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Glaucoma > Open Angle Glaucoma > Flashcards

Open Angle Glaucoma Flashcards

1
Q

Define primary OAG

A

a chronic slowly progressive optic neuropathy with characteristic patterns of ON damage and VF loss

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2
Q

What are risk factors for primary OAG

A
  • Increased IOP
  • Decreased Ocular Perfusion Pressure (BP-IOP)
    -Decreased CCT
  • advanced age
    • Fam Hx
      +/- Myopia
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3
Q

What are some characteristics of primary open angle glaucoma?

A 
Insidious onset
Slow Progression
Painless
Usually asymmetric
Central vision relatively unaffected until late in disease
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4
Q

How do you diagnose primary open angle glaucoma?

A

diagnose via appearance of OD and VF

VF deficit should correlate with OD appearance

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5
Q

How does CCT affect IOP?

A

thicker corneas resist flattening, leading to artificially increased IOP readings.

Thick CCT– artificially high IOP
Thin CCT- artificially low IOP

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6
Q

What did the Baltimore Eye Study show?

A

It showed that there was increased prevalence of glaucoma in patients with increased age, particularly among African Americans

prevalence >11% in patients older than 80

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7
Q

What did the collaborative initial glaucoma treatment study show regarding VF defects?

A

it found that defects were 7x more likely to progress in patients older than 60 (compared to those < 40)

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8
Q

What relationship did the OHTS reveal between OAG and age?

A

with increased age, there is increased risk of developing OAG

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9
Q

What affect does race have on development of glaucoma?

A

AA and Hispanics have a 3-4x increased risk of developing disease than Caucasians

risk of bilateral blindness in AAs=4x higher)

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10
Q

What relationship b/w siblings and glaucoma was elicited by the Baltimore Eye Study?

A

The risk of developing glaucoma in an individual with an affected sibling is 10%

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11
Q

What retinal disease process do OAG and OHTN put patients at risk for?

A

Central Retinal Venous Occlusion

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12
Q

What is the prevalence of blindness in patients with glaucoma?

A 
AA's= 8%
Caucasian = 4%
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13
Q

What are characteristics of NTG?

A

usually bilateral but often asymptomatic

OD hemorrhages more common compared to POAG patients and those with increased IOP

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14
Q

What are the two sub groups of NTG? How are they distinguished?

A

Distinguished by appearance of neuroretinal rim

Senile “Shallow” sclerotic group = shallow, pale, sloping neuroretinal rim

Focal Ischemic Group= deep focal notching of neuroretinal rim

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15
Q

What is the characteristic appearance of VF deficits in patients with NTG?

A

VFs more likely to be focal, deeper, and closer to fixation and occur earlier in disease (compared to OAG patients)

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16
Q

What is Ocular HTN?

A

condition where IOP>21 mm Hg but there is no OD/rNFL/VF abnormalities

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17
Q

What did the OHTS study reveal?

A

topical Rx shown to decrease risk of progression to glaucoma in patients with OHTN

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18
Q

How much does each mm Hg affect the risk of glaucomatous damage?

A

each 1 mm Hg increased the risk of glaucomatous changes by 10%

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19
Q

How do changes in the vertical C/D ration affect the risk of progression to glaucoma?

A

For each 0.1 mm incremental increase, the risk of progressing to glaucoma increases by 32%

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20
Q

What risk factors did the OHTS study identify for developing glaucoma?

A
  • increased age
  • increased IOP
  • decreased CCT
  • increased PSD on perimetry
  • increased C/D at baseline
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21
Q

What is exfoliation syndrome?

A

disease characterized by deposition of distinctive fibrillar material in the anterior segment of the eye, either bilaterally or unilaterally

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22
Q

What genetic mutation is associated with exfoliation syndrome? What does the mutation effect?

A

LOXL1 gene is mutated

causes reduced/abnormal synthesis of elastin fibers

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23
Q

How does exfoliation syndrome cause increased IOP?

A

IOP becomes increased 2/2 fibrillar material obstructing and damaging the TM/Uveoscleral pathway

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24
Q

What are some characteristic findings in exfoliation syndrome?

A

Deposition of fibrillar material in a “target-like” pattern on the anterior lens capsule

Heavily brown pigmented TM

Peripupillary atrophy with TIDs

Sampoalesi Line = inferior pigmented line usually anterior to schwalbes line

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25
Q

How does exfoliation syndrome relate to OAG? Is there a population/s that is at specific risk?

A

Exfoliaton syndrome is associated with OAG, accounting for 50% of OAG in Scandinavia

Typically occurs in patients > 70 y/o

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26
Q

How can you manage Exfoliation Syndrome?

A

Laser Trabeculoplasty

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27
Q

What is Pigment Dispersion Syndrome?

A

Disease characterized by pigment deposition on the corneal endothelium (in a vertical spindle pattern, aka Krukenberg Spindle), TM, or on the lens

28
Q

What do Krukenberg spindles form on the corneal endothelium?

A

the vertical spindle known as the krukenberg spindle forms due to the convection currents of the aqueous and phagocytosis by the corneal endothelium

29
Q

What are other s/sx of PDS other than the Krukenberg spindle?

A
  • Peripheral radial iris TIDs
  • Gonio: homogenously densely pigmented TM
  • increased iridozonular contact (2/2 posterior bowing of iris)
  • Zentmeyer Line = pigment deposits on zonular fibers, Anterior hyaliod, or near the lens equator (only seen with dilated pupils)
  • Halos
  • intermittent vision blurring
  • ocular pain
30
Q

What is the risk of developing glaucoma from PDS?

A

25-50%

31
Q

What population does PDS most commonly occur in?

A

Caucasian myopic males aged 20-50

32
Q

How does PDS cause increased IOP?

A

pigment is released into the aqueous (i.e. exercise, dilation, etc) and clogs the TM

33
Q

What treatment modalities can be used to treat PDS?

A

Topical medications
Laser Trabeculoplasty
Filtering surgery

34
Q

What are the different types of Lens-Induced OA Glaucoma?

A

1- Phacolytic
2- Lens Particle
3- Phacoantigenic

35
Q

What is Phacolytic Glaucoma?

A

inflammatory open angle glaucoma caused by leakage of lens proteins through the capsule of a mature/hypermature cataract that obstruct the TM

P/w sudden onset pain, conjunctival hyperemia, and worsening vision

No Keratic Precipiates (vs phacoantigenic)

36
Q

What is Lens Particle Glaucoma?

A

occurs when cortex parcels obstruct the TM s/p CE, capsulotomy, or ocular trauma

usually occurs within weeks of surgery (however, can occur months- years later)

37
Q

What are the clinical findings of lens particle glaucoma?

A
  • Free cortical material in the AC
  • increased IOP
  • moderate AC reaction
  • microcystic K edema
  • posterior synechiae/PAS
38
Q

What is phacoantigenic glaucoma?

A

the patient becomes sensitized to their own lens proteins following surgery or penetrating trauma, causing granulomatous inflammation

39
Q

What are the signs/symptoms of phacoantigenic glaucoma?

A

Moderate AC reaction with KP (on K endothelium and Anterior Lens surface)
low grade vitrifies
synechiae formation
residual lens material in AC

40
Q

What is the treatment for phacoantigenic glaucoma?

A

Corticosteroids and aqueous suppressants

41
Q

How can intraocular tumors cause glaucoma?

A
  • Direct invasion of Angle
  • Angle closure 2/2 CB rotation/lens displacement
  • intraocular hemorrhage
  • NVA
  • Depositon of tumor cells, inflammatory cells, and cellular debris into the TM
42
Q

How can choroidal/retinal tumors cause angle closure?

A

Angle closure can occur due to the forward shift of the lens-iris interface

43
Q

What is the most common cause of glaucoma in patients with either primary or metastatic intraocular tumors?

A

Direct invasion of the CB

44
Q

How does glaucoma occur in uveitis?

A

Mainly occurs 2/2 increased IOP occurs when TM dysfunction > CB hypo secretion

  • TM edema
  • TM endothelial dysfunction
  • blockage of TM by fibrin and inflammatory cells
  • PG mediated breakdown of blood-aqueous barrier
  • PAS
  • blockage of schlemm canal by inflammatory cells
  • steroid induced decrease in aqueous flow through TM
45
Q

What uveitides are associated with glaucoma?

A 
Fuchs heterochromic iridocyclitis
Herpes Zoster Iridocyclitis
HSV keratouveitis
Toxoplasmosis
Juvenile Idiopathic Arthritis
Pars Planitis
46
Q

In the face of active inflammation, what should increased IOP be attributed to?

A

assume its inflammatory related

47
Q

What is glaucomatocyclitic crisis?

A

aka Posner-Schlossman Syndrome
= uncommon form of OAG characterized by recurrent bouts of markedly increased IOP and low grade AC inflammation

Usually presents in middle age patients with unilateral blurred vision, mild pain, mild iritis, and a few KP that are small round and discrete

48
Q

What is Fuchs Heterochromic iridocyclitis?

A

a rare, chronic condition characterized by iris heterochromia with loss of pigment in affected eye

often affects hypo chromatic eye

49
Q

What are the s/sx of Fuchs heterochromic iridocyclitis?

A

low grade AC reaction with small stellate KP
posterior subcapsular cataracts
secondary OAG
Gonio: multiple fine vessels that cross the TM (not associated with fibrous membrane, PAS, or secondary angle closure)

50
Q

What is the treatment for Fuchs Heterochromic Iridocyclitis?

A

Aqueous suppressants

51
Q

What is normal episcleral venous pressure?

A

5-9 mm Hg

52
Q

What are signs of elevated EVP?

A

chronic red eye without discomfort or allergies

tortuous dilated episcleral vessels

unilateral or bilateral

Gonio: blood in schlemm canal

53
Q

What is the treatment for elevated EVP?

A

PG analogs or aqueous suppressants

54
Q

What are possible accidental/surgical causes of glaucoma?

A 
hyphema
angle recession
iridodialysis
iris sphincter tear
cyclodialysis
lens subluxation
55
Q

In patients with sickle cell disease, why do RBCs tend to sickle in the AC?

A

due to the low pH of the aqueous

56
Q

How do you treat an uncomplicated hyphema? What about hyphema with increased IOP?

A

Uncomplicated: eye shield, limited activity, and head elevation

Hyphema with increased IOP: aqueous suppressants and hyper osmotic agents

57
Q

What is hemolytic glaucoma? Ghost cell glaucoma?

A

Conditions that occur s/p vitreous hemorrhage

Hemolytic = Hbg-laden macrophages block the trabecular outflow channels

Ghost Cell= secondary OAG due to degenerated RBCs blocking TM

58
Q

What is angle recession? How does angle recession relate to glaucoma?

A

= tear in the CB, usually b/w the ciliary and longitudinal muscles

causes a chronic unilateral OAG (therefore, consider as a part of Ddx in all patients with unilateral increased IOP)

Increased angle recession is associated with increased risk of glaucoma

59
Q

What are the gonio findings in angle recession?

A
  • brown colored broad angled recess
  • absent/torn iris processes
  • white glistening scleral spur
  • depression in overlying TM
  • PAS @ border of recession
60
Q

What is Uveitis-Glaucoma-Hyphema Syndrome?

A

a secondary inflammatory glaucoma 2/2 chronic inflammation related to a malpositioned or rotating ACIOL

P/W chronic inflammation, CME, NVI, and recurrent hyphemas

61
Q

How are glaucoma and PKP surgery related?

A

Secondary glaucoma is a common complication of surgery related to wound distortion of the TM and a progressive angle closure

62
Q

What is Schwartz Syndrome (Schwartz-Matsuo Syndrome)?

A

increased IOP associated with rhegmatogenous RD

thought to be caused by migration of photoreceptor outer segments through the tear into the AC, and eventually causing obstruction in the TM

63
Q

How do steroids cause increased IOP?

A

they increase resistance to outflow in the TM

can develop at any time during steroid administration

64
Q

What did the collaborative initial glaucoma treatment study show?

A

Purpose of the study was to evaluate if initial medial or surgical treatment was better for OAG

Results: both resulted in similar VF outcomes

65
Q

What did the OHTS study show

A

showed that topical medications resulted in lower IOP, and also established RFs for OHTN patients to develop glaucoma

66
Q

What are some of the RFs the OHTS study linked to progression to glaucoma in OHTN patients?

A 
increased age
increased horizontal/vertical cupping
PSD (0.2 dB caused an increased relative risk of 22%)
increased IOP
decreased CCT
67
Q

What did the early manifest glaucoma trial show?

A

compare the immediate treatment v observation on the progression of newly detected OAG

Results: increased progression of observation group to glaucoma compared to Tx group

progression risk decreased by 10% for every 1 mm Hg decrease in IOP

Glaucoma (8 decks)

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