Non metallic poisons

NON METALLI

C POISON

S

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?

• 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

• 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

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

• 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

• 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

Ethylene Glycol

• 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

• 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

• 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

Vitamin C

rarely see stone formation in kidney and bladder

large dose - liver problems and jaundice

Niacin

• 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

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

Environmental Pollutants• very lipophilic and highly

stable, poorly metabolized• very resistant to

environmental degradation• bioaccumulates in food

chain.

THANK YOU