1. Toxic Plants
Plants containing Cardiac glycosides

2. Cardiac Glycosides
Cardiac glycosides are divided into two main types: * Bufadienolides are C24 steroids,
The primary cardiac glycoside present in Helleborus is the bufadienole, hellebrin.
Hellebrigenin, the aglycone of hellebrin is more potent than the glycoside itself.

4. Cardenolides have a hormonal nature as substances
Cardenolides have a hormonal nature as substances. Their effects are on the heart and kidney.
Strong, bitter and disagreeable taste.
Cardiotonic = affect contractions of the heart muscle.
Break down in fermentation by enzymatic action.
Treatment: atropine and activated charcoal, lidocaine for H. viridis
Assumed mechanism of action: inhibition of the Na+, K+-ATPase resulting in increased intracellular sodium and subsequent intracellular calcium leading to enhanced muscle contraction in cardiac tissue.

5. Cardenolides are classified according to the chemical composition of their aglycones as lanataglucosides A, B, C, D and E. OnlyDigitalis lanata, the woolly foxglove contains all five forms.e. The entire foxglove plant is toxic. Symptoms of poisoning include dizziness, vomiting, irregular heart beat, and delerium or halucinations.

6. Digitalis
Digitoxin, a glycoside which stimulates the heart. A carefully prescribed dose often has miraculous effects on people with heart conditions, but an overdoes may be FATAL

7. Digitalis lanata

8. POISON LOCATION:
Sap, flowers, seeds, and leaves of Foxgloves, but the greatest concentration of the toxin occurs in the leaves, even dried ones.

9. TYPICAL POISONING SCENARIO:
Accidental consumption of leaves or flowers by livestock, or children who are attracted by the showy flowers, or the nectar, both of which contain the glycoside poison. The sugar in the glycoside breaks down during digestion, releasing the active chemical. Adults are occasionally poisoned by the misuse of herbal preparations- tea from dried Foxglove leaves is traditionally a diuretic- or by overdoses of prescribed digitalis . Like any other medicine, digitalis must be kept out of the hands of children.

10. Another possible cause of poisoning is misidentification
Another possible cause of poisoning is misidentification. The leaves of Foxgloves are easily mistaken for those of Comfrey, which are traditionally brewed for tea; both share the same general form and a coasely hairy surface. Additional confusion occurs because, in its first year, Foxgloves produce only leaves, no flowers. Foxglove leaves, however, have finely toothed edges, whereas Comfrey leaves are smooth. Digitoxin is dangerous, so Foxgloves must be treated with caution .

11. Nerium oleander Common name: دفلة Scientific name: Nerium oleander L.
Family: Apocynaceae

13. Toxic ingredient:
It contains cardiac glycosides (oleandrin, neriin, folinerin, digitoxigenin, rosagenin, nerigoside), oleandrin is one of the major glycosides present in the plant.

14. Toxic parts:
All parts of the plant, including the leaves, flowers, sweet nectar and twigs are poisonous
The highest percentages of cardiac glycosides are found in the seeds, stems and roots followed by the fruit and leaves which contain the greatest oleandrin concentrations.
The nectar makes a toxic honey.
The bark contains rosagenin which has strychninelike actions.
Four CNS depressant cardenolides including a new cardenolide, neridiginoside and three known constituents, nerizoside, neritaloside and odoroside-H, have been isolated from the leaves which exhibited CNS depressant activity in mice at a dose of 25 mg/kg.

15. Toxic dosage:
Fatal oleander poisonings have been reported in humans 4,8, but the human mortality associated with oleander ingestion is generally very low, even in cases of intentional consumption (suicide attempts) 9.
A child who ingested three leaves developed a partial right bundle branch block but was able to leave the hospital after 24 hours.
Seeds: the absorption of 10 has led to serious symptoms 2.

16. Exposure:
Modes of exposure to the plant include accidental ingestions by children, as well as intentional administration in foods, drinks or medicinal preparations from its leaves which have been used as treatments for malaria, leprosy, venereal diseases, and to induce abortions Oleander has also been used in suicide attempts 4,9, in criminal poisonings and in rat poison.

17. Children have been poisoned by chewing leaves and sucking the nectar from flowers.
Adults have been poisoned after eating meat roasted on oleander stems used as skewers 5, consumption of stagnant water contaminated by leaves or flowers, or inhalation of smoke from burning wood and leaves 2.

18. Manifestations:
Symptoms of oleander intoxication are very similar to those of digoxin, in that nausea and vomiting are followed by potentially lethal cardiotoxicity 4.
Nausea and vomiting usually occur within several hours .
Serious toxicity results from cardiotoxicity and specifically from cardiovascular collapse and ventricular ectopy.
Conduction delays may persist 3-6 days, displaying classical digitalis toxicity as characterized by increased ectopy and conduction delay (e.g. supraventricular tachycardia with atrioventricular block) 9
Bradycardia may be as down as beats/min, the pulse is weak and irregular.

19. Other toxic effects of the oleander include burning of the mucous membranes of the eyes, mouth and gastrointestinal tract 4, bloody diarrhea 4,5, xanthopsia (yellow vision) 2,4, convulsions, respiratory paralysis and loss of consciousness 4,5 .
Clinical tests reveal a more or less pronounced hyperkalemia.

20. Treatment:
Supportive, gastric lavage (but should be avoided after the onset of cardiac symptoms).
Fluid administration, atropine (which in young victims, or when small quantities ingested) is sufficient to prevent bradycardia and allows the cardiac rhythm to return to normal within a few hours.
Isoproterenol, antiarrhythmics and early administration of activated charcoal may be useful, sometimes in combination with sorbitol.

21. Mechanism of action -
Inhibition of Na,K-ATPase activity by the cardiac glycosides.
Cardiac glycosides interfere with transport of Na+ and Ca+2 out of the cell. They bind with high affinity to an inhibitory site on the portion of Na, K-ATPase structure that faces the outside of the cell. Consequently, sodium and potassium transport is blocked.

22. Squill: Common name: عيصلان , بوصلان, بصول, عود الري
Scientific name: Urginea maritima (L.) Baker Syn. Drimia maritima (L.) Stearn Syn. Scilla maritima (L.)
Family: Liliaceae 1

24. Squill Bulb

25. Toxic ingredients:
The principal compounds are glycosides of scillarenin (scillaren A, glucoscillaren A and proscillaridin A) and of scilliphaeosidin (glucoscilliphaeoside), scilliphaeoside and epi-scilliphaeoside together with scillicyanoside 2 .
Toxic parts:
The bulb, but possibly the whole plant contains several cardioactive glycosides 3.
Manifestations:
Squills are rarely implicated in poisoning, yet, fatal cases were reported due to the consumption of the bulbs of the plant

26. The toxic effects of squill are similar to those of digitalis glycosides.
Vital signs
- Bradycardia or tachycardia may be seen; either could lead to secondary hypotension.
- In absence of concomitant ingestion, environmental exposure, thyroid disorder, or underlying infection, patient generally is normothermic.
- Lungs: Examination findings typically are normal in the absence of preexisting disease, but rales have been reported.

27. - Heart
Bradydysrhythmias or tachydysrhythmias can occur, typically with increased automaticity and depressed conduction.
Hypotension and shock may ensue.
Pulses may be weak, thready, and irregular.
Abdomen
Abdomen is generally soft.
Vomiting and diarrhea may be noted.
Emesis may contain plant material.

28. Neurologic
Findings may include an altered level of consciousness, hypotonia, hyporeflexia, dysarthria, ataxia, horizontal nystagmus, and generalized seizures.
The patient typically is nonfocal with pupillary reflexes intact.
Skin: Skin may be pale, diaphoretic, and cool.

29. Other Plants
Strophanthus
Veratrum virid
Lilly of the Valley