Glaucoma Flashcards

(212 cards)

1
Q

<p>What two structures make up the ciliary body?</p>

A

<p>Pars plana and pars plicata</p>

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2
Q

<p>How wide are the pars plana and pars plicata respectively?</p>

A

<p>4mm (pars plana)2mm (pars plicata)</p>

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3
Q

<p>What 3 structures make up the pars plicata?</p>

A

<p>ciliary muscles, ciliary vessels, ciliary processes</p>

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4
Q

<p>What are the 3 types of muscles that make up the ciliary muscle?</p>

A

<p>Longitudinal, radial and circular</p>

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5
Q

<p>Where do longitudinal muscles insert?</p>

A

<p>scleral spur</p>

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6
Q

<p>How does the longitudinal muscle affect IOP?</p>

A

<p>affects outflow facility (contraction of muscle increases outflow)</p>

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7
Q

<p>Which muscle fibers of the ciliary body are responsible for accommodation?</p>

A

<p>Circular</p>

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8
Q

<p>What is the blood supply of the ciliary body?</p>

A

<p>Anastomosis between branches of anterior and long posterior ciliary arteries</p>

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9
Q

<p>How many ciliary processes?</p>

A

<p>70</p>

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10
Q

<p>Name 5 functions of the ciliary body:</p>

A

<p>1. Suspends and alters shape of lens2. Produces aqueous3. Affects aqueous outflow4. Makes acid mucopolysaccharide component of vitreous5. Maintains blood aqueous barrier </p>

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11
Q

<p>Contraction of the longitudinal muscle creates what change in the lens?</p>

A

<p>shifts the lens forward and shallows the AC (DOES NOT CHANGE LENS SHAPE)</p>

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12
Q

<p>Contraction of the circular muscle creates what change in the lens? What refractive change?</p>

A

<p>relaxes the zonules making the lens more round with more refractive power (accommodation)</p>

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13
Q

<p>Relaxation of the circular muscle creates what change in the lens? What refractive change?</p>

A

<p>tightens the zonules making the lens flatter with less refractive power </p>

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14
Q

<p>By what method is aqueous humor produced?</p>

A

<p>Active secretion via Na+/K+ pump and carbonic anhydrase </p>

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15
Q

<p>How does glucose enter aqueous humor?</p>

A

<p>passive diffusion</p>

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16
Q

<p>What is the rate of aqueous production?</p>

A

<p>2-3microliters/min</p>

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17
Q

<p>What is the anterior chamber and posterior chamber volumes respectively?</p>

A

<p>250 microliters, 60 microliters</p>

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18
Q

<p>What is the rate of aqueous humor turnover?</p>

A

<p>1% per minute</p>

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19
Q

<p>What is fluorophotometry? What is it used for?</p>

A

<p>direct optical measurement of decreasing fluorescein concentration. Used to measure the rate of aqueous production.</p>

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20
Q

<p>How does the production of aqueous change daily and over a lifetime?</p>

A

<p>Decreases about 45% with sleep.Decreases about 2%/decade (counterbalanced by decrease outflow with increasing age)</p>

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21
Q

<p>What is the pH of aqueous?</p>

A

<p>7.2</p>

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22
Q

<p>Vitamin C concentration in aqueous is higher or lower than in plasma??</p>

A

<p>Much higher! 15x higher</p>

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23
Q

<p>Protein concentration in aqueous is higher or lower than in plasma??</p>

A

<p>Lower (provides optical clarity)</p>

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24
Q

<p>Name 3 functions of the aqueous?</p>

A

<p>1. Maintains IOP2. Provides nutrition to the lens/cornea3. removes metabolic waste</p>

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25

Blood/aqueous barrier is maintained by what cells in the ciliary body?

outer pigmented epitheliuminner non pigmented epithelium

26

Outer pigmented epithelium is continuous with what structure posteriorly?

RPE (basal lamina continuous with Bruch's)

27

Inner nonpigmented epithelium is continuous with what structure posteriorly?

neurosensory retina (basal lamina continuous with ILM) Site of active secretion

28

How do the inner and outer pigmented epithelium relate to each other?

Apex to apex

29

What is flare in the AC?

increase in concentration of protein

30

How does atropine decrease flare?

By closing tight junctions of the blood/aqueous barrier

31

What is the traditional aqueous outflow pathway? What percentage of aqueous outflow is via the traditional pathway?

Outflow via the TM80-85%

32

Give the structural pathway of the traditional aqueous outflow path.

uveoscleral meshwork -> corneoscleral meshwork-> juxtacanalicular connective tissue -> scheme's canal -> collector channels -> aqueous veins -> episcleral and conj veins -> anterior ciliary and superior ophthalmic veins -> cavernous sinus

33

What structure provides the greatest resistance to aqueous outflow?

Juxtacanalicular tissue (4-7micrometer pore size)

34

How many collector channels are there from Schlemm's canal?

30

35

Uveoscleral outflow accounts for how much of the total aqueous outflow?

15-20%

36

Aqueous passes through what angle structure in the uveoscleral outflow tract?

CB -> suprachoroidal space -> CB veins, choroidal veins and scleral veins

37

A cyclodialysis cleft increases aqueous outflow through what mechanism?

increase uveoscleral outflow

38

What affect do cycloplegics have on aqueous outflow?

increase uveoscleral outflow

39

What affect do miotic agents have on aqueous outflow?

Decrease uveoscleral outflowIncrease TM outflow

40

Why are angle structures only visible on gonioscopy?

total internal reflection of the air/cornea

41

Anatomically, Schwalbe's line is...

Termination of Descemet's membrane

42

Name causes of increased pigmentation of TM.

Pseudoexfoliation syndrome, pigment dispersion syndrome, uveitis, melanoma, trauma, hyphema, darkly pigmented patients, age

43

Ddx of blood in Schlemm's canal

elevated episcleral venous pressure, oculodermal melanocytosis, hypotony, congenital ectropion uvea, neurofibromatosis

44

Name 7 cases of PAS

1. angle closure2. uveitis3. NVA4. flat AC5. ICE syndrome6. ciliary body tumors7. mesodermal dysgenesis

45

How do you tell a normal angle vessel from an abnormal angle vessel?

abnormal angle vessels cross scleral spur

46

DDx for abnormal vessels in the angle?

1. Neovascularization2. Iris neoplasm3. Fuch's heterochromic iridocyclitis (Amsler sign)

47

Angle recession is disinsertion of what two structures?

tear between longitudinal and circular fibers of the ciliary muscle

48

What percentage of patients with traumatic hyphema have angle recession?

60-90%

49

What percentage of patient's with angle recession have glaucoma?

5%

50

A cyclodialysis cleft is separation of what 2 structures?

ciliary body and scleral spurDIRECT COMMUNICATION BETWEEN AC AND SUPRACHOROIDAL SPACE

51

How are cyclodialysis clefts treated?

cycloplegics to relax ciliary body, argon laser, cryotherapy, suture CBB to SS, intravitreal air bubble to close superior cleft

52

Iridodialysis is....

disinsertion of the iris root

53

How many axons make up the adult optic nerve?

1.2 million

54

Retinal nerve fiber layer blood supply?

Central retinal artery

55

Prelaminar and laminar optic nerve blood supply?

Short posterior ciliary arteries

56

What is the Goldmann Fick equation?

IOP= F/C +EVPF is rate of aqueous formationC is facility of outflowEVP is episcleral venous pressure

57

Facility of outflow is measured by what?

tonography

58

Facility of outflow increases or decreases with age?

Decreases

59

What is normal EVP?

8-12 mmHg

60

What can cause EVP to increase?

venous obstruction, AV shunt

61

How do you measure EVP?

manometry

62

What is the distribution of IOP?

Non gaussian, skewed towards higher IOP

63

What is a normal range of diurnal variation of IOP?

2-6mmHg

64

How does season affect IOP?

IOP is higher in winter than in summer

65

How does posture affect IOP?

IOP is higher when you are laying down compared to sitting up

66

How does refractive error affect IOP?

IOP is typically higher in myopes

67

Name 3 types of tonometry.

1. Applanation2. non-contact3. indentation

68

What is a Schiotz tonometer?

A known weight indents the cornea and displaces a volume of fluid within the eye. Amount of indentation determines pressure.Falsely low with eyes with low rigidity: high myopia, retinal detachments, intraocular gasFalsely high with scleral rigidity and hyperopia

69

What is the Imbert Fick principle and what is it used for?

P = F/Afor an ideal thin-walled sphere, pressure inside sphere equals force necessary to flatten its surface divided by area of flattening

70

What is the diameter of the application tip?Why?

3.06mmAt this diameter corneal rigidity and tear meniscus pull of tonometer cancel each other out

71

Thick corneas overestimate IOP by about how much?

5mmHg per 70micrometersSame is true for thin corneas

72

If the patient has astigmatism, what changes need to be made with application?

if >1.5D of astigmatism, must align red mark with axis of MINUS cylinder

73

What is a Perkin's tonometer?

Portable form of a Goldmann tonometer

74

What is a Mackay-Marg tonometer? What are some examples?

Applanates a small area so good for corneal scars. Ex: tonopen and pneumotonometer

75

What is the Scheie classification for gonioscopy?

Grade 1- wide open (CBB)Grade 2- SS visibleGrade 3- only ATM visibleGrade 4- closed

76

What is the Schaffer classification system for gonioscopy?

Grade 1- 10% open Grade 2- 20% open Grade 3- 30% open Grade 4- 40% open

 

 

77

What is the first element of the Spaeth classification system for gonioscopy?

First element is a CAPITAL LETTERA- anterior to TMB- at TMC- at SSD- CBB visibleE- large CBB with indentation gonioscopy, put first impression then indent and write actual insertion in (_)

78

What is the 2nd element of the Spaeth classification for gonioscopy?

iridocorneal angle width in degrees from 5-45

79

What is the 3rd element of the Spaeth classification for gonioscopy?

Peripheral iris configurationr= regular (flat)s= steep (convex)q= queer (concave)

80

What is the 4th element of the Spaeth classification for gonioscopy?

Amount of pigmentation graded from 0 to 4

81

Which gonioscopy lens gives a direct view of the angle?

Koeppe

82

Which lenses can perform indentation gonioscopy?

Zeiss, Posner, Sussman

83

Which indirect viewing lens CANNOT perform indentation gonioscopy?

Goldmann (too big)

84

What is the degree or extent a person with normal visual fields can see in all directions?

Nasal- 60Superior- 60Inferior 70-75Temporal 100-110

85

Define fixation loss.

patient responds to target that is displayed in the blind spot

86

Define false positive

patient responds when there is no stimulus

87

Define false negative

patient does not respond to a super threshold stimulus at a spot that was previously responded to (lack of attention, cloverleaf)

88

What is mean deviation?

the average departure of each test point from the age-adjusted normal value

89

what is the background illumination for HVF?

31.5 apostilbs

90

what is the stimulus duration for HVF?

0.2s

91

What is the technical name for a nasal step?

Nasal step of Ronne

92

What is a seidel scotoma?

Small scotoma connected to the blind spot.

93

When performing direct ophthalmoscopy and looking at the RNFL, what is the best setting/light to visualize the RNFL?

red free

94

What cells die in glaucoma?

ganglion cells, amacrine and muller

95

Where do you find the earliest histological changes in glaucoma?

lamina cribrosa

96

What is Schnabels Cavernous Optic Atrophy? What causes it?

atrophy of neural element of the optic nerve and replacement with hyaluronic acid.

Glaucoma or atherosclerotic disease and normal IOP

97

Schnabels Cavernous Optic Atrophy stains classically __________ with ___________.

Hyalouronic acid (mucopolysaccharide) with colloidal iron (blue)

98

Glaucoma is the _______ leading cause of blindness in the US.

(first, second, third or fourth)

Second

99

Steroid responders have __% chance of developing glaucoma in the next 5 years.

31%

100

If a patient has glaucomatous damage in one eye, what is the risk of developing glaucoma in the fellow eye in 5 years?

29%

101

What is the most common genetic cause of POAG?

OPTN (optineurin) mutation

102

JOAG has been mapped to what gene?

MYOC/TIGR on chromosome 1q21-q31

103

Name 6 risk factors for glaucoma

1. age

2. increased C/D

3. thin CCT (<550)

4. family hx (6x increase in 1st degree relatives)

5. increased IOP

6. race (6x increased risk in African Americans)

7.  Possibly DM, HTN, migraines??

104

Decrease in what two colors is the first to occur with glaucomatous damage?

blue - yellow

105

Name 5 causes of secondary open angle glaucoma.

1. clogging of TM  (RBCs, macrophages, neoplastic cells, pigment, lens proteins, photoreceptor outer segments, visco)

2. Toxic/medication (steroids, siderosis, chalcosis)

3. Inflammation (uveitis, interstitial keratitis)

4. Increased EVP 

5. Trauma (angle recession, chemical injury)

106

_______% risk of glaucoma is hyphema is more than 50% the AC volume

_________% risk of glaucoma with total hyphema

27%, 52%

107

What class of medication should be avoided in patients with sickle cell and hyphema?

Carbronic anhydrase inhibitors.

increase vitamin C in AC (decreases pH) and increases sickling

108

Non-clearing VH causes what type of glaucoma?

Ghost cell, khaki colored degenerated RBCs

109

What does "lytic" mean when referring to glaucoma?

macrophages filled with something are obstructing the TM

Hemolytic (hemosiderin)

Phacolytic (lens proteins)

Melanomalytic (melanin from malignant glaucoma)

Melanocytomalytic (melanin from necrotic melanocytoma)

 

110

What is phacolytic glaucoma? What cause it?

When lens proteins leak through the capsule in the setting of a hypermature cataract, macrophages engulf lens proteins and then become stuck in TM

111

Who is your typical patient with pigmentary glaucoma?

young myopic male

112

What percentage of patient with pigment dispersion develop pigmentary glaucoma?

50%

113

How is pigment dispersion syndrome inherited?

AD

114

What is the mechanism of pigment dispersion?

Reverse pupillary block. Iris bows back wards and there is mechanical rub against the pigmented posterior iris

115

What corneal abnormalities can be present in PDS?

Kruckenberg spindle (endothelium metabolizes released melanin)

116

Describe the TIDs of PDS.

Midperipheral, spoke like, radial

117

Patients with PDS have a higher liklihood of having what 2 retinal pathologies?

Lattice (20%), RD (5%)

118

What is the treatment for PDS?

miotics, excellent response to SLT

119

True or False: SLT is recommended in patients with PDS.

True! respond very well to SLT

120

What is the gene for pseudoexfoliation?

LOXL1

121

What percentage of patients with Pseudoexfoliation Syndrome have secondary glaucoma?

50%

122

True/False: PXE is a systemic disease.

True! 

123

What finding on gonioscopy is typical of PXE?

Sampaolesi's line

(band of pigment anterior to schwalbe's line)

124

PXE is most common in what ethnic group?

Scandinavians

125

In PXE, what changes can you see in the iris?

1. blood-aqueous barrier defect

2. pseudouveitis

3. iris rigidity

4. posterior synechiae

5. poor dilation

126

In PXE, what changes can you see in the cornea?

1. Reduced endothelial cell count (interesting huh?)

2. endothelial decompensation

3. endothelial proliferation over TM

127

True/False: PXE can cause both open and closed angle glaucoma.

True! weak zolunes can allow anterior movement of the lens and can cause intermittent angle closure glaucoma

128

Treatment for PXE?

usually have a very good response to laser trabeculopasty

usually have higher initial IOP and more difficult to control IOP with medical treatment alone compared to POAG

129

What is Schwartz's syndrome?

high IOP associated with RRD

130

What material blocks TM outflow in Schwartz syndrome?

photoreceptor outer segments and pigment release from RPE

131

What is the treatment for Schwartz syndrome?

repair RRD

132

What is lens particle glaucoma?

lens particles block TM following trauma or cataract surgery (retained lens fragments). Greater inflammation than with phacolytic glaucoma

133

What are some typical findings of lens particle glaucoma?

very high IOP, PAS, posterior synechiae and inflammatory membranes

134

What is alpha-chymotrypsin?

How does it induce glaucoma?

An enzyme used to melt the zonules in intracapsular cataract extraction (ICCE)

Zonular fragments accumulate in TM, alpha-chymotrypsin itself does not cause damage

135

Who gets steroid induced glaucoma?

1. Patients with POAG

2. Patients with Fam Hx

3. Older patients

4. High myopes

5. DM

136

True or False: Oral steroids raise IOP more than topical steroids.

FALSE

137

Siderosis (iron) and chalcosis (copper) cause glaucoma how?

TM toxicity and scarring from IOFB

138

Name 4 types of non-infectious uveitis that are notorious for causing glaucoma.

1. JRA (20% develop glaucoma)

2. Posner Schlossman syndrome (episodic trabeculitis)

3. Fuch's heterochromic iridocyclitis (60% develop high IOP, glaucoma more common in those with spontaneous hyphema and bilateral disease)

4. UGH

139

Glaucoma develops in ___% of patients that have >180 degrees of angle recession.

10%

140

True or False: Acidic burns cause scarring of the TM more commonly than basic burns.

FALSE

141

A patient with TAO is in your clinic and you notice that in upgaze the patients IOP in about 5mmHg higher than in primary gaze. Why?

calse elevation of IOP caused by IR fibrosis and resistance to upgaze

142

What are some etiologies of elevated episcleral venous pressure?

CC fistula, cavernous sinus thrombosis, Sturge-Weber, NF, orbital mass, TAO, superior vena cava obstruction, mediastinal tumors and syndromes

143

Elevated episcleral venous pressure can cause what finding on gonioscopy?

blood in Schlemms canal

144

What is the mechanism of pupillary block?

In susceptible patients, iridolenticular touch causes resistance of aqueous flow from posterior to anterior chamber causing increased posterior pressure. When pupil in MID-DILATED (stress, low ambient light, sympathomimetric or anticholinergic meds), elevated posterior chamber pressure causes peripheral iris to bow forward and occlude angle

145

What ethnic group comes to mind that is particularly known for having ACUTE angle closure?

Eskimos and Asians

146

What racial group comes to mind that more commonly has CHRONIC angle closure?

African Americans more than asians

147

At what age is a patient at highest risk for angle closure?

55-65 years old 

5% of patients over age 60 have angles that can be occluded and 0.5% of those patients with occludable angles will develop angle closure

148

Is angle closure glaucoma usually unilateral or bilateral?

Bilateral. 75% risk of untreated fellow eye in 5 years

149

What anatomic features predispose to angle closure?

1. small anterior segment (hyperopia, nanophthalmos, microcornea, microphthalmos)

2. Hereditary narrow angle

3. anterior iris insertion (eskimos, asians and AA)

4. Shallow AC (large lens, plateau iris, loose or dislocated lens)

150

You decide to treat a patient that you suspect is in acute angle closure with glycerin. What co-morbidity do you need to check the patients chart for before administering glycerin?

DM

151

True or False: Acute angle closure glaucoma can cause optic nerve edema.

True

152

After an episode of acute angle closure, what are some findings you may see in the lens? Iris?

Lens- glaukomflecken

Iris- atrophy from focal iris stromal necrosis, dilated irregular pupil from sphincter necrosis

153

What do you call focal anterior lens epithelial necrosis after an episode of acute angle closure?

Glaukomflecken

154

If you suspect a patient may be susceptible to angle closure, what are some in office tests you may consider?

Prone test

Darkroom test

Prone darkroom test

pharmacologic pupillary dilation

155

You suspect a patient may be suseptible to angle closure so you decide to put them in a dark room, prone in your office. After 1 hour you check the IOP and it has risen by 6mmHg from baseline. Is this a positive or negative test?

Negative. IOP has to rise >8mmHg to be positive

156

You suspect a patient is in acute angle closure and decide to give IV mannitol. What adverse events could possibly occur?

cardiovascular

157

You give a patient with acute angle closure pilocarpine and nothing happens. Why?

You give a patient with acute angle closure pilocarpine and the IOP goes up. Why?

1. sphincter ischemia

2. iris lens diaphram moves forward and worsens pupillary block

158

What is the difinitive treatment of angle closure?

PI

159

You suspect a patient is in angle closure. Besides drops and lasers, what other treatment options do you have?

compression gonioscopy. Can force aqueous through block and open angle

160

In a patient with angle closure glaucoma... if the iris is in ________ position, an LPI will not be as effective treatment of a treatment. Instead you should try what type of laser?

Plateau iris.

Laser iridoplasty

161

What is a potential serious adverse reaction to IV mannitol?

cardiovascular adverse effects

162

In a patient in acute angle closure in one eye, what is the chance of ACG in the other eye in the next 5 years?

75%

163

Name 2 exam findings you could see in a patient with a history of previous AACG or intermittent angle closure glaucoma.

PAS and glaukomflecken

164

What is glaukomflecken?

gray-white epithelial and anterior cortical lens opacities that occur following an episode of markedly elevated IOP. Histopathologically, glaukomflecken are composed of necrotic lens epithelial cells and degenerated subepithelial cortex.

165

Name a few causes on Secondary Angle-Closure glaucoma WITH PUPILLARY BLCOK.

Phacomorphic

dislocated lens

seclusio pupillae

nanophthalmos

SO

microspherophakia

166

Name a few causes of Secondary Angle Closure WITHOUT PUPILLARY BLOCK and with posterior pushing mechanism.

Posterior pushing:

1. Anterior rotation of CB:

      inflammation (scleritis, uveitis, s/p PRP)

     choroidal effusion (uveal effusion, hypotony)

     suprachoroidal hemorrhage

2. Aqueous misdirection (AKA Malignant glaucoma)

3. Pressure from posterior segment

    tumor, expansive gas, exudative RD

4. Contracture of retrolental tissue

    PHFV, ROP

167

Name a few causes of Secondary Angle Closure WITHOUT PUPILLARY BLOCK with anterior pulling mechanism.

1. Epithelial downgrowth

2. endothelial downgrowth (ICE syndrome, PPMD)

3. NVG

4. adhesion from prior trauma

168

Define nanophthalmos:

Hyperopia of....

axial length of....

corneal diameter of....

Hyperopia of >10D

axial length of <20mm

corneal diameter of  <10.5mm

169

Name some risk factors for development of malignant glaucoma.

uveitis

angle closure

nanophthalmos

hyperopia

s/p laser or incisional surgery in patients with PAS or CACG

170

What clinical findings do you see in malignant glaucoma?

entire AC is shallow (vs with angle closure only the periphery is shallow)

IOP higher than expected

patent iridectomy

no suprachoroidal fluid or blood

171

On POD1 after glaucoma surgery you do a Bscan on a patient and are concerned for a choroidal detachment. What patient SYMPTOM would be more indicative of a choroidal hemorrhage than a choroidal effusion? What CLINICAL FINDING?

Symptom: Pain more indicative of suprachoroidal hemorrhage. No pain with choroidal effusion.

 

Exam Finding: IOP elevated with suprachoroidal hemorrhage and low with effusion.

172

What percentrage of cases of malignant glaucoma resolve with medical therapy alone?

50%

173

Name 3 different laser/surgical options for management of malignant glaucoma.

1. Argon to ciliary process (shrink them?)

2. YAG to anterior hyaloid face

3. PPV with disruption of anterior hyaloid face

174

What is the most common mechanism by which an intraocular malignant melanoma produces glaucoma?

Direct invasion of the TM (can induce NVA and melanin laden macrophages can obstruct the TM (malanomalytis)

175

What is melanomalytic glaucoma?

Secondary open angle glaucoma caused by obstruction of TM with melanin laden macrophages (intraocular malignant melanoma of uveal tract)

176

This endothelial dystrophy looks like "snail tracks" and causes glaucoma by what mechanism?

BONUS: How is it inherited?

Posterior Polymorphous Corneal Dystrophy (PPMD) (don't think about the letters too hard)

Abnormal corneal endothelial cells migrate into angle 

 

Autosomal dominant

 

177

Name 4 proposed mechanisms of NTG.

Nocturnal hypotension (compromised blood supply to nerve)

Autoimmune (increased incidence of proteinemia and autoantibodies)

Vasospasm

Previous hemodynamic crisis (excessive blood loss)

178

What exam finding is more commong in patients with NTG than POAG and can be a sign that IOP is not adequately controlled?

optic nerve splinter hemorrhages

179

In NTG, visual fields differ from POAG in what way?

deeper defects, closer to fixation

180

In ALT, what are the settings?

Power?

spot size?

Duration?

# of spots over what area?

400-1200mW power

50micrometers spot size

duration 0.1s

50 spots over 180 degrees

181

On average, ALT reduces IOP by what percentage?

30%

182

If a burn is placed too posterior with ALT, what is a risk?

PAS

183

ALT is successful most often in what type of glaucoma?

PXG (best) > PG > POAG > NTG > aphakic (worst)

184

On gonioscopy, the more _________, the more likely ALT is to lower IOP.

pigment

185

ALT may worsen IOP in what conditions?

uveitic glaucoma, angle recession, ACG, congenital glaucoma, steroids glaucoma

186

The majority of glaucoma is inherited in a _________ fashion. The exception is ___________ glaucoma, which is inherited __________.

The majority of glaucoma is inherited in an autosomal dominate fashion. The exception is congenital glaucoma, which is inherited autosomal recessive.

187

SLT parameters:

spot size?

power?

number of shots over what degree?

400 micrometer spot size

power 0.6-0.9mJ

50 shots over 180 degrees

188

You can do an LPI with either YAG or Argon laser (or both). What is the benefit and risk of each?

YAG bleed more but close less

Argon bleeds less, more pronounced iritis

189

What are the laser settings for iridoplasty?

power?

spot size?

duration?

200-400 mW power

500 micrometer spot size

duration 0.5-1.0 seconds

190

What patients are at higher risk of bleb failure with trabeculectomy?

previous surgical failure, darker skin, hx of keloid, younger, intraocular inflammation, scarred conjunctiva, hyperopia, shallow AC

191

Mitomycin C is an antibiotic isolated from _________.

streptomyces caespitosus

192

What is MMC mechanism of action?

intercalates with DNA and prevents replication, suppresses fibrosis and vascular ingrowth after exposure to the filtation site. Toxic to fibroblast in all stages of cell cycle, 100x more potent than 5-FU

193

What happens if MMC gets in the eye?

corneal decompensation due to endothelial damage

AC inflammation

necrosis of CB

retinal toxicity

194

What is 5-FUs mechanism of action?

affects the S-phase of the cell cycle

195

What happens if 5-FU gets in the eye?

nothing at normal concentrations

196

If IOP is high post operatively after trabeculectomy, what do you do?

laser suturelysis or digital massage

197

POD1 trabeculectomy. 

Bleb high, IOP low.

What is DDx and Tx?

DDx: overfiltration

Tx: revision

198

POD1 trabeculectomy. 

Bleb flat, IOP low.

What is DDx and Tx?

DDx: choroidal detachment

Tx: cycloplegics, steroids and +/- drainage

 

DDx: bleb leak

Tx: Antibiotis, IOP suppressants, stop steroid, reform AC, pressure patch, glue, surgery?

199

POD1 trabeculectomy. 

Bleb flat, IOP elevated.

What is DDx and Tx?

DDx: suprachoroidal hemorrhage.... Tx: Drainage

DDx: pupillary block.... Tx: cycloplegics, steroid, PI

DDx: malignant glaucoma..... Tx: cycloplegics, aqueous suppressants, PI, YAG to anterior hyaloid, PPV

 

200

POD1 trabeculectomy. 

Bleb high, IOP high.

What is DDx and Tx?

Dx: encapsulated bleb

Tx: needling, aqueous suppressants, bleb revision

201

Most common organism to cause blebitis?

Staphylococcus

202

Treatment of blebitis?

aggressive topical antibiotics, observe daily for endophthalmitis

203

Bacteria most commonly associated with bleb associated endophthalmitis?

streptococcus or H flu

204

Bleeding of this vessel causes a suprachoroidal hemorrhage after trab.

long posterior ciliary artery stretches until it ruptures

205

What are risk factors for suprachoroidal hemorrhage after trabeculectomy?

increased age, HTN, CAD, aphakia

206

What was the main conclusion of the Advanced Glaucoma Intervention Study? (AGIS)

African Americans: ATT

(ALT then trab then trab)

Caucasians: TAT

(trab first)

207

What was the main conclusion from the Ocular Hypertension Treatment Study? (OHTS)

At 5 years, the risk of development of POAG in a patient with ocular HTN decreases from 9.5% to 4.4% with treatment of ocular hypertension.

208

What was the main conclusion from the Collaborative Initial Glaucoma Treatment study (CIGTS)?

Initial treat of POAG with surgery or medical therapy results in similar VFs at 5 years. 

VA loss was initially worse in the surgical group, but evened out by 5 year follow up.

209

What was the main conclusion of the Early Manifest Glaucoma Trial?

Each 1mmHg of IOP suppression resulted in 10% decreased risk of progression.

Treatment of early glaucoma halves the chance of progression

210

What was the main conclusion of the Glaucoma Laser Trial? (GLT)

initial treatment with ALT is at least as good as initial treatment with timoptic

211

What was the main outcome of the Collaborative Normal Tension Glaucoma Study?

IOP is a factor the pathogenesis of NTG and lowering IOP by 30% is beneficial.

212

In NTG, what are the factors that increase the rate of progression?

female gender, hx of migrains, disc hemorrhages