2nd YEAR BIOCHEMISTRY – TOPICAL PAST

PAPERS (2005-22)
Compiled by;
• 2005-17 questions by Shahroze Ahmed, N-66, NMU
• 2018-22 questions by ZAIN ALI, M ABDURREHMAN ANJUM
MUZAMIL FIAZ, SHAHAB ZAFAR from BATCH ’25, AIMC

▪ BIOENERGETICS
1. Enumerate the cytochromes of mitochondrial respiratory chain, mention the
free mobile and membrane embedded separately.
2. At which level of respiratory chain, cyanide acts and blocks energy
production?
3. How the reducing equivalents NADH produced in the glycolytic pathway of
cytosol are transferred to mitochondria for further oxidation?
4. Draw electron transport chain.
5. Name any four inhibitors of electron transport chain.
6. How uncouplers of oxidative phosphorylation produce their effect?
7. Give all pathways through which high energy phosphate is transferred to ADP
for formation of ATP.
8. What is meant by oxidation phosphorylation?
9. Write down uncouplers of oxidative phosphorylation.
10. What is chemiosmotic theory?
11. Describe complex V of electron transport chain along with its two inhibitors.
12. What is the role of ATP synthase in ATP production?
13. Define respiratory chain and give its location.
14. Describe the components and functions of complexes of ETC which act as
proton pumps.
15. Write down the chemiosmotic theory of oxidative phosphorylation.
16. A worker of H2S gas industry became unconscious and brought to medical
emergency where he was declared a case of H2S gas poisoning.
A) Which complex of mitochondrial respiratory chain is blocked in this
patient?
B) Give the components of this complex.
17. An unskilled worker in a water garden/plant nursery was sent to sweep up a
spill of a white powder in the storage shed. Later he was found with labored
breathing and convulsions. On further examination, the white powder was
identified as rotenone.
A) What is the cause of respiratory distress on rotenone exposure?
B) Name other inhibitors of oxidative phosphorylation.
18. Draw a figure showing the sites of inhibition of electron transport chain by
drugs.
19. A child accidentally took cyanide and was brought to the hospital in coma.
What is the effect of this poison on mitochondrial respiration?
20. Give the mechanism of ATP production by ATP synthase.
21. What is cytochrome oxidase, what is its function?
22. What is substrate level phosphorylation? Elaborate with the help of any two
examples.
23. How the electrons flow through the respiratory chain complexes with entry
points of reducing equivalents from important substrates? Draw diagram.
24. Write down NADH generating reactions of citric acid cycle. Give the role of
this cycle in fatty acid synthesis.
25. Define substrate level phosphorylation, name three reactions related to this
phenomenon.

▪ CARBOHYDRATE METABOLISM
Glycolysis
1. Write down three irreversible reactions of glycolysis.

2. Write down the reaction catalyzed by the enzyme pyruvate kinase.

3. What is the cause of hemolytic anemia in pyruvate kinase deficiency?

4. What happens in pyruvate kinase deficiency?

5. Give the regulatory enzymes of hepatic glycolysis, how these are regulated?

6. Write the regulatory enzymes with their reactions in glycolysis.

7. Differentiate between glucokinase and hexokinase

8. glycolysis. Give its hormonal regulation.

9. Write two reactions of glycolysis containing substrate level phosphorylation.

10. How is 2,3-Biphosphoglycerate synthesized

11. What is substrate level phosphorylation?Elaborate with the help of any two
example

Oxidation of Pyruvate
1. Give different fates of pyruvate.
2. Give different components of pyruvate dehydrogenase complex.

3. How lactic acidosis occur in pyruvate dehydrogenase deficiency?

4. Why neurological disturbance occur in pyruvate dehydrogenase deficiency?

5. How pyruvate is converted to acetyl CoA? Give it regulation.

6. A chronic alcoholic has been brought to medical emergency.Blood

biochemistry reveals lactic acidosis.Deficiency of pyruvate dehydrogenase
complex is suspected.Give the reaction catalyzed Pyruvate dehydrogenase
complex with its mechanism.Why thiamine deficiency leads to deficient
activity of PDH complex?
TCA Cycle
1. What is the role of various B-complex vitamins in TCA cycle?

2. What is the significance of TCA cycle?

3. Enlist the reactions mediating ATP formation in TCA cycle

Glycogen Metabolism
1. Why is only a little amount of free glucose formed from glycogen degradation
In muscles?
2. How glycogen is synthesized in the liver?
3. How glycogen synthesis is regulated?
4. What is reciprocal regulation of glycogen metabolism?
5. Outline the steps of breakdown of glycogen.
6. Enlist glycogen storage diseases.
7. Which disorder occurs due to deficiency of glucose-6-phosphatase?
8. What are glycogen storage diseases and what are their biochemical defects?
9. Outline the sequence of reactions involved in the breakdown of glycogen in
the skeletal muscles,explain the purpose served by this process.
10. How the process of glycogenesis occur in the liver?Name the factors affecting
glycogen content of the body.
11. A 4 months old infant was brought to the hospital with jittery spells and
irritability several hours after feeding.Physical examination revealed enlarged
liver.The laboratory reports indicated that he developed fasting
hypoglycemia.Large deposits of glycogen with shorter than normal branches
were seen in biopsy specimen from the liver.What is the probable
 diagnosis?Name the deficient enzyme.How glycogen synthesis and
degradation is allosterically regulated especially in liver and muscle?

Gluconeogenesis & Control of Blood Glucose

1. Define gluconeogenesis.

2. How gluconeogenesis is suppressed after feed and enhanced during fasting?

3. How do gluconeogenic precursors glycerol and lactate enter gluconeogenic

Pathway?

4. Describe the process of gluconeogenesis from alanine.

5. How alanine, glycerol and lactate are converted to glucose?

6. What is the significance of gluconeogenesis?

7. Which metabolic pathways are activated to provide energy during period of

Starvation?

8. Write three specific enzymes which are required to convert amino acids to
Glucose

9. Enumerate the tissue/cellular sites, sources, enzymes, nutritional control and

Metabolic sequences of gluconeogenesis.

10. How availability of energy yielding nutrients is regulated in the body during
Fasting?

11. the precursors of gluconeogenesis.What are the irreversible steps of

glycolysis which are reversed during the process of gluconeogenesis?

12. Define gluconeogenesis.Write down its substrates along with their sources.

Pentose Phosphate Pathway

1. What is the biochemical cause of hemolysis in patient with G6PD deficiency?
2. Write down the reaction catalyzed by G6PD.
3. What is the role of G6PD in RBCs?
4. Enumerate functions of pentose phosphate pathway.
5. What are the consequences of G6PD deficiency?
6. How is nitric oxide synthesized in the body?
7. Enumerate various roles of nitric oxide.
8. Define oxidative and non-oxidative phase of hexose monophosphate
pathway, Giving importance of each.
9. Write down the uses of NADPH in the body (atleast 5)
10. Give the first two reactions of pentose phosphate pathway.Give the
importance of oxidative and non oxidative phases of this pathway.
11. A patient develops severe intravascular hemolysis after taking antimalarian
drugs.What is the cause of this hemolysis?
12. What is G6PD deficiency?
13. A patient after taking antimalarian drugs developed severe intravascular
hemolysis.Name the enzyme deficient in this patient.Why its deficiency leads
to hemolysis?

Fructose and Galactose Metabolism

1. How does high fructose diet leads to flooding of cells with cholesterol and
Triacylglycerol? Give the mechanism.
2. How lactose is synthesized in mammary glands?
3. How will you manage a patient with lactose intolerance?
4. In a controlled study, sucrose fed rats developed more atherosclerosis than
The glucose fed rats. Explain the mechanism.
5. What are the enzyme deficiencies in essential fructosuria and hereditary
Fructose intolerance? Write down reactions catalyses by these enzymes.
Which One leads to severe hypoglycemia of fructose and why? What is the
cause of Hyperuricema in this condition?
6. What are the biochemical events involved in causation of cataracts in
Uncontrolled diabetes mellitus?
7. How galacatose component of lactose is converted to glycogen in the liver?
8. Which defect cause galactosemia?
9. How high fructose intake for prolonged time is more atherogenic than
Glucose?
10. Give hepatic metabolism of fructose and its regulation.

Diabetes Mellitus + Obesity

1. What are the effects on hepatic glycolysis and gluconeogenesis in a patient
with type 1 DM?

2. Give the reactions of glycolysis and gluconeogenesis that are affected in type
1 DM

3. A patient of uncontrolled DM developed fatty liver. What is the mechanism?

4. What tests are needed to confirm diabetes?

5. is the difference between juvenile and maturity onset diabetes?

6. Explain how insulin reduces plasma glucose levels.

7. What is the cause of ketonuria and glucosuria in DM?

8. Explain metabolism of diabetic ketoacidosis.

9. is the effect of obesity on lipid profile and how would it be reorganized to

normal levels?

10. A known diabetic brought to emergency ward with rapid repiratory rate.His
blood glucose was 480mg/dl.Urine was positive for ketone bodies and
glucose.Hos blood pH was 7.30.Which energy producing nutrient isn’t properly
utilized in this case?Which energy producing nutrient is rapidly mobilized from
storage site and utilized for production of energy?Why hormone sensitive
lipase is active in this case?

11. An apparently healthy man on a routine checkup had a fasting blood glucose
level of 80mg/dl with normal urine ezxamination.One and half hour after
heavy breakfast his blood glucose was 140mg/dl but benedicts test was
positive on the urine.What is the possible diagnosis?How will you further
investigate?What is the course of this disease?

12. A 32 years old male patient of type-1 Diabetes Mellitus developed symptoms
of dry mouth,nausea and vomiting after he left medication against medical
advice.He was brought to emergency in semicomatose state.On examination
he was found dehydrated,hypotensive and has kussmaul
breathing.Investigations revealed very high blood glucose level
415mg/dl,presence of ketone bodies in the urine and decreased blood pH
7.09.What is the most likely diagnosis?How ketone bodies Are produced and
utilized in the body?

13. Hyperglycemia and ketoacidosis are the hallmarks of untreated type 1

diabetes mellitus.Give biochemical cause of hyperglycemia and ketoacidosis in
these patients
▪ LIPID METABOLISM
Oxidation of Fatty Acids & Ketogenesis
1. How long chain fatty acids are transported in mitochondria?
2. Calculate total energy produced when one molecule of palmitic acid is oxidized
by beta-oxidation.
3. What is beta oxidation?
4. How is beta-oxidation regulated?
5. How ketone body (3-hydroxy-butyrate) is utilized in extrahepatic tissues?
6. Write down the similar reactions of ketogenesis and cholesterol biosynthesis
occurring in mitochondria and cytosol respectively.
7. Write down complete reaction for synthesis and utilization of ketone bodies.
8. Name and draw structures of ketone bodies.
9. What is the role of carnitine shuttle?
10.How fatty acids brought in hepatocytes from adipose tissues is activated and
transferred to mitochondrial matrix for further oxidation? Give its regulation.
11.Write three fates of acetyl CoA.
12.How are ketone bodies synthesized?
13.What are the various roles of peroxisomes in lipid metabolism?
14.How ketone body acetoacetate serve as a fuel for extrahepatic tissue?
15. Write down the names of enzymes involved in beta oxidation. What do you
know about alpha oxidation and Refsum disease?
16. A known diabetic brought to emergency ward with rapid respiratory rate. His
blood glucose was 480 mg/dL. (Normal = 80-120 mg/dl). Urine was positive for
ketone bodies and glucose. His blood pH was 7.30 (Normal = 7.35 – 7.35).
a Which energy producing nutrient is not properly utilized in this case?
b Which energy producing nutrient is rapidly mobilized from storage
site and utilized for production of energy?
 c Why hormone sensitive lipase of adipocytes is active in this case?
17. A 32-year-old patient of type 2 diabetes mellitus developed symptoms of
dry mouth, nausea and vomiting after he left the medication against medical
advice. He was brought to emergency in semi-comatose state. On examination
he was found dehydrated, hypotensive and had Kussmaul breathing.
Investigations revealed very high blood glucose level (415 mg/dl), presence of
ketones in the urine and decreased pH of blood to 7.09.
a What is the most likely diagnosis?
b How are ketone bodies produced and utilized in the body?
18. Elevated levels of ketone bodies can be found in the blood of people with
untreated type 1 diabetes and individuals on severe diets. What are the names
of ketone bodies circulating in the plasma?
19. How are ketone bodies produced and utilized by extrahepatic tissues?
20. Name the ketone bodies. How are they synthesized in the human body?
21. Discuss the sources and fate of acetyl CoA

Biosynthesis of Fatty Acids & Eicosanoids

1. How is cytosol acetyl CoA produced for de novo synthesis of fatty acid?
2. Write biochemical functions of Eicosanoids.
3. Give the sources of reducing equivalent NADPH required for lipogenesis.
4. How insulin regulates lipogenesis?

5. How fatty acid synthesis is regulated? Write down the regulatory steps of fatty
acid synthesis.

6. Which fatty acid is the primary end product of fatty acid synthase activity?
Give summary of total energy yield from the oxidation of this fatty acid

Metabolism of Acylglycerols & Sphingolipids

1. Name the products of lipolysis and give their fate.
2. How lipolysis is increased in a patient of DM?

3. Give an account of lipid storage diseases.

Lipid Transport & Storage
1. How is VLDL synthesized in the liver?
2. Which substances block the synthesis and release of VLDL?
3. What is HDL? Enumerate its various types.
4. How is HDL synthesized?
5. Which plasma lipid will be increased or decreased in lipoprotein lipase
deficiency?
6. How are chylomicrons cleared from plasma?
7. How cholesterol is transported from extrahepatic tissues to liver?
8. Classify lipoproteins. What is their role in health and disease?
9. What is the fate of nascent VLDL released from liver?
10. A patient of Diabetes Mellitus developed fatty liver. What is the mechanism?
11. Define lipotropic factors and give their relationship with fatty liver.
12. Describe fatty liver.
13. How ethanol causes fatty liver?

14. Write down the site of production, composition, and metabolism of very low
density lipoproteins (VLDL).

15. Enumerate all transport vehicles responsible for transport of neutral lipids in
plasma. Which one of them transports digested and absorbed dietary lipids to
liver and extrahepatic tissues?

16. Why is HDL called good lipoprotein, what are its various types, how it is
formed and what are its functions?

17. Give the metabolism of low density lipoproteins (LDL).

18. What is HDL? What are its various types? How is it formed? What are its
functions?

19. Give the metabolism of HDL particles.

20. What is fatty liver? Discuss the causes and prevention of fatty liver.
Cholesterol Synthesis, Transport & Storage
14. How cholesterol synthesis is regulated in man?
15. How cholesterol is transported from extrahepatic tissues to liver?
16. How is cholesterol transport affected in LCAT deficiency?
17. How cholesterol causes atherosclerosis?
18. Name various diseases in which prolonged elevation of blood levels of
cholesterol-rich proteins occur?
19. Write down the regulatory steps in cholesterol biosynthesis.
20. Write various factors affecting the activity of the regulatory enzyme in
cholesterol biosynthesis.
21. Write down the similar reactions of ketogenesis and cholesterol biosynthesis
occurring in mitochondria and cytosol respectively.
22. How is 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase regulated as a
rate limiting enzyme of cholesterol biosynthesis?
23. Draw structure of cholesterol. What is its importance in health and disease?
24. A patient presents to physician with history of chronic constipation and on
investigation cholesterol level is too high, doctor advises him use of fiber on
regular basis, what are various types of fiber and their action in the body, from
where these fibers can be obtained?
25. Give the reaction of hepatic cholesterol biosynthesis upto the level of
mevalonate. How the regulation of cholesterogenesis occurs at this level?

▪ PROTEIN & AMINO ACID METABOLISM

Amino Acids: Disposal of Nitrogen
1. Give extramitochondrial steps of urea synthesis.
2. Give the regulation of hepatic urea biosynthesis
3. Explain the abnormality that arises in urea biosynthesis if the ornithine
transporter of inner mitochondrial membrane is defective.
4. Enumerate the two pathways for the degradation of tissue proteins inside the
cell and describe the ATP dependent pathway.
5. Write down reactions of urea cycle occurring in mitochondrial matrix.
6. How is urea cycle regulated?
7. Name the genetic defects in urea cycle.
8. What are the sources of ammonia in the body?
9. How is ammonia transported to the liver?
10. Why ammonia is toxic to brain tissue?
11. How ammonia is buffered in brain and liver?
12. How ammonia detoxification is regulated in liver?
13. Give the pathway by which ammonia is detoxified in the liver.
14. What is hyperammonemia? Give its type and defect involved in each type.
15. How proteins are degraded in our body?

Amino Acid Degradation and Synthesis

1. Give biochemical events leading to characteristic clinical manifestations in
patients with Phenylketonuria.
2. Write the reaction catalyzed by the enzymes phenylalanine hydroxylase.
3. Suggest management of a patient with Phenylketonuria.
4. Why does phenylalanine appear in urine in large amounts in Phenylketonuria?
5. . What is the source of phenylpyruvate and phenyllactate
6. What are Phenylketonuria and Alkaptonuria?
7. How will you diagnose Alkaptonuria from urine sample of a patient?
8. Enumerate various inherited disorders of tyrosine metabolism.
9. How is S-Adenosyl Methionine synthesized?
10.Write four products derived from phenylalanine
11.How branched chain amino acids are catabolised in the body and how their
metabolism differs from the other amino acids?
12.Which disease may result due to deranged metabolism of branched chain
amino acids?
13.Name the glucogenic and ketogenic amino acids.
14.What enzymes are deficient in Alkaptonuria and homocystinuria? Write down
the reactions catalyzed by these deficient enzymes.

Conversion of Amino Acids to Specialized Products

1. How creatine and creatinine are formed in the body? What is their fate?
2. How catecholamines are synthesized from tyrosine?
3. How creatine phosphate is synthesized?
4. Enumerate the amines of biological importance produced from histidine,
tyrosine and tryptophan.
5. Write down the steps involved in the biosynthesis of catecholamines and their
mechanism of action.
6. Which neurotransmitters are synthesized from amino acids? Give at least two
examples.
7. Name the compounds formed from tyrosine.
8. Outline the steps of catabolism of catecholamines. What is VMA and what is
its diagnostic value?

Other
1. Write the biochemical functions of Methionine.
2. Enumerate four major biochemical functions of glycine.
3. What is nitrogen balance? What are its various types along with conditions
associated with abnormal nitrogen balance?

▪ NUCLEOTIDE METABOLISM
1. What is the role of adenosine deaminase?

2. Give the biochemical mechanism by which adenosine deaminase deficiency

Leads to severe combined immunodeficiency.

3. Write down the steps in the degradation of purine nucleotides.

4. How is allopurinol helpful in the treatment of gouty arthritis?

5. products are increased in plasma when uric acid production is blocked By

allopurinol?

6. In the process of de novo pyrimidine biosynthesis, how CTP (cytidine

Triphosphate) is synthesized from orotic acid?

7. Methotrexate blocks the de novo biosynthesis of which nucleotides and at

Which level?

8. Give the purine salvage pathway from purine bases. Which metabolite will
accumulate in the body if the enzymes of this pathway become deficient?

9. List the end products formed after degradation of purine and pyrimidine
Bases.

10. What should be the appropriate treatment for a child with severe combined
Immunodeficiency (SCID)?

11. Which enzyme is deficient in Orotic Aciduria? What is normal biochemical

Function of this enzyme in our body?

12. How does a person with Lesch-Nyhan Syndrome develop hyperuricemia?

13. Name the defective enzyme in Lesch-Nyhan syndrome and write down the
Reaction catalyzed by this enzyme.

14. How is 5’-phosphoribosyl-1-pyrophosphate (PRPP) synthesized?

15. Name the amino acids taking part in purine formation.

16. Write down the complete reaction of synthesis of uric acid from its immediate
Precursor.
17. How is inosine formed from adenosine in the course of synthesis of uric acid?

18. How uric acid is formed in the body?

19. What are the disadvantages of increased uric acid level?

20. Write down the catabolic end products of purine and pyrimidines.How
purines are catabolized?

21. A 2 year old boy showed signs of delayed motor development and was
brought for consultation,his mother has noticed sand like crystals on
diaper,history revealed that the child has compulsive urge to bite his lips and
fingers.Urinary and serum uric acid levels were abnormally high for the boys
age.What could be the possible diagnosis for such patient also showing
behavioral disturbances and hyperuricemia?Also narrate biochemical aspects
and other clinical manifestations associated with disease.

22. A patient of 5 years presented with swollen and painful joints especially the
joints of toes of his feet.His plasma uric acid was 12.5mg/dl.On detailed
investigations he was diagnosed as a case of Lesch Nyhan syndrome.Which
enzyme is deficient in this case?Give the biochemical reason of developing
hyperuricemia.

23. Write down the the reaction involved in the conversion of ribonucleotides to
deoxyribonucleotides along with its regulation.

24. Give normal blood uric acid levels in both males and females.Plasma uric acid
levels are raised in Lesch Nyhan syndrome.Give the biochemical reason for
hyperuricemia in this disorder.

25. Why Allopurinol is used to treat hyperuricemia in patients who are

“overproducers” of uric acid?
26.A baby of 6 months off and on developing severe infection was diagnosed a
case of severe combined immunodeficiency due to deficiency of adenosine
deaminase enzyme.What is the role of this enzyme?Give the biochemical
mechanism by which this enzyme deficiency leads to severe combined
immunodeficiency

▪ GENETICS
DNA Synthesis, Replication, and Repair
1. What type of DNA damage is caused by ultraviolet light? How this damage is
repaired in a normal individual?
2. What is DNA supercoiling? Give its effects.
3. How the problem created by DNA supercoiling is solved in Prokaryotes and
Eukaryotes?
4. What is pre-priming complex in prokaryotic DNA replication? Give the role of
each component of this complex.
5. Enlist the pre-requisites for replication process.
6. How proof-reading occurs once DNA is formed?
7. Write various enzymes and their functions involved in DNA replication.
8. What is primosome? Give its components.
9. A patient presented with severe urinary tract infection. He was prescribed
Ciprofloxacin. How does this drug help in killing bacteria?
10. Name five classes of eukaryotic DNA polymerases along with principle
functions in DNA replication and repair.
11. Write down the steps of replication of DNA.
12. What is reverse transcriptase? What is its biochemical mechanism of action?
13. How damaged DNA is repaired?

14. Briefly discuss various DNA repair mechanisms?

15. How replication of DNA is started in prokaryotes. Give role of topoisomerases

in this process?
16. A) What you know about prepriming complex?

B) Enumerate eukaryotic DNA polymerases along with their principal

functions.

17. What is replication? How damaged DNA is repaired?

18. Define primosome and give its functions?

19. A 48 years old man had a history of skin cancer. In the past 6 years, he has had
over 30 neoplasms removed from the sun exposed areas. Skin had scattered
areas of hyperpigmentation. He has been diagnosed as a case of xeroderma
pigmentation.

(a) What is the biochemical lesion resulting from UV radiation?

(b) How this lesion is repaired?

20. Write down the Wobble Hypothesis. How the breaks in double stranded DNA
are repaired?

RNA Structure, Synthesis, and Processing

1. Give the components of prokaryotic RNA polymerase mentioning the role of
each component.
2. What are post-transcriptional modifications required to convert pre-mRNA to
mature RNA?
3. Give the mechanism of removal of introns from pro-mRNA.
4. How termination of transcription process takes place?
5. Write down the autoantibodies produced in Systemic Lupus Erythematosus.
6. What is the role of small nuclear ribonucleoprotein particles?
7. What is meant by splicing?
8. What is transcription?
9. What enzymes does Rifampicin inhibit? What is the structure and function of
this bacterial enzyme?
10.What is rho-dependent termination of RNA synthesis?
11.What is the function of RNA polymerase?
12.What are the various RNA polymerases in eukaryotes? Give the role of each.

13.What is the process of splicing?

14.What is transcription and reverse transcription?

15.Q9. A 32 years old male with sore throat, respiratory infections, 37. 8°C
temperature and WBCs 200/mm^3 has infection secondary to HIV.

(a) HIV is abbreviation to which pathogen?

(b) This pathogen requires which enzyme to act?

© What is biochemical mechanism?

(d) Structure of RNA polymerase?

16.What is transcription? How mRNA is modified after transcription?

Protein Synthesis
1. Define silent, missense and nonsense mutations.
2. What is the role of eIF-2 in regulation of protein synthesis in eukaryotes?
3. What is frame-shit mutation? Give example.
4. From transcription to translation to post-translation modifications, give an
outline of protein synthesis in eukaryotes.
5. Describe two types of post-translational modifications in polypeptide chains.
6. Enumerate the characteristics of genetic code.
7. Name four inhibitors of protein synthesis indicating their site of action.
8. Write notes on post-translational modification of protein.
9. Define mutation. What are its types?

10.What are mutations? Discuss its various types?

11.Erythromycin is the antibiotic of choice when treating respiratory tract
infections in whooping cough, and pneumonia because of its ability to inhibit
protein synthesis in certain bacteria. How Erythromycin inhibit protein
synthesis.

12.Define mutations. What are its types? What is sickle cell anemia?

13.Write note on Degeneracy of code?

14.15 Years old female with sickle cell anemia, severe pain and Hb -7. 1 g/dl.
What is the molecular genetics behind this disorder?

15.Give mechanisms of following antibiotics:

(a) Streptomycin

(b) Tetracyclines

(c) chloramphenicol

Regulation of Gene Expression

1. How does lactose regulate its own utilization when administered to a bacterial
colony in nutritional media?

Biotechnology and Human Disease

1. Enlist the steps of Polymerase Chain Reaction (PCR).
2. Define plasmid and cosmid.
3. What is Polymerase Chain Reaction? Give the steps of this technique. What
are its applications?
4. What is sickle cell anemia?
5. What is the molecular genetics behind sickle cell anemia?
6. What is biochemical explanation of pain crisis in sickle cell anemia
7. Give an account of Recombinant DNA technology?
8. Define PCR ; give the steps of this technique?

▪ ENDOCRINOLOGY
Chemical nature and mechanism of action of hormones
1. Write the classification of hormones on the basis of chemical diversity.
2. How adenylyl cyclase is regulated by peptide hormones
3. Classify hormones according to their mechanism of action with examples.
What is the mechanism of action of steroid hormones?
4. Name any 4 hormones that bind intracellular receptors.

Pituitary and Hypothalamic Hormones

1. Give the effects of vasopressin (ADH) on kidney to regulate to water
Reabsorption.

2. How will the body compensate hypovolemia and hyponatremia due to heavy
Perspiration?

3. Discuss the site of stimulus, mechanism of biosynthesis, discharge, transport,

Binding to receptors, signal transduction and metabolic functions of ADH.

4. Diabetes insipidus

5. Where is ADH synthesized? What is its nature? What is its mechanism of

Action?

6. Growth hormone is the most abundantly produced hormone of anterior

Pituitary. Give its regulation, structure, mechanism of action and effects of
Hyperproduction.

7. Write down the mechanism of action of prolactin.

8. What are trophic hormones?Name trophic hormones of anterior pituitary.

9. A 32 years old man was admitted in emergency department suffering a
concussion and head trauma from motor vehicle accident.The patient was
stabilized in the emergency department and transferred to ICU for
observation.On second day ICU nurse informed that the patient had a large
amout of urine.Osmolality was ordered and was low.Physician on duty
remarked that kidneys are not concentrating the urine normally.What is the
most likely diagnosis for increasing dilute urine output?What is the
biochemical mediator that is responsible for this disorder?Where this
biochemical mediator is synthesized?What is the nature of biochemical
mediator?What is the mechanism of action of this biochemical mediator?

Thyroid Hormones
1. What is the relationship of thyroid hormone with obesity?

2. Give synthesis and regulation of thyroid hormone.

3. Give types of thyroid hormones? Which one is active? How its active form is
Produced from prohormone?

4. Give the regulation of biosynthesis and release of thyroid hormones.

5. Enlist the tests to evaluate thyroid gland.

6. Enlist thyroid hormones.Which one is most active?How its active form is

produced from prohormone?

7. A 50 year old school lady complains of hoarness of voice and feeling of

tiredness.She also admitted that she has also gained weight and feel
comfortable in warm weather.What is the most probable cause?What are the
investigations to be done in this patient.How the related hormone is
synthesized in the body?

PARATHYROID HORMONE
 1. A 50 years old female presented with severe body aches and pain.X ray
picture shows marked osteoporosis.Plasma level of calcium was
20mg/dl.CT scan of neck shows an enlarged mass of gland which is involved
in regulation of blood calcium.The size and function of thyroid is
normal.She is suffering from hypertrophy of which gland?Which plasma
hormone will you advise to determine in lab for diagnosis?How the
increased secretion of this gland causes osteoporosis and hypercalcemia?

Adrenal Cortical Hormones

1. Write the mechanism of action of cortisol.

2. What are the effects of cortisol on carbohydrates and lipid metabolism?

3. the effects of cortisol on carbohydrates metabolism in early and late Fasting

state.

4. Give the steps in the biosynthesis of cortisol in the adrenal cortex. Give its
regulation.

5. How does ACTH control the synthesis of cortisol and other cortical hormones?

6. How does aldosterone cause the retention of sodium which contributes to

increase in B.P?

7. What are effects of cortisol?

8. Give effects of glucocorticoids in tabulated form.

9. How mineralocorticoid are synthesized?

ADRENAL MEDULLA

1. Name the hormones made from tyrosine.

2. Write down the steps involved in the biosynthesis of catecholamines and
their Mechanism of action.
3. Outline the catabolism of catecholamines.
 4. What is VMA and what is its diagnostic value?

5.What is pheochromocytoma?How it is diagnosed?

Catecholamines
1. Name the hormones made from tyrosine.
2. Write down the steps involved in the biosynthesis of catecholamines and their
mechanism of action.
3. Outline the catabolism of catecholamines.
4. What is VMA and what is its diagnostic value?

Pancreatic Hormones
1. How lipolysis is increased in a patient having uncontrolled DM?

2. Explain the mechanism of diabetic ketoacidosis.

3. Give an outline of insulin structure. What is the mechanism of action of

Insulin? How insulin secretion is regulated?

4. Explain how insulin could reduce the elevated blood glucose concentration in
a Patient of DM?

5. How can you explain ketonuria and glucosuria in a patient of DM?

Calcium Regulating Hormones

1. How the increased secretions of enlarged parathyroid glands cause
Hypercalcemia and osteoporosis.

2. Write a note on regulation of serum calcium level.

Reproduction
1. What is corpus luteum? What is the role in menstrual cycle and pregnancy?
▪ BIOCHEMISTRY OF GIT
Gastric Juice
1. Give chemical composition of gastric juice.
2. Write any three functions of HCl.
3. After taking meal, plasma bicarbonate of a man increased from 22mEq to
27mEq. What is the reason? (Alkaline tide)
4. Name the organic constituents of gastric juice and give their functions.
5. What is achlorhydria?

Pancreatic Juice
1. Give composition of pancreatic juice. How bicarbonate component of
pancreatic juice is regulated?
2. Give the effect of Cholecystokinin and secretin on secretions of pancreatic
juice.
3. Enumerate proteases of pancreatic juice, give specificity of each.
4. Name various lipolytic enzymes present in pancreatic juice and elaborate their
digestive mechanism on dietary lipomes (lipids).
5. Enumerate the endopeptidases of pancreatic juice and give the specific role of
each.
6. Name various proteolytic enzymes present in pancreatic juice and intestinal
juice with their specific actions in protein digestion.
7. What are functions of pancreatic phopholipase A2 and alpha amylase?
8. Give chemical composition and functions of pancreatic juice.

Intestinal Juice
1. Name various proteolytic enzymes present in pancreatic juice and intestinal
juice with their specific actions in protein digestion.
Digestion & Absorption of Carbohydrates
1. Give the digestion of dietary carbohydrates.
2. How dietary hexoses are actively absorbed from intestinal lumen?

3. How milk sugar “ lactose” is digested and absorbed in milk feed of new born.
What is effect of lactase deficiency?

4. A new born baby developed diarrhea, abdominal distension and foul smell in
breath after breast feeding. Stools contains reducing substances and hydrogen
breath test is positive. Which enzyme is deficient in this patient?

Digestion & Absorption of Lipids

1. How dietary TAG is digested and absorbed in the small intestine?
2. Name various lipolytic enzymes present in pancreatic juice and elaborate
their digestive mechanism on dietary lipomes (lipids)
3. How lipids are Digested in the body?
4. How lipids are Digested and absorbed in gastrointestinal tract in human?

Digestion & Absorption of Proteins

1. Enumerate the proteases of gastrointestinal tract. Which enzyme hydrolyses
the dietary protein by breaking the endopeptide formed by carboxylic side of
basic amino acids?
2. Enumerate the proteases present in various GIT juices along with respective
source organs,

3. A five year old child reports to paediatric OPD with muscle wasting, edema
and distended abdomen. He is diagnosed as patient of Kwashiorkor. Besides
protein non-availability, this condition can occur due to decreased protein
digestive enzymes required to produce amino acids for new protein synthesis.
Name pro-enzymes and active enzymes of GIT for protein digestion along with
converting factor of each pro-enzyme.
Gastrointestinal Hormones
1. Write down major actions of gastrin, secretin and Cholecystokinin.
2. Give the effect of Cholecystokinin and secretin on secretions of pancreatic
juice.

▪ WATER-ELECTROLYTE & ACID-BASE BALANCE

1. What is the normal plasma level of potassium? How body regulated this
electrolyte?
2. Enlist any four causes of respiratory alkalosis. How is it compensated?
3. What is plasma anion gap?
4. Give the role of kidney in relations to reabsorption and synthesis of
Bicarbonate.Enlist the 4 factors which can affect bicarbonate reabsorption
from kidneys.
5. Plasma bicarbonate of a male was 22mEq/L before meal which became
27mEq/L after meals. How rise in bicarbonate occurred after taking routine
Food?
6. A 24 year old diabetic male was brought to Emergency Room. His blood
glucose on arrival was 780mg/dL. He had been started on an insulin drip and
had received one amp of bicarbonate. ABG results are: pH=7.33 (N=7.34-7.45),
HCO3=12 mEq/L (N=22-26),PaO2=89, PaCo2=25 (35-45)
(a)What Acid Base imbalance is this patient suffering from?
(b) Is it compensated? Justify your answer.
7. Write down the various roles of kidney in acid-base balance.
8. How is filtrated bicarbonate from renal golmeruli reabsorbed?
9. What is acidosis? Differentiate between metabolic and respiratory acidosis.
10. What is the normal level of plasma sodium?How the body regulates sodium
balance?
11. What is the role of renal buffers in maintaining plama pH?
12. A 21 year old girl was admitted to the casualty department with the history of
excessive Panadol intake.On examination found hyperventilating.Blood
reports are; Na+ 134 mmol/L , K+ 6 mmol/L , HCO3 10mmol/L , Cl- 93mmol/L ,
 glucose 5.3mmol/L. Arterial blood gas analysis pH 7.2,pp CO2 3.18 pKa , pp 02
13.1 pKa.What is most probably diagnosis? Calculate Anion gap.
13. A 52 years old male with end stage renal disease is brought to emergency
department feeling weak and dizzy.His heart rate is 50 and ECG shows tall
peaked T waves with narrow base in precordial leads,shortened QT interval,
and ST segment depression .His blood potassium levels are 6 mEq/L .What is
diagnosis and give 4 cause of this electrolyte imbalance?
14. Arterial blood gas analysis shows pH7.48 , pCO2 28 mmHg , HCO3 22mEq/L
give acid base disorder
15. An unconscious diabetic patient while during management by intravenous
insulin and glucose infusion developed prolonged PR interval, T wave
flattening on ECG.Which plasma electrolyte abnormality he developed,its
cause and normal values?
16. What is normal blood Ph? Explain the role of plasma buffers and renal
mechanisms in acid base regulation of body?
17. Enlist various causes of respiratoy acidosis.
18.A patient of chronic renal failure was brought in state of unconsciousness. The
ECG picture displaying on cardiac monitor shows widening of QRS complex and
tall tented “T” wave.
(a) From which electrolyte abnormality he is suffering from?
(b) What are the normal plasma levels of this electrolytes due to to abnormality
of which he presented abnormal ECG pattern?
(c ) How body regulate this electrolyte?
26.Define metabolic acidosis. Give its causes and compensation?
▪ CANCER & XENOBIOTICS
1. A xenobiotic was transported through circulation into the liver. How liver will
metabolize it to convert it into water soluble excretable form?
2. Define tumor suppressor genes. How these are linked to carcinogenesis?
3. Enumerate the mechanism through which proto-oncogenes are converted to
oncogenes.
4. Write a note on tumor markers.
5. Define oncogenes and tumor suppressor genes. Give their relationship with
cancer.

6. Enlist different tumor markers along with the associated malignancies in which
their levels are raised.

7. Define oncogenes and tumor suppressor genes of the body. Give their
association with high incidence of cancer formation.

8. Define carcinogenesis. Which four basic concepts are involved in the process
of carcinogenesis?

9. In the process of detoxification of drugs what is the role of cytochrome P450

monooxygenase system, how induction of cytochrome P450 affects heme
synthesis, give its clinical implications.

10. Enlist five conjugation reactions which prepare xenobiotics for excretion in
phase 2 of their metabolism.

11. Elaborate the role of glucuronic acid and glutathione in the metabolism of
xenobiotics. Polymorphic forms of which phase 2 enzyme affect isoniazid
metabolism and how?

12. The hydroxylated products of phase 1 of Xenobiotics metabolism are

converted to soluble metabolites by help of phase 2 reaction by a process
called conjugation. Discuss the role of conjugating agents in detoxification
reactions.

13. Proto-oncogenes are normally present genes on DNA giving no harm to the
cells during their life and replication. When these proto-oncogenes are
mutated to oncogenes the products of these mutated genes become
uncontrolled and lead to cancer formation. Enumerate the mechanisms
through which proto-oncogenes are converted to oncogenes.

14. Define proto-oncogenes? Give three mechanisms of activation of proto-

oncongenes?