1. Inorganic irritants like phosphorus, iodine, chlorine, and powdered glass act locally to damage tissues through various mechanisms like extracting water, coagulating proteins, and directly corroding surfaces.
2. Phosphorus poisoning can cause serious and potentially fatal effects within 12-48 hours from just 1 gram ingested. Chronic exposure leads to "phossy jaw" bone necrosis.
3. Aluminum phosphide used as a fumigant is highly toxic and a common cause of suicide, with mortality rates over 50% even from a single tablet. It liberates phosphine gas which is cytotoxic.
Heavy metal poisoning can involve multiple systems and be caused by various metals like arsenic, lead, mercury, and copper. Arsenic poisoning presents with gastrointestinal symptoms like vomiting and diarrhea as well as skin lesions. Lead poisoning commonly affects the nervous system causing issues like decreased IQ and hyperactivity. Mercury poisoning can cause pulmonary toxicity and kidney damage. Copper poisoning results in liver injury and haemolysis. Diagnosis involves measuring metal levels in blood and urine. Treatment focuses on decontamination, chelation therapy, and supportive care.
1. Copper and copper compounds like copper sulfate and copper subacetate are toxic heavy metals that can cause acute and chronic poisoning through ingestion, inhalation, or skin exposure.
2. Acute copper poisoning causes gastrointestinal symptoms like vomiting and diarrhea as well as liver and kidney damage. Chronic poisoning can result in conditions like anemia, bronchitis, and corneal ulcers.
3. Iron and thallium are also toxic heavy metals that can cause multiple organ damage and even death in acute overdoses. Their absorption is followed by stages of toxicity affecting the gastrointestinal tract, liver, kidneys, and other organs.
4. Potassium permanganate is a toxic compound of manganese that
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
Arsenic toxicity in animals can occur through ingestion, inhalation, or dermal exposure. The document discusses the sources, clinical signs, post-mortem findings, diagnosis, and treatment of arsenic poisoning in various animal species. It provides lethal dose information for different animals and details the mechanisms of toxicity, which involve inhibition of enzymatic reactions through binding to sulfhydryl groups. Distribution is widespread in the body with high concentrations in the liver, kidneys, and other organs.
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.
The document provides information on metallic poisons arsenic and barium. It discusses the forms, mechanisms of action, absorption, excretion, signs and symptoms of acute and chronic poisoning, laboratory investigations, treatment, and post-mortem findings for both arsenic and barium poisoning. It also covers the medical-legal importance of arsenic as a homicidal poison due to its tasteless and odorless properties.
The document discusses various household poisons including aluminium phosphide (ALP), bleach, and pyrethrins. It provides details on the mechanism of action, signs and symptoms, diagnosis, and treatment of poisoning from these substances. ALP poisoning results from phosphine gas release in the stomach and causes metabolic acidosis, organ damage, and often death within 24 hours. Bleach contains hypochlorite and hydrogen peroxide and can cause irritation or burns depending on concentration. Pyrethrins are insecticides that prolong sodium channel activation and may cause allergic reactions, respiratory issues, or seizures from ingestion.
Heavy metal poisoning can involve multiple systems and be caused by various metals like arsenic, lead, mercury, and copper. Arsenic poisoning presents with gastrointestinal symptoms like vomiting and diarrhea as well as skin lesions. Lead poisoning commonly affects the nervous system causing issues like decreased IQ and hyperactivity. Mercury poisoning can cause pulmonary toxicity and kidney damage. Copper poisoning results in liver injury and haemolysis. Diagnosis involves measuring metal levels in blood and urine. Treatment focuses on decontamination, chelation therapy, and supportive care.
1. Copper and copper compounds like copper sulfate and copper subacetate are toxic heavy metals that can cause acute and chronic poisoning through ingestion, inhalation, or skin exposure.
2. Acute copper poisoning causes gastrointestinal symptoms like vomiting and diarrhea as well as liver and kidney damage. Chronic poisoning can result in conditions like anemia, bronchitis, and corneal ulcers.
3. Iron and thallium are also toxic heavy metals that can cause multiple organ damage and even death in acute overdoses. Their absorption is followed by stages of toxicity affecting the gastrointestinal tract, liver, kidneys, and other organs.
4. Potassium permanganate is a toxic compound of manganese that
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
Arsenic toxicity in animals can occur through ingestion, inhalation, or dermal exposure. The document discusses the sources, clinical signs, post-mortem findings, diagnosis, and treatment of arsenic poisoning in various animal species. It provides lethal dose information for different animals and details the mechanisms of toxicity, which involve inhibition of enzymatic reactions through binding to sulfhydryl groups. Distribution is widespread in the body with high concentrations in the liver, kidneys, and other organs.
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.
The document provides information on metallic poisons arsenic and barium. It discusses the forms, mechanisms of action, absorption, excretion, signs and symptoms of acute and chronic poisoning, laboratory investigations, treatment, and post-mortem findings for both arsenic and barium poisoning. It also covers the medical-legal importance of arsenic as a homicidal poison due to its tasteless and odorless properties.
The document discusses various household poisons including aluminium phosphide (ALP), bleach, and pyrethrins. It provides details on the mechanism of action, signs and symptoms, diagnosis, and treatment of poisoning from these substances. ALP poisoning results from phosphine gas release in the stomach and causes metabolic acidosis, organ damage, and often death within 24 hours. Bleach contains hypochlorite and hydrogen peroxide and can cause irritation or burns depending on concentration. Pyrethrins are insecticides that prolong sodium channel activation and may cause allergic reactions, respiratory issues, or seizures from ingestion.
This document discusses arsenic poisoning. It begins by defining arsenic and describing its characteristics, including that it is colorless, odorless, and tasteless. It then discusses sources of arsenic exposure like contaminated water or food, occupational exposure, and arsenic's movement in the environment. The document outlines both acute and chronic health effects of arsenic poisoning, including cancers, neurological effects, and vascular disease. It provides details on treatment options like chelation therapy and hemodialysis. In the end, it discusses some case studies on arsenic exposure in Latin America and links between high exposure levels and various adverse health outcomes.
This document discusses toxic minerals including lead, arsenic, mercury, and cadmium. It describes the sources of exposure, absorption, distribution, toxicity effects, and treatment options for poisoning from each of these heavy metals. Lead is discussed in most depth, outlining its various non-occupational exposure sources and noting the EPA limits for levels in drinking water, soil, and air. Symptoms of lead toxicity and chelation therapy using dimercaprol are also summarized.
This document summarizes information about irritant poisons, focusing on phosphorus and iodine. It describes their properties, mechanisms of toxicity, symptoms, treatment, and autopsy findings. Phosphorus is a waxy yellow substance that is luminous in the dark and has a garlic odor. It causes necrosis of liver cells. Iodine occurs as brown crystals with violet vapors and acts by precipitating proteins. Both cause severe abdominal pain and vomiting when ingested. Phosphorus poisoning can lead to liver and kidney failure within days, while iodine poisoning symptoms appear more rapidly but death typically occurs within 24 hours.
Arsenic poisoning can occur through ingestion, inhalation, or skin absorption of arsenic compounds. Acute arsenic poisoning causes gastrointestinal symptoms like vomiting and diarrhea, while chronic exposure can lead to skin lesions, peripheral vascular disease, and cancer. Diagnosis is made through laboratory tests of urine, blood, hair, nails, and tissue samples, which detect elevated arsenic levels. Treatment for acute poisoning involves gastric lavage, administration of chelating agents like BAL, and supportive care, while chronic cases require removing the source of exposure and long-term chelation therapy along with symptom management. Autopsy findings may show inflammation of the gastrointestinal tract and liver congestion in acute deaths.
This document summarizes information about phosphorous and its different allotropes (forms), properties, toxicity, and treatment. It discusses three main allotropes - white, red, and violet phosphorous. White phosphorous is highly toxic, flammable, and causes injuries/death by burning, inhaling its fumes, or ingestion. Symptoms of ingestion include vomiting, diarrhea, and liver damage. Treatment involves decontamination, supportive care, and monitoring for toxicity and bleeding tendencies.
Iron toxicity occurs when excess iron is ingested and circulating levels exceed the body's iron-binding capacity. This can lead to direct injury of the gastrointestinal tract and multiple organ failure. Symptoms progress through four stages, initially causing vomiting and diarrhea and potentially leading to coma and death from hepatic failure. A diagnosis is suggested by elevated serum iron levels above 150 mcg/100 mL or a positive chelating challenge test showing iron excretion in urine. Treatment focuses on gastric decontamination and chelation therapy with deferoxamine to remove unbound iron from circulation.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
This presentation gives the description that which heavy metals are toxic for human health and how they interact with the metabolic processes and cause different diseases in human beings. There are also the threshold values given to help prevent the toxicity....
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.
Lead is a toxic heavy metal that can cause lead poisoning when levels become elevated in the body. Lead poisoning was common historically from sources like lead paint and gasoline, and it still impacts an estimated 500,000 children in the US. Symptoms range from vague issues to encephalopathy and death. Diagnosis is made via blood lead level testing. Treatment focuses on chelation therapy, prevention of further exposure, and supportive care, though long-term effects can be permanent. While efforts have reduced exposure, lead poisoning remains an important public health issue.
Zinc phosphide is a rodenticide that causes poisoning by reacting with stomach acid to form phosphine gas, a toxic protoplasmic poison. Symptoms include vomiting, breathing difficulties, circulatory collapse, coma and death within 24 hours due to respiratory or hepatic failure. Treatment involves gastric lavage, activated charcoal, antacids and correcting metabolic acidosis. Zinc phosphide poisoning is often used for suicide or homicide and can cause fatty liver changes, jaundice and renal failure upon autopsy. Chronic zinc oxide vapor inhalation in industrial settings causes metal fume fever with influenza-like symptoms.
COPPER POISONING
Appear within 15-30 min
Metallic taste
Increased salivation
Burning pain in stomach
Nausea, vomiting (vomited matter : blue / green colour)
Diarrhoea with much straining (motions are liquid and brown)
Oliguria, haematuria, albuminuria, acidosis, uraemia
In severe cases, haemolysis, jaundice, pancreatitis, convulsions, spasm of legs
Breathing difficulty, cold perception, severe head ache
Death due to HEPATIC or RENAL failure or both
This document discusses childhood anemia, including its definition, causes, signs and symptoms, diagnostic tests, treatment, and iron metabolism. Some key points:
- Anemia is defined as low red blood cell or hemoglobin levels. It poses health risks in children and is commonly caused by iron deficiency.
- Diagnosis involves blood tests showing microcytic, hypochromic anemia and low iron stores.
- Treatment consists of oral iron supplements initially, with parenteral options for severe cases. Absorption can be improved by vitamin C and hindered by certain foods.
This document discusses various types of rodenticides, including their classification, mechanisms of action, clinical signs, diagnosis, and treatment. It covers both inorganic rodenticides such as arsenic, phosphorus, and thallium sulfate as well as organic rodenticides like anticoagulants, fluoroacetate derivatives, vitamin D compounds, ANTU, bromethalin, metaldehyde, and strychnine. For each rodenticide, a brief overview of its mechanism of toxicity, associated clinical signs in poisoned animals, and recommended treatment approaches are provided. The document serves as a comprehensive reference for information on different rodenticide chemicals that are commonly used.
clinical features and management of heavy metal poisoning .pptxvuyyuribhaargavi
Lead poisoning is the commonest metal involved in chronic poisoning. lead is one of the 1st metals known to man and has been widely used during the last 2000 yrs for domestic, industrial, and therapeutic purposes.
Abundant in soil, being distributed throughout the earth’s crust.
Their salt forms are coloured powders or liquids, widely used in industry and at home, producing cumulative toxicity on chronic exposure. lead combines with sulfhydryl enzymes leading to interference with their action. it also decreases haeme synthesis by inactivating the enzymes like aminolaevulinic acid dehydrogenase, aminolaevulinic acid synthetase etc resulting in anaemia.
ARSENIC POISONING
Arsenic is thought to occur throughout the universe
Arsenic is today the commonest source of acute heavy metal poisoning, and is second only to lead in the incidence of chronic toxicity
While arsenic does not cross the blood-brain barrier easily, it crosses the placenta readily and can give rise to intrauterine death of the foetus.
Arsenic replaces phosphorus in the bone where it may remain for years. It also gets deposited in hair
This document discusses Perls stain, which is used to identify iron deposits in tissue samples. It provides background on pigments in living tissue, including endogenous pigments like hemosiderin and hematogenous pigments. The history of Prussian blue and its use as Perls stain is described. The principle of the stain is that hydrochloric acid releases ferric ions from hemosiderin, which then react with potassium ferrocyanide to form insoluble Prussian blue pigment. Staining protocols, quality control, and clinical applications for identifying iron deposits in organs are covered.
Arsenicosis is a world wide health problem.
it may be acute poisoning and chronic poisoning.
chronic poisoning show up with rain drop pigmentation, palmoplantar hyperkeratosis, and other skin , hair, nail and systemic treatment. No specific treatment is yet established for chronic arsenic poisoning.
Pesticides are substances used to control pests and include insecticides, herbicides, fungicides, and rodenticides. They work through various mechanisms such as inhibiting acetylcholinesterase, disrupting sodium channels, or inhibiting plant processes like photosynthesis. While effective, many pesticides can be toxic, especially to non-target organisms. The toxicity of organophosphates, carbamates, pyrethroids and other pesticides is described. Their treatment and mechanisms of toxicity are discussed. The toxicity of other pesticide classes like organochlorines, herbicides and fungicides is also summarized.
The document describes three cataract extraction techniques: intracapsular cataract extraction (ICCE), extracapsular cataract extraction (ECCE), and manual small incision cataract surgery (SICS). ICCE involves removing the entire lens and capsule, while ECCE removes most of the lens leaving the posterior capsule. SICS performs ECCE through a small, sutureless incision. The document then details the steps for ECCE and SICS, and explains that phacoemulsification differs by using a smaller incision, continuous curvilinear capsulorrhexis, hydrodissection, and emulsifying/aspirating the nucleus with phacoemulsification before removing cortex
The document describes the anatomical structures located in different regions of the horizontal section of the brain, including the anterior region containing the head of the caudate nucleus and genu of the corpus callosum, the medial region containing the thalamus, and the lateral region containing the lentiform nucleus, internal capsule, external capsule, and insular lobe. It also notes the posterior region contains the posterior horn of the lateral ventricle, tail of the caudate nucleus, and splenium of the corpus callosum. The document concludes by providing brief descriptions of how structures appear on CT and T1-weighted MRI scans.
This document discusses arsenic poisoning. It begins by defining arsenic and describing its characteristics, including that it is colorless, odorless, and tasteless. It then discusses sources of arsenic exposure like contaminated water or food, occupational exposure, and arsenic's movement in the environment. The document outlines both acute and chronic health effects of arsenic poisoning, including cancers, neurological effects, and vascular disease. It provides details on treatment options like chelation therapy and hemodialysis. In the end, it discusses some case studies on arsenic exposure in Latin America and links between high exposure levels and various adverse health outcomes.
This document discusses toxic minerals including lead, arsenic, mercury, and cadmium. It describes the sources of exposure, absorption, distribution, toxicity effects, and treatment options for poisoning from each of these heavy metals. Lead is discussed in most depth, outlining its various non-occupational exposure sources and noting the EPA limits for levels in drinking water, soil, and air. Symptoms of lead toxicity and chelation therapy using dimercaprol are also summarized.
This document summarizes information about irritant poisons, focusing on phosphorus and iodine. It describes their properties, mechanisms of toxicity, symptoms, treatment, and autopsy findings. Phosphorus is a waxy yellow substance that is luminous in the dark and has a garlic odor. It causes necrosis of liver cells. Iodine occurs as brown crystals with violet vapors and acts by precipitating proteins. Both cause severe abdominal pain and vomiting when ingested. Phosphorus poisoning can lead to liver and kidney failure within days, while iodine poisoning symptoms appear more rapidly but death typically occurs within 24 hours.
Arsenic poisoning can occur through ingestion, inhalation, or skin absorption of arsenic compounds. Acute arsenic poisoning causes gastrointestinal symptoms like vomiting and diarrhea, while chronic exposure can lead to skin lesions, peripheral vascular disease, and cancer. Diagnosis is made through laboratory tests of urine, blood, hair, nails, and tissue samples, which detect elevated arsenic levels. Treatment for acute poisoning involves gastric lavage, administration of chelating agents like BAL, and supportive care, while chronic cases require removing the source of exposure and long-term chelation therapy along with symptom management. Autopsy findings may show inflammation of the gastrointestinal tract and liver congestion in acute deaths.
This document summarizes information about phosphorous and its different allotropes (forms), properties, toxicity, and treatment. It discusses three main allotropes - white, red, and violet phosphorous. White phosphorous is highly toxic, flammable, and causes injuries/death by burning, inhaling its fumes, or ingestion. Symptoms of ingestion include vomiting, diarrhea, and liver damage. Treatment involves decontamination, supportive care, and monitoring for toxicity and bleeding tendencies.
Iron toxicity occurs when excess iron is ingested and circulating levels exceed the body's iron-binding capacity. This can lead to direct injury of the gastrointestinal tract and multiple organ failure. Symptoms progress through four stages, initially causing vomiting and diarrhea and potentially leading to coma and death from hepatic failure. A diagnosis is suggested by elevated serum iron levels above 150 mcg/100 mL or a positive chelating challenge test showing iron excretion in urine. Treatment focuses on gastric decontamination and chelation therapy with deferoxamine to remove unbound iron from circulation.
Toxicology on aluminium phosphide, the characteristics, fatal dose,fatal period, sign and symptoms, postmortem appearance and medicolegal importance are discussed.
This presentation gives the description that which heavy metals are toxic for human health and how they interact with the metabolic processes and cause different diseases in human beings. There are also the threshold values given to help prevent the toxicity....
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.
Lead is a toxic heavy metal that can cause lead poisoning when levels become elevated in the body. Lead poisoning was common historically from sources like lead paint and gasoline, and it still impacts an estimated 500,000 children in the US. Symptoms range from vague issues to encephalopathy and death. Diagnosis is made via blood lead level testing. Treatment focuses on chelation therapy, prevention of further exposure, and supportive care, though long-term effects can be permanent. While efforts have reduced exposure, lead poisoning remains an important public health issue.
Zinc phosphide is a rodenticide that causes poisoning by reacting with stomach acid to form phosphine gas, a toxic protoplasmic poison. Symptoms include vomiting, breathing difficulties, circulatory collapse, coma and death within 24 hours due to respiratory or hepatic failure. Treatment involves gastric lavage, activated charcoal, antacids and correcting metabolic acidosis. Zinc phosphide poisoning is often used for suicide or homicide and can cause fatty liver changes, jaundice and renal failure upon autopsy. Chronic zinc oxide vapor inhalation in industrial settings causes metal fume fever with influenza-like symptoms.
COPPER POISONING
Appear within 15-30 min
Metallic taste
Increased salivation
Burning pain in stomach
Nausea, vomiting (vomited matter : blue / green colour)
Diarrhoea with much straining (motions are liquid and brown)
Oliguria, haematuria, albuminuria, acidosis, uraemia
In severe cases, haemolysis, jaundice, pancreatitis, convulsions, spasm of legs
Breathing difficulty, cold perception, severe head ache
Death due to HEPATIC or RENAL failure or both
This document discusses childhood anemia, including its definition, causes, signs and symptoms, diagnostic tests, treatment, and iron metabolism. Some key points:
- Anemia is defined as low red blood cell or hemoglobin levels. It poses health risks in children and is commonly caused by iron deficiency.
- Diagnosis involves blood tests showing microcytic, hypochromic anemia and low iron stores.
- Treatment consists of oral iron supplements initially, with parenteral options for severe cases. Absorption can be improved by vitamin C and hindered by certain foods.
This document discusses various types of rodenticides, including their classification, mechanisms of action, clinical signs, diagnosis, and treatment. It covers both inorganic rodenticides such as arsenic, phosphorus, and thallium sulfate as well as organic rodenticides like anticoagulants, fluoroacetate derivatives, vitamin D compounds, ANTU, bromethalin, metaldehyde, and strychnine. For each rodenticide, a brief overview of its mechanism of toxicity, associated clinical signs in poisoned animals, and recommended treatment approaches are provided. The document serves as a comprehensive reference for information on different rodenticide chemicals that are commonly used.
clinical features and management of heavy metal poisoning .pptxvuyyuribhaargavi
Lead poisoning is the commonest metal involved in chronic poisoning. lead is one of the 1st metals known to man and has been widely used during the last 2000 yrs for domestic, industrial, and therapeutic purposes.
Abundant in soil, being distributed throughout the earth’s crust.
Their salt forms are coloured powders or liquids, widely used in industry and at home, producing cumulative toxicity on chronic exposure. lead combines with sulfhydryl enzymes leading to interference with their action. it also decreases haeme synthesis by inactivating the enzymes like aminolaevulinic acid dehydrogenase, aminolaevulinic acid synthetase etc resulting in anaemia.
ARSENIC POISONING
Arsenic is thought to occur throughout the universe
Arsenic is today the commonest source of acute heavy metal poisoning, and is second only to lead in the incidence of chronic toxicity
While arsenic does not cross the blood-brain barrier easily, it crosses the placenta readily and can give rise to intrauterine death of the foetus.
Arsenic replaces phosphorus in the bone where it may remain for years. It also gets deposited in hair
This document discusses Perls stain, which is used to identify iron deposits in tissue samples. It provides background on pigments in living tissue, including endogenous pigments like hemosiderin and hematogenous pigments. The history of Prussian blue and its use as Perls stain is described. The principle of the stain is that hydrochloric acid releases ferric ions from hemosiderin, which then react with potassium ferrocyanide to form insoluble Prussian blue pigment. Staining protocols, quality control, and clinical applications for identifying iron deposits in organs are covered.
Arsenicosis is a world wide health problem.
it may be acute poisoning and chronic poisoning.
chronic poisoning show up with rain drop pigmentation, palmoplantar hyperkeratosis, and other skin , hair, nail and systemic treatment. No specific treatment is yet established for chronic arsenic poisoning.
Pesticides are substances used to control pests and include insecticides, herbicides, fungicides, and rodenticides. They work through various mechanisms such as inhibiting acetylcholinesterase, disrupting sodium channels, or inhibiting plant processes like photosynthesis. While effective, many pesticides can be toxic, especially to non-target organisms. The toxicity of organophosphates, carbamates, pyrethroids and other pesticides is described. Their treatment and mechanisms of toxicity are discussed. The toxicity of other pesticide classes like organochlorines, herbicides and fungicides is also summarized.
The document describes three cataract extraction techniques: intracapsular cataract extraction (ICCE), extracapsular cataract extraction (ECCE), and manual small incision cataract surgery (SICS). ICCE involves removing the entire lens and capsule, while ECCE removes most of the lens leaving the posterior capsule. SICS performs ECCE through a small, sutureless incision. The document then details the steps for ECCE and SICS, and explains that phacoemulsification differs by using a smaller incision, continuous curvilinear capsulorrhexis, hydrodissection, and emulsifying/aspirating the nucleus with phacoemulsification before removing cortex
The document describes the anatomical structures located in different regions of the horizontal section of the brain, including the anterior region containing the head of the caudate nucleus and genu of the corpus callosum, the medial region containing the thalamus, and the lateral region containing the lentiform nucleus, internal capsule, external capsule, and insular lobe. It also notes the posterior region contains the posterior horn of the lateral ventricle, tail of the caudate nucleus, and splenium of the corpus callosum. The document concludes by providing brief descriptions of how structures appear on CT and T1-weighted MRI scans.
Peripheral vascular disease (PVD) refers to narrowed, blocked, or spasming blood vessels outside the heart and brain. It is commonly caused by atherosclerosis which leads to the buildup of fatty plaques in the arteries (atherosclerotic plaques). Symptoms range from mild intermittent leg pain with walking (intermittent claudication) to severe leg or foot pain at rest or skin ulcers/gangrene of the lower leg or foot. Treatment involves lifestyle changes, medications to reduce pain, plaque, or clotting, and potentially minimally invasive or open surgical procedures to restore blood flow if more conservative options are ineffective.
This document discusses normal growth and factors that affect growth. It defines growth and development and explains their significance. Factors that influence prenatal and postnatal growth are described, including genetic, environmental, hormonal, and social factors. The document outlines the phases of growth, growth patterns, and growth parameters seen at different ages. It also discusses growth standards and recommended growth charts.
This document provides information on the adrenal gland and adrenal disorders including:
1) The adrenal gland is a paired organ that produces hormones important for stress response and electrolyte balance. Diseases include primary adrenal insufficiency (Addison's disease) and Cushing's syndrome.
2) Pheochromocytoma is a rare catecholamine-producing tumor that causes symptoms of headache, sweating, and palpitations. Preoperative management with alpha-blockade is important to prevent postoperative hypotension.
3) Adrenocortical carcinoma is a rare malignant tumor most commonly presenting as Cushing's syndrome or virilization in adults. Surgical resection is the main treatment when possible
This document discusses benign breast disorders occurring in different reproductive periods in females. It describes conditions like fibroadenoma and fibrocytstadenosis.
Fibroadenoma is a benign encapsulated tumor occurring commonly in females under 30 years of age. It is an aberration in normal lobule development. Fibrocystadenosis is now called cyclic mastalgia with nodularity, which is an estrogen dependent condition causing painful, cystic swelling of the breast tissue.
The document provides details on the clinical features, investigations, classifications, and treatment options for these common benign breast conditions like fibroadenoma and fibrocytstadenosis.
Pneumothorax is the presence of air in the pleural cavity, which occurs when there is a breach in the parietal or visceral pleura. It can be classified as primary or secondary, and also as acute, chronic, small, large, partial or complete. Primary spontaneous pneumothorax typically occurs in young, tall, thin males and results from a rupture of a pulmonary bleb or bulla. Management depends on factors such as size, symptoms and underlying cause, and may include observation, aspiration, tube thoracostomy, chemical or surgical pleurodesis, or thoracoscopic procedures. Complications can include failure to reexpand, recurrence, infection or respiratory failure.
This document summarizes abnormalities of the pupil. It begins with general considerations on pupil embryology and function. It then discusses various morphological abnormalities and conditions that cause unequal pupil size (anisocoria). These include physiologic anisocoria as well as pathological causes like Horner's syndrome and Adie's tonic pupil. The document also reviews normal and abnormal pupillary reflexes, including afferent and efferent pathway defects as well as dissociations between light and near reflexes.
Exploiting Artificial Intelligence for Empowering Researchers and Faculty, In...Dr. Vinod Kumar Kanvaria
Exploiting Artificial Intelligence for Empowering Researchers and Faculty,
International FDP on Fundamentals of Research in Social Sciences
at Integral University, Lucknow, 06.06.2024
By Dr. Vinod Kumar Kanvaria
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
Thinking of getting a dog? Be aware that breeds like Pit Bulls, Rottweilers, and German Shepherds can be loyal and dangerous. Proper training and socialization are crucial to preventing aggressive behaviors. Ensure safety by understanding their needs and always supervising interactions. Stay safe, and enjoy your furry friends!
বাংলাদেশের অর্থনৈতিক সমীক্ষা ২০২৪ [Bangladesh Economic Review 2024 Bangla.pdf] কম্পিউটার , ট্যাব ও স্মার্ট ফোন ভার্সন সহ সম্পূর্ণ বাংলা ই-বুক বা pdf বই " সুচিপত্র ...বুকমার্ক মেনু 🔖 ও হাইপার লিংক মেনু 📝👆 যুক্ত ..
আমাদের সবার জন্য খুব খুব গুরুত্বপূর্ণ একটি বই ..বিসিএস, ব্যাংক, ইউনিভার্সিটি ভর্তি ও যে কোন প্রতিযোগিতা মূলক পরীক্ষার জন্য এর খুব ইম্পরট্যান্ট একটি বিষয় ...তাছাড়া বাংলাদেশের সাম্প্রতিক যে কোন ডাটা বা তথ্য এই বইতে পাবেন ...
তাই একজন নাগরিক হিসাবে এই তথ্য গুলো আপনার জানা প্রয়োজন ...।
বিসিএস ও ব্যাংক এর লিখিত পরীক্ষা ...+এছাড়া মাধ্যমিক ও উচ্চমাধ্যমিকের স্টুডেন্টদের জন্য অনেক কাজে আসবে ...
Main Java[All of the Base Concepts}.docxadhitya5119
This is part 1 of my Java Learning Journey. This Contains Custom methods, classes, constructors, packages, multithreading , try- catch block, finally block and more.
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2. Intro…
• Corrosive – Substance which erodes and destroys any surface in
contact with.
• *Almost acts exclusively locally.
• True mainly in case of inorganic acids and alkalis.
• MOA:
• Extraction of water from tissues.
• Coagulation of cellular proteins.
• Conversion of Hb to Hematin.
3. Corrosive v/s Irritants
• Diluted corrosives behaves like irritants and vice versa.
• Compared to corrosives, irritants are less severe*.
• MOA: Mainly gastroenteritis with variable systemic.
14. Acute poisoning
• 0.1-1gm intake
• Nausea, vomiting and diarrhea. The vomitus and stools are luminous and may
emit fumes (SMOKY STOOL SYNDROME).
• Garlicky or sulphurous odor in the breath.
• Intense thirst.
• Abdominal pain
• Delayed symptoms due to latency
• Same as above
• Hepatomegaly and jaundice
• Abnormal bleeding (hypoprothrombinaemia)
• Yellow atrophy of liver
• Ranal failure
• Convulsions and delirium
• Death
15. Chronic Poisoning
• Occupational Hazards
• Not common now due to safety matches
• Inhalation of fumes of phosphorus over time.
• Tooth ache, ulcerative stomatitis, loosening of teeth
• Phossy jaw: Necrosis of jawbone with osteomyelitis resulting in multiple sinus
formation , discharging foul smelling pus. By Bristowe
• Fatal dose: 1mg/kg body weight.
16. Rx
Fulminant & Acute Poisoning:
• Stomach wash : Pot. permanganate + Hydrogen peroxide / Copper
sulphate
• No oily demulcents / oily foods.
• Calcium gluconate: 5-10ml of 10% Solution
• Vitamin B-complex, K and C
• Soda bicarb – acidosis
• Low fat and high carb – liver stress
• Supportive measures
• Skin – copious washing with 2% sod.bicarb / 1% copper sulphate
19. MLI
• Accidental: in children and Unqualified medical practitioners.
• Suicide: old by using match heads, now by rodenticides.
• Homicidal: by adulteration.(Ricketts Case)
• Arson
20. Aluminium Phosphide
• Marketed in India under trade names – Alphos, Celphos, Chemfume, Delicia,
Fumigran, Phosphotek, Phostoxin, Quickfos, Synfume etc.,
• Available as greyish green tablets of 3gm each, mixed with urea and
ammonium carbonate.
• Each tablet liberates 1gm of phosphine.
21. Uses
Most ideal grain preservative – cheap and very effective in repelling pests.
AIP + 3H2O Al(OH)3 + PH3
*Traces of phosphite and hypophosphite of Aluminium may be present, but they are non-toxic.
Fatal dose – 1-3tablets
22. C/f
Same as acute poisoning in Pure form.
• CVS – hypotension, tachy/bradycardia and ECG
abnormalities
• R.S – distress
• CNS – coma
• Cyanosis, cold and clammy skin.
Systemic effects
High mortality if taken >3 tablets.
25. Biological
Test
5-10ml gastric aspirate / 5-10gm liver - sample
Taken in a steam distiller and equal amount of water is added
and then acidified with HCl /H2SO4 and then heating up to 50 C
for 15 min.
The distillate is received through ice cold receiver
containing silver nitrate
If Phosphine present – the solution turns black
For confirmation – add Nitric acid to black precipitate and boil,
after sol. Is clear add ammonium molybdate and heat for a
minute – yellow colour confirms phosphine
26.
27. Autopsy
findings
Hypoxic organ damage – congestion &
petechiae
Stomach- hemorrhagic with mucosal
shredding and garlicky odor
Microscopic necrosis in liver and kidney
Heart – toxic myocarditis + fibrillar
necrosis
Lungs – ARDS with pul.edema
28. Significance
• AlP is a fumigant for stored cereal grains, used to kill insects and
rodents.
• Cases of AlP poisoning is under-reported. AlP is cheap, readily
available, highly toxic.
• AlP is the most common cause of suicidal death in North India.
• Mortality rates from AlP poisoning vary from 40-80%, usually >50%.
• The toxicity of aluminium phosphide is attributed to the liberation of
phosphine gas.
• Phosphine (PH3) is a colorless gas with a disagreeable odor of fish or
garlic. It is a cytotoxic compound that causes free radical mediated
injury, inhibits vital cellular enzymes and is directly corrosive to
tissues. CDC has classified phosphine as immediately dangerous to
life at 50 parts per million.
29. Hepatotoxic
Poisons
• Alcohol
• Aminoglycosides
• Anabolic steroids
• Arsenic
• Carbon tetrachloride
• Iron
• Paracetamol
• Paraquat
• Phosphorus
• Naphthalene
• Oral contraceptives
• Sulphonamides
A SOAP IN A CAPP
34. Rx
• Emetics or stomach wash with warm water containing soluble starch and
albumen
• Sodium thisulphate
• NaCl
• Supportive
• Skin lesion with 20% alcohol.
35. P.M Appearances
• Mucosa of bowel – inflamed, excoriated and brown.
• Fatty degeneration – heart, liver & kidney
• Edema of brain.
36. Chronic poisoning
• Pain over frontal sinus
• Running nose, conjunctivitis, bronchial catarrh
• salivation, nausea, vomiting, purging
• emaciation, lymphadenopathy, parotid swelling (iodide mumps)
• wasting of breasts, testes etc.,
• acne or erythematous patches on the skin, urticaria etc., (ioderma)
37. Chlorine
• greenish – yellow gas, unpleasant irritating odor
• Exposure – laboratories, factories and chemical works.
• Oxidizing agent – destruction of organic tissue.
38. C/f
• Inhaled – irritant and suffocative effect
• Acute – irritation of eyes, throat and mucous mem. Of respiratory tract with
violent coughing & extreme dyspnea
• Nausea, vomiting and glottis spasm
• Death – cardiac failure – edema of lungs and Pul. congestion.
42. Powdered Glass
• C/f:
• Sharp burning pain in throat, stomach, intestine, usually constipation but rarely
diarrhea.
• Death – shock as a result of bowel perforation
• Fatal dose & period – uncertain
• P.M Appearances –
• erosions of bowel
• Sticky mucous over stomach along with glass particles
• Inflamed and congested gastric mucosa
• MLI
• rarely suicide or homicide
• Used as cattle poison.