116 Exam Questions Answers and
Detailed Rationales
Question 1 — Renal Physiology
A 24-year-old man develops severe diarrhoea and vomiting
for 3 days. His blood pressure is 88/54 mmHg, and laboratory
studies show elevated BUN and creatinine. The fractional
excretion of sodium is 0.4%. Which renal adaptation is most
likely responsible for maintaining his glomerular filtration rate
during the early stages of volume depletion?
A. Constriction of the afferent arteriole
B. Increased renal prostaglandin degradation
C. Dilation of the afferent arteriole mediated by
prostaglandins
D. Increased resistance of the efferent arteriole caused by
nitric oxide
Rationale: In volume depletion, renal prostaglandins promote
afferent arteriolar dilation, helping preserve renal blood flow
and GFR. Sympathetic activation and angiotensin II
preferentially constrict the efferent arteriole, while
prostaglandins counteract excessive afferent vasoconstriction.
NSAIDs can impair this compensatory mechanism and
precipitate acute kidney injury.
,Question 2 — Immunology
A patient with recurrent infections is found to have a
mutation affecting the CD40 ligand expressed on activated T
lymphocytes. Which immunoglobulin abnormality is most
likely?
A. Increased IgA with decreased IgM
B. Increased IgE with decreased IgG
C. Increased IgM with decreased IgG, IgA, and IgE
D. Decreased IgM with increased IgG and IgA
Rationale: CD40 ligand on T cells interacts with CD40 on B
cells and is required for immunoglobulin class switching.
Deficiency causes hyper-IgM syndrome, characterised by
elevated or normal IgM with reduced IgG, IgA, and IgE.
Patients are susceptible to recurrent bacterial and
opportunistic infections.
Question 3 — Pharmacology
A 67-year-old patient with hypertension and benign prostatic
hyperplasia is started on a medication that improves urinary
flow but causes dizziness upon standing. Which receptor
blockade most directly explains this adverse effect?
A. β1-adrenergic receptor
B. M2 muscarinic receptor
C. α2-adrenergic receptor
D. α1-adrenergic receptor
,Rationale: α1 blockers such as tamsulosin and prazosin cause
vasodilation by preventing norepinephrine-mediated
contraction of vascular smooth muscle. This can produce
orthostatic hypotension. Tamsulosin is relatively selective for
α1A receptors in the prostate and therefore has less systemic
hypotension than nonselective α1 blockers.
Question 4 — Biochemistry
A child develops severe hypoglycaemia after prolonged
fasting. Laboratory testing reveals increased fatty acid
oxidation but inadequate ketone production. A deficiency of
which enzyme is most likely?
A. Glucose-6-phosphatase
B. Carnitine acyltransferase I
C. Mitochondrial HMG-CoA synthase
D. Hormone-sensitive lipase
Rationale: Mitochondrial HMG-CoA synthase catalyses a key
step in ketone-body synthesis. Deficiency prevents adequate
ketogenesis during fasting despite increased fatty acid
oxidation, producing hypoketotic hypoglycaemia. This
contrasts with defects in fatty acid oxidation, which also
produce impaired ketone formation but reduce fatty acid
utilisation itself.
Question 5 — Neurology
, A 72-year-old man develops sudden weakness of the right
face, arm, and leg. He also has loss of vibration and
proprioception on the right side of the body. Which vascular
territory is most likely affected?
A. Left anterior cerebral artery
B. Left posterior cerebral artery
C. Right posterior inferior cerebellar artery
D. Left middle cerebral artery
Rationale: The left MCA supplies the lateral cerebral
hemisphere, including the primary motor and sensory cortices
representing the contralateral face and upper limb, with
variable leg involvement. A large MCA infarct can therefore
cause contralateral hemiparesis and hemisensory loss.
Dominant-hemisphere involvement may additionally produce
aphasia.
Question 6 — Endocrinology
A woman with weight loss, tremor, heat intolerance, and
palpitations has a suppressed TSH and elevated free T4.
Radioactive iodine uptake is diffusely increased throughout
the thyroid gland. Which mechanism is responsible?
A. Destruction of thyroid follicles by cytotoxic T cells
B. Autonomous secretion of TSH by a pituitary adenoma
C. Autoantibodies stimulating the TSH receptor
D. Excessive conversion of T4 to reverse T3
Rationale: Graves disease results from thyroid-stimulating
immunoglobulins that bind and activate the TSH receptor.