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Pathopharmacology > Unit 2 Pathophysiology - Chapter 13 Cancer epidemoiology > Flashcards

Unit 2 Pathophysiology - Chapter 13 Cancer epidemoiology Flashcards

1
Q

Dietary factors

A

r/t cancer development; how it interacts w/ genomics, epigenomics, transcription factors, proteomics (proteins), and metabolic factors => nutrigenomics

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2
Q

What can influence risks of developing cancer and other diseases?

A

What you eat, weight, and how much they move!

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3
Q

Food components w/ cancer preventing potential

A
  • polyphenols
  • selenium
  • methyl group donors
  • retinoids
  • isothiocyanates
  • allyl compounds
  • mono- , poly- unsaturated fatty acids
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4
Q

Source of carcinogenic substances

A

cooking fat, meat or protein
plants - alkaloids or mold byproducts

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5
Q

Dietary components as mutagens?

A

Some components can act directly as mutagens or interfere w/ mutagen elimination

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6
Q

Dietary factors can affect what specfically?

A

cell cycle, differentiation, DNA damage and repair, stem cell renewal, hormonal axes, cellular proliferation, and cell death, cell signaling/inflammation/immunity

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7
Q

Xenobiotics

A

toxic, mutagenic, and carcinogenic chemicals found in human diet

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8
Q

What other food and nutrition tips can change carinogen metabolism?

A

sulforaphane (Sulforaphane is found in cruciferous vegetables like broccoli, cauliflower, and kale. It may offer anticancer, antidiabetes, and other benefits.) and isoflavonoids (Evidence suggests that eating a diet rich in soy foods may offer protection against certain cancers and cardiovascular disease. Isoflavones also appear to play a role in preventing bone loss — legume seeds or lentils, beans, peas)

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9
Q

Diets high in red meat and processed meat

A

colorectal cancer; N-nitroso compounds can increase nitogenous residues in colon and cause DNA damage

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10
Q

Undernutrition

A

factor in cancer d/t infectious agents

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11
Q

Obesity at risk for?

A

At risk for liver, advanced prostate, ovarian, gallbladder, kidney, colorectal, esophageal (adenocarcinoma), postmenopausal breast, pancreatic, endometrial, and stomach cancer.

lower body fatness lowers cancer risk for thyroid and multiple myeloma

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12
Q

3 main factors r/t to obesity and cancer

A

insulin-insulin-like growth factor axis, sex hormones, and adipokines (cytokines produced by adipose)

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13
Q

Obseity and metabolic changes

A

insulin resistance, hyperglycemia, dyslipidemia, hypoxia, anad chronic inflammation

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14
Q

Adipocyte dysfunction and obesity

A

secretions of abnormal levels of cytokines linked to insulin resistance, impairments in triglyceride storage and increases in lipolysis

adipocyte function as endocrine cells (alpha cells which secrete glucagon, beta cells which secrete insulin, and delta cells which inhibit the secretion on glucagon and insulin) and shape tumor microenvironment

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15
Q

Obesity and immune cell recruitment

A

increased cytokine production, inflammation, and fibrosis and reduced response to chemotherapy

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16
Q

obesity and aromatase expression

A

Aromatase is an enzyme that converts androgens into estrogens,

increased estradiol levels, promote growth of estrogen-dependent cancers

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17
Q

Warburg effect

A

tumors consume tons of glucose => to make cellular building blocks

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18
Q

Food metabolism and circadian cycles

A

linked; impairment of clock dysregulates metabolism

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19
Q

Alcohol and cancer

A

mouth, pharynx, esophagus, and liver; colorectal cancer in men and postmenopausal breast cancer

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20
Q

Factors that l/t alcohol-induced cancer developmetn

A

acetaldehyde (broken down from ETOH), oxidative stress, nutritional deficiency (folate and vitamin B)

21
Q

Abberrant patterns (deviating) of DNA methylation

A

contribute to alcohol-induced carcinogenesis

22
Q

Physical activity

A

reduce risk of breast cancer, colon cancer, and endo metrial cancer

23
Q

Other protective effects of exercise

A

decrease insulin, IGF levels (aging)
* decrease obesity
* increase free-radical scavenger systems
* change inflammatory mediators
* decrease oncogenes
* decrease metabolic hormones and circulating sex hormones
* improve immune fx
* enhance cytochrome p-450 fx (detoxification and metabolism of foreign material and drugs) => modify carcinogen activation and increase gut motility

24
Q

Exposure to outdoor air pollution and to particulate matter (PM in outdoor air

A

carcinogenic to humans and causes lung cancer; fine or ultrafine particles absorbed by lungs and phagocytosed by macrophages and neutrophils that release tissue-damaging inflammatory mediators

25
Q

Mechanisms of adverse cellular effects d/t PM particulate matter

A
  • cytotoxicity via oxidative stress
  • ROS generation
  • DNA oxidative damage
  • mutagenicity (ability to induce mutagens)
  • stimulation of proinflammatory factors
  • induce cell senescence (eventually stop multiplying, don’t die off)
26
Q

Indoor air pollution environmental tobacco smoke (ETS; passive smoking)

A

form reactive oxygen free radicals and thus DNA damage; ETS => human carcinogen

27
Q

2012 Diesal exhaust

A

carcinogen as well

28
Q

Central hypothesis for cancer pathogenesis via respiratory

A
  1. insoluble particles => pulmonary inflammation
  2. oxidative stress
  3. oxidation of DNA
  4. proliferative response => tissue remodeling via fibrosis
  5. tumor development
29
Q

Atomic bomb exposure in japan

A

acute leukemias in adults and children; increased thyroid and breast carcinomas including lung, stomach, colon, esophageal, and urinary tract cancers + multiple myeloma

30
Q

Ionizing radiation (IR) in radiation carcinogenesis

A
  • initiator of premaligant cell clones
  • promoter of preexisting premalignant cell alterations
31
Q

Ionizing radiation

A

mutagen and carcinogen => penetrate cells and tissues and deposit energy in tissues @ random in form of ionizations

32
Q

Exposure to ionizing radiation induces?…

A

apoptosis and senescence; evident in endothelial cells and radiation induced CV disease

33
Q

innocent bystander cells

A

radiation may induce type of genomic instability to progeny of directly irradiated cells over many cell generations

34
Q

Epigenetic events after radiation

A

altered pathways:
* cell adhesion
* extracellular matrix interactions
* cell-to-cell communication

35
Q

Sun and UV radiation

A

basal cell carcinoma and squamous cell carcinoma

36
Q

Intermittent acute sun exposure l/t

A

sunburn associated w/ increased risk of melanoma

37
Q

degree of damage in skin

A

intensity and wavelength content - ultraviolet A (UVA) or ultraviolet B (UVB)

38
Q

Pathogenesis of nonmelanoma skin cancers

A

involves:
* specific gene mutations
* DNA methylation and histone modifications
* oxidative stress
* inflammation
* reduced immune surveillance

39
Q

Inflammation and ROS

A

ROS can induce # of transcription factors:
* activator protein 1 [AP-1]
* NF-KB

and increasea regulating genes that induce inflammation => critical in tumor progression

40
Q

EMR controversey

A

non ionizing and low-frequency radiation

41
Q

Radiofrequency-EMF

A

Electromagnetic field

possibly carcinogenic to humans
* genotoxicity
* impaired immune
* gene and protein expression
* cell signaling
* oxidative stress
* apoptosis
* blood-brain barrier

42
Q

Certain viruses, bacteria, and parasite

A

main contributor to cancer worldwide (15.4% in 2012)

43
Q

Helicobacter pylori (H pylori), human papillomavirus (HPV), hepatitis B virus (HBV), hepatitis C (HCV), and Epstein-barr virus (EBV)

A

top notable infection and cancer cases

EBV => affect a person’s blood and bone marrow. The virus can cause the body to produce an excessive number of white blood cells called lymphocytes (lymphocytosis). EBV can also weaken the immune system

44
Q

Large majority of liver cancer diagnoses

A

Hepatitis B and hepatitis C

45
Q

Reproductive tract viral infection

A

HPV; most for both genders will be infected at some point and may be repeatedly infected

46
Q

75% of stomach cancer

A

H. pylori

47
Q

EBV

A

associated w/ subset of hodgkin lymphoma (white blood cells called lymphocytes grow out of control, causing swollen lymph nodes in neck, chest, or armpits, and growths throughout the body) and burkitt lymphoma (non-Hodgkin lymphoma, cancer of lympathic system, makes abnormal B lymphocytes, start anywhere in the body)

If a specific type of cell called a Reed-Sternberg cell is seen, the lymphoma is classified as Hodgkin’s. If the Reed-Sternberg cell is not present, the lymphoma is classified as non-Hodgkin’s. Many subtypes of lymphoma exist.

48
Q

HPVs

A

13 are cancer causing; types 16 and 18 - high risk or oncogenic cause 70% of cervical cancers and precancerous cervical lesions

also linked w/ anus, vulva, vagina, and penis cancer
infection w/ HPV-16 precedes several years diagnosis of oropharyngeal cancer

49
Q

Factors that inc risk for cancer following high-risk HPV infection

A

smoking, decreased immunity, having multiple children, long-term oral contraceptive, poor oral hygiene, chronic inflammation

Pathopharmacology (99 decks)

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