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Block 3 Up To Quiz 1 > Neuromuscular Pharmacology Pt1 > Flashcards

Neuromuscular Pharmacology Pt1 Flashcards

1
Q

Steps neuromuscular transmission

A
  1. Nerve action potential depolarizes presynaptic terminal of neuromuscular junction
  2. Voltage-sensitive Ca2+ channels open
  3. Ca2+ enters presynaptic terminal
  4. Exocytosis of synaptic vesicles containing acetylcholine
  5. Acetylcholine diffuses across synaptic cleft; 1/3 acetylcholine molecules degraded by acetycholinesterase
  6. Remainng acetylcholine molecules reach postsynaptic membrane where interact with acetylcholine receptors embedded in post synaptic membrane
  7. Binding of acetylcholine to acetylcholine receptor -> opening nonspecific cation channel -> depolarization postsynaptic muscle membrane
  8. Remaining acetylcholine degraded by acetylcholinesterase
  9. Depolarization of muscle membrane -> action potential and release of Ca2+ from internal stores into cytoplasm
  10. Increased cytoplasmic calcium binds to troponin
  11. Actin and myosin filaments slide -> muscle contraction
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2
Q

synaptic cleft neuromuscular

A

500 angstrom synaptic cleft; there is basal laminal fold ion cleft with acetylcholine esterase on it 1/3 of acetylcholine will get destroyed when crossing

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3
Q

excitatory postsynaptic potential (EPSP)

A
  • depolarization of postsynaptic (muscle) membrane
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4
Q

Sites of drug action neuromuscular transmission

A
  1. CNS
  2. Motor neuron axon
  3. Acetylcholinesterase
  4. Nicotinic acetylcholine receptor
  5. Skeletal muscle
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5
Q

drugs/ substances acting on neuromuscular transmission of CNS and muscle relaxation

A
  • drugs can cause muscle relaxation by acting on internuncial spinal neurons to depress polysynaptic pathways
  • these drugs also work on higher brain centers as anti anxiety agents
  • unknown if muscle relaxation due to acton on spinal cord or anti-anxiety effects
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6
Q

drugs/ substances acting on CNS neuromuscular transmission used to treat

A
  • drugs in this category used to treat muscle spasm (spasmolytics)
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7
Q

drugs/ substances acting on CNS neuromuscular transmission

A
  • Diazepam
  • Methocarbamol
  • Glycerol Guaiacolate
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8
Q

Diazepam

A
  • addictive
  • muscle relaxant
  • relaxes muscle w/o blocking it
  • works on neuromuscular transmission of CNS
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9
Q

drugs/ substances acting on motor neuron axon transmission what do they do

A
  • interfere with conduction of action potentials 2 ways
    1. Blockade propagation of action potential
    2. Facilitation of propagation of action potential
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10
Q

Blockade propagation of action potential drugs

A
  1. Local anesthetics

2. Toxins (tetrodotoxin, saxitotoxin, scorpion toxin, brevitoxin)

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11
Q

Local anestetics (motor neuron axon)

A

have to use ALOT of this to get motor neuron blocked bc preference is for sensory

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12
Q

Toxins (motor neuron axon) effects

A
  • agents block motor neurons in some cases can -> death
  • skeletal muscle block
  • D+
  • Convusions
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13
Q

Tetrodetoxin

A
  • made in liver of puffer fish
  • blocks Na+ channel
  • kills b/c paralyzes diaphragm muscles
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14
Q

Saxitoxin and Brevitoxin

A
  • found single celled algae that lead to red tide
    Saxitotoxin blocks Na+
    Brevitoxin leaves Na+ channels on all the time blocking action potneital
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15
Q

Aminopyridines

A
  • facilitate propagation action potential

- block K+ channels -> stronger action potential

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16
Q

Aminopyridines clinical use

A

useful in MS pateients

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17
Q

drugs/ substances effecting neurotransimission motor neuron terminal

A
  • hemicholinum
  • botulinum toxin
  • latrotoxin
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18
Q

hemicholinum

A
  • blocks uptake of choline and synthesis of acetylcholine
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19
Q

botulinum toxin

A
  • inhibits release of acetylcholine
  • v potent toxin; protease that can enter presynaptic terminal and cleave proteins involved in release presynaptic terminal -> inhibition release acetylcholine
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20
Q

Latrotoxin

A
  • black widow spider venom
  • causes massive release acetylcholine followed by decreased synthesis and release acetylcholine
  • interacts with presynaptic terminal forming pore allowing Ca2+ in -> massive acetylcholine release which uses up all acetyl choline and turns off presynaptic terminal -> paralysis
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21
Q

Acetylcholinesterase inhibitors types

A

Reversible and irreversible

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22
Q

Reversible acetylcholine esterase inhibitors

A

pyridostigmine, physostigmine, neostigmine, edrophonium

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23
Q

edrophonium mechanism of action

A
  • reversible acetylcholinesterase inhibitor

- reversibly binds to acetycholinesterase (no covalent modification therefore readily reversed)

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24
Q

Pyridostigmine, Physostigmine, and neuostigmine mechanism of action

A
  • reversible acetylcholinesterase inhibitors

- enzyme covalently modified (carbamylated), this is reversible over several hours

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25
Q

Reversible acetylcholinesterase inhibitors clinical use

A
  • pyridostigmine- treatment myasthenia gravis
  • edrophonium- diagnosis of myasthenia gravis
  • all 4: reversal of some neuromuscular blockers
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26
Q

Irreversible acetylcholinesterase inhibitors

A
  • organophosphate compounds
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27
Q

irreversible acetylcholinesterase inhibitor mechanism of action

A
  • enzyme covalently modified (phosphorylation)
  • in some organophosphates covalent modification spontaneously reversibles in others it can be reversed by 2-PAM but after loss of alkyl group from organophosphate -> “aging” modification can’t be reversed and only new enzyme synthesis will restore function
28
Q

irreversible acetylcholinesterase inhibitor uses

A

nerve gas and insecticises

29
Q

acetylcholine receptor blockers

A

non depolarizing blockers

depolarizing blockers

30
Q

non depolarizing blockers

A
  • bind to acetylcholine receptor but does not produce response (competitive antagonist)
31
Q

depolarizing blockers

A
  • bind to acetylcholine receptor and produce response but rapidly desensitize the receptor -> temporarily blocking further activation of receptor
  • these are agents that don’t get broken down by acetylcholineesterase
32
Q

environmental toxicology and acetylcholine receptor blcokers

A
  • anatoxin-a (very fast death factor)
  • hemoanatoxin
  • both are potent agonists of nicotinic acetylcholine receptors and are produced by cyanobacteria
  • mainly neuronal acetylcholine receptor agonist
  • also interacts with muscle nicotinic acetylcholine receptor will eventually work as blocker and can kill by blocking respiratory system -> respiratory failure by blocking skeletal muscle and therefore diaphragm
33
Q

acetylcholine receptor blockers fx

A

-most useful agents for sx (both classes) bc ensures patent will be totally still especially useful with spinal sx ect.

34
Q

neuromuscular blockers and pain releif

A
  • MUST use analgesia with neuromuscular blockers bc they don’t provide pain relief so if doing sx using them must also use analgesic
35
Q

blocker of acetylcholinesterase in presence depolarizing blocker

A

will make it worse bc even more acetylcholine to desensitize receptor

36
Q

non depolarizing blockers exmaples

A
  • types acetylcholine receptor blockers
  • 2 major classes:
  • Benzylisoquinolines
  • Ammonio steroids
37
Q

Benzylisoquinolines

A
  • includes first neuromuscular blocker to be used (d-tubocurarine + blockers used extensively clinically (atracurium and mivacurium)
38
Q

D-tubocurarine side effects

A
  • 1st neuromuscular blocker used
  • Benzylisoquinolines
  • side effects: hypotension (bc vasodilation bc blocking autonomic ganglia -> reduced vasomotor tone and bc histamine release)
39
Q

why not use D-tubocuraine more

A
  • not very specific to acetylcholine receptor at skeltal muscle
  • unpleasant side effects like histamine release if used in Sx so came up with different molecules
40
Q

Atracurium

A
  • Benzylisoquionlines
  • pretty specific for muscle acetyl choline receptor
  • shorter acting and exhibits less ganglionic blockade and histamine release than D-tubocuraine
41
Q

mivacurium

A
  • Benzylisoquionlines
  • related to atracurium
  • developed as neuromuscular blocker in humans, duration of action prolonged in some species (dogs have less seroaminoeserase and have diff AA sequence for serocholinoesterase than humans)
42
Q

Ammino steroids

A
  • class of non depolarizing blockers
  • these drugs exhibit no histamine release but some vagal blockade occurs bc interaction with muscarininc acetylcholine receptors (possible tachycardia)
43
Q

Ammino steroids agents

A 
- pancuronium- prototypic drug
New ones (shorter acting more easily reversed)
- vecuronium
- rapacuronium
- rocuronium
44
Q

non depolarizing acetylcholine receptor blockers absorption

A
  • quaternary ammonium= poorly absorbed if given orally, must give IM or IV
  • do not cross blood brain barrier
45
Q

non depolarizing acetylcholine receptor blockers excretion

A
  • Most excreted largely unchanged in urine (complications in animals with renal issues)
  • Atracurium and mivacurium = can be degraded by plasma cholinesterase
46
Q

non depolarizing acetylcholine receptor blocker following IV injection

A
  1. onset 2-6 minutes
  2. duration depends on drug (atracurium= about 40min)
  3. Weakness for up to 24hrs
47
Q

non depolarizing acetylcholine receptor blocker pharmacological effects

A
  • skeletal muscle blockade by competitive antagonism of effects of acetylcholine
48
Q

non depolarizing acetylcholine receptor blocker pharmacological effects reversal

A
  • blockade reversed by administration of acetylcholinesterase inhibitors
49
Q

Clinical uses non depolarizing acetylcholine receptor blocker

A
  • skeletal muscle relaxation in sx at low levels of anesthesia
  • relief of spasm while setting fractures
50
Q

Clinical uses non depolarizing acetylcholine receptor blocker without ventilation and analgesia

A

is malpractice

51
Q

non depolarizing acetylcholine receptor blocker drug interactions

A
  • phenothiazines, local anesthetics, general anesthetics, and antibiotics can potentiate activity of neuromuscular blockers b/c noncompetitive blockade of acetylcholine receptor by the above drugs and a competitive block by neuromuscular blockers
52
Q

acetyl choline depolarizing blockers vs acetyl choline competitive antagonists (non depolarizing blocker) acetylcholinesterase inhibitors

A
  • depolarizing blockers not reversed by acetylcholinesterase inihibitors
  • competitive antagonists are reversed by acetylcholinesterase
53
Q

acetyl choline depolarizing blockers vs acetyl choline competitive antagonists serum cholinesterase

A
  • depolarizing blockers broken down by serum cholinesterase

- competitive antagonists some broken down by serum cholinesterase some by liver metabolism

54
Q

acetyl choline depolarizing blockers vs acetyl cholinecompetitive antagonists (non depolarizing blockers) pain relief

A

neither type gives pain relief

55
Q

acetyl choline Depolarizing blockers examples:

A
  • Decamethonium

- Succinylcholine

56
Q

Succinylcholine

A
  • v rapidly acting
  • acetyl choline depolarizing blocker
  • w/ in 5 min animal is back to normal
57
Q

route of administration acetyl choline depolarizing blockers

A

IM or IV bc quaternary ammoniums

58
Q

succinylcholine degredation

A
  • degreased by pseudocholinesterase in serum
  • pseudocholinesterase made in liver so hepatic damage can -> decreased enzyme level in serum -> complications with use succinylcholine
59
Q

acetylcholine depolarizing blockers following IV injection

A
  • onset between 1-2 min

- duration between 5-10 min

60
Q

do acetylcholine depolarizing blockers cross blood brain barrier

61
Q

pharmacological effects acetylcholine depolarizing blocekrs

A
  • depolarization and muscle twitching followed by repolarization and relaxation
62
Q

Are acetylcholine depolarizing blockers reversed by acetylcholinesterase inhibitors?

63
Q

use of acetylcholine depolarizing blockers without ventilation and anlagesia is

A

malpractice

64
Q

drug interactions of acetylcholine depolarizing blockers

A
  • phenothiazines, local anesthetics, general anesthetics, and antibiotics can potentiate activity of neuromuscular blockers b/c noncompetitive blockade of acetylcholine receptor by the above drugs and a competitive block by neuromuscular blockers
65
Q

Dantorlene fx

A
  • reduces contraction of skeletal muscle by decreasing amount of Ca2+ released into cytoplasm from sarcoplasmic reticule by interactions with ryanodine receptors
  • used in malignant hyperthermia
66
Q

malignant hyperthermia

A
  • mutation in ryanodine receptor found in ppl, horses, and pigs
  • this mutation has effect during sx bc some combinations anesthetics can activate it
  • Ca2+ release -> muscle contraction = increase body temp.
  • triggered by exposure to volatile anesthetic and depolarizing muscular blockers

Block 3 Up To Quiz 1 (24 decks)

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