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Pharm > Neuromuscular Blocking Drugs & Reversal > Flashcards

Neuromuscular Blocking Drugs & Reversal Flashcards

1
Q

How many molecules of a nondepolarizing NMB must bind to an alpha subunit to produce a neuromuscular block?

A

One molecule to one alpha subunit

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2
Q

How does succ produce membrane hyperpolarization?

A

Produces prolonged depolarization of endplate region resulting in desensitization of nicotinic ACh receptors

Inactivation of voltage gated Na channels at NMJ

Increase in K permeability

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3
Q

What catalyze the hydrolysis of succinylcholine?

A

Plasma cholinesterase

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4
Q

Majority of NMBD are synthetic alkaloids except?

A

Tubocurarine

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5
Q

Long acting NMBD

A

D-Tubocurarine

Pancuronium

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6
Q

Intermediate-acting NMBD

A

Rocuronium
Vecuronium
Atracurium
Cisatracurium

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7
Q

Short-acting NMBD

A

Mivacurium

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8
Q

Most important curare alkaloid (Benzylisoquinolinium)

A

Tubocurarine

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9
Q

Where do steroidal compounds interact with nicotinic ACh receptors?

A

Postsynaptic muscle membrane

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10
Q

Tubocurarine

A

Monoquarternary, long acting Benzylisoquinolinium

O: slow
D: long
Recovery: slow

E: unchanged in urine; liver secondary (not suitable for renal or liver failure)

Int: 0.5-0.6 mg/kg
Maint: 0.1-0.2 mg/kg

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11
Q

Atracurium elimination

A

Depend on liver (70% excreted in bile; impaired in pts w/ biliary obstruction)

Designed to undergo spontaneous degradation at physiologic temp and pH by Hofmann elimination to Laudanosine & monoquarternary acrylate metabolite

Laudanosine easily crosses BBB & stimulates CNS

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12
Q

Cisatracurium undergoes how much Hoffman elimination?

A

77% of clearance

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13
Q

Mivacurium

A

Only currently available short-acting NMBD
D/c in US

May produce Histamine release if given rapidly

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14
Q

Pancuronium

A

Potent long acting

Vagolytic & butyrylcholinesterase inhibiting

E: around 50% kidneys; 11% bile; 15-20% deacetylation in liver

Remains stable for 6 months at room temp

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15
Q

Accumulation of what metabolite is responsible for prolongation of the duration of Pancuronium?

A

3-OH

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16
Q

Vecuronium

A

Monoquarternary with intermediate duration of action

Slight decrease in potency compared to panc
Loss of vagolytic properties
Molecular instability in solution explaining shorter duration
Increased lipid solubility=greater biliary excretion (30-40%)

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17
Q

____ has 80% the neuromuscular blocking potency of Vec & w/ prolonged administration may contribute to prolonged neuromuscular blockade

A

3-OH

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18
Q

Rocuronium

A

Intermediate acting monoquaternary with fast onset

6 times less potent than Vec

E: liver & bile, 30% unchanged in urine

Remains stable for 60 days at room temp

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19
Q

What order do inhalation anesthetics potentiate neuromuscular blocking effect?

A

Des> Sevo> Iso > Halothane > Nitrous oxide, barbiturates, propofol

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20
Q

Mechanisms for potentiation:

A

Central effect on alpha motoneurons & interneuronal synapses

Inhibition of postsynaptic nicotinic ACh receptors

Augmentation of antagonist’s affinity at receptor site

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21
Q

Which antibiotics potentiate neuromuscular blockade and how?

A

Aminoglycoside
Polymyxins
Lincomycin
Clindamycin

Inhibiting the prejunctional release of ACh & depressing postjunctional nicotinic ACh receptor sensitivity

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22
Q

What antibiotic potentiate neuromuscular blockade by exhibiting post junctional activity only?

A

Tetracycline

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23
Q

How can high magnesium concentrations potentiate NMBD?

A

It inhibits Ca channels at presynaptic nerve terminals that trigger release of ACh

24
Q

Onset of action is inversely proportional to?

A

Potency of NMBD

25
Q

Low potency=?

A

Rapid onset

26
Q

High potency=?

A

Slow onset

27
Q

Molar potency is highly predictive of a drugs time to onset of effect except for which drug?

A

Atracurium

28
Q

Buffered diffusion

A

The process in which diffusion of a drug is impeded b/c it binds to extremely high-density receptors within a restricted space

Can be seen w/ high potency drugs

29
Q

Tubocurarine is associated with marked ganglion blockade resulting in:

A

Histamine manifestations (hypotension, reflex tachycardia, bronchospasm) in asthmatics

30
Q

What class of NMB cause histamine release? Except?

A

Benzylisoquinoliniums; except cisatricurium

31
Q

Which NMB are benzylisoquinoliniums?

A

Tubocurarine
Atracurium
Cisatracurium
Mivacurium

32
Q

Which NMB are steroidal compounds?

A

Pancuronium (long acting)
Vecuroniumn (intermediate acting)
Rocuronium (intermediate acting)

33
Q

What antibodies are involved in anaphylactic reactions?

A

Immunoglobulin E antibodies fixed to mast cells

34
Q

Treatment of anaphylaxis

A

100% O2
IV Epi 10-20 mcg/kg
Consider early tracheal intubation if angioedema develops
Fluids (crystalloids &/or colloids)
NorEpi or Phenylephrine may be needed until fluid status restored
Treat dysrhythmias
Antihistamines & steroids controversial

35
Q

Half-life of succ

A

47 sec

36
Q

Which order kinetics does succ follow

A

First order (fractionated)

37
Q

How does succ cause bradycardia, junctional rhythm, and sinus arrest?

A

Mimics physiologic effects of ACh at cardiac muscarinic cholinergic receptors

Usually when 2 doses give < 5 min apart

38
Q

Not widely accepted in open eye cases. Why?

A

Succinylcholine; can increase IOP

39
Q

Succ Phase I

A

Skeletal muscle paralysis occurs b/c depolarized post junctional membrane & inactivated Na channels cannot respond to release of ACh

Absence of fade and tetanic to TOF

40
Q

Succ Phase II

A

Present when post junctional membrane has become repolarized but still does NOT respond normally to ACh

Has more characteristics of NDMB & fade is seen in response to TOF

41
Q

What causes leaking of K from interior of cells with Succ?

A

Sustained opening of Na channels

42
Q

Succinylcholine should not be given to pts 24-72 hrs after:

A

Major burns

Trauma

Extensive denervation of skeletal muscles

43
Q

what decreased likelihood of cardiac responses to succ?

A

Atropine 13 min before

44
Q

Twitches with drug

A 
4= 75% or less receptors blocked
3= 85% or less receptors blocked
2= 95% or less receptors blocked
1= 99% or less receptors blocked
0= 100% receptors blocked
45
Q

Onset matches for AChe inhibitors and anticholinergics:

A

Atropine 7-10 mcg/kg & Endrophonium 0.5-1.0 mg/kg (both rapid)

Glycopyrrolate 7-15 mcg/kg & Neostigmine 40-70 mcg/kg (both slower)

46
Q

Why do we give glycopyrrolate with Neostigmine?

A

Anticholinergic to minimize muscarinic CV side effects of AChe inhibitors

47
Q

Neostigmine supply

A

5mg/5ml

48
Q

Anticholinergic effects

A

Flushing, dry secretions, mydriasis (blurred vision), confusion, hyperthermia

49
Q

Cholinergic effects (SLUDGEM)

A 
Saliva
Lacrimation (tearing)
Urination
Defecation/Diarrhea
GI effects/ cramping
Messi
Miosis (pinpoint pupils)/ Muscle cramping
50
Q

Robinul supply

A

0.2mg/ml

51
Q

Neostigmine

A

Usually 1mg/ml

52
Q

How much glyco & Neostigmine for full reversal stick?

A

0.8 mg (4ml) of glyco + 5mg (5ml) Neostigmine

53
Q

Suggamadex most effective to least order

A

Roc> Vec > Pancuronium

54
Q

Sugammadex should be avoided in?

A

Pts with creatinine clearance < 30ml/min

55
Q

Sugammadex supply

A

100mg/ml - 200mg/2ml vial or 500mg/5ml vial

Pharm (15 decks)

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