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pharmacy Topic wise MCQs

Hematology MCQ’s ( Megaloblastic Anemias )

Hematology MCQ’s ( Megaloblastic Anemias )

369 Element found at the center of corrin ring in cobalamin is ?
A. Copper
B. Cadmium
C. Cobalt
D. Calcium
Explanation:- All forms of Cobalamin (vit. B12) have a cobalt atom at the center of corrin ring.

370 Which form of cobalamin is present in human plasma & in cell cytoplasm ?
A. Cobalamin
B. Methylcobalamin
C. Hydroxocobalamin
D. Adocobalamin
Explanation:- Cobalamin (vitamin B12) exists in a number of different chemical forms. Methylcobalamin is the form of cobalamin in human plasma & in cell cytoplasm.

371 Methylcobalamin is the cofactor for ?
A. Cystathionine synthase
B. Methionine synthase
C. Serine – glycine hydroxymethylase
D. All of the above
Explanation:- Methylcobalamin is the cofactor for methionine synthase.

372 Which of the following about cobalamin is false ?
A. Copper atom is situated within a corrin ring
B. Cannot be synthesized in human body
C. Only dietary source is animal products
D. Daily requirement is ~ 1 – 3 μg
Explanation:- Cobalamin is a complex organometallic compound in which a “cobalt” atom is situated within a corrin ring. It cannot be synthesized in human body & must be supplied in diet of animal products (meat, fish, and dairy products). Daily requirement for cobalamin is ~ 1 – 3 μg.

373 Body stores of cobalamin can suffice for how many years after supplies are completely cut off ?
A. 1 to 2 years
B. 2 to 3 years
C. 3 to 4 years
D. 5 to 7 years
Explanation:- Body stores of 2 – 3 mg are sufficient for 3 – 4 years if supplies are completely cut off essentially due to enterohepatic cycle & size of liver stores. There is a permanent liver reserve of 1 mg.

374 Deficiency of cobalamin is almost always due to ?
A. Dietary deficiency
B. Malabsorption
C. Alcohol abuse
D. Specific congenital enzyme deficiencies
Explanation:- Dietary intake of cobalamin is more than adequate for body’s requirements, except in complete vegetarians & their breast-fed infants. Deficiency of cobalamin is almost always due to malabsorption.

375 Normal active physiologic mechanism of cobalamin absorption occurs in ?
A. Buccal mucosa
B. Duodenal mucosa
C. Ileal mucosa
D. All of the above
Explanation:- Cobalamin absorption can be passive through buccal, duodenal & ileal mucosa. More efficient normal physiologic active mechanism is through ileum mediated by gastric intrinsic factor (IF).

376 Which of the following is a family of cobalamin-binding proteins ?
A. Glucocorrins
B. Enterocorrins
C. Haptocorrins
D. All of the above
Explanation:- Dietary cobalamin combines rapidly with a salivary glycoprotein that belongs to the family of cobalamin-binding proteins known as haptocorrins (HCs).

377 In intestine, haptocorrin is digested by which of the following enzyme ?
A. Pancreatic trypsin
B. Pancreatic amylase
C. Pancreatic lipase
D. Pancreatic colipase
Explanation:- In intestine, haptocorrin is digested by pancreatic trypsin to release cobalamin which is transferred to IF.

378 IF is produced in ?
A. Gastric parietal cells
B. Gastric chief cells
C. Gastric endocrine cells
D. Gastric enterochromaffin cells
Explanation:- IF is produced in the acid-secreting gastric parietal cells located in oxyntic gland of fundus & body of stomach. Its secretion parallels that of hydrochloric acid.

379 Name of the receptor that mediates intestinal absorption of cobalamin-IF complex is ?
A. Spirulin
B. Humulin
C. Cubulin
D. Cobalin
Explanation:- Cubilin is a specific receptor on microvillus membrane of enterocytes. IF-cobalamin attaches to it and enters the ileal cell, where IF is destroyed..

380 Endocytic receptor protein related to cubulin is ?
A. Amnionless (AMN)
B. Leptin receptor
C. Asialo-GM1
D. Glycophorin A
Explanation:- Cubulin acts through amnionless (AMN), an endocytic receptor protein that directs sublocalization and endocytosis of cubulin with its ligand IF-cobalamin complex.

381 Cubilin also is present in ?
A. Cardiomyocyte
B. Renal proximal tubular epithelium
C. Islet of Langerhans
D. All of the above
Explanation:- Cubilin also is present in yolk sac and renal proximal tubular epithelium.

382 Gastric R binder is found in which of the following secretions ?
A. Saliva
B. Gastric juice
C. Bile
D. All of the above
Explanation:- Cobalamin in food is released and forms a stable complex with gastric R binder that is found in secretions like saliva, milk, gastric juice and bile.

383 Intrinsic factor (IF) catalyzes the conversion ?
A. Methionine to homocysteine
B. Homocysteine to methionine
C. Serine to glycine
D. Glycine to serine
Explanation:- On entering the duodenum, the cobalamin-R binder complex is digested, releasing the cobalamin, which then binds to intrinsic factor (IF), a 50-kDa glycoprotein which catalyzes the conversion of homocysteine to methionine.

384 Most circulating cobalamin is bound to ?
A. Gastric R binder
B. Transcobalamin (TC) I
C. Transcobalamin (TC) II
D. Intrinsic factor (IF)
Explanation:- TC I is derived from specific granules in neutrophils. Normally, it is ~ two-thirds saturated with cobalamin, which it binds tightly. TC I does not enhance cobalamin entry into tissues.

385 Which of the following is not related to “absorption” of cobalamin in humans ?
A. Gastric R binder
B. Intrinsic factor (IF)
C. Transcobalamin (TC) I
D. Transcobalamin (TC) II
Explanation:- Two main cobalamin transport proteins in human plasma are TC I & TC II. TC II carries cobalamin in plasma & gives up cobalamin to marrow, placenta, and other tissues.

386 The common name for pteroylmonoglutamic acid is ?
A. Folic acid
B. Vitamin B12
C. Ascorbic acid
D. Pyridoxine
Explanation:- Folic acid is the common name for pteroylmonoglutamic acid.

387 Which of the following is primary dietary source of folic acid ?
A. Fruits and vegetables
B. Eggs
C. Milk
D. Meat
Explanation:- Fruits and vegetables are the primary dietary source of folic acid. Folate concentrations is highest in liver, yeast, spinach, other greens, and nuts.

388 Which of the following is the major body store of folic acid ?
A. Liver
B. Bone marrow
C. Spleen
D. Kidney
Explanation:- Total-body folate in the adult is ~10 mg, liver containing the largest store.

389 Normally, minimum daily requirement of folic acid is about ?
A. 100 μg
B. 200 μg
C. 300 μg
D. 400 μg
Explanation:- Daily requirement is normally about 100 μg, but this may be increased several fold during periods of enhanced metabolic demand such as pregnancy, infancy, malignancy, increased hematopoiesis (chronic hemolytic anemias), chronic exfoliative skin disorders, hemodialysis.

390 Body stores of folate can suffice for how many months after supplies are completely cut off ?
A. 1 to 2 months
B. 2 to 3 months
C. 3 to 4 months
D. 5 to 7 months
Explanation:- Total-body folate in adult is ~10 mg. Daily adult requirement is ~100 μg, so stores are sufficient for 3 – 4 months, if severe folate deficiency develops rapidly.

391 Site of absorption of Folic acid is ?
A. Stomach
B. Proximal jejunum
C. Terminal Ileum
D. Colon
Explanation:- Folates in food are largely conjugated to a chain of glutamic acid residues which impair its intestinal absorption. Conjugases ( -glutamyl carboxypeptidases) in gut lumen convert polyglutamates to mono- & diglutamates, which are readily absorbed in proximal jejunum.

392 All dietary folates are converted to which of the following before entering portal plasma?
A. N5-methyltetrahydrofolate
B. N10-methyltetrahydrofolate
C. N15-methyltetrahydrofolate
D. N20-methyltetrahydrofolate
Explanation:- Plasma folate is primarily in the form of N5-methyltetrahydrofolate. All dietary folates are converted to 5-methyl THF (5-MTHF) within small-intestinal mucosa before entering portal plasma.

393 N5-methyltetrahydrofolate is a type of ?
A. Monoglutamate
B. Diglutamate
C. Triglutamate
D. Polyglutamate
Explanation:- N5-methyltetrahydrofolate is a monoglutamate.

394 The prime function of folate compounds is ?
A. To transfer single-carbon moieties to organic compounds
B. Factor for methionine synthase & methylmalonyl coenzyme
A (CoA) synthase
C. Conversion of methylmalonyl CoA to succinyl CoA
D. Conversion of succinyl CoA to methylmalonyl CoA
Explanation:- Primary function of folate compounds is to transfer single carbon moieties such as methyl and formyl groups to various organic compounds. The sources of these 1-carbon moieties is usually serine which reacts with tetrahydrofolate to produce glycine and N5,10 methylenetetrahydrofolate.

395 Gamma-glutamyl carboxypeptidases in gut lumen convert ?
A. Polyglutamates to mono & diglutamates
B. Diglutamates to monoglutamates
C. Polysaccharides to mono and disaccharides
D. Disaccharides to monosaccharides
Explanation:- Conjugases (-glutamyl carboxypeptidases) in the gut lumen convert polyglutamates to monoand diglutamates, which are readily absorbed in the proximal jejunum.

396 Folate is essential for the de-novo synthesis of ?
A. Purines
B. Deoxythymidylate monophosphate (dTMP)
C. Methionine
D. All of the above
Explanation:- Folate is essential for the de novo synthesis of purines, deoxythymidylate monophosphate (dTMP), and methionine, serving as an intermediate carrier of 1-carbon fragments used in the biosynthesis of these compounds.

397 Active form of folic acid is ?
A. Dihydrofolate
B. Trihydrofolate
C. Tetrahydrofolate
D. Pentahydrofolate
Explanation:- Active form of folate is tetrahydrofolate (THF).

398 Folate coenzymes are essential in which of the following biochemical reactions ?
A. Purine synthesis
B. Pyrimidine synthesis
C. Serine – glycine interconversion
D. All of the above
Explanation:- Folate coenzymes are essential in Formate activation, Purine synthesis (formation of glycinamide ribonucleotide and formylation of aminoimidazole carboxamide ribonucleotide (AICAR), Pyrimidine synthesis (Methylation of deoxyuridine monophosphate (dUMP) to thymidine monophosphate (dTMP), Amino acid interconversion (serine – glycine interconversion, homocysteine to methionine and forminoglutamic acid to glutamic acid in histidine catabolism).

399 Which of the following drugs inhibit DHF reductase ?
A. Methotrexate
B. Pyrimethamine
C. Trimethoprim
D. All of the above
Explanation:- 5,10-methylene-THF is oxidized to DHF (dihydrofolate). Enzyme DHF reductase converts DHF to THF. Methotrexate, pyrimethamine, and trimethoprim inhibit DHF reductase that prevents formation of active THF coenzymes from DHF.

400 Which of the following about megaloblastic anemias is false ?
A. Caused by impaired DNA synthesis
B. Hematopoietic precursors & GI epithelial cells affected
C. Megaloblastic cells have increased DNA to RNA ratio
D. Ineffective erythropoiesis
Explanation:- Megaloblastic anemias are caused by impaired DNA synthesis in cells with rapid turnover like hematopoietic precursors & gastrointestinal epithelial cells. Cell division becomes sluggish but cytoplasmic development progresses normally, so megaloblastic cells tend to be large, with an increased ratio of RNA to DNA. Megaloblastic erythroid progenitors are destroyed in marrow whose cellularity is increased but production of RBC is decreased (ineffective erythropoiesis).

401 In deficiencies of either folate or cobalamin, there is failure to convert ?
A. dUMP to dTMP
B. dTMP to dUMP
C. dUMP to dUTP
D. dUTP to dUMP
Explanation:- In deficiencies of either folate or cobalamin, there is failure to convert deoxyuridine monophosphate (dUMP) to deoxythymidine monophosphate (dTMP), the precursor of dTTP because folate is needed as the coenzyme 5,10-methylene – THF polyglutamate for conversion of dUMP to dTMP.

402 Which of the following is a cobalamin-requiring reaction ?
A. Purines synthesis
B. Deoxythymidylate monophosphate (dTMP) synthesis
C. Methionine synthesis
D. All of the above
Explanation:- THF acquires 1-carbon fragment from serine which is converted to glycine. For purine synthesis, the 1-carbon fragment is first oxidized to the level of formic acid, then transferred to substrate. For methionine synthesis, a cobalamin-requiring reaction, the 1-carbon fragment is first reduced to the level of a methyl group, then transferred to homocysteine. In these reactions the cofactor is released as THF, which can immediately participate in another 1-carbon transfer cycle. During the production of dTMP from dUMP, the 1-carbon fragment is reduced from formaldehyde to a methyl group during transfer reaction. Hydrogen atoms used for this reduction come from the cofactor, which is released, not as THF, but as dihydrofolate (DHF). To participate further in the 1-carbon transfer cycle, DHF has to be re-reduced to THF, a reaction catalyzed by dihydrofolate reductase.

403 Methylmalonyl CoA isomerization requires which of the following ?
A. Adocobalamin
B. Methylcobalamin
C. 5-MTHF
D. All of the above
Explanation:- Methylmalonyl CoA isomerization requires adocobalamin, and the methylation of homocysteine to methionine requires both methylcobalamin and 5-MTHF.

404 Which of the following abnormalities of folate metabolism occur in cobalamin deficiency ?
A. High serum folate
B. Low cell folate
C. Positive purine precursor aminoimidazole carboxamide ribonucleotide (AICAR) excretion
D. All of the above
Explanation:- Abnormalities of folate metabolism that occur in cobalamin deficiency include high serum folate, low cell folate and positive purine precursor aminoimidazole carboxamide ribonucleotide (AICAR) excretion.

405 Which of the following statements about megaloblastic anemia due to folate deficiency is true ?
A. Raised serum methylmalonic acid, elevated homocysteine
B. Reduced serum methylmalonic acid, reduced homocysteine
C. Normal serum methylmalonic acid, reduced homocysteine
D. Normal serum methylmalonic acid, elevated homocysteine

406 Which of the following statements about megaloblastic anemia due to cobalamin deficiency is true ?
A. Raised serum methylmalonic acid, elevated homocysteine
B. Reduced serum methylmalonic acid, reduced homocysteine
C. Raised serum methylmalonic acid, reduced homocysteine
D. Reduced serum methylmalonic acid, elevated homocysteine

407 Most frequently affected tissues in cobalamin and folate deficiencies is ?
A. Epithelial cell surfaces of the mouth
B. Bone marrow
C. Peripheral nerves
D. Epithelial cell surfaces of the small intestine
Explanation:- Most frequently affected tissue in cobalamin and folate deficiencies is the bone marrow followed by the epithelial cell surfaces of the mouth, stomach, and small intestine and the respiratory, urinary, and female genital tracts.

408 What dose of folic acid provides protective effect against Neural Tube Defects (NTDs) at conception ?
A. 0.1 mg daily
B. 0.2 mg daily
C. 0.3 mg daily
D. 0.4 mg daily
Explanation:- 0.4 mg daily of folic acid provides protective effect against NTDs at conception. Folic acid (400 μg daily, should be given as a supplement before and throughout pregnancy. In women who have had a previous fetus with a neural tube defect, 5 mg daily is recommended when pregnancy is contemplated and throughout the subsequent pregnancy.

409 To prevent neural tube defects, folic acid supplements must be started at ?
A. Conception
B. First 4 weeks of pregnancy
C. First 8 weeks of pregnancy
D. First 12 weeks of pregnancy
Explanation:- To prevent neural tube defects, folic acid supplements must be started at the time of conception and in the first 12 weeks of pregnancy. It reduces the incidence of neural tube defects (NTDs) (anencephaly, meningomyelocele, encephalocele, and spina bifida) in the fetus by 70%.

410 In NTD fetuses, which of the following maternal folate metabolic abnormality has been identified ?
A. Mutations in methionine synthase
B. Mutations in serine – glycine hydroxymethylase
C. Autoantibodies to folate receptors
D. Reduced activity of 5,10-methylene-THF reductase (MTHFR)
Explanation:- In NTD fetuses, reduced activity of the enzyme 5,10-methylene-THF reductase (MTHFR) has been identified as the maternal folate metabolic abnormality.

411 Deficiency of which of the following enzymes can cause homocystinuria ?
A. Methionine synthase
B. MTHFR
C. Cystathionine synthase
D. All of the above
Explanation:- Severe homocystinuria may be due to deficiency of methionine synthase, MTHFR, or cystathionine synthase. Homocystinuria is a rare metabolic defect in the conversion of homocysteine to cystathionine. Folate deficiency is due to excessive utilization because of compensatory increased conversion of homocysteine to methionine.

412 Individuals with which of the following enzyme deficiency have an increased risk of vascular disease ?
A. Methionine synthase
B. MHTFR
C. Cystathionine synthase
D. All of the above
Explanation:- Children with deficiency of enzyme methionine synthase, MHTFR or cystathionine synthase have an increased risk of vascular disease.

413 Meta-analysis has suggested that folic acid supplementation reduces the risk of stroke by ?
A. 4 %
B. 8 %
C. 18 %
D. 25 %
Explanation:- Meta-analysis has suggested that folic acid supplementation reduces the risk of stroke by 18%.

414 Prophylactic folic acid in pregnancy reduces subsequent incidence of which of the following ?
A. Acute lymphoblastic leukemia (ALL)
B. Hodgekin’s lymphoma
C. Astrocytoma
D. Hemangioma
Explanation:- Prophylactic folic acid in pregnancy reduces the subsequent incidence of acute lymphoblastic leukemia (ALL) in childhood.

415 Clinical features of cobalamin deficiency involve which of the following ?
A. Blood
B. Gastrointestinal tract
C. Nervous system
D. All of the above
Explanation:- The clinical features of cobalamin deficiency involve the blood, the gastrointestinal tract, and the nervous system.

416 Hematologic manifestations of cobalamin deficiency are due to ?
A. Anemia
B. Leucopenia
C. Thrombocytopenia
D. All of the above
Explanation:- The hematologic manifestations are almost entirely the result of anemia, although very rarely purpura may appear, due to thrombocytopenia.

417 Which of the following pathological situations can be seen in cobalamin deficiency ?
A. Demyelination
B. Axonal degeneration
C. Neuronal death
D. All of the above
Explanation:- Initial pathology is demyelination, followed by axonal degeneration & eventual neuronal death.

418 Involvement of which of the following structures is uncommon in cobalamin deficiency ?
A. Peripheral nerves
B. Spinal cord
C. Cerebellum
D. Cerebrum
Explanation:- Sites of involvement include peripheral nerves; the spinal cord, where the posterior and lateral columns undergo demyelination; and the cerebrum itself.

419 Earliest neurologic manifestation of cobalamin deficiency is ?
A. Numbness and paresthesia in extremities
B. Motor weakness
C. Ataxia
D. Sphincter disturbances
Explanation:- Signs and symptoms of cobalamin deficiency include numbness and paresthesia in the extremities (the earliest neurologic manifestations), weakness, and ataxia. There may be sphincter disturbances.

420 Neutrophils nucleus of >=6 lobes is suggestive of ?
A. Megaloblastic anemia
B. CML
C. AML
D. Multiple myeloma
Explanation:- Hypersegmented nuclei of neutrophils is a characteristic finding of megaloblastic anemia. A single cell with a nucleus of six lobes or more raises suspicion of a megaloblastic anemia.

421 Which of the following provides evidence of ineffective erythropoiesis ?
A. Reduced haptoglobins
B. Positive urine hemosiderin
C. Raised serum lactate dehydrogenase
D. All of the above
Explanation:- Raised urine urobilinogen, reduced haptoglobins and positive urine hemosiderin, and a raised serum lactate dehydrogenase provides evidence of ineffective erythropoiesis.

422 What value of MCV is diagnostic of megaloblastic anemia ?
A. > 80 fL
B. > 90 fL
C. > 100 fL
D. > 110 fL
Explanation:- Significant and marked macrocytosis (MCV > 100 fL) suggests presence of a megaloblastic anemia. Macrocytosis is less marked with concurrent iron deficiency or thalassemia. Reticulocyte index is low, & leukocyte and platelet count may also be decreased, particularly in severely anemic patients. PBF shows marked anisocytosis & poikilocytosis, with macroovalocytes, which are large, oval, fully hemoglobinized erythrocytes typical of megaloblastic anemias.

423 Causes of macrocytosis include all except ?
A. Hemolysis
B. Aplastic anemia
C. Liver disease
D. Hyperthyroidism
Explanation:- Macrocytosis occurs in hemolysis, liver disease, alcoholism, hypothyroidism & aplastic anemia.

424 Megaloblastoid morphologic picture of RBC series is seen in ?
A. Hemolysis
B. Pernicious anemia
C. Myelodysplasia
D. All of the above
Explanation:- Myelodysplasia produces a distinct morphologic picture most apparent in orthochromatic normoblasts in which a megaloblastic nucleus is associated with severely hypochromic cytoplasm. This variant is called “megaloblastoid” meaning presence of both nuclear & cytoplasmic maturation defects. “Megaloblastoid” does not mean “mildly megaloblastic.”

425 Megaloblastic anemia is seen in all except ?
A. Hereditary TC I deficiency
B. TC II deficiency
C. Orotic aciduria
D. Imerslund-Grasbeck disease

426 Which of the following is not a finding in bone marrow examination in folate or B12 deficiency megaloblastic anemia ?
A. Hypercellularity
B. Increased myeloid / erythroid ratio
C. Nuclear-cytoplasmic asynchrony in RBC precursors
D. Fenestrated nuclear chromatin in RBC precursors
Explanation:- In B12 deficiency megaloblastic anemia, bone marrow is hypercellular with decreased myeloid / erythroid ratio & abundant stainable iron. RBC precursors are abnormally large & have nuclei that appear much less mature than would be expected from the development of cytoplasm (nuclearcytoplasmic asynchrony). Nuclear chromatin is more dispersed & it condenses in a peculiar fenestrated pattern that is very characteristic of megaloblastic erythropoiesis. Abnormal mitoses may be seen. Granulocyte precursors are also affected appearing as giant bands and metamyelocytes. Megakaryocytes are decreased & show abnormal morphology.

427 Incidence of pernicious anemia is increased in ?
A. Graves’ disease
B. Myxedema
C. Thyroiditis
D. All of the above

428 Incidence of pernicious anemia is increased in ?
A. Addison’s disease
B. Vitiligo
C. Hypoparathyroidism
D. All of the above
Explanation:- Incidence of pernicious anemia is increased in patients with other diseases of immunologic origin like Graves’ disease, myxedema, thyroiditis, Addison’s disease, vitiligo & hypoparathyroidism.

429 Which of the following about pernicious anemia is false ?
A. Gastric atrophy does not affect antrum of stomach
B. 90% of patients have antiparietal cell antibody
C. ~80% of patients have anti-IF antibody
D. None of the above
Explanation:- ~90% patients with PA have antiparietal cell antibody directed against H+,K+-ATPase, while IF antibodies are detected in gastric juice in ~80%. In patients with gastric atrophy without pernicious anemia, antiparietal cell antibody is found in 50%, but anti-IF antibody is usually absent. Antiparietal cell antibody is found in 10 – 15% of random patient population.

430 Which of the following about pernicious anemia is false ?
A. Hypergastrinemia
B. Pentagastrin-fast achlorhydria
C. Relatives have increased incidence of disease
D. It is uncommon in patients with agammaglobulinemia
Explanation:- PA is associated with hypogammaglobulinemia, with premature graying or blue eyes, and in persons of blood group A. Gastric output of hydrochloric acid, pepsin, and IF is severely reduced. Serum gastrin level is raised, and serum pepsinogen I levels are low.

431 Which of the following is false about pernicious anemia ?
A. Rare under the age of 30 years
B. Average age of presentation is 60 years
C. Men more affected than women
D. Caused by the absence of IF
Explanation:- Pernicious anemia is the most common cause of cobalamin deficiency. It is caused by absence of IF, due to atrophy of gastric mucosa or autoimmune destruction of parietal cells. Ratio of incidence of PA in men and women among whites is 1:1.6. Average age of presentation is 60 (disease of elderly) & is rare < 30 years of age.

432 Which of the following about pernicious anemia is false ?
A. Unusually common in agammaglobulinemia
B. Helicobacter pylori infection is infrequent
C. Gastric atrophy spares the antrum
D. None of the above
Explanation:- Pernicious anemia is unusually common in patients with agammaglobulinemia. Helicobacter pylori does not cause parietal cell destruction in pernicious anemia. Most characteristic finding in pernicious anemia is gastric atrophy affecting the acid- and pepsin-secreting portion of the stomach while sparing the antrum.

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433 Which of the following about pernicious anemia is false ?
A. Gastric epithelium atypia common
B. Hypergastrinemia common
C. Gastric polyps common
D. None of the above
Explanation:- Abnormalities in gastric epithelium appear as cellular atypia that must be distinguished from cytologic abnormalities of gastric malignancy. Hypergastrinemia & pentagastrin-fast achlorhydria occur secondary to gastric atrophy. Incidence of gastric polyps & stomach cancer is increased.

434 Which of the following about juvenile pernicious anemia is false ?
A. Gastric atrophy
B. Achlorhydria
C. Serum IF antibodies present
D. Parietal cell antibodies present
Explanation:- In Juvenile PA, gastric atrophy, achlorhydria and serum IF antibodies are present, but parietal cell antibodies are usually absent.

435 Removal of what length of terminal ileum causes malabsorption of cobalamin ?
A. 0.2 meter
B. 0.5 meter
C. 0.8 meter
D. 1.2 meter
Explanation:- Removal of 1.2 meters of terminal ileum causes malabsorption of cobalamin.

436 Disease due to mutation in cubulin receptor leading to selective defect in cobalamin absorption is ?
A. Stickler syndrome
B. Imerslund-Gräsbeck Syndrome
C. Cogan’s syndrome
D. Menkes’ syndrome
Explanation:- Imerslund-Gräsbeck syndrome is a congenital disorder (autosomal recessive) of selective defect in cobalamin absorption accompanied by nonspecific proteinuria but renal functions are normal. Mutation occurs in cubulin receptor that mediates intestinal absorption of cobalamin-IF complex. Patients have normal amounts of IF & gastric acid as are other tests of intestinal absorption.

437 Combined deficiencies of cobalamin and folic acid is seen in which of the following conditions ?
A. Gastric achlorhydria
B. Tropical sprue
C. Regional enteritis
D. Pregnancy
Explanation:- Combined deficiencies of cobalamin & folic acid is seen in tropical sprue. Gastric achlorhydria produces cobalamin deficiency by malabsorption due to defective release of cobalamin from food. Regional enteritis produces cobalamin deficiency by malabsorption due to terminal ileum malfunctioning. Pregnancy produces folate deficiency due to increased requirements.

438 Fish tapeworm – D. latum causes megaloblastic anemia due to ?
A. Defective release of cobalamin from food
B. Inadequate production of intrinsic factor (IF)
C. Competition for cobalamin
D. Intestinal stasis
Explanation:- Megaloblastic anemia or cobalamin neuropathy is seen in persons heavily infested by fish tapeworm, Diphyllobothrium latum, due to competition by the worm for cobalamin. Individuals acquire the worm by eating raw or partly cooked fish. Destruction of the worm eliminates the problem.

439 Infestations by fish tapeworm “Diphyllobothrium latum” is common in which of the following countries ?
A. South East Asia
B. Scandinavia
C. South Africa
D. South America
Explanation:- Individuals acquire fish tapeworm, Diphyllobothrium latum by eating raw or partly cooked fish. Infestation is common around the lakes of Scandinavia, Germany, Japan, North America & Russia.

440 Acute megaloblastic anemia can be seen after ?
A. Nitrous oxide anesthesia
B. Halothane anesthesia
C. Chloroform anesthesia
D. Ether anesthesia
Explanation:- Nitrous oxide irreversibly oxidizes methylcobalamin to an inactive precursor which inactivates methionine synthase.

441 Malabsorption of folate is seen with which of the following drugs ?
A. Salazopyrine
B. Cholestyramine
C. Triamterene
D. All of the above
Explanation:- Malabsorption of folate occurs in patients receiving salazopyrine, cholestyramine & triamterene. Antifolate drugs include anticonvulsant drugs (phenytoin, primidone, barbiturates), sulphasalazine, Nitrofurantoin, and tetracycline.

442 Neonatal folate level falls rapidly to the lowest values at ?
A. 6 weeks of age
B. 12 weeks of age
C. 24 weeks of age
D. 32 weeks of age
Explanation:- Neonatal folate level falls rapidly to the lowest values at about 6 weeks of age.

443 Folic acid deficiency is due to ?
A. Inadequate intake
B. Increased demand
C. Malabsorption
D. All of the above

444 Conditions that increase demand of folic acid are all except ?
A. Chronic hemolytic anemias
B. Pregnancy
C. Hemodialysis
D. Tropical sprue
Explanation:- The mechanism of folic acid deficiency in tropical sprue is malabsorption. Rest of the above conditions lead to increased folic acid requirements and cause megaloblastic anemia.

445 Folate deficiency frequently occurs in which of the following ?
A. Sickle cell disease
B. Autoimmune hemolytic anemia
C. Congenital spherocytosis
D. All of the above
Explanation:- Folate deficiency frequently occurs in chronic hemolytic anemia, particularly in sickle cell disease, autoimmune hemolytic anemia, and congenital spherocytosis.

446 Alcohol causes folic acid deficiency by which of the following mechnism ?
A. Inadequate intake
B. Increased requirements
C. Malabsorption
D. Impaired metabolism
Explanation:- Alcohol interferes with folate metabolism. Distilled spirits are devoid of folic acid, while beer and wine do not contain enough of vitamin for daily requirement.

447 Which of the following drugs is an inhibitor of dihydrofolate reductase ?
A. Zidovudine
B. Methotrexate
C. Azathioprine
D. All of the above

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448 Which of the following drugs is an inhibitor of dihydrofolate reductase ?
A. Pentamidine
B. Trimethoprim
C. Pyrimethamine
D. All of the above
Explanation:- Drugs that inhibit DHF reductase include methotrexate, pyrimethamine & trimethoprim. Methotrexate has the most powerful action against the human enzyme, whereas trimethoprim is most active against the bacterial enzyme and is only likely to cause megaloblastic anemia when used in conjunction with sulphamethoxazole in patients with preexisting folate or cobalamin deficiency. The activity of pyrimethamine is intermediate.

449 In megaloblastic anemia due to folate antagonists, which of the following is given ?
A. Folic acid
B. Folinic acid
C. Pyridoxine
D. All of the above
Explanation:- Megaloblastic anemia due to folate antagonists that inhibit dihydrofolate reductase can be counteracted by folinic acid [5-formyl tetrahydrofolate (THF)] in a dose of 100 to 200 mg/day, which circumvents the block in folate metabolism by providing a form of folate that can be converted to 5,10-methylene THF. For the megaloblastic forms of sideroblastic anemia, pyridoxine in pharmacologic doses (~300 mg/day) can be tried. Folinic Acid (5-Formyl-THF) is a stable form of fully reduced folate. It is given orally or parenterally to overcome the toxic effects of methotrexate or other DHF reductase inhibitors.

450 The normal range of cobalamin in serum is ?
A. 5 to 100 ng/L
B. 100 to 200 ng/L
C. 160 to 1000 ng/L
D. 1000 to 2500 ng/L
Explanation:- The normal range of serum cobalamin in serum is 160 – 1000 ng/L. Values between 100 & 200 ng/L are regarded as borderline.

451 Serum homocysteine is raised in all except ?
A. Chronic renal disease
B. Hyperthyroidism
C. Alcoholism
D. Pyridoxine deficiency
Explanation:- Serum homocysteine is raised in early cobalamin & folate deficiency, CKD, alcoholism, smoking, pyridoxine deficiency, hypothyroidism, steroid & cyclosporine therapy. Levels are higher in serum than in plasma, in men than in premenopausal women, in women taking HRT or oral contraceptives. Homocysteine levels are not used for diagnosis of cobalamin or folate deficiency.

452 Levels of which of the following is raised in patients with cobalamin deficiency ?
A. Calcium
B. Iron
C. Serum methylmalonate (MMA)
D. Glycine
Explanation:- In patients with cobalamin deficiency sufficient to cause anemia or neuropathy, serum methylmalonate (MMA) level is raised.

453 Normal serum folic acid levels are ?
A. 6 to 20 ng / mL
B. 30 to 40 ng / mL
C. 60 to 80 ng / mL
D. 80 to 100 ng / mL

454 Normal range of serum folate is ?
A. 2 to 15 μg / L
B. 12 to 25 μg / L
C. 25 to 45 μg / L
D. 42 to 75 μg / L
Explanation:- Normal range of serum folate is 2 to 15 μg/L.

455 In folate deficiency due to drugs inhibiting dihydrofolate reductase, tissue folate concentrations are ?
A. Normal
B. Elevated
C. Reduced
D. Any of the above
Explanation:- Various drugs can inhibit dihydrofolate reductase thereby producing folate deficiency. However, tissue folate concentrations remain normal.

456 What value of folic acid is diagnostic of folate deficiency ?
A. <=1 ng/mL
B. <=2 ng/mL
C. <=3 ng/mL
D. <=4 ng/mL

457 Which is a better index of folate stores ?
A. Serum folate level
B. RBC folate level
C. WBC folate level
D. Platelet folate level
Explanation:- Normal serum folic acid ranges from 6 to 20 ng/mL. Values <=4 ng/mL are considered diagnostic of folate deficiency. Measurement of RBC folate level is not subject to short-term fluctuations in folate intake & is better than serum folate as an index of folate stores.

458 For cobalamin maintenance therapy, 1000 μg of hydroxocobalamin IM is given ?
A. Once a month
B. Once every 2 months
C. Once every 3 months
D. Once every 6 months

459 For cobalamin maintenance therapy, 1000 μg of cyanocobalamin IM is given ?
A. Once a month
B. Once every 2 months
C. Once every 3 months
D. Once every 6 months
Explanation:- Replenishment of body stores of cobalamin is complete with six 1000-μg IM injections of hydroxocobalamin given at 3- to 7-day intervals. For maintenance therapy, 1000 μg hydroxocobalamin IM once every 3 months is satisfactory. Because of the poorer retention, cyanocobalamin is given 1000 μg IM, monthly.

460 Oral dose of folic acid in folate deficiency is ?
A. 5 – 15 mg for ~ 1 month
B. 5 – 15 mg for ~ 4 months
C. 5 – 15 mg for ~ 8 months
D. 5 – 15 mg for ~ 12 months
Explanation:- Oral dose of folic acid in folate deficiency is 5-15 mg daily for ~4 months because all folatedeficient RBC’s will be eliminated in this time.

461 Long-term folic acid therapy is required in which of the following ?
A. Chronic dialysis
B. Hemolytic anemias
C. Gluten-induced enteropathy
D. All of the above
Explanation:- Long-term folic acid therapy is required in chronic dialysis, hemolytic anemias and gluteninduced enteropathy that does not respond to gluten-free diet.

462 Adenosylcobalamin is required for the conversion of ?
A. Methylmalonyl CoA to succinyl CoA
B. Succinyl CoA to Methylmalonyl CoA
C. Propionyl CoA to Methylmalonyl CoA
D. Methylmalonyl CoA to Propionyl CoA
Explanation:- Adenosylcobalamin is required for the conversion of methylmalonyl CoA to succinyl CoA. Lack of this cofactor leads to large increases in the tissue levels of methylmalonyl CoA and its precursor, propionyl CoA. As a consequence, nonphysiologic fatty acids containing an odd number of carbon atoms are synthesized and incorporated into neuronal lipids. This biochemical abnormality may also contribute to the neurologic complications of cobalamin deficiency.

463 Pathway deranged in cobalamin deficiency is ?
A. Methyltetrahydrofolate to tetrahydrofolate
B. N5-methenyltetrahydrofolate to N5-methylenetetrahydrofolate
C. N5-methylenetetrahydrofolate to Dihydrofolate
D. Dihydrofolate to tetrahydrofolate
Explanation:- Due to IF deficiency, cobalamine is deficient thereby impairing conversion of homocysteine to methionine. Cobalamin is essential for the conversion of methyltetrahydrofolate to tetrahydrofolate. Its absence deranges folate metabolism. Defect in DNA synthesis and megaloblastic maturation pattern in patients who are deficient in cobalamin is due to this mechanism (Folate trap hypothesis).

464 Which of the following about cobalamin is false ?
A. Cobalamin is an essential cofactor for methionine synthase & methylmalonyl-CoA synthase
B. Methylcobalamin and adenosylcobalamin are metabolically active forms
C. Therapeutically available as cyanocobalamin
D. Cyanocobalamin is biologically active

465 Cobalamin deficiency without anemia is common in ?
A. Infants
B. Adolescents
C. Adults
D. Elderly

466 Which isoenzyme of plasma lactic acid dehydrogenase is increased in enhanced intramedullary destruction of erythroblasts ?
A. Isoenzyme 1
B. Isoenzyme 2
C. Isoenzyme 3
D. Isoenzyme 4
Explanation:- Enhanced intramedullary destruction of erythroblasts results in an increase in unconjugated bilirubin and lactic acid dehydrogenase (isoenzyme 1) in plasma.

467 Which of the following manifestations occur with cobalamin deficiency but not with folic acid deficiency ?
A. Gastrointestinal
B. Neurologic
C. Hematologic
D. All of the above
Explanation:- Patients with folic acid deficiency are more malnourished than those with cobalamin deficiency. Gastrointestinal, hematologic manifestations are similar. Neurologic abnormalities do not occur with folic acid deficiency.

468 Folic acid supplementation is required in patients on chronic hemodialysis because ?
A. Folate is lost in dialysate
B. Heparin reduces folate levels in blood
C. Protamine reduces folate levels in blood
D. All of the above
Explanation:- Patients on chronic hemodialysis require folate supplementation to replace that lost in dialysate.

469 Normally, what percentage of RBC precursors are destroyed in bone marrow ?
A. 10 – 15 %
B. 25 – 30 %
C. 50 – 60 %
D. 75 – 80 %
Explanation:- Megaloblastic anemias are characterized by ineffective erythropoiesis. In a severely megaloblastic patient, as many as 90% of RBC precursors may be destroyed before they are released into the bloodstream, compared with 10 to 15% in normal individuals.

470 Clinically significant deficiency of cobalamin is present when its levels are ?
A. < 100 pg / mL
B. < 200 pg / mL
C. < 300 pg / mL
D. < 400 pg / mL
Explanation:- Values <200 pg/mL indicate clinically significant cobalamin deficiency.

471 Reticulocytosis after intramuscular cyanocobalamin therapy for megaloblastic anemia due to cobalamin deficiency peaks at about ?
A. Day 3
B. Day 5
C. Day 7
D. Day 10
Explanation:- Reticulocytosis begins 4 to 5 days after intramuscular cyanocobalamin therapy is started & peaks at ~ day 7. If reticulocytosis does not occur, or if it is less brisk than expected from the level of hematocrit, other factors contributing to anemia (infection, coexisting iron and/or folate deficiency, or hypothyroidism) need to be looked.

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