Ophthalmology Flashcards
What is the typical presentation of keratitis and what is it?
Keratitis = infection of the cornea.
Presents with a GRITTY SENSATION, painful red eye + photophobia.
What are the typical organisms that cause keratitis?
Bacterial - staph aureus = most common. pseudomonas aeruginosa in contact wearers (a risk factor)
Amoeba - Acanthomoebic keratitis - 2ndary to eye exposure to contaminated water/soil - pain is disproportionate
Parasitic - onchocercal keratitis (river blindness)
Viral - herpes simplex keratitis
How to manage suspected keratitis?
Same day referral to an eye specialist for slit lamp examination. Topical antibiotics (quinolones). Don’t use contacts until healed.
How should squint (strabismus) in children be managed?
In children < 3 months with intermittent squint and no other visual concerns = reassure, is normal
If > 3 months and persistent squint +/- other concerns regarding vision then = ophthalmology referral, may trial an eyepatch
What is blepharitis?
Blepharitis = inflammation of the eyelid margins
Presents w/ dry, gritty eyes, normally bilateral, may have red eyelid margins, may have sticky discharge in the morning.
Blepharitis -> can either be posterior blepharitis (more common = dysfunction of the meibomian gland [secretes lipids to stop your tear film evaporating]) or anterior blepharitis (less common, 2ndary to seborrheic dermatitis or a staph aureus infection in which case tends to present with SWOLLEN eyelids)
Mx of blepharitis -> hot compress, artificial tears, mechanical cleaning of the eyelids with cotton buds dipped in cooled boiled water and baby shampoo.
If the eyelids are swollen this can suggest a staph aureus infection (anterior blepharitis) and may require abx.
Which drugs commonly cause colour disturbance of vision?
Digoxin -> Yellow vision
Sildenafil / Viagra -> blue vision (‘the blue pill’)
What is the most common cause of blindness in adults in the DEVELOPED world?
Diabetic retinopathy
What is the different types of diabetic eye disease?
- Diabetic maculopathy:
More common in Type II DM.
Hard exudates in the macula (centre of the retina, responsible for central vision and detailed vision) but with the rest of the retina normal on fundoscopy. - Non-proliferative diabetic retinopathy (microvascular + BM dysfunction but no neovascularization yet)
Mild NPDR: microaneurysm/s only in the retina
Moderate NPDR: at least 1 microaneurysm or area of haemorrhage PLUS hard exudate or cotton wool spot (lighter areas caused by nerve fibre infarcts) or venous beading
Severe NPDR: any of the following: (the 4:2:1 rule)
- > 20 sites of haemorrhage in each of the 4 quadrants of the retina
- venous beading in 2 or more quadrants
- IRMA in 1 or more quadrants (intraretinal microvascular abnormalities = abnormal branching from existing vessels)
- Proliferative diabetic retinopathy
(sometimes this develops FROM non-proliferative, sometimes proliferative can appear de nova!!)
Ischaemia (due to microthrombi / poor perfusion due to the macular oedema) -> VEGF -> neovascularisation -> prone to rupture / haemorrhage
EITHER: - Neovascularisation
or - Vitreous / Preretinal haemorrhage
on fundoscopy
What are risk factors for diabetic retinopathy?
Type I DM Poor glycaemic control Pregnancy HTN Dyslipidaemia Smoking Co-existent diabetic nephropathy
What is management of diabetic retinopathy?
Non-proliferative:
- Improved Glycaemic Control: target HbA1C is <6.5% in Type I, < 6.5% in Type II that diet-controlled or controlled with 1 medication not associated with hypoglycaemia, <7% in Type II on meds associated with hypoglycaemia (HbA1C target in Type II might be further relaxed if reduced life expectancy, high risk of hypos eg driving heavy machinery)
- Monitoring
Proliferative diabetic retinopathy:
- Pan-retinal photocoagulation (laser treatment that reduces the risk of tractional retinal detachment)
- Anti-VEGF injections (Ranibizumab, Bevacizumab)
What are common causes of tunnel vision (LOSS OF PERIPHERAL VISION)
1) Glaucoma (progressive optic neuropathy, caused by increased intraocular pressure killing retinal ganglion cells)
2) Retinitis pigmentosa -> genetic condition, presents in childhood with initially loss of night vision and peripheral vision and then goes onto complete vision loss.
3) Chorioretinitis (inflammation of the choroid = the vascular layer of the eye between the sclera and the retina -> when inflamed [bacteria, AIDs, newborn eye infections] can affect blood supply to the retina leading to visual loss)
4) Optic atrophy in tabes dorsalis (tertiary syphilis)
5) Papilloedema (optic disc swelling 2ndary to ^ ICP -> tumour, haemorrhage, cerebral venous sinus thrombosis)
What is the pathophysiology of macular degeneration and how does it present?
Macular degeneration = degenerative condition of the macula leading to irreversible CENTRAL vision loss.
Risk factors: Biggest = age. Current smoker. Family history of MD.
High BMI / cardiovascular risk / HTN. Deficiency of Vitamins A, C, E, Omega 3 fatty acids + zinc.
2 types:
1) Dry macular degeneration - 90% of MD. Presents with more GRADUAL, SLOW vision loss.
Pathophysiology -> Blockage of secretions from the RPE of the retina = backlog of secretions = clump to form soft drusen = atrophy of RPE and surrounding photoreceptors
Presentation = graudal loss of central vision, difficulty with dark-light adaption (worse in dawn and late night), fluctant visual loss
Clinical findings -> Drusen on fundoscopy, distorted line perception on Amsler grid testing
NO SPECIFIC TREATMENT
It is possible to subsequently develop wet macular degeneration from dry.
2) Wet macular degeneration (aka exudative / neovascular) - presents with more SUDDEN vision loss. Carries WORSE PROGNOSIS.
Wet MD -> can use anti-vascular endothelial growth factor
Basic anatomy of the eye
3 layers to the eye.
1) Sclera
2) Choroid
3) Retina - innermost lining -converts light into neuronal signals sent via the optic nerve
Structure of retina:
* Retinal Pigment Epithelium (RPE) - adjacent to the choroid
* Rods (detect motion, black and white vision, function well in low light) and cones (colour vision, concentrated in the macula, perform best in bright light)
* Ganglion cells -> conjoin to form the optic nerve
* Macula = centre of the retina, responsible for central + fine acuity vision - high concentration of cones
Central retinal ARTERY occlusion presentation?
SUDDEN and PAINLESS vision loss
Fundoscopy: prominent fovea ( cherry red spot), retinal pallor, reduced pupillary light response
central retinal VEIN occlusion presentation?
more GRADUAL vision loss
Fundoscopy: ‘pizza fundoscopy’ with lots of red dilated venous vessels
presentation of blepharitis?
swelling of the eyelids
not always infected by when it is tends to be staph aureus
presentation of stye?
VERY tender + red lump due to infection of follicle
presentation of chelazion?
blocked oil gland, firm swelling, non-tender
Typical presentation of anterior scleritis?
INTENSE eye pain + blurred vision+ photophobia
typical presentation of posterior scleritis?
PAINLESS vision loss + swollen eyelid + swollen optic disc
Tx = NSAIDs / steroids
