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Ophthalmology > Pathology of the retina and choroid > Flashcards

Pathology of the retina and choroid Flashcards

1
Q

What is pathologic myopia?

A

Type of myopia that begins during childhood and progressively worsens, resulting in severe myopia by adulthood with an axial length >/= 26mm or refractive error >/= -6.00D)

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2
Q

What are some factors that can cause pathologic myopia?

A
  • Environmental and genetic influences cause increased axial growth of the eyeball
  • Often accompanied by degenerative changes in the retina
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3
Q

How does pathologic myopia present?

A
  • Blurred vision
  • Scleral thinning
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4
Q

What will fundoscopy show in pathologic myopia?

A
  • Lacquer cracks
  • Subretinal haemorrhage
  • Fuschs’ spot - degeneration of the macula; occurs due to proliferation of RPE associated with choroidal haemorrhage
  • Posterior staphyloma - outpouching of scleral tissue typically involving the optic disc or macula
  • RPE/choroid atrophy
  • Degeneration - cystoid, paving stone, lattice
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5
Q

What is shown?

A

Pathologic myopia

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6
Q

What is shown?

A

Pathologic myopia - Evaluates development of choroidal neovascularisation

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7
Q

How is pathologic myopia managed?

A
  • Annual checkups if stable
  • If CNV develops - anti-VEGF
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8
Q

What are some causes of retinal tears?

A
  • Age-related degeneration of the retina
  • Myopia
  • Eye injuries
  • Eye surgery e.g. cataract
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9
Q

What is a retinal hole?

A

An area of progressive thinning of the retina due to chronic retinal atrophy

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10
Q

What is a retinal break?

A

A full thickness defect in the sensory retina; when a retinal break is associated with vitreous traction (PVD), it is termed a retinal tear

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11
Q

How does retinal tear present?

A
  • Asymptomatic
  • May have photopsia or see floaters
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12
Q

How are retinal tears managed?

A
  • Management ofretinal tearsaims to create adhesions between the retina and the choroid to prevent detachment
  • This can be done using laser therapy or cryotherapy
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13
Q

What is a possible complication of retinal tear?

A

Retinal detachment

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14
Q

What is retinal detachment?

A

Refers to the detachment of the inner layer of the retina from the retinal pigment epithelium

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15
Q

What are the 2 forms of retinal detachment?

A

Rhegomatogenous
Non-rhegomatogenous

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16
Q

What is a rhegmatogenous retinal detachment?

A

Detachment of the retina caused by a tear or hole, with acute posterior vitreous detachment and predisposing peripheral retinal degeneration

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17
Q

What are some risk factors of rhegmatogenous retinal detachment?

A
  • Posterior vitreous detachment
  • Pathological myopia
  • Previous intraocular surgery
  • Trauma
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18
Q

What is non-rhegmatogenous retinal detachment?

A

Detachment without any retinal tears

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19
Q

What are the 2 forms of non-rhegmatogenous retinal detachment?

A

Tractional
Exudative

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20
Q

Describe the pathophysiology of tractional retinal detachment

A
  1. Formation of vitreoretinal bands (most commonly due to proliferative diabetic retinopathy)
  2. Pressure on the band during eye movement or as a result of sudden decrease in intraocular pressure
  3. Retinal detachment
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21
Q

Describe the pathophysiology of exudative retinal detachment

A

Subretinal fluid accumulation without retinal tears

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22
Q

What are some causes of non-rhegmatogenous retinal detachment?

A
  • Choroidal tumours - primary or metastatic
  • Intraocular inflammation - Harada disease, posterior scleritis
  • Systemic - toxaemia of pregnancy, hypoproteinaemia
  • Iatrogenic - RD surgery, excessive retinal photocoagulation
  • Miscellaneous - choroidal neovascularisation, uveal effusion sydrome
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23
Q

What are some symptoms of retinal detachment?

A
  • Painless, progressive visual field loss
  • Patients may describe a curtain/shadow descending or ascending on field of vision
    • Shadow corresponds to area of detached retina
  • If detachment affects macula, central vision will be lost
  • Sudden onset of floaters/flashes can preceed visual loss - indicates posterior vitreal detachment
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24
Q

What is a possible sign of retinal detachment?

A

RAPD

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25
Q

What are some signs of rhegmatogenous retinal detachment on fundoscopy?

A
  • Retinal tear may be visible
  • Detatched retina takes a convex shape
  • Deep mobile elevation extending to ora serrata (junction between retina and ciliary body)
  • Slightly opaque with dark blood vessels
  • Loss of choroidal pattern
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26
Q

What are some signs of non-rhegmatogenous retinal detachment on fundoscopy?

A
  • Detatched retina takes a convex shape
  • Smooth elevation
  • May be very mobile deep with shifting fluid
  • Subretinal pigment (leopard spots) after flattening
  • No retinal tear visible
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27
Q

What is shown?

A

Rhegmatogenous retinal detachment

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28
Q

What is shown?

A

Non-rhegmatogenous retinal detachment

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29
Q

How is retinal detachment managed?

A

Various surgical options which aim to reattach the retina and reduce any traction or pressure that may cause it to detach again

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30
Q

What is posterior vitreous detachment?

A

Detachment of the posterior vitreous cortex from the internal limiting membrane of the retina

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31
Q

What are some causes of posterior vitreous detachment?

A
  • Age-related degeneration of the vitreous body (most common cause)
  • Myopia
  • Eye injury
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32
Q

How does posterior vitreous detachment present?

A
  • Usually asymptomatic
  • Photopsia with eye movements - caused by partially detached vitreous tissue pulling on the retina
  • Floaters - collection of deposits in the vitreous body of the retina perceived as spots or strings drifting through the visual field
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33
Q

What is shown?

A

Posterior vitreous detachment

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34
Q

What is shown?

A

Posterior vitreous detachment

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35
Q

How is posterior vitreous detachment managed?

A

No treatment necessary - symptoms improve as brain adjusts

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36
Q

What is a possible complication of posterior vitreous detachment?

A

Can predispose to patients developing retinal tears and retinal detachment

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37
Q

What is vitreomacular traction?

A

Incomplete posterior vitreous detachment with the persistently adherent vitreous exerting tractional pull on the macula and resulting in morphologic alterations and consequent decline of visual function

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38
Q

How does vitreomacular traction present?

A
  • Metamorphopsia
  • Decreased vision
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39
Q

What investigation is required in vitreomacular traction?

A

Optical coherence tomography (OCT)

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40
Q

How is vitreomacular traction managed?

A

Options include observation, surgical management and medical therapy

41
Q

What is central serous chorioretinopathy?

A

Serous retinal detachment at the posterior pole of the eyeball (macula or perimacular region) due to a defect in the pigment epithelium which allows fluid to leak from the sclera into the subretinal space

42
Q

Who is most commonly affected by central serous chorioretinopathy?

A

Men 30-50 years old

43
Q

How does central serous chorioretinopathy present?

A
  • Hyperopia
  • Metamorphopsia
44
Q

How will central serous chorioretinopathy present on fundoscopy?

A

Roundish detachment of central retina

45
Q

What is shown?

A

Central serous chorioretinopathy

46
Q

How will central serous chorioretinopathy present on fluorescein angiography?

A

Most common finding is a small, focal hyperfluorescent RPE leak

47
Q

What is shown?

A

Central serous chorioretinopathy - Most common finding is a small, focal hyperfluorescent RPE leak

48
Q

What is epiretinal membrane?

A

Scar tissue formation across the inner surface of the retina which can cause visual problems

49
Q

What causes epiretinal membrane?

A
  • Scar tissue most commonly forms due to age-related vitreous retraction
  • Can also form following eye surgery or inflammation inside the eye
50
Q

How does epiretinal membrane present?

A
  • Metamorphopsia
  • Decreased acuity
51
Q

How will epiretinal membrane present on fundoscopy?

A
  • Retinal striae
  • Subretinal fluid or cystic damage
  • Almost always associated with PVD
52
Q

What is shown?

A

Epiretinal membrane

53
Q

How is epiretinal membrane managed?

A

Surgery indicated if patient has significant visual complaints of visual decline and /or metamorphopsia

54
Q

What is a macular hole?

A

Central small break in the macula

55
Q

What are some causes of macular hole?

A
  • Idiopathic
  • Secondary e.g. due to vitreous detachment, trauma
56
Q

How will macular hole present?

A
  • Metamorphopsia
  • Central visual field losses
  • Severe reduction of visual acuity
57
Q

How will macular hole present on fundoscopy?

A
  • Depending on the stage, a subfoveal spot or ring can be noted
  • In more advanced cases, a partial or full-thickness macular break is observed
58
Q

What is shown?

A

Macular hole

59
Q

How is macular hole managed?

A

There are conservative, medical and surgical options depending on the stage of the hole

60
Q

What is cystoid macular oedema?

A

Retinal thickening of the macula due to accumulation of fluid in the outer plexiform layer

61
Q

What are some causes of cystoid macular oedema?

A
  • Postoperative
  • Uveitis
  • Retinal venous occlusive disease
  • Choroidal neovascularisation
  • Epiretinal membrane /VMT
  • Retinitis pigmentosa
62
Q

How does cystoid macular oedema present?

A

Blurred/decreased central vision

63
Q

How is cystoid macular oedema managed?

A

Majority (95%) of cases spontaneously resolve

64
Q

What is chorioretinitis?

A

Inflammatory and exudative condition of the choroid and the retina (form of posterior uveitis)

65
Q

What are some causes of chorioretinitis?

A
  • Most often seen in immunodeficient patients e.g. HIV/AIDS
  • Usually a response to viral, bacterial, fungal or protozoal infection
66
Q

What are some forms of chorioretinitis?

A

Acute retinal necrosis
Endogenous chorioretinitis
Toxoplasma gondii
Ocular toxocaracanis

67
Q

What causes acute retinal necrosis?

A

HSV/HZV

68
Q

What causes endogenous chorioretinitis?

A
  • 50% bacterial, 50% fungal e.g. candida
  • Associated with bacterial endocarditis or indwelling catheters including central lines
69
Q

What causes toxoplasma gondii chorioretinitis?

A
  • Congenital or acquired
  • Associated with contaminated soil and undercooked meat
70
Q

How can toxoplasma gondii chorioretinitis present?

A
  • Results in a mild flu-like illness and rarely causes any further problems
  • In immunocompetent patients it enters latent phase with cysts forming, can reactivate
71
Q

What causes ocular toxocaracanis (Roundworm)?

A
  • Ingestion with toxocara eggs (parasite hosted by cats and dogs) leads to systemic and ocular infection
  • Reactive inflammatory processes lead to the organism’s encapsulation and the formation of eosinophilic granulomas - can cause irreversible visual loss if the egg has migrated to the eye
  • No proven treatment
72
Q

What is shown?

A

Acute retinal necrosis

73
Q

What is shown?

A

Endogenous chorioretinitis

74
Q

What is shown?

A

Endogenous chorioretinitis

75
Q

What is shown?

A

Toxoplasma gondii chorioretinitis

76
Q

What is shown?

A

Ocular toxoxaracanis (Roundworm)

77
Q

How will will older patients present with chorioretinitis?

A
  • Older patients commonly present with reduced visual acuity with floaters
    • Degree of symptoms depends on where the inflammatory lesions lie
    • Symptoms are usually unilateral and tend to develop over several days
78
Q

How will congenital chorioretinitis present?

A

Congenital infections may present insidiously, with little history and few symptoms

79
Q

What investigations are required in chorioretinitis?

A
  • Swab - culture (bacterial/viral), serology for toxoplasma and toxocara
  • Serology for toxoplasma and toxocara
80
Q

How is chorioretinitis managed?

A

May involve observation or antimicrobials ± topical steroid treatment - depends on causative pathogen and other criteria

81
Q

How is toxoplasma gondii chorioretinitis managed?

A

Systemic treatment if sight-threatening (clindamicin/azithromycin +/- steroids)

82
Q

What is the most common cause of blindness in individuals over 65 in developed countries?

A

Age-related macular degeneration

83
Q

What is thought to be the cause of ARMD?

A

Not clear - age-related, underlying inflammatory process

84
Q

What are some risk factors of ARMD?

A
  • Increasing age
  • Smoking
  • Positive family history
  • Poor nutrition
85
Q

What are the 2 main types of ARMD?

A

Dry ARMD
Wet ARMD

86
Q

Describe the pathophysiology dry ARMD?

A

Deposition of drusden (accumulation of byproducts - proteins, lipids, and inflammatory mediators) in RPE and between RPE and Bruch membrane results in slow progressive atrophy of the local RPE

87
Q

How does dry ARMD present?

A
  • Gradual decline in vision
  • Central vision ‘missing’ (scotoma)
88
Q

What is shown?

A

Scotoma (Central vision loss)

89
Q

What will be seen on fundoscopy in dry ARMD?

A
  • Drusen
  • Atrophic patches of retina
90
Q

What is shown?

A

Dry ARMD

91
Q

How is dry ARMD managed?

A
  • No cure - treatment is supportive with low vision aids e.g. magnifiers
    • Magnifiers increase retinal image size, making object easier to see as scotoma stays the same size
92
Q

Describe the pathophysiology of wet ARMD

A
  • Neovascularisation in choroid, mediated by VEGF
  • New vessels are small and fragile → more likely to haemorrhage so more likely to result in visual loss
93
Q

How does wet ARMD present?

A
  • Rapid central visual loss
  • Distortion (metamorphopsia)
94
Q

What will be shown on fundoscopy in wet ARMD?

A

Haemorrhage/Exudate

95
Q

What will be shown on fluorescein angiography in wet ARMD?

A
96
Q

What will be shown on OTC in wet ARMD?

A
97
Q

How is wet ARMD managed?

A

Anti-VEGF

98
Q
A

Ophthalmology (9 decks)

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