Glaucoma Flashcards

Question

What is POAG characterized by?

Answer 1

*Retinal nerve fibre layer thinning. *Glaucomatous optic nerve damage. *Characteristic visual field loss as damage progresses. *An open anterior chamber angle. *Absence of signs of secondary glaucoma or a non-glaucomatous cause for the optic neuropathy. *IOP is a key modifiable risk factor.

Answer 2

European/African

Answer 3

1) High IOP. Asymmetry >4 significant 2) Older age 3) Difficult to control in black than white people 4) FH POAG- sibling 4x, offspring 2x risk 5) Myopia 6) Anti VEGF injections risk of IOP elevation. More with bevacizumab than ranibizumab 7) Contraceptive pill- blocks protective oestrogen effect 8) Vascular disease 9) Translaminar pressure gradient- difference in level of IOP and orbital CSF pressure increase likelihood and progression of glaucoma damage due to associated deformation of lamina cribrosa 10) Optic disc area- large discs more vulnerable to damage 11) Ocular perfusion pressure. Large difference between arterial BP and IOP increase risk and progression of glaucoma

Answer 4

MYOC gene coding for myocillin protein in trabecular meshwork and OPTN gene coding for optineurin

Answer 5

Retinal ganglion cell death through apoptosis rather than necrosis. Preterminal event is calcium ion influx into cell body and rise in intracellular nitric oxide. After injury, astrocyte and glial cell proliferation and alteration in ECM of lamina cribrosa and optic nerve remodelling.

Answer 6

1) Direct mechanical damage to retinal nerve fibres at ONH as they pass through lamina cribrosa 2) Ischaemic damage due to compression of blood vessels at ONH. 3) Both mechanisms lead to reduced axoplasmic flow

Answer 7

Refractive status- myopia increased risk of POAG, hypermetropia PACG Causes of secondary glaucoma eg ocular trauma or inflammation. Previous eye surgery eg refractive surgery which can affect IOP readings

Answer 8

Focal ischaemic discs: Localised superior and or inferior notching and associated with localised field defects with early threat to fixation Myopic disc with glaucoma- tilted shallow disc with temporal crescent of PPA + glaucoma damage. Sense superior/inferior scotomas are common. Sclerotic discs- shallow saucerized cups and gently sloping NRR, variable PPA + peripheral VF loss. Concentrically enlarging discs- fairly uniform NRR thinning and diffuse field loss. IOP significantly elevated at presentation

Answer 9

Disc haemorrhages- extend from NRR onto retina inferotemporally. Common in NTG Baring of blood vessels- space between NRR and superficial blood vessels Bayoneting- double angulation of blood vessel. With NRR, a vessel entering disc from retina may angle sharply backwards into disc then turn towards original direction to run across lamina cribrosa Collaterals between 2 veins at the disc loss of Nasal NRR Lamina dot sign- advancing glaucoma. Grey dot like fenestrations in lamina cribrosa become exposed as NRR recedes. Can be seen in normal eyes too.

Answer 10

○Alpha (outer) zone is characterized by superficial retinal pigment epithelial changes. It tends to be larger and possibly more common in glaucomatous eyes.

Answer 11

characterized by chorioretinal atrophy. It is distinct from the scleral rim, the white band of exposed sclera central to the beta zone. The beta zone is larger and more common in glaucoma and is a risk factor for progression. The location of beta-zone PPA seems to indicate the orientation of likely visual field loss.

Answer 12

Papillomacular bundle

Answer 13

SWAP Frequency doubling technology (FDT)

Answer 14

Small paracentral depressions Nasal step Temporal wedge Arcuate defects Ring scotoma End stage changes- small island of central vision with temporal island. 10-2 monitors residual central field

Answer 15

Glaucoma hemifield test outside normal limits or >2 occasions consecutively. Assesses points in sup and inf field Cluster of 3 or more non edge points in a location typical for glaucoma all of which are depressed on PSD<5% level and one depressed at PSD<1% level on 2 consecutive occasions CPSD in less than 5% normal individuals on 2 consecutive fields

Answer 16

Early MD<-6dB Mod -6 to -12 dB Severe >-12 dB

Answer 17

<18 based on Advanced Glaucoma Intervention Study (AGIS) found that significant visual field progression is unlikely to occur in most patients in the medium term if IOP can be kept below 18 mmHg at all times.

Answer 18

a 10% reduction in the risk of progression (when measured from presentation to the first follow-up visit).

Answer 19

Perimetry every 6-12 months sufficient

Answer 20

Annually, as anterior chamber angle narrows with age.

Answer 21

Occult adherence failure Undetected diurnal variation Impaired optic nerve perfusion Alternative pathology eg: compressive lesions

Answer 22

IOP consistently equal to or less than 21mmHg on diurnal testing Signs of ON damage in characteristic glaucoma pattern VF loss as damage progresses consistent with ON appearance Open anterior chamber angle

Answer 23

Aetiological factors distinct from POAG not conclusive but mechanisms including anomalies of local and systemic vascular function, structural ON anomalies and autoimmune disease. NTG in some patients explained by low CCT.

Answer 24

1) Age- older than those with POAG 2) Gender- females highter 3) Race- Japanese 4) Family Hx- POAG greater in families of patients with NTG than normal. 5) Mutations in OPTN gene identified in NTG. 6) CCT lower in NTG than POAG 7) Abnormal vasoregulation eg migraine, Raynauds 8) Systemic hypotension EMGT trial confirms low BP risk factor for NTG 9) OSA associated with poor ocular perfusion 10) Autoantibody levels higher in NTG patients 11) Translaminar pressure gradient higher than POAG 12) Ocular perfusion pressure lower than POAG 13) Myopia increases risk of glaucoma and progression

Answer 25

Angle closure- dark room gonio Low CCT underestimation of IOP POAG with diurnal fluctuation Previous episodes raised IOP Masking by systemic treatment like oral beta blocker Spontaneously resolved pigmentary glaucoma Progressive RNFL defects not due to glaucoma eg myopic degeneration and optic disc drusen Congenital disc anomalies- optic disc pit/ coloboma Neurological lesions Previous AION/GCA Previous acute ON insult hypovolemic shock Inflammatory/infiltrative and drug induced

Answer 26

Loss of VA out of proportion to cupping Loss of colour vision on Ishihara VF loss not consistent with RNFL drop out NRR pallor Rapid progression despite normal IOP

Answer 27

50% at 5-7 years

Answer 28

Prostaglandins first line. Brimonidine- neuroprotective effect Betaxolol choice to prevent BP drop SLT reasonable Surgery if progression despite IOP in low teens. Control of systemic vascular disease- diabetes/hyperlipidaemia Systemic CCB Antihypotensive measures- increase salt intake Sleep in head up position Ginkgo biloba useful in some cases

Answer 29

Higher in flat position than 30 degrees head up position

Answer 30

occlusion of the trabecular meshwork by the peripheral iris (iridotrabecular contact – ITC), obstructing aqueous outflow.

Answer 31

superiorly

Answer 32

Grade 4 (35-45 deg)- widest angle characteristic of myopia and pseudophakia. Ciliary body seen without tilting the lens Grade 3 (25-35 deg)- open angle, scleral spur visible Grade 2 (20 deg)- trabeculum but not the scleral spur seen Grade 1 (10 deg)- very narrow angle only Schwalbe line and top of trabeculum seen Grade 0 (0 deg)- Iridocorneal contact

Answer 33

Detailed but underused. Formal description of position of iris insertion, angular approach and peripheral iris curvature

Answer 34

Refers to angle structures visible allocating Roman numeral acordingly. IV suggests narrow angleW

Answer 35

Uses slit lamp alone: Thin but bright light approximately perpendicular to corneal surface Beam estimates ratio of corneal thickness to most peripheral part of AC Overestimates angle in patients with plateau iris configuration

Answer 36

Gonioscopy shows three or more quadrants of ITC associated with raised IOP/and or PAS, best evaluated using indentation gonioscopy Normal optic disc and field Further classified into non ischeamic and ischaemic. Ischaemic shows higher IOP elevation such as iris changes/glaukomflecken

Answer 37

ITC in 3 or more quadrants associated with glaucomatous optic neuropathy ON damage from episode of severe IOP elevation eg PAC

Answer 38

Relative pupillary block Non pupillary block Lens induced angle closure Retrolenticular Combined mechanism Reduced aqueous outflow

Answer 39

Failure of aqueous flow through pupil leads to pressure differential between anterior and posterior chambers with anterior iris bowing. Relieved by peripheral iridotomy

Answer 40

Important in many asian patients Associated with deeper AC than those with pure pupillary block Eg: plateau iris younger than those with pure pupillary block

Answer 41

characterized by a flat or only slightly convex central iris plane, often in association with normal or only slightly shallow central anterior chamber depth. The angle recess is typically very narrow, with a sharp backward iris angulation over anteriorly positioned and/or orientated ciliary processes. A characteristic ‘double hump’ sign is seen on indentation gonioscopy, the central hump being due to the underlying central lens supporting the iris and the peripheral hump resulting from the underlying ciliary processes.

Answer 42

persistence of gonioscopic angle closure despite a patent iridotomy in a patient with morphological plateau iris.

Answer 43

Appositional obstruction by iris Degeneration of TM due to chronic or intermittent contact with iris or damage sustained due to elevated IOP Permanent occlusion of TM by PAS.

Answer 44

Age- 62 years, non pupillary block presents earlier Females affected more than males Race- Far eastern and Indian asians FH: increased prevalence Refraction- pure pupillary block usually hypermetropic. Axial length- short eyes have shallower AC. Nanophthalmic eyes are at risk (AL<20mm)

Answer 45

Precipitating factors- watching TV in dark room, pharmacological mydriasis, rarely miosis. Intermittent blurring haloes, acute decreased vision, periocular pain/headaches. May be asymptomatic in chronic/intermittently elevated IOP

Answer 46

VA 6/60 to HM IOP 50-80 Conj hyperaemia with violaceous circumcorneal injection Corneal epithelial oedema AC shallow, aqueous flare present Non dilated vertically oval pupil classic Fellow eye shows occludable angle.

Answer 47

Early- low IOP - ciliary body shutdown, folds in DM if IOP rapidly reduced. Optic nerve head congestion ,choroidal folds. Late- iris atrophy with spiral configuration, glaucomflecken (white foci of necrosis on sueprficial lens) other forms of cataract and irregular pupil due to iris sphincter/dilator damage and posterior synechiae. Greater duration of attack and PAS formation, lower likelihood of IOP control with medication alone

Answer 48

Intermittent episodes spontaenously resolving mild/moderate APAC in patients with pupillary block.

Answer 49

AS- OCT- AC depth measurement Biometry if lens extraction needed Posterior segment ultrasonography in atypical cases to exclude other cases of secondary angle closure Provocative testing eg when plateau iris suspected.

Answer 50

patient sits on dark room, face down for 1 hour without sleeping (sleep induces miosis). IOP checked before and immediately after the test. Rise in IOP >8mm considered significant. Gonioscopy without indentation used to confirm closure of angle. If test positive in patient with prior PI, likely plateau iris confirmed with OCT scan.

Answer 51

Lens induced angle closure Malignant glaucoma (aqueous misdirection) Neovascular glaucoma Hypertensive uveitis (herpetic/CMV/Posner Schlossman) Scleritis with or without angle closure PDS/PXF Orbital/retroorbital lesions eg inflammation/retrobulbar haemorrhage

Answer 52

Lie down in supine position Diamox 500mg IV if IOP>50. Orally if IOP <50 Contraindications are sulphonamide allergy/PAC due to topiramate Single dose Apraclonidine 0.5%/1%, Timolol Pred/Dexamethasone Pilocarpine 1 drop repeated after 30 mins Analgesia and antiemetic

Answer 53

CC indentationwith squint hook or indentation goniolens to force aqueous into angle. Epithelial oedema cleared with 50% glycerol Mannitol 20% 1-2g/kg IV over 1 hour, PO glycerol 50% 1g/kg, PO isosorbide 1-1.5g/kg Early laser iridotomy after clearing corneal oedema with glycerol Paracentesis effective but small risk of lens damage

Answer 54

Pilocarpine 2% QDS to affected eye and 1% QDS to fellow eye Topical steroids QDS if eye acute inflamed Consider Timolol, Iopidine, TDS, Diamox 250mg PO QDS. Bilateral PI once cornea clear and Acute attack cleared, IOP normal. Continue steroids for at least 1 week. Repeat gonio to confirm angle open Trab may be needed if IOP persistently raised

Answer 55

Laser PI has a modest prophylactic effect only offered to those with highest risk of developing PAC. If significant ITC persists after iridotomy, observe, laser iridoplasty and long term pilocarpine prophylaxis. Consider lens extraction if symptomatic cataract.

Answer 56

clear lens extraction with IOL implantation shows greater efficacy and is more cost-effective than laser peripheral iridotomy in patients with primary angle closure and IOP >29 mmHg or in patients with primary angle-closure glaucoma.