Neuromuscular Blocking Agents and Fibromyalgia/Spasticity - Sweatman Flashcards

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1
Q

What are the isoquinolone derivatives used for neuromuscular blocking?

A

1) Atracurium
2) Cisatracurium

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2
Q

What are the steroid derivatives used in neuromuscular blocking?

A

1) Pancuronium
2) Rocuronium
3) Vecuronium

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3
Q

What is the only depolarizing agent used in neuromuscular blocking?

A

Succinylcholine

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4
Q

What drugs are used to reverse neuromuscular blocking?

A

1) Edrophonium
2) Pyridostigmine
3) Neostigmine
4) Sugammedex (not approved in US yet)

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5
Q

What receptor do the neuromuscular blocking agents act on?

A

Nicotinic M receptor –> found on skeletal muscle

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6
Q

What is the physiological role of the nicotinic acetylcholine receptor?

A

Ligand-gated Na+ channel that opens during depolarization –> 2 Ach bind per receptor

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7
Q

What is the mechanism of action of the non-depolarizing neuromuscular blockers?

A

Stabilize the closed conformation of the Nicotinic M receptor to prevent Na+ influx

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8
Q

What is the mechanism of action of the depolarizing neuromuscular blocker?

A

Stabilizes the Nicotinic M channel in the open conformation –> blocks depolarization of the membrane

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9
Q

What is unique about the inactivation of the isoquinolone drugs?

A

It undergoes hepatic metabolism and Hoffman elimination

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10
Q

What advantage does cisatracurium have over atracurium?

A

Cisatracurium does no produce the toxic metabolite associated with seizures (laudanosine)

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11
Q

How is succinylcholine metabolized?

A

Rapidly metabolized by cholinesterase’s in the plasma or liver (5-10 minute duration of action)

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12
Q

What is the major “off target” action of pancuronium and rocuronium?

A

Cardiac M receptor blocking –> Pancuronium is worse Decreased rate and force of contraction

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13
Q

What are the major adverse effects of succinylcholine?

A

1) Hyperkalemia
2) Malignant hyperthermia
3) Myoglobinuria

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14
Q

What causes malignant hyperthermia when using neuromuscular blockers?

A

Uncontrolled release of Ca2+ from sarcoplasmic reticulum

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15
Q

What is the treatment for malignant hyperthermia?

A

1) Dantrolene
2) Stop giving NM blocker
3) Correct hyperkalemia, acidosis, and cool core temp

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16
Q

What are the major drug-drug interactions (3) of neuromuscular blockers?

A

1) Volatile anesthetics –> Malignant hyperthermia
2) Aminoglycosides –> Enhanced blockade
3) Local anesthetics –> block pre-junctional neural effect

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17
Q

What are the three acetylcholinesterase inhibitors and their recommended anticholinergics?

A

1) Neostigmine –> Glycopyrolate
2) Edrophonium –> Atropine
3) Pyridostigmine –> Glycopyrolate

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18
Q

What are acetylcholinesterase inhibitors used for?

A

To reverse non-depolarizing neuromuscular blockade

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19
Q

What is the mechanism of action of Sugammadex?

A

Traps steroid-based neuromuscular blockers to stop their action

20
Q

What is the biggest difference between the non-depolarizing neuromuscular blockers and succinylcholine?

A

Non-depolarizing drugs have a longer duration of action and fewer adverse effects

21
Q

What are the drugs used to treat fibromyalgia?

A

1) Duloxetine (SNRI)
2) Milnacipran (SNRI)
3) Pregabalin (Ca2+ Channel Blocker)
4) Amitriptyline (tricyclic antidepressant)
5) Cyclobenzaprine (fucks you up; alcohol +++)
6) Fluoxetine (SSRI)

22
Q

What is the mechanism of action of duloxetine and milnacipran? What are their selectivities?

A

Both are serotonin-norepinephrine reuptake inhibitors; duloxetine is more selective for serotonin and milnacipran is more selective for norepinephrine

23
Q

How is duloxetine metabolized and why is that important?

A

Mainly Cyp2D6 and also mildly inhibits –> possible drug-drug interactions

24
Q

What are the cautions/contraindications of duloxetine and milnacipran?

A

1) Mild increase in HR and BP –> pre-existing CV issues
2) Uncontrolled closed angle glaucoma
3) Hyponatremia secondary to SIADH
4) BBW for suicide

25
Q

What is the mechanism of action of pregabalin?

A

Inhibit alpha-2-delta subunits of L-type Ca2+ channels in presynaptic nerves –> inhibits excitatory transmission by glutamate

26
Q

How is pregabalin eliminated?

A

Renal elimination –> reduce dose with renal dysfunction/failure

27
Q

What are the cautions and things that should be monitored with pregabalin?

A

1) Rebound symptoms with drug withdrawal
2) Potentially addictive
3) Depression/suicide risk
4) Monitor serum creatinine

28
Q

How do amitriptyline and fluoxetine help in fibromyalgia?

A

It is thought they restore the neurotransmitter imbalance –> used off label

29
Q

What drugs are used as muscle relaxers?

A

1) Carisoprodol
2) Cyclobenzaprine
3) Methocarbamol
4) Tizanidine

30
Q

What is the mechanism of action of carisoprodol?

A

CNS action in reticular activating system and spinal cord leading to sedation and altered perception of pain –> NO DIRECT EFFECT ON MUSCLES

31
Q

What are the cautions and monitoring parameters for carisoprodol?

A

1) Drowsiness/dizziness most common
2) Additive sedation with other drugs
3) Monitor serum creatinine and BUN

32
Q

What is the mechanism of action of cyclobenzaprine?

A

Similar to amitriptyline (sereotnin/norepi reuptake inhibitor) –> central action possible at level of brain stem

33
Q

What are the cautions association with cyclobenzaprine?

A

1) Significant anti-cholinergic effects
2) Additive CNS depression with other drugs/alcohol (don’t give to Kendall)
3) GI symptoms are MOST significant (paralytic ileum)
4) May increase QT interval

34
Q

What is the mechanism of action of methocarbamol?

A

Effects thought to be due to generalized sedative action –> altered pain perception No direct action on muscles

35
Q

What is the elimination route for methocarbamol?

A

Hepatic dealkylation and hydroxylation with renal elimination –> significant hepatic/renal dysfunction can cause toxicity

36
Q

What caution is associated with methocarbamol?

A

Additive CNS depression with other drugs and alcohol (sorry Kendall)

37
Q

What is the mechanism of action of tizanidine?

A

Agonist for pre-synaptic alpha-2 receptor –> decreased activation of polysynaptic spinal cord motor neurons –> reduced muscle tone but not strength

38
Q

What elimination problem is associated with tizanidine?

A

Decreased clearance in renal dysfunction and elderly –> should titrate to effective dose

39
Q

What cautions and monitoring parameters are associated with tizanidine?

A

1) Hepatotoxicity –> Monitor LFTs
2) Taper cessation to avoid rebound
3) Additive CNS depression

40
Q

What drugs are used to treat muscle spasticity?

A

1) Baclofen
2) Botulinum toxin
3) Dantrolene
4) Tizanidine

41
Q

What is the mechanism of action of Baclofen?

A

GABAB agonist producing inhibitory or hyper polarizing signals which reduce excitatory polysynaptic pathways

42
Q

What elimination issue is associated with baclofen use?

A

Can’t use in renal dysfunction –> drug accumulation leads to encephalopathy , abdominal pain, seizures, respiratory depression

43
Q

What cautions are associated with baclofen use?

A

1) Abrupt discontinuation leads to rebound neural activity (confusion, seizures, psychiatric disturbances and spasticity occur) –> taper over 2 weeks
2) Additive hypotension with antihypertensives and MAOIs
3) May increase blood glucose (fuckin diabetics)

44
Q

What is the mechanism of action of dantrolene?

A

Directly interferes with Ca2+ release from sarcoplasmic reticulum –> blocks the ryanodine receptor

45
Q

What elimination issues are associated with dantrolene?

A

Crosses placenta causing “floppy baby syndrome”

May cause hepatic dysfunction so monitor LFTs

46
Q

What cautions are associated with dantrolene?

A

1) Additive CNS depression
2) When given IV and combined with CCBs may cause Vfib and CV collapse