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Ophthalmology OPEX > Uveitis > Flashcards

Uveitis Flashcards

1
Q

What does ACAID stand for?

A

Anterior Chamber- Associated Immune Deviation

-Affords the immune privilege of the internal eye

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2
Q

First identified association between HLA genes and human disease?

A

HLA-B27 and Anterior Uveitis

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3
Q

STRONGEST association between HLA genes and human disease ever described (224x risk)

A

HLA-A29 and Birdshot Chorioretinopathy

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4
Q

Birdshot Chorioretinopathy: associated HLA subtype?

A

HLA-A29 (“ABI the bird”)

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5
Q

HLA-B27: associated ophtha disease?

A

Acute Anterior Uveitis: Ankylosing Spondylitis and Reiter’s Syndrome (“BinugBoG na Reiter”)

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6
Q

HLA-B51/B5: associated ophtha disease?

A

Behçet’s Disease (“BEA Behçet”)

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7
Q

Vogt-Koyanagi-Harada Syndrome, Sympathetic Ophthalmia: associated HLA subtype?

A

HLA-DR4: (“DR. 4 Vicky So”)

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8
Q

Specialized dendritic cells in the Conjunctiva

A

Langerhans Cells

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9
Q

Hypersensitivity Type 1: Immediate/IgE-mediated diseases

A

Seasonal Allergic Conjunctivitis, Giant Papillary Conjunctivitis, Vernal Keratoconjunctivitis, Atopic Keratoconjunctivitis

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10
Q

Hypersensitivity Type 2: Cytotoxic diseases

A

Mooren’s Ulcer, Mucous Membrane Pemphigoid

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11
Q

Hypersensitivity Type 3: Immune Complex-mediated diseases

A

Stevens-Johnson Syndrome, Sjogren’s Syndrome, Peripheral Ulcerative Keratitis, Scleritis

(Triple S PUK)

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12
Q

Hypersensitivity Type 4: Delayed Hypersensitivity diseases

A

Giant Papillary Conjunctivitis, Vernal Keratoconjunctivitis, Atopic Keratoconjunctivitis, Sympathetic Ophthalmia, Phlyctenulosis, Contact Dermatoblepharitis, Graft Rejection

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13
Q

Hypersensitivity Type 5: Stimulatory diseases

A

Thyroid-related Eye Disease

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14
Q

Acute course

A

Sudden-onset and limited duration

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15
Q

Recurrent course

A

Repeated episodes separated by periods of inactivity WITHOUT treatment ≥ 3 months in duration

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16
Q

Chronic course

A

Persistent Uveitis with relapse in < 3 months after DISCONTINUING treatment

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17
Q

Worsening activity

A

2-step increase in level of inflammation OR

increase from Grade 3+ to 4+

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18
Q

Improved activity

A

2-step decrease in level of inflammation OR decrease from Grade 1+ to 0

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19
Q

Anterior Chamber Cells Classification

A

Marker of activity

0: <1
0.5+/trace: 1-5
1+: 6-15
2+: 16-25
3+: 26-50
4+: >50

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20
Q

Anterior Chamber Flare Classification

A
  • Not a marker of activity
  • Protein transudation due to breakdown of the B-O-B
0: None
1+: Faint
2+: Moderate (Iris and Lens details CLEAR)
3+: Marked (Iris and Lens details HAZY)
4+: Intense (Fibrin or Plasmoid Aqueous)
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21
Q

Vitreous Flare Classification

A

0: None
1+: Hazy RNFL details (Clear details of the Optic Disc and Vessels)
2+: Hazy details of the Optic Disc and Vessels
3+: Only the Optic Disc is visible
4+: Optic Disc NOT visible

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22
Q

Granulomatous Morphology

What size of KP?
Nodules?
Severity?

A
  • Large mutton fat KPs
  • With Busacca, Koeppe and Berlin nodules
  • Usually chronic and severe
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23
Q

Large and mutton-fat keratic precipitates are made up of what?

A

Macrophages and Giant Cells

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24
Q

Infectious etiologies of granulomatous uveitis

A

TTT Fudge Lasang Herpes Siya

TB, Syphilis, Toxoplasma, Toxocara, Herpes, Fungal, Leprosy

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25
Q

Non-Infectious etiologies of granulomatous uveitis

A

(Very sterile sterile man)

VKH, SO, Sarcoidosis, Masquerade

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26
Q

Non-Granulomatous morphology size?

A

Small to medium-sized Keratic Precipitates

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27
Q

Small to medium-sized Keratic Precipitates are made up of what?

A

PMNs (Neutrophils) & Lymphocytes

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28
Q

Diseases with red eyes

A

JIA-associated Uveitis, Fuchs Heterochromic Iridocyclitis, Posner-Schlossman Syndrome, Intermediate, Posterior uveitis

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29
Q

Uveitic diseases with hypopyon

A

Behçet’s Disease, HLA-B27-associated Uveitis, Herpes Zoster/Herpes Simplex Keratouveitis, Toxoplasmosis, Toxocariasis, Masquerade (Endophthalmitis, Retained IOFB)

(TT HHMB)

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30
Q

Differential of broad based posterior synechiae

A

Tuberculous uveitis

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31
Q

Occlusio Pupillae

A

membrane covering the entire pupil

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32
Q

Iris BombĂŠ

A

Anterior bowing of the Iris due to a pupillary block from either an occlusio or seclusio pupillae

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33
Q

Seclusio Pupillae

A

360-degree posterior synechiae

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34
Q

Location of Busacca nodules

A

Iris stroma

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35
Q

Location of Koeppe nodules

A

Pupillary border

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36
Q

Location of Berlin nodules

A

Angle

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37
Q

What are keratic precipitates?

A

Collection of inflammatory cells at the Corneal Endothelium

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38
Q

Stellate KP differentials

A

“HIT”

Intraocular Viral Infections (i.e. Herpes)
Toxoplasmosis
Fuchs Heterochromic Iridocyclitis

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39
Q

Etiologies of Band Keratopathy and Treatment

A 
Chronic Inflammation (i.e. Childhood Chronic Iridocyclitis)
Silicone Oil in Aphakic patients
Hypercalcemia
Hyperphosphatemia
Hereditary
Exposure to Mercurial vapors

Tx: EDTA

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40
Q

What is a band keratopathy and where is it located?

A

Deposits of calcium in Bowman’s layer

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41
Q

What comprises snowballs?

A

Epithelioid Cells and Giant Cells

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42
Q

What is a snowbank?

A

Accumulation of a FIBROGLIAL MASS over the Pars Plana and adjacent Retina; can have vessels crossing over it

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43
Q

MOST COMMON cause of decreased vision in Intermediate Uveitis in adults

A

Cystoid Macular Edema

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44
Q

MOST COMMON cause of decreased vision in Intermediate Uveitis in children

A

Optic disc edema

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45
Q

Diseases causing perivascular sheathing of arterioles

A

ARN, Toxoplasmosis

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46
Q

Diseases causing perivascular sheathing of venules

A

CMV

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47
Q

Entity causing candlewax drippings

A

Sarcoidosis

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48
Q

4 entities causing Retinitis + Vasculitis

A

Behçet’s, HSV, VZV, CMV

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49
Q

Disease causing geographic choroiditis + retinitis

A

TB

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50
Q

Diseases causing choroiditis + exudative RD

A

VKH, SO, CSCR

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51
Q

Give baseline uveitic workup

A 
CBC w/ Platelet &amp; Differential Count
ESR, CRP
Chest X-Ray, PPD, Quantiferon Gold, GeneXpert 
VDRL/RPR, FTA-ABS
Urinalysis
FBS, AST, ALT, Crea
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52
Q

Special test to request for ankylosing spondylitis?

A

Sacroiliac Joint X-Ray

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53
Q

Special test to request for Granulomatosis with Polyangiitis?

A

c-ANCA (Proteinase 3)

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54
Q

Special test to request for Polyarteritis Nodosa?

A

p-ANCA (Myeloperoxidase)

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55
Q

Special tests to request for Viruses, Toxoplasma, Toxocara?

A

PCR of Intraocular Fluid/serum antigenemia

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56
Q

Special tests to request for Sarcoidosis?

A

Serum Angiotensin Converting Enzyme (ACE), Lysozyme, Kveim Test, Gallium scan, Chest CT-Scan

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57
Q

Why should steroids be given in the morning between 6-10AM?

A

To mimic the normal diurnal cycle and reduce the risk of adrenal suppression

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58
Q

What is the ideal glucocorticoid?

A

No mineralocorticoid activity

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59
Q

Complication if steroid dose decreased too quickly

A

Adrenal crisis

60
Q

Steroids causing less IOP increasing effects?

A

Fluorometholone, Rimexolone, Loteprednol

61
Q

Common side effects of steroids

A
  • Increase in IOP: mainly caused by outflow resistance

- Cataract formation: Posterior Subcapsular type

62
Q

Absolute indications of IMT

A
  • Behçet’s Disease
  • Vogt-Koyanagi-Harada Disease
  • Sympathetic Ophthalmia
  • Necrotizing Scleritis
  • Rheumatoid Sclerouveitis
  • Granulomatosis with Polyangiitis
  • Polyarteritis Nodosa
  • Relapsing Polychondritis
63
Q

Relative Indications of IMT

A
  • Intermediate Uveitis (esp. in children)
  • Chronic Iridocyclitis
  • Birdshot Chorioretinopathy
  • Serpiginous Choroidopathy
  • Multifocal Choroiditis and Panuveitis
  • Juvenile Idiopathic Arthritis associated Uveitis
64
Q

Steroids: Start ___, then ____

A

Start HIGH, then taper

65
Q

IMTs: Start ____, then ____

A

Start LOW, then increase in dose

-Given concurrently with steroids because full effects are seen within 2-3 weeks from intake

66
Q

Antimetabolites and side effects

A
  • Methotrexate: Hepatotoxicity
  • Azathioprine: Hepatotoxicity and GI upset
  • Mycophenolate Mofetil: GI upset
67
Q

T Cell Signalling Inhibitors and side effects

A
  • Cyclosporine: Nephrotoxicity and HTN
  • Tacrolimus: Nephrotoxicity and HTN
  • Sirolimus: GI upset
68
Q

Alkylating agents and side effects

A
  • Cyclophosphamide: HEMORRHAGIC CYSTITIS, MYELOSUPPRESSION, STERILITY, BLADDER CA
  • Chlorambucil: MYELOSUPPRESSION, STERILITY, INCREASED RISK OF CA
69
Q

Biologics and side effects

A
  • Infliximab: TB REACTIVATION, MALIGNANCY

- Rituximab: NEUTROPENIA

70
Q

Treatment options for Cataract with No flare; Few Posterior Synechiae

A

Phaco, CCC, Acrylic IOL in the bag

71
Q

Treatment options for Cataract with (+) Flare; >270-degree Posterior Synechiae

A

Pars Plana Lensectomy, Aphakic

72
Q

Treatment options for JIA associated cataract

A

IMT, Phaco, +/- Acrylic IOL in the bag

73
Q

How long should pre-treatment be done for cataract surgery?

A

3-6 months

74
Q

When does exacerbation of inflammation post-op start?

A

3 days post-op

75
Q

3 main complications of cataract sx post-op

A

Moderate anterior chamber reaction, hyphema, ocular hypertension

76
Q

3 uses of atropine

A

(1) Decreases pain from ciliary spasm
(2) Prevents formation of posterior synechiae
(3) Stabilizes the blood-ocular barrier

77
Q

MOST COMMON known cause of Acute Anterior Uveitis

A

HLA-B27 Associated anterior uveitis

78
Q

HLA-B27 Associated anterior uveitis

More common in males or females?

____ Decade of life

A

Male predominance; 2nd-5th decade of life

79
Q

Finding on sacroiliac xray of Ankylosing Spondylitis

A

Bamboo-spine deformity

80
Q

Symptoms of Inflammatory LBP of ankylosing spondilitis

A
  1. ) Morning stiffness > 30 minutes
  2. ) Improvement of back pain with exercise but not with rest
  3. ) Awakening from back pain during the second half of the night only
  4. ) Alternating buttock pain
81
Q

Ankylosing Spondylitis: RF positive or negative?

A

Negative

82
Q

Reactive Arthritis/Reiter’s Disease findings

A

Can’t See (Conjunctivitis, Iritis, Keratitis), Can’t Pee (Urethritis), Can’t Climb a Tree (Arthritis)”

Other major findings: Keratoderma blenorrhagicum,
Balanitis circinata

83
Q

Inflammatory Bowel Disease signs

A

Anterior Uveitis, Conjunctivitis, Peripheral Ulcerative Keratitis, Episcleritis/Scleritis, Vitritis, Retinal Vasculitis

84
Q

What is the cause of HTN uveitis?

A

Due to Trabeculitis or PAS formation

85
Q

3 Conditions with HTN uveitis

A
  1. Fuchs Heterochromic Iridocyclitis
  2. Posner-Schlossman Syndrome
  3. Herpetic Uveitis (HSV, VZV, CMV)
86
Q

FUCHS HETEROCHROMIC IRIDOCYCLITIS

A

(+) Formation of abnormal vessels in the anterior chamber angle (fine & fragile)

  • Diffuse white stellate KPs
  • Mild Anterior chamber cellular reaction
  • Mild increase in IOP
  • Diffuse Iris stromal atrophy
  • NO Posterior synechiae formation
  • +/- Vitritis
  • Cataract formation is common
87
Q

Hyphema formation during intraocular surgery

A

AMSLER- VERREY SIGN

88
Q

Treatment for FHI

A

Steroids, anti-glau (Avoid PGA), cataract sx

89
Q

Posner Schlossman Syndrome pathology

A

Glaucomatocyclitic process

90
Q

Posner Schlossman Syndrome presentation

A
  • Unilateral, recurrent attacks of markedly elevated IOP and very mild anterior chamber cellular reaction
  • NO posterior synechiae formation or posterior segment involvement
91
Q

Treatment for Posner Schlossman Syndrome

A
  • Topical Corticosteroids
  • Topical Anti-glaucoma medications (PGAs are avoided)
  • Surgical intervention if indicated
92
Q

Herpetic anterior uveitis presentation

A
  • Iritis, Iridocyclitis, Keratouveitis
  • Stellate KPs at Arlt’s triangle
  • Diffuse/sectoral iris atrophy
93
Q

Hutchinson Sign

A
  • Indicate Nasociliary nerve involvement and a greater likelihood that the eye will be affected
  • In VZV keratouveitis

Tx:
HSV & VZV:
-Oral Acyclovir 400mg 5x/day - HSV; 800mg 5x/day - VZV

-Oral Valacyclovir 500mg 3x/day - HSV; 1g 3x/day - VZV

  • Oral Acyclovir (as maintenance for chronic & recurrent
    cases) - 800mg/day

-Topical Corticosteroids, Topical Mydriatic-Cycloplegic

94
Q

CMV Anterior Uveitis presentation and treatment

What is the pattern of the KPs?

Topical, oral, intravitreal tx?

A

Endotheliitis (KPs form a coin-shaped pattern)

TX:
-Topical Ganciclovir gel - recommended first-line treatment;
-Topical Corticosteroids
-Oral Valganciclovir 900mg 2x/day for 6 weeks, then
maintained at 450mg 2x/day
-Intravitreal Ganciclovir

95
Q

Treatment of herpetic anterior uveitis

A
  • Epithelial: Topical Anti-viral + Oral Prophylaxis (BID)
  • Stromal/Endothelial: Topical Anti-viral + Topical Corticosteroids + Oral Prophylaxis (BID) + Topical Cycloplegics
  • Keratouveitis: Topical Anti-viral + Topical Corticosteroids + Oral Acyclovir (400mg 5x/day for HSV; 800mg 5x/day for VZV) + Topical Cycloplegics
96
Q

Juvenile Idiopathic Arthritis-associated Uveitis risk factors

A
  • Pauciarticular or Oligoarticular type of JIA (≤ 4 joints involved) -RF negative, ANA positive
  • Female predilection
  • Younger age of onset of Arthritis (< 5 years old)
97
Q

Juvenile Idiopathic Arthritis-associated Uveitis most common presentation

A

Chronic iridocyclitis

98
Q

Complications of JIA

A
  • Band Keratopathy
  • Posterior Synechiae formation
  • Cataract formation
  • Glaucoma or Hypotony
  • Macular Edema
99
Q

Screening for JIA should be done every ____ months

A

Every 2 months from onset of arthritis, for 6 months

100
Q

JIA Treatment

A
  • Topical or Periocular Corticosteroids (Systemic if severe)
  • Topical Cycloplegics
  • IMTs (Methotrexate, Azathoprine, Mycophenolate mofetil, Cyclosporine)
  • Cataract surgery for visually significant cataracts (3 months quiet)
101
Q

Scleritis commonly associated with _____

Predominance?

A

Systemic vasculitides
(Rheumatoid Arthritis, SLE, GPA, PAN, Relapsing Polychondritis)

Female

102
Q

New name of Wegener’s Granulomatosis

A

Granulomatosis with Polyangiitis (GPA)

103
Q

Triad of GPA

A
  1. ) Necrotizing Granulomatous vasculitis of the upper and lower respiratory tract
  2. ) Focal Segmental Glomerulonephritis
  3. ) Necrotizing vasculitis of small arteries and veins

(+) c-ANCA

104
Q

Polyarteritis Nodosa most common symptom

A 
Mononeuritis Multiplex
(Weight loss (> 4kg), Livedo reticularis, Testicular pain,
Increased Diastolic BP, (+) Hepatitis B infection)

(+) p-ANCA

105
Q

Most common symptom of scleritis

A

Severe boring pain

106
Q

Hue of scleritis and episcleritis

A

Scleritis: Bluish purple due to deep vascular involvement

Episcleritis: Bright red hue

DOES NOT BLANCH with 10% Phenylephrine instillation

107
Q

Types of anterior scleritis

A
  • Non-Necrotizing - Nodular (localized)
  • Non-Necrotizing - Diffuse (extensive)
  • Necrotizing - Extreme pain and tenderness; severe vasculitis with scleral thinning
  • Scleromalacia Perforans-painless; avascular sclera; scleral thinning
108
Q

Posterior scleritis presentation

What sign on ocular UTZ?

A

Thickening of the sclera posterior to rectus muscle insertions

“T-sign” on Ocular Ultrasound (retrobulbar edema surrounding the Optic Nerve)

109
Q

Tx of anterior scleritis

A

Anterior Non-Necrotizing - Diffuse: Oral NSAIDs, Topical/Oral Corticosteroids

Anterior Non-Necrotizing - Nodular, Anterior Necrotizing & Posterior Scleritis: Oral Corticosteroids with IMT (Cyclophosphamide, Azathioprine)

110
Q

Intermediate uveitis: unilateral or bilateral?

A

Bilateral

111
Q

What haplotype is associated with intermediate uveitis?

A

HLA DR15

112
Q

Primary complaint of intermediate uveitis and cause?

A

BOV and/or floaters due to vitritis and CME

113
Q

What are always present in intermediate uveitis?

A

Vitreous cells in vit and peripheral retina

114
Q

Other manifestations of intermediate uveitis?

A

Snowballs and vitreous flare

115
Q

Exudate accumulation on the pars plana

A

Pars planitis

116
Q

Pars planitis

A

snowbank and snowball formation over the pars plana and ora serrata

117
Q

What comprises a snowbank formation and where is its location? How is it best seen?

A

Fibroglial mass

inferiorly

Scleral depression or 3-mirror gonioscopy to see neovascularizations

118
Q

Pars planitis compared to other intermediate uveitis:

Worse _____
More severe _____
Worse _____

A

Worse vitritis

More severe macular edema Worse prognosis

119
Q

How does vitreous hemorrhage occur in pars planitis?

A

Result of NVs from vitreous base, pars plana or peripheral retina, crossing over the formed snowbank extending through breaks in the Inner Limiting Membrane of the vitreous base

120
Q

4 Step Approach for intermediate uveitis

A
  1. Intravitreal or Periocular Corticosteroid injection (FIRST LINE) +/- Oral NSAIDs or Systemic Corticosteroids
  2. ) Pars Plana Cryotherapy or Transpupillary Thermotherapy
  3. ) Pars Plana Vitrectomy
  4. ) Immunomodulatory Therapy
121
Q

True or false: Topical Steroids are effective for phakic patients

A

False

122
Q

What is the first line drug of immunomodulators for IU and indication?

A

Cyclosporine for those who are resistant to corticosteroid therapy or require chronic corticosteroid treatment

123
Q

Other name for VOGT-KOYANAGI-HARADA SYNDROME?

A

Uveomeningitis

124
Q

VKH pathology?

A

Systemic, autoimmune disease where the main targets are the melanin- containing cells of the eyes, ears, meninges, skin

125
Q

VKH is a bilateral, chronic, ______ panuveitis with ________ involvement

A

Bilateral, chronic, granulomatous panuveitis with choriocapillaris involvement

126
Q

Male or female predilection for VKH?

Which decade of life?

A

Female

20-40

127
Q

Systemic manifestations:
Meninges: _____
Ears: ______
Skin:______

A

Meninges: Headache, orbital pain, stiff neck (CSF pleocytosis)

Ears: Auditory deficits

Skin: Vitiligo (60-65%), Poliosis (80-90%), Alopecia (70-75%), should not precede the onset of the ocular manifestations

CHECK AXILLA

128
Q

Ocular manifestation of VKH

A
  • Acute granulomatous manifestation with mutton fat KPs and iris nodules
  • ON swelling
  • Exudative non rhegmatogenous detachment
  • Dalen Fuchs nodules (Nummular chorioretinal depigmented scars)
  • Sunset glow fundus
  • Sugiura’s sign
129
Q

Perilimbal vitiligo in VKH

A

Suguira’s sign

130
Q

Cause of sunset glow fundus?

A

Chorioretinal depigmentation from RPE loss & perturbation

131
Q

Phases of VKH

A

Prodromal, acute uveitic, convalescent, chronic recurrent

132
Q

Prodromal phase clinical features

A

Headache, Fever, Nausea, Vomiting, Meningismus, Vertigo, Auditory Disturbances, Sensitivity of Skin or Scalp to touch (Hyperesthesia), CSF Pleocytosis

133
Q

Acute uveitic phase clinical features

A

Sudden-onset bilateral granulomatous panuveitis, multiple focal serous retinal detachments, choroidal thickening, optic disc edema

134
Q

Convalescent phase clinical features

A

Ocular: Perilimbal Depigmentation (Sugiura Sign), Chorioretinal Depigmentation (Sunset Glow Fundus), Nummular Chorioretinal Depigmented Scars; Systemic: Vitiligo, Poliosis, Alopecia

135
Q

Chronic Recurrent

A

Complications: Cataract, Posterior Synechiae, Glaucoma, Band Keratopathy, RPE proliferation, Subretinal Fibrosis, CNVM formation

136
Q

Diagnostic criteria: Early manifestations of VKH

A
  1. Evidence of diffuse Choroiditis (Focal areas of Subretinal Fluid or Bullous Serous RD)
  2. Both of the following (if with equivocal fundus findings)

a.) Fluorescein Angiography:
Focal areas of delay in choroidal perfusion > Multifocal areas of pinpoint leakage > Large placoid areas of Hyperfluorescence > Pooling within Subretinal Fluid > Optic Nerve Staining

b.) Ultrasonography: Diffuse choroidal thickening WITHOUT evidence of Posterior Scleritis

137
Q

Diagnostic criteria: Late manifestations of VKH

A
  1. History suggestive of prior presence of findings from 3A and either both 2 &3 below,
    or multiple signs from 3
  2. Ocular Depigmentation: Sunset Glow Fundus or Sugiura’s Sign
  3. Other Ocular Signs: Nummular Chorioretinal Depigmented Scars, RPE Clumping or migration, Recurrent or chronic anterior uveitis
138
Q

Differentials of VKH

A

Non-Infectious
-Sympathetic Ophthalmia (SO), Behçet’s Disease (BD), Sarcoidosis, Central Serous Chorioretinopathy (CSCR), Retinochoroidal mass (i.e. Retinoblastoma, Lymphoma)

Infectious
-Tuberculosis, Syphilis, Bartonellosis

139
Q

Treatment for VKH

A

High dose systemic corticosteroids - MAINSTAY

Early treatment (about 2-3 weeks from onset of symptoms), 1-1.5 mg/kg/day

Maintained for 2-4 weeks then tapered gradually and maintained for at least 6 months

Others:
Topical corticosteroids, cycloplegics, IMTs

140
Q

When can sympathetic ophthalmia occur?

A

Within 1 year

141
Q

Part that is spared in sympathetic ophthalmia?

A

Choriocapillaris

This is due to production of anti-inflammatory
molecules by the RPE > TGF-β & RPE protective protein > suppress generation of superoxides by phagocytes

142
Q

4 Initial symptoms of SO

A
  1. Photophobia
  2. Decreased accommodation
  3. Redness
  4. Pain
143
Q

Treatment for SO

A
  1. High-dose systemic corticosteroids for 3 months - FIRST LINE; tapered over the next 3-6 months
  2. Immunomodulatory therapy 3. Enucleation > Evisceration
144
Q

Differentiate SO and VKH

A

VKH

  • No history of trauma or surgery
  • Plasma cells observed

SO

  • History of trauma or surgery
  • Plasma cells observed
  • Sparing of choriocapillaris
145
Q

Characteristic of Behcet’s Disease

A

Obliterative/occlusive vasculitis involving both arteries & veins

Ophthalmology OPEX (1 decks)

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