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NTRN 364 > Midterm Study Guide > Flashcards

Midterm Study Guide Flashcards

1
Q

How are vitamins classified (i.e. by what)?

A

-biological and chemical activity

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2
Q

What is a vitamin? What about a provitamin?

A

Vitamin refers to ..
organic compounds essential for normal physiological functions and needed in small amounts

Provitamins are compounds that ….
-can be converted into the bioactive form of the vitamin in your body

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3
Q

What are the following characteristics of vitamins?

A

-functions are highly specific and needed in small quantities
-food forms usually require some metabolic transformation to functional/bioactive form
-vary chemically and functionally
-do not have structural function and are not catabolized for energy

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4
Q

What is a primary vs. secondary vitamin deficiency?

A

Primary-an organism does not get enough of the vitamin from its food;varied diet will unlikely cause a severe primary deficiency

Secondary-underlying disorder that prevents or limits the absorption or use of the vitamin
-lifestyle factors: smoking; excessive alcohol consumption; use of medications that interfere with the absorption or use of the vitamin
-genetics/SNPs

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5
Q

What are the DRI’s?

A

DRI is an umbrella term that includes AI, EAR, RDA, UL
-DRI’s are recommendations for healthy population.

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6
Q

What are the similarities and differences between EAR, RDA, AI? What reference values can individuals use?

A

-EAR;estimated average requirements- a value that meets the requirements of 50 percent of healthy poeple in their target group within a given life stage or particular sex. These values become the scientific foundation upon whihc RDA values are set
-RDA; recommended daily allowance-set to meet the needs of 97-98 percent of the target healthy population in life stage or gender group, used as a goal for usual dialy intkae by individuals
-AI; adequate intake- created for nutrients when there is insufficient consistent scientific evidence to set an EAR fot the entire population; used as a goal for individuals

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7
Q

What are the stages of deficiency?

A

-interruption in source— reduction in body storage (reserves vary)—-impairments in biochemical functioning—-alteration in function/morphology
-result: clinical manifestations; clinical manifestations target every organ

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8
Q

How do we assess vitamin status in general?

A

-refers to the degree of balance between supply (this includes intake and body stores) and biological need
-goal: stable, satisfactory or positive status

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9
Q

What are the different forms of vitamin A?

A

-retinol (alcohol) or retinal (aldehyde)

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10
Q

what is vitamin A

A

-nutritional term for compounds that enhibit biological activity of all trans-retinol

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11
Q

What is the relationship between the carotenoids and the active form of vitamin A?

A

Retinal or active form of vitamin A from animal sources
provitamin a; beta carotene and other carotenoids come from plant sources

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12
Q

What has the highest Vitamin A activity coming from plant sources?

A

-B-carotene

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13
Q

beta-carotene turns into …. which is required for…. which is then turned into…. which is required for…..which is then turned into…. which is stored in the ….

A

beta-carotene turns into retinal which is required for vision which then is turned into retinol(vitamin a) which is required for reproduction, which is then turned into retinol palmitate which is stored in the liver

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14
Q

What are the differences in bioavailability of preformed vs pro-vitamin forms?

A

Carotenoids-provitamin a, are less bioavailable than retinoids-pre formed vitamin a; Retinyl palmitate is a form of preformed vitamin A.

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15
Q

What do we know about the absorption between the preformed and the pro-vitamin A sources?

A

Absorption of dietary preformed Vit A( retinyl esters) is about 70-90% if meal contains fat
Absorption of cartenoids varies greatly(type of food consumed, food processing)

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16
Q

What are the food sources of provitamin A?

A

-dark green and yellow fruits and vegetables
-ex. Spinach, carrots, sweet potato, squash, cantaloupe

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17
Q

What are the food sources of preformed vitamin A retinoids?

A

-egg yolk, dairy products (milk fat), organ meats and meats, fatty fish oils, fortified foods

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18
Q

Why is there use of the RAE?

A

RAE- retinol activity equivalents and is a unit of measure for the vitamin A content of food. It reflects the amount of active vitamin A provided by the different types of food sources
1 mcg RAE= 12 mcg beta carotene in foods and 24 mcg other carotenoids in foods

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19
Q

What other deficiency usually coexists with Vitamin A deficiency?

A

-Iron deficiency

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20
Q

What is the relationship between zinc and vitamin a?

A

zinc deficiency and influence vitamin a absorption because it is part of rbp (transporting to cells) and required for the enzyme that converts retinol to retinal

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21
Q

What is the plasma transporter for vitamin A?

A

-retinol binding protein (RBP)

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22
Q

Summarize the function of Retinoid binding protein (RBP)

A

-The relative abundance of RBP is highest in liver
-in plasma, RBP function to solubulize retinol and to deliver it to cells
-RBP concentrations vary with disease (PEM, liver diseases, Vitamin A deficiency)

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23
Q

What do we know about RBP and the various bioactive forms of Vitamin A? RBP is tightly regulated by what specific factors?

A

RPB is homeostatically maintained: regulation via RPB, renal and the variety of enzymes esterify and hydrolyze. RPB is governed by many factors including adequacy of zinc, quantity of vitamin A stores, protein status,kidney function ect..

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24
Q

What is associated with decreased RBP?

A

-Protein Malnutrition

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25
Q

What is Holo-RBP?

A

When R-OL binds, the complex is known as Holo-RBP
Holo-RBP binds to TTR for transport to target cells (transthyretin)
TTR bound to Holo-RBP protects it from being filtered by the kidney and favors cellular uptake

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26
Q

What are the functions of Vitamin A

A

-Vision, immune function, epithelial cell differentiation, gene regulation, bone growth(bone growth will not be covered)

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27
Q

What are some key clinical indicators of vitamin A deficiency?

A

-Eye Signs: Conjuctival Xerosis with Bitot’s Spots in young children
-dietary assessment
-epithelial cell differentiation (inc. keratin forming cells)
-impaired reproductive capacity and immune function

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28
Q

Are there concerns about toxicity with the different forms of vitamin A? Why/why not?

A

Yes, because vitamin A is a fat soluble vitamin there is the risk of the body storing too much to the point of toxicity. As well, preformed vitamin A, such as in the form of supplements, is the form of vitamin A associated with toxicity.

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29
Q

What was learned from the deplete/replete study?

A

-Plasma A levels do not appear to be useful in ascertaining vitamin A deficiency, as plasma levels did not reflect inadequacy immediately or within a reasonable time period.
-There was a wide range of plasma levels that reflected various symptoms. This could be due to a various number of factors, such as diet, and body fat storage. Above 20 mcg/100 mL symptoms did not manifest, but subjects reached this point at varying times
-Retinol does a more effective job at increasing levels of plasma A
-it’s unlikely that the DRI recommendations are solely based on plasma levels of vitamin A. Plasma A may play some role in adequacy status, but due to the high variability of vitamin A repletion and depletion rates in different people other factors such as liver vitamin A reserve also have an impact.

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30
Q

What is the active form of Vitamin D?

A

-Calcitriol (1alpha,25 dihydroxycholecalciferol)

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31
Q

What is the plant derived form of Vitamin D?

A

-D2(ergocalciferol)(not active form)

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32
Q

What is the form of vitamin D that is synthesized from sunlight and skin and found in animal sources?

A

-Cholecalciferol or Vitamin D3 (not active form)

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33
Q

Give examples of food sources of vitamin D?

A

-salmon, fortified cereal, fortified milk, egg yolk, irradiated mushrooms

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34
Q

Describe what happens in the body when responding to hypercalcemia

A

-calcitonin levels increase
-osteoblasts build bone using calcium(take calcium from plasma to decrease levels)
-kidney increases calcium excretion
-feedback inhibition of 1 alpha hydroxylase to slow rate of active D formation

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35
Q

Describe the vitamin D targets of action-calcium homeostasis in Bone, intestines and kidney

A

-Bone: PTH +D =stimulates osteoclasts
-Intestines: D dependent increases calcium absorption
-Kidney: PTH +D= increases calcium absorption
Vitamin D and PTH work in tandem to raise plasma calcium to retain calcium homeostasis

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36
Q

What is the interaction between calcium and vitamin D?

A

increases calcium reabsorption in kidneys, increases absorption in the gut, mobilizes calcium from bones

37
Q

How is the inactive form of Vit.D activated? Where does this occur and how exactly (including enzymes)?

A

Vitamin D3 is activated after 2 hydroxylations-liver and kidney

38
Q

Why is there an upper limit (UL)? Are food sources a concern for vitamin D toxicity? What happens with toxicity?

A

-If toxicity happens, it is typically from high supplement doses are a genetic sensitivity to Vit. D
What is the upper level of Vitamin D?
-4,000 IU
-symptoms include nausea, vomiting, weakness and altered level of consciousness, excessive thirst

39
Q

What is the process of endogenous or cutaneous Vitamin D production?

A

Epidermis absorbs UV-B light (280-310nm), & dehydrocholesterol converted to inert isomers, Carbon bonds break, slowly converts to Vitamin D3, non-enzymatic photo-isomeric conversion into choecalciferol, temperature dependent (1-2 days), carried via DBP in plasma to liver for metabolism

40
Q

What are some of the factors that affect the body’s ability to synthesize vitamin D?

A

UVB light not sufficient at high latitudes during certain winter months Clothing and sunscreen, higher melanin content, skin temperature, burn patients,obesity and aging

41
Q

What are the main risk factors for a vitamin D deficiency?

A

African American Women are 20 times more likely to have low D3 levels vs Caucasian women, burn patients have lower levels of 7-dehyrochlosterol in post burn scar tissue, aging- the epidermis of 77-88 year olds has lower 7-dehydocholesterol levels, Obesity decreases bioavailibilty of stores because adipose tissue sequesters vit D.

42
Q

What clinical signs might be associated with insufficient vitamin D? What can deficiency lead to in children and adults?

A

Clinical signs potentially associated include difficulty walking and muscle pain, as vitamin D deficiency can lead to improper calcium levels due to decreased absorption of calcium in the small intestine and altered PTH homeostasis. Altered calcium levels lead to poorer bone health. Calcium is also important for muscle function, specifically muscle contractions.
Lead rockets in children and osteoporosis in adults

43
Q

What is the Vitamin D deficiency disease?

A

-Rickets

44
Q

How do you determine status? What form of vitamin D is used for assessment?

A

Vitamin D is assessed by plasma 25-OH-D3 levels as this is the most active form in the plasma.

45
Q

What should be considered when purchasing dietary supplements of vitamin D?

A

What type of vitamin D it is. It is better to have supplement with cholecaciferol (D3) because of better bioavailability. Also the IU because a lot of supplements go over the DRI recommendations.

46
Q

Vitamin E is also known as a

A

-tocopherols and tocotrienols

47
Q

What are the characteristics of the tocopherols vs tocotrienols?

A

Tocopherols have no double bonds and tocotrienols do. alpha tocopherol meets vitamin E requirements. the forms are not convertible

48
Q

What is the main factor impacting which form of the vitamin has the most biologic activity?
What form of Vitamin E meets Human requirements?

A

-alpha-tocopherol because it can be transported by the alpha tocopherol transfer protein in the liver

49
Q

What does all-rac vs RRR forms of the vitamin mean?

A

The natural form is the molecular form RRR-alpha-tocopherol while the synthetic form is in the molecular form all rac-alpha-tocopherol.

50
Q

What are the differences between natural vs synthetic forms of vitamin E?

A

a natural source
-is the single isomer (d-alpha-tocopherol)
-Synthetic is a mixture of eight isomers
-Natural source has twice the bioavailability of synthetic

51
Q

What are good sources of Vitamin E?

A

-Sunflower Oil(1 tablespoon); Almonds (1 oz.); Avocado (1 med. sized)

52
Q

What does the tocopherol transfer protein (TTP) do? Where is it located? What form of Vitamin E does it have the highest affinity for?

A

located in liver, plays an integral role in whole-body Vitamin E status; TPP has the highest affinity for alpha-tocopherol; TPP for intracell trafficking of vitamin

53
Q

How is vitamin E carried in the plasma? Is there a carrier protein?

A

Alpha tocopherol transfer protein for vitamin E is primarily located in the liver. It functions to transfer alpha tocopherol from the hepatocyte membrane to plasma via chylomicrons/lipoproteins.
Vittamin E is transported solely by chylomicrons, which contain a high concentration of hydrophobic molecules, mainly fatty acids. Vitamin E is not transported by its own unique transport protein like A and D. The most analogous thing for vitamin E is the alpha-tocopherol transfer protein, but that only transports in the liver.

54
Q

What are the main functions of Vitamin E?

A

-boosts antioxidant defense, protects cell membranes, enhances immune function

55
Q

What other vitamins can Vitamin E interact with?

A

-Vitamin K; A negative result is that high levels of Vitamin E can cause bleeding

56
Q

How does vitamin E function as an antioxidant

A

-its an antioxidant by contributing a hydrogen from its hydroxy group, to neutralize the free radicals; vitamin C then contributes a hydrogen to restore vitamin E’s hydroxyl group to its natural form.

57
Q

Vitamin E protects … from lipid peroxidation

A

-long-chain poly-unsaturated fatty acids (PUFAS)

58
Q

What are factors that affect bioavailability of Vitamin E?

A

-genetics(alpha TPP), lifestyle(smoking, obesity), gender, age, intake, absorption and transport, metabolism(interaction with drugs)

59
Q

Vitamin E absorption efficiency is

A

-low; less than 50%

60
Q

How is vitamin E assessed? What are the challenges with this?

A

Assessed by testing plasma levels. The limitation is that alpha tocopherol levels may be in the normal range in patients with elevated cholesterol and triglyceride concentrations but the individual may actually be deficient
You could look for increased red cell hemolysis and increased expired ethane or pentane.

61
Q

What is the UL based on? How is toxicity of Vitamin E different from Vitamins A & D?

A

The UL was set based on rate studies. Few side effects <2,000 mg of alpha tocopherol byt lacking long term human studies
Vitamin E absoprtion efficiency is low <50% and is lowest of fat soluble vitamins .
It is fat soluble so it can be stored but it will not accumulate in liver to toxic lvels. Stored in many places throughout the body

62
Q

What are the 2 primary vitamers of Vitamin K?

A

Phyllo Quinone (K1), plant, low absorption (<20%)
Menaquinones (K2), animal source

63
Q

Where do we find sources of phylloquinone, menaquinone?

A

-K1(phylloquinone): Kale, canola oil
-K2(menaquinone): fermented soybeans

64
Q

Highest phylloquinone content in most diets are

A

-green leafy vegetables(spinach, lettuce, broccoli)

65
Q

What is Vitamin K2 labeled as and which one has the longer half-life?

A

-known as MK-4 or MK-7
-MK-7 seems to have the longer half life so MK-7 is often the standard form used in dietary supplements

66
Q

How is vitamin K carried in plasma?

A

Mainly carried in the blood by lipoproteins, no transporter proteins. Essentially it is packaged into mixed micelles, absorbed by enterocytes, packaged into chylomicrons, goes to liver via lymphatic system, repackaged into VLDLs then delivered to tissue by lipoproteins

67
Q

Why is recycling of vitamin k important?

A

Body pool of K is very small hence cycling of vitamin K plays important role in maintaining body levels

68
Q

What is the molecular role of Vitamin K?

A

-post translational ycarboxylation
-K is a co-factor for vitamin K dependent carboxylase, y glutamyl carboxylase

69
Q

What is the active form of the vitamin k used as the cofactor for the gamma carboxylation of glutamic acid?

A

The enzyme uses the hydroquinone form of K and catalyzes a gamma-carboxylation of glutamic acid residues in several different proteins. Therefore, vitamin K becomes a key co-factor for proper modification of the function of clotting proteins. To form the actual blood clot, the precursor proteins found in the liver need vitamin K to convert the precursors into clotting factors (catalyzing the carbon dioxide incorporation into specific residues of glutamate in specific precursor proteins aka gamma-carboxylation).

70
Q

What are some examples of GLA proteins?

A

Clotting proteins, Hepatic K dependent proteins, bone protein involved in calcification

71
Q

What is the best assessment of Vitamin K status?

A

-Presence of undercarboxylated proteins (PIVKA-II protein induced in Vitamin K absence)

72
Q

What does INR stand for and what does it tell us?

A

International normalization ratio
-patient’s PT time/ mean normal patient PT time (prothrombin time)
-inc. INR =increased clotting time
-inc. Vit K intake can cause INR to dec.
-dec. In Vit K intake can cause INR to increase

73
Q

Why are long-term antibiotics a concern for vitamin K status?

A

It causes insufficient intestinal microbiome(decreased gut bacteria production)

74
Q

Why are babies at birth routinely given a dose of Vitamin K?

A

Newborns are at high risk for Vitamin K deficiency due to an immature hemostasis system, their gut bacteria still developing, and poor placental transfer from their mothers. These are the reasons why a dose at birth of Vitamin K is crucial to making sure that newborns do not undergo a hemorrhagic disease.

75
Q

What is the link between Vitamin K and anticoagulant therapy? How does warfarin affect the Vitamin K cycle?

A

-It interrupts in the third step of the Vitamin K cycle where the Vitamin K epoxide needs to be reactivated and is reduced to Vitamin K quinone and then Vitamin K quinone is reduced to hydroquinone(active form)
-Warfarin blocks both reductases

76
Q

What is Prothrombin Time? (PT)

A

-Prothrombin is produced by the liver and is one of the VKDPs involved in blood clotting
-clinically used test determines how long it takes for one’s blood to clot

77
Q

What is the difference between total C and vitamin C?

A

-Total Vitamin C refers to both Ascorbic Acid (AA) and Dehydroascrorbic acid (DHAA) forms(no biologic activity)
-vitamin C refers to water soluble L-Ascorbic Acid form of the vitamin with biological activity of ascorbic acid

78
Q

What is the bioactive form of this vitamin C ?

A

L-Ascorbic acid form is the bioactive form
DHAA is considered to have biologic activity only in that it can convert back into AA.

79
Q

What is an excellent source of Vitamin C?

A

-fruits and vegetables
Ex: Strawberries, orange,kiwi, cantaloupe, Broccoli, Raw green and red peppers,

80
Q

What is the major metabolic role of Vitamin C? What are the enzymatic vs. non-enzymatic functions of the vitamin?

A

Enzymatic function: Vit. C is a co-factor for 14 different enzymes that are either monooxygenases, or dioxygenases
Non-enzymatic functions:
-Its an antioxidant, immune functions, prevents LDL oxidation

81
Q

What is Vitamin C interactions with iron?

A

-Vitamin C aids in iron absorption
-Vitamin C sources enhances non-heme iron absorption by reducing ferric to ferrous
-Reducing inhibition from inhibitors such as tea, coffee, calcium.phosphate
-increase absorption but not iron status

82
Q

What is the role of this vitamin C in collagen synthesis and wound healing?

A

Vitamin C is a co-factor for 3 enzymes in collagen synthesis including prolyl 4-hyroxylase
Vitamin C acts as a cofactor in 3 enzymes involved in collagen synthesis, specifically by reducing the iron center to activate the enzyme. In this way, vitamin C is vital for the formation of collagen and is thus important for wound healing where more collagen needs to be constructed.

83
Q

When there is an increased need for Vitamin C?

A

-Infections, burns(collagen for scar tissue), intake of toxic metals (lead, mercury),smoking

84
Q

How do we determine status for vitamin C ?
What is the best way to see recent dietary intake and what is the best way to see longer term?

A

plasma vit. C concentration reflects recent dietary intake
-leuokocyte vitamin C reflects tissue stores (but difficult to assess)

85
Q

What is the deficiency for vitamin C called?

A

Scurvy

86
Q

What are the earliest signs of vitamin C deficiency? What are the clinical features of scurvy?

A

-Bleeding from the gums, petechiae, and fatigue are some of the earliest signs of vitamin C deficiency.
-Clinical signs of scurvy include bleeding and inflamed gums, hair and tooth loss, joint pain, and impaired wound healing. One way to remember the clinical features of scurvy is the 4 H’s: hemorrhage, hyperkeratosis, hypochondriasis, and hematologic disorders.

87
Q

What do the 4 H’s reference?

A

4 H’s: hemorrhage, hyperkeratosis, hypochondriasis, and hematologic disorders.

88
Q

How is vitamin C linked to Vitamin E?

A

Vitamin E protects against LDL oxidation and then is regenerated by Vitamin C.

89
Q

What is the UL based on for Vit C

A

-The UL of Vitamin C of 2 g/d is based on preventing adverse GI effects

NTRN 364 (7 decks)

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