POAG Flashcards

1
Q

Principal site of insult in POAG

A

Laminar region of ONH

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2
Q

What diurnal variation is common in POAG?

A

> 5 mmHg

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3
Q

T/F: IOP asymmetry is more common in secondary GLC compared to primary GLC

A

TRUE

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4
Q

How much asymmetry is common in GLC?

A

≥ 3 mmHg

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5
Q

Primary cause of elevated IOP in GLC

A

Reduced outflow facility

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6
Q

Fundamental cause for the increased resistance to outflow in POAG is not known, but is believed to be a consequence of alterations in…

A

Juxtacanicular region of TM

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7
Q

OHT is associated with higher incidence of ___ (inc/dec) CCT

A

Increased (>555 mmHg)

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8
Q

NTG is associated with higher incidence of ___ (inc/dec) CCT

A

Decreased (<555µm)

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9
Q

POAG is diagnosed if angles are open/normal; however Gonio should still be performed on these pts. Why? And especially if they are…

A

May develop angle closure due to lens changes, esp in HYPEROPES

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10
Q

What is the single most important clinical feature to establish Dx of POAG?

A

ONH appearance

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11
Q

Floor Effect

A

RNFL thinning stops (“Reaches its floor”) at 60µm despite progression

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12
Q

OCT features of POAG:
1. RNFL defects
2. Thinning of GCs
3. Decrease in NRR
4. ???

A

Loss of macular and peripapillary capillaries

visible on OCT angiography but not widely used in practice

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13
Q

Most common meridian for RNFL defects

A

Inf Temp

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14
Q

What is the difference between local and diffuse RNFL defect in RNFL?

A

30º

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15
Q

Trans-laminar cribosa pressure gradient becomes higher when the lamina is ___, as in the case of high ___

A

Thinner; myopia

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16
Q

Low blood pressure is associated with ___ (hi/lo) CSFP

A

Low

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17
Q

How can a benign tumor in the chiasmal region produce GLC-like optic discs:

A

Obstructs ON/CSF canal —> Inc TLPD —> thin NRR + large PPA

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18
Q

SVP pulsation occurs in tandem with the ___ pulse

A

CSF

(Collapses during CSFP diastole, expands during systole)

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19
Q

SVP is ___ (less/more) common in GLC

A

LESS

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20
Q

Absence of SVP may be ___ (protective/RF) of GLC

A

RF

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21
Q

Strain in Lamin Cribosa triggers what CT remodeling? Via Via what receptors?

A
  1. LC stiffens
  2. Post mvmt of LC

Via integrin receptors

22
Q

Other than VF loss, what other visual dysfunction?

A

Decreased CS, color, and motion perception in early stages
VA affected later stages

23
Q

How many test locations in a 30-2?

24
Q

How many test locations in a 24-2?

25
Clinical use of 10-2?
Advanced GLC, macular involvement
26
What results would you expect in a VEP of a GLC pt?
VEP latency
27
What results would you expect in a ERG of a GLC pt?
Abnormal pattern/flicker w/ VF progression
28
What results would you expect in a PhNR ERG of a GLC pt?
< 50% b-wave amplitude —> suggest GC abnormality
29
T/F: VF is a *requirement* for the Dx of GLC
FALSE; not all pts are able to provide reliable fields (electrophysiology may be used in its place)
30
According to OHTS, 3 RFs that significantly increase risk of conversion from OHT to GLC
1. Higher baseline IOP (<25 mmHg) 2. Thinner CCT (< 555 µm) 3. Larger VCDR (>0.5)
31
According to OHTS study, 20% reduction in IOP reduces risk of GLC by ___ in whites, ___ in blacks, and overall: ___.
36% in white 58% in black 50% overall
32
OHTS: High risk suspects have **any** of the following… + a ___% risk of conversion
1. IOP > 30 mmHg 2. CCT < 555 [+IOP > 25 *or* VCD > 0.5] 3. RNFL defect on OCT 4. VF defect, consistent w/ GLC > 20% conversion
33
TX for Low-Risk
No Tx Pt edu F/u: 6-12 mo RTC x 1 yr CEE + OCT/VF
34
TX for Medium-Risk
No Tx (if OCT/VF reliable) Maybe Tx trial (if unreliable) F/u: every 6 months
35
TX for High-Risk
Tx rec’d — 15% reduction Consider: life expectancy, expense, or risk of tx F/u: every 6 months
36
NTG suspect might exhibit:
1. Cupping 2. RNFL loss 3. VF defects But normal IOP
37
What IOP is normal for NTG?
High end of normal (18-20 mmHg)
38
T/F: Decreased VA in a NTG suspect is indicative of progression to GLC
FALSE; suspicious for non-GLC disease bc dec VA not expected until late stage GLC
39
Case HX that may indicate NTG in suspect
1. Hypotension 2. Prior IOP elevation 3. Vasospasms (Migraines, Raynaud’s) 4. FOHX of GLC
40
Central scotomas suggest
ON compression
41
Why is a peripheral retina exam important in GLC eval?
Scars/lesions may produce VF defects
42
Pathognomonic sign for GLC
Does not exist
43
T/F: GLC Dx is urgent and requires immediate TX
FALSE; “time is on your side”
44
T/F: POAG is diagnosed independent of IOP
FALSE; IOP must be > 21 mmHg Otherwise, consider NTG
45
___% of adults in US have vCDR < 0.6
98%
46
98% of adult pop in US has vCDR asymmetry < ___ Each ___ increase in vCDRE asymmetry increases odds of GLC by ___x
0.2 0.1; 2.5x
47
T/F: (-) ISNT can be found in non-GLC pt
TRUE; 5-10% of gen pop
48
T/F: Cirrus = RNFL + GC + IPL
FALSE GCC = RNFL + GC + IPL Cirrus = GC + IPL
49
Rim area < ___ is **always** suspicious
< 1.0 mm^2
50
Fovea lies about ___º below ONH
10º
51
5 steps to manage GLC
1. Establish baseline 2. Set IOP target 3. Lowe pressure 4. Long term f/u 5. Modify as needed
52
T/F: IOP lowered below threshold shows no add’l benefit, once threshold already met
TRUE