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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

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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 left 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

It reveals 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.

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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.

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.

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.

85
Q

True or False: The choriocapillaris contains melanocytes.

A

False

The choriocapillaris does not contain melanocytes.

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.

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.

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.

89
Q

What is the thickness of Bruch’s membrane?

A

About 2 microns thick

This thinness is significant for its function and structure.

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.

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.

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.

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.

94
Q

What is Leber congenital amaurosis?

A

A rod-cone disorder characterized by vision loss

It may initially show a normal-appearing fundus.

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.

96
Q

What does ERG reveal in cases of Leber congenital amaurosis?

A

ERG is markedly abnormal or flat

This finding is crucial for establishing the diagnosis.

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.

98
Q

What are dilated vessels associated with?

A

Retinal edema and non-ischemic central retinal vein occlusion

Dilated vessels are a clinical sign observed in non-ischemic central retinal vein occlusion.

99
Q

What are flame-shaped hemorrhages?

A

A type of retinal hemorrhage found in non-ischemic central retinal vein occlusion

These hemorrhages can be observed in all four quadrants of the retina.

100
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.

101
Q

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

A

Formation of a thrombus near or at the lamina cribrosa

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

102
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.

103
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.

104
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.

105
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.

106
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.

107
Q

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

A

Women aged between 60-80 years

108
Q

What is postulated to cause idiopathic macular holes?

A

Traction on the macular region by the vitreous

109
Q

What classification system is used for idiopathic macular holes?

A

Gass classification system

110
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

111
Q

What characterizes Stage 1B of idiopathic macular holes?

A

Appearance of a yellow ring along with a foveal detachment

112
Q

What defines Stage 2 of idiopathic macular holes?

A

Small foveal defects measuring less than 400 um in diameter

113
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

114
Q

What are the characteristics of Stage 4 idiopathic macular holes?

A

Macular defects larger than 400 um, complete posterior vitreous detachment, yellow deposits at the level of the RPE may be observed in the center of the hole, border of the hole may appear elevated

115
Q

What protozoa causes Toxoplasmosis?

A

Toxoplasma gondii

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

116
Q

Who is particularly at risk from Toxoplasmosis and why?

A

Pregnant mothers

An infection in the mother can potentially harm the unborn fetus

117
Q

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

A

Blindness

Retinal damage can result from the infection

118
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

119
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

120
Q

What symptoms may patients with active retinitis from Toxoplasmosis report?

A

Floaters, blurry vision, photophobia

Patients typically do not experience pain

121
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

122
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

123
Q

What additional problems may immunocompromised persons experience with Toxoplasmosis?

A

Encephalitis and chorioretinitis

These patients may not display vitritis

124
Q

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

A

False

Toxoplasmosis rarely leads to illness in healthy individuals

125
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

126
Q

What organism causes presumed ocular histoplasmosis?

A

Histoplasma capsulatum

This organism typically enters the body via inhalation into the lungs.

127
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.

128
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.

129
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.

130
Q

Do patients suffering from histoplasmosis manifest vitritis?

A

No

Patients with histoplasmosis will never show signs of vitritis.

131
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.

132
Q

Are most cases of retinoblastoma sporadic or familial?

A

Most cases are sporadic

Occasionally, the malignancy may be familial in origin.

133
Q

What percentage of retinoblastoma cases may be observed bilaterally?

A

30%

The majority of cases present unilaterally.

134
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.

135
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.

136
Q

What additional testing should be included for patient taking plaquenil?

A
  1. 10-2 VF
  2. Multifocal ERG
  3. Mac OCT
  4. Ishihara color vision
137
Q

What additional testing should be included for patient taking plaquenil?

A
  1. 10-2 VF
  2. Multifocal ERG
  3. Mac OCT
  4. Ishihara color vision
138
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

139
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

140
Q

What are choroidal nevi typically considered?

A

Congenital

Choroidal nevi are rarely observed in younger children.

141
Q

At what stage do choroidal nevi usually become clinically apparent?

A

Puberty

142
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.

143
Q

What may develop over time on choroidal nevi?

A

Overlying drusen

144
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.

145
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.

146
Q

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

A

Approximately 1%

147
Q

What can serous fluid in the form of an overlying retinal detachment indicate?

A

Higher likelihood of the nevus becoming a melanoma

148
Q

What increases the chance of transformation from nevus to melanoma?

A

Development of orange pigment on the surface of nevi

149
Q

Where are nevi more likely to become melanomas?

A

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

150
Q

What additional indicators may suggest a nevus is more likely to transform into melanoma?

A

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

151
Q

What is a predictive factor for nevus to melanoma formation?

A

Absence of drusen

152
Q

What do drusen indicate regarding choroidal nevi?

A

Chronicity and benignity

Lesions with drusen rarely transform into melanomas.

153
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.

154
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.

155
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.

156
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.

157
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.

158
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.

159
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.

160
Q

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

A

color vision changes and Amsler grid abnormalities.

161
Q

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

A

Paracentral scotoma

162
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.

163
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.

164
Q

What imaging technique enables the detection of disruption of the parafoveal ellipsoid zone in early stages?

A

Optical coherence tomography (OCT)

OCT can reveal abnormalities affecting various retinal layers.

165
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.

166
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.

167
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.

168
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.

169
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.

170
Q

What defects have been reported in relation to ganglion cell complex and peripapillary RNFL?

A

Defects associated with hydroxychloroquine retinopathy

These defects are indicative of retinal damage and functional impairment.

171
Q

What is candidiasis caused by?

A

Candidiasis is caused by a yeast fungus, Candida albicans.

172
Q

Where is Candida albicans frequently encountered in humans?

A

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

173
Q

In which patients might retinal involvement occur due to candidiasis?

A

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

174
Q

What symptoms might patients with retinal involvement from candidiasis notice?

A

Floaters and blurred vision unilaterally.

175
Q

How do lesions from retinal candidiasis appear?

A

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

176
Q

What can happen to lesions if they are left untreated?

A

They may coalesce together and extend into the vitreous, causing the appearance of suspended ‘cotton balls.’

177
Q

What serious conditions may ensue if candidiasis is left untreated?

A

Endophthalmitis, retinal necrosis, and detachment.

178
Q

True or False: Candidiasis can only affect the skin.

A

False

179
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.

180
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.

181
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.

182
Q

What causes 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.

183
Q

What does CRAO stand for?

A

Central retinal artery occlusion

184
Q

What is the primary consequence of central retinal artery occlusion?

A

Acute, painless loss of vision

185
Q

What percentage of CRAO cases present unilaterally?

A

99%

186
Q

What type of defect is observed in CRAO?

A

Afferent pupillary defect

187
Q

How does the retina appear in cases of CRAO?

A

More pale/white superficially

188
Q

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

A

Cherry red spot

189
Q

Is CRAO typically associated with retinal hemorrhages?

A

No

190
Q

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

A

central retinal artery

191
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
192
Q

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

A

1-2 months for 6 months

193
Q

RTC for CRVO if VA is worse than 20/200

A

1 month for 6 months

194
Q

What is a sub-Tenon’s injection?

A

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

195
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.

196
Q

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

A

Toward the globe.

197
Q

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

A
  • Vitritis
  • Posterior uveitis
  • Cystoid macular edema
198
Q

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

A

2 to 3 mm from the inferotemporal fornix.

199
Q

What should be avoided when penetrating the bulbar conjunctiva?

A

Nick any of the subconjunctival vessels.

200
Q

What should be done with the needle tip after penetrating the conjunctiva?

A

Move it back and forth to safeguard against penetration of the sclera.

201
Q

What is the purpose of withdrawing the plunger before injecting?

A

To ensure that the tip of the needle is not located within a vessel.

202
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]

203
Q

Watzke-Allen sign

A

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

204
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

NBEO Part 2 (15 decks)

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