Glaucoma Flashcards

Question

Classification of Secondary Open Angle Glaucoma?

Answer 1

* Anatomically like POAG w/ free access to trab meshwork but something causes malfunction of trab meshworks ability to drain aqueous at normal rate o Pseudoexfoliation syndrome/glaucoma o Pigment dispersion syndrome/ pigmentary glaucoma o Steroid induced glaucoma (topical, creams, systemic) o Phacolytic glaucoma – related to leakage of lens protein in mature cataract o Ghost cell glaucoma/Hyphaema – bleeding in eye either in vitreous or AC leading to blockage of trab meshwork by RBCs o Uveitis – can cause secondary open angle or closed angle glaucoma – sometimes steroids for it cause the glaucoma o Trauma – can result in damage to trab meshwork or inflammation of trab meshwork – can be chronic leading to damage to optic nerve & field over time o Raised episcleral venous pressure  causes back pressure of venous system in orbit, translates through into Schelmm’s canal & to trab meshwork making it more difficult for aqueous to get out  ↑IOP  E.g. Sturge-Weber Syndrome (inherited)  Dysthyroid Eye Disease (DED) – swelling in orbit & thickened muscles which leads to raised IOP & pressure on venous system * More than just these examples

Answer 2

* Anatomically similar but not identical to PACGs – access to trab meshwork is retricted by some anatomical change secondary to usually another ocular disease or abnormality o Phacomorphic – swelling of lens over time, in pxs with already smaller angles e.g. hyperopic – can result in gradual closing and raise in IOP o Post-vitreoretinal or post-corneal graft surgery (mainly penetrating keratoplasty) o Ectopia lentis – displacement of lens in eye (due to Marfans, Ehlers Danlos, trauma) o Post segment tumours – can push iris-lens diaphragm forward o Aniridia – absence of iris or bunch up of iris can block angle o Aqueous misdirection syndrome – can happen following intraocular surgery o Uveitis – w/ chronic inflammation in eye, iris can gradually become adhered to trab meshwork & cause peripheral anterior synechiae & scar tissue formation, resulting in gradual closing up of angle o Rubeosis iridis – often secondary to ischaemia e.g. diabetic retinopathy, vein occlusions --> NV in iris & angle, gradually causes closing of angle & ↑IOP

Answer 3

* Tend to arise from birth/infancy or in children & young adults o Congenital glaucoma – autosomal recessive inheritance o May see haab’s striae – linear cracks in Descemet’s membrane o Anterior segment dysgenesis syndrome like Iridocorneal Endothelial syndrome (ICE) or Axenfeld-Reiger syndrome o May see corectopia pupil o Juvenile Onset glaucomas

Answer 4

* Signs: o Raised (POAG) or normal (NTG) IOP o Open angle or deep anterior chamber o Abnormal optic disc cupping o Abnormal VF (can often be normal in early stages when disc shows changes) * Symptoms: o None until advanced or paracentral VF defect (may then become aware)

Answer 5

* Presentation v similar to POAG but anatomical clinical findings are v different yet sometimes subtle & can develop over time in pxs previously diagnosed w/ POAG or NTG * Signs: o Raised or normal IOP o Open but narrow angle or moderate/deep AC (can sometimes be shallow) o Abnormal optic disc cupping o Abnormal VF o Shallow AC o 3 plus Quadrants of ITC on gonioscopy o Hypermetropia – usually goes hand in hand with small eye & more crowded anterior segment * Symptoms: o None as per POAG

Answer 6

* Signs: o Raised or normal IOP o Narrow angle o +/- abnormal optic disc cupping o +/- abnormal VF o Shallow AC – narrow angle on Van Herick’s or gonioscopy o 3 plus quadrants ITC on gonioscopy o Hypermetropia * Symptoms: o Intermittent brow ache o Haloes o Often resolve after short period of time

Answer 7

* Signs: o Red eye o Fixed mid-dilated pupil o Hazy blue/green cornea – due to corneal oedema o Iritis – associated with high IOP o IOP>40mmHg o Shallow AC – hard to see with hazy cornea * Symptoms: o Blurred vision/haloes o Brow ache/headache o Nausea * Medial ophthalmic emergency as visual loss is rapid & condition must be referred EMERGENCY * Px generally unwell * Images show typical appearance of eye at risk or fellow eye & eye is affected * Gonioscopy shows closed/narrow angle in other eye or eye at risk & an anterior segment OCT

Answer 8

Loss of retinal GCs & their axons leading from optic nerve to brain o Both glial & nerve cells are affected * Ischaemic changes at ONH as well as raised IOP & development of inflammatory changes at ONH in form of release of free radicals (nitrous oxide & glutamate) which cause further neuronal loss o Some of these changes may also be toxic changes where dying cells (due to ↑ IOP/ischaemia) release toxic substances which affect adjacent cells & cause them to become sick & eventually die * Apoptosis – programmed cell death

Answer 9

* Always involves ↑ IOP but many of other mechanisms e.g. ischaemia, neurodegeneration & apoptosis are probably also in play after initial high pressure insult * Limited access to trab meshwork is initially main cause followed over time by trab dysfunction even after successful tx of underlying anatomical issues of angle closure * Restricted access to trab meshwork: o Hypermetropia (e.g. +2.00) o Shallow anterior chamber o Small eyes (short axial length) o Anteriorly inserted iris o ↑ in lens size o Dilatation of pupil – can precipitate bunching up of iris in angle & lead to angle closure (happens physiologically when pupil dilates or pharmacologically when px is dilated) o Trab dysfunction --> may be able to open up drainage angle in eye by doing iridotomy but sometimes IOP will still be elevated & continue to climb o Narrow gonioscopic angle

Answer 10

Iris slowly comes into contact w/ ↑ area of trab meshwork, resulting in trab meshwork dysfunction & gradual rise in IOP

Answer 11

o Angle is narrow but open, but certain physiological states (producing dilation – e.g. dim light) lead to transient rises in IOP which resolve over variable periods of time (~20-30mins)  Often produces transient symptoms of acute angle closure – experience headache/brow ache around eye or haloes then resolve o Eventually this type of eye will develop either CACG or more acutely AACG o Pupil block which occurs spontaneously resolves

Answer 12

o Dilation of pupil (physiological or otherwise) leads to angle becoming closed o Marked rise in IOP due to:  Pupil block  Peripheral iris tissue occluding angle  (Often both present simultaneously) o Similar to intermittent ACG but attack is permanent & can be devastating to site & subsequent successful management of px o This type of attack can & freq occurs w/ no previous hx of IAC attacks o Underlying mechanism in IACG and AACG attacks is something known as Pupil block  Pupil is in a physiological mid dilated state & comes into contact with lens  Temporarily in these px prevents aqueous from making its way from posterior chamber into the AC and to trab meshwork.  Trapped aqueous pushes peripheral iris forward & further shallows peripheral AC and blocks access to the trab meshwork. o Treatment of this condition requires relief of the pupil block and iridotomy is the definitive treatment

Answer 13

* Caused by iridolenticular contact * Usually relative but may be absolute as in the case of posterior synechiae * Usually asymptomatic but if appositional closure occurs w/o an acute rise of IOP then PAS may form leading to chronic angle closure * If pupillary block becomes absolute, IOP in posterior chamber rises pushing the peripheral iris forward to cover trab meshwork w/ an ensuing greater rise in IOP & acute ACG * In nearly all cases of ACG, some element of pupil block is present

Answer 14

* Anatomical iris configuration o Anteriorly displaced ciliary body position o Anteriorly inserted or thicker iris * The central AC is usually not shallow, & the iris plane is flat or slightly convex * Angle appears narrow and crowded on gonioscopy * Gonioscopy shows a “double hump” sign * Hard to diagnose/detect as central AC is often normal depth

Answer 15

-ACG associated w/ plateau iris is usually cured by YAG laser Peripheral Iridoplasty (PI) -Plateau iris syndrome is where post-PI, angle closure recurs w/ elevated IOP attacks Requires different tx e.g. ALPI (argon laser peripheral irdoplasty), pilocarpine long term or lens extraction

Answer 16

* Take several systematic & clinical findings into account to arrive at correct diagnosis o Glaucoma refers to collective term for several different conditions w/ similar & related features * Take: o H&S  Ocular & systemic o Family Hx o Refraction  Myopic: more likely to get POAG  Hyperopic: more likely to get ACG o IOP & CCT o Ant chamber & gonio (or Van Hericks) o Discs, VFs, OCT

Answer 17

* ISNT rule – normal disc rim is thickest inferiorly then superiorly and then nasally then temporally  IF NOT FOLLOWED, DOES NOT MEAN PX HAS GLAUCOMA * Notice rim colour – pallor should correspond or be slightly less than cup * Tilted discs are difficult to interpret – common in myopes & astigmats o Look carefully for glaucomatous features and correlate VF  (SuperTemporal VF defects – tilted disc VF does not normally encroach on central (this would usually be due to cupping)) * Note size of optic disc: o Disc size can be measured with normal disc being 1.5 to 2mm in vertical diameter or assessed in relation to the calibre of BVs which are fairly constant in size o Small discs in hyperopes apparently normal CD ratio may be misleading o Large discs have large cups - look at NRR CANNOT RELY ON C:D ALONE

Answer 18

- Is there any definite evidence of glaucomatous nerve damage? E.g apon or notch - Is there any difference in appearance of 2 optic nerves – asymmetry often sign in glaucoma (>0.2C:D between eyes) - Is there a reason other than glaucoma for any apparent difference in appearance of the 2 optic nerves? E.g. px may be myopic in one eye & not other - Does appearance of optic nerve indicate any acquired change? Progressive? – PPA v common feature, but if see notch or haemorrhage this is a sign of change

Answer 19

1. CD ratio: vertical height of cup to vertical height of disc – 0.5 C:D is potentially suspect but have to think where position of cup is & if it is a large nerve or not 2. BV Position: BVs can give clue to where edge of cup is in glaucoma – if see BV bayoneting over edge of contour then suggests that’s where edge of cup is o BVs tend to come out of nasal side of cup – as lose nerve fibre layer & rim, BVs tend to fall away with loss of tissue – see change in position of BVs over time o BV contrast important: “baring of BVs” – when BV overlies NRR, NRR usually pink & BV red so not lot of contrast  as NRR disappears &dies away, red BV outline starker against paler background of cup 3. Rim Thickness: shows where deficit is in NRR – if v thin then NOTE this 4. Pallor: of NRR can be sign of glaucoma or other optic neuropathies 5. Peri-papillary atrophy (PPA): where get loss of NRR, get more PPA in that area – WEAK sign as v common 6. APON: acquired pit of optic nerve – areas of highly focal loss of tissue – seen mainly in pxs w/ NTG – often associated w/ paracentral VF defects 7. Optic disc haemorrhages: strong correlation w/ glaucoma (~40% of pxs) – not exclusive though (e.g. PVD, systemic hypertenstion) 8. Nerve fibre layer defects: see on volk & red-free light – hard to see though – use photos/OCT 9. Notch: highly focal loss of tissue – gradual shelving & loss of nerve fibre layer 10. Laminar (cribosa) dots: often seen in base of notch, normal to see in central part of cup – round – if see them more peripherally in optic nerve (appear more oval) – sign suggests loss of NRR

Answer 20

* Shift in position of BVs * Thinning of NRR * Developing notch (strong sign) * Haemorrhage crossing disc rim * Developing focal pallor – often develops in pxs w/ v high IOP * Change in peripapillary atrophy – does occur naturally overtime

Answer 21

* Based on: o 1. Size of disc – measure & state if small, medium, large – use graticule on SL & volk o 2. Thinning of NRR (inverse of CD ratio) in thinnest areas & degrees of involvement

Answer 22

* Volk: 66D-1.0 60D-0.88 78D-1.2 90D-1.33

Answer 23

- DDLS stage 4 or more: refer - Medium size disc: stage 4: NRR of 0.1 to 0.19 in thinnest area --> suspect glaucoma for referral - Small optic disc measuring <1.25mm  stage 4: NRR of 0.2 to 0.29 --> suspect glaucoma - Large disc: <0.1 NRR thickness - Look at all sign of glaucoma

Answer 24

* Say cup:disc starts at C:D ~0.3 --> increasing as px develops glaucoma (e.g. C:D~0.5) --> then becomes e.g. C:D~0.8 w/ v thin rim inferotemporally, temporally & slightly superotemorally * Difficult to say if px has glaucoma in early stages * If saw 1st disc probs wouldn’t say had glaucoma but if px returned 2yrs later w/ 2nd disc then you would see the CHANGE * If saw 3rd disc as presentation: would almost certainly say it is glaucoma

Answer 25

Variant of concentric cupping – principal loss of NRR on temporal side

Answer 26

* Common pattern seen in glaucomatous optic nerve development * Start with small, central cup – enlarges superiorly or inferiorly

Answer 27

* Like vertical extension but w/ v highly focal loss of tissue in that region either inferiorly or temporally * May see lamina cribosa dots extending into periphery & v oval

Answer 28

* Highly focal loss of tissue like notch, develops generally at inferotemporal or superotemporal part of optic disc * May see little BVs disappearing into pits & popping out again on other side * More common in NTG than POAG * A congenital Pit: occur on central or temporal part of optic disc, tend to be larger than APON

Answer 29

* Variant of concentric cupping – preferential loss of NRR on nasal side * Nasalisation of BVs * May see BVs in central trunk fall away to nasal side as no NRR left

Answer 30

* Type of glaucomatous change seen in v elderly pxs (90s) * Don’t see lots of signs of obvious cupping but see gradual saucerisation of optic disc * Will also see development of pallor across whole nerve due to ischaemic changes of age * Development of generalised PPA * Disc may appear like saucer, generalised gradual concentric cupping occurs w/ extreme pallor

Answer 31

Sometimes see in glaucoma but occurs in other conditions/optic neuropathies which may be more important/serious than glaucoma

Answer 32

* Excavated Disc Abnormalities: o Optic nerve coloboma o Congenital optic nerve pit o Morning glory syndrome o Tilted disc syndrome o Peri-papillary staphyloma – can sometimes be mistaken for disc cupping * Pale Optic Discs: o AION – anterior ischaemic optic neuropathy o CRAO o Heredofamilial optic atrophies like dominant optic atrophy o Other optic neuropathies (inflammatory, infectious, toxic, nutritional, compressive e.g. due to pituitary tumour or optic nerve tumour) * When see pallor, need to exclude these through history & other examinative tests Papilloedema Pituitary tumour (NRR v pale & almost yellow in colour, C:D normal)

Answer 33

* Disease of change (slow) – with normal IOPs – start follow-up and watch for signs of change (particularly in pxs w/ normal IOPs) * Perform disc photography and store on computer or case records * Never in isolation - consider risk factors (age, fam Hx, IOP, myopia, central corneal thickness, VFs)

Answer 34

90-100° temporally & 60° nasally Superiorly ~60° & inferiorly ~75°

Answer 35

* Most defects occur within central 30 degrees but peripheral VF often involved * VF loss may be focal or generalised or both * Retinal GC axons follow an arcuate path to ONH. Field defects are direct result of axonal damage at level of ONH  Axonal damage will always respect horizontal midline * VF loss pattern is characteristic & tends to correlate w/ typical ONH excavation seen in glaucomatous optic neuropathy

Answer 36

Frequent in early glaucoma & may account for 70% of early VF defects usually in superior VF between 10-20°

Answer 37

Slightly more advanced than paracentral defects & occur in arcuate or Bjerrum’s area usually superior > inferior

Answer 38

o Highly suggestive of glaucomatous aetiology o Defined as within 10° of fixation o More common in NTG o Significant AMD can also produce a similar result

Answer 39

Up to 40% of pxs w/ glaucomatous loss have nasal steps (usually superior)

Answer 40

Uncommon – tend to be correlated with significant nasal cupping

Answer 41

Many different causes from neurological to ocular (including PPA) but in glaucoma may manifest as elongation (in superior or inferior direction) of blind spot in an arcuate fashion

Answer 42

o Due to ↓sensitivity of retina secondary to diffuse loss of nerve fibres throughout optic nerve o Accounts for up to 38% of VF defects o Generalised depression especially nasally o ↓mean deviation scores o Can be due to media opacities e.g. cataract

Answer 43

* Check px data (refraction, pupil) * Check reliability indices – make sure px doesn’t have too many fixation losses or false +ves * Look at grayscale (overall impression) * Rule out possible artefacts (ptosis, lens, lens rim artefacts, px factors) * Observe numerical graph – look at dB values * Analyse total deviation probability plot (looking for diffuse loss of sensitivity – could be due to glaucoma or due to lens opacities) * Look at Pattern deviation plot (localised) * Analyse global indices – mean deviation & pattern standard deviation (confirm depth & extent of VF loss) * Check GHT (glaucoma hemifield test) – looks at asymmetry between superior & inferior VF * Compare VF to clinical info to see if it correlates

Answer 44

- VF abnormalities should be repeatable before being considered as real & true defect - Changes at optic disc will commonly present before any VF defect manifests in early glaucoma  correlate any VF defect seen to other info for e.g. if have thinning of NRR in optic disc inferiorly then expect to see a superior VF defect  also look at retina for other abnormalities that may be causing the VF defect - VF defects should be considered as possible glaucomatous if they fit w/ appearances of optic disc neuropathy & have characteristic patterns - Any VF defect that is not typical of glaucoma & does not correlate w/ optic disc abnormalities should prompt a search for other ocular (retinal) or visual pathway pathology --> e.g. look for VF defect respecting vertical midline which may suggest it is of neurological origin & px may need to be referred for neuorophthalmic assessment & possibly scanning of brain

Answer 45

- If have pxs w/ early disease, can achieve quite significant reduction in pxs progressing by a smaller reduction in IOP. - If have pxs w/ v advanced disease, need to achieve much lower target IOPs in order to keep them stable. - If need v low target pressures, surgery may be preferable over medical tx. Even w/ medical tx, if get pressure low enough, pxs can do v well. - With ocular hypertension, reducing IOP is important mainly in pxs in high-risk category for progression. - With all factors; IOP, CCT, age --> can stratify pxs into: * High risk for progression & treat them * Low risk can discharge * Medium risk can monitor

Answer 46

SAME DAY: acute red-eye & high IOP (acute glaucoma) URGENT: IOP >30mmHg ROUTINE: IOP <30mmHg w/ suspicious disc/fields OHT w/ IOP>22mmHg as per NICE guidelines IOP must be by contract tonometry Referral on fields alone must be repeatbale All glaucoma referrals must include: IOP + FIelds + Disc assessment

Answer 47

* Topical hypotensives (monotherapy (1 agent) to maximal therapy (as required)) * YAG iridotomy if narrow angles (ITC) – may also require topical hypotensives afterwards * Selective Laser Trabeculoplasty (SLT) – as long as angle is wide enough that can treat trab meshwork  used if px not controlled on drops or intolerant to drops * Trabeculectomy/Deep Sclerectomy – if not controlled w/ drops & laser & is still progressing then tend to proceed towards surgery – some pxs not suitable for surgery or in short term before have surgery may need stronger IOP lowering agents * Oral Acetazolamide – carbonic anhydrase inhibitor – tend to have side-effects & long-term effects on px’s health  generally not used except in short-term * Angle Surgery (Phaco, istent, trabectome, canaloplasty) – to try & improve drainage through trab meshwork * Cyclodiode Laser Ciliary Ablation * Tube or valve surgery – put in silicone tube/valve into eye, drains into reservoir or base-plate which sits under the conjunctiva & on surface of sclera --> reserved for pxs w/ more complex glaucomas where trabeculectomy is likely to fail or pxs who have had previous surgery already w/ trabeculectomy which has failed & there is significant scar tissue

Answer 48

* 1st Line: Prostaglandin analogue (most effective in terms of % IOP reduction) or Beta-Blocker o Uniocular trials – some pxs – if other eye is not much at risk – start tx in worse eye to see what effect is compared to other eye, if makes difference then tx other eye too * 2nd Line: Prostaglandin analogue or Beta-Blocker  add in which ever didn’t start the 1st time so px on 2 meds * 3rd Line: Carbonic anhydrase inhibitor (less side-effects) or alpha 2 agonist (more side-effects) * 4th Line: Rarely as 3 above or pilocarpine

Answer 49

* Latanoprost (Xalatan, Generic, Monopost) od * Travoprost (Travatan) od * Bimatoprost 0.01/0.03% (Lumigan) od * Tafluprost (Saflutan) od * Increased uveoscleral outflow by ciliary muscle relaxation * 30-35% reduction in IOP o Mild conjunctival hyperaemia --> particularly 1st few weeks then decreases over time o Mild punctate keratopathy o Foreign body sensation o Ocular irritation o Lengthening of eyelashes – most pxs don’t mind this – some pxs end up w/ them rubbing on back of spectacles (trim lashes) o Cystoid macular oedema (pseudo or aphakic pxs) – may need to stop txs if doing cataract surgery or where CMO develops o Very rarely exacerbation of asthma – prostaglandin analogues are tx of choice in pxs w/ asthma as avoiding using a beta-blocker – if get exacerbation, need to stop tx

Answer 50

* Timolol * Levobunolol * Betaxolol * Decreased aqueous production from ciliary epithelium * 25-30% reduction in IOP * Suffer from tachyphylaxis – over period of time may become less effective o Ocular Side Effects (these may be due to the preservatives in the drops):  Corneal hypaesthesia  Punctate keratopathy  Dry eye syndromes  Burning/stinging  Pseudopemphigoid * Systemic Side effects: - Severe bradycardia - Arrhythmia - Heart failure – can exacerbate ability of heart to pump - Dyspnoea - Exacerbation of asthma - Anxiety - Hallucinations - Disorientation * Some pxs MUST NOT be prescribed beta-blockers – specifically if pxs have arrythmia or problems w/ heart rate

Answer 51

* Dorzolamide (trusopt) tds * Brinzolamide (azopt) bd * 18% reduction in IOP – act as adjunct to other drops * Reduce aqueous secretion from ciliary epithelium * Possible improved optic nerve perfusion due to local vasodilatation * Side Effects: o Transient burning/stinging (33%) o Bitter taste (26%) – due to agent going down nasolacrimal duct through puncta & into nasopharynx o Ocular allergy – compared to timolol & prostaglandins which have v low rates of allergy o Superficial punctate keratitis (10%) – gives rise to dry-eye type symptoms o Blurred vision o Dryness o Hair loss – particularly woman on Brinzolamide – if caught early & stopped often reverses – can sometimes be stopped but not reversed * Systemic Side Effects:  Rare and more relevant to systemic CAIs like acetazolamide o Sulphonamide hypersensitivity o Stevens-Johnson syndrome o Toxic epidermal necrosis o Aplastic anaemia  These 4 conditions can potentially be fatal

Answer 52

* Apraclonidine (used as short-term adjunct to control IOP before px receives surgery) and Brimonidine (used more long-term) * Reduction in aqueous production * 25% reduction in IOP (more effective than CAIs but bad SIDE-EFFECTS) * Side Effects: o High rate of allergy (15-25% for brimonidine – can be in initial stages or can be months later) o Conjunctival hyperaemia or blanching o Follicular conjunctivitis (10%) – can give rise to itchy & uncomfortable eyes & red eyes o Systemic blood pressure reduction (never use in children) o Avoid with mono amine oxidase inhibitors or anti-depressants (depression)

Answer 53

* ↑ trabecular outflow via ciliary muscle contraction plus some minor ↓ in aqueous inflow * Pilocarpine 1-4% qds o ~ 20% reduction in IOP from baseline * ↑ trabecular outflow via ciliary muscle contraction plus some minor ↓ in aqueous inflow * Pilocarpine 1-4% qds o ~ 20% reduction in IOP from baseline SIDE EFFECTS OF PILOCARPINE: o Only really used to treat ACG in short term & v rarely used as a long-term tx * Ciliary muscle spasm * Brow ache * Accommodative myopia * Miosis with constriction of VFs – significant in pxs who have already visual loss due to macular disease or advanced glaucoma * Increased risk of retinal detachment * Bradycardia, nausea, sweating, diarrhoea, bronchospasm – if px is elderly & over-dosed on pilocarpine * Acute or chronic angle closure – even though used in ACG, pilocarpine can facilitate pupil block & acute or chronic angle closure

Answer 54

* Cosopt (Timolol and Dorzolamide) * Xalacom (Timolol and Latanoprost) * Combigan (Timolol and Brimonidine) * Duotrav (Timolol and Travoprost) * Ganfort (Timolol and Bimatoprost) * Azarga (Timolol and Brinzolamide) * Simbrinza (Brimonidine and Brinzolamide) (alpha-agonist & CAI) * Taptiqom (Timolol and Tafluprost)

Answer 55

* Simpler tx regimens – use combined preparation where possible, minimal amount of drop tx is required * Use agents w/ least side-effects * Educate px on why they are receiving the tx as most pxs w/ glaucoma are asymptomatic & are not aware they have a visual problem – px may feel side-effects from drops that they previously didn’t have * Reinforcement when px returns to clinic that their tx is working * Regular review & reassurance – so they understand importance of coming back for check ups * Realistic expectations of tx – sometimes pxs return after starting tx saying they stopped the tx because they didn’t notice any improvement in their eyesight – px has to understand that the tx is ↓ IOP & preserving their glaucoma from deteriorating over long period of time rather than improving their sight

Answer 56

* Preservative related (Irritation, redness, dryness) * Idiosyncratic – px may come with additional problem or side-effect that is not common – individual reactions that others don’t have * Remember nasolacrimal duct occlusion – if px reports bitter taste in their mouth or if want to minimise absorption of beta-blocker into the system --> can press on medial side of lower lid to occlude puncta (& thus nasolacrimal duct) to stop the drops draining into throat --> do for ~1min after applying the drops * Vaseline to lids – for dryness & excoriation – put on before putting drops in, acts as barrier to stop drops from irritating skin * Drops at least 5 mins apart (ideally 10-15mins apart) – if px on multiple drops – prevents one drop washing other drop out or diluting it * Close eyes for 1 to 3 mins after drop – helps w/ absorption & efficacy * Avoid dabbing eyes with tissue immediately after putting drop in as this can result in tissue taking medication out of eye  dab skin if spills onto skin but not eye

Answer 57

* Preservatives e.g. Benzalkonium Chloride are harmful in long term to ocular surface * Intolerance/irritation – particularly in elderly pxs who have ocular surface disease anyway * Allergy – so pxs who are allergic to multiple drops are often allergic to the preservative rather than the medical agent * Exacerbates dryness especially in susceptible pxs & those on multiple drops * Vogue for prescribing preservative free glaucoma meds (long-term)

Answer 58

* Timolol (MSD and Thea -Tiopex 0.1%, Eysano-Aspire) * Monopost (Latanoprost pres free) * Tafluprost (Saflutan)/Taptiqom (saflutan and timolol) * Lumigan UD/ Ganfort UD (Bimatoprost/Timolol) * Eyreida (bimatoprost 0.3%) * Travatan (BAK free – Polyquad) * Cosopt and Eylamdo (dorzolamide/timolol) Dorzolamide (Eydelto) * Pilocarpine 2% * Apraclonidine (Iopidine 0.5% and 1%)

Answer 59

All medications have side effects but if those are tolerable, not causing harm, & medication is effective then px should continue w/ that treatment

Answer 60

* Different types of glaucoma * Red eye * Different types of open angle * Different types of closed angle * Secondary glaucoma * Lens related glaucoma * Glaucoma w/ raised IOP * Glaucoma w/ normal IOP

Glaucoma Flashcards

(84 cards)