Muscle Paralytics and activators Flashcards

1
Q

What effect will anticholinesterases have on skeletal muscle? WHat disease are they used in?

A

They will increase skeletal muscle contraction by reducing ACh degradation.

used for rmyasthenia gravis

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2
Q

What are the three acetylcholinesterases that we talked about? Which is used most often? Which is used as a diagnostic?

A

Neostigmine

Pyridostigmine (used more often)

Edrophonium (used to test)

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3
Q

What is used to treat muscle spasms by blocking acetylcholine release?

A

botulinum toxin

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4
Q

Which anticholinesterase has been used to prevent nerve gas action?

A

pyridostigmine

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5
Q

What will happen in an edrophonium test if the patient has myasthenia gravis? How about if they have a cholinergic crisis?

A

MG = muscle strength will increase

CHolinergic crisis = muscle strength will decrease

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6
Q

What are the anticholinesterase side effects?

A

SLUDGE

sweating

lacrimation

urination

diarrhea

GI distress

Emesis

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7
Q

WHat are the two competitive ACh blockers we need to know about?

A

d-tubocurarine (from curare)

mivacurium

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8
Q

What is the depolarizing agent that works as a neuromuscular blocker?

A

Succinylcholine

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9
Q

Which can be reversed: the competitive blockers or the depolarizing agents? How?

A

THe competitive blockers can be reversed by giving an anticholinesterase

the depolarizing agent can’t be reversed -you have to just wait until the body works it out

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10
Q

Specifically what does succinylcholine do?

A

it depolarizes the end plate of the muslcle by causing chronic Na+ influx. This results in continuous depolarization sot aht the receptor can eventually no longer fire

You’ll sed fasciculations preceding flaccid paralysis

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11
Q

Why wouldn’t you want to give succinylcholine to a burn patient?

A

burned skin has an increase in nicotiinc receptors, so if you give them succinylcholine they will release too much K+

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12
Q

Besides anticholinesterases, what can you give to slightly reverse a competitive blockade using either tubocurarine or mivacurium?

A

epinephrine or norepinephrine

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13
Q

What are some of the toxic effects of the neuromuscular plockers (paralytics)?

A

apnea (paralysis of diaphragm)

hitamine release in anaphylaxis

CV collapse

malignant hyperhtermia (especially with succinylcholine)

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14
Q

What is the treatment for malignant hyperthermia? How does it work?

A

it blocks calcium release from the sarcoplasmic reticulum by blocking the ryanodine receptor

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15
Q

All paralytics are metabolized by the kidneys except….

A

atracurium - so give this one for people in renal failure

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16
Q

What structure do the competitive inhibitors have?

A

quaternary ammonium ion structures

17
Q

Are the competitive inhibitors have short or long duration?

A

short - which is nice, because you can just stop infusing them when you don’t need their action anymore

18
Q

Vecuronium is another competitive inhibitor paralytic like tubocurararine, but with what added benefits?

A

it doesn’t block the vagal effects on the heart

won’t release histamine

19
Q

Which patients will be somewhat resistant to the effects of succinylcholine? WHy?

A

People with myasthenia gravis - they have fewer nicotinic receptors to block

20
Q

How is the action of succinylcholine stopped?

A

degradation by a native enzyme - butyrylcholinesterase

21
Q

Because of its rapid action, succinylcholine is preferred for what procedure?

A

intubation

22
Q

WHat is the most lethal toxin known?

A

botulinum toxin

worrisome because we only have antisera against 3 out of 8 types

23
Q
A