Midterm Review Flashcards
Describe the metabolism of alcohol. What enzymes are involved?
Alcohol diffuses easily across all membranes and is thus completely absorbed by the GI tract in the stomach and upper intestine.
95% of alcohol is metabolized by the enzyme alcohol dehydrogenase (ADH) and the other 5% is excreted through the lungs
85% is metabolized in the liver and 15% is metabolized by first-pass metabolism
Max metabolism is 170g/24hours or 7-8g (10mL)/1hr
- ADH converts alcohol to acetaldehyde.
- Acetaldehyde dehydrogenase (ALDH) converts acetaldehyde to acetic acid.
- Acetic acid is broken down into carbon dioxide and water
How long does it take for an adult to metabolize the alcohol in a 1oz glass of 80 proof whiskey? A 4oz glass of wine? A 12oz bottle of beer? and a pint of 7% microbrew?
1 hour
Is a man safe to drive if he is 200lbs and has had 6 drinks in 4 hours?
BAC of 200lbs man after 6 drinks = .11
Alcohol burned up after 4 hours = .060
0.11 - 0.60 = 0.05
He is not safe to drive as he is over the legal limit
Is the claim ‘men can handle their alcohol better!” true?
For the majority, yes.
Women have a lower level of ADH and thus less or broken down and more alcohol gets into the blood stream
Men typically have a greater ratio of muscle to fat which means they have a larger vascular compartment and thus more blood = more dilution
Women have higher body fat which concentrates alcohol is plasma
What are the pharmacodynamics of alcohol (GABA and Glu)?
Alcohol has been shown to affect the Glutamate and GABA systems and the intracellular transduction process
Alcohol depresses the responsiveness of the NMDA glutamate receptor - an excitatory receptor
Alcohol binds to the GABAA receptor, resulting in increased inhibition (reducing panic and anxiety)
- GABA inhibition induces opioid release which triggers DA in the reward system
Is the stimulation people feel from drinking alcohol pharmacological or psychological?
Psychological - alcohol is a depressant
What are the pharmacodynamics in chronic alcohol users?
Chronic exposure leads to:
- Upregulation of NMDA receptors - Acamprosate interacts with these NMDA receptors to reduce neuronal hyper excitability (seizures, nerve damage and loss)
- An antagonistic effect on 5-HT increasing its activity (remaining in the cleft) - impulsivity and dependence
- Formation of NT anandamide which activated the cannabinoid receptor, causing down-regulation and hyperactive activation (cravings)
What are the pharmacological effects of alcohol?
- Graded (worsens with increase of dose) reversible depression of behaviour and cognition
- Depression of respiration
- Additive effects with other sedative-hypnotic compounds
- Reduction of circulation function (dilates blood vessels)
- Increased risk for coronary artery disease and drugs
- Increase of HD-lipoprotein and HD-choleseterol (good fat and cholesterol)
What are the psychological effects of alcohol?
- Activates GABA system to reduce anxiety
- Activates DA system so impulse control is reduced and aggression is increased
- Depressed Glutamate system causing impaired cognitive function, alcohol myopia (short sightedness), and cognitive and attentional deficits
What are the different types of tolerance?
Metabolic tolerance - body’s ability to adapt to alcohol
Tissue/functional tolerance
Homeostatic tolerance - environmental cues
What are some side effects of alcohol use?
Acute use: clouded sensorium, impaired judgement, anterograde amnesia
High/chronic use: delusions, hallucinations, unconscious
Physical effects: liver damage, dementia (nerve damage), Wenicke Korsakoff syndrome, digestive problems, cancer
Describe some of the fetal effects of alcohol. Is there a ‘safe’ level of drinking during pregnancy?
There is no safe limit. Alcohol exposure can cause FAS or alcohol related neurodevelopment disorder (ARND)
FAS is marked by CNS dysfunction, retardation, body growth deficiency, FAS facial/body features
Facial features: microencephaly, palperbral tissue (short opening of eye), epicanthal folds, mid face (flat), low nasal bridge, philtrium (flat upper lip(, micrognathia (small jaw), railroad track ears)
Summarize some of the drugs used in treating alcoholism
Alcohol ingestion decreases Glutamate and increases GABA. Alcohol rebound/withdrawl increases glutamate and decreases GABA
- Benzos treat withdrawal by increasing GABA
- Antipsychotics alleviate delirium, haullucinosis, and seizures
- Anticonvulsants treat alcohol dependency
- Drugs used to maintain abstinence: antabuse, naltrexone, acamprosate,DA drugs (wellbutrin), 5-HT drugs
What differences does Type A and Type B have on alcohol use?
Type A are later onset drinkers and Type B drinkers start at a younger age
Alcohol treatment is more difficult with Type B personalities as they started younger.
What is a BrAC?
Breath alcohol concentration
If a BAC ratio is .08BAC/..02BrAC what is their BAC is their BrAC is .03
X BAC .08 BAC
——— = ————–
.03 BrAC .02 BrAC
x = (.08 BAC)(.03 BrAC)
—————————–
.02 BrAC
x = 0.12
What is the reaction that occurs in a brethalyzer?
Potassium Dichromate is the reactive agent that changes colour
Sulfuric acid is what is measured in the breath
Silver nitrate is the catalyst that speeds up the reaction without parking
A rapid change of air temperature can impact a breathalyzer reading
True or False
True - requires frequent calibration
Holding your breath will decrease you BAC levels
True or False
False - in concentrated it
Running will decrease your BAC levels
True or False
True - it decreases the amount of air to expel
Rinsing with mouthwash will increase your BAC
True or False
True - it creates false positives because there is alcohol in it
Describe the mechanism action of bentos and how it differs from that of barbiturates
Barbituates and benzos are both GABA receptor agonists.
Barbiturates bind to the GABAA receptor and result in an increased duration of the opening of the cl- channel. They also act as an NMDA receptor antagonist, blocking glutamate transmission (blocking excitation)
Benzos bind to an adjacent GABA binding site and cause a 3-dimensional conformation change that increases the affinity (binding) of GABA, increasing the inhibitory action resulting in an influx of Cl- ions hyperpolarizng the postsynaptic neuron depressing excitability
Since barbiturates do not require the presence of GABA they are more toxic