Help
Options
Question
four ways of naming drugs
click to flip
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't know
Question
definition of drugs
Remaining cards (364)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
PSY 3142 DRUGS
drugs and behaviour final
| Question | Answer |
|---|---|
| four ways of naming drugs | chemical name, generic name, trade name and street name |
| definition of drugs | as a substance that alters the physiology of the body but is not a food or nutrient |
| 3 ways of getting drugs to market | preclinical testing (animal testing before humans), human clinical testing (small groups of ppl being tested) and use & off label use (realizing a drug works for something else and using it for that) |
| caveat | metabolic rates of animals differing - larger animals metabolize more slowly and require lower doses smaller the animal --> larger the dose |
| dose response curve | small change at low dose (big effect), small change at high dose (small effect) BLUE GRAPH |
| continuous variables | y axis |
| ED50 | Median effective dose |
| LD50 | median lethal dose |
| purpose of ED50 and LD50 | distance between them determine how safe a drug is. further LD50 is from ED50 the safer the drug is. Closer the LD50 to the ED50 the more dangerous the drug. |
| Therapeutic Index | how safe drug is (ratio of LD50 and ED50) higher the number the safer the drug is LD50/ED50 |
| Potency | amount of drug needed to produce any given effect |
| effectiveness | if the drug produces a functional response at its functional location it is effect |
| drug with lower ED50 | more potent, therefore you need less to acheive the same effect |
| primary effect | desired effect |
| side effect | any other effect that happens due to the drug |
| Antagonism | one drug reduces the effect of another |
| Additive | effects together - they increase the effect |
| potentiation (superadditive effect) | when effect of two drugs together is greater than might be expected from their individual effects |
| 4 main types of parental routes | subcutaneous (arm or thigh for humans), intramuscular (into muscle), intraperitoneal (in stomach cavity not good for humans), intravenous (needle into vein right into bloodstream, usually done inside elbow). |
| Other types of parental routes | intrathecal (drug into CSF not for humans), intracerebroventricular (into CSF via ventricle), intracerebral (into brain tissue) |
| capillaries | small branches that have blood carried to them by arteries and away from them by veins, they pass through pores in their walls. drugs pass through their pores through diffusion. |
| more capillaries ??? | more rapid absorption |
| diffusion | substances moving from area of high concentration to areas of low concentration |
| factors that affect absorption into circulatory system | volume of blood flow (greater flow faster absorption), heat, amount of capillaries (more capillaries = faster absorption) |
| problem with smoke particles | drug cannot be exhaled |
| more problems with inhalation route | can damage lungs or reduce ability to absorb oxygen or eliminate CO2, CO is present - blocks ability of blood to carry oxygen. carbon monoxide blocks ability of blood to carry oxygen |
| inhalation | returning blood is pumped to lungs, CO2 released and oxygen absorbed, blood returns directly to heart |
| what does diffusion do for gas movement in lungs | more in air then blood - gas will enter, more in blood than air- gas will be exhaled |
| oral administration | mouth to digestive system - pills are the easiest exmaple |
| other methods that act on digestive system | intranasal (by nose), buccal (in mouth not swallowed), intearectal |
| how does oral administration work | stomach breaks down drug using strong acid and enzymes, most drugs are better absorbed by intestines, drugs absorbed in blood by capillaries that line intestines |
| what does food do to absorption? | food slows absorption |
| cell membrane | have lipid bilayer (2 layers of fat molecules) |
| atom cluster (or heads) | hydrophilic (water loving) |
| tails | hydrophobic (water repelling |
| lipid solubility | how well a drug dissolves on a fatty substance |
| Ions | molecule or atom with a net of electric charge due to loss or gain of one or more electrons - not lipid soluble |
| damital | weak acid, becomes more highly ionized as pH is more basic (higher number) |
| Endital | weak base, becomes more highly ionized at acid Phs |
| Transdermal route | epidermis (outer skin) lipid soluble and has capillaries underneath |
| distribution of drugs | process of concentration/segregation of a drug in different areas of body. |
| what can drug distribution be impacted by | lipid solubiltiy, ionization. BB barrier, transport mechanisms, blood proteins, placenta |
| ion trapping | anywhere with membrane separating fluids with different pH values, depending on acidicity or bacidity of drug more concentrated on one side than the other |
| CNS | BB barrier blocks pores in capillaries (exception: postrema (for vomiting)) |
| Passive transport | through channels or attached to carrier proteins (no energy required) |
| active transport | ion pumps |
| protein binding | drugs become attached to large proteins in blood |
| placental barrier | fetus has little protection from drugs |
| Elimination of drugs actors | liver and kidneys |
| what do liver and kidneys do to eliminate drugs | metabolize and excrete. liver uses enzymes to metabolize drugs. metabolites are filtered out of blood by kidneys (excretion) |
| liver | contains enzymes that control chemical reactions (modify molecules) |
| metabolism | restructuring of molecules |
| metabolites | product of molecules |
| kidneys | maintain water/salt balance, filters everything and reabsorbs what is required then excrete unwanted substances through urine |
| nephron function | nephron takes proteins and cells that cannot pass through capillaries that surround it, majority of substances are reabsorbed into nephron the remainder is excreted |
| what is done in nephrons | diffusion, lipid solubility, transport |
| rates of elimination | as concentration goes down, rate slows high concentration of drug, high rate of metabolism |
| elimination kinetics | movement of drugs out of organism |
| stimulate enzyme systems | enzyme levels increased by previous drug exposure |
| depress enzyme systems | two drugs compete for enzyme |
| therapeutic window | range of blood concentrations of a medicine above level that is ineffecitve (therapeutic level) and below level with toxic side (toxic level) |
| large therapeutic window | drug absorbs and excretes slowly |
| narrow therapeutic window | drug moves rapidly though system |
| where do we get caffeine | plants |
| how much of world population regularly consumes coffee | 80% |
| main 2 coffee species | Arabica and Robusta |
| is Robusta or Arabica contain more caffeine | Robusta |
| where does high quality tea come from | more caffeine close to bud |
| where does low quality tea come from | further from bud |
| where do tea leaves come from | Camellia Sinesis plant |
| where does cocoa come from | theobroma cocoa tree |
| how is cocoa made | beans get fermented, heat up, germinated and die (dried) |
| Other natural caffeine sources | Ilex plant (makes mate), Cassina (makes yaupon, tea), Gurana (dried paste), Cola |
| Theophylline | respiratory stimulant for infants and people suffering from asthma or chronic obstructive pulmonary disease (COPD) |
| important points about energy drinks | sold as dietary supplements, may contain up to 200 mg of caffeine (more than one coffee in each can), contain many herbal ingredients |
| history of coffee | 12th-15th century in Africa, went to Europe 1650 coffee associated with intellectuals, this went to US English switched to tea |
| history of tea | grown and sold in China by 780 CE, shipped to Europe (Netherlands) in 1600s created tax on tea - tea was factor in American revolution (1770s) |
| history of cocoa | started in mexico/peru reserved for wealthy, considered aphrodisiac, called chocolate (contained corn and spices) 1500s europe - sugar added very expensive most comes from Africa now |
| methylxanthines absorption | slow from stomach, rapid from intestines |
| peak blood levels of caffeine | 30 mins and all is absorbed (only 2% excreted and unchanged) |
| methylxanthines distribution | crosses BB barrier more quickly than theophylline or theobromine - reaches all organs - 10-30% binds to proteins and stays in blood |
| where is most caffeine metabolized | liver |
| mean half life of caffeine | 3.5 hours |
| mean half life of theophylline and theobromine | 6-7 hours |
| one thing that effects methylxanthines excretion | genetic differences: fast metabolizers - do not experience effects of coffee as much, slow metabolizers - cannot have coffee past noon or cannot sleep (expereince more effects of caffeine), |
| second thing that effects methyxanthines excretion | enzyme inihibition by meds or food; slowed by alcohol (and grapefruit and some antibiotics), metabolism speeded by broccoli and by smoking |
| differences in excretion of methyxanthines in women | half life of caffeine is longer after ovulation, doubled for women taking oral contraceptives, slows during pregnancy |
| methyxanthines and infants | half life is 4 days, cannot metabolize until 7-9 months |
| how does caffeine impact adenosine receptors | caffeine blocks receptors that adenosine bind to |
| 4 types of adenosine receptors | A1 in brain, A2A in striatium (basal ganglia), A2B, A3 |
| what does 2 cups of coffee a day for 5 days do | upregulation of adenosine receptors - brain will make more adenosine receptors to try to get them to regular amount |
| mosaics | places where receptors attach to each other and therefore influence each other |
| receptor mosaics | 2 receptors are attached when you look at them under microscope, you see two different ones that are tied together, they influence eachother |
| how do methyxanthines effect the body | release of epinephrine from adrenal gland which leads to a sympathetic action, voluntary muscles strengthen, smooth muscles relax, reduced muscle fatigue, increase rate and depth in breathing |
| how does caffeine affect the body | reduces headaches (constricts blood vessels in brain), dilates blood vessels in body, increases frequency and urgency of urination |
| subjective effects of caffeine for energy & confidence vs anxiety and tension | positive effects when; person used low dose of caffeine or did not use caffeine, decreases sleepy feelings, high dose can cause anxiety and panic attacks (in those who have anxiety disorder) |
| caffeine effects on human cognitive performance | caffeine reverses deficits caused by boredom and fatigue, some improvements in attention and working memory, improvements in reaction time on visual and cognitive tasks, caffeine withdrawal - usually massive headache |
| caffeine effects on atheletic performance | improves performance on endurance type sports like cross country skiing, long distance running and cycling, works best at low doses |
| methyxanthines effects on sleep | takes longer to fall asleep, sounds wake people easily , counteracts sleep effects of pentobarbital, since caffeine blocks adenosine receptors sleep center is not as well triggered - wakefulness |
| how long can 2 cups of coffee keep a person awake | 2 hours |
| uconditioned effects of caffeine on non human animals | high doses causes rats to attack other rats, high doses cause death from seizure |
| conditioned effects of caffeine on non human animals | increase in excitability, increases avoidance responding, increases spontaneous motor activity in mice (run around more) |
| discrimination of caffeine | for rats dicriminate caffeine from saline also their dopamine receptor blockers interfere with animals ability to discriminate caffeine from saline (at low doses). for humans can discriminate caffeine at low doses but range of ability to do this |
| tolerance of caffeine in rats | tolerance shown - dose response curve well to right |
| tolerance of caffeine in humans | tolerance shown different effects and different times mostly cardiovascular and sleep effects but these dissapear in a week |
| caffeine withdrawal in humans | headaches, fatigue, sometimes depressed mood |
| how long does caffeine withdrawal last in humans | felt within a day, peaks at 2 days and lasts up to 9 days |
| how to self administer caffeine for non humans | primates often need infusions at first, often abstain and don't increase dose overtime |
| how to self administer caffeine for humans | low doses are more reinforcing |
| harmful effects of caffeine | low birth rate, slowed fetal growth (correlational studies), linked to risk of heart attack , reduction in bone density in post menopausal women who drink coffee, 5-10 cups can lead to sensory disturbance, for those with anxiety increase anxiety |
| what does more than 1g of caffeine per day do? | can lead to agitation, twitching, irregular heart rhythm, rambling speech |
| harmful effects of energy drinks | dangerous when combined with other drugs, heavy consumption; dizziness, vomiting, diarrhea, palpitations, heart attack, stroke, spontaneous abortion, hallucinations and more |
| benefits of caffeine | may be protective against parkinson's disease may cause weight loss or prevent weight gain, 6 cups per day correlated with reduced risk of developing Type 2 diabetes (works w decaf), 3-5 cups - correlates fairly big reduction in risk for later cog disease |
| where is cocaine from | leaves of coca bush in south america |
| cathinone (khat) | from plant 'catha edulis' (plant is a shrub can also grow as a tree) |
| ephedrine | from huang plant |
| isomer | chemical term to describe molecules that contain same number of atoms of each element, have different arrangements of their atoms |
| types of isomers | d-amphetamine and l-amphetamine. mixing them is called dl-amphetamine |
| what are isomers prescribed for | treating ADHD and narcolepsy adderall (dl-amph), dextrine (d-amph) |
| non amphetamine stimulant | methylphenidate (Ritalin) |
| history of cocaine | found leaves in burial sites from 2500 BCE incas made coca sacred from 10th century coca was used as payment for labour during spanish conquest europe in 1860 tried to find medical use for coke freud proposed treatment for addiction and depression |
| more on history of cocaine | anaestheic properties in cocaine and found it could be injected with morphine and be used as stimulant for creativity, 1860s Italians added to wine |
| when did US ban cocaine | 1914 used undergound but after WWII increased use |
| history of amphetamines | ephedrine used in china 5,000 years ago approved in USA during WWII for narcolepsy, depression, asthma and weight loss |
| chen and schmidt 1924 | amphetamine - chemical structure similar to adrenalin so they used it to treat asthma |
| what are amphetamines used for today | prescriptions limited to ADHD and narcolepsy |
| history of cathinone (khat) | started being used around time of Alexander the Great (300 BCE) introduced in europe around 1600s |
| where is cathinone popular | middle east (chew it there) |
| slow absorption | oral administration (to prevent sleep and fatigue) |
| fast absorption | injection, chewing of leaves (coca, khat), sniffing, smoking and inhalation of vapours |
| what do the percentage of ions depend on | whether drug is weak acid or weak base, whether fluid is an acid of base, the pKA (ph at which half of molecules are ionized) |
| what are the percentage of ions for psychostimulants | drugs are weak bases, pKa of 9 or 10, half are ionzed, PH of solution |
| Traditional methods of absorption | incas sucked on rolled coca lead with lime from wood ash or ground shells - this increases PH of saliva and digestive tract, reduces ionization and increases absorption |
| current methods of cocaine absorption | cocaine being sold as salt, crack cocaine mixed with solution of baking soda after evaporation chunks are heated and vapours are inhaled |
| peak blood levels of amphetamines | after oral administration, 30 minutes |
| peak blood levels of cocaine | after sniffing - 10-20 mis, after smoking uncertain but probably fast |
| psychomotor stimulants distribution | cross BB barrier; concentrate in kidney, spleen and brain |
| excretion of amphetamines | long half lives, depends on PH of urine. acidic drug is not reabsorbed from nephron and has a half life of 7-14 hours. basic the drug is reabsorbed from nephron and shifts to liver and has a half life of 16-34 hours |
| excretion of cocaine | fast!!! half life of 45-75 mins depends on acidity of urine |
| Agonist and amphetamine | amphetamine is an agonist that blocks DA and NE reuptake |
| 3 different types of monoamine transporters | dopamine transporter, norepineprine transporter, serotonin transporter |
| what occurs when MA is transported into vesicle by a transporter | prevents enzymatic degradation in synapse, preserve NT for later use when an action potential occurs |
| reuptake blocker (monoamines) | an example of this is cocaine. this occurs when the monoamine transporters are being blocked which leaves more monoamine in the cleft |
| subtrate-releasing agent | an example of this is amphetamine. this occurs when the drug is preventing storage of MA in the vesicle, this causes a release of MA into the cell which causes a reverse action of the monoamines transporters (bringing them back to the cleft) |
| where does cocaine bind to | DA transporter, NE transporter and SERTs |
| where do methylphenidates bind to | DA transporters, NE transporters and high concentrations of SERTs |
| where do amphetamines and methamphetamines bind to | most potent in NE transporters, then DA transporters then SERTs |
| which drug acts in a similar way to cocaine | antidepressants (bcuz SNRIs block SERTs and NETs and can act on DATs) |
| psychomotor stimulants behavioural effects | CNS - increased release of DA in mesolimbic and nigrostriatal system (to get high about half transporters have to be blocked) PNS- stimulants act on epinephrine synapses, result is sympathetic arousal (fight or flight) |
| Anaesthetic effects of psychomotor stimultants | cocaine blocks Na+ channels, action potentials are prevented (basis for anaesthetic effects) |
| basic body effects of psychomotor stimulants | increase heart rate and BP, vasodilation and bronchodilation, reduced appetite (cause feeling of fullness). Less of these effects in methamphetamine has fewer of these effects than d- or l- amphetamine |
| sleep effects of psychomotor stimulants | block fatigue, increase attention, amphetamines cause insomnia (some are used to treat narcolepsy) |
| subjective effects of psychomotor stimulants | improved mood, decreased fatigue, clarity in thought (felt more when blood levels are rising), acute tolerance to pleasurable effects after one use |
| damage risk criteria for amphetamines | feel stimulated, like the drug, feel friendly and talkative, do not feel sluggish/fatigue |
| subjective rush with amphetamines and cocaine | with iv and inhalation, very dramatic effects and often reported to have sexual component , rush followed by crash (mild depression), cocaine initial numbing sensation followed by 20-30 min high then crash |
| punding | repeated behaviours (e.g., cleaning, re-sorting things, taking things apart, putting them back together) |
| other things that occur during punding | people get angry if interrupted, caused by stimulation of nigrostriatal DA system |
| monoamine psychosis (high doses) | looks like schizophrenia (hallucinations, delusions, paranoia; also flattened affected depression), resolves in hours to days, common symptom formication (sense that bugs are crawling under the skin) |
| sensory effects of stimulants on performance | increase in visual acuity, slight improvements in auditory flicker fusion |
| general effects of stimulants on performance | increased endurance, reduced fatigue |
| amphetamine effects on behaviour and performance | improved reaction time, improved vigilance and attention, improved short memory, impaired divided attention, impaired performance at high doses (inflexibility, inability to change strategies, distraction and impaired judgement) |
| ADHD treatments | attention improved by low dose amphetamine and methyphenidate (ritalin in US- 9% of boys, 4% of girls), stimulants increase DA and NE activity in prefrontal cortex. Improvement in attention and impulse control, better control of behaviour. |
| stimulants effects on driving | twice as likely to be killed in a car accident, drifting, weaving, speeding, reduced ability in driving |
| stimulants effects on sports | banned from sports due to improvements in swimming times, results for track and field sports |
| stimulant effects on rats | low dose leads ton increase in locomotor and exploratory activity and in high dose increase in locomotor activity followed by SMA (head bobbing, sniffing, rearing, itching) |
| stimulant effects on monkeys | SMA more complex than rats. Low dose leads to reduced consumption of food and water. High dose leads to auto-mutilation |
| Dews 1985 | Pigeons who take amphetamines increase responding on fixed-interval schedule (behaviour reinforced only when a certain amount of time has passed) , decreases responding on fixed ratio schedule (behaviour reinforced after a certain number of responses) |
| amphetamines and dissociation | amphetamines cause dissociation (lack of memory for what was learned under influence of drug) |
| discrimination in rats | they can discriminate drugs from saline, poor discrimination when mesolimbic D1/D2 receptors blocked |
| sevak et al 2009 | did human experiment on discriminaiton. humans could discriminate amphetamine from the placebo |
| acute tolerance to cocaine in humans | subjective effect of improved mood, if they take too much coke (10-12 hours later) no longer improved moods. do not feel heart rate and bp effects so may risk toxic effects |
| chronic tolerance in humans | some effects tolerate with time and continued administration, no tolerance for blocking sleep, sensitization |
| withdrawal of stimulants | depression and lethargy, sleep problems, increased appetite, vivid dreams. chronic use leads to severe depression. begins 24 hours of stopping and mostly complete in a week. depression and appetite changes may persist for months |
| cocaine self administration in humans | large quantities for a short period of time (run-abstinence cycle) enjoy mixing drugs with cocaine with heroin, benzos or hallucinogens. |
| amphetamine self administration in humans | like run abstinence cycle (large quantities for a short period of time), for staying awake, high doses for euphoria (lasts 24-48 hours then big crash) |
| cocaine non human animals self administration | cocaine has few withdrawal symptoms but reinforcing , lab animals will administer cocaine to point of death, binging does not occur when availability is restricted |
| direct harmful effects of cocaine | liver damage, damage to mucous membranes (sniffing) |
| direct harmful effects of amphetamines (short term) | confusion, restlessness, punding, stroke in some individuals |
| direct and indirect harmful effects of chronic use of stimulants | heartbeat, BP (may lead to stroke), indirect effect on small blood vessels in brain; potential death of DA cells |
| indirect harmful effects of cocaine | disease in IV users (hepatitis and HIV/AIDS), poor diet, lack of sleep, anti social behaviours, 6x normal death rate |
| harmful effects of stimulants on reproduction | more risky sexual behaviours, high dose disrupt sexual activity, when used during pregnancy birth abnormalities and behavioural problems in kids, cocaine correlated with 10x occurence of early placental development |
| cocaine overdose (caine reaction) | depends on route of administration, genetic differences caine reaction has 2 phases 1- excitement/seizure then loss of conciousness/heart failure |
| 3 main therapies for stimulants | behavioural, pharma (looking for non-addictive drug or one taken orally and has longer half life), immunization (in testing phase) |
| why does the textbook not use the word narcotic? | negative connotation associated with older interpretations of the word, negative images of addicts |
| where is opium from | poppy sap in seed pods, only available 10 days of life cycle then they are pressed into cakes and dried |
| what contains opium | morphine, codeine, thebaine |
| when were morphine and codeine isolated | morphine-1800s, codeine- 1830 |
| morphine | opium sap (10% of weight), salt form, available only by prescription |
| codeine | opium sap (0.5% of weight), available in Canada in small quantities over the counter (cough or pain meds) |
| hydrocodone | derived from codeine, most commonly prescribed opioid in USA, suppresses cough, relives pain and can be combined with other pain relievers, common one Vicodin |
| natural opioid | morphine and codeine made from opium (from poppy) |
| semi-synthetic opioids | hydrocodone, thebaine and heroin |
| thebaine | occurs naturally in tiny quantities, source of oxycodone, known as percocet when combined with acetaminophen, crushed and injected (causes accidental overdose and addiction) |
| heroin (diamorphine) | made by adding to morphine molecule, 10x more potent and more lipid soluble (so crosses BB barrier, gets to brain quicker) |
| synthetic opioids | act same as morphine just chemically different and vary in effectiveness. many based on fetanyl molecule. examples include; methadone, fetanyl, meperidine. |
| history of opium | farmed since 5000 BCE, originated in middle east, first smoked in china in 1600s, 19th century freely available in britain |
| history of heroin | invented by Bayer (Germany) company that invented aspirin, discovered heroin same way, banned in US in 1920, Canada recently started prescribing heroin |
| how they made aspirin | they were experimenting with acetyl groups to reduce corrosive properties of salicylic acid - aspirin |
| jan 2016-march 2022 | 30,834 opioid toxicity deaths between jan and march 21 deaths per day mostly involved fetanyl |
| how much did opioid deaths increase by over covid pandemic | 91%, could be due to toxic drug supply, isolation, stress, anxiety, limited services |
| what is canada doing to prevent opioid deaths | sued makers of oxycontin to cover health costs for those addicted, pushing for safe use sites during pandemic |
| administration routes of cocaine | weak base so not readily absorbed by oral route, only 15% available in digestive tract and liver, advantageous oral administration allows maintenance of constant blood levels |
| administration routes of heroin | mainly parental/inhalation; snuff, pipe, smoking, injection |
| administrations of antagonists (e.g., naloxone) | parentally bcuz too slow via digestive track |
| distributions of opioids in brain | concentrated in basal ganglia, amygdala and periaqueductal gray |
| distributions of heroin | highly lipid soluble, goes to brain quick but cannot act there, rapidly metabolized |
| excretion of morphine | 10% excreted unchanged, half life is 2 hours, 90% is gone in 24 hours |
| excretion of methadone | 10% excreted unchanged, half life of 10-25 hours , bound to blood proteins, long action- useful as maintenance therapy |
| excretion of nalaxone | completely metabolized in liver, very short half life of 1.5 hours, effects may wear off too soon |
| neurophysiology history | first receptors discovered in 1973 |
| what were opioids derived from | polypeptides (large molecules that can be NTs or hormones) |
| 4 known types of opioid endorphines or enkephalins | Mu (μ), kappa (k), delta (δ) and ‘opioid receptor-like’ (ORL1)all metabotropic and release second messengers |
| effects opioid endorphines have on cell | activate potassium channels, inhibit certain voltage gated calcium channels, inhibit production of cAMP second messenger and activates kinases and may alter gene expression (endocytosis) |
| different types of effects of opioids | mu (agonists or antagonists), agonists or antagonists or more receptor types, some are mixed ago |
| locations of cells and outcomes | mu - limbic system, thalamus, locus coeruleus, VTA, PAG, delta- limbic system, cortex, hypothalamus, Nacc, medulla, kappa- nacc, VTA, hypothalamus, thalamic |
| mu receptors | where most opioids act, responsible for analgesia and sedation effects and responsible for many side effects |
| naloxone opioid replacement | pure opioid antagonist at mu, delta and kappa receptors, mild effect, used to treat opioid overdose |
| three important sites of actions | 1 analgesia (PAG) different types of pain are relived by different types of drugs 2 reinforcement (reward path), mu receptors in VTA inhibit GABA interneurons (more DA), most reinforcing and 3 vital life function (brain stem); respiratory, vomiting etc |
| opioid effects on body | vomiting nausea (first time use), constricted pupils, lower bp, constipation, reduced sex hormone, disturbed sleep patterns |
| opioid subjective effects | many vivid dreams, 19th century opium oral administration produced feelings of happiness, improved vision and improved hearing. some suggests opium increased creativity. Samuel Taylor Coleridge(took combo alcohol and opium) |
| opioid mood effects | initial positive feelings then negative, felt good until tolerance developed, felt worse + psychiatric symptoms after few days, relief only 30-60 mins, less social activity, more aggression |
| human performance on opioids | slowed psychomotor performance and some cog performance, most tasks tolerance develops |
| opioid effects on animal behaviour | low dose increase SMA, high dose decrease SMA (except in mice), low dose - increase responding, high dose - decreased responding, antagonists block effects at low dose, avoidance slow high dose, don't increase behaviour surpressed by punishment |
| opioid tolerance | rapid and extensive tolerance, 3 or 4 months may increase 10 times. |
| types of opioid tolerance | acute tolerance; thought due to removal of opioid receptors (endocytosis), long-term tolerance; recycling of receptors (altered sensitivity), context dependent (via learning), cross tolerance (with other mu opioids, alcohol not other drugs) |
| withdrawal of opioids | never fatal, always unpleasant, starts in 6-12 hours peaks at 3 days (restless, yawning, chills, goosebumps, short breaths), then deep sleep 8-12 hours then vomiting, sweating twitching PAG INVOLVED (reduces symptoms of heroin withdrawal) |
| addicted humans self administration of opioids | begins with curiousity, preoccupied with getting drug |
| opioid use without doctors | 56% friends/family, 80% were originally prescribed |
| overdose of opioids | can kill you by depressing breathing, half of overdose deaths in US, heroin leading cause of death people with 5-10 years of expereince, laced with quinine, combining with bezo or alc or loss of tolerance (after not using or new env) |
| more harmful effects of opioids | increase risk of cancer, reduced fertility, abnormal brain activation, pregnancy - withdrawal harms fetus, serious health problems, low birth weight and premature |
| lifestyle and complex interactions with opioids | more accidents, more death from disease, more homicide, more suicide, more cancer deaths and add to this poor social support and poverty |
| opioid treatment | detoxification (abstinence or opioid antagonist) or using methadone to help make withdrawal symptoms less bad, maintenance therapy (methadone- antagonist to heroin lasts 24 hours), antagonist therapy |
| antipsychotics purpose | to treat schizophrenia and other psychotic disorders |
| schizophrenia positive symptoms | hallucinations, delusions, paranoia, incoherent thoughts and speech |
| schizophrenia negative symptoms | diminished expressiveness, lack of interest in work/social life, uncommunicative, no feelings of pleasure |
| other schizophrenia symptoms | problems with learning, memory and problem solving |
| brain abnormality theory behind schizophrenia | double normal size lateral and third ventricles, potentially due to loss of brain tissue volume elsewhere, loss is progressive can occur before birth, children exhibit warning signs |
| 1960s dopamine hypothesis schizophrenia | results from excessive DA activity in brain (3 revelevant DA systems nigrostriatal, neocortical, mesolimbic), drugs that increase DA function can cause psychosis |
| Newer DA theory | due to overactivity of DA especially in D2 receptors. blocking DA does not relieve symptoms right away, slow changes may be involved, negative and cog symptoms do not improve |
| most recent DA theory | excessive DA in mesolimbic pathay explains positive symptoms, lack of DA activity in mesocortical pathway explains negative symptoms |
| glutamate hypothesis 1950s | synthesis of phenyclidine and ketamine, produced psychosis like symptoms, bind at GLU NMDA, PCP antagonizes with NMDA binding sites |
| glutamate in relation to schizophrenia | genetic differences may predispose people to reduced glutamate activity, glutamate levels same as healthy individuals |
| current view on schizophrenia | develops gradually, cog and neg symptoms first then positive, development may be explained by neural pathway changes, happens at various NT sites in brain |
| proposed current schizophrenia theory | brain deterioration (moved along by synaptic pruning), deterioration results in loss of glutamate synapses (glutamate dysregulation) and glutamate no longer activates mesocortical DA neurons (neg symptoms), glutamate no longer inhibits interneurons (excit |
| when were antipsychotic meds discovered | accidentally in 1950s |
| how were antipsychotic meds discovered | search for anxiety treatment to prevent surgical shock (wanted to block epinephrine and Ach) |
| first antipsychotic | chlorpromazine - promoted artifical hiberantion |
| impact of antipsychotics | 80% reduction in numbers of people in mental institutions, replaced barbiturates, electric shock and being placed in mental institution |
| typical antipsychotic | developed first as dopamine antagonists (D2 blockers). Associated with motor problems and often causes non-compliance. 1/3 of ppl do not respond |
| atypical antipsychotic | developed in 1975 dopamine and 5-HT antagonists EPS atypical so there are fewer motor problems. Weak affinity for D2 receptors and high affinity for D3 and D4 receptors. clozapine was first. |
| third generation antipsychotics | 2002- aripiprazole. modulates D2, D3 and D4 receptors. DA activity is low (prefrontal cortex) - it is an agonist and where DA activity high (mesolimbic path) it is an antagonist. Can treat positive and negative symptoms. Not better than other types. |
| routes of administration for antipsychotics | treating psychosis is taken orally, for surgical treatment (sedation) is intramuscular and intravenous, in cases of non compliance, IV or depot injection |
| absorption of antipsychotics | most are easily absorbed, cross BB barrier and in body fat, slowly released from body fat |
| absorption of typical antipsychotics | in oil accumulate in body fat and can take weeks or months to reach steady state |
| absorption of atypical antipsychotics | not in oil do not accumulate as much in body fat- peak 4-28 days |
| variable effects of antipsychotics | effect of single drug varies from person to person, they are hard on the body |
| side effects of typical antipsychotics | EPS,inability to stay still, tics, problems regulating temp, sun sensitivity, weight gain, heart problems, dry mouth, impaired vision, dizziness, constipation, jaundice and seizure risk clozapine - dramatically reduce white blood cell count |
| side effects of atypical antipsychotics | weight gain, diabetes, increased cholesterol, heart problems, dry mouth, problems regulating temp, dizziness, nausea, cataracts |
| side effects of third generation antipsychotics | far fewer side effects, mainly nausea and dizziness |
| EPS (extra pyramidal signs) | looks like parkinson's disease; tremor, loss of coordination, slow movement, flat facial expression. reported in up to 40% of people who take typicals |
| akathisia | restlessness, compulsive movement, protruding tongue, facial grimace. seen in 20% of people taking typical antipsychotics |
| tardive dyskinesia | involuntary tics, movement in face, tongue flicking, smacking lips, symptoms are permanent (even when drug is stopped) |
| antipsychotics effects on sleep | no changes in sleep cycle, can be sedating and can lengthen sleep |
| typical antipsychotic effects on behaviour | described as unpleasant, chlorpromazine; confusion, difficulty concentrating, dejection, anxiety, irritability, feeling tired. haloperidol; restless and having difficulty moving |
| is atypical or typical antipsychotics effects more unpleasant | typical |
| antipsychotics effect on performance | potential impairment in attention due to sedative effects, impairment of attention |
| animals and antipsychotics | avoid antipsychotics |
| other uses for antipsychotics | prevent nausea and vomiting , pre surgical sedatives, treats huntington's disease, tourette's, tardive dsykinesia |
| major depressive episode | feeling of sadness, loss of appetite, anhedonia (no interest in normal activities), lack of energy, guilt, sleep problems, suicidal ideation |
| major depressive disorder | same as depressive episodes symptoms just do not go away |
| dysthymic disorder | chronic mild depression |
| history of depression | since early greek civilization, 13-17% will experience, women double likelihood of having depression in life time |
| depression for males vs females | male= 12% in lifetime, feel tired and irritable. females= 24% in lifetime, feel sad and guilty |
| suicide and depression | 5x more risk for suicide. females attempt more, males suceed more |
| original monoamine theory | depression caused by reduced activity in 5HT, NE and DA, drugs that deplete monoamines cause depression, depleting 5HT cause depression |
| problems with monoamines theory | antidepressants act on monoamines but relief may not be felt for weeks or months, only affects mood in some ppl (with family history of depression) |
| additions to monoamine theory | norephineprine and 5HT dysregulated in depression, 5HT, NE & DA may influence other systems, second messenger systems, hormones and immune system all can increase risk of depression. depression complex disorder |
| updates on monoamine theory | low levels of 5HT, low levels of tryptohan, low levels of tryptophan metabolite, decreased numbers of 5HT transporter reuptake proteins, abnormalities in number and function of 5HT receptors |
| glucocoricoid theory of depression | hypothalamic-pituitary-adrenal axis (HPA), stress response in hypothalamus leads to activation of pituitary and release of cortisol from adrenal cortex, cortisol travels to hippocampus, amygdala, prefrontal cortex, buildup cortisol - increase risk depre |
| interaction monoamine & glucocoticoid processes | connections from amygdala to 5HT & NE in midbrain & hindbrain - overexcite override prefron cortex, high levels stress - reduce 5HT hippocampus, adrenalectomy - upregulation 5HT receptors |
| what do antidepressants do | increase number of cortical receptors, improves feedback and ultimately lowers level of stress hormone, normalization happens before person feels relief, if normalization does not occur person relapses |
| first generation antidepressants | monoamine oxidase inhibitors (MAOIs) and tricyclic antidepressants (TCAs) |
| second generation antidepressants | more recent many different chemical structures. includes selective serotonin inhibitors (SSRIs) |
| third generation antidepressants | includes both 5HT and NE reuptake inhibitors (SNRIs) |
| Monoamine oxidase inhibitors (MAOIs) | first one 1950s. originally tuberculosis med. fell out of favour, supposedly, caused liver damage, ineffective (correct dose neither r true) newer ones available |
| tricyclic antidepressants (TCAs) | discovered accidentally during research on antipsychotics, thought to be safer than MAOIs - so replaced them, block reuptake transporter proteins 5HT NE act on NT system many side effects |
| second generation antidepressants | first SSRI 1987 (prozac) slightly different than TCAs- fewer side effects, treat anxiety |
| third generation antidepressants | SNRI enhanced NE activity and reduce symptoms of fatigue, do not alter Ach so fewer side effects |
| first generation antis and monoamines | block enzyme activity and breaks free floating monoamines (NE, DA and 5HT) 2 types of enzymes MAO-A (degrades all 3 types) MAO-B (degrades DA) |
| second generation antis and monoamines | SSRI block reuptake transporter for 5HT, cause buildup of 5HT in synapse, act only on 5HT but everywhere, delayed effect on these drugs |
| third generation antis and monoamines | block reuptake of 5HT, NE and sometimes DA, some modified to induce sedation |
| main antidepressant actions | monoamine oxidase inhibitors, tricyclics, second generation; selective serotonin reuptake inhibitors |
| absorption of antidepressants | all the drugs have similar absorption, TCA peak in blood 1-3 hours, SSRIs/SNRIs peak at 4-8 hours, first pass metabolism in liver/digestive tract |
| excretion of MAOIs | short half life 2-4 hours, |
| excretion of TCAs | half life of 24 hours |
| excretion of second & third generation | half life of 15-25 hours |
| are antidepressants effective | most effective for ppl who are severely depressed, often have to try several before finding one that works for them. 60-70% expereience relief, placebo effects high |
| MAOIs side effects | tremors, weight gain, dry mouth, postural hypotension, insomnia or sedation, breaks down tyramine in food (cheese, beer, wine, chocolate), can cause cheese effect - serious condition in which BP rises may cause internal bleeding, serotonin syndrome |
| tricyclic side effects | fluid retention, constipation, dry mouth, dizziness, low BP, weight gain, reduced seizure threshold, can cause nightmares and can cause heart attack |
| SSRI and third generation effects | SSRI; nausea, headache, nervousness agitation, gastro problems, weight lose, vivid dreams, insomnia third generation; increase appetite, weight gain, gastro problems, may cause sedation |
| subjective and behavioural effects of antidepressants | feeling of apathy, no euphopria, driving and other vigilance tasks are affected by TCAs, personality changes (questionable) |
| tolerance and withdrawal of antidepressants | TCAs have to be gradually withdrawn can include restlessness and anxiety, SSRIs; anxiety, headache, fatigue and others and SNRIs; serious withdrawals, psychiatric symptoms |
| other treatments for depression instead of antidepressants | herbal treatments (lavender, chamomile); not large effect, electroconvulsive therapy, deep brain stimulation, transcranial magnetic stimulation, exercise, CBT, psychotherapy (reduce cortisol), hallucinogens |
| female cannabis plant | shorter with more leaves |
| 2 species of cannabis plant | cannabis sativa and cannabis indica |
| history of cannabis | native to central asia, grown in europe for medicine, 19th century used to treat psychiatric and neurological disorders, 1970 no medical potential, strong potential for abuse |
| cannabinoids | main ingredient delta-9-tetrahydrocannabinol, anything that binds to endocannabinoid receptor |
| phytocannabinoids | from plant |
| endocannabinoids | endogenous to body, are triggered when one consumes cannabis. THC effects of cannabis (psychoactive effects) |
| synthocannabinoid | synthesized made in lab, legal and illegal varieties, some treat anorexia associated with AIDS |
| THC | psychoactive and appetite inducing |
| CBD | non psychoactive and may be therapeutic |
| oral administration of cannabis | lipid soluble, slow absorption, first-pass metabolism in the liver, peak of effects in 1-3 hours |
| inhalation of cannabis | normal smoking 10-25% of cannabinoids to lungs (all absorbed) |
| cannabis vaporizers | heats plants - safer because cannabinoids vaporize at lower temp than tar/carcinogens |
| cannabis distribution | highly lipid soluble so distributed to fat concentrations in lungs, kidneys, only 1% concentrated in brain |
| cannabis excretion | metabolism mainly in liver, delta-9-THC is converted to 11-hydroxy-delta-9-THC, CBD and CBN interact with THC slows metabolism in liver |
| THC half life | biphasic half life; drop in first 30 mins followed. by 20-30 hour half life |
| cannabis neurpharmacology | receptors found in 1990s two receptors CB1 (in CNS), CB2 (found in immune system and some in brain) |
| where cannabis acts in brain | cerebellum (movement), hippocampus (memory) and maybe mesolimbic DA system (via opioids) |
| effects of moderate dose of cannabis | bloodshot eyes, drooping eyelids, dry mouth/thirst, hunger (3 hours after use), altered perceptions & good feelings, increased heart rate, drowsiness, high dose cause sleep disturbance |
| medical uses of cannabis | glaucoma, helps reduce nausea with chemo, reduces muscle spasms, improves subjective pain ratings |
| cannabis effects on human behaviours | euphoria, hilarity, placid dreaminess, avoid physical activity, sensory distortions, loss of sensitivity to pain, experience time as passing more quickly, long term use associated with reduction in hippocampal volume, no effect on creativity |
| cannabis tolerance | fairly rapid 5-6 days in animals, down regulation in CB1 receptors |
| cannabis withdrawal | not severe in animals or humans in humans appetite change, restlessness, craving |
| synthetic cannabis toxic effects | more dangerous agitation, confusion, psychosis, paranoia |
| cannabis gateway theory | more cannabis use associated with use of other drugs, no causal relationship |
| some harmful effects of cannabis | high doses - panic attack, may accelerate schizophrenia occurs in people who already may be vulnerable, effects may be permanent on developing brain |
| types of hallucinogens | classic hallucinogens; lysergic acid amide (LSD), psilocybin, MDMA (ecstasy), ketamine, dextromenthorphan |
| sources of classic hallucinogens | LSD- morning glory seeds and ergot fungus grains, psilocybin - mushrooms |
| sources of other hallucinogen | toad, vines, plants, nutmeg, mace |
| pre LSD history | Ergotism (sickness from ingesting grains that have been infected) causes hallucinations, delirium and feeling of excessive warmth during middle ages (500-1500 CE) |
| LSD history | Albert Hoffman 1940 accidentally ingested and had the first trip. they thought it could be used to treat mental disorders because it looked similar to serotonin |
| Timothy Leary | Psych prof at harvard experimented with psilocybin in Mexico thought hallucinogens could lead to great psychic improvement |
| history of psilocybin | Aztecs (14th century) used in religious ceremonies |
| administration of LSD | oral gel tabs effective at 20-80 µg for intense visuals 200 µg takes effect in about 30-60 mins mostly metabolized by liver felt for about 12 hours |
| administration of psilocybin | oral in dried form |
| hallucinogens and the CNS | LSD - serotonin receptor agonist only at certain receptor subtypes. Psilocybin also agonist but at more serotonin receptor subtypes |
| Locus coeruleus and hallucinogens | drugs can surpress also enhance response to novelty |
| cortex and hallucinogens | drugs act on glutamate to increase duration of action potentials esp prefrontal cortex |
| raphe nuclei and hallucinogens | inhibits 5 HT release |
| phantasticant perceptual effects | effect of hallucinogens means feeling as though expereience is significant (emotionally or to world events), enhaced expereince of music and art |
| etactogenic and empathogenic | insight into one's own feelings and mind and insight leading to empathy with others |
| Tolerance of hallucinogens | rapid 1-3 days, sensitivity then develops |
| withdrawal symptoms of hallucinogens | none |
| harmful effects of hallucinogens | designer versions can be dangerous, psychedelic crisis, flashbacks |
| History of MDMA | synthesized by Merck 1914 |
| administration of MDMA | oral administration ~100mg, effects felt in about half an hour and peak in an hour or 2, half life of 8 hours and effects can persist for days |
| excretion of MDMA | either in urine or being metabolized to MDA |
| neuropharmacology of MDMA | prevents reuptake of DA, NE and 5HT, in humans increases levels of serotonin, stimulant and euphoric effects related to increased DA transmission, empathy due to enhanced release of oxytocin, heavy use - higher cortisol |
| effects of MDMA on non human animals | rats; increased locomotor activity, increase in anxiety, avoidance behaviours impairment of object recognition memory monkeys; increased locomotor activity, more social grooming behaviour |
| effects of MDMA on humans | low dose- effects like cannabis, high associated with social inhibition, openess, self-confidence, emotional warmth, empathy, energy and euphoria, rapid tolerance |
| acute withdrawal of MDMA | 'crash' associated with lethargy, irritability, depression, insomnia and memory problems |
| MDMA effects on body | short term - pupil dilation, headache, teeth grinding heavy use - tachycardia (HR over 100 beats per min) can cause hyperthermia in warm env, excercising extra sweat brain swelling ' |
| Neurotoxic effects of DA on mice | degeneration of axon terminals in nigro-striatal DA path early life (adolescent) exposure leads to greater vulnerability later on |
| Neurotoxic effects of DA on humans | effects on DA less obvious; future Parkinson's disease may be result |
| Neurotoxic effects of 5HT on humans | can lead to impulsivity, problems with memory, emotion and cognition |
| Neurotoxic effects of 5HT on monkeys | damages serotonin neurons in many brain regions - damage persists for 7 years in some species of monkeys |
| history of ketamine | synthesized in 1960 - mainly used by veterinarians |
| administration of ketamine | oral liquid or capsule but can be inhaled from power. effects only last about an hour |
| neuropharmacology of ketamine | blocking glutamate receptive, therefore glutamate is ineffective |
| behavioural effects of ketamine | usual dose- sedation, tingling, numbness, euphoria, feeling of floating date rape drug high dose- psychosis, catatonic excitation, sudden mood change |
| more effects of ketamine | some will be injured if they do not feel pain, in rats kills fetus |
| lethal dose ketamine | 40x usual dose |
| dextromethorphan | synthetic cough supressant - found in cold and cough drugs very large doses blocks NMDA receptors increases 5HT (should not b taken w antidepressants) rapid tolerance |
Created by:
faythk23