Glaucoma Flashcards

1
Q

What is glaucoma?

A

A group of progressive optic neuropathies that have characteristic changes at the optic nerve head and retinal nerve fiber later in the absence of optic nerve disease.

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2
Q

Classic triad of glaucoma?

A
  1. Increased IOP
  2. Loss of visual fields
  3. Cupping of optic disc
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3
Q

Is glaucoma treatable?

A

Yes

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4
Q

Types of glaucoma?

A
  1. Open angle (POAG, NTG, Pigment dispersion, PXF)
  2. Closed angle
  3. Secondary (Uvetic, trauma, neovascularization)
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5
Q

Primary open angle glaucoma common in what race?

A

African- American

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6
Q

Characteristics of glaucoma?

A
  1. Optic disc cupping
  2. Visual field defect- due to loss of retinal ganglion cells.
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7
Q

Risk factors of primary open angle glaucoma?

A
  1. Elevated IOP
    2, Increasing age
  2. Black race
  3. Family history of glaucoma
  4. Myopia
  5. Migraine an vasospasm
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8
Q

What is pigment dispersion syndrome?

A

Type of open angle glaucoma, characterized by spontaneous dispersion of pigment granules from the pigment epithelium of the iris, which gets deposited in the anterior segment.

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9
Q

How does pigment dispersion syndrome look on retroillumiation and normal exam?

A

Retroillumination: spoke-like defects
Slit lamp: Pigment granules

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10
Q

What is pseudoexfoliative syndrome (PXF)? How does it look?

A

Protein like material in anterior segment of the eye, most noticed in the anterior capsule.
Looks like dandruff on the iris bundles. because TBM is blocked.

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11
Q

PDS vs PXF?

A

Differentiated by pigment deposition in the eye.
PDS: Spindle- shaped pattern (Krukenberg’s spindle) - tends to affect younger myopic patients
PXF: Dandruff like - tends to affect older population.

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12
Q

What is it when patients have increased IOP, Px has no changes vision, but no glaucoma?

A

Ocular hypertension

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13
Q

How does raised IOP cause optic nerve head damage?

A

It causes mechanical changes to lamina cribrosa

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14
Q

Eyes not treated for glaucoma IOP can fluctuate upto?

A

10-15mmHg

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15
Q

True or false? - glaucoma causes stress to the optic nerve head?

A

True

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16
Q

What happens to optic nerve head in glaucoma?

A

Alteration of optic nerve head flow and nutrient supply causing retinal ganglion cell death

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17
Q

Why does the neural retinal rim thin?

A

Due to nerve death

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18
Q

Why does glaucoma cause cupping of optic nerve head?

A

Nerves die causing the nerve head to excavate.

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19
Q

What regulates IOP in the eye?

A

Ciliary body- it forms aqueous and drains it to the front and back. For aqueous to move to the anterior chamber it needs to pass through the iris then pas to the pupil and move to the front where it drains through meshwork.

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20
Q

2 places where obstruction of aqueous occurs?

A
  1. Pupil block
  2. Schlemms canal
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21
Q

How is a suspected galucoma confirmed?

A

Monitor for progression

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22
Q

What is a notch of optic nerve?

A

Degeneration of blood vessels results in a notch along neuroretinal rim

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23
Q

What is bayoneting of blood vessels in glauacoma?

A

When blood vessels bend or kink sharply as they pass over the edge of the cup.
It is a sign of erosion or loss of NRR.

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24
Q

True or false- cup/disc ratio varries with disc size?

A

True

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25
Q

Congenital optic nerve head pit results from? What type of defect does it cause?

A

Result from an imperfect closure of the superior edge of the embryonic fissure.
It is a small pocket or hole near the optic nerve.
Altitudinal defect

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26
Q

HRT vs OCT- why is OCT better?

A

OCT allows RNFL + Macular imaging

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27
Q

Relation between pictures and OCT results for glaucoma dignoses?

A

If OCT and pictures do not match= not glaucoma .
Visual feilds helps identify if thinning is the same place corresposing to picture - if match = glaucoma confirmed

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28
Q

Subtypes of angle closure glaucoma?

A
  1. Acute angle closure
  2. Chronic angle closure
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29
Q

Characteristics of angle closure glaucoma?

A
  1. Females > males
  2. > 40 years
  3. Painful + vomiting
  4. Acute loss of vision
  5. Intermittent blur
  6. Haloes around bright light
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30
Q

ACG Subtypes/ stages?

A
  1. Latent- asymptomatic (IOP normal)
  2. Subacute- intermittent angle closure (may develop acute or chronic angle closure)
  3. Acute (Sent to A&E)- Congestive (Sudden total angle closure), Post congestive (follow acute attack)
  4. Chronic- creeping or latent angle closure
  5. Absolute - no PL following acute attack
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31
Q

ACG: Predisposing factors?

A

Convex iris lens diaphragm causes shallow anterior chambers (eclipise sign).
Narrow approach to angle. (Narrow van herick)

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32
Q

ACG Mechanism?

A
  1. Increase in physiological pupil block
  2. Dilation of pupil renders peripheral iris more flaccid.
  3. Increased pressure in posterior chamber causes iris bombe
  4. Angle obstruction by peripheral iris and rise in IOP.
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33
Q

What is subacute or intermittent angle closure glaucoma?

A

brief episodes of angle closure that resolve spontaneously. Patients experience the above symptoms of acute angle closure, but on a milder scale.

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34
Q

Signs seen on acute (congestive) ACG?

A
  1. Corneal oedema
  2. Dilated and undilated pupils
  3. Tonic pupils (pupil doesn’t move)
35
Q

Treatment / Rx of glaucoma?

A
  1. Medical (tropical drops, pilocarpine, suspension of aqueous production, diamox)
  2. YAG peripheral iridotomy
36
Q

What does YAG peripheral iridotomy do?

A

Equalise pressure in anterior and posterior chamber

37
Q

Signs of congenital glaucoma?

A
  1. Corneal oedema
  2. Lacrimation
  3. Photophobia
  4. Bupthalmos (large eye balls)
38
Q

What is Haab’s stiae?

A

Horizontal breaks in Descemet’s membrane, which may be single or multiple. Caused in primary congential glaucoma

39
Q

Axenfeld-Rieger syndrome

A

Pupil displacement
Small- displaced teeth
A rare, congenital, ocular defect caused by anterior segment dysgenesis and characterized by anteriorly displaced Schwalbe’s line and iris bands extending into the cornea.

40
Q

Peters anomaly?

A

a rare congenital disorder characterized by central corneal opacity with a relatively clear peripheral cornea.
Congenital defect

41
Q

aniridia

A

a partial or complete absence of the iris.

42
Q

How does sturge webers syndrome look like?

A

is condition in which there is usually a birthmark (port wine stain) involving the forehead or eye lid area, a layer of extra blood vessels over the surface of the brain

43
Q

sturge webers syndrome- what does it cause?

A

Increased episcleral venous pressure, backflow problems (episcleral venous pressure high)

44
Q

Can blood enter Schlemm’s canal?

A

Blood can enter Schlemm’s canal when the IOP becomes lower relative to the episcleral venous pressure

45
Q

Why is it important to lower pressure in glaucoma?

A

Reduce risk of progression, visual field loss. Lowering IOP improves visual prognosis.

46
Q

Convential and unconvential outflows are?

A

Convential: TM
Unconvential: Uveoscleral

47
Q

Most 2 common drugs to treat glaucoma?

A
  1. Prostaglandin analogues
  2. Prostaglandin analogues + Beta blockers
48
Q

Side effects of medical rx in glauacoma?

A

periorbital fat atrophy & pink eye
if beafy red colour eye = px is allergic to the drug.

49
Q

Is YAG Peripheral iridotomy used to treat glaucoma?

A

Not used for treatment, but used to prevent angle closure.
Burns around the edge of the angle, burns iris and pupil- it pulls away from the angle. not used in the UK.

50
Q

What is cyclodiode laser?

A

Kill ciliary body because it produces aqueous

51
Q

Filtration surgery can cause?

A

bleb

52
Q

Aqueous humour leaves through which 2 routes?

A
  1. TB (90%)0 Trabecular meshwork
  2. Schlemm cannal
53
Q

IOP is determined by?

A

Balance between aqueous production and rate of outflow

54
Q

Key modifiable factor in glaucoma?

A

IOP

55
Q

IOP varries with?

A

Time of day, BP, Respiration

56
Q

Mean IOP?

A

16mmHg

57
Q

Goal of glaucoma treatment?

A

Slow rate of progression to maintain visual functions.

58
Q

How to determine if it is open vs closed glaucoma?

A

Determined by aqueous outflow

59
Q

POAG Characteristics

A
  1. Optic nerve head damage
  2. RNFL thinning
  3. Open anterior chambers
  4. European/ African decent
  5. Both genders affected equally
60
Q

What asymmetry between IOP is significant?

A

4mmHg

61
Q

Risk factors of POAG?

A
  1. IOP- High IOP= more risk
  2. Age- more common in old ppl
  3. Race- Black
  4. Family history of POAG
  5. Diabetes mellitus
  6. Myopia
  7. Anti-VEGF Therapy: px’s undergoing anti-VEGF therapy for age related macular changes or diabetic macular oedema are ay higher risk of increased IOP.
  8. Long use of contraceptive pill- increases risk of glaucoma
  9. Large optic discs are more prone to damage.
62
Q

Are visual symptoms notes in px’s with glaucoma?

A

Absent unless damage is significant

63
Q

Myopia vs hypertropia in risk of glaucoma?

A

Myopia: high risk of POAG
Hypermetropia: High risk of PACG (Primary angle closure glaucoma).

64
Q

How does family history relate to glaucoma?

A
  1. POAG or Ocular hypertension
  2. Other ocular family histroy
65
Q

What 7 examinations are carried out to confirm glaucoma?

A
  1. VA- Likely to be normal unless glaucoma is advanced.
  2. Pupils- RAPD initally -ve but can become +ve if substainial progression
  3. Colour vision assesement
  4. Slit lamp examination- to look for secondary changes like pigmentary or pseudo exfoliation
  5. Tonometry- before patchmetry, note time
  6. Gonioscopy
  7. Optic disc exmaintion- on dilated eyes
66
Q

What is neuroretinal rim?

A

orange/ pink tissue between outer edge of cup and disc margin

67
Q

Optic nerve changes in glaucoma cause?

A

Irreversible decrease in nerve fibres, glial cells and blood vessels causing cupping.

68
Q

How is optic disc evaluated in galaucoma?

A
  1. Look for optic disc cupping
  2. Look for neuroretinal thinning, is ISNT rule followed?
  3. What is the CD ratio?
  4. Asymmetry between discs?
  5. Optic disc size
69
Q

What population has the largest optic discs?

A

African

70
Q

What are the non-specific optic disc glauacoma chnges?

A
  1. Disc haemorrhages
  2. Barring of circymlinear blood vessels
  3. Boyoneting
  4. Collaterals between 2 veins at the disc
  5. Loss od nasal NRR
  6. Laminar dot sign
71
Q

Large vs small discs- which one is likely to be damaged ?

A

Large discs at higher risk of damage

72
Q

Disc Haemorrhages common in what location and common in what type of glaucoma?

A

Inferiorly
NTG

73
Q

Characteristics of NTG?

A
  1. IOP Equal or less than 21mmHG
  2. Signs of optic nerve head damage characteristic of glaucoma pattern
  3. Visual field loss
  4. Open anterior chamber
  5. No features of secondary glaucoma
74
Q

NTG which gender is affected more?

A

Females

75
Q

NTG which race is affected most?

A

Japanese

76
Q

Optic nerve head large in NTG or POAG?

A

NTG

77
Q

PAGC caused by?

A

Occlusion of TMB by peripheral iris, obstructing aqueous flow.

78
Q

PAGC Common in what race?

A

East Asian and Indian Asian

79
Q

PACG vs POAG - which one is likely to cause visual loss?

A

PACG

80
Q

PACG Symptoms

A

blurred vision, halos around lights, eye pain, headache, nausea, and possibly vomiting.

81
Q

PXS Common in what gender?

A

woman

82
Q

true or false PXS can progress more rapidly than primary open angle glaucoma?

A

True, it can also result in significant visual loss.

83
Q

Neovascular glaucoma occurs as a result of?

A

Aggressive iris neovasculrisation (rubeosis iridis), which leads to progressive angle closure and rapid glaucomatous atrophy. Cause: diffused, chronic ischemia.

84
Q

Causes of neovascular glaucoma?

A
  1. Ischamic central retinal vein occlusion
  2. Diabetes mellitus
  3. Arterial retinal vascular disease