Lecture 16 Flashcards

1
Q

Describe the upper level of intake for vitamins?

A

It is the level in which if we were to take any more vitamins we would be in the marginal-danger of toxicity to our body zone.

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2
Q

Describe RDI or AI for vitamins?

A

RDI is a safety net. The figures are arbitrary, we don’t really know what the RDI or AI is. Basically RDI is in the safety zone for our body.

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3
Q

Describe an EAR?

A

This is the estimate average requirement. This is in the marginal to safety zone of vitamins required for our body. Basically if we had any lower we would be in danger of deficiency.

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4
Q

Describe water-soluble vitamins transportation?

A

These are vitamins that are digested by mucosal hydrolyses. They are absorbed into the mucosal cell (sometimes subjected to modification) where they are transported into the portal vein to reach the liver.

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5
Q

Describe lipid-soluble transportation?

A

These vitamins undergo the same components as triglycerides and cholesterol. Initially the vitamins form minor components of micelles, this depends on the presence of vile salts and pancreatic lipase (attacking triglycerides) before this can occur. After uptake into the mucosal cell they’re exported into the lymphatic system and ultimately into the plasma as chylomicrons. They eventually end up being stored as body lipids, sometimes as fatty acid esters.

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6
Q

What are water-soluble vitamins?

A
  1. Vitamin C (ascorbic acid)
  2. Thiamin (Vitamin B1)
  3. Riboflavin (Vitamin B2)
  4. Niacin (Vitamin B3)
  5. Pantothenic acid (Vitamin B5)
  6. Pyridoxine (Vitamin B6)
  7. Cobalamin (vitamin B12)
  8. Folate (Folic Acid - Vitamin B4)
  9. Biotin (Vitamin B7)
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7
Q

What are lipid-soluble vitamins?

A
  1. Vitamin A (retinol, carotenes).
  2. Vitamin D (cholecalciferol).
  3. Vitamin E (tocopherols and tocotrienes).
  4. Vitamin K (phylloquinone, menaquinone, menadione).
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8
Q

What happens in water-soluble vitamins in regards to absorption?

A

Directly into the blood.

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9
Q

What happens to water-soluble vitamins in regards to transport?

A

Travel freely.

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10
Q

What happens to water-soluble vitamins in regards to storage?

A

Circulate freely in water-filled parts of the body.

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11
Q

What happens to water-soluble vitamins in regards to excretion?

A

Kidneys detect and remove excess in urine.

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12
Q

What happens to water-soluble vitamins in regards to toxicity?

A

Possible to reach toxic levels when consumed from supplements.

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13
Q

What happens to water-soluble vitamins in regards to requirements?

A

Needed in frequent doses (1-3 days).

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14
Q

What happens to lipid-soluble vitamins in regards to absorption?

A

First into the lymph, then the blood.

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15
Q

What happens to lipid-soluble vitamins in regards to transport?

A

Many require protein carriers.

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16
Q

What happens to lipid-soluble vitamins in regards to storage?

A

Stored in the cells associated with fat.

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17
Q

What happens to lipid-soluble vitamins in regards to excretion?

A

Less readily excreted; tend to remain in fat-storage sites.

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18
Q

What happens to lipid-soluble vitamins in regards to toxicity?

A

Likely to reach toxic levels when consumed from supplements.

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19
Q

What happens to lipid-soluble vitamins in regards to requirements?

A

Needed in periodic doses (perhaps weeks or even months).

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20
Q

What are the factors the affect bioavailability?

A
  1. Efficiency of digestion/transit time.
  2. Previous nutrient intake and nutritional status.
  3. Other foods consumed simultaneously.
  4. Food preparation method.
  5. Source of the nutrient - synthetic or natural.
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21
Q

What is the active form of Vitamin B1?

A

Thiamine pyrophosphate.

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22
Q

What is the major function of Vitamin B1?

A

Coenzyme of carbohydrate metabolism - energy yielding.
Oxidative decarboxylations.
Transketolases (PPP).

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23
Q

What is the primary deficiency of Vitamin B1?

A

Beriberi - wet and dry.

Wernicke’s encephalopathy.

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24
Q

What is a common food source of Vitamin B1?

A

Whole grain cereals, fortified cereals, pork, sunflower seeds, legumes.

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25
Q

What is the active form of Vitamin B2?

A

Riboflavin - FMN FAD

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26
Q

What is the major function of Vitamin B2?

A

Coenzyme of carbohydrate metabolism. Intermediates via red/ox reactions.

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27
Q

What is the primary deficiency of Vitamin B2?

A

Inflammation of mouth and tongue - aribofalvinosis, cracks at the corner of mouth, eye disorders.

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28
Q

What is the common food source of Vitamin B2?

A

Milk products, fortified cereals, liver, mushrooms.

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29
Q

What is the active form Vitamin B3?

A

Niacin - NAD+ NADP+

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30
Q

What is the major function of Vitamin B3?

A

Coenzyme of energy metabolism.
Coenzyme of fat synthesis.
Coenzyme of fat breakdown.

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31
Q

What is the primary deficiency of Vitamin B3?

A

Pellagra: diarrhoea, dermatitis, dementia, death.

32
Q

What is the common food source of Vitamin B3?

A

Milk, eggs, meat, poultry, tuna, salmon, and fortified cereals.

33
Q

What is the active form of Vitamin B5?

A

Pantothenic acid.

34
Q

What is the major function of Vitamin B5?

A

Constituent of coenzyme A.

35
Q

What is the active form of Vitamin B6?

A

Pyridoxal phosphate.

36
Q

What is the major function of Vitamin B6?

A

Coenzyme of protein metabolism.
Phosphorylase modification.
Neurotransmitter synthesis.
Haemoglobin synthesis.

37
Q

What is the common food source of Vitamin B6?

A

Meat, fish, poultry, potatoes, legumes, non-citrus fruits, salmon, seeds, spinach.

38
Q

What is the active form of Vitamin B7?

A

Biotin - Amide link to lysine.

39
Q

What is the major function of Vitamin B7?

A

Coenzyme of glucose production.

Coenzyme of fat production (carboxylations - ATP dependent).

40
Q

What is the primary deficiency of Vitamin B7?

A

Depression, lethargy, dermatitis, anaemia.

41
Q

What is the common food source of Vitamin B7?

A

Cheese, organ meats, egg yolks, soybeans, fish, wholegrain cereals, GI bacteria.

42
Q

What is the active form of Vitamin B9?

A

Folate - Tetrahydrofolate.

43
Q

What is the major function of Vitamin B9?

A

Coenzyme involved in DNA synthesis (one carbon transfers).

44
Q

What is the primary deficiency of Vitamin B9?

A

Microcytic (megaloblastic) anaemia.
Homocysteinuria
Poor growth
Inflammation.

45
Q

What is the common food source of Vitamin B9?

A

Animal products (meat, fish, poultry, milk, cheese, eggs) and fortified cereals.

46
Q

What is the active form of Vitamin B12?

A

Cobalamin.

47
Q

What is the major function of Vitamin B12?

A

Coenzyme of folate metabolism - methylmalonyl CoA -> succinyl CoA Homocysteine -> methionine (THF dependent).

48
Q

What is the primary deficiency of Vitamin B12?

A

Microcytic anaemia (pernicious anaemia causes B12 deficiency).

49
Q

What are the states of BeriBeri (Thiamine Deficiency)?

A

Wet.
Dry.
Infantile.

50
Q

What is Wet beriberi characterised by?

A

Edema (reduction pressure.
Press finger on the skin and you’ll get an indentation.
People look puffy - due to accumulation of fluid around the abdomen.
Disorientated and confused state.

51
Q

What is dry beriberi characterised by?

A
Protein energy malnutrition. 
Peripheral neuropathy.  
Loss of sensation - tingling. 
Vomiting.
Convulsions. 
Loss of muscle function in lower legs.
52
Q

What is the main cause of thiamine deficiency in the western world?

A

Alcohol. Alcohol causes there to be not enough thiamine reaching the liver.

53
Q

What is Wernicke-encephalopathy?

A

It is an alcohol related brain damage. Language problems, walking difficulty, unusual eye movement as well.

54
Q

What is Korsakoff syndrome?

A

Amnesia, inability to learn and confabulation.

55
Q

What does folate naturally occur in foods?

A

As polyglutamate. It occurs as mono glutamate in fortified foods and supplements.

56
Q

What happens to folate in the intestine?

A

Digestion breaks glutamates off and adds a methyl group. Folate is absorbed and delivered to cells.

57
Q

Describe folate deficiency?

A
Megaloblastic anaemia (large RBCs).
Neural tube defects (NTDs) during fatal developments e.g. spinal bifida. 
(?) Elevated risk of cancer and heart disease and to mental abnormalities.
58
Q

What are the causes of folate deficiency?

A
  1. Low dietary intake.
  2. Reduced intestinal absorption.
  3. Anticonvulsant drugs; some lipid lowering drugs.
  4. Folate antagonists - methotrexate.
  5. High alcohol intake - leading to decreased absorption, increased catabolism, often accompanied by poor diet.
  6. Pregnancy - due to increased folate requirement.
59
Q

What is the rate of neural tube defect affected pregnancies in NZ and countries with mandatory fortification?

A
NZ = 12-14 per 10,000.
Other = 7-9 per 10,000.
60
Q

What is the requirement of Folic Acid before and when pregnant?

A
Before = 800 micrograms a day 4-12 weeks prior to pregnancy.
During = 5000 micrograms a day.
61
Q

What foods are retinyl esters found in?

A

Animal foods.

62
Q

What happens to retinyl esters once in the body?

A

Becomes retinol, which supports reproduction. Retinol then can become retinal which can help vision.

63
Q

What foods is beta-carotene found in?

A

Plant foods.

64
Q

What happens to beta-carotene once in the body?

A

Becomes retinal, which supports vision.

65
Q

What happens to retinal?

A

It can become retinoid acid, which can regulate growth.

66
Q

What happens when light enters the eye?

A

Pigments within the cells of the retina absorb the light.

67
Q

What is vitamin A deficiency?

A

Night Blindness. Common in parts of the pacific, india and south east asia.

68
Q

Describe Vitamin A’s role in the body?

A

Vitamin A maintains healthy cells in the mucous membranes. Without vitamin A, the normal structure and function of the cells in the mucous membranes are impaired.

69
Q

What is a Vitamin A deficiency symptom?

A

Keratinisation. This is where you get little chicken bumps on the skin.

70
Q

Describe Beta-Carotene toxicity?

A

Beta-carotene is found in may fruits and vegetables. Toxicity occurs when there is overconsumption from food with Beta-carotene in it or if there is inefficient conversion of it. The person tends to get an orange colour on their skin.

71
Q

Describe Retinol toxicity?

A

Overconsumption from supplements. This toxicity is not reversible.

72
Q

What are other names of Vitamin D?

A
  1. Calciferol.
  2. 1,25 - dihydroxy Vitamin D (calcitriol).
  3. Animal version = Vitamin D3 or Cholecalciferol.
  4. Plant version = Vitamin D2 or ergocalciferol.
73
Q

How do we get Vitamin D?

A

We have a precursor made in our liver from cholesterol called:
7-dehydrocholesterol. Once UV from the sun hits it, it becomes Provitamin D3. We then eat foods, making it become Vitamin D3 (inactive form). It then travels to the liver where hydroxylation occurs and we now have 25-hydroxy vitamin D3. It then travels to the kidneys where hydroxylation occurs and we get 1,25-hydroxy Vitamin D3.

74
Q

Describe the amount of Vitamin D in food (IU)?

A
  1. Cod liver oil - 1Tbsp = 1,360 IU.
  2. Cooked Salmon - 100g = 360 IU.
  3. Milk (fortified - anlene) - 250mL = 200 IU.
  4. Sardines in oil - 100g = 345 IU.
  5. Cooked beef or liver - 100g = 30 IU.
  6. Raw mushrooms - 1/2 cup = 27 IU.
  7. Egg - 1 whole = 20 IU.
75
Q

What are the functions of Vitamin D?

A
  1. Regulation of cel growth (cancer prevention).
  2. Regulation of immune function (diabetes type 1, MS, RA autoimmune disease prevention).
  3. Regulation of blood pressure.
  4. Insulin production (heart disease and diabetes prevention.
76
Q

What is vitamin D deficiency?

A
Children = rickets - bowed legs due to the long bones of the legs bending outwards as weight bearing activities occur, such as walking. 
Adults = Osteomalacia.
77
Q

Who are the people that need vitamin and mineral supplements?

A
  1. Poor nutrient intake (elderly, dieters, adolescents, vegetarians).
  2. Increased nutrient requirements (children, pregnancy/lactation).
  3. Increased metabolic demands (surgery/trauma/fracture).
  4. Maldigestion or malabsorption (liver disease, GI, diarrhoea).
  5. Drug-nutrient interactions (prednisone/vita D, diuretics/K, Mg).
  6. Medical treatment interactions (chemo/radiation).