• Water-soluble vitamins
        • Vitamins serve as cofactors for enzymes.
        • Thiaminepyrophosphate
          • Thiamine pyrophosphate(TPP) is formed from ATP and the vitamin thiamine.
          • TPP isinvolvedintheoxidativedecarboxylationofalpha ketoacids.
          • The alpha-carbon of the alpha-ketoacid becomes covalently attached to TPP, and the carboxyl group is released as CO2.
          • Thiamine pyrophosphate is the cofactor for transketolaseof the pentose-phosphate pathway (MCQ)
        • Lipoicacid
          • Lipoic acid is not derived from a vitamin
          • is involved in oxidative decarboxylationreactions.(MCQ)
          • Lipoicacidparticipatesintheoxidationoftheketogroupofadecarboxylated alpha – ketoacid
          • After an alpha-ketoacid is decarboxylated, the remainder of the compound is oxidized as it is transferred from TPP to lipoic acid, forming a thioester with lipoate. The compound is then transferred to the sulfur of coenzyme A.
          • Lipoate is limiting in the cell
            • so reduced lipoate is reoxidizedfor reuse.
            • It is reoxidized by FAD, which generates FADH2. (MCQ)
            • The FADH2 is reoxidized by NAD+, generating NADH.
        • NADPH (the reduced form of NADP+) (MCQ)
          • provides reducing equivalents for the
          • synthesis of fatty acids
          • reduction of glutathione.
        • Biotin
          • Biotin is involved in the carboxylation of (MCQ)
            • pyruvate(which forms oxaloacetate)
            • acetyl coenzyme A (CoA) (which forms malonyl CoA
            • propionyl CoA(which forms methyl- malonyl CoA)
        • Pyridoxal phosphate
          • Pyridoxal phosphate is derived from vitamin B6 (pyridoxine).(MCQ)
          • Pyridoxal phosphate, an aldehyde, interacts with an amino acid to form aSchiff base.
          • Amino acids are transaminated, decarboxylated, or deaminatedin pyridoxal phosphate–requiring reactions.(MCQ)
        • Tetrahydrofolate
          • Tetrahydrofolate is synthesized from the vitamin folate
          • transfers one-carbon units(MCQ)
            • from compounds such as serine(MCQ)
            • to compounds suchas deoxyuridine monophosphate (dUMP) to form thymidine monophosphate (dTMP)(MCQ)
        • Vitamin B12
          • SourcesofvitaminB12
            • Vitamin B12 is produced by microorganisms but not by plants.
            • Animals obtain vitamin B12 from their intestinal flora, from bacteria in their food supply or by consuming the tissues of other animals.(MCQ)
            • Intrinsic factor
              • produced by gastric parietal cells(MCQ)
              • required for absorption of vitamin B12 by the intestine.(MCQ)
            • Vitamin B12 is stored and efficiently recycled in the body.
        • FunctionsofVitaminB12
          • Vitamin B12 containscobaltin a corrin ring that resembles aporphyrin.
          • Vitamin B12 is the cofactor for methylmalonyl CoA mutase(MCQ)
              • catalyzes the rearrangement of methylmalonyl CoA to succinyl CoA.(MCQ)
              • Amino acids whose degradation pathways lead to succinyl CoA (such as valine, isoleucine, threonine, and methionine) do so by forming methylmalonyl CoA.(MCQ)
              • Propionyl CoAformed by the oxidation of fatty acids with an odd number of carbons(MCQ)
              • propionyl CoA is converted to methylmalonyl CoA by propionyl CoA carboxylase, a biotin requiring enzyme.(MCQ)
          • Vitamin B12 facilitates the transfer of methyl groups from FH4 to homocysteine to form methionine.(MCQ)
      • Vitamin C (ascorbic acid)
        • It is involved in hydroxylation reactions, such as the hydroxylation of prolyl residues in the precursor of collagen.(MCQ)
        • Itfunctionsintheabsorptionofiron(MCQ)
        • Itisanantioxidant(MCQ)



        • Fat-soluble vitamins
          • Vitamin K activates precursors of prothrombin and other clotting factors by carboxylation of glutamate residues.(MCQ)
          • Vitamin A is necessary for
            • Vision
              • 11-cis-Retinal binds to the proteinopsin, forming rhodopsin
              • Light causes conversion of 11-cis-retinal to all-trans-retinal, which dissociates from opsin, causing changes allowing light to be perceived by the brain.(MCQ)
            • for normal growth and reproduction(MCQ)
            • for differentiationand maintenance of epithelial tissues.
            • Retinoicacid,themostoxidizedformofvitaminA,actslikeasteroidhormone.
          • Vitamin E
            • serves as an antioxidant.(MCQ)
            • It prevents free radicals from oxidizing compounds such as polyunsaturated fattyacids.
            • Maintains integrity of membranes by preventing free radical–induced oxidation of the fatty acid residues in phospholipids.


A 57-year-old alcoholic man with chronic pancreatitis is admitted to the hospital for treat- ment. The absorption of which one of the fol- lowing vitamins may be affected with pancreatitis?

(A) Vitamin B12 (cobalamin)

(B) Folic acid

(C) Vitamin B2 (riboflavin)

(D) Vitamin B6 (pyridoxine)

(E) Vitamin D

The answer is E. Although alcoholics are often malnourished with various nutrient deficiencies, pancreatitis will affect the role of the exocrine pancreas in the absorption of fat-soluble vitamins. Vitamin D is the only vitamin listed that is fat soluble; the other vitamins listed are water soluble. With the lack of pancreatic lipase dietary fat cannot be digested, and the fat-soluble vitamins cannot be released from the lipids. The vitamins thus pass through the intestine, nonabsorbed. The other fat-soluble vitamins are vitamins E, K, and A.

6. A 74-year-old living in Retired home is brought into the clinic by a family member. They are concerned because of impaired memory, diarrhea, and a rash on the face, neck, and dorsum of the hands. Which vitamin deficiency do these symptoms represent?

(A) Niacin


(C)Folic acid

(D) Vitamin C

(E) Vitamin E

1. The answer is A. The patient presents with the classic presentation of pellagra, or niacin defi- ciency, with diarrhea, dementia, and dermatitis. Niacin is synthesized from the essential amino acid tryptophan, which is particularly deficient in corn-based diets. However, niacin is still required in the diet because the amount of niacin derived from tryptophan is insufficient for daily needs. A cobalamin deficiency (vitamin B12) will lead to megaloblastic anemia along with methylmalonic acidemia. Folic acid deficiency often manifests with megaloblastic anemia. Vita- min C deficiency results in scurvy. Vitamin E deficiency is rare and can result in neurologic symptoms.

A 32-year-old woman presents to the physi- cian with extreme fatigue and vague neurologic complaints. On examination, it is found that she has decreased positional and vibrational sense, and her complete blood count reveals a mega- loblastic anemia. She relates a history of gastric resection 4 years ago for severe stomach ulcers. Which vitamin deficiency does this represent?

(A)Vitamin C

(B) Vitamin D

(C) Vitamin K

(D) Vitamin B12

(E) Folate

The answer is D. Both folate and vitamin B12 deficiency lead to a megaloblastic anemia second- ary to a reduction in DNA synthesis. Only vitamin B12 deficiency causes neurologic dysfunction associated with damage to the dorsal spinal columns. The history of gastric resection is consist- ent with a deficiency of intrinsic factor required for reabsorption of vitamin B12 in the terminal il- eum. Vitamin C, D, and K deficiencies will not lead to megaloblastic anemia.

@ 9. A 45-year-old alcoholic man walks into the emergency room with a clumsy, wide-based gait and appears confused. He has pronounced nystagmus, and laboratory tests are significant for a metabolic acidosis and a serum blood alcohol level of 0.13. This patient should most probably be treated with IV fluids containing which of the following?

a) Thiamine

b) Riboflavin

c) Niacin

d) Pantothenic acid

e) Biotin

The answer is A. Wernicke encephalopathy, with the classic triad of ataxia, confusion, and oph- thalmoplegia (and nystagmus), is due to thiamine deficiency. Thiamine is an essential coen- zyme in carbohydrate metabolism, including the pentose-phosphate pathway (transketolase) and the TCA cycle (pyruvate dehydrogenase and a-ketoglutarate dehydrogenase). Riboflavin deficiency is possible in malnourished alcoholics, causing cheilosis, glossitis, and corneal changes. Niacin deficiency causes diarrhea, dementia, and dermatitis. Deficiencies of pantothenic acid and biotin are rare, although a biotin deficiency will lead to hypoglycemia and mild ketosis.

A postpartum woman from a rural community recently gave birth to a baby boy with the aid of a midwife at home. She now brings the baby to the hospital because of continued bleeding and oozing from the umbilical stump.

a) Vitamin A

b) Vitamin C

c) Vitamin K

d) Vitamin D

Ans C

A child with bowing of the long bones and growth in the lowest fifth percentile

a) Vitamin A

b) Vitamin C

c) Vitamin K

d) Vitamin D

Ans D

A child with dark, purplish spots on the legs, bleeding gums and gingivitis with tooth loss, epistaxis, and profuse diarrhea

a) Vitamin A

b) Vitamin C

c) Vitamin K

d) Vitamin D

Ans B

A child from a developing country with visual impairment and poor skin healing

a) Vitamin A

b) Vitamin C

c) Vitamin K

d) Vitamin D

Ans A

@ Methylmalonic aciduria is seen in Vitamin B12 deficiency .The fact is best reconciled by which of the following explanations?

a. Vitamin B12 is a precursor for methylmalonic acid synthesis

b. Vitamin B12 is a prosthetic group for the enzyme methylmalonic acid Co A 

c. Vitamin B12 is a cofactor for the MMACoA mutase enzyme

d. Vitamin B12 is a competitive inhibitor of MMACoA mutase enzyme

e. Vitamin B12 is a feedback inhibitor of MMACoA mutase enzyme

The answer is c. Small molecules may be inte- gral parts of enzymes (prosthetic groups) or cofactors that participate in enzyme-substrate interaction or conversion. Prosthetic groups cannot be dis- sociated from the enzyme by dilution and thus will not be obvious compo- nents of the enzyme reaction when reconstitituted in the test tube. Cofactors, like vitamin B12 for methylmalonyl CoA mutase, associate reversibly with enzymes or substrates and can be added in vitro to obtain enhancement of the catalyzed reaction(s). Competitive or feedback inhibitors interact at substrate or allosteric binding sites of the enzyme, reducing effective substrate concen- tration and reaction rate or converting the enzyme to a less active conforma- tion. Vitamin B12 (cyanocobalamin) is a cofactor for MMACoA mutase, accelerating the conversion of methylmalonic acid to succinyl CoA through activity of its cobalt group. Certain defects in MMACoA mutase can be ame- liorated by intramuscular B12 injections so that effective B12 concentration and mutase activity are increased.

@ The biochemical defect in Vitamin C deficiency is which of the following?

(A) Creating lysine cross-links in collagen

(B) Mobilization of calcium into bone

(C) Hydroxylation of proline residues in collagen

(D) Glycosylation of fi brillin

(E) Conversion of glycine to proline in collagen

10 The answer is C:

Hydroxylation of proline residues in collagen. Limes provided vitamin C, which is a required cofactor for prolyl hydroxylase, the enzyme which hydroxylates proline residues in collagen. Lysine crosslinks in collagen do not require vitamin C (although lysine hydroxylation, for the purpose of glycosylation, does). Vitamin C does not affect calcium mobilization (that is vitamin D), and fibrillin is not the problem in vitamin C deficiency. Glycine residues in collagen cannot be converted to proline within the polypeptide.

@ A patient, who was recently diagnosed with cystic fi brosis, displays an increased blood clotting time. This is most likely due to which of the following?

(A) Lack of proline hydroxylation

(B) Inability to catalyze transaminations

(C) Lack of dolichol and an inability to glycosylate serum proteins

(D) Inability to carboxylate glutamic acid side chains

(E) Reduction in the synthesis of blood clotting factors due to lack of lipids for energy production

11 The answer is D:

Inability to carboxylate glutamic acid side chains. Cystic fi brosis patients have a thickening of the pancreatic duct, leading to nutrient malabsorption, as pancreatic enzymes have diffi culty reaching the intestinal lumen. Lipid malabsorption syndromes frequently lead to defi ciencies in fat-soluble vitamin uptake (vitamins E, D, K, and A). Vitamin K is required for the carboxylation of glutamic acid side chains on blood clotting proteins. This provides a means for these proteins to chelate calcium, and to bind to platelet surfaces. In the absence of gamma-carboxylation of glutamate, the clotting complexes cannot form, and a clotting disorder is observed. Vitamin C is required for proline hydroxylation, and as vitamin C is a watersoluble vitamin, lipid malabsorption does not affect vitamin C uptake. Transaminations require vitamin B6, another water-soluble vitamin. Dolichol can be synthesized in the body, so its absorption is not an issue under these conditions. Endogenous fatty acids will provide energy for protein synthesis in individuals with lipid malabsorption problems.

Vitamin K is involved in the post translational modification of?

A. Glutamate

B. Aspartate

C. Proline

D. Lysine

Ans A

Vitamin B12 is absorbed primarily in the

a. Stomach

b. Duodenum

c. Jejunum

d. Ileum

e. Colon

Ans D

Bile salts and Vitamin B12

are absorbed from:

1. Proximal intestine

2. Mid-intestine

3. Distal small intestine

4. Caecum

Ans C

Vitamin B12 and folic acid

supplementation in megaloblastic

anemia leads to the improvement of

anemia due to

1. Increased DNA synthesis in bone


2. Increased Hemoglobin production

3. Erythroid hyperplasia

4. Increased iron absorption

Ans A

The vitamin essential in tissue 
culture medium include all except

(A) Pyridoxine

(B) Thiamine

(C) Nicotinic acid

(D) Inositol

Ans D

vitamins most used in the cell and tissue culture media include: thiamin (B1), nicotinic acid and pyridoxine (B6).

vitamin k helps in activation of all EXCEPT

A)factor VII

B)factor VIII

C)factor IX

D)Protein C

Ans B

Vitamin K is an essential factor to a hepatic gamma-glutamyl carboxylase that adds a carboxyl group to glutamic acid residues on factors II, VII, IX and X, as well as Protein S, Protein C and Protein Z. In adding the gamma-carboxyl group to glutamate residues on the immature clotting factors Vitamin K is itself oxidized. Another enzyme, Vitamin K epoxide reductase, (VKORC) reduces vitamin K back to its active form. Vitamin K epoxide reductase is pharmacologically important as a target of anticoagulant drugs warfarin and related coumarins such as acenocoumarol, phenprocoumon, and dicumarol. These drugs create a deficiency of reduced vitamin K by blocking VKORC, thereby inhibiting maturation of clotting factors. Vitamin K deficiency from other causes (e.g., in malabsorption) or impaired vitamin K metabolism in disease (e.g., in hepatic failure) lead to the formation of PIVKAs (proteins formed in vitamin K absence) which are partially or totally non-gamma carboxylated, affecting the coagulation factors’ ability to bind to phospholipid.

A 40-year-old man with a 20-year history of alcohol abuse is brought to the hospital by his friends because he was difficult to rouse. He ate a large meal several hrs ago. He is emaciated and lethargic. Exam’n shows severely restricted horizontal eye movements and ataxia of both upper extremities. The most likely cause of these findings is a deficiency of which of the following nutrients?

A. Folic acid

B. Vitamin A

C. Vitamin B1 (thiamine)

D. Vitamin B6 (pyridoxine)

E. Vitamin B12 (cobalamin

Ans C

@ A 12-year-old girl, who lives on a farm, started to have shaking and sweating episodes. Upon physical examination, she was found to be hypoglycemic under fasting conditions and positive for ketones in her blood and urine. She has the habit of eating one or two raw eggs every morning. This had been going on for the past 6 weeks or so. A reasonable explanation for her laboratory results is which one of the following?

(A) Reduced levels of electron acceptors in her system, leading to reduced glucose production

(B) Reduced effectiveness of carboxylation reactions, leading to reduced glucose production

(C) Reduced effectiveness of acyl activation, leading to reduced glucose production

(D) Reduced effectiveness of protein hydroxylation, leading to reduced enzymatic activity and reduced glucose production

(E) Reduced levels of electron donors in her system, leading to reduced glucose production

4 The answer is B:

Reduced eff ectiveness of carboxylation reactions, leading to reduced glucose production. Raw eggs contain a potent binding partner to biotin, avidin, which, while bound to biotin, blocks biotin’s participation in carboxylation reactions. This leads to reduced activity of pyruvate carboxylase, a necessary step in many gluconeogenic pathways, thereby leading to a reduced ability of the liver to properly maintain blood glucose levels. As oxaloacetate levels drop due to the need of oxaloacetate for gluconeogenesis, acetyl-CoA derived from fatty acid oxidation increases, leading to ketone body formation. Avidin does not affect NAD+ or FAD levels, nor does it interfere with coenzyme A or vitamin C.

@ A toddler has been diagnosed with a mild case of Leigh syndrome. One possible treatment is which of the following?

(A) Increased carbohydrate diet

(B) Additional B6 in the diet

(C) Decreased lipoamide in the diet

(D) Additional thiamine in the diet

(E) Decreased fat diet

7 The answer is D:

Additional thiamine in the diet. Leigh syndrome can result from a deficiency of pyruvate dehydrogenase (PDH) activity, leading to lactic acidosis. In some cases, the enzyme has a reduced affinity for thiamine pyrophosphate, a required cofactor for the enzyme. Adding thiamine to the diet may overcome this deficiency by raising the concentration of thiamine pyrophosphate such that it will bind to the altered enzyme. Increasing the carbohydrate in the diet will make the disease worse, as more pyruvate would be generated due to the increase in the glycolytic rate. Vitamin B6 does not play a role in glycolysis or the PDH reaction. Lipoamide is a required cofactor for the PDH reaction, so reducing lipoamide would have an adverse effect on the activity of PDH. Decreasing the fat content of the diet may be harmful, particularly if the calories are replaced as carbohydrate.

@ A chronic alcoholic presents to the emergency department with nystagmus, peripheral edema, pulmonary edema, ataxia, and mental confusion. The physician orders a test to determine if there is a vitamin defi ciency. An enzyme used for such a test can be which of the following?

(A) Transaldolase

(B) Aldolase

(C) Transketolase

(D) β-ketothiolase

(E) Acetylcholine synthase

4 The answer is C:

Transketolase. The patient is experiencing the symptoms of vitamin B1 (thiamine) defi ciency. Ethanol blocks thiamine absorption from the gut, so in the United States, one will usually only see a B1 deficiency in chronic alcoholics. One assay for B1 deficiency is to measure transketolase activity (which requires B1 as an essential cofactor) in the presence and absence of added B1. If the activity level increases when B1 is added, a vitamin defi ciency is assumed. None of the other enzymes listed (transaldolase, aldolase, β-ketothiolase, and acetylcholine synthase) require B1 as a cofactor, and, thus, could not be used as a measure of B1 levels. A reaction catalyzed by transketolase is shown below (note the breakage of a

carbon bond, and then the synthesis of a carbon–carbon bond to generate the product of the reaction).


@ Routine newborn screening identifi ed a child with elevated levels of α-ketoacids of the branched-chain amino acids. A certain subset of such children will respond well to which of the following vitamin supplementation?

(A) Niacin

(B) Ribofl avin

(C) B12

(D) B6

(E) Thiamine

7 The answer is E:

Thiamine. The child has maple syrup urine disease, a defect in the branched-chain α-keto acid dehydrogenase step that utilizes all three branchedchain α-keto acids as substrates. The reaction catalyzed by this enzyme is an oxidative decarboxylation reaction, which requires the same fi ve cofactors as do pyruvate and α-ketoglutarate dehydrogenase; thiamine, NAD+, FAD, lipoic acid, and coenzyme A. A subset of patients with this disorder has a mutation in the E1 subunit of the enzyme, which has reduced the affi nity of the enzyme for vitamin B1. Increasing the concentration of B1 can therefore overcome the effects of the mutation and allow the enzyme to exhibit suffi cient activity to reduce the buildup of the toxic metabolites. While niacin and ribofl avin are required for the enzyme, the mutation in the enzyme is such that the affi nity of these cofactors for the enzyme has not been altered. B12 and B6 are not required for this reaction.

Treatment with which of the following vitamins may be successful in controlling homocytinuria?

(A) B1

(B) B2

(C) B3

(D) B6

(E) B12

11 The answer is D:

B6. Cystathionine β-synthase is a B6 requiring enzyme (the reaction is a β-elimination of the serine hydroxyl group, followed by a β-addition of homocysteine to serine; both types of reactions require the participation of B6). In some mutations, the affi nity of the cofactor for the enzyme has been reduced, so signifi cantly increasing the concentration of the cofactor will allow the reaction to proceed. The enzyme does not require the assistance of B1, B2, B3 (niacin), or B12 to catalyze the reaction.


@ Consider a 23-year-old medical student has just initiated a 24 h fast asking Government to change its policies in medical education . Which of the following cofactors are necessary so that his blood glucose levels can be kept constant?

(A) B6, biotin, and niacin

(B) B6, niacin, and vitamin D

(C) B6, biotin, and vitamin D

(D) Biotin, niacin, and B12

(E) Biotin, niacin, and vitamin K

1 The answer is A:

B6, biotin, and niacin. Biotin is required for pyruvate carboxylase (the enzyme that converts pyruvate to oxaloacetate), an enzyme necessary for gluconeogenesis from any TCA cycle precursor (and pyruvate). The B6 is required for glycogen phosphorylase (the ability to produce glucose from glycogen) and for transamination reactions, which are necessary for amino acids (such as alanine, aspartic acid, and glutamic acid) to provide carbons for gluconeogenesis. The niacin is required to produce NADH, which is needed to reverse the glyceraldehyde- 3-phosphate dehydrogenase step during gluconeogenesis. It is also needed for lactate to be converted to pyruvate, and lactate (provided by the red blood cell) is a major gluconeogenic precursor. The lipid-soluble vitamins (D and K) are not required for glucose production and release (vitamin D is needed for calcium metabolism, and vitamin K is required for the carboxylation of glutamic acid side chains of proteins involved in blood clotting). Vitamin B12 is not required for glucose production directly, and its absence does not lead to hypoglycemia.

@ 2     The hypoglycemia is a result of which of the following in vitamin B6 deficiency?

(A) Inhibition of phosphoenolpyruvate carboxykinase

(B) Inhibition of pyruvate carboxylase

(C) Reduced activity of glucose-6-phosphatase

(D) Reduced activity of liver glycogen phosphorylase

(E) Reduced insulin secretion

2 The answer is D:

Reduced activity of liver glycogen phosphorylase. Glycogen phosphorylase requires pyridoxal phosphate (derived from vitamin B6) as an essential cofactor. The role of B6 in the mechanism of the phosphorolysis reaction is still controversial, but it may play a role in general acid-base catalysis. B6 is not required for the PEP carboxykinase reaction, the pyruvate carboxylase reaction (which requires biotin), or the glucose-6-phosphatase reaction. B6 is also not involved in regulating insulin secretion.

@ A patient has been diagnosed with abetalipoproteinemia. A possible defi ciency in which of the following vitamins could occur in this patient?

(A) Vitamin B1

(B) Vitamin B2

(C) Vitamin C

(D) Vitamin E

(E) Niacin

5 The answer is D:

Vitamin E. Abetalipoproteinemia is a disorder in which neither nascent chylomicrons nor nascent VLDL can be produced due to a defect in the microsomal triglyceride transfer protein. Fat-soluble vitamins are delivered to tissues via chylomicrons; in the absence of chylomicron formation, the fat soluble vitamins will remain in the intestinal epithelial cell, or not even be absorbed from the intestinal tract. Vitamin E is believed to be a major antioxidant factor in cells. All of the other vitamins listed (B1, B2, C, and niacin) are water-soluble vitamins, and do not require chylomicron formation for vitamin delivery.

@ 6     A deficiency in which of the following vitamins will lead to a functional folate deficiency?

(A) Thiamine

(B) Niacin

(C) Ribofl avin

(D) B12

(E) Vitamin C

6 The answer is D:

B12. A B12 defi ciency will block the methionine synthase reaction, in which homocysteine reacts with N5-methyltetrahydrofolate (THF) to regenerate methionine and free THF. In the absence of such an activity, the N5-methyl THF accumulates, and as that form is the most stable form, eventually all folate will be “trapped” as the N5-methyl derivative. N5-methyl THF cannot go back to N5, N10-methylene THF; once the N5-methyl form is synthesized, the folate is trapped in that form until the methionine synthase reaction occurs. Thus, folate is still available, but in the wrong form; the levels of N5, N10-methylene THF are too low to allow for thymidine synthesis, and the levels of N10-formyl THF are too low to allow for suffi cient purine synthesis. Thus, a functional folate defi ciency occurs. Defi ciencies in the other vitamins listed (thiamine, niacin, ribofl avin, and C) will not lead to a functional folate defi ciency. The reaction involving folate and vitamin B12 is diagrammed below, along with other reactions involved in homocysteine metabolism.


@ The neurotransmitters GABA, dopamine, and histamine are all derived from an amino acid precursor. The generation of these neurotransmitters from the appropriate amino acids requires which one of the following cofactors?

(A) NAD+

(B) B1

(C) B2

(D) B6

(E) B12

10 The answer is D:

B6. All three neurotransmitters (GABA, dopamine, and histamine) are derived via decarboxylation of an amino acid precursor. Such amino acid decarboxylation reactions require pyridoxal phosphate (derived from B6). GABA is derived from the decarboxylation of glutamate, dopamine from the decarboxylation of dihydroxyphenylalanine, and histamine from the decarboxylation of histidine. NAD, thiamine (B1), riboflavin (B2), or cobalamin (B12) are not required for any of these reactions to occur.


@ An individual has developed pancreatitis, and with it, steatorrhea. The patient also reports problems with his night vision, although visual acuity appears normal. Another expected fi nding in this patient would be which of the following?

(A) Nystagmus

(B) Easy bruising

(C) Dermatitis

(D) Loss of teeth

(E) Orange tonsils

12 The answer is B:

Easy bruising. The patient, due to the pancreatitis, is not able to adequately digest triglycerides in the intestinal lumen, which is what leads to the steatorrhea. Fat-soluble vitamin absorption is dependent upon triglyceride digestion and absorption, so under these conditions, the patient can become defi cient in fat-soluble vitamins (A, D, E, and K). The loss of night vision is an early warning for lack of vitamin A. If the patient is becoming defi cient for vitamin K, bruising would become a problem, due to ineffective clotting with slight internal damage. Nystagmus is a symptom of vitamin B1 deficiency, a water-soluble vitamin. Dermatitis is a symptom of niacin defi ciency (vitamin B3). Loss of teeth can occur with a vitamin C deficiency, and orange tonsils is not due to a vitamin defi ciency, but rather to a lack of ABC-1 activity, and is indicative of Tangier disease.

@ A 9-month-old child of strict vegan parents is brought to the pediatrician due to perceived muscle weakness. Due to their strict dietary beliefs, the child has not been given vitamin supplements. An image of the anterior of the knee reveals cupped and widened metaphyses. As the child is very fair skinned, the parents always cover up the child when they go outside such that minimal skin is exposed to the sun. In order to correct these problems the physician prescribes treatment with which of the following?

(A) Vitamin D

(B) Vitamin K

(C) Folic acid

(D) Vitamin B12

(E) Vitamin E

15 The answer is A:

Vitamin D. The child has rickets, which is due to a lack of vitamin D. Vitamin D is synthesized via a circuitous route (see the fi gure below), and due to the parents’ (and child’s) diet, there is insufficient vitamin D for the child to form healthy bones. UV light is required to form the active form of vitamin D, and the child is also lacking exposure to sunlight. While, due to the diet, the child may become deficient for vitamin B12, lack of B12 does not lead to these symptoms. The symptoms are also not consistent with a lack of vitamin K (which would lead to bleeding problems), folic acid (which would lead to anemia), or E (loss of protection against oxidative radicals). The pathway of active vitamin D formation is shown below



@ Warfarin exerts its effect by blocking which of the following?

(A) Platelet biogenesis

(B) Phospholipid synthesis

(C) Clotting factor synthesis

(D) Vitamin E activity

(E) Formation of γ-carboxyglutamate

16 The answer is E:

formation of g-carboxyglutamate. Warfarin is a vitamin K antagonist, and blocks the regeneration of active vitamin K after it has participated in its reaction of creating a γ-carboxyglutamate residue (see below). In the absence of this side-chain modifi cation, clotting proteins cannot bind to platelets, and the clotting cascade is inhibited. Warfarin does not interfere with platelet synthesis, nor does it alter phospholipid biosynthesis. Warfarin does not alter the transcription or translation of the clotting factors, and has no relationship with vitamin E, which protects against radical damage within cells and tissues. As seen in the fi gure below, warfarin blocks the activity of vitamin K epoxide reductase.


83.       Which coenzyme is required by transketolase enzyme:

A.         Pyridoxal phosphate (PLP)

B.         Thiamine pyrophosphate (TPP)

C.         Coenzyme A

D.         Biotin

ANS:    83.       B.Thiamine pyrophosphate (TPP) is a coenzyme for transketolaseenzyme in hexose monophosphate shunt (HMP Shunt). The following reactions are catalyzed by transketolase


Pyridoxal phosphate (PLP) is a coenzyme for decarboxylation, transamination, deamination, transsulfuration reactions. Biotin is a carrier of Co2 group in carboxylation reactions. Coenzyme A serves as a carrier of activated acyl or acetyl groups.

84.       Which one of the following is a non vitamin coenzyme:

A.         Methylcobalamin

B.         Tetrahydrofolate (THF)

C.         S-Adenosylmethionine

D.         Pyridoxal phosphate

ANS:    84.       C. S-adenosyl methionine (SAM) is a non vitamin coenzyme. Most of the metabolic reactions utilize SAM, transfers the methyl group from tetrahydrofolate. It is synthesized by the transfer of the adenosyl group from ATP to the sulfur of methionine. In methylation reactions by transfer of methyl group, SAM converted to S-adenosylhomocysteine. By the transfer of a methyl group from N5-methyl tetrahydrofolate to homocysteine regenerates the methionine.

101.     Thiazole ring is present in:

A.         Riboflavin

B.         Thiamine

C.         Pyridoxine

D.         Pantothenic acid

ANS:    101.     B. Thiamine (Vitamin Bt) contain a pyrimidine ring and a thiazole ring, linked together by methylene bridge. Thiamine is a water soluble vitamin. In alkaline medium it is oxidized with potassium ferricyanide to thiochrome. Thiamine has fluorescence in ultraviolet light.

102.     Which one of the following reaction requires thiamine pyrophosphate as a coenzyme:

A.         Citrate —> a-ketoglutarate

B.         Succinyl CoA —> Succinate

C.         a-ketoglutarate —> Succinyl CoA

D.         Acetyl CoA —>Citrate

ANS:    102.     C. All the reactions given in the question are in TCA cycle, out of

these citrate —>a-ketoglutarate, sucdnyl CoA -> succinate, acetyl CoA -> citrate does not require thiamine pyrophosphate as a coenzyme. Succinyl CoA and CO2 are produced from a-ketoglutarate by oxidative decarboxylation. It is an analogous reaction to the conversion of pyruvate to acetyl CoA.


103.     All the following cofactors are required by pyruvate dehydrogenase complex EXCEPT:

A.         Thiamine pyrophosphate

B.         FAD

C.         Pyridoxal phosphate

D.         Lipoicacid

ANS:    103.     C. Pyruvate dehydrogenase complex (PDH) is an association of different enzymes which are pyruvate dehydrogenase, dihydrolipoyl trans acetylase, dihydrolipoyl dehydrogenase. PDH requires thiamine pyrophosphate as its cofactor. Dihydrolipoyl transacetylase requires lipoic acid and CoA. Dihydrolipoyl dehydrogenase has an FAD prosthetic group that is reoxidised by NAD+. Pyridoxal phosphate is not a coenzyme for pyruvate dehydrogenase complex.

104.     Wernicke- korsakof f syndrome can be reversed by administration of:

A.         Vitamin B2

B.         Vitamin Bx

C.         Vitamin B6

D.         Vitamin B12

ANS:    104.     B. Wernicke-korsakoff syndrome results from deficiency of thiamine, seen in chronic alcoholics. It is mainly due to insufficient intake of nutritive food leading to thiamine deficiency, characterized by clinical features of encephalopathy and psychosis.

105.     Beri- beri is the deficiency manifestation of:

A.         Thymine

B.         Thiamine

C.         Tryptophan

D.         Serine

ANS:    105.     B. Thiamine deficiency produces beri-beri. It is characterized by cardiovascular symptoms, polyneuritis with muscular atrophy and edema. Thymine is a base in deoxyribonucleic acid. In tryptophan deficiency we observe pellagra type of symptoms. Serine is polar head group of phospholipids, it is treated by supplying food like yeast products, whole grains, nuts which are rich with thiamine.

106.     Which one of the following is required for the conversion of acetyl CoA to malonyl CoA:

A.         Pantothenic acid

B.         Biotin

C.         Pyridoxal phosphate

D.         TPP

ANS:    106.     B. Carboxylation of acetyl CoA to malonyl CoA is the key

enzymatic step in the fatty acid synthesis; this is an ATP dependent reaction and requires biotin for CO2 fixation. The carboxyl group of biotin is covalently bound with the e- amino acid group of a lysine residue of acetyl CoA carboxylase. The reaction occurs in two stages.

            1.         Carboxylation of Biotin enzyme

            Biotin – Enz + ATP + HCO3   ► CO2 – biotin – enzyme + ADP + Pi

            2.         Formation of malonyl CoA from acetyl CoA

            CO2-biotin-enzyme++Acetyl CoA    ► Malonyl CoA + biotion – enzyme

            CO2- is transferred form C02- biotin – enzyme to aoetyl CoA


107.     Which one of the following is required for transfer of acetyl or acyl groups?

A.         Pantothenic acid

B.         Biotin

C.         Pyridoxal phosphate

D.         Lipoicacid

ANS:    107.     A. Coenzyme A is involved in transfer of acetyl or acyl group A strand for acetylation. It is composed of pantothenic acid linked to adenosine diphosphate and cysteine. Acyl groups are linked to CoA by a thioester bond, which forms the acetyl CoA.

108.     Isoalloxazine ring is present in:

A.         FAD

B.         TPP

C.         Coenzyme A

D.         Biotin

 ANS:   108.     A. Flavin mononucleotide, flavin adeninedinucleotide, isoalloxazine ring is the functional unit of both the coenzymes, serves as an acceptor of the two hydrogen atoms and participate in many redox reactions. FMN and FAD on accepting two hydrogen atoms form FMNH2 and FADH2.

109.     All the following enzymes require coenzyme derived from the vitamin shown below EXCEPT:

A.         Glutamate dehydrogenase

B.         HMG CoA reductase

C.         Isocitrate dehydrogenase

D.         Xanthine oxidase


ANS:    109.     D. The structure shown in the question is that of niacin. The active coenzyme forms of niacin are nicotinamide adeninedinucleotide (NAD+) and nicotinamide dinudeotide phosphate (NADP). NAD is a coenzyme required by all dehydrogenases. NADPH is produced by pentose phosphate pathway. Xanthine oxidase does not require niacin as a coenzyme.

110.     Niacin deficiency produces:

A.         Beriberi

B.         Glossitis

C.         Pellagra

D.         Gopalan’s syndrome

ANS:    110.     C. Niacin deficiency produces a disease called pellagra. The symptoms o f pellagra are commonly described as 3Ds; dermatitis, diarrhoea and dementia. Dermatitis found in the areas of the skin exposed to sunlight. Diarrhoea may be with blood and mucus; this may lead to weight loss. Dementia includes irritability, insomnia and anxiety.

111.     Deficiency of tryptophan is seen in:

A.         Pulses

B.         Cereals

C.         Maize and corn

D.         Topioca

ANS:    111.     C.Maize contains zein protein. It is an incomplete protein, lacks amino acid tryptophan. Niacin coenzymes can not be synthesized from tryptophan, this results in a condition called pellagra. Dietary niacin requirement increases in high corn and maize eaters.

112.     Burning feet syndrome is the deficiency manifestation of:

A.         Biotin

B.         Riboflavin

C.         Pantothenic acid

D.         Folk acid

ANS:    112.     C. Burning feet syndrome is the deficiency manifestation of pantothenic acid. It is characterized by numbness and pain in the toes, fatigue and sleeplessness. Deficiency manifestations are very rare in human beings.

113.     All the following vitamins and vitamin like comounds have sulphur in their structure EXCEPT:

A.         Riboflavin

B.         Thiamine

C.         Biotin

D.         Lipoicacid


ANS:113.        A. Thiamine contains pyrimidine ring and thiazole ring held by a methylene bridge. Sulphur is present in thiazole ring. Biotin is a hetero cyclic sulfur containing vitamin with monocarboxylic acid. Imidazole and thiophene rings are present in biotin structure. Lipoic acid is a sulfur containing fatty acid, chemically it is 6,8 di thiooctanoic acid. Riboflavin does not contain any sulphur.

114.     Which one of the following enzyme requires coenzyme derived from the vitamin structure shown above:

A.         HMG CoA reductase

B.         Glutamate Dehydrogenase

C.         Pyruvate dehydrogenase

D.         Alcohol dehydrogenase

ANS:    114.     C. The structure shown in the question is that of riboflavin vitamin. Two coenzyme forms of riboflavin are flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD). Structure of coenzymes contains the sugar alcohol ribitol. Pyruvate dehydrogenase is a multi enzyme complex, contains the enzyme dihydrolipoyl dehydrogenase also contain tightly bound two molecules of FAD per molecule of enzyme, transferring the reducing equivalents to FAD. FADH2 in turn transfers the reducing equivalents to NAD+. In the overall reaction, the reduced FAD is reoxidised by NAD+. HMG CoA reductase, glutamate dehydrogenase, alcohol dehydrogenase all use nicotinamide dinucleotide coenzyme.

40.       Corrin ring is present in:

A.         Folicacid

B.         Biotin

C.         Cyanocobalamin

D.         Niacin

ANS:    40.       C. Corrin ring consists of four pyrrole rings surrounding a single cobalt atom, present in vitamin cyanocobalamin. Cyanide group is bound to cobalt atom is called as cyanocobalamin, if OH group -CH3 and adenosine replace cyanide group in that case, it is called hydroxyl cobalamin, methyl cobalamin and adenosyl cobalamin respectively. Folk acid, biotin and niacin does not contain corrin ring.

41.       Which one of the following statement is a incorrect statement regarding vitamin B12:

A.         Intrinsic factor is required for absorption

B.         Only found in food of animal origin

C.         Deficiency results pellagra

D.         Cofactor for methyl malonyl CoA mutase

ANS:    41.       C. Deficiency of vitamin B12 results in pernicious anemia and neurological symptoms. Pernicious anemia is due to an absence of intrinsic factor. Neurological symptoms are due to inadequate myelin synthesis and nerve degeneration. Intrinsic factor (IF) is released by gastric parietal cells required for absorption of vitamin B12, it is not present in vegetables, that’s why vegetarians are at risk of vitamin B12 deficiency. Methyl malonyl CoA mutase requires deoxy adenosyl cobalamin as a coenzyme to convert D-methyl malonyl CoA to succinyl CoA.

42.       Homocysteine methyl transferase enzyme requires which coenzyme form of vitamin B12:

A.         5′-Deoxy adenosyl cobalamine

B.         Methyl cobalamine

C.         Hydroxy cobalamine

D.         None of the above

ANS:    42.       B.Homocysteine methyl transferase enzyme catalyses the methylation of homocysteine to methionine. It requires methyl cobalamin as the coenzyme. This reaction also reverses the methyltrap, regenerating tetrahydrofolate (THF) from N5 -methyl tetrahydrofolate. 5′-deoxy adenosyl cobalamin is a coenzyme of methyl malonyl CoA mutase, which converts methyl- malonyl CoA into succinyl CoA. Hydroxycobalamin is not an active coenzyme form of vitamin B12 (if the cyanide group in the structure of cyanocobalamin is substituted by hydroxyl group is known as hydroxycobalamin)

43.       In vitamin B12 deficiency which one of the following compound is excreted in urine:

A.         Phenyl pyruvate

B.         Methyl malonic acid

C.         Formimino glutamate

D.         Xanthurenic acid

ANS:    43.       B. Phenylpyruvate is excreted in phenylketonuria. Formimino glutamate is excreted in f olic acid deficiency and xanthurenic acid in pyridoxal deficiency. In vitamin B^ deficiency methyl malonyl CoA accumulates and is excreted in urine as methyl malonic acid.

44.       Which one of the following test is not used to diagnose deficiency state of vitamin:

A.         Schilling test

B.         Histidine loading test

C.         Hollenders test

D.         Dark adaptation test

ANS:    44.       C. Hollander’s test is the confirmatory test for vagotomy. Schilling test, measures the absorption of vitamin B12. Folk add deficiency, is assessed by histidine loading test and dark adaptation test is used to diagnose vitamin A levels.

45.       Folic acid deficiency leads to:

A.         Burning foot syndrome

B.         Beri-Beri

C.         Macrocytic anemia

D.         Pellagra

ANS:    45.       C. In macrocytic anaemia DNA synthesis is impaired due ID decreased production of purines and dTMP because of block in DNA synthesis, slowed down the maturation of erythrocyle leading to macrocytic anemia with megaloblastic bone marrow changes but it does not produce neurological manifestations like vitamin B12.

46.       Deficiency of which vitamin leads to excretion of formimino glutamate (FIGLU) in urine:

A.         Pantothenic acid

B.         Folic acid

C.         Riboflavin

D.         Thiamine

ANS:    46.       B. Formimino glutamate (FIGLU) is formed in histidine metabolism. Formimino group is removed by tetrahydro folk acid to produce N5- formimino THF. In f olic acid deficiency, this can not be carried out; FIGLU accumulates and is excreted in urine. FIGLU excretion in urine is a biochemical index of folk acid deficiency.

47.       Which one of the following vitamin is involved in one carbon metabolism:

A.         Riboflavin

B.         Pantothenic acid

C.         Folic acid

D.         Biotin

ANS:    47.       C. Folk acid consists of pteridine ring, p-aminobenzoic acid and glutamic acid. Coenzyme form of folk acid is tetrahydrofolate(THF). Humans are unable to synthesize pteridine ring, which they are obtain from intestinal flora or from the diet. THF can serve as acceptor or donor of one carbon units, these carbon units include methylene (-CH2), methyl (-CH3), formyl (-CHO) and formimino (-CH=NH). Deficiency of folk acid causes purine macrocytic anemia by retarding purine synthesis and the conversion of deoxy uridine monophosphate (dUMP) to deoxy thymidine monophosphate (dTMP), this leads to inhibition of DNA synthesis.

48.       Which one of the following pyridoxine antagonists used for the treatment of tuberculosis:

A.         Deoxy pyridoxine

B.         Methoxy pyridoxine

C.         Isoniazid

D.         Oxythiamine

ANS:    48.       C. Isoniazid (isonicotinic acid hydrazide), used for the treatment of tuberculosis, it binds with pyridoxal phosphate (PLP) from hydrazone complex, which inhibits PLP dependent enzyme. Long term use of isoniazid in tuberculosis patients develop peripheral neuropathy, which is reversed by pyridoxine administration. Deoxypyridoxine and methoxypyridoxine are the antagonists of pyridoxine but not used in treatment of leprosy. Oxythiamine is an antagonist of thiamine.

49.       Pyridoxal phosphate (PLP) is required as a coenzyme in the following reaction EXCEPT:

A.         Transamination

B.         Dehydrogenation

C.         Decarboxylation

D.         Deamination

ANS:    49.       B. Pyridoxal phosphate (PLP) is the coenzyme form of pyridoxine (vitamin B6). PLP participates in metabolic reactions like transamination, decarboxylation, transulfuration and deamination reactions.

50.       L-gulonolactone oxidase is required for synthesis of:

A.         Riboflavin

B.         Folic acid

C.         Thiamine

D.         Ascorbic acid

ANS:    50.       D. L- gulono lactone oxidase required for synthesis of ascorbic acid (vitamin C) via uronic add pathway by utilizing glucose. Man, primates, guinea pigs can not synthesize ascorbic acid due to deficiency of enzyme L-gulono lactone oxidase.

51.       Pick out the incorrect statement regarding vitamin C:

A.         Coenzyme in hydroxylation reactions

B.         It is a non reducing agent

C.         It is an antioxidant

D.         Deficiency causes anemia

ANS:    51.       B. Vitamin C (ascorbate) is a powerful reducing agent, reduces inactive Fe3+ to active state Fe2+ in the gut and is absorbed. Deficiency of vitamin C leads to anemia. It is a coenzyme in hydroxylation of proline and lysine in collagen synthesis and also for dopamine beta-hydroxylase in epinephrine and nor epinephrine synthesis. It inactivates free radicals which damage lipid membranes, DNA and proteins.

27.       Which vitamin is required to form prothrombin in liver:

A.         Vitamin-C

B.         Vitamin-K

C.         Vitamin-A

D.         Vitamin-D

ANS:    27.       B. Vitamin K is required to form prothrombin (Factor II) from inactive preprothrombin. Prothrombin activity is measured as prothrombin time. Vitamin C, A and D are not required for prothrombin formation. Prothrombin formation is effected in obstructive jaundice due to absence of bile salts, inturn inhibiting absorption of vitamin K. By administration of adequate amounts of vitamin K parenterally returns the prothrombin time to normal in obstructive jaundice.

28.       A patients with alcoholic cirrhosis:

A.         Plasma cholinesterase activity is often increased

B.         Plasma [albumin] not a good index of severity in the later stages of the disease

C.         A prolonged prothrombin time usually fails to revert to normal in response to parenteral vitamin K

D.         Plasma immune globulins are decreased

ANS:    28.       C. Plasma cholinesterase activity is low in case of alcoholics cirrhosis. Plasma [albumin] provides a good index of severity in the later stages of the disease. Plasma immunoglobulin levels are increased especially IgA- increased in cirrhosis, plasma IgG- in chronic active hepatitis. IgM- increased in primary biliary cirrhosis. In alcoholic cirrhosis a prolonged prothrombin time is observed which is not reverts to normal in response to parenteral administration of vitamin K.

29.       Carboxylation of glutamate requires:

A.         O2

B.         CO2

C.         Vitamin K

D.         All of the above

ANS:    29.       D. In the liver, clotting factor II (Prothrombin), VII (Proconvertin stable factor), IX (Christmas factor) and X (Stuart-power factor) synthesized as inactive precursor molecules, for activation requires vitamin K-dependent carboxylation of glutamic acid residues to a-carboxyglutamate (absence of carboxylation, the coagulant proteins fail to bind calcium and clotting is incomplete). This activation reaction requires O2, CO2 and hydroquinone of vitamin K; this reaction is inhibited by dicumarol (natural anticoagulant) and warfarin (synthetic analog of vitamin K).

30.       Which one of the following statement is correct regarding vitamin K:

A.         It is a water soluble vitamin

B.         It plays an important role in thrombosis

C.         Newborns can synthesize vitamin K from intestine

D.         It acts as an antioxidant

ANS:    30.       B. Carboxylation of glutamate residues of prothrombin to a- carboxyglutamate binds with calcium and form prothrombin-calcium complex. This complex is able to bind phospholipids essential for blood clotting on the surface of platelets, favours proteolytic conversion of prothrombin to thrombin.

31.       Serum glutamate oxaloacetate transaminase (aspartate transaminase) requires which of the following coenzyme:

A.         FAD

B.         ATP

C.         NAD

D.         Pyridoxal phosphate

ANS:    31.       D. Aspartate transaminase or glutamate oxaloacetate transaminase catalyses the transamination reaction in which glutamate and oxaloacetate are converted to a-ketoglutarate and aspartate. Thus they can be used for synthesis or degradation of AAs. This reaction is reversible and requires pyridoxal phosphate as a coenzyme.

32.       Which of the following compounds are substrates for alanine transaminase:

A.         Pyruvate and glutamate

B.         Alanine and oxaloacetate

C.         oc-Ketoglutarate and aspartate

D.         Serine and threonine

ANS:    32.       A. Alanine transaminase (glutamate pyruvate transaminase) converts pyruvate and glutamate to alanine and oxaloacetate. It is a reversible transamination reaction and requires pyridoxal phosphate as a coenzyme.










Vitamins And Their Importance
How do vitamins work? – Ginnie Trinh Nguyen
An overview of vitamins: water soluble vitamins and lipid soluble vitamins.
A list of their functions, deficiency, toxicity and pathways.
Understanding Vitamins and Minerals
Do Vitamins Really Improve Health
Vitamin supplements are everywhere, touting that a normal food diet doesn’t provide the entire nutrition we need. Supplementing with vitamins will make us healthier and will prolong our lives. But is this actually true? And could we be doing more harm than good by swallowing all these extracts each day?