1.

DIGITALIS GLYCOSIDES
BACKGROUND OF ORIGIN: Cardiac glycosides are found in certain flowering plants, such as
oleander and lily-of-the-valley. Indigenous people in various parts of the world have used many
plant extracts containing cardiac glycosides as arrow and ordeal poisons. The ancient Egyptians
used squill (Urginea maritime) as a medicine. The Romans employed it as a diuretic, heart tonic,
emetic, and rat poison. Digitalis, or foxglove, was mentioned in the year 1250 in the writings of
Welsh physicians. Fuchsius described it botanically 300 years later and named it Digitalis
purpurea.William Withering published his classic account of foxglove and some of its medical
uses in 1785, remarking upon his experience with digitalis. He recognized many of the signs of
digitalis toxicity, noting, "The foxglove, when given in very large and quickly repeated doses,
occasions sickness, vomiting, purging, giddiness, confused vision, objects appearing green or
yellow; increased secretion of urine, slow pulses, even as low as 35 in a minute, cold sweats,
convulsions, syncope, death."
MEDICINAL USES: Digitalis is a plant-derived cardiac glycoside commonly used in the treatment
of chronic heart failure (CHF), atrial fibrillation, and reentrant supraventricular tachycardia.
MECHANISM OF TOXICITY: Digoxin blocks the sodium/potassium ATPase pump. The
mechanism by which this decreases AV conduction is not clear but is perhaps due to increased
vagal tone. Intracellular calcium within the cardiac myocytes is increased by digoxin, resulting in
increased inotropy, or contractility. Digoxin toxicity causes hyperkalemia, or high potassium.
The sodium/potassium ATPase pump normally causes sodium to leave cells and potassium to
enter cells. Blocking this mechanism results in higher serum potassium levels. In states of
hypokalemia, or low potassium, digoxin toxicity is worsened because digoxin normally binds to
the ATPase pump on the same site as potassium. When potassium levels are low, digoxin can
more easily bind to the ATPase pump, exerting the inhibitory effects.
CLINICAL PRESENTATION: Visual aberration often is an early indication of digitalis toxicity.
Yellow-green distortion is most common, but red, brown, blue, and white distortions also
occur. Drug intoxication also may cause the following: Snowy vision, Photophobia, Photopsia,
Decreased visual acuity, Yellow halos around lights (xanthopsia), Transient amblyopia or
scotomata.Central nervous system (CNS) symptoms of digitalis toxicity include the following:
Drowsiness, Lethargy, Fatigue, Neuralgia, Headache, Dizziness, Confusion or giddiness.
DIAGNOSIS: Serum digoxin level, Electrolytes, Electrocardiography
ANTIDOTE: Digoxin immune Fab

2. ATROPINE
BACKGROUND OF ORIGIN: Deadly Nightshade is a part of the Solanacae family of flowering
plants which includes tomatoes, potatoes, eggplants and more, and can be found growing
throughout most of the northern hemisphere. To the untrained eye, this perennial looks
perfectly normal, but don’t be deceived, this is far from your average shrub. The beauty tonic
was also used to dilate women’s pupils, a look and practice that was fashionable at the time.
It’s from this popularity as a cosmetic that the Deadly Nightshade established its formal name,
Atropa Belladonna, meaning “Beautiful Lady” in Italian.
MEDICINAL USES: drug of choice for treatment of organophosphate nerve agent & insecticide
intoxication Adjuvants, Anesthesia; Anti-Arrhythmia Agents; Antidotes; Bronchodilator Agents;
Muscarinic Antagonists; Mydriatics; Parasympatholytics
MECHANISM OF TOXICITY: Competitive antagonist of M1 and M2 muscarinic cholinergic
receptor. Toxic effects from antagonism of the nicotinic cholinergic system is not a component
of the syndrome. s an extension of the pharmacologic effects, which is due to extensive
antagonism of the central and peripheral muscarinic acetylcholine receptors.
CLINICAL PRESENTATION:
MILD SYMPTOMS of nerve agent or insecticide exposure include the following:
-Blurred vision, miosis
-Excessive unexplained teary eyes
-Excessive unexplained runny nose
-Increased salivation such as sudden unexplained excessive drooling
-Chest tightness or difficulty breathing
-Tremors throughout the body or muscular twitching
-Nausea and/or vomiting
SEVERE SYMPTOMS of exposure to nerve agent or insecticides include the following:
-Strange or confused behavior
-Severe difficulty breathing or severe secretions from your lungs/airway
-Severe muscular twitching and general weakness
-Involuntary urination and defecation (feces)
-Convulsions
-Unconsciousness
DIAGNOSIS: No specific diagnostic studies exist for anticholinergic overdoses. Laboratory
studies that may be helpful include the following:
Acetaminophen and salicylate screening - in all intentional poisonings
Blood and urine cultures – in febrile patients
Serum chemistry and electrolyte analysis
Electrolyte and arterial blood gas (ABG) analysis
Urine pregnancy test - in all women of childbearing age
ANTIDOTE:Physostigmine

3. QUININE
BACKGROUND OF ORIGIN: For centuries, the plant was used by Peruvians, including the Incas,
to treat malaria, digestive problems, and fevers. It is also known to stimulate salivary secretions
and digestive juices.It was the Incas who taught the Spanish how to cure fevers with the bark.
In 1640, the wife of the Viceroy of Peru, the Condesa de Chincón, sent word back to Spain
extolling the wondrous powers of the bark. The remedy soon became known as "chincona" in
her honour. Later, when the Jesuits brought large quantities of the powdered bark back to
Europe, it was sold as "polvos de la condessa", the countess's powders.
MEDICINAL USES: on-narcotic analgesics; antimalarial; central muscle relaxants. It is also used
as flavor in carbonated beverages.
MECHANISM OF TOXICITY: Inhibition of the sodium channels may result in widening of the QRS
complex, and inhibition of the potassium channels may predispose patients to torsade de
pointes. Alpha-adrenergic blockade may cause hypotension. Because of its oxytocic effects, it
may act as an abortifacient. Quinine is directly toxic to the retina and causes inhibition of
hearing by various mechanisms. It also inhibits ATP-sensitive potassium channels in pancreatic
beta cells causing insulin release similar to sulfonylureas, resulting in hyperinsulinemia and
hypoglycemia. However, this is usually limited to high dose intravenous treatment.
CLINICAL PRESENTATION: MILD TO MODERATE TOXICITY: In mild overdose, patients present
with skin flushing, gastrointestinal upset (nausea and vomiting is common), and cinchonism
(tinnitus, deafness, vertigo, headache, and visualdisturbances)
SEVERE TOXICITY: Patients can develop ataxia, CNS depression, coma, seizures, respiratory
arrest, hypotension, PR prolongation, QRS widening, QT prolongation, ST depression, AV blocks,
and various ventricular dysrhythmias. CNS toxicity seems to be more marked in children than
adults; children frequently present with seizures following an overdose. Cardiac toxicity
resembles toxicity secondary to quinidine.Retinal toxicity may also result approximately 9 to 10
hours postingestion. Patients complain of blurred vision, tunnel vision, visual field constriction
diplopia, alteration in color perception, photophobia, scotomata, and frank blindness.
Respiratory depression may occur. Visual complaints usually resolve without treatment.
DIAGNOSIS:
A)Specific laboratory studies for confirming quinine
ingestion are not readily available in most clinical
laboratories, and are not generally useful for guiding
therapy.
B) Monitor serum electrolytes, BUN, creatinine, glucose,
CBC, CPK, urinalysis, and ECG.
C) In the acutely ill patient, blood gas analysis may
demonstrate metabolic acidosis. Lactate is also usually
elevated.
ANTIDOTE:No specific antidote, Supportive care and Activated charcoal

4. NICOTINE
BACKGROUND OF ORIGIN: Nicotine was isolated from tobacco leaves (Nicotiana tabacum)
in 1828, but the powerful effects of nicotine were already well recognized. The tobacco plant is
native to the Americas and its use as a medicine and stimulant goes back at least 2000 years
and most likely many millennia before that. South American temple carvings show Mayan
priests enjoying the benefits of this drug from smoking tobacco through a pipe. Tobacco
appears to part of the healing arts and sacred rituals of many of the native peoples of the
Americas. (Image:Aztec women are handed flowers and smoking tubes before eating at a
banquet, Florentine Codex, 16th century.)
MEDICINAL USES:Smoking cessation
MECHANISM OF TOXICITY: Toxic effects are dose-related and result from overstimulation of
nicotinic receptors, often causing inhibition of receptor action following initial stimulatory
effects.
CLINICAL PRESENTATION: MILD TO MODERATE TOXICITY: GI upset, nausea, vomiting, dizziness,
headache, tremor, diaphoresis, tachycardia, pallor, and hypertension are common events.
SEVERE TOXICITY: Seizures, confusion, weakness, bradycardia, hypotension, and respiratory
muscle paralysis can develop.
DIAGNOSIS:
A) No testing is required in patients with mild or no
symptoms.
B) Serum chemistries, creatine kinase, lactate, urinalysis
should be performed in patients with severe poisonings.
C) Obtain an ECG and institute continuous cardiac monitoring
in all symptomatic patients.
ANTIDOTE: No specific antidote, Supportive care and Activated charcoal
5. RICIN
BACKGROUND OF ORIGIN: The castorbean plant (Ricinus communis) has been cultivated for
centuries for the oil produced by its seeds. The Egyptians burned castor oil in their lamps more
than 4,000 years ago.Thought to be native to tropical Africa, the plant is a member of the
spurge family. The seeds with hulls removed contain 35 to 55% oil. The seeds, leaves, and stems
of the plant contain ricin and ricinine, which are poisonous to humans and animals. Eating a
castorbean causes nausea and eating several may cause death. These toxic compounds are not
present in the oil.
MEDICINAL USES: The beans from Ricinus communis (ricin) are a commercial source of castor
oil and the remaining powder (pomace) is used as a fertilizer. Castor oil and its derivatives,
which are used in a variety of products and extracted from the seeds of the castor plant, have
ricin removed as part of the purification process.
MECHANISM OF TOXICITY: Ricin is a protein consisting of 2 approximately equal in size
subunits (A and B) bound by disulfide bonds. The B part of the toxin binds to galactose
containing receptors in the cell wall,allowing the intact ricin protein to be actively transported
into a cell. The A part then inhibits protein synthesis by disabling the 60S ribosomal units.
Disruption of protein synthesis inhibition is considered the primary mode of toxicity. Other
mechanisms that may contribute include activation of apoptotic pathways, direct cell
membrane damage, and release of cytokine inflammatory mediators. ABRIN: Abrin, a
toxalbumin that can be found in the seeds of the Abrus precatorius plant acts via a similar
mechanism and function to ricin. However, abrin is considered more potent.
CLINICAL PRESENTATION: MILD TO MODERATE TOXICITY: CASTOR BEANS or ABRUS SEEDS:
Significant toxicity is not expected after ingestion of intact or whole seeds Nausea, vomiting,
diarrhea and abdominal pain may develop. SEVERE TOXICITY: CASTOR BEARS or ABRUS SEEDS:
The majority of patients that ingest castor beans abrus precatorius seeds recover with
supportive care However, there have been reports of severe toxicity. Nausea, vomiting and
diarrhea generally develop within hours of severe overdose, and may lead to volume depletion
and hypotension. Severe irritation of the GI mucosa may develop, which may result in
gastrointestinal hemorrhage and sloughing of tissue. Electrolyte abnormalities may occur.
Fever may develop early. Severe exposures may ultimately result in death reflecting the severe
cytotoxic effects of the toxins to the liver, central nervous system, and kidneys.
DIAGNOSIS:
A) Monitor vital signs and mental status.
B) Monitor serum electrolytes, renal function, and liver
 enzymes in symptomatic patients.
C) Laboratory radioimmunoassay is available to measure ricin
levels after ingestion, however, specific ricin
concentrations are neither readily available nor useful
in guiding therapy.
ANTIDOTE: No specific antidote, Supportive care and Activated charcoal

6. Convallarin
BACKGROUND OF ORIGIN: Lily of the valley, (Convallaria majalis), fragrant perennial herb and
only species of the genus Convallaria in the asparagus family (Asparagaceae). Native to Eurasia
and eastern North America, lily of the valley is cultivated in shaded garden areas in many
temperate parts of the world. The plants often grow closely together, forming a dense mat, and
are sometimes used as ground cover.
MEDICINAL USES: congestive heart failure and for ventricular rate control in atrial fibrillation.
MECHANISM OF TOXICITY: The effects in overdose are an extension of
the therapeutic effects. Increased intracellular calcium
leads to early afterdepolarization, cardiac
irritability, and dysrhythmias. Increased vagal and
decreased sympathetic tones lead to bradycardia and
heart block. Inhibition of the sodium-potassium ATPase
pump causes hyperkalemia.
CLINICAL PRESENTATION:
MILD TO MODERATE TOXICITY: Toxicity from cardiac
glycosides can be acute (from a single overdose due to
accidental ingestion by a child or due to a self-harm
attempt by an adult) or chronic toxicity (due to
increased dosing or decreased drug clearance). The
manifestations and treatment are slightly different.
The most common symptoms following acute ingestion are
nausea, vomiting, abdominal pain, lethargy, and
bradycardia. With chronic toxicity, patients often
present with bradycardia, malaise, nausea, anorexia,
delirium, and vision changes.
2) SEVERE TOXICITY: Patients with acute poisoning may
develop severe bradycardia, heart block, vomiting, and
shock. Hyperkalemia is a marker of severe acute
toxicity and serum potassium is the best predictor of
cardiac glycoside toxicity after acute overdose. Severe
chronic toxicity causes ventricular dysrhythmias and
varying degrees of heart block, but hyperkalemia is
uncommon.

DIAGNOSIS: Monitor serial serum digoxin concentrations and serum

electrolytes every hour, until patient is improved and
 digoxin concentrations are clearly declining towards
therapeutic. False positive digoxin concentrations have
been reported in patients with pregnancy, liver disease,
and hypothermia.

ANTIDOTE: Digoxin immune Fab

7. COLCHICINE
BACKGROUND OF ORIGIN: Autumn Crocus has a long history of use, although writing in his Des
Materia Medica in the first century AD, Dioscorides records that it is a poison. Despite this
knowledge, it was used in the Byzantine Empire for joint problems such as rheumatism and
arthritis. It was the Arabs who first realized that it could be used to treat gout effectively.
MEDICINAL USES: antimitotic and anti-inflammatory agent used to treat gout, familial
Mediterranean fever, secondary amyloidosis, and scleroderma
MECHANISM OF TOXICITY: Colchicine inhibits mitosis of dividing cells and functions as a
microtubule or spindle poison. In overdose, it preferentially affects rapidly dividing
cells. In high concentrations it is a general cellular poison.
CLINICAL PRESENTATION:
MILD TO MODERATE POISONING: Mild overdose causes
mainly nausea, vomiting, diarrhea, and abdominal pain.
SEVERE POISONING: Severe overdose causes clinical
findings in 3 phases but may be delayed initially a
few hours:
a) PHASE I (0 TO 24 HOURS) - GASTROINTESTINAL: Nausea,
vomiting, diarrhea (bloody), abdominal pain,
dehydration, leukocytosis, volume depletion, and
hypotension.
b) PHASE II (1 TO 7 DAYS) - MULTIORGAN SYSTEM FAILURE:
Possible risk of sudden cardiac death, dysrhythmias;
confusion, coma, seizures; pancytopenia, renal
failure, hepatic failure, sepsis, acute lung injury,
electrolyte imbalances, rhabdomyolysis. Patients with
severe overdose may die during this phase.
c) PHASE III (OVER 7 DAYS) - RECOVERY OR DEATH:
Alopecia; myopathy, neuropathy, myoneuropathy, or
rebound leukocytosis; death usually is caused by
respiratory failure, intractable shock, dysrhythmias,
and cardiovascular collapse.
DIAGNOSIS: Monitor serial serum electrolytes, BUN, creatinine,
glucose, CBC, CPK, liver enzymes, INR, and urinalysis.
B) Obtain an ECG and institute continuous cardiac monitoring
in symptomatic patients.
C) Specific drug levels are not clinically useful or widely
available.
ANTIDOTE: There is no current antidote,
 8. Brucine & Strychnine
BACKGROUND OF ORIGIN: Scientific name “strychnos” from no less a mind than Carl Linnaeus,
who classified it back in 1753, but it was known to the population of India way before then. Nux
vomica originates in India, a surprising fact, considering the bulk of stories about strychnine
poisoning don’t come from India. Perhaps the lack of stories shows the reticence of record
keepers rather than a lack of ingenuity among Indian murderers. Or perhaps the poisoners in
India came up with the most subtle way to use strychnine. While there are no famous particular
poisonings,one book from 1900 speaks of a kind of black market for strychnine hidden in plain
sight. Those who know where to go could get a drug called “kurchi”—a bitter but harmless
tonic for mild ailments. Those who really knew where to go would find kurchi cut with the
powdered pulp of the nux vomica. That would get the poison into a victim.
MEDICINAL USES: Used mainly as a pesticide and a rodenticide. Also, used in some laboratories
as a research tool to study glycine receptors.
MECHANISM OF TOXICITY: Competitively inhibits glycine binding to
the alpha-subunit of the glycine-regulated chloride
channel in the spinal cord. Glycine acts as an
inhibitory neurotransmitter in the spinal cord. It
opens chloride channels allowing the influx of chloride
into cells leading to hyperpolarization and inhibition.
Thus, inhibition of glycine binding to this receptor
causes excitation of the muscle directly stimulated by
the spinal cord.
CLINICAL PRESENTATION: GASTROINTESTINAL: Nausea and vomiting occur
uncommonly. CNS EFFECTS: Bilateral horizontal
nystagmus and blurred vision have been reported.
Muscle tightness/cramps, agitation, and heightened
sensitivity to stimulation may precede severe
neurologic toxicity. Neurologic symptoms occur quickly
(within 15 to 30 minutes) and include agitation,
severe hypertonicity of muscles, opisthotonos, and
painful muscle spasms. Trismus and risus sardonicus
are also reported. The patient usually remains alert
throughout this convulsive activity. Auditory,
tactile, or visual stimulation may trigger a violent
motor response. OTHER: Tachycardia, hypertension,
tachypnea, and hyperthermia are seen commonly
secondary to neuromuscular hyperactivity. RESPIRATORY
FAILURE: Patients may also present with bradycardia
and hypotension in cases of respiratory
failure/arrest. Involvement of the respiratory muscles
leads to diaphragm paralysis resulting in hypoxia and
hypercarbia. RENAL FAILURE: Acute renal failure can
occur secondary to myoglobinuria, rhabdomyolysis, and
DIAGNOSIS: Monitor vital signs, including continuous monitoring of
core temperature in any patient with muscle spasms.
B) Monitor serum electrolytes, creatine kinase, renal
function, liver enzymes, urinalysis and urine output in
symptomatic patients.
ANTIDOTE:No specific antidote

9. AMYGDALIN
BACKGROUND OF ORIGIN: The substance amygdalin (from the Greek word for almond,
amygdále) was first isolated from bitter almonds (Prunus dulcis) by two French scientists,
Robiquet and Boutron-Charlard in 1830, appearing in pharmacopoeias[*] by the year 1834.
The first reference to the use of a laetrile-like substance against cancer can be found in a 19th
century medical journal[1]. Professor T. Inosemtzeff of Moscow Imperial University described
two cases of cancer successfully treated with an emulsion of bitter almonds, one of which
survived more than three years, the other for eleven years.
MEDICINAL USES:Cancer Treatment
MECHANISM OF TOXICITY: Amygdalin is the cyanogenic diglucoside
D-mandelonitrile- beta-D-gentiobioside and is not toxic
until it is metabolized by the enzyme emulsin which is
present in the seeds of these plants. Inadvertent
ingestion of whole seeds or pits is unlikely to result
in acute cyanide toxicity. Toxicity occurs after
enzymatic hydrolysis in the GI tract. Onset of symptoms
is often delayed up to 2 hours or more after ingesting
masticated pits that contain amygdalin. The most common
plants to produce human cyanide toxicity in the US are
the seeds of the Rosacea family, including apricots
(Prunus armeniaca) bitter almond (Prunus amygdalus),
peach (Prunus persica), pear (Pyrus communis), apple
(Malus sylvestris) and plum (Prunus domestica).
CLINICAL PRESENTATION:
MILD TO MODERATE TOXICITY: Signs and symptoms
association with ingestion of significant amount of
masticated pits containing amygdalin include dyspnea,
cyanosis, weakness, and lightheadedness.
SEVERE TOXICITY: Coma, seizures, stupor, dysrhythmias,
cardiovascular collapse, and metabolic acidosis.
CHRONIC TOXICITY: Chronic consumption of cyanogenic
glycoside containing plants as a food staple may result
in chronic polyneuropathies which includes spastic
paresis and tropical ataxic neuropathy. Spastic paresis
is characterized by bilateral and symmetrical
involvement of the pyramidal tracts affecting the lower
 extremities resulting in spastic gait, paraplegia,
extensor plantar responses, spastic bladder,
constipation and impotence, with visual involvement
rarely reported. Chronic poisoning should be considered
when nonspecific or neurologic symptomatology is
associated with a large or chronic ingestion of
cyanogenic plants.
DIAGNOSIS:
A) Monitor serum chemistry and lactate concentrations.
B) Monitor arterial and venous blood gases.
C) Cyanide levels can be measured to confirm the diagnosis,
but are usually not available in a timely manner to be
clinically useful.
D) Institute continuous cardiac monitoring and obtain an
ECG.
E) Methemoglobin should also be monitored frequently in
patients receiving intravenous sodium nitrite.
F) Consider a head CT for comatose patients.
ANTIDOTE: hydroxocobalamin OR the
sodium nitrite/sodium thiosulfate kit, should be
administered to symptomatic patients (metabolic
acidosis, depressed mental status, hypotension,
dysrhythmias, seizures).
10. PODOPHYLLOTOXIN
BACKGROUND OF ORIGIN: Roots of the mayapple were used by Native Americans and early
settlers as a purgative, emetic, “liver cleanser”, and worm expellent. Roots were also used for
jaundice, constipation, hepatitis, fevers and syphilis.
Mark Catesby, the 18th century artist and naturalist, described it as “an excellent Emetic”. “It
flowers in March,” he wrote. “The fruit is ripe in May, which has occasioned it in Virginia to be
called May-Apple.” (Catesby, Natural History, vol. 1. p. 24).
MEDICINAL USES: Podophyllum resin (podophyllin) is extracted from
the May apple rhizomes and roots (mandrake) and is used
as a topical keratolytic to treat external genital and
perianal warts, papillomas, and fibroids. It is
dispensed as 25% podophyllum resin in benzoin tincture
or alcohol. Derivatives are used as anticancer agents
(etoposide and teniposide).
MECHANISM OF TOXICITY: Similar to colchicine, podophyllum arrests
cell division by inhibiting microtubule formation and
polymerization. It inhibits cell division similarly to
a chemotherapeutic agent, and causes toxicity in
rapidly dividing cells first. It also inhibits
axoplasmic transport, protein, RNA, and DNA synthesis,
and oxidation enzymes in the tricarboxylic acid cycle.
CLINICAL PRESENTATION: Toxicity occurs rapidly (within a few hours) after
ingestion but is delayed up to 12 to 24 hours
following dermal absorption. Nausea, vomiting,
diarrhea, and abdominal pain develop first, along with
confusion, delirium, coma, tachycardia, orthostatic
hypotension, and metabolic acidosis. Hematologic
findings (pancytopenia) occur and nadir within 4 to 7
days of exposure. Neurologic findings include cranial
nerve palsy, peripheral sensorimotor axonopathy, and
loss of reflexes. Autonomic dysfunction, ileus, and
urinary retention may persist for several months after
recovery from severe poisoning.
DIAGNOSIS:
A) Monitor serum electrolytes, BUN, creatinine, glucose,
CBC, urinalysis, and ECG.
B) Monitor vital signs and mental status.
C) Monitor neurologic function, over several weeks, in
patients who develop severe toxicity.
D) Obtain nerve conduction studies if peripheral neuropathy
develops.
ANTIDOTE:No specific antidote