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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
Q

Transillumination more obvious in ___ eyes

A

Light

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26
Q

Why is it important to record post-dilation IOP in PDS pts?

A

Acute IOP spikes can occur due to pigment cloud in AC

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27
Q

Why heterochromia in PDS?

A

Pigment deposition may occur on
the anterior iris surface

28
Q

Scheie stripe (or Zentmayer Line)

A

Seen in PDS

Pigment deposition at site of Ant Hyaloid attachment to post lens

29
Q

Pigment Reversal Sign

A

In PDS, with age, pigment clears, esp inferiorly —> sup darker than inf

30
Q

T/F: Pts in Active Pigment Dispersion Phase (prior to conversion to GLC) can get LPI as prophylactic tx

31
Q

Increased pigment dispersion may occur due to… (3)

A
  1. Exercise
  2. Stress
  3. Dilation
32
Q

Most important factor in conversion from PDS to GLC

33
Q

Advantages of Pilocarpine to TX PDS

A
  1. Lower IOP
  2. Reverse bowing
  3. Inhibit exercised-induced IOP spike
34
Q

Disadvantages of Pilocarpine to TX PDS

A
  1. Accommodative spasm
  2. Inc risk of RD
35
Q

Advantage of PGA to TX PDS

A

Lower IOP (bypasses TM)

36
Q

Disadvantages of PGA to TX PDS

A

Does not directly affect IZC or PD

37
Q

Why might aqueous suppressants increase ICZ?

A

Dec PC pressure

38
Q

T/F: Laser iridotomy can slow progression of established PG

39
Q

PDS candidates for prophylactic LPI

A
  1. Concave iris
  2. Clinically detectable pigment releasing on dilation
  3. Normal IOP w/o tx
40
Q

Describe efficacy of SLT in PG

A

Very effective in lowering IOP but short lives
Most effective in young

41
Q

Pathophysiology of Steroid-induced GLC?

A
  1. Changes in TM structure
  2. Increased deposit of ECM in TM
  3. Dec Phagocytic activity of TM endo cells
42
Q

Time to IOP response: topical

43
Q

Time to IOP response: IV

44
Q

Time to IOP response: systemic

45
Q

RF for steroid-induced GLC?

A
  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
Q

Why should PGA and pilo be avoided in steroid-induced GLC?

A

Pro-inflammatory

47
Q

Manage Steroid Induced GLC

A

Stop steroid, tx IOP

48
Q

Why might a uveitic pt initially present with low IOP?

A
  1. Prostaglandin-mediated inc in UVO
  2. CB inflamed —> dec in AH prod
49
Q

Uveitis can elevate IOP via (4)

A
  1. TM endo dysfunction
  2. Fibrin and inflamm cells block TM
  3. Steroid Tx
  4. PAS
50
Q

Which drug class should be avoided with Posner-Schlossman?

A

PGA (inflammation)

51
Q

Posner Schlossman Syndrome

A

Acute unilateral IOP elevation (40-50 mmHg)
(+) blurred vision, mild pain
w/ trabeculitis

52
Q

Fuchs Heterochromic Iridocyclitis

A

Rare chronic unilateral uveitis
1. Heterochromia
2.Uveitis
3. PSC
4. 2ºOAG

53
Q

Phacolytic GLC

A

Mature CAT —> leakage of proteins —> obstructs TM

54
Q

Pseudohypopyon

A

Accumulation of proteins that leaked from mature CAT in Phacolytic GLC

55
Q

Lens Particle GLC is caused by

A

Retention of lens material, following CAT extraction that obstructs TM

56
Q

TX for Lens Particle GLC

A
  1. Aqueous suppressants
  2. Mydriatics (inhibits Posterior Synechia)
  3. Steroids
  4. Surgically remove lens material
57
Q

Phacoantogenic/Phacoanaphylactic GLC

A

Pt sensitive to own lens proteins after surgery or penetrating trauma w/
- Low grade vitritis
- Posterior + Anterior Synechia

58
Q

In phacoantigenic GLC, if cortex remains:

A

Bomb w/ steroids

59
Q

In phacoantigenic GLC, if nucleus remains,

A

BACK TO SURGERY

60
Q

In Hyphemia, IOP elevation occurs due to obstruction by:

A
  1. RBC
  2. Inflammatory cells
  3. Fibrin
61
Q

Sickle Cell pts should avoid which drugs?

A
  1. CAIs
  2. Hyperosmotics
  3. AAs
62
Q

TX for Hyphema

A
  1. Head elevation, eye shield, + limited activity to settle blood
  2. Steroids (Pred)
  3. Cyclo (Pain)
  4. Tx IOP (eg Timolol)
63
Q

GLCs caused by vitreous hemorrhage

A
  1. Hemolytic GLC (RBCs)
  2. Ghost cell GLC (Degenerated RBCs)
64
Q

IOL associated GLCs

A
  1. UGH — inflammation
  2. Secondary Pigmentary
  3. Pseudophakic Pupillary Block
65
Q

Causes of elevated EVP

A
  1. Sturge Weber (AV malformation)
  2. Venous obstruction
  3. Sup VC Syndrome
  4. Idiopathic*

Z. Glaucoma — Class Final (8 decks)

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