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Glaucoma
- 1.
- 2. GLAUCOMA A disease ofprogressive optic neuropathy with loss of retinal neurons and the nerve fiber layer, resulting in blindness if left untreated.
- 3. There is adose-responseThere is a dose-response relationship between intraocularrelationship between intraocular pressure and the risk of damagepressure and the risk of damage to the visual field.to the visual field. What causes it?What causes it?
- 4. The IOP refersto the pressure exerted by the intraocular fluids on the coats of the eyeball Normal IOP is 10-21mm Hg (mean 16±2.5mmHg)
- 5.
- 6. AQUEOUS AND ANATOMY Aqueousis continuously produced by the ciliary body Aqueous flows from the posterior chamber through the pupil into the anterior chamber Aqueous filters largely through the trabecular meshwork (90%) Aqueous also exits to a smaller extent through the ocular venous system (10%) Uveoscleral outflow (ciliary body, choroid, scleral vessels)
- 7. Types of glaucoma I.Primary: A. Congenital B. Hereditary C. Adult (common types) 1. Narrow angle 2. Open angle II. Secondary A. Inflammatory B. Traumatic C.Phacolytic etc.
- 8. Congenital Glaucoma Onset: antenatallyto 2 years old SymptomsSymptoms IrritabilityIrritability PhotophobiaPhotophobia Poor visionPoor vision Signs Elevated IOP Buphthalmos Corneal clouding Glaucomatous cupping Field loss
- 9. Congenital Glaucoma Buphthalmos andcloudy corneasBuphthalmos and cloudy corneas
- 10. Congenital Glaucoma Buphthalmos, glaucomatous cupping, and cloudycornea OD Haab’s striae
- 11. Narrow Angle Glaucoma Onset:50+ years of ageOnset: 50+ years of age SymptomsSymptoms Severe eye/headacheSevere eye/headache painpain Blurred visionBlurred vision Red eyeRed eye Nausea and vomitingNausea and vomiting Halos around lightsHalos around lights Intermittent eye acheIntermittent eye ache at nightat night SignsSigns Red, teary eyeRed, teary eye Corneal edemaCorneal edema Closed angleClosed angle Shallow ACShallow AC Mid-dilated, fixedMid-dilated, fixed pupilpupil Iris atrophyIris atrophy AC inflammationAC inflammation
- 12. Narrow Angle Glaucoma Mid-dilated,fixed pupilMid-dilated, fixed pupil
- 13. Open Angle Glaucoma Onset:50+ years of ageOnset: 50+ years of age SymptomsSymptoms Usually noneUsually none May have loss of centralMay have loss of central and peripheral visionand peripheral vision latelate SignsSigns Elevated IOPElevated IOP Visual field lossVisual field loss Glaucomatous disk changesGlaucomatous disk changes
- 14. Open Angle Glaucoma HISTORY: Positivefamily history African American background History of trauma History of steroid use Risk factorsRisk factors
- 15. Parasympathetic Innervations tothe Eye 2/19/201015
- 16.
- 17. AUTONOMIC NERVOUS SYSTEM Sympatheticregulation Fight and flight 2 main classes of receptors Beta receptors (ß1 and ß2) Alpha receptors (α1 and α2) Parasympathetic regulation
- 18. AUTONOMIC NERVOUS SYSTEM Pupilis controlled by both Sympathetic system dilates the pupil by stimulating the contraction of dilator muscle Parasympathetic system constricts the pupil by causing contraction of the sphincter muscle. Ciliary body is controlled by both Sympathetic system for aqueous production Parasympathetic system causing ciliary body muscle movement
- 19. Drugs used intreatment of glaucoma DRUGS MOA DOSE REG. Directly acting cholinomimetics PILOCARPINE 1) Ciliary muscle contraction. 2) Pupillary constriction 3) Pulling of iris 4) Opening of Trabecular meshwork All causes increased drainage of aqueous humor and causes decrease in IOP 0.5 – 4% topically TDS
- 20. Reversible Anti- AchE PHYSOSTIGMINE-DO- 0.25 – 5% topically TDS Irreversible Anti- AchE Ecothiophate -DO- 0.05 – 0.25% topically once in 2 weeks Beta- blockers a)Timolol b)Butaxolol c)Levovunolol d)Carteolol Reduce the aqueous humor Formation by blocking b2 receptors Present on ciliary epithelium 0.25 – 5% BD
- 21. NONSELECTIVE α agonist 1)Epinephrine 2)dipivefrine Facilitate outflowof Aqueous Humour Better penetration through cornea’ longer duration of action 0.15 – 0.25% topically 0.1%-tds SELECTIVE α2 Agonist 1)APRACLONIDINE 2)BRIMONIDINE Reduce the formation of aqueous Humour .do not cross blood brain barrier. Hence no systemic effects. 0.5 to 1% topically 0.2%topically .use restricted for acute rise in IOP after laser trabeculoplasty
- 22. Prostaglandin F2α analogues Latanoprost bimatoprost Increase fluid outflowthrough ocular venous system (uveoscleral outflow 0.005% OD Carbonic Anhydrase inhibitors Acetazolamide Dorzolamide Reduces AH formation by decreasing the formation of HCO3 ion in ciliary epithelium 250-500 mg 3 times daily 1% sol BD
- 23. Prostaglandins Systemic side effectsare extremely rare Allergy is extremely rare Most side effects are local and cosmetic Conjunctival hyperemia Iris pigmentation Periorbital darkening Eyelash growth/thickening/darkening
- 24. WHEN PROSTAGLANDINS AREYOUR FIRST CHOICE Primary Open Angle Glaucoma Ocular Hypertension Pigmentary Glaucoma
Editor's Notes
- #4 But pressure certainly plays a role. Glaucoma is just too complicated to fit a nice simple definition.
- #6 Normal anatomy. The aqueous humor is made in the posterior chamber and escapes through the trabecular meshwork of the anterior chamber.
- #8 This lecture covers only congenital and adult varieties of glaucoma but it is important to realize there are many other causes.
- #9 Haab’s striae are found only in congenital glaucoma.
- #10 The right eye in each patient has congenital glaucoma.
- #12 The classical signs and symptoms of narrow angle glaucoma.
- #13 Mid-dilated, fixed pupils and cloudy corneas during an angle closure attack.
- #14 Remember: most patients with open angle glaucoma have no symptoms. This is the best reason to have periodic eye examinations with pressure checks and optic nerve evaluations.