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glaucoma Flashcards

1
Q

where is the ciliary body and what does it produce

A

pars plicata anteriorly and pars plana posteriorly.

The aqueous humour is formed by the ciliary processes in the pars plicata.

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2
Q

what are the mechanisms of secretion

A

Diffusion: Due to a concentration gradient.

Ultrafiltration: Pressure gradient between oncotic and hydrostatic pressures (capillary versus intraocular pressures).

Active (∼80%): Active transport is mediated by transmembrane aquaporin activated by Na+/K+ ATPase enzyme and carbonic anhydrase enzyme.

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3
Q

aqueous secretion is innervated by what

A

sympathetic (adrenergic innervation) system. β2 receptor stimulation increases aqueous secretion

however, α2 receptor stimulation decreases aqueous secretion.

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4
Q

function of the aqueous humour

A

Supplies essential nutrients for the cornea and lens.
● It fills the anterior chamber (volume of 0.25 mL; tends to become shallower
with age and in people with hypermetropia) and posterior chamber (smaller
than the anterior chamber).

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5
Q

composition of aqeous humor

A
  • Water constitutes >99% of normal aqueous humour.
  • Lower concentrations of protein and glucose than plasma.
  • Higher concentrations of ascorbic acid, chloride and lactate than plasma.
  • Similar concentration of sodium to plasma.
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6
Q

what are the aqeous outflow routes

A

● Trabecular outflow (∼70%): The conventional aqueous route in the eye going through the trabecular meshwork (TM) and Schlemm’s canal to the episcleral veins.

● Uveoscleral outflow: Aqueous humour passes through the ciliary muscle to the suprachoroidal space and is eventually drained by choroidal veins, emissary canals of the sclera (vortex veins) or veins of the ciliary body.

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7
Q

what are the three parts of the trabecular meshwork

A

● Uveal meshwork (innermost): Contains relatively large holes.
● Corneoscleral meshwork: Contains smaller holes, accounting for greater
resistance.
● Juxtacanalicular meshwork (outermost): Connects the trabecular meshwork
with the Schlemm canals. It contains narrow intercellular spaces, thus supplying the major part of the normal aqueous outflow resistance.

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8
Q

role of the schlemms canal

A

endothelial-lined oval canal situated circumferentially in the scleral sulcus. It contains holes for collector channels which terminate in the episcleral veins.

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9
Q

what is the neuroretinal rim

A

● Refers to the area of the optic disc, between the margins of the central cup and the disc, containing retinal neuronal cells.
● The rim is thickest Inferiorly, followed by Superiorly, Nasally and Temporally (the ‘ISNT rule’).
● During glaucomatous changes, thinning of this neuroretinal rim occurs.

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10
Q

what is cup to disc (C/D) Ratio

A

● Defined as the vertical diameter of the optic cup divided by the vertical diameter of the optic disc.
● The normal C/D ratio is 0.3. Some individuals may have physiological cupping of 0.6 or 0.7 without glaucomatous changes.

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11
Q

what is trabeculotomy

A

IOP-lowering surgical technique which involves the creation of a fistula for aqueous outflow from the anterior chamber to the sub-Tenon space, creating a bleb

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12
Q

what may be used to prevent bleb failure and examples of them

A

use of antimetabolites may be used to slow the healing process in order to prevent bleb failure. Such antimetabolites are:

  • 5-fluorouracil (5-FU): A pyrimidine analogue which inhibits fibroblasts by blocking DNA synthesis.
  • Mitomycin C: An alkylating agent which also inhibits fibroblasts.
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13
Q

what is ocular HTN

A

Raised IOP (>21 mmHg)
open angles
without glaucomatous damage.

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14
Q

RFS for ocular HTN goin to glaucoma

A

● Older age.
● Higher IOP.
● Large cup/disc ratio.
● A thinner CCT: Patients with relatively thin central corneal thickness (CCT)
(≤555 μm) had 3.4 times higher risk of conversion than patients with CCT
>588 μm.
● African American origin, males and heart disease.
- sterioid use

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15
Q

Mx for ocular HTN

A

● Regular monitoring.
● Medical treatment is indicated in cases with persistent IOP >30 mmHg or
with high-risk profile patients.

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16
Q

what is primary open-angle glaucoma

genetic causes

RFs

A

chronic disorder characterized by glaucomatous visual field defects due to optic nerve damage.

MYOC and OPTN gene mutations have the potential to cause POAG.

  • age >40
  • myopia
  • Diabetes Mellitus
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17
Q

features
Sx
Signs
of primary open -angle glaucoma

A
  • falling visual acuity
  • difficulty moving from bright to dark rooms

● Open anterior chamber angle
● High C/D ratio and thinning of the neuroretinal rim
● Raised IOP (>21 mmHg)
● Glaucomatous VF defects

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18
Q

Ix for primary open-angle glaucoma

A

● Fundoscopy: Evaluate the optic disc.
● Gonioscopy: Assessment of angle.
● Pachymetry: Measure CCT.
● Perimetry: Visual field testing.

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19
Q

Mx for primary angle glaucoma

A

● Topical IOP-lowering agents, such as prostaglandin analogues or beta-blockers.
● Laser trabeculoplasty.
- minimally invasive glaucoma surgery
● Trabeculectomy if failure of other treatments.

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20
Q

what is normal tension glaucoma,Ix and Mx

A

progressive optic neuropathy despite a normal or low IOP

same as primary open-angle glaucoma

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21
Q

RFs of primary normal tension glaucoma

A

● Age: Commonly older than patients with POAG.
● Race: East Asian (e.g. Japanese).
● CCT: Commonly lower than patients with POAG.
● Systemic vascular disease: Conditions such as Raynaud phenomenon,
migraines and systemic hypotension (use beta-blockers carefully due to their effect on blood pressure) are more associated with NTG rather than POAG.

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22
Q

differences between NTG and POAG

A

● Optic nerve head can be larger in patients with NTG.

● Flame-shaped haemorrhages on optic nerve rim are more common in NTG. — Drance haemorrhages

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23
Q

what is primary angle-closure glaucoma

A

iris blocks the TM - 👈obstruction of aqueous flow with the potential of causing a rise in IOP and optic nerve damage.

peripheral anterior synaechiae + elevated IOP + glaucomatous changes adn VF defects

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24
Q

what is Primary angle closure suspect

A

A narrow angle in which the peripheral iris is almost touching the TM. No peripheral anterior synechiae (PAS) present (PAS refers to the adherence of the peripheral iris anteriorly in the anterior chamber).

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25
What is PAS
peripheral anterior synaechiae + IOP NO glaucomatous optic nerve changes
26
RFs of primary angle-closure glaucoma
``` ● Increasing age ● East Asian race ● Hypermetropia ● Family history ● Short axial length of the eye ```
27
pathophysiology of primary angle closure glaucoma
● Relative pupillary block Failure of the normal aqueous flow through the pupil causes an increase in pressure difference between the posterior and anterior chambers = anterior bowing of the peripheral iris (BOMBE) = subsequent TM obstruction Risk is highest in a mid-dilated pupil due to maximum contact between iris and lens at this level. ● Plateau iris configuration (non-pupillary block): Important pathophysio- logical mechanism in the East Asian descents. Characterized by a flat iris, normal anterior chamber depth and anteriorly positioned ciliary processes which displaces the iris base leading to a narrow/closed angle.
28
Mx of primary angle-closure glaucoma
``` ● Acute: Supine position - systemic acetazolamide - topical beta-blockers ± alpha-2 agonists ± topical prednisolone. ``` ● Bilateral peripheral Nd: YAG laser iridotomies to be performed after resolution of acute attack. ● Cataract extraction has shown to be effective in lowering IOP in both acute and chronic stages of the disease.
29
what is neovascular glaucoma
known as 100 day glaucoma cause of either secondary open- or closed- angle glaucoma. NVG occurs due to proliferation of fibrovascular tissue in the anterior angle and results from rubeosis iridis
30
causes if neovascular glaucoma
● Ischaemic central retinal vein occlusion (CRVO) (NVG usually occurs about 3 months after onset of CRVO ‘100-day glaucoma’). ● Central retinal artery occlusion (CRAO). ● Diabetes mellitus. ● Ocular ischaemic syndrome. ● Retinal detachment.
31
pathophysiology of neovascular glaucoma
● Retinal ischaemia. ● Hypoxia to the retina cells. ● Release of angiogenic factors (VEGF and IL-6). ● The result is neovascularization of the anterior segment (iris and iridocorneal angle) with subsequent overlying fibrovascular membrane formation.
32
features of neovascular glaucoma
● New radially orientated vessels on iris surface and pupillary margins - rubeosis iridis - conjunctival injection ● PAS and posterior synechiae can form. ● Corneal oedema. ● Elevated IOP with open angle at the beginning but progression will lead to fibrovascular tissue proliferation leading to PAS formation and angle closure.
33
Ix for neovascular glaucoma
● Establish the cause of retinal ischaemia.
34
Mx for neovascular glaucoma
● PRP ± intravitreal anti-VEGF injections to reduce neovascularisation. ● Medical treatment - Similar to POAG. - Avoid miotic agents, as they can worsen synechial angle closure. - Use prostaglandin analogues carefully because they may exacerbate ocular inflammation. - Osmotic agents can be used for corneal oedema. ● Surgery (if medical treatment fails) If good visual prognosis = glaucoma drainage device (tube). - If bad visual potential = cyclodiode laser (destruction of the ciliary body epithelium leading to reduction of aqueous humour secretion). - Trabeculectomy can often result in bleb failure due to scarring.
35
what is pigmented dispersion syndrome
bilatera ocular characterized by excessive ‘shedding’ of pigmented material of the iris deposited throughout the anterior segment - thru aqueous flow dynamics It is more common in myopic males.
36
features of pigment dispersion syndrome
- Blurred vision and haloes on exertion - deeper AC due to iris bowing -> rubs w lens zonules ● Mid-peripheral spoke-like defects of the iris on transillumination ● Increased IOP and glaucomatous damage. ● Vertical oval-shaped pigments on the corneal endothelium (Krukenberg spindles). ● TM pigmentation. ● Sampaolesi line may be present (a band of pigmented anterior to the Schwalbe line on gonioscopy). ● Concave peripheral iris.
37
Mx of pigment dispersion syndrome
● Avoid extraneous exercise. ● Medical treatment is similar to POAG. Prostaglandin analogues are generally the preferred medical treatment for patients, although other topical medications may be used. ● Pilocarpine has shown to be a prophylactic measure to prevent exercise- induced elevation of IOP. However, the use of miotics (pilocarpine) can induce myopia and have risk of retinal detachment. ● Laser trabeculoplasty. ● Trabeculectomy.
38
what is psuedoexfoliation syndrome asssociated w
cause of secondary open-angle glaucoma in which grey-white fibrillar deposits block the anterior chamber angle. Associated with mutation in the LOXL1 (enzyme that contributes to elastin formation).
39
Ix for pseudoexfoliation syndrome
● Fundoscopy: Evaluate the optic disc. ● Gonioscopy: Assessment of angle. ● Pachymetry: Measure CCT. ● Perimetry: Visual field testing.
40
Mx for pseudoexfoliation syndrome
● Topical IOP-lowering agents, such as prostaglandin analogues or beta-blockers. ● Laser trabeculoplasty. ● Trabeculectomy if failure of other treatments.
41
pseudoexfoliation syndrome seen in who
Scandinavians, females and age >50.
42
associations of pseudoexfoliation syndrome
● Hearing loss ● Alzheimer disease ● High plasma homocysteine levels ● Low folate intake
43
features of pseudoexfoliation syndrome
● Increased IOP and glaucomatous damage. ● Flaky white deposits on the anterior lens capsule - pupil, iris ● Sampaolesi line - TM pigment ● Peripupillary defect on transillumination slit lamp - loss of iris shape
44
what is psoner-schlossman syndrome
A rare disorder characterized by recurrent unilateral acute attacks of IOP elevation and may cause secondary open-angle glaucoma (uncommon, only if repeated attacks).
45
psoner-schlossman syndrome is associated with
CMV or Helicobacter pylori infection and HLA-BW5.
46
features of psoner-schlossman syndrome
● Discomfort, haloes and blurred vision. ● Anterior chamber inflammation. ● Mydriasis.
47
Mx of psoner-schlossman syndrome
● Topical steroids and IOP-lowering agents.
48
what is phacolytic glaucoma
A secondary open-angle glaucoma caused by trabecular obstruction due to leakage of lens protein from a hypermature cataract.
49
features of phacolytic glaucoma
● Painful red eye with photophobia and decreased vision. ● Corneal oedema, mature cataract and white particles may be seen in the anterior chamber due to an inflammatory response against the lens protein present in the anterior chamber.
50
Mx for phacolytic glaucoma
● Topical or systemic IOP-lowering agents. | ● Definitive treatment: cataract extraction.
51
what is phacomorphic glaucoma
An acute secondary angle-closure glaucoma due to a swelling of a cataractous lens potentiating a pupillary block. Presentation is similar to acute PACG.
52
Mx for phacomorphic glaucoma
● IOP reduction: Same as acute PACG (avoid miotics: can potentiate pupillary block). ● Definitive treatment: Cataract extraction.
53
what is red cell glaucoma
A hyphema (collection of blood inside the anterior chamber) can form, usually following blunt trauma to the eye, which leads to blockage of the TM leading to raised IOP and secondary open angle glaucoma. A secondary bleed may occur 3–7 days post initial injury. early onset - obstruction uet ot blood/pupil block late onset - tears, synaechiae SIGNS - SC haemorrhage - ectopia lentis - iridodialysis - angle recession - cuclodialysis cleft - vitreous haemorrhage - retinal detachment MX - stabilise: protective eye shield, head elevation, BP control medical -cycloplegics, steroids Surgical - laser, trab, TM reco
54
what is ghost cell glaucoma
A type of secondary open-angle glaucoma occurring 2–4 weeks after a vitreous haemorrhage due to TM obstruction with red blood cells.
55
what is angle recession glaucoma
A cause of chronic secondary open-angle glaucoma due to ciliary body rupture caused by blunt trauma. Gonioscopy shows irregular widening of the ciliary body face. The risk of glaucoma occurring is about 10% after 10 years following the traumatic incident.
56
what is sturge-weber syndrome
A congenital neuro-oculocutaneous disorder that can cause secondary open- angle glaucoma.
57
pathophysiology of glaucoma
Anterior chamber angle malformation (causes early-onset glaucoma during the first year of life) or increased episcleral venous pressure (causes later-onset glaucoma).
58
features of sturge weber syndrome
● Cutaneous: Port wine stain, typically along CNV1 and CNV2. ● Neurological: Seizures and learning disability. ● Ocular: Choroidal haemangiomas and glaucoma ipsilateral to the cutaneous lesion.
59
Mx for sturge-weber syndrome
● Early-onset glaucoma: Goniotomy or trabeculotomy or combined trabeculotomy-trabeculectomy. ● Late-onset glaucoma: Medical therapy first, then trabeculectomy if medical therapy fails.
60
what is primary congenital glaucoma
rare bilateral (two-thirds of patients) condition due to malformation of the anterior chamber angle that occurs in the first year of life.
61
epidemiology of primary congenital glaucoma
● More common in boys. ● Mostly sporadic, however, can be AR. ● Prevalence higher in patients with CYP1B1 gene.
62
features of primary congenital glaucoma
● Photophobia, epiphora and blepharospasm. ● Corneal oedema. ● Large corneal diameter (>12 mm). ● Buphthalmos: Large eyes due to elevated IOP. ● Haab striae: Healed breaks in Descemet’s membrane due to corneal oedema. Best seen on retroillumination.
63
Ix for primary congential glaucoma
● IOP measurement (normal IOP in newborns is 10–12 mmHg). ● Optic disc evaluation for cupping: Look for asymmetry or a ratio of >0.3. ● Corneal diameter measurement (normal range is 9.5–10.5 mm in newborns).
64
Mx for primary congential glaucoma
● Angle surgery: Goniotomy if the cornea is clear. If the cornea is cloudy, then trabeculotomy can be tried.
65
what is glaucoma known in western world
no.1 cause of irreversible blindness in western society 2nd most common cause of visual repairment in the over 65s
66
``` what is 1st 2nd 3rd cause of registration of visual impairment in the over 65s ```
1st AMD & macular degeneration 2nd glaucoma 3rd DR
67
what is the optic cup
anatomical depression in ONH that is not occupied by axons
68
what is the lamina cribrosa
a mesh like structure at the optic nerve head that surrounds and supports the retinal ganglion cell axons as they form the optic nerve
69
resistance to outflow of aqueous humour primarily occurs where
1. ednothelium - uses transcytosis to transpost material across cells 2. juxtacanalicular - which uses collagen beams and GAG proteins to slow water
70
classical signs of normal tension glaucoma
optic disc cupping - visual field defects - pericapillary atrophy - focal notching/thinning - drance haemorrahges
71
classical signs of primary closed angle galucoma
``` headache acute painful red eye acute vision loss haloes around light N&V ```
72
what is uveitic glaucoma
causes local inflammation and leaky blood vessels (loss of blood-aqueous barrier)
73
causes of uveitis glaucoma
``` JIA seronegative arthropathies infection - TB, syphillis, herpetic sarcoidosis lens-induced - aphakic ocualr disorders - fuchs ```
74
classical signs of uveitic glaucoma
- synechiae - bulky ciliary body - acute or chronic uveitis (nodules, perilimbal injections, pupil block) - systemic signs
75
what is malignant glaucoma
characterised by a shallow AC PLUS raised IOP - despite Mx usually follows penetrating surgery to the eye
76
signs of malignant glaucoma
shallow AC NO iris bombe high IOP normal posterior segment
77
Mx of malignant glaucoma
topical cycloplegia topical ocular anti hypertensives oral hyperosmotic agents laser/surgery to disrupt the anterior hyaloid face (including vitrectomy)

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