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101 Cards in this Set

  • Front
  • Back
causes of oxygen deficiency
1) low inspired fraction (FiO2)
2) increased diffusional barrier
3) hypoventilation
4) V/Q mismatch
hypoxia causes:
1) increased ventilation
2) sympathetic stimulation
3) pulm. vasoconstriction to optimize V/Q
4) impaired CNS function
5) anaerobic metabolism
sympathetic stimulation causes:
tachycardia, but decreased PVR - local effect
anerobic metabolism
1) increase lactic acid
2) decrease ionic gradients
3) increase cell H, Ca, Na
4) cell death
oxigen toxicity from over-exposure probably due to:
peroxide formation
CO2 is carried in blood as part of:
bicarbonate buffer system
1) constrict cerebral vessels
2) decrease brain size
3) used in neurosurgery
cardiac Sx uses CO2 to decrease:
air (insoluble N2) around heart
nitric oxide
1) signaling molecule used in cells
2) main drive mech for vasodilation of many arterioles
nitric oxide can cause:
large pulmonary vasodilation with minimal systemic effects (binds and inactivates oxyhemoglobin)
main use of helium:
1) pulmonary function testing
2) laser airway Sx
3) diving
sedative cause
1) mild suppression of arousal and behavior
2) slight decrease in alertness and response to stimuli
hypnotic cause
1) pronounced sedative effects including the induction of sleep
1) Ethanol
2) Ethchlorvynol
3) Chloral hydrate
1) Thiopental
2) Pentobarbital
3) Phenobarbital
1) Diazepam
2) Lorazepam
3) Midazolam
1) Meprobamate
2) Methaqualone
3) Paraldehyde
4) Deoperidol
5) Etomidate
6) Propofol
MOA of sedative/hypnotics
1) very complex in the CNS, not completely clear
2) most act mainly on POLYsynaptic pathways
sedative usually function to increase:
PREsynaptic inhibition
MOA, most believed to enhance the:
pre- and post-synaptic effects of GABA
2 phases of normal sleep
1) slow wave sleep (SWS)
2) rapid eye movement sleep (REM)
slow wave sleep (SWS)
EEG shows mainly high-voltage synchronous activity
rapid eye movement sleep (REM)
1) skeletal muscles are relaxed (inhibited)
2) eyes move back and forth rapidly
3) accounts for ~25% of sleep
4) most of dreaming occurs
hypnotic sleep differs:
1) SWS patterns are altered and shortened
2) REM sleep is decreased
3) total sleep time is prolonged
barbiturates bind to:
GABA(A) receptor complex
barbiturates decrease:
the dissociation rate of GABA from its binding site, thus increasing the duration of action of GABA at the receptor, and increasing Cl conductance
barbiturates inhibit:
excitatory glutamate AMPA receptors
barbituric acid
1) the parent compound of barb.
2) no sedative powers
barb. exists in:
keto and enol forms (tautomers)
addition of various functional groups onto position 5 alters:
the sedative/hypnotic properties
replacement of C-2 oxygen with sulfur results in the:
thiobarbiturates (greater lipid solubility)
addition of a phenyl group at C-5 enhances:
anticonvulsant activity (ex. phenobarbital)
addition of a methyl group to the ring N atom shortens:
duration of action (ex. methohexital)
1) long duration
Phenobarbital (Luminal)
2) intermediate duration
1) Pentobarbital (Nembutal)
2) Secobarbital (Seconal)
3) short or ultra-short duration
1) Methohexital (Brevital)
2) Thiopental (Pentothal)
lipid solubility
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 [ ]
barbituates are:
weak acids
barbs are usually packaged as:
sodium salt, which is the basic form
(high pH of solution makes itself bacteriostatic)
stability of solutions (barb) limited to a couple weeks after opened and exposed to air due to:
precipitation of acid form caused by CO2 in air altering pH of solution
barb. metabolism
most metabolized to a large extent
primary metabolic pathway is:
hydroxylation to inactive metabolites
t1/2 of phenobarbital
86 hrs
occurs to a larger extent in oriental populations
barbs are potent inducers of the:
hepatic microsomal enzyme system
clinical uses of barb.
1) induction anesthesia
2) anticonvulsants
3) neuropsychiatric exams (Wada Speech Test) prior to neurosurgery
4) cerebral edema and brain protection
Wada Speech Test
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.
barb. use in pregnancy
1) fetal blood levels usually well under maternal level
2) placental transfer does occur
3) fetal elimination much slower than mother
decline in barb. use due to:
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.
primary uses of barb.
1) thrapeutic/diagnostic aids in psychiatry
2) reduction of cerebral edema following Sx, head injury or cerebral ischemia
3) antiepileptic use
uses of benzodiapepins
1) sedative
2) antiaxiety
3) anticonvulsant
4) muscle relaxant properties
with large doses of benzos:
hypnosis and unconciousness may be produced
benzos which widely used for preanesthetic medication:
1) Diazepam (Valium)
2) Lorazepam (Ativan)
3) Midazolam (Versed)
half-lives of benzos
varying half-lives ranging from 1 hr for midazolam to more than 24 hrs for diazepam
many of benzos metabolized via:
microsomal N-demethylation (diazepam)
Oxazepam eliminated rapidly primarily via:
glucuronide conjugation
Midazolam is metabolized rapidly mainly via:
microsomal hydroxylation
Benzo's half-life can be greatly altered in pts with:
1) liver disease
2) taking other drugs which induce or inhibit metabolism
Diazepam is converted into:
several active metabolites
(increase the period of clinical effect)
Benzos act on specific receptor sites located at the:
interface of the alpha and beta subunits of the GABA receptor in the CNS
gamma subunit
required for activity, but does not appear to be the binding site
Benzos enhance:
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
Benzos have minimal effects in other areas of the body because:
the receptors are found almost exclusively on post-synaptic regions in the CNS
receptor density greatest in:
1) cerebral cortex
2) areas assosiated with memory formations
What is seen after use of benzo.?
memory effects (amnesia)
Benzo: effects on other tissues
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
rapid IV infusion of Diazepam will cause:
transient apnea
clinical uses of Benzo.
1) pre-op meds
2) induction of anesthesia
3) IV sedation
4) anticonvulsant
5) Tx of delirium tremens
6) skeletal muscle relxation
Benzo use in pregnancy
Benzo cross placenta well, and leads to fetal depression
Is benzo used as anesthetics?
No. used as adjunct to balanced anesthesia
abuse potential of benzo is relatively:
high, and long-acting agents (Diazepam) can lead to true physical dependence
Benzo. #1 (oral and IV)
1) Diazepam (Valium)
2) Lorazepam (Ativan)
3) Midazolam (Versed)
Benzo. #2 (oral)---pam
1) Clonazepam (Klonopin)
2) Flurazepam (Dalmane)
3) Oxazepam (Serax)
4) Quazepam (Doral)
5) Temazepam (Restoril)
Benzo. #3 (oral) ---zolam
1) Estazolam (Prosom)
2) Triazolam (Halcion)
Benzo. #4 (oral)
1) Chlordiazepoxide (Librium)
2) Clorazepate (Tranxene)
competitive Benzo antagonist (IV)
Flumazenil (Romazicon)
What is SE of Flumazenil?
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.
Ethanol increases:
cutaneous blood flow when applied topically
high dose of ethanol injection near nerves blocks:
conduction by decreasing Na and K conductance
ethanol effects are greatest of the:
up-swing of the plasma [ ] curve
Why ethanol is not used as a general anesthetics?
due to small therapeutic window
ethanol decreases:
mental and physical abilities by a "top-down" CNS depression
Ethanol raises:
pain threshold and causes euphoria
Ethanol depresses:
medullary sensing of plasma CO2 levels, and thus may affect respiration
high dose of ethanol depresses:
central temp. control mechanisms
(potentially fatal in cold weather)
high plasma [ ] of ethanol causes:
cardiac depression by both central and direct mechanisms
ethanol and skeletal muscle
1) small doses - increase total work ability via central mecha.
2) larter doses - decrease work and are also damaging to the muscle directly
~20 % concentration of alcohols increas:
gastric blood flow and secretions
high [ ] of alcohols cause:
severe gastric irritation and erosion
vomiting due to large ingestions of alcohols due to:
local irritant effect
alcohols increase synthesis of:
1) fat in liver, leading to "fatty liver"
2) ling-term abuser - cirrhosis
ethanol is converted via _____ to ______.
via alcohol dehydrogenase to acetaldehyde
alcohol dehydrogenase
a liver enzyme that contains zinc, and requires NAD as a cofactor
acetaldehyde is converted via _____ to ______.
via aldehyde dehydrogenase to acetic acid (used as an energy source)
methanol is converted via _____ to ______.
via alcohol dehydrogenase to formaldehyde
formaldehyde is converted via ______ to ______.
via aldehyde dehydrogenase to formic acid
formaldehyde damages:
retinal cells and leads to blindness
(15 ml dose of methanol)
formic acid
can not be utilized by body, and build-up leads to acidosis, which can be fatal
Tx of methanol toxicity
large dose of ethanol to "tie-up" metabolizing enzymes until excreted in urine
Formepizole, Antizol
newer agent; inhibitor of alcohol dehydrogenase and may replace ethanol use