Ophthalmology: Anatomy Physiology and Pharmacology

• Outer eye: The Orbit | Eyelids | Tears and the Lacrimal System | Cornea, Conjunctiva and Sclera
• Inner eye: Uvea and Aqueous Humour | Intraocular Pressure and the Drainage Angle | Lens, Focusing and Refraction | Vitreous, Retina and Macula | Blood Supply of the Eye
• Vision and nerves: How We See — Photoreceptors and Visual Function | The Visual Pathway and Field Defects | Pupils and Their Nerves | Eye Movements — III, IV and VI | Basic Eye Assessment
• Pharmacology: Getting Drugs into the Eye | Glaucoma Drugs | Dilating Drops, Anaesthetics and Stains | Antibiotics, Antivirals, Steroids and Lubricants | Anti-VEGF and Other Specialist Treatments | Eye Side Effects of Systemic Drugs
• Revision: Eye Anatomy and Drugs at a Glance | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

👁️ Ophthalmology anatomy, physiology and pharmacology — the foundation page for the Ophthalmology chapter. The eye is small, but its anatomy explains almost every eye presentation — why a blowout fracture causes double vision, why some drops can trigger acute glaucoma, why a third nerve palsy with a big pupil is an emergency. Many systemic drugs harm the eye, and some eye drops cause systemic effects. This page covers the structures, how vision works, and the drugs used in and around the eye.
Your four questions for every eye problem: Which part of the eye or visual pathway is affected? Is vision, the pupil or eye movement affected — and is it sight-threatening? Could a drug (local or systemic) be the cause? Is this a treatment I can start, or does it need an ophthalmologist?

The Orbit

• Bony orbit — seven bones forming a cone pointing backwards.
  • Floor (maxilla) — thin — blowout fracture after a blow from a ball or fist: infraorbital nerve numbness (cheek and upper lip), restricted upgaze with vertical diplopia (inferior rectus entrapment — urgent in children: "white-eyed blowout" with vomiting and bradycardia), enophthalmos.
  • Medial wall — paper-thin lamina papyracea (ethmoid) — ethmoid sinusitis spreads into the orbit (orbital cellulitis in children); surgical emphysema after nose-blowing with a fracture.
  • Roof — anterior cranial fossa above.
• Openings:
  • Optic canal — optic nerve (II) and ophthalmic artery.
  • Superior orbital fissure — III, IV, VI, V1 (ophthalmic division) and the superior ophthalmic vein — lesions here (or in the cavernous sinus) cause multiple cranial nerve palsies with forehead numbness.
  • Inferior orbital fissure — infraorbital nerve and vessels.
• Orbital septum — fibrous sheet from the orbital rim to the eyelids — separates preseptal (periorbital) cellulitis (lids only — oral antibiotics) from orbital cellulitis (behind the septum — proptosis, painful or restricted eye movements, reduced vision, RAPD — emergency: IV antibiotics, CT, ENT and ophthalmology).
• Proptosis — thyroid eye disease (commonest — bilateral or unilateral; enlarged extraocular muscles), orbital cellulitis, tumours (lymphoma, metastases), carotid–cavernous fistula (pulsatile, bruit, red eye).
• Venous drainage — ophthalmic veins drain to the cavernous sinus (no valves) — facial infections can spread (cavernous sinus thrombosis).

Eyelids

• Functions — protect the eye, spread the tear film with blinking, drain tears towards the puncta.
• Muscles:
  • Levator palpebrae superioris — oculomotor nerve (III) — main lid elevator — complete ptosis in third nerve palsy.
  • Müller's muscle (superior tarsal) — sympathetic — 1–2 mm of elevation — partial ptosis in Horner's syndrome.
  • Orbicularis oculi — facial nerve (VII) — closes the eye — can't close the eye in Bell's palsy (exposure keratopathy).
• Causes of ptosis — ageing (levator aponeurosis disinsertion — commonest), III palsy, Horner's, myasthenia gravis (fatigable, variable), myotonic dystrophy, mitochondrial myopathy (CPEO), congenital (amblyopia risk in children).
• Lid glands:
  • Meibomian glands (in the tarsal plate) — oil layer of tears — blockage causes a chalazion (painless lump); blepharitis (meibomian gland dysfunction) — warm compresses, lid hygiene.
  • Glands of Zeis and Moll (lash follicles) — infection causes a stye (external hordeolum).
• Lid position — entropion (inturning — lashes rub the cornea) and ectropion (outturning — watering, exposure) — common in older people; surgery.
• Lid lumps — basal cell carcinoma is the commonest malignant lid tumour (lower lid, medial canthus — pearly, ulcerated, lash loss); sebaceous gland carcinoma mimics chalazion (recurrent "chalazion" — biopsy).
• Lid lacerations involving the margin or the medial canthus (canaliculus) — ophthalmic repair.

Tears and the Lacrimal System

• Tear film (three layers):
  • Lipid (outer) — meibomian glands — slows evaporation.
  • Aqueous (middle) — lacrimal gland — nutrients, antimicrobials (lysozyme, IgA), washing.
  • Mucin (inner) — conjunctival goblet cells — helps tears spread and stick.
• Lacrimal gland — in the superolateral orbit; parasympathetic supply from the facial nerve (greater petrosal nerve → pterygopalatine ganglion) — a proximal facial nerve lesion reduces tear production.
• Drainage — puncta (medial lids) → canaliculi → lacrimal sac → nasolacrimal duct → inferior meatus of the nose.
  • Congenital nasolacrimal duct obstruction — sticky, watery eye in infants — most resolve by 12 months (massage; probing if persistent).
  • Acquired obstruction — watering eye in older adults; dacryocystitis (painful swelling at the medial canthus — antibiotics, later DCR surgery).
• Dry eye disease — evaporative (meibomian gland dysfunction — commonest) or aqueous-deficient (Sjögren's, ageing, drugs — anticholinergics, antihistamines, isotretinoin, beta-blockers); symptoms worse with screens, wind and air conditioning; reflex watering is common in dry eye.
• Schirmer's test — filter paper measures tear production.
• Corneal exposure — Bell's palsy, thyroid eye disease, sedated ICU patients (lid taping, lubricants).

Cornea, Conjunctiva and Sclera

• Cornea — the clear front window:
  • Provides about two-thirds of the eye's focusing power (about 43 dioptres) — refractive surgery reshapes it.
  • Avascular — oxygen from tears and air (contact lens overwear causes hypoxia and neovascularisation); transparency depends on regular collagen and a dehydrated stroma.
  • Layers — epithelium (regenerates within days — abrasions heal quickly), Bowman's layer, stroma (90% — scars here are permanent), Descemet's membrane, endothelium (pumps water out — doesn't regenerate; loss causes corneal oedema — Fuchs' dystrophy, surgical trauma).
  • Most densely innervated tissue in the body (V1) — abrasions and ulcers are very painful; corneal reflex — afferent V1, efferent VII (lost early in cerebellopontine angle tumours).
  • Keratitis risks — contact lenses (Pseudomonas, Acanthamoeba — tap water and swimming), HSV (dendritic ulcer), herpes zoster ophthalmicus, trauma, dry eye, exposure — urgent ophthalmology.
• Conjunctiva — thin vascular membrane covering the sclera (bulbar) and lining the lids (palpebral); conjunctivitis — infective (bacterial — purulent; viral — watery, follicles, preauricular node, very contagious) or allergic (itch, papillae); subconjunctival haemorrhage (painless, harmless — check BP and INR if recurrent).
• Limbus — the corneoscleral junction — ciliary (circumcorneal) injection (redness concentrated at the limbus) suggests serious disease — keratitis, anterior uveitis, acute angle-closure glaucoma — rather than conjunctivitis.
• Sclera — tough white coat; episcleritis (mild discomfort, sectoral redness — benign, self-limiting) vs scleritis (severe, boring pain, tender, deep violet redness — associated with rheumatoid arthritis and vasculitis (GPA) — urgent ophthalmology; risk of perforation).

Uvea and Aqueous Humour

• Uveal tract — pigmented, vascular middle layer:
  • Iris — controls pupil size — sphincter pupillae (parasympathetic — III — constricts) and dilator pupillae (sympathetic — dilates).
  • Ciliary body — ciliary muscle (parasympathetic — accommodation) and ciliary epithelium (makes aqueous humour).
  • Choroid — highly vascular — supplies the outer retina (photoreceptors).
• Uveitis:
  • Anterior (iritis) — painful red eye, photophobia, small pupil, ciliary injection, cells and flare in the anterior chamber (hypopyon if severe) — associated with HLA-B27 (ankylosing spondylitis, reactive arthritis, IBD, psoriasis), sarcoidosis, JIA (asymptomatic — children need screening), Behçet's, herpes — topical steroids and cycloplegics (ophthalmology).
  • Intermediate and posterior — floaters, blurred vision — sarcoidosis, MS, toxoplasmosis, TB, syphilis, CMV (immunosuppressed).
• Aqueous humour:
  • Production — ciliary epithelium (active secretion — Na⁺/K⁺-ATPase, carbonic anhydrase, beta-adrenergic and alpha-2 receptors — the targets of glaucoma drugs).
  • Flow — posterior chamber → through the pupil → anterior chamber → drainage angle.
  • Outflow — trabecular meshwork → Schlemm's canal (conventional — most) and uveoscleral outflow (through the ciliary muscle — increased by prostaglandin analogues).
  • Functions — nourishes the lens and cornea, maintains eye shape and pressure.
• Ocular melanoma — the commonest primary intraocular malignancy in adults (choroid) — often found on routine eye examination.

Intraocular Pressure and the Drainage Angle

• Normal intraocular pressure (IOP) — about 10–21 mmHg; depends on the balance of aqueous production and outflow; measured by tonometry (Goldmann applanation); corneal thickness affects readings.
• Glaucoma — progressive optic neuropathy with characteristic optic disc cupping and visual field loss; raised IOP is the main modifiable risk factor (but "normal-tension glaucoma" exists).
• Primary open-angle glaucoma — the angle is open but outflow through the trabecular meshwork is reduced — painless, slowly progressive peripheral field loss (central vision lost late) — risk factors: age, family history (first-degree relatives — free NHS eye tests from 40), Black African or Caribbean ancestry, myopia, diabetes, steroids. Detected by optometrists (IOP, discs, fields).
• Primary angle-closure glaucoma — the peripheral iris blocks the angle:
  • Risk factors — hypermetropia (small eye, shallow anterior chamber), older age, women, East Asian ancestry, growing cataract.
  • Triggers — pupil dilation — dim light, anticholinergics, antihistamines, tricyclics, sympathomimetics, dilating eye drops, topiramate (different mechanism — ciliary body swelling).
  • Acute attack — severe eye pain, headache, nausea and vomiting, haloes around lights, red eye, fixed mid-dilated pupil, hazy cornea, rock-hard eye — emergency (see Ophthalmology emergencies).
  • Definitive treatment — laser peripheral iridotomy (both eyes) or lens extraction.
• Secondary glaucoma — steroids, uveitis, trauma, neovascular (diabetes, CRVO), pigment dispersion.
• Congenital glaucoma — large cloudy eyes (buphthalmos), watering, photophobia in infants.

Lens, Focusing and Refraction

• Lens — clear, avascular, biconvex, held by zonules from the ciliary body; provides about one-third of focusing power and all of the adjustable focus.
• Accommodation (focusing on near objects) — ciliary muscle contracts (parasympathetic — III) → zonules relax → lens becomes rounder (more powerful); with pupil constriction and convergence (the near triad).
• Presbyopia — age-related stiffening of the lens — reading difficulty from the 40s — reading glasses.
• Refractive errors:
  • Myopia (short-sighted) — eye too long — images focus in front of the retina — concave (minus) lenses; increased risk of retinal detachment, open-angle glaucoma and myopic maculopathy; rising in children (near work, less time outdoors).
  • Hypermetropia (long-sighted) — eye too short — convex (plus) lenses; risk of angle closure; in children — squint and amblyopia.
  • Astigmatism — unequal corneal curvature — cylindrical lenses.
  • A pinhole improves vision reduced by refractive error (not by disease) — quick bedside test.
• Cataract — opacity of the lens — gradual painless blurring, glare, faded colours — ageing (commonest), diabetes, steroids (posterior subcapsular), trauma, UV light, smoking, uveitis, radiation, congenital (rubella, galactosaemia — absent red reflex in a baby is urgent).
  • Treatment — phacoemulsification with intraocular lens implant (day case, local anaesthetic) when vision affects daily life (NICE NG77).
  • Complications — posterior capsule opacification (laser capsulotomy), endophthalmitis (rare — painful red eye with reduced vision days after surgery — emergency), retinal detachment, cystoid macular oedema.
• Lens dislocation — trauma, Marfan syndrome (upwards), homocystinuria (downwards).

Vitreous, Retina and Macula

• Vitreous — clear gel filling the back of the eye; liquefies with age:
  • Posterior vitreous detachment — new floaters and flashes (traction on the retina) — common after 50 and in myopes — needs same-day or next-day examination to exclude a retinal tear.
  • Vitreous haemorrhage — sudden floaters or loss of vision — proliferative diabetic retinopathy, retinal tear, trauma.
• Retina — neural tissue lining the back of the eye:
  • Photoreceptors (rods and cones) → bipolar cells → ganglion cells (axons form the optic nerve); retinal pigment epithelium supports photoreceptors (recycles visual pigment).
  • Optic disc — where ganglion cell axons leave — no photoreceptors (blind spot); swelling (papilloedema — raised ICP; disc swelling — optic neuritis, AION) or cupping (glaucoma).
  • Macula — central retina responsible for detailed and colour vision; the fovea at its centre is packed with cones and has no blood vessels.
• Retinal detachment — flashes, floaters, then a "curtain" or shadow spreading across the vision — emergency (same day) — especially before the macula detaches ("macula-on").
• Age-related macular degeneration — the commonest cause of blindness registration in the UK:
  • Dry (geographic atrophy) — slow central loss — no proven treatment in the UK (low vision aids; stop smoking; AREDS supplements may slow intermediate disease).
  • Wet (neovascular) — sudden central distortion (straight lines look wavy — Amsler grid), blurring — urgent referral (within 1 week — rapid access) for anti-VEGF injections.
• Diabetic retinopathy — microaneurysms, haemorrhages, exudates, cotton wool spots → proliferative (new vessels — bleeding, detachment) and maculopathy (the commonest sight-threatening form) — NHS Diabetic Eye Screening (annual or 2-yearly retinal photography for everyone with diabetes aged 12+).
• Hypertensive retinopathy — arteriolar narrowing, AV nipping, flame haemorrhages, cotton wool spots, papilloedema (malignant hypertension — emergency).

Blood Supply of the Eye

• Ophthalmic artery — the first branch of the internal carotid artery — enters through the optic canal; branches:
  • Central retinal artery — supplies the inner retina; an end artery — occlusion causes sudden painless profound loss of vision: pale retina with a cherry-red spot at the fovea (the fovea is supplied by the choroid) — a form of stroke — urgent stroke pathway (and exclude giant cell arteritis in older people).
  • Posterior ciliary arteries — supply the choroid (outer retina) and the optic nerve head — giant cell arteritis occludes them — arteritic anterior ischaemic optic neuropathy (pale swollen disc, sudden visual loss) — high-dose steroids immediately (the other eye is at risk).
  • Cilioretinal artery (present in some people) — from the choroidal circulation — may spare central vision in central retinal artery occlusion.
  • Lacrimal, ethmoidal and muscular branches; anterior ethmoidal artery — nosebleeds (see ENT page).
• Amaurosis fugax — transient monocular visual loss ("curtain coming down") from emboli (carotid stenosis, AF) — a TIA — urgent stroke assessment and carotid imaging.
• Venous drainage — central retinal vein and ophthalmic veins → cavernous sinus.
  • Retinal vein occlusion — "stormy sunset" / "blood and thunder" haemorrhages (CRVO) — risk factors: age, hypertension, diabetes, glaucoma, hyperviscosity — manage risk factors; anti-VEGF for macular oedema; neovascular glaucoma risk.
• Retinal circulation is the only place where small vessels can be seen directly — signs of hypertension, diabetes, emboli (cholesterol Hollenhorst plaques), raised ICP and vasculitis.

How We See — Photoreceptors and Visual Function

• Rods — about 120 million; peripheral retina; very sensitive — night and peripheral vision; contain rhodopsin (needs vitamin A — deficiency causes night blindness and xerophthalmia — a major cause of childhood blindness worldwide).
• Cones — about 6 million; concentrated at the fovea; colour (red, green and blue cone types) and fine detail; work in bright light.
• Phototransduction — light isomerises retinal (11-cis to all-trans) → activates transducin → closes sodium channels → photoreceptor hyperpolarises → signal to bipolar and ganglion cells.
• Dark adaptation — takes about 20–30 minutes (rhodopsin regeneration) — impaired in vitamin A deficiency and retinitis pigmentosa (inherited rod–cone dystrophy — night blindness, tunnel vision, bone-spicule pigmentation).
• Colour vision deficiency — X-linked red–green (about 8% of men, 0.5% of women); acquired colour loss — optic neuritis (red desaturation), ethambutol, macular disease.
• Visual acuity — mainly foveal function; Snellen (6/6 normal — fraction of distance the patient reads at versus a normal eye) or LogMAR charts.
• Binocular vision — the brain fuses images from both eyes (depth perception); misalignment (squint) in children causes amblyopia ("lazy eye") if not treated before about 7–8 years (patching, glasses, atropine penalisation).
• UK driving standard (DVLA, group 1) — read a number plate at 20 metres (about 6/12 binocular acuity, with glasses if needed) and an adequate binocular visual field (at least 120° horizontally) — field loss from glaucoma, stroke or retinal disease must be reported.

The Visual Pathway and Field Defects

• Visual pathway — retina → optic nerve → chiasm (nasal retinal fibres — temporal fields — cross) → optic tract → lateral geniculate nucleus (thalamus) → optic radiations (temporal and parietal lobes) → primary visual cortex (occipital).
• Pupil fibres leave the optic tract before the lateral geniculate nucleus (to the pretectal nucleus) — so cortical blindness spares the pupil light reflexes.
• Bilateral occipital infarcts — cortical blindness, sometimes with denial (Anton's syndrome).
• See the Neuro-ophthalmology page for clinical detail.

Pupils and Their Nerves

• Pupillary light reflex:
  • Afferent — optic nerve (II) → pretectal nucleus (both sides).
  • Efferent — Edinger–Westphal nucleus → parasympathetic fibres in the oculomotor nerve (III) → ciliary ganglion → short ciliary nerves → sphincter pupillae — both pupils constrict (direct and consensual).
• Relative afferent pupillary defect (RAPD) — swinging torch test — the affected pupil dilates when the light swings to it — optic nerve disease or extensive retinal disease (not cataract or refractive error).
• Sympathetic pathway (three neurones) — hypothalamus → brainstem and spinal cord to T1 → (1st order) → sympathetic chain → superior cervical ganglion (2nd order — passes the lung apex) → along the internal carotid artery (3rd order) → dilator pupillae and Müller's muscle.
  • Horner's syndrome — miosis, partial ptosis, (anhidrosis — depends on level), apparent enophthalmos — causes: Pancoast tumour, carotid dissection (painful Horner's — emergency), lateral medullary stroke, cervical cord lesions, neck surgery, cluster headache.
• Abnormal pupils:
  • Third nerve palsy with a dilated pupil — compression (posterior communicating artery aneurysm, uncal herniation) — emergency CT angiography; the pupillary fibres run on the outside of the nerve.
  • Pupil-sparing third nerve palsy — usually microvascular (diabetes, hypertension).
  • Holmes–Adie (tonic) pupil — young women, large pupil that reacts slowly, absent ankle reflexes — benign.
  • Argyll Robertson pupils — small, irregular, accommodate but don't react to light — neurosyphilis (also diabetes).
  • Drugs — pinpoint pupils (opioids, organophosphates, pilocarpine); dilated (anticholinergics, sympathomimetics, cocaine, amphetamines, tricyclic overdose, mydriatic drops, nebulised ipratropium — accidental).
  • Physiological anisocoria — up to 1 mm difference, equal in light and dark.

Eye Movements — III, IV and VI

• Six extraocular muscles — "LR6 SO4, the rest 3":

  Muscle	Nerve	Main action (testing position)
  Lateral rectus	VI	Abduction
  Medial rectus	III	Adduction
  Superior rectus	III	Elevation (best in abduction)
  Inferior rectus	III	Depression (best in abduction)
  Inferior oblique	III	Elevation (best in adduction)
  Superior oblique	IV	Depression in adduction (looking down and in — reading, walking downstairs); intorsion

• Third (oculomotor) nerve palsy — eye "down and out", complete ptosis, ± dilated pupil.
• Fourth (trochlear) nerve palsy — vertical diplopia worse looking down and in (stairs), head tilt away from the affected side — trauma (long thin intracranial course), congenital, microvascular.
• Sixth (abducens) nerve palsy — horizontal diplopia worse looking towards the affected side, failure of abduction — microvascular, raised intracranial pressure (a "false localising sign" — long intracranial course), tumours, MS, Wernicke's.
• Conjugate gaze — the medial longitudinal fasciculus links VI and III nuclei — lesion causes internuclear ophthalmoplegia (failure of adduction with nystagmus of the abducting eye — MS in the young, stroke in the old).
• Restrictive causes of diplopia — thyroid eye disease (inferior and medial recti — restricted upgaze), blowout fracture; neuromuscular — myasthenia gravis (fatigable, variable, pupils normal).
• Monocular diplopia (persists with the other eye covered) — ocular cause (cataract, refractive) — not neurological.

Basic Eye Assessment

• Visual acuity — always first (and documented — medicolegal) — each eye separately, with glasses or pinhole; if unable to read the top letter — count fingers, hand movements, perception of light.
• Pupils — size, shape, reactions, RAPD.
• Visual fields — confrontation (red pin for central scotoma and chiasmal lesions); formal perimetry.
• Eye movements — H-pattern, diplopia, nystagmus.
• Anterior segment — lids, conjunctiva, cornea (fluorescein stains epithelial defects green under blue light — abrasions, ulcers, dendritic herpes ulcer), anterior chamber (hypopyon, hyphaema), pupil.
• Red reflex — absent or white in cataract, retinoblastoma (leukocoria), vitreous haemorrhage — newborn and 6–8 week checks.
• Fundoscopy — optic disc (colour, cup, swelling), vessels, macula, retina — dilated examination is best.
• Amsler grid — distortion or missing areas — macular disease.
• Colour vision — Ishihara plates — optic nerve disease, ethambutol monitoring.
• Intraocular pressure — tonometry (optometrist or ophthalmology); a stony-hard eye on gentle palpation in acute angle closure.
• Red flags — sudden loss of vision, painful red eye with reduced vision, photophobia, chemical injury (irrigate immediately — before anything else), penetrating trauma, new diplopia with headache, flashes and curtain.

Getting Drugs into the Eye

• Routes:
  • Topical drops and ointments — most eye treatment; the cornea is a barrier (lipophilic epithelium, hydrophilic stroma); a drop is about 50 microlitres but the eye holds only about 10 — one drop is enough; separate different drops by 5 minutes; ointments last longer but blur vision (use at night).
  • Periocular and intracameral injections — subconjunctival, sub-Tenon's steroid; intracameral antibiotic at cataract surgery (cefuroxime).
  • Intravitreal injections — anti-VEGF, steroids, antivirals — reach the retina.
  • Systemic — oral acetazolamide, steroids (GCA, uveitis, optic neuritis), antivirals (herpes zoster ophthalmicus), antibiotics (orbital cellulitis, endophthalmitis).
• Systemic absorption of eye drops — drops drain through the nasolacrimal duct to the nasal mucosa and are absorbed directly into the circulation (bypassing first-pass metabolism) — timolol drops can cause bronchospasm and bradycardia.
  • Reduce it — punctal occlusion (press on the inner corner of the eye for 1–2 minutes) or simply closing the eyes after instillation.
• Preservatives (benzalkonium chloride) — damage the ocular surface with long-term or frequent use — preservative-free drops for frequent dosing, dry eye and long-term glaucoma therapy if intolerant.
• Contact lenses — remove before drops (preservatives absorb into soft lenses); don't wear during eye infections.
• Adherence — technique is often poor (especially older people with arthritis or tremor) — drop aids, teaching, simplified regimens, combination drops.
• Expiry — most multidose bottles are discarded 28 days after opening.

Glaucoma Drugs