EYE CONDITIONS
A patient presents with a headache, which ACUTE ANGLE CLOSURE GLAUCOMA
came on suddenly. She feels nauseous, PATHOPHYS: the flow of aqueous humour out of
the eye is blocked -> IOP rapidly increases,
has blurry vision and complains of haloes
damaging optic nerve
around lights. She has recently been RISK FACTORS: hypermetropia, pupillary dilatation,
taking amitriptyline for back pain. lens growth associated with age, female, FHx,
medications (tricyclic, anticholinergic, adrenergic)
CLINICAL FEAT: severe, sudden, orbital pain and
frontal headache rapidly progressive visual loss,
N&V, halos around lights due to corneal oedema,
pupil fixed and dilated, hard, red eye, hazy cornea,
usually at night due to mid-dilation of pupils->
blockage.
IX: immediate ophthalmologic evaluation, slit lamp,
OCT, visual field analyser, GAT to check IOP
MX: initial (lie pt on their back without a pillow,
pilocarpine eye drops 2% blue and 4% brown eyes,
beta-blocker, apha-2-agonist, 500mg IV
acetazolamide, analgesia, anti-emetic), definitive
(laser iridotomy)
A 57-year-old patient presents with PRIMARY OPEN ANGLE GLAUCOMA
progressive visual loss around her PATHOPHYS: normal angle between the iris and the
cornea. POAG is the most common form of
peripheries and blurred vision. They glaucoma, raised IOP normally but not invariably
currently have T2DM and myopia. What is present
the likely diagnosis? RISK FACTORS: increasing age, Afro-Caribbean,
raised IOP, diabetes, HTN, FHx, myopia,
corticosteroids, thin cornea
CLINICAL FEAT: peripheral visual field loss (nasal
scotomas progressing to ‘tunnel vision’, decreased
visual acuity, optic disc cupping
FUNDOSCOPY: optic disc cupping (cup-to-disc ratio
>0.7), optic disc pallor (atrophy), bayonetting of
vessels, cup notching, disc haemorrhages
IX: automated perimetry for visual field, slit lamp,
tonometry for IOP, central corneal thickness
measurement, gonioscopy
MX: to prevent visual loss, prostaglandin analogues
(1st line), beta-blocker, sympathomimetics, carbonic
anhydrase inhibitor, miotics, surgery or laser
A 67-year-old patient presents to the GP CATARACTS
PATHOPHYS: protein aggregates disrupt the crystalline
complaining of glare when looking at fibres in the lens, causing, clouding, light scattering and
lights and poor vision at night. She also visual obstruction
reports that she no longer needs reading CLINICAL FEAT: visual loss of acuity, blurred vision,
poor night vision, sensitivity to light and glare, seeing
glasses, but her distance vision has ‘halos’ around lights, polyopia, reduction in colour
worsened. She has a PMHx of T2DM intensity, changes in glasses prescription
controlled with metformin SIGNS: loss of red reflex, white/ grey pupil, nystagmus.
Cortical, post subscapular, ulcer, or mature cataracts
IX: ophthalmoscopy after pupil dilation (normal
findings), slit lamp examination (visible cataract)
MX: early stages (stronger glasses/ contacts, use
brighter lighting) but surgery only effective
management to replace the lens
COMPLICATIONS: endophthalmitis, posterior capsule
opacification, retinal detachment, posterior capsule
rupture
, A 70-year-old lady presents DRY AMD
complaining of gradual loss of vision. PATHOPHYS: geographic atrophy. Drusen are
lipid and protein waste products of
She reports that over recent years, photoreceptors deposited on Bruch’s
her vision has deteriorated to the membrane on the choroid. Thickening of the
point where she is worried it is not just membrane and impairing blood supply to the
old age. She has a hx of cataracts, RPE. Ischemia and degeneration of
photoreceptors occurs in the macula.
which have been treated with surgery. CLINICAL FEAT: progressive visual
O/E, you note no pupillary defects. disturbance, gradual loss of central vision,
Fundoscopy shows appearance of peripheral vision retained, they may also suffer
yellow deposits in macules. from photopsia
SIGNS: distortion of line perception may be
noted on Amsler grid testing, fundoscopy has
drusen
IX: slit lamp microscopy IX of choice,
fluorescein angiography, OCT to visualise
retina in 3D
MX: combo of zinc and anti-oxidant vitamins
A, C and E
A 60 year old lady presents WET AMD
complaining of rapid vision loss. She PATHOPHYS: growth of new, abnormally
located blood vessels (choroidal
reports that she cannot see people’s neovascularisation), sudden loss of vision is
faces directly in front of her and due to leakage of fluid or by haemorrhage
straight lines are distorted. She is a RISK FACTORS: advancing age, smoking,
current FHx, HTN, dyslipidaemia, diabetes
CLINICAL FEAT: carries worst prognosis,
smoker and profound, sudden central visual loss, distortion
has history of straight lines, (same as dry AMD but more
of HTN. sudden)
IX: slit-lamp microscopy, fluorescein
angiography (used if neovascular ARMD), OCT
MX: photodynamic therapy, anti-VEGF
intravitreal injection, laser, irradiation, surgery
A 65 year old patient presents with DIABETIC RETINOPATHY
PATHOPHYS: hyperglycaemia increases retinal
painless, gradual visual loss, mainly blood flow and abnormal metabolism in the retinal
central. She also complains of seeing vessel walls. This precipitates damage to endothelial
cells and pericytes. Endothelial dysfunction leads to
‘black floating things’. She currently increased vascular permeability -> exudates.
has type 2 diabetes mellitus Pericyte dysfunction predisposes to formation of
microaneurysms. Growth factors due to retinal
ischaemia cases neovascularisation
CLASSIFICATION: non-proliferative (mild, mod,
severe), proliferative, maculopathy
CLINICAL FEAT: microaneurysm and dot
haemorrhages, exudates, cotton wool spots, retinal
oedema, dull retina, loops, doubling and beading
neovascularization
IX: OCT, fundoscopy
MX: diabetic eye screening once a year, optimise
glycaemic control, control BP and lipid, maculopathy
(anti-VEGF), non-prolif (observe laser if severe),
prolif (laser, anti-VEGF, vitreoretinal surgery if
severe)
