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MOD > Chapter 9 Part 1 > Flashcards

Chapter 9 Part 1 Flashcards

1
Q

Definition of global disease burden

A

estimates burden imposed by environmental diseases including communicable and nutritional diseases

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2
Q

Disability adjusted life year

A

sum of years of life lost due to premature mortality and disability

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3
Q

What is the leading global cause of health loss?

A

Undernutrition

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4
Q

What is the leading cause of death in developed countries?

A

Ischemic heart diseases and cerebral vascular disease

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5
Q

What is the leading cause of death in developing countries?

A

Infectious disease

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6
Q

What are the three preventable conditions attributed to nearly 50% of all deaths in kids <5?

A

pneumonia, malaria, diarrheal dz

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7
Q

Key trends in the changing burden of disease?

A

Increase in CV, cancer, HIV/AIDS related deaths, Decrease in neonatal conditions and infectious disease deaths

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8
Q

Definition of emerging infectious disease

A

Infectious disorder whose incidence has recently increased or is expected to increase in the future

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9
Q

Categories of emerging infectious diseases

A

Newly evolved strains, pathogens endemic to other species that have passed to humans, diseases that have been present but are recently increasing

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10
Q

Key ways climate change impacts CV and resp diseases

A

worsened by heatwaves and air polution

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11
Q

Key ways climate change impacts gastroenteritis, cholera, other food and waterborne dzs

A

contamination from flood and disruption of clean water supply

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12
Q

Key way vector-borne infectious dzs are impacted by climate change

A

increase temp, crop failure and more extreme variations in weather increase malaria and Dengue fever

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13
Q

Key way malnutrition impacted by climate change

A

disrupted crop production

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14
Q

Definition of toxicology

A

“science of poisons”, distribution, effects, and mechanisms of toxic agents

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15
Q

Definition of poison

A

quantitative concept dependent on dosage

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16
Q

Definition of xenobiotics

A

exogenous chemicals in environment that may be absorbed into body

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17
Q

What is a key property of solvents and drugs that facilitates their transport in the blood and through plasma membrane?

A

lipophilicity

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18
Q

Phase I reactions of CYPs

A

hydrolysis, oxidation, reduction; make compound water soluble

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19
Q

Phase II reactions of CYPs

A

glucuronidation, sulfation, methylation, conjugation

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20
Q

Primary location of CYP450 enzymes

A

ER of liver, skin, lungs, GI mucosa, and other organs

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21
Q

Main action of P-450 system

A

catalyze reactions to detoxify xenobiotics or to make it into an active metabolite

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22
Q

Factors that decrease CYP activity

A

fasting and starvation

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23
Q

Major pollutants monitored by the EPA

A

sulfur dioxide, carbon monoxide, ozone, nitrogen dioxide, lead, and particulate matter

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24
Q

How is ozone produced?

A

Interaction of UV radiation and oxygen in the atmosphere

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25
Q

What is ground level ozone?

A

gas formed by reaction of nitrogen oxides and volatile organic presents in sunlight, chemicals injure epithelial cells in resp tract and type 1 alveolar cells and release inflammatory mediators

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26
Q

Populations at risk for ozone effects

A

Healthy adults and children (decreased lung fxn and increased airway reactivity), athletes, outdoor works and asthmatics (decreased exercise capacity and increased hospitalizations)

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27
Q

What makes up the “witches’ brew”?

A

ozone and particulate matter/sulfur dioxide

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28
Q

Where is sulfur dioxide released from?

A

power plants that use fossil fuels, copper smelting, and byproduct of paper mills

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29
Q

Clinical symptoms of sulfuric acid and sulfuric trioxide

A

burning in nose and throat, difficulty breathing, asthma attacks

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30
Q

Populations at risk for health effects of sulfur dioxide and effects

A

Healthy adults: increased resp sxs
Individuals with chronic lung disease: increased mortality
Asthmatics: increased hospitalizations, decreased lung functions

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31
Q

What are the main effects of particulate matter inhalation?

A

pulmonary inflammation and secondary CV effects

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32
Q

Carbon monoxide

A

nonirritating, colorless, tasteless, odorless gas produced when there is incomplete oxidation of hydrocarbons

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33
Q

What is the most important environmental source of CO?

A

automotive engines, furnaces, cigarettes

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34
Q

Who is at risk for chronic CO poisoning?

A

People who work in tunnels, underground garages, highway toll booths with high exposures to automobile fumes

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35
Q

Who is at risk for acute CO toxicity?

A

someone in a small, closed garage with a running car or those who use gas-powered generators improperly

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36
Q

How does CO kill?

A

Induces CNS depression and causes widespread ischemic changes esp in basal ganglia and lenticular nuclei

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37
Q

How much Hgb saturation with CO is needed to develop systemic hypoxia?

A

20-30%

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38
Q

How much Hgb saturation with CO is needed to cause unconsciousness and death?

A

60-70%

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39
Q

Permanent neurological sequelae caused by CO?

A

impaired memory, vision, hearing, and speech

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40
Q

Characteristic color change in acute CO poisoning?

A

cherry-red color of skin and mucous membranes

41
Q

Morphological changes in rapidly occurring death due to CO poisoning

A

NONE

42
Q

Morphological changes in longer survival in CO poisoning

A

edematous brain, punctate hemorrhages, hypoxia-induced neuronal changes

43
Q

Common sources of CO in home

A

furnace, water heater, dryer, BB!, stove, car, blocked vents

44
Q

Common symptoms of CO poisoning>

A

headache, dizziness, fatigue, confusion, blurry or double vision, SOB, chest pain, N/V

45
Q

Carcinogen in wood smoke

A

polycyclic hydrocarbons

46
Q

Examples of bioaerosols

A

Legionnaires Dz, viral pneumonia, pet dander, fungi, molds

47
Q

Radon derivative and risk

A

derived from uranium, increases lung CA risk

48
Q

Where is formaldehyde typically found?

A

building materials, esp poorly ventilated trailers

49
Q

What is sick building syndrome and what may cause it?

A

HA, chest infection, chest congestion, nasal congestion; caused by common mold, damp homes

50
Q

How does lead effect the body?

A

binds to sulfhydryl groups in proteins and interferes with calcium metabolism; hematologic, skeletal, neuro, GI, and renal toxicities

51
Q

Common means of Pb exposure?

A

flaking led paint and soil, occupational exposure

52
Q

Where is Pb commonly absorbed?

A

bone and developing teeth, competes with Ca

53
Q

Effects of low levels of Pb

A

subtle deficits in intellect, behavioral problems, hyperactivity, poor organizational skills in kids, brain damage

54
Q

Effects of CNS disturbances due to Pb poisoning in adults?

A

peripheral neuropathies–wrist drop, foot drop

55
Q

Clinical anomalies that occur due to Pb poisoning

A

lead lines, hypochromic mycrocytic anemia, basophilic stippling, and ring sideroblast (Fe laden mt), lead “colic” (poorly localized abd pain), proximal tubule damage and possible failure

56
Q

Level of lead required to decrease Hgb synthesis

A

40 ug/mL

57
Q

Level of lead required for death

A

150 ug/mL

58
Q

Level of lead to see developmental toxicity?

A

10 ug/mL

59
Q

What enzymes does Pb interfere with?

A

delta-ALA dehydratase, ferrochelatase

60
Q

How does mercury effect the body?

A

binds sulfhydryl groups, damage CNS and kidney

61
Q

Main sources of mercury

A

contaminated fish, mercury fapors

62
Q

Minamata disease sxs and cause

A

CP, deafness, blindness, mental retardation, and major CNS defects; caused by methyl mercury in fish

63
Q

Sxs of mercury poisoning

A

gingivitis, tremor, bizarre behavior; muscle weakness, poor coordination, numbness in hands and feet, skin rashes, anxiety, memory problems, trouble speaking

64
Q

How does arsenic effect the body?

A

Interferes with cellular metabolism, toxicities are most prominent in GI tract, nervous system, skin, and heart

65
Q

Main environmental sources of arsenic

A

soil, water, wood preservatives, herbicides, herbal medicines

66
Q

Common sx 2-8 weeks post arsenic exposure

A

sensorimotor neuropathy resulting in paresthesia, numbness, pain

67
Q

Skin changes due to arsenic exposure

A

hyperpigmentation, hyperkertaosis

68
Q

Common CAs from arsenic exposure

A

lungs, bladder, skin (palms and soles)

69
Q

How does cadmium effect the body?

A

Preferentially toxic to kidneys and lungs via mechanisms that cause increased ROS

70
Q

Common sources of cadmium

A

mining, electroplating, production of nickel-cadmium batteries, soil-> food

71
Q

Principle toxic effects of cadmium excess

A

obstructive lung disease, renal tubular damage, skeletal abnormalities

72
Q

Itai-Itai

A

Dz in postmenopausal women in japan due to cadmium-containing water, osteoporosis and osteomalacia associated with renal disease

73
Q

Diseases associated with CO toxicity

A

heart disease

74
Q

Diseases associated with lead toxicity

A

peripheral neuropathies, heart disease, infertility

75
Q

Diseases associated with asbestos

A

lung CA, fibrosis

76
Q

Diseases associated with mercury

A

peripheral neuropathies, ataxic gate, renal toxicity, teratogenesis, female infertility

77
Q

Diseases associated with benzene toxicity

A

leukemia

78
Q

Disease associated with vinyl chloride toxicity

A

liver angiosarcoma

79
Q

Health risks of organic solvents

A

chloroform and carbon tetrachloride in decreasing and dry cleaning agents cause dizziness and confusion, CNS depression and coma

80
Q

Effect of benzene on body

A

broken down by CYP2E1 to toxic metabolites that disrupt differentiation of hematopoietic differentiation, increasing risk of leukemia

81
Q

Polycyclic hydrocarbons

A

come from the combustion of fossil fuels and are implicated in lung, scrotal, and bladder cancers

82
Q

Organochlorines

A

lipophilic products often used as pesticides, disrupt hormone balance

83
Q

Dioxins and PCBs

A

folliculitis and chloracne, characterized by hyperpigmentation, hyperkeratosis and abnormalities in liver and CNS

84
Q

Mineral dusts

A

pneumonconioses, asbestosis, mesothelioma, ferruginous bodies (asbestos coated with iron and Ca

85
Q

BPA

A

potential endocrine disruptor

86
Q

Leading exogenous cause of human cancer

A

tobacco

87
Q

Pack-years = ?

A

ppd x number years smoking

88
Q

Nicotine

A

alkaloid substance in tobacco responsible for addictive properties of tobacco, binds to nAchR in brain stimulates release of catecholamines; responsible for increase HR and BP

89
Q

AE of smoking

A

CA of oral cavity, larynx, esophagus, lungs, pancreas, bladder; chronic bronchitis, atherosclerosis, MI, peptic ulcer

90
Q

Substance in tobacco that cause toxicity to cilia

A

formaldehyde, nitrogen oxides

91
Q

Main effects of agents in smoke

A

inflammation and increased mucus production, leukocyte recruitment

92
Q

Polycyclic hydrocarbons and nitrosamines

A

potent carcinogens involved in development of lung CA

93
Q

Lung CA has a higher incidence in what 2 populations of workers

A

Asbestos and uranium miners (10x higher)

94
Q

Multiplicative interaction of tobacco and alcohol

A

increase risk of laryngeal and oral CAs

95
Q

Effect of tobacco intermediates during CYP reaction

A

may form DNA adducts that cause mutations in oncogenes and tumor supressors

96
Q

Most common diseases caused by cigarette smoking

A

emphysema, chronic vronchitis, COPD

97
Q

Factors that greatly increase MI risk in smokers

A

HTN and hypercholesterolemia

98
Q

Risks associated with maternal smoking

A

spontaneous abortions, preterm births, intrauterine growth retardation

99
Q

Risk of lung CA in exposed nonsmoker compared to unexposed nonsmoker

A

1.3x

MOD (34 decks)

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