Toxicology Flashcards

(63 cards)

1
Q

This elucidates the cellular, molecular, and biochemical effects of xenobiotics within the context of a doseresponse relationshipbetween the xenobiotic and the adverse effect.

A

Mechanistic Toxicology

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2
Q

is the study of the adverse effects of xenobiotics in humans

A

Toxicology

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3
Q

include chemicals and drugs that are not normally found or produced in the body.

A

Xenobiotics

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4
Q

This uses the results from animal experiments to predict what level of exposure will cause harm in humans. This process is known as risk assessment.

A

Descriptive Toxicology

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5
Q

Interpretation of combined data from mechanistic and descriptive studies is used to establish standards that define the level of exposure that will not pose a risk to public health or safety.

A

Regulatory Toxicology

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6
Q

oversees human safety issues associated with therapeutic drugs, cosmetics, and food additives.

A

Food and Drug Administration

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7
Q

has regulatory oversight with regard to pesticides, fungicides, rodenticides, and industry-related chemicals that may threaten safe drinking water and clean air.

A

U.S. Environmental Agency

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8
Q

is responsible for ensuring safe and healthy work environments.

A

Occupational Safety and Health Administration(OSHA)

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9
Q

regulates household chemicals

A

Consumer Product Safety Commission

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10
Q

oversees transporting of chemical hazards.

A

Department of Transportation

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11
Q

wanted the toxic’ warning symbol to be “memorable but meaningless”.

A

Charles L. Baldwin

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12
Q

Charles L. Baldwin developed The ‘toxic’ warning symbol in

A

1966

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13
Q

health engineers in the The ‘toxic’ warning symbol

A

Charles L. Baldwin of Dow Chemicals

Robert S. Runkle of the National Institutes of Health

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14
Q

study of interrelationships between xenobiotics and disease states

This area emphasizes not only diagnostic testing but also therapeutic intervention

A

Clinical Toxicology

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15
Q

Is concerned with themedicolegal consequences of exposure to chemicals or drugs. A major focus of this area is establishing and validating the analytic performance of the methods used to generate evidence in legal situations, including the cause of death.

A

Forensic Toxicology

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16
Q

Includes the evaluation of environmental chemical pollutants and their impact on human health. This is a growing area of concern as we learn more about the mechanisms of action of these chemicals, monitor occupational health, and increase public health biomonitoring efforts nationwide.

A

Environmental Toxicology

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17
Q

is usually considered a specialty of clinical chemistry

A

toxicology

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18
Q

are defined as exogenous agents that may have an adverse effect on a living organism. Examples include antibiotics, antidepressants, and environmental exposures of concern such as perfluorinated (non-stick pans, waterproof furniture, etc.) and brominated compounds (insecticides, fumigants, dyes, pool sterilizers, etc.)

A

Xenobiotics

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19
Q

This term is more often used when describing animal, plant, mineral, or gas poisons. Examples include venom from poisonous snakes, poison hemlock, arsenic, or carbon monoxide poisonings, respectively.

A

Poisons

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20
Q

are substances that are biologically synthesized either in living cells or in microorganisms. Examples include botulinum toxin produced from the microorganism, Clostridium botulinum, hemotoxinsproduced from venomous snakes, and mycotoxinsproduced from fungus.

A

Toxins

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21
Q

can become protonated in gastric acid. The result is a nonionized species, which can be absorbed in the stomach.

A

Weak acids

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22
Q

favor absorption in the intestine, where the pH is largely neutral or slightly alkaline.

A

Weak bases

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23
Q

have the ability to diffuse across cell membranes and, therefore, can be absorbed anywhere along the gastrointestinal tract.

A

Hydrophobic substances

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24
Q

cannot passively diffuse across membranes.Other factors can influence absorbance of

A

Ionized substances

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25
factors can influence absorbance of toxins from the gastrointestinal tract
-rate of dissolution -gastrointestinal motility -resistance to degradation in the gastrointestinal tract -interaction with other substances.
26
—a Swiss physician and alchemist (1493 to 1591)—pioneered the use of chemicals in medicine and coined the term “the dose makes the poison.
Paracelsus
27
dose that would be predicted to be effective or have a therapeutic benefit in 50% of the population.
ED50
28
dose that would be predicted to produce a toxic response in 50% of the population
TD50
29
dose that would predict death in 50% of the population
LD50
30
the ratio of the TD50 or LD50 to the ED50. ( TI = TD50/ED50)
therapeutic index
31
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING: Super Toxic
<5 mg per kg
32
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING:Extremely Toxic
5-50 mg per kg
33
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING:Very Toxic
50-500 mg per kg
34
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING:Moderately Toxic
0.5-5 g per kg
35
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING:Slightly Toxic
5-15 g per kg
36
36
LETHAL ORAL DOSE IN AVERAGE ADULT for TOXICITY RATING:Practically Non-Toxic
>15 g per kg
37
are terms used to relate the duration and frequency of exposure to observed toxic effects.
Acute toxicity and chronic toxicity
38
usually associated with a single, short-term exposure to a substance, the dose of which is sufficient to cause immediate toxic effects.
Acute toxicity
39
repeated frequent exposure for extended periods for greater than 3 months and possibly years,
Chronic toxicity
40
testing includes examples such as when environmental risk of exposure is known, to support the investigation of a known exposure (e.g., spill, fire, suicide attempt), to comply with occupational regulations or guidelines (e.g., OSHA), and to confirm clinical suspicions of poisoning.
Targeted testing
41
As such, the predicted toxicokinetics of the individual element(s) involved must be coordinated with
the selection of specimen, and timing of specimen collection, relative to the time of exposure.
42
Preanalytical Variables to Consider:
o Elimination patterns o Analyte stability o Specimen collection
43
Common Sources of External Contamination:
Common Sources of External Contamination: o Patient clothing o Skino Hair o The collection environment (e.g., dust, aerosols, and antiseptic wipes) o Specimen handling variables (e.g., container, lid, and preservatives)
44
certified “trace element–free” collection tubes
royal blue top for most elements; tan top for lead
45
commonly used for screening of drugs.
Immunoassays
46
is a relatively simple, inexpensive method of detecting various drugs and other organic compounds.
Thin-Layer Chromatography
47
is a widely used, well-established technique for the qualitative andquantitative determination of many volatile substances
Gas Chromatography (GC)
48
The reference method for the quantitative identification of most organic compounds
Gas Chromatography/Mass Spectrometry (GC/MS).
49
causes disorientation, confusion, and euphoria, which can progress to unconsciousness, paralysis, and, with high-level exposure, even death.
ALCOHOL
50
Excessive consumption, with its associated consequences, is a leading cause of economic, social, and medical problems throughout the world. The economic impact is estimated to exceed $100 billion per year in terms of lost wages and productivity. Many social and family problems are associated. The burden to the health-care system is significant.
Ethanol
51
The determination of blood ethanol concentration by the laboratory in cases of drunk driving requires an appropriate:
chain of custody, documentation of quality control, and proficiency testing records.
52
what blood alcohol concentration causes adverse effects such as impaired judgement and movement with lower alertness
0.05%-0.08%
53
what blood alcohol concentration causes adverse effects such as speech slurred, loss of balance and muscle control, slow reaction time, visual attention impaired, unstable emotions, nausea, vomiting
0.08%-0.15%
54
what blood alcohol concentration causes adverse effects such as unable to walk without help, feeling sleepy, difficulty breathing, unable to remember events, loss of bladder control, loss of consciousness
0.15%-0.30%
55
what blood alcohol concentration causes adverse effects such as coma and death
>0.30%
56
Blood Alcohol Content, or BAC, refers to the percentage of alcohol in a person's bloodstream, and can be measured within _________ minutes after drinking.
30-70 minutes
57
Alcohol consumption's pathologic sequence starts with
the accumulation of lipids in hepatocytes.
58
Alcohol consumption's pathologic sequence starts with the accumulation of lipids in hepatocytes. With continued consumption, this may progress to
alcoholic hepatitis
59
fibrosis leading to a loss of functional hepatic mass.
Cirrhosis
60
- increased liver size due to fat deposits - perivenular fibrosis
Steatosis
61
- fibrosis - hepatocyte destruction
Cirrhosis
62
Alcoholic Hepatitis
- increased liver size due to fat deposits - hepatocyte necrosis