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74 Cards in this Set
- Front
- Back
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Toxicology
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The study of the adverse effects of xenobiotics (chemicals) on living systems
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Toxicity
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The inherent capacity of a substance ot produce injury
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Hazard
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The practical certainty that injury will occur when a substance is used in stated quantity and set of conditions: Proportionate risk
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Safety
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The practical certainty that injury will not occur when a substance is used in stated quantity and set of conditions:
Acceptable risk |
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Toxicological Hazard
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Routes of exposure
Duration of exposure Presence of Mixtures |
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All substances are poisons: There is none which is not a poison. The right __ differentiates a poision from a remedy
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dose
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Route of exposure
__ most common in children and in intentional poisoning |
Ingestion
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Route of exposure
__ is the major route in occupational settings followed by __ contacts |
Inhalation is the major route in occupational settings followed by topical contacts
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Duration of exposure
__ toxicity: rapid exposure to high dose with rapid course of injury |
Acute toxicity:
usually accidental: 5000 to 10,000 deaths get years reported to the poison control center Some homicidal or suicidal: Ingestion Some occupational: Inhalation or dermal |
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Duration of exposure
__ toxicity: slowly developing injury that is often progressive and irreversible |
Chronic toxicity
1. Frequently occupational: dermatoses, cancer, delayed neurological dz, obstructive lung dz, reproductive impairment 2. Environmental: Chronic bronchitis, excess cardiopulmonary mortality 3. Sources: Bioaccumulation, air pollution, buidling materials, industrial accidents |
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Bioaccumulation
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Accumulate in the tissue/ increasing concentration
Ex. mercury in tuna fish |
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Dose response possibilities
Threshold model |
Regulated by body defense mechanism
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Hormetic model
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When dose is low, it is beneficial
ex. meds, vitamins |
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Bio-transformation
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The process whereby a substance is changed from one chemical to another (transformed) by a chemical reaction within the body
May increase, decrease, or change |
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Primary chemical reactions leading to toxic actions
1. Block __ 2. Alter__ 3. Alter __ 4. Free __ formation and __ 5. Formation of ___ 6. Binding to critical __ |
1. Block oxygen transport or utilization
2. Alter enzyme activity 3. Alter selective permeability of membranes 4. Free radical formation and lipid peroxidation 5. Formation of reactive oxygen species 6. Binding to critical macromolecules 7. Hapten (small molecule that stimulates the production of antibody molecules only when conjugated to a larger molecule) and antigen formation |
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Mechanisms of antidotal action
1. complexation with __ 2. Acceleration of bioconversion to __ 3. Block formation of more __ 4. Accelerate __ 5. Block or compete for essential __ 6. Bypass effect of __ |
1. Complexation with poison
2. Acceleration of bioconversion to nontoxic metabolite 3. Block formation of a more toxic metabolite 4. Accelerate excretion 5. Block or compete for essential receptors 6. Bypass effect of the poison |
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Reaction with oxygen transport systems
Carbon monoxide forms __ |
Carboxyhemoglobin
Cannot transport O2 |
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__ of CO for hemoblobin is 210 times that of oxygens's
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Net affinity of CO
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Concept of Cooperativity
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In the tetrameric form of normal adult hemoglobin, the binding of oxygen is, thus, a cooperative process. The binding affinity of hemoglobin for oxygen is increased by the oxygen saturation of the molecule, with the first oxygens bound influencing the shape of the binding sites for the next oxygens, in a way favorable for binding.
Destroys cooperativity kills people |
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Antidote for CO
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Oxygen at high partial pressure displaces CO from Hb
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Exposure to nitrates, aromatic amines and nitro compounds forms __
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Methemoglobin formation results from exposure to nitrates, aromatic
amines and nitro compounds. • Hb (Fe++) + NO2 Hb (Fe+++) • hemoglobin methemoglobin |
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Methemoglobin antidote
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Antidote - methylene blue acts as electron donor to reduce ferric form of hemoglobin to ferrous form.
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Cyanide
The effects from cyanide poisoning are those of progressive histotoxic tissue __ by binding to the active site of __ thereby stopping aerobic cell __ |
those of progressive histotoxic tissue hypoxia by binding to the active site of cytochrome oxidase thereby stopping
aerobic cell metabolism |
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Cyanide ion (CN) reacts with ferric (Fe+++) form of cytochrome oxidase.
This rapidly disrupts cellular energy metabolism which is manifast by ___ and ___ dysfunction. |
Cyanide ion (CN) reacts with ferric (Fe+++) form of cytochrome oxidase.
This rapidly disrupts cellular energy metabolism which is manifast by CNS and cardiac dysfunction. |
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Antidote of Cyanide
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Antidote is two step: 시안은 에미에게 소금을 뿌려
• amylnitrites inhaled to produce methemoglobin Hb (Fe+++) which competes with cytochrome oxidase for free CN; cyanmethemoglobin so formed is nontoxic • sodium thiosulfate to form thiocyanate ion (SCN) which is relatively nontoxic and is readily excreted |
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nitrates, aromatic
amines and nitro compounds |
Methemoglobin formation
Hb (Fe++) + NO2 -> Hb (Fe+++) |
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Antidote of nitrate, aromatic
amines and nitro compounds |
Methylene blue acts as 나이트 블루
electron donor to reduce ferric form of hemoglobin to ferrous form |
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Antidote for Nitroglycerin
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Methylene blue
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Reaction with biocatalysts
Paraoxon insecticide |
phosphorylates
the enzyme acetylcholinesterase. This leads to an accumulation of acetylcholine and a cholinergic crisis. : |
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Paraoxon
Antidote is three phase |
팔아 옥스 앞으로 팜...Atropine sulfate blocks acetylcholine at muscarinic receptors
(It inhibits actions of acetylcholine at postganglionic parasympathetic neuroeffector sites) Pralidoxine (PAM) dephosphorylates acetylcholinesterase and restores active enzyme PAM reacts directly with paraoxon rendering it inert |
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Damaging membrane function
Solvents (gasoline, kerosene, paint thinner) S/S |
솔번트 (하인이 꿀꺽 삼키다 폐렴에 걸림)
CNS depression **Aspiration-induced pneumonitis Can sensitize the myocardium |
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Iron
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Corrosive (effect on the lining of the stomach and small intestines)
***Period of apparent recovery 아연 맨은 겉으로 괜챦아 보일때가 있다. |
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Intoxication from kerosene or gasoline S/S
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가솔린/케로신으로 인해 행동이 무질서 밴을 타고 CNS 무너짐
CNS depression similar to that of ethanol Incoordination, restlessness, resp. arrest, death Ventricular fibrillation (inhalation of vapors can sensitize the myocardium and precipitate ventricular filbrillation) |
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TX of solvents. petroleum distillates (kerosene, gasoline, diesel oil and paint thinner)
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Tx is mostly supportive. B/C danger of aspiration, emesis or gastric lavage should not be considered
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Heavy metals
Iron |
Ferrous form absorbed readily, coverted to ferric form and bound by protein
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Iron toxicity results when binding sites become
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saturated
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S/S of Iron toxicity
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Corrosive action on GI mucosal cells leading to coagulative necrosis, hemmorhage, hypovolemic shock, and hepatic dysfunction
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Iron
Corrosive action on __ leading to |
Corrosive action on GI mucosal cells leading to coagulative necrosis, hemmorhage, hypovolemic shock and hepatic dysfunction
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Phases of Iron poisoning
Phase 1 |
30-2 hr
Irritability, seizures, restlessness, Abd pain, vomiting, Bloody diarrhea, Tachypnea, Tachycardia |
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Phases of Iron poisoning
Phase 2 (immediately follows Phase 1) |
**Period of apparent recovery
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Phases of Iron poisoning
Phase 3 |
8-16 hr after Phase 1
Shock, Refractive acidosis Cyanosis, Fever |
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Phases of Iron poisoning
Phase 4 |
2-4 days post ingestion
Hepatic necrosis Elevated SGOT, SGPT |
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Phases of Iron poisoning
Phase 5 |
2-4 weeks post ingestion
GI obstruction |
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Mercury
Speciation Elemental mercury Inorganic mercury Organic mercury |
Speciation crucial to toxicity
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Elemental mercury
(quicksilver and vapor) |
Hg is uncharged, easily crosses cell membranes, and preferentially targets the CNS. Non toxic when ingested.
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Inorganic mercury
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Hg +1 and Hg -2
Agricultural antifungal, dental amalgums, cathartic , rat poison, curative in felt hat industry: Targets the kidney |
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Organic mercury (Methymercury)
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Lipid soluble, Target both CNS and Kidney
Created from inorganic mercury by anaerobic bacteria Bioaccumulation in food chain, acute exposure rate |
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Elemental Mercury poisoning
Route Target organ S/S TX |
Inhalation
CNS, Kidney Bronchial inhalation Pneumonitis Stomatitis Gingivitis Excessive salivation Erethism Tremors Tubular necrosis (kidney) TX BAL, CaNa, EDTA |
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Inorganic Mercury poisoning
Route Target organ S/S TX |
Oral
Kidney Metalic taste Stomatitis Gastroentaritis Urticaria Vesication Tubular necrosis BAL |
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Organic Mercury poisoning
Route Target organ S/S TX |
Oral and food chain
CNS, Liver Alaxia, Chorea, Athetosis, Tremor, Convulsions, Paresthesias, Erethism Chalators are not effective |
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Lead
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Kidney damage
Learning and emotional disability |
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Lead
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Accumulated in bone, hair, and teeth but can be re-mobilized by factors which affect calcium metabolism
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Acute lead poisoning (rare)
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Sweat metallic taste
Salivation Vomiting Intestinal colic |
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Chronic lead poisoning (Plumbism)
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Hematological
-Basophillic stippling -Hypochronic normocytic anemia Neurological (lead encephalopathy) Alaxia, N/V, Restlessness, Irritability, Conculsions, coma GI (Lead colic) Anorexia, Constipation, Metalic taste Neuromuscular (Lead palsy) Wrist drop, Foot drop, Fatigue, Muscular weakness Renal Fanconi-like syndrome (reversible) Chronic nephritis (irreversible) |
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Cadmium
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One of the greatest modern day toxicologic concerns
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Cadmium
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Widely used in numerous industrial process including elecroplating
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Cadmium exhibits enzymes including alpha1 antirypsin, resulting in severe __
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Lung damage
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S/S Cadmium
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Osteomalacia
(Ouch-Ouch dz) Immunosuppressant, Growth retardation, Testicular damage, Carcinogenesis |
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Calcium disodium EDTA
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For lead and Iron poisoning
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Long term of using Calcium disodium EDTA cause __
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Arrhythmias
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Calcium disodium EDTA: Beware of __ and __
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Hypocalcemia and severe proximal nephron degeneration
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BAL (dimercaprol)
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For mercury and Lead
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Antidote to arsenical gas
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BAL (dimercaprol)
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Deferoxamine
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for Iron poison
Can provoke histamine release |
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Penicillamine
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Moderately useful for a number of metals, but not first choice
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For Lead poisoning __ __
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Calcium disodium EDTA
BAL (dimercaprol) |
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For Iron poisoning __ __
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Calcium disodirum EDTA
Deferoxamine |
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Corrosive S/S
Ingestion |
Burning pain in mouth, throat and abd, vomiting, bloody diarrhea, dysphagia, drooling, hypotension
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Corrosive S/S
Inhalation |
Bronchial irritation, pulmonary edema, frothy sputum, moist rales, hypotension, dyspnea
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Corrosive S/S
Dermal |
Staining of skin, burning pain
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Corrosive S/S
Ocular |
Conjuctivitis, corneal destruction, pain, lacrimation, photophobia
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Lipid peroxidation and reactive oxygen
Carbon Tetrachloride (solvent) |
P450 metabolism to free radical
liver damage CNS depression Ventricular fibrillation |
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Lipid peroxidation and reactive oxygen
Paraquat |
Lung toxicity
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Depletion of essential intermediates
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Acetaminaphen
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