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Flashcards in Glaucoma Deck (149)
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1
Q

Pilocarpine : Mechanism of Action

A

Parasympathomimetic - Pilocarpine directly stimulates cholinergic receptors, acting on a subtype of muscarinic receptor (M3) found on the iris sphincter muscle, causing the muscle to contract and produce miosis. timulates the sphincter pupillae in the iris and the ciliary muscle, resulting in displacement of the scleral spur, opening of the trabecular meshwork and/or Schlemm’s canal, and enhancement of conventional aqueous outflow.

2
Q

Beta-Blockers: MOA

A

Beta-blockers decrease aqueous humor production by the ciliary body and hence reduce IOP.

3
Q

Carbonic Anhydrase Inhibitors

A

Carbonic anhydrase is an enzyme that catalyzes the reaction of H2O and CO2 in equilibrium with H+ and HCO3−. The net effect of the enzyme on aqueous production is to generate bicarbonate ions, which are transported actively across the ciliary epithelial membrane into the posterior chamber (sodium is the primary cation); an osmotic gradient is established. Water passively follows because of the presence of the gradient, which results in aqueous production. Inhibition of this enzyme results in lower IOP because aqueous production is decreased approx 50% or more;aqueous outflow and episcleral venous pressure are affected little or not at all.

4
Q

Alpha-Adrenergic Agonists

A

Apraclonidine decreases aqueous production but is also associated with an increase in outflow facility and a decrease in episcleral venous pressure. Brimonidine is 23 times more alpha-2 selective than apraclonidine and 12 times more selective than clonidine. Its mechanism of action includes a reduction in aqueous formation as well as an increase in uveoscleral outflow

5
Q

Relate Ciliary Body Anatomy to demonstrate the difference between Angle Recession, cyclodialysis and irido-dialysis

A

Angle recession is a separation between the longitudnal and radial muscles of the ciliary body. (you see a wide CB band but otherwise N structures) Cyclodialysis is when the longitudnal muscles separate from the scleral spur and ca cause hypotony and haemorrhage. Irido dialysis is separation of the iris root and the ciliary body.

6
Q

OHTS found 5 significant risk factors that increased the risk of POAG

A
  • age
  • higher iop
  • CDR
  • greater pattern standard deviation
  • reduced CCT
7
Q

What were the pressure lowering goals of OHTS and CNTGS

A

OHTS: 20% from baseline

CNTGS: 30% from baseline

8
Q

What are the risk factors for steroid responders (5)

A
  • known POAG
  • family hx
  • age
  • DM
  • myopia
9
Q

DDx of arcuate defects

A
Glaucoma
ONH drusen
NAION, AAION
Myelinated NFL
Hemiretinal vein occlusions
BRAO
Optic nerve colobomas, pit
Laser scars to one area of retina
10
Q

DDx of enlarged blind spot

A
ONH drusen
Papilledema
Diabetic papillitis
Hypertensive papillitis
Optic neuritis
MEWDS/IEBSS
Megalopapilla
High myopia (PPA)
11
Q

Glaucomatous nerve features

A
High CDR
Assymetric CDR
Notch
Loss of NFL
Optic disc hg
Bayonetting of vessels
Nasalisation of vessels
Vertical elongation of the cup
Laminar dots (?)
12
Q

Systemic associations with drusen

A

Autosomal dominant
PXE
Sickle cell

13
Q

DDx of glaucomatous nerve

A

Physiologic cupping
Tilted discs

Anything that causes nerve damage...
Glaucoma (open or closed)
Optic neuropathies
compression
toxic/metabolic
vascular insults
14
Q

Disc hg ddx

A
Glaucoma (esp NTG)
Hemorrhagic PVD
Papilledema
NAION
AAION
Diabetes
HTN
Valsalva
15
Q

Thickest rim

A

I>S>N>T

16
Q

Most suspectible to glaucoma (parts of the rim)

A

I>S>T>N

17
Q

Angle most open

A

Inferior

18
Q

Angle most pigmented

A

Inferior

19
Q

Deep AC in who

A

Myopes
Young
Male
(basically everyone who gets PDS)

20
Q

Shallow AC in who

A

Old
female
hyperopes
Eskimo/Asians

21
Q

Steroid responder risks (5)

A
POAG
Family history
Age
Myopia
DM
22
Q

CDN guidelines for suspect, early, mod, and adv glaucoma (dx and management)

A

Class; CDR; VF; Tmax you want; lower by

Suspect; — ; — ; 24; 20%
Mild; 10deg from fixation; 20; 25%
Moderate; 10 deg from fixation; 17; 30%
Severe: >0.9, within 10 deg of fixation; 14; 30%

23
Q

Dose of MMC for trab

A

0.01% for 2 min (in real life this varies but this is a reasonable exam answer)

24
Q

Two types of VF testing

A

Static (Humphrey or Goldmann)

Kinetic (Goldmann)

25
Q

DDx of hyphema in adult

A
Trauma
Bleeding diathesis
Leukemia
Ocular surgery
Fuch's
Other NVI/NVA
UGH
26
Q

PXF cataract risks

A
Poor dilation
Stiff pupil
Zonular weakness
Increased risk of phacodynesis and vitreous loss
Capsular fragility
Lower endothelial cell count
Unstable IOP post-op (spikes)
Post-op inflammation
27
Q

Findings in PXF

A
Poor dilation
Ring of pigment on anterior lens capsule
PXF material on pupil margin
Pupil margin TID
Pigmented angle
Sampolessi line
28
Q

Membrane over angle

A

ICE
Epithelial ingrowth
PAS (uveitis, bad ALT, chronic ACG)
NVI

29
Q

ICE clinical variants

A

Chandler - mostly cornea
Iris nevus - membrane on iris tents up normal stroma to look like nevi (not actually nevi)
Essential iris atrophy (correctopia/polycoria)

30
Q

3 lytic glaucomas

A

Lytic = macrophages clog up TM with junk

Phacolytic - lens particles
Hemolytic - RBC from hyphema
Melanomalytic - pigmented melanocytes (or something) from melanoma cells floating around

31
Q

Secondary glaucomas after IOL implantation

A

UGH
Pupil block angle closure
Secondary pigmentary glaucoma

32
Q

Pigmented TM in who

A
Pigmented people
Older people
PXF
PDS
Melanomas
33
Q

IOP formula

A

IOP = F/C + EVP

34
Q

Types of tonometry

A

Indentation - Schiotz

Applanation - tonopen, Goldmann, Perkins, pneumotonometer (don’t let this last one throw you - unless they say AIR PUFF, it’s still a contact tonometer)

Non-contact - air puff

35
Q

Glaucoma with pigment

A
PXF
PDS
Pigmented people with open angles
Pigment on endothelium from old inflammation, cataract surgery, trauma, hyphema 
ICE
Melanoma
36
Q

Intermittent ACG findings

A
Hx of intermittent ACG
\+/-Normal IOP
PAS
Glaucomflecken
Signs of glaucmatous damage to ON
37
Q

Risk of ACG in the fellow eye after AACG

A

75%. So always do prophylactic LPI

38
Q

Segmental iris atrophy

A
Cataract surgery
Trauma
HSV, EBV, CMV, VZV
ICE syndrome
Axenfeld reiger
PPMD
39
Q

Iridodenesis

A

Separation of iris from CB
Usually result of trauma or surgery
Rx with coloured CL or surgically re-insert

40
Q

Causes of ectropion uveae

A
ICE
Axenfeld reiger
Uveitis
PPMD
NF-1
Epithelial downgrowth
NVG
uveitis
41
Q

How do you tell epithelial ingrowth vs fibrous downgrowth

A

Epithelial ingrowth turns white with YAG

42
Q

Lens induced glaucomas

A

Phacomorphic - angle closure with pupil block
Phacolytic - lens particles leak through intact capsule. Minimal inflammation, but macrophages ingest the particles and obstruct. NO KP.
Phacoanaphylactic - broken capsule. Maybe after surgery. Some books call this the same as lens particle glaucoma. LOTS OF INFLAMMATION with KP’s.
Lens particle - basically the same thing. Maybe it’s more after cataract surgery with some lens left behind.

UGH - from IOL
Dislocated lens (if dislocates anteriorly, causes ACG)
Same with microspherophakia causing ACG

43
Q

Cyclodialysis def’n and treatment

A

Separation of CB from SS
Result of either trauma or surgery
Gonio to confirm
Rx with cycloplegics, most will close on their own in 6/52
Cause hypotony in the meantime, +/- spike when its closing

44
Q

Risks for OHTN progression

A
Age
High IOP
High CDR
High pattern standard deviation
Low CCT
45
Q

CCT definition in OHTS

A

588 = thick

46
Q

RF for OAG

A
Age
High IOP
Family history
Race
Other: HTN, DM, Myope, migraines?
47
Q

RF for AACG

A
Female
Age
Previous ACG
Race - inuit or asian
Hyperopic
Nanophthalmos
Family history
48
Q

RF for NTG

A
Female
Disc hg
migraine
vasospasm/raynauds
smoking
49
Q

DDx of NTG

A

IOP is high, but you’re not measuring it:

  • uncalibrated equipment
  • low CCT
  • corneal edema

IOP is high sometimes but you’re missing it:

  • diurnal fluctuations
  • intermittent ACG
  • Posner Schlossman episodes

IOP was high before but its ok now:

  • burned out OAG (PDS, PXF)
  • old AACG

It’s not glaucoma at all:

  • ONH drusen
  • old optic neuritis, NAION, AION, etc
  • compressive lesion (do a CT - nerve to chiasm)
  • infiltrative lesion of the nerve (sarcoid, TB, lyme, etc)

Only if you’ve ruled all that out can you call it NTG.

50
Q

Acute IOP rise ddx

A

After laser (LPI, SLT, etc)
After surgery (retianed visco, retained lens particles)
Inflammatory (HSV, CMV, Posner Schlossman, Fuch’s)
Steroid responder
After hyphema
AACG

51
Q

Characteristics of plateau iris and treatment

A

Deep central AC, shallow periphery
Flat iris
Bunched up iris in angle
No change in configuration despite LPI

Rx:

  • always make sure they have an LPI first
  • Argon iridoplasty to pull the iris out of the angle
  • miotics
52
Q

DDX of increased EVP

A

AV malformation: CCF, SWS, orbital varix
Lesion compressing SOV: thyroid, tumor, orbital vein thrombosis, cavernous sinus thrombosis, SVC syndrome
Idiopathic: posture (lying down), familial EVP

53
Q

DDx of blood in Schlemm’s

A

High EVP (AV issues, something compressing SOV)
Hypotony (inflammation, hypotony, following trab)
Normal with compression gonioscopy (occludes episcleral veins)

54
Q

DDx of axenfeld-reiger

A
ICE
Aniridia
Isolated posterior embryotoxin (N in 15%?)
Peter's anomaly
Ectopia lentis et pupillae (no glaucoma)
55
Q

Systemic findings in axenfeld reiger

A

Microdontia

Redundant peri-umbilical skin

56
Q

Schabel’s optic atrophy def’n and ddx

A

Hyaluronic acid infiltation of the nerve (stains with colloidal iron, alcian blue)
either from end-stage glaucoma or ischemic optic neuropathy (NAION, AION, etc)

57
Q

Posterior pushing mechanisms of ACG

A
Choroidal effusions
Vitreous overfill from gas
Ciliary body mass
Supra-choroidal hemorrhage
Malignant glaucoma
Contraction of retro-lental tissue (ROP, PHPV)
58
Q

DDx of NVI/NVA

A
Fuch's heterochromic iridocyclitis
DM, radiation retinopathy, OIS
CRVO, BRVO, CRAO
RB!!! Always think RB
ROP/FEVR/Eales
Sickle cell
59
Q

Types of ONH analysers

A

Surface topography - HRT

Cross section - OCT

60
Q

Types of setons

A

Valved (Ahmed)

Non-valved (Baerveldt, Molteno)

61
Q

Pilocarpine for ACG - what types of ACG?

A

Really just for pupil block or plateau iris
Everything else you dilate (malignant, CACG, NVG, cyclodialysis)

Also, pilo won’t work in IOP > 40 because iris muscle is ischemic. Need to lower IOP first

62
Q

Malignant glaucoma risks

A
Hyperopia
Female
Nanophthalmos
Previous ACG
Recent surgery (5d)
63
Q

Malignant glaucoma rx

A

Always do an LPI first to resolve any component of pupil block
Dilate
Decrease IOP with aq suppressants or hyperosmotics
If pseudophake/aphake, can YAG anterior hyaloid face
If phakic, need vitrectomy

64
Q

Injuries with anterior segment trauma

A
Conj laceration
Scleral perforation
Corneal perforation
Hyphema
Traumatic iritis
Traumatic mydriasis
Angle recession
Cyclodialysis
Iridodialysis
PVD
RT, GRT
RD
Retinal dialysis
65
Q

Nanophthalmos - what do you get in the eye and how do you treat

A
  • Large lens - gives phacomorphic ACG. LPI. Can dilate to pull the lens back a bit.
  • Thick sclera - get uveal effusions. Can do sclerectomies
  • Malignant glaucoma - LPI, dilate, YAG hyaloid/vitrectomy
  • Can also get high EVP from outflow obstruction through thick sclera - aq suppressants
66
Q

Why cycloplege in uveitis

A

Reduces pain
Reduces PS
Reduces PAS by deepening the AC
Stabilise blood-aq barrier

67
Q

Deadly effects of atropine

A

Red as a beet, dry as bone, mad as hatter, hot as hades, blind as a bat

Red - vasodilation, flushing, tachycardia
Dry - dry eyes, dry mouth, constipation
Mad - delerium
Hot - fever
Blind - cycloplegia

Rx with acetylcholinesterase inhibitor - e.g. physostigmine

68
Q

Side effects of phospholine iodide

A

Iris cysts and ASC cataracts

69
Q

Side effects of b-blockers

A

ASTHMA AND DECREASED HR/heart block

- always ask about asthma and check HR before giving BB

70
Q

Side effects of brimonidine (and C/I)

A

NEVER GIVE TO CHILDREN - causes respiratory distress/apnoea, CNS depression, hypotension

Adult s/e:

  • allergy
  • increased HR
  • HTN
  • vasodilation/flushing
71
Q

Side effects of CAI (and C/I)

A

Know this cold.

  • SJS
  • metallic taste
  • tingling in hands/feet
  • APLASTIC ANEMIA
  • renal failure
  • metabolic acidosis
  • renal stones
  • SICKLE CELL CRISIS

Don’t give to sickle cell ppl or kidney failure

72
Q

Cloudy cornea infant ddx

A

G-STUMPED

73
Q

Congenital ocular anomalies with assoc glaucoma

A

Anterior segment anomalies:

  • ICE
  • axenfeld reiger
  • aniridia
  • nanophthalmos, high hyperopia
  • microspherophakia

Cornea:
- sclerocornea, megalocornea

Retina:
- PHPV, ROP

Systemic things:

  • Lowe’s (cataract + glaucoma)
  • Rubella (cataract OR glaucoma, never both)
74
Q

Schwartz syndrome

A

Photoreceptor OS’s from old RD clog the TM and cause glaucoma. Resolves after RD repaired.

75
Q

Hemosiderotic glaucoma

A

Hemosiderin from hyphema/vit hx clog TM

76
Q

Thymoxamine - whats it used for

A

Causes pupil constriction without shifting iris-lens diaphragm forward. So you can see the effect of un-bunching iris from the angle without changing the position.

Helps you decide if prophylactic LPI would actually be helpful
(never actually used, i don’t think)

77
Q

Photophobia/tearing child

A

Glaucoma
Lid/eyelash malposition
Corneal irritation, trauma, abrasion, infection
Dacryocystitis, congenital NLDO, canalliculitis, etc

78
Q

Congenital glaucoma triad and signs

A

Tearing, blepharospam, photophobia

enlarged K diam
cloud K
Haab striae (horizontal)
high IOP
high CDR
increasing myopia
79
Q

Definition of congenital vs infantile vs juvenile glaucoma

A
Congenital = 0-3 mos
Infantile = 3 mos - 3 years
Juvenile = 3 yrs+
80
Q

Descemet tears - diff types

A

Forceps trauma - vertical
Haab striae (glaucoma) - horizontal
Vogt’s striae (KC) - concentric to cone
Hydrops, PBK

81
Q

Options for painful blind eye

A

Always do yearly B-scan to rule out mass if there’s no view

  • atropine/PF
  • cyclophotocoagulation
  • retro-bulbar alcohol or chlorpromazine
  • enucleation/evisceration
82
Q

GA effects on IOP measurement

A

Ketamine and succinylcholine increase IOP
(KISS of high IOP)

Others lower it

83
Q

Glaucoma surgery in kids - when to do what

A

Medical management is just temporizing in kids. Start with CAI. Never give brimonidine.

  • goniotomy - needs clear K
  • trabeculotomy - don’t need clear K
  • trabeculectomy - if the others fail
84
Q

6 reasons to do an LPI

A
  • acute ACG
  • prophylactic if other eye has ACG
  • occludable angles
  • malignant glaucoma
  • plateau iris
  • if silicone oil in an aphakic eye (do it inferiorly. SO rises so a superior one will get plugged with SO)
  • with ACIOL
85
Q

Define false positive

A

Patient presses the button when there is no stimulus provided

Max acceptable = 30%

86
Q

Define false negative

A

Patient doesn’t press the button despite it being suprathreshold and in the same area as where they previously saw it

Max acceptable = 30%

87
Q

Define fixation loss (2 ways)

A
  1. There’s a pupil tracker on most machines that follows where the patients eye is moving
  2. Patient sees a spot that’s in the blind spot that was already mapped out

Max acceptable = 1/3

88
Q

What is short term fluctuation on VF

A

10 points are re-tested 2x each
It measures the difference in brightness that the patient responds to

Can reflect inattention or advanced dz

89
Q

What is MD on visual field

A

Average of the deviation of all the patient’s spots from age-matched control. Measure of the total drop in VF (could be due to glaucoma or cataract/etc)

90
Q

What is PSD on visual field

A

Measure of the standard deviation of the difference in the patient vs age-matched control. An estimate of the depression in the hill of vision

91
Q

How would a scotoma look if BCVA is

A

Wider and deeper

92
Q

What happens to the VF if pupil

A

Globally depressed

93
Q

How do you define a scotoma on VF

A

Area of vision >3 degrees that is depressed >6 db

Or 1 pt on Humphrey > 10 db depressed
or 2 adj points > 5 db each

94
Q

What is the definition of legal blindness

A

BCVA in the BETTER eye

95
Q

what doubles in FDT

A

It’s basically a bunch of wide stripes that they flicker really fast in different areas of the VF

So it’s high temporal frequency, low spatial frequency
What doubles is the temporal frequency

96
Q

What cells do FDT preferrentially test for

A

M cells (may be affected first in glaucoma so it may be more sensitive as a screening tool than humphrey)

97
Q

What are the 4 types of VF testing algorithms

A

Acronym - STER (like a STER-case that we know is used in VF testing)

  1. Threshold: staircase of up 4 db, then down 2 db until it reverses again
  2. Supra threshold: screening test that shows bright spots higher than threshold. Only picks up severe defects as a screening tool.
  3. Efficient threshold: estimates threshold for age-matched and tests those first. Subsequent spots up/down based on what was seen. Only one reversal @ each spot (=SITA)
  4. Threshold-related: Threshold determined for a few points then hill of vision determined from those. Then shows 6 db brighter at all spots than threshold - i.e. again just a screening tool for mod/adv dz.
98
Q

How do you classify ACG

A

Primary or secondry, pupil block or not

Primary pupil block: AACG
Primary non pupil block: chronic ACG, plateau iris

Secondary pupil block: phacomorphic, PS, bombe, lens dislocation/microspherophakia, IOL pupil block

Secondary non-pupil block:

  • Anterior pulling: PAS, NVG, ICE, PPMD, epithelial downgrowth
  • Posterior pushing: choroid (effusion or anterior rotation), vitreous pressure (silicone oil, gas, tumors, aq misdirection), retro-lental membranes (ROP, PHPV)
99
Q

What did GLT show

A

L = laser, T = timolol

Laser (ALT) vs drops as first line therapy. Both are ok.

100
Q

What did CIGTS show

A

T = timolol, S = surgery

For initial glaucoma, is medical therapy better or surgery?

Surgery was worse initially but both had equal Va and IOP control and VF changes at 5 years

101
Q

What did EMGT show

A

T = timolol (vs nothing)

Is lowering IOP even helpful for glaucoma?
Used timolol +/- ALT needed

Answer is yes, obviously.
53% progressed (62% with no rx, 45% with rx)

102
Q

What did AGIS show

A

S = surgery

This was primarly a surgical trial looking at ALT vs trab in advanced glaucoma that had failed medical therapy.

Results based on race:

  • Blacks: ALT is better initially (because they scar a lot - think keloids - so trab is not going to be good)
  • Whites: trab is better initially

ALT failure assoc with young age, high IOP
Trab failure: young age, higher IOP, DM, post-op complications (IOP, inflammation, etc)

103
Q

What did TVT show

A

Looked at people with glaucoma who either had prev cataract or prev trab surgery

Randomized to get a trab (with MMC) or tube as the next step

Both groups did well. Therefore, tubes can be used earlier than previously thought.

104
Q

What did OHTS show

A

Inclusion: IOP 24-32, normal field, normal nerve

Lowering IOP by 20% reduces progression from 9.5% to 4.5% over 5 years

Risks for progression:

  • age
  • lower cct (
105
Q

What did NTGS show

A

Lowering IOP by 30% is helpful in reducing progression

Risks of progression:

  • female
  • disc hg
  • migraine
106
Q

What are the laser settings for ALT

A
Argon
Spot size 50um
Power 400 mw
Time 0.1 s
50 spots x 180 deg
107
Q

What are the laser settings for SLT

A

YAG laser on SLT setting
400 um size
power - start at 0.6-0.9 mJ, want champagne bubbles on some shots
50 spots / 180 deg

108
Q

What are the laser settings for iridoplasty

A

Argon
500 um size
400 mw power
0.5 - 1.0 seconds (whoa, long)

Think of iridoplasty as 10x argon...
same power (400 mw)
10x spot size (500 vs 50)
10x time (1 sec vs 0.1 sec)
109
Q

What is total deviation on VF

A

Map of deviation of each point from an age-matched control

110
Q

What is pattern deviation on VF

A

Take the total deviation, subtract the 7th BEST point and apply that subtraction to all points

Should remove media opacities or general depressions and help you see the hill of glaucoma defects

111
Q

Gene for PXF

A

LOXL-1

112
Q

2 types of outflow and relative contributions

A

Trabecular = 90%
UVS = 10%
(% vary depending on source)

113
Q

What drops have an effect on which outflows

A

PG’s: increase UVS
Alpha ag: increase UVS
Cycloplegics: increase UVS

Miotics: increase TM outflow

114
Q

Greatest site of resistance to outflow

A

Juxta-canalicular meshwork (part of UVS pathway)

115
Q

Outflow measurement called what

A

Tonography

116
Q

Outflow rate normally

A

0.22-0.28 ul/min/mmHg

117
Q

GAT size

A

3.06 diam

118
Q

Ideal cct for GAT

A

520 um

119
Q

How to clean GAT

A

alcohol wipe

or 5 min soak with:

  • 70% etoh
  • 1:10 bleach
  • 3% hydrogen peroxide
120
Q

Schaeffer grading system for narrow angle

A
I = narrow
IV = open
121
Q

What supplies ONH

A

short posterior ciliary arteries

122
Q

NFL supplied by what

A

recurrent branches from CRA

everything OPL and forward is from CRA

123
Q

2 theories of glaucoma damage

A
  1. mechanical: compression of NFL axons from high IOP causes damage
  2. ischemic: poor blood flow to NFL axons causes them to die
124
Q

% normals with CDR > 0.6

A

5%

125
Q

% normals with assym CDR > 0.2

A

1%

126
Q

Hemifield assymetry on VF

A

compares top half of VF to bottom half
sup is normally 1-2 db less than inferior
(see better inferiorly)

anything different is suspicious

127
Q

Narrow angle provocative tests

A

Prone-dark test (30-60 min lying prone in the dark)

128
Q

SLT best for who

A

Pigmented glaucoma and angles

PXF and PDS

129
Q

PDS - risk of glaucoma

A

25-50%

130
Q

Who gets PDS

A

young, myopic, males

131
Q

Compare Fuch’s vs Posner Schlossman

A

Fuch’s:

  • presents with blurred vision
  • fine stellate KP
  • min AC rxn
  • iris heterochromia
  • fine angle vessels that bleed easily
  • treat IOP, steroids don’t really help

PS:

  • mild AC rxn
  • no KP
  • no heterochromia
  • episodic unilateral pain
  • rx with steroid (IOP should come down on its own)
132
Q

Sickle cell - how to treat IOP

A

avoid CAI

avoid alpha-1 ag (apraclonidine). alpha-2 ok (brimonidine)

133
Q

Abx in kids - whats not ok

A

Tetracyclines def not ok

134
Q

When do you get ghost cell glaucoma

A

1-3 months after vit hx

135
Q

How do you treat ACG from microspherophakia

A

DILATE the pupil (flattens the lens and pulls it back)

136
Q

How to treat fibrous ingrowth/epi downgrowth over the angle

A

If blocks the angle, treat with meds first

Can’t do laser

137
Q

Rx for topamax induced ACG

A

dilate the pupil (rotate CB backwards)

138
Q

how to treat glaucoma in pregnancy

A
All drugs class C except brimonidine (class B)
better to do laser first if you can

Stop brimonidine once she starts nursing

139
Q

ALT stats

A

Decreases IOP by 20-25%
80% ppl respond
50% success at 5 years (10% per year drop off)

140
Q

Bleb endopht risks

A

young age
male
blepharitis
dacryocystitis, NLDO

141
Q

Bleb endopht bugs

A

Strep pneumo, H flu

142
Q

How to treat bleb endophth

A

tap and inject + fortified topicals

EVS PPV results don’t really apply. So might do PPV earlier I think?

143
Q

Rate of aq production

A

2-3 ul/min = 3 ml/day

144
Q

AC vol

A

250 ul

145
Q

Fluorophytometry is what

A

Measures rate of aq production

146
Q

Decreased aq production with:

A

age
sleep (45% less!)
inflammation, surgery, trauma, meds

147
Q

Aq humor compared to plasma

A

15X more ascorbate (remember this one)
Less protein, less ca, less phosphorous
everything else the same

148
Q

Blood:CB barrier is…

A

fenestrated

149
Q

CB = what layers

A

Inner non-pigmented epithelium (equiv to retina - inner and non-pig)
Outer pigmented epithelium (continuous with RPE - think outer, pigmented)