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ChM > glaucoma > Flashcards

glaucoma Flashcards

1
Q

What are the 3 components of trabecular meshwork

A

uveal (at iris root), corneoscleral (sheets spanning from scleral spur to scleral sulcus), juxtacanalicular (major site of outflow resistance; next to canal of schlem)

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2
Q

What are the 3 mechanisms that aqueous enters the posterior chamber?

A

active secretion (via Na-K pumps), ultrafiltration (hydrostatic and oncotic pressures), and diffusion (movement of ions down concentrations gradient

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3
Q

aqueous production is via what kind of cells?

A

non pigmented ciliary cells

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4
Q

what is the Goldmann Equation of IOP?

A

IOP=(formation of aqueous-pressure insensitive uveoscleral pathway)/(Pressure sensitive trabecular pathway+episcleral venous pressure)

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5
Q

what are the two pathways of aqueous outflow?

A

via trabecular meshwork (schlem to episcleral veins) and uveoscleral pathway (root of iris/ciliary body to suprachoroidal space)

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6
Q

POAG risk factors

A

elevated IOP, African American, FMHx, thin corneas, age, decreased perfusion pressure, ischemic vascular diseases (HTN, DM…etc)

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7
Q

PACG risk factors

A

women, hyperope, inuit/asian

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8
Q

when is peak IOP during the day

A

early AM; decreases by half during sleep.

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9
Q

What is the rate of aqueous production

A

2-3microliters/min

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10
Q

what is the venous outflow path from canal of schlem?

A

schlemm to episcleral veins to anterior ciliary and superior ophthalmic veins then to cavernous sinus

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11
Q

what happens to cross section of canal of schlemm as IOP increases

A

cross section decreases as trabecular meshwork expands

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12
Q

uveoscleral drainage decreases with age and glaucoma. What increases uveoscleral drainage?

A

cycloplegics, adrenergic, prostaglandins.

Miotics decreases uveoscleral outflow

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13
Q

what 4 conditions increase episcleral vein pressure?

A

cavernous-carotid fistula, cavernous thrombosis, sturge weber, thyroid eye disease

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14
Q

what are factors influencing IOP?

A

time of day
body position, exercise, HR, BP, respiration
Fluid intake
Meds

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15
Q

what principle is tonometry based on?

A

Imbert Fick Priciniple

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16
Q

What is the inbert fick principle?

A

The pressure in a dry thin walled sphere equals the force necessary to flatten its surface divided by the area of flattening. P=F/A

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17
Q

What is the area that is flattened on Goldman application

A

3.06 mm diameter of the cornea

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18
Q

too much fluoresceine on Goldmann applanation leads to what falsely high or low pressures

A

high

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19
Q

what is CCT

A

central corneal thickness

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20
Q

whats normal CCT

A

520 microns

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21
Q

why are tonopens and pneumatic tonometers (both are Mackay Marg Type tonometers) useful for patients with corneal edema or scars?

A

because it only interacts with a small area of the cornea

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22
Q

what kind of tonometer is good for Peds?

A

rebound tonometer because it doesn’t require topical anesthesia

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23
Q

How does the Schiotz tonometer work?

A

It indents the cornea with a known weight to be converted to IOP

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24
Q

what are three ways to clean tonometer prisms?

A

1:10 bleach, 3% hydrogen peroxide, 70% isopropyl alcohol for 5 mins.

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25
Q

Hyperemia in a patient with glaucoma you should think of what two causes?

A

elevated IOP or their drops

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26
Q

what are some adverse affects of IOP lowering drops?

A

follicular reaction, decreased tear production.

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27
Q

What characteristics of a bleb should you look at?

A

height, size, degree of vascularization, integrity, Seidel test

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28
Q

what are breaks in the decemets membrane secondary to enlargement of the cornea called?

A

Haabs striae (found in glaucoma patients at times)

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29
Q

Characteristic eye driness from glaucoma meds

A

infranasal PEEs

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30
Q

what’s Van Herrick’s method

A

fast method of estimating angle with thin slit lamp beam

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31
Q

In what situations can blood from episcleral veins enter the canal of schlemm?

A

whenever episcleral vein pressure is higher than IOP. In hypotony, sturge-weber, cavernous carotid fistula

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32
Q

What are normal vessels that can traverse the angle? how are they usually oriented?

A

radial iris vessels, ciliary body arterial circle, vertical branches of the anterior ciliary arteries.
Either vertically or radially.

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33
Q

what does PAS stand for? What could you possibly confuse this for at the angle?

A

peripheral anterior synechiae (more solid sheet like)

Can be confused with normal iris processes (uveal meshwork–which are open and lacy)

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34
Q

what is sampaolesi line?

A

pigment deposition anterior to Schwalbe’s line from pseudo exfoliation syndrome.

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35
Q

what are the names of the two most common gonio grading systems?

A

Schaffer and Spaeth

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36
Q

Criteria for angle recession glaucoma diagnosis on gonio?

A
  1. abnormally wide ciliary body band
  2. increased prominence of scleral spur
  3. torn iris processes
  4. marked variation of the ciliary face width and depth in 4 quadrants
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37
Q

what is cyclodialysis?

A

separation of ciliary body from scleral spur

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38
Q

diameter of anterior optic nerve?

A

1.5 mm

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39
Q

diameter of posterior optic nerve

A

3-4 mm

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40
Q

what are the 3 types of retinal ganglion cells in primates?

A 
M cells (magnocellular neurons)
P cells (Parvocellular neurons)
Bistriated cells (koniocellular neurons)
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41
Q

What are M Cells? what kind of vision does it provide? where does it synapse?

A

They are large axonal cells of the retinal ganglion layer; responsible for dim changes in luminance–thus motion detection. They synapse on the Magnocellular layer of the lateral geniculate ganglion

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42
Q

What are P cells? where do they synapse? what are their function

A

They are located in the central retina with small diameter axons with slow conduction velocity. They synapse on the parvocellular layer of the lateral geniculate ganglion. They discern color and details. Best in luminance conditions.

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43
Q

what is the bistriated cells’ function?

A

discerning blue-yellow oppnency. Activated when blue cones are stimulated and suppressed with red-green cones.

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44
Q

what are the 4 layers of anterior optic nerve?

A

nerve fiber layer–essentially same as RNFL
prelaminar layer–juxtaposed to the peripapillary choroid
laminar layer- juxtaposed to sclera and lamina cribosa
retrolaminar layer-Becomes myelinated and leptomeninges wraps around

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45
Q

how can you visualize the nerve fiber layer?

A

red free filter (green)

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46
Q

What is lamina cribosa?

A

structural layer of the optic nerve as it exits the eye along the Laminar portion of the optic nerve. It has extraceullar matrix for support, vessels for nourishment. Fenestrations allow traversing central retinal A and V to pass through

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47
Q

What is ring of Elschnig?

A

connective tissue ring layer next to the sclera/choroid supporting the optic nerve.

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48
Q

lamina cribosa is thinnest where?

A

superior and inferiorly

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49
Q

What are the two types of peripapillary atrophy (PPA)? Which is concerning

A

Alpha (normal and in glaucoma with hyper and hypopigmentation. Beta zone is associated with glaucoma and have atrophic RPE and largest in areas of neuroretinal loss

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50
Q

What is the ganglion cell complex?

A

Retinal layers including RNFL and ganglion cell layer and inner plexiform layer

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51
Q

What are the two other imaging techniques for RNFL/ONH other than OCT?

A

Confocal scanning laser ophthalmoscopy, scanning laser polarimetry

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52
Q

Clover leaf VF indicates what

A

Inattentive patient or malingering

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53
Q

What are the classic VF patterns of glaucomatous change?

A

Arcuate defect (Bjerrum scotoma), nasal step, paracentral scotoma, altitudinal defect, generalized depression, temporal wedge

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54
Q

What is trend based analysis

A

looking at all VFs throughout time.

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55
Q

what is event based analysis

A

looking at VFs against a baseline test

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56
Q

what are ways to measure progression based on Visual fields?

A

mean deviation, visual field index progression plot

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57
Q

What is FDT perimetry?

A

Frequency doubling technology perimetry. selectively evaluates M pathway for contrast sensitivity toward motion

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58
Q

What is SWAP?

A

short wavelength automated perimetry. uses narrow blue-violet stimulus against a bright yellow background to test the koniocellular layers projecting toward lat gen ganglion

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59
Q

What is FDF

A

flicker defined form perimetry. stimulates M pathway and may be useful for early glaucoma detection.

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60
Q

What is UBM and AS-OCT? what’s good about each?

A

US biomicroscopy and ant seg-OCT. AS OCT has higher resolution. however AS OCT doesn’t penetrate sclera well…thus UBM is better for ciliary body structures

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61
Q

How was the normal IOP range determined?

A

average IOP of 15.5 with +/- 2SD on either side. This is based on European studies

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62
Q

whats the average CCT?

A

540

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63
Q

what are the major associations risk factors for POAG?

A

age, race, family history, CCT, IOP

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64
Q

what is the association of HTN and POAG?

A

young people are protected against POAG and older are more susceptible

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65
Q

Which study found association of DM with POAG? which showed it’s protective against POAG?

A

Beaver Dam showed DM is associated with POAG. OHTS showed it’s protective

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66
Q

what are more obscure conditions associated with POAG?

A

migraines, thyroid, sleep apnea, HLD, low CSF pressure, corneal hysteresis, Raynaud

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67
Q

what characteristic of a POAG patient puts them at most likelihood of blindness?

A

visual field loss at the time of diagnosis

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68
Q

what’s the technical term for normal tension glaucoma?

A

POAG without elevated IOP

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69
Q

normal tension glaucoma can be split in to which two categories?

A

Senile sclerotic group-pale sloping neuroretinal rim

Focal ischemic group- deep focal notching of rim

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70
Q

How does VF differ in a NTG pt vs POAG?

A

NTG tend to be more dense centrally early on

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71
Q

Collaborative NTG Study (CNTGS) found what?

A

reducing IOP by 30% reduced progression of VF from 35% to 12%… after adjusting for the effect of cataracts

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72
Q

what kind of glaucoma has incisional surgery as first line of treatment?

A

primary congenital glaucoma

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73
Q

What’s the general mechanism of Laser trabeculoplasty surgery?

A

increase outflow via targeting the trabecular meshwork

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74
Q

How does ALT work?

A

Thermal damage to trabecular meshwork leading to scarring and release of TNFa, INFb leading to stretching of adjacent areas of trabecular meshwork

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75
Q

How does SLT work?

A

targets pigmented cells only leading to increased inflammation and trabecular meshwork adjacent to areas targeted.

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76
Q

what are glaucoma suspects?

A

abnormal nerve appearance OR abnormal fields

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77
Q

pseudo exfoliation syndrome is associated with what gene?

A

LOXL1; but it’s a multifactorial disease.

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78
Q

Classic pattern on exam for pseudo exfoliative syndrome?

A
  • bullseye pattern
  • transillumination defect
  • Poor pupillary dilation
  • weak zonules–phacodonesis, iridodonesis
  • Pigment deposition (sampaolesi line) at the angle
  • Krukenberg spindles
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79
Q

Intraop (cataract surgery) complications of pseudo exfoliation?

A

zone dehiscence, lens dislocation, vitreous loss

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80
Q

association of increase risk for progression in pseudoexfoliation syndrome in development of glaucoma was shown in what study?

A

Early management of glaucoma trial

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81
Q

prognosis of pseudo exfoliative glaucoma vs POAG?

A

pseudo is worse

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82
Q

What population is pseudoexfoliation syndrome associated with?

A

Scandinavians (up to 50% of glaucomas)

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83
Q

What are classic exam signs of pigment dispersion syndrome?

A
  • transillumination defect
  • pigment deposition (krukenberg spindle and in trabecular meshwork)
  • Sampaolesi line
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84
Q

Zentamayer ring or scheme stripe is?

A

deposition of pigment on zoneules and equatorial region of lens in pigment dispersion syndrome.

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85
Q

How is pigmentary dispersion syndrome affected by age.

A

It may get better given pigment is reduced.

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86
Q

posterior bowing of iris seen in what glaucoma condition

A

pigment dispersion

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87
Q

Pigmentary dispersion glaucoma responds well to what?

A

medical, laser, and trabeculectomy filtering surgery (however caution in young myopes)

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88
Q

How can you distinguish phacoantigenic and phacolytic glaucoma?

A

phacolytic is nontraumatic/disturbed lens and NO KPs

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89
Q

How can tumors cause glaucoma?

A

direct angle invaions, angle closure, hemoorhage, NV, inflammation

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90
Q

how to treat retained lens particle glaucoma?

A

medical therapy to control IOP when the particle resorbs… If cannot be controlled then take it out

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91
Q

Hallmarks of Posner scholssman

A

High IOP in 40-50s, mild AC reaction, unilateral in middle age person

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92
Q

What is a theoretical cause of Fuch’s heterochromic uveitis?

A

Rubella

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93
Q

Does fuch’s heterochromic uveitis respond to steroids?

A

typically no

94
Q

Classic findings in Fuch’s heterochromic uveitis?

A

mild inflammation (stellate KPs), elevated IOP, asymptomatic, fine vessels crossing the trabecular meshwork but NO PAS

95
Q

why are sickle cell patients at an elevated risk of IOP elevation after hyphema?

A

acidic aqueous induces sickling and traps RBCs in trabeculum. Sickle cell patients’ optic nerves also are more prone to damage.

96
Q

which two patient population with hyphema should you consider early surgical intervention

A
  1. sickle cell as their optic nerves are more susceptible to damage
  2. Young children to avoid corneal staining/amblyopia
97
Q

what’s the difference between traumatic hyphema, hemolytic glaucoma, and ghost cell glaucoma

A

hyphema is layering in AC, hemolytic glaucoma is AC RBCs from vitreous hemorrhage, ghost cells are degenerated hemolytic RBCs

98
Q

glaucoma is a frequent side effect of PKP. why?

A

wound distortion of the trabecular meshwork and progressive PAS formation

99
Q

what’s IOP like in most rhegmatogenous RD? What is the issue if it’s high? How do you treat this?

A

IOP is usually low. High IOP can be seen with Schwartz Syndrome given outer segment photoreceptor migration to AC and decreases aqueous outflow.

Retina reattachment to treat

100
Q

What is Schwartz syndrome

A

migration of outer segment photoreceptors to AC and decreasing aqueous outflow thereby increasing IOP

101
Q

what are risk factors for corticosteroid induced glaucoma? 6

A

POAG, first degree relative with POAG, young age <6 years, connective tissues disease, Type 1 DM, myopia

102
Q

CIGTS trial. Purpose? Results/big points?

A

collective initial glaucoma tx study
Purpose: medical vs filtering surgery for initial treatment of POAG
Results: surgery lowered IOP more, but progression were about the same long run. Worse baseline VF and surgery resulted in less progression

103
Q

OHTS trial. purpose? results/big points

A

ocular hen study
purpose: efficacy and safety of topical antihypertensives in ocular HTN.

topical were effective preventing onset of POAG.
5 year risk of OAG risks were: older, CDR/morphology, higher pattern standard deviation, baseline IOP. CCT.

104
Q

EMGT trial. purpose and big points

A

early manifest glaucoma trial
Purpose: effectiveness of IOP lowering with new, early OAG
Results: no tx progressed more than tx.. risk factors for progression –age, high IOP, pseudo exfoliation, more advanced field loss, bilateral glaucoma

105
Q

primary angle closure suspect (PACS) definition

vs primary angle closure (PAC) vs Primary angle closure glaucoma (PACG)

A

iridotrabecular contact >180deg no trabecular/optic nerve damage.
iridotrabecular contact with IOP elevation or PAS, no optic nerve damage
iridotrabecular contact AND optic neuropathy

106
Q

population most susceptible to angle closure glaucoma

A

Asian females (inuits the highest)

107
Q

name some secondary causes of angle closure glaucoma?

A

NVG, intumescent lens. lax zonules–marfans/pseudoexfoliation, chronic uveitis, corneal endothelial migration, epithelial ingrowth, posterior mass

108
Q

most common cause of angle closure?

A

pupillary block

109
Q

anterior chamber depth of less that what depth is prone to PAC

A

2.5mm

110
Q

biometric parameters predisposing to PAC?

A

short AL, shallow AC (2.5mm), thick lens, small K diameter

111
Q

which gene is associated with PACG?

A

ABCC5

112
Q

general risk factors for PACG?

A

female, Asian, biometric measures, FMHx, hyperopes

113
Q

when should you definitely do an LPI for an anatomical narrow angle patient?

A

appositional closure, PAS, increased segmental trabecular meshwork pigmentation, hx of previous angle closure, high risk factors

114
Q

PAC symptoms/signs

A

eye pain, blurry vision, halos, HA

high IOP, mid dilated pupil, K edema, shallow AC

115
Q

strategies to break an PAC attack.

A

miotics cholinergic (with care, this may worsen some types without pupillary block), beta blockers, alpha2 agonists, prostaglandins, carbonic anhydrase inhib, globe compression with gonio, LPI

116
Q

lowered IOP after an acute angle closure attack doesn’t necessarily mean angle is open…why?

A

ciliary body ischemia may lead to decreased aqueous production leading to lowered IOP…therefore you need to gonio to make sure anle is open

117
Q

what is subacute angle closure

A

also called intermittent angle closure… angle closes now and then and resolves –esp while sleeping (miosis). Pt has intermit HA, IOP elevation, eye pain

118
Q

what is chronic angle closure glaucoma? how do you treat it?

A

slow progression of PAS at angle. can be confused with POAG. must do LPI

119
Q

what is double hump sign

A

plateau iris

120
Q

how to treat plateau iris?

A

LPI, lensectomy, iridoplasty

121
Q

treatment phacomorphic glaucoma?

A

cataract surgery vs LPI then cataract surgery

122
Q

iris bombe treatment

A

LPI 180 degrees apart. then lensectomy

123
Q

Why does pseudophakic, aphakic, and AC IOL angle closure occur?

A

vitreous pushes forward to these interphases

124
Q

what is capsular block?

A

fluid or visco enters capsular bag and pushes IOL forward narrowing the angle.

125
Q

NVG occurs mostly with which conditions?

A

DR, CRVO, BRVO, ocular ischemic syndrome

126
Q

NVG and ICE both can cause ectropion uvea and PAS in the angle. what feature distinguishes them?

A

in NVG PAS ends at the Schwalbe line. ICE extens to corneal endothelium.

127
Q

what conditions causes NVI that’s not associated with retinal ischemia?

A

Fuch’s heterochromic uveitis., pseudoexfoliation, iris melanoma

128
Q

what is Schwabe’s line

A

where descemet meets trabecular meshwork

129
Q

what is posterior embryotoxon

A

thin gray arcuate line marking anteriorly displaced schwalbes line

130
Q

what are some contraindications for incisional filtering surgery?

A

conj scarring/surgery, active scleritis/uveitis, active anterior segment NV

131
Q

whats the definitive treatment for NVI

A

PRP, antiVEGF

132
Q

What are the triads of ICE syndrome.

A

iris atrophy, angle closure, corneal edema

133
Q

patient population of ICE syndrome

A

middle age, women, unilateral

134
Q

What are the three clinical variants of ICE syndrome?

A

Essential progressive iris atrophy, Cogan-Reese syndrome, Chandler syndrome

135
Q

What is unique about PAS formed in ICE syndrome?

A

high PAS reaching pass schwalbe’s line

136
Q

what is essential progressive iris atrophy?

A

clinical variant of ICE syndrome characterized by extreme iris atrophy: heterochromia, corectopia, ectropion uveal,, iris stromal atrophy, holes

137
Q

What is Chandler syndrome

A

ICE variant characterized by corneal edema and angle closure mostly with minimal iris atrophy

138
Q

What is Cogan Reese syndrome?

A

ICE variant characterized by tan pedunculate nodules on iris surface

139
Q

what is the percentage of patients with ICE who develop glaucoma?

A

50%

140
Q

two conditions with beaten bronze endothelium appearance?

A

Fuch’s, ICE

141
Q

Treatment for ICE? medical? surgical?

A

targeting K edema and ACG. Hypertonic topicals, aqueous suppressant, prostaglandins. Filtering surgery is good. YAG can be used if endothelial cells grow over filtering fistula

142
Q

what is malignant glaucoma?

A

AKA aqueous misdirection or ciliary block. mostly postop with sudden onset pain/IOP, diffusely shallowing of the AC–AVOID miotics

143
Q

what’s the definitive treatment for malignant glaucoma? what about in the interim prior to definitve tx.

A

vitrectomy with anterior hyaloidozonulectomy and deepening the AC.
-can do topicals, YAG to disrupt anterior vitreous in pseudophakics, and Argon photocoagulation of ciliary processes in the interim

144
Q

How do you confirm a diagnosis of epithelial ingrowth?

A

argon laser produces white burns on epithelium

145
Q

define nanophthalmos. other features?

A

axial length <20mm. small cornea, lens is relatively large compared to eye, thick sclera (impede vortex veins drainage)

146
Q

surgical risks of nanophthalmic eyes

A

choroidal effusion, nonrhegmatogenous RD, angle closure

147
Q

what can topiramate cause? how to treat?

A

bilateral sudden onset angle closure and myopic shift. usually bilateral. Stop topiramate and get IOP down

148
Q

what are meds that can cause secondary acute angle closure?

A

topiramate, Bactrim, acetazolamide/methazolamide,

149
Q

what should you think of with bilateral angle closure and myopic shift.

A

topiramate

150
Q

what are the 4 categories of primary pediatric glaucomas?

A
  1. congenital open angle glaucoma
  2. juvenile open angle glaucoma
  3. glaucoma due to ocular anomalies
  4. glaucoma due to systemic diseases
151
Q

three classic features of primary congenital glaucoma (PCG?)

A

high IOP, large cornea, haabs striae

152
Q

whats the time frame of new born primary congenital glaucoma?

A

at birth or witin 1 month of age

153
Q

whats the time frame of late diagnosed primary congenital glaucoma?

A

up to 2 years of life

154
Q

what’s the time frame of juvenile open angle glaucoma? what’s it associated with? general prognosis?

A

after 2 years of life (4-35 usually) associated with anterior segment abnormalities. px most will end up need trabs and tube shunts.

155
Q

juvenile open angle glaucoma is associate with what genes?

A

TIGR, MYOC –both of GLC1A locus

156
Q

mode of inheritance of primary congenital glaucoma?

A

sporadic and autosomal rescessive

157
Q

mode of inheritance of juvenile open angle glaucoma?

A

autosomal dominant

158
Q

genetic association of aniridia?

A

PAX6, usually autosomal dominant

159
Q

genetic associations of axenfeld rieger?

A

PITX2, FOXC1

160
Q

genetic associations of Peter’s syndrome

A

PAX6, FOXC1, PITx2, CYP1b1

161
Q

gender association of primary congenital glaucoma?

A

boys (65%)>girls

162
Q

good prognostic factors in primary congenital glaucoma?

A

diagnosis between 3 mo and 1 year

163
Q

bad px factors in primary congenital glaucoma?

A

dx at birth or after 1 year, K diameter >14mm

164
Q

classic presenting triad of congenital glaucoma?

A

photophobia, blepharospasm, epiphora

165
Q

why are corneas large in congenital glaucoma?

A

IOP elevation causes K and scleral stretch up to 3 years old–leading to large K and bulthalmos. Causing K edema and Haab’s striae

166
Q

what origin are trabecular meshwork cells?

A

neurocrest

167
Q

what is axenfeld anomaly

A

posterior embryotoxon with peripheral iris strands

168
Q

what is Rieger anomaly?

A

axenfeld anomaly (Posterior embryotoxon) +corectopia, iris atrophy, ectropion uvea

169
Q

what is axenfeld-Rieger syndrome?

A

ocular( posterior embryotoxon, corectopia, iris atrophy, glaucoma), dental malformation, maxillary hypoplasia, redundant periumbilical folds, hypospadias, pituitary abnl

170
Q

eye manifestations of Peter’s anomaly

A

leukoma (stromal, decemet, endothelial abnls), iris strands, aniridia,

171
Q

systemic manifestation of Peter’s anomaly?

A

cardiac, urogenital, musculoskeletal, ear, palate, spine

172
Q

Peters anomaly mode of inheritan

A

sporadic– both autos dom and rece also exist

173
Q

what percent of Peters anomaly patients develop glaucoma? What about Axenfeld rieger?

A

50% for both

174
Q

why is aniridia associated with glaucoma?

A

angle closure occurs when rudimentary iris stomp rotates forwards and forms PAS over time

175
Q

aniridia is associated with what cornea abnl?

A

limbal stem cell deficiency–>pannus formation

176
Q

aniridia mode of transmission? associated genes?

A

autosomal dominant. PAX6, WT1 (wilms tumor)

177
Q

systemic syndromes associated with aniridia?

A

Wagr (wilms tumor, aniridia, genitourinary, retardation)-autosomal dom
Gillespie: autos recessive-aniridia, cerebellar ataxia, retardation

178
Q

sturge weber– % associated with glaucoma? why glaucoma?

A

30-70%. increased episcleral venous pressure and malformation of the trabecular meshwork

179
Q

associations of sturge weber (systemic)

A

leptomeningeal angioma, choroidal cavernous hemangioma, calcifications, seizures, focal neurologic deficits, cognitive impairement

180
Q

ocular surgical risk in patients with sturge weber?

A

choroidal effusion, choroidal hemorrhage

181
Q

neonate with ectropion uvea– you should work them up for what?

A

NF1

182
Q

NF1 ocular findings? systemic findings?

A

Lisch nodules, optic nerve gliomas, eyelid neurofibromas, glaucoma.

café aulait spots, cutaneous nerofibromas, axillary freckling

183
Q

aphakic glaucoma risk factors?

A

cataract surgery within 1st year of life, post op complications, small K diameter

184
Q

normal corneal diameter in new born and 1 year old?

A

9.5-10.5 at birth, 11-12 mm at 1 year

185
Q

anesthesia all lower IOP except for what? and what increases IOP

A

chloral hydrate.

ketamine incrases IOP

186
Q

what are the therapies of choice for primary congenital glaucoma?

A

surgical: goniotomy (for clear corneas) or trabeculotomy (for cloudy corneas)

70-80% success for patients diagnosed 3 mo to 12 mo.

187
Q

trabeculectomy or tube shunts are reserved for which pediatric patients?

A

if they have failed two conservative surgeries (goniotomy/trabeculotomy)

188
Q

what are some complications of cyclodestruction

A

phthisis bulbi, uveitis, hypotony, RD

189
Q

what is trabeculotomy?

A

sclerotomy and then cannulating the canal of schlem 360.

190
Q

what is goniotomy?

A

incision at the uveal trabecular meshwork with a gonio lens in place and through a clear corneal incision

191
Q

trabeculectomy has a low success rate in which patients?2

A

younger than 2 y/o and aphakic

192
Q

what are the aqueous suppressing meds?

A

alpha agonist, beta blocker, carbonic anhydrase

193
Q

side effects of betablockers?

A

bronchospasm, hypotension

194
Q

what are side effects of carbonic anhydrase? who should NOT be given these?

A

diarrhea, hypokalemia, sickle cell crisis, SJS, aplastic anemia

sulfa allergies, poor renal function

195
Q

side effect of alpha blockers? contraindications?

A

crosses BBB, therefore apnea, hypotension, bradycardia, hypothermia, hypotonia, somnolence, follicular conjunctivitis with long term use

contraindicated in children <3

196
Q

which are the outflow promoters?

A

alpha agonists, prostaglandins, cholinergics

197
Q

possible side effect of prostaglandins?

A

exacerbates uveitis.
hypertrichosis, trichiasis, conj hyperemia, periocular pigmentation, darkening of iris color, prostaglandin associated periorbitaopathy (sunken in eyes), CME

198
Q

general rule of thumb with target IOP in glaucoma pts?

A

> 25%, but should be individualized

199
Q

what are the 6 classes of glaucoma meds?

A

alpha agonist, beta blocker, carbonic anhydrase, prostaglandin, cholinergics, hyperosmotics

200
Q

what are the 4 prostaglandins and what’s special about each

A

latanoprost/travoprost: lowers by 25-32%
bimatoprost: lowers by 27-33%
Tafluprost: only preservative free

201
Q

what’s special about betaxolol

A

it’s a beta 1 selective inhibitor. less effective than the nonselectives

202
Q

pilocarpine is used for what?

A

plateau iris syndrome, pigmantart glaucoma

203
Q

serious side effects of hyperosmolars?

A

CHF, MI, confusion, subdural/subarachnoid hemorrhage. Contraindicated in renal failure

204
Q

which glaucomas are good for laser trabeculoplasty?

A

POAG, steroid induced, pseudoexofliation, pigmentary

205
Q

which glaucomas should not be treated with laser trabeculoplasty?

A

developmental, inflammatory, NVG, ICE

206
Q

which is the only category B glaucoma med in pregnancy?

A

brimonidine

207
Q

what are the 3 lasers used for laser trabeculoplasty?

A

argon (ALT), nd;yag (SLT), iodide

208
Q

what is peripheral iridotomy used for?

A

primary angle closure, pupillary block, or PAC suspects

209
Q

contraindications of LPI?

A 
completely flat chamber--avoid K damage
hazy view
secondary angle closures w/o pupillary block
360 PAS
NVI
210
Q

how do you deal with bleeding during LPI?

A

push laser lens on the eye to tamponade the bleed. if that doesn’t work use argon laser to coagulate it

211
Q

what is gonioplasty/iridoplasty?

A

argon laser to the peripheral iris to allow AC to deepen by causing stromal shrinkage. This is done after LPI in angle closure/plateau iris

212
Q

what are the cyclodestruction techniques

A

endoscopic cyclophotocoagulation
transscleral cyclophotocoagulation
cyclocryotherapy (higher risk of phthisis, hypotony)

213
Q

when do you do cyclodestruction

A

poor visual potential, poor candidate for incisional surgery. “painful NLP eye”

214
Q

methods of treating painful NLP eyes?

A

retrobulbar alcohol, retrobulbar chlorpromazine, enucleation, transscleral cyclophotocoagulation

215
Q

what are the contraindications of external cyclodestruction?

what are contraindications of endoscopic cyclophotocoagulation?

A

external (cryo, transscleral): contraindicated in good vision, NV–> high risk of phthisis
endoscopic CP: contraindicated in blind eyes due to sympathetic ophthalmia risk

216
Q

what are indications for incisional surgery

A

uncontrolled IOP, progression of field loss, medication nonadherence

217
Q

contraindications for trabeculectomy. 3

A

active uveitis/infection, bad conj/sclera, blind eye

218
Q

whats the most common cause of vision loss s/p trabeculectomy? what are other causes?

A

cataract formation. others include macular edema, hypotony maculopathy, “wipe out” loss of vision for no apparent reason, blebitis/endophthalmitis

219
Q

short term complications of trabeculectomy?

A

wound leak, hypothyroidism, shallow AC, choroidal effusion/hemorrhage.

220
Q

long term complications of trabeculectomy

A

blebitis, endophthalmitis, bleb leak/failure/scaring/over hang, hypotony associated maculopathy, choroidal hemorrhage, eye lid issues, dellens, contact fitting issues

221
Q

risk factors for bleb related endophthalmitis

A

chronic bleb leak, blepharitis, conjunctivitis, trauma, nasolacrimal duct obstruction, CL use, male, young

222
Q

risk factors for bleb failure?

A

young, African American, aphasia, uveitis, anterior NV, prior cataract surgery, prior failed filtering surgery

223
Q

name the two nonvalved tube shunts?

A

molten, baervaldt

224
Q

name a valved tube shunt

A

ahmed

225
Q

what did the tube vs trabecular study show?

A
  • both were similar in terms of IOP and required medications
  • tube was more successful in eyes with prior intraocular surgery
  • tubes required fewer additional procedures
226
Q

indications for tubes?

A
  • failed trabeculectomy
  • active uveitis
  • NVG
  • inadequate conj
  • aphakia
  • CL lens use
227
Q

contraindications of tube shunts?

A

poor corneal endothelial function

228
Q

tube shunt complications?

A

hypotony, corneal touch, tube obstruction, plate migration, tube erosion, endophthalmitis

229
Q

which is more likely for leaks? fornix based or limbus based trabeculectomy?

A

fornix based is more likely to leak bc the incision is at the limbus

230
Q

when is surgical iridectomy indicated?

A

when laser iridotomy can’t be done– cloudy cornea, shallow/flat AC, inadequate pt cooperation

231
Q

goniosynechialysis can be done in PAS of what duration?

A

6-12 months

ChM (59 decks)

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