Fat Soluble Vitamins Flashcards

1
Q

natural form of vit A

A

retinol

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2
Q

what do the retinoids include

A
  1. retinol: storage form of Vit A, found in animal tissues. is a primary alcohol
  2. retinal: aldehyde derivative of retinol when oxidised
  3. retinoic acid: acid derived from oxidation of retinal. cannot be produced in body
  4. beta-carotene: plant foods contain it.
    - AKA provitamin A.
    - oxidatively cleaved in intestine to give 2 retinal molecules.
    - has antioxidant activity
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3
Q

sources of vitamin A

A
  • liver
  • kidney
  • cream
  • butter
  • egg yolk
  • yellow, orange, daark green vegertables and fruits good sources of carotenes
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4
Q

vit A absorption and transport to liver

A
  • retinyl esters -> retinol and FFA
  • b-carotene -> retinal -> reduced to retinol
  • both these retinols re-esterified in enterocytes using fatty CoA
  • secreted as component of chylomicrons in lymphatic system.
  • chylomicron remnants containing retinyl esters taken up by and stored in liver
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5
Q

release from liver

A
  • retinol binding protein complexed with transthyretin transports retinol through blood
  • binds to transp protein on surface of peripheral tissue cells, allows retinol to enter
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6
Q

retinoic acid mechanism of action

A
  • retinol oxidised to retinoic acid
  • binds to receptor acid receptors RAR in nucleus
  • retinoic acid-RAR complex binds to response elements on DNA and regulates RNA synthesis
  • allows control of specific protein eg keratin
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7
Q

functions of vit A

A
  • vision maintenance (retinoic acid not involved)
  • epithelial cell maintenance - differentiation - mucus secretion - immune syst
  • reproduction; supports spermatogenesis and prevents fetal resorption in females (retinoic acid not involved)
  • bone growth
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8
Q

describe visual cycle vit A

A
  • 11-cis retinal + opsin -> rhodopsin
  • light + rhodopsin -> all-trans retinal + opsin
  • all-trans retinal -> all trans retinol -> all-trans retinyl esters -> 11-cis retinol -> 11-cis retinal
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9
Q

effects of vit A deficiency

A
  • earliest sign: nyctalopia (night blindness)
  • prolonged deficiency = permanent loss of visual cells
  • severe deficiency xerophthalmia ; untreated = blindness
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10
Q

what is xerophalthamia

A
  • pathologic dryness of conjunctiva and cornea caused in part by inc keratin synthesis
  • untreated -> corneal ulceration -> blindness due to formation of opaque scar tissue
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11
Q

which vit A is used to treat mild acne + skin aging

A

all-trans retinoic acid (tretinoin) oral too toxic

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12
Q

what is oral tretinoin used for

A

acute promyelocytic leukemia

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13
Q

what is isotretinoin used for

A
  • severe cystic acne.
  • is teratogenic, should be avoided in women of child-bearing capacity
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14
Q

how is psoriasis treated

A

oral synthetic retinoid

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15
Q

excess of vitamin A

A
  • hypervitaminosis A
  • skin dry and pruritic ( decreased keratin)
  • liver enlarged - can become cirrhotic
  • CNS-> rise in intracranial pressure can mimic symptoms of brain tumour.
  • decreased bone mineral density + increased risk of fractures
  • teratogenesis in pregnant women
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16
Q

which retinoid functions as a hormone

A

retinol

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17
Q

active form of vitamin E

A

alpha-tocopherol

18
Q

function of vit E

A
  • antioxidant in prevention of nonenzymic oxidations, eg oxidation of LDL and peroxidation of polyunsaturated FA
19
Q

effect of vit C on vit E

A

C regenerates active vit E

20
Q

sources of vit E

A
  • vegetable oils rich source
  • liver and eggs moderate source
21
Q

vit E deficiency

A
  • newborns can obtain from breast milk/supplements to prevent haemolysis and retinopathy
  • in adults, usually due to defective lipid absorption/transport
  • abetalipoproteinemia caused by defecr in formation of chylomicrons result in vit E deficiency
22
Q

what is the least toxic fat sol vitamin

A

vit E

23
Q

active molecule of vitamin D

A
  • calcitriol
24
Q

vit D distribution

A
  • collagen synthesis intermediate converted to vit D3 in dermis + epidermis when exposed to sunlight, transp to liver by vit d-binding protein
  • diet; vit d2 found in plants and vit d3 found in animal tissues. dietary vit D packaged into chylomicrons
25
Q

how is vit d formed

A
  • vit d2 + d3 converted to calcitriol by 2 sequential hydroxylation reactions
  • 1st in liver forms calcidiol
  • 2nd in kidneys form calcitriol
26
Q

functions of vit D

A
  • maintain adequate ca2+ serum levels
  • inc ca2+ mobilisation from bone
  • inc renal resorption ca2+
  • dec renal excretion of ca2+
  • inc intestinal absorption of ca2+
27
Q

how does vit d increase intestinal absorption of calcium

A
  • calcitriol binds to cytosolic receptor in intestinal cell and interacts w/ response elements on DNA
  • increases gene expression of calbindin
28
Q

sources of vit D

A
  • fatty fish
  • liver
  • egg yolk
29
Q

Vit D deficiency

A

diet causes:
- rickets in children - continual formation of collagen matrix but not mineralisation - soft and pliable bones
- osteomalacia in adults - demineralisation of bones increases susceptibility to fracture -bow legs

mutation in vit d receptor causes hereditary vit d-deficient rickets

30
Q

Renal osteodystrophy causes, effects and treatment

A
  • caused by chronic kidney disease
  • decreased vit D formation, hyperphosphatemia and hypocalcemia
  • low ca2+ = increase in PTH -> associated bone demineralisation
  • treated with vit d supplementation + PO43- reduction therapy
31
Q

what is hypoparathyroidism + treatment

A
  • lack of PTH causes hypocalcemia and hyperphosphatemia as PTH increases phosphate excretion
  • treated with vit D
32
Q

Vit D toxicity symptoms

A
  • loss of appetite
  • nausea
  • thirst
  • weakness
  • hypercalcemia - ca2+ deposits in soft tissue (metastatic calcification)
  • excess vit d produced in skin is converted to inactive form so doesnt cause toxicity
33
Q

principal role of vit K

A
  • coenzyme in carboxylation of glutamic acid residues to gamma-carboxyglutamate (Gla) in post-translational protein modification
  • req y-glutamylcarboxylase, O2, CO2, hydroquinone form of vit K (gets oxidised to epoxide form)
  • Gla residues also used to form osteocalcin + matrix Gla protein in bones
34
Q

active forms of vit K

A
  • plants as phylloquinone (K1)
  • intestinal bacteria as menaquinone (K2)
  • menadione (synthetic form of vit K) can be converted to K2
35
Q

what can inhibit formation of Gla residues

A

warfarin - synthetic analog of vit K (inhibits VKOR, enzyme req to regenerate functional form hydroquinone form of vit K

36
Q

what blood clotting proteins is vit k involved in formation of

A
  • prothrombin
  • FVII
  • FIX
  • FX
37
Q

vitamin K sources

A
  • cabbage
  • kale
  • spinach
  • egg yolk
  • liver
  • intestinal bacteria
38
Q

vitamin K deficiency

A
  • unusual as adequate amounts in diet and bacteria
  • decrease in bacterial gut population eg by antibiotics -> leads to hypoprothrombenima -> bleeding tendency therefore may need vit K supplementation
    cephalosporin antibiotics have warfarin-like mechanism, inhibits VKOR
  • deficiency can also affect bone health
39
Q

why can newborns have vit K deficiency

A
  • sterile intestines + breastmilk provides only 1/5th of req amount
  • therefore single intramuscular dose as prophylaxis against haemorrhagic disease of the newborn
40
Q

Vit K excess

A
  • prolonged admin of large doses of menadione can cause haemolytic anaemia and jaundice in infants due to RBC membrane damage