Q.N.1- 20 multiple choice questions on a separate sheet.
Q.N.2- a) What are the salient features of an a-helix? Name two amino acids that destabilize this structure.
b) Give an account of the biochemical changes in the blood of a phenylketonuric subject. How will you proceeds for the diagnosis and treatment of this disease?
c) Outline 3 metabolic roles of glycine.
Q.N.3– a) Describe the steps of de novo synthesis of fatty acids? How is this process regulated?
b) Explain the significance of the enzyme b-hydroxy-b-methylglutaryl CoA (HMG-CoA) Reductase.
Q.N.4- a) Explain why are the following compounds toxic: (i) Rotenone (ii) 2, 4-dinitrophenol (iii) Atractyloside.
b) Explain how alcohol consumption by an undernourished person can cause hypoglycemia.
c) Explain why the breath of an untreated diabetic smells of acetone.
d) Explain how the monitoring of glycosylated hemoglobin (HbAIc) levels is useful in the treatment of diabetes mellitus.
Q.N.5- Write short notes on-
a) Visual cycle
b) One carbon metabolism.
c) Enzyme Inhibition
Q.N.6- a) Briefly discuss the mechanism of iron absorption from the intestinal lumen. What is its biological and clinical significance?
b) Give an example of:
(i) cyclic fatty acid
(ii) polyunsaturated fatty acid and
c) Give the biochemical explanation for the presence of high levels of (i) Ketone and (ii) Methylmalonic acid in the urine.
Multiple Choice Questions
Q.N.1- Which of the following monosaccharide is not an aldose?
Q.N.2- Which of the following enzymes catalyzes a reaction that involves a decarboxylation reaction?
b) Isocitrate dehydrogenase
c) α-keto glutarate dehydrogenase
d) all of the above.
Q.N.3- In the enzyme catalyzed reactions when the conc. of the substrate is too high the reaction order is-
a) Zero order
b) First order
c) Second order
d) Third order.
Q.N.4-. The primary defect which leads to sickle cell anemia is:
a)An abnormality in porphyrin part of hemoglobin.
b Replacement of glutamate by Valine in β-chain of HbA.
c).A nonsense mutation in the β -chain of HbA.
d)Substitution of Valine by glutamate in the α -chain of HbA.
Q.N.5-Which of the following is a sugar alcohol?
a) Gluconic acid
Q.N.6- In Tangier’s disease-
a) HDL is more in plasma
b) HDL is less in plasma
c) LDL is more in plasma
d) LDL is lesst in plasma.
Q.N.7- All are nitrogen containing compounds except-
b) Thyroid hormones
Q.N.8- Absorption of calcium is enhanced by the presence of vitamin-
Q.N.9- All are proteins that include a porphyrin ring except-
Q.N.10-Enzymes of TCA cycle are found in-
d) None of the above.
Q.N.11- Histidine is catabolized by opening the ring to produce-
a) Formimino Glutamic acid
c) γ-amino butyric acid
d) p- amino benzoic acid
Q.N.12-Which metal is responsible for imparting red color to vitamin B12-
Q.N.13- Zinc is a part of the structure of the following enzyme-
b) Carbonic Anhydrase
d) Cytochrome Oxidase.
Q.N.14- Pellagra is characterized by-
c) Aplastic anemia
d) Exfoliative dermatitis.
Q.N.15- Creatine is present in urine in-
c) Myasthenia Gravis
d) All of the above.
State True or False
Q.N.16- Tay Sach’s disease is a Glycogen Storage disease.
Q.N.17- Serotonin is derived from Tryptophan.
Q.N.18-Ammonium ion is toxic to the brain.
Q.N.19-Muscles can efficiently synthesize glucose.
Q.N.20- 131ATP molecules are produced by the complete oxidation of one molecule of Palmitic acid.
Q.N.1-(Multiple Choice Questions)
Q.N.2-a)-Salient features of Alpha helix-
1) The Alpha helix is a spiral structure.
2) The structure is stabilized by Hydrogen bonds between NH and C=O groups of the main chain.
3) Each turn is formed by 3.6 residues.
4) The distance between each amino acid residue is 1.5A.
5) It is generally right-handed.
6) In proteins like Hb and Myoglobin the alpha helix is abundant.
7) Two amino acids that disrupt the helix are proline and hydroxy proline.
Diagram and the list of participating amino acids / amino acids causing disruption of helix are to be given
b) Biochemical changes in the blood of a phenylketonuric subject- Phenyl Alanine can’t be converted to Tyrosine , it accumulates and alternate minor pathways are opened. Phenyl pyruvate, phenyl lactate and phenyl acetate accumulate in blood and are excreted in urine.
Diagnosis is made by blood phenyl Alanine levels, Guthrie test and urine ferric chloride test.
Treatment is based on early detection. The principle of treatment is to provide a diet containing low phenyl Alanine. Gene therapy is the permanent cure.
Details of reactions are needed
c) 3 metabolic roles of glycine.
1) Formation of Haem
2) For detoxification of toxic substances
3) For the formation of bile salts.
Reactions and the clinical significance of each is needed.
Q.N.3-a) steps of de novo synthesis of fatty acids- all the steps of incorporation of acetyl co A and Malony co A to the enzyme. The steps of reduction, dehydration and reduction are to be explained. The repetition of cycles and the energy yield etc is to be explained.
b)- significance of enzyme b-hydroxy-b-methylglutaryl CoA (HMG-CoA) Reductase- it is a key regulatory enzyme of cholesterol synthesis. It is regulated by feed back inhibition, covalent modification, allosteric modification and by diet induced induction or repression. It is competitively inhibited by statins which are used for lowering plasma cholesterol levels.
Reaction and some details are needed.
Q.N.4- a)The following compounds are toxic because
(i) Rotenone – It inhibits the first complex of ETC, thus there is no ATP formation and death occurs due to metabolic derangements.
(ii) 2, 4-dinitrophenol- It is an uncoupler of oxidative phosphorylation
(iii) Atractyloside- inhibits ATP/ADP translocase.
b) Alcohol consumption by an undernourished person can cause hypoglycemia- Alcohol is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase, which utilize NAD+, as a result NADH accumulates and all the reactions where NAD+ is utilized are inhibited and the reactions where NADH is utilized are promoted. Hence oxaloacetate and pyruvate are converted to malate and lactate respectively limiting the substrates for Gluconeogenesis resulting in to hypoglycemia.
c) why the breath of an untreated diabetic smells of acetone- untreated diabetes mellitus leads to hyperglycemia. Non utilization of glucose leads to lipolysis. The excess acetyl co A is utilized for ketogenesis. Acetone, the Ketone body is excreted through lungs, that’s why the breath of the untreated diabetics smells of acetone.
d) How the monitoring of glycosylated hemoglobin (HbAIc) levels is useful in the treatment of diabetes mellitus– The degree of hyperglycemia can be depicted by the conc. of glycosylated hemoglobin (HbAIc). The target of therapy is based on lowering the levels of glycosylated HbA1c . It is a better parameter than estimating blood sugar levels.
Q.N.5- Short notes on-
a) visual cycle – The steps of disintegration of Rhodopsin and reformation are to be explained.
b) One carbon metabolism- Sources and various acceptors of one carbon are to be explained. Various forms of folic acid acting as carriers of one carbon group are to be discussed.
c) Enzyme Inhibition– various types of inhibitions like competitive, non competitive, feed back, allosteric inhibition etc are to be discussed.
Q.N.6- a) Mechanism of iron absorption from the intestinal lumen- Mucosal block theory is to be explained.
b) Give an example of: (i) cyclic fatty acid – Chaulmoogric acid and hydnocarpic acid
(ii) Polyunsaturated fatty acid – Arachidonic acid
(iii) Glycolipids-Glucocerebrosides, Glucocerebrosides, Gangliosides.
c)The biochemical explanation for the presence of high levels of (i) Ketone bodies
The possible causes are starvation, uncontrolled diabetes mellitus, high fat feeding etc.
(ii) Methylmalonic acid in the urine- It is excreted in the deficiency of vitamin B12. L-methyl malonyl co A is not converted to suucinyl co A, it accumulates and is thus excreted excessively in urine.
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