Lecture 5: Neurobiology of Specific Substances Flashcards
etoh
chemical name
CDC Drinking Guidelines
Moderate Drinking = Potential Health Benefits?
* Small amounts still ↑ risk of Cardiovascular-related illnesses
Moderate drinking guidelines (CDC)
* Females = up to 1 drink per day
* Males = up to 2 drinks per day
Heavy Drinking
* Females = 8 or more per week
* Males = 15 or more per week
Binge Drinking (in 2-3 hours)
* Females = 4 or more
* Males = 5 or more
National Institute on Alcohol Abuse and Alcoholism (NIAAA) Stats
140,000 people in the U.S. die from alcohol-related deaths each year.
4th leading preventable cause of death in the US.
Rates of daily heavy drinking are higher among the following ethnic groups:
* Hispanics:33.9%
* Native Americans:28.4%
* Whites:27.3%
*Asians at 19.2%
Different to alcohol dependence rates:
* Whites (13.8 percent) > Blacks (8.4 percent) and Hispanics (9.5 percent)to develop alcohol dependence in their lifetime.
* Genetics of alcohol dehydrogenase indicate resistance has arisen independently in different cultures.
ETOH: hangovers
5-23% of pop are hangover “resistant”.
Hangover severity may be correlated with Cogener levels
ETOH: asians
Approximately 36% of East Asian subjects experience an alcohol-induced flush reaction d/t deficient enzyme levels of aldehyde dehydrogenase.
ETOH: SES
highest at each end of SES spectrum
ETOH: Marketing
Marketing between 2006-2012 = ↑ 38.5% targeting young women
* Sugar = ↓ absorption (prolongs effects)
* Carbonation = ↑ absorption
* Menstruation = ↓ etoh metabolism
Pharmacokinetics: ADME
Absorption
Distribution
Metabolism
Excrection
Pharmacokinetics of Ethanol: Absorption
Absorption – GI Tract = 20% stomach & 80% small intestine (several variables)
* Food inhibits absorption by causing oxidation of alcohol & closing the pyloric sphincter
* Irritates gastric mucosa –> slowed absorption
* Impacts vitamin absorption
Pharmacokinetics of Ethanol: metabolism
Metabolism = Primarily hepatic (90%)
* Metabolized by Alcohol Dehydrogenase (ADH) (requires B vitamins) Acetaldehyde
* Acetaldehyde (toxic, carcinogenic, prevents absorption of nutrients) metabolized by aldehyde dehydrogenase (ALDH) Acetate
Pharmacokinetics of Ethanol: excretion
Excretion = Urine
Diuretic properties decreased nutrients & dehydration
Pharmacokinetics of Ethanol: intoxication
Intoxication = consuming etoh faster than liver can break it down
*1 standard drink per hour
What do most people with AUD have?
80% of ind. With AUD = Thiamine Deficiency D/T ↓ Vitamin Absorption & ↑ Thiamine use by ADH
1) decrease vitamin
2) metabolize
3) prevents absorbtion
4) diuretic
Neural effects - alcohol
Alcohol: how different amounts have different effects
Biphasic Model = low amounts and high amounts have different effects
Wernicke-Korsakoff Syndrome
Caused by thiamine deficiency
Thiamine plays roles in brain cell energy production & maintenance and synthesis of myelin
Technically 2 conditions
* Wernicke’s Encephalopathy (WE) – ACUTE phase = delirium, incoordination, ataxia, decreased consciousness, memory deficits, abnormal gait
* Korsakoff Psychosis – can develop after (WE) or without – CHRONIC phase = impacts anterograde memory more significantly than retrograde memory & confabulation * NOT treatable –> yellow string test: no string, but that person will see a yellow string and reach for it
Alcoholic Neuropathy
Peripheral nerve damage
Stimulant Pharmacokinetics
Stimulants impact the brain’s levels of epinephrine/norepinephrine (E/NE), dopamine (DA), and serotonin (5-HT).
* Stimulants impact each to a varying degree (selectivity).
* Cause alertness, attention, energy.
Several medical uses and rich history (Freud’s Uber Coca)
* Pain management, ADHD, asthma, obesity, narcolepsy
Stimulant risk factors
Primary risk factors:
* Reduced seizure threshold (more likely to have a seizure)
* ↑ BP, HR, HTN = ↑ risk of stroke, myocardial infarction
* Poor appetite, mood swings, anxiety, insomnia
* Toxic levels = paranoia, psychosis
Betel Nut
