This document discusses alcohol absorption, effects, and treatment. It notes that alcohol is absorbed primarily in the small intestine and lists factors that influence absorption. It then summarizes some of alcohol's effects on the nervous system, cardiovascular system, liver, and ability to fight infections. The document outlines treatments for alcohol dependence including medications like acamprosate, naltrexone, disulfiram, topiramate, and ondansetron. It provides details on how several of these medications work and clinical trial results on their effectiveness in reducing cravings and relapse.

1. Dr. RAGHU PRASADA M S
MBBS,MD
ASSISTANT PROFESSOR
DEPT. OF PHARMACOLOGY
SSIMS & RC. 1

2.  Absorption in stomach 20%
 Absorption in small intestine 80%
 Factors that influence absorption
▪ Concentration of the drink
▪ Amount consumed
▪ Food in the stomach
▪ Mood
▪ Pylorospasm (spasm of valve)

3. Uniformly distributed throughout tissues and body
fluids
Readily crosses placenta, to exposure fetus

4.  Decision making skills impaired
 Alcohol lowers inhibitions, impairing ability to make
wise decisions
 Immediate effects of alcohol
 Reduces frequency of nerve transmissions
 Dehydration
 Water is lost from cerebrospinal fluid
 Alcohol irritates the gastrointestinal system
 Hangovers

5.  Effects on the Nervous System
 Cardiovascular Effects
 Liver disease
▪ Cirrhosis
▪ Alcoholic hepatitis
 Cancer
 Chronic inflammation of pancreas
 Impairs ability to recognize and fight bacteria and
viruses

6.  GI tract/Liver: Fatty liver, hepatitis, cirrhosis,
esophagitis, gastritis
pancreatitis, cancers
 Nervous system: Brain: Hepatic encephalopathy,
Wernicke-Korsakoff syndrome(thiamine deficiency),
cerebellar degeneration, central pontine
myelinolysis, dementia

7.  Nutrition: Deficiencies of
Vitamins: Folate, thiamine, pyridoxine, niacin,
riboflavin
Minerals: Magnesium, zinc, calcium
Protein
 Metabolites and electrolytesHypoglycemia,
ketoacidosis, hyperlipidemia, hyperuricemia,
hypomagnesemia, hypophosphatemia

8.  Neuromuscular: Neuropathy, myopathy
 Cardiovascular: Arrhythmia, cardiomyopathy,
Hypertension
 Bone marrow: Macrocytosis, anemia,
thrombocytopenia, leukopenia

9.  Endocrine: Pseudo-Cushing's syndrome, testicular
atrophy, amenorrhea, DM?,
Osteopenia/osteoporosis
cancers (i.e., breast)
 Traumatic injury
Fetal alcohol syndrome

10.  Brain neurotransmitter physiology is
abnormal………..
 Effective treatments lead to
 2/3rds reduction in alcohol problems
 50% reductions in consumption at one year
(with 1/3rd abstinent or drinking moderately)
 beneficial when given in addition to non
pharmacological therapies
10

11. • Tremor
• Nausea
• Irritability
• Agitation
• Tachycardia
• Hypertension
• Seizures
• Hallucinations

12. Careful monitoring and supportive care
Ample fluids (p/o or IV fluids if dehydrated)
Correction of electrolyte imbalance
Parenteral Thiamine(100 mg p.o or i.v or i.m) daily
Restrict access to addicting substances
12

13.  Cross tolerant medications with alcohol
 Benzodiazepines
 Diazepam and Chlordiazepoxide
Lorazepam and oxazepam - short acting patients
with liver problems, in elderly)
 Others (more than 150 agents, carbamazepine;
valproate, ß adrenergic antagonists etc.,)
 Emerging: Baclofen
13

14. Ethanol AcetateAcetaldehyde
•Flushing
•Headache
•Palpitations
•Dizziness
•Nausea
ADH ALDH
14
DISULFIRAM

15. Causes antabuse reaction due to accumulation of
acetaldehyde
The effect lasts for 7-14 days
Metronidazole, chlorpropamide, tolbutamide,
griseofulvin, cephalosporins and phenylbutazole
Contra indication- liver disease

16. structure similar to GABA amino acid.
 Restores the GABA activity.
 reduce glutamate surges that excite
NMDA- Rs.
 acts as a neuro-protectant and protect
neurons from damage caused by
alcohol withdrawal
 Prevent relapse in heavy drinking
16

17. Stabilizes activity in the glutamate system
 Affinity for GABA A and GABA B receptors
 Inhibits glutamate effect on NMDA receptors
BUT cannot be used in liver disease
17
NMDA
receptor
ETHANOL
glutamate
GABAA Receptor
GABA
Cl-

18. Volpicelli, 1992
 Opiate blocker
 Evidence for reduced cravings and relapse rates
 23% relapsed vs. 54% placebo during 12 week study
 Definition of relapse

19. a 5-HT3 antagonist that exerts its antidrinking effects
through cortico-mesolimbic dopamine system
modulation.
improve drinking outcomes in patients with early-
onset alcoholism.
Adverse events are mild
starting dosage of 4 mcg/kg twice daily should be
maintained throughout treatment.
19

20.  GABA, glutamate receptors (?)
 Some efficacy in those not abstinent at start of
medication
 Used for other psych disorders

21. Single agent
Acamprosate
Naltrexone
Disulfiram
 Aimed at complete abstinence ,
can be started at any time
including withdrawal phase,
 may be started immediately
during first consultation
 Early onset with family loading,
helps in heavy drinking and may be
choice in which acamprosate trial has
failed,
 Liver function test is mandatory
 Patient completely motivated and
with good social support, still low
acceptability
21

22.  Benzodiazepines
 Clonidine
 Baclofen

23.  It is used to denature ethyl alcohol
 No therapeutic value
 Methanol formaldehyde formic acid
 Manifestations
 Vomiting headache, vertigo, sev abdominal pain,
hypotension, delurium, acidosis, coma

24.  Correction of acidosis
 Protect eyes
 Gastric lavage
 Blood pressure maintainance
 Ventilation
 Ethyl alcohol
 Fomepezole
 hemodialysis

25. (National Geographic, George Steinmetz, Feb 1992)