Nicotinic cholinergic transmission, NMBA Flashcards

1
Q

Excitation contraction coupling

A

Process by which an action potential in a motor neuron leads to contraction of a muscle

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2
Q

Polarized membrane

A

Positive charge on the outside, negative charge on the inside

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3
Q

Steps in muscle contraction

A

Action potential at NMJ release ACH, ACH binds to nicotinic m, end plates depolarize, depol over muscle membrane happens, release of calcium ions from SR, calcium permits actin/myosin to bump uglies and cause muscle contraction, ach quickly dissociates from receptors on motor end plate, calcium take into SR causing relaxation

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4
Q

Non depolarizing compete with

A

binding to nicotinic M receptors

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5
Q

Order of paralysis

A

Eyes face first, then limbs, abdo and glottis. Last is respiratory muscles

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6
Q

Hypotension

A

NMBA can cause hypotension due to blockade of nicotinic m receptors, also from histamine release. Can’t cross BBB

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7
Q

Succs paralysis

A

4-6 minutes (at 1.5mg/kg)

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8
Q

Succ degraded by

A

Pseudocholinesterase which is present in plasma

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9
Q

Succ peaks

A

1 minute after administration, lasts no longer than 10 minutes

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10
Q

Psuedocholinesterase

A

Can be deficient

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11
Q

MH

A

Rare, potentially fatal, triggered by succ, 1:25,000 Muscle rigidity, extremely high temp (up to 43C)

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12
Q

MH cause in a nutshell

A

Increased calcium from SR causing prolonged muscle rigidity

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13
Q

Succ hyperK+

A

Rarely can cause hyperk+ on its own Significant hyperK+ from burns, trauma (crush injuries) rhabdo

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14
Q

Succ trade name

A

Anectine

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15
Q

Succ contras

A

Hypersensitivity known or suspected hyperK+, family hx of MH or pseudocholinesterase deficiency, myopathies with elevated CK

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16
Q

Succ dose

A

1.5mg/kg IV/IO max of 150mg Ped 1.5-2.0mg/kg IV/IO

17
Q

Succ considerations

A

Sedation/analgesia first Withhold in difficult predicted airway Drug takes 60-90 for full effect Acute airway burns are not a cause for hyperK+

18
Q

This chart

A
19
Q
A