non metallic poisons
TRANSCRIPT
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NON METALLI
C POISON
S
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A substance that is capable of causing illness or death of a living organism when introduced or absorbed in the body.
What is a Poison?
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• Carbon Monoxide• Cyanide• Methanol• Ethylene Glycol• Acetaminophen• Vitamin A, C and D• Niacin• Chlorinated Hydrocarbon Insecticide• Organophosphorius• Carbamate Insecticide• Environmental Pollutants
Types of Non-Metallic Poisons
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• SOURCES: CAR EXHAUST, GAS FURNACE, CHARCOAL FIRES
• MECHANISM OF ACTION: HB-CO>HB-O2
• SYMPTOMS: HEADACHE, UNCONSCIOUSNESS/COLLAPSE->DEATH CV-MI, ARRTHYMIAS, BRAIN, RESP.
• TREATMENT: HIGH PRESSURE OXYGEN- FACE MASK
Carbon Monoxide
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Cyanide• Sources: Apricot pits, Synthetic Rubber,
nitrogen containing fires, metal cleaners, insecticides, rodenticides.
• Symptoms: low dose: headache palpitations, n/vmoderate dose: ataxia convulsions, deathhigh doses: Instant unconsciousness and death
• Diagnosis: History, Bitter almond breath, abruptness of onset.
• MOA: CN bind ferric iron of cyt oxidase in
mitochondria-> stop oxidation->hypoxia
• Treatment: 1. Fe pooling2. Amyl or Sodium Nitrate 3. Oxygen inhalation
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• Sources : paint remover, solvents, antifreeze
• MOA : more slowly oxidized vs. Ethanol Methanol->formaldehyde (blindness) and formic acid (cardiotoxin)• Symptoms: like ethanol , vision
disturbed. mydriasis, pupils unresponsive to light, acidosis CV and respiratory failure and permanent blindness• Treatment: Warmth, no light, sodium
bicarbonate for acidosis, give ethanol to compete for alcohol dehydrogenase
Methanol
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• Sources: Anti-freeze• MOA: metabolized by alcohol
dehy. -> oxalate -> Renal injury formic acid formation -> Acidosis (a cardiotoxin)
• Treatment: gastric lavage, sodium bicarb, ethanol to compete, hemodialysis
Ethylene Glycol
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Ethylene Glycol
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• Sources: Tylenol• Pk: absor. in GI. Metabolized to a
glucuronide and sulfate conjugates. Some first hydroxylated then conjugated with Glutathione peroxidase (GSH). when GSH depleted -> cellular necrosis
• Symptoms: toxic doses 1-2 days pallor, 2-4 days: hepatic damage
• Diagonosis: plasma levels, monitor liver function
• Treatment: N-acetylcystein (sulfhydrl cmpd) - binds APAP or replenishes GSH in liver.
Acetaminophen
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• Symtoms:GI/CNS disturbance, dermatitis, joint and muscle pain, hypercalemia and premature epiphyseal closure.
chronic exposure leads to irreversible liver damage • Treatment : symptomatic
Vitamin A
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• Most toxic of all vitamins• Symtoms: elevated
plasma calcium (hypercalemia) - deposition in kidneys and heart. increase MI in men
• Treatment: symptomatic, decrease calcium intake
Vitamin D
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Vitamin C
rarely see stone formation in kidney and bladder
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large dose - liver problems and jaundice
Niacin
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• Example: DDT• fat soluble, low molecular
weight, low water solubility and high fat solubility;
• poor biodegradability (t1/2=10years)
• interferes with inactivation of sodium channel (rapid AP firing- CNS stimulation
• persist in environment; • bioaccumulate
Chlorinated hydrocarbon insecticides
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Organophosphorus insecticides• used in environment, absorbed
through the skin and GI, highly toxic
• MOA: inhibits AChE by phosphorylating esteratic site.
• Symptoms: due to overstimulation of cholinergic sites, salivation, lacrimation, urination, rest of them are given in Diagram on next slide
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Environmental Pollutants• very lipophilic and highly
stable, poorly metabolized• very resistant to
environmental degradation• bioaccumulates in food
chain.
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