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Mo and Mik > m and m 11 - NMB > Flashcards

m and m 11 - NMB Flashcards

1
Q

What type of presynaptic channels are activated by the action potential, Leading to fusion of vessicles?

A

Voltage gated calcium channels

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2
Q

What types of Ach receptors are at the postsynaptic junction, muscarinic or nicotinic?

A

Nicotinic

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3
Q

Activation of approximatly what percentage of postsynapic AchR is needed for muscle contraction?

A

About 10%

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4
Q

How many subunits of the mature AchR? WHat are they? What binds the Ach?

A

5 subunits
2 alpha, 1 beta, delta and epsilon
2 alphas each bind one Ach

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5
Q

What happens if only one Ach is bound? What happens after 2 bind?

A

One ach binds, Nothing

Two bind, Then channel oppens and allows sodium and calcium influx, potassium efflux

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6
Q

How is fetal AchR different from mature AchR?

A

Fetal has a gamma unit instead of the epsilon seen in the mature receptor

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7
Q

Explain the process of depolarizing the perijunctional membrane

A

In response to Ach binding, the receptor Becomes sensitive to extracellular calcium ion concentrations. If enough receptors are activated, then the perijunctional membrane is activated, causing depolarization by activating perijunctional sodium channels (voltage gated)

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8
Q

Explain propagation of the action potential from the motor end plate

A

Voltage gated sodium channel activation causes depolarization, which propagates along the muscle membrane and T-tubule system. This opens downstream sodium channels, which causes release of calcium from the sarcoplasmic reticulum. Ca++ from sarcoplasmic reticulum allows for activation of actin and myosin

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9
Q

The end plate depolarization causes release of 10x number of ions/NT needed for action potential propagation. What happens in myesthenia gravis and Eaton Lambert?

A

MG - reduced AchR at the end plate

EL - Decreased presynaptic calcium channels (P/Q-type)

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10
Q

What is the general structure of the neuromuscular blocking agents?

A

Quaternary ammonium compounds

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11
Q

Why is the action of succx different from Ach?

A

AChE is able to metabolize Ach, terminating its action. The same doesn’t apply to Succx

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12
Q

What is the mechanism of a phase 1 block?

A

The persistent presence of a depolazing stimulus prevents the end-plate from “resetting”, keeping the channels in the open state and preventing repolarization.

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13
Q

What is the effect of “prolonged” end plate depolarization?

A

Can cause phase 2 block, resembles the block of a non-depolarizing agent

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14
Q

True or false, binding of non-depolarizing NMB to the AchR causes a conformational change in the receptor

A

False, this conformational change only happens with Ach or Succx binding

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15
Q

True or false, neuromuscular blockade will occur with only one alpha receptor bound to a NMB

A

True - channel activation requires 2 Ach binding, which can’t happen if one of the alpha channels is occupied by a non-depol NMB

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16
Q

In diseases where there is chronic decrease in Ach release (e.g. muscle denervation), there is compensation by increasing the number of AchR. These diseases will show [increased / decreased] sensitivity of depolarizing neuromuscular blockers

A

Increased - these upregulated immature channels show low channel conductance, but prolonged opening times

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17
Q

In diseases where there is decreased expression of post-synaptic AchR (e.g. MG), there will be increased [sensitivity / resistance] to depolarizing agents and increased [sensitivity / resistance] to non-depol agents

A

Increased resistance to depol agents (not enough binding spots)
Increased sensitivity for non-depol (they will overwhelm the synapse, out-compete the Ach for what few receptors are available)

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18
Q

While not clinically relevant some drugs can cause closed channel blockade. What is closed channel blockade, what drugs can cause this in the lab (4)?

A

Closed channel blockade is when a receptor pore is plugged by a substance, preventing cation flow.
Neostigmine, some abx, cocaine and quinidine

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19
Q

What is the major ways that succx effect is terminated?

A

Diffusion from the junction and metabolism by pesurocholinesterase, plasma cholinesterase and butyrylcholinesterase

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20
Q

Mivacurium metabolism is unique among non-depol NMB. Why?

A

It is metabolized by pseudocholinesterase

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21
Q

What is the mechanism of reversal after neuromuscular blockade with medications?

A

These reversal drugs block AchE activity, allowing for accumulation of Ach, which will then out-compete the neuromuscular blocker

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22
Q

What can happen is you use a reversal agent after blockade with Succx? What is the exception?

A

Can prolong block by causing more depolarization. The exception is if you have a phase 2 block with Succx, Then a reversal agent may be warranted

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23
Q

What is the mechanism of suggamadex?

A

It is a cyclodextran that is able to bind the steroid side chains of the steroid containing NMBs (roc, vec)

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24
Q

If you use a peripheral nerve stimulator and see fade, what what administered? (2)

A

A non-depol blocker

Succinylcholine in a phase 2 block

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25
Q

What is the proposed mechanism of fade?

A

non-depol NMBs cause a decrease in the amount of NMB available for release

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26
Q

You can monitor fade with sustained tetanic stimulation, double burst, train of 4 or repeated twitches. Which is the best way to monitor fade (2)?

A

The first 2, tetanic stim and double burst

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27
Q

After which of the following can you see increase in the degree of evoked potential: tetanic stimulation, double burst, train of 4 or repeated twitches?

A

After tetanic, it is called post tetanic stimulation

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28
Q

True or false, you can have post tetanic stimulation even with a succinylcholine block?

A

False, only occurs with non-depol block

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29
Q

What structures make up succx?

A

2 acetylcholine molecules

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30
Q

True or false, succx has a very high volume of distribution, which underlies its rapid onset of action.

A

False, low Vd, therefore fast onset of action. This low Vd applies to other NMBs

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31
Q

What is the enzyme that metabolizes Suxxc?

A

Pseudocholinesterase

32
Q

True or false, majority of succx that is injected into a patient gets to the NMB, underlying the rapid onset of action

A

False, majority of the succx injected is metabolized by pseudocholinesterase, and thus just a small fraction reaches the NMJ

33
Q

What is the effect of temperature on succx metabolism?

A

Low temps decreases the rate of metabolism (hydrolysis)

34
Q

What health conditions are associated with decreased pseudocholinesterase? (3)

A

Pregnancy, liver dz, renal failure

35
Q

Dibucaine inhibits the normal pseudocholinesterase by what percent? What about the abnormal pseudocholinesterase? How does this relate to dibucaine number?

A

Inhibits normal by 80%, abnormal by 20%. “Normal” dibucaine number is 80, homozygote abnormal is 20 and heterozygote is 40-60

36
Q

What are 2 mechanisms by which cholinesterase inhibitors prolong Succx block?

A

Increase Ach at the NMJ, causing more depolarization

Inhibit pseudocholinesterase

37
Q

What is the significance of echothiophate re: succx blockade?

A

Echothiophate is an organophosphate. Used to be used for glaucoma, it irreversibly inhibits AchE and can this prolong the block by succx

38
Q

How do small vs large doses of non-depol NMB affect the block by succx?

A

Small doses will antagonize block by succx by occupying some of the receptors, preventing succx from depolarizing as strongly as it ordinarily would. Large doses, if given after, would potentiate a phase 2 block

39
Q

True or false, children require a larger / kg dose of succx compared to adults

A

True - they have more extracellular space, thus a larger volume of distribution

40
Q

Why can succx cause both bradycardia and tachycardia?

A

The Ach-like nature will allow it to activate both sympathetic and parasympathetic ganglia (both nicotinic AchR) as well as muscarinic receptors in the sinoatrial node of the heart (SA node activation will cause brady cardia)

41
Q

How can you prevent succx induced bradycardia?

A

Pretreatment with atropine, this makes sense since the bradycardia is from too much cholinergic activation

42
Q

How can you prevent fasciculations by succx? How does this affect succx dosing?

A

Prevent with pretreatment with non-depol relaxant. Will need to increase the dose of succx as the pretreatment will antagonize its effects

43
Q

Generally, a dose of succx is expected to increase serum K+ by about how much?

A

0.5 MeQ

44
Q

Per M and M, 15 conditions with increased suceptibility to succx induced hyperkalemia. Name them

A
  • Burns (after 24 hrs)
  • massive trauma
  • severe intra-abd infection
  • spinal cord injury
  • encephalitis
  • stroke
  • Guillian Barre
  • Severe Parkinsons
  • Tetanus
  • Prolonged immobilization
  • ruptured cerebral aneurysm
  • polyneuropathy
  • closed head injury
  • hemorrhagic shock with metabolic acidosis
  • myopathies
45
Q

Theoretically, what is the effect of succx on an open globe?

A

The fasciculations will increase intraoccular pressure and can theoretically cause extrusion of eye contents. Has never been documented

46
Q

When treating a patient with succx and you find an abnormally rigid jaw, what should you suspect / be wary of?

A

While some jaw stiffness may be expected, a markedly increased degree of stiffness may signal malignant hyperthermia

47
Q

True or false, succx is a potent triggering agent for malignant hyperthermia

A

True - avoid in patients with Increased risk

48
Q

What are the three main classes non non-depol NMDs? Clinical characteristics, broadly?

A

Steroidals - (Panc, Vec, Roc) - Vagolytics
Benzylisoquinolones - Atra and Cisat - Release histamine
Chlorofumarate - Gantacurium

49
Q

What are 2 ways to increase onset of action for paralysis so as to use non-depol NMBs for intubation?

A

Increase the dose

Use a priming dose (about 10% of intubating dose)

50
Q

Approximately what percentage of receptors need to be blocked for a clinically significant paralysis?

A

75-80% of receptors

51
Q

True or false, priming dose of non-depol NMB can cause dyspnea, diplopia, dysphagia and dyspnea.

A

True - if this happens, move forward with intubation without delay

52
Q

Which recovers faster from NMB, laryngeal muscles or adductor pollicis longus?

A

Laryngeal muscles. Generally, one of the last of the monitored muscles to cover is the adductor pollicus, longer than the obicularis oculi, diaphragm, jaw, larynx

53
Q

How can you prevent fasciculations and myalgias from succx? What is the most common agent used for this purpose?

A

Can pretreat with non-depol NMB (10% intubating dose). Most commonly done with rocuronium, but can be done with other agents as well.

54
Q

True or false, inhalational agents augment the effects on NMBs.

A

True. Des>Sevo>iso>halothane (reverse order of the MAC potency)

55
Q

True or false, Non-depol NMBs of the same class are synergistic with each other

A

False, usually agents from different classes. Agents of the same class are generally additive

56
Q

Among the currently used non-depol NMBs, one specific agent is associated with tachycardia. What is this agent and what is the mechanism?

A

Pancuronium - associated with tachycardia because it blocks the muscarinic receptors in the SA node. Also a direct sympathomimetic

57
Q

What is the relationship between cis-atracurium and atracurium?

A

Cisatra is an isomer of atracurium. Advantage of cisatra is that is doesn’t cause the degree of histamine release seen with atracurium (bronchospasm, skin flusing and hypotension)

58
Q

What are the two non-depol NMBs with clinically significant metabolites?

A

Pancuronium and vecuronium, will have prolonged elimination in patients with liver disease

59
Q

In patients with liver failure, which of the non-depol NMBs will have a longer duration of action?

A

Pancuronium and rocuronium

60
Q 
Which potentiate neuromuscular blockade?
Hypo/hyperthermia? 
Acidosis/Alkalosis? 
Hyper/Hypokalemia?
Hyper/Hypocalcemia? 
Hyper/Hypomagnesemia?
A

Prolonged Blockade with

  • Hypothermia
  • Acidosis
  • Hypokalemia
  • Hypocalcemia (need Ca at NMJ)
  • Hypermagnesemia (competes with Ca at NMJ)
61
Q

Liver Dz and Renal Dz can affect NMB in what ways, generally speaking?

A

Can both cause greater volume of distribution, meaning more drug may be needed for initial effect. However, due to decreased excretion of specific agents, maintenance doses may be decreased.

62
Q

True or false, all NMBs have quarternary groups that prevent crossing of the cell membrane

A

True

63
Q

Atracurium is extensively metabolized and less than 10% of it is excreted unchanged. What are the 2 mechanisms of metabolism?

A

Ester hydrolysis - By non-specific esterases (NOT pseudocholinesterase or acetylcholinesterase)

Hoffmann degradation - spontaneous non-enzymatic degradation at physiological pH and temp

64
Q

What are CV side effects of atracurium? How can these be prevented?

A

Can cause tachycardia and Hypotension, independent of histamine release. Prevent with slow injection

65
Q

Why should you avoid the use of atracurium in asthmatics?

A

Release of histamine associated with bronchospasm

66
Q

What is the significance of laudanosine toxicity re: NMBs?

A

This is a product of atracurium and cisatracurium Hofmann degradation. Can cause CNS excitation, which at minimum increases MAC and at its worse, will cause seizures

67
Q

Under what conditions may laudanosine become clinically significant?

A

Patient who have received a large cumulative dose of cistatracurium or atracurium, or patient who have hepatic failure

68
Q

What is the significance of avoiding hypothermia in patient treated with cis/atracurium?

A

Both are extensively metabolized by Hofmann degradation, which relies on ideal temp (and pH). Hypothermia will prolong duration of action

69
Q

True or false, Cisatracurium doesn’t cause as much histamine release as atracurium, however, it is a lot less potent

A

False, it doesn’t cause as much histamine release AND it is more potent (4x)

70
Q

Which will cause more laudonosine production for the same amount of neuromuscular blockade and why, cisatra or atra?

A

Atra - less potent, more will have to be used, causing more substrate for laudanosine production

71
Q

Structurally, how does pancuronium differ from vecuronium and rocuronium?

A

Pancuronium contains 2 quaternary amines while the others have one each

72
Q

Why should pancuronium be used carefully in patients where tachycardia is not desirable?

A

It is a vagolytic and can also be a direct sympathomimetic (stimulates ganglions, increases catecholamine release from nerve terminals and decreases re-uptake of catecholamines)

73
Q

Why is the use of vecuronium in ICU patients significant?

A

Long term use in ICU patients can result in prolonged blockade, mainly because of the accumulation of its metabolite that is clinically active

74
Q

Which is the most potent of the steroid NMBs? Which has the fastest onset?

A

Potency? Panc = Vec

Fastest? Roc

75
Q

What NMB is metabolized By pseudocholinesterase, although not clinically used/ available in the US?

A

Mivacurium

76
Q

Pipercuronium and pancuronium are both long acting NMBs. What is a clinically significant difference?

A

Pipercuronium is not a vagolytic, therefore won’t cause the same tachycardia as with pancuronium

Mo and Mik (9 decks)

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