Neuromuscular Junction PPT-Josh Flashcards by Diana Hathaway

Q

What is the function of the neuromuscular junction?

A

to conduct propagated impulses to the muscle cell

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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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Q

Motor end plate Potential:

how many protein sub-units are there?

A

5

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Q

Motor end plate Potential:

what are the 5 sub units

A

2 alpha
beta
delta
gamma

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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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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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Q

Muscle Relaxants:

which type produce NO fade on TOF

A

DMR

(SCh)

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Q

Muscle Relaxants:

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

A

2 ACh’s

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Q

Muscle Relaxants:

what type produces fade on TOF

A

NDMR

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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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Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Normal Tv

A

80%

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Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 50Hz

A

75-80%

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Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

TOF, DBS

A

75-80%

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Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Holds tetanus 100Hz

A

50%

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Q

SAY WHAT % OF RECEPTORS ARE STILL BLOCKED

Head lift x 5 sec.s

A

33%

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Q

Myasthenia Gravis (MG):

the alteration is where?

A

Post-juntional

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Q

Myasthenia Gravis (MG):

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

A

Decrease #

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Q

Myasthenia Gravis (MG):

the onset is usually presents w/ what signs?

A

Pharyngeal and ocular weakness

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Q

Myasthenia Gravis (MG):

what happens with exercise? worse or better?

A

worse

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Q

Myasthenia Gravis (MG):

treatment?

A

Anticholinesterases (edrophonium)

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Q

Myasthenia Gravis (MG):

undertreatment causes what?

A

Myasthenic crisis (weakness)

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Q

Myasthenia Gravis (MG):

what occurs w/ SCh

A

resistance (Slight)

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Q

Myasthenia Gravis (MG):

what happens w/ NDMR

A

Sensitive (very)

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Q

Cholinergic Crisis:

is due to what?

A

An excess administration of Anticholenesterase drugs (usually pyridastigmine)

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## Footnote Cholinergic Crisis: S/S

Increaseing weakness muscarinic affects (SLUDGE) Salivation Lacrimation Urination Defication Gastric upset Emesis (add miosis)

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\*\*

Myasthenic Syndrome/ Eaton Lambert Syndrome: where is the alteration in the junction

Pre-juntional

Myasthenic Syndrome/ Eaton Lambert Syndrome: what is the main problem r/t ACh or ACh recptors?

Decreased ACh release

Myasthenic Syndrome/ Eaton Lambert Syndrome: usually associated w/ underlying malignancy. what is that malignancy?

Oat cell Ca

Myasthenic Syndrome/ Eaton Lambert Syndrome: What muscles are usually affected

peripheral and pelvic

Myasthenic Syndrome/ Eaton Lambert Syndrome: what happens w/exercise? (better or worse)

Improves

Myasthenic Syndrome/ Eaton Lambert Syndrome: will the symptoms improve w/ anticholenesterases?

* nope

Myasthenic Syndrome/ Eaton Lambert Syndrome: what is their response to NDMR?

sensitive

Myasthenic Syndrome/ Eaton Lambert Syndrome: what is their response to DMR

sensitive

Muscular Dystrophy: what is teh most prevalent

Duchene's

Muscular Dystrophy: there is a defect in what?

the muscle fiber

Muscular Dystrophy: is their muscle weakness progressive?

yes

Muscular Dystrophy: response to SCh

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

Muscular Dystrophy: response to NDMR

HyperSensitive ## Footnote

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

Ca++ Cytoplasmic reticulum

Myotonias: is there a risk of MH?

Unclear, but should assume the risk

## Footnote Myotonias: response to SCh

* Bad * Hyperkalemia * Worse muscle contractions

Myotonias: response to NDMR

Normal

Multiple Sclerosis: is the ______ os the corticospinal tracts in the brain

Demylination

Multiple Sclerosis: what are the causes?

Possibly autoimmune

Multiple Sclerosis: is the Peripheral nervous system affected?

Nope

Multiple Sclerosis: what in the OR can worsen the Symptoms?

increased Temp

## Footnote Multiple Sclerosis: what is their response to all MR

unpredictable

Multiple Sclerosis: Response to SCh (or compication)

poss Hyperkalemia

Guillan-Barre: (acute idiopathic polyneuritis) is the demylination of the _____ nerves

Peripheral

Guillan-Barre: (acute idiopathic polyneuritis) Causes

? autoimmune

Guillan-Barre: (acute idiopathic polyneuritis) S/S

Sudden onset of weakness in legs and spreads cephalad

Guillan-Barre: (acute idiopathic polyneuritis) there is an autonomic dysfunction that causes what r/tVS

wide swings in VS

Guillan-Barre: (acute idiopathic polyneuritis) response to SCh

Hyperkalemia

Guillan-Barre: (acute idiopathic polyneuritis) response to NDMR

prolonged response

Amyotropic Lateral Sclerosis (ALS): \_\_\_\_ and _____ motor neuron dysfunction

Upper and lower

Amyotropic Lateral Sclerosis (ALS): get atrophy of _____ muscle

Skeletal

Amyotropic Lateral Sclerosis (ALS): what are the causes

* Viral * Toxin * Immune dysfunction * Trauma * DNA

Amyotropic Lateral Sclerosis (ALS): Response to SCh

hyperkalemia

Amyotropic Lateral Sclerosis (ALS): response to NDMR

Prolonged

Spinal Cord Transection: up regulation after \_\_\_-\_\_\_ hrs

48-72 hrs

Spinal Cord Transection: up regulated for 48-72 hrs, risks for \_\_-\_\_months

3-6 mths

Spinal Cord Transection: ACUTE SCh use?

* effective * Safe w/in 1st 24 hrs

Spinal Cord Transection: ACUTE NDMR use?

* Safe * effective

Spinal Cord Transection: Chronic SCh use?

* Hyperkalemia risk 1st 6 months

## Footnote Spinal Cord Transection: Chronic NDMR use?

* safe * effective

Burn Injuries: there is up-regulation of the ________ cholinergic receptors

Extrajunctional

Burn Injuries: SCh use SE

Hyperkalemia

Burn Injuries: SCh SE of JHyperkalemia peaks in what days

10-50

Burn Injuries: w/ NDMR there is a 3 fold resistance in a TBSA % \> what?

\>30%

Parkinson's Disease: Degeneration of the ___ \_\_\_\_ \_\_\_

Central nervous System

## Footnote Parkinson's Disease: there is a ________ depletion in the basal Ganglia

Dopamine

Parkinson's Disease: S/S

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

Parkinson's Disease: response to all MR

no alterations

Key Points: Depolarizers are _______ at the NMJ

Agonistic

Key Points: NDMR are ________ at the NMJ

Antagonistic

Key Points: What is the MOST indicitive sign of adequate muscle relaxant reversal

5 sec. Head lift (33%)

Key Points: Myasthemia Gravis has DECREASED \_\_\_\_\_\_\_?

ACh receptors

Key Points: Myasthenic Syndrome or Eatin-Lambert Disease has a DECREASED \_\_\_\_\_\_?

ACh Molecules

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

1-10mg edrophonium IV Improvement= Myasthenic Crisis

Key Points: Avoid ____ w/ Muscular dystrophies and Myotonias

SCh

Key Points: Avoid ____ w/ spinal cord and Burn injuries

SCh

Key Points: Avoid ____ w/ ALL demyelinating Diseases

SCh

Thats it and now flip for your reward