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GLAUCOMA
This document provides information about glaucoma, including: 1. Glaucoma is the second leading cause of blindness worldwide and is characterized by increased intraocular pressure, optic nerve damage, and visual field defects. 2. There are two main types - open angle glaucoma, which has no pain and slow vision loss, and angle closure glaucoma, which causes sudden, painful vision loss. 3. Treatment involves medications like prostaglandin analogs to lower pressure or surgery like trabeculectomy if medications are not effective. New gene therapies are also being explored to treat glaucoma at the cellular level.
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GLAUCOMA
- 1. GLAUCOMA NIDHIL NARAYANAN TBILISI STATEMEDICAL UNIVERSITY
- 2. 2nd most causeof BLINDNESS in the world. • Classical triad of glaucoma( atleast 2 of 3 ) • 1. increase IOP (>21mm of Hg) • 2. visual field defects • 3. optic disk damage • Only inc IOP - ocular HTN • VFD + ODD – inc IOP = Normal tension low tension glaucoma
- 3. MECHANISM -Inc IOP- Compression ofoptic disk visual field defect.
- 6. GLAUCOMA • PRIMARY • IDIOPATHIC •MORE COMMON • Therefore we reduce the IOP • SECONDARY • UVEITIS (ant causes max—blocking angle,steroid & blockage of T meshwork) • NEOVASCULAR • LENS INDUCED • TRAUMA • STEROID INDUCED We reduce the underlying cause not IOP directly.
- 7. • PRIMARY CHILDHOOD ADULT •( > 40YRS) CONGENITAL JUVENILE OAG ACG BUPHTHAMUS (BIRTH- 3YRS) (3YRS- 40YRS)
- 8. Congenital glaucoma (buphthalmias) BARKANSMEMBRANE – congenital anomaly TRIAD- lacrimation-photophobia-blepharospasm • Large eye – HAZY cornea due to corneal edema (inc IOP CAUSES) • HAAB'S STRIAE – rupture of Descemet's membrane • Treatment -- --- CORNEA • CLEAR HAZY • • GONIOTOMY TRABECULOTOMY AUTOSOMAL RECESSIVE CONSANGUINEOUS MARRIAGE
- 9. ADULT GLAUCOMA OAG (openangle galucoma) ACG (angle closure glaucoma) 3 : 1 Dangerous Painful but not Dangerous
- 10. ANGLE CLOSURE GLAUCOMA •RISK FACTOR • Middle aged ( coz growing lens ) Women ( d/t shallow ant chamber) • Hypermetropia (small eyeball + small /shallow angle) Mid dilated pupil – relaxed iris --- falls on lens --- blocks pupil --- -- inc post chamber IOP (15mm – 60 mm in 30 mins) ACUTE ANGLE CLOSURE GLAUCOMA (seen in the evening /night /pain in movie theater) SEVERE PAIN LOSS OF VISION / COLORED HALOS D/T CORNEAL EDEMA VOMITING SIGNS –STONY HARD EYE STEAMY CORNEA OVAL,MID DILATED ,NON REACTING PUPIL
- 11. OPEN ANGLE GLAUCOMA (silentthief of sight ) • RISK FACTORS • Thin cornea( will show falsely low IOP ) • colored races , myopic , middle aged , • trabecular meshwork fibrosis ( blocks the outflow of AH) • SYMPTOM • NO PAIN (slow rise in pressure ,yrs. ) • Clear cornea ( no corneal edema ) • NO LOSS OF VISSION & NO COLORED HALLOS DIAGNOSIS - 1) MEASURE IOP EVERY YEAR 2) PERIMETRY – VISUAL FIELD (mostly accidental findings coz late appearance of signs ) Presentation - TUNNEL VISION/TUBULAR VISION ( end stage glaucoma) ONLY SYMPTOM – frequent change in presbyopic glasses
- 12. ANGLE CLOSURE GLAUCOMAOPEN ANGLE GLAUCOMA • FEMALE PREDOMINANCE • MIDDLE AGE • HYPERMETROPIC • SUDDEN,PAINFUL, • COLORED HALOS • PUPILLARY BLOCK • NO GENDER PREDISPOSITION • MIDDLE AGE • MYOPIC • SLOW, PAINFUL • NO SYMPTOMS • TRABECULAR FRIBROSIS
- 13. VISUAL FIELD DEFECTIN GLAUCOMA (due to optic nerve damage –negative scotoma) • Para central scotoma (earliest ) • Bjerrum scotoma (blind spot in arc @ central 30 degree meridian) • Generalized constriction of field / concentric constriction of isotopes • Nasal step (step like field defect in nasal side) • Arcuate scotoma (in shape of arc) 1st field to be destroyed in glaucoma –NASAL FIELD Last to get destroyed – TEMPORAL FIELD Most are ARC shaped Follows an horizontal meridian –sup or inf
- 14. Optic disc • NEURORETINAL RIM • Contains neurons of optic nerve . • Each nerve ( 1.2 M neurons ) • Raised IOP destroys the NNR . • Reddish pink • CUP DISK RATIO (n) - 0.3 -0.6 • ( TELLS US DISTRUCTION OF OPTIC DISK ) • CENTRAL CUP • Contains 1 cental retinal artery & 1 central retinal vein .( vein pulsates) CUP SIZE INCREASES IN GLAUCOMA. IRREGUAL MARGINE – EDEMA
- 15. OPTIC DISC CHANGESIN GLAUCOMA • 1. CDR increased(cup expands) • 2. DISC PALLOR • 3. SPLINTER HAEMORRHAGE • 4. SIGN OF NASALIZATION • (apparent shift of the temporal vessels to nasal side) • 5.SIGN OF BAYONETTING • (apparent discontinuity of blood vessels) • 6. GLAUCOMATOUS OPTIC ATROPHY
- 18. DIAGNOSTIC METHODS • 1.PACHYMETRY • 2. TONOMETER • 3. FINCHAM'S TEST • (distinguish colored halos of cataract and glaucoma) • 4. HUMPHREY'S PERIMETER • 5. GONIOSCOPY • 6. OPHTHALMOSCOPE
- 19. TREATMENT (OPEN ANGLE GLAUCOMA) •MEDICAL MANAGEMENT • INC OUT FLOW DEC PRODUCTION • PILOCARPINE • PG ANALOGEUS • SURGICAL MANAGEMENT • ALT ( argon laser trabeculoplasty) • TRABECULECTOMY
- 20. ANTI GLAUCOMA DRUGS •1. CHOLINERGIC AGONIST (PILOCARPINE ) • Inc trabecular outflow • S/E :- • Uveitis ( not used in inflamed eye) • Ciliary spasm ( pain ) • Myopia ( ciliary ms contracts ) • Retinal detachment • 2 membranes of polyethylene-co-vinyl acetate • Ring of pilocarpine • Placed in inferior fornix • B BLOCKERS (non-selective –TIMOLOL / LEVO BUNOLOL selective –BETAXOLOL • Dec production • S/E - C/I - bronchial asthma , COPD • Arrythmias/ cardiac problem • Dry eyes , depression
- 21. • EPINEPHRINE • Inctrabecular outflow & dec production • S/E - sweating , palpitation , tachycardia ,HTN , nervousness . Tremors • OCULAR – CME in aphakia ,pupil dilation • C/I - HTN AND ACG • Prodrug – DIPIVEFRINE • No systemic S/E • CARBONIC ANHYDRASE INHIBITORS • ACETAZOLAMIDE (SYSTEMIC) • S/E - SULFA ALERGY , ACIDOSIS , KIDNEY STONE, HYPOKELIMIA • (TOPICAL ) DORZOLAMIDE & BRINZOLAMIDE • Safest DOC children • S/E -CONRNEAL DECOMPENSATION (destroy corneal endothelial cells ) • Dec production
- 22. • 2-alpha agonists( Alpha-2 Adrenergic Agonists) :(apraclonidine, brimonidine) • MOA- dec IOP by reducing production of aqueous humor.& inc outflow. • S/E:. HTN tachycardia, allergic conjunctivitis, local irritation head ache. • C/I- CHILDREN • 5- prostaglandin analogs: (latanoprost, bimatoprost, unoprostone, travoprost)(pgf2alpha) • MOA : increase the uveoscleral outflow • . Side Effects: -Iris pigmentation - local irritation -increased growth of eyelashes ,uveitis , CME • DOC- OAG & LTG
- 23. • HYPEROSMOTICS (extracts waters from vitreous humor ) • MANNITOL ( IV – fastest acting ) • DOC – ACUTE ACG (C/I-CHF) GLYCEROL Oral syrup ( C/I -DM) Advantage Used in Emergency / pre-op Limitations Reduce IOP only transiently
- 24. TREATMENT (ANGLE CLOSURE GLAUCOMA) •1. Dec IOP - SYSTEMIC DRUGS- MANNITOL(DOC) ACETAZOLAMIDE GLYCEROL • 2. PROPHYLACTIC PI/LI OF SECOND EYE • 3. PI/LI OF ATTACKED EYE after IOP Dec and cornea is clear
- 25. • SURGICAL MANAGEMENT •MOLTENO TUBE :- • Drainage tube placed between cornea and iris • Exits at junction of cornea & sclera • ALT(ARGON LASER TRABECULOPLASTY) • TRABECULECTOMY • PERIPHERAL IRIDECTOMY • ND-YAG LASER IRIDOTOMY • PI/LI- PROPHYLACTIC TREATMENT
- 26. SECONDARY GLAUCOMA (LENS INDUCEDGLAUCOMA ) PHACOMORPHIC GLAUCOMA ACG MATURE CATARACT ( absorbs water ---pushes iris forward ) SHALLOW AC Rx- cataract extraction • PHACOLYTIC GLAUCOMA • OAG • HYPERMATURE CATARACT ( lens shrinks – microleaks – lens matter blocks T meshwork ) • DEEP AC • Rx- cataract extraction
- 27. NEOVASCULAR GLAUCOMA • RETINA( needs too much o2) • Hypoxia – VEGF – neovascularization ( retina – vitreous – iris – RUBEOSIS IRIDIS ) • Pulls iris close to cornea ( ACG) • Causes - • DIABETES • CRVO (central retinal Venus occlusion) • OCULAR ISHEMIC DS • TUMOR • SICKEL CALL ANEMIA
- 28. • EARLY MANAGEMENT •STOP NEOVASCULARIZATION • ANTI VEGF • BEVACIZUMAB • RANIBIZUMAB • PAN RETINAL PHOTOCOAGULATION ( for hypoxia) • Coagulation except macula • DEC IPO – DRUG OR TRABECULECTOMY • LATE MANAGEMENT • ABSOLUTE GLAUCOMA – LOST VISION . • PAIN ( CYCLODESTRUCTION ) DLCP ( diod cyclo photocoagulation ) • CYCLOCRYOPLEXY • ( cold -80dec probe distruction )
- 29. GENE THERAPY Target tissue Gene Targetprotein/ mechanism Cellular/molecular changes Trabecular me shwork DN Rho Inhibiting Rho Disruption of cellular adhesio ns in cultured cells C3 Inactivating Rho by rebosylation DNRK Inhibiting Rho kinase caldesmon Inhibiting actin-myosin activating myosin Mg ATPase Ciliary meshw ork PG synthase ↑MMP ase expression Degrade ECM Retina ErK Mediate neuroprotective activity of extracellular factors ↑RGC survival MeK1 Upstream activity of Erk CNTF neuroprotection TNF Alpha Inhibit CNTF BRICK-4 Inhibit caspases
- 30. Why new drugs? ••Neural damage irreversible – need for neuroprotective agents • •Patients with asthma, bradycardia, cataract, allergy to sulfa drugs or topical brimonidine – not much options left other than SX • •Need for preservative free drugs • •Benzalkonium – punctate / ulcerative keratopathy • •Thiomersal – hypersensitivity • •Drugs for newer drug delivery systems
- 31. References • https://www.ncbi.nlm.nih.gov/books/NBK538217/ • DeepakSambhara et. al. Glaucoma management: relative value and place in therapy of available drug treatments • https://pubmed.ncbi.nlm.nih.gov/28577860/ • http://www.icoph.org/downloads/ICOGlaucomaGuidelines.pdf • https://www.glaucoma.org/news/blog/recent-advances-in-glaucoma- treatment-what-do-they-mean-for-patients.php
- 32. THANKYOU !! :) HAVEA GOOD DAY .
Editor's Notes
- #14 Island of vision with sea of darkness = visual field