tox test 2 Flashcards

1
Q

cancer

A
2nd most common death in the u.s 
men-prostate,lung,colorectal
women-breast,lung,colorectal 
cancer death rate is lower and survival rate higher 
sir Percivall Pott (chimney sweeps)
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2
Q

IARC (international agency for research on cancer)

A

identifies carcinogens into five groups

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3
Q

tumor

A

solid mass of cancer cells

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4
Q

benign tumor

A

not potentially lethal

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5
Q

malignant

A

potentially spread and kill

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6
Q

Staging

A

looking at a biopsy to see how advanced and how much (put into a 1-4 category T1-T4)

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7
Q

Gleason scale

A

1-10(12) the lower the better they compare normal cancer to biopsy

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8
Q

carcinogenesis

A

process which cancer develops

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9
Q

mutational theory

A

most accepted theory in three phases

  1. initiation
  2. promotion
  3. progression
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10
Q

initiation

A

damage to DNA random or induced

transformed into neoplastic cell

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11
Q

promotion

A

further cellular changes leading to a tumour (monoclonal)

can involve promoters to stimulate cell division

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12
Q

progression

A

tumour becomes malignant

metastasis

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13
Q

carcinogens

A

agent/factor that causes cancer

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14
Q

genetic carcinogen

A

have damage to DNA (chemical/virus/radiation insert into DNA)

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15
Q

epigenetic carcinogens

A

some place other than DNA (normally affecting proteins)

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16
Q

procarcinogens

A

some carcinogens must be activated before they are carcinogenic

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17
Q

Alkylation of DNA bases

A

covalent bond formed between base and alkyl group(added)

base pairing becomes impaired and mistakes happen during replication by DNA polymerase

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18
Q

Dioxin

A
  • DIrty dozen
  • binds to cytosolic receptor protein; complex moves to the nucleus, binds to a DNA receptor binding site induces transcription of the gene for arylhydrocarbon hydroxylase (AH) and other genes)
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19
Q

Methyltransferase enzymes

A

repair damage DNA by removing methyl groups from Guanine

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20
Q

Nucleotide excision repair systems

A
  • endonucleases

- open DNA strand to allow removal of the damages or mispaired base.

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21
Q

polymerase

A

insert correct base

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22
Q

Ligase

A

reseals the strand

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23
Q

Mismatch repair

A

-everyone has mismatches

recognizes and corrects incorrectly paired bases

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24
Q

Ames test

A

tests for mutagenicity (uses bacteria to test if chemical can cause mutations in DNA)
not every mutagen is a carcinogen

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25
Q

threshold model

A

a small dose can be beneficial

dose that begins to show effect

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26
Q

non-threshold model

A

based on biological responses at high radiation doses and dose rates

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27
Q

testes

A

sperm formation begins at puberty

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28
Q

tight junctions (blood testis barrier)

A

between adjacent sertoli cells of the SI tubules

  • provides limited protection
  • testes have P450 activity making it stuff more lethal
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29
Q

sperm production

A

can be inhibited, lower sperm counts, or be deformed

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30
Q

SI epithelium

A

can be injured or destroyed

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31
Q

Affects energy in Sertoli cells

A

ex. Phthalates, m-DNB, DNT

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32
Q

Heavy metals

A

Pb (lead) and Cd (cadmium) cause infertility, chromosome damage, testicular necrosis

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33
Q

ethanol

A

delays testicular development

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34
Q

damage to oocytes

A

anthineoplastics agents, heavy metals, PAH’s, radiation, tobacco, pesticides, chlorinated hydrocarbons, aromatic solvents

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35
Q

theo colborn

A

“our stolen future” (1996)

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36
Q

Enviromental estrogens

A

low concentration in the environment

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37
Q

endocrine disruptor

A

chemical that mimics or disrupts hormone

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38
Q

anabolic steroids

A

decrease male fertility

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39
Q

puberty

A

average age of puberty onset in humans is decreasing

40
Q

Bisphenol A (BPA)

A

commonly used in plastics as a plasticizer

significant baby birth defects linked to prenatal exposure

41
Q

Dichlorodiphenyltrichloroethane (DDT)

A

first organic that was a success as a pesticide
benzene rings and chloride
paul herman muller
pestcide against colorado potato beetles
ww2 malaria mosquitoes

42
Q

Rachel Carson /DDT

A

wrote silent spring (1962)
DDT thing of bird eggs and bald eagle
-beginning of modern environmental movement
-very long half-life in enviroment
-biomagnification (toxins in organism because of eating other plants or animals with toxin)(interference with food chain)

43
Q

Birth control

A

act on reproduction hormone system -mix of estrogen and progesterone

  • inhibts ovulation because inhibits FSH and LH
  • many side effects (thromboembolism, stroke)
44
Q

Teratology

A

study of birth defects

45
Q

Teratogens

A

enviromental agent which produces birth defects

  1. doage/exposure level
  2. timing
46
Q

Infectious

A

passed through infections (rubella,syphilis,CMV)

47
Q

medications

A

thalidomide,accutane (medicines)

48
Q

Drugs of abuse

A

alcohol, cocaine

49
Q

external agents

A

radiation, hyperthermia

50
Q

Maternal

A

diabetes,lupus, PKU (passed from mother)

51
Q

Pregnancy

A
  • During pregnancy any exposure to toxicants is considered to be problematic
  • placenta is not much of a barrier
  • first three months are most crucial
  • dose that do not harm the mother can harm the embryo
52
Q

embryo

A

there is little phase 1 and phase 2 reactions because enzymes are at very low levels

53
Q

Exposure to embryo

A
  • early embryonic exposure is lethal
  • exposre in 3rd trimester growth problems
  • each body system/organ has a critical period of development
54
Q

Diethylstilbesterol (DES)

A

-synthetic estrogen
prevent miscarriages
-rare vaginal cancer (clear cell adenocarcinoma)
-reproductive tract problems in offspring and grandchildrem

55
Q

Ethanol

A

fetal alcohol syndrome (1970’s)

problems associated when mother had intake of 1 oz/day

56
Q

cleft palate

A

incomplete joining of maxillary and palatine

57
Q

TCDD

A

binding to cytosol proteins and blocking programmed cell death

58
Q

cocaine

A

blocks reuptake of norepinephrine
create vasocontraction and decreased blood flow
leads to premature contractions and births

59
Q

Thalidomide

A

•Synthesized in 1954; similar to barbituarates•Best selling sedative and antiemetic by 1961•Not sold in the U.S.

60
Q

respiratory tox. two categories

A

gases

particulates

61
Q

effects

A

immediate(asthma attack,watery eyes,runnynose)

delayed(cancer,cough)

62
Q

air toxins cause

A

death, irreparable damage, discomfort

63
Q

exposure times

A

acute (few seconds/hours)

chronic (day in/day out)

64
Q

Upper respiratory tract

A

cilia and mucus trap particles

particles consumed by macrophages(attack bacteria)

65
Q

mucocilary escalator

A

cilia move particles like escalator

66
Q

club (clara)cells

A

_Bronchiolar exocrine cells (secrete chemicals into bronchials)
-dome-shaped, small villi, small granules
-secrete gags for protection
P450 activity in SER

67
Q

Exposure levels

A

estimated based on concentration of gas and length of exposure

68
Q

gases

A

measured in ppm

69
Q

particulates

A

measured in weight/ volume (Mg/M^3)

70
Q

Exposure level types based off american conference of governmental and industrial hygenists

A
  • TLV-TWA :time weighted average over an 8 hour day
  • TLV-STEL: MAx allowable concentration over a 15 min period
  • TLV-c(ceiling)- concentration never to be exceeded
71
Q

Deposition of gases

A
  • water soluble gases absorb quickly into mucus of URT

- other gases (lipophilic) continue into LRT

72
Q

deposition of large particulates

A
  • size is the key property
  • fibers and very large particles (5micrometers in diameter)attach to walls of nasal cavity or the pharynx
  • PM10 (particulate matter)
73
Q

medium particulates

A

(1-5 micrometers) settles in trachea as sediment

-PM2.5

74
Q

small particulates

A

(<1micrometer) go to alveoli

75
Q

nanoparticles

A

(less than 100 nm)lung cancer

76
Q

five cardinal signs of inflammation

A
redness
warmth
swelling
adema
pain
77
Q

immediate responses

A

enlarged blood vessels , accumulation of immune cells, cell death, sneezing, coughing, bronchioconstriction

78
Q

Radical oxygen species

A

free radicals produced by toxicants unstable molecule that contains oxygen and that easily reacts with other molecules in a cell

79
Q

nitric acid

A

produced in lungs using the enzyme nitric oxide synthase
conc. increase because of toxicant exposure
protective or damaging

80
Q

upper airway effects

A

sulfur dioxide

formaldehyde

81
Q

sulfur dioxide

A

swelling and edema in URT
bronchioconstrictor
mucus formation

82
Q

Formaldehyde

A

URT irritant and carcinogen -nasopharyngeal cancer and leukemias
very observable
aggravates asthma,skin problems, irritates eye
1oz ingestion can cause death

83
Q

immediate response lower airway

A

mucus peoduction in alveoli interferes with gas exchange

  • nitrogen dioxide
  • paraquat
84
Q

nitrogen dioxide and ozone

A

oxidants-lipid peroxidation

85
Q

paraquat

A
  • herbicide
  • ends up in lungs no matter what route
  • produces superoxide anions in type 2 respir. epithelial cells
86
Q

Asthma

A

exact cause of signs and symptoms unclear

vasoconstriction

87
Q

Byssinosis

A

brown lung
1 to 2 day delay
cotton dust

88
Q

hypersensitivity pneumonitis

A

very sensitive to allergens
shortness of breathe, fever, chills
exposure to organic materials (mold,fungus)

89
Q

Bronchitis

A

inflammation of bronchial tubes (allergens)

90
Q

Emphysema

A

lungs loose flexibility and cant expand

91
Q

Chronic obstructive pulmonary disease (COPD)

A

smoking or exposure to smoke
cause complex
increase in protease activity

92
Q

Squamous cell carcinoma

A

Cancer caused by an uncontrolled growth of abnormal squamous cells.

93
Q

types of lung cancer

A

squamous cell carcinoma
adenocarcinoma
large cell carcinoma
small cell carcinoma

94
Q

adenocarcinoma

A

cancer that starts in mucus-producing glandular cells of your body(most common)

95
Q

small cell carcinoma

A

A fast-growing type of lung cancer commonly caused by smoking.(most agressive)

96
Q

large cell carcinoma

A

lack the cytologic and architectural features of small cell

97
Q

smoking

A

greatist risk factor
10-20x higher
69 known carcinogens