( to become an extra bad badass what is the 7th don’t need to know for test but for knowledge)

A 
Curare
Pancuronium
veruronium
pocuronium
atracurium
cis-atracurium
BONUS
--------Mivacurium
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12
Q

what is a special note about Curare

A

its the origional NDMBD

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13
Q 
*******************************************
Must know the doses of the following
Cis-atracurium
Rocuronium
Pancuronium
Vecuronium
A 
in order per potency (Pink Vagina Can-Always Rebound)
Pancuronium-0.08-0.1
Vercuronium-0.08-0.1
Cis-Atracurium- 0.15-0.2 mg/kg
Rocuronium- 0.6-1.2 mg/kg
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14
Q

Depolarizers (Sux’s) resemble and mimic ______ at the Ach receptor

A

Acetylcholine

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15
Q

how do DMBDs work (Sux’s)

A
  • mimic ACh at teh ACh receptor
  • cause sustained depolarization rendering the NMJ unable to conduct further impulses which = muscle relaxation
  • fasiculations
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16
Q

Sux’s (DMBDs) has how many phases

A

2

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17
Q

what is a phase I block of DMBDs

A

sustained opening of receptor channels in depolarized post junctions membrane cannot respond to further ACh

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18
Q

what is phase II block of DMBDs

A

desensitized repolarized post-junctional membrane remains unresponsive to ACh. (occurs after a large or repeated sux’s doses)

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19
Q

when does phase II blocks occur

A

After large or repeated doses of sux’s

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20
Q

what is the mechanis that causes phase II blocks

A

Unknown

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21
Q

Side effects of DMBDs (sux’s)

A

-the sustained depolarization causes K+ to be releases from cells (remember most K+ is stored in the cell)

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22
Q

Hyperkalemia is an increased risk with Sux’s administration,but this risk is increased with what type of pt’s

A

Upregulated

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23
Q

the massive K+ release associated with DMBDs (sux’s) is released from where

A

extra junctional receptors

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24
Q

Sux’s is metabolized by what? and where?

A

psuedocholinesterase

in the plasma

25
Q

plasmacholinesterase (what metabolizes sux’s) is also called what

A

psuedocholinesterase

butyrocholinesterase

26
Q

Sux’s is metabolized rapidly into ___________ upon injection into the blood, thus only a fraction actually reaches the NMJ

A

Succinylmonocholine

27
Q

what accounts for th longer duration of action of depolarizers (sux’s) compared to ACh

A

b/c depolarizers must diffuse away from the NMJ to the plasma to be metabolized
(kinda of confusing, if you want clarification look at slide 19, basic take home message is that sux’s last longer than ACh)

28
Q

2 types of psuedocholinesterase deficiency’s

A

1) Heterozygous atypical

2) Homozygous atypical

29
Q

what drug would a psuedocholinesterase deficiency affect and why?

A

Sux’s, b/c thats what metabolizes all DMBDs AKA sux’s

30
Q

2 things to know about psuedocholinesterase deficiency

Heterozygous atypical

A

-1 abnormal gene ( way to remember HETER 1 male 1 female)
-prolonged block 20-30 minutes after sux’s administration
(side note occurs 1:50 pts)

31
Q

2 things to know about psuedocholinesterase deficiency Homozygous atypical

A

-2 abnormal genes ( way to remember 2 fags= homo)
-prolonged blockake 6-8 hours after sux’s
(side note occurs 1:3000 pts)

32
Q

which type of psuedocholinesterase deficiency is most common

A

heterozygous

33
Q

in relation to psuedocholinesterase deficiency the __________ number represents the percentage inhibition of pseudocholinesterease

A

Dibucaine

34
Q

what is DIBUCAINE

A

a local anesthetic that inhibits normal pseudocholinesterase by 80%, heterozygous by 40-60% and homoxygous by 20%

35
Q

NDMBDs 3 facts about their distribution

A

1) highly ionized (low lipophilicity)
2) low volume of distribution (extracellular fluid)
3) do NOT cross the BBB, placental barrier, or GI

36
Q

Chemical structures of all NDMBDs

A

J/K see slide 24 ( just look at and see basic make up..

37
Q

NDMDs action 4 simple steps

A
  • competative antagonism
  • binds to ACh receptors (but exert no effect)
  • Block action of ACh
  • then diffusion away from NMJ site to site of metabolism
38
Q 
NDMBDs duration (not individual just est from ppt slides on all overal )
short, intermediate, long acting
A

short acting 5-20 min
intermediate acting 25-55 min
long acting 60 min and >

39
Q

Metabolism of NDMBD

A 
metabolized in 
Liver
Kidney
Plasma
and spontaneously
40
Q

how are NDMBDs excreated in active or inactive forms

A

Both

41
Q

how does Pregnancy affect PK of NDMBDs

A
  • no change in PK

- UNLESS os MgSO4 (this results in increased potency and duration)

42
Q

how does temperatire affect NDMBDs

A

hypothermia causes INCREASED duration of action

43
Q

how does AGE effect PK of NDMBDs

A

Vd larger in children

elderly can have longer duration with organ clearance drugs

44
Q

how does obesity effect PK of NDMBDs

A

Vd and clearance reduced

45
Q 
Must Know ********************************
SUCCINYLCHOLINE
ED 95 mg/kg
intubation dose
time to intubation
duration
elimination 
histamine release
A 
ED 95 mg/kg---0.25 MG/KG
intubation dose--1-1.5 MG/KG
time to intubation--30-20SEC
duration 5-10 MIN
elimination -- PLASMACHOLINESTERASE
histamine release--YES
46
Q 
Must Know ********************************
PANCURONIUM (pavulon)
ED 95 mg/kg
intubation dose
time to intubation
duration
elimination 
histamine release
A 
ED 95 mg/kg --0.07 MG/KG
intubation dose--0.08-0.1 MG/KG
time to intubation--3-5 MIN
duration--80-100 MIN
elimination -- 80% RENAL; 20% BILIARY
histamine release--NOPE
47
Q 
Must Know ********************************
VECURONIUM (norcuron)
ED 95 mg/kg
intubation dose
time to intubation
duration
elimination 
histamine release
A 
ED 95 mg/kg--0.06 MG/KG
intubation dose--0.08-0.1
time to intubation--2-3 MIN
duration--25-30 MIN
elimination-- 20% RENAL; 80% BILARY
histamine release-- NO

HINTS ( vec and pan are very similar- dose is the same time to intubate close to the same. main differences is PAN is LONG acting, VEC is INTERMEDIATE acting and eliminatin is inversed)

48
Q 
Must Know ********************************
ROCURONIUM (zemuron)
ED 95 mg/kg
intubation dose
time to intubation
duration
elimination 
histamine release
A 
ED 95 mg/kg--0.3 MG/KG
intubation dose-- 0.6-1.2 MG/KG
time to intubation--1-3 MIN
duration--30 MIN
elimination --30% RENAL; 70% BILIARY
histamine release--NO
49
Q

Most NDMBDs are metabolised where?

A

renal and biliary

50
Q

*** must know**

of the NDMBDs which one should NOT be used with renal failure and why??

A
  • Pancuronium (pavulon)

- b/c 80% excreated by renal

51
Q

side note from shores (and to make sure that we speak MORE ON A GRADUATE LEVEL per Nancy) how should we say NDMBDs are metabolized in the liver

A

Say BILIARY TRACT

52
Q

**must know****

Cis-atracurium (Nimbex) is just like atracurium, but is better and more frequently used why????

A

has less histamine release

he said that is all we need to know about it

53
Q

**must know***
shores stated in his lecture that we are not to larn the doseage but must know the following
what is good and bad about Atracurium (tracrium)

A
  • good for kidney and hepatic factors

- bad for histamine release

54
Q

**must know****

what is important to know about Mivacurium

A

short acting
has histamine release
no organ clearance (cleared via plasma cholinesterase)

55
Q

**** must know***

how is Nimbex (cis-atacurium) eliminated

A

Hoffman elimination

56
Q

should defiently know this*

what is the relationship between ED95 and intubation dose of muscle relaxants

A 
the intubating dose is 3 xs the ED 95 (you will be pimped)
 except for VEC and PAN (but close)
Roc ED95 0.3 intubating dose 0.6-0.12 (3 times the ED95=0.9 hmm in the middle)
Nim ED95 0.05 intibating dose 0.15-0.2
(he said this in class it works 50/50 do what you wish i mean all NDMBDs except Vec and Pan follow this)
57
Q

what is ED95

A

a dose causing muscle relaxation suitable for intubation in 95% of the population

58
Q

** great tip

if someone says how many cc’s of Vec would you give a pt who weighs 70 kg say 7, but then give what rational

A

most muscle relaxants ( not suxs) can be given in a ratio of 1ml per 10 kg of pt for example
Vec is prepared as 1 mg/ml in bottle and the intubating dose is 0.1 mg/kg so a 70 kg pt would get 7 mg for a dose (0.1 x 70=7mg) so give 7 ml of vec or 7mg
–or Roc 0.9 mg/kg (intubating dose) 70kg x 0.9 mg/kg = 63mg. it comes in 10mg/ml so give 6.3 mls very close to 7

Anesthesia Pharm 1-Josh (10 decks)

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