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Principles 4 > Neuromuscular Junction PPT-Josh > Flashcards

Neuromuscular Junction PPT-Josh Flashcards

1
Q

What is the function of the neuromuscular junction?

A

to conduct propagated impulses to the muscle cell

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2
Q

Definitions for following cards

NM=Neuromuscular

NDMR= non-depolerizing muscle relaxant

DMR= depolarizing muscle relaxant

A

thats for you dwayne

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3
Q

Motor end plate Potential:

how many protein sub-units are there?

A

5

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4
Q

Motor end plate Potential:

what are the 5 sub units

A
  • 2 alpha
  • beta
  • delta
  • gamma
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5
Q

Motor end plate Potential:

ACh binds to what subunit? and how many of the subunits? to open to ion channels

A
  • aplha
  • 2
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6
Q

Motor end plate Potential:

what the ACh binds to the 2 alpha subunits and opens the ion channels, what ions are exchanged?

A
  • k+ out
  • Na+ and Ca+ in
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7
Q

Muscle Relaxants:

which type produce NO fade on TOF

A

DMR

(SCh)

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8
Q

Muscle Relaxants:

basically all SCh is, is the combination of what 2 molecules?

A
  • 2 ACh’s
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9
Q

Muscle Relaxants:

what type produces fade on TOF

A

NDMR

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10
Q

Nerve Stimulation/ Monitoring:

what is the purpose of it?

A

To evaluate degree of muscle paralysis or recovery from paralysis

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11
Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Normal Tv

A

80%

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12
Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 50Hz

A

75-80%

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13
Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

TOF, DBS

A

75-80%

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14
Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 100Hz

A

50%

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15
Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Head lift x 5 sec.s

A

33%

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16
Q

Myasthenia Gravis (MG):

the alteration is where?

A

Post-juntional

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17
Q

Myasthenia Gravis (MG):

there is an autoimmune response to ACh receptors.so what happens to their receptors?

A

Decrease #

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18
Q

Myasthenia Gravis (MG):

the onset is usually presents w/ what signs?

A

Pharyngeal and ocular weakness

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19
Q

Myasthenia Gravis (MG):

what happens with exercise? worse or better?

A

worse

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20
Q

Myasthenia Gravis (MG):

treatment?

A

Anticholinesterases (edrophonium)

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21
Q

Myasthenia Gravis (MG):

undertreatment causes what?

A

Myasthenic crisis (weakness)

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22
Q

Myasthenia Gravis (MG):

what occurs w/ SCh

A

resistance (Slight)

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23
Q

Myasthenia Gravis (MG):

what happens w/ NDMR

A

Sensitive (very)

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24
Q

Cholinergic Crisis:

is due to what?

A

An excess administration of Anticholenesterase drugs (usually pyridastigmine)

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25
Q

Cholinergic Crisis:

S/S

A

Increaseing weakness

muscarinic affects

(SLUDGE)

Salivation

Lacrimation

Urination

Defication

Gastric upset

Emesis

(add miosis)

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26
Q

Myastenic crisis vs Cholinergic Crisis:

How can you differentiate b/t the 2

A
  • Give edrophonium 1-10 mgIV
  • Improves= Myasthenic crisis
  • Worsens= Cholinergic crisis

** makes sense Myasthenis crisis- the onder streament so it would help, cholinergic crisis too much anticholinesterase thus more would make it worse**

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27
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

where is the alteration in the junction

A

Pre-juntional

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28
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what is the main problem r/t ACh or ACh recptors?

A

Decreased ACh release

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29
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

usually associated w/ underlying malignancy. what is that malignancy?

A

Oat cell Ca

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30
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

What muscles are usually affected

A

peripheral and pelvic

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31
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what happens w/exercise? (better or worse)

A

Improves

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32
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

will the symptoms improve w/ anticholenesterases?

A
  • nope
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33
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what is their response to NDMR?

A

sensitive

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34
Q

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what is their response to DMR

35
Q

Muscular Dystrophy:

what is teh most prevalent

A

Duchene’s

36
Q

Muscular Dystrophy:

there is a defect in what?

A

the muscle fiber

37
Q

Muscular Dystrophy:

is their muscle weakness progressive?

38
Q

Muscular Dystrophy:

response to SCh

A
  • Bad
  • Hyperkalemia
  • MH
  • Rhabo (I added this one)
39
Q

Muscular Dystrophy:

response to NDMR

A

HyperSensitive

40
Q

Myotonias:

There is a defect in the Re-uptake of ___ by the _____ _____ thus sustained skeletal mucle contraction

A

Ca++

Cytoplasmic reticulum

41
Q

Myotonias:

is there a risk of MH?

A

Unclear, but should assume the risk

42
Q

Myotonias:

response to SCh

A
  • Bad
  • Hyperkalemia
  • Worse muscle contractions
43
Q

Myotonias:

response to NDMR

44
Q

Multiple Sclerosis:

is the ______ os the corticospinal tracts in the brain

A

Demylination

45
Q

Multiple Sclerosis:

what are the causes?

A

Possibly autoimmune

46
Q

Multiple Sclerosis:

is the Peripheral nervous system affected?

47
Q

Multiple Sclerosis:

what in the OR can worsen the Symptoms?

A

increased Temp

48
Q

Multiple Sclerosis:

what is their response to all MR

A

unpredictable

49
Q

Multiple Sclerosis:

Response to SCh (or compication)

A

poss Hyperkalemia

50
Q

Guillan-Barre: (acute idiopathic polyneuritis)

is the demylination of the _____ nerves

A

Peripheral

51
Q

Guillan-Barre: (acute idiopathic polyneuritis)

Causes

A

? autoimmune

52
Q

Guillan-Barre: (acute idiopathic polyneuritis)

S/S

A

Sudden onset of weakness in legs and spreads cephalad

53
Q

Guillan-Barre: (acute idiopathic polyneuritis)

there is an autonomic dysfunction that causes what r/tVS

A

wide swings in VS

54
Q

Guillan-Barre: (acute idiopathic polyneuritis)

response to SCh

A

Hyperkalemia

55
Q

Guillan-Barre: (acute idiopathic polyneuritis)

response to NDMR

A

prolonged response

56
Q

Amyotropic Lateral Sclerosis (ALS):

____ and _____ motor neuron dysfunction

A

Upper and lower

57
Q

Amyotropic Lateral Sclerosis (ALS):

get atrophy of _____ muscle

58
Q

Amyotropic Lateral Sclerosis (ALS):

what are the causes

A
  • Viral
  • Toxin
  • Immune dysfunction
  • Trauma
  • DNA
59
Q

Amyotropic Lateral Sclerosis (ALS):

Response to SCh

A

hyperkalemia

60
Q

Amyotropic Lateral Sclerosis (ALS):

response to NDMR

61
Q

Spinal Cord Transection:

up regulation after ___-___ hrs

62
Q

Spinal Cord Transection:

up regulated for 48-72 hrs, risks for __-__months

63
Q

Spinal Cord Transection: ACUTE

SCh use?

A
  • effective
  • Safe w/in 1st 24 hrs
64
Q

Spinal Cord Transection: ACUTE

NDMR use?

A
  • Safe
  • effective
65
Q

Spinal Cord Transection: Chronic

SCh use?

A
  • Hyperkalemia risk 1st 6 months
66
Q

Spinal Cord Transection: Chronic

NDMR use?

A
  • safe
  • effective
67
Q

Burn Injuries:

there is up-regulation of the ________ cholinergic receptors

A

Extrajunctional

68
Q

Burn Injuries:

SCh use SE

A

Hyperkalemia

69
Q

Burn Injuries:

SCh SE of JHyperkalemia peaks in what days

70
Q

Burn Injuries:

w/ NDMR there is a 3 fold resistance in a TBSA % > what?

71
Q

Parkinson’s Disease:

Degeneration of the ___ ____ ___

A

Central nervous System

72
Q

Parkinson’s Disease:

there is a ________ depletion in the basal Ganglia

73
Q

Parkinson’s Disease:

S/S

A
  • Rigidity
  • tremors
  • d/t inhibition of extrapyramidal motor impulses
74
Q

Parkinson’s Disease:

response to all MR

A

no alterations

75
Q

Key Points:

Depolarizers are _______ at the NMJ

76
Q

Key Points:

NDMR are ________ at the NMJ

A

Antagonistic

77
Q

Key Points:

What is the MOST indicitive sign of adequate muscle relaxant reversal

A

5 sec. Head lift

(33%)

78
Q

Key Points:

Myasthemia Gravis has DECREASED _______?

A

ACh receptors

79
Q

Key Points:

Myasthenic Syndrome or Eatin-Lambert Disease has a DECREASED ______?

A

ACh Molecules

80
Q

Key Points:

Differentiating Myastenic Crisis (low ACh) from Cholinergic Crisis (High ACh) give what?

A

1-10mg edrophonium IV

Improvement= Myasthenic Crisis

81
Q

Key Points:

Avoid ____ w/ Muscular dystrophies and Myotonias

82
Q

Key Points:

Avoid ____ w/ spinal cord and Burn injuries

83
Q

Key Points:

Avoid ____ w/ ALL demyelinating Diseases

84
Q

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Principles 4 (20 decks)

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