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Substance Use & Addiction, Eating Disorders Shreya Mehta sm3622@ic.ac.ukLECTURE TIMELINE 1.Substance 2. 3.Alcohol Use 4. Eating Use, Model of Disorders Addictions & Opoid Use Addiction & disorders DependenceTypes of substance use Hazardous use • likelyto causeharmif it continuesatthislevel Harmfuluse • causes damage tothe health-mental orphysical-of the userinthe absence of diagnosisof dependencesyndrome, involving adversesocial consequences and/orbingeing Addiction:compulsivedrugusedespiteharmful consequences vs Dependence: aphysical adaptationtoa substance–tolerance/withdrawal; canbe dependenton something butnotnecessarilyaddictedDependance Syndrome ICD-10 diagnosticcriteria(need 3or moresymptomsfordiagnosis) 1. Strong desire/compulsiontotake substance 2. Lack of controlof substancetaking behaviour 3. Aphysiologicalwithdrawalstate whensubstanceusereduces 4. Evidence of tolerance-needtotakemore toget sameeffect 5. Progressiveneglectof alternativeinterests 6. Choosing to ignore evidence of harmful consequencesandpersistwith substanceuseModels of addiction THREEMAIN MODELS OF ADDICTION 1. Positive reinforcement (Rewarddeficiency) 2. Negativereinforcement(Overcomingadversestate egwithdrawal, anxiety) 3. Impulsivity/compulsivity • Dopamineisthemain hormoneinvolved in‘pleasure-reward-motivation’ system thatfuels addiction • Key modulator is opoidsystem (mu-opoidmediates pleasurableeffects)Positive reinforcement Rewardsincreasedopaminein theventraltegmental area, which actsonthe ventralstriatum(natural-food, unnatural-drugs) Addiction = reward deficient statePositive reinforcement Howdo drugs of abuse increase dopamine?(from VT Ato V entral striatum) 1. Blockre-uptakeof DA • Cocaine,amphetamine 2 2. Enhance releaseof DA 1 • Amphetamine 3. Increase DA neuron firing in AT • Alcohol,opiates,nicotine 3Negative reinforcement Change from positive to negativereinforcementasaddiction/dependence develops POSITIVE REINFORCEMENT At first, you take drugs because it gets you high Then, the ‘highs’ are less but the lows are lower Now , addiction is driven by trying to escape the lows NEGATIVE REINFORCEMENTNegative reinforcement Howare the ‘lows’ created? The 3 stages of the addiction cycle Withdrawal andnegativeemotionalstates: Dysregulationin amygdalais key(arousaland stress system) • Increasein kappa/dynorphinopioidactivity • Increasein noradrenergicactivity (arousal) • Increasein corticotropin-releasing factor(stress) Evidence: Heightened brainresponse in amygdala toaversive imagesinabstinentpolydrug addictsImpulsivity/ compulsivity Change from voluntary drug use to more habitualand compulsive drug use involvestransitionfrom: • Prefrontal tostriatalcontrolover drug taking i.e.prefrontal ‘top-down’controlis diminished withgreaterstriatal reward drive • Ventral(limbicoremotional)to dorsal (habit)striatum Alcohol alters the balance between the brain’s excitatory Alcohol addiction and inhibitory systems Excitatory Inhibitory Normal Neurotransmitter: Glutamate Neurotransmitter: GABA Acute alcohol Blocks excitatory system Boosts inhibitory system • Causing impaired memory • Anxiolysis and Sedation Chronic alcohol Neuroadaptation: Neuroadaptation: ↑ number of NMDA receptors ↓ inhibitory function = tolerance Withdrawal ↑ NMDA receptors = ↑ Ca2+ ↓ inhibitory function • Hyperexcitability (seizures) • GABA function reduced • Cell death (atrophy) Treatment Acamprosate Benzodiazepines (eg. Lorazepam, Diazepam ) • Reduces NMDA function • Boosts GABA functionAlcohol use disorder Alcoholusedisorder(AUD) =is amedicalcondition characterizedbyan impairedabilityto stopor control alcoholusedespiteadverse social,occupational, or healthconsequences.It encompassesalcoholabuse, alcohol dependence and alcoholaddiction. CAGE screening 1. Haveyoueverfeltyou neededto Cutdownon yourdrinking? 2. HavepeopleAnnoyedyou by criticizing yourdrinking? 3. HaveyoueverfeltGuiltyabout drinking? 4. Haveyoueverfeltyou neededadrink firstthinginthemorning (Eye-opener)Alcohol assessment History Examination Investigations • Alcohol-related • Jaundice • Bloods(LFT s,U&Es,GGT , seizures • Anaemia lipids,amylase) • DeliriumTremens • Clubbing • Breathalyser (hallucinations) • SpiderNaevi • Urine drug screen • Alcoholpsychosis • Oedema • Haematemesis • Ascites Treatment: • Melaena Benzodiazepines & Neurological signs Acamprosate • Wernicke’ sencephalopathy • Korsakoff’ssyndrome Chlorodiazepoxide in inpatient % strength x ml/1000 = units Safe recommended limits for men and women is 14 units per weeknt settingsAlcohol withdrawal More dangerous thanopiate withdrawal - Hallucinations canoccurat anytime - Delirium Tremensisa latesignAlcohol withdrawal Minor Moresevere • Tremulousness(hands, tongue,eyelids) • Alcoholic hallucinosis • Diaphoresis(sweating) • Withdrawalseizures • Fever • DeliriumTremens • Anxietyandagitation o Hallucinations(auditory,visual) • GI:nausea,vomitingand retching o Confusion and disorientation o Hypertension o Agitation o T achycardia o Fever o Severetremorin handsandbody Opiate use assessment Opiates… 1. Relievepain Opoidagonists:heroin, 2. Createsense of euphoria methadone, fentanyl,codeine Partialagonists:buprenoprhine • Mimic releaseofendorphins (endogenous opiates) Antagonists:naltrexone • Actonopoidreceptors (mu, delta,kappa) Examination Investigations • Collapsed veins/track marks • Bloods(LFT s,U&Es,GGT ,Glucose) • Infectiveendocarditis • Blood culture(!endocarditis) • Skin abscesses • Breathalyser • Hepatitis/HIV • Urinedrug screen • Pneumonia • Sexual healthscreening/BBVOpioid overdose Symptoms: 1. Notmoving andcan’tbe woken 2. Slow orno breathing 3. Choking, gurglingsounds orsnoring 4. Constrictedpupils (overdose) 5. Clammyor coldskin 6. Blue lips and nails Treatment: Naloxone injectionintoupperthigh/arm-opioidreceptorantagonist, reversesanopioid overdose Provideairway support&recovery positionOpiate withdrawal • Dilatedpupils (withdrawal) • Rhinorrhea • Goosefleshskin • Tachycardia • Sweating • Restlessness • Bone aches • GIupset • Tremor • Yawning • Anxiety/irritabilityEating disorders • =Mental disorders • ‘A persistent disturbance of eating behaviour or behaviour intended to control weight, which significantly impairs physical health or psychosocial functioning’ • Driven by fear of fatness or extreme distress about eating Eating disorders impact physical health? (5) Eating disorders impact Impact growth & development psychosocial function? (3) Stop periods Impact work Effect on brain Impact relationships Distress Osteoporosis Higher mortalityEating disorders • ANOREXIA NERVOSA Epidemiology: • BULIMIA NERVOSA Common in childhood & adolescence Incidence of AN & BN stabilising• BINGE ETING DISORDER Incidence of OSFED & BED increasing • OSFED • ARFID AN most common ED in clinics • RUMINA TION DISORDER/SYNDROME • PICAAnorexia FOUR KEY CHARACTERISTICS: • Restriction of energy intake relative to requirements -> low body weight for that age/sex/gender/developmental stage • Intense fear of gaining weight/becoming fat • Persistent behaviour that interferes w/ weight gain • Disturbance in experience of weight/shape; constant self-evaluation; lack of recognition of seriousness of low body weightBulimia Nervosa FOUR KEY CHARACTERISTICS: • Over-eating episodes • Inappropriate compensatory mechanisms -> i.e. self-induced vomiting; excessive exercise • Body image disturbance -> guilt/shame • Episodes occur 1 x week, for at least 3 weeksBinge Eating Disorder THREE KEY CHARACTERISTICS: • Over-eating episodes • No compensation (! Key difference w/ bulimia nervosa) • Frequently overweightOSFED - i.e. Purging Disorder TWO KEY CHARACTERISTICS: • Recurrent “purging” behaviour to influence weight • Self-induced vomiting • Misuse of laxatives, diuretics, insulin • In the ABSENCE OF BINGE-EATING • Weight normal OSFEDs (other specified feeding & eating disorders) include purging disorder, atypical AN, atypical BN, night-eating syndrome*ARFID =avoidant/restrictive food intake disorder Used to be called Feeding Disorders of Infancy & Early Childhood TWO KEY CHARACTERISTICS: • Feeding/Eating disturbance • Significant weight loss • Significant nutritional deficiency • Dependance on enteral feeding & nutritional supplements • Marked interference w/ psychosocial functions No concerns about weight/shapeCauses & Interventions Interventions: In Children/Young People… • ED focussed family therapy Causes that increase risk of EDs? • CBT • Adolescent focussed therapy (only in AN treatment) • Psychological • Anxiety disorder → increased risk of AN In Adults… • MANTRA (for AN) • ADHD, Hx of depression → increased • Specialist integrative therapy risk of BN • SSCM • Bullying, social pressure • Specialist supportive clinical management → talking to a therapist • Trauma • CBT • Sexual abuse → binge/purge disorder Can also use medication (! NOT ON ITS OWN) • SSRIs for anxiety & depression • Olanzapine or aripiprazole to reduce emotional dysregulation during refeedingGeneral Management of EDs Role of medical team: • Safely re-feeding • Manage fluid & electrolyte imbalance • Arrange discharge w/ mental health team • Manage behaviours in patients Role of mental health team: • Assess & treat patients under compulsion • Address family concerns • Advise appropriate onward care following medical stabilisation • Advise patients on complex co-morbidityComplications of EDs Long term complications Growth stunting Death (if pre-pubertal Osteoporosis onset) Mental health Pregnancy Dental erosion comorbidities complications including substance misuseSBA 1 A 17-year-old girl comes into the clinic. She appears very thin and shorter than she should be. She tells you that she has been going on 5km runs every day to maintain her weight. She does not seem concerned at all by her low weight. What is the most likely diagnosis? a) Anorexia Nervosa b) Bulimia Nervosa c) OSFED d) Purging disorder e) DepressionSBA A 17-year-old girl comes into the clinic. She appears very thin and shorter than she should be. She tells you that she has been going on 5km runs every day to maintain her weight. She does not seem concerned at all by her low weight. What is the most likely diagnosis? a) Anorexia Nervosa b) Bulimia Nervosa c) OSFED d) Purging disorder e) DepressionSBA 2 A 21 year old man comes into A&E with alcohol withdrawal. He is very confused, disoriented and reports “seeing figures and hearing vo. BP is 160/130mmHg, HR 120bpm. How long has it been since the patient’s cessation of alcohol? a) 2 hours b) 10 hours c) 24 hours d) 36 hours e) 48 hoursSBA A 21 year old man comes into A&E with alcohol withdrawal. He is very confused, disoriented and reports “seeing figures and hearing vo. BP is 160/130mmHg, HR 120bpm. How long has it been since the patient’s cessation of alcohol? a) 2 hours b) 10 hours c) 24 hours d) 36 hours e) 48 hours Patient is in DT (delirium tremens).SBA 3 Which of the following is not a feature of chronic alcohol addiction? a) Upregulation of NMDA receptors b) Reduced inhibitory system function c) Hyperexcitability d) Increased uptake of Ca2+ e) Impaired memorySBA 3 Which of the following is not a feature of chronic alcohol addiction? a) Upregulation of NMDA receptors b) Reduced inhibitory system function c) Hyperexcitability d) Increased uptake of Ca2+ e) Impaired memory Impaired memory is due to inhibition of excitatory system in acute alcohol addictionFeedback ☺