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MSK II > NMJ pharm > Flashcards

NMJ pharm Flashcards

1
Q

nondepolarizing NM blocking agents

A

isoquinoline derivatives

steroid derivates

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2
Q

Nondepolarizing isoquinoline derivatives

A 
Cisatracurium
tubocurarine 
atracurium
doxacurium
metocurine
mivacurium
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3
Q

nondepolarizing steroids derivatives

A

pancuronium
pipecuronium
recuroinum
vecuronium

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4
Q

depolarizing NM blocking agents

A

succinylcholine

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5
Q

mm relaxants/spasmolytics

A

dantorlene

botulinum

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6
Q

AChEinhibitors

A 
echotophate
edrophonium
neostigmine
physostigmine
pyridostigmine
ambenonium
donepezil
galantamine
rivastigmine
tacrine
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7
Q

antimuscarinic compounds

A

atropine

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8
Q

cholinesterase reactivators

A

pralidoxime

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9
Q

neuromuscular blockers

A

antinicotinic drugs
interfere with NMJ do not have CNS activity
adjuncts to general anesthesia for mm relaxation
all are highly polar and inactive orally so must be administered parenterally

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10
Q

spasmolytics

A

used to reduce spasticity in a variety of neurological conditions
aka ‘centrally acting’ mm relaxants

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11
Q

neuromuscular blocking agents MOA

A

competitive antagonists at nAChR

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12
Q

which mm are affected first?

A

smaller mm, larger mm (diaphragm) are last to be affected and first to recover

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13
Q

reversal of neuromuscular blockade

A

AChE inhibitors
neostigmine and pyridostigmine
edrophonium (less effective)
administer anticholinergic agents with AChE inhibitors to minimize adverse cholinergic effects effects d/t increased ACh at mAChR

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14
Q

adverse effects of nondepolarizing agents

A
  • some produce H2 -> wheals, bronchospasm, hypotension, bronchial and salivary secretion can co-administer antiH2
  • large doses tubocurarine and metocurine can prodcuce AChR blockade at autonomic ganglia and adrenal medulla -> hypotension and tachy
  • b/c tubocurariene causes sign H2 release not really used anymore
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15
Q

NM blockers and anesthetics

A

inhaled anesthetics potentiate the NM blockade produced by nondepolarizing mm relaxants
dose dependent

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16
Q

NM blockers and abx

A

aminoglycosides enhance NM blockade

some abx reduce release of ACh

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17
Q

aminoglycosides

A

gentamicin
tobramycin
amikacin
streptomycin

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18
Q

phenytoin and carbamazepine

A

significantly increase requirement for nondepolarizing NMBAs by unknown mech

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19
Q

NMBAs in pts >70

A

must be reduced d/t decreased metabolism and clearance

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20
Q

pts with severe burns and UMN disease

A

resistant to NMBAs likely d/t decreased nAChRs

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21
Q

atracurium

A 
intermediate acting
breakdown product laudanosine can cross BBB and cause seizures 
only an issue with prolonged Tx
can be used in renal or hepatic failure
less H2 release
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22
Q

cisatracurium

A

isomer of atracurium, but 3x as potent
intermediate acting with fewer side effects
can used used with significant renal/hepatic failure
devoid of CV efects

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23
Q

micacurium

A

shortest duration of action of all nondepolarizing agents
large dose can cause profound H2 release and CV effects
not really used

24
Q

intermediate acting steroid derivatives

A

vecuronium and rocuronium
more depend on biliary excretion or hepatic meta and used more often then long acting steroid derivatives
low H2 release

25
Q

long acting derivatives

A

pancuronium
pipcuronium
low H2 release

26
Q

prolonged steroidal derivative use

A

several days

3-hydroxy metabolite can cause prolonged paralysis b/c has longer half life

27
Q

pancuronium

A

intermediate onset, long acting, high potency

DOC for pts w/normal renal and hepatic fnx requiring paralysis >1hr

28
Q

rocuronium

A

most rapid onset, intermediate acting, and low potency
alternative to succinylcholine
devoid of CV effects

29
Q

vecuronium

A

slower onset, intermediate duration, high potnecy
acceptable alternative to competitive nondepolarizing blocker to rocuronium
commonly used in critically ill pts for >24hrs
no CV effects

30
Q

succinylcholine

A

only depolarizing blocking drug used clinically

31
Q

PK of succinylcholine

A

ultra-short acting d/t rapid hydrolysis and inactivation by plasmacholinesterase so only small percentage of dose reaches NMJ
not effectively metabolized by AChE at NMJ

32
Q

PD of succinylcholine

A

phase 1: depolarizing-> mm contraction -> cannot be redepolarized -> flaccid paralysis
phase 2: desensitization of AChR

33
Q

uses of succinylcholine

A

rapid sequence induction (emergency surgery) and for quick surgical procedures

34
Q

reversal of succinylcholine

A

plasma cholinesterases

35
Q

CV adverse effects of succinylcholine

A

cardiac arrythmias when administered with halothane anesthesia
neg inotropic and chronotropic effects
large doses can cause pos inotropic and chronotropic effects

36
Q

other adverse effects of succinylcholine

A 
hyperkalemia (most common)
increased intraocular pressure
increased intraepigastric pressure 
mm pain
H2 release
37
Q

hyperkalemia

A

most common adverse effect of succinylcholine
pts with burns, nn damage, NM disase, closed head injury, and truama are more at risk for hyperkalemia which can lead to cardiac arrest

38
Q

CI to succinylcholine

A

personal or FHx of MH
myopathies associated with elevated CPK
acute phase of injury, majro burns, multiple trauma, neuro injury

39
Q

black box warning of succinylcholine

A

cardiac arrest
d/t rhabdomylosis with hyperkalemia
usually males <8yrs

40
Q

succinylcholine and anesthetics

A

MH

41
Q

dantrolene MOA

A

inhibits RyR

42
Q

adverse rxns dantrolene

A

mm weakness
sedation
hepatits (don’t give orally if pt has hep)

43
Q

dantrolene uses

A

MH

44
Q

butyrylcholinesterase

A

aka pseudocholinesterase or plasma cholinesterase
synthesized by liver absent in NMJ and CNS
also inhibited by cholinesterase inhibitors

45
Q

3 subgroups of AChE inhibitors

A

alcohols
carbamic acid esters (carbamates)
organophosphates

46
Q

alcohols

A

contain alcohol and quaternary ammonium group- positively charged
edrophonium
bind noncovalently and reversibly

47
Q

carbamates

A

quaternary or tertiary ammonium groups (pos or neutral)
neostigmine, pyridostigmine, physostigmine, and carbaryl
bind noncovalently and reversibly

48
Q

organophosphates

A

neutral and highly lipid soluble

bind covalently and irreversibly

49
Q

quaternary and charged AChE inhibitors

A

parenteral administration
no CNS
duration determined by stability of inhibitor-enzyme complex, not meta or excretion
neostigmine, pyridostigmine, edrophonium, echothiophate, ambenonium

50
Q

tertiary and uncharged AChE inhibitors

A

well absorbed from all sites
CNS
more toxic then quaternary
physostigmine, donepezil, tacrine, rivastigmine, galantamine

51
Q

organophosphates

A

lipid soluble
very toxic everywhere
must regenerate AChE

52
Q

alcohols duration of action

A

relatively weak interactions and short lived 2-10min

53
Q

carbamic acid esters duration of action

A

2-step hydrolysis

2nd step- formation of covalent bond requires 30min-6hrs

54
Q

uses of AChE inhibitors

A 
MG
reversal of pharm paralysis
glaucoma
dementia
antimuscarinic antidote
55
Q

succinylcholine and AChE inhibitors

A

phase 1 block enhanced by AChE inhibitors

phase 2 block inhibited

56
Q

beta blockers and AChE inhibitors

A

enhanced bradycardia

57
Q

systemic corticosteroids and AChE inhibitors

A

enhance mm weakness seen in MG

MSK II (19 decks)

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