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Glaucoma > Secondary Glaucomas > Flashcards

Secondary Glaucomas Flashcards

1
Q

What is secondary glaucoma?

A

glaucoma caused by some other entity, characterized by site of aqueous obstruction

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2
Q

What are sites of aqueous obstruction?

A

pre-trabecular, trabecular, post-trabecular

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3
Q

What are pre-trabecular glaucomas?

A

neovascular, ICE syndrome and epithelial ingrowth

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4
Q

What are trabecular glaucomas?

A

hyphema, pigmentary, pseudoexfoliation

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5
Q

What are post-trabecular glaucomas?

A

episcleral venous pressure

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6
Q

What are other names for neovascular glaucoma?

A

hemorrhagic, congestive, thrombotic

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7
Q

What are main causes of rubeosis?

A

DM, retinal vascular occlusive disease, carotid artery disease, RD, sickle cell retinopathy, uveitis

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8
Q

What is 90 day glaucoma?

A

rubeosis in first 3 months after CRVO

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9
Q

Rubeosis mechanism:

A

ischemic retina, release of VEGF produced by muller cells, VEGF travels through pupil and over the iris and into the angle

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10
Q

NVG treatment:

A

treat underlying etiology in pre-angle closure stages, aka PRP or tx of carotid disease, use aqueous suppressants and filters/drainage devices, anti-VEGF

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11
Q

How does anti-VEGF work?

A

avastin injections showed excellent regression of NVI, good resolution of open angle NVG (still need some filtering), resolves neo in closed angle but IOP is not improved

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12
Q

Which medications reduce aqueous production?

A

alpha agonist, beta blocker, CAI

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13
Q

What is ICE syndrome?

A

iridocorneal endothelial syndrome- abnormal corneal endothelium forms membrane over angle

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14
Q

What are ICE demographics?

A

middle age female, possible association with HSV, EBV trigger, associated with progressive iris atrophy and cogan reese and chandler (most common)

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15
Q

What is the pathology of ICE?

A

collagenous layer bound to the posterior aspect of Descemet’s membrane, a cellular membrane develops over angle, yields synechiae further blocking the AC angle, cellular membrane on the iris

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16
Q

What is a corneal sign of Chandlers?

A

thickened endothelial layer

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17
Q

How is ICE diagnosed?

A

consider specular microscopy for better eval of corneal endothelial cells

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18
Q

What is the treatment of ICE?

A

topical aqueous suppressants, trabeculectomy, filtering procedures, PKP, descemet stripping automated endothelial keratoplasty, deep lamellar endothelial keratoplasty, descemets membrane endothelial keratoplast

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19
Q

What are characteristics of ICE?

A

sporadic, usually unilateral, W>M, 20-50 years old

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20
Q

What is epithelial ingrowth?

A

rare, post surgical or trauma, corena or conj grows into anterior chamber, epithelium of K or conj can get into wound and proliferate to block the TM, membrane covers angle

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21
Q

What are the surgical interventions for epithelial ingrowth?

A

remove/destruct epithelium or filtering procedure

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22
Q

How does a hyphema affect IOP?

A

less than 1/2 of AC filled= 4% incidence of IOP increase, greater than 1/2 of AC filled= 85% incidence of IOP increase

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23
Q

What is the etiology of hyphema induced glaucoma?

A

most commonly traumatic, post surgical

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24
Q

What is the therapy for hyphema?

A

stop anticoagulant/aspirin (consult PCP), rest no strenuous activity, upright posture, aqueous suppressants, topical steroid

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25
Q

What is the controversy of mydriasis as hyphema therapy?

A

may cause vasoconstrictive effect to reduce the persistence of a hyphema or pushing iris forward into angle which could potentially further narrow angle

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26
Q

When should you do a surgical anterior chamber wash?

A

with a total hyphema lasting more than 5 days

27
Q

What is PDS?

A

bilateral pigment release from posterior iris, irido-zonular contact

28
Q

Who is PDS more common in?

A

myopes and caucasians

29
Q

What are signs of PDS?

A

Krukenberg spindle, pigment granules on iris, open angle with pigment/sampaolesi’s line, iris TID, sheie ring on anterior lens

30
Q

What is the pathophysiology of PDS?

A

excessive pigment in angle causing IOP increase and ONH damage, IOP spikes with exercise

31
Q

What are characteristics of PDS?

A

symptomatic in 40s, M>W, may be asymmetric

32
Q

What is the PDS therapy?

A

miotics if tolerable, topical GLC med, PI, laser trabeculoplasty, trabeculectomy

33
Q

What is the risk of pilo in PDS?

A

pilo stretches iris to pull it away form the lens zonules, there are SEs like accommodative spasm and risk of RD in high myopia

34
Q

What is a good GLC med for PDS?

A

reduce production/alternative outflow, rho kinase inhibitors are good as they work at TM to open up the spaces and increase contractibility of TM

35
Q

What is true of ALT and SLT in PDS?

A

pigment absorbs energy

36
Q

What is pseudoexfoliative glaucoma?

A

extracellular material develops in anterior chamber clogging the TM

37
Q

What are signs of PXE?

A

moth eaten pupillary ruff, bulls eye pattern on lens, flare appearance, corneal endo deposits possible, dandruff like debris on gonio

38
Q

What does moth eaten pupillary ruff describe?

A

TIDs close to pupillary border

39
Q

What is the hallmark sign of PXE?

A

bulls eye pattern on lens, iris starts to rub off the material on the lens so you see a bulls-eye appearance on the lens from iris constriction and dilation

40
Q

What are characteristics of PXE?

A

Scandinavian descent, more females have the syndrome but more males have glaucoma as a result, genetic predisposition of LOXL1, 7th decade of life, unilateral/asymmetric, 20% with syndrome develop glaucoma

41
Q

What is PXG therapy?

A

topical GLC meds, ALT/SLT, filtration sx, poorer prognosis than POAG due to fluctuations and IOP spikes/greater risk of treatment failures

42
Q

What is not curative for PXG?

A

phaco IOL is not curative, you just don’t see deposition as readily due to not having deposition for a plethora of years

43
Q

What is inflammatory glaucoma?

A

IOP spike with AC inflammation, may have initial low IOP due to CB dysfunction in inflammatory attack, WBC/RBC/debris in TM

44
Q

What is the etiology of inflammatory glaucoma?

A

traceculitis

45
Q

What does inflammatory glaucoma lead to?

A

PAS and PS

46
Q

What are therapies for inflammatory glaucoma?

A

treat inflammation/disease (caution with steroid b/c IOP elevation possible), mydriasis, NO PGA, beta blocker or CAI or alpha agonist good, LPI, filtration surgery

47
Q

Why is a LPI likely to close in inflammatory glaucoma?

A

due to inflammation and scarring

48
Q

What are phaco glaucomas?

A

phacolytic and phacoantigenic

49
Q

What is phacolytic?

A

high molecular weight proteins leak from lens with intact capsule and deposit in the angle, macrophages lodge in angle

50
Q

What is phacoantigenic?

A

lens proteins leak through ruptured capsule, inflammatory response, post sx with retained material

51
Q

What are signs of traumatic glaucoma?

A

disruption of angle structure/integrity, hyphema, angle recession

52
Q

What is acute and long with angle recession?

A

acute: trauma can pull TM directly and damage schlemm’s canal to reduce outlfow// longterm: scarring of TM and schlemm’s causing later stage IOP elevation

53
Q

What is the pathophysiology of traumatic glaucoma?

A

direct trauma to TM, debris in TM yield scarring, migration of endothelial cells over TM

54
Q

What is treatment of traumatic glaucoma?

A

POAG more common in opposing eye, treatment with aqueous suppressants or filtration surgery

55
Q

What is the typical episcleral venous pressure?

A

8-10 mmHg

56
Q

What is the normal drainage process?

A

outflow requires a pressure gradient so an area of higher pressure can drain into an area of lower pressure, if EVP is elevated, we don’t have as much of a gradient so we get reduced outflow

57
Q

What two things cause increased EVP?

A

carotid cavernous fistula and sturge weber syndrome

58
Q

What is a carotid cavernous fistula?

A

abnormal communication of arterial and venous flow in cavernous sinus, increase pressure in sinus leads to poor venous drainage

59
Q

What is the treatment of CC fistula?

A

surgical tx of fistula is high risk because it is in the middle of the brain, tx IOP with aqueous suppressants, if neo filtration procedure

60
Q

What is sturge-weber?

A

phacomatosis, vascular hamartoma leading to increased EVP, may also have angle malformation

61
Q

What is the most obvious sign of sturge-weber?

A

port wine stain along trigeminal distribution, noted at birth/early age

62
Q

What is the glaucoma incidence with sturge-weber?

A

50% esp if ophthalmic and maxillary divisions are involved

63
Q

What is the mechanism of sturge weber glaucoma?

A

anomalous development of angle, neo possible (requires goniotomy at young age to remove TM), small fistulas in episcleral vessles… if eyelid is involved glaucoma is more common

64
Q

What is therapy for sturge weber glaucoma?

A

pharm therapy if later onset, filtration surgery often needed for younger patients esp with neo present

Glaucoma (4 decks)

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