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Pharmacology > Neuromuscular Physiology and Pharmacology > Flashcards

Neuromuscular Physiology and Pharmacology Flashcards

1
Q

Depolarizing Muscle Relaxant

A

Succinylcholine, Mimics the action of ACh

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2
Q

Depolarizing Muscle Relaxant

A

Succinylcholine, Mimics the action of ACh

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3
Q

Succinylcholine Metabolism

A

Hydrolyzed by plasma cholinesterase
• AKA pseudocholinesterase or butyrocholinesterase – not present in the NMJ, drug must be cleared from
plasma

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4
Q

NM ‘blockade’ occurs because…(DMR, Sux)

A

the depolarized post‐junctional membrane cannot respond to additional agonist (Ion flux is an important consideration)

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5
Q

Clearance from the junctional cleft occurs by…(DMR, Sux)

A

diffusion (Sux molecules can repeatedly bind to receptors until the diffuse away from the NMJ)

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6
Q

Desensitization

A

Occurs when agonists bind to α subunits but do not cause a conformational change to open the Na+ pore (These receptors are unable to transmit the chemical signal to the muscle membrane)

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7
Q

Closed channel blockade

A

Drug reacts around the mouth of the channel and prevents passage of ions
– Seen with cocaine, some antibiotics, quinidine, etc.

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8
Q

Open channel blockade

A

Drug enters an open channel but does not pass all the way through (“gets stuck”)
– Impedes the flow of ions – Ex. NDMRs in large doses

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9
Q

Extrajunctional Receptors (number)

A

Normally not present in large numbers
– Synthesis is suppressed by normal neural activity
• May proliferate if normal neural activity is decreased
– Trauma,sepsis,prolongedbedrest,burninjury,spinalcordinjury,etc.

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10
Q

Extrajunctional Receptors (Differ from nAChRs)

A

-change in the epsilon
subunit—structurally different from nAChRs
-stay open longer (AllowlargeramountsofK+effluxafteradministrationofDMR • Hyperkalemic arrest is well documented after SCh adm)
-Spread across the entire muscle membrane (not just at the NMJ)

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11
Q

Succinylcholine Metabolism

A

Hydrolyzed by plasma cholinesterase
• AKA pseudocholinesterase or butyrocholinesterase – not present in the NMJ, drug must be cleared from
plasma

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12
Q

Succinylcholine (activity termination)

A

Activity is terminated by diffusion of the drug away from the NMJ

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13
Q

NM ‘blockade’ occurs because…(DMR, Sux)

A

the depolarized post‐junctional membrane cannot respond to additional agonist (Ion flux is an important consideration)

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14
Q

Clearance from the junctional cleft occurs by…(DMR, Sux)

A

diffusion (Sux molecules can repeatedly bind to receptors until the diffuse away from the NMJ)…sustained opening

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15
Q

Desinsitization

A

Occurs when agonists bind to α subunits but do not cause a conformational change to open the Na+ pore (These receptors are unable to transmit the chemical signal to the muscle membrane)

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16
Q

Closed channel blockade

A

Drug reacts around the mouth of the channel and prevents passage of ions
– Seen with cocaine, some antibiotics, quinidine, etc.

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17
Q

Open channel blockade

A

Drug enters an open channel but does not pass all the way through (“gets stuck”)
– Impedes the flow of ions – Ex. NDMRs in large doses

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18
Q

Extrajunctional Receptors (number)

A

Normally not present in large numbers
– Synthesis is suppressed by normal neural activity
• May proliferate if normal neural activity is decreased
– Trauma,sepsis,prolongedbedrest,burninjury,spinalcordinjury,etc.

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19
Q

Extrajunctional Receptors (Differ from nAChRs)

A

-change in the epsilon
subunit—structurally different from nAChRs
-stay open longer (AllowlargeramountsofK+effluxafteradministrationofDMR • Hyperkalemic arrest is well documented after SCh adm)
-Spread across the entire muscle membrane (not just at the NMJ)

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20
Q

Extrajunctional Receptors (agonist/antagonists)

A

Highly sensitive to agonists, but less sensitive (resistant) to antagonists

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21
Q

Prejunctional Receptors

A

nAChRs on prejunctional membranes

• Believed to regulate release of ACh from presynaptic membrane

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22
Q

Stimulation of Prejunctional Receptors

A

inhibits release of ACh from presynaptic
membrane
– May stimulate production of more ACh in the nerve terminal

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23
Q

nAChRs vs. mAChRs

A

All cholinergic receptors are responsive to acetylcholine

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24
Q

Nicotinic receptors are located…

A

-At the synapse betw preganglionic and postganglionic
parasympathetic nerves
-At the synapse betw preganglionic and postganglionic sympathetic nerves
-At the NMJ

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25
Q

Muscarinic receptors are located…

A

At the synapse betw postganglionic parasympathetic nerves and the end organ/tissue

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26
Q

Drugs which have affinity for cholinergic receptors may produce effects at….

A

mAChRs or nAChRs… or both ( This explains many of the side effects of many NDMRs and DMR outside the NMJ
• E.g., autonomic side effects)

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27
Q

primary pharmacologic effect of NMBAs is to…

A

interrupt transmission of nerve impulses at the NMJ (NMDR or DMR)

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28
Q

All NMBAs…

A
  • Contain quaternary ammonium groups
  • Limited Vd
  • Do not cross the BBB
  • Do not cross the placenta
  • No CNS effects
  • Oral administration not effective
  • Minimal renal reabsorption
  • Ionized Water-soluble, Limited lipid solubility
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29
Q

NMBA P‐kinetics: Vd and E 1/2T influences by…

A

Age,

Hepatic or renal disease

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30
Q

NMBA Vd

A

Generally, NMBAs have a Vd that is equivalent to the extracellular compartment (~14L) (not highly protein bound)

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31
Q

NDMR (effect)

A

Antagonize the effects of ACh

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32
Q

NMDR Long Acting

A

Pancuronium, Pipecuronium, Doxacurium

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33
Q

NMDR Intermediate Acting

A

Atracurium, Rocuronium, Vecuronium, Cisatracurium

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34
Q

NMDR Short Acting

A

Mivacurium

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35
Q

NMBA and Volatile Anesthetics (halothane, des, iso, sevo) PK

A

Do not directly alter the p‐kinetics of NMBAs

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36
Q

NMDR and Volatile Anesthetics (halothane, des, iso, sevo) PD

A

NDMRs are enhanced via pharmacodynamic action of VA
• Volatile anesthetics potentiate the effects of NDMRs via Ca++ channels
• Decreased dosing required for NDMRs in the presence of VAs

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37
Q

Clinical Uses NMBA

A

– Facilitate tracheal intubation
– Enhance surgical conditions
– Decrease oxygen utilization in critically ill patients who have limited reserve
– Treat laryngospasm (suxtiny dose!)
– Treat truncal rigidity associated with large doses of opioids

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38
Q

ED95

A

– The dose necessary to produce 95% suppression of a single twitch in response to peripheral nerve stimulator
– 2xED95 for NDMRs is the recommended dose to facilitate tracheal intubation (intubating dose)
• 90% depression is adequate for surgical relaxation

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39
Q

Choice of relaxant is determined based on…(4 things)

A

– Speed of onset
– Duration of action
– Side effect profile of the drug
– Patient’s health history

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40
Q

Inadequate return of function (residual paralysis)

A
  • Difficulty focusing/diplopia
  • Inability to swallow/dysphagia • Unable to protect airway
  • Ptosis
  • Weakness of mandibular muscles
  • Low VT (hypoxia)
  • floppy
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41
Q

All NMBAs (structure)

A 
– Are structurally similar to ACh
– Are compounds that have at least one N which binds to the α subunit of the AChR
• Quaternary ammonium group
– Are ionized
– Have Vd similar to Extracellular Fluid
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42
Q

cause the majority of anaphylactic reactions during anesthesia

A

NMBAs…The biggest offenders are Succinylcholine and Rocuronium

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43
Q

Benzylisoquinoliniums (NDMR classification)

A
  • Atracurium
  • Cisatracurium
  • Mivacurium

More likely to evoke histamine release d/t tertiary amine

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44
Q

Aminosteroids (NDMR classification)

A
  • Pancuronium • Vecuronium
  • Rocuronium

Do not possess any hormonal activity

45
Q

Electrostatic attraction between AChRs(‐) and NH4+ groups

A

Occurs at all cholinergic sites including cardiac mAChRs and autonomic ganglion nAChRs which may cause cardiac side effects

46
Q

the length of the carbon chain separating the + ammonium groups influences the degree of CV effects (structure/activity relationship)

A

-Longer chains are more specific to the nAChRs of the NMJ
– Maximal autonomic blockade when NH4+ groups are
separated by 6 Cs (hexamethonium)
– NM blockade is maximal when 10 Cs are present (decamethonium)

47
Q

Succinylcholine chloride (intubation dose)

A

– 1‐1.5 mg/kg
• General dosing for tracheal intubation
• 1.5 mg/kg is the dose for rapid sequence intubation

48
Q

Sux MOA

A

• Attaches to one or both α subunits of the nAChR where it mimics the actions of ACh
• Hydrolysis by pseudocholinesterase in the plasma is slow
– Depolarization is sustained and the depolarized membrane/receptors cannot respond to additional agonist
• This is referred to as Phase I blockade
• Fasciculations occur due to sustained depolarization

49
Q

Sux and K

A

• Sustained depolarization is associated with leakage of K+ from the muscle cell
– plasma K+ increases 0.5 mEq/L (nrl response)

50
Q

Sux Overdose

A

• A single large dose, repeated doses, or an infusion may cause postjunctional membranes to respond abnormally to ACh (overdose)
– Mechanism for this is unclear
• May be due to desensitization, ion channel blockade, or entry of Sux into skeletal muscle cytoplasm. Blockade characteristics change to Phase II Blockade

51
Q

Phase I Blockade with SCh

A
  • Decreased contractile force in response to a single twitch
  • Sustained tetany with decreased amplitude
  • TOF ratio >0.7 (~1.0)
  • No Post Tetanic Facilitation
  • Fasciculations
  • Augmentation after admin anticholinesterase
52
Q

Phase II Blockade with SCh

A
  • Decreased contractile force in response to a single twitch
  • Decreased amplitude and tetanic fade to sustained stimulus
  • TOF ratio <0.7
  • No fasciculations
  • Can be antagonized by anticholinesterase
  • Abrupt onset manifests as tachyphylaxis and increased dose requirements
53
Q

Sux—Phase II (te)

A

Tetanic stimulation before & after administration of a LARGE dose of Sux is similar to the normal response to a NDMR
POST TETANIC FACILITATION

54
Q

Sux—Phase I (te)

A

Tetanic stimulation before and after administration of an DMR

NO POST TETANIC FACILITATION

55
Q

Post Junctional Receptor Agonists

A

ACh, Sux (depolarizing)

56
Q

Post Junctional Receptor Antagonists

A

NDMRs (non-depolarizing)

57
Q

cholinesterase inhibitors

A

inhibit acetylcholinesterase enzyme activity (reverse NDMR, prolong Sux)

58
Q

fade

A

nondepolarizing block (d/t decrease in ACH from prejunctional receptors) OR phase II block Sux

59
Q

parasympathetic (ganglionic fibers)

A

long pre-ganglionic fiber, short post-ganglionic fiber

60
Q

sympathetic (ganglionic fibers)

A

short pre-ganglionic fiber, short post-ganglionic fiber

61
Q

Sux metabolized by _____________ to produce ____________ and ______________.

A
  • plasma cholinesterase

- succinylmonocholine and choline (succinic acid and choline)

62
Q

plasma cholinesterase in sysnthesized by the….

A

liver

63
Q

Sux duration of action is prolonged d/t…

A
  • decreased synthesis of plasma cholinesterase, drug induced inhibition of the enzyme, atypical plasma cholinesterase
  • <75% normal serum levels necessary to prolong plamsa cholinesterase
64
Q

Atypical Plasma Cholinesterase

A

• Often discovered after administration of SCh produces prolonged effect
• Several variants of the enzyme exist
– Dibucaine‐related variants are most clinically
important
– Dibucaine “test” permits diagnosis of atypical plasma cholinesterase

65
Q

Dibucaine

A

• Anamidelocal anesthetic
Dibucaine # 80
Significance
• Inhibitstheactivityof normal plasma cholinesterase by approximately 80%
Confirms normal plasma cholinesterase enzyme
• Inhibitstheactivityof atypical plasma cholinesterase by ~20%

  • 80: Confirms normal plasma cholinesterase enzyme
  • 40-60: Indicates heterozygous for atypical plasma cholinesterase (1:480). Modest increase in DOA
  • 20: Indicates homozygous for atypical plasma cholinesterase (1:3200). NMB may last hours
66
Q

resistance to SCh may be seen in patients with…

A

Myasthenia Gravis…d/t decrease in functional nAChRs

67
Q

Sux AE (histamine)

A
  • histamine release (large, rapid dose)

- face/trunchal flushing, bronchospasm, reduction in blood pressure, anaphylaxis/anaphylactoid reactions

68
Q

Sux AE (cardiac dysrhythmias)

A

– Sinus bradycardia, junctional rhythm, and sinus arrest have been observed
• Due to stimulation of cardiac postganglionic mAChRs
• More common after a second dose of Sux is
administered soon after the first or in pediatric pop
• Pretreatment with a NDMR or atropine decreases the incidence
– Increases in HR and BP may occur
• Reflect activity at sympathetic ganglia

69
Q

Sux AE (hyperkalemia)

A

– Occurs reliably in patients with
• Muscular dystrophy, 3rd degree burns, denervation injurymuscle atrophy, trauma, sepsis, upper motor neuron lesions, prolonged bed rest/mechanical ventilation…
– Due to proliferation of extrajunctional receptors
– Cardiac arrest may occur
– Pretreatment with NDMR does not protect against hyperK+ and related sequelae
– Using a smaller dose of Sux DOES NOT attenuate hyperkalemic response.

70
Q

Sux AE (myalgia)

A

• Myalgia
– Esp. neck, back, abdomen, pharynx
– Apparently due to fasciculations
– Young, healthy, athletic more susceptible
– Pretreatment with a NDMR (a defasciculating dose) can reduce the severity
– May be treated with NSAIDS (if approp) – IV NSAID (ketorolac)

71
Q

Sux AE (IOP)

A

• Increased IOP
– Onset: 2‐4 min after administration – Duration: 5‐10 min
– Unknown mechanism
– Theoretical basis
• Some avoid sux in patients with open globe injury to prevent extrusion of ocular contents

72
Q

Suz AE (ICP)

A

• Increased ICP

– Not a consistent observation

73
Q

Sux AE (intragastric pressure)

A

• Increased intragastric pressure
– Possible risk of aspiration
– Probably due to fasciculations and abdominal
muscle contraction
– May be prevented by defasciculating doses of NDMRs

74
Q

Sux AE (sustained muscle contraction)

A

• Sustained muscle contraction
– Esp. masseter muscle (Trismus) • Common in children
• Sux is NOT recommended in peds
– Must be differentiated from Malignant Hyperthermia

75
Q

Sux AE (malignant hyperthermia)

A

• Malignant Hyperthermia
– Rare, life‐threatening Autosomal Dominant pharmacogenetic disorder involving defective ryanodine receptors which control release of Ca++ in the sarcoplasmic reticulumhypermetabolism
– Often discovered after administration of a trigger (Sux or volatile anesthesics)
– Manifests as muscle rigidity, hyperpyrexia, hypermetabolism and 02 consumption, hypercarbia, tachycardia, metabolic acidosis, rhabdomyolysis
– Prompt diagnosis and treatment with dantrolene decreases mortality significantly

76
Q

NDMRs (MOA)

A

– Bind to nAChRs in the NMJ without causing activation of the ion channel. Compete with ACh at the α subunits. Hi doses can cause channel blockade
– 70% receptor occupation does not produce evidence of NM blockade by single twitch
– 80‐90% receptor occupation required to interrupt transmission of the chemical signal
-steep dose response curve

77
Q

Characteristics of NDMR blockade

A 
– Decreased twitch to single stimulus
– Tetanic fade
– TOF ratio < 0.7
– Post‐tetanic facilitation TOF TOF – Potentiation of other NDMRs
– Antagonism by anticholinesterase drugs
-resembles phase II
78
Q

NMDR SE (CV)

A

CV effects related to
– Histamine, prostacyclin release
– Antagonism of muscarinic receptors and/or nicotinic receptors in the ANS

79
Q

Autonomic Margin of Safety

A

the difference between the required dose for NM blockade and the dose for circulatory effects

  • pancuronium has very narrow autonomic margin of safety
  • Vec, roc, and cis have much wider autonomic margins of safety
80
Q

NMDR interactions (VA)

A

• Volatile anesthetics (not nitrous)
– Cause dose‐dependent potentiation of NDMRs (not sux)
• Iso=Des=Sevo>Halo>N2O(none)
• Long‐acting > intermediate‐acting
• Perhaps due to VA interaction with Ca++ channelsdecreased sensitivity of post junctional membrane to depolarization
– Pharmacodynamic, not p‐kinetic interaction

81
Q

NMDR interactions (drugs…)

A 
• Antibiotics
– Aminoglycosides enhance NDMRs (& DMR)
• May decrease prejunctional release of ACh by competing with
Ca++
• Local Anesthetics enhance NDMRs(&DMR)
• Antidysrhythmics enhance NDMRs (&DMR)
• Diuretics enhance NDMRs
– Furosemide inhibits cAMP↓ACh output
• Magnesium enhances NDMRs (esp.vec) (hypermagnesia- competes with calcium at the motor end plate) 
• Lithium enhances NDMRs (&DMR)
• Phenytoin decreases NDMR effect
• Cyclosporin prolongs NDMRs
• Ganglionic blockers delay onset and prolong DOA of NDMRs
• Hypothermia enhances NDMRs
• Increased K+enhances DMR, causes
resistance to NDMRs
• Decreased K+resistance to DMRs and enhances NDMRs

82
Q

NMDR interactions (injury)

A
  • Thermal injury resistance to NDMRs after 10 days (not r/t prolif of ejrs)
  • Paresis/hemiplegia resistance to NDMRs on the affected side
83
Q

NMDR and NMDR interaction

A
  • Some NDMRs have synergistic effects with other NDMRs
  • Panc + dTC or metocurine
  • Vec + dTC
  • Males are less sensitive to NDMRs than women – Women require 22% less vec than men!
  • d/t mucsle mass
84
Q

Pancuronium Bromide (structure)

A

• Long‐acting,bisquaternaryaminosteroid

85
Q

Pancuronium Bromide DOA

A

60-90min (long) – Prolonged with renal dz, cirrhosis, biliary obstr, aging

86
Q

Pancuronium Bromide Metabolism/Elimination

A

• Renalelimination(80%unΔinurine) • Hepaticdeacetylation(10‐40%)
– 3‐desacetylpancuronium is 50% as potent as panc • Cumulative effects may occur with repeat dosing

87
Q

Pancuronium Bromide CV effects

A

• CV effects
– ↑HR, MAP, CO
• Due to antagonism of cardiac mAChRs (SA node)
• More profound increases with AV conduction abns • Increased myocardial O2 consumption
– Can contribute to ischemia in pts with CAD
• No histamine release
• No ganglionic blockade

88
Q

Intermediate acting NDMR

A

• Efficiently cleared
– Less cumulative effects than long‐acting
• Speed of onset can be hastened by administration of a priming dose
– ~10% of the ED95 prior to induction
– After induction, the balance of the intubating dose is adm
• Onset of intubating conditions is faster • Defasciculating dose (on the other hand)
– ~10% of the ED95 of NDMR prior to induction – However, a larger dose of Sux is required

89
Q

Vecuronium Bromide (structure)

A

intermediate acting, monoquaternary aminosteroid

90
Q

Vecuronium Bromide (metabolism, elimination)

A

• RenalandHepaticelimination
– Deacetylation to 3‐desacetylvecuronium which is 50‐70% as potent as vec
– Prolonged in patients with renal and/or hepatic disease

91
Q

Vercuronium Bromide (facts…)

A

• Does not antagonize mAChRs
• Does not cause mast cell degranulation
• Unstableinsolution
– Supplied as a powderrequires reconstitution
• Cumulative effects (esp. with renal dz) – Panc > Vec > atracurium

92
Q

Vecuronium Bromide (peds, elderly)

A

• Pediatric considerations – Similar potency c/t adults
– More rapid onset in infants – Longer DOA in infants
• Elderly consideration
– Prolonged DOA d/t lower clearance

93
Q

Rocuronium Bromide (structure)

A

Intermediate‐acting monoquaternary aminosteroid

94
Q

Rocuronium Bromide (excretion)

A

• ExcretedunΔinbile
• Renalexcretion(>30%)
– Liver and/or renal dz can prolong effects

95
Q

• The only NDMR which can serve as an alternative to Sux when rapid onset is needed for RSI

A

Rocuronium Bromide….– Quality of relaxation is less than with Sux but still adequate.

96
Q

Rocuronium Bromide SE

A
  • No CV effects
  • No histamine release
  • Highest incidence of anaphylaxis among NMBAs—actually among all drugs used perioperatively!
97
Q

Atracurium Bromide (structure)

A

Intermediate-acting bisquaternary benzylisoquinolinium (mixture of 10 stereoisomers in solution)

98
Q

Atracurium Bromide (metabolism, elimination)

A

• Cleared by Hofmann Elimination & hydrolysis by non‐specific plasma esterases
– Both pathways produce laudanosine
• CNS stimulant
– Increases MAC in animal models
– May be epileptogenic
– Laudanosine cleared renally !

99
Q

Atracurium Bromide (CV effects)

A

• CVeffects
– Rapid administration of >2x ED95 results in ↑HR and ↓BP • Facial and truncal flushing accompany histamine release at 3x ED95

100
Q

Atracurium Bromide (pediatric, elderly considerations)

A 
• Pediatric considerations
– Infants 1‐6 mos, decrease dose by 50% for same effect as
full dose in adults
– Recovery is more rapid in infants
• Elderly considerations
– No change in pharmacokinetics
101
Q

Cisatracurium Bromide (structure)

A

• Intermediate‐acting benzylisoquinolinium
– Purified form of one of the 10 stereoisomers of atracurium

-Similar NM blocking profile to atracurium except slower onset and no histamine release

102
Q

Cisatracurium Bromide (elimination)

A
  • Hofmann elimination at physiologic temp and pH to laudanosine (less than atracurium)
  • No metabolism by nonspecific esterases
  • May be adm to patients with renal/he pdz w/o prolonged effect.
103
Q

Cisatrabromide (CV effects)

A

• CV Effects
Cisatracurium bromide
– No histamine release
– Indistiguishable from the CV effects of vec in patients with CAD

104
Q

Mivacurium (structure)

A

Short‐Acting NDMR—Mivacurium
• BenzylisoquinoliniumNDMR
– Mixture of 2 stereoisomers
– Trans‐trans and cis‐trans are most active and are equipotent
– Cis‐cis is 1/10 as potent as the others

drug no longer available

105
Q

Mivacurium (hydrolysis)

A

• Hydrolyzed by plasma cholinesterase

106
Q

Mivacurium (CV effects)

A

• CV effects
– Minimal at clinically relevant doses
– Rapid administration of 3x ED95 produces
histamine release↓MAP (transiently)

107
Q

Defective receptor is malignant hyperthermia

A

Ryanodine

108
Q

Treatment malignant hyperthermia

A

Dantrolene

Pharmacology (9 decks)

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