B2 Glaucoma Flashcards

1
Q

define glaucoma

A

it is the disease of the optic nerve head characterised by:

  • loss of optic nerve head fibres (NFL) and its corresponding visual field defects
  • potentially raised IOP
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2
Q

state normal IOP (range and mean) and diurnal variation

A

normal: 10-21 mmHg (range), 16 +- 2.5 mmHg (mean)

diurnal variation: higher in the morning than afternoon, 4-6 mmHg (normal variation)

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3
Q

how is IOP measured

A

by tonometry

highly influenced by corneal thickness (thicker cornea -> higher IOP)

when assessing IOP, risk factors must be taken into account ie. medication, refractive surgery

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4
Q

state and explain 2 pathophysiological aspects to glaucoma

A

mechanical theory: IOP increase causes damage to retinal GLC axons which cause NFL to eventually die leading to ONH atrophy

vascular theory: IOP increase causes blood vessels at ONH to be squeezed, hence ONH undergoes infarction/ischemia (lack of O2). splinter haemorrhages may be seen but will subside if IOP returns to normal

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5
Q

state classifications of glaucomatous changes

A

ONH damage (enlarged cupping, neural rim changes, signs of peripapillary atrophy, optic disc haemorrhage, laminar dot sign, b/v changes, NFL loss) …

…and its corresponding VF defects

others: corneal oedema/thickness changes/AC angle changes

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6
Q

explain ONH changes (glaucomatous)

A
  1. c-d ratio: 0.3 to 0.4 (normal), >0.5 suspicious, asymmetry > 0.2 suspicious
  2. neuroretinal rim thickness: loss (notching/thinning) of sequence in thickness (ISNT) can indicate loss of NFL ((glaucoma usually causes vertical thinning))
  3. peripapillary atrophy: common in high myopes, RPE (alpha zone) and choroidal (beta zone) degeneration which happens when the RPE pulls away from the ONH revealing the choroid or sclera. in the beta zone, chorio retinal atrophy may be associated with glaucoma
  4. haemorrhage (drance/splinter): occurs where NF present, often adjacent to NF thinning, temporary (IOP stabilises)
  5. lamina cribosa dot sign: becomes more obvious due to receding NRR/loss of NRR (loss of NFL)
  6. blood vessels: nasal sweep, baring (hangs over ONH, poor support to BV), bayoneting (sharp exit from ONH)
  7. NFL loss: different in colour can be seen in fundus imaging to show NFL loss or bvs appear darker and sharply defined. normally starts at inferior (recall NF never cross temporal raphe). diffused/localised, striations are absent
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7
Q

state 5 R’s for glaucoma evaluation

A

(scleral) RING - observe optic disc size
(neuroretinal) RIM - observe NRR size&shape / i.s.n.t.

RNFL

REGION of peripapillary atrophy

(hemo)RRHAGES - presence of retinal or optic disc haemorrhages

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8
Q

instruments to detect for possible glaucoma

A

VF analyser (stages of glaucoma): starts off with enlarged blind spot/paracentral scotoma, nasal step, (superior/inferior) arcuate field loss, entire (superior/inferior) arcuate field loss, superior & inferior arcuate field loss

frequency doubling perimeter (early glaucoma): measures ganglion M cells which are bigger in diameter and more susceptible to glaucomatous changes. loss of these cells causes considerable loss of visual function

OCT & HRT (structural loss): capture the images of the optic disc to measure the CD ratio, NRR thickness and the Retinal Nerve Fiber Layer (RNFL) thickness.

gonioscopy: gold standard for AC angle assessment, this technique allows actual visualisation of AC angle structures unlike other methods.

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9
Q

what are some symptoms of glaucoma (if not asymptomatic)

A

pain, redness, watering of eyes

blurred vision

nausea & vomitting

haloes

bumping into objects while walking (due to diminishing peripheral vision)

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10
Q

explain referral guideline & management for glaucoma

A

van herick angle <0.25: symptomatic of ACG (haloes, headache, blurred vision) refer within 3 days, asymptomatic is non-urgent referral

disc >0.7/thinning or notching of NFL/asymmetry >0.2: non urgent referral and advice accordingly to sheet

IOP > 22mmHg (avg of 4 readings and taken on 3 different occasions): 22-25 non urgent, 25-35 early, >35 3 days, AACG immediate, and according to advice sheet

glaucomatous VF defect: according to urgency appropriate to clinical assessment

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11
Q

explain ocular hypertension

A

when the patient’s IOP is higher than normal but show no detectable glaucomatous change.

4-7% of individuals older than 40 have OHTN. OHTN has 10% chance of progressing to glaucoma in 5 years

risk factors of progression from OHT to glaucoma: IOP >/= 30mmHg, greater age, thin central corneal thickness, larger c/d ratio

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12
Q

describe POAG

A

most common, chronic, usually bilateral but asymmetrical

AC angle is open but outflow is slow. meaning AC angle structures may be blocked ie. TM

risk factors: more in black people, age 40-60 and risk increasing with age, high myopia, fm hx 1st degree 1/10 risk, systematic diseases (DM, HTN), smoking, steroid use, ocular (constantly high IOP, higher myopia, large cd ratio, retinal disease CRVO RP)

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13
Q

explain ssx of POAG

A

signs: glaucomatous changes, open & normal filtration angle
symptoms: usually asymptomatic though they may start to lose their peripheral vision with time (by then 40% damage is done). therefore, regular eye exams and hx taking important

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14
Q

explain ssx of POAG

A

signs: glaucomatous changes - IOP may be normal, open & normal filtration angle
symptoms: usually asymptomatic though they may start to lose their peripheral vision with time (by then 40% damage is done). therefore, regular eye exams and hx taking important

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15
Q

explain management of POAG

A

IOP reduction: the greater the damage, the greater the IOP reduction

urgent referral for medical Tx (first choice)

regular follow up: 6-12 months

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16
Q

describe ACG

A

[pathogenesis] iris recedes during pupillary dilation (this itself starts to narrow the AC angle). the crystalline lens has also moved anteriorly (aging). iris buries itself into the lens when pupil dilates (aka iris bombe) and there is now relative pupil block. this prevents the AQ from flowing into the anterior chamber and hence builds up in the posterior chamber. the AQH build up in posterior chamber pushes the iris anteriorly, narrowing the filtration angle this causes a rise in IOP and hence inflicting eye pain, corneal oedema (hazy, seeing halos), conjunctival infection/redness to the patient.

17
Q

explain risk factors for ACG

A

more in south-east asians, Chinese, eskimos

older than 40, hyperopes/shorter axial length, females, fx history, larger crystalline lens size, dim illumination, post pupil dilation, emotional disturbance

18
Q

explain ssx of ACG

A

signs: shallow/closed AC angle, oval non-reactive mid-dilated pupil, conjunctival infection/red eye, corneal oedema
symptoms: blur vision, haloes & hazy vision, severe eye pain, headaches, nausea & vomitting,

19
Q

explain management of ACG

A

immediate referral to drop IOP

required surgical Tx followed by drugs

follow up every 3 months

peripheral iridotomy is 1st choice

20
Q

explain sub-acute angle closure glaucoma

A

intermittent episodes of blurred vision and ocular discomfort with narrow angles

repeated sub acute attacks may result in PACG

same management as ACG

21
Q

explain treatment of glaucoma

A

IOP is regulated by AQH production and outflow. hence treatment is to decrease production OR increase outflow

aim: lower IOP, avoid nerve damage, save sight

done by medical/drug treatment

22
Q

explain congenital glaucoma

A

caused by mal-development of the AC angle, usually manifested by 3rd otherwise 16th birthday. CG is sporadic, primary

ssx: corneal haze, photophobia, megalocornea, high myopia etc
tx: paediatrics ophthalmologist, surgical tx

23
Q

explain pigment dispersion syndrome

A

caused by pigments from iris epithelium clogging filtration angle, young and middle age onset. associated with exercise, mechanical friction from IOL etc

ssx: loss of pupillary ruff, iris transillumination, TM/iris surface hyperpigmentation etc
tx: same as POAG treatment

24
Q

explain pseudo exfoliation

A

recall: it is the grey/white granular material on the pupillary margin, anterior lens and posterior cornea

elderly onset, more in females, high incidence in Scandinavia

tx: same as POAG treatment

25
Q

explain neovascular glaucoma

A

secondary to iris rubeosis due to chronic severe retinal ischemia

tx: surgical tx

26
Q

explain secondary glaucoma

A

phakocytic glaucoma: caused by rupturing of morgagnian cataract which causes pupillary block. referral needed

uveitic glaucoma: secondary to posterior synechiae where the iris is adherent to the anterior lens

haemolytic glaucoma: caused by hyphema (bleeding in The Eye)

steroid induced glaucoma: involves ocular inflammation