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Flashcards in Water-Soluble Vitamins Deck (135):
1

What are vitamins?

Organic, essential molecules that are required in tiny amounts to maintain normal growth, development, and metabolism

2

Can we synthesize vitamins?

We cannot synthesize them or cannot synthesize them in adequate mounts

3

Which vitamins are synthesized by our gut bacteria?

Vitamin K and biotin

4

Which vitamins are synthesized by our body from precursors?

Vitamin D (from cholesterol) and niacin (from tryptophan)

5

What are the water-soluble vitamins?

B-complex and vitamin C

6

How are vitamins different from carbohydrates, fats, and proteins?

Organic, no calories, micronutrients

7

Factors influencing bioavailability?

efficiency of digestion and time of transit in the GI-tract, method of food preparation, previous nurtrient intake and nutrition status, source of nutrient (synthetic, fortified, or naturally occurring), other foods consumed at same time

8

In food, what are most water-soluble vitamins bound to?

protein

9

Where is the unbound vitamin absorbed (excluding vitamin B12)?

Unbound free vitamins are absorbed in the upper portion of the small intestine

10

Where is unbound vitamin B12 absorbed?

Vitamin B12 is absorbed in the ileum

11

Once absorbed into intestinal cells, where do vitamins go (excluding vitamin B12)?

Once absorbed, they are delivered directly into the portal vein and transported to the liver and sent out into circulation

12

Once absorbed, what happens to vitamin B12?

Vitamin B12 is stored in the liver

13

Which two vitamins are not excreted from the body quite rapidly through the kidneys?

Vitamin B12 and vitamin B6 (pyridoxine) - takes longer to develop a deficiency

14

How are water-soluble vitamins packaged?

Water soluble vitamins travel freely in the blood stream and they are absorbed into the blood directly. (remember, fat soluble vitamins require chylomicrons)

15

Are most water soluble vitamins stored?

No. We do not store most of the water-soluble vitamines, but we store the fat-soluble itamins in the liver and adipose tissue.

16

Is encountering toxicity with water soluble vitamins likely?

No. Since we do not store water soluble vitains, we do not encounter toxicities unless they are consumed as mega dose supplement.

17

What are cofactors?

accessory molecules that are important for protein or enzyme function; can be inorganic molecules such as minerals or organic molecules which are called coenzymes

18

What are coenzymes?

organic cofactors

19

Mnemonic for B-vitamins?

The rhythm nearly proved fully contagious

20

Name for vitamin B1

Thiamin

21

Sources of thiamin?

Meat, sunflower seeds, grains, cereal (result of fortification)

22

Active form of thiamin?

Thiamin pyrophosphate

23

What reduces the absorption of thiamine?

Alcohol consumption and in individuals with folate deficiency

24

Where is thiamine found in the body?

skeletal muscles, liver, heart, kidneys, and brain

25

Functions of thiamine?

(1) helps the body's cells convert carbohydrates into energy
(2) non-enzyme roles of thiamine and its phosphorylated derivatives
(3) 4 enzymes that use thiaine as coenzymes

26

What are the 4 enzymes that use thiamine as coenzymes?

Three are dehydrogenases: pyruvate dehydrogenase, alpha-ketoglutarate dehydrogenase, branched-chain alpha-ketoglutarate dehydrogenase. The last enzyme is transketolase which is an enzyme involved in the hexose monophosphate pathway or pentose phosphate pathway

27

Who usually has a thiamin deficiency?

malnourished, homeless patients, in alcoholics and also in patients on weight-loss diets such as Atkins, Ornish and LEArN plans

28

Early symptoms of thiamin deficiency?

poor appetite, irritability, apathy, confusion and weight loss

29

Prolonged symptoms of thiamin deficiency

Beriberi

30

What are the advanced stages of beriberi?

Wet beriberi and dry beriberi

31

Discuss wet beriberi

Wet beriberi affects the cardiovascular system and there are abnormalities with heart leading to edema

32

Discuss dry beriberi

in dry beriberi, there is muscle wasting, and pain, numbness and tingling of the lower extremities making walking difficult

33

What is the disease associated with alcoholism and thiamin deficiency?

In alcoholics, the symptoms can progress to give rise to Wernicke-Korsakoff syndrome with encephalopathy and psychosis (Psychosis is a serious mental disorder characterized by thinking and emotions that are so impaired, that they indicate that the person experiencing them has lost contact with reality.)

34

The other name of vitamin B2?

Riboflavin

35

Sources of vitamin B2?

beef liver, mushrooms, spinach

36

What destroys riboflavin?

UV light and irradiation

37

What doesn't destroy riboflavin?

heat

38

How does riboflavin circulate in the body?

Bound to albumin or other serum proteins

39

Where and to what is riboflavin converted to?

Once in the cell, riboflavin is converted to flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)

40

What are the active forms of riboflavin?

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

41

Functions of vitamin B2?

(1) prosthetic groups for many enzymes
(2) involved in oxidation and reduction reaction - example TCA cycle

42

Main characteristic of riboflavin deficiency?

Inflammation of membranes

43

What are some of the inflammation of membranes caused by a riboflavin deficiency?

Cheilosis which means cracks at the corners of the mouth, glossitis which means inflammation of the tongue, stomatitis which means inflammation of the mouth and lips

44

Besides inflammation to membranes, what else does riboflavian deficiency cause?

Sensitivity to bright light, seborrheic dermatitis

45

What is seborrheic dermatitis?

skin condition that causes flaky, white to yellowish scales to form on oil areas such as the scalp, face or inside the ear

46

Is there toxicity report for riboflavin?

No. No toxicity is reported

47

Other name for vitamin B3?

Niacin

48

Source for vitamin B3?

fortified foods - cereal and chicken

49

What are the active forms of niacin?

NAD and NADP

50

Niacin refers to which two structures?

Nicotinic acid and nicotinamide

51

What is unique about vitamin B3?

Our body can make it from trytophan which is an essential amino acid

52

What is the form of vitamin B3 that circulates in the blood?

Nicotinamide (which is the major form of niacin in blood)

53

Function of vitamin B3?

more than 200 oxidation and reduction reactions (production and breakdown of glucose, fats, amino acids and DNA)

54

Causes of a mild deficiency in vitamin B3?

alcohol intake or corn-based diets (corn is low on both tryptophan and niacin)

55

What develops because of niacin deficiency?

Pellagra

56

What is pellagra?

Pellagra means rough skin. Pellagra is a deficiency disease caused by a lack of nicotinic acid or its precursor tryptophan in the diet. It is characterized by dermatitis, diarrhea, and mental disturbance, and is often linked to overdependence on corn as a staple food.

57

what are the symptoms of pellagra?

4 D's - diarrhea, dermatitis, dementia, and death

58

What is unique with the dermatitis in pellagra?

Bilateral, symmetrical development on those body parts sensitive to the sun. Casal's necklace - dermatitis developed around the neck.

59

Side effects of taking mega doses of niacin?

Niacin flushing and itching (treated with low dose aspirin or ibuprofen (advil))

60

How does someone take too much niacin?

Nicotinic acid lower LDL, triacylglycerol and increases HDL

61

Other name for vitamin B6?

Pyridoxine

62

Sources of pyridoxine?

Potatoes, oatmeal, bananas, pistachios, pinto beans
(Think Boppp)

63

What are the three forms of pyridoxine?

Pyridoxal, pyridoxine, and pyridoxamine (al, ine, amine)

64

What happen to the three forms of pyridoxine?

Converted to pyridoxal phosphate

65

Importance of pyridoxal phosphate?

amino acid metabolism

66

Where is vitamin B6 stored?

Stored exclusively in muscle tissue

67

Which reactions are pyridoxine involved in?

transamination and deamination reactions

68

What is transamination?

transamination reactions involves removal of amine group from an amino acid and placing it to a keto acid

69

What is deamination?

deamination reactions stops at the removal of the amine group from the amino acid

70

What is the relationship between pyridoxine and niacin?

Pyridoxine is important for the conversion of trytophan (an amino acid) to niacin

71

What else does pyridoxine synthesize?

Pyridoxine is essential for the synthesis of many neurotransmitters such as serotonin, dopamine, norepinephrine, and histamine.

72

What is the relationship between pyridoxine and heme synthesis?

Pyridoxine is used in the committed step as a coenzyme for ALA synthase.

73

Which drugs affect reabsorption of vitamin B6

isoniazid (treatment for tuberculosis) and penicillamine (treatment of rheumatoid arthritis)

74

Presentation of patient with deficiency in vitamin B6?

Cheliosis, glossitis, pellagra-like dermatitis, depression and confusion (remember that pyridoxine deficiency may lead to niacin deficiency, hence explaining some of the common symptoms)

75

Pharmacological use of pyridoxine?

treat carpal tunnel syndrome, PMS, asthma, depression, during pregnancy to control nausea and diabetic neuropathy

76

Side effects of high doses?

Irreversible nerve damage

77

Other name for vitamin B9?

Folate

78

Sources of folate?

orange juice, lentils, fortified cereal

79

What is folic acid?

Folic acid is used instead of the natural form of folates due to its stability

80

Structure of a folate?

Ring structure known as pteridine, Para-aminobenzoic acid (PABA) which is a bridge molecule, glutamate (usually 3-5 glutamates at the end)

81

Describe folate in foods

In foods, folate naturally occurs as polyglutamate

82

Describe folate in the intestine

In the intestine, digestion breaks glutamates off and adds a methyl group

83

Describe folate in cells

In cells, folate is trapped in its inactive form

84

Who activates folate?

Vitamin B12 activates folate in the cells. Because of this, vitamin B12 picks up a methyl group and is now activated

85

Functions of folate?

(1) synthesis of DNA, RNA, some amino acids
(2) regnerate methionine from homocysteine
(3) red blood cell maturation

86

Symptoms of folate deficiency?

weakness, fatigue, headache, palpitations, shortness of breath - all due to macrocytic anemia

87

What may cause a folate deficiency?

may develop when there is an increased demand by the growing fetus during pregnancy, inadequate absorption due to problems in epithelial cells of the gut such as celiac disease and Crohn disease, cancer therapy and alcoholism, antacids

88

What are examples of folate analogs? What are they used for?

Folate analogs known as antifolates such as methotrexate are commonly used in cancer treatment (leukemias)

89

Treatment for folate deficiency?

Should give both folic and vitamin B12

90

What is the methymalonic acid test?

Methymalonic acid accumulation is an indication of vitamin B12 deficiency.

91

Insufficient folate in pregnant mothers

Results in neural tube defects - main neural tube defect encountered in these babies are spina bifida in which the neural tube does not close completely and anencephale which the brain and skulll are underdeveloped

92

Relationship between folate and heart disease

Folate deficiency leads to increased homocysteine levels. Homocysteine is a known independent risk factor to atherosclerosis.and cardiovascular disease

93

Relationship between strokes and folic acid

Smokers may also benefit from folic acid supplementation which is shown to decrease the risk of strokes

94

Other name for vitamin B12?

Cobalamin

95

Sources of vitamin B12?

animal products only or fortified or fermented foods such as soy milk

96

Synthetic form of cobalamin?

Cyanocobalamio

97

Two active forms of cobalami?

Methylcobalamia and deoxyadenosylcobalamin

98

How is vitamin B12 absorbed? What proteins and factors are involved?

In stomach, 3 things happen: vitamin B12 is released
from its protein partner and it binds to R protein. At the same time another molecule called Intrinsic factor (IF) is released from the parietal cells. Then R-protein bound
vitamin B12 and IF moves to duodenum. Here pancreatic enzymes cleaves R-protein enabling Vitamin B12 to bind to IF. From here to ileum, Vitamin B12 is bound to IF.
At ileum, IF receptors allows internalization of vitamin B12. In the ileal epithelial cells, Vitamin B12 is released from IF and released to hepatic circulation and it is
transported bound to transcobalamin II to be delivered to liver. Due to enterohepatic circulation, vitamin B12 can be sufficient for several years.

99

Who produces R-protein?

Salivary glands

100

Where is the R-protein broken up?

In the duodenum

101

Where is the intrinsic factor released?

In the stomach via the parietal cells

102

Who does vitamin B12 bind to?

First - R-protein
Second - Intrinsic factor
Third - Transcobalamine II

103

Symptoms of vitamin B12 deficiency?

pernicious anemia develops (result of destruction of parietal cells - autoimmune disease), nerve damage including tingling in the hands and feet, painful swollen tongue

104

Malabsorption of vitamin B12?

leads to megaloblastic anemia. Mega meaning large, blastic means containing nucleus.

105

Functions of Biotin (B7)

(1) co-enzyme that adds CO2 to compounds
(2) required for metabolism of carbohydrates, fats and proteins
(3) ABC carboxylases - ATP, Biotin, CO2

106

What causes a biotin deficiency?

loss/inactivation of the enzyme important for recycling the active form of biotin (enzyme is biotindiase enzyme). Described in patients who are taking excessive amounts of raw eggs

107

Why do eggs lead to biotin deficiency?

In egg white there is a molecule called avidin which binds to biotin very tightly

108

Is there evidence of toxicity in biotin?

No

109

What is the result of a biotinidase deficiency?

Inability to recycle biotin

110

What causes a biotinidase deficiency?

It is a genetic disorder and it is passed on in an autosomal recessive manner

111

Symptoms of biotinidase deficiency?

Muscle weakness, seizures, eczema, alopecia, developmental delays and lactic acidosis

112

Soures of Pantothenic acid (B5)?

Meat, milk and many vegetables

113

Form of pantothenic acid (B5)?

Coenzyme A

114

Importance of coenzyme A?

essential for activation of fatty acids; therefore important in fat metabolism

115

Function of pantothenic acid (B5)?

Synthesis of fatty acids, triacylglycerol, cholesterol, acetylcholine and cell membranes

116

Deficincy in pantothenic acid? Toxicity in pantothenic acid?

Neither deficiency nor toxicity is known

117

Relationship between vitamins B2 and B6

FMN (riboflavin coenzyme) is important for the conversion of pyridoxine (B6) to pyridoxal phosphate

118

What is needed for conversion of Trp to niacin?

FMN, PLP and iron are required for conversion of Trp to niacin

119

Other name for vitamin C?

Ascorbic acid

120

Symptoms of scurby?

muscle weakness, joint pain, impaired wound healing, loose tooth, bleeding, swollen gums bruised skin and fatigue

121

Source of vitamin C?

many our of veggies and fruits

122

Functions of vitamin C?

formation of collagen, water soluble antioxidant, synthesis of neurotransitters, synthesis of carnitine (important for fatty acid degradation), increases the bioavailability of iron from foods by enhancing intestinal absorption of non-heme iron

123

What does collagen formation include?

Strengthening bones and blood vessels, anchoring teeth into gums, tissue repair and wound healing

124

Why is vitamin C a great antioxidant?

Readily donates it's eletrons to free radicals to reactive oxygen species. Also, reversibility - reduced back to its active form.

125

Importance of antioxidant function?

protects proteins, nucleic acids, carbohydrates and lipid damage from oxidation

126

What is oxidation?

loss of electrons

127

In collagen synthesis, what is vitamin C's role?

Vitamin C is used as a cosubstrate by peptidyl-proplyl hydroxylase and peptidyl-lysyl hydroxylase. Prolyl
hydroxylase catalyzes the selective modification
of proline to hydroxyproline and lysyl hydroxylase catalyzes the conversion of lysine to hydroxylysine.
These modifications are essential for proper collagen folding. Consequently, the lack of vitamin C results in the formation of non-functional collagen in blood vessels and bones, which accounts for most of the severe bone and
blood vessel related symptoms.

128

Relationship between vitamin c and neurotransmitters

Vitamin C is a co-substrate for multiple enzymes involved in neurotransmitter biosynthesis such as norepinephrine. Lack of neurotransmitters helps explain the neurological dysfunction symptoms of scurvy.

129

Where may a vitamin c definicy develop?

Vitamin C deficiency may develop in urban areas with little or no access to fresh fruits and vegetables and in poor older adults

130

What decreases vitamin C?

alcohol decreases absorption of vitamin C, smoking depletes tissue levels

131

How are patients with severe burns and fractures treated with respect to vitamin C?

Increased dosage of vitamin C with patient with severe burns or fractures (they may develop vitamin C deficiency with normal intake)

132

What are pinpoint hemorrhages?

Another symptom of vitamin C deficiency due to internal bleeding

133

What are scorbutic gums?

symmetrical appearance without infection; result of vitamin C deficiency; seen in patients with scurvy

134

Who should be concerned about excess vitamin C?

People with a tendency with developing oxalate stones (vitamin C is metabolized to oxalic acid)

135

Vitamin C as medicine?

(1) doesn't prevent the common cold but may reduce the severity of the infection
(2) reduces oxidation of LDL cholesterol
(3) As for its role in reducing LDL levels or cancer risk, more research is needed