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Pharm > NMBD's > Flashcards

NMBD's Flashcards

1
Q

True or False: Nicotinic receptors are located only on the post-synaptic end-plate.

A

False, located both pre and post synaptic.

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2
Q

Where are acetylcholinesterase molecules found?

A

Around post synaptic nicotinic receptors and in the synaptic cleft

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3
Q

Acetylcholine is synthesized from _____ and ____ through the action of _____

A

AcetylCoA and Choline, Choline Acetyltransferase (ChAT)

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4
Q

Release of Ach depends on the entry of ____ in to the terminal

A

Calcium

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5
Q

What does Calcium do once inside the nerve terminal?

A

causes vesicles to fuse with nerve cell membrane and exocytosis of Ach

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6
Q

What happens when Ach binds to a pre-synaptic nicotinic Ach receptor?

A

A positive feedback loop-it increases synthesis and release of Ach.

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7
Q

____ number of molecules of Ach must combine with 2 ____ subunits on the nicotinic receptor.

A

2, alpha

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8
Q

When both nicotinic subunits are occupied by Ach, the channels snap open and __ and ____ flow into the cell and ____ flows out.

A

Na and Ca flow into, K flows out

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9
Q

Acetylcholinesterase splits Ach into ___ and ____

A

acetate and choline

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10
Q

____ is transported back to the pre-synaptic terminal where it’s reconverted to Ach. ____ diffuses away.

A

Choline, acetate

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11
Q

What are extrajunctional nicotinic receptors?

A

Proliferate in response to paralysis, dystrophies, upper/lower motor neuron injury, major burns.

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12
Q

What happens as a result of extrajunctional nicotinic receptors?

A

Channels stay open 4x longer and upregulate-causes hyperkalemia

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13
Q

What are the subunits of a nicotinic receptor?

A

2 alpha, 1 beta, 1 delta, 1 epsilon

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14
Q

Depolarizing muscle relaxants act as acetylcholine receptor ______

A

Agonists

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15
Q

Non-depolarizing muscle relaxants act as ____ ____

A

competitive antagonists

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16
Q

Which medication is a depolarizing muscle relaxant?

A

Succinylcholine

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17
Q

Which medication is a long acting non-depolarizing muscle relaxant?

A

Pancuronium

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18
Q

Which medications are intermediate acting non-depolarizing muscle relaxants? (4)

A

Atracurium, Cisatracurium, rocuronium, vecuronium

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19
Q

Which medication is a short acting non-depolarizing muscle relaxant?

A

Mivacurium

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20
Q

What is the mechanism of action for Succinylcholine?

A

It mimics Ach. It works on the pre-synaptic receptors to mobilize ach and works at post synaptic receptors to open channels-Na/Ca enters the cell, K leaves the cell. This creates a prolonged depolarization.

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21
Q

What is the absolute refractory period?

A

action potentials cannot be initiated in the skeletal muscle until it REpolarizes. Voltage gated sodium channels in the membrane adjacent to the post synaptic terminal (motor end plate) snap in to the inactivated state.

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22
Q 
What is the following for Succinylcholine?
Dose:
Onset:
Duration:
What is it broken down by?
A

0.5-1mg/kg
30sec
3-5 min
Plasma Cholinesterase (aka pseudocholinesterase or butyrocholinesterase)

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23
Q

What is the metabolite of succinylcholine?

A

Succinylmonocholine

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24
Q

What percent of succinylcholine actually reaches the neuromuscular junction? or What percent isn’t metabolized?

A

10%

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25
Q

What is the name of the enzyme that breaks down succinylcholine?

A

Pseudocholinesterase (aka plasma cholinesterase, butyrocholinesterase)

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26
Q

What are some example of situations that will have a prolonged blockage by succinylcholine?

A

Atypical plasma cholinesterase, severe liver disease, use of anticholinesterase medications

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27
Q

What are some drugs that lower plasma cholinesterase, which would prolong the effect of succinylcholine?

A 
Metaclopramide
Esmolol
Neostigmine & Pyridostigmine
Echothiophate
Oral contraceptives/estrogen
Cyclophosphamide
MAOI's
N2 Mustard
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28
Q

What are some conditions that lower plasma cholinesterase?

A 
Atypical Anticholinesterase
Severe Liver disease
Chronic kidney disease
burns
advanced age
Organophosphate poisoning
neoplasm
malnutrition
late pregnancy
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29
Q

What does a dibucaine number tell you?

A

reflects the percentage of plasma cholinesterase that is inhibited when dibucaine is given. It has NO effect on atypical plasma cholinesterase.

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30
Q

Does a dibucaine number tell you the quantity or quality of the plasma cholinesterase enzyme?

A

Quality

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31
Q

About how long does it take to recover is your dibucaine number is above 80? 40-60? 20 and below?

A

above 80: 5-10 min. normal response
40-60: 20-30 min
20 and below: 4-8hr

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32
Q

What is a way to minimize fasciculations that may cause myalgias?

A

Give 1/10 of the ED 95 dose of a non-depolarizing muscle relaxant. (Ex. Roc, vec.) 3-5 min before giving succinylcholine

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33
Q

What are side effects of succinylcholine?

A 
Bradycardia
Tachycardia
Hypertension
Hyperkalemia
Myalgias
Myo-globinuria
Increased intra gastric pressure
Increased intracranial pressure
Increased intraocular pressure
Malignant Hyperthermia
Masseter Spasm
Prolonged respiratory paralysis (with atypical plasma cholinesterase)
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34
Q

Which receptors are being stimulated if succinylcholine causes bradycardia?

A

Muscarinic receptors

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35
Q

Which receptors are being stimulated in succinylcholine causes tachycardia and hypertension?

A

Autonomic ganglia nicotinic receptors

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36
Q

What are factor that prolong the depolarizing block of succinylcholine?

A 
Antibiotics (especially aminoglycosides)
local anesthetics
Anticholinesterase agents (increases Ach
Hyperkalemia
Hypermagnesemia
Inherited pseudo-cholinesterase effect
Lithium
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37
Q

What are potential conditions that accentuate succinylcholine -induced hyperkalemia?

A 
Undiagnosed muscular dystrophy
burn (7-10 days post acute burn)
Severe abdominal infections
Severe metabolic acidosis
Conditions with up-regulation of extra-junctional acetylcholine receptors (para/hemipalegia, muscular dystophies, gullain-barre, upper motor neuron lesions/injuries, CVA, etc)
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38
Q

What are the subunits on an extra-junctional nicotinic receptor?

A

7 alpha subunits and a gamma subunit (instead of an epsilon)

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39
Q

What is the mechanism of action for non-depolarizing muscle relaxants at the pre-synaptic area?

A

Inhibits mobilization of acetylcholine to be ready for exocytosis. This causes FADE

40
Q

What is the mechanism of action for non-depolarizing muscle relaxants at the post-synaptic area?

A

Binds to Ach receptors, competitively blocking Ach from attaching. Channels stay CLOSED, no electrolyte influx/eflux. No depolarization of the muscle.

41
Q

Are non-depolarizing muscle relaxants hydrophilic or lipophilic?

A

Hydrophilic

42
Q

Are non-depolarizing muscle relaxants ionized or non-ionized?

A

ionized

43
Q

T or F? Non-depolarizing muscle relaxants cross the blood brain barrier and can cross the placenta.

A

False

44
Q

How are non-depolarizing muscle relaxants excreted?

A

Renal and liver

45
Q

What are the two classes of non-depolarizing muscle relaxants?

A

Steroidal and Benzylisoquinolinium

46
Q

What are the 3 non-depolarizing muscle relaxants classified as steroidal?

A

Pancuronium, Vecuronium, Rocuronium

47
Q

Of the following, which are short, intermediate, and long acting?

A

Pancuronium (long), Vec & Roc (intermed)

48
Q

What are the 3 non-depolarizing muscle relaxants classified as benzylisoquinolinium?

A

Atracurium, Cisatricurium, Mivacurium

49
Q

Of the following, which are short, intermediate, and long acting?

A

Atracurium (Intermed), Cisatricurium (intermed), Mivacurium (short)

50
Q

How are atracurium and cisatricurium metabolized?

A

Atracurium: 66% ester hydrolysis, 33% Hoffman
Cisatricurium: 77% Hoffman, no ester hydrolysis

51
Q

Which category of non-depolarizing muscle relaxants is dependent on hepatic/renal function for elimination?

A

Aminosteroids

52
Q

Where are benzylinsoquinoliniums metabolized?

A

by enzymes in the plasma

53
Q

What is the metabolite of atracurium?

A

Laudanosine

54
Q

With what condition should you not give atracurium to a patient? Why?

A

Hx of seizures because of laudanosine.

55
Q

Which steroid non-depolarizing muscle relaxant should not be given with liver disease? What percent is eliminated by the liver?

A

Rocuronium, >70%

56
Q

Which steroid non-depolarizing muscle relaxant should not be given with renal disease? What percent is eliminated by the kidneys?

A

Pancuronium, 85%

57
Q

What percent of vecuronium in metabolized by which organ?

A

30-40% by the liver

58
Q

Which non-depolarizing muscle relaxants have the primary route of elimination of metabolism?

A

Succinylcholine, atracurium, cisatricurium

59
Q

Which non-depolarizing muscle relaxants have the primary route of elimination of the liver?

A

Vecuronium, Rocuronium

60
Q

Which non-depolarizing muscle relaxant has the primary route of elimination of the kidneys?

A

Pancuronium

61
Q

Which non-depolarizing muscle relaxant releases histamine?

A

Atracurium

62
Q

Which two non-depolarizing muscle relaxants are metabolized by ester hydrolysis and Hoffman elimination, thus not affected by kidney or liver impairment?

A

Atracurium (ester) and Cisatracurium (Hoffman)

63
Q

Which two non-depolarizing muscle relaxant rely on biliary excretion?

A

Roc and Vec

64
Q

Which non-depolarizing muscle relaxant is excreted by the kidneys?

A

Pancuronium

65
Q

Which non-depolarizing muscle relaxant has the most affect on the vagal blockade? Which one has an affect but not as strong?

A

Pancuronium, Rocuronium

66
Q

If Hoffman elimination:
Alkalosis and hyperthermia=
Acidosis and hypothermia=

A

faster metabolism, shorter duration of action

slower metabolism, longer duration of action

67
Q

What are the side effects of the histamine release from atracurium?

A

hypotension, tachycardia

68
Q

Which non-depolarizing muscle relaxant is most associated with tachycardia?

A

Pancuronium (vagal blockade)

69
Q

Which non-depolarizing muscle relaxant is most associated with anaphylaxis?

A

Succinylchloline

70
Q

Which two non-depolarizing muscle relaxant release histamine?

A

succ and atracurium

71
Q

Which paralytic would you avoid in a patient with idiopathic hypertrophic sub-aortic stenosis? Why?

A

Pancuronium. The tachycardia can cause the leaflet to block the left ventricular outflow tract, thus decreasing cardiac output and blood pressure.

72
Q

Your patient is undergoing a stone extraction with a urinary stent and has Stage 3 kidney disease. Which paralytic would you use?

A

Cisatricurium. Both benzlisoquinoliniums do not rely on liver or kidney elimination, they are metabolized by ester hydrolysis and hoffman elimination. Cisatricurium is 16% renal elimination, atracurium is 10-40%.

73
Q 
What is the following for Pancuronium?
Dose: 
-Intubating dose:
-Maintenance dose:
Onset:
Duration:
Metabolite:
Elimination:
A

-Intubating dose: 0.1mg/kg
-Maintenance dose: .01 mg/kg
Onset: 3-5 min
Duration: 45-90 min
Metabolite: 3-OH
Elimination: 85% kidneys

74
Q 
What is the following for Vecuronium?
Dose: 
-Intubating dose: 
-Maintenance dose:
Onset:
Duration:
Metabolite:
Elimination:
A

-Intubating dose: 0.1mg/kg
-Maintenance dose: 0.01mg/kg
Onset: <3 min
Duration: 25-30 min
Metabolite: 3-OH
Elimination: liver 50-60%

75
Q 
What is the following for Rocuronium?
Dose: 
-Intubating dose: 
-Maintenance dose:
Onset:
Duration:
Metabolite:
Elimination:
A

-Intubating dose: 1mg/kg
-Maintenance dose: .1 mg/kg
Onset: 45-90 sec
Duration: 15-30 min (dose dependent)
Metabolite: ??
Elimination: liver 70%

76
Q

What is an alternative paralytic to use for RSI instead of succinylcholine?

A

Rocuronium but longer duration of action (15-30 min)

77
Q

What does it mean by a “priming dose”?

A

Give 10% of of the total dose, give induction med, then remaining 90% of the dose

78
Q 
What is the following for Atracurium?
Dose: 
-Intubating dose: 
-Maintenance dose:
Onset:
Duration:
Metabolite:
Elimination:
A

-Intubating dose: .5mg/kg
-Maintenance dose: .1mg/kg
Onset: <3 min
Duration: 20-35 min
Metabolite: Laudanosine (CNS excitation)
Elimination: 66% ester hydrolysis, 33% hoffman elimination

79
Q

What are 3 scenarios where you would NOT use atracurium due to the histamine release?

A 
Hypertrophic cardiomyopathy (b/c of tachycardia)
Aortic Stenosis (because of hypotension)
Sever asthmatics (increases airway pressures)
80
Q 
What is the following for Cisatracurium?
Dose: 
-Intubating dose: 
-Maintenance dose:
Onset:
Duration:
Metabolite:
Elimination:
A

-Intubating dose: .2mg/kg
-Maintenance dose: .1mg/kg
Onset: <3 min
Duration: 30-60 min
Metabolite: ??
Elimination: Hoffman elmination 77%. Smallest amount of renal clearance compared to others.
*Good for renal impairment pts

81
Q

What are drugs that potentiate NDMR’s?

A 
Drugs:
aminoglycoside abx (polymyxins, clindamycins)
local anesthetics (large doses)
volatile gases (des, sevo, iso, N2O)
mag sulfate
lithium 
loop diuretics
antiarrhythmic agents (quinidine, propranolol, procainamide)
82
Q

What are patient factors that potentiate NDMR’s?

A 
hypothermia
female gender (from make-up)
83
Q

What are electrolyte conditions that potentiate NDMR’s?

A

high magnesium
low calcium
low potassium

84
Q

What are factors that decrease the effects of NDMR’s?

A

Chronic anticonvulsant therapy
Hyperparathyroidism and hypercalcemia
hyperkalemia

85
Q

What response to paralytics will people with Myasthenia Gravis have?

A

They have less functional Ach receptors due to damage from antibodies-this makes them more sensitive to non-depolarizing muscle relaxants. They will be resistant to succinylcholine

86
Q

What response to paralytics will people who have muscle denervation injuries have?

A

they have a chronic decrease in Ach release with a compensatory increase in Ach-nicotinic post-synaptic receptors (up regulation)
Resistance to NDMR’s (they have more Ach receptors that need to be blocked)
Exaggerated response to succ (more Ach receptors being depolarized)

87
Q

What is the best location to check twitches for onset?

A

Facial nerve

88
Q

What is the best location to check twitches for recover?

A

Ulnar nerve

89
Q

What muscles are you checking with twitches at the facial nerve? What’s the action it causes?

A 
Orbicularis Oris (closes eyelid)
Corregator Supercilii (furrows brow)
90
Q

What muscle are you checking with twitches at the ulnar nerve? What’s the action it causes?

A

Adductor Pollicis (Adducts thumb)

91
Q

What is the pneumonic to remember the order in which muscles recover after paralytic is given? What do the letters stand for?

A 
Vocal Cords Die Out After Adding Muscle Paralysis Externally
Vocal Cords
Diaphragm
Orbicularis Oris
Abdominal Rectus
Adductor Pollicis
Masseter
Pharyngeal
Extra-ocular

In order of 1st to recover, last to block

92
Q

How can you distinguish between a Phase 1 or Phase II Succinylcholine block?

A

Phase II has fade

93
Q

What train of four ratio is needed for safe extubation?

A

> 0.9

94
Q 
What percentage of receptors are blocked with the following train of four responses:
0 twitches
1 twitch 
2 twitches
3 twitches
4 twitches
A 
0=100%
1=90%
2=80%
3=75% (3 twitches present and still 75%blocked)
4=<70%
95
Q

Which test most closely indicates a train of four ratio of 0.9?

A

Sustained jaw clench on tongue blade

Pharm (12 decks)

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