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Pharm Fall 2019 > Ex4 NMBA > Flashcards

Ex4 NMBA Flashcards

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1
Q

when nerve potential reaches the nerve terminal, _______ occurs

A

ACh is released into synaptic cleft near nAChRs

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2
Q

ACh is synthesized in nerve terminal from

A

choline + acetyl-coenzyme A

*in the presence of choline acetyltransferase

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3
Q

80% of ACh is stored in

A

synaptic vesicles

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4
Q

20% of ACh is stored in

A

nonvesicular reserve

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5
Q

post junctional receptor agonists

A

ACh

Sux

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6
Q

post junctional receptor antagonits

A

NDMRs

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7
Q

Subunits of post junctional receptors

A

2 alpha
1 beta
1 epsilon
1 delta

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8
Q

depolarizing muscle relaxant

A

Succinylcholine

nAChR agonist

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9
Q

nAChR antagonist

A

NMDRs

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10
Q

receptor activation occurs when

A

both alpha subunits are occupied by (2) agonists

  • 1ACh + 1 Sux
  • 2ACh
  • 2Sux
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11
Q

1 NMDR + 1 ACh
or
1NDMR + 1 Sux

A

won’t open channel at receptor site

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12
Q

NDMRs work by

A

prevent depolarization of skeletal muscle by binding to 1 or both alpha units

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13
Q

NMDRs may also block

A

an open receptor pore

*especially after a large dose

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14
Q

After NDMRs bind to site, ____ occurs

A
  • ACh competitively inhibited, opening of receptor pore does not occur
  • muscle cell does not depolarize
  • no ion influx
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15
Q

NDMRs are competitive inhibitors of ______ at _______

A

acetylcholine at alpha subunit of presynaptic Nn receptor

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16
Q

depolarizing muscle relaxant

A

succinylcholine

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17
Q

succinylcholine mimics the action of ____

A

ACh

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18
Q

Succinylcholine is hydrolyzed by

A

plasma cholinesterase

**NOT AChEase

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19
Q

Succinylcholine must be terminated in the _____

A

plasma

*plasma cholinesterase is not present in NMJ

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20
Q

Activity of sux must be terminated by ____ of drug

A

diffusion of drug away from NMJ

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21
Q

NM blockade from Sux occurs because

A

the depolarized post-junctional membrane cannot respond to additional agonist

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22
Q

closed channel blockade

A

drug reacts around mouth of channel and prevents passage of ions
*ie cocaine, antbx, quinidine

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23
Q

open channel blockade

A

drug enters an open channel but does not pass all the way thru “gets stuck” - impedes flow of ions
*ie NDMRs in large doses

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24
Q

extrajunctional receptors

A
  • normally not present in large numbers (synthesis suppressed by normal neural activity)
  • may proliferate if normal neural activity is decreased (sepsis, prolonged bedrest)
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25
extrajunctional receptors differ from nAChRrs
- change in the epsilon subunit - structurally different from nAChRs - stay open longer (allow larger amounts of K+ efflux after administration of DMR)
26
Risk of extrajunctional receptors after SCh administration
hyperkalemic arrest
27
prejunctional membranes
- nAChRs | - regulate release of ACh from presynaptic membrane
28
stimulation of prejunctional receptors results in
- inhibits release of ACh from presynaptic membrane | - may stimulate production of more ACh in nerve terminal
29
effect of NDMRs on prejunctional membranes
- antagonize pre-JRs - inhibit ACh production - -explains tetanic fade after NDMR (ACh depletion)
30
tetanic stimulation before and after administration of NDMR
post-tetanic facilitation
31
tetanic stimulation before and after administration of DMR
NO post-tetanic facilitation
32
All NMBAs contain
quaternary ammonium group (NH4+)
33
All NMBAs are _____ soluble
ionized, water soluble, limited lipid solubility
34
NMBAs characteristics
- limited Vd - do not cross BBB - PO not effective - do not cross placenta - no CNS effects - minimal renal reabsorption
35
NMBA P-kinetics
- Not highly protein bound | - influenced by age, hepatic/renal dx
36
NMBAs have a Vd that is equivalent to
Extracellular compartment (~14L)
37
NMBAs + volatile anesthetics
- do not directly alter p-kinetics | - NDMRs are enhanced via pharmacodymanic actions of VAs
38
volatile anesthetics ______ the effects of NDMRs via _____
1. potentiate | 2. Ca2+ channels
39
______ dosage required for NDMRs in presence of VAs
decreased
40
ED95
dose necessary to produce 95% suppression of a single twitch in response to peripheral nerve stimulator
41
recommended dose to facilitate tracheal intubation (intubating dose)
2 x ED95
42
________ depression is adequate for surgical relaxation
90%
43
standard of care - degree of NM blockade is evaluated by
monitoring the evoked response to electrical stimulation using a peripheral nerve stimulator (PNS)
44
Residual paralysis
inadequate return of function - difficulty focusing/diplopia - *inability to swallow/dysphagia (unable to protect airway) - ptosis - weakness of mandibular muscles - low VT (hypoxia) - "floppy"
45
NMBAs lack ______ effects
CNS/analgesic
46
NMBAs are all structurally similar to
ACh
47
which portion of the NMBA binds to the alpha subunit of the AChR?
N (from quaternary ammonium group)
48
NMBAs cause the majority of ______ during anesthesia
anaphylactic reactions
49
most likely to evoke histamine release
benzylisoquinoliniums - d/t tertiary amine atracurium cisatracurium mivacurium
50
benzylisoquinoliniums all end in
"urium"
51
aminosteroids all end in
"curonium"
52
Succinylcholine chloride ED95
0.25-0.5 mg/kg
53
Sux onset
rapid 30-60s
54
Sux DOA
Short: 5-10 minutes
55
Sux: general dosage for tracheal intubation
1-1.5mg/kg
56
Sux: dosage for RSI
1.5mg/kg
57
depolarization is sustained, the depolarized membrane/receptors cannot respond to additional agonist
Sux: Phase I blockade
58
Fasciculations occur due to
sustained depolarization
59
Sux - sustained depolarization is associated with
leakage of K+ from muscle cell
60
approximate plasma K+ plasma increase d/t Sux
0.5 mEq/L
61
overdose to Sux is d/t
- single large dose - repeated doses - infusion * leads to postjunctional membranes responding abnormally
62
OD to Sux results in
characteristics change to Phase II Blockade
63
Phase I Blockade - Sux
- Decreased contractile force in response to single twitch - sustained tetany w/ decreased amplitude - TOF ratio >0.7 (~1.0) - no post tetanic facillitation - fasciculations - augmentation after admin anticholinesterase
64
Phase II Blockade - Sux
- Decreased contractile force in response to single twitch - decreased amplitude/tetanic fade to sustained stimulus - TOF ratio<0.7 - no fasciculations - can be antagonized by anticholinesterase - abrupt onset manifests as tachyphylaxis/increased dose reqmts
65
Which phase of Sux resembles characteristics of NDMRs?
Phase II
66
Sux Phase II Characteristics
Post tetanic facilitation
67
Sux Phase I characteristics
NO post tetanic facilitation
68
Biggest offenders of anaphylactic rxn during anesthesia
Sux, Roc
69
NMBAs Vd
similar to ECF
70
NMBAs: ionized or nonionized
ionized
71
aminosteroids
pancuronium vecuronium rocuronium
72
benzylisoquinoliniums
atracurium cisatracurium mivacurium
73
Which Rx do not possess any hormonal activity?
Aminosteroids pancuronium vecuronium rocuronium
74
How is Sux metabolized?
hydrolyzed via pseudocholinesterase in plasma | -slow
75
TOF ratio
TOF last twitch/first twitch
76
TOF graph - which will produce 4 twitches at equal height?
Sux
77
TOF graph - which will produce 4 twitches at sequentially smaller heights?
NDMR
78
Sux hydrolyzed into
succinylmonocholine + choline
79
termination of action of sux d/t
diffusion of drug away from site of action
80
plasma cholinesterase is sythesized by
liver
81
sux DOA may be prolonged d/t
-decreased synthesis of enzyme -Rx induced dec. of enzyme -atypical plasma cholinesterase < 75% norm serum levels necessary to prolong plasma cholinesterase
82
atypical plasma cholinesterase
-dibucaine test
83
dibucaine # that confirms normal plasma cholinesterase
80
84
dibucaine # that indicates NMB lasting hours
20
85
Resistance to Sux in which patients
myasthenia gravis d/t decreased fxnal nAChRs
86
NMBA w/ greatest histamine release
Sux
87
Large/Rapid dose of Sux may result in
face/truncal flushing *bronchospasm decreased bp/anaphylaxis rxns
88
Cardiac AE to Sux
- cardiac dysrhythmias (sinus brady, junctional, sinus arrest) - increased HR/BP
89
AEs to Sux
- HyperK - Myalgia - increased intragastric pressure (risk for aspiration)
90
MH is d/t
ryanodine receptors = defective
91
MH manifests
rigidity, hyperpyrexia, hypermetabolism/O2 consumption, hypercarbia, tachycardia, metabolic acidosis, rhabdomyolysis
92
MH Tx
dantrolene
93
MOA NDMRs
-competitive antagonist at nAChRs in NMJ
94
high doses of NDMRs can cause
channel blockade
95
receptor occupation required to interrupt transmission of signal
80-90%
96
80% receptors occupied
VT 5mL/kg
97
70% receptors occupied
TOF = no fade | VC at least 20 mL/kg
98
60% receptors occupied
Sustained tetany = no fade | DBS = no fade
99
50% receptors occupied
Head Lift - 180 degrees, 5s | Hand grip - sustained 5s
100
Characteristics of NDMR blockade
``` Decreased twitch to single stimulus tetanic fade TOF ratio < 0.7 post-tetanic facilitation potentiation of other NDMRs ```
101
NDMRs are antagonized by
anticholinesterase drugs
102
difference between required dose for NM blockade and dose for circulatory effects
autonomic margin of safety
103
very narrow autonomic margin of safety
pancuronium
104
wider autonomic margins of safety
vec, roc, cis
105
NDMR Rx intxn: VAs
dose dependent potentiation | biggest = Des
106
NDMR Rx intxn: antibiotics
aminoglycosides: enhance NDMRs+DMRs | may be via decr. prejunctional release of ACh by competing w/ Ca++
107
NDMR/DMR Rx intxn: enhances
``` local anesthetics antidysrhythmics lithium not Sux: diuretics magnesium hypothermia cyclosporin ```
108
NDMR Rx intxn: decreases
phenytoin
109
increased K+ effects NDMR/DMR how?
Increased K+ --> enhances DMR, resistance to NDMR
110
decreased K+ effects NDMR/DMR how?
decreased K+ --> enhances NDMR, resistance to DMR
111
Resistance to NDMRs
``` Thermal injury (10 days) paresis/hemiplegia (affected side) ```
112
males are _____ sensitive to NDMRs than women
less
113
women require _______ than men
22% less vec

Pharm Fall 2019 (33 decks)

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