water soluble vitamins Flashcards
general facts
not stored in the body (b12 exception) chronic intakes do alter tissue levels toxicity usually low (B6 exception) Absorption usually high Excrete via urine breast milk reflects maternal intake (folate is exception)
Thiamine (B1) function
Thiamine Diphosphate (TDP or thiamin pyrophosphate TPP)- coenzyme for rglycolysis, TCA cycle, amino acid metabolism; specifically in decarboxylation and transketolation reactions; TTP thought to bind at Na+ channel in nerve membranes; many function in nerve conduction
Riboflavin B2
“Part of 2 co-enzymes, flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) which function in oxidation/reduction reactions in TCA cycle and oxidative phosphorylation;
Amino acid & fatty acid metabolism; metabolism of vit K, folate B6, and niacin.”
Niacin B3
Nicotinamide is substituent of the critical electron carrying substances * NAD & NADP*; functions in multiple energy related pathways, including glycolysis, TCA cycle and oxidative phosphorylation and fatty acid synthesis and oxidation.
Folate
1-carbon transfers, esp. in synthesis of nucleic acids and for metabolism of certain amino acids; conversion homocysteine → methionine
Methyl-donor, epigenetics
Vit b12 (cobalmin)
”- Closely related to folate metabolism 1-C transfers;
- Metabolism of odd chain length fatty acids;
- Re-form THF from methylfolate (in formation of methionine);
- Isomerization of methylmalonyl Co-A to succinyl Co-A (essential to lipid & CHO metabolism).
- Interaction essential for protein & nucleic acid synthesis.
- Absorption and Homeostasis*: - Cleavage of vit from dietary protein & binding to “intrinsic factor” (IF) secreted by gastric parietal cells. -Cobalamin - IF complex absorbed from distal ileum. Absorbed into portal circulation, transported bound to transcobalamin II.
- Liver stores 1-10 mg* (vs RDA!); Can take years to develop deficiency, unless damage to stomach, ileum, pancreas”
Vit B6
critical in amino acid metabolism, interconversions
Vit C
antioxidant/reducing agent (=electron donor);
Collagen synthesis;
reduction of Fe3+ → Fe2+ & enhanced Fe absorption; Norepinephrine synthesis
Absorption & Homeostasis: Through active (saturable) process; dose dependent: at low doses ( 1.5 g/d, absorption ~50%; at 10 g/d, absorption ~15 %. ∴
*** if large total intake, better to take divided in 80 mg/d; maximum pool size ~ 2000 mg; intakes > 400-500 mg/d → minimal further increase in plasma a.a. concentrations.
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Neuro symptoms
Vit E, Niacin, Vit B12, Vit B6, Vit C
Anemia
B12, folate, vit b6, vit C, vit E, Vit K
Mouth lesions
folate, vit b6, vit b12, vit C, riboflavin
rash/skin findings
niacin, vit C, vit A, vit K
energy releasing vitamins
Thiamine (b1)
Thiamine sources
Esp. rich in whole grains (high in germ), enriched grains, lean pork, legumes
Riboflavin B2 sources
“Richest sources: liver, wheat germ;
Dairy = largest contribution to intake in US diet (UV light destroys the vitamin),
meats & poultry;
leafy greens”
Niacin B3 sources
Meats, poultry, fish, peanut butter, legumes are major sources of preformed niacin.
Tryptophan = precursor;
diets w/ liberal amounts of milk and eggs (rich in tryptophan) are likely adequate for niacin, even if low in preformed niacin.
Folate sources
“foliage” - deep green leaves, broccoli, orange juice, whole grains
(easily destroyed w/ prolong cooking); fortification of grains in U.S. in 1998 → ↑intakes
Vit B12 sources
Animal products only!
Vit B6 sources
animal products, vegetables, whole grains (lost in processing, not enriched)
Vit C sources
“Fruits and vegetables: broccoli, green pepper, citrus, potatoes.
US diet:
39% from fruits, 15% potatoes,
38% other veg;
> 80% vit C in Western diet from F/V
(Paleolithic diet about 600 mg/d)”
Deficiency Toxicity Vit C
- Scurvy*: defective collagen formation in capillary basement membranes & loss of precursors of catecholamines and other vasoactive and neurotropic substances.
- Symptoms: petechiae, bleeding gums, anemia, bruising; painful joints*
Deficiency Toxicity Vit B6
anemia, seizures, glossitis; +/- depression?;
Risk of toxicity: doses > 500 mg/d associated with sensory ataxia, impaired position/vibratory sensation; symptoms partially reversed with d/c of supplement
Deficiency Toxicity Vit B12
Macrocytic anemia, hypersegmented neutrophils, Neurologic disturbances: paresthesias, gait problems, depression
*Note: hematologic effects reversible, but neurologic effects are irreversible with longstanding deficiency. Treatment with folate will correct anemia but has NO effect on neurologic symptoms.
Macrocytic anemia should not be treated with folate unless B12 deficiency has been ruled out.
Deficiency Toxicity Folate
Macrocytic anemia, hypersegmented neutrophils, glossitis,
↑ increased plasma homocysteine;
↑ occurrence & recurrence of neural tube defects; risk partly hereditary, partly polygenic;
Individuals w/ MTHFR gene ↑’s requirement
Deficiency Toxicity Niacin B3
Pellagra: “The 4 D’s:”
Dermatitis: characteristic symmetric pattern; aggravated by sun, heat exposure (hypo and hyper pigmented areas
Dementia- confusion, dizziness, and hallcucinations
Diarrhea
Death
Toxicity: Relatively nontoxic in doses of 3 6 grams/d of nicotinic acid; used to lower serum cholesterol (esp LDL); initially causes peripheral vasodilation & flushing; less common: ↑ serum uric acid, glucose intolerance, liver damage.”
Deficiency Toxicity Riboflavin B2
Deficiency signs: oral-ocular-genital syndrome - cheilosis (cracking of lips) and angular **stomatitis (sores at corner of mouth), **increased vascularization of conjunctiva and photophobia, and seborrheic dermatitis and ***scrotal dermatitis.
Thiamine B1 deficiency
“Classical syndrome: Beriberi;
Dry (paralytic/nervous) beriberi: peripheral neuropathy w/ impairment of sensory, motor, and reflex functions; affects distal > proximal limbs; muscle tenderness, weakness/ atrophy, foot/wrist drop
Wet (cardiac) beriberi: edema and high output cardiac failure (tachycardia, cardiomegaly and CHF) + signs/sxs of dry beriberi
Wernicke-Korsakoff syndrome (cerebral beriberi):
“Triad” – ocular signs (nystagmus, ophthalmoplegia), ataxia, and amnesia/mental confusion. Retentive memory impaired out of all proportion to other cognitive function; only partially reversible with pharmacologic doses of thiamin; genetic predisposition for different susceptibility, unmasked by EtOH abuse, dietary deficiency. Neuro sxs may be only partially reversible (ophthalmoplegia quickly responds)”
which vitamins are involved in energy production
Thiamine, riboflavin, niacin
found enriched grains
Berberi
dry-neuropathy muscle tenderness weakness atrophy foot drop.
wet- edema, circulatory collapse, CHF
wernicke korsakoff- ataxia, memory loss, opthalmoplegia, confusion
B1 deficiency
who is at risk for B1 deficiency
alcoholics, bariatric surgery, TPN, anorexia, refeeding,
endemic in southeast asia
6 mo old breastfed infant vomiting, opthalmoplegia, CHF
B1 deficiency (berberi)
5 yr old eats burgers and milk, now limping and cant walk, rash
vitamin C (Scurvy)
alcoholic found down altered mental status, anemic
Thiamine maybe b12
15 mo old breast fed infant that doesnt want to walk, growth faltering
b12- baby not getting it in milk
obese adolescentbariatric surgery, cant walk falls down
thiamine, maybe b12
adult with rash and diarrhea
pallagra, niacin deficiency
