Primary Open Angle Glaucoma and Normal Tension Glaucoma

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Comprehensive set of 90 practice flashcards reviewing Primary Open Angle Glaucoma (POAG) and Normal Tension Glaucoma (NTG), covering definitions, risk factors, clinical features, tonometry, visual field defects, OCT imaging, differential diagnoses, and referral guidelines.

Last updated 6:29 PM on 10/13/26
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90 Terms

1
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What percentage of aqueous humour drainage occurs via the trabecular route?

90%90\% of aqueous outflow occurs via the trabecular route.

2
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What percentage of aqueous humour drainage occurs via the uveoscleral route?

10%10\% of aqueous outflow occurs via the uveoscleral route.

3
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What constitutes the optic nerve head (ONH), and what are its three anatomical regions?

The ONH is the intraocular segment of the optic nerve, consisting of the surface nerve fibre layer, the prelaminar region, and the lamina cribrosa.

4
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What is the lamina cribrosa and what functions does it provide to the retinal nerve fibre layer (NFL)?

It is a band of connective tissue that provides mechanical support, protection, and nutrients to the nerve fibre layer.

5
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What vertical optic disc diameter measurement defines a small disc?

A vertical disc diameter of <1.5 mm<1.5\,\text{mm}.

6
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What vertical optic disc diameter measurement defines a large disc?

A vertical disc diameter of >2.2 mm>2.2\,\text{mm}.

7
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What is the general classification definition of glaucoma?

A group of eye diseases that cause progressive optic neuropathy.

8
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What two primary pathological features characterise progressive optic neuropathy?

Distinctive excavation of the ONH (pathological cupping / loss of retinal NFL) and visual field defects.

9
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How is primary glaucoma defined?

Glaucoma that has no association with any other ocular or systemic disease.

10
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How is secondary glaucoma defined?

Glaucoma that occurs secondary to the presence of another ocular or systemic disease, abnormality, or injury.

11
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What characterizes the drainage apparatus in open angle glaucoma?

The anterior chamber angle is open and aqueous humour has free access to the drainage apparatus, but blockage occurs at or within the trabecular meshwork.

12
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What characterizes the drainage apparatus in closed angle glaucoma?

The anterior chamber angle is closed, which prevents aqueous humour from reaching the trabecular meshwork.

13
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Which six subtypes of secondary glaucoma are listed in the lecture notes?

Pseudoexfoliative glaucoma, Pigmentary glaucoma, Steroid-induced glaucoma, Neovascular glaucoma, Inflammatory glaucoma, and Congenital glaucoma.

14
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What is the definition of Primary Open Angle Glaucoma (POAG), and what parameter is notably omitted from it?

A slowly progressive neuropathy characterised by a distinctive excavation of the optic nerve head and progressive visual field loss; intraocular pressure (IOP) is notably not mentioned in the definition.

15
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What is the epidemiological significance of POAG in terms of prevalence and blindness worldwide?

POAG is the most prevalent type of glaucoma and the 2nd2\text{nd} leading cause of blindness globally.

16
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What are the four diagnostic criteria for chronic POAG (high tension)?

IOP >21 mmHg>21\,\text{mmHg}, glaucomatous optic nerve damage, an open anterior chamber angle, and no secondary causes.

17
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What are the five diagnostic criteria for Normal Tension Glaucoma (NTG)?

IOP consistently <21 mmHg<21\,\text{mmHg}, glaucomatous optic nerve damage, an open anterior chamber angle, characteristic visual field loss, and no secondary causes.

18
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What are the diagnostic criteria for Ocular Hypertension (OHT)?

IOP >21 mmHg>21\,\text{mmHg} (referred and treated if >21 mmHg>21\,\text{mmHg} with Goldmann Applanation Tonometry), with no glaucomatous optic disc damage and no visual field loss.

19
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What overlap and clinical distinction is noted between POAG and NTG?

There is clinical overlap between POAG and NTG, but NTG tends to have a more distinct clinical profile and more vascular associations.

20
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How does the nature of progression differ between POAG and NTG?

Progression in POAG is more pronounced and correlates with the level of IOP, whereas progression in NTG is less pronounced or even non-progressive.

21
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<p>Based on the comparative table, what specific clinical features, structural changes, and visual field defects are circled as characteristic of NTG?</p>

Based on the comparative table, what specific clinical features, structural changes, and visual field defects are circled as characteristic of NTG?

Clinical profile: lower body weight, detail-orientated and health conscious; Risk factors: female gender, Japanese descent, hypotension, altered ocular blood flow (OBF), vasospasm/vascular dysregulation; ONH changes: predominantly inferotemporal NRR thinning and disc haemorrhages; VF defects: deep, steep, paracentral defects; Progression: less pronounced or non-progressive.

22
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What specific patient clinical profile is associated with Normal Tension Glaucoma (NTG)?

Lower body weight, as well as being detail-orientated and health conscious.

23
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How do ethnic risk factor associations differ between POAG and NTG in the comparative chart?

African descent is asterisked as a significant risk factor for POAG, whereas Japanese descent is asterisked as a significant risk factor for NTG.

24
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Which gender is noted with an asterisk as an increased risk factor in NTG?

Female gender.

25
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What structural neuroretinal rim (NRR) change is predominantly observed in NTG compared to POAG?

Inferotemporal NRR thinning predominantly, accompanied by disc haemorrhages.

26
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How do the characteristic visual field defects differ between POAG and NTG?

POAG presents with arcuate scotomas with paracentral locations involved at later stages, whereas NTG presents with deep, steep, paracentral defects earlier on.

27
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What cellular event represents the core underlying pathogenesis of POAG?

Progressive retinal ganglion cell (RGC) death.

28
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What is the primary mechanism proposed by the mechanical theory of POAG?

Damage is induced by raised IOP exerting physical force on the lamina cribrosa and the axons of the optic nerve head, with greater force exerted at higher pressures.

29
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What four sequential pathological outcomes occur according to the mechanical theory of POAG?

  1. Deformation of lamina cribrosa plates; 2. Disturbance of axonal transport; 3. Compression of nerve fibre bundles; 4. Nerve fibre damage and loss.
30
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What is the primary mechanism proposed by the vascular theory of POAG?

Damage is induced by the failure of the microvasculature to nourish the ONH nerve fibres, leading to cellular death.

31
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What four potential systemic or vascular causes are cited for microvasculature failure in POAG?

Faulty autoregulation, hypotension, vasospasm, and cardiovascular disease.

32
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Which specific vascular risk factors are marked with an asterisk for NTG in comparison to POAG?

Hypotension, altered ocular blood flow (OBF), and vasospasm/vascular dysregulation.

33
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What are the four general risk factors for POAG?

Increased IOP, older age, African descent, and a positive family history in a 1st1\text{st} degree relative.

34
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What degree of relative is specifically noted as a general family history risk factor for POAG?

A 1st1\text{st} degree relative.

35
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What are the three ocular risk factors for POAG listed in the lecture notes?

Myopia, large optic nerve head (ONH), and thinner central corneal thickness.

36
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What systemic risk factors are associated with POAG?

Hypertension/hypotension, vasospasm (Raynaud's syndrome), history of cardiovascular disease, and sleep apnea.

37
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Why is POAG typically asymptomatic during its early stages?

The anterior eye is usually quiet, and initial visual field loss is nasal and masked/covered by the overlapping field of the other eye.

38
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At what stage do visual symptoms usually arise in a patient with POAG?

Symptoms typically arise once visual field loss becomes significant.

39
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What four clinical assessments need to be considered when evaluating POAG?

Optic nerve head (ONH), intraocular pressure (IOP), visual fields (VF), and optical coherence tomography (OCT).

40
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What is the ISNT rule for a normal optic disc, and what occurs to it in POAG?

In normal eyes, neuroretinal rim thickness follows Inferior >> Superior >> Nasal >> Temporal; in POAG, there is a loss of the ISNT rule.

41
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What two patterns of neuroretinal rim (NRR) thinning are seen in POAG?

Diffuse (generalised) thinning and focal thinning (notching).

42
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What is vascular 'baring' in the context of glaucomatous ONH changes?

A sign where circumlinear vessels no longer run coincident with the cup margin and are left unsupported or 'bared'.

43
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What is 'bayonetting' of a retinal blood vessel at the optic disc?

A sharp change of angle (sharp bend) of a blood vessel as it passes from the neuroretinal rim into the optic cup.

44
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What is 'overpassing' in glaucomatous optic disc vascular signs?

A vascular sign where a blood vessel courses over the cup margin without dipping down.

45
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What is 'nasalisation' of vessels at the optic disc and why does it occur?

Displacement of blood vessels toward the nasal side of the optic disc due to progressive loss of supportive neuroretinal rim tissue.

46
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What are the appearance and duration of disc haemorrhages seen in glaucoma?

They are splinter- or flame-shaped haemorrhages that are transient, lasting between 1 to 8 months1\text{ to }8\,\text{months}.

47
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What morphological cup changes are characteristic signs of POAG?

Vertical cupping, a large or enlarging cup-to-disc (c/d) ratio, deep or deepening cupping, and changes in the lamina cribrosa pores.

48
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What cup-to-disc ratio asymmetry between eyes is considered suspicious for glaucoma?

An asymmetry of >0.2>0.2 between eyes.

49
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What causes peripapillary atrophy (PPA)?

Chorioretinal thinning and disruption of the retinal pigment epithelium (RPE).

50
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In what percentage of normal healthy eyes is peripapillary atrophy present as part of the ageing process?

Up to 80%80\% of normal eyes.

51
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What are the anatomical characteristics of the Alpha zone in peripapillary atrophy?

The outer crescent with irregular hypopigmentation and hyperpigmentation, commonly found in normal eyes.

52
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What are the anatomical characteristics of the Beta zone in peripapillary atrophy?

The inner zone adjacent to the disc showing visible sclera, choroidal vessels, and total loss of RPE; it is more clinically significant for glaucoma.

53
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How do the Alpha and Beta zones of PPA compare in normal eyes versus glaucomatous eyes?

In normal eyes, alpha >> beta and is temporal; in glaucoma, both zones are significantly larger, and the beta zone is more frequently present.

54
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In which type of optic disc is the presence of a Beta zone of PPA a particularly sensitive indicator of glaucoma?

In an optic disc with a small cup-to-disc (c/d) ratio.

55
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How does the anatomical location of peripapillary atrophy relate to optic nerve damage in glaucoma?

The location of the peripapillary atrophy relates directly to the damaged region of the optic nerve head.

56
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What is a choroidal crescent in the differential diagnosis of PPA?

A crescent seen when the retinal pigment epithelium (RPE) stops short of the optic nerve head.

57
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What is a scleral crescent in the differential diagnosis of PPA?

A crescent seen when both the RPE and the choroid stop short of the optic nerve head.

58
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What is a pigment crescent in the differential diagnosis of PPA?

A crescent seen where the retinal pigment epithelium (RPE) thickens or folds.

59
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What congenital anomaly can be confused with PPA on fundus photographs?

Myelinated nerve fibres, which appear brighter in fundus photos.

60
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What optical lighting technique makes subtle retinal nerve fibre layer (RNFL) defects more visible on fundus photos?

Red-free illumination.

61
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What two morphological patterns of retinal nerve fibre layer defects are observed?

Localised wedge-shaped defects and diffuse defects.

62
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What is the typical clinical timeline of RNFL defects relative to visible ONH changes and visual field loss?

RNFL defects often precede the development of visible optic nerve head changes and visual field loss.

63
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At what absolute intraocular pressure level is glaucoma more likely to be suspected on contact tonometry?

An IOP of >24 mmHg>24\,\text{mmHg} (actual value obtained via contact tonometry and pachymetry).

64
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What degree of diurnal IOP variation on diurnal phasing raises clinical suspicion of glaucoma?

A diurnal variation of >5 mmHg>5\,\text{mmHg}.

65
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What degree of IOP asymmetry between the two eyes raises suspicion of glaucoma?

An asymmetry between eyes of >4 mmHg>4\,\text{mmHg}.

66
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What action should always be taken whenever a suspicious IOP reading is recorded?

Suspicious IOP readings should always be repeated.

67
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What proportion of patients with glaucoma may have normal intraocular pressure readings?

15 to 25%15\text{ to }25\% of glaucoma patients (representing Normal Tension Glaucoma).

68
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What is the average central corneal thickness (CCT) cited in the notes?

545 μm545\,\mu\text{m}.

69
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What approximate numerical conversion relates corneal thickness variation to measured IOP?

10 μm10\,\mu\text{m} of corneal thickness difference corresponds approximately to 0.5 mmHg0.5\,\text{mmHg} of measured IOP.

70
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How does a cornea that is thicker than average affect the measured IOP reading?

It produces an artificially high IOP reading.

71
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How does a cornea that is thinner than average affect the measured IOP reading?

It produces an artificially low IOP reading.

72
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Why is prior corneal refractive surgery a critical consideration when evaluating IOP?

Post-refractive surgery central corneal thickness will be thinner than it was previously, leading to artificially low IOP readings.

73
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Besides corneal thickness, what other ocular surface factor can affect tonometry IOP readings?

The amount of tears.

74
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What four characteristic visual field defects occur in POAG?

Paracentral scotoma, Nasal step, Arcuate scotoma, and Tunnel vision (with macula sparing).

75
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What two criteria must a visual field defect fulfill to be considered diagnostically valid in glaucoma?

The defect should be reproducible and consistent with the optic disc appearance.

76
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What threshold criteria define a reliable visual field plot?

<20%<20\% fixation losses, <33%<33\% false positives, and <33%<33\% false negatives.

77
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In what percentage of early glaucoma cases does a paracentral scotoma appear, and where is it located?

It appears in 70%70\% of early cases within the central 10 to 20∘10\text{ to }20^\circ of fixation, usually adjacent to the nasal and superior sections of the blind spot, respecting the horizontal midline.

78
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What is a nasal step defect, and how does it evolve as glaucoma progresses?

A difference in visual sensitivity above and below the midline in the nasal field that arcs towards the blind spot as it progresses.

79
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How does an arcuate scotoma form, and what anatomical pathway does it follow?

It forms from the coalescence of paracentral scotomas or the extension of a nasal step, following the arcuate pattern of the retinal nerve fibre layer.

80
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What visual field defect results when an arcuate scotoma expands to involve both the superior and inferior quadrants?

A ring scotoma.

81
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Why is 'macula sparing' observed in advanced POAG tunnel vision?

Because the papillomacular bundle is the last nerve bundle to be affected by glaucomatous damage.

82
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What is the ultimate visual outcome if visual field loss in POAG progresses completely unchecked?

The entire visual field is lost, resulting in no perception of light.

83
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What structural evaluation does OCT provide in glaucoma management?

An automated evaluation of cross-sectional retinal thickness at the optic nerve head to measure the thickness of inner retinal layers.

84
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Which specific anatomical components of retinal ganglion cells correspond to the three inner retinal layers measured on OCT?

RGC axons correspond to the retinal nerve fibre layer (RNFL), RGC cell bodies correspond to the ganglion cell layer (GCL), and RGC dendrites correspond to the inner plexiform layer (IPL).

85
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What three anatomical variations can cause false-positive glaucomatous RNFL thinning on OCT?

Variations in axial length, optic disc size or tilt, and the angle between the optic nerve head and the fovea.

86
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What refractive error range is included in standard OCT normative databases?

Refraction values between +5.00 D+5.00\,\text{D} and −5.00 D-5.00\,\text{D}.

87
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What three retinal layers comprise the 'Ganglion Cell Complex' (GCC) measured at the macula on OCT?

Retinal nerve fibre layer (RNFL), ganglion cell layer (GCL), and inner plexiform layer (IPL).

88
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Why is taking OCT measurements at the macula advantageous compared to the optic nerve head?

Macular scans are more reliable, more stable, less affected by axial length, and sample the region with the highest density of retinal ganglion cells where early cell loss can be detected.

89
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What clinical examinations are used to evaluate the anterior chamber angle, ONH/RNFL, IOP, and visual fields in a glaucoma workup?

Angle: Van Herrick's, gonioscopy; ONH/RNFL: slit-lamp biomicroscopy, fundus photography, OCT; IOP: applanation tonometry, pachymetry; VF: threshold visual fields.

90
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What are the five differential diagnoses for POAG listed in the notes, and what is the 5-year5\text{-year} risk of untreated OHT developing glaucoma?

Ocular hypertension, physiological cupping, tilted discs, anterior ischemic optic neuropathy, and congenital ONH anomalies; approximately 10%10\% of untreated OHT patients develop glaucoma within 5 years5\,\text{years}.