Glaucoma Flashcards
1
Q
What is the definition of glaucoma?
A
condition characterised by optic disc cupping and visual field loss, in which intraocular pressure (IOP) is sufficiently raised to impair normal optic nerve function
2
Q
What are 2 groups into which glaucoma can be classified?
A
Primary and secondary
3
Q
What is the difference between primary and secondary glaucoma?
A
In primary there is no cause apparent, but in secondary a cause is apparent e.g. trauma
4
Q
What 2 groups can both primary and secondary types of glaucoma be classified into?
A
Open angle and closed angle
5
Q
What are the 4 general groups used to talk about glaucoma?
A
- Primary open angle glaucoma (POAG) 2. Primary acute angle-closure glaucoma (AACG) - due to hypermetropia 3. Secondary glaucoma - inflammatory, trauma, neurovascular 4. Congenital glaucoma
6
Q
What is the definition of primary open angle glaucoma?
A
Raised IOP>21mmHg (normal is 10-21) with open aqueous drainage angle
7
Q
What is meant by open aqueous drainage angle in POAG?
A
no macroscopic blockage of aqueous outflow - through trabecular meshwork and through ciliary body
8
Q
What are 2 clinical features which define POAG?
A
Pathological cupping of optic disc and glaucomatous visual field loss
9
Q
What is the definition of ocular hypertension?
A
Raised IOP>21mmHg but normal optic disc and field
10
Q
What is the prevalence of glaucoma?
A
About 65 million people worldwide; predicted 7 million would be blind. note: in developed countries only 50% diagnosed
11
Q
What is thought to be the proportion of people with POAG with blindness?
A
4.4-7.9% (it varies)
12
Q
How does intra ocular normally vary throughout the day?
A
rises during the morning then falls again in the afternoon, by 7pm in the evening dramatically rises again, drops off at 11pm
13
Q
What are 2 places where drainage of aqueous humour occurs and what is the proportion of each?
A
- Conventional route: 85% drains through trabecular meshwork into the canal of Schlemm in anterior chamber angle 2. Uvoscleral route: 5% drains through ciliary route and into ciliary circulation
14
Q
What is the direct mechanical theory for the pathogenesis of open angle glaucoma?
A
raised IOP mechanically damages the nerve
15
Q
What is the indirect ischaemic theory for open angle glaucoma?
A
raised IOP interferes with microcirculation, perfusion pressure is too low to compensate
16
Q
What are the two theories for optic nerve damage in primary open angle glaucoma?
A
- direct mechanical theory 2. indirect ischaemic theory
17
Q
What are 3 contributing causes to POAG?
A
- Ageing (increased evidence with increasing age, rare <40y) 2. corticosteroids - topical and systemic 3. Inherited (dominant)
18
Q
What are 3 types of associations of POAG?
A
- family history 2. ocular - high myopia, central retinal vein occlusion 3. system e.g. diabetes mellitus
19
Q
What are the systems of POAG?
A
usually none, never pain, white eye. Visual loss when condition advanced
20
Q
What are three things to perform on examination in POAG and what will be seen?
A
- visual acuity: usually normal, reduced in advanced 2. Goldmann applanation tonometry: raised IOP 3. Gonioscopy (looking at drainage angle with goniolens and slit lamp) open drainage angle
21
Q
What is the Goldmann applanation tonometer found as part of?
A
slit lamp
22
Q
How is pressure measured with the applanation tonometer?
A
shine a blue light on eye, apply pressure using knob you can twist until 2 semicircles that you can see just touch - gives you the pressure (see picture)
23
Q
How do you measure cup: disc ratio?
A
in pathology there will be little inner circle in the optic disc; vertical length of inner circle divided by whole disc vertical length
24
Q
What is a pathologically cupped disc ratio defined as and how does it appear? 5 features
A
- Cup:disc ratio>0.5 2. Pallor 3. Asymmetry of C:D ratio 4. Nasal shift of vessels, 5. Haemorrhages (see image)
25
What are 2 possible complications of glaucoma?
retinal vein occlusion, blind eye(s)
26
How does glaucomatous visual field loss occur?
Initially nasal step then superior and inferior arcuate scotomas; temporal and central islands then turns to complete field loss i.e. blindness
27
What is a scotoma?
partial los of vision in an otherwise normal visual field; little patch of visual loss
28
What are Goldmann fields?
Patient has head against bar looking into bowl; operators look through hole to see if patient looking at intended target not moving eyes around. Operator moves thing around, patient presses button each time they see light. Plot it and join it up (see Goldmann chart)
29
How are scotomas/ areas of visual loss shown on a Goldmann field chart?
dark purple filled in blob
30
What are Humphrey fields?
(see image) automated version; patient puts chin rest on machine looking at bowl. computer program shies light in different fields and works out visual field loss
31
Is glaucoma treatable/curable?
treatable but not curable
32
What will happen to incidence of glaucoma in the future?
will become more prevalent as more of population living longer
33
Why might early disease or ocular hypertension not be picked up?
Because asymptomatic
34
What 4 things can cause ocular hypertension patients to develop POAG?
1. raised age 2. Greater cup: disc ratio 3. Central corneal thickness reduced 4. Raised level of IOP
35
What should be done to try and pick up more glaucoma?
patients \>40 should have regular checkups at an optometrist, particularly if there is a family history of glaucoma
36
What 3 things can be monitored to asses glaucoma patients?
1. IOP 2. Optic disc - C:D ratio, pallor, haemorrhages and shift 3. visual fields
37
How frequently should visual fields in assessed in glaucoma?
Six monthly to yearly assessment using kinetic (Goldmann) or static (Humphrey) perimetry and must be reliable, reproducible, able to detect progression of any loss
38
Why is it important to try and achieve a lower IOP in glaucoma patients/ those at risk?
If pressure \>17.5, as time goes on you get more visual field loss than detected on visual field test - aim of treatment is to keep pressure as low as possible
39
What is the theory behind medical ways to lower IOP?
decrease production of aqueous, and/or increased aqueous outflow
40
What is the surgical mechanism to lower IOP?
Increase aqueous outflow
41
What is the protocol for medical treatment to lower IOP?
topical drops are mainstay; start with one type of drop then add another or two if not controlled. (plus systemic medication; usually temporary or emergency due to systemic side effects)
42
What are 4 types of topical medication for lowering IOP e.g. in glaucoma?
1. Prostaglandin F2 analogues (commonest) e.g. latanoprost 2. Beta blockers (second commonest) e.g. timolol 3. Carbonic anhydrase inhibitors e.g. dorzolamide (acetazolamide is systemic) 4. Alpha-2 agonist e.g. brimonidine
43
How does latanaprost (prostaglandin F2 alpha analogue) work to treat POAG?
increase uveo-scleral outflow
44
How does timolol (beta blocker) work to treat POAG?
reduce aqueous production
45
How does dorzolamide (topical carbonic anhydrase inhibitor) work to treat POAG?
reduce aqueous production
46
How does brimonidine (alpha-2 agonist) work to treat POAG?
reduce aqueous production and increase uveo-scleral outflow
47
What is a systemic medication that can be given to reduce IOP?
acetazolamide - carbonic anhydrase inhibitor (oral, IV for angle-closure glaucoma)
48
What area 3 types of surgery that can be used for glaucoma?
1. trabulectomy - surgical formation of fistula connecting anterior chamber to sub-conjunctival space. provide alternative path for aqueous escape 2. augmentation - topical chemotherapy applied at time of surgery (5-fluoro-uracil, mitmycin C) prevents scar formation, increases both success rate and risk of complications 3. Laser to trabecular meshwork
49
What intervention can be used for more advanced or resistant cases of glaucoma?
Glaucoma drainage tubes
50
What do glaucoma drainage tubes for more advanced/resistant cases involve?
tube with or without valve, to release aqueous from anterior chamber into subconjunctival space
51
Which factor most increases the patient's risk of glaucoma?
Family history: increases risk significantly, approximately 4x for siblings or 2x for children
52
What 4 examinations are most helpful in confirming a diagnosis of primary open angle glaucoma?
1. Goldmann applanation tonometry to measure IOP
2. Gonioscopy
3. Ophthalmoscopy
4. Visual field assessment
53
What does Goldmann applanation tonometry involve?
requires slit lamp and surface of eye to be anaesthetised; used in conjunction with fluorescein dye
54
What does gonioscopy involve?
Checking if angle open or closed; with patient on the slit lamp, surface of eye is anaesthetised and small lens with mirrors placed on cornea. mirrors allow view into aqueous drainage angle (see image)
55
What would you expect to find on ophthalmoscopy in POAG?
pathological cupping of the optic disc, i.e. vertical cup to disc ratio (VCDR) \>0.5
56
What causes pathological optic disc cupping in POAG?
loss of retinal nerve fibres, resulting in a thin neuroretinal rim
57
What are 2 ways to perform visual field assessment when diagnosing POAG?
1. Confrontational visual fields (during examiniation)
2. Formal visual field teseting
58
Why is it unlikely that visual confrontational visual fields will be helpful in the diagnosis of glaucoma?
visual defects are initially too subtle
59
How does visual field deterioration occur in POAG?
Earliest glaucomatous field defect is a nasal step. With increasing damage to optic nerve head, arcuate scotomas (superior and inferior) develop, then only temporal and central islands of vision remain and if the IOP is not controlled then eventually all vision is lost
60
What are 2 key types of investigations that are appropriate in POAG?
1. **Visual fields**: static perimetry (Humphrey) and kinetic perimetry (Goldmann)
2. **Central corneal thickness**
61
How does static perimetry/ Humphrey fields work?
* **Automated** device displays a number of spots of light of varying brightness, patient asked to **press a buzzer** when they can see a light
* Requires a good deal of concentration and engagement
* Each eye tested in turn
62
How does kinetic perimetry/ Goldmann fields work?
63
Why must central corneal thickness be measured in POAG?
* All methods of measuring IOP measure the force required to indent the cornea, since this force is related to the pressure inside the eye
* A number of assumptions are made and the largest confounder is thickness of the cornea
* In a thinner cornea, less force is required to indent it regardless of IOP so when we measure IOP it will be artificially low
64
Can any damage that has already occurred to the optic disc in POAG be reversed?
No but medication can slow down progression of the disease
65
What are 3 other treatment options available for POAG in addition to topical ocular anti-hypertensives?
1. Oral ocular anti-hypertensives
2. Laser treatment: selective laser trabeculoplasty SLT
3. Surgery: trabeculectomy
66
When and why are oral ocular anti-hypertensives used for POAG?
Only used temporarily or as emergency treatment due to systemic side effects (acetazolamide)
67
How does laser treatment (selective laser trabeculoplasty) work to treat POAG?
Used to **open up trabecular meshwork;** _not first line_ and may _only give modest reduction_ in IOP
68
How many times can laser treatment (selective laser trabeculoplasty) be performed in POAG?
Can only be **repeated once** and if still unsuccessful is unlikely to have further effect
69
When is trabeculectomy used in POAG?
reserved for the most recalcitrant cases when medical therapy has failed
70
How does trabeculectomy work for POAG?
aim is to reduce pressure by creating an artificial drainage channel for aqueous to drain out of the eye
not without risks but is gold standard treatment
71
What is the gold standard treatment for POAG?
Surgery (trabeculectomy)
72
How long does a patient with POAG need to be under the care of the hospital?
Lifelong - if treatment stops, IOP will rise and optic disc will be at risk again so treatment needs to be lifelong
73
What are 4 examinations that you should perform on a patient with suspected acute angle closure glaucoma?
1. General observation: patient in pain - lying/standing, being sick, wearing thick glasses
2. Visual acuity
3. Slit lamp + gonioscopy
4. Measure IOP
74
What are 4 things that you are likely to find on slit lamp examination + gonsioscopy in AACG?
1. Conjunctiva **red** and inflamed
2. cornea hazy due to oedema of corneal epithelium
3. **Pupil fixed, mid-dilated,** not responding to light
4. Anterior chamber is shallow
75
How can intraocular pressure be assessed without any specialised equipment?
**Digital intraocular pressure:** i.e. use fingers; ask patient to close eyes and look down, use index finger of both hands on upper lid of eye and ballot eye from one index finger to the other. If IOP high, eye will feel harder than other
76
What are 2 ways to accurately measure IOP?
1. Goldmann applanation tonometry
2. Non-contact tonometry: performed by optometrists, air puff tonometry that doesn't require topical anaesthesia
77
How high could pressure become in an eye with AACG?
up to 60mmHg
78
What causes haloes and reduced vision in AACG?
cornea becoming oedematous
79
What is the mechanism behind primary angle closure in AACG?
* Hyper metropic eye, eye small so drainage angle narrow
* with age thickness of crystalline lens increases and pushes iris forwards, further narrows angle
* in dim light, pupil is mid-dilated and iris bunches up causing closure of the angle
* aqeous can't drain out so pressure in the eye increases
80
What is the treatment required for AACG that attempts to reverse the initiating event?
Miotic drops e.g. pilocarpine, to constrict pupil (as initiating event is pupil dilation)
81
Why might pupil constricting medication (miotics) not initially work to treat AACG?
iris is ischaemic in the eye with high pressure, so difficult to constrict iris. therefore pressure must be rapidly brought down
82
How can IOP be rapidly lowered in AACG, in order to reduce iris ischaemia and for pilocarpine drops to work? 2 key ways
1. Oral ocular anti-hypertensives: acetazolamide (carbonic anhydrase inhibitor), initially given IV then orally (also other topical ocular anti-hypertensives to try and reduce pressure e..g beta blockers)
2. Corticosteroid drops: eye inflamed
83
What are the aims of treatment of AACG?
Dilate pupil and open the drainage angle to break the angle closure attack and reduce pressure. Reduce iris ischaemia by clearing cornea and allowing pilocarpine to work
84
What are the 3 definitive forms of treatment for AACG?
1. Laser YAG iridotomy
2. Surgical iridectomy
3. Cataract surgery and IOL implantation
85
How does laser YAG iridotomy work to treat AACG?
Nd:YAG laser used to create hole in the iris, re-establishes communication between posterior and anterior chambers so prevents further acute angle closure attacks
Should perform on both eyes as usually have similar refractive error, prophylactic on second eye
86
Should laser iridotomy just be performed on the affected eye in AACG?
no, perform on both; both eyes usually have similar refractive rror and so are similar in size, prophylactic on unaffected eye to prevent future attack
87
How does surgical iridectomy work to treat AACG?
iridotomy usually successful, but requires the cornea to be clear if the attack can't be broken with medication and the cornea remains cloudy, surgical iridectomy might be needed
88
Why can cataract surgery and intra-ocular lens (IOL) implantation be used as a definitive treatment for AACG?
since age-related lens growth causes angle closure, cataract surgery and IOL implantation replaces the thick crystalline lens with a much thinner artificial lens. this can prevent further angle closure attacks
