Final Study: Chapter 10: Tobacco PDF

final study Created @December 11, 2024 11:45 PM Class HPEX 352 Chapter 10: Tobacco 1. Psychoactive chemical- Nicotine; Safer cigarettes. 2. Health hazards and carcinogens & poisons in tobacco/tobacco smoke....

final study Created @December 11, 2024 11:45 PM Class HPEX 352 Chapter 10: Tobacco 1. Psychoactive chemical- Nicotine; Safer cigarettes. 2. Health hazards and carcinogens & poisons in tobacco/tobacco smoke. -affects nearly every part of the body; mouth, brain, stomach, reproductive system. -contains 100s of damaging chemicals such as; acetone, ammonia, hexamine. cigarette tar: condensed particles in the cigarette producing a stick brown mass. carcinogens combined with other chemicals can cause cancer. some forms of it :Benzo(a)pyrene, Nitrosamine, Urethane poisonous substances: Arsenic and Hydrogen cyanide 3. Smokeless tobacco & health concerns; e-cigarettes & health concerns. smokeless tobacco packaging carry warning labels. the health hazards are increased risk of dental disease and oral cancer. -contents potent carcinogens such as nitrosamines which causes leukoplakia. final study 1  E-cigs are a nicotine delivery system; it turns nicotine and other chemicals into a vapor that is inhaled. 4. Long-term effects of smoking tobacco on the lungs, heart, blood vessels, and other organs. -the greatest avoidable cause of death; risk increases for those who start young and smoking for a long time. -COPD; chronic bronchitis- inflammation of the airways -nicotine affects the blood vessels; plaque buildup in the blood vessels. -if you’re diabetic it can cause insulin resistance. 5. Environmental Tobacco Smoke, components of ETS-mainstream, sidestream, thirdhand smoke;Effects of ETS on health; Smoking and pregnancy. second hand smoking; cigarette smoke inhaled from the environment of others. Environmental tobacco smoke is classified as a class A carcinogen. mainstream:the smoke exhaled by the smoker sidestream: the smoke rising from the ash of a cigarette. thirdhand: residual nicotine and other chemicals left on indoor surfaces by tobacco/ vapes. Effects -develop cough, headaches, eye irritation, and sinus problems. -causes 3400 deaths due to lung cancer and 46000 heart disease deaths. final study 2  -effects on children that are exposed to this are likely to have bronchitis(even later in life) pneumonia, and SIDS. -reduced lung functions; asthma -effects on pregnancy increased the risk of miscarriage, low birth weight, and sudden infant death syndrome(SIDS). 6. Nicotine pharmacology, absorption, metabolism, and mechanism of action on the brain. -An active ingredient in tobacco; a natural occured liquid alkaloid that is colorless and volatile -tolerance and dependence develops quickly; lethal dose = 60mg—a cigar contains twice that much. inhalation- very effective and 90% of inhaled nicotine is absorbed. -80-90% of nicotine is deactivated in the liver and then excreted via the kidneys. -use of nicotine increases the activity of liver enzymes responsible for nicotine deactivation; contributes to tolerance, enough dose to be lethal. inhibitors of cyp2a6— cotinine—-3-hydroxycotinine nicotine has a short half life- 24-84 minutes (short duration of action.) cotinine is the active metabolite/ 3-hydroxycotinine is an inactive metabolite. Mechanism of action -mimics acetylcholine; first stimulates and then blocks receptor sites -causes a release of dopamine and the release of adrenaline and has an indirect sympathomimetic effect. final study 3  7. Physiological & behavioral effects; Challenges to quitting smoking; Treatments (pharmacological and replacement therapy). CNS and circulatory system effects -increased heart rate and blood pressure -increased oxygen need of the heart. -decreased oxygen-carrying ability of blood which causes shortness of breath. reduced hunger; inhibition of hunger contractions, increased blood sugar behavioral effects -nicotine has both stimulant and calming effects. within minutes of quitting your heart rate drops, 24 hours later; the nicotine level in the blood drops to zero etc. replacement therapy; delivering nic without the tar and carbon monoxide; produced in gum, patches, inhalers. pharmacological therapy; bupropion(zyban) Chapter 11: Caffeine -most used psychoactive drug and belongs to the class chemicals known as xanthines. 1. Xanthine- caffeine, theophylline, theobromine, and the three main sources of xanthine. xanthine; a purine base found in most human body and other organisms. final study 4  coffee plant(middle east), tea plant (grown in china), and cacao plant( central america)-contains xanthines. plant derivatives are; caffeine, theophylline, and theobromine. 2. Xanthine content in coffee, tea, and chocolate. caffeine is the xanthine derived from the coffee plant; an average cup contains 90-95mg of caffeine. tea has more caffeine than coffee; has about 40-60 mg of caffeine per cup depending on the type and strength of the brew. -1 ibs of tea leaves= 200 cups of tea -1 ibs of coffee= 50-60 cups of coffee. Theophylline is another xanthine found in tea -very small amount- 0.3% by mass -in high doses, theophylline is used as an asthma medication. theobromine is the xanthine unique to chocolate; similar to caffeine but less potent. -an average cup contains 200 mg in caffeine an average cup of cocoa contains 4mg. 3. Pharmacology (effect on cardiovascular & central nervous system, dependence, mechanism of action on the brain, and physiological & behavioral effects), Caffeinism. the three key xanthines; caffeine, theophylline, and theobromine-soluble in water. final study 5  CNS Effects -greatest stimulant effect- caffeine; have a less stimulating effect on our cns- theobromine/ theophylline. Cardiovascular effects -theophylline and theobromine has the most potent cardiac stimulating effect. -caffeine has the least potent cardiac stimulating effect. time course fast absorption if taken orally the peak levels reached in 30 minutes and the (metabolism) half life is about 3 hours -duration of action is also short, fast onset effect. dependence -withdrawal symptoms; fatigue and headache. -dsm-5 does not list caffeine under substance use disorder. mechanism of action -xanthines block the adenosine receptors in our brain. adenosine; produce a behavioral sedation; inhibitory neurotransmitter that modulates the release of other neurotransmitters(dopamine and epinephrine.) physiological effects -stimulates the cns and skeletal muscles and causes sleep disturbances. -constricts blood vessels in the brain. behavioral effects final study 6  cognitive/psychomotor performances; caffeine partially offsets the effects of fatigue but it may not improve performance in well rested individuals. Chapter 13: Opioids 1. Opioid (its effects & examples), Analgesic & Anesthetic; Classification of opioids. -a naturally occuring substance derived from the poppy plant. -relieves pain and delivers pleasure and relief from anxiety. Analgesic; relief from pain and might be targeted toward a specific anatomical region. Anesthetic; lack of sensation removing feeling from the body; affects the entire body. classification; natural forms: morphine, codeine, and thebaine semisynthetic; heroin, oxymorphone, and hydromorphone synthetic (man made and highly potent mimicing the natural opiod; meperidine, methadone, morphinians, and benzamorphans. 2. Opiate & Opioid, Agonist & Antagonist (examples). opiates- more natural than the other has the first connection to the plant.;opium, morphine, codeine opioids- opioids are in everything. ie: heroin, fentanyl, morphine. angonists- drugs that occupy receptors and activate them final study 7  antagonists-drugs that occupy receptors but do not activate them-blocks the receptors and get no effect. partial agonist- its not completely blocked but you get some affects from the drug. 3. Morphine, Codeine, Heroin, Fentanyl. morphine is the active ingredient in opium- 10x potent as opium. -clinically useful as a strong analgesic; pure chemical and potency is as strong as a strong full agonist. -soldiers would use this drug during 1853 a lot; it became addictive. codeine is a secondary active alkaloid. -known as methyl morphine -much less analgesic than morphine more antitussive -a cough suppressant. -can cause respiratory distress and death when taken in high doses. -codeine is strong full opiate agonist 4. Mechanism of Action on the brain, Opioid receptors, Opioid Antagonist. enkephalins; morphine-like neurotransmitters found in the brain and adrenals. endorphins; morphine-like neurotransmitters found in the brain and pituitary gland. -both bind to the opioid receptors in the brain. target these opioid receptors; mu, delta, kappa and target the brain rewards system by triggering dopamine and blocking gaba & norepinephrine receptors. Mu; physical dependence,sedation, euphoria, analgesia(CNS, most opioids) Kappa; miosis, sedation, dysphoria, analgesia(PNS, most opioids) Delta; antidepressant effects, analgesia(PNS, most opioids) final study 8  Antagonist blocks the action of opioids- naltrexone, nalorphine, and naloxone. -reverse depressed respiration from opioid overdose, precipitate with drawls syndrome. an overdose happens when too much of an opioid(heroin, oxycontin) fits in too many receptors which stops the persons breathing. -naltrexone knocks the opioids off the receptors for a short time, this allows the person to breathe again the reverse the overdose. 5. Beneficial/Medical uses, Dependence potential, Acute & Chronic toxicity, Misconceptions. -used as a pain relief; educed the emotional response to pain and diminshes the patient’s awareness of and response to the aversive stimulus. treatment for intestinal disorders; counteracts diarrhea and the resulting dehydration. cough suppressant; codeine is used for it’s antitussive properties and dextromethorphan(OTC antitussive) is an opioid analogue. acute toxicity -opioids depress respiration, occasionally nausea and vomiting, can be counteracted with naloxone. chronic toxicity associated with injection and infections and the spread of blood borne diseases. dependence potential final study 9  tolerance: cross tolerance exist among all the opioids and the higher doses need to maintain effects. physical dependence; withdrawal is unpleasant but rarely life threatening and it can be prevented with any opioid agonist. psychological dependence; positive reinforcement: positive effects reliably follow use of the drug and negative reinforcement; use of the drug removes withdrawals symptoms. misconceptions -withdrawal is always excruciating-similar to a mild case of the intestinal flu(true). -after one injection you are hooked. Chapter-14: Psychedelics 1. Psychedelics (its effects & examples), depersonalization, flashbacks, synesthesia. the oldest known drugs that have been used for their ability to alter human perceptions and moods. -used to treat mental health illness. Examples: LSD, psiocybin, MDMA. lsd and psilocybin belong to the chemical groupings of indole the sensation of experiencing sounds as pictures or of seeing movements produced by musical rhythms is known as synethesia 2. Factors considered for the classification of psychedelics. chemical structure pharmocological properties how dangerous how much loss of awareness they cause final study 10  3. Two major groups of psychedelics and their subgroups (indole, catechol). Phantastica; alter perceptions while allowing the user to remain communication with the present world. ie:LSD, psilocybin, MDMA, and mescaline indole; drugs that have the same basic indole structure of the neurotransmitter serotonin ie: LSD. catechol; drugs that have the same catechol structure of the neurotransmitters norepinephrine and dopamine ie: mdma(ecstasy or molly) Deliriants; produce more mental confusion, greater clouding of consciousness and loss of touch with reality. ie:PCP and ketamine 4. Phantastica [LSD (highly potent), psilocybin, mescaline, MDMA] - absorption, metabolism, mechanism of action, dependence, and physical and psychological/behavioral effects. physical effects -dilated pupils, higher body temperature, increased heart rate and blood pressure. psychological effects of LSD -feelings of spirituality; thinking they can connect with something else. -experience sever, terrifying thoughts and feelings. synesthesia(mixing of senses); ie sounds may appear as visual images. mechanism of action lsd acts by stimulating serotonin-21 receptors- acts on dopamine, nor- epinephrine, and glutamate. final study 11  -metabolized by the liver, half life is about 3 hours, takes affect within 30 minutes and it can last up to 12 hours. -less than.001 gram of LSD produces extreme hallucinations. time course of effects -typically last 6-12 hours; first 20 mins: autonomic responses occur, next 30-40 mins: alterations in mood, perception, and sensation begin. within the first hour; full intoxication occurs (loss of self awareness & control may occur). psilocybin- is a primary active ingredient , known as the magic mushroom. -lasts about 6-10 hours, similar to LSD *mescaline- is the primary active ingredient in peyote ( small, spineless, carrot shaped cactus) -rapidly absorbed after oral administration, dosen’t cross the blood brain barrier easily and same physical effects as LSD. -half life is about 6 hours and typically lasts up to 12 hours. MOA- Acts on the synapse to increase the activity of dopamine and norepinephrine and small amount of serotonin. -low does effects are primarily euphoric and higher doses cause the full set of hallucinogenic effects. MDMA-close to amphetamines, its effects are increased heart rate and blood pressure, increased euphoria and sociability. mechanism of action; acts on the synapse to increase the activity of dopamine, norepinephrine and high amount of serotonin. -immediate after effects, 4-8 hours in duration. 5. Deliriants- Physical and behavioral effects, mechanism of action on the brain. phantastica- have similar effects and acts primarily through the serotonin, dopamine, norepinephrine. final study 12  delirants have a greater tendency to produce mental confusion and a loss of touch with reality. acts on different brain mechanisms -Sigma receptors(agonist) -GABA(agonist) -Kappa opioid receptors (agonist) -NMDA Antagonists-glutamate physiological and behavioral effects -blocks production of mucus in the nose and throat and prevents salivation. -eyes dilates and heart rate increases. -at high does, behavior pattern resembles toxic psychosis(delirium, mental confusion). 6. PCP and other PCP-like drugs; Medical uses of psychedelics. generic name ; phencyclidine; used as anesthetic for animals. MOA- binds selectively to the sigma receptors and other delirants bind to this receptor. -acts on glutamate, opioid receptors. medical use -used for mental illness -relieve memories and experiences directly helps those with PTSD, social anxiety Chapter 15: Marijuana final study 13  1. Marijuana (its effects); Cannabis, Marijuana, THC difference. -a schedule 1 drug marijuana is derived from cannabis Cannabis-plant: contain chemicals that can be used for medical purposes. Marijuana is a preparation of leafy material. THC; a chemical in cannabis that gives you head high/ addiction. Marijuana falls underneath its own category. 2. Cannabinoids- Psychoactive ingredients & other types of cannabinoids. Cannabinoids- unique to the cannabis plant and has medical use; 70 chemicals. CBD; dosen’t give you the feeling of highness but has a bunch of medical uses; pain reliever, neuroprotective affect. THC: the most pharmacolically used type of cannabinoids 3. Pharmacology- metabolites, smoking and oral THC difference (time course and metabolism). -metabolized by liver enzymes -CYP450-3A4. -11-hydroxy-delta-9-THC is more potent than THC After smoking -thc is absorbed rapidly by the blood and travels to the brain then the rest of the body. -peak mood effects occurs within 5-10 minutes, within 30 minutes most thc is gone from the brain. lasts about 1-3 hours. after oral administration - its absorbed much more slower, peak effects occur about 90 minutes , effects last about 8-10 hours -more thc is metabolized by the liver and less thc reaches the brain. final study 14  after a week 25-30% of thc and its metabolites remains in the body. 4. Mechanism of action on the brain, Endocannabinoids and their receptors. thc and cannbiniods bind to two receptors CB1 & CB2 Recpetors -causes increased dopamine release and it mostly binds to CB1 receptors triggering anandamine. anandamine- endocannabiniods; endogenous substance isolated from the brain tissue with marijuana like effects. CB1- concentrated in the brain and CNS CB2- mostly in the perepheral organs especially cells associated with the immune system. 5. Medical uses of Cannabis; Physiological effects. safe and effective medicine for patients suffering from chronic conditions. Dronabinol; oral thc prepration , used as an antiemetic (prevent nausea and vomiting) in 1985 -in 1993 it was used to stimulate appetite. Physiological effects -increased heart rate occurs after smoking and ingesting. pulmonary effects; bronchodilation- acute exposure to marijuana -reddening of the eyes and dryness of the mouth. -munchies; increase in appetite afterwards. euphoria” being high” peak effects after 5-10 minutes and lasts about 2 hours. -oral has similar effects but different time course. final study 15  6. Abuse potential & dependence; Acute & Chronic toxicity. -oral thc dosent have an abuse potential due to its different time course effect. -tolerance usually comes after high levels of usage. -withdrawals isn’t life threatening but unpleasant, begins after 1 day after the last dose and last about 4-12 days. Symptoms include anxiety, irritability, disrupted sleep. acute and chronic effects -increased heart rate and risky for someone with preexisting cardiovascular disease. -chronic lung exposure from marijuana exposure; daily smoking damages your air flow in and out of your lungs. -testosterones is reducing in men the more they smoke and diminishes your sperm and abnormal sperm count in men. -lower birth rate in women final study 16