Anesthesia Med Sheet MOA/INFO Flashcards by Elisabeth Tribeck

Q

Etomidate S/E, metabolism and other

A

CV stable, less myocardial depression than propofol

S/E: myoclonus/pain on injection, cv stable, epileptic foci

METABOLISM: plasma esterases and hepatic enzymes; a single induction dose may inhibit 11 BH leading to adrenocortical suppression

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Q

ketamine S/E, metabolism and other

A

hallucinations
increased CO
increased HR
increased salivation
decreased BP
analgesia

metabolism: liver cyp450; redistribution

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Q

methohexital/brevital S/E, metabolism, other

A

porphyria
do not give with asthma

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Q

propofol S/E, metabolism and other

A

pain on injection
no use in egg/soy allergy
antiemetic
decreases CV

metabolism: liver and lungs

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Q

midazolam S/E, metabolism and other

A

decreased respiration
amnesia
1/2 life: 1-4 hrs
H2O soluble
benzo

eliminated renal

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Q

dexmedetomidine info to know

A

alpha 2 agonist

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Q

succinylcholine S/E, metabolism, other

A

short-acting depolarizing
can cause MH
locks NA channel

met: plasma pseudocholinesterase

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Q

mivacurium info to know

A

short-acting non depolarizing

met: plasma cholinesterase

can cause histamine release

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Q

atracurium info to know

A

intermediate acting nondepolarizing

metabolism: hoffman/ ester hydrolysis

can cause histamine release

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Q

vecuronium info to know

A

intermediate acting; nondepolarizing

metabolism: liver>kidney

high lipid solubility

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Q

rocuronium info to know

A

intermediate acting; nondepolarizing

metabolism: liver >kidney

painful on injection
shortest acting NDNMB

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Q

ciastracurium info to know

A

intermediate acting; nondepolarizing

met: hoffman/esterase hydrolysis

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Q

pancuronium info to know

A

long acting; nondepolarizing

metabolism: renal

increase HR- no NOREPI reuptake

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Q

fentanyl info to know

A

pulm 1st pass
can cause rigid chest

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Q

sufentanil info to know

A

can cause rigid chest
most potent
pulm 1st pass

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Q

remifentanil info to know

A

metabolized by hydrolysis esterase
ultra short acting
1/2 life: 6 min

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Q

meperidine info to know

A

metabolite = seizures
no with MAOIs
crosses placenta
increase HR
treats post op shivering

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Q

ketorolac info to know

A

bleeding/ inhibits COX

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Q

morphine info to know

A

can cause Nausea and vomitting
most allergies: +histamine
can cause biliary spasm

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Q

hydromorphone info to know

A

can cause N/V
+histamine
antitussive
1mg=7mg MSO4 (morphine sulfate)

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Q

etomidate MOA

A

GABA mimetic

binds to GABA receptor and enhances receptors affinity for GABA

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Q

Ketamine MOA

A

non competitively binds to NMDA (glutamate receptor)

inhibits glutamate receptor (excitatory)- decreases presynaptic release of glutamate and potentiates GABA release

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Q

methohexital MOA

A

barbituate

acts on GABA receptors

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Q

propofol MOA

A

modulates GABA receptors
increases transmembrane Cl- conduction- hyperpolarizes post-synaptic cell membrane
sedation and hypnosis

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midazolam MOA

Works on the GABA receptor To increases frequency of Cl-channel influx and hyperpolarizes targeted cell

MOA of dexmedetomidine

Alpha 2 agonist Binds with pre and postsynaptic alpha 2a agonist receptors Decreases norepi levels; causes sedation and analgesia Alpha 2 agonist Decreases cAMP which inhibits the locus coeruleus in the pons = sedation

MOA of succinylcholine

Binds to one or both alpha subunits of nicotinic ACh receptors and mimics action of ACh Depolarizes the membrane

MOA of mivacurium

binds competitively to cholinergic receptors to antagonize the action of ACh and cause neuromuscular blockade

MOA atracurium

reversibly competitive antagonism of ACh

MOA of vecuronium

reversibly competitive antagonism of ACh

MOA of rocuronium

reversibly competitive antagonism of ACh

MOA of cisatracurium

reversibly competitive antagonism of ACh

MOA of pancuronium

reversibly competitive antagonism of ACh

info about ephedrine

direct/indirect beta and alpha 1 agonist can have tachyphylaxis dont give with fast HR dont give with MAOI decreases uterine blood flow

info about phenylephrine

alpha 1 agonist can cause reflex bradycardia (baroreceptor reflex)

info about epinephrine ( think hemodynamics)

direct beta1, beta2, alpha 1 agonist causes increased CO increased HR increased contractility increased SVR

info about dopamine

alpha1, beta1,beta2 and dopamine (renal perfusion) receptor agonist avoid with MAOIs 400mg/250ml bag= 1600mcg/ml

info about dobutamine

selective beta1 inotrope

info about atropine

increases HR causes mydriasis (pupil dilation) tertiary ammonium (crosses BBB)

info about glycopyrrolate

decreases secretions quaternary ammonium (DOES NOT CROSS BBB)

info about neostigmine

max dose 5mg cholinergic syndrome decreases HR hepatic metabolism

info about physostigmine

crosses BBB (tertiary amine) dont give with asthma renal excreted

info about edrophonium

do not give with glycopyrrolate renal excreted can diagnose MG true reversible

info about flumazenil

benzo antagonist repeat 0.2mg q 1min (3mg/hr max)

info about naloxone

reversal for opioids

info about hydralazine

Arteriole vasodilation causes increased cGMP increased HR increased CO decreases SVR increased RENIN DOC with normal to low HR (beta blockers preferred for HTN with increased HR)

info about labetalol

alpha, beta1, beta2 antagonist ratio 1:7 alpha to beta IV decreases HR, give slow

info about esmolol

beta1 antagonist metabolized by plasma hydrolysis t1/2 9min

info on ondansetron

5HT3 antagonist admin slowly to prevent headache

info about droperidol

paradoxical reaction( restless anxious) decreases BP change in dopamine in CNS (dont give with parkinsons)

info about dexamethasone

decreases inflammation decreases immunity

muscarinic effects

decrease HR bronchoconstriction increased salivation decreased BP MIOSIS (pupil constriction) intestinal spams

MOA of fentanyl

opioid mu receptor agonist

MOA of sufenta

opioid mu receptor agonist

MOA of ultiva/remifentanil

opioid mu receptor agonist

MOA of meperidine

synthetic opioid agonist at mu and kappa receptors

MOA of toradol

nonselective NSAID inhibits COX1 and COX2

MOA of morphine

mostly mu agonist inhibits ascending pain pathways

MOA of hydromorphone

mostly mu agonist and some kappa receptors

MOA of ephedrine

direct: alpha and beta agonist indirect: causes release of endogenous catecholamines stored in nerve terminals

MOA of epinephrine

beta 2> beta1> alpha1 beta1: inotropy, chronotropy beta2: vasodilation (skeletal muscles) and bronchodilation alpha1: vasoconstriction

MOA of dopamine

adrenergic agonist inotropic precursor to norepi alpha1, beta1, beta2, dopaminergic

MOA of atropine

inhibits postganglionic muscarinic receptors competes with ACh at the muscarinic receptor sites as an antagonist increases firing of SA node and conduction through the AV node by blocking the action of the vagus nerve

MOA of glycopyrrolate

competitively antagonizes ACh at muscarinic receptors

MOA of bridion/sugammadex

noncovalently binds to the steroidal muscle relaxant prevents NDNMBs from binding to nicotinic ACh immediate reversal of NDNMB

MOA of neostigmine

-anticholinesterase- accumulation of ACh at nicotinic receptors in NMJ -does this by the formation of carbamyl esters -reverses and restores neuromuscular transmission

MOA of physostigmine

-anticholinesterase- increases ACh at nicotinic receptors in NMJ -does this by formation of carbamyl esters -more neurotransmitters available for interaction with cholinergic receptors

MOA of edrophonium

anticholinesterase- competitive inhibition through electrostatic attachment to the anionic site on the acetylcholinesterase enzyme (presynaptic)

MOA of flumazenil

competitive GABA antagonist prevents or reverses effects of benzos

MOA of naloxone

competitively antagonizes mu, kappa, delta opioid receptors greatest affinity for MU

MOA of hydralazine

activates guanylate cyclase increases cGMP decreases intracellular Ca ateriolar relaxation

MOA of labetalol

selective alpha 1 nonselective beta1 and beta 2 blocker

MOA of esmolol

selective B1 blocker

MOA of ondansetron

5HT3 antagonist blocks serotonin centrally at the CRTZ and peripherally

MOA of droperidol

butyrophenone dopamine antagonist at GABA in CRTZ

MOA of dexamethasone

-glucocorticoid steroid -derivative of prednisolone -reduces surgery-induced inflammation due to inhibition of prostaglandin synthesis

what medication has less myocardial depression than propofol

etomidate

what medication can lead to adrenocortical suppression

etomidate

what are some CV considerations of etomidate

CV stable less myocardial depression than propofol

what are side effects of etomidate

myoclonus pain on injection epileptic foci

how is etomidate metabolized

plasma esterases and hepatic enzymes

how does etomidate cause adrenocortical suppresssion

inhibits 11 beta hydroxylase

what does ketamine do to HR, CO and BP

HR increases BP decreases CO increases

what is a metabolism consideration with ketamine

redistribution

what are 3 side effects of ketamine

hallucinations analgesia increase salivation

what are the contraindications off methohexital

porphyria asthma

what are signs and symptoms of porphyria

hyponatremia peripheral neuropathy severe abdominal pain psych problems

where is propofol metabolized

lungs and liver

how is versed eliminated

renal

what is the half life of versed

1-4 hrs

is versed water soluble

yes

what are the short NMBs

succs mivacurium

what are the intermediate NMBs

atracurium vec roc cisatracurium

what is the long action NMB

pancuronium

what is the shortest onset non depolarizing muscle blocker

roc

what are considerations for succinylcholine?

metabolized by plasma pseudocholinesterase locks sodium channel can cause MH

what is the specific temperature and pH called that causes spontaneous degradation of atracurium

hofman elimination

what two NDNMB increase histamine release

mivacurium atracurium

what two NMB are eliminated by Hofman elimination or ester hydrolysis

cisatracurium atracurium

what are considerations for vecuronium

metabolized more in liver than kidney increased lipid solubility

what are considerations for rocuronium

metabolized more in liver than kidney painful injection shortest onset NDNMB

what are considerations for pancuronium

increases HR blocks norepi reuptake eliminated in the kidneys

what are considerations for fentanyl

rigid chest pulmonary 1st pass effect

what is pulmonary 1st pass effect

loss of drug on first circulation through the lungs

what are considerations for giving sufentanil

rigid chest pulm 1st pass effect MOST POTENT

what are considerations for remifentanil

ultra short acting 6.5 min half life metabolized by hydrolysis esterase

what are considerations for merperidine

DO NOT GIVE WITH MAOIs crosses placenta metabolite can cause seizures increase HR used for post op shivering

what bp med is selective b1 and a positive inotrope

dobutamine

what are considerations for ephedrine admin

does not increase uterine blood flow direct/indirect betal and alpha1

what should be done after admin of sugammadex

ptc postetanic count aka twitches

what side effects should you look for with neostigmine

cholinergic syndrome decreased HR

what class of drug is famotidine

H2 receptor antagonist

MOA of famotidine

H2 receptor antagonist that produces selective and reversible inhibition of H2-mediated secretion of hydrogen ions produced by the stomach

what is half life and peak of famotidine

half life: 2.5-4 hrs peak: 1-3.5 hrs

What NDNMB are supplied in 10mg/ml

Atracurium Rocuronium

What NDNMBs are supplied in 2 mg/ml

Mivacurium Cisatracurium And sometimes pancuronium

What NDNMBs are supplied in 1mg/ml

Pancuronium Vecuronium

Edrophonium MOA

Anticholinesterase Competitive inhibition through electrostatic attachment to the anionic site on the acetylcholinesterase enzyme (presynaptic)

MOA of phenylephrine

directly activates alpha1 constricts arteries and veins Veins>arteries alpha 1>alpha2