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Calotropis
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Calotropis / Giant Milkweed: Calotropis / Giant Milkweed: Common name: عشير Common name: عشير Scientific name: Calotropis procera (Ait.) Ait. fil. Scientific name: Calotropis procera (Ait.) Ait. fil. Family: Asclepiadaceae Family: Asclepiadaceae
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Toxic ingredient: Toxic ingredient: The plant contains active cardiac glycosides. The plant contains active cardiac glycosides. The latex contains a no. of cardioactive glycosides, calactin, calotropin, calotoxin, uscharin, uscharidine, voruscharin, tannins, flavonoids, sterols and /or triterpenes. The latex contains a no. of cardioactive glycosides, calactin, calotropin, calotoxin, uscharin, uscharidine, voruscharin, tannins, flavonoids, sterols and /or triterpenes. The leaves and stalks contain calotropin, calotropagenin. The leaves and stalks contain calotropin, calotropagenin. A new norditerpenyl ester, named Calotropterpenyl ester, and two pentacyclic triterpenoids, namely calotropursenyl acetate and A new norditerpenyl ester, named Calotropterpenyl ester, and two pentacyclic triterpenoids, namely calotropursenyl acetate and calotropfriedelenyl acetate have been isolated from the root bark of Calotropis procera. calotropfriedelenyl acetate have been isolated from the root bark of Calotropis procera. The glycoside calotropin is extremely potent. The glycoside calotropin is extremely potent.
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Toxic parts: Toxic parts: Latex: can be strong irritant to skin and mucous membranes, it exhibits inflammation and iridocyclitis, cardiotoxicity, liver damage, testicular necrosis Latex: can be strong irritant to skin and mucous membranes, it exhibits inflammation and iridocyclitis, cardiotoxicity, liver damage, testicular necrosis
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Nicotiana Nicotiana: Nicotiana: Common name: شجرة تمباك, دخان شجري Scientific name: Nicotiana glauca R.C. Graham Common name: شجرة تمباك, دخان شجري Scientific name: Nicotiana glauca R.C. Graham Nicotiana rustica (L.) Nicotiana rustica (L.) Nicotiana tabacum (L.) Nicotiana tabacum (L.) Family: Solanaceae Family: Solanaceae
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N. tabacum: Nicotine is the major toxic alkaloid with a concentration in leaves ranging from 1.5%-4% by dry weight 2. N. tabacum: Nicotine is the major toxic alkaloid with a concentration in leaves ranging from 1.5%-4% by dry weight 2. N. glauca: Anabasine and nicotine are the dominant alkaloids, fruits and leaves are richest in anabasine ( leaf contains 1.3% by weight) 2, followed by roots, flowers and stems 3. N. glauca: Anabasine and nicotine are the dominant alkaloids, fruits and leaves are richest in anabasine ( leaf contains 1.3% by weight) 2, followed by roots, flowers and stems 3. Nicotine is the water-soluble alkaloid ((S)-3-(1- methyl-2-pyrrolidinyl) pyridine) and has an alkaline pKa of 8.5; it belongs to the pyridine/piperidine alkaloids. Nicotine is the water-soluble alkaloid ((S)-3-(1- methyl-2-pyrrolidinyl) pyridine) and has an alkaline pKa of 8.5; it belongs to the pyridine/piperidine alkaloids. Anabasine (1-(3-pyridyl) piperidine) is pharmacologically similar to nicotine. Anabasine (1-(3-pyridyl) piperidine) is pharmacologically similar to nicotine.
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Nicotine Nicotine Anabasine Anabasine
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Toxic parts: Leaves. Toxic parts: Leaves. Toxic dose: Toxic dose: Nicotine is highly toxic, 2-5 mg may cause nausea, 40-60 mg may be lethal 4. Nicotine is highly toxic, 2-5 mg may cause nausea, 40-60 mg may be lethal 4. Nicotine is well absorbed from the skin, lungs and gastrointestinal tract, it appears to be poorly absorbed in the acidic pH of the stomach 2. Nicotine is well absorbed from the skin, lungs and gastrointestinal tract, it appears to be poorly absorbed in the acidic pH of the stomach 2. Cases of intoxication by ingesting the plant are infrequent, they can occur as the result of an error, or deliberate ingestion which leaded to death due to consumption of N. glauca leaves Cases of intoxication by ingesting the plant are infrequent, they can occur as the result of an error, or deliberate ingestion which leaded to death due to consumption of N. glauca leaves
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Mechanism of action: Mechanism of action: Nicotine exerts its effects by binding to a subset of cholinergic receptors, the nicotinic receptors, which are located in ganglia at the neuromuscular junction, and also within the central nervous system, where the psychoactive and addictive properties reside 7. Nicotine exerts its effects by binding to a subset of cholinergic receptors, the nicotinic receptors, which are located in ganglia at the neuromuscular junction, and also within the central nervous system, where the psychoactive and addictive properties reside 7.
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Initially, and only briefly, nicotine is stimulating to the autonomic nervous system ganglia and neuromuscular junction. The most prominent effects relate to stimulation of the adrenal medulla, central nervous system, cardiovascular system (release of catecholamines), gastrointestinal tract (parasympathetic stimulation), salivary and bronchial glands and the medullary vomiting center. Initially, and only briefly, nicotine is stimulating to the autonomic nervous system ganglia and neuromuscular junction. The most prominent effects relate to stimulation of the adrenal medulla, central nervous system, cardiovascular system (release of catecholamines), gastrointestinal tract (parasympathetic stimulation), salivary and bronchial glands and the medullary vomiting center. There is subsequent blockade of autonomic ganglia and the neuromuscular junction transmission, inhibition of catecholamine release from the adrenal medulla, and central nervous system depression. There is subsequent blockade of autonomic ganglia and the neuromuscular junction transmission, inhibition of catecholamine release from the adrenal medulla, and central nervous system depression.
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Manifestations: Manifestations: ▫ Nicotine is an extremely lethal poison. ▫ Nicotine is an extremely lethal poison. ▫ Symptoms of nicotine poisoning may develop within 15 min., the onset of symptoms much more rapid after ingestion of liquid nicotine (e.g. insecticides) compared with nicotine – contained in organic material (plant parts). ▫ Symptoms of nicotine poisoning may develop within 15 min., the onset of symptoms much more rapid after ingestion of liquid nicotine (e.g. insecticides) compared with nicotine – contained in organic material (plant parts). ▪ The onset of symptoms begins with gastrointestinal distress (vomiting, nausea, salivation, abdominal pain, and diarrhea). ▪ The onset of symptoms begins with gastrointestinal distress (vomiting, nausea, salivation, abdominal pain, and diarrhea). ▪ CNS: headache, confusion, dizziness, ataxia, agitation, restlessness and incoordination develop initially after serious nicotine overdose. ▪ CNS: headache, confusion, dizziness, ataxia, agitation, restlessness and incoordination develop initially after serious nicotine overdose. Later, in severe poisoning, convulsions and coma may occur. Later, in severe poisoning, convulsions and coma may occur.
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Respiratory system: Initial tachypnea, but late dyspnea, decreased respiratory rate and cyanosis may be seen. Respiratory system: Initial tachypnea, but late dyspnea, decreased respiratory rate and cyanosis may be seen. Respiratory arrest may occur and results into death. Respiratory arrest may occur and results into death. ▪ Cardiovascular system: A transient increase in blood pressure followed by hypotension, bradycardia, paroxysmal atrial fibrillation or cardiac standstill is observed. ▪ Cardiovascular system: A transient increase in blood pressure followed by hypotension, bradycardia, paroxysmal atrial fibrillation or cardiac standstill is observed.
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● Green tobacco sickness: ● Green tobacco sickness: It is an occupational disorder that affects specifically the workers who harvest tobacco. It is an occupational disorder that affects specifically the workers who harvest tobacco. It is characterized by weakness, dizziness, headache, lightheadedness, abdominal pain, nausea, vomiting and in many cases respiratory difficulties. It is characterized by weakness, dizziness, headache, lightheadedness, abdominal pain, nausea, vomiting and in many cases respiratory difficulties. The manifestations are associated with the transdermal absorption of nicotine. The manifestations are associated with the transdermal absorption of nicotine. The disease is self-limited and resolves by the following day. The disease is self-limited and resolves by the following day. There is high incidence of the occurrence of the disease when the tobacco leaves, the skin or both are damp (dew, rain, sweat). There is high incidence of the occurrence of the disease when the tobacco leaves, the skin or both are damp (dew, rain, sweat). Wearing gloves and protective clothing is recommended 8. Wearing gloves and protective clothing is recommended 8.
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POTATO Potato: Potato: Common name: بطاطا Common name: بطاطا Scientific name: Solanum tuberosum Scientific name: Solanum tuberosum Family: Solanaceae. Family: Solanaceae.
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Glycoalkaloid solanine. Glycoalkaloid solanine. Solanine designates a mixture of six compounds, three solanines and three chaconines. Solanine designates a mixture of six compounds, three solanines and three chaconines. The aglycone common to all of the alkaloids is solanidine The aglycone common to all of the alkaloids is solanidine Solanidine is structurally similar to steroids; its proposed biosynthetic pathway is from acetate through cholesterol. Solanidine is structurally similar to steroids; its proposed biosynthetic pathway is from acetate through cholesterol. α- solanine and α- chaconine represent 90%-95% of the alkaloids occurring in the plant. α- solanine and α- chaconine represent 90%-95% of the alkaloids occurring in the plant. Solanine is water-soluble and is removed by boiling but not baking. Solanine is water-soluble and is removed by boiling but not baking. It is poorly absorbed from the gastrointestinal tract. It is poorly absorbed from the gastrointestinal tract. Elimination occurs rapidly in the feces and to lesser extent in urine. It concentrates in tissues in the following order: spleen, kidney, liver, lung, fat, heart, brain, blood Elimination occurs rapidly in the feces and to lesser extent in urine. It concentrates in tissues in the following order: spleen, kidney, liver, lung, fat, heart, brain, blood
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Toxic parts: Toxic parts: Ripe fruit contains the least amount of solanine, which appears in a nontoxic amount. Ripe fruit contains the least amount of solanine, which appears in a nontoxic amount. Human poisoning occurs after consumption of green or stressed potatoes. Human poisoning occurs after consumption of green or stressed potatoes. The toxic alkaloids are produced by the periderm, the cortex and areas of high metabolic activity such as the eyes and sprouts, green skin and stems The toxic alkaloids are produced by the periderm, the cortex and areas of high metabolic activity such as the eyes and sprouts, green skin and stems
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Exposure: Exposure: Solanine poisoning is rare except in times of food shortages. Solanine poisoning is rare except in times of food shortages. Although most solanine is removed by peeling and boiling, a few outbreaks occurred as a result of catering errors or unusual conditions Although most solanine is removed by peeling and boiling, a few outbreaks occurred as a result of catering errors or unusual conditions
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Factors that increase solanine concentration: Factors that increase solanine concentration: Although solanine exists throughout the plant, its concentration varies over a wide range because of a host of environmental and genetic factors. Although solanine exists throughout the plant, its concentration varies over a wide range because of a host of environmental and genetic factors. Studies revealed that the following factors increase alkaloid concentration: Studies revealed that the following factors increase alkaloid concentration: 1. Storage in lighted areas: exposure to sunlight for 6 hours multiplies the concentration of solanine by four (from 5 to 20 mg/100g), after 72 hours of exposure to sunlight, the concentration can reach 45mg/100g 1,2,3. 2. Species variation.
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3. Physiological stress. 4. mmaturity (i.e. green potatoes). 5. Storage conditions: potatoes are well kept in dark between 9-15 ◦C and in a dry atmosphere. 6. Trauma: any minor damage (cuts or crushing) leads to a 200%-300% increase in the solanine concentration.
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Toxic dose in humans is estimated to be between 2-5 mg/kg of solanine. Toxic dose in humans is estimated to be between 2-5 mg/kg of solanine. LD50 in humans was found to be 75 mg/kg via IP route. LD50 in humans was found to be 75 mg/kg via IP route.
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Manifestations: Manifestations: Gastrointestinal and neurologic symptoms predominate in cases of solanine poisoning depending on the amount ingested. Gastrointestinal and neurologic symptoms predominate in cases of solanine poisoning depending on the amount ingested. Vomiting, diarrhea, anorexia, malaise, headache and flushing are the most common symptoms. Vomiting, diarrhea, anorexia, malaise, headache and flushing are the most common symptoms. Non-gastrointestinal-- symptoms may include fever, altered mental status (drowsiness, confusion, delirium), restlessness and hallucinations. Non-gastrointestinal-- symptoms may include fever, altered mental status (drowsiness, confusion, delirium), restlessness and hallucinations. Some patients may have hypotension, tachycardia and stupor. Some patients may have hypotension, tachycardia and stupor.
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Nonspecific symptoms and visual blurring may develop. Nonspecific symptoms and visual blurring may develop. Allergic symptoms of immediate urticaria and angioedema related to contact with raw potato was described. A prick-by-prick test with potato pulp and rub test were positive. Specific IgE to potato was positive 5. The major potato allergen is patatin, Sol t 16. Allergic symptoms of immediate urticaria and angioedema related to contact with raw potato was described. A prick-by-prick test with potato pulp and rub test were positive. Specific IgE to potato was positive 5. The major potato allergen is patatin, Sol t 16. Deaths have been associated with consumption of toxic potatoes, but these reports involved malnourished patients who may not have received adequate care. Deaths have been associated with consumption of toxic potatoes, but these reports involved malnourished patients who may not have received adequate care.
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Treatment : Treatment : ▪ Gut decontamination (syrup of ipecac/ lavage, charcoal, cathartics) may be useful for those patients who are seen early (4 hours) and who don ’ t have spontaneous vomiting and diarrhea. ▪ Gut decontamination (syrup of ipecac/ lavage, charcoal, cathartics) may be useful for those patients who are seen early (4 hours) and who don ’ t have spontaneous vomiting and diarrhea. ▪ General supportive care: fluid status should be evaluated in every patient by means of orthostatic pulse and blood pressure. Electrolytes should be checked on those patients who exhibit profound changes or who take medications that alter the fluid or electrolyte balance. ▪ General supportive care: fluid status should be evaluated in every patient by means of orthostatic pulse and blood pressure. Electrolytes should be checked on those patients who exhibit profound changes or who take medications that alter the fluid or electrolyte balance.
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An intravenous line should be established on those patients who exhibit orthostatic hypotension or neurologic signs. An intravenous line should be established on those patients who exhibit orthostatic hypotension or neurologic signs. Seriously ill patients who don ’ t respond to fluid replacement, may need cardiac monitoring and vasopressors. Seriously ill patients who don ’ t respond to fluid replacement, may need cardiac monitoring and vasopressors. Seizures are treated by diazepam. Seizures are treated by diazepam. Patients with neurologic signs or orthostatic changes should be admitted for at least 24 hours of observations. Patients with neurologic signs or orthostatic changes should be admitted for at least 24 hours of observations.
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