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Z. Glaucoma — Class Final > SOAG > Flashcards

SOAG Flashcards

1
Q

Without exception, all secondary
glaucomas arise due to

A

Abnormality in outflow

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2
Q

T/F: XFS is age-related

A

TRUE

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3
Q

XFS is characterized by deposition of ___ material throughout the body

A

Extracellular fibrillar (beta amyloid)

described as razor blades, not fluffy

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4
Q

Men or women: XFS more common

A

Women

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5
Q

T/F: LOXL1 is a useful screening tool for XFS

A

FALSE

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6
Q

Describe the latitude, climate, and solar impact on XFS

A

Higher latitude (upper US), colder climate, and more time outside —> RF

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7
Q

What is the most consistent and important Dx feature of XFS?

A

Deposits on ant surface of lens

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8
Q

Describe classic XFS pattern on lens (when dilated)

A

Central zone (relatively homogenous), intermediate clear zone, then peripheral (granular/patchy) layer

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9
Q

In XFS, why is phacodenesis and lens dislocation common?

A

Weak zonules

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10
Q

Features of XFS on iris

A
  1. XFM on iris sphincter (may be subtle)
  2. Pigment loss from iris sphincter
  3. Iris blood vessel abnormalities (eg rubeosis) **NVA is rare
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11
Q

What can be found on cornea in XFS?

A

Flakes of XFM on endo surface + increased CCT

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12
Q

Increased TM pigmentation is a prominent sign of XFS. Unlike PDS, the distribution of the pigment
tends to be …

A

Uneven, splotchy

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13
Q

How to diff between XFS and Capsular Delamination?

A
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14
Q

Capsular Delamination is associated with ___ due to ___.

A

CAT; heat exposure

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15
Q

T/F: POAG has a more severe clinical course and worse prognosis than XFG .

A

FALSE; XFG progression is worse than POAG

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16
Q

Target pressure for XFS

A

17

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17
Q

Why CAI CI’d w/ XFS?

A

Compromised endo

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18
Q

___ is the procedure of choice for XFG

A

Trabeculectomy

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19
Q

Classic triad of PDS:

A
  1. Corneal endo pigment (Krukenberg)
  2. Mid-peripheral transillumination defects
  3. Dense homogenous pigment of TM
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20
Q

PDS/PG occurs almost exclusively in ___ (race)

A

Caucasians

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21
Q

Flap Valve Effect

A

AH can pass from PC to AC but not back —> higher pressure in AC —> displaces iris posteriorly

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22
Q

Why does burnout phase of PG occur?

A

As lens gets larger and Miosis occurs, iris pulled away from zonules

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23
Q

T/F: IOP elevation in PDS is sue to pigment blockage

A

FALSE; phagocytosis of TM cells overload —> TM cells die —> meshwork collapses

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24
Q

T/F: Krukenerg pathognomonic of PDS

A

FALSE; but seen in 95% of PDS

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25
Transillumination more obvious in ___ eyes
Light
26
Why is it important to record post-dilation IOP in PDS pts?
Acute IOP spikes can occur due to pigment cloud in AC
27
Why heterochromia in PDS?
Pigment deposition may occur on the anterior iris surface
28
Scheie stripe (or Zentmayer Line)
Seen in PDS Pigment deposition at site of Ant Hyaloid attachment to post lens
29
Pigment Reversal Sign
In PDS, with age, pigment clears, esp inferiorly —> sup darker than inf
30
T/F: Pts in Active Pigment Dispersion Phase (prior to conversion to GLC) can get LPI as prophylactic tx
TRUE
31
Increased pigment dispersion may occur due to… (3)
1. Exercise 2. Stress 3. Dilation
32
Most important factor in conversion from PDS to GLC
IOP > 21
33
Advantages of Pilocarpine to TX PDS
1. Lower IOP 2. Reverse bowing 3. Inhibit exercised-induced IOP spike
34
Disadvantages of Pilocarpine to TX PDS
1. Accommodative spasm 2. Inc risk of RD
35
Advantage of PGA to TX PDS
Lower IOP (bypasses TM)
36
Disadvantages of PGA to TX PDS
Does not directly affect IZC or PD
37
Why might aqueous suppressants increase ICZ?
Dec PC pressure
38
T/F: Laser iridotomy can slow progression of established PG
FALSE
39
PDS candidates for prophylactic LPI
1. Concave iris 2. Clinically detectable pigment releasing on dilation 3. Normal IOP w/o tx
40
Describe efficacy of SLT in PG
Very effective in lowering IOP but short lives Most effective in young
41
Pathophysiology of Steroid-induced GLC?
1. Changes in TM structure 2. Increased deposit of ECM in TM 3. Dec Phagocytic activity of TM endo cells
42
Time to IOP response: topical
Weeks
43
Time to IOP response: IV
Months
44
Time to IOP response: systemic
Years
45
RF for steroid-induced GLC?
1. Pre-existing POAG/suspect status *(30% of suspects & 90% of POAG develop ≥6 mmHg in after 4 weeks of dexamethasone)* 2. Age (rly young, rly old)
46
Why should PGA and pilo be avoided in steroid-induced GLC?
Pro-inflammatory
47
Manage Steroid Induced GLC
Stop steroid, tx IOP
48
Why might a uveitic pt initially present with low IOP?
1. Prostaglandin-mediated inc in UVO 2. CB inflamed —> dec in AH prod
49
Uveitis can elevate IOP via (4)
1. TM endo dysfunction 2. Fibrin and inflamm cells block TM 3. Steroid Tx 4. PAS
50
Which drug class should be avoided with Posner-Schlossman?
PGA (inflammation)
51
Posner Schlossman Syndrome
Acute *unilateral* IOP elevation (40-50 mmHg) (+) blurred vision, mild pain w/ **trabeculitis**
52
Fuchs Heterochromic Iridocyclitis
Rare chronic unilateral uveitis 1. Heterochromia 2.Uveitis 3. PSC 4. 2ºOAG
53
Phacolytic GLC
Mature CAT —> leakage of proteins —> obstructs TM
54
Pseudohypopyon
Accumulation of proteins that leaked from mature CAT in Phacolytic GLC
55
Lens Particle GLC is caused by
Retention of lens material, following CAT extraction that obstructs TM
56
TX for Lens Particle GLC
1. Aqueous suppressants 2. Mydriatics (inhibits Posterior Synechia) 3. Steroids 4. Surgically remove lens material
57
Phacoantogenic/Phacoanaphylactic GLC
Pt sensitive to own lens proteins after surgery or penetrating trauma w/ - Low grade vitritis - Posterior + Anterior Synechia
58
In phacoantigenic GLC, if cortex remains:
Bomb w/ steroids
59
In phacoantigenic GLC, if nucleus remains,
BACK TO SURGERY
60
In Hyphemia, IOP elevation occurs due to obstruction by:
1. RBC 2. Inflammatory cells 3. Fibrin
61
Sickle Cell pts should avoid which drugs?
1. CAIs 2. Hyperosmotics 3. AAs
62
TX for Hyphema
1. Head elevation, eye shield, + limited activity to settle blood 2. Steroids (Pred) 3. Cyclo (Pain) 4. Tx IOP (eg Timolol)
63
GLCs caused by vitreous hemorrhage
1. Hemolytic GLC (RBCs) 2. Ghost cell GLC (Degenerated RBCs)
64
IOL associated GLCs
1. UGH — inflammation 2. Secondary Pigmentary 3. Pseudophakic Pupillary Block
65
Causes of elevated EVP
1. Sturge Weber (AV malformation) 2. Venous obstruction 3. Sup VC Syndrome 4. Idiopathic*

Z. Glaucoma — Class Final (8 decks)

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