Transcript Poison

Poisoning
(intoxication)
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Poisoning
Outline of lecture:
1.
2.
3.
4.
5.
Definition
Epidemiology
Clinical symptoms
Treatment – antidotes
Types of poisoning: Chemicals
Drugs
Animal toxins
Plant and bacterial toxins
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Poisoning
Poisoning is a morbidity induced by the presence of venom
(nox) in the organism.
 acute poisoning: results from exposure (ingestion, inhalation,
injection) of an effective amount of poison (e.g. consumption of
toadstools green, snakebite)
 chronic poisoning: resulting as a consequence of long-term
income of low doses of cumulative poison (eg. heavy metal
poisoning).
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Basic principles of toxicology
The dose makes the poisioning
(Paracelsus 1493-1541)
LD50: lethal dosis 50% specifies the relative toxicity of
substances
The concentration of the substance at which 50% of animals dies
within 24 hours after administration of the poison (approximate value
depends on weight and condition of the individual).
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Epidemiology
• In the Czech Republic ~ 100-200 000 intoxications per year
(excluding recreational use of cannabis and ethanol).
• Accidental (unintentional): usually children under 6 years
• Attempted suicide (intentional self-harm)
• Improper use or abuse of freely available medicaments
(excessive dosing, combinations, expectations of euphoric effect ...)
• Mortality:
– <1% of all intoxicated individuals
– 1-2% of suicide attempts
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Clinical symptoms
Non-specific symptoms of acute poisoning:
➢ Gastrointestinal discomfort, vomiting, abdominal pain,
diarrhea
➢ Headache
➢ Respiratory disorders
➢ Sweating, salivation
➢ Convulsions
➢ Cardiac arrhythmias
➢ Loss of consciousness
➢ Hallucinations (LSD = lysergic acid diamid, Psilocybin,
MDMA aka Ecstasis, Cannabis...)
➢ Mydriasis / Miosis
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Clinical symptoms
The pacient may be:
Agitated/ Excited:

Increased heart rate, blood pressure, respiratory rate, temperature
and neuromuscular activity (e.g. cocaine, selective beta-agonists,
hallucinogens, but also withdrawal symptoms)
Inhibited:
Decreased heart rate, blood pressure, respiratory rate, temperature
and neuromuscular activity (e.g. sympatholytic, opiates, cholinergic
agents – stimulants of muscarinic and nicotinic receptors, sedatives,
hypnotics)
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Clinical signs of poisoning
Discordant:
– simultaneous occurrence of stimulation and inhibition of
physiological functions, or a gradual transition from one state to
another
– e.g. substances causing hypoxia/ asphyxia (CO, carbon
monoxide), substances causing metabolic acidosis (methanol,
ethylene glycol, salicylates) substances leading to liver failure,
kidney failure or respiratory disorders
Normal:
– substances that are slowly absorbed, distributed, and
metabolically activated or affect metabolic processes
(e.g. paracetamol, cumulative poisons), poisoning as by
"toxic time bomb"
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Diagnosis

Recognition of the poisoning

Identification of inducing substances
(analysis of urine, blood, vomit...)

Determination of clinical impact and
appropriate management
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Treatment

Support of vital functions (O2, intravenous fluids)

Preventing further absorption of the poison
(decontamination)

Support of elimination of the poison from the body

Administration of the antidotes
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2 phases of poisoning:
1. PRERESORPTIVE – inactivation and removal of
unabsorbed toxic substace. E.g. vomiting, flushing of
stomach, washing the the skin...
2. POSTRESORPTIVE (managing of consequences of poisoning)
a) inactavation of toxic substance: antidotes
b) blocking of subsatnce toxic effects
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Types of intoxication
Foreign substance = xenobiotic
Poison = noxa
 Chemicals – alcohols, heavy metals, anions,
pesticides and other industrial chemicals
 Pharmaceuticals
 Addictive substances (drugs)
 Animal and plant poisons
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Most frequent intoxications
• Paracetamol (Acetaminophen)
– the most common intoxication requiring
hospitalization.
• CO (carbon monoxide)
– the most common lethal intoxication/ death usually occurs prior
to the hospitalization.
– 1st place among accidental poisoning in Europe.
– in the Czech Republic CO poisoning causes 140-150 deaths per
year.
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Paracetamol
Characterization: Paracetamol
(Acetaminophen, N-acetyl-p-aminofenol)
-component of analgetics, antipyretics
(COLDREX, KORYLAN, PANADOL…)
-the therapeutic dose for adults – from 325 to 650 mg/ 1 dose,
max. 4 g/ day.
- the therapeutic plasma level from 5-20 mg/ ml.
- after oral administration the dose is absorbed within 0,5 to 1 hour.
- maximum plasma concentration is reached within 1 hour after
administration
- passes well tissue including the placenta, overdose threatens the fetus
Toxic dose: 100 mg/kg; adults: 7,5 g
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Paracetamol
Symptoms of acute poisoning:
•
Within few hours (0,5 - 24) after the overdose: nausea,loss of
apettite, vomiting, sweating and drowsiness.
•
In extreme doses of 75-100 g for an adult may lead to coma and
metabolic acidosis as early as 3-4 hours after ingestion.
•
After 3-4 days: increase in aminotransferases ALT, AST
•
After 5 and more days: liver and kidney failure, metabolic acidosis,
myocardial injury, neurological symptoms and hematlogical disorders
(trombocytopenia).
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Paracetamol
Mechanism:
Paracetamol is hepatotoxic, toxicity
increases in combination with alcohol.
Paracetamol is metabolized in the liver
by cytochrome P450 enzyme into the
highly reactive metabolite N-acetyl-pbenzochinonimin (NAPQI), which is
inactivated under physiological condition
by conjugation with glutathione
and excreted by the kidneys as cysteine.
 In overdose – fast depletion of
available glutathione (decrease supplies
under 30 %)- NAPQI metabolite attacks
covalently cellular proteins in hepatocytes
and causes their apoptosis.
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Paracetamol
First Aid:
-Gastric lavage, vomiting, immediate administration of
charcoal (50-100g) which binds well paracetamol.
-Antidote is N-acetylcysteine - supplements glutathione
reserves in the liver and renal tubular cell and thereby
ensures inactivation of toxic metabolite NAPQI.
-Administration of antidote up to 10 hrs after ingestion
almost completely prevents fatal liver damage.
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Carbon monoxide (CO)
Characterization
-Carbon monoxide is colorless and odorless, arises from incomplete
combustion.
-CO is part of each flue gas.
-Exhaust gases gasoline or diesel engines contain a high percentage of
CO.
- CO in the atmosphere is normally present at a concentration of less
0,001% (or 10 ppm)
-the most common cause of death for reasons of intoxication
(death usually occurs prior to admission).
-in the Czech Republic die for CO poisoning 140-150 pers./year
(LD50): the concentration in air of 0.05% is already dangerous
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Carbon monoxide (CO)
Symptoms: - facial flushing, headache, vomiting, dizziness,
visual disturbances, rapid breathing and heartbeat
disturbances and loss of consciousness.
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Carbon monoxide (CO)
Concentration
Symptoms
35 ppm
(0.0035%)
Headache and dizziness within six to eight hours of constant
exposure
100 ppm (0.01%)
Slight headache in two to three hours
200 ppm (0.02%)
Slight headache within two to three hours; loss of judgment
400 ppm (0.04%)
Frontal headache within one to two hours
800 ppm (0.08%)
Dizziness, nausea, and convulsions within 45 min; insensible
within 2 hours (700 ppm – Mars atmosphere)
1,600 ppm
(0.16%)
Headache, tachycardia, dizziness, and nausea within 20 min;
death in less than 2 hours
3,200 ppm
(0.32%)
Headache, dizziness and nausea in five to ten minutes. Death
within 30 minutes.
6,400 ppm
(0.64%)
Headache and dizziness in one to two minutes. Convulsions,
respiratory arrest, and death in less than 20 minutes.
12,800 ppm
(1.28%)
Unconsciousness after 2-3 breaths. Death in less than three
minutes.
Carbon monoxide (CO)
Mechanism:
• CO binds to hemoglobin forming karbonylhemoglobin
(karboxyhemoglobin, COHb).
• Affinity of CO to hemoglobin is 200–300x greater than the
afinitty of oxygen. CO binds with the same affinity to muscle
myoglobin and heart myoglobin.
• Physiological concentration of COHb is 1-2%, for heavy
smokers up to 10%).
• CO blocks the binding sites of hemoglobin for oxygen and
causes tissue hypoxia.
• Physiologically CO as well as NO and SH2 acts as a
neurotransmiter (vasodilatory effect) and participate in the
inflammatory response.
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Carbon monoxide(CO)
Mechanism II:
• CO causes tissue hypoxia, tissue with high comsupntion of
Oxygen (myocardium and brain) are the most affected.
• CO blocks the activity of enzymes including P-450 and
triggers metabolic acidosis.
• Can cause neuronal apoptosis and consequently severe
neurological disability leading to death.
• CO is especially toxic to the fetus, which display a low
partial pressure of Oxygen
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Carbon monoxide (CO)
First aid:
- Ensuring the supply of fresh air or artificial respiration (due to high affinity
of CO to Hb has CO a long dissociation).
- Medical first aid involves the administration of oxygen.
- Hyperbaric oxygen therapy (HBO, application of 100% Oxygen under
high pressure).
- HBO accelerstes the dissociation of COHb (from 90 to 20 min) and
significantly reduces the risk of ischemia-reperfusion injury.
- In severe poisoning after initiation reoxygenation are developed
reoxygenation, or ischemia-reperfusion injury (leads to execute a
series of pathophysiological cascades, as activation neutrophil
adhesion to endothelium and subsequent capillary damage, as well as
the neuronal apoptosis).
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Cyanide potassium
Characterization:
 Cyanide potassium (KCN): potassium salt of hydrocyanic acid.
 White, crystalline, hygroscopic substance, lethal dose of 100–250 mg.
 Reaction of KCN with atmosperic carbon dioxide forms extremely poisonous
gas hydrogen cyanide (HCN), smelling of bitter almonds.
2 KCN + CO2 + H2O (vzd.) → K2CO3 + 2 HCN
 Potassium cyanide poison was used for executions during WW2 (cyklonB) or
suicides of chieftains of the Nazi regime (Heinrich Himmler and Hermann
Göring).
 HCN may arise as a photodissociation product of the decay of nitroglycerin
(angina pectoris).
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Cyanide potassium
Mechanism:
In the stomach the interaction of KCN with hydrochloric acid (HCl)
releases highly poisonous hydrogen cyanide HCN.
 Toxic
effect: blocking the enzymes of respiratory chain in
mitochondria.
most important is the inhibition of cytochromeoxidase. - CN- binds to
the ferric iron (Fe3+) contained in cytochromeoxidase thus blocking cellular
respiration. Asa consequence the lactate concentration is increasing causing
the metabolic acidosis, resulting in tissue suffocation, especially the brain
centers.
 The
 Transport
of oxygen in blood is maintained, because the iron in the
hemoglobin is in the divalent form (Fe2 +).
 Poisoning
after ingestion of small amounts may take up to several
hours.
 When
a large dose of hydrogen cyanide is released in the body (or
when inhaled) death occurs in a few seconds.
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Cyanide potassium
First Aid:
After contact of KCN with skin, wash the affected area by water.
If swallowed, and the victim is conscious, induce vomiting immediately.
Antidotes:
 i.v. administration of hydroxocobalamin (compound of B12) at high
dose (~grams). The exchange of hydroxide group forms non-toxic
cyanocobalamin.
 thiosulphate sodium - forms non-toxic thiocyanate
(rhodanide),excreted in the urine.
 Isoamylester of nitrous acid mediates binding of HCN to
methemoglobin containing Fe3+ to form nontoxic kyanohemoglobin
(HbCN).
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Ethanol
Characteristic: ethyl alcohol, alcohol CH3CH2OH
•Colorless hydrophilic liquids, lighter than water, former by fermentation
of sugar by east (especially Saccharomyces genus)
•It is easily absorbed (stomach, small intestine), and rapidly enters into
the circulation.
• The euphoric effects known from Middle Ages.
Metabolism:
• ~10 % of the dose is excreted in the urine and breath
• Most of the dose is metabolized in the liver by the enzyme
alcohol dehydrogenase to produce highly toxic metabolite:
acetaldehyde - attacking S-S bridges of proteins – crosslinking
cellular proteins, causing apoptosis of hepatocytes
• final metabolites: acetate, CO2, H2O, fatty acids
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Ethanol
Stages of intoxication:
The excitation stage
Increased mental and physical activity. Impaired coordination of movements with
the extension of reaction time.
The narcotic stage
Vasodilatory effects, i.e. engorgement and redness of the skin, particularly on the
face. Double vision and dizziness, especially when eyes are closed and lying.
Increases blood pressure and pulse. Vomiting may occur and diuresis. After the
previous euphoria started a major downturn, indifference and passivity
accompanied by a loss of sense of reality.
The comatose stage
Started coma with complete motor weakening. Breathing is deep and slow (due to
respiratory acidosis). When vomiting danger of aspiration of gastric contents and
apnea.
Alcohol hypoglycemic coma
Ethanol inhibits gluconeogenesis from amino acids, lactic acid and glycerol
In liver. Hypoglycemia occur 4-12 hours after ingestion.
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Ethanol
Physiological action:
• toxic is particularly the metabolite acetaldehyde.
• damage of hepatocytes, liver cirrhosis
• damage to other organs, peripheral nerve disorders of brain activity
Treatment:
• early vomiting.
• gastric lavage.
• hemodialysis.
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Methanol
Characteristic: methyl alcohol, wood alcohol CH3OH
Colourless, alcoholic smelling liquid unlimitedly miscible with water. Volatile,
flammable and highly toxic.
Solvent, an ingredient of antifreeze solutions, denaturant.
Mechanism:
The toxicity of methanol is based on the action of its metabolites.
Very slow metabolism, elimination about 7 times slower than ethanol.
Is metabolized in the liver by alcohol dehydrogenase forming the toxic
formaldehyde. This is further converted by aldehyde dehydrogenase into the
formic acid. The ultimate metabolite is carbon dioxide.
Peak levels of formic acid - about 2 days after ingestion.
Result: metabolic acidosis, impaired cell metabolism by formic acid and lactate.
disablement of CNS (similar to Parkinson symptoms), impaired vision, retinal
disorders -light-sensitive nerve endings and the basal ganglia, where HCOOH
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accumulates.
Methanol
Symptoms :
Early symptoms: narcotic intoxication, drunkenness, drowsiness.
After 8 to 36 hours: headache, dizziness, coma or convulsions.
First Aid:
Gastric lavage
As soon as possible after ingestion – enzyme saturation by innfusion of
ethanol, (competitive oxidation of ethanol, 20x higher affinity for alcohol
dehydrogenase than methanol), maintaining blood ethanol levels of about
1,5g/kg
Antidote also fomepizole = 4-methylpyrazole, a specific
inhibitor of alcohol dehydrogenase. 15 mg/kg after 12hours,
level doesn`t has to be monitored.
Long term hemodialysis (recommended approximately 5 days).
Regulation of plasma pH, natrium bicarbonate infusion + folic acid,
which accelerates the oxidation of formic acid.
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Ethyleneglycol
Characteristic: 1,2-ethandiol
• Viscous liquid, sweet taste, odorless and colorless.
• Substance of antifreeze solution in the cars (Fridex).
Symptoms of poisoning:
•
CNS depression, euphoric intoxication, narcotic effects as alcohol, later
GI problems, the development of acute renal failure
•
Toxic metabolites are: glycolaldehyde, glyoxylate, oxalate
•
Metabolites cause acidosis, anuria, pulmonary edema and brain, acute
renal failure.
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Ethyleneglycol
First Aid:


Gastric lavage
Blocking the formation of toxic metabolites – antidotes administration:
ethanol
(per os, intravenous) maintain the level of 1-2 g/kg, fomepizole (15
mg/kg ).


Hemodialysis in severe poisoning
Correction of acidosis – Sodium bicarbonate infusion (NaHCO3).
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Organophosphates
Characteristics:
Organophosphates are phosphoric acid esters.
• The most widely used organic phosphorus compounds.
• Series of essential biomolecules, including DNA and RNA and many
cofactors, e.g. Adenosine triphosphaet (ATP), nucleotiesy (ATP, UTP,
GTP, CTP and their deoxy derivatives)
• Basis of - insecticides: (malathion, parathion, diazinon, fenthion,
dichlorvos, chlorpyrifos)
- herbicides (tricresylphosphates)
- nerve paralysis weapons (soman, sarin, tabun
nebo VX).
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Organophosphates
Mechanism:
• nerve paralytic
• Inhibitors of acetylcholinesterase (AChE), which catalyzes the
degradation of the neurotransmitter acetylcholine into choline and
acetate in the synaptic cleft.
• The result is accumulation of acetylcholine in the synaptic clefts and
subsequent neuromuscular paralysis (sustained contraction of the
muscles) throughout the body.
• Death by suffocation
Symptoms:
Salivation, lacrimation, urinary urgency and defecation, motility of the
digestive system, vomiting and download the pupils. May occur
bronchospasm and bradycardia.
First Aid:
Antidote: atropine, blocks peripheral action of acetylcholine
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Heavy metals
Lead, mercury, copper, cadmium
Characterization:
•The cumulative poisons, minimaly excreted and stored in the body, e.g. In fat,
hair, bones, livers.
•During the food chain leads to increasing concentrations in organisms.
•Carcinogenic.
Lead: Plumbum Pb
Symptoms of poisoning: facial pallor, constipation, loss of appetite, colic,
anemia, headache, convulsions, chronic nephritis, brain damage and disorders
of the central brain system
- Disruption of porphyrin metabolism (ALAD, FCH – sideroblasts)
Treatment: consists in the formation of the complex and the masking Pb by
strong chelating agent.
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.
Heavy metals
Mercury: Hydrargyrum, Hg
•The use of dental amalgam fillings.
Is stored primarily in the kidney and to a lesser extent in the liver and
spleen. In the organism persists for decades.
Symptoms of chronic poisoning are often nonspecific:
•hair loss, digestive disorders, neurological and psychiatric problems,
anemia, chronic candidiasis treatment contrary, rheumatic disease, or
kidney disease (glomerular).
•When a single high dose of mercury always occur abdominal pain,
diarrhea and vomiting.
Treatment: milk or white (insoluble precipitates Hg-albuminate),
chelating agents (dimerkaptopropan sulfonate), hemodialysis
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Animal poisons
1.Snakes
2.Amphibians
1.Insects
2.Coelenterates
4.Microorganisms
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Animal poisons - snakes
Poisonous snakes inject venom by canals in teeth. Venom is formed in gland
located on the oral floor. Gland evolved from the salivary glands and has
externally and internally secretory function.
Venom composition: highly viscous, sticky liquid, white to orange colour.
Multicomponent.The main toxic component are enzymes, amino acids and
peptides, which acts as:
-neurotoxines (pre a post synaptic)
-cardiotoxin
-vasoaktivní -cirkulační toxines
-hemolysiny
-component affecting coagulation
Enzymes:
•Hyaluronidase: cleaves ECM
•Phospholipase: cleaves lipids. It works neurotoxic (bungarotoxin, taipotoxin,
myotoxic or heamolytic.
•Proteolytic enzymes: decomposition of the tissue protein, tissue damage and
circulatory disturvances. They may affect the coagulation, e.g. Thrombin or
anticoagulant activity.
Hemorhaginy cause re-endothelializationof blood and lymphatic capillaries. Also
cause the release of histamine and bradykinine (vasodilatation).
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Animal poisons - snakes
European adder (Vipera berus) – the only venomous snake
of the Czech Republic. Forests, meadows, clearings and
stony and rocky terrain of the Central Europe to 1500m.
-Aktive mostly in the daytime and at nightfall.
-Poison contains mainly hemorhagine, circulating toxins and coagulation-active
substances.
Bite: Vipers regulate the amount of venom injected at defensive bites
intoxication occurs in less than 50 % of cases.
For an adult does not mean most serious threat.
In the Czech Republic, dozens of bites/year.
Symptoms: swelling (due to paralysis lymphatics vessels), greater response
to pain lymph nodes, nausea, vomiting, sweating, elevated temperature.
When possible allergic reaction, anaphylactic shock, circulation shock,
contraction of smooth muscle in the gastrointestinal tract and bronchi due to
histamine and subsequent asphyxia, colic, diarrhea.
Symptoms generally persist for longer than 48 hours.
First Aid: immobilization of the affected limb, sedatives,
analgesics, rest, fluids
Antidote: the specific recombinant antibody.
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Animal poisons - snakes
Indian cobra (Naja naja): India, 1-2m,
•The distinctive marking on the cephalothorax
•Poison - synaptic neurotoxins that paralyze
muscles thus affecting the respiratory and cardiac
activity.
•Bite symptoms manifest from 15 minutes to 2 hours
and can be fatal in less than one hour.
Black mamba (Dendroaspis polylepis) 2-4m, the
most venomous snake in Africa.
•Poison contains neurotoxins, paralysis, high death
rate.
•Immediate life support, antiserum most difficult to
reach.
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Animal poisons - snakes
Eastern diamondback rattlesnake (Crotalus
adamanteus)
Vipers, the most venomous snake and the largest in
North America. Occurrence southeast USA.
Poison: proteolytic enzymes
Symptoms: Intense local reaction with severe
hemorrhages to necrosis (leads to expose the long bones
of the limbs).
For the overall reaction is characterized by severe
coagulopathy and hypovolemic shock.
Coastal taipan (Oxyuranus scutellatus). The family of
the coral
Up to 3 meters, are among the most venomous snakes of
the world.
Occurance: coast of Australia and Papua-New Guinea
-Mortality bite approaching 90%.
-the Antiserum, early application provides a high chance
of rescue.
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Animal poisons - frogs
Kokoe poison frog (Phyllobates aurotaenia) South American
frog – skin glands contain steroidal alkaloid batrachotoxin.
• The secretion is used as a South American Indians curare.
• Venom is excreted in colorless glands located at the back.
• Frogs don`t synthesize the venom, but they ingest in the food.
• Batrachotoxin: selectively activates the Na+ion channel
without reciprocal changes K and Ca ions, which leads to
depolarization of neuronal membranes and subsequent
paralysis.
• One of the most toxic poisons: lethal dose of less than 200 pg.
~ 15x more potent than curare.
• Neurotoxic (CNS and periphery) cardiotoxic (arrhythmia to
cardiac arrest). There is no antidote
• Used by the Indians of western Colombia for hunting (used to
produce poisoned arrows into blowpipes).
• Common toad (Bufo bufo): skin glands contain the steroids
bufotoxin and bufogenine. Influence of ion transport in the
cardiac muscle. Arrhythmias, dizziness. Due to the low
concentration of neurotoxins - minimal danger.
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Insect
•Hymenoptera
•Spiders
•Scorpions
Hymenoptera
Bees, wasps, hornets, ants
Sting contains:
•Biogenic amines: histamine, serotonin, acetylcholine
•peptides: melitin to 50% by volume (disruption of membrane mast cell,
degranulation), kinin (vasodilation, muscle contraction)
enzymes: hyaluronidase, phospholipase A (ECM cleavage, disruption of
membranes, allow the penetration of tissues other components poison.
The fundamental problem that causes an allergic reaction, anaphylactic
shock, apnea.
Treatments: Desinfection injection, antihistamines, glucocorticoids
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Insect - spiders (Arachnida)
Black widow (Latrodectus mactans) the most common venomous
representative of the American continent also occurs in southern Europe, for
example Croatia.
Poison: a-latrotoxin (neurotoxin, affects neuromuscular endings) further
protease, hyaluronidase, phosphodiesterase.
Symptoms: edema, erythromycin, pain, tremor, dyspnoe. The bite is not
fatal, there is an effective antidote.
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Insect - spiders (Arachnida)
Funnel-web spider (Atrax robustus)
- Astralian funnel-web spider, one of the largest in the world, it occurs primarily
in New South Wells (Sydney).
Poison: robustoxin - neurotoxin acts on presynaptic terminals,
atrotoxin, acts on neuromuscular terminals and releasing neurotransmitters,
hyaluronidase.
Symptoms: spasms of whole muscle groups in the upper half of the body,
abdominal cramps bites to lower limbs. Irritation of the parasympathetic
nervous systém, increased secretion of glands: sweating, tearind and
overproduction of mucus in the airways.
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Coelenterates
•Octopus
•Corals
•Anemones
Poison of coelenterates form mostly proteolytic enzymes, low molecular
weight peptides and glycoproteins - e.g. congestin, thalassin,
eginatoxin.
Cnidocysts (nematocysts) - unicellular poison glands, covering tentacles
and sometimes all over the body
•Inside is the spiral fiber with a thin tip that coelenterates shoot into the body
of animals. Fiber and tip are dipped into poison.
•After touching the local reaction occurs (stinging, erythema to vesicles),
tissue necrosis.
•On the mucous membranes and corneal can occur ulceration, which is only
slowly healing. When massive intoxication - the overall reaction with nausea
and vomiting, muscle cramps, breathing disorders, kidney damage, heart
failure.
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Jellyfish
Sea wasp (Chironex fleckeri)
Deadly species of sea jellyfish from the family of
Chirodropidae
Lives in coastal waters of Australia.
Head approximetaly 25 cm in diamater.
Up to 3 meters long, thin sticky tentacles covered by
number of stinging cells.
Stinging cells in contact with the human skin causes
severe pain followed by swelling and often shock, causing
heart failure leading to drowning swimmer
Portuguese man o' war
(Physalia physalis)
Atlantic shore of Portugal and Spain.
Accidentaly passes gibraltar in to the
Mediterranean Sea.
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Octopus
Blue-ringed octopus and Greater blue-ringed octopus ( species of
Hapalochlaena )
They occur in shallow waters from northern Australia to Japan.
Size to 20cm
Poison is consists of tetrodotoxin(TTX) – a neurotoxin, blocks the fast Na+
channels during depolarization, is among the strongest animal poisons.
hurt and intoxication beak.
Symptoms: numbness of the tongue, blurred vision, subsequent blindness.
Poison paralyses the muscles. Systemic paralysis occurs within three minutes,
including respiration. Cyanosis, choking.
 Octopuses have two venom glands
(comparable in size with the brain), and
each has a different composition toxins.
First gland produces a toxin which stuns
prey, which then feeds. Poison from the
second gland is used as a defense.
There is still no antidote !
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Octopus
Blue-ringed octopus and Greater blue-ringed octopus (species of
Hapalochlaena )
First Aid: is necessary immediate and long-term support of vital functions,
artificial respiration and heart massage. If the patient is treated, the poison is
eliminated from the body upon 24 hours without sequelae.
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Fish: Fugu
Fugu (Takifugu rubripes), blowfish :
Occurance: the Sea of Japan
Venom: tetrodotoxin
liver and sexual organs, meat and skin.
In attack: swell
The meat of this fish is non-toxic out of the reproductive period, and in Japan
is considered a special delicacy.
First aid: necessary immediate and long-term support of vital functions,
artificial respiration and heart massage.
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Plant poisons: Mushrooms
Death cap: amantine
faloidin
Hepatonefrotoxic syndrome
Fly amanita: amantine
Halucinogenic syndrome
Magic mushroom: psilocybine
Hallucinogenic syndrome
Satans mushroom:
Gastroenteritic syndrome
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Death cap (Amanita phalloides)
Mechanism: Phalloidin binds to intracellular membranes, especially the
endoplasmic reticulum, vacuoles causes an autolytic degradation of cytoplasm
and subsequent necrosis of hepatocytes.
Amanitin (a, b) specifically binds RNA-polymerase II and inhibits transcription
in hepatocytes and kidney tubules.
Treatment: fast gastric and intestines lavage.
•High doses of penicillin G (aprox. one million units per kg body weight), which
displaces amanitin of binding to serum albumin and than hepatoprotectives
(silymarin).
•Early intervention is important – chance of a complete cure, if there is a full
development of severe poisoning – permanent disability
•Poisoning is fatal in 40 – 50 % cases.
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Plant poisons
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Plant poisons: mushrooms
Death cap (Amanita phalloides)
Most venomous and dangerous fungus
of Europe and North America!
– causes most lethal poisoning.
Poison: faloidin, α a β amanitine
Symptoms:
•the first symptoms appear only when the poison is absorbed and are already
severely affected liver.
•tiredness, nausea, dizziness, headache, feeling cold
Delayed: stomach pain, severe diarrhea resulting in dehydration to
circulatory failure. This is especially for children immediate cause of death.
•In the second stage the liver and possibly kidney failure.
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Plant poisons
Yew (Taxus baccata)
• mixture of alkaloids (taxine)

whole plant is poisonous, except red fleshy follicle fetus
• Foxglove (Digitalis purpurea)
• glycosides, steroid aglycone
• cardiotonics, influencing myocardial contractility (ionotropid effect)
inhibitory effect on the sodium-potassium pump
(Na+/K+-ATPase)
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Continued counseling for intoxication:
Toxicological Information
Centre (TIS).
Klinika pracovního lékařství VFN a 1. LF UK
Na Bojišti 1, 120 00, Praha 2
Nonstop line
224 91 92 93, 224 91 54 02
http://www.tis-cz.cz/
E-mail: [email protected]
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