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Substance abuse power presentation

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Substance abuse, also known as drug abuse, is a patterned use of a drug in which the user consumes the substance in amounts or with methods which are harmful to themselves or others, and is a form of the substance-related disorder.

Substance abuse, also known as drug abuse, is a patterned use of a drug in which the user consumes the substance in amounts or with methods which are harmful to themselves or others, and is a form of the substance-related disorder.

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Substance abuse power presentation

  1. 1. Substance relatedSubstance related DisordersDisorders
  2. 2. Psychoactive SubstancePsychoactive Substance Psychoactive (psychotropic)Psychoactive (psychotropic) substancesubstance isis any substance which after absorptionany substance which after absorption has influence on mental processes bothhas influence on mental processes both cognitive and affectivecognitive and affective..
  3. 3. Substance abuseSubstance abuse  Substance abuse can be defined as usingSubstance abuse can be defined as using a drug in a way that is inconsistent witha drug in a way that is inconsistent with medical or social norms and despitemedical or social norms and despite negative consequences.negative consequences.
  4. 4. DetoxificationDetoxification  Detoxification is the process of safelyDetoxification is the process of safely withdrawing from a substance.withdrawing from a substance.
  5. 5. IntoxicationIntoxication  Intoxication is use of a substance thatIntoxication is use of a substance that results in maladaptive behavior.results in maladaptive behavior.
  6. 6. Withdrawal syndromeWithdrawal syndrome  Withdrawal syndromeWithdrawal syndrome refers to therefers to the negative psychological and physicalnegative psychological and physical reactions that occur when use of areactions that occur when use of a substance ceases or dramaticallysubstance ceases or dramatically decreases.decreases.
  7. 7. BlackoutBlackout  It is an episode during which the personIt is an episode during which the person continues to function but has no consciouscontinues to function but has no conscious awareness of his or her behavior at theawareness of his or her behavior at the time nor any later memory of the behavior.time nor any later memory of the behavior.
  8. 8. ToleranceTolerance  Tolerance is defined as the need forTolerance is defined as the need for increasingly larger or more frequent dosesincreasingly larger or more frequent doses of a substance in order to obtain theof a substance in order to obtain the desired effects originally produced by adesired effects originally produced by a lower dose.lower dose.
  9. 9. DependenceDependence  DependenceDependence A compulsive or chronicA compulsive or chronic requirement. The need is so strong as torequirement. The need is so strong as to generate distress (either physical orgenerate distress (either physical or psychological) if left unfulfilled.psychological) if left unfulfilled.
  10. 10. Substance ClassesSubstance Classes  AlcoholAlcohol  CaffeineCaffeine  CannabisCannabis  HallucinogensHallucinogens  PCPPCP  othersothers  InhalantsInhalants  OpioidsOpioids  Sedatives, hypnotics,Sedatives, hypnotics, and anxiolyticsand anxiolytics  StimulantsStimulants  TobaccoTobacco  OtherOther
  11. 11. EtiologyEtiology  Biological factorBiological factor  Social factorsSocial factors  Psychological factorPsychological factor  Psychiatric disordersPsychiatric disorders  Environmental factorsEnvironmental factors
  12. 12. Biological FactorsBiological Factors 1.Genetics1.Genetics  Children of alcoholics are three timesChildren of alcoholics are three times more likely than other children to becomemore likely than other children to become alcoholicsalcoholics  Biological offspring of alcoholic parentsBiological offspring of alcoholic parents have a significantly greater incidence ofhave a significantly greater incidence of alcoholism than offspring of nonalcoholicalcoholism than offspring of nonalcoholic parents.parents.
  13. 13.  Monozygotic twins have a higher rate forMonozygotic twins have a higher rate for concordance of alcoholism than dizygoticconcordance of alcoholism than dizygotic
  14. 14. 2. Biochemical factors2. Biochemical factors  Norepinephrine and dopamine have beenNorepinephrine and dopamine have been implicated in opioid, cocaine and ethanolimplicated in opioid, cocaine and ethanol dependence.dependence.  Abnormalities in alcohol dehydrogenase inAbnormalities in alcohol dehydrogenase in alcohol dependencealcohol dependence
  15. 15. Psychological factorsPsychological factors  LonelinessLoneliness  Unmet needsUnmet needs  Low self esteemLow self esteem  Desire to escape from realityDesire to escape from reality  Sense of adventureSense of adventure  Pleasure seekingPleasure seeking  Sense of inferioritySense of inferiority  Poor impulse controlPoor impulse control
  16. 16. Social factorsSocial factors  Religious reasonsReligious reasons  Peer pressurePeer pressure  UrbanizationUrbanization  Extended period of educationExtended period of education  UnemploymentUnemployment  OvercrowdingOvercrowding  Poor social supportPoor social support  Effect of tv and other mass mediaEffect of tv and other mass media
  17. 17.  Occupation: barmen, executives,Occupation: barmen, executives, salesmen, actors, entertainers, armysalesmen, actors, entertainers, army personnel, medical personnel.personnel, medical personnel.
  18. 18. Psychiatric disordersPsychiatric disorders  DepressionDepression  Anxiety disorderAnxiety disorder  SchizophreniaSchizophrenia  Personality disorder.Personality disorder.
  19. 19. Social and EnvironmentalSocial and Environmental FactorsFactors  laws,laws,  cost, and availabilitycost, and availability
  20. 20. Substance-Related DisordersSubstance-Related Disorders  2 Groups:2 Groups:  Substance Use DisordersSubstance Use Disorders • Abuse or dependenceAbuse or dependence  Substance-Induced DisordersSubstance-Induced Disorders  Intoxication, withdrawal, delirium, dementia,Intoxication, withdrawal, delirium, dementia, amnesia, psychosis, mood disorder, anxietyamnesia, psychosis, mood disorder, anxiety disorder, sexual dysfunction, and sleepdisorder, sexual dysfunction, and sleep disordersdisorders
  21. 21. ComorbidityComorbidity  Up to 50% of addicts have comorbidUp to 50% of addicts have comorbid psychiatric disorderpsychiatric disorder  Antisocial PDAntisocial PD  DepressionDepression  SuicideSuicide
  22. 22. Options for where to treatOptions for where to treat  Hospitalization-Hospitalization- -Due to drug OD, risk of severe withdrawal, medical-Due to drug OD, risk of severe withdrawal, medical comorbidities, requires restricted access to drugs,comorbidities, requires restricted access to drugs, psychiatric illness with suicidal ideationpsychiatric illness with suicidal ideation  Residential treatment unitResidential treatment unit -No intensive medical/psychiatric monitoring needs-No intensive medical/psychiatric monitoring needs -Require a restricted environment-Require a restricted environment -Partial hospitalization-Partial hospitalization  Outpatient Program -No risk of med/psych morbidity andOutpatient Program -No risk of med/psych morbidity and highly motivated patienthighly motivated patient
  23. 23. TreatmentTreatment  Behavioral InterventionsBehavioral Interventions Motivation to changeMotivation to change Group TherapyGroup Therapy Individual TherapyIndividual Therapy Self-Help Recovery Groups (AA)Self-Help Recovery Groups (AA) Therapeutic CommunitiesTherapeutic Communities Aversion TherapiesAversion Therapies Family Involvement/TherapyFamily Involvement/Therapy Relapse PreventionRelapse Prevention
  24. 24. TreatmentTreatment  Pharmacologic InterventionPharmacologic Intervention  Treat Co-Occurring Psychiatric DisordersTreat Co-Occurring Psychiatric Disorders  50% will have another psychiatric disorder50% will have another psychiatric disorder  Treat Associated Medical ConditionsTreat Associated Medical Conditions  cardiovascular, cancer, endocrine, hepatic,cardiovascular, cancer, endocrine, hepatic, hematologic, infectious, neurologic,hematologic, infectious, neurologic, nutritional, GI, pulmonary, renal,nutritional, GI, pulmonary, renal, musculoskeletalmusculoskeletal
  25. 25. AlcoholAlcohol
  26. 26. AlcoholismAlcoholism  Alcoholism refers to the use of alcoholicAlcoholism refers to the use of alcoholic beverages to the point of causing damagebeverages to the point of causing damage to the individual, society or both.to the individual, society or both.
  27. 27. PHYSIOLOGIC EFFECTS OFPHYSIOLOGIC EFFECTS OF LONG-TERM ALCOHOL USELONG-TERM ALCOHOL USE  Cardiac myopathyCardiac myopathy  •• PancreatitisPancreatitis  •• EsophagitisEsophagitis  •• HepatitisHepatitis  •• CirrhosisCirrhosis  •• LeukopeniaLeukopenia  •• ThrombocytopeniaThrombocytopenia  Protein malnutritionProtein malnutrition  Vitamin deficiencyVitamin deficiency
  28. 28. Cont….Cont….  Sexual dysfunctionSexual dysfunction  Fetal alcohol syndrome(low birth weightFetal alcohol syndrome(low birth weight and inteligency)and inteligency)  Social problemsSocial problems  Financial problemFinancial problem  Occupational problemOccupational problem  CriminalityCriminality  Marital dishormonyMarital dishormony
  29. 29. Psychiatric disorders due toPsychiatric disorders due to alcohol dependencealcohol dependence
  30. 30. 1. Acute Intoxication1. Acute Intoxication  Blood Alcohol Level -Blood Alcohol Level - 0.08g/dl0.08g/dl  Progress from moodProgress from mood lability, impairedlability, impaired judgment, and poorjudgment, and poor coordination tocoordination to increasing level ofincreasing level of neurologic impairmentneurologic impairment (severe dysarthria,(severe dysarthria, amnesia, ataxia)amnesia, ataxia)  Can be fatal (loss ofCan be fatal (loss of airway protectiveairway protective reflexes, pulmonaryreflexes, pulmonary aspiration, profound CNSaspiration, profound CNS depression)depression)
  31. 31. 2. Alcohol Withdrawal syndrome2. Alcohol Withdrawal syndrome  EarlyEarly  anxiety, irritability, tremor, insomnia, nausea,anxiety, irritability, tremor, insomnia, nausea, tachycardia, HTN, hyperthermia, hyperactive reflexestachycardia, HTN, hyperthermia, hyperactive reflexes  SeizuresSeizures  generally seen 24-48 hoursgenerally seen 24-48 hours  most often Grand malmost often Grand mal  Withdrawal Delirium TremensWithdrawal Delirium Tremens  generally between 48-72 hoursgenerally between 48-72 hours  altered mental status, hallucinations, markedaltered mental status, hallucinations, marked autonomic instabilityautonomic instability  life-threateninglife-threatening
  32. 32. Alcohol Withdrawal (cont.)Alcohol Withdrawal (cont.)  BenzodiazepinesBenzodiazepines  GABA agonist - cross-tolerant with alcoholGABA agonist - cross-tolerant with alcohol  reduce risk of SZ; provide comfort/sedationreduce risk of SZ; provide comfort/sedation  AnticonvulsantsAnticonvulsants  reduce risk of SZreduce risk of SZ  Carbamazepine or Valproic acidCarbamazepine or Valproic acid  Thiamine supplementationThiamine supplementation  Risk thiamine deficiency (Wernicke/Korsakoff)Risk thiamine deficiency (Wernicke/Korsakoff)
  33. 33. 3.Alcohol induced amnestic3.Alcohol induced amnestic disorderdisorder  Thiamine deficiency is most frequentThiamine deficiency is most frequent cause of amnestic disorder.cause of amnestic disorder.  Wernicke’s encephalopathy:Wernicke’s encephalopathy:  Cerebral ataxiaCerebral ataxia  66thth cranial nerve palsycranial nerve palsy  Periperal neropathyPeriperal neropathy
  34. 34.  Korsakoff’s psychosisKorsakoff’s psychosis  Gross memory disturbanceGross memory disturbance  DisorientationDisorientation  ConfusionConfusion  Confabulation: the unconscious filling ofConfabulation: the unconscious filling of memory gaps by imagined or untruememory gaps by imagined or untrue experience due to memory lossexperience due to memory loss  Poor attention spanPoor attention span  Impaired insightImpaired insight
  35. 35. 4. Alcohol induced psychiatric4. Alcohol induced psychiatric disorderdisorder  Alcohol induced dementiaAlcohol induced dementia  Alcohol induced mood disorderAlcohol induced mood disorder  Alcohol induced anxiety disorderAlcohol induced anxiety disorder  Suicidal behaviourSuicidal behaviour  Pathological jealousyPathological jealousy  Alcoholic seizuresAlcoholic seizures  Alcoholic hallucinosis: auditoryAlcoholic hallucinosis: auditory
  36. 36. Alcohol treatmentAlcohol treatment  Outpatient CD treatment:Outpatient CD treatment:  support, education, skills training, psychiatricsupport, education, skills training, psychiatric and psychological treatment, AAand psychological treatment, AA  Medications:Medications:  DisulfiramDisulfiram  NaltrexoneNaltrexone  AcamprosateAcamprosate
  37. 37. Medications-alcohol deterrentMedications-alcohol deterrent therapytherapy  Disulfiram (antabuse) 250mg-500mg po dailyDisulfiram (antabuse) 250mg-500mg po daily  Inhibits aldehyde dehydrogenase andInhibits aldehyde dehydrogenase and dopamine beta hydroxylasedopamine beta hydroxylase  Aversive reaction when alcohol ingested-Aversive reaction when alcohol ingested- vasodilatation, flushing, hypotenstion/ HTN,vasodilatation, flushing, hypotenstion/ HTN, coma / deathcoma / death  Psychiatric side effects - psychosis,Psychiatric side effects - psychosis, depression, confusion, anxietydepression, confusion, anxiety  Dermatologic rashes and itchingDermatologic rashes and itching  Watch out for forms of alcohol - sauces,Watch out for forms of alcohol - sauces, mouth wash, cough meds, alcohol basedmouth wash, cough meds, alcohol based hand sanitizers, etchand sanitizers, etc
  38. 38. MedicationsMedications  Naltrexone 50mg po dailyNaltrexone 50mg po daily  Opioid antagonist thought to block mu receptorsOpioid antagonist thought to block mu receptors reducing intoxication euphoria and cravingsreducing intoxication euphoria and cravings  Hepatotoxicity at high doseHepatotoxicity at high dose  Acamprosate(Campral) 666mg po tidAcamprosate(Campral) 666mg po tid  Unknown MOA but thought to stabilize neuronUnknown MOA but thought to stabilize neuron excitation and inhibition - may interact with GABA andexcitation and inhibition - may interact with GABA and Glutamate receptor - cleared renally (check kidneyGlutamate receptor - cleared renally (check kidney function)function)
  39. 39. Benzodiazepine( BZD)/Benzodiazepine( BZD)/ BarbituratesBarbiturates
  40. 40. Benzodiazepine( BZD)/Benzodiazepine( BZD)/ BarbituratesBarbiturates  IntoxicationIntoxication  Similar to alcohol but less cognitive/motorSimilar to alcohol but less cognitive/motor impairmentimpairment  Variable rate of absorption (lipophilia) andVariable rate of absorption (lipophilia) and onset of action and duration in CNSonset of action and duration in CNS  The more lipophilic and shorter the duration ofThe more lipophilic and shorter the duration of action, the more "addicting" .action, the more "addicting" .
  41. 41. BenzodiazepineBenzodiazepine  WithdrawaWithdrawall  Anxiety, irritability, insomnia, fatigue, HA,Anxiety, irritability, insomnia, fatigue, HA, tremor, sweating, poor concentrationtremor, sweating, poor concentration  Common detox mistake is tapering too fast;Common detox mistake is tapering too fast; symptoms worse at end of tapersymptoms worse at end of taper  Convert short elimination BZD to longerConvert short elimination BZD to longer elimination half life drug and then slowly taperelimination half life drug and then slowly taper  Outpatient taper- decrease dose every 1-2Outpatient taper- decrease dose every 1-2 weeks and not more than 5 mg Diazepamweeks and not more than 5 mg Diazepam dose equivalentdose equivalent
  42. 42. BenzodiazapinesBenzodiazapines  AlprazolamAlprazolam  OxazepamOxazepam  TemazepamTemazepam  ClonazepamClonazepam  LorazepamLorazepam  ChlordiazepoxideChlordiazepoxide  DiazepamDiazepam
  43. 43. OpiodsOpiods
  44. 44. OPIOIDSOPIOIDS  The commonly abused opioids(narcotics)The commonly abused opioids(narcotics) are heroin(brown sugar).are heroin(brown sugar).  Synthetic preparation like pethidine,Synthetic preparation like pethidine, fortwin.fortwin.
  45. 45. OPIOIDSOPIOIDS Bind to the Opioid receptor in the CNS to modulate painBind to the Opioid receptor in the CNS to modulate pain  Intoxication-Intoxication- pinpoint pupils, sedation, constipation,pinpoint pupils, sedation, constipation, bradycardia, hypotension and decreased respiratory ratebradycardia, hypotension and decreased respiratory rate  Withdrawal-Withdrawal-  Not life threatening unless severe medical illness butNot life threatening unless severe medical illness but extremely uncomfortable.extremely uncomfortable.  dilated pupils lacrimation, goosebumps, diarrhea,dilated pupils lacrimation, goosebumps, diarrhea, myalgias, arthralgias, dysphoria or agitationmyalgias, arthralgias, dysphoria or agitation
  46. 46.  Neuroadaptation:Neuroadaptation: increased DA andincreased DA and decreased NEdecreased NE
  47. 47. Treatment - Opiate Use DisorderTreatment - Opiate Use Disorder  RxRx- symptomatically with antiemetic, antacid,- symptomatically with antiemetic, antacid, antidiarrheal, muscle relaxantantidiarrheal, muscle relaxant (methocarbamol), NSAIDS, clonidine and(methocarbamol), NSAIDS, clonidine and maybe BZDmaybe BZD  support, education, skills building, psychiatricsupport, education, skills building, psychiatric and psychological treatment.and psychological treatment. 
  48. 48.  MedicationsMedications  Methadone (opioid substitution)Methadone (opioid substitution)  NaltrexoneNaltrexone  Buprenorphine (opioid substitution)Buprenorphine (opioid substitution)
  49. 49. Treatment - Opiate Use DisorderTreatment - Opiate Use Disorder  NaltrexoneNaltrexone  Opioid blocker, mu antagonistOpioid blocker, mu antagonist  50mg po daily50mg po daily  MethadoneMethadone  Mu agonistMu agonist  Start at 20-40mgStart at 20-40mg  Average dose 80-100mg dailyAverage dose 80-100mg daily  BuprenorphineBuprenorphine  Partial mu partial agonistPartial mu partial agonist Mu= opioid receptorMu= opioid receptor
  50. 50. StimulantsStimulants
  51. 51.  Stimulants (Amphetamines, Cocaine,Stimulants (Amphetamines, Cocaine, Others)Others)  Stimulants are drugs that stimulate orStimulants are drugs that stimulate or excite the central nervous system.excite the central nervous system.
  52. 52. STIMULANTSSTIMULANTS  Intoxication (acute)Intoxication (acute)  Psychological signsPsychological signs  euphoria, hyperactivity, restlessness, interpersonaleuphoria, hyperactivity, restlessness, interpersonal sensitivity, anxiety, tension, anger, impaired judgmentsensitivity, anxiety, tension, anger, impaired judgment  Physical signsPhysical signs  tachycardia, papillary dilation, HTN, diaphoresis,tachycardia, papillary dilation, HTN, diaphoresis, chills, weight loss, chest pain, cardiac arrhythmias,chills, weight loss, chest pain, cardiac arrhythmias, confusion, seizures, comaconfusion, seizures, coma
  53. 53. STIMULANTSSTIMULANTS (cont.)(cont.)  Chronic intoxicationChronic intoxication  affective blunting, fatigue, sadness, socialaffective blunting, fatigue, sadness, social withdrawal, hypotension, bradycardia, musclewithdrawal, hypotension, bradycardia, muscle weaknessweakness  WithdrawalWithdrawal  Not severe but have exhaustion with sleepNot severe but have exhaustion with sleep (crash)(crash)  Treat with rest and supportTreat with rest and support
  54. 54. CocaineCocaine  Route: nasal, IV or smokedRoute: nasal, IV or smoked  Has vasoconstrictive effects that may outlastHas vasoconstrictive effects that may outlast use and increase risk for CVA and MIuse and increase risk for CVA and MI  Neuroadaptation:Neuroadaptation: cocaine mainly preventscocaine mainly prevents reuptake of DAreuptake of DA
  55. 55. Treatment - Stimulant UseTreatment - Stimulant Use Disorder (cocaine)Disorder (cocaine)  Treatment including support, education,Treatment including support, education, PsychotherapyPsychotherapy  PharmacotherapyPharmacotherapy  Amyl nitrite is an antidoteAmyl nitrite is an antidote  AntidepressentAntidepressent
  56. 56. AmphetaminesAmphetamines  Similar intoxication syndrome to cocaine butSimilar intoxication syndrome to cocaine but usually longerusually longer  Route - oral, IV, nasally, smokedRoute - oral, IV, nasally, smoked  No vasoconstrictive effectNo vasoconstrictive effect  NeuroadaptationNeuroadaptation  inhibit reuptake of DA, NE, SE - greatest effect on DAinhibit reuptake of DA, NE, SE - greatest effect on DA
  57. 57.  Chronic use results in neurotoxicityChronic use results in neurotoxicity possibly from glutamate and axonalpossibly from glutamate and axonal degenerationdegeneration  Can see permanent amphetamineCan see permanent amphetamine psychosis with continued usepsychosis with continued use  Treatment similar as for cocaine but noTreatment similar as for cocaine but no known substances to reduce cravingsknown substances to reduce cravings
  58. 58. Treatment – Stimulant UseTreatment – Stimulant Use Disorder (amphetamine)Disorder (amphetamine)  Treatment: including support, educationTreatment: including support, education  No specific medications have been foundNo specific medications have been found helpful in treatmenthelpful in treatment
  59. 59. TobaccoTobacco
  60. 60. TobaccoTobacco  Most important preventable cause of death /Most important preventable cause of death / diseasedisease  45% of smokers die of tobacco induced disorder45% of smokers die of tobacco induced disorder  Second hand smoke causes death / morbiditySecond hand smoke causes death / morbidity  Psychiatric pts at risk for Nicotine dependence-Psychiatric pts at risk for Nicotine dependence- 75%-90 % of Schizophrenia pts smoke75%-90 % of Schizophrenia pts smoke
  61. 61. Tobacco (Tobacco (cont.)cont.)  No intoxication diagnosisNo intoxication diagnosis  initial use associated with dizziness, nauseainitial use associated with dizziness, nausea  NeuroadaptationNeuroadaptation  nicotine acetylcholine receptors on DA neurons innicotine acetylcholine receptors on DA neurons in ventral tegmental area release DAventral tegmental area release DA  ToleranceTolerance  rapidrapid  WithdrawalWithdrawal  irritability, anxiety, decreased concentration,irritability, anxiety, decreased concentration, insomnia, increased appetiteinsomnia, increased appetite
  62. 62. Treatment – Tobacco UseTreatment – Tobacco Use DisorderDisorder  Cognitive Behavioral TherapyCognitive Behavioral Therapy  Agonist substitution therapyAgonist substitution therapy  nicotine gum , transdermal patch, nasal spraynicotine gum , transdermal patch, nasal spray  MedicationMedication  Bupropion 150mg po bid,Bupropion 150mg po bid,
  63. 63. Inhalants or volatileInhalants or volatile solventssolvents
  64. 64. Commonly used solvents are:Commonly used solvents are:  PetrolPetrol  AerosolsAerosols  ThinnersThinners  Industrial solventsIndustrial solvents
  65. 65. IntoxicationIntoxication  EuphoriaEuphoria  ExcitementExcitement  Slurring of speechSlurring of speech  Impaired judgementImpaired judgement
  66. 66. Withdrawal symptomsWithdrawal symptoms  AnxietyAnxiety  DepressionDepression
  67. 67. COMPLICATIONSCOMPLICATIONS  Liver, kidney and brain damageLiver, kidney and brain damage  Peripheral neuropathyPeripheral neuropathy
  68. 68. TreatmentTreatment  ReassuranceReassurance  Diazepam for intoxicationDiazepam for intoxication
  69. 69. BarbituratesBarbiturates
  70. 70.  Commonly abused are:Commonly abused are:  SecobarbitalSecobarbital  PentobarbitalPentobarbital  AmobarbitalAmobarbital
  71. 71. IntoxicationIntoxication  Inco-ordinationInco-ordination  Slurred speechSlurred speech  Attention and memory impairmentAttention and memory impairment  IrritabilityIrritability
  72. 72. ComplicationComplication  IV route use can cause cellulites,IV route use can cause cellulites, embolism, abscesses.embolism, abscesses.
  73. 73. Withdrawal syndromeWithdrawal syndrome  Delirium tremensDelirium tremens  SeizuresSeizures  RestlessnessRestlessness
  74. 74. TreatmentTreatment  Symptomatic treatmentSymptomatic treatment  Induction of vomitingInduction of vomiting  Use activated charcoal to reduce aUse activated charcoal to reduce a absorptionabsorption
  75. 75. HallucinogensHallucinogens
  76. 76. HALLUCINOGENSHALLUCINOGENS  Naturally occurring - Peyote cactus; magicNaturally occurring - Peyote cactus; magic mushroom- oralmushroom- oral  Synthetic agentsSynthetic agents  LSD (lysergic acid diethyamide) - oralLSD (lysergic acid diethyamide) - oral  DMT (dimethyltryptamine) - smoked, snuffed, IVDMT (dimethyltryptamine) - smoked, snuffed, IV  MDMA (3,4-methyl-enedioxymethamphetamine)MDMA (3,4-methyl-enedioxymethamphetamine) – oral– oral
  77. 77. MDMAMDMA  Designer club drugDesigner club drug  3-6 hour duration3-6 hour duration  Tolerance develops quickly and unpleasant sideTolerance develops quickly and unpleasant side effects with continued use (teeth grinding) soeffects with continued use (teeth grinding) so dependence less likelydependence less likely
  78. 78. IntoxicationIntoxication  illusions, sensitivity of touch, taste/ smellillusions, sensitivity of touch, taste/ smell altered, tearfulness, euphoria, panic,altered, tearfulness, euphoria, panic, impairment judgmentimpairment judgment
  79. 79. MDMAMDMA ..  NeuroadaptationNeuroadaptation- affects serotonin (5HT), DA,- affects serotonin (5HT), DA, NENE  PsychosisPsychosis  Hallucinations generally mildHallucinations generally mild  Paranoid psychosis associated with chronic useParanoid psychosis associated with chronic use  Serotonin neural injury associated with panic, anxiety,Serotonin neural injury associated with panic, anxiety, depression, flashbacks, psychosis, cognitive changes.depression, flashbacks, psychosis, cognitive changes.  WithdrawalWithdrawal – unclear syndrome– unclear syndrome
  80. 80. CannabisCannabis
  81. 81. Cannabis (Marijuana/ ganja)Cannabis (Marijuana/ ganja)  Cannabis sativa is the hemp plantCannabis sativa is the hemp plant  Cannabis is most often smoked inCannabis is most often smoked in cigarettes but it can be eaten(bang).cigarettes but it can be eaten(bang).  lipid soluble;lipid soluble;  long half life of 50 hourslong half life of 50 hours
  82. 82. CANNABISCANNABIS  IntoxicationIntoxication-- Appetite and thirst increaseAppetite and thirst increase Colors/ sounds/ tastes are clearerColors/ sounds/ tastes are clearer Increased confidence and euphoriaIncreased confidence and euphoria RelaxationRelaxation Increased libidoIncreased libido Transient depression, anxiety, paranoiaTransient depression, anxiety, paranoia Tachycardia, dry mouth,Tachycardia, dry mouth, Slowed reaction time/ motor speedSlowed reaction time/ motor speed Impaired cognitionImpaired cognition PsychosisPsychosis
  83. 83. CANNABIS (cont.)CANNABIS (cont.)  NeuroadaptationNeuroadaptation  Neuromodulator effect; decrease uptake of GABANeuromodulator effect; decrease uptake of GABA and DAand DA  WithdrawaWithdrawal - insomnia, irritability, anxiety, poorl - insomnia, irritability, anxiety, poor appetite, depression, physical discomfortappetite, depression, physical discomfort
  84. 84. CANNABIS (cont.)CANNABIS (cont.)  TreatmentTreatment -Detox and rehab-Detox and rehab -Behavioral model-Behavioral model -No pharmacological treatment but-No pharmacological treatment but maymay treat other psychiatric symptomstreat other psychiatric symptoms
  85. 85. PCPPCP
  86. 86. PHENACYCLIDINE ( PCP)PHENACYCLIDINE ( PCP) "Angel Dust""Angel Dust"  Dissociative anestheticDissociative anesthetic IntoxicationIntoxication::  severe dissociative reactionssevere dissociative reactions – paranoid delusions,– paranoid delusions, hallucinations, can become very agitated/ violent withhallucinations, can become very agitated/ violent with decreased awareness of pain.decreased awareness of pain.  Cerebellar symptomsCerebellar symptoms - ataxia- ataxia  With severe over doseWith severe over dose - mute, catatonic, muscle rigidity,- mute, catatonic, muscle rigidity, HTN, hyperthermia, coma and deathHTN, hyperthermia, coma and death
  87. 87. PCP cont.PCP cont.  TreatmentTreatment  antipsychotic drugs or BZD if requiredantipsychotic drugs or BZD if required  Low stimulation environmentLow stimulation environment  NeuroadaptationNeuroadaptation  opiate receptor effectsopiate receptor effects  No tolerance or withdrawalNo tolerance or withdrawal

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