Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm Fall 2019 > Ex4 NMBA > Flashcards

Ex4 NMBA Flashcards

1
Q

when nerve potential reaches the nerve terminal, _______ occurs

A

ACh is released into synaptic cleft near nAChRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACh is synthesized in nerve terminal from

A

choline + acetyl-coenzyme A

*in the presence of choline acetyltransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

80% of ACh is stored in

A

synaptic vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

20% of ACh is stored in

A

nonvesicular reserve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

post junctional receptor agonists

A

ACh

Sux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

post junctional receptor antagonits

A

NDMRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Subunits of post junctional receptors

A

2 alpha
1 beta
1 epsilon
1 delta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

depolarizing muscle relaxant

A

Succinylcholine

nAChR agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

nAChR antagonist

A

NMDRs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

receptor activation occurs when

A

both alpha subunits are occupied by (2) agonists

  • 1ACh + 1 Sux
  • 2ACh
  • 2Sux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

1 NMDR + 1 ACh
or
1NDMR + 1 Sux

A

won’t open channel at receptor site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

NDMRs work by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NMDRs may also block

A

an open receptor pore

*especially after a large dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

NDMRs are competitive inhibitors of ______ at _______

A

acetylcholine at alpha subunit of presynaptic Nn receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

depolarizing muscle relaxant

A

succinylcholine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

succinylcholine mimics the action of ____

A

ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Succinylcholine is hydrolyzed by

A

plasma cholinesterase

**NOT AChEase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Succinylcholine must be terminated in the _____

A

plasma

*plasma cholinesterase is not present in NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Activity of sux must be terminated by ____ of drug

A

diffusion of drug away from NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

NM blockade from Sux occurs because

A

the depolarized post-junctional membrane cannot respond to additional agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

closed channel blockade

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

extrajunctional receptors differ from nAChRrs

A
  • change in the epsilon subunit - structurally different from nAChRs
  • stay open longer (allow larger amounts of K+ efflux after administration of DMR)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Risk of extrajunctional receptors after SCh administration

A

hyperkalemic arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

prejunctional membranes

A
  • nAChRs

- regulate release of ACh from presynaptic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

stimulation of prejunctional receptors results in

A
  • inhibits release of ACh from presynaptic membrane

- may stimulate production of more ACh in nerve terminal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

effect of NDMRs on prejunctional membranes

A
  • antagonize pre-JRs
  • inhibit ACh production
  • -explains tetanic fade after NDMR (ACh depletion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

tetanic stimulation before and after administration of NDMR

A

post-tetanic facilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

tetanic stimulation before and after administration of DMR

A

NO post-tetanic facilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

All NMBAs contain

A

quaternary ammonium group (NH4+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

All NMBAs are _____ soluble

A

ionized, water soluble, limited lipid solubility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

NMBAs characteristics

A
  • limited Vd
  • do not cross BBB
  • PO not effective
  • do not cross placenta
  • no CNS effects
  • minimal renal reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

NMBA P-kinetics

A
  • Not highly protein bound

- influenced by age, hepatic/renal dx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

NMBAs have a Vd that is equivalent to

A

Extracellular compartment (~14L)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

NMBAs + volatile anesthetics

A
  • do not directly alter p-kinetics

- NDMRs are enhanced via pharmacodymanic actions of VAs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

volatile anesthetics ______ the effects of NDMRs via _____

A
  1. potentiate

2. Ca2+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

______ dosage required for NDMRs in presence of VAs

A

decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ED95

A

dose necessary to produce 95% suppression of a single twitch in response to peripheral nerve stimulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

recommended dose to facilitate tracheal intubation (intubating dose)

A

2 x ED95

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

________ depression is adequate for surgical relaxation

A

90%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

standard of care - degree of NM blockade is evaluated by

A

monitoring the evoked response to electrical stimulation using a peripheral nerve stimulator (PNS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Residual paralysis

A

inadequate return of function

  • difficulty focusing/diplopia
  • *inability to swallow/dysphagia (unable to protect airway)
  • ptosis
  • weakness of mandibular muscles
  • low VT (hypoxia)
  • “floppy”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

NMBAs lack ______ effects

A

CNS/analgesic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

NMBAs are all structurally similar to

A

ACh

47
Q

which portion of the NMBA binds to the alpha subunit of the AChR?

A

N (from quaternary ammonium group)

48
Q

NMBAs cause the majority of ______ during anesthesia

A

anaphylactic reactions

49
Q

most likely to evoke histamine release

A

benzylisoquinoliniums - d/t tertiary amine
atracurium
cisatracurium
mivacurium

50
Q

benzylisoquinoliniums all end in

A

“urium”

51
Q

aminosteroids all end in

A

“curonium”

52
Q

Succinylcholine chloride ED95

A

0.25-0.5 mg/kg

53
Q

Sux onset

A

rapid 30-60s

54
Q

Sux DOA

A

Short: 5-10 minutes

55
Q

Sux: general dosage for tracheal intubation

A

1-1.5mg/kg

56
Q

Sux: dosage for RSI

A

1.5mg/kg

57
Q

depolarization is sustained, the depolarized membrane/receptors cannot respond to additional agonist

A

Sux: Phase I blockade

58
Q

Fasciculations occur due to

A

sustained depolarization

59
Q

Sux - sustained depolarization is associated with

A

leakage of K+ from muscle cell

60
Q

approximate plasma K+ plasma increase d/t Sux

A

0.5 mEq/L

61
Q

overdose to Sux is d/t

A
  • single large dose
  • repeated doses
  • infusion
  • leads to postjunctional membranes responding abnormally
62
Q

OD to Sux results in

A

characteristics change to Phase II Blockade

63
Q

Phase I Blockade - Sux

A
  • 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
Q

Phase II Blockade - Sux

A
  • 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
Q

Which phase of Sux resembles characteristics of NDMRs?

A

Phase II

66
Q

Sux Phase II Characteristics

A

Post tetanic facilitation

67
Q

Sux Phase I characteristics

A

NO post tetanic facilitation

68
Q

Biggest offenders of anaphylactic rxn during anesthesia

A

Sux, Roc

69
Q

NMBAs Vd

A

similar to ECF

70
Q

NMBAs: ionized or nonionized

A

ionized

71
Q

aminosteroids

A

pancuronium
vecuronium
rocuronium

72
Q

benzylisoquinoliniums

A

atracurium
cisatracurium
mivacurium

73
Q

Which Rx do not possess any hormonal activity?

A

Aminosteroids
pancuronium
vecuronium
rocuronium

74
Q

How is Sux metabolized?

A

hydrolyzed via pseudocholinesterase in plasma

-slow

75
Q

TOF ratio

A

TOF last twitch/first twitch

76
Q

TOF graph - which will produce 4 twitches at equal height?

A

Sux

77
Q

TOF graph - which will produce 4 twitches at sequentially smaller heights?

A

NDMR

78
Q

Sux hydrolyzed into

A

succinylmonocholine + choline

79
Q

termination of action of sux d/t

A

diffusion of drug away from site of action

80
Q

plasma cholinesterase is sythesized by

A

liver

81
Q

sux DOA may be prolonged d/t

A

-decreased synthesis of enzyme
-Rx induced dec. of enzyme
-atypical plasma cholinesterase
< 75% norm serum levels necessary to prolong plasma cholinesterase

82
Q

atypical plasma cholinesterase

A

-dibucaine test

83
Q

dibucaine # that confirms normal plasma cholinesterase

A

80

84
Q

dibucaine # that indicates NMB lasting hours

A

20

85
Q

Resistance to Sux in which patients

A

myasthenia gravis d/t decreased fxnal nAChRs

86
Q

NMBA w/ greatest histamine release

A

Sux

87
Q

Large/Rapid dose of Sux may result in

A

face/truncal flushing
*bronchospasm
decreased bp/anaphylaxis rxns

88
Q

Cardiac AE to Sux

A
  • cardiac dysrhythmias (sinus brady, junctional, sinus arrest)
  • increased HR/BP
89
Q

AEs to Sux

A
  • HyperK
  • Myalgia
  • increased intragastric pressure (risk for aspiration)
90
Q

MH is d/t

A

ryanodine receptors = defective

91
Q

MH manifests

A

rigidity, hyperpyrexia, hypermetabolism/O2 consumption, hypercarbia, tachycardia, metabolic acidosis, rhabdomyolysis

92
Q

MH Tx

A

dantrolene

93
Q

MOA NDMRs

A

-competitive antagonist at nAChRs in NMJ

94
Q

high doses of NDMRs can cause

A

channel blockade

95
Q

receptor occupation required to interrupt transmission of signal

A

80-90%

96
Q

80% receptors occupied

A

VT 5mL/kg

97
Q

70% receptors occupied

A

TOF = no fade

VC at least 20 mL/kg

98
Q

60% receptors occupied

A

Sustained tetany = no fade

DBS = no fade

99
Q

50% receptors occupied

A

Head Lift - 180 degrees, 5s

Hand grip - sustained 5s

100
Q

Characteristics of NDMR blockade

A 
Decreased twitch to single stimulus
tetanic fade
TOF ratio < 0.7
post-tetanic facilitation
potentiation of other NDMRs
101
Q

NDMRs are antagonized by

A

anticholinesterase drugs

102
Q

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

A

autonomic margin of safety

103
Q

very narrow autonomic margin of safety

A

pancuronium

104
Q

wider autonomic margins of safety

A

vec, roc, cis

105
Q

NDMR Rx intxn: VAs

A

dose dependent potentiation

biggest = Des

106
Q

NDMR Rx intxn: antibiotics

A

aminoglycosides: enhance NDMRs+DMRs

may be via decr. prejunctional release of ACh by competing w/ Ca++

107
Q

NDMR/DMR Rx intxn: enhances

A 
local anesthetics
antidysrhythmics
lithium
not Sux:
diuretics
magnesium
hypothermia
cyclosporin
108
Q

NDMR Rx intxn: decreases

A

phenytoin

109
Q

increased K+ effects NDMR/DMR how?

A

Increased K+ –> enhances DMR, resistance to NDMR

110
Q

decreased K+ effects NDMR/DMR how?

A

decreased K+ –> enhances NDMR, resistance to DMR

111
Q

Resistance to NDMRs

A 
Thermal injury (10 days)
paresis/hemiplegia (affected side)
112
Q

males are _____ sensitive to NDMRs than women

A

less

113
Q

women require _______ than men

A

22% less vec

Pharm Fall 2019 (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions