psyc 115 final

Anxiogenics

drugs that increase anxiety

Nicotine absorption and where it is concentrated in the body

- gets concentrated in the kidneys, liver, salivary glands and stomach - Smoking: absorbed in the lungs, distributed rapidly though the blood/body and then brain

Genetic influence of nicotine and effects that genetics has on its effects

-16-25% of people have a genetic defect in their ability to metabolize nicotine -People with this defect are less likely to be smokers, and if they are, they smoke less

Cannabis effects on the body, sleep, and performance

-Bloodshot eyes (dilation of small vessels) -Droopy eyelids -Dry mouth -compulsion to drink something -Munchies, 3 hours after (many report sooner) -HR increase fluctuations in BP, and BT -Higher doses -headaches -nausea -vomiting -Small doses, increases drowsiness and sleep time -Large doses interferes with sleep (restlessness) -High doses, it can have hallucinogenic effects, but usually produces a pleasureable 'high' -can't store new information in the short term, and is often distracted -Can interfere with driving ability (usually drive very slow!!) -Tolerance occurs, for all effects of the drug

4 theories of Nicotine addiction

-Constant Blood Level Theory -Nicotine Bolus Theory -Dual Reinforcement Model -Withdrawal

Effects of methylxanthines on humans (positive and negative)

-Increase sympathetic nervous system activity -physiological changes in vascular tone, heart rate, and body temperature -smooth (involuntary) muscles tend to relax, and striated (voluntary) muscles increase in strength -either dilate or constrict blood vessels -increases the urgency and frequency of urination, decreases the sensation of a full bladder, and increases flow rate and volume of voided urine -increased anxiety, tension, jitteriness, and nervousness -positive effects, such as increased sense of well-being, energy, motivation for work, and self-confidence -can also cause panic attacks and increase anxiety in people with panic and anxiety disorders (but not in non-anxious individuals) -Tea: relaxation, peaceful mood -Caffeine interacts with some of the various other ingredients typically added to these beverages and dietary supplements. Glucose, for instance, has been found to counteract the effect of caffeine on enhancing hostility, but to increase caffeine-induced tension. The addition of taurine counteracts caffeine's stimulatory impact on mood, fatigue, alertness, and vigor. In combination with caffeine, L-theanine, which is also present in tea, increases alertness and decreases headache. -Caffeine improves attention and speeds both simple and choice reaction times. -Research shows that administration of caffeine alone decreased mental fatigue and improved information processing, while the addition of L-theanine further enhanced cognitive performance, as demonstrated by improvements in reaction time, working memory, long-term memory, and a decrease in headache -methylxanthines can produce insomnia and impact regular sleep patterns; impacts memory consolidation because of reduced REM

Conditioned Bx effects of caffeine on taste preference

-Taste preference: When a reinforcer is repeatedly paired with a neutral stimulus, this stimulus can also acquire reinforcing properties by virtue of respondent (i.e., Pavlovian) conditioning. -through conditioning certain flavors are preferred when paired with flavor

The endogenous cannabinoid

-a neuromodulator whose action is mimicked by THC and other drugs present in marijuana -anandamide

Genetics and caffeine dependence

-appears to be influenced by genotype. -Studies comparing twins have shown heritabilities of caffeine use, tolerance, and withdrawal ranging from 35% to 77%.

opponent-process theory

-compensatory reaction -comedown -cancelling out positive state

incentive-sensitization theory

-craving -motivation -psychological desire/ habitual nature of addiction -focusing on actual behaviors of addiction

Withdrawal from nicotine

-decreased heart rate -increased eating causing weight gain -lack of concentration -insomnia and increased awakenings from sleep -craving for cigarettes and urge to smoke; -alterations in mood, including anxiety, irritability, restlessness, anger, frustration, aggression, and depression, -nervousness, tremor, headaches, dizziness, nausea, light-headedness, and drowsiness -cognitive impairments.

Psychomotor effects of Bx

-improve mood -When amphetamine or cocaine is used in high doses it causes a big mood lift, or rush. But, once the drug wears off, a depression occurs -When taken continuously, the psychomotor stimulants cause stereotypic behavior (the senseless repetition of a meaningless act) -In humans, high does can also cause paranoia and psychosis -In low doses, amphetamines and cocaine can actually improve performance in certain activities --They may eliminate the fatigue that occurs with long cognitive or perceptual tasks (like studying) or with athletic activity

Antidepressants/ Mood Stabilizers Routes of Admin

-max blood concentration on TSA is after ~3hrs. -Max blood concentration on SSR is after ~ 4-8 hrs. Much of it is destroyed by the digestive system

Opioids routes of admin

-oral -inhalation (smoking) -intranasal administration (snorting) -parenteral. Is less effective when given orally than when the same dose given parenterally

hedonic disregulation

3 stages: -intocxication/ impulse -withdrawls -anticipation -focuses on negative reinforcement -incentives to use

harmful effects of vaping

i. cancer-causing carcinogens, like formaldehyde and acetaldehyde ii. affect the ability of cells to destroy bacteria iii. May cause trouble breathing, headache, cough, dizziness, sore throat, nose bleeds, chest pain, heart palpitations, and allergic reactions such as itchiness and lip swelling

Cocaine NT

Dopamine; cocaine blocks DA transporters and DA binds again and again to the cell overstimulating the cell

Anxiolytics

Drugs that treat agitation and anxiety disorders. Also used for alcohol withdrawal and in anesthesia (tranquilizers)

b. Indolamines

Family of neurotransmitters that share a common molecular structure. A classification of monomine neurotransmitter along with catecholamines and ethylamine

Alcohol NT

GABA inhibitory NT; Glutamate excitatory NT; alcohol interacts with GABA receptors making them more inhibitory and binds to Glutamate receptors prevents Glutamate from exciting the cell

Heroin NT

Inhibitory NTs stop DA from being released. Without inhibition, DA can be released. Heroin mimics natural opiates, DA floods synapse

Marijuana NT

Inhibitory transporters already active before marijuana intake, they inhibit DA from being released. Body's native cannabinoid (anandamide) cause cannabinoid receptors to turn off the release of inhibitory NTs, now DA can be released. THC mimics anandamide and binds to cannabinoid receptors. Inhibition is turned off and DA now allowed into synapse.

Methamphetamine NT

Meth mimics DA and is taken into the cell by DA transporters; Meth enters the DA vesicles forcing the DA molecules out; DA pumped out of cell and into synapse (reverse of normal flow). Excess DA becomes trapped in synaptic cleft, over stimulates the cell as it binds again and again to the receptors

Opioid antagonists

Naloxone, naltrexone

Opioid metabolism

Opioids are metabolized by digestive system enzymes, primarily in the liver but also in the intestinal tract, and the resulting metabolites are excreted by the kidneys

Changes in marijuana potency over time

Over the past 50 years, the potency of typical marijuana has increased by about 50% as a result of crossbreeding

Effects of nicotine on the CNS and PNS

PNS: -Nicotine stimulates receptors in the neuromuscular junction - muscle tremors -Decreases some reflexive movements (knee jerk) -Increases HR and BP, constricts vessels in the skin -Decreases skin temp (may lead to more wrinkling/aging) -Stimulates bowels, but decreases blood flow to them! (herniation risk) -CNS: Stimulates release of adrenalin (epinephrine), resulting is CNS arousal -Respiration increases -Stimulates brain stem emesis centers -Cells in the VTA connecting to NA dopamine releasing cells contain a subtype of nicotinic receptors -Thus, nicotine stimulates cells in VTA, causing an excessive release of dopamine in NA -Nicotine also effects the serotonergic neurotransmitter system

Anxiolytics routes of admin

Readily absorbed after oral or parenteral administration

the effect of anxiolytics on unconditioned animal behavior

Reduces defensive aggression but not unprovoked aggression

Effects of opioids, in general and on Bx

a. Analgesia: Reduces thermoceptive pain (caused by extreme heat or cold), mechanical pain (due to physical damage to muscles, skin, and joints), and visceral nociception (associated with organ damage) -Opioids also reduce the aversive emotional aspect of pain -Reward: VTA and Nacc are thought to be important for the motivational and rewarding effects of opioids -Vital life functions: Usually opioid overdose deaths are due to respiratory depression -Acute lethal effects: At high doses, opioids produce a comatose state with severe depression of breathing, which can eventually cause death. -Chronic effects: indirect harm that arises from the lifestyle of most addicts, expensive, illegal, HIV/AIDS -YPLL (Years of potential life lost) method calculates the number of years of potential life that are lost within a specific segment of the population.; heroin users lose an avg of 18.3 years of potential life before the age of 65 years b. Body: nausea and vomiting because of effects on CNS and PNS; miosis; may slow heart rate and influence function indirectly by stimulating the vagus nerve or the release of histamine; long-term may increase risk of heart attack; lower blood pressure; flushed, warm face; sweating; impacts the endocrine system which can lead to impaired sexual function, decreased libido, infertility, and osteoporosis; atrophy of secondary sex characteristics in males and stopped menstruation in women; interfere with urination; serious pregnancy complications (anemia, cardiac disease, swelling, liver disease, hypertension, pneumonia, tuberculosis, and infections of the urogenital system, such as bladder infections and venereal disease). Babies have low birth weight, irritability, respiratory distress, yawning, sneezing, tremors, difficulty in sucking and swallowing, peculiar high-pitched cry, seizures. • Sleep: somnolence (drowsiness), lethargy, and nodding throughout the day; cause insomnia, sleep deprivation, increased muscular tension during sleep, and altered sleep patterns including more time spent in light sleep and a reduction in delta (deep) and REM (rapid eye movement) sleep, sleep apnea • Cognitive performance: inattention, difficulty concentrating, perceptual distortions, memory deficits, executive dysfunction, and psychomotor impairment; extreme cognitive dysfunction can result in hallucinations, delirium (confusion, decreased alertness, loss of comprehension), and coma; higher risk of driving-related accidents. • Subjective effects: increased sensitivity in both hearing and vision; The rush (this intense momentary feeling of pleasure experienced when high concentrations of opioid molecules are delivered suddenly to the brain. Rushes are usually described as sexual, rather like an orgasm in the stomach or in the entire body). • Mood and liking: positive feelings do not last long and are quickly replaced with emotions that are mostly negative; decrease in physical activity and social interaction and an increase in aggressive behavior and social isolation

3 broad categories of anxiolytics and order of addiction risk

a. Barbiturates: More dangerous b. Benzodiazepines: Less dangerous c. Z Drugs and Others; Even less dangerous

Nicotine routes of administration

Smoking Chewing Dipping (snuff) Trans-dermal patch Chewing gum Nasal spray

Psychomotor Stimulants routes of admin

When used medically to treat ADHD or sleep disorders, orally because amphetamines are weak bases they can be absorbed in the digestive tract, slow rate of absorption. -oral (for ADHD or sleep disorders) -snorted -smoked -anal/ vaginal suppositories -intravenously -easily distributed throughout the body and metabolized by the liver and exerted in the urine. -Amphetamines and cocaine cross blood brain and the placental barriers. -Remain concentrated in the spleen, kidneys, and brain. Cocaine has a shorter half life than amphetamines. Crack cocaine is non-ionized so is rapidly absorbed and distributed

Chronic tolerance of anxiolytics; relations to GABA

With repeated administration benzodiazepines become less effective in their ability to modulate the effects of GABA

Cocaine and acute and chronic tolerance

a. Acute tolerance: continuous cocaine sniffing every 20-30 minutes for 10-12 hours results in formation of acute tolerance The drugs no longer gives the rush and becomes ineffective at improving mood Called a 'coke-out'. Usually why people stop when at the end of a binge. This is cleared up after 24 hours, and the person can start again with the normal drug effects b. Chronic tolerance: After 2 weeks of use with coke or meth...some of the appetite loss goes away, and the effects on HR and BP decreases over time. Lethal doses go up... over time a consistent user can intake doses that would be lethal in a new user

Where do opioids concentrate

a. After absorption into the blood, opioids become concentrated in the heart, lungs, kidney, liver, spleen and, to a lesser extent, the muscles and brain. Within the brain, opioids become concentrated in the basal ganglia, the amygdala, and the periaqueductal gray, an area closely associated with the sensation of pain. • After absorption and rapid distribution to bodily organs and tissues, these drugs are later slowly redistributed to muscles and fat, though some molecules may persist in body tissues and organs, such as the liver

Stimulants and monoamines

a. Amphetamines (including crystal meth) b. Ephedrine c. Cocaine d. cathinone

Opioid stats according to slide

a. Between 30 and 80% of drug abusers overdose at some point and nearly half experience multiple overdoses within a short period of only a few months b. For every fatal drug overdose, there are an additional 20 or more non-fatal drug poisonings c. Every year, an estimated 1.1 million people visit a U.S. emergency department due to drug overdose. Most b/t the ages of 20 and 34 years, w males and females represented in roughly equal proportions d. Males are more likely to experience unintentional drug poisoning, whereas roughly equal proportions of females require emergency care due to unintentional or self-inflicted drug overdose e. Opioids are directly implicated in roughly 14% of drug poisonings that require an emergency room visit; 5.7% are caused by heroin and methadone f. Risk of overdose is increased by numerous factors, including high frequency of drug use (e.g., daily or binge use); higher drug purity; injecting drugs, as opposed to administering them orally or by inhalation; and polydrug use, especially the combining of opioids with amphetamines, cocaine, alcohol, or benzodiazepines

Factors that affect methylxanthine metabolism

a. Caffeine metabolism slowed by alcohol and grapefruit juice, sped up by smoking (nearly twice as fast) and broccoli b. In woman, caffeine metabolism varies based on monthly-cycle related hormone levels

Adenosine receptors and methylxanthines

a. Caffeine metabolism slowed by alcohol and grapefruit juice, sped up by smoking (nearly twice as fast) and broccoli b. In woman, caffeine metabolism varies based on monthly-cycle related hormone levels c. It is metabolized in the liver and slowly eliminated (half life 3.5 hours) d. caffeine tricks your body into thinking that it's not yet time for sleep by acting like adenosine

Harmful effects of tobacco

a. Cancer b. Heart and Pulmonary disease c. Reproduction: infertility and birth defects; SIDS d. Nicotine poisoning e. Environmental Tobacco Smoke AKA Secondhand smoke f. Mainstream smoke g. Sidestream smoke h. Thirdhand smoke

Harmful effects of psychomotor stimulants

a. Cocaine: liver damage, inflammation and ulceration of mucous membranes in the nasal passages Huge money losses...people can lose all judgment and often buy coke till they have no more money Also, while in a run, bad effects include: hallucinations, paranoia, cravings, antisocial behavior, concentration/attentional problems, blurred vision, weight loss b. Amphetamine: short term: restlessness, excessive talking, confusion, dizziness, tremors Long term: paranoid psychotic behavior, possibly also due to lack of sleep and food. Irrational thinking, increase BP and maybe stroke. Brain damage to dopaminergic neurons, only after 4 uses!

Distinguish between detox, in-patient, and out-patient programs of tx

a. Detox a must and may include hospitalization...where first the acute withdrawal problems are cared for, then the person is put on (then weaned off) depressant drugs (like valium) b. After that, outpatient programs (less successful) or... c. Inpatient programs where the person is observed/treated both physiologically and psychologically

Maintenance therapy and antagonist therapy for opioid addiction

a. Detoxification: eliminate the physical dependence by helping the addict get through withdrawal b. Maintenance Therapies: addicts are provided with an opioid agonist, which is made continuously available, like Methadone c. Antagonist Therapies: first detox, then kept abstinent for 7 to 10 days. This is followed by the relapse-prevention phase. Addicts are given daily doses of the antagonist, naltrexone, when they come for therapy; Outpatient day program with educational seminars, recreational activities, and group therapy.

Types of opioid receptors, what are they, where are the located?

a. Four types of opioid receptors—three "classical receptors," referred to as mu (μ), kappa (κ), delta (δ), and one more recently discovered "non-classical receptor" called the "opioid receptor-like" (ORL1 ) receptor b. Activation of all four types of opioid receptors results in reduced excitability of the postsynaptic neuron and a diminution in neurotransmission and neurotransmitter release. -On presynaptic neurons, receptor activation impedes the flow of Ca2+ and thereby the release of many different neurotransmitters such as glutamate, GABA, glycine, norepinephrine, dopamine, and acetylcholine. This means that opioids are both inhibitory neurotransmitters and inhibitory neuromodulators of many other transmitters. -Activation of endogenous mu opioid receptors results in the prototypic opioid effects of reward, withdrawal, and analgesia -Opioid receptors are located in the central and peripheral nervous system. Activation of mu receptors in the central nervous system results in responses such as respiratory depression, analgesia, euphoria, and miosis. Stimulation of peripheral mu opioid receptors, in smooth muscle of the bronchi and intestines, results in cough suppression and opioid-induced constipation.

Cannabis medicinal effects

a. Glaucoma: by reducing eyeball pressure Anti-emetic: people using chemo Spasticity: like in MS, or other movement disorders Pain, weight and appetite loss in people with cancer and AIDS

4 types of Nicotine addiction treatment

a. Nicotine Replacement Therapy b. Pharmacotherapies c. Immunization d. Behavioral Interventions

Harmful effects of cannabis

a. No real evidence for marijuana causing violent or aggressive behavior -Large doses can cause paranoia or anxiety, even panic attacks -Long term use: cannabis dementia, memory loss...and similar brain volume reduction as seen with alcoholics -Amotivational syndrome Progression to other drugs -Reproduction: may lower testosterone, possibly leading to lower fertility rates in men -In woman, may prevent egg implantation after fertilization -Prenatal exposure may cause hyperactivity, cognitive and behavioral disorders, first observed at pre-school ages -When combined with cigarette smoking, it is in increased risk factor for earlier development of lung cancer

Anxiolytics: effects of human bx

a. Psychomotor impairment and disorientation b. Muscle relaxation c. Ataxia (a lack of motor coordination) and muscle tremor are unwanted side effects; injuries d. Anticonvulsant properties e. Increased appetite and weight gain f. Less time spent in rapid eye movement (REM) sleep; slow-wave (deep) sleep, but this effect diminishes within a few weeks of continued use g. Euphoria (feeling good) h. Anterograde amnesia, a loss of memory for information presented while under the influence of a benzodiazepine i. Impairs explicit but not implicit memory (except lorazepam) j. Impaired working and short-term memory k. Impaired attention, psychomotor performance (RT) l. can improve performance in highly anxious m. Z drugs may cause sleepwalking, sleep-driving, and hallucinations; increased risk of dementia n. Residual effects

Harmful effects of antidepressants

a. Reproduction: TCAs affect male ejaculation b. Teratogenic effects: SSRIs cause heart defects c. Prozac and TCAs, women twice as likely to miscarry (compared to controls) d. Violence and suicide: Some anecdotal reports and case studies have shown Prozac to cause violence and suicide, but controlled studies with large subject numbers do not show the effect e. overall findings inconclusive, lots of 3rd variables, like the fact that agitation and suicide is often goes along with depression f. Overdose g. If SSRIs are combined with other antidepressants or psychomotor stimulants it can lead to serotonin syndrome, which if left untreated, can lead to respiratory, circulatory and kidney failure. Alone, no deaths attributed to SSRI overdose

Cannabinoid metabolism and the body's organs

a. Some metabolism in the lungs, but most in the liver The delta-9 THC is converted in the liver to a more potent form, one that crosses the blood-brain barrier easily b. Complete excretion is slow, can be detected in the body 30 days after a single use

Which stimulants are synthesized, semi synthesized, and naturally occurring

a. Synthesized: Amohetamines b. Semi synthesized: cocaine c. Natural: Ephedrine and cathinone

Sensitization and opioids

a. The endogenous opioid system undergoes adaptive changes that lead to the development of tolerance and physical dependence, sensitization, and, during abstinence, symptoms of withdrawal. b. Sensitization: Hyperalgesia, or the enhanced sensitivity to painful stimuli, is one manifestation of opioids' sensitizing effects on neural mechanisms (increased pain sensitivity as a result of opioid-induced sensitization)

Withdrawal: methylxanthines and opioids

a. With repeated use, humans show tolerance to the effects of caffeine. b. Withdrawal symptoms can get severe when a serious user goes cold turkey c. These include: headaches, restlessness, anxiety d. Withdrawal peaks between 20-48hrs without caffeine and can last a week.

Positive reinforcement model

b. assumes that drugs are self-administered, at least initially, because they act as positive reinforcers and that the principles that govern behavior controlled by other positive reinforcers apply to drug self-administration; Drug addiction is conceptualized as a disorder that develops when behavior initially maintained by positive reinforcement (intoxication) progresses to being motivated by negative reinforcement—that is, drug-taking as a means of alleviating the unpleasant emotional state experienced during withdrawal

LSD NT

binds to serotonin receptors (serotonin receptor 1 and 2); acts differently on receptors (sometimes inhibits and sometimes excites); that's why effects vary and effect perception

MDMA effects

f. MDMA short term use . Immediate (post-administration) i. Hyperthermia, ii. dehydration iii. overhydration/hyponatraemia (low sodium) iv. Safety issues v. Overdose g. Ecstasy overdose . FLUID RETENTION / RENAL FAILURE i. AGITATION, CONFUSED MENTAL STATE, DISORDERED SPEECH, PSYCHOSIS, HALLUCINATIONS, CONVULSIONS, SEVERE HEADACHE ii. TACHYCARDIA (RESTING HEART RATE >120 BPM) iii. HYPERTENSION / HYPOTENSION iv. HYPERTHERMIA (TEMP >38.6O C ) v. NAUSEA OR VOMITING vi. EXCESSIVE FLUID CONSUMPTION vii. MUSCLE RIGIDITY viii. DEATH. h. Dependence on Ecstasy . LOW LIKELIHOOD OF PHYSICAL DEPENDENCE i. TOLERANCE TENDS TO RESULT IN REDUCED EFFECTS, REDUCED ENJOYMENT, AND 'LOSS OF THE ECSTASY MAGIC' AS LIFETIME USE INCREASES. i. GHB Effects . SMALL DOSE (1-3 G) 1. DECREASED INHIBITIONS 2. INCREASED LIBIDO 3. EUPHORIA SIMILAR TO ECSTASY 4. SEDATIVE EFFECTS 5. MEMORY LOSS (SEDATION) 6. SYNERGISTIC EFFECT WHEN COMBINED WITH ALCOHOL (SIGNIFICANTLY INCREASES RISK OF OVERDOSE). • LARGER DOSE (4-5 G) • POWERFUL SEDATIVE EFFECTS • NAUSEA AND VOMITING • STIFFENING OF MUSCLES • DISORIENTATION • PROFOUND SEDATION • CONVULSIONS • COMA • RESPIRATORY COLLAPSE. j. GHB Overdose and Long-term-use i. OVERDOSE RISK IF MIXED WITH OTHER CNS DEPRESSANTS: - RESPIRATORY DEPRESSION 1. - DIAPHORESIS (SWEATING) 2. - 'EYES ROLLING' 3. - MUSCULAR SPASMS, CONVULSIONS ii. POTENTIAL FOR DEPENDENCE, WITH SYMPTOMS SIMILAR TO ALCOHOL iii. OTHER LONG-TERM CONSEQUENCES UNKNOWN.

Antipsychotics on human Bx

i. Each drug's effectiveness as an antipsychotic and the sorts and intensity of side effects vary considerably from person to person; no pharmacological cure for psychosis and treatment is often lifelong • Extrapyramidal Symptoms (EPS)—disturbances in movement that resemble the symptoms of Parkinson's disease • dulled facial expression, rigidity and tremor in the limbs, loss of coordinated movement, weakness in the extremities, and a slowing of movements ii. Akathisia, a condition characterized by uncontrolled restlessness, constant compulsive movement, and sometimes a protruding tongue and facial grimacing. iii. Tardive dyskinesia: involuntary, tic-like, repetitive movements of the face, such as muscle twitching, smacking of the lips, or flicking of the tongue, sometimes dozens of times per minute; can be permanent; more common in women and elderly; less common with atypicals. iv. Agranulocytosis, a potentially fatal loss of white blood cells and decline in immune system function due to the suppression of bone marrow activity; 1-2% of patients v. Trouble regulating temperature; sunburns, weight gain, changes in cardiac function and blood pressure (due to the effect of these drugs on NE receptors), dry mouth, impaired vision, dizziness, constipation (due to anticholinergic effects), and jaundice. In certain susceptible individuals, there is an increased risk of seizures. vi. Subjective effects: often unpleasant so rarely abused. Antipsychotics represent a group of drugs for which there is considerable difficulty gaining patient compliance

LSD effects

i. Largely sympathomimetic 1. PUPILLARY DILATATION 2. ↑ BP 3. TACHYCARDIA 4. HYPER-REFLEXIA 5. TREMOR 6. NAUSEA 7. PILOERECTION (GOOSEBUMPS) 8. MUSCULAR WEAKNESS 9. ↑ TEMPERATURE. ii. Non-sympathomimetic: 1. Dizziness 2. Weakness 3. drowsiness 4. paraesthesia 5. emotional 6. Lability b. LSD Chronic Effects . FLASHBACKS (EXPERIENCED BY 15% OF USERS) i. NO EVIDENCE OF LONG-TERM TOXICITY ii. SOME EVIDENCE FOR REDUCED CAPACITY FOR ABSTRACT THINKING WITH REPEATED USE iii. TOLERANCE TO SUBJECTIVE AND BEHAVIORAL EFFECTS DEVELOPS RAPIDLY BUT NOT TO AUTONOMIC EFFECTS (REGULATION OF BODILY FUNCTIONS) iv. RISK OF DEPENDENCE IS LOW. c. LSD Mental Effects . COLORFUL 'VISIONS', OFTEN IN TUNNELS OR SPIRALS i. RAPID SUCCESSION IF VARIOUS 'SCENES' ii. MYSTICAL RELIGIOUS FEELINGS iii. STRONG EMOTIONS, GOOD FEELINGS iv. PLEASURE IN VIEWING ART OR LISTENING TO MUSIC v. FEELINGS OF LOVE AND EMPATHY FOR OTHERS vi. ENHANCED SENSORY AWARENESS (KEEN PERCEPTION) d. LSD Behavior and Performance . IMPAIRS REACTION TIME i. AND OFTEN CREATES AN INATTENTIVENESS, SO DRIVING IS DANGEROUS ii. PERFORMANCE CAN IMPROVE, THOUGH, ON SOME REPETITIVE MOTOR TASKS e. LSD Tolerance and Withdrawal . AFTER 1-2 DAYS OF CONSTANT INGESTION, THE DRUG STOPS WORKING i. BUT, SENSITIVITY TO THE DRUG CAN REBOUND IN A COUPLE DAYS ii. NO KNOWN WITHDRAWAL SYMPTOMS, BUT PEOPLE HAVE REPORTED FLASHBACKS WITH LSD

Antidepressants on Bx

i. do not stimulate NS, like psychomotor stimulants, but block activity in the parasympathetic NS - Results in dry mouth, constipation, dizziness, irregular heart beat, blurred vision, ringing in the ears, urine retention, excessive sweating, and sometimes tremors ii. SSRIs: nausea, headache nervousness, insomnia iii. Occasional effect: serotonin syndrome: caused by an acute increase in serotonin transmission... disorientation, agitation, confusion, fever, shivering diarrhea. This usually occurs when doubling up different SSRIs or combining with psychomotor stimulants iv. TCAs cause sleepiness - High doses of TCAs can cause extreme nightmares - Wellbutrin increases REM sleep - Most other ADs decreases REM sleep, which is hypothesized to improve depression - Some people on SSRIs complain about being sleepy all the time

Antipsychotics Routes of Admin

oral= pills, parenteral (before surgery (sleep0 or depot injections)

Caffeine/ Methylxanthines Routes of Admin

orally, rectally, parentally, transdermally.

Ecstasy/MDMA NT

serotonin removes old 5-HTP molecules from cleft, ecstasy mimics serotonin and it taken up by serotonin transporters; Transporter stops transporting 5-HTP out of cell, excess gets trapped in cleft, binds again and again to receptors overstimulating the cell

Constant Blood Level Theory

smokers adjust their cigarette use to maintain a constant blood level of nicotine (i.e., one high enough to avoid withdrawal symptoms, but below a level that has toxic or aversive effects)

Nicotine Bolus Theory

the sudden delivery of highly concentrated nicotine to the brain intensifies the pleasure and enhances the reinforcing effects of smoking

Compute half-life

the time it takes for the concentration of the drug in the plasma or the total amount in the body to be reduced by 50% ... Watch video

Dual Reinforcement Model

three processes at work during nicotine reinforcement