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Ocular Disease III > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

T/F: Primary Open Angle Glaucoma (POAG) is typically asymptomatic at the time of diagnosis

A

True

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2
Q

Is visual acuity affected by glaucoma?

A

Sometimes

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3
Q

What is Krukenberg spindle, and why do we care about it in glaucoma?

A

Pigment deposition on the corneal endothelium that is an indication of pigment dispersion syndrome

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4
Q

Rubeosis iridis (iris neovascularization) can be seen in glaucoma. What common conditional also causes rubeosis iridis?

A

Diabetes Mellitus

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5
Q

What is a normal IOP? Abnormal?

A

“Normal” range is 10-21mmHg. Mean is 16mmHg. However, 4-5% of population has IOP > 21mmHg. 50% of POAG patients have IOP

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6
Q

Okay okay that last card was a bit unfair. Here’s something more concrete. What IOP by itself is concerning enough to start treatment?

A

30mmHg

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7
Q

What is a normal central corneal thickness?

A

545 microns

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8
Q

What central corneal thickness readings are associated with a higher risk of glaucoma? Lower?

A

588 microns - Lower risk

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9
Q

What retinal sign is pathonogmonic for glaucoma?

A

Progressive thinning of the neural rim of the optic disk

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10
Q

A (small/large) optic disk is a greater risk for glaucoma?

A

small disk –> more risk

It’s less room for all those fibers to get through

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11
Q

What C/D ratio makes you concerned about glaucoma

A

Approaching 0.6

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12
Q

Your patient has C/D ratios that vary by only 0.1 between their eyes. Is this a big deal?

A

It is! A 0.1 difference is seen in only 8% of normals, but 70% of early glaucoma

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13
Q

Is glaucoma typically bilateral?

A

Yes! However it is also typically asymmetric. That’s why different C/Ds between eyes is such a problem

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14
Q

(Vertical/Horizontal) elongation of the cup is more of a concern for glaucoma?

A

Vertical

Vertical notching is a red flag

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15
Q

Free Card: The nerves can look normal and you can still have glaucoma. You can also have glaucomatous cupping without field loss.

A

Free Card

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16
Q

How do NFL defects appear in glaucoma?

A

Dark slits or wedges from the disk rim. Inferior temporal wedges are the most obvious but also the least common

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17
Q

What retinal finding is a common association with normotensive glaucoma?

A

Drance (spinter) Hemorrhage

It is however a poor prognostic sign: they’re seen in already active disease

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18
Q

Back to visual fields from 1st year. Tell me about decibels and apostilbs. What do they mean when they’re high or low?

A

Apostilbs are the brightness of the light.

Decibels are the sensitivity of the patient

These terms are inverse to each other

High apostilbs means high brightness light, which means low sensitivity, which means low decibels.

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19
Q

What’s the standard field to run?

A

White-on-white Humphrey 30-2 or 24-2

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20
Q

What are (usually) the first scotomas to show up on visual fields in glaucoma?

A

Paracentral in 5-20 degrees of fixation

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21
Q

Free card: diseases other than glaucoma can cause visual fields that look like glaucoma. If your results are uncertain, it is prudent to repeat the fields

A

Tarjeta Gratis

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22
Q

What is MD (Mean Deviation) in a visual field?

A

MD is a measure of the average elevation or depression in the overall field compared to norms

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23
Q

What is PSD (Pattern Standard Deviation) in a visual field?

A

PSD is a measure of the irregularity of an overall field compared to norms

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24
Q

What is SF (Short-term fluctuation) in a visual field?

A

SF is a measure of consistency between responses, tested twice at 10 pre-selected points

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25
Q

What is CPSD (Corrected Pattern Standard Deviation) in a visual field?

A

CPSD is a measure of intra-test variability of field shape to reference while taking consistency into account

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26
Q

What is an FDT perimeter and why is it important to glaucoma?

A

FDT (frequency-doubling technology) perimetry has a stimulus of fluctuating bars of low spatial frequency. The flickering effect isolates Magoncellular neurons, which may be the first to be affected in glaucoma. This helps us catch glaucoma earlier.

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27
Q

What is a Humphrey Matrix?

A

Has the same visual field area and tests the same points as the 30-2, but uses the same principle as the FDT

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28
Q

What does the GDx Analyzer do?

A

It uses low-intensity polarized light to measure NFL thickness

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29
Q

What is the GCC in a retinal OCT?

A

GCC = Ganglion Cell Complex. It measures the thickness of the 3 innermost retinal layers (NFL, GCL, IPL), which are particularly affected by glaucoma.

For reference, those 3 layers are different parts of the ganglion cells

NFL = axons
GCL = cell bodies
IPL = dendrites
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30
Q

What is “provocative testing” in the realm of glaucoma?

A

If a patient has narrow angles, dilate them to see if you can induce angle closure. Treat the angle closure in office if it occurs. It’s better that it happens in your chair and for you to fix it and know about it versus it happening to the patient sometime.

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31
Q

Free Card: None of the tests we have are definitive in diagnosing glaucoma. There is no cure and early diagnosis is critical. ODs are often the first to spot it, so get good at it and save a future patient’s vision

A

Free Card

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32
Q

What is the flow of glaucoma treatment in the USA?

A

Medications –> Laser Treatment –> Surgery

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33
Q

What are the 3 theories of nerve damage in glaucoma?

A

1) IOP directly damages nerve
2) IOP cuts off circulation to nerve
3) Genetic apoptosis

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34
Q

What two classes of drugs reduce aqueous outflow?

A

Beta blockers and Carbonic anhydrase inhibitors

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35
Q

What suffix is common to many CAIs?

A

-zolamide

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36
Q

What suffix is common to many BBs?

A

-olol

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37
Q

What drug is the only B1 selective BB? What is this helpful for?

A

Betaxolol

Reduces side effects for asthmatics

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38
Q

Which BB is the “gold standard”?

A

Timolol

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39
Q

Which BB has the longest 1/2 life?

A

Levobunolol

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40
Q

Which BB does not cross the BBB, and has the bonus of not hurting as much when put in the eye?

A

Carteolol

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41
Q

What is the common dosing for BBs?

A

1 gtt, either QD or BID

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42
Q

How much does treatment with BB typically lower IOP?

A

22-33%

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43
Q

What are some BB side effects?

A

CNS: depression, fatigue, decreased libido, HA, hallucinations, dizziness

Ocular: sting/burn, blurred vision, SPK

Heart: bradycardia, arrhythmia, palpitation, CHF

Lungs: bronchospasm, short of breath, respiratory failure

Hematological: aggravate lipid levels, mask hypoglycemia

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44
Q

Do oral BBs work for glaucoma too?

A

They do have the beneficial effect of reducing IOP, but are not prescribed for glaucoma

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45
Q

How much do CAIs typically reduce IOP?

A

15-20%

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46
Q

T/F: CAIs are often used as monotherapy for glaucoma?

A

False: they’re rarely used on their own

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47
Q

What are the 2 topical CAIs to know about?

A

Dorzolamide and Brinzolamide

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48
Q

What are the 3 systemic CAIs to know about?

A

Acetazolamide, Methazolamide, Dichlorophenamide

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49
Q

Which CAI is good for dropping IOP quickly in emergencies? What IOP would constitute an emergency?

A

Acetazolamide, >40mmHg

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50
Q

Which systemic CAI has less side effects?

A

Mthazolamide

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51
Q

What type of drug allergy do you have to worry about with CAIs?

A

Sulfa allergy

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52
Q

What ocular conditions contraindicate CAI use?

A

Corneal surgery patients, or patients with endothelial disease. CAIs disrupt endothelial function

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53
Q

What systemic conditions contraindicate CAIs?

A

Sickle cell disease or other blood dycrasias

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54
Q

What are the 5 classes of drugs that increase aqueous outflow

A

1) Adrenergic agonists
2) Cholinergic agonists
3) Prostaglandins
4) Docosanoids?
5) Hyperosmotics

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55
Q

What drug class is Dipivefrin? How does it help with glaucoma?

A

Adrenergic agonist. Increases uveoscleral outflow

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56
Q

What drug class is Apraclonadine? How does it help with glaucoma?

A

Adrenergic agonist. Increases uveoscleral outflow and decreases aqueous production

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57
Q

What drug class is Brimonidine? How does it help with glaucoma?

A

Adrenergic agonist. Increases uveoscleral outflow and decreases aqueous production

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58
Q

What is Combigan?

A

Combo of Brimonidine and Timolol. Shown to be better than those drugs individually, but not as well as taking both of them together otherwise

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59
Q

What is currently the only combo glaucoma drop that does not include Timolol?

A

Simbrinza. It’s bronzolamide and bromonidine

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60
Q

What drug class is Pilocarpine? How does it help with glaucoma? What are it’s contraindications?

A

Parasympatholytic. Increases aqueous outflow.

Indicated for POAG, ACG, and Pigmentary glaucoma

Contraindicated for patients under 40, RD history, high myopes, cataracts, and inflammatory/uveitic/neovascular glaucoma

61
Q

What drug is often the first choice medication for lowering IOP?

A

Latanoprost. Extremely safe. First prostaglandin to be released. Increases uveoscleral outflow

62
Q

What drug class is Travaprost?

A

Prostaglandin analog. More effective on blacks

63
Q

What drug class is Bimatoprost?

A

Prostaglandin. May reduce IOP more than others in the class

64
Q

What drug class is Tafluprost?

A

Prostaglandin. Is preservative free

65
Q

What are some prostaglandin side effects?

A

Irreversible iris darkening (6-12 mo onset). Lash/periocular hair thickening. Eyelid/periocular skin darkening. CME in aphakes/pseudophakes. Uveitis. Onset of herpes simplex ocular infection

Possible eyelid darkening/deepening of eyelid sulcus.

66
Q

What is Uniprostone?

A

Docosanoid class. Safest glaucoma drug out there! Additive therapy

67
Q

What are hypersmotics used for in glaucoma? Give some examples (4).

A

Solutions that osmotically pull water from tissues into bloodstream. Temporary and immediate use for emergency situations.

Examples: glycerol, isosorbide, mannitol, and urea

68
Q

What role do steroids have in glaucoma treatment?

A

Steroids can increase IOP, but they also lower it in certain inflammatory conditions

69
Q

What is the minimum follow up time for stabilized glaucoma?

A

3 months

70
Q

Glaucoma is a category of widely varying group of ocular disease. What is the commonality of these diseases?

A

Acquired, progressive optic neuropathy, often associated with abnormal IOP. These conditions lead to ONH damage, ganglion cell loss, and therefore visual field loss and potential blindness

71
Q

What does a “primary” glaucoma mean?

A

It’s not associated with any other apparent ocular or systemic disorder

72
Q

What is the most common form of adult glaucoma?

A

Open angle

73
Q

What is the order you see structures, posterior to anterior, on gonioscopy? Assume all structures are visible

A

1) Ciliary Body
2) Scleral Spur
3) Trabecular Meshwork
4) Schwalbe’s Line

74
Q

Pigmentary Glaucoma (PG) and Pigmentary Dispersion Syndrome (PDS) are different things. What do they have in common? What is different between them?

A

They both feature pigment accumulation in TM, leading to dysfunction, blockage of outflow, and ocular HTN. This can occur without optic neuropathy with is PDS, or with optic neuropathy, which is PG.

75
Q

What portion of people with PDS develop PG?

A

~35%

30%-50% in literature

76
Q

What are the two theories of how pigment is dispersed in PG/PDS?

A

1) Pigment release due to abnormalities of iris pigment epithelium
2) Mechanical disruption of iris pigment epithelium as folds rub against lens capsule and/or zonules

77
Q

What is the most common age of diagnosis of PG/PDS?

A

20-40 years old

78
Q

What ethnic group is predisposed to PDS?

A

Caucasians

79
Q

What is the sex predilection for PDS/PG?

A

PDS is equal M/F. PG is more common in Males

80
Q

What ocular condition has a strong association with PDS?

A

Myopia. ~90% of PDS patients are myopic

81
Q

Patients with (wider / narrower) angles are more predisposed to PDS?

A

Deeper angles, interestingly

82
Q

What are the symptoms of PDS/PG?

A

Typically asymptomatic. However, rapid IOP spikes can cause pain, corneal edema, intermittent blurry vision, and halos around lights. This can happen after exercise, as pigment is liberated by physical activity, and settles in TM during rest

83
Q

What is the classic triad of PDS/PG?

A

1) Krukenberg spindle
2) Iris transillumination defects
3) Pigment deposition in TM

84
Q

What is Sampaolesi’s line?

A

Darkened schwalbe’s line due to pigment deposition in the angle

85
Q

What is Zentmeyer ring (aka Scheie’s line)

A

Pigment deposition on mid-peripheral anterior lens capsule in PG/PSD

I think this is correct?

86
Q

Pseudoexfoliative Glaucoma (PXG) and Pseudoexpholiation Syndrome (PXE) are different conditions. What’s different about them? What is the same?

A

PXE does not have increased IOP, glaucomatous VF loss, or optic nerve changes. PXG does have the these consequences.

Both are characterized by psuedoexfoliative material accumulating in corneal anterior segment structures

87
Q

What is pseudoexfoliative material (PXM) made of?

A

The exact origin is uncertain, but it is though to come from iris pigment epithelium, ciliary epithelium, and peripheral anterior lens epithelium.

88
Q

What is the common age of onset of PXG/PXE?

A

Most common onset is 60-80, and is rarely seen before age 50

89
Q

What fraction of people with PXE develop PXG?

A

The risk is cumulative over time. About 15% of patients with PXE develop PXG after 10 years

90
Q

What is the main objective sign of PXE/PXG?

A

3-ring sign on the lens. Shows in a “bull’s-eye-pattern” on the anterior lens surface. Best seen when the eye is dilated. The 3 rings are the central translucent disk, the intermediate clear zone, and the peripheral granular zone

91
Q

Other than the 3-ring lens sign what are the objective findings in PXE/PXG?

A

Lens subluxations (10-15%)

Cataracts

“Moth eaten” pupillary ruff appearance

PXM deposition in various anterior segment structures

Any signs associated with PDS/PDG, which can be caused secondarily by PXE/PXG

92
Q

Where is PXM found most prominently in PXE/PXG?

A

Inferior angle

93
Q

What nutritional supplement is sometimes used with PXE/PXG

A

B-12 and folic acid supplements can decrease hyperhomocysteinemia

94
Q

What is the typical cause of the fibrovascular membrane in neovascular glaucoma?

A

RETINAL hypoxia/ischemia and resulting release of angiogenic factors

95
Q

What are the major conditions that predispose patients to neovascular glaucoma?

A

CRVO, Diabetic retinopathy, Carotid artery dissection, and CRAO

96
Q

What is the first sign of neovascularization of the iris (NVI)?

A

Small, tortuous vessels at the pupillary margin. Use 25-40X on SLEx to see. Look for these: early detection is essential in neovascular glaucoma. This sign is considered the “early phase”

97
Q

What is considered the “middle phase” of neovascular glaucoma?

A

The angle becomes involved. This is neovascularization of the angle (NVA). This can occur without the pupil ever should neovascularization

98
Q

What is considered the “late phase” of neovascular glaucoma?

A

The fibrovascular membrane results in peripheral anterior synechia. It can progress to 360 degree angle closure.

99
Q

T/F: IOP increases early in the disease of neovascular glaucoma

A

False! IOP often remains normal

100
Q

What is the first line therapy for retinal hypoxia (which leads to NVG)

A

Panretinal photocoagulation

Anti-VEGF injections are often used in conjunction

101
Q

To define acute angle closure glaucoma, the patient needs 2 of a list of symptoms, and 3 of a list of signs. What are these signs and symptoms?

A

Symptoms: Ocular pain, N/V, Hx of intermittent vision blur with halos

Signs: IOP>21mmHg, Conj. injection, Corneal epithelial edema, Mid-dilated non-reactive pupil, Shallower chamber in presence of occlusion.

102
Q

What is the state of the iris when most pupil blocks occur?

A

Mid-dilated

103
Q

Which refractive condition is more susceptible to angle closure? Male vs Female?

A

Hyperopes and females

104
Q

What is the main symptom of acute angle closure?

A

Severe eye pain!

105
Q

Reduces sense of color and brightness is a trait of macular or optic nerve dysfunction?

A

Optic nerve

106
Q

What drug is used to drop ICP?

A

Acetazolamide

107
Q

How do you treat demyelinating optic neuritis?

A

We (ODs) don’t do it. IV methylprednisolone. Orals don’t work as well

108
Q

What is the most common hereditary retinal dystrophy?

A

Retinitis pigmentosa

109
Q

What is different about autosomal dominant and autosomal recessive RP?

A

Recessive: more common, more severe. Peripheral loss in childhood, central vision loss by adulthood.

Dominant: less common, less severe. Central vision intact until 40s or or 50s.

110
Q

T/F: 30-40% of cases of RP are part of a systemic syndrome

A

True

111
Q

What is the initial symptom of RP?

A

Night blindness (Nyctalopia)

112
Q

What is the initial sign of RP?

A

Aterial attenuation (shrinking)

113
Q

What test will be abnormal in RP before there are any retinal signs?

A

Scotopic ERG

114
Q

What is Usher Syndrome?

A

Congenital sensori-neural hearing loss plus RP

115
Q

How do you treat RP?

A

No cure. Slow progression with nutrient supplements. Vit A, Omega 3, Lutein, B-carotene.

Short wavelength blocking tints help too

116
Q

What other condition is Leber’s Congenital Amaurosis like?

A

It’s similar to RP, but congenital or very early onset

117
Q

What is the typical presentation of Leber’s

A

Visually unresponsive baby with nystagmus

118
Q

How is Leber’s treated?

A

Sub-retinal injection of RPE65 with viral vector. It’s gene therapy!

119
Q

Are acuities affected in CSNB?

A

Mild, usually 20/30 - 20/60

120
Q

What test is diagnostic for CSNB?

A

Pattern ERG

121
Q

What is Oguchi’s disease?

A

Varient of CSNB found in Japanese populations. The retina appears yellow-grey, which is reversed by dark adaptation

122
Q

What is Gyrate Dystrophy

A

A hereditary choroidal disease. Causes high myopia, night blindness (in 20s). On fundoscopy, bare sclera acan be seen. RP-like vision loss is seen.

Treatment: B6 supplements, low protein diet

123
Q

What is Choroideremia?

A

X linked disease that causes night blindness at age 5-10. RPE and choroid atrophy, leaving bare sclera. Central field lost in 40s-50s

124
Q

What is Starget’s Macular Dystrophy?

A

Like a juvenile AMD. Onset is 8-16 years, with poor acuity. 25% of cases have later onset, with better outcomes. Macular changes are subtle at first and acuity loss will be way worse than it looks like it should be

125
Q

What are the retinal findings in Sargart’s

A

FLR lost. Oval area of atrophic RPE appears at macular. Beaten bronze fundus at end stage. Yellow pisciform lesions in posterior pose develop.

126
Q

What is the prognosis for Stargart’s

A

Usually the condition stabilizes in early 20s with acuities in 20/200 - 20/400 range

127
Q

What is fundus flavimaculatus?

A

A variant of Stargart’s where the pisciform lesions develop sooner and acuity loss is later (40s-50s)

128
Q

What is Best’s disease? (Vitelliform Dystrophy)

A

Retinal disease with stages that begins in early childhood

Previtilliform: abnormal ERG

Vitilliform: Yellow spots coalesce into “egg yolk.” VAs still normal here

Pseudohypopion: lesion partially reabsorbs

Vitellifruptive: lesion breaks up into “scrambled egg” and VA drops significantly (20/200 range)

129
Q

Treatment for Best’s

A

Anti-VEGF

130
Q

What are the two forms of achromatopsia?

A

1) Rod monochromatism (AR)

2) Blue cone monochromatism (X-link)

131
Q

What are the features of achromatopsia?

A

Photophobia, nystagmus, 20/100 - 20/200 VAs, lack of color vision. Photopic ERG diminished

132
Q

Treatment for symptoms in achromatopsia?

A

Red tint (magenta for blue-cone). Acuity and comfort both improved.

133
Q

What is progressive cone dystrophy?

A

Condition with reduced VAs (20/60 - 20/200), photophobia, BULLS EYE MACULAR LESION, and diminished photopic ERG.

134
Q

What is the main factor affecting acuity in albanism?

A

Foveal hypoplasia

135
Q

What are the shapes for retrovitreal hemorrhages?

A

Boat-like and blob-like

136
Q

What is a “roth spot”?

A

A flame-shaped (or other) heme with a white center, which is presumed to be immune cells

137
Q

What is the followup protocol for macroaneurysms?

A

Asymptomatic w/o exudate or heme: 6mo

Asymptomatic w/ exudate or heme: 1-3mo

Symptomatic and threatens macula: retinal consult

138
Q

What are cotton wool spots? How do they appear on angiography?

A

Areas of NFL ischemia. Appear black on FA

139
Q

What is IRMA?

A

Intra-retinal microvascular anomaly. It’s basically pre-neovascularization. Tortuous capillaries form in an area of severe capillary non-perfusion. These new vessels do not leak or bleed, and are not an immediate threat to vision, but need referral for laser of anti-VEGF treatment

140
Q

How are shunts and collaterals different?

A

Collateral: A-A or V-V

Shunt: A-V or V-A

141
Q

What does all quadrant vs sectoral retinal vascular tortuosity indicate?

A

Diffuse: congenital

Sectoral: acquired

142
Q

Which has poor visual outcomes: AAION or NAION?

A

AAION

143
Q

When do retinal changes occur in anemia

A

When Hg concentration falls to 1/2 normal value

144
Q

What causes pernicious anemia?

A

Vit B12 deficiency

145
Q

What condition causes sea fan neovascularization?

A

Sickle cell disease

146
Q

What is polycythemia vera?

A

Bone-marrow over-production of blood cells

147
Q

What is secondary polycythemia?

A

Kidney overproduction of EPO, which causes overproduction of blood cells

148
Q

Why is polycythemia so bad for the retina?

A

Increased blood viscosity (up to 4x) can lead to ischemia

149
Q

What is the typical retinal appearance of polycythemia?

A

Dilated, tortuous vessels and a dark visible choroid

Ocular Disease III (1 decks)

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