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Daddy Pharm > NMB (Exam 2) > Flashcards

NMB (Exam 2) Flashcards

1
Q

Ganglionic Blockers originally used for

A

BP control

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2
Q

Ganglionic Blockers act on

A

ganglionic nicotinic (ionophore) receptor
in BOTH symp & parasymp

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3
Q

What happens when a drug blocks both symp & parasym?

A

(ie: Ganglionic Blockers)

-lose nearly all homeostatic control & fine tuning
-assumes predominant tone
-tissues lose self-regulation
-very easily shifted from one mode to the other

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4
Q

Ganglia function is much more complex than the simple idea of

A

a cholinergic nerve entering & acting on a ganglionic nicotinic (ionophore) receptor.

There are several receptors in ganglia.

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5
Q

Ganglionic Blockers
specificity
SEs

A

very non-specific
lots of SEs
“heavy hitters”

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6
Q

“heavy hitters”

A

lots of associated SEs

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7
Q

Ganglionic Blockers were effective at BP control bc…

A

predominant tone of BV is sympathetic
it blocks this
parasymp takes over
slight vessel relaxation

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8
Q

Dominant tone of blood vessels

A

sympathetic

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9
Q

Sympathetic stimulation
cutaneous vessels
skeletal muscle

A

cutaneous vessels: constrict (prevent blood loss; preserve BP)

skeletal muscle: dilate vessels to increase O2

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10
Q

Parasympathetic effects & BVs

A

prevents constriction by symp.
cant really dilate further unless muscles fatigued or with specific medication

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11
Q

Ganglionic Blockers
cardiac effects

A

dominant tone parasympathetic
blocks this completely
↑HR

bizarre heart activity; hard to predict
many systems control heart (hormones, renal fxn, ions, symp., etc)

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12
Q

T/F
Ganglionic Blockers alter hormonal circulation.

A

False
partially why their SEs are hard to predict

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13
Q

T/F
Multiple receptor types exist within the cholinergic ganglion.

A

True
not only nicotinic receptors

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14
Q

Only _____ can trigger an output & cause an axon to fire. But ____ & ____ can modulate/attenuate/fine tune it.

A

nicotinic receptors

norepi & muscarinic inputs

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15
Q

EPSP

A

excitatory post-synaptic potential

firing of a signal inside the cell

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16
Q

Only _____ can generate an EPSP.

A

nicotinic receptor (N2, ganglionic nAChR)

muscarinic & norepi receptors can control it

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17
Q

hexamethonium

A

standard ganglionic blocking drug
not used clinically

blocks nicotinic generated EPSP

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18
Q

ACh binds to a nicotinic receptor and allows influx of ___.

A

Na

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19
Q

Secondary receptors on the ganglia

A

ganglia (muscarinic, adrenergic, & others)

amplify or suppress (modulate) EPSP signal

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20
Q

Only ____ ganglionic blockers can completely block the transmission through ganglia.

A

nicotinic

all others can only modulate

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21
Q

Depolarizing type blockers
moA

A

initially stimulate the ganglia (like ACh)

followed by longer term block due to a persistent depolarization
(i.e. nicotine)

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22
Q

hexamethonium blockade

A

non-depolarizing (no receptor stimulation)

only acts by competing for ACh binding site

“plugs” the ion channel after it opens

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23
Q

Mecamylamine
moA

A

non-depolarizing blocker
non-competitive

acts at a secondary site to decrease ACh binding (negative allosterism)

(Mecamylamine = Meek (wont compete or stimulate, just binds to secondary site)

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24
Q

T/F
Mecamylamine is a non-competitive, non-depolarizing blocker by acting at the ACh site.

A

false
Does not act at ACh site
Allosterically changes ACh site

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25
Q

nicotine
cardiac fx

A

↑ HR by initial stimulation of the sympathetic ganglia
or
depressing the parasympathetic cardiac ganglia,
and vice versa

-chemoreceptors & medullary centers:
send increased or decreased signals to the heart via compensatory responses

-triggers epi release from adrenal medulla:
↑ HR & BP

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26
Q

Nicotine
overall SE

A

hard to predict

depends on state of person at that moment

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27
Q

hexamethonium is an example of which type of block?

A

non-depolarizing

ganglionic

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28
Q

Symptoms of ganglionic block

A

ie: hexamethonium

↑ skin bloodflow (warm and pink)
↓ sweating, lacrimation, salivation, GI tone/motility
mydriasis & cycloplegia
↓BP
urinary retention
constipation
hypoglycemia

(Use with any other drug can completely change Sx)

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29
Q

What causes warm pink skin seen with ganglionic blockade?

A

vascular predominant tone = sympathetic
blocking this = dilation
dilation = warm, pink skin

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30
Q

Bodily fluids predominant tone

A

Parasympathetic

ganglionic blockade:
↓ sweating, lacrimation, salivation
urine retention

atropine (anti ACh) = dry mouth

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31
Q

Eye predominant tone

A

parasympathetic (constricted pupil)

ganglionic blockade:
blocks parasymp→dilates pupil (mydriasis) & cycloplegia

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32
Q

cycloplegia

A

inability to focus eyes close for near vision

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33
Q

.

A
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34
Q

T/F
Arterial status contributes most to CO.

A

False

primary controller of CO are the veins
no venous return = no CO

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35
Q

controls lens of the eye

A

ciliary muscle

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36
Q

T/F
Ganglionic blockers can give you a stiffy!

A

False
decreased erection
decreased blood floow

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37
Q

T/F
Ganglionic blockade is not seen with drugs currently on the market due to safety concerns.

A

False
Some drugs currently used cause a certain extent of ganglionic blocker

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38
Q

Only ganglionic blocker still on the market

A

Mecamylamine

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39
Q

Mecamylamine
uses (past & current)
current status

A

OG usage: severe & malignant HTN
(safer & better drugs now)

~cocaine and nicotine addictions

Orphan drug status (FDA) for:
specific nicotine-responding neurological disorders (ie: Tourette’s)

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40
Q

Orphan drug status (FDA)

A

not many people use (3-5k ppl/month)
drug companies do as pro-bono
no profit made back

Manufctr benefit: prohibits generic status so the company can still make some sort of profit

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41
Q

T/F
nicotinic receptors can be found in the brain

A

True

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42
Q

T/F
Tourette’s syndrome is a muscarinic-responding neurological disorder

A

False
nicotine-responding

treat with Mecamylamine

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43
Q

Mecamylamine
does it cross the CNS?
what receptors does it affect?

A

Crosses CNS easily
blocks nicotinic receptors in brain & ganglia

note: acts at secondary site to decrease ACh binding (negative allosterism)

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44
Q

Mecamylamine
brain fx

A

blockade:
↓ dopamine & norepi release
modulates neuroendocrine responses

note: mecamylamine also blocks nicotinic rcptrs in the ganglia

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45
Q

Mecamylamine
At low doses…

A

CNS effects are seen with few peripheral side effects

bc amount given isnt enough to block all peripheral receptors; concentrates in brain

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46
Q

neuroendocrine/neurohormonal

A

affects other cells at a distance

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47
Q

Mecamylamine
C/A

A

potential peripheral activity

Hx MI, glaucoma, cerebrovascular Dz (i.e. stroke)

Avoid sudden d/c (rebound hypersensitivity effects possible)

pregnancy (crosses placenta)

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48
Q

Mecamylamine
adverse rxns

A

nausea and vomiting
anorexia
constipation
mydriasis
syncope
weakness
fatigue

Larger dose = peripheral fx

49
Q

peripheral effects can be seen with (small/large) doses of Mecamylamine

A

large

50
Q

NMB

A

blocks nicotinic receptors, but they are at the NMJ (N1/NMnicotinicR)

51
Q

Ganglia and NMJ both respond to ___.
but what makes them different?

A

nicotine

both ionophore
but
spacing & structure different

52
Q

d-tubocurarine chloride
derived from…

A

a plant extract of Chondodendron Tomentosum

53
Q

Curare

A

generic term for arrowhead poison that can kill using skeletal muscle paralysis

54
Q

Curare is a plant ___.

A

alkaloid

55
Q

Curare
first use in humans

A

in 1932
treat tetanus & spasticity

56
Q

How curare became part of anesthesia

A

1940’s
discovered to give adequate skeletal muscle relaxation during operative anesthesia without using excessive amounts of general anesthetics

57
Q

tubocurarine
uses

A

aid to mechanical respiration
prevent trauma in electroconvulsive therapy
aids diagnosis of myasthenia gravis

58
Q

d-tubocurarine chloride
current status

A

taken off market; cost and better agents exist

59
Q

Suxx structure

A

succinate on choline molecule

60
Q

currently used NMB with curare-like properties

A

Suxx

61
Q

Suxx breakdown

A

ester hydrolysis → Succinic acid + choline

(Do not confuse with ACh: acetic acid & choline)

62
Q

example of NMB developed and utilized over the last 50 years

A

Pancuronium

63
Q

competitive nondepolarizing neuromuscular blocking agents

A

atracurium
cisatracurium
rocuronium
vecuronium
etc

64
Q

NM site
Adult subunits

A

pentameric

2 Alpha-1
Beta
Delta
Epsilon

16 variations but this most common

65
Q

Where does ACh form a momentary fairly strong bond using its ester component?

A

esteratic site
Alpha subunit

bond is not as strong as covalent

66
Q

How many ACh sites at NMJ?

A

2

66
Q

Where does the qua+ernary amine portion of ACh bind to?

A

delta & epsilon (the negative charges here attract it)

67
Q

binding of …. allows ACh to open NMJ receptors and allow influx of ___.

A

ester portion to 2 A1 subunits
quat amine to delta & epsilon subunits

Na

68
Q

Decamethonium
structure and how it works

A

Depolarizing
any initial stimulation = insignificant

Quat amine sites on delta and epsilon (like ACh)

but w/ 10 C spacer:
fits perfectly across channel to block Na influx

69
Q

Pancuronium
structure & how it works

A

steroid nucleus
1 quat amine (to epsilon)
2 esters (to Alpha subunits)
also stretches across & blocks Na

“ronium → ‘roids → steroid”

70
Q

Two types of depolarizing blockers

A

Succinylcholine
Decamethonium (stimulation very little)

71
Q

Depolarizing blockers
moA

A

initial stimulation (depolarization)

followed by long-term blockade
(d/t keeping receptor depolarized, and not able to repolarize for re-stimulation).

72
Q

Suxx
main benefit

A

its very short duration (1 - 2 minutes)

73
Q

Decamethonium

A

(experimental only; nicotinic blocker)

10 C chain separating two tri-methyl amines (Quats).

74
Q

Decamethonium vs Suxx

A

both:
Depolarizing
work at NMJ
quat amines

Suxx: dual ester provides same spacing but allows quick metabolism!

75
Q

Ganglionic blocker vs NMB
Hexamethonium vs Decamethonium

A

both block nicotinic receptors!

ganglionic: blocked by hexamethonium
(6C spacer between 2 quat/trimethyl amines)

NMJ: blocked decamethonium
(10C spacer between 2 quat/trimethyl amines)

spacers show these receptors are not the same!
decamethonium too big to work on ganglionic

76
Q

Which are competitive antagonists of ACh?
non-depolarizing
depolaring

A

non-depolarizing

depo = suxx = mimics ACh
non-D = roc,vec,etc = compete with ACh @ NMJ

77
Q

Non-Depolarizing blockers

A

competitive antagonists of ACh @ NMJ

blocks ACh from stimulating muscle @ motor end plate
↓
muscle weakness (lower doses)
paralysis (higher doses)

78
Q

What gives Non-D NMBs their lack of stimulating properties & competitive nature?

A

lipid soluble groups at both ends
repeatedly release and rebind, going to diff locations

79
Q

Has steroidal nucleus

A

Panc
Roc

P.R.: personal record (gym) = steroids

80
Q

chemical blueprint for paralytic spacers

A

dont memorize

81
Q

Shortest onset & duration

A

Suxx

82
Q

Succinylcholine (Anectine)

A

Unique in its depolarizing mechanism
shortest-acting NMB
good ETT conditions w/in 60 sec, lasts 2—3 min

83
Q

Suxx
SEs

A

transient sinus brady
hypotension
arrhythmias
tachycardia
possible cardiac arrest by increased vagal stimulation

Primarily d/t relatively strong depolarization

Can also cause hyperkalemia.

84
Q

🔷(I dont understand)
Suxx
pretreament

A

anticholinergic agents, e.g., atropine, may reduce the occurrence of bradyarrhythmias.

increases ACh that can compete with suxx

85
Q

Can we give Suxx to a severely asthmatic pt?

A

no
significant histamine-release

Asthmatics very sensitive to histamine
↓
B.constriction

86
Q

Rocuronium

A

short-acting(?)
nondepolarizing

effective RSI alternative to Suxx (short onset & fairly short doA)

87
Q

Mivacurium was removed and put back on the market bc…

A

removed d/t manfcturing & patent issues

Short DoA made it a better agent than others so we brought it back

88
Q

considered short-acting with a longer onset time but shorter duration than Rocuronium

A

Mivacurium

89
Q

Intermediate-acting agents

A

Atracurium
Cisatracurium (Nimbex)
Vecuronium

DoE: 30 to 60 minutes

90
Q

long-acting agent

A

Pancuronium

DoE: 60-120 min

91
Q

Atracurium
metab

A

nonspecific serum esterases
Hofmann elimination
metabolized somewhat in tissues
small amount eliminated unchanged

! Laudanosine

92
Q

mainly metabolized by Hofmann elimination

A

Cisatracurium

93
Q

Cisatracurium
metab

A

mainly Hofmann degradation

greater potency & lower doses
↓
limited laudanosine risk

94
Q

Mivacurium
metab

A

primarily plasma esterases

95
Q

Hofmann Elimination

A

spontaneous

chemical deamination
(moving double bond & remove amine)

naturally occurs in aqueous environments
specific temperatures and pH

increases with high T & pH

96
Q

T/F
Atracurium should not be given in liver or renal failure.

A

False
Hoffman + non-specific esterase degradation

the patient’s liver and renal function is not critical

97
Q

Increases Hoffman elimination

A

hot & basic
high T & pH

98
Q

Ester Metab products
(Atracurium)

A

hydrolysis
split ester off
↓
Pentamethylene-1,5-diol & 2 Quat structures

99
Q

Hoffman elimination products
(Atracurium)

A

removes amine
↓
2 laudanosine molecules & spacer

100
Q

T/F
Ester hydrolysis requires adequate renal and liver fxn.

A

False

101
Q

Renally eliminated agents

A

Pancuronium

may require dosage reduction and careful monitoring in patients with renal impairment.

Panc = Peepee

102
Q

primarily excreted by hepatic metabolism or biliary excretion

A

Rocuronium & Vecuronium

precautions if hepatic Dz

(“LVR” = Liver Vec Roc)

103
Q

Myasthenia Gravis
What is it?
How does it affect NMB dosing?

A

slower destruction of NM ACh receptors

Have less receptors
Block more fully with lower doses
SMALL DOSES can cause complete paralysis

104
Q

Electrolyte imbalances that potentiate NMB

A

low Na
high K

“KANP”
K Alta N Pequeno

105
Q

pseudocholinesterase deficiency:

A

Increases HL of compound
Potential accumulation

106
Q

Mg & Ca salts

A

Mag inhibits the Ca

107
Q

Conditions/Meds that can prolong/potentiate

A

myasthenia gravis
renal impairment
hepatic disease
pseudocholinesterase deficiency

potentiate nondepolarizing:
lithium
calcium salts
magnesium salts
IAs
certain antibiotics
LAs (quinidine, procainamide, lidocaine)

108
Q

Histamine release

A

Suxx: moderate

Atracurium: mild-moderate
Cisatracurium: minimal

generally dose-related

CAUTION: asthma & cardiac Dz cardiopulmonary adverse effects:
flushing
hypoTN
sinus tachycardia (reflex to ↓TN)
bronchospasm

109
Q

Agents which lack significant histamine-releasing effects and do not block cardiac muscarinic receptors

A

Rocuronium & Vecuronium

110
Q

Prolonged blockade can result in…

A

muscle paralysis
apnea
dyspnea
respiratory depression

111
Q

Patients at risk for prolonged neuromuscular blockade

A

conditions/medications:

-impairing neuromuscular function
(e.g., myasthenia gravis)

-potentiating NMB
(e.g., electrolyte imbalance; Low Na, high K)

112
Q

Tachycardia is most common with ____, due to…

A

Pancuronium
blockade of muscarinic receptors

worsened by:
age, electrolyte imbalance, and renal or hepatic failure.

113
Q

T/F
Phlebitis and pain is a/w depolarizing neuromuscular blockers.

A

False
non-depolarizing

114
Q

asthmatic patients on steroids & steroidal neuromuscular blockers while on ventilator

A

(e.g., Vecuronium, Pancuronium)

acute myopathy lasting days to weeks

Exact cause not known

115
Q

Malignant Hyperthermia

A

IAs
Suxx

triggered by combo of certain anesthetics & NMBs

initiated by uncontrolled release of Ca++ from the sarcoplasmic reticulum in skeletal muscle

more commonly with depolarizing + anesthetic
still possible w/ suxx or IA alone

116
Q

Sugammadex (Bridion)

A

first in a new class known as SRBA’s

designed for Roc reversal agent
fairly good @ vecuronium & pancuronium too

117
Q

Sugammadex (Bridion)
FDA approval

A

12/15/2015

multiple rejections for allergic reactions
(Low occurrence & minor reaction)

118
Q

Sugammadex (Bridion)
structure

A

complex cyclodextrin ‘cage’
high lipophilicity
binds NMB & allows removal

roids bind inside cage and rapidly removed from body

Daddy Pharm (13 decks)

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