Neuromuscular Blocking Agents and Fibromyalgia/Spasticity - Sweatman Flashcards Preview

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Flashcards in Neuromuscular Blocking Agents and Fibromyalgia/Spasticity - Sweatman Deck (46):
1

What are the isoquinolone derivatives used for neuromuscular blocking?

1) Atracurium

2) Cisatracurium

2

What are the steroid derivatives used in neuromuscular blocking?

1) Pancuronium

2) Rocuronium

3) Vecuronium

3

What is the only depolarizing agent used in neuromuscular blocking?

Succinylcholine

4

What drugs are used to reverse neuromuscular blocking?

1) Edrophonium

2) Pyridostigmine

3) Neostigmine

4) Sugammedex (not approved in US yet)

5

What receptor do the neuromuscular blocking agents act on?

Nicotinic M receptor --> found on skeletal muscle

6

What is the physiological role of the nicotinic acetylcholine receptor?

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

7

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

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

8

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

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

9

What is unique about the inactivation of the isoquinolone drugs?

It undergoes hepatic metabolism and Hoffman elimination

10

What advantage does cisatracurium have over atracurium?

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

11

How is succinylcholine metabolized?

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

12

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

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

13

What are the major adverse effects of succinylcholine?

1) Hyperkalemia

2) Malignant hyperthermia

3) Myoglobinuria

14

What causes malignant hyperthermia when using neuromuscular blockers?

Uncontrolled release of Ca2+ from sarcoplasmic reticulum

15

What is the treatment for malignant hyperthermia?

1) Dantrolene

2) Stop giving NM blocker

3) Correct hyperkalemia, acidosis, and cool core temp

16

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

1) Volatile anesthetics --> Malignant hyperthermia

2) Aminoglycosides --> Enhanced blockade

3) Local anesthetics --> block pre-junctional neural effect

17

What are the three acetylcholinesterase inhibitors and their recommended anticholinergics?

1) Neostigmine --> Glycopyrolate

2) Edrophonium --> Atropine

3) Pyridostigmine --> Glycopyrolate

18

What are acetylcholinesterase inhibitors used for?

To reverse non-depolarizing neuromuscular blockade

19

What is the mechanism of action of Sugammadex?

Traps steroid-based neuromuscular blockers to stop their action

20

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

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

21

What are the drugs used to treat fibromyalgia?

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

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

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

23

How is duloxetine metabolized and why is that important?

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

24

What are the cautions/contraindications of duloxetine and milnacipran?

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

What is the mechanism of action of pregabalin?

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

26

How is pregabalin eliminated?

Renal elimination --> reduce dose with renal dysfunction/failure

27

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

1) Rebound symptoms with drug withdrawal

2) Potentially addictive

3) Depression/suicide risk

4) Monitor serum creatinine

28

How do amitriptyline and fluoxetine help in fibromyalgia?

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

29

What drugs are used as muscle relaxers?

1) Carisoprodol

2) Cyclobenzaprine

3) Methocarbamol

4) Tizanidine

30

What is the mechanism of action of carisoprodol?

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

31

What are the cautions and monitoring parameters for carisoprodol?

1) Drowsiness/dizziness most common

2) Additive sedation with other drugs

3) Monitor serum creatinine and BUN

32

What is the mechanism of action of cyclobenzaprine?

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

33

What are the cautions association with cyclobenzaprine?

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

What is the mechanism of action of methocarbamol?

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

35

What is the elimination route for methocarbamol?

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

36

What caution is associated with methocarbamol?

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

37

What is the mechanism of action of tizanidine?

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

38

What elimination problem is associated with tizanidine?

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

39

What cautions and monitoring parameters are associated with tizanidine?

1) Hepatotoxicity --> Monitor LFTs

2) Taper cessation to avoid rebound

3) Additive CNS depression

40

What drugs are used to treat muscle spasticity?

1) Baclofen

2) Botulinum toxin

3) Dantrolene

4) Tizanidine

41

What is the mechanism of action of Baclofen?

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

42

What elimination issue is associated with baclofen use?

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

43

What cautions are associated with baclofen use?

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

What is the mechanism of action of dantrolene?

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

45

What elimination issues are associated with dantrolene?

Crosses placenta causing "floppy baby syndrome"

May cause hepatic dysfunction so monitor LFTs

46

What cautions are associated with dantrolene?

1) Additive CNS depression

2) When given IV and combined with CCBs may cause Vfib and CV collapse