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NBEO Part 2 > More Retina/Choroid/Vitreous > Flashcards

More Retina/Choroid/Vitreous Flashcards

1
Q

Characteristics of birdshot retinopathy

A

White dot syndrome
idiopathic
F>M, middle age
(+)HLA-A29

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2
Q

Signs and symptoms of birdshot retinopathy (name at least 4)

A

Symptoms:
1) blur ~20/40
2) floaters
3) photopsia
4) nyctalopia

Signs:
5) uveitis/ vitritis
(Vitritis triad: CME, ERM, cataracts)
6. Disc edema
7. ERG abnormal

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3
Q

What is the age range for APMPPE?

A

20-40 years
*Acute posterior multifocal placoid pigment epitheliopathy
* white dot syndrome

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4
Q

What is the sex ratio for APMPPE?

A

F = M

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5
Q

What is the laterality of APMPPE?

A

Bilateral
*Acute posterior multifocal placoid pigment epitheliopathy

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6
Q

What HLA type is associated with APMPPE?

A

B7, DR2

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7
Q

What is the level of vitritis in APMPPE?

A

Mild

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8
Q

Describe the lesions in APMPPE.
(Acute Posterior Multifocal Placoid Pigment Epitheliopathy)

A

Large, geographic, gray white; shallow pigmented scars within 1-2 weeks
* white dot syndrome

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9
Q

What is the prognosis for APMPPE?

A

Good

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10
Q

What treatment is recommended for APMPPE?

A

None

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11
Q

What is the age range for MEWDS?
(Multiple evanescent white dot syndrome)

A

20-30 years

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12
Q

What is the sex ratio for MEWDS?

A

F > M

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13
Q

What is the laterality of MEWDS?

A

Unilateral

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14
Q

What HLA type is associated with MEWDS?

A

None

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15
Q

What is the level of vitritis in MEWDS?

A

Mild

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16
Q

Describe the lesions in MEWDS.

A

Small, soft, graywhite dots; no scarring

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17
Q

What is the macula appearance in MEWDS?

A

Granularity

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18
Q

What is the prognosis for MEWDS?

A

Good

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19
Q

What treatment is recommended for MEWDS?

A

None

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20
Q

What is the age range for Serpiginous?

A

30-50 years

*rare, bilateral, idiopathic inflammatory disorder
* results in geographic destruction of RPE, retina and choriocapillaris
*~M>F
* HLA-B7

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21
Q

What is the sex ratio for Serpiginous?

A

F = M

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22
Q

What is the laterality of Serpiginous?

A

Bilateral

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23
Q

What HLA type is associated with Serpiginous?

A

B7

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24
Q

What is the level of vitritis in Serpiginous?

A

Mild

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25
Q

Describe the lesions in Serpiginous.

A

Active, geographic, graywhite patches; deep scars with fibrosis

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26
Q

What is the macula appearance in Serpiginous?

A

Subretinal scars

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27
Q

What percentage of patients develop CNV in Serpiginous?

A

25%

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28
Q

What is the prognosis for Serpiginous?

A

Poor

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29
Q

What treatments are recommended for Serpiginous?

A

Steroids, laser CNV

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30
Q

What is the age range for Birdshot?

A

40-60 years

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31
Q

What is the sex ratio for Birdshot?

A

F > M

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32
Q

What is the laterality of Birdshot?

A

Bilateral

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33
Q

What HLA type is associated with Birdshot?

A

A29

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34
Q

What is the level of vitritis in Birdshot?

A

Chronic, moderate

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35
Q

Describe the lesions in Birdshot.

A

Deep, creamy spots; indistinct margins; yellow scars without pigmentation

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36
Q

What is the macula appearance in Birdshot?

A

CME rare, CNV rare

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37
Q

What is the prognosis for Birdshot?

A

Fair

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38
Q

What treatments are recommended for Birdshot?

A

Steroids?, Cyclosporine

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39
Q

What is the age range for Multifocal Choroiditis with Panuveitis?

A

30-40 years

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40
Q

What is the sex ratio for Multifocal Choroiditis with Panuveitis?

A

F > M

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41
Q

What is the laterality of Multifocal Choroiditis with Panuveitis?

A

Bilateral

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42
Q

What is the level of vitritis in Multifocal Choroiditis with Panuveitis?

A

Chronic, moderate

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43
Q

Describe the lesions in Multifocal Choroiditis with Panuveitis.

A

100-200 um white-yellow spots; mixture of old scars and new spots

44
Q

What is the macula appearance in Multifocal Choroiditis with Panuveitis?

A

CME 35%, CNV rare

45
Q

What is the prognosis for Multifocal Choroiditis with Panuveitis?

46
Q

What treatments are recommended for Multifocal Choroiditis with Panuveitis?

A

Steroids?, Laser CNV

47
Q

What percentage of patients develop CNV in Atrophic scars?

48
Q

What is the prognosis for Atrophic scars?

49
Q

What treatments are recommended for Atrophic scars?

A

Steroids?, Laser CNV

50
Q

What condition may look similar to vitreomacular traction on an OCT scan?

A

Fibrovascular proliferation

Conditions include proliferative diabetic retinopathy, retinopathy of prematurity, and sickle cell retinopathy.

51
Q

How does fibrovascular proliferation appear compared to the posterior hyaloid face?

A

Denser and more irregular

This difference helps differentiate it from vitreomacular traction.

52
Q

What is more apparent on a fundus exam, fibrovascular proliferation or vitreomacular traction?

A

Fibrovascular proliferation

This visibility aids in diagnosis.

53
Q

What are common associations of fibrovascular proliferation?

A
  • Vitreous hemorrhages
  • Preretinal hemorrhages
  • Neovascularization

These associations are important for clinical evaluation.

54
Q

Risk factors for amelanotic choroidal melanoma

A

Sun exposure
Fair skin, unable to tan
Pre-existing nevi
Ocular or oculodermal melanocytosis

55
Q

What syndrome accounts for approximately one half of the cases of patients who are both visually and hearing impaired?

A

Usher syndrome

56
Q

How many subtypes of Usher syndrome are there?

A

Three subtypes

57
Q

What factors vary among the three subtypes of Usher syndrome?

A

Age of onset of vision loss, severity of hearing loss, absence or presence of vestibular function

58
Q

What is indicated by delayed developmental milestones such as walking in a patient with Usher syndrome?

A

Balance problems

59
Q

Which type of Usher syndrome is associated with abnormal vestibular function?

A

Type 1 Usher syndrome

60
Q

In which types of Usher syndrome is vestibular function normal?

A

Types 2 and 3

61
Q

When does vision loss occur in patients with type 1 Usher syndrome?

A

During the first decade of life

62
Q

When does vision loss occur in patients with types 2 and 3 Usher syndrome?

A

In the second decade of life

63
Q

What is the nature of hearing loss in patients with type 1 Usher syndrome?

A

Total to profound hearing loss that is non-progressive and present at birth

64
Q

What type of hearing loss do patients with type 2 Usher syndrome have?

A

Moderate hearing loss

65
Q

What is Usher syndrome?

A

A genetic condition characterized by hearing loss and progressive vision loss.

Usher syndrome is divided into different types, each with varying degrees of severity.

66
Q

What may type 1 patients of Usher syndrome eventually experience?

A

Severe vision loss.

This progressive vision loss can significantly impact the patient’s quality of life.

67
Q

What type of instruction may be needed for patients with Usher syndrome?

A

Braille instruction.

Braille instruction is essential for patients who experience significant vision loss.

68
Q

What is the role of genetic counseling in Usher syndrome?

A

To determine which type of Usher syndrome the patient has and to help with emotional acceptance of the condition.

Genetic counseling can provide valuable information and support to patients and their families.

69
Q

What is the inheritance pattern of Usher syndrome?

A

Autosomal recessive

This means that a child must inherit two copies of the mutated gene, one from each parent, to be affected by the condition.

70
Q

How many different gene mutations are known to cause Usher syndrome?

A

At least 10

These mutations can vary and contribute to the different types of Usher syndrome.

71
Q

What must be true about the parents for a child to be born with Usher syndrome?

A

Each parent must be a carrier of identical gene mutations

This means both parents must have at least one copy of the mutated gene.

72
Q

Fill in the blank: For a child to inherit Usher syndrome, they must receive _______ from each parent.

A

one copy of the identical gene mutation

This is necessary for the condition to manifest in the offspring.

73
Q

What is the first component of the classic clinical triad associated with retinitis pigmentosa?

A

Arteriolar attenuation

The triad specifically mentions arteriolar attenuation, not dilation.

74
Q

What is the second component of the classic clinical triad associated with retinitis pigmentosa?

A

Retinal bone-spicule pigmentation

This pigmentation pattern is a key indicator of the disease.

75
Q

What is the classic clinical triad associated with retinitis pigmentosa?

A

Waxy optic disc pallor
Attenuated arterioles
Bone spicules

76
Q

Name an ocular finding that may occur at any time during the disease of retinitis pigmentosa.

A

Posterior subcapsular cataracts

These cataracts can affect vision and may require surgical intervention.

77
Q

What type of cataracts are commonly observed in all types of retinitis pigmentosa?

A

Posterior subcapsular cataracts

These cataracts are treatable via lensectomy.

78
Q

What is the common refractive error found in patients with retinitis pigmentosa?

A

Myopia

Myopia is frequently observed and should be monitored for spectacle correction.

79
Q

What vitreous changes are commonly seen in patients with retinitis pigmentosa?

A

Posterior vitreous detachments and uveitis

These changes are part of the ocular findings associated with the disease.

80
Q

True or False: Hyperopia is frequent in the population with retinitis pigmentosa.

A

False

Myopia, not hyperopia, is the common refractive error in this population.

81
Q

Fill in the blank: The classic clinical triad associated with retinitis pigmentosa includes arteriolar attenuation, retinal bone-spicule pigmentation, and _______.

A

waxy optic disc pallor

82
Q

Which quadrant is the most common site for CHRPEs?

A

Temporal quadrant

83
Q

Pathophysiology of RP?

A

Progressive loss of photoreceptors and RPE function

84
Q

What are hard drusen?

A

Hyaline deposits located between basement membrane of RPE and inner collagenous layer of Bruch’s

85
Q

Polypoidal choroidal vasculopathy signs

A
  • subretinal orange-red nodules with polyps seen on ICGA
  • unilateral mostly
  • on OCT multiple pigment epithelial detachments “string of pearls” of hyper reflective material under RPE
86
Q

What are the characteristics of severe non-proliferative diabetic retinopathy?

A

Any of the following in the absence of proliferative retinopathy:
* >20 intraretinal hemorrhages in each quadrant
* 2 quadrants of venous beading
* 1 quadrant of prominent intraretinal microvascular abnormalities (IRMA)

Severe non-proliferative diabetic retinopathy is a critical stage that requires monitoring and intervention.

87
Q

What defines clinically significant macular edema?

A

Defined as any one of the following:
* Retinal thickening within 500 microns (1/3 disc diameter) of the center of the fovea
* Hard exudates within 500 microns of the center of the fovea, if associated with adjacent retinal thickening
* Thickening of the retina with a size greater than 1 disc area, part of which is within 1 disc diameter of the foveal center

Clinically significant macular edema can lead to vision loss if not managed.

88
Q

What observations are included in high-risk proliferative diabetic retinopathy?

A

Includes one of the following observations:
* NVD with a size greater than 1/4 to 1/3 of the optic disc
* Any degree of NVD if an associated pre-retinal or vitreous hemorrhage is present
* NVE greater than 1/2 the size of the optic disc when associated with a pre-retinal or vitreous hemorrhage

High-risk proliferative diabetic retinopathy indicates a significant risk for severe vision loss.

89
Q

Fill in the blank: Severe non-proliferative diabetic retinopathy involves more than _______ intraretinal hemorrhages in each quadrant.

A

> 20

This threshold is critical for diagnosis.

90
Q

True or False: Clinically significant macular edema can occur without retinal thickening.

A

False

Retinal thickening is a key component of clinically significant macular edema.

91
Q

What is the significance of NVD greater than 1/4 to 1/3 of the optic disc in diabetic retinopathy?

A

It is an observation that indicates high-risk proliferative diabetic retinopathy.

NVD stands for neovascularization of the disc.

92
Q

True or false
Uncontrolled diabetes is the most commoncause of vitreous hemorrhaging in adults

A

TRUE
*trauma is most common in young people

93
Q

What is malignant hypertension?

A

The most severe presentation of hypertension with extremely high blood pressure and associated retinal hemorrhages and exudates, with or without papilledema.

94
Q

What are the typical blood pressure readings in malignant hypertension?

A

Systolic blood pressure above 180 mmHg and diastolic blood pressure above 120 mmHg.

95
Q

What condition is likely associated with malignant hypertension in this text?

A

Renal failure from a history of IgA nephropathy.

96
Q

How do retinal arterioles and capillaries respond to hypertension?

A

They have autoregulatory mechanisms and tight junctions that maintain the blood-ocular barrier.

97
Q

What happens to the blood-ocular barrier in high levels of hypertension?

A

Leakage of blood and lipoprotein occurs, resulting in hemorrhages, cotton-wool spots, hard exudates, and capillary occlusion.

98
Q

Do choroidal arterioles and capillaries exhibit autoregulation?

A

No, they do not exhibit autoregulation but have fenestrations.

99
Q

What changes occur in hypertensive choroidopathy?

A

Fibrinoid changes in the choriocapillaris lead to areas of focal nonperfusion and ischemia of the outer retina and retinal pigment epithelium (RPE).

100
Q

What can exudation through the injured RPE lead to?

A

Neurosensory detachments.

101
Q

What characteristics do vessels of the optic nerve head possess?

A

They exhibit autoregulation but have an incompetent blood-ocular barrier.

102
Q

What is thought to cause disc edema in severe hypertension?

A

Ischemia and axoplasmic stasis caused by vasoconstrictive agents released in response to elevated blood pressure.

103
Q

What conditions can be observed in patients with malignant hypertension?

A

Hypertensive retinopathy, choroidopathy, and optic neuropathy.

104
Q

What type of changes can occur surrounding the macular area in malignant hypertension?

A

Circinate edematous changes.

105
Q

What is the etiology of CWS?
Cotton wool spots

A

Occlusion of terminal retinal arterioles
*usually resolve 3-6 weeks

NBEO Part 2 (23 decks)

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