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
Effects of Alcohol on the Liver
Reversible damage (increased fatty acid / lipid deposition -> hepatitis).
ascites,
esophageal varicosities.
May see decreased synthesis of clotting proteins, thus increased bleeding time.
Cirrhosis occurs in ______ of chronic alcoholics (5-25 yrs)
20%
High doses of ethanol can decrease absorption of _________.
amino acids, glucose, folic acid, thiamine, B12
Alcohol-induced increases in digestive secretions can produce ________.
pancreatitis
Prolonged ethanol use may cause serious ulceration of the gastric mucosa, ranging from ______to actual ________.
gastritis,
hemorrhage
Alcohol exerts a diuretic effect by ___________.
inhibiting the secretion of antidiuretic hormone
Heavy drinkers have increased risk of cancers of the
_____________ .
mouth, pharynx, larynx, esophagus, liver, and lung
can get ethanol Cross tolerance with other CNS depressants such as ______ & _____
anesthetics,
benzodiazepines
what are early withdrawal Sx’s of ethanol (0-48Hr)
anxiety
tremor,
mild agitation
what are some late alcohol withdrawal Sx’s (24-150 Hrs)
extreme overactivity,
disorientation,
confusion
In __________. Patients display progressive external ophthalmoplegia, nystagmus, ataxia of gait, pain, loss of sensation, and weakness of the arms and legs. Results from thiamine deficiency that is secondary to alcohol intake; responds quickly to thiamine administration
Wernicke’s Disease
___________. Symptoms include severe amnesia and personality alterations. Amnesic syndrome may result from interaction of thiamine deficiency with direct neurotoxic effects of alcohol.
Korsakoff’s psychosis
what are the Major effects of ethanol by pregnancy trimester?
1st: Major morphologic abnormality
2nd: Increased risk of spontaneous abortions
3rd: Decreased fetal growth
Ethanol can promote ______ if taken with aspirin.
GI bleeding
If alcoholic with normal liver function -> faster metabolism (enzyme induction, CYP2E1); may reduce concomitant drug effect and can potentiate ______ toxicity.
acetaminophen
•NMDA receptor drugs _________. Produces SOME reduction in alcohol craving and relapse rates in combination with psychotherapy.
Acamprosate
Opioid antagonists _______ Shown to reduce alcohol craving, consumption, and relapse rates when used in combination with psychotherapy.
Naltrexone
