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Toxicology Flashcards

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1
Q

Toxicology

A

Science of adverse effects of chemicals on living organisms

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2
Q

Major areas of toxicology

A

Descriptive- toxicity testing in cells, animals, humans
Mechanistic- how chemicals cause adverse effects and how the body protects against them
Regulatory- rule making and compliance

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3
Q

Food and Drug Administration (FDA)

A

Drugs, medical devices, cosmetics, food additives

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4
Q

Environmental Protection Agency (EPA)

A

Pesticides, toxic chemicals, hazardous wastes, and toxic pollutants in water and air

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5
Q

Occupational Safety and Health Administration (OSHA)

A

Determines whether or not employers are providing working conditions that are safe for employees

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6
Q

Forensic toxicology

A

Combines analytical chemistry and fundamental toxicology to investigate postmortem the cause or circumstances of death, concerned with medicolegal aspects of chemicals

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7
Q

Clinical toxicology

A

Treat patients who are poisoned by drugs and other chemicals and develop new techniques for diagnosis and treatment of intoxications

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8
Q

Signs and symptoms can be caused by toxic chemicals

A

From administered therapeutic agents and/or the environment

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9
Q

Dose-response relationship in individual

A

Graded dose-response relationship

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10
Q

Dose-response relationship in population

A

Quantal dose-response relationship, extremely important in toxicology, LD50 is determined experimentally

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11
Q

Shape of dose-response curve in individual

A

Shape of graded dose response relationship in an individual is U-shaped, low doses have high level adverse effect, too high of a dose has different adverse effect

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12
Q

Hormesis

A

Nonnutritional toxic substances that may impart beneficial or stimulatory effects at low doses but produce adverse effects at high doses (ex- alcohol)

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13
Q

Dose-response curve of alcohol

A

Chronic consumption increases risks of esophageal, stomach, and liver cancer, low-moderate consumption may reduce incidence of coronary heart disease and stroke

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14
Q

Therapeutic index (TI)

A

TD50 / ED50

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15
Q

Margin of safety

A

LD1 / ED99

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16
Q

Mechanism of toxicity- delivery

A

Toxication- biotransformation to harmful products

Detoxication- biotransformation that eliminates the ultimate toxicant or prevent formation

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17
Q

Mechanism of toxicity- reaction

A

Reaction of toxicant with target molecule or biological microenvironment

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18
Q

Mechanism of toxicity- cellular dysfunction and resulting toxicities

A

Cell regulation (signaling), cell maintenance (survival)

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19
Q

Cell regulation (signaling)

A

Dysregulation of gene expression- inappropriate cell division, apoptosis, or protein synthesis
Dysregulation of ongoing cell function- inappropriate neuromuscular activity, tremors, convulsion, arrhythmia, paresthesia

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20
Q

Cell maintenance (for survival)

A

Impaired internal maintenance- ATP synthesis, membrane function, protein synthesis
Impaired external maintenance- impaired function of integrated systems

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21
Q

Mechanism of toxicity- repair or disrepair

A

Repair- molecular, cellular, tissue repair

Disrepair- necrosis, fibrosis, carcinogenesis

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22
Q

Prevention of acute poisonings

A

Most poisonings from drugs can be prevented by physicians providing common sense instructions, patients or parents of patients accepting the advice

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23
Q

Division of toxic agents

A

Those for which specific treatment antidote exist
Those for which there is no treatment- majority of drugs and chemicals, require medical care that supports vital functions

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24
Q

Supportive therapy

A

Most important aspect of treatment of drug poisoning

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25
Strategy for treatment of poisoned patient
Clinical stabilization of patient, clinical evaluation, prevention of further toxic absorption, enhance toxin elimination, administration of antidote, supportive care and clinical follow-up
26
Stabilization
First priority, assessment of vital signs and respiration/circulation, ventilation support, circulation support, oxygenation, in critically ill, treatment interventions must be initiated before patient is stable
27
Clinical evaluation
Determine the substance and time of exposure, get information from family, EMT, etc, assume maximal level of exposure, unobtainable history proceeds as unknown ingestion poisoning
28
Physical examination
Assess patient's condition, mental status, trauma, infection, initiation of rational treatment based on most likely toxin responsible
29
Laboratory evaluation
Some drugs or chemicals are available for immediate measurement in a hospital facility, number of agents is limited
30
Anion gap
Difference between concentrations of serum Na ion and the sum of serum Cl and HCO3 ion, normal is <12, metabolic acidosis and elevated anion gap suggest toxicity
31
Osmol gap
Numerical difference between the measured and calculated serum osmolality, normal is <10 mOsm, elevated osmol gap suggests presence of osmotically active substances in the plasma not accounted for by Na, glucose, or BUN
32
Radiographic examination
Use is limited, may detect ingested substances, may detect lesions to specific organs
33
Prevention of further toxin absoprtion
Toxins from inhalation- remove patient from environment Toxins from contact- remove clothing, wash skin Toxins from ingestion- methods of emesis, gastric lavage (dilution), charcoal administration, whole bowel irrigation
34
Enhance toxin elimination
Alkalinization of urine, hemodialysis, hemoperfusion, hemofiltration, hemodiafiltration, plasma exchange or exchange transfusion, serial oral activated charcoal
35
Alkalinization of the urine
Ionize weak acids for elimination
36
Hemodialysis
Remove toxins by passing blood through semipermeable dialysis membrane
37
Hemoperfusion
Remove toxins by passing blood through a cartridge containing absorptive material
38
Hemofiltration
Removal of ultrafiltrate of plasma and replacement with sterile solutions
39
Hemodiafiltration
Hemodialysis plus removal of ultrafiltrate of plasma and replacement with sterile solutions
40
Plasma exchange or exchange transfusion
Removal of plasma and replacement with frozen donor plasma, albumin, or both
41
Serial oral activated charcoal
Remove toxins by serving as "sink" for toxins
42
Administration of antidote
Small number of specific antidotes are available clinically in the treatment of poisoning, antidotes may be chelators, antagonists, reactive chemicals to increase detoxifying capacity for the toxins
43
Supportive care
Some toxins have delayed toxicity, some exhibit multiple phases of toxicity, close monitoring can detect later-phase complications, psychiatric assessment to prevent future poisoning
44
Environmental toxicants
Air pollutants, pesticides, plant toxins
45
Pollutants that account for most of air pollution
Carbon monoxide, sulfur oxides, nitrogen oxides, volatile organic compounds, particulate matter
46
Reducing type of pollution
Sulfur dioxide and smoke from incomplete combustion of coal and by conditions of fog and cool temperatures
47
Oxidizing type of pollution
Hydrocarbons, oxides of nitrogen, photochemical oxidants from automobile exhaust in areas with intense sunlight, causing photochemical reactions
48
Carbon monoxide (CO)
Colorless, odorless, tasteless, nonirritating gas from incomplete combustion of organic matter, produced from forest fires, ocean microorganisms, inadequate furnace venting, automobiles, cigarette smoke
49
Toxicology of carbon monoxide
Binding site of hemoglobin is ferrous heme that can reversibly bind oxygen, CO prevents oxygen binding by forming a bond with ferrous heme significantly stronger than oxygen-heme bond
50
Mechanism of CO poisoning
When 50% of O2 binding sites on hemoglobin are occupied by CO, no more than 50% saturation of O2, at tissue, hemoglobin saturation is still over 35%, less than 15% of heme sites can deliver O2 to tissues
51
CO2 poisoning
In addition to interference with O2 delivery, CO binds to cellular cytochromes in respiratory enzymes and myoglobin and interfere with enzyme function, anemic individuals are more susceptible, signs of CO poisoning mimic hypoxia
52
Pathology of CO poisoning
Tissues most affected are those most sensitive to O2 deprivation- permanent damage to brain and heart, headache due to cerebral edema and increased intracranial pressure
53
Diagnosis of CO poisoning
Facilitated by circumstantial evidence, living patient is commonly cyanotic and pale, "cherry-red cyanosis" seen only at autopsy (CO hemoglobin is cherry-red)
54
Excretion of CO
Once exposure to CO is terminated, it will be excreted from lungs, CO concentration of blood decreases with half-time of 320 min in room air, 100% O2 is 80 min, hyperbaric is <25 min
55
Treatment of CO poisoning
Transfer patient to fresh air, artificial respiration if respiration failed, 100% oxygen or hyperbaric oxygen
56
Prolonged low-level CO exposure
Shift from aerobic to anaerobic metabolism, increased incidence of atherosclerosis, impaired vigilance test, long term exposure can cause development of polycythemia
57
CO exposure and fetus
Fetus is susceptible, gas readily crosses the placenta, gross damage to brain, neurological sequelae
58
Toxicity of sulfur dioxide
Burning of fossil fuels contains sulfur, water soluble upper airway irritant, stimulates mucus secretion and bronchoconstriction
59
Mechanism of sulfur dioxide toxicity
Portion of SO2 converted in atmosphere to sulfuric acid (H2SO4), ammonium sulfate, and other sulfates, sulfuric acid irritates upper airway due to acidity- more bronchoconstriction than SO2, chronic exposure injuries phagocytes and endothelial cells, can cause bronchitis
60
Donora fog
Mainly comprised of ammonium sulfate, more bronchoconstriction than SO2, associated with increased mortality
61
Toxicity of nitrogen dioxide (NO2)
Deep lung irritant, can produce pulmonary edema if inhaled at high concentrations, causes bronchiole inflammation, high concentration damages bronchiole epithelial cells and cause loss of ciliated cells and secretory granules
62
Volatile organic compounds (VOC)
Gases emitted from certain solids or liquids under normal indoor pressure and temp, higher concentration indoors, cause eye and respiratory tract irritation, headaches, dizziness, visual disorders, memory impairment
63
Sources of VOC
Paints and lacquers, paint strippers, cleaning supplies, pesticides, building materials, furnishings, office equipment, craft materials, tobacco smoke
64
Formaldehyde
Act via sensory nerves that signal through trigeminal nerve, induce bronchoconstriction through vagus nerve, associated with nasopharyngeal cancer in humans, linked to leukemia and sinonasal cancer
65
Sources of formaldehyde
Product of construction materials such as plywood, furniture, polymerized urea-formaldehyde from insulation
66
Particulate matter
Combination of organic, inorganic, biological material, causes pneumoconiosis- restrictive lung diseases caused by inhalation of dust particles
67
Pneumoconiosis
Most common is silicosis, macrophages proliferate and migrate to site of reaction to release cytokines and other growth factors, cause replication of fibroblasts and collagen synthesis
68
Asbestos
Long-term inhalation of dust, causes three forms of lung disease: asbestosis, bronchial lung cancer, malignant mesothelioma
69
Asbestosis
Pulmonary fibrosis, develops first in areas adjacent to bronchioles, formation of fibrous pleuritis, dyspnea, tachypnea, cough
70
Bronchial lung cancer
Occur 20-30 years after exposure, increased incidence with cigarette smoking
71
Malignant mesothelioma
Cancer of thin cell wall lining internal organs, occurs 25-40 years after exposure
72
Pesticides
Include insecticides, rodenticides, fungicides, herbicides, fumigants, major insecticides: organochlorine, organophosphorus
73
Organochlorine
Chlorophenothane (DDT)- highly lipophilic, stored in fat, major environmental effect, declining bird population, banned form US in 1972
74
Organophosphates
Parathion, malathion- do not persist in environment, low carcinogenic potential, inhibits cholinesterases through phosphorylation of esteratic active site
75
Signs and symptoms of organophosphate toxicity
Cholinergic symptoms- sweating, salivating, bronchiole secretion and constriction, miosis, increased GI motility, diarrhea, tremors, muscle twitching, severe poisoning may cause respiratory collapse
76
Treatment of organophosphate toxicity
IV atropine to prevent excessive muscarinic action and pralidoxime to prevent aging
77
Agent orange
Herbicide, used in Vietnam war to defoliate forests, causes vomiting, burning of mouth, abdominal pain, hypotension, and CNS effect including coma, causes soft-tissue sarcoma, non-Hodgkin's lymphoma, chronic lymphocytic leukemia
78
Paraquat
Accumulates in lungs and kidney, poorly metabolized and excreted unchanged in urine
79
Paraquat toxicity
Damages alveolar epithelial cells within 24 hours, leads to loss of alveolar epithelium, alveolar edema, interstitial inflammatory cells infiltration, death due to anoxia
80
Signs of paraquat toxicity
1st phase- extensive proliferation of fibroblasts in the lung 2nd phase- attempted alveolar epithelium regeneration, intensive fibrosis
81
Rodenticides
Compound 1080, causes CNS and heart toxicity, anticoagulants- warfarin/coumarin derivatives, dispersed in grain-based baits
82
Fumigants
Active against insects, mites, nematodes, weed seeds, fungi, rodents, liquids readily vaporize, may cause respiratory, GI, neurologic symptoms
83
Plant toxins- skin
Allergic dermatitis caused by plants, flower growers at risk, major allergen in natural rubber latex from rubber tree
84
Plant toxins- respiratory tract
Pollen causes summer rhinitis (hay fever, pollinosis), workers that handle peppers- capsaicin depletes neuropeptide P, increase incidence of cough
85
Plant toxins- GI system
Nausea, vomiting, diarrhea, cholchicine is major alkaloid in autumn crocus- Gi effects, antimitotitic, confusion, delirium, hematuria, neuropathy, bone marrow aplasia, renal failure
86
Plant toxins- cardiovascular system
Cardioactive glycosides (digitalis)- found in plants, when eaten may present with nausea, vomiting, cardiac arrhythmias, ergots- fungus parasitics on grains of rye, cause vasoconstriction in extremities followed by gangrene
87
Plant toxins- liver
Most deaths from mushroom poisoning are due to liver damage, A. phalloides has phalloidin- combines with muscle cell actin to interfere with muscle function (diarrhea), and amatoxins- strong affinity for hepatocytes where it binds to RNA polymerase II, inhibiting protein synthesis, liver failure, death
88
Plant toxins- bladder
Bracken fern contains carcinogen ptaquiloside, alkylates adenines and guanines of DNA, increased incidence of epithelial and bladder tumor, esophageal and stomach cancers
89
Plant toxins- kidney
Woodland fungi cause acute degenerative tubular lesions with inflammatory interstitial fibrosis, acute renal failure
90
Plant toxins- nervous system
Cicuta maculata (water hemlock)- contains cicutoxin, binds GABA-gated chloride channels, cause tonic-clonic convulsions, some mushrooms- muscarine, causes parasympathetic stimulation, some plants- anticholinergic alkaloids, parasympathetic blockade
91
Plant toxins- skeletal muscle
Some plants contain nicotine- prolonged depolarization of NMJ, causes muscle weakness, respiratory compromise, muscle spasm, GI irritation, curare- neuromuscular blocking agent, stops respiration, blocks AChR

Pharmacology (15 decks)

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