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Alcohol class
- 1.
- 2. Alcohols are hydroxyderivatives of aliphatic hydrocarbons Ethyl Alcohol (Ethanol) Methyl Alcohol (Methanol)
- 3. How Manufactured ? •Fermentation – Sugar to Alcohol and Carbon dioxide C6H12O6→ 2(CH3-CH2-OH) + 2CO2 (Yeasts +sugar + water = CO2 + ethanol) • Yeasts are living micro-organisms which die in concentrations of alcohol greater than 10 to 15% Starch Maltose • Commercially - obtained from Mollases Convertase
- 4. Alcoholic Beverages MaltedLiquors: Fermentation of germinating cereals (malts) – mostly Barley – Beers (3-6%) Wines: fermentation of Natural Sugars – grapes, apples and other fruits No distillation, <15% Fortified (port) – up to 22% Champagne – 12-16% (effervescent wine) Spirits (Distilled after fermaentation) – Rum, Whisky, Brandy and Gin 40 - 55% v/v Standard 42.8% v/v or 37% w/w Sources: Whiskey - distilled grain Rum - distilled molasses Gin – any sugar source Brandy – Distilled wine (Grapes) Vodka – fermentation of any of grain, rye, wheat, potatoes, grapes, sugar beet or mollases
- 5. Alcohol – PercentageCalculations Alcohol content of beverages: specific gravity of alcohol is 79 Therefore, 1 litre alcohol weighs 790g Percent may be by weight or by volume By volume: 1 litre alcohol add 1 litre water = 50% (vol) By weight: 1 litre alcohol (790g), add 790g water = 50% (weight) 40% alcohol by weight = 50% by volume
- 6. 1litre water 1litre alcohol + = 2litres 50% (volume) 1 kilo water 1 kilo alcohol 2 kilos 50% (weight) + = 40% alcohol by weight = 50% by volume
- 7. Pharmacological actions of alcohol- Local 1. Rubefacient and counterirritant to skin 2. Irritant – soft skin and mucus membrane 3. Pain, inflammation and necrosis – injection 4. Astringent: Antiseptic (20 – 90%) 100% is dehydrating 5. No action on spores
- 8. Effects of alcoholconsumption - Acute CNS: Neuronal depressant – dose dependent manner Plasma concentration Expected effects 30 – 100 mg/dl Anxiolytic, euphoria and excitation, Hesitation, restraint, caution and self – critisim are lost Impaired coordination – mood and feelings are altered 100 -150 mg/dl Mental clouding, ataxia, disorganization of thought and impairment of memory and drowsiness 150 – 200 mg/dl Sloppy, ataxia and drunkenness - Slurring of speech, loss of judgment and inhibition 200 – 300 mg/dl Stupor and unconsciousness
- 9. Effects of alcoholconsumption (acute) - contd. Impaired performance, slowing of reflexes and fine discrimination impaired Induces sleep – but not ideal hypnotic Analgesic – but no ideal analgesic Anticonvulsant action – but not ideal anticonvulsant Mechanism: GABAA receptor mediated synaptic inhibition by chloride channel opening Inhibition of NMDA excitatory amino acid receptor Stimulates 5-HT3 receptors
- 10. Effects of alcoholconsumption (acute) - contd. CVS: Small doses – cutaneous vasodilatation, flushing Medium dose – tachycardia and mild rise in BP Large dose - Vasodilatation due to direct vascular smooth muscle dilatation and vasomotor centre depression (clinical implication) Respiration: Stimulation of Respiration – by irritation of pharyngeal and buccal mucosa Central action – depression Blood: Moderate drinking increases HDL-cholesterol level Decrease in LDL oxidation Anaemia (Folate Metabolism)
- 11. Effects of alcoholconsumption (acute) - contd. GIT: Dilute alcohol at low doses - stimulate GI secretion – flavour, aroma or direct action on gastrin secretion Higher doses inhibit GI secretion Acute consumption – pylorospasm, gastritis, vomiting, reflux etc Mallory-Weiss lesion
- 12. Effects of alcoholconsumption – (acute) - contd. Kidney: Diuresis – increased water ingestion and inhibition of ADH Uterus: Relaxation of uterine muscles Endocrine: Low dose – Adrenaline release and hyperglycemia High dose – Hypoglycemia Sex - Aphrodisiac
- 13. Rapidly absorbedfrom small intestine, and colon but slowly from stomach First pass metabolism in stomach and liver Maximal blood concentration within 30 to 90 minutes Can be absorbed through the lungs Can be absorbed through skin Absorption
- 14. Uniformly distributedthroughout tissues and body fluids Readily crosses placenta, to exposure fetus Crosses BBB readily Distribution Elimination Urinary Excretion Exhalation Metabolism
- 15. Metabolism I CH OH Ethanol H H C H H CH H H CO H = Acetaldehyde (ADH – Alcohol Dehydrogenase) ADH
- 16. Metabolism II CH H H C O H = Acetaldehyde (ALDH– Acetaldehyde Dehydrogenase) ALDH Acetate CH H H C O OH =
- 17. Metabolism III 80-90%Metabolized Also metabolized in small amounts by hepatic microsomal enzyme Rate is constant (not increased by concentrations in the blood) – zero order (8-12 ml/H of absolute alcohol) About 30 ml (1 oz) in 3 hours Concentration in exhaled air is 0.05% of blood concentration – used in medico legal purposes
- 18. Adverse Effects ofAlcohol Acute Effects Nausea, Vomiting, hangover and traffic accidents CNS Depressant Depression of inhibitory control Vasodilatation, warm, flushed, reddish skin Emotional outbursts Decreased memory & concentration Poor judgment Decreased reflexes Decreased sexual response
- 19. Adverse Effects ofAlcohol – contd. Acute Alcohol Intoxication: Estimated ED50: 150 mg/100 ml and LD50 = 500 mg/100ml Therapeutic index about 3.5 Hypotension, hypoglycemia, respiratory depression coma and death Death due to respiratory depression or inhaled vomit Treatment: Gastric lavage Endotracheal intubations Fluid and electrolyte balance Glucose infusion Thiamine injection 100 mg in 500 ml of glucose IV Haemodialysis
- 20. Toxic Effects -Chronic Alcoholism GIT: Gastritis and damage to the mucosa – anaemia Intestinal damage: Lack of absorption - Deficiency of water soluble vitamins and amino acids (protein deficiency) Less or no food intake (enough calorie) - Vitamin and Protein deficiency
- 21. Chronic Alcoholism –contd. Liver cirrhosis – scarring of liver Usually fatal if drinking is not stopped Fatty infiltration (excess in NADH) Oxidative stress and cellular necrosis Damage to hepatocytes and inflammation – aldehyde Glutathione depletion Microsomal enzyme induction
- 22. Chronic Alcoholism –contd. Neurological: Polyneuritis, pellagra, tremors, seizures, loss of brain mass, Korsakoff`s psychosis (Alcholic Dementia) CVS: Hypertension, cardiomyopathy, CHF arrhythmias and stroke Hormonal: Impotence, gynaecomastia and infertility Acute pancreatitis
- 23. Chronic Alcoholism –contd. Reproduction Alcohol is a teratogen, it causes birth defects. Fetal Alcohol Syndrome (FAS) or Fetal Alcohol Effects (FAE), or Alcohol-Related Birth Defects (ARBD) Symptoms include retardation, poor coordination, loss of muscle tone, low birth weight, slow growth, malformation of internal organs and peculiar facial characteristics
- 24. Fetal Alcohol Syndrome(FAS) Characteristics Growth retardation Facial malformations Small head Greatly reduce intelligence
- 25. • Craving: Astrong need, or compulsion, to drink • Loss of control: The inability to limit one’s drinking on any given occasion • Tolerance: The need to drink greater amounts of alcohol in order to “get high” – pharmacokinetic or cellular tolerance • Physical dependence: Withdrawal symptoms, such as nausea, sweating, shakiness, sleep impairment, hallucinations, delirium tremens and anxiety, occur when alcohol use is stopped after a period of heavy drinking • Withdrawal syndromes: long acting BZDs like chlordizepoxide and diazepam • Naltrexone (50 mg) Chronic Alcoholism - features
- 26. Ethanol – Usefulness: 1.Local: antiseptic, rubefacient and counterirritant in sparins and to prevent bedsores antiperspirant and aftershave Alcohol sponges – to reduce body temperature 2. Appetite stimulant and carminative: 30 – 60 ml of 7-10% 3. Neuralgias: severe cancer pain – injection round the nerve 4. Protection from cold 5. Alcohol may have a protective effect from heart attack 6. Methanol Poisoning
- 27. Disulfiram (Antabuse) Internationallymarketed as antabuse ALDH enzyme inhibitor Alcohol + disulfiram rise in concentration of aldehyde in blood and tissue distressing aldehyde syndrome Symptoms: flushing, burning sensation, throbbing headache, perspiration, dizziness, vomiting, visual disturbance, mental confusion, fainting and circulatory collapse Uses: aversion technique in chronic alcoholics: only to motivated persons Technique: abstain alcohol overnight and start with 1 gm on day 1 followed by 0.75 gm next day and 0.50 gm next day and so on. Effects start within few hrs of 1st dose and lasts for 2 weeks Mechanism: irreversible inhibition of ALDH and synthesis of new enzyme takes time and thus person resolves not to drink for distressing symptoms Available as 250 mg tablets
- 28. Ethanol as Antidote Methanol, Ethylene glycol, Diethylene glycol Methanol poisoning – toxicological importance – unscrupulous mixing with alcoholic beverages Formic acid is toxic: above 50 mg/dl, lethal dose 75 – 100 ml, even 15 ml can cause blindness Methanol poisoning: vomiting, epigastric pain dyspnoea, bradycardia, acidosis – permanent retinal damage and Death Mechanism: Ethanol saturates alcohol dehydrogenase enzyme - no metabolism of Methanol to form Formic acid Methanol formaldehyde Formic acidADH ALDH
- 29. Methanol Poisoning treatment Patientin dark room, Ventilation and BP supportive measures Gastric lavage with sodibicarb if brought immediately IV sodibicarb to combat acidosis – large quantity may be required Ethanol 10% in water – nasogastric tube with loading dose of 0.7 ml/kg followed by 15 ml/kg/hr by infusion – continue treatment for several days (methanol is oxidized slowly) Potassium chloride if hypokalemia occurs Folinic acid or Calcium leucovorin ijection 50 mg IV every 6 Hrly – to enhance oxidation of formic acid 4-methylpyrazole – specific inhibitor of ALD – 15 mg/kg IV and 10 mg/kg 12 Hrly. till methanol level is <20 mg/dl Haemodialysis
- 30. Summary Alcohol isa neuronal depressant Long term exposure to alcohol brings about adaptive changes in the neuronal system Chronic alcoholism causes toxic effects on all the organs especially liver Withdrawal syndrome in alcoholics are treated by BZDs and Naltrexone Antbuse/disulfiram is the drug is use as aversion technique in chronic alcoholics Ethanol is used as antidote in Methanol Poisoning
Editor's Notes
- #18 The drunkometer collected a motorist's breath sample directly into a balloon inside the machine. The breath sample was then pumped through an acidified potassium permanganate solution. If there was alcohol in the breath sample, the solution changed colour. The greater the colour change, the more alcohol there was present in the breath.