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Intoxication Case Analysis

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    Case analysis

    Alcohols

    Cyanide

    Arsenic

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    Case 1

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    Question 1

    One man, Alexander Zhbckov, 28, died atthe Bodrum State Hospital as doctors were

    unable to stabilize her condition, afterdringking alcohol. Weight: 70 kg, Alcoholconcentration 50g. How much blood

    alcohol level?

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    Alcohols

    Ethanol is beverage alcohol

    Metanol and isopropanol are also available in theenvironment or workplace and may contribute tohuman injury

    Ninety minutes after ethanol ingestion is theapproximate time to the achievement of peak bloodlevels

    Cp (blood concentration) = D(g)/(Vd(L/kg)xW(kg))

    D: dose; Vd: Volume of distribution (0,7 in man and 0,6in women); W: body weight in killograms

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    Toxicology of AlcoholAlcohol is absorbed through the stomach and

    intestine

    Once absorbed, alcohol is: Oxidized- in liver by alcohol dehydrogenase

    Excreted- by breath, perspiration, and kidneysturnedinto carbon dioxide and water

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    Assessment of Ethanol Impairment Blood alcohol concentration:

    10-50 mg/dL: Impairment detectable by special tests

    30-120 mg/dL: Beginning of sensory-motor impairment

    90-250 mg/dL: Sensory-motor incoordination;impaired balance

    180-400 mg/dL: Increased muscular incoordination;apathy; lethargy

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    Assessment of Ethanol Impairment Blood alcohol concentration:

    250-400 mg/dL: Impaired consciousness; sleep; stupor

    350-500 mg/dL: Complete unconsciousness; coma 450 and greater mg/dL: Death from respiratory arrest

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    Case 2

    -What is the name of this phenomenon?-What is the name of poison?

    -In cyanide poisoning, what is the componentthat form that phenomenon?

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    Cyanide

    Cyanide is dangerous because it binds to ferric ionsin cytochrome oxidase, an enzyme in the electrontransport system within the mitochondria of cells

    Cherry red livor mortis because of

    cyanomethaemoglobin formation Forensic laboratories can tes for cyanide in whole

    blood and its concentration correlates well withseverity of poisoning.

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    Arsen Industrial processes Semiconductor manufacturing (gallium arsenide)

    Fossil fuels

    Wood treated with arsenic preservatives Smelting (copper, zinc, lead) and refining of metals and

    ores

    Glass manufacturing

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    ArsenicAcute Poisoning Ingestion of large doses (70180 mg) of inorganic

    arsenic can be fatal

    Symptoms of acute intoxication include:Fever

    Anorexia

    Hepatomegaly

    Melanosis

    cardiac arrhythmia

    in fatal cases, eventual cardiac failure

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    nifestation

    sofacutearsenic

    poisoning

    Bodily system affected Symptoms or signs Time of onset

    Systemic ThirstHypovolemia, Hypotension

    MinutesMinutes to hours

    Gastrointestinal Garlic or metallic tasteBurning mucosaNausea and vomitingDiarrhea

    Abdominal pain

    HematemesisHematochezia, melenaRice-water stools

    ImmediateImmediateMinutesMinutes to hoursMinutes to hours

    Minutes to hoursHoursHours

    Hematopoietic system HemolysisHematuriaLymphopeniaPancytopenia

    Minutes to hoursMinutes to hoursSeveral weeksSeveral weeks

    Pulmonary(primarily in inhalationalexposures)

    Cough

    DyspneaChest PainPulmonary edema

    Immediate

    Minutes to hoursMinutes to hoursMinutes to hours

    Liver JaundiceFatty degenerationCentral necrosis

    DaysDaysDays

    Kidneys ProteinuriaHematuria

    Acute renal failure

    Hours to daysHours to daysHours to days

    rsen cAcute Poisoning

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    ArsenicChronic ToxicitySkin Diffuse or spottedhyperpigmentation and, alternatively,

    hypopigmentation can first appear between 6 months to 3

    years with chronic exposure to arsenic

    Skin cancer is common with

    protracted high-level arsenical exposure

    Palmar-plantar hyperkeratosis usuallyfollows the initial appearance of arsenic-induced pigmentation changes within a

    period of years

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    ArsenicChronic ToxicityLiver Characteristic of long-term or chronic arsenic

    exposure, manifests :jaundice

    abdominal pain

    hepatomegalyprogress to cirrhosis and ascites

    even to hepatocellular carcinom

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    ArsenicChronic ToxicityPeripheral neurophathy Repeated exposure to low levels of inorganic arsenic

    can produce This neuropathy usually begins with :

    sensory changes

    numbness in the hands and feetpainful pins

    and needles sensationmotor nerves be affected

    muscle tenderness

    weaknes progressing from proximal to distal

    muscle groupss

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    ArsenicChronic Toxicitycardiovascular disease Peripheral vascular disease has been observed in

    persons with chronic exposure to inorganic It is manifested :

    acrocyanosis

    progress to endarteritis andgangrene of the lower extremities

    (Blackfoot disease).

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    Reference

    Abdul Munim Idries, dkk, 1979 : Ilmu KedokteranKehakiman , cetakan I, Jakarta.

    Ariens E.J.,dkk., 1993 : Toksikologi umum

    (pengantar), Gadjah Mada University Press,Yogyakarta. Flanagan R.J., dkk., 1995 : Analisis Toksikologi

    Dasar, International Programme on ChemicalSafety, WHO, Geneva.


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