Glaucoma drugs Flashcards
What causes open angle glaucoma?
Caused by clogging of the trabecular
meshwork with decreased drainage of the aqueous humor.
Often undetected by patients until it is advanced, because it is
not painful. Causes elevated eye pressures, optic nerve
atrophy, and decreased vision once disease is advanced.
What causes closed angle (acute) glaucoma?
A MEDICAL EMERGENCY. Patients can lose all vision in the eye within hours. Most common
mechanism is a pupillary block. The lens is attached to the iris, and pushes the iris anteriorly, which closes the angle between the
iris and the cornea. As the iris-corneal angle closes, the trabecular meshwork gets blocked. With no exit pathway, fluid builds up in
the chambers and creates a pressure gradient rapidly and acutely, which then damages the optic nerve.
Presentation: Acute eye pain, red eye, poorly reactive pupil, seeing halos, Increased Intra-Ocular Pressure (IOP), N/V
What are the prostaglandin analogues?
Latanaprost, travaprost, bimatoprost, unoprostone.
“Prost” drugs
What is MOA of prostaglandin analogues?
Lower IOP by increasing the rate of fluid outflow from the eye by increasing uveoscleral outflow (space between choroid and sclera) - Increases the rate of fluid outflow from traditional meshwork outflow
Prostaglandin analogues: Indications
Can be used with all glaucomas (with rare exceptions). Contraindicated with herpes keratitis (viral infection of the eye caused by HSV; causes rare inflammatory glaucoma).
Prostaglandin analogues: Side Effects
- Ocular irritation and conjunctival injection
- Increased iris and periocular skin pigmentation
with longer. Thicker eyelashes
POSSIBLY DANGEROUS:
- Uveitis
- Possible herpes activation
- Cystoid macular edema
What are beta-blockers used for glaucoma treatment?
Timolol (Non-selective), carteolol (non-selective), levobunolol (non-selective), metipranolol (non-selective), betaxolol (selective)
Beta-blockers: MOA
All are eyedrops. Reduce IOP by blocking beta-adrenergic R’s within the ciliary body epithelium to reduce the production of aqueous fluid.
Beta-blockers: Indications
All types of glaucoma. Non-selectives are absolutely contraindicated with asthma, COPD and greater than 1st degree heart block.
All beta-blockers are
absolutely contraindicated with
CHF.
Relative contraindication with sinus
bradycardia, hypotension, hx of syncope, hx of life threatening
depression, brittle insulin dependent
diabetes, impotence.
Beta-blockers: Side effects
- Due to topical route: corneal toxicity and
allergic reaction. - Non-selective (1st 4) can be absorbed
systemically and have SE’s of
SOB/bronchospasm/CHF; decreased
libido/impotence’ arrhythmias, bradycardia;
depression.
To reduce level of beta-blocker absorbed into systemic circulation, pts should be taught
nasolacrimal occlusion method of eye drop
application.
What are the alpha-2-agonists?
Brimonidine and apraclonidine
Alpha-2-agonists: MOA
Decrease IOP by: Lowering amount of aqueous fluid produced and increasing the
outflow through the
uveoscleral outflow
pathway.
Alpha-2-agonists: Indications
Use brimonidine for all types of
glaucoma.
Use apraclonidine for IOP spikes
following laser surgery for glaucoma.
Contraindicated with MAO-inhibitor
use and for patients less than 2 yrs.
Side effects of brimonidine?
Dry mouth, fatigue, ocular redness,
ocular irritation.
Side effects of apraclonidine?
Severe allergic blepharitis,
tachyphyalaxis with chronic use, mydriasis, eyelid
retraction and conjunctival branching.
Which drugs can cause systemic side effects?
Prostaglandin analogues, beta-blockers and CAIs can case systemic side effects
• α-2-agonists don’t have many systemic effects unless used chronically, but do drip into mouth -> dry mouth
Which drugs reduce IOP by decreasing amt of aqueous fluid produced?
Beta-blockers and CAIs reduce IOP by reducing the amount of aqueous fluid produced
Which drugs reduce IOP by increasing outflow of fluid from eye?
Prostaglandins reduce IOP by increasing the outflow of fluid from the eye
Which drugs reduce production of aqueous fluid and increase outflow?
Alpha-2 agonist reduce the production of aqueous fluid AND increase the outflow
What reaction does carbonic anhydrase catalyze?
Hydration of CO2 and dehydration of bicarbonate.
Parietal cells use CA to secrete stomach into acid.
Pancreatic duct cells use CA to secrete bicarbonate.
RBC convert CO2 to bicarbonate fro transport then back to CO2 to be exhaled by lungs using CA.
Renal tubules secrete H+ to maintain acid-base and fluid balance using CA.
Cells producing CSF, aqueous fluid in eye, endolymph of semicircular canals, cochlear duct, perilymph of scala vestibuli and scala tympnai all contain high levels of CA.
What are the carbonic anhydrase inhibitors (CAIs)?
Dorzolamide (topical)
Brinzolamide (topical)
Acetazlamide (oral)
Methazolamide (oral)
CAI: MOA
Inhibiting CA in ciliary body
epithelium. Decreases IOP.
CAI: Indications
Acetazolamide was first CAI used,
the “prototype”, used as diuretic.
Has remained in popular use worldwide for effects on specific tissues as described above, and today’s main use is in the tx of glaucoma.
Used topically for all glaucomas. Can be used orally for rapid lowering of acute increases in IOP; when a patient has poorly tolerated other topical glaucoma medications
Absolute contraindication:
sulfonamide allergy, SCD, aplastic
anemia, thrombocytopenia
Relative contraindication: adrenal insufficiency, hepatic failure, chronic respiratory acidosis, renal failure, metabolic acidosis, repeated kidney stones.
CAI: Side Effects
TOPICAL: Stinging, burning, redness /dermatitis / conjunctivitis, allergy, transient
myopia, metallic taste.
ORAL: Parasthesis, frequent urination,
metabolic acidosis, metallic taste.
These drugs are structurally similar to
sulfonamides – so if a patient has an allergy, they
should not take CAIs.
