Vitamin Thiamine h) Riboflavin (8,) Niacin (B3) Pyridoxine (By) Cobalamin (Bz) Folate Vitamin C Biochemical Function Cofactor for pyruvate and a-ketogluta dehydrogenase Precursor to the coenzymes flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD) Required for the production of NAD* and NADP* as well as numerous dehydrogenases Required for several transaminase and decarboxylation reactions Required for some carboxylation reactions Required by methylmatony! CoA mutase and methionine synthase Reduced by dihydrofolate reductese to tetrahydrofolate (THF), which functions as a one-carbon donor in many biosyn- thetic pathways Hydroxylation of proline residues in ‘collagen end aids in iron absorption Clinical Consequence of Vitamin Deficiency Beriberi: high-output heart failure (wet beriberi) and peripheral neuropathy (dry beriberi) Wernicke-Korsakolf syndrome: deficiency in chronic alcoholics manifesting with ataxia, ophthalmoplegia, confusion, and confabulation Rare deficiency because grain and cereal prod- ucts are fortified with riboflavin. Deficiency is associated with atrophy of the tongue (glossi- tis), fissures of the comer of the mouth (cheilo- sis), dermatitis, and corneal ulceration, Deficiency results in pellagra, characterized by diarrhea, dementia, and dermatitis. Deficiency can result from the antituberculoid medic: isoniazid, Hartnup disease, or carcinoid syndrome, Most severe symptoms due to the requirement for decarboxylating glutamic acid to the inhibitory ‘neurotransmitter GABA, resulting in seizures. Deficiency can be associated with isoniazid or penicilamine use. Deficiency is rare because biotin is synthesized gastrointestinal bacteria, although defi- the consumption of raw eggs, contai din, that binds and inhibits absorption of biotin. Deficiency associated with lack of intrinsic fac- tor, produced by parietal cells ofthe stomach. Deficiency resutts in a block in purine and thy- rmidine biosynthesis, resulting in megaloblastic ‘anemia and subacute combined degeneration ofthe spinal cord. It also causes a functional Lack of folate results in impaired thymidine mono- phosphate (4TMP) synthesis, with arest of DNA synthesis in rapidly dividing cels, ike he- matopoietic cells, resulting in jaloblastic anemia. Pregnant patients require more folate; deficiency results in neurotubule defects, such ‘as spina bifida in the developing fetus. Deficiency can resuitin scurvy, which is charac terized swollen gums, hemorrhage, andClinical Consequence of Vitamin Deficiency Vitamin A Vitamin D Vitamin E Vitamin K Biochemical Function Required for growth and differentiation; required for the production ofthe light-absorbing protein rhodopsin. Regulation of gone expression for the absorption ‘of calcium from the gastrointestinal tract Functions as an antioxidant and free radi scavenger Required for the y-carboxylation of coagulation factors Il, Vil, IX, and X Defici \cy results in night blindness, dry eyes corneal damage, and urinary stones Rickets in children results in detective bone mineral- ization with a “squared” head, chest deformity, spine abnormalities, and bowing of the legs. In ‘adults, osteomalacia can occur, with weakening ‘of bone and increased incidence of fracture. Rare; however, lack of vitamin E can contribute to the development of atherosclerosis and cardiovascu- lar disease. Deficiency is seen in newboms because vitamin K is produced by the yet undeveloped gastrointestinal flora, resulting in hemorrhage and bleeding diathe- sis. The blood thinner warfarin, used to treat blood clots, antagonizes the vitamin's actions.