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Molecules to Cells > LEC 44 Lipid Soluble Vitamins > Flashcards

LEC 44 Lipid Soluble Vitamins Flashcards

Identify the biochemical active moieties in the structure of the lipid-soluble vitamins Describe the functions of each lipid-soluble vitamin Describe the signs and symptoms of deficiency Relate the sources and circumstances leading to deficiency Describe the signs and symptoms of toxicity

1
Q

What are the 4 lipid soluble vitamins?

A

A, D, E, & K

Slide 1

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2
Q

What are the requirements to be considered a vitamin?

A
  • Organic compounds distinct from lipids, carbohydrates and proteins
  • Natural components of foods (usually in minute quantities)
  • Essential for normal physiological function
  • Deficiency causes specific syndromes
  • Not synthesized by the host in sufficient amounts to meet normal physiological needs

Slide 5

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3
Q

How are lipid soluble vitamins carried in the blood to this tissues?

A

using lipoproteins

namely chylomicrons b/c they come from diet

He said this during lecture

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4
Q

Retinol (vit A) is derived from what compound?

A

beta-carotene

The smaller building unit is called isoprene

Slide 7 & 9

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5
Q

How is β-carotene converted to Vitamin A?

Enzymes & Intermediates

A
  1. β-carotene dioxygenase converts β-carotene to Retinaldehyde (Retinal) using bile salts and an O2
  2. Retinaldehyde Reductase converts retinaldehyde to Retinol using NADPH

Slides 9 & 10

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6
Q

Aside from retinol, retinal can also convert to what?

What does this compound act like?

A

Retinoic Acid

acts like a steroid hormone

Slide 12

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7
Q

In the visual cycle, what enzyme converts trans-Retinal to Δ11-cis-Retinal?

A

Retinal Isomerase

Slide 13

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8
Q

After storage in the tissues, how is vitamin A mobilized in the blood?

A

using retinol-binding protein (RBP)

From the Brick & slide 14

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9
Q

What is the major transport (circulating) & storage form of Vitamin A?

A

Retinol

Brick & Slide 12

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10
Q

How does retinal contribute to the visual cycle?

A
  • a component of rhodopsin, the light-sensing biological pigment in the rods of the retina
  • On exposure to light, rhodopsin triggers a G-protein cascade that allows the human eye to sense the amount of light in the environment

Brick

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11
Q

What is the cellular retinol binding protein involved in intestinal absorbtion?

A

CRBP II

Slide 14

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12
Q

Which cellular retinoic acid binding proteins are involved in embryogenesis?

A

CRABP I & II

Slide 14

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13
Q

What is promyelocytic leukemia?

A
  • the majority of cases involve a translocation of chromosomes 15 and 17
  • genetic fusion of the retinoic acid receptor (RAR) gene to the promyelocytic leukemia (PML) gene
  • PML protein is responsible for promoting immature myeloid cells differentiation into more mature cells
  • Fusion defeats normal regulation
  • Responds to RA treatment

Slide 17

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14
Q

How does vitamin A deficiency present?

A
  • Night blindness
  • Xerosis (dry conjunctivae)
  • Keratomalacia (softening and ulcerations of the cornea)
  • Rough scaly skin
  • Periosteal overgrowth
  • Nephritis
  • Fetal death and reabsorption
  • Ataxia and increased CSF pressure
  • Microcytic, hypochromic anemia

Slide 19

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15
Q

How does vitamin A toxicity present?

A
  • Birth defects (neural crest dysfunction)
  • Muscle and joint pain
  • Alopecia and skin erythemia
  • Liver dysfunction
  • Stunted growth
  • Bone fractures

Slide 21

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16
Q

What are 3 things that can happen with the eyes due to vitamin A deficiency?

A
  • Bitot’s Spots
  • Xeropthalmia
  • Keratomalacia

Slide 22

17
Q

What form of vitamin A is associated with teratogenesis in excess amounts?

Accutane

A

13-cis-retinoic acid

Slide 23

18
Q

What is the role of Vitamin D?

A
  • Maintains plasma calcium & phosphorous concentrations
  • Supports cellular processes, neuromuscular and immune function, & bone ossification
  • Enhances calcium & phosphorous absorption from small intestine & mobilization from bone
  • Acts like a hormone with receptors and target tissues

Slide 24

19
Q

Where is vitamin D stored?

A

Liver

Slide 26

20
Q

Vitamin D must undergo what type of reaction to leave the liver?

A

Hydroxylation

Slide 26

21
Q

What is the circulating form of vitamin D?

A

25(OH)D3

25-hydroxy Vit D

Slide 26

22
Q

How does Rickett’s occur?

A
  • Inborn error with the 1-alpha-hydroxylase in the kidney
  • No production of 1,25(OH)2D3

Slide 27

23
Q

What happens when serum calcium is low?

with regards to vitamin D

A
  • 1,25-(OH)2 D & PTH stimulate calcium release from bone and 1,25-(OH)2 D promotes absorption of calcium in the gut
  • PTH tells kidney to make more 1,25-(OH)2 D and to inhibit calcium excretion and to excrete phosphate

Slide 28

24
Q

What happens when serum calcium is high?

Low PTH(Parathyroid) and High CT(calcitonin)

A
  • CT inhibits calcium release from the bone
  • decreased calcium absorption in gut
  • CT tells kidney to excrete calcium
  • decreased PTH tells kidney to make more 24,25(OH)2 D instead of 1,25

Slide 29

25
Q

How does vitamin D regulate genes?

A

interacts with VDR nuclear receptor in target tisues

Slide 30

26
Q

Vitamin D deficiency causes what 3 diseases?

A
  • Rickets
  • Osteomalacia
  • Osteoporosis

Slide 33

27
Q

What happens with vitamin D toxicity?

A
  • Hypercalcemia
  • Calcinosis (soft tissue calcification)
  • Polyuria, headaches, vomiting

Slide 37

28
Q

What is the current adult recommendation for vitamin D?

A

400-600 IU/d

Slide 39

29
Q

Why is Vitamin E so important and required for all mamalian cells?

A
  • PROTECTS AGAINST REACTIVE OXYGEN SPECIES
  • PROTECTS AGAINST CHAIN REACTIONS IN LIPID OXIDATIONS
  • PROTECTS AGAINST FREE RADICALS FORMED BY IONIZING RADIATIONS

Slide 40

30
Q

What other vitamins does vitamin E need to do its job?

A

Vitamin C & Vitamin B3

Glutathione is also required

Slide 42

31
Q

How does vitamin E deficiency present?

A
  • In infants interventricular hemorrhage
  • Red cell hemolysis
  • Myopathies
  • White muscle disease in lower mammals

Slide 43

32
Q

Describe vitamin E toxicity.

A
  • Humans and other animal can tolerate high dosages of Vitamin E with little adverse effect
  • High doses of vitamin E can interfere with the action of the other lipid soluble vitamins. Increasing the dose of the other vitamins overcomes the interference.

Slide 44

33
Q

Where does vitamin K come from?

A
  • Synthesized by green plants
    (phylloquinones)
  • Synthesized by bacteria including those in the human gut (menaquinones)

Slide 45

34
Q

How does Warfarin work?

A

it inhibits Vitamin K epoxide reductase and Vitamin K Reductase which disrupts formation of Gla residues and in turn the clotting process

Slide 47 & 51

35
Q

What does Vitamin K-dependent Carboxylase do?

A

uses a glutamate residue & vitamin KH2 to produce vitamin K epoxide and a carboxylated prozymogen (γ-carboxyglutamate)

Slide 47

36
Q

How do calcium and γ-Carboxyglutamate (Gla) interact to promote clotting?

A
  • Gla is a high affinity calcium chelator
  • the complex interacts with acidic membrane lipids that fold it into correct structures that are recognized by factors in the clotting pathways

Citrate prevents calcium chelation and is therefore an anticoagulant

Slide 49

37
Q

How does vitamin K deficiency present?

A
  • Hemorrhage (trauma-induced; intramuscular, skin ecchymoses, spontaneous GI bleeding)
  • Especially neonatal hemorrhagic disease

Slide 53

38
Q

What are the effects of vitamin K toxicity?

A
  • Liver damage at high doses but not much else
  • High levels of Vit K make it very difficult to achieve adequate anticoagulation with warfarin

Slide 54

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