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ANTI GLAUCOMA DRUGS
Bikash Sapkota16th batch B. Optometry
Maharajgunj Medical CampusNepal
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Presentation Layout
Introduction to glaucoma Anti glaucoma drugs: Classification Indications Contraindications Summary
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Introduction
VISUAL FIELD LOSS
OPTIC NERVE
DAMAGE
GLAUCOMA
INCREASE
IOP
Glaucoma refers to a group of diseases characterized by
• Optic neuropathy• Specific pattern of visual field
defect• Raised IOP
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Aqueous production and drainage Secretion of aqueous humour -ciliary body (posterior chamber) Route of drainage -primary (90%) : trabecular meshwork -uveo-scleral outflow(10%)
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Purpose of initiating glaucoma therapy
The ultimate goal of glaucoma treatment is
To preserve enough vision during the patient’s lifetime to meet their functional needs
Ideally, treatment should also delay glaucomatous process
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MEDICAL ASPECTS OF GLAUCOMA THERAPY
o When to treat ? - when glaucomatous damage is documented or future
damage is likelyo What to prescribed ? - best to try one drug with least ocular & systemic side
effects
- use least amount of medication
- in emergency use 2 drugs
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Mechanisms of action of anti glaucoma agents
Chief therapeutic measure is to lower IOP to the target level either by o Reducing aqueous production in the ciliary bodyo Promoting aqueous humour outflow through the
trabecular meshwork o Promoting aqueous humour outflow via the uveoscleral
pathway
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Beta blockers e.g. timolol, carteolol, betaxolol,levobunolol and metipranolol
Classification of anti glaucoma drugs
Adrenergic agonists e.g. epinephrine, dipivefrin, brimonidine and apraclonidine
Prostaglandin analoguee.g. latanoprost, bimatoprost ,unoprostone
Cholinergic agents e.g. pilocarpine, carbachol,demecarium bromide and echothiophate iodide
Carbonic anhydrase inhibitors e.g. dorzolamide and brinzolamide
Topical Drops
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Carbonic anhydrase inhibitors e.g. acetazolamide and methazolamide
Osmotic agents e.g. glycerine, mannitol and urea
Systemic Drops
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Beta blockers First drug of choice for POAG Lower IOP by reducing aqueous secretion due to their
effect on β2 receptors
Non selective β1 & β2
Timolol
Levobunolol
Metipranolol
Carteolol
Selective β1 blockers
Betaxolol
Pindolol
Metaprolol
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β-blockers are ineffective during sleep
Topical β-blockers reduce aqueous formation by 24% to 48% in
awake humans
Antagonize the effect of catecholamines
Reduction in aqueous secretion
Mechanism of action
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Beta blockers TimololMost commonly used agentNon-selective β blockerAs a salts of : maleate, Hemihydrate Efficacy oIOP decrease : 20% to28%oPeak – 2-3 hrsoWashout : 1 month
Concentration: 0.25% & 0.5%,
1-2 times daily
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Beta blockers Short term escape:
Marked initial fall in IOP followed by transient rise with moderate fall in IOP
Long term drift:
Slow rise in IOP in patients who were well controlled with many months of therapy
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Beta blockers Carteolol Non selective beta blockerAs effective as timolol Intrinsic sympathomimetic activity and ability to partially
activate β-receptors in the absence of catecholamines
Advantages oLess stingingoBest choice in pt. with POAG having associated hyperlipidemias
or atherosclerotic cardiovascular disease
Concentration : 1% drop, 1-2 times daily
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Beta blockers Levobunolol Reduces IOP by oReducing aqueous humor formation
Advantage oAction lasts the longest, so is more reliable for once a day use than timolol
Contraindications oPts. predisposed to cardiac or respiratory disease
Concentration : 0.25 – 0.50% drop,
once daily
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Beta blockers Betaxolol First selective β1 blocker used
in ophthalmology Long term effect is slightly less than Timolol and Levobunolol
Advantage oInitial therapy in pts. with asthma and other pulmonary problems
Concentration : 0.25% drop,
2 times daily
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Adverse effects of β-blockers
Cardiovascular-Bradycardia-Conduction arrhythmias-Hypotension-Raynaud’s phenomenon-Fluid retention
Pulmonary-Bronchoconstriction/ bronchospasm-Asthma-Dyspnea
Central nervous systemAmnesiaDepressionConfusionHeadacheImpotenceInsomniaMigraine prophylaxisMyasthenia gravis
GastrointestinalDiarrheaNausea
DermatologicAlopeciaNail pigmentationUrticariaLichen planus
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Ocu
lar
side
eff
ects
Beta blockers Allergic blepharoconjunctivitis
Dry eye/decreased tear breakup time
Corneal anesthesia
Macular edema (aphakics)Macular hemorrhage/retinal
detachmentUveitis
Cataract progression
Allergic blepharoconjunctivitisDry eye/decreased tear breakup
timeCorneal anesthesia
Macular edema (aphakics)Macular hemorrhage/retinal
detachmentUveitis
Cataract progression
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Beta blockers Open angle Glaucoma
Angle closure Glaucoma
Secondary Glaucoma
Glaucoma in children
Indications
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Beta blockers
Bronchial asthmaHistory of bronchial asthmaSevere COPDBradycardia Severe heart blockOvert cardiac failureChildren & infants
Contraindications
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Beta blockers
Clinical issues Preferred drugBest IOP control Avoid BetaxololCost Generic Timolol
MetipranololTimolol hemihydrate
Comfort CarteololHypercholesterolemia CarteololCOPD BetaxololPregnancy Avoid all
Selection of β-Blockers
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Adrenergic agonist Mode of action Decreasing aqueous formation by constricting the
ciliary blood vessels Increasing uveoscleral outflow by an increase in
prostaglandin synthesis
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Adrenergic agonist
α and β agonist
Epinephrine
Dipivefrin
Phenylephrine
α2 selective
Apraclonidine
Brimonidine
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Adrenergic agonist
EpinephrineNonselective α- and β-adrenergic agonist Onset of action occurs at 1 hr Peak effect at 4 hours Ocular hypotensive effect may last up to 72 hoursIOP control : 20 -25 %
Concentration : 0.5-2% drop,
2 times daily
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Adrenergic agonist Side effects of epinephrine StingingBrowacheConjunctival hyperemiaAdenochrome depositsAllergic lid reactions Macular edema Blepharoconjuntivitis Systemic hypertensionArrythmia
Contraindications o Severe Hypertensiono Cardiac Diseaseso Thyrotoxicosis
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Adrenergic agonist DipivefrinProdrugPenetration across the cornea is 17 times more than epinephrineBetter tolerated than epinephrineOnset of action : 30 minutes, Peak effect : 1hr IOP reduction :20-24%
AdvantageoLower cardiovascular side effects oCan be used in pts. of asthma, in young pts. intolerant to
miotics and in those with cataracts
Concentration : 0.1% drop,
2 times daily
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Adrenergic agonist Phenylephrine Acts on α1 adrenergic receptors MOA : Induce vasoconstriction and mydriasis to break posterior
synechiae Can produce mydriasis even in pts. treated with strong
miotics
Concentration : 0.125-10 %drop
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Adrenergic agonist Apraclonidineα2-adrenergic agonist Para amino derivative of clonidineIOP control : 20 % -30 % Maximal effect is produced 3-5 hours after dosing
Not used as primary treatment due to significant tachyphylaxis Mainly indicated in acute pressure spikes in case of laser iridotomy, trabeculoplasty, and posterior capsulotomy
Concentration : 1% and 0.5%, twice daily
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Adrenergic agonist BrimonidineSmall effect on uveoscleral
outflowNeuroprotection IOP control: 20-30%
AdvantageoCan be used as primary drug in POAGoLess tachyphylaxis & less rate of allergic
reactions than apraclonidine
Concentration :tartrate 0.2%, tartrate in purite 0.1%BD, TID
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Adrenergic agonist
OcularoAllergyoContact dermatitis oBlurred visionoBurning/ stingingoFollicular conjunctivitisoHyperemia/itchingoPhotophobia
Side effects SystemicoDry mouthoFatigueoDrowsinessoHeadacheoHypotensionoBradycardia in neonatesoHypothermia in neonates
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Cholinergic drugs
contraction of the longitudinal fibers of the ciliarymuscle, producing tension on the scleral spur: (Opening the trabecular meshwork) and facilitating aqueous outflow
Contraction of the circular fibers of the ciliary muscle, relaxing the zonular tension on thelens equator : Accommodation
Contraction of the iris sphincter: Constricts the pupil (miosis)
Mec
hani
sm o
f acti
on
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Classification of Cholinergic AgonistsDirect-actingAcetylcholineMethacholinePilocarpine ▪ drop- 0.5, 1, 2, 4, 6 %,gel-4%
Carbachol ▪ drop-1.5, 3%
Indirect-acting (cholinesterase inhibitors)ReversiblePhysostigmineNeostigmineEdrophoniumDemecariumIrreversibleEchothiophate ▪ drop-0.125%Diisopropylfluorophosphate
▪ Formulated for topical ocular use
Activate cholinergic receptors directly at the neuroeffector junctions of the iris sphincter muscle and ciliary body
Exert their cholinergic effects primarily by inhibitingcholinesterase, thereby making increased amountsof acetylcholine available at cholinergic receptors
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Cholinergic drugs Pilocarpine Derived from the plant Pilocarpus
MicrophyllusIOP decrease : 15-25%Peak : 1 ½ - 2hrsEffect lasts up to : 6-8 hrs Gel form at bedtime
Concentration : 0.25- 10% drop QID, 4% gel, ocusert:20-40µg/hr
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Ocular pigmentation influences
Blue eyes show maximal ocular hypotensive responses
Darkly pigmented eyes demonstrate a relative resistance to IOP reduction
may require pilocarpine solutions in concentrations exceeding 4%
Cholinergic drugs
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Cholinergic drugs
Acute and chronic narrow angle glaucoma Open angle glaucoma For prophylaxis of primary angle-closure glaucoma until a
peripheral iridotomy can be performed
Indications
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Ocular Side Effects Accommodative spasm Miosis Follicular conjunctivitis Pupillary block with
secondary angle-closure glaucoma
Band keratopathy Allergic
blepharoconjunctivitis Retinal detachment Conjunctival injection Lid myokymia Anterior subcapsular
cataract Iris cyst formation
Systemic Side Effects Headache Browache Marked salivation Profuse perspiration Nausea Vomiting Bronchospasm Pulmonary edema Systemic hypotension Bradycardia Generalized muscular
weakness Abdominal pain, diarrhea
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o Presence of cataracto Patients younger than 40 years of ageo Neovascular and uveitic glaucomao History of retinal detachmento Asthma or history of asthmao High myopiao Known hypersensitivity to the drug
Cholinergic drugs
Contraindications
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It is a dual acting parasympathomimetic Direct action- by stimulation of end plate potential Indirect action- by inhibition of acetylcholine esterase
Ocular pain, impaired vision due to induced accommodation & myopia
1% for intracameral use during surgery
Carbachol
Acetylcholine
Cholinergic drugs Concentration : 0.75-3%, TID
Side effects
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It is an indirect acting parasympathomimetic
Constriction of sphincter pupillae muscle around
the pupillary margin and thus increases aqueous outflow
Retinal detachment, miosis, cataract, pupillary
block glaucoma, iris cyst, browache and punctal stenosis
Physostigmine
Cholinergic drugs Concentration : 0.25-0.5% drop
Mechanism
Side effects
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Prostaglandin AnalogueOriginally discovered in the eye as mediators of the ocular
inflammatory responsePro-drugsConverted to active compound by corneal esterasesMOA: Increases uveoscleral outflowPG stimulates collagenase and metalloproteinase to degrade the
extracellular matrix between ciliary muscle bundles, which in
turn leads to the reduction of hydraulic resistance to uveoscleral
flow
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Prostaglandin analogueLatanoprost (Xalatan)
Lowers IOP 27-30% with peak at 10-14 hrs Maximum effect usually by 4-6 weeks, may have further
decrease after 3-4 months Latanoprost tends to be less effective in lowering IOP in
children than in adults
Concentration : 0.005% drop, Once daily
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Prostaglandin analogue Travoprost (Travatan)
Lowers IOP 7-9 mmHg (27-33%) Maximum IOP lowering effect achieved within 2
weeks
.
Concentration : 0.004% drop, once daily in evening
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Prostaglandin analogue
Bimatoprost (Lumigan)
Prostamide analog Better IOP control than Latanoprost Maximum IOP effect within 1-2 weeks
.
Concentration : 0.03% drop, Once in the evening
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Prostaglandin analogue
Indications Contraindications
o Primary open angle glaucoma o Normal tension glaucoma o Chronic closed angle glaucoma o Pigment dispersion syndrome o Exfoliation glaucoma
o Allergy o Pregnant and nursing mothero Children o Uveitic glaucoma o Immediate postoperative
period o Pt. with healed or active
herpes simplex keratitis
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Ocular side effects Systemic side effects
o Cornea: punctate erosions, corneal pseudodendrites, recurrent herpes keratitis
o Conjunctiva : hyperemiao Eyelash : lengthening, thickening,o hyperpigmentationo Iris : irreversible hyperpigmentation o periorbital skin : hyperpigmentationo CME after cataract surgeryo Allergyo Anterior uveitis
o Occasional headacheo Skin rasho URTI
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AdvantageoOnce daily dosingoLack of cardiopulmonary side effectsoAdditivity to other anti glaucoma medications
Prostaglandin analogue
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Carbonic anhydrase inhibitor
99% inhibition of CA – decrease aqueous production
• Inhibit enzyme carbonic anhydrase
• Reducing aqueous humour formation
Mechanism of actionMechanism
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Carbonic anhydrase inhibitor
Systemic Acetazolamide
Methazolamide
Ethoxzolamide
Dichlorphenamide
Topical
Dorzolamide
Brinzolamide
Lodoxamide
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Carbonic anhydrase inhibitor
Oral/IV preparationIOP decrease : 15-20% Peak : 2-4 hrs (oral), 30 mins (IV)Washout : 12 hrs (oral ),4 hrs (IV)
Acetazolamide
o Oral : 125mg & 250mg tablet- 6 hrlyo 500mg sustained-release capsules -2 timeso For children(5-10mg/kg)-6 to 8 hrlyo IV preparation- 500mg
Concentration
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Systemic Numbness and tingling of
extremities and perioral region Metallic taste Symptom complex Decreased libido Depression Fatigue Malaise Weight loss Gastrointestinal irritation Metabolic acidosis Hypokalemia Renal calculi Blood dyscrasias Dermatitis
OcularTransient myopia
Side Effects of Acetazolamide
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Clinically significant liver disease Severe chronic obstructive pulmonary
disease Certain secondary glaucoma Renal disease, including kidney stones Pregnancy Known hypersensitivity to sulfonamides
Contraindications to Acetazolamide
Carbonic anhydrase inhibitor
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Potency > acetazolamide Improved intraocular penetration Higher water and lipid solubilities Increased half life and plasma concn
Can be given at lower doses than acetazolamideo Dose : 25-50mg x BD/TDSo Indication : chronic IOP reduction
Carbonic anhydrase inhibitorMethazolamide
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Topical Dorzolamide 2% & Brinzolamide 1%Efficacy IOP decrease : 15-20%peak : 2-3 hrswashout : 10-18 hrsDose : 2-3 times daily
Carbonic anhydrase inhibitor
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Carbonic anhydrase inhibitorOcular side effectsoInduced myopiaoStinging sensationoKeratitis, conjunctivitisoDermatitis
Contrainidications Pt with known hypersensitivity to sulfonamide
Systemic side effectso Similar to oral CAI but less likely
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Hyperosmotic agents IV : Mannitol , urea Oral : glycerol, isosorbide
Mechanism of action
Increase blood osmolality
Osmotic gradient between blood and vitreous
Water is drawn out of vitreous
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Hyperosmotic agents IV Preparation Mannitol
20% solution 1-2gm/kg or 5(2.5-7)ml/kg over 20 minOnset:15-30minPeak:30-60min Last : 6hrs
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Hyperosmotic agents Oral Preparation
Glycerol50% solution ,1gm/kg or 1.5-3 ml/kgOnset: 20min Peak:45mins -2 hrs Duration:4-5hrscaution in Diabetics
Isosorbide
45% solution1.5-4 ml/kg
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Hyperosmotic agents Side effects Gastrointestinal systemoNausea,vomiting,abdominal cramp
Cardiovascular systemoCHF,angina
CNSoSubdural hematoma, Headache, confusion,
disorientation,fever RenaloDiuresis, anuria, potassium loss
OthersoDiabetic ketoacidosis ,urticaria.
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Summary
Open angle glaucoma
1.β-blockers :Timolol, Betoxolol, Levubunolol
2.Miotic : Pilocarpine
3.α adrenergic agonist : Adrenaline, Dipiverdine, Brimonidine
4.Carbonic anhydrase inhibitors : Acetazolamide, Dorzolamide
5.Prostaglandin : Latanoprost
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Angle closure glaucomaCombination of vigorous therapy is employed
1.Beta blocker –Timolol eye drop
2.Miotic – Pilocarpine eye drop every 10 min
3.Hypertonic- mannitol injection (20%)
4.Acetazolamide orally
5.Apraclonidine eye drop
Summary
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Mode of action of anti glaucoma drugs
Beta blocker-decrease aqueous secretionMiotics -increase trabecular outflowAdrenergic agonist-decrease aqueous secretionProstaglandin-increase trabecular and uveaoscleral outflowCarbonic anhydrase inhibitor-decrease aqueous secretion
Summary
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References Clinical Ocular Pharmacology by Jimmy D Balett Ophthalmic Drugs by Graham Hopkins & Richard Pearson Comprehensive Ophthalmology by A.K. Khurana AAO-Section 10-Glaucoma AAO-Section 2-Fundamentals & Principles of Ophthalmology Internet
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