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NMBD Special Flashcards

1
Q

Succinylcholine
Benefit, Effect of MG

A

Benefit: Very Fast on/off (10 min off),
AE: Downregulated Receptors (MG): decreased sensitivty -> more dose

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2
Q

Rocuronium
Benefit, AE

A

short onset (useful for RSI) can inc duration if double duration, AE:

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3
Q

Pancuronium
|System, Benefit, AE,

A

Benefit: Long acting, Slow onset (poor intubating choice)
AE: Duration Inc with R+H impair

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4
Q

Vecuronium
Benefits, AE,

A

Benefit: Intermediate
AE: Hepatic clearance, LF means long duration. Has Active metabolite, avoid long duration due to weakness

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5
Q

Atricuronium
Benefit, AE,

A

Benefit:

AE: metabolite lidanosine (hepatic + renal excrete),
Histamine (hypoten, tachycardia, bronchospasm)

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6
Q

Cisatricuronium System,
Benefit, AE,

A

Benefit: ICU friendly, recovery independent of duration

AE: May Lead to Ladanosine inc sz threshold (hep metabolism, renal ex)

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7
Q

Succinylcholine
MOA, Termination, Elimination

A

MOA: Mimic ACh by binding to nicotinic cholinergic R -> ion channel open Initially leads to fasiculation (prolong depol), Preoccupied receptor cannot react to release of ach -> paralysis

Termination: Diffusion
Elimination: Pseudocholinesterase

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8
Q

Rocuronium
Chem Structure, System

A

Chem Structure: Aminosteroid;
System: No CVS effect or H release

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9
Q

Pancuronium
Chem Structure, System:

A

Chem Structure: Aminosteroid;
System: Dose -Vasolytic (inc HR, BP, CO), No H-Release

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10
Q

Vecuronium
Chem Structure, System; Metabolism Significant

A

Chem Structure: Aminosteroid;
System: No CVS effect or H release

Has active metabolite of 3-deaceytl-veucornium (80% of efficacy)

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11
Q

Atricuronium
Chem Structure,System:

A

Chem Structure:Benzylisoquinolines;
System: Histamine release

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12
Q

Cisatricuronium
Chem Structure, System:

A

Chem Structure: Benzylisoquinolines
System: no histamine release, min CVS changed

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13
Q

Depolarization Nerve Stim Characteristic:

A

Phase I: TOF ratio > 70%, decreased amplitude but sustained response to tetany; no post no posttetanic faciliation of twitches

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14
Q

NonDepolarizing Meds
MOA: AE:

A

MOA: Compeititve ACH receptor antagonist, increasing ACh in the synaptic cleft;

AE: Upregulation of receptor (burns, dennervate): more desensitive, need higher dose

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15
Q

Indication for RSI:

A

Risk of aspiration :

  • full stomach,Obesity, Pregger
  • trauma, DM, Hitial Hernia
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16
Q

AE of Succinylcholine:

A
  • MH trigger;
  • Inc Intraocular and ICP,
  • HyperK ( e.g. burn patients s/p 1d to 6 mo of event or CVA)
  • Anaphylaxsis
  • Peds: BradyC
  • Muscle Soreness/ Rhabdo./ Prolonged Paralysis
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17
Q

Succ + HyperK; ergo bad in:

A

K inc by 0.5 to 1.

burn, crush, acidosis, infect,

Immobile (trauma or due to myotonia, muscular dz),

Nerve Pathology (dennervation, cva, spinal cords)

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18
Q

Massesster Spasm:
When, Dangerous ddx

A
  1. complication during intubation;
  2. may be a sign of early MH but not low specificity
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19
Q

Edrophonium,
Benefits, AE

A

Benefits: AE:

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20
Q

Neostigmine
Notes, AE

A

Note: Relies on adequate Level of Nondepols or else phase 2 may occur

AE: Neuro: Occular Side Effect (genetic), Arthralgia, Fasiculation, Laryngospasm, Muscle Cramps
Cardio: BradyC +/- AV block, Flushing, Hypotension, Syncope
GI: Diarrhea, Dysphagia, Flatulence, Peristalsis, N/V

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21
Q

Pyridostigmine

AE; Benefit

A

AE: penetrates through b-brain-bar -> central chloinergic effect -> Delirium, SZ, AMS, Resp depression

Benefit: tx for central anticholinergic syndrome)

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22
Q

Common AE of antiCHE:

A

Cardiac muscarinic: (bradyC, Sinus Arrest), minimized with dosing of A/G (G to N), (A to E);
Parasymp: Bronchospasms (inc secretion), miosis, nausea, inc peristaslsis;
Nicotinic effect: (paradoxical muscle weakness with large dose)

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23
Q

Common AE of antiCHE in Fetal

which med, cause tx and sx:

A

Neostigminie can cross placenta -> fetal bradycardia

(need to use atropine here instead of glyco)

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24
Q

Most sen to NBMD Muscle/CN:

A
  1. EOM (CN3, most sen)
  2. Pharyngeal (CNX)
  3. Masseter (CN5)
  4. Adductor Pollicis
  5. ABD rectus
  6. Orbicularis oculi
  7. Diaphgram
  8. Larynx
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25
Speed of Onset Muscles
1. Larynx (fastest onset) 2. diaphgram 3. orbicularis oculi 4. adductor Pollicis
26
Fastest Recovery
1. Larynx (fast recovery) 2. Orbicularis Oculi = Diaphgram 3. Adductor Pollis
27
Sugammadex: MOA
Selective relaxant binding agent- cyclodextrin that captures nmbd (esp rocuronium and vecuronium); Has Lipophilic Core with hydrophilic periphery with Quaternary Nitrogen binding to the Core.
28
Cholesterase Inhibitor MOA:
1. Inhibits ACHe -\> inc ACh in NMJ 2. overcoming comp inhibition
29
Cholinestaerase Inhib Warning
Recurarization: Increased weakness due to lasting effect of NMBD (Tip: check duration of NMBD and reverse agent)
30
Sugammadex Benefits; AE
Benefits:Useful in administration of roc esp in fast recovery of profound NMB [Cannot intubate cannot ventilate] AE:Rare BradyC; hypersensitivty rxn. Blocks OCP (need condom x 7 days s/p)
31
Most Reliable NBMD Montior; TOF \>0.9
Theoretically: Peripheral Nerve Stim (TOF at CN7\>Ulnar) Threshold for TOF to paralyze: 90
32
TOF 2 HZ x4 Two burst of 3 separated by 750 msec ( preserved as two sep twitches) 5 secs of 50 Hz (response fades)
33
Test for TOF \<0.3; Dobule Burst Test for TOF\>0.7; Tetanus
34
35
Prolong ScH Causes
genetic defect of PCE, Dx via dibucaine, Liver Dz (less pce), Drugs, organophosphate poisoning, Excessive dose/Phase 2 blocks, Hypothermia
36
Alerted Pseudocholinesterase- Dibucaine #
Dibucaine: % blocking of pseudocholinesterase when given dibucaine; Number ~ function of pseudocholinesterase Normal 80 (5-10 duration); HEterozygous 40-60 (20-30 duration, 1 in 30,50); Homozygous 20 (3-6h, 1-2k 3); Decreased plasma vs level: 80 (\<25 min)
37
Depolarizing Muscle Relaxant MOA
Binds to Nicotinic Receptor and Remain Depolarized with CHannel opening -\> Postjunctional unable to respond to subsequent release (desentiization of receptor)
38
TOF vs TOFC
TOF: 4 x 2hz no less than 10 sec apart; Calc Amp of Response 4th /1st TOFC: COunts Evoked Responses 1Count:
39
Tetanus vs PTC
Tetanus: stim 30Hz x 5 seconds PTC: Tetanus + ST Stimuli at 1hz x 20 secs Used if TOFC is 0
40
Double Burst Stimulation
2 mini tetanic burst 0.75 secs apart (less painful)??
41
Succ Phase 2 block
Post Junctional Membrane potential moves back to normal despite continued activation of ach (due to inc na/k pump). Desensitization of the receptor
42
Chemical Subtype of nond- NMBD and Elimination of each
Steroidal: Pancuronium; Vecuronium; Rocuronium Hepatic +/- Renal Elimination Benzylisoquinolinium: Atracurium; Cisatricurium Hoffman Elimination
43
Nondepol NMBD relation between Onset and Duration
Longer Onset correlates with Longer duration
44
45
Acquired Factors affecting Dibucaine
Increase PseudoCHE: Obesity, ETOH abuse Decrease: PseudoCHE: 75% preggers; 57% postpartum Inhibited PseudoCHE: Organophosphate (insecticide)
46
Congential Myopathy and NMBD
NonDepol: Needs more dose (too effective) Depolarization: Risk of MH
47
Effect of Lambert Eaton?? and MG
MG: Less effective Receptors. -\> Succ less effective (more dose) Nondepol: More effective (need less dose)
48
Factors that Upregulate receptors Effect on nondepolarizing and Depolarizing
Upregulation: Increases sensitivity for Depolarizing (need less, do not give due to hyperK) and Decrease sensitivity for Nondepol (require more) - Spinal Cord Inury S/p 24 hours - Burns s/p 24 hours up to 1-2 years - GBS, NMO, MS (demyelination and axonal degradation; also have autonomic dysfunction which requires to maintain adequate preload)
49
Neostigmine vs Pyrdrostigmine site of interaction
Neostigmine: Peripheral NS only Pydriostigmine: Crosses BBB; (CNS also)
50
Mivacurium Metabolism
Pseudochholinesterase
51
Neostigmien then Succ effect
Prolong Duration of phase I blockade (30 min)
52
Phase 2 block of succ
A phase II block is likely due to the interaction of succinylcholine on the prejunctional acetylcholine receptors. Prejunctional receptors are blocked by the higher concentration of succinylcholine leading to a decrease in cholinergic transmission and competition with the drug at the postsynaptic receptors.
53
Combination of NMBD effects
Synergistic Effect. Cis + Roc; Additive Effects Cis+atra
54
Combination of Succ + NMBD
If Defasiculating of NMBD is given, Subsequent dose of succ must be increased due to antagonism; If Blockade is deep: Antagonism with Succ, Block is shallow: potentiation with succ is more likely.
55
Reglan + NMBD
Inhibitory effect on plasma cholinesterase: Prolong Duration of Succ and Mivacurium.
56
MC Variants of Pseudocholinesterase Deficiency
A, and K variants
57
double succ effects
small then large will decrease fasiculation but not myalgia incidence
58
decrease succ myalgia factors
pre succ, lidocaine, periop vit c, ca.
59
physiostigmine severe AE
sz esp eith nicotinic receptor agonists (varenicline)
60
RF of allergy to NMBD
Cosmetic (or toothpaste, detergents, shampoo) to Aminosteroid
61
Trisomy 21 Effecton NMBD
Less requirement due to hypotonia
62
Succ with pretreatment of NDNB affect most but what AE
tachy/brady (former 2/2 catecholamine); IOP inc.
63
Myasthenia Gravis vs Syndrome Meds concerns
MG: insensitive to Succ; MS: insensitive to neostigmine
64
Muscle relaxant potentiation via inhalants
desflurane \> sevoflurane \> isoflurane \> halothane \> TIVA
65
Neostigmine AE that is not blocked by antimuscularinic
Paradoxical Musclar Weakness, following the complete recovery of neuromuscular function, or a second dose is administered in patients with a small degree of residual blockade.
66
Elderly Considerations in NMBD
Prolong onset, Longer Duration, Less requirement for nmbd.
67
Termination of Succ
Diffusion from NMJ
68
Concerns of Succ with Infants
possibility of hyperkalemia 2/2 undiagonsed muscular dystrophy.
69
effect on TOF ratio on chronically paralyzed limb
TOF ratio increases due to less weaker effect of nondepol on limb due to extracellular ach junction
70
MC effect of succ on peds
bradyc esp up to 1 yo
71
peds vs adult pseudocholinesterase and clinical effect
only 0.5 of adult levels, no clinical effect.
72
TOFC relation to percentage of blocked receptors
0 is 100%, 1 is 90; 2 is 80, 3 is 70 to 80, 4 is at most 70
73
neostigmine dose for succ sleep apnea in atypical plasma cholinesterase
0.03 mg/kg at most for phase 2 block only
74
effect of atypical pseudocholinesterase in pts.
usual phase 1 block can lead to phase 2 block.
75
precurarization dosage for a nondepolarizing agent
10% of the ED95 (2.5% to 5% of Intubation) , given about 3-5 minutes prior to succinylcholine.
76
Precuraization purpose
the increase in intragastric pressure due to fasciculations can reach levels as high as 40 cmH2O, which may lead to aspiration of gastric contents; precuraization reduces this. But will need to increase from 1.0 mg/kg to 1.5mg/kg of succ
77
ED 95 of NNMBD define
the dose that causes 95% twitch suppression in 50% of the population.
78
10% of intubating dose effect
Will lead to dyspnea and the dose that causes 95% twitch suppression in 50% of the population.
79
succ relation to peds strabismus
Increased risk of masseter ridigidty syndrome
80
ACGE-I Blocking Pairing Neo Edrophonium Pyridostigmine
81
82
Twitch Monitoring Table
83

Pharmacology (21 decks)

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