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84 Cards in this Set
- Front
- Back
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Optic nerve anatomy
where does early glaucomatous thinning occur? |
1.2 million axons, cells body of ganglion cells in ganglion cell layer
Early glaucomatous thinning inferotemporally |
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Blood supply of optic nerve
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NFL- Central retinal artery
Prelaminar- capillaries of short post ciliary artery Laminar-dense plexus short post ciliary artery Retrolaminar-supplied by both ciliary and retinal circulation |
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Outflow pathway: trabecular meshwork.
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1. trabecular meshwork path
uveoscleral meshwork --> corneosclera --> juxtacanalicular --> schlemm's --> collector channels --> aqueous veins --> episcleral/conj veins --> anterior ciliary and sup ophthalmic veins --> cavernous sinus Juxtacanalicular tissue has greatest resistance site. |
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Outflow pathway: uveoscleral outflow
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accounts 15-20% outflow. Aqueous pass through the face of ciliary body in angle -> ciliary muscle --> suprachoriodal space --> rain by veins cilary body, choroid, and sclera
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Describe pathway from blood stream to post chamber
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Ciliary epithelium bilayer. Capillary BM --> pigmented epithelium BM --> pigmented epithelium --> non-pigmented epithelium --> nonpigmented epithelium BM
Within ciliary processes, plasma enters from thin fenestrated endothelium of the capillary core --> passes stroma --> 2 layers epithelium with apposing apical surfaces. outer pigmented layer - continuous with RPE Inner non pigmented layer - equivalent to sensory retina |
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DDx Blood in schlemm;s canal
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1. elevated venous pressure (carotid-cavernous fistula, sup vena cava syndrome, sturge weber)
2. oculodermal melanocytosis 3. neurofibromatosis 4. congenital ectropion uveae 5. hypotony 6. gonioscopy |
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Plateau iris
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caused by anterior positioned ciliary processes that narrow the anterior chamber by pushing the peripheral iris forward
Angle anatomy results in deep central AC and shallow peripheral AC Finding: present with acute or chronic angle closure, ant positioned ciliary process. Have a deep chamber centrally and flat iris contour with sharp drop off peripherally. Dilation casues peripheral iris to bunch into the angle occluding the TM, compression gonio difficult to open angle. Treat with LPI, laser iridoplasty, miotics. |
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Limbus anatomy
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Limbus is transition between the cornea and sclera. conjunctiva and tenons is fused over the limbus.
-Termination of descemets and bowmans Surgeons perspective: anterior to blue zone (through conjunctival insertion) --> enter AC through descemets Posterior the white zone --> enters AC through TM |
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Aqueous humor production
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Production via non pigmented epithelium of ciliary body
aqeous production primarily by active secretion. Both Na/K pump and carbonic anhydrase invovled. rate 2-3microliter/min AC vol=250microliter Post chamber vol= 60microliters aqueous production decreases with sleep, age, inflammation, surgery, trauma, drugs |
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Aqueous humor composition
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15x more ascorbate than plasma
low protein low calcium and phosphorus (Na, K, Mg, iron, zinc, copper similar to plasma) Cl, HCO3 vary ** aqueous is slightly acidic |
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causes of pigmented TM
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Pigment dispersion
pseudoexfoliation trauma uveitis intraocular surgery laser treatment diabetes |
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Which cell and retinal layer is affected most by glaucoma?
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Ganglion cells and nerve fiber layer
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Optic nerve drusen
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Superficial or buried hyaline bodies in the prelaminar portion of optic nerve. Sporatic or AD. 75% bilateral, common in white.
Assoc with angiod streaks, RP, Alagille's syndrome Finding: nodular appearance to nerve head, visual field defect (enlarge blind spot, arcuate, sectoral scotoma). Transient visual obscurations, RAPD, calcification with age. pathology: hyaline bodies become calcified, stain with amino acid, calcium, mucopolysaccharides, hemosiderin. NOT AMYLOID. Diagnosis: Bscan, CT, FA shows autofluorecense |
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IOP diurnal variation
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Normal IOP vary 2-6mmhg over 24 hours, diurnal variation >10mmhg suggests glaucoma. many reach peaks in morning hours.
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Goldman equation
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IOP = (F/C) +EVP
F=rate formation (2-3microl/min) C=rate of outflow (0.28microl/min/mmhg) EVP= 8-12mmhg |
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Goldman tonometer
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Measures force necessary to flatten 3.06mm diameter of cornea. At this diameter the resistance of the cornea counterbalanced by capillary attraction of tear film.
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Conditions that change the goldman tonometry IOP reading
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1. excess fluorecein=high IOP
2. little fluorecein= low IOP 3. K edema= low IOP 4. K scar= high IOP 5. over soft CL = low IOP 6. post scleral buckle= low IOP 7. High CCT=high IOP 8. Low CCT=Low IOP 9. PRK, Lasik= low IOP 10. >3D against rule astigmatism= high IOP 11. >3D with the rule astigmatism= low IOP |
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What is the adjustement of IOP in low and high CCT?
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For every 10micrometers change .5mmhg
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glaucoma visual defect
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Visual defect defined by 3 degree wide, 6 decibels deep.
On HVF 1 point >10dB or 2 points depressed at least 5dB |
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Goldmann visual field
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Can be kinetic or static
test distance .33m Object size: I to V, each increment is 2x diameter and 4x area Light filters: 1-4, 5dB increments a-e, 1dB increments |
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humphrey visual field
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Static perimetry, testing at .33m. stimulus size 3, duration .2sec
Reliability index: 1. fixation loss: pt responds to target at blind spot. 2. false positive: responds when no stimulus (white area) 3. false negative: fails to respond to stimulus expected to be seen (loss attn, fatigue, clover leaf pattern) Global indices: 1. Mean deviation: avg departure of each test pt from the age ajusted normal 2. pattern std deviation: standard deviation difference between threshold and expected value 3. short term fluctuation- variability of response from same patient tested, a measure of consistency. 4. Long term fluctuation- variability of repsonse from one test to another. 5. corrected pattern Std Dev: adjusted PSD by subtracting short term fluctuation |
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Visual fields
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Perimetry measures topographic respresentation of differential light sensitivity.
2 types: 1. Kinetic- moving stimulus, contants intensity (horizontal cross section hill version) 2. Static-fixed stimulus with constant or variable intensity (vertical cross section hill of vision) Goldmann: kinetic and static Humphry: static |
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Optimal pupil diameter for HVF
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3mm
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Congenital glaucoma
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Mutation CYP1B1 accounts 85% congenital glaucoma. 70% BL 70% M, affected parent 5% change to have child with glaucoma.
symptoms: tearing, photophobia, blepharospasm, eye rubbing. have >21 IOP, high C/D (reversible), buphthalmos, enlarge cornea >13mm, haab striae, lens subluxation. Can be assoc with angle malformations (neural crest abnormalities). Diagnosis: EUA. definite treatment is surgical, goniotomy, trabeculotomy amblyopia can occur due to: corneal edema, breaks in descemets, myopia, astigmatism, anisometropia, ON damage |
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congenital glaucoma with associated syndromes
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sturge weber
neural crest abnormalities (axenfield/riegers/peters) lowe's rubella aniridia neurofibromatosis homocysteinuria PHPV |
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Primary open angle glaucoma
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A progressive, bilateral, optic neuropathy with open angles, cause typical pattern nerve bundle defect leading to visual loss. IOP >21 not caused by any other disease.
POAG is the most common form glaucoma, mutation OPTN 17% risk factors: increase IOP, increase C/D, thin cornea <550, FHx, old age, African american. Have increase IOP, increase C/D ratio (rim notching, asymmetry C/D, vertical elongation), nerve fiber loss, disc splinter heme, visual loss defect, optic nerve damage. Loss of yellow/blue color vision first |
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Risk factors of POAG
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1. elevated IOP
2. increased c/d ratio 3. family history 4. thin corneas <550 5. african american Possible risks: DM, myopia, hypertension, migraines |
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Ocular hypertension
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elevated IOP in absence of optic nerve damage, visual field loss. IOP > 21mmhg but no optic nerve defect, nerve fiber layer defect, or visual field loss.
approx 7% of US population have ocular hypertension. IOP distribution curve is skewed to the higher IOP |
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Trabeculectomy
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risk factors for failure: previous surgical failure, dark skin, keliod formation, neovascular changes, young age, intraocular inflammaiton, scarring conjunctiva, high hyperopia, shallow AC, cannot use steroids post op.
Use antimetabolite for patients at risk failure 1. mitomycin-c- intercalate DNA, prevents replication suppress fibrosis, vascular growth, more potent 100x than 5FU, 5-FU- affect S-phase of cell cycle. higher complications: in hyperopic, nanophthalmos, chronic angle closure, can roll ciliary process anteriorly and block ostium during surgery. |
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treatment of shallow or flat AC following trabeculectomy
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1. Elevated bleb and low iop = (excess filtration) revise bleb
2. Flat bleb and low iop = a. choridal detachment: must drain, start steroids, cycloplegia b. bleb leak: treat with antibiotics, aqueous suppressants, stop steroid, pressure patch, bandage contact lens, AC formation, glue, laser, autologous blood injection. 3. Flat bleb and high IOP a. suprachoroidal heme: drain b. pupillary block: PI c. malignant glaucoma: along with shallow ac, treat with cycloplegia, aqueous suppresant, PI, yag anterior hyaloid, vitrectomy 4. elevated bleb, high IOP: encapsulated bleb, needling, aqueous suppresants, bleb revision |
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treating a bleb leak
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antibiotics
aqueous suppresants stop steroids reforem AC if needed pressure patch bandage contact lens trichloroacetic acid glue laser autologous blood injection *if impending failure of bleb such as flat chamber, with corneal decompensation, kissing choroidals, progressive cataract needs surgical repair of the wound and drain choroidals |
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drainage impants
What types available? What indications? |
Non-valved - molteno, schocket, baerveldt. (these need temporary occlusion with suture
Valved - ahmed, kropin Indications: trab failure, active uveitis, neovascular glaucoma, inadequate conjunctiva, aphakic |
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What is most frequent cause of trabeculectomy failure?
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bleb scarring due to episcleral fibrosis
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Blebitis
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infection of filtering bleb, most common with staph.
Cause red eye, photophobia, discharge, marked conjunctival injection, seidel +, moderate AC cells and flare. no vitreal involvement. treatment: topical antibiotics, repair wound leak, observe for signs of endophthalmitis |
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Selective laser trabeculectomy (SLT)
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Settings:
Power .7 - .9 Spot fixed 400 50 applications /180 straddle TM Produce less tissue destructon than ALT so SLT is repeatable Targets only melanin containing cells in TM SLT is equivalent to ALT to in IOP reduction |
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Argon Laser trabeculectomy (ALT)
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Setting:
Power 400-1200mW Spot 50 duration .1 sec titrate to small bubble, aim at junction of non-pigmented and pigmented TM. 50 spots/180 avg of 30% decrease IOP can be repeated. Use Iopidine post op to avoid IOP spike and topical steroids. 25% fail to control IOP at 1 week. Approximately 10% patients have some increase in pressure each year, average durationj is approx 5 years . |
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What are the risk of pressure spike in ALT?
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posterior laser burn
dense TM pigment low outflow 360 treatment |
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Which glaucoma has best success with ALT?
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1. PXE (Best)
2. pigmentary glaucoma 3. POAG 4. NTG 5. aphakic (WORST) more pigment in angle better result. |
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What are factors that cause poor respond in ALT?
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older patients, inflammatory glaucoma, angle receesion, angle closure, congenital glaucoma, steroid induced, large amount PAS (contraindicated)
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Primary angle closure glaucoma
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Glaucoma caused by peripheral iris blocking TM, most common is pupillary block
common in eskimo, asians cause blurry vision, color halos on lights, pain, redness, nausea, vomiting, headache Find: increase IOP, cornea edema, conj injection, mid dilated pupil, shallow AC, MILD AC C/F, closed angle, optic nerve swelling, arterial pulsation Treatment: peripheral iridotomy, compression gonioscopy, pilo (not effective >40mmhg), reduce IOP with B-blocker, alpha agonist, CAI, hyperosmotic agent, IV mannitol, topical steroids. laser PI fellow eye , 75% chance of attach on fellow eye |
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anatomic features, predisposing to angle closure
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1. small anterior segment: hyperopia, nanophthalmos, microcornea, microphthalmos
2. hereditary narrow angle 3. anterior iris insertion (eskimo, asians, african americans) 4. shallow AC (large lens, plateau risi, loose or dislocated lens) |
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Laser iridotomy
types of laser used |
Perform in: narrow angles, iris bombe, synechial angle closure, plateau iris, malignant glaucoma
Laser types: Yag- bleed more, closes less, power 1-12mj Argon- reaction is pigment related, needs more energy and total application than yag. thermal effect. Less bleeding, closes off more, iritis pronounced |
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types of provocative tests for angle closure glaucoma
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Prone test, dark room, prone dark room, pharmacologic pupillary dilation
*positive if IOP rises >8mmhg thymoxamine test: alpha adrenergic antagonist, use to distinguish narrow angles with angle closure. It blocks iris dilator leading to miosis but does not decrease IOP, so decrease IOP suggests miosis removed iris from outflow channel reversing angle closure. |
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angle recession
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tear in anterior face of ciliary body between longitutinal and circular ciliary muscles.
most common source hemorrhage, no blunt trauma. Treat with with topical glaucoma meds, avoid pilocarpine can worsen, SLT/ALT does not help |
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cyclodialysis
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separation of ciliary body fomr the scleral spur, allows aqueous into the suprachoriodal spiace, leading to hypotony.
TReat with atropine, argon laser,surgical repair (suture, scleral buckle) spontaneous closure can casue spike in IOP |
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phacomorphic glaucoma
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lens induced angle closure
rapid, acute glaucoma precipiated by lens swelling as result of cataract formation, development of pupillary block in eye not disposed to closure Treatment: laser iridectomy, cataract extraction |
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Phacolytic glaucoma
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hypermature, morgaganian cataract, denatured lens protein leak form intact lens capsule.
macrophages ingest lens material and block TM, milky substance in AC. Needs surgical removal or lens reduce inflammation pre-op with topical steroid, cycloplegic, and ocular hypotensive meds |
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Pigmentary glaucoma
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AD, occurs in young myopic males. 50% of patients with pigment dispersion syndrome develop glaucoma.
Mechanism: reverse pupil block bows iris against zonules, iris movement result in pigment liberation. Pigment obstructs TM, Pigments release in exercise. Findings: halos, blurry vision with IOP spoke, krukenburg spindle (melanin phagocytes by cornea endothelium) Heavy TM deposition, iridonesis, mid-peripheral TI defects Assoc: lattice 14%, RD Treatment: miotics minimize iris-zonule touch (risk of RD). Great response to laser trabculoplasty, LPI helps with reduction of posterior bowing of iris |
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Lens particle glaucoma
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Lens material blocks TM after trauma or cataract surgery.
has more inflammation than phacolytic. can have PAS, posterior synechiae, inferior membranes, IOP very high. can see fluffy lens material in AC treatment: cycloplegics, steroids (will slow down les absroption), ocular hypotensive meds |
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Pseudoexfoliation glaucoma
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LOXL1, high incidence open angle glaucoma, common in scandinavians
amyloid-like substance deposit in eye clogs TM. substance also in other organs Find: iridopathy, keratophaty, sampaolesi's line (prominent inferior), weak zonules, lens capsule fibrillar material deposition, pupillary border TI defects. Treat with: great response to laser trabeculoplasty, PXE usually has higher IOP and more difficult to control than POAG. Pathology: amorphous eosinophils material lines up in perpendicular to lens (iron filings) Cataract surgery can have higher risk of capsular rupture. |
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Normal tension glaucoma
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glaucoma with normal angles and IOP.
mechanism: 1. noctornal systemic hypotension 2. autoimmune 3. vasospasm 4. previous blod loss, cardiac shock Must rule out intracranial process and other causes for optic neuropathy dx: diurnal curve, neuro work up, CBC, ESR, ANA, VDRL, FTA-abs, carotid eval, brain imaging. NTG has VF steeper slope, greater depth, closer to fixation than poag. splinter heme more common, and more difficult treating. |
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Optic nerve cupping occurs
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AION, Chiasmal compression, optic neuritis, methanol toxicity
(these tend to lose central VA and color vision first) |
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Neovascular glaucoma
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retinal or ocular ischemia causing fibrovascular membrane in iris leading to adherence of iris to TM. blocking TM outflow.
Causes: DM (33%), CRVO (33%), carotid occlusive (13%), tumors (RB (50%), melanoma, reticulum cell sarcoma, Metastasis, chronic RD. treat: aqueous suppressant, hyperosmotics, atropine (helps increase uveoscleral flow), PRP, peripheral retinal cryo can be done if poor view of retina (50% will get phthisical) Tube shunt 70% success. AVOID miotics |
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Iridocorneal Endothelial syndrome
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non-hereditary, abnormal corneal endothelium
occurs unilateral, middle age women. Abnormal corneal endothelium grows over angle, iris causing a block TM, distorts and contracts iris, making iris nodules. Beaten metal appearance of endothelium. 3 types 1. iris nevus (cogan-reese) - iris nodules composed of normal iris cells, bunched up due to overlying membrane. 2. Chandler's syndrome - corneal edema with normal IOP 3. Essential atrophy - endothelium produce broad PAS, corectopia, ectropion uveae, iris hole. Pathology - growth of endothelium and descemets over TM and iris |
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Ghost cell glaucoma
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Occurs when there is posterior vitreous. Degenerated RBCs, pass through hyaloid face. Khaki colored cells us much less pliable than RBC cannot pass through TM leading to glaucoma.
Can have layer of cells causing pseudohypopyon |
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Steroid induced glaucoma
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Risk factors: open angle glaucoma, fhx, glaucoma, DM, high myopia
Topical steroids cause more pressure effect than systemic steroids There is 31% risk of developing glaucoma withing 5 years in steroid responders |
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Which steroids cause less increase in steroids
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FML
Rimexolone Loteprednol |
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Malignant glaucoma
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Ciliary process rotate forward against lens cause anterior displacement of lens-iris diaphram.
Risk factors: Uveitis, angle closure, nanophthalmos, hyperopia. Occurs after surgery: intraocular surgery, laser, hyaloid face not broken. also when mydriatics stopped and miotics added. Finding: shallow AC (both central and peripheral), IOP high, patent iridectomy, absent suprachoriodal fluid, blood. Treat with mydriatics (cycloplegics) helps pull iris-diaphram posteriorly. Aqueous suppresants, peripheral iridotomy, miotics contraindicated. Surgical treatment: photocoagulation ciliary process, YAG hyaloid face, vitrectomy Treat: |
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iridoplasty
indications settings |
can be indicated in:
1. narrow angles 2. plateau iris 3. help stretch iris away from angle setting: Power 200-400mW Spot: 500 micron duraton: .5-1.0 sec |
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nanophthalmos
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small eye w/ normal features
lens size is normal, sclera is thickend, though to impede vortex vein drainage. Assoc: hyperopia, angle closure, choroidal effusion during surgery, exudative detachement |
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Intraocular tumors / malignant melanoma and glaucoma
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- intraocular tumors can push angle closed from the posterior
- malignant melanoma of anterior uveal tract can cause glaucoma by: 1. direct invasion TM 2. neovascularizaton 3. TM obstructed by melanin filled macrophages 4. Tumor seeding in outflow channels Other mechanisms - pigment - inflammation - hemorrhage |
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Expulsive suprachoroidal hemorrhage
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caused by progressive serous choroidal detachment leads to stretching of long posterior ciliary artery until rupture.
Can occur during intraocular surgery or days later Risk factors: elderly, HTN, atherosclerosis, DM, sudden drop IOP during surgery, high myopia, vitreous loss, fellow eye with hx expulsive hemorrhage, glaucoma, aphakia, post-op valsalva. find: forward movement of intraocular contents in surgery, loss of red reflex, subretinal heme, choriodal detachment, extrusion of ocular contents. Treatment: close wound rapidly, surcial drainage |
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suprachoroidal hemorrahge after trabeculectomy
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Occurs usually couple days after trabeculectomy surgery. Has acute pain often when straining, nausea, vomiting, decrease vision
Mechanism - serous choroidal detachment, stretches the long posterior ciliary artery until rupture. Risk factor: aphakia, HTN, cardiovascular disease, old age. |
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How to prevent suprachoroidal hemorrhage?
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decompress the eye pre op
small wound control bp in surgery prevent buckling of patients in surgery |
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Ocular ischemic syndrome
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reduction of blood flow to globe causing anterior and posterior segment ischemia. Carotid occlusion is most common
Assoc:DM, HTN, CAD, CVA cause-amaurosis fugax, decrease in vision, dull pain. anterior segment: chronic conjunctivitis, rubeiosis, PAS, AC cells, corneal edema, cataract, low IOP post segment: vitreous cells, NV, disc pallor, Optic nerve swelling, mid peripheral heme, CME, cherry spots, altered vessels. Diagnosis: digital pressure on eye --> arterial pulsation. FA- delay in filling of retina, choroid. ophthalmodynamometry, carotid ultrasound. treatment: lower IOP helps increase perfusion, carotid surgery, PRP. |
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1. Study: North American symptomatic carotid endarterectomy trial collaborators
2. Study: European carotid surgery trial colloarative group |
1. symptomatic patients (hx amaurosis fugax, TIA, CVA) with 70%-94% carotid artery stenosis have 2 years of stroke rate. 9% endarterectomy group vs. 26% control antiplatelets only
2. symptomatic group carotid stenosis 0-29% no benefit to carotid stenosis, symptomatic 50-69% stenosis 5 year stroke rate 16% endarterectomy va 22% treated medically |
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Study: Glaucoma Laser Trial
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Evaluated the efficacy treating POAG initially with ALT vs timolol
1. initial treatment of POAG w/ ALT is at least as effective as initial treatment with timolol. 2. 2 years into study 56% laser treated eyes needed supplemental medical control of IOP. -laser treated eyes had lower mean IOP |
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Study: Collaborative initial glaucoma treatment study
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Evaluate effectiveness of medical treatment vs. trab for treatment of newly diagnosed open angle glaucoma (primary, pigmentary, PXE)
Visual field loss not significantly different with either treatment. Trabeculectomy has initial increase in significant visual loss but by the 4th year the VA was equal in both groups. IOP avg is lower in surgicla group cataract rate is higher in surgical group. |
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Study: Advanced Glaucoma Intervention Study
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Evaluated ALT vs. Trab as initial surgery in patients with advanced open angle glaucoma.
1. african americans best result with ATT 2. Caucasians best result with TAT 3. Visual field was more severe in African Americans. 4. Eyes with IOP <18mmhg at all visits had no progression of VF loss 5. Trab increased risk cataract by 78% 6. risk faliure ALT: young age, high IOP 7. risk failure trab: young age, high IOP, DM, post op complications 8. Bleb encapsulation, male sex, previous ALT |
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Study: Ocular Hypertension Treatment Study
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Evaluate effect of topical medication in delaying or preventing POAG in patients with ocular hypertension.
Goal was to reduce IOP at least 20% from baseline, taget pressure of at least <24mmhg. primary outcome measure: VF loss, ON damage IOP reduction 22% in medicine group vs 4% observed At 5 years risk of developing POAG treated 4.4% vs. Observed 9.5% Conclusion: topical hypotensive is effective in preventing POAG in eyes with ocular HTN. Predictive factors to develop POAG: 1. baseline IOP 2. Age 3. C/D ratio 4. CCT |
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Study: Early Manifest Glaucoma Trial
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Evaluate effectiveness of reducing IOP on progression of newly diagnosed open angle glaucoma.
treated group recieved ALT and betaxolol. treated gropu had 5.1mmhg (25%) reduction rate. progression is less in the treated (45% vs 62%) Each 1mmhg of IOP lowering from baseline reduce risk progression by 10% Treatment halves risk of progression. risk factors for progression: higher baseline IOP, exfoliation, bilateral disease, old age, disc heme |
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Study: Collaborative Normal Tension Glaucoma Study
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Evaluate if IOP is a factor in NTG.
goal for treatment group was to reduce IOP by 30% (either with meds, laser, or surgery) Lowering of IOP 30% is beneficial, IOP is a factor in NTG factors that increase rate progression: female, migraine, disc heme |
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Alpha agonists
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aproclonidine - Iopidine
brimonidine - alphagan Mechanism: reduces aqueous production, a vasocontrictor Avoid with MAO inhibitors can cause hypertensive crisis side effects: allergy, dry mouth, dry eye, lethargy, mydraiasis, hypotension, lid retraction |
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Beta blockers
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reduce aqeous production by inhibiting Na/K pump. lose effectiveness in time by upregulation of beta receptors
side effect: bradycardia, heart block, bronchospasm, impotence, lethargy, mask hypoglycemia. 1. non-selective: timolol, levobunolol, metipranolol, carteolol 10% do not hav therapeutic effect decrease in HDL, systemic Beta blockers use may decrease effect Cadioselective- Betaxolol, have fewer pulmonary side effects. Use in pulmonary patients. Carteolol less effect on plasma lipids |
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epinephrine and dipiveprin
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epinephrine - improves aqueous outflow, has slight reduction of aqueous production. cause allergy, CME in aphakia, HTN, tachycardia, arrythmias, adrenochrome deposits
can cause CME and arrythmia Dipivefren- prodrug of epinephrine. Is converted to epinephrine in cornea by esterase. Less toxic, fewr side effects. causes allergy, CME in aphakia, HTN, tachycardia, fewer systemic side effects |
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Miotics used in glaucoma
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increase aqueous outflow due to contraction of ciliary muscle opening TM. It decreases uveoscleral outflow.
1. Pilocarpine: acetylcholine agonist, cause HA, brow ache due to accomodative spasm, myopia, pupil block, follicular conjunctivitis, retinal tear. 2. Carbachol - Ach agonist and acetylcholinesterase inh, stronger and longer duration. Poor cornea penetration, miostat an intraocular formula Echothiophate (Phospholine Iodide)- cholinesterase inhibitor, used of accom esotropia. 3 week duration. side effects: obicularis, ciliary, iris muscle spasm, cataract, iris cysts, decrease serum pseudocholinesterate activity cause increase succinylcholine effects during general anesthesia Generally contraindicated in patients with retinal holes and those with risk of RD |
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Carbonic anhydrase inhibitors
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decrease bicarb formation in ciliary body epithelium. Bicarb formation linked to Na and fluid transport. CAI decreases aqueous producton. A sulfonamide
99% carbonic anhydrase inhibited to decrease IOP. Methazolamide: naptazine PO, more lipid soluble decrease in toxicity compared to diamox side effects: matabolic acidosis, kidney stones, hypokalemia (avoid digoxin worsen hypokalemia), parasthesia, GI upset, loss of libido, metal taste, aplastic anemia, SJS, transient myopia Topical: most common burning burning, bitter taste, allergy. metallic taste, parasthesia, malaise, wt loss, depression, skin rash, corneal edema |
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hyperosmotic agents for glaucoma
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increase serum osmolarity draws fluid out of the eye reducing vitreous volume.
side effect: HA, thirst, nausea, vomiting, diarrhea, diuresis, dizzy, subarachnoid hemorrhage. 1. urea: extravasation cause tissue necrosis (no commonly used) 2. mannitol: most potent, CHF 3. glycerin: hyperglycemia, do not use in diabetes 4. isosorbide: can use in diabete, 95% unchanged in urine |
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Prostaglandin analogue
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cause increase in uveoscleral outflow
1. latanoprost (xalatan) 2. bimatoprost (lumigan) 3. travoprost (travatan) 4. unoprostone (isopropyl) 5. recula (prostaglandin F2alpha) side effects: flu lke symptoms, hyperemia, lash growth, periocular skin, iris hyperpigmentation (Increase melanocytes), CME, reactivate HSV keratitis. contraindicated in Uveitis, CME, pregnant women |
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glaucoma allergy
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1. iopidine
2. epinephrine 3. propine 4. brimonidine 5. b-blocker 6. pilo |
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Conditions and medications that cause acute abdomen in a glaucoma patients
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acute angle closure
CAI pilocarpine echothiophate |
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dapripazole
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alpha adrenergic antagonist, used to reverse pupillary dilation
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beta blockers have additive effect in combination with whitch meds?
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adrenergic agonist (alphagan) most
carbonic anhydrase inhibitors (substancial effect) Miotics hypotensive lipid (undetermined magnitude) |
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glaucoma meds that can aggravate inflammation after cataract surgery
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adrenergic agonist (epinephrine, dipivefrin)
miotics prostaglandins (xalatan) |
