Biochem Block 1 Vitamins

davidwurbel7's version from 2015-04-19 09:54

Section 1

Question Answer
Vitamins C and B complexesWater Soluble Vitamins
Vitamins A, D, E and KFat Soluble Vitamins
Predominantly eating polished riceThiamine deficiency
Chronic alcoholismThiamine deficiency
VegansCobalamin deficiency
Fat MalabsorbationVitamin A, D, E and K deficiency
Pyruvate dehydrogenase complex requires this vitaminThiamine
Alpha-ketoglutarate dehydrogenase complex requires this vitaminThiamine
Branched chain-alpha-ketoacid dehydrogenase complex requires this vitaminThiamine
Transketolase reaction in pentose phosphate pathway requires this vitaminThiamine
Deficiency of Thiamine Beriberi
Mainly involves cardiovascular systemWet beriberi
High output cardiac failure, four chamber dilated heartWet beriberi
Dependent edema, breathlessness, palpitation, orthopneaWet beriberi
Acute circulatory failure, deathWet beriberi
Central nervous system mainly involvedDry beriberi
Polyneuritis, peripheral neuropathyDry beriberi
Progressive muscle wasting, foot drop, wrist drop, loss of reflexes, parasthesiaDry beriberi
Difficulty in walking, bedriddenDry beriberi
Born to thiamine deficient motherInfantile beriberi
Sleepiness, restlessnessInfantile beriberi
Cyanosis, breathlessness, cardiac failureInfantile beriberi
Sudden death cardiac failureInfantile beriberi
Key signs: vision changes, ataxia and impaired memory. Seen as secondary to alcoholismWernicke-Korsakoff Syndrome
Nystagmus, ophthalmoplegia, cerebellar ataxia, confusion, loss of memory (anterograde and retrograde amnesia) and confabulatory psychosisWernicke-Korsakoff Syndrome
Biologically active forms are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD)Riboflavin
Component of electron transport chain complexesRiboflavin
Important for the metabolism of fat, carbohydrates, proteins. Riboflavin
Plays a role in drug and steroid metabolism, including detoxification reactionsRiboflavin
Reversibly accepts hydrogen atoms to become reduced to FADH2 and FMNH2Riboflavin
Extremely light sensitiveRiboflavin
Biologically active derivatives are NAD+, NADH, NADP+, NADPHNiacin
Deficiency is manifested principally by lesions of the mucocutaneous surfaces of the mouth and skin. Cheilosis, Angular cheilitis and stomatitis, glossitis, Corneal neovascularization, Seborrhic dermatitis, Anemia, and personality changesRiboflavin
NAD(H) dehydrogenases catalyze oxidative pathways Niacin
NADP(H) reductases catalyze reductive biosynthesisNiacin
Tryptophan can be converted to this vitamin with an efficiency of 60:1 by weightNiacin
Late signs and symptoms: Diarrhea (involvement of enterocytes), dermatitis (skin) and dementia (neuronal degeneration)Pallagra - Niacin deficiency
Early signs and symptoms: loss appetite, generalized weakness and irritability, abdominal pain, and vomitingPallagra - Niacin deficiency
Component of coenzyme A (CoA) which transfers acyl groups.Pantothenic acid
Deficiency manifestations – very rare, non-specific signs like fatigue, weakness, numbness, paresthesia, and muscle cramps, restlessness, malaise, sleep disturbance, painful burning sensation in foot (burning foot syndrome)Pantothenic acid
Biologically active form is pyridoxal phosphate (PLP).Pyridoxine
Deficiency seen in chronic alcoholics, Isoniazid therapy for TB, Women taking oral contraceptive pills, infants fed with deficient formulasPyridoxine
Peripheral neuropathy, personality changes including depression, confusion, convulsions, insomnia, restlessness, microcytic hypochromic anemia, homocysteinemia and increased risk of cardiovascular eventsPyridoxine
Acts as a coenzyme for all carboxylases; carrier of CO2 in the carboxylase catalyzed reaction also requires ATP and Mg2+Biotin
Deficiency manifestation: non-specific, dermatitis, glossitis, alopecia, loss of appetiteBiotin
Rapidly absorbed from intestine, not significantly stored, excreted as diketogulonic acid and oxalic acid.Ascorbic acid
Biologically active forms dehydroascorbic acid and ascorbic acidAscorbic acid
Smoking, hemodialysis, pregnancy, and stress increase requirementAscorbic acid
Coenzyme for prolyl hydroxylase and lysyl hydroxylaseAscorbic acid
Coenzyme for dopamine beta-hydroxylaseAscorbic acid
Participates in carnitine biosynthesisAscorbic acid
Are converted to 5-methyl tetrahydrofolate (THF) within the small intestinal mucosa before entering portal plasmaFolic acid
Acts as coenzymes in the transfer of single carbon unitsFolic acid
Involved in purine biosynthesisFolic acid
involved in the conversion of homocysteine to methionineFolic acid
Causes for deficiency include pregnancy, poor intestinal absorption, chronic alcoholism, cvercooking of green leafy vegetables, treatment with methotrexateFolic acid
Megaloblastic anemia, hypochromic RBCs, macrocytosis, hypersegmented neutrophils, anisocytosis, poikilocytosisFolic acid
Requires R-binder and intrinsic factor (IF) for absorption and absorbed in the last distal IleumCobalamin
Deficiency is usually due to malabsorption and protental to arises in vegans Cobalamin
Atrophic gastritis with pernicious anemia, congenital IF deficiency, gastrectomy, food malabsorption, intestinal malabsorption, abnormalities in metabolismCobalamin
Intestinal causes of malabsorption: e.g. ileal resection, tropical sprue, celiac disease, small bowel bacterial over growth syndrome, fish tape worm infestation Cobalamin
Abnormalities of metabolism: congenital transcobalamin II deficiency, nitrous oxide inhalation Cobalamin
Deficiency manifestations include megaloblastic anemia, neurologic manifestations including bilateral neuropathy or degeneration (demyelination) of the dorsal and lateral spinal columns, methylmalonic acidemia and aciduriaCobalamin
Retinol, Retinal, Retinoic acid and Β-carotene are all forms ofVitamin A
Loaded on to APO B48, secreted as chylomicronsRetinol
Binds with rhodopsin producing neuronal signal in the eyeRetinol
Component of the visual pigment in photoreceptor of rod cells., maintains bone development and growth in children, essential for normal reproduction; male spermatogenesis, fetal development in females and essential for normal differentiation of epithelial tissues and mucus secretionRetinol
Xerophthalmia, night blindness, conjunctival xerosis, Bitot’s spots, corneal ulceration and necrosis, Keratomalacia, follicular hyperkeratosis, poses an increased risk of mortality from diarrhea, dysentery, measles, and respiratory disease, can compromise barrier and innate and acquired immune defenses to infectionRetinol
Acute toxicity: increased intracranial pressure, vertigo, diplopia, bulging fontanels in children, seizures, and exfoliate dermatitis; it may result in death.Retinol
Chronic toxicity: dry skin (scaly dermatitis), cheilosis, glossitis, vomiting, alopecia, bone demineralization and pain, hypercalcemia, lymph node enlargement, hyperlipidemia, amenorrhea, hepatosplenomegaly, and features of pseudotumor cerebri with increased intracranial pressure and papilledema.Retinol
Toxicity during pregnancy can lead to congenital malformations (abortions, craniofacial anomalies, valvular heart disease).Retinol
The skin can produce this vitamin when exposed to UVB lightCholecalciferol
Hydroxylated at its 25th carbon in the liver by 25-hydroxylaseCholecalciferol
Hydroxylated at its 1st carbon in the kidneys by 25(OH)D3-1α-hydroxylaseCholecalciferol
Long standing deficiency results in hypocalcemia accompanied by secondary hyperparathyroidism, impaired mineralization of the skeleton and proximal myopathy, most common cause of rickets and osteomalacia.Cholecalciferol
Important naturally occurring antioxidants, stored in fat deposits, accumulate on cell membranes and transported through VLDL.Tocopherol
Prevents oxidation of LDL and play an important role in reducing the risk of cardiovascular disease.Tocopherol
Plays a role in cellular respiration by stabilizing ubiquinone.Tocopherol
Deficiency is seen in only severe and prolonged fat malabsorptive diseases, such as celiac disease, or after small intestinal resection, cystic fibrosis, abetalipoproteinemia.Tocopherol
Deficiency manifestations: peripheral neuropathy, hemolytic anemia, skeletal myopathy, degeneration of myelinated axonsTocopherol
Required for the posttranslational carboxylation of glutamic acidMenaquinone
Newborns are susceptible to Hemorrhagic disease of newborn because of a deficiency ofMenaquinone
Deficiency can manifest in patients with cystic fibrosis, Celiac disease and Crohn’s disease, with obstructed biliary tracts, after small bowel resection, prolonged broad spectrum antibiotic treatmentMenaquinone
Deficiency manifests with hemorrhagic episodes, prolonged prothrombin time, and reduced clotting factorsMenaquinone

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