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Fahad Alosaimi MBBS, SSC-Psych Psychosomatic medicine Consultant Assistant professor King Saud University.

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Presentation on theme: "Fahad Alosaimi MBBS, SSC-Psych Psychosomatic medicine Consultant Assistant professor King Saud University."— Presentation transcript:

1 Fahad Alosaimi MBBS, SSC-Psych Psychosomatic medicine Consultant Assistant professor King Saud University

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3 ارتفاع نسبة الادمان في شرق السعودية 300% خلال عامي

4 CNN وقال ماثيو نايس، خبير مكافحة المخدرات في المكتب، إن الكميات الأكبر من الأمفيتامين يجري مصادرتها في المملكة العربية السعودية، وأضاف، في حديث لـ CNN أن الرياض صادرت خلال 2008 أكثر من 12.8 طن متري من الأمفيتامين من أصل 15.3 مليون طن على مستوى المنطقة ككل أما علي الحقوي، الطبيب في مستشفي الملك سعود بن عبدالعزيز، فقال إن المرضى لديه يقولون بأن الاتجاه الأكبر للإدمان هو على الكحول، ومن ثم الأمفيتامين.

5 What is addiction? In Aug 2011, The American Society of Addiction Medicine (ASAM) has officially recognized Addiction as mostly: a) a social problem b) a moral problem c) a criminal problem d) a primary chronic brain problem e) a behavioral disorder occur as the result of other causes such as emotional or psychiatric problems. Addiction is not a choice, but choice still plays an important role in getting help.

6 Terminology Abuse: Self-administration of any substance in a culturally disapproved manner that causes adverse consequences. Dependence: The physiological state of neuroadaptation produced by repeated administration of a drug, necessitating continued administration to prevent the appearance of the withdrawal state. Addiction: A nonscientific term that implies dependence. Intoxication: Withdrawal: Tolerance:

7 Substance Use Disorders (DSM IV-TR) Substance Abuse:  Repetitive problems in  1 major life areas Substance Dependence (  3 criteria):  Tolerance  Withdrawal   Amount /  time  Urges, failure to cut down  Excessive time obtaining, using & recovering  Activities given up  Use despite problems

8 Common Routes of Substance Abuse Routesubstances Oral  alcohol  hypnotics - sedatives  stimulants  hallucinogens Injections  Opioids  stimulants Smoking  cannabis  PCP Sniffing  cocaine  volatile substances

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10 Photo courtesy of the NIDA Web site. From A Slide Teaching Packet: The Brain and the Actions of Cocaine, Opiates, and Marijuana.

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13 Case of Mr.A 26 year old male. He came to ER with a runny nose, stomach cramps, dilated pupils, muscle spasms, chills despite the warm weather, elevated heart rate and blood pressure, and is running a slight temperature. He has no other adverse medical problem and no psychological problems. At first he is polite and even charming to you and the staff. He’s hoping you can just give him some “meds” to tide him over until he can see his regular doctor. However, he becomes angry and threatening to you and the staff when you tell him you may not be able to comply with his wishes.

14 Case of Mr.B He is an older man in his late sixties and was a bit disheveled in appearance. He came to ER accompanied by his neighbour. The neighbour tells you that he found him earlier this evening trying to enter his apartment door. He was sweaty, his eyes where dilated, and his hands were trembling so badly that he could not get the key in the door. He kept calling his neighbour by another name and saying he was trying to get into his office to do some work though he retired years ago. He can correctly identify himself but, also appears confused & unable to tell you the month or season. His demeanor is polite and apologetic to you and the staff. He tells you he has never had a problem with ???? but scored high on the ???? assessment test. He then admits to an occasional ???? every now and then.

15 Questions What preliminary Axis I diagnosis would give each of your patients and why? What, if any, medical danger(s), do you see or should you consider for either patient? Why? Management?

16 Assessement Collateral history. Urine screening tests. blood screening tests (alcohol, barbiturates). Pattern of Abuse:  What? (type, dose, route, effect: nature and duration).  How? (frequency, duration, how long, source, and situation)  Why? (? psychosocial problems).  Dependence? Complications :  Psychosocial…..  Physical…..

17 Classes of Substances Alcohol Sedatives, hypnotics or anxiolytics Inhalants (Volatile Solvents) CNS depressants Amphetamines, Cocaine Khat (Qat) Caffeine, Nicotine (Tobacco) Cannabis Opioids Hallucinogens, Phencycldine CNS stimulants

18 Alcohol أم الخبائث

19 Alcohol Kills More Than AIDS, TB or Violence-WHO report (Feb 2011) Alcohol causes nearly 4% of deaths worldwide, more than AIDS, tuberculosis or violence. Alcohol is the world's leading risk factor for death among males aged 15-59," Alcohol is a causal factor in 60 types of diseases and injuries. Now we have strong evidence of a causal relationship between drinking and breast cancer.

20 20 Epidemiology dependence is most common in those aged 40 – 55 years. In USA : 13 % men and 4 % women age  % hospital admissions Alcoholics who continue drinking have a shortened life-span of 15 years why?

21 Assessment

22 Risk factors of Alcohol abuse Vulnerable personality: impulsive, gregarious, less conforming, isolated or avoidant persons. Vulnerable occupation: senior businessmen, journalists, doctors. Psychosocial stresses: social isolation, financial, occupational or academic difficulties, and marital conflicts. Emotional problems: anxiety, chronic insomnia depression.

23 Is your patient ETOH dependent? CAGE questionnaire C = Have you ever felt you must Cut down your drinking? A = Have people Annoyed you by criticizing your drinking? G = Have you ever felt Guilty about your drinking? E = Have you ever had a drink first thing in the morning as an “Eye opener”?

24 Laboratory Tests Identify acute and/or heavy drinking (> 5 drinks/day):  Blood Alcohol Levels (BAL).  Gamma-glutamyltransferase (GGTP > 35 IU/L)  Carbohydrate Deficient Transferrin (CDT > 20 IU/L)  Erythrocyte mean corpuscular volume (MCV >91.5  3 )  High AST/ALT *** CDT + GGTP best diagnostic combination.

25 Alcohol intoxication Ethanol plasma concentrations Vs. CNS effects Ethanol plasma concentration (per mill) Effect 0.2 Feeling of relaxation 0.3 Slight euphoria 0.5 Slight motor incoordination 1ataxia 3stupor >4>4>4>4 Coma, death due to the respiratory failure

26 Alcohol withdrawal 70 % of AD patients &  Rate in the elderly. No gender/ethnic differences 85% mild-to-moderate 15% severe and complicated:  Seizures  Delirium Tremens Features : Tremulousness (hands, legs and trunk). Nausea, retching and vomiting. Sweating, tachycardia and fever. Anxiety, insomnia and irritability. Cognitive dysfunctions. Thinking and perceptual disturbances.

27 Course of AW Stages I (24 – 48 hours): II (48 – 72 hours): III (72 – 105 hours): IV (> 7 days): Symptoms  Peak severity at 36 hours 90% of AW seizures Most cases self-limited   Stage I symptoms  “Delirium Tremens”  Protracted withdrawal

28 Delirium Tremens Features: delirium. gross tremor. autonomic disturbances. dehydration and elecrolyte disturbances.. marked insomnia. Course : peaks on third or fourth day, lasts for 3 – 5 days, worsens at night, and followed by a period of prolonged deep sleep, Complications : seizures. chest infection, aspiration. violent behaviour. coma. death; mortality rate: 5-15%. Why ?

29 Complications of chronic ETOH abuse MedicalpsychiatricSocial  Neurological  Cerebellar degeneration  Seizures  Periphral neuropathy  Optic nerve atrophy  head trauma  Alimentary  Tumours (oesophagus, liver..)  gastritis, peptic ulcer  Pancreatitis  hepatitis, cirrhosis  Others:  cardiomyopathy  anaemia  obesity  impotence  gynaecomastia  amnesic disorder  delirium  dementia  psychosis  depression  reduced sexual desire  insomnia  personality deterioration  suicide  morbid jealousy  social isolation  job loss  marital conflicts  family problems  legal troubles  social stigma  others

30 Treatment Treating Alcohol Intoxicated Patient: Conscious : supportive, antipsychotic if agitated. Unconscious: ABC Treating Alcohol Withdrawal: Supportive, thiamine & long acting BDZ (Why?) ± anticonvulsants for seizure. Maintaining Abstinence: Medciations: Disulfiram – blockade of aldehydedehydrogenase  cummulation of acetaldehyde - nausea, flushing, tachycardia, hyperventilation, panic… Naloxone – reduces alcohol-induced reward. Acamprosate – anti-craving effects. Psychological: group Tx, AA, relapse prevention.

31 Sedatives, Hypnotics, and Anxiolytics Similar clinical manifestations to alcohol. withdrawal from short-acting substancet (e.g. triazolam) can begin within hours. Alcohol and all drugs of this class are brain depressants any risk?, are cross-tolerant and cross-dependant. withdrawal can be accomplished safely using diazepam, phenobarbital, and pentobarbital, dose reduced in steps (about 1/4 - 1/10 of daily benzodiazepine dose, every two weeks). BDZ have a large margin of safety & less addiction potentials. Flumazenil is a BDZ receptor antagonists used in BDZ overdose.

32 Inhalants (Volatile Solvents ) Examples : Lighter fluids,Spray paints,Cleaning fluids,Glues,Typewriter correction fluids,Fingernail polish removers. The active compounds : acetone, benzene or toluene. brain depressants, effects appear within 5 – 10 minutes and may last for several hours. Common among adolescents in lower socioeconomic groups, usually as occasional experimentation. features of recent abuse : unusual breath or odour, rashes around the nose and the mouth or the residue on the face, hands or clothing.

33 Inhalants Acute effectsLong term effects  Euphoria  excitement disinhibition **High dose:  disturbed conciousness  perceptual disturbances  Impulsiveness  Assultiveness  impaired judgement  Sedation  slurred speech  nystagmus,  ataxia,  incoordiantion  nausea, vomiting.  Irreversible multi-organ damages (brain, lungs, liver, kidneys, muscles, peripheral nerves and bone marrow).  Psychological dependence.  Death because of:  respiratory depression  asphyxiation  aspiration of vomitus  cardiac arrhythmia  serious injury *Course of abuse: short * Treatment : supportive.

34 STIMULANTS Enhance DA & NE, sympathomimitics peripherally. amphetamine, Khat (Qat), caffeine, cocaine & nicotine (tobacco). Therapeutic uses : ADHD, narcolepsy,depression & obesity. Abused by students, long distance drivers..etc. Crack ( smoked, cocaine ) is highly addictive why? Mild w/drawal Sx : low mood and dec. energy. * In severe cases : depression, anxiety, lethargy, headache, sleep disturbances & craving.

35 STIMULANTS (Clinical effects) Psychological Physical  Enhanced cognitive functions  Elevated mood  Hyperactivity  Over-talkativeness  Increased confidence, self-esteem  Insomnia. In high doses / prolonged use:  Restlessness, irritability  Paranoid psychosis  Aggressiveness, hostility  Reduced sense of fatigue  Reduced appetite (anorexia)  Dilated pupils  Tremor In high doses / prolonged use:  Nausea, vomiting, cardiac arrhythmia. hypertension, CVA, seizures, dizziness, hyperthermia, respiratory distress, cyanosis.  rebound rhinitis, nose bleeds & perforated nasal septum(cocaine snorting) Treatment * Intoxication: supportive ( sedation, antiarrhythmic drugs, Antipsychotics & urine acidification why? * Planed Withdrawal : counseling,sedatives & Antidepressants if needed..

36 Other stimulants Khat: * The fresh leaves are chewed for their stimulant effect( Cathinone ). * Chronic use : infection & loss of appetite. Caffeine * Intoxication >250 mg. : restlessness * excitement * agitation insomnia * diuresis * GI upset tachycardia * muscle twitching * flushed face * Withdrawal (after prolonged use and abrupt cessation) headache * nausea * vomiting * anxiety dysphoria * fatigue * drowsiness

37 Nicotine CNS stimulants,agonist at the nicotinic subtype of Ach receptors and activating DA and NE. & a skeletal muscle relaxant. Why people like smoking? improved attention, learning, reaction time, and problem - solving ability. Withdrawal features ( peak in 1-2 days, few weeks): irritability * frustration * poor concentration insomnia * dysphoric mood * increase appetite. Smoking causes cancer of the lung, upper respiratory tract, bladder, pancreas, oesophagus and probably kidney and stomach. Cigarette smoking can induce liver microsomal enzymes and reduce plasma concentrations of antipsychotic agents.

38 OPIOIDS This group include: heroin morphine codeine pethidine methadone. The medical use of opioids ( e.g. pethidine) is mainly for analgesia. They are abused for their powerful euphoriant effects. Tolerance develops rapidly & diminishes rapidly which is serious why? Opioid Withdrawal: flulike Sx, craving.. They are very distressful but not serious medically. including:  lacrimation  muscle and joint pain  cold and hot flushes  nausea, vomiting and diarrhoea  piloerection

39 Opioids ( clinical effects) PsychologicalPhysical  euphoria  relaxation  hyperactivity  drowsiness  analgesia  reduced sexual desire  small pupil  bradycardia  reduced appetite  constipation  respiratory depression  I.V use: *AIDS * hepatitis * endocarditis * septicemia * Acute local infections Treatment: *Opioid overdose : supportive +naloxone *Opioid Withdrawal: symptomatic treatment, Counseling, individual or group therapy * Harm reduction strategies: methadone,buprenophine

40 CANNABIS (clinical effects) PsychologicalPhysical  sense of well being  euphoria  relaxation  enhancement of aesthetic experiences through hightened perceptual awareness  impaired memory  impaired psychomotor performance.  dysphoria, depression  anxiety, panic attacks  amotivation syndrome ? (chronic use)  psychosis (risk factor for SCZ)  tachycardia  reddening of the conjunctiva  dry mouth  respiratory tract irritation  increased appetite

41 CANNABIS The active ingredient “9-tetrahydrocannibinol” (THC). With high dose & prolong abuse, tolerance psychological dependence may occur. Withdrawal from high doses gives rise to a syndrome of nausea, anorexia, irritability and insomnia. Chronic use of cannabis can lead to a state of apathy and amotivation (amotivation syndrome) but this may be more a reflection of patient’s personality structure than an effect of cannabis. Treatment : Symptomatic, support & counseling.

42 HALLUCINOGENS (clinical effects) PsychologicalPhysical  marked perceptual distortion ( changing shapes, colours…)  hallucinations ( visual, tactile… )  false sense of achievement an strength  depersonalization, derealization  euphoria, anxiety, panic  paranoid ideation  homicide and suicide tendencies  flashbacks after abstinence  Delirium PCP  euphoria and peaceful floating sensations.  delirium  agitation and aggressive behaviour.  tachycardia  hypertension  cerebellar signs  wide pupils  hyperemic conjuncitva  blurred vision  hyperthermia  Piloerection PCP  hypertensive crisis  status epilepticus  malignant hyperthermia

43 HALLUCINOGENS Hallucinogenes can be natural, e.g. Psilocybin (magic mushroom) or synthetic, e.g. Lysergic acid diethylamide (LSD). Phencyclidine(PCP) is a dissociative anaesthetic with hallucinogenic effects (a separate category in DSM IV). Tolerance develops rapidly& reverses quickly in few days. Abuser can develop a psychological dependence. Treatment: Supportive & symptomatic.

44 Questions What preliminary Axis I diagnosis would give each of your patients and why? What, if any, medical danger(s), do you see or should you consider for either patient? Why? Management?

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