13.Alcohol Use Disorders Lecture no. 2.pptx

Lecture on alcohol use disorders

1. SUBSTANCE USE DISORDERS Dr Michelle Dube

2. ALCOHOL Purposeful production of ethyl alcohol through fermentation of grain, fruit or honey has been a part of many cultures for centuries Alcohol is a psychoactive substance with dependence-producing properties The harmful use of alcohol ranks among the top five risk factors for disease, disability and death throughout the world and is a causal factor in numerous disease and injury states (3.3million deaths/year)

3. HARMFUL USE OF ALCOHOL The harmful use of alcohol causes a large disease, social and economic burden in societies Alcohol-related harm is determined by the volume of alcohol consumed, the pattern of drinking, and, on rare occasions, the quality of alcohol consumed Harmful use of alcohol is linked with development of infectious diseases such as tuberculosis and HIV/AIDS

4. VULNERABILITY FACTORS Age - children, adolescents and the elderly are more vulnerable to alcohol related harm early initiation associated with 3-4 times increased risk of alcohol dependance, unintentional injury, memory and cognitive impairment Gender - 7.6% of male deaths in 2012 were attributable to alcohol vs 4% of female deaths Men drink more frequently and in larger quantities than women and more likely to get injured However, for health outcomes such as cancers, gastrointestinal diseases or cardiovascular diseases, the same level of consumption leads to more pronounced outcomes for women

5. GENDER The vulnerability of women may be explained by a wide range of factors women typically have lower body weight, smaller liver capacity to metabolize alcohol, and a higher proportion of body fat, which together contribute to women achieving higher blood alcohol concentrations than men for the same amount of alcohol intake. Women are also affected by interpersonal violence and risky sexual behaviour as a result of the drinking problems and drinking behaviour of male partners Alcohol use has been shown to be a risk factor for breast cancer Also many societies hold more negative attitudes towards women’s drinking alcohol than men’s drinking, and especially towards their harmful drinking which, depending on the cultural context, may increase women’s vulnerability to social harm. Finally, women who drink during pregnancy may increase the risk of fetal alcohol spectrum disorder (FASD)

6. FAMILIAL VULNERABILITY A family history of alcohol use disorders is considered a major vulnerability factor for both genetic and environmental reasons Multiple genes influence alcohol use initiation, metabolism and reinforcing properties in different ways, contributing to the increased susceptibility to psychoactive and dependence-producing properties of alcohol in vulnerable groups Heavy drinking by parents affects family functioning, the parent–child relationship and parenting practices, which in turn affects child development adversely

7. SOCIO-ECONOMIC FACTORS There are more drinkers, more drinking occasions and more drinkers with low-risk drinking patterns in higher socioeconomic groups, while abstainers are more common in the poorest social groups. However people with lower socioeconomic status (SES) appear to be more vulnerable to tangible problems and consequences of alcohol consumption

8. HARMFUL ALCOHOL USE Harmful use of alcohol is defined as a pattern of alcohol use that is causing physical or mental damage to health. Alcohol dependence is a cluster of behavioural, cognitive, and physiological phenomena that develop after repeated alcohol use that typically include: a strong desire to consume alcohol, difficulties in controlling its use, persisting in its use despite harmful consequences, a higher priority given to alcohol use than to other activities and obligations, increased tolerance, and sometimes a physiological withdrawal state

9. IDENTIFYING RISKY DRINKING IN PRIMARY CARE routine screening various screening tools available - AUDIT, ASSIST, DAST

10. SCREENING FOR A.U.D Screening for alcohol consumption among patients in primary care carries many potential benefits. It provides an opportunity to educate patients about low-risk consumption levels and the risks of excessive alcohol use. Information about the amount and frequency of alcohol consumption may inform the diagnosis of the patient's presenting condition alert clinicians to the need to advise patients whose alcohol consumption might adversely affect their use of medications and other aspects of their treatment. Screening also offers the opportunity to take preventative measures that have proven effective in reducing alcohol-related risks.

11. DSM 5 CRITERIA FOR A.U.D Alcohol is taken in larger amounts or over a longer period than was intended Persistent desire or unsuccessful efforts to cut down or control alcohol use. A great deal of time is spent in activities to obtain, use or recover from effects of alcohol Craving, or a strong desire or urge to use alcohol Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home.

12. DSM 5 CRITERIA FOR A.U.D Continued alcohol use despite having persistent /recurrent social problems caused or exacerbated by the effects of alcohol. Important social, occupational, or recreational activities are given up or reduced because of alcohol use Recurrent alcohol use in situations in which it is physically hazardous Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol Tolerance and Withdrawal

13. A.U.D SEVERITY The presence of at least 2 of these symptoms indicates an Alcohol Use Disorder (AUD). The severity of the AUD is defined as: Mild - The presence of 2 to 3 symptoms Moderate - The presence of 4 to 5 symptoms Severe - The presence of 6 or more symptoms

14. Investigations AST, ALT Gamma Glutamyl Transferase Carbohydrate deficient transferrin MCV

15. Short term effects of Alcohol Enters the bloodstream quickly through small intestine Metabolized by the liver slowly at 1 ounce of 100 proof per hour Effects vary by concentration Concentration varies by gender, height, weight, liver efficiency, food in stomach Size of drink defined by alcohol content 12 oz. glass of beer, 5 oz. glass of wine, and 1.5 oz. of hard liquor are equal in alcohol content Interacts with several neural systems Stimulates GABA receptors Reduces tension Increases dopamine and serotonin Produces pleasurable effects Inhibits glutamate receptors Produces cognitive difficulties (e.g., slowed thinking, memory loss) Effect of ingesting large amounts (intoxication) Significant motor impairment Poor decision making Poor awareness of errors made

16. Alcohol and the Brain Alcohol use affects the two major neurotransmitters, GABA and glutamate. GABA ( у -aminobutyric acid) is the main inhibitory neurotransmitter causing a calming or sedative effect. Alcohol takes over this function causing increased sedation. Glutamate is an excitatory (NMDA) neurotransmitter which increases brain activity and energy levels. Alcohol suppresses the release of glutamate, causing increased sedation With chronic use, there is downregulation of GABA activity and up regulation of glutamate receptors.

17. Pathophysiology of alcohol withdrawal With cessation of alcohol use: Neurons are taking in larger amounts of excitatory glutamate. the excess glutamate causes brain hyperexcitability seen as: anxiety, HTN, tremors, insomnia, irritability, hallucinations, palpitations, diaphoresis, headache, and GI upset. The symptoms will vary depending on the amount of alcohol intake and recent drinking habits.

18. Symptoms of AWS Symptoms Time from cessation of alcohol Minor: insomnia, tremors, GI upset 6 – 12 hours Visual/auditory/ttactile hallucinations 12 – 24 hours Withdrawal seizures 24 – 48 hours Delirium Tremens 48 – 72 hours

19. Complications of alcohol withdrawal Seizures – 70% risk of recurrence of seizures with each consecutive time a patient withdraws Delirium tremens - Severe mental and neurological changes, including psychosis and seizures typically occurring within 72 hours after the last drink of alcohol. History of daily heavy alcohol use, previous DTs or withdrawal seizures, older age, abnormal liver function, and more severe withdrawal symptoms on admission is at higher risk for developing DTs.

20. Risk factors for sever AWS Previous episodes of alcohol withdrawal Previous alcohol withdrawal seizures History of delirium tremens History of alcohol rehabilitation treatment Previous episodes of blackouts Concomitant use of CNS-depressant agents or illicit drugs Recent alcohol intoxication Blood Alcohol Level > 200mg/dL Evidence of increased autonomic activity

21. Long term effects of Alcohol Malnutrition Calories from alcohol lack nutrients Alcohol interferes with digestion and absorption of vitamins from food Deficiency of B-complex vitamins causes Amnestic syndrome Severe loss of memory for both long-and-short-term information Cirrhosis of the liver Liver cells engorged with fat and protein, impeding functioning Cells die, triggering scar tissue which obstructs blood flow Damage to endocrine glands and pancreas Heart failure Erectile dysfunction Hypertension Stroke Capillary hemorrhages - Facial swelling and redness, especially in nose Destruction of brain cells - Especially areas important to memory

22. INTERVENTIONS FOR ALCOHOL USE DISORDERS treatment is administered with the goal of allowing the affected individual to resume normal functioning. the most successful approaches include brief interventions and motivational enhancement, followed by pharmacotherapy and skills therapy.

23. MEDICAL MANAGEMENT FOR WITHDRAWAL Withdrawal consists of a cluster of symptoms developing within 1–3 days after the last drink. In the mild form of the syndrome tremor, hyperactivity, anxiety, tachycardia, sweating and sleep disturbances are seen. Without treatment, patients may develop more severe symptoms like hallucinations, seizures and delirium tremens, which is a potentially lethal condition with a mortality rate of 1–5% Adequate treatment of AWS is important for the adherence of patients with addictions to treatment as patients' fear of getting symptoms can be an obstacle to seeking alcohol treatment Detoxification can be done on an out-patient or in-patient setting depending on the severity of the symptoms

24. DETOXIFICATION benzodiazepines can prevent seizures and delirium tremens - diazepam, lorazepam and chlordiazepoxide They increase GABA activity and produce an inhibitory effect In general, long-acting benzodiazepines with active metabolites seem to result in a smoother course with less chance of recurrent withdrawal or seizures. Lorazepam or oxazepam is preferred for the treatment of patients with advanced cirrhosis or acute alcoholic hepatitis. The shorter half-life of lorazepam and the absence of active metabolites with oxazepam may prevent prolonged effects if oversedation occurs. symptom triggered therapy is preferred as it shortens duration of detox.

25. SYMPTOM TRIGGERED MEDICATION With this method patients with overt or suspected alcohol withdrawal are objectively assessed for presence of significant withdrawal at regular intervals. Severity of withdrawal is assessed using a standardised CIWA Scale found to have significant withdrawal (CIWA =10), the patient is given a stat dose of a benzodiazepine (diazepam 20mg). This procedure of standardised assessment and treatment is repeated every ninety minutes until the patient is no longer in withdrawal and detoxification is complete when there are 3 consecutive CIWA scores less than 10

26. FIXED DOSE REGIMENS Symptom triggered medications require repeated observation and may be inappropriate where there is staff shortage Fixed dose regimens give tapering doses of benzodiazepines over a period of 10 days

27. THIAMINE REPLACEMENT Wernicke-Korsakoff Syndrome (WKS) is a degenerative neurological syndrome of Vitamin B1 deficiency. 100mg Thiamine for prophalaxis against Wernicke-Korsakoff Syndrome should be given to all alcohol dependant in-patients intravenously once daily for 3 days. It should be diluted in 100ml saline or dextrose (infused over 30 minutes). In patients with signs of possible WKS, (ie acute delirium, ataxia, gaze palsy, nystagmus), give thiamine three times daily and continue for as long as symptoms are improving.

28. ADJUNCTIVE AGENTS Haloperidol can be used to treat agitation and hallucinations. Atenolol in conjunction with oxazepam has been shown to improve vital signs more quickly and to reduce alcohol craving more effectively than the use of oxazepam alone Adjunctive treatment with a beta blocker should be considered in patients with coronary artery disease, who may not tolerate the strain that alcohol withdrawal can place on the cardiovascular system. Clonidine also has been shown to improve the autonomic symptoms of withdrawal. Naltrexone 50mg-100mg daily improves abstinence in motivated patients Disulfiram as an aversive agent also helps patients remain abstinent

29. Anti- craving medications Naltrexone Acamprosate Mechanism of Action Mu-opioid receptor antagonist Glutamate receptor modulator Indication Alcohol use disorder Opioid use disorder Alcohol use disorder Clinical Evidence Reduced likelihood of return to any and heavy drinking; Fewer drinking days overall; Reduced subjective experience of “craving” Decreased likelihood of returning to drinking after achieving abstinence; Fewer drinking days Pre-treatment Workup Check hepatic function Measure serum creatinine Dosing Oral tablet: 50mg PO daily for most; up to 100mg daily for some 25 mg PO daily then 50mg PO daily for women due to potential GI side effects 666mg PO TID

30. Disulfiram Mechanism of Action Inhibitor of aldehyde dehydrogenase When the patient consumes alcohol while taking disufiram, the accumulation of acetaldehyde causes a physical response such as tachycardia, flushing, headache, nausea, and vomiting Pre-treatment Workup ECG, physical exam, hepatic function Dosing First dose 12 hours after the last drink; 500mg PO each morning for 1-2 weeks, then 250mg PO each morning Recommend involving a family or roommate as an observer of daily medication adherence Physical reaction can be precipitated by alcohol containing products (e.g., cold medicine, mouthwashes) and certain medications (e.g., sertraline oral concentrate, metronidazole, ritonavir)

31. Non-pharmacological treatment Motivational interviewing Cognitive behavioural therapy Peer support groups e.g. Alcoholics Anonymous

32. PSYCHIATRIC ILLNESS ASSOCIATED WITH ALCOHOL USE depression anxiety HIV/AIDS and TB Multiple drug use

33. SUBSTANCE USE

34. 10 classes of substances Alcohol Caffeine Cannabis Hallucinogens Inhalants Opioids Sedatives, Hypnotics and anxiolytics Stimulants Tobacco Other

35. Substance Related disorders Divided into 2: Substance use disorders Substance induced disorders e.g. Symptoms occur only when in Intoxication, withdrawal

36. Substance Use Disorders Cognitive, behavioural and physiological symptoms indicating continued use despite significant substance related disorders. Underlying changes to the brain circuits may persist beyond detoxification resulting in repeated relapses.

37. S.U.D Criteria Impaired control over substance use is the theme of criteria 1- 4. Substance use in larger amounts or over longer period than intended Persistent desire to cut down or regulate substance use and may have multiple failed attempts to discontinue Much time spent procuring, using or recovering from the substance Uncontrollable cravings (a prognostic indicator of imminent relapse) Social impairment is the theme of criteria 5 – 7. Recurrent failure to fulfill major role obligations Continued use despite persistent social or interpersonal problems caused or exacerbated by substance use Important social, occupational or recreational activities may be given up because of substance use

38. SUD Criteria continued Risky use of substance use is the theme of criteria 8 - 9 Recurrent use of substances In physically hazardous conditions Continued use despite knowledge of having a persistent physical or mental problem caused or worsened by substance use i.e failure to abstain despite the problems it is causing . Pharmacological criteria are the theme of 10 and 11(not required for a Dx of SUD) Tolerance - requiring markedly increased dose of substance to achieve the desired effect (history + lab tests can assist) Withdrawal – a syndrome that occurs as blood or tissue concentrations of a substance decline in an individ

39. Tobacco Use Disorder Nicotine Addicting agent of tobacco Stimulates dopamine neurons in mesolimbic area Involved in reinforcing effect 18% prevalence Smoking is among the most preventable causes of premature death Lung cancer is most common cancer 87% caused by smoking Cigarettes also cause or exacerbate: Emphysema, cancers of larynx, esophagus, pancreas, bladder, cervix, stomach, cardiovascular disease Sudden infant death syndrome and pregnancy complications

40. Marijuana Drug derived from dried and ground leaves and stems of the female hemp plant ( Cannabis sativa ) Hashish Stronger than marijuana Produced by drying the resin exudate of the tops of plants In DSM-5, called Cannabis use disorder Most frequently used illicit drug Greater use by men than women Rates of daily use are on the rise May be related to varying degrees of legal status

41. Effects of Marijuana Major active ingredient THC (delta-9-tetrahydrocannabinol) Psychological Feelings of relaxation and sociability Rapid shifts of emotion Interferes with attention, memory, and thinking Decline in IQ over time Heavy doses can induce hallucinations and panic Difficult to regulate dosage Effects take 30 minutes to appear Smoke more than intended waiting for effects Interfere with cognitive functioning Impairs memory, complex motor skills Physiological Bloodshot and itchy eyes Dry mouth and throat Increased appetite Reduced pressure within the eye Increased BP Damage to lung structure and function in long-term users

42. Marijuana and the Brain Two cannabinoid brain receptors CB1 and CB2 High concentration in hippocampus Increased blood flow to emotion regions Amygdala and anterior cingulate Habitual use leads to tolerance Withdrawal symptoms also observed

43. Therapeutic Effects of Marijuana Reduces nausea and loss of appetite caused by chemotherapy Relieves discomfort of AIDS, chronic pain

44. Opiate Use Disorder Group of addictive sedatives that in moderate doses relieve pain and induce sleep Opium Morphine Heroin- Estimated over half a million individuals addicted to heroin in U.S contributing 62 to 82% of drug-related hospital admissions Codeine Opiates legally prescribed as pain medications include: Hydrocodone , Oxycodone the basis for OxyContin, 6.8 million pain meds users for nonmedical purposes

45. Psychological and Physical Effects of Opiates Produce euphoria, drowsiness, and lack of coordination Loss of inhibition, increased self-confidence Severe letdown after about 4 to 6 hours Heroin and OxyContin Rush Intense feelings of warmth and ecstasy following injection Stimulate receptors of the body’s opioid system Stimulate nucleus accumbens Tolerance develops and withdrawal occurs Muscle soreness and twitching, tearfulness, yawning Become more severe and also include cramps, chills/sweating, increase in HR and BP, insomnia, and vomiting Withdrawal lasts about 72 hours

46. Psychological and Physical Effects of Opiates 29-year follow-up of 500 heroin addicts 28% dead by age 40 Half by suicide, homicide, or accident One-third by overdose Many users resort to illegal activities to obtain money for drugs Theft, prostitution, dealing drugs Exposure to infectious diseases via shared needles e.g., HIV Evidence suggests that free needles reduce infectious diseases associated with IV drug use

47. Stimulants: Amphetamines Increase alertness and motor activity; reduce fatigue Amphetamines Trigger release and block reuptake of norepinephrine and dopamine Produce high levels of energy, sleeplessness Reduce appetite, increase HR, constrict blood vessels in skin and mucous membranes High doses can lead to: Nervousness, agitation, irritability, confusion, paranoia, hostility Tolerance can develop after only 6 days’ use

48. Stimulants: Methamphetamine Methamphetamine (aka crystal meth) Amphetamine derivative Can be taken orally, intravenously, or intranasally (snorting) Chronic use damages brain Impacts dopamine and serotonin systems Reduction in hippocampus volume

49. Stimulants: Cocaine Crack Form of cocaine that quickly become popular in the ’80s Rock crystal that is heated, melted, and smoked Cheaper than cocaine Alkaloid obtained from coca leaves Reduces pain Produces euphoria Heightens sexual desire Increases self-confidence and indefatigability Blocks reuptake of dopamine in mesolimbic areas of brain Overdose: Chills, nausea, insomnia, paranoia, hallucinations; possibly heart attack and death Not all users develop tolerance Some become more sensitive May increase risk of OD

50. Hallucinogens, Ecstasy, and PCP LSD d -lysergic acid diethylamide Hallucinogen effects include : Colorful visual hallucinations Psychedelic trip: expansion of consciousness Only 1-2% regular users African Americans less likely to use than others Flashbacks Hallucinogen persisting perception disorder (HPPD) Most common during stress Other hallucinogens: Mescaline Active ingredient of peyote Psilocybin Extracted from mushroom psilocybe mexicana Ecstasy (MDMA) and Molly Methylenedioxymethamphetamine Increase feelings of intimacy and enhances mood Increases muscle tension, nausea, anxiety, and depression Chemically similar to mescaline and amphetamines Acts on serotonin PCP (phencyclidine) Angel dust Animal tranquilizer Causes severe paranoia and violence

51. Process of Becoming a Drug Abuser

52. Etiology of Substance-Related Disorders: Genetic Factors Relatives and children of problem drinkers have higher-than-expected rates of alcohol abuse or dependence Greater concordance in MZ than DZ twins Ability to tolerate large quantities of alcohol may be an inherited diathesis Asians have low rates of alcohol abuse Deficient enzymes (ADH or alcohol dehydrogenases) Genes and smoking People with SLC6AS less likely to smoke and more likely to quit Smokers with defect in CYP2A6 gene less likely to become dependent

53. Etiology of Substance-Related Disorders: Neurobiological Factors Nearly all drugs, including alcohol, stimulate the dopamine system in the brain, particularly the mesolimbic pathway Produce rewarding or pleasurable feelings Some evidence that people dependent on drugs or alcohol have a deficiency in the dopamine receptor DRD2 Vulnerability in the dopamine system leads to substance use or substance use leads to dopamine system problems People take drugs to avoid the bad feelings associated with withdrawal Explains frequency of relapse Incentive-sensitization theory Distinguish Wanting (craving for drug) from Liking (pleasure obtained by taking the drug) Dopamine system becomes sensitive to the drug and the cues associated with drug (e.g., needles, rolling papers, etc.) Sensitivity to cues induces and strengthens wanting Brain imaging studies show that cues for a drug (needle or a cigarette) activate the reward and pleasure areas of the brain involved in drug use

54. Etiology of Substance-Use Disorders: Psychological Factors Mood alteration Crying in one’s beer Expectancies about drug effects People who expect alcohol to reduce stress and anxiety are most likely to drink Drinking and positive expectancies influence each other positively Genetic and shared environmental risk factors interact

55. Etiology of Substance-Use Disorders: Personality Personality factors that predict onset of substance-related disorders: Negative emotionality or negative affect Desire for increased arousal and positive affect Kindergarten children who were rated high in anxiety and novelty seeking more likely to get drunk, smoke, and use drugs in adolescence

56. Etiology of Substance-Use Disorders: Sociocultural Factors Men consume more alcohol than women but differences vary by country Availability Usage is higher when alcohol and drugs are easily available

57. Etiology of Substance-Use Disorders: Sociocultural Factors Family factors Parental alcohol use Marital discord, psychiatric or legal problems in the family linked to substance use Lack of emotional support from parents increases use of cigarettes, marijuana, and alcohol Lack of parental monitoring linked to higher drug usage

58. Etiology of Substance-Related Disorders: Sociocultural Factors Social network Having peers who drink influences drinking behavior ( social influence) but individuals also choose friends with drinking patterns similar to their own ( social selection) Advertising and media Countries that ban ads have 16% less consumption than those that don’t

59. Treatment of Substance Use Disorders: Alcohol Use Disorders Couples therapy Found to be more effective than individual treatment approaches Cognitive and behavioral treatments Contingency-management therapy Patient and family reinforce behaviors inconsistent with drinking e.g., avoiding places associated with drinking Teach problem drinker how to deal with uncomfortable situations e.g., refusing the offer of a drink Relapse prevention Strategies to prevent relapse Motivational interveiwing

60. Treatment of Substance Use Disorders: Nicotine Dependence Peer behavior important If others in social network stop smoking, increases likelihood that individual will also stop Physician’s advice By age 65, most smokers have quit Scheduled smoking Reduce nicotine intake gradually over a few weeks Nicotine replacement treatments Gum, patches, or inhalers Reduce craving for nicotine Combining patch with antidepressants (Wellbutrin) improved success rate

61. Treatment of Drug Use Disorders Motivational interviewing or enhancement therapy Self-help residential homes Non-drug environment Group therapy Guidance and support from former users

62. Treatment of Drug Use Disorders: Drug Replacement Treatments and Medications Heroin substitutes Synthetic narcotics Methadone, buprenophine Used to wean heroin users from dependence Opiate antagonists Naltrexone Prevents feeling high

63. Prevention of Substance-Use Disorders Often aimed at adolescents Utilize some or all of the following elements: Enhancing self-esteem Social skills training Peer pressure resistance training Parental involvement in school programs Warning labels on alcohol bottles Education regarding alcohol impairment Testing for drugs and alcohol at school or work Correction of beliefs and expectations Inoculation against mass media messages Peer leadership