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Pharm Block 10 > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

What neuromuscular blocking drugs that we talk about target the CNS

A

Baclofen
Tizanidine
Diazepam

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2
Q

What neuromuscular blocking drugs target the actual muscle

A

Dantrolene

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3
Q

Why is it clinically necessary to block tranmission at the neuromuscular end plate of Ach

A

Needed for surgical relaxation, tracheal intubation, and control of ventilation

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4
Q

What is the process of Ach getting across the synapse

A
  • AP sent down nerve, inside becomes more positive and causes Ca2+ channels to open
  • Ca2+ comes in it becomes more positive, which activated the vesicles contains Ach and cause Ach to be released
  • once ACh goes across synapse, it binds to the Na+ channels to open them (Nm is Na channel)
  • Na+ influx into the muscle fiber
  • small amount of K flux out of fiber
  • this causes contraction
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5
Q

Ach receptor

A

2 alpha subunits that Ach has to bind

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6
Q

What are the two types of neuromuscular blocking drugs

A
  1. Non-depolarizing

2. Depolarizing

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7
Q

No depolarizing neuromuscular blocking drugs

A 
Tubocurarine 
Atracurium 
Pancuronium 
Vecuronium
Rocuronium 
Cisatracurium
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8
Q

MOA of nondepolarixing neuromuscular blocking drugs

A

Nicotinic antagonist-competitive antagonists, compete with Ach for receptor

  • prevent action of Ach at NMJ.
  • competitive blockers, can be overcome by increasing Ach
  • bind to and block the Nm receptor, no Na can get in, cause relaxation
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9
Q

What is a nondepolarizing neuromuscular blocking drug reversed with

A

Achase inhibitor

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10
Q

What are the effects of nondepolarizing neuromuscular blocking drugs on the cardiac and smooth muscle

A

None because it only works on No receptors

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11
Q

CNS effects of nondepolarizing neuromuscular blocking drugs

A

None

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12
Q

Analgesia and sedation with nondepolarizing neuromuscular blocking drugs

A

They dont have these affects. Have to give these first before the nondepolarizing drug so the patient doesn’t feel pain

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13
Q

Clinical use for nondepolarixing neuromuscular blocking drugs

A

Used mainly in anesthesia protocols or in the ICU to afford muscle relaxation and or immobility

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14
Q

Atracurium

A
  • nondepolarizing neuromuscular blocking drugs

- forms laudanosine, which can cause seizures

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15
Q

Cisatracurium

A
  • Nondepolarizing neuromuscular blocking drug
  • forms less laudanosine than atracurium
  • one of the most commonly used muscle relaxants in clinical practice
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16
Q

What is the most commonly used muscle relaxant in clinical practice

A

Cisatracurium

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17
Q

What’s the difference between atracurium and cisatracurium

A

Cisatracurium does not produce as much laudanosine, which means less risk of seizures

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18
Q

Duration of action of nondepolarizing neuromuscular blocking drugs

A
  • long acting ones are more potent and require low concentrations. Tubocurarine, pancuronium
  • intermediate actions of vecuronium, rocuronium, atracurium, cisatracurium
  • most are pretty short acting
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19
Q

Reversal of non-depolarizing agents

A
  • neostigmine: Achase inhibitor, allows more Ache to be in the cleft to compete with drug
  • sugammadex: encapsulates and binds with molecules of rocuronium or vecuronium, thereby rapidly reversing their neuromuscular blocking effect
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20
Q

Depolarizing (non-competitive) neuromuscular blocking drugs

A

Succinylcholine

21
Q

What is succinylcholine

A

Depolarizing (non-competitive) neuromuscular blocking drug

-2 Ach stuck together

22
Q

MOA of succinylcholine

A

Classic depolarizing agent

  • stimulates all cholinergic receptors
  • binds directly to the postsynaptic Ach receptors of the NMJ causing continuous stimulation of these receptors.
  • leads to transient fasciculations followed by muscular paralysis
  • composed of 2 Ach molecules
  • STRONG ACH RECEPTOR AGONIST
  • sustained depolarization and prevents muscle contraction
  • acts like a nicotinic agonist and depolarizes the NMJ
23
Q

What is succinylcholine broken down by

A

Pseudocholinesterase

24
Q

What is a problem with succinylcholine?

A

Since it stays bound to the Nm receptor, the receptor stays open, allowing Na to go in and K to come out, too much K going out can cause hyperkalemia
-people need tested to make sure K levels are not increased

25
Q

Clinical use of succinylcholine (depolarizing neuromuscular blocking drugs)

A

Used extensively in the emergency setting, due to its rapidity of onset and offset, and the consistent intubating conditions it provides

26
Q

Side effects of succinylcholine (depolarizing neuromuscular blocking drug)

A

-hyperkalemia

27
Q

When is succinylcholine contraindicated

A 
Inherited myopathies 
Malignant hyperthermia family HS
Stroke over 72 hours 
Rhabdomyolysis 
Hyperkalemia 
Burns, after 72 hours 
Crush injuries, after 72 hours

The last two things cause a lot of K to be released into the body due to cell damage and lysis

28
Q

Dosing of succinylcholine

A

It is far better to overestimate the dose than underestimate
-larger doses result in the same level of paralysis and do not increase the risk to the patient; inadequate doses can leave the patient inadequately paralyzed and difficult to intubate

29
Q

Succinylcholine is absolutely contraindicated in people with a family history of __________

A

Malignant hyperthermia and in patients deemed to be at high risk of developing severe hyperkalemia
-Ca2+ channels staying open generates heat, muscle damage also increases K levels

30
Q

What can be used as a rescue medication is bradycardia occurs when taking succinylcholine

A

Atropine

31
Q

A myopathic metabolic disorder that is characterized by sympathetic hyperactivity, muscular rigidity, acidosis, and hyperthermia

A

Malignant hyperthermia

32
Q

Reversal of blockade (depolarizing neuromuscular blocking drug)

A

Phase I

Phase II

33
Q

Phase I of reversal of blockade (depolarizing neuromuscular blocking drug)

A

Depolarization, fasciculation, prolonged depolarization, flaccid paralysis

34
Q

Phase II of reversal of blockade (depolarizing neuromuscular blocking drug

A

Desensitization

35
Q

What phase of depolarizing neuromuscular blocking drugs does achase inhibitors increase

A

Phase I

  • succinylcholine is bound, so achase inhibitors are not going to work.
  • there could be Ach and succinylcholine bound to the same receptor. Ach can just keep binding, but if the succinylcholine is there, it wont matter
36
Q

What phase of depolarizing neuromuscular blocking drugs do achase inhibitors possibly reverse

A

Phase II

-receptor kinda numb, Ach may or may not bind. Will eventually wear off

37
Q

GABA a

A

Ion gated

38
Q

GABA B

A

G coupled proteins

39
Q

Examples of centrally acting skeletal muscle relaxants

A

Benzodiazepines

Baclofen

40
Q

What do benzodiazepines target

A

GABA a

41
Q

What does baclofen target

A

GABA b

42
Q

Spasmolytic drugs

A

Do not resemble Ach in structure or effect
Act in CNS
Block NT release, no AP release, will never reach muscle.

43
Q

Slide effects of spasmolytics

A

drowsiness, confusion, fatigue

44
Q

Dantrolene

A

RyR1 receptor blocked, no Ca2+ flowing. Good for malignant hyperthermia

45
Q

What drug is good to use with malignant hyperthermia

A

Dantrolene

46
Q

What drug is not good to use with malignant hyperthermia

A

Succinylcholine

47
Q

Treatment for malignant hyperthermia

A

Dantrolene

48
Q

Botox

A
  • inhibits release of Ach out of vesicles

- can reduce pain caused by severe spasm

49
Q

What are the drugs used for chronic spasm

A

Baclofen
Diazepam
Dantrolene
Botox

Pharm Block 10 (6 decks)

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