Nutrition Flashcards
Which are the liposoluble vitamins?
A, D, E and K, their absorption depends on the gut and pancreas. They accumulate in fat, so toxicity is more common than with the hidrosoluble.
Malabsorption with steatorrhea (CF, celiac) or mineral oil intake can cause deficit.
Which are the hidrosoluble vitamins?
All the B complex and C (ascorbic acid).
Easy wash from body, except for B12 (in liver for 3-4 years) and B9 (for 3-4 months).
Can be coenzymes or precursors to coenzymes.
Which is the B complex?
B1 (thiamine TTP) B2 (rivoflavin FAD, FMN) B3 (niacin NAD+) B5 (pantothenic acid: CoA) B6 (pyridoxine PLP) B7 (biotin) B9 (folate) B12 (cobalamin). Its deficiencies may result in glossitis, dermatitis and diarrhea.
What does vitamin B1 (thiamine) do and how do its alterations manifest?
Thiamine pyrophosphate (TPP), cofactor for dehydrogenase enzyme reactions: [Be APT]
Branched-chain ketoacid dehydrogenase
Alpha-ketoglutarate dehydrogenase (TCA cycle)
Pyruvate dehydrogenase (links glycolisis to TCA cycle)
Transketolase (HMP shunt)
Deficit: impaired glucose breakdown, ATP depletion worsened by glucose infusion, highly aerobic tisues affected.
Thiamine before dextrose in alcoholic to prevent Wernicke.
Dx: High RBC transketolase activity following B1 admin.
Wernicke-Korsakoff sx: triad: confusion, ophtalmoplegia, ataxia; confabulation, personality change, permanent memory loss, damage of mammilary bodies, medial dorsal nucleus of thalamus.
Dry Beriberi: polyneuropathy, symmetrical muscle wasting.
Wet Beriberi: high output cardiac failure, edema.
Ber1 Ber1.
What does vitamin B7 (biotin) do and how do its alterations manifest?
It serves as a cofactor for carboxylation enzymes, which add a l-carbon group.
- Pyruvate carboxylase: pyruvate (3C) = oxaloacetate (4C).
- Acetyl-CoA carboxylase: acetyl-CoA (2C) = malonyl-CoA (3C)
- Propionyl-CoA carboxylase: propionyl-CoA (3C) = methylmalonyl-CoA (4C)
Deficit is uncommon, dermatitis, enteritis, alopecia.
Due to long term antibiotic uso or excess of raw egg whites.
AVIDin in egg whites AVIDly binds biotin.
What does vitamin B9 (folate) do and how do its alterations manifest?
Its converted to tetrahydrofolic acid (TFH), coenzyme for l.carbon transfer/methylation reactions.
In leafy greens, absorbed in jejunum, FOLate from FOLiage. Pool in liver.
Synthesis of nitrogenous bases in DNA and RNA.
Deficit: Macro, megaloblastic anemia, hypersegmented PMN, glossitis, no neuro signs, high homocysteine, alcoholism and pregnancy.
B phenytoin, sulfonamides, MTX.
Maternal folic acid at least a month prior to conception and early pregnancy.
B9 = 9 months preg.
What does vitamin B12 (cobalamin) do and how do its alterations manifest?
Cofactor for methionine synthase (CH3 groups as mathylcobalamin) and methylmalonyl-CoA mutase.
DNA synthesis.
In animal products, only synthesized by microorganisms.
Large pool in liver.
Deficit: due to malabsorption, lack of IF, absence of terminal ileum, drugs like metformin, veganism.
Macro and megaloblastic anemia, hypersegmented PMN, paresthesias, subacute combined degeneration due to abnormal myelin.
High serum homocysteine and methylmalonic acid, secondary folate deficit.
If prolonged: irreversible nerve damage.
Anti-IF ABs: dx for pernicious anemia.
Folate supplementation masks hematologic symptoms, not neurological.
What does vitamin C (ascorbic acid) do and how do its alterations manifest?
Antioxidant, iron absorption by reducing it to Fe2. Hydroxylation of proline and lysine in collagen synthesis.
Necessary for dopamine ß-hydroxlase to convert dopamine to NE. Fruits and vegetables.
Tx for methemoglobinemia, Fe3 to Fe2.
Deficit: Scurvy, swollen gums, easy bruising, anemia, poor wound healing, corkscrew hair, weak immune response.
vit C deficit Causes sCurvy due to Collagen synthesis defect.
Excess: N/V, diarrhea, fatigue, ca oxalate nephrolitiasis. Increases Fe toxicity in predisposed.
What does vitamin D do and how do its alterations manifest?
D3 (cholecalciferol) exposure to sunlight, fish, milk, plants.
D2 (ergocalciferol) from plants, fungi, yeast.
Converted to 25OH D3 (storage form) in liver
What does vitamin D do?
D3 (cholecalciferol) exposure to sunlight, fish, milk, plants.
D2 (ergocalciferol) from plants, fungi, yeast.
Converted to 25OH D3 (storage form) in liver and active form 1,25(OH)2 D3 (calcitriol) in kidney.
Increases intestinal absorption of Ca and phosphate, bone mineralization at low levels and resorption at higher levels.
High PTH, low Ca and phosphate increase 1,25(oh)2D3 production in kidney and negative feedback.
Increase in PTH increases Ca reabsorption and lows phosphate reabsorption in kidney.
How are deficit and excess of vitamin D manifested?
Deficit: rickets in kids, deformity, bowlegs, in adults is osteomalacia (bone pain, muscle weakness), hypocalcemic tetany.
Malabsorption, low sun exposure, poor diet, CKD, liver disease.
Oral vitamin to breastfed.
Exacerbated by pigmented skin, premature birth.
Excess: hypercalcemia, hypercalciuria, loss of apetite, stupor. In granulomatous diseases, more activation of vit D by epithelioid macrophages.
What does vitamin E (tocopherol and tocotrienol) do and how do its alterations manifest?
Antioxidant, protects membranes from free radical damage.
Deficit: hemolytic anemia, acanthocytosis, muscle weakness, demyelination of posterior columns (less position and vibration), spinocerebellar tract.
Excess: risk of enterocolitis in kids, supplementation may alter metabolism of vit K: increases warfarin effects.
What does vitamin K do and how do its alterations manifest?
Phytomenadione, phylloquinone, phytonadione, menaquinone.
Its activated by epoxide reductase to reduced form, cofactor for gamma-carboxylation of glutamic acid residues on proteins for clotting. Synthesized by gut flora.
K = koagulation.
Maturation of II, VII, IX, X, protein C and S. Warfarin inhibits vit K dependent synthesis.
Deficit: neonatal hemorrhage, increased PT and aPTT, but normal bleeding time. Sterile gut, no flora to synthesize it. After broad spectrum antibiotics too.
What is zinc and how do its alterations manifest?
Mineral for activity of >100 enzymes. Formation of zinc fingers (transcription factor motif).
Deficit: delayed wound healing, suppressed immunity, male hypogonadism, little adult hair, dysgeusia, anosmia. Acrodermatitis anteropathica.
Predisposes to alcoholic cirrhosis.
What is Kwashiorkor?
Protein malnutrition = skin lesions, edema (low oncotic pressure), liver malfunction (fatty change, low apolipoprotein synthesis). Small kid, swollen belly. Protein deficient MEALS: Malnutrition Edema Anemia Liver (fatty) Skin (hyperkeratosis, dyspigmentation).
