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Pharmacology > Neuromuscular Blocking Agents > Flashcards

Neuromuscular Blocking Agents Flashcards

1
Q

Under which category does the neuromuscular blockers fall under?

A

Somatic Nervous System under the Peripheral Nervous System

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2
Q

Somatic Fiber ?

A

-Has no ganglia, indirectly innervates muscle
-Has nicotonic receptor
-Has Ach as a neurotransmitter

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3
Q

Neuromuscular Junction?

A

Synapse between presynaptic motor neuron and postsynapatic muscle membrane

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4
Q

General anethesia?

A

Includes analgesia, amnesia, loss of consciousness, inhibition of sensory and automatic reflexes and skeletal muscle relaxtion.

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5
Q

Where are neuromuscular blockers used?

A

Used in anaesthesia and artificial ventilation

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6
Q

Somatic Nervous System innervation?

A

Skin, sensory, organs and skeletal muscle-transmits information from CNS to the rest of the body

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7
Q

Two major neuron types?

A

*Sensory neurons (afferent
neurons): body -CNS

*Motor neurons (efferent
neurons): brain and
spinal cord muscle
fibers throughout the body

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8
Q

Normal neuromuscular transmission?

A
  1. Action potential (AP) conducted along the motor neuron
  2. Depolarization
  3. Ca2+ influx
  4. ACh release from storage vesicles into a synaptic cleft
  5. ACh binds on nicotinic receptors on the motor end plate
  6. Na+ channels on motor end plate open
  7. Na+ influx and depolarization (end plate potential (EPP))
  8. AP produced
  9. Muscle contraction occurs
  10. ACh hydrolyzed by AChE from motor end plate and process starts again
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9
Q

Which step of neuromuscular transmission do neuromuscular blockers ?

A

Step 5
5. ACh binds on nicotinic receptors on the motor end plate

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10
Q

Skeletal Muscle Relaxtants types?

A
  1. Peripherally-acting agents
    -Depolarising NMBD’S
    -Nondepolarising NMBDs
  2. Centrally-acting agents
    -act on the CNS
  3. Directly-acting agents
    -act on the muscle
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11
Q

Structure of NMBD’S?

A

Structurally polar-do not cross blood brain barrier

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12
Q

NMD administration?

A

All administered parenterally

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13
Q

NMD action?

A

Relax voluntary skeletal muscles, diaphragm and laryngeal muscles

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14
Q

General MOA of NMB?

A

structurally similar to ACh
act at the post-junction nicotinic receptors

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15
Q

NMB agonists or antagonists?

A

*agonists = depolarizing NMBDs
mimic ACh
persisting state of depolarization

*antagonists = non-depolarizing NMBDs
competitive inhibitors of ACh
prevent depolarization

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16
Q

Types of Peripherally acting NMB?

A
  1. Depolarizing NMBDs
  2. Non-depolarizing NMBDs
    Can be identified by “cur”
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17
Q

NMB Depolarising drugs?

A

*Succinylcholine (suxamethonium)

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18
Q

NMB non-depolarising drugs types?

A

a) Isoquinoline derivatives

b) Steroid derivatives

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19
Q

NMB Isoquinoline derivative drugs?

A

MAD

*Mivacurium
*Atracurium
*d-tubocurarine

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20
Q

NMB Steroid derivatives drugs?

A

Very Running People

Vecuronium
Rocuronium
Pancuronium

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21
Q

Succinylcholine MOA?

A

only depolarizing NMBD in clinical use
causes ↑ EPP rapid muscle contraction,
clinically observed as muscle fasciculation
this is followed by flaccid paralysis within 30-
60 sec and lasts for 3-5 min
with repeated dose, receptors reach
tolerance rapid and complete muscle
relaxation

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22
Q

Succinylcholine (SCh) phases?

A

Phase I

ACh agonist
triggers EPP via the ACh cascade
Voltage-gated Na+ channels open depolarization
increase Ca2+ release from sarcoplasmic reticulum
rapid muscle contraction (muscle fasciculations/twitches)
followed by muscle relaxation (flaccid paralysis)

Phase II

continued SCh exposure (repeated doses)
Na+ channels non-responsive to the stimulus repolarization
rapid and complete muscle relaxation

23
Q

How long does the phase one of Succinylcholine ?

A

lasts for 3-5 min

24
Q

Succinylcholine hyrolysed by?

A

not hydrolyzed by AChE)

Hydrolysed by plasma pseudocholinesterase

25
Q

Succinylcholine duration?

A

resolves spontaneously within 10 minutes

26
Q

Succinylcholine P/K?

M & E

A

Metabolism: liver (CYP450),
plasma (pseudocholinesterases)

*Excretion: renal, only 10% excreted
unchanged

27
Q

Succinylcholine DI?

A

*Cholinesterase inhibitors
*Digoxin

28
Q

Succinylcholine A/E?

A

*Malignant
hyperthermia
*myalgia
*Bradycardia
*Hypotension
*Increased IOP
*Increased
intragastric
pressure
*Increased
salivation

29
Q

Succinylcholine stimulate which othe receptors and what is their effects?

A

Stimulation of autonomic muscarinic receptors
bradycardia
Hypotension
Increased salivation

30
Q

What is the solution to succinylcholine to avoid muscuranic effects?

A

Atropine prior to repeated doses or continuous infusion of SCh to counteract these effects

competitively antagonize muscarinic activity
prevent bradycardia and hypotension

31
Q

Nondepolarizing NMBDs MOA?

A

competitively antagonize ACh
prevent EPP
prevent Ca2+ release from
sarcoplasmic reticulum
muscle relaxation

32
Q

Nondepolarizing Irr/reversible?

A

Reversible

33
Q

Nondepolarizing Administeration?

A

All administered IV
They do not cross the placenta and BBB

34
Q

Tubocuraine?

A

Tubocurarine is a toxic alkaloid from curare historically known for its use as an arrow poison. a prototype from which many synthetic nondepolarizing NMBDs were synthesized
rarely used in clinical medicine

35
Q

What do non-depolarising drugs release and what is the exception?

A

Most nondepolarizing NMBDs (except rocuronium) release histamine and exhibit histamine-related side effects

36
Q

What are histamine S/E?

A

Hypotension
Bronchospasm

37
Q

Non-depolarising duration?

A

Short acting:
Mivacurium(“Move Mivacurium)

Intermediate-acting: Really Very Aware

Rocuronium
Vecuronium
Atracurium

Long-acting: Paced DRugs

Pancuronium
d-tubocurarine

38
Q

Which non-depolarising NMB is the most rapid onset of action?

A

Rocuronium

39
Q

Which non-depolarising NMB is the most slowest but has the longest duration?

A

Pancuronium

40
Q

Which non-depolarising NMB is the most potent in releasing histamine?

A

Mivacuronium

41
Q

Mivacuronium metabolism?

A

Plasma cholinesterase

42
Q

Mivacuronium S/E?

A

Bronchospasm, Hypotension, prolonged neuromuscular blocker

43
Q

Atracurium P/K?

M, E & DI

A

M: spontaneous (Hoffman)
degradation at body temp. and pH
 Drug of choice in liver failure
E: renal mainly
DI: incompatible with thiopental
sodium (used in GA induction phase)

44
Q

Vecuronium P/K?

M& E

A

M: liver
E: bile mainly

45
Q

Vecuronium S/E?

A

Bronchospasm,
Anaphylaxis

46
Q

Rocuronium P/K?

M, E & DI

A

M: liver
E: bile
DI: Phenytoin, carbamazepine may
cause recovery

47
Q

Rocuronium S/E?

A

Anaphylaxis

48
Q

Tubocurarine P/K?

M & E

A

M: Hoffman degradation and hepatic
E: renal mainly

49
Q

Tubocurarine S/E?

A

Hypotension, bronchospasm

50
Q

Pancuronium P/K?

M&E

A

M: liver (small amount)
E: renally mainly unchanged

51
Q

Pancuronium S/E?

A

Tachycardia, elevation in BP

52
Q

NMJ Blockade reversal?

A

Acetycholinesterase iNhibitors

Eg:Neostigmine

53
Q

NMJ Blockade reversal action?

A
  1. block ACh hydrolysis
  2. accumulation of ACh
  3. NMJ blocker displacement
54
Q

What antimuscuranic agent may need to be used to block musarinic effects?

A

Antimuscarinic agent, atropine, may need to be concurrently used
to block the muscarinic effects of ACh i.e. bradycardia

Pharmacology (44 decks)

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