Retina/Choroid/ Vitreous Flashcards

(515 cards)

1
Q

RTC for CSR?

A

1 month then monitor on monthly basis until stable, longer than 3-6 months = chronic CSR

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2
Q

CSR on FA shows what shape?

A

Smoke stack

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3
Q

Which condition is leakage from choriocapillaris into sub-retina, causing serous detachment of neuro sensory retina of macula? And appears as a “smoke stack on FA”

A

Central serous chorioretinopathy

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4
Q

Demographic for CSR?

A

Middle age men (30-50 y.o) with high anxiety, stress, type A personalities.
* on systemic steroids
* HTN
* lupus

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5
Q

Criteria for CSME?

A
  1. Retina thickening within 500 microns of center of fovea
  2. Hard exudates within 500 microns of center of fovea, if associated with adjacent retinal thickening
  3. Thick retina greater than 1 DD, within 1DD of center of fovea
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6
Q

4-2-1 Rule?

A

Severe vs Very severe non-proliferative DR
4 quadrants of intra-retinal hemes
2 quadrants of venous beading
1 quadrant of IRMA (intraretinal microvascular abnormalities)

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7
Q

What conditions can cause falsely LOW A1c?

A

Hemolytic anemia
CKD, liver disease
Vitamin C and E
Pregnancy
Rheumatoid arthritis
Hypertriglyceridemia
** conditions that shortens lifespan of RBCs

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8
Q

Cotton wool spots will be hyper or hypo under FA?

A

Hypo fluorescent

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9
Q

Areas of neovascularization will be hyper or hypo on FA?

A

Hyper fluorescent

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10
Q

Microaneurysms and areas of retinal edema will be hyper or hypo on FA?

A

Hyper fluorescent

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11
Q

Which layers of the retina are supplied by the choriocapillaris?

A

Outer retina
RPE
PR
ELM
ONL
OPL

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12
Q

Layer of retina supplied by both choroid and central retinal artery

A

Outer plexiform layer

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13
Q

CSR tends to be associated with Type-A personalities and stress but it can also occur in? (5)

A
  • Pregnancy
  • HTN
  • Steroid use
  • Cushing Syndrome
  • Lupus
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14
Q

Which condition is most frequently observed in chorioretinal coloboma?

A

Microphthalmia
* abnormal small eye

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15
Q

Which condition is most frequently observed in chorioretinal coloboma?

A

Microphthalmia

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16
Q

Why is plaquenil toxic to the eyes?

A

It is an anti-malaria drug (melatropic medication)

prolonged use can cause it to concentrate in melanin-containing structures like the choroid and RPE

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17
Q

In order to be classified as having Charles Bonnet Syndrome, a patient must have?

A

Intact cognition with no history of psychiatric disorders, neurological abnormalities, drug abuse, toxic, metabolic or infectious etiologies or dementia

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18
Q

True or False
Patients with Charles Bonnet syndrome do not experience hallucinations that involve hearing or smell

A

True

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19
Q

What’s a major difference between Charles Bonnet Syndrome and senile dementia?

A

In CBS patients are aware of the unreal nature of the hallucinations

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20
Q

What ocular condition has the HIGHEST association with Charles Bonnet Syndrome?

A

AMD

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21
Q

What is the most common type of visual hallucination in Charles Bonnet Syndrome?

A

Faces

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22
Q

Talc retinopathy affects what type of patients?

A

Long term intravenous drug users

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23
Q

Toxocariasis is caused by what organism?

A

Parasitic nematode called Toxocara canis
** think Canis = canines 🐶
** parasite found in dog feces

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24
Q

Hollenhorst plaques are commonly located where on a retinal artery?

A

At the bifurcation of a retinal artery

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25
The most common source of a retinal embolism is?
Ulceration and release of material from atheromatous plaque of the carotid bifurcation
26
What does cholesterol emboli look like?
Appear as bright, refractive golden yellow orange crystals
27
Why does cholesterol emboli cause amaurosis fugax?
Cholesterol plaques are malleable, allows blood to flow through but may result in fleeting vision loss that last seconds/minutes due to temporary blockage of retinal artery
28
Calcific emboli originate from?
Atheromatous plaques in the ascending aorta, carotid arteries or from calcified heart valves
29
Which type of emboli is most dangerous, because it can cause permanent occlusion?
Calcific emboli (Look like single white plugs of material close to optic disc)
30
Patients with s/s of retinal embolus must undergo what investigations? (5)
1. Pulse (to detect atrial fibrillation) 2. Blood pressure 3. Carotid evaluation (to detect bruit) 4. Electrocardiogram (EKG) 5. Blood testing (CBC, FBG, lipids and ESR)
31
Management for Hollenhorst plaque
1. Report findings to PCP 2. Refer patient for vascular work up within 48-72 hours
32
Indications for anterior chamber paracentesis
CRAO Acute glaucoma Uveitis or endophthalmitis
33
Paracentesis
Penetrate corneal near limbus with a needle to allow outflow of aqueous from globe to relieve high IOP in emergencies or to obtain fluid samples for diagnosis
34
Attenuation of RPE leading to loss of melanin granulates allows for increased what?
Visibility of underlying choroid aka window defect
35
Inheritance pattern of gyrate atrophy
Autosomal recessive
36
Tx for RPE window defect
Monitor annually * may enlarge as patient gets older but no Tx because will not cause vision loss
37
What are the 3 types of RD?
- Tractional - Rhegmatogenous - Exudative
38
What is the most common systemic disease associated with angioid streaks?
Pseudoxanthom elasticum * connective tissue disorder, elastin affected
39
Gronblad-Strindberg syndrome
Pseudoxanthoma elasticum and angioid streaks
40
Pathophysiology of angioid streaks
Small dehiscences (small openings) in collagenous and elastic portions of Bruch’s membrane
41
2 fundus findings associated with angioid streaks
1. Peau d’orange 2. optic disc drusen *1. mottled fundus appearance, yellow, speckled pinpoint areas that look like a leopard skin-spotting
42
6 conditions that can cause CNVM
CHBALA Choridal rupture Histoplasmosis Best disease AMD Lacquer cracks Angioid streaks
43
Angioid streaks are associated with what systemic conditions (5)
PEPSI Pseudoxanthoma elasticum Ehler’s Danlos syndrome Paget’s Sickle cell Idiopathic
44
Tx & management of Angioid streaks
Perform FA to check for CNVM If clear, close monitoring If CNVM present Tx with anti-VEGF if subfoveal
45
CME formation following cataract surgery
Irvine Gass Syndrome * 6 weeks to 3 months post op
46
Fluid accumulates in which layers of the retina in cystoid macular edema?
Outer plexiform layer and inner nuclear layer
47
Chronic longstanding CME can lead to?
Lamellar macular hole (partial, hole doesn’t go through all layers of retina) * cystic spaces coalesce and progress to form macular hole
48
On FA: small hyperfluorescent spots in early phase with flower-petal pattern of hyperfluorescence in late stage
cystoid macular edema
49
On FA: well demarcated lacy hyperfluorescence in early phase with increasing leakage in late phase
Choroidal neovascular membrane
50
On FA: smoke-stake appearance
Central serous retinopathy
51
Which hereditary retinal disease is most commonly associated with CME?
Retinitis pigmentosa
52
Tx of CME secondary to YAG cap following CE
* topical NSAID and topical steroids Example: 1 gtts ketorolac QID 1 gtts prednisolone acetate QID
53
Detachment of neurosensory retina from RPE secondary to full thickness retinal break
RRD
54
Detached retina will appear concave with a smooth surface
Tractional RD
55
Tobacco dust seen in anterior vitreous is a sign for?
Rhegmatogenous retinal detachment
56
IOP is lower in affected eye by 5mmHg compared to fellow eye in which type of RD?
RRD * if IOP extremely low, an associated choroidal detachment is suspected
57
Talc can deposit in small blood vessels of which organs?
Lungs Liver Spleen Kidneys Lymph nodes * talc retinopathy in long term IV drug abuse with cocaine and heroin
58
What additional tests should be ordered in a patient with talc retinopathy?
- Chest X-ray (pulmonary complications) - fluorescein angiography (evaluate for possible vasculature leakage or non-perfusion
59
What retinal complications can arise from talc deposits?
Retinal ischemia * develop hemorrhages, CWS, peripheral neovascularization, vitreous hemorrhages and tractional RD
60
Degenerative retinoschisis is between which layers of the retina?
outer plexiform layer and inner nuclear layer
61
What is the visual prognosis of choroideremia?
Visual acuity will remain stable until later in life when it is expected to become significantly affected
62
What is the most common initial symptom of patients with choroideremia?
Nyctalopia or night blindness
63
Snail track degeneration is commonly located in which retinal quadrants?
ST and SN peripheral quadrants of myopic eyes
64
What is the 2nd most common ocular opportunistic infection of AIDS patients?
PORN: progressive outer retinal necrosis * varicella zoster variant, very aggressive
65
White without pressure is most commonly seen in which areas of the retina?
Inferior and temporal * located at the vitreous and ora serrata
66
What is Central Serous Chorioretinopathy (CSR)?
CSR occurs as a result of fluid leaking from the choriocapillaris into the subretinal area, causing a serous detachment of the neurosensory retina. ## Footnote Occasionally, a detachment of the retinal pigment epithelium may also develop.
67
What are the common demographics associated with CSR?
CSR typically occurs in middle-aged males with a type 'A' personality, experiencing high levels of emotional stress, increased cortisol levels, hypertension, or systemic lupus erythematosus. ## Footnote This condition is generally unilateral in presentation.
68
List the symptoms of Central Serous Chorioretinopathy.
* Reduced visual acuity * Metamorphopsia (distortion of objects) * Abnormal color vision * Patients may be asymptomatic if the macular region is not involved.
69
What clinical signs may indicate CSR? (Name at least 3)
* Loss of foveal reflex * Hyperopic shift * Potential relative scotoma * Distortion on Amsler grid testing * Hyperfluorescence in fluorescein angiography (smoke stack appearance) * Blister-like elevation of the neurosensory retina in posterior pole evaluation.
70
True or False: CSR frequently requires intervention.
False ## Footnote CSR frequently spontaneously regresses within 6 months, and intervention is rarely required.
71
What treatments are available for CSR?
* Photocoagulation * Photodynamic therapy ## Footnote These treatments are performed for patients experiencing profound levels of decreased acuity or blurred vision for prolonged periods of time, as long as the area is not within the foveal avascular zone.
72
Fill in the blank: Argon laser photocoagulation or photodynamic therapy will decrease the _______ of CSR but will not alter the resultant visual outcome.
[recovery time]
73
What is a potential result of fluorescein angiography in CSR?
hyperfluorescence in a smoke-stack formation. ## Footnote This finding is characteristic of CSR.
74
RTC for CSR
Monthly until resolution
75
What is the choroid?
A heavily pigmented and highly vascularized layer of the eye positioned interior to the sclera and exterior to the retinal tissue ## Footnote It is part of the uveal tract, which includes the iris, ciliary body, and choroid.
76
What are the four layers of the choroid, listed from most external to most internal?
* Suprachoroid * Stroma (vessel layer) divided into Haller’s layer and then Sattler’s layer * Choriocapillaris * Bruch's membrane ## Footnote These layers play distinct roles in the structure and function of the choroid.
77
What is the function of the suprachoroid?
Serves as a transition junction between the sclera and the choroid ## Footnote Comprised of 10-15 layers of collagen binding to the lamina fusca of the sclera.
78
What types of cells are found in the suprachoroid?
* Melanocytes (produce melanin, pigment) * Fibroblasts (connective tissue) ## Footnote These cells contribute to the structure and pigmentation of the choroid.
79
What constitutes the vessel layer of the choroid?
Haller's layer and Sattler's layer ## Footnote This layer primarily consists of blood vessels.
80
What is Haller's layer?
The layer external to Sattler's layer containing larger blood vessels ## Footnote It plays a role in the vascular supply of the choroid. *part of the stroma of the choroid
81
What is Sattler's layer?
The layer possessing smaller blood vessels in the choroid ## Footnote The diameter of the blood vessels decreases from the outer to the inner edge of the stroma in choroidal
82
What causes the brown appearance of the stroma in the choroid?
Melanocytes present in the stroma ## Footnote These cells contribute to the pigmentation of this layer.
83
What is the choriocapillaris?
A network of capillaries that maintain the outer retina ## Footnote The capillaries in this layer are larger than those in the rest of the body.
84
What is unique about the capillaries in the choriocapillaris?
They allow the passage of several blood cells simultaneously ## Footnote This feature is important for the metabolic needs of the outer retina.
85
True or False: The choriocapillaris contains melanocytes.
False ## Footnote The choriocapillaris does not contain melanocytes.
86
Fill in the blank: The choroid is a common site for ocular _______ that may develop into melanomas.
nevi ## Footnote Routine examination of the choroid is warranted due to this risk.
87
What is Bruch's membrane?
A thin, complex membrane located between the choriocapillaris of the choroid and the retinal pigment epithelium of the retina ## Footnote It is about 2 microns thick.
88
List the five components of Bruch's membrane from outermost to innermost.
* Basement membrane of the choriocapillaris * Outer collagenous zone * Elastic layer * Inner collagenous zone * Basement membrane of the retinal pigment epithelium ## Footnote These layers play a role in the structural support of the retina.
89
What is the thickness of Bruch's membrane?
About 2 microns thick ## Footnote This thinness is significant for its function and structure.
90
True or False: Bruch's membrane is located between the sclera and the choroid.
False ## Footnote Bruch's membrane is located between the choriocapillaris of the choroid and the retinal pigment epithelium.
91
What is the function of the outer collagenous zone in Bruch's membrane?
Provides structural support ## Footnote It is one of the five layers that contribute to the integrity of the membrane.
92
Fill in the blank: The _______ is the layer of Bruch's membrane that is elastic.
[Elastic layer] ## Footnote This layer is important for the flexibility of Bruch's membrane.
93
What layers are found in the choroid alongside Bruch's membrane?
* Haller's layer * Sattler's layer ## Footnote These layers are part of the vascular structure of the choroid.
94
What is Leber congenital amaurosis?
A rod-cone disorder characterized by vision loss ## Footnote It may initially show a normal-appearing fundus.
95
What ocular findings are associated with Leber congenital amaurosis by childhood?
* Narrowing of retinal blood vessels * optic disc pallor * pigmentary changes ## Footnote These findings can be observed during an ocular examination. * congenital retinal dystrophy, affects rods and cones, severe impairment in ability to convert light into electrical signals * ERG abnormal The Visual Cycle is a series of enzymatic reactions between the retinal pigment epithelium (RPE) and the neurosensory retina to metabolize dietary vitamin A into 11-cis retinal to generate photopigment. Without 11-cis retinal, the phototransduction cascade cannot be initialized; thus, visual neuronal signals are not propagated to the visual cortex. A dysfunctional mutation of any of the genes encoding for proteins that catalyze any of the series of enzymatic reactions to generate 11-cis retinal can block the Visual Cycle and lead to symptoms of LCA.
96
What does ERG reveal in cases of Leber congenital amaurosis?
ERG is markedly abnormal or flat ## Footnote *reduced or absent electrical response from retina when stimulated by light. Reflecting impaired photoreceptor function
97
What is the inheritance pattern of Leber congenital amaurosis?
Autosomal recessive ## Footnote This means that the disorder typically requires two copies of the mutated gene for manifestation.
98
Which layer of the retina are flame-shaped hemorrhages?
Nerve fiber layer * seen in HTN retinopathy, CRVO
99
What is disc edema?
Swelling of the optic disc often associated with retinal conditions ## Footnote It is frequently present in cases of non-ischemic central retinal vein occlusion.
100
What is the most common cause of non-ischemic central retinal vein occlusion? (Pathophysiology)
Formation of a thrombus near or at the lamina cribrosa ## Footnote This thrombus compresses the central retinal vein, impeding blood flow return. Associated with HTN, coronary artery disease, diabetes, hyperlipidemia, POAG, smoking
101
What symptoms do patients with non-ischemic CRVO typically report?
Acute, painless, unilateral loss of vision ## Footnote This symptom is a key indicator of the condition.
102
What clinical signs are associated with non-ischemic CRVO?
1. Decreased VA > 20/200 2. Neovasc rare 3. Dot-blot hemorrhages 4. Flame-shaped hemorrhages 5. Disc and macular edema 6. Dilated and tortuous vessels * no APD * CWS rare * better prognosis than ischemic CRVO * lower risk for neovasc
103
What is the visual acuity level typically seen in non-ischemic CRVO?
Generally better than 20/400 ## Footnote This indicates that while vision is impaired, it is not as severely affected as in ischemic cases.
104
What is the typical age demographic for individuals affected by non-ischemic CRVO?
Majority are 65 years of age or older ## Footnote Age is a significant risk factor for this condition.
105
What are common symptoms reported by patients with a full thickness macular hole?
Decreased vision centrally, possible scotoma, or metamorphopsia on the Amsler grid ## Footnote Flashes of light may also be experienced due to possible vitreo-retinal traction.
106
At what age group are idiopathic macular holes most commonly observed?
Women aged between 60-80 years
107
What is postulated to cause idiopathic macular holes?
Traction on the macular region by the vitreous
108
What classification system describes idiopathic macular holes by clinical findings?
Gass classification system
109
Describe Stage 1A of the Gass classification for idiopathic macular holes.
Difficult to detect clinically, marked by an intraretinal cyst, may appear as a small yellow spot in the center of the fovea, best observed with OCT
110
What characterizes Stage 1B of idiopathic macular holes?
Appearance of a yellow ring along with a foveal detachment
111
What defines Stage 2 of idiopathic macular holes?
Small foveal defects measuring less than 400 um in diameter * stage 2 always progresses to stage 3 * VA varies 20/50 to 20/400
112
What is noted in Stage 3 of idiopathic macular holes?
Defects greater than 400 um with posterior vitreous still attached, holes surrounded by a cuff of edema, yellow deposits at the level of the RPE may be observed in the center of the hole
113
What are the characteristics of Stage 4 idiopathic macular holes?
- Macular defects larger than 400 um - complete PVD - yellow deposits at the level of the RPE may be observed in the center of the hole - border of the hole may appear elevated
114
What protozoa causes Toxoplasmosis?
Toxoplasma gondii ## Footnote T. gondii is commonly associated with improper handling of raw meat or cat fecal matter
115
Who is particularly at risk for Toxoplasmosis and why?
Pregnant mothers ## Footnote An infection in the mother can potentially harm the unborn fetus
116
What serious consequence can Toxoplasmosis lead to if enough retinal damage occurs?
Blindness ## Footnote Retinal damage can result from the infection
117
What clinical appearance do old lesions of Toxoplasmosis have?
Circular areas of chorioretinal atrophy surrounded by pigmentation ## Footnote Areas of atrophy are generally stable
118
What symptoms may patients with active retinitis from Toxoplasmosis report?
Floaters, blurry vision, photophobia ## Footnote Patients typically do not experience pain
119
What is a characteristic observation in cases of active retinal Toxoplasmosis?
A yellow-white lesion next to an old chorioretinal scar ## Footnote This is typically associated with vitritis
120
What may happen to the anterior chamber in active retinal Toxoplasmosis?
Vitritis may spill over into the anterior chamber ## Footnote Vitritis is inflammation of the vitreous body
121
What additional problems may immunocompromised persons experience with Toxoplasmosis?
Encephalitis and chorioretinitis ## Footnote These patients may not display vitritis
122
True or False: Healthy individuals are likely to become seriously ill from Toxoplasmosis.
False ## Footnote Toxoplasmosis rarely leads to illness in healthy individuals
123
Fill in the blank: Toxoplasmosis is primarily associated with improper handling of _______ or _______.
raw meat or cat fecal matter ## Footnote These are common sources of T. gondii infection
124
What organism causes presumed ocular histoplasmosis?
Histoplasma capsulatum ## Footnote This organism typically enters the body via inhalation into the lungs. * associated with bats * fungus
125
In which geographical areas is presumed ocular histoplasmosis most prominent?
Ohio-Mississippi River valley region and southern United States ## Footnote These regions have higher incidences of the disease.
126
What are the three ocular findings associated with retinitis from presumed ocular histoplasmosis?
* Histo spots * Peripapillary atrophy * Choroidal neovascular membrane ## Footnote Two of these findings must be present for diagnosis.
127
What is required for a diagnosis of presumed ocular histoplasmosis?
Two of the three ocular findings must be present ## Footnote The findings include histo spots, peripapillary atrophy, and choroidal neovascular membrane.
128
Do patients suffering from histoplasmosis manifest vitritis?
No ## Footnote Patients with histoplasmosis will never show signs of vitritis.
129
What is the most frequently occurring intraocular tumor in children?
Retinoblastoma ## Footnote This condition is critical for early detection due to its high mortality rate.
130
Are most cases of retinoblastoma sporadic or familial?
Most cases are sporadic ## Footnote Occasionally, the malignancy may be familial in origin.
131
What percentage of retinoblastoma cases may be observed bilaterally?
30% ## Footnote The majority of cases present unilaterally.
132
What clinical features are commonly observed in patients with retinoblastoma?
* Leukocoria * Strabismus * White retinal lesion * Iris neovascularization (in ~20% of cases) These features are crucial for clinical recognition
133
Why is early detection and prompt treatment vital for retinoblastoma?
Due to the high mortality rate associated with this tumor ## Footnote Timely intervention can significantly impact patient outcomes.
134
What additional testing should be included for patient taking plaquenil?
1. 10-2 VF (if Asian 24-2 or 30-2) 2. Multifocal ERG 3. Mac OCT 4. Ishihara color vision
135
What additional testing should be included for patient taking plaquenil? (4)
1. 10-2 VF 2. Multifocal ERG 3. Mac OCT 4. Ishihara color vision *multifocal ERG is a diagnostic test that measures electrical activity in retina cells
136
Ocular complications of lupus include?
CRVO BRVO CRAO BRAO Exudative retinal detachments Toxic maculopathies (secondary to plaquenil) * retinal diseases associated with lupus mimic T2DM and HTN
137
What are the greatest risk factors for transformation of a choroidal nevus to a malignant choroidal nevus?
Thickness >2mm Fluid subretinal Orange pigment (lipofuscin) Symptoms (reduced VA) Location in posterior pole = proximity to optic disc * remember mnemonic: To Find Small Ocular Melanoma Do Imaging
138
Are choroidal nevi acquired or congenital?
Congenital
139
At what age does choroidal nevi usually become clinically apparent?
Puberty
140
What are the characteristics of choroidal nevi?
Flat or minimally elevated, pigmented or amelanotic ## Footnote They usually measure between 1.5 to 5mm in diameter and less than 2mm thick.
141
What may develop over time on choroidal nevi?
Overlying drusen
142
What is the histopathological composition of a choroidal nevus?
Low-grade, spindle-shaped, ovoid or round melanocytes ## Footnote These melanocytes have varying amounts of cytoplasmic pigmentation.
143
What is a statistical risk factor for the transformation of a choroidal nevus into a melanoma?
Tumor thickness greater than 2 mm ## Footnote Other factors include the presence of subretinal fluid, orange pigmentation, proximity to the optic disc, and the presence of symptoms.
144
What percentage of nevi measuring 2.5 mm in thickness become melanomas per month?
Approximately 1%
145
What increases the chance of transformation from choroidal nevus to melanoma?
Development of orange pigment on the surface of nevi
146
Where on the retina are nevi more likely to become melanomas?
Towards the posterior portion of the eye (closer to the optic disc)
147
What additional indicators may suggest a nevus is more likely to transform into melanoma? (FA, symptoms, visual field)
Hot spots on fluorescein angiography, decreased vision, or a visual field defect
148
What do drusen indicate regarding choroidal nevi?
Chronicity and benignity ## Footnote Lesions with drusen rarely transform into melanomas.
149
What occurs during the pre-maculopathy stage of hydroxychloroquine toxicity?
Visual acuities remain unaffected, but there is a noticeable loss of the foveal reflex. Granular changes within the macula may result in color vision changes and Amsler grid abnormalities. ## Footnote If the medication is discontinued at this time, the associated retinal changes are reversible.
150
What happens if hydroxychloroquine is continued during the pre-maculopathy stage?
Early maculopathy occurs, linked to a decrease in visual acuity and RPE atrophy surrounding the fovea. ## Footnote Fluorescein angiography at this stage will reveal a window defect.
151
What is the consequence of reaching the early maculopathy stage in hydroxychloroquine toxicity?
Retinal damage is not reversible upon cessation of the medication. ## Footnote This stage is marked by a decrease in visual acuity.
152
What visual changes are noted as hydroxychloroquine toxicity progresses?
Moderate decrease in vision and a 'bull's eye' macular lesion is visible on fundus examination. ## Footnote This indicates progression to severe maculopathy.
153
What characterizes the severe maculopathy stage in hydroxychloroquine toxicity?
Significant reduction in visual acuity and RPE atrophy adjacent to the fovea. ## Footnote This stage leads to more severe visual impairment.
154
What are the features of end-stage maculopathy in hydroxychloroquine toxicity?
Very poor visual acuity, attenuation of arterioles, increased choroidal visibility due to RPE atrophy, and clumping of pigment in the retinal periphery. ## Footnote This stage represents the most advanced form of retinal damage.
155
True or False: The retinal changes associated with hydroxychloroquine toxicity are always reversible.
False. ## Footnote Changes are reversible only if the medication is discontinued during the pre-maculopathy stage.
156
Fill in the blank: Granular changes within the macula during the pre-maculopathy stage of plaquenil toxicity may result in _______.
color vision changes and Amsler grid abnormalities.
157
What type of visual field defect frequently manifests in early stages of plaquenil toxicity?
Paracentral scotoma
158
Which tests are MOST useful in the diagnosis and management of hydroxychloroquine retinopathy? (Select 2)
* Optical coherence tomography (OCT) * Multifocal electroretinogram (mERG) ## Footnote These tests help detect early signs of retinal damage, allowing for timely intervention.
159
What is the key to maintaining visual integrity in patients with hydroxychloroquine retinopathy?
Early detection ## Footnote Early detection alerts clinicians to discontinue the medication before permanent retinal damage occurs.
160
In later stages of hydroxychloroquine retinopathy, which retinal layers may show abnormalities?
* Parafoveal outer nuclear layer * Inner plexiform layer * External limiting membrane ## Footnote These layers can exhibit structural changes as the disease progresses.
161
What sign associated with hydroxychloroquine toxicity can be observed on OCT?
Flying saucer sign ## Footnote This sign indicates preservation of outer retinal layers subfoveally with perifoveal loss.
162
What is the purpose of the multifocal electroretinogram (mERG) in the context of retinal health?
To detect paracentral retinal damage ## Footnote mERG provides an objective measure of retinal function.
163
What does fundus autofluorescence (FAF) identify in patients with hydroxychloroquine retinopathy?
Areas of retinal pigment epithelium (RPE) dysfunction ## Footnote FAF is useful for visualizing RPE health.
164
What is candidiasis caused by?
Candidiasis is caused by a yeast fungus, Candida albicans.
165
Where is Candida albicans frequently encountered in humans?
On the skin and in the digestive tract, mouth, and vagina.
166
In which patients might retinal involvement occur due to candidiasis?
Immunocompromised patients, IV drug users, or those with long-term indwelling catheters.
167
What symptoms might patients with retinal involvement from candidiasis notice?
Floaters and blurred vision unilaterally.
168
How do lesions from retinal candidiasis appear?
As areas of small, white, round lesions with indistinct borders.
169
What serious conditions may ensue if candidiasis is left untreated?
Endophthalmitis, retinal necrosis, and detachment.
170
True or False: Candidiasis can only affect the skin.
False
171
What are the clinical signs of an ischemic Central Retinal Vein Occlusion (CRVO)?
Multiple cotton wool spots, widespread retinal hemorrhages, dilated tortuous vessels, optic disc edema, macular and retinal edema, a relative afferent pupillary defect (APD), and poor visual acuity (usually 20/400 or worse) ## Footnote Ischemic CRVO indicates a more severe form of vein occlusion and often results in significant visual impairment.
172
Signs for non-ischemic Central Retinal Vein Occlusion (CRVO)? List at least 2
- Dot-blot hemes and flame-shaped hemorrhages in all four quadrants - dilated and tortuous vessels - optic disc and macular edema *typically absent APD and cotton wool spots *generally better visual acuity than 20/400 ## Footnote Non-ischemic CRVO is usually less severe and may have a better prognosis than ischemic CRVO.
173
What is the typical age demographic for individuals suffering from a CRVO?
65 years or older ## Footnote Age is a significant risk factor for CRVO, with older adults being more susceptible.
174
Pathophysiology of arteritic anterior ischemic optic neuropathy (AION)?
Infarction of the prelaminar and laminar segment of the optic nerve ## Footnote AION is often associated with conditions like giant cell arteritis.
175
What does CRAO stand for?
Central retinal artery occlusion
176
What are the symptoms of central retinal artery occlusion?
Acute, painless vision loss
177
What percentage of CRAO cases present unilaterally?
99%
178
What type of pupillary defect is observed in CRAO?
Afferent pupillary defect
179
How does the retina appear in cases of CRAO?
More pale/white superficially with cherry red spot macula
180
What is the pronounced appearance of the fovea in CRAO known as?
Cherry red spot
181
Is CRAO typically associated with retinal hemorrhages?
No
182
Fill in the blank: CRAO is an obstruction of the _______.
central retinal artery
183
Potential complications of CRVO
- persistent Mac edema - NVD - NVE - NVI *therefore monitor for “90 day glaucoma” from NVI which may occur 2-4 months after initial CRVO * neovascularization can cause recurrent pre-retinal and vitreous hemes, RD and open angle or closed angle glaucoma
184
RTC for pt’s with CRVO and have a VA 20/40 or better
1-2 months for 6 months
185
RTC for CRVO if VA is worse than 20/200
monthly for the next 6 months
186
What is a sub-Tenon's injection?
An injection using a long needle where the tip is obscured from view.
187
What happens if a needle bends during a tangential injection?
It will enter tissue away from the bevel and may penetrate further into the tissue.
188
How should the bevel of the needle be positioned during a sub-Tenon's injection?
Toward the globe.
189
What conditions is a sub-Tenon's injection typically reserved for?
* Vitritis * Posterior uveitis * Cystoid macular edema
190
Where should the needle be placed for a sub-Tenon's injection?
2 to 3 mm from the inferotemporal fornix.
191
What should be avoided when penetrating the bulbar conjunctiva?
Nick any of the subconjunctival vessels.
192
Complete the sentence: A sub-Tenon's injection uses a long needle in which the tip, when properly inserted, is _______.
[obscured from view]
193
Watzke-Allen sign
Patient sees a “break” in a Thin slit-beam shone over macula * positive test for full thickness macular hole
194
Shafer sign
Release of pigment into vitreous chamber from a retinal tear, a break in retina releases retinal pigment epithelial cells * patient cues them as sudden increase in floaters
195
What are the two forms of macular drusen associated with dry AMD?
Hard or soft drusen
196
What is a common observation in the outer retina of patients with dry AMD?
Areas of pigment clumping
197
What occurs in RPE atrophy related to dry AMD?
Underlying choroidal vessels may appear more visible
198
What is geographic atrophy in the context of dry AMD?
Regions of confluent retinal and choriocapillaris atrophy
199
How does visual acuity in dry AMD compare to wet AMD?
Typically less affected
200
What is a classic OCT finding in dry AMD?
Ripples formed under the RPE due to drusen
201
What is the appearance of cystoid macular edema on fundus evaluation?
Irregular, blunted foveal light reflex and thickening in the central macular region
202
What additional signs may be observed in severe cases of cystoid macular edema?
- Vitreous cells - swelling of the optic nerve - hemorrhages - lamellar macular holes
203
What ocular conditions can lead to cystoid macular edema? (6)
* Diabetic retinopathy * BRVO and CRVO * Uveitis * Retinitis pigmentosa * Retinal vasculitis * Certain medications (ex: prostaglandins)
204
What OCT finding is characteristic of cystoid macular edema?
Loss of foveal contour due to cystic spaces within the retina
205
What is the typical presentation of central serous retinopathy?
Localized serous detachment of the neurosensory retina in the macula
206
What visual acuity range is common in patients with central serous retinopathy?
20/20 to 20/80
207
What may Amsler grid testing reveal in central serous retinopathy?
Distortion of straight lines and a possible central scotoma
208
What are the clinical signs of idiopathic polypoidal choroidal vasculopathy? (Name at least 3)
* Subretinal red-orange polyp-like lesions * Circinate subretinal exudates * Choroidal neovascular membrane * Subretinal or sub-RPE blood * Vitreous hemorrhages * Subretinal fibrosis * Subretinal fluid * Multiple serous pigment epithelial detachments
209
How can idiopathic polypoidal choroidal vasculopathy be distinguished from AMD?
Occurs at a younger age without significant drusen or geographic atrophy
210
In which races is polypoidal choroidal vasculopathy more commonly observed?
Asians and African Americans
211
In which demographic is choroidal melanoma most commonly found?
Occurs most commonly in Caucasians with a median age of 55
212
What are some risk factors for developing choroidal melanoma?
Risk factors include: * Sun exposure (or arc welding) * Fair skin with inability to tan * Pre-existing choroidal nevi * Ocular or oculodermal melanocytosis
213
True or False: Genetic factors may predispose patients to choroidal melanoma.
True
214
What symptoms may indicate the presence of choroidal melanoma?
Symptoms include: * Decreased visual acuity * Metamorphopsia * Flashing lights (photopsia) * Scotomas
215
What can cause decreased visual acuity in patients with choroidal melanoma?
Causes include: * Involvement in the macular area * Subretinal fluid * Media opacities (hemorrhage, vitreal tumor seeding, cataract, corneal pacification from secondary glaucoma)
216
What characteristics are typical of melanomas observed in the fundus?
Melanomas are typically: * Elevated * Subretinal mass lesions * Color can vary from amelanotic to very darkly pigmented
217
What shape is associated with choroidal melanoma due to a rupture in Bruch's membrane?
Collar-button or mushroom shape
218
What is the differential diagnosis for choroidal melanoma?
Differential diagnosis includes: * Choroidal nevus * Congenital hypertrophy of the retinal pigment epithelium (CHRPE) * Melanocytoma * Disciform scar * Subretinal or subRPE hamartoma * Choroidal hemangioma * Posterior scleritis * Retinal gliosis * Ocular melanocytosis
219
What characteristics of a lesion suggest it is a choroidal melanoma?
Suggestive characteristics include: * Thickness of >2 mm * Presence of subretinal fluid * Orange surface pigmentation * Visual symptoms * Proximity to the optic disc or macula **Documented history of growth**
220
What procedure would be most helpful in diagnosis and evaluation of melanocytic choroidal nevus?
B-scan Characteristics: * dome or mushroom-shaped tumor * steep angle kappa * attenuation of signals * choroidal excavation * orbital shadowing
221
What are the most common risk factors for development of choroidal melanoma?
* increased sun exposure * oculodermal melanocytosis * pre-existing uveal nevus
222
What are adverse prognostic factors in patients diagnosed with choroidal melanomas?
Histological features, chromosomal abnormalities, appearance of tumor, local tumor recurrence ## Footnote These factors are critical for assessing the prognosis of patients with choroidal melanomas.
223
What histological feature indicates a poor prognosis in choroidal melanoma?
Large number of epithelioid cells ## Footnote Epithelioid cells are more associated with aggressive tumor behavior compared to spindle cells.
224
What tumor appearance factors contribute to poor prognosis in choroidal melanoma?
Larger size of tumor, extrascleral extension, growth through Bruch's membrane, optic nerve extension, lack of pigmentation, more anterior location ## Footnote These factors often correlate with advanced disease at the time of diagnosis.
225
True or False: Lymphocytic infiltration is a favorable histological feature in choroidal melanoma.
False ## Footnote Lymphocytic infiltration is typically associated with a worse prognosis.
226
Fill in the blank: A large number of _______ cells in choroidal melanoma is a poor prognostic factor.
epithelioid ## Footnote Epithelioid cells are more aggressive compared to spindle cells.
227
What is the significance of local tumor recurrence in choroidal melanoma?
It indicates a poorer prognosis ## Footnote Local recurrence suggests that the disease is more aggressive and difficult to manage.
228
What does the appearance of closed vascular loops within the tumor indicate?
Poor prognosis ## Footnote Closed vascular loops are a histological feature that correlates with aggressive tumor behavior.
229
What is the implication of a tumor's anterior location in choroidal melanoma?
It is associated with larger tumor size at diagnosis ## Footnote Tumors located more anteriorly, especially involving the ciliary body, are often larger due to lead time before diagnosis.
230
Once diagnosis of choroidal melanoma has been made what’s the next series of systemic tests to rule out possible metastasis? (3)
- Blood testing - chest x-ray - abdominal CT scan
231
CSME criteria
1. Retinal edema within 500 microns of fovea 2. Hard exudates within 500 microns of fovea 3. Retinal edema within an area of at least 1500 microns within 1DD of the fovea * 1/3DD = 500 um * 1 DD = 1500 um
232
4-2-1 rule
4 quadrants of hemorrhages 2 quadrants of venous beading 1 quadrant of IRMA (intraretinal microvascular abnormalities) * meet at least 1 criteria = severe NPDR * meet 2 criteria = very severe NPDR
233
RTC for NPDR
Every 6 months
234
RTC for PDR
Every 3 months
235
Hemorrhages in patients with Valsalva retinopathy are located where?
Between the retina and posterior vitreous face * subhyaloid And/or sub-internal limiting membrane (between ILM and NFL) * mostly occur in macular area
236
What is the pathophysiology of Valsalva maneuver?
Elevation of intra-abdominal pressure leads to increase in ocular venous pressure, resulting in ruptures of superficial retinal capillaries
237
What is a Valsalva maneuver?
A forcible exhalation against a closed glottis that increases intrathoracic or intra-abdominal pressure ## Footnote This maneuver can interfere with venous return to the heart.
238
What behaviors are typically associated with the Valsalva maneuver?
Strenuous exertion from behaviors such as: * Emesis (vomiting) * Violent coughing * Constipation * Labor * Heavy lifting * Blowing musical instruments * Crush or compression injuries ## Footnote These activities can lead to the forcible exhalation characteristic of the Valsalva maneuver.
239
What happens to ocular venous pressure during a Valsalva maneuver?
There is a rapid rise in ocular venous pressure ## Footnote This can lead to rupture of superficial retinal capillaries.
240
What is a possible consequence of elevated ocular venous pressure?
Rupture of superficial retinal capillaries leading to hemorrhaging into the subhyaloid space ## Footnote This can cause sudden and painless disruption of vision.
241
What are some differential diagnoses for Valsalva retinopathy?
Differential diagnoses include: * Posterior vitreous detachment * Purtscher retinopathy * Hypertensive retinopathy * Diabetic retinopathy * Terson retinopathy ## Footnote Each of these conditions has distinct mechanisms that can lead to retinal hemorrhaging.
242
What causes posterior vitreous detachment?
Mechanical traction due to compression and detachment of the vitreous body ## Footnote This can lead to damage of retinal vasculature and subsequent hemorrhaging.
243
What is Purtscher retinopathy?
Multiple patches of retinal whitening, large cotton wool spots and hemorrhages that surround optic disc after multiple long-bone fractures with fat emboli or severe compressive injuries to trunk or head *due to occlusion of small arterioles by intravascular microemboli from a compression injury ## Footnote This condition is associated with trauma.
244
What causes hypertensive retinopathy?
Chronic elevation in retinal arteriolar pressure ## Footnote This results in damage to the capillary wall endothelium and leakage of blood and fluid.
245
What is diabetic retinopathy characterized by?
Increased vascular permeability due to changes in microvasculature structure ## Footnote This leads to leakage of blood and fluid into the retina.
246
What triggers Terson retinopathy?
Increase in intracranial pressure leading to elevation in intraocular pressure ## Footnote This results in compression of the central retinal vein and can cause hemorrhaging.
247
If pre-retinal hemorrhage from Valsalva maneuver does not spontaneously resolve over several weeks, what treatment would be indicated?
Nd:YAG laser disruption of posterior hyaloid face
248
What is cobblestone degeneration?
A benign thinning/atrophy of the peripheral retina, retinal pigment epithelium, and choriocapillaris
249
In which individuals is cobblestone degeneration more frequently seen?
Myopic individuals
250
How is cobblestone degeneration commonly observed in terms of laterality?
It commonly occurs bilaterally
251
Which part of the retina is most frequently involved in cobblestone degeneration?
Inferior temporal aspect
252
What symptoms are associated with cobblestone degeneration?
Asymptomatic condition
253
What clinical signs are observed during the evaluation of the fundus in cobblestone degeneration?
White/yellow circular areas of atrophy; halo of pigment surrounding lesions
254
What may happen to regions of degeneration in cobblestone degeneration?
They may coalesce together to form a large band of atrophy
255
Is cobblestone degeneration associated with ocular complications?
No, it is not associated with ocular complications
256
What is the recommended follow-up for patients with cobblestone degeneration?
Annual evaluation
257
What is another name for macular epiretinal membrane (ERM) when the membrane is slight?
Cellophane maculopathy
258
What does the term 'macular pucker' refer to?
A denser ERM that results in diminished acuity
259
What causes the formation of epiretinal membranes (ERMs)?
Disruption of the internal limiting membrane (ILM)
260
What type of cells proliferate to form the membrane in ERM?
Glial cells
261
What is the appearance of the membrane in the early stage of ERM?
A glistening area of transparent tissue
262
What symptoms are commonly associated with macular epiretinal membranes?
Decreased and/or distorted vision
263
What percentage of ERM cases may be bilateral?
Up to 20%
264
What clinical signs indicate the presence of mild epiretinal membranes?
Glistening tissue overlying or next to the macula
265
What are the sequelae of a severe macular pucker?
Cystoid macular edema or a tractional retinal detachment
266
True or false The majority of patients with ERM are asymptomatic
True
267
What are some causes of ERM formation? List at least three.
* Idiopathic origin * Posterior vitreous detachment * Uveitis * Trauma, intraocular surgery, or laser treatment * Diabetic retinopathy * Retinal breaks * Retinal vascular diseases
268
What visual disturbances can be caused by a mature ERM?
Metamorphopsia and reduced visual acuity
269
What is another name for Epiretinal Membrane?
Cellophane Maculopathy ## Footnote This term describes the appearance of the membrane on the retina.
270
When is treatment recommended for patients with Epiretinal Membrane?
If the patient is symptomatic and suffers from reduced visual acuity or experiences a large amount of metamorphopsia ## Footnote Treatment is not recommended for asymptomatic patients with visual acuity of 20/40 or better.
271
What surgical procedure is warranted for symptomatic patients with Epiretinal Membrane?
Pars plana vitrectomy followed by a membrane peel ## Footnote This procedure helps alleviate symptoms related to the membrane.
272
What is the expected outcome of surgery for patients with Epiretinal Membrane?
Patients will typically experience an improvement in their postoperative acuity ## Footnote However, acuity is not expected to fully return to pre-membrane levels, especially in chronic cases.
273
What tool may be given to patients for monitoring distortion after treatment?
Amsler grid ## Footnote This grid helps patients detect changes in their vision.
274
OCT of patient with familiar drusen would show?
Thickening of RPE-Bruch’s membrane complex with an intact photoreceptors layer
275
Tx for CME secondary to YAG cap following CE
Topical NSAID Topical steroid Oral CAI Example: 1 gtt ketorolac QID and 1 gtt prednisolone acetate QID
276
Tx for CME in patients with retinitis pigmentosa
Oral CAI
277
What does CME look like on FA in early and late stages?
Small hyper fluorescent spots in early stages 'flower-petal' pattern in the late stage. ## Footnote This pattern is indicative of cystoid macular edema (CME) observed during FA.
278
Which imaging techniques are valuable for identifying patients with CME?
Fluorescein angiography (FA) and optical coherence tomography (OCT). ## Footnote These techniques are particularly useful when the diagnosis is uncertain.
279
What does the early arteriovenous phase of FA show in patients with CME?
Capillary dilation and leakage of fluid. ## Footnote This leads to the visibility of small hyperfluorescent spots.
280
What occurs in the later phase of FA for patients with CME?
Fluorescein dye accumulates within the microcystic spaces in the outer plexiform layer of the retina. ## Footnote This accumulation results in characteristic staining petalloid patterns
281
What is the classic perifoveal staining pattern observed in CME during the late phase of FA?
'Petaloid' or 'spoke-wheel' staining pattern. ## Footnote This pattern is a key diagnostic feature of CME.
282
In cases of CME, what additional leakage may be observed?
Optic nerve head leakage. ## Footnote This is most commonly associated with Irvine-Gass syndrome.
283
What appearance do outer cystoid spaces show in severe cases of CME?
'Honeycomb' appearance. ## Footnote This is due to larger fused cystoid spaces extending outside the perifoveal region.
284
What is the appearance of a classic choroidal neovascular membrane (CNVM) in the early phase of angiography?
Clearly visible and well-demarcated 'lacy' hyperfluorescence. ## Footnote This feature helps differentiate CNVM from other conditions.
285
What is the appearance of fluorescein angiography in central serous retinopathy?
Smoke-stack appearance. ## Footnote This distinct appearance helps in the diagnosis of central serous retinopathy.
286
What is the most common ocular complication of Behcet disease?
Uveitis * bilateral, non-granulomatous uveitis
287
ERG and EOG in best disease
Normal ERG Abnormal EOG
288
ERG and EOG in stargardt
Normal ERG Normal EOG
289
ERG and EOG in familial drusen * familial drusen is autosomal dominant
Normal ERG Abnormal EOG (in advanced familial drusen)
290
ERG and EOG in choroideremia
Abnormal ERG abnormal EOG
291
What is choroideremia?
An X-linked recessive condition that leads to degeneration of the retina, specifically the choriocapillaris and retinal pigment epithelium (RPE).
292
Who typically presents with choroideremia?
Typically presents in males in the 1st to 2nd decade of life.
293
What is the most common entering complaint of choroideremia?
Nyctalopia, or night blindness.
294
What are early signs of choroideremia?
Typically occur in the first or second decade of life.
295
What visual symptoms progress throughout the patient's life in choroideremia?
Restriction of peripheral vision.
296
When does visual acuity typically remain favorable in choroideremia?
Until late in the disease when macular involvement can occur.
297
What is the characteristic appearance of the fundus early in choroideremia?
Pigment granules scattered throughout the fundus, sparing the macular region (salt-and-pepper fundus).
298
What happens to the RPE as choroideremia progresses?
Patches of RPE atrophy in the mid-peripheral retina become confluent and progressive.
299
Choroideremia is a degeneration of what structures?
choriocapillaris and RPE * diffuse progressive degeneration
300
In end-stage choroideremia, what can be seen extending from the posterior pole to the periphery?
Visibility of the sclera.
301
What visual function do patients commonly maintain until later in the disease?
Central vision.
302
What is a common finding in female carriers of choroideremia?
Mid-peripheral mottling of the RPE that tends to be static.
303
What is the 'moth-eaten' appearance associated with in choroideremia?
The RPE, along with RPE pigment clumping and degeneration.
304
What is observed in late-stage ERG for choroideremia?
No recordable scotopic function and a greatly reduced photopic response.
305
Fill in the blank: Choroideremia is an _______ condition.
X-linked recessive
306
True or false A successful treatment for choroideremia does not currently exist
True
307
What is Leber's Congenital Amaurosis?
A progressive autosomal recessive rod-cone dystrophy and the most common congenital cause of blindness in children ## Footnote It involves the loss of retinal photoreceptors, outer segments, and outer nuclear layers.
308
What are the early symptoms of Leber's Congenital Amaurosis?
- Roving eye within the first few months of life - reduced acuity and color perception - nyctalopia - photophobia ## Footnote Nyctalopia refers to difficulty seeing in low light conditions. *group of hereditary disorders, onset birth or early childhood * severe visual impairment (20/40 to NLP) * vascular attenuation, salt and pepper fundus, RP appearance
309
What range of visual acuity is typically seen in patients with Leber's Congenital Amaurosis?
From 20/40 to no light perception (NLP), with the average being 20/200 ## Footnote Visual acuity is a measure of the eye's ability to resolve detail.
310
What are some ocular signs associated with Leber's Congenital Amaurosis?
* Attenuated vessels * Chorioretinal atrophy * Significant macular pigmentation * Pigmentary retinopathy * Yellow flecks * Tapetal metallic sheen * Sluggish pupils * Nystagmus * Constricted visual fields * High hyperopia * Keratoconus * Keratoglobus * Posterior subcapsular cataracts * Oculo-digital sign (eye rubbing) ## Footnote The oculo-digital sign may lead to atrophy of orbital fat and enophthalmos.
311
What systemic findings can occur with Leber's Congenital Amaurosis?
* Deafness * Skeletal and muscular anomalies * Renal/kidney abnormalities * Endocrine dysfunction * Mental handicap * Epilepsy ## Footnote These systemic issues may vary in severity and presentation.
312
What is the prognosis for patients with Leber's Congenital Amaurosis?
Poor, with no treatment available ## Footnote Management typically involves referral to a low vision specialist.
313
ERG in Leber’s congenital amaurosis
Abnormal *severely reduced * loss of retinal photoreceptors, outer segments and outer nuclear layers
314
FA on stargardt disease
“Silent choroid” * choroidal hypo-fluorescence with prominent retinal vasculature * dark choroid
315
Tx for stargardt
Prescribe low vision aids * with daily Amsler, RTC ASAP if changes
316
Macular disease may cause what color vision deficiency?
Blue-yellow
317
WWOP is mostly seen in which area of the retina?
Inferior and temporally
318
4 bright bands on OCT Mac
1. ELM 2. PIL (photoreceptor integrity line) 3. Interdigitation zone (RPE complex) 4. RPE (interacts with Burch’s membrane)
319
Paving stone degeneration most commonly seen in which areas of the retina?
Inferior and temporal
320
RP triad
1. Attenuation of arterioles 2. Bone-spicule pigmentation of retina 3. Waxy pallor of optic nerve *subcapsular cataract common in RP
321
What type of cataract commonly develops in RP?
Subcapsular cataract
322
How many layers compose the retina?
10 layers ## Footnote The layers include the retinal pigment epithelium, photoreceptors, and others.
323
What is the first outermost layer of the retina?
Retinal pigment epithelium (RPE) ## Footnote This is the outermost layer of the retina.
324
List the layers of the retina from outermost to innermost.
* Retinal pigment epithelium (RPE) * Photoreceptors * External limiting membrane (ELM) * Outer nuclear layer (ONL) * Outer plexiform layer (OPL) * Inner nuclear layer (INL) * Inner plexiform layer (IPL) * Ganglion cell layer (GCL) * Nerve fiber layer (NFL) * Internal limiting membrane (ILM) ## Footnote These layers play various roles in processing visual input.
325
What is the role of the retinal pigment epithelium (RPE)?
Forms part of the blood-retinal barrier, phagocytosis of fragments from shed photoreceptor discs, metabolizes and stores vitamin A ## Footnote Vitamin A is crucial for the formation of rhodopsin photopigment.
326
What happens due to vitamin A deficiency?
Prolonged dark adaptation ## Footnote Vitamin A is essential for converting light into electrical signals. *pts with retinitis pigmentosa supplement vitamin A to help with dark adaptation because pts are symptomatic for nyctalopia
327
What does the photoreceptor cell layer contain?
Outer and inner segments of rods and cones ## Footnote These segments are characterized by high levels of metabolic activity.
328
Fill in the blank: The _______ converts radiant energy into electrical energy.
photoreceptor cell layer ## Footnote This conversion is essential for visual processing.
329
True or False: The inner layers of the retina absorb light before it reaches the photoreceptors.
False ## Footnote Light is refracted by the cornea and lens and passes through the inner layers before being absorbed by photoreceptors.
330
What is the external limiting membrane?
Consists of intercellular junctions of the photoreceptor cells ## Footnote It delineates the inner segments of the photoreceptors and their respective nuclei.
331
What cells does the outer nuclear layer contain?
The cell bodies and nuclei of the rods and cones
332
What is the function of the outer plexiform (synaptic) layer?
Site where photoreceptor cells synapse with the dendrites of horizontal and bipolar cells from the inner nuclear layer
333
What cell types are found in the inner nuclear layer?
Bipolar, horizontal, amacrine, and Muller cells
334
What role do Muller cells play in the retina?
Create tight junctions and contribute to the formation of the external limiting membrane
335
What does the inner plexiform (synaptic) layer encompass? (Which cells and which part of those cells?)
The synapses of bipolar, ganglion, and amacrine cells' axons
336
What is contained within the ganglion cell layer?
Ganglion cell bodies
337
What does the nerve fiber layer contain?
The axons of ganglion cells
338
What forms the internal limiting membrane?
Radial feet processes of Muller cells and other glial cell constituents
339
Where do Muller cells' processes extend in the retina?
Throughout the length of the retina except for the retinal pigment epithelium
340
What types of cells do amacrine cells amalgamate information from?
Ganglion and bipolar cells
341
Where are horizontal cell bodies located?
At the outer edge of the inner nuclear layer
342
What information do horizontal cells combine?
Information obtained from rods and cones
343
How many different types of horizontal cells are there?
At least two or three different types
344
What is a potential complication of retinal laser photocoagulation treatment?
Choroidal detachment ## Footnote May lead to angle-closure glaucoma.
345
What are the complications associated with retinal laser photocoagulation treatment? (Name 3)
* Choroidal detachment * Rhegmatogenous retinal detachment * Cystoid macular edema * Macular pucker * Exudative retinal detachment * Retinal hemorrhage (rare) ## Footnote Complications typically occur due to overtreatment of large regions of the retina.
346
What complication of retinal laser treatment is rare?
Retinal hemorrhage ## Footnote Occurs in rare cases.
347
What is a common complication of cryotherapy?
Eyelid edema ## Footnote Occurs almost 100% of the time.
348
Which complication of cryotherapy occurs almost 100% of the time?
Chemosis ## Footnote This condition involves swelling of the conjunctiva.
349
Fill in the blank: Transient diplopia may be caused by accidental treatment of an _______ muscle.
extracular ## Footnote This refers to muscles outside of the eye.
350
List some complications of cryotherapy.
* Eyelid edema * Chemosis * Transient diplopia * Vitritis * Maculopathy (very rare) ## Footnote Maculopathy is considered very rare.
351
What is vitritis?
Inflammation of the vitreous body ## Footnote It can occur as a complication of cryotherapy.
352
True or False: Maculopathy is a common complication of cryotherapy.
False ## Footnote Maculopathy is described as very rare.
353
stargardt on FA
Choroidal hypofl with prominent retinal vasculature “Silent choroid”
354
What is Stargardt disease most commonly caused by?
Mutations in the ABCA4 gene ## Footnote ABCA4 gene mutations are primarily responsible for Stargardt disease.
355
What type of protein does the ABCA4 gene encode?
ATP-binding cassette transmembrane protein ## Footnote This protein is specifically expressed by rod outer segments.
356
What is the role of the ABCA4 gene in the retina?
Involved in the transport of all-trans-retinal ## Footnote This transport is crucial for proper photoreceptor function.
357
What happens as a result of mutations in the ABCA4 gene?
Accumulation of all-trans-retinal in the photoreceptors and retinal pigment epithelium ## Footnote This accumulation leads to various retinal pathologies.
358
What is lipofuscin and why is it significant in Stargardt disease?
A component that accumulates and is toxic to RPE and photoreceptors ## Footnote Lipofuscin accumulation leads to cellular damage and vision loss.
359
Fill in the blank: The ABCA4 gene mutations lead to the _______ of lipofuscin.
accumulation ## Footnote This accumulation is detrimental to retinal health.
360
What is Stargardt disease?
A genetic eye disorder that results in a decrease in visual acuity, typically presenting in the first to second decades of life. ## Footnote It is characterized by specific retinal changes and accumulation of lipofuscin-like material.
361
What are the initial symptoms of Stargardt disease?
Decreased vision, which may be mistaken for malingering due to a normal appearing fundus. ## Footnote Children may report decreased vision before any noticeable retinal changes occur.
362
What appearance does the macula take on as Stargardt disease progresses?
It may appear mottled and eventually develop a 'beaten-bronze' appearance, potentially surrounded by yellowish flecks. ## Footnote This progression indicates worsening of the disease.
363
What is the characteristic pattern of geographic atrophy in Stargardt disease?
'Bull's eye' pattern. ## Footnote This pattern is associated with significant loss of visual acuity.
364
What accumulates at the level of the retinal pigment epithelium in Stargardt disease?
Unusual lipofuscin-like material. ## Footnote This accumulation is a key feature of the disease.
365
What is the typical finding in the electroretinogram (ERG) of patients with Stargardt disease?
Characteristically normal, but may be atypical in advanced cases. ## Footnote The ERG tests the electrical responses of the retina. Normal ERG and normal EOG until diseases advances
366
How does the electro-oculogram (EOG) change as Stargardt disease progresses?
It is likely normal in early stages but becomes increasingly abnormal as the disease progresses. ## Footnote The EOG measures the electrical potential of the retina.
367
What is Best disease also known as?
Vitelliform dystrophy. ## Footnote It is a rare retinal condition that affects the macular area.
368
What occurs during the pre-vitelliform stage of Best disease?
The child is asymptomatic, the fundus appears normal, but the EOG reading is abnormal. ## Footnote This stage may be detected through testing even if no symptoms are present.
369
Describe the vitelliform stage of Best disease.
Egg yolk stage! Occurs in the first or second decade of life with a small decrease in vision and a macular lesion resembling an egg yolk. **This stage is typically bilateral.
370
What characterizes the pseudohypopyon stage in Best disease?
A blister-like lesion where lipofuscin may gravitate inferiorly, causing the appearance of a pseudohypopyon. ## Footnote This stage usually occurs in the second to third decades of life.
371
What happens in the vitelliruptive stage of Best disease?
Scrambled eggs! The 'egg yolk' breaks apart, leading to a decrease in visual acuity. ** This stage indicates further progression of the disease.
372
What defines the atrophic stage of Best disease? (End stage)
Macular scarring and potential formation of choroidal neovascular membranes (CNVM) and/or geographic atrophy. ## Footnote Visual acuity is typically very poor at this stage.
373
What is fundus flavimaculatus?
A variant of Stargardt disease characterized by white-yellow flecks in the posterior pole instead of macular involvement. ## Footnote Visual acuity remains fairly good as long as the macula is clear.
374
In fundus flavimaculatus, what happens to visual acuity?
It tends to remain fairly good as long as the macula remains clear and geographic atrophy is absent. ## Footnote This is in contrast to Stargardt disease where visual acuity decreases significantly.
375
Tx for retinal detachment
Focal Laser photocoagulation * multiple rows of treatment burns to ensure longevity and stability
376
Pneumatic retinopexy is used to treat?
Small retinal breaks associated with uncomplicated retinal detachment in upper 2/3rds of peripheral retina *procedure performed by injecting an expanding gas bubble into vitreous cavity * gas placed against break which seals it closed
377
Tx for CRVO RTC after initiation of treatment
Refer for intravitreal anti-VEGF injection * treat macular edema * injections every 6 weeks RTC: if VA 20/40 or better 1-2 months for 6 months RTC if VA worse than 20/200 monthly for 6 months
378
RTC for wet AMD with active CNVM
1-3 months until CNVM inactive (based on OCT and FA)
379
What is Ocular Ischemic Syndrome (OIS) also known as?
Venous Stasis Retinopathy ## Footnote This term is considered outdated.
380
What is the average age of patients affected by Ocular Ischemic Syndrome?
65 years ## Footnote Epidemiology shows >50 years as the demographic.
381
What is the male to female ratio in cases of Ocular Ischemic Syndrome?
2:1 ## Footnote Males are affected more frequently than females.
382
What is the 5-year mortality rate for patients with Ocular Ischemic Syndrome?
40% ## Footnote This indicates a significant risk associated with the syndrome.
383
What are the common risk factors for developing Ocular Ischemic Syndrome?
* Hypertension * Hyperlipidemia * Diabetes Mellitus * Giant Cell Arteritis ## Footnote These conditions contribute to the development of OIS.
384
What pathophysiological condition leads to Ocular Ischemic Syndrome?
Chronic ocular hypoperfusion due to severe internal carotid artery stenosis ## Footnote This can also involve insufficiency or thrombosis of the internal carotid artery.
385
What percentage of internal carotid artery stenosis is associated with Ocular Ischemic Syndrome?
>70% ## Footnote Significant stenosis is critical for the development of OIS.
386
What happens to the central retinal artery (CRA) perfusion pressure in Ocular Ischemic Syndrome?
It is reduced by 50% ## Footnote This reduction leads to ischemic conditions in the eye.
387
What is a consequence of low perfusion pressure in OIS?
Induces oxidative stress damage ## Footnote This damage affects both the retina and choroid.
388
What are the symptoms of Ocular Ischemic Syndrome?
* Gradual loss of vision over weeks or months * Decrease in visual acuity (VA) ranging from mild to severe * Asymptomatic cases are possible ## Footnote Visual acuity can vary significantly among patients.
389
What defines 'mild' visual acuity loss in Ocular Ischemic Syndrome?
20/25 - 20/40 ## Footnote This indicates the range of mild loss in visual acuity.
390
What defines 'severe' visual acuity loss in Ocular Ischemic Syndrome?
20/400 or worse ## Footnote Severe cases can lead to significant impairment in vision.
391
What type of visual loss may occur in Ocular Ischemic Syndrome?
Transitory monocular visual loss ## Footnote This type of loss may recover over time.
392
What percentage of OIS patients report transient monocular visual loss (TMVL)?
10-15% ## Footnote TMVL is a significant symptom in ocular ischemic syndrome (OIS) patients.
393
What is the hallmark of carotid insufficiency?
Amaurosis fugax ## Footnote Amaurosis fugax is an older term for TMVL.
394
How long does TMVL typically last? (Transient monocular visual loss)
5 minutes or less ## Footnote This duration is characteristic of transient monocular visual loss.
395
What proportion of patients with amaurosis fugax have significant ipsilateral carotid artery obstruction?
1/3rd ## Footnote Specifically, these patients have an obstruction of ≥75%.
396
What visual symptoms may patients with OIS complain of?
Blur, dimming, or darkened vision ## Footnote Patients may describe a curtain coming down over the eye.
397
What is ocular angina?
Ocular and/or periocular pain ## Footnote This symptom occurs in approximately 40% of OIS patients.
398
What visual phenomenon might patients experience after bright light exposure?
Slow adaptation ## Footnote This is a common symptom in OIS.
399
What are the typical signs of OIS in the posterior segment?
1. Typically unilateral (80%) 2. Dilated retinal veins 3. Mid-peripheral hemorrhages (80% of cases) 4. Cherry-red spot (12% of eyes) ## Footnote Other signs may include narrowed arteries and rare cases of flame hemes, CWS, optic disc edema, and macular edema.
400
What is a cherry-red spot associated with in OIS?
Embolic occlusion of the CRA or increased IOP *embolism causes a blockage in CRA ## Footnote It may occur in neovascular glaucoma.
401
True or False: Retinal hemorrhages in OIS are usually in the posterior pole.
False ## Footnote Midperipheral hemorrhages are more common than those in the posterior pole.
402
Fill in the blank: OIS symptoms may include _______ after bright light exposure.
Worsening of vision ## Footnote This worsening can also occur with postural changes.
403
What is the most common sign of Ocular Ischemic Syndrome (OIS)?
NVI (iris rubeosis) is most common (65-85%) ## Footnote NVI stands for Neovascularization of the Iris.
404
What is the order of anterior chamber reaction in OIS?
flare > cells > KPs (20%) ## Footnote KPs refer to Keratic Precipitates.
405
What percentage of OIS cases may present with neovascular glaucoma?
50% of OIS cases ## Footnote Neovascular glaucoma may not have very high intraocular pressure due to poor ciliary body perfusion.
406
What is a common IOP finding in unilateral OIS?
Unilateral low IOP (non-neovascular) ## Footnote This finding can help differentiate OIS from other conditions.
407
What are some signs of Ocular Ischemic Syndrome (OIS) in the anterior segment? (List at least three)
* Diffuse episcleral injection * Corneal edema * Iris atrophy with poor reacting pupil (mid-dilated) ## Footnote These signs indicate ischemic changes in the eye.
408
What is a differential diagnosis (DDx) for OIS?
* Central Retinal Vein Occlusion * Diabetic Retinopathy ## Footnote Both conditions can present with similar vascular disorders.
409
What laboratory tests should be ordered for OIS evaluation?
* CBC * Fasting glucose * HbA1C * Fasting lipids * Sed Rate * C-reactive protein ## Footnote These tests help assess overall health and identify potential underlying causes.
410
What diagnostic imaging study is recommended if the carotid ultrasound is inconclusive?
MRA ## Footnote MRA stands for Magnetic Resonance Angiography.
411
What happens to the carotid arteries during a venous stasis evaluation?
Ask patient to hold breath ## Footnote This maneuver helps visualize blood flow and detect abnormalities.
412
At what stenosis level can a bruit be heard during carotid auscultation?
50-60% stenosis ## Footnote A bruit may not be heard if stenosis is less than 50%.
413
True or False: A bruit can be detected if stenosis is less than 50%.
False ## Footnote Bruits are typically not audible at less than 50% stenosis.
414
What is the management strategy for inflammation in the anterior segment?
Treat inflammation with topical steroid QID and homatropine 5% BID (cycloplegic) ## Footnote QID means four times a day, and BID means twice a day.
415
What should be done when neovascularization develops?
Refer to OMD for Panretinal Photocoagulation (PRP) 500um spots when neovascularization develops ## Footnote OMD refers to an ophthalmic medical doctor.
416
What is the recommended treatment for macular edema?
Intravitreal anti-VEGF agents may be beneficial for macular edema ## Footnote Anti-VEGF agents are used to inhibit vascular endothelial growth factor.
417
What is indicated for significant carotid blockage?
Carotid endarterectomy or stent surgery if significant blockage ## Footnote This is to restore normal blood flow in the carotid artery.
418
When is Carotid Endarterectomy (CEA) indicated?
Symptomatic patients with 70-99% carotid stenosis, asymptomatic minimum of 60% stenosis ## Footnote CEA may be considered on a case-by-case basis for 50-69% stenosis.
419
What is the perioperative risk of stroke or death for CEA?
<6% and 3% ## Footnote These percentages indicate a low risk for surgery.
420
Why is endarterectomy not performed in cases of total (100%) obstruction?
Because it is dangerous due to collateral blood supply having occurred ## Footnote This means that alternative pathways for blood flow have developed, complicating surgery.
421
What are the signs of Ocular Ischemic Syndrome (OIS)?
Mid-peripheral hemes Neovasc of the angle Flare in anterior chamber Corneal edema * Dilated non-tortuous veins * Arterial attenuation * Hemorrhages (midperipheral > PP) * Neovascularization (Iris > angle > NVD > NVE) * Mild anterior uveitis * Neovascular Glaucoma ## Footnote NVD refers to neovascularization of the disc, and NVE refers to neovascularization elsewhere.
422
How is the diagnosis of OIS typically made?
Based on fundus appearance and history of systemic disease ## Footnote Fundus examination is key in identifying changes associated with OIS.
423
True or False: TMVL and retinal artery occlusions are considered medical emergencies.
True ## Footnote They necessitate emergent vascular and brain imaging.
424
True or False Pts with stargardt should avoid Vitamin A supplements
TRUE, Unable to process excess Vitamin A, causes accumulation of deposits in macula
425
Mortality rate for OIS
After 5 years, mortality rate it 40%
426
What is retinoschisis?
Retinoschisis is defined as splitting of the layers within the retina.
427
How does retinoschisis differ from retinal detachment?
Retinal detachment is when the retina is split from the choroid, while retinoschisis involves splitting within the retina.
428
What type of lesions does retinoschisis typically create?
Dome shaped lesions in the retinal periphery.
429
What visual field defects are associated with retinoschisis?
Absolute visual field defects with sharp borders.
430
What visual field defects are associated with retinal detachments?
Relative visual field defects.
431
What testing/ imaging can help differentiate retinoschisis from retinal detachment?
* Threshold visual field * Scleral depression * OCT
432
Can fluorescein angiography be used to differentiate retinoschisis from retinal detachment?
No, fluorescein angiography cannot be used for differentiation.
433
What sign is absent in retinoschisis that may be seen in retinal detachment?
Tobacco dust/Shafer's sign.
434
Can retinoschisis present with rhegmatogenous retinal detachments?
Yes, retinoschisis can rarely present with rhegmatogenous retinal detachments.
435
What are the two types of retinoschisis?
* Acquired Age Related * Juvenile (X-linked recessive)
436
What characterizes acquired age-related retinoschisis?
More common, presents bilaterally and symmetrically; splitting between inner nuclear and outer plexiform layers.
437
What characterizes juvenile retinoschisis?
Less common, located in the nerve fiber layer; presents with progressively decreasing VA from 20/25 to 20/80.
438
What conditions can juvenile retinoschisis cause? (3)
* Amblyopia * Nystagmus * Strabismus
439
What does juvenile retinoschisis look like on OCT?
Stellate maculopathy (spoke-like foveal cysts).
440
What may juvenile retinoschisis present with due to the longevity of the disease?
A pigment demarcation line.
441
What symptoms may patients with retinoschisis report?
Patients may be asymptomatic or complain of blurry vision.
442
What are the three categories of non-proliferative diabetic retinopathy (NPDR)?
Mild NPDR, moderate NPDR, severe NPDR
443
What is mild NPDR associated with?
Hard exudates, microaneurysms, isolated dot/blot hemorrhages
444
What characterizes moderate NPDR?
Greater degree of ischemia and vascular leakage, increased hemorrhages, venous beading/tortuosity, cotton wool spots, intraretinal microvascular abnormalities (IRMA)
445
What are the features of severe NPDR?
Dot/blot hemorrhages and microaneurysms in all four quadrants, venous beading in at least two quadrants, IRMA in at least one quadrant
446
What occurs in proliferative diabetic retinopathy (PDR)?
Development of new, abnormal, preretinal blood vessel growth and proliferation
447
Where can neovascularization be observed in PDR?
At the optic nerve (neovascularization of the disc), greater than 1 disc diameter away (neovascularization elsewhere), new blood vessel growth at the iris (rubeosis iridis)
448
What type of hemorrhages are associated with PDR?
Large preretinal hemorrhages (keel or boat-shaped)
449
What complication may arise from the proliferation of fibrovascular tissue in PDR?
Tractional retinal detachment
450
Fill in the blank: Mild NPDR is associated with what retinal findings? (3)
* isolated dot/blot hemorrhages * hard exudates * microaneurysms
451
True or False: Severe NPDR includes venous beading in at least one quadrant.
False
452
What are the three categories of non-proliferative diabetic retinopathy (NPDR)?
Mild NPDR, moderate NPDR, severe NPDR
453
What is mild NPDR associated with?
Hard exudates, microaneurysms, isolated dot/blot hemorrhages
454
What characterizes moderate NPDR?
Greater degree of ischemia and vascular leakage - increased hemorrhages - venous beading/tortuosity - cotton wool spots - intraretinal microvascular abnormalities (IRMA)
455
What are the features of severe NPDR?
Dot/blot hemorrhages and microaneurysms in all four quadrants, venous beading in at least two quadrants, IRMA in at least one quadrant
456
What occurs in proliferative diabetic retinopathy (PDR)?
Development of new, abnormal, preretinal blood vessel growth and proliferation
457
Where can neovascularization be observed in PDR?
At the optic nerve (neovascularization of the disc), greater than 1 disc diameter away (neovascularization elsewhere), new blood vessel growth at the iris (rubeosis iridis) NVD NVE NVI
458
What type of hemorrhages are associated with PDR?
Large preretinal hemorrhages (keel or boat-shaped)
459
What complication may arise from the proliferation of fibrovascular tissue in PDR?
Tractional retinal detachment
460
Fill in the blank: Mild NPDR is associated with _______.
hard exudates, microaneurysms, isolated dot/blot hemorrhages
461
True or False: Severe NPDR includes venous beading in at least one quadrant.
False
462
What is the inheritance pattern of Juvenile retinoschisis?
X-linked recessive * affects males * females are carriers
463
Tx/Mgmt of juvenile retinoschisis
Close monitoring + retina Patient education about avoiding head trauma and high impact sports because increased risk of RD If RD Tx with scleral buckling If vitreous heme Tx with vitrectomy
464
What is preretinal hemorrhage?
Leakage of blood into either the subhyaloid space between the posterior vitreous face and retina, or beneath the internal limiting membrane ## Footnote Usually presents with a boat-shaped hemorrhage which obscures the underlying retina.
465
What are the common findings in malignant hypertension related to the retina?
* Hard exudates in a macular star formation * optic nerve edema * flame-shaped retinal hemorrhages * retinal edema * cotton- wool spots ## Footnote Requires immediate medical treatment. Malignant HTN = systolic >180 And/or >120 diastolic
466
Fundus evaluation of Valsalva retinopathy will show?
Single or multiple hemorrhages beneath the internal limiting membrane, most commonly noted in the area of the macula ## Footnote Usually associated with a history of heavy lifting, coughing, vomiting, or straining.
467
What are the signs of ocular ischemic syndrome?
Mid-peripheral retinal hemorrhages with dilated and irregular retinal veins ## Footnote Disc neovascularization may be present.
468
What symptoms are commonly associated with ocular ischemic syndrome?
History of transient visual loss, transient ischemic attacks, or orbital pain ## Footnote These symptoms indicate potential underlying vascular issues.
469
What is preretinal hemorrhage?
Leakage of blood into either the subhyaloid space between the posterior vitreous face and retina, or beneath the internal limiting membrane ## Footnote Usually presents with a boat-shaped hemorrhage which obscures the underlying retina.
470
What are the common findings in malignant hypertension related to the retina?
Hard exudates in a macular star formation, optic nerve edema, flame-shaped retinal hemorrhages, retinal edema, and cotton-wool spots ## Footnote Requires immediate medical treatment.
471
What characterizes Valsalva retinopathy?
Single or multiple hemorrhages beneath the internal limiting membrane, most commonly noted in the area of the macula ## Footnote Usually associated with a history of heavy lifting, coughing, vomiting, or straining.
472
What are the signs of ocular ischemic syndrome?
Mid-peripheral retinal hemorrhages with dilated and irregular retinal veins *flare in anterior chamber and corneal edema ## Footnote Disc neovascularization may be present.
473
What symptoms are commonly associated with ocular ischemic syndrome?
History of transient visual loss transient ischemic attacks or orbital pain ## Footnote These symptoms indicate potential underlying vascular issues.
474
What characterizes severe non-proliferative diabetic retinopathy?
*1 category from the 4-2-1 rule Any of the following in the absence of proliferative retinopathy: *intraretinal hemorrhages in all 4 quadrants * 2 quadrants of venous beading * 1 quadrant of prominent intraretinal microvascular abnormalities (IRMA) ## Footnote These criteria help in the diagnosis of severe non-proliferative diabetic retinopathy.
475
What is defined as clinically significant macular edema?
Defined as any one of the following: * Retinal thickening within 500 microns (1/3 disc diameter) of the center of the fovea * Hard exudates within 500 microns of the center of the fovea, if associated with adjacent retinal thickening * Thickening of the retina with a size greater than 1 disc area, part of which is within 1 disc diameter of the foveal center ## Footnote Clinically significant macular edema can lead to vision impairment if not treated.
476
What observations indicate high-risk proliferative diabetic retinopathy?
Includes one of the following observations: * NVD with a size greater than 1/4 to 1/3 of the optic disc * Any degree of NVD if an associated pre-retinal or vitreous hemorrhage is present * NVE greater than 1/2 the size of the optic disc when associated with a pre-retinal or vitreous hemorrhage ## Footnote These criteria are critical for determining treatment approaches such as parenteral laser photocoagulation.
477
Fill in the blank: Severe non-proliferative diabetic retinopathy can involve _______ intraretinal hemorrhages in each quadrant.
>20 ## Footnote This specific number is part of the diagnostic criteria for severe non-proliferative diabetic retinopathy.
478
True or False: Clinically significant macular edema can occur without retinal thickening.
False ## Footnote Retinal thickening is one of the key definitions of clinically significant macular edema.
479
What is NVD in the context of diabetic retinopathy?
Neovascularization of the disc (NVD) ## Footnote NVD is a critical indicator of high-risk proliferative diabetic retinopathy.
480
Fill in the blank: High-risk proliferative diabetic retinopathy includes NVE greater than _______ the size of the optic disc when associated with a pre-retinal or vitreous hemorrhage.
1/2 ## Footnote NVE stands for neovascularization elsewhere and is a significant factor in assessing the severity of diabetic retinopathy.
481
What condition may occur even following uneventful cataract surgery?
Cystoid macular edema ## Footnote Cystoid macular edema is a condition characterized by fluid accumulation in the eye.
482
What results in the formation of a small cyst in cystoid macular edema?
Buildup of fluid between the outer plexiform layer and the inner nuclear layer adjacent to the macula ## Footnote This fluid accumulation leads to the characteristic cyst formation seen in this condition.
483
How long does cystoid macular edema commonly self-resolve?
Within six months ## Footnote Most cases of cystoid macular edema resolve spontaneously without treatment.
484
What treatments may be prescribed if a patient with cystoid macular edema is symptomatic?
Topical NSAIDs or steroids ## Footnote Non-steroidal anti-inflammatory drugs (NSAIDs) and steroids are used to reduce inflammation and symptoms. If no response Tx with oral NSAIDs and/or oral acetazolamide
485
What can happen if cystoid macular edema is longstanding?
Cysts may enlarge and coalesce, causing a lamellar macular hole ## Footnote Prolonged cystoid macular edema can lead to more serious complications affecting vision.
486
What appearance does cystoid macular edema have on fluorescein angiography during the late phase?
Flower-like or clover-like appearance ## Footnote This distinctive appearance helps in the diagnosis of cystoid macular edema.
487
What characteristic appearance is observed in fluorescein angiography for central serous maculopathy?
Smoke stack appearance ## Footnote The smoke stack appearance is a key diagnostic feature in central serous maculopathy.
488
What factor influences the fluorescein angiography presentations in proliferative diabetic retinopathy?
Area(s) of leakage ## Footnote Different areas of leakage can result in varied fluorescein angiography findings in this condition.
489
What does the fluorescein angiography for bull's eye maculopathy display?
RPE window defects surrounding the fovea in a ring-like fashion ## Footnote This ring-like pattern is characteristic of bull's eye maculopathy.
490
What is AS sickle cell trait?
Found in 8% of the African-American population, requires extreme hypoxia to cause sickling.
491
What is SS sickle cell anemia?
Found in 0.4% of the African-American population, associated with severe systemic complications but only mild ocular problems.
492
What is SC sickle cell C disease?
Found in 0.2% of the African-American population.
493
What is sickle cell thalassaemia (Sthal)?
Both SC and SThal result in mild systemic complications but are associated with advanced ocular conditions.
494
How many stages are there in proliferative retinopathy associated with sickle cell disease?
5 stages.
495
What occurs in Stage 2 of proliferative retinopathy?
Peripheral arteriovenous anastomoses.
496
What is observed in Stage 3 of proliferative retinopathy?
Neovascularization of the anastomoses resulting in a 'sea-fan' appearance; 40-50% of 'sea-fans' will unexpectedly involute.
497
What happens in Stage 4 of proliferative retinopathy?
Vitreous hemorrhage.
498
What is the outcome in Stage 5 of proliferative retinopathy?
Proliferation of fibrovascular tissue and rhegmatogenous or tractional retinal detachment.
499
What is AS sickle cell trait?
Found in 8% of the African-American population, requires extreme hypoxia to cause sickling.
500
What is SS sickle cell anemia?
Found in 0.4% of the African-American population, associated with severe systemic complications but only mild ocular problems.
501
What is SC sickle cell C disease?
Found in 0.2% of the African-American population.
502
What is sickle cell thalassaemia (Sthal)?
Both SC and SThal result in mild systemic complications but are associated with advanced ocular conditions.
503
How many stages are there in proliferative retinopathy associated with sickle cell disease?
5 stages.
504
What occurs in Stage 1 of proliferative retinopathy?
Occlusion of the peripheral arterioles.
505
What occurs in Stage 2 of proliferative retinopathy?
Peripheral arteriovenous anastomoses.
506
What is observed in Stage 3 of proliferative retinopathy?
Neovascularization of the anastomoses resulting in a 'sea-fan' appearance; 40-50% of 'sea-fans' will unexpectedly involute.
507
What happens in Stage 4 of proliferative retinopathy?
Vitreous hemorrhage.
508
What is the outcome in Stage 5 of proliferative retinopathy?
Proliferation of fibrovascular tissue and rhegmatogenous or tractional retinal detachment.
509
What are some toxic/metabolic disorders that may cause visual hallucinations?
• Drug and alcohol withdrawal syndromes • Medications with toxic side effects • Metabolic encephalopathies due to endocrine disturbances, vitamin deficiency, inflammatory and infectious diseases, cardiopulmonary insufficiency ## Footnote Toxic/metabolic disorders encompass a range of conditions affecting the body's metabolism and can lead to hallucinations.
510
Name two psychiatric disorders that can cause visual hallucinations.
• Acute psychosis • Schizophrenia ## Footnote Psychiatric disorders often involve disturbances in perception, which can manifest as hallucinations.
511
Fill in the blank: _______ is a condition that may lead to visual hallucinations and involves intense emotional states.
[Affective disorder]
512
What neurologic disorder is associated with visual hallucinations?
• Parkinson disease • Migraine • Dementia • Epilepsy • Brain-stem lesions • Hemispheric lesions ## Footnote Neurologic disorders can disrupt normal brain function, leading to various perceptual disturbances, including hallucinations.
513
True or False: Sensory deprivation can cause visual hallucinations.
True ## Footnote Sensory deprivation removes external stimuli, which can lead to the brain generating its own perceptions, including visual hallucinations.
514
What is the condition characterized by visual hallucinations without any other sensory stimuli (hearing or smell)?
• Charles Bonnet syndrome ## Footnote Charles Bonnet syndrome typically affects individuals with significant vision loss and can lead to vivid visual hallucinations. *can be simple or complex *mostly faces not scary
515
List some miscellaneous conditions that may cause visual hallucinations.
• Sensory and sleep deprivation • Intense emotional states (grief, stress) ## Footnote Miscellaneous conditions can be varied and often intersect with psychological and physiological factors.