Glaucoma 2 - Presentation and Pathogenesis Flashcards

1
Q

Primary Open Angle Glaucoma/Normal tension Glaucoma (POAG/NTG) Signs and Symptoms?

A

SIGNS
• Raised or normal intra-ocular pressure
• Open angle or deep anterior chamber
• Abnormal optic disc cupping
• Abnormal visual field
SYMPTOMS
• None until advanced or paracentral visual field defect

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2
Q

Chronic Angle Closure Glaucoma (CACG) Signs and Symptoms?

A

SIGNS
•Raised or normal IOP
Open but narrow angle or moderate/deep AC
• Abnormal optic disc cupping
• Abnormal visual field
• Shallow AC
•3+ quadrants of ITC on gonioscopy
•Hypermetropia

SYMPTOMS
•None as per POAG

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3
Q

Intermittent Angle Closure Glaucoma (IACG) Signs and Symptoms:

A

SIGNS
• Raised or normal IOP
• Narrow angle
• +/-Abnormal optic disc cupping
• +/- Abnormal visual field
• Shallow AC
• 3+ Quadrants ITC on gonioscopy
• Hypermetropia

SYMPTOMS
• Intermittent brow ache
•HALOES

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4
Q

Acute Angle Closure Glaucoma (AACG) : Signs and symptoms:

A

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

SYMPTOMS
• Brow ache/headache
•Blurred vision/haloes
• Nausea

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5
Q

Pathogenesis of POAG theories?

A

• Pressure theory
• Vascular theory
• Mixed mechanism
• Neurodegenerative and apotptosis

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6
Q

What does the pressure theory state?

A

•Trabecular dysfunction
- Trabecular meshwork gradually becomes less effective in allowing aqueous to pass through to Schlemm’s canal (increased outflow resistance)

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7
Q

Ocular Perfusion Supply:

A

• The posterior segment of the eye is supplied by 2 different circulatory systems
- Retina: Central retinal artery
- Choroid: Short posterior ciliary arteries
- Optic disc: both
• Vasoactive drugs can reach the optic nerve via the choroid
A reduced bloodflow to the optic nerve increases the eye’s sensitivity to IOP

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8
Q

Mixed Mechanism theory

A

•Combination of Pressure theory and Vascular Theory

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9
Q

Neurodegenerative and Apoptosis theory

A

•With time as px get older, the nerves get damaged

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10
Q

Mechanism of damage:

A

The exact mechanism in glaucoma is not understood completely:
•Loss of retinal ganglion cells
•Ischaemc changes at the ONH/free radicals
•Apoptosis

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11
Q

Pathogenesis Primary Angle Closure Glaucoma (PACG) (8 total)

A

Restricted access to trabecular meshwork
• Hypermetropia (eg + 2.00)
• Shallow anterior chamber
• Small eyes (short axial length)
• Anteriorly inserted iris
• Increase in lens size
• Dilatation of pupil
• Trabecular Dysfunction
• Narrow gonioscopic angle

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12
Q

What occurs during Angle Closure?

A

•Obstructed trabecular meshwork
•The angle between the iris and the cornea narrows or closes
•Iris pushing forward
•Cornea

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13
Q

PACG: ChronicAngle Closure (CAC):

A

• The Iris slowly comes into contact with an increasing area of TM, resulting in TM dysfunction and a gradual rise in IOP

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14
Q

PACG: Intermittent angle closure mechanism:

A

• The angle is narrow but open, but certain physiological states (producing dilation) lead to transient rises in IOP which resolve over variable periods of time
• This often produces transient symptoms of acute angle closure

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15
Q

PACG: Acute Angle Closure - Mechanism

A

•Dilation of the pupil (physiological or otherwise)leads to the angle becoming closed
• Marked rise in IOP due to:
• pupil block
• peripheral iris tissue occluding the angle (often both present simultaneously)

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16
Q

What causes Plateau Iris?

A

• Anatomical iris configuration
- anteriorly displaced ciliary body position
- anteriorly inserted or thicker iris
• The central AC is usually not shallow and the iris plane is flat or slightly convex
- Angle appears narrow and crowded
- Gonioscopy shows a “double hump” sign

17
Q

What is Plateau Iris Syndrome?

A

• ACG associated with plateau iris is usually cured by YAG peripheral iridotomy
• Plateau iris syndrome is where post-peripheral iridotomy the angle closure recurs with elevated IOP attacks

18
Q

Key points in diagnosing glaucoma:

A

• History and symptoms
- ocular and systemic
• Family Hx
• Refraction
• IOP and CCT
• Ant Chamber and Gonio
• Discs, fields, OCT

19
Q

AC Depth Assessment

A

• Peripheral
- Van Herick Technique
- Correlates well with gonioscopy
•Central
- Redmond smith technique

20
Q

Gonioscopy In Clinic + Technique

A

•Indirect Visualisation of angle structures
• Dim/dark room illumination
• Reduced slit lamp illumination & beam height
• Carried out in primary position
• Indentation
- Gentle pressure on the central cornea forces aqueous into the angle and peripheral iris
- Differentiates between appositional and synechial closure

21
Q

Grading Gonioscopy angle Width:

A

Aim
• Evaluate functional status of the angle
• Degree of closure
• Risk of closure

Evaluate
• Geometric angle width
• Shape & contour of the iris
• Most peripheral structure seen
• Presence of peripheral anterior synechiae
• Amount of trabecular pigmentation

22
Q

Types of Grading Techniques with Gonioscopy

A

• Shaffer
- Simple but functional
- Commonly used throughout Ophthalmology

• Spaeth
- Complex but comprehensive
- Used by glaucoma specialists

23
Q

What can you see with Gonioscopy?

A

In order from Iris upwards:
•Iris
•Ciliary Body Band (Pigmented)
•Scleral Spur Band (white)
•Pigmented Trabecular Meshwork Band
•Non-pigmented Trabecular Meshwork
•Schwalbes Line

24
Q

Iris in relation to Gonioscopy

A

IRIS
most posterior structure visible. Gonio assessment of the angle should include its insertion and contour.

25
Q

Ciliary Body Band

A
  • production of aqueous and the regulation of its outflow
  • Amount visible dependant on the level of iris insertion- related to eye size. Wider in myopia, narrower hypermetropia
  • Varies in colour from greyish white to brown in appearance.
  • Normal radial blood vessels can be seen in 2/3 patients with blue eyes and 10% brown.
26
Q

Scleral Spur

A

The most anterior portion of the sclera, visible as a narrow, often shiny white band It is an important landmark as it appears consistent in different eyes

27
Q

Trabecular Meshwork portions?

A
  • The posterior: Pigmented TM (Approx 90% of aqueous flows out via this route)
  • Anterior non-pigmented portion: Varies in appearance from little or no pigmentation to densely pigmented.
  • Cases of raised EVP and trauma, can have a red appearance as blood visible in schlemms canal, which sits posteriorly to PTM.
    Angle generally considered occludable if TM cannot be seen in more than 90 degrees of the angle
28
Q

Schwalbes Line

A

The most anterior structure- represents the transition between the TM and the cornea.
Appears as an opaque flat white line, variable amount of pigment.
When pigment deposits- known as Sampaolei’s line, common finding in conditions with pigment dispersion

29
Q

Corneal Wedge

A

• 2 light reflections create a wedge shaped line which intersect at the sclero-corneal junction
• Locates Schwalbe’s line
• Imperative for localisation in difficult angles

30
Q

What Pathological Findings can you find In Angle?

A

• Peripheral Anterior Synechiae
- PACG, anterior uveitis, ICE
• New vessel formation
- Neovascular glaucoma, Fuchs heterochromic cyclitis, anterior
uveitis
•Hyperpigmentation
- PDS, pseudophakic pigment dispersion, PXF, blunt trauma,
anterior uveitis, post acute angle closure, post YAG PI
•Trauma
- Angle recession, post trabeculectomy, post cyclodialysis, foreign body