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Pharmacology > Toxicology > Flashcards

Toxicology Flashcards

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
Q

Strategy for treatment of poisoned patient

A

Clinical stabilization of patient, clinical evaluation, prevention of further toxic absorption, enhance toxin elimination, administration of antidote, supportive care and clinical follow-up

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26
Q

Stabilization

A

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

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27
Q

Clinical evaluation

A

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

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28
Q

Physical examination

A

Assess patient’s condition, mental status, trauma, infection, initiation of rational treatment based on most likely toxin responsible

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29
Q

Laboratory evaluation

A

Some drugs or chemicals are available for immediate measurement in a hospital facility, number of agents is limited

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30
Q

Anion gap

A

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

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31
Q

Osmol gap

A

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

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32
Q

Radiographic examination

A

Use is limited, may detect ingested substances, may detect lesions to specific organs

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33
Q

Prevention of further toxin absoprtion

A

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

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34
Q

Enhance toxin elimination

A

Alkalinization of urine, hemodialysis, hemoperfusion, hemofiltration, hemodiafiltration, plasma exchange or exchange transfusion, serial oral activated charcoal

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35
Q

Alkalinization of the urine

A

Ionize weak acids for elimination

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36
Q

Hemodialysis

A

Remove toxins by passing blood through semipermeable dialysis membrane

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37
Q

Hemoperfusion

A

Remove toxins by passing blood through a cartridge containing absorptive material

38
Q

Hemofiltration

A

Removal of ultrafiltrate of plasma and replacement with sterile solutions

39
Q

Hemodiafiltration

A

Hemodialysis plus removal of ultrafiltrate of plasma and replacement with sterile solutions

40
Q

Plasma exchange or exchange transfusion

A

Removal of plasma and replacement with frozen donor plasma, albumin, or both

41
Q

Serial oral activated charcoal

A

Remove toxins by serving as “sink” for toxins

42
Q

Administration of antidote

A

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
Q

Supportive care

A

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
Q

Environmental toxicants

A

Air pollutants, pesticides, plant toxins

45
Q

Pollutants that account for most of air pollution

A

Carbon monoxide, sulfur oxides, nitrogen oxides, volatile organic compounds, particulate matter

46
Q

Reducing type of pollution

A

Sulfur dioxide and smoke from incomplete combustion of coal and by conditions of fog and cool temperatures

47
Q

Oxidizing type of pollution

A

Hydrocarbons, oxides of nitrogen, photochemical oxidants from automobile exhaust in areas with intense sunlight, causing photochemical reactions

48
Q

Carbon monoxide (CO)

A

Colorless, odorless, tasteless, nonirritating gas from incomplete combustion of organic matter, produced from forest fires, ocean microorganisms, inadequate furnace venting, automobiles, cigarette smoke

49
Q

Toxicology of carbon monoxide

A

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
Q

Mechanism of CO poisoning

A

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
Q

CO2 poisoning

A

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
Q

Pathology of CO poisoning

A

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
Q

Diagnosis of CO poisoning

A

Facilitated by circumstantial evidence, living patient is commonly cyanotic and pale, “cherry-red cyanosis” seen only at autopsy (CO hemoglobin is cherry-red)

54
Q

Excretion of CO

A

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
Q

Treatment of CO poisoning

A

Transfer patient to fresh air, artificial respiration if respiration failed, 100% oxygen or hyperbaric oxygen

56
Q

Prolonged low-level CO exposure

A

Shift from aerobic to anaerobic metabolism, increased incidence of atherosclerosis, impaired vigilance test, long term exposure can cause development of polycythemia

57
Q

CO exposure and fetus

A

Fetus is susceptible, gas readily crosses the placenta, gross damage to brain, neurological sequelae

58
Q

Toxicity of sulfur dioxide

A

Burning of fossil fuels contains sulfur, water soluble upper airway irritant, stimulates mucus secretion and bronchoconstriction

59
Q

Mechanism of sulfur dioxide toxicity

A

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
Q

Donora fog

A

Mainly comprised of ammonium sulfate, more bronchoconstriction than SO2, associated with increased mortality

61
Q

Toxicity of nitrogen dioxide (NO2)

A

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
Q

Volatile organic compounds (VOC)

A

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
Q

Sources of VOC

A

Paints and lacquers, paint strippers, cleaning supplies, pesticides, building materials, furnishings, office equipment, craft materials, tobacco smoke

64
Q

Formaldehyde

A

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
Q

Sources of formaldehyde

A

Product of construction materials such as plywood, furniture, polymerized urea-formaldehyde from insulation

66
Q

Particulate matter

A

Combination of organic, inorganic, biological material, causes pneumoconiosis- restrictive lung diseases caused by inhalation of dust particles

67
Q

Pneumoconiosis

A

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
Q

Asbestos

A

Long-term inhalation of dust, causes three forms of lung disease: asbestosis, bronchial lung cancer, malignant mesothelioma

69
Q

Asbestosis

A

Pulmonary fibrosis, develops first in areas adjacent to bronchioles, formation of fibrous pleuritis, dyspnea, tachypnea, cough

70
Q

Bronchial lung cancer

A

Occur 20-30 years after exposure, increased incidence with cigarette smoking

71
Q

Malignant mesothelioma

A

Cancer of thin cell wall lining internal organs, occurs 25-40 years after exposure

72
Q

Pesticides

A

Include insecticides, rodenticides, fungicides, herbicides, fumigants, major insecticides: organochlorine, organophosphorus

73
Q

Organochlorine

A

Chlorophenothane (DDT)- highly lipophilic, stored in fat, major environmental effect, declining bird population, banned form US in 1972

74
Q

Organophosphates

A

Parathion, malathion- do not persist in environment, low carcinogenic potential, inhibits cholinesterases through phosphorylation of esteratic active site

75
Q

Signs and symptoms of organophosphate toxicity

A

Cholinergic symptoms- sweating, salivating, bronchiole secretion and constriction, miosis, increased GI motility, diarrhea, tremors, muscle twitching, severe poisoning may cause respiratory collapse

76
Q

Treatment of organophosphate toxicity

A

IV atropine to prevent excessive muscarinic action and pralidoxime to prevent aging

77
Q

Agent orange

A

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
Q

Paraquat

A

Accumulates in lungs and kidney, poorly metabolized and excreted unchanged in urine

79
Q

Paraquat toxicity

A

Damages alveolar epithelial cells within 24 hours, leads to loss of alveolar epithelium, alveolar edema, interstitial inflammatory cells infiltration, death due to anoxia

80
Q

Signs of paraquat toxicity

A

1st phase- extensive proliferation of fibroblasts in the lung
2nd phase- attempted alveolar epithelium regeneration, intensive fibrosis

81
Q

Rodenticides

A

Compound 1080, causes CNS and heart toxicity, anticoagulants- warfarin/coumarin derivatives, dispersed in grain-based baits

82
Q

Fumigants

A

Active against insects, mites, nematodes, weed seeds, fungi, rodents, liquids readily vaporize, may cause respiratory, GI, neurologic symptoms

83
Q

Plant toxins- skin

A

Allergic dermatitis caused by plants, flower growers at risk, major allergen in natural rubber latex from rubber tree

84
Q

Plant toxins- respiratory tract

A

Pollen causes summer rhinitis (hay fever, pollinosis), workers that handle peppers- capsaicin depletes neuropeptide P, increase incidence of cough

85
Q

Plant toxins- GI system

A

Nausea, vomiting, diarrhea, cholchicine is major alkaloid in autumn crocus- Gi effects, antimitotitic, confusion, delirium, hematuria, neuropathy, bone marrow aplasia, renal failure

86
Q

Plant toxins- cardiovascular system

A

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
Q

Plant toxins- liver

A

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
Q

Plant toxins- bladder

A

Bracken fern contains carcinogen ptaquiloside, alkylates adenines and guanines of DNA, increased incidence of epithelial and bladder tumor, esophageal and stomach cancers

89
Q

Plant toxins- kidney

A

Woodland fungi cause acute degenerative tubular lesions with inflammatory interstitial fibrosis, acute renal failure

90
Q

Plant toxins- nervous system

A

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
Q

Plant toxins- skeletal muscle

A

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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