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603 > glaucoma L1 > Flashcards

glaucoma L1 Flashcards

1
Q

acquired open angle glaucoma

A
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2
Q

Acquired close angle glaucoma

A
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3
Q

What are the 2 types of glaucoma?

A

acquired and congenital

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4
Q

What is open angle glaucoma?

A

Anterior chamber angle is open, aqueous humour can drain through the trabecular meshwork… BUT there is
Blockage occurs at/within the trabecular meshwork

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5
Q

What is closed angle glaucoma?

A

Anterior chamber angle is closed, aqueous humour is prevented from reaching the trabecular meshwork

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6
Q

What does primary mean?

A

No association with any other disease

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7
Q

What does secondary mean?

A

Occurs secondary to the presence of another ocular or systemic disease, abnormality or injury

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8
Q

What is the function of aqueous humour?

A

» maintains structural integrity of the globe
» maintains the position of the refractive surfaces relative to each other
* Nutrition of the avascular lens and cornea
* Removal of waste products from lens and cornea

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9
Q

What produces aqueous humor?

A

-ciliary body

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10
Q

What is the pathway of aqueous humour?

A

Ciliary body → Posterior chamber → Pupil → Anterior chamber ↓
Drainage apparatus ( out trab meshwork and schlemms canal)

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11
Q

What are th2 2 drainage routes of aqueous humour?

A

trabecular route
uveoscleral route

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12
Q

Describe the trabecular drainage route?

A

90% of outflow
* Aqueous flows through trabecular meshwork, into the canal of sclemm and away via the episcleral veins
* Pressure sensitive route

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13
Q

Describe the uveoscleral route?

A

10% of aqueous outflow
* Aqueous passes across the face of ciliary body into the suprachoroidal space and away via venous circulation of ciliary body, choroid and sclera

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14
Q

What is POAG?

A

slowly progressive optic neuropathy characterised by a distinctive excavation of the optic nerve head and progressive visual field loss

-most common type
-chronic
-2nd leading cause of blindnesss in the world

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15
Q

What are the sub divisions of POAG?

A

1.Normal tension glaucoma (NTG)

  1. Ocular hypertension (OHT)
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16
Q

summarise POAG

A
  • IOP > 24mmHg at some point
  • Glaucomatous optic nerve damage
  • An open anterior chamber angle
  • Characteristic visual field loss
  • No secondary causes
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17
Q

Summarise NTG

A
  • IOP consistently ≤ 24mmHg
  • Glaucomatous optic nerve damage * An open anterior chamber angle
  • Characteristic visual field loss * No secondary causes
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18
Q

Summarise OHT

A

IOP > 24mmHg
* No glaucomatous optic nerve damage
* No visual field loss

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19
Q

What is the difference between NTG and POAG?

A

-Considerable overlap between the 2

-NTG tends to have a more classic clinical profile and more vascular associations (but not always)

Less pronounced or even non-progressive

Inferotemporal NRR thinning predominantly
- Disc haemorrhages
NTG accounts for approx 15-25% POAG cases

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20
Q

What is the pathogenesis of POAG?

A

caused by progressive retinal ganglion cell death caused by mechanical or vascular damage

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21
Q

What is the mechanical theory?

A

increases/raised IOP puts pressure on the lamina cribosa and the optic nerve head.

-this damages the lamina cribs and the axons of the ONH

1.compression of the nerve fibre bundles= nerve fibre damage/loss

  1. disturbance of the axonal transport
  2. deformation of lamina cribs plates
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21
Q

What is the mechanical theory?

A

increases/raised IOP puts pressure on the lamina cribosa and the optic nerve head.

-this damages the lamina cribs and the axons of the ONH

1.compression of the nerve fibre bundles= nerve fibre damage/loss

  1. disturbance of the axonal transport
  2. deformation of lamina cribs plates
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22
Q

What is the vascular theory?

A

. Ocular blood flow may be reduced/innsufficient due to elevated IOP.

which causes compression of the capillaries supplying the ONH.

Damage induced by failure of the microvasculature to nourish ONH nerve fibres – cell death

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23
Q

What are the potential causes of the vascular theory?

A
  • Faulty autoregulation
  • Hypotension
  • Vasospasm
  • Cardiovascular disease
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24
Q

What are the risk factors of POAG?

A
25
Q

what are the symptoms of POAG?

A

Asymptomatic
* Anterior eye is white and quiet
➢ Initial field loss is usually nasal and covered by other eye
➢ Symptoms may arise once visual field loss becomes significant

26
Q

What are the key 4 signs of POAG?

A
  • Optic Nerve Head
  • Visual Field
  • Intraocular pressure
  • OCT
    ➢ Usually bilateral but asymmetric
27
Q

What does the NRR look like in POAG?

A

NRR:
– Loss of ISNT rule
– Diffuse (generalised) thinning
– Focal thinning (notching)

28
Q

What does the cup look like in POAG?

A

Cup:
– Vertical cupping
– Large or enlarging c/d ratio
– Deep or deepening cupping
– Change in lamina cribrosa pores
– Asymmetry (>0.2)
– Progression over time

29
Q

What are the vascular changes in POAG?

A

– Baring
– Bayonetting
– Overpassing
– Nasalisation
– Disc haemorrhages

30
Q

What is diffuse loss of the NRR?

A

concentric enlargement of cup
Diffuse (generalised) thinning

31
Q

What is a focal loss of the NRR?

A

Thinning or notching in a certain region
Inferior rim usually affected first, followed by superior rim

32
Q
A

Early stages: loss of ISNT rule, inferior thinning of NRR, vertical enlargement of cup

33
Q
A

Superior notching of NRR

34
Q
A

inferior notching

35
Q

reduced iop

A

reduced progression of glaucoma

36
Q
A

Barring

circumlinear vessels no longer run coincident with the cup margin and are ‘bared’

37
Q
A

Bayonetting
retinal vessels may disappear as they make a sharp turn into the cup

change of angle of blood vessel as it passes from NRR to optic cup (sharp bend)

If blood vessels bend or kink sharply when they pass over the edge of the cup= sign of erosion or loss of nor

38
Q
A

Overpassing:

blood vessel isolated from disc margin and floor and is left ‘hanging’ in the volume of the cup (bridges the cup)

39
Q
A

Nasalisation of vessels:
– Progressive loss of NRR tissue leads to loss of support for blood vessels

40
Q
A

Disc haemorrhages:
– Splinter or flame shaped
– Transient (1-8 months)
– High risk of future damage
– Precede notching, NFL defects and/or visual field loss
– NTG?

40
Q
A

Disc haemorrhages:
– Splinter or flame shaped
– Transient (1-8 months)
– High risk of future damage
– Precede notching, NFL defects and/or visual field loss
– NTG?

41
Q

What are nerve fibre layer defects?

A

Subtle defects – more visible with red-free illumination
* Often precede development of visible ONH changes and visual field loss
* Two patterns:
– Localised wedge shaped defects
– Diffuse defects

42
Q

What is Peripapillary atrophy (PPA)?

A
  • Caused by chorioretinal thinning and disruption of RPE
  • Present in up to 80% of normal eyes (ageing process)
    Divide peripapillary region into two zones: alpha and beta zone
43
Q

What is the alpha zone?

A

Alpha:
– outer crescent
– irregular hypo and hyper- pigmentation
– common in normal eyes

44
Q

What is the beta zone?

A

– area adjacent to disc
– visible sclera, choroidal vessels and total loss of RPE
– more significant to glaucoma

45
Q
A

Peripapillary atrophy (PPA)

46
Q

What does PPA look ike when someone has glaucoma?

A

– Both zones significantly larger
– Beta zone more frequently present
– Sensitive indicator if present in a disc with small c/d ratio
– Location relates to damaged region

47
Q

Differential diagnosis of PPA?

A

Choroidal crescent: seen if RPE stops short of ONH
* Scleral crescent: seen if both RPE and choroid stop short of ONH
* Pigment crescent: seen where RPE thickens or folds

48
Q

End stage POAG

A
49
Q

Suspect glaucoma

A

IOP > 24mmHg (actual value- contact tonometry + pachymetry)

Diurnal variation of >5mmHg (on phasing- testing IOP at phases during the day)

  • Asymmetry between eyes of >5mmHg
50
Q

sus readings

A

Suspicious readings should always be repeated
- Level of IOP that causes damage can vary between individuals
- Consider corneal thickness
- 15-25% of patients with glaucoma may have normal IOP (NTG)

51
Q

What is the average corneal thickness

A
  • Average corneal thickness = 550 microns
  • 10 microns = 0.5mmHg (very approximate)
52
Q

How does CCT affect IOP?

A

Thicker than average cornea: artificially high IOP reading

  • Thinner than average cornea: artificially low IOP reading
53
Q

What are the characteristic visual field defects in POAG?

A

– Paracentral scotoma
– Nasal step
– Arcuate scotoma
– Tunnel vision (Macula sparing)

54
Q

Defect should be

A

Defect should be: * Reproducible
* Consistent with optic disc appearance
* Visual field plot should be reliable
(<20% fixation losses, <33% false +ves and false –ves)

55
Q

What are the 3 visual field defects in POAG

A
  1. paracentral scotoma
    2.nasal step
  2. arcuate scotoma
56
Q
A

paracentral scotoma

57
Q
A

nasal step

58
Q
A

arcuate scotoma

59
Q

What is likely to cause false readings in OCT?

A

➢ Axial length*
➢ Optic disc size or tilt
➢ Angle between optic nerve head and fovea

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