Q. What is the source of thiamine?
A. Aleurone layer of cereals (food grains) is a rich source of thiamine. Whole wheat flour and
unpolished rice and yeast are very good sources.
Q. Thiamine pyrophosphate is required for which reactions ?
A. Transketolase, pyruvate dehydrogenase, and alpha keto glutarate dehydrogenase.
Q. Which Vitamin is required for oxidative decarboxylation?
A. Thiamine pyrophosphate.
Q. In thiamine deficiency, what alterations are seen in blood ?
A. Increased pyruvic acid level and increased transketolase activity.
Q. What are the clinical manifestations of thiamine
deficiency?
A. Beriberi, Wernick’s syndrome, and polyneuritis.
Q. Beberi is due to the deficiency of which Vitamin?
A. Thiamine.
Q. What is the daily requirement of Vitamin B1 (thiamine) ?
A. 1 to 1.5 milligram.
Q. Chronic alcoholism may lead to the deficiency of which Vitamin?
A. Vitamin B1.
Q. Wernicke’s encephalopathy is due to the deficiency of which Vitamin?
A. Vitamin B1.
Q. What is the co-enzyme function of riboflavin ?
A. FMN and FAD dependent enzymes.
Q. What are the FAD dependent enzymes?
A. Succinate dehydrogenase, acyl CoA dehydrogenase,xanthine oxidase, glutathione reductase,
glycine cleavage system, pyruvate dehydrogenase,and alpha ketoglutarate dehydrogenase.
Q. What are the manifestations of riboflavin deficiency?
A. Glossitis, cheilosis, angular stomatits, andcircumcorneal vascularisation.
Q. What is the dietary sources of riboflavin?
A. Rich sources are liver, dried yeast, egg, and milk.
Q. What is the daily requirement of riboflavin?
A. 1.5 mg per day.
Q. Which Vitamin is synthesised in the body?
A. Niacin.
Q. What is the co-enzyme function of niacin?
A. NAD and NADP.
Q. Name some important NAD dependent enzymes.
A. Lactate dehydrogenase, glyceraldehyde-3-phosphate dehydrogenase, pyruvate dehydrogenase,
beta hydroxy acyl CoA dehydrogenase,and mitochondrial isocitrate dehydrogenase.
Q. Name the NADPH generating reactions.
A. Glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malic enzyme, and
cytoplasmic isocitrate dehydrogenase.
Q. What are the important NADPH utilising reactions?
A. Beta keto acyl ACP dehydrogenase, alpha, betaunsaturated ACP dehydrogenase, HMGCoA
reductase, met-hemoglobin reductase, dihydrofolatere ductase, and phenylalanine hydroxylase.
Q. Pellagra is seen in the deficiency of which Vitamin?
A. Niacin.
Q. What are the features of pellagra ?
A. Dermatitis, diarrhea, and dementia.
Q. What is the precursor of niacin?
A. Tryptophan.
Q. Tryptophan will give rise to how much niacin?
A. About 60 mg of tryptophan will yield 1 mg of niacin.
Q. Tryptophan is deficient in which food stuff?
A. Maize and corn.
Q. Which conditions will lead to symptoms of pellagra?
A. Isoniazid therapy, low tryptophan content in diet,niacin deficiency, hartnup disease, and carcinoid
syndrome.
Q. What is the dietary sources of niacin?
A. Natural sources of niacin are dried yeast, rice polishing,liver, peanut, whole cereals, legumes, meat and fish. About half of the requirement is met by the conversion of tryptophan to niacin. About 60 mg of tryptophan will yield 1 mg of niacin.
Q. What is the daily requirement of niacin?
A. The R.D.A is 20 mg/day.
Q. Transamination reaction requires which Vitamin?
A. Pyridoxal phosphate.
Q. Pyridoxal phosphate is required for what reactions?
A. Transamination reactions, decarboxylation of amino acids, ALA synthase, glycogen phosphorylase.
Q. Give an example of transamination reaction.
A. Alanine transaminase (ALT) will catalyse the reaction, alanine to pyruvate.
Q. What is its clinical significance?
A. Blood level of ALT is increased in liver diseases,AST is increased in myocardial infarction.
Q. Give some examples of decarboxylation reactions.
A. Glutamate to GABA (gamma aminobutyric acid),histidine to histamine, 5-hydroxy tryptophan to
serotonin, cysteine to taurine, and serine to ethanol amine.
Q. Xanthurenic acid in urine is seen in the deficiency of which Vitamin?
A. Pyridoxal deficiency.
Q. What are the manifestations of pyridoxal deficiency?
A. Infantile convulsions, peripheral neuritis,pellagra, and anemia.
Q. What is the reason for infantile convulsions in pyridoxal deficiency?
A. Pyridoxal phosphate is required for the formation of GABA, and it is an inhibitory neurotransmitter,
absence of which leads to hyper-excitation
and convulsions.
Q. What is the reason for peripheral neuritis in pyridoxal deficiency?
A. PLP is involved in the synthesis of sphingolipids,so B6 deficiency leads to demyelination of nerves
and consequent peripheral neuritis.
Q. What is the reason for pellagra-like disease in pyridoxal deficiency?
A. Since niacin is produced from tryptophan, one of the enzymes of this pathway is PLP dependent.
So B6 deficiency in turn leads to niacin deficiency which is manifested as pellagra.
Q. Can you give an exmple of one Vitamin deficiency leading to another Vitamin deficiency?
A. PLP deficiency in turn leads to niacin deficiency which is manifested as pellagra.
Q. What is the reason for anemia in pyridoxal deficiency?
A. PLP is required for ALA synthase. In adults hypochromic microcytic anemia may occur due
to the inhibition of heme biosynthesis.
Q. What are the drugs which cause pyridoxal deficiency?
A. Isonicotinic acid hydrazide (INH) (isoniazid),cycloserine, penicillamine and oral contraceptives
act as B6 antagonists. Ethanol in the body is converted to acetaldehyde, which inactivates PLP.
Q. What are the dietary sources of pyridoxal?
A. Rich sources are yeast, rice polishing, wheat germs, cereals, legumes (pulses), egg, milk, meat,
fish and green leafy vegetables.
Q. What is the daily requirement of pyridoxal phosphate?
A. 1 to 2 mg/day.
Q. What is the co-enzyme form of pantothenic acid?
A. Co-enzyme A.
Q. What is the function of CoA?
A. Oxidation of pyruvic acid and activation of acylgroups.
Q. Deficiency of pantothenic acid leads to what?
A. Burning foot syndrome.
Q. What are the donors for acetyl CoA pool?
A. Pyruvate, fatty acid, and amino acids.
Q. Acetyl CoA is used for what purposes?
A. Oxidation in TCA cycle, fatty acid synthesis,cholesterol synthesis, steroid synthesis, and
ketone body formation.
Q. Succinyl CoA is used for what purposes?
A. Oxidation in TCA cycle, heme synthesis, and activation of acetoacetate.
Q. What is the function of biotin?
A. Carboxylation reactions.
Q. Name some reactions dependent on biotin.
A. Acetyl CoA carboxylase, propionyl CoA carboxylase, and pyruvate carboxylase.
Q. What is the antagonist for biotin?
A. Avidin.
Q. What is its use in laboratory?
A. Biotin-avidin reaction is used in immunosorbent assays.
Q. What is the chemical nature of folic acid?
A. Pteroyl glutamic acid (pteridine + PABA + glutamic acid).
Q. What is PABA?
A. Para amino benzoic acid.
Q. What is the co-enzyme form of folic acid?
A. Tetrahydro folic acid.
Q. What is the main function of folic acid?
A. Tetrahydro folic acid is the carrier of one carbon units.
Q. What are the causes of folate deficiency?
A. Pregnancy, defective absorption (sprue, celiac disease), anticonvulsant drugs (hydantoin,
dilantin, phenytoin, phenobarbitone), hemolytic anemias, and dietary deficiency.
Q. What is the major manifestation of folic acid deficiency?
A. Macrocytic anemia.
Q. Folic acid deficiency in pregnancy is associated with what?
A. Folic acid deficiency during pregnancy may lead to neural tube defects in the fetus. Folic acid
prevents birth defects (fetal malformations such as spina bifida).
Q. What are the other minor effects of folic acid?
A. Folic acid is also useful to reduce the level of homo-cysteine in blood, and therefore helps in
preventing heart diseases. Folic acid is beneficial in prevention of cancer.
Q. What are the laboratory findings in folic acid deficiency?
A. (1) Normal folic acid level in serum is decreased.(2) FIGLU is excretion is more, especially after
histidine load. (3) AICAR excretion in urine. (4) Peripheral blood picture shows macrocytic anemia. (5)
Homocysteine level in blood is increased
Q. What are the sources of folic acid?
A. Yeast, liver, egg, green leafy vegetables, cereals,and pulses.
Q. What is the daily requirement of folic acid?
A. The RDA of free folate is 200 mg/day. In pregnancy the requirement is increased to 400 mg/day.
Q. What is the mechanism of action of sulphonamides?
A. They are anti-bacterial agents. They have structural similarity with PABA. Therefore they competitively
inhibit the enzyme responsible for the incorporation of PABA into folic acid.
Q. What is the mechanism of action of trimethoprim?
A. It inhibits the folate reductase and so formation of THFA is reduced. It is bactericidal agent.
Q. What is mechanism of action of methotrexate?
A. It inhibits folate reductase, and is a powerful anticancer drug.
Q. What are inhibitors of folic acid?
A. Methotrexate, trimethoprim, pyrimethamine and sulphonamide.
Q. Name a water soluble Vitamin, which is stored in the body.
A. Vitamin B12.
Q. What is the metal present in Vitamin B12?
A. Cobalt.
Q. What is the ring system present in Vitamin B 12?
A. Corrin ring.
Q. Vitamin B12 is absorbed from where?
A. Ileum.
Q. What is the transport form of Vitamin B12?
A. Methyl B 12.
Q. What is the carrier of Vitamin B12 in blood?
A. Transcobalamin-II, a glycoprotein, is the specific carrier.
Q. What is the storage form of Vitamin B12?
A. It is stored in the liver cells, as ado-B12 form, in combination with transcobalamin-I or transcorrin.
Q. What is the co-enzyme function of Vitamin B 12?
A. Methyl malonyl CoA isomerase, and homocysteine methyl transferase.
Q. What abnormalities are seen in Vitamin B 12 deficiency?
A. Methyl malonic aciduria, accumulation of methylmalonic acid, breakdown of myelin sheaths and
interruption in nerve transmission. Homocysteinuria is also seen.
Q. What abnormal compound is excreted in Vitamin B12 deficiency?
A. Methyl malonic acid in urine.
Q. What is folate trap?
A. The production of methyl THFA is an irreversible step. Therefore, the only way for generation of free
THFA is methyl THFA to THFA, by a Vitamin B12 dependent step. When B12 is deficient, this
reaction cannot take place. This is called the methyl folate trap.
Q. What is the clinical importance of folate trap?
A. This leads to the associated folic acid scarcity in B12 deficiency.
Q. What is the explanation of demyelination in Vitamin B12 deficiency?
A. In Vitamin B12 deficiency, there is non-availability of active methionine. Therefore, methylation
of phosphatidyl ethanolamine to phosphatidylcholine is not adequate. This leads to
deficient formation of myelin sheaths of nerves.
Q. What are the causes of B12 deficiency?
A. Nutritional B12 deficiency, decrease in absorption,addisonian pernicious anemia, atrophy of
gastric epithelium, and pregnancy.
Q. What is the cause for pernicious anemia?
A. It is an autoimmune disease with a strong familial background. Antibodies are generated against
intrinsic factor. So IF is deficient, leading to defective absorption of B12.
Q. What are the manifestations of Vitamin B12 deficiency?
A. Megaloblastic anemia and subacute combined egeneration.
Q. What is the difference in folate deficiency and B12 deficiency?
A. In folate deficiency, there is macrocytic anemia,and in B12 deficiency, there is additional
neurological symptoms also.
Q. What is the daily requirement of Vitamin B12?
A. One to two microgram/per day.
Q. A patient who has undergone gastrectomy is likely to develop deficiency of which Vitamin?
A. Vitamin B12.
Q. In Vitamin B12 deficiency, what are the abnormalities seen in urine?
A. Urine may contain methyl malonic acid, homocystine,cystathione, and formimino glutamic acid.
Q. Which is the Vitamin totally absent in plant sources?
A. Vitamin B12.
Q. What are the sources of Vitamin B12?
A. Liver, meat, fish, and curd.
Q. What is the chemical structure of Vitamin C?
A. L-ascorbic acid.
Q. How it is synthesised?
A. Man and primates cannot synthesise ascorbic acids. Lower animals could synthesise it from
glucose through glucuronic acid pathway.
Q. What are the major functions of ascorbic acid?
A. Ascorbic acid promotes collagen formation through its action on post-translational
hydroxylation of proline and lysine residues.
Q. What are the other functions of ascorbic acid?
A. Parahydroxy phenyl pyruvate oxidation to homogentisic acid, iron absorption from the intestine,
reconversion of methemoglobin to hemoglobin,and adrenal steroidogenesis.
Q. Which Vitamin is required for post-translational modifications?
A. Ascorbic acid.
Q. What is the daily requirement of ascorbic acid?
A. 75 mg per day.
Q. Scurvy is due to the deficiency of which Vitamin?
A. Ascorbic acid.
Q. What are the important features of scurvy?
A. Hemorrhagic tendency, microcytic anemia, bone pain, bleeding gums
------------------------------------------ Best Wishes: Dr.Ehab Aboueladab, Tel:01007834123 Email:ehab10f@gmail.com,ehababoueladab@yahoo.com ------------------------------------------
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