PSY365 Quiz 3 Review Sheet PDF

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1 pear1.Adderall is RACEMIC (combination of two amphetamines) amphetamine and dextroamphetamine 2.Caffeine the 1st most taken drug , alcohol is the 2nd, and Nicotine the 3rd 3.T or F: Psychiatric symptoms can be observed under high levels of caffeine. TRUE 4.CAFFEINE IS THE ONLY LEGAL OVER THE COUNTER STIMULANT - True. Isn't nicotine a stimulant? 5.Strattera works differently than other drugs. Inhibits reuptake of NE 6. Area Postrema not protected by the blood brain barrier** & is the “vomit center” of the brain

Can someone make a quizlet for Exam 3? Found this studyblue online… could be useful. https://www.studyblue.com/#flashcard/view/12618001 https://quizlet.com/163040568/psy-365-exam-3-flash-ca rds/

~Half life of Cocaine, Nicotine, Amphetamines….?? (Usually on test) - Cocaine - 30 to 90 min - quickly out of blood after 6 hours - Nicotine - frequent smokers: 1 to 2 hours - For non smokers is 10 to 20 mins - Caffeine 4-6 hrs - Amphetamines - Smoked (Crystal Meth) - 12 hours - Ritalin 2-4 hrs - Adderall 7-8 hours 1. Review the different types of cocaine. How do the routes of administration differ for each type? - Erythroxylon coca leaf : each leaf itself has maybe 1% percent cocaine (.5%) . chew dose= 200 mg - some people rub on gums to get a numb feeling - similar high to snorting - increase endurance, alleviate hunger, social and religious background **was used as a local anesthetic before novocaine - paste: 60-80% percent cocaine - Cocaine Hydrochloride: commonly snorted, or injected - commonly cut with talcum and baking soda - also levanisol (dewormer) - can lead to agranulocytosis (damage to WBC)= immunodeficiencies - Levamisole: 70% cocaine is cut with this drug used to deworm animals. Why? Because it is similar texture of cocaine. It looks like cocaine. It’s a big problem for chronic users. It destroys white blood cells. White blood cells fight infections. people get skin sores and flu like symptoms. - NOT stable when heated (not smoked) - You can put it in a water solution, dissolve it, and inject it. - salt/rock (powder) version of cocaine - this process removes cocaine from leaves by adding hydrochloric acid - when snorted getting 25-100 mg - cocaine molecules is going to constrict blood vessels (vasoconstrictor) - 20-30% of cocaine snorted actually makes it to the blood stream - 20-30 min to peak in the blood stream - 10-15 min to start the effects. - feeling high for a couple of hours

2 - you can see the cocaine in the plasma for about 6 hours. - when injected: - bypass all barriers of absorption. every molecule is gonna get into the blood. - 30sec to 60sec to hit. persist for 30 min. high is pretty similar to smoking it. - it can cause a blood clot because not all chemicals in it are soluble in blood. - i.e. if cut with baby/talcum powder, they’re not soluble in water → can cause clot/stroke cocaine hydrochloride will not hold up in heat, which is why it has to be made into a different form (freebase or crack) in order to be smoked! - freebase: usually smoked, sometimes snorted (highly concentrated) - take away hydrochloride. this is done with ammonia and ether - inhaled into lungs; rapidly and nearly completely absorbed - rush within 15-20 sec. - Peak in 5 min - Persist for 30-45 min before coming down - Crack: usually smoked, sometimes snorted, rarely injected - “safer/cheaper/easier to make” - made with baking soda. Hydrochloride binds with the baking soda rather than the cocaine molecules. Called crack because it sounds like a cracking noise when burned. - can be 80-90% concentrated (the expensive type) - Snorting: 25-100 mg - Smoking: 250-1000 mg 2. Is cocaine found in a plant or is it synthesized in a lab? ➢ Cocaine is naturally found on the molecular level in the leaves of the Erythroxylon coca (E. coca) plant ○

cocaine we know is completely synthesized

3. What is the difference between crack cocaine and freebase cocaine in terms of the how the two drugs are made (just the basics here…)? ➢ essentially they make the same form of drug. crack has baking soda with it tho. ➢ free base: takes off hydrochloride molecule with ether or ammonia(can explode) ● very dangerous to make because ether is very flammable ➢ crack: extraction process is done with baking soda (safer) ○ Baking soda bonds with hydrochloride to remove from cocaine 4. How was cocaine used in the late 1800s and early 1900s? ➢ Freud used it to treat depression and chronic fatigue (1884) + morphine addiction ○ note: he also created Formication- bug crawling ○ “3rd worst drug behind alcohol and heroin” ➢ was actually in Coca Cola, toothache drops, wine ➢ used as a local anesthetic until rise of novocaine (1918) ➢ became a schedule 2 drug in (1914, Harrison Narcotic Act) ➢ housewife stimulant to get chores and duties done, I remember him saying this about amphetamine is it true for cocaine as well? yes. 5. How is cocaine metabolized and what is the metabolite? How is cocaethylene formed? - Metabolized by liver (takes 8 hours to get out of the brain), can also be metabolized in blood plasma - Benzoylecgonine: inactive metabolite that comes out in urine, is what is detected in tests (up to 72 hours) - Benzoylecgonine is detected up to 48-72 hrs after in UA (up to 2 wks for chronic users), and 90 days in hair follicle analysis - Cocaine when taken with alcohol - Cocaethylene: active metabolite produced when coke and alcohol are used together, can be super charged version of cocaine and more addicting, worse on your heart - increases withdrawal symptoms (severity) and dependency/toxic levels

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Cocaine is rapidly metabolized by the liver and plasma. The metabolite is Benzoylecgonine. - confirmed in the discussion board by the TA (that’s the inactive one though, the active one is cocaethylene) 6. Which neurotransmitters are affected by cocaine and how are the neurotransmitters affected in the brain? ➢ Dopamine, serotonin, & norepinephrine: blocks reuptake ➢ also keep in mind that it binds to the receptors to increase neurotransmitters in synapse, more psycho stimulation ➢ dopamine is also involved in reinforcement which leads to addiction. 7. What are the three primary actions of cocaine (hint: vasoconstriction is one to get you started)? ➢ Local anesthetic: numbness in gums, sinuses and back of throat and perhaps a choking sensation (blocks Sodium channels on axons like novocaine) ➢ Vasoconstrictor: constricts blood vessels/cardiovascular problems and possibly death ○ 8-30% actually gets in blood stream ○ because cocaine is a vasoconstrictor, when snorted the blood vessels in the nose get further from the surface. That means the more you snort, the less will be absorbed. That is a barrier to absorption ○ vasoconstriction can lead to cardiovascular problems & death ➢ Psychostimulant: creates euphoria and a rush, which is why people use it (blocks reuptake of dopamine, norepinephrine, and serotonin) ○ Reinforcing effect that leads to abuse/dependence (dopamine) 8. What is a speedball? rip john m ➢ a mixture of cocaine and heroin. It is injected and responsible for many overdoses. ➢ a fatal example of a bad drug interaction ➢ most chemically toxic 9. Which drugs are used to treat cocaine dependence and withdrawal? ➢ Anticraving agents: zofran ○ effects serotonin, antagonist to serotonin R3 receptor ○ also helpful for anti nausea ➢ Treatment of comorbid disorders: antidepressants & antipsychotics ○ background into why they started using ➢ Cocaine vaccine: blocks cocaine's euphoric effects (only effective in the minority of patients (about 40%). In the cases where it is effective, it makes cocaine less reinforcing) ○ effective in 40% of patients ○ contains antibodies that block the euphoric feeling ○ not meant for long-term use; use during withdrawal symptoms/early treatment to decrease dependency ➢ Anti-withdrawal: Ritalin (blocks reuptake of dopamine and norepinephrine) ○ helps balance DA and NE levels ○ decrease severity of symptoms 10. What is the “crash” observed in cocaine users and what effect does it have on mood?Full blown mania -> full blown depression (aka crash) They start using cocaine because they are depressed, they snort cocaine (25-100mg) and they come off cocaine and get sad again. They repeat this cycle. Then they start to increase the dose. Then, when they come down, they come down to full-blown depression. This promotes abuse and using high doses. During the crash, people usually feel deep depression, anxiety, fatigue, and agitation. (The higher you get, the further you fall) called “cocaine blues” 11. How was amphetamine first discovered and how is it made? ➢ dates back almost 5000 years to Chinese medical herb called ma-huang (used to clear airways) ○ active ingredient of ma-huang: ephedra vulgaris ➢ isolated by German scientists (ephedrine) from mahuang ○ synthesized ephedrine= amphetamine (by Gordon Alles) ➢ made into a pharmaceutical drug ○ 1930 Benzedrine - racemic dextro/levo- amphetamine mixture) as a CNS stimulant ■ used as decongestant (over the counter at that time) but had multiple uses ● smoking cessation, schizo treatment, headaches, etc

4 ○ 1937: Benzedrine used to treat ADHD rx ➢ 1940: methadrine came out (pill version of methamphetamine) ➢ 1970: because of US Drug Regulation Act & Control Act; became a regulated Schedule II drug 12. What are some differences between the different forms of amphetamine? How do the routes of administration differ for each type? ➢ Dextroamphetamine: (prescription version) taken orally, more potent. ○ Used for adderall (racemic amphetamine:= dextroamphetamine + amphetamine) ○ Dexedrine: (brand name dextroamphetamine) is an amphetamine ■ used to be prescribed for weight loss, depression (can be taken orally, rectally, snorted, or IV). ADD treatment ➢ Levamphetamine: taken orally, less potent than D-amphetamine; can be taken orally, snorted, or IV). ○ left-sided enantiomers cause more side effects in general and doesn’t do as much as Dexedrine ➢ Methamphetamine hydrochloride: (chemical still used, methyl group crosses the blood brain barrier faster, more of it gets into the brain more efficient, stronger than D & L-amphetamines). ○ has the strongest effect because it readily crosses the Blood Brain Barrier. ○ Called meth, speed, or crank. Not CRYSTAL METH So what is crystal meth? Free based methamphetamine i think? So like cocaine one has to remove the HCL that makes it a salt (water soluble) in order to free base and smoke meth ○ Desoxyn ■ pharmaceutical version= 5 mg tablets prescribed ■ Treat narcolepsy and sometimes ADHD and morbid obesity. ■ Schedule 2 drug 13. What is the primary difference between amphetamine and methamphetamine in terms of crossing the blood brain barrier? ➢ methamphetamine is very fat soluble so it can cross the blood brain barrier quickly (faster and more efficient than amphetamine) ○ why it’s useful in pharmacology ➢ stronger than amphetamine ➢ Methamphetamine is also a methylated version of amphetamine 14. How is amphetamine metabolized and what are the metabolites? ➢ metabolized in the mainly liver ○ most excreted as amphetamine itself about 70%, very little gets broken down ■ if broken: methaphetamine and amethpetamine ■ testable up to 4 days 15. Which neurotransmitters are affected by amphetamine and what effect does it have on the neurotransmitters? - increase release of dopamine and norepinephrine -Both STIMULATE RELEASE (more is going to get released by making the vesicles leaky) and both BLOCK REUPTAKE (slows/minimizes it) Add for crystal meth: 50% reduction in dopamine AND serotonin receptors in frontal (more aggressive behavior)

lobe and basal ganglia= movement disorders 16. What effects does amphetamine have on the autonomic nervous system? -the effects can be prolonged in the sympathetic nervous system, these effects are: increased respiration, increased heart rate, increased hyperthermia, and elevated blood pressure. all last about 8-12 hours. 17. What is amphetamine psychosis? -a set of symptoms, including hallucinations, paranoia, violence, mood swings and disordered thinking, resulting from high doses of amphetamines. usually from inability to sleep, no sleep = hallucinations

5 18. Which drugs are used to treat ADHD? What are some basic differences between how the drugs affect neurotransmitters in the brain? -Methylphenidate (Ritalin) – half life is 2-4 hours. -blocks reuptake of dopamine and norepinephrine. -slightly increases release of DA and NE as well -Methylphenidate SR (Concerta): is released over 10 hours; it's not an amphetamine and blocks reuptake of DA and NE like cocaine does and slightly increases release of DA and NE like amphetamine. -Daytrana (Ritalin patch; SR) --how the drugs affect neurotransmitters in the brain? -Dexmethylphenidate (Focalin)- pro-drug, body metabolizes it into methylphenidate how the drugs affect neurotransmitters in the brain? -Racemic Amphetamine (Adderall): a combo of 2 amphetamines (amphetamine and dextroamphetamine) half life of 78 hours; more likely to cause dependence compared to Ritalin -XR = extended release -Vyvanse: lisdexamphetamine; prodrug, similar to Adderall -Dextroamphetamine (Dexedrine)how the drugs affect neurotransmitters in the brain? -Strattera: blocks NE reuptake -antidepressant- like; but known to increase suicidal thoughts New for ADHD treatment: -Intuive: anti hypertension drug; unknown why it helps treat ADHD -Nuvigil/Provigil: treats narcolepsy and apnea; focuses on dopamine 19. What are some basic side effects of drugs used to treat ADHD? How do these drugs affect individuals who do not have ADHD when the drugs are taken as “study aides”. -side effects: loss of appetite, insomnia, mood swings, delayed growth, headache, stomach ache, irritability -Ritalin: stunts growth, reduced appetite, rebound hyperactivity, headache, GI irritability, sleep problems, slight blood pressure increase -Adderall (usually mild side effects when used as prescribed): tachycardia, GI upset, increase in blood pressure, weight loss (more so than Ritalin), increase psychomotor activity -study aide side effects: Individuals who don't suffer from ADHD, but are using ADHD medication will be able to stay awake for a long period of time, but it doesn't mean that they will be able to retain information better. Students who take ADHD medication might overstimulate themselves leaving them unable to concentrate DODSON GRAPH- Cognitive performance vs. Excitation -Want to have a certain level of excitation to maximize cognitive performance, can disrupt excitation if over-stimulated; goldilocks issue, either not enough stimulation or too much or just right -Goal of medications to have optimal performance/excitation -Use of Adderall and Ritalin as study aids for non-ADHD individuals

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20. Review the differences in the amount of caffeine found in various products (e.g. coffee, soft drinks, Red Bull, etc). You do not need to know specific numbers but know roughly which products have high vs. lower amounts of caffeine.j -decaf coffee, chocolate bar, soft drinks, tea/instant coffee, drip brewed coffee, energy drinks -lower to higher HIGH: Coffee/Brewed Starbucks, Red Bull, 5 Hour Energy, 4-Lokos MEDIUM: Soft drinks, Tea, baking chocolate LOW: Decaf Coffee, milk/sweet chocolate, Cocoa TA on Discussion Board mentioned this will be an exam question: Nodoz and Vivarin are Over The Counter and contain approx 200mg of caffeine. They also contain more caffeine than most soft drinks or energy drinks. That will be an exam question. 21. Where might you find theophylline or theobromine? -theobromine: a xanthine stimulant found in chocolate -theophylline: a xanthine stimulant found in small amounts in tea, it is used as an antiasthma medication 22. Which type of receptors does caffeine affect in the brain? -Main Mechanism of Action: in both low and high doses, caffeine blocks adenosine (plays a role in sleep) -in low doses of caffeine, it really has no effect on the cAMP - what is the cAMP ← stands for Cyclic 7 Adenosine Monophosphate; a “messenger” in cellular responses -cAMP is only affected at high doses by inhibiting the phosphodiesterase (enzyme that breaks down cAMP). -high doses: -increase in calcium release (more getting into receptors and neurons) -blocks GABA-A receptors -at really high doses: inhibition of phosphodiesterase (enzyme that breaks down cAMP) -low/regular doses: -blocks adenosine receptors → decreases sleepiness -secondary effect: may indirectly activate NE channels, and may increase release of DA & serotonin 23. How is caffeine metabolized and what are the metabolites? -Caffeine is broken down by the CYP1A2 enzyme in the liver. -98-99% of caffeine gets broken down. 95% of caffeine is excretfed through urine and 5% as poop. caffeine is mostly cleared from circulation during sleep. -metabolites:

7 -Theophylline (found in tea) -Paraxanthine: mildly psychoactive, very weak -Theobromine (found in chocolate): 1/10th strength of theophylline 24. What are some of the effects that caffeine can have on physiology in the body (e.g. blood pressure, blood vessels, etc.)? -Enlarges coronal blood vessels, -increases intracellular calcium -releases nitric (or is it nitrous?) oxide in smooth vascular muscles -constricts cerebral blood vessels (Adenosine makes blood vessels in brain smaller) -decreases blood flow to brain (at a dose of around 100-200mg) -increases blood pressure (small effect at normal dose) -increased respiration -diuresis (increased water excretion, which can lead to dehydration) -affects ADH (antidiuretic hormone) in kidneys -increased effects on epinephrine & sympathetic system restricts the blood vessels to the brain (cerebral blood vessels), which can help with headaches. 25. Although caffeine is a fairly safe chemical, which demographic in the population (group of people) may suffer adverse effects of caffeine and what kinds of problems can it cause in some individuals? -ELDERLY: leads to osteoporosis and bone fractures -May benefit people with PARKINSON’S DISEASE -PREGNANT WOMEN: caffeine consumption during first months is related to low birth weight, increase miscarriages -CHILDREN: deficiencies in calcium/phosphorus for normal bone growth, behavior problems such as anxiety, nervousness, insomnia 26. How might caffeine help to alleviate headaches? - caffeine constricts blood vessels (vasoconstrictor) in the brain => this reduces pressure => this overall alleviates the headache. 27. Review some potential dangers associated with energy drinks containing caffeine. -usually labeling is deceiving: higher caffeine/stimulant levels than easily readable, multiple servings per can -Rockstar drinks have lots of vitamin B along with other vitamins, if you’re drinking a 24 oz multiply 3x the recommended daily dosage of normal vitamin B, and you get that much in one drink! -don’t need more vitamin B12 than what our body produces, consuming more does nothing -guarine is typically not listed under caffeine, so you might be getting more caffeine than what is labeled (TA made a comment to focus on dangers on the DB, so here they are..) boost heart rate and blood pressure which can lead to arrhythmia 28. What is caffeinism? -a dangerous state of overstimulation from a very large dose of caffeine (1,000-2,000MG) ● experience symptoms similar to an anxiety attack -characterized by restlessness, nervousness, insomnia, tachycardia (rapid heart rate), and an upset GI. -the first case was in the 1890’s. 29. What are the major diseases associated with cigarette smoking? -cardiovascular/Heart disease (#1 killer in USA) -Atherosclerosis - plaque buildup; thrombosis - (blood clotting) arteriosclerosis - hardening of the arteries -pulmonary (Lungs) disease

8 - bronchitis/emphysema (Chronic obstructive pulmonary diseases) -cancer

Emphysema, heart disease, cancer, lung diseases 30. Which type of receptors does nicotine bind to and where are these receptors found in the body? -in the ANS -Which: acetylcholine nicotinic receptors (Nicotinic AcH) -Where: Brain (ANS) and Neuromuscular junction

31. What effects does nicotine have on the autonomic nervous system? -sympathetic ns: decreased appetite, increases blood pressure, and heart rate -parasympathetic ns: it activates the stomach to releas...