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Using Fig. 4.113, design a problem to help other students

Fundamentals of Electric Circuits | 5th Edition | ISBN: 9780073380575 | Authors: Charles Alexander ISBN: 9780073380575 128

Solution for problem 4.46 Chapter 4

Fundamentals of Electric Circuits | 5th Edition

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Fundamentals of Electric Circuits | 5th Edition | ISBN: 9780073380575 | Authors: Charles Alexander

Fundamentals of Electric Circuits | 5th Edition

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Problem 4.46

Using Fig. 4.113, design a problem to help other students better understand Norton equivalent circuits.

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Chapter 10 - Marijuana Marijuana  Medicinal uses documented back to ancient times… Cannabis sativa There are 2 varieties of this plant:  Psychoactive o Growing o Weaker fabric o High cannabinoid content o Delta-9-tetrahydrocannabinol and 66 other cannabinoids.  Non-psychoactive (hemp) o Easy and fast growing o Strong plant fiber o Little cannabinoid o Many industrial uses Cannabis sativa L. There are two sub-species:  Cannabis sativa: higher THC content. o More euphoria.  Cannabis indica: higher Cannabidol (CBD) content. o More medicinal aplications (muscle relaxation, analgesia, sleep aid) Marijuana in America  Classified as controlled substance iwht no medicinal value in 1970. Today  Most commonly used legal drug. o More than 83 million Americans report trying at least once.  18 million in the past month. o Is associated with cigarette and alcohol use. o The number 1 cash crop in America.  2015 revenue in CO. Cannabis sativa: Psychoactive forms  Marijuana: Dried leaves and flowers. o Usually smoked; may be baked into foods. o Wide range of THC content (5-15% THC) o Sinsemilla: without seeds (25 to 35% THC)  Bhang: Entire remainder of plant after top has been picked. o Ground into a powder. o Often mixed into drinks. 2  Ganja: Made of the tops of the female plants; resin is still present.  Hashish: resign from top of female plant. o Dried and then smoked or baked into foods.  Hash Oil: Solvents are used to extract the cannabinoids o Tends to have high THC content (15 to 70%)  Dab o Concentrated hash oil  Infuse marijuana with butane gas o 80-90% pure THC  20 to 25% Absorption  Highly lipid (fat) soluble; will hardly dissolve in water.  Oral: o SLOW o Oil in foods help to speed absorption. o Peak effects in 1-3 hours; may last up to 6 hours.  Inhalation: o 10 to 25% of cannabinoids are absorbed. o Blood levels peak in 15 minutes. o Effects last 30 to 60 minutes. 3 o Depth of inhalation is more important than length. Distribution  Only 1% enters the brain.  Distributed all over the body. Where does it work in the brain  Currently know about two cannabinoid receptors. o CB 1– Found primarily in brain o CB 2– Found primarily in periphery o These work to influence GABA, endorphins, and dopamine.  Endogenous agents: endocannabinoids o Anadamide o 2-AG (2-arachindonoylglycerol)  2-AG is the primary endocannabinoid. Why not develop CB 1 and CB 2(ant)agonists  There has been development of various CB1 and CB2 agonists and antagonists.  They seem to be less effective than the effects observed from cannabis. o The medicinal value of cannabis is not simply the stimulation of CB 1and CB 2 receptors… 4 Efficacy of cannabis  Pharmacodynamic interaction of THC and Cannabidiol (CBD) o THC’s psychotropic effect can be blunted by CBD. o Extremely difficult to mimic medicinal value of cannabis. Excretion  Most metabolism takes place in the liver.  Converted to metabolites that rapidly cross into the brain.  Takes 20-30 hours to remove ½ the dose.  May be detected in the body up to 30 days later. Effects of 9 THC  Psychological – euphoria, relaxation, sleepiness, “insight”  Perceptual – altered perception of space and time, mood changes, introspection, and more “creative”.  Physical – increased heart rate, reddening of eyes, increased appetite, decreased coordination, dry mouth, and possible headache.  Cognitive Effects: o Impairment of short term memory during use. o Long term is more controversial.  May cause damage to neurons in the hippocampus.  May cause deficits in the ability to organize and integrate complex information. 5 Long Term Effects Crean et al., 2011  Heavy use impairs cognitive function for 2-3 weeks after stopping. o Attention, concentration, inhibition.  Less information is available for 3 weeks and beyond. o Suggests a similar trend. Effects of 9 THC  Motivational effects o AMS – amotivational syndrome.  Characterized by amotivational, apathetic mood; not achievement oriented. Tolerance  Studies suggest tolerance occurs o Develops rapidly in laboratory animals. o Down regulation of cannabinoid receptors in the brain. o Not as clear in humans.  Sensitization and novice effects.  Hirvonon et al., 2012 (in humans): o Down regulation of CB1 in receptors in cortical areas. o Correlation between smoking frequency and down regulation. 6 o Effect was reversed with 4 weeks of abstincence. Withdrawal  Animals: Cannabinoid antagonist results in withdrawal. o Increase in stress hormones.  Humans – Maybe with high doses… o Increased anxiety, irritability, decreased appetite.  Recent evidence suggest it occurs in about 10% of people who have ever tried it. o Daily users have a 50% chance of developing dependence. Treatment  Typically, outpatient treatment  Relapse rates are similar to other drugs of abuse.  Antidepressants and oral THC may help. Long Term effects of Marijuana  Fairly minimal to date.  Inflammation and cell injury in lungs. o Contains 50-70% more carcinogens than cirarettes. o May be a risk factor for cancer, but now empirical evidence.  THC suppresses the immune system. 7  Reproductive function o Females it decreases gluttonizing hormones. In males it decrease testosterone.  Marijuana smoke may be a source of cellular oxidative stress. Long Term Effects in Adolescents  Significant relationship between early heavy use and the development of psychotic disorders in adulthood.  Regular marijuana may alter adolescent brain development. Possible Therapeutic Value  Nausea and vomiting o An effective antiemetic drug (for reducing nausea) associated with chemotherapy. o Marinol, and Cesamet: Available for medical use in oral form of chemotherapy–induced nausea. Other Therapeutic Uses  Glaucoma o Reduces fluid pressure.  Asthma  Multiple Sclerosis (MS) and spinal cord injury.  Traumatic brain injury.  Marijuana smoke may contain antioxidants.  CBD may slow the growth of cancer cells. 8 Chapter 5 – Nicotine Routes of Administration  Potent poison and bitter flavor. o Tobacco leaves contain up to 10% nicotine.  Snuff: Sniffed into the nostrils  Dip: Placed inside the cheek.  Chew: Absorbed through membrane of the mouth. o All 3 are absorbed through mucus membranes.  Cigarettes and cigars: smoked o Nicotine is vaporized and is in the ash and smoke. o Absorbed in the lungs. Absorption  Lungs  Heart  Brain o Rapid o 90% of nicotine inhaled reaches the brain. Distribution  Smoke contains: o Carbon monoxide: Reduces oxygen o Tar: Sticks to cells in the lungs and prevents elimination of foreign materials. o Nicotine: Oily psychoactive compound.  60mg of pure nicotine would kill an adult.  7 to 9 mg in a cigarette.  Average about 1 mg per cigarette is absorbed into bloodstream/brain. Distribution and Excretion  Half life ~30 minutes.  30 to 40% eliminated in urine.  Remaining metabolized in liver.  No day to day accumulation.  Crosses placenta and is found in breast milk. Where does it work in the brain  Binds to nicotine receptors for acetylcholine. o Many different brain regions.  Stimulates release of epinephrine, dopamine, and serotonin. Effects  Physical: Increases heart rate and blood pressure, constricts blood vessels in the skin (cold touch and wrinkles), laxative, increased respiration, nausea. o Increases metabolic rate and decrease appetite.  Nesbitt’s paradox: Causes physiological arousal: yet report relaxation. o For non-users it causes arousal, tension, dizziness and/or nausea.  Performance: Improves performance of smokers on tasks that require vigilance and attention. o Speeds information processing. o Improves performance on learning tasks.  Tolerance does develop. Withdrawal  Decreased heart rate, increased appetite, difficulty concentrating, trouble sleeping, craving, anxiety, anger, depression.  Last about 1 month (except for craving).  May last up to 6 months. 2 Smoking Cessation  Most surveys show that the majority of smokers want to quit…  Physical and psychological addiction. Pharmacotherapies  Substitution and weaning (reliably increase long term abstinence). o Nicotine patch. o Nicotine gum. o Nicotine inhaler. o Nicotine nasal spray. Other things  Zyban (buproprion) – Approved in 1997 for smoking cessation. o Originally an antidepressant (Wellbutrin). o Mechanism of action not well understood.  Chantix (varenicline) – approved in 2006 for smoking cessation. o Partial agonist for a portion of the nicotine receptor. o Prevents nicotine from occupying receptors. o Results in sustained low level of dopamine release while preventing withdrawal. Topics Hallucinogens ~14 questions Marijuana ~12 questions Nicotine ~8 questions. 3 Chapter 11 – Alcohol What is a Hallucinogen  All drugs that cause users to have hallucinations.  Abrams (1996) defined psychedelics: o Any agent that causes alterations in perception, cognition, and mood as its primary psychobiological actions in the presence of an otherwise clear sensorium. Psychedelic drugs  Many (but not all) psychedelics structurally resemble one of five neurotransmitters: 1. Serotonin Catecholamine’s 2. Norepinephrine 3. Dopamine 4. Glutamate 5. Opiate LSD  LSD – synthesized in 1938 o Serotonin-like psychedelic drug. o Albert Hofmann synthesized a series of lysergic compounds, with no interesting findings. o LSD-25 o Later decided to deliberately ingest 0.25mg. o Recorded the first human experience with LSD in 1943.  Uses of LSD: 1953-1966 o LSD used as adjunct to psychotherapy.  Initial LSD research  Timothy Leary o Clinical Psychologist o Conducted Psilocybin and LSD experiments at Harvard University. o Asked to leave Harvard in 1963. o “Turn on, tune in, and drop out…”  Pharmacokinetics o Absorption rapid – oral route most common. o ½ life ~ 3 hours o Metabolized in liver o Only 1% reaches the brain.  Tolerance – Develops very rapidly. o Recover is also usually rapid (so weekly use of same dose is possible)  Cross tolerance – LSD with psilocybin, mescaline.  No obvious withdrawal.  Mechanisms of action: o Initially thought LSD worked by action on serotonin (5-HT) receptors. o 5-HT receptors ARE primary, but NOT only binding sites for LSD.  Some cases working as agonist and some as antagonist. 2  LSD Experience: o Typically last 6-9 hours. o Mostly visual/perceptual changes.  Colored lights, distorted images; synesthesia (see sounds, hear colors… Senses are blended). o Altered sense of time o Depersonalization (outside of themselves). o Dilated pupils, elevated temperature and blood pressure. o Restlessness, euphoria, and sensation that inner tenstion has been released.  Adverse Effects: o Panic reaction o Flashbacks.  Quite variable and unpredictable. o LSD psychosis  Rare and usually occur when the person is: o Unaware of taking the drug. o Mentally unstable before taking the drug.  Pharmacology of LSD: o Extremely potent of 0.03-0.1mg o No OD death reported in humans. Serotonin-like 3  LSD  Mushrooms (psilocybin)  Peyote  DMT  Ayahuasca  Nutmeg  Mescaline *Serotonin is a monoamine. Psilsoybin (mushrooms)  Mild and doesn’t last long.  “Magic mushrooms”.  Long history in religions and ceremonial use.  Isolated by Albert Huffman and then synthesized it.  4mg yield pleasant experience with relaxation and some bodily sensation.  Similar to LSD, but now as potent. Current research with psychedelics  Therapy for fear and anxiety. Peyote  Mescal buttons 4  Wed in spiritual ceremonies (Native-Americans church) Pharmokinetics  Readily absorbed if taken orally, but does not get into the brain easily. 1  2,000 as potent as LSD 1  - ~ 2 hours 2 Effects  Nausea and vomiting.  Tremors and lack of coordination.  After about an hour have LSD-like effects for several hours  Death results from seizures and respiration affects. DMT  Extremely potent.  Serotonin is a monoamine.  Typically solid in power form and smoked.  Structurally similar to serotonin.  Peak during effects very widely by route: o Smoking: 1-5 minutes o Injections: 10-15 minutes (might be more intense). o Orally or pill form: 2-3 hours. 5 5-Med-DMT (cousin)  Might be called “foxy”.  4 to 10 fold more potent than DMT.  Peak effects about 30-45 minutes after inhalation. Licking Toad  Squeeze road and secretes 5-med-DMT.  Both DMT and 5-med-DMT are only midley active if taken orally. o Must take in with a monoamine oxidase inhibitor (mao-I, hamaline). o Unlike LSD, both DMT and 5-med-DMT can be fatal if taken in combination and or in combination with MAD-Is o MAO-Monamine oxidase: Enzyme that breaks down monoamines monoamine oxidase destroyes excess monoamines in the terminal so have more serotonin available  too much  death from heart attack due to rise in blood pressure. Ayahuasca o Drink in South America that combines plants with DMT with plants with MAO-Is o Effects last 6-12 hours 3 phases of the experience 1. Vivid visual imagery. Dizziness and nausea with vomiting. 2. Contact with the spirit world 3. Fading of visions, a decrease in nausea, and exhaustion. Nutmeg 6  Myristin likely active in ingredient. o Can cause changes in visual perceptions, visual hallucinations, depersonalization, euphoria BUT…  Need a high dose (at least 1 tablespoon).  Side effects; vomiting, nausea, unconsciousness, tremors that last up to 12 hours. Mescaline  Found in San Pedro cactus.  5-HT receptor agonist.  Rapidly and completely absorbed when taken (orally).  Significant concentrations achieved in the brain within 1-2 hours.  Trips can last 10 hours.  Induces nausea and vomiting. Hallucinogens 2.Catechol hallucinogens  Catechols – dopamine and norepinephrine. 3.Other hallucinogens  Opiate, glutamate, etc. Salvia divinorum  Common effects 7 o Uncontrollable hysterical laughter. o Overlapping realities. The perception that one is in several locations at once. o Salvinorin A – active ingredient  Does not work on the same neurotransmitters as other hallucinogens. o Kappa Opioid Receptor Agonist. PCP and Ketamine  Both are anesthetic agents  Work on the glutamate system o NMDA antagonists o This also results in dopamine release. PCP  “Angel dust”  Power or pill form  Dissociation from the body.  Strong emotional response (positive or negative).  Cognitive disorganization. Ketamine  Less portent than PCP.  Short acting (lasts 30-60 minutes).  Marked dissociative state. o Lose all contact with body. o Sensation of lights coming through the body. o Complete loss of time. o Altered perception of “body consistency”. o Sudden insight into the mysteries of existence.  Compulsive daily use can develop.  Tolerance does develop.  Repeated use causes neuronal changes, including cell death.  Recent studies have found that a single iv dose of ketamine markedly improves depression. 8

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Chapter 4, Problem 4.46 is Solved
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Textbook: Fundamentals of Electric Circuits
Edition: 5
Author: Charles Alexander
ISBN: 9780073380575

The answer to “Using Fig. 4.113, design a problem to help other students better understand Norton equivalent circuits.” is broken down into a number of easy to follow steps, and 15 words. Fundamentals of Electric Circuits was written by and is associated to the ISBN: 9780073380575. This textbook survival guide was created for the textbook: Fundamentals of Electric Circuits, edition: 5. Since the solution to 4.46 from 4 chapter was answered, more than 248 students have viewed the full step-by-step answer. The full step-by-step solution to problem: 4.46 from chapter: 4 was answered by , our top Engineering and Tech solution expert on 11/10/17, 05:48PM. This full solution covers the following key subjects: better, Circuits, Design, equivalent, fig. This expansive textbook survival guide covers 18 chapters, and 1560 solutions.

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Using Fig. 4.113, design a problem to help other students