skeletal muscle relaxers Flashcards

1
Q

two groups of skeletal muscle relaxers

A

depolarizing and non-depolarizing

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2
Q

5 steps of normal neuromuscular function

A
  1. Axn potential arrives at nerve terminal
  2. influx of Ca++ and release of Ach
  3. Ach diffuses across synaptic cleft
  4. Nicotine receptors activated on nerve endplate
  5. Muscle contracts
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3
Q

what are the non-depolarizing (antagonist) agents ?

A

” - curiums” and “-roniums”

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4
Q

what is the depolarizing (agonist) agent ?

A

succinylcholine

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5
Q

MOA of neuromuscular blocking agents

A

Agents block cholinergic transmission between motor nerve ending and nicotinic receptors on skeletal muscle

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6
Q

uses for neuromuscular block?

A

Facilitate tracheal intubation
Provide complete muscle relaxation
adjunct to anesthesia (decreased anesthesia dose and faster recovery)

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7
Q

what are the two groups of non-depolarizing (antagonist) neuromusc. blocking agents?

A
short acting ( 30-60min) 
long acting( 60-120min)
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8
Q

what are the short-acting non-depolarizing NM blocking agents?

A

Atracurium
Cisatracurium
Rocuronium (VERY rapid onset, short DOA)
Vecuronium

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9
Q

what is the long-acting non-depolarizing NM blocking agent?

A

Pancuronium

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10
Q

MOA of non-depol. NM blockers

A

competitive antagonists - block Ach from binding to receptor and activating it

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11
Q

clinical effect of non-depol NM blockers

A

progression- muscle weakness then complete muscle paralysis

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12
Q

large or small muscles more resistant to NM blockade ? what does this mean?

A

large muscles, paralyzed last but recover first

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13
Q

all NM blocking agents (depol and nondepol) are polar or nonpolar, why is this significant?

A

polar: can’t get into CNS when given orally so NEED to be IV.

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14
Q

you can get an increase NM blockade when giving nondepol agents with _______

A

antibiotics (usually aminoglycosides- GNATS)

- the abx DECREASE the release of Ach which enhances the blockade but INCR. RESPIRATORY DEPRESSION

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15
Q

how can you reverse the effect of nondepol NM blockers?

A

they are competative antagonists, so you can FLOOD with an agonist (Ach)
- give acetylcholinesterase inhibitors (e.g. neostigmine) so you have more Ach

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16
Q

what is the MOA of succinylcholine?

A

this is our “agonist” depolarizing agent.
- mimics Ach to depolarize NM, stays attached and constantly is depolarizing… unable to depol again while this drug is present.

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17
Q

when are you using succinylcholine?

A

adjunct to general anesthesia
- help tracheal intubation, skeletal muscle relaxation during surgery or mechanical ventilation in adequately sedated patients

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18
Q

what is the metabolism of of succinylcholine (depol NM block) ?

A

Metabolized by plasma pseudocholinesterase
DOA: 4-30 minutes
-drug disappears rapidly after discontinuation

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19
Q

what is the “genetic variant” for succinylcholine?

A

some people (w/ this variant) have PROLONGED effects from the drug

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20
Q

4 ADRs of depolarizing NM blocker (succinycholine)?

A
  1. apnea
  2. hyperkalemia
  3. muscle pain
  4. malignant hyperthermia
21
Q

how can succinycholine cause apnea?

A

Deficiency/atypical form of plasma cholinesterase leads to prolonged apnea from diaphragm paralysis

22
Q

how can succinycholine cause hyperkalemia? why is this significant?

A

Succinylcholine increases K+ release from intracellular stores.

  • Damaged tissue ( burns, nerve damage, trauma, etc) has rapid loss of K+
  • can lead to cardiac arrest
23
Q

what 4 things can cause malignant hyperthermia ?

A

inhaled anesthetics + succinylcholine OR

-Genetic excitation-contraction coupling defect, burn victims, muscular dystrophy

24
Q

what is malignant hyperthermia? what can it ultimately lead to?

A

Uncontrolled increased in skeletal muscle metabolism with SUDDEN, PROLONGED RELEASE OF Ca++
(overwhelm’s body’s capacity to supply O2, remove CO2 and regulate temp)
-fast rise in BODY TEMP, SEVERE MUSCLE CONTRACTIONS
- circulatory collapse and death !!

25
Q

what would you use to txt succinylcholine+inhaled anesthetic - induced malignant hyperkalemia?

A

dantrolene

26
Q

“when you hear allergy to Ach-drug think of ….”

A

malignant hyperthermia!

  • if pt has allergy to a cholinergic, could potentially get malignant hyperthermia from inhaled anesthesia + succinycholine
  • txt with dantrolene!
27
Q

MOA of Dantrolene

A

a direct acting skeletal muscle RELAXANT

-prevents release of Ca+ in skel. muscle

28
Q

two clinical uses of Dantrolene

A
  1. Txt of spasticity associated with upper motor neuron disorders (eg, spinal cord injury, stroke, cerebral palsy, or multiple sclerosis)
  2. Malignant hyperthermia - IV
29
Q

All Spasmolytics are _____ _______ except for dantrolene. why is this significant?

A

centrally acting
-Provide significant relief from painful muscle spasm but don’t really help improve meaningful function
E.g., mobility or returning to work

30
Q

what is Diazepam (Valium) used for?

A

Spasmolytic:

relief of skeletal muscle spasm due to inflammation, trauma or upper motor neuron disorders (cerebral palsy, MS)

31
Q

ADR of Diazepam (valium) ?

A

Significant CNS sedation at doses needed for spasm relief

32
Q

MOA of Baclofen?

A

A spasmolytic: Agonist of GABAb receptor

= decrease release of excitatory NT and decrease Ca++ influx

33
Q

MOA of Tizanidine (Zanaflex)

A

Alpha-2 agonist
Decrease spasticity be increasing presynaptic inhibition to reduce muscle spasms
Overall: decrease facilitation of spinal motor neurons

34
Q

what are the “non-spasmolytic” “other” drugs use to treat muscle spasm?

A
Cyclobenzaprine (Flexeril), the protoype
Orphenadrine (Norflex)
Carisoprodol (Soma)
Metaxalone (Skelaxin)
Methocarbamol (Robaxin)
35
Q

what do we use “other” drugs for muscle spasm for in particular? what do we NOT use them for?

A
  • Relief of acute muscle spasm caused by tissue trauma or strain (**nonspecific back pain) NOT for spasm from spinal cord or brain
  • Don’t use in spinal cord or brain injuries
36
Q

what is the major ADR of the “other” drugs for muscle spasm?

A

Strongly antichlolinergic (anti sludgemm),

37
Q

what 4 drugs are used for true severe muscle spasm due to neurologic injury?

A

Diazepam, Baclofen, Tizanidine, Dantrolene

38
Q

what population should spasmolytics and the “other” spasm drugs be used in caution with?

A

elderly:

little clear benefit and the ADRs are more pronounced in the elderly ( we do use these but really should not)

39
Q

4 types of anesthesia

A

Local: +/- sedation
Conscious sedation
Regional
General

40
Q

what is used for conscious sedation?

A

IV pain med and mild sedative are used (not local)
S-H (midazolam), fentanyl, morphine
*pt is sleepy but can maintain airway

41
Q

what is regional anesthesia?

A

block sensation to particular part of body

42
Q

4 goals of general anesthesia

A

Smooth, rapid induction with rapid recovery
Drug to maintain anesthesia
Wide therapeutic margin
Few side effects

43
Q

what is most commonly used as pre-medication (step 1) for anesthesia?

A

midazolam (S-H) that sedates, decreases anxiety and often causes amnesia

44
Q

what is often used for anesthesia induction? (step 2)

A

pre-oxygentate then…

IV use ultra short acting barbiturates (methohexital/brevital) or Propofol

45
Q

principle of maintenance (step 3)

A

Use inhaled anesthetics and/or intravenous combined with IV agents in regimens of balanced anesthesia

46
Q

what are the 3 spasmolytic drugs that we care about?

A

diazepam (valium)
baclofen (Lioresal)
Tizanidine (Zanaflex)

47
Q

which spasmolytic is AS effective as Valium but with less CNS sedation?

A

Baclofen

48
Q

what is zanaflex used for?

A

spasticity from cerebral or spinal injury

49
Q

when is baclofen used?

A
  • severe spastic disorders

- used for alcohol abstinence to decrease cravings