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Gastrointestinal System > Fat Soluble Vitamins > Flashcards

Fat Soluble Vitamins Flashcards

1
Q

general properties of fat soluble vitamins

A

vitamins A, D, E, K

  • require an emulsifier: bile or other fats
  • more diverse fx than Bs (“energy metabolism”)
  • excess stored in liver and adipose tissue
    • stores can last months-yrs
  • not easily excreted
    • higher toxicity risk
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2
Q

emulsifier

A

main example: bile

has hydrophilic head and hydrophobic tail to be in phase with GI secretions and fat-soluble vitamins

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3
Q

digestion and absorption of fat-soluble vitamins

A
  1. stomach: vitamins bound to proteins when we eat them. proteins are degraded in stomach, vitamins are released
  2. jejunum: fat-sol vitamins for micelles with bile salts, are passively transported into intestinal enterocytes
  3. intestinal enterocytes: packaged into chylomicrons and released into lymphatic system
  4. lymphatic system: chylomicrons trael up thoracic duct and empty into L subclavian v to enter circulation
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4
Q

vitamin A

  • sources
  • forms
A

retinyl esters (animal foods: liver) ⇔ beta-carotene (plant foods: carrots, sweet potato)

  • conversion between these two forms is reversible
  • conversion from retinol to retinoic acid is irreversible

forms

  • retinol - alcohol
  • retinal - aldehyde
  • retinoic acid - carboxylate group
  • beta-carotene - two retinals joined at tail
    • sometimes cleavage happens at wrong carbon, so you don’t get the 2 vit A molecules expected
    • absorption of beta-carotene less effective than vit A
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5
Q

vitamin A: absorption, transportation, excretion

A

absorption

  • packaged in chylomicrons (as retinyl ester), transported to liver (converted to retinol in hepatocytes)
  • moved to stellate cells for storage
    • located in space of Disse between sinusoidal endothelial cells and heptatic epithelial cells (5-8% of liver cells)
    • in healthy liver, largest reservoir of vit A in body

transport

  • transported as retinoids (bound to retinol-binding protein)

excretion

  • small amounts excreted in urine
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6
Q

vitamin A functions

A

main fx

  • vision
  • maintenance of cornea, epithelial cells, mucous membranes, skin
  • important lipid-soluble antioxidant

diff forms, diff fx

  • retinol
    • ​supports reproductin
    • major transport and storage form
  • retinal
    • _​_role in vision
  • retinoic acid
    • regulates transcription for cell diff, growth, embryonic devpt
  • beta-carotene
    • ​antioxidant
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7
Q

retinoic acid as a transcription factor

A

retinoic acid and vit D are unique in fx as transcription factors

RA-mediated transcription​

  1. RA/retinoid binds to ligand-binding site
  2. receptor dimerization (heterodimer formation = RAR:RXR)
  3. DNA binding (RA response elements bind heterodimers)
  4. chromatin remodeling and recruitment of transc machinery to effect transcriptional modulation
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8
Q

vitamin A and mucous membranes

A

protects mucous membranes lining mouth, stomach, intestines, bladder, uterus, urethra, etc by promoting differentiation of epithelial cells and goblet cells

in absence of vitamin A, goblet cells can’t fx properly = flattened/abnormal epi cells

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9
Q

pharmacological uses of vitamin A

A
  • retinoic acid
    • treatment of acute promyelocytic anemia
  • All Trans Retinoic Acid (ATRA) (tretinoin)
    • RetinA: topical cream tx for acne, age spots
  • 13-cis retinoic acid (isotretinoin)
    • Accutane: oral tx for severe acne but also TERATOGENIC ⇒ requires use of effective contraception
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10
Q

vitamin A and vision

A

retinal

maintains cornea, aids in conversion of light energy to nerve impulses

  • rod cells in retina contain rhodopsin (opsin + retinal)
    • critical for night vision/B&W vision
  • light + rhodopsin = conversion of retinal from cis to trans, which releases it from opsin
    • opsin initiates signal transduction cascade to nerve cells that communicate with visual center
  • trans retinal is converted back to cis; rhodopsin is reformed

takeaway: vitamin A critical for night vision

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11
Q

vitamin A deficiency

A
  • might occur through…
    • inadequate intake (primary def)
    • poor absorption of fats - CF, Crohn’s disease, liver disease, high alcohol intake (secondary def)
  • vit A status depends on other factors
    • stores in liver
    • ability to make retinol binding proteins (for transport)
  • see symptoms in eyes, epithelial tissue, immune fx
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12
Q

vit A defiency symptoms

A

EYES

  • night blindness (inadequate retinal in retina)
  • progression to blindness (xerophthalmia)
    • inadequate vit A at cornea
  • stages
    • xerosis: corneal drying
    • Bitot spots: triangular gray spots on eye (keratin buildup on conjunctiva)
    • keratomalacia: softening of cornea
    • xerophthalmia: corneal degen and blindness

EPITHELIAL CELLS

  • keratinization/hyperkeratosis: affects skin, GI tract, resp tract, urinary tract epi cells
    • change in size/shape
    • dry, rough, scaly skin
    • abnormal digestion/absorption in GI
    • weakened defenses in resp tract, vagina, inner ear, urinary tract

IMMUNE SYSTEM

  • impaired immunity (prone to infection diseases)
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13
Q

vit A toxicity

A

risk factors include…

  • frequent consumption of liver
  • systemic use of retinoic acid analogues
    • birth defects: cranofacial malformations, CNS/thymus/heart issues

**beta-carotene: no tox!

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14
Q

beta-carotene excess

A

beta-carotene is not efficiently converted; excess is stored in the fat under skin

NOT HARMFUL

symptoms: yellowing of skin due to accumulation

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15
Q

vitamin D

  • name
  • why it’s called “conditional”/a “prohormone”
  • how it’s made
A

calciferol

body can synthesize it from cholesterol with UV light given exposure to sun for 10-15min x 2-3 times/wk

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16
Q

vitamin D synthesis

A
  • on sunlight exposure:

pro-vitamin D3 (7-dehydrochol) → pre-vitamin D3

  • vitamin D3 (either pre-D3 that’s isomerized or ingested D3) binds to DBP (vit D binding protein) in bloodstream, and is transported to liver
  • in liver: hydroxylation[enzyme: liver 25-hydroxylase]

D3 → 25-hydroxycholecalciferol

  • in kidney: hydroxylation [enzyme: 25-hydroxyvitamin D3-1-OHase]

25-hydroxycholecalciferol → active 1,25(OH)2D3 (calcitriol)

17
Q

vitamin D sources

A

diff types of fish, fortified milk, mushrooms

18
Q

vitamin D functions

A
  • Ca, PO4 homeostasis
    • increases Ca absorption (sm intestines)
    • helps release Ca from bone (if req)
  • bone health
  • immune fx
  • reduction of inflammation and apoptosis
  • bp regulation
  • regulation of gene expression [prohormone]
    • binds to VDR (vit D receptor) and interacts with target gene promoters
19
Q

vitamin D deficiency risk factors

A
  • dark skin (pigment reduced vitD synth)
  • limited sun exposure
  • elderly (lose ability to activate D)
  • people with little or no [fortified] milk in diet (vegans, lactose-intolerant) or breastfeeding moms who aren’t supplementing

can lead to rickets and osteomalacia

20
Q

rickets

A

vitamin D deficiency

  • most children (worldwide; rare in US - breastfed black babies with poor vitD intake, reduced ability to synth)
  • symptoms
    • inadequate calcification of bones
      • growth retardation, skeletal abnormalities (bowed legs)
    • lax muscles (protruding abd) and muscle spasms
    • beaded ribs (poor bone/cartilage interface)
    • delayed closure of fontanels: rapid head enlargement
21
Q

osteomalacia/osteoporosis

A

vitamin D deficiency : poor mineralization leading to soft, brittle, deformed bones

  • affects adults
  • causes
    • long-term usage of anticonvulsants (phenobarbital, phenytoin): increased breakdown of vit D in liver
    • chronic kidney disease: low production of calcitriol
  • symptoms
    • soft, brittle, deformed bones
    • ​progressive weakness
    • pain in pelvis, lower back, legs
22
Q

vitamin D toxicity

A

most likely of the vitamins to have toxic effects when consumed in excess!!!

NOT FROM SUNLIGHT/DIETARY SOURCES - supplementation only

  • excess vit D leads to increased blood Ca
    • precipitate in soft tissues (blood vessels, kidney, heart, lungs) - can cause death
23
Q

vitamin E

A

aka tocopherol

tocopherol is actually a general term for 8 related compounds (4 tocopherols, 4 tocotrienols) of which one has vitamin E activity…

D-ISOMER OF ALPHA TOCOPHEROL

*found in nuts/oils - easily destroyed by oxygen and heat [ex. frying]

24
Q

vitamin E functions

A
  • most effective lipid-soluble antioxidant
    • protects polyunsat FAs in cell membranes from peroxidation
  • prevents platelet aggregation and monocyte adhesion
  • helps maintain fertility
25
Q

vitamin E: antioxidant activity & regeneration

A
  • ROS accumulate in body, wreak havoc
    • mitochondrial ETC generates majority (superoxide, hydrogen peroxide)
    • sequential reduction of oxygen (superoxide anion, peroxide, hydroxyl radical)
  • ROS target cellular membranes’ unsaturated FAs via lipid peroxidation
    • vitamin E donates H to lipid radicals to protect membrane integrity
  • active vitamin E is regenerated by vitamin C
    • vit E is dependent on vit C for activity
26
Q

vit E deficiency

A
  • primary deficiency is rare (can occur in premature infants)
    • preterm infants given supplemental vitamin E!
  • can occur due to fat malabsorption (CF, pancreatic insufficiency)
  • symptoms
    • erythrocyte hemolysis due to oxidation of polyunsat FAs
    • leads to ​hemolytic anemia
27
Q

vit E toxicity

A

non-toxic except in HUGE doses

hard to develop from food; might be able to develop with huge exogenous supplemental doses

  • excess vit E interferes with vitamin K’s role in blood clotting (risk of hemorrhage)
  • can lead to nerve damage
28
Q

vitamin K

A
  • menaquinones (animal source) - synthesized by gut bacteria
  • phylloquinones (plant form) - green leafy feg, broccoli, peas, green beans, oils
29
Q

vitamin K function

A
  • required cofactor for post-translational carboxylation of Glu

Glu → gamma-carboxylglutamate (Gla)

  • rxn catalyzed by gamma-glutamyl carboxylase
  • product (Gla) has key roles in blood clotting and bone mineralization (osteocalcin)
    • involved in both intrinsic and extrinsic pathways of clotting

vitamin K dependent proteins (VKD proteins) require several Gla residues (9-13) for normal fx

30
Q

vitamin K deficiency

A
  • newborns have low stores
    • ​receive vit K dose at birth due to sterile intestinal tract, lack of gut bacteria to make it!
  • secondary deficiency can occur due to antibiotics or malabsorption
  • symptoms
    • ​hemorrhage
    • bruisability
    • mucosal bleeding
31
Q

vitamin K toxicity

A

no toxicity known, BUT pts taking warfarin/coumadin should be careful eating vitamin K rich foods

  • warfarin works by decreasing vit K activity, lengthening clotting time
32
Q

interrelationships of fat-soluble vitamins

A
  • vitamin E protects vitamin A from oxidation
  • vitamin C protects vitamin E from oxidation
  • vitamins A, D, K all play roles in bone growth/remodeling

Gastrointestinal System (35 decks)

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