This document summarizes the duties and responsibilities of doctors in cases of suspected poisoning. It describes relevant sections of the Indian Penal Code and Criminal Procedure Code, including requirements to preserve evidence and inform authorities. It also provides guidance on treating specific types of poisoning through gastric lavage, activated charcoal, and antidotes. Common poisons discussed include organophosphates, heavy metals, acids, and other toxic substances. Post-mortem findings are also outlined.
1. Alcohol is a depressant that slows down the body and mind, affecting reaction time, decision making, and judgment. Its effects are felt quickly upon consumption as it is absorbed into the bloodstream within 5-10 minutes.
2. Drinking alcohol can damage many organs, especially the brain and liver. Even low doses can impair functions while high doses can cause loss of consciousness, coma, or death. The liver is responsible for filtering alcohol but can only process about one drink per hour.
3. Binge drinking and underage drinking are especially dangerous and illegal, increasing risks of injuries, alcohol poisoning, liver disease, and other health issues. The safest amount of alcohol is none. Treatment
This document discusses neurotics and alcohol. It describes different categories of neurotics including cerebral, spinal and peripheral neurotics. It then discusses alcohol in depth, including its absorption, distribution, metabolism, excretion, actions, acute and chronic poisoning, and treatment for alcohol poisoning. Key points include alcohol is primarily metabolized in the liver, it has depressant effects on the central nervous system, and chronic alcohol use can lead to organ damage and conditions like cirrhosis of the liver.
This document discusses neurotics and alcohol. It defines different categories of neurotics such as cerebral, spinal, and peripheral neurotics. It then discusses alcohol in depth, including its absorption, distribution, metabolism, excretion, actions, acute and chronic poisoning, and treatment. It defines terms like inebriation and provides details on ethyl alcohol including its production, consumption levels, and percentages in different alcoholic beverages.
The document discusses various types of alcohols such as ethyl alcohol and methyl alcohol, how alcohols like ethanol are manufactured through fermentation, and the pharmacological effects of acute and chronic alcohol consumption including intoxication, organ damage, and diseases like cirrhosis as well as the potential benefits and uses of alcohol in small amounts.
This document summarizes information on arsenic and lead poisoning. It discusses the sources, physical properties, uses, and toxic effects of arsenic and lead. For both poisons, it describes the absorption, distribution, and mechanisms of toxicity. The clinical manifestations of acute and chronic poisoning are outlined for each element. Diagnosis involves measuring levels in blood and urine. Treatment of arsenic poisoning involves chelation therapy with BAL, penicillamine or DMSA. For severe lead poisoning, chelation with CaNa2EDTA or BAL is recommended along with supportive care. Mild to moderate lead poisoning is treated with oral chelation agents like D-penicillamine.
This document discusses various corrosive poisons including acids and alkalies. It describes their properties, clinical effects, post-mortem findings, and medicolegal aspects. Major acids discussed are sulfuric acid, nitric acid, hydrochloric acid, oxalic acid, and carbolic acid. Their local tissue-destroying effects and systemic toxicity are outlined. Major alkalies covered are ammonia, potassium hydroxide, sodium hydroxide, and sodium/potassium carbonates. Their caustic properties, inhalation dangers, and causes of death are summarized. The document provides details on evaluating and treating corrosive poisoning cases.
This document summarizes the duties and responsibilities of doctors in cases of suspected poisoning. It describes relevant sections of the Indian Penal Code and Criminal Procedure Code, including requirements to preserve evidence and inform authorities. It also provides guidance on treating specific types of poisoning through gastric lavage, activated charcoal, and antidotes. Common poisons discussed include organophosphates, heavy metals, acids, and other toxic substances. Post-mortem findings are also outlined.
1. Alcohol is a depressant that slows down the body and mind, affecting reaction time, decision making, and judgment. Its effects are felt quickly upon consumption as it is absorbed into the bloodstream within 5-10 minutes.
2. Drinking alcohol can damage many organs, especially the brain and liver. Even low doses can impair functions while high doses can cause loss of consciousness, coma, or death. The liver is responsible for filtering alcohol but can only process about one drink per hour.
3. Binge drinking and underage drinking are especially dangerous and illegal, increasing risks of injuries, alcohol poisoning, liver disease, and other health issues. The safest amount of alcohol is none. Treatment
This document discusses neurotics and alcohol. It describes different categories of neurotics including cerebral, spinal and peripheral neurotics. It then discusses alcohol in depth, including its absorption, distribution, metabolism, excretion, actions, acute and chronic poisoning, and treatment for alcohol poisoning. Key points include alcohol is primarily metabolized in the liver, it has depressant effects on the central nervous system, and chronic alcohol use can lead to organ damage and conditions like cirrhosis of the liver.
This document discusses neurotics and alcohol. It defines different categories of neurotics such as cerebral, spinal, and peripheral neurotics. It then discusses alcohol in depth, including its absorption, distribution, metabolism, excretion, actions, acute and chronic poisoning, and treatment. It defines terms like inebriation and provides details on ethyl alcohol including its production, consumption levels, and percentages in different alcoholic beverages.
The document discusses various types of alcohols such as ethyl alcohol and methyl alcohol, how alcohols like ethanol are manufactured through fermentation, and the pharmacological effects of acute and chronic alcohol consumption including intoxication, organ damage, and diseases like cirrhosis as well as the potential benefits and uses of alcohol in small amounts.
This document summarizes information on arsenic and lead poisoning. It discusses the sources, physical properties, uses, and toxic effects of arsenic and lead. For both poisons, it describes the absorption, distribution, and mechanisms of toxicity. The clinical manifestations of acute and chronic poisoning are outlined for each element. Diagnosis involves measuring levels in blood and urine. Treatment of arsenic poisoning involves chelation therapy with BAL, penicillamine or DMSA. For severe lead poisoning, chelation with CaNa2EDTA or BAL is recommended along with supportive care. Mild to moderate lead poisoning is treated with oral chelation agents like D-penicillamine.
This document discusses various corrosive poisons including acids and alkalies. It describes their properties, clinical effects, post-mortem findings, and medicolegal aspects. Major acids discussed are sulfuric acid, nitric acid, hydrochloric acid, oxalic acid, and carbolic acid. Their local tissue-destroying effects and systemic toxicity are outlined. Major alkalies covered are ammonia, potassium hydroxide, sodium hydroxide, and sodium/potassium carbonates. Their caustic properties, inhalation dangers, and causes of death are summarized. The document provides details on evaluating and treating corrosive poisoning cases.
This document provides information on corrosive poisons including sulfuric acid, oxalic acid, phenol, and nitric acid. It describes their physical and chemical properties, mechanisms of action, clinical features of poisoning, treatment approaches, causes of death, and post-mortem appearances. It also discusses their judicious and injudicious uses and medicolegal significance. The document is intended to educate about these dangerous corrosive poisons through detailed descriptions and comparisons.
Mercury is a liquid metal that is highly toxic, especially in its vaporized form and when ingested as certain mercury compounds. The document discusses mercury's properties and various forms, how mercury poisoning affects the body and can cause damage to organs like the kidneys and brain, symptoms of both acute and chronic mercury toxicity, treatment options, and postmortem findings related to mercury poisoning.
Ethanol acts as a central nervous system depressant by enhancing the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. It is metabolized in the liver by alcohol dehydrogenase and aldehyde dehydrogenase. Acute intoxication can cause impairment, loss of coordination, and respiratory depression, while chronic use is associated with conditions like cirrhosis of the liver and cardiomyopathy. Treatment for acute intoxication involves maintaining airway and circulation, gastric lavage, glucose supplementation, and benzodiazepines for seizures. Chronic alcoholism is treated with supervised withdrawal, benzodiazepine substitution, psychotherapy, and disulfiram to produce an aversive reaction if alcohol is consumed. Methanol poisoning is treated
This document discusses various post-mortem changes that can help estimate time since death, including lividity, rigor mortis, decomposition, and biochemical changes in vitreous humor, blood, and cerebrospinal fluid over time. Measurement of facial hair growth or food digestion can also provide clues to estimate how long someone survived after their last shave or meal. Radiocarbon dating of bone can also potentially estimate time of death for skeletal remains.
Methanol poisoning causes metabolic acidosis, optic neuritis, renal toxicity, and CNS depression. Symptoms include odor on breath, acid urine with acetone and albumin, retinal ganglion cell degeneration, and convulsions. Death is mainly due to metabolic acidosis from formic acid production and respiratory depression from CNS effects.
Inorganic (non metallic) irritant Poisons by Sunil Kumar Dahasunil kumar daha
Please find the power point on Inorganic (non metallic) irritants poisons. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
A presentation on Arsenic Poisoning, from a brief history, compounds, uses, circumstances of poisoning, types with clinical symptoms, diagnosis, treatment and postmortem findings. Subject from Forensic Medicine and Toxicology.
#arsenicpoisoning #arsenic
This document summarizes information about gastric acid secretion and factors that influence it. It discusses:
1) Gastric acid is produced by parietal cells in the stomach and plays a key role in protein digestion. Parietal cells secrete acid in response to gastrin, histamine, and acetylcholine.
2) Peptic ulcers are caused by an imbalance between gastric acid and the protective mucus lining, often due to H. pylori infection. Antacids and proton pump inhibitors are used to treat ulcers by reducing acid.
3) Proton pump inhibitors irreversibly block the proton pump in parietal cells, strongly inhibiting gastric acid secretion.
This document discusses corrosive poisoning from ingesting or contacting strong acids and bases. It notes that these chemicals can erode and destroy surfaces and cause systemic effects. Treatment involves dilution, avoiding gastric lavage, and symptomatic care. Complications can be acute like perforations or chronic like strictures. Death typically occurs from circulatory collapse within 12-24 hours. Postmortem findings include blackened and eroded stomach lining with potential perforations. The document also discusses vitriolage, which is the malicious throwing of corrosives like sulfuric acid to disfigure victims, which causes severe burns.
1. The document discusses acid-base disturbances and defines acids, bases, and pH. It explains how acids and bases are produced and balanced in the body to maintain a normal blood pH.
2. When there is excess acid or base in the blood, compensation mechanisms attempt to return the pH to normal through buffers, lungs, and kidneys. However, disease can cause acidosis or alkalosis if the imbalance persists.
3. Respiratory and metabolic acidosis and alkalosis are described based on their causes and effects on pH, pCO2, and HCO3 levels. Compensation and treatment approaches are also outlined.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
Most people can recover from burns without serious health consequences, depending on the cause and degree of injury. More serious burns require immediate emergency medical care to prevent complications and death
This document provides information about gastrointestinal agents (GI agents), which are drugs used to treat GI disorders. It discusses the classifications of GI agents including acidifying agents, antacids, protectives, adsorbents, and cathartics. It then describes common antacids including aluminum hydroxide gel, calcium carbonate, and magnesium salts. The ideal characteristics of antacids are outlined. Common calcium-containing and magnesium-containing antacids are also discussed in more detail.
Heavy metal poisoning, especially from arsenic, is a major global health issue. Arsenic is commonly found in soil, water, and foods in some areas. It interferes with cellular energy production. Acute arsenic poisoning causes nausea, vomiting, and diarrhea resembling cholera. Chronic arsenic poisoning over years causes skin pigmentation, keratosis, and neurological symptoms. The diagnosis is confirmed by detecting high arsenic levels in urine, hair, and nails. Treatment involves removing the patient from exposure and giving dimercaprol as an antidote.
Uric acid is the end product of purine metabolism and is excreted in urine. It is produced from the breakdown of purines from food and cells. There are two main methods for determining serum uric acid levels - the Caraway method which uses phosphotungstic acid and measures absorbance at 700nm, and the enzymatic method using uricase and peroxidase to produce a colored product measured at 500-540nm. Normal serum uric acid levels are 3.5-7.2 mg/dl for males and 2.5-6.2 mg/dl for females. Hyperuricemia can be caused by reduced excretion due to renal disorders or increased production from metabolic disorders and diseases
This document provides information about antacids, including their mechanism of action, classification, and examples. It discusses how antacids work by neutralizing gastric acid through chemical reactions or by forming protective coatings in the stomach. Antacids are classified as systemic or non-systemic. Systemic antacids like sodium bicarbonate can cause alkalosis while non-systemic antacids like aluminum hydroxide, magnesium hydroxide, and magnesium carbonate act locally in the stomach without systemic absorption. Common antacids are discussed in detail with their chemical reactions, effects, uses, and side effects.
This document summarizes post-mortem changes that can help estimate time of death. It describes immediate changes that occur within 30 minutes of death, early changes within 36 hours such as algor mortis (body cooling), rigor mortis (muscle stiffening), and livor mortis (post-mortem lividity). Late changes after 36 hours include decomposition stages of bloating, decay, and skeletonization. Specific changes in the skin, eyes, and potassium levels in vitreous humor are also noted.
This document discusses acidifying agents used to treat conditions caused by low stomach acid such as achlorhydria. It describes two main acidifying agents - ammonium chloride and hydrochloric acid. Ammonium chloride is used as a systemic acidifier, expectorant, and diuretic. It is prepared by neutralizing hydrochloric acid with ammonia. Hydrochloric acid is used as an acidifying agent, solvent, and catalyst. It is prepared by reacting sulfuric acid with sodium chloride. Both agents work to increase stomach acid levels and support digestion when acid production is impaired.
Gastrointestinal agents are classified into different groups based on their mechanism of action. These include acidifying agents, antacids, adsorbents, laxatives, cathartics, purgatives, and protective agents. Acidifying agents like dilute hydrochloric acid are used to increase acid levels in the stomach. Antacids like aluminum hydroxide gel and magnesium hydroxide are used to neutralize excess stomach acid in conditions like hyperacidity. Laxatives, cathartics and purgatives help promote bowel movements and treat constipation.
How to Manage Reception Report in Odoo 17Celine George
A business may deal with both sales and purchases occasionally. They buy things from vendors and then sell them to their customers. Such dealings can be confusing at times. Because multiple clients may inquire about the same product at the same time, after purchasing those products, customers must be assigned to them. Odoo has a tool called Reception Report that can be used to complete this assignment. By enabling this, a reception report comes automatically after confirming a receipt, from which we can assign products to orders.
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Similar to Acid and Alkali Poisoning.pdf ////////////
This document provides information on corrosive poisons including sulfuric acid, oxalic acid, phenol, and nitric acid. It describes their physical and chemical properties, mechanisms of action, clinical features of poisoning, treatment approaches, causes of death, and post-mortem appearances. It also discusses their judicious and injudicious uses and medicolegal significance. The document is intended to educate about these dangerous corrosive poisons through detailed descriptions and comparisons.
Mercury is a liquid metal that is highly toxic, especially in its vaporized form and when ingested as certain mercury compounds. The document discusses mercury's properties and various forms, how mercury poisoning affects the body and can cause damage to organs like the kidneys and brain, symptoms of both acute and chronic mercury toxicity, treatment options, and postmortem findings related to mercury poisoning.
Ethanol acts as a central nervous system depressant by enhancing the effects of the inhibitory neurotransmitter GABA at GABA-A receptors. It is metabolized in the liver by alcohol dehydrogenase and aldehyde dehydrogenase. Acute intoxication can cause impairment, loss of coordination, and respiratory depression, while chronic use is associated with conditions like cirrhosis of the liver and cardiomyopathy. Treatment for acute intoxication involves maintaining airway and circulation, gastric lavage, glucose supplementation, and benzodiazepines for seizures. Chronic alcoholism is treated with supervised withdrawal, benzodiazepine substitution, psychotherapy, and disulfiram to produce an aversive reaction if alcohol is consumed. Methanol poisoning is treated
This document discusses various post-mortem changes that can help estimate time since death, including lividity, rigor mortis, decomposition, and biochemical changes in vitreous humor, blood, and cerebrospinal fluid over time. Measurement of facial hair growth or food digestion can also provide clues to estimate how long someone survived after their last shave or meal. Radiocarbon dating of bone can also potentially estimate time of death for skeletal remains.
Methanol poisoning causes metabolic acidosis, optic neuritis, renal toxicity, and CNS depression. Symptoms include odor on breath, acid urine with acetone and albumin, retinal ganglion cell degeneration, and convulsions. Death is mainly due to metabolic acidosis from formic acid production and respiratory depression from CNS effects.
Inorganic (non metallic) irritant Poisons by Sunil Kumar Dahasunil kumar daha
Please find the power point on Inorganic (non metallic) irritants poisons. I tried to present it on understandable way and all the contents are reviewed by experts and from very reliable references. Thank you
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This document summarizes information about gastric acid secretion and factors that influence it. It discusses:
1) Gastric acid is produced by parietal cells in the stomach and plays a key role in protein digestion. Parietal cells secrete acid in response to gastrin, histamine, and acetylcholine.
2) Peptic ulcers are caused by an imbalance between gastric acid and the protective mucus lining, often due to H. pylori infection. Antacids and proton pump inhibitors are used to treat ulcers by reducing acid.
3) Proton pump inhibitors irreversibly block the proton pump in parietal cells, strongly inhibiting gastric acid secretion.
This document discusses corrosive poisoning from ingesting or contacting strong acids and bases. It notes that these chemicals can erode and destroy surfaces and cause systemic effects. Treatment involves dilution, avoiding gastric lavage, and symptomatic care. Complications can be acute like perforations or chronic like strictures. Death typically occurs from circulatory collapse within 12-24 hours. Postmortem findings include blackened and eroded stomach lining with potential perforations. The document also discusses vitriolage, which is the malicious throwing of corrosives like sulfuric acid to disfigure victims, which causes severe burns.
1. The document discusses acid-base disturbances and defines acids, bases, and pH. It explains how acids and bases are produced and balanced in the body to maintain a normal blood pH.
2. When there is excess acid or base in the blood, compensation mechanisms attempt to return the pH to normal through buffers, lungs, and kidneys. However, disease can cause acidosis or alkalosis if the imbalance persists.
3. Respiratory and metabolic acidosis and alkalosis are described based on their causes and effects on pH, pCO2, and HCO3 levels. Compensation and treatment approaches are also outlined.
Burns are one of the most common household injuries, especially among children. The term “burn” means more than the burning sensation associated with this injury. Burns are characterized by severe skin damage that causes the affected skin cells to die.
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This document provides information about gastrointestinal agents (GI agents), which are drugs used to treat GI disorders. It discusses the classifications of GI agents including acidifying agents, antacids, protectives, adsorbents, and cathartics. It then describes common antacids including aluminum hydroxide gel, calcium carbonate, and magnesium salts. The ideal characteristics of antacids are outlined. Common calcium-containing and magnesium-containing antacids are also discussed in more detail.
Heavy metal poisoning, especially from arsenic, is a major global health issue. Arsenic is commonly found in soil, water, and foods in some areas. It interferes with cellular energy production. Acute arsenic poisoning causes nausea, vomiting, and diarrhea resembling cholera. Chronic arsenic poisoning over years causes skin pigmentation, keratosis, and neurological symptoms. The diagnosis is confirmed by detecting high arsenic levels in urine, hair, and nails. Treatment involves removing the patient from exposure and giving dimercaprol as an antidote.
Uric acid is the end product of purine metabolism and is excreted in urine. It is produced from the breakdown of purines from food and cells. There are two main methods for determining serum uric acid levels - the Caraway method which uses phosphotungstic acid and measures absorbance at 700nm, and the enzymatic method using uricase and peroxidase to produce a colored product measured at 500-540nm. Normal serum uric acid levels are 3.5-7.2 mg/dl for males and 2.5-6.2 mg/dl for females. Hyperuricemia can be caused by reduced excretion due to renal disorders or increased production from metabolic disorders and diseases
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This document summarizes post-mortem changes that can help estimate time of death. It describes immediate changes that occur within 30 minutes of death, early changes within 36 hours such as algor mortis (body cooling), rigor mortis (muscle stiffening), and livor mortis (post-mortem lividity). Late changes after 36 hours include decomposition stages of bloating, decay, and skeletonization. Specific changes in the skin, eyes, and potassium levels in vitreous humor are also noted.
This document discusses acidifying agents used to treat conditions caused by low stomach acid such as achlorhydria. It describes two main acidifying agents - ammonium chloride and hydrochloric acid. Ammonium chloride is used as a systemic acidifier, expectorant, and diuretic. It is prepared by neutralizing hydrochloric acid with ammonia. Hydrochloric acid is used as an acidifying agent, solvent, and catalyst. It is prepared by reacting sulfuric acid with sodium chloride. Both agents work to increase stomach acid levels and support digestion when acid production is impaired.
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2. Acids
concentration, time of act
precipitation and dissolving proteins – coagulation
necrosis
cause dehydratation of tissue and with water some acids
are heat up and create termic changes
after consume of acid it can immediately come collapse
and quickly death
Autopsy finding: constricted stomach, stomach wall is
oedematous and fat up to 1cm. Vessels are filled by black
altered blood, up to tarry clots (acid hematin).
3. Sulphuric acid - H2SO4
deadly dose is dependent on concentration
approximately 4 – 6 g
symptoms immediately after swallow - burning pain in the mouth,
neck, oesophagus, stomach and in the abdomen, very painful and
continuous, than man screaming of pain and faint
soon after consume begin vomiting of acid
intestine constipation and in the urinary blader is only little of urine
intensive thirst with swallowing disorders, attempt to drink lead to
new vomiting
dehydratation occur
heavy and noisy breathing, hoarse voice, speaking latter impossible
after absorbtion – nervous symptoms, alcali of blood decrease
4. Hydrochloric acid - HCl
Deadly dose at concentrate acid is 10 – 15 g,
at children approximately 2 g
Symptoms are similar as at sulphuric acid
5. Nitric acid - HNO3
Deadly dose is approximately 8 g, death be
coming approximately 12 hours after consume.
Vomit liquid has lemon up to orange coloration.
Autopsy: at nose is yellow foam, finding is
similar as at another acids, but epithelium is
yellow.
6. Acetic acid - CH3COOH
Deadly dose is approximately 12 g, death be coming 1,5
hours up to 2 days after consume.
Symptoms: burning pain in the mouth and pharynx, pain in
the stomach and abdomen. Becam thirst, vomiting, noisy
breathing, irritable cough, temperature grow up.
Nervous signs – tremors, paralysis of the extremites.
Autopsy: similar finding on the body as at anorganic acids.
7. Oxalic acid - (COOH)2 -
CH3COOH
Deadly dose is 15- 20 g, death be coming after 10
minutes up to 30 hours.
After consume begin burning in the mouth and in
the oesophagus, vomiting, pains in the abdomen, hoarse
voice. Vomit liquid is greenbrown up to black. Rising
consciousness disorders, fibrilations of muscles,
spasms, paleness, skin is cold, temperature go down.
Autopsy finding: basicly same as at acid. Oxalic acid
uptake calcium from tissue and form insoluble calcium
oxalate, calcium oxalate crystals can find under
epithelium of stomach and intestine. Body loss calcium,
it lead to muscle malfunction. In the kidney we can see
crystals already macroscopically.
8. Lemon, tartaric and lactic acid
Deadly doses
30 g lemon acid
10 g tartaric acid
Rising acidosis and cause of death is
methaemoglobinaemia and production of acid
haematin.
10. Alkali
Hydroxide create with proteins alkalic substances
(albuminates) and not coagulate proteins.
Dissolving proteins, thereby rising gelatine masses
and colliquative necrosis, which is sticky.
Acid create coagulation necrosis!!!
11. Potassium and sodium hydroxide
KOH & NaOH
Deadly dose: 80 – 100 g
Symptoms: burn on the skin or necrosis, healing by scars.
Per os: promptly burning pain in the mouth, oesophagus,
stomach and in the abdomen. Vomit liquid have strong alkali
reaction and there are parts of epithelium and blood. Cold
feelings, salivation and tremor.
Autopsy finding: burn around mouth, epithelium in the
stomach is incrassate(fat) and sticky. Lining is gelatinous,
toxic damage of myocardium, in the liver necrosis.
