Alcohol and alcoholism

Alcohol and Alcoholism
Moderator DR POONAM GUPTA (MD)
ANIL KUMAR G

Introduction
• Alcohol (beverage ethanol ) distributes
throughout the body , affecting almost all
systems and altering nearly every neurochemical
process in the brain.
• Low doses of alcohol have some health benefit.
• The intake of more than three standard drinks per
day on a regular basis enhances the risk for
cancer and vascular disease, and alcohol use
disorders decrease the life span about 10 years.
1.HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392
alcohol and alcoholism no 3456-3552.

Epidemiology
• Worldwide, an estimated 2.3 million people die
from alcohol related causes.
• 3.7% of all deaths, of this 6.1% among men and 1.1
% among women
• WHO estimated 2 billion people worldwide
consume & 76.3 million with disorder arising out of
harmful use.
• In India around 20-30 % of adult males and around
5 % adult females use alcohol.
PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental
health- alcoholism and drug dependence no 774.

PHARMACOLOGY AND NUTRITIONAL IMPACT OF ETHANOL
• Blood levels of ethanol are expressed as mg or gm of ethanol per dL (e.g., 100
mg/dL = 0.10 g/dL)
• With values of 0.02 g/dL resulting from the ingestion of one typical drink. In
round figures, 340 mL (12 oz) of beer, 115 mL (4 oz) of nonfortified wine, and 43
mL (1.5 oz) (a shot) of 80-proof beverage such as whisky, gin, or vodka
• Each contain 10–15 g of ethanol and represent a standard drink
• 0.5 L (1 pint) of 80-proof beverage contains 160 g (about 16 standard drinks), and
750 mL of wine contains 60 g of ethanol.
 One unit = 10 gm of alcohol
 One oz = 30ml
 Proof =2*%ethanol by volume
 One drink = 44ml of whiskey(80%proof), 3- 5oz wine or 12 oz beer.
 BAC –blood alcohol conc.
 0.1%BAC =100 mg alcohol in 100ml blood. .
 HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and alcoholism no
3456-3552

Absorption
 GIT ,20% in stomach, rest in small intestine
 80%-90% absorption within 30-60mins.
 Absorption also depends on other factors
 Females attain higher blood alcohol level.
 BAC decreases by 15-25 mg /100ml/ hr.
 Inhalation –pulmonary vascular bed.
PHARMACOLOGY
 C2H5OH
 Colorless, odourless liquid
 M.Wt - 46
1gm ethyl alcohol – 7.1 kcal energy .HARRISONS PRINCIPLES OF
INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and alcoholism no 3456-
METABOLISM

• Alcohol supplies calories (a drink contains 300 kJ, or
70–100 kcal), these are devoid of nutrients such as
minerals, proteins, and vitamins. In addition,
alcohol can also interfere with absorption of
vitamins in the small intestine and decreases their
storage in the liver with modest effects on folate
(folacin or folic acid), pyridoxine (B6), thiamine (B1),
nicotinic acid (niacin, B3), and vitamin A.
• A heavy ethanol load in a fasting, healthy individual
is likely to produce transient hypoglycemia within
6–36 h, secondary to the acute actions of ethanol
on gluconeogenesis. This can result in temporary
abnormal glucose tolerance tests.
• HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and alcoholism
no 3456-3552

Alcoholics may have thiamine deficiency because of
the following:
• Inadequate nutritional intake: Alcoholics tend to intake less than the
recommended amount of thiamine.
• Decreased uptake of thiamine from the GI tract: Active transport of thiamine
into enterocytes is disturbed during acute alcohol exposure.
• Liver thiamine stores are reduced due to hepatic steatosis or fibrosis.
• Impaired thiamine utilization: Magnesium, which is required for the binding of
thiamine to thiamine-using enzymes within the cell, is also deficient due to
chronic alcohol consumption. The inefficient utilization of any thiamine that
does reach the cells will further exacerbate the thiamine deficiency.
• Ethanol per se inhibits thiamine transport in the gastrointestinal system and
blocks phosphorylation of thiamine to its cofactor form (ThDP).
Butterworth RF, Gaudreau C, Vincelette J et al. (1991). "Thiamine deficiency and wernicke's encephalopathy in
AIDS". Metab Brain Dis 6 (4): 207–12.

• The other most prominent actions relate to boosting GABA activity,
especially in GABAA receptors.
• Enhancement of this complex chloride channel system contributes to
anticonvulsant, sleep-inducing, antianxiety, and muscle relaxation
effects of all GABA-boosting drugs.
• Continued use of this drug increases density of GABAA receptors,
while alcohol withdrawal states are characterized by decreases in
GABA-related activity.
• Ability of acute alcohol to inhibit postsynaptic N-methyl-d-aspartate
(NMDA) excitatory glutamate receptors, while chronic drinking and
desistance are associated with an upregulation of these excitatory
receptor subunits.
• Relationships between greater GABA and diminished NMDA receptor
activity during acute intoxication and diminished GABA with
enhanced NMDA actions during alcohol withdrawal explain much of
intoxication and withdrawal phenomena.
HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and
alcoholism no 3456-3552.

• Drinking alcohol acutely increases dopamine levels in the
brain, changes in dopamine pathways are also linked to
increases in "stress hormones," including cortisol and
adrenocorticotropic hormone (ACTH) during intoxication
and decreases in these hormones during withdrawal.
• Such alterations are likely to contribute to both feelings of
reward during intoxication and depression during falling
blood alcohol concentrations.
• Alcohol-induced changes in opioid receptors, with acute
alcohol also causing release of beta endorphins.
HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and

Pathophysiology
 GABA ↑. Glutamate ↓.
 ↑NADH/NAD ratio.
 ↑ketogenesis.
 ↓gluconeogenesis
 ↑glycogenolysis
 Fluid & electrolyte imbalance.

Behavioral Effects and Tolerance
• "Legal intoxication" with alcohol in most states requires a blood
alcohol concentration of 0.08 g/dL, while levels of 0.04 or even lower
are cited in other countries. In INDIA 0.15g/dL.
• Effects of Blood Alcohol Levels in the Absence of Tolerance.
Blood level g/dL Usual Effect
Less then 0.03 Not noticeable
0.03-0.05 Selective impairment
0.05-0.10 Slight impairment
0.10-0.15 Under the influence
0.15-0.20 Drunk
0.20-.30 Very drunk
0.30-0.35 Stupor to coma
Over 0.35 Comatose to death
ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS DEPRESSANTS no 497-514

Selective impairment: (0.03-0.05gm/dL) increase in reaction time; impairment of
complex skills such as flying an aircraft or driving a motor vehicle. Detectable
only on detailed examination
Slight impairment: (0.05-0.10gm/dL) flushed face; dilated pupils; euphoria; loss of
restraint
Under the influence: (0.10-0.15gm/dL) flushed face; dilated pupils; euphoria; loss
of restraint ; test errors; stagger on sudden turning.
Drunk: (0.15-0.20gm/dL) flushed face; dilated sluggish/inactive pupils; clouding of
intellect; incoordination of thought, speech and action; staggering gait with
reeling and lurching while making sudden turns.
Very drunk:(0.20-.30gm/dL) flushed or pale face; pupil inactive, contracted or
dilated; mental confusion; marked incoordination of thought, speech and
action; staggering gait with reeling and lurching while making sudden turns ,
vomiting amnesia.
.PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental health-
alcoholism and drug dependence no 774.

Repeated use of alcohol contributes to acquired tolerance, at least three
types of compensatory mechanisms.
(1) After 1–2 weeks of daily drinking, metabolic or pharmacokinetic
tolerance can be seen, with up to 30% increase in the rate of hepatic
ethanol metabolism.
(2) Cellular or pharmacodynamic tolerance develops through
neurochemical changes that maintain relatively normal physiologic
functioning despite the presence of alcohol. Subsequent decreases in
blood levels contribute to symptoms of withdrawal.
(3) Individuals learn to adapt their behavior so that they can function
better than expected under influence of the drug (learned or behavioral
tolerance).
1.HARRISONS PRINCIPLES OF INTERNAL MEDICINE 18th edition vol 2; chapter 392 alcohol and

Different alcohol poisonings.
 Acute ethanol intoxication
 Acute methanol poisoning.
 Acute ethylene glycol poisoning.
 Acute isopropyl alcohol poisoning

Acute ethyl poisoning
• Ethyl alcohol depresses central nervous system irregularly
in descending order from cortex to medulla.
• 1. Stage of excitement: (0.03-0.10%) feeling of well being and
pleasure resulting from inhibition of higher centres. Drinker
converses well , laughs and smiles readly or becomes angry easily. He
may disclose secrets.
• 2. Stage of incoordination: (0.10-0.30%) incoordination of
thought, speech, and action, which manifest as impaired judgement,
confusion, slurred speech, and staggering gait. May become morose ,
euphoric or irritable depending on his inherent emotions. Nausea
and vomiting are common. Pupils dilated. Offences committed in this
stage. Impaired judgment may lead to accidents, sexual excesses,
violence and crime.
.PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION , chapter 18 mental health-

• 3.Stage of narcosis: pt passes into deep sleep and
responds only to strong stimuli. Pulse is rapid,
temperature subnormal, breathing Sertorius, &
pupils may contracted. Macewans sign seen. If this
stage lasts for more then 12hrs, death ensues from
paralysis of cardiac or respiratory center or later
from effects of pulmonary edema.
• Recovery occurs with acute depression and
gastrointestinal irritation which continue for 24hrs
or longer. Headache is also present as an hang over
effect and is due to cerebral edema. Hang-over
means a temporary state of indisposition usually
following recovery from drunkenness.
3.PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental

• Fatal dose : depend on age and habits of the pt and
the strength of liquor taken. Death usually occurs
from large quantity taken in short time.
Concentration of 0.35gm/dL & above of alcohol in
blood is generally sufficient to cause death.
• Fatal period: usually 12 to 24 hrs though death may
be delayed for 5 to 6 days.
• Cause of death : depression of respiratory center.
May be lethal at relatively lower blood levels when
combined with other CNS depressants such as
barbiturates, carbon monoxide, or morphine, & in
presence of some natural disease of heart or lungs.
3.PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental health-

Associated acute problems
 Alcoholic ketoacidosis.
Alcoholic hypoglycemia.
Fluid & electrolyte imbalance.
Wernicke’s encephalopathy
 Acute effects on heart.
Acute GI effects.
Acute alcoholic myopathy.
Trauma
Associated other substance poisoning.
2.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS
DEPRESSANTS no 497-514.

Alcoholic ketoacidosis:
 High anion gap acidosis
Normal or low glucose level
Chronic alcoholics
Binge drinking wks before symptoms
Dehydration, starvation due to vomiting ,gastritis
 Altered mental status
Kussumal breathing
Ketotic breath
Lab finding
high anion gap acidosis
↑beta hydroxybutyrate : acetoacetate
↓insulin level
Exclude other causes of ↑A;G acidosis
.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS

• Alcohol poor food intake dehydration
↓ ↓ ↓
Acetaldehyde glycogenolysis ↑counter
regulatory
↓ hormones
Acetate ↓ ↓
↓
↑NADH/NAD ↑glucagon
ratio ↓insulin
↓
• ↓gluconeogenesis
ketogenesis

 Chronic alcoholic found unresponsive
Symptoms
neuroglycopenic →confusion,fatigue,seizure,
loss of consciousness→death
autonomic responses → palpitation ,tremor ,
sweating
Signs
pallor ,diaphoresis
tachycardia,raised systolic B.P
transient focal neurological signs
Alcoholic hypoglycemia

Water and electrolytes disorders
Immediate ↑ in urine volume followed by ↑ADH.
 Hydration also depends on
-diet, nonalcoholic fluids, type of drinks
-vomiting, diarrhea, infection
 Water intoxication & hyponatremia in severe chronic
alcoholics→seizure & altered sensorium
 Central pontine mylenolysis
• Other electrolytes abnormalities
 Hypomagnesemia
Hypophosphatemia
Hpokalemia
Hypocalcemia

Wernicke-korsakoff’s syndrome
 As high as 12.5% in alcoholics.
 Major reversible cause of death.
 If untreated 10-20% mortality rate.
 Thiamine deficiency is the root cause.
 Magnesium deficiency in thiamin resistant cases.
 Clinical features
global confusion
ocular abnormalities
ataxia
.Neurology in Clinical Practice e-dition, 5th Edition Bradley, Daroff, Fenichel & Jankovic;
chapter 61 Deficiency Diseases of the Nervous System no 1650-1654.

Acute effect on heart
 Direct negative inotropic effect & vasodilation.
 PR & QT prolongation
 Both supraventricular & ventricular arrhythmia.
 “holiday heart syndrome”
 Various degree of heart block.
 Acute alcoholic myopathy
 Acute muscle necrosis mainly in binge drinkers
 Alcoholism is the most common cause of rhabdomyolysis
 Raised CKMM, myoglobinuria,
 Acute tubular necrosis→↑urea ,creatinine
ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS DEPRESSANTS no

Acute gastrointestinal effect
 Acute gastritis & esophagitis.
 Epigastric distress and gastrointestinal bleeding.
 Mallory-weiss tear.
 Acute hepatitis & pancreatitis.
2.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter
30 CNS DEPRESSANTS no 497-514.

Differential diagnosis in acutely intoxicated
patient.
 Toxic
Metabolic
Infectious diseases
Neurologic
Miscellaneous
Trauma

Management
 Airway
 Breathing
 Circulation
 Intubate if poor gag reflex
 Finger stick glucose , iv dextrose
 Thiamin 100 mg im/ iv stat.
 iv dextrose
 magnesium
.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter

 . 2 mg naloxone
 Exclude other causes of intoxication
 ABG
 Osmolar gap.
 2Na+ + BUN/2.8 + Glu/18 + Eth/4.6
 Serum electrolytes
 Anion gap.
 Correct other electrolyte abnormalities
 Phenytoin
 CT scan
ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS DEPRESSANTS
no 497-514.

 Blood alcohol conc (BAC)
 Enhanced elimination
evacuation after 1 hr little benefit
activated charcoal.
fructose
haemodialysis
metadoxine (300-900mg iv) (VIBOLIV, ALCOLIV)
(pyridoxine–pyrrolidone carboxylate)

Methanol poisoning
 CH3OH(wood alcohol)
 Solvent ,antifreeze, paint
remover.
 Epidemics of methanol toxicity.
 Poisoning mainly by ingestion
Clinical effects
 Inebriated but lack of euphoria.
 1-72 hrs of latent period.
 Fatal dose 60-240 ml.
 Vertigo ,nausea, vomiting, diarrhea, abdominal
pain,dyspnea,agitation.
Blurred vision, photophobia, ↓
visual acuity
Bradycardia, blindness, seizures,
coma
ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS

 Physical examination
constricted visual field, fixed & dilated pupils,
retinal edema & hyperemia of disc
resp apnea , opisthotonus & seizure in pts dying of
Methanol intoxication
 Lab finding
high anion gap acidosis (correlates with
mortality)
high osmolar gap
serum methanol> 20 mg/dl symptoms
> 50 mg/ dl serious
> 100 mg/ dl ocular signs

 Specific treatment
aggressive tt of acidosis
ethanol
achieve BAC of 100- 150mg
/100ml
loading 0.8gm/ kg of 5 – 10%
ethanol
followed by 130mg/kg/hr.
oral loading if no iv preparation
if dialysis,250-350 mg/kg/hr.
ethanol indications
methanol >20
mg/100ml,symptomatic
acidosis, need for HD.
ingestion >o.4ml/kg
 Folic acid 30 mg iv every 4 hrly
 Leucovorin 1-2mg/kg iv
 4-methyl pyrazole(fomepizole ) 15-20
mg/kg iv
 Haemodialysis not haemoperfusion
 Haemodialysis indications:
methanol>20-50mg/100ml
acidosis not responsive to
bicarbonate
formate levels > 20 mg/100ml
visual impairment
renal impairement
 Dialysis till methanol level≈0mg/100ml
and acidosis clears.

Alcoholism (Alcohol Abuse or Dependence)
• Alcohol dependence is defined in DSM-IV as repeated alcohol-related
difficulties in at least three of seven areas of functioning that cluster
together over a 12-month period. Two of these seven items, tolerance and
withdrawal, may have special importance as they are associated with a
more severe clinical course.
• Alcohol abuse is defined as repetitive problems with alcohol in any one of
four life areas—social, interpersonal, legal, and occupational—or repeated
use in hazardous situations such as driving while intoxicated in an individual
who is not alcohol dependent. About 50% of those with alcohol abuse
continue to have alcohol problems 2–5 years later, but only 10% of these
patients—including adolescents—go on to develop alcohol dependence.
• The lifetime risk for alcohol dependence in most Western countries is about
10–15% for men and 5–8% for women.
alcoholism no 3456-3552

Current risk terms
Abstinence : no alcohol use
Moderate drinking :
Men: no more than 2 standard drinks per drinking d
Women: no more than 1 std drink per drinking d
Elder persons(>65y): no more than 1 std drink per drinking d
Risky or hazardous drinking :
Men : More than 4 std drink per drinking d/ More than 14 std drink per drinks per wk
Women : More than 3 std drink per drinking d/ More than 7 std drink per drinks per wk
Elder persons(>65y): More than 3 std drink per drinking d/ More than 7 std drink per drinks per wk
.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS- ALCOHOLISM no 921-927.

Three types of chronic alcohol abuse seen
1. regular daily excessive drinking
2.regular heavy drinking on weekends only
3.long periods of sobriety interspersed with binges that last days, weeks,
months.
Familial influence
1. a family history of alcoholism , son of an alcoholic father
2. family history of teetotalism (i.e, avoidance of alcohol under any
circumstance)
3. an alcoholic spouse
.NMS PSYCHIATRY 5th edition JOUHUA T. THORNHILL 4, chapter 5 substance related disorder
chapter 7 no 158-159

Screening
• Alcohol Use Disorders Identification Test
(AUDIT)
• CAGE questionnaire
• TWEAK questionnaire
• CRAFFT questionnaire
• S-MAST-G questionnaire
.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS- ALCOHOLISM
no 921-927.

Screening
Add all scores to obtain a total > 8 for men or > 4 for women indicates a higher risk of alcohol use disorder
• Alcohol Use Disorders Identification Test (AUDIT)

CAGE questionnaire
.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS-
ALCOHOLISM no 921-927.

• Two or more points indicate possible alcohol problem

CRAFFT questionnaire
One yes response indicates need for further assessment; two yes
responses indicates risk of alcohol use disorder
.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS- ALCOHOLISM no 921-
927.

The Short MAST-GERIATRIC VERSION (SMAST-G)
PleaseanswerYes or No to the followingquestions: Yes No
1. Whentalkingwithothers,doyoueverunderestimatehowmuchyoudrink?
2. Aftera fewdrinks,haveyousometimesnoteatenorbeenabletoskipa meal
becauseyoudidn’tfeel hungry?
3. Doeshavinga fewdrinkshelpdecrease yourshakinessortremors?
4. Doesalcohol sometimesmakeithardfor youto rememberpartsoftheday or
night?
5. Do youusuallytakea drinkto calmyour nerves?
6. Do youdrinkto take yourmindoffyourproblems?
7. Haveyou everincreasedyourdrinkingafterexperiencingalossinyour life?
8. Has a doctoror nurseeversaidtheywereworriedorconcernedaboutyour
drinking?
9. Haveyou evermaderulestomanageyour drinking?
10. Whenyoufeel lonely,doeshavingadrinkhelp?
SCORING:
Score1 pointfor each‘yes’answerandthentotal theresponses
2+ points = are indicativeof an alcohol problem
.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS- ALCOHOLISM
no 921-927.

Diagnosis of alcohol use problems
• Alcohol abuse (> 1 in last year )
• Alcohol has caused or contributed to repeated: failure to
fulfil obligation at home, school, or work.;arrests or other
legal problems; physical fights; driving ,swimming.
• Alcohol dependence (>3 in the last 12 mnth):
development of physical tolerence,;binging episodes;
reduced time in other pleasurable activities; drinking
persists despite physical or psychological problems.
• Alcohol withdrawal (> 2 within hours to days after
lowered blood alcohol levels ): autonomic hyperactivity;
hand tremor; insomnia; anxiety; seisures;hallicinations;
nausea vomiting

Intervention
• Assess: screen patients with AUDIT or with CAGE or CRAFFT or S-
MAST-G questionnaires as appropriate and compute average
drinks per week.
• Advise: give feed back in the form of concern, direct conclusions,
and recommendations
• Agree: when the patient concurs that a change in drinking would
be beneficial, agree on a specific goal to cut down to a particular
daily and weekly limits for low risk drinking or to stop drinking.
Agreement should be recorded and a copy given to the pt both as
a reminder and motivator for behavioural change.
• Assist : work with the pt to formulate concrete steps to
implement the drinking reduction plan, how to avoid high risk
drinking situation , keep a record of alcohol intake.
• Arrange: set up follow up support and counseling visits or refer
pts meeting dependence criteria for specifically treatment. Seek
medical treatment if withdrawal symptoms occur.

• Pharmacological therapy:
• Benzodiazepines – diazepam 10-20mg(valium) &
chlordiazepoxide 50-100mg(librium) CIWA-Ar score
less then 8.
• Long acting barbiturates , phenobarbital (120mg
loading followed by 60mg 6hrly) for CIWA-Ar score
of 10 or more.
• Thiamine 100mg/day for 3 days counter act
thiamine deficiencies

• Asssessment of motivation : pt who is willing to consider
abstaining completely for 1 month has at least some
motivation to give up.
Medication management:
• Disulfiram(antabuse) – works by inhibiting the metabolism of
alcohol, causing build up of acetaldehyde, a noxious
substance .( 125-500mg/day).
• Naltrexone : reduction of craving of alcohol, (vivitrol long
acting I.M, once monthly 300mg reduces non compliance)
• Acamprosate(campral): taurine analogue works on GABA and
glutamate neurotransmission, reduce relapse to drinking, two
333mg tab 3 times daily who have ceased alcohol at least
5days.
• Topiramite (topamax): titrated over 5wks between 50mg and
300mg daily.

Involvement of family:
• A family intervention in which all family members
confront the patients drinking, help the patient to deal
with denial.
• Refusal by spouse to remain with the pt unless he or
she stops drinking
Alcoholics anonymous (AA): highly useful treatment
group and found most effective treatment model.
Behaviour therapy : punishing drinking (e.g disulfirum)
and rewarding sobriety (e.g. by paying the pt for
abstinence)
On going emotional support by primary physician.

Alcohol liver disease
• Risk factors:
• Drinking pattern- >80gm of alcohol / day
• Sex- women
• Genetics – HLAB8 , hep B & C acts as co factor
• Nutrition- alcohol increases daily requirement of
cholin, folic acid, protein deficiency promotes
the toxic of alcohol
.SLEISENGER AND FORDTRANS 9th edition gastrointestinal and liver disease Vol2 Section IX –
Liver;CHAPTER 84 – Alcoholic Liver Disease no 1394.

• Mechanism of liver injury
1. direct toxic effect of alcohol
2. acetaldehyde: binds with phospholipids, amino residues, &
sulphydryl groups and thus becomes reactive and toxic; binds to tubulin
and impairs the microtubules of cytoskeleton.
OTHER MECHANISM
1. Changes in intracellular redox potential
2. Mitochondrial swelling
3. Liver cell water protein retention
4. Hypermetabolic state
5. Increased liver fat
6. Immunological liver damage
7. Fibrosis
8. Cytokine mediated injury.

Morphological change
• Fatty liver: presence of more than 5gm of fat/ 100gm of liver tissue.
Lab features
a. Hyperbilirubinemia
b. AST/ALT > 2 in 80% ( due to pyridoxine deficiency)
c. ALP elevated in the absence of cholestasis
d. GGT/ALP ratio 5 or higher in 50% cases
e. GGT blood levels > 30U & Carbohydrate Deficient Transferrin > 20U
( specificity and sensitivity > 70 % )
f. Other blood increased MCV > 91 and sr uric acid > 7mg/dl

Alcohol hepatitis:
• c/f: anorexia, nausea, weakness, icterus, weight loss or fever.
• Morphological change : liver cell damage, neutrophilic infiltration,
pericellular & perivenular fibrosis, mallory hyaline or mallory body.
• Physical signs: hepatomegaly(95%), hepatic tenderness (50-60%), signs of
portal htn (40-70%) jaundice, fever, upper GI bleeding (30%) & evidence of
hepatic encephalopathy.
• Lab features: bilirubin increase , AST & ALT elevated, PT prolonged.
Hepatic cirrhosis:
• Morphological change : micronodular type.
• c/f: asymptomatic 10-20%, commonly presents with complications and
stigmata of CLD
• Lab features: transaminases incresed, hypoalbuminaemia , PT prolonged.
• Prognosis : Discriminant function = 4.6 *increased PT (sec) + sr bilirubin
(mg)

Treatment
• Dicremination factor > 32 can be tried with steroids
prednisone 40mg/day for four weeks and then taper or
pentoxyphylline.
• Abstinence from alcohol
• Dietary supplementation
• Avoid precipitating factors( infection)
• Treatment of withdrawal syndrome
• Treatment of complications ( ascites, SBP, hepatorenal
syndrome, hepatic encephalopathy, upper GI bleed)
• hepatic transplantation in selected cases

Fetal alcohol syndrome(FAS)
Any unborn child, male
or female of any race
might be affected by the
alcohol that a mother
consumes while she is
pregnant.
FAS in 1 to 2 births /
1,000 in U.S each year.

Drunkenness
• Is a condition produced in a person, who as taken
alcohol in a quantity sufficient to cause him to
lose control of his faculties to such an extent, that
he is unable to execute safely, the occupation in
which he was engaged at the particular time.
• Model scheme of medical examination:
suggested by special committee of British
Medical Association “the drinking driver” 1965.

1. Exclusion of injuries and pathological state: head injury,
metabolic disorder, neurological condition, drugs, pre-existing
psychological disorder.
2. History: relevant events obtained from accused person while
observing him. The amount and time of liquor taken should be noted.
3. General behaviour: state of dress, speech, self control.
4. Memory and mental alertness: memory of recent events,
calculations
5. Hand writing: time taken, repetition or omission of words , ability to
read his own hand writing, sign his name.
6. Pulse: rapid and usually bounding.
7. Temperature: surface temp is usually raised.
8. skin: moist, dry, flushed or pale
9. Mouth: smell of breath
10. Eyes: general, visual acuity, intrinsic muscles (pupils ) ,extrinsic
muscle (nystagmus)
.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS DEPRESSANTS
no 497-514.

11. Ears: gross impairment of hearing
12. Gait: manner of walking, reaction time to
direction to turn, manner of turning
13. Stance. Romberg's sign
14. Muscular coordination: placing finger to nose,
placing finger to finger, picking medium sized objects
from the floor.
15. Reflexes: knee and ankle delayed or sluggish.
Planter reflex may be extensor or flexor
16. Pulmonary, cardiovascular and git systems :
presence or absence of disease
17. Tests: nerve conduction speed, pupillary reflex
time ..ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS

• 18. Lab invest :
Blood: preserved in 100mg sodium fluoride and 30 mg potassium
oxalate for 10ml.
Widmark: evolved a formula which takes into account the size and
sex of person and the type of alcohol liquor consumed,
a=prc
a-weight of alcohol(gm) in body; p-body weight (in kg); c-
concentration of alcohol on blood (mg/kg); r- is constant (0.6 for
men, 0.5 for women)
1. kozelka and hine test is macro method 2. cavett test is a micro
method. ( in a test tube 1ml of unknown solution+ one drop
sulphuric acid + one ml of acetic acid, heat gently for one min,
strong fruity odour is positive.
.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS DEPRESSANTS
no 497-514.

Sample Relative concentration of alcohol at
equilibrium
Whole blood 1
Plasma/serum 1.12 to 1.2
alveoli 0.0021
Spinal fluid 1.1 to 1.27
brain 0.8
vitreous 1.3
Urine 1.3
Liver 0.8

• Breath: alcohol absorbs radiation in infrared region of
spectrum and that the amount of infrared light absorbed
by vapour is proportional to concentration of alcohol in
that vapour.
60-100ml of breath is received in dry balloon and analysed
by drunkometer, drunkotester, intoximeter, alcometer. The
end portion of a prolonged forced expiration gives correct
results. Alcohol in deep lung air is dependent on that of
arterial blood (2100-2300 of alveolar blood contains same
amount of alcohol in 1ml of blood)

Urine: in order to compare the urine and blood, a
ratio of 1.3:1.0 is usually accepted when urine and
blood are in equilibrium.
Disadvantages: 1.time lag before equilibrium
between blood and urine reached; max concentration
reached 20-25 min later than in blood.
Vitreous: not change after death due to putrefaction,
at equilibrium , for every unit of alcohol in blood ,
there are 1.2 units in vitreous
.ESSENTIALS OF FORENSIC MEDICINE K S NARARYAN REDDY 28TH EDITION ; chapter 30 CNS

References
4.CONNS CURRENT THERAPY BOPE KELERMAN 2013, SECTION 16 PSYCHIATRIC DISORDERS- ALCOHOLISM no
921-927.
5.SLEISENGER AND FORDTRANS 9th edition gastrointestinal and liver disease Vol2 Section IX –
6.Neurology in Clinical Practice e-dition, 5th Edition Bradley, Daroff, Fenichel & Jankovic;
chapter 61 Deficiency Diseases of the Nervous System no 1650-1654.
7.PARIKHS TEXT BOOK OF MEDICAL JURISPRUDENCE FORENSIC MEDICINE AND TOXICOLOGY, 6TH
EDITIOIN PART 5 CLINICAL AND FORENSIC TOXICOLOGY SECTION 10, CHAPTER 50 INEBRIANT
POISONS 10.14-10.34.
8.NMS PSYCHIATRY 5th edition JOUHUA T. THORNHILL 4, chapter 5 substance related disorder chapter 7
no 158-159

Ethylene glycol poisoning
 Colourless, odourless ,nonvolatile,water
soluble.
 Paints,polishes, cosmetics,antifreeze.
 Viscous & sweet –poorman’s substitute for
alcohol.
 Minimal lethal dose 1-1.5ml/kg.
 Peak level 1-4 hr.
• Clinical effects
 Stage 1– inebriated without odour of alcohol.
(1-12hrs) other CNS symptoms.
 Stage 2-- CVS changes
(12-24 hrs)
 Stage3-- ARF
(24-72 hrs)
 Lab finding:
oxalate crystals in urine.
hypocalcemia
↑A: G acidosis
tt mainly on history & clinical
symptoms.
 Specific treatment:
ethanol
pyridoxine
thiamine
magnesium
4-methyl pyrazole(antidote)
HD

Isopropyl alcohol poisoning
 2-propanol,isopropanol.
 Clear, volatile ,bitter taste,aromatic
odour
 Solvent, & disinfectant.
 2nd to ethanol as most commonly
ingested alcohol.
 Twice potent than ethanol as CNS
depressant.
 Toxic dose--- 1ml/kg of 70 % solution.
 Lethal dose---2-4ml/kg.
 80% absorbed from GIT in 30 mins.
 Dermal absorption & inhalation.
.PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental health- alcoholism and drug dependence no 774.

 Diagnosis
inebriated with –ve or low
ethanol.
elevated osmolar gap
ketosis without acidosis
 >50mg/dl toxic,200-
400mg/dl lethal.
 Treatment:
GI evacuation.
dialysis if 3-4 ml /kg of
70% solution
blood level
>400mg/dl
unrespnsive
hypotension
renal
failure,coma.
.
PARKS TEXTBOOK OF PREVENTIVE AND SOCIAL MEDICINE ; 21 EDITION ,CHAPTER 18 mental health-

Alcohol and alcoholism

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