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Pharmacology > NMBD Special > Flashcards

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
Q

Speed of Onset Muscles

A
  1. Larynx (fastest onset)
  2. diaphgram
  3. orbicularis oculi
  4. adductor Pollicis
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26
Q

Fastest Recovery

A
  1. Larynx (fast recovery)
  2. Orbicularis Oculi = Diaphgram
  3. Adductor Pollis
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27
Q

Sugammadex: MOA

A

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.

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28
Q

Cholesterase Inhibitor MOA:

A
  1. Inhibits ACHe -> inc ACh in NMJ
  2. overcoming comp inhibition
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29
Q

Cholinestaerase Inhib Warning

A

Recurarization: Increased weakness due to lasting effect of NMBD

(Tip: check duration of NMBD and reverse agent)

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30
Q

Sugammadex
Benefits; AE

A

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)

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31
Q

Most Reliable NBMD Montior; TOF >0.9

A

Theoretically: Peripheral Nerve Stim (TOF at CN7>Ulnar)

Threshold for TOF to paralyze: 90

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32
Q

TOF 2 HZ x4
Two burst of 3 separated by 750 msec ( preserved as two sep twitches)

5 secs of 50 Hz (response fades)

A
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33
Q

Test for TOF <0.3; Dobule Burst

Test for TOF>0.7; Tetanus

A
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34
Q
A
35
Q

Prolong ScH Causes

A

genetic defect of PCE, Dx via dibucaine,

Liver Dz (less pce),

Drugs, organophosphate poisoning,

Excessive dose/Phase 2 blocks,

Hypothermia

36
Q

Alerted Pseudocholinesterase- Dibucaine #

A

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
Q

Depolarizing Muscle Relaxant MOA

A

Binds to Nicotinic Receptor and Remain Depolarized with CHannel opening -> Postjunctional unable to respond to subsequent release (desentiization of receptor)

38
Q

TOF vs TOFC

A

TOF: 4 x 2hz no less than 10 sec apart; Calc Amp of Response 4th /1st

TOFC: COunts Evoked Responses
1Count:

39
Q

Tetanus vs PTC

A

Tetanus: stim 30Hz x 5 seconds

PTC: Tetanus + ST Stimuli at 1hz x 20 secs
Used if TOFC is 0

40
Q

Double Burst Stimulation

A

2 mini tetanic burst 0.75 secs apart
(less painful)??

41
Q

Succ Phase 2 block

A

Post Junctional Membrane potential moves back to normal despite continued activation of ach (due to inc na/k pump). Desensitization of the receptor

42
Q

Chemical Subtype of nond- NMBD and Elimination of each

A

Steroidal: Pancuronium; Vecuronium; Rocuronium
Hepatic +/- Renal Elimination

Benzylisoquinolinium: Atracurium; Cisatricurium
Hoffman Elimination

43
Q

Nondepol NMBD relation between Onset and Duration

A

Longer Onset correlates with Longer duration

44
Q
A
45
Q

Acquired Factors affecting Dibucaine

A

Increase PseudoCHE: Obesity, ETOH abuse

Decrease: PseudoCHE: 75% preggers; 57% postpartum

Inhibited PseudoCHE: Organophosphate (insecticide)

46
Q

Congential Myopathy and NMBD

A

NonDepol: Needs more dose (too effective)
Depolarization: Risk of MH

47
Q

Effect of Lambert Eaton?? and MG

A

MG: Less effective Receptors. -> Succ less effective (more dose)
Nondepol: More effective (need less dose)

48
Q

Factors that Upregulate receptors
Effect on nondepolarizing and Depolarizing

A

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
Q

Neostigmine vs Pyrdrostigmine site of interaction

A

Neostigmine: Peripheral NS only
Pydriostigmine: Crosses BBB; (CNS also)

50
Q

Mivacurium Metabolism

A

Pseudochholinesterase

51
Q

Neostigmien then Succ effect

A

Prolong Duration of phase I blockade (30 min)

52
Q

Phase 2 block of succ

A

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
Q

Combination of NMBD effects

A

Synergistic Effect. Cis + Roc; Additive Effects Cis+atra

54
Q

Combination of Succ + NMBD

A

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
Q

Reglan + NMBD

A

Inhibitory effect on plasma cholinesterase: Prolong Duration of Succ and Mivacurium.

56
Q

MC Variants of Pseudocholinesterase Deficiency

A

A, and K variants

57
Q

double succ effects

A

small then large will decrease fasiculation but not myalgia incidence

58
Q

decrease succ myalgia factors

A

pre succ, lidocaine, periop vit c, ca.

59
Q

physiostigmine severe AE

A

sz esp eith nicotinic receptor agonists (varenicline)

60
Q

RF of allergy to NMBD

A

Cosmetic (or toothpaste, detergents, shampoo) to Aminosteroid

61
Q

Trisomy 21 Effecton NMBD

A

Less requirement due to hypotonia

62
Q

Succ with pretreatment of NDNB affect most but what AE

A

tachy/brady (former 2/2 catecholamine); IOP inc.

63
Q

Myasthenia Gravis vs Syndrome Meds concerns

A

MG: insensitive to Succ; MS: insensitive to neostigmine

64
Q

Muscle relaxant potentiation via inhalants

A

desflurane > sevoflurane > isoflurane > halothane > TIVA

65
Q

Neostigmine AE that is not blocked by antimuscularinic

A

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
Q

Elderly Considerations in NMBD

A

Prolong onset, Longer Duration, Less requirement for nmbd.

67
Q

Termination of Succ

A

Diffusion from NMJ

68
Q

Concerns of Succ with Infants

A

possibility of hyperkalemia 2/2 undiagonsed muscular dystrophy.

69
Q

effect on TOF ratio on chronically paralyzed limb

A

TOF ratio increases due to less weaker effect of nondepol on limb due to extracellular ach junction

70
Q

MC effect of succ on peds

A

bradyc esp up to 1 yo

71
Q

peds vs adult pseudocholinesterase and clinical effect

A

only 0.5 of adult levels, no clinical effect.

72
Q

TOFC relation to percentage of blocked receptors

A

0 is 100%, 1 is 90; 2 is 80, 3 is 70 to 80, 4 is at most 70

73
Q

neostigmine dose for succ sleep apnea in atypical plasma cholinesterase

A

0.03 mg/kg at most for phase 2 block only

74
Q

effect of atypical pseudocholinesterase in pts.

A

usual phase 1 block can lead to phase 2 block.

75
Q

precurarization dosage for a nondepolarizing agent

A

10% of the ED95 (2.5% to 5% of Intubation) , given about 3-5 minutes prior to succinylcholine.

76
Q

Precuraization purpose

A

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
Q

ED 95 of NNMBD define

A

the dose that causes 95% twitch suppression in 50% of the population.

78
Q

10% of intubating dose effect

A

Will lead to dyspnea and the dose that causes 95% twitch suppression in 50% of the population.

79
Q

succ relation to peds strabismus

A

Increased risk of masseter ridigidty syndrome

80
Q

ACGE-I Blocking Pairing

Neo
Edrophonium
Pyridostigmine

A
81
Q
A
82
Q

Twitch Monitoring Table

A
83
Q
A

Pharmacology (21 decks)

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