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rhemuatology > NMB's musc/rheum > Flashcards

NMB's musc/rheum Flashcards

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
Q

which eleiminiation of steroidal NonDep is quicker

A

hepatic is quicker than renal

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26
Q

duraiton of action of the non-depol agents

A

related to halflife….action on receptor is short lived…effects are tissue receptor density dependent

27
Q

mechanism of inactivtion for isoquinolone drugs

A

Nonenzymatic chemical reaction

28
Q

toxic metabolite (laudanosine) is a concern for

A

atracurium–>seizures

*avoided by cisatricurium-> relies on hepatic metabolism less , less laudanisin and less histamine release

29
Q

hepatic metabolism and hoffman elimination

A

atracurium

30
Q

how are steroids metabolised

A

less potent 3-oh intermediates

31
Q

Duration of ation for succinyl choline

A

5-10 minutes
diffuses from cleft what small amount reaches
cholinesterase influences durability

32
Q

break down of succinylcholine

A

butyrylcholinesterase in the liver

pseudocholinesterase in the plasma

33
Q

dubicaine test used for

A

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
Q

why is Succ preferred for rapid sequence intubation

A

SHORT duration of effect < 8 minutes

35
Q

longest duration

A

tubocurarine

36
Q

all the others have a duration of effect of about

A

20-44 minutes

37
Q

hepatically eliminated (90%)+ renal (10%)

A

rocuronium

vecuronium

38
Q

renally eliminated

A

pancuronium

tubucorarine

39
Q

spontaneously eliminated

A

atracurium

cisatracurium

40
Q

the most potent NMB

A

steroids (6) rucuronium and vecuronium
isoquinolones (1.5) atricurium and cisatricurium
* as compared to tubocurarin (1)
succinylcholine=4

41
Q

NMB which can cause heart block

A

Pancuronium

42
Q

activation of the M2 receptor in the heart is important for

A

closing the calcium channels to reduce force and rate of contraction …can lead to diminished CV capability

43
Q

which NMB’s can lead to histamine release and hypotension

A

atracurium, tubocurarine, and succinyl choline

44
Q

off target effect of this drug includes stimulation of ganglia

A

succinycholine

45
Q

off target effect of this drug is weak block of autonomic ganglia

A

tubocurarine

46
Q

adverse effects of succinyl choline

know for the test

A 
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
Q

drug that causes malignant hyperthermia by resulting in unctontrolled release of Ca2+ from SR

A

succinylcholine

*also seen in desfluance and svoflurance

48
Q

what symptoms are involved in malignant hyperthermia

A

Rigor
Heat
CO2
Lactate

49
Q

how do you reverse malignant hyperthermia

A 
Dantrolene
02
avoid CCB's
correct hyperK and acidosis
cool core body temp
50
Q

what happens with you give Succ with a small dose of nondepol. agent

A

the depol effect of Succ is antagonized (makes sense because the binding site is occupied)

51
Q

Name the ACHEi’s

A

neostigimine
edrophonium
pyrostigimine-not typically used in anethstetics

52
Q

do ACHEi’s cross BBB

A

hell naw bruh

53
Q

who are anticholinergic co-administered with ACHEi’s?

A

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
Q

Recommended anticholinergics for each ACHEi

A

neostigimine-glycopyrrolate
edrophonium-atropine
pyrostigimine-glycopyrrolate

55
Q

reversal agent causing marked sedation and antisialogogue

A

scopalamine

56
Q

reversal agent causing market tachycardia

A

atropine

57
Q

reversal agent causing marked antisialogogue

A

glycopyrrolate

58
Q

ACHEi’s can cause what off target effects

A

DUMMBBELLS…not gonna go thru these here you know them

59
Q

MOA for Suggamedex

A

rapidly encapsulated steroid NMB’s like rocuronium and vecuronium
*reverses any depth of NMB

60
Q

Suggamedex is inactive against…

A

non-steroidal NMB’s like Succinyl Choline and cisatricurium

61
Q

Do NMB’s provide pain relief or amnesia

A

NO

62
Q

why do we use NMB’s

they only acomplish paralysis!!

A
  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
Q

administration of NMB’s is by

A

IV…not orally active

64
Q

two main reversal agents

A
  1. suggamedex

2. AcheI’s

rhemuatology (2 decks)

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