Pharmacology of Ethanol Flashcards
Ethanol Absorption is rapid throughout entire GI tract; and extremely rapid in the ________.
•
small intestine
The more rapid the ethanol _______ , the more rapid the absorption (dependent on concentration gradient)
ingestion
Ethanol is water soluble and distributed in ________
total body water (will also cross the placenta)
Distribution / equilibration is most rapid in areas of high ________. Initial CNS effects within 5 min; peak effects within 15-60 min.
blood flow (brain, liver, kidney, lung)
Fat contains less water and thus less alcohol._______ is a factor that corrects for the volume of distribution of alcohol
[r]
r = \_\_\_\_\_\_ for men, r = \_\_\_\_\_\_ for women.
- 68,
0. 55
Women given the same g/kg dose of ethanol as a man of equal weight will have a _______ blood alcohol concentration
higher
Metabolism is responsible for _______ of disappearance of alcohol from body.
90-98%
First pass metabolism in _________ may be important in sex differences in BAC
gastric mucosa
Metabolism occurs at a __________ of 7-10 grams of alcohol per hour
constant rate (zero order kinetics)
which enzyme is the main metabolizer of ethanol in the liver
Alcohol dehydrogenase
________ accounts for 10-25% of ethanol metabolism at higher BACs
CYP2E1 (previously known as Microsomal Ethanol Oxidizing System [MEOS]);
Aldehyde dehydrogenase is inhibited by ________
disulfiram
__________ converts acetaldehyde to acetate.
Aldehyde dehydrogenase
acetate is converted to ______. then metabolized into fatty acids and cholesterol, CO2, H2O, and energy
Acetyl CoA
what are the adverse effects of increased acetaldehyde levels
nausea/vomiting,
respiratory and cardiovascular collapse,
convulsions
Mitochondrial oxidation of NADH to NAD is insufficient with the increased levels of _______, caused by alcohol
NADH
increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Blood lactate =________
acidosis -> behavioral disturbances
Increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Mg++ excretion can lead to _______
Decreased Uric acid excretion may precipitate ______
convulsions,
gout attacks
Increased levels of NADH leads to disruptions in hepatic metabolic pathways:
Increased Acetyl CoA leads to _________ fatty acid synthesis combined with decreased fat breakdown leads to fatty liver.
Increased NADH leads to Decreased Krebs cycle activity, -> Decreased gluconeogenesis -> ______
Increased,
hypoglycemia
Alcohol produces a dose-dependent __________ effect similar to ________
CNS depressant
barbiturates
Ethanol is not a stimulant at any dose, but depression of _________ neurons is seen first, resulting in a relative stimulatory phase prior to depressive actions.
inhibitory cortical
The CNS effects of low-to-moderate doses of ethanol (0.05-0.250 g/dl [50-250 mg %]) are mediated via interactions with ______ and _________ receptor coupled ion channels.
GABA (potentiation), glutamate NMDA (inhibition)
alcohol may precipitate convulsions; and is ________ in epilepsy
contraindicated
