Mydriatics  Amphotericin B: cause electrolyte imbalance

 Short –acting: phenylephrine and tropicamide and cell death; may be reversed by osmotic
 Intermediate-acting: cyclogyl control of the cell
 Long-acting: atropine  Natamycin: accumulates in the cell
 Indications: refraction, dx’c & tx’c dilation membrane; disrupts phospholipid film; not
 ADR: HPN, glaucoma in NOA’s, psychosis, reversible
nightmares, flushing, palpitation, fever  Azoles: fluconazole, itraconazole, miconazole,
ketoconazole
Miotics  Interferes with synthesis of ergosterol in
 Pilocarpine fungal membrane; direct action causing
 Indications: treatment of angle closure glaucoma, membrane to be leaky
aids in ophthalmic laser procedures (iridotomies,  Flucytosine: incorporated into fungal RNA, interferes
refractive laser) with protein synthesis
 ADR: retinal detachment in high myopes
Antibiotics: ADR’s
Antibiotics  Toxicities
 Anti-bacterial, anti-virals, anti-fungals  Punctate or filamentary keratitis
 Indications: tx of infection (name 7 possible types of  Hypersensitivities: contact blepharodermatitis
periocular or ocular infections)  Ocular discomfort in anti-fungals
 Preparation: drops or ointments  Generally:
 Routes of administration: topical, subconjunctival,  ointments more toxic than drops
intravitreal (*oral)  Anti-virals and anti-fungals more toxic than
 Anti-bacterials: anti-bacterials
 Erythromycin, erythromycin-colistin, fucidic  Aminoglycosides most toxic among
acid, tobramycin, gentamycin, antibacterials
sulfacetamide, sulfacetamide-
chloramphenicol, polymyxin-neomycin- Topical steroids
gramicidin/bacitracin combinations,  ANTI-INFLAMMATORY effect
quiniolones (ciprofloxacin, ofloxacin,  INJURY (traumatic, infectious, autoimmune
levofloxacin, etc.)  Infiltration by inflammatory cells
 Edema
Anti-bacterials:  New vessel formation
Mechanism of Action  Corneal melting
 Penicillins, cephalosporins, vancomycin, bacitracin:
inhibit bacterial cell wall synthesis; disruption of The role of PMN’s in tissue injury
bacterial cell wall  Inflammatory Cell infiltration (PMN’s
 Polymyxin, colistin: alters bacterial cell wall  Release of hydrolytic enzymes
permeability, leakage of intracellular compounds
 Denaturation of protein and necrosis of tissue
 Chloramphenicol, tetracycline, erithromycin: o Corneal melting
reversible inhibition of protein systhesis
o Formation of scar tissue
 Aminoglycosides: alteration of protein synthesis by
o Visual loss
binding to 30s bacterial ribosome unit leading to cell
o Final healing
death
o Termination of inflammation
 Quinilones: interruption of bacterial nucleic acid
metabolism through inhibition of DNA supercoiling
Steroids: MOA
and systhesis
 Steroids control PMN’s by:
 Sulfonamides: blockage of specific metabolic steps
essential to the microorganism  Producing involution of inflammatory cells
 Suppressing migration of additional PMN’s
Anti-virals and MOA  Inhibit release of hydrolytic enzumes from
 trifluorothymidine: Inhibits thymidylate synthetase inflammatory cells
and thus DNA sysnthesis, incorporated into viral
DNA; more effective in treating steroid treated ulcers Steroids: Indications
 idoxuridine: resembles thymidine; incorporated into  External diseases of the eye: allergic conjunctivitis,
viral DNA; affects virus-infected cells and normal corneal graft rejection, sympathetic ophthalmia,
cells mucous membrane diseases, marginal corneal melts,
 Acyclovir/ gancyclovir: cells infected with HSV disciform keratitis, padi keratitis, scleritis, phlycten,
specifies an enzyme, thymidine kinase which allergic contact dermatitis
mediates the phosphorylation of acyclovir into an  Glaucoma: phacolytic glaucoma, glaucomato-
active form; phosphorylated acyclovir is incorporated iridoclyclitic crisis, acute angle closure glaucoma
into viral DNA chain and disrupts further viral  Diseases of the orbit and optic nerve: thyroid-related
replication orbitopathy, orbital pseudotumor, optic neuritis,
retrobulbar neuritis
 Trauma: acute chemical burns
Anti-virals  REMEMBER: except for adrenal insufficiency,
 Failure to heal of viral corneal ulcer: corticosteroids are neither curative nor specific
 Resistant infection
 Toxicity Steroids: Routes of administration:
 Least toxic and most specific of anti-virals: acyclovir  Topical:
and gancyclovir  Mild steroids: flurometholone
 Moderately strong:
Anti-fungals: MOA dexamethasone, prednisolone
 Polyenes: bind to ergosterols in fungal cell acetate 0.5%
membrane  Strong steroids: predisolone
acetate 1%
  Subconjunctival/Subtenon’s- triamcinolone
 Intravitreal- dexamethasone phosphate
 Oral: prednisone 5 or 10 mg tabs
 ADR: cataract and glaucoma

Topical NSAID’s
 Examples: diclofenac, ketorolac
 Indication: anit-inflammatory action in patients where
steroids are too strong or contraindicated (steroid-
responders); to maintain intra-operative mydriasis
 ADR: punctate keratitis

Combination Steroid-Antibiotics
 Examples:
 prednisolone acetate-neomycin-polymyxin;
 gentamycin-flurometholone
 Dexamethasone-neomycin-polymyxin
 Tobramycin-dexamethasone
 For use in inflammatory conditions of the eye where
antibiotic prophylaxis is desired
 Viral conjunctivitis
 Post-op patients to control inflammation

Anti-glaucoma Meds
 Indication: to control intraocular pressure in
glaucoma patients
 MOA:
 Beta blockers: (betaxolol, timolol,
levobunolol, metopranolol)- decreases
aqeuos humor formation
 Pilocarpine
 Mannitol, acetazolamide, dorzolamide:
increases outflow of aqueous humor
 Prostaglandin analogs: latanoprost,
travoprost- increases uveoscleral outflow or
aqueous humor
 Alphagan: aqueous suppressant also like PG
analog

Anti-allergic Meds
 Antihistamines:
 Mast cell stabilizers
 Examples: olopatadine, cromolyn sodium, ketotifen

Artificial Tears
 For dry eye problems
 E.g.’s : tears naturale, refresh, lacryvisc, genteal,
vidisic gel, hialid, systane, etc.
 With allergies or toxicities if with preservatives