Biochemistry First year MBBS viva style 40 questions and answers on topic carbohydrates and its metabolism for revision and also writes down high yield theory exam questions based on PGIMS university rohtak

Reading File

Finding Sources

Searching the Web

PGIMS Rohtak university biochemistry first year MBBS syllabus carbohydrates metabolism exam pattern

Finding Sources

Reading File

I now have enough from the textbooks to compile a thorough, exam-oriented Q&A set. Let me generate the complete response now.

Biochemistry - Carbohydrates & Metabolism

First Year MBBS | Viva + Theory Exam Preparation

(Based on Standard 1st Year MBBS Curriculum | PGIMS Rohtak Pattern)

PART A: VIVA QUESTIONS & ANSWERS (40 Q&A)

SECTION 1: Chemistry of Carbohydrates

Q1. Define carbohydrates. A: Carbohydrates are polyhydroxy aldehydes or ketones, or compounds that yield them on hydrolysis. General formula is (CH2O)n. They serve as the primary energy source, structural components (cellulose, chitin), and signaling molecules (glycoproteins, glycolipids).

Q2. How are carbohydrates classified? Give examples. A:

Class	Definition	Examples
Monosaccharides	Cannot be hydrolyzed further	Glucose, Fructose, Galactose
Disaccharides	Yield 2 monosaccharides on hydrolysis	Sucrose, Lactose, Maltose
Oligosaccharides	Yield 3-10 monosaccharides	Raffinose
Polysaccharides	Yield >10 monosaccharides	Starch, Glycogen, Cellulose

Q3. What is the difference between aldoses and ketoses? A: Aldoses have an aldehyde group (e.g., glucose, galactose). Ketoses have a ketone group (e.g., fructose). The position of the carbonyl group determines this classification.

Q4. What are epimers? Give an example. A: Epimers are monosaccharides that differ in configuration at only ONE carbon atom (other than the anomeric carbon). Example: Glucose and Galactose are epimers - they differ at C-4. Glucose and Mannose differ at C-2.

Q5. What are anomers? What is mutarotation? A: Anomers are isomers that differ in configuration only at the anomeric carbon (C-1 in aldoses, C-2 in ketoses). Alpha (α) form has -OH below the plane; Beta (β) form has -OH above the plane (in Fischer projection). Mutarotation is the spontaneous interconversion between α and β anomers in solution until equilibrium is reached (e.g., glucose equilibrates to ~36% α and ~64% β).

Q6. What are reducing sugars? Which disaccharides are non-reducing? A: Reducing sugars have a free anomeric carbon (free aldehyde or ketone group) that can reduce oxidizing agents (Cu²⁺ in Benedict's/Fehling's test). All monosaccharides are reducing. Lactose and Maltose are reducing disaccharides. Sucrose is non-reducing because both anomeric carbons are involved in the glycosidic bond.

Q7. Differentiate between starch and glycogen. A:

Feature	Starch	Glycogen
Source	Plant	Animal/Fungi
Branching	Less (every 25-30 glucose)	More (every 8-12 glucose)
Components	Amylose + Amylopectin	Only glycogen
Iodine test	Blue-black	Reddish-brown
Chain length	Longer	Shorter

Q8. What is the composition of sucrose, lactose, and maltose? A:

Sucrose: Glucose + Fructose (α1→β2 glycosidic bond)
Lactose: Galactose + Glucose (β1→4 glycosidic bond) - "milk sugar"
Maltose: Glucose + Glucose (α1→4 glycosidic bond) - product of starch digestion

Q9. What is the significance of the GLUT transporters? A: Glucose enters cells via facilitated diffusion through GLUT proteins (GLUT-1 to GLUT-14), which are Na+/ATP-independent uniporters:

GLUT-1: Most tissues; RBCs, brain (basal uptake)
GLUT-2: Liver, kidney, pancreatic β-cells (low affinity, high capacity - acts as glucose sensor)
GLUT-3: Brain (high affinity)
GLUT-4: Muscle and adipose - insulin-dependent (most important clinically)
GLUT-5: Fructose transport (jejunum, testes)

GLUT-4 is the key insulin-responsive transporter - its defective action underlies Type 2 DM.

SECTION 2: Glycolysis

Q10. Define glycolysis. Where does it occur? A: Glycolysis is the metabolic pathway that converts one molecule of glucose (6C) into two molecules of pyruvate (3C), generating 2 ATP and 2 NADH. It occurs in the cytoplasm (cytosol) of all cells. It is universal - present in all organisms.

Q11. What are the 3 irreversible (regulatory) steps of glycolysis? A:

Step 1: Glucose → Glucose-6-phosphate (enzyme: Hexokinase/Glucokinase, uses ATP)
Step 3: Fructose-6-phosphate → Fructose-1,6-bisphosphate (enzyme: Phosphofructokinase-1 / PFK-1 - the rate-limiting step)
Step 10: Phosphoenolpyruvate → Pyruvate (enzyme: Pyruvate Kinase)

Mnemonic: "HePK" - Hexokinase, PFK-1, Pyruvate Kinase.

Q12. What is the net ATP yield from one molecule of glucose in glycolysis? A: - 2 ATP consumed (steps 1 & 3) - 4 ATP produced (steps 7 & 10) - Net = 2 ATP + 2 NADH per glucose molecule.

Q13. What is the difference between Hexokinase and Glucokinase? A:

Feature	Hexokinase	Glucokinase
Location	Most tissues	Liver, pancreatic β-cells
Km for glucose	Low (~0.1 mM) - high affinity	High (~10 mM) - low affinity
Inhibition	Product-inhibited by G-6-P	NOT inhibited by G-6-P
Km	Not induced by insulin	Induced by insulin
Function	Traps glucose at low levels	Glucose sensor; handles high post-meal glucose

Q14. What is PFK-1 and how is it regulated? A: Phosphofructokinase-1 (PFK-1) catalyzes the rate-limiting step of glycolysis (Fructose-6-P → Fructose-1,6-bisphosphate).

Activated by: AMP, ADP, Fructose-2,6-bisphosphate (most potent), Pi, low pH (mild)
Inhibited by: ATP, Citrate, low pH (severe), glucagon (via decreased F-2,6-BP)

F-2,6-bisphosphate is the most potent allosteric activator - formed by PFK-2 (bifunctional enzyme).

Q15. What happens to pyruvate under aerobic vs anaerobic conditions? A:

Aerobic conditions: Pyruvate enters mitochondria → converted to Acetyl-CoA by pyruvate dehydrogenase complex (PDH) → enters TCA cycle
Anaerobic conditions (or RBCs): Pyruvate → Lactate (catalyzed by Lactate Dehydrogenase, LDH), regenerating NAD+ for continued glycolysis

Q16. What is the Pasteur effect? A: The Pasteur effect is the inhibition of glycolysis (and lactate formation) by oxygen. Under aerobic conditions, oxidative phosphorylation produces ATP efficiently, raising ATP levels which inhibit PFK-1, thereby slowing glycolysis. In anaerobic conditions, glycolysis is maximally activated to compensate for low ATP production.

Q17. What is the Warburg effect? A: Cancer cells preferentially use aerobic glycolysis (glycolysis → lactate, even in the presence of O2) rather than oxidative phosphorylation. This "aerobic glycolysis" or Warburg effect provides rapid ATP production and biosynthetic intermediates for rapidly dividing cells. This is the basis for PET scan (tumor cells uptake more [18F]-FDG).

SECTION 3: Pyruvate Dehydrogenase & TCA Cycle

Q18. What cofactors are required by the Pyruvate Dehydrogenase Complex (PDC)? A: PDC requires 5 cofactors derived from B vitamins:

TPP (Thiamine Pyrophosphate) - Vitamin B1
Lipoic acid (Lipoamide)
FAD - Vitamin B2 (Riboflavin)
NAD+ - Vitamin B3 (Niacin)
CoA - Pantothenic acid (Vitamin B5)

Mnemonic: "TL FNC" = TPP, Lipoate, FAD, NAD+, CoA

Q19. What is the product of PDC reaction and how much energy is generated? A: Pyruvate + CoA + NAD+ → Acetyl-CoA + CO2 + NADH. Each NADH produces ~2.5 ATP in the ETC. PDC is irreversible - it is the "metabolic bridge" committing pyruvate to the TCA cycle. Deficiency of PDC (e.g., B1 deficiency) causes lactic acidosis.

Q20. Name all the enzymes of the TCA cycle in order. A:

Citrate synthase (OAA + Acetyl-CoA → Citrate)
Aconitase (Citrate → Isocitrate)
Isocitrate dehydrogenase (rate-limiting; 1st CO2, 1st NADH)
α-Ketoglutarate dehydrogenase (2nd CO2, 2nd NADH)
Succinyl-CoA synthetase (produces GTP = 1 ATP equivalent)
Succinate dehydrogenase (produces FADH2) - embedded in inner mitochondrial membrane
Fumarase (Fumarate → Malate)
Malate dehydrogenase (3rd NADH)

Q21. What is the total ATP yield per acetyl-CoA in the TCA cycle? A: Per turn of TCA cycle (one Acetyl-CoA):

3 NADH × 2.5 ATP = 7.5 ATP
1 FADH2 × 1.5 ATP = 1.5 ATP
1 GTP = 1 ATP
Total = 10 ATP per Acetyl-CoA

Q22. What is the total ATP yield from complete oxidation of one glucose molecule? A:

Glycolysis: 2 ATP + 2 NADH (cytoplasmic)
PDC: 2 NADH (mitochondrial)
TCA (×2): 6 NADH + 2 FADH2 + 2 GTP
Total ATP = ~30-32 ATP (modern estimate using P/O ratios of 2.5 for NADH and 1.5 for FADH2)

Old textbook value: 38 ATP. PGIMS exams may accept 36-38.

Q23. Which TCA enzyme is inhibited by fluoroacetate (rat poison)? A: Fluoroacetate is converted to fluorocitrate in the cell, which inhibits aconitase - causing citrate accumulation and blocking the TCA cycle. This is clinically relevant as a case of poisoning.

SECTION 4: Gluconeogenesis

Q24. What is gluconeogenesis? What are its major substrates? A: Gluconeogenesis is the synthesis of glucose from non-carbohydrate precursors. It occurs mainly in the liver (90%) and kidney cortex (10%). Major substrates (glucogenic precursors):

Lactate (most important - Cori cycle)
Glycerol (from triglyceride breakdown)
Alanine & Glutamine (most important gluconeogenic amino acids - glucose-alanine cycle)
Other glucogenic amino acids
Propionate (from odd-chain fatty acids)

Note: Fatty acids (even-chain) CANNOT be used for gluconeogenesis.

Q25. What are the 3 bypass reactions in gluconeogenesis (that bypass irreversible glycolytic steps)? A:

Glycolytic step	Gluconeogenic bypass enzyme
Pyruvate Kinase	Pyruvate Carboxylase (Pyr → OAA) + PEPCK (OAA → PEP)
PFK-1	Fructose-1,6-bisphosphatase (F-1,6-BP → F-6-P)
Hexokinase/Glucokinase	Glucose-6-phosphatase (G-6-P → Glucose) - liver only

Q26. What is the role of biotin in gluconeogenesis? A: Biotin is the cofactor for Pyruvate Carboxylase, which catalyzes the first step of gluconeogenesis in the mitochondria: Pyruvate + CO2 + ATP → Oxaloacetate. This is a carboxylation reaction requiring biotin as the CO2 carrier. Biotin deficiency impairs gluconeogenesis.

Q27. What is the Cori cycle? What is its physiological significance? A: The Cori cycle (lactic acid cycle) describes the recycling of lactate between muscle and liver:

Muscle performs anaerobic glycolysis → lactate → released into blood
Liver takes up lactate → converts to glucose via gluconeogenesis → glucose released to blood → muscle

Significance: Allows muscle to continue working under anaerobic conditions. The energy cost: liver uses 6 ATP to regenerate glucose, muscle uses only 2 ATP - net energy transfer from liver to muscle.

SECTION 5: Glycogen Metabolism

Q28. What is the structure of glycogen? Name the key enzymes. A: Glycogen is a branched homopolysaccharide of glucose:

Main chain: α1→4 glycosidic bonds
Branch points: α1→6 glycosidic bonds (every 8-12 glucose units)
Key synthesis enzymes: Glycogen synthase (α1→4 bonds), Branching enzyme (creates α1→6 branch points)
Key degradation enzymes: Glycogen phosphorylase (cleaves α1→4), Debranching enzyme (cleaves α1→6)
Primer protein: Glycogenin (self-glucosylating protein that initiates glycogen synthesis)

Q29. What activates and inhibits glycogen synthase and glycogen phosphorylase? A:

	Glycogen Synthase (synthesis)	Glycogen Phosphorylase (breakdown)
Activated by	Glucose-6-P, Insulin (dephosphorylation)	Glucagon/Epinephrine (phosphorylation), AMP, Ca²+
Inhibited by	Glucagon, Epinephrine (phosphorylation)	Glucose-6-P, Glucose, ATP, Insulin

Key rule: Phosphorylated form of glycogen phosphorylase (a) = ACTIVE; Phosphorylated glycogen synthase = INACTIVE.

Q30. What is the role of UDP-glucose in glycogen synthesis? A: UDP-glucose is the activated form of glucose used in glycogen synthesis. Glucose-1-phosphate + UTP → UDP-glucose + PPi (catalyzed by UDP-glucose pyrophosphorylase). Glycogen synthase then transfers glucose from UDP-glucose to the non-reducing end of the glycogen chain, forming an α1→4 linkage and releasing UDP.

Q31. What are Glycogen Storage Diseases (GSDs)? Name clinically important ones. A: GSDs are inherited enzyme deficiencies causing abnormal glycogen accumulation. Key ones:

Type	Name	Deficient Enzyme	Features
I	Von Gierke's	Glucose-6-phosphatase	Hypoglycemia, hepatomegaly, lactic acidosis
II	Pompe's	Lysosomal α-1,4-glucosidase (acid maltase)	Cardiomegaly, hypotonia - only GSD with lysosomal involvement
III	Cori's	Debranching enzyme	Milder than Type I
V	McArdle's	Muscle phosphorylase	Exercise intolerance, myoglobinuria, no rise in blood lactate on exercise
VI	Hers'	Liver phosphorylase	Hepatomegaly, mild hypoglycemia

SECTION 6: HMP Shunt (Pentose Phosphate Pathway)

Q32. What is the HMP shunt? What are its products and significance? A: The HMP shunt (Hexose Monophosphate pathway / Pentose Phosphate Pathway) is an alternative pathway of glucose oxidation in the cytoplasm.

Products: NADPH (reducing power) and Ribose-5-phosphate (precursor for nucleotides)
Occurs in: Liver, RBCs, adrenal cortex, mammary gland, testes (metabolically active tissues)
Clinical significance: NADPH is needed for:
- Reductive biosynthesis (fatty acid, steroid synthesis)
- Regeneration of reduced glutathione (protects RBCs from oxidative damage)
- NADPH oxidase (phagocyte killing)

Q33. What is G6PD deficiency? What is its clinical significance? A: Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is the most common enzyme deficiency worldwide (X-linked recessive). G6PD catalyzes the first step of HMP shunt (G-6-P → 6-Phosphoglucono-δ-lactone), generating NADPH.

Without NADPH, RBCs cannot regenerate reduced glutathione → oxidative stress → hemolysis.

Triggers: Primaquine, dapsone, fava beans, infections
Lab finding: Heinz bodies (denatured hemoglobin in RBCs), bite cells on blood smear
Test: Brilliant cresyl blue dye decolorization

Q34. Why is the HMP shunt important in the adrenal cortex? A: Steroidogenesis requires NADPH for cytochrome P450 hydroxylation reactions. The adrenal cortex has very high HMP shunt activity to supply NADPH for steroid hormone synthesis.

SECTION 7: Regulation of Blood Glucose

Q35. What is the normal blood glucose level? How is it regulated? A:

Fasting blood glucose: 70-110 mg/dL (3.9-6.1 mmol/L)
Postprandial (2-hr): <140 mg/dL

Regulation:

Lowering: Insulin (only hypoglycemic hormone)
Raising: Glucagon, Epinephrine (Adrenaline), Cortisol, Growth Hormone, Thyroid hormones - the "counter-regulatory hormones"

Q36. What is the biochemical basis of diabetes mellitus? A:

Type 1 DM: Autoimmune destruction of β-cells → absolute insulin deficiency → no GLUT-4 recruitment → hyperglycemia, lipolysis, ketogenesis → DKA
Type 2 DM: Peripheral insulin resistance → relative insulin deficiency → hyperglycemia; Glucokinase is reduced in β-cells → impaired glucose sensing

Key biochemical features: Hyperglycemia, glycosuria (when blood glucose exceeds renal threshold ~180 mg/dL), ketonemia, ketonuria (Type 1).

Q37. What is HbA1c and why is it clinically important? A: HbA1c (glycated hemoglobin) is formed by non-enzymatic glycosylation of hemoglobin A (at the N-terminal valine of beta chains). It reflects average blood glucose over the previous 2-3 months (lifespan of RBC).

Normal: <5.7%
Pre-diabetes: 5.7-6.4%
Diabetes: ≥6.5%

It is the gold standard for monitoring long-term glycemic control in diabetic patients.

Section 8: Fructose & Galactose Metabolism

Q38. What are the disorders of fructose metabolism? A:

Essential fructosuria: Deficiency of Fructokinase - benign, fructose appears in urine - no symptoms
Hereditary Fructose Intolerance (HFI): Deficiency of Aldolase B - accumulation of Fructose-1-phosphate → inhibits glycogenolysis and gluconeogenesis → severe hypoglycemia after fructose/sucrose intake; liver damage

Key distinction: HFI is serious; essential fructosuria is benign.

Q39. What is Galactosemia? How does it present? A: Galactosemia is a disorder of galactose metabolism due to deficiency of Galactose-1-phosphate uridyltransferase (GALT) - classic galactosemia (most common and severe).

Galactose-1-P accumulates → toxic to liver, brain, lens
Presents in neonates: jaundice, vomiting, E. coli sepsis, cataracts, intellectual disability
Cataracts occur due to galactitol accumulation in the lens (via aldose reductase)
Screening: Newborn screening test; treatment = lactose-free diet

Q40. What is the glucose-alanine cycle? A: The glucose-alanine cycle is the equivalent of the Cori cycle but involving amino acids:

Muscle: Pyruvate from glycolysis + glutamate → Alanine (transamination via ALT)
Alanine released into blood → liver
Liver: Alanine → Pyruvate + glutamate (transamination) → Pyruvate → Glucose (gluconeogenesis)
Glucose returns to muscle

Significance: Transfers nitrogen from muscle to liver (for urea synthesis) and carbon skeleton for hepatic gluconeogenesis. This is why plasma alanine rises during fasting/starvation.

PART B: HIGH-YIELD THEORY EXAM QUESTIONS

(PGIMS Rohtak Pattern - 1st Year MBBS Biochemistry)

LONG ESSAY QUESTIONS (10 Marks)

Describe glycolysis in detail - mention all steps, enzymes, energetics, regulation, and clinical significance of anaerobic glycolysis. Add a note on the Warburg effect.
Write an essay on gluconeogenesis - substrates, pathway, bypass reactions, key enzymes, regulation by glucagon and cortisol. Describe the Cori cycle and glucose-alanine cycle.
Describe glycogen synthesis and degradation. Include the role of glycogenin, UDP-glucose, branching/debranching enzymes, hormonal regulation (insulin vs glucagon/epinephrine), and classify glycogen storage diseases with clinical features.
Write in detail about the TCA (Krebs) cycle - reactions, enzymes, cofactors, energy yield, amphibolic nature, and clinical importance (anaplerotic reactions, relationship to amino acid metabolism).

SHORT ESSAY QUESTIONS (5 Marks)

HMP shunt (Pentose Phosphate Pathway) - reactions, significance, and NADPH roles.
G6PD deficiency - pathophysiology, clinical features, trigger factors, lab findings.
Classification of carbohydrates with examples.
Pyruvate Dehydrogenase Complex (PDC) - components, cofactors, reaction, regulation.
Regulation of blood glucose level - hormonal and metabolic mechanisms.
Hereditary Fructose Intolerance vs Essential Fructosuria - comparison.
Galactosemia - enzyme defect, pathophysiology, clinical features, treatment.
Glucose transporters (GLUTs) - types, tissue distribution, clinical relevance.
Hexokinase vs Glucokinase - differences and clinical significance.
Regulation of glycolysis at PFK-1 - role of F-2,6-bisphosphate.

SHORT ANSWER QUESTIONS (2-3 Marks)

What are anomers? Define mutarotation.
Name the irreversible steps of glycolysis and their enzymes.
What is the net ATP yield from glycolysis?
What is the Pasteur effect?
Name the cofactors of Pyruvate Dehydrogenase Complex.
What is the rate-limiting enzyme of the TCA cycle?
Name the two enzymes unique to gluconeogenesis.
What is glycogenin?
Name glycogen storage diseases with their enzyme defects.
What is the Cori cycle? Name the organs involved.
What is the renal threshold for glucose?
Define HbA1c. What does it reflect?
What is the difference between McArdle's disease and Von Gierke's disease?
What are Heinz bodies?
Name products of the HMP shunt and their uses.
What are non-reducing sugars? Give one example.

IMPORTANT ONE-LINERS FOR VIVA / SPOT QUESTIONS

Question	Answer
Rate-limiting enzyme of glycolysis	PFK-1
Rate-limiting enzyme of TCA cycle	Isocitrate dehydrogenase
Only hypoglycemic hormone	Insulin
Enzyme unique to gluconeogenesis	Pyruvate carboxylase, PEPCK, F-1,6-BPase, G-6-Pase
Enzyme committing glucose to glycolysis	PFK-1
Glucose stored as in liver/muscle	Glycogen
Only GSD with lysosomal involvement	Pompe's disease (Type II)
Primer for glycogen synthesis	Glycogenin
Most potent activator of PFK-1	Fructose-2,6-bisphosphate
Vitamin required by pyruvate carboxylase	Biotin (B7)
Substrate level phosphorylation in TCA	Succinyl-CoA synthetase
Enzyme inhibited by fluoroacetate	Aconitase
Classic galactosemia - enzyme defect	Galactose-1-P uridyltransferase
Benign fructose disorder	Essential fructosuria (fructokinase deficiency)

Sources: Lippincott Illustrated Reviews Biochemistry (8th ed), Basic Medical Biochemistry - A Clinical Approach (6th ed), Harper's Illustrated Biochemistry (32nd ed). All content aligned with the standard 1st year MBBS syllabus as prescribed under MCI/NMC guidelines followed at PGIMS Rohtak.

This is a shared conversation. Sign in to Orris to start your own chat.