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OD3 (S1&2) > DIS - Posterior Uveitis I - Week 4 > Flashcards

DIS - Posterior Uveitis I - Week 4 Flashcards

1
Q

Define posterior uveitis (4).

A

Inflammation posterior to the vitreous base
-choroid
-choroid and retina
-vitreous
-possible accompanying anterior uveitis

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2
Q

What are the two classifications of posterior uveitis? How does this change the relevancy of chronic vs acute? Explain.

A

Active vs resolved
Most posterior uveitis is chronic or slow moving
-acute vs chronic is less relevant

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3
Q

List the two main types of posterior uveitis by cause.

A

Infectious
Distinct inflammatory disorders of uncertain aetiology

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4
Q

List the four classifications of infectious posterior uveitis. Give at least three examples for each.

A

Viral
-CMV, HSV, HZV, rubella
Bacterial
-syphilis, TB, strep/staph, lyme
Fungal
-candida, aspergilla, histoplasmosis, crptococcus
Parasitic
-toxoplsmosis, toxocara, onchocerciasis

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5
Q

Is diagnosis of posterior uveitis easy or difficult?

A

Often difficult

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6
Q

List three ocular causes of unifocal chorioretinitis.

A

Toxoplasmosis
Toxocara
Candida

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7
Q

List four ocular causses of diffuse chorioretinitis.

A

CMV
ARN
PORN

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8
Q

What are the four aims of assessing a patient with posterior uveitis?

A

Diagnose the ocular condition
Diagnose the systemic condition
Diagnose the cause of visual loss
Management - referral/treatment

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9
Q

What is the main role of optometry in posterior uveitis?

A

Mainly detection and appropriate referral

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10
Q

What is intermediate uveitis? Is it generally acute or chronic?

A

Pars planitis
-chronic

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11
Q

Does pars planitis have a common HLA error like other forms of uveitis?

A

No

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12
Q

In what four ways does pars planitis differ from other forms of uveitis (aside from HLA)?

A

Bilateral in 95%
Different inflammatory cells involved
Limited ciliary body inflammation
Few, if any, systemic associations

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13
Q

What are three possible systemic associations of pars planitis?

A

MS
Sarcoidosis
Syphilis

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14
Q

List three symptoms of pars planitis. Note the most dominant first.

A

Floaters
Blurred vision
Reduced VA
-if CMO is present

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15
Q

List three signs of pars planitis.

A

Exudation in to the vitreous
-cells in the vitreous
Small gelatinous snowballs/cottonballs
Grey/white plaque snow banking

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16
Q

Where are small gelatinous snowballs/cottonballs generally seen in pars planitis?

A

Inferior vitreous

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17
Q

Where is grey/white snow banking generally seen in pars planitis? What is it? What is needed to see it?

A

Overlying inferior pars plana
Is a fibroglial membrane
Only seen with scleral depression
-unless very extensive

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18
Q

What kind of diagnosis is pars planitis?

A

Diagnosis of exclusion

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19
Q

List at 7 differential diagnoses for pars planitis.

A

Sarcoidosis
Lymphoma
Infectious posterior uveitis
Behcets disease
VKH
Exudative vitreoretinopathy
Retinoblastoma

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20
Q

List four labs tests often used for exclusion in pars planitis.

A

ACE/chest Xray
CBC
FTA-ABS
Infection titres

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21
Q

What is the most common cause of infectious retinochoroiditis? What kind of organism is it?

A

Toxoplasmosis gondii
-protozoan

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22
Q

How does toxoplasmosis initially enter humans?

A

By crossing mucosal surfaces
-the gut

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23
Q

Which animal is the reservoir for toxoplasmosis and what is required for reproduction? How do they spread from this reservoir and in what form?

A

The cat
Feline intenstinal mucosa needed for reproduction
Resistant oocysts shed in faeces

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24
Q

List 5 common ways that toxoplasmosis is contracted.

A

Non-pasteurised milk
Transfusion/transplant
Poorly/partly cooked meat infected by cysts
Unwashed fruit
Cat faeces

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25
Q

describe congenital toxoplasmosis infections of the eye and the percentage risk of foetal infection. When is infection required for tis to occur? What type of foetal tissue is infected?

A

Occurs in non-immunised pregnant women
-is trans-placental
40% risk of foetal infection if the mother is infected just before conception or during pregnancy
Likes foetal neural tissue

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26
Q

List four foteal effects of congenital toxoplasmosis.

A

Stillbirth/spontaneous abortion
Multiorgan disability
Asymptomatic offspring but neurological/ocular sequelae later in life

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27
Q

Is post-natal acquired toxoplasmosis common or rare?

A

Rare allegedly

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28
Q

Note the two forms of toxoplasmosis gondii and whether or not they are infectious.

A

Trophozoites
-infectious
Cysts/oocysts
-non-infectious

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29
Q

Are trophozoites responsible for acute or chronic disease?

A

Acute

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30
Q

What are toxoplasmosis oocysts? Where do they concentrate (3) and what happens if they rupture?

A

Cysts containing many trophozoites
Concentrate in heart, muscle, neural tissue (including retinal)
If ruptured, leads to inflammation

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31
Q

Describe how txoplasmosis is able to persist in a reservoir animal host (4).

A

Survives stomach acids and invades gut wall
Cysts are impervious to host immune system/drugs
Bradyzoites live inside cells without killing or being killed by the host
Transmits to another host via faeces or when host is consumed by a predator
-cats eating rats, humans eating pork

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32
Q

When toxoplasmosis reaches the eye, what happens as the host immune system responds (3)? Is anything visible?

A

Organism converts to cyst form
Resistant to immune system
Chronic latent infection
Nothing visible

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33
Q

When toxoplasmosis reaches the eye and the host immune system response, what happens if for some reason the immune system declines (3)?

A

Cyst wall rupture, releasing organism
Fresh infection locus
Satellites with reactivation

34
Q

How does toxoplasmosis infections look once healed?

A

A chorioretinal scar

35
Q

Is acquired post-natal toxoplasmosis generally self-limiting or require urgent treatment (4)? Explain.

A

Generally is benign, self-limiting, subclinical, and asymptomatic

36
Q

In individuals with symptoms, list 6 symptoms of acquired post-natal systemic toxoplasmosis.

A

Flu-like illness
-lymphadenopathy
-fever
-malaise
-myalgia
-sore throat
-papillo-macular rash

37
Q

List three individuals who generally show symptoms of acquired post-natal systemic toxoplasmosis (6).

A

Adults without antibodies
-with cats
-farming
-unwashed vegetables
Pregnant women without antibodies
Immunocompromised
-HIV

38
Q

What does positive toxoplasmosis serology show? Will patients with other forms of uveitis be positive or negative?

A

Shows only previous exposure
Patients with other forms of uveitis will be positive

39
Q

What immunoglobin levels are elevated with acquired toxoplasmosis?

A

High IgM

40
Q

What percentage of systemic toxoplasmosis infections cause ocular toxoplasmosis?

A

1-3%

41
Q

Can the high incidence of toxoplasmosis infection in some countries (like Brazil) be explained by transplacental infection?

A

No

42
Q

What was found to be a cause of an acquired toxoplasmosis epidemic in southern India?

A

Contaminated drinking water

43
Q

What is the classical look of congenital ocular toxoplasmosis? What shape and colour does it have and where is it usually found?

A

An atrophic scar
Round/oval with pigmented edge
Often at/near the macula

44
Q

List 8 features of active ocular toxoplasmosis.

A

Satellite lesions near the scar
Cyst rupture
Fresh focus of necrotising retinochoroiditis
Vitreous
-cells/exudates
-damage
Retinal thickening
Cells in the anterior chamber
-mild anterior uveitis
Vasculitis with fresh infection
-frosted branch angiitis

45
Q

What is there a risk of with active ocular toxoplasmosis?

A

SRN

46
Q

Is congenital toxoplasmosis generally uni-or bilateral?

A

Can be bilateral

47
Q

Is acquired toxoplasmosis generally uni-or bilateral?

A

Usually unilateral

48
Q

Where are lesions typically found in acuired toxoplasmosis?

A

Distant from the fovea

49
Q

Is recurrence common or rare with toxoplasmosis?

A

Common

50
Q

How long does active ocular toxoplasmosis last?

A

1-2 months
-self-limiting

51
Q

List four indications for treatment/intervention of active ocular toxoplasmosis.

A

Significant reduction in VA
Threat to macula
Intense inflammation
-marked vitritis
Large lesion

52
Q

What is the medical management of active ocular toxoplasmosis (3)? List in order and note drug names if applicable (2).

A

High dose antibiotics for 24h before any steroid
-clindamycin
-sulphonamide drugs + pyrimathamine
Oral steroids

53
Q

Are oral steroids ever given alone for treating active toxoplasmosis?

A

Never - risk of ARN

54
Q

What surgery is available for treating active toxoplasmosis (2) and when is it indicated? List two risks associated with these interventions.

A

Cryopexy/laser
-useful when drug therapy is contraindicated
Risk of vitreous contraction and epiretinal membranes

55
Q

What causes toxocariasis? What kind of organism is it? What is a reservoir animal?

A

Infection by toxocara canis
-parasitic roundworm
Infects gut of dogs, especially puppies

56
Q

How do children typically get toxocariasis?

A

Eating dirt
-geophagia

57
Q

What two organs are involves with systemic toxocariasis?

A

Liver and spleen

58
Q

List three systemic manifestations of toxocariasis.

A

Fever
Pulmonary effects
-coughing, athsma-like attacks
Neurological symptoms
-convulsions, meningitis

59
Q

In what age are most cases of toxocariasis found (include percentage)?

A

80% in <16 years

60
Q

What is the ocular manifestation of toxocariasis and where is it found (2)? What does it resemble and in what percentage of cases is it found?

A

A granuloma resembling a retinoblastoma near the posterior pole in about 50% of cases
Can also be found in the periphery (causes dragged disc)

61
Q

List four features of a toxocariasis granuloma including colour, size, and elevation.

A

White elevated lesion
Variable size
Adacent exudate, haemorrhage, sensory RD
Well defined mass with healing

62
Q

List three ocular manifestations of toxocariasis aside from a granuloma. Explain why they occur if applicalbe (1).

A

Vitritis - severe
-immune response to dead worms
Peripheral retinitis/perivasculitis
Endophthalmitis

63
Q

Should you refer toxciariasis?

A

Yes

64
Q

How is toxocariasis treated (2)?

A

Steroids
Anti-helminthics
-thiabendazole/diethylcarbamazine

65
Q

What is sarcoidosis characterised by (4)?

A

Non-caseating granulomas
-little or no necrosis
-resolves completely or fibrosis

66
Q

What percentage of sarcoidosis cases involve the eye?

A

40%

67
Q

What often precedes systemic onset of sarcoidosis?

A

Uveitis

68
Q

Is sarcoidosis granulomatous or non-granulomatous?

A

Granulomatous

69
Q

Which is less common, posterior or anterior segment in sarcoidosis? Which is more visually disabling?

A

Posterior segment to both

70
Q

List 7 posterior ocular manifestations of sarcoidosis

A

Vitritis
-clump of cells/protein resembling snowballs
Granuloma
Cystoid macular oedema
-chronic
Periphlebitis
-may resemble BVO
Peripheral neovascularisation
Candle wax exudates
Disc swelling/atrophy

71
Q

Describe candle wax exudates in posterior sarcoidosis.

A

Exudates dripping from sclerosed/white retinal vessels

72
Q

List a treatment option for sarcoidosis. Is spintaneous improvement common or rare?

A

Spontaneous improvement common
Corticosteroids
-low dose, long term

73
Q

What is the most common cause of VA loss in sarcoidosis?

A

Cystoid macular oedema

74
Q

List 3 ocular manifestations of behcets disease when it affects the posterior uvea. Is the visual prognosis good or poor with posterior uvea changes?

A

Diffuse vascular leakage
Retinal vasculitis
-periphlebitis
Retinitis
Poor visual prognosis from posterior changes

75
Q

What is ocular histoplasmosis caused by? What kind of organism is it, where is it found (environment) and what country is it endemic to?

A

Histoplasma capsulatum
-fungus
Found in rivers and valleys worldwide
Endemic to mid-west USA

76
Q

In what age group is ocular histoplasmosis commonly found?

A

Middle aged people

77
Q

What is histoplasmosis primarily? What does it resemble?

A

A lung disease
-resembles TB

78
Q

Are there any visual symptoms of ocular histoplasmosis (2)?

A

No, unless the macula is involved

79
Q

What are the four main features of ocular histoplasmosis?

A

Disseminated choroiditis
-punctate atrophic lesions
Macular lesions
-simulates CSR
Peripapillary atrophy
-with SRN
Complete absence of vitreous cells

80
Q

What is treatment of ocular histoplasmosis limited to? List three treatment options.

A

Limited to macular lesions
-steroids
-laser/surgical removal if SRN is present
-antiVEGF

OD3 (S1&2) (114 decks)

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