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Pharmacology > neuromuscular junction > Flashcards

neuromuscular junction Flashcards

1
Q

pyramidal and extrapyramidal are voluntary or involuntary?

A

pyramidal - voluntary

extrapyramidal - involuntary

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2
Q

what does central pathology look like

A
  • increase muscle tone
  • spastic paralysis
  • hyper-reflexia
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3
Q

what does peripheral pathology look like

A
  • decrease muscle tone
  • flaccid paralysis
  • hypo-reflexia
  • muscle atrophy
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4
Q

NMJ is under voluntary or unvoluntary? pyramidal or extrapyramindal?

A

voluntary and pyramidal

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5
Q

what part of the brain is under involuntary extrapyramidal system

A

basal ganglia

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6
Q

pathology of basal ganglia

A

rigidity, akinesia/diskinesia

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7
Q

which receptor is involved in NMJ

A

nicotinic muscular (Nm) receptor

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8
Q

what happens with miniature endplate potentials (MEPPs)

A

triggered by release of small number of Ach vesicles (leakage)

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9
Q

how many vesicles involved in action potential

A

200 Ach vesicles

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10
Q

what do muscle relaxants work on (central or peripheral)

A

peripheral

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11
Q

what does muscle relaxants do

A
  • reduce muscle spasm

- cause muscle paralysis

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12
Q

example of peripheral drug muscle relaxant

A
  • d-tubocurarine (curare)

- succinylcholine

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13
Q

3 uses of muscle relaxants

A
  1. surgical procedures
  2. assist ventilation
  3. use with GA
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14
Q

spasmolytic drugs act on peripheral or central?

A

central

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15
Q

what do spasmolytic drugs do

A

decrease muscle spasms

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16
Q

example of central drug muscle relaxant

A
  • benzodiazepine

- baclofen

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17
Q

what is central (spasmolytic) drugs used to treat

A
  • back/neck pain

- fibromyalgia

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18
Q

NMJ peripheral are divided into which two types

A
  • non-depolarizing

- depolarizing

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19
Q

non-depolarizing NMJ blockers for Nn

A

hexamethonium
trimethaphan
mecamylamine

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20
Q

non-depolarizing NMJ blockers for Nm

A

curare (d-tubocurarine)

decamethonium

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21
Q

non-depolarizing NMJ Nm blockers

A
  • curare
  • atracurium
  • rocuronium
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22
Q

curare prevents the action potential from

A

shhooting up and depolarizing

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23
Q

curare versus atracurium overtime (onset and duration)

A

curare has a slower onset and longer duration

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24
Q

which drugs can protect against non-dep blockers

A

Muscarinic antagonist:

  • atropine
  • glycopyrrolate
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25
Q

how do muscarinic antag protect against NMJ blocker

A

protect against:

  • excessive secretions
  • bronchospasms
  • bradycardia
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26
Q

does glycopyrrolate (a 4ry amine) cross BBB?

A

no!

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27
Q

Tx indications for atropine and glycopyrrolate

A
  • inhibit salivation, respiratory secretion, bradycardia
  • rapid sequence intubation
  • musc/organophosphate poisoning
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28
Q

reversal of non-dep blockers

A
  • AchE inhibitors

- sugammadex

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29
Q

why is neostigmine advantagous

A

doesnt cross BBB

30
Q

duration of edrophonium compared to neostigmine

A

-edrophonium is much shorter

31
Q

sugammadex reverses which type of NMJ blocker

A

STEROIDAL

32
Q

how does sugammedex physically block drugs from receptors

A

forms a ring around them

33
Q

example of depolarizing NMJ blocker

A

succinylcholine

34
Q

what does succinylcholine do prior to causing blockade

A

causes muscle fasciculation (ie. twitching)

35
Q

how does succinylcholine “fool the system”

A

acts as Ach but doesn’t cause full depolarization

36
Q

what breaks down succinylcholine

A

plasma cholinesterase (NOT ACHase!!)

37
Q

why is succinylcholine good for sugeries

A
  • fast onset

- short duration

38
Q

adverse effects of succinylcholine

A
  • bradycardia
  • increase IOP
  • hyperkalemia
  • MALIGNANT HYPERTHERMIA**
39
Q

what is the tx for malignant hyperthermia

A

DANTROLENE**

40
Q

how does dantrolene work

A
  • block ryanodine receptor (RyR) in calcium channel in SR
  • decrease calcium levels in cytoplasm
  • decrease muscle contraction
41
Q

what is dantrolene used to treat

A
  • malignant hyperthermia
  • neuroleptic malignant syndrome
  • ecstasy-induced hyperthermia
42
Q

NMJ blockers use in dentistry

A
  • laryngospasm
  • mandibular fractures
  • trismus
  • endotracheal intubation in GA
43
Q

what is the first choice of drug for laryngospasm

A

succinylcholine

44
Q

spasmolytic drugs can be divided into

A
  • gaba a ag

- non-gaba a ag

45
Q

what type of receptor is Gaba a

A
  • ionotropic

- ROC

46
Q

what does benzodiazepine do to channel opening

A

increase frequency of Cl- channel opening

47
Q

what blocks benzodiazepine effects (ie. antagonist to the site)

A

flumazenil **

48
Q

duration of benzodiazepines (name, classification, time, administration)

A
  • diazepam (long acting, 100 hours), PO
  • lorazepam (intermediate acting, 10-20 hours), PO
  • midazolam (short acting, 1-4 hours), IV or IM
  • triazolam (short acting, 1.5- 5.5 hours), PO
49
Q

diazepam tx

A
  • muscle spasticity
  • anxiety
  • pre-op
  • seizures
  • alcohol withdrawal
50
Q

lorazepam tx

A
  • anxiety
  • pre-op
  • seizures
51
Q

midazolam tx

A

pre-op ONLY!

52
Q

triazolam tx

A

dental pre-procedure oral sedation

53
Q

short term use of triazolam can cause

A

insomnia

54
Q

what does barbiturates do

A

increase length of Cl- channel opening

55
Q

3 examples of barbiturates and their tx

A
  • thiopental (anaesthesia, lethal injection)
  • pentobarbital (sedative)
  • phenobarbital (sedative, anesthesia, anticonvulsant)
56
Q

GABA B receptor classification

A
  • metabotropic

- G i PCR with Ca and K channels

57
Q

selective Ag for GABA B receptor

A

baclofen

58
Q

selective Antag for GABA B receptor

A

phaclofen

59
Q

list of CNS-acting spasmolytic drugs

A
  • benzodiazepines
  • barbiturates
  • baclofen
  • methocharbamol
  • cyclobenzaprine
  • gabapentin
  • pregabalin
60
Q

methocharbamol effect

A
  • central muscle relaxant

- does NOT act on muscle cells or NMJ

61
Q

cyclobenzaprine effect

A
  • central muscle relaxant

- does NOT act on muscle cells or NMJ

62
Q

adverse effects of cyclobenzaprine

A
  • increase HR
  • sedation
  • increase effect of NE
63
Q

cyclobenzaprine tx

A

-short-term tx of muscle spasm (from acute musculoskeletal conditions)

64
Q

what do gabapentin and pregabalin bind to

A

-N-type voltage-gated calcium channels

65
Q

what do gabapentin and pregabalin do

A

-inhibit presynaptic release of glutamate

66
Q

what do gabapentin and pregabalin used to tx

A

antiepileptic

67
Q

signs and symptoms of myasthenia gravis

A
  • painless fluctuating muscle weakness
  • muscle fatigue
  • respiratory failure
  • ptosis, diplopia
  • dysarthria, dysphagia
68
Q

how does edrophonium treat myasthenia gravis

A

blocks AchE => more Ach is available

69
Q

etiology of myasthenia gravis

A
  • autoimmune disease (SLE, RA)
  • auto-antibodies against Ach receptors at NMJ
  • thymic hyperplasia, thymomas, hyperthyroidism
70
Q

tx for myasthenia gravis

A
  • AchE inhibitors: neostigmine, pyridostigmine
  • immunosuppressant
  • plasmapheresis (removes the auto-antibody)
  • thrymectomy

Pharmacology (17 decks)

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