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rhemuatology > NMB's musc/rheum > Flashcards

NMB's musc/rheum Flashcards

(64 cards)

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1
Q

NON-depol-ISOQUINOLONE DERIVATIVES

A

ATRACURIUM
CISATRICURIUM
(D-TUBOCURARINE NOT USED)

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2
Q

NON-depol-STEROID DERIVATIVES

A

PANCURONIUM
ROCURONIUM
VECURONIUM

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3
Q

DEPOLARIZATING AGENT

A

SUCCINYLCHOLINE

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4
Q

REVERSAL AGENTS

A

EDROPHONIUM
PYROSTIGIMINE
NEOSTIGIMINE
SUGGAMEDEX–> FOR STEROID AGENTS ONLY

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5
Q

WHERE all are muscarinic receptors found

A

Nm= neuromuscular end plate in skeletal muscle

Nn=autonomic ganglia

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6
Q

where all are muscarinic receptors found

A

Nerves, Heart and smooth muscle, gland and epithelium

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7
Q

action of paralytics

A

Nm receptor blockade (hopefully wit no Nn blockade…but obvi, not possible)

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8
Q

where is the ryanodine receptor located

A

sarcoplasmic triad and controls the release of Ca2+

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9
Q

depolarization and phase II blockade

A

succinyl choline and pancuronium

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10
Q

what type of channel in Nm receptor

A

multi-subunit, ligand gates ion (Na+) channel

–> takes TWO ach molecules for activation

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11
Q

blockade of mucle contraction

A

dantrolene

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12
Q

reversals that inhibit ACHE accomplish what

A

allow Ach to linger in the cleft…more time to generate an AP..reversal of Nm inhibition

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13
Q

fundamental different between non-depol and depol agents

A

ROCURONIUM: non-depols prevent ANY activation of muscle contraction
SUCC CHOL: depols- gates for initial muscle contraction but persisists on the receptor, disallowing reconfiguration and repoening…therfore flaccid paralysis ensues because the OPEN Na channel is physically blocked by another molecule of the drug

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14
Q

DESCRIBE FADE

A

TOF TECHNIQUE: WHEN NON-DEPOLARIZING DRUGS OCCUPYING NEUROMUSCULAR BLOCKERS–> the strength of the fourth twitch is less than the first until eventually the muscle does not twitch with the 4th stim
(normally the first and the fourth ar equal intensity w/o blockade)

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15
Q

titration of doses of NMB’s in the ICU is

A

typically two or three of four trwitches are sought (usually this takes place at around 70-85% of the receptors being occupied)…

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16
Q

Define PTP

A

Post tetanic potentiation seen in sustained stimulation peripheral nerve stimulation

  • -> represents synaptic palsticity caused by Ca dependent activation of PKC…increases the # of release Ach vesicles (quantal content) by increasing release probablity and o the readily released pool size
  • increasing the release quantal content…is able to out-compete, briefly< witht eh NMBloackade with Non-depols and in phase II with succ
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17
Q

which drugs exhibit clean fade

A

NON-depols

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18
Q

Succinyl CHoline in the TOF phase I

A

phase 1–> no fade…constant but diminished

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19
Q

succinyl choline in the TOF phase II

A

fade

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20
Q

AchE inhibition in phase one

A

augments

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21
Q

AchE inhibition in phase II

A

reverses or antagonizes

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22
Q

muscle response in phase I

A

fasciculations nd then paralysis

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23
Q

muscle response in Phase II

A

flaccid paralysis

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24
Q

NON-depol metabolic fate

A

duration of action correlates with I/2 life

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25
which eleiminiation of steroidal NonDep is quicker
hepatic is quicker than renal
26
duraiton of action of the non-depol agents
related to halflife....action on receptor is short lived...effects are tissue receptor density dependent
27
mechanism of inactivtion for isoquinolone drugs
Nonenzymatic chemical reaction
28
toxic metabolite (laudanosine) is a concern for
atracurium-->seizures | *avoided by cisatricurium-> relies on hepatic metabolism less , less laudanisin and less histamine release
29
hepatic metabolism and hoffman elimination
atracurium
30
how are steroids metabolised
less potent 3-oh intermediates
31
Duration of ation for succinyl choline
5-10 minutes diffuses from cleft what small amount reaches cholinesterase influences durability
32
break down of succinylcholine
butyrylcholinesterase in the liver | pseudocholinesterase in the plasma
33
dubicaine test used for
to judge genetic variants of plasma cholinesterase __if cholinesterase is bad--> potential for lond duration of effect of succinyl choline * dubicaine inhihits normal ezyme by 80% and the abnormal one by only 20%
34
why is Succ preferred for rapid sequence intubation
SHORT duration of effect < 8 minutes
35
longest duration
tubocurarine
36
all the others have a duration of effect of about
20-44 minutes
37
hepatically eliminated (90%)+ renal (10%)
rocuronium | vecuronium
38
renally eliminated
pancuronium | tubucorarine
39
spontaneously eliminated
atracurium | cisatracurium
40
the most potent NMB
steroids (6) rucuronium and vecuronium isoquinolones (1.5) atricurium and cisatricurium * as compared to tubocurarin (1) succinylcholine=4
41
NMB which can cause heart block
Pancuronium
42
activation of the M2 receptor in the heart is important for
closing the calcium channels to reduce force and rate of contraction ...can lead to diminished CV capability
43
which NMB's can lead to histamine release and hypotension
atracurium, tubocurarine, and succinyl choline
44
off target effect of this drug includes stimulation of ganglia
succinycholine
45
off target effect of this drug is weak block of autonomic ganglia
tubocurarine
46
adverse effects of succinyl choline | *know for the test*
``` bradycardia tachycardia ventricular arryhtmias HTN HYPERKALEMIA with large burns, crush inury? phase II blockase prolonged increased intraoccular and intrcranial P muscle pain MYOGLOBINURIA Malignanthyperthermia Anaphylaxis ```
47
drug that causes malignant hyperthermia by resulting in unctontrolled release of Ca2+ from SR
succinylcholine | *also seen in desfluance and svoflurance
48
what symptoms are involved in malignant hyperthermia
Rigor Heat CO2 Lactate
49
how do you reverse malignant hyperthermia
``` Dantrolene 02 avoid CCB's correct hyperK and acidosis cool core body temp ```
50
what happens with you give Succ with a small dose of nondepol. agent
the depol effect of Succ is antagonized (makes sense because the binding site is occupied)
51
Name the ACHEi's
neostigimine edrophonium pyrostigimine-not typically used in anethstetics
52
do ACHEi's cross BBB
hell naw bruh
53
who are anticholinergic co-administered with ACHEi's?
to reduce the off-target effects *we want to reverse it but not too much REVERSAL ONLY REQUIRES THE LOCAL CHOLINERGIC EXCESS PROVIDED BY THE ACHEi FOR ACH TO OUTCOMPETE WITH THE NMB DRUG...WHAT WE DONT WANT IS FOR ALL THIS NEW ACH TO THEN GO OUT AND ACT ON MUSCARINC RECEPTORS
54
Recommended anticholinergics for each ACHEi
neostigimine-glycopyrrolate edrophonium-atropine pyrostigimine-glycopyrrolate
55
reversal agent causing marked sedation and antisialogogue
scopalamine
56
reversal agent causing market tachycardia
atropine
57
reversal agent causing marked antisialogogue
glycopyrrolate
58
ACHEi's can cause what off target effects
DUMMBBELLS...not gonna go thru these here you know them
59
MOA for Suggamedex
rapidly encapsulated steroid NMB's like rocuronium and vecuronium *reverses any depth of NMB
60
Suggamedex is inactive against...
non-steroidal NMB's like Succinyl Choline and cisatricurium
61
Do NMB's provide pain relief or amnesia
NO
62
why do we use NMB's | they only acomplish paralysis!!
1. as adjuvants in sxical anethesia less adverse effect and allows us use less anethesia 2. short Ortho procedures (setting breaks) 3. ENDOTRACH. TUBING 4.
63
administration of NMB's is by
IV...not orally active
64
two main reversal agents
1. suggamedex | 2. AcheI's

rhemuatology (2 decks)

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