7270362
Description
Flashcards by Liam Musselbrook, updated more than 1 year ago
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Created by Liam Musselbrook
almost 8 years ago
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| Question | Answer |
| What are is the normal range for intra-ocular pressure? | 10-21 mmHg May vary by ~5mmHg through the day Typically higher at night (dilatation) |
| Assessment/screening of glaucoma | Visual fields test Optic disc visualisation: asymmetrical cupping suggests glaucoma, as does vertical elongation of the cup, notching of the rim and haemorrhage IOP testing: Goldmann tonometer |
| What is the 'ISNT' rule of the optic disc? | In a normal disc, size of inferior > superior > nasal > temporal |
| Primary Open Angle Glaucoma (POAG) | 2nd commonest cause of sight loss Visual field defects (initially peripheral) Asymptomatic until almost blind Raised IOP not required for diagnosis (normal tension glaucoma) |
| Risk Factors for POAG | Raised IOP Family history Myopia (shortsightedness) African-Carribean race Diabetes Steroids |
| What is the pathogenesis of POAG? | Raised IOP and/or vascular factors (e.g. DM) Ischaemic loss of retinal nerve fibres Optic disc cupping Visual field defects Tunnel vision Blindness |
| Clinical features of POAG | Increased cup:disc ratio Pale disc: progressed (optic atrophy) Arcuate scotoma and nasal step Open angle Raised IOP Generally bilateral |
| Prognosis of POAG if untreated | IOP >30 - blind in 3 years IOP 25-30 - blind in 6 years IOP 21-25 - blind in 15 years |
| Name types of drugs used to medically treat POAG | Prostaglandin analogues Beta-blockers Alpha-adrenergic agonists Carbonic anhydrase inhibitors Miotics |
| How do beta blockers and carbonic anhydrase inhibitors help? | Decrease aqueous production |
| What do prostaglandin analogues do? | Increase uveoscleral aqueous outflow |
| How do alpha-adrenergic agonists treat glaucoma? | Decreases aqueous production and increases uveoscleral aqueous flow |
| What are the surgical treatment options for POAG? | Argon laser trabeculectomy Surgical trabeculectomy |
| What is the pathophysiology of Acute Angle Closure Glaucoma? | Lens becomes pushed up against iris -> pupillary block Build of of aqueous in posterior chamber and bulging of iris Closure or irido-corneal angle Blocks trebecular meshwork Overhydration of cornea -> clouding Vesicles form on cornea |
| Risk factors for AACG | More common in females (4:1), and Asians Shallow anterior chamber Shorter axial length |
| Secondary causes of AACG | Inflammatory - eg. uveitis Neovascular - eg. in DM, retinal vein occlusion (rubeotic glaucoma) Pigment dispersion syndrome Traumatic hyphaema |
| Symptoms of AACG | Pain (periocular/headache) Nausea and Vomiting Blurred vision |
| Signs of AACG | Brick-red eye Cloudy cornea Fixed mid-dilated pupil IOP >21mmHg Closed iridocorneal angle |
| Management of AACG | Urgent referral to ophthalmologist Reduce aqueous secretions: acetazolamide Induce pupil constriction: topical pilocarpine Steriod e.g. prednisolone |
| What systemic treatment is given for AACG? | IV carbonic anhydrase inhibitor IV hyperosmotic agent Analgesia Anti-emetic |
| Medium-term treatment for AACG? | Laser iridotomy - two small holes in iris for drainage Trabeculectomy |
| Management of POAG | Prostaglandin analogues (e.g. Latanoprost) - ↑ uveoscleral outflow, may cause brown pigmentation Beta-blockers (e.g. Timolol) - ↓ aqueous production, avoid in asthmatics and heart block Sympathomimetics (e.g. brimonidine) - ↓ aqueous production + ↑ increase outflow, avoid if taking MAOI or tricyclic antidepressants, poss. hyperaemia Carbonic anhydrase inhibitors (e.g. Dorzolamide) - ↓ aqueous production, may cause sulphonamide-like reactions Miotics (e.g. pilocarpine) - ↑ uveoscleral outflow, constricted pupil, headache and blurred vision |
| What drops can precipitate AACG? | Mydriatic drops |
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