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Flashcards in MCP 5 Deck (34)
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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.


thiamine function

vitamin B1. required cofactor for several enzymes in cellular energy metabolism. particularly critical in nervous system


thiamine deficiency

mild: GI symptoms, depression, fatigue.
moderate: Wernicke korsakoff syndrome
severe: beriberi


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


riboflavin function

B2. precursoe of FAD and FMN, key coenzymes for redox reactions involved in energy metabolism.


riboflavin deficiency

ariboflavinosis: rash around nose, inflammation of mouth and tongue, burning and itchy eyes, light sensitivity. susceptible groups are alcoholics, deficiency is quite uncommon


niacin function

B3. precursor of NAD and NADP. coenzymes important in redox reactions of energy metabolism. given to patients with hypercholesterolemia or hypertriglyceridemia


niacin deficiency

B3. pellagra, characterized by dermatitis, diarrhea, and mental symptoms (confusion, memory loss, mania)

susceptible groups are those with corn or millet based diets


biotin function

coenzyme for several carboxylases


biotin deficiency

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