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PLANT POISONING

PLANT POISONING. Dr. Hisham Zein Alabdin. POISONOUS PLANTS. The active principles in most of these plants are alkaloids but glycosides ( digitales ) and resinous materials, as cannabis also exist.

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PLANT POISONING

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  1. PLANT POISONING Dr. Hisham Zein Alabdin

  2. POISONOUS PLANTS • The active principles in most of these plants are alkaloids but glycosides (digitales) and resinous materials, as cannabis also exist. • The plant poisons have mainly remote action after their absorption. The route of poisoning is usually the oral one, so gastric lavage is indicated . each plant poison has its specific physiological antidote.

  3. Atropine poisoning Atropa belladonnas. Daturafastiosa, Daturastrammonium ( thorn apple), • Plant contains ; atropine, hyoscine and hyoscayamine. All parts of the plant contain the active substance. • Atropine has 2 actions: 1. central action causes stimulation of the CNS . In large toxic doses it causes depression. 2. peripheral action anticholenergic: atropine blocks nicotinic and muscarinic effects of acetycholine.

  4. Uses A- Therapeutic: • Pre- anesthetic. • Antispasmodics. • In the treatment of peptic ulcer. • Ophthalmic use. • Nocturnal enuresis • Toxicological use: as antidote in phosphate esters, digitalis, aconite poison. B- Non therapeutic: by addicts.

  5. Toxicokinetics • Absorption : slowly absorbed from the gut. • Metabolism: is in the liver and muscle to tropine tropic acid. • Excretion: is via the kidney in the urine, partly unchanged and partly metabolized.

  6. Pathophysiology A-Central action: stimulation followed by depression of CNS. Except hyoscine has depressant action only. B- Peripheral action: By blocking the muscarinic action of acetylcholine at the post ganglionic nerves whether parasympathetic or sympathetic (sweat glands)

  7. Clinical picture 1- Central effects: A- Stimulation phase: 1-Delirium ,disorientation, confusion, loss of short term memory, talkativeness(acute toxic psychosis). 2-Ataxia, in-coordination, hallucination(Lilliputian type) 3-Occupational purposeless movements (picking or grasping) 4- Tremors and convulsions.

  8. B- Depressant phase: it follows pre-existing stimulation phase . Patient is calm and falls into sleep then into stupor and coma. The respiration becomes slow and irregular. The end result will be central asphyxia and death.

  9. II- Peripheral effects: 1- Vital signs: • Increased respiration. • Increased blood pressure. • Increased temperature up to atropine fever resulting from anhydrosis. • Rapid pulse and may be cardiac arrhythmia.

  10. 2- Diminished secretion: • saliva dryness of the mouth with dysarthria and dysphagia. • Sweat dry skin • GIT constipation (decreased secretion and motility) • Urinary oliguria and retention of urine

  11. 3- Blood vessels: Peripheral vasodilatation to increase heat loss , leading to atropine flush which may be misdiagnosed as scarlet fever. 4-Eye changes: • Dilation and fixed pupils blurred vision. • Loss of accommodation due to cycloplegia (ciliary muscle paralysis) • Diplopia and photophobia • Loss of light reflex.

  12. The eye symptoms may be the earliest ones, thus the anticholinergic syndrome of parasympathetic paralysis can be remembered • Blind as a Bat. • Red as a Beet. • Dry as a Bone. • Hot as a Hare. • Mad as a Hen.

  13. Treatment • Support respiration. • Control convulsion if present by diazepam. • Stop further absorption by inducing emesis or by gastric lavage. • The physiological antidotes ( physostigmine, pilocarpine.). • Treat hyperthermia by ice packs • IV fluids to maintain urine output

  14. DIGITALIS (FOX GLOVE) Uses: • As cardiac tonic for cases of congestive heart failure. • As diuretic. • As an anti-arrhythmic especially in atrial flutter and. fibrillation as well as in paroxysmal tachycardia

  15. Toxicokinetics • Digitalis preparations are rapidly absorbed from the GIT and injection sites . Metabolism takes place in the liver . Excretion is via the renal route mainly, a small part in the bile ( enterohepatic circulation).

  16. Pathophysiology Digitalis toxicity is an exacerbation of the drug Pharmacological actions: • Positive inotropic action: it increases the force and velocity of myocardial contraction by increasing intracellular Ca++ . This increase in the excitability and contractility of the atria and ventricles may result in extrasystoles and tachyarrhythmias.

  17. Negative chronotropic action: (rate) It increases the vagal tone in the early stage leading to decreased heart rate. • Negative dromotropic action: (conduction velocity) It slows AV node conduction velocity that can be depressed resulting in Saor AV block. • It increases the refractory periods of AV node and depresses that of the atria and ventricles, resulting in prolonged PR interval , AV block and shortened QT interval. • Alteration of impulse formation with suppressant and excitatory effects.

  18. Mechanism of action: • Digitalis inhibit active transport of Na+ ,K+ across cell membranes by binding to the Na+ - K+ ATP ase , and inhibiting Na+ - K+ pumps . • The net result • Increase extracellular potassium • Increase intracellular sodium. • Increase intracellular calcium

  19. Predisposing factors • Patient factor: (old age, myocardial infarction, core pulmonale, renal failure.) • Electrolyte abnormalities: ( hypo and hyperkalemia, hypomagnesemia, hyper and hypocalcemia.) • Drug interaction: (diuretics, antibiotics, quinidine , reserpine.)

  20. Clinical picture • Asymptomatic period of several minutes to several hours follows a single oral toxic dose. The toxic effects include non cardiac and cardiac effects A- Non cardiac : • GIT: may be the first complaints. (nausea, vomiting, abduminal pain and diarrhea) • CNS: headache, trigeminal neuralgia, confusion, delirium, disorientation, drowsiness and hallucination.

  21. Visual transient amblyopia, diplopia, blurring, scotoma and abnormal colour vision including yellow halos (xanthopsia). • Endocrine : Gynecomastia. • Allergic : Urticaria.

  22. B- Cardiac: Early slow full pulse (vagus) , with hypotension, followed by any type of dysrhythmia (altration in cardiac rate and rhythm): • AV block. • Atrial tachycardia with AV block. • Sino-atrial block. • Atrial flutter, fibrillation. • Ventricular premature extrasystoles , flutter.

  23. Digoxin toxicity

  24. MANAGEMENT Investigations: 1-ECG: • Prolonged PR interval • Shortened QT interval • ST segment depression, inverted T wave. 2-Laboratory : • Electrolytes (K+ ) • Serum digoxin: toxic level is above 2ng/ml and is above 25ng/ml for digitoxin.

  25. Treatment • Stop drug administration. • monitor the patient in an ICU. • Establishment of respiration. • Dicontamination. • Atropine sulphate 1-2mg IM for bradycardia. • Phenytoin or diphenylhydantoin is the drug of choice for tachyarrhythmia. • Cholestyramine help excretion of digitalis

  26. Determine electrolytes hourly and correct electrolytes and acid base disturbances. • For hypokalaemia: potassium chloride5g in fruit juice every hour until ECG show improvement or peaking of T wave. • For hyperkalaemia : give 20 units of insulin with 5% Dextrose. • For hypocalcemia: avoid replacement because intracellular calcium is very high.

  27. Antidotal therapy: Digoxin specific antibody (Digibind).They bind to the free digoxin and increase the renal excretion of digoxin bound to FAB fragment. • Indications for (DIGIBIND ) • Hyperkalaemia (k + > 5 mEq/L). • Bradyarrhythmias unresponsive to atropine. • High degree AV block. • Life threatenting ventricular tachycardia and ventricular fibrillation.

  28. THANK YOU

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