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Pathology-my one > AMD > Flashcards

AMD Flashcards

1
Q

What is AMD?

A

Eye condition which affects the central retina causing vision ,oss

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2
Q

What is the macula and how big is it ?

A

The central area of the posterior pole, subtends an area of 15-20 degrees.

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3
Q

What is the fovea?

A

The fovea is right at the centre of the macula subtending an area of 5 degrees of your visual field.

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4
Q

What areas surround the fovea?

A

Surrounding the fovea is the parafovea and the perifovea is around the parafovea.

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5
Q

From centre going out, name the structures of the central retina

A

Fovea-parafovea-perifovea-macula

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6
Q

What are the non-modifiable risk factors of AMD?

A

Age >50

FH

Genetic

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7
Q

What are the modifiable risk factors of AMD?

A

Smoking

HTN, High fat diet, Lack of exercise

Cataract sx

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8
Q

How does cataract surgery affect AMD?

A

Can be a risk for speeding up any AMD present.If a px has any signs of AMD they’ll be made aware of the risk of it progressing more quickly if they have cataract surgery)

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9
Q

Give 5 tests you can do in a suspected AMD px

A

BCVA – ETDRS chart

Amsler

Reading speed

Mircoperimetry/gross perim = field test for central vision loss

Fundus BIO and OCT

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10
Q

What are the 2 symptoms of dry AMD?

A

Reduced VA

Distortion on amsler

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11
Q

What are the 3 symptoms of wet AMD?

A

Sudden onset of distortions and reduced vision in the affected eye.

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12
Q

Why may the symptoms of wet AMD go unnoticed?

A

This may not be immediately notice if the fellow eye is unaffected, which is why patients at risk of wet AMD are advised to monitor their vision monocularly on a daily basis.

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13
Q

What is the very first sign of AMD?

A

Drusen

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14
Q

What are the signs of early AMD?

A

Soft drusen ≥63µm

RPE hyper/hypo pigmentation

RPE atrophy(cell death)

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15
Q

What are the signs of late dry AMD?

A

Geographic atrophy (GA)

Sharply demarcated area of atrophy

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16
Q

What is another name for dry AMD?

A

Atrophic/non-neovascular

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17
Q

What are the signs of wet AMD?

A

Choroidal neovascularisation

Macular oedema

SRF=sub retinal fluid

Haemorrhages=Sub, intra or pre retinal

Serous detachment of neurosensory retina

RPE detachment (PED) or tear

Exudates

Scarring (disciform)(a neovasuclar scar can form)

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18
Q

What are basal laminar deposits?

A

An sign of early AMD

Lipid deposition in Bruch’s membrane

19
Q

What causes basal laminar deposits to form?

A

Failure of RPE to process cell debris

20
Q

How are basal laminar deposits seen?

A

Using electron microscopy so you won’t be able to use OCT to see it

21
Q

What are drusen?

A

Earliest visible sign

Round yellow deposits

22
Q

Where are drusen located?

A

Between RPE and bruch’s membrane

23
Q

What are drusen made of?

A

Deposits of lipofuscin, amyloid, complement factors so they’re waste products

24
Q

How can drusen be described?

A

Size:
Small <63µm= Very common, ~80% >age 30 yrs

Large ≥63µm=Hallmark of AMD, 26% >age 70 yrs have large drusen

Apperance:
Hard, soft or confluent

25
Q

What is the difference between Hard, soft or confluent drusen?

A

Hard drusen have well defined margins and soft drusen have ill define margins.

Confluent is combination of both

26
Q

How can u measure drusen?

A
  • On a fundus photograph using suitable tools

- On OCT which have calaerpers and can measure the width of the drusen

27
Q

When is drusen normal vs abnormal?

A

Hard drusen in small numbers= part of normal ageing process/NOT AMD

When numerous hard drusen present= risk factor for soft drusen and AMD

28
Q

What are pigmentary changes caused by?

A

Increased melanin content of RPE, RPE cell profileration, RPE cell migration.

29
Q

What is geographic atrophy?

A

GA are regions of RPE cell death causing death of photoreceptors causing scotoma

Inner retinal layer then start to die too

30
Q

How fast is the vision loss with GA occuring?

A

Gradual loss of central vision leads to eventual scotoma.

31
Q

How is GA seen in a hospital?

A

Increased autofluorescence on Fundus Autofluorescence.

32
Q

What are the two features that increase the risk of progression to wet AMD?

A

Larger, increased number and more confluent drusen with pigmentary changes associated with increased risk progression to advanced AMD

33
Q

Signs of WET AMD?

A

Choroidal neovascularisation

Macular oedema

SRF=sub retinal fluid

Haemorrhages=Sub, intra or pre retinal

Serous detachment of neurosensory retina

RPE detachment (PED) or tear

Exudates

Scarring (disciform)(a neovasuclar scar can form)

34
Q

What causes choroidal neovascularisation?

A

Hypoxia caused by deposits build up leads to choroidal neovascularisation (haemorrhages which leak under RPE, or subretinal space causes RPE detachment, leaves area of atrophy).

35
Q

What can repeated leakage cause?

A

Repeated leakage form disciform scar-complete scotoma/untreatable. Macular oedema, exudates

36
Q

How does CNV appear on fundus?

A

CNV may be seen as a green/grey lesion on a fundus photograph

But is easier to detect either using as binocular stereoscopic viewing strategy, such as volk, or on OCT, where the disrupted, raised RPE is clearly visible, and the hyperreflective neovascular membrane is seen beneath

37
Q

What are the first symptoms of wet AMD?

A

Sudden onset of distortions and reduced vision in the affected eye. This may not be immediately notice if the fellow eye is unaffected, which is why patients at risk of wet AMD are advised to monitor their vision monocularly on a daily basis.

38
Q

Can you get CNV in early AMD?

A

Yes, CNV develops in 10-15% of people with early AMD.

39
Q

Why causes sub or intraretinal haemorrhages, hard exudates, intra-retinal fluid, or retinal pigment epithelial detachment to form?

A

The fragile nature of the new vessels means that sub or intraretinal haemorrhages, hard exudates, intra-retinal fluid, or retinal pigment epithelial detachment are common.

40
Q

Where are these new blood vessels growing from and where do they grown into?

A

From the choroidal circulation, through breaks in Bruch’s membrane, to proliferate beneath the RPE. They can also break through the RPE to grow into the subretinal space.

41
Q

What causes a PED in wet AMD?

A

It’s a separation which occurs between the basement membrane of the RPE and Bruch’s membrane.

42
Q

What is the prognosis of a PED?

A

May flatten over time, but 1 in 10 is also likely to tear.

Either way, the prognosis is poor, and the PED usually leaves an area of atrophy or subretinal scar tissue formation.

43
Q

How do you differentiate wet AMD from hypertensive retinopathy?

A

CNV leakage causes exudate in the area so it can start to look hypertensive retinopathy.

The difference is that Wet AMD is confined to the macula area and it can be bilateral so look in ur history and symptoms whether px has told u that they have hypertensive ret or high blood pressure

44
Q

What are the main symptom differences between dry and wet?

A

DRY= Gradual loss in central vision, amsler distortion may be reported in later stage

WET=Sudden painless loss in central vision, monocular likely but can be binocular, distortion

Pathology-my one (12 decks)

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