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Biochem-Metabolism Quiz 4 > Lecture 45 & 46: Vitamins > Flashcards

Lecture 45 & 46: Vitamins Flashcards

1
Q

In what types of patients are you likely to see vitamin deficiencies?

A
  • alcohol abusers
  • elderly patients
  • patients with small bowel resections
  • food faddists
  • malnourished people in the developing world
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2
Q

What is an RDA?

A

Recommended Daily Allowance; not true % for everyone as individual needs vary; really a unit of measure, just there for comparison

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3
Q

What are the water soluble vitmains?

Where can you find them in your diet?

How long does it take for deficiencies to manifest?

A

The B-complex vitmains + vitamin C

Usually found in plants (except B12)

~deficiencies noticed w/in weeks (except B12) b/c of low body stores

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4
Q

Describe the classification of the B vitamins.

A

Energy-releasing

  • B1 (thiamine)
  • B2 (riboflavin)
  • B3 (niacin)
  • B5 (pantothenic acid)
  • B7 (biotin)

Hematopoietic

  • B9 (folate)
  • B12 (cobalamin)

Other

  • B6 (pyridoxine, pyridoxamine, pyridoxal)
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5
Q

What is Vitamin B1?

What is it used for?

A

B1 = thiamine

Used as a coenzyme in carbohydrate metabolism specifically:

  • a-ketogluatarate DH
  • pyruvate DH
  • transketolase
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6
Q

What is Wernicke’s syndrome? How do you treat it? Why?

A

Wernicke’s syndrome is seen in patients with alcoholism who have thiamine deficiency.

  • Sx include: nystagmus, ataxia, confusion and weakness

Treat w/ glucose PLUS THIAMINE (banana bag)

  • Why? Because B1 (thiamine) is needed as a co-factor in the CAC, so if you give straight glucose, the thiamine-deficient patient’s neurons will metabolize it anaerobically causing rapid built up of lactic acid and neuronal cell death, especially in the mammilary bodies of the brain. This is called Korsakoff’s syndrome
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7
Q

What is thiamine deficiency like in those who are third-world countries?

S/sx?

Tx?

A

Called beriberi. Often resuts from diets of only polished rice (the thiamine-containing husk is removed)

S/sx

  • dialated cardiomyopathy: tachy, SOB, flushed look due to high-output heart failure
  • peripheral neuropathy: drop foot, loss of sensation in the feet bilat

Tx = emergent i.v. thiamine

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8
Q

What is vitamin B2? What is it used for?

A

Vit b2 = riboflavin

Used in FAD and FMN (Flavin mononucleotide); for are oxidizing agents that can accept 2 H+ ions each.

They are used as cofactors for “flavoenzymes” that are involved in redox rxns

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9
Q

What are the s/sx of riboflavin deficiency?

A
  • cheliosis (fissuring at angle of mouth)
  • dry, skin rash
  • smooth, purple tongue

Really not a big deal, though where there is one vitamin deficiency there are likely others.

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10
Q

What is vitamin b3?

What’s it for?

A

b3 = niacin or nicotinic acid

**technically not a vitamin b/c we can make it from tryptophan

Needed to make NAD+ and NADP+

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11
Q

How is niacin deficiency manifested?

Who do you see this deficiency in?

A

Niacin deficiency causes pellagra (Italian for “sour skin”)

  • FOUR D’S: DERMATITIS (photosensitive), DIARRHEA, DEMENTIA, DEATH

Seen in pts w/ carcinoid (tumor that alters trytophan metabolism); Hartnup dz (decr. niacin uptake)

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12
Q

What is Vitamin B4? What is it used for?

A

Trick question! no such thing

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13
Q

What is Vit B5?

What’s it used for?

What is deficiency called?

A

panthotenic acid

component of Coenzyme A

• Widely distributed in food; deficiency syndrome has not been characterized.

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14
Q

What is Vitamin B6?

What’s it used for?

A

B6 = pyridoxine, pyridoxal, and pyridoxamine

It’s a cofactor for enzymes that metabolize amino acids.

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15
Q

Name an iatrogenic cause of B6 deficiency.

A

Binds to the antituberculous drug isoniazid; therefore B6 is routinely prescribed together with isoniazid to prevent functional deficiency, characterized by seizures.

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16
Q

What is vit B7? What’s it used for?

A

B7 = biotin

Covalently bonds to enzymes involved in carboxylation rxns.,

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17
Q

What causes B7 deficiency? What’s it look like?

A

eating >20 raw eggs/day (b/c their “avidin” protein binds biotin)

s/sx = dermatitis, glossitis, and nausea.

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18
Q

What is B9 and what’s it for?

A

B9 = folic acid

Needed for one-carbon metabolism (e.g. purines and thymidine metabolism and therefore DNA synth)

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19
Q

What does folate deficiency cause?

A

megaloblastic anemia

neural tube defects in utero

20
Q

Who gets folate deficiency?

What are processes that prevent folate deficiency?

A

most common vitamin deficiency in the U.S.: pregnant women, people who abuse alcohol

prevention

  • commensal bacteria make some and many foods are now enriched with it
  • commensal-produced not enough in times of high demand (i.e. high DNA synth, i.e. pregnancy)
  • pre-natal vitamins
21
Q

What cancer drug interfers with folate f(x)?

A

Methotrexate competitively inhibits dihydrofolate reducatase

also used as abortifacient

22
Q

How do you “rescue” a patient in folate deficiency post-methotrexate tx?

A

give straight up THF (leukovorin)

23
Q

What is Vitamin B12?

How do we get it?

How do we metabolize it?

What’s it used for?

A

b12 = cobalamin

not found in plants; animal proteins

intrinsic factor from gastric parietal cells

Uses-precursor for two coenzymes:

  • methylcobalamine used in synth of homocysteine—>Methionine in blood cells
  • deoxyadenosylcobalamin, which is needed for fatty acid metabolism in brain cells
24
Q

How long to B12 stores last?

A

years

25
Q

What does B12 deficiency cause?

A

Deficiency causes:

  • megaloblastic anemia by functionally trapping folate (see below)
  • subacute combined degeneration of the spinal cord
  • dementia.
26
Q

What is pernicious anemia, and what causes it?

Tx?

A

megaloblastic anemia due to autoimmune attack of parietal cells—decreased intrinsic factor production—>decreased b12 uptake—>prevents DHF-to-THF

Tx w/ IM B12 b/c you bypass need for intrinsic factor

27
Q

What is the etiology of megaloblastic anemia in vitamin B12 deficiency?

A

(the folate trap hypothesis)

  • During methionine synthesis, N5-methyl-tetrahydrofolate transfers a methyl group to homocysteine forming Met
    • vitamin B12 is co-factor and does the actual transfer methylcobalamin = i)
  • rxn also req’d to metabolize N5-methyl-tetrahydrofolate
    • Lack of B12 blocks the metabolism of N5-methyl-tetrahydrofolate, which cannot be used for DNA synthesis
28
Q

Why can’t you treat B12 deficiency with straight Folate/THF?

A

folate supplemenation would mask the megaloblastic anemia but it does not prevent/tx subacute combined degeneration

  • perm spinal cord damage
  • due to increased folate supplementation in enriched foods! also in pregnant women being given pre-natal vitamins
29
Q

Vitamin B12 deficiency looks similar to what other deficiecny?

A

folate deficiency

30
Q

In what groups is b12 def common?

A

long-term vegans, ppl w/ the autoimmune dz “pernicious anemia”

31
Q

What is vitamin C?

what does it do?

A

Vit c = ascorbic acid

needed for:

  • hydroxylation of proline and lysine residuce: cross-linking in collagen
  • antioxidant
    *
32
Q

What is Vit C deficiency called?

S/sx?

A

vit c deficiency = scurvy

  • bleeding gums
  • hemorrhages around corkscrew hair follicles
  • bone/joint pain (bleeding under peri-ost.)
  • poor wound healing
33
Q

What can excessive Vitamin C cause?

A

oxalic acid kidney stones

34
Q

What are the fat-soluble vitamins?

How long do stores of them last?

A

Vitamins A, D, E & K

stores last for months in adipose

35
Q

In what type of patients are fat-sol vit def common?

A

Often seen in patients with fat malabsorption syndromes (pancreatic insufficiency or small intestine disease)

36
Q

What is Vitamin A?

Where do we get it?

What does it do?

A

retinoic acid, retinol and retinal

get it from ß-carotene in plants or from animal sources

Roles:

  • retinoic acid - necessary to maintain differentiation of epithelial cells
  • retinal - component of visual protein rhodopsin
  • retinol - doesn’t saw
37
Q

How does Vit A deficiency first manifest?

Later sx?

A

Manifests as night blindness which can be rapidly reversed w/ emergent vit a supp

Later sx:

  • Dry Eyes (wrinkles and loss of shine)
  • Bitot’s spots (patches of little gray bubbles on the sclera) Corneal ulceration
  • Keratomalacia (soft or bulging cornea)
38
Q

Who should NOT get Vitamin A? Why?

A

pregnant women b/c it’s a teratogen

39
Q

S/sx of hypervitaminosis A?

A

dry skin, liver damage, and raised intracranial pressure

40
Q

What is Vitamin D?

How do we get it to its active form?

What does it do?

A

Vitamin D3—liver—kidney—>calcitrol (active form; unique b/c it’s a hormone)

We can get D3 through diet, or:

  • by metabolizing D2 from diet, or
  • by making it in the skin from endogenous precursors with exposure to UV light

Calcitrol increases intestinal Ca2+ absorption and decrease renal excretion of Ca2+

41
Q

How does vitamin D deficiency present?

A

In kids: rickets

in adults: osteomalacia (brittle bones)

42
Q

Problems with treating osteomalacia with calcitrol?

A

hypercalcemia: bones (pain), stones, and abdominal moans

43
Q

Risk factors for Vitamin D deficiency?

A

Risk factors

  • lack of milk consumption (fortified with vitamin D) due to lactose intolerance, vegan diet, etc.
  • dark skin color
  • low sun exposure (northern latitudes)
44
Q

What is Vitamin E?

What does it do?

What does deficiency look like?

A

tocopherol

Antioxidant that protects lipid membranes

Deficiency can cause red blood cell fragility.

45
Q

What does vitamin K do?

Where do we get it?

Deficiency causes…

A

Vitamin K is needed for carboxylation of glutamate, which is req’d for Ca2+ binding by several blood clotting factors, including prothrombin

Our commensal gut bacteria make it.

Deficiency leads to hemorrhage with a long prothrombin time

  • serious complications include cerebral, pulmonary, and gastrointestinal hemorrhage)
46
Q

What therapies involve Vitamin K?

A

Vit K is given to premies with no commensal bacteria and increased bleeding

Vit K is blocked w/ warfarin (rat poison when used in high doses!)

Biochem-Metabolism Quiz 4 (3 decks)

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