PHM 431 EXAM 2 UPDATED ACTUAL QUESTIONS AND
CORRECT ANSWERS
Question:
How does alcohol differ from other drugs?
Answer:
Large amounts are needed for pharmacological effect
Question:
Blood alcohol level (BAL)
Answer:
0.08% (80 mg of alcohol per 100 ml of blood) ~18mM
Question:
Blood alveolar air partition coefficient
Answer:
2000:1
Question:
T/F: alcohol is absorbed into the portal blood (blood draining the
gastrointestinal tract and passing through the liver)
Answer:
true
Question:
T/F: alcohol is absorbed from the stomach and small intestine
Answer:
true
Question:
Characteristics of alcohol being absorbed in stomach/small intestine
Answer:
absorption from the stomach is relatively slow
anything that delays emptying the stomach (food) will delay alcohol
absorption
,Question:
Characteristics of alcohol being ingested orally
Answer:
relatively long onset to time of peak plasma concentration
Question:
T/F: alcohol is subject to large first pass effect
Answer:
true
Question:
Two routes of alcohol metabolism
Answer:
cytochrome P450 subtype CYP2E1: CYP2E1 generates reactive oxygen species
(ROS) which can damage hepatocytes (liver cells)
alcohol dehydrogenase: main route of metabolism, in cytosol of hepatocytes,
produces acetaldehyde
Question:
T/F: alcohol is slowly metabolized
Answer:
false
Question:
Acetaldehyde effects
Answer:
produces effects of hangovers: nausea, vomiting, aversion to light/sound
Question:
Alcohol pathway in liver cell
Answer:
Ethanol in cytoplasm (2 paths): (1) becomes acetaldehyde (using alcohol
dehydrogenase)
(2) transported to endoplasmic reticulum and turned into CYP2E1 using
NADPH + H + O2 which is turned into acetaldehyde using ROS + H2O
Acetaldehyde transported into mitochondria where it is oxidized by aldehyde
dehydrogenase to produce acetic acid
Question:
Progression of alcoholic liver disease
,Answer:
alcohol ingestion -> fatty liver -> alcoholic hepatitis -> cirrhosis
Question:
T/F: 90-98% of consumed ethanol is excreted as acetate by the kidney
Answer:
true
Question:
How do high levels of alcohol dehydrogenase alter the re-dox state of
hepatocytes
Answer:
increasing the NADH/NAD+ ratio
excess NADH increases fatty acid synthesis in the liver (leads to hepatitis and
eventually cirrhosis)
Question:
Role of disulfiram (alcohol)
Answer:
aldehyde dehydrogenase inhibitor
used to treat alcoholism, ingesting alcohol when taking disulfiram causes
immediate nausea and vomiting (due to high concentrations of acetaldehyde)
Question:
Role of CYP2E1 (alcohol)
Answer:
secondary route for alcohol metabolism
induced by alcohol exposure (enzyme levels increase)
two jobs increase alcohol metabolism, allows for alcohol tolerance
Question:
Tylenol interaction with alcohol
Answer:
drug-drug interaction
impacts CYP2E1 levels when taken with alcohol
Question:
Rate of elimination for alcohol
Answer:
zero order elimination kinetics, constant per unit time
allows for estimation of BAL for a certain time
Question:
T/F: alcohol crosses the blood brain barrier
, Answer:
true
Question:
How does alcohol cross the blood brain barrier?
Answer:
freely distributes throughout body because it is uncharged
high levels of consumption = large diffusion gradient from blood towards
tissues
weakly polar, small molecule = facilitates diffusion across the blood brain
barrier
Question:
Disulfiram is an effective alcoholism treatment because it blocks:
Answer:
aldehyde dehydrogenase
Question:
Alcohol is one of very few drugs metabolized by 0 order kinetics because:
Answer:
metabolic enzymes are saturated
Question:
Principle molecular targets for alcohol effects in the brain
Answer:
GABAa (Y amino butyric acid A) receptors
Question:
T/F: GABA is the most important inhibitory neurotransmitter in the brain
Answer:
true
Question:
Characteristics of GABAa receptors
Answer:
ligand gated Cl- channels (Cl- concentrations higher outside than inside cell)
when activated: Cl- enters the cell (down concentration gradient) making the
cell more negative -> inhibitory (causing membrane potential moving
away from -50 mV, activation potential for sodium channels, action potential
generation)
Question:
Why are GABAa re-ceptors highly modulated
Answer:
many drug binding sites (including site for EtOH)
Question:
T/F: EtOH causes inhibitory responses caused by GABA? why?
Answer:
true
Cl- entry is increased -> making membrane potential more negative -> unlikely
to fire action potential (no output)
CORRECT ANSWERS
Question:
How does alcohol differ from other drugs?
Answer:
Large amounts are needed for pharmacological effect
Question:
Blood alcohol level (BAL)
Answer:
0.08% (80 mg of alcohol per 100 ml of blood) ~18mM
Question:
Blood alveolar air partition coefficient
Answer:
2000:1
Question:
T/F: alcohol is absorbed into the portal blood (blood draining the
gastrointestinal tract and passing through the liver)
Answer:
true
Question:
T/F: alcohol is absorbed from the stomach and small intestine
Answer:
true
Question:
Characteristics of alcohol being absorbed in stomach/small intestine
Answer:
absorption from the stomach is relatively slow
anything that delays emptying the stomach (food) will delay alcohol
absorption
,Question:
Characteristics of alcohol being ingested orally
Answer:
relatively long onset to time of peak plasma concentration
Question:
T/F: alcohol is subject to large first pass effect
Answer:
true
Question:
Two routes of alcohol metabolism
Answer:
cytochrome P450 subtype CYP2E1: CYP2E1 generates reactive oxygen species
(ROS) which can damage hepatocytes (liver cells)
alcohol dehydrogenase: main route of metabolism, in cytosol of hepatocytes,
produces acetaldehyde
Question:
T/F: alcohol is slowly metabolized
Answer:
false
Question:
Acetaldehyde effects
Answer:
produces effects of hangovers: nausea, vomiting, aversion to light/sound
Question:
Alcohol pathway in liver cell
Answer:
Ethanol in cytoplasm (2 paths): (1) becomes acetaldehyde (using alcohol
dehydrogenase)
(2) transported to endoplasmic reticulum and turned into CYP2E1 using
NADPH + H + O2 which is turned into acetaldehyde using ROS + H2O
Acetaldehyde transported into mitochondria where it is oxidized by aldehyde
dehydrogenase to produce acetic acid
Question:
Progression of alcoholic liver disease
,Answer:
alcohol ingestion -> fatty liver -> alcoholic hepatitis -> cirrhosis
Question:
T/F: 90-98% of consumed ethanol is excreted as acetate by the kidney
Answer:
true
Question:
How do high levels of alcohol dehydrogenase alter the re-dox state of
hepatocytes
Answer:
increasing the NADH/NAD+ ratio
excess NADH increases fatty acid synthesis in the liver (leads to hepatitis and
eventually cirrhosis)
Question:
Role of disulfiram (alcohol)
Answer:
aldehyde dehydrogenase inhibitor
used to treat alcoholism, ingesting alcohol when taking disulfiram causes
immediate nausea and vomiting (due to high concentrations of acetaldehyde)
Question:
Role of CYP2E1 (alcohol)
Answer:
secondary route for alcohol metabolism
induced by alcohol exposure (enzyme levels increase)
two jobs increase alcohol metabolism, allows for alcohol tolerance
Question:
Tylenol interaction with alcohol
Answer:
drug-drug interaction
impacts CYP2E1 levels when taken with alcohol
Question:
Rate of elimination for alcohol
Answer:
zero order elimination kinetics, constant per unit time
allows for estimation of BAL for a certain time
Question:
T/F: alcohol crosses the blood brain barrier
, Answer:
true
Question:
How does alcohol cross the blood brain barrier?
Answer:
freely distributes throughout body because it is uncharged
high levels of consumption = large diffusion gradient from blood towards
tissues
weakly polar, small molecule = facilitates diffusion across the blood brain
barrier
Question:
Disulfiram is an effective alcoholism treatment because it blocks:
Answer:
aldehyde dehydrogenase
Question:
Alcohol is one of very few drugs metabolized by 0 order kinetics because:
Answer:
metabolic enzymes are saturated
Question:
Principle molecular targets for alcohol effects in the brain
Answer:
GABAa (Y amino butyric acid A) receptors
Question:
T/F: GABA is the most important inhibitory neurotransmitter in the brain
Answer:
true
Question:
Characteristics of GABAa receptors
Answer:
ligand gated Cl- channels (Cl- concentrations higher outside than inside cell)
when activated: Cl- enters the cell (down concentration gradient) making the
cell more negative -> inhibitory (causing membrane potential moving
away from -50 mV, activation potential for sodium channels, action potential
generation)
Question:
Why are GABAa re-ceptors highly modulated
Answer:
many drug binding sites (including site for EtOH)
Question:
T/F: EtOH causes inhibitory responses caused by GABA? why?
Answer:
true
Cl- entry is increased -> making membrane potential more negative -> unlikely
to fire action potential (no output)
