Ophthalmology: Eye Conditions 1 Flashcards
Glaucoma, macular degeneration, cataracts
What is glaucoma?
Glaucoma is a group of eye diseases that cause progressive optic neuropathy. It is characterised by visual field defects and characteristic changes to optic nerve head(e.g. pathological cupping or pallor of the optic disc). Commonly associated with raised intraocular pressure (IOP) but may occur without raised IOP.
*NICE definition
Glaucoma can be classified in numerous different ways; state 4 ways it can be classified
- Age of onset: congenital, infantile, juvenile or adult
- Cause: primary or secondary
- Rate of onset: acute, subacute or chronic
- Angle between the iris and cornea in the anterior chamber: open or closed angle
*One we will focus on
What is the normal intraocular pressure?
What creates/maintains this pressure?
- 10-21mmHg
- Resistance to flow through trabecular meshwork and canal of Schlemm
Describe the pathophysiology of open-angle glaucoma
- Aqueous humour produced by ciliary body; then flows under iris and through the pupil into the anterior chamber. Then drains through trabecular meshwork into canal of Schlemm and eventually drains into systemic circulation
- Gradual increase in resistance through trabecular meshwork
- Reduces drainage of aqueous humour
- Slow increase in IOP
State some risk factors for open-angle glaucoma
- Increasing age
- FH
- Black ethnic origin
- Near-sightedness/short-sighted/myopia
- Long term topical corticosteroids
State some symptoms of open-angle glaucoma/describe the typical presentation
How else may a patient present?
Present with gradual onset of:
- Tunnel vision/reduced peripheral vision (GLAUCOMA AFFECTS PERIPHERAL VISION FIRST)
- … above may progress to decreased visual acuity
- Halos around lights (particularly at night)
- Blurred vision
- Headaches
- Fluctuating pain
It can be asymptomatic for a long time so may be picked up during routine optometry appointments.
What might you find on examination of someone with open-angle glaucoma?
- Raised intraocular pressure
- Cupping of optic disc (optic cup is >0.5 size of the optic disc)
- Optic disc pallor (indicates optic atrophy)
****In centre of optic disc is the optic cup; this is a small indent that is normally <0.5x size of optic disc. When IOP is raised, pressure causes the indent to become wider and deeper- known as ‘cupping’
How do we diagnose open-angle glaucoma?
- Visual field assessment: looking for tunnel vision
- Fundoscopy: assess for optic disc cupping & optic nerve health
- Measure IOP: Goldmann applanation tonometry is gold standard
- Gonioscopy: measure anterior chamber depth
Explain how each of the following work to measure intraocular pressure:
- Non-contact tonometry
- Goldmann applanation tonometry
Non-contact tonometry: shoot puff of air at cornea and measure corneal response to that air (less accurate than Goldmann applanation tonometry but helpful for general estimate/screening)
Goldmann applanation tonometry: special device mounted to slit lamp. Makes contact with cornea and applies different pressures to get an accurate measure of IOP (gives an accurate measure of IOP so is GOLD STANDARD)
What are the NICE recommendations in relation to screening pts with first degree relatives who have open angle glaucoma?
People older than 40 years of age who have a first-degree relative (parent, sibling, or child) with open angle glaucoma should be examined annually - free examination is available through the NH
Discuss the management of open-angle glaucoma
Aim is to reduce IOP. Usually start treatment when IOP is >/=24mm/Hg and follow up to assess response to treatment. Options include:
- First line= prostaglandin eye drops (e.g. latanoprost)
- Second line:
- Beta blockers (e.g. timolol)
- Carbonic anhydrase inhibitors (e.g. dorzolamide)
- Sympathomimetics (e.g. brimonidine)
- If eye drops don’t work, trabeculetomy surgery or laser treatment
Explain the mechanism of action of each of the following eye drops when used in open-angle glaucoma:
- Prostaglandins
- Beta blockers
- Carbonic anhydrase inhibitors
- Sympathomimetics
- Prostaglandins (e.g. latanoprost): increase uveoscleral outflow
- Beta blockers (e.g. timolol): reduce production of aqueous humour
- Carbonic anhydrase inhibitors (e.g. dorzolamide): reduce production of aqueous humour
- Sympathomimetics (e.g. brimonide [alpha-2 agonist]): reduce production of aqueous humour & increase uveoscleral outflow
State some common side effects of prostaglandin eye drops used in open-angle glaucoma
- Eyelid pigmentation
- Iris pigmentation
- Increased eyelash length
Who should you avoid using beta blocker eye drops in?
- Asthmatics
- Heart block
Who should you avoid using sympathomimetic eye drops in?
Those taking TCAs or MAOIs
Explain what trabeculectomy surgery involves and how it works for open-angle glaucoma
- Create new channel from anterior chamber through sclera to a location under conjunctiva
- Forms/creates a bleb under conjunctiva where aqueous humour can drain
- Aqueous humour then reabsorbed from the bleb into general circulation
Describe the pathophysiology of acute-angle glaucoma
- Iris bulges forwards and seals off/blocks trabecular meshwork
- Hence, aqueous humour can’t drain out of anterior chamber (through trabecular meshwork as usual)
- Increase in IOP
- Pressure particularly increases in posterior chamber which worsens the closure of the angle as it further pushes the iris forwards
State some risk factors for acute-angle glaucoma
- Increasing age
- Females (4:1)
- FH
- Chinese & East asian origin (rare in those of black ethnic origin unlike open-angle)
- Shallow anterior chamber
- Hypermetropia
- Medications
- Mydriatic drops
- Adrenergic e.g. NA
- Anticholinergics e.g. oxybutynin, solifenacin
- TCAs e.g. amitriptyline (have anticholinergic side effects)
State some symptoms of acute-angle glaucoma/describe the typical presentation
Short/acute history of:
- Severely painful red eye
- Blurred vision
- Halos around lights
- Associated symptoms: nausea/vomiting, headaches
What might you find on examination of someone with acute-angle glaucoma?
- Red eye
- Teary
- Hazy cornea (due to corneal oedema)
- Fixed pupil size
- Dilatation of pupil on affected side
- Firm/hard eyeball on palpation
- Decreased visual acuity
Acute-angle glaucoma is an ophthalmological emergency; true or false?
True; requires urgent referral to ophthalmologist to prevent permanent vision loss
What investigations would you do for someone with suspected acute angle glaucoma?
- Gonioscopy is the gold standard investigation for assessing the angle between the iris and cornea
- Goldmann applanation tonometry
Discuss the immediate management of acute-angle glaucoma
Urgent referral to ophthalmologist. Aim is to reduce IOP:
- Combination of eye drops:
- Parasympathomimetic/mitotic e.g. pilocarpine
- Beta blocker e.g. timolol
- Sympathomimetic/alpha-2 agonist e.g. brimonidine
- Carbonic anhydrase inhibitor e.g. dorzolamide
- PO or IV carbonic anhydrase inhibitor e.g. acetazolamide
*See separate FC for NICE guidance on what to do if immediate admission to ophthalmology is not possible
Discuss the definitive management of acute-angle glaucoma
- Laser iridotomy (use laser to make hole in the iris so that aqueous humour can flow from posterior chamber into anterior pressure. Relieves pressure that was pushing iris against cornea.)
What are the four layers of the macula?
- Choroid layer
- Bruch’s membrane
- Retinal pigment epithelium
- Photoreceptors
Describe the pathophysiology of ARMD; include any differences between wet and dry
Some features are common to both wet & dry AMD:
- Drusen: yellow deposits of proteins & lipids that appear between Bruch’s membrane and retinal pigment epithelium. Some small drusen are normal; however, larger and greater numbers of drusen are an early sign of AMD
- Atrophy of retinal pigment layer
- Degeneration of photoreceptors
Features only in wet AMD:
- New vessels grow from choroid layer into the retina: can leak fluid or blood → oedema and more rapid loss of vision
Summary of pathophysiology of ARMD
What do drusen look like on fundoscopy?
Describe typical presentation of cataracts (include symptoms & signs- such as those on fundoscopy)
Usually asymmetrical symptoms (both eyes are affected separately):
- Very gradual reduction in visual acuity
- Change of colour vision with colours becoming more brown or yellow
- Starbursts around lights/glare (particularly at night)
- Loss of red reflex (grey or white)
Briefly outline how cataract/lens replacement surgery is done
- Make small in incision in anterior capsule
- Use high frequency ultrasound to emulsify lens (phacoemulsification)
- Aspirate old lens out
- Insert folded new artificial lens into capsule and allow to unfold
State some potential complications of cataract surgery
- Retinal detachment
- Posterior capsule rupture
- Endophthalmitis
- Posterior capsule opacification (thickening of lens capsule. Shown in image)
***Not exactly a complication but once had cataract surgery may then be able to diagnose other pathology e.g. AMD, diabetic retinopathy etc… this may be reason for vision not improving
