Glaucoma Flashcards
Pilocarpine : Mechanism of Action
Parasympathomimetic - Pilocarpine directly stimulates cholinergic receptors, acting on a subtype of muscarinic receptor (M3) found on the iris sphincter muscle, causing the muscle to contract and produce miosis. timulates the sphincter pupillae in the iris and the ciliary muscle, resulting in displacement of the scleral spur, opening of the trabecular meshwork and/or Schlemm’s canal, and enhancement of conventional aqueous outflow.
Beta-Blockers: MOA
Beta-blockers decrease aqueous humor production by the ciliary body and hence reduce IOP.
Carbonic Anhydrase Inhibitors
Carbonic anhydrase is an enzyme that catalyzes the reaction of H2O and CO2 in equilibrium with H+ and HCO3−. The net effect of the enzyme on aqueous production is to generate bicarbonate ions, which are transported actively across the ciliary epithelial membrane into the posterior chamber (sodium is the primary cation); an osmotic gradient is established. Water passively follows because of the presence of the gradient, which results in aqueous production. Inhibition of this enzyme results in lower IOP because aqueous production is decreased approx 50% or more;aqueous outflow and episcleral venous pressure are affected little or not at all.
Alpha-Adrenergic Agonists
Apraclonidine decreases aqueous production but is also associated with an increase in outflow facility and a decrease in episcleral venous pressure. Brimonidine is 23 times more alpha-2 selective than apraclonidine and 12 times more selective than clonidine. Its mechanism of action includes a reduction in aqueous formation as well as an increase in uveoscleral outflow
Relate Ciliary Body Anatomy to demonstrate the difference between Angle Recession, cyclodialysis and irido-dialysis
Angle recession is a separation between the longitudnal and radial muscles of the ciliary body. (you see a wide CB band but otherwise N structures) Cyclodialysis is when the longitudnal muscles separate from the scleral spur and ca cause hypotony and haemorrhage. Irido dialysis is separation of the iris root and the ciliary body.
OHTS found 5 significant risk factors that increased the risk of POAG
- age
- higher iop
- CDR
- greater pattern standard deviation
- reduced CCT
What were the pressure lowering goals of OHTS and CNTGS
OHTS: 20% from baseline
CNTGS: 30% from baseline
What are the risk factors for steroid responders (5)
- known POAG
- family hx
- age
- DM
- myopia
DDx of arcuate defects
Glaucoma ONH drusen NAION, AAION Myelinated NFL Hemiretinal vein occlusions BRAO Optic nerve colobomas, pit Laser scars to one area of retina
DDx of enlarged blind spot
ONH drusen Papilledema Diabetic papillitis Hypertensive papillitis Optic neuritis MEWDS/IEBSS Megalopapilla High myopia (PPA)
Glaucomatous nerve features
High CDR Assymetric CDR Notch Loss of NFL Optic disc hg Bayonetting of vessels Nasalisation of vessels Vertical elongation of the cup Laminar dots (?)
Systemic associations with drusen
Autosomal dominant
PXE
Sickle cell
DDx of glaucomatous nerve
Physiologic cupping
Tilted discs
Anything that causes nerve damage... Glaucoma (open or closed) Optic neuropathies compression toxic/metabolic vascular insults
Disc hg ddx
Glaucoma (esp NTG) Hemorrhagic PVD Papilledema NAION AAION Diabetes HTN Valsalva
Thickest rim
I>S>N>T
Most suspectible to glaucoma (parts of the rim)
I>S>T>N
Angle most open
Inferior
Angle most pigmented
Inferior
Deep AC in who
Myopes
Young
Male
(basically everyone who gets PDS)
Shallow AC in who
Old
female
hyperopes
Eskimo/Asians
Steroid responder risks (5)
POAG Family history Age Myopia DM
CDN guidelines for suspect, early, mod, and adv glaucoma (dx and management)
Class; CDR; VF; Tmax you want; lower by
Suspect; — ; — ; 24; 20%
Mild; 10deg from fixation; 20; 25%
Moderate; 10 deg from fixation; 17; 30%
Severe: >0.9, within 10 deg of fixation; 14; 30%
Dose of MMC for trab
0.01% for 2 min (in real life this varies but this is a reasonable exam answer)
Two types of VF testing
Static (Humphrey or Goldmann)
Kinetic (Goldmann)
DDx of hyphema in adult
Trauma Bleeding diathesis Leukemia Ocular surgery Fuch's Other NVI/NVA UGH
PXF cataract risks
Poor dilation Stiff pupil Zonular weakness Increased risk of phacodynesis and vitreous loss Capsular fragility Lower endothelial cell count Unstable IOP post-op (spikes) Post-op inflammation
Findings in PXF
Poor dilation Ring of pigment on anterior lens capsule PXF material on pupil margin Pupil margin TID Pigmented angle Sampolessi line
Membrane over angle
ICE
Epithelial ingrowth
PAS (uveitis, bad ALT, chronic ACG)
NVI
ICE clinical variants
Chandler - mostly cornea
Iris nevus - membrane on iris tents up normal stroma to look like nevi (not actually nevi)
Essential iris atrophy (correctopia/polycoria)
3 lytic glaucomas
Lytic = macrophages clog up TM with junk
Phacolytic - lens particles
Hemolytic - RBC from hyphema
Melanomalytic - pigmented melanocytes (or something) from melanoma cells floating around
Secondary glaucomas after IOL implantation
UGH
Pupil block angle closure
Secondary pigmentary glaucoma
Pigmented TM in who
Pigmented people Older people PXF PDS Melanomas
IOP formula
IOP = F/C + EVP
Types of tonometry
Indentation - Schiotz
Applanation - tonopen, Goldmann, Perkins, pneumotonometer (don’t let this last one throw you - unless they say AIR PUFF, it’s still a contact tonometer)
Non-contact - air puff
Glaucoma with pigment
PXF PDS Pigmented people with open angles Pigment on endothelium from old inflammation, cataract surgery, trauma, hyphema ICE Melanoma
Intermittent ACG findings
Hx of intermittent ACG \+/-Normal IOP PAS Glaucomflecken Signs of glaucmatous damage to ON
Risk of ACG in the fellow eye after AACG
75%. So always do prophylactic LPI
Segmental iris atrophy
Cataract surgery Trauma HSV, EBV, CMV, VZV ICE syndrome Axenfeld reiger PPMD
Iridodenesis
Separation of iris from CB
Usually result of trauma or surgery
Rx with coloured CL or surgically re-insert
Causes of ectropion uveae
ICE Axenfeld reiger Uveitis PPMD NF-1 Epithelial downgrowth NVG uveitis
How do you tell epithelial ingrowth vs fibrous downgrowth
Epithelial ingrowth turns white with YAG
Lens induced glaucomas
Phacomorphic - angle closure with pupil block
Phacolytic - lens particles leak through intact capsule. Minimal inflammation, but macrophages ingest the particles and obstruct. NO KP.
Phacoanaphylactic - broken capsule. Maybe after surgery. Some books call this the same as lens particle glaucoma. LOTS OF INFLAMMATION with KP’s.
Lens particle - basically the same thing. Maybe it’s more after cataract surgery with some lens left behind.
UGH - from IOL
Dislocated lens (if dislocates anteriorly, causes ACG)
Same with microspherophakia causing ACG
Cyclodialysis def’n and treatment
Separation of CB from SS
Result of either trauma or surgery
Gonio to confirm
Rx with cycloplegics, most will close on their own in 6/52
Cause hypotony in the meantime, +/- spike when its closing
Risks for OHTN progression
Age High IOP High CDR High pattern standard deviation Low CCT
CCT definition in OHTS
588 = thick
RF for OAG
Age High IOP Family history Race Other: HTN, DM, Myope, migraines?
RF for AACG
Female Age Previous ACG Race - inuit or asian Hyperopic Nanophthalmos Family history
RF for NTG
Female Disc hg migraine vasospasm/raynauds smoking
DDx of NTG
IOP is high, but you’re not measuring it:
- uncalibrated equipment
- low CCT
- corneal edema
IOP is high sometimes but you’re missing it:
- diurnal fluctuations
- intermittent ACG
- Posner Schlossman episodes
IOP was high before but its ok now:
- burned out OAG (PDS, PXF)
- old AACG
It’s not glaucoma at all:
- ONH drusen
- old optic neuritis, NAION, AION, etc
- compressive lesion (do a CT - nerve to chiasm)
- infiltrative lesion of the nerve (sarcoid, TB, lyme, etc)
Only if you’ve ruled all that out can you call it NTG.
Acute IOP rise ddx
After laser (LPI, SLT, etc)
After surgery (retianed visco, retained lens particles)
Inflammatory (HSV, CMV, Posner Schlossman, Fuch’s)
Steroid responder
After hyphema
AACG
Characteristics of plateau iris and treatment
Deep central AC, shallow periphery
Flat iris
Bunched up iris in angle
No change in configuration despite LPI
Rx:
- always make sure they have an LPI first
- Argon iridoplasty to pull the iris out of the angle
- miotics
DDX of increased EVP
AV malformation: CCF, SWS, orbital varix
Lesion compressing SOV: thyroid, tumor, orbital vein thrombosis, cavernous sinus thrombosis, SVC syndrome
Idiopathic: posture (lying down), familial EVP
DDx of blood in Schlemm’s
High EVP (AV issues, something compressing SOV)
Hypotony (inflammation, hypotony, following trab)
Normal with compression gonioscopy (occludes episcleral veins)
DDx of axenfeld-reiger
ICE Aniridia Isolated posterior embryotoxin (N in 15%?) Peter's anomaly Ectopia lentis et pupillae (no glaucoma)
Systemic findings in axenfeld reiger
Microdontia
Redundant peri-umbilical skin
Schabel’s optic atrophy def’n and ddx
Hyaluronic acid infiltation of the nerve (stains with colloidal iron, alcian blue)
either from end-stage glaucoma or ischemic optic neuropathy (NAION, AION, etc)
Posterior pushing mechanisms of ACG
Choroidal effusions Vitreous overfill from gas Ciliary body mass Supra-choroidal hemorrhage Malignant glaucoma Contraction of retro-lental tissue (ROP, PHPV)
DDx of NVI/NVA
Fuch's heterochromic iridocyclitis DM, radiation retinopathy, OIS CRVO, BRVO, CRAO RB!!! Always think RB ROP/FEVR/Eales Sickle cell
Types of ONH analysers
Surface topography - HRT
Cross section - OCT
