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PUBH 6011 Final Exam: Key Public Health Concepts, Exams of Biology

A comprehensive overview of key concepts in public health, covering topics such as cell death, genetics, epigenetics, mutations, immunity, toxicology, and drug metabolism. It presents a series of questions and answers that are relevant to the final exam for pubh 6011, offering valuable insights into the course material. Particularly useful for students seeking to reinforce their understanding of fundamental public health principles and prepare for their final exam.

Typology: Exams

2024/2025

Available from 01/11/2025

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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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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

2 /

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

5 /

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

  1. 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

  1. eosinophils: destroy invaders, especially antibody coated parasites
  2. monocytes and macrophages: ingest and destroy invaders, antigen presenta-

tion

56. dendritic cells: recognize pathogen and activate other immune cells by antigen

presentation

7 /

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

  1. 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

14 /

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

  1. 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

16 /

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

17 /

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

19 /

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

  • water quality indicator

20 /

  • 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