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ns 1400 > Prelim #1 > Flashcards

Prelim #1 Flashcards

1
Q

Health

A

state of physical, mental, and social well-being; not merely the absence of disease.

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2
Q

Biological Determinants of Health

A

Innate (genetics), Structural (anatomy), Functional (physiology)

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3
Q

Genetics

A

genes, genetic variation, heredity

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4
Q

Anatomy

A

study of structure

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5
Q

Physiology

A

study of functioning

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6
Q

Disease

A

deviation from the normal structural and functional state of an organism; associated with symptoms

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7
Q

Socioecological model

A

individual, interpersonal, organizational, community, public policy

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8
Q

Causes of health disparity

A

poverty & LES, injustice, and culture

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9
Q

Economics

A

study concerning the allocation of resources among competing ends

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10
Q

Opportunity Cost

A

forgone benefit from the option not chosen

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11
Q

Non-biological factors Affecting Health

A

Occupation, Education, Income

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12
Q

LARA

A

Listen, Affirm, Respond, Add info

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13
Q

Obesity Origins

A

19th-century life insurance companies needed to determine what type of people die at what ages.

They used the correlation b/w (Wt/Ht) ratio and life expectancy.

Later on, the correlation b/w subcutaneous fat and (Wt/Ht) ratio called the Quetelet Index became BMI.

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14
Q

BMI Formula

A

(kg/m2) = (lbs/in2)*703

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15
Q

Underweight BMI

A

> 18.5

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16
Q

Normal BMI

A

18.6-24.9

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17
Q

Overweight BMI

A

25-29.9

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18
Q

Obese BMI

A

</= 30

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19
Q

BMI Advantages

A
  • ease of use
  • inexpensive
  • non-invasive
  • easily understood
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20
Q

BMI Criticisms

A
  • predominantly white male population sample
  • does not account for lean mass to total BW
  • %Body fat and BMI correlation not perfect
  • Asian population have risk at lower BMI
  • better methods
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21
Q

BMI Survey

A

NHANES

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22
Q

Obesity Prevalence Trends

A

Sex, race, education, income

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23
Q

% of people obese worldwide

A

13%

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24
Q

% of people obese and overweight

A

39%

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25
Q

Causes of Obesity

A

changes in food systems
- sweet beverages
- cheap fast food
- ease of access
individual behavior
- reduced activity
- less meal prep

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26
Q

Economic Costs of Obesity

A

direct medical costs, economic productivity costs, higher medical premiums

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27
Q

Characteristics of Disease

A

1) organs, systems affected
2) nutritional, environmental, and genetic causes
3) group of symptoms
4) deviates from normal function

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28
Q

Is obesity a disease?

A

meets essential criteria for a disease, ICD code assigned, and increases the risk of other diseases.

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29
Q

Obesity

A

disproportionate body weight for height due to excess accumulation of adipose tissue

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30
Q

Metabolic Syndrome

A

a cluster of symptoms that increase the risk of CVD, stroke, and diabetes.

HIGH BP, HIGH TG, LARGE WAIST, LOW HDL, HIGH BLOOD SUGAR

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31
Q

Diagnosis of Obesity

A

requires body composition assessment

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32
Q

Body Composition Assessments

A

densitometry, image-based methods, anthropometry

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33
Q

Densitometry: Hydrostatic Weighing

A

fat less dense than lean mass; displaces less water

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34
Q

DEXA

A

measures fat, lean mass, and bone. (gold standard)
- informs fat distribution

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35
Q

Direct Measurement Disadvantages

A
  • expensive
  • trained professionals
  • inaccessible
  • invasive
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36
Q

WHR

A

better predictor of CVD

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37
Q

Compartments of Adipose Tissue

A

subcutaneous, visceral

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38
Q

Subcutaneous Fat

A
  • under the dermis of the skin
  • <80% of total body fat
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39
Q

Visceral

A
  • surrounding organs
  • intra-abdominal, perirenal, and pericardial
  • CVD risk increases
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40
Q

Android Obesity

A

increase in intra-abdominal AT, decrease in subcutaneous AT -> altered metabolic profile -> CVD risk increases

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41
Q

Gynoid Obesity

A

increase in subcutaneous AT, decrease in intra-abdominal AT -> normal metabolic profile -> CVD risk decreases

42
Q

1st Law of Thermodynamics

A

Energy is not created nor destroyed: conserved.

43
Q

Energy Balance

A

Intake = Energy Expenditure

44
Q

Deviation from Energy Homeostasis (obesity)

A

low activity, high intake

45
Q

energy intake factors

A

nervous system, endocrine system, microbiota

46
Q

EE factors

A

REE, thermic effect of food, activity-related EE

47
Q

Physiological Influences

A

hunger

48
Q

Sensory Influences

A

seek food & start meal

49
Q

Cognitive Influences

A

keep eating

50
Q

post-ingestive influences

A

satiation: end meal

51
Q

post-absorptive influences

A

satiety: several hours later

52
Q

gut

A

digest and absorbs nutrients (ghrelin)

53
Q

pancreas

A

facilitates digestion and produces insulin

54
Q

adipose

A

releases stored nutrients and releases leptin

55
Q

endocrine network

A

involving peripheral organs and the CNS
- hormones maintain balance between intake and EE

56
Q

negative feedback system

A

food intake is counter-regulated to offset deviation in energy balance

57
Q

hypothalamus

A

control center; receives chemical signals and coordinates a response.
- hunger and thirst
- satiety

58
Q

arcuate nucleus (ARC)

A

primary site for integrating endocrine signals
- orexigenic
- anorexigenic

59
Q

orexigenic neurons

A
  • appetite stimulating in a fasted state
  • AgRP/NPY
60
Q

anorexigenic neurons

A
  • appetite suppressing in a fed state
  • POMC/ α-MSH
61
Q

Leptin

A

adipose hormone released proportional to fat stores
-> inhibits AgRP/NPY and activates POMC
-> inhibits food intake and increases EE

62
Q

Insulin

A
  • pancreas hormone that regulates glucose homeostasis
  • binds to ARC and changes neuronal sensitivity
  • potentiates satiety action of leptin
63
Q

Ghrelin

A
  • produced by stomach to stimulate food intake
  • activates AgRP/NPY
64
Q

Intestine Hormones & Function

A
  • GLP-1, PYY, CCK
  • inhibit food intake in fed state
65
Q

Microorganisms

A
  • trillions
  • most are symbiotic
  • benefit health: detoxify compounds, make Vit, yield SCFA’s
66
Q

Total Energy Expenditure (TEE) is a sum of:

A

1) Resting EE
2) Thermic effect of food
3) Activity-related EE

67
Q

Resting EE

A
  • RMR -> energy requirements of body
  • Thermogenesis -> heat produced due to environment
68
Q

Thermic Effect of Food

A

post-prandial thermogenesis -> energy needed to metabolize food
-> Protein: highest TEF 20-30%
-> Fat: lowest TEF 0-3%

69
Q

Activity-related EE

A
  • non-exercise, exercise
  • second-largest contribution to EE
  • most modifiable component
70
Q

Adipose Tissue Functions

A
  • Binding, Protection, Storage
71
Q

Adipose Tissue Types

A

WAT, BAT, Beige

72
Q

WAT

A
  • energy reservoir
  • most abundant
  • maintains energy homeostasis
  • acts as endocrine organ
73
Q

BAT

A
  • thermogenic center (generates heat)
  • least abundant
  • important for EE
  • lots of mitochondria
74
Q

Beige AT

A
  • energy storage and thermogenic based on environment
  • aging reduces Beige AT
75
Q

Healthy AT

A
  • vascularization
  • 60-70% AT, immune cells
  • O2 increase, inflammation decrease
76
Q

hypertrophy

A
  • increase in size
  • deleterious
77
Q

hyperplasia

A
  • increase in number
  • protective against ectopic fat deposition
78
Q

hypoxia

A

enlargement -> O2 down, Inflammation up
-> chronic low-grade inflammatory state

79
Q

Fibrotic AT

A
  • AT undergo cell death -> loss of normal function
80
Q

Adipokines

A

proteins/hormones that regulate function
- paracrine local effect
- endocrine distant effect

81
Q

adipokine pathway

A

dysfunctional AT -> pro-inflammatory adipokine
-> atherogenesis & insulin resistance

82
Q

Why is only intra-abdominal fat accumulation associated with metabolic syndrome?

A

Pro-inflammatory adipokines are produced.

83
Q

Ectopic fat deposition

A

accumulation of TG in non-adipose tissue -> dysfunction, impaired metabolism, lipoxicity

84
Q

AT Impact on organ function

A

greater pharyngeal soft tissue, mechanical load on joints, intra-abdominal pressure

85
Q

Adiposity Increase (Pathways)

A

adipokine synthesis -> pro-inflammatory cytokines -> insulin resistance -> type II diabetes -> CVD
-> lipid production
-> mechanical stress
-> metabolic syndrome

86
Q

Genetics of Obesity

A
  • 70% of BW due to genetic makeup
  • MZ twins more similar in BW
87
Q

gene

A

unit of heredity
- every person has two copies of each gene

88
Q

Monogenic Obesity

A
  • mutation in one gene
  • rare
  • characterized by early-onset obesity
  • predominantly hyperphagic condition (hungry)
89
Q

Polygenic Obesity

A
  • SNP associated with obesity traits
  • GWAS identified >300 genetic loci (small impact)
  • FTO gene variants have largest, but overall small effect on obesity
90
Q

EOSS

A

five stage system of obesity

91
Q

Stage O (NO risks)
Stage 1 (Existing Risk)

A

lifestyle intervention

92
Q

Stage 2 (Pronounced Risk)

A
  • lifestyle intervention
  • consider behavioral, drug, and surgical
93
Q

Stage 3 (Significant End Organ Damage)
Stage 4 (Chronic Disease)

A
  • lifestyle intervention
  • drug and surgical interventions
94
Q

First Line Therapy

A

Lifestyle intervention
- meal plan, physical activity, behavior

95
Q

Drug Therapy

A
  • adjunct to lifestyle changes
  • combination has additive effect
  • decreases appetite by mimicking GLP-1 (Wegovy, Ozempic)
  • also for concurrent complications
96
Q

Bariatric Surgery

A
  • anatomical manipulation -> restrict size and nutrient absorption
    sleeve (50-80%)
    bypass (60-85%)
    banding (40%)
    duodenal switch (75-90%)
97
Q

Case Report

A

description of individual report.
- unusual or novel occurance

98
Q

Children BMI

A

expressed by same age and sex
5, 5-85, 85-95, 95

99
Q

Body habitus

A

physical characteristics of body

100
Q

Results of Case Study

A

Rapid Onset, sustained for long period

101
Q

Does leptin result in weight loss for common obesity?

A

No. Obesity associated with increased leptin
- may cause leptin resistance

ns 1400 (1 decks)

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