MORAN - Glaucoma OKAP

Prostaglandin analogues
- What are the two prostaglandin analogues that are pro drugs?
- What is the mechanism of prostaglandin analogues?
- What two diseases can prostaglandin analogues exacerbate?
- What response do you see in 1% of patients?
Click the card to flip 👆
1 / 35
Terms in this set (35)
Prostaglandin analogues
- What are the two prostaglandin analogues that are pro drugs?
- What is the mechanism of prostaglandin analogues?
- What two diseases can prostaglandin analogues exacerbate?
- What response do you see in 1% of patients?
- Latanoprost + travaprost = pro drugs (LT was a PRO football player)
- Mechanism = increases uveoscleral outflow
- Can exacerbate HERPES KERATITIS + CME
- Uveitis is an idoiosyncratic response in 1% of patients
Beta-Blockers
- Which is B2 selective?
- Mechanism?
- When is the effect highest? Lowest?
- Side effects (10)
- What disease can this worsen?
- What can this also mask?
- Betaxolol = B2 selective
- Mechanism = aqueous suppressant that decreases cAMP
- Most effective during the day, minimal IOP lowering effect at night
- S/E = bronchospasm, bradycardia, increased heart block, hypotension, reduced exercise tolerance, CNS depression, mood lability, worsening depression, impotence, worsening dry eye, increase serum lipids
- Worsening of myasthenia gravis
- Masks hypoglycemia
Alpha Adrenergic agonists
- What are the 2 choices?
- Which has more alpha 2 selective?
- What is the mechanism?
- What are 2 common ocular side effectS? What are 2 systemic side effects?
- What is a relative contraindication to this drop?
- Which age can you give it to children?
- Brimonidine + Apraclonidine
- Brimonidine = more alpha2 selective than apraclonidine
- Mechanism = aqueous suppressant and lowers EVP
- Ocular: Blepharodermatitis, follicular conjunctivitis
- Systemic: Dry mouth, lethargy
- Relative contraindication: Use of MAOI or TCA
- Brimonidine okay after age 4...
Carbonic anhydrase inhibitors:
- What is the mechanism of action?
- What has to happen before IOP lowering effect is seen?
- What are 3 common side effects?
- Dorzolamide is more likely to cause ___________, and brinzolamide is more likely to give _____________.
- What do these meds to do the cornea?
- What are 8 systemic side effects?
- Which oral CAI is metabolized in the kidney? Liver?
- What are the 2 meds that you AVOID Rx Diamox?
CAI mechanism = Aqueous suppressant by targeting ciliary epithelial carbonic anhydrase
- 90% of carbonic anhydrase has to be blocked before IOP lower effect is seen
- Ocular s/e: bitter taste, blurry vision, PEE
- Dorzolamide more likely to cause burning, brinzolamide more likely to give white flecks
- Cornea = worsening corneal edema in pts with compromised endothelial cell function
- Systemic s/e: metabolic acidosis, hypokalemia, abdominal pain, nausea, vomiting, diarrhea, impotence, severe depression, renal stones
- Diamox = kidneys, Methazolamide = liver
- AVOID diamox in patients with thiazide and loop diuretics
Parasympathomimetics
- What is the mechanism of action?
- What are 8 ocular side effects?
- What are 4 systemic side effects?
- What can this paradoxically cause?
Mechanism: Contracts the longitudinal ciliary muscle —> Pulls scleral spur —> Tightens TM —> increases outflow
- Ocular: brow ache, ciliary spasm, miosis, RD, cataract, iris cysts in children, epiphora, increase bleeding during ocular surgery, increased inflammation, worsening uveitis
- Systemic: diarrhea, abdominal cramps, increased salivation, enuresis, bronchospasm
- Paradoxical angle closure because of forward movement of lens-iris interface
Pregnancy and IOL drops:
- Which gtts are category C? Category B?
- What can PGAs cause?
- What can CAIs cause?
- Which is the safe drop to use?
- Which drop do you avoid in breastfeeding?
- All glaucoma gtts are category C except Brimonidine, which is category B
- PGA —> early uterine contractions
- CAIs —> neural tube defects in animals
- Timolol = thought to be safe in pregnant women
- Breastfeeding = no brimonidine because of CNS depression + Betablockers concentrate in breastmilk and should be avoided
Prostaglandin analogues:
- In what colour eyes is the iris colour changes most likely to occur?
- What is the risk for blue-eyed patients?
- What is the OVERALL % risk of pigment changes?
- How long does it take for the iris changes to reverse after starting the drop?
- Yellow most likely, next is Hazel
- Risk for blue-eyed is < 8%
- Overall risk = 33%
- Iris pigmentary changes DON'T reverse!
How does Netarsudil work in reducing the IOP?
First medication to reducing IOP by working at the TM
POAG
- What are 5 risk factors?
- What did the CNTGS study find for lowering IOP for this disease?
- Risk factors: OHT, Age, Myopia, FHx, Race
- CNTGS: lowering IOP by 30% reduces 5 years risk of VF progression from 35% to 12%
PXF
- What gene is associated with PXF?
- Where do you see the transillumination defects? What do you see in the angle?
- How do these patients respond to SLT?
- LOX1 gene
- TID at the PUPILLARY MARGIN + Sampaeolesi line
- SLT: can be very effective because less power required, but effects don't last as long and more prone to post-treatment IOP spike
Pigment Dispersion - What would you see in the TM? - What is a classic sign of this disease? - Where do you see the TIDs? - What kind of iris conformation do you see on gonio? - What is the typical patient that's at risk? What do they do to make their spikes worse? - What's the typical treatment? - Why do you have to be more careful with these patients for surgery?- Densely pigmented TM + sampaolesi line - Krukenberg spindle - Mid-peripheral spoke-like iris TID - CONCAVE iris on gonio - Typical patient = young, myopic male. IOP spikes after exercise - Treatment = SLT - They're higher risk of hypotony with filtering surgery!Differentiate between phacolytic, lens particle, phacomorphic, and phacoantigenic glaucoma in terms of: - Angle status - Mechanism - Status of the lens - Presence of KPChoose phacolytic, lens particle, or phacoantigenic for the following: - KP present + absent lens/post trauma - KP absent + hypermature cataract- Phacoantigenic - PhacolyticFor Possner-Schlossman and Fuchs heterochromic, what is common in the angle? - In which similar disease is the angle the opposite? - When do you get PAS in P-S or Fuchs heterochromic? - Which viruses do they think is involved in P-S? - Which virus do they think is involved in Fuchs heterochromic?It's always open! ICE syndrome = angle is closed - P-S and Fuchs do not have PAS - P-S = ?HSV or CMV - Fuchs heterochromic = ?RubellaWhat is your DDx for elevated EVP?Elevated EVP: - AV fistula - Orbital varix - Sturge weber - Retrobulbar tumour - TED - Superior vena cava syndromeWhat do you commonly see in Schlemm's Canal with elevated EVP > IOP?Blood in schlemm canalWhat treatment is not effective in elevated EVP?SLT is NOT effective!Differentiate between Hemolytic and Ghost cell glaucoma in terms of: - When it happens - What is blocking TM - Coloured cells in the AC?- Both happen after VH - Hgb laden macrophages in Hemolytic vs Degenerated RBC block TM in Ghost cell - Red tinged cells in AC in Hemolytic vs. Khaki coloured cells in AC in Ghost cellWhat is the most common mechanism for angle closure glaucoma? - What is a treatment option if used at a lower concentration? What if you use a higher concentration? - What is the definitive treatment?Pupillary block —> aqueous flow obstructed at the level of the LENS IRIS interface, which leads to peripheral bowing (iris bombe) - Mild cholinergic (pilocarpine 1%) to induce miosis... but at higher concentrations it can increase vascular congestion and rotate the lens/iris interface anteriorly - Definitive treatment is LPIWhat is the mechanism for chronic angle closure? What is the treatment?Chronic angle closure = creeping PAS advance circumferentially Treatment is iridotomy/iridectomyWhat are 2 types of medications that can induce angle closure? Give a few examplesAdrenergic (sympathomimetics) or anticholinergics (parasympatholytic) meds Allergy and cold medicines, antidepressants, urological medicationsPlateau iris - Describe the pathophysiology of this - What kind of description do you watch out for to suspect plateau iris? - What would you see on UBM? - What is different about the PAS that form in this disease? - What is the treatment? (3)Plateau iris = anteriorly positioned ciliary process pushes peripheral iris forward OR more anterior junction of the iris dilator muscle and ciliary epithelium Suspect this when AC looks deep and iris looks flat, but angle looks narrow Double hump sign on UBM PAS can begin at Schwalbe line and extend posteriorly over the TM Treatment - LPI, but this usually doesn't work... so - Miotics to pull pupil away from angle - Argon peripheral laser iridoplastyICE syndrome - Does it tend to be unilateral or bilateral? - What is the typical sex and age of patient? - What is different about the PAS that form? - Which forms of ICE is the glaucoma 50% worse?- Unilateral - Women ages 20-50 - HIGH PAS that extend over Schwalbe line because endothelium is abnormal - Glaucoma is 50% more severe in essential iris atrophy + cogan reeseWhat kind of AC do you typically see in aqueous misdirection? - What clinical scenario does this tend to occur? - How do you treat this condition? - What % of these patients will resolve without surgery?- UNIFORM flattening of AC - Post-surgical eye Treatment - Intense cycloplegia - YAG anterior hyaloid - PPV with anterior hyaloido-zonulectomy 50%What is the most appropriate initial treatment of pupillary block in a patient with microspherophakia?Dilation drops! —> Moves lens diaphragm posteriorlyExplain why the following medications should be avoided in patients with hyphema and sickle cell disease - CAIs - Alpha1 agonists - Mannitol - Pilocarpine- CAIs = increases sickling by lowering pH - Alpha1 agonists cause anterior segment ischemia via vasoconstriction - Hyperosmotics can induce global sickle cell crisis - Parasympathomimetics should b eavoided in any hyphemaWhat's the mechanism of angle recession (traumatic) glaucoma?Angle recession isn't damage to the angle itself that causes elevated IOP, but rather a sign that the TM sustained severe injury and the angle recession is just a marker of that injuryWhat is the % of patients that will get a steroid spike on gtts?BCSC = 30%What is the mechanism that is thought to be the etiology of glaucoma in aniridia patients?Anterior rotation and eventual adhesion of iris tissue to the angleWhat is the relationship between uveoscleral outflow and IOP?Uveoscleral outflow is INDEPENDENT of IOP!What is the Goldmann equation?Po = F/C + Pv Po = IOP in mmHg F = rate of aqueous formation C = facility of outflow Pv = episcleral venous pressureWhat % of the outflow is uveoscleral responsible for?20%What are the 3 lens types that can do compression gonioscopy?Zeiss, Possner, and SussmanWhat is the rate of aqueous production per minute?2 microL per minuteWhat do the following things measure? 1. Tonography 2. Manometry 3. Tonometry 4. FluorophotometryTonography = aqueous outflow Manometry = EVP Tonometry = IOP Fluorophotometry = aqueous formation