Ocular Physiology In Depth: Tear Film, Cornea, Aqueous, Lens, Retina and Vision
Last updated: November 2026
Physiology explains why diseases look the way they do and how our drugs and operations work. This in-depth guide covers each part of the eye in turn, from the tear film to the visual cortex, with the mechanisms and numbers that examiners ask.
Tear film
Component
Source
Function
Lipid layer
Meibomian glands (and Zeis)
Reduces evaporation, stabilises the film
Aqueous-mucin gel
Main and accessory lacrimal glands (Krause, Wolfring); goblet cells
Membrane-bound mucins (MUC1, MUC4, MUC16) of the epithelium
Makes the surface wettable
Tear volume about 7 µL; secretion about 1.2 µL/min; turnover about 16% per minute.
Reflex secretion: afferent V1, efferent parasympathetic fibres from the superior salivatory nucleus via CN VII, the greater petrosal nerve and the pterygopalatine ganglion.
Tear osmolarity normally about 300 mOsm/L; above about 308 or an inter-eye difference of more than 8 suggests dry eye.
Drainage depends on the lacrimal pump: blinking compresses the canaliculi and sac.
Cornea
Transparency: stromal collagen fibrils of uniform diameter, spaced less than half a wavelength apart, so scattered light cancels out (Maurice's lattice theory); no vessels; non-keratinised epithelium; and relative dehydration.
Deturgescence (about 78% water) is kept by the endothelial pump (Na+/K+-ATPase and bicarbonate transport) and the barrier function of the epithelium and endothelium. Stromal swelling pressure is about 50–60 mmHg.
The endothelium does not divide; cells spread to cover gaps. Decompensation occurs below about 500 cells/mm².
Oxygen comes mostly from the tear film (air) with eyes open and from the palpebral conjunctiva with eyes closed: why overnight contact lens wear causes hypoxia.
Epithelial wound healing: cells slide in hours, proliferate and stratify over days; Bowman layer does not regenerate.
Aqueous humour and IOP
Aqueous is made by the ciliary processes and leaves through the trabecular meshwork or the uveoscleral route.
Process
Details
Production
About 2–3 µL/min by the non-pigmented ciliary epithelium: active secretion (the major part; needs Na+/K+-ATPase and carbonic anhydrase), ultrafiltration and diffusion. Lower at night.
Composition
Low protein (about 1/200 of plasma), high ascorbate (about 15–20 times plasma, protects against UV and oxidation), lactate; glucose slightly below plasma
Conventional outflow
Trabecular meshwork to Schlemm canal: pressure-dependent, most of the outflow; resistance mainly in the juxtacanalicular tissue
Uveoscleral outflow
Through the ciliary muscle into the suprachoroidal space: pressure-independent; increased by prostaglandin analogues, reduced by pilocarpine
Outflow facility
About 0.2–0.3 µL/min/mmHg; falls with age and in POAG
Episcleral venous pressure
About 8–10 mmHg; raised in carotid-cavernous fistula and Sturge-Weber syndrome
Goldmann equation: IOP = (F ÷ C) + Pv. IOP is normally about 10–21 mmHg, with a diurnal variation of 3–6 mmHg (often highest in the early morning, partly when lying down). Ocular perfusion pressure = blood pressure − IOP.
Blood-ocular barriers
Blood-aqueous barrier: tight junctions of the non-pigmented ciliary epithelium and the iris vessel endothelium; breaks down in uveitis and after surgery (flare).
Inner blood-retina barrier: tight junctions of retinal capillary endothelium (breaks down in diabetic macular oedema and vein occlusion).
Outer blood-retina barrier: tight junctions of the RPE (breaks down in CSCR, choroidal neovascularisation).
Fenestrated choroidal capillaries leak fluorescein freely; retinal vessels do not, which is why FFA shows retinal leakage clearly.
Lens
Avascular and anucleate in its core; energy mainly from anaerobic glycolysis (about 80% of glucose), plus the hexose monophosphate shunt for NADPH.
Antioxidant defences: glutathione (very high concentration), ascorbate, superoxide dismutase.
Transparency: tightly packed fibres with few organelles and crystallin proteins (alpha, beta, gamma) at high concentration (about 33% of lens weight, the highest protein content of any tissue). Alpha-crystallin acts as a chaperone.
Ion balance by Na+/K+-ATPase in the epithelium (pump-leak system).
Cataract mechanisms: oxidation and protein cross-linking (age, UV), osmotic swelling from sorbitol via aldose reductase (diabetes, galactosaemia), steroids (posterior subcapsular), and hydration changes.
Vitreous
A gel of type II collagen fibrils kept apart by hyaluronan; liquefies with age (synchysis) and collapses (syneresis), leading to posterior vitreous detachment, usually after age 50 (earlier in myopes).
It acts as a metabolic reservoir and a barrier to diffusion and cell migration; vitrectomy speeds lens oxidation (nuclear cataract) and drug clearance.
Failure leads to debris and degeneration (some RP genes)
Recycles retinal (visual cycle: RPE65)
RPE65 Leber amaurosis treated with gene therapy
Pumps fluid from subretinal space to choroid
Subretinal fluid in CSCR when the pump or barrier fails
Forms the outer blood-retina barrier
Leakage on FFA
Secretes growth factors (VEGF towards choroid, PEDF towards retina)
Basis of choroidal neovascularisation and anti-VEGF therapy
Müller cells span the retina: structural support, potassium and glutamate buffering, and they contribute to the ERG b-wave.
Macular pigment (lutein, zeaxanthin) in the Henle fibre and inner layers filters blue light (the dark spot on FAF).
The retina has one of the highest oxygen consumptions in the body; the outer retina is supplied by the choroid, the inner retina by the retinal circulation.
Phototransduction
A photon isomerises 11-cis-retinal to all-trans-retinal in rhodopsin (peak absorption about 498 nm).
Activated rhodopsin activates transducin (a G protein), which activates phosphodiesterase.
cGMP falls, cGMP-gated sodium channels close, and the "dark current" stops.
The photoreceptor hyperpolarises and releases less glutamate; bipolar cells respond (ON cells depolarise, OFF cells hyperpolarise).
Recovery: rhodopsin kinase and arrestin stop the cascade; calcium-dependent feedback restores cGMP.
All-trans-retinal is carried to the RPE, converted back to 11-cis-retinal (RPE65 isomerase) and returned: the visual cycle. Cones also use a Müller cell pathway for faster regeneration.
Adaptation and colour vision
Dark adaptation: a cone phase (best in 5–10 minutes), the rod-cone break at about 7–10 minutes, then the rod phase reaching maximum sensitivity at about 30–40 minutes. Delayed in vitamin A deficiency, RP and AMD.
Light adaptation is faster (seconds to minutes).
Photopic vision uses cones (peak sensitivity 555 nm), scotopic vision uses rods (507 nm); the shift is the Purkinje shift.
Trichromacy: S cones (about 420 nm), M cones (530 nm) and L cones (560 nm); then opponent processing (red-green, blue-yellow, light-dark) in the retina and LGN.
Congenital red-green defects are X-linked (about 8% of men); acquired optic nerve disease tends to cause red-green defects and retinal disease blue-yellow (Kollner rule).
Pupil and accommodation
Light reflex: retina, optic nerve and tract (pupillary fibres leave before the LGN), pretectal nuclei (bilateral, giving the consensual response), Edinger-Westphal nuclei, CN III, ciliary ganglion, short ciliary nerves, sphincter.
Near triad: accommodation, convergence and miosis; the near pathway runs more ventrally, explaining light-near dissociation.
Accommodation (Helmholtz): the ciliary muscle contracts, zonular tension falls, and the lens rounds up, especially its anterior surface. Amplitude falls from about 14 D at age 10 to about 1 D at age 60 (presbyopia).
Sympathetic dilation via the three-neuron pathway; the pupil is the balance of sphincter and dilator tone.
Ocular blood flow
The retinal circulation is autoregulated (no autonomic innervation) and has a high oxygen extraction; the choroidal circulation has very high flow, low extraction and sympathetic control, and is poorly autoregulated.
Failure of autoregulation and low perfusion pressure are proposed in normal-tension glaucoma.
Fluorescein reaches the choroid about 1 second before the retinal arteries (arm-retina time about 10–15 seconds).
Visual function
Visual acuity is limited by foveal cone spacing (about 0.5 minute of arc) and optics; 6/6 corresponds to resolving 1 minute of arc.
Contrast sensitivity peaks at about 3–5 cycles per degree.
Binocular single vision needs normal retinal correspondence and fusion within Panum fusional area; stereopsis arises from horizontal disparity.
Electrophysiology basis: ERG a-wave from photoreceptors, b-wave from bipolar and Müller cells, oscillatory potentials from amacrine cells; EOG from the RPE (light rise / dark trough, the Arden ratio); VEP from the visual cortex. See electrophysiology made easy.
Where residents slip
Saying photoreceptors depolarise to light.
Thinking prostaglandins act on the trabecular route (mainly uveoscleral).
Forgetting that the endothelium does not regenerate.
Confusing the photopic (555 nm) and scotopic (507 nm) peaks.
Saying the retinal circulation has autonomic control (it is autoregulated).