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GI > Fat-Soluble Vitamins > Flashcards

Fat-Soluble Vitamins Flashcards

1
Q

What are the Fat Soluble Vitamins?

A

ADEK

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2
Q

General properties for fat soluble vitamins?

A
  • require bile and fats for absorption
  • excess stored in liver and adipose tissue
  • not readily excreted (because of efficient enterohepatic circulation); results in increased risk of toxicity
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3
Q

How are vitamins unbound to proteins?

A

Vitamins are bound to proteins as we eat them, but once in the stomach, proteins are degraded into small peptides releasing vitamins.

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4
Q

Where does absorption occur for fat-soluble vitamins?

A

In the jejunum

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5
Q

Explain how absorption of fat-soluble vitamins occur

A

In the jejunum, fat-soluble vitamins forms micelle with bile salts allowing them to be passively transported into the intestinal enterocytes.

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6
Q

What occurs once the micelle enters the intestinal enterocyte?

A

In the enterocytes, micelles are packaged into chylomicrons and released into the lymphatic system. Once inside the lymphatic system, chylomicrons travel up the thoracic duct and enter the left subclavian vein.

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7
Q

Where do we obtain vitamin A from?

A

Either from animal foods in the form of retinyl esters or from plant foods as beta carotene

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8
Q

Discuss the conversion of the different forms of vitamin A in the body.

A

Retinol (which comes from retinyl esters) to retinal (which comes fro beta-carotene) is reversible. Retinal to retinoic acid is irreversible.

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9
Q

Sources of vitamin A

A

liver, sweet potatoes and carrots

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10
Q

Does the ingestion of equal amounts of beta carotene and retinyl esters yield similar amounts of vitamin A?

A

No. The absorption of beta carotene is not as efficient as that of retinyl ester

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11
Q

What is the form of vitamin A circulating in chylomicrons?

A

Retinyl ester

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12
Q

Where is retinyl ester converted to retinol?

A

In the hepatocyte

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13
Q

After conversion from retinyl ester to retinol, where is retinol stored?

A

Retinol is transported into stellatte cells for storage

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14
Q

What are stellate cells?

A

Account for 5%-8% of the cells in the liver. In a healthy liver, stellate cells are quiescent and contain numerous vitamin A lipid droplets, constituting the largest reservoir of vitamin A in the body

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15
Q

Function of retinol?

A

Supports reproduction and major transport and storage form

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16
Q

Function of retinal?

A

Active in vision

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17
Q

Function of retinoic acid?

A

Regulates cell differentiation, growth, and embryonic development

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18
Q

Function of beta-carotene?

A

Antioxidant

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19
Q

Why is retinoic acid unique?

A

Retinoic acid functions as a transcription factor, which means it participates in protein synthesis and cell differentiation through regulating gene expression (via RAR - its nuclear receptor)

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20
Q

Name specific cells affected by retinoic acid

A

Retinoic acid promotes differentation of both epithelial cels and goblet cells which protects mucous membranes

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21
Q

Pharamacological use of retinoids?

A
  1. Retinoic acid - treatment of acute promyelocytic anemia
  2. Tretionin - specifically Retin-A - treatment for acne, agining, dark pigments
  3. Isotretinoin - specifically accutane - oral treatment for cystic acne but is a teratogenic, therefore women who are using Accutane are required to use reliable forms of birth control
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22
Q

What is the pigment molecule found in rods (a cell of the retina)

A

Rhodopsin

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23
Q

What is rhodopsin?

A

Rhodopsin is composed of a protein caled opsin which is bonded to a molecule of retinal.

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24
Q

Explain how light affects the conformation of rhodopsin

A

As light interacts with rhodopsin, retinal changes from cis to trans configuration. Configuration change (cis to trans) releases retinal from opsin. Alone, opsin initiates a signal transduction cascade to nerve cells that communicate with the brain’s visual center. Trans retinal is enzymatically converted back to cis retinal which combines with opsin to regenerate rhodopsin.

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25
Q

What is a primary deficiency?

A

Inadequate intake

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26
Q

What is a secondary deficiency?

A

Poor absorption of fats

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27
Q

What is a deficiency in vitamin A called?

A

Hypovitaminosis A

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28
Q

What diseases can cause a secondary deficiency in vitamin A?

A

Cystic fibrosis, Crohn’s disease, liver disease, excessive alcohol intake

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29
Q

Symptoms of vitamin A deficiency?

A

Night blindness . If left untreated, it can progress to complete blindness known as xerophthalmia

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30
Q

Explain how a deficiency in vitamin A can lead to dry eyes.

A

Reduction in goblet cells and production of mucin leads to dry eyes.

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31
Q

Other changes developing with vitamin A deficiency

A

Bitot spots, corneal ulcer and keratomalacia

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32
Q

What causes corneal ulcers (keratitis)?

A

Due to inflammation of cornea

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33
Q

What causes keratomalacia?

A

Due to softening of the cornea

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34
Q

How is immunity affected in patient with a vitamin A deficiency?

A

Immunity is impaired

35
Q

What is keratinization?

A

Kertinization, also known as hyperkeratosis, results from a vitamin A deficiency. The skin becomes dry, rough and scaly.

36
Q

Results of toxiticy of vitamin A

A

birth defects

37
Q

What are the birth defects in a child whose mother took accutane?

A

Cranofacial malformations and malformations of the CNS, thymus, and heart

38
Q

Symptoms of Beta-carotene excess

A

Not harmful. Excess beta-carotene is stored in the fat under skin

39
Q

How is vitamin D different from other nutrients?

A

Vitamin D can be synthesized in the body with the help of UV light using cholesterol as a precursor

40
Q

Describe what occurs in the skin that leads to vitamin D3 formation.

A

In response to sunlight exposure, pro-vitamin D3 (7-dehydrocholesterol) is converted to pre-vitamin D3. Pre-vitamin D3 undergoes isomerization to become Vitamin D3 (cholecalciferol).

41
Q

What form of vitamin D is food?

A

Vitamin D3 (cholecalciferol)

42
Q

Describe what occurs in the liver, with regard to vitamin D.

A

Vitamin D3 binds to a vitamin D-binding protein in the bloodstream and is transported to the liver. D3 is hydroxylated by the liver. Enzyme responsible is 25-hydroxylase. The result is 25(OH)D3

43
Q

Describe what occurs in the kidney, with regard to vitamin D.

A

25(OH)D3 is further hydroxylated in the kidney by (1-OHase). This yields the active 1,25 (OH)2D3 which is calcitriol

44
Q

Sources of vitamin D?

A

Several types of fish, mushrooms, and fortified milk

45
Q

Functions of vitamin D?

A

calcium and phosphorus homeostasis (main), bone health (main), immune function, reduction of inflammation and apoptosis, blood pressure regulation, regulation of gene expression as a pro-hormone

46
Q

How does vitamin D modulate gene transcription?

A

The active form of vitain D, calcitriol, can modulate gene transcription following binding to its cognate nuclear receptor, the vitamin D receptor (VDR)

47
Q

Factors that contribute to a vitamin D deficiency

A

Dark skin, breastfeeding without supplementation, lack of sunlight, use of non-fortified milk, lose ability to active vitamin D (elderly), little or no milk in diet, vegan diet

48
Q

Diseases resulting from a vitamin D deficiency

A

Rickets, osteomalacia, osteoporosis

49
Q

Symptoms of Rickets?

A

(1) Growth retardation, skeletal abnormalities such as bowing of the legs. (2) Poorly formed attachments of bones to cartilage. (3) Delayed closure of fontanel resulting in rapid enlargement of head

50
Q

Who in the US is more suspectible to rickets?

A

young, breast-fed black children. Breast milk does not have much vitamin D and pigments in dark skin reduce vitamin D synthesis

51
Q

What is osteomalacia?

A

poor mineralization of bones due to vitamin D deficiency leads to soft, brittle and deformed bone

52
Q

How can osteomalacia develop?

A

Result of taking anticonvulsants such as phenobarbital and phenytoin for a long period of time. Also, in patients with chronic kidney disease where the production of the active form of vitamin D is greatly reduced

53
Q

What causes toxiticis in vitamin D?

A

occurs with supplementation; cannot occur via sunlight or dietary sources

54
Q

Harm from increased vitamin D?

A

Excess vitamin D increases the concentration of blood calcium which tends to precipitate in the soft tissues suh as blood vessels, kidney, heart, lungs where it can cause death

55
Q

Another name for vitamin E?

A

Tocopherol

56
Q

What is tocopherol?

A

Tocopherol is a general term describing 8 related compounds (4 tocopherols: alpha, beta, gamma & delta and 4 tocotrienols), one of which has vitamin E activity.

57
Q

Which compond has vitamin E activity?

A

D-isomer of alpha tocopherol

58
Q

Sources of vitamin E?

A

Nuts and oils

59
Q

Functions of vitamin E?

A

effective lipid soluble antioxidant (main), inhibition of platelet aggregation and monocyte adhesion, assisting in maintenance of fertility

60
Q

How is vitamin E an effective lipid soluble antioxidant?

A

Protects polyunsaturated fatty acids within cell membranes from peroxidation

61
Q

What is lipid peroxidation?

A

Lipid peroxidation is the oxidative degradation of lipids. It is the process in which free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage.

62
Q

Common target for peroxidation?

A

Unsaturated fatty acids present in membrane phospholipids

63
Q

How does vitamin E stop peroxidation?

A

Vitamin E stops peroxidation by donating a hydrogen to lipid radicals

64
Q

What is vitamin C’s role in aiding vitamin E?

A

After donating its hydrogen, active vitamin E is regenerated by vitamin C

65
Q

Who generates the most reactive oxygen species?

A

The mitochondrial electron transport chain generates most of the reactive oxygen species such as superoxide or hydrogen peroxide

66
Q

Results from a deficiency in vitamin E?

A

characterized by the premature destruction of red blood cells leading to hemolytic anemia

67
Q

How could a vitamin E deficiency occur?

A

inadequate intake (rare) or fat malabsrption because of cystic fibrosis or pancreatic insufficiency (secondary deficiency) or in preterm infants

68
Q

How can vitamin E toxicity occur?

A

rare; but may develop when exogenously supplemented

69
Q

Results of excess vitamin E?

A

(1) interference with vitamin K which can lead to issues with clotting and increase likelihood of a hemorrhage
(2) nerve daage

70
Q

How is vitamin K unique?

A

Synthesized by the bacteria in our gut

71
Q

Animal source of vitamin K?

A

menaquinones (also the form synthesized by gut bacteria)

72
Q

Plant source of vitamin K?

A

phylloquinones

73
Q

Sources of vitamin K?

A

Green, leafy vegetables and oils

74
Q

Function of vitamin K?

A

involved in blood clotting and bone mineralization

75
Q

What is vitamin K’s main role as a cofactor?

A

Vitamin K is a required cofact for the posttranslational modification of glutamate to the unusual amino acid, gamma-carboxyglutamate (Gla)

76
Q

Which enzyme catalyzes the conversion of glutamate to gamma-carboxyglutamate (Gla)?

A

Gamma-glutamyl carboxylase

77
Q

What is the importance of gamma-carboxyglutamate (Gla) ?

A

Several blood proteins require the presence of nine to thirteen Gla residues for normal function; these are the so called vitamin K-dependent (VKD) proteins

78
Q

Role of vitamin K in blood coagulation?

A

Vitamin K participates in both the intrinsic and extrinsic blood-clotting pathways

79
Q

Causes of a possible deficiency in vitamin K?

A

Deficiency of vitamin K may develop with the use of antibiotics and malabsorption. Newborns have low stores of vitamin K at birth due to the laack of gut bacteria.

80
Q

Symptoms of vitamin K deficiency?

A

hemorrhaging, bruisability, mucosal bleeding

81
Q

How could a patient have a toxicity in vitamin K?

A

Toxicity may develop in patients taking warfarin. Warfarin works by decreasing the activity of vitamin K

82
Q

What do vitamins A, D, and K have in common?

A

Play important role in bone growth and remodeling

83
Q

What is the relationship between vitamin E and A?

A

Vitamin E protects vitamin A from oxidation

GI (27 decks)

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