Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Rheum/Musculoskeletal/Derm Week 1 > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

What are the non-depolarizing isoquinoline derivatives?

A
  • atracurium
  • cisatracurium
  • D-tubocurarine (off the market)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the non-depolarizing steroid derivatives?

A
  • Pancuronium
  • Rocuronium
  • Vecuronium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the only depolarizing agent?

A

Succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the reversal agents for NMBs?

A
  • Edrophonium
  • Pyridostigmine
  • Neostigmine
  • Sugammedex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are reversal agents used for?

A

They are given post‐procedurally to reverse the residual effects of the paralytic agent and restore normal neuromuscular activity and tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the types of cholinergic receptors?

A

nicotinic receptors

and muscarinic receptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where do paralytic agents act?

A

nicotinic M receptors found on post-synaptic skeletal muscle (the other type is the nicotinic N receptors- can be found on pre-synaptic terminal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the nicotinic acetylcholine receptor.

A

It is a multimeric ligand-gated ion channel for sodium influx into the cell, leading to depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What must occur for the nicotinic acetylcholine receptor to activate?

A

2 molecules of Ach must bind

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are depolarizing paralytics different from non-depolarizing paralytics?

A

Non-depolarizers bind the receptor and prevent the opening of the receptor channel (thus preventing initial activation of muscle contraction) while depolarizing agents actually open the gate and causes persistent depolarization which prevents gate closure and repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the result of depolarizing paralytics (i.e. succinylcholine)?

A

The initial, intense muscle contraction is replaced by flaccid paralysis from preventing repolarization to occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does a peripheral nerve stimulator (PNS) work?

A

It delivers 4 sequential stimuli at 2 Hz. Each stimuli causes release of Ach from synaptic vesicles. In the absence of neuromuscular blockade, the 4th twitch of the adductor polices muscle is as strong as the first. This is called ‘fade’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Only the first twitch is registered in a PNS when what percentage of receptors is bound?

A

85-90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which twitches can be seen when 70-8% of receptors are bound?

A

between 2-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How are the non-depolarizing drugs metabolized?

A

rapid initial distribution into tissue with slower elimination and duration of action correlated closely with half life.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How are the non-depolarizing drugs eliminated?

A

more rapidly eliminated via liver than kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is a potential downside of Atracurium?

A

it is intermediate acting with hepatic metabolism and Hofmann elimination which produced laudanosine, a metabolite linked to seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the advantages of Cisatracurium over atracurium?

A

it is less dependent on hepatic inactivation, thus producing less laudanosine and it also releases less histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How is succinylcholine eliminated?

A

broken down in situ by pseudocholinesterase enzyme (not present in synaptic cleft) (plasma) or by hydrolysis by butyrylcholinesterase (liver)

decreased pseudocholinesterase may be seen in older patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How long does succinylcholine act?

A

only 5-10 minutes. However, Note the predisposition of some patients, with variant pseudocholinesterase activity, to experience prolonged drug action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When else has increased duration of action been seen in succinylcholine?

A

with ester-type anesthetic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What test can be performed to identify the extent of pseudocholinesterase activity?

A

Dibucaine test (inhibits normal enzyme by 80% and abnormal by only 20%)

Alternatively a simplified colorimetric screening test can be performed using the Acholest Test Paper, a substrate-impregnated test paper, a similar colorimetric reaction occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are atracurium and cisatracurium eliminated? Tubocurarine?

A

spontaneously at site of action (tubocurarine is really mostly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which isoquinolone lasts longest? shortest?

A

longest- tubocurarine (50+ min)

shortest- atracurium (20-35 min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How are the steroidal eliminated?

A

mostly renal in pancuronium with rocuronium and vecuronium being mostly hepatic elimination

26
Q

Which isoquinolones can cause Ach binding to other receptors?

A

atracurium and tubocurarine (more so) can cause histamine release and tubocurarine can weakly block autonomic ganglia

27
Q

Which steroidals can cause Ach binding to other receptors?

A

pancuronium can cause slight block of cardiac M receptors to cause tachycardia

28
Q

What do cardiac M receptors do?

A

The activation of the M2 receptor in the heart is important for closing calcium channels in order to reduce the force and rate of contraction, so inactivation can lead to diminished CV capability.

29
Q

What can succinylcholine cause Ach binding to other receptors?

A

stimulation of autonomic ganglia, cardiac M receptors and slight histamine release

30
Q

AEs of succinylcholine?

A
  • hemodynamic changes (brady, tachycardia, HTN)
  • hyperkalemia
  • prolonged neuromuscular blockade
31
Q

What conditions can hyperkalemia be seen in with succinylcholine?

A
  • large burn injuries, trauma

- upper or lower motor neuron injuries, muscular dystrophy, or prolonged immobilization

32
Q

Why would hyperkalemia only been seen in these states?

A

Normally, the acetylcholine receptors (AChRs) are located only in the junctional area. In certain pathologic states, such as those listed here, there is up-regulation (increase) of AChRs spreading throughout the muscle membrane, with the additional expression of two new isoforms of AChRs. The depolarization of these AChRs that are spread throughout the muscle membrane by succinylcholine and its metabolites leads to potassium efflux from the muscle, leading to hyperkalemia

33
Q

Other AEs of succinylcholine?

A
  • muscle pain
  • myoglobinuria
  • malignant hyperthermia (MT)
  • anaphylaxis (histamine release)
34
Q

What causes malignant hyperthermia?

A

drugs that cause an uncontrolled release of calcium from the SR

35
Q

What drugs can cause MT?

A
  • succinylcholine

- all volatile (liquid at room temp) anesthetic agents including desflurane and iso/sevoflurane

36
Q

How is MT treated?

A
  • dantrolene (Dantrium)
  • hyperventilate with O2
  • avoid CCBs
  • correct hyperkalemia and acidosis from lactate production, cool core temp
37
Q

How can aminoglycosides affect neuromuscular function?

A

Enhancement of blockade (pre-junctional P-type Ca2+ channels) and Depressed Ach release similar to that caused by magnesium

38
Q

How can local anesthetics affect neuromuscular function?

A

Can depress via a pre-junctional neural effect and can block neuromuscular transmission in large doses

39
Q

The depolarizing effect of succinylcholine can be antagonized by administering a small dose of what?

A

a non-depolarizing blocker

40
Q

What is a main way to reverse neuromuscular blockade?

A

increase levels of Ach by preventing metabolism of this endogenous ligand by AchE.

41
Q

What are the AchE inhibitors used to reverse neuromuscular blockade?

A
  • Neostigmine
  • Edrophonium
  • Pyridostigmine
42
Q

What is the recommended anticholinergic to give with Neostigmine?

A

Glycopyrrolate

43
Q

What is the recommended anticholinergic to give with Edrophonium?

A

Atropine

44
Q

What is the recommended anticholinergic to give with Pyridostigmine?

A

Glycopyrrolate

45
Q

What is the quickest onset AchE inhibitor?

A

Neostigmine and Edrophonium act within 5-10 min (period- 10-20 min)

46
Q

DOA of AchE inhibitors?

A

Neo- 45-90 min
Edro- 30-60 min
Pyrido- 60-120 min

47
Q

Can any AchE inhibitor cross the BBB?

A

No

48
Q

Which anticholinergic given with a AchE inhibitor is most likely to prevent bradycardia?

A

Atropine (others can work if needed, Glycopyrrolate over Scopolamine)

49
Q

Which anticholinergic given with a AchE inhibitor is most likely to prevent bronchoconstriction?

A

Atropine or Glycopyrrolate (scopolamine can work if needed)

50
Q

Which anticholinergic given with a AchE inhibitor is most likely to promote sedation?

A

scopolamine (glycopyrrolate will not help at all and atropine can work if needed)

51
Q

Which anticholinergic given with a AchE inhibitor is most likely to promote antisialogogue (decrease saliva secretions)?

A

scopolamine or glycopyrrolate (atropine can work if needed)

52
Q

AEs of AchE inhibitors?

A
  • decreased HR
  • bronchospasm, increased secretions
  • diffuse cerebral excitation
  • increased peristalsis and bladder tone
  • pupillary constriction
53
Q

What is the effect of Sugammadex?

A

Rapidly encapsulates steroids like rocuronium and vecuronium to cause reversal of any depth of neuromuscular blockade, including profound blockade

54
Q

T or F. Sugammadex is inactive against non-steroidal neuromuscular blocking agents, like succinylcholine and cisatracurium

A

T.

55
Q

What are some of the uses of NMBs?

A

As adjuvant in surgical anesthesia
(Permits lower doses of anesthetics; reduced adverse events. Does not substitute for anesthetic. No relief of pain, no amnesia)

For short orthopedic procedures
Dislocations; alignment of fractures

Endotracheal intubation
Laryngoscopy, bronchoscopy, esophagoscopy

56
Q

What parts of the body are affected first by NMBs?

A

Small, rapidly moving muscles such as those of the eyes, jaw, and larynx relax before those of the limbs and trunk.

Ultimately, the intercostal muscles and finally the diaphragm are paralyzed, and respiration then ceases

Recovery of muscles usually occurs in the reverse order to that of their paralysis, and thus the diaphragm ordinarily is the first muscle to regain function.

57
Q

How are NMBs given?

A

IV

58
Q

What is the function of nicotinic N receptors?

A

help mobilize pre-synaptic vesicles to the pre-synaptic surface to be ready to be released with the next impulse (these are also blocked with NMBs and is the basis of ‘fade’)

59
Q

NMBs act upon which type of receptors?

A

Nicotinic M

60
Q

What is the difference between nicotinic and muscarinic receptors?

A

nicotinic receptors are ion channels and muscarinic receptors are g-coupled receptors

61
Q

What is a classic sign of MT?

A

coca-cola urine and muscle rigidity

62
Q

T or F. Patients who have adequate NMB are comfortable and pain free

A

FALSE. No pain relief whatsoever

Rheum/Musculoskeletal/Derm Week 1 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions