Flashcards in MCP 5 Deck (34):
how do vitamin deficiencies arise?
poor nutrition, increased demand, problem with absorption of one or more vitamins, interactions with medications
lipid soluble vitamins
A, D, K, and E. structure resembles lipids. generally are stored more efficiently than water soluble. deficiencies dont arise as quickly. toxicity may be a problem, especially with D and A.
water soluble vitamins
B and C. more hydrophillic structure. in general, deficiencies can arise more rapidly if vitamin is unavailable since they are excreted efficiently. less likely to be toxic
vitamin A functions
visual cycle: rhodopsin and cone opsins. synth of certain glycoproteins and mucopolysaccharides. retinoic acid: acts as a hormone. antioxidant
vitamin A deficiency
night blindness early, xerophtalmia (thickening of conjunctiva) advanced. follicular hyperkeratosis (goosebumps that dont go away). anemia despite normal iron intake. poor growth in children. increased suceptibility to infection and cancer. susceptible groups are poor, malnourished, and premature babies
vitamin A toxicity
accumulates in liver. excess intake can be toxic. symptoms include nausea, diarrhea, bone pain, scaly skin, and orange cast to skin.
vitamin D functions
maintaining bone. calcium homeostasis. acts as a hormone: receptors are present in many tissues but full range of activity is unknown
vitamin D deficiency
rickets in children, osteomalacia in adults. increased susceptibility to breast and other canceres, metabolic syndrome/diabetes, and infection. susceptible groups are poor, elderly, alcoholics
synth of active vitamin D
needs three organ systems: skin (sunlight), liver, and kidney (both hydroxylation)
active form is called calcitriol
vitamin D and cancer
low serum vitamin D in post menopausal women is correlated with increased risk of breast cancer. polymorphisms of D receptor and breastcancer links have been amde. D effects are postulated to arise from cell cycle signalling effects through the D receptor
vitamin K functions
localization of enzymes required during blood clotting. helps catalyze addition of gamma-carboxyglutamate to clotting enzymes.
vitamin K deficiency
results in easy bruising, bleeding, and hemorrhage. susceptible groups are newborn infants, patients on long term antibiotics, elderly and other with defects in fat absorption. babies lack bacteria that make vitamin K and deficiency can lead to brain bleed. given shot at birth. In adults, long term antibiotics can kill the bacteria that make K.
vitamin K in blood clotting
essential for enzymes involved in GLA modification of several clotting enzymes
vitamin E function
antioxidant. scavenges free radicals. protects membranes from damage. prevents oxidation of LDL
vitamin E deficiency
cardiovascular disease. neurological symptoms. susceptible groups include patients with severe, prolonged defects in absorption (celiac) or genetic effects
vitamin C function
cofactor for oxidases involved in collagen formation. required for synthesis of steroids in stress response. aids in absorption of iron. has antioxidant activity.
vitamin C deficiency
mild: bruising, immunocompromise
severe: scurvy (decreased would healing, osteoporosis, hemorrhage and anemia, fatigue, corkscrew hairs, pinpoint hemorrhages, periodontal disease)
susceptible groups: people with poor diet, smokers, pirates
energy releasing B complex vitamins
thiamine (B1), riboflavin (B2), niacin (B3), pantothenic acid (B5), pyridoxine (B6)
hematopoietic B complex vitamins
Folate (B9) and Cobalamin (B12)
energy releasing B vitamin deficiencies
symptoms show up first in rapidly growing tissue: skin (dermatitis, red tongue, swollen, glossitis), GI (diarrhea)
nervous system affected due to high energy demand. peripheral neuropathy or tingling of extremities, depression, confusion, lack of coordination, malaise.
vitamin B1. required cofactor for several enzymes in cellular energy metabolism. particularly critical in nervous system
mild: GI symptoms, depression, fatigue.
moderate: Wernicke korsakoff syndrome
wenicke korsakoff syndrome
moderate/severe thiamine deficiency. seen in alcoholics. mental disturbance, unsteady gate, uncoordinated eye movements. occasionally congestive heart failure
severe thiamine deficiency. seen in japan when they had polished rice. extreme muscle weakness, polyneuropathy, heart failure. wet beriberi has edema
B2. precursoe of FAD and FMN, key coenzymes for redox reactions involved in energy metabolism.
ariboflavinosis: rash around nose, inflammation of mouth and tongue, burning and itchy eyes, light sensitivity. susceptible groups are alcoholics, deficiency is quite uncommon
B3. precursor of NAD and NADP. coenzymes important in redox reactions of energy metabolism. given to patients with hypercholesterolemia or hypertriglyceridemia
B3. pellagra, characterized by dermatitis, diarrhea, and mental symptoms (confusion, memory loss, mania)
susceptible groups are those with corn or millet based diets
coenzyme for several carboxylases
rare, but can be caused by eating a lot of raw eggs. eggs contain avidin which binds biotin very tightly, causing it to not function
pantothenic acid function
B5. required for synth of CoA. CoA is a coenzyme for a ton of things. required for TCA cycle and metabolism of all fats and proteins
pantothenic acid deficiency
B5. very rare. symptoms are typical of B vitamins. B5 is found in a ton of foods so the deficiency is rare
precursor of pyridoxal phosphate. required for glycogen breakdown and synthesis of GABA and heme.