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143 Cards in this Set
- Front
- Back
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what is the blood-gas coefficient for desflurane
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0.45
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what is the blood-gas coeffcient for N20
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0.47
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what is the blood-gas coefficient for sevoflurane
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0.65
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what is the blood-gas coefficient for isoflurane
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1.4
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what is the blood-gas coefficient for enflurane
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1.8
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what is the blood-gas coefficient for halothane
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2.5
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what is the blood-gas coefficient for methoxyflurane
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15
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what is the blood-brain partition coefficient range for the IA
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1-2
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what is the muscle-blood partition coefficient range for the IA
is there any exceptions? |
*2-3.5
*N20 which is 1.2 |
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what is the fat-blood partition coefficient for the IA?
with what exception? |
*27-51
*N20 is 2.3 |
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what body tissue acts as a reservoir for inhalation agents
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fat
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what IA is the best choice for obesity
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N20
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which body tissue takes up inhalation agents for a long period of time
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fat
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quadrupuling cardiac output has what effect on solubility
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it quadrupules solubilty and will decrease pressure in alveoli
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with high inspired cocentration what occurs with pressure in the alveoli
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there is a rapid rate of rise
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with low inspired concentration what occurs with pressure in the alveoli
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rate of rise in alveoli follows solubility coefficient
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what factor drives uptake
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concentration NOT solubility
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what are the routes that anesthesia leaves the body
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1-lungs (main)
2-metabolism (liver) 3-percutaneous/visceral loss |
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what is metabolite recovery
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looks at metabolites in pts urine
-it is the difference b/t what is breathed out and what is left in the urine |
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what is mass balance
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collection of all exhaled gases metabolism is considered the amt NOT recovered in the exhaled gases
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when measuring metabolism what is the reason for the difference in metabolism numbers
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methods of measuring metabolism
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which IA has the largest metabolism range
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halothane
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what % of desflurane is biodegraded
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0-0.02
(100% metabolized) |
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what % of isoflurane is biodegraded
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0-0.2
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what % of sevoflurane is biodegraded
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5-8
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what is mac awake
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max concentration at which pt will open eyes to command
**pt can maintain airway** |
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what is MAC awake for isoflurane
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0.35% or 1/3 MAC
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what is MAC awake for desflurane
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2% or 1/3 MAC
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what is MAC awake for sevoflurane
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0.6% or 1/3 MAC
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how would you know a pt can maintain there own airway
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they can follow commands
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what are the factors that influence time to discharge
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1-pain level
2-N/V 3-surgical implications |
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increased ventilation affects FA how
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increase rate of rise
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physiological changes have LESS imapact on what type of agent
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poorly soluble
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the more slow or rapid alveolar ventilation the more rapid washin will be
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the more RAPID
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which agent can have a dramatic sympathomemetic effect esp if non-gradual changes in concentration are made
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desflurane
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which agent can cause increased CO, BP and HR
how long do these changes last? |
*desflurane
*3-4 min |
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what are some events that impact CO
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*cardiac stimulants
*hypovolemia *cardiogenic shock *blood loss *changes in surgical stimulation *IA agents |
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what changes do cardiac stimulatants cause
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increase in uptake of IA and decrease in FA
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what changes does hypovolemia cause
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DECREASE in uptake of IA and increase in partial pressure of alveoli
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what changes does blood loss cause
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DECREASE in uptake of IA and increase in partial pressure of the alveoli
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what changes does cardiogenic shock cause
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DECREASE in uptake and increase in partial pressure of the alveoli
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which IA can dilute the amt of O2 given to a pt
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desflurane
-b/c desflurane is given in higher concentrations |
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what can occur at high levels of halothane
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profound depression of CO
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if you increase the concentration of halothane from 0.3% to 6% what would occur
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a decrease in CO and a more rapid rise of FA/FI
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what happens as rate of rise of halothane increases in contolled ventilation
this is an example of what |
*CO is severely depressed
*positive feedback |
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what happens to metabolism of IA as body size increases
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it decreases
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what is the FA/FI ratio in children compared to adults
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it is higher
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in children a great proportion of blood flow goes to which tissue group
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VRG
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which agent showed NO difference in flow changes r/t tissue volumes
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N20 (least soluble agent)
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though MAC is higher in children why is anethesia induced more rapidly
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blood flow to brain is higher and time constant is shorter
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what factors may cause changes in cerebral blood flow and alter the rate of induction
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changes in circulation and ventilation
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increased ventilation will do what to alveolar concentation?
this is esp true for what type of agent? |
*increase it
*high soluble agents |
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what does hyperventilation do in emergence
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it does NOT "blow off" the drug b/c it causes cerebral vasoconstriction
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increased CO does what to uptake
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increases it
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increased CO does what to pressure in alveoli
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decreases it
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increased CO does what to induction rate
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SLOWS it
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which type of IA are more affected by shunts
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least soluble agents
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which types of IA are the easiest to titrate with a shunt
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more soluble agents
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what is the half life of NO gas
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short--6-10 sec
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what occurs with OONO (perioxynitrite)
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DNA fragmentation and cell death
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the Meyer-Overton hypothesis proposed that IA act where
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in the hydrophobic (lipid) portion of the neurons
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according to the Meyer-Overton hypothesis anesthestic potentency correlates closely with what
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the affinity of the anesthetic for a lipid phase and thus implies an action in a lipid-like phase
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regarding preposed mech of action MAC correlates with what
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the lipid /gas partition coefficient
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what is the 5-angstrom theroy
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proposed by Egar and collegues states that anesthetics produce anesthesia by an action on 2 sites seperated by a distance of approx 5 angstroms or 5carbons
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what is the cellular role of GABA-a receptors
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*increased Cl- permeability
*membrane hyperpolarization *INHIBITION of excitation |
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what is the behavioral, physilogical and pharmacologic role of GABA-a
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enhanced activity associated with anxiolysis, sedation, amnesia, myorelaxation & anticonvulsant
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what is the cellular role of glycine receptors
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*increased Cl- permeability
*membrane hyperpolarization *INHIBITION of excitation |
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what is the behavioral, physilogical and pharmacologic role of glycine
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*spinal reflexes and startle reponses
*major inhibitory receptor in spinal cord |
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what is the cellular role of neuronal nicotinic Ach receptors
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*high permeablitiy to non-covalent cations and Ca+
*release of NT |
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what is the behavioral, physilogical and pharmacologic role of neuronal nicotinic Ach receptors
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*association w/ memory & nociception
*mutations linked to sz disorders *autonomic fxns |
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what is the cellular function of muscle nicotonic Ach receptors
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neuromuscular transmission
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what is the behavioral, physilogical and pharmacologic role of muscle nicotinic Ach receptors
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skeletal muscle contraction
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what is the cellular role of serotonin type 3 receptors
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enhance excitability by inhibiting resting K leak currents
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what is the behavioral, physilogical and pharmacologic role of serotonin type 3 receptors
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*arousal
*possible role in emesis |
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what is the cellular role of glutamate/NMDA receptors
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*fast EXCITATORY transmission
*cation conductance for Ca+ and Mg+ |
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what is the behavioral, physilogical and pharmacologic role of glutamate/NMDA receptors
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*perception
*learning and memory *nociception |
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isoflurane binds to what receptor
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GABA-a a1
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propofol binds to what receptor
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GABA-a b2
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what is picrotoxin
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a GABA-a antagonist
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what happens to effects of GABA when an IA is given
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it is potentiated
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which K channel IS sensitive to IA
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K2p
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what receptor is associated with malignant hyperthermia
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RYR1
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what test can be done to check for malignant hyperthermia
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halothane caffeine contracture test
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halogenated alkanes and ethers have what effect on GABA-a
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enhancement
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non-halogenated alkanes have what effect on GABA-a
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no effect
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N20 has what effect on GABA-a
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no effect
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halogentated alkanes and ethers have what effect on glycine receptors
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enhancement
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non-halogenated alkanes have what effect on glycine receptors
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no effect
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N20 has what effect on glycine receptors
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no effect
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halogentated alkanes and ethers have what effect on neuonal nicotinic Ach receptors
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strong INHIBITION
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non-halogentated alkanes have what effect on neuronal nicotinic Ach receptors
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strong INHIBITION
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N20 has what effect on neuronal nicotinic Ach receptors
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ND
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halogenated alkanes and ethers have what effect on muscle nicotinic Ach receptors
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INHIBITION
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non-halogenated alkanes have what effect on muscle nicotinic Ach receptors
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INHIBITION
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N20 has what effect on muscle nicotinic Ach receptors
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ND
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halogenated alkanes and ethers have what effect on serotonin receptors
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weak INHIBITION
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non-halogenated alkanes have what effect on serotonin receptor
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ND
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N20 has what effect on serotonin receptors
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no effect
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halogentated alkanes and ethers have what effect on glutamate NMDA receptors
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INHIBITION
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non-halogenated alkanes have what effect on glutamate NMDA receptors
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INHIBITION
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n20 has what effect on glutamate NDMA receptors
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INHIBITION
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halogenated alkanes and ethers have what effect on glutamate a-amino-3hydroxy-5methyl-4isoxazole propionic acid and kainate
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INHIBITION
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non-halogentated alkanes have what effect on glutamate a-amino-3hydroxy-5methyl-4isoxazole propionic acid and kainate
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ND
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N20 has what effect on glutamate a-amino-3hydroxy-5methyl-4isoxazole propionic acid and kainate
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no effect
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halogentated alkanes and ethers have what effect on background K+ channels
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enhancement or no effect
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non-halogenated alkanes have what effect on background K+ channels
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ND
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N20 has what effect on background K+ channels
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ND
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halogenated alkanes and ethers have what effect on voltage-activated K+ channels
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inhibition or no effect
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non-halogenated alkanes have what effect on voltage-gated K+ channels
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ND
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N20 has what effect on voltage-gated K+ channels
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no effect
|
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halogentated alkanes and ethers have what effect on ATP-activated K+ channels
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enhancement or no effect
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non-halogenated alkanes have what effect on ATP-activated K+ channels
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ND
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N20 has what effect on ATP-activated K+ channels
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ND
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halogenated alkanes and ethers have what effect on voltage-activated Na+ channels
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weak inhibition
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non-halogenated alkanes have what effect on voltage-activated Na+ channels
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weak inhibition
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N20 has what effect on voltage gated Na+ channels
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ND
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halogenated alkanes and ethers have what effect on voltage-gated Ca+ channels
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weak inhibition
|
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non-halogenated alkanes have what effect on voltage-gated Ca+ channels
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ND
|
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N20 has what effect on voltage-gated Ca+ channels
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no effect
|
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halogentated alkanes and ethers have what effect on ryanodine-activated Ca+ channels
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enhancement or inhibition
|
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non-halogenated alkanes have what effect on ryanodine-activated Ca+ channels
|
ND
|
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N20 has what effect on ryanodine-activated Ca+ channels
|
ND
|
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what amino acids make up the receptor to which isoflurane binds
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*Ala291
*Tyr415 *Leu232 *Ser270 |
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what amino acids make up the receptor to which propofol binds
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*Met286
*Tyr445 *Asn265 |
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how is a gas carrried in the body (bound)
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to a specific protein
|
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the largest amt of CO2 is transported how
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as HCO3 so it is "captured"
|
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smaller amts of CO2 in the body are transported how
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as Hgb and Co2
|
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NO binds to what as its "carrier"
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guanylyl cyclase (a protein)
|
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nitric oxide has to do what to be activated
|
bind to a protein (guanylyl cyclase)
|
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how is cGMP inactivated
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by phosphodiaesterase that converts it to 5-GMP (inactive)
|
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what a pathological effect of nitric oxide
|
OONO
|
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MAC is similar of equivalent to what
|
ED50
|
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why do you have to use higher concentrations of N20 to see effects
|
b/c it has a low potency
|
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what is needed inside the GABAa receptor for inhaled agents to work
|
critical amino acids
|
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if critical amino acids are not present within a GABAa receptor will an inhalation agent work
|
YES--you would just need increase the concentration of the agent
|
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what occurs with picotoxin or bicuculline and inhibition of tonic current if isoflurane (or IA agent) is present
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inhibition of tonic current still occurs
|
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with the nicotinic Ach receptor where does the IA impact
|
the "pore"
|
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what do inhalation agents do to voltage gated Na channels
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impact them
|
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what do inhalation agents do to the NMDAr receptor
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inhibit it
|
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what is the ryanodine receptor involved in
|
Ca+ induced Ca+ release from the SR
|
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what are the "parameters" for the halothane caffeine contracture test
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1 min and 1 gm of strength
|
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what is the incidence of malignent hyperthermia in the US
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1:10,000
|
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what is the incidence of malignent hyperthermia in Australia
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1:200
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