Neuromuscular Junction PPT-Josh Flashcards Preview

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Flashcards in Neuromuscular Junction PPT-Josh Deck (84):
1

What is the function of the neuromuscular junction?

 

to conduct propagated impulses to the muscle cell

 

2

Definitions for following cards

NM=Neuromuscular

NDMR= non-depolerizing muscle relaxant

DMR= depolarizing muscle relaxant

thats for you dwayne

3

Motor end plate Potential:

how many protein sub-units are there?

5

4

Motor end plate Potential:

what are the 5 sub units

  • 2 alpha
  • beta
  • delta
  • gamma

5

Motor end plate Potential:

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

  • aplha
  • 2

6

Motor end plate Potential:

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

  • k+ out
  • Na+ and Ca+ in

7

Muscle Relaxants:

which type produce NO fade on TOF

DMR

(SCh)

8

Muscle Relaxants:

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

  • 2 ACh's

9

Muscle Relaxants:

what type produces fade on TOF

NDMR

10

Nerve Stimulation/ Monitoring:

what is the purpose of it?

 

 

To evaluate degree of muscle paralysis or recovery from paralysis

 

11

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Normal Tv

 

80%

12

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 50Hz

75-80%

13

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

TOF, DBS

75-80%

14

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 100Hz

50%

15

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Head lift x 5 sec.s

33%

16

Myasthenia Gravis (MG):

the alteration is where?

Post-juntional

17

Myasthenia Gravis (MG):

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

Decrease #

18

Myasthenia Gravis (MG):

the onset is usually presents w/ what signs?

Pharyngeal and ocular weakness

19

Myasthenia Gravis (MG):

what happens with exercise? worse or better?

worse

20

Myasthenia Gravis (MG):

treatment?

Anticholinesterases (edrophonium)

21

Myasthenia Gravis (MG):

undertreatment causes what?

Myasthenic crisis (weakness)

22

Myasthenia Gravis (MG):

what occurs w/ SCh

resistance (Slight)

23

Myasthenia Gravis (MG):

what happens w/ NDMR

 

Sensitive (very)

 

24

Cholinergic Crisis:

is due to what?

An excess administration of Anticholenesterase drugs (usually pyridastigmine)

25

 

Cholinergic Crisis:

S/S

Increaseing weakness

muscarinic affects

(SLUDGE)

Salivation

Lacrimation

Urination

Defication

Gastric upset

Emesis

(add miosis)

 

26

Myastenic crisis vs Cholinergic Crisis:

How can you differentiate b/t the 2

  • 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**

27

Myasthenic Syndrome/ Eaton Lambert Syndrome:

where is the alteration in the junction

Pre-juntional

28

Myasthenic Syndrome/ Eaton Lambert Syndrome:

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

Decreased ACh release

29

Myasthenic Syndrome/ Eaton Lambert Syndrome:

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

Oat cell Ca

30


Myasthenic Syndrome/ Eaton Lambert Syndrome:

What muscles are usually affected

peripheral and pelvic

31

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what happens w/exercise? (better or worse)

Improves

32

Myasthenic Syndrome/ Eaton Lambert Syndrome:

will the symptoms improve w/ anticholenesterases?

  • nope

33


Myasthenic Syndrome/ Eaton Lambert Syndrome:

what is their response to NDMR?

sensitive

34

Myasthenic Syndrome/ Eaton Lambert Syndrome:

what is their response to DMR

sensitive

35

Muscular Dystrophy:

what is teh most prevalent

Duchene's

36

Muscular Dystrophy:

there is a defect in what?

the muscle fiber

37

Muscular Dystrophy:

is their muscle weakness progressive?

yes

38

Muscular Dystrophy:

response to SCh

  • Bad
  • Hyperkalemia
  • MH
  • Rhabo (I added this one)

39

Muscular Dystrophy:

response to NDMR

 

HyperSensitive

 

40

Myotonias:

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

Ca++

Cytoplasmic reticulum

41

Myotonias:

is there a risk of MH?

Unclear, but should assume the risk

42

 

Myotonias:

response to SCh

  • Bad
  • Hyperkalemia
  • Worse muscle contractions

43

Myotonias:

response to NDMR

Normal

44

Multiple Sclerosis:

is the ______ os the corticospinal tracts in the brain

 

Demylination

45

Multiple Sclerosis:

what are the causes?

Possibly autoimmune

46

Multiple Sclerosis:

is the Peripheral nervous system affected?

Nope

47

Multiple Sclerosis:

what in the OR can worsen the Symptoms?

increased Temp

48

 

Multiple Sclerosis:

what is their response to all MR

unpredictable

49

Multiple Sclerosis:

Response to SCh (or compication)

poss Hyperkalemia

50

Guillan-Barre: (acute idiopathic polyneuritis)

is the demylination of the _____ nerves

 

Peripheral

51

Guillan-Barre: (acute idiopathic polyneuritis)

Causes

? autoimmune

52

Guillan-Barre: (acute idiopathic polyneuritis)

S/S

Sudden onset of weakness in legs and spreads cephalad

53

Guillan-Barre: (acute idiopathic polyneuritis)

there is an autonomic dysfunction that causes what r/tVS

wide swings in VS

54

Guillan-Barre: (acute idiopathic polyneuritis)

response to SCh

Hyperkalemia

55

Guillan-Barre: (acute idiopathic polyneuritis)

response to NDMR

prolonged response

56

Amyotropic Lateral Sclerosis (ALS):

____ and _____ motor neuron dysfunction

 

 

Upper and lower

57

Amyotropic Lateral Sclerosis (ALS):

get atrophy of _____ muscle

Skeletal

58

Amyotropic Lateral Sclerosis (ALS):

what are the causes

  • Viral
  • Toxin
  • Immune dysfunction
  • Trauma
  • DNA

59

Amyotropic Lateral Sclerosis (ALS):

Response to SCh

hyperkalemia

60

Amyotropic Lateral Sclerosis (ALS):

response to NDMR

Prolonged

61

Spinal Cord Transection:

up regulation after ___-___ hrs

 

48-72 hrs

62

Spinal Cord Transection:

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

3-6 mths

63

Spinal Cord Transection: ACUTE

SCh use?

 

  • effective
  • Safe w/in 1st 24 hrs

64

Spinal Cord Transection: ACUTE

NDMR use?

  • Safe
  • effective

65

Spinal Cord Transection: Chronic

SCh use?

  • Hyperkalemia risk 1st 6 months

66

 

Spinal Cord Transection: Chronic

NDMR use?

  • safe
  • effective

67

Burn Injuries:

there is up-regulation of the ________ cholinergic receptors

Extrajunctional

68

Burn Injuries:

SCh use SE

Hyperkalemia

69

Burn Injuries:

SCh SE of JHyperkalemia peaks in what days

10-50

70

Burn Injuries:

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

>30%

71

Parkinson's Disease:

Degeneration of the ___ ____ ___

Central nervous System

72

 

Parkinson's Disease:

there is a ________ depletion in the basal Ganglia

Dopamine

73

Parkinson's Disease:

S/S

 

  • Rigidity
  • tremors
  • d/t inhibition of extrapyramidal motor impulses

74

Parkinson's Disease:

response to all MR

no alterations

75

Key Points:

Depolarizers are _______ at the NMJ

Agonistic

76

Key Points:

NDMR are ________ at the NMJ

Antagonistic

77

Key Points:

What is the MOST indicitive sign of adequate muscle relaxant reversal

5 sec. Head lift

(33%)

78

Key Points:

Myasthemia Gravis has DECREASED _______?

ACh receptors

79

Key Points:

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

ACh Molecules

80

Key Points:

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

1-10mg edrophonium IV

Improvement= Myasthenic Crisis

81

Key Points:

Avoid ____ w/ Muscular dystrophies and Myotonias

SCh

82

Key Points:

Avoid ____ w/ spinal cord and Burn injuries

SCh

83

Key Points:

Avoid ____ w/ ALL demyelinating Diseases

SCh

84

Thats it and now flip for your reward

 

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