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Term Definition
Ethanol -A psychoactive drug
-Similar in most respects to other sedative-hypnotic compounds
-Used primarily for recreational purposes rather
than medical purposes
Pharmacology of Alcohol:pharmacokinetics /absorption1 how does it absorb? Soluble in both water & fat
-contains calories
Diffuses easily across all biological membranes
Rapidly & completely absorbed from entire gastrointestinal tract
Presence of food in stomach slows the speed of absorption
Pharmacology of Alcohol:pharmacokinetics /absorption2 where in the body 20% of a single dose absorbed directly from stomach & remaining 80% absorbed rapidly & completely from upper intestine
Distribution:of alcohol after absorption what happens -After absorption, alcohol evenly distributed throughout all body fluids & tissues
-Once it reaches the brain, it crosses blood-brain barrier almost immediately
-Freely distributed across placenta & will easily enter the brain of fetus
Excretion:of alcohol About 95% of alcohol ingested is enzymatically metabolized by enzyme alcohol dehydrogenase
5% is excreted mainly through lungs, sweat, & urine
Metabolism of alcohol where in the body is it metabolized 85% of metabolism occurs in the liver
Up to 15% of the metabolism is done by gastric alcohol dehydrogenase enzyme located in stomach lining
Excretion of alcohol (breakdown) Alcohol—-> Acetaldehyde–> acetic acid–> carbon dioxide & water
The average person metabolizes 6 to 8 grams of 100% (200 proof) alcohol per hour
It would take an adult 1 hour to metabolize the amount of alcohol that is contained in… 1.5 oz. shot of 80 proof hard liquor
5 oz. of wine
12 oz. bottle of beer
= 1 drink!
Women have higher
blood ethanol concentrations than men
Women have a lower
level of gastric alcohol dehyrdogenase enzyme
Blood Alcohol sat_flash_1
Dependent on:
-Presence of food
-Rate of consumption
– Concentration of alcohol
-Drinker’s body composition
Ethanol is a potent inhibitor of the function of glutamate receptors
how does ethanol disrupt It disrupts by depressing the responsiveness of NMDA receptors to release glutamate
Removal of ethanol’s inhibitory effects results in withdrawal signs like seizures
GABA receptors:
Behavioral results include
sedation, muscle relaxation, and inhibition of cognitive & motor skills
Increased levels of GABA have what effects on the brain Increased levels of GABA have positive effects of reward center in brain
Serotonin:Chronic alcohol consumption results in? augmentations in activity
Serotonin dysfunction may role in? pathogenesis alcoholism
Effects of alcohol are graded, reversible depression of CNS function
Effects of Alcohol Moderate Use: Disinhibition, sedation, mood swings
Effects of Alcohol Heavy, Long-Term Use Erratic behavior, blackouts
Acute Effects of Alcohol:1 – Hypoglycemia
Irritant & promotes flow of gastric juices
Effects pituitary gland which tells kidneys to produce more than normal amounts of dilute urine (diuretic)
Presence of alcohol interferes with metabolizing medication
Chronic Effects of Alcohol:
Visible symptoms:
-Thin, bloated appearance
-Hyperpigmented or jaundiced skin
-Multiple bruises
-Hoarse voice
-Ankle swelling, hemorrhoids, loss of pubic hair -Testicles may shrink
-Dilated capillaries & acne lesions
-Enlarged bulbous nose
Chronic Effects of
2. Irritation, Bleeding, & Malabsorption:
-Alcohol irritates stomach lining
-Irritates esophagus resulting in mild chest pain
-Causes ulcers and stomach bleeding
Chronic Effects of
3. Liver Disease:
-Fatty liver
-Alcoholic hepatitis (jaundice)
-Cirrhosis of the liver (non reversible)
Chronic Effects of Alcohol:
5. Cardiovascular System:
-AHMD (alcoholic heart muscle disease)
-Shortness of breath & dramatic enlargement of heart
-Increase risk of stroke
mental expectations and setting become what due to alcohol Mental expectations & setting become less important at increased doses due to sedative effects
is alcohol an aphrodisiac Alcohol is NOT an aphrodisiac
Low doses:of alcohol – Memory, concentration, & insight are dulled
– Confident, social ability, & courage increased
??Blackouts caused by alcohol:
– Serve as a warning sign
– Tend to occur after RAPID consumption of alcohol, or
how fast BAC level rises
—Not ‘how much you drink’ but ‘how fast you drink’
-Can involve a person’s level of tolerance
– Person cannot create/store NEW memories
Binge drinking defined:
Other terms: High-risk drinking
Drinking that increases the risk of consequences legally, physically, personally and/or academically
-For men: 5 or more drinks in one sitting
-For women: 4 or more drinks in one sitting
how much more likely are binge drinkers to miss class Compared to non-binge drinkers, frequent bingers are 17 times more likely miss a class as a result of their drinking
The extent of tolerance depends on amount, pattern, & extent of alcohol ingestion
CNS adapts to the continual presence of alcohol
— Need more alcoholto achieve same affect
Little or no tolerance: Ingest intermittently
Marked tolerance: Ingest large amounts
Tolerance Three types: 1. Metabolic Tolerance: Liver increases its amount of drug-metabolizing enzyme
Tolerance Three types: 2. Tissue, or Function Tolerance: -Neurons in brain adapt to amount of drug present
-Display blood alcohol levels about twice those of non-tolerant people at similar level of intoxication
Tolerance Three types:3. Associative, Contingent, Homeostatic Tolerance: Environmental manipulations can counter effects of ethanol
After physical dependence is established, withdrawal symptoms can occur
Withdrawal Symptoms
-Severity of symptoms widely depends on alcohol abuse
Hangover is a mini-withdrawal Tremors
Rapid pulse
Increased body temperature Depression
Addictive Process Availability -Sedative -Tolerance
-Physical dependence
-Memory programming –
– Depressive effect of alcohol on brain
Alcohol & Pregnancy
Fetal Alcohol Syndrome (FAS) :
Developmental disorder that occurs in children of mothers who drank during pregnancy
Mother does not need to be an alcoholic
No safe level of alcohol intake during pregnancy
Alcohol & Pregnancy
Fetal Alcohol Syndrome (FAS) : babies have:
Facial abnormalities
Retarded growth
Heart defects
CNS dysfunction, low intelligence
Behavioral abnormalities

-Damage is irreversible

Uppers (stimulants) include: 1. very strong stimulants: cocaine & amphetamines 2. moderate: diet pills & Ritalin
3. milder plant stimulants: ephedra & khat
4. legal mild stimulants: caffeine
uppers: stimulants 1 name and example ?Cocaine (hydrochloride, crack, freebase)
Amphetamines (speed, meth, ice)
Amphetaminecongeners(Ritalin ,dietpills, e.g., fen-phen)
uppers: stimulants2 name and example Plant stimulants (khat, betel nut, yohimbe)
Caffeine (coffee, tea, soft drinks, OTC meds)
Nicotine (cigarettes, cigars, smokeless tobacco)
Behavioral Stimulants
-Cocaine and the amphetamines are powerful psycho-stimulants that affect mental functioning and behavior.
-To exert their acute behavioral stimulant effects these drugs act to augment the action of several neurotransmitters, most important :dopamine
Cocaine and the amphetamines, in addition to other actions, increase dopaminergic activity on the nucleus accumbens, other limbic structures, and the limbic cortex associated with behavioral reinforcement, compulsive abuse, drug dependency, and cue-induced drug craving.
Cocaine and the amphetamines are therefore widely recognized as important drugs of compulsive abuse.
These drugs also have a variety of therapeutic uses, although today, reasonable alternatives are available for most of them.
All psycho-stimulants have significant side effects, toxicities, and patterns of abuse.
In low doses, cocaine and other psycho- stimulants evoke an alerting, arousing, or behavior-acting response that is not unlike a normal reaction to an emergency or stress.
what isthe most commonlyconsumed psychoactive drug in the world caffeine
In the U.S caffeine consumed daily by up to 80% of the adult population.
Caffeine is found in significant concentrations in: coffee, tea, cola drunks, chocolate candies, fortified waters, and cocoa.
Caffeine is one of the most widely used stimulants in sports, with documented efficacy and safety.
The average cup of coffee contains about 100 milligrams of caffeine
a 12-ounce bottle of cola contains about 40 milligrams of caffeine
The caffeine sat_flash_1 of chocolate may be as high 25 milligrams per ounce
Toxic Effects of Stimulant Drugs
• Psychological & Behavioral
1. Mood elevation
2. Enhanced alertness & increased attention
3. Sleep disturbances
4. Analeptic effects(increased psychomotor stimulation) 5. Anxiety & paranoid schizophrenic
6. Diminished appetite 7. Drug withdrawal: depression
8. Dependency synd
Toxic Effects of Stimulants •
Physiological Effects

1.—-• Cardiovascular

-cardiac arrhythmia
-increased systolic & diastolic blood pressure -circulatory collapse
-cerebral hemorrhage
Toxic Effects of Stimulants •
Physiological Effects
2.—-• Central nervous system
– Seizures
– Intracranial hemorrhage
– Movement disorders
Toxic Effects of Stimulants
• Physiological Effects
3. Pulmonary Effects
– Bronchodilation
– Increased oxygen consumption
Toxic Effects of Stimulants
• Physiological Effects
4, Renal Effects
– Increased urinary retention
Toxic Effects of Stimulants
• Physiological Effects
5.metabolic effects
– Hyperglycemia
– Increased metabolic rate (large drug doses)
– Elevated lipolysis
• Physiological Effects (eyes) • Mydriasis (pupillary dilation)
• Altered Thermoregulatory Capacity
• Physiological Effects
– Maternal, Fetal, & Neonatal complications
• Maternal
– Spontaneous abortion
– Still birth
• Fetal
– Growth retardation
– Cerebral infarction or hemorrhage
– Premature birth
• Neonatal
– Drug withdrawal,seizures
– Cardiovascular system complications
History Of Cocaine
Pure Food & Drug Act limited cocaine for medical use only
History Of Cocaine
Harrison Narcotic Act labeled cocaine as a narcotic
History Of Cocaine
Controlled Substance Act made cocaine use or possession a federal crime
Most street cocaine is adulterated which
complicates the pharmacology
• Common Adulterants:
Effects of Cocaine Depend on: 1. Dosage
2. Form in which drug is taken 3. Route of administration
4. Frequency of administration 5. User expectations
6. Setting
7. History & personality of user
Pharmacologic Actions:blockage of: initiation or conduction of nerve impulses (local anesthetic)
CNS stimulation caused by dose & route of administration -Euphoria & feeling of well being
-Motor coordination decreases with increased dose
-Fatigue is masked by central stimulation
-Weight loss
-Higher doses cause depression/reparatory failure
-Chronic administration cause paranoia
-Dental hygiene decr
Pharmacologic Effects
cardiovascular effects
• Cardiovascular effects:
•– Small doses may slow heart rate
•– Moderate doses increase heart rate
• –Increased blood pressure
•– Muscle fatigue is a direct toxic effect on heart
— Conduction disturbances
Pharmacologic Effects
?other effects
• Increased body temperature
• Dilated pupils
• Increases glucose availability
Mechanism of Action of Cocaine • Action of nerve impulse& conduction
• Blockade of neurotransmitter reuptake of dopamine, serotonin norepinephrine, & epinephrine
•– Similar to amphetamine
•– Increase epinephrine, increases physical energy
?Dosage Forms 1. Cocaine Hydrochloride • Water-soluble salt form for intranasal & intravenous use
Dosage Forms 2. Cocaine Base Crystals • Water-insoluble “crack” a ready to smoke base form of cocaine which vaporizes when heated at high temperature. Can be used intravenously.
Dosage Forms 3. Cocaine Alkaloid Paste • Water-insoluble “freebase” can also be smoked like “crack”
Routes of Administration • MucousMembrane –-ORAL
• Duration of high is 45-90 min and slowly diminishes
• Rapid absorption & peek euphoria in 15-30 min
• Perforation of nasal septum with chronic use
• Continual snorting limits absorption due to vasoconstriction of blood ves
Routes of Administration
• Intravenous
• Initial onset of action
– 30-45sec
• Duration of high
– 10-20min
• Initial euphoria followed by “crash” of extreme dysphoria & intense craving 40 – 60 min after injection
• Can lead to hepatitis, AIDS, endocarditis, addiction, & risk of overdose
Routes of Administration
• Smoking
• Euphoria more intense
• Initial onset of action – 8–10sec
• Duration of high – 5–10min
• Followed by a “crash” similar to intravenous injection
• Leads to chronic addiction
• Can cause pulmonary disease
Detoxification & Metabolism • Rapidly distributes to brain
• Metabolized in liver
Half-life OF COCAINE in plasma only 30 – 90 min
Half-life of cocaine with alcohol 150 min
1.Overdose can occur
2.Average lethal dose is
1.by any route of administration.
2. 500mg, but is variable.
Symptoms:of cocaine – Excitement
– Panic, Paranoia – Restlessness
– Chills
– Fever
– Nausea
– Vomiting
– Irregular heart rhythms
– Respiration&mentalconfusion
• Treatment: for cocaine – No antidote for cocaine
– Sedatives (Valium) can be used to decrease CNS stimulation
Monitoring Use : urine
Snorting & Intravenous
Positive urine for 2-4 days
Monitoring Use : urine
• Positive urine for 8-12 days
Chronic Cocaine Use & Withdrawal • Dopamine depletion • Rapid heart beat
• Hypertension
• Paranoia
• Sleep deprivation
• Withdrawal almost never fatal
• Not physically dependent
cocaine • Withdrawal Symptoms • Decreased energy
• Excessive sleeping
• Irritable mood
• Depression
• Psychomotor retardation • Nausea/vomiting
what is the primary active ingredient in tobacco. nicotine
Nicotine One of 4000 active compounds in tobacco
Is an extremely toxic, clear, & oily liquid
Accounts for only acute pharmacological effects of smoking
Routes of Administration: nicotine
Oral route (snuff, chewing tobacco)
Inhalation (cigars, cigarettes)
–Chemical by products of smoking
Nicotine is readily absorbed from every site on / in our body: including Lungs
Gastrointestinal tract
how is nicotine absorbed Quickly absorbed throughout body & body fluids and penetrates all barriers
Smoking is highly regulated behavior

Goal is to maintain steady-state brain levels of highly addictive psychoactive agent
Smokers “self-regulate” level of nicotine in system
Smoker regulates:
Frequency of breaths
Depth of breath
Time the smoke is held in lungs
#of cigs

half life of cig/nicotine 2 hours
Mechanism of Action:
-stimulates hypothalamus to increase dopamine levels
Dopamine accounts for the behavioral reinforcement, stimulant, antidepressant, and addictive properties of the drug
-Evidence shows nicotine as a powerful drug of addiction like heroine alc coke
only pharmacologically aactive drug in tobacco is: nictoine
Outside CNS, nicotine increases Respiration rate
Heart rate
Blood pressure
Coronary blood flow
in CNS, nicotine increases Cognitive functioning
Increase psychomotor activity
Sensorimotor performance
Attention & memory consolidation
Pharmacological Effects of nicotine Reduces activity of afferent nerve fibers coming from muscles
Reduction in muscle tone
Involved in relaxation experience of smoking
Antidepressant effects
Reduces appetite
Reduces weight gain
Low doses of nicotine: Relaxation
Increases vigilance
Rapid information processing
High doses of nicotine: Nervousness
Increase panic attacks
Psychological Effects of nicotine Increased concentration
Decrease in perceived level
of tension
Ability to cope with over stimulating environment
Pleasure, relaxation
Quick bursts of energy
when tired
Enjoyable tactile sensations
Toxicity cigarettes Tar:
in tobacco
mainly responsible for diseases associated
with long-term tobacco use
Person’s life is shortened 14 minutes for every cigarette smoked
Leading causes of death from smoking: Heart disease
Cerebrovascular disease
Lung disease
how does smoking effect the lungs Pack-a-day smoker pours 1 full cup of tar into his lungs a year
Tar thickens cells in mucous membranes in throat & destroys delicate air sacs (alveoli)
Smoking paralyzes lungs’ natural cleansing process
Increases risk of emphysema
how does smoking effect cardiovascular Pulse quickens
Heart beats extra 10-25 times per minute which strains the heart
Blood vessels constrict & blood pressure increases by 10-15%
Stress on the heart increases risk of heart attack & stroke
Health Effects of Smoking
Decrease in blood flow causes
Takes longer to heal wounds
Health Effects of Smoking blood Carbon monoxide decreases oxygen
Health Effects of Smoking
Become yellow from smoke and tar
Health Effects of Smoking
Men- erection problems, decreased
sperm count, altered shape of sperm Women- 43% decrease in fertility
health effects of smoking lung and mouth irritation shortness of breath
smokeless tobacco health effects moth sores
smokeless tobacco health effectsBlood vessel constriction grayish complexion
Tolerance & Dependence
/ nicotine and tobacco
Nicotine induces physiological &
Cessation of smoking causes cravings &
Nicotine causes physical addictio
Getting Help
Pharmacotherapies: nicotine/tobacco
Nicotine gum
Nicotine inhaler
Nicotine nasal spray
Nicotine patch
Benefits from Quitting
Within 36 hours
blood carbon monoxide levels
return to normal
Nicotine-Cardiovascular Disease carbon monoxide in smoke decreases amount of oxygen delivered to heart muscle,nicotine increases the amount of work heart does increasing heartrate/bloodpressure
carbon monoxide and nicotine increaseincidence of atherosclerosis, narrowing and thrombosis
Nicotine-Cardiovascular Disease cigarette smoke Cigarette smoke has been firmly established as an independent risk factor for atherosclerosis and other vascular diseases. Data suggests nicotine releases VEGF through nicotinic Acetylcholine Receptors. VEGF may contribute to risk of cardiovascular diseas
Nicotine-Cardiovascular Disease The carbon monoxide in smoke decreases the amount of oxygen delivered to the heart muscle, while nicotine increases the amount of work the heart must do by increasing the heart rate and blood pressure.
Nicotine-Cardiovascular Disease
Both carbon monoxide and nicotine increase the incidence of
atherosclerosis, narrowing and thrombosis clotting in the coronary arteries.
Theses three actions and others as well seem to underlie the dramatic increase in the risk of heath from coronary heart disease in smokers compared to nonsmokers.
Cigarette smoke has been firmly established as an independent risk factor for atherosclerosis and other vascular diseases. Data suggest that nicotine releases VEGF through nicotinic Acetylcholine Receptors. VEGF may contribute to the risk of cardiovascular diseases in cigarette smokers.
Cigarette Smoking & Risk of Stroke Cigarette smoking: a major cause of stroke by:
– increasing clotting factors in the blood
– decreasing HDL cholesterol levels
– increasing triglyceride levels damaging lining of blood vessels.
risk for stroke increases
as # of cigs smoked increases
Effects of Secondhand Smoke secondhand smoke also negatively affects cardiovascular health by:
– decreasing exercise endurance
– damaging blood vessel walls
– increasing the tendency of blood platelets to clot
Cigarette smokers
a 50% increase in the progression of atherosclerosis when compared with people who have never smoked.
Contrary to public perception, smoking-caused heart disease actually results in more deaths per year than smoking-caused lung cancer.
cigarette smokers/heart disease stats 30% of all heart disease deaths are caused by cigarette smoking.
Smoking is the single largest preventable cause of heart disease in the United States.
Study Drugs Today psychostimulants CNS stimulant drugs having anti- depressant or mood elevating properties. Including:
n Adderall
??????n n n
n n
adderall Ritalin
These medications are prescribed to treat
depression, obesity, narcolepsy, and ADHD
study drugs are classified as: Schedule II due to their high potential for addiction.
Psychostimulants Today In a high pressure college environment where a GP A can determine one’s fate, study drugs are often used.
n Certain drugs can allow users to remain focused and awake for hours, giving students what they perceive to be superhuman mental strength
Paradox: Stimulants pacify hyperactivity? “Hyperactivity may develop when the relationships between dopamine and serotonin is imbalanced Elevating serotonin restores the delicate balance between dopamine and serotonin and supposedly pacifies hyperactivity”
stimulating underperming areas of brain
Adderall Methamphetamine back bone with extra methly(CH3) group attached to the amine(NH2).
Extra methyl(CH3) group on the amine(NH3) -This extra group gives molecules better fat solubility and therefore quicker entry to the brain
-This makes the “high” far more intense
-The faster the rate of uptake, the greater potential for addiction
Adderall and Cocaine
n immediate effects include:
-increased energy, feelings of well-being , superiority, increased concentration, alertness, verbose, mood elevation, increase heart rate, breath/min, and blood pressure, dilated pupils, dry mouth, perspiration.
adderall and cocaine -have ability to block dopamine transporters
the reuptake of catecholamine noradrenalin and dopamine are blocked leaving them in the synapse in increased concentration
How it Works
n The ADHD brain supposedly works
by blocking the reuptake of dopamine and norepinephrine into the presynaptic neuron and increasing their release from the presynaptic neuron into the extr neronal space
The increased flow of dopamine and norepinephrine into the extra neuronal space causes the patients' brain to experience a more intense level of concentration, causing an increased ability to focus for extended periods of time, and a heightened interest in performing focus based tasks.
ADHD medications are designed to have different effects than what? -methamphetamines and cocaine,
because of their time released nature and low doses they are
???prescribed in
n However, when crushed, snorted, or taken in high doses the pills may produce a high that parallels meth/amphet or cocaine.
How The Body is affected increased flow dopamine/norepinephrine into extra neuronal space causes patients brain toexperience a more intense level of concentration, causing ability to focus for extended periods of time, and a heightened interest in performing focus based tasks.
Adderall works by blocking the euptake of dopamine and norepinephrine into the presynaptic neuron and increasing their release from the presynaptic neuron into the extra neuronal space.
what does adderall cause the body to do? symptoms Increased alertness, motivation, confidence, loquaciousness, reduced appetite, dilated pupils
For the “ADHD brain” dopamine is believed
People with ADHD are believed to have a deficiency in dopamine causing them to be hyperactive and to look for stimulation in the environment.
n Adderall is thought to provide those with ADHD the dopamine level needed for normal functioning.
has adhd been scientifically proven? no
Psychopharmacology “…field of medicine that addresses the use of medications to help correct or control mental illnesses and drug addiction”
Psychoactive drugs: Focus on opiates and common combinations
what is the the 2nd most often illicitly abused drug in the U.S. opioids
history what happened in 1914 concern began to grow
§ Harrison Narcotic Act passed, restricting opioids to
only medical use
What are Opiates? Opium The exuded substance from the poppy Papaver Somniferum
What are Opiates? opiates Natural opium extracts and semi-
synthetic opium preparations
What are Opiates? opiods Synthetic opium-like compounds
Common Opiates Used in College § Morphine
§ Codeine
§ Oxycodone
§ Use to make Percodan® and Oxycontin®
§ Hydrocodone
§ Used to make Vicodin®
§ Hydrocodone most widely prescribed opioid
§ Heroin
Effects of Opiates •Desired Effects v.s. Side Effects § Pain relief
§ Suppresses coughs
§ Controls diarrhea (constipation)
§ Euphoria
§ Slurred speech
§ Depressed respiration & heart rate § Miosis
?Effects of Opiates
Toxic Effects
§ Addiction
§ Overdose
§ Drug contamination & adulterants > infection § Abscesses
§ STDs
§ Fetal effects
How it works: Neurotransmission
smallest functional unit of the nervous system
How it works: Neurotransmission
cell body
contains the nucleus; processes information that is received by the dendrites
How it works: Neurotransmission
-extension of the cell body that conducts an action potential
How it works: Neurotransmission
small space between axon terminal of one neuron & dendrite of another neuron or postsynaptic target
Biological Basis of Pain
pain signals damage
Neurotransmitter called substance P carries pain message
Biological Basis of Pain
Natural opioids help protect the body: Endorphins are?
Endorphins:enkephalins, dynorphins, beta endorphins
biological basis of pain:
Exogenous opioids work by reacting with the same receptor sites which are?
Mu,kappa,delta, nociceptin
Opioids also effect emotional pain in what way? § Decrease anxiety
§ Sense of detachment
§ Deadening of unwanted emotions
Opioid users take the drug for some of these effects: Reward/control pathway activated telling body to repeat these actions during stressful periods
—– Can lead users to become opioid abusers/addicts
what are Opioid Effects on Pleasure Reward/control pathway tells body to repeat actions that are good for survival

Cells in brain monitor action and when need filled, send signal to stop
Exogenous opioids mimic endorphins tell body to reuse drugs

opioid effects on pleasure
Natural opioids effect what pathway? example?
Reward/control pathway tells body to repeat actions that are good for survival


opioid effects on pleasure
strong opiates like heroin do what?
disrupt stop switch
They overload the stop switch causing it to malfunction “Drug abusers use past the point of pain relief…” (Inaba)
Routes of Administration Smoking: 7-10 seconds to reach the brain
Injection:15-30 seconds
Snorting:5-8 minutes
Oral:20-30 minutes
factors affecting distribution Properties of drug, Body weight/size,Age, Gender, Genotype (diabetes example), Health condition, Nutritional status
-Pharmacological state
– Environmental setting
-Psychological disposition: Personality, Expectation about drug effects
Students commonly combine opiates with what? alcohol or anti-anxiety meds
opiates, alcohol and anti-anxiety meds are all considered depressants. side effects? Control pain, reduce anxiety, promote sleep, lower inhibition, induce euphoria,depress circulatory, respiratory, and
muscular systems
–Additive effects
Prescription painkillers (opiates) are often mixed with what? alcohol
Opiates and Alcohol
Both substances depress the respiratory system increasing the risk of:
Cyanosis, cell death, and coma
— Also, one could simply stop breathing
Some slow-release opioids can be dissolved by alcohol, what does this do? releases a day’s worth of opioid in a matter of minutes
Today the most widely used sedative- hypnotics in the U.S.is? Benzodiazepines
— However, now they are usually only prescribed for short-term and for specific conditions–Can be very addictive, dangerous withdrawal symptoms
–Anxiety also treated with serotonin-type antidepressants and mood stabilizers
What are Benzodiazepines?
used in medicine for?
– Manage anxiety
– Treat sleep problems
– Control muscular spasms and seizures § Subdue symptoms of alcohol withdrawal
What are Benzodiazepines?
used recreationally for:
– Anxiety relief
– Induce mild euphoria
-Lower inhibitions
Common benzodiazepines: xanax,valium,rohpnol
xanax:what does it do? relieve symptoms of generalized anxiety disorder, panic disorder, and depression resulting from anxiety
valium: what does it do? Treat anxiety, gain relief from musculoskeletal spasms, control seizures such as those that occur during severe alcohol or barbiturate withdrawal
rohypnol: what does it do? Produces anxiety relief, sedation, and amnesia, especially when taken with alcohol
Benzodiazepines and Brain Areas:
The anxiolytic effects result from the actions at
limbic centers
Benzodiazepines and Brain Areas:
Actions at other regions result in side effects such as
sedation, cognitive impairment, muscle relaxation, and increased seizure threshold
Benzodiazepines and Brain Areas:
The amygdala, orbitofrontal cortex, and insula are associated with
the production of behavioral responses to fearful stimuli and the central mediation of anxiety and panic
—Inhibition due to GABA reduces stimulation of these areas leading to decreased anxiety
Mechanism of Action:GABA A GABA receptor agonist
-Does not directly stimulate GABA receptor
MECHANISM OF ACTION: GABA, since it does not directly stimulate the GABA receptor what does it do? -Binds to an adjacent site and increases the affinity of GABA for receptor
– This increases the inhibitory synaptic action of GABA, facilitating the influx of chloride ions, causing hyperpolarization of the postsynaptic neuron, depressing its excitabilit

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