neuromuscular blocking agents

Question 1

Neuromuscular blocking agents

Answer 1

drugs used to immobilize patients for surgery, certain procedures and paralyze skeletal muscle and are high alert

Question 2

effects of IV competitive blocking agent

Answer 2

motor weakness progresses to total flaccid paralysis, small moving muscels relax before larger until paralysis - recovery moves in the opposite direction

Question 3

___ is the NT involved in skeletal muscle activation

Answer 3

ach

Question 4

process of skeletal muscle action

Answer 4

ach released from a somatic neuron and activates Nm receptors - allowing for the influx of sodium depolarizing the t-tubule and promotes an increase in intracellular calcium contraction

Question 5

Nm belongs to a family of _____

Answer 5

ligand-gated ion channels which also include GABA, 5HT, glycine

Question 6

the general structure of Nm receptor

Answer 6

pentamer composed of 5 subunits, 2 ACh molecules are required to open the cahnnel and the binding site for ach is on the ALPHA (when it binds it opens), each subunit has a single peptide chain with with 4 membrane spanning units

Question 7

how many configurations of neuronal nicotinic receptors

Answer 7

16

Question 8

drugs that interact with the Nm receptor

Answer 8

they usually have two portions of the molecule which resemble ach. (N + ester) bc the molecule will bind to both sides to block it

Question 9

succinylcholine

Answer 9

Nm receptor blocker depolarizing unit, resistant to AChE, rapidly metabolized by cholinesterase resulting in a short half-life

Question 10

atracurium

Answer 10

non-depolarizing unit, more rigid in structure, Nm receptor blocker

Question 11

the only depolarizing NMBA

Answer 11

succinylcholine - causes a muscle fasiculations because the cell membrane becomes depolarized, ion chanels on the membrane become refractory and the muscle become resistant to further stimulation (flaccid paralysis

Question 12

phase 1 block

Answer 12

depolarizing agent immediately after admin- muscle becomes resistant to flaccid paralysis because the cell membrane becomes refractory
(depolarized to -55mV, immediate, lower dose dependent, rapid recovery, no fade, augments (inc) ach inhibition, fasiculations to paralysis)

Question 13

phase 2 block

Answer 13

due to high doses of depolarizing NM agents, resembles non-polarizng NMBA (replarization towards -80mV, slow transition, usually higher or follows prolonged infusion, more prolonged, fade, reverse ach inhib, flaccid paralysis)

Question 14

how would admin of AChE inhibitor effect the actions of succinyl choline

Answer 14

inch ach, turn off the receptor, one agent not reversed by cholinesterase inhibitor

Question 15

amino steroids

Answer 15

drugs end in -uronium (rocuronium, vecuronium, pncuronium)

Question 16

benzylisoquinolines

Answer 16

drugs end in -cruium (mivacruium, (cis)aracurium)

Question 17

all _____ are competitive antagonists at the Nm receptor

Answer 17

non-depolarizing

Question 18

would non-depolarizing cause muscle fasiculation

Answer 18

no, not depolarizing

Question 19

would non-depolarizing be reversed by AChE inhibitor

Answer 19

yes, inc in Ach, compete off the drug

Question 20

which non-depolarizing drugs have the shortest half life

Answer 20

succinylcholine, mivacurium both by BchE

Question 21

what non-depolarizing drugs should be does independ

Answer 21

succ, atra, cis atra

Question 22

where would non-depolarizing drugs primarily distribute throughout the body

Answer 22

total body water

Question 23

mivacurium

Answer 23

met - renal, BuChE, short duration

Question 24

cisatracurium / atracurium

Answer 24

met- hofman degration (except atra also has ester hydrolysis)
intermediate duration

Question 25

panuronium

Answer 25

met- renal, some hepatic | long duration

Question 26

rocuronium

Answer 26

met- hepatic (bile), renal | intermediate duration

Question 27

succinylcholine

Answer 27

met- BuChE | short duration

Question 28

vecuronium

Answer 28

met- hepatic, some renal | intermediate duration

Question 29

hofmann degradation

Answer 29

atracurium/cisatracurim both undergo spontaneous degradation without any enzymes!

Question 30

incresed fluid volume leads to

Answer 30

inc fluid volume bc of hepatic or renal disease will have a higher vd and will need a higher dose

Question 31

t 1/2 =

Answer 31

0.693 x vd / Cl

Question 32

hyperkalemia

Answer 32

concern with NMBA admin, associated with succinylcholine, prolonged depolarization of the membrane results in the efflux of potassium from within the muscle cells

Question 33

depolarization =

Answer 33

cell trying to repolarize and k+ goes into the plasma

Question 34

increased intragastric pressure

Answer 34

succinyl choline- abdomen contracts and stomach muscle contracts, may result in vomiting and issues with the airway

Question 35

histamine release

Answer 35

succinylcholine and atracurium are most associated with a decrease in BP

Question 36

myalgias

Answer 36

muscle pain caused by succinylcholine

Question 37

all agents

Answer 37

combinded admin with inhaled anesthetic may make the pt more sensitive to the medications and reduce the dose of the NMBA

Question 38

reversal of non-depolarizing block

Answer 38

neostigmine- Ach inhibitor- reverse paralysis

Question 39

what is the rational for admin neostigmine? why not work for succinylcholine reversal

Answer 39

inc ach- compete with neuromuscular blocker

Question 40

what is the rationale for administering neostigmine -

Answer 40

increase ach and compete with a NM blocker

Question 41

what is the rationale for admin of a musc ADR from neostig -

Answer 41

getting ach - GI discomfort and bladder loss salivary increased

Question 42

if the patient is bradycardia why should anti-muscurinic agent always be admin first

Answer 42

HR would be too low just with neostigmine, give anti muscurinic first then give the other

Question 43

aged enzyme

Answer 43

resistant to hydrolysis- permentantly phosphorylated ser-o-p, isopropyl leaves - hardly any electrophilicity,

Question 44

definition of depolarizing

Answer 44

Depolarizing muscle relaxants acts as ACh receptor agonists. They bind to the ACh receptors and generate an action potential. However, because they are not metabolized by acetylcholinesterase, the binding of this drug to the receptor is prolonged resulting in an extended depolarization of the muscle end-plate. As the muscle relaxant continues to bind to the ACh receptor, the end plate cannot repolarize, resulting in a phase I block. The ACh receptor can also undergo conformational and ionic changes after a period of time, resulting in a phase II block.

Question 45

definition of non-depolarizing

Answer 45

competitive antagonists. They bind to the ACh receptors but unable to induce ion channel openings. They prevent ACh from binding and thus end plate potentials do not develop.