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substance abuse m2
midterm 2
| Term | Definition |
|---|---|
| Ethanol | -A psychoactive drug -Similar in most respects to other sedative-hypnotic compounds -Used primarily for recreational purposes rather than medical purposes |
| Pharmacology of Alcohol:pharmacokinetics /absorption1 how does it absorb? | Soluble in both water & fat -contains calories Diffuses easily across all biological membranes Rapidly & completely absorbed from entire gastrointestinal tract Presence of food in stomach slows the speed of absorption |
| Pharmacology of Alcohol:pharmacokinetics /absorption2 where in the body | 20% of a single dose absorbed directly from stomach & remaining 80% absorbed rapidly & completely from upper intestine |
| Distribution:of alcohol after absorption what happens | -After absorption, alcohol evenly distributed throughout all body fluids & tissues -Once it reaches the brain, it crosses blood-brain barrier almost immediately -Freely distributed across placenta & will easily enter the brain of fetus |
| Excretion:of alcohol | About 95% of alcohol ingested is enzymatically metabolized by enzyme alcohol dehydrogenase 5% is excreted mainly through lungs, sweat, & urine |
| Metabolism of alcohol where in the body is it metabolized | 85% of metabolism occurs in the liver Up to 15% of the metabolism is done by gastric alcohol dehydrogenase enzyme located in stomach lining |
| Excretion of alcohol (breakdown) | Alcohol----> Acetaldehyde--> acetic acid--> carbon dioxide & water |
| The average person metabolizes | 6 to 8 grams of 100% (200 proof) alcohol per hour |
| It would take an adult 1 hour to metabolize the amount of alcohol that is contained in... | 1.5 oz. shot of 80 proof hard liquor 5 oz. of wine 12 oz. bottle of beer = 1 drink! |
| Women have higher (metabolism) | blood ethanol concentrations than men |
| Women have a lower (metabolism) | level of gastric alcohol dehyrdogenase enzyme |
| Blood Alcohol Content Dependent on: | -Presence of food -Rate of consumption - Concentration of alcohol -Drinker’s body composition |
| Ethanol is a potent inhibitor of | the function of glutamate receptors |
| how does ethanol disrupt | It disrupts by depressing the responsiveness of NMDA receptors to release glutamate |
| Removal of ethanol’s inhibitory effects | results in withdrawal signs like seizures |
| GABA receptors: Behavioral results include | sedation, muscle relaxation, and inhibition of cognitive & motor skills |
| Increased levels of GABA have what effects on the brain | Increased levels of GABA have positive effects of reward center in brain |
| Serotonin:Chronic alcohol consumption results in? | augmentations in activity |
| Serotonin dysfunction may role in? | pathogenesis alcoholism |
| Effects of alcohol are | graded, reversible depression of CNS function |
| Effects of Alcohol Moderate Use: | Disinhibition, sedation, mood swings |
| Effects of Alcohol Heavy, Long-Term Use | Erratic behavior, blackouts |
| Acute Effects of Alcohol:1 | - Hypoglycemia Irritant & promotes flow of gastric juices Effects pituitary gland which tells kidneys to produce more than normal amounts of dilute urine (diuretic) Presence of alcohol interferes with metabolizing medication |
| Chronic Effects of Alcohol: Visible symptoms: | -Thin, bloated appearance -Hyperpigmented or jaundiced skin -Multiple bruises -Hoarse voice -Ankle swelling, hemorrhoids, loss of pubic hair -Testicles may shrink -Dilated capillaries & acne lesions -Enlarged bulbous nose |
| Chronic Effects of Alcohol: 2. Irritation, Bleeding, & Malabsorption: | -Alcohol irritates stomach lining -Irritates esophagus resulting in mild chest pain -Causes ulcers and stomach bleeding |
| Chronic Effects of Alcohol: 3. Liver Disease: | -Fatty liver -Alcoholic hepatitis (jaundice) -Cirrhosis of the liver (non reversible) |
| Chronic Effects of Alcohol: 5. Cardiovascular System: | -AHMD (alcoholic heart muscle disease) -Shortness of breath & dramatic enlargement of heart -Arrhythmias -Increase risk of stroke |
| mental expectations and setting become what due to alcohol | Mental expectations & setting become less important at increased doses due to sedative effects |
| is alcohol an aphrodisiac | Alcohol is NOT an aphrodisiac |
| Low doses:of alcohol | - Memory, concentration, & insight are dulled - Confident, social ability, & courage increased |
|  Blackouts caused by alcohol: | - Serve as a warning sign - Tend to occur after RAPID consumption of alcohol, or how fast BAC level rises ---Not ‘how much you drink’ but ‘how fast you drink’ -Can involve a person’s level of tolerance - Person cannot create/store NEW memories |
| Binge drinking defined: Other terms: High-risk drinking | Drinking that increases the risk of consequences legally, physically, personally and/or academically -For men: 5 or more drinks in one sitting -For women: 4 or more drinks in one sitting |
| how much more likely are binge drinkers to miss class | Compared to non-binge drinkers, frequent bingers are 17 times more likely miss a class as a result of their drinking |
| The extent of tolerance depends on | amount, pattern, & extent of alcohol ingestion |
| CNS adapts to | the continual presence of alcohol -- Need more alcoholto achieve same affect |
| Little or no tolerance: | Ingest intermittently |
| Marked tolerance: | Ingest large amounts |
| Tolerance Three types: 1. Metabolic Tolerance: | Liver increases its amount of drug-metabolizing enzyme |
| Tolerance Three types: 2. Tissue, or Function Tolerance: | -Neurons in brain adapt to amount of drug present -Display blood alcohol levels about twice those of non-tolerant people at similar level of intoxication |
| Tolerance Three types:3. Associative, Contingent, Homeostatic Tolerance: | Environmental manipulations can counter effects of ethanol |
| After physical dependence is established, | withdrawal symptoms can occur |
| Withdrawal Symptoms -Severity of symptoms widely depends on alcohol abuse | Hangover is a mini-withdrawal Tremors Seizures Rapid pulse Sweating Increased body temperature Depression Insomnia Vomiting Illusion/hallucinations |
| Addictive Process | Availability -Sedative -Tolerance -Physical dependence -Memory programming – - Depressive effect of alcohol on brain Advertisements- |
| Alcohol & Pregnancy Fetal Alcohol Syndrome (FAS) : | Developmental disorder that occurs in children of mothers who drank during pregnancy Mother does not need to be an alcoholic No safe level of alcohol intake during pregnancy |
| Alcohol & Pregnancy Fetal Alcohol Syndrome (FAS) : babies have: | Facial abnormalities Retarded growth Heart defects CNS dysfunction, low intelligence Behavioral abnormalities -Damage is irreversible |
| Uppers (stimulants) include: | 1. very strong stimulants: cocaine & amphetamines 2. moderate: diet pills & Ritalin 3. milder plant stimulants: ephedra & khat 4. legal mild stimulants: caffeine |
| uppers: stimulants 1 name and example | Cocaine (hydrochloride, crack, freebase) Amphetamines (speed, meth, ice) Amphetaminecongeners(Ritalin ,dietpills, e.g., fen-phen) |
| uppers: stimulants2 name and example | Plant stimulants (khat, betel nut, yohimbe) Caffeine (coffee, tea, soft drinks, OTC meds) Nicotine (cigarettes, cigars, smokeless tobacco) |
| Behavioral Stimulants example/neurotransmitter | -Cocaine and the amphetamines are powerful psycho-stimulants that affect mental functioning and behavior. -To exert their acute behavioral stimulant effects these drugs act to augment the action of several neurotransmitters, most important :dopamine |
| Cocaine and the amphetamines, in addition to other actions, | increase dopaminergic activity on the nucleus accumbens, other limbic structures, and the limbic cortex associated with behavioral reinforcement, compulsive abuse, drug dependency, and cue-induced drug craving. |
| Cocaine and the amphetamines are therefore widely recognized | as important drugs of compulsive abuse. These drugs also have a variety of therapeutic uses, although today, reasonable alternatives are available for most of them. |
| All psycho-stimulants have significant | side effects, toxicities, and patterns of abuse. |
| In low doses, cocaine and other psycho- stimulants evoke | an alerting, arousing, or behavior-acting response that is not unlike a normal reaction to an emergency or stress. |
| what isthe most commonlyconsumed psychoactive drug in the world | caffeine |
| In the U.S caffeine consumed daily by up to | 80% of the adult population. |
| Caffeine is found in significant concentrations in: | coffee, tea, cola drunks, chocolate candies, fortified waters, and cocoa. |
| Caffeine is one of the most widely used stimulants in | sports, with documented efficacy and safety. |
| The average cup of coffee contains about | 100 milligrams of caffeine |
| a 12-ounce bottle of cola contains about | 40 milligrams of caffeine |
| The caffeine content of chocolate may be as high | 25 milligrams per ounce |
| Toxic Effects of Stimulant Drugs • Psychological & Behavioral | 1. Mood elevation 2. Enhanced alertness & increased attention 3. Sleep disturbances 4. Analeptic effects(increased psychomotor stimulation) 5. Anxiety & paranoid schizophrenic 6. Diminished appetite 7. Drug withdrawal: depression 8. Dependency synd |
| Toxic Effects of Stimulants • Physiological Effects 1.----• Cardiovascular | -cardiac arrhythmia -increased systolic & diastolic blood pressure -circulatory collapse -cerebral hemorrhage -hypertension -tachycardia |
| Toxic Effects of Stimulants • Physiological Effects 2.----• Central nervous system | – Seizures – Intracranial hemorrhage – Movement disorders |
| Toxic Effects of Stimulants • Physiological Effects 3. Pulmonary Effects | – Bronchodilation – Increased oxygen consumption |
| Toxic Effects of Stimulants • Physiological Effects 4, Renal Effects | – Increased urinary retention |
| Toxic Effects of Stimulants • Physiological Effects 5.metabolic effects | – Hyperglycemia – Increased metabolic rate (large drug doses)\ – Elevated lipolysis |
| • Physiological Effects (eyes) | • Mydriasis (pupillary dilation) • Altered Thermoregulatory Capacity  |
| • Physiological Effects – Maternal, Fetal, & Neonatal complications | • Maternal – Spontaneous abortion – Still birth • Fetal – Growth retardation – Cerebral infarction or hemorrhage – Premature birth • Neonatal – Drug withdrawal,seizures – Cardiovascular system complications |
| History Of Cocaine 1906 | Pure Food & Drug Act limited cocaine for medical use only |
| History Of Cocaine 1914 | Harrison Narcotic Act labeled cocaine as a narcotic |
| History Of Cocaine 1970 | Controlled Substance Act made cocaine use or possession a federal crime  |
| Most street cocaine is adulterated which complicates the pharmacology • Common Adulterants: | -Methamphetamine -Mannitol -Lactose -Lidocaine -Procaine  |
| Effects of Cocaine Depend on: | 1. Dosage 2. Form in which drug is taken 3. Route of administration 4. Frequency of administration 5. User expectations 6. Setting 7. History & personality of user  |
| Pharmacologic Actions:blockage of: | initiation or conduction of nerve impulses (local anesthetic) |
| CNS stimulation caused by dose & route of administration | -Euphoria & feeling of well being -Motor coordination decreases with increased dose -Fatigue is masked by central stimulation -Weight loss -Higher doses cause depression/reparatory failure -Chronic administration cause paranoia -Dental hygiene decr |
| Pharmacologic Effects cardiovascular effects | • Cardiovascular effects: •-- Small doses may slow heart rate •-- Moderate doses increase heart rate • --Increased blood pressure •-- Muscle fatigue is a direct toxic effect on heart -- Conduction disturbances |
| Pharmacologic Effects other effects | • Increased body temperature • Dilated pupils • Increases glucose availability |
| Mechanism of Action of Cocaine | • Action of nerve impulse& conduction • Blockade of neurotransmitter reuptake of dopamine, serotonin norepinephrine, & epinephrine •-- Similar to amphetamine •-- Increase epinephrine, increases physical energy |
| Dosage Forms 1. Cocaine Hydrochloride | • Water-soluble salt form for intranasal & intravenous use |
| Dosage Forms 2. Cocaine Base Crystals | • Water-insoluble “crack” a ready to smoke base form of cocaine which vaporizes when heated at high temperature. Can be used intravenously. |
| Dosage Forms 3. Cocaine Alkaloid Paste | • Water-insoluble “freebase” can also be smoked like “crack” |
| Routes of Administration • MucousMembrane | –-ORAL • Duration of high is 45-90 min and slowly diminishes --INTRANASAL SNORT • Rapid absorption & peek euphoria in 15-30 min • Perforation of nasal septum with chronic use • Continual snorting limits absorption due to vasoconstriction of blood ves |
| Routes of Administration • Intravenous | • Initial onset of action – 30-45sec • Duration of high – 10-20min • Initial euphoria followed by “crash” of extreme dysphoria & intense craving 40 - 60 min after injection • Can lead to hepatitis, AIDS, endocarditis, addiction, & risk of overdose |
| Routes of Administration • Smoking | • Euphoria more intense • Initial onset of action – 8–10sec • Duration of high – 5–10min • Followed by a “crash” similar to intravenous injection • Leads to chronic addiction • Can cause pulmonary disease |
| Detoxification & Metabolism | • Rapidly distributes to brain • Metabolized in liver |
| Half-life OF COCAINE in plasma | only 30 – 90 min |
| Half-life of cocaine with alcohol | 150 min |
| Toxicology 1.Overdose can occur 2.Average lethal dose is | 1.by any route of administration. 2. 500mg, but is variable. |
| Symptoms:of cocaine | – Excitement – Panic, Paranoia – Restlessness – Chills – Fever – Nausea – Vomiting – Irregular heart rhythms – Respiration&mentalconfusion |
| • Treatment: for cocaine | – No antidote for cocaine – Sedatives (Valium) can be used to decrease CNS stimulation |
| Monitoring Use : urine Snorting & Intravenous | Positive urine for 2-4 days |
| Monitoring Use : urine Smoking | • Positive urine for 8-12 days |
| Chronic Cocaine Use & Withdrawal | • Dopamine depletion • Rapid heart beat • Hypertension • Paranoia • Sleep deprivation • Withdrawal almost never fatal • Not physically dependent |
| cocaine • Withdrawal Symptoms | • Decreased energy • Excessive sleeping • Irritable mood • Depression • Psychomotor retardation • Nausea/vomiting |
| what is the primary active ingredient in tobacco. | nicotine |
| Nicotine | One of 4000 active compounds in tobacco Is an extremely toxic, clear, & oily liquid Accounts for only acute pharmacological effects of smoking |
| Pharmacokinetics Routes of Administration: nicotine | Oral route (snuff, chewing tobacco) Inhalation (cigars, cigarettes) --Chemical by products of smoking |
| Nicotine is readily absorbed from every site on / in our body: including | Lungs Buccal Nasal Skin Gastrointestinal tract |
| how is nicotine absorbed | Quickly absorbed throughout body & body fluids and penetrates all barriers |
| Smoking is highly regulated behavior | Goal is to maintain steady-state brain levels of highly addictive psychoactive agent Smokers “self-regulate” level of nicotine in system Smoker regulates: Frequency of breaths Depth of breath Time the smoke is held in lungs #of cigs |
| half life of cig/nicotine | 2 hours |
| Mechanism of Action: Nicotine | -stimulates hypothalamus to increase dopamine levels Dopamine accounts for the behavioral reinforcement, stimulant, antidepressant, and addictive properties of the drug -Evidence shows nicotine as a powerful drug of addiction like heroine alc coke |
| only pharmacologically aactive drug in tobacco is: | nictoine |
| Outside CNS, nicotine increases | Respiration rate Heart rate Blood pressure Coronary blood flow |
| in CNS, nicotine increases | Cognitive functioning Increase psychomotor activity Sensorimotor performance Attention & memory consolidation |
| Pharmacological Effects of nicotine | Reduces activity of afferent nerve fibers coming from muscles Reduction in muscle tone Involved in relaxation experience of smoking Antidepressant effects Reduces appetite Reduces weight gain |
| Low doses of nicotine: | Relaxation Increases vigilance Rapid information processing |
| High doses of nicotine: | Nervousness Tremors Seizures Increase panic attacks |
| Psychological Effects of nicotine | Increased concentration Decrease in perceived level of tension Ability to cope with over stimulating environment Pleasure, relaxation Quick bursts of energy when tired Enjoyable tactile sensations |
| Toxicity cigarettes | Tar: in tobacco mainly responsible for diseases associated with long-term tobacco use Person’s life is shortened 14 minutes for every cigarette smoked |
| Leading causes of death from smoking: | Heart disease Cancer Cerebrovascular disease Lung disease |
| how does smoking effect the lungs | Pack-a-day smoker pours 1 full cup of tar into his lungs a year Tar thickens cells in mucous membranes in throat & destroys delicate air sacs (alveoli) Smoking paralyzes lungs’ natural cleansing process Increases risk of emphysema |
| how does smoking effect cardiovascular | Pulse quickens Heart beats extra 10-25 times per minute which strains the heart Blood vessels constrict & blood pressure increases by 10-15% Stress on the heart increases risk of heart attack & stroke |
| Health Effects of Smoking Skin: | Decrease in blood flow causes wrinkles Takes longer to heal wounds |
| Health Effects of Smoking blood | Carbon monoxide decreases oxygen levels |
| Health Effects of Smoking teeth | Become yellow from smoke and tar |
| Health Effects of Smoking fertility | Men- erection problems, decreased sperm count, altered shape of sperm Women- 43% decrease in fertility |
| health effects of smoking lung and mouth irritation | shortness of breath |
| smokeless tobacco health effects moth | sores |
| smokeless tobacco health effectsBlood vessel constriction | grayish complexion |
| Tolerance & Dependence / nicotine and tobacco | Nicotine induces physiological & psychological dependence Cessation of smoking causes cravings & relapse Nicotine causes physical addictio |
| Getting Help Pharmacotherapies: nicotine/tobacco | harmacotherapies: Nicotine gum Nicotine inhaler Nicotine nasal spray Nicotine patch |
| Benefits from Quitting Within 36 hours | blood carbon monoxide levels return to normal |
| Nicotine-Cardiovascular Disease | carbon monoxide in smoke decreases amount of oxygen delivered to heart muscle,nicotine increases the amount of work heart does increasing heartrate/bloodpressure carbon monoxide and nicotine increaseincidence of atherosclerosis, narrowing and thrombosis |
| Nicotine-Cardiovascular Disease cigarette smoke | Cigarette smoke has been firmly established as an independent risk factor for atherosclerosis and other vascular diseases. Data suggests nicotine releases VEGF through nicotinic Acetylcholine Receptors. VEGF may contribute to risk of cardiovascular diseas |
| Nicotine-Cardiovascular Disease | The carbon monoxide in smoke decreases the amount of oxygen delivered to the heart muscle, while nicotine increases the amount of work the heart must do by increasing the heart rate and blood pressure. |
| Nicotine-Cardiovascular Disease Both carbon monoxide and nicotine increase the incidence of | atherosclerosis, narrowing and thrombosis clotting in the coronary arteries. Theses three actions and others as well seem to underlie the dramatic increase in the risk of heath from coronary heart disease in smokers compared to nonsmokers. |
| Cigarette smoke has been firmly established as | an independent risk factor for atherosclerosis and other vascular diseases. Data suggest that nicotine releases VEGF through nicotinic Acetylcholine Receptors. VEGF may contribute to the risk of cardiovascular diseases in cigarette smokers. |
| Cigarette Smoking & Risk of Stroke | Cigarette smoking: a major cause of stroke by: - increasing clotting factors in the blood - decreasing HDL cholesterol levels - increasing triglyceride levels damaging lining of blood vessels. risk for stroke increases as # of cigs smoked increases |
| Effects of Secondhand Smoke | secondhand smoke also negatively affects cardiovascular health by: - decreasing exercise endurance - damaging blood vessel walls - increasing the tendency of blood platelets to clot |
| Statistics Cigarette smokers | a 50% increase in the progression of atherosclerosis when compared with people who have never smoked. Contrary to public perception, smoking-caused heart disease actually results in more deaths per year than smoking-caused lung cancer. |
| cigarette smokers/heart disease stats | 30% of all heart disease deaths are caused by cigarette smoking. Smoking is the single largest preventable cause of heart disease in the United States. |
| Study Drugs Today psychostimulants | CNS stimulant drugs having anti- depressant or mood elevating properties. Including: n Adderall n n n n n Ritalin Concerta |
| adderall Ritalin Concerta These medications are prescribed to treat | depression, obesity, narcolepsy, and ADHD |
| study drugs are classified as: | Schedule II due to their high potential for addiction. |
| Psychostimulants Today | In a high pressure college environment where a GP A can determine one’s fate, study drugs are often used. n Certain drugs can allow users to remain focused and awake for hours, giving students what they perceive to be superhuman mental strength |
| Paradox: Stimulants pacify hyperactivity? | “Hyperactivity may develop when the relationships between dopamine and serotonin is imbalanced Elevating serotonin restores the delicate balance between dopamine and serotonin and supposedly pacifies hyperactivity” stimulating underperming areas of brain |
| Adderall | Methamphetamine back bone with extra methly(CH3) group attached to the amine(NH2). |
| Extra methyl(CH3) group on the amine(NH3) | -This extra group gives molecules better fat solubility and therefore quicker entry to the brain -This makes the “high” far more intense -The faster the rate of uptake, the greater potential for addiction |
| Adderall and Cocaine n immediate effects include: | -increased energy, feelings of well-being , superiority, increased concentration, alertness, verbose, mood elevation, increase heart rate, breath/min, and blood pressure, dilated pupils, dry mouth, perspiration. |
| adderall and cocaine | -have ability to block dopamine transporters the reuptake of catecholamine noradrenalin and dopamine are blocked leaving them in the synapse in increased concentration |
| How it Works n The ADHD brain supposedly works | by blocking the reuptake of dopamine and norepinephrine into the presynaptic neuron and increasing their release from the presynaptic neuron into the extr neronal space |
| The increased flow of dopamine and norepinephrine into the extra neuronal space causes the patients' brain to | experience a more intense level of concentration, causing an increased ability to focus for extended periods of time, and a heightened interest in performing focus based tasks. |
| ADHD medications are designed to have different effects than what? | -methamphetamines and cocaine, because of their time released nature and low doses they are prescribed in n However, when crushed, snorted, or taken in high doses the pills may produce a high that parallels meth/amphet or cocaine. |
| How The Body is affected | increased flow dopamine/norepinephrine into extra neuronal space causes patients brain toexperience a more intense level of concentration, causing ability to focus for extended periods of time, and a heightened interest in performing focus based tasks. |
| Adderall works by blocking the | euptake of dopamine and norepinephrine into the presynaptic neuron and increasing their release from the presynaptic neuron into the extra neuronal space. |
| what does adderall cause the body to do? symptoms | Increased alertness, motivation, confidence, loquaciousness, reduced appetite, dilated pupils |
| n For the “ADHD brain” dopamine is believed  | deficient  |
| People with ADHD are believed to have a deficiency in | dopamine causing them to be hyperactive and to look for stimulation in the environment. |
| n Adderall is thought to provide those with ADHD | the dopamine level needed for normal functioning. |
| has adhd been scientifically proven? | no |
| Psychopharmacology | “...field of medicine that addresses the use of medications to help correct or control mental illnesses and drug addiction” |
| Psychoactive drugs: | Focus on opiates and common combinations |
| what is the the 2nd most often illicitly abused drug in the U.S. | opioids |
| history what happened in 1914 | concern began to grow § Harrison Narcotic Act passed, restricting opioids to only medical use |
| What are Opiates? Opium | The exuded substance from the poppy Papaver Somniferum |
| What are Opiates? opiates | Natural opium extracts and semi- synthetic opium preparations |
| What are Opiates? opiods | Synthetic opium-like compounds |
| Common Opiates Used in College | § Morphine § Codeine § Oxycodone § Use to make Percodan® and Oxycontin® § Hydrocodone § Used to make Vicodin® § Hydrocodone most widely prescribed opioid § Heroin |
| Effects of Opiates •Desired Effects v.s. Side Effects | § Pain relief § Suppresses coughs § Controls diarrhea (constipation) § Euphoria § Slurred speech § Depressed respiration & heart rate § Miosis |
| Effects of Opiates Toxic Effects | § Addiction § Overdose § Drug contamination & adulterants > infection § Abscesses § STDs § Fetal effects |
| How it works: Neurotransmission neuron | smallest functional unit of the nervous system |
| How it works: Neurotransmission cell body | contains the nucleus; processes information that is received by the dendrites |
| How it works: Neurotransmission axon | -extension of the cell body that conducts an action potential |
| How it works: Neurotransmission synapse | small space between axon terminal of one neuron & dendrite of another neuron or postsynaptic target |
| Biological Basis of Pain pain signals damage | Neurotransmitter called substance P carries pain message |
| Biological Basis of Pain Natural opioids help protect the body: Endorphins are? | Endorphins:enkephalins, dynorphins, beta endorphins |
| biological basis of pain: Exogenous opioids work by reacting with the same receptor sites which are? | Mu,kappa,delta, nociceptin |
| Opioids also effect emotional pain in what way? | § Decrease anxiety § Sense of detachment § Deadening of unwanted emotions |
| Opioid users take the drug for some of these effects: | Reward/control pathway activated telling body to repeat these actions during stressful periods ----- Can lead users to become opioid abusers/addicts |
| what are Opioid Effects on Pleasure | Reward/control pathway tells body to repeat actions that are good for survival Cells in brain monitor action and when need filled, send signal to stop Exogenous opioids mimic endorphins tell body to reuse drugs |
| opioid effects on pleasure Natural opioids effect what pathway? example? | Reward/control pathway tells body to repeat actions that are good for survival endorphins |
| opioid effects on pleasure strong opiates like heroin do what? | disrupt stop switch They overload the stop switch causing it to malfunction “Drug abusers use past the point of pain relief...” (Inaba) |
| Routes of Administration | Smoking: 7-10 seconds to reach the brain Injection:15-30 seconds Snorting:5-8 minutes Oral:20-30 minutes |
| factors affecting distribution | Properties of drug, Body weight/size,Age, Gender, Genotype (diabetes example), Health condition, Nutritional status -Pharmacological state - Environmental setting -Psychological disposition: Personality, Expectation about drug effects |
| Students commonly combine opiates with what? | alcohol or anti-anxiety meds |
| opiates, alcohol and anti-anxiety meds are all considered depressants. side effects? | Control pain, reduce anxiety, promote sleep, lower inhibition, induce euphoria,depress circulatory, respiratory, and muscular systems --Additive effects --synergism |
| Prescription painkillers (opiates) are often mixed with what? | alcohol |
| Opiates and Alcohol Both substances depress the respiratory system increasing the risk of: | Cyanosis, cell death, and coma -- Also, one could simply stop breathing |
| Some slow-release opioids can be dissolved by alcohol, what does this do? | releases a day’s worth of opioid in a matter of minutes |
| Today the most widely used sedative- hypnotics in the U.S.is? | Benzodiazepines --- However, now they are usually only prescribed for short-term and for specific conditions--Can be very addictive, dangerous withdrawal symptoms --Anxiety also treated with serotonin-type antidepressants and mood stabilizers |
| What are Benzodiazepines? used in medicine for? | - Manage anxiety - Treat sleep problems - Control muscular spasms and seizures § Subdue symptoms of alcohol withdrawal |
| What are Benzodiazepines? used recreationally for: | - Anxiety relief - Induce mild euphoria -Lower inhibitions |
| Common benzodiazepines: | xanax,valium,rohpnol |
| xanax:what does it do? | relieve symptoms of generalized anxiety disorder, panic disorder, and depression resulting from anxiety |
| valium: what does it do? | Treat anxiety, gain relief from musculoskeletal spasms, control seizures such as those that occur during severe alcohol or barbiturate withdrawal |
| rohypnol: what does it do? | Produces anxiety relief, sedation, and amnesia, especially when taken with alcohol |
| Benzodiazepines and Brain Areas: The anxiolytic effects result from the actions at | limbic centers |
| Benzodiazepines and Brain Areas: Actions at other regions result in side effects such as | sedation, cognitive impairment, muscle relaxation, and increased seizure threshold |
| Benzodiazepines and Brain Areas: The amygdala, orbitofrontal cortex, and insula are associated with | the production of behavioral responses to fearful stimuli and the central mediation of anxiety and panic ---Inhibition due to GABA reduces stimulation of these areas leading to decreased anxiety |
| Mechanism of Action:GABA | A GABA receptor agonist -Does not directly stimulate GABA receptor |
| MECHANISM OF ACTION: GABA, since it does not directly stimulate the GABA receptor what does it do? | -Binds to an adjacent site and increases the affinity of GABA for receptor - This increases the inhibitory synaptic action of GABA, facilitating the influx of chloride ions, causing hyperpolarization of the postsynaptic neuron, depressing its excitabilit |
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