Vitamin Questions

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.

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?

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.

Which vitamin supplementation is given to treat morning sickness of pregnancy?

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

Name the enzyme required for the conversion of carotene to Retinal.

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.

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

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.

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

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.

Total non vegetarian diet can produce scurvy, is it true or false?

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.

Which vitamin deficiency is associated with lactic acidosis?

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.

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

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.

Which forms of Cobalamine is required for the methylation of Homocysteine to Methionine ?

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

Which vitamin deficiency is associated with Neural tube defects?

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.

Name the coenzyme for the reaction for the conversion of Pyruvate to alanine.

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

Which vitamin deficiency is associated with egg white injury?

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.

Name the active form/forms of Riboflavin.

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.

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

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).

For which defect in the body, Schilling test is carried out?

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.

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?

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.

What is the possible link between intake of polished rice and sudden cardiac failure?

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.

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?

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.

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?

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.

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

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.

What is the absorbable form of Thiamine?

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).

Which type of Transcobalamine is required for the transportation of vitamin B12?

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.

What is the cause of hyperkeratinization in vitamin A deficiency?

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.

Which vitamin deficiency is associated with sub acute combined degeneration of spinal cord?

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.

Which vitamin deficiency is detected by intradermal dye test?

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).

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

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.

Which vitamin participates in the absorption of calcium from gut?

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.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?

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.

What are the clinical manifestations of B12 deficiency?

he 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.

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

itamin 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..

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

lves 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.