Toxicology 3

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Toxicology 3

• Insecticides
• Snail Baits

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Chlorinated HydrocarbonsDDT others
Discovered by Dr Paul Muller 1939 Awarded a Nobel
Peace Prize in 1948 Saved more human lives from
Malaria Infections than any chemical ever
produced Termite control products were used in
the United States until the 1980s. Some of
these products Are still active 60 years after
they were applied Unfortunately it accumulates
in the environment And is magnified up the food
chain In 1962 Rachael Carlson, an American
Biologist Wrote Silent Spring, describing the
magnification Of this pesticide in the food chain
and its effects On the Bird population
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Chlorinated HydrocarbonInsecticides

• Symptoms
• Acts as a CNS Stimulant
• 1. Neuromuscular tremors and convulsions
• 2. Rapid increase in body temperature
• 3. Hypersalivation and Urinary incontinence

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Chlorinated HydrocarbonsDiagnosis

• 1. Exposure to products (cats being bathed in
  Lindane products)
• 2. Tissue samples of the kidney, fat, liver and
  especially the brain

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Chlorinated HydrocarbonInsecticides

• Treatment
• 1. There are no antidotes for this type of
  insecticide.
• 2. Treatment is symptomatic and Supportative

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Chlorinated HydrocarbonInsecticides

• Overview
• These products are still being used in developing
  countries to control mosquitoes and other vectors
  of human disease. Very few products are
  currently available for purchase in the United
  States.

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Chlorinated HydrocarbonMedical Uses

• As a treatment for Cushings Disease
• (Lysodren) Mitotane, o,p-DDD

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Organophosphates

• First Synthesized in the 1850s
• Modern Products trace back to development in
  Germany in the 1930s
• Potent Insecticide
• Poisonous to mammals, birds, reptiles and fish
• Is the component in biological agents called
  Nerve Gasses

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OrganophosphatesRocky Mountain Arsenal
Militarys produced and stockpiled These products
in World War 2 Nazi Germany had A huge plant
and Storage facility but Did not use the gas
in World War 2 Tabun, Sarin
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OrganophosphatesPhoto of Rocky Mountain Arsenal
Sarin Gas Organophosphate Manufactured
for Biological warfare Terrorist used this
in Tokyo in a subway
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OrganophosphateToxicity

• Organophosphate poisoning results from the
  blocking of the enzyme acetylcholenesterase.
• Symptoms Develop in 3 Categories
• 1. Muscarinic-
• 2. Nicotinic-
• 3. Central-

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Organophosphate ToxicitySymptoms

• Muscarinic (SLUDGE)
• 1. Hypersalivationprofuse drooling
• 2. Vomiting, Diarrhea
• 3. Urinating
• 4. Difficult Breathing
• 5. Bronchiospasms

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Organophosphate ToxicitySymptoms

• Nicotinic
• 1. Muscle Weakness
• 2. Muscle tremors, facilitations

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Organophosphate ToxicitySymptoms

• Central
• 1. Ataxia (in coordination)
• 2. Nervousness, Apprehension
• 3. Seizures

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Organophosphate ToxicityDiagnosis

• Exposure to products
• Symptoms
• Laboratory analysis
• 1. Cholenesterase levels

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Organophosphate ToxicityTreatment

• 1. Emesis, Cathartics, Absorbents (activated
  charcoal)
• 2. Bathing if dermal exposure
• 3. Antidotes
• A. Atoprine
• B. 2-PAM

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OrganophosphatesMedical Uses

• 1. Glaucoma treatments
• 2. Myesthenia Gravis
• 3. Potential uses in Alzheimers disease and
  dementia

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Organophosphates
Dont last as long in the environment As
chlorinated hydrocarbons Many need to go 1st to
the liver to Be activated Atoprine and 2-PAM
are antidotes
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OrganophosphateIntoxication

• Prognosis
• Good if caught in time. Antidotes are very
• Effective.

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CarbamatesInsecticides

• These insecticides are for agricultural and home
  use.
• They act similar to organophosphates in that they
  inhibit cholenesterase a nerve junctions.
• Their bond with the acetylcholenesterase is more
  fragile than the ops
• They are more easily biodegradable than the
  organophosphates
• The are lower dermal toxins

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Carbamate Toxicity

• Symptoms (similar to organophosphates)
• 1. Increased salivation
• 2. Increased GI mobility
• 3. (vomiting, diarrhea)
• 4. Cyanosis to mucous membranes
• 5. Miosis (constricted pupils)

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Carbamate Toxicity

• Treatment
• 1. Atoprine
• 2. Decrease absorption, increase elimination
• Cathartics, Emetics, Activated Charcoal, bathing
  and rinsing off the product

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Snail BaitMetaldehyde
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Metaldehyde Toxicity

• Metaldehyde is considered the most common
  poisoning in dogs in California.
• The chemical is in snail and slug poisons in a
  granular or pelleted form. These pellets are
  flavored with bran or molasses which makes them
  attractive to pets.
• Less than 1 teaspoon is toxic to a 10 dog
• Some of the product is metabolized to
  acetaldehyde. Metaldehyde and acetylaldehyde
  cause metabolic acidosis and CNS stimulation

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Metaldehyde ToxicitySymptoms

• Shake and Bake
• 1. Extreme twitching
• 2. Hyperthermia
• 3. Salivation, Vomiting
• 4. Nystagmus
• 5. Hepatic failure (long term)
• Symptoms Can appear like strynine

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Metaldehyde ToxicityDiagnosis

• Exposure to toxin
• Symptoms (Shake and Bake)
• Stomach contents (frozen)

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Metaldehyde ToxicityTreatment

• These dogs can rapidly overheat and die from the
  tremors
• 1. Sedate/Anesthetize
• 2. Gastric Lavage
• 3. Activated Charcoal /- cathartic
• 4. Muscle relaxants (Roboxin)
• 5. Cold Water/ Alcohol bath
• Treatment is symptomatic as no pure antidote
  exists.

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Metaldehyde ToxicityPrognosis

• 1. This is a true emergency condition. The
  sooner the pet is sedated and cooled down the
  better the prognosis
• 2. Some dogs incur hepatic damage due to this
  toxin and may go into liver failure later on

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StrychninePoisoning

• Pesticide
• Derived from the seeds of Strychnos nux-vomica
  and Strychnos ignatii
• Has been used for centuries as both a medicine
  and poison
• This plants alkaloids (poison) are one of the
  most bitter compounds known

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Strychnine TreeNative to Southeast Asia
Seeds contain a very Bitter alkaloid. This is
The poison. Product has become a Restricted
use pesticide But can still be purchased Over the
counter in home Centers.
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Strychnine
Medicine Herbal Txs Poisoning
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Strychnine

• Symptoms
• Violent tetanic seizures May be induced by
  physical, visual or auditory stimuli
• Muscle Stiffness
• Facial Deformity risus sardonicus

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Risus Sardonicus
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Strychnine PoisoningPathophysiology

• Strychnine inhibits the action of glycine in the
  Renshaw cells of the Central Nervous System.
  Consequently, animals receive excessive sensory
  input and have exaggerated motor responses

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Strychnine PoisoningDiagnosis

• 1. Seizure activity in exposed animals
• 2. Urine
• 3. Stomach Contents
• 4. Liver (postmortem)

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Strychnine PoisoningTreatment

• 1. Anesthesia
• 2. Gastric Lavage
• 3. Activate Charcoal
• 4. Anticonvulsants (long acting )
• 5. Roboxin
• 6. IV Fluids
• 7. Dark, Quiet Confinement

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Strychnine PoisoningPrognosis

• 1. Fair if caught early and 24 hour supervision
  is available (dogs and cats may need to be
  anesthetized for up to 2 days)
• This compound is still a common cause of
  Malicious poisoning in the Southwest..

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Considered a Restricted Use PesticideIs
still Available in hardware stores
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Grains are usually colored Green or Blue VERY
TOXIC TO BIRDS AND WILDLIFE
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Arsenic Toxicity

• Potent Heavy Metal Toxin
• King of Poisons, Poison of Kings
• Herbicides, insecticides,

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ArsenicGrants Ant Stakes
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Arsenic Poisoning

• Acute, Highly toxic heavy metal
• King of Poisons, Poison of Kings
• Compound is found in herbicides, insecticides,
  wood preservatives, and treatment for blood
  parasites.
• Has a long history of medicinal uses

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Arsenic PoisoningSymptoms

• 1. Abdominal pain
• 2. Vomiting
• 3. Weakness
• 4. Diarrhea, frequently with blood and mucous
• 5. Hypothermia
• 6. Collapse
• 7. Death

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Arsenic PoisoningDiagnosis

• 1. Known Exposure
• 2. Urine test (acute)
• 3. Kidney and Liver testing (sub acute)
• 4. Hair (chronic poisoning) (Napoleon)

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Arsenic PoisoningPathology

• Gastrointestinal Lesionscommon and severe.
• Liversoft and yellow
• Lungscongested and edematous
• Skin lesionscutaneous exposureblistering,
  edema, cracking with secondary infections

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Arsenic Poisoning

• 1. Induce emesis or gastric Lavage
• 2. IV fluids to support kidneys
• 3. GI protectorates ( Kaolin-pectin)
• 4. Maintain body temperature
• 5. BAL (Dimercaprol)

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BAL
British anti-Lewisite (dimercaprol) was developed
during world War 1 to combat the Lewisite gas
(Acetylene and arsenic) called The Dew of Death
This gas was a biproduct of attempts to Develop
synthetic rubber.It was never used in War Fare
but the Antidote has proven a great aid in heavy
metal poisoning