Inhalational Anesthetics Pharm Final

Front 1

MAC (minimum alveolar concentration)

Back 1

1) more lipid-soluble agents have lower MAC values
2) at steady state, correlates to 500 umoles per 100 ml of membrane for each agent

Front 2

Unitary Theory of Narcosis

Back 2

all anesthetics have a common method of action

Front 3

Meyer-Overton Theory

Back 3

1) strong correlation between lipid solubility and potency
2) more lipid soluble agents are more potent anesthetics
3) points to a lipophilic action in some region of the brain
4) most likely site is membrane, affecting fluidity

Front 4

Meyer-Overton Theory suggests what cause the effect?

Back 4

the # of molecules dissolved in the membrane, and not the specific agent which cause the effect

Front 5

Critical volume hypothesis (Mullins)

Back 5

1) binding of anesthetic agent into membranes causes membrane to expand
2) alters the action of receptors and/or ion channel proteins locked into membrane

Front 6

other theory additions

Back 6

1) larger molecule size increases membrane expansion
2) binding of agent to memb. proteins in lipophilic regions alters protein (Na ion channel) function

Front 7

Membrain concentration rule

Back 7

1) provides quantitative explanation

Front 8

Membrain concentration rule suggests?

Back 8

1) when memb. excitability is blocked, the [ ] of the agent in the memb. is 500 umoles per 100 ml of memb. volume
2) equals 3 x 10(20th) molecules per 500 umoles

Front 9

problems with physical theories

Back 9

impossible to explain why some entantiomers have different anesthetic potencies or effects

Front 10

CNS effects r/t inhalational anesthetics

Back 10

1) unconsciousness - via peripheral neurons, SC, brainstem, other brain areas
2) immobilization - by action of SC
3) unconciousness - via depression of thalamic neurons
4) amnesia - via depression of hippocampal neurons

Front 11

activation of which receptors in the BRAIN triggers hyperpolarization?

Back 11

GABA-mediated chlorida ionophores

Front 12

cell hyperpolarization

Back 12

less likely to be able to be stimulated, thus decreasing passage of signals between neurons

Front 13

activation of which receptors in the BRAINSTEM and SC triggers hyperpolarization?

Back 13

Glycine-mediated chloride ionophores

Front 14

inhalational anesthetics inhibit?

Back 14

1) glutamate-mediated excitatory calcium channels (NMDA channels)
2) inhibit postsynaptic release of some neurotransmitters

Front 15

GABA A receptor complex composed of?

Back 15

1) GABA site
2) Benzodiazepine site
3) Steroid site
4) Barbiturate site
5) Picrotoxin site

Front 16

main structures of inhalational anesthetics

Back 16

1) alkanes
2) ethers
3) chlorinated/ fluorinated

Front 17

general anesthesia is?

Back 17

1) the loss of all perception
2) chara. by sleep, loss of pain sensation, inhibition of visceral reflexes, and muscle relaxation

Front 18

characteristics that make up a good general anesthetic

Back 18

1) rapid induction
2) good muscle relaxation
3) amnesia
4) analgesia
5) rapid emergence

Front 19

balanced anesthesia

Back 19

the mixture of different compounds for their different required effects, thus allowing less toxic doses of any one agent to be used

Front 20

anesthesia will depend on

Back 20

the partial pressure of the agent in the inspired air, and it's physiochemical properties

Front 21

partition coefficient (blood:gas)

Back 21

used to discuss the agents solubility between the gaseous phase and solubility into blood

Front 22

MAC values

Back 22

1) used to compare potencies of anesthetic agents
2) are at equilibrium (steady state), and are not related to time to reach anesthesia

Front 23

the onset of anesthesia is related to?

Back 23

blood/gas solubility (more rapid for less soluble agents)

Front 24

Ethylene and Cyclopropane

Back 24

1) older agents - no longer used
2) flammable

Front 25

Nitrous Oxide

Back 25

1) non-irritating gas
2) slightly sweet odor
3) non-explosive or flammable
4) MAC = 104 %

Front 26

advantages of N2O

Back 26

1) good relaxant at 10-30 % in air
2) excellent analgesic - as good as morphine

Front 27

N2O act by?

Back 27

inhibiting NMDA glutamate excitatory recetors, not by GABA enhancement

Front 28

solubility of N2O

Back 28

very low solubility in blood, therefore rapidly reaches equilibrium, and is rapidly eliminated (excreted unchanged in lungs)

Front 29

long term use of N2O lead to?

Back 29

1) inactivation of vitamin B12 lead to
2) megaloblastic anemia
3) leukopenia
4) thromobocytopenia

Front 30

Diethyl Ether

Back 30

1) no longer used in U.S.
2) stimulate catecholamine release - maintain BP, but can cause arrythmias
3) very irritating to bronchioles (>secretions)
4) explosive

Front 31

CNS effects of halogenated alkanes and ethers

Back 31

1) inhibit post-syna. excitatory responses
2) enhances post-syna. inhibitory response
3) pre-syna. effects leading to inhibition of NTM release

Front 32

Halothane (Fluothane)

Back 32

1) pleasant smelling
2) non-irritaing
3) non-explosive
4) soluble to some extent in rubber, and thus is taken up into some parts and tubing of anes. equipment

Front 33

MAC of Halothane

Back 33

0.76 %

Front 34

rapid induction and maintenance of Halothane

Back 34

1) rapid induction = 4 % v/v of air
2) maintenance = 0.5 - 2%

Front 35

elimination of Halothane

Back 35

80 % cleared b lungs, with remainder undergoing liver biotransformation

Front 36

SE of Halothane

Back 36

1) respiratory depression
2) decreases TV (cause short rapid breaths)
3) cardiac depression (<BP)
4) some vascular smooth muscle relaxation (<BP)
5) sensitizes the heart to catecholamines (trigger arrythmias)
6) post-op hepatitis
7) trigger MH
8) poor skeletal muscle relxant

Front 37

Methoxyfluorane (Penthrane)

Back 37

1) D/C ed
2) liver metabolism, via P-450 2E1 isomer mainly (50% of dose) releases free fluoride, whch can lead to kedney toxicity - (this has caused it to be removed from US market)

Front 38

actual cause of nephrotoxicity is belived due to?

Back 38

release of free fluoride in nephron by kidney metabolism (not due to liver metabolism)

Front 39

Isofluorane (Forane)

Back 39

1) widely used
2) pleasant smelling
3) non-irritating
4) non-explosive

Front 40

MAC of Isofluorane

Back 40

1.16 %

Front 41

induction and maintenance [ ] of Isoflurane

Back 41

1) induction [ ] = 2-4 % (v/v)
2) maintenance [ ] = 1-2 % (v/v)

Front 42

metabolism of Isoflurane

Back 42

very little metabolized < 1 %

Front 43

effects of Isoflurane

Back 43

1) mild analgesic effects
2) mild skeletal muscle relaxation (potentiates NMB)

Front 44

SE of Isoflurane

Back 44

1) some cardiac depression
2) < BP
3) no sensitization of the myocardium to catecholamines (Ether structure)

Front 45

Which structure of volatile anesthetics cause sensitization of the heart to catecholamines?

Back 45

Alkane types
(ex) Halothane

Front 46

Enflurane (Enthrane)

Back 46

1) similar (isomer) to Isoflurane
2) no longer widely used in U.S.
3) MAC = 1.68 %

Front 47

high doses of Enflurane stimulate

Back 47

the CNS, leading to seizure-like twitching of muscles

Front 48

metabolization of Enflurane

Back 48

~2% metabolized, and the release of free fluoride ions in long Sx procedures may lead to kidney toxicity(?)

Front 49

Desflurane (Suprane)

Back 49

1) low solubility (rapid induction & emergence)
2) one of most widely used agents today

Front 50

MAC of Desflurane

Back 50

6.0 %

Front 51

vapor pressure of Desflurane

Back 51

1) high vapor pressure (~700 mmHg at 20C)
2) requires specialized vaporizer

Front 52

Is Desflurane good for induction?

Back 52

No! due to pungent odor

Front 53

cardiac effects of Desflurane

Back 53

1) < BP
2) no sensitization of heart to catecholamine (Ether)

Front 54

metabolization of Desflurane

Back 54

very little metabolized (~0.02 %)

Front 55

Sevoflurane (Ultrane)

Back 55

1) newest agent approved in U.S.
2) low solubility (rapid induction & emergence)
3) rapidly become one of the most preferred agents

Front 56

MAC of Sevoflurane

Back 56

1.71 %

Front 57

cardiac effects of Sevoflurane

Back 57

1) < BP
2) no sensitization of heart to catecholamines (Ether)

Front 58

metabolization of Sevoflurane

Back 58

1) ~3% metabolized
2) release free fluoride due to liver metabolism (does not appear to be as nephrotoxic as methoxyflurane)

Front 59

nephrotoxicity of free fluoride

Back 59

1) in nephron by kidney meta. - more toxic
2) produced by liver meta. - less toxic

Front 60

Carbon dioxide absorbents

Back 60

1) used in gas machine to allow rebreathing and save anesthetic
2) cause chemical breakdown of all halogenated anesthetics
3) below 40C, little breakdown of modern anesthetics except for Sevoflurane

Front 61

what reaction causes CO2 absorbents to increase the temperature?

Back 61

reaction of soda lime or Baralyme with water vapor and CO2 causes temp. to increase to 40-60C normally, and thur allow breakdown (due to NaOH or KOH in the absorbant)

Front 62

compound A

Back 62

is formed from Sevoflurane is nephrotoxic and requires higher gas flow rates and limits anesthesia times

Front 63

Carbon monoxide

Back 63

1) is another degradation product of halogenated anesthetics with dry absorbents
2) appears worse on Monday

Front 64

carbon monoxide can lead to

Back 64

carboxyhemoglobinemia

Front 65

which agent appears to cause the most CO production?

Back 65

Desflurane
(not as much seen with Sevo. or Halothane)