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PY11.1-7 | Special Senses — Gate Quiz
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In the visual pathway, fibres from the nasal half of each retina cross at the optic chiasma. A lesion of the optic chiasma (as in a pituitary tumour) causes:
Correct! The nasal retinal fibres (carrying temporal visual field information) cross at the optic chiasma. A chiasmal lesion (e.g., pituitary adenoma compressing the chiasma from below) damages these crossing fibres → bitemporal hemianopia (loss of both temporal visual fields — "tunnel vision").
Key concept: Visual pathway lesions — (1) Optic nerve: monocular blindness; (2) Optic chiasma: bitemporal hemianopia (pituitary tumour); (3) Optic tract/optic radiation/occipital cortex: homonymous hemianopia (with macular sparing if cortical). Nasal retina sees temporal field; temporal retina sees nasal field. Nasal fibres cross at chiasma; temporal fibres do not. Superior quadrantanopia (inferior radiation/temporal lobe): "pie in the sky."
Incorrect. A chiasmal lesion damages the crossing nasal retinal fibres (which carry temporal field information) → bitemporal hemianopia. This is characteristic of pituitary tumours (most common cause of bitemporal hemianopia).
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Rod photoreceptors in the retina are responsible for:
Correct! Rods (120 million per retina) contain rhodopsin, are highly sensitive to light (one photon can activate a rod), operate in low light (scotopic vision), and provide monochromatic (black and white) vision. They are concentrated in the peripheral retina. Vitamin A deficiency impairs rhodopsin regeneration → night blindness (nyctalopia).
Key concept: Photoreceptors — Rods: ~120 million, peripheral retina, rhodopsin (opsin + 11-cis retinal, from vitamin A), scotopic vision, monochromatic, high sensitivity; Cones: ~6 million, concentrated in fovea centralis, 3 types (L=red, M=green, S=blue), photopic vision, colour discrimination, high acuity. Macular degeneration: foveal cones lost → central vision loss. Retinitis pigmentosa: peripheral rods lost → tunnel vision.
Incorrect. Rods are responsible for scotopic (dim light) vision — highly sensitive but monochromatic. Cones (3 types: L, M, S) provide colour vision and high acuity in bright light (photopic vision) in the fovea.
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Sound transduction in the cochlea occurs when basilar membrane vibration causes deflection of hair cell stereocilia, leading to:
Correct! Basilar membrane deflection → stereocilia tip links stretch → mechanically gated K⁺ channels open → K⁺ influx (from endolymph, which has uniquely high [K⁺] = 150 mEq/L) → hair cell depolarisation → voltage-gated Ca²⁺ channels open → Ca²⁺ influx at basolateral membrane → glutamate released onto spiral ganglion (cochlear nerve) fibres.
Key concept: Cochlear hair cell transduction — Endolymph (unique: high K⁺ 150 mEq/L, +80 mV endocochlear potential from stria vascularis) provides driving force for K⁺ influx when channels open. Frequency coding (tonotopy): base = high frequency; apex = low frequency. Inner hair cells (IHC) = primary sensory (3500, connected to 95% of cochlear nerve fibres). Outer hair cells (OHC) = amplifiers (motor function via prestin).
Incorrect. Hair cell transduction: stereocilia deflection → tip-link tension → mechanically gated K⁺ channels open → K⁺ influx (from K⁺-rich endolymph) → depolarisation → Ca²⁺ influx → glutamate release → cochlear nerve activation.
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In Rinne's test, a 512 Hz tuning fork is placed on the mastoid process (bone conduction) and then held near the ear (air conduction). A patient hears air conduction LESS WELL than bone conduction (Rinne negative). This indicates:
Correct! Rinne negative (BC > AC) = conductive hearing loss. In conductive loss, the middle ear (ossicular chain, tympanic membrane) cannot efficiently transmit sound, reducing air conduction. Bone conduction bypasses the middle ear and reaches the cochlea directly — hence BC > AC in conductive hearing loss.
Key concept: Hearing tests — Rinne: AC > BC = normal (Rinne+); BC > AC = conductive loss (Rinne−); AC > BC but reduced = sensorineural loss (Rinne+ but bilateral reduced). Weber (midline tuning fork): lateralises to affected ear in conductive loss (bone conduction better in blocked ear); lateralises to good ear in sensorineural loss. Causes of conductive loss in India: otitis media with effusion, wax impaction, otosclerosis. Sensorineural: noise-induced, presbycusis, drugs (aminoglycosides, cisplatin).
Incorrect. Rinne negative (BC > AC) = CONDUCTIVE hearing loss. Rinne positive (AC > BC) is NORMAL or sensorineural loss. In conductive hearing loss, the middle ear pathway is impaired but bone conduction still reaches the cochlea.
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The five basic taste qualities detected by taste receptor cells include all of the following EXCEPT:
Correct! The five basic tastes are: sweet, sour, salty, bitter, and umami (savoury). Spicy/pungent sensation from capsaicin is mediated by TRPV1 (transient receptor potential vanilloid 1) pain/heat receptors — NOT a taste receptor. It is a chemosensory nociceptive sensation, not a classical taste quality.
Key concept: Five basic tastes — Sweet (T1R2/T1R3 GPCRs, cAMP), Salty (Na⁺ through ENaC channels), Sour (H⁺ ions, PKD2L1 channels), Bitter (T2R family GPCRs, protective against toxins), Umami (T1R1/T1R3, L-glutamate). Taste buds on papillae (fungiform, circumvallate, foliate). Tastants → cranial nerves VII (anterior 2/3 tongue), IX (posterior 1/3), X (epiglottis) → nucleus tractus solitarius → thalamus → insular cortex.
Incorrect. The five basic tastes are sweet, sour, salty, bitter, and umami. Spicy (capsaicin) is mediated by TRPV1 pain receptors on the tongue — it is a pain/heat sensation, not a taste quality.
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The semicircular canals of the inner ear detect:
Correct! The three semicircular canals (anterior/superior, posterior, lateral/horizontal) detect angular (rotational) acceleration. Each canal is oriented in a different plane; rotation moves endolymph, deflecting the cupula and bending hair cell stereocilia → generating signals in the ampullary nerve. The utricle and saccule detect linear acceleration and gravity.
Key concept: Vestibular apparatus — Semicircular canals (3, ampullae): angular acceleration (rotation); Utricle: horizontal linear acceleration + static head position; Saccule: vertical linear acceleration + gravity. Mechanism: endolymph inertia deflects cupula/otolith membrane → hair cell mechanotransduction → CN VIII → vestibular nuclei → cerebellum, spinal cord, extraocular muscles (VOR). Benign paroxysmal positional vertigo (BPPV): otoconia displaced into posterior canal → triggered by position change.
Incorrect. Semicircular canals detect angular (rotational) acceleration. Linear acceleration and gravity are detected by the otolith organs — the utricle (horizontal linear acceleration) and saccule (vertical linear acceleration/gravity).
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A 60-year-old man is found to have elevated intraocular pressure (IOP = 26 mmHg) and optic disc cupping on examination. His condition (open-angle glaucoma) results from:
Correct! IOP is maintained by the balance between aqueous humour production (by ciliary body epithelium) and drainage through the trabecular meshwork → canal of Schlemm → episcleral veins. In open-angle glaucoma, progressive trabecular meshwork resistance reduces drainage → ↑IOP → compression of optic nerve axons at the optic disc → optic disc cupping and visual field loss.
Key concept: Aqueous humour — Produced by ciliary body epithelium; flows from posterior → anterior chamber → trabecular meshwork → canal of Schlemm → episcleral veins. IOP normally 10–21 mmHg. Open-angle glaucoma: trabecular meshwork resistance ↑, gradual painless vision loss; Angle-closure glaucoma: acute, painful, red eye. Treatment: β-blockers (↓production), prostaglandin analogues (↑uveoscleral outflow), pilocarpine (↑trabecular outflow). NOT related to systemic BP.
Incorrect. Primary open-angle glaucoma = impaired aqueous outflow through the trabecular meshwork → elevated IOP → optic nerve damage. The angle between iris and cornea is open (unlike angle-closure glaucoma where it is physically blocked).
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The most common form of colour blindness is:
Correct! Red-green colour blindness (deuteranopia = absent green M-cones, or protanopia = absent red L-cones) is the most common form, affecting ~8% of males and ~0.5% of females. It is X-linked recessive (genes for L and M cones are on the X chromosome). Males have one X chromosome — if the gene is defective, they are colour blind.
Key concept: Colour vision defects — Red-green (most common): X-linked, males >>females; Protanopia: missing L-cones (red); Deuteranopia: missing M-cones (green); Tritanopia: missing S-cones (blue), autosomal dominant, rare. Test: Ishihara colour plates. Trichromacy: normal 3-cone vision. Young-Helmholtz trichromatic theory: colour perceived by relative stimulation of L, M, S cones. Opponent process theory: how signals are processed centrally.
Incorrect. Red-green colour blindness (8% of males, X-linked recessive) is the most common type of colour vision deficiency. Blue-yellow (tritanopia, autosomal) and complete colour blindness are much rarer.
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Olfactory receptor neurons detect smell by:
Correct! Olfactory receptors are GPCRs (Golf protein) on olfactory cilia. Odourant binding → Golf → adenylyl cyclase III → ↑cAMP → opens CNG (cyclic nucleotide-gated) channels → Na⁺/Ca²⁺ influx → depolarisation → action potential in olfactory receptor neurons → olfactory nerve (CN I) → olfactory bulb → primary olfactory cortex (piriform cortex).
Key concept: Olfactory receptor neurons (ORNs) — bipolar neurons in nasal olfactory epithelium; axons form CN I → pass through cribriform plate → olfactory bulb (first synapse with mitral cells) → lateral olfactory tract → piriform cortex, amygdala, entorhinal cortex. >400 functional olfactory receptor genes (largest gene family). One ORN expresses ONE type of receptor. Anosmia: head injury (cribriform plate fracture), viral (COVID-19), Parkinson's (early symptom), Kallmann syndrome (no GnRH development).
Incorrect. Olfactory transduction: odourant → GPCR (olfactory receptor) → Golf → ↑cAMP → CNG channels open → Na⁺/Ca²⁺ influx → depolarisation → olfactory nerve.
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A 50-year-old software engineer finds difficulty reading close text but sees distant objects clearly. He requires reading glasses with convex lenses. This is consistent with:
Correct! Presbyopia is the age-related (typically begins in 40s) reduced ability to focus on near objects due to progressive loss of lens elasticity and reduced ciliary muscle effectiveness. The lens cannot increase its curvature (accommodation) sufficiently for near vision. Corrected with convex (plus) lenses for reading. Near-perfect distant vision distinguishes it from hypermetropia.
Key concept: Accommodation — ciliary muscle contracts → zonular fibres relax → lens becomes rounder (↑refractive power) for near vision. Accommodation controlled by parasympathetic (CN III, ciliary ganglion). Presbyopia: lens hardens with age → reduced accommodation. Refractive errors: Myopia (axial too long / lens too powerful): near objects clear; Hypermetropia (axial too short): all objects blurred; Astigmatism: irregular lens/cornea curvature; Presbyopia: accommodation failure in older age.
Incorrect. Presbyopia = age-related loss of lens elasticity → impaired accommodation → difficulty reading close objects. Normal distance vision. Corrected with convex (plus) reading glasses. Very common presentation in adults aged >40.
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