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Pharmacology > Neuromuscular Blockers > Flashcards

Neuromuscular Blockers Flashcards

1
Q

Which cholinergic receptor is involved in neuromuscular blockade?

A

Nicotinic receptor

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2
Q

What binds to the nicotinic receptor to create muscle movement?

A

Acetylcholine (ACh)

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3
Q

What part of the ACh actually makes the connection to the receptor site?

A

The Positively charged Nitrogen ion

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4
Q

Which cholinergic receptor is involved more with rest and digest and associated with slowing down cardiac cells?

A

Muscarinic

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5
Q

What deactivates acetylcholine?

A

Acetylcholinesterase

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6
Q

What does acetylcholinesterase break ACh down into?

A

Choline and Acetate

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7
Q

How much neuromuscular blockage is typically deemed appropriate for surgery?

A

90% suppression single twitch response

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8
Q

Describe succinylcholine chemically?

A

It is basically two ACh molecules stuck together. Two Positively charged Nitrogen groups

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9
Q

What is ED95?

A

Effective dose 95. Dose of NMBA necessary to produce 95% suppression of the single twitch response

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10
Q

How much of ED95 dose is required for tracheal intubation?

A

2x ED95 dose

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11
Q

What is the order of effect for NMB?

A

Small, rapidly moving muscles first (eyes, fingers) and larger muscle last (diaphragm, abdomen).

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12
Q

What is the order of muscle NMB recovery?

A

Recovery is in reverse order.

Larger muscle groups first, then smaller muscles.

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13
Q

Why do large muscles recover faster than smaller muscles after NMB?

A

More blood flow

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14
Q

What is a good prediction of larynx paralysis?

A

Eye muscle TOF

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15
Q

Are NMBAs hydrophillic or lipophillic?

A

Other than vec=lipophilic, they are all hydrophilic and ionized, water soluble.

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16
Q

What part of the nicotinic receptor do NMBA bind?

A

Both alpha subunits of the nicotinic receptor

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17
Q

What is an example of a drug interaction related to pharmacokinetics?

A

CYP enzymes

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18
Q

What is an example of a drug interaction related to pharmacodynamics?

A

Membrane stabilization or something that enhances or inhibit the medication directly at the receptor site.

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19
Q

What are examples of long-acting non-depolarizing NMBA?

A

Pancuronium.
Doxacurium.
Pipecuronium.

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20
Q

What are examples of intermediate-acting non-depolarizing NMBA?

A

Atracurium.
Vecuronium.
Cisatracurium.
Rocuronium.

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21
Q

What are examples of short-acting non-depolarizing NMBA?

A

Mivacurium.

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22
Q

What are examples of aminosteroid non-depolarizing NMBA?

A

Pancuronium.
Pipecuronium.
Vecuronium.
Rocuronium.

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23
Q

What are examples of benzylysoquinolinium non-depolarizing NMBA?

A

Doxacurium.
Atracurium.
Cisatracurium.
Mivacurium.

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24
Q

Which NMBA has the most intense rapid paralysis?

A

Succinylcholine.

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25
Q

What is onset, peak, and duration of succinylcholine?

A

Onset 30-60sec.
Peak 5min.
Duration 3-5min.
Full duration 10min

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26
Q

How is succinylcholine broken down in the body?

A

Acetylcholinesterase

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27
Q

Is most of succinylcholine’s MOA presynpactic or postsynaptic?

A

Postsynaptic mostly.

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28
Q

What NMBA use Phase 1 Blockade?

A

Depolarizing NMBA-succinycholine

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29
Q

What NMBA uses Phase 2 blockade?

A

Non-depolarizing agents

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30
Q

What is dose for succinylcholine for tracheal intubation?

A

1mg/kg

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31
Q

How likely is prolonged (by hours) NMB after succinylcholine?

A

1:3,200

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32
Q

What common drug decreases plasma cholinesterase? and What does this do for succinylcholine use?

A

Reglan decreases it.

Allows for slower metabolism of succinylcholine.

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33
Q

What patient population has higher levels of plasma cholinesterases?

A

Obese patients

34
Q

What can be done to reduce side effects of succinylcholine?

A

Pretreatment with a non-depolarizer- Priming principle.

35
Q

What are the primary side effects of succinylcholine on CV?

A

Sinus brady, sinus arrest.

Cardiac muscarinic receptors- mimics ACh.

36
Q

What are secondary (potential) side effects of succinycholine on CV?

A

Tachycardia and hypertension d/t ANs ganglia stimulation.

37
Q

What medications cannot effectively be used to treat bradycardia resulting from succinylcholine administration?

A

Atropine

38
Q

What side effect is increased if a 2nd dose of succinylcholine is used?

A

Arrhythmias=bradycardia

39
Q

Why is hyperkalemia a side effect of succinylcholine?

A

Because receptor opens up and Na+ rushes in, so the cells balance that out by kicking out K+.

40
Q

Which patients are at a higher risk of hyperkalemia as a side effect of succinylcholine?

A

Muscular dystrophy.
Third Degree burns.
Skeletal muscle atrophy/severe trauma.
Upper motor neuron lesions.

41
Q

Why are patients with muscular dystrophy at increased risk of hyperkalemia as a side effect of succinylcholine?

A

The body creates excess nicotinic receptors. These receptors cannot participate in muscle movement, but can participate in ion movement. The succinylcholine binds to all off them and worsens the hyperkalemia because of the extra junctional sites.

42
Q

Who is at very high risk for hyperkalemia as a side effect of succinylcholine with undiagnosed myopathy?

A

Male children.

43
Q

What are the major side effects of succinylcholine?

A

Myalgias.
Hyperkalemia.
Increased pressure (IOP, IAP, ICP).
Arrhythmias.

44
Q

Where are the most noted areas of myalgia following succinylcholine administration?

A

Neck, back, abdomen

45
Q

Who are at high risk of myalgia from succinylcholine?

A

Young adults, minor surgical procedures, and early ambulation.

46
Q

What three things will have increased pressure from succinylcholine administration?

A

IAP. ICP. IOP.

47
Q

Which of the three increased pressures is at higher risk and what are the issues it causes?

A

Intragastric (IAP).

Increases risk of aspiration.

48
Q

T/F: non-depolarizing NMBA are competive antagonists?

A

True

49
Q

Which NMBAs are more commonly associated with critical myopathies?

A

Aminosteroids.

Higher risk with corticosteroids simultaneously.

50
Q

T/F: Males have a higher incidence of allergic reactions to ND NMBA?

A

False.

D/t soaps and cosmetic use

51
Q

Do sympathomimetic drugs increase or decrease NMB effect?

A

Increase d/t increased blood flow.

52
Q

What alters the effect of NMBA in an enhancing way?

A 
Volatile anesthetics.
Local anesthetics.
Aminoglycosides(gentamicin).
Antiarrythmics.
Diuretics.
Magnesium
Lithium.
Sympathomimetics
53
Q

What are the effects of temperature on NMB response?

A

Hypothermia=prolonged duration.

By every 1 degree Celsius in either direction, you can change duration by 5-15 minutes

54
Q

What is serum potassium’s alterative effects on NMB?

A 
HypoK+ :
Resistance to SCh.
Increased sensitivity to NDNMBA.
HyperK+ :
Increased SCh effect
Opposes NDNMBA.
55
Q

If a patient has paresis or hemiplegia, you can use half as much NMBA to cause paralysis: T/F?

A

False. Have more receptors and would require same or more.

56
Q

There are two groups of NDNMBA based off chemical structure. What are they?

A

Steroids and benzylisoquinoliniums.

57
Q

How can you determine if a NDNMBA is a steroid or a benzyl?

A

Benzyl=Curiums

Steroids=Curoniums

58
Q

What are the only two NMBAs that are monoquaternary (1 Nitrogen group?

A

Rocuronium and Vecuronium.

59
Q

What is the average onset and duration of long-acting NMBA?

A

Onset: 3-5min
Duration: 60-90min

60
Q

(though all relatively safe) Which long acting NMBA is less safe CV wise than the others?

A

Pancuronium.

61
Q

What are the effects of pancuronium on CV?

A 
Increased HR.
Increased MAP.
Increased CO.
Vagal nerve blockade.
SNS activation.
Muscarinic interference.
62
Q

How are pancuronium, doxacurium, and pipecuronium metabolized?

A

80% unchanged in urine.

Half as potent metabolite, but not much effect since mostly eliminated unchanged in urine.

63
Q

How would hepatic cirrhosis/ascites effect long Pancuronium effects?

A

Would need higher loading dose because the drug is hydrophillic and will enter that water filled area.

64
Q

What are advantages to using intermediate NDNMB?

A 
Better clearance.
More predictable.
1/3 duration of long acting.
Minimal CV side effects.
Reliably reversible by anticholinesterases.
65
Q

Of the intermediate NDNMBA, which is the only one with a different onset time?

A

Rocuronium 1-2 minutes.

66
Q

How does the priming principle work for NDNMBA ?

A

Small dose binds spare receptors with no clinical effect.

4 minutes later, give rest of dose and onset will resemble SCh=very quickly.

67
Q

Which is the first intermediate NDNMBA created?

A

Atracurium.

68
Q

How is atracurium different than all others?

A

82% protein bound. Albumin plays a large role in its effect.

69
Q

Which two NMBA are eliminated via Hoffman Elimination (HE)?

A

Atracurium and Cisatracurium.

70
Q

What is Hoffman Elimination?

A

Essentially the body’s natural way of breaking the molecule down to a much smaller molecule so that it can be eliminated via the kidneys.

71
Q

In what patient population would Hoffman Elimination be helpful?

A

Kidney and liver disease because they are not metabolized there.

72
Q

What are some of the smaller molecules that Hoffman Elimination breaks atracurium and cisatracurium down into?

A

Laudanosine and Electrophillic acrylates.

73
Q

When Hoffman elimination breaks them down into laudanosine what are potential complications?

A

CNS stimulant.
Peripheral vasodilation.
Increase MAC of volatile anesthetics.

74
Q

What are atracurium’s CV effects?

A

Increase HR.
Decrease MAP
Histamine release.

75
Q

Rocuronium, cisatracurium, vecuronium all have histamine release: T/F?

A

False

76
Q

Atracurium and Mivacurium have no histamine release?

A

False

77
Q

Cisatracurium is almost exactly like atracurium except for what factor?

A

Cisatracurium does not cause any histamine release.

78
Q

How is vecuronium metabolized?

A

Hepatic and renal.

79
Q

What other NMBA is rocuronium most like?

A

Vecuronium except with faster onset.

80
Q

What is the onset and duration of mivacurium?

A

2-3 min onset

12-20 min duration

81
Q

How is mivacurium metabolized?

A

Plasma cholinesterases.
Hepatic.
and Renal.

Pharmacology (9 decks)

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