NRE Step 1 Physiology MCQs
12 sample questions from the 235 Physiology questions in NRE-1 Prep. Choose an answer to see why it is right and why each other option is wrong.
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Sample Physiology questions
1. A 30-year-old man has had profuse watery diarrhoea for 3 days. ABG: pH 7.28, PaCO₂ 30 mmHg, HCO₃⁻ 14 mmol/L. Na⁺ 138, Cl⁻ 114 mmol/L. What is the acid–base disturbance?
Answer: Normal anion gap metabolic acidosis. pH low with low HCO₃⁻ = metabolic acidosis. Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻) = 138 − (114 + 14) = 10, which is normal (≈8–12). Diarrhoea loses bicarbonate and the kidney retains chloride, giving a hyperchloraemic picture. Respiratory compensation is appropriate: Winter’s formula predicts PaCO₂ = 1.5 × 14 + 8 = 29 ± 2 mmHg.
- High anion gap metabolic acidosis: The anion gap is 138 − (114 + 14) = 10, which is normal.
- Respiratory acidosis: Respiratory acidosis needs a raised PaCO₂; here it is low, reflecting compensation for a metabolic acidosis.
- Mixed metabolic and respiratory alkalosis: The pH of 7.28 is acidaemic, so any alkalosis cannot be the primary disturbance.
2. Five years after a total gastrectomy for gastric cancer, a 60-year-old man has tiredness, a sore tongue and numbness in his feet. MCV is 112 fL. Which loss explains his anaemia?
Answer: Loss of intrinsic factor. Parietal cells in the stomach body secrete both acid and intrinsic factor. Vitamin B12 must bind intrinsic factor to be absorbed in the terminal ileum. After total gastrectomy B12 stores (2–5 years’ supply) run out, causing macrocytic anaemia and subacute combined degeneration of the cord. Patients need lifelong intramuscular hydroxocobalamin.
- Loss of duodenal iron uptake: Gives microcytosis and no neuropathy.
- Loss of gastric acid for folate: Folate deficiency doesn’t cause neuropathy.
- Loss of gastrin: Losing gastrin reduces acid stimulation but does not cause anaemia; macrocytosis with neuropathy is B12 deficiency from loss of intrinsic factor.
3. A blood film shows a white cell with a bilobed nucleus and large orange-red granules. The patient has asthma and a worm infestation. Which cell is this?
Answer: Eosinophil. Eosinophils have bilobed nuclei and orange-red (eosin-staining) granules containing major basic protein. They fight helminths and are raised in allergy/asthma, parasites, drug reactions, Addison’s and some cancers (Hodgkin). Basophils have dark blue-purple granules (histamine) and are raised in CML. Neutrophils are multilobed with pale granules.
- Basophil: Dark purple granules; raised in CML.
- Neutrophil: 3–5 lobes, pale granules; bacterial infection.
- Monocyte: Monocytes are large cells with a kidney-shaped nucleus and no orange granules.
4. In a ventricular myocyte action potential, which ion movement produces the plateau (phase 2), and which drug class prolongs repolarisation (phase 3) by blocking K⁺ channels?
Answer: Ca²⁺ influx — class III. Ventricular myocyte action potential: phase 0 — rapid Na⁺ influx (fast Na⁺ channels; class I drugs block); phase 1 — transient K⁺ efflux; phase 2 — plateau from L-type Ca²⁺ influx balanced by K⁺ efflux (Ca²⁺ triggers contraction; prevents tetany by long refractory period); phase 3 — repolarisation by delayed rectifier K⁺ efflux (IKr/hERG — class III drugs and many QT-prolonging drugs block); phase 4 — resting (IK1). QT prolongation (drugs, low K/Mg/Ca, congenital) → torsades de pointes → IV magnesium.
- Na⁺ influx — class I: Phase 0; class I blocks Na⁺.
- Ca²⁺ influx — class IV: Class IV blocks Ca²⁺, not K⁺.
- K⁺ efflux — class II: K⁺ efflux causes repolarisation, and class II drugs are beta-blockers.
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5. In the testis, which cells produce testosterone and which hormone stimulates them; which cells support spermatogenesis and respond to FSH?
Answer: Leydig (LH) testosterone; Sertoli (FSH). Leydig (interstitial) cells: LH → testosterone (local high concentration needed for spermatogenesis; negative feedback on LH/GnRH). Sertoli cells (within seminiferous tubules): FSH + testosterone → support and nourish developing sperm, blood–testis barrier, androgen-binding protein, inhibin B (negative feedback on FSH), AMH (fetal regression of Müllerian ducts). Spermatogenesis takes ~74 days (so repeat semen analysis after ~3 months). Exogenous testosterone/anabolic steroids suppress LH/FSH → testicular atrophy and azoospermia. 5α-reductase converts testosterone to DHT (prostate, external genitalia, hair).
- Sertoli (LH) testosterone; Leydig (FSH): Cells reversed — Leydig cells (LH) make testosterone; Sertoli (FSH) support sperm.
- Leydig (FSH) testosterone; Sertoli (LH): The hormones are reversed: LH stimulates Leydig cells and FSH stimulates Sertoli cells.
- Spermatogonia make testosterone: Germ cells (spermatogonia) do not make testosterone.
6. Which enzyme from the duodenal brush border starts the activation of pancreatic proteases?
Answer: Enteropeptidase. Enterokinase (brush border of duodenum) converts trypsinogen → trypsin; trypsin then activates more trypsinogen and other zymogens (chymotrypsinogen, procarboxypeptidase, proelastase, prophospholipase). Pancreatic trypsin inhibitor (SPINK1) prevents premature activation in the pancreas — mutations (and PRSS1) cause hereditary pancreatitis. Congenital enterokinase deficiency → protein malabsorption, oedema, failure to thrive.
- Trypsin inhibitor: Trypsin inhibitor prevents activation.
- Gastric pepsin: Pepsin acts in the stomach.
- Duodenal secretin: Secretin is a hormone, not an enzyme.
7. Which receptors respond mainly to a fall in arterial PO₂ (below ~8 kPa) to increase ventilation?
Answer: Carotid and aortic bodies. Peripheral chemoreceptors (carotid bodies — glossopharyngeal nerve; aortic bodies — vagus): sense low PaO₂ (especially < 8 kPa), also high PaCO₂ and H⁺ — rapid response; only receptors responding to hypoxia. Central chemoreceptors (ventral medulla): respond to H⁺ in CSF from CO₂ (CO₂ crosses BBB) — main drive in health; adapt in chronic hypercapnia (COPD), leaving hypoxic drive. J receptors (juxtacapillary): pulmonary congestion → dyspnoea, tachypnoea. Hering–Breuer: inflation reflex.
- Central medullary chemoreceptors: Central chemoreceptors respond to CO₂ and H⁺.
- Pulmonary stretch receptors: Stretch receptors mediate the Hering–Breuer reflex.
- J receptors: J receptors respond to interstitial oedema.
8. Atrial stretch in heart failure releases a hormone that increases sodium excretion and causes vasodilation. Which is it?
Answer: Atrial natriuretic peptide. ANP (atria) and BNP (ventricles) are released with myocardial stretch → natriuresis, diuresis, vasodilation, inhibit renin/aldosterone/ADH — counter-regulatory to RAAS. BNP/NT-proBNP used to diagnose heart failure (high negative predictive value; raised also in renal failure, AF, age; lower in obesity). Neprilysin degrades natriuretic peptides — sacubitril (neprilysin inhibitor) with valsartan (ARNI) in HFrEF.
- Adrenal aldosterone: Aldosterone retains sodium.
- Angiotensin II peptide: Angiotensin II causes vasoconstriction.
- Antidiuretic hormone: ADH retains water.
9. Rubbing an injured area reduces pain because large-diameter Aβ fibres activate inhibitory interneurons in which region?
Answer: Substantia gelatinosa. Gate control theory (Melzack and Wall): Aβ (touch) fibres activate inhibitory interneurons in the substantia gelatinosa (lamina II) of the dorsal horn, reducing transmission from nociceptive Aδ (fast, sharp) and C (slow, burning) fibres to projection neurons; descending inhibition from periaqueductal grey and rostral ventromedial medulla (endogenous opioids, serotonin, noradrenaline) also gates pain. Basis of TENS, acupuncture, rubbing.
- Ventral horn grey matter: The ventral horn is motor.
- Ventral posterior thalamus: The thalamus is a relay, not the gate.
- Primary motor cortex: The motor cortex does not gate pain.
10. In smooth muscle, Ca²⁺ binds calmodulin to activate which enzyme that initiates contraction?
Answer: Myosin light-chain kinase. Smooth muscle: Ca²⁺ (from extracellular influx and SR via IP3) binds calmodulin → activates myosin light-chain kinase (MLCK) → phosphorylates myosin light chain → cross-bridge cycling; relaxation via myosin light-chain phosphatase (activated by NO → cGMP → PKG; inhibited by Rho kinase). Skeletal/cardiac muscle: Ca²⁺ binds troponin C → tropomyosin shifts. Nitrates/PDE5 inhibitors relax smooth muscle via cGMP; β2-agonists via cAMP (inhibit MLCK).
- Troponin C complex: Troponin C acts in skeletal and cardiac muscle.
- Myosin phosphatase: Myosin phosphatase causes relaxation.
- Phospholamban protein: Phospholamban regulates cardiac SERCA.
11. Light shone in the left eye causes constriction of both pupils. Which nerve carries the efferent limb?
Answer: Oculomotor nerve (CN III). Pupillary light reflex: afferent — retina → optic nerve → optic tract → pretectal nucleus (bypasses LGN) → both Edinger–Westphal nuclei (consensual response); efferent — parasympathetic fibres in oculomotor nerve → ciliary ganglion → short ciliary nerves → sphincter pupillae. RAPD (Marcus Gunn): afferent defect (optic neuritis, severe retinal disease) — swinging light test. Efferent defect (CN III palsy): dilated pupil, no direct or consensual constriction in that eye.
- Optic nerve (CN II): The optic nerve is the afferent limb.
- Trochlear nerve (CN IV): The trochlear nerve supplies superior oblique.
- Ophthalmic division of CN V: V1 is the afferent limb of the corneal reflex.
12. Six months after a C6 spinal cord injury, a man has high-pressure bladder contractions while his external sphincter contracts at the same time, causing retention and hydronephrosis. Why?
Answer: Loss of pontine coordination. Micturition: sacral reflex arc (S2–S4 parasympathetic → detrusor); pontine micturition centre coordinates detrusor contraction with sphincter relaxation; cortex provides voluntary control. Lesion types: suprapontine (stroke, dementia) → uninhibited detrusor overactivity with coordinated sphincter (urge incontinence, low pressure); suprasacral spinal cord (after spinal shock) → detrusor overactivity with detrusor–sphincter dyssynergia (high pressure, reflux, renal damage — needs intermittent catheterisation, antimuscarinics); sacral/cauda equina/peripheral → atonic bladder with overflow.
- Destruction of the sacral reflex arc: A sacral arc lesion causes a flaccid, areflexic bladder.
- Isolated loss of cortical inhibition: Suprapontine lesions keep sphincter coordination.
- Hyperactive bladder sensory afferents: Hyperactive afferents are not the main mechanism.
Topics covered
Neurophysiology, Cardiovascular, Blood, Respiratory, Renal, Endocrine, Nerve & muscle, Special senses, GI, Reproduction, Respiratory physiology, Endocrine physiology, Cardiovascular physiology, Renal physiology, Reproductive physiology, Body fluids, Gastrointestinal physiology, GI physiology, Homeostasis, Acid–base, Thermoregulation, Haematology physiology, Cell physiology, Membrane transport, Cell, Measuring renal plasma flow, Measuring body fluid compartments, Fastest cardiac conduction, Somatomedin C, Suprachiasmatic nucleus, Enterokinase, Pituicytes, Water intoxication, Brunner glands, Haemoglobin cooperativity, Bohr and Haldane effects, Peripheral chemoreceptors, Methacholine challenge, Frank–Starling law, Pressure–volume loop
Frequently asked questions
How many NRE Step 1 Physiology questions are in the bank?
There are 235 Physiology questions in NRE-1 Prep, each with an explanation for every option.
Are these past paper questions?
No. Every question is original, written by us and mapped to the published PMDC NRE syllabus.
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