Poisonous Plants PDF
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Iqra Noor Khan
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This document provides information about poisonous plants, specifically focusing on those found in Pakistan. It covers various aspects of these plants, including classifications, toxic components, symptoms of poisoning, and treatment.
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Poisonous Plants With special reference of pakistan IQRA NOOR KHAN DEFINITION: Poisonous plants consist of a group of plants, when these plants are introduced into human body toxic effects are produced. Poisonous plants are those plants which are capable...
Poisonous Plants With special reference of pakistan IQRA NOOR KHAN DEFINITION: Poisonous plants consist of a group of plants, when these plants are introduced into human body toxic effects are produced. Poisonous plants are those plants which are capable of producing a toxic reaction or death There are many plants available in northern areas & ground areas of Pakistan. Theses plants have the ability to produce some drastic effects on the human body. Classification of poisonous plants These are classified on the basis of the systems these plants are effecting Plants acting on GIT Plants acting on CNS Plants acting on CVS Plants producing Atropine like action Plants producing Nicotine like action Cyanogenetic plants Plants Causing GIT Toxicity It can further be classified as following Gastro Enteric Irritant Plant Plants toxic to gastric mucosa Plants irritant to intestinal mucosa Plants causing delayed gastroenteritis Gastroenteric plants Arisaema triphyllum Colocasia esculanta Arum jacquemonti Arisaema triphyllum Family “Araceae Habitat Sindh Gilgit Swat Ayubia Nathiagali Common name Indian turnip, saanp booti Colocasia esculenta Family “Araceae Habitat Sindh Gilgit Swat Ayubia Nathiagali Common name Taro, elephant-ear Arum jacquemonti Family “Araceae Habitat Sindh Gilgit Himalaya Parachanar Nathiagali Common name Arum Toxicology Toxic principle is Raphides. The oxalic acid is poisonous if ingested. The plant contains calcium oxalate crystals as in all parts, and because of this, consumption of the raw plant material results in a powerful burning sensation. It can cause irritation of the mouth and digestive system, and on rare occasions the swelling of the mouth and throat may be severe enough to affect breathing. Care is needed to avoid confusion with poison ivy, which has three leaflets per leaf somewhat similar in appearance. Symptoms Intense burning sensation Dermatitis Blister on tongue Increase salivation Loss of voice is also reported Plants toxic to Gastric Mucosa This group includes those plants which regulate spontaneous emesis upon ingestion. Narcissus tazetta Amaryllus vittae Crinum asiatcum Narcissus tazetta Family : “Amaryllideaceae” Habitat Gilgit Lower Swat Wally Common name: paper white Amaryllus vittae Family : “Amaryllideaceae” Habitat Punjab Sindh Common name: belladonna lily, Jersey lily, Crinum asiatcum Family : “Amaryllideaceae” Habitat Punjab Sindh Common name: Crinum Lily Toxicology There are various alkaloids in these plants but lycorine is the most dangerous one, that cause multiple symptoms. It also has fungicidal properties. Symptoms Inflammation and burning sensation of mouth Gastritis Headache Increase salivation Increased nasal secretion Convulsion insensibility Plants irritant to Intestinal Mucosa This group includes plants which induces emesis and colic (abdominal pain within one hour of ingestion) Aseculus indica Podophyllum emodi Podophyllum paltatum Ranunculus scleratus Taxus baccata Aseculus indica Plant name Aseculus indica Family Hippocastanaceae Habitat Kashmir Ziarat Quetta Muree Swat. Aseculus indica Toxicity It contain saponin glycoside “aesculin” which is found in nut leaves and bark of Aseculus indica. Aseculus indica Symptoms Inflammation of gastric mucosa Peptic ulcer Duodenal ulcer Inflammation eye. (Conjunctivitis) Vomiting Fever Headache Severe sneezing Podophyllum emodi Family Berberidaceae Habitat Swat Chitral Murree Ziarat Common name Himalayan May Apple Podophyllum emodi Toxicity The reason of toxicity is the presence of a resin “podophyllin” which is present in the rhizome. Medicinal value Podophyllum emodi/ paltatum can be used as anti cancer. Podophyllum emodi Symptoms Inflammation of gastric mucosa Peptic ulcer Duodenal ulcer Inflammation eye. (Conjunctivitis) Vomiting Fever Headache Severe sneezing Taxus baccata Plant name Taxus baccata Family Taxacacae Habitat Kashmir, Gilgit Muree Swat. Taxus baccata Toxicity There are many alkaloid present in taxus baccata but the reason of toxicity is “taxine” which is present in the leaves. Medicinal value Taxus also has anti cancer properties. Taxus baccata Symptoms Inflammation of gastric mucosa Peptic ulcer Duodenal ulcer Inflammation of eye. (Conjunctivitis) Vomiting Fever Headache Plants causing delayed gastroentritis Abrus precatorius Ricinus communis Rheum webbianum Rheum ribes Abrus precatorius Plant name Abrus precatorius Family Fabacae Habitat Sindh, and Kashmir.it found at 3000__5000 altitude. Common name Ratti, rosary pea Abrus precatorius Toxicology Seeds of this plant contain abrin, which is a phytotoxin. Abrin is neither degraded nor altered by gastric juices. It is a lethal cytotoxin Ingestion of a single seed, well chewed, can be fatal to both adults and children. It has a tendency to be invasive where it has been introduced. The toxin abrin is a dimer consisting of two protein subunits ricin, termed A and B. The B chain facilitates abrin's entry into a cell by bonding to certain transport proteins on cell membranes, which then transport the toxin into the cell. Abrus precatorius Ricin A, probably because of its peculiar binding potential is selectively transported by the neurons. This type of transport is known as suicidal transport. Treatment can be attempted with arecoline. Abrus precatorius Symptoms Even small amount of ingestion of seeds can cause cardiac Arrest especially in children. Severe gastroenteritis Nausea Vomiting Trembling of hands Muscular weakness Abrus precatorius Treatment Because no antidote exists for abrin, the most important factor is avoiding abrin exposure in the first place. If exposure cannot be avoided, the most important factor is then getting the abrin off or out of the body as quickly as possible. Abrin exposure can be prevented when it is present in large quantities by wearing appropriate personal protective equipment. Abrin poisoning is treated with supportive care to minimize the effects of the poisoning. Abrus precatorius This care varies based on the route of exposure and the time since exposure. For recent ingestion, administration of activated charcoal and gastric lavage are both options. Using an emetic (vomiting agent) is not a useful treatment. In cases of eye exposure, flushing the eye with saline helps to remove abrin. Oxygen therapy, airway management, assisted ventilation, monitoring, IV fluid administration, and electrolyte replacement are also important components of treatment Ricinus communis Plant name Ricinus communis Family Euphorbiaceae Habitat Punjab Sindh Common name castor bean, ارنڈ ۔ Ricinus communis Toxicology The toxic principle behind ricinus communis is the presence of a glycoprotein “Ricin” which is present in seeds. Fatal dose 5-10 crushed seeds 6 mg of ricin Fatal period 2 to several days Medicinal value It can also be used as purgative. Ricinus communis Symptoms Inflammation and burning sensation of mouth Gastritis Headache Increase salivation Increased nasal secretion Ricinus communis Treatment The treatment includes Gastric lavage Activated charcoal Symptomatic treatment Rheum webbianum Plant name Rheum webbianum Family Polygonacae Habitat In Pakistan it grows on slopes at an elevation of 2,000–4,500 metres above sea level. Gilgit Kpk Common name Chotal, ishpar , rhubarb Rheum ribes Plant name Rheum ribes Family Polygonacae Habitat In Pakistan it grows on slopes at an elevation of 2,000–4,500 metres above sea level. Gilgit Kpk Common name Rawash, Syrian rhubarb Rheum Toxicology The leaf blades of rhubarb contain enough oxalic acid to cause poisoning. Acute renal failure has been associated with long-term use. Symptoms Burning sensation Gastroentritis Diarrhea Emesis Rheum Toxic dose 3.5 mg-6 mg Treatment Gastric lavage Activated charcoal Plants causing cvs disturbance That produce CVS disturbance i.e, effect the heart functions due to their toxicity Some of these plants are: Digitalis Aconitum Nerium indicum DIGITALIS COMMON NAME: ENGLISH: Foxglove URDU: Berge-Lafta SOURCE: Digitalis purpurea Digitalis lanata FAMILY: Scrophulariaceae DIGITALIS purpurae PLANT DESCRIPTION: Biennial Erect plant Height is 2-6 feet or 30-150 cm FLOWERS: White or purple in color Digitalis lanata PLANT DESCRIPTION: Biennial Erect plant Height is 2-3 feet (60-90 cm) Digitalis CHEMICAL CNSTITUENTS: Digitalis leaves contain glycosides also known as Cardiac Glycosides Important glycosides are: Digitoxin Gitoxin Lannatoside C Digitalis ABSORPTION & EXCRETION: Absorption of glycosides is irregular Digitoxin is completely & rapidly absorbed through GIT Excreted very slowly through urine in 20 days Digitalis POISONING: Cardiac glycosides can cause cardiac toxicity It arrests the heart Poisoning occurs due to overdose of the medication In case of children, the poisoning occurs due to ingestion of leaves, seeds or sucking the flowers Digitalis SYMPTOMS: Low dose can cause Decrease in heart rate Headache & Nausea Anorexia Digitalis High dose can cause: Increase in heart rate Vomiting Diarrhea Abdominal pain Yellow vision Other visual disturbances Difficult breathing Unconsciousness & coma Death due to heart arrest after fibrillation (abnormal action of heart muscles) Digitalis LETHAL DOSE: Crude leaves-----2g Digitoxin ----------5mg Digoxin------------10mg Digitalis TREATMENT: Gastric lavage Activated charcoal 20g ------ given in slurry (thick liquid) mixed with water Saline catharsis (purgatives containing salts Phenytoin sodium 1-3 mg /kg body weight is given slowly through i/v injection which is effective against cardiac arrythmias Propranolol is also effective against digitalis poisoning Either given through i/v injection (0.5-2 mg)/minute Through mouth from 10-30 mg every 8 hours ACONITUM LOCAL NAME: URDU: Atis PUNJABI: Bonga B.O: Aconitum napellus Aconitum hetrophyllum FAMILY: Ranunculaceae ACONITUM PLANT DESCRIPTION: Perennial herb Bright green in color FLOWERS: Blue or purple in color ACONITUM CHEMICAL CONSTITUENTS: Aconitum contains the following alkaloids ACONITINES: The ester of poly-hydric amino alcohols Very poisonous All the species are extremely poisonous ATISINES: Amino alcohols Less poisonous ACONITUM TOXICITY: All parts of plants contain Aconitine & other alkaloids But the roots contain greater amount & concentration of poisonous Aconitine Roots are the most poisonous part Leaves are greatly poisonous just before flowering Toxic dose 2mg ACONITUM SYMPTOMS: After ingestion of the plant part following symptoms may be observed Tingling (a thrilling sensation) Burning sensation of the lips, mouth & tongue Salivation Nausea Vomiting Palpitation Arrythmia Slow & weak pulse Respiratory failure Numbness Convulsion Death may occur within 2 hours due to ventricular fibrillation & respiratory failure ACONITUM TREATMENT: Gastric lavage Saline catharsis Atropine Lidocaine Nerium indicum: Plant name Nerium indicum: Family Apocynaceae Habitat Gilgit Kpk Common name OLEANDER Nerium indicum TOXIC PRINCIPLE Leaves and roots of this plant contain a mixture of glycosides which are chemically and physiologically related to digitalis glycosides. Among these Oleandrin is a major toxic principle Nerium indicum Severe gastroenteritis Dizziness and drowsiness Increased pulse rate Abdominal pain Irregular weakend heart Vomiting and respiratory depression PLANTS ACTING ON CNS The following plants are responsible for CNS toxicity. Cicuta virosa Melia azadirachta, Melia azadarach Cannabis sativa OR Cannabis indica Cicuta virosa Common name: Water hemlock Family : Umbelliferae TOXIC PRINCIPLE: This plant contains a unsaturated alcohol called Cicutoxin distributed through the plant but highly concentrated in stem and rhizome. Cicuta virosa POISONING: Flowers of this plant are only slightly toxic. Cicutoxin acts slowly as it is sparingly soluble in water and thus slowly absorbs but once completely absorbed its actions are violent. SYMPTOMS OF TOXICITY: Increased salivation, nausea and vomiting. Tremor respiratory paralysis which is usual cause of death Melia azadirachta Plant name Melia azadirachta Family Meliacae Habitat Gilgit Kpk Common name chinaberry tree, neem Melia azadirachta Toxicology It contains neurotoxin and unidentified resins. It contains four tetranortriterpenes(meliatoxin) Symptoms of toxicity Faintness Mental confusion Emesis meliatoxin Diarrhea Cannabis sativa/indica Common name: Cannabis sativa/indica Family : Cannabaceae Habitat Found throughout Pakistan i.e, Punjab Sind KPK Baluchistan Usually found on road sides Best quality found in Gilgit & chitral Common name Bhang Cannabis sativa/indica ACTION: Sedative Hypnotic Hallucinant ABSORPTION & EXCRETION: Cannabinol is absorbed from inhaled smoke Excreted very slowly through urine Cannabis sativa/indica Toxic principle Toxic principle in this plant is narcotic resin i.e. Cannabis resin which contains over 60 various compounds. Cannabinoids principle of which are Cannabiol, Cannabidiol and tetrahydrocannabinol. Tetrahydrocannabinol is a euphoric principle Cannabinol Cannabidiol Cannabidiolic acid (precursor of THC) These are sedative principles Fresh plant contains reserved Cannabidiolic acid which is the precursor of THC i.e, cannabidiolic acids are transformed to THC during drying, storage or extraction Cannabis sativa/indica Tetrahydrocannabinol Cannabis sativa/indica TOXIC EFFECTS: Toxicity of the drug depends upon the potency of the drug & route of administration When taken orally , the following symptoms are observed Anxiety Confusion Disorientation Auditory hallucination Toxic dose More than 10 mg Cannabis sativa/indica Heavy dose may cause vertigo. When resin is administered through injection following symptoms may be observed after 15-20 minutes Rigors, a sudden feeling of cold Fever Tachycardia Tremors Hypotension Nausea Vomiting Diarrhea CYANOGENETIC PLANTS These plants contain cyanogenetic or cyanophoric glycosides, which only on hydrolysis produce HCN and Benzaldehyde. First isolated cyanogenic glycoside is Amygdalin 1mg/kg of HCN is lethal. Following are the plants which are cyanogenetic. Prunus amygdalus OR Prunus persica Manihot utilissima OR Manihot esculentus Prunus amygdalis Plant name Prunus amygdalis FAMILY: Rosaceae LOCAL NAME: Badam Geographical location in pakistan Wild in Baluchistan, Chitral, Gilgit, cultivated in these areas Prunus amygdalis PLANT DESCRIPTION: Small tree which grows to a height of 15 feet Bark is smooth, shiny, having Slate Purple color CHEMICAL CONSTITUENTS: Dried seeds contain 50% fixed oil 3-4% Amygdalin 0.5-0.8% essential oil which contains 4-7% of Hydrogen Cyanide Prunus amygdalis Mechanism of toxicity It contain enzyme emulsin which in the presence of water act on the two soluble glucosides amygdalin prunasin And yield glucose, cyanide and the essential oil of bitter almonds, which is nearly pure benzaldehyde, the chemical causing the bitter flavor. Bitter almonds may yield 4–9 mg of hydrogen cyanide per almond and contain 42 times higher amounts of cyanide than the levels found in sweet almonds Prunus amygdalis TOXICITY: Few mg of HCN may be fatal to humans because it blocks the ability of cells to use Oxygen HCN inhibits the action of an enzyme i.e, Cytochrome Oxidase which is Respiratory catalyst or enzyme which links atmospheric Oxygen with metabolic respiration Thus HCN poisoning causes asphyxia (lack of Oxygen causing death or loss of consciousness) at cellular level Prunus amygdalis Lethal dose Extract of bitter almond was once used medicinally but even in small doses, effects are severe or lethal, especially in children; the cyanide must be removed before consumption. The acute oral lethal dose of cyanide for adult humans is reported to be 0.5–3.5 mg/kg (0.2–1.6 mg/lb) of body weight (approximately 50 bitter almonds), so that for children consuming 5–10 bitter almonds may be fatal Prunus amygdalis Symptoms of toxicity Generally cyanide poisoning causes: Difficulty in breathing Spasm (an involuntary & painful contraction of a muscle) Coma Sudden & unexpected death Large doses of HCN may cause; Unconsciousness within a few seconds Prunus amygdalis Smaller doses Giddiness(sensation of whirling and tendency to fall) Staggering Headache Dilation of pupils Palpitations Unconsciousness Death may occur within 15 minutes to an hour after ingestion Prunus amygdalis TREATMENT: Must be given immediately Immediate diagnosing may be made by characteristic cyanide odor of the breath of the patient but it is always not detectable Patient should be given amyl nitrite inhalations for 15-30 seconds each minute Just after the inhalations, Cobalt edetate injection should be administered. It is immediately followed by 50 ml of Dextrose injection Stomach should be emptied by aspiration & lavage using 0.02% solution of Pot. Permangante or 5% solution of Sodium thio-sulphate 300 ml of 25% Sodium thiosulphate solution should be left in the stomach Prunus amygdalis CYANIDE EMERGENCY KIT: It is an ampoule kit containing injection of Cobalt edate, dextrose & with Amyl Nitrite & Ancillary equipment Manihot utilissima/esculantus) Plant name Manihot utilissima/esculantus FAMILY: Euphorbiaceae LOCAL NAME: Cassava Geographical location in Pakistan Punjab Sindh Manihot utilissima/esculantus) PLANT DESCRIPTION Herb Woody, hairy 5m or rarely more Tuberous roots Plant occurs in two verities Sweet species Bitter species (poisonous) Manihot utilissima/esculantus) CHEMICAL CONSTITUENTS: Roots & leaves contain a high concentration of cyanogenic glycosides & HCN, Sufficient to cause death due to cyanide poisoning Roots also contain starch called Cassava starch, which is used as important foodstuff in many regions In order to remove the poison from the roots, the roots are peeled & cooked During cooking process the water is replaced several times by fresh water Manihot utilissima/esculantus TOXICITY: The toxic principle is LINAMARIN and LOTAUSTRALIN. Both these toxins are decomposed by LINAMARASE ,naturally occuring ezyme liberating Cyanide. In 1830, the cyanogenetic glycosides i.e, Manihotoxin was isolated from Manihot Manihotoxin consist of acetone, cyanohydrin & glucoside On hydrolysis, manihotoxin yields HCN Manihot utilissima/esculantus A few milligrams of HCN maybe fatal to humans, Because it blocks the ability of cells to use Oxygen HCN inhibits the action of an enzyme i.e, Cytochrome Oxidase Cytochrome oxidase is a respiratory catalyst or enzyme which links atmospheric Oxygen with metabolic respiration HCN causes asphyxia (lack of Oxygen causing death or loss of consciousness) at the cellular level Manihot utilissima/esculantus TOXIC EFFECTS OR SYMPTOMS: Generally the cyanide poisoning causes: Difficulty in breathing Spasm Goiter Partial paralysis Coma Sudden & unexpected death LARGE DOSES MAY CAUSE: Unconsciousness within a few seconds Smaller doses Giddiness Staggering Headache Dilation of the pupils Palpitations Death may occur within 15 minutes to an hour, after ingestion Manihot utilissima/esculantus TREATMENT: Must be given immediately. Immediate diagnosis may be made by characteristic cyanide odor of the breath of the patient, but it is not always detectable Amyl nitrite inhalations for 15-30 minutes Just after inhalations Cobalt edetate injection should be administered It is immediately followed by 50 ml of dextrose injection The stomach should be emptied by aspiration & lavage using 0.02% solution of Potassium Permanganate or 5% solution of Sodium thiosulphate. 300 ml of 25% Sodium thiosulphate solution should be left in the stomach Manihot utilissima/esculantus CYANIDE EMERGENCY KIT: It is an ampoule kit containing injection of Cobalt edate, dextrose & with Amyl Nitrite & Ancillary equipment ATROPINE CONTAINING PLANTS These are solanaceous alkaloids which contain atropine, hyoscyamine and hyoscine. These alkaloids are mostly found in seeds, leaves berries and rhizome. Atropa belladona Datura alba OR Datura stramonium OR Datura fastousa Hyoscyamus niger Atropa belladona Plant name Atropa belladona FAMILY: Solanacae LOCAL NAME: deadly nightshade Geographical location in Pakistan Kurram Dir Sawat Hazara Muree Azad kashmir Atropa belladona TOXIC PART: Belladonna is one of the most toxic plants found in the Eastern Hemisphere. All parts of the plant contain tropane alkaloids. The berries pose the greatest danger to children because they look attractive and have a somewhat sweet taste. The consumption of two to five berries by a human adult is probably lethal. The root of the plant is generally the most toxic part, though this can vary from one specimen to another. Ingestion of a single leaf of the plant can be fatal to an adult. Datura stramonium Plant name Datura stramonium FAMILY: Solanacae LOCAL NAME: thorn apple, jimsonweed TOXIC PART: All plant parts are toxic DISTRIBUTION: Sindh Punjab KPK Balochistan Commonly found in weedy places Hyoscyamus niger Plant name Hyoscyamus niger FAMILY: Solanaceae TOXIC PART: All the plant parts are toxic Geographical location in Pakistan Sindh Baluchistan Punjab KPK Hyoscyamus niger Common name Stinking nightshade, henbane PLANT DESCRIPTION: Perennial Erect Branched Hairy herb Height is about 30-90 cm Whole plant body is covered with soft wooly hair Toxicity Atropine increases firing (The rate at which the SA node generates impulses) of the sinoatrial node (is a group of cells known as pacemaker cells, located in the wall of the right atrium of the heart). Opposes the action of vagus nerve (longest nerve of the autonomic nervous system which regulate many physiological functions e.g heart rate etc) Blocks acetylcholine receptor sites (anticholinergic). In general atropine lowers the parasympathetic activity of all muscles and glands regulated by parasympathetic system Toxicity Lethal dose 2 mg to 3 mg (maximum 0.03 mg/kg to 0.04 mg/kg) Signs and symptoms Signs and symptoms of toxicity depends on the amount of toxic material ingested. Early symptoms include Visual disturbances. Dryness of mouth and throat intense thirst. Skin becomes hot, dry and flushed. High temperature may be upto 105 degrees Fahrenheit accompanied by headache, marked confusions and muscular incoordination. In severe intoxication: slow respiration, irregular pulse, cyanosis and death by respiratory failure. Treatment Emergency help with atropine poisoning or poisonous plants (getting it through the mouth) - gastric lavage. The patient is given to drink 2-3 liters of warm water with crushed tablets of activated carbon or the slightly pink solution of potassium permanganate. Simultaneously, the ambulance crew is called. The unconscious patient is turned on its side to avoid suffocation when sticking the tongue. Treatment if, as a patient, it is not possible to do a gastric lavage, a subcutaneous injection of apomorphine (an emetic) is done in order to quickly remove toxic residues. In cases of impaired respiratory function, artificial lung ventilation or may be indicated. For removal of the sucked poison they perform forced diuresis. As an antidote physostigmine can be used. PLANTS PRODUCING NICOTINE LIKE ACTION Conium maculatum Lobelia inflata Nicotianna tobaccum Conium maculatum Plant name Conium maculatum FAMILY: Apiaceae Geographical location in Pakistan Mardan Swabi Peshawar Hazara kashmir Conium maculatum Toxic part All parts of the plant are toxic, especially the seeds and roots when ingested.. Common name hemlock, poison hemlock Conium maculatum CONSTITUENTS: Poison hemlock contains coniine and some similar poisonous alkaloids, and is poisonous to all mammals (and many other organisms) that eat it. C. maculatum is known for being extremely poisonous. Its tissues contain different alkaloids. In flower buds, the major alkaloid found is γ-coniceine Poison hemlock is most poisonous in the spring when the concentration of γ-coniceine (the precursor to other toxins) is at its peak. Conium contains the piperidine alkaloids coniine, N methylconiine, conhydrine, pseudoconhydrine and gamma-coniceine which is the precursor of the other hemlock alkaloids. Conium maculatum TOXICITY symptoms Overdose may cause fatal neuromuscular dysfunction failure of the respiratory system Oxygen deprivation LETHAL DOSE: For an adult, the ingestion of more than 100 mg (0.1 gram) of coniine (about six to eight fresh leaves, or a smaller dose of the seeds or root) may be fatal. Conium maculatum Treatment Gastric lavage Activated charcoal Nicotiana tobaccum LOCAL NAME: Tumbacco B.O: Nicotiana tobaccum FAMILY: Solanaceae Nicotiana tobaccum Geographical location in pakistan Cultivated in Pakistan Mardan Swabi Peshawar CONSTITUENTS: Contain following alkaloids.6-9% of Nicotine ----- Pyridine alkaloids Due to presence of pyridine ring Nor-nicotine Precursor of N-nitrosonornicotine (carcinogen) Nicotyrine Nicotinic acid Nicotinic acid Nicotiana tobaccum ACTION: Nicotine is CNS stimulant & then depressant Nicotine exerts its action as a stimulant leading to depression & thereafter paralysis It has a paralytic action on the skeletal muscles Nicotiana tobaccum TOXICITY: Overdose may cause Local irritation paralysis Overdose can occur through combined use of nicotine patches or nicotine gum & cigarettes at the same time Spilling a high concentration on skin can cause intoxication or even death Because nicotine readily passes into blood stream It is Carcinogenic and teratogenic Nicotiana tobaccum Treatment Gastric lavage Activated charcoal LOBELIA Also called as Indian Tobacco B.O: Lobelia inflata (American species) Lobelia frutescence FAMILY: Lobeliaceae HABITAT: Pkistan & india at altitude of 700-2200 m CHEMICAL CONSTITUENTS: Fourteen alkaloids Major & important one is Lobeline In Indian Lobelia it is found about 0.8% Lobeline is in the form of colorless crystals Slightly soluble in water Readily soluble in hot alcohols USES: Respiratory stimulant Effects are short in duration Lobelia sulphate (0.5-1.5 mg) in tablets & lozenges to break smoking habit ACTION: CNS stimulant Nicotinic in nature Acts as local irritant SYMPTOMS: Dryness of throat Nausea Vomiting Abdominal pain Sweating Rapid pulse Tremors Muscular twitching & convulsion Death due to respiratory failure LETHAL DOSE: Injection is 10mg Ingestion of dried herb ----50 mg Tincture 1ml TREATMENT: Gastric lavage Saline cathartics with Potassium Permangnate (.05%) Saline catahrtics are useful which cause vomiting (30 g of sodium sulphate in 250 ml water) Ethopropazine 100 mg is also effective----- given through mouth Assisted respiration Injected overdose may be treated with Assisted respiration Ethopropazine is given orally Diazepam 5-10 mg through i/v or deep i/m injection is helpful to treat convulsion