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Biochemistry > Nutrition > Flashcards

Nutrition Flashcards

1
Q

What vitamin is related to Retinol?

A

Vitamin A

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2
Q

Where does Vitamin A come from?

A

There are 2 sources. Preformed vitamin A and Provitamin A carotenoids, which are cleaved in the middle to create Vitamin A.

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3
Q

What are the three caretenoids that are cleaved to make vitamin A?

A

Alpha carotene, beta carotene and cryptoxanthin

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4
Q

Where is vitamin A found?

A

animal foods, dairy, eggs. (things with a face or a mother), or the caretonoids are found in green leafy veggies, or brightly colored fruits

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5
Q

Biological Roles of Vitamin A: both the preformed and carotenoids

A

Carotenoids have antioxidant activity. The preformed Vitamin A is important in Immune functions, bone growth, epithelium (kornification), reproduction, vision

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6
Q

Where is vitamin A stored?

A

in da liva!

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7
Q

how is Vitamin A transported?

A

It is bound to retinol binding protein or be transported on VLDL / LDL. The carotenoids are transported in and our of the liver on lipoproteins.

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8
Q

Risks of deficiency of Vitamin A

A

Priamry deficiency: A deficiency in Zinc can lead to a deficiency in Vitamin A or from an impoverished diet. A secondary deficiency can come from very low fat diets or pancreatic insufficiency

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9
Q

How do you get Vitamin A toxicity?

A

From supplements or from Chronic Kidney Disease

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10
Q

What are symptoms of Vitamin A toxicity?

A

increased cranial pressure, abdominal pain, nausea,headaches, coma,
chronic: osteoperosis, liver dysfunction, teratogenicity, hair loss, bleeding

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11
Q

What is the upper limit of Carotenoid before it becomes toxic?

A

NO SUCH THING AS AN UPPER LIMIT, YOU FOOL!

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12
Q

Where does Vitamin D come from?

A

There are two forms:
D2 / erocalciferol which comes from plants, fortified foods, and invertabrea,
D3 / cholecalciferol- which is made in the skin in response to sun light

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13
Q

How it Vitmain D metabolized?

A

Vitamin D is made into pre-vitamin D in the skin by sunlight. This preD is hydroxylated first by the liver and then by the kidney (due to the action of Parathyroid hormone) to make active vitamin D. Vitamin D, which is responsible for faciliating the absorption of calcium and phosphate

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14
Q

What is the role of vitamin D?

A

vitamin D triggers a nuclear receptor to increase calcium and phosphate absorption in the small intestine, and to increase calciu reabsoprtion in the kideny and from bone

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15
Q

Risks of Vitamin D deficiency?

A

Limited Sun exposure, obesity, infants that are exclusively breast fed, people who are lactose intolerant, liver or kidney diseases

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16
Q

Manifestations of Vitamin D deficiency

A

In children: Rickets, and adults: osteomalcia

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17
Q

Manifestations of Vitamin D toxicity?

A

kidney stones!

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18
Q

assessing Vitamin D

A

23(OH)D since it has a longer half-life, looking at calcium levels, PTH levels and DEXA scan

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19
Q

What forms does Vitamin E come in?

A

Alpha, beta, gamma and delta

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20
Q

Where is vitamin E found?

A

Nuts, seeds, vegetable oils, green leafy vegetables, supplements, olives

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21
Q

How is vitamin E distributed and absorbed?

A

It is absorbed as part of chylomicrons, and stored in the liver. It is necessary to have alpha tocopherol transfer protein to load vitamin E onto VLDL

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22
Q

What roles does Vitamin E play?

A

It functions as an antioxidant, prevents hemolysis, DNA repair

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23
Q

What is needed to regenerate Vitamin E?

A

Vitamin C is needed to make it an active antioxidant again

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24
Q

Risks of Vitamin E deficiency

A

defect in Alpha-tocoperol transfer protein, or a lipid disorder where you dont secrete VLDL, and so you dont secrete vitmain E

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25
Q

Symptoms of vitmain E deficiency:

A

neuropathy, ataxia, retinopathy, RBC homolysis

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26
Q

How do you get Vitamin E toxicity?

A

supplement use, bro!

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27
Q

Risks of toxicity

A

excessive bleeding. do not use this before surgery.

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28
Q

What are the two dietary forms of Vitmain K?

A

Phylloquinone: found in plants/ green leafy vegetables

menaquinones: found in fermented foods, dairy and animal foods

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29
Q

Where is vitamin K stored?

A

in da liver!

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30
Q

What is the biochemical function of vitamin K?

A

It is carboxylated to GLA, which allows it to bind to calcium and trigger the clotting cascade

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31
Q

What does Warfarin do?

A

It prevents clotting by preventing regeneration of the active Vitamin K.

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32
Q

What are risk factors of having a vitamin K deficiency?

A

Malabsoprtion, liver disease, serosis, alcoholism

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33
Q

Symptoms of deficiency

A

bleeding,

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34
Q

What are the manifestations of vitaminK toxicity?

A

there arent any!!!

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35
Q

How is heme-iron abdorbed?

A

It is absorbed by heme carrier protein 1 in the small intestine. the heme is removed form iron and it is bound to ferratin

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36
Q

how is non-heme iron absorbed?

A

the fe3+ form that was liberated from the food matrix must be reduced by DcytB at the brush border. Vitamin C also helps to reduce the iron. The Fe2+ form is now absorbed by DCT1/ DMT1

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37
Q

What are factors that enhance non-heme iron absoprtion

A

Vitmain C and acids

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38
Q

What are some inhibitors of heme absorption?

A

oxalate (grains fruits and veggies), phytates (legumes, grains, rice) and polyphenols (tanic acid, tea and red wine), zinc and other divalent ions such as manganese and calcium.

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39
Q

What do vegetarians have to be careful of?

A

Vegetarians are in trouble because not only do they have decreased iron intake, but they also eat a great deal of the heme inhibitors.

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40
Q

How is iron regulated?

A

Hepcidin is released by the liver. Hepcidin interacts with ferroportin on the basolateral side of the membrane and signlas the cell to internalize it, thus decreasing the release of iron form the cell. These enterocytes are then sloughed off, and iron is released from the body.

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41
Q

Symptoms of Iron deficiency

A

anemia, fatigue, cold intolerance, impaired immunity, microcytic anemia. glossitis : atrophic tongue, angular stomatitis, concave nails

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42
Q

Iron Overload

A

Could happen due to a defect in hepcidin release from the liver, leading to way too much iron in the blood. blood letting helps

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43
Q

Where is copper absorbed

A

in the stomach and duodenum

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44
Q

Sources of copper?

A

liver, shellfish, meats, whole grains

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45
Q

What are some functions of copper?

A

It helps transport iron out of the enterocyte and into the blood stream, and it also acts as a cofactor for multiple enzymes in nerve function and transport of iron.

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46
Q

What are the transporters of copper?

A

CTR and DMT1

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47
Q

Describe the absorption of copper

A

it is absorbed in the enterocyte and bound to metallothionein until it is transported across the basolateral membrane

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48
Q

What do high doses of zinc lead to? How?

A

a deficiency in copper. High doses of copper upregulate metallothionen, but metallothionen binds to copper moer tightly than zinc, so all of the copper will be bound as a result of the zinc induced increase in metallothionen.

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49
Q

What causes a deficiency in copper?

A

upper GI surgery, zinc supplements, Menkes disease

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50
Q

what is menkes disease

A

A disease of transport into peripheral cells, where copper is stuck in the cell an cant be transported

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51
Q

what vitamin deficiency symptoms are similar to that of copper?

A

B12

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52
Q

Symptoms of copper defieicny

A

peripheral neuropathy, macro, micro or normo anemia, liver disease

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53
Q

Recommendations of weight gain for women who are

1. underweight, 2. normal weight, 3. overweight 4. obese

A
  1. 28-40 lbs
  2. 25-35 lbs
  3. 15-25 lbs
  4. 11-20 lbs
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54
Q

what is fetal programming?

A

development of many diseases begins in the development of the fetus

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55
Q

how many more calories should a woman in her second and third trimester consume?

A

in the second trimester, an additional 340 kcal/day

in the third trimester, an additional 450 kcals/day

56
Q

how much additional protein should a pregnant woman take?

A

25 g/day

57
Q

how much additional fluids should a pregnant woman consume

A

3 L/day to maintain blood volume and termpature

58
Q

How much folate should be added to a pregnant woman’s diet

A

neural tube defects can be prevented by taking 360-800 mcg/day in the periconceptual period. doesnt matter during the actual pregnancy.

59
Q

The RDA of which minerals increase in pregnancy?

A

Iron, Zinc, Iodine, Folate, fluid, protiein, energy

60
Q

Manifestations of iodine deficiency in gestation/ adulthood

A

cretinism in development, goiter as an adult

61
Q

Teratogens during pregnancy

A

vitamin A, alcohol, caffeine, sugar substitutes,

62
Q

the needs of what goes down in breastfeeding women?

A

iron and folate because a lady is not menstruating

63
Q

What is breast milk low in?

A

Vitamin D and iron

64
Q

…most children double their birth weight in

A

4-6 months

65
Q

height should be doubled in

A

12 months

66
Q

What is supplemeted in breast fed infants?

A

Iron at 4 months, Vitamin D and flouride at one year.

67
Q

What should be supplemeted in formula fed babies?

A

iron and flouride 6 mo. - 1 yr

68
Q

definition of organic v. non-organic FTT

A

organic: child with underlying problem

non-organic: no known medical problem

69
Q

When does a toddlers appeptite begin to decrease from the insanely high needs?

A

around 1 years

70
Q

Vat is ze female athlete triad?

A

disordered eating, amenorrhea (no period), osteoperosis

71
Q

sarcopenia

A

a decrease in FFM, increase in fat

72
Q

what do you measure when assessing pancreatitus

A

amylase of lipase

73
Q

congenital lactase deficiency

A

infants dont have lactase

74
Q

congenital lactose intolerance

A

defect in absoprtion.. absorbed in the stomach and goes into circulation. not good.

75
Q

Primary LNP

A

permanent loss of lactase

76
Q

secondary LNP

A

associated with actue damage to the bowel, irreversible

77
Q

how is the severity of LNP determined?

A

the ability to fermet short chain FA

78
Q

how to treat LNP

A

with Beta-galactosidase, you fool!

79
Q

an unexplained iron deficiency could be indicative of?

A

celiacs disease due to the destruction of the mucosal lining

80
Q

causes of pancreatitus

A

alcohol, abdominal injury, gall stones , all of which stop the release of pancreatic enzymes

81
Q

When should protein be restricted in the setting of kidney disease?

A

Only when the patient is on dialysis should protein be supplemented. restrict protein when not on dialysis.

82
Q

secondary hyperparathyroidism

A

in kideny disease the low amounts of calcium in the blood due to the inability of the kidney to activate vitamin D which increases calcium absorption, so PTH is released to increase calciums stoers.

83
Q

albumin is linked to ?

A

hydration status. if someone is over hydrated, albumin decreases

84
Q

In CKD sodium should be

A

decreased

85
Q

In CKD potassum should be

A

maintained. hyperkalemia can be life threatening

86
Q

erythropoiten is a consideration in which disease?

A

Kidney disease.

87
Q

Another name for Vitmain D

A

D2: ergo calciferol
D3: cholecalciferol

88
Q

Another name for Vitamin K

A

Phyllaquinon and Menaquinone. Remeber the Q..theres a Q in qumadin, which is involved in blood clotting.

89
Q

How does one get rickets?

A

from a calcium assocaited vitamin D deficiency

90
Q

What are some functions of Vitamin C?

A

iron absorption, collagen synthesis

91
Q

What are symptoms of vitamin D deficiency?

A

impraied bone growth, swollen gums and teeth

92
Q

upperlimit of vitamin c? what does it cause?

A

Diarrhea, bloating, 2g/day

93
Q

Another name for Thiamin?

A

B!

94
Q

Where is thiamin found?

A

whole grains

95
Q

what is thiamin important for?

A

NADPH biosynthesis: transketolae in the PPP, energy metabolism: pyruvate dehydrogenase, synthesis of acetycholine glutamate, GABA

96
Q

Diseases associated with Thiamin deficiency

A

Beriberi wet –> tachychardia, edema, herat failure, dry: peripheral neuropathy and calf tenderness. Wenicke encepalopathy and karsakoff’s psychosis: confabulation

97
Q

Sources of Niacin

A

tryptophan, whole grains

98
Q

What is niacin important for?

A

synthesis of FA, DNA repair, glutamate synthesis , people with hartnups disease

99
Q

manifestations of niacin deficiency

A

pellegra, the 4 Ds

100
Q

What is folate important in?

A

Nucelotide synthesis and methylation. also the conversion of homocysteine to methionine. methyl THF –> THF

101
Q

symptoms of deficiency

A

megaloblastic anemia, neural tube defect

102
Q

Why is B12 important?

A

if it a cofactor for methionine synthesis

103
Q

Who is at risk for deficiency?

A

Elderly due to GI problems and lack of instinsic factor,

104
Q

manifestations of copper deficiency

A

neuropathy and periphral neuropathy?

105
Q

What do saturated fats do?

A

They increase total LDL and HDL

106
Q

What do trans fats do?

A

They increase LDL and either reduce or dont change HDL

107
Q

What do MUFAs and PUFAs do?

A

They reduce LDL and remain neutral to HDL.

108
Q

Importance of fiber in CVD?

A

Fiber delays gastric emptying, it triggers the ileal break, It also binds bile acis and cholesterol for excretion

109
Q

high intake of Fructose shown to

A

cause VLDL synthesis, increased TAGs, liver fat,obesity and insulin reistanc

110
Q

Components of the dash diet?

A

low sodium, supplement potassium, low saturated fats and cholesterols, fiber and morderate protein

111
Q

Vegans require supplementation of

A

b12, fe, calcium and vitamin D

112
Q

definition of under weight

A

low weight for age

113
Q

definition of wasting

A

low weight/height

114
Q

definition of stunting

A

low hight for age

115
Q

ascites accompanies what diease?

A

liver disease

116
Q

what is ascites due to?

A

it is due to the accumulation of fluid in the peritoneal space and it also due to elevated hydrostatic pressure from portal hypertension and from decreased plasma pressure from decreased albumin

117
Q

how to treat ascites?

A

treat with paracentesis, diuretcs, and dietary restriction of sodium

118
Q

NAFLD is caused by?

A

failrue to supress lipolysis of adipose tissue, and insulin resistance, along wth increased TG syntheis and FA oxidation is inhibitied

119
Q

reestrct orotein with or withour encephalopathy?

A

only restrict protein if encepalopathy exists

120
Q

encepalopathy and ascites are in which disease?

A

liver disease

121
Q

When do you supplement protein in renal disease?

A

only when GFR <25

122
Q

actiavted vitamin D does what in the body?

A
  1. calcium and po4 release from the bone
  2. calcoum reabsorption and po4 excretion from kideny
    intestinal ca and po4 absoprtion
123
Q

patients not on dialysis should have how much protein?

A

.6-.8

124
Q

types of LNP

A

primary: irreversible
seconday: with disease, reverisble

125
Q

which is more scientific. the RDA or the AI?

A

the RDA

126
Q

wha is the primary determinant of BEE

A

ffm

127
Q

is albumin a measure of nutritional status in the setting of acute illlness

A

no!

128
Q

Who benefits from nutritional support?

A

pre-op patients with severe PEM. inpatients with alcoholic liver disease, patients undergoing bonemarrow, patients with moderate to severe malnutrition who can tmeet those needs wthin 48 hours, an acutely ill patient but unlikely to meet needs within next 7-10 days

129
Q

leptin

A

is made by fat cells, so is proportional to fat, and acts on the hypothalmus to decrease food intake

130
Q

thiamin participates in the synthesis of

A

GABA and acetylcholine

131
Q

B12 and folate are responsbile of the conversion of what?>

A

homocysteine to methionine

132
Q

folate deficiency results in what type of anemia?

A

macrocytic anemia

133
Q

thiamin participates in the synthesis of?

A

GABA and acetylcholine

134
Q

folate converts

A

homocysteine to methionine

135
Q

folate deficiency results in what kin dof anemia?

A

macrocytic

Biochemistry (3 decks)

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