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OC DZ 3rd year > MT 1 > Flashcards

MT 1 Flashcards

1
Q

CME with leakage on FA

A

Diabetic Retinopathy, BRVO, Idiopathic retinal telangiectasia, psuedophakia or aphacia

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2
Q

CME without leakage on FA

A

macular hole, neovascularization, RP, nicotinic acid maculopathy.

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3
Q

Cause of Macular hole

A

Idiopathic-premenstrual women. Myopia-staphyloma Trauma, solar retinopathy

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4
Q

Cause of epiretinal membrane

A

Retinal vascular dz, intraocular inflammation, trauma, retinal procedures

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5
Q

Stage I of Macular hole

A

Decreased or absent foveal depression, yellow deposits, Macular cyst. no hole

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6
Q

Stage II of macular hole

A

Peripheral macular detachment. Increased yellow deposits. Takes weeks-months to get here from I.

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7
Q

Stage III of macular hole

A

Macular hole. Quick from II. 1/3DD punched out area. 20/200 or worse. May see operculum.

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8
Q

Stage IV of macular hole

A

May get better VA with lessening of edema. Complete hole cuff. Complete PVD. May see operculum.

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9
Q

What layers of retina get fluid in CME

A

OPL and INL.

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10
Q

Criteria for CSME

A
  1. Retinal edema within 500 nanometer of fovea 2. hard exudates within 500 nanometers of fovea with adjacent edema 3. edema 1 DD (1500) that is within 1DD to the fovea.
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11
Q

Central Serous Retinopathy vs. Pigment Epithelial Detachment

A

Central serous the RPE is still in place. PED the RPE is also displaces

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12
Q

What do you see on FA with CSR

A

Umbrella or smokestack.

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13
Q

How long does CSR typically recover

A

1-6 months. Can do photocoagulation for quicker results. Can also give low plus for hyperopic shift.

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14
Q

Selective Retinal Therapy

A

For CSR with PED. Treats RPE and spares photo.

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15
Q

Dioxide laser therapy

A

Can also be used to treat CSR.

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16
Q

Lacquer cracks

A

Breaks in brush’s membrane. Can lead to choroid neovascularization.

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17
Q

Findings with Myopic Macular Degeneration

A

Posterior staphyloma, lacquer cracks, fuch’s spots.

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18
Q

Plaqunil/hydroxycholorquine/cholorquine screening

A

Baseline DFE, DFE within one year, DFE every year after 5 years if no risk factors. Run 30-2 or 24-2 on Asians and 10-2 on all other patients.

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19
Q

Risk factors for plaqunil maculopathy

A

550 mg every day for 3 years. Worse with tamoxifine.

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20
Q

Where does plaqunil deposit

A

REP and chord. Pigment areas.

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21
Q

Cinchonism

A

Cause by an overdose of quinie. Fixed dilated pupils, retinal edema, VF restriction, ON atrophy, VA loss.

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22
Q

Thioridazine + chlorpromazine

A

Used to treat psychosis. 2400> of chlorpromazine and 800> thioridazine. Salt and pepper retinopathy. Decreased VAs and poor dark adaption. Pigmentation of macula–> geographical defects of RPE.

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23
Q

Tamoxifene

A

Drug used to treat breast cancer. Rarely vortex keratopathy and ON. Can get yellow crystal deposits in macula with VA loss.

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24
Q

Canthaxathin

A

Promotes suntanning. Can get yellow deposits in retina. Typically benign.

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25
Q

Talc maculopathy

A

Filler in tablets. Asymptotic primarily. Consult for pulmonary exam. Drug counseling. Yearly DFE and photos.

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26
Q

Micro talc Retinopathy

A

Glaucoma like loss. Finer. Ends up in NFL.

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27
Q

Solar Retinopathy

A

2 weeks after exposure. Lamellar hole or foveal cyst. VAs can be normally but central scotoma seen. Start as foveal edema or exudate. Resolve in 1-6 months.

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28
Q

Histoplasmosis

A

Ohio-Missisipi Area. Chicken Poop. Classic Triad 1. Histo spots 2. peripapillary atrophy 3. CNVM. The CNVM is normally late. Treat with photocoagulation. FA and Amsler for other eye as can spread.

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29
Q

Toxocara Canis

A

Granuloma central or by ON. Can have bands connecting them.

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30
Q

Toxoplasmosis

A

When active have car lights in a fog. When quite: pigmented atrophic scar.

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31
Q

Toxoplasmosis tx

A

Pyrimethamine, sulfadiazine, clindamycin, steroid, vitrecotmy, photocoagulation.

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32
Q

Angoid Associated Findings

A
  1. Peur’d orange or leopard spot-temporal to macula. May precede angoid. 2. Salmon spot: peripapillary atrophy 3. ON Drusen
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33
Q

Angoid Streaks

A

Break in brush’s membrane secondary to REP/Chorio changes. Hyperfluoo on FA.

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34
Q

Angoid Streak Complications

A
  1. Neovascularization 2. Rupture of choroid 3. Foveal involvement.
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35
Q

Granbold-straddleberg syndrome

A

PXE + Angoid

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36
Q

PXE

A

Inherited connective tissue disease. 4 kinds. 80% have angoid streaks. Have chicken skin (esp. on neck), cardio dz, and GI hemorrhages.

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37
Q

Paget’s Syndrome

A

Osteogenesis imperfecti. large skulls, kyphosis, deformed bones. Deafness is common. Angoid streaks in 2%.

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38
Q

Ehlers-Dalos Syndrome

A

Rare AD disease. Hyper flexible joints and skin. Have high myopia, epicanthal folds, keratoconus, blue sclera, lens sublimation, RD. Angoid streaks associated.

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39
Q

Sickle Cell and Thalesemmia

A

See angoid streaks.

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40
Q

Choroid Rupture

A

Occurs with trauma. White and concentric to ON. If greater than 200 from fovea can do photocoagulation if neovascularization. Neo is the main complication. Can occur d to weeks following trauma. Monitor with amsler.

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41
Q

Choroidal Folds

A

Normally horizontal. Can cause decreased VA or metamorphism. Common around macula.

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42
Q

What cause choroidal folds

A
  1. idiopathic-common with hyper 2. Orbital dz. 3. Choroidal tumor 4. decreased IOP chronic. Also associated with Retinopathy of prematurity.
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43
Q

Idiopathic Juxtafoveal Retinal Telangectasia

A

Mildest rare retinal vascular anomalies. Have retinal v. dilation, exudates, aneurysm.

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44
Q

Leber’s Miliary Aneuyrsm

A

Moderate retinal v. anomolies

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45
Q

Coat’s Disease

A

Severe retinal v. anomalies.

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46
Q

Groups of IJT

A
  1. Men and seen by Dr. 2. Either gender. VA poor. FA helps. 3. Rarest. Poor macula O2. CNS strokes.
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47
Q

AREDS Category 1

A

Total area of less than 5 small (<63 micrometers) of drusen. 20/32 or better VA in both eyes.

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48
Q

ARED Category 2

A

Multiple small drusen, non extensive (<20) intermediate (63-124) drusen, pigment changes, or any combination. VA 20/32 or better in both eyes.

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49
Q

AREDS Category 3

A

At least one large drusen (<125), extensive intermediate drusen (63-124), geographic atrophy not in macula center. At least one eye at 20/32 or better.

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50
Q

AREDS Category 3a

A

Both eyes meet the AREDS Category 3 criteria

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51
Q

AREDS Category 3B

A

One eye has reduced vision not from AMD or a disqualifying condition.

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52
Q

AREDS Category 4a

A

Geographic atrophy in the macular center or neo

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53
Q

AREDS Category 4b

A

VA worse than 20/32 with AMD the cause.

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54
Q

What categories benefited in the AREDS study

A

3 and 4

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55
Q

Smoking increases risk of geographic atrophy by ____ and CNV by ____

A

2x geo and 3x neo.

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56
Q

What does obesity put you at a greater risk for and by how much

A

93% more likely to develop chorioretinal geographic atrophy.

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57
Q

AMD and Diet

A

50% decrease risk with omega fatty acids. 36% decrease with fruit.

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58
Q

AREDS 2

A

Can eliminate beta carotene and decrease zine dose.

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59
Q

LAST Study

A

Lutein supplementation can help recover function.

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60
Q

Recommendations with AMD Test

A
  1. If no CFH and 1 or 2 ARMS2 alleles–> zinc 2. If 1 or 2 CFH and no ARMS2 alleles–>vitamins.
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61
Q

Macular photocoagulation study

A

Found that all VA was better than observed eye. Not good for subfoveal and good initial VA.

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62
Q

Visudyne laser therapy

A

Inject visudyne in arm and trace back and laser fires and clogs the neo. Dries up and dies. Very effective. Good VAs as long as Neo is not too big and VAs weren’t good initially (<20/50).

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63
Q

Macugen/pegaptanib

A

Anti-VEGF. Used to be very popular. Does decrease vision loss.

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64
Q

Macugen

A

Pegatpamnib

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65
Q

Lucentis

A

ranibizumab

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66
Q

Avastin

A

bevacizumab

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67
Q

Eylea

A

afibercept. Only have to inject every other month.

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68
Q

Triamcinolone on AMD

A

Not effective

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69
Q

FOVISTA

A

Use with lucentis. Inhibits PDGF for better tx.

70
Q

Ambler Grid

A

Each box subtends one degree at 30 cm. 20 degrees total.

71
Q

Foresee PHP

A

14 degrees total field. Can detect early neovascularization.

72
Q

FU for Dry AMD

A

Category 1: 1 year Category 2-3: 4-6 months Category 4: 3-4 months.

73
Q

How many pt. with glaucoma are not diagnosed?

A

50%

74
Q

Hallmarks of glaucoma

A

VF loss and optic atrophy

75
Q

Risk factors for glaucoma

A

Age (normally older but pigment dispersion with younger), African Americans, IOP, Thin corneas

76
Q

Average IOP decrease with drops

A

30%

77
Q

Tmax

A

highest IOP that has been recorded.

78
Q

Can you diagnose glaucoma based on IOP alone?

A

NO. Need to evaluate many factors.

79
Q

The first most important factor in diagnosing glaucoma

A

Risk factors. Then ONH appearance.

80
Q

POHTS central thickness and glaucoma

A

71% increased risk of glaucoma with 40 micron decrease

81
Q

POHTS age and glaucoma

A

For every 10 years there is 22% increase.

82
Q

POHTS sex and glaucoma

A

Increase risk with male

83
Q

POHTS A. American and glaucoma

A

increased risk

84
Q

POHTS heart disease and glaucoma

A

Increased risk

85
Q

POHTS caveats

A

Only applicable to ocular hypertension patients.

86
Q

Average corneal thickness

A

545

87
Q

Risk factors caveates

A

May want to take into account best and worst case scenarios, Risk is also not linear over time, calculator also ignores some important variables (i.e. willingness to take drops)

88
Q

Genetic basis of gluacoma

A

maternal stronger than paternal. Sibling is very strong. Positive family history in 50%.

89
Q

Peripheral vascular disease and glaucoma

A

3x risk with ED. Lack of perfusion to nail beds associated with glaucoma risk. Related to NFL.

90
Q

LOW BMI in Females

A

increased risk for glaucoma.

91
Q

Floppy eyelid syndrome

A

Occurs in patients with floppy eyelid syndrome. Low cerebrospinal fluid. May be associated with NTG.

92
Q

Pupils and glucoma

A

Pupils can affect VF results.

93
Q

Pseudo exfoliation glaucoma

A

Categorize as this once you see ONH changes. Near the border.

94
Q

Pigmentary dispersion glaucoma

A

Occurs in the mid of the iris.

95
Q

How do cataracts increase risk of glaucoma

A

The lens swells and decreases the angle. Can also restrict VF.

96
Q

High specificity

A

No false positives. Do not want a lifelong diagnosis

97
Q

High sensitiviy

A

No false negatives. Prevent risk of blindness.

98
Q

Can you rely on one test alone?

A

NO! you need to rely on multiple tests.

99
Q

Laser Scanner

A

Helps to dx glaucoma.

100
Q

Can you dx glaucoma if no VF change and no ON change?

A

NO.

101
Q

VF and ON atrophy

A

ON atrophy occurs before VF loss is detected.

102
Q

Is FDT good for glaucoma screening?

A

Yes! Especially if threshold.

103
Q

When is an FDT Abnormal?

A
  1. Andy defect in central 5 2. 2 or more mild defects in outer twelve 3. one or more moderate or severe defect in outer twelve 4. Takes longer than 90s to perform the best on one eye.
104
Q

24-2 vs. 30-2

A

24-2 is quicker. 30-2 shows peripheral points that can start to change first.

105
Q

Reliability on Humphrey

A

Blind spot=20% or less. False positives=33% or less. False negatives=33% or less.

106
Q

Poor reliability on a patient with a scotoma

A

Blur the scotoma and make it less noticeable. Has effect on false negatives.

107
Q

Pattern standard deviation

A

Smoothness of hill of vision

108
Q

Standard deviation

A

Overall depression or elevation.

109
Q

Most common early VF loss with glaucoma

A

partial arcuate, paracentral, nasal step (begins on temporal retina), temporal wedge. PPNT.

110
Q

Most common later VF loss with glaucoma

A

Arcuate and altitudinal.

111
Q

Fovea threshold

A

35-40 decibels

112
Q

Degrees between spots in 24-2 or 30-2.

A

six degrees but central spit into two so 3 degrees.

113
Q

Degrees between spots in 10-2

A

2 degrees

114
Q

Partial arcuate loss

A

When the NFL bundle is affected. Defect connected the blind spot to midline. Must have one abnormal spot in temporal field.

115
Q

Paracentral

A

Not contagious with blind spot or nasal. Does not include spots outside 15 degrees that are adjacent to nasal. ST is the most common.

116
Q

Nasal step

A

Limited to nasal horizontal meridian. One or more abnormal spot outside 15 degrees. Cannot have greater than 2 abnormal on temporal side.

117
Q

Temporal wedge

A

Small defect temporal to blind spot. From nasal disc damage.

118
Q

Arcuate

A

Extend from blind spot to at least one point outside 15 degrees and nasal.

119
Q

Altitudinal

A

Severe VF loss in one hemifeld.

120
Q

VF data significant for glaucama

A
  1. 1 non edge point at 0.5% 2. 2 adjacent non edge points at 5% and one at 1% 3. 3 adjacent non-edge points at 5% 4. Horizontal points that differ by 10 decibels 5. CSPD greater than 5%. 6. GHT abnormal.
121
Q

What cornea thickness is GAT designed for

A

520

122
Q

What race has thicker corneas

A

caucasans.

123
Q

NTG tends to have ____ than normal corneal thickness

A

Thinner

124
Q

HTG tends to have ____ than normal corneal thickness

A

thicker

125
Q

____ corneas with OHT have a greater chance of developing POAG

A

Thin

126
Q

AIOP

A

Changing the IOP based off of cornea thickness. use several different equations.

127
Q

Sensimed triggerfish

A

continuously measure the IOP by cornea changes.

128
Q

capsize must be determined by

A

contour NOT color

129
Q

ISNT RUle

A

I>S>N>T

130
Q

Average disc size

A

1.88 V and 1.77 H

131
Q

How much aniso between eyes in C/D is suspiscious

A

0.2

132
Q

What ON defects occur with glaucoma

A

in the lamina cribosia. excavation.

133
Q

Where do ON defects typically occur with glaucoma

A

IT and then ST.

134
Q

Ratio of Horizontal C/D to Vertical C/D

A

Should be greater than 1.

135
Q

Where is the most common position of the central retinal artery trunk

A

superior nasal.

136
Q

Why is the CRA position important

A

tissue first lost is most likely opposite this position.

137
Q

Drance/Splinter Hemorrhage

A

Flame when just off the ONH. Dot when on the ONH. Commonly associated with glaucoma. Inferior pole most common. Can resolve in 10 weeks. Indicates notching. Indication for VF progression. Bad prognosis.

138
Q

Drance/Splinter Hemorrhage more likely found in ____

A

normotensive.

139
Q

Glaucomatous Peripapillary Atrophy

A

Mottling in the RPE that occurs around the ON. Alpha and Beta Zones. Associated with damage and rim loss in same sector.

140
Q

Beta Zone

A

Borders the nerve and bad. Marked atrophy of RPE and choriocapillaris. Visibility of large choroidal vessels and sclera.

141
Q

Alpha zone

A

Irregular hypo and hyper pigment. Touches the healthy retina. Temporally in normal eyes sometimes.

142
Q

Acquired Pits

A

I and S lamina are bigger. Stretch can damage them. More common in NTG. Most likely in IT. Found in areas of pallor.

143
Q

Gonio

A

Perform on all suspect glaucoma and yearly on confirmed glaucoma.

144
Q

Corneal wedge

A

Joins at Schwalbe’s line.

145
Q

Normal NFL

A

Casts a whitish haze over underlying structures. Makes eyes bright. Brightness related to thickness.

146
Q

Slit Defects

A

Focal damage of NFL at lamina. Can be seen in up to 1-% of normals.

147
Q

Wedge Defects

A

Represents expanding loss of NFL. Normally in same quadrant as notch defect. Correlates with VF defect. More narrowed toward disc.

148
Q

Diffuse NFL Atrophy

A

Most common pattern seen. More common in HT glaucoma. Occurs in superior and inferior arcades. Zones appear thin or raked.

149
Q

NLF Reversal

A

Seen with NFL atrophy. Brightest in papillomacular area and dimmest by the disc (what is normally seen)

150
Q

What size nerves do you miss glaucoma with

A

small nerves as their C/D will be smaller.

151
Q

Order of changes in glaucoma

A

NFL then ON changes and then VF.

152
Q

Normal IOP

A

12-22

153
Q

Enhanced Depth Imaging

A

Allows for imaging of the choroid and structures below the RPE. Heidelberg and Cirrus do this. Can detect lamina cribs changes.

154
Q

Glaucoma and choroid

A

Thinner.

155
Q

Cirrus OCT

A

Have a normative data base of NFL, macula thickness, and ON parameter. Only adjusted by age and not race or other factors.

156
Q

Optic disc cube scan

A

6 x 6 scan.

157
Q

Calculation Center

A

automatically centers and places a circle around the ONH for repeatable measures.

158
Q

How does the cirrus calculation the termination of the Optic nerve?

A

The end of brush’s membrane.

159
Q

Important things to look at in NFL

A

Symmetry index and average NFL thickness

160
Q

Guided progression analysis (GPA)

A

greatest thing to come up with glaucoma management

161
Q

If you find a drance heme and the patients has not been dx with glaucoma what is the chance he will be dx

A

5x

162
Q

If you are treating for glaucoma and see a drance heme what is the rate of progression

A

2x

163
Q

How long for dance heme to show up on VF

A

6-8 weeks. Can start meds ASAP.

164
Q

Sirus ganglion cell layer

A

Different as it pulls out the NFL and the complex is only GCL and IPL.

165
Q

Best tool for monitoring advanced glaucoma

A

VF as nothing to scan in OCT if advanced.

166
Q

Flicker Defined Form

A

Good for dx glaucoma.

167
Q

MultiColor Scanning

A

IR, Green, Blue scans. Gives you detail of different pathologies in different layers.

168
Q

Revue database

A

Unique as compare to age, signal strength, and OD size.

169
Q

FLV%

A

Detects localized thinning using a pattern deviation

170
Q

GLV%

A

Detects thinning of GCC using pattern deviation

171
Q

FLV and GCC importance

A

Great predictor of glaucoma advancements. 41% suspects have glaucoma and 60% glaucoma have VF defects.

172
Q

Normal change in NFL or GGC per year

A

.2 microns

OC DZ 3rd year (2 decks)

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