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Ophthalmology > 8 - Uveitis > Flashcards

8 - Uveitis Flashcards

1
Q

What are the 3 ways to classify uveitis?

A
  1. Anatomical classification based on primary site of inflammation
    a) anterior (anterior chamber) - iritis, iridocyclitis, anterior cyclitis
    b) intermediate (vitreous) - pars planitis, posterior cyclitis
    c) posterior (choroid or retina) - retinitis, choroiditis, retinal vasculitis, chorioretinitis, neuroretinitis
    d) paneveitis - involves all layers
  2. Etiology of inflammation

a) infectious
- bacterial
- viral
- fungal
- parasitic

b) non-infectious
- idiopathic
- w. a known systemic association

c) masquerade
- neoplastic
- non-neoplastic

  1. Timing of “
    - Onset
    a) sudden
    b) insidious
  • Duration
    a) limited
    b) persistent
  • Clinical course
    a) acute
    b) chronic
    c) recurrent
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2
Q

What is uveitis?

A

the inflammation of the uvea, which is the middle vascular layer of the eye, just beneath the sclera.

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3
Q

What is the step-by-step approach to uveitis? (flow chart)

A
  1. Pt hx
    - pain characteristics
    - fam hx
    - contact w/ infective patients or wild animals
    - travels to exotic places
  2. Ocular exam (slit lamp) –> of anterior and posterior segment of eye –> for anatomical classification of uveitis
  3. Once you know if it is infectious,
    autoimmune or non-infectious, –> Additional lab and instrumental work-up, with treatment response –> to understand etiology and hence reach
    a definitive diagnosis.
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4
Q

What is anterior uveitis & what are the 2 types?

A

inflammation of anterior uveal tract –> iris and anterior part of ciliary body (pars plicata).
most common and most unspecific form of uveitis. (children & adults)

  1. acute (AAU)
    - most common
    - rapid unilateral photophobia, pain, blurry vision, watery discharge
    - classic sign = red, painful eye with small pupil
  2. chronic (CAU) anterior uveitis
    - much slower and gradual symptoms → the absence of symptoms (white eye) –> leads to detection of a COMPLICATION AS A 1ST SIGN of uveitis (cataract, glaucoma, band keratopathy).
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5
Q

What are the various presentation of anterior uveitis? (seen at slit lamp exam)

A
  1. Conjunctival/ciliary injection
  2. Keratin precipitates
  3. CA inflammation (anterior chamber)
  4. Fibrinous exudate/ Hypopyon
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6
Q

Anterior uveitis must be divided into _________ & non-_________ to define the ______ & assess the ______.

A

granulomatous
non-granulomatous
cause
severity

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7
Q

Which is more severe & which is more frequent? (anterior non-granulomatous vs anterior granulomatous uveitis)

A

more severe = granulomatous

more frequent = non-“

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8
Q

What is the clinical presentation of anterior granulomatous uveitis?

A
  • thicker keratic precipitates
  • fatty-like deposits
  • nodules in the pupil sphincter and in the iris stroma.

When unilateral –> usually assoc. to Herpes Viruses –> many diff manifestations and

Toxoplasma –> typical retinal lesion easy to identify; when bilateral it is usually assoc with Sarcoidosis, Tuberculosis and Syphilis.

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9
Q

What is the clinical presentation of anterior non-granulomatous uveitis?

A

keratic precipitates, anterior chamber flares and cells,
hypopyonand synechiae4

. When unilateral it is usually associated with HLA-B27-related uveitis, when

bilateral5
it is usually associated with autoimmune diseases.

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10
Q

In order to see the posterior part of the eye, you need to dilate the ______

A

FUNDUS

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11
Q

What is the laboratory work-up for anterior uveitis? (AU)

A

is tailored to each patient and directed by clinical features

  1. HLA: tissue typing to look for HLA-B27 (cell
    surface protein with peptides to T cells)
  2. MRI of the sacroiliac region if patients have
    some kind of inflammatory pain (meaning the
    feeling of rigidity and immobility)
  3. Serology for sarcoidosis, tuberculosis, Herpetic viruses, syphilis and Toxoplasma.
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12
Q

Treatment of anterior uveitis (AU).

A

aim = stop inflammation.

  • AAU: corticosteroid drops + cycloplegics or
    mydriatics (by dilating the iris ciliary body, decrease stress & inflammation).

Initial treatment –> strong + aggressive to cut off the inflammatory reaction –> gradually lower the treatment.

(If you don’t start off aggressive, then you’ll have a low-grade inflammation that will keep on relapsing → be aggressive to avoid recurrency.)

Mydriatic agents –> needed to dilate the pupil preventing posterior synechiae

  • give maintenance therapy when recurrencies are v frequent, or when they are causing
    complications
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13
Q

What is juvenile idiopathic arthritis (JIA) uveitis?

A

= Autoimmune arthritis of unknown etiology typical of children < 16 y.o
- it persists for at least 6 weeks.
- chronic uveitis
- classified into oligoarticular / polyarticular / systemic according to the extent of joint involvement during
the first 6 months.
- most common systemic dx associated to childhood AU

(probability for JIA pt to develop
uveal complications is indirectly related to extent of joint inflame)

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14
Q

Treatment of juvenile idiopathic arthritis (JIA) uveitis

A

must be very aggressive, and recurrency is frequent when it starts in the eye

  • Steroid drops –> but they speed up cataract (complication), so need systemic therapy or kids might develop cataract
  • Another complication = glaucoma, may also be caused by steroid drops –> alter the distribution
    of the trabecular meshwork.
  • If after 3 weeks –> no increase in the intraocular pressure, you won’t have glaucoma dev, but still have risk of dev cataract.
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15
Q

What is viral anterior uveitis caused by?

A 
Herpes simplex virus -- a neurotropic virus, travels through nerves into the eye and may cause
corneal problems (corneal keratitis) or anterior uveitis or retinitis.
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16
Q

How is viral anterior uveitis diagnosed?

A
  • diagnosis –> based on clinical appearance.
  • Serology usually confirms viral infection, but rarely an active stage of disease.
  • If it seems very relapsing –> tap the anterior
    chamber with a needle, aspirate some liquid and do a PCR to see if we find some viral RNA.
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17
Q

Therapy of viral anterior uveitis.

A

Depending on the severity of the disease you can use antivirals.
Treatment is differentiated based on the extent of the infection:

1) If it is intraocular, only anterior, without epithelial involvement, it is considered as an immune-
mediated reaction and treated with topical corticosteroids, cycloplegics and hypotensive meds (if

pressure is high)
2) If the inflammation is severe as a first line is used topical ganciclovir, and as a second line is used
systemic valganciclovir.

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18
Q

What is Fuchs uveitis?

A
  • unilateral, chronic
  • characterized by a stellate deposition of pigmented epithelium precipitate
  • very low-grade inflammation
  • heterochromia iridis/ iris atrophy, loss of eyes’ color
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19
Q

Treatment of Fuchs uveitis.

A

Rarely need to treat them, bc treatment would cause more complications than the dx.

Only treatment = managing the two major complications –> cataract and glaucoma.

20
Q

What is intermediate uveitis (IU)?

A
  • chronic, relapsing dx
  • insidious onset
  • vitreous = primary site of inflammation.

can be:

  1. idiopathic (called Pars Planitis)
  2. assoc to a systemic dx (multiple sclerosis, sarcoidosis, Lyme disease, Syphilis, TB).
21
Q

What are the 2 types of intermediate uveitis (IU)?

A

can be:

  1. idiopathic (called Pars Planitis)
  2. assoc to a systemic dx (multiple sclerosis, sarcoidosis, Lyme disease, Syphilis, TB).

The diagnosis is CLINICAL.
❖ Pars Planitis –> typical snow banking and/or snowball formation

❖ Associated with systemic disease
➔ Serology for granulomatous uveitis
➔ Investigation for multiple sclerosis
(intermediate uveitis may precede other symptoms of demyelination)

Multiple sclerosis suspected –> esp women 20-50, and in case of suspicion –> perform cranial MRI

22
Q

Treatment of intermediate uveitis (IU).

A

STEROIDS

a. Intraocular steroids –> intraocular slow-release dexamethasone –> prevents
many complications of systemic corticosteroids.

b. Systemic steroids –> consider contraindications and potential adverse effects: osteoporosis, hypertension, diabetes etc → to avoid these give a fast and
intense systemic steroid therapy followed by another immunosuppressor –> saves pt from steroid dependency.

  • Intermediate uveitis responds pretty well to ADALIMUMAB (subcutaneous monoclonal antibodies).
  • For severe and resistant vitreous inflammation –> may need pars plana vitrectomy
23
Q

What is posterior uveitis (PU)?

A
  • most severe forms of uveitis
  • lesions on the retina and on the choroid.
  • encompasses: retinitis, choroiditis and retinal vasculitis.
  • lesions may originate primarily in retina or choroid but often both are involved (retinochoroiditis and chorioretinitis).

▪ Granulomatous pavuveitis
▪ Predominant retinal vascular component
▪ Herpetic retinitis
▪ Idiopathic inflammatory chorioretinopathies

Investigated w/

  • fluorescein angiography (FA)13
  • indocyanine green angiography (ICG).
24
Q

What are the 2 investigations for posterior uveitis (PU)? Explain each.

A
  1. Fluorescein angiography FA
    - fluorescent dye is bound to serum proteins, the dye diffuses only through fenestrated choriocapillaris, Bruch’s membrane or damaged ocular tissue.
    - Hypofluorescence – indicate blockage or vascular filling defect.
    - Hyperfluorescence can indicate windows defects,
    leakage, pooling, staining or abnormal retinal/choroidal vessels.
    - FA signs of uveitis: papillitis, vascular retinal staining, vascular retinal leakage, cystoid macular edema,
    inflammation of retinal capillaries, peripheral retinal vasculitis.

(Occlusive vasculitis seen in
cytomegalovirus infection)
- FA allows to define the location & extension of posterior inflammation
- Generally FA patterns are not diagnostic or pathognomonic of a specific dx

  1. Indocyanine green angiography ICG
    - ICG molecule is almost completely bound to large proteins (lipoproteins).
    - In the choroid it slowly leaks from fenestrated choriocapillaris –> ICG- protein complex is then slowly reabsorbed in circulation.
    - As the ICG remains entrapped in choroid –> a background fluorescence can be seen.
    - +ve of ICGA = thanks to its wavelength it can go deeper compared to FA –> the choroid can be observed to look for inflam & changes, also retinal tumors filling
    - ICG fluorescence is distributed by choroidal inflammatory lesions, only major vessels cause ICG to leak out from retinal vessels.
    - Diseases seen w/ ICGA = white dot syndromes (aka choriocapillaropathies)

➔ FA ↔ retinal angiography. IGC ↔ choroidal angiography

25
Q

What are white dot syndromes (choriocapillaropathies)?

A

= inflammatory diseases characterized by the presence of white dots on the fundus,

  • due to early absence of perfusion of the choriocapillary layer.
  • appreciated just for the few initial days –> then the filling of the background causes diffused hyperfluorescence.
  • are differentiated from the stromal choroiditis (another disease which can be seen with ICGA) bc it follows the large vessels patterns, so the foci are much deeper.
26
Q

What is sympathetic ophthalmia?

A
27
Q

What is Tuberculosis uveitis?

A
28
Q

What are the intraocular signs of Tuberculosis uveitis?

A
29
Q

What are the investigations done for Tuberculosis uveitis?

A
30
Q

What is sarcoidosis uveitis?

A
31
Q

What are the intraocular signs of sarcoidosis uveitis?

A
32
Q

Treatment of sarcoidosis uveitis.

A
33
Q

What is Syphilis uveitis? Diagnosis? Intraocular signs?

A

=

Diagnosis –>

34
Q

What is Toxoplasmosis uveitis?

A
35
Q

What are the 3 forms of Toxoplasmosis uveitis?

A
36
Q

What are the ocular signs of Toxoplasmosis uveitis?

A
37
Q

What is the typical lesion in Toxoplasmosis uveitis?

A
38
Q

Treatment of Toxoplasmosis uveitis.

A
39
Q

What is Vogt-Koyanagi-Harada?

A
40
Q

What are the 4 phases of Vogt-Koyanagi-Harada?

A
41
Q

What is the differential diagnosis b/w Vogt-Koyanagi-Harada (VKH) & sympathetic ophthalmia ?

A
42
Q

Treatment of Vogt-Koyanagi-Harada (VKH).

A
43
Q

What is Herpetic retinitis?

A
44
Q

What are the 3 types of Herpetic retinitis?

A
45
Q

What is Adamantiades-Behcet’s disease (ABD)? Key pathogenic component? Therapy?

A

Ophthalmology (12 decks)

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