alcohol class ppt useful for medical students

alcohol class ppt useful for medical students

1. Ethanol
Alcoholism is a complex disorder with genetic
and environmental determinants.
Ethanol is absorbed from the upper GIT and
distributed in the body water.
The majority is oxidized, primarily in the liver;
breath contains 0.05% of blood.
It follows zero order kinetics (220mmol/hr).

2. Estimates of Blood Alcohol Estimates of Blood Alcohol
LevelsLevels
A typical adult (70 kg/150 lb) can metabolize 7-10 g of alcohol/hourA typical adult (70 kg/150 lb) can metabolize 7-10 g of alcohol/hour
Blood alcohol levels of a 70 kg male will increase by 20 mg% per drinkBlood alcohol levels of a 70 kg male will increase by 20 mg% per drink
12 oz beer (3 % EtOH) = 9 g EtOH12 oz beer (3 % EtOH) = 9 g EtOH
3 oz wine (12 % EtOH) = 9 g EtOH3 oz wine (12 % EtOH) = 9 g EtOH
1 oz whisky(40 % EtOH)= 9 g EtOH1 oz whisky(40 % EtOH)= 9 g EtOH
A 70 kg adult male will be legally intoxicated after 4 drinks in one hourA 70 kg adult male will be legally intoxicated after 4 drinks in one hour
Total body water in lean males=68%Total body water in lean males=68%
Total body water in females = 55 %Total body water in females = 55 %
BAC =BAC =Amount of EthanolAmount of Ethanol
(Body weight)(% body water)(Body weight)(% body water)

3. Ethanol metabolism
 The Alcohol
Dehydrogenase
(ADH) pathway in
the cytosol.
 The Microsomal
Ethanol Oxidizing
System (MEOS)
located in the smooth
endoplasmic
reticulum.

4. Ethanol
Alcohol Dehydrogenase Pathway in Liver
The major pathway of alcohol metabolism converts
alcohol into acetaldehyde and leads to generation of
NADH.
The rate of ethanol oxidation is determined by the
capacity to re-oxidize NADH.
If the ability of the liver to maintain redox
homeostasis is overwhelmed, then a number of
metabolic disturbances arise including lactic acidosis,
↑uric acid and abnormalities of lipid metabolism.

5. Ethanol

6. Ethanol
MEOS (Cytochrome P 450) :
Its role in ethanol metabolism is very less, when
blood ethanol concentrations are low (<100mg%).
Chronic alcohol is associated with an induction of
the MEOS system; can account for up to 10% of
ethanol oxidation

7. Ethanol
Mechanism of action: Ethanol
Ethanol enhances the action of GABA through
GABA-A receptor
It also inhibits NMDA receptor
Ethanol potentiates the action of BZD and
barbiturates and can result in fatal CNS depression.

8. Ethanol
Central nervous system effects :
Ethanol inhibits the release of ADH from pituitary
and produce diuresis.
It produces vasodilatation and hypothermia.
Thiamine deficiency occurs due to poor diet and
decreased absorption leading to nerve
demyelination.

9. Cardiovascular Effects of EthanolCardiovascular Effects of Ethanol
ACUTE EFFECTS:ACUTE EFFECTS:
Cutaneous vasodilation with increased blood flow to the skinCutaneous vasodilation with increased blood flow to the skin
Increased coronary blood flow, Depressed myocardial contractilityIncreased coronary blood flow, Depressed myocardial contractility
Acetaldehyde induce cathecholamine release result in tachycardiaAcetaldehyde induce cathecholamine release result in tachycardia
Vasoconstriction in cerebral and renal vascular bedsVasoconstriction in cerebral and renal vascular beds
CHRONIC EFFECTSCHRONIC EFFECTS
Dilated cardiomyopathy, Ventricular hypertrophyDilated cardiomyopathy, Ventricular hypertrophy
Atrial & Ventricular arrhythmiasAtrial & Ventricular arrhythmias
Mild Anemia from Folate deficiencyMild Anemia from Folate deficiency

10. Gastrointestinal Effects of EthanolGastrointestinal Effects of Ethanol
Gastrin release and gastric acid secretionGastrin release and gastric acid secretion
Inflammation and bleeding by ulceration of the stomach linningInflammation and bleeding by ulceration of the stomach linning
Retards intestinal absorption of glucose, amino acid, folic acid, thiamine Retards intestinal absorption of glucose, amino acid, folic acid, thiamine
& vitamin B& vitamin B
12 12 (alcoholics)(alcoholics)
Chronic CNS effects (Korsakoff Psychosis & Wernicke encephalopathy Chronic CNS effects (Korsakoff Psychosis & Wernicke encephalopathy
occurs from thiamine deficiencyoccurs from thiamine deficiency
Liver acidosis, hypoglycemia, increased fatty acid and lactate formation; Liver acidosis, hypoglycemia, increased fatty acid and lactate formation;
steatosissteatosis
Alcoholic hepatitis; Liver Cirrhosis; Liver failure (Alcoholism) Alcoholic hepatitis; Liver Cirrhosis; Liver failure (Alcoholism)

11. Cell & Organ damage by EthanolCell & Organ damage by Ethanol

12. Ethanol
Toxicity of Ethanol:
Acetaldehyde acts as a poison by inhibiting oxidative
phosphorylation.
Lactic acidosis.
Hypoglycemia.
All redox reactions are perturbed
Death can occur when the blood alcohol levels is
>400-500mg/dl.

13. Ethanol
BAC

14. Ethanol
Withdrawal syndrome of alcohol
Tremors, hallucinations, seizures, insomnia,
hyperthermia, nausea/vomiting
Delirium tremens or withdrawal syndrome is
treated by chlordiazepoxide or diazepam.

15. Craniofacial features associated with fetal alcohol
syndrome
Malformation of skeletal, cardiovascular, renogenital systemMalformation of skeletal, cardiovascular, renogenital system

16. Fetal Alcohol SyndromeFetal Alcohol Syndrome

Specific pattern Specific pattern
of facial featuresof facial features

Pre- and/or Pre- and/or
postnatal growth postnatal growth
deficiencydeficiency

Evidence of Evidence of
central nervous central nervous
system system
dysfunctiondysfunction

17. Ethanol
Disulfiram :
Acts by inhibiting aldehyde dehydrogenase and thus
acetaldehyde is accumulated.
It should not administered with alcohol.
It results in flushing, headache, tachycardia,
vomiting, confusion and convulsions.
Naltrexone helps to abstain from alcoholism by
decreasing craving and relapse.

18. FOMIPEZOLE

19. Disulfiram
Ethanol

20. Ethanol
Drugs used to treat alcohol dependence
To render alcohol unpleasant Disulfiram
To reduce alcohol craving Naltrexone &
Acamprosate

21. Ethanol
Drugs causing disulfiram like effect:
Metronidazole
Cefotetan
Cefoperazone
Chlorpropamide
Griseofulvin

22. Therapeutic UsesTherapeutic Uses
TOPICALTOPICAL
To cleanse the skinTo cleanse the skin
To denature protein and toughen skin with 50-70 % EtoH in bed To denature protein and toughen skin with 50-70 % EtoH in bed
sores.sores.
To reduce body temperature during high feverTo reduce body temperature during high fever
Antiseptic 70 % EtOH (needle puncture, cavity preparation)Antiseptic 70 % EtOH (needle puncture, cavity preparation)
SYSTEMICSYSTEMIC
Mild Sedative, Digestive aidMild Sedative, Digestive aid
Trigeminal neuralgia (to destroy painful facial nerves)Trigeminal neuralgia (to destroy painful facial nerves)
Pulmonary Edema (to collapse airway foam)Pulmonary Edema (to collapse airway foam)

23. Methanol
Methyl alcohol ‘Wood alcohol’ is widely used
in the industrial production of organic
solvents (windshield washing products).
The most characteristic feature of methanol
poisoning is a delayed visual disturbance.

24. Methanol
The treatment of methanol poisoning includes –
1. Suppression of metabolism by alcohol
dehydrogenase – Ethanol and Fomipezole
Fomipezole is an alcohol dehydrogenase
inhibitor, approved for the treatment of methanol
and ethylene glycol poisoning.
2. Methanol concentration in excess of 50 mg/dl is
an absolute indication for hemodialysis.

25. Ethylene glycol
Ethylene glycol is widely used as an automotive
antifreeze, engine coolants and hydraulic brake
fluids. .
Ethylene glycol is toxic, and its ingestion should be
considered a medical emergency.
Fomipezole
Renal failure
Ca Oxalate stones