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Viva questions

Q.1- Which vitamin deficiency is associated with sub acute combined degeneration of spinal cord?

Answer- Vitamin B12 deficiency is associated with sub acute combined degeneration of spinal cord. Peripheral nerves are usually affected first, and patients complain initially of paresthesias. The posterior columns next become impaired, and patients complain of difficulty with balance. In more advanced cases, cerebral function may be altered as well. An accumulation of Methylmalonyl-CoA in serum, has been suggested as a possible cause of neurologic defects seen in cobalamin deficiency by decreasing lipid synthesis.

Impaired biosynthesis of phosphatidyl choline due to decreased levels of methionine and S-adenosylmethionine (SAM) may also play a role in the neurologic symptoms of cobalamin deficiency by compromising the repair of demyelination.

Q.2- Which vitamin participates in the absorption of calcium from gut?

Answer- Vitamin D has an active role in the absorption of calcium from gut. Vitamin D promotes the synthesis of calbindin protein that promotes the absorption of calcium from gut. This action is brought about through nuclear receptors. it acts like a steroid hormone, binding to nuclear receptors and enhancing gene expression, although it also has rapid effects on calcium transporters in the intestinal mucosa

Q.3- A 2-year- old child presents with chronic cough, bronchitis, growth failure, chronic diarrhea and growth failure. A deficiency of which vitamin should be considered?

 Answer- The child is probably suffering from Vitamin A deficiency.

The child has chronic cough, bronchitis, growth failure and passage of light-colored, foul-smelling stools. All these symptoms are due to increased susceptibility to infections as a result of the keratinization of mucous membranes in the respiratory, GI, and urinary tracts. The thickened mucosa cracks easily and the risk for bacterial infections increases. During infection the synthesis of retinol binding protein is reduced in response to infection since it is a negative ‘Acute phase protein’, that results in decreased circulatory concentration of the vitamin with further deterioration of the immune system.

Q.4- A 2-year- old child has been brought to Pediatric O.P.D with the complaint of painful and difficult walking. General examination reveals bow legs and prominent costochondral junctions. Which vitamin supplementation should be given as a part of the treatment?

Answer- Vitamin D supplementation is needed as a part of treatment since the child seems to be suffering from Rickets. In young infants, rickets causes softening of the entire skull (Craniotabes). In older infants with rickets, sitting and crawling are delayed, as is Fontenelle closure; there is bossing of the skull and costochondral thickening. Costochondral thickening can look like bead like prominences along the lateral chest wall (rachitic rosary). In children 1 to 4 yr, epiphyseal cartilage at the lower ends of the radius, ulna, tibia, and fibula enlarge; Kyphoscoliosis develops, and walking is delayed. In older children and adolescents, walking is painful; in extreme cases, deformities such as bowlegs and knock-knees develop.

Q.5- Which vitamin deficiency is associated with Neural tube defects?

Answer- Neural tube defects are observed are due to maternal folic acid deficiency. Neural Tube Defects (NTDs) are birth defects of the brain and the spinal cord (malformations of the brain and spinal cord, causing anencephaly, spina bifida or encephalocele).It has been demonstrated that periconceptional (before and during the first 28 days after conception) supplementation of women with folic acid can decrease the risk of neural tube defects. Therefore, a daily intake of 400 µg folic acid in addition to a healthy diet 8 weeks prior to and during the first 12 weeks after conception is recommended. There is evidence that adequate folate status may also prevent the incidence of other birth defects, including cleft lip and palate, certain heart defects and limb malformations. To reduce the risk of neural tube defects, cereal grains are fortified with folate in some countries.

Q.6- Which vitamin deficiency is associated with egg white injury?

Answer- Raw egg whites contain Avidin, a glycoprotein that strongly binds to biotin and prevents its absorption. Thus, the ingestion of large quantities of raw egg white over a long period can result in a biotin deficiency.

Q.7- Name the coenzyme for the reaction for the conversion of Pyruvate to alanine.

Answer- Pyruvate to Alanine conversion is catalyzed by Transaminase (SGPT- Alanine transferase), that requires vitamin B6-P as a coenzyme.

Q.8- The bone marrow smear of a strict vegetarian female patient, presenting with weakness, fissured tongue and paralysis reveals megaloblastic anemia. Which vitamin deficiency is expected?

Answer- The patient is suffering from megaloblastic anemia. The cause seems to be B12 deficiency. Although it is synthesized exclusively by microorganisms, for practical purposes vitamin B12 is found only in foods of animal origin, there being no plant sources of this vitamin. This means that strict vegetarians (Vegans) are at risk of developing B12 deficiency.

Q.9- A 56 – year-old male on Isoniazid therapy for tuberculosis has developed rashes on the exposed parts of the body. What is the probable cause for these rashes?

Answer- The patient has developed pellagra. Prolonged treatment with the anti-tuberculosis drug, Isoniazid, can cause niacin deficiency. Isoniazid may induce a state of pyridoxine deficiency by combining with pyridoxine and generating inactive isoniazid-pyridoxal hydrazones, thus depleting the supply of pyridoxine. Pyridoxine is needed in the endogenous pathway of niacin synthesis. Thus diminished synthesis of niacin ultimately produces pellagra.

Q.10- Why is it said that babies undergoing phototherapy for physiological jaundice are prone to develop riboflavin deficiency?

Answer- Riboflavin is stable when heated and is not easily destroyed in the ordinary processes of cooking but it is light-sensitive so it is degraded easily by light, that is why infants undergoing phototherapy for jaundice  get prone to this deficiency. Loss of riboflavin is also seen if foods are left out in sunlight or in UV light. Because of this light sensitivity, riboflavin rapidly disappears from milk kept in glass bottles exposed to the sun or bright daylight (85% within 2 hours).

Q.11- A child from a very poor socio economic background has reported with loss of vision.Make a probable diagnosis. What is the underlying cause for blindness?

Answer- As the child is from a family with poor socio economic background, perhaps he is suffering from vitamin A deficiency.The earliest symptom of vitamin A deficiency is impaired dark adaptation, or night blindness. Severe deficiency causes xerophthalmia, ultimately resulting in corneal ulcers, scarring and blindness.

Q.12- What is the possible link between intake of polished rice and sudden cardiac failure?

Answer- The link between intake of polished rice and sudden cardiac failure is thiamine deficiency (wet beriberi).Polished rice or highly refined carbohydrates are poor sources of thiamine.

Thiamine deficiency is most commonly observed in chronic alcoholics or people subsisting on polished rice or high carbohydrate refined diets.

Q.13- Name an FMN dependent enzyme

Answer- L- amino acid oxidase that catalyzes the oxidative decarboxylation of amino acids requires the presence of FMN as a coenzyme.

Q.14- What are folate antagonists? Enlist a few clinically important Folate antagonists.

 Answer- Folate antagonists were originally developed as antileukemic agents, but are now being used and/or investigated in the treatment of a wide range of cancerous and non-cancerous diseases. Sulfanilamide and Trimethoprim are antibiotics, Pyrimethamine is antimalarial while Methotrexate is an anticancer drug.

Q.15- Cancer patients on Methotrexate therapy, develop Glossitis and oral ulcers, what is the possible reason?  

Answer- Methotrexate, an analog of 10-methyl-tetrahydrofolate, inhibits dihydrofolate reductase and has been exploited as an anti-cancer drug.  Methotrexate blocks the cell’s ability to regenerate THF, leading to inhibition of these biosynthetic pathways. The lack of nucleotides prevents DNA synthesis, and these cancer cells cannot divide without DNA synthesis.

Unfortunately, the effects of Methotrexate are nonspecific and other rapidly dividing cells such as epithelial cells in the oral cavity, intestine, skin, and blood cells are also inhibited. This leads to the side effects associated with methotrexate (and other cancer chemotherapy drugs) such as mouth sores, low white blood cell counts, stomach upset, hair loss, skin rashes, and itching.


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Q.1- Name the vitamin that acts as a coenzyme for the post translational modifications of prothrombin.

Answer- The post translational modifications of prothrombin are carried out by gamma carboxylation of its glutamic acid residues. The reaction is catalyzed by carboxylase enzyme  which requires vitamin K as a coenzyme. CO 2 and O2 are also required for this carboxylation process.The ability to bind calcium ions (Ca2+) is required for the activation of the seven vitamin K-dependent clotting factors, or proteins, in the coagulation cascade. Vitamin K-dependent gamma-carboxylation of specific glutamic acid residues in those proteins makes it possible for them to bind calcium.

Q.2- Treatment of pregnant women with warfarin can lead to fetal bone abnormalities (fetal warfarin syndrome), what is the cause for this disorder?

Answer-  Warfarin is a vitamin K antagonist; its mechanism of action involves inhibition of vitamin K cycle producing vitamin K deficiency.The fetus gets the supply of vitamin K from maternal circulation as there are no other sources, so the maternal vitamin K deficiency results in fetal deficiency. There is gross impairment of gamma carboxylation of fetal vitamin K dependent proteins. Under carboxylation adversely affects the capacity to bind the bone mineral that is the reason for the malformed bones.

Q.3- Vitamin B6 deficiency leads to niacin deficiency also, suggest the reason for it.

Answer- vitamin B6 is required as a coenzyme for the enzyme kynureninase, which is an enzyme of the pathway of biosynthesis of niacin from tryptophan. In B6 deficiency, niacin is inappropriately synthesized,B6 being unavailable at the Kynureninase step, hence niacin deficiency also sets in and clinical manifestations of deficiencies of both vitamins are observed..

Q.4- Name a water-soluble vitamin that is required for the synthesis of collagen.

Answer- Vitamin C is required for the synthesis of collagen. The enzymes Prolyl and lysyl hydroxylases require vitamin C for their actions to form hydroxy proline and hydroxy lysine from proline and lysine  respectively. These post translational modifications are required for the formation of triple helical structure of collagen. Deficiency of vitamin C leads to impaired hydroxylation reactions with the resultant formation of a weak collagen.

Q.5- What is the cause of hyperkeratinization in vitamin A deficiency?

Answer- Vitamin A (Retinoic acid) regulates the synthesis of keratin by regulating its gene expression. In vitamin A deficiency keratin is excessively synthesized resulting in hyperkeratinization of mucus membranes which can easily crack to allow bacterial invasion with the resultant increased frequency of infections in vitamin A deficiency. Since vitamin A decreases the expression of keratin gene, vitamin A is given therapeutically for the treatment of acne.

Q.6- What is the absorbable form of Thiamine?

Answer- Thiamine occurs in the human body as free thiamine and in various phosphorylated forms: thiamine monophosphate (TMP), thiamine triphosphate (TTP), and thiamine pyrophosphate (TPP), which is also known as thiamine diphosphate. Thiamine pyro phosphate is the active form of Thiamine. It is rapidly converted to its active form, in the brain and liver by a specific enzyme, TPP synthetase. The synthesis of TPP from free thiamine also requires the presence of magnesium and adenosine triphosphate (ATP).

Q.7- Name the active form/forms of Riboflavin.

Answer- Riboflavin (B2) exists in two active forms FMN (flavin mono nucleotide) and FAD (flavin adenine dinucleotide). In the body, riboflavin occurs primarily as an integral component of the enzymes. These coenzymes participate in a large majority of the reactions in the body.

Q.8- Which forms of Cobalamine is required for the methylation of Homocysteine to Methionine ?

Answer- Methyl Cobalamine form is required for the methylation of homocysteine to Methionine.

Q.9- Which vitamin deficiency is associated with lactic acidosis?

Answer-  Lactate, a product of anaerobic glucose metabolism, is generated from pyruvate with lactate dehydrogenase as a catalyst. Pyruvate is normally aerobically metabolized to CO2 and H2O in the mitochondrion. Initially pyruvate is converted to Acetyl co A with pyruvate dehydrogenase complex acting as a catalyst requiring thiamine, niacin, riboflavin, pantothenic acid and lipoic acid as coenzymes. Acetyl co A is completely oxidized in the Krebs cycle.

Normally, pyruvate is in a state of equilibrium with lactate and under condition like thiamine deficiency, when PDH complex becomes less active, the equilibrium is shifted towards production of lactate. Lactate is cleared from blood, primarily by the liver, with the kidneys (10-20%) and skeletal muscles to a lesser degree. Lactic acidosis results from an increase in blood lactate levels when lactate production exceeds consumption and body buffer systems become overburdened.

Q.10- Which vitamin supplementation is given to treat morning sickness of pregnancy?

Answer- B6 is given to treat morning sickness of pregnancy. It is also given to treat radiation sickness, muscular dystrophies and epileptiform convulsions.

Q.11- Total non vegetarian diet can produce scurvy, is it true or false?

Answer-  It is true. Vitamin C is mainly present in citrus fruits and green leafy vegetables. Hence a pure non vegetarian diet can precipitate vitamin C deficiency.

Q.12- Name the enzyme required for the conversion of carotene to Retinal.

Answer- Carotene-β- dioxygenase catalyzes the conversion of beta carotene to form retinal. The conversion is inefficient and also Beta carotene has 1/6th activity as that of retinol. Due to this reason, excess carrots ingestion(carrots are rich in beta carotene) does not lead to vitamin A toxicity.

Q.13- What are the clinical manifestations of B12 deficiency?

Answer- The hallmark of symptomatic vitamin B12 deficiency is megaloblastic anemia. The megaloblastic state also produces changes in mucosal cells, leading to glossitis, as well as other vague gastrointestinal disturbances such as anorexia and diarrhea. Cobalamine deficiency also can present with numerous neurologic manifestations including: numbness, paresthesias, weakness, ataxia, abnormal reflexes and diminished vibratory sensation.

Q.14- For which defect in the body, Schilling test is carried out?

Answer- Scilling test is carried out for the diagnosis of pernicious anemia. The Schilling test can determine if the deficiency is due to absence of intrinsic factor, or some malabsorption disorder. The Schilling test measures Cbl (cobalamine)absorption by increasing urine radioactivity after an oral dose of radioactive Cbl.

Q.15- Which vitamin deficiency is detected by intradermal dye test?

Answer- Vitamin C deficiency is detected by intradermal dye test. Intradermal injections of 2,6-dichlorophenol indophenol are given and the time is noted for the decolorization of the injected area. The dye is expected to be reduced by vitamin C and upon reduction the dye becomes colorless. Abnormally long persistence of blue color in cutaneous wheal indicates sub saturation of vitamin C (vitamin C deficiency).


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Q.1- Which type of Transcobalamine is required for the transportation of vitamin B12?

Answer- Three plasma transport proteins have been identified. Transcobalamine I and III (differing only in carbohydrate structure) are secreted by white blood cells. Although approximately 90% of plasma vitamin B12 circulates bind to these proteins, only Transcobalamine II is capable of transporting vitamin B12 into cells.

Q.2- Name any two inhibitors of conjugase enzyme, that is required for the removal of extra Glutamic acid residues from the dietary folic acid?

Answer- Conjugase (γ-glutamyl carboxypeptidase) in the intestinal lumen cleaves off extra Glutamic acid residues, and folate is absorbed by the mucosa of the small intestine. Alcohol and Anticonvulsant drugs, such as Dilantin, interfere with mucosal conjugase, hence impair folate absorption.

Q.3- Which form of folic acid is required for the de novo synthesis of purine nucleotide?

Answer- Two different forms of folate are required for different aspects of nucleotide biosynthesis. N10-formyl THF provides the C-2 and C-8 carbons for the de novo synthesis of purine rings, and thus is critical for DNA metabolism. The Methylene form, N5,N10-methylene THF, is required for the production of dTMP from dUMP (pyrimidine nucleotide) .

Q.4- Which form of vitamin B12 is present in plasma ?

Answer- Cobalamin (vitamin B12) exists in a number of different chemical forms. All have a cobalt atom at the center of a corrin ring. In nature, the vitamin is mainly in the 2-deoxyadenosyl (ado) form, which is located in mitochondria. It is the cofactor for the enzyme Methylmalonyl CoA mutase. The other major natural cobalamin is methylcobalamin, the form in human plasma and in cell cytoplasm. It is the cofactor for methionine synthase. There are also minor amounts of hydroxocobalamin to which methyl- and Adenosyl cobalamin are rapidly converted by exposure to light.

Q.5- Why is it said that the requirement of riboflavin increases with the increasing protein load ?

Answer-Riboflavin is required for the catabolism especially the  oxidative deamination of amino acids. Thus its requirement increases with the increasing protein load.

Q.6- Why is it said that the maize eaters must supplement with niacin ?

Answer- Maize lacks tryptophan which is a precursor of niacin in the body (60 mg of tryptophan is required for the synthesis of 1 mg of niacin). Maize does contain niacin but it is present in the bound form and is thus not available for biological use. Thus Maize eaters  generally manifest pellagra like rashes due to underlying niacin deficiency.

Q.7-What is the basis of using B6-P as a drug for treating infantile convulsions?

Answer- B6-P is required for the decarboxylation of amino acids. Glutamic acid undergoes decarboxylation under the activity of decarboxylase enzyme in the presence of B6-P to form GABA (gamma amino butyric acid) which is an inhibitory neurotransmitter. Thus there is relief of convulsions which is a state of hyper excitation, by B6P through promoting the synthesis of GABA.

Q.8-Which vitamin is required for the absorption of amino acids from the gut?

 Answer- Vitamin B6 is required for the active absorption of amino acids from the gut.

Q.9- Which vitamin is required as coenzyme for the activity of lactate dehydrogenase enzyme?

Answer- Lactate dehydrogenase catalyzes the interconversion of pyruvate and lactate. Niacin in the form of NAD+ is required as a coenzyme for the activity of lactate dehydrogenase enzyme.

Q.10-Name the enzyme catalyzing the activation of vitamin B6

Answer- Pyridoxal kinase catalyzes the conversion of B6 to B6-P, the metabolically active form of Vitamin B6.

Q.11- Name the synthetic form of vitamin K.

Answer- Three compounds have the biological activity of vitamin K phylloquinone, the normal dietary source, found in green vegetables; menaquinones, synthesized by intestinal bacteria, with differing lengths of side chain; and menadione and menadiol diacetate, synthetic compounds that can be metabolized to phylloquinone.

Q.12- Achlorhydria can precipitate the deficiency of Vitamin B12,  is it true?

Answer- Intrinsic factor (IF) is required for the absorption of vitamin B12 which is secreted by the parietal cells of stomach, In conditions of gastric atrophy due to genetic causes or auto immune destruction, apart from HCl , intrinsic factor is also not synthesized with the resultant impaired absorption of vitamin B12 and pernicious anemia as a consequence.

Q.13- Name the inhibitors of vitamin K that act as anticoagulants.

Answer- Although vitamin K is a fat-soluble vitamin, the body stores very little of it, and its stores are rapidly depleted without regular dietary intake . The oral anticoagulants, such as Dicumarol and warfarin, inhibit coagulation through antagonism of the action of vitamin K.

Q.14-The synthesis of which vitamin is inhibited by Sulphonamides?

Answer- The synthesis of folic acid is inhibited by sulphonamides (sulphanilamides).  Because its shape is similar to that of p-aminobenzoic acid, sulfanilamide inhibits the growth of bacteria by interfering with their ability to use p-aminobenzoic acid to synthesize folic acid. Sulfa drugs were the first antimetabolites to be used in the treatment of infectious disease. Because humans don’t make folic acid, sulfanilamide is not toxic to humans in the doses that inhibit bacteria. This ability to inhibit bacteria while sparing humans made them useful in preventing or treating various infections.

Q.15- Which form of vitamin A -11 cis Retinal or 11-cis Retinol is required for vision?

Answer- Vitamin A, in the strictest sense, refers to retinol. However, the oxidized metabolites, retinaldehyde and retinoic acid, are also biologically active compounds. The term retinoids includes all molecules (including synthetic molecules) that are chemically related to retinol. Retinaldehyde (11-cis) is the essential form of vitamin A that is required for normal vision, whereas retinoic acid is necessary for normal morphogenesis, growth, and cell differentiation.


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 Q.1- Which vitamin deficiency affects the synthesis of carnitine in the muscle?

Answer- Vitamin C is required for the synthesis of carnitine. Carnitine ( β hydroxy-γ-trimethyl ammonium butyrate), (CH3)3N+—CH2—CH(OH)—CH2—COO, is widely distributed and is particularly abundant in muscle. Carnitine facilitates the beta-oxidation of fatty acids, through its role in transporting long chain fatty acids from the cytoplasm into the mitochondrial matrix of cardiac and skeletal muscle. Vitamin C dependent trimethyllysine and -γ butyrobetaine hydroxylases are required for the synthesis of carnitine. Vitamin C acts as a reducing agent in these reactions.

Q.2- Why is it said that Niacin and vitamin D are not true vitamins?

Answer- The distinguishing feature of the vitamins is that they generally cannot be synthesized by mammalian cells and, therefore, must be supplied in the diet.Vitamin D, which is formed in the skin after exposure to sunlight, and niacin, which can be formed from the essential amino acid tryptophan, do not strictly comply with this definition. However, the ability to utilize tryptophan for niacin synthesis is inefficient (60 mg of tryptophan are required to synthesize 1 mg of niacin).

Q.3- What is the cause of bleeding tendencies in obstructive jaundice?

Answer- In obstructive jaundice there is obstruction to the outflow of bile. Bile salts are needed for the absorption of fat soluble vitamins. Vitamin K, a fat soluble vitamin has an active role in coagulation of blood. In conditions of malabsorption or obstructive jaundice, Vitamin K deficiency sets in with the resultant impaired coagulation of blood and bleeding tendencies.

Q.4- Which form of vitamin B2 (Riboflavin) is required for the activity of succinate dehydrogenase enzyme of TCA cycle ?

Answer- Succinate dehydrogenase catalyzes the conversion of succinate to fumarate; FAD form of vitamin B2 is required as a coenzyme for this reaction.

Q.5- Which vitamin is required for the activity of muscle glycogen phosphorylase enzyme?

Answer- B6-P is required for the activity of muscle glycogen phosphorylase enzyme. Approximately 80% of the body’s total vitamin B6 is present in muscle, mostly associated with glycogen phosphorylase. This is not available in deficiency, but is released in starvation, when glycogen reserves become depleted, and is then available, especially in liver and kidney, to meet increased requirement for gluconeogenesis from amino acids.

Q.6-  Which vitamin is required in higher amount with increasing carbohydrate load?

Answer- The requirement of thiamine increases with heavy carbohydrate diet. Because thiamine is required for enzymes involved in glucose metabolism such as Pyruvate dehydrogenase complex, Alpha keto glutarate dehydrogenase complex and transketolase, so its requirement also increases with the increasing carbohydrate load for the proper functioning of these enzymes. The severe thiamine deficiency disease known as Beriberi is the result of a diet that is carbohydrate rich and thiamine deficient. In subjects on a relatively high carbohydrate diet, this results in increased plasma concentrations of lactate and pyruvate which may cause life-threatening lactic acidosis.

Q.7- Which vitamin is required for the synthesis of Sphingol required for the formation of sphingomyelin?

Answer- Vitamin B6-P is required for the formation of Sphingol (an amino alcohol) required for the synthesis of sphingomyelins (Sphingophospholipids).

Q.8- Name a vitamin required for as a coenzyme for the activity of SGOT?

Answer- SGOT- Serum Glutamate Oxalo acetate transaminase is B6-P dependent and catalyzes the reversible transamination reaction involving glutamate and oxaloacetate for the formation of aspartate and alpha ketoglutarate.

Q.9-Name a vitamin required for the activity of dihydrofolate reductase?

Answer- Dihydrofolate reductase as the name indicates is associated with folic acid and catalyzes the conversion of dihydrofolate to Tetrahydrofolate (active form). Methotrexate acts as a competitive inhibitor of this enzyme and is used as an anticancer drug.

Q.10- Name a vitamin, the deficiency of which is detected by Reduced Red cell Glutathione reductase activity.

Answer- The deficiency of vitamin B2 is detected by estimating RBC Glutathione reductase enzyme.

Q.11- What should be the clinical outcome if Riboflavin deficiency is detected?

Answer- Most prominent effects are seen on the skin, mucosa and eyes: Glossitis (magenta tongue, geographical tongue), cheilosis, angular stomatitis (fissures at the corners of the mouth), sore throat, burning of the lips, mouth, and tongue ,inflamed mucous membranes, pruritus (itching) and seborrheic dermatitis (moist scaly skin inflammation) are the symptoms commonly observed in deficient individuals.

Q.12- Name a vitamin/ Vitamins required for the activity of Pyruvate dehydrogenase complex.

Answer- Pyruvate dehydrogenase, a multienzyme complex, catalyzes the oxidative decarboxylation of pyruvate to form Acetyl co A. It requires Thiamine pyrophosphate (TPP), pantothenic acid, lipoic acid, riboflavin and niacin for it’s activity. The deficiency of any of these vitamins can affect the activity of this enzyme complex. Most common out of these is thiamine deficiency.

Q.13- Name the vitamin that is required as a coenzyme for the conversion of Acetyl co A to Malonyl co A?

Answer- The conversion of Acetyl co A to malonyl co A , the first step of fatty acid synthesis, is catalyzed by Acetyl co A carboxylase enzyme, that requires biotin as a cofactor. It is a carboxylation reaction.

Q.14- Which enzyme is inhibited by Dicoumarol and what is the mode of inhibition?

Answer- Dicoumarol acts as an anti coagulant. It is a competitive inhibitor of Epoxide reductase, the enzyme that catalyzes the conversion of epoxide form of vitamin K to quinone form. Quinone form is further reduced to hydroquinone form (functional form) that can be further utilized for gamma carboxylation of glutamic acid residues. In the presence of dicoumarol, the functional form of vitamin K is not regenerated and hence coagulation cascade is not triggered.

Q.15- Which vitamin/vitamins participate in the synthesis of catecholamines?

Answer- Vitamin C and B6 are required for the synthesis of catecholamines. B6 is required for the decarboxylation and vitamin C is required for the hydroxylation reactions.


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1- Name two vitamin B-6 Phosphate dependent enzymes.

Answer- Vitamin B6 serves as a coenzyme of approximately 100 enzymes that catalyze essential chemical reactions in the human body. It plays an important role in protein, carbohydrate and lipid metabolism. Pyridoxal phosphate is a coenzyme for many enzymes involved in amino acid metabolism, especially transamination, deamination and decarboxylation reactions. It is also the cofactor of glycogen phosphorylase.

2- Which out of the two oxidases, L-Amino acid Oxidase or D- amino acid Oxidase, require FMN as a prosthetic group?

Answer- L-amino acid oxidases require FMN while FAD is required by D- Amino acid oxidases.

3- What is the cause for neurological manifestations in B6P deficiency?

Answer- It is required for the synthesis of neurotransmitters like Serotonin, GABA (Gamma amino butyric acid) and also Dopamine, norepinephrine and epinephrine . These are produced by decarboxylation reactions .B6-P is also required for the synthesis of sphingomyelins and other sphingolipids that are required for the formation of myelin sheath. Therefore deficiency of B6-P results in impairment of such reactions and hence neurological deficit.

4- What are the different forms in which the disease Beriberi can be manifested ?

Answer- Beriberi is the outcome of vitamin B1(thiamine) deficiency. It is manifested as dry, wet, infantile, cerebral (Wernicke’s Korsakoff syndrome) or shoshin beriberi.

5- Which vitamin deficiency, B6 or B12 is associated with Homocystinuria?

Answer- Homocystinuria is associated with deficiencies of both B6 and B12. It is also associated with folic acid deficiency. The remethylation of homocysteine back to methionine is B12 and folic acid dependent, (Homocystine is a dimer), while further metabolism of homocysteine is B6 dependent. Thus deficiency of any of these vitamins can cause accumulation of homocysteine in blood and also excessive excretion in urine (dimeric form).

6- Which vitamin is required for the synthesis of bile salts from cholesterol?

Answer- Vitamin C (ascorbic acid) is required for the activity of 7-α hydroxylase, the key regulatory enzyme of bile acid synthesis from cholesterol. Bile salts are produced from bile acids.

7- Name the vitamin required as a coenzyme for the conversion of Pyruvate to Oxaloacetate?

Answer- Biotin is required as a coenzyme, since it is a carboxylation reaction catalyzed by pyruvate carboxylase enzyme. This is the first step of gluconeogenesis.

8- What is the cause of reduced RBC Transketolase activity in Thiamine deficiency?

Answer- Transketolase enzyme is the enzyme of HMP pathway, a pathway of glucose utilization. Thiamine as TPP (active form- Thiamine pyrophosphate form) is required as a coenzyme for the functioning of this enzyme. In thiamine deficiency, the activity of this enzyme goes down and that is estimated in red blood cells to diagnose the underlying deficiency.

9- Why are alcoholics more prone to Thiamine deficiency?

Answer- Reduced dietary intake and  impaired absorption are the important causes of thiamine deficiency in chronic alcoholics.

10- Which vitamin deficiency can be detected by Tryptophan load test?

Answer- Tryptophan load test is undertaken to diagnose underlying B6-P deficiency. Tryptophan is given as a loading dose and the amount of xanthurenic acid excreted in urine is estimated. In B6 deficiency, the amount of xanthurenic acid excreted in urine is increased (Xanthurenic acid is normally produced in a very small amount, but it is produced in excess in B6 deficiency.)

11- Which water soluble vitamin participates in the transfer of one carbon fragments?

Answer- Folic acid is the carrier of one carbon fragments. Tetrahydrofolate can carry one-carbon fragments attached to N-5 (formyl, formimino, or methyl groups), N-10 (formyl) or bridging N-5–N-10 (methylene or methenyl groups).

12-Which vitamin participates in decarboxylation reactions of amino acids?

Answer- Decarboxylation reactions  of amino acids are catalyzed by decarboxylases that require B6 as a coenzyme. The neurotransmitters serotonin, GABA, Dopamine, norepinephrine and epinephrine are produced by decarboxylation of amino acids.

13- Which vitamin deficiency leads to impaired coagulation of blood?

Answer- Vitamin K is required for coagulation of blood. Vitamin K deficiency is the cause of bleeding tendencies and impaired coagulation of blood.

14- What is the basis of supplementation with Folic acid, B12 and B6 to prevent IHD?

Answer- Folic acid, B12 and B6 participate in the metabolism of homocysteine. Excess of homocysteine has atherogenic effect and increases the tendency for ischemic heart disease in the high risk people or people having family history of IHD. Deficiency of any of these vitamins can cause accumulation of homocysteine in blood, thus as a precaution these vitamins are supplemented to prevent the trigger of atherosclerosis by hyperhomocysteinemia.

15- What are the toxic effects of high dose niacin therapy?

Answer- Prostaglandin-mediated flushing due to binding of the vitamin to a G protein–coupled receptor has been observed at daily doses as low as 50 mg of niacin when taken as a supplement or as therapy for dyslipidemia. It may be more intense after alcohol ingestion, aerobic activity, sun exposure, and consumption of spicy foods.  There is no evidence of toxicity from niacin derived from food sources. Flushing always starts in the face and may be accompanied by skin dryness, itching, paresthesias, and headache. Premedication with aspirin may alleviate these symptoms. Nausea, vomiting, and abdominal pain also occur at similar doses of niacin. Hepatic toxicity is the most serious toxic reaction due to niacin and may present as jaundice.


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1- What is the expected clinical outcome of niacin deficiency ?

Answer- Niacin deficiency in severe form is manifested as Pellagra. Disoriented memory (dementia), diarrhea and dermatitis are the signs of pellagra. In untreated cases it leads to death (4 Ds)

2- Why should milk be preferably stored in dark bottles?

Answer- Riboflavin (B1) present in milk is photosensitive, it is destroyed upon exposure to light. Hence to avoid, milk should be stored in dark bottles.

3- Why are premature infants given vitamin K injections immediately after birth?

Answer- Newborn infants, in general, have low vitamin K status for the following reasons:

a) Vitamin K is not easily transported across the placental barrier;

b) The newborn’s intestines are not yet colonized with bacteria that synthesize menaquinones; and

c) The vitamin K cycle may not be fully functional in newborns, especially premature infants.

4- The patients suffering from Carcinoid syndrome generally manifest pellagra like rashes, what could be the reason for this?

Answer- In carcinoid syndrome, tryptophan metabolism is diverted towards serotonin production and less is available for the synthesis of niacin. Niacin deficiency is thus manifested as dementia, dermatitis and diarrhea (pellagra).

5- Which vitamin deficiency is associated with Methyl malonic aciduria?

Answer- Vitamin B12 deficiency is required as a coenzyme for the activity of methyl malonyl co A mutase enzyme that catalyzes the conversion of L-Methyl malonyl co A to Succinyl co A. In vitamin B12 deficiency this conversion is impaired with the resultant excessive accumulation of methyl malonic acid in serum as well as excretion in urine.

6- Which Carboxylation reaction does not require Biotin for its activity?

Answer- Generally biotin is required as a coenzyme for the carboxylation reactions , but gamma carboxylation of specific glutamic acid residues in certain proteins is vitamin K dependent, as in factor II, VII, IX and X of coagulation cascade and osteocalcein (calcium binding proteins).

7- Name two TPP dependent enzymes.

Answer- TPP (Thiamine pyro phosphate), the active form of thiamine is required as a coenzyme for enzymes such as Pyruvate dehydrogenase, Alpha-ketoglutarate dehydrogenase, and branched chain keto acids (BCKA) dehydrogenase complexes and Transketolase.

8- Which vitamin deficiency is associated with Sideroblastic anemia?

Answer- Vitamin B6 deficiency is associated with sideroblastic anemia as it is required as a coenzyme in the pathway of heme biosynthesis (for ALA synthase enzyme).Deficiency leads to impaired heme synthesis and thus reduced Hb synthesis. Deranged heme synthesis in the developing red cell leads to decreased hemoglobin production with the formation of hypochromic and microcytic red cells and other misshaped erythrocytes. These red cells are the progeny of the ring sideroblasts that constitute the diagnostic hallmark of any sideroblastic anemia. 

9 – Which vitamin is known to participate in Carnitine synthesis?

Answer- Vitamin C is required for the synthesis of carnitine. Carnitine is required for the transportation of fatty acid across the inner mitochondrial membrane in to the mitochondrial matrix where the oxidation of fatty acids takes place.

10 – Name the antioxidant vitamins.

Answer-An antioxidant is a substance that significantly decreases the harmful effects of “reactive species”, such as reactive oxygen and nitrogen molecules that disrupt normal physiological function on a cellular level in humans. Examples include the antioxidant vitamin C, vitamin E, and the carotenoids (vitamin A). Selenium is also an antioxidant.  A multitude of other nutrients, including minerals such as copper, manganese, and zinc, flavonoids, and coenzyme Q10, also possess antioxidant properties.

11- What are the clinical findings in a case of Rickets?

Answer- Rickets is caused by a failure of osteoid to calcify in growing children. It occurs due to vitamin D deficiency.  The clinical manifestations include-frontal bossing,bow legs, knock-knees, rachitic rosary along the costochondral junctions, Harrison groove and in more severe instances in children older than 2 years, vertebral softening leading to Kyphoscoliosis. In the long bones, laying down of uncalcified osteoid at the metaphysis leads to spreading of those areas, producing knobby deformity.

12- What are the target organs /tissues for the action of vitamin D ?

Answer- The target organs for vitamin D are bone, intestine and kidney. The basic function of vitamin D is to promote the reabsorption of calcium so as to maintain the serum calcium levels and to promote the mineralization of bones.

13- Which vitamin is known to participate in the oxidative deamination reactions of amino acids?

Answer- Riboflavin is required for the oxidative deamination reactions. FMN form is required for L-amino acid oxidases while FAD is required for D-amino acid oxidases.

14- Which water soluble vitamin is stored in liver ?

Answer- Vitamin B12 is the only water soluble vitamin that is stored in the body (in the liver). The liver contains 2000–5000 mcg of stored vitamin B12. Since daily losses are 3–5 mcg/d, the body usually has sufficient stores of vitamin B12 so that vitamin B12 deficiency develops more than 3 years after vitamin B12 absorption ceases.

15- Why is vitamin D considered a hormone?

Answer- Vitamin D is actually a hormone since its mechanism of action resembles that of hormones. Like hormones it is required only in small amount. Most if not all actions of vitamin D are mediated through a nuclear transcription factor known as the vitamin D receptor (VDR) similar to hormones.


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1- A homeless person has been brought to emergency. Blood biochemistry reveals highf lactate levels. An impaired activity of PDH complex is suspected. Which vitamin deficiency can cause such symptoms ?

Answer- It is a case of thiamine (B1) deficiency. PDH complex catalyzes the conversion of Pyruvate to Acetyl co A . The multienzyme complex requires the presence of thiamine, lipoic acid, pantothenic acid, riboflavin and niacin. A deficiency of thiamine (TPP- active form) which is very common in alcoholics usually presents with lactic acidosis. Due to impaired activity of PDH complex alternatively pyruvate is converted to lactate causing lactic acidosis.

2. A 22-year-old female has presented with seborrheic dermatitis. Blood biochemistry reveals reduced activity of Glutathione reductase enzyme. Which vitamin deficiency is suspected in this patient ?

Answer- It is a case of Riboflavin (B2) deficiency.  Riboflavin is essential for healthy skin, nails, hair growth and general good health. Characteristic symptoms of riboflavin deficiency include lesions of the skin, especially in the corners of the mouth, and a red, sore tongue. Assessment of Riboflavin status can be done by erythrocyte glutathione reductase activity.

3.What would be the clinical outcome if vitamin C is deficient?

Answer- Vitamin C deficiency can occur as part of general under nutrition, but severe deficiency (causing scurvy) is uncommon. Symptoms include fatigue, depression, and connective tissue defects (eg, gingivitis, petechiae, rash, internal bleeding, impaired wound healing). In infants and children, bone growth may be impaired. Severe deficiency results in scurvy, a disorder characterized by hemorrhagic manifestations and abnormal osteoid and dentin formation. Diagnosis is usually clinical. Treatment consists of oral vitamin C

4.- Name a confirmatory test to diagnose underlying Thiamine deficiency.

Answer- R.B.C Transketolase activity and 24-h urinary thiamine excretion may be measured  to diagnose underlying thiamine deficiency.

5 – Which vitamin is known to participate in the Carboxylation reactions?

Answer- Biotin participates in the carboxylation reactions. The enzymes like Pyruvate carboxylase, Acetyl  co A carboxylase and Propionyl co A carboxylase require Biotin as a coenzyme. These carboxylation reactions require CO2 and ATP as a source of energy.

6- What is the active form of vitamin B6?

Answer- Vitamin B6, also called pyridoxine is active in the pyridoxal-phosphate form. There are six forms of vitamin B6: pyridoxal (PL), pyridoxine (PN), pyridoxamine (PM), and their phosphate derivatives: pyridoxal 5′-phosphate (PLP), pyridoxine 5′-phosphate (PNP), and pridoxamine 5′-phospate (PNP). PLP is the active coenzyme form, and has the most importance in human metabolism.

7- Which vitamin deficiency is associated with Burning feet syndrome?

Answer- Mostly deficiency of Pantothenic acid is associated with burning feet syndrome.

8- Name a folate antagonist used as an anticancer drug.

Answer- Methotrexate , a folate antagonist is used as an anticancer drug. Methotrexate, an analog of 10-methyl-tetrahydrofolate, inhibits dihydrofolate reductase and has been exploited as an anti-cancer drug. Methotrexate blocks the cell’s ability to regenerate THF, leading to inhibition of these biosynthetic pathways.The lack of nucleotides prevents DNA synthesis, and these cancer cells cannot divide without DNA synthesis.

9-Which vitamin is known to participate in the hydroxylation reactions?

Answer- Vitamin C, also known as ascorbic acid participates in the hydroxylation reactions. Vitamin C  is the coenzyme for two groups of hydroxylases. These are copper-containing hydroxylases and the α -ketoglutarate-linked iron-containing hydroxylases.

10-Name the vitamins, the deficiencies of which can be manifested as megaloblastic anemia.

Answer- Both folate and cobalamine deficiencies have similar megaloblastic  anemia and GI symptoms. However, cobalamine deficiency also can present with numerous neurologic manifestations including: numbness, paresthesias, weakness, ataxia, abnormal reflexes and diminished vibratory sensation.

11- Which vitamin deficiency would be precipitated by a complete vegetarian diet?

Answer- Since vitamin B12 is present in all foods of animal origin, dietary vitamin B12 deficiency is extremely rare and is seen only in vegans—strict vegetarians who avoid all dairy products as well as meat and fish

12- Which vitamin deficiency would be precipitated by a complete non vegetarian diet?

Answer- Folic acid and vitamin C deficiencies are expected in persons with a complete non vegetarian dietary pattern  as these vitamins are mostly of plant origin.

13- New born infants exposed to blue light for phototherapy generally develop Riboflavin deficiency, suggest the reason for it.

Answer- Riboflavin is sensitive to light and becomes inactive upon exposure that is why deficiency is precipitated.

14- Which vitamin deficiency is known to cause bleeding gums?

Answer- Vitamin C deficiency causes bleeding gums. Gums may become swollen, purple, spongy, and friable; they bleed easily in severe deficiency.

15- Name a vitamin which is used therapeutically as a lipid lowering drug

Answer- Niacin reduces plasma triglyceride and LDLc levels and raises the plasma concentration of HDLc. Niacin is also the only currently available lipid-lowering drug that significantly reduces plasma levels of Lp (a). If properly prescribed and monitored, niacin is a safe and effective lipid-lowering agent.


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