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Top Shelf Drugs > Neuromuscular blocker agents > Flashcards

Neuromuscular blocker agents Flashcards

It seemed silly to redo the cards for these drugs since it's solid information. Feel free to add or change things.

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 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

cholinesterasesee 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 ortrue 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 binds to 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

Depolarizersnon-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

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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13
Q

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

A

Acetylcholine

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14
Q

how do DMBDs work (Sux’s)

A

-mimic ACh at the ACh receptor-cause sustained depolarization rendering the NMJ unable to conduct further impulses which = muscle relaxation-fasiculations

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15
Q

Sux’s (DMBDs) has how many phases

A

2

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16
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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17
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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18
Q

when does phase II blocks occur

A

After large or repeated doses of sux’s

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19
Q

what is the mechanism that causes phase II blocks

A

Unknown

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20
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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21
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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22
Q

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

A

extra junctional receptors

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23
Q

Sux’s is metabolized by what? and where?

A

psuedocholinesterasein the plasma

24
Q

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

A

psuedocholinesterasebutyrocholinesterase

25
Q

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

A

Succinylmonocholine

26
Q

what accounts for the 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)

27
Q

2 types of psuedocholinesterase deficiency’s

A

1) Heterozygous atypical 2) Homozygous atypical

28
Q

what drug would a psuedocholinesterase deficiency affect and why?

A

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

29
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)

30
Q

2 things to know about psuedocholinesterase deficiency Homozygous atypical

A

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

31
Q

which type of psuedocholinesterase deficiency is most common

A

heterozygous

32
Q

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

A

Dibucaine

33
Q

what is DIBUCAINE

A

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

34
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

35
Q

Chemical structures of all NDMBDs

A

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

36
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

37
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 >

38
Q

Metabolism of NDMBD

A

metabolized in Liver Kidney Plasma and spontaneously

39
Q

how are NDMBDs excreated in active or inactive forms

A

Both

40
Q

how does Pregnancy affect PK of NDMBDs

A

-no change in PK -UNLESS os MgSO4 (this results in increased potency and duration)

41
Q

how does temperatire affect NDMBDs

A

hypothermia causes INCREASED duration of action

42
Q

how does AGE effect PK of NDMBDs

A

Vd larger in children elderly can have longer duration with organ clearance drugs

43
Q

how does obesity effect PK of NDMBDs

A

Vd and clearance reduced

44
Q

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–30-20 SEC duration 5-10 MIN elimination – PLASMACHOLINESTERASE histamine release–YES

45
Q

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

46
Q

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–0.08-0.1time 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 eliminatoin is inversed)

47
Q

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

48
Q

Most NDMBDs are metabolised where?

A

renal and biliary

49
Q

Which NDMBDs should NOT be used with renal failure and why??

A

-Pancuronium (pavulon)-b/c 80% excreated by renal

50
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

51
Q

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)

52
Q

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

A

-good for kidney and hepatic factors-bad for histamine release

53
Q

what is important to know about Mivacurium

A

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

54
Q

how is Nimbex (cis-atacurium) eliminated

A

Hoffman elimination

55
Q

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)

56
Q

what is ED95

A

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

57
Q

** great tipif 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

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