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*Pharmacology > Apex- Neuromuscular blockers > Flashcards

Apex- Neuromuscular blockers Flashcards

1
Q

Which subunits MUST be occupied to open the nicotini receptor at the motor endplate?

A. Alpha and alpha
B. Alpha and gamma
C. Alpha and delta
D. Alpha and epsilon

A

A. Alpha & Alpha

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2
Q

What is the NMJ?

A

It’s a synaptic connection between a motor nerve and skeletal muscle.

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3
Q

Which is present on the neurons vs motor end plate/skeletal muscle?

Nm or NN
(which is 1 and 2)

A

Nm (N1) [1 n] - M for motor end plate

Nn (N2) [2ns] - N for neuron

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4
Q

What does a peripheral nerve stimulator actually do?

A

It sends an action potential to depolarize the axon terminal and release stores of ACH into the synpatic cleft

>sodium ions flood in
>cell is now more positive on the inside which
>opens CA+ ion channels
>calcium goes in and releases ACH into the synaptic cleft

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5
Q

What happens when ACH binds to the presynaptic nicotinic receptors?

A

It speeds up the release of ACH stores

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6
Q

What hydrolyzes ACH as soon as it diffuses away from it’s receptors?

A

acetylcholinesterase

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7
Q

What is ACH metabolized into?

A

Choline + acetate

>choline is recycled back into the presynpatic neuron and used to synthesize more ACH

>acetate diffuses away from the NMJ

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8
Q

How does sux work?

A

it binds to the post-synpatic nicotinic receptor and depolarizes the motor end plate

it mimics ACH but binds to the receptor for a much longer period of time

-so it depolarizes the motor end plate (muscle contraction) and then it can’t be stimulated again until sux dissociates away from the receptor

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9
Q

How is the action of sux terminated?

A

after it diffuses away from the nicotonic receptors at the motor endplate

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10
Q

How do non-depolarizers work?

A

They block the nicotonic receptors at the motor endplate and prevent ACH from binding

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11
Q

What happens when ACH binds to the 2 alpha subunits on the post synaptic nicotinic receptor?

A

sodium and calcium flood flood into the myocyte and K+ leaves

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12
Q

what happens when the myocyte is depolarized?

A

(meaning calcium and na have flooded inside)

>The sarcoplasmic reticulum releases calcium into the cytoplasm where it engages with myofilaments and initiates muscle contraction

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13
Q

What enzyme terminates the effect of ACH

A

acetylcholinesterase

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14
Q

All of hte following statements regarding extrajunctional nicotinic receptors are true EXCEPt:

A. it is opened by choline
B. an epsilon subunit replaces a gamma subunit
C. It opens for a longer period of time
D. Denervation allows for it’s proliferation

A

B. an epsilon subunit replaces a gamma subunit

*extrajunctional (extra post-synaptic nicotinic receptors have a gamma subunit instead of a epsilon subunit

*This structural change impacts how it responds to sux

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15
Q

What two things can lead to proliferation of extrajunctional nicotinic receptors?

(aka- upregulation?)

A
  • Denervation
  • Prolonged immobility

<2yo, stroke, burns “thermal injury”

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16
Q

The the absence of exgtrajunctional receptors, sux can transiently increase the serum K by __ - ___mEq/L for up to ____-____ minutes.

A

0.5-1 mEq/L
10-15 minutes

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17
Q

In the event of a denervation injury, sux is best avoided ______ hours following the injury up to how long after?

A

after 24 hours up to a year

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18
Q

Pt with upregulated extrajunctional receptors are (sensitive/resistant) to nondepolarizers.

Does this increase or decrease the potency of these drugs?

A

they are resistanct to non-depolarizers (more receptors that need coverage)

  • reduced potency of the drug
  • more is needed
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19
Q

Which is pathologic of the nicotinic receptor - gamma or epsilon

A

gamma = pathologic
(think gamma knife is required for pathologic things)

epsilon = normal

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20
Q

Conditions where sux is contraindicated (9)

A
  1. upper or lower motor neuron injury
  2. SCI
  3. Burns
  4. Skeletal muscle trauma
  5. CVA
  6. Tetanus
  7. Severe sepsis
  8. Muscular dystrophy
  9. Prolonged chemical denervation (mag, long term NMB infusion, clostridal toxin)
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21
Q

Fade during TOF stimulation is caused by:

A. agonism of the presynaptic nicotinic receptors

B. antagonism of hte presynaptic nicotinic receptors

C. Impaired presynaptic acetylcholine reuptake

D. decreased acetylcholine synthesis

A

B. antagonism of hte presynaptic nicotinic receptors (Nn)

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22
Q

Why do you get fade with non-depolarizers but no fade with depolarizers?

A

non-depolarizers = antagonists
>fade is from blocking the presynaptic Nn receptor which results in less release of ACH from the presynaptic nerve terminal

depolarizers = agonists
>agonism of the presynaptic Nm receptor mobilizes ACH stores and therefore wont produce fade

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23
Q

Acetylcholine is synthesized from _____ & _____ in the presence of what?

A

choline & acetyl CoA

in the presence of choline acetyltransferase (ChAT)

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24
Q

Identify the statement that BEST characterizes a phase 2 block following succinylcholine (select 2)

  • fade with tetany
  • post-tetanic potentiation is absent
  • constant but diminsed response to double burst stimulation
  • prolonged duration
A

-fade with tetany

&

-prolonged duration

(a phase 2 block occurs with excessive dosease of sux)

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25
Q

Does Sux produce a phase 1 or phase 2 block?

A

Phase 1 block

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26
Q

What distinguishes a phase 1 from a phase 2 block?

A

The presecne of fade

phase 1 block = no fade
phase 2 block = fade

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27
Q

nondepolarizers - phase 1 or phase 2 block?

A

phase 2 (+fade)

  • think depolarizers = 1
  • non-de polarizers = 2
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28
Q

2 circumstances where sux can produce a phase 2 block

A

high doses
infusion of it

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29
Q

T/F: a phase one block will result in post-tetonic potentiation

A

False- present with a phase 2 block

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30
Q

Idenify the MOST sensitive indicator of recovery form NMB

A. 4/4 twitches with no fade
B. TV 6ml/kg
C. VC > 20ml/kg
D. Inspiratory force better than -40cm h20

A

D. Inspiratory force better than -40cm h20

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31
Q

The best place to measure the onset and recovery of blockade

Muscle vs nerve

A

onset:

Nerve:

-Facial nerve

Muscle:
>obicularis oculi (closes eyelid)
>corrugator supercilii (eyebrow twitch)

recovery:

Nerve:

-Ulnar nerve or posterior tib nerve

Muscle:

  • Adductor pollicis (thumb adduction)
  • Flexor hallucis (big toe flexion)
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32
Q

Stimulation of the _________ nerve results in closure of the eyelid (which muscle)

A

Facial nerve

  • obicularis oculi
  • closes eyelid
  • onset/intubation conditions- first to go, first to come back

(corrugator supercilii twtiches eyebrow)

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33
Q

Stimulation of the _________ nerve results in twitching of the eyebrown (which muscle)

A

facial nerve

  • corrugator supercilii
  • onset/intubating conditions
  • first to go/first to come back
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34
Q

Stimulation of the _________ nerve results in adduction of the thumb (which muscle)

A

ulnar nerve

-adductor pollicis

-extubating conditions/return of airway function

-last to go, last to come back

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35
Q

Stimulation of the _________ nerve results in big toe flexion (which muscle)

A

posterior tibular nerve

  • flexor hallucis
  • extubating conditions/return of upper airway muscle function
  • last to go, last to come back
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36
Q

Recovery from NMB is defined as a TOF ratio of what

A

>/= 0.9

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37
Q

T/F- the return of normal tidal volume is a poor endpoint for assessing the retun of neuomuscular function

A

true

-whoops do it all the time

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38
Q

4 best qualitative bedside tests of recovery and degree of blockade association

A
  1. sustained tetany > 5 seconds
  2. sustained head lif > 5 seconds
  3. Sustained hand grip same as pre-induction > 5 seconds
  4. pt’s ability to hold a gongue blade in his mouth agaisnt force (whos doing such things)

50% blocked/50% recovered

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39
Q

placement of TOF stickers- is it red to the head or red to the heart

A

red to the heart

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40
Q

T/F - NMB is defined as a TOF ratio of < 0.9

A

True

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41
Q

TV of 6ml/kg correlates with ___% of receptors still being occupied

A

80% still bocked

-only 20% recovered

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42
Q

TOF without fade correlates to ____% of receptors still being blocked

how much recovered

A

70% still blocked

only 30% recovered

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43
Q

VC >/= 20ml/kg correlates to ____% of receptors still being blocked

how much recovered

A

70% still blocked

only 30% recovered

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44
Q

What 2 tests correlate with 60% of receptors still being occupied and the pt only being 40% recovered?

A

Sustained tetanus @ 50hz without fade &

DBS with no fade

*so these are more accurate predictors of recovery compared to TOF without fade

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45
Q

identify the statement that demonstrates the MOST accurate understanding of SUX

A. HTN is a normal side effect

B. It’s an absolute contraindication with an open globe injury

C. Severe sepsis increases the risk of hyperkalemia

D. Masseter spasm warrents cancellation of the planned procedure

A

A. HTN is a normal side effect

B. It’s an absolute contraindication with an open globe injury

C. Severe sepsis increases the risk of hyperkalemia

D. Masseter spasm warrents cancellation of the planned procedure

  • sux is not absolutely conraindicated with open globe injury; the risk of eye injury is low and securing airway is the top priority
  • masseter spasm may be a warning sign of MH but it’s also a normal effect of sux. In the absence of other signs suggesting MH, the case may proceed
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46
Q

An inspiratory force better than -40cm H20 is associated with what % of receptors being blocked vs recovered

A

50% blocked and recovered

(a more negative number is better)

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47
Q

T/F- masseter spasm is a normal effect of sux

A

true

-given no other signs of MH, it’s okay to proceed with case

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48
Q

T/F- HTN is a nomal side effect of sux

A

True!

-news to me lol

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49
Q

Why are kids more susceptible to bradycardia with sux and when should you administer atropine before giving sux?

A

bc kids have a higher baseline vagal tone

-give atropine before sux if a second dose is required

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50
Q

T/F sux is safe for the renal failure patient

A

true- as long as they have a normal K level

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51
Q

What 5 things can sux increase?

A
  1. Heart rate
  2. BP
  3. K+
  4. Intraocular pressure
  5. Intracranial pressure
  6. Intragastic pressure
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52
Q

What is sux made of?

A

2 acetylcholine molecules bound together

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53
Q

Mechanism by which sux can cause bradycardia or asystole

What increases this risk and why?

A

by stimulating the M2 receptor in the SA node

a second dose of sux increases this risk thought to be due to accumulation of it’s primary metabolite- succinylmonocholine

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54
Q

Primary metabolite of sux

A

succinylmonocholine (accumulation with a second dose of sux can lead to bradycardia or asystole and can be prevented or relieved with an antimuscarinic)

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55
Q

Mechanism by which sux causes tachycardia and HTN (mainly in adults)

A

by mimicking the action of Ach at the sympathetic ganglia

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56
Q

Sux transiently increases IOP by ____ - _____mHg for up to _____minutes

A

5-15mmHg for up to 10 minutes

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57
Q

How can you midigate the risk of increased ICP with SUX

A

Giving a de-fasiculating dose of NDMR; however, now that sugammadex is available, might as well just give that lol

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58
Q

since sux causes the contraction of abdominal muscles which increases intragastric pressure, does this increase the risk for aspiration?

A

no- bc it also increases lower esophageal sphincter tone

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59
Q

Why does sux stay at the NMJ longer than acetylcholine?

A

Bc it’s metabolized by pseudocholinesterase which is in the plasma and has to be delivered to the NMJ whereas ACH is metabolized by acetylcholinesterase which is immediately available at the NMJ to metabolize it

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60
Q

What metabolizes acetylcholine vs sux?

A

Acetylcholine

  • acetylcholinesterase
  • true, type 1, genuine, specific cholinesterase (the real og)

SUX (+ mivacurium and ester LA’s)

  • pseudocholinesterase
  • false, type 2, plasma cholinesterase

+ butryrylcholinesterase

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61
Q

Does butrylcholinesterase metabolize ach or sux?

A

sux

62
Q

What 6 drugs increase the duration of sux? How?

(Mneumonic)

A

COME-EN (& stay a while bc you suck)

  • Cyclophosphamide
  • Oral contraceptives

-Metoclopramide

-Esmolol

-Echothiopate

-Neostigmine

They decrease pseudocholinesterase activity

-less pseudocholinesterase available to metabolize sux , stays at the NMJ longer and binds to the receptor longer

63
Q

What stage pregnancy can lead to an increased DOA of sux and why?

A

late-stage pregnancy

  • reduced pseudocholinesterase activity (think sharing with a fully developed baby)
  • less pseudocholinesterase to break down sux = increased DOA
64
Q

T/F- obesity increases the DOA of sux

A

false- DECREASES

-bc obesity results in increased pseudocholinesterase activity

65
Q

Mysthenia gravis is assoicated with a (sesnsitivity/resistance) to sux

A

Resistnace to sux

(due to a reduced number of nicotinic receptors at the NMJ)

  • wouldn’t you need less then??? idk)
66
Q

A patient with a dibucaine number of 20 received sux; this patient:

A. is heterozygous for pseudocholineserase

B. Fails to produce pseudocholinesterase in sufficient quantity

C. Should receive FFP

D. Will be paralyzed for 8 hours

A

D. Will be paralyzed for 8 hours

67
Q

What 5 conditions lead to reduced pseudocholinesterase activity. Why is this important? Mnemonic?

A

B-PANS (Jenns kid, condition)

Burns

Pregnancy (late stage-)

Atypical PChE

Neoplasm

Severe liver disease

-decreased pseudocholinesterase activity = decrease metabolism of sux = prolonged duration of sux

68
Q

Is Atypical Pseudocholinesterase a quantative or qualitative defect?

A

Qualatative defect - PChE is produced in sufficient quantity, however the enzymee produzed is not functional

69
Q

T/F- Dibucaine is a ester local anesthetic

What is it used for and how does it work?

A

False- it’s an amide local anesthetic and is used to diaghose atypical PChE.

It inhibits normal PChE, but has no effect on atypical PChE

70
Q

What is the Dibucaine numbers associated with:

Typical homozygous (normal)

Heterozygous varient

Atypical homozygous

-How long will each group be paralyzed for?

(What does the number signify?)

A

Typical homozygous (normal) = 70-80

Heterozygous varient - 50- 60

Atypical homozygous - 20-30

Number reflects the % of normal enzyme that is inhibited by dibucaine.

71
Q

T/F - Atypical PChE varients cannot hydrolyze sux

A

True- so DOA will be prolonged

72
Q

What is the best treatment for a patient with atypical PChE who has received sux?

A

sedation, mechanical ventilation, and time for it to wear off

73
Q

What would you think if you checked twitches after giving somone sux an hour ago and they have none

A
74
Q

Normal vs Abnormal Dibucaine numbers

A

Normal = 80 - 80% of PChE was inhibited by dibucaine

Abnormal- 20% - dibucaine did not inhibit the PChE

75
Q

Sux has a black box warning that the risk of cardiac arrest and sudden death secondary to _____________ in children with undaignosed ___________.

What’s the most common cause?

A

hyperkalemic rhabdomyolysis

skeletal muscle myopathy

76
Q

Because of the black box warning, sux is generally avoided in kids under what age?

A

<8yo

77
Q

Sux-induced hyperkalemia typically presents with which ekg change?

A

peaked T-waves and sudden cardiac arrest.

78
Q

What are your goals if you give sux to a kid and they die

A
79
Q

4 ways to shift K into the cells

(mneumonic)

A

GASH

  1. Glucose & Insulin
  2. Albuterol
  3. Sodium Bicarb
  4. Hyperventilate

GASH on A BIG DICK

80
Q

Duchenne’s is an X-linked, (autosomal/recessive) disease that results from the absence of what protein?

A

X- lined

Recessive

Dystrophin protein (stabalizes skeletal and cardiac myocytes - it’s absence results in destabilization of the sarcolemma and allows CK and myglobin to enter systemic circulation; CA++ can then freely enter the cell)

81
Q

Calcium chloride vs Calcium Gluconate given for hyperkalemia and how much elemental calcium do each have?

A

Calcium Chloride

  • 20mg/kg
  • 10% contains 27.2mg/mL of elemental calcium

Calcium Gluconate

  • 60mg/kg
  • 10% contains 9mg/mL of elemental calcium

(calcium gluconate 60/9 - think on the floor you always gave the weaker one and that has 9mg/ml and calcium chloride contains 3 x as much, so you need 3x less)

82
Q

How much Sodium Bicarb to give to treat hyperkalemia?

A

1-2mmol/kg

83
Q

How much glucose and insulin to give in life threatening hyperkalemia?

A

Glucose

  • 0.3-0.5g/kg as 10% glucose solution

Insulin

  • 1 unit per 5g of insulin
84
Q

What are the 5 types of muscular dystrophy?

A

“Dont Boys Fucking Lick Everything”

Duchenne

Becker

Facisoscapulohum

Limb-girdle

Emery-Dreifuss

85
Q

Who has the highest risk of developing myalgia after sux administration?

A

Young adults (WOMEN>men) undergoing ambulatory surgery.

86
Q

T/F- men have a higher rate of developing myalgia after sux

A

false- women

87
Q

What 3 groups of patient have the lowest incidence of sux-induced myalgia?

A
  1. Kids
  2. Elderly
  3. Preggo
88
Q

How long can sux-induced myalgia persist for after surgery?

A

24-48 hours

89
Q

Are people who work out and are fit or fat and lazy more prone to postop myalgia from sux

A

fat and lazy

aka: “do not routinely engage in stenuous activity”

90
Q

T/F- using a lower dose of sux will decrease the risk of postop myalgia

A

False! - actually using a higher dose will

91
Q

How should you adjust your sux dose after giving a defasiculating dose of a non- depolarizer and why?

A

increase sux dose to 1.5-2.0mg/kg

92
Q

Who shouldn’t receive a defasiculating dose of sux?

A

those with pr-existing skeletal muscle weakness such as:

myesthenia gravis

93
Q

T/F- opioids reduce the incidence of sux-induced postop myalgia

A

false

-but NSAIDs and lidocaine do

94
Q

____ of the ED95 of a NDMR will reduce sux fasiculations

Roc -

Atracurium-

Vec-

How much time should lapse between defasic dose and suxs?

A

1/10th of the ED95

  • Roc - 2mg
  • Atra- 1.5mg
  • Vec - 0.3mg

3-5 minutes - ha!

95
Q

Myasthenia gravis patients are resistant/sensitive to which relaxants?

A

MG = Resistant to SUX (need more)

Sensitive to NDMR (need less)

96
Q

What specific condition poses sensitivity to BOTH depolarizers and nondepolarizers?

A

Huntington chorea

97
Q

6 conditions with a increased sensitivy to NDMR in which you would give less

A
  1. ALS
  2. Duchenne’s
  3. Guillain-Barre
  4. Huntington Chorea
  5. MS
  6. Mysthenia Gravis
98
Q

Sux induced hyperkalemia with:

Myotonic dystrophy

A

No- just increased muscle contractions which poses a potential issue with airway management

99
Q

Sux induced hyperkalemia with:

Charcot-Marie-tooth

A

Yes

-postassium in marie’s teeth

100
Q

Sux induced hyperkalemia with:

Guillian Barre

A

Yes - weakness - upregulation of extajunctional receptors

101
Q

Sux induced hyperkalemia with:

Myasthenia gravis

A

NOOOOO

  • how am I gonna remember that
  • Myasthenia gravis is already in the GRAVE so it gives no fucks and won’t increase K
  • i suppose i could figure out the disease process and make sense of it- maybe later , but for now , GRAVE - NO K
102
Q

Sux induced hyperkalemia with:

MS

A

YES

-upregulation in extrajunctional receptors

103
Q

Sux induced hyperkalemia with:

ALS

A

YES

104
Q

Sux induced hyperkalemia with:

Huntington chorea

A

NO - but SENSITIVE to BOTH sux and NDMR

105
Q

Rank the NDMR in terms of potency with 1 being the most potent and 4 being the least

  • Roc
  • Pancuronium
  • Atracurium
  • Cisatricurium
A
  1. Cisatracurium (Chuck norris = most potent)
  2. Pancuronium (He’ll hit you on the head with a PAN)
  3. Atracurium (then you scream AHHHHH)
  4. Roc (Roc shows up late to help save you)
106
Q

In the contenxt of NMBs, the ED95 is the dose at what?

A

there is a 95% decrease in twitch height

107
Q

The dose of NMB required to provide optimal conditions for tracheal intubation is _____ x the ED95

A

2-3X the ED95

108
Q

The higher the ED95, the (higher/lower) the potency and the (faster/slower) the onset

A

higher ED95 = lower potency (more drug required to get an effect)

Faster onset- bc more molecules are available to diffuse from the plasma to the NMJ

-explains why roc has the fastest onset and why high-dose roc 1.2mg/kg has a similar onset to Sux

109
Q

Short acting NDMR

  • intubating dose
  • onset
  • duration
A

Mivacurium

  • 0.15mg/kg

3 minutes

15 minutes

110
Q

Intubating doses of the 4 intermediate acting NDMRs

A
  1. Cisatracurium - 0.1
  2. Vecuronium- 0.1
  3. Atracurium- 0.5
  4. Roc- 0.6
111
Q

Long-acting NDMR

  • intubating dose
  • onset
  • duration
A

Pancuronium

  • 0.08mg/kg
  • 3 minutes
  • 90 minutes
112
Q

Match each drug with the primary event that terminates its effect:

Atracurium

Cisatracurium

Rocuronium

Pancuronium

[billiary excretion, renal excretion, non-specific ester hydrolysis, hoffman elimination]

A

Atracurium> Non-specific ester hydrolysis

Cisatracurium > Hoffman Elimination

Rocuronium > biliary excretion

Pancuronium > renal excretion

113
Q

The 3 benzylisoquinolinium NDMBs

A
  1. Cisatracurium
  2. Atricurium
  3. Mivacurium
114
Q

3 Aminosteroid NDMBs

A
  1. Roc
  2. Vec
  3. Panc
115
Q

Short acting NDMR

A

Mivacurium

116
Q
A
117
Q

What is Laudanosine?

A

A metabolite of Atracurium > Cisatracurium

-CNS stimulant - can produce seizures

118
Q

What is a better NDMR for someone with hepatic or renal dysfunction?

A

Cisatracurium, Atricurium, or Mivacurium

(dont rely on liver or renal for excretion- hoffmans and non-specific ester hydrolysis

119
Q

What drugs are broken down by non-specific esterases (3)

A

Remi, Esmolol, Atracurium

120
Q

T/F = patients with a pseudocholinesterase deficiency will experience a prolonged block with atracurium

A

False

-Atracurium is broken down by non-specific plasma esterases- NOT pseudocholinesterase (sux, ester local anesthetics)

121
Q

What is the only NDMR metabolized by pseudocholinesterase?

A

Mivacurium (explains it’s short DOA)

122
Q

T/F- a reversal agent may not be necessary when giving mivacurium

A

True

123
Q

Key things surrounding Atracurium

A
  • Non-specific esterases (66%)
  • Hoffman’s elimination (33%)
  • Launosinde (CNS stimulant)
124
Q

Key facts about Cisatracurium

A
  • Hoffmans elmination (77%)
  • Luanosine (CNS stimulant)
    • Less than atracurium
125
Q

Hoffman’s elimination is faster/slower with (acidosis/alkalosis) and (hyper/hypothermia)

A

Faster

  • Alkalosis & Hyperthermia
  • (Faster = increased; increased PH & increased T)

Slower:

  • Acidosis & Hypothermia
    • (Slower = decreased, decreased pH & decreased T)
126
Q

T/F- Roc does snot undergo signficant deacetylation by the liver

A

True -

-the primary method of elmination is through bilary excretion as an unchanged molecule.

127
Q

Vec undergoes hepatic deacetylation to ____________________; which is half as potent as it’s parent compoud but rapidly metablized into inactive metabolites

A

3-OH vecuronium

128
Q

T/F- Roc doesn’t undergo any significant metabolism

A

True- it is primarily excreted unchanged in the bile.

129
Q

4 NMBs that undergo organ-depedent elimination

A

Atracurium

Cisatracurium

Mivacurium

Sux

130
Q

T/F- Duration of NMB can be prolonged by phenytoin

A

False- shortened

(induces P450 enzymes, gets metabolized faster)

131
Q

6 drug classes that can protentiate your NMB

A
  1. Volatile anesthetics
    * Des > Sevo > Iso > N20 > Prop
  2. Antibiotics
    * Aminoglycosides, polymixins, clindamycin, lincomycin, tetracycline
  3. Anti-dysrhythmics
    * Verapamil, amlodipine, lidocaine, quinidine
  4. Local anesthetics
  5. Diuretics
    * Furosemide
  6. Other
    * Dantrolene, cyclosporin, tamoxifen
132
Q

How does lithium affect your NMB?

A

It increases/potentiates it

-Lithium activates K+ channels > hyperpolarizes > harder to generate AP

133
Q

How do Mag, K, and Ca affect your NMB?

A

Mag - potentiates it (antagonist at the pre-synaptic calcium channel, less calcium to go in and generate an AP)

CA- low ca = potentiation (less calcium to go in and generate AP)

K+ hypokalemia = increased K in the cells, lower RMP, harder to generate AP

134
Q

T/F - women are more senssitive to the NMBs compared to men

A

true

135
Q

T/F- hypothermia potentiates NMB

A

True - decreased clearence and metabolism

136
Q

Which inhaled anesthetic potentiates NMBs the least?

A

N20

(Des>Sevo>Iso>N20)

137
Q
A
138
Q

What condition precludes the use of pancuronium?

  1. Aortic regurgitation
  2. Hypertrophic cardiomyopathy
  3. 1st degree AV block
  4. Bradycardia
A

2. Hypertrophic cardiomyopathy

  • Panc is a vagolytics (increases HR)
  • in the patient with hypertrophic cardiomyopathy, tachycardia reduces blood flow through the LVOT, ultimately reducing cardiac output
139
Q

Which NMBs have a histamine release (3)

A

MMAST

Morphine

Meperidine

Mivacurium

Atracurium

Sux

Thiopental

140
Q

By which mechanism does Panc produce a vagolytic effect in the SA node?

A

It stimulates the release of catecholamines and inhibits catecholamine reuptake in the adrenergic neuons

141
Q

How long does the histamine release from NMBs typially last?

How can you minimize it?

A

1-5 minutes

-give it slow

142
Q

Which NMB is MOST likely to cause anaphylaxis?

  • Atracurium
  • Cisatracurium
  • Sux
  • Roc
A

Sux

143
Q

T/F- NMB are the most common cause of perioperative allergic reactions

A

True

-data is mixed but sux and roc are assoicated with the highest incidence of anaphylaxis

144
Q

Lab to measure anaphylaxis as a differential diagnosis

A

Tryptase (peaks in 15-120 mins after exposure)

145
Q

T/F- the structures of NMBs contain one or more antigenic quarternary ammonia groups that interact with Ig-G, causing mast cell and basophil degrandulation.

A

False- Ig- E

(E= eisoniphil = allergy)

146
Q

Cross sensitivity may occur in up to ____% of those who have had a prior allergic response to NMBs

A

70%

147
Q

What 2 conditions necessitate a dose reduction for Rocuronium?

  • Charcot-Marie tooth
  • MS
  • Duchenne muscular systrophy
  • Hypeerkalemia periodic paralysis
A
  • MS
  • Duchenne muscular systrophy
148
Q

What NMB should be avoided in the patient with a spinal cord transection that ocured 3 months ago?

  • Sux
  • Roc
  • Atracurium
  • Mivacurium
A

Sux

-avoided 24-48 hours following a denervation injury to at least 1 year after

149
Q

Which NMB does NOT produce an active metabolite?

  • Vec
  • Atracurium
  • Roc
  • Sux
A

Roc

Vec > 3-OH vec

Atracurium > laudanosine

Sux > succinylmonocholine

150
Q
A
151
Q

Which antiemetic can prolong sux DOA

  • Metoclopramide
  • Odansetron
  • Droperidol
  • Scopalamine
A

-Metoclopramide

152
Q
A

*Pharmacology (25 decks)

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