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Methanol 
Formaldehyde 
Formic Acid 
Metabolic Acidosis
Renal Toxicity 
 Distributed in the tissues having 
high water content, high conc. Is 
found in vitreous body and optic 
nerve, hence causes optic neuritis.
General signs of poisoning 
 Odour present in breath. 
 Effects on CNS is well marked
Urine is strongly acidic and contain 
acetone and trace of albumin. 
 Metabolic acidosis: Due to excess 
of lactic acid and respiratory 
depression
Retinal ganglion cells and optic disc 
shows degenerative changes. 
 In fatal cases: Convulsions 
 Death may occur from respiratory 
depression
Cause of death: 
 Death is mainly due to metabolic 
acidosis resulting from production of 
organic acids mainly, Formic Acid. 
 CNS depression leading to respiratory 
depression.
 Also known as alcohol or ethyl 
alcohol 
 Considered the same whether 
beverage is wine, beer or hard liquor 
 Classified as a food but contains 
empty calories
 Not digested like other foods 
 It can go directly into the 
bloodstream 
 Alcohol absorption throughout the GI 
tract 
 It is quickly distributed throughout the 
body
 Can be absorbed into the 
bloodstream at: 
• Mouth 
• Esophagus 
• Stomach 
• Small Intestine
 About 20% to 25% is absorbed 
 Factors that influence absorption: 
the rate of intake 
presence of food 
the rate of gastric emptying
 75-80% is absorbed. 
 This absorption is extremely rapid.
 Alcohol Dehydrogenase (ADH) 
• Stomach 
• Liver 
 Microsomal Ethanol Oxidizing System 
(MEOS) 
› Liver
 In the cytoplasm, ADH converts 
ethanol to acetaldehyde 
CH3-CH2-OH + NAD+ CH3-CHO + NADH + H+ 
Ethanol ADH Acetaldehyde
 In the mitochondria, acetaldehyde is 
converted to acetate and in turn acetate is 
converted to acetyl CoA which leads the 
two-carbon molecule into the TCA cycle 
CH3-CHO + NAD+ CH3-COOH + NADH + H+ 
Acetaldehyde ADH Acetate
 Alternate pathway used, in addition to 
ADH, when alcohol intake is excessive 
 End products include: 
• Ethanol  acetaldehyde 
• NADPH + H+  NADP+ 
No ATP formation = Energy Wasteful
LIVER 
 Fatty liver 
 Cirrhosis 
 Hypoglycemia (low blood sugar)
Central Nervous System 
 When intoxication occurs it affects emotional 
and sensory function, judgment, memory and 
learning ability 
 Smell and taste are dulled 
 Ability to withstand pain increases 
 Long term effects include tolerance, 
dependency and irreversible damage 
 Brain is most affected
Blood 
 Blood-Sludging 
 Anemia 
 Weakness of bone structure 
 Decrease resistance to infection and 
inability to fight off infections
Muscles 
 Reduced blood flow. Causing muscle weakness 
and deterioration 
 Irregular heartbeat, sluggish heart, and muscle 
aches
Endocrine 
 Sedates glands 
 Sexual functioning 
-Low doses decrease 
inhibitions 
-High doses decrease 
sexual functioning for 
men and women
Acetyl salicylate 
Acetylsalicylate inhibits prostaglandin 
and thromboxane production by human 
platelets suspended in plasma or buffer. 
Acetylsalicylate inhibits arachidonate-induced 
aggregation of human platelets 
suspended in plasma 
This compound belongs to the 
phenol esters. These are aromatic 
compounds containing a benzene ring 
substituted by an hydroxyl group and an 
ester group.
Absorption 
Absorption is generally rapid and 
complete following oral administration but may 
vary according to specific salicylate used, 
dosage form, and other factors such as tablet 
dissolution rate and gastric or intraluminal pH.
Mechanism of action 
Acetylsalicylic acid's antirheumatic ( anti-inflammatory) 
actions are a result of its analgesic 
and anti-inflammatory mechanisms. 
the therapeutic effects are not due to 
pituitary-adrenal stimulation. 
The platelet aggregation-inhibiting effect of 
acetylsalicylic acid specifically involves the 
compound's ability to act as an acetyl donor to 
cyclooxygenase. 
the nonacetylated salicylates have no 
clinically significant effect on platelet aggregation.
Effects of overdose 
 abdominal pain, 
hypokalemia, 
hypoglycemia, 
pyrexia, 
hyperventilation, 
dysrhythmia, 
hypotension, 
hallucination, 
renal failure, 
 confusion, 
seizure, 
coma, 
 death.
Forensic methanol gopi
Forensic methanol gopi

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Forensic methanol gopi

  • 1.
  • 2.
  • 3.
  • 4. Methanol Formaldehyde Formic Acid Metabolic Acidosis
  • 5. Renal Toxicity  Distributed in the tissues having high water content, high conc. Is found in vitreous body and optic nerve, hence causes optic neuritis.
  • 6. General signs of poisoning  Odour present in breath.  Effects on CNS is well marked
  • 7. Urine is strongly acidic and contain acetone and trace of albumin.  Metabolic acidosis: Due to excess of lactic acid and respiratory depression
  • 8. Retinal ganglion cells and optic disc shows degenerative changes.  In fatal cases: Convulsions  Death may occur from respiratory depression
  • 9. Cause of death:  Death is mainly due to metabolic acidosis resulting from production of organic acids mainly, Formic Acid.  CNS depression leading to respiratory depression.
  • 10.
  • 11.  Also known as alcohol or ethyl alcohol  Considered the same whether beverage is wine, beer or hard liquor  Classified as a food but contains empty calories
  • 12.  Not digested like other foods  It can go directly into the bloodstream  Alcohol absorption throughout the GI tract  It is quickly distributed throughout the body
  • 13.  Can be absorbed into the bloodstream at: • Mouth • Esophagus • Stomach • Small Intestine
  • 14.  About 20% to 25% is absorbed  Factors that influence absorption: the rate of intake presence of food the rate of gastric emptying
  • 15.  75-80% is absorbed.  This absorption is extremely rapid.
  • 16.  Alcohol Dehydrogenase (ADH) • Stomach • Liver  Microsomal Ethanol Oxidizing System (MEOS) › Liver
  • 17.  In the cytoplasm, ADH converts ethanol to acetaldehyde CH3-CH2-OH + NAD+ CH3-CHO + NADH + H+ Ethanol ADH Acetaldehyde
  • 18.  In the mitochondria, acetaldehyde is converted to acetate and in turn acetate is converted to acetyl CoA which leads the two-carbon molecule into the TCA cycle CH3-CHO + NAD+ CH3-COOH + NADH + H+ Acetaldehyde ADH Acetate
  • 19.  Alternate pathway used, in addition to ADH, when alcohol intake is excessive  End products include: • Ethanol  acetaldehyde • NADPH + H+  NADP+ No ATP formation = Energy Wasteful
  • 20. LIVER  Fatty liver  Cirrhosis  Hypoglycemia (low blood sugar)
  • 21. Central Nervous System  When intoxication occurs it affects emotional and sensory function, judgment, memory and learning ability  Smell and taste are dulled  Ability to withstand pain increases  Long term effects include tolerance, dependency and irreversible damage  Brain is most affected
  • 22. Blood  Blood-Sludging  Anemia  Weakness of bone structure  Decrease resistance to infection and inability to fight off infections
  • 23. Muscles  Reduced blood flow. Causing muscle weakness and deterioration  Irregular heartbeat, sluggish heart, and muscle aches
  • 24. Endocrine  Sedates glands  Sexual functioning -Low doses decrease inhibitions -High doses decrease sexual functioning for men and women
  • 25. Acetyl salicylate Acetylsalicylate inhibits prostaglandin and thromboxane production by human platelets suspended in plasma or buffer. Acetylsalicylate inhibits arachidonate-induced aggregation of human platelets suspended in plasma This compound belongs to the phenol esters. These are aromatic compounds containing a benzene ring substituted by an hydroxyl group and an ester group.
  • 26. Absorption Absorption is generally rapid and complete following oral administration but may vary according to specific salicylate used, dosage form, and other factors such as tablet dissolution rate and gastric or intraluminal pH.
  • 27. Mechanism of action Acetylsalicylic acid's antirheumatic ( anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms. the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase. the nonacetylated salicylates have no clinically significant effect on platelet aggregation.
  • 28. Effects of overdose  abdominal pain, hypokalemia, hypoglycemia, pyrexia, hyperventilation, dysrhythmia, hypotension, hallucination, renal failure,  confusion, seizure, coma,  death.