NS 1400 Exam 1 Flashcards

1
Q

what are the 4 characteristics of a disease?

A
  1. Disease is a condition of the body, its parts, organs, or systems or an alteration thereof
  2. Results from infection, parasites, nutritional, environmental, genetic, or other causes
  3. Has a characteristic, identifiable, marked group of signs or symptoms
  4. Deviates from normal structure or function
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2
Q

is obesity a disease?

A

yes, meets essential criteria for disease

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3
Q

what is to obesity characterized by?

A

disproportionate body weight for height, owing to an excessive accumulation of adipose tissue

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4
Q

what are the two primary cardio-metabolic health risks of obesity?

A

Type II diabetes and hypertension/cardiovascular disease

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5
Q

what is metabolic syndrome characterized by?

A

excess of accumulation of fat (outside the adipose tissue) that results in several metabolic disturbances

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6
Q

true or false, low triglycerides are associated with metabolic syndrome?

A

false, high triglycerides are a result of the excess accumulation of fat during metabolic syndrome

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7
Q

what are the two direct measurements of body composition?

A
  1. densitometry
  2. dual X-ray absorptiometry
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8
Q

what is the advantage of dual X-ray absorptiometry compared to other composition measurements?

A

it can discriminate across more body compartments including fat, lean mass, and bone

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9
Q

true or false, direct measurements of total body fat are affordable and easily accessible?

A

false, challenging, and expensive

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10
Q

what is a more feasible alternative to direct composition measurement?

A

anthropometry

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11
Q

what are the three anthropometric measurements commonly used for body composition?

A
  1. BMI
  2. anatomical fat deposition
  3. waist to hip ratio
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12
Q

what does BMI measure?

A

relative measure of total body weight to height

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13
Q

true or false, BMI is clinically feasible?

A

true, shown to moderately correlate with directly measurements of body fat

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14
Q

what is the equation for BMI in both kg/m and lb/in?

A

BMI = weight (kg)/height (m)^2

BMI = weight (lbs) / height (in)^2 x 703

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15
Q

what BMI is considered obese?

A

> = 30

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16
Q

does BMI account for the impact of lean muscle mass to total body weight?

A

No

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17
Q

does BMI account for body fat distribution?

A

no

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18
Q

true or false, measurements of waist-to-hip ratio are a better predictor of cardiovascular disease and events than BMI

A

true

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19
Q

what are the two types of adipose tissue distribution?

A

subcutaneous adipose tissue &
visceral adipose tissue

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20
Q

which type of adipose tissue is more concerning towards obesity related health risk?

A

visceral accumulation of fat

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21
Q

where does visceral tissue surround?

A

internal organs

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22
Q

where does subcutaneous tissue lie?

A

under the dermis of the skin

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23
Q

what percentage of total body fat does subcutaneous adipose tissue make up?

A

> 80%

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24
Q

what are the two types of fat distribution?

A

android and gynoid

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25
Q

what is excess central adiposity called?

A

android obeisty

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26
Q

what shape is android obesity associated with?

A

apple shape

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27
Q

what shape is gynoid obesity associated with?

A

pear shape

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28
Q

what is associated with a greater risk of health complications, gynoid or android obesity?

A

android

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29
Q

android obesity is associated with higher/lower intra-abdominal AT and higher/lower subcutaneous AT?

A

higher, lower

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30
Q

what basically causes excessive fat deposition?

A

deviations of energy balance, when amount of energy consumed (calories) is greater than the amount of energy the body expends/requires

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31
Q

describe the negative feedback loop of body weight regulation?

A

senses positive/negative fluctuating in energy balance either nutrient or hormone related. initiates counter response to set off the deviation in energy balance (food intake or alteration in metabolism)

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32
Q

what is the role of the hypothalamus?

A

to receive chemical signals (hormones) and to coordinate a response to those signals

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33
Q

what is the primary site for integrating endocrine signals in the hypothalamus?

A

arcuate nucleus

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34
Q

what are the two types of ARC neurons that regulate food intake and energy balance?

A

orexigenic neurons and anorexigenic neurons

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35
Q

what do orexigenic neurons do?

A

stimulate appetite in the fasted state

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36
Q

what do anorexigenic neurons do?

A

suppress appetite in the fed state

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37
Q

what are the two types of orexigenic neurons?

A

agouti-related peptide (AgRP)

neuropeptide Y (NPY)

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38
Q

what are the two types of anorexigenic neurons?

A

pro-opiomelanocortin (POMC)

a-MSH

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39
Q

neural circuits are regulated by the peripheral cues from where?

A

gut, pancreas, and fat

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40
Q

what hormone is produced in adipose tissue?

A

leptin

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41
Q

what is leptin levels proportional too?

A

fat stores

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42
Q

what neurons does leptin activate and what neurons does it inhibit?

A

directly activates POMC expression and inhibits AgRP/NPY expression

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43
Q

what is the net effect of leptin of food intake and energy expenditure?

A

inhibits food intake and increases energy expenditure

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44
Q

what hormone is secreted in the beta cells of the pancreas?

A

insulin

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45
Q

what does insulin do to neurons?

A

activates insulin receptors on POMC and AgRP/NPY neurons that change neuronal sensitivty

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46
Q

what is the function of insulin?

A

insulin potentates the satiety action of leptin

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47
Q

true or false, gut hormones are short term regulators which have both orexigenic and anorexigenic effects that fluctuate between meals?

A

true

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48
Q

what gut hormone stimulates food intake?

A

ghrelin

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49
Q

what are the three gut hormones that inhibit food intake?

A
  1. glucagon like peptide (GLP-1)
  2. Peptide YY 3-36 (PYY)
  3. Cholecystokinin (CCK)
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50
Q

true or false, most microbes in the body exist in a symbiotic way?

A

true

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51
Q

what are three ways that microbiota can benefit health?

A
  1. detoxify compounds
  2. synthesize vitamins
  3. digest indigestible foods
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52
Q

what can microbiota produce that acts as an additional nutrient source and prevents chronic disease?

A

short chain fatty acids

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53
Q

Total energy expenditure (TEE) is the sum of what three components?

A
  1. resting energy expenditure
  2. thermal effect of food
  3. activity-related energy expenditure
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54
Q

what is resting metabolic rate?

A

energy requirements of the body to maintain vital functions when at rest

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55
Q

what refers to heat production in response to environmental changes?

A

adaptive thermogenesis

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56
Q

what is post-prandial thermogenesis?

A

energy needed to metabolize meals

57
Q

what foods have the highest Thermic effect of food (TEF)

A

proteins, fats have the lowest

58
Q

true or false, energy spent in physical activity makes the largest contribution towards TEE?

A

false, second most but it is the most modifiable component

59
Q

what types of tissue is adipose tissue?

A

connective support tissue

60
Q

what type of adipose tissue is responsible for energy reservoirs?

A

White adipose tissue (WAT)

61
Q

what two types of adipose tissue are responsible for thermogenic centers?

A

brown adipose tissue (BAT) and
beige adipose tissue

62
Q

what is the most abundant type of adipose tissue?

A

White adipose tissue

63
Q

what are three histological features of WAT?

A

small cytoplasm, flattened, non-centrally located nuclei, large fat droplets

64
Q

when energy is abundant what do white adipocytes do?

A

store excess E in the form of triacylglycerol

65
Q

when energy is scare what do white adipocytes do?

A

break down triacylglycerols to FFA and glycerol to generate ATP

66
Q

what are three histological features of brown adipocytes?

A

fat droplets of varying sizes, central nuclei, large cytoplasm, numerous mitochondira

67
Q

what is the least abundant adipocyte?

A

brown adipose tissue

68
Q

why are brown adipocytes important for thermogenesis?

A

rich in uncouple protein 1 and broken down fatty acids generated by BAT are used to generate heat

69
Q

what do BAT generate their color from?

A

high vascularization and high presence of mitochondria

70
Q

what does aging do to beige adipocytes?

A

reduces depots of beige adipose tissue

71
Q

what does obesity do to adipose tissue?

A

expands it

72
Q

what is hypertrophy?

A

increase in cell size

73
Q

what is hyperplasia?

A

increase in cell number

74
Q

is hyperplasia good or bad?

A

good, protective

75
Q

is hypertrophy good or bad?

A

bad, damaging

76
Q

what does expansion of adipose tissue cause?

A

enlarges adipocytes which impede circulation and promotes hypoxia

77
Q

what does hypoxia cause?

A

low oxygen triggers release of pro-inflammatory cytokines and migration of immune cells

78
Q

what happens if hypoxia is not released?

A

adipocytes undergo cell death and excess extracellular matrix proteins accumulate causing scar tissue buildup. This causes loss of normal function

79
Q

what are adipokines?

A

proteins or hormones that regulate a variety of physiological functions

80
Q

when are adipokines produced?

A

in response to anatomical and physiological changes in adipose tissue

81
Q

what type of adipokines does dysfunctional adipose tissue produce?

A

pro-inflammatory adipokines

82
Q

what are the two main effects of pro-inflammatory adipokines?

A

insulin resistance and atherogenesis (vascular remodeling: stroke, myocardial infarction, peripheral artery disease)

83
Q

why is visceral fat the only type that causes increased risk of metabolic syndrome?

A

visceral fat has PRO-inflammatory adipokines and also reduced anti-inflammatory adipokines

84
Q

what is ectopic fat deposition?

A

accumulation of triglycerides in non-adipose tissue

85
Q

what happens to hypertrophied adipocytes?

A

become saturated and cannot store additional fat

86
Q

how does hyperplasia help against harmful ectopic fat?

A

acts as a metabolic sink that prevents lean tissue against fat

87
Q

what does ectopic fat lead to?

A

local cell dysfunction, impaired metabolism, cell death (lipotoxicity)

88
Q

true of false, body weight is highly heritable evidenced by the fact that monozygotic twins have more concordant body weight than that of dizygotic twins?

A

true

89
Q

what is a gene?

A

basic physical and functional unit of hereditary, composed of DNA, that can act as a set of instructions to make proteins

90
Q

what are small differences in the same gene called?

A

alleles

91
Q

what is characteristic of monogenic obesity?

A

single mutation in one gene

92
Q

is monogenic early-onset or delayed onset?

A

early-onset

93
Q

is monogenic obesity severe or normal?

A

severe

94
Q

what are some common behaviors of monogenic obesity?

A

constant hunger, lack of satiety, food seeking behavior, increased food consumption

95
Q

what is polygenic obesity?

A

hundred of variants in or near many genes

96
Q

how to identify polygenic obesity?

A

screening the entire genome in large sample study, identify single nucleotide polymorphism associated with BMI and other obesity traits

97
Q

what are the genome wide association studies?

A

identified >300 genetic loci that confer obesity susceptibility

98
Q

is polygenic obesity severe or common?

A

common

99
Q

what is the name of the 5 stage system of obesity classification that considers metabolic, physical, and physiological parameters to determine optimal obesity treatment

A

Edmonton Obesity Staging System

100
Q

what are the 4 parameters of the system?

A
  • signs of obesity related risk factors
  • physical symptoms
  • physiological symptoms
  • functional limitations
101
Q

what are the three classes of WHO’s obesity scale based on BMI?

A

obese class 1 = 30-35
obese class II = 35-40
obese class III = >40

102
Q

in general what are stage 0 and stage 1 patients parameters?

A

either NO or MILD risk factors, symptoms and limitations

103
Q

what is the treatment for stage 0 & 1?

A

lifestyle intervention, counseling, monitoring health risks

104
Q

in general what are stage 2 patients parameters?

A

pronounced risk factors requiring care, moderation functional limitations or moderate psychological symptoms

105
Q

what is the treatment for stage II?

A

lifestyle intervention, counseling, consideration of behavioral, drug, and surgical options

106
Q

in general what are the parameters of stage 3 and 4 patients?

A

significant end organ damage, severe or grave functional limitations and physiological symptoms

107
Q

what is the treatment for stage 3 and 4?

A

implementation of drug and surgical interventions

108
Q

what are the three lifestyle interventions?

A

first-line therapy, drug therapy, bariatric surgery

109
Q

what are the three components of first line therapy?

A
  1. meal plan
  2. physical activity
  3. behavior
110
Q

is drug therapy best implemented alone or in combination?

A

combination therapy has an additive effect on weight loss and metabolic risks

111
Q

true or false, bariatric surgery is highly effective and reduces long term obesity related mortality?

A

true

112
Q

what are the 4 types of bariatric surgery?

A
  1. gastric sleve
  2. RNY gastic bypass
  3. Gastric banding
  4. duodenal switch
113
Q

which of the 4 types of bariatric surgery are reversible?

A

gastric banding

114
Q

why is weight by age more effective for children?

A

body composition in children varies with age and gender so BMI needs to be expressed relative to other children of the same age and sex

115
Q

how was the patient treated?

A

recombinant leptin administration

116
Q

what were the results?

A

rapid onset reductions in body weight within 2 weeks, sustained over 12 month period

117
Q

why did leptin result in weight loss?

A

exogenous leptin treatment introduces the missing satiety factor.

118
Q

who discovered leptin?

A

Jeffery M. Friedman

119
Q

can leptin administration result in weight loss for individuals without deficiency?

A

no, common obesity is associated with increased serum leptin. Become insensitive to leptin suggesting a defect in LEPR signaling

120
Q

how does leptin induce satiety?

A

LEP directly activated LEPR on POMC neurons to promote aMSH which acts on MC4R to induce satiety

121
Q

how do you define health?

A

the ability to adapt and to self manage in pursuit of physical, mental and social well-being

122
Q

what are the three subclasses of the biological determinants of health?

A
  1. innate
  2. structural
  3. functional
123
Q

what branch of biology studies the innate determinant?

A

genetics

124
Q

what branch of study covers the structural determinant?

A

anatomy

125
Q

what branch of study covers the functional determinant?

A

physiology

126
Q

what are the 4 types of genetic determinants?

A
  1. single gene
  2. chromosomal
  3. multifactorial
  4. mitochondrial DNA linked
127
Q

what are the 4 classifications of diseases?

A

congenital vs acquired
acute vs chronic

128
Q

what are the two categories of acquired disease?

A

communicable & non-communicable

129
Q

what are communicable acquired diseases?

A

includes contagious and non-infectious diseases

130
Q

what are non-communicable diseases?

A

includes non-infectious diseases that develop slowly and persist from several weeks to years

131
Q

what are acute disease?

A

suddenly appear and last short time

132
Q

what are chronic diseases?

A

slow development and is long lasting

133
Q

what are the three main causes of health disparity?

A
  1. poverty
  2. social injsutice
  3. culture
134
Q

what is the premise of economics?

A

allocation of scare resources among competing ends

135
Q

what is opportunity cost?

A

forgone benefit that would have been derived by an option not chosen

136
Q

advantages of using BMI?

A

easy to do, non-invasive, inexpensive, can be readily understood

137
Q

criticism of BMI?

A

almost all work done on male caucasians, does not distinguish between muscle mass and fat, correlation between % body fat and BMI is not perfect, more accurate ways

138
Q

why is there an upward trend in obesity? two views?

A
  1. obesogenic environment (enables weight gain and restricts weight loss)
  2. changes in individual behavior