Sedative

Front 1

causes of oxygen deficiency

Back 1

1) low inspired fraction (FiO2)
2) increased diffusional barrier
3) hypoventilation
4) V/Q mismatch

Front 2

hypoxia causes:

Back 2

1) increased ventilation
2) sympathetic stimulation
3) pulm. vasoconstriction to optimize V/Q
4) impaired CNS function
5) anaerobic metabolism

Front 3

sympathetic stimulation causes:

Back 3

tachycardia, but decreased PVR - local effect

Front 4

anerobic metabolism

Back 4

1) increase lactic acid
2) decrease ionic gradients
3) increase cell H, Ca, Na
4) cell death

Front 5

oxigen toxicity from over-exposure probably due to:

Back 5

peroxide formation

Front 6

CO2 is carried in blood as part of:

Back 6

bicarbonate buffer system

Front 7

hypocarbia

Back 7

1) constrict cerebral vessels
2) decrease brain size
3) used in neurosurgery

Front 8

cardiac Sx uses CO2 to decrease:

Back 8

air (insoluble N2) around heart

Front 9

nitric oxide

Back 9

1) signaling molecule used in cells
2) main drive mech for vasodilation of many arterioles

Front 10

nitric oxide can cause:

Back 10

large pulmonary vasodilation with minimal systemic effects (binds and inactivates oxyhemoglobin)

Front 11

main use of helium:

Back 11

1) pulmonary function testing
2) laser airway Sx
3) diving

Front 12

sedative cause

Back 12

1) mild suppression of arousal and behavior
2) slight decrease in alertness and response to stimuli

Front 13

hypnotic cause

Back 13

1) pronounced sedative effects including the induction of sleep

Front 14

alcohols

Back 14

1) Ethanol
2) Ethchlorvynol
3) Chloral hydrate

Front 15

barbiturates

Back 15

1) Thiopental
2) Pentobarbital
3) Phenobarbital

Front 16

benzodiazepines

Back 16

1) Diazepam
2) Lorazepam
3) Midazolam

Front 17

miscellaneous

Back 17

1) Meprobamate
2) Methaqualone
3) Paraldehyde
4) Deoperidol
5) Etomidate
6) Propofol

Front 18

MOA of sedative/hypnotics

Back 18

1) very complex in the CNS, not completely clear
2) most act mainly on POLYsynaptic pathways

Front 19

sedative usually function to increase:

Back 19

PREsynaptic inhibition

Front 20

MOA, most believed to enhance the:

Back 20

pre- and post-synaptic effects of GABA

Front 21

2 phases of normal sleep

Back 21

1) slow wave sleep (SWS)
2) rapid eye movement sleep (REM)

Front 22

slow wave sleep (SWS)

Back 22

EEG shows mainly high-voltage synchronous activity

Front 23

rapid eye movement sleep (REM)

Back 23

1) skeletal muscles are relaxed (inhibited)
2) eyes move back and forth rapidly
3) accounts for ~25% of sleep
4) most of dreaming occurs

Front 24

hypnotic sleep differs:

Back 24

1) SWS patterns are altered and shortened
2) REM sleep is decreased
3) total sleep time is prolonged

Front 25

barbiturates bind to:

Back 25

GABA(A) receptor complex

Front 26

barbiturates decrease:

Back 26

the dissociation rate of GABA from its binding site, thus increasing the duration of action of GABA at the receptor, and increasing Cl conductance

Front 27

barbiturates inhibit:

Back 27

excitatory glutamate AMPA receptors

Front 28

barbituric acid

Back 28

1) the parent compound of barb.
2) no sedative powers

Front 29

barb. exists in:

Back 29

keto and enol forms (tautomers)

Front 30

addition of various functional groups onto position 5 alters:

Back 30

the sedative/hypnotic properties

Front 31

replacement of C-2 oxygen with sulfur results in the:

Back 31

thiobarbiturates (greater lipid solubility)

Front 32

addition of a phenyl group at C-5 enhances:

Back 32

anticonvulsant activity (ex. phenobarbital)

Front 33

addition of a methyl group to the ring N atom shortens:

Back 33

duration of action (ex. methohexital)

Front 34

barbiturates
1) long duration

Back 34

Phenobarbital (Luminal)

Front 35

2) intermediate duration

Back 35

1) Pentobarbital (Nembutal)
2) Secobarbital (Seconal)

Front 36

3) short or ultra-short duration

Back 36

1) Methohexital (Brevital)
2) Thiopental (Pentothal)

Front 37

lipid solubility

Back 37

more lipid soluble agents have shorter onset due to rapid increase in brain [ ], followed by rapid redistribution to other body fatty tissues with a concomitant drop in brain [ ]

Front 38

barbituates are:

Back 38

weak acids

Front 39

barbs are usually packaged as:

Back 39

sodium salt, which is the basic form
(high pH of solution makes itself bacteriostatic)

Front 40

stability of solutions (barb) limited to a couple weeks after opened and exposed to air due to:

Back 40

precipitation of acid form caused by CO2 in air altering pH of solution

Front 41

barb. metabolism

Back 41

most metabolized to a large extent

Front 42

primary metabolic pathway is:

Back 42

hydroxylation to inactive metabolites

Front 43

t1/2 of phenobarbital

Back 43

86 hrs

Front 44

N-glucosylation

Back 44

occurs to a larger extent in oriental populations

Front 45

barbs are potent inducers of the:

Back 45

hepatic microsomal enzyme system

Front 46

clinical uses of barb.

Back 46

1) induction anesthesia
2) anticonvulsants
3) neuropsychiatric exams (Wada Speech Test) prior to neurosurgery
4) cerebral edema and brain protection

Front 47

Wada Speech Test

Back 47

The Wada (intracarotid amobarbital) test is done to localize speech and memory functions in some candidates for epilepsy surgery. The internal carotid vascular distribution of half of the brain is put to sleep through injection of a quick-acting barbiturate into the internal carotid artery (via a catheter placed in the femoral vein at the groin).



During the next 5 - 15 minutes, speech and memory are tested. Surgery can be performed on the temporal lobe of the speech-dominant side, but not as much brain can safely be removed as on the non-dominant side. Global amnesia after injecting one internal carotid artery is a danger signal for surgery, because this result suggests that there may be severe memory problems after the operation. Not every surgical candidate requires a Wada test.

Front 48

barb. use in pregnancy

Back 48

1) fetal blood levels usually well under maternal level
2) placental transfer does occur
3) fetal elimination much slower than mother

Front 49

decline in barb. use due to:

Back 49

1) benzos are safer and just as effective
2) drug interactions (due to enzyme induction)
3) tolerance development
4) greater abuse potential
5) less CNS specificity than benzo.

Front 50

primary uses of barb.

Back 50

1) thrapeutic/diagnostic aids in psychiatry
2) reduction of cerebral edema following Sx, head injury or cerebral ischemia
3) antiepileptic use

Front 51

uses of benzodiapepins

Back 51

1) sedative
2) antiaxiety
3) anticonvulsant
4) muscle relaxant properties

Front 52

with large doses of benzos:

Back 52

hypnosis and unconciousness may be produced

Front 53

benzos which widely used for preanesthetic medication:

Back 53

1) Diazepam (Valium)
2) Lorazepam (Ativan)
3) Midazolam (Versed)

Front 54

half-lives of benzos

Back 54

varying half-lives ranging from 1 hr for midazolam to more than 24 hrs for diazepam

Front 55

many of benzos metabolized via:

Back 55

microsomal N-demethylation (diazepam)

Front 56

Oxazepam eliminated rapidly primarily via:

Back 56

glucuronide conjugation

Front 57

Midazolam is metabolized rapidly mainly via:

Back 57

microsomal hydroxylation

Front 58

Benzo's half-life can be greatly altered in pts with:

Back 58

1) liver disease
2) taking other drugs which induce or inhibit metabolism

Front 59

Diazepam is converted into:

Back 59

several active metabolites
(increase the period of clinical effect)

Front 60

Benzos act on specific receptor sites located at the:

Back 60

interface of the alpha and beta subunits of the GABA receptor in the CNS

Front 61

gamma subunit

Back 61

required for activity, but does not appear to be the binding site

Front 62

Benzos enhance:

Back 62

the ability of GABA to bind to its receptor, thus increasing the ability of the Cl ionophore to admit more Cl ions into the cell, r/i hyperpolarization which makes them more resistant to excitation

Front 63

Benzos have minimal effects in other areas of the body because:

Back 63

the receptors are found almost exclusively on post-synaptic regions in the CNS

Front 64

receptor density greatest in:

Back 64

1) cerebral cortex
2) areas assosiated with memory formations

Front 65

What is seen after use of benzo.?

Back 65

memory effects (amnesia)

Front 66

Benzo: effects on other tissues

Back 66

1) caused by action in the CNS
2) mild CV effects
3) minor decrease in SBP and vascular resistance
4) HR < or >
5) relaxation of spastic skeletal muscle activity

Front 67

rapid IV infusion of Diazepam will cause:

Back 67

transient apnea

Front 68

clinical uses of Benzo.

Back 68

1) pre-op meds
2) induction of anesthesia
3) IV sedation
4) anticonvulsant
5) Tx of delirium tremens
6) skeletal muscle relxation

Front 69

Benzo use in pregnancy

Back 69

Benzo cross placenta well, and leads to fetal depression

Front 70

Is benzo used as anesthetics?

Back 70

No. used as adjunct to balanced anesthesia

Front 71

abuse potential of benzo is relatively:

Back 71

high, and long-acting agents (Diazepam) can lead to true physical dependence

Front 72

Benzo. #1 (oral and IV)

Back 72

1) Diazepam (Valium)
2) Lorazepam (Ativan)
3) Midazolam (Versed)

Front 73

Benzo. #2 (oral)---pam

Back 73

1) Clonazepam (Klonopin)
2) Flurazepam (Dalmane)
3) Oxazepam (Serax)
4) Quazepam (Doral)
5) Temazepam (Restoril)

Front 74

Benzo. #3 (oral) ---zolam

Back 74

1) Estazolam (Prosom)
2) Triazolam (Halcion)

Front 75

Benzo. #4 (oral)

Back 75

1) Chlordiazepoxide (Librium)
2) Clorazepate (Tranxene)

Front 76

competitive Benzo antagonist (IV)

Back 76

Flumazenil (Romazicon)

Front 77

What is SE of Flumazenil?

Back 77

seizure

Front 78

Ethanol

Back 78

1) locally cause dehydration of cell protoplasm (astringent)
2) cooling effect on skin due to rapid evapolation
3) potent CNS depressant
4) bactericidal effect by disruption of cell memb.

Front 79

Ethanol increases:

Back 79

cutaneous blood flow when applied topically

Front 80

high dose of ethanol injection near nerves blocks:

Back 80

conduction by decreasing Na and K conductance

Front 81

ethanol effects are greatest of the:

Back 81

up-swing of the plasma [ ] curve

Front 82

Why ethanol is not used as a general anesthetics?

Back 82

due to small therapeutic window

Front 83

ethanol decreases:

Back 83

mental and physical abilities by a "top-down" CNS depression

Front 84

Ethanol raises:

Back 84

pain threshold and causes euphoria

Front 85

Ethanol depresses:

Back 85

medullary sensing of plasma CO2 levels, and thus may affect respiration

Front 86

high dose of ethanol depresses:

Back 86

central temp. control mechanisms
(potentially fatal in cold weather)

Front 87

high plasma [ ] of ethanol causes:

Back 87

cardiac depression by both central and direct mechanisms

Front 88

ethanol and skeletal muscle

Back 88

1) small doses - increase total work ability via central mecha.
2) larter doses - decrease work and are also damaging to the muscle directly

Front 89

~20 % concentration of alcohols increas:

Back 89

gastric blood flow and secretions

Front 90

high [ ] of alcohols cause:

Back 90

severe gastric irritation and erosion

Front 91

vomiting due to large ingestions of alcohols due to:

Back 91

local irritant effect

Front 92

alcohols increase synthesis of:

Back 92

1) fat in liver, leading to "fatty liver"
2) ling-term abuser - cirrhosis

Front 93

ethanol is converted via _____ to ______.

Back 93

via alcohol dehydrogenase to acetaldehyde

Front 94

alcohol dehydrogenase

Back 94

a liver enzyme that contains zinc, and requires NAD as a cofactor

Front 95

acetaldehyde is converted via _____ to ______.

Back 95

via aldehyde dehydrogenase to acetic acid (used as an energy source)

Front 96

methanol is converted via _____ to ______.

Back 96

via alcohol dehydrogenase to formaldehyde

Front 97

formaldehyde is converted via ______ to ______.

Back 97

via aldehyde dehydrogenase to formic acid

Front 98

formaldehyde damages:

Back 98

retinal cells and leads to blindness
(15 ml dose of methanol)

Front 99

formic acid

Back 99

can not be utilized by body, and build-up leads to acidosis, which can be fatal

Front 100

Tx of methanol toxicity

Back 100

large dose of ethanol to "tie-up" metabolizing enzymes until excreted in urine

Front 101

Formepizole, Antizol

Back 101

newer agent; inhibitor of alcohol dehydrogenase and may replace ethanol use