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NBEO Part 2 > Retina/Choroid/ Vitreous > Flashcards

Retina/Choroid/ Vitreous Flashcards

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?

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
Q

The most common source of a retinal embolism is?

A

Ulceration and release of material from atheromatous plaque of the carotid bifurcation

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26
Q

What does cholesterol emboli look like?

A

Appear as bright, refractive golden yellow orange crystals

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27
Q

Why does cholesterol emboli cause amaurosis fugax?

A

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

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28
Q

Calcific emboli originate from?

A

Atheromatous plaques in the ascending aorta, carotid arteries or from calcified heart valves

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29
Q

Which type of emboli is most dangerous, because it can cause permanent occlusion?

A

Calcific emboli
(Look like single white plugs of material close to optic disc)

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30
Q

Patients with s/s of retinal embolus must undergo what investigations? (5)

A
  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)
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31
Q

Tx for Hollenhorst plaque

A
  1. Report findings to PCP
  2. Refer patient for vascular work up within 48-72 hours
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32
Q

Indications for anterior chamber paracentesis

A

CRAO
Acute glaucoma
Uveitis or endophthalmitis

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33
Q

Paracentesis

A

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

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34
Q

Attenuation of RPE leading to loss of melanin granulates allows for increased what?

A

Visibility of underlying choroid aka window defect

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35
Q

Inheritance pattern of gyrate atrophy

A

Autosomal recessive

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36
Q

Tx for RPE window defect

A

Monitor annually
* may enlarge as patient gets older but no Tx because will not cause vision loss

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37
Q

What are the 3 types of RD?

A
  • Tractional
  • Rhegmatogenous
  • Exudative
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38
Q

What is the most common systemic disease associated with angioid streaks?

A

Pseudoxanthom elasticum
* connective tissue disorder, elastin affected

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39
Q

Gronblad-Strindberg syndrome

A

Pseudoxanthoma elasticum and angioid streaks

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40
Q

Pathophysiology of angioid streaks

A

Small dehiscences (small openings) in collagenous and elastic portions of Bruch’s membrane

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41
Q

2 fundus findings associated with angioid streaks

A

Peau d’orange & optic disc drusen
*’mottled fundus appearance, yellow, speckled pinpoint areas that look like a leopard skin-spotting

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42
Q

6 conditions that can cause CNVM

A

CHBALA

Choridal rupture
Histoplasmosis
Best disease
AMD
Lacquer cracks
Angioid streaks

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43
Q

Angioid streaks are associated with what systemic conditions (5)

A

PEPSI

Pseudoxanthoma elasticum
Ehler’s Danlos syndrome
Paget’s
Sickle cell
Idiopathic

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44
Q

Tx & management of Angioid streaks

A

Perform FA to check for CNVM
If clear, close monitoring

If CNVM present Tx with anti-VEGF if subfoveal

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45
Q

CME formation following cataract surgery

A

Irvine Gass Syndrome
* 6 weeks to 3 most post op

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46
Q

Fluid accumulates in which layers of the retina in cystoid macular edema?

A

Outer plexiform layer and inner nuclear layer

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47
Q

Chronic longstanding CME can lead to?

A

Lamellar macular hole
* cystic spaces coalesce and progress to form macular hole

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48
Q

On FA: small hyperfluorescent spots in early phase with flower-petal pattern of hyperfluorescence in late stage

A

cystoid macular edema

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49
Q

On FA: well demarcated lacy hyperfluorescence in early phase with increasing leakage in late phase

A

Choroidal neovascular membrane

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50
Q

On FA: smoke-stake appearance

A

Central serous retinopathy

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51
Q

Which hereditary retinal disease is most commonly associated with CME?

A

Retinitis pigmentosa

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52
Q

Tx of CME secondary to YAG cap following CE

A

1 gtts ketorolac QID
1 gtts prednisolone acetate QID
* topical NSAID and topical steroids

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53
Q

Detachment of neurosensory retina from RPE secondary to full thickness retinal break

A

RRD

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54
Q

Detached retina will appear concave with a smooth surface

A

Tractional RD

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55
Q

Tobacco dust seen in anterior vitreous is a sign for?

A

Rhegmatogenous retinal detachment

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56
Q

IOP is lower in affected eye by 5mmHg compared to fellow eye in which type of RD?

A

RRD
* if IOP extremely low, an associated choroidal detachment is suspected

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57
Q

Talc can deposit in small blood vessels of which organs?

A

Lungs
Liver
Spleen
Kidneys
Lymph nodes
* talc retinopathy in long term IV drug abuse with cocaine and heroin

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58
Q

What additional tests should be ordered in a patient with talc retinopathy?

A

Chest X-ray (pulmonary complications)
And fluorescein angiography (evaluate for possible vasculature leakage or non-perfusion

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59
Q

What retinal complications can arise from talc deposits?

A

Retinal ischemia
* develop hemorrhages, CWS, peripheral neovascularization, vitreous hemorrhages and tractional RD

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60
Q

Degenerative retinoschisis is between which layers of the retina?

A

outer plexiform layer and inner nuclear layer

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61
Q

What is the visual prognosis of choroideremia?

A

Visual acuity will remain stable until later in life when it is expected to become significantly affected

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62
Q

What is the most common initial symptom of patients with choroideremia?

A

Nyctalopia or night blindness

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63
Q

Snail track degeneration is commonly located in which retinal quadrants?

A

ST and SN peripheral quadrants of myopic eyes

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64
Q

What is the 2nd most common ocular opportunistic infection of AIDS patients?

A

PORN: progressive outer retinal necrosis
* varicella zoster variant, very aggressive

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65
Q

White without pressure is most commonly seen in which areas of the retina?

A

Inferior and temporal
* located at the vitreous and ora serrata

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66
Q

What is Central Serous Chorioretinopathy (CSR)?

A

CSR occurs as a result of fluid leaking from the choriocapillaris into the subretinal area, causing a serous detachment of the neurosensory retina.

Occasionally, a detachment of the retinal pigment epithelium may also develop.

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67
Q

What are the common demographics associated with CSR?

A

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.

This condition is generally unilateral in presentation.

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68
Q

List the symptoms of Central Serous Chorioretinopathy.

A
  • Reduced visual acuity
  • Metamorphopsia (distortion of objects)
  • Abnormal color vision
  • Patients may be asymptomatic if the macular region is not involved.
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69
Q

What clinical signs may indicate CSR?

A
  • 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.
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70
Q

True or False: CSR frequently requires intervention.

A

False

CSR frequently spontaneously regresses within 6 months, and intervention is rarely required.

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71
Q

What treatments are available for CSR?

A
  • Photocoagulation
  • Photodynamic therapy

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.

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72
Q

Fill in the blank: Argon laser photocoagulation or photodynamic therapy will decrease the _______ of CSR but will not alter the resultant visual outcome.

A

[recovery time]

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73
Q

What is a potential result of fluorescein angiography in CSR?

A

hyperfluorescence in a smoke-stack formation.

This finding is characteristic of CSR.

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74
Q

RTC for CSR

A

Monthly until resolution

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75
Q

What is the choroid?

A

A heavily pigmented and highly vascularized layer of the eye positioned interior to the sclera and exterior to the retinal tissue

It is part of the uveal tract, which includes the iris, ciliary body, and choroid.

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76
Q

What are the four layers of the choroid, listed from most external to most internal?

A
  • Suprachoroid
  • Stroma (vessel layer)
  • Choriocapillaris
  • Bruch’s membrane

These layers play distinct roles in the structure and function of the choroid.

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77
Q

What is the function of the suprachoroid?

A

Serves as a transition junction between the sclera and the choroid

Comprised of 10-15 layers of collagen binding to the lamina fusca of the sclera.

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78
Q

What types of cells are found in the suprachoroid?

A
  • Melanocytes
  • Fibroblasts

These cells contribute to the structure and pigmentation of the choroid.

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79
Q

What constitutes the vessel layer of the choroid?

A

Haller’s layer and Sattler’s layer

This layer primarily consists of blood vessels.

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80
Q

What is Haller’s layer?

A

The layer external to Sattler’s layer containing larger blood vessels

It plays a role in the vascular supply of the choroid.
*part of the stroma of the choroid

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81
Q

What is Sattler’s layer?

A

The layer possessing smaller blood vessels

The diameter of the blood vessels decreases from the outer to the inner edge of the stroma.

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82
Q

What causes the brown appearance of the stroma in the choroid?

A

Melanocytes present in the stroma

These cells contribute to the pigmentation of this layer.

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83
Q

What is the choriocapillaris?

A

A network of capillaries that maintain the outer retina

The capillaries in this layer are larger than those in the rest of the body.

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84
Q

What is unique about the capillaries in the choriocapillaris?

A

They allow the passage of several blood cells simultaneously

This feature is important for the metabolic needs of the outer retina.

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85
Q

True or False: The choriocapillaris contains melanocytes.

A

False

The choriocapillaris does not contain melanocytes.

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86
Q

Fill in the blank: The choroid is a common site for ocular _______ that may develop into melanomas.

A

nevi

Routine examination of the choroid is warranted due to this risk.

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87
Q

What is Bruch’s membrane?

A

A thin, complex membrane located between the choriocapillaris of the choroid and the retinal pigment epithelium of the retina

It is about 2 microns thick.

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88
Q

List the five components of Bruch’s membrane from outermost to innermost.

A
  • Basement membrane of the choriocapillaris
  • Outer collagenous zone
  • Elastic layer
  • Inner collagenous zone
  • Basement membrane of the retinal pigment epithelium

These layers play a role in the structural support of the retina.

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89
Q

What is the thickness of Bruch’s membrane?

A

About 2 microns thick

This thinness is significant for its function and structure.

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90
Q

True or False: Bruch’s membrane is located between the sclera and the choroid.

A

False

Bruch’s membrane is located between the choriocapillaris of the choroid and the retinal pigment epithelium.

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91
Q

What is the function of the outer collagenous zone in Bruch’s membrane?

A

Provides structural support

It is one of the five layers that contribute to the integrity of the membrane.

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92
Q

Fill in the blank: The _______ is the layer of Bruch’s membrane that is elastic.

A

[Elastic layer]

This layer is important for the flexibility of Bruch’s membrane.

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93
Q

What layers are found in the choroid alongside Bruch’s membrane?

A
  • Haller’s layer
  • Sattler’s layer

These layers are part of the vascular structure of the choroid.

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94
Q

What is Leber congenital amaurosis?

A

A rod-cone disorder characterized by vision loss

It may initially show a normal-appearing fundus.

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95
Q

What ocular findings are associated with Leber congenital amaurosis by childhood?

A

Narrowing of retinal blood vessels, optic disc pallor, and pigmentary changes

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

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96
Q

What does ERG reveal in cases of Leber congenital amaurosis?

A

ERG is markedly abnormal or flat

*reduced or absent electrical response from retina when stimulated by light. Reflecting impaired photoreceptor function

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97
Q

What is the inheritance pattern of Leber congenital amaurosis?

A

Autosomal recessive

This means that the disorder typically requires two copies of the mutated gene for manifestation.

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98
Q

Which layer of the retina are flame-shaped hemorrhages?

A

Nerve fiber layer
* seen in HTN retinopathy, CRVO

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99
Q

What is disc edema?

A

Swelling of the optic disc often associated with retinal conditions

It is frequently present in cases of non-ischemic central retinal vein occlusion.

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100
Q

What is the most common cause of non-ischemic central retinal vein occlusion?
(Pathophysiology)

A

Formation of a thrombus near or at the lamina cribrosa

This thrombus compresses the central retinal vein, impeding blood flow return.

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101
Q

What symptoms do patients with non-ischemic CRVO typically report?

A

Acute, painless, unilateral loss of vision

This symptom is a key indicator of the condition.

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102
Q

What clinical signs are associated with non-ischemic CRVO?

A
  • Dot-blot hemorrhages
  • Flame-shaped hemorrhages
  • Retinal edema
  • Dilated and tortuous vessels

Other signs include the presence of disc and macular edema, and typically absent APD and cotton wool spots.

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103
Q

What is the visual acuity level typically seen in non-ischemic CRVO?

A

Generally better than 20/400

This indicates that while vision is impaired, it is not as severely affected as in ischemic cases.

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104
Q

What is the typical age demographic for individuals affected by non-ischemic CRVO?

A

Majority are 65 years of age or older

Age is a significant risk factor for this condition.

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105
Q

What are common symptoms reported by patients with a full thickness macular hole?

A

Decreased vision centrally, possible scotoma, or metamorphopsia on the Amsler grid

Flashes of light may also be experienced due to possible vitreo-retinal traction.

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106
Q

At what age group are idiopathic macular holes most commonly observed?

A

Women aged between 60-80 years

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107
Q

What is postulated to cause idiopathic macular holes?

A

Traction on the macular region by the vitreous

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108
Q

What classification system is used for idiopathic macular holes?

A

Gass classification system

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109
Q

Describe Stage 1A of the Gass classification for idiopathic macular holes.

A

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

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110
Q

What characterizes Stage 1B of idiopathic macular holes?

A

Appearance of a yellow ring along with a foveal detachment

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111
Q

What defines Stage 2 of idiopathic macular holes?

A

Small foveal defects measuring less than 400 um in diameter

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112
Q

What is noted in Stage 3 of idiopathic macular holes?

A

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

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113
Q

What are the characteristics of Stage 4 idiopathic macular holes?

A
  • 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
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114
Q

What protozoa causes Toxoplasmosis?

A

Toxoplasma gondii

T. gondii is commonly associated with improper handling of raw meat or cat fecal matter

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115
Q

Who is particularly at risk for Toxoplasmosis and why?

A

Pregnant mothers

An infection in the mother can potentially harm the unborn fetus

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116
Q

What serious consequence can Toxoplasmosis lead to if enough retinal damage occurs?

A

Blindness

Retinal damage can result from the infection

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117
Q

What clinical appearance do old lesions of Toxoplasmosis have?

A

Circular areas of chorioretinal atrophy surrounded by pigmentation

Areas of atrophy are generally stable

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118
Q

What can cause damage to adjacent healthy retinal tissue in Toxoplasmosis?

A

Rupture of bradyzoite cysts releasing tachyzoites

This can occur in chronic infections

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119
Q

What symptoms may patients with active retinitis from Toxoplasmosis report?

A

Floaters, blurry vision, photophobia

Patients typically do not experience pain

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120
Q

What is a characteristic observation in cases of active retinal Toxoplasmosis?

A

A yellow-white lesion next to an old chorioretinal scar

This is typically associated with vitritis

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121
Q

What may happen to the anterior chamber in active retinal Toxoplasmosis?

A

Vitritis may spill over into the anterior chamber

Vitritis is inflammation of the vitreous body

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122
Q

What additional problems may immunocompromised persons experience with Toxoplasmosis?

A

Encephalitis and chorioretinitis

These patients may not display vitritis

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123
Q

True or False: Healthy individuals are likely to become seriously ill from Toxoplasmosis.

A

False

Toxoplasmosis rarely leads to illness in healthy individuals

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124
Q

Fill in the blank: Toxoplasmosis is primarily associated with improper handling of _______.

A

raw meat or cat fecal matter

These are common sources of T. gondii infection

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125
Q

What organism causes presumed ocular histoplasmosis?

A

Histoplasma capsulatum

This organism typically enters the body via inhalation into the lungs.
* associated with bats

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126
Q

In which geographical areas is presumed ocular histoplasmosis most prominent?

A

Ohio-Mississippi River valley region and southern United States

These regions have higher incidences of the disease.

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127
Q

What are the three ocular findings associated with retinitis from presumed ocular histoplasmosis?

A
  • Histo spots
  • Peripapillary atrophy
  • Choroidal neovascular membrane

Two of these findings must be present for diagnosis.

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128
Q

What is required for a diagnosis of presumed ocular histoplasmosis?

A

Two of the three ocular findings must be present

The findings include histo spots, peripapillary atrophy, and choroidal neovascular membrane.

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129
Q

Do patients suffering from histoplasmosis manifest vitritis?

A

No

Patients with histoplasmosis will never show signs of vitritis.

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130
Q

What is the most frequently occurring intraocular tumor in children?

A

Retinoblastoma

This condition is critical for early detection due to its high mortality rate.

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131
Q

Are most cases of retinoblastoma sporadic or familial?

A

Most cases are sporadic

Occasionally, the malignancy may be familial in origin.

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132
Q

What percentage of retinoblastoma cases may be observed bilaterally?

A

30%

The majority of cases present unilaterally.

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133
Q

What clinical features are commonly observed in patients with retinoblastoma?

A
  • Leukocoria
  • Strabismus
  • White retinal lesion
  • Iris neovascularization (in ~20% of cases)

These features are crucial for clinical recognition.

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134
Q

Why is early detection and prompt treatment vital for retinoblastoma?

A

Due to the high mortality rate associated with this tumor

Timely intervention can significantly impact patient outcomes.

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135
Q

What additional testing should be included for patient taking plaquenil?

A
  1. 10-2 VF (if Asian 24-2 or 30-2)
  2. Multifocal ERG
  3. Mac OCT
  4. Ishihara color vision
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136
Q

What additional testing should be included for patient taking plaquenil? (4)

A
  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

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137
Q

Ocular complications of lupus include?

A

CRVO
BRVO
CRAO
BRAO
Exudative retinal detachments
Toxic maculopathies (secondary to plaquenil)
* retinal diseases associated with lupus mimic T2DM and HTN

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138
Q

What are the greatest risk factors for transformation of a choroidal nevus to a malignant choroidal nevus?

A

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

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139
Q

What are choroidal nevi typically considered?

A

Congenital

Choroidal nevi are rarely observed in younger children.

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140
Q

At what stage do choroidal nevi usually become clinically apparent?

A

Puberty

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141
Q

What are the characteristics of choroidal nevi?

A

Flat or minimally elevated, pigmented or amelanotic

They usually measure between 1.5 to 5mm in diameter and less than 2mm thick.

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142
Q

What may develop over time on choroidal nevi?

A

Overlying drusen

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143
Q

What is the histopathological composition of a choroidal nevus?

A

Low-grade, spindle-shaped, ovoid or round melanocytes

These melanocytes have varying amounts of cytoplasmic pigmentation.

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144
Q

What is a statistical risk factor for the transformation of a choroidal nevus into a melanoma?

A

Tumor thickness greater than 2 mm

Other factors include the presence of subretinal fluid, orange pigmentation, proximity to the optic disc, and the presence of symptoms.

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145
Q

What percentage of nevi measuring 2.5 mm in thickness become melanomas per month?

A

Approximately 1%

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146
Q

What increases the chance of transformation from nevus to melanoma?

A

Development of orange pigment on the surface of nevi

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147
Q

Where are nevi more likely to become melanomas?

A

Towards the posterior portion of the eye (closer to the optic disc)

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148
Q

What additional indicators may suggest a nevus is more likely to transform into melanoma?
(FA, symptoms, visual field)

A

Hot spots on fluorescein angiography, decreased vision, or a visual field defect

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149
Q

What do drusen indicate regarding choroidal nevi?

A

Chronicity and benignity

Lesions with drusen rarely transform into melanomas.

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150
Q

What occurs during the pre-maculopathy stage of hydroxychloroquine toxicity?

A

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.

If the medication is discontinued at this time, the associated retinal changes are reversible.

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151
Q

What happens if hydroxychloroquine is continued during the pre-maculopathy stage?

A

Early maculopathy occurs, linked to a decrease in visual acuity and RPE atrophy surrounding the fovea.

Fluorescein angiography at this stage will reveal a window defect.

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152
Q

What is the consequence of reaching the early maculopathy stage in hydroxychloroquine toxicity?

A

Retinal damage is not reversible upon cessation of the medication.

This stage is marked by a decrease in visual acuity.

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153
Q

What visual changes are noted as hydroxychloroquine toxicity progresses?

A

Moderate decrease in vision and a ‘bull’s eye’ macular lesion is visible on fundus examination.

This indicates progression to severe maculopathy.

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154
Q

What characterizes the severe maculopathy stage in hydroxychloroquine toxicity?

A

Significant reduction in visual acuity and RPE atrophy adjacent to the fovea.

This stage leads to more severe visual impairment.

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155
Q

What are the features of end-stage maculopathy in hydroxychloroquine toxicity?

A

Very poor visual acuity, attenuation of arterioles, increased choroidal visibility due to RPE atrophy, and clumping of pigment in the retinal periphery.

This stage represents the most advanced form of retinal damage.

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156
Q

True or False: The retinal changes associated with hydroxychloroquine toxicity are always reversible.

A

False.

Changes are reversible only if the medication is discontinued during the pre-maculopathy stage.

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157
Q

Fill in the blank: Granular changes within the macula during the pre-maculopathy stage of plaquenil toxicity may result in _______.

A

color vision changes and Amsler grid abnormalities.

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158
Q

What type of visual field defect frequently manifests in early stages of plaquenil toxicity?

A

Paracentral scotoma

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159
Q

Which tests are MOST useful in the diagnosis and management of hydroxychloroquine retinopathy? (Select 2)

A
  • Optical coherence tomography (OCT)
  • Multifocal electroretinogram (mERG)

These tests help detect early signs of retinal damage, allowing for timely intervention.

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160
Q

What is the key to maintaining visual integrity in patients with hydroxychloroquine retinopathy?

A

Early detection

Early detection alerts clinicians to discontinue the medication before permanent retinal damage occurs.

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161
Q

In later stages of hydroxychloroquine retinopathy, which retinal layers may show abnormalities?

A
  • Parafoveal outer nuclear layer
  • Inner plexiform layer
  • External limiting membrane

These layers can exhibit structural changes as the disease progresses.

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162
Q

What sign associated with hydroxychloroquine toxicity can be observed on OCT?

A

Flying saucer sign

This sign indicates preservation of outer retinal layers subfoveally with perifoveal loss.

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163
Q

What is the purpose of the multifocal electroretinogram (mERG) in the context of retinal health?

A

To detect paracentral retinal damage

mERG provides an objective measure of retinal function.

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164
Q

What does fundus autofluorescence (FAF) identify in patients with hydroxychloroquine retinopathy?

A

Areas of retinal pigment epithelium (RPE) dysfunction

FAF is useful for visualizing RPE health.

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165
Q

Fill in the blank: Increased thickness of the retinal pigment epithelium and _______ has been observed in early stages of retinopathy.

A

Bruchs membrane

These changes can signal the onset of retinopathy.

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166
Q

What is candidiasis caused by?

A

Candidiasis is caused by a yeast fungus, Candida albicans.

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167
Q

Where is Candida albicans frequently encountered in humans?

A

On the skin and in the digestive tract, mouth, and vagina.

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168
Q

In which patients might retinal involvement occur due to candidiasis?

A

Immunocompromised patients, IV drug users, or those with long-term indwelling catheters.

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169
Q

What symptoms might patients with retinal involvement from candidiasis notice?

A

Floaters and blurred vision unilaterally.

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170
Q

How do lesions from retinal candidiasis appear?

A

As areas of small, white, round lesions with indistinct borders.

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171
Q

What serious conditions may ensue if candidiasis is left untreated?

A

Endophthalmitis, retinal necrosis, and detachment.

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172
Q

True or False: Candidiasis can only affect the skin.

A

False

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173
Q

What are the clinical signs of an ischemic Central Retinal Vein Occlusion (CRVO)?

A

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)

Ischemic CRVO indicates a more severe form of vein occlusion and often results in significant visual impairment.

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174
Q

What are the characteristics of a non-ischemic Central Retinal Vein Occlusion (CRVO)?

A

Dot-blot and flame-shaped hemorrhages in all four quadrants, retinal edema, dilated and tortuous vessels, optic disc and macular edema, typically absent APD and cotton wool spots, and generally better visual acuity than 20/400

Non-ischemic CRVO is usually less severe and may have a better prognosis than ischemic CRVO.

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175
Q

What is the typical age demographic for individuals suffering from a CRVO?

A

65 years or older

Age is a significant risk factor for CRVO, with older adults being more susceptible.

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176
Q

Pathophysiology of arteritic anterior ischemic optic neuropathy (AION)?

A

Infarction of the prelaminar and laminar segment of the optic nerve

AION is often associated with conditions like giant cell arteritis.

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177
Q

What does CRAO stand for?

A

Central retinal artery occlusion

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178
Q

What is the primary consequence of central retinal artery occlusion?

A

Acute, painless loss of vision

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179
Q

What percentage of CRAO cases present unilaterally?

A

99%

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180
Q

What type of pupillary defect is observed in CRAO?

A

Afferent pupillary defect

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181
Q

How does the retina appear in cases of CRAO?

A

More pale/white superficially

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182
Q

What is the pronounced appearance of the fovea in CRAO known as?

A

Cherry red spot

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183
Q

Is CRAO typically associated with retinal hemorrhages?

A

No

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184
Q

Fill in the blank: CRAO is an obstruction of the _______.

A

central retinal artery

185
Q

Potential complications of CRVO

A
  • 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
186
Q

RTC for pt’s with CRVO and have a VA 20/40 or better

A

1-2 months for 6 months

187
Q

RTC for CRVO if VA is worse than 20/200

A

monthly for the next 6 months

188
Q

What is a sub-Tenon’s injection?

A

An injection using a long needle where the tip is obscured from view.

189
Q

What happens if a needle bends during a tangential injection?

A

It will enter tissue away from the bevel and may penetrate further into the tissue.

190
Q

How should the bevel of the needle be positioned during a sub-Tenon’s injection?

A

Toward the globe.

191
Q

What conditions is a sub-Tenon’s injection typically reserved for?

A
  • Vitritis
  • Posterior uveitis
  • Cystoid macular edema
192
Q

Where should the needle be placed for a sub-Tenon’s injection?

A

2 to 3 mm from the inferotemporal fornix.

193
Q

What should be avoided when penetrating the bulbar conjunctiva?

A

Nick any of the subconjunctival vessels.

194
Q

Complete the sentence: A sub-Tenon’s injection uses a long needle in which the tip, when properly inserted, is _______.

A

[obscured from view]

195
Q

Watzke-Allen sign

A

Patient sees a “break” in a Thin slit-beam shone over macula
* positive test for full thickness macular hole

196
Q

Shafer sign

A

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

197
Q

What are the two forms of macular drusen associated with dry AMD?

A

Hard or soft drusen

198
Q

What is a common observation in the outer retina of patients with dry AMD?

A

Areas of pigment clumping

199
Q

What occurs in RPE atrophy related to dry AMD?

A

Underlying choroidal vessels may appear more visible

200
Q

What is geographic atrophy in the context of dry AMD?

A

Regions of confluent retinal and choriocapillaris atrophy

201
Q

How does visual acuity in dry AMD compare to wet AMD?

A

Typically less affected

202
Q

What is a classic OCT finding in dry AMD?

A

Ripples formed under the RPE due to drusen

203
Q

What is the appearance of cystoid macular edema on fundus evaluation?

A

Irregular, blunted foveal light reflex and thickening in the central macular region

204
Q

What additional signs may be observed in severe cases of cystoid macular edema?

A
  • Vitreous cells
  • swelling of the optic nerve
  • hemorrhages
  • lamellar macular holes
205
Q

What ocular conditions can lead to cystoid macular edema?

A
  • Diabetic retinopathy
  • BRVO and CRVO
  • Uveitis
  • RP
  • Retinal vasculitis
  • Certain medications
206
Q

What OCT finding is characteristic of cystoid macular edema?

A

Loss of foveal contour due to cystic spaces within the retina

207
Q

What is the typical presentation of central serous retinopathy?

A

Localized serous detachment of the neurosensory retina in the macula

208
Q

What visual acuity range is common in patients with central serous retinopathy?

A

20/20 to 20/80

209
Q

What may Amsler grid testing reveal in central serous retinopathy?

A

Distortion of straight lines and a possible central scotoma

210
Q

What are the clinical signs of idiopathic polypoidal choroidal vasculopathy?

A
  • Subretinal red-orange polyp-like lesions
  • Subretinal or sub-RPE blood
  • Vitreous hemorrhages
  • Circinate subretinal exudates
  • Subretinal fibrosis
  • Subretinal fluid
  • Choroidal neovascular membrane
  • Multiple serous pigment epithelial detachments
211
Q

How can idiopathic polypoidal choroidal vasculopathy be distinguished from AMD?

A

Occurs at a younger age without significant drusen or geographic atrophy

212
Q

In which population is idiopathic polypoidal choroidal vasculopathy more commonly observed?

A

Asian populations

213
Q

In which demographic is choroidal melanoma most commonly found?

A

Occurs most commonly in Caucasians with a median age of 55

214
Q

What are some risk factors for developing choroidal melanoma?

A

Risk factors include:
* Sun exposure (or arc welding)
* Fair skin with inability to tan
* Pre-existing choroidal nevi
* Ocular or oculodermal melanocytosis

215
Q

True or False: Genetic factors may predispose patients to choroidal melanoma.

A

True

216
Q

What symptoms may indicate the presence of choroidal melanoma?

A

Symptoms include:
* Decreased visual acuity
* Metamorphopsia
* Flashing lights (photopsia)
* Scotomas

217
Q

What can cause decreased visual acuity in patients with choroidal melanoma?

A

Causes include:
* Involvement in the macular area
* Subretinal fluid
* Media opacities (hemorrhage, vitreal tumor seeding, cataract, corneal pacification from secondary glaucoma)

218
Q

What characteristics are typical of melanomas observed in the fundus?

A

Melanomas are typically:
* Elevated
* Subretinal mass lesions
* Color can vary from amelanotic to very darkly pigmented

219
Q

What shape is associated with choroidal melanoma due to a rupture in Bruch’s membrane?

A

Collar-button or mushroom shape

220
Q

What is the differential diagnosis for choroidal melanoma?

A

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

221
Q

What characteristics of a lesion suggest it is a choroidal melanoma?

A

Suggestive characteristics include:
* Thickness of >2 mm
* Documented history of growth
* Presence of subretinal fluid
* Orange surface pigmentation
* Visual symptoms
* Proximity to the optic disc or macula

222
Q

What procedure would be most helpful in diagnosis and evaluation of melanocytic choroidal nevus?

A

B-scan

Characteristics:
* dome or mushroom-shaped tumor
* steep angle kappa
* attenuation of signals
* choroidal excavation
* orbital shadowing

223
Q

What are the most common risk factors for development of choroidal melanoma?

A
  • increased sun exposure
  • oculodermal melanocytosis
  • pre-existing uveal nevus
224
Q

What are adverse prognostic factors in patients diagnosed with choroidal melanomas?

A

Histological features, chromosomal abnormalities, appearance of tumor, local tumor recurrence

These factors are critical for assessing the prognosis of patients with choroidal melanomas.

225
Q

What histological feature indicates a poor prognosis in choroidal melanoma?

A

Large number of epithelioid cells

Epithelioid cells are more associated with aggressive tumor behavior compared to spindle cells.

226
Q

What chromosomal gain is associated with a favorable prognosis in choroidal melanoma?

A

Gains in short arm of chromosome 6

These gains can indicate a better survival outcome.

227
Q

What tumor appearance factors contribute to poor prognosis in choroidal melanoma?

A

Larger size of tumor, extrascleral extension, growth through Bruch’s membrane, optic nerve extension, lack of pigmentation, more anterior location

These factors often correlate with advanced disease at the time of diagnosis.

228
Q

True or False: Lymphocytic infiltration is a favorable histological feature in choroidal melanoma.

A

False

Lymphocytic infiltration is typically associated with a worse prognosis.

229
Q

Fill in the blank: A large number of _______ cells in choroidal melanoma is a poor prognostic factor.

A

epithelioid

Epithelioid cells are more aggressive compared to spindle cells.

230
Q

What is the significance of local tumor recurrence in choroidal melanoma?

A

It indicates a poorer prognosis

Local recurrence suggests that the disease is more aggressive and difficult to manage.

231
Q

What does the appearance of closed vascular loops within the tumor indicate?

A

Poor prognosis

Closed vascular loops are a histological feature that correlates with aggressive tumor behavior.

232
Q

What is the implication of a tumor’s anterior location in choroidal melanoma?

A

It is associated with larger tumor size at diagnosis

Tumors located more anteriorly, especially involving the ciliary body, are often larger due to lead time before diagnosis.

233
Q

Once diagnosis of choroidal melanoma has been made what’s the next series of systemic tests to rule out possible metastasis?

A
  • Blood testing
  • chest x-ray
  • abdominal CT scan
234
Q

CSME criteria

A
  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
235
Q

4-2-1 rule

A

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
236
Q

RTC for NPDR

A

Every 6 months

237
Q

RTC for PDR

A

Every 3 months

238
Q

Hemorrhages in patients with Valsalva retinopathy are located where?

A

Between the retina and posterior vitreous face
* subhyaloid
And/or sub-internal limiting membrane (between ILM and NFL)

  • mostly occur in macular area
239
Q

What is the pathophysiology of Valsalva maneuver?

A

Elevation of intra-abdominal pressure leads to increase in ocular venous pressure, resulting in ruptures of superficial retinal capillaries

240
Q

What is a Valsalva maneuver?

A

A forcible exhalation against a closed glottis that increases intrathoracic or intra-abdominal pressure

This maneuver can interfere with venous return to the heart.

241
Q

What behaviors are typically associated with the Valsalva maneuver?

A

Strenuous exertion from behaviors such as:
* Emesis (vomiting)
* Violent coughing
* Constipation
* Labor
* Heavy lifting
* Blowing musical instruments
* Crush or compression injuries

These activities can lead to the forcible exhalation characteristic of the Valsalva maneuver.

242
Q

What happens to ocular venous pressure during a Valsalva maneuver?

A

There is a rapid rise in ocular venous pressure

This can lead to rupture of superficial retinal capillaries.

243
Q

What is a possible consequence of elevated ocular venous pressure?

A

Rupture of superficial retinal capillaries leading to hemorrhaging into the subhyaloid space

This can cause sudden and painless disruption of vision.

244
Q

What are some differential diagnoses for Valsalva retinopathy?

A

Differential diagnoses include:
* Posterior vitreous detachment
* Purtscher retinopathy
* Hypertensive retinopathy
* Diabetic retinopathy
* Terson retinopathy

Each of these conditions has distinct mechanisms that can lead to retinal hemorrhaging.

245
Q

What causes posterior vitreous detachment?

A

Mechanical traction due to compression and detachment of the vitreous body

This can lead to damage of retinal vasculature and subsequent hemorrhaging.

246
Q

What is Purtscher retinopathy?

A

Hemorrhages due to occlusion of small arterioles by intravascular microemboli from a compression injury

This condition is associated with trauma.

247
Q

What causes hypertensive retinopathy?

A

Chronic elevation in retinal arteriolar pressure

This results in damage to the capillary wall endothelium and leakage of blood and fluid.

248
Q

What is diabetic retinopathy characterized by?

A

Increased vascular permeability due to changes in microvasculature structure

This leads to leakage of blood and fluid into the retina.

249
Q

What triggers Terson retinopathy?

A

Increase in intracranial pressure leading to elevation in intraocular pressure

This results in compression of the central retinal vein and can cause hemorrhaging.

250
Q

If pre-retinal hemorrhage from Valsalva maneuver does not spontaneously resolve over several weeks, what treatment would be indicated?

A

Nd:YAG laser disruption of posterior hyaloid face

251
Q

What is cobblestone degeneration?

A

A benign thinning/atrophy of the peripheral retina, retinal pigment epithelium, and choriocapillaris

252
Q

In which individuals is cobblestone degeneration more frequently seen?

A

Myopic individuals

253
Q

What percentage of normal eyes can exhibit cobblestone degeneration?

A

Up to 25%

254
Q

How is cobblestone degeneration commonly observed in terms of laterality?

A

It commonly occurs bilaterally

255
Q

Which part of the retina is most frequently involved in cobblestone degeneration?

A

Inferior temporal aspect

256
Q

What symptoms are associated with cobblestone degeneration?

A

Asymptomatic condition

257
Q

What clinical signs are observed during the evaluation of the fundus in cobblestone degeneration?

A

White/yellow circular areas of atrophy; halo of pigment surrounding lesions

258
Q

What may happen to regions of degeneration in cobblestone degeneration?

A

They may coalesce together to form a large band of atrophy

259
Q

Is cobblestone degeneration associated with ocular complications?

A

No, it is not associated with ocular complications

260
Q

What is the recommended follow-up for patients with cobblestone degeneration?

A

Annual evaluation

261
Q

What is another name for macular epiretinal membrane (ERM) when the membrane is slight?

A

Cellophane maculopathy

262
Q

What does the term ‘macular pucker’ refer to?

A

A denser ERM that results in diminished acuity

263
Q

What causes the formation of epiretinal membranes (ERMs)?

A

Disruption of the internal limiting membrane (ILM)

264
Q

What type of cells proliferate to form the membrane in ERM?

A

Glial cells

265
Q

What is the appearance of the membrane in the early stage of ERM?

A

A glistening area of transparent tissue

266
Q

What symptoms are commonly associated with macular epiretinal membranes?

A

Decreased and/or distorted vision

267
Q

What percentage of ERM cases may be bilateral?

A

Up to 20%

268
Q

What clinical signs indicate the presence of mild epiretinal membranes?

A

Glistening tissue overlying or next to the macula

269
Q

What may occur due to severe macular pucker?

A

Cystoid macular edema or a tractional retinal detachment

270
Q

True or false
The majority of patients with ERM are asymptomatic

A

True

271
Q

What are some causes of ERM formation? List at least three.

A
  • Idiopathic origin
  • Posterior vitreous detachment
  • Uveitis
  • Trauma, intraocular surgery, or laser treatment
  • Diabetic retinopathy
  • Retinal breaks
  • Retinal vascular diseases
272
Q

What happens to the fibrocellular tissue as the membrane matures?

A

It may opacify and contract further

273
Q

What visual disturbances can be caused by a mature ERM?

A

Metamorphopsia and reduced visual acuity

274
Q

What is the appearance of a membrane that is round and condensed directly over the macula?

A

Pseudohole

275
Q

What is another name for Epiretinal Membrane?

A

Cellophane Maculopathy

This term describes the appearance of the membrane on the retina.

276
Q

When is treatment recommended for patients with Epiretinal Membrane?

A

If the patient is symptomatic and suffers from reduced visual acuity or experiences a large amount of metamorphopsia

Treatment is not recommended for asymptomatic patients with visual acuity of 20/40 or better.

277
Q

What surgical procedure is warranted for symptomatic patients with Epiretinal Membrane?

A

Pars plana vitrectomy followed by a membrane peel

This procedure helps alleviate symptoms related to the membrane.

278
Q

What is the expected outcome of surgery for patients with Epiretinal Membrane?

A

Patients will typically experience an improvement in their postoperative acuity

However, acuity is not expected to fully return to pre-membrane levels, especially in chronic cases.

279
Q

What tool may be given to patients for monitoring distortion after treatment?

A

Amsler grid

This grid helps patients detect changes in their vision.

280
Q

Patients should be instructed to return if _______ occurs.

A

changes in their vision

This ensures timely follow-up and management of any new symptoms.

281
Q

OCT of patient with familiar drusen would show?

A

Thickening of RPE-Bruch’s membrane complex with an intact photoreceptors layer

282
Q

Tx for CME secondary secondary to YAG cap following CE

A

Topical NSAID
Topical steroid
Oral CAI

Example: 1 gtt ketorolac QID, 1 gtt and prednisolone acetate QID

283
Q

Tx for CME in patients with retinitis pigmentosa

A

Oral CAI

284
Q

What does CME look like on FA in early and late stages?

A

Small hyper fluorescent spots in early stages

‘flower-petal’ pattern in the late stage.

This pattern is indicative of cystoid macular edema (CME) observed during FA.

285
Q

What percentage of CME cases may go undiagnosed with clinical examination alone?

A

5-10%.

Clinical examination is often insufficient for diagnosis, highlighting the importance of imaging techniques.

286
Q

Which imaging techniques are valuable for identifying patients with CME?

A

Fluorescein angiography (FA) and optical coherence tomography (OCT).

These techniques are particularly useful when the diagnosis is uncertain.

287
Q

What does the early arteriovenous phase of FA show in patients with CME?

A

Capillary dilation and leakage of fluid.

This leads to the visibility of small hyperfluorescent spots.

288
Q

What occurs in the later phase of FA for patients with CME?

A

Fluorescein dye accumulates within the microcystic spaces in the outer plexiform layer of the retina.

This accumulation results in characteristic staining petalloid patterns

289
Q

What is the classic perifoveal staining pattern observed in CME during the late phase of FA?

A

‘Petaloid’ or ‘spoke-wheel’ staining pattern.

This pattern is a key diagnostic feature of CME.

290
Q

In cases of CME, what additional leakage may be observed?

A

Optic nerve head leakage.

This is most commonly associated with Irvine-Gass syndrome.

291
Q

What appearance do outer cystoid spaces show in severe cases of CME?

A

‘Honeycomb’ appearance.

This is due to larger fused cystoid spaces extending outside the perifoveal region.

292
Q

What is the appearance of a classic choroidal neovascular membrane (CNVM) in the early phase of angiography?

A

Clearly visible and well-demarcated ‘lacy’ hyperfluorescence.

This feature helps differentiate CNVM from other conditions.

293
Q

What happens to the leakage in the late phase of angiography for CNVM?

A

There is an increasing amount of leakage.

This progression is a key characteristic of CNVM.

294
Q

What is the appearance of fluorescein angiography in central serous retinopathy?

A

Smoke-stack appearance.

This distinct appearance helps in the diagnosis of central serous retinopathy.

295
Q

Most common ocular complication of Behcet disease?

A

Uveitis
* bilateral, non-granulomatous uveitis

296
Q

ERG and EOG in best disease

A

Normal ERG
Abnormal EOG

297
Q

ERG and EOG in stargardt

A

Normal ERG
Normal EOG

298
Q

ERG and EOG in familial drusen
* familial drusen is autosomal dominant

A

Normal ERG
Abnormal EOG (in advanced familial drusen)

299
Q

ERG and EOG in choroideremia

A

Abnormal ERG
abnormal EOG

300
Q

What is choroideremia?

A

An X-linked recessive condition that leads to degeneration of the retina, specifically the choriocapillaris and retinal pigment epithelium (RPE).

301
Q

Who typically presents with choroideremia?

A

Typically presents in males in the 1st to 2nd decade of life.

302
Q

What is the most common entering complaint of choroideremia?

A

Nyctalopia, or night blindness.

303
Q

What are early signs of choroideremia?

A

Typically occur in the first or second decade of life.

304
Q

What visual symptoms progress throughout the patient’s life in choroideremia?

A

Restriction of peripheral vision.

305
Q

When does visual acuity typically remain favorable in choroideremia?

A

Until late in the disease when macular involvement can occur.

306
Q

What is the characteristic appearance of the fundus early in choroideremia?

A

Pigment granules scattered throughout the fundus, sparing the macular region (salt-and-pepper fundus).

307
Q

What happens to the RPE as choroideremia progresses?

A

Patches of RPE atrophy in the mid-peripheral retina become confluent and progressive.

308
Q

What is the initial loss observed in choroideremia?

A

Loss of choriocapillaris.

309
Q

In end-stage choroideremia, what can be seen extending from the posterior pole to the periphery?

A

Visibility of the sclera.

310
Q

What visual function do patients commonly maintain until later in the disease?

A

Central vision.

311
Q

What is a common finding in female carriers of choroideremia?

A

Mid-peripheral mottling of the RPE that tends to be static.

312
Q

What is the ‘moth-eaten’ appearance associated with in choroideremia?

A

The RPE, along with RPE pigment clumping and degeneration.

313
Q

What is observed in late-stage ERG for choroideremia?

A

No recordable scotopic function and a greatly reduced photopic response.

314
Q

Fill in the blank: Choroideremia is an _______ condition.

A

X-linked recessive

315
Q

True or false
A successful treatment for choroideremia does not currently exist

A

True

316
Q

What is Leber’s Congenital Amaurosis?

A

A progressive autosomal recessive rod-cone dystrophy and the most common congenital cause of blindness in children

It involves the loss of retinal photoreceptors, outer segments, and outer nuclear layers.

317
Q

What are the early symptoms of Leber’s Congenital Amaurosis?

A

Roving eye within the first few months of life, reduced acuity and color perception, nyctalopia, and photophobia

Nyctalopia refers to difficulty seeing in low light conditions.

318
Q

What range of visual acuity is typically seen in patients with Leber’s Congenital Amaurosis?

A

From 20/40 to no light perception (NLP), with the average being 20/200

Visual acuity is a measure of the eye’s ability to resolve detail.

319
Q

What are some ocular signs associated with Leber’s Congenital Amaurosis?

A
  • 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)

The oculo-digital sign may lead to atrophy of orbital fat and enophthalmos.

320
Q

What systemic findings can occur with Leber’s Congenital Amaurosis?

A
  • Deafness
  • Skeletal and muscular anomalies
  • Renal/kidney abnormalities
  • Endocrine dysfunction
  • Mental handicap
  • Epilepsy

These systemic issues may vary in severity and presentation.

321
Q

What is the prognosis for patients with Leber’s Congenital Amaurosis?

A

Poor, with no treatment available

Management typically involves referral to a low vision specialist.

322
Q

ERG in Leber’s congenital amaurosis

A

Abnormal
*severely reduced
* loss of retinal photoreceptors, outer segments and outer nuclear layers

323
Q

FA on stargardt disease

A

“Silent choroid”
* choroidal hypo-fluorescence with prominent retinal vasculature
* dark choroid

324
Q

Tx for stargardt

A

Prescribe low vision aids
* with daily Amsler, RTC ASAP if changes

325
Q

Macular disease may cause what color vision deficiency?

A

Blue-yellow

326
Q

WWOP is mostly seen in which area of the retina?

A

Inferior and temporally

327
Q

4 bright bands on OCT Mac

A
  1. ELM
  2. PIL (photoreceptor integrity line)
  3. Interdigitation zone (RPE complex)
  4. RPE (interacts with Burch’s membrane)
328
Q

Paving stone degeneration most commonly seen in which areas of the retina?

A

Inferior and temporal

329
Q

RP triad

A
  1. Attenuation of arterioles
  2. Bone-spicule pigmentation of retina
  3. Waxy pallor of optic nerve

*subcapsular cataract common in RP

330
Q

What type of cataract commonly develops in RP?

A

Subcapsular cataract

331
Q

What is the retina?

A

A multi-layer neural structure that gathers and filters visual information

The retina transmits data to higher processing centers within the visual pathway.

332
Q

How many layers compose the retina?

A

10 layers

The layers include the retinal pigment epithelium, photoreceptors, and others.

333
Q

What is the first layer of the retina?

A

Retinal pigment epithelium (RPE)

This is the outermost layer of the retina.

334
Q

List the layers of the retina from outermost to innermost.

A
  • 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)

These layers play various roles in processing visual input.

335
Q

What is the role of the retinal pigment epithelium (RPE)?

A

Forms part of the blood-retinal barrier, phagocytosis of fragments from shed photoreceptor discs, metabolizes and stores vitamin A

Vitamin A is crucial for the formation of rhodopsin photopigment.

336
Q

What happens due to vitamin A deficiency?

A

Prolonged dark adaptation

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

337
Q

What does the photoreceptor cell layer contain?

A

Outer and inner segments of rods and cones

These segments are characterized by high levels of metabolic activity.

338
Q

Fill in the blank: The _______ converts radiant energy into electrical energy.

A

photoreceptor cell layer

This conversion is essential for visual processing.

339
Q

True or False: The inner layers of the retina absorb light before it reaches the photoreceptors.

A

False

Light is refracted by the cornea and lens and passes through the inner layers before being absorbed by photoreceptors.

340
Q

What is the external limiting membrane?

A

Consists of intercellular junctions of the photoreceptor cells

It delineates the inner segments of the photoreceptors and their respective nuclei.

341
Q

What does the outer nuclear layer contain?

A

The cell bodies and nuclei of the rods and cones

342
Q

What is the function of the outer plexiform (synaptic) layer?

A

Site where photoreceptor cells synapse with the dendrites of horizontal and bipolar cells from the inner nuclear layer

343
Q

What cell types are found in the inner nuclear layer?

A

Bipolar, horizontal, amacrine, and Muller cells

344
Q

What role do Muller cells play in the retina?

A

Create tight junctions and contribute to the formation of the external limiting membrane

345
Q

What does the inner plexiform (synaptic) layer encompass?

A

The synapses of bipolar, ganglion, and amacrine cells’ axons

346
Q

What is contained within the ganglion cell layer?

A

Ganglion cell bodies

347
Q

What does the nerve fiber layer contain?

A

The axons of ganglion cells

348
Q

What forms the internal limiting membrane?

A

Radial feet processes of Muller cells and other glial cell constituents

349
Q

Where do Muller cells’ processes extend in the retina?

A

Throughout the length of the retina except for the retinal pigment epithelium

350
Q

How do amacrine and horizontal cells integrate information?

A

Integrate information laterally, summating horizontally across the retina

351
Q

What types of cells do amacrine cells amalgamate information from?

A

Ganglion and bipolar cells

352
Q

How many different types of amacrine cells exist?

A

At least 35 different types

353
Q

Where are horizontal cell bodies located?

A

At the outer edge of the inner nuclear layer

354
Q

What information do horizontal cells combine?

A

Information obtained from rods and cones

355
Q

How many different types of horizontal cells are there?

A

At least two or three different types

356
Q

How do ganglion, bipolar, and photoreceptor cells transmit information?

A

Transmit information across layers and not within them

357
Q

What is a potential complication of retinal laser photocoagulation treatment?

A

Choroidal detachment

May lead to angle-closure glaucoma.

358
Q

What are the complications associated with retinal laser photocoagulation treatment?

A
  • Choroidal detachment
  • Rhegmatogenous retinal detachment
  • Cystoid macular edema
  • Macular pucker
  • Exudative retinal detachment
  • Retinal hemorrhage (rare)

Complications typically occur due to overtreatment of large regions of the retina.

359
Q

What complication of retinal laser treatment is rare?

A

Retinal hemorrhage

Occurs in rare cases.

360
Q

What is a common complication of cryotherapy?

A

Eyelid edema

Occurs almost 100% of the time.

361
Q

Which complication of cryotherapy occurs almost 100% of the time?

A

Chemosis

This condition involves swelling of the conjunctiva.

362
Q

Fill in the blank: Transient diplopia may be caused by accidental treatment of an _______ muscle.

A

extracular

This refers to muscles outside of the eye.

363
Q

List some complications of cryotherapy.

A
  • Eyelid edema
  • Chemosis
  • Transient diplopia
  • Vitritis
  • Maculopathy (very rare)

Maculopathy is considered very rare.

364
Q

What is vitritis?

A

Inflammation of the vitreous body

It can occur as a complication of cryotherapy.

365
Q

True or False: Maculopathy is a common complication of cryotherapy.

A

False

Maculopathy is described as very rare.

366
Q

stargardt on FA

A

Choroidal hypofl with prominent retinal vasculature
“Silent choroid”

367
Q

What is Stargardt disease most commonly caused by?

A

Mutations in the ABCA4 gene

ABCA4 gene mutations are primarily responsible for Stargardt disease.

368
Q

What type of protein does the ABCA4 gene encode?

A

ATP-binding cassette transmembrane protein

This protein is specifically expressed by rod outer segments.

369
Q

What is the role of the ABCA4 gene in the retina?

A

Involved in the transport of all-trans-retinal

This transport is crucial for proper photoreceptor function.

370
Q

What happens as a result of mutations in the ABCA4 gene?

A

Accumulation of all-trans-retinal in the photoreceptors and retinal pigment epithelium

This accumulation leads to various retinal pathologies.

371
Q

What is the conversion product of all-trans-retinal that contributes to lipofuscin accumulation?

A

N-retinylidene-N-retinylethanolamine (A2E)

A2E is a significant component of lipofuscin, which is toxic.

372
Q

What is lipofuscin and why is it significant in Stargardt disease?

A

A component that accumulates and is toxic to RPE and photoreceptors

Lipofuscin accumulation leads to cellular damage and vision loss.

373
Q

Fill in the blank: The ABCA4 gene mutations lead to the _______ of lipofuscin.

A

accumulation

This accumulation is detrimental to retinal health.

374
Q

What is Stargardt disease?

A

A genetic eye disorder that results in a decrease in visual acuity, typically presenting in the first to second decades of life.

It is characterized by specific retinal changes and accumulation of lipofuscin-like material.

375
Q

What are the initial symptoms of Stargardt disease?

A

Decreased vision, which may be mistaken for malingering due to a normal appearing fundus.

Children may report decreased vision before any noticeable retinal changes occur.

376
Q

What appearance does the macula take on as Stargardt disease progresses?

A

It may appear mottled and eventually develop a ‘beaten-bronze’ appearance, potentially surrounded by yellowish flecks.

This progression indicates worsening of the disease.

377
Q

What is the characteristic pattern of geographic atrophy in Stargardt disease?

A

‘Bull’s eye’ pattern.

This pattern is associated with significant loss of visual acuity.

378
Q

What accumulates at the level of the retinal pigment epithelium in Stargardt disease?

A

Unusual lipofuscin-like material.

This accumulation is a key feature of the disease.

379
Q

What is the typical finding in the electroretinogram (ERG) of patients with Stargardt disease?

A

Characteristically normal, but may be atypical in advanced cases.

The ERG tests the electrical responses of the retina.

Normal ERG and normal EOG until diseases advances

380
Q

How does the electro-oculogram (EOG) change as Stargardt disease progresses?

A

It is likely normal in early stages but becomes increasingly abnormal as the disease progresses.

The EOG measures the electrical potential of the retina.

381
Q

What is Best disease also known as?

A

Vitelliform dystrophy.

It is a rare retinal condition that affects the macular area.

382
Q

What occurs during the pre-vitelliform stage of Best disease?

A

The child is asymptomatic, the fundus appears normal, but the EOG reading is abnormal.

This stage may be detected through testing even if no symptoms are present.

383
Q

Describe the vitelliform stage of Best disease.

A

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.

384
Q

What characterizes the pseudohypopyon stage in Best disease?

A

A blister-like lesion where lipofuscin may gravitate inferiorly, causing the appearance of a pseudohypopyon.

This stage usually occurs in the second to third decades of life.

385
Q

What happens in the vitelliruptive stage of Best disease?

A

The ‘egg yolk’ breaks apart, leading to a decrease in visual acuity.

This stage indicates further progression of the disease.

386
Q

What defines the atrophic stage of Best disease?

A

Macular scarring and potential formation of choroidal neovascular membranes (CNVM) and/or geographic atrophy.

Visual acuity is typically very poor at this stage.

387
Q

What is fundus flavimaculatus?

A

A variant of Stargardt disease characterized by white-yellow flecks in the posterior pole instead of macular involvement.

Visual acuity remains fairly good as long as the macula is clear.

388
Q

In fundus flavimaculatus, what happens to visual acuity?

A

It tends to remain fairly good as long as the macula remains clear and geographic atrophy is absent.

This is in contrast to Stargardt disease where visual acuity decreases significantly.

389
Q

Tx for retinal detachment

A

Focal Laser photocoagulation
* multiple rows of treatment burns to ensure longevity and stability

390
Q

Pneumatic retinopathy is used to treat?

A

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

391
Q

Tx for CRVO
RTC after initiation of treatment

A

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

392
Q

RTC for wet AMD with active CNVM

A

1-3 months until CNVM inactive (based on OCT and FA)

393
Q

What is Ocular Ischemic Syndrome (OIS) also known as?

A

Venous Stasis Retinopathy

This term is considered outdated.

394
Q

What is the average age of patients affected by Ocular Ischemic Syndrome?

A

65 years

Epidemiology shows >50 years as the demographic.

395
Q

What is the male to female ratio in cases of Ocular Ischemic Syndrome?

A

2:1

Males are affected more frequently than females.

396
Q

What is the 5-year mortality rate for patients with Ocular Ischemic Syndrome?

A

40%

This indicates a significant risk associated with the syndrome.

397
Q

What are the common risk factors for developing Ocular Ischemic Syndrome?

A
  • Hypertension
  • Hyperlipidemia
  • Diabetes Mellitus
  • Giant Cell Arteritis

These conditions contribute to the development of OIS.

398
Q

What pathophysiological condition leads to Ocular Ischemic Syndrome?

A

Chronic ocular hypoperfusion due to severe internal carotid artery stenosis

This can also involve insufficiency or thrombosis of the internal carotid artery.

399
Q

What percentage of internal carotid artery stenosis is associated with Ocular Ischemic Syndrome?

A

> 70%

Significant stenosis is critical for the development of OIS.

400
Q

What happens to the central retinal artery (CRA) perfusion pressure in Ocular Ischemic Syndrome?

A

It is reduced by 50%

This reduction leads to ischemic conditions in the eye.

401
Q

What is a consequence of low perfusion pressure in OIS?

A

Induces oxidative stress damage

This damage affects both the retina and choroid.

402
Q

What are the symptoms of Ocular Ischemic Syndrome?

A
  • Gradual loss of vision over weeks or months
  • Decrease in visual acuity (VA) ranging from mild to severe
  • Asymptomatic cases are possible

Visual acuity can vary significantly among patients.

403
Q

What defines ‘mild’ visual acuity loss in Ocular Ischemic Syndrome?

A

20/25 - 20/40

This indicates the range of mild loss in visual acuity.

404
Q

What defines ‘severe’ visual acuity loss in Ocular Ischemic Syndrome?

A

20/400 or worse

Severe cases can lead to significant impairment in vision.

405
Q

What type of visual loss may occur in Ocular Ischemic Syndrome?

A

Transitory monocular visual loss

This type of loss may recover over time.

406
Q

What percentage of OIS patients report transient monocular visual loss (TMVL)?

A

10-15%

TMVL is a significant symptom in ocular ischemic syndrome (OIS) patients.

407
Q

What is the hallmark of carotid insufficiency?

A

Amaurosis fugax

Amaurosis fugax is an older term for TMVL.

408
Q

How long does TMVL typically last?

A

5 minutes or less

This duration is characteristic of transient monocular visual loss.

409
Q

What proportion of patients with amaurosis fugax have significant ipsilateral carotid artery obstruction?

A

1/3rd

Specifically, these patients have an obstruction of ≥75%.

410
Q

What visual symptoms may patients with OIS complain of?

A

Blur, dimming, or darkened vision

Patients may describe a curtain coming down over the eye.

411
Q

What is ocular angina?

A

Ocular and/or periocular pain

This symptom occurs in approximately 40% of OIS patients.

412
Q

What visual phenomenon might patients experience after bright light exposure?

A

Slow adaptation

This is a common symptom in OIS.

413
Q

What percentage of patients with symptomatic carotid occlusion show retinal vascular changes?

A

Approximately 30%

These changes are usually asymptomatic.

414
Q

What are the typical signs of OIS in the posterior segment?

A
  1. Typically unilateral (80%)
  2. Dilated retinal veins
  3. Retinal hemorrhages (80% of cases)
  4. Cherry-red spot (12% of eyes)

Other signs may include narrowed arteries and rare cases of flame hemes, CWS, optic disc edema, and macular edema.

415
Q

What is a cherry-red spot associated with in OIS?

A

Embolic occlusion of the CRA or increased IOP

It may occur in neovascular glaucoma.

416
Q

True or False: Retinal hemorrhages in OIS are usually in the posterior pole.

A

False

Midperipheral hemorrhages are more common than those in the posterior pole.

417
Q

Fill in the blank: OIS symptoms may include _______ after bright light exposure.

A

Worsening of vision

This worsening can also occur with postural changes.

418
Q

What is the most common sign of Ocular Ischemic Syndrome (OIS)?

A

NVI (iris rubeosis) is most common (65-85%)

NVI stands for Neovascularization of the Iris.

419
Q

What is the order of anterior chamber reaction in OIS?

A

flare > cells > KPs (20%)

KPs refer to Keratic Precipitates.

420
Q

What percentage of OIS cases may present with neovascular glaucoma?

A

50% of OIS cases

Neovascular glaucoma may not have very high intraocular pressure due to poor ciliary body perfusion.

421
Q

What is a common IOP finding in unilateral OIS?

A

Unilateral low IOP (non-neovascular)

This finding can help differentiate OIS from other conditions.

422
Q

What are some signs of Ocular Ischemic Syndrome (OIS) in the anterior segment? (List at least three)

A
  • Diffuse episcleral injection
  • Corneal edema
  • Iris atrophy with poor reacting pupil (mid-dilated)

These signs indicate ischemic changes in the eye.

423
Q

What is a differential diagnosis (DDx) for OIS?

A
  • Central Retinal Vein Occlusion
  • Diabetic Retinopathy

Both conditions can present with similar vascular disorders.

424
Q

What laboratory tests should be ordered for OIS evaluation?

A
  • CBC
  • Fasting glucose
  • HbA1C
  • Fasting lipids
  • Sed Rate
  • C-reactive protein

These tests help assess overall health and identify potential underlying causes.

425
Q

What imaging study is recommended if the carotid ultrasound is inconclusive?

A

MRA

MRA stands for Magnetic Resonance Angiography.

426
Q

What happens to the carotid arteries during a venous stasis evaluation?

A

Ask patient to hold breath

This maneuver helps visualize blood flow and detect abnormalities.

427
Q

At what stenosis level can a bruit be heard during carotid auscultation?

A

50-60% stenosis

A bruit may not be heard if stenosis is less than 50%.

428
Q

True or False: A bruit can be detected if stenosis is less than 50%.

A

False

Bruits are typically not audible at less than 50% stenosis.

429
Q

What is the management strategy for inflammation in the anterior segment?

A

Treat inflammation with topical steroid QID and homatropine 5% BID (cycloplegic)

QID means four times a day, and BID means twice a day.

430
Q

What should be done when neovascularization develops?

A

Refer to OMD for Panretinal Photocoagulation (PRP) 500um spots when neovascularization develops

OMD refers to an ophthalmic medical doctor.

431
Q

What is the recommended treatment for macular edema?

A

Intravitreal anti-VEGF agents may be beneficial for macular edema

Anti-VEGF agents are used to inhibit vascular endothelial growth factor.

432
Q

What is indicated for significant carotid blockage?

A

Carotid endarterectomy or stent surgery if significant blockage

This is to restore normal blood flow in the carotid artery.

433
Q

When is Carotid Endarterectomy (CEA) indicated?

A

Symptomatic patients with 70-99% carotid stenosis, asymptomatic minimum of 60% stenosis

CEA may be considered on a case-by-case basis for 50-69% stenosis.

434
Q

What is the perioperative risk of stroke or death for CEA?

A

<6% and 3%

These percentages indicate a low risk for surgery.

435
Q

What are the age and life expectancy criteria for CEA?

A

40-75 years old and life expectancy of at least 5 years

Patients outside this age range or with a shorter life expectancy may not be candidates for CEA.

436
Q

Why is endarterectomy not performed in cases of total (100%) obstruction?

A

Because it is dangerous due to collateral blood supply having occurred

This means that alternative pathways for blood flow have developed, complicating surgery.

437
Q

What are the signs of Ocular Ischemic Syndrome (OIS)?

A
  • Dilated non-tortuous veins
  • Arterial attenuation
  • Hemorrhages (midperipheral > PP)
  • Neovascularization (Iris > angle > NVD > NVE)
  • Mild anterior uveitis
  • Neovascular Glaucoma

NVD refers to neovascularization of the disc, and NVE refers to neovascularization elsewhere.

438
Q

How is the diagnosis of OIS typically made?

A

Based on fundus appearance and history of systemic disease

Fundus examination is key in identifying changes associated with OIS.

439
Q

True or False: TMVL and retinal artery occlusions are considered medical emergencies.

A

True

They necessitate emergent vascular and brain imaging.

440
Q

True or False
Pts with stargardt should avoid Vitamin A supplements

A

TRUE,
Unable to process excess Vitamin A, causes accumulation of deposits in macula

441
Q

Mortality rate for OIS

A

After 5 years, mortality rate it 40%

442
Q

What is retinoschisis?

A

Retinoschisis is defined as splitting of the layers within the retina.

443
Q

How does retinoschisis differ from retinal detachment?

A

Retinal detachment is when the retina is split from the choroid, while retinoschisis involves splitting within the retina.

444
Q

What type of lesions does retinoschisis typically create?

A

Dome shaped lesions in the retinal periphery.

445
Q

What visual field defects are associated with retinoschisis?

A

Absolute visual field defects with sharp borders.

446
Q

What visual field defects are associated with retinal detachments?

A

Relative visual field defects.

447
Q

What procedures can help differentiate retinoschisis from retinal detachment?

A
  • Threshold visual field
  • Scleral indentation
  • OCT
448
Q

Can fluorescein angiography be used to differentiate retinoschisis from retinal detachment?

A

No, fluorescein angiography cannot be used for differentiation.

449
Q

What sign is absent in retinoschisis that may be seen in retinal detachment?

A

Tobacco dust/Shafer’s sign.

450
Q

Can retinoschisis present with rhegmatogenous retinal detachments?

A

Yes, retinoschisis can rarely present with rhegmatogenous retinal detachments.

451
Q

What are the two types of retinoschisis?

A
  • Acquired Age Related
  • Juvenile (X-linked recessive)
452
Q

What characterizes acquired age-related retinoschisis?

A

More common, presents bilaterally and symmetrically; splitting between inner nuclear and outer plexiform layers.

453
Q

What is the etiology of acquired age-related retinoschisis?

A

The etiology seems to be unclear.

454
Q

What characterizes juvenile retinoschisis?

A

Less common, located in the nerve fiber layer; presents with progressively decreasing VA from 20/25 to 20/80.

455
Q

What complications can juvenile retinoschisis cause?

A
  • Amblyopia
  • Nystagmus
  • Strabismus
456
Q

What is a common presentation of juvenile retinoschisis?

A

Stellate maculopathy (spoke-like foveal cysts).

457
Q

What may juvenile retinoschisis present with due to the longevity of the disease?

A

A pigment demarcation line.

458
Q

What symptoms may patients with retinoschisis report?

A

Patients may be asymptomatic or complain of blurry vision.

NBEO Part 2 (20 decks)

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