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Pharm Oral > NMB and reversals > Flashcards

NMB and reversals Flashcards

1
Q

Atricurium MOA

A

competitively inhibits/blocks ACh at the post junctional nicotinic cholinergic receptor in the NMJ by binding to 2 alpha subunits, preventing opening of the channel, depolarization and contraction

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2
Q

Atricurium/Tracurium class

A

Intermediate acting bisquarternary benzyllisoquinoline NDMR

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3
Q

Atricurium Pharmacokinetics

A

PB= 82%, onset 1-3min, DOA 20-50min, E1/2 20min, water soluble, metabolized 2/3 by ester hydrolysis and 1/3 Hofmanns elimination, excreted in urine, metabolite Laudanosine- (liver metabolized) can accumulate in renal failure and cause CNS problems like sz

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4
Q

SE Atricurium

A

Histamine release; decrease bp and increase HR, skin flushing; BRONChospasm

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5
Q

Atricurium CI/Cautions

A

conscious patient, hypersensitivity, cautious with asthma and COPD &pts unable to handle histamine release- CAD, sz history, muscle weakness, metabolite can accumulate with liver/renal problems
NMB can be prolonged with IA, abc, and anti-convulsants, LA, steriods, and immunosuppressants
Resistance can occur in burn PTs- up to 3 months; resistance with muscle trauma, denervation, immobilized

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6
Q

Atricurium dose

A

initial 0.5mg/kg iv, maintanance- 0.1mg/kg q 20-45min; continuous 9-10mcg/kg/min

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7
Q

Cisatracurium/Nimbex class

A

intermediate acting NDMR; stereoisomer of Atricurium

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8
Q

Cisatracurium PK

A

Vd= .12-.2l/kg, onset 3-5min, DOA 20-90min, e1/2 20-30min, water soluble, metabolized 80% by hoffmann elimination, excreted in urine and feces, metabolite Laudanosine 1/5 that of atriucurium (can accumulate in RF and cause CNS problems like szs)

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9
Q

Cisatracurium SE

A

no histamine release, lacks cv effects, laudanosine production less likely than with atr, anaphylaxis

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10
Q

Cisatracurium Ci/cautions

A

conscious patient , hypersensitivity, electrolye/acid/base abnormalities, muscle weakness, metabolite can accumulate with liver/renal problems
enhancedNMB with some abx, LI, LA, procainamide, mg
Decreased action with PTs on phenytoin/carbamazepine

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11
Q

Cisatracurium dose

A

initial 0.2mg/kg; maintenance- 0.03mg/kgq 40-60min, continous 1-3mcg/kg/min

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12
Q

Rocuronium class

A

short/intermediate acting monoquatinary aminosteriod ND NMB

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13
Q

Rocuronium MOA

A

competes with ACh for alpha subunits on the nicotinic receptor and inhibits a conformational change which prevents depolarization and contraction

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14
Q

Rocuronium PK

A

1/6 the potency of vecuronium, Not highly protein bound- 30-50%, VD 0.25L/KG, onset 60-90 sec, DOA 30-90, E1/2t 1-2hr, metabolized in liver by deacetylation to 17-desacetylrocuronium (5-10% activity of parent) 30% excreted in the urine unchanged, 20% hepatic degradation, billary excretion is primary up to 50%- don’t need to decrease dose in renal disease

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15
Q

Rocuronium SE

A

anaphylactic reactions, little affect on cardiac system- no histamine release, Hypertension or hypotension, arrhythmia, apnea, bronchospasm, hiccups, salivation

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16
Q

Rocuronium CI/Cautions

A

conscious patient, hypersensitivity, underlying neuromuscular disorder, children (2-12) need larger dose because shorter DOA, elderly prolonged effect, burns greater than 30% 3rd degree and Anticonvulsants will have resistance;
potentiated by IA, some abx, lasix, LA, antidsyrhythmics, dantroline, ketamine, anticonvulsants and Mag2+•
esmolol admin before will increase onset time
ephedrine given before will decrease onset time
Ach inhibitors diminish effects

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17
Q

Rocuronium dose

A

defaciculating- 0.06-0.1mg/kg, 0.6-1.2mg/kg intubating, maintenance 0.2mg/kg; continuous 10-12mcg/kg/min

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18
Q

Vecuronium/Norcuron- class

A

intermediate acting steriod type NDMR

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19
Q

Vecuronium PK

A

60-80% PB, Vd 0.2-0.2L/kg, onset 2-3 min, DOA 20-35min, e1/2 70min, hepatic metabolism; 30% excreted unchanged in the urine and primary excretion is billiary - active metabolite= 3-desacetyl vecuronium- 1/2 potency of parent

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20
Q

Vecuronium SE

A

No histamine release, bronchospasm, can cause SA node exit block

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21
Q

Vecuronium CI/cautions

A

hypersensitivity, caution with liver and renal disease, NMB blockade enhanced with INH Agents and increase effects of some abc (amino glycosides, anticonvulants, thiazides, and mag)

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22
Q

Vecuronium dose

A

defaciculating dose- 0.01mg/kg, 0.1mg/kg, maintenance 0.01mg/kg q25-45min, continuous 1mcg/kg/min

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23
Q

Pancuronium/Pavulon

A

longacting steriod type bisquarternary aminosteriod NDMR

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24
Q

Pancuronium PK

A

little PB, onset 2-3min, DOA 60-90 min, e1/2 2hours, 10-20% hepatic metabolism with renal excretion (80% excreted unchanged), 3 active metabolites= most 3-desacetyl pancurounium ( 1/2 potency parent)

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25
Q

Pancuronium SE

A

no histamine release, not CV stable- increase hR/arrhythmias- even if beta blocked, htn, bronchospasm, allergic rxn

26
Q

Pancuronium CI

A

hypersensitivity, conscious pt, underlying skeletal muscle disease, CV disease, hyperparathyroid, pheochromocytoma, renal disease, prolonged excretion in renal biliary or hepatic disease elderly and obese
. can be prolonged with IA, abc, BB, LI, diuretics, anticonvulsants, and TCAs

27
Q

Pancuronium dose

A

initial 0.1mg/kg, maintenance 0.01mg/kg q 40-60min, infusion 1mcg/kg/min

28
Q

Mivicurium/Mivacron class

A

short acting quaternary ammonium ND NMB

29
Q

Mivicurium Pk

A

highly ionized, water soluble= decreased lipid solubility so it doesn’t cross the BBB, Ed95=80mcg/kg, onset 2-3min, doa 12-20min, e1/2 55min, hydrolyzed by plasma cholinesterase’s ~88% the rate of sux, 7% excreted unchanged in the urine

30
Q

Mivicurium SE

A

slight histamine release, transient hypotension, increase HR, vasodilation, bronchospasm

31
Q

Mivicurium CI

A

atypical plasma esterase deficiency- prolong duration, hypersensitivity, asthma, COPD

32
Q

Mivicurium dose

A

initial 0.2mg/kg, maintenance 0.01-0.1mg/kg, continuous 6-7mcg/kg/min

33
Q

succinycholine class

A

depolarizing NMB with rapid onset and ultrashort acting

34
Q

sux MOA

A

mimics ACh at alpha subunits on the nicotinic receptor and produces a sustained depolarization of the post junctional membrane- keeping the channel open and unable to respond to other APs, effects are terminated when sux diffuses away from the NMJ

35
Q

sux PK

A

onset 30-60sec, DOA 8-15min, e1/2 2-4min, small vd and little PB, rapidly hydrolyzed by plasma esterase’s when diffuses away form NMJ and excreted in the urine,

36
Q

sux SE

A

increased ICP, IOP, IGP, decrease HR and BP, histamine release, hyperkalemia, masseter muscle spasm, myalgias, fasciculations, rhabdomyolysis, myoglobuneria, systole, MH

37
Q

sux ci

A

muscular dystrophy, pt with history or family history of MH or plasma esterase deficiency, only for emergency use in children, pts with increased K like renal pts, myopathies, pts with increased ICP, IOP, IGP, hypersensitivity, histamine release so caution with asthma/COPD, not for burns/trauma/extensive deinervation with skeletal muscle for 24-72 hours

38
Q

sux dose

A

20-40mg for larngospasm
intubation 1-1.5mg/kg for RSI
maintenance 0.04-0.07 mg/kg q5-10min

39
Q

Neostigmine class

A

NMB reversal/ anticholinesterase quarternary ammonia that is a competitive acetylcholinesterase inhibitor

40
Q

Neostigmine MOA

A

competitively and irreversibly covalently binds to the carbamyl group of the acetylcholinesterases inhibiting the breakdown of Ach in the NMJ- increasing the availability of ACh at the motor end plate; used to antagonize the affects of NMBs. it’s the most reliable med for a deep block

41
Q

Neostigmine PK

A

onset 3min, peak 7-10min, DOA 1hr, e1/2 70min, metabolized by plasma and liver esterase’s 50% and excreted unchanged 50% in the urine

42
Q

Neostigmine SE

A

decrease HR, BP, SVR, N/V, increased salivation, bronchoconstriction, increase gastric secretions, seizures

43
Q

Neostigmine CI

A

renal failure will increase DOA, GI/GU obstruction, asthma, caution in CAD

44
Q

Neostigmine dose

A

0.05-0.07mg/kg

and with glycopyrolate 0.01mg/kg IV

45
Q

Pyridostigmine- class

A

Competitive anticholinesterase/ NMB reversal

quaternary ammonia

46
Q

Pyridostigmine- MOA

A

reversibly binds to acetylcholinesterase, inhibiting its action and increasing the concentration of acetylcholine at the motor end plate for use on the nicotinic receptors—- attracted to the electrostatic interaction bt + charged Nitrogen and - charged catalytic site of the enzyme; forms a covalent bond to the carbamyl group on the acetylcholinesterases inhibiting the b/d of ACh @ the NMJ. increases ACh at the NMJ…… can be given orally to myasthenia gravis

47
Q

Pyridostigmine PK

A

onset 10min, DOA 60-120, e1/2= 112 minutes, 25% hepatic metabolism by microsomal enzyme system and 75% excreted unchanged in the urine

48
Q

Pyridostigmine SE

A

muscarinic effects- decreased HR/dysthrhythmias, BP, SVR, N/V, increased salivation, bronchospasm, increase gastric secretions, seizures

49
Q

Pyridostigmine CI

A

hypersensitivity, Renal failure will increase DOA, GI/GU obstruction, asthma, caution with CAD
BB= potentiate decrease bp

50
Q

Pyridostigmine dose

A

0.1-0.2mg/kg
15mg PO
IV with glycopyrolate 0.01mg/kg

51
Q

Edrophonium class

A

quaternary ammonia NMB reversal/ anticholiensterase

52
Q

Edrophonium MOA

A

reversable H+ binding to the acetylcholinesterases forming an electrostatic attachment increasing ACh at the NMJ

53
Q

Edrophonium PK

A

less severe muscarinic effects in this class, onset fast, DOA short at 1 receptor but binds to multiple receptors before being elimated which prolongs the DOA, peak 1-2min, 25% hepatic metabolism, 75% renal excretion unchanged

54
Q

Edrophonium SE

A

decreases HR, BP, SVR, N/V. increases salivation and gastric secrtions, seizures

55
Q

Edrophonium CI

A

renal failure prolongs actions, GI/GU obstruction, asthma, caution with CAD

56
Q

Edrophonium dose

A

0.5-1mg/kg

with atropine 0.01mg/kg

57
Q

Physostigmine- class

A

medium duration central acting tertiary amine anticholinesterase,

58
Q

Physostigmine MOA/uses

A

reversible binding forms a carbamyl ester complex at the esoteric site of the acetylcholinesterases increasing concentration of ACh at the NMJ; also used for atropine toxicity, MG, and glaucoma

59
Q

Physostigmine PK

A

vd= 1L/kg- lipid soluble and crosses BBB, onset 5 min, DOA 1-5hr, e1/2 30min, hydrolyzed at ester linkage by cholinesterase’s, renal excretion is minimal

60
Q

Physostigmine SE

A

decrease HR, bp, svr, n/v. increase salivation any gastric secretions, seizures

61
Q

Physostigmine CI

A

use with another anti cholinesterase, Gi/GU obstruction, asthma, caution with CV disease

62
Q

Physostigmine dose

A

15-60mg/kg IV q 1-2 hours- for anticholinergic syndrome

Pharm Oral (10 decks)

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