Optho pharm Flashcards
Ocular antihypertensives
Anti-glaucoma drops
- Hits ciliary body (“pump of eye”)
- Turns off the faucet
Classes:
- Beta-blockers (#2 prescribed glaucoma drops after prostaglandin-analogs)
- Prostaglandin analogs
Timoptic, Betagan, Betoptic S, Ocupress, Optipranolol
Ocular beta-blockers (formerly 75% of all glaucoma drops used)
MOA:
- Decrease aqueous production
- Antagonize circulating catacholamines at the B1 and B2 receptors at the ciliary epithelium
Side effects:
- decreased heart rate and BP, shortness of breath,
- fatigue, depression (20 cases of acute suicidal depression),
- decreased libido
- adverse effect on lipid profiles
- Asthma/pulmonary dz, bradycardia, myasthenia gravis, ?IDDM
** Carteolol (Ocupress) nonselective BB with intrinsic sympathomimetic activity (ISA)
- theoretically decreased side effects and less adverse effect on lipids
** Betoptic S (Betaxolol) cardioselective B1
theoretically less breathing problems, 1/10 potency of timolol and levobunalol
BUT, if want to avoid these side effects, use prostaglandin analogs!
Ocular Prostaglandin analog
MOA:
- Increase uveoscleral outflow (relaxation of ciliary muscle and changes in the ECM between muscle fibers) by upregulating matrix metalloproteinases
- *Quickly became first-line (now FDA approved for that) and most prescribed glaucoma medication
- Greater IOP reduction than with beta blocker
- Once a day dosing
Xalatan (Latisse)
Prostagladin analog for glaucoma
7-16% hazel irides turn brown
- Increased size not number of melanocytes
- Hypertrichosis, hyperemia (bedtime dosing), periorbital skin darkening reversible cystoid macular edema (CME), uveitis
Trusopt, Azopt, Diamox, Neptazane
Carbonic anhydrase Inhibitors
- Sulfonamide derivative
MOA:
- Decrease aqueous humor production
- Carbonic anhydrase (CA) present in pigmented and nonpigmented epithelium of ciliary body
AEs:
- Systemic effects:
- Metallic taste, stomach upset, loss of libido, drowsiness, tingling, renal stones, metallic acidosis, hypotension, anemia - Ocular effects:
- Burning, redness, SPK, induced myopia (CB swelling)
Contraindications:
- History of sulfa allergy, renal stones, liver or kidney disease, Addison’s disease or adrenal insufficiency
- Use of thiazide diuretics, steroids, digitalis
- ASA and Diamox (CA inhibitor) may lead to acid-base imbalance and salicylate toxicity
Iopidine, Alphagan P
Alpha-adrenergic agonists
MOA:
- Decreases aqueous production
- ? neuroprotection and increase in uveoscleral outflow
AEs:
- Transient dry mouth and nose, syncope, eyelid retraction, mydriasis, conjunctival blanching, allergic reaction (redness, itching, etc) 13-36%
- Alphagan has primarily Alpha 2 activity
- contraindicated in children and with MAOIs
- Allergy rate 10% (less than with Iopidine)
Pilocarpine, Carbachol, Ocusert
Cholinergic agents= Miotics
- Increases outflow (vs turning off pump) like prostaglandin analogs
MOA:
- Miosis and accommodation
- Longitudinal fibers of the ciliary muscle attach to the TM and scleral spur; contraction of the muscle fibers opens up the TM widening the trabecular spaces to aqueous outflow
- Increased trabecular outflow
AEs:
- Intense miosis and accommodative spasm, iritis, iris cysts, lens induced myopia and anterior chamber shallowing, pupillary block, corneal haze
- Pilocarpine toxicity: salivation, lacrimation, sweating, N/V/D, bronchiolar spasm/pulmonary edema
- Worsens Parkinson’s disease
Atropine, Homatropine, Scopolamine, Cyclopentolate, Tropicamide
Mydriatics/Cycloplegics:
Anticholinergics block effect of acetylcholine
MOA:
- Paralyze the parasympathetic iris sphincter and circular muscle of ciliary body
- Move the lens-iris diaphragm
- Stabilizes blood-aqueous barrier
AEs:
- Atropine toxicity: hot as a hare, red as a beet, dry as a bone, blind as a bat, mad as a hatter
- Decreased GI motility, increased gastric secretions, dry mucous membranes, urinary retention (careful elderly men with BPH), tachycardia, confusion, restlessness
** Atropine= LONG acting
Phenylephrine
Alpha agonist (sympathomimetic) - Mydriatic (dilates pupil) without cycloplegia (no difficulty focusing)
AEs:
- Acute hypertension, pulmonary edema, arrhythmia, death
- Never use 10% in infants
- Avoid in patients with sympathetic denervation (MAOIs, diabetics with neuropathy)
** Could precipitate angle-closure attack in pre-disposed individual with narrow angle
Anti-inflammatory agents
To decrease pressure in acute glaucoma before surgery
Steroids- COMPLICATIONS:
- Watch for steroid-induced glaucoma (accumulation of glycosaminoglycans in the trabecular meshwork)
- Cataract (PSC)
- Delayed wound healing, enhanced microbial/fungal proliferation, punctate keratopathy
NSAIDs:
- Can worsen ocular herpes
- Associated with corneal melting
Antibiotics for ocular problems
Fluoroquinolone= good psuedomonas coverage
- Used in Contact-lens wearer with infection
- Trauma with plant material (scratch on branch)
Anti-VEGF
VEGF= Vascular endothelial growth factor
- Homodimeric protein secreted by a variety of cells in response to hypoxia/ischemia and other signaling molecules
- Induces vascular permeability and angiogenesis
Anti-VEGF= Agents to treat cancer
Shown to have promising effects in treating ocular diseases associated with neovasculaization:
- macular degeneration
- diabetic retinopathy
- retinal vein occlusions, etc.
- injected frequently (often monthly)
Agents:
- Ranibizumab= Lucentis
- Targets VEGF-A (designed for intraocular use)
- Used for macular degeneration
- Expensive, frequency and duration of treatment unknown
- Possible increased risk of thromboembolic events - Bevacizumab (Avastin)
- Less expensive, off-label, widely used
AEs:
- blurred vision, pain, redness of the eye, sensitivity to light
- increased intraocular pressure
- cataract (injection), infection, retinal detachment (injection in posterior part of eye)
- allergic reaction
? increased risk of thromboembolic events
