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Biochemistry and nutrition medical question bank

Practise every biochemistry and nutrition topic with explained SBAs.

Recall Engine has 1,000+ biochemistry and nutrition questions across 50+ topics in 6 body systems. Every question explains each option.

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Biochemistry and nutrition by body system

Biochemistry and nutrition has 50+ topics in 6 body systems. Each section shows how many questions it has and every topic it covers.

Cardiovascular

7 questions across 1 topic. It also has 1 topic note.

  • Cardiac biomarkers: troponin and CK

Respiratory

20+ questions across 1 topic. It also has 1 topic note.

  • Gas exchange in red blood cells

Endocrine and metabolic

300+ questions across 10+ topics. It also has 10+ topic notes.

  • Adrenal steroids: synthesis and action
  • Biochemical assay of cholesterol
  • Biochemical assay of glucose
  • Body mass index charts
  • Cholesterol assay and lipid profile
  • Control of blood glucose
  • Diabetes: insulin resistance and tests
  • Diabetes: types, glucose tests, and HbA1c
  • Hormone transport and signalling
  • Introduction to obesity
  • Nuclear hormone receptors
  • Undernutrition: starvation and protein-energy malnutrition
  • Vitamins: functions and deficiency

Musculoskeletal

90+ questions across 4 topics. It also has 4 topic notes.

  • Collagen, elastin, and bone matrix
  • Connective tissue: fibrous proteins
  • Muscle fuel selection and collagen disorders
  • Muscle proteins and contractile mechanisms

Blood and cancer

30+ questions across 3 topics. It also has 3 topic notes.

  • Glucose-6-phosphate dehydrogenase deficiency
  • Haemoglobinopathies
  • The red blood cell membrane

General principles

500+ questions across 20+ topics. It also has 20+ topic notes.

  • Amino acids and protein structure
  • Amino acids and their side chains
  • Carbohydrate metabolism: glycolysis, glycogen, and gluconeogenesis
  • Citric acid cycle: reactions and energy accounting
  • Citric acid cycle: regulation and metabolic integration
  • DNA, mRNA, and protein synthesis
  • Enzyme catalysis and kinetics
  • Enzyme regulation, inhibitors, and assays
  • Fat digestion and metabolism
  • Fat metabolism
  • Formation of ATP
  • Free radicals and antioxidants
  • Glucose transport and glycolysis
  • Glycogen and gluconeogenesis
  • Hormone immunoassays and reference intervals
  • Integration and control of metabolism: hormone signalling
  • Introduction to clinical biochemistry lab tests
  • Levels of protein structure
  • Macronutrients
  • Minerals: iron, iodine, zinc, and selenium
  • Molecular biology
  • Muscle fuel selection
  • Nutrients: requirements and sources
  • Overview of metabolism
  • Protein structure and function
  • Synthesis and storage of fat as an energy reserve
  • The integration and control of metabolism
  • The urea cycle and its control

Biochemistry and nutrition sample questions

These 4 are published biochemistry and nutrition questions shown exactly as students see them. Open an answer to see why it is right and why every other option is wrong.

Question 1 · Biochemistry and nutrition, Preclinical

Which role does phosphodiesterase play in G-protein coupled hormone signalling?

  1. A. It removes phosphate from phosphorylated proteins
  2. B. It phosphorylates proteins at serine or threonine
  3. C. It converts GTP into GDP on the α subunit
  4. D. It converts ATP into cAMP
  5. E. It converts cAMP into 5′-AMP
Show the answer and explanation

Answer: E. It converts cAMP into 5′-AMP

Phosphodiesterase converts cAMP into 5′-AMP. This degrades the second messenger and reverses the activation of PKA, which is one of three ways the hormonal action is terminated.

Why the other options are wrong

  • A. It removes phosphate from phosphorylated proteins: Phosphatases remove phosphate from phosphorylated proteins.
  • B. It phosphorylates proteins at serine or threonine: PKA phosphorylates cellular proteins at serine or threonine.
  • C. It converts GTP into GDP on the α subunit: The GTPase activity of the α subunit converts GTP into GDP.
  • D. It converts ATP into cAMP: Adenylyl cyclase catalyses the formation of cAMP from ATP.

Key point: Phosphodiesterase ends cAMP signalling by converting cAMP into 5′-AMP.

References

Question 2 · Biochemistry and nutrition, Preclinical

Fasted volunteers receive equal infusions of either propionate (a three-carbon fatty acid) or octanoate (an eight-carbon fatty acid). Hepatic glucose output rises with propionate but not with octanoate, although both are oxidised. Which explanation best accounts for the difference?

  1. A. Propionate is converted directly to glycerol in the liver
  2. B. Octanoate inhibits glucose-6-phosphatase in hepatocytes
  3. C. Octanoate cannot be oxidised by hepatic mitochondria
  4. D. Propionate raises insulin, which stimulates gluconeogenesis
  5. E. Propionyl-CoA becomes succinyl-CoA, a cycle intermediate
Show the answer and explanation

Answer: E. Propionyl-CoA becomes succinyl-CoA, a cycle intermediate

Odd-chain fatty acids such as propionate give propionyl-CoA, which is carboxylated to methylmalonyl-CoA and rearranged to succinyl-CoA. Succinyl-CoA is a citric acid cycle intermediate that adds net carbon to oxaloacetate, which can leave for gluconeogenesis. Even-chain octanoate yields only acetyl-CoA, which cannot give net glucose because the pyruvate dehydrogenase step is irreversible and the cycle loses two carbons as CO2.

Why the other options are wrong

  • A. Propionate is converted directly to glycerol in the liver: Propionate is not converted to glycerol; glycerol comes from triacylglycerol breakdown in adipose tissue.
  • B. Octanoate inhibits glucose-6-phosphatase in hepatocytes: Even-chain fatty acids do not inhibit glucose-6-phosphatase; they fail because they yield only acetyl-CoA.
  • C. Octanoate cannot be oxidised by hepatic mitochondria: The stem states that both are oxidised; medium-chain fatty acids are readily oxidised by the liver.
  • D. Propionate raises insulin, which stimulates gluconeogenesis: Insulin suppresses gluconeogenesis rather than stimulating it, so a rise in insulin would lower glucose output.

Key point: Gluconeogenic substrates include lactate, glycerol, glucogenic amino acids, and propionyl-CoA from odd-chain fatty acids, which enters the cycle as succinyl-CoA; acetyl-CoA from even-chain fatty acids gives no net glucose.

References

Question 3 · Biochemistry and nutrition, Preclinical

Inactive protein kinase A is an R2C2 hetero-tetramer. Which event frees its catalytic subunits so that they can phosphorylate cellular proteins?

  1. A. Binding of PIP3 to a PH domain
  2. B. Binding of four cAMP molecules to the two R subunits
  3. C. Hydrolysis of GTP to GDP by the Gα subunit
  4. D. Cross-phosphorylation of receptor tyrosine residues
  5. E. Exchange of GDP for GTP on the Gα subunit
Show the answer and explanation

Answer: B. Binding of four cAMP molecules to the two R subunits

Protein kinase A is an R2C2 hetero-tetramer. Binding of four cAMP molecules to the two R subunits makes them dissociate from the catalytic subunits, activating them.

Why the other options are wrong

  • A. Binding of PIP3 to a PH domain: PIP3 allows PDK1 and PKB to associate with the membrane via their PH domains.
  • C. Hydrolysis of GTP to GDP by the Gα subunit: The Gα subunit hydrolyses GTP to GDP and becomes inactive again.
  • D. Cross-phosphorylation of receptor tyrosine residues: On hormone binding, receptor tyrosine kinase monomers cross-phosphorylate each other.
  • E. Exchange of GDP for GTP on the Gα subunit: A hormone-bound receptor causes the exchange of GDP for GTP, activating the Gα subunit.

Key point: Four cAMP molecules binding the two R subunits release and activate the catalytic subunits of PKA.

References

Question 4 · Biochemistry and nutrition, Preclinical

A 15-month-old boy has failure to thrive and a firm, enlarged liver with signs of portal hypertension. Fasting glucose is usually normal. Liver biopsy shows cirrhosis and deposits of abnormal glycogen with long outer chains and very few branch points, which is poorly soluble. Which enzyme deficiency best explains these findings?

  1. A. Liver glycogen synthase
  2. B. Glycogen branching enzyme
  3. C. Glucose-6-phosphatase
  4. D. Liver glycogen phosphorylase
  5. E. Muscle glycogen phosphorylase
Show the answer and explanation

Answer: B. Glycogen branching enzyme

The branching enzyme moves a block of residues to make alpha-1,6 branches. Without it, glycogen forms long, poorly branched chains that are insoluble and accumulate as abnormal deposits, especially in liver, muscle, and heart. In the liver they damage cells and cause progressive cirrhosis with portal hypertension. Hypoglycaemia is not the main feature because glycogen breakdown and gluconeogenesis are largely intact.

Why the other options are wrong

  • A. Liver glycogen synthase: Glycogen synthase deficiency means little glycogen is made, so there would be no abnormal glycogen deposits in the liver.
  • C. Glucose-6-phosphatase: Glucose-6-phosphatase deficiency stores glycogen of normal structure and causes severe fasting hypoglycaemia, not early cirrhosis.
  • D. Liver glycogen phosphorylase: Liver phosphorylase deficiency stores normally structured glycogen and usually follows a mild course that improves with age.
  • E. Muscle glycogen phosphorylase: Muscle phosphorylase deficiency affects muscle during exercise and does not cause liver cirrhosis.

Key point: Branching enzyme deficiency produces long, poorly branched, insoluble glycogen that accumulates in liver, muscle, and heart, causing progressive cirrhosis rather than marked hypoglycaemia.

References

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