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GI Skildum > Vitamins and lipids (1.15) > Flashcards

Vitamins and lipids (1.15) Flashcards

1
Q

What are the 4 fat soluble vitamins?

A

A
D
E
K

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2
Q

What is the active form of vitamin A?

A

all-trans-retinol

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3
Q

What are the dietary forms of vitamin A? What foods?

A

Carotenoids
Retinyl-acyl esters

Red, yellow, and orange fruits and vegetables

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4
Q

How is dietary vitamin A converted into free carotenoid and free retinol in the intestine?

A

Dietary protein-bound carotenoids and retinyl esters enter stomach –proteases–> carotenoid and retinyl esters enter duodenum –hydrolases, esterases, and lipases–> free carotenoids and free retinol

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5
Q

What happens in the intestine after free carotenoids and free retinols are formed? Why?

A

Fatty acids, phospholipids, monoacylglycerol, and/or cholesterol are added

Gets incorporated into micelle

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6
Q

In what two forms does vitamin A leave the intestinal cell?

A

Retinoic acid…to liver via blood albumin

CRBPII-retinyl-palmitate…lymphatics in chylomicron –> to liver as chylomicron-remnant

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7
Q

Why does retinoic acid go to the liver?

A

The liver stores vitamin A in stellate cells…controls vitamin A homeostasis (30-86ug/dL)

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8
Q

After retinyl esters enter a hepatic parenchymal cell, how can the leave?

A 
Stellate cells (to/back to storage)
VLDL (to tissues)
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9
Q

After retinyl esters enter a hepatic parenchymal cell, they can be converted to retinol. How does retinol leave?

A

Retinol complexes with transthyretin and retinol binding protein (RBP) to go out to the serum

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10
Q

After retinyl esters enter a hepatic parenchymal cell, they can be converted to retinoic acid. How does retinoic acid leav?

A

Goes out to serum complexed with albumin…like it did from the intestinal cell

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11
Q

What kind of receptors are Retinoic Acid Receptors (RAR), Retinoic X Receptors (RXR), and some Peroxisome proliferator activated receptor (PPAR)?

A

Ligand activated transcription factors

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12
Q

What are the effects of RAR, RXR, and PPAR?

A

Increased differentiation of goblet cells
Decreased keratinization
Apoptosis of cancer cells
Maturation of dendritic cells
Recruitment of antibody secreting B cells to small intestine

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13
Q

How can carotenes be helpful if they are not cut?

A

Act as antioxidants…their double bonds can neutralize singlet oxygen and free radicals

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14
Q

What are the symptoms of vitamin A deficiency?

A 
Anorexia
Retarded growth
Increased susceptibility to infections
Alopecia
Keratinization of epithelial cells
Night blindness*
Xeropthalmia (dry eyes d/t keratinization)*
Bitot's spots (something with eyes)*
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15
Q

How is vitamin A deficiency diagnosed?

A

The Relative Dose Response (RDR)

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16
Q

How is the RDR calculated?

A

Measure plasma retinol –> give an oral bolus of retinyl-palmitate –wait 5 hours–> measure plasma retinol…bb for “before bolus” and ab for “after bolus”

RDR = retinol - retinol / retinol

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17
Q

At what point is an RDR indicative of a deficiency?

A

RDRs > 20%

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18
Q

What is the Tolerable Upper Limit (TUL) of vitamin A?

A

3000ug/day

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19
Q

What can happen if vitamin A TUL is exceeded for a period of time?

A 
Nausea/Vomiting
Blurred vision*
Headache
Desquamation of skin
Alopecia
Ataxia
Liver damage (from excess stellate cell growth and proliferation)
Conjunctivitis/eye pain
Teratogen at very high doses (Accutane--an acne medication)
20
Q

What are the two forms of vitamin E? What food?

A

Tocopherols (saturated 16C acyl chains)
Tocotrienols (polyunsaturated 16C acyl chains)

Plant oils and wheat germ

21
Q

How does vitamin E get into the liver?

A

Similar to vitamin A

Pancreatic lipase does its thing so vitamin E can enter intestinal epi cells…leaves as chylomicron for tissues…then to the liver in a chylomicron remnant

22
Q

How is vitamin E sent to the tissues after being in the liver?

A

RRR steroisomers can be incorporated into and exported in VLDL

23
Q

What is vitamin E’s function?

A

Antioxidant activity (d/t phenolic hydroxyl) in lipid bilayers

24
Q

What other two vitamins does vitamin E interact with?

A

Vitamin C reduces oxidized vitamin E to active form

Vitamin K absorption and metabolism are INHIBITED by vitamin E

25
Q

What are the symptoms of vitamin E deficiency?

A

Myopathy
Hemolytic anemia
Peripheral neuropathy
Ataxia…loss of vibratory sense

26
Q

What can cause vitamin E deficiency?

A

Absorptive problems–premies, Crohn’s, short bowel syndrome

Inherited lipoprotein disorders

27
Q

What are the two main forms of dietary vitamin K?

A

Phylloquinone (main form…in leafy greens)

Menaquinones (produced by fermentation…cheese)

28
Q

What is a synthetic form of vitamin K used in animal feed that can be toxic to humans?

A

Menadione (liver toxicity)

29
Q

What is the digestion/absorption process for vitamin K?

A

Same as E…which is the same as A…which is the same as fat

30
Q

Where is vitamin K stored?

A

Cellular membranes–lung, kidney, bone marrow, and adrenal glands

31
Q

What is vitamin K’s function?

A

Co-factor for gamma-glutamyl carboxylase –> activates clotting proteins (Factors IX, VIIa, and X)

32
Q

What are the symptoms of vitamin K deficiency?

A

Coagulation disorder (increased PTT and bleeding)

33
Q

What foods contain vitamin D?

A

Foods of animal origin

34
Q

Besides the diet, how else can vitamin D be obtained?

A

Synthesized de novo from cholesterol

35
Q

What is needed to make active vitamin D3?

A

Metabolism of skin, liver, and kidney

36
Q

What is the main function of vitamin D?

A

Calcium homeostasis

37
Q

Vitamin D is taken to the liver via the expected route, but how is it activated (start with de novo steps)?

A

Cholesterol + sunlight (skin) –> dietary form of vitamin D –liver–> 25-Hydroxycholecalciferol (main form circulating in blood) –kidney (PTH 1-alpha hydroxylase–> 1,25-OH D3 (active form)

38
Q

When does the parathyroid secrete the PTH necessary to activate vitamin D?

A

When serum calcium is low (<8.5mg/dL)

39
Q

How does vitamin D increase serum calcium levels?

A

Reabsorption from bones

Increased absorption in the gut

40
Q

How does vitamin D increase intestinal calcium absorption?

A

Vitamin D Receptor acts as a ligand activated transcription factor –> tsl of calcium transport proteins (TRPV6 at brush border, calbindin in cytoplasm, and Ca ATPases at basolateral membrane…and alters claudin–tight junctions–to be more permeable to calcium)

41
Q

If vitamin D causes increased translation of proteins, how can there be a response within seconds to minutes?

A

There is a transcription-independent rapid response… binds to other plasma membrane receptors

42
Q

What are the symptoms of vitamin D deficiency?

A

Rickets (seizures, growth retardation, osteomalacia)

43
Q

What can cause vitamin D deficiency?

A

Diet
Genetics
Absorption problem (Crohn’s)

44
Q

What are the symptoms of vitamin D toxicity (most likely vitamin toxicity)?

A

Calcification of soft tissues
Hyperphosphatemia
Hypertension

45
Q

What is the TUL of vitamin D in people >9?

GI Skildum (8 decks)

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