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Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
Eye disorders
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Eye disorders
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Eye disorders

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  • Sclera
    Is the white, dense. Fibrous , protective coating.
    Episclera
    A thin layer of loose connective tissue, contains blood vessels that cover and nourish the sclera.
    Conjunctiva
    Is a mucous membrane that covers the anterior portion of the eye and lines the eyelids.
  • In people with glaucoma damage, because of increased pressure in the eye and/or loss of blood flow to the optic nerve, these nerve fibers begin to die. This causes the cup to become larger in comparison to the optic disc, since the support structure is not there. Optic nerve cupping progresses as the cup becomes larger in comparison to the optic disc
  • outflow channels (i.e.,the trabecular meshwork and Schlemm's canal)
  • Examination of the anterior chamber angle by gonioscopy, assists in differentiating between open-angle glaucoma and angle-closure glaucoma.
    gonioscopy, using a corneal contact lens, a magnifying device (e.g., a slitlamp
    microscope), and a light source,
    Photo showing conjunctival vessels dilated at the corneal edge (ciliary flush, circumcorneal flush) and hazy cornea characteristic of acute angle closure glaucoma
  • Transcript

    • 1. Alieh Bazi Eye Disorders
    • 2. glaucom a Conjunctivit is
    • 3. OCULAR ANATOMY
    • 4. GLAUCOMA Silent thief of sight • Glaucoma, a leading cause of blindness worldwide. • It is normally associated with increased fluid pressure in the eye . • Is a nonspecific term used for a group of diseases that can irreversibly damage the optic nerve resulting in visual field loss.
    • 5. GLAUCOMA  Risk Factors : • Increased intraocular pressure (lOP)  Is the most common risk factor.  Even people with "normal“ lOPs can experience vision loss from glaucoma. • Increasing age. • African American race. • family history. • Thinner central corneas. • larger vertical cup-disk ratios.
    • 6. Intraocular Pressure • lOP is influenced by:  The production of aqueous humor by the ciliary processes  The outflow of aqueous humor through the trabecular meshwork. • Generally, an lOP of 10 to 20 mmHg is considered normal. • An lOP of 22 mmHg or higher should arouse suspicion of glaucoma. • Although a more rare form of glaucoma is associated with a low lOP.
    • 7. Ocular Hypertension • Ocular hypertension has been defined as an :  lOP >21 mmHg. • Only a small percentage of patients with ocular hypertension develop open-angle glaucoma. • Diagnosis of glaucoma can be applied when pathologic cupping of the optic nerve is observed.
    • 8. Open-Angle Glaucoma • Prevalence: • Occurs in about 1.8% of people older than 40 years of age in the United States. • However, glaucoma can affect other age groups. • About 2.2 million people in the United States have glaucoma. • This number likely will increase to about 3.3 million by The year 2020 as the population ages
    • 9. Primary Open-Angle Glaucoma • In patients with primary open-angle glaucoma (POAG) :  Aqueous humor outflow from the anterior chamber is continuously subnormal .  Primarily because of a degenerative process in the trabecular meshwork.  The decreased outflow appears to be worsen with the passage of time .  The lOP can vary in the course of a day from normal to significantly high pressures.  In rare cases, the outflow is normal even during a phase of elevated lOP,
    • 10. Open-Angle Glaucoma • The onset of POAG usually is gradual and asymptomatic. • A defect in the visual field examination may be present in early glaucoma. • Loss of peripheral vision usually is not seen until late in the course of the disease. • Visual field defects correlate well with changes in the optic disc . • Which help differentiate glaucoma from ocular hypertension in patients with increased lOP.
    • 11. Angle-Closure Glaucoma • Angle-closure glaucoma accounts for approximately 5% to 10% of all primary glaucoma cases. • The sole cause of the elevated lOP in angle-closure glaucoma is closure of the anterior chamber angle. • Angle-closure glaucoma is a medical emergency. • Usually presents as an acute attack with a     Rapid increase in lOP Blurring or sudden loss of vision Appearance of haloes Around lights And pain that is often severe.
    • 12. Angle-Closure Glaucoma • When patients are predisposed to angle-closure glaucoma:  Their pupils should not be dilated (e.g., during an ophthalmic examination).  They should be taught the signs and symptoms of angle closure. • Acute attacks can terminate without treatment. • But if the lOP remains high, the optic nerve can be irreparably damaged.
    • 13. Angle-Closure Glaucoma • Patients with chronic angle closure generally :  Experience a gradual closure of aqueous humor outflow channels.  patients can be asymptomatic until the glaucoma is in an advanced stage. • Permanent medical management of acute or chronic angle closure glaucoma is difficult:  surgical procedures (e.g., peripheral iridectomies) often are needed.
    • 14. Secondary Glaucoma  Prolonged use of steroids (steroid-induced glaucoma)  Conditions that severely restrict blood flow to the eye, such as : Severe diabetic retinopathy and central retinal vein occlusion (neovascular glaucoma)  Ocular trauma  Uveitis (uveitic glaucoma)
    • 15. Diagnosis
    • 16. Diagnosis • Testing for glaucoma should include :  Measurements of the intraocular pressure via tonometry. Is based upon the pressure required to flatten a small area of the central cornea.  Changes in size or shape of the eye, anterior chamber angle examination or gonioscopy.  And examination of the optic nerve to look for any visible damage to it (Imaging).  Visual field test.
    • 17. t nt me at re
    • 18. Primary Open-Angle Glaucoma drugs • Initial Therapy • • • • • β-ADRENERGIC BLOCKERS PROSTAGlANDIN ANALOGS α-ADRENERGIC AGONISTS TOPICAL CARBONIC ANHYDRASE INHIBITORS ANIICHOLINESTERASE AGENTS
    • 19. β-ADRENERGIC BLOCKERS Timolol, levobunolol, metipranolol, carteolol, betaxolol, levobetaxolol • β -adrenergic blockers have been the most commonly prescribed first-line agents for the treatment of POAG. • Block the β -adrenergic receptors in the ciliary epithelium of the eye . • Lower lOP primarily by decreasing aqueous humor production.
    • 20. Timolol(timopotol, betimol, blocarden) •A nonselective β 1- and β 2-adrenergic antagonist. •Is one of the most commonly prescribed glaucoma medications. •Therapy usually is initiated with a 0.25% solution administered as one drop BID.
    • 21. con,… • Timolol has been associated with :  A modest reduction of resting pulse rate (5-8 beats/minute).  Worsening of congestive heart failure.  And adverse pulmonary effects (e.g., dyspnea, airway obstruction, pulmonary failure).  Uveitis
    • 22. Betoxolol (Betoptic) Levobetoxolol (Betoxon)
    • 23. Prostaglandin Analogs  Latanoprost (Xalatan), travoprost (Travatan), and bimatoprost(Lumigan) Mechanism:  Increase uveoscleral outflow of aqueous humor and, thereby, decrease IOp.  Often are prescribed as first-line agents for the treatment of POAG, because they are at least as effective as the β-blockers.  Can be administered once a day, and are associated with minimal adverse effects.  Unlike the β-blockers, generic versions of these drugs are not yet available
    • 24. Latanaprost (Xalatan)  Is approved for the initial treatment of POAG or ocular hypertension.  administered once daily in the evening,latanoprost is at least as effective as timolol in decreasing lOP.  When the effectiveness of latanoprost 0.005% once daily was compared with timolol 0.5% BID, the IOP lowering effects of latanoprost were superior to timolol.  the nocturnal control of lOP with latanoprost was superior to that with timolol.
    • 25. Con…  Additive effects when administerate with β-blockers (e.g., timolol), carbonicanhydrous inhibitors (e.g., dorzolamide), α2-adrenergic agonists (e.g., brimonidine,apraclonidine), and dipivefrin.  Adjunctive ophthalmic for patients who are unable to adequately lower their lOP with single-agent therapy. Becuase When added to existing therapy, decreases lOP an additional 2.9 to 6.1 mmHg.
    • 26. α-adrenergic agonist • Apraclonidine (Iopidine) and Brimonidine (Alphagan) are selective α2adrenergic agonists similar to clonidine. • Appear to lower lOP by decreasing the production of aqueous humor and by increasing uveoscleral outflow. • Should be used with caution in patients with cardiovascular disease, orthostatic hypotension,depression, and renal or hepatic dysfunction. • Longterm lOP control should be monitored closely in patients on α 2-adrenergic agonists because tachyphylaxis can occur.
    • 27. Apraclonidine • Is less lipophilic than clonidine and brimonidine • Does not cross the blood-brain barrier as readily • Apraclonidine I% is indicated to control or prevent postsurgical elevations in lOP after argon laser trabeculoplasty or iridotomy. • The 0.5% apraclonidine solution is indicated for short-term adjunctive therapy in patients on maximally tolerated medical therapy
    • 28. Brimonidine • Is more highly selective for α 2-adrenergic receptors than clonidine or apraclonidine and, theoretically, should be associated with less ocular side effects. • Is an alternative first-line agent in the treatment of POAG. • It may also be used as adjunctive therapy in patients not responding to other agents. • Brimondine(Alphagan P) is now available with purite as a preservative which facilitates drug delivery into the eye allowing use of alower drug concentration.
    • 29. Con,… • The lOP-reduction effects (peak and trough) of brimonidine 0.2% BID is 14% to 28%. • Although the approved dosing schedule of brimonidine is TID, brimonidine 0.2% BID lowers lOP comparably to timolol 0.5% BID, and both are slightly better than betaxolol 0.25% BID. • The combination of brimonidine and timolol is equally tolerable and effective as the combination of dorzolamide and timolol. • The FDA-approved Combigan ophthalmic solution combines α-adrenergic agonist (brimonidine tartrate 0.2%) with β-adrenergic blocker (timolol maleate 0.5%).
    • 30. Side effects of α-adrenergic agonist • Common ocular side effects include : burning, stinging, blurring, and an allergic-like reaction consisting of hyperemia, pruritus, edema of the lid and conjunctiva, and foreign body sensation. • apraclonidine has less systemic side effects (e.g., hypotension,decreased pulse, dry mouth). • ocular side effects are less common with brimonidine than with apraclonidine. • systemic side effects (e.g., dry nose and mouth, mild hypotension, decreased pulse, and lethargy) are more common with brimonidine.
    • 31. Topical Carbonic Anhydrase Inhibitors dorzolamide (Trusopt) brinzolamide (Azopt)
    • 32. Topical Carbonic Anhydrase Inhibitors • Carbonic anhydrase occurs in high concentrations in the ciliary processes and retina of the eye. • Carbonic anhydrase inhibitors (CAIs) lower IOP is by decreasing bicarbonate production  the flow of bicarbonate, sodium, and water into the posterior chamber of the eye resulting in a 40% to 60% decrease in aqueous humor secretion. • Although CAIs have been used orally for many years in the treatment of elevated IOPs, they have been replaced by the topical ophthalmic CAIs, dorzolamide (Trusopt) and brinzolamide (Azopt), which are safer and better tolerated. • Topical CAIs are excellent alternatives to β-blockers in the initial management of elevated IOPs, and are effective as adjunctive agents.
    • 33. Con,… • The IOP-reduction effects (peak and trough) of dorzolamide 2% TID is 16% to 25%. Brinzolamide and dorzolamide are approved for TID dosing; however, BID dosing may be adequate. • Dorzolamide provides additional IOP-lowering effects when added to existing βblocker therapy. • An ophthalmic solution of dorzolamide hydrochloride and timolol maleate is marketed as Cosopt. • The combined use of topical dorzolamide and oral acetazolamide does not result in additive effects and might increase the risk of toxicity. Therefore, the concomitant use of topical and oral CAIs is not advised.
    • 34. Con,… • The topical CAIs are well tolerated with few systemic side effects. • The most common adverse effects reported with dorzolamide are ocular burning, stinging, discomfort and allergic reactions, bitter taste, and superficial punctate keratitis. • Brinzolamide causes less burning and stinging of the eyes than dorzolamide, because its pH more closely resembles that of human tears. • Dorzolamide and brinzolamide are sulfonamides and may cause the same types of adverse reactions attributable to sulfonamides. These drugs should not be used in patients with renal or hepatic impairment.
    • 35. Pilocarpine • Pilocarpine (IsoptoCarpine)  was an initial treatment of choice, but with the introduction and widespread use of newer agents  pilocarpine has fallen out of favor as an initial treatment. • Pilocarpine is a direct-acting cholinergic (parasympathomimetic) that causes contraction of ciliary muscle fibers attached to the trabecular meshwork and scleral spur. This opens the trabecular meshwork to enhance aqueous humor outflow. • There also may be a direct effect on the trabecular meshwork. Pilocarpine causes miosis by contraction of the iris sphincter muscle, but the miosis is not related to the decrease in IOP.
    • 36. Epinephrine • • • • Epinephrine (Glaucon, Eppy/N, Epitrate) is a sympathomimetic that stimulates both α-and β-receptors. The β-adrenergic stimulation is responsible for increasing aqueous humor outflow and is the probable basis of epinephrine's ability to lower IOP. In contrast, the βadrenergic blockers decrease aqueous humor production. The α-adrenergic effect of epinephrine predominantly decreases the inflow of aqueous humor, which is not as significant as the increase in aqueous humor outflow. Patients in whom systemic effects of this drug could potentiate pre-existing problems should be monitored closely. Dipivefrin is an epinephrine prodrug that is better tolerated and absorbed than epinephrine. Dipivefrin or epinephrine is often used in younger patients or patients with cataracts in which miosis and the resultant decreased vision from cholinergic agents are a problem. Both are second or thirdline drugs in the therapy of POAG and are used most often as second agents in combination regimens rather than as monotherapy.
    • 37. Anticholinesterase Agents • If control of IOP is not achieved with optimal use of other topical monotherapy and combination therapy agents, then anticholinesterase agents may be prescribed as a last topical therapy option. • Anticholinesterase agents inhibit the enzyme cholinesterase, thereby increasing the amount of acetylcholine and its naturally occurring cholinergic effects.
    • 38. Echothiophate Iodide • an irreversible cholinesterase inhibitor • Echothiophate iodide is the most widely used cholinesterase inhibitor for openangle glaucoma and can be used if maximal doses of other agents and combination therapy are ineffective. • Echothiophate iodide has a long duration of action that affords good control of IOP • side effects miosis and myopia • Concentrations higher than 0.06% are associated with a significant increase in subjective complaints (e.g., brow ache).
    • 39. Treatment of Angle-Closure Glaucoma • pilocarpine 2% to 4%, one drop every 5 minutes for four to six administrations • It is recommended that the puncta be covered during administration to decrease the possibility of systemic absorption • Stronger miotics are contraindicated, because they may potentiate angle closure • Topical timolol also has been used in acute angle-closure glaucoma, commonly in combination with pilocarpine
    • 40. Hyperosmotic Agents • Hyperosmotic agents act by creating an osmotic gradient between the plasma and ocular fluids. • side effects of hyperosmotic agents: headache, nausea, vomiting, diuresis, and dehydration • the patient not be allowed to drink because this will counteract the osmotic effects of these agents • Precipitation of pulmonary edema and CHF has been reported with hyperosmotic agents, and an allergic reaction has been reported with mannitol
    • 41. Nasolacrimal Occlusion • Occlusion of the puncta (through the application of slight pressure with the finger to the inner corner of the eye closest to the nose for 3 to 5 minutes during and after drug instillation) can minimize systemic absorption of ophthalmic medications
    • 42. Conjunctivitis
    • 43. Conjunctivitis • • Is a common external eye problem that involves inflammation of the conjunctiva. Redness, Pruritis, Discharge, FB sensation Classification: • Infectious: Viral & Bacterial & Fungal & Parasitic • Noninfectious: Allergic & Toxins & Chemicals & Trauma & Autoimmune disease & Neoplastic • • • • • • Most commenly viral Affects all ages, genders, social status. But more common in kids. Permanent visual or structural damage infrequent Highly contagious Patients with pain, decreased vision, unequal distribution of redness, irregular pupils, or opacity should be referred immediately to an ophthalmologist. The infection usually starts in one eye and is spread to the other by the hands. Or other persons.
    • 44. Bacterial conjunctivitis • • • • • • • • • Most cases: S. aureus, Streptococcus pneumococcus, Haemophilus aegyptius. Typically with less pruritis Unilateral > bilateral Unlike bacterial conjunctivitis, corneal infections can obliterate vision rapidly; therefore, accurate diagnosis is important. Treatment: Eye drops: 7 to 10 days: Quinolone or trimethoprim-polymyxin Erythromycin ointment in peds. Contact lens: need pseudomonal coverage: Quinolone first line Supportive care, warm compresses & irrigation No eye patches
    • 45. Bacterial conjunctivitis
    • 46. Viral conjunctivitis • • • • • • • • Significant redness and pruritis Less discharge that bacterial Progresses bilateral in 24-48 hours Contagious for 2 weeks Self limited Education on hand washing Treatment: Symptomatic: artificial tears, Cold compresses, vasoconstrictor antihistamine combinations for pruritis.
    • 47. Viral conjunctivitis
    • 48. Allergic conjunctivitis • • • • • • • Removal of allergen from the enviroment Cold compresses Topical vasoconstrictors (nephazoline, tetrahydrozoline) with or without antihistamines (antazoline, pheniramine).but not be used longer than 72h because rebound congestion. Topical mast cell stabilizers (nedocromil, lodoxamide, ketotifen%0.025 BIDtoQID, cromolyn sodium%2) Topical antihistamines (levocabastine BIDtoQID, azalastine, emedastine QID, olopatadine BID) Antihistamine tablets or syrup. Ophthalmic corticosteroides
    • 49. Allergic conjunctivitis
    • 50. viral conjunctivitis vs bacterial vs allergic conjunctivitis

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