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Clinical Ophthalmology > Glaucoma > Flashcards

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
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2
Q

Glaucoma - Incidence

A
  • 2nd most common visual impairment in the UK
  • higher incidence of cases for older px’s
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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
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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)
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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
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6
Q

Types of POAG

A
  • High pressure (POAG)
  • Normal pressure (NTG)
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7
Q

POAG Symptoms

A
  • asymptomatic
  • none until there is an advanced paracentral VF defect
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8
Q

POAG Signs

A
  • raised IOP (or normal if NTG)
  • open angle and deep AC
  • abnormal OD
  • abnormal VF
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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
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10
Q

POAG Pathogenesis - Vascular Theory

A
  • some px’s develop damage due to ischaemia/poor blood supply to ONH
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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
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12
Q

POAG Pathogenesis - Mixed Mechanism

A
  • damage occurs due to combination of IOP and blood supply
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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
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14
Q

Types of PACG

A
  • Acute angle closure glaucoma
  • Intermittent angle closure glaucoma
  • Chronic angle closure glaucoma
  • Plateau iris syndrome
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15
Q

PACG Symptoms

A
  • blurred vision
  • halos around lights
  • pain
  • nausea
  • redness
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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
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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
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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
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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
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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
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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
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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
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23
Q

Acute ACG Symptoms

A
  • blurred vision
  • brow ache/headache
  • nausea
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24
Q

Acute ACG Signs

A
  • Red eye
  • Fixed mid-dilated pupil
  • Hazy blue/green cornea
  • Iritis
  • IOP >40 mmHg
  • Shallow AC
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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
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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
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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
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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
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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
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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
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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
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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
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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

Clinical Ophthalmology (10 decks)

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