Structure and Functions of Nucleotides
Q1. A nucleotide is composed of:
A. Nitrogenous base only
B. Nitrogenous base + sugar
C. Nitrogenous base + phosphate
D. Nitrogenous base + sugar + phosphate
Q2. The sugar present in RNA nucleotides is:
A. Glucose
B. Deoxyribose
C. Ribose
D. Fructose
Q3. Which of the following is a purine base?
A. Cytosine
B. Thymine
C. Guanine
D. Uracil
Q4. Which of the following is not a function of nucleotides?
A. Energy currency (e.g., ATP)
B. Coenzyme components (e.g., NAD⁺)
C. Storage of amino acids
D. Signal transduction (e.g., cAMP)
Q5. The phosphate group in a nucleotide is attached to which carbon of the pentose sugar?
A. 1′
B. 2′
C. 3′
D. 5′
Q6. The difference between nucleoside and nucleotide is the presence of:
A. Sugar
B. Nitrogenous base
C. Phosphate group
D. Peptide bond
Q7. cAMP functions as a:
A. DNA precursor
B. Coenzyme
C. Secondary messenger in hormonal signaling
D. Protein
Q8. Which of the following nucleotides serves as the energy currency of the cell?
A. NAD⁺
B. ATP
C. cAMP
D. GMP
Q9. Which of the following is not a component of DNA nucleotides?
A. Adenine
B. Thymine
C. Ribose
D. Deoxyribose
Q10. In nucleotides, the nitrogenous base is attached to the sugar at which carbon position?
A. 1′
B. 2′
C. 3′
D. 5′
Answer Key
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D. Nitrogenous base + sugar + phosphate
-
C. Ribose
-
C. Guanine
-
C. Storage of amino acids
-
D. 5′
-
C. Phosphate group
-
C. Secondary messenger in hormonal signaling
-
B. ATP
-
C. Ribose
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A. 1′
Purine Salvage Pathway & Lesch-Nyhan Syndrome
Q1. The enzyme deficient in Lesch-Nyhan syndrome is:
A. Adenosine deaminase
B. Xanthine oxidase
C. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
D. Carbamoyl phosphate synthetase II
Q2. The purine salvage pathway helps in:
A. De novo synthesis of purines
B. Recycling of free purine bases to form nucleotides
C. Degradation of purines
D. Synthesis of pyrimidines
Q3. Which of the following enzymes is involved in the purine salvage pathway?
A. Ribonucleotide reductase
B. HGPRT
C. PRPP synthetase
D. Carbamoyl phosphate synthetase I
Q4. A clinical feature of Lesch-Nyhan syndrome is:
A. Hypouricemia
B. Self-mutilation
C. Hypoglycemia
D. Hyperammonemia
Q5. Which compound is overproduced in Lesch-Nyhan syndrome?
A. Uric acid
B. Ammonia
C. Bilirubin
D. Lactate
Q6. PRPP (phosphoribosyl pyrophosphate) is required in:
A. Only pyrimidine synthesis
B. Only purine degradation
C. Both de novo and salvage pathways of purine synthesis
D. Glycogen synthesis
Q7. In the salvage pathway, guanine is converted to GMP by:
A. Xanthine oxidase
B. Adenylosuccinate synthetase
C. HGPRT
D. Adenosine deaminase
Q8. Lesch-Nyhan syndrome is inherited in which pattern?
A. Autosomal dominant
B. Autosomal recessive
C. X-linked recessive
D. Mitochondrial
Q9. A consequence of HGPRT deficiency is:
A. Decreased PRPP levels
B. Increased salvage of purines
C. Decreased uric acid formation
D. Increased de novo purine synthesis
Q10. Which of the following symptoms is specific to Lesch-Nyhan syndrome and not seen in simple hyperuricemia?
A. Gout
B. Renal stones
C. Neurological defects and self-mutilation
D. Joint pain
Answer Key
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C. Hypoxanthine-guanine phosphoribosyltransferase (HGPRT)
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B. Recycling of free purine bases to form nucleotides
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B. HGPRT
-
B. Self-mutilation
-
A. Uric acid
-
C. Both de novo and salvage pathways of purine synthesis
-
C. HGPRT
-
C. X-linked recessive
-
D. Increased de novo purine synthesis
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C. Neurological defects and self-mutilation
Purine De Novo Synthesis
Q1. The purine ring is built upon which molecule during de novo synthesis?
A. ATP
B. PRPP (Phosphoribosyl pyrophosphate)
C. AMP
D. GMP
Q2. The first committed step of purine de novo synthesis is catalyzed by:
A. PRPP synthetase
B. Adenylosuccinate synthetase
C. Glutamine-PRPP amidotransferase
D. HGPRT
Q3. Which of the following is not a donor of atoms in the purine ring?
A. Aspartate
B. Glycine
C. Glutamate
D. Formyl-THF
Q4. The end products of purine de novo synthesis are:
A. UMP and CMP
B. AMP and GMP
C. Hypoxanthine and xanthine
D. IMP and PRPP
Q5. Which of the following vitamins is essential for purine synthesis due to its role in one-carbon transfer?
A. Vitamin B2
B. Vitamin B12
C. Folic acid (Vitamin B9)
D. Vitamin C
Q6. IMP (inosine monophosphate) is a precursor for:
A. Only AMP
B. Only GMP
C. Both AMP and GMP
D. UMP
Q7. The nitrogen at position 9 of the purine ring is contributed by:
A. Glycine
B. Aspartate
C. Glutamine
D. CO₂
Q8. Which enzyme converts IMP to AMP?
A. GMP synthetase
B. Adenylosuccinate synthetase
C. IMP dehydrogenase
D. PRPP amidotransferase
Q9. Feedback inhibition of de novo purine synthesis is primarily exerted by:
A. PRPP
B. ATP
C. AMP and GMP
D. Uric acid
Q10. Purine de novo synthesis mainly occurs in which organ?
A. Kidney
B. Muscle
C. Liver
D. Brain
Answer Key
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B. PRPP
-
C. Glutamine-PRPP amidotransferase
-
C. Glutamate
-
B. AMP and GMP
-
C. Folic acid (Vitamin B9)
-
C. Both AMP and GMP
-
C. Glutamine
-
B. Adenylosuccinate synthetase
-
C. AMP and GMP
-
C. Liver
Gout: Primary, Secondary & Treatment
Q1. Gout is primarily caused by elevated levels of:
A. Urea
B. Creatinine
C. Uric acid
D. Ammonia
Q2. The deposition of monosodium urate crystals in joints leads to:
A. Osteoarthritis
B. Gouty arthritis
C. Rheumatoid arthritis
D. Rickets
Q3. Primary gout is mainly due to:
A. High protein diet
B. Uric acid underexcretion
C. Inherited metabolic enzyme defects
D. Kidney failure
Q4. Secondary gout is usually associated with:
A. Genetic deficiency of HGPRT
B. Overproduction or underexcretion of uric acid due to another disease
C. High purine diet only
D. Idiopathic causes
Q5. Which of the following diseases is commonly associated with secondary gout?
A. Diabetes mellitus
B. Myeloproliferative disorders
C. Hypothyroidism
D. Cirrhosis
Q6. A drug used to treat gout by inhibiting xanthine oxidase is:
A. Colchicine
B. Probenecid
C. Allopurinol
D. Aspirin
Q7. Which of the following drugs increases uric acid excretion (uricosuric)?
A. Allopurinol
B. Probenecid
C. Colchicine
D. Indomethacin
Q8. Colchicine is used in acute gout attacks because it:
A. Inhibits xanthine oxidase
B. Increases uric acid excretion
C. Prevents urate crystal formation
D. Inhibits neutrophil migration and inflammation
Q9. In gout, uric acid is derived from:
A. Amino acid metabolism
B. Carbohydrate metabolism
C. Purine metabolism
D. Fatty acid metabolism
Q10. The first-line drug for chronic management of gout is:
A. Colchicine
B. Indomethacin
C. Probenecid
D. Allopurinol
Answer Key
- C. Uric acid
- B. Gouty arthritis
- C. Inherited metabolic enzyme defects
- B. Overproduction or underexcretion of uric acid due to another disease
- B. Myeloproliferative disorders
- C. Allopurinol
- B. Probenecid
- D. Inhibits neutrophil migration and inflammation
- C. Purine metabolism
- D. Allopurinol
Case Based and Analytical MCQs
Q1.
A 5-month-old male infant presents with self-mutilation, hyperuricemia, and developmental delay. Urine analysis reveals orange sand-like crystals. Enzyme assay shows a near-total deficiency of hypoxanthine-guanine phosphoribosyltransferase (HGPRT).
Which pathway is primarily defective in this condition?
A. De novo purine synthesis
B. Pyrimidine degradation
C. Purine salvage pathway
D. Urea cycle
Q2.
A patient with recurrent infections and partial albinism is diagnosed with a rare immunodeficiency syndrome. Laboratory testing shows accumulation of dATP, leading to inhibition of ribonucleotide reductase.
Which enzyme deficiency is most likely responsible for the findings?
A. Adenosine deaminase
B. Xanthine oxidase
C. HGPRT
D. Carbamoyl phosphate synthetase II
Q3.
An adult male is prescribed allopurinol for recurrent gout attacks. Allopurinol acts by inhibiting which of the following enzymes in the purine degradation pathway?
Identify the enzyme inhibited.
A. Adenosine deaminase
B. Xanthine oxidase
C. Ribonucleotide reductase
D. HGPRT
Q4.
A newborn presents with macrocytic anemia and megaloblastosis. Laboratory tests show decreased levels of thymidine and abnormal dTMP synthesis.
Which enzyme is most likely deficient?
A. Dihydrofolate reductase
B. Thymidylate synthase
C. Orotidine monophosphate decarboxylase
D. Ribonucleotide reductase
Q5.
An infant is diagnosed with orotic aciduria, which is unresponsive to urea cycle defect treatment. Genetic analysis shows a defect in pyrimidine synthesis.
Which of the following is the deficient enzyme in this condition?
A. Ornithine transcarbamylase
B. CPS I
C. Orotate phosphoribosyltransferase
D. Xanthine oxidase
Q6.
A patient with acute leukemia is being treated with 6-mercaptopurine. The drug acts by interfering with which step of nucleotide metabolism?
What is its mechanism of action?
A. Inhibition of ribonucleotide reductase
B. Inhibition of purine degradation
C. Inhibition of de novo purine synthesis
D. Stimulation of pyrimidine salvage
Q7.
In purine synthesis, PRPP (phosphoribosyl pyrophosphate) acts as a key molecule. Overproduction of PRPP can lead to:
Which of the following clinical outcomes?
A. Megaloblastic anemia
B. Hypouricemia
C. Gout
D. Immunodeficiency
Q8.
A child presents with severe combined immunodeficiency (SCID). One mechanism involves impaired DNA synthesis due to buildup of deoxyadenosine triphosphate.
Which step in nucleotide metabolism is primarily affected in this variant?
A. Inhibition of PRPP synthetase
B. Inhibition of xanthine oxidase
C. Inhibition of ribonucleotide reductase
D. Inhibition of carbamoyl phosphate synthetase II
Q9.
A cancer drug inhibits dihydrofolate reductase (DHFR), leading to decreased availability of tetrahydrofolate.
Which of the following processes is directly affected?
A. Conversion of UMP to CMP
B. Conversion of dUMP to dTMP
C. Conversion of IMP to AMP
D. Salvage of adenine
Q10.
A patient on chemotherapy develops megaloblastic anemia due to folate antagonism. Supplementation with which compound bypasses the blocked step and restores nucleotide synthesis?
Choose the correct rescue therapy.
A. Folic acid
B. Vitamin B12
C. Leucovorin
D. SAMe
🔹 Answer Keys
| Q.No | Answer | |
|---|---|---|
| Q1 | C | |
| Q2 | A | |
| Q3 | B | |
| Q4 | B | |
| Q5 | C | |
| Q6 | C | |
| Q7 | C | |
| Q8 | C | |
| Q9 | B | |
| Q10 | C |