1. Drugs for diseases and disorders of eyes

3. Fluorescine
Detection of corneal lesions and foreign bodies
Adult: Apply 1% or 2% solution as eye drops or as sterile papers impregnated with fluorescein sodium. May also be given in combination with a local anaesthetic: as a 0.25% solution with oxybuprocaine HCl or proxymetacaine HCl.

4. Topical Drugs Used for Diagnosis: Fluorescin Dye
Fluorescein strip:
water soluble
No systemic complications
Beware of contact lens staining
Cobalt blue light
Orange becomes green
Eye with corneal ulcer

5. Anesthetics Example: Uses: Side effects:
Propracaine Hydrochloride 0.5%
Tetracaine 0.5%
Uses:
Anesthetize cornea within 15 sec, last 10 mins
Remove corneal foreign bodies
Perform tonometry
Examine damaged corneal surface
Side effects:
Allergy: local or systemic
Toxic to corneal epithelium ( inhibit mitosis, migration)

6. Mydriatics (pupil dilation)
Two classes:
Cholinergic-blocking ( parasympatholytic)
Adrenergic-stimulating (sympathomimetic)
Iris sphincter constrict pupil
Pupillary dilator muscles

7. Cholinergic-Blocking drugs
Action
Dilate by paralyzing iris sphincter muscle
Cycloplegia by paralyzing ciliary body muscles
Tropicamide
Max pupil dilatation 30 min
Effect diminishes 4-5 hrs
Side effects:
Rare
Nausea / vomiting
Pallor vasomotor collapse
Other examples:
Homatropine hydrobromide 1% or 2%
Atropine sulfate 0.5% or 1%
Scopolamine hydrobromide 0.25% or 5% (last 1-2 wks)

8. Adrenergic Stimulating Drugs
Phenylephrine 2.5% or 10%
Dilates in 30 mins, no effect on accommodation
Pupil remains reactive to light
Combine with Tropicamide for maximal dilatation
Infants combine Cyclopentolate 0.2% & Phenylephrine 1%
Side effects:
acute hypertension or MI (with 10%)

9. Topical Therapeutic Drugs
Anti-allergics
Combination naphazoline+antazoline
Decongestant+antihistamine
Mast cell stabilizers
Anti-inflammatory
Topical steroids should NEVER be prescribed by primary care physician
Non steroidals: e.g. diclofenac
Uses : ocular itch, macular edema, prevent pupil constriction during cataract Sx
Decongestants:
Over the counter weak adrenergic-stimulating drugs
Vasoconstriction = white eyes temporarily
E.g. Naphazoline % Phenylephrine 0.12% Tetrahdrozaline0.05%
Side effect
rebound vasodilatation, common
acute angle closure glaucoma, rare

10. Ocular side effects of systemic drugs
Steroids
Anti-inflammatory
PSCC,
Steroid induced glaucoma
Chloroquine
Rx of RA, SLE
Corneal deposits
Bull’s eye maculopathy
250mg qd, or 300g total
Digitalis (Digoxin)
Atrial Fibrillation
Yellow vision most common sign of intoxication
Amiodarone
Cardiac arrhythmias
Cornea verticillata (whorls)
Diphenylhydantoin
Seizure
Horizontal nystagmus in lateral gaze, vertical nystagmus in up gaze
Ethambutol
TB chemotherapy
Optic neuropathy
Chlorpromazine
Schizophrenia
Punctate Corneal epithelial opacities
Thioridazine
psychosis
Pigmentary retinopathy

11. Many drugs can increase IOP
The potential to induce or worsen glaucoma depends on the type of glaucoma and on whether it is adequately controlled.
Closed-angle glaucoma occurs when there is a physical blockage of the trabecular meshwork, resulting in increased IOP.

12. Drugs That May Induce or Potentiate Increased IOP
Closed-angle glaucoma
Topical anticholinergics
Topical sympathomimetics
Systemic anticholinergics
Heterocyclic antidepressants
Low-potency phenothiazines
Antihistamines
Ipratropium
Benzodiazepines (low risk)
Theophylline (low risk)
Vasodilators (low risk)
Systemic sympathomimetics (low risk)
CNS stimulants (low risk)
Selective serotonin reuptake inhibitors
Imipramine
Venlafaxine
Topiramate
Tetracyclines (low risk)
CAIs (low risk)
MOA inhibitors (low risk)
Topical cholinergics (low risk)
Open-angle glaucoma
Ophthalmic corticosteroids (high risk)
Systemic corticosteroids
Nasal/inhaled corticosteroids
Fenoldopam
Ophthalmic anticholinergics
Succinylcholine
Vasodilators (low risk)
Cimetidine (low risk)

13. TREATMENT OF OCULAR HYPERTENSION AND OPEN-ANGLE GLAUCOMA
Treatment is indicated for ocular hypertension if the patient has a significant
risk factor such as IOP greater than 25 mm Hg, vertical cup-disk ratio greater than 0.5, or central corneal thickness less than 555 micrometers. Additional risk factors to be considered include family history of glaucoma, black race, severe myopia, and presence of only one eye.
Treatment is indicated for all patients with elevated IOP and characteristic
optic disk changes or visual field defects.
Drug therapy is the most common initial treatment and is initiated in a
stepwise manner, starting with a single well tolerated topical agent (Table
66-2). Historically, β-blockers (e.g., timolol) were the treatment of choice
and continue to be used if there are no contraindications to potential
β- blockade caused by systemic absorption.
β-Blockers have the advantage of
low cost owing to generic formulations. •

14. Newer agents are also suitable for first-line therapy.
Prostaglandin analogs
(e.g., latanoprost, bimatoprost and travoprost) have the advantage of strong potency, unique mechanism suitable for combination therapy, good safety profile, and once-a-day dosing.
Brimonidine has the theoretical advantage of neuroprotection, which has not yet been demonstrated in humans.
Topical CAIs are also suitable for first-line therapy.

15. Pilocarpine and dipivefrin, a prodrug of epinephrine, are used as thirdline therapies because of adverse events or reduced efficacy as compared with newer agents.
Carbachol, topical cholinesterase inhibitors, and oral CAIs (e.g., acetazolamide)
are used as last-resort options after failure of less toxic options.
The optimal timing of laser or surgical trabeculectomy is controversial, ranging from initial therapy to after failure of third- or fourth-line drug therapy.
Antiproliferative agents such as fluorouracil and mitomycin C are used to modify the healing process and maintain patency.

16. TREATMENT OF CLOSED-ANGLE GLAUCOMA
Acute closed-angle glaucoma with high IOP requires rapid reduction of IOP. Iridectomy is the definitive treatment, which produces a hole in the iris that permits aqueous flow to move directly from the posterior to the anterior chamber.
Drug therapy of an acute attack typically consists of an osmotic agent and secretory inhibitor (e.g., β-blocker, α2 agonist, latanoprost, or CAI), with or without pilocarpine.
Osmotic agents are used because they rapidly decrease IOP. Examples : glycerin, 1 to 2 g/kg orally, and mannitol, 1 to 2 g/kg IV.
Although traditionally the drug of choice, pilocarpine use is controversial as initial therapy. Once IOP is controlled, pilocarpine should be given every 6 hours until iridectomy is performed.
Topical corticosteroids can be used to reduce ocular inflammation and synechiae.
Epinephrine should be used with caution because it can precipitate acute closed-angle glaucoma, especially when used with a
β-blocker.

17. EVALUATION OF THERAPEUTIC OUTCOMES
Successful outcomes require identifying an effective, well-tolerated regimen; closely monitoring therapy; and patient adherence.
Whenever possible, therapy for open-angle glaucoma should be started as a single agent in one eye to facilitate evaluation of drug efficacy and tolerance. Many drugs or combinations may need to be tried before the optimal regimen is identified.
Monitoring therapy for open-angle glaucoma should be individualized.
IOP response is assessed every 4 to 6 weeks initially, every 3 to 4 months
after IOPs become acceptable, and more frequently after therapy is
changed. The visual field and disk changes are monitored annually, unless glaucoma is unstable or worsening.
Patients should be monitored for tachyphylaxis, especially with
β-blockers or apraclonidine. Treatment can be temporarily discontinued to monitor its benefit.
There is no specific target IOP because the correlation between IOP and
optic nerve damage is poor. Typically, a 25% to 30% reduction is desired.

18. The target IOP also depends on disease severity and is generally less than 21 mm Hg for early visual field loss or optic disk changes, with progressively lower targets for greater damage. Targets as low as less than 10 mm Hg are desired for very advanced disease, continued damage at higher IOPs, normal tension glaucoma, and pretreatment pressures in the low- to mid-teens.
Using more than one drop per dose increases the risk of adverse events and cost, but not efficacy.
Patients should be educated about possible adverse effects and methods for preventing them.

19. Patients should be taught how to administer topical therapy
Patients should be taught how to administer topical therapy. With a forefinger pulling down the lower eyelid to form a pocket, the patient should place the dropper over the eye, look at the tip of the bottle, and then look up and place a single drop in the eye. To maximize topical activity and minimize systemic absorption, the patient should close the lid for 1 to 3 minutes after instillation and place the index finger over the nasolacrimal drainage system in the inner corner of the eye.
If more than one topical drug is required, instillation should be separated by 5 to 10 minutes to provide optimal ocular contact.
Adherence to drug therapy should be monitored because it is commonly inadequate and a cause of therapy failure.

20. Systemic Side Effects of Glaucoma Meds
Beta blockers
Timolol, levobunolol, metapranolol, carteolol
Nonselective
↓ Aqueous production
Bronchospasm  Ø Asthma, COPD
Bradycardia  Precipitate or worsen cardiac failure
Betaxolol
Cardio selective  avoids pulm. side effects
Cholinergic-stimulating drugs
Pilocarpine
↑aqueous outflow
Side effects
Miosis
Headache
Systemic: lacrimation, N/V, diarrhea
Echothiophate
Long acting anticholinestrase
Inactivates plasma cholinestrase,  pt more susceptible to effect of succinylcholine
Prolonged apnea or death reported

21. Systemic Side Effects of Glaucoma Meds
Alpha-2 adrenoceptor agonist
Brimonidine: (Alphagan)
↓ aqueous production, ↑uveoscleral outflow
Hypotension & apnea in infants
Local allergic conjunctivitis
Dry mouth, fatigue, headache
Apraclonidine: (Iopidine)
Used against pressure spikes after iris laser
Orthostatic hypotension
High allergic conjunctivitis
Adrenergic-stimulating drugs: (Epinephrine, Dipivefrin)
Arrhythmias, HTN,
Prostaglandin analog
Latanoprost (Xalatan) PGF2α
↑ uveoscleral outflow
Iris darkening
Elongation of eye lashes
CME
Carbonic anhydrase inhibitors
Oral Acetazolammide (Diamox)
Sulfur allergy
Parasthesia, anorexia, metallic taste, renal calculi
Topical Dorzolamide (Trusopt)
Same side effects but lower