Download PUBH 6011 Final Exam: Key Public Health Concepts and more Exams Biology in PDF only on Docsity!
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PUBH 6011 final Exam
Questions with Correct
Answers.
1. Two types of cell death: apoptosis: programmed cell death
necrosis: cell damage and death
2. Virus vs bacteria: virus: only active within host cells which they need to repro-
duce bacteria: single-celled organisms that produce own energy and can reproduce on their own
3. DNA base pairing: A-T
G-C
4. DNA strands held together by...: hydrogen bonds
5. DNA to protein: DNA encodes the sequence of proteins carried in DNA
6. Gene: DNA coding (for protein, for trait)
7. Protein functions: structural support, storage, transport, cellular communica-
tions, movement, and defense against foreign substances
8. Protein sequence: determines how protein will fold
9. Protein structure: determines function
10. Enzyme: enhances rate of chemical reaction in body; catalysts, so not used up
in reaction
11. Process of DNA to protein: DNA > transcription > RNA > transcription > protein
12. Genome: all of an organism's genetic material
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13. Epigenetics: the study of influences on gene expression that occur without a
DNA change determines which genes are expressed
14. Epigenetics results in: heritable changes in the phenotype without changes to
DNA sequence/structure (genotype)
15. Can epigenetic modifications be transferred from generation to genera- tion?:
YES
16. Three mechanisms of epigenetics: 1. DNA methylation
2.histone modification
3.micro-RNAs
17. DNA methylation: adding a methyl group to DNA to switch off the gene
possible connection between DNA methylation of 5 genes and PM 2.
18. Histone: protein molecule around which DNA is tightly coiled in chromatin
19. Histone modification: changes in the structure of histones that make it more
or less likely that a segment of DNA will be transcribed acetyl group allows for transcription
20. Epigenetic factor that binds to histone tail: acetyl group; allows for transcrip- tion
21. Micro-RNAs: bind to complementary RNA to prevent translation
22. Mutation: heritable changes in genetic information
genotype change
23. Microlesions: base pair substitution
24. 2 types of microlesions: change in DNA sequence
change in codon (if coding region)
25. Change in codon - 3 outcomes: no effect = degenerate code
missense mutation = change amino acid, sometimes function
4 / can change function of proteins
36. Health effects of mutation: germ cells/ova: point mutations may be lethal
somatic cells: source of variability (polymorphism); concern = carcinogenesis
37. How does cancer arise?: DNA mutations in cells
uncontrolled proliferation
38. Proto-oncogene mutation: leads to altered forms of normal cellular genes
39. tumor suppressor gene: mutation
can promote apoptosis can act as "brake" to regulate proliferation of normal cells
40. Genotoxic compounds: directly alter DNA
point mutations chromosomal aberrations
41. point mutation: gene mutation in which a single base pair in DNA has been
changed
42. nongenotoxic compound: do not directly alter DNA but can increase cancer
risk increase chance of replication errors and increase number of cells at risk
43. cancer types with highest mortality in US: women: lung, breast, colon
men: lung, prostate, colon
44. innate immunity: - immunity that is present before exposure and effective from
birth
- responds to a broad range of pathogens physical barriers help prevent entry 0-12 hours after infection -- immediate
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45. adaptive immunity: - the ability to recognize and remember specific antigens
and mount an attack on them detects molecules (usually proteins) on surface of cells and learns to ignore self proteins delayed
46. non-self proteins: antigens, substance that can promote immune response
- what type of cell makes antibodies?: B lymphocytes
can there be multiple antigens on one pathogen?: YES
49. antigen: a toxin or other foreign substance that induces an immune response
in the body, especially the production of antibodies
50. antibody: a substance produced by the body that destroys or inactivates an
antigen that has entered the body
51. Antigen reaction: - a decrease in BP
- a release of epinephrine and norepinephrine from the adrenal medulla
- an increase in the Heart Rate and vasoconstriction occurs
- an increase in the BP
52. basophils and mast cells: release chemicals that mediate inflammation and
allergic responses
53. neutrophils: ingest and destroy invaders
- eosinophils: destroy invaders, especially antibody coated parasites
- monocytes and macrophages: ingest and destroy invaders, antigen presenta-
tion
56. dendritic cells: recognize pathogen and activate other immune cells by antigen
presentation
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65. mechanistic study: answers "How does this system work?"
study of potential modes of action in lab animals (in vivo) or tissues, cells, etc (in vitro)
66. in vivo studies in tox: ADME studies
effect of different dosing levels
67. in vitro studies in tox: mutagenic potential
molecular mechanisms of action
68. strengths and weaknesses of mechanistic studies: strengths: com-
pound-specific information, cross-species extrapolation, dose extrapolation weaknesses: difficult to rule out alt theories; often lack data for humans
69. dose-effect relationship: the relationship between drug dose and blood, or
other biological fluid concentrations
70. dose-response relationship: the relationship between the different doses and
the responses they generate
71. how is toxicity quantified?: dose-effect and dose-response relationships
72. LD50: the point at which 50 percent of the test organisms die from a
toxin lethal dose in mg/kg used to compare relative acute toxicity
73. LC50: concentration of a substance needed to kill 50% of the organisms within
a specified period of time lethal concentration in ppm or mass/volume
74. ADD: average daily dose
75. ADD formula: C x IR / BW = average daily dose in mg/kg/day
8 / C= concentration IR= intake rate BW= body weight
76. NOAEL and LOAEL: No Observed Adverse Effect Level
Lowest Observed Adverse Effect Level
77. CSF: cancer slope factor
0.10/LED
provides estimate of increase in cancer risk per mg/kg/day of ADD
78. rise and run in CSF: rise: 10% increase in risk
run: dose associated with that risk increase
79. interpretation of CSF: if CSF = 1.5 x 10^- 3
if I have exposure to chemical at 1mg/kg/day ADD for a lifetime, my risk of cancer increases by 0.001 from background risk
80. acute toxicity and exposure pattern/level: adverse effects that occur within a
short period after exposure to a toxicant rapid effects, usually after one dose, including death, CNS effects, irritation
very high on dose/effect relationship
81. chronic toxicity and exposure pattern/level: adverse effects that occur some time
after exposure to a toxicant or after extended exposure to the toxicant result of prolonged exposure, usually lower dose than acute, can lead to organ damage, cancer...
82. local toxicity vs systemic toxicity: local: toxic effect occurs at site of exposure
systemic: requires absorption of toxicant into body, then distribution (usually via bloodstream) to organs where toxic effect occurs
10 / like dissolves like
91. distribution (ADME) + 3 things that influence it: is the process by which the drug
becomes available to body fluids and tissues. directly influenced by: blood flow drug affinity to tissue protein binding effect.
92. metabolism (ADME): enzymatic alteration of the chemical structure of a mole-
cule, usually to make them easier to excrete
93. two primary systems for elimination: phase I reactions and phase II reactions
94. Phase I reactions + result: oxidation, reduction, or hydrolysis of drug
- add polar groups
- overlapping specificity of Phase I enzymes result: converts to more polar molecule and is more reactive
95. Phase II reactions + results: conjugation reactions make molecules bigger by
adding on other large molecules
- increase water solubility >>> increase biliary or urinary excretion
- enzymes inducible reactions that increase water solubility by conjugation of the drug molecule
96. 4 reasons we care about metabolism in tox: 1. it changes amount of chemical
present in body
2.influences rate of excretion
3.can make a molecule more or less toxic
4.rates can vary between individuals and populations
97. Excretion (ADME): process in which drug elimination, mainly through the kid-
11 / neys(urine).
13 / latency irreversible lesions become dependent of dose cancer = NONTHRESHOLD example: more exposure to benzene does not mean the cancer you may get will be worse, it just increases your chances of getting the cancer in the first place
108. threshold dose response model: a threshold dosage must be reached before
any detectable harmful effects occur
109. threshold: often short
latency often reversible lesions may be dependent of dose severity depends on dose assumption for non-cancer = THRESHOLD
110. 2 types of exposure assessments: 1. measured: more precise, $$$$, source
must be present
- modeled: rely on models, require assumptions, allow better incorporation of time in exposure estimates
111. exposure pathway examples: ingestion of soil, water, food, or particles; in-
halation of air or particles; dermal contact with soil, sediment, water, or air
112. IARC Carcinogen Classification: 1: carcinogenic to humans
2A: probably carcinogenic to humans 2B: possibly carcinogenic to humans 3: not classifiable 4: probably not carcinogenic
113. Non-cancer risk assessment: 1. identify available data
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2.evaluate endpoints and dose-response relationships
3.choose critical effect in critical study (one sex, one species, one outcome;
usually most sensitive)
4.identify POD for critical effect
114. Point of Departure (POD): non-cancer risk estimates build from POD on
dose-response curve dose-response point that marks the beginning of a low-dose extrapolation
115. non-cancer risk estimates build from a .....: point of departure on the
dose-response curve
116. 2 approaches to setting POD: 1. NOAEL
- benchmark dose
117. Benchmark Dose Approach: begins with dose at "benchmark" levels of re-
sponse instead of NOAEL uses dose-response modeling to try to estimate a place to start non-cancer risk assessment process: identify dose at "benchmark" response and apply appropriate uncertainty factors to benchmark dose LED10 - lowest effective dose causing response in 10% of animals ED10 - effective dose causing response in 10% of animals
118. uncertainty factor approach: trying to figure out which dose is safe for hu-
mans; used to derive RfD; usually a factor of 10 as "usual uncertainty factor" take POD (NOAEL or BMDL10) and divide by appropriate UF
usual UF = 10
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126. freshwater: does not contain any saltwater and can be rivers,
lakes, streams,ponds, and wetlands
127. groundwater: water that fills the cracks and spaces in underground soil
and rock layers
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128. Surface water flow: runoff stays above ground when surface is not porous
or precipitation falls fast
129. Clean Water Act (CWA): 1972; set maximum permissible amounts of
water pollutants that can be discharged into waterways; aims to make surface waters swimmable and fishable
130. NPDES (National Pollutant Discharge Elimination System): set water qual- ity
standards for surface waters
131. point source pollution: pollution that comes from a specific site
primarily from industrial sources and WWT plants
132. CSO: Combined Sewer Overflow
when volume of wastewater overwhelms plant, water may be discharged directly via CSO untreated
133. how are point sources regulated?: CWA requires permit from NPDES
134. Safe Drinking Water Act (SDWA): 1974; set maximum contaminant levels
for pollutants in drinking water tha may have adverse effects on human health
135. National Primary Drinking Water Regulations (NPDWR): legally enforceable
health standards for public drinking water supplies that are implemented uniformly primary standards
136. National Secondary Drinking Water Regulations (NSCWR): nonenforce-
able guidelines that include cosmetic and aesthetic effects, incl. taste secondary standards
137. CCL: contaminant concern
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146. household water treatment options (4): - chlorination-Safe Water Systems
(SWS)
- combined flocculent/ disinfectant
- ceramic and biosand filtration
- solar/SODIS, boiling
147. WASH: water, sanitation, hygiene
148. MDG (Millennium Development Goals) Goal 7: ensure environmental sus-
tainability, incl. halving proportion of people w/o sustainable access to drinking water and basic sanitation
149. improved drinking water source: piped water, public tap, protected dug
well, protected spring, rainwater
150. improved sanitation: flush or pour-flush to piped sewer system, septic
tank, pit latrine
151. how does availability of water affect health?: significant increase in illness
risk in people living far from water source
152. non-point source pollution: water pollution that does not have a specific
point of origin not regulated under NPDES ex: bacteria, virus
153. primary nutrients of concern in NPS pollution: nitrogen and phosphorus
help plants grow, but if too high can lead to eutrophication (algae bloom) >> ANOXIA/DEAD ZONE
154. Biological Oxygen Demand (BOD): tests nutrients in water
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- the amount of oxygen used by microorganisms in aerobic oxidation
- lower is better; raw sewage = 800 mg/L; river usually below 1 mg/L
- can lead to hypoxia or anoxia/dead zones
155. why do marine dead zones develop?: NPS pollution
156. wastewater treatment stages: Primary treatment, Secondary Treatment, Ter-
tiary (Advanced) Treatment
157. primary treatment of wastewater: the removal of large particles and organic
materials (up to 60% of solids) from the wastewater by using a screening process
158. secondary treatment of wastewater: removes up to 90% of the oxygen-de-
manding wastewater, by degrading the waste aerobically using oxygen and bacteria
159. Tertiary treatment of wastewater: removal of inorganic minerals and plant
nutrients (nitrates) after primary and secondary treatment of sewage (expensive process, but increasingly necessary)
160. Key Waterborne Disease Agents: protozoa -- can exist as cysts, resistant to
disinfection; ex = giardia bacteria -- mostly from sewage; ex = typhoid, cholera, e. coli virus -- norovirus, polio, viral hep A other -- arsenic, nitrate, pesticides, DBPs
161. fecal-oral route: feces > fluids, fingers, flies, fields, floors > food >
ingested by human
162. preventative measures for fecal-oral transmission: sanitation, clean water
supply, hygiene/hand washing effectiveness point of use water treatment: 30-50% reduction in child DD safe storage: 21% reduction hand washing with soap: 43% reduction
