An obese man faints whenever he wears a shirt with a tight collar or turns his head sharply. What is the mechanism?
Answer: Carotid sinus hypersensitivity
Pressure on the carotid sinus stretches its baroreceptors. Impulses travel in the glossopharyngeal nerve (sinus nerve of Hering) to the medulla, which increases vagal output and reduces sympathetic tone. Heart rate and blood pressure fall, and the patient faints. In some older people the reflex is exaggerated (carotid sinus hypersensitivity).
Baroreceptor reflex
Carotid sinus → IX (Hering); aortic arch → X
Stretch ↑ → vagus ↑ + sympathetic ↓ → HR and BP ↓
Carotid body = chemoreceptor (O₂, CO₂, pH)
Remember Sinus senses Stretch; Body senses Breath (gases).
Why the other options are wrong
Vertebral artery compression Vertebrobasilar insufficiency causes dizziness on extension, not on collar pressure.
Internal jugular vein compression Venous compression does not cause sudden syncope.
Carotid body stimulation Chemoreceptors respond to low O₂ and high CO₂, not pressure.
Vasovagal response to pain Triggered by pain, fear or standing, not neck pressure.
Question 2Hard
A man with faecal peritonitis remains hypotensive despite fluids and high-dose noradrenaline; his arterial pH is 7.18. A low-dose vasopressin infusion raises his blood pressure markedly. Which of the following best explains its effectiveness?
Answer: Relative vasopressin deficiency in sepsis
In early septic shock vasopressin levels rise, but stores in the posterior pituitary are soon exhausted, leaving a relative deficiency. Sepsis and acidosis also down-regulate and desensitise adrenergic receptors, while vasopressin acts through separate V1 receptors on vascular smooth muscle via Gq and calcium. Low doses therefore raise vascular tone and allow the noradrenaline dose to be reduced. At high doses it can cause digital, mesenteric and coronary ischaemia.
Vasopressin in septic shock
Pituitary stores exhausted
V1 receptors, not adrenoceptors
Works in acidosis when catecholamines fail
Spares noradrenaline dose
Remember Vasopressin uses a different receptor.
Exam trap It is a catecholamine-sparing add-on, not a replacement first-line vasopressor.
Why the other options are wrong
Vasopressin increases cardiac contractility It has no direct inotropic action and may reduce output.
Vasopressin stimulates α1 receptors It acts on V1 receptors, not adrenoceptors.
Vasopressin blocks nitric oxide release Its effect is not mainly through blocking nitric oxide.
Question 3Medium
A 70-year-old man has heaviness and pain in both legs after walking 200 m, relieved by sitting or leaning forward on a shopping trolley. Pedal pulses are normal. Which of the following explains why spinal flexion relieves his symptoms?
Answer: Flexion enlarges the spinal canal
In lumbar canal stenosis, degenerate bulging discs, hypertrophied facet joints and a thickened ligamentum flavum narrow the central canal and lateral recesses. In extension, as in standing and walking upright, the ligamentum flavum buckles inwards and the disc bulges back, so the canal and foramina narrow further and the cauda equina roots become congested and ischaemic, causing neurogenic claudication. Flexion stretches the ligamentum flavum taut and opens the canal and foramina, so symptoms ease when the patient sits or stoops. Vascular claudication eases on standing still and is accompanied by weak pulses.
Lumbar canal stenosis
Disc, facets and ligamentum flavum narrow the canal
Extension narrows it further
Flexion opens the canal
'Shopping trolley' relief, normal pulses
Remember Leg pain eased by stooping, pulses normal: spinal stenosis.
Exam trap Cycling is often well tolerated in spinal stenosis because the spine is flexed; uphill walking may also be easier than downhill.
Why the other options are wrong
Flexion improves iliac artery flow Pulses are normal and posture does not change arterial flow in this way.
Flexion relaxes piriformis on the nerve Piriformis syndrome causes buttock pain, not posture-related bilateral claudication.
Flexion closes the facet joints Flexion opens the facet joints rather than closing them.
Flexion lowers CSF pressure in the sac CSF pressure is not the mechanism of neurogenic claudication.
Question 4Medium
A 22-year-old vegetarian woman with iron deficiency asks why her doctor says iron from meat is absorbed better than iron from lentils and spinach. What is the main reason?
Answer: Haem iron is taken up by a separate pathway
Non-haem iron in plants is mostly ferric, poorly soluble at duodenal pH, and must be reduced to ferrous iron by duodenal cytochrome b before DMT1 can take it up. It is strongly inhibited by phytates, tea polyphenols and calcium, and enhanced by vitamin C. Haem iron is taken up intact by a separate route and its iron released inside the cell by haem oxygenase, so it is absorbed more efficiently and is little affected by other foods. Both forms leave the enterocyte through ferroportin, which hepcidin controls.
Two kinds of dietary iron
Non-haem: ferric, needs reduction
Inhibited by phytate, tea, calcium
Haem: separate, efficient uptake
Both exit via ferroportin
Remember Vegetarians should take vitamin C with iron-rich meals and avoid tea with them.
Exam trap Spinach contains iron, but most of it is non-haem iron bound by oxalate and poorly absorbed.
Why the other options are wrong
Plant iron is mostly in the ferrous form Plant iron is mostly ferric.
Meat increases intrinsic factor secretion Intrinsic factor is for B12, not iron.
Haem iron does not need the duodenum Haem iron is also absorbed in the duodenum.
A 30-year-old woman has frequent migraines and starts a monthly injection of a monoclonal antibody for prevention. Which neuropeptide released from trigeminal nerve endings does this treatment target?
Answer: Calcitonin gene-related peptide
In migraine, activation of the trigeminovascular system releases calcitonin gene-related peptide (CGRP) from trigeminal nerve endings around meningeal vessels. CGRP dilates vessels and sensitises pain pathways. Antibodies against CGRP or its receptor, and small-molecule receptor blockers, reduce migraine frequency. Triptans also reduce CGRP release through 5-HT1D receptors.
CGRP and migraine
Trigeminal endings release CGRP
Vasodilatation and pain sensitisation
Antibodies block CGRP or its receptor
Triptans reduce CGRP release
Remember Migraine prevention now targets CGRP.
Exam trap Triptans are avoided in coronary disease because they constrict coronary arteries.
Why the other options are wrong
Substance P Substance P antagonists failed in migraine trials.
Vasoactive intestinal peptide VIP is not the main migraine target.
Neuropeptide Y Neuropeptide Y is mainly a sympathetic cotransmitter.
Somatostatin Somatostatin is not used for migraine.
Question 6Medium
A woman's left ureter was unknowingly tied during a hysterectomy. Over the next week her urine output and serum creatinine stay almost normal until a scan shows left hydronephrosis. Why did the creatinine barely rise?
Answer: The right kidney increased its filtration
Serum creatinine depends on total GFR from both kidneys. When one ureter is blocked, filtration on that side falls as Bowman space pressure rises, but the healthy kidney increases its single-nephron GFR through hyperfiltration and maintains total clearance close to normal. Urine output and creatinine therefore change little, which is why unilateral ureteric injury is easily missed and why imaging is needed when injury is suspected. Creatinine production from muscle is unchanged.
Unilateral obstruction
Obstructed side: GFR falls
Other kidney hyperfilters
Creatinine and output near normal
Needs imaging to detect
Remember One kidney can hide an injury to the other ureter.
Exam trap Normal creatinine after pelvic surgery does not exclude a unilateral ureteric injury.
Why the other options are wrong
The ligated kidney kept filtering normally Filtration falls on the obstructed side as Bowman pressure rises.
Urine was reabsorbed into the blood via lymph Pyelolymphatic backflow is minor and does not maintain clearance.
Creatinine was excreted through the gut Gut excretion of creatinine is trivial.
Ligation reduced creatinine production Muscle creatinine production is unaffected.
Question 7Hard
After a road traffic accident with a basal skull fracture, a 26-year-old woman develops amenorrhoea and milky nipple discharge. MRI shows transection of the pituitary stalk. Which hormone pattern is expected?
Answer: Low LH and FSH with raised prolactin
Cutting the stalk interrupts the hypophyseal portal supply. Hormones that need a hypothalamic releasing hormone (GnRH, CRH, TRH, GHRH) fall, so LH and FSH drop and ovulation stops. Prolactin is the exception: it is under tonic inhibition by hypothalamic dopamine, so losing the portal dopamine releases lactotrophs and prolactin rises, causing galactorrhoea. The raised prolactin further suppresses GnRH. Diabetes insipidus may also occur.
Stalk section effect
Releasing hormones lost: LH, FSH fall
Dopamine lost: prolactin rises
Galactorrhoea, amenorrhoea
May get diabetes insipidus
Remember Cut the stalk: everything falls except prolactin.
Exam trap Mild hyperprolactinaemia with a large non-functioning tumour may be stalk effect, not a prolactinoma.
Why the other options are wrong
High LH and FSH with low prolactin Gonadotrophins depend on GnRH and fall.
High LH and FSH with raised prolactin Gonadotrophins fall without GnRH.
Low LH and FSH with low prolactin Prolactin rises when dopamine is lost.
Normal LH and FSH with raised prolactin LH and FSH cannot stay normal without GnRH.
Question 8Hard
In a research study, women whose plasma levels of a placental peptide rise unusually steeply at 20–30 weeks tend to deliver preterm. The peptide is stimulated, not suppressed, by cortisol. Which peptide is this?
The placenta secretes CRH, which rises exponentially in the second half of pregnancy and peaks at labour, acting as a 'placental clock'. Unlike hypothalamic CRH, placental CRH is stimulated by cortisol, so it forms a positive feedback loop with the fetal adrenal. It drives fetal adrenal DHEA sulphate and cortisol output and stimulates prostaglandin production in the membranes. A faster rise predicts preterm birth, and a slower one post-term birth.
Placental CRH
Rises exponentially to term
Cortisol stimulates it
Drives fetal adrenal and prostaglandins
Steep rise: preterm birth
Remember Placental CRH is the clock of pregnancy.
Exam trap Cortisol suppresses hypothalamic CRH but stimulates placental CRH.
Why the other options are wrong
Placental human chorionic gonadotrophin Peaks at 10 weeks and then falls.
Human placental lactogen Rises with placental mass; not linked to labour timing.
Relaxin from the corpus luteum Made mainly by the corpus luteum.
Inhibin A from the placenta Not the placental clock.
Question 9Medium
After a long labour with an epidural, a woman is found to have a blistered burn on her calf where a hot water bottle had been placed; she says she felt nothing. Through which pathway would she normally have felt the heat?
Answer: Lateral spinothalamic tract
Heat and cold, like pain, are detected by free nerve endings with A-delta and C fibres. These synapse in the dorsal horn, and second-order fibres cross in the anterior white commissure to ascend in the lateral spinothalamic tract to the thalamus. Epidural local anaesthetic blocks these thin fibres in the nerve roots, so thermal sensation is lost below the block and a hot object can burn without being felt. Warming devices must not be placed on blocked areas.
Thermal sensation
Free endings: A-delta and C
Cross in anterior white commissure
Ascend in lateral spinothalamic tract
Lost under neuraxial block
Remember Temperature travels with pain.
Exam trap Patients with dense blocks cannot protect numb skin from heat or pressure.
Why the other options are wrong
Dorsal column–medial lemniscus Carries fine touch, vibration and position sense.
Spinocerebellar tracts Carries unconscious proprioception to the cerebellum.
Corticospinal tract Descending motor pathway.
Vestibulospinal tract Descending pathway for posture.
Question 10Easy
In uterine artery Doppler at 22 weeks, the frequency-shifted echoes that make up the waveform are reflected mainly by which moving targets?
Answer: Red blood cells
Red cells are the most numerous particles in blood and act as tiny scatterers. When they move towards or away from the probe, the echoes they return are shifted in frequency in proportion to their velocity. The spectrum of shifts from many red cells forms the Doppler waveform. Wall motion produces a low-frequency, high-amplitude signal that machines remove with a wall filter.
Doppler signal source
Scatterers: red blood cells
Shift ∝ red cell velocity
Wall motion removed by wall filter
Spectrum shows range of velocities
Remember Doppler listens to moving red cells.
Exam trap The vessel wall produces clutter, not the flow signal.
Why the other options are wrong
Arterial wall Wall motion is slow and is filtered out.
Plasma proteins Proteins are far too small to scatter ultrasound usefully.
Platelets Far fewer than red cells.
Endothelial cells Stationary lining cells produce no Doppler shift.
Question 11Medium
A man is stabbed in the back, and the left half of his spinal cord is cut at the T8 segment. He has weakness and loss of vibration and position sense in the left leg. What sensory loss is found on the right side?
Answer: Pain and temperature below about T10
Dorsal column fibres for vibration and proprioception ascend on the same side and cross in the medulla, so they are lost on the side of the lesion. Spinothalamic fibres for pain and temperature enter the cord, rise one or two segments and cross in the anterior white commissure to the opposite side. A left hemisection therefore causes loss of pain and temperature on the right from one or two segments below the lesion, with left-sided weakness and dorsal column loss.
Brown-Séquard
Same side: weakness
Same side: vibration, position lost
Opposite side: pain, temperature lost
Starts 1–2 segments below
Remember Hemisection: motor and dorsal columns same side, pain opposite.
Exam trap The level of pain loss on the opposite side is one or two segments lower than the cord lesion.
Why the other options are wrong
Vibration and position sense in the right leg Dorsal column loss is on the side of the lesion, the left.
Light touch only, at T8 alone Touch is carried in both pathways and is usually only reduced.
All sensation below T8 Complete loss on one side would need more than a hemisection.
No sensory loss on the right The crossed spinothalamic fibres are damaged, so right-sided pain loss occurs.
Question 12Medium
A 50-year-old man with several rib fractures breathes rapidly and shallowly: tidal volume 250 mL at 32 breaths/min. His anatomical dead space is 150 mL. What is his alveolar ventilation?
Answer: 3.2 L/min
Alveolar ventilation is (tidal volume minus dead space) multiplied by respiratory rate. Here it is (250 - 150) x 32 = 3,200 mL/min. His minute ventilation is 8 L/min, which looks generous, but most of each small breath only fills the conducting airways. Rapid shallow breathing therefore wastes ventilation and allows CO2 to rise.
Alveolar ventilation
VA = (VT minus VD) x RR
Here: 100 mL x 32 = 3.2 L/min
Minute ventilation 8 L/min
Shallow breaths waste ventilation
Remember Subtract dead space from every breath before multiplying.
Exam trap Minute ventilation can be normal while alveolar ventilation is low.
Why the other options are wrong
8.0 L/min This is minute ventilation, ignoring dead space.
4.8 L/min This uses dead space wrongly or the rate wrongly.
