Ex4 Reversal Agents Flashcards
1
Q
Ganglia
A
group of nerve cells forming a nerve center, especially one outside brain/spinal cord
2
Q
in both spine + brain, back (posterior) is always
A
sensory
3
Q
in both spine + brain, front (anterior) is always
A
motor
4
Q
mnemonic for PNS
A
SAME DAVE sensory-dorsal afferent-afferent motor-ventral efferent-efferent
5
Q
site of action for NMBAs
A
NMJ in skeletal muscle (somatic/voluntary) portion of efferent peripheral pathways
6
Q
thoracolumbar ANS
A
sympathetic
7
Q
craniosacral ANS
A
parasympathetic
8
Q
effects of thoracolumbar NS
A
fight/flight/fright
- redistribution of blood flow from vicera to skeletal muscle
- increased cardiac fxn
- decreased salivation
- pupillary dilation (mydriasis)
9
Q
effects of craniosacral NS
A
rest + digest (maintenance of fxns)
- digestive fxns (increased salivation/mucus secretion, GI motility)
- GU fxns
10
Q
receptors in ANS are classified by
A
- neurotransmitters with which they react
2. described in terms of location (pre/post-synaptic)
11
Q
adrenergic receptors react with
A
NE or Epi
12
Q
adrenergic receptors are subdivided into
A
alpha1, alpha2, beta1, beta2
also dopaminergic receptors (D1-D5)
13
Q
cholinergic receptors react with
A
ACh
14
Q
cholinergic receptors subdivided into
A
muscarinic, nicotinic
15
Q
Cholinergic nerves include
A
-all motor nerves that innervate skeletal muscle (somatic)
- all preganglionic para/symp neurons
- all postganglionic parasymp neurons
- some postgangl symp neurons: sweat glands/certain blood vessels
- preganglionic symp neurons that originate from grtr splanchnic nerve + innervate adrenal medulla
- central cholinergic neurons
16
Q
most organs have _____ innervation
A
dual (symp + parasymp)
17
Q
anticholinergic Rx combine _____ with ____ receptors to compete with _____
A
combine reversibly with
muscarinic receptors
to compete with ACh
18
Q
antimuscarinic Rx may enhance _____ activity
A
sympathetic
19
Q
antimuscarinic Rx block all ______ effects
A
muscarinic
20
Q
DOC - tx of reflex bradycardia
A
Atropine
21
Q
tx of anticholinergic syndrome
A
physostigmine 15-60 mcg/kg IV
22
Q
causes of anticholinergic syndrome
A
scopolamine
atropine
23
Q
s/s anticholinergic syndrome
A
restlessness, somnolence, hallucinations, unconsciousness
24
Q
atropine - caution in patients with
A
narrow angle glaucoma
prost hypertrophy
bladder neck obstruction
25
atropine uses
premedication- antisialogogue
tx for bradyarrhythmias
minimize effects of anticholinesterases
potent effects on heart/bronchial smooth muscle
26
how to minimize effects of anticholinesterases
add atropine, scopolamine, or glycopyrrolate
27
atropine premedication dosage
0.01-0.04 mg IM
28
max dose atropine
up to 0.4-0.6 mg total (adults)
29
max dose atropine w/ edrophonium
10mcg/kg
30
scopolamine premedication dose
0.4-0.6 mg IM
31
scopolamine - caution in
patients with:
| narrow (closed) angle glaucoma, prost hypertrophy, bladder neck obstruction
32
additional use for scopolamine
prevention of PONV + motion sickness
33
glycopyrrolate premedication dose
up to 0.3mg IM
34
glycopyrrolate DOA
2-4 hours after IV adm
35
glycopyrrolate effects
increased HR
36
glycopyrrolate max dose
up to 0.01-0.012 mg/kg IV
| with neostigmine or pyridostigmine
37
effect of anticholinesterase administration
massive parasympathetic response
38
actual s/s of anticholinesterase administration
```
salivation
weeping
wheezing
vomiting
urinating
defecating
seizing
```
39
only endogenous compound that causes simultaneous bradycardia/hypotension
ACh
40
muscarinic effects of ACh are similar to
vagal stimulation
41
effects of ACh
- generalized vasodilation (including cor/pulm circ)
- negative chrono/dromotropic effects
- inhibition of NE release from adrenergic nerves
- smooth muscle contraction (bronch/int/gu)
- relaxation of sphincters
- contraction of iris
- lacrimal, trach/bronch, salivary, dig, exocrine secretion
42
primarily used for reversal of residual NMB by NDMRs
anticholinesterases (or cholinesterase inhibitors)
43
goal of anticholinesterases
inhibition of AChE ("true cholinesterase")
44
when is reversal appropriate?
SAFE - only after evidence of spontaneous recovery from NDMRs
45
what must be present in order to reverse with anticholinesterases?
a single twitch on TOF
| 2/4 TOF = better
46
in absence of NDMRs, what can anticholinesterases produce?
- fasciculations of skeletal muscles
| - excess ACh may cause desensitization after admin
47
cholinergic crisis/anticholinesterase OD
often by organophosphate insecticides
48
cholinergic crisis/anticholinesterase OD s/s
```
bradycardia, miosis, abdominal cramps
loss of bowel/bladder control
weakness, confusion, ataxia
coma, seizures, vent depression
SLUDGE
```
49
SLUDGE mnemonic
Salivation, Lacrimation, Urination, Defacation, GI upset, emesis
50
Tx: cholinergic crisis
supportive (intubate/mech vent)
anticholinergic rx
administration of AChE reactivator (pralidoxime)
51
MOA Pralidoxime
antagonizes CNS effects of excessive ACh
52
effects of anticholinesterases
primarily reflect muscarinic effects
- bradycardia/decreased SVR
- salivation/hyperperistalsis
- bronchial secretions/bronchoconstriction
- miosis
53
antimuscarinic drugs are not effective where?
NMJ
54
neostigmine dosage
up to 0.07mg/kg (no more than 5mg total)
55
who should not receive neostigmine?
patient with profound NMB
56
pt with no twitches but + tetanic facilitation
no reversal
57
neostigmine peak
10 minutes
58
neostigmine DOA
> 1 hour
| prolonged in CRI/CRF
59
if incomplete reversal at peak of neostigmine
you MUST wait for full recovery prior to extubation (take patient to PACU intubated)
60
preferred antimuscarinic given with neostigmine
glycopyrrolate d/t slower time to onset
61
neostigmine effect on elderly/peds
more sensitive to effects, rapid onset, smaller dose
| elderly only: prolonged DOA
62
pyridostigmine is ______ as potent as neostigmine
20%
63
pyridostigmine dosage
up to 0.35 mg/kg
| up to 20mg in adults
64
pyridostigmine onset
10-15 minutes
65
pyridostigmine DOA
> 2 hours
| prolonged in CRI/CRF
66
Endrophonium dosage
up to 1mg/kg
67
Endrophonium onset
1-2min
| *fastest in class
68
Endrophonium + atropine
co-administered
69
Endrophonium + glycopyrrolate
glyco administered several minutes prior
70
Endrophonium DOA
> 1 hour in large doses
| prolonged in CRI/CRF
71
tx for anticholinergic toxicity caused by atropine/scopolamine
Physostigmine
72
unique for physostigmine
tertiary amine group
| *lipid soluble = only anticholinesterase that can access CNS
73
large doses of physostigmine may cause
central cholinergic crisis
74
physostigmine dosage
up to 0.03 mg/kg
75
what should be available with physostigmine administration?
atropine + glco d/t bradycardia (infrequent)
76
physostigmine onset
5 minutes
77
physostigmine DOA
30-300 minutes
78
physostigmine metabolism
plasma esterases
| *unique for class
79
physostigmine AEs
salivation, vomiting, convulsions
80
echothiophate is used for
eye gtt
combines irreversibly w/ AChE
inhibits plasma cholinesterase, may prolong DOA SCh
81
Sugammadex characteristics
- modified gaba-cyclodextrin
- 3d, hollow cone shape
- hydrophobic cavity, hydrophylic exterior (drugs go in but not back out)
82
Sugammadex MOA
encapsulates steroidal NMBA
| Roc>Vec>Pan
83
sugammadex is biologically _____
inactive
84
sugammadex metabolism
biologically inactive, rapid excretion, does not bind to plasma proteins
75% eliminated thru urine
~70% excreted w/in 6h, > 90% in 24h
85
sugammadex is capable of reversing _____ depth of NMBA induced by ____ or _____ to a TOF ratio of _____ within ____ (time)
any depth
roc/vec
> or = 0.9
within 3 minutes
86
sugammadex is ineffective against
```
Sux
Benzylisoquinolinium NMBAs (miva/atra/cistracurium)
```
87
Sugammadex dosage: RSI wtih Roc
16mg/kg
88
Sugammadex dosage: TOF 0/4
4mg/kg
89
Sugammadex dosage: TOF 2/4
2mg/kg
90
Sugammadex AEs
```
Anaphylaxis
Marked bradycardia
Residual blockade
Risk of coagulopathy
not recommended - severe renal impairment (CrCl < 30mL/min)
```
