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NUTR-455 > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

What is the main energy source: Brain (CNS)

A

Glucose, ketone bodies

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2
Q

What is the main energy source: red blood cells

A

glucose

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3
Q

What is the main energy source: skeletal muscle

A

glucose
ffa
tag

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4
Q

What is the main energy source: adipose tissue

A

glucose

tag

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5
Q

What is the main energy source: liver

A 
amino acids
ffa
lactate
glycerol
glucose
ethanol
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6
Q

Review what hapens to glucose, fat, and protein metabolism throughout the various stages

A

okay

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7
Q

How does insulin affect: glycolysis

A

inhibits

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8
Q

How does insulin affect: gluconeogenesis

A

promotes

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9
Q

How does insulin affect: glycogenesis

A

promotes in muscle and liver

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10
Q

How does insulin affect: glycogenolysis

A

inhibits in muscle and liver

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11
Q

How does insulin affect: amino acid uptake

A

inhibits in muscle

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12
Q

How does insulin affect: lipoprtein lipase

A

promotes in adipose

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13
Q

How does insulin affect: lipolysis

A

inhibits in adipose

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14
Q

fatty acid beta oxidation is inhibited by this

A

high glucose

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15
Q

Increases in AMPK in the liver lead to these 3 things

A

decreased FA synth
decreased cholesterol synth
decreased gluconeogenesis

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16
Q

increases in AMPK in the muscle leads to this

A

increased glucose uptake

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17
Q

This stimulates AMPK

A

Increases in AMP

Decreases in ATP

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18
Q

This compound is a key building block for FA synth

A

malonyl CoA

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19
Q

this compound inhibits carnitine:palmitate transferase-2

A

malonyl CoA

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20
Q

Formation of malonyl CoA is inhibited by

A

AMPK

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21
Q

Can fatty acids be converted to glucose

A

No

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22
Q

Role of ketogenesis in the fed state

A

Nonexistent to limited

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23
Q

role of ketogenesis in the post-absorptive state

A

Nonexistent to limited

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24
Q

Role of ketogenesis in the fasting state

A

ketones begin to be used as an energy substrate after prolonged fasting

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25
Q

Role of ketogenesis in the starvation state

A

ketone concentration remains the same as prolonged fasting, but makes up a greater percent of the energy substrate for the brain ect

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26
Q

This compound is used in energy production, fat synthesis, cholesterol synthesis, and ketone body formation

A

Acetyl CoA

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27
Q

How do amino acids contribute to energy production

A

They are coverted to gluconeogenic substrates, and ketonic substrates (leucine, lysine) to form substrates which are usable in energy production

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28
Q

energy sources during exercise (order)

A

atp-cp
lactic acid system
aerobic system

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29
Q

Exercise increases insulin sensitivity due to this

A

activation of AMPK

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30
Q

this system is used in high-intensity, short duration activites (

A

Cp-ATP system

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31
Q

This system is used in high-intensity, relatively short duration activities (1-3min)

A

lactic acid system (anaerobic)

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32
Q

This system is used in low-intensity, longer term activities (>3 min)

A

aerobic

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33
Q

these are the 4 fuel sources used during exercise

A

muscle glycogen
plasma glucose
plasma fatty acids
intramuscular triacylglycerols

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34
Q

This intensity level uses muscle TAG and plasma FA

A

low intensity (2-30% VO2max)

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35
Q

this intensity level uses increased FA OX mostly due to muscle TG

A

moderate (~65%VO2max)

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36
Q

This intensity level uses increased CHO ox and shows an increase in lactate production

A

high (85% VO2max)

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37
Q

Metabolic adaptations to exercise training: aerobic training

A

increased ability to perform more work at the same exercise intensity

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38
Q

4 examples of physiological training adaptations

A

increased muscle mitochondria density
increased capacity to store muscle glycogen
increased oxygen uptake and transport
increased fat utilization

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39
Q

this substrate is used much more in trained vs untrained individuals

A

intermuscular triglycerides

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40
Q

this supstrated is used much less in trained vs untrain individuals

A

carbohydrates

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41
Q

Maximal fat oxidation occurs at this %VO2max

A

65%

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42
Q

How does CHO intake affect exercise/sport performance

A

if increases in glycogen stores are seen than it can increase the duration of exercise

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43
Q

Released by a fall in plasma sodium, chloride, ECF volume, or blood pressure

A

renin

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44
Q

what releases renin

A

afferent glomerulus

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45
Q

renin activates this enzyme

A

angiotensinogen

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46
Q

activated form of angiotensinogen

A

angiotensin 1

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47
Q

this converts angiotensin I to angiotensin II

A

angiotensin-converting enzyme

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48
Q

Angiotensin II stimulates these two tissues

A

hypothalamus

adrenal cortex

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49
Q

This is released by the hypothalamus in response to angiotensin II

A

vasopressin

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50
Q

vasopressin does this

A

increases water retention in the kidney

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51
Q

this is released by the adrenal cortex in response to angiotensin II

A

aldosterone

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52
Q

Aldosterone does this

A

increases sodium retention and potassium excretion in the kidney

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53
Q

What is the effect of the renin-angiotenstin aldosterone system on blood pressure

A

blood pressure is increased

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54
Q

What is vasopressing

A

a hormone that acts as a anti-diuretic

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55
Q

How do natriuretic peptides affect blood pressure

A

lower blood pressure by lowering cardiac output and reducing peripheral vascular resistance

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56
Q

natriuretic peptides lower blood pressure by doing this

A

promoting sodium and water excretion

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57
Q

in which part of the nephron are electrolytes reabsorbed

A

ascending loop of henly

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58
Q

in which part of the nephron is water reabsorbed

A

decending loop of henly

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59
Q

How does Na affect blood pressure

A

sodium increases blood pressure

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60
Q

how does K+ affect blood pressure

A

lowers blood pressure

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61
Q

These 3 systems regulate pH

A

Buffer system
Respiratory center
Renal regulation

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62
Q

3 dietary treatments for high blood pressure

A

lower sodium intake

increase potassium and vit d intake

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63
Q

How does the kidney regulate acid-base 3balance

A

long term control of bicarb system
secretion of H+
synthesizing ammonium ions

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64
Q

pH of urine

A

5.5-6.5

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65
Q

Formula for calculation of BMI

A

(weight in kg)/(height in m)^2

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66
Q

lbs to kg

A

lbs/2.2

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67
Q

inches to cm

A

inches x 2.54

68
Q

underweight bmi

69
Q

normal weight bmi

70
Q

overweight bmi

71
Q

obese bmi

72
Q

mobidly obese bmi

73
Q

Body weight: a change in this reflects this

A

weight

energy balance

74
Q

BMI is not useful in these situations

A

extreme end of physical fitness

75
Q

what is a better measure of health in heavily muscled individuals

A

body composition

76
Q

IBW men =

A

106lb + 6lb/in (>5ft)

77
Q

IBW woment =

A

100 + 5/in (>5ft)

78
Q

%IBW =

A

(actual weight/ideal weight) x 100

79
Q

normal % bodyfat in men

80
Q

normal % bodyfat in woment

81
Q

normal weight circumference in women and men

82
Q

What body comp measure utilizes the principles that lean body is denser than fat, weight in air vs weight under water, and water displaced

A

hydrostatic weighing

83
Q

This tool is similar to hydrostatic weighing

A

air displacement (bodpod)

84
Q

Considered the gold standard of body composition measures

A

dual xray absorptiometry (dexa)

85
Q

This measure of body comp is widely available, less accurate in obese, and has more operator error

A

skinfold thickness

86
Q

resistance to current is inversely proportional to fat-free mass (conductivity is greater in lean tissue than fat)

A

bioelectrical impedance

87
Q

total combustable energy value of food

A

total energy intake

88
Q

this percent of food energy is lost in fecese

89
Q

energy that is absorbed from the gi tract

A

digestible energy intake

90
Q

percent of digestible or absorbed energy lost in urine, etc

91
Q

what is available for use by cells of the body or caloric value of foods

A

metabolized energy

92
Q

percent of heat lost to biochemical inefficiency of converty fuel energy into ATP

93
Q

energy converted to high-energy bonds of ATP, and the percent of metabolizable energy

A

energy available to couple to work

40%

94
Q

percent of heat loss due to biochemical inefficiency of coupling ATP to work

95
Q

mechanical work such as respiration and circulation: transport work, synthetic work, muscle contraction, and percent metabolizable energy

A

energy actually used to accomplish work

16%

96
Q

percent of energy lost through dissipation of heat in the body as a consequence of internal work and muscle contraction to generate force for external work

97
Q

percent of metabolizable energy that is used to do external work on the environment

98
Q

What affects BMR

A

energy expenditure for respiration, heartbeat, renal function and blood circulation

99
Q

What effects the thermic effect of food

A

nutrient composition of food

100
Q

according to the thermic effect of food protein increases energy expenditure by this %

101
Q

according to the thermic effect of food CHO increases energy expenditure by this %

102
Q

according to the thermic effect of food fat increases energy expenditure by this %

103
Q

4 components of energy expendiuture

A

BMR and REE
Thermic effect of food
physical activity
thermoregulation

104
Q

BEE accounds for this much of total daily EE

105
Q

T/F: RMR is slightly lower than BEE

106
Q

BEE for woment

A

1300 +/- 120 kcal

107
Q

BEE

A

Basal energy expenditure at complete rest in the morning after sleep

108
Q

T/F: lean body mas affects BEE

109
Q

T/F: brain, liver, kidney, and heart are most metabolically active organs at rest

110
Q

T/F: skeletal muscle REE is low (20-40% of BEE) but represents 40% of total body mass

111
Q

T/F: genetics do not play a major role in influencing BEE

112
Q

T/F: various physiological factors can affect BEE

113
Q

measures dissipation of heat from the body

A

direct calorimetry

114
Q

measures comsumption of O2 and expiration of Co2

A

indirect calorimetry

115
Q

uses stable isotopes of water, and measures their disaapearance in the blood and urine for 3 weeks

A

doubly labeled water

116
Q

Repiratory quotient for CHO, TAG, PRO

117
Q

maximal exercise results in an RQ closer to this value

118
Q

This is the only orexigenic hormone

119
Q

Ghrelin does this

A

makes you feel hungry, makes you eat

120
Q

Leptin is secreted from this type of tissue

121
Q

leptin does this

A

suppresses hunger

122
Q

leptin affects this portion of the brain

A

arcreate nucleus or hypothalamus

123
Q

T/F: over secretion of leptin can cause the body to become resistant to it

124
Q

Ghrelin is produced here

A

stomach and duodenum

125
Q

adiponectin is produced here

A

adipocytes

126
Q

T/F: adiponectin levels increase with increased fat mass, and deress with decreased fat mass

127
Q

this hormone protects against insulin resistance, glucose intolerance, and dyslipidemia

A

adiponectin

128
Q

main thing insulin does

A

insulin binding to receptors causes GLUT4 transporters to work on muscle and adipose tissue

129
Q

abnormality in glucose homeostatsis

130
Q

insulin deficiency

A

type 1 diabetes

131
Q

reduced insulin sensitivity

A

insulin resistance

132
Q

mismatch betwen insuling produciton and requirements

A

type 2 diabetes

133
Q

Type 1 makes up this % of cases

134
Q

This occurs in type 1

A

B-cells of the pancreas are attacked by the immune system

135
Q

End result of T1DM

A

hyperglycemia

ketoacidosis

136
Q

reduced signaling to GLUT4 after insulin binding

A

insulin resistance

137
Q

This can affect the sensitivity of insulin receptors

A

inflammation

138
Q

4 steps of progression to T2DM

A

insulin resistance
compensatory B-cell hyperplasia
B-cell failure (early)
b-cell failure (late)

139
Q

Characteristics of cempnsatory b-cell hyperplasia

A

increased insulin in blood with normoglycemia

140
Q

Characteristics of B-cell failure (early)

A

falling insulin levels leading to impaired glucose tolerance

141
Q

characteristics of lat B-cell failure

A

little to no insulin leading to diabetes

142
Q

this disease has a strong association with obesity and inactivty

143
Q

T/F: down regulation of insulin receptors plus defects within cells are characteristics of T2DM

144
Q

T/F: Ketoacidosis is very common with T2DM

145
Q

4 diagnostic symptoms of diabetes

A

polyuria
polydipsia
polyphagia
weight loss (fat and protein stores being used)

146
Q

2 short term complications of DM

A

hypoglycemia

hyperglycemic diabetic ketoacidosis

147
Q

microvascular disease, macrovascular disease, dyslipidemia, hypertension

A

long-term complications of DM

148
Q

Blood test for diagnosis of DM

149
Q

HbA1c checks for this

A

glycated hemoglobin

150
Q

T/F: HbA1c is a measure of short term blood glucose control

A

F, long term control 2-3 months

151
Q

A1c, FPG, OGTT for diabetes

A

> 6.5%
126
200

152
Q

A1c, FPG, OGTT for pre-diabetes

A

5.7-6.4
100-125
140-199

153
Q

A1c, FPG, OGTT for normal

154
Q

absolute insulin requirement

155
Q

insulin resistance, impaired beta cell function

156
Q

DM that develops during pregnancy

A

gestational diabetes

157
Q

goals of treatments for T2DM

A

reduce blood glucose

158
Q

treatment for T1DM

A

insulin therapy

159
Q

General diabetes treatment

A

lose excess body fat
exercise
eat balanced diet

160
Q

T/F: all overweight people are insulin resistant

161
Q

T/F: insulin sensitivity improves with weight loss

162
Q

T/F: Low-fat, high CHO diet requires less insulin which is good for those who are insulin resistanct

163
Q

medicine type for T2Dm

A

oral hypoglycemic agents

164
Q

this number of risk factors for MS is grounds for diagnosis

165
Q

5 risk factors for metabolic syndrome

A

elevated waist circumference
elevated TAG (>=150)
reduced HDL (=130(and/or)/85)
elevated fasting glucose (>=100 mg/dl)

NUTR-455 (4 decks)

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