Glaucoma Flashcards
1
Q
Glaucoma Definition
A
- group of disorders with characteristic optic neuropathy changes at the ONH and loss of RNFL ganglion cells
- leading to eventual VF defects with characteristic patterns consistent with the loss of RNFL ganglion cells
- IOP is often a factor
2
Q
Glaucoma - Incidence
A
- 2nd most common visual impairment in the UK
- higher incidence of cases for older px’s
3
Q
Glaucoma - Prevalence
A
- higher in those of African Caribbean descent
- severity of glaucoma at presentation is the major factor in the development of glaucoma blindness
4
Q
Glaucoma - Genetics
A
- 6x more likely to develop POAG if 1st degree relative has glaucoma
- racial factors - POAG (African descent), ACG (Asians, Chinese)
5
Q
Glaucoma - Risk Factors
A
- IOP
- Age
- FH
- Rx
- CCT
- Pseudoexfoliation
- Pigment dispersion
- Shallow AC
- Other systemic factors
- Drug hx
- Migraine
- Raynaud’s
- Vascular hx
6
Q
Types of POAG
A
- High pressure (POAG)
- Normal pressure (NTG)
7
Q
POAG Symptoms
A
- asymptomatic
- none until there is an advanced paracentral VF defect
8
Q
POAG Signs
A
- raised IOP (or normal if NTG)
- open angle and deep AC
- abnormal OD
- abnormal VF
9
Q
POAG Pathogenesis - Pressure Theory
A
- raised IOP (due to trabecular dysfunction) causes mechanical damage to the ON
- due to pressure pressing against nerve fibres
- TM gradually becomes less effective in allowing aqueous to pass through to Schlemm’s canal
10
Q
POAG Pathogenesis - Vascular Theory
A
- some px’s develop damage due to ischaemia/poor blood supply to ONH
11
Q
POAG Pathogenesis - Vascular Theory (Ocular perfusion)
A
- posterior segment of the eye supplied by 2 different circulatory systems
- Retina - CRA
- Choroid - short PCA’s
- OD - both
- reduced blood flow to the ON increases sensitivity of the eye to IOP
12
Q
POAG Pathogenesis - Mixed Mechanism
A
- damage occurs due to combination of IOP and blood supply
13
Q
POAG Pathogenesis - Neurodegenerative and Apoptosis
A
- neurogenerative changes to ONH as px ages
- apoptosis (natural cell death) - some cells programmed to die at certain time in px’s life
14
Q
Types of PACG
A
- Acute angle closure glaucoma
- Intermittent angle closure glaucoma
- Chronic angle closure glaucoma
- Plateau iris syndrome
15
Q
PACG Symptoms
A
- blurred vision
- halos around lights
- pain
- nausea
- redness
16
Q
PACG Signs
A
- Raised or normal IOP
- Open but narrow angle or moderate/deep AC
- Abnormal VF
- Shallow AC
- 3 + quadrants of ITC on gonioscopy
- Hyperopia (goes hand in hand with a small eye - tend to get a more crowded anterior segment)
- FIXED DILATED PUPIL
- AC flare and cells
- lenticular opacities
17
Q
PACG Mechanism
A
- iris slowly comes into contact with an increasing area of TM
- results in TM dysfunction, and gradual rise in IOP
18
Q
Pupil Block
A
- AH unable to pass through pupil due to occlusion of the gap between posterior iris and anterior lens
- This causes a build-up of pressure bulging the iris forward (iris bombe)
- The anterior iris then may come into contact with the posterior cornea (anterior synechiae)
- This occludes the AC angle and leads to a sharp rise in IOP
19
Q
Intermittent ACG Symptoms
A
- intermittent brow ache (lasts 30ish mins, often in evening when lights dim, resolves itself)
- halos
- episode of pupillary block resolves spontaneously after several hrs
20
Q
Intermittent ACG Signs
A
- Raised or normal IOP
- Narrow angle
- Abnormal/normal OD cupping
- Abnormal/normal VF
- Shallow AC
- 3 + quadrants of ITC on gonioscopy
- Hypermetropia
21
Q
Intermittent ACG Mechanism
A
- Angle narrow but open, certain physiological states (producing dilation) lead to transient rises in IOP which resolve over periods of time (pupil block which occurs spontaneously resolves)
- Often produces transient symptoms of acute angle closure
22
Q
Acute ACG
A
- Medical ophthalmic emergency
- Visual loss is rapid, must be referred and dealt with without delay
- Similar to intermittent ACG but attack is permanent
- caused by a blockage in aqueous drainage
23
Q
Acute ACG Symptoms
A
- blurred vision
- brow ache/headache
- nausea
24
Q
Acute ACG Signs
A
- Red eye
- Fixed mid-dilated pupil
- Hazy blue/green cornea
- Iritis
- IOP >40 mmHg
- Shallow AC
25
Q
Acute ACG Mechanism
A
- Dilation of the pupil (physiological or otherwise) leads to angle becoming closed
- Marked rise in IOP due to:
- Pupil block
- Pupil comes into contact with the lens in a mid-dilated state, this temporarily prevents the aqueous making its way from the posterior to the AC and to the TM
- The trapped aqueous pushes the peripheral iris forwards which blocks access to the TM
- Peripheral iris tissue occluding the angle
- Often both present simultaneously
26
Q
Plateau Iris Configuration
A
- Anatomical iris configuration
- Anteriorly displaced ciliary body
- Anteriorly inserted or thicker iris
- Central AC is usually not shallow and iris plane is flat or slightly convex
- Angle appears narrow and crowded
- Gonioscopy shows a ‘double hump’ sign
27
Q
PACG Pathogenesis
A
- Restricted access to TM
- Hypermetropia (e.g. + 2.00D)
- Shallow AC
- Small eyes (short axial length)
- Anteriorly inserted iris
- Increase in lens size (as px’s get older past 40) - can crowd angle further by pushing iris anteriorly towards cornea
- Dilation of pupil - can cause bunching up of iris and the angle and lead to angle closure
- Physiologically - when pupil dilates
- Pharmacologically - when px is dilated
- Trabecular Dysfunction
- Narrow gonioscopic angle
28
Q
Key Points from the Ocular Examination that help diagnose Glaucoma
A
- H&S - ocular and systemic
- FH - gives clues to risk of developing glaucoma, px’s sometimes follow progression patterns of family members
- Refraction - myopic (OAG more common) or hyperopic (ACG more common)
- IOP - type of glaucoma, risk of progression
- CCT - risk of progression for those with OHT
- AC depth and gonioscopy - OAG or ACG
- Discs, fields, OCT - clues to whether damage has occurred and whether they have developed glaucoma itself
29
Q
Gonioscopy
A
- can grade both peripheral and central AC depth
- essential on all px’s with suspicion of glaucoma to ensure correct diagnosis
30
Q
Gonioscopy - AC Assessment
A
- peripheral - VH
- central - Redmond Smith technique
- however, these give an impression of the angle and don’t actually visualise it
31
Q
Gonioscopy in clinic
A
- Gives an indirect visualisation of angle structures
- Dim/dark room illumination (angle at its physiologically narrowest)
- Reduced SL illumination and beam height (prevent unwanted pupil constriction and angle widening)
- Carried out in primary position (avoid tilting lens, may indent artificially opening the angle)
- Indentation
- Gentle pressure on the central cornea forces aqueous into the angle and peripheral iris
- Differentiates between appositional and synechial closure
32
Q
Gonioscopy - Grading of Angle Width
A
- Evaluate geometric angle width (in all 4 quadrants)
- Shape & contour of the iris
- Most peripheral structure seen
- Presence of peripheral anterior synechiae
- Amount of trabecular pigmentation
33
Q
Gonioscopy - Grading of Angle Width (Shaffer’s Technique)
A
- Simple but functional
- Based on visible angle structures
- Gives a number - fails to characterise important qualitative aspects of angle, may need recorded separately
- Commonly used throughout ophthalmology
34
Q
Gonioscopy - Grading of Angle Width (Spaeth’s Technique)
A
- Complex but comprehensive
- Grading is more descriptive
- Used by glaucoma specialists
35
Q
AC Angle Anatomy - Iris
A
- Most posterior structure
- Gonio assessment should include its insertion and contour
36
Q
AC Angle Anatomy - Ciliary Body
A
- Important in production and regulation of outflow of aqueous
- Visible area on gonio - ciliary body band
- Amount visible related to eye size (wider in myopia, narrower in hyperopia, very wide in angle recession)
- Greyish white to brown appearance
37
Q
AC Angle Anatomy - Scleral Spur
A
- Most anterior portion of sclera
- Visible as soft, shiny, white band
- Appears consistent with different eyes
38
Q
AC Angle Anatomy - Trabecular Meshwork
A
- Posterior pigmented TM (90% of aqueous flows through this route)
- Anterior non-pigmented TM
- Varies in appearance from little/no pigmentation to densely pigmented
- Angle considered occludable if TM cannot be seen in more than 90 degrees of the angle
39
Q
AC Angle Anatomy - Schwalbe’s Line
A
- Most anterior structure - represents transition between TM and cornea
- Opaque flat white line, variable amount of pigment
- Pigment deposits (Sampaolei’s line) are a common finding in conditions with pigment dispersion
- When heavily pigmented may be mistaken for TM
- Corneal wedge
- Used in cases of poorly pigmented angles where difficult to identify SL
- A thin slit of light at an angle of 10-15 degrees
40
Q
Pathological Findings in the Angle
A
- peripheral anterior synechiae
- neovascularisation
- hyperpigmentation
- trauma
41
Q
Optic Disc Changes
A
- Changes in OD and RNFL usually precede onset of VF defects with standard white on white perimetry
42
Q
Normal Optic Disc
A
- ISNT rule - thickest inf, then sup etc
- rim colour - pallor should correspond or be slightly less than cup
- size - 1.5-2mm vertical diameter
43
Q
Justified large/small C:D
A
- Small discs in hypermetropes can have an apparently normal C:D which may be misleading
- Large discs have large cups, can appear to be cupping, so look at NRR, can’t rely on C:D alone
44
Q
Glaucomatous Optic Disc
A
- C:D - anything over 0.5 suspicious
- BV position
- Rim thickness
- Pallor
- Peri-papillary atrophy (tends to be more where there is loss of NRR)
- APON (acquired pits of the ON)
- Haemorrhages
- NFL defects
- Notch
- Laminar dots
45
Q
Optic Disc - Signs of change
A
- Shift in position of BV’s
- Thinning of NRR
- Developing notch
- Haemorrhage crossing disc rim
- Developing focal pallor
- Change in peripapillary atrophy
- Concentric enlargement of cup
46
Q
Tilted Discs
A
- common in myopes and px’s with high astigmatism
- can produce supratemporal VF defects - tend not to encroach central VF
47
Q
Temporal/Nasal Unfolding
A
- variant of central cupping
- loss of NRR on temporal/nasal side
48
Q
Vertical Extension
A
- central cup starts enlarging inferiorly or superiorly
49
Q
Notching
A
- similar to vertical extension but focal loss of tissue either inferiorly or superiorly
50
Q
APON (Acquired Pit of Optic Nerve)
A
- Highly focussed loss of tissue like a notch which develops generally at the infero-temporal or supero-temporal parts of the OD
- Tend to see BV’s disappearing into these pits and then popping out again at the other side
- More common in NTG
51
Q
Congenital Disc Pit
A
- occur on central or temporal part of OD
- tend to be larger than acquired pits (which tend to appear on superior and inferior portions of OD and are smaller)
52
Q
Laminar Dots
A
- round dots normal in central cup
- oval dots in peripheral cup suggestive of glaucoma
53
Q
Senile Sclerosis
A
- Pallor across the whole nerve due to ischaemic changes or age
- Development of generalised peripapillary atrophy
- More common in very elderly px’s
- Gradual saucerization of OD
54
Q
Pale Optic Disc - Differential Diagnosis
A
- AION
- CRAO
- Heredofamilial optic atrophies
- Other optic neuropathies (inflammatory, infectious, toxic, compressive)
55
Q
Visual Field Changes
A
- Changes in OD and RNFL usually precede onset of VF defects with standard white on white perimetry
- Even with advanced changes in ON morphology VF changes may or may not be present
56
Q
Visual Field Sensitivity (Recap)
A
- The sensitivity of the eye is not constant across the whole of the VF and depends on:
- Eccentricity
- Adaptation level
- Nature of test stimuli
- Maximal sensitivity in the fovea and no sensitivity in the blind spot
- Followed by gradual decrease in sensitivity as we move to the nasal and temporal sides
57
Q
Visual Field Strategies (Recap)
A
- Kinetic - stimulus moves into VF from periphery
- Static - stimulus presented at different points and intensities
58
Q
Factors affecting Visual Field
A
- Pupil size - can be due to meds (e.g. pilocarpine), small pupils dims instesnsity of stimulus
- Lens/media opacities - scatter incoming light and reduce amount of light that reaches retina, reducing contrast of stimuli
- Refractive errors - result in defocus especially small central stimuli, correct errors > 1D
- Lens rim artefacts - normally at edge of VF, mimic RNFL defect appearance, can be due to lens decentration, common in elderly and those with deep sunken eyes
- Lids/lashes/brows - droopy upper lid can encroach onto visual axis and give superior defects
- Px experience - px often don’t perform well in first ever VF, if test is long can fatigue px and result in threshold increase
59
Q
Visual Field in Glaucoma
A
- VF loss can be focal, generalised or both
- Retinal ganglion cell axons follow an arcuate path to the ONH
- Field defects are a result of axonal damage at the level of the ONH
- Axonal damage always respects the horizontal midline (based on the way the nerve fibres are arranged in the retina)
60
Q
Visual Field Defects in Glaucoma
A
- Bjerrum’s area defects
- Arcuate defects
- Paracentral defects
- Nasal step
- Temporal wedge
- Enlargement of blind spot
- Overall depression
61
Q
Visual Field Defects in Glaucoma - Bjerrum’s area
A
- frequent in early glaucoma
- may account for 70% of early VF defects usually in superior VF between 10-20 degrees
62
Q
Visual Field Defects in Glaucoma - Paracentral defects
A
- Highly suggestive of glaucoma
- Defined as within 10 degrees of fixation
- More common in NTG
- Significant AMD can also produce a similar result
63
Q
Visual Field Defects in Glaucoma - Arcuate defects
A
- Slightly more advanced than paracentral defects and occur in arcuate or Bjerrum’s area
- Usually superior more commonly than inferior
64
Q
Visual Field Defects in Glaucoma - Nasal step
A
- Up to 40% of px’s with glaucoma have nasal steps
- Usually superior
65
Q
Visual Field Defects in Glaucoma - Temporal wedge
A
- Uncommon
- Associated with nasal cupping
66
Q
Visual Field Defects in Glaucoma - Enlargement of blind spot
A
- Many different causes
- In glaucoma, elongation of the blind spot in an arcuate fashion
67
Q
Visual Field Defects in Glaucoma - Overall depression
A
- Due to reduced sensitivity of the retina secondary to diffuse loss of nerve fibres throughout ON
- Accounts for up to 38% of VF defects
- Generalized depression especially nasally
- Reduced mean deviation scores
- Can be due to media opacities (e.g. cataract)
68
Q
Visual Field Global Indices (Recap)
A
- Mean deviation
- Weighted average of total deviation values
- Reflection of the general VF sensitivity
- Often used to monitor signs of progression in px’s over time
- Pattern standard deviation
- Measure of the variability of the hill of vision
- High when a localised defect is present
69
Q
Systematic Visual Field Assessment
A
- Check px data (refraction, pupil)
- Check reliability indices
- Look at grayscale (overall impression of any VF loss)
- Rule out possible artefacts (ptosis, lens, px factors)
- Observe numerical graph
- Analyse TD probability plot (looking for diffuse loss of sensitivity)
- Look at PSD (localised)
- Analyse the global indices (confirm depth and extent of VF loss)
- Check GHT (looks for asymmetry between the superior and inferior VF’s)
- Compare VF to clinical information
70
Q
General Treatment for Glaucoma
A
- Only proven treatment is reduction of IOP
- Target IOP - the IOP that is expected to confer ON stability in a px with glaucoma
- Greater damaged ON’s require greater IOP reduction
71
Q
Target IOP Modifications
A
- Severity of existing ON damage
- How high the IOP is
- Rate of progression (how rapidly the damage has occurred)
- Additional risk factors present
- Life expectancy
72
Q
Rough Target IOP based on ON damage
A
- Mild damage - 30%
- Moderate damage - 35%
- Severe damage - 40%
- Once target IOP selected, may need modified depending on px response to treatment (e.g. severely damaged eye may require greater reduction for stability)
73
Q
Management - Order of Prescribing
A
- 1st Line - Prostaglandin analogue or Beta-blocker
- Sometimes start treatment on worse eye and observe effect, once effective begin treatment on both eyes
- 2nd Line - Prostaglandin analogue or Beta-blocker (would then be on 2 agents)
- 3rd Line - Carbonic anhydrase inhibitor (have less side effects than ->) or alpha 2 agonist
- 4th Line - rarely as 3 above or pilocarpine
74
Q
1st Line - Prostaglandin Analogues
A
- Latanoprost (Xalatan, Generic, Monopost) od
- Increased aqueous outflow through the uveoscleral route by ciliary muscle relaxation
- 30-35% reduction in IOP
75
Q
1st Line - Prostaglandin Analogues (Side effects)
A
- Mild conjunctival hyperaemia
- Mild punctate keratopathy
- FB sensation
- Ocular irritation
- Increased iris pigmentation (20%)
- Lengthening of eyelashes (significant side effect, most px don’t mind)
- CMO (pseudophakic or aphakic, may wish to stop treatment if undergoing cataract surgery or if CMO develops)
- Reactivation of HSK (may stop if this happens)
- Exacerbation of asthma very rarely (stop if this happens)
- Exacerbation of uveitis (may need to stop if uveitis persisting)
76
Q
1st Line - Adrenergic Agents (Beta Blockers)
A
- Timolol and others
- Decreased aqueous production
- 25-30% reduction in IOP
- Suffer from tachyphylaxis (med provides lessened response than once did)
77
Q
1st Line - Adrenergic Agents (Beta Blockers Side effects)
A
- Ocular (very rare)
- Corneal hypaesthesia
- Punctate keratopathy
- DE syndromes
- Burning/stinging
- Pseudopemphigoid
- Systemic (more common)
- Severe bradycardia
- Arrhythmia
- Heart failure
- Dyspnoea
- Exacerbation of asthma
- Anxiety
- Depression
- Avoid in px’s with heart problems, asthma, or shortness of breath!
78
Q
3rd Line - Carbonic Anhydrase Inhibitors
A
- Reduce aqueous secretion from the ciliary epithelium
- Dorzolamide (trusopt) tds (3 times daily)
- Brinzolamide (azopt) bd (2 times daily)
- 18% reduction in IOP
- Possible improved ON perfusion due to local vasodilatation
79
Q
3rd Line - Carbonic Anhydrase Inhibitors (Side Effects)
A
- Transient burning/stinging (33%)
- Bitter taste (26%) - goes down nasolacrimal duct and into the puncta
- Ocular allergy
- SPK (10%)
- Blurred vision
- Dryness
- Tearing
- Photophobia (1-5%)
- Hair loss
*Use in caution if unhealthy endothelium as may cause corneal thickening and loss of clarity
80
Q
General Principles of Compliance
A
- Simpler treatment regimens
- Least side effects
- Educate importance of using drops
- Reinforce reason for using drops
- Regular review and reassurance (make px aware of importance of attending review appts)
- Realistic expectations of treatment
81
Q
3 stages of primary angle closure glaucoma
A
- primary angle closure suspect
- primary angle closure
- primary angle closure glaucoma
