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88 Cards in this Set
- Front
- Back
What is the definition of Dependence?
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A progressive pharmacological/physiological adaptation to a drug resulting in tolerance
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What is the definition of Tolerance?
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The same dose of drug producing a smaller effect each subsequent time it is taken
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How do you know if someone is dependent?
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Manifests by the appearance of withdrawal symptoms
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What is the definition of Addiction?
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A behavioural pattern characterized by compulsive use and obsession with obtaining the drug and its use, as well as a high relapse rate after withdrawal, despite the physical, emotional and societal damage the drug causes to the individual
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Does it mean that a patient taking opioids for pain is addicted if they show tolerance or dependence?
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No!
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What influences the risk for Addiction?
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Biology, Social Environment, Age and Stage of Development
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What are the neural pathways that mediate positive reinforcement of drugs of abuse?
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The mesolimbic dopamine system is the prime CNS target of addictive drugs.
DA neurons in the VTA discharge and release DA onto the nucleus accumbens and the prefrontal cortex |
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What are the three distinct classes of molecular targets that addictive drugs engage in the Ventral Tegmental Area?
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1) G-protein Coupled Receptors (GPCRs)
2) Ionotropic receptors and Ion channels 3) DA Transporter |
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How do drugs activate the GPCRs of the Ventral Tegmental Area?
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Addictive drugs cause postsynaptic hyperpolarization (inhibition) and presynaptic regulation (suppression) of transmitter release
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How do drugs activate the Ionotropic and Ion channels of the Vegmental Trigemntal Area?
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Addictive drugs enhance the release of DA from DA neurons
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How do drugs activate the Transporter of the Ventral Tegmental Area and Nucleus Accumbens?
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Addictive drugs block the reuptake or stimulate non-vesicular release of DA causing an accumulation of extracellular dopamine in target structures
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Which drugs activate the GPCRs of the Ventral Tegmental Area?
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Opioids, THCs, GHB
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Which drugs activate the Ionic Channels of the Ventral Tegmental Area?
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Benzodiazepines, Nicotine, Ehtanol
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Which drugs activate the Transporters of Ventral Tegmental Area and Nucleus Accumbens?
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Cocaine, Amphetamines, Ecstasy
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Which of the commonly abused Opioids is more common in health care professionals?
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Meperidine
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What is the MOA of Opioids for Abuse?
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Mu receptors in the VTA are selectively expressed on GABA neurons
(which they inhibit leading to disinhibiton and increased release of DA) |
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Why do K-opiods agonists cause Euphoria while K agonists cause dysphoria?
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Mu opioid receptors inhibit GABA neurons and so increase release of DA.
K opioid receptors inhibit DA neurons. |
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What is the definition of Detoxification?
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Refers to the treatment of acute withdrawal symptoms
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What are the options of Detoxification?
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1) Switch to long acting opioid (methadone) and wean off slowly
2) Clonidne to relieve physical symptoms (DOES NOT RELIEVE CRAVINGS) |
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What is the recommended Opioid addiction Treatment?
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i) Switch to Methadone or other long acting opioid and wean off
ii) Clonidine, relieves some physical symptoms but not helpful for cravings iii) If patient is not treated after detoxification there is high chance of relapse |
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How long can withdrawal symptoms of opiod addiction last?
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Can persist for up to 6 months
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What are the withdrawal symptoms of opioid addiction?
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Anxiety, Insomnia, Cravings, Cyclic Changes in weight, pupil size, respiratory center sensitivity
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What are the benefits of Buprenorphine for Opioid Addiction Treatment?
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A partial agonist at mu receptors;
1) Low abuse potential 2) Low risk with overdose 3) Minimal withdrawal upon discontinuation 4) Can block heroin effects |
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What is the relative risk of addiction with Opioids?
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4 out of 5
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What are the signs of Acute Opioid Toxicity?
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Coma, Miosis, Depressed Respiration
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What are the treatment options for Opioid Toxicity?
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1) Naloxone is an opioid antagonist which reverses morphine/heroin effects within minutes
2) Long acting opioids (Methadone, Buprenorphine) usually administered in supervised setting |
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How is Marijuana prepared?
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Prepared from the dried flowering tops and leaves.
Hashish (2-20%) from the dried cannabis and compressed flowers extracted for its resin Hashish oil (15-80%) |
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Which of the cannabinoids in Marijuana is a powerful psychoactive substance?
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Δ9-Tetra Hydrocannabinol (THC)
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How much THC is in local BC Marijuana?
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10-20%
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What is the CNS MOA of Marijuana?
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1)Endogenous cannabinoids bind to CB1 receptors in CNS
2) THC binds to CB receptors in the brain which causes disinhibtion of DA neurons 3) Mainly presynaptic inhibition of GABA neurons in the VTA which releases DA in reward/pleasure centers |
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How is Marijuana usually administered?
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Usually smoked and ~3 times more potent by this route compared to the oral route
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How do the onsets of actions of Marijuana compare ?
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1) Onset with smoking in seconds/minutes CNS effect duration lasts 2-3 hours
2) Onset with oral administration is within 30min-2hrs , CNS effects last 5-12hrs |
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What are the dose related CNS effects of Marijuana?
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i) 2mg smoked/5mg Oral: Euphoria well being, relaxation, disinhibtion, fragmented thinking, exaggerated laughter altered time passage perception
ii) >7mg smoked: Marked alteration of time sense akin to LSD sensory changes: lights visual, auditory clarity iii) >15mg smoked: Psychotic like symptoms, fragmented thinking, impaired memory paranoia, depersonalization, hallucinations, marked sedation |
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What are the other pharmacological effects of Marijuana?
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1) Tachycardia (dose related)
2) Conjunctival Inflammation (red eyes) 3) Minimal drop in body temperature 4) Minimal decrease in blood pressure 5) Dy mouth and Throat; Irritation in chronic users 6) Increased appetite, anti-emetic actions, decreased IOP and relief of Chronic Pain |
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What are the symptoms of Marijuana withdrawal syndrome?
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Restlessness, Irritability, Mild Agitation, Insomnia, Nausea and cramping
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What is the relative risk of addiction with Marijuana?
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2 out of 5
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What are long term consequences of Marijuana use?
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1) Brionchiole/Lung tissues
2) Tolerance/Dependence 3) Mild Withdrawal 4) Apathy, loss of desire to work, decreased productivity, energy, tiredness 5) Impaired memory cognition, relationships 6) Immune system may be compromised, hormone changes |
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What preparations of Marijuana are available?
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i) Dronabinol; Cannabinoid Agonist, Antiemetic, Appetite Stimulant
ii) Nabilone: Older Δ9-THC analog-Antiemetic |
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What are the adverse effects of Marijuana?
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Drowsiness, Orthostatic Hypotension, Dry Mouth, Dizziness, Disorientation
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What are the uses of Marijuana?
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i) Analgesic
ii) Glaucoma (Decreased IOP) iii) Ant-convulsant iv) Hypertension v) Sedative |
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What are the Hallucinogens?
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Lysergic Acid Diethylamide (LSD), Mescaline, Peyote alters one's state of consciousness
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What are the central effects of Hallucinogens?
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1) Altered Perception
2) After images are prolonged 3) Visual illusions perhaps progressing to Hallucinations 4) Subjective Responses: Increased color perception 5) Non logical thought Sequences 6) Synesthesia 7) Loss of Boundaries 8) Disorientation 9) Feeling of being outside oneself 10) Effect comes in and out 11) Initial feelings of Anxiety and Apprehension |
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What are the factors of a good trip with Hallucinogens?
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Good set, Setting, Good Quality Drug, Guide or Guardian nearby
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What are the factors of a bad trip with Hallucinogens?
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Bad set, Fear, Anxiety, Impure drugs, Anxiety --> Psychosis (most are acute panic reactions)
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What is the relative risk of addiction with Hallucinogens?
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Hallucinogens do NOT lead to addiction/physical dependence
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What are the effects of Hallucinogens outside the CNS?
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1) Pupillary dilation 2) Tachycardia 3) Facilitation of monosynaptic reflexes 4) Increased body temperature, pulse rate, respiratory rate and systolic BP
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What is the MOA of Hallucinogens?
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Interacts with 5HT2 receptors as an agonist currently though to activate Thalamic 5HT2 receptors causing disruption of Thalamic gating with sensory overloads of the cortex.
LSD mimics 5HT at 5HT1A autoreceptors on raphe cell bodies, producing a marked slowing of the firing rate of serotonergic neurons |
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What are the characteristics of Tolerance for Hallucinogens?
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i) Develops rapidly
ii) Dissipates rapidly iii) Cross tolerance with Mescaline and Psylocybin iv) No cross tolerance with Cannabis or Amphetamine |
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What are the Toxicity signs of Hallucinogens?
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1) Most are psychological problems and dose related.
2) Flashbacks (Hallucinogen, Persisting, Perception Disorder) 3) Chromosomal Breakage 4) Teratogenic/Miscarriages 5) Epileptic Foci Activation 6) Problems while under the influence |
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What are the prescription uses of LSD in Canada?
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There are currently no approved uses of LSD for any of these scenarios
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What are the preparations of LSD-like drugs?
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i) Mescaline (Peyote) 200-500mg; Nausea,
Vomitting more prominent i i) Psilocybin or Psilocin 10-50mg: From Magic Mushroom |
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"Alcohol is likely to contribute to more morbidity, mortality and public health costs than all of the illicit drugs combined" True or False?
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TRUE
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What is the definition of Alcoholism?
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The compulsive and uncontrolled consumption of alcoholic beverages, usually to the detriment of the drinkers health, personal relationships and social standing
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What are the Environmental factors that may increase risk of Alcoholism?
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i) Economic, Social Factors
ii) Employment, Educational Factors iii) Legal drinking age iv) Cost of Alcohol v) Alternative activities for Pleasure |
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What are the Genetic factors that may increase risk of Alcoholism?
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i) Tolerance
ii) Personality iii) Predisposition does NOT mean predestination |
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What are the Premorbid condition factors that may increase risk of Alcoholism?
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i) Maleness
ii) Societal iii) Related to an Alcoholic iv) Anti-social people; lack control of environment v) Unhappy Childhood |
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What are the treatment options for Alcoholics?
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We cannot treat alcoholics, Alcoholics recover because they want to treat themselves
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What is the CNS MOA of Alcohol?
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1) A principal CNS depressant agent
2) Enhances pre & postsynaptic GABA-A inhibition 3) Depresses excitatory transmission (blocks NMDA receptor mediated excitation) 4) Increases the release of DA in the reward center of the brain 5) Releases β endorphins, activation of μ receptors 6) Increases 5HT synaptic levels 7) Increased CB1 activity--> Changes in DA, GABA, Glutamate activity 8) Alcohol increases ACh in VTA with a subsequent increase in the DA in the nucleus accumbens |
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What are the CNS behavioural effects of Alcohol?
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1) Affects discrimination, memory, concentration, insight, coordination proportionally to blood concentration
2) Increases confidence, decreases ability , increases risk taking behaviour 3) Emotional Swings (happy but also belligerent aggressive) 4) Heavy Drinkers (blackouts, memory deficits) >14 drinks/week |
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Does the behavioural effects of alcohol correlate with Blood Alcohol Concentrations?
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Yes
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What level of BAC is the BC driving impairment level?
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0.05 g/dL
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What are the characteristics of a BAC of 0.05 g/dL?
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i) Approximate threshold for impairment of motor coordination ii) Relaxation iii) Lowering of Inhibitions
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What are the characteristics of a BAC of 0.05-0.15 g/dL?
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i) A progressive increase in the impairment of motor function (staggering) ii) Slowing of visual accommodation iii) Slurring of Speech iv) Deficits in performance, particularly in focusing attention v) Confusion
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What are the characteristics of a BAC of 0.15-0.30 g/dL?
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i) Marked Staggering ii) Irrational Behaviour iii) Blackouts iv) Amnesia
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What are the characteristics of a BAC of 0.3-0.5 g/dL?
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i) Anesthesia ii) Respiratory Depression iii) Cardiovascular Depression
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What are the characteristics of a BAC of 0.5-0.7 g/dL?
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Death
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What are the steps of Alcohol metabolism?
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Alcohol --(Alcohol Dehydrogenase)--> Acetaldehyde --(Aldehyde Dehydrogenase)--> CO2 +H20
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How is Alcohol dehydrogenase elimination essentially linear(zero order)?
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Alcohol Dehydrogenase is saturated at low concentrations and therefore the elimination of alcohol is essentially linear
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What are the effects of Alcohol on the Cardiovascular System?
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1) Vasodilation of skin, redness, heat loss
2) Hypertension possible when drinking, Hypotension afterwards 3) Chronic Capillary Enlargement "Whiskey Nose" 4) 1-2 drinks/day decreases occurrence of myocardial infarction |
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"1-2 drinks/day decrease the occurrence of MI" True or False?
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TRUE
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What are the effects of Alcohol on the GIT?
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1) Irritating, Increases Acid, Pepsin can lead to Aspiration, Vomitting
2) Diarrhea/Constipation 3) Interacts with NSAIDs |
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What are the effects of Alcohol on the Liver?
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1) Interacts with Acetaminophen
2) Increases mobilization of Fat, Accumulates in Liver (fatty liver) 3) Can go on Hepatitis Cirrhosis |
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What are the effects of Alcohol on the Kidney?
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1) Diuretic Action
2) Blocks ADH release 3) Lose more fluid than one takes in leading to Dehydration |
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What are the effects of Alcohol on the Brain?
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1) Directly toxic to Brain (worsened by Thiamine deficiency
2) Wernicke's Disease 3) Korsakoff's Psychosis |
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What is Wernicke's Disease?
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Damage to the Thalamus, Mammary Bodies resulting in Psychosis
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What is Korsakoff's Psyhosis?
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Impaired memory, loss of contact with reality
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What is the effect of Alcohol on Sex/Hormones?
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1) Decreased Inhibitions, Promotes Desires, Decreases performance 2) Causes Testicular Damage, Decreases Testosterone 3) Gynecomastia (Decreased Testosterone, Decreased LH, ICSH, Increased Prolactin)
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What is the life expectancy of Alcoholics?
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Decreased Life Expectancy of 15 years
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Why is the life expectancy of Alcoholics shorter than the general population?
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1) Heart Disease 2) Cancers (esophagus, mouth, lungs , stomach) 3) Suicide 4) Anemia (Folic Acid Deficiency) |
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What are the issues with Chronic Alcoholisms?
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1) Thiamine Deficiency
2) Seizures 3) Decreased Life Expectancy |
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What are the signs of Alcohol withdrawal syndrome?
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i) 12-16hours: Tremors, Anxiety, Restlessness, Weakness, Cramps, Nausea, Vomitting, Hypotension, Fainting ii) 24+ Hours: Delirium, Convulsions
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What are the Agents for managing Alcoholism?
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a) Disulfram
b) Naltrexone c) Ondansetron |
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What is use of Disulfram?
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Reinforces one's motivation to abstain Alcohol by accumulating Acetaldehyde
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What is the MOA of Disulfram for managing Alcoholism?
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Interferes with the conversion of Acetaldehyde to Acetyl CoA. Acetaldehyde accumulates and produces distressing effects.
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What are the signs of Acetaldehyde accumulation?
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1) Flushing 2) Palpitations 3) Dyspnea 4) Nausea and Vomitting 5) Severe Headaches 6) Marked Hypotension
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What is the MOA of Naltrexone for managing Alcoholism?
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Decreases the high and desire to drink
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What is the MOA of Ondansetron for managing Alcoholism?
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Decreases the desire to drink
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What are the prescription uses of Alcohol?
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1) As a solvent 2) Externally as a cooling agent 3) Skin Disinfectant 4) Neurolytic agent used locally to destroy nerves (Trigeminal Neuralgia) 5) Manage Methanol Poisoning
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