NBCE Part I Practice Questions (2026) — Free Sample Questions with Answers

Answer: B

Lunate: The lunate is the carpal bone that most often dislocates, and it can undergo avascular necrosis (Kienböck disease). However, it lies proximal to the capitate, not in the snuffbox, and lunate fractures are uncommon.

Scaphoid: Correct. The scaphoid forms the floor of the anatomical snuffbox and is the carpal bone fractured most often. Its blood supply enters distally and runs retrograde, so the proximal pole is at risk of avascular necrosis and nonunion.

Hamate: Hook-of-hamate fractures usually come from grip sports such as golf or batting. They cause hypothenar pain, not snuffbox tenderness.

Trapezium: The trapezium sits at the base of the thumb, distal to the scaphoid. Fractures are uncommon and lack the classic retrograde blood-supply problem.

Snuffbox tenderness after a fall on an outstretched hand means a scaphoid fracture until proven otherwise. Retrograde blood flow puts the proximal pole at risk of avascular necrosis.

Answer: C

Right-sided loss of pain and temperature; left-sided loss of vibration and spastic weakness: This reverses the tracts. The spinothalamic tract has already crossed, so its loss is contralateral. The dorsal columns and corticospinal tract are uncrossed in the cord, so their loss is ipsilateral.

Bilateral loss of pain and temperature with preserved vibration sense and normal strength: This describes a central cord lesion, such as a syrinx, that interrupts crossing fibers in the anterior white commissure. It is not a hemisection.

Right-sided spastic weakness and loss of vibration; left-sided loss of pain and temperature: Correct. This is Brown-Séquard syndrome. The dorsal columns and lateral corticospinal tract are ipsilateral in the cord. Spinothalamic fibers cross within one to two segments, so pain and temperature are lost on the opposite side starting a level or two below the lesion.

Left-sided spastic weakness and loss of vibration; right-sided loss of pain and temperature: This mirror image would come from a left hemisection, not a right one. Both the side of the motor loss and the side of the sensory loss are reversed.

Brown-Séquard: ipsilateral motor loss and loss of proprioception/vibration, contralateral loss of pain and temperature, because only the spinothalamic tract has crossed within the cord.

Answer: D

Increased carotid sinus firing, which raises vagal tone and slows the heart: A fall in pressure reduces stretch of the carotid sinus, so baroreceptor firing decreases, not increases. Raising vagal tone would make the hypotension worse.

Decreased carotid sinus firing, which lowers sympathetic outflow and dilates arterioles: Lower baroreceptor firing disinhibits the vasomotor center, so sympathetic outflow rises, not falls. The arterioles constrict.

Increased carotid sinus firing, which raises sympathetic outflow and constricts arterioles: The efferent response is right, but the afferent step is wrong. Lower arterial pressure reduces, rather than increases, carotid sinus firing.

Decreased carotid sinus firing, which raises sympathetic outflow and heart rate: Correct. Less stretch means fewer afferent impulses (CN IX from the carotid sinus). The medulla responds by increasing sympathetic and decreasing vagal outflow, which raises heart rate, contractility and peripheral resistance.

Baroreceptor reflex: a fall in pressure → less stretch → less firing → more sympathetic and less parasympathetic outflow → blood pressure returns toward normal.

Answer: B

Km unchanged; Vmax decreased: This is noncompetitive inhibition. The inhibitor binds a site other than the active site and lowers the amount of functional enzyme.

Km increased; Vmax unchanged: Correct. A competitive inhibitor raises the apparent Km (more substrate is needed to reach half-maximal velocity). Enough substrate outcompetes it, so Vmax is unchanged.

Km decreased; Vmax decreased: Both parameters fall in uncompetitive inhibition, where the inhibitor binds only the enzyme–substrate complex.

Km increased; Vmax decreased: This combination describes mixed inhibition, in which the inhibitor binds both the free enzyme and the ES complex with different affinities.

Competitive: Km ↑, Vmax unchanged (Lineweaver–Burk lines cross on the y-axis). Noncompetitive: Vmax ↓, Km unchanged (lines cross on the x-axis).

Answer: B

Positive rheumatoid factor: Rheumatoid factor is typical of rheumatoid arthritis. The spondyloarthropathies are seronegative.

HLA-B27 positivity: Correct. Inflammatory back pain in a young man with bilateral sacroiliitis suggests ankylosing spondylitis. About 90% of patients of European ancestry with AS carry HLA-B27.

Anti-cyclic citrullinated peptide: Anti-CCP antibodies are highly specific for rheumatoid arthritis. They are not associated with axial spondyloarthritis.

Elevated serum uric acid: Hyperuricemia is linked to gout, which usually affects peripheral joints such as the first MTP. It does not cause bilateral sacroiliitis.

Ankylosing spondylitis: young man, inflammatory back pain that improves with activity, bilateral sacroiliitis, HLA-B27, and later a 'bamboo spine' from syndesmophytes.

Answer: B

Blocking acetylcholine release at the neuromuscular junction: This is the action of botulinum toxin, which causes descending flaccid paralysis, not spasms.

Blocking GABA and glycine release from spinal inhibitory interneurons: Correct. Tetanospasmin from Clostridium tetani travels retrograde to the CNS and cleaves synaptobrevin in Renshaw and other inhibitory interneurons. Unopposed motor neuron firing causes spastic paralysis, trismus and opisthotonos.

ADP-ribosylating elongation factor 2 in motor neurons: ADP-ribosylation of EF-2 is how diphtheria toxin and Pseudomonas exotoxin A act. They inhibit protein synthesis and do not cause spasms.

Persistently activating adenylate cyclase in skeletal muscle: Raised cAMP through G-protein activation is how cholera and pertussis toxins act. Neither causes tetanic spasms.

Tetanus toxin blocks inhibitory neurotransmitter release (spastic paralysis). Botulinum toxin blocks ACh release (flaccid paralysis). Both are zinc proteases that cleave SNARE proteins.