Biochemistry End-of-Year 2013 (2) — Past Paper OmpathStudy

Revise Biochemistry End-of-Year 2013 (2) with structured exam questions and available answers for focused medical revision. Kenya, Africa and global rev...

Bchem EOY 2013 (2) — Past Paper Questions & Answers University of Nairobi, First Year Examinations 2012/2013 — HBC 100 / UPC 102 / VBC 100: Biochemistry. This paper carries no printed answer key; model answers below are written from standard biochemistry references, not copied from a marking scheme. --- Section A: Essay Questions (Attempt any THREE) — 30 Marks Question 1 (a) Briefly describe oxidative deamination of amino acids. [5 marks] (b) State the sources of amino acids in the "amino acid pool". [5 marks] Model answer: (a) Oxidative deamination removes the α-amino group of an amino acid as free ammonia (NH₃), regenerating the corresponding α-keto acid. It is catalyzed mainly by glutamate dehydrogenase (in liver mitochondria), which uses NAD⁺ or NADP⁺ as coenzyme. Glutamate + NAD⁺ + H₂O → α-ketoglutarate + NADH + NH₄⁺ — this is the main reaction funnelling amino groups (collected via transamination) into free ammonia for urea synthesis. (b) Sources of amino acids in the body's "amino acid pool": Dietary protein digested by gastric, pancreatic and intestinal proteases/peptidases. Breakdown (turnover) of the body's own tissue/cellular proteins. De novo synthesis of the nonessential amino acids from metabolic intermediates. --- Question 2 (a) Describe the oxidative phase of the pentose phosphate pathway (PPP). [5 marks] (b) State three goals of the PPP. [3 marks] (c) State two diseases associated with the PPP. [2 marks] Model answer: (a) Glucose-6-phosphate → 6-phosphogluconolactone, catalyzed by glucose-6-phosphate dehydrogenase (G6PD), generating the first NADPH. 6-phosphogluconolactone → 6-phosphogluconate (via lactonase, a hydrolysis step). 6-phosphogluconate → ribulose-5-phosphate + CO₂, catalyzed by 6-phosphogluconate dehydrogenase, generating a second NADPH. (b) Goals of the PPP: Generate NADPH for reductive biosynthesis (e.g. fatty acid and cholesterol synthesis). Generate NADPH for antioxidant defence (keeping glutathione reduced, protecting cells — especially red cells — from oxidative damage). Generate ribose-5-phosphate for nucleotide and nucleic acid synthesis. (Non-oxidative phase also interconverts sugars to match the cell's relative need for NADPH vs. ribose-5-phosphate.) (c) Diseases: G6PD deficiency (causes hemolytic anemia/favism under oxidative stress); certain cancers (tumour cells upregulate the PPP for NADPH and ribose supply to support rapid proliferation). --- Question 3 Nucleotides are essential for all cells, discuss: (a) The biological significance of nucleotides. [5 marks] (b) The medical significance of nucleotide metabolism in humans. [5 marks] Model answer: (a) Biological significance: Building blocks of DNA and RNA — storage and transfer of genetic information. Energy carriers/currency — ATP, GTP. Components of key coenzymes — NAD⁺, FAD, coenzyme A. Second messengers — cAMP, cGMP. Allosteric regulators of metabolic enzymes. (b) Medical significance: Gout — excess purine catabolism raises uric acid, which crystallizes in joints. Lesch-Nyhan syndrome — HGPRT deficiency in purine salvage. Severe combined immunodeficiency (SCID) — adenosine deaminase (ADA) deficiency. Orotic aciduria — defect in pyrimidine synthesis (UMP synthase). Many chemotherapy and antimicrobial drugs (5-fluorouracil, methotrexate, acyclovir) target nucleotide metabolism. --- Question 4 Giving an example of each, explain biological roles of proteins. [10 marks] Model answer: Structural — collagen (connective tissue), keratin (skin/hair/nails). Enzymatic/catalytic — amylase, pepsin, DNA polymerase. Transport — haemoglobin (O₂), albumin (fatty acids/drugs), transferrin (iron). Hormonal — insulin, glucagon, growth hormone. Immune/defence — immunoglobulins (antibodies). Contractile/motility — actin and myosin (muscle contraction). Storage — ferritin (iron storage), casein (amino acid storage in milk). Receptor — insulin receptor, GPCRs. Buffering — plasma proteins help maintain blood pH. --- Question 5 (a) Draw a clearly labeled diagram of a replication fork. [4 marks] (b) Identify any three functional differences between DNA polymerases and RNA polymerase. [1.5 marks] (c) Why is DNA repair important? [1 mark] (d) Briefly explain how thymine dimers in DNA are repaired. [3.5 marks] Model answer: (a) Replication fork (described, since a hand-drawn diagram can't be reproduced here): Helicase unwinds the parental duplex ahead of the fork; single-strand binding proteins keep the separated strands from reannealing; topoisomerase relieves the supercoiling generated ahead of the fork. The leading strand is synthesized continuously in the 5'→3' direction, following the fork. The lagging strand is synthesized discontinuously, away from the fork, as a series of Okazaki fragments, each started by an RNA primer (primase) and later joined by DNA ligase after RNA primers are removed and gaps filled. (b) Functional differences: DNA polymerase requires a primer to begin synthesis; RNA polymerase can initiate RNA synthesis de n
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