alcohol and road

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    Alcohol and road traffic

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    45% of car accidents are caused at an

    alcoholemy of

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    The alcohol is dangerous because its effects:

    negative psichological (optimism, exagerated

    selfconfidence, reduced selfcriticism and

    selfcontrol

    physiological (reflex deprimation)

    sensorial (diminuation of visual field, difficulties in

    estimating the distances and speed of thecomming vehicles)

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    Reaction time at noticing an obstacle is 0.75 s,

    at alcoholemy level this value is three times

    bigger

    The braking distance at 100 km/h is 75 m ->

    will become 225 m

    0.5g% alcoholemy doubles the risks of car

    accident, it will double at every 0.5g%

    alcoholemy

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    Alcoholometry

    The alcoholometry estimates the alcohol level in theorganism by measuring its concentration in the expiredair

    It is a chemical reaction of oxidation -> the

    alcoholometer becomes green (it contains bichromatof potassium)

    This permits only sanctions, it has not the character ofan evidence at the justice

    Modern alcoholometers are based on one of theproperties of the alcohol: the intensity absorbtion ofinfrared light is directly proportional with theconcentration of alcohol in the expired air

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    2.1 l alveolar air contains the same ammount

    of alcohol as 1 ml blood

    blood/alcohol in expired air =1/2100

    Blood Expired Air

    0.80 g%o 0.40 g%o

    1.20 g%o 0.60 g%o

    2.00 g%o 1.00 g%o

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    Alcohology notions

    Chemically the alcohols conatin C, O, H and havethe capacity to bind directly with acids

    The alcohols are largely used in many domains

    We are interested in the per os use of alcoholicdrinkables, nutritive value of alcohol, acute andchronic intoxication with alcohol, acuteintoxication with ethanol, therapeutic use of

    alcohol Many of there problems have medico-legal and

    major juristic implications

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    1. Classification of alcoholic drinks and

    their nutritive values

    A. The way of preparation Examples

    Fermented alcoholic drinks direct fermentation of the sugar grape wine, beer

    Distilled alcoholic drinks distillation of fermentated drinks brandy, cogniac, plum

    brandy (uic)Industrial alcoholic drinks fermentation of a must or potato or

    cereals juice

    B. Ammount of alcohol

    Strong alcoholic drinks 25-30% alcohol plum brandy, rom,

    cogniac, whiskyMedium strength alcoholic

    drinks

    8-12% alcohol wine

    Light alcoholic drinks 1-9% alcohol beer, some fruit juices

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    As calory source the alcohol can cover some of

    these kind of necessity:

    In Germany it covers 8%

    In France it covers 10%

    It can cover 50%, but the avitaminoses are

    cauzed by the alcohols reduced ammount of

    vitamins

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    2. Therapeutic use of alcohol

    Solvent for drugs

    Reduces transpiration, good extern desinfectant(in 70% conc.)

    It is used in ganglionar alcoholisation Increases the apetite, decreases the meteorism

    and colicas

    In inhalation it decreases the pulmonary edemaby decreasing the superficial tension

    Sedative and anesthetic

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    I. Pharmacokinetiks and

    pharmacodynamicsI.1. Absorbtion

    Ethanol is rapidly absorbed from the gastrointestinal tract(gastric20% - and duodenal80% - mucosa) by diffusion

    Also at the buccal mucosa

    Small cantities in the lungs

    Absorbtion speed in the gastric and duodenal mucosadepends of: The concentration of the alcohol in the ingested drink

    Speed and rhytm of ingestion

    The absence or presence of food in the stomac and their type: Fat, proteins and milk slow the absorbtion

    Anti-cholinergics, neuroleptics, triciclic antidepressants slows downthe absorbtion

    Diseases of the stomach

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    At the begining of the ingestion theabsorbtion speed is high (expecially strongdrinks) then slows down -> the absorbtion

    may last 2-6 hours Following the ingestion on an empty stomach,

    peak levels occur in to 2 hours

    Ethanol rapidly distributes into the body waterand equilibrates very rapidly with it targetorgans

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    I.2.Distribution of the alcohol in the organism.Alcoholemy

    Reaches the vena portae and liver -> is distributed in

    the organisms liquids: extra- and intracellular fluids Repartisation in tissues is done based on the tissueswater and fat content -> more watermore alcohol

    The alcohol concentration in plasma is bigger than inRBC so the alcohol determination is done onanticoagulated blood

    The concentration is bigger in arterial blood than invenous

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    Ethanol blood concentration may be used to

    estimate the level of ethanol in the brain

    The equilibrium between the concentration of

    ethanol in the blood and in the expired air is

    attained rapidly

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    Alcoholemy curve

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    Alocoholemy reaches the maximum level after 30-120 minsfrom ingestion

    Alcohol concentration in any tissue results from: diffusionspeed / oxidation speed

    The time and values of maximum levels of alcohol variesdepends in the same time of the detoxification processes

    Based on the nature of the alcohol the period when thealcoholemy is at maximum level varies from 30 mins to 90mins

    Around 90-95% of absorbed alcohol is oxidated, the rest 5-10% is eliminated in the urine, respiration, saliva and sweat

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    1 g%o alcoholemy is reached by ingestion of 1g

    alcohol/kg

    Concetrated alcoholic drinks are absorbed quickly

    At an adult with average weight 45 g ingerated

    alcohol (as whisky) with empty stomac results a

    0.650.90 g/o alcoholemy, but in case of alimentconsumption the alcoholemy would be

    approximatelly half of this value

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    Consumed aliments and their type influences

    the alcoholemy:

    Fat and sugar flattens the curve

    Proteins lowers the alcoholemy

    Ingestion of a greater cantity of fruits results a

    0.48g%o alcoholemy

    At diabetics the alcoholemy may be much greaterafter the ingestion of the same alcohol as a

    healthy person

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    I.3. Elimination of the alcohol or post-absorbtionphase

    Ethil-oxidation coeficiency: cantity of oxidated

    alcohol on minute/kg body The elimination is low at the begining of the

    absorbtion period, it will end in 24 hours afterthe ingestion, being dependent of many fators

    (also constitutional) The ethil-oxidation coeficiency is constant for the

    same person

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    The elimination of the alcohol is cantitatively proportionalwith its concentration in the blood

    The curve is different in small alcoholemies and hugealcoholemies

    An adult eliminates 6.33 g alcohol/h (3.6-10.6g) Women eliminates more alcohol than men

    Urine/alcohol in blood=1.30-1.40

    Concentration of alcohol in blood/alveolar air=1/2000

    The smell of alcohol is from the aromatic substances

    0.5-2% of the ingerated alcohol is eliminated in the lungs: inthe lungs the organism eliminates 1g alcohol/hour (if thealcoholemy and hiperventilation are raised

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    Mean value of metabolic rate at the descendingphase is: 0.15g/1.000 ml/hour (0.110.22 g/1000ml/hour)

    men

    0.18 g/1000ml/hour women

    It has huge variations, so juridically it isconsidered that tha elimination rate is

    0.15g/1000ml/hour At chronic alcoholists the elimination rate is

    0.27g/1000ml/hour (0.16-0.43g/1000ml/hour

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    Elimination can be appreciated with Michaels-

    Menten equation:dC = VmaxC

    dt Km+ C

    Where the elimination rate (dC/dt) depends on the

    maximum elimination rate (Vmax), Michaelis

    constant (Km)and concentration. The Michaelis

    constant is the substrate concentration at which

    the reaction rate is half of Vmax.

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    I.4. Metabolisation process of the alcohol

    Absorbtion -> oxidation (quick process)in liver throughthe ADH (alcohol-dehidrogenase system); also atmicrosomal level and catalase-peroxidase system

    I.4.1. Alcohol-dehidrogenase (ADH) Large specificity enzyme including the steroids

    dehidrogenase and a megaoxidation of fatty acids.

    Most of it is in the liver and participate in the process

    of transforming the ethanol in the liver Codehydraseis a coenzyme which is a NAD (nikotine-

    adenine-dinucleotide) which is the receptor of H

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    The oxidation process in the liver

    1st phase: alcohol -> acetic-aldehide (the alcohol loses2H)

    2nd phase: acetic-aldehide -> acetate

    The 1st phase is catalised by the ADH which is in thehepatic citosole, it cannot be found in the blood

    In the kidney the concentration of ADH is very high -> canassure the degradation of alcohol until CO2 and H2O

    ADH is a metalic (Zn++) ezyme, which is incorporated

    through biosynthesis -> element which gives possibility toform an active complex of enzyme-coenzyme (thecoenzyme is is phosphorilated-NAD)

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    Rate: 15mg/h

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    The acetate transforms in acetil-coenzyme A

    which oxidates in Krebs cycle

    Micro-somal system: 20% of the alcohol is

    burned

    The catalase-peroxidase system intervines in

    high alcoholemies

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    In some of the oriental people there is an

    immediate hypersensitivity to alcohol

    ingestion, named oriental reaction or flash

    reaction, due to acetaldehyde accumulationbecause of the alcohol dehydrogenises

    increasing or acetaldehyde dehydrogenises

    diminution. This is a state due to thehallucinogen effect of acetaldehye, but is

    different from the pathological drunkenness

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    Simptomatoloy of acute ethilic

    intoxication

    Alcoholemy level Intoxication signs

    4.0 g%o death - cardio-respirator stop

    Entrance ways:

    orally (by ingestion)the most common way

    inhalationvery rarely

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    Simptomatology

    Actions on the CNS Acute doses of ethanol depress the excitability at all

    levels of the CNS enhancing GABA neurotransmission

    Ethyl-alcohol determines a state of hypoxia to the

    neural cells, reducing their activity The depressant action begins in the superior parts of

    the brain (the most developed) amd goes downthrough the bulb

    If only superior parts of the brain are affected, thebehavior will be more primitive and understainedwhich seems to be a false simulator efect (the inferiorparts of the brain being controlled byy the superiorparts due to their inhibition

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    Actions on gastrointestinal tract

    Chronic alcoholic is associated with

    Malabsorption of fat, folic acid, thiamine and vit B12

    Accumulation of fat in the liver and cirrhosis

    Cancer of the liver and of the GI tract

    Effects on kidney

    Produces diuresisinhibits the antidiurethichormone

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    Ethanol intoxication

    The ethanol intoxication is produced in 3clinical phases:

    1. Until an amount of 1g%o - excitation of

    intellectual functions, euphoria,vasodilatation, tachicardia, psycho-motorexaltation, diminished reflex activity,decreased reaction speed, midriasis,

    nystagmus, perspiration, the sensation ofwarmth

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    2. Alcohol level between 12.50 %oProfound

    psycho-sensorial disturbances. The

    disturbances affects the intelligence,

    guidance and motricityIt is also called the medico-legal phase, because in

    this phase are commited many antisocial acts

    and accidents.

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    The alcohol is the intelligences poison: theautocritics is abolished, intelectual-rationalment functions, attention, memory

    are altered, words are incoherent, absurd.Instincts and passions are takeing control.Vestibulo-labirintial disturbances are present,also agression. Vomiting and hiccups are

    indicating the involment of the medullaoblongata. Increased heart and respiratoryrhytm

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    3. Comatose phaseabove 3.0 g%o alcoholemy

    decrease in alkaline reserves -> marked acidosis;decrease of the ureea level in blood;

    hipercholesterolaemia;profound sleep, anesthesia, hypothermia, coma

    - Death is caused by the respiratory depression,hypotension, hypothermia, hypoglycemia

    - Lethal dose: 300-500 ml (equivalent to about alitre of whisky) if taken in less than an our

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    Death can also be caused by an acute methabolicdecompensation of alcoholic ketoacidosis (AKA)or alcoholic lacticacidosis (ALA) type

    Common simptoms: nausea, vomiting, abdominalpain, tachicardia and Kussmaul type respiration

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    Alcoholic ketoacidosis (AKA)

    Excessive ingestion of alcohol increases the

    NADH/NAD+ratio which inhibits the

    gluconeogenesis and utilisation of free fatty

    acids. Simultaniously decreased ingestion ofcarbohidrates causes a depletion of glycogen and

    reduction of gluconeogenesis, with decreased

    release of insulin -> increased lipolysis ->

    increase of ketonic bodies.

    Normal values of ketonic bodies: 2.33.5 mg/l

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    Alcoholic lacticacidosis (ALA)

    It is determined by the increase of theNADH/NAD+ratio with the increase of lactateor piruvate, diminished gluconeogenesis and

    decrease of hepatic reconversion of lactate.Major causes are malnutrition and thiaminedeficiency at chronic alcoholics. At alcoholics,ALA cand be triggered by hypothermia.

    Diagnosis is put when the sum of glucose +lactate in the vitreous humour is bigger than300mg/dl

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    Laboratory diagnosis

    1.1 Measuring/Dosage of the alcohol in theexpired air:

    Henrys law: at a given temperature, the mass ofgas disolved in the volume of a liquid isproportional with the pressure exerted of the gason the liquid

    Ratio of alcohol: 1/2000 -> 1ml blood contains asmuch alcohol as 2000 ml alveolar air

    Alcohol tests!

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    1.2. Measuring/Dosage of the alcohol in the

    blood:

    Cromatography, titrimetrybased on the

    property of alcohol that it can be oxidated by asulfo-cromic mixture, like Nicloux method

    The official method in Romania is the CORDEBARD

    method (the nitro-chromic oxidation) it needs at least 10 ml venous blood for

    determinatios

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    1.3. Interpreting the results and some medico-legal problems regarded to the alcoholemy

    a. Factor RWIDMARKto calculate the total

    cantity of alcohol in the organism:

    concentration of alcohol in organism (whole body)alcoholemy

    normal value= 0.70; if the alcoholemy is multiplied withthe R factor and the weight of the body, the total cantityof alcohol is obtained

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    Practically the determination of the total

    ammount of ingested alcohol depends of

    many factors, but using this formula we can

    deduce:

    alcoholemy (g%o) x body weight (kg)

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    Another problem is calculating the alcoholemy

    for the moment when the traffic happening

    was produced, knowing the time elapsed until

    taking the blood sample.

    Taking in consideration the ethil-oxidation

    factor (0.120.18 g%o/h) this is possible for a

    5-6 hours period. (IML Bucuresti)

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    1. Calculation of the alcoholemy based on the

    ingestion datas (without lab exam of the blood

    sample):alcohol conc. In blood g%o= A/B

    A= ingested alcohol

    B=body weight

    A= TxVxd/100 d=alcohol density0.8- When more types of alcohol are consumed A will be the

    sum of each type

    - In case of strong alcohols the value increases with 30%

    - Maximum level of alcoholemy with empty stomac isreached in 30 mins, with full stomac in 90-120 mins

    (based on the way of consuption and type of alcohol

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    2. Retrospective calculation of the alcoholemy

    - This is effectuated for the eliminatory phase of

    alcohol, when from the traffic event and blood

    sample had passed an interval of time (more

    then 30-60 mins)

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    The alcoholemy value is given by the relation:

    alcoholemy g%o = alcohol conc. g%o + BxT

    B=coeficiency of ethil-oxidation 0.15 g%o/hour

    T=time between traffic event and blood sample

    It is done max. 7-8 hours retroactiveabove this

    period it has only informative value

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    Treatment

    Symptomatic

    Correction any physiological dysfunctions, as

    possible acid-basic or electrolytic disorders,

    hypoglycemia, hypovitaminosis

    Maintaning respiratory tracts open

    Metadoxine has been used with succes

    accelerates the urinary elimination of ethanol

    and acetaldehyde

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    Alcohol and traffic accidents

    Traffic accidents: 250000 death/year; 10 mill.injuries/year40% remains with infirmities

    In Romania 58.25% of the accidents are thedrivers fault and 10.2 % are caused by alcohol

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    Legislative problems: Art. 38. Driving an automobile on public roads by a

    person who has in his blood an alcohol inhibitionabove the legal limit (alcoholemy >0.8 g%o) or which

    is in drunkennes condition, is punished with 1-5 yearsof imprisonment.

    Evasion from taking biological samples to determinethe alcoholemy is punished with 1-5 years ofimprisonment

    Art.41. The right of driving an automibile is suspendedin case of: driving an automobile under the influenceof alcoholic drinks..(>0.8g%o)

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    Medical examination of the driver to determinethe condition of alcoholic intoxication

    The alcoholtest is a way of sorting, it is based onoxidation (sulpho-chromic content of the tube) ofthe expired alcohol with the alveolar air, whichmanifests in changing the colour (green,dependending of the alcoholemy: green it >0.40g%o alcoholemy)

    The legal limit of infractionality in Romania is>0.80 g%o

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    Juridical regime in alcoholism: In acute volunteer drunkennes the person has

    responsability for his acts

    Intentioned drunkennes (drinks to make courage) isan agravant factor

    Acute accidental drunkenness excuses the personfrom the responsability for his acts

    In pathological drunkenness there is no responsabilityfor the persons acts

    Psychotic manifestations of chronic alcoholics doesnot involve penal liability