DEFINITION:- ALIPHATIC ALCOHOLS ARE HYDROXY DERIVATIVES OF ALIPHATIC HYDRO CARBONS.

TYPES:MONO-HYDROXY EG. ETHYL ALCOHOL, METHYL ALCOHOL. DI-HYDROXY EG. ETHYLENEGLYCOL, PROPYLENE GLYCOL TRI-HYDROXY EG. GLYCEROL POLY-HYDROXY EG.MANNITOL, SORBITOL.
COMMONLY

USED ALCOHOL IS ETHYL ALCOHOL. RELEASED DURING DIGESTION OF FAT.

GLYCEROL IS

DIFFERENT FORMS OF ALCOHOLS

1.ABSOLUTE ALCOHOL:- 99% W/W ETHANOL 2.RECTIFIED SPIRIT:- 90%W/W ETHANOL 3.PROOF SPIRIT:- 49.29%W/W/ ALCOHOL

ALCOHOLIC BEVERAGES:MALTED LIQUOR:- EXAMPLE IS BEER. 4-6%V/V OF ALCOHOL WINES:- MORE THAN 16% OF ALCOHOL, PREPARED BY FORTIFICATION WITH NEUTRAL SPIRIT. SPIRITS:- THESE ARE DISTILLED AFTER FERMENTATION. EXAMPLE:-RUM, GIN. VODKA ETC ALCOHOL CONC IS 40-55%W/W

ETHYL ACOHOL

COLORLESS, VOLATILE, INFLAMMABLE LIQUID. MAIN CONSTITUENT OF ALL KINDS OF ALCOHOLIC BEVERAGES. GENERALLY OBTAINED BY FERMENTATION OF SUGARS BY YEAST. AND IS SEPERATED BY SIMPLE DISTILLATION.

LOCAL ACTIONS OF ETHYL ALCOHOL:

IT SHOWS COOLING AND REFERESHING EFFECT. USED IN COSMETIC PREPERATIONS LIKE AFTER SHAVE, NAIL REMOVERS ETC. AT CONC. OF 40-50% IT HAS RUBIFACIENT AND MILD IRRITANT PROPERTIES. AT HIGH CONCS IT IS USED AS ASTRINGENT. CONC. 70% USED AS AN ANTISEPTIC TO VEGETATIVE FORMS OF ORGANISMS

PHARMACOLOGICAL ACTIONS OF ETHYL ALCOHOL:GIT:1. 2.

3. 4. 5.

6.

IT HAS IRRITANT ACTION ON GASTRIC MUCOSAL MEMBRANE. 7-10%% OF ALCOHOL INCREASES GASTRIC SECRETION BY RELEASING HISTAMINE, GASTRIN FROM ANTRUM OF STOMACH. ABOVE 15% INHIBIT BOTH MOTILITY AND SECRETIONS WHICH PERSIST FOR MANY HOURS. ABOVE 20% REDUCES ENZYME ACTIVITY OF GASTRIC AND INTESTINAL JUICES. 40% AND MORE LEADS TO DIRECT TOXIC EFFECT ON GASTRIC MUCOUS MEMBRANE WHICH MAY PRECIPITATE GASTRITIS GIVING RISE TO NAUSEA, VOMITING. MANY CHRONIC ALCOHOLICS SUFFER FROM GASTRITIS, ACHLORHYDRIA.

C.N.S:1.

2. 3. 4. 5.

6.

7.

PRIMARILY ACTS AS CNS DEPRESSANT EITHER BY ENHANCING THE GABA OR ANTAGONISING THE GLUTAMATE NEURO TRANMISSION. IT EFFECTS FUNCTIONING OF RECEPTORS LIKE DOPAMINE, 5-HT3, NORADRENALINE, ENDORPHINE. PROTEINS ARE PRIMARY SITE FOR ALCOHOLS. PLEASURABLE AND STIMULANT EFFECTS ARE MEDIATED BY DOPAMINERGIC PATHWAY. CRAVING IS DEFINED AS CONSCIOUS DESIRE TO DRINK ALCOHOL HAS BEEN LINKED TO DOPAMINERGIC 5-Htergic, OPIOID SYSTEMS THAT MEDIATE THE RE INFORCEMENT AND THE GABAminergic , GLUTAMATE ERGIC, NORADRENERGIC SYSYEMS THAT MEDIATE THE WITHDRAWAL. CHRONIC ALCOHOL ABUSE CAUSES SHRINKAGE OF BRAIN BY ITS NEUOTOXIC ACTION. IT ALSO REDUCES BRAIN NORADRENALINE. IT REDUCES VISUAL ACTIVITY, IMPAIRS ABILITY OF BRAIN TO COORDINATE THE MOTOR ACTIVITY.

C.V.S:1.

2.

3.

REGULAR CONSUMPTION LEADS TO HYPERTENSION. IT ALSO EFFECTS CONDUCTION SYSYEM OF HEART AND MAY PRECIPITATE ARRYTHMIA . EPIDIMOLOGICAL EVIDENCES SUGGEST THAT DRINKING WINE MAY HAVE SOME CARDIO PROTECTIVE EFFECTS LINKED WITH ELEVATION OF PLASMA HDL LEVELS. CHRONIC ALCOHOLISM CAUSES CARDIO MYOPATHY BY DIRECT TOXIC ACTION ON CARDIAC MYOCYTES.

LIVER:1.

2.
3.

IT CAUSES DOSE RELATED TOXIC EFFECTS COMMONLY ARE FATTY INFILTRATION, HEPATOMEGALY. IMPAIRED GLUCONEOGENESIS, DIMINISHED FATTY ACID OXIDATION, INCREASED SYNTHESIS OF VLDL. INHIBITION OF HEPATIC MICROSOMAL CYTOCHROME P450 ENZYME SYSTEM.

KIDNEY:INCREASES URINE OUTPUT BY DECREASING TUBULAR REABSORPTION OF WATER BY REDUCING THE ADH RELEASE.

TERATOGENIC EFFECT:DRINKING DURING PREGNANCY CAN CAUSE DAMAGE TO FOETUS THAT IS FOETAL ALCOHOL SYNDROME.

SKELETAL MUSCLE:DECREASES MUSCLE STRENGTH, CAUSES IRREVERSIBLE DAMAGE TO MUSCLE TISSUE.

ABSORPTION FATE EXCRETION:1. 2. 3. 4.

ABSORBED VERY RAPIDLY FROM STOMACH, DUODENUM, SMALL INTESTINE. PARTLY METABOLISED BY GASTRIC AND HEPATIC ADH ENZYME. RATIO OF ALCOHOLIC CONC IN BLOOD : ALVEOLAR AIR IS 2100:1 90-95% OF ALCOHOL IS METABOLISED IN LIVER BY NON MICROSOMAL CYTOSOLIC ENZYME. REST IS EXCRETED BY KIDNEYS AND LIVER.

ETHYL ALCOHOL + NAD

ALCOHOL DEHYDROGENASE

ACETALDEHYDE + NADH + H
ALDEHYDE DEHYDROGENASE

CO2 + H20 + ENERGY

AT LOW CONC. IT FOLLOWS FIRST ORDER KINETICS.

INTERACTIONS:1. 2. 3.

INSULIN AND SULHONYL UREA : ALCOHOL ENHANCES HYPOGLYCEMIA ACUTELY. ACUTE ALCOHOL INHIBITS, WHILE CHRONIC INTAKE INDUCES TOLBUTAMIDE,PHENYTOIN METABOLISM. ALCOHOLICS ARE MORE PRONE TO PARACETAMOL TOXICITY DUE TO ENHANCED GENERATION OF ITS TOXIC METABOLITE.

CONTRA INDICATIONS:ALCOHOL IS SELDOM PRESCRIBED MEDICALLY HOWEVER ITS CONSUMPTION SHOULD BE AVOIDED BY :PEPTIC ULCER, HYPER ACIDITY. EPILEPTICS. SEVERE LIVER DISEASE PATIENTS. PREGNANT WOMAN : FOETAL ALCOHOLIC SYNDROME. UNSTABLE PERSONALITIES: THEY ARE LIKELY TO ABUSE IT AND BECOME EXCESSIVE DRINKERS.

1. 2. 3. 4. 5.

TOXICITY:SIDE EFFECTS OF MODERATE DRINKING:NAUSEA, VOMITING, FLUSHING, TRAFFIC ACCIDENTS.

ACUTE ALCOHOLIC INTOXICATION:HYPOTENSION, GASTRITIS, HYPOGLYCEMIA, COLLAPSE, RESPIRATORY DEPRESSION, COMA, AND DEATH.

CHRONIC ALCOHOLISM:ON CHRONIC INTAKE TOLERANCE DEVELOPS TO SUBJECTIVE AND BEHAVIORAL EFFECTS OF ALCOHOL. PSYCHIC DEPENDANCE OCCURS EVEN WITH MODERATE DRINKING.

TREATMENT OF ALCOHOL DEPENDENCE:ITS MAINLY TWO TYPES:DETOXIFICATION AND REHABILITATION. DETOXIFICATION CAN BE ACHIEVED BY USING DRUGS WHICH CAN BE CLASSIFIED INTO 1. AVERSION DRUG EG. DISULFIRAM 2. OPIOID ANTAGONISTS EG. NALTREXONE, NALMEPHENE. 3. DOPAMINERGIC ANTAGONISTS EG. TIAPRIDE 4. MISCELANEOUS EG, ACAMPROSATE. 5. SUPPORTING DRUGS EG. LITHIUM, CARBAMAZEPINE/

REHABILITATION:PSYCHOTHERAPY INSTITUTIONAL THERAPY.

DISULFIRAM:ENSURE THAT ALCOHOL HAS NOT BEEN CONSUMED FOR ATLEAST 12HOURS BEFORE INITIATING THERAPY. TREATMENT IS INITIATED WITH A DOSE OF 800mg AS A SINGLE DOSE ON FIRST FIVE DAYS. AFTER THE FIFTH DAY MAINTENACE DOSE OF 100-200mg IS GIVEN DAILY FOR ABOUT AN YEAR. SEVERE REACTIONS CAN OCCUR EVEN WITH THE FIRST DOSE AND HENCE TREATMENT IS CARRIED OUT IN HOSPITALS. MOA:ACTS BY INHIBITING ADLEHYDE DEHYDROGENASE. SIDE EFFECTS:INDUCES RASHES. METALIC TASTE, NERVOUSNESS, ABDOMINAL UPSET, INHIBITS NUMBER OF OTHER ENZYMES.

METHYL ALCOHOL:

METHYL ALCOHOL IS ADDED TO RECTIFIED SPIRIT TO RENDER IT UNFIT FOR DRINKING. IT IS ONLY FOR TOXICOLOGICAL IMPORTANCE. UNSCRUPULOUS MIXING OF METHYLATED SPIRIT WITH ALCOHOLIC BEVERAGES OR ITS INADVERTENT INGESTION RESULTS IN METHANOL POISONING/ METHANOL IS METABOLISED TO FORMALDEHYDE AND FORMIC ACID BY ALCOHOL AND ALDEHYDE DEHYDROGENASE RESPECTIVELY. IT FOLLOWS ZERO ORDER KINETICS. T1/2 IS 20-60 HRS. METHANOL IS A C.N.S DEPRESSANT BUT LESS POTENT THAN ETHANOL. TOXIC EFFECTS OF METHANOL ARE LARGELY DUE TO FORMIC ACID SINCE ITS METABOLISM IS SLOW AND FOLATE DEPENDENT. MANIFESTATIONS OF METHANOL POISIONING ARE VOMITING, HEADACHE, EPIGATRIC PAIN, DYSPNOEA SPECIFIC TOXICITY OF FORMIC ACID IS RETINAL DAMAGE.

TREATMENT:KEEP THE PATIENT IN A QUITE DARK ROOM PROTECT EYES FROM LIGHT. GASTRIC LAVAGE WITH SODIUM BICARBONATE ETHANOL100mg/dl IN BLOOD SATURATES ALCOHOL DEHYDROGENACE AND RETARDS METHANOL METABOLISM. THIS HELPS IN REDUCING THE GENERATION OF TOXIC METABOLITIES. ETHANOL IS ADMINISTERED THROUGH A NASOGASTRIC TUBE , LOADING DOSE IS 0.7 ml/kg MAINTAINANCE DOSE IS 0.15ml/kg. HAEMODIALYSIS CLEARS METHANOL AS WELL AS FORMATE AND HASTENS RECOVERY. FOMEPIZOLE SPECIFIC INHIBITOR OF ALCOHOL DEHYDROGENASE,RETARDS METHANOL METABOLISM FOLATE THERAPY:A PROMISING ADJUANT APPOACH, CALCIUM LEUCOVORIN 50mg GIVEN.