Water Soluble Vitamins Flashcards
(41 cards)
Thiamine B1 Vitamin
THIAMINE (B1)
a. Functions: Thiamine Diphosphate (TDP or thiamin pyrophosphate TPP): coenzyme central to intermediary metabolism in all cells, esp. glycolysis, TCA cycle, amino acid metabolism; decarboxylation; transketolation reactions; TTP thought to bind at Na+ channel in nerve membranes; many function in nerve conduction
b. Food sources: Esp. rich in whole grains (high in germ), enriched grains, lean pork, legumes
c. Requirements/intake recommendations: RDA: 1.1-1.2 mg/d.
d. Biochemical evaluation: Erythrocyte transketolase activity; blood thiamine levels
e. Treatment for deficiency: 50-100 mg intramuscular or intravenous.
Deficiency of B1 (Thiamine)
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.
i. 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.
ii. Neuro sxs may be only partially reversible (ophthalmoplegia quickly responds)
Populations at risk of B1 deficiency
Populations at risk of deficiency:
a. Alcoholics most at risk in US (low intake, poor intestinal absorption, defective metabolism)
b. elderly may have relatively high incidence of mild deficiency;
c. chronic renal dialysis patients
d. adults on high carbohydrate diet derived mainly from milled rice or unenriched grains; refeeding after starvation may precipitate deficiency as body “stores” insufficient to handle increased demand to metabolize CHO/energy load; bariatric surgery (assoc. w/ bypass, banding, and gastric sleeve).
e. Dietary deficiency still common in many Asian countries with high reliance on refined rice.
Riboflavin (B2)
a. Functions: 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.
i. Amino acid & fatty acid metabolism; metabolism of vit K, folate B6, and niacin.
b. Food sources: Richest sources: liver, wheat germ; Dairy = largest contribution to intake in US diet (UV light destroys the vitamin), meats & poultry; leafy greens
Intake recommendations: RDA: 1.1-1.3 mg/d
c. Deficiency/Toxicity: Deficiency signs: oral-ocular-genital syndrome - cheilosis (cracked lips) and angular stomatitis (sores at corner of mouth), increased vascularization of conjunctiva and photophobia, and seborrheic dermatitis and scrotal dermatitis.
d. Biochemical eval: Erythrocyte glutathione reductase activity co-efficient (EGRAC) ( in def)
Riboflavin B2 Deficiency
Deficiency signs: oral-ocular-genital syndrome
i. cheilosis (cracked lips) and angular stomatitis (sores at corner of mouth),
ii. increased vascularization of conjunctiva and photophobia, and seborrheic dermatitis and scrotal dermatitis.
Things to Look for in B2 deficiency
a. cheilosis (cracked lips) and angular stomatitis (sores at corner of mouth),
b. increased vascularization of conjunctiva and photophobia
Vitamin 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
Niacin (B3)
NIACIN (B3)
a. Functions: Nicotinamide is substituent of the electron carrying substances NAD & NADP; functions in multiple energy related pathways, including glycolysis, TCA cycle and oxidative phosphorylation and fatty acid synthesis and oxidation.
b. Food sources: Meats, poultry, fish, peanut butter, legumes are major sources of preformed niacin.
i. Tryptophan = precursor; diets w/ liberal amounts of milk and eggs (rich in tryptophan) are likely adequate for niacin, even if low in preformed niacin.
c. Intake recommendations: RDA: 14-16 mg/d; Niacin equivalents (NE): 1 NE = 1 mg niacin or 60 mg tryptophan.
d. Deficiency treatment: 50-100 mg 3x/day for 3-4 days
e. Biochemical evaluation: urinary excretion of N1-methylnicotinamide and 2-pyridone (ratio < 1.0 = def); serum niacin
Niacin (B3) Deficiency
a. Deficiency/Toxicity:
Pellagra: “4 D’s:”
- Dermatitis: characteristic symmetric pattern; aggravated by sun, heat exposure
- Dementia: confusion, dizziness, and hallucinations
- Diarrhea
- Death
b. 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;
i. less common: Increased serum uric acid, glucose intolerance, liver damage.
Niacin (B3) Deficiency- Pellagra
“4 D’s:”
- Dermatitis: characteristic symmetric pattern; aggravated by sun, heat exposure
- Dementia: confusion, dizziness, and hallucinations
- Diarrhea
- Death
Water Soluble Vitamins
a. Generally not “stored” in body
i. (B12 = exception)
b. Chronic intakes do alter tissues levels
c. Toxicity usually low (B6 = exception)
d. Absorption usually high
e. Excretion typically via urine
f. Breast milk reflects maternal intake/status
(folate = exception)
What’s the risk/Dx?
Water soluble vitamin deficiency are rare, happen in unique cases
- 6 mo old breastfed infant, vomiting, ophthalmoplegia, congestive heart failure
- 5 yr old child only eats burgers (w/ bun) & milk, now limping & refusing to walk, ~ rash
- Alcoholic, “found down”, altered mental status, anemic
- Obese adolescent, s/p bariatric surgery, can’t walk; falls down
- Adult, low SES, chronic diarrhea/malabsorption, rash on arms, hands, neck
Thiamin (B1) /Riboflavin (B2) /Niacin (B3)
a. Functions:
i. All involved in glycolysis/TCA cycle
ii. TPP, FAD, NAD; decarboxylation, oxidation-reduction
b. Food sources: whole & enriched grains
i. Thiamin: legumes, rice bran, grains
- (decreased polished rice)
ii. Riboflavin: dairy, eggs, meats
iii. Niacin: meat/poultry; tryptophan = precursor
- (corn = poor source unless alkaline-treated)
Thiamin (B1) Deficiency
Beriberi - nervous & cardiovascular systems
1. “Dry:” peripheral neuropathy; muscle tenderness (esp legs), weakness & atrophy; foot drop;
- “Wet:” edema, circulatory collapse, congestive heart failure
- Wernicke-Korsakoff (cerebral): confusion, ophthalmoplegia, ataxia, memory loss (complete correction 25%; partial 50%); peripheral neuropathy
Thiamin Deficiency – Who’s at Risk
B1 Vitamin
Alcoholics
Vomiting
(e.g. s/p bariatric surgery (esp 1st 6 mo post-op)
TPN (total parenteral nutrition), w/o thiamin
(deficiency occurs w/in 2-3 wk)
Anorexia nervosa
Re-feeding
Endemic in So Asia (maternal & BF infant) – polished rice diet;
Thiamin Deficiency:
Dry beri-beri
a. Peripheral neuropathy
b. Muscle weakness/atrophy
c. Foot drop
d. Eventual inability to walk w/o falling
Thiamin Deficiency:
Cerebral beri-beri
Wernicke-Korsakoff
- Ophthalmoplegia
- Ataxia
- Confusion
- Memory loss
Infantile beriberi
a. Infant formula w/o thiamin
b. 9 infants (2-12 mo) present w/
- Infection
- Vomiting
- Lethargy/restlessness
- Ophthalmoplegia
- Low thiamine pyrophosphate, acidosis
c. Prompt response to high dose (50 mg/d x 2 wk)
Riboflavin (B2) Deficiency:
- Cheilosis–> Inflammation and small cracks in one or both corners of the mouth.
- Angular stomatitis–> is inflammation of one or both corners of the mouth.
i. Often the corners are red with skin breakdown and crusting.
B2 def–>Low dairy, animal products; common in low resource settings
Niacin (B3) Deficiency: Pellagra Predisposing Factors
a. Nutritional/dietary restriction
i. Cornmeal (w/o germ) based diet (esp w/o alkaline/lime treatment)
ii. Food faddism / restriction
b. Malabsorption syndromes
c. Alcoholism
d. Metabolic “shunting” (carcinoid tumor ↑ serotonin tryptophan)
Pellagra: The “4 D’s”
Niacin (B3) Deficiency
- Diarrhea
- Dermatitis
i. symmetric, scaling w/ areas depigmentation & hyperpigmentation
ii. aggravated by sun exposure (“Casal’s necklace”; reflects ↓ DNA repair, UV-light damage) - Dementia
i. confusion, dizziness, hallucination - Death
Folic Acid
a. Functions: single C transfers
i. nucleic acid synthesis
ii. amino acid metabolism
iii. DNA Methylation – regulation of gene expression / epigenetics
b. Food sources:
i. “foliage,” deep green veg
ii. orange juice
iii. whole grains
(Grains enriched in US since 1998)
(Easily destroyed in prolonged cooking)
Situations with Risk of
Folate Deficiency
a. Inadequate intake or increased destruction in food
b. Alcoholics
c. Pregnancy – globally, high rates deficiency; WHO: routine supplementation, women of reproductive age
d. Hematopoietic conditions
e. Drug/nutrient interactions
Signs/symptoms of
Folate Deficiency
- *Macrocytic anemia
- *Hypersegmented neutrophils
- *Glossitis, irritability
- *Homocysteinemia
- Neural tube defects (occurrence/recurrence)
- Reversible with correction of deficiency
- cannot reverse the neural tube deffects
