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Alcohol use disorder


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Academic base harrisons 19th edition

Published in: Health & Medicine
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Alcohol use disorder

  2. 2. greater than three standard drinks per day enhances the risk for cancer and vascular disease, and alcohol use disorders decrease the life span by about 10 years 2 .
  3. 3. ROUND FIGURES A standard drink is 10–12 g as seen in 1. 340 mL of beer 2. 115 mL of wine 3. 43 mL of whisky 0.5 L (1 pint) of 80-proof beverage contains ~160 g of ethanol (about 16 standard drinks), and 750 mL of wine contains ~60 g of ethanol. Congeners include methanol, butanol, acetalde-hyde, histamine, tannins, iron, and lead 3
  4. 4. METABOLISM OF ALCOHOL Absorbed from 1. Mucous membranes of mouth & esophagus (in small amounts) 2. Stomach and large bowel (in modest amounts) 3. Proximal portion of the small intestine (the major site). The rate of absorption is increased by 1. Rapid gastric emptying (as seen with carbonation) 2. Absence of proteins, fats or carbohydrates (which interfere with absorption) 3. Dilution to a modest percentage of ethanol (maximum at ~20% by volume). 4
  5. 5. METABOLISM OF ALCOHOL 1. Ethanol is excreted directly through the lungs, urine, or sweat 2. Most of it metabolized to acetaldehyde, in liver. 3. The most important pathway occurs in the cell cytosol where alcohol dehydrogenase (ADH) produces acetaldehyde, 4. which is then rapidly destroyed by aldehyde dehydrogenase (ALDH) in the cytosol and mitochondria 5
  6. 6. A second pathway occurs in the microsomes of the smooth endoplasmic reticulum (microsomal ethanol-oxidizing system i.e. MEOS) It is responsible for ≥10% of ethanol oxidation at high blood alcohol concentrations 6
  8. 8. 1. Although a drink contains ~300 kJ, or 70–100 kcal 2. These are devoid of minerals, proteins, and vitamins. 3. In addition, alcohol interferes with: • Absorption of vitamins in the small intestine and • Decreases their storage in the liver E.g. Folate (folacin or folic acid), Pyridoxine (B6), Thiamine (B1), Nicotinic acid (niacin, B3) Vitamin A 8
  9. 9. ALCOHOLIC KETOACIDOSIS Heavy drinking in a fasting, can produce transient hypoglycemia within 6–36 h, because ethanol inhibits hepatic gluconeogenesis Alcohol ketoacidosisc (AKA) d/t decrease in fatty acid oxidation + poor diet or recurrent vomiting, can be misdiagnosed as diabetic ketosis. AKA: 1. patients show an increase in serum ketones along with a mild increased glucose but a large anion gap, a mild to moderate increase in serum lactate. 2. β-hydroxybutyrate/lactate ratio of between 2:1 and 9:1 (with normal being 1:1). 9
  10. 10. NEUROTRANSMITTER CHANGES Alcohol affects almost all neurotransmitter systems. Boosting GABA activity, especially at GABA-A receptors. Enhancement of chloride channel system Anticonvulsant, sleep-inducing, antianxiety, and muscle relaxation effects of all GABA-boosting drugs. 1. Acutely administered  produces a release of GABA, and 2. Continued Alcohol use  increases density of GABA A receptors 3. Withdrawal states  decreased GABA activity.. 10
  11. 11. Acute alcoholism  Inhibit postsynaptic NMDA (N-methyl-d- aspartate) excitatory glutamate receptors Chronic drinking  upregulate NMDA excitatory receptors. The relationships between greater GABA and diminished NMDA receptor activity during acute intoxication and diminished GABA with enhanced NMDA actions during alcohol withdrawal explain intoxication and withdrawal phenomena. 11
  12. 12. Alcohol acutely increases dopamine levels in the ventral tegmentum and related brain regions, and this effect plays an important role in continued alcohol use, craving, and relapse. The changes in dopamine also increases “stress hormones” including cortisol & ACTH during intoxication and withdrawal. Such alterations contribute to both feelings of reward during intoxication & depression during falling blood alcohol concentrations. 12
  13. 13. BEHAVIORAL EFFECTS, TOLERANCE & WITHDRAWAL “Legal intoxication” with alcohol requires a blood alcohol concentration of 0.08 g/dL 1. Behavioral, psychomotor, cognitive changes are seen at 0.02–0.04 g/dL (i.e. after one to two drinks) 2. Deep & disturbed sleep can be seen at 0.04 – 0.08g/dl. 3. Death can occur with levels between 0.30 - 0.40 g/dL. 13
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  15. 15. ACQUIRED TOLERANCE Repeated use of alcohol Acquired tolerance iInvolve 3 compensatory mechanisms. (1) Metabolic tolerance After 1–2 weeks of daily drinking, up to 30% increase in the rate of hepatic ethanol metabolism (2) Cellular tolerance develops through neurochemical changes that maintains relatively normal physiologic functioning despite the presence of alcohol. Subsequent decreases in blood levels contribute to symptoms of withdrawal. (3) Behavioral tolerance Individuals learn to adapt their behavior so that they can function better than expected under influence of the drug (learned T.) 15 .
  16. 16. THE EFFECTS OF ETHANOL ON ORGAN SYSTEMS Low doses of alcohol (1 or 2 drinks / day) beneficial effects :- 1. Increasing high-density lipoprotein cholesterol 2. Decreasing aggregation of platelets 3. Resulting decrease in risk for occlusive coronary disease and embolic strokes. Red wine has potential health-promoting qualities at low doses due to flavinols and related substances. Modest drinking decrease risk for : vascular dementia & Alzheimer’s disease. 16
  17. 17. NERVOUS SYSTEM 1) Approximately 35% experience a blackout, an episode of temporary anterograde amnesia, in which the person forgets all or part of what occurred during a drinking evening. 2) disturbed sleep:- initially help a person fall asleep, it disrupts sleep. The stages of sleep are altered, Time spent in REM & deep sleep is reduced. 3) Alcohol relaxes muscles in the pharynx, which cause snoring and exacerbate sleep apnea; 75% of alcoholic men older than age 60. 4) impaired judgment & coordination 5) Hangover : headache, thirst, nausea, vomiting, and fatigue the following day 6) Brain atrophy, evident as ventricular enlargement and widened cortical sulci on MRI are usually reversible if abstinence is maintained. 17
  18. 18. PSYCHIATRIC 1. Impulsivity and disinhibition 2. Intense sadness lasting for days to weeks 3. Severe anxiety 4. Auditory hallucina-tions and/or paranoid delusions 18
  19. 19. GIT 1. Inflammation of esophagus & stomach causing epigastric distress and gastrointestinal bleeding, hemorrhagic gastritis. 2. Violent vomiting :-- Mallory-Weiss lesion 3. Acute pancreatitis (~25 per 1000 per year)  3 fold higher in alcoholics 4. Alcohol impairs gluconeogenesis in the liver, increased lactate production, and decreased oxidation of fatty acids. This L/T fat accumulation in liver cells. 5. With repeated exposure to ethanol, causes alcohol- induced hepatitis, perivenular sclerosis, and cirrhosis 6. Vulnerability to infections 19
  20. 20. HEMATOPOIETIC SYSTEM 1. Increase in red blood cell size MCV 2. If folic acid deficiency, there can also be • Hyper segmented neutrophils • Reticulo cytopenia • Hyperplastic bone marrow 20
  21. 21. CVS decreases myocardial contractility peripheral vasodilation Resulting mild decrease in blood pressure and a compensatory increase in cardiac output. Cardiac oxygen consumption is higher. Dose-dependent increase in blood pressure, which normalised within weeks of abstinence. Chronic heavy drinkers have 6 fold increased risk for CAD & cardiomyopathy. 21
  22. 22. CVS Symptoms : 1. Unexplained arrhythmias in the presence of left ventricular impairment 2. Heart failure 3. Dilation of all four heart chambers with associated mural thrombi and mitral valve regurgitation. Atrial or ventricular arrhythmias, especially paroxysmal tachycardia, temporarily after heavy drinking with no other evidence of heart disease— known as the “holiday heart” 22
  23. 23. GENITOURINARY SYSTEM CHANGES, SEXUAL FUNCTIONING, AND FETAL DEVELOPMENT 1. Affect normal sexual development & reproductive onset. 2. At any age, modest ethanol doses (e.g. 0.06 g/dL) can increase sexual drive but decrease erectile capacity in men 3. Irreversible testicular atrophy & shrinkage of the seminiferous tubules, decreases in ejaculate volume & lowers sperm count 4. Women  amenorrhea, a decrease in ovarian size, infertility, & spontaneous abortion. 23
  24. 24. Heavy drinking during pregnancy  rapid placental transfer of both ethanol and acetaldehyde Fetal alcohol syndrome (FAS) ~5% 1. facial changes with 1. epicanthal eye folds 2. poorly formed ear concha 3. small teeth with faulty enamel 2. Cardiac : atrial or ventricular septal defects 3. Aberrant palmar crease 4. Limitation in joint movement 5. Microcephaly with mental retardation. 24
  25. 25. OTHER EFFECTS Skeletal muscle weakness i.e. acute alcoholic myopathy improves with abstinence. Effects on skeletal system :-- 1. Changes in calcium metabolism, lower bone density, and decreased growth in epiphyses 2. Increased risk for fractures and osteonecrosis femoral head 25
  26. 26. ALCOHOL USE DISORDER • Alcohol use disorder is defined as 1. Repeated alcohol-related difficulties 2. In at least 2 of 11 life areas 3. That cluster together in the same12-month period • Criterias were taken directly from the 7 dependence and 4 abuse criteria in DSM-IV • The lifetime risk is about 10–15% for men and 5–8% for women • Severity of an alcohol use disorder 1. Mild - two or three items 2. Moderate - four or five 3. Severe - six or more 26
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  28. 28. TREATMENT The approach to treating alcohol-related conditions is relatively straightforward: (1) recognize that at least 20% of all patients have an alcohol use disorder; (2) learn how to identify and treat acute alcohol-related conditions; (3) know how to help patients begin to address their alcohol problems; and (4) know enough about treating alcoholism to appropriately refer patients for additional help. 28
  29. 29. IDENTIFICATION OF THE ALCOHOLIC by asking questions about alcohol problems & noting laboratory test results. The two blood tests with ≥60% sensitivity and specificity for heavy alcohol consumption are 1. γ-glutamyl transferase (GGT) (>35 U) and 2. Carbohydrate deficient transferrin (CDT) (>20 U/L or >2.6%) Other useful blood tests high-normal : MCVs (≥91 μm3) & uric acid (>416 mol/L, or 7 mg/dL). 29
  30. 30. 30
  31. 31. TREATMENT : ALCOHOL-RELATED CONDITIONS ACUTE INTOXICATION Assess vital signs Manage respiratory depression Cardiac arrhythmias or Blood pressure instability Aggressive behavior T/t : reassurance & low doses of a short- acting benzodiazepine such as lorazepam (e.g., 1–2 mg PO or IV) & repeated as needed. An alternative approach : antipsychotic (e.g., 0.5–5 mg of haloperidol PO or IM every 4–8 h as needed, or olanzapine 2.5– 10 mg IM repeated at 2 and 6 h, if needed). 31
  32. 32. INTERVENTION Two main elements : motivational interviewing and brief interventions. 1. Motivational interviewing:- clinician helps patient to think through the assets (e.g., comfort in social situations) & liabilities (e.g., health- and interpersonal-related problems) of the current pattern of drinking, helping to weigh options & encouraging the patient to take responsibility for needed changes. 2. Brief intervention:- summarized as FRAMES: 32
  33. 33. BRIEF INYTERVENTION FRAMES Feedback to the patient Responsibility to be taken by patient Advice, on what needs to be done Menus of options that might be considered; Empathy for understanding patient’s thoughts and feelings & Self-efficacy, i.e., offering support for the capacity of the patient to make changes. 33
  34. 34. INTERVENTION Once the patient begins to consider change, the emphasis shifts to brief interventions. Discussions focus on 1. consequences of high alcohol consumption 2. approaches to stopping drinking 3. help in recognizing and avoiding situations likely to lead to heavy drinking. carried out in 15-min sessions, multiple meetings to explain the problem, discuss optimal treatments and explain the benefits of abstinence 34
  35. 35. ALCOHOL WITHDRAWAL If the patient stop drinking, can produce withdrawal symptoms. Features include 1. Tremor of the hands (shakes) 2. agitation and anxiety 3. autonomic nervous system overactivity (increase in pulse, respiratory rate, sweating, and body temperature; and insomnia.) Symptoms 1. begin within 5–10 h of decreasing ethanol intake, 2. peak on day 2 or 3, and 3. improve by day 4 or 5 4. may persist for 4–6 months (protracted abstinence Syndrome) 35
  36. 36. About 2% of alcoholics experience a withdrawal seizure & similar rate of delirium tremens mental confusion, Agitation fluctuating levels of consciousness associated with tremor and autonomic overactivity 36
  37. 37. PHYSICAL EXAMINATION IN ALL ALCOHOLICS 1. Search for evidence of liver failure 2. Gastrointestinal bleeding 3. Cardiac arrhythmia 4. Infection 5. Glucose or electrolyte imbalances.  Adequate nutrition and oral multiple B vitamins  50–100 mg thiamine daily for a week or more 37
  38. 38. 1. Rapid removal of alcohol 2. Administer depressant in doses that decrease symptoms (e.g., a rapid pulse and tremor) and then tapering the dose over 3–5 days. 3. Benzodiazepines have the highest margin of safety and lowest cost 4. Short-half-life benzodiazepines for patients with serious liver impairment / significant brain damage, given every 4 h to avoid risk for seizures. 5. use drugs with longer half-lives 1. Chlordiazepoxide 25–50 mg or 2. Diazepam 10mg given PO every 4–6 h on the first day doses then decreased over the next 5 days. 38
  39. 39. TREATMENT OF DELERIUM TREMENS 1. Challenging & Likely to run a course of 3–5 days regardless of the therapy 2. High dose benzodiazepine max 800 mg/d of chlordiazepoxide has been given. 3. Use of antipsychotics E.g. haloperidol or olanzapine • Antipsychotics are less likely to exacerbate confusion but may increase risk of seizure • they have no role in treatnig mild withdrawal symptoms. • Little evidence anticonvulsants such as phenytoin or gabapentin are more effective in drug-withdrawal seizures 39
  40. 40. REHABILITATION OF ALCOHOLICS ≥60% of alcoholics, maintain abstinence for at least a year, and many achieve lifetime. The core of treatment Cognitive-behavioral approaches motivation toward abstinence Instructing family members to stop protecting the patient from problems caused by alcohol. try self-help groups as Alcoholics Anonymous (AA) to help them to learn how to deal with life’s stresses 40
  41. 41. RELAPSE PREVENTION helps the patient identify situations in which a return to drinking is likely formulate ways of managing these risks develop coping strategies that increase the chances of a return to abstinence if a slip occurs. Counseling focuses on improving functioning in the absence of alcohol Helping to manage free time without alcohol Develop a nondrinking peer group & handle stresses. 41
  42. 42. INSOMNIA Teach elements of “sleep hygiene” :- Maintaining consistent schedules for bedtime and awakening. Sedating antidepressants (e.g., trazodone); not be used because they interfere with cognitive functioning & disturb the normal sleep architecture. 42
  43. 43. MEDICATIONS FOR REHABILITATION 1. Naltrexone(Opioid antagonist) 50–150 mg/d orally  shorten relapses, oral form or as once per month 380-mg injection MOA: By blocking opioid receptors, decreases dopaminergic activity in the ventral tegmental reward system & decreases pleasure . 2. Acamprosate ~2 g/d divided into three oral doses : similar effects MOA: inhibits NMDA receptors, decreasing symptoms of withdrawal. 3. Disulfiram (ALDH inhibitor) 250 mg/d : produces vomiting and autonomic nervous system instability with alcohol. Can be dangerous in patients with heart disease, stroke, diabetes mellitus or hypertension. S/E:- depression, psychotic symptoms, peripheral neuropathy, and liver damage 43
  44. 44. OTHER DRUGS 1. Opioid antagonist - nalmefene 2. Nicotinic receptor agonist - varenicline, 3. Serotonin antagonist - ondansetron 4. α-adrenergic agonist - prazosin 5. GABAB receptor agonist - baclofen 6. Anticonvulsant - topiramate 7. Cannabinol receptor antagonists 44
  45. 45. THANK YOU 45