Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

excitatory postsynaptic potential (EPSP)

A
  • depolarization of postsynaptic (muscle) membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sites of drug action neuromuscular transmission

A
  1. CNS
  2. Motor neuron axon
  3. Acetylcholinesterase
  4. Nicotinic acetylcholine receptor
  5. Skeletal muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

drugs/ substances acting on CNS neuromuscular transmission used to treat

A
  • drugs in this category used to treat muscle spasm (spasmolytics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

drugs/ substances acting on CNS neuromuscular transmission

A
  • Diazepam
  • Methocarbamol
  • Glycerol Guaiacolate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diazepam

A
  • addictive
  • muscle relaxant
  • relaxes muscle w/o blocking it
  • works on neuromuscular transmission of CNS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Blockade propagation of action potential drugs

A
  1. Local anesthetics

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Local anestetics (motor neuron axon)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Toxins (motor neuron axon) effects

A
  • agents block motor neurons in some cases can -> death
  • skeletal muscle block
  • D+
  • Convusions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Tetrodetoxin

A
  • made in liver of puffer fish
  • blocks Na+ channel
  • kills b/c paralyzes diaphragm muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Aminopyridines

A
  • facilitate propagation action potential

- block K+ channels -> stronger action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Aminopyridines clinical use

A

useful in MS pateients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

drugs/ substances effecting neurotransimission motor neuron terminal

A
  • hemicholinum
  • botulinum toxin
  • latrotoxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

hemicholinum

A
  • blocks uptake of choline and synthesis of acetylcholine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acetylcholinesterase inhibitors types

A

Reversible and irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Reversible acetylcholine esterase inhibitors

A

pyridostigmine, physostigmine, neostigmine, edrophonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

edrophonium mechanism of action

A
  • reversible acetylcholinesterase inhibitor

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pyridostigmine, Physostigmine, and neuostigmine mechanism of action

A
  • reversible acetylcholinesterase inhibitors

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Reversible acetylcholinesterase inhibitors clinical use
- pyridostigmine- treatment myasthenia gravis - edrophonium- diagnosis of myasthenia gravis - all 4: reversal of some neuromuscular blockers
26
Irreversible acetylcholinesterase inhibitors
- organophosphate compounds
27
irreversible acetylcholinesterase inhibitor mechanism of action
- 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
irreversible acetylcholinesterase inhibitor uses
nerve gas and insecticises
29
acetylcholine receptor blockers
non depolarizing blockers | depolarizing blockers
30
non depolarizing blockers
- bind to acetylcholine receptor but does not produce response (competitive antagonist)
31
depolarizing blockers
- 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
environmental toxicology and acetylcholine receptor blcokers
- 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
acetylcholine receptor blockers fx
-most useful agents for sx (both classes) bc ensures patent will be totally still especially useful with spinal sx ect.
34
neuromuscular blockers and pain releif
- MUST use analgesia with neuromuscular blockers bc they don't provide pain relief so if doing sx using them must also use analgesic
35
blocker of acetylcholinesterase in presence depolarizing blocker
will make it worse bc even more acetylcholine to desensitize receptor
36
non depolarizing blockers exmaples
- types acetylcholine receptor blockers - 2 major classes: - Benzylisoquinolines - Ammonio steroids
37
Benzylisoquinolines
- includes first neuromuscular blocker to be used (d-tubocurarine + blockers used extensively clinically (atracurium and mivacurium)
38
D-tubocurarine side effects
- 1st neuromuscular blocker used - Benzylisoquinolines - side effects: hypotension (bc vasodilation bc blocking autonomic ganglia -> reduced vasomotor tone and bc histamine release)
39
why not use D-tubocuraine more
- 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
Atracurium
- Benzylisoquionlines - pretty specific for muscle acetyl choline receptor - shorter acting and exhibits less ganglionic blockade and histamine release than D-tubocuraine
41
mivacurium
- 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
Ammino steroids
- 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
Ammino steroids agents
``` - pancuronium- prototypic drug New ones (shorter acting more easily reversed) - vecuronium - rapacuronium - rocuronium ```
44
non depolarizing acetylcholine receptor blockers absorption
- quaternary ammonium= poorly absorbed if given orally, must give IM or IV - do not cross blood brain barrier
45
non depolarizing acetylcholine receptor blockers excretion
- Most excreted largely unchanged in urine (complications in animals with renal issues) - Atracurium and mivacurium = can be degraded by plasma cholinesterase
46
non depolarizing acetylcholine receptor blocker following IV injection
1. onset 2-6 minutes 2. duration depends on drug (atracurium= about 40min) 3. Weakness for up to 24hrs
47
non depolarizing acetylcholine receptor blocker pharmacological effects
- skeletal muscle blockade by competitive antagonism of effects of acetylcholine
48
non depolarizing acetylcholine receptor blocker pharmacological effects reversal
- blockade reversed by administration of acetylcholinesterase inhibitors
49
Clinical uses non depolarizing acetylcholine receptor blocker
- skeletal muscle relaxation in sx at low levels of anesthesia - relief of spasm while setting fractures
50
Clinical uses non depolarizing acetylcholine receptor blocker without ventilation and analgesia
is malpractice
51
non depolarizing acetylcholine receptor blocker drug interactions
- 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
acetyl choline depolarizing blockers vs acetyl choline competitive antagonists (non depolarizing blocker) acetylcholinesterase inhibitors
- depolarizing blockers not reversed by acetylcholinesterase inihibitors - competitive antagonists are reversed by acetylcholinesterase
53
acetyl choline depolarizing blockers vs acetyl choline competitive antagonists serum cholinesterase
- depolarizing blockers broken down by serum cholinesterase | - competitive antagonists some broken down by serum cholinesterase some by liver metabolism
54
acetyl choline depolarizing blockers vs acetyl cholinecompetitive antagonists (non depolarizing blockers) pain relief
neither type gives pain relief
55
acetyl choline Depolarizing blockers examples:
- Decamethonium | - Succinylcholine
56
Succinylcholine
- v rapidly acting - acetyl choline depolarizing blocker - w/ in 5 min animal is back to normal
57
route of administration acetyl choline depolarizing blockers
IM or IV bc quaternary ammoniums
58
succinylcholine degredation
- degreased by pseudocholinesterase in serum - pseudocholinesterase made in liver so hepatic damage can -> decreased enzyme level in serum -> complications with use succinylcholine
59
acetylcholine depolarizing blockers following IV injection
- onset between 1-2 min | - duration between 5-10 min
60
do acetylcholine depolarizing blockers cross blood brain barrier
no
61
pharmacological effects acetylcholine depolarizing blocekrs
- depolarization and muscle twitching followed by repolarization and relaxation
62
Are acetylcholine depolarizing blockers reversed by acetylcholinesterase inhibitors?
NO
63
use of acetylcholine depolarizing blockers without ventilation and anlagesia is
malpractice
64
drug interactions of acetylcholine depolarizing blockers
- 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
Dantorlene fx
- 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
malignant hyperthermia
- 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions