Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
73 Cards in this Set
- Front
- Back
What amount of alcohol is considered 'moderate drinking'?
|
2 drinks/day for men, 1 drink/day for women.
|
|
What is considered a short-acting, weak sedatohypnotic?
|
Alcohol-->its short-acting causing it to have a bad withdrawal like the short-acting barbituates.
|
|
How many Americans suffer from Alcohol Use Disorders?
|
18 million
|
|
In every ten people, how many engage in high-risk drinking patters?
|
3 out of even 10 US adults.
|
|
How do you define 'binge drinking'?
|
Pattern of drinking that brings BAC to 0.08% or above. For the typical adult, this is 5 or more drinks (male) or 4 or more drinks (female) in 2 hrs. Its dangerous for drinker and society.
|
|
What 2 factors influenze alchol use and dependence?
|
-genetic (50%) and environmental (50%)
|
|
How does alcohol consumption affect the brain?
|
The cortex stops growing @ 25 and many in their teens and early twenties consume large amounts of alcohol. The limbuc system governing emotions matures earlier than frontal cortex, responsible for planning, self-control, & decision making.
|
|
What are the consequencers of adolescent alcohol abuse on the developing human brain.
|
Binge-like drinking-->affects memory, alters sensitivity to motor impairment, & damanges frontal-anterior cortical regions.
-Prolonged ethanol exposure produces long-lasting neurophysiological changes in cortex & hippocampus (@ gene level) |
|
What is the relationship b/w alcohol use, nicotine, & cannabis?
|
There is a huge correlation b/w nicotine & alcohol users. Nicotine is a weak stimulant, alcohol is a sedatohypnotic, and marijauna most closely resebles alcohol.
|
|
Compared to adults, who sensitive are adolescent to alcohol?
|
Adolescents are less sensitve to some of the aversive effects of acute alcohol intoxication (sedation, hangover, ataxia), but more sensitive to alcohol's effects on:
social facilitation, disruption of spatial memory. |
|
What 5 factors does BAC depend on?
|
-Amt & alcohol concentration of beverage.
-Rate of drinking -Food consumption & composition -Gastric emptying & gastric metabolism -Hepatic first pass |
|
Where is alcohol absorbed?
|
Rapidly absorbed thru duodenum.
|
|
Do you need a lot of alcohol to get an effect?
|
Yes
|
|
What order kinetics is alcohol?
|
Zero order kinetics.
|
|
Some of the alcohol is destroyed by what enzyme in the stomach?
|
Alcohol dehydrogenase. (ADH)-->known as first pass metabolism. Solid food in stomach slows absorption of alcohol.
|
|
After a few drinks, does absorption rate increase or decrease?
|
Incease.
|
|
What does carbonation do for alcohol absorption?
|
Passage of alcohol thru stomach may be facilitated by carbonation--like 'kick i' in champagne.
|
|
How does a high alcohol concentration affect diffusion/absorption?
|
Diffusion rates of alcohol increases w/ inc concentration, but very high concentrations interferes w/ absorption by slowing rates at which stomach empties its contents into intestines.
|
|
What are the gender difference in alcohol absorption for men and women?
|
Women have lower levels of ADH in their stomach than men to break some of the alcohol down. Men also have more total body water b/c of the higher testosterone level.
|
|
Does alcohol cross the BBB?
|
Yes, alcohol is evenly distributed in body fluid and crosses teh BBB and the placental barrier w/o difficulty.
|
|
How do you calculate BAL?
|
mg/100mL of blood
|
|
Define zero order kinetics.
|
Drugs that metabolize w/ zero order kinetics @ a constant rate regardless of the size of initial dose. (like alcohol!)
|
|
Where does most of alcohol get metabolised?
|
Liver.
|
|
What is alcohol's elimination rate?
|
7 g/hr
|
|
What breaks down alcohol to acetaldehyde?
|
Alcohol dehydrogenase (usually not rate limiting)
|
|
What causes aldehyde dehydrogenase inhibition?
|
Disulfiram
|
|
Accumulation of acetaldehyde is associated w/ what symptoms?
|
HA, gastritis, nausea, dizziness (hangover)--can also be from dehydration.
|
|
What happens when alcohol is being metabolized?
|
You generate a lot of hydrogens and get a lot of metabolic acidosis.
|
|
Polymorphism occurs at which 2 ADH loci?
|
ADH2 and ADH3
|
|
Why do 15% of African Americans have an increased alcohol metabolic rate?
|
B/c they have ADH 2*3 allele.
|
|
95% of White Americans have which ADH allele?
|
ADH2*1
|
|
50% of Asians have which ALDH (aldehyde dehydrogenase) allele causing them to have decreased elimination of acetaldehyde & alcohol as well as a flushing response?
|
ALDH2
|
|
What is the rate limiting step of alcohol metabolism?
|
Alcohol dehydrogenase.
|
|
What is the Microsomal Ethanol-Oxidizing System?
|
Uses p450 system to metabolize alcohol. Handles 5-10% @ low blood levels. Its activity rises @ higher centers of blood alcohol accounting for 50-65% of inc alcohol metabolism inducing by heavy drinking, which partly accounts for alcohol tolerance. Also responsible for metabolism of other drugs like barbituates.
|
|
What CNS effects does alcohol have from depression of inhibitory control mechanisms in the brain?
|
Euphoria, impaired thought proceses, dec mechanical efficiency.
|
|
What is the MOA of ethanol?
|
Works on ion channels--especially by inhibiting glutamate-NMDA excitatory NT receptor & potentiating GABAa inhibitory NT receptor
|
|
What does chronic alcohol consumption induce?
|
Chronic ethanol consumption reduces GABA-mediated inhibition & abolishes ethanol potentiation
|
|
Ethanol inhibits or facilitates which receptors?
|
Ethanol inhibits: adenosine transporter & NE transporter
Ethanol facilitates: DA transporter & 5-HT transporter |
|
What gives pregnant black-American women who drink while pregnant a protective effect against alcohol-related birth defects?
|
ADH2*3-->higher alcohol metabolism
|
|
Waht effects does ethanol have on the GABA system?
|
Interaction w/ GABAA receptor-->facilitation of GABA transmission-->activation of DA neurons in mesolimbic system--> sedative & anxiolytic effecgts, rebound hyperexcitability seen w/ withdrawal.
|
|
explain zero-order kinectics.
|
a constant amount of drug is metabolized per unit of time regardless of a drug concentration; alcohol will be metabolized 1 drink per hour or about 10grams of EtOH an hour; aspirin and alcohol follow zero-order kinetics
|
|
explain alcohol's first pass metabolism.
|
alcohol follows first-pass metabolism. it begins it metabolism in the gut by alcohol dehydrogenase; the majority 90-98% is metabolized in the liver; both stomach and liver use the enzyme alcohol dehydrogenase (ADH is a NAD dependent enzyme that breaksdown alcohol at a fixed rate (zero-order) of 7-10g/hr
|
|
what two enzymes are responsible for metabolizing alcohol into its final waste product acetate?
|
alcohol --> ALCOHOL DEHYDROGENASE --> acetaldehyde (associated with headache, gastritis, nausea, hangover) --> ALDEHYDE DEHYDROGENASE --> acetate (eliminated in urine)
|
|
what drug will inhibit the breakdown of acetaldehyde --> acetate, thus working by inhibiting the enzyme aldehyde dehydrogenase?
|
disulfiram
|
|
what allele is associated with persons of asian decent that will cause a decreased elimination of acetaldehyde/alcohol/and flushing?
|
50% of asians have a polymorphism at the ALDH2 gene that depletes them of the enzyme aldehyde dehydrogenase
|
|
what is the rate-limiting step in alcohol metabolism?
|
alcohol dehydrogenase (ADH) - 1st and slowest step in breaking down EtOH
|
|
what enzyme is found mostly in the liver and increases in response to chronic ethanol exposure (which may attribute to tolerance).
|
MEOS - microsomal ethanol oxidizing system (also responsible for metabolizing barbituates)
|
|
how many drinks will it take you to get to a BAC of 0.08?
|
1 drink per 50lbs per hour to get a BAC of 0.08
|
|
what is a letal BAC?
|
BAC of 0.4 is normally lethal.
|
|
explain ethanol's MOA.
|
ethanol inhibits glutamate-NMDA excitatory neurotransmitter receptors and potentiates the GABAa inhibitory neurotransmitter receptor.
|
|
chronic alcohol intake will do what to ethanol's normal action on GABA?
|
chronic ethanol use will reduce the GABAa-mediated inhibition. the brain adjusts
|
|
what is ethanol's relationship with neurotransmitter release?
|
ethanol enhances dopamine release from the ventral tegmental area and teh nucleus accumbens; explaining the reward
|
|
name the two types of postsynaptic receptors and list examples of each.
|
1)LIGAND-GATED ion channels (fast): GABAa, glycine, glutamate, AcH (nicotinic) 2) METABOTROPIC RECEPTORS (slow): norE, GABAb, serotonin, dopamine, AcH (muscarinic), purinergic (adenosine)
|
|
what does alcohol do to blood vessels, sleep, and antidiuretic hormone?
|
dilates blood vessels; decreases REM, and inhibits ADH (reason for constant urinating while drinking)
|
|
when the BAL is rising what type of feelings to people have? what about when the BAL is falling?
|
RISING: stimulation, euphoria and elation; FALLING BAL: sedation, anger, and depression
|
|
at 60mg/100ml, what generally happens to a person's stance?
|
positive Romberg sway test
|
|
what is the term to describe the inability to convert short term into long term memory; it occurs in heavy drinkers.
|
blackout
|
|
what is the term to describe when you cannot remember events that happened while drunk but can remember then again if reminded?
|
greyout - this is likely a result of dissociation
|
|
at what BAL will driving performance be effected?
|
50-80mg/100ml of blood
|
|
functional MRIs will show a weakened connection between what two CNS structures?
|
frontal lobes and striatum
|
|
how long does it take to develop maximum tolerance?
|
few weeks; tolerance disappears in a couple of weeks if alcohol is taken away
|
|
define alcohol abuse.
|
in a 12 month period must have one of the following: 1 failure to carry out major obligations at work, home, or school; 2.repated use even when it is physically dangerous 3.repeated legal problems due to EtOH, 4. continued use despite knowing it has caused or worsened social or interpersonal problems
|
|
repeated use of EtOH will cause tolerance to alcohol and cross-tolerance to what?
|
other drugs (sedatives)
|
|
if you combine alcohol with sedatives what will it do to the response and TI?
|
increase the response and decrease the TI(ratio of drug's toxic dose/theraputic dose); it will take less time to kill you;;;;even combined, alcohol will still metabolize at 1 drink/hr (zero order)
|
|
name some signs of alcohol poisoning?
|
mental confusion, stupor, coma, no response to pinching, vomiting while asleep, seizures (knocked out GABA -opposite of MOA; burst of glutamate), bluish tint to skin, cold hands
|
|
what is the final thing that will kill a person from alcohol poisoning?
|
respiratory failure
|
|
name some detrimental side-effects of alcohol use.
|
alcoholic hepatitis--> cirrhosis (ascities-abdominal distention), korsakoff's syndrome (due to lack of B1/thiamine); FAS fetal alcohol syndrome, alcoholic cardiomyopathy, ulcers, CA, pancreatitis, volume depletion
|
|
describe the facies of a fetal alcohol baby.
|
flat midface, short nose, thin upper lip, low nasal bridge, micrognathia (small chin), minor ear abnormalities, epicanthal folds
|
|
name this term that describes a chronic alcoholic with tremor, anxiety, tachycardia, delusions, and agitation. what do they have?
|
delirium tremens - this occurs when chronic alcoholics are suddenly deprived of alcohol - need to treat
|
|
what drug class do we treat alcohol withdrawal with?
|
benzodiazepines - helps to tx the tremors, tachycardia, hypertension and seizures
|
|
what drugs do we use to prevent drinking?
|
Disulfiram (blocks aldehyde dehydrogenase enzyme); Naltrexone (injection-binds to opioid receptors and blocks craving/reward$$); acamprosate (in withdrawl)(blocks craving by decreasing the release of glutamate); Benzodiazepines, SSRIs
|
|
what is the name of the behavioral-psychosocial treatment that treats alcoholism as a disease model?
|
Alcoholics Anonymous
|
|
name the drug that inhibits neuronal hyperexicitability by decreasing the release of glutamate and decreasing the post-synaptic excitability of glutamate. it inhbits Ca influx through NMDA glutamate receptors and voltage dependent ca channels.
|
acamprosate (used during withdrawl - decrease glutamate) - reason it works: chronic EtOH increases NMDA glutamate and Voltage dependent Ca2+ channels
|