GLAUCOMA

GLAUCOMA (PPT)
Brief on glaucoma for medical students .

1. GLAUCOMA NIDHIL NARAYANAN   TBILISI STATE MEDICAL UNIVERSITY

2. 2nd most cause of 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 of optic disk  visual field defect.

4. 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.

5.                                                   PRIMARY                           CHILDHOOD                             ADULT                                                                                           ( > 40YRS)    CONGENITAL\     JUVENILE            OAG                 ACG                        BUPHTHAMUS     (BIRTH- 3YRS)      (3YRS- 40YRS)        

6. Congenital glaucoma (buphthalmias) BARKANS MEMBRANE – 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

7. ADULT GLAUCOMA                OAG  (open angle galucoma)                     ACG (angle closure glaucoma)                   3                                       :                           1           Dangerous                                                 Painful but not Dangerous

8.    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

9. OPEN ANGLE GLAUCOMA (silent thief 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  

10. ANGLE CLOSURE GLAUCOMA                     OPEN 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 

11. VISUAL FIELD DEFECT IN 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 

12. Optic disc   NEURO RETINAL 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 

13. OPTIC DISC CHANGES IN 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

14. 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

15. TREATMENT (OPEN ANGLE GLAUCOMA) MEDICAL MANAGEMENT INC OUT FLOW      DEC PRODUCTION PILOCARPINE    PG ANALOGEUS    SURGICAL MANAGEMENT ALT ( argon laser trabeculoplasty)  TRABECULECTOMY  

16. 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 

17. EPINEPHRINE Inc trabecular 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 

18. 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 analog s: ( 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

19. 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

20. 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

21. 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

22. SECONDARY GLAUCOMA (LENS INDUCED GLAUCOMA ) 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 

23. 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 

24. 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 )

25. GENE THERAPY  Target tissue Gene Target protein/ mechanism Cellular/molecular changes T r ab e c ular  me s h w ork DN Rho Inhibiting Rho Disruption of  cellular  adhesions in  cultured cells C3 Inactivating Rho by rebosylation DNRK Inhibiting Rho kinase caldesmon Inhibiting actin-myosin activating myosin  Mg ATPase Ciliary  me s h w 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

26. 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

27. References https://www.ncbi.nlm.nih.gov/books/NBK538217/ Deepak Sambhara 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

28. THANKYOU !! :)  HAVE A GOOD DAY .