Opthamology Flashcards
Where is aqeuous humor produced
Ciliary body - travels through the anterior chamber, trabecular meshwork and into the canal of schlemm before reaching general circulation
Pathophys of open-angle gluacoma
Gradual increase in resistance through the trabecular meshwork makes it more difficult for aqeuous humor to flow through the meshwork + exit the eye therefore the pressure slowly builds up within the eye
Pathophys of closed-angle glaucoma
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing any aqueous humor from draining away = opthamological emergency (continuous build up of pressure)
What opthalmoscopy finding suggests increased pressure
Cupping of the optic discs
Open-angle glaucoma
Sx;
* Often diagnosed by routine screening as remains asymptomatic for a long while
* Gradual loss of peripheral vision / blurred vision
* Fluctuating pain / headaches
* Halo’s appear around lights particularly at nightime
Invx;
1. Gold standard = Goldmann applanation tonometry (measures intraocular pressure)
2. Fundoscopy - optic disc cupping
Management;
–> commence when intraocular pressure is 24mmHg +
1. Prostaglandin analogue eye drops (latanoprost)
2. Beta-blockers (to reduce production of aqueous humor)
3. Carboic anhydrase inhibitors (dorzolamide)
Surgery = trabeculectomy (when eyedrops become ineffective)
Side effects of latanoprost
Eyelash growth
Eyelid pigmentation
Iris browning
Closed-angle glaucoma
Risk factors = Age / Long-sightedness (hypermetropia) / Pupil dilation / female / FHx / Chinese / Shallow anterior chamber / Medications (e.g TCAs & anticholingerics)
Sx; Rapid onset of
* severely painful red eye
* blurred vision
* Decreased visual acuity
* Halo’s around lights & symptoms worsened with mydriasis
* Associated headache & nausea & vomitting
O/E - the eye will be red & teary with a **hazy cornea + fixed dilated pupil. Eyeball is firm to touch. **
Diagnosis = Both Tanometry + Gonioscopy (slit lamp) are needed
Management;
* same day referral to opthamology
* **Lie patient on back + Pilocarpine eye drops (Inc dose for brown eyes) + Acetazolamide
**
Definitive management = Laser iridotomy
How does Pilocarpine help in close-angle glaucoma
= Cholingeric agonsit
It causes miosis (constriction) which therefore contracts the ciliary muscles - opens the trabecular meshwork + increases outflow of aqueous humor
Other uses = Sjogren’s syndrome & Radiotherapy induced dry mouth
Macular degeneration
Most common cause of blindness in UK. Common in pts over 75yrs.
2 types;
1. Wet - 10% - worse prognosis and more acute & have development of new vessels (can bleed) stimulated by VEFG.
2. Dry - 90% - characterised by drusen
RF = Age / Smoking / White or Chinese / Fhx / CVD
Presentation;
* Difficulties in dark adaptation
* Gradual worsening of central vision loss
* Reduced visual acuity
* Crooked or wavy appearance to straight lines.
O/E = Reduced visual acuity + scotoma.
* Amsler grid test = distortion of straight lines
* Fundoscopy = Drusen
Diagnosis = slit-lamp fundus examination + optical coherence tomography (1st line for Wet AMD)+/- Fluroscein angiography (2nd line to diagnosed wet AMD)
Management;
–> Refer to opthamology
Dry AMD = conservative management
Wet = Anti-VEGF medication (Ranibizumab, bevacizumab) - *needs to be commenced <3months in to be effective *
Layers of the macula
- Choroid layer - contains the blood vessels which supply blood to the macula
- Bruchs membrane
- Retinal pigment epithelium
- Photoreceptors
What are drusen
Yellow deposits of proteins/lipids between the retinal epithelium + photoreceptors. Normally they are small and hard but get bigger and more of them in macular degeneration.
What is the most common cause of blindness among 35-65yr olds
Diabetic retinopathy
How does Diabetes cause retinopathy
Prolonged hyperglycemia causes damage to small vessels in the retina + endothelium. It increases vascular permeability which causes leakage to blood from blood vessels (blot haemorrhages) and lipid deposits (hard exudates)
Damage to blood vessel walls causes **microaneurysms + venous bleeding. **
Damage to retinal nerve fibres causes Cotton wool spots
As the disease progresses there is neovascularisation (Due to VEGF)
Features/Staging of non-proliferative diabetic retinopathy
Mild = microaneurysms
Moderate = microaneurysms + Blot haemorrhages + Hard exudates + cotton-wool spots
Severe = Microaneurysm/blot haemorrhage in 4 quadrants + cotton-wool spots in 2
Management = Generally just observe + prevent it getting worse. if severe = laser photocoagulation.
Proliferative Diabetic retinopathy
Presence of Neovascularisation (may lead to vitreous haemorrhage)
May have macular oedema
Management = Panretinal laser photocoagulation
Consider Anti-VEGF (e.g ranibizumab)
If vitreous haemorrhage = vitreoretinal surgery
Keith-Wagner classification of Hypertensive retinopathy
Stage 1 = Silver-wiring
Stage 2 = AV nipping
Stage 3 = Flame/blot haemorrhages (macular star) + Cotton-wool spots + hard exudates
Stage 4 = Papillodema