S2 L7-8 Poisonous plants of Sri Lanka

  • Published on

  • View

  • Download


S2 L7-8 Poisonous plants of Sri Lanka. Anna Drew & Peradeniya University BPharm Batch 2005/6 (8 July 2008) with slide contribution from: Ruben Thanacoody, www.wikitox.org. Paracelcus 1493-1541. - PowerPoint PPT Presentation


  • S2 L7-8 Poisonous plants of Sri LankaAnna Drew

    & Peradeniya University BPharm Batch 2005/6

    (8 July 2008)

    with slide contribution from: Ruben Thanacoody, www.wikitox.org

  • Paracelcus 1493-1541All substances are poisons; there is none which is not a poison. The right dose differentiates a poison from a remedy.

  • Thevetia peruvianaFamily: Apocyanaceae

    Sinhala name/s: kaneru

    Tamil name/s: manjal alari

    English/common name/s: yellow oleander, lucky nut

    Plant habitat:often used for hedging in Sri Lanka native of Central & S.America but now grown throughout tropical and subtropical regions

    Toxic part of the plant: seed (although all parts toxic)

    Lethal dose: kernel of one fruit (or 2 leaves for a child)

    Main toxic constituent/s: thevetin A, thevetin B

    Constituent type: cardiac glycosides

    Mode of action: inhibit sodium-potassium ATPaseincreased intracellular sodium and serum potassiumnegative chronotropic, positive inotropic effects

  • Representative Cardiac CellNa+ channelVoltage dependentL-type Ca2+ channelNa+/K+ ATPaseNa+/Ca2+ exchangerHeart muscleK+ channel(s)3 Na+Ca2+-adrenergic receptor

  • Cell ElectrophysiologyCa2+Phase 2Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+3 Na+Ca2+

  • 3 [Na+]2 [K+]Therapeutic & Toxic MoACa2+Phase 2Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Ca2+Na+K+

  • Clinical features of poisoning: digoxin-likeEarly on: burning sensation in mouth, tingling of tongue, dry throat, giddiness, nausea vomiting, diarrhoeaCardiovascular: sinus bradycardia, first and second degree heart block, junctional rhythms, atrial and ventricular extrasystoles, ventricular fibrillationOther: yellow vision, anxiety, convulsions, coma

    Diagnosis:cardiac glycoside blood levels seed remnants, vomitus, gastric aspirate may help identifymonitor serum potassium and electrolytes

    Treatment of poisoning:induce emesis at home (ipecac)gastric lavage within 1 hour or activated charcoalatropine 0.5mg IV for bradycardia, repeatedcardiac pacing for third degree heart blockanti-digoxin Fab antibodies in severe casesReferences: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006; IPCS Inchem. Thevetia peruviana. Dated March 1990 [Accessed at http://www.inchem.org/documents/pims/plant on 29 June 2008]; www.wikitox.org

  • Datura metel


  • Scientific name:Datura metel Synonyms:Datura fastuosa (L.) Datura alba (Nees.) Family:Solanaceae Sinhala name:Ela-attana Tamil name:Ayigam Common names:Devil's trumpet, downy thorn-apple, black datura, angel's trumpet

  • Plant habitat:Native to China, India and South East Asia.It is a common weed in waste and cultivated land in Sri-lanka and now it is used in landscaping and gardening .

    Plant description: Shrub-like annual herb with large flowers, typically white or yellow with deep purple accents. Leaves are alternate and simple.

    Traditional use: Leaves/dried flowers are used to relieve asthma or wheezing like symptoms in many cultures eg Chinese herbal medicine (yng jn hu).Leaf poultices are applied to engorged breasts to relief excess milk production, rheumatic swelling of joints and lumbago.Powdered root is rubbed into gums or stuffed into cavities for toothache.

    Toxic part of the plant : all parts.

    Main toxic constituents : tropane alkaloids

  • Leaves/flowers - mainly atropine Seeds/roots - mainly hyoscyamine Fruits scopolamine

    Dose:Accidentally (or intentionally) ingesting even a single leaf could lead to severe side effects

    Symptoms: anticholinergicThirst, dry mouth, blurred vision, photophobia, urinary retention occur soon after ingestion. Skin is hot, dry and flushed. Pupils are dilated and fixed. Cardiovascular effects are sinus tachycarida, hypertension, supra/ventricular arrhythmias, orthostatic hypertension.Severe poisoning causes disorientation, agitation, violent behaviour, convulsions, delirium, visual and auditory hallucinations, ataxia, respiratory depression, coma.

  • Mode of action: It stimulates the central nervous system and simultaneously depresses peripheral nerves and dilates the pupils by peripheral action. The most probable action in this case is paralysis of the occulomotor nerve ending or its myoneural junction.Treatment of poisoning:Ipecac to induce emesis or gastric lavage.Activated charcoal to reduce absorption of toxic substances.Catheterization to empty bladder if necessaryDiazepam for hallucinations and delirium. References:www.wikipedia.org/wiki/Datura_metel www.ces.ncsu.edu/depts/hort/consumer/poison/Daturme.htm www.people.vcu.edu/~asneden/tropane%20alkaloids.pdf waynesword.palomar.edu/ww0703.htm DMA Jayaweera. Medicinal plants used in Ceylon Parts 1-5. Colombo: National Science Foundation, 2006Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • D. NiyangodaT.A. Ekanayaka

  • Scientific name: Abrus precatorius L.

    Synonyms: A.minor, A.pauciflorus

    Family: Leguminosae

    Sinhala name: Olinda

    Tamil name: Adisamiyai

    Common names:Abrus seed, crabs eye, Indian bead, Indian liquorice, wild liquorice, lucky bean, prayer or rosary beads, precatory bean, weather plant, jumble beads, jequirity bean

    Plant description: slender perennial twiner

    Habitat: grows wild in dry regions of Sri Lanka at low elevations

    Traditional use:To cure itch, sores and wounds due to bites of dogs, cats and ratsLeaves: conjunctivitis, painful swellings; ground with lime for acne, boils, abscesses and tetanusSeeds: diabetes, Brights disease

  • Toxic part of the plant: seedThe most poisonous parts of the plant involved in poisoning are the small, scarlet seeds, that have a black eye at the hilum

    Toxicity: One seed well masticated can cause fatal poisoning (adults and children)

    Main toxins: Abrin - concentrated in seeds

    Mode of action:

    Abrin exerts its toxic action by attaching itself to the cell membranesIt has a direct action on parenchymal cells (eg liver and kidney cells) and red blood cells

    Clinical effects:

    Early features of toxicity - burning of the mouth and oesophagus, and severe gastroenteritis with vomiting, diarrhoea and abdominal pain. Haematemesis and melaena are less common

    Later - drowsiness, disorientation, weakness, stupor, convulsions, shock, hepatotoxicity, cyanosis, retinal haemorrhages, haematuria, and acute renal failure (oliguria) can occur

    (Contact with the eyes can cause conjunctivitis and even blindness)

  • Diagnosis:

    Diagnosis is made by the presence of the typical manifestations following ingestion: gastroenteritis with risk of dehydration, haematemesis and melaena. Drowsiness and convulsions may occur.Toxicological analysis of body fluids for the poison is not helpful.Plant material, seeds or remnants of seeds, vomitus and gastric aspirate should be collected in clean bottles for identification.

    Main risks and target organs:

    The main risk is the severe gastroenteritis leading to dehydration and shock. Ingested seeds can affect the gastrointestinal tract, the liver, spleen, kidney, and the lymphatic system.


    Administration of fluids and electrolytes will alleviate dehydration.

    References:Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science Foundation, 2006http://www.inchem.org/documents/pims/plant/abruspre.htm [accessed 03/07/2008]

  • Myristica fragrans

    M. JayasingheC.M.C. Indrajith

  • Scientific name: Myristica fragrans

    Family: Myristicaceae

    Sinhala name: Sadikka, Wasawasi (aril)

    Tamil name: Adipam, Attigam, Kasam, Sadi, Sadikkay

    English/common names: Nutmeg, Mace tree

    Plant habitat:A native of E.Moluccas and other Indian IslandsNow cultivated in Sri Lanka, Malaya, Philippines, W.Indies & South America

    Traditional use: As a spice in foodsAs a traditional medicine for diarrhoea

    Toxic part of the plant: seeds (nutmeg) and, to a lesser extent, the aril (mace)

    Lethal dose:Humans: 1-3 nutmegs (5-15g) for adults, 2 nutmegs for childrenAnimals: oral dose of 24mg nutmeg oil per kg body weightMain toxins: myristicin & elemicin


  • Mode of action:Elemicin undergoes oxidation of its oleficin side chain to produce TMA (3,4,5-trimethoxyamphetamine), a psychotropic drug agentMyristicin produces MMDA which is metabolised to form TMA. MMDA has a higher potency than TMANutmeg has monoamineoxidase inhibition properties and anti-prostaglandin synthesis effectsClinical features of poisoning:symptoms are usually seen within 3-6 hours after ingestion and vary according to the dose taken and the variability between different samples of nutmegsintoxication resembles anti-cholinergic intoxication ie profuse sweating, flushed face, dry mouth, burning epigastric pain, tachycardia, restlessness, giddiness, hallucinationsunlike anti-cholinergic symptoms pupils constrict

    Diagnosis:Blood monitoring (electrolytes, liver enzymes, renal function) and urinalysis

    Treatment of poisoning: symptomatic and supportiveInduce emesis (with ipecac) or gastric lavageActivated charcoalDiazepam for restlessness or hallucinationsReferences: http://www.rain tree nutmeg.com/plant images/myristica pic.htm [01.07.2008]; http://www.inchem.org/documents/pims/plants/pim335.htm [1.07.2008]; http://en.wikipedia.org/wiki/ [1 July 2008] ; Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science Foundation, 2006

  • Alocasia macrorrhiza


  • Scientific name: Alocasia macrorrhiza

    Synonyms: A.odora, A.commutata, Colocasia macrorrhiza, Caladium glycyrrhizum, Philodendron peregrinum, Arum grandiflorum

    Family: Araceae (Magnoliophyta)

    Sinhala name: Habarala

    Tamil name: Parum sembu

    English/common names: giant taro, elephant ear, ape flower

    Plant habitat:grows in all tropical countries including India, Sri Lanka, Malaya & Philippines

    Traditional use:Acrid juice of the leaf gives instant relief to stings of the giant nettleChopped leaves & roots used as an application on painful jointsCut stem + lime/water applied to dogs bitesDried stems for haemorrhoids & chronic feversCrystals destroyed on boiling or roasting so starch in stem can be used as a foodsource

    Flower of the Alocasia plantTaro corms

  • Toxic part of the plant: all parts

    Main toxic constituent/s:all parts of the plant contain specialized cells containing bundles of needle-like calcium oxalate crystals and toxic proteins

    Mode of action: When the plant is chewed the sharp crystals injure the mucous membrane allowing toxic proteins to penetrate

    Lethal dose: The extreme oropharyngeal response generally limits the amount of plant ingested and oxalate absorbed through the oral mucosa is unlikely to cause systemic poisoning

    Symptoms:Eating parts of the plant causes a severe burning in mouth and throat. Other symptoms may include:Redness, swelling, pain, burning pain of the tongue and mucous membranes, profuse salivation, dysphagiaSwelling can rarely cause obstruction and respiratory compromiseLoss of speech may last several days and swelling more than a week

    Treatment of poisoning:wipe out the mouth with a cold, wet cloth and give milk to drinkantihistamines, mouthwashes, antiseptics and steroids may be usedReferences: http://en.wikipedia.org/wiki/Alocasia [3 July 2008]; Jayaweera DMA. Medicinal plants used in Ceylon. Part 1. Colombo: The National Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Nicotiana tabacumSanduni SudusingeUthpala SiriwardhaneMano Wickramarathne

  • Scientific nameNicotiana tabacumFamilySolanceaeSinhalese nameDum kola

    Tamil namePhaielai English nameTobaccoPlant habitat native of tropical and subtropical America but it is now commercially cultivated worldwide

    Traditional use- as an insecticide - intestinal worms or constipation- dried tobacco leaves for chewing, snuffing or smoking

    Toxic part of the plantleaves, stems, roots and flowers

    Main toxic constituentsnicotine

    Constituent type alkaloid

    Lethal dose0.5-1 mg/kg body weight nicotine (~ 40 - 60 mg)

  • Mode of actionNicotine binds stereo specifically to acetylcholine receptors at autonomic ganglia, the adrenal medulla, the neuromuscular junction and the brainThis evokes the release of catecholaminenicotine produces ganglionic blockade, vagal afferent nerve stimulation, or direct depressor effects mediated by action on the brain

    Clinical features of poisoningMild: salivation, nausea, dizziness, drowsiness, headache, vomiting, diarrhoea, hand tremorSerious: mental confusion, circulatory collapse (shallow rapid pulse, cold sweating), convulsions, loss of consciousness, cardiac arrest, respiratory paralysis

    DiagnosisBlood monitoring (blood gases) and urinanalysis

    Treatment of poisoninginduced emesis (ipecac) or gastric lavage and activated charcoalsupportive therapy directed towards maintaining respiration and blood pressure (IV fluids) and controlling convulsionsReferences: www.wikipedia.com; www.inchem.org; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Scientific name : Strychnos nux-vomica Synonyms : S.lucida, S.colbrina, S.aromatica Family : Loganiaceae Sinhala name : Godakaduru, Visha kaduru Tamil name : Eddi, Etti, Kagodi English/common name : Poison nut, Nux vomica, Quaker buttons Plant habitat : dry forests of Ceylon, flowers in August A moderate sized or large tree with an erect trunk, Slide 5 Bark Wood Leaves Flowers Fruit

    Traditional use :Root - cures fever and bites of venomous snakes Used for preparation of homeopathic medicine

    Toxic part of the plant : seed (although all parts toxics)

    Wathsala Wimalasena Kanishka Jayaweera

  • Main toxic constituents : strychnine, (brucine)

    Constituent type : alkaloids

    .Lethal dose : plant poisoning is rare possibly due to bitter taste The quantity of strychnine in one seed could be fatal If seeds are swallowed uncrushed they are not poisonous

    Mode of action : Strychnine is a potent convulsant. It causes increased reflex excitability in the spinal cord

    Brucine resembles strychnine activity but it is less potent

    Clinical features of poisonings : Symptoms appear within 15 - 30 min of ingestion - Initial symptoms bitter taste in mouth, feeling of suffocation - Twitching of the muscles in neck, body and limbs - Extreme contractions affecting all muscles in the body - The patient is conscious and has intense pain. - Complications - lactic acidosis, rhabdomyolysis, acute renal failure - Death is caused by asphyxia or muscular paralysis

  • Diagnosis : Based on history of ingestion and development of muscular stiffness

    Strychnine (and brucine) can be measured chemically but there is no time to perform this procedure before treatment

    Measure acidosis, serum potassium, SGOT, LDH, CPK etc

    Treatment of poisonings : Activated charcoal Support respiratory and cardiovascular functions If convulsions cannot be controlled with diazepam (IV or rectal), or if they recur, administer phenobarbitone or phenytoin. Intubation with suxamethonium chloride may be necessary When convulsions and hyperactivity are completely controlled, gastric lavage can be performed safely

    References : http://www.inchem.org/documents/pims/plant [accessed 29 June 2008]; Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science Foundation, 2006; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • LeafFlowerFruitBarkSeed

  • Scientific name: Gloriosa superba

    Synonyms: G.simplex, Methonica doniana, Eugonia superba

    Family: Colchicaceae, Liliaceae

    Sinhala name: Niyangala

    Tamil: Karththigaikkilangu, Illangalli

    English/common names:flame lily, glory lily, tiger claw

    Plant habitat:native of tropical Africa, India, Malaya, etcfound in low country Sri Lanka

    Traditional use:tuber bruises and sprains

    Poisonous parts of the plant:The entire plant, especially the tubers, are extremely poisonous

  • Main toxic constituents: colchicine (+ gloriosine in tubers)

    Constituent type: alkaloid

    Mode of action:Colchicine has an antimitotic effectIt stops cell division by disrupting the spindle apparatus during the metaphaseCells with rapid turnover are affected (bone marrow, intestinal epithelium, hair-producing cells -> hair loss)It can alter neuromuscular function(It can withstand drying, storage and boiling - tubers not a foodsource!)

    Clinical features of poisoning:Initial symptoms develop within 6-12 hours of ingestionburning pain, numbness, itching and tingling around the mouth and throat with thirstnausea, intense vomitingabdominal pain, severe diarrhoea with blood and mucusThese lead toelectrolyte imbalance, dehydration, hypovolaemic shock manifested hypotension and tachycardia

  • After 24 hours patients developMuscle weakness, myoglobinuria, bronchial constriction, leucopenia, thrombocytopenia, clotting defects with bleeding, polyneuropathy cardiac arrhythmias, hepatic insufficiency, acute renal failureIn severe cases there may beRespiratory depression, confusion, delirium, convulsions, comaDeath occurs due to shock or respiratory failure

    Diagnosis:Toxicological, biomedical, blood gas, haematological analyses

    Treatment of poisoning:hospitalize the patient immediately induce vomiting (ipecac) / gastric lavagegive repeated activated charcoalsupportive care eg IV fluid, assisted ventilation may be needed

    References: Jayaweera DMA. Medicinal plant use in Ceylon - Part 3. Colombo: The National Science Foundation, 2006; http://www.inchem.org/documents/pims/plant (Accessed 4 July 2008]; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Poisonus plants of Sri lanka Ricinus communis


  • Scientific name: Ricinus communis Linn. Synonyms: Ricinus africanus Willd., Ricinus communis L. var. viridis (Willd.) Mll. Arg., Ricinus inermis Jacq., Ricinus lividus Jacq., Ricinus macrocarpus G. Popova, Ricinus microcarpus G. Popova, Ricinus persicus G. Popova, Ricinus speciosus Burm.,Ricinus viridis Willd., Ricinus vulgaris Mill., Ricinus zanzibaricus G. Popova, Croton spinosus

    Family: Euphorbiaceae (spurge family)

    Sinhala name/s: Erandu, Tel-erandu, beheth endaru, thel endaru

    Tamil name/s: Amanakku, Muttu-kottai, Andagam

    English/common name/s: castor bean, castor-oilplant, Palma Christii

    Plant habitat:Cultivated as a decorative plant in village gardens in Sri lankaProbably of African origin but now grows in tropical, subtropical and temperate areas Commercially cultivated mainly in Brazil, India, Italy, etc.

    Traditional use:In Sri lanka the root of the plant is used in pleurodynia (muscular rheumatism) and rheumatic pains while seeds are used for lumbago and sciaticaAfricans use the bark for stitching up wounds & as a dressing for soresLocal application of fresh leaves to the lactating breast is said to produce a powerful galactogogic action. They are also used headachesThe root is a remedy for abdominal pains and diarrhoea while root bark (and seed oil) is a purgative also used for skin diseases and sores

  • Toxic part of the plant: seeds are the most toxic part (leaves are also poisonous)

    Lethal dose: 1mg/kg pure ricin in manIngestion of a single well chewed bean has caused death1-3 seeds can be fatal to a child2-4 seeds cause severe poisoning in an adultpoisoning is unlikely if seeds are swallowed without chewing

    Main toxic constituent/s: Ricin

    Constituent type: Glycoprotein or a toxalbuminmember of a class of plant toxins known as type 2 ribosome inactivating proteins

    Mode of action: Ricin impairs chain elongation in protein synthesis, causing cell death and tissue damage

    Clinical features of poisoning: Early on - burning sensation of the mouth and throat occursAfter 3-6 hrs - nausea, vomiting, severe abdominal pain and diarrhoea resulting in dehydration electrolyte imbalance and shockCardiovascular - hypotention, tachycardia, ECG changes and circulatory failureOther - prostration, blurring of vision, loss of consciousness, convulsions, haemolysis, uraemia and liver necrosis

  • Diagnosis: Blood gases and electrolytes analysisClose monitoring of renal, hepatic hematological systems & blood clotting.Botanical & pharmacognostical identification of a sample of the plant or vomitusRadioimmunoassay with antiricin antibodies labeled with iodine 125 for ricin in plasma or urine

    Treatment of poisoning: Induce emesis at home (ipecac)Immediate gastric lavage or activated charcoalCorrect fluid & electrolyte imbalance immediatelyIn case of bronchial asthma, oxygen, B2-agonist eg salbutamol and corticosteroids may be necessary (if acute poisoning occurred by inhalation) Antihistamines or corticosteroids may be beneficial in treating skin lesions (if acute poisoning occurred by skin exposure)References:Jayaweera DMA. Medicinal plants used in Ceylon. Part 2. Colombo: The National Science Foundation, 2006 http://www.inchem.org/documents/pims/plant.htmwww.wikipedia.orgLucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Scientific name: Manihot utilissimaSynonyms: Jatropha manihot (Kunth), Manihot manihot (Cockerell), Manihot melanobasis (Muell)Family: Euphhorbiaceae Sinhala name: "Manyokka" Tamil names: Maravalli AlavalliEnglish /common name: cassava, manioc, tapioca

    Plant description: shrub with a big tuberous root Plant habitat: The sweet and bitter cassava plants are indigenous to Southern and Central America but have been introduced to almost all tropical countriesTraditional use : Used as a food source. American Indians use the brown juice for burnsBy : J.S.R.Sherif E.M.A.K.Ekanayaka

    Manihot utilissima

  • Toxicity of the plant : The leaves and roots contain free and bound forms of the cyanogenic glycoside linamarin, which is converted to cyanide in the presence of linamarinase, a naturally occurring enzyme in cassava or via exposure to the atmosphere. (Slide 5)Two varieties Sweet - contains as little as 20 milligrams of cyanide (CN) per kilogram of fresh rootsBitter - may produce more than 50 times as much (1 g/kg)The paralytic neurological disease caused by long-term consumption of cassava is called mantakassa. Yam that is cut, washed and boiled in an open container at 72C for long enough will destroy the enzyme and any hydrocyanic acid formed will evaporate. Lethal dose : One dose of pure cassava cyanogenic glucoside (40mg) is sufficient to kill even a cow. Hence about 300 grams of fresh root is enough to kill an adult human and about 125 grams of fresh root would be enough to kill a child

    Mode of action :A "large" sudden dose (HCN) is highly poisonous to all humans and animals because it rapidly inactivates cellular respiration thereby causing death. This means that it stops cells from being able to use oxygen. The heart, respiratory system and central nervous system are most susceptible to cyanide poisoning and cease to function as a result of lack of oxygen.

  • Clinical features of poisoning :Acute: Within 3-6 hours of ingestion burning epigastric pain, vomiting, flushing of skin, dry mouth, tachycardia, pupil constriction, restlessness, giddiness and hallucinations occur.Chronic: initial symptoms are described as tremor, cramps, a heavy feeling and/or weakness in the legs, a tendency to fall down and difficulty remaining uprightThere is a visible hypertonic gait when walking or runningOccasionally there will be lower back pain, blurred vision, speech difficulties and/or paresthesia of the legs, but they disappear within a month, later some people will develop dysarthria, abnormalities of eye movement, hypertonicity of the arms

    DiagnosisAcute poisoning: signs of extreme metabolic acidosisChronic poisoning: a visible hypertonic gait when walking or running, bilateral brisk knee and Achilles tendon reflexes without signs of vertebral lesions The onset of the disease takes less than one week and then remains stableUrinary concentrations of (thiocyanate and linamarin are elevated) (Cyanide (CN-) is normally converted thiocyanate (SCN-) by the enzyme rhodanase)

    Treatment of poisoning There is no known treatment for cyanide poisoning . Treatment with sodium thiosulphate (Na2S2O3), a cyanide antidote, gave disappointing results. A good and varied diet, high dose multivitamins (specially B12 ,it detoxifies the HCN) and physical rehabilitation are advised.

    References Affran DK. Cassava and its economic importance. Ghana Farmer 1968; 12(4): 172-178; Bellotti AC et al. Recent advances in cassava pest management. Ann Rev Entomol 1999; 44: 343-370; Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Presented by: M.M.JAYARATHNA H.V.N.LAKMALIBotanical Name:Peganum harmala FamilyName:ZygophyllaceaeLocal Name: Ispandur Urdu Name: HarmalSinhala name: Rata aruda English name: Wild Rue Tamil name: SimaiyarawandiPart used: Whole plant Flowering: May - June

  • Plant habitatUS states ofArizona,California Montana, Texas - grows in salt deserts and shrub lands. Grows in India, Persia,Mediterranean region, Central Asia, Arabia, North Africa

  • Multibranched, leafy, perennial,bright green, succulent herb.Leaves divided, seed angled,Flowers white, single.Constituent type: alkaloidsHarmalineHarmine HarmalolTetrahydroharmine VasicineMode of action:Harmaline is a reversible monoamine oxidase inhibitor found especially in higher quatities in ripe seedsThe plant also has antibacterial, antioxidant, anti-inflammatory and antitumour activity

  • CLINICAL FEATURESOverdose is potentially comprised of hallucinations and neurosensorial syndromes, bradycardia, low blood pressure, raised body temperature and gastrointestinal disturbances such as nausea and vomitingDIAGNOSIS ONPhysical examination

    TREATMENTSSupportive therapyIV fluidsAntacids (or H2 antagonists)

    References: IPCS Inchem.Peganum harmala [Accessed at http://www.inchem.org/documents/pims/plant 04 July 2008 ]Massoud M et al. Toxicity of Peganum harmala: Review and a Case Report. Iranian Journal of Pharmacology & Therapeutics 2002: 1(1); 1-4

  • Adenia palmataSynonyms: Adenia hondala, Granadilla hondala, Modecca palmata

    Family: Passifloraceae

    Sinhala name/s: hondala

    Tamil name/s: kondala

    English/common name/s: ?

    Plant habitat:large aerial plant climbing by tendrils attached to large trees growing in the wet and dry zones along forest edges

    Traditional use: ?

    Toxic part of the plant: fruit (which closely resembles passion fruit -> accidental ingestion by children)

    Lethal dose: ?

    Main toxic constituent/s: a cyanogenic glycoside, a toxalbumin and emulsin (an enzyme)

    Constituent type: cyanogenic glycoside

  • Mode of action:1st phase hydrocyanic acid2nd phase local toxalbumin effects3rd phase - hypersensitivity reaction

    Clinical features of poisoning:1st phase vomiting, fever, restlessness, dizziness, disorientation, abdominal pain and diarrhoea within one hour2nd phase necrotising enteritis -> diarrhoea with blood and mucus, abdominal colic and right iliac fossa tenderness after a variable period of time3rd phase myocarditis with ECG changes, tender hepatomegaly, retinopathy with papilloedema, exudates and haemorrhages may be seen 2-3 weeks after ingestion all transient

    Diagnosis:cardiac glycoside blood levels seed remnants, vomitus, gastric aspirate may help identifymonitor serum potassium and electrolytes

    Treatment of poisoning:if no vomiting occurs induce emesis with ipecac syrup or perform gastric lavageactivated charcoal will help with the absorption of toxic substancesIV fluid therapy may be neededantidotes for cyanide poisoning not usually necessaryblood transfusion may be necessary in the 2nd phaseReference: Lucas GN, De Silva TUN. Poisonous plants of Sri Lanka. Colombo: Sri Lankan College of Paediatricians, 2006

  • Datura metelatropine, hyoscine, hyoscyaminealkaloidsseed (all)Gloriosa superbacolchicinetuberNicotiana tabacumnicotineleaf (all)Pagiantha dichotoma? narcotic, datura-likeseed(Peganum harmala)harmalineseedStrychnos nux vomicastrychnineseedAlocasia macrorrhizacalcium oxalate crystals (needle-like), toxic proteinsleaf/stem (all)Anthurium sp.Dieffenbachia sp.Scindapsus aureusZantedeschia aethiopicaCerbera manghascerberine, odollum,thevetincardiac glycosidesfruit kernelThevetia peruvianathevetin A, theventin BfruitAdenia palmatacyanogenic glycoside, toxalbumin, emulsin enzymecyanogenic glycosidesfruitManihot utilissimalinamarin, (linase enzyme)tuberAbrus precatoriusabrintoxalbuminsseedJatropha curcascurcinseed (all)Jatropha multifidaJatrophinRicinus communisricinEucalyptus robustaoil of eucalyptus (eugenol)volatile oilsallMyristica fragransmyristicinseed (aril)Amanita phalloidesphalloidin, phalloin, phallolysinalpha, beta, gamma amanitinphlallatoxins amatoxins aerial parts (mushroom)


    Digoxin inhibits Na+/K+ ATPase (exchange pump)Increased intracellular [Na+], and increased extracellular [K+]Leads to decreased Na+/Ca++ exchangeWhich leads to increased intracellular [Ca++]Leading to increased contractility

    ToxicologicExcessive intracellular [Ca++]Less negative membrane potential (closer to threshold = depolarization)Increased automaticityTachydysrhythmias*Therapeutic:

    Digoxin inhibits Na+/K+ ATPase (exchange pump)Increased intracellular [Na+], and increased extracellular [K+]Leads to decreased Na+/Ca++ exchangeWhich leads to increased intracellular [Ca++]Leading to increased contractility

    ToxicologicExcessive intracellular [Ca++]Less negative membrane potential (closer to threshold = depolarization)Increased automaticityTachydysrhythmias*Therapeutic:

    Digoxin inhibits Na+/K+ ATPase (exchange pump)Increased intracellular [Na+], and increased extracellular [K+]Leads to decreased Na+/Ca++ exchangeWhich leads to increased intracellular [Ca++]Leading to increased contractility

    ToxicologicExcessive intracellular [Ca++]Less negative membrane potential (closer to threshold = depolarization)Increased automaticityTachydysrhythmias*


View more >