Neuromuscular Blocker Review Flashcards

1
Q

What part of the Ach attaches to the Nicotinic receptor?

A

Binds to the alpha sub unit through the + charged Nitrogen atom

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2
Q

What is the synthesis of Ach?

A

Its a reaction between Choline and Acetyl CoA via the enzyme cholineacetyltransferase

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3
Q

What is the active structure of Ach?

A

The quaternary ammonium ester group with a + charged Nitrogen

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4
Q

What are the 2 categories of NMB’s

A

NDNMB, DNMB

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5
Q

Suc’s is metabolized by?

A

Pseudocholinesterase

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6
Q

For Suc’s to work it must occupy _______ receptors?

A

Both Alpha receptors

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7
Q

How many receptors do NDNMB occupy?

A

They only need to occupy 1 alpha subunit receptor

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8
Q

When both alpha subunits are occupied by Suc’s causes the Na+ channels to stay_____by attaching to 2 alpha subunits?

A

open

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9
Q

When a NDNMB attaches to a alpha subunit it causes the Na+ channels to stay______?

A

Closed

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10
Q

Pancuronium and Vecuronium, are metabolized by?

A

deacetylation in the liver and excreated in the bile and via the kidneys

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11
Q

Suc’s is metabolized into?

A

Choline and Succinylmonocholine

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12
Q

What ends a NDNMB efect?

A

Redistribution, renal and hepatic metabolism, Hoffman elimination and plasma cholinesterase.

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13
Q

What eliminates DNMB?

A

Pseudocholinesterase

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14
Q

Which agents release Histamine?

A

(SAM) Suc’s, Atricurium, and Mivacurium

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15
Q

Histamine release is attenuated by?

A

Administration of H1 and H2 blockers

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16
Q

Major side effect of Suc’s?

A

faciculations releasing K+ and inhibiting the closure of the Na+ channels allowing leaking of K+ from the Cells

17
Q

How is the depolarization of Suc”s terminated?

A

Diffusion away from the the neuromuscular junction and metabolized by plasma cholinesterase (pseudocholinesterase)

18
Q

Is Ach metabolized by pseudocholinesterase?

A

No, it is metabolized by true cholinesterase or acetylcholinesterase

19
Q

Pseudocholinesterase deficiency will prolong Suc’s effects by?

A

Aprox 6-8 hours (PP slide 21)

20
Q

What drugs will potentiate NDNMB?

A

VAA, Aminoglycosides, LA, Antiarrythmics, Mag, Lithium, dantrolene

21
Q

Which muscle relaxants are ultra short acting?

22
Q

Which muscle relaxants are short acting?

A

Mivacurium

23
Q

Which muscle relaxants are intermediate acting?

A

Vec, Roc, Atracurium, Cisatracurium

24
Q

Which muscle relaxants are long acting?

A

Pancuronium

25
Where do Muscle relaxants work?
Post synaptic motor end plate
26
Depolarizers resemble and mimic _________?
Ach
27
The sustained opening of receptor channels in a depolarized post-junctional membrane is called a _____?
Phase 1 block
28
Desensitized repolarized post junctional membrane that remains unresponsive to Ach occurs after ___________ and is called _______?
Repeated or large doses of Suc's and is called a Phase 2 block
29
Types of Patients that would have extra junctional receptors?
Denervation p 24-28 hrs, Burns p 2 days, immobilization p 3 days.
30
Up regulated junctional receptors can cause ________ when given Suc's?
Massive release of K+ up to 0.5meq into the circulatory system
31
NDNMB don't cross the _____, _______, _____?
Blood brain barrier, Placental barrier and GI
32
to decrease the side effects of Suc's, pretreatment with a ______ may decrease cardiac arrythmias, Myalgias, and fasiculations
NDNMB
33
Will pretreatment with a NDNMB before giving SUC's decrease the K+ release?
NO, because K+ is released because the cells are depolarized and allow K+ to leak out while the Na+ channels are open
34
To impair motor nerve conduction > then ______% of Ach receptors must be blocked
75
35
Total flaccidity is at what % of Ach receptors are blocked?
99%
36
Twitch monitoring on the head is using what nerve?
Facial Nerve( CN VII)
37
The twitch monitor triggers what muscle through the facial nerve?
Curragator Supercilli
38
The placement of the electrodes over the ulnar nerve stimulates what muscle?
Adductor Pollicis
39
Stimulation of the Posterior tibia nerve stimulates what muscle?
Flexor Hallucis