Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nutrition > Exam 1: Fat Soluble Vitamins > Flashcards

Exam 1: Fat Soluble Vitamins Flashcards

1
Q

Fat soluble vitamins

A

Vitamins A, D, E, K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F Vitamins A, D, E, and K require 5-10 grams of fat for bile secretion in digestion and absorption

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fat-soluble vitamins are absorbed by _______ diffusion

A

Passive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Fat soluble vitamins are transported with _____ in ________

A

Lipids

Lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fat soluble vitamins are able to be stored in the _______ and ________ which means they can be toxic in large amounts

A

Liver

Adipose tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Emulsifier made from cholesterol in the liver and stored in the gallbladder.

A

Bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What causes secretion of bile?

A

Fat-rich chyme entering the small intestine signals the release of CCK which stimulates gallbladder contraction and releasing of bile through the Sphincter of Oddi into the small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Another name for Vitamin A is ______

A

Retinoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Types of Vitamin A and what each types best known function is

A
  • Retinol (alcohol form) = Reproduction and growth
  • Retinal (aldehyde form) = Vision
  • Retinoic acid (carboxylic form) = Cell differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Vitamin A that comes from animal products attached to an ester. Is this considered active or inactive?

A

Preformed (Retinol Esters)

Active

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the usual preformed retinol ester?

A

Palmitic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Precursor to vitamin A that comes from plant products. Used only when we don’t get enough preformed vitamin A in the diet

A

Proformed vitamin A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Main proformed vitamin A precursor that comes from plants.

A

Carotenoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

T/F Carotenoids are antioxidants

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

It takes __ times as much proformed vitamin A to equal preformed vitamin A activity

A

12x

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What % of carotenoids can be converted to retinol?

A

<10% (of 600 known carotenoids)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Carotenoids are usually bound to a _____ while Retinol esters are bound to both a _______ and _______ in food

A

Carotenoids = fatty acid (carotenoid ester)

Retinol Esters = fatty acid and protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Make vitamin A soluble

A

Bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What kinds of enzymes are able to remove fatty acids and protein from retinol esters?

A

Fatty acids = Lipases (esterace)

Protein = Proteases (pepsin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where do proteases and lipases act on retinol esters in the body?

A 
Proteases = stomach and small intestine 
Lipases = small intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Free retinol and carotenoids are incorporated into _____

A

Micelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where in the small intestine is vitamin A absorbed by passive diffusion?

A

Duodenum and jejunum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is retinol bound to after passive diffusion into the enterocyte?

A

Cellular-retinol binding protein (CRBP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

After being bound to CRBP, retinol is reesterified to a retinol ester in the enterocyte by:

A

Lecithin: Retinol Acyl Transferase (LRAT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Reesterified Retional esters in the enterocyte are incorporated into:

A

Chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What happens if retinol intake is low?

A

1) Carotenoids are metabolized into 2 retinals
2) Retinals are either bound to CRBP, reduced to retinol, esterified via LRAT and incorporated into chylomicrons OR retinal is oxidized to retinoic acid and travels to the liver bound to a protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What protein binds to retinoic acid and transports it to the liver when retinol intake is low?

A

Albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What happens if retinol intake is adequate?

A

Carotenoids are incorporated into chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

T/F Patients with low protein status cannot mobilize retinol out of the liver

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How does vitamin A deficiency cause night blindness?

A

Retinal is combined with Opsin to form rhodopsin, which is important for vision in dim light and highly concentrated in the rods of the retina. Low vitamin A means low Retinal, low retinal means low rhodopsin which causes night blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How does a vitamin A deficiency cause Hyperkeratinization?

A

Retinoic acid from vitamin A is important for rapidly dividing cells by directing keratin synthesis (causes immature keratinocytes to mature into mature cells). Low vitamin A prevents the creation of mature mucus-secreting cells in respiratory, GI, and urinary tracts from keratin producing cells causing Hyperkeratinization (dry eyes, dry mouth, constipation, and dry mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

_____ vitamin A stimulates osteoblast activity while ______ vitamin A stimulates osteoclast activity, both of which can cause an increased risk of pathologic fractures.

A

Low (deficiency) = stimulates osteoblasts

High (excessive) = stimulates osteoclasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

T/F Retionic acid interacts with ribosomes in the rough ER to stimulate production of enzymes and growth factors

A

FALSE.

Retionic acid interacts with the DNA in the nucleus into stimulate production of enzymes and growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Low levels of this impact sperm mobility and quality

A

Retinol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

This stimulates phagocytosis, cytokine production, and maintains natural killer cell concentrations

A

Retinoic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Function of carotenoids

A
  • Antioxidant (quenches ROS)

- Cell growth and differentiation (some may inhibit growth and proliferation of several cancer lines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Preformed Vitamin A sources

A

Liver
Fish
Fortified dairy
Eggs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Proformed Vitamin A sources

A 
Carrots
Dark green leafy veggies 
Sweet potatoes 
Tomatoes
Cantaloupe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Primary and secondary cause of hypovitaminosis A

A

A.k.a. Vitamin A deficiency
Primary = inadequate intake
Secondary = fatty malabsorption (inadequate fat or abnormality in bile production, enzymes, liver diseases, etc. prevents proper absorption)

40
Q

Vitamin A deficiency symptoms

A
  • Night blindness
  • Xerophthalmia (dry eyes = inadequate mucus production [hyperkeratosis)
  • Bitot’s spots
  • Permanent blindness (MC in developing countries)
  • Impaired reproduction
  • Depressed immune symptom
  • Skin problems (hyperkeratosis)
41
Q

Who is at risk of vitamin A deficiency?

A
  • Children in developing countries

- Patient with fat malabsorption

42
Q

Major symptom of someone with fatty malabsorption?

A

Steatorrhea (fat in stools = stinky mineral colored stool)

43
Q

Symptoms of acute hypervitaminosis A

A

A.k.a. Vitamin A toxicity

  • nausea, vomiting, headache, *double vision, dizziness
  • Taking a single dose of over 200,000 RAE
44
Q

Symptoms of chronic hypervitaminosis A

A

A.k.a. Vitamin A toxicity

  • No specific symptom to indicate toxicity
  • Chronic intake of >7000 RAE/day
45
Q

T/F Vitamin A is safe for women to megadose during pregnancy

A

FALSE.

Vitamin A toxicity can cause birth defects (teratogenic)

46
Q

Acne medication that contains retinoic acid and is teratogenic

47
Q

T/F The TUL limit for Carotenoid is 3,000 RAE per day

A

FALSE.

Carotenoid has no TUL

48
Q

Major symptom of ingesting 4-5 ounces of carrots per day for several months

A

Yellow/orange skin (Carotenoid toxicity)

49
Q

T/F While considered safe in plant based foods, supplements of carotenoids does increase your risk of lung cancer, heart disease, and death in smokers and former smokers

50
Q

What did high levels of alpha-tocopherol (high vitamin E) and beta-carotene have on cancer prevention?

A
  • AT decreased prostate cancer by 32%

- BC increased risk of lung cancer in heavy smokers and light drinkers by 18%

51
Q

What did the trial showing high levels of beta-carotene and retinol show?

A

Increased risk of lung cancer, cardiovascular disease, and all-cause mortality (1.28, 1.26, 1.17, respectfully)
-Trial was stopped 2 years early, but even after 6 years, the female risk for all 3 issues was increased by 40%

52
Q

Known as the sunshine vitamin. Made from cholesterol

53
Q

Animal form of vitamin D

A

Cholecalciferol (Vitamin D3)

54
Q

Plant form of Vitamin D

A

Ergocalciferol (Vitamin D2)

55
Q

50% of Vitamin D from food is absorbed into the small intestine (mostly ___ ) by means of ________

A

Ileum

Passive diffusion

56
Q

Of the 50% of vitamin D absorbed from food, what happens next?

A

40%- bound to vitamin D binding protein (DBP) and sent to the liver
60%- packed into chylomicrons and sent to the liver

57
Q

How is vitamin D3 absorbed from the skin reach the liver?

A

Vitamin D3 is bound to DBP and sent to the liver (similar to 40% of vitamin D from food)

58
Q

Enzymes used to convert inactive vitamin D to its active form

A

Hydroxylases

59
Q

Hydroxylases belong to what part of enzymes in the liver?

A

Cytochrome P450 enzymes

60
Q

T/F Calcidiol has a shorter half life than Calcitrol

A

FALSE.

  • Calcidiol (inactive 25-hydroxy vitamin D3)= 60 day 1/2 life
  • Calcitrol (active 1,25-hydroxy vitamin D3)= 4-6 hour 1/2 life
61
Q

Enzyme found in all cells that limits amount of active calcitriol (active 1,25-hydroxy vitamin D3)

A

24-hydroxylase

62
Q

Where is the highest concentration of 24-hydroxylase found?

63
Q

A mutation in gene coding for 24-hydroxylase leads to ______

A

Hypercalcemia

64
Q

What organs contain Vitamin D3, Calcidiol, and Calcitriol?

A

Vitamin D3 = Skin
Calcidiol = Liver
Calcitriol = Kidneys

65
Q

T/F Only the skin, liver, and kidneys contain vitamin D receptors

A

FALSE.

All cells contain vitamin D receptors (known to control >200 genes)

66
Q

Vitamin D functions

A
  • Calcium and phosphorus homeostasis (via gene expression)
  • Cell differentiation and growth (prevents cancerous cells from replicating and important for immune system, nerves and prevention of CVD, MS, etc.)
67
Q

Hormone secreted from this gland in response to low blood calcium

A

Parathyroid hormone (PTH) from the parathyroid gland

68
Q

How does release of PTH cause increased calcium absorption and decreased calcium excretion?

A
  • PTH induces hydroxylase in kidneys
  • Hydroxylase activates calcitriol
  • Calcitriol stimulates synthesis of calcium-binding proteins
  • Calcium binding proteins increase calcium absorption and decreases calcium excretion
69
Q

Vitamin E Vitamers

A

Tocopherol

Tocotrienol

70
Q

Most common Vitamin E vitaminers that we eat or gain in supplements

A

Tocopherol

71
Q

Difference between natural and synthetic vitamin E

A

Natural- only biological active isomers present

Synthetic- fatty acid attached and is a racemic mixture of isomers

72
Q

T/F Natural Vitamin E contains alpha-tocopherol only while Vitamin E supplements contains a mixture of tocopherols and tocotrienols

A

FALSE.

  • Natural vitamin E contains a mixture of tocopherols and tocotrienols
  • Vitamin E supplements contain only alpha-tocopherol only
73
Q

T/F Vitamin E supplements do not prevent cancer, heart disease, all-cause mortality, etc.

74
Q

The fatty acid is removed from tocopherols and tocotrienols by the enzyme:

75
Q

About 50% of tocopherols and tocotrienols and absorbed by ___________ in the small intestine (mostly the ______)

A

Passive diffusion

Jejunum

76
Q

After being absorbed in the small intestine, tocopherols and tocotrienols are packaged into _________ and sent to the _____

A

Chylomicrons

Liver

77
Q

What protein is added to the tocopherols and tocotrienols after being packaged and sent to the liver as chylomicrons?

A

alpha-tocopherol transport protein (a-TTP)

78
Q

Most alpha-tocopherol and some gamma-tocopherol and tacotrienals and incorporated into _____

79
Q

T/F 10% of vitamin E is stored in adipose tissue

A

FALSE.

90% of vitamin E is stored in adipose tissue

80
Q

Function of Vitamin E

A

Antioxidant (regeneration of vitamin E has shown to decrease risk of heart disease, cancer, age-related macular degeneration, etc.)

81
Q

What part of the cell uses vitamin E to donate H+?

A

Plasma membrane (protects PUFA’s from free radicals)

82
Q

T/F The ratio of vitamin E to unsaturated fats in the cell is about 1:10

A

FALSE.

Closer to 9:1,000-2,000

83
Q

Overall, what is the best source of vitamin E?

A

Plant oils

84
Q

Who is at risk most of developing hypovitaminosis E?

A

1) Patients with fat malabsorption disorders (CF, pancreatic cancer, bile disorders)
2) Premature infants

85
Q

Symptoms of hypervitaminosis E

A

Bleeding
Nausea
Diarrhea
Fatigue

86
Q

Majority of Vitamin K found in plants

A

Phylloquinone (K1)

87
Q

Majority of vitamin K found in bacteria

A

Menaquinone (K2)

88
Q

K1 and K2 (phylloquinone and menaquinone, respectively) are absorbed by __________ in the small intestine (mostly _______)

A

Passive diffusion

Jejunum

89
Q

K1 and K2 are absorbed and sent to the ______ packaged as ________. From there they can be incorporated in ________

A

Liver
Chylomicrons
VLDL

90
Q

Where most vitamin K is stored

A

Liver (others include heart, lungs, kidneys)

91
Q

Functions of vitamin K

A

1) Coenzyme for Blood clotting (makes calcium binding sites found on clotting factors, prothrombin, and osteocalcin)
2) Coenzyme for Bone formation (makes calcium binding sites on osteocalcin)

92
Q

Carboxylated by vitamin K to facilitate calcium binding (when synthesis is stimulated by vitamin D)

A

Osteocalcin

93
Q

Vitamin K adds a carboxylic acid group to _______ residues in specific proteins to make __________ (also known as calcium binding sites)

A

Glutamate

Carboxylglutamates

94
Q

Food sources for K1 and K2

A

K1 (Phylloquinones) = plants

K2 (Menaquinones) = meat, cheese, yogurt, egg yolks

95
Q

People at risk for Vitamin K deficiency

A

1) Newborns
2) Patients with fat malabsorption
3) Patients chronically treated with antibiotics

96
Q

T/F Oral vitamin K has the highest efficacy

A

FALSE.

Intramuscular injection vitamin K has the highest efficacy

97
Q

Symptoms of vitamin K toxicity

A

None (no established safe upper limit)

Nutrition (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions