Vitamin A Flashcards

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1
Q

What do retinoids include

A
  • retinol - retinal - retinoic acid - retinyl esters - synthetic analogues
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2
Q

Examples of sources of Vitamin A

A

liver, dairy, fish, eggs

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3
Q

Stability of Vitamin A

A

degraded by oxygen light and heat

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4
Q

Bioavailability of Vitamin A

A

70-90% of Vitamin A is absorbed as long as the meal contains at least 10 g of FAT

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5
Q

During digestion of Vitamin A, what is retinol typically bound to?

A

fatty acid esters

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6
Q

what are the retinyl esters complexed with in the diet

A

proteins

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7
Q

how is retinol absorbed

A

the protein + retinyl esters need to be removed

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8
Q

how is the protein and retinyl ester removed?

A

by proteolytic enzymes in ST or duo.

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9
Q

what do retinol esters form once they are released from the proteins

A

fat globules

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10
Q

why do retinol esters form fat globules

A

because they are fat soluble

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11
Q

what happens to the fat globules after release from retinol esters

A

bile and phospholipids help emulsify to form micelles. brush border enzymes break off fatty acid chains to form free retinol

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12
Q

where is vitamin A absorbed?

A

in the duod and jejun

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13
Q

what is vitamin A absorbed by?

A

low doses - protein carrier high doses - passive diffusion

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14
Q

True or false - vitamin A can be absorbed through the skin

A

TRUE - topical applications

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15
Q

What does retinol require for transportation

A

esterification

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16
Q

what is esterification in the transport of retinol regulated by?

A

cellular retinol binding protein (CRBP)II

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17
Q

how is retinol bound to CRBP II converted to retinyl esters

A

LRAT ARAT

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18
Q

what are retinyl esters in the enterocyte incorporated into for transport

A

chylomicrons

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19
Q

what do chylomicrons carry the retinyl esters to?

A

peripheral cells and tissues in the body. the remaining retinyl esters are then brought to the liver in the chylomicron remnants

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20
Q

When needed, what do retinyl esters do?

A

they are transported out of the liver in the blood via RBP and tranthyretin

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21
Q

what do RBP and tranthyretin do

A

carry retinol fom liver back to extrahepatic tissue

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22
Q

why is RBP bound to tranthyretin?

A

to prevent its filtration by the kidney

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23
Q

RBP levels are dependent on what

A

protein, retinol, zinc

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24
Q

True or false retinoic Acid can enter circulation through portal vein

A

true - it is bound to albumin for transport. retinol CANNOT

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25
Q

Where is esterified retinol stored

A

in the liver bound to CRBP - in the stellate cells- (some also in parenchymal)

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26
Q

The liver contains ___ of the bodys total vitamin A stores

A

90% - about 500,000IU in storage - able to last several years.

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27
Q

When does hypervitaminosis A develop

A

when stellate cells cannot take up anymore vitamin A and as a result serum levels start to rapidly increase

28
Q

Is retinol or retinoic acid involved in dark adaptation

A

retinol

29
Q

how is retinol transported to the retina

A

via circulation - where it moves into retinal pigment epithelial cells

30
Q

what happens when retinol arrives at retinal pigment epithelial cells

A

LRAT converts retinol into all-trans retinyl esters - that can be stored

31
Q

when retinyl esters are needed- what are they converted to

A

11-cis retinOL - and then into 11-cis retinAL

32
Q

11-cis retinal is transported where?

A

rod cells

33
Q

once in a rod cell, 11-cis retinal combines with what?

A

opsin

34
Q

11-cis retinal + opsin

A

rhodopsin

35
Q

once a photon is absorbed 11- cis retinal is converted to what?

A

11-trans retinal

36
Q

once photon is absorbed, what happens to the opsin attached to the retinal

A

it is separated as a nerve impulse is sent to the optic cortex of the brain ( via optic nerve)

37
Q

all-trans retinal is converted to what?

A

all trans retinol

38
Q

after all trans retinal is converted to all trans retinol, it is released from what? and to where?

A

rod cells - back into pigment epithelium of retina - where it can be converted to cis-retinal

39
Q

how is vitamin A involved with normal cell differentiation

A

maintenance of integrity and function of epithelial tissues

40
Q

What happens to squamous and keratinized cells during vitamin A deficiency

A

they increase

41
Q

what happens to mucous secreting collumnar and cuboidal cells during vitamin A deficincy

A

they decrease

42
Q

What type of immunity is Vitamin A involved in

A

humoral and cell mediated immunity WBC differentiation, activation of T-lymphocytes

43
Q

Retinol or retinoic acid are required for spermatogenesis

A

RETINOL

44
Q

during excretion retinol is oxidized and conjugated to make what

A

polar, non soluble metabolites

45
Q

after retinol is oxidized and conjugated into polar non soluble metabolites, where is it exctreted?

A

60% urine 40% feces

46
Q

Vitamin A deficiency is common in what age group

A

children under the age of 5 in developing worlds

47
Q

Symptoms of Vitamin A deficiency

A

follicular hyperkeratinosis

delayed growth

impaired spermatogenesis

increased infections blindness

48
Q

children who are deficient in vitamin A have a higher incidence of what?

A

respiratory disease and diarrhea + mortality

49
Q

what is the leading cause of blindness in developing worlds?

A

vitamin A deficiency

50
Q

what is the earliest evidence of vitamin A def

A

impaired dark adaptaion

51
Q

mild vitamin A deficiency results in what

A

changes in the conjunctiva called Bitots spots

52
Q

what do disappearance of goblet cells in conjuctiva result in

A

dryness from inadequate mucin production

53
Q

what does inadequate mucin production in the eyes result in

A

enlargement and keratinization of epithelial cells and the appearance of bitots spots over the keratinized epithelia

54
Q

severe or prolonged Vitamin A deficiency can result in what

A

xerophthalmia (dry eyes)

55
Q

what is xerophthalmia characterized by

A

changes in cells of the cornea that result in corneal ulcers, scarring, and blindness

56
Q

who has an increased risk of vitamin A deficiency

A
  • hypothyroidism
  • fat malabsorptive disorders
  • LV or GB dz
  • renal dz
  • protein malnutr
  • alcoholics
57
Q

Clinical indications of Vitamin A supplementation

A
  • retinitis pigmentosa
  • diseases of the skin
  • acute promyelocytic leukemia
58
Q

Toxicuty of cause by the overconsumption of vitamin a or carotenoids

A

vitamin a

59
Q

true or false, with vitamin A supplementation, teratogenicity is reported in newborn babies, therefore high doses are CI in pregnant women

A

true

60
Q

early warning signs of vitamin A toxicity

A
  • dry skin
  • fatigue
  • headache
  • jt, mm, bone pain
61
Q

Conraindications

A
  • high doses in pregnant women
  • end stage renal dz
  • lv dz
  • malnutrition
  • alcoholism
62
Q

ACUTE signs and sx of hyperviatminosis A

A

increase intracranial pressure n/v altered mental status H/A dizzy double vision weak jt, mm, bone pain

63
Q

CHRONIC signs and sx of hyperviatminosis A

A

increase intracranial pressure ataxia anorexia H/A dry itchy skin alopecia, brittle nails conjunctivitis jt, mm, bone pain bone fractures LV damage

64
Q

What happens to iron when there is Vitamin A deficiency

A

there is decrease iron incorporation into RBCs

65
Q

___ is required as a cofactor for the conversion of retinol to retinal

A

Zn

66
Q

What does the RDR test?

A

measures plasma retinol levels before and 5 hours after oral administration