Nucleic Acid Structure
DNA is double-stranded. Why does the sequence on one strand determine the other?
Complementary base pairing (A-T, G-C) ensures sequence on one strand dictates the other.
DNA replication is semi-conservative. What does this mean?
Each new DNA molecule contains one old strand and one newly synthesized strand.
Proteins are made of amino acids. Why is sequence critical?
Determines folding → function.
Blood pH = 7.3. Slightly acidic. Classify as acidosis or alkalosis.
Acidosis.
Vitamin C deficiency → scurvy. Explain molecular reasoning.
Collagen hydroxylation impaired → weak connective tissue → bleeding gums, bruising
RNA has uracil instead of thymine. Predict how this affects hydrogen bonding and stability compared to DNA
Uracil forms normal H-bonds with A; RNA less stable due to single-stranded nature and lack of 5-methyl group.
mRNA is synthesized from DNA. If RNA polymerase reads the template strand 3'-5', what direction is the RNA sythesized?
5'-3' direction
Polysaccharide with β-linkages. Predict digestibility in humans.
Humans lack β-glycosidase → cannot digest
Metabolic acidosis: HCO₃⁻ low. Predict compensatory respiratory change.
Hyperventilation → decreased CO₂ to raise pH.
Vitamin D deficiency → rickets. Explain link to calcium absorption.
Reduced intestinal Ca²⁺ absorption → weak bones.
A patient has a mutation that adds extra methyl groups to DNA bases. How could this affect replication and gene expression?
Methylation may block polymerase binding or transcription factors leading to altered replication and gene silencing.
A mutation in a tRNA’s anticodon loop occurs. Predict the effect on translation.
Misreading of codons → wrong amino acid incorporation → defective proteins.
Lipid bilayer: why amphipathic nature essential for membrane formation?
Hydrophilic heads face water, hydrophobic tails inside → spontaneous bilayer formation
Patient has vomiting-induced alkalosis. Explain mechanism.
Loss of H⁺ from stomach → increased blood pH → metabolic alkalosis
Vitamin B12 deficiency → neurological symptoms. Explain reasoning.
Impaired myelin synthesis → nerve dysfunction.
Circular DNA of mitochondria is more prone to mutations than nuclear DNA. Explain using structure and repair mechanisms.
Mitochondrial DNA lacks protective histones, has less repair machinery so higher mutation rate.
Topoisomerase inhibitor drug blocks DNA replication in cancer cells. Explain the molecular mechanism.
Prevents relaxation of supercoiled DNA → replication fork stalls → apoptosis in rapidly dividing cells.
Misfolded protein accumulates. Predict cellular consequences.
ER stress, unfolded protein response, potential apoptosis.
Diabetic ketoacidosis patient: pH drops. Explain respiratory compensation.
Kussmaul breathing → deep rapid breaths → blow off CO₂ → partially correct pH
Vitamin K needed for clotting. Predict effect of warfarin therapy.
Inhibits vitamin K recycling → decreased clotting factor activation → bleeding tendency
In a cancer patient, guanine oxidation leads to mispairing during replication. Predict the base-pairing error and its consequence.
A damaged DNA base (8‑oxoG) can pair with the wrong partner, causing a G to be replaced by a T in the DNA.
A patient has a nonsense mutation in a critical enzyme gene. Predict molecular consequence and link to potential clinical symptoms.
Premature stop codon → truncated nonfunctional protein → enzymatic deficiency → clinical phenotype
Glycoprotein mutation disrupts N-linked glycosylation. Predict the effect on cell-cell communication.
Impaired recognition/signalling → altered immune or adhesion responses.
Mixed disorder suspected: pH low, HCO₃⁻ low, pCO₂ high. Use logic to predict mixed respiratory/metabolic disorder.
Primary metabolic acidosis with respiratory acidosis compensation failing → mixed disorder
Hypervitaminosis A → headache, nausea, liver damage. Explain molecular basis
Excess stored in liver → hepatotoxicity and intracranial pressure; fat-soluble → accumulates.