Chapter 6: Alcohol Flashcards
According to Dr. D. Musto, Alcohol consumption in america tends to:
tends to peak every 60-70 years, followed by a decline in use. The decline was often accompanied by preoccupation with health and morality and by public concern over the harm of alcohol. (ex/ start of MADD)
What is BAC? what’re its units? how do you convert to percent alcohol?
BAC= Blood-alcohol concentration. Units in mg/100 ml of blood, but SI mmol/L. You can convert mg/ml by moving the decimal 3 places to the left to find alcohol percentage.
ex/ BAC of 80mg/100ml
T/F alcohol absorption is effected by PH of the stomach
false. Alcohol cannot ionize
What organ is the site of first pass metabolism for alcohol?
the stomach. NOT THE LIVER. There are high levels of alcohol dehydrogenase in the stomach, which breaks down alcohol before it gets absorbed into the blood and taken to the liver.
Why does eating before drinking prevent you from getting drunk?
because alcohol will spend more time in the stomach,making it exposed to first pass metabolism even further.
How does carbonation aid in alcohol absorption?
carbonation and carbonated drinks help pass alcohol through the stomach and into the blood stream faster.
How does Histidine H2 receptor antagonists effect alcohol absorption?
H2 antagonists reduce stomach levels of alcohol dehydrogenase and significantly reduces the amount of first pass metabolism, meaning the alcohol will arrive in larger concentrations into the blood stream
How to antacids such as Zantac affect alcohol absorption?
reduces stomach acidity and levels of first pass metabolism by reducing the amount of alcohol dehydrogenase present in the stomach, results in increased BAC levels
Why do women show higher levels of BAC even if they consumed the same amount as a male?
because they have less amounts of alcohol dehydrogenase, the alcohol is not metabolized as fast before entering the blood stream.
Additionally, because alcohol is distributed and excreted through body water, which women have less of (they have more fat), alcohol reaches higher concentrations in the blood since their is less body water to dilute the alcohol.
Why does alcohol inhalation cause higher BACs that oral ingestion of alcohol?
AWOL (alcohol without liquid) causes higher BACs because first pass metabolism is passed- the alcohol goes directly to the blood stream without going through the stomach.
Why would individuals that have a lesser % of muscle have higher levels of BAC compared to an individual who is ripped?
because alcohol is distributed, excreted and carried entirely in body water. A person with more fat will have higher BACs because the body with more fat has less water (in the muscles) to dilute the EtOH in the blood.
How does alcohol distribution get affected with age?
BAC’s increase as individuals get older because their fat: muscle ratio goes up, even if their body weight does not change. Fat= less body water= alcohol does not get diluted as much= higher concentrations.
What major organ is responsible for alcohol to be completely metabolized?
the liver; although the stomach is where first pass metabolism takes place, the liver is where most of it is metabolized.
What is the rate limiting step/ slowest step of alcohol metabolism?
the conversion of alcohol to acetaldehyde via alcohol dehydrogenase.
In addition to alcohol dehydrogenase, what other system helps the body metabolize alcohol?
the Microsomal Ethanol Oxidizing System (MEOS). A much smaller component of alcohol metabolism than alcohol dehydrogenase. MEOS is stimulated in heavy drinkers.
T/F Eating speeds up the rate of metabolism
TRUE. Eating speeds up the rate of metabolism but not absorption. This is a result of increased blood flow to the liver caused by food in the stomach
Two main neurotransmitters affected by alcohol
GABA and glutamate
Two ways that alcohol interacts with GABA or glutamate receptors
1) interacting with a pocket: an alcohol sensitive area on the receptor site
2) blocking the entire ion channel itself
Alcohol is a GABA ____
Alcohol is a GABA agonist. EtOH stimulates GABA activity and then decreases brain activity
2 types of GABA receptors
GABAa receptors- ionotropic
GABAb receptors- metabotropic
How is the function of the GABAa regulated in terms of structure?
the receptors are made of different types of subunits, alpha beta delta etc. Different varieties of subunits result in different GABAa receptor configurations. The variety of receptors determines its functions and how the receptor is affected by alcohol and other GABAergic drugs
Difference between orthosteric site and allosteric site
orthosteric site: binding site on the GABAa receptor where the natural ligand (aka GABA) binds to. When activated, the receptor opens its ion channel and permits an influx of Cl- ions, creating hyperpolarization of the cell. (More neg charge= more inhibition)
allosteric site: GABAa has alternative binding sites for alcohol and benzodiazepines, which creates conformational change, affecting the orthosteric site. Modification at the allosteric site by alcohol can change GABA binding affinity to GABAa.
Alcohol is a _____ modulator of GABAa receptors.
Alcohol is a positive allosteric modulator that enhances the ability of GABAa to open its ion channels via interaction of allosteric sites.
What kind of subunit must be present in order for alcohol to be able to allosterically modulate GABAa? Where are most of these subunit-containing GABAa receptors found?
EtOH only acts on GABAa receptors that have DELTA subunits.
DELTA-containing GABAa subunits are predominantly found in the cerebellum (PURKINJE NEURONS), which is involved in fine motor control, balance and coordination– issues that are compromised when a person has been drinking.
What type of neuron is found in the cerebellum and are found to interact with alcohol?
Purkinje Neurons are cerebellum neurons that are stimulated at low doses of alcohol, when alcohol acts on GABAa receptors. This causes the impairments in motor control.
What are the three varieties of GABAb receptors? Which one of these types of GABAb receptors can be modulated by alcohol?
1) autoreceptor GABAb= located on PREsynaptic cell and stimulates/modulates GABA release
2) located on the POST synaptic cell= blocks release of other neurotransmitters by altering the calcium channels
3) dopamine-stimulating GABAb receptors
EtOH alters GABAb receptors located on dopamine synapses that stimulate the release of dopamine.
Alcohol is a glutamate _____
alcohol is a glutamate antagonist
Which type of glutamate receptor is affected by the presence of alcohol? How is it affected?
NMDA receptors. Alcohol blocks the NMDA ion channels, which is responsible for excitatory responses. This results in the depression of the function of the glutamate ion channel. Magnesium release from ion channel of NMDA receptor is also disrupted.
What does chronic use of alcohol do to a person’s NMDA receptors? How might this contribute to withdrawal symptoms?
Chronic exposure UPREGULATES NMDA receptor-ion channel functioning. the brain thus becomes more sensitive to glutamate as a means for compensating for the prolonged depression caused by alcohol. When a person stops drinking, they are still very sensitive to glutamate (excitatory), which may responsible for the increased anxiety and agitation.
How does alcohol interfere with long term potentiation and prevention of new neuronal formation?
alcohol can affect hippocampus and memory formation because of its interactions with NMDA receptors.