Anesthesia Flashcards
What are opiod receptors?
G coupled proteins

What are the endogenous opiod ligands?
Endorphins, enkephalins and dynorphins
How does activation of opiod receptors decrease neuronal activity?
Influk K+, decrease Ca+⇒
decreases release neurotransmittors (subsatance P, glutamate) in presynaptic cell ⇒
hyperpolarization of postsynaptic cell
How much does an opiod reduce the inhalent requirement?
40-60%
Potentcy of hydromorphone, oxymorphone, meperidine, methadone, fentanyl and buprenorphine in relation to morphine?
Hydro 8x greater
Oxymorphone 10x greater
Meperidine 10x less
Methadone 2x greater
Fentanyl 100x morphine
Buprenorphine 40x greater at the Mu agonist but binds to receptor without fully activating resulting reduced analgesia
Side effects of serotonin syndrome?
hyperthermia, anxiety, shock, rhabdomyolysis and ARF
MOA methadone?
Mu receptor agonist
NMDA receptor antagonist (N-methyl-D-aspartate)
What is unique about remifentanyl?
Metabolized by plasma esterases
No hepatic or renal metabolism
Very short half life - good for rapid awakening
MOA of naloxone
Binds competatively to Mu, Kappa, and Delta receptors
MOA benzodiazepines?
Enhance GABA (gamma-aminobutyric acid), an inhibitory NT
The GABA receptor allows Cl to enter the neuro, hyperpolarizing the cell and preventing action potentials.
What effects do benzodiazepines have?
muscle relaxation
narcosis
amnesia
no analgesia, cardio or respiratory depression
excitement = central disinhibitory effect
What are the active metabolites of diazepam and midazolam? How is this clinically relavent?
Diazepam = nordiazapem, oxazepam (both sedative with same duration as diazepam but slow clearence)
Midazolam = 1 hydroxymethyl midazolam (no activity)
Midazolam better for patients with hepatic dysfunction (ie decreased clearence)
What is acepromazine (drug class)?
phenothiazine
MOA acepromazine?
Depresses dopamine activity in the reticular activating system
alpha 1 receptor antagonist = vasodilation and hypotension and protective for some cardiac arrhythmias
Clinical effects of ACE?
moderate sedation
some muscle relaxation
no analgesia
antihistaminic
antiemetic
Dexmedetomidine MOA
Alpha 2 angonist = decrease Norepi release in CNS = sedation, analgesia and muscle relaxation
Peripheral alpha 1 agonist = vasocontriction, hypertension, arrhythmogenicity and paradoxical excitation
Hypertension = reflex bradycardia which can be compounded by decreased central sympathetic output = hypotension
Other SE: hyperglycemia, diuresis, respiratory depression
How does medetomidine effect cats different than dogs?
Dogs = hypertension and increased myocardial work
Cats = minimal hypertension; HR,CO,SV decrease alot
MOA propofol
GABA receptor agonist increasing inhibition throughout CNS
What is in propofol emulsion?
soybean oil, glycerol, egg lecithin
What is propofol infusion syndrome?
Occurs in people (not reported in animals)
Effects mitochondria - severe metabolic acidosis, refractory bradycardia, and rhabdomyolysis
MOA ketamine
NMDA receptor ANTAgonist - decrease dorsal horn windup
Dissociative anesthestic - separation between higher and unconcious function (eg muscle riditiy), maintains respiratory center sensitivity to CO2
Mild sympathomimetic (increased sympathetic) = may increase myocardial work, decrease CO
Bronchodilation
Clinical effects of ketamine?
Increase myocardial work
Decrease CO
Increase ICP
Increase intraocular pressure
Muscle rigidity
Laryngeal function maintained
Bronchodilation
How is ketamine eliminated?
Metabolized to active metabolic (norketamine) which is renally excreated (aka not good to use with severe renal disease as may be long to recover)
Only 50% converted in cats, rest excreated unchanged
What is telazol?
Tiletamine (like ketamine)
Zolazepam (benzo)


