Vitamins Flashcards

1
Q

Water Soluble Vitamins

Features

A
  • Most water-soluble vitamins are precursors of coenzymes involved in intermediary metabolism.
  • All water-soluble vitamins except for vitamin B12 are present in vegetables.
  • Deficiency of all water-soluble vitamins except for vitamin B12 produces clinical symptoms within weeks due to low body stores.
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2
Q

Examples of Water Soluble Vitamins

A
  • Vitamin B1 (Thiamine)
  • Vitamin B2 (Riboflavin)
  • Vitamin B3 (Niacin)
  • Vitamin B5 (Pantothenic acid)
  • Vitamin B6
  • Vitamin B7 (Biotin)
  • Vitamin B9 (Folate)
  • Vitamin B12 (Cobalamin)
  • Vitamin C (ascorbic acid)
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3
Q

Vitamin B1 (Thiamine)

A

• Thiamine pyrophosphate is a coenzyme for enzymes involved in carbohydrate metabolism, specifically pyruvate dehydrogenase,
α-ketoglutarate dehydrogenase, and transketolase.
• Deficiency causes Korsakoff’s syndrome in alcohol abusers. Thiamine should always be administered together with glucose to alcohol abusers.
• Beriberi- peripheral neuropathy and dilated cardiomyopathy.

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4
Q

Vitamin B2 (Riboflavin)

A
  • Precursor of flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) coenzymes.
  • Deficiency causes fissuring at the angles of the mouth, dermatitis, and purple tongue.
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5
Q

Vitamin B3 (Niacin)

A
  • Collective term for two compounds- nicotinamide or nicotinic acid.
  • Precursors of nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) coenzymes.
  • Strictly not a vitamin because humans can synthesize niacin from tryptophan.
  • Deficiency causes pellagra (Italian for “sour skin”)- dermatitis, diarrhea, dementia, and death.
  • Seen in some patients with Hartnup disease (diminished tryptophan uptake) and patients with carcinoid syndrome (altered tryptophan metabolism).
  • Used therapeutically to lower LDL and VLDL cholesterol in type IIb hyperlipoproteinemia.
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6
Q

Vitamin B5 (Pantothenic acid)

A
  • Component of coenzyme A

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

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7
Q

Vitamin B6

A
  • Collective term for pyridoxine, pyridoxal, and pyridoxamine.
  • Precursors of pyridoxal phosphate, a coenzyme catalyzing reactions involving amino acids.
  • 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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8
Q

Vitamin B7 (Biotin)

A
  • A coenzyme in carboxylation reactions, which is covalently bound to specific lysine residues of biotin-containing enzymes.
  • Deficiency caused by eating >20 raw eggs per day (which contains the biotinbinding protein avidin): dermatitis, glossitis, and nausea.
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9
Q

Vitamin B9 (Folate)

A
  • Necessary for one-carbon metabolism, including purine and thymidine (and therefore DNA) synthesis.
  • Deficiency causes megaloblastic anemia in adults and neural tube defects in fetuses.
  • Given therapeutically before and during 1st trimester of pregnancy to prevent neural tube defects.
  • Supplemented in “enriched” foods since 1998.
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10
Q

Vitamin B12 (Cobalamin)

A
  • Precursor of methylcobalamin, which is needed to synthesize methionine from homocysteine in blood cells, and deoxyadenosylcobalamin, which is needed for fatty acid metabolism in brain cells.
  • Not produced by plants.
  • Requires intrinsic factor for intestinal absorption.
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11
Q

Deficiency of Vitamin B12

A

• A common deficiency- seen in vegans and patients with pernicious anemia (lacking intrinsic factor).
• Deficiency causes megaloblastic anemia by functionally trapping folate, subacute combined degeneration of the spinal cord, and dementia.
• Etiology of megaloblastic anemia in vitamin B12 deficiency (the folate trap hypothesis): During methionine synthesis, N5-methyl-tetrahydrofolate transfers a methyl group to vitamin B12 to form methylcobalamin. This reaction is also required to metabolize N5-methyl-tetrahydrofolate. Lack of vitamin B12 blocks the metabolism of N5-methyl-tetrahydrofolate, which cannot be used for DNA
synthesis.
• Clinical symptoms become manifest only after years of deficiency due to large body stores.
• Treat pernicious anemia with intramuscular B12 injections, which circumvents the
need for intrinsic factor.

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12
Q

Folate supplementation

A

Folate supplementation ameliorates megaloblastic anemia caused by deficiencies of either vitamin B12 or folate. However, folate supplementation does not treat subacute combined degeneration of the spinal cord caused by vitamin B12 deficiency.

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13
Q

Vitamin C (ascorbic acid)

A
  • Necessary for post-translational hydroxylation of proline, especially in collagen.
  • Deficiency causes scurvy- bleeding gums, hemorrhages around corkscrew hair follicles, bone pain caused by bleeding underneath periosteum, poor wound healing.
  • Mega-doses can cause oxalic acid kidney stones.
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14
Q

Fat Soluble Vitamins

Features

A
  • In the United States, deficiencies of fat-soluble vitamins are often present in patients with fat malabsorption syndromes.
  • Fat-soluble vitamins are stored in the body and metabolized slowly, and therefore deficiency usually develops only after months of inadequate intake.
  • Excess consumption of either vitamin A or D leads to toxicity.
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15
Q

Examples of Fat Soluble Vitamins

A
  • Vitamin A
  • Vitamin D
  • Vitamin E
  • Vitamin K
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16
Q

Vitamin A

A

• Collective term for retinol, retinal, the essential visual pigment, and retinoic acid, which is necessary to maintain differentiation of epithelial cells.
• Vitamin A can be obtained from animal sources or derived from β-carotene
present in plants.

17
Q

Vitamin A Deficiency

A

Deficiency causes 1.2 million cases of permanent blindness each year in the developing world. First symptom is night blindness, which can be rapidly
improved with emergency vitamin A therapy.
• Important physical signs of vitamin A deficiency caused by corneal epithelial cell dedifferentiation/keratinization include xeropthalmia and Bitot’s spots.

18
Q

Effects of Vitamin A

A
  • Used in treatment of acne and psoriasis
  • Hypervitaminosis A causes skin rash, liver damage, and raised intracranial pressure
  • Vitamin A is teratogenic: avoid giving to pregnant patients
19
Q

Vitamin D

A

• Vitamin D can be produced endogenously in the skin by uv irradiation, or obtained from either animal or plant tissues. Vitamin D is converted to its active
form, calcitriol, by two successive hydroxylation reactions: first in the liver, and subsequently in kidney, bone, or placenta.
• Calcitriol is a steroid hormone that increases calcium absorption by the intestine epithelium.
• In the United states, milk is fortified with vitamin D

20
Q

Vitamin D Deficiency

A
  • Deficiency causes demineralization of formed bone in adults, leading to osteomalacia (bone pain, microfractures and compression fractures), and failure to mineralize developing bones in children, leading to rickets (bowed legs).
  • Risk factors for deficiency = lack of milk consumption (often due to lactose intolerance), dark skin color, low sun exposure.
  • Calcitriol is given as therapy, but often causes hypercalcaemia: “bones, stones, and abdominal moans.”
21
Q

Vitamin E (tocopherol)

A
  • Antioxidant that protects lipid membranes.

* Deficiency can cause red blood cell fragility.

22
Q

Vitamin K

A
  • Needed for post-translational carboxylation of glutamate, which is required for calcium binding by several blood clotting factors, including prothrombin.
  • Produced by intestinal bacteria.
23
Q

Effects of Vitamin K

A
  • Deficiency leads to hemorrhage with a long prothrombin time (PT).
  • Clinically administered to premature infants, who lack the intestinal bacteria that provide vitamin K, and adults on long-term antibiotic therapy.
  • In some clinical scenarios, Vitamin K action is intentionally blocked by the drug coumarin, a vitamin K antagonist, to prevent clotting (e.g. in patients with prosthetic heart valves).