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pharmacology > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

1
Q

Structure of NMB

A

Quaternary Ammoniums
Structurally related to Ach
Synthetic Alkaloids
except Tubocuraine

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2
Q

Structure of Succinylcholine

A

Two ACh molecules linked by acetate methyl groups

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3
Q

Dose of Succinylcholine

A

1.0mg/kg

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4
Q

How long does Succinylcholine take to work?

A

60 seconds

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5
Q

How long does it take to recover 90% muscle strength?

A

9-13 minutes

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6
Q

Metabolism of Succinylcholine

A

short action due to rapid hydrolysis

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7
Q

Enzyme that breaks down Succinylcholine

A

butrylcholinesterase

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8
Q

Metabolites of Succinylcholine

A

Succinylmonocholine and choline

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9
Q

Succinylmonocholine is a

A

weak NMB; succinic acid and choline

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10
Q

Where does recovery from succinylcholine motor blockade occur?

A

as it drifts away from NMJ down a concentration gradient

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11
Q

Where is butyrylcholinesterase metabolized?

A

liver and found in plasma

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12
Q

What is butyrylcholinesterase responsible for the metabolism of?

A

succinylcholine, mivacurium, procaine, chloroprocaine, tetracaine, cocaine and heroin

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13
Q

Factors that decrease butyrylcholinesterase activity?

A 
advance liver disease
age
malnutrition
pregnancy
burns
oral contraceptives
MAO inhibitors
echothiophate
cytotoxic drugs
neoplastic disease
anticholinersterase drugs
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14
Q

Beta Blockers will

A

cause a mild prolongation of Succinylcholine

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15
Q

Genetic variations with the administration of succinylcholine

A

will significantly prolongation

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16
Q

Dibucaine

A

local anesthetic that inhibts typical PchE

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17
Q

Reflects the typical PChE not quantity

A

dibucaine number

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18
Q

Heterogenous for atypical gene

A

dibucaine number 40-60

Prolongs block 1.5-2times longer

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19
Q

Homogenous for atypical gene

A

dibucaine number less then 30

prolonged for 4-8 hours

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20
Q

Cardiac Side Effects of Succinylcholine

A 
bradycardia,
tachycardia
junctional rhythm
sinus arrest
due to muscarinic receptors  on cardiac cells
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21
Q

Cardiac effects due to succinylochine are more likely to occur

A

second dose within 5 minutes of first dose

pediatric patients

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22
Q

Stimulation of autonomic ganglia may cause

A

ventricular dysrhythmias
tachycardia
increased BP

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23
Q

Hyperkalemia

A

0.5-1mEq/L increase in plasma concentration
More severe in: burns, abdominal infectinos, metabolic acidosis, closed head injury and conditions with upregulation of nAChR (paraplegia, muscular dystrophy, Gullian-Barre)

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24
Q

Myoglobinuria

A

damage to skeletal muscle especially pediatric patients

Most found to have muscular dystrophy or by malignant hyperthermia susceptible

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25
Q

Increased intraocular pressure

A

peaks 2-4 minutes; pressure returns to normal by 6 minutes

not widely accepted in open eye injury

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26
Q

Increased intragastric and lower esophageal pressures

A

related to intensity of fasciculations of abdominal muscles
Prevented by prior administration of ND-NMB
does not increase risk of regulation

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27
Q

Increased intracranial pressure

A

can be attenuated with pre-treatment of ND-NMB

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28
Q

Masseter Spasm

A

trigger for MH

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29
Q

Myalgias

A

prominent in skeletal muscle of the neck, back and abdomen
greater in young adults females and ambulatory surgery patients
not well understood possible muscle injury to fasciculations
pretreatment with ND-NMV lidocaine or NSAIDs
myalgias occur even in absence of succinylcholine

30
Q

Elderlys (sux)

A

onset slower due to decreased circulation
reduced levels of PChE
certain alzheimer medications may prolong actions

31
Q

Pediatrics (suc)

A

avoided in pediatric patients (<5 yrs)
Duchenne muscular dystrophy
Cardiac arrest him from hyperkalemic rhabdomyolysis

32
Q

Atricurium

A

Histamine Release

33
Q

Structure of Cis

A

cis isomer of atracuurium

34
Q

Onset of action of Cis

A

intermediate

35
Q

Intubation Dose of Cis

A

0.1mg/kg

36
Q

Cis is metabolized

A

by Hoffman elimination

No ester hydrolysis

37
Q

Does cis cause histamine release?

A

no

38
Q

DOA of Mivacurium

A

short acting non-deplorizing available

39
Q

Intubating dose of mivacurium

A

0.15mg/kg

40
Q

Mivacurium is metabolize by

A

butyrylcholinesterase
70-88% rate of succinylcholine
monoester, dicarboxylic acid

41
Q

Mivacurium produces

A

histamine release

42
Q

Steriodal compounds include

A

pancuronium
vecuronium
rocuronium

43
Q

Steriodal compounds structure

A

acetyl ester thought to facilitate interaction with NaChR

essential that one of two nitrogen atoms are quarternized

44
Q

DOA of Pancuronium

A

Potent long acting neuromuscular blocking drug

45
Q

Intubation dose of Pancuronium

A

0.08mg/kg

46
Q

Onset time to max block of pancuronium

A

2.9 minutes

47
Q

Majority of Pancuronium is cleared

A

by the kidney

48
Q

Other small amount of Pan is

A

deacteylated by the liver

49
Q

3-OH metabolite

A

Pancuronium

accumulation is responislbe for block prolongation

50
Q

DOA of Vec

A

intermediate Acting

51
Q

Intubating dose of VEc

A

0.1mg/kg

52
Q

Onset time to max block of Vec

A

2.4 minutes

53
Q

What drug is Vec similar

A

pancuronium without quaternized methyl group

54
Q

What are the differences in properties between vec and pan?

A

slight decrease in potency
loss of vagolytic properties
Molecular instability (shorter DOA)
increase lipid solubility

55
Q

Where is Vec metabolized

A

principally by the liver

3-OH metabolites has 80% of neuromuscular potency

56
Q

DOA of Roc

A

Intermediate

57
Q

Intubation dose of Roc

A

0.6mg/kg

58
Q

Time to Max block in roc

A

1.7 minutes

59
Q

Roc has a faster onset than

A

pan or vec

60
Q

Roc potency is x times less potent then

A

pan or vec

61
Q

Roc is primarily metabolized

A

in the liver

approximately 30% executed in the urine

62
Q

NMB Potency increased

A 
inhalational agents
antibiotics
hypothermia
magnesium sulfate
local anesthetic
quinidine
63
Q

Factors that decrease NMB potency

A

chronic anticonvulsant administration
hyperparathyroidism and hypercalcemia
(decreased atracurium sensitivity)

64
Q

With NMB potency and onset

A

have an inverse relationship

65
Q

Buffered Diffusion seen with

A

high density drugs

drug diffusion is impeded because it binds to high density receptors in a confined space

66
Q

Autonomic Effects of NMB

A

block nicotinic receptors within sympathetic and parasympathetic nervous system
bradycardia and hypotension
histamine release (flushing, hypotension, reflex tachycardia and bronchospasm)

67
Q

Vagolytic effects occur

A

pancurium
block muscarinic receptors
inhibition of negative feedback system where catecholamine release is modulated or prevented

68
Q

Histamine Release

A

seen in benzylisoquinolinium (miv, atra, tubo)
short duration
slow administration or pretreatment with H1 and H2 blockers to reduce cardiovascular effects

69
Q

Respiratory effects of NMB

A

related to histamine release in patients with reactive airways disease
increasd airway resistance and bronchospasm

70
Q

Allergic Reactions

A

cross reactivity =- food, cosmetics, disinfections, and industrial materials

71
Q

treatment of allergic reaction

A 
o2
IV epi
intubation
fluids 
sympathomimetic drug

pharmacology (14 decks)

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