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MBBS II MSS > L14 - Neuromuscular blocking agents and Local anaesthetics > Flashcards

L14 - Neuromuscular blocking agents and Local anaesthetics Flashcards

1
Q

What is the dose response curve of an agonist added with a competitive antagonist?

A

Curve shifts to the right compared to agonist alone

Same maximal response because increase in agonist concentration overcomes the action of the comp. antagonist

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2
Q

Describe the dose response curve of an agonist added with a non-competitive antagonist?

A

Diminished maximal response compared to agonist alone

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3
Q

What are the 3 increasing degree of anaesthesia?

A

Hypnosis (unconsciousness)
Analgesia (pain relief)
Paralysis

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4
Q

Describe a depolarizing neuromuscular blocking agent structure?

A

Succinylcholine = Similar to ACh, bind to AchR

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5
Q

What are the 2 categories of NMBs?

A

Depolarizing and Non-depolarizing

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6
Q

Give an example of Depolarizing NMB

A

Succinylcholine

(diacetylchloine)

Causes transient depolarization/ contraction before paralysis

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7
Q

Describe the onset and offset of Succinylcholine?

A

Onset = Rapid, 60sec

Offset = Rapid (10-15 min)

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8
Q

Why is succinylcholine declining in popularity?

A

Numerous side effects

Action on muscarinic and nicotinic receptors cause ANS effects

Quaternary ammonium compounds, can cause severe allergy

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9
Q

List some Cardiovascular effects of succinylcholine?

A
  • Arrthythmias, sinus bradycardia, ventricular arrthymias
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10
Q

What ionic imbalance results from succinylcholine?

A

extrajunctional AchR stimulated causing increase influx of K+

> > exacerbates Hyperkalemia secondary to burns, trauma, neuromuscular disease, closed head injury, intra-abdominal infections

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11
Q

What adverse effects results from the transient depolarization caused by succinylcholine?

A

Increase intra-ocular pressure
Increase intragastric pressure
Myalgias

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12
Q

What is the most threatening side effet of succinylcholine?

A

Anaphylaxis > High incidence

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13
Q

List 3 newer non-steroidal NMBs with fewer systemic side effects than Succinylcholine and why?

A

Mivacurium
Atracurium
Cis-atracurium

Both are Non-depolarizing NMBs

Both bind to nicotinic AchR only, No Muscarinic side effects, Effects are only localized on NMJ

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14
Q

Name 2 new steroidal NMBs?

A

Rocuronium

Vecuronium

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15
Q

List some new Short and intermediate and Long acting NMBs?

A

Short = Mivacurium

Intermediate = Atracurium, Cis-atracurium, Rocuronium (steroidal)

Long = Pancuronium, Tubocurare

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16
Q

Why are long acting new NMBs rarely used?

A

No place because need muscle power to recover promptly when we wake up the patient

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17
Q

What is the duration of action of newer short and intermediate acting NMBs?

A
  • Short acting = 5-10 mins
  • Intermediate acting = 20-30 mins

short duration does not mean rapid onset

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18
Q

Why is mechanical ventilation needed during used of NMB?

A

Paralyze diaphragm and intercostal muscles, cannot breathe

> > Need intubation and mech. ventilation

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19
Q

Ach injection can be used to overcome the effects of competitive antagonist NMBs. True or False?

A

False

Increase [Ach] can overcome effect but cannot inject Ach directly due to short half-life and lots of ANS side effects

20
Q

What can overcome the effects of competitive NMB agents?

A

Inhibit acetylcholinesterase to lower the breakdown of Ach in the synaptic cleft

21
Q

What are some drugs that can overcome the effects of competitive NMB agents?

A

neostigmine, edrophonium, pyridostigmine

Also used to treat Myasthenia gravis

22
Q

What are the 3 ways to terminate the effects of non-depolarizing NMBs?

A

1) Wait for metabolism + elimination of NMB
2) Inject acetylcholinesterase inhibitors/ anticholinesterases (i.e. neostigmine) to increase [Ach] in synaptic cleft
3) Chelators (e.g. synthetic γ-cyclodextrin / sugammadex) to remove NMB at NMJs

23
Q

Describe the principal of neuromuscular monitoring?

A

Monitor twitch response/ muscle power over time after admin. NMB

Electrodes stimulate ulnar nerve:

if NMJ works, adductor pollicis should contract and give signal to transducer: count number of responses

If [NMB] is hight, effects may not terminate with anticholinesterases, no twitch response

24
Q

Run through the pain pathway.

A

1) Nociceptors detect change in pain, temperature
2) pain fibers in skin, deep tissues signal primary afferent neuron
3) dorsal root ganglion
4) second-order neurons in dorsal horn (sensory)
5) brainstem, thalamus to be perceived as pain

25
Q

Describe the MoA of local anesthetics?

A

Need to diffuse across neuronal cellular membrane to bind to voltage-gated Na+ channel intracellularly** (exam)

> > No Na+ influx
No AP generated
Reduce pain

26
Q

List some essential properties of local anesthetics?

A

Must bind to Na+ channels intracellularly

> > Must be non-polar, lipid soluble to pass neuronal membrane

27
Q

If the Body pH is 7.4, and the local anesthetic pKa is 7.4, what is the speciation of the drug?

A

Difference between pH and pKa is 0

50% of drug is protonated, 50% is in free base

28
Q

If the body pH is lower than the pKa of a drug, what form does the drug exist in?

A

Protonated form

Harder to pass through cell-membrane

29
Q

Explain why more inflammation/ more severe infection means local anaesthetics have less effect?

A

More inflammation = more acidic

pH of tissue is much lower than pKa of local anesthetic

most of drug in protonated form» cannot cross cell membrane for action

30
Q

What is the solution to increase the effect of local anesthetics in inflamed/ infected tissue?

A

Add sodium bicarbonate along with local anesthetics to increase tissue pH

More of drug in free base form, better for crossing cell membrane for action

31
Q

Local anesthetics can be given systemically by IV to achieve systemic analgesia. True or False?

A

False

Local anesthetics must never be given by IV

Highly toxic and fast spread

32
Q

What are some toxic systemic effects if local anesthetics are mistakenly injected into blood?

A

Increasing severity:

Muscle twitching > unconsciousness > convulsions > coma > respiratory arrest > CVS depression

33
Q

What technique to used to ensure local anesthetics do not reach blood?

A

Always aspirate to see if there if blood

Never inject too much to prevent diffusion into capillaries and vessels

34
Q

What are the classes of local anesthetics?

A

Ester (e.g. cocaine, Benzocaine, Procaine), more likely to cause allergy

Amide (e.g. Lignocaine, Bupivacaine, Ropivacaine), less likely to cause allergy

35
Q

What are the 3 most clinically used local anesthetics?

A

Lignocaine
Bupivacaine
Ropivacaine

36
Q

What are the routes of admin of local anesthetics?

A

LOCAL admin:

  • Topical (onto mucosa: eye, throat, esophagus)
  • Infiltration (needle pierce skin to reach nociceptors)
  • Nerve/plexus block
  • Epidural/spinal

(IV, but not used and very dangerous)

37
Q

Give two examples of topical local anesthetic formula?

A

EMLA - Eutectic Mixture of Local Anesthetics: Lignocaine + prilocaine

Lidocaine patch (e.g. for post shingles pain)

38
Q

What is the advantage of Eutectic mix of local anesthetics?

A

Lower melting point in mixture, half liquid form in room temp

Can mix into high concentration liquid form (not aqueous form so not highly soluble) at room temp to penetrate skin

Can contain higher conc. at lower dose

39
Q

What LA dosage is injected into where for an arm nerve block?

A

Axillary approach – put 15-20mL LA at brachial plexus to block the arm

40
Q

What are the dose limits of Lignocaine and Bupivacaine?

A

• Lignocaine
– 4 mg/kg
– 7 mg/kg with adrenaline (epinephrine)

• Bupivacaine (Marcain)
– 2.5 mg/kg

41
Q

Why is Adrenaline given with LA sometimes?

A

Adrenaline causes vasoconstriction of capillaries

Slow down LA absorption into blood and can give higher dose locally

Dose limit is higher but harder to calculate, depends on patient factor and injection site

42
Q

Adrenaline-mixed LA can be given to end arteries when operating on areas like fingers or penis. True or False?

A

False

Must not give Adrenaline - mixed LA to end-arteries

Severe vasoconstriction causes ischaemia&raquo_space; penile block or digital block

43
Q

Side effects of LA?

A

Toxicity from metabolites
Allergy
Motor block
Sympathetic block (especially peripheral nerves)

44
Q

What are the metabolites of common LA that can cause toxicity?

A

– Lignocaine (monoethylglycinexylidide)

– Prilocaine (o-toluidine)

45
Q

What are the considerations when choosing which LA to use?

A
  • Onset
  • Duration
  • Route of admin and availability
  • Safety
46
Q

What are the considerations when choosing what concentration of LA to use?

A

Motor block - extent
Duration
Volume required and dose limit

MBBS II MSS (31 decks)

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