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NUTR 315 > Under-nutrition (2/19) > Flashcards

Under-nutrition (2/19) Flashcards

1
Q

What accounts for over half of the world’s disease burden?

A

malnutrition

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2
Q

What is malnutrition?

A

too much food or hunger

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3
Q

How many kcals/day does adults need to support healthy life?

A

2100

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4
Q

What is hidden hunger?

A

micronutrient deficiencies

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5
Q

What does under-nutrition do?

A

physical and mental activity declines, growth slows and ceases altogether, muscle & fat wasting occurs, the immune system weakens, death rates rise

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6
Q

What are health consequences of undernutrition?

A

poor people may eat and absorb too little nutritious food, making them more disease prone; inadequate or inappropriate food leads to stunted development or premature death; nutrient-deficient diets provoke health problems; disease decreases people’s ability to cultivate or purchase nutrient foods; sickness and loss of livelihood

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7
Q

What are the complex causes of world hunger?

A

AIDs; rapid depletion of natural resources; poor infrastructure; high external debt; extreme imbalances in the food/population ratio; war and political/civil unrest

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8
Q

What is food insecurity?

A

limited or uncertain access to nutritious safe foods necessary to lead a healthy lifestyle

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9
Q

What does households that experience food insecurity have?

A

reduced quality or variety of meals and may have irregular food intake

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10
Q

What are food insecurities in the US linked to?

A

obesity (especially in women) and higher risk of chronic diseases (e.g, diabetes)

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11
Q

What is high household food security?

A

no indications of food access problems or limitations

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12
Q

What is marginal household food security?

A

1 or 2 indications of food access problems (anxiety, shortage of food); little or no change in diets or food intake

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13
Q

What is low household food security?

A

reduction in quality, variety, desirability of diet; little or no reduced food intake

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14
Q

What is very low household food security?

A

multiple indications of disrupted eating patterns and reduced food intake

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15
Q

What are the nutrient deficiency diseases that are commonly accompanying undernutrition?

A

xerophthalmia, rickets, beriberi, ariboflavinosis, pellagra, megaloblastic anemia, scurvy, iron deficiency anemia, goiter, protein-energy malnutrition

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16
Q

What vitamin deficiency causes xerophthalmia?

A

vitamin A

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17
Q

Where is xerophthalmia commonly seen?

A

asia, africa

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18
Q

What vitamin deficiency causes rickets?

A

vitamin D

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19
Q

Where is rickets commonly seen?

A

asia, africa (due to clothing)

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20
Q

What vitamin deficiency causes beriberi?

A

thiamin

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21
Q

Where is beriberi commonly seen?

A

areas of famine

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22
Q

What vitamin deficiency causes ariboflavinosis?

A

riboflavin

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23
Q

Where is ariboflavinosis commonly seen?

A

areas of famine

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24
Q

What vitamin deficiency causes pellagra?

A

niacin

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25
Q

Where is pellagra commonly seen?

A

areas of famine

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26
Q

What vitamin deficiency causes megaloblastic anemia?

A

folate

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27
Q

Where is megalobastic anemia commonly seen?

A

asia, africa

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28
Q

What vitamin deficiency causes scurvy?

A

vitamin C

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29
Q

Where is scurvy commonly seen?

A

areas of famine

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30
Q

Where is iron deficiency anemia commonly seen?

A

worldwide

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31
Q

What vitamin deficiency causes goiter?

A

iodine

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32
Q

Where is goiter commonly seen?

A

south america, eastern europe, africa

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33
Q

What are vitamins?

A

organic compounds required by the body in trace amounts that perform specific metabolic funcitons

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34
Q

Are vitamins dietary essentials?

A

yes, they are not synthesized by the body or are not synthesized in sufficient quantity

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35
Q

What are the fat soluble vitamins?

A

ADEK

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36
Q

What are the water soluble vitamins?

A

thiamin, riboflavin, niacin, B6, B12, folic acid, pantothenic acid, biotin, ascorbic acid (C)

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37
Q

How do we get vitamin A?

A

some comes preformed in animal tissues others can be “made” from provitamins found in plant tissue (carotenoids)

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38
Q

What is a food that contains both forms of vitamin A?

A

milk fat and egg yolk

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39
Q

What are the 3 forms of vitamin A?

A

retinol, retinal (all trans), and beta-carotene

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40
Q

What are carotenoids?

A

yellow-orange pigmented materials in fruits and vegetables

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41
Q

How is retinoids absorbed?

A

preformed vit. A in animal foods as retinol and retinyl ester; retinyl ester is hydrolyzed in small intestine to retinol and fatty acid; 90% of retinol is absorbed into the cells of the small intestine via a specific carrier protein and is re-esterified; newly formed retinyl esters are packaged to chylomicrones, enter the lymph circulation, and are delivered to tissues for storage (liver)

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42
Q

How much vit. A does the liver store?

A

enough to last for several months and protect from deficiencies

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43
Q

What happens to vitamin A once it is released from the liver?

A

goes into the bloodstream and is then bound to retinol binding protein (RBP); RBP is attached to transthyretin (TTR) in circulation; RBP and TTR deliver vit. A to cells; vit A is then transferred to one of several cellular retinoid-binding proteins (CRBP) which direct vit. A to functional sites in the cells.

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44
Q

How is carotenoids absorbed?

A

dietary carotenoids are attached to proteins that are then cleaved by digestive enzymes in the small intestine; carotenoids are then absorbed mainly by passive diffusion; inside the intestinal cell, carotenoids are cleaved to form retinal or retinoic acid; retinal is converted to retinol which is re-esterified and transported to the liver. retinoic acid can enter the bloodstream directly for transport to the liver

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45
Q

What does nuclear retinoid receptors do?

A

bind to response elements in DNA, regulate formation of mRNA from vit. A responsive genes, and broad spectrum of functions

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46
Q

What are the types of nuclear retinoid receptors?

A

RXR and RAR

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47
Q

What are the physiological functions of vit. A?

A

visual cycle, maintenance of epithelial tissues, growth/differentiation, reproduction, immunity

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48
Q

What is the retinol activity equivalents?

A

1 RAE = 1 microgram all trans retinol, 12 microgram all trans beta-carotene, or 24 micrograms other carotenoids

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49
Q

What is the RDA for vit. A?

A

900 microgram/day RAE for men and 700 microgram/day RAE for women

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50
Q

What is the UL for vit A?

A

3000 microgram RAE

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51
Q

What are vit. A deficiency sympotms?

A

night blindness, keratinizaiton of epithelial tissue, xerophthalmia, blindness

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52
Q

What are acute toxicity symptoms for vit. A?

A

gastrointestinal upset/nausea, headaches, dizziness, muscle uncoordination

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53
Q

What are chronic toxicity symptoms for vit. A?

A

liver damage, hair loss, bone/muscle pain, loss of appetite, dry skin and mucous membranes, hemorrhages, coma, fractures

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54
Q

What are teratogenic toxicity symptoms for vit. A?

A

fetal malformation and spontaneous abortion

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55
Q

What is nyctalopia?

A

night blindness

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56
Q

How does night blindness occur?

A

blood retinol levels too low to replace retinal in visual cycle, thus rods regenerate rhodopsin more slowly, slower adjustment to low light

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57
Q

What is xerosis?

A

dryness at mucous membrane covering the front surface of the eye

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58
Q

What does xerosis progress too?

A

bitot’s spots

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59
Q

What are bitot’s spots?

A

foamy gray spots on the eye consisting of hardened epithelial cells

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60
Q

What do bitot’s spots progress to?

A

keratomalacia

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61
Q

What is keratomalacia?

A

softening of the cornea and scaring

62
Q

What is xerophthalmia?

A

irreversible blindness

63
Q

What does keratin do?

A

protects the inner layers and reduces water loss

64
Q

What is follicular hyperkeratosis?

A

hair follicles plugged with keratin giving dry, rough, sandy texture to the skin

65
Q

What is keratinizaiton?

A

low retinoic acid leads to deterioration of mucous-forming cells. keratinized cells replace the normal mucous forming cells

66
Q

What was the international initiative to decrease vitamin A deficiency?

A

promoting breastfeeding, fortification of foods, educational programs to increase home gardening of vit. A rich foods and veggies, providing vit. A supplements to populations at risk

67
Q

What are symptoms of acute vit A toxicity?

A

GI upset, nausea, headaches, etc.

68
Q

What are symptoms of chronic vit. A toxicity?

A

liver damage, hair loss, bone muscle pain, etc.

69
Q

What are symptoms of teratogenic vit. A toxicity?

A

fetal malformation, spontaneous abortion

70
Q

What needs to come together to form an active enzyme?

A

inactive enzyme and vitamin coenzyme

71
Q

What is the coenzyme form of thiamin?

A

thiamin pyrophosphate (TPP)

72
Q

What was the cure for beriberi?

A

rice polishings

73
Q

how is thiamin absorbed?

A

through active transport

74
Q

is thiamin needed in the diet daily?

A

yes, due to only a little being stored

75
Q

how is thiamin excreted?

A

in urine

76
Q

What energy generating reactions is TPP involved in?

A

decarboxylation reactions; 20 other reactions in carbs, lipids, and protein metabolism; conversion of tryptophan to niacin

77
Q

What is the RDA for thiamin?

A

1.2 mg/d for men or 1.1 mg/d for women

78
Q

What are the food sources that we can get thiamin?

A

pork, legumes, wheat germ, dried yeast, enriched flour and other products

79
Q

What does enriched mean?

A

thiamin, niacin, riboflavin, and iron added to a grain product to level present prior to processing

80
Q

What does fortified mean?

A

vitamins and/or minerals added to a food product in excess of what was originally found in the product.

81
Q

What enzyme destroys thiamin?

A

thiaminase enzyme

82
Q

Where can thiaminase enzyme by found?

A

some species of fresh fish and shellfish

83
Q

What foods are antagonists for thiamin?

A

coffee, tea, blueberries, and beets

84
Q

What is beriberi disease?

A

deficiency of thiamin

85
Q

what is symptoms of beriberi?

A

anorexia, weight loss, apathy, loss of short-term memory, confusion, irritability, peripheral neuropathy, muscle weakness

86
Q

What is wernicke-korsakoff syndrome?

A

reduced absorption of thiamin, increased excretion of thiamin, poor diet

87
Q

What are symptoms of wernicke-korsakoff syndrome?

A

ataxia, deranged, nystagmus

88
Q

What is the coenzyme form of riboflavin?

A

flavin adenine dicucleotide (FAD)

89
Q

How is riboflavin absorbed?

A

active transport into intestinal mucosal cells, phosphorylated in mucosal cells, transported to liver, further phosphorylated

90
Q

T/F: riboflavin is not absorbed better with food

A

false, it is absorbed better

91
Q

What is riboflavin synthesized by?

A

intestinal bacteria but not known to be absorbed

92
Q

What are riboflavins coenzyme forms?

A

FMN (flavin mononucleotide) and FAD (flavin adenine dinucleotide)

93
Q

What is the RDA for riboflavin?

A

1.3 mg/d for men and 1.1 mg/d for women

94
Q

What are the food sources of riboflavin?

A

milk, organ meats, green leafy vegetables, enriched flour and other products

95
Q

T/F: riboflavin is light sensitive

A

true

96
Q

What is riboflavin deficiency?

A

ariboflavinosis

97
Q

What is symptoms of ariboflavinosis?

A

cheilosis (dry skin around nose and mouth), glossitis, low levels in RBCs

98
Q

What diseases is common with ariboflavinosis?

A

cancer, CVD, diabetes, alcoholism, malabsorption disorders

99
Q

How is niacin absorbed?

A

diffusion and active transport in the stomach and small intestine

100
Q

What is niacin converted to in tissues?

A

NAD+ and NADP+

101
Q

Where are niacin coenzymes stored?

A

in the liver

102
Q

Where is excess niacin excreted?

A

in urine

103
Q

What does NAD play a role in?

A

hydrogen acceptor in glycolysis and citric acid cycle

104
Q

What does NADP play a role in?

A

hydrogen donor in fatty acid and cholesterol synthesis

105
Q

What is the DRI for niacin?

A

6.6 mg/1000 kcal

106
Q

What is the RDA for niacin?

A

16 mg/d for men and 14 mg/d for women

107
Q

What is the UL for niacin?

A

35 mg/d

108
Q

What are food sources for niacin?

A

meat, poultry, fish > fruits, veggies, grains > dairy, eggs

109
Q

What disease is caused from niacin deficiency?

A

pellagra

110
Q

What are symptoms of pellagra?

A

the 4Ds… dermatitis, diarrhea, dementia, death

111
Q

How was pellagra eradicated in the US?

A

through enrichment of grains and protein-rich foods

112
Q

When can pellagra be observed today?

A

in severe malabsorption, chronic alcoholism, Hartnup disease

113
Q

What is hartnup disease?

A

genetic disorder where tryptophan to niacin pathway is blocked

114
Q

how is folate absorbed?

A

glutamic acid residues removed in upper intestine and then absorbed immediately

115
Q

What is the rate of absorption of folate reduced by?

A

increased number of glutamic acid residues

116
Q

What is the function of folate?

A

transfer of single carbon units (nucleic acid synthesis and some amino acids)

117
Q

What is the coenzyme form of folate?

A

tetrahydrofolate (THF)

118
Q

What is the RDA of folate?

A

400 micrograms/d

119
Q

What does the requirement of folate increase with?

A

increased levels of cell replication (pregnancy, growth)

120
Q

What is food sources of folate?

A

green vegetables, liver, fish, poultry, legumes

121
Q

What happens with folate deficiency?

A

megaloblastic anemia and neural tube defects

122
Q

how is cobalamin absorbed?

A

b12 released by HCl and pepsin in stomach and then combines with R-protein from salivary glands for travel to duodenum, pancreatic proteases free B12 to combine with intrinsic factor which was synthesized in stomach and then travels to ileum where B12 is absorbed by a receptor

123
Q

What transports cobalamin to tissues?

A

transcobalamin II

124
Q

What are the functions of cobalamin?

A

single carbon unit metabolism, recycle folate coenzymes, and nervous system function

125
Q

What is the RDA for cobalamin?

A

2.4 micrograms/d

126
Q

What are food sources of cobalamin?

A

all of bacterial origin, liver, seafood, meat, eggs, milk

127
Q

What disease does cobalamin deficiency lead to?

A

pernicious anemia

128
Q

What is pernicious anemia?

A

lack of intrinsic factor

129
Q

How is vitamin B6 absorbed?

A

dephosphorylated in intestine, absorbed (by diffusion) and transported in free form to the liver, phosphorylated when enters cells to PLP by pyridoxal oxidase, transported in blood as PLP on albumin, main storage in muscle

130
Q

how is excess B6 excreted?

A

in urine

131
Q

What functions is B6 involved in?

A

amino acid metabolism (transamination, decarboxylation, transsulfuration, side chain transfers) and phosphorylase which mobilizes glucose form glycogen, hemoglobin synthesis, neurotransmitter synthesis, tryptophan to niacin

132
Q

what is the RDA for B6?

A

1.3 mg/d

133
Q

What is the UL for B6?

A

100 mg/d

134
Q

What are food sources for B6?

A

yeast, organ meats, whole grains, cereals, legumes, bananas

135
Q

What are antagonists of B6?

A

antitubercular drugs, antibiotics, oral contraceptive pills

136
Q

What happens with B6 deficiency?

A

microcytic hypochromic anemia, marginal deficiency, pregnancy and lactation

137
Q

What is microcytic hypochromic anemia?

A

reduced hemoglobin synthesis, small RBCs, muscle weakness, irritability, depression, confusion, and dermatitis

138
Q

What is the toxicity for B6?

A

2-6 g/d for 6 months

139
Q

how is ascorbic acid absorbed?

A

by active transport and diffusion into portal blood

140
Q

how much ascorbic acid is stored in the liver, spleen, and adrenals?

A

1500 mg

141
Q

how is ascorbic acid excreted?

A

in urine

142
Q

What is the functions of ascorbic acid?

A

collagen formation, antioxidant, neurotransmitter synthesis, iron absorption, immune function, cancer prevention

143
Q

What is collagen formation?

A

conversion of proline and lysine to hydroxyproline and hydroxylysine

144
Q

how much ascorbic acid needed to prevent scurvy?

A

10 mg/d

145
Q

What is the RDA for ascorbic acid?

A

90 mg/d for men and 75 mg/d for women

146
Q

What is the UL of ascorbic acid?

A

2000 mg/d

147
Q

What increases the requirement of ascorbic acid?

A

smoking

148
Q

What are food sources of ascorbic acid?

A

citrus fruits, potatoes, green veggies

149
Q

What is scurvy?

A

abnormal collagen synthesis, fatigue, pinpoint hemorrhage, bleeding gums

150
Q

What are symptoms of ascorbic acid toxicities?

A

GI disturbances (nausea, cramps, diarrhea) and some questionable symptoms reported with megadoses (kidney stones, excess iron absorption, B12 deficiency, dental enamel erosion, allergic response, etc.)

NUTR 315 (22 decks)

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