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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.