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YAY ALMOST DONE > Vitamins > Flashcards

Vitamins Flashcards

1
Q

Vitamins definition

A

organic chemicals that must be supplied by exogenous sources to achieve adequate functional amounts (exception: vitamin D)

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2
Q

Which are fat soluble and water soluble vitamins?

A

fat soluble: A, D, E, K
water soluble: B and C

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3
Q

What is the cause for primary and secondary deficiencies?

A

primary: due to inadequate intake
- usually not seen in countries with adequate nutrition availability

secondary: due to improper absorption, drug-nutrient interactions, or increased requirements
- pregnancy - need more
- puberty
- old age - need less and less

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4
Q

PK - Absorption of fat soluble vitamins

A
  • similar to fat absorption
  • bile salts enhance it or are required
  • reduced absorption with increased intake with vitamin E
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5
Q

Transport of fat soluble vitamins

A
  • vitamin E transported in blood by plasma b-lipoproteins
  • vitamin A and b-carotene transported from intestine in chylomicrons via lymph
  • vitamin A released into plasma as retinol bound to specific retinol binding protein (RBP)
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6
Q

Storage of fat soluble vitamins

A
  • vitamin A and E mainly in liver, some in muscle, kidney, adipose, lung
  • Vitamin E and D mobilized slowly from adipocytes
  • Vitamin K storage limited, can be depleted in 10-20 days
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7
Q

What are the consequences for dosing or intake of a vitamin being fat soluble vs water soluble?

A

water soluble vitamins
- excess removed through urine

fat soluble vitamins
- excess sit in fat stores
- testing vitamins through circulation is an incomplete representation of fat soluble vit.
- need to be careful with dose escalations

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8
Q

Vitamin A Source

A
  • b-carotene from plants –> 15,13- dioxygenase coverts to retinal –> dehydrogenase converts to retinol (carrot, broccoli, papaya)
  • retinal used in visual system - rhodorphins
  • retinol from animal products (eggs, dairy, fish)
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9
Q

Vitamin A RDA

A

700ug/d females
900ug/d males

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10
Q

Vitamin A functions

A
  1. cellular differentiation (developmental, immunity)
  2. visual pigments (opsin binds retinal = rhodopsin)
  3. regulation of gene expression via retinoic acid
    - all trans retinoic acids bind to RAR (retinoic acid R)
    - RAR and RXR (retinoid X R) bind to RARE (retinoic acid response elements)
    - RARE regulates gene expression
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11
Q

Vitamin A deficiency

A
  • leading cause of blindness in developing nations (dietary deficiency)
  • increased infectious diseases (respiratory, GI)
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12
Q

Pharmacologic Uses

A
  • acute promyelocytic leukemia (RAR mutations, impaired differentiation of promyelocytes)
  • skin conditions, acne, fine lines and blemishes
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13
Q

Vitamin A Toxicity

A
  • results from excessive supplementation
  • acute effects of single dose of 200,000: blurred vision, vertigo, nausea
  • long term toxicity: liver damage, birth defects, skin and joint damage
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14
Q

Vitamin E Structure

A
  • 4 tocopherols (saturated) and 4 tocotrienes (unsaturated) (a, b, gamma, sigma)
  • a-tocopherol most nutritional significance
  • d-a-tocopherol highest biological activity
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15
Q

Vitamin E sources and RDA

A
  • vegetable oils, nuts, wheat germ, apricots
  • RDA: 15mg/d a-tocopherol
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16
Q

Vitamin E functions

A
  1. antioxidant
  2. prevents destruction of membrane lipids through oxidation
  3. inhibits protein kinase C (cell signalling)
  4. inhibits platelet aggregation
  5. enhances vasolidation
  6. affects activity of immune and inflammatory cells
17
Q

Vitamin E deficiency Prevalence and Symptoms

A

prevalence
- rare in healthy adults
- chronic fat malabsorption and b-lipoprotein deficiency
- premature infants –> due to limited storage and absorption

symptoms
- anemia –> impaired erythrocyte survival
- progressive neurological disorder –> impaired balance and neuropathy

18
Q

Vitamin E Therapeutic Use

A

treatment of susceptible individuals - prevention of CV disease (vit E enhances vasodilation)

19
Q

Vitamin E PK

A

50% absorption
circulates to B-lipoprotein
storage in liver, muscle, fat

20
Q

Vitamin E toxicity

A
  • limited when intake is less than 2000mg a-tocopherol a day
  • can exacerbate vitamin K deficiency –> may impair clotting and lead to hemorrhage
21
Q

Vitamin E interactions

A
  • anticoagulant therapry
  • antiplatelet drugs
  • vitamin K deficient individuals
22
Q

Vitamin K: forms, sources, RDA, PK

A

two naturally occurring forms
1. plants: phyloquinone –> vitamin K1
- green leafy vegetables
2. bacteria: menaquinone-n –> vitamin K2
- egg yolk, liver, fermented foods, microbiota

RDA: 90ug/day

PK: limited storage (10-20 days), reused by oxidation and reduction cycles

23
Q

Vitamin K epoxide cycle

A
  1. vitamin K –quinone reductase–> reduced vit K hydroquinone –carboxylase–> vit K epoxide –epoxide reductase–> vit K
  • carboxylase important in making y-carboxylated proteins
    • clotting factors: dysfunction in vit K deficiency
    • matrix gla (carboxylased glutamate) proteins : needed to stop innappropriate calcification (seen in old age diseases)
24
Q

What is the effect of warfarin on the Vit K epoxide cycle?

A
  • inhibits quinone reductase and epoxide reductase
  • acts as vitamin K antagonist: impairs clotting factor function
25
Q

Vitamin K functions

A
  • coagulation (vit K dependent clotting factors are synthesized in the liver –> acts as a coenzyme for y-carboxylation of glutamic acid into y-carboxyglutamic acid)
  • calcium binding function of some proteins - roles in bone mineralization and cellular growth and regulation
26
Q

Vitamin K deficiency causes and symptoms

A

deficiency
- malabsorption (insufficient fat absorption)
- vitamin K antagonist (warfarin)
- chronic use of cephalosporin antibiotics

symptoms
- increased prothrombin time (PTT) - bleeding will appear in GI tract first
- hemorrhagic disease of newborn

27
Q

Vitamin K therapeutics

A
  • increase biosynthesis of clotting factors by liver
  • prevent hemorrhagic disease of newborn
  • antidote for anticoagulant toxicity
28
Q

Vitamin D Sources

A
  • not true vitamin –> can be synthesized by body
  • derived from cholesterol
  • D2 (ergocalciferol) from plants
  • D3 (cholecalciferol) from animals
29
Q

Vitamin D synthesis in the body

A

7-dihydrocholesterol –(UVB from sun in skin)–>cholecalciferol D3 –(liver)–> 25-hydroxyvitamin D3 –(kidney)–> 1,25-dihydroxyvitamin D3 (active form)

30
Q

Vitamin D regulation of gene transcription

A
  1. calcitriol forms complex with vitamin D receptor (VDR) in nucleus
  2. complex binds with retinoic acid X receptor (RXR) to form heterodimer
  3. heterodimer binds to vitamin D responsive elements (VDRE)
  4. changes in gene transcription (bone related genes, p21, 24-hydroxylase, TGFB2 and more)
31
Q

Vitamin D actions

A
  • increase calcium absorption from gut
  • increase bone mineralization
  • regulation of immune function
32
Q

Vitamin D deficiency Causes and Outcomes

A
  • insufficient UVB to generate vitamin D occurs during nov-feb in toronto
  • conservative estimates for insufficiency are <40nmol/L
  • but thee is no stimulation of PTH at <80nmol/L
  • at <25nmol/L one is deficient: bone loss

in children
- rickets: insufficiency or mutations in VDR
in adults
- osteomalacia
- decrease in bone mineral content: bones are more pliable and don’t fracture as much - less weight bearing
- bone pain and soft bones: bowing of legs

33
Q

Vitamin D toxicity causes and consequences

A
  • can occur due to chronic high dose supplementation (esp. calcitriol)

adverse effects from elevated blood calcium levels
- generalized symptoms: fatigue, headache, diarrhea, hypercalcemia

disruption in mineralization system: - demineralization of bone
- calcification of organs such as heart, kidney, lungs, BVs and skin
- growth arrest

34
Q

Hypocalcemia - range, symptoms, causes

A

range: <2.05mM (2.2-2.7 is normal)

symptoms: related to increased neuromuscular irritability
- numbness/tingling in toes and fingers
- muscle cramps, tetany, convulsions
- irritability, impaured mental capacity
- laryngospasm, bronchospasm, cardiac arrest

common causes
- hypoparathyroidism (PTH deficiency)
- vitamin D deficiency
- vitamin D resistance

35
Q

Hypercalcemia - range, symptoms, causes

A

range: >2.9mM (normal is 2.2-2.7)

symptoms: related to decreased neuromuscular activity
- lethargy, lack of concentration, sleep
- headache, muscle weakness
- vomiting, diarrhea, polyuria, nocturia

common cause
- hyperparathyroidism
- malignancies (ex. increased 1-hydroxylase)
- ectopic vitamin D production

36
Q

Vitamin D therapy and considerations

A
  1. drisdol (ergocalciferol) 25-hydroxyvitamin D2
  2. calciferol
  3. calcitriol 1,25-hydroxyvitamin D3

considerations
- time to reach equilibrium
- fat malabsorption
- hepatobiliary disease
- renal disease

37
Q

Drug interactions with vitamin D

A

anticonvulsants: inhibit hydroxylation in liver
glucorticoids: inhibit actions of vitamin D at VDR

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