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Pharmacotherapy of glaucoma
Glaucoma is a chronic progressive optic neuropathy caused by an imbalance between the rate of aqueous humor formation and drainage, leading to damage of the optic nerve and loss of vision. It is defined as an intraocular pressure of over 21 mmHg. The aqueous humor is produced by the ciliary epithelium and normally drained through two routes - the conventional trabecular route which drains around 90% and the uveoscleral pathway which drains around 10%. Glaucoma is diagnosed by tonometry and treated through lifelong drug therapy, laser treatment, or surgery to lower intraocular pressure and prevent further vision loss.
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Pharmacotherapy of glaucoma
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- 2. Derived from Greekword “Glaukoma” Affects 12 million Indians annually Define:- “ Glaucoma is a chronic progressive optic neuropathy caused due to imbalance between rate of formation of aqueous humor by the ciliary epithelium and the rate of drainage conditions which lead to damage of optic nerve with loss of visual function ’’ • Intraocular pressure(IOP):- more than 21 mmHg (Normal range – 10-21 mmHg) ( pressure in vascular supply of patient’s retina with hypoxic damage to retina, very fragile neural tissue, causes Blindness) Introduction M3
- 3. Aqueous humor productionfrom the base of iris i.e. ciliary epithelium
- 4. Derived from Greekword “Glaukoma” Affects 12 million Indians annually Define:- “ Glaucoma is a chronic progressive optic neuropathy caused due to imbalance between rate of formation of aqueous humor by the ciliary epithelium and the rate of drainage conditions which lead to damage of optic nerve with loss of visual function ’’ • Intraocular pressure(IOP):- more than 21 mmHg (Normal range – 10-21 mmHg) ( pressure in vascular supply of patient’s retina with hypoxic damage to retina, very fragile neural tissue, causes Blindness) Introduction β1 M3 M3 α1, α2 Prostanoid receptors
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- 6. Drainage of aqueoushumor occurs by 2 routes:- (1)Conventional route through the trabecular network into the canal of Schlemm, it drains about 90%. (2) Uveo-scleral pathway through the ciliary body into the suprachoroidal space, it drains about 10%
- 7. -:Risk Factors:- Age- above40-45yr. Family history of Glaucoma Physical injuries-Eye trauma Disease condition- Diabetes mellitus, Cataract, Cardiovascular disease, Hypothyroidism, Sleep apnoea, Sickle cell anaemia, Leukaemia Drug induced-corticosteroid use, anti-histaminic drug Emotional stress Thin cornea
- 8. Due to:- Raised IOPinduced mechanical changes Disturbed auto regulation of optic nerve head vasculature
- 9. GLAUCOMA: OPTIC NERVEDAMAGE Rise in IOP > 21 mm Hg Mechanical back pressure on optic nerve/retina Loss of blood supply to optic nerve head Retinal ganglion cell loss
- 10. Diagnosis Tonometry examination:- Condition IOP Normalrange- 10-20mmHg(usually 15.5mmHg) Open angle glaucoma 22-40mmHg Close Angle glaucoma >60 mmHg
- 11. Drainage of aqueoushumor occurs by 2 routes Diagnosis Drug treatment:- lifelong therapy –cant be cured to ↓ IOP - ↓ secretion of aqueous humor - promote its drainage MANAGEMENT DRUGS LASER SURGICAL
- 12. Drainage of aqueoushumor occurs by 2 routes Types of Glaucoma Glaucoma Narrow (closed) angle glaucoma/Acute Congestive glaucoma wide (open) angle glaucoma/chronic simple glaucoma
- 13. Narrow angle/Close angleAcute Congestive glaucoma Acute painful Emergency condition It is due to lack of drainage of aqueous humor through the canal of schlemm resulted in IOP Irish is clamping next to the canal of schlemm and physicall obstructing the aqueous humor axis Treatment:- • usually treated surgically by iridotomy • Emergency drug treatment prior to surgery • Drugs are used to lower IOP before surgery
- 14. Iridotomy Opening is madeon iris to improve outflow Lasers Iridotomy perform-light energy used
- 15. Drainage implants orshunts Its is a open tubes implanted in the anterior chamber to shunt aqueous humor to an attached place in the conjunctive place
- 16. Open angle /wideangle/chronic simple) glaucoma Genetically predisposed degenerative condition- mutation in myocilin gene(GLC1A). Progressive (painless) visual loss untreated Blindness Irido-corneal angle is normal but the patency of the trabecula meshwork is disrupted Slow progressive raise of BP & usually chronic and is treated medically
- 18. DRUGS USED INGLAUCOMA ↓ Aqueous secretion Aqueous Outflow β-blockers α2-agonists Brimonidine Apraclonidine Carbonic anhydrase inhibitors Acetazolamide Dorzolamide Brinzolamide Trabecular outflow Uveo-scleral outflow Latanoprost Bimatoprost Cardioselective Betaxolol Levo-betaxolol Non-selective Timolol Levobunolol Carteolol Miotics Pilocarpine Physostigamine α2-agonists Dipevefrine
- 19. Narrow angle glaucoma:- 1.Shortacting miotics:- Pilocarpine (DOC) , Physostigmine, carbachol. 2.Dehydrating agents (osmotic agents):- Mannitol, magnesium sulphate, isosorbide 3.Carbonic Anhydrase Inhibitors: dorzolamide acetazolamide 4.Alpha 2 agonists:- Brimonidine Wide angle glaucoma:- 1. β-Blockers:- Timolol, Betaxolol, levobunolol, carteolol 2.Sympathomimetic (α-Agonists)- Adrenaline, Dipivefrine α2-Agonists :-Apraclonidine, Brimonidine 3.PGF2α-analogues:- latanoprost, travoprost, bimatoprost 4.Carbonic Anhydrase Inhibitors:- Dorzolamide, brinzolamide, acetazolamide, dichlorophenamide 5.Muscarinic agonists- Physostigmine, Carbachol,bethanechol,pilocarpine,neosti gmine,demecurium DRUGS USED IN GLAUCOMA
- 20. MUSCARINIC AGONISTS(PARASYMPATHOMIMETICS)-MIOTICS Pilocarpine (0.5%) Topical Mechanismof action:- Activation of M3 receptor causes contraction of ciliary muscle drainage of aqueous humor # Echothiaophate :- AChE inhibitors - outflow WIDE ANGLE GLAUCOMA
- 21. SE:- diminishedvision headache, brow pain spasm of accommodation Current status:- several drawbacks they are now used only as the last option
- 22. (α1-Agonists):- adrenaline (topical) formationof aqueous humor by vasoconstriction. AE:- irritation and pigmentation of conjunctiva. Dipivefrine:- prodrug converted into adrenaline inside the eye. Dipivefrine Adrenaline α1 and α2 receptor Sympathomimetic + Aqueous secretion Reduction of IOP Advantage:- Better tolerated and longer acting than adrenaline Uveoscleral outflow(β)
- 23. Use topically(1%) asan adjunct α2 Agonist-Apraclonidine Reduction of IOP Side effects:- Itching Lid dermatitis Follicular conjunctivitis Mydriasis Eye lid retraction Dryness of mouth & nose Apraclonidine α2 Agonist formation of aqueous humor
- 24. PGF2α-analogues • First linedrug • Once daily dosing Mechanism:- 1.PG analogues Prostanoid receptors (ciliary muscle) Decreases IOP 2. Uveoscleral outflow SE:- Conjunctival hyperemia Eyelash growth stimulation Pregnant women should avoid prostaglandin analogues (which can cause uterine contractions)
- 25. Once dailyadministration in evening Potent IOP lowering effect Mean IOP reduction(by 25-35%) Advantage:- good efficacy once daily application absence of systemic complications PG-analogues have become the first choice drugs in developed countries
- 26. Non-selective -Timolol maleate Levobunolol Metipranolol Carteolol Selective β1-blocker - Betaxolol -blockers Drugs:- Timolol(0.5% topical), Betaxolol, carteolol , levobunolol, (betaxolol, timolol) having neuroprotective action β-blockers blunt the ganglion cell death in glaucoma .eg- Levobetaxolol People with asthma should avoid beta-blockers and parasympathomimetics (which can cause bronchospasm)
- 27. Advantages over miotics:- nochange in pupil size – no headache no fluctuations in i.o.p once / twice daily administration Mechanism:- block β-receptors in ciliary body ↓c-AMP aqueous humor
- 28. Integral partof glaucoma management 2nd line medication Work well when added to prostaglandins If twice daily dosing required early morning and then 12 hrs later Use in clinical practice
- 29. BETAXOLOL Selective β1- blocker Less likely to cause bronchospasm Less likely to cause systemic side effects Neuroprotective effect- Ca⁺⁺-channel blocker effect
- 30. 1. Topical –Dorzolamide , Brinzolamide 2. Oral – Acetazolamide, Methazolamide Mechanism:- These drugs inhibit carbonic anhydrase enzyme Reduces formation of HCO₃⁻ IOP reduction Carbonic anhydrase inhibitors
- 31. Malaise, fatigue,nausea, loss of appetite, taste alteration Confusion, drowsiness, hearing dysfunction Renal stones & polyuria Hyponatremia Hypokalemia Severe kidney or liver dysfunction Adrenal gland failure Hyperchloremic alkalosis Pregnancy-teratogenic effect Adverse Effect:- Contraindication:-
- 32. Short actingmiotics:- pilocarpine (drug of choice) , physostigmine, carbachol. Carbonic Anhydrase Inhibitors: given locally as dorzolamide or orally as acetazolamide Alpha 2 agonists as Brimonidine. osmotic agents :- Mannitol , Urea Mannitol – i.v 1.5-2g/Kg infusion over 30min Urea – i.v 1-1.5g/Kg slow infusion CLOSED ANGLE GLAUCOMA
- 33. Note:- Avoid mydriaticsin closed angle glaucoma.(Q). Recently Beta blockers are used with pilocarpine. Drugs Contraindicated in Glaucoma: Antimuscarinic drugs:- atropine, hyoscine, and synthetic substitutes homatropine, tropicamide, and cyclopentolate. Ganglion blockers:-e.g trimethaphan. Drugs with atropine- like action: 1st-generation antihistaminics- antiarrhythmic drugs-Disopyramide Tricyclic antidepressants-Phenothiazine antipsychotics Glucocorticoids: such as cortisol, may also cause cataract. Vasodilators: as nitrates and fenoldopam. Succinylcholine: depolarizing neuro-muscular blocker.
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Editor's Notes
- #32 Evening time glacoma ppt more coz evening time puple dialate more