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229 Cards in this Set
- Front
- Back
|
what type of anticholinesterase is neostigmine
|
carbamic acid ester with quaternary nitrogen
|
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can neostigmine enter the CNS?
|
NO
|
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what is the onset of Neostigmine?
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intermediate
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what is the duration of neostigmine?
|
intermediate
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is neostigmine synthetic
|
yes
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what is the mechanism of action of neostigmine?
|
works at the esteratic site of AchE
|
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what are the clinical uses of neostigmine?
|
reversal of NMB agents and treatment of myasthenia Gravis
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what is the standard conc of neostigmine?
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0.5-1mg/mL
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what is the dose of neostigmine?
|
0.04-0.08mg/kg
|
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is neostigmine lipid soluble
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no
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what is the metabolism of anticholinesterases?
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hepatic hydrolysis and conjugation to inactive metabolites
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what is the clearance of anticholinesterases?
|
renal 50-75%
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what are the uses of anticholinesterases
|
NMBD reversal, tx of myasthenia gravis, glaucoma, central anticholinergic syndrom, Alzheimer's, paralytic ileus, nerve gas, insecticides, anesthetic somnolence
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what type of anitcholinergic is edrophonium
|
quaternary ammonium alcohol
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can edrophonium enter the CNS
|
no
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what is the onset of edrophonium
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rapid
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what is the duration of edrophonium
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intermediate
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is edrophonium synthetic
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yes
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what is the mechanism of action of edrophonium
|
electrostatic attachment to the anionic site of AchE
-works presynaptic |
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what is the clinical uses of edrophonium
|
NMBD reversal and diagnosis of MG
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what is the standard con of edrophonium
|
10mg/mL
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what is the standard dose of edrophonium
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0.5-1mg/kg
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what is the lipid solubility of edrophonium
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poor
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what type of antichoilnesterase is physostigmine
|
carbamic acid ester with a tertiary amine
|
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can physostigmine go into the CNS
|
yes
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what is the onset of physostigmine
|
slow
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what is the duration of physostigmine
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long
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what is the mechanism of action of physostigmine
|
reversible inactivation of AchE through formation of carbamolyated intermediate
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what are the clinical uses for physostigmine
|
anesthetic somnolence, intestinal and bladder atony, tx of central antichoinergic syndrom and GHB intoxication
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what is the standard conc of physostigmine
|
1mg/mL
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what is the dose of physostigmine
|
15-60 mcg/kg
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what is the lipid solubility of physostigmine
|
good
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synthetic organophosphates mechanism of action and use
|
covalently bind to AchE creating long lasting Ach increase
used for glaucoma tx |
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what type of cholinergic antagonist is atropine
|
natural antimuscarinic
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is atropine lipid soluble
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yes
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what is the structure of atropine
|
tertiary amine
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what is the elimination of atropine
|
hepatic hydrolysis
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what is the standard conc of atropine
|
0.1-0.4mg/ml
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what is the dose of atropine
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0.01-.03mg/kg
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what are the uses of atropine
|
opthalmic, gastric antispasmodic, anticholinesterase adjunct, insectiside or nerve gas poisoning, antisecretory, brady and asystole
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what type of cholinergic antagonist is scopolamide?
|
natural antimuscarinic
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is scopolamide lipid soluble?
|
yes
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what is the structure of scopolamide
|
tertiary amine
|
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what is the metabolism of scopolamide
|
hepatic hydrolysis
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what is the standard conc of scopolamide
|
0.2mg/ml
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what is the dose of scopolamide
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0.2mg
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what are the uses of scopolamide
|
motion sickness and anmestic
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what type of cholinergic antagonist is glycopyrrolate?
|
synthetic antimuscarinic
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is glycopyrrolate lipid soluble
|
no
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what is the structure of glycopyrrolate
|
quaternary ammonium
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what is the elimination of glycopyrrolate
|
unchanged in the urine
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what is the standard con of glycopyrrolate
|
0.2mg/ml
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what is the dose of glycopyrrolate
|
.01-.02mg/kg
|
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what is glycopyrrolate used for
|
anticholinesterase adjunct, antisecretory and bradycardia tx
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what is the structure of succinylcholine?
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2 cholines esterified at a central di-carboxylic acid
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what is the mechanism of action of succinylcholine
|
mimics Ach at the alpha subunit causing sustained depolarization preventing the return to resting state, causes fasciculation's, slower hydrolysis than Ach
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onset of succinylcholine
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<1 min
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duration of succinylcholine
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4-5 min
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what are the side-effects of succinylcholine
|
bradycardia, hyperkalemia, myalgia, masseter spasm, increased intragastric,intraoccular, and intracranial pressure, myoglobinuria
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what is the conc of succinylcholine
|
20mg/ml
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what is the dose of succinylcholine
|
IV=1-2mg/kg
IM=2-4mg/kg |
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why does sux have a short duration?
|
b/c of rapid hydrolysis by pseudochoinesterase
only a small concentration administered actually reaching the junction and blockaid terminated by diffusion into the extracellular fluid |
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|
Dibucain #
what it means normal and abnormal readings |
-tests the quality of pseudocholinesterase
-normal is 80% abnormal is 20% -abnormal in 1 in 3,200pts |
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what type of NMBD is pancuronium
|
Bisquaternary aminosteroid
|
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what is the onset of pancuronium
|
3-5 min
|
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what is the duration of pancuronium
|
60-90 min
|
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what is the metabolism of pancuronium
|
hepatic de-acetylation
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where is elimination of pancuronium
|
kidney
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what is the conc of pancuronium
|
2mg/ml
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what is the dose of pancuronium
|
.1-.2mg/kg
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what is unique about pancuronium
|
it is a cardiovascular stimulant causing increased HR and CO
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what type of NMBD is vecuronium
|
monoquaternary aminosteroid
|
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what is the onset of vecuronium
|
3-5 min
|
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what is the duration of vecuronium
|
30-60 min
|
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what is the metabolism of vecuronium
|
hepatic de-acetylation
|
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where is elimination of vecuronium
|
kidneys and biliary
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what is the conc of vecuronium
|
10mg/ml diluted in 10cc NS ti 1mg/ml
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what is the dose of vecuronium
|
IV=.08-.12mg/kg
Inf=1-1.5mcg/kg/min |
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what type of NDMR is cisatracurium
|
benzylisoquinolinum
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what is the onset of cisatracurium
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3-5 min
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what is the duration of cisatracurium
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30-60 min
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what is the metabolism of cisatracurium
|
hoffmann elimination
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where is the elimination of cisatracurium
|
hoffmann and <16% in the kidneys
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what is the conc of cisatracurium
|
2mg/ml
|
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what is the dose of cisatracurium
|
IV=.08-.12
Inf=0.4-4mcg/kg/min |
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what is unique about the benzylisoquinolinium cisatracurium
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it does not release histamine like other benzyls do
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what type of NMBR is rocuronium
|
monoquaternary aminosteroid
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what is the onset of Roc
|
1-2 min
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what is the duration of roc
|
20-35 min
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what is the metabolism of roc
|
hepatic clearance
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where is the elimination of roc
|
kidneys and biliary
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what is the conc of roc
|
10mg/ml
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what is the dose of roc
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IV=0.6-1.2mg/kg
Inf= 3-12mcg/kg/min |
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what is the mechanism of action for nondepolarizing NMBR
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competative antagoinsm at the alpha subunit of postjunctional nicotinic Ach receptor
-occupies as much as 70% before clinical effect |
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what do VA do to NMBR
|
enhance the duration and magnitude of NDMR
-skeletal muscle relaxation at the spinal cord |
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what do aminoglycosides do to NDMR
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stimulate presynaptic receptors causeing decreased release of Ach, depress the post junx membrane
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what do local anesthetics do to NDMR
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interfere with prejunctional release of Ach, depress skeletal musc fibers, compete for plasma cholinesterase
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what does the antiarrhythmic drug quinidine do to NDMR
|
depress the prejunx release of Ach
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what do diuretics do to NDMR
|
forosemide depresses release of ach
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what does magnesium do to NDMR
|
stabalize the postjunctional membrane
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what other 2 things effect the NDMR
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lithium and prior sux administration
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what do anticonvulsants do to NDMR
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increase hepatic clearance, protein binding and enzyme production
-decrease duration |
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what do cyclosporins do to NDMR
|
depress the release of ACh
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what does hypothermia do to NDMR
|
decrease the clearance, slow rate of effect site equilibrium
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what does a brain injury do to NDMR
|
alter the affinity of receptor for Ach
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what is the structure of benzodiazapines
|
benzene ring fused to a 7 membered diazepine ring
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what is the mechanism of action of benzos
|
bind to the GABA receptor at the benzo binding site, GABA binds and Cl- flows into the cell
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what are the clinical uses of benzos
|
anxiolysis, sedation, anticonvulsant, mild musc relaxant, antergrade amnesia, sleep disorders
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what are the cardiac effects of diazepam
|
mild decrease in BP
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what are the resp effects of diazepam
|
mild depressant effects
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CNS effects of diazepam
|
sedation and anticonvulsion
|
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what is the dose of diazepam
|
IV=.05-.2mg/kg
IM=.1 PO=20-30mg |
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what is the conc of diazepam
|
5-10mg/ml
|
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solubility, Vd and protein binding of diazepam
|
highly for all
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metabolism of diazepam
|
hepatic P450 demethylation creating highly active metabolite
*venoirritant |
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cardiac effects of midazolam
|
decrease in SVR and BP
|
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resp effects of midazolam
|
ventilatory depression
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CNS effects of midazolam
|
decrease in CMRO2, CBF, ICP
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dose of medazolam
|
IV=.025-.06mg/kg
PO= 0.5 |
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concentration of medazolam
|
1-5mg/ml
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potency and affinity for receptor compared to diazepam
|
2-3x more potent 2x affinity for rec
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is midazolam lipid or water soluble and high or low protein binding
|
water, high
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duration of action and speed of redistribution of midazolam
|
short, rapid
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metabolism of midazolam
|
rapid hepatic P450
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what is Flumazenil
|
benzo antagonist
|
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conc of flumazenil
|
0.05-.1mg/ml
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dose of flumazenil
|
8-15mcg/kg
.2mg every min up to 1mg Inf=.1-.4mcg/kg/min |
|
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what is Dexmetomidine
|
selective specific and potent alpha 2 agonist used for IV sedation
|
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what is the loading dose and infusion for dexmetomidine
|
L: .5-1mcg/kg
Inf= .5-5mcg/kg/hr |
|
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mech of action for pentothal
|
enhances inhibatory effects of GABA in RAS (prevents dissociation of GABA from rec)
|
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clinical uses of pentothal
|
induction of anesth, tx if increased ICP, anticonvulsant, cerebral protection
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metabolism of pentothal
|
liver to hydroxy-thiopental and carboxylic acid
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cardio effects of pentothal
|
decreased BP due to dec SVR, increased HR
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resp effects of pentothal
|
decrease minute ventilation due to dec Vt and RR
|
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CNS effects of pentothal
|
dec ICP, due to dec CBF and CMRO2
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hepatic effects of pentothal
|
mild decrease in HBF
|
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renal effects of pentothal
|
mild dec in RBF and GFR
|
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conc of pentothal
|
25mg/ml
|
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dose of pentothal
|
3-5mg/kg
|
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what type of drug is pentothal
|
barbiturate, derivative of barbitureic acid, it is basic
|
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why does pentothal have prompt awakening?
|
redistribution from VRG to inactive tissues
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cations of pentothal
|
placental transfer and trigger for acute intermittent porphyria
|
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mech of action of propofol
|
selective GABA activation, decreased rate of dissociation of GABA from receptor, increased hyperpolarization of membranes
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clinical uses of propofol
|
induction of anesth, IV concious sedation, ICU sedation, anesth maintenance, and anticonvulsant, decreases bronchoconstriction, antiemetic
|
|
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metabolism of propofol
|
hepatic by P450 to inactive water soluble form, or pulmonary reuptake
|
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cardio effects of propofol
|
decrease SVR, CO, and BP
|
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resp effects of propofol
|
dec Vt and RR
|
|
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CNS effects of propofol
|
dec CMRO2, CBF, ICP
|
|
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hepatic effects of propofol
|
none
|
|
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renal effects of propofol
|
none
|
|
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dose of propofol
|
IV=1.5-2.5 mg/kg
Inf= 25-100mcg/kg |
|
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conc of propofol
|
10mg/ml
|
|
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what type of drug is propofol
|
diisopropylphenol
|
|
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why is there a risk of infection and allergic rxn with propofol
|
b/c its stored in fat embolism which can grow bacteria
-it has soybean oil and egg lecithin |
|
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mech of action of etomidate
|
enhance the affinity of GABA for its receptors
|
|
|
metabolism of etomidate
|
hepatic and plasma esterase
|
|
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cardio effects of etomidate
|
mild to no change in SVR
|
|
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resp effects of etomidate
|
dec Vt incr RR
|
|
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CNS effects of etomidate
|
dec CMRO2, ICP and CBF
|
|
|
renal effects of etomidate
|
none
|
|
|
hepatic effects of etomidate
|
none
|
|
|
conc of etomidate
|
2mg/ml
|
|
|
dose of etomidate
|
.1-.4mg/kg
|
|
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what type of drug is etomidate
|
carboxylated imidazole
|
|
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how long for etomidate to reach peak brain levels
|
<1min
|
|
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why does etomidate have fast awakening
|
redistribution and rapid metabolism
|
|
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is etomidate high or low protein bound
|
high 76%
|
|
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what is a side effect of etomidate
|
inc N/V
|
|
|
mech of action of ketamine
|
binds to NMDA
|
|
|
clinical uses for ketamine
|
induction, analgesia, neuaxial anesth, burn pt changes, restless leg syndrome
|
|
|
metabolism of ketamine
|
hepatic 1st pass effect
demethylation by P450 to norketamine which is 1/3 as active |
|
|
cardia effects of ketamine
|
increased HR, SVR, CO
|
|
|
resp effects of ketamine
|
mild dec in RR
bronchodilation, inc in PVR |
|
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CNS effects of ketamine
|
inc CMRO2, ICP, and CBF
|
|
|
renal effects of ketamine
|
none
|
|
|
hepatic effects of ketamine
|
none
|
|
|
conc of ketamine
|
5-100mg/ml
|
|
|
dose of ketamine
|
IV=1-2.5mg/kg
IM= 4-8mg/kg Maintenance+ 15-30mcg/kg/min |
|
|
what type of drug is ketamine
|
phencyclidine
|
|
|
lipid solubility, Vd of ketamine
|
high and rapid transfer across BBB
|
|
|
clinical effects of ketamine
|
emergance delerium
prosialogogue nystamus(rapid eye movement) inhibits plt aggregation decreases amt of NMBR needed |
|
|
metabolism of sufentanil
|
hepatic dealkylation and demethylation to desmethylsulfentanil
-significant 1st pass effect |
|
|
cardio effects of sufentanil
|
dec HR and mild dec CO
|
|
|
resp effects of sufentanil
|
vent depression, dec RR inc Vt
|
|
|
CNS effects of sufentanil
|
mild Inc in ICP
|
|
|
conc of sufentanil
|
50 mcg/ml
|
|
|
dose of sufentanil
|
IV=.05-.2mcg/kg
Inf=0.1-0.4mcg/kg/hr |
|
|
onset, redistribution and lipid solubility of sufentanil
|
high for all
smaller Vd than fentanyl |
|
|
metabolism of fentanyl
|
hepatic P450 demethylation to norfentanil
high first pass effect |
|
|
cardio effects of fentanyl
|
dec HR mild dec CO
|
|
|
resp effects of fentanyl
|
vent depression dec rr inc Vt
|
|
|
CNS effects of fentanyl
|
mild inc ICP
|
|
|
dose of fentanyl
|
IV=.5-2 mcg/kg
intrathecal=5-25mcg sublingual=5-20mcg/kg Inf=1.5-3mcg/kg/hr |
|
|
conc of fentanyl
|
50mcg/ml
|
|
|
clinical effects of fentanyl
|
synergism w/ benzos
reflex coughing skeletal musc regidity |
|
|
onset, potency duration lipid solubility of fentanyl
|
rapid onset, highly potent, short duration due to high lipid solubility
|
|
|
metabolism of Meperidine
|
absorbed from GI
hepatic demethylation to normeperidine, accumulation can cause selerium renal excretion |
|
|
cardio effects of Meperidine
|
dec BP inc HR, myocardial depression
|
|
|
resp effects of Meperidine
|
ventilatory depression
|
|
|
CNS effects of Meperidine
|
delirium, seziures, hyperreactive reflexes
|
|
|
conc of Meperidine
|
50mg/ml must be diluted
|
|
|
dose of meperidine
|
.5-2mg/kg
|
|
|
clinical effects of Meperidine
|
mydriasis, dry mouth, interactions w/ MAOI drugs, dependance, analgesia, postop shivering due to stimulating alpha 2 agonist decreasing the shivering threshold
|
|
|
Site of action for Morphine
|
mu recpetors in CNS and PNS
kappa in substantia gelatinosa inhibits release of excitatory neurotransmitters |
|
|
cardio effects of Morphine
|
dec HR and dec BP at large doses
myocardial dpression when used with N2O |
|
|
resp effects of Morphine
|
dec RR inc Vt, vent depr
|
|
|
CNS effects of Morphine
|
dec CBF with dec ICP
inc PaCO2 inc ICP |
|
|
conc of Morphine
|
1mg/ml epi and IV
0.2 mg/ml spinal |
|
|
dose of Morphine
|
IV=.05-.2mg/kg
EP=2-4mg Spi= .05-2mg |
|
|
clinical effects of Morphine
|
histamine release
cough suppresent skeletal musc regidity biliary spasm miosis dec gastric emptying constipation emesis |
|
|
when is Morphine more effective
|
when given before painful stim
for releaving constant dull pain |
|
|
lipid solubility, ionization, protein binding, of morphine
|
poor lip sol, highly ionized, high pro
|
|
|
metabolism of Morphine
|
hepatic conjugation w/ glucuronic acid forming morphine-6-glucuronide which is a highly active metabolite
|
|
|
potency duration effect site equilibration ionization vd of alfentanil compared to fent
|
20% of the potency of fent
30% of the duration of fent rapid effect site equilib 90% nonionized at phys pH small Vd compared to fent |
|
|
metabolism of alfentanil
|
hepatic w/i 1 hr
|
|
|
conc of alfentanil
|
500mcg/ml
|
|
|
dose of alfentanil
|
IV=15-30 mcg/kg
inf=15-25mcg/kg/hr |
|
|
potency and duration of remifentanil compared to fentanyl
|
the same
|
|
|
Vd, clearance of remifentanyl
|
small Vd, rapid clearance (6 min)
|
|
|
metabolism of remifentanyl
|
dealkylation by nonspecific plasma and tissue esterase
|
|
|
conc of remifentanyl
|
2mg/ml
|
|
|
dose of remifentanyl
|
IV=0.25mcg/kg
inf= .1-.5mcg/kg/hr |
|
|
drugs used for mild to moderate pain
|
codeine
tramadol propoxyphene |
|
|
drugs used for moderate to sever pain
|
hydrocodone
oxycodone meperidine |
|
|
Characteristics of Narcan
|
-pure opioid receptor antagoinst at mu receptor
-displaces agonist and binds at receptor |
|
|
onset and duration of Narcan
|
O- <60 sec
D-30-45 min |
|
|
clinical considerations of Narcan
|
associated w/ N/V after rapid IV
cardiovascular stim neonatal withdrawl |
|
|
narcan conc
|
.4mg/ml
|
|
|
narcan dose
|
IV=1-4mcg/kg
Inf=5mcg/kg/hr |
