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Summary Ophthalmology summaries

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Summary document containing ophthalmology conditions for medical student finals. Contains information about clinical features of each condition, as well as relevant diagnostic tests and investigations, risk factors, causes and management guidelines. Everything has been cross referenced with passm...

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  • November 20, 2023
  • 17
  • 2023/2024
  • Summary
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saskiahogan
OPHTHALMOLOGY




Microsoft Office User
[COMPANY NAME] [Company address]

,CATARACTS



AETIOLOGY PATHOPHYSIOLOGY
Ocular causes Any light-scattering opacity within the lens
- Trauma Can cause visual loss if extensive or lying on the visual
- uveitis axis
- high myopia Most treatable cause of blindness worldwide
- steroid eye drops
- intraocular tumour Lens is mostly made of water + protein. The protein is
arranged to let light pass through and focus on the
systemic causes retina. If the proteins clump together it can start to
- diabetes, other metabolic disorders cloud a small area of the lens, blocking some light from
- systemic steroids, chlorpromazine reaching the retina and interfering with vision
- XR
- Congenital rubella
- Atopic dermatitis
- Myotonic dystrophy CLINICAL FEATURES
- Down’s syndrome - Painless loss of vision
Risk factors - Glare
- Age - Change in refraction
- Smoking - Altered colour vision
- Long term UV exposure - Decreased VA (especially in bright light)
- FHx - Difficulty driving at night
- Dark silhouette against red reflex
- Loss of red reflex



DIAGNOSIS MANAGEMENT
Look for systemic cause if < 60 years, or unilateral Surgery – phacoemulsification
cataract Uses US to break up cataract and replace with an
Biometry to enable accurate intraocular lens power artificial intraocular lens
(IOL) calculatory




COMPLICATIONS OF SURGERY
1/1000 have reduced sign
1/10,000 lead to loss of eye
- Iris prolapse
- Posterior capsule opacification
o Decreased VA over months
o Treated with laser capsulotomy – hole created in posterior capsule in the pupillary axis
- Endophthalmitis – vitreal infection
- Cystoid macular oedema
o Severe decreased VA
o Treated with steroids, NSAIDs
- Vitreous loss and retinal detachment

, DIABETIC RETINOPATHY



SUMMARY PATHOPHYSIOLOGY
Affects 40% of diabetic population Microangiopathy with damage to small vessels.
T1DM > T2DM Intracellular accumulation of sorbitol  cellular
damage.
Proliferative DR affects about 10% of the diabetic
population – T1DM particularly at risk - Death of pericytes
- Thickening of capillary BM
Risk factors - Loss of vascular smooth muscle cells
- Duration of diabetes - Proliferation of endothelial cells
- Poor diabetes control - Abnormal RBCs
- Pregnancy, sometimes associated with rapid - Increased plasma viscosity
progression All of which lead to capillary occlusion and leakage
- HTN
- Nephropathy Capillary non-perfusion causes retinal hypoxia 
- Smoking release of VEGF  neovascularisation
- Obesity Release of VEGF also causes breakdown in the blood-
retinal barrier which can cause diabetic macular
oedema
PRESENTATION
Visual symptoms CLASSIFICATION
- Asymptomatic 1. Non-proliferative DR
- Decreased VA 2. Diabetic maculopathy – foveal oedema,
- Distortion exudates, or ischaemia
- Floaters a. Most common cause of visual
Non-proliferative: dot/blot haemorrhages around impairment in diabetes (particularly T2)
the periphery, microaneurysms b. Diffuse – caused by extensive capillary
leakage
- Cotton wool spots
c. Local – focal leakage from
- Hard exudates
microaneurysms and dilated capillaries
- Blot haemorrhages
3. Proliferative DR – neovascularisation within 1 disc
diameter and/or new vessels elsewhere in the
fundus
MANAGEMENT 4. Advanced diabetic eye disease – tractional
Non-proliferative: observation retinal detachment, significant persistent
vitreous haemorrhage, neovascular glaucoma
Diabetic macular oedema
- Centre-spared = macular laser therapy
- Centra-involved = COMPLICATIONS
o VA < 6/9 = anti-VEGF injection - Retinal haemorrhage
o VA > 6/9 = observation - Vitreous haemorrhage
Proliferative DR = panretinal photocoagulation - Rubeosis iridis (formation of new blood vessels in
the iris)
Anti-VEGF injections can’t be used as it only lasts ~1
- Optic neuropathy
months (not practical). PRPC aims to decrease
- Cataracts
oxygen requirement of retina by destroying the
peripheral retina and leaving the macular –
preventing release of VEGF
It does cause a decrease in the visual field. Since the
peripheral retina is largely made of red cells –
ablation of the periphery means patient will be
night-blind.

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