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Year 2 - Pharmacology and Therapeutics > Neuromuscular Blocking Drugs > Flashcards

Neuromuscular Blocking Drugs Flashcards

1
Q

What do NM blocking drugs deal with?

A

SOMATIC NS

NOT the ANS

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2
Q

Describe NM transmission

A
  1. Production of ACh using CAT
  2. AP propagation
  3. Ca2+ influx
  4. ACh exocytosis
  5. ACh binds to receptors
  6. Na+ influx
  7. ACh esterase breaks down ACh
  8. Recycling by uptake
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3
Q

3 most important NM-blocking drugs?

A

COMPETITIVE
• tubocurarine
• atracurium

DEPOLARISING
• suxamethonium

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4
Q

Why can we develop drugs that have some degree of selectivity for somatic nAChr?

A

The NMJ nAChR is DIFFERENT IN STRUCTURE to the ganglionic (ANS) nAChR
• so can develop selective drugs just for somatic NS

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5
Q

Describe the structure of the nAChR

A 
5 subunits in the receptor
 • A1
 • A2
 • B
 • DELTA
 • GAMMA

ACh ONLY binds to the ALPHA-receptors

Large extracellular domain
Slightly smaller intracellular domain

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6
Q

Where is the density of the nAChR highest?

A

At the MOTOR-END PLATE

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7
Q

5 sites of drug action?

A
  1. Central Processes
  2. Conduction of nerve AP in motor neurone
  3. ACh release
  4. Depolarisation of motor end-plate AP initiation
  5. Propagation of AP along muscle fibre & muscle contraction
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8
Q

Drug that works for relaxant effect on the 1ST drug site?

A
  1. Central Processes

= SPASMOLYTICS
• e.g. Diazepam, Baclofen

They relieve spasm of the muscles
• reduce generation of AP around cell bodies (so before it enters the pre-synaptic neurone)
• work on SC so centrally acting

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9
Q

Drug that works for relaxant effect on the 2ND drug site?

A
  1. Conduction of nerve AP in motor neurone

= LOCAL ANAESTHETICS
• Inhibit influx of Na+
• so reduces the propagation of the AP along the nerve
• MORE effective around sensory fibres rather than motor fibres

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10
Q

Drug that works for relaxant effect on the 3RD drug site?

A
  1. ACh release

= Hemicholinium
= Ca2+-entry blockers
= Neurotoxins
• ALL inhibit re-uptake of Ca2+

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11
Q

Drug that works for relaxant effect on the 4TH drug site?

A
  1. Depolarisation of motor end-plate AP initation

= Tubocurarine
= Suxamethonium
• these react on the post-synpatic membrane

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12
Q

Drug that works for relaxant effect of the 5TH drug site?

A
  1. Propagation of AP along muscle fibre & muscle contraction

= Spasmolytics
• e.g. Dantrolene

Acts INSIDE the skeletal muscle (rather than the SC like the 1ST one does!)
• reduces Ca2+ release from sacroplasmic reticulum = relaxes muscles = reduces spascity

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13
Q

2 main groups of Post-synaptic NM-blocking drugs?

A
  1. Non-depolarising (competitive antagonists)
    • e.g. tubocurarine & atracurium
  2. Depolarising (agonist)
    • e.g. suxamethonium (succinylcholine)
    - good at stimulating due to its VERY SIMILAR STRUCTURE to ACh
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14
Q

What is special about the 2 main groups of post-synaptic NM-blocking drugs?

A

Do NOT affect consciousness OR pain sensation
• so NO analgesic properties - simply relax the muscles
• true for NM relaxants in general!

ALWAYS need to assist respiration
• until drug is inactive OR antagonised

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15
Q

Difference between antagonists & agonists in terms of structure?

A

Antagonists have a RIGID structure
• less free rotation
• bind onto receptor & block it

Agonists have MORE free rotation
• so can bind & allow for efficacy

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16
Q

Why is Suxamethonium an agonist?

A

Has 2 ACh groups on either side

17
Q

MOA of Suxamethonium?

A

Causes an EXTENDED end-plate depolarising block
• takes a long time to break-down in synaptic cleft
• overstimulates the nAChR so shuts it down (compared to enzyme inhibitor which would not e.g. organophosphate)

Also causes fasciculations (brief twitches of muscle fibres)
• which turns into FLACCID PARALYSIS (loss of tone)

18
Q

Pharmokinetics of Suxamethonium?

A

ROA = IV
• as it is highly-charged

Duration of paralysis is short
• ~5 mins

Metabolised by pseudo-cholinesterase
• in the liver & plasma
• remember, AChcholinesterase is SPECIFIC to ACh so cannot be used for this!

19
Q

Uses of Suxamethonium?

A

Endotracheal intubation
• relaxes vocal chords

Muscle relaxant for ECT
• electro convulsive therapy - for severe clinical depression treatment
• across bi-temporal lobe

20
Q

Unwanted effects of Suxamethonium?

A

Post-operative muscle pains

Bradycardia
• direct muscarinic action of the heart (as similar in shape to ACh)
BUT
• ATROPINE normally given as well so blocks it

Hyperkalaemia
• soft tissue injury or burns –> ventricular arrhythmias/MI
• if reduce cholinergic innervation, leads to denervation supersensitivity (as more nACHR = bigger Na+ influx = bigger K+ efflux)

Increase in IOP
• so avoid for eye injuries/glacucoma as causes constriction of extra-ocular muscles

21
Q

If have glaucoma, what drug should be used?

A

NON-DEPOLARSING BLOCKER

as the DP agonist causes an increase in IOP

22
Q

What is true about ALL Non-depolarising blockers?

A

Have similar MOA & side-effects

• BUT have DIFFERENT DOA

23
Q

Where is Tubocurarine found?

A

Naturally occurring 4o ammonium compound found in S.ameria plants

24
Q

MOA of Tubocurarine?

A

A COMPETITIVE nAChR antagonist

A block of 70-80% necessary
• to cause effect of skeletal muscle relaxation
• so EP potential is insufficient to fire an AP

25
Q

Effects of Tubocurarine?

A

Tubocurarine –> flaccid paralysis

The flaccid paralysis then affects the muscles in a particular order:
• extrinsic eye muscle (double vision)
• small muscles of face,limbs, pharynx
• respiratory muscles

Recovery of this effect then works backwards and rewinds the effects
i.e. eye muscle blocked first BUT recovers last

26
Q

Uses of Tubocurarine?

A

Relaxation of skeletal muscles during surgical operations
• so less anaesthetics needed

Permits artificial ventilation
• as it relaxes the respiratory muscles (so does NOT work against the ventilator)

27
Q

How can the effects of Non-depolarsing NM blockers be reversed?

A

Using ANTICHOLINESTERASES
• e.g. Neostigmine (+ atropine)

As normally inhibit ACh, so increase endogenous ACh to overcome the block as COMPETITIVE BLOCK
• also shot with atropine as want to BLOCK muscrainic action

28
Q

Neostigmine?

A

Same as phyigostimine

BUT

has a LONGER DOA

29
Q

Can you reverse depolarising NM blockers?

A

NO - as NOT competitive antagonists

30
Q

Pharmokinetics of Tubocurarine?

A

ROA = IV
• as highly charged

Does NOT cross BBB or placenta
• so can be used in pregnant women

DOA is long
• ~1-2hr

NOT metabolised
• but it IS excreted (70% urine, 30% bile)
• need to be careful is have renal or hepatic impairment as less excreted = more stays in system = so use lower one

31
Q

Atracurium?

A

Exactly same as Tubocurarine

BUT

Chemically unstable at certain pH
• so breaks down and inactivates itself
• use if have renal/hepatic impairment

32
Q

Unwanted effects of Tubocurarine?

A

Causes a
• GANGLION block (if give higher dose see this)
AND
• HISTAMINE release (from mast cells)

SO
o Hypotension
• ganglion blockade LOWERS TPR
• histamine release = vasoDILATION

o Tachycardia
• reflex tachycardia (due to hypotension)
• also blocks the vagal ganglia

o Bronchospasm & excessive secretions (bronchial & salivary)
• histamine release = bronchoconstriction

o Apnoea
• thus ALWAYS assist respiration

33
Q

The clinical use of neuromuscular blocking drugs will most likely involve interference with which of following physiological processes?

A: Kidney function
B: Consciousness
C: Body temperature regulation
D: Pain sensation
E: Respiration
A

E

34
Q

Which of the following effects would be observed with a non-depolarising neuromuscular block?

A: Initial muscle fasciculations
B: Irreversible nAChR blockade
C: The block would be enhanced by anti-cholinesterase drugs
D: A flaccid paralysis
E: Increased arterial pressure
A

D

Year 2 - Pharmacology and Therapeutics (9 decks)

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