Exam 1 Flashcards
1
Q
T/F: Primary Open Angle Glaucoma (POAG) is typically asymptomatic at the time of diagnosis
A
True
2
Q
Is visual acuity affected by glaucoma?
A
Sometimes
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
4
Q
Rubeosis iridis (iris neovascularization) can be seen in glaucoma. What common conditional also causes rubeosis iridis?
A
Diabetes Mellitus
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
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
7
Q
What is a normal central corneal thickness?
A
545 microns
8
Q
What central corneal thickness readings are associated with a higher risk of glaucoma? Lower?
A
588 microns - Lower risk
9
Q
What retinal sign is pathonogmonic for glaucoma?
A
Progressive thinning of the neural rim of the optic disk
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
11
Q
What C/D ratio makes you concerned about glaucoma
A
Approaching 0.6
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
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
14
Q
(Vertical/Horizontal) elongation of the cup is more of a concern for glaucoma?
A
Vertical
Vertical notching is a red flag
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
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
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
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.
19
Q
What’s the standard field to run?
A
White-on-white Humphrey 30-2 or 24-2
20
Q
What are (usually) the first scotomas to show up on visual fields in glaucoma?
A
Paracentral in 5-20 degrees of fixation
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
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
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
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
25
What is CPSD (Corrected Pattern Standard Deviation) in a visual field?
CPSD is a measure of intra-test variability of field shape to reference while taking consistency into account
26
What is an FDT perimeter and why is it important to glaucoma?
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.
27
What is a Humphrey Matrix?
Has the same visual field area and tests the same points as the 30-2, but uses the same principle as the FDT
28
What does the GDx Analyzer do?
It uses low-intensity polarized light to measure NFL thickness
29
What is the GCC in a retinal OCT?
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
```
30
What is "provocative testing" in the realm of glaucoma?
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.
31
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
Free Card
32
What is the flow of glaucoma treatment in the USA?
Medications --> Laser Treatment --> Surgery
33
What are the 3 theories of nerve damage in glaucoma?
1) IOP directly damages nerve
2) IOP cuts off circulation to nerve
3) Genetic apoptosis
34
What two classes of drugs reduce aqueous outflow?
Beta blockers and Carbonic anhydrase inhibitors
35
What suffix is common to many CAIs?
-zolamide
36
What suffix is common to many BBs?
-olol
37
What drug is the only B1 selective BB? What is this helpful for?
Betaxolol
Reduces side effects for asthmatics
38
Which BB is the "gold standard"?
Timolol
39
Which BB has the longest 1/2 life?
Levobunolol
40
Which BB does not cross the BBB, and has the bonus of not hurting as much when put in the eye?
Carteolol
41
What is the common dosing for BBs?
1 gtt, either QD or BID
42
How much does treatment with BB typically lower IOP?
22-33%
43
What are some BB side effects?
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
44
Do oral BBs work for glaucoma too?
They do have the beneficial effect of reducing IOP, but are not prescribed for glaucoma
45
How much do CAIs typically reduce IOP?
15-20%
46
T/F: CAIs are often used as monotherapy for glaucoma?
False: they're rarely used on their own
47
What are the 2 topical CAIs to know about?
Dorzolamide and Brinzolamide
48
What are the 3 systemic CAIs to know about?
Acetazolamide, Methazolamide, Dichlorophenamide
49
Which CAI is good for dropping IOP quickly in emergencies? What IOP would constitute an emergency?
Acetazolamide, >40mmHg
50
Which systemic CAI has less side effects?
Mthazolamide
51
What type of drug allergy do you have to worry about with CAIs?
Sulfa allergy
52
What ocular conditions contraindicate CAI use?
Corneal surgery patients, or patients with endothelial disease. CAIs disrupt endothelial function
53
What systemic conditions contraindicate CAIs?
Sickle cell disease or other blood dycrasias
54
What are the 5 classes of drugs that increase aqueous outflow
1) Adrenergic agonists
2) Cholinergic agonists
3) Prostaglandins
4) Docosanoids?
5) Hyperosmotics
55
What drug class is Dipivefrin? How does it help with glaucoma?
Adrenergic agonist. Increases uveoscleral outflow
56
What drug class is Apraclonadine? How does it help with glaucoma?
Adrenergic agonist. Increases uveoscleral outflow and decreases aqueous production
57
What drug class is Brimonidine? How does it help with glaucoma?
Adrenergic agonist. Increases uveoscleral outflow and decreases aqueous production
58
What is Combigan?
Combo of Brimonidine and Timolol. Shown to be better than those drugs individually, but not as well as taking both of them together otherwise
59
What is currently the only combo glaucoma drop that does not include Timolol?
Simbrinza. It's bronzolamide and bromonidine
60
What drug class is Pilocarpine? How does it help with glaucoma? What are it's contraindications?
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
What drug is often the first choice medication for lowering IOP?
Latanoprost. Extremely safe. First prostaglandin to be released. Increases uveoscleral outflow
62
What drug class is Travaprost?
Prostaglandin analog. More effective on blacks
63
What drug class is Bimatoprost?
Prostaglandin. May reduce IOP more than others in the class
64
What drug class is Tafluprost?
Prostaglandin. Is preservative free
65
What are some prostaglandin side effects?
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
What is Uniprostone?
Docosanoid class. Safest glaucoma drug out there! Additive therapy
67
What are hypersmotics used for in glaucoma? Give some examples (4).
Solutions that osmotically pull water from tissues into bloodstream. Temporary and immediate use for emergency situations.
Examples: glycerol, isosorbide, mannitol, and urea
68
What role do steroids have in glaucoma treatment?
Steroids can increase IOP, but they also lower it in certain inflammatory conditions
69
What is the minimum follow up time for stabilized glaucoma?
3 months
70
Glaucoma is a category of widely varying group of ocular disease. What is the commonality of these diseases?
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
What does a "primary" glaucoma mean?
It's not associated with any other apparent ocular or systemic disorder
72
What is the most common form of adult glaucoma?
Open angle
73
What is the order you see structures, posterior to anterior, on gonioscopy? Assume all structures are visible
1) Ciliary Body
2) Scleral Spur
3) Trabecular Meshwork
4) Schwalbe's Line
74
Pigmentary Glaucoma (PG) and Pigmentary Dispersion Syndrome (PDS) are different things. What do they have in common? What is different between them?
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
What portion of people with PDS develop PG?
~35%
| 30%-50% in literature
76
What are the two theories of how pigment is dispersed in PG/PDS?
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
What is the most common age of diagnosis of PG/PDS?
20-40 years old
78
What ethnic group is predisposed to PDS?
Caucasians
79
What is the sex predilection for PDS/PG?
PDS is equal M/F. PG is more common in Males
80
What ocular condition has a strong association with PDS?
Myopia. ~90% of PDS patients are myopic
81
Patients with (wider / narrower) angles are more predisposed to PDS?
Deeper angles, interestingly
82
What are the symptoms of PDS/PG?
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
What is the classic triad of PDS/PG?
1) Krukenberg spindle
2) Iris transillumination defects
3) Pigment deposition in TM
84
What is Sampaolesi’s line?
Darkened schwalbe's line due to pigment deposition in the angle
85
What is Zentmeyer ring (aka Scheie's line)
Pigment deposition on mid-peripheral anterior lens capsule in PG/PSD
*I think this is correct?*
86
Pseudoexfoliative Glaucoma (PXG) and Pseudoexpholiation Syndrome (PXE) are different conditions. What's different about them? What is the same?
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
What is pseudoexfoliative material (PXM) made of?
The exact origin is uncertain, but it is though to come from iris pigment epithelium, ciliary epithelium, and peripheral anterior lens epithelium.
88
What is the common age of onset of PXG/PXE?
Most common onset is 60-80, and is rarely seen before age 50
89
What fraction of people with PXE develop PXG?
The risk is cumulative over time. About 15% of patients with PXE develop PXG after 10 years
90
What is the main objective sign of PXE/PXG?
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
Other than the 3-ring lens sign what are the objective findings in PXE/PXG?
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
Where is PXM found most prominently in PXE/PXG?
Inferior angle
93
What nutritional supplement is sometimes used with PXE/PXG
B-12 and folic acid supplements can decrease hyperhomocysteinemia
94
What is the typical cause of the fibrovascular membrane in neovascular glaucoma?
RETINAL hypoxia/ischemia and resulting release of angiogenic factors
95
What are the major conditions that predispose patients to neovascular glaucoma?
CRVO, Diabetic retinopathy, Carotid artery dissection, and CRAO
96
What is the first sign of neovascularization of the iris (NVI)?
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
What is considered the "middle phase" of neovascular glaucoma?
The angle becomes involved. This is neovascularization of the angle (NVA). This can occur without the pupil ever should neovascularization
98
What is considered the "late phase" of neovascular glaucoma?
The fibrovascular membrane results in peripheral anterior synechia. It can progress to 360 degree angle closure.
99
T/F: IOP increases early in the disease of neovascular glaucoma
False! IOP often remains normal
100
What is the first line therapy for retinal hypoxia (which leads to NVG)
Panretinal photocoagulation
Anti-VEGF injections are often used in conjunction
101
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?
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
What is the state of the iris when most pupil blocks occur?
Mid-dilated
103
Which refractive condition is more susceptible to angle closure? Male vs Female?
Hyperopes and females
104
What is the main symptom of acute angle closure?
Severe eye pain!
105
Reduces sense of color and brightness is a trait of macular or optic nerve dysfunction?
Optic nerve
106
What drug is used to drop ICP?
Acetazolamide
107
How do you treat demyelinating optic neuritis?
We (ODs) don't do it. IV methylprednisolone. Orals don't work as well
108
What is the most common hereditary retinal dystrophy?
Retinitis pigmentosa
109
What is different about autosomal dominant and autosomal recessive RP?
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
T/F: 30-40% of cases of RP are part of a systemic syndrome
True
111
What is the initial symptom of RP?
Night blindness (Nyctalopia)
112
What is the initial sign of RP?
Aterial attenuation (shrinking)
113
What test will be abnormal in RP before there are any retinal signs?
Scotopic ERG
114
What is Usher Syndrome?
Congenital sensori-neural hearing loss plus RP
115
How do you treat RP?
No cure. Slow progression with nutrient supplements. Vit A, Omega 3, Lutein, B-carotene.
Short wavelength blocking tints help too
116
What other condition is Leber's Congenital Amaurosis like?
It's similar to RP, but congenital or very early onset
117
What is the typical presentation of Leber's
Visually unresponsive baby with nystagmus
118
How is Leber's treated?
Sub-retinal injection of RPE65 with viral vector. It's gene therapy!
119
Are acuities affected in CSNB?
Mild, usually 20/30 - 20/60
120
What test is diagnostic for CSNB?
Pattern ERG
121
What is Oguchi's disease?
Varient of CSNB found in Japanese populations. The retina appears yellow-grey, which is reversed by dark adaptation
122
What is Gyrate Dystrophy
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
What is Choroideremia?
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
What is Starget's Macular Dystrophy?
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
What are the retinal findings in Sargart's
FLR lost. Oval area of atrophic RPE appears at macular. Beaten bronze fundus at end stage. Yellow pisciform lesions in posterior pose develop.
126
What is the prognosis for Stargart's
Usually the condition stabilizes in early 20s with acuities in 20/200 - 20/400 range
127
What is fundus flavimaculatus?
A variant of Stargart's where the pisciform lesions develop sooner and acuity loss is later (40s-50s)
128
What is Best's disease? (Vitelliform Dystrophy)
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
Treatment for Best's
Anti-VEGF
130
What are the two forms of achromatopsia?
1) Rod monochromatism (AR)
| 2) Blue cone monochromatism (X-link)
131
What are the features of achromatopsia?
Photophobia, nystagmus, 20/100 - 20/200 VAs, lack of color vision. Photopic ERG diminished
132
Treatment for symptoms in achromatopsia?
Red tint (magenta for blue-cone). Acuity and comfort both improved.
133
What is progressive cone dystrophy?
Condition with reduced VAs (20/60 - 20/200), photophobia, *BULLS EYE MACULAR LESION*, and diminished photopic ERG.
134
What is the main factor affecting acuity in albanism?
Foveal hypoplasia
135
What are the shapes for retrovitreal hemorrhages?
Boat-like and blob-like
136
What is a "roth spot"?
A flame-shaped (or other) heme with a white center, which is presumed to be immune cells
137
What is the followup protocol for macroaneurysms?
Asymptomatic w/o exudate or heme: 6mo
Asymptomatic w/ exudate or heme: 1-3mo
Symptomatic and threatens macula: retinal consult
138
What are cotton wool spots? How do they appear on angiography?
Areas of NFL ischemia. Appear black on FA
139
What is IRMA?
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
How are shunts and collaterals different?
Collateral: A-A or V-V
Shunt: A-V or V-A
141
What does all quadrant vs sectoral retinal vascular tortuosity indicate?
Diffuse: congenital
Sectoral: acquired
142
Which has poor visual outcomes: AAION or NAION?
AAION
143
When do retinal changes occur in anemia
When Hg concentration falls to 1/2 normal value
144
What causes pernicious anemia?
Vit B12 deficiency
145
What condition causes sea fan neovascularization?
Sickle cell disease
146
What is polycythemia vera?
Bone-marrow over-production of blood cells
147
What is secondary polycythemia?
Kidney overproduction of EPO, which causes overproduction of blood cells
148
Why is polycythemia so bad for the retina?
Increased blood viscosity (up to 4x) can lead to ischemia
149
What is the typical retinal appearance of polycythemia?
Dilated, tortuous vessels and a dark visible choroid
