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Duke Elder 2020 > Medical Retina > Flashcards

Medical Retina Flashcards

1
Q

What is the vitreous cavity in the retina?

A

LARGEST CAVITY 4.0-4.4 ML IN ADULTHOOD

CONTAINS VISCOELASTIC GEL MADE OF MOSTLY WATER

CONTAINS MAINLY HYALURONIC ACID AND TYPE II COLLAGEN

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2
Q

What is the vitreous derived from?

A

Embryologically from the diencephalon

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3
Q

What does the diencephalon give rise to?

A

Optic vesicle and then optic cup

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4
Q

What are the two layers of the retina?

A

Retinal Pigment Epithelial Layers

Neurosensory Retina

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5
Q

Why does retinal detachment occur?

A

weak connection between RPE and NSR

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6
Q

What are the 9 layers of the retinal pigment epithelium? (Internal to external)

A
  1. Internal limiting membrane
  2. Nerve fibre Layers
  3. Ganglion cell layer
  4. Inner plexiform layer
  5. Inner nuclear layers
  6. Outer plexiform layer
  7. Outer nuclear layer
  8. External limiting membrane
  9. Photoreceptor layer
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7
Q

What is the function of the internal limiting membrane?

A

SEPARATES THE RETINA FROM THE VITREOUS

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8
Q

What is the function of the nerve fibre layer?

A

CONTAINS GANGLION CELL AXONS THAT COME TOGETHER TO FORM THE OPTIC NERVE,

PRESENT IN THE MACULAR AREA AND TRAVELS NASALLY TO THE OPTIC NERVE DIRECTLY THROUGH THE PAPILLOMACULAR BUNDLE

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9
Q

What is the function of the ganglion cells layer?

A

CONTAINS THE CELL BODIES OF THE GANGLION CELLS, INVOLVED IN TRANSMITTING VISUAL INFORMATION TO THE BRAIN INCLUDING STIMULUS REQUIRES FOR LIGHT PUPILLARY RESPONSE

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10
Q

What is the function of the inner plexiform layer?

A

SYNAPTIC LAYER BETWEEN SECOND AND THIRD ORDER NEURONS

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11
Q

What is the function of the inner nuclear layer?

A

CONTAINS CELL BODIES OF BIPOLAR CELLS AND CELL BODIES OF MULLER CELLS

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12
Q

What is the function of the outer plexiform layer?

A

SYNAPTIC LAYER BETWEEN PHOTORECEPTORS AND BIPOLAR CELLS

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13
Q

What is the function of the outer nuclear layer?

A

CONTAINS CELL BODIES OF RODS AND CONES

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14
Q

What is the function of the external limiting membrane?

A

CONNECTIONS BETWEEN PHOTORECEPTORS AND MULLER CELLS CREATE THE ELM

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15
Q

What is the function of the photoreceptor layer?

A

contains rods and cones

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16
Q

What is the RPE composed of?

A

SINGLE LAYER OF A CUBOIDAL EPITHELIAL CELLS CONTAINING MELANOSOMES AND HAS MANY FUNCTIONS

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17
Q

What are the functions of the RPE?

A

ABROBS LIGHTS AND PREVENTS THE SCATTERING OF LIGHT WITHIN THE EYE

REPLENSIHES THE MOLECULES NEEDED FOR PHOTOTRANSDUCTION

CONTAINS A BLOOD RETINAL BARRIER WHICH PROVIDES A SELECTIVELY PERMEABLE MEMBRANE TO SUPPLY NUTRIENTS TO THE PHOTORECEPTORS AND MAINTAIN HOMEOSTASIS

-BLOOD RETINAL BARRIER IS MAINTAINED BY THE ZONULAE OCCLUDENTES

PHAGOCYTOSIS OF PHOTORECEPTOR OUTER SEGMENT MEMBRANES

TRANSPORT AND STORAGE OF METABOLITES AND VITAMINS

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18
Q

What is the macula lutea?

A

MACULA IS PIGMENTED, ROUNDED AREA AT THE POSTERIOR POLE OF THE RETINA, LOCATED TEMPORAL TO THE OPTIC DISC

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19
Q

What is the macula lutea made of?

A

SEVERAL LAYERS OF GANGLION CELLS (peripheral retinal only has one layer of ganglion cells)

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20
Q

What is the fovea?

A

DEPRESSION AT THE CENTRE OF THE MACULA THAT CONTAINS ONLY CONES AND REPRESENTS THE RETINA’S HIGHEST VISUAL ACUITY

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21
Q

What is unique about the centre of the fovea?

A

CENTRE OF THE FOVEA IS AVASCULAR AND IS DEPENDENT ON THE UNDERLYING CHORIOCAPILLARIS FOR BLOOD SUPPLY VIA DIFFUSION

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22
Q

How many rods are there?

A

120 million

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23
Q

How many cones are there?

A

6 million

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24
Q

What is the pigment in rods?

A

rhodopsin

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25
Q

What is the pigment in cones?

A

iodopsin

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26
Q

What is the wavelength of maximum absorbance in rods?

A

498

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27
Q

What is the wavelength of maximum absorbance in cones?

A

SHORT (420) - blue

MEDIUM (534) - green

LONG (564) - red

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28
Q

Describe the bipolar connection of rods

A

ONE BIPOLAR CELL CAN RECEIVE STIMULI FROM MULTIPLE RODS

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29
Q

Describe the bipolar connection of cones

A

FORMS A 1:1 RATIO WITH BIPOLAR CELLS

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30
Q

Describe the function of rods

A

SENSITIVE IN DARK-DIM ILLUMINATION

RESPONSIBLE FOR NIGHT AND PERIPHERAL VISION

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31
Q

Describe the function of cones

A

SENSITIVE TO BRIGHT LIGHT

RESPONSIBLE FOR CENTRAL AND COLOUR VISION

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32
Q

Describe the blood supply to the retina

A

OUTER THIRD OF RETINAL LAYERS, INCLUDING PHOTORECEPTORS AND RPE ARE SUPPLIED BY THE SHORT POSTERIOR CILIARY ARTERY

INNER TWO THIRD OF RETINAL LAYERS ARE SUPPLIED BY THE CENTRAL RETINAL ARTERY

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33
Q

Describe the variation in blood supply to the retina

A

N SOME PATIENTS, THE INNER LAYER OF THE MACULA MAY HAVE A DUAL BLOOD SUPPLY BY THE CILIORETINAL ARTERIES (BRANCH OF THE SHORT POSTERIOR CILIARY ARTERY

WHEN UNAFFECTED, CENTRAL VISION MAY BE CONSERVED IN CASES OF CENTRAL RETINAL ARTERY OCCLUSION (CRAO)

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34
Q

What is the most common microvascular complication of diabetes?

A

diabetic retinopathy and maculopathy

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35
Q

What is the most common cause of blindess in in adults aged 35-65 in developed countries?

A

diabetic retinopathy and maculopathy

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36
Q

Describe the pathogenesis of diabetic retinopathy and maculopathy

A

HYPERGLYCAEMIA CAUSES INCREASED RETINAL BLOOD FLOW AND DAMAGE TO ENDOTHELIAL WALLS AND PERICYTES

ENDOTHELIAL DYSFUNCTION CAUSES VASCULAR PERMEABILITY AND HARD EXUDATIVE FORMATION (LIPOPROTEINS IN THE OUTER PLEXIFORM LAYER)

PERICYTE DAMAGE PREDISPOSES TO THE FORMATION OF MICROANEURYSMS, WHICH ARE LEAKAGES OF BLOOD FROM CAPILLARY WALLS AND FLAME HAEMORRHAGES DUE TO RUPTURE OF THE CAPILLARY WALLS WHICH TRACK ALONG THE NERVE FIBRE LAYER

COTTON WOOL SPOT FORMATION: AXONAL DEBRIS AT MARGINS OF ISCHAEMIC INFARCTS

NEOVASCULARISATION OCCURS THROUGH ANGIOGENIC FACTORS SUCH AS VASCULAR ENDOTHEALIAL GROWTH FACTORS IN RESPONSE TO ISCHAEMIA

CYSTOID MACULAR OEDEMA: MOST LAYERS CAN BE AFFECTED PARTICULARLY THE OUTER PLEXIFORM LAYER

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37
Q

What is the most important risk factor in the development of diabetic retinopathy and maculopathy?

A

duration of diabetes

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38
Q

What are the risk factors for diabetic retinopathy and maculopathy?

A

duration of diabetes

diabetic control

pregnancy

smoking

hyperlipidaemia

hypertension

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39
Q

What are the features of diabetic retinopathy and maculopathy?

A

MOST PATIENTS WILL BE ASYMPTOMATIC

CAUSES OF VISION LOSS INCLUDE:

GRADUAL ONSET:

  • ANY TYPE OF DIABETIC RETINOPATHY
  • DIABETIC MACULAR OEDEMA: MOST COMMON CAUSE OF VISUAL IMPAIRMENT
  • CATARACT

ACUTE ONSET:

  • PAINLESS: SIMILAR TO VITREOUS HAEMORRHAGE OR TRACTIONAL RETINAL DETACHMENT (FLASHES AND FLOATERS MAY PRECEDE VISUAL LOSS)
  • PAINFUL: SIMILAR OT NEOVASCULAR GLAUCOMA PRECIPITATED BY RUBEOSIS IRIDIS
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40
Q

How is DR classified?

A

MODIFIED AIRLINE HOUSE Classification

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41
Q

describe mild non-proliferative DR

A

AT LEAST ONE MICROANEURYSM

INRTARETINAL HAEMORRHAGES

EXUDATES

COTTON WOOL SPOTS

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42
Q

describe moderate non-proliferative DR

A

INTRARETINAL HAEMORRHAGES (IN 1-3 QUADRANTS) OR MILD INTRARETINAL MICROVASCULAR ABNORMALITY

VENOUS BEADING (IN 1 QUADRANT ONLY)

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43
Q

Describe severe non-proliferative DR

A

FOLLOWS THE 4-2-1 RULE; ONE OR MORE OF

INTRARETINAL HAEMORRHAGES IN 4 QUADRANTS

VENOUS BEADING > 2 QUADRANTS

MODERATE IRMA > 1 QUADRANT

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44
Q

Describe non high risk proliferative DR

A

NEOVASCULARISATION ON DISC OR ELSEWHERE

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45
Q

Describe high risk proliferative DR

A

FULFILS ONE OF THE FOLLOWING

NV > 1/3 DISC AREA

NVD (neovasc disc) PLUS VITREOUS HAEMORRHAGE

NVE (neovasc elsewhere) > ½ DISC AREA PLUS VITREOUS HAEMORRHAGE

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46
Q

Describe advanced proliferative DR

A

Tractional retinal detachment

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47
Q

What is diabetic maculopathy?

A

PRESENCE OF DIABETIC MACULAR OEDEMA

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48
Q

How is diabetic maculopathy classified?

A

CENTRE INVOLVING DIABETIC MACULAR OEDEMA OR

EXTRA-FOVEAL DIABETIC MACULAR OEDEMA MEETING CLINICALLY SIGNIFICANT MACULAR OEDEMA DEFINED BY THE ETDRS

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49
Q

What investigations are used for diabetic maculopathy?

A

OPTICAL COHERENCE TOMOGRAPHY FOR ASSESSING AND MONITORING DMO

FLUORESCENCE ANGIOGRAPHY MAINLY USED TO ASSESS FOR RETINAL ISCHAEMIA

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50
Q

What is the management of diabetic maculopathy?

A

GLYCAEMIC AND BLOOD PRESSURE CONTROL (USE FOR EFFECTIVE ANTIHYPERTENSIVES SUCH AS LISINOPRIL)

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51
Q

What is the management of non proliferative dr

A

MONITORING IN SCREENING PROGRAMMES OR SECONDARY CARE RANGING FROM ANNUAL (FOR MILD-MODERATE) TO 4MONTHLY SEVERE

CONSIDER PAN RETINAL PHOTOCOAGULATION (PRP) FOR SEVERE NONPROLIFERATIVE IN ELDERLY PATIENTS WITH TYPE 2 DIABETES OR IF POOR ATTENDANCE OR PRIOR TO CATARACT SURGERY

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52
Q

What is the management for non high risk proliferative dr?

A

REGULAR ROUTINE REVIEW +/- PRP

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53
Q

What is the management for high risk proliferative DR?

A

PRP WITHIIN TWO WEEKS

TREAT DMO IF COEXISTS AT THE SAME TIME OR BEFORE

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54
Q

What is the management for vitreous haemorrhage?

A

TREAT AS HIGH RISK Proliferative DR

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55
Q

What is the management for traction retinal detachment or persistent vitreous haemorrhage?

A

PARS PLANA VITRECTOMY

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56
Q

What is the treatment for maculopathy?

A

TREATED WITH INTRAVITREAL ANTI-VEGF (RANIBIZUMAB OR AFILBERCEPT, NOT THE LATTER HAS A HIGHER MOLECULAR WEIGHT AND IS SECOND LINE) IF THERE IS DMO ON OCT AND THE VISION AFFECTED

CONSIDER USING MODIFIED ETDRS LASER IF ANTI-VEGF IS CONTRAINDICATED (E.G. PREGNANCY)

DIABETIC RETINOPATHY AND CATARACT SURGERY: TREAT Clinically significant macular oedema AND PDR OR NEOVASCULARISATION OF IRIS BEFORE CATARACT SURGERY

IF THERE IS NO FUNDAL VIEW PERFORM B SCAN ULTRASOUND

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57
Q

What is hypertensive retinopathy?

A

chronic hypertension - atherosclerotic changes and vasoconstriction - endothelial damage –> retinopathy

CHRONIC HYPERTENSIVE RETINOPATHY CAN INCLUDE SIMILAR SIGNS TO DIABETIC RETINOPATHY

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58
Q

How is Hypertensive Retinopathy managed?

A

BP control

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59
Q

What are the stages of hypertensive retinopathy?

A

ARTERIOLAR NARROWING

ARTERIOVENOUS NIPPING (FIGURE 14.3) OR ATHEROSCLEROSIS WITH THICKENING OF RETINAL ARTERIOLES (‘COPPER / SILVER WIRING’)

STAGE 2 PLUS FLAME HAEMORRHAGES, COTTON WOOL SPOTS OR EXUDATES

STAGE 3 PLUS PAPILLOEDEMA

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60
Q

What other vascular conditions is hypertension associated with?

A

RETINAL ARTERY AND VEIN OCCLUSION AND COMPOUNDS COMPLICATIONS OF DIABETIC RETINOPATHY

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61
Q

What is retinal vein occlusion?

A

SECOND MOST COMMON RETINAL VASCULAR DISORDER AFTER DIABETIC RETINOPATHY

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62
Q

How is retinal vein occlusion classified?

A

CENTRAL RETINAL VEIN OCCLUSION VERSUS BRANCH RETINAL VEIN OCCLUSION: AN OCCLUSION AT OR PROXIMAL TO THE LAMINA CRIBROSA WHERE THE RETINAL ARTERY EXITS THE EYE LEADS TO CRVO

AN OCCLUSION OF ONE OF THE BRANCHES OF CENTRAL RETINAL VEIN LEADS TO BRVO

ISCHAEMIC VS NON ISCHAEMIC

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63
Q

What are the risk factors for retinal vein occlusion?

A

AGE

MICROVASCULAR: HYPERTENSION, HYPERLIPIDAEMIA AND DM

COMBINED ORAL CONTRACEPTIVE PILL

GLAUCOMA

64
Q

Describe non-ischaemic central retinal vein occlusion

A

SUDDENT, PAINLESS dVA (>6/60)

FUNDOSCOPY: TORTUOSITY AND DILATATION OF ALL BRANCHES OF CENTRAL RETINAL VEIN, DOT/BLOT AND FLAME HAEMORRHAGES OF ALL FOUR QUADRANTS, PROMINENTS IN THE PERIPERHY WITH OPTIC DISC AND MACULAR SWELLING

65
Q

Describe ischaemic central retinal vein occlusion

A

SUDDENY, PAINLESS SEVERE dVA (6/60)

RELATIVE AFFERENT PUPILLARY DEFECT

SIGNIFICANT TORTUOSITY AND DILATATION OF ALL FOUR QUADRANTS WITH SEVERE FLAME HAEMORRHAGES, DISC AND MACULAR OEDEMA

RUBEOSIS IRIDIS IN ABOUT 50% OF PATIENTS WHICH CAN LEAD TO NVG

66
Q

What is the most common location of branch retinal vein occlusion?

A

SUPEROTEMPORAL, FOLLOWED BY INFEROTEMPORAL

67
Q

describe the features of branch retinal vein occlusion

A

DVA, METAMORPHOPSIA, VF DEFECT (ALTITUDINAL)

RETINAL HAEMORRHAGE IN AFFECTED QUADRANT

68
Q

What are the complications of branch retinal vein occlusion?

A

CMO AND NEOVASCULARISATION

69
Q

What is the management for branch retinal vein occlusion?

A

MACULAR OEDEMA WITH MINIMAL ISCHAEMIA

  • WITHIN 3 MONTHS OF ONSET: CONSIDER OZURDEX OR ANTI-VEGF
  • AFTER 3 MONTHS OF ONSET: CONSIDER MACULAR GRID LASER OF OZURDEX OR ANTI-VEGF

MACULAR OEDEMA WITH MARKED ISCHAEMIA: NO IMMEDIATE TREATMENT

ISCHAEMIC BRVO WITH NEOVASCULARISATION: PRP

70
Q

What is retinal artery occlusion?

A

OPTHALMIC EMERGENCY

71
Q

What is the most common cause of retinal artery occlusion?

A

Atheroscleorisis and GCA

72
Q

Describe the features of central retinal artery occlusion

A

SUDDEN PAINLESS LOSS OF VISION (VA USUALLY COUNTING FINGERS, UNLESS CILIORETINAL IS SPARED) WITH MARKED RAPD

73
Q

Describe the fundoscopy findings of central retianl artery occlusion

A

FUNDOSCOPY:

  • SWOLLEN, PALE AND OPAQUE RETINA, -‘CHERRY RED’ SPOT AT THE MACULE
  • ARTERIOLAR ATTENUATION
74
Q

Describe the management of central retinal artery occlusion

A

IRREVERSIBLE RETINAL INFARCTION USUALLY OCCURS WITHIN 90 MINUTES OF OCCLUSION OF THE ARTERY:

THUS OCULAR MASSAGE,
Anterior Chamber PARACENTESIS,
IOP-LOWERING INTERVENTION SUCH AS IV ACETAZOLAMIDE OUTSIDE OF THIS WINDOW HAVE QUESTION EFFICACY

75
Q

Describe features of branch retinal artery occlusion

A

MOST COMMONLY DUE TO EMBOLIC CAUSES

SUDDEN PAINLESS ALTITUDINAL FIELD LOSS

SWOLLEN WHITE RETINA ALONG THE AFFECTED VESSEL WITH ARTERIOLAR ATTENUATION

76
Q

What is ocular ischaemic syndrome?

A

can be thought of as angina of the eye

MAJORITY OF CASES CAUSED BY ATHEROSCLEORTIC-STENOSIS OF THE CAROTID ARTERY

77
Q

Describe the features of ocular ischaemic syndrome

A

UNILATERAL SUBACUTE dVA AND PERIOCULAR PAIN

ANTERIOR SEGMENT: CONJUNCTIVAL INJECTION, AC CELLS AND RUBEOSIS IRIDIS (IOP MAY REMAIN LOW DUE TO HYPOPERFUSION)

POSTERIOR SEGMENT: CAN BE DECEPTIVELY SIMILAR TO CRVO, CHERRY RED MACULA, RETINAL ARTERY ATTENUATION AND ENOVASCULARISATION OF THE DISC ARE SEEN

78
Q

Describe non proliferative sickle cells changes to the eye

A

INCLUDES SIGNS OF INTRARETINAL HAEMORRHAGES (‘SALMON PATCHES’) OR PATCHES OF RPE HYPERPLASIA (BLACK SUNBURSTS)

79
Q

Describe proliferative sickle cell changes to the eye

A

PERIPHERAL ARTERIOLAR OCCLUSION

ARTERIOVENOUS ANASTOMOSIS

NEOVASCULARISATION WITH A ‘SEA FAN’ APPEARANCE

VITREOUS HAEMORRHAGE

TRACTIONAL / RHEGMATOGENOUS RETINAL DETACHMENT

80
Q

what IS THE LEADING CAUSE OF BLINDNESS IN THE ELDERLY IN DEVELOPED COUNTRIES ?

A

age related macular degeneration

81
Q

What is the hallmark of age related macular degeneration?

A

LARGE CONFLUENT SOFT DRUSEN

82
Q

How does cell death occur in age related macular degeneration?

A

apoptosis

83
Q

Describe the pathological changes in dry age related macular degeneration

A

DRUSEN: YELLOW DEPOSITS BETWEEN BRUCH’S MEMBRANE AND RPE

ATROPHY OF RPE, PHOTORECEPTOR LAYERS ANC CHORIOCAPILLARIES

GEOGRAPHIC ATROPHY: THE END POINT OF DRY ARMD, CHARACTERISED BY LARGE ATROPHIC AREAS WITH VISIBILITY OF UNDERLYING CHOROID

84
Q

Describe the pathological changes in wet age related macuular degeneration

A

INGROWTH OF CHOROIDAL VESSELS INTO RPE AND SUBRETINAL SPACE (CHOROIDAL NEOVASCULARISATION)

DISCIFORM MACULAR DEGENERATION IS THE END POINT OF WET ARMD

THIS IS FIBROUS SCARRING DUE TO SUB-RPE NEOVASCULARISATION (SUBRETINAL FIBROSIS)

85
Q

Describe the pathological changes in polypoidal choroidal vasculopathy

A

A VARIANT OF WET ARMD

CHARACTERISED BY POLYPOIDAL DILATTION OF THE CHOROIDAL VASCULATURE

PROGRESSES TO SUBRETINAL HAEMORRHAGE AND MULTIPLE PEDs

MORE COMMON IN MIDDLE AGED ASIAN POPULATION AND IS UNILATERAL IN PRESENTATION

86
Q

What are the risk factors for age related macular degeneration

A

INCREASING AGE: MOST IMPORTANT RISK FACTOR

GENETICS: CFH AND ARMS2 GENES

SMOKING

HYPERMETROPIA

HYPERTENSION

FEMALE

WHITE RACE

87
Q

What are the features of dry age related md

A

GRADUAL dVA AND CENTRAL SCOTOMA

INTERMEDIATE OR LARGE SOFT DRUSEN (>63 MICRONS OR >125 MICRONS) NOTE: SMALL, HARD DRUSEN ARE OF LIMITED SIGNIFICANCE AND MAY REFLEXT NORMAL AGE-RELATED CHANGES

GEOGRAPHIC ATROPHY OF RPE

88
Q

What are the features of wet age related md?

A

DECREASED VA, METAMORPHOPSIA AND CENTRAL SCOTOMA OF SUDDEN ONSET

SUBRETINAL OR SUB-RPE HAEMORRHAGE AND EXUDATION

RPE AND OR EXUDATIVE RETINAL DETACHMENT

CMO

SUBRETINAL FIBROSIS

89
Q

What investigations are used in age related md

A

OCT: MOST WIDLEY USED TEST TO MONITOR DISEASE PROGRESS

ICG IF PCV SUSPECTED: BRANCHING VASCULAR NETWORK MAY BE SEEN ON EARLY FRAMES WITH HYPERFLUORESCENCE POLYPS IN LATE FRAMES

90
Q

How is dry age related md managed?

A

INVOLVES MANAGEMENT OF MODIFIABLE RISK FACTORS

AGE RELATED EYE DISEASE STUDY 2 (9): VITAMIN C, VITAMIN E, LUTEIN, ZEAXANTHIN AND ZINC PROVIDED TO REDUCE THE PROGRESSION OF ARMD

AMSLER GRID: TO RULE OUT PROGRESSION TO WET ARMD

91
Q

How is wet age related md managed?

A

INTRAVITREAL ANTI-VEGF INJECTIONS (E.G. RANIBIZUMBA OR AFLIBERCEPT)

92
Q

What are two aids for low vision?

A

MAGNIFIERS: FOR READING E.G. LOOP OR SPECTACLE MAGNIFIERS

TELESCOPES: FOR DISTANCE VISION E.G. GALILEAN TELESCOPES

93
Q

What is choroidal neovascularisation?

A

ABNORMAL GROWTH OF VESSELS FROM THE CHORIOCAPILLARIES THROUGH BRUCH MEMBRANE INTO SUB-RPE (TYPE 1) OR SUBRETINAL (TYPE 2) SPACE

94
Q

Describe the presentation of choroidal neovascularisation

A

DVA, METAMORPHOPSIA AND SCOTOMA

95
Q

What are the causes of choroidal neovascularisation?

A

DEGENERATIVE: ARMD (MOST COMMON CAUSE) MYOPIC DEGENERATION AND ANGIOID STREAK

CENTRAL SEROUS CHORIORETINOPATHY

INFLAMMATORY CONDITIONS: BIRDSHOT CHOROIDOPATHY, VKH, POHS

BEST DISEASE

IDIOPATHIC

96
Q

What is degenerative myopia?

A

DEGENERATIVE CHANGES MAY OCCUR IN PATIENTS WITH PROGRESSIVE / PATHOLOGICAL MYOPIA

THOSE ARE A SUBSET OF PATIENTS WITH MYOPIA > -6D IN WHICH THE AXIAL LENGTH OF THE EYE MAY NEVER STABILISE

97
Q

What disease is degenerative myopia associated with?

A

STICKLER, MARFAN, EHLERS-DANLSO AND DOWN SYNDROMES

98
Q

What are the features of choroidal neovascularisation?

A

CHOROIDAL ATROPHY WITH VISIBILITY OF UNDERLYING CHOROIDAL VESSELS

CNV

RHEGMATOGENOUS RETINAL DETACHMENT

MACULAR HOLE

POSTERIOR STAPHYLOMA

99
Q

What is a posterior staphyloma?

A

AN OUTPOUCHING OF THE POSTERIOR WALL OF THE EYE THAT HAS A DIFFERENT RADIUS OF CURVATURE THAN THE REST OF THE EYE

ONE OF THE HALLMARKS OF PATHOLOGICAL MYOPIA, ASSOCIATED WITH POOR PROGNOSIS

100
Q

What are angiooid streaks?

A

USUALLY BILATERAL SYMMETERICAL IRREGULAR ATROPHIED STREAKS DEEP TO THE RETINA, RADIATING FROM THE OPTIC DISC

RESULT FROM BREAKS IN THE BRUCH MEMBRANE

101
Q

How do angioid streaks present?

A

PERIPAPILLARY ATROPHY WITH MULTIPLE IRREGULAR STREAKS RADIATING IN A CIRCULAR PATTERN

102
Q

What are some causes of angioid streaks?

A

IDIOPATHIC

PSEUDOXANTHOMA ELASTICUM: MOST COMMON SYSTEMIC ASSOCIATION

MUTATIONS IN THE ABCC6 GENE

PRESENTS WITH YELLOW PAPULAR LESIONS WITH EXCESSIVE WRINKLING (PLUCKED CHICKEN APPEARANCE) OF SKIN USUALLY IN THE NECK, INGUINAL FOLDS AND ANTECUBITAL FOSSA

EHLER-DANLOS SYNDROME

PAGET DISEASE

103
Q

What is cystoid macular oedema?

A

RETINAL THICKENING OF THE MACULA DUE TO ABNORMALITIES OF THE BLOOD RETINAL BARRIER WHICH LEADS TO LEAKAGE OF FLUID WITHIN THE INTRACELLULAR SPACES OF THE RETINA, TYPICALLY IN THE OUTER PLEXIFORM LAYER

104
Q

What are some symptoms of cystoid macular oedema?

A

dVA, METAMORPHOPSIA AND SCOTOMA

105
Q

What investigation is used in cystoid macular oedema?

A

OCT

106
Q

What are some causes of cystoid macular oedema?

A

DIABETIC MACULE OEDEMA

CRVO AND BRVO

ARMD

UVEITIS TYPICALLY PARS PLANITIS BUT ALSO OCCURS IN ANTERIOR AND POSTERIOR UVEITIS

RETINITIS PIGMENTOSA

IRVINE-GASS SYNDROME

DRUGS

107
Q

What is central serous chorioretinopathy?

A

BUILDUP OF CENTRAL SUBRETINAL FLUID DUE TO RETINAL PIGMENT EPITHELIUM DYSFUNCTION AND CHOROIDAL HYPERPERMEABILITY

108
Q

What are some risk factors for central serous chorioretinopathy?

A

MALES AGED 20-50

TYPE A PERSONALITY

CORTICOSTEROID RELATED: IATROGENIC OR CUSHING DISEASE

109
Q

What are some features of central serous chorioretinopathy?

A

UNILATERAL DROP IN VA METAMORPHOPSIA, CENTRAL SCOTOMA

SLOW RECOVERY FROM BRIGHT LIGHT

COMPLICATIONS INCLUDE SEROUS (EXUDATIVE) RD AND CNV

110
Q

What are the investigations used for central serous chorioretinopathy?

A

OCT: TRIANGLE SHAPED SUBRETINAL FLUID COLLECTION WITH NEUROSENSORY RETINAL DETACHMENT

FA: PROGRESSIVE LEAKAGE WITH ‘INKBLOT’ OR ‘SMOKESTACK’ APPEARANCE

111
Q

What is the management used for central serous chorioretinopathy?

A

OBSERVE (SPNTANEOUS RESOLUTION) WITH MANAGEMENT OF RISK FACTORS

CONSIDER PHOTODYNAMIC THERAPY (VERTEPORFIN) WHEN THERE IS AISGNIFICANT VISUAL DISTURBANCE OR CHRONIC CSCR

112
Q

What is Eales Disease?

A

IDIOPATHIC PERIPHERAL RETINAL PERIPHLEBITIS THAT TYPICALLY OCCURS IN YOUNG INDIAN MALES

113
Q

How does Eales Disease present?

A

USUALLY WITH RECURRENT VITREOUS HAEMORRHAGES

114
Q

What is a risk factor for Eales Disease?

A

TUBERCULAR PROTEIN EXPOSURE (TUBERCULIN SENSITIVITY) MAY BE A RISK FACTOR FOR DEVELOPING THIS DISEASE

115
Q

What is Best Disease?

A

BEST VITELLIFORM MACULAR DYSTROPHY IS AN AD DEGENERATION OF THE MACULA

116
Q

What is Best Disease associated with?

A

LIPOFUSCIN ACCUMULATION IN THE RPE AND ATROPHY OF THE PHOTORECEPTOR LAYER OF THE RETINA

117
Q

What are the features of Best Disease

A

BILATERAL CONDITION ASSOCIATED WITH HYPERMETROPIC PATIENTS

EGG YOLK LESION IN MACULA: YELLOW-ORANGE ELEVATED LESION

ELECTRORETINOGRAM (ERG): NORMAL

ELECTRO-OCULOGRAM (EOG): ABNORMAL

CAN BE COMPLICATED BY CNV WHICH LEADS TO DVA

118
Q

What is stargardt disease?

A

AN AR CONDITION ASSOCAITED WITH A MUTATION IN THE ABCA4 GENE ON CHROMOSOME 1 THAT CAUSES MACULAR DEGENERATION

119
Q

How does stargardt disease present?

A

PRESENTS WITH READING DIFFICULTIES IN PATIENTS UNDER 20

120
Q

What are the features of stargardt disease?

A

NORMAL-APPEARING FUNDUS IN EARLY STAGES OF THE DISEASE

LATE FUNDAL APPEARANCE

  • BEATEN BRONZE APPEARANCE OF THE MACULA THAT CAN PROGRESS TO GEOGRAPHIC ATROPHY WITH A BULL’S EYE PATTERN
  • YELLOW WHITE FLECKS IN RPE

FA: DARK CHOROID (REDUCED CHOROIDAL CIRCULATION)

121
Q

What is lebers congenital amaurosis?

A

A RECESSIVE CONDITION THAT PRESENTS WITH SEVERE VISUAL LOSS AT BIRTH, NYSTAGMUS AND ABSENT PUPILLARY REFLEXES

122
Q

Describe the fundoscopy findings in lebers congenital amauruosis?

A

EARLY DISEASE; NORMAL

LATE DISEASE: SALT AND PEPPER RETINOPATHY AND BULL’S-EYE MACULOPATHY

123
Q

What is albinism?

A

HEREDITARY GROUP OF DISEASES THAT AFFECTS A MELANIN SYNTHESIS O THE EYE ONLY (OCULAR LABINISM – XL INHERITENCE) OR, MORE COMMONLY, THE EYE, SKIN AND HAIR (OCULOCUTANEOUS ALBINISM – AR INHERITENCE)

124
Q

What are the features of albinism?

A

SYMPTOMS: dVA DUE TO FOVEAL HYPOPLASIA

SIGNS: NYSTAGMUS, STRABISMUS AND IRIS / FUNDAL HYPOPIGMENTATION RESULTING IN A ‘PINK EYE’ APPEARANCE

OPTIC CHIASM CONTAINS MORE CROSSED FIBRES THAN NORMAL

125
Q

What is retinitis pigmentosa?

A

A CONDITION THAT IS CHARACTERISED BY PHOTORECEPTOR DYSFUNCTION (RODS THEN CONES) AND PROGRESSIVE ATROPHY DEGENERATION OF RETINAL TISSUE

126
Q

What is retinitis pigmentosa caused by?

A

MOST COMMONLY DUE TO A MUTATION IN THE RHODOPSIN GENE IN THE LONG ARM OF CHROMOSOME 3

INHERITENCE CAN BE AD (MOST COMMON BUT LEAST SEVERE) AR OR XL INHERITENCE (WORST PROGNOSIS)

127
Q

What are the features of retinitis pigmentosa?

A

SYMPTOMS: NYCTALOPIA (LIGHT BLINDNESS) AND PERIPHERAL CISION LOSS (TUNNEL VISION IN LATE DISEASE)

TRIAD: PALE OPTIC DISC (WAXY DISC) + BOHNY SPICULES + ARTERIOLAR ATTENUATION

ERG (CONFIRMS DIAGNOSIS AND MONITORS DISEASE PROGRESSION) AND EOG ARE ABNORMAL

128
Q

What are the associations with retinitis pigmentosa?

A 
OPTIC DISC DRUSEN, 
MYOPIA, 
POSTERIOR SUBSCAPULAR CATARACT, 
CMO, 
OPEN ANGLE GLAUCOMA
KERATOCONUS
129
Q

What are retinitis-pigmentosa like conditions?

A

A GROUPS OF AR CONDITIONS CHARACTERISED BY PHOTORECEPTORS DYSFUNCTION WITH SIMILAR FEATURES TO RP

130
Q

How do retinitis pigmentosa like conditions present?

A

ALL PRESENT WITH NYCTALOPIA AND TUNNEL VISION WITH ASSOCIATED EXTRAOCULAR FEATURES

131
Q

What is Usher Syndrome?

A

MOST COMMON INHERITED CAUSE OF COMBINED DEAFNESS (SENSORINEURAL) + BLIDNESS

132
Q

What is Refsum Syndrome?

A

ACCUMULATION OF PHYTANIC ACID

ASSOCIATED ANOSMIA, PERIPHERAL NEUROPATHY AND ICHTHYOSIS

133
Q

What is bardet-biedel syndrome?

A

RP-LIKE RETINOPATHY OR BULL’S EYE MACULOPATHY (CONE-ROD DYSTROPHY MORE COMMON)

ASSOCIAED LEARNING DISABILITY, POLYDACTYLY AND OBESTIY

134
Q

What is Bassen Kornzweig syndrome?

A

ABNORMAL ABSORPTION OF FAT-SOLUBLE VITAMINS

ASSOCIATED SPINOCEREBELLAR ATAXIA AND ACANTHOCYTOSIS

135
Q

What are some causes of leukocoria?

A

CONGENITAL CATARACT

RETINOBLASTOMA

PERSISTENT FETAL VASCULATURE

RETINOPATHY OF PREMATURITY

COATS DISEASE

TOXOCARIASIS

(white pupil / absence of red reflex)

136
Q

What is a retinoblastoma?

A

MOST COMMON PRIMARY INTRAOCULAR MALIGNANCY IN CHILDREN

137
Q

What is a retinoblastoma?

A

MOST COMMON PRIMARY INTRAOCULAR MALIGNANCY IN CHILDREN

138
Q

What does retinoblastoma originate from?

A

ARISES FROM EMBRYONAL PHOTORECEPTOR CELLS OF THE RETINA WITH A MUTATION IN THE TUMOUR SUPPRESSION GENE RB1 ON THE LONG ARM OF CHROMOSOME 13

MOST COMMONLY SPORADIC IN INHERITENCE BUT CAN BE AD

139
Q

Describe the histopathology of retinoblastoma

A

FLEXNER ROSETTES ARE CLASSIC BUT HOMER-WRIGHT ROSETTES ARE FLURETTES MAY EXIST

140
Q

Describe the features of retinoblastoma

A

AVERAGE AGE OF DIAGNOSIS IS 3 YEARS, PARENTS OFTEN NOTICE LOSS OF RED REFLEX IN PHOTOS

141
Q

Describe the diagnostic features of retinoblastoma

A

UNILATERAL (SOMETIMES BILATERAL) LEUKOCORIA + STRABISMUS +/- RED EYE AND dVA

FUNDUSCOPY: WHITE ROUND MASS WITH EITHER ENDOPHYTIC (TOWARDS VITREOUS) OR EXOPHYTIC GROWTH (TOWARDS RPE / CHOROID)

ULTRASOUND SCAN: CAN SHOW CALCIFICATION WITH HIGHER INTERNAL REFLECTIVITY AND CAN HELP DETERMINE TUMOUR THICKNESS

142
Q

What is persistent fetal vasculature?

A

ALSO KNOWN AS PERSISTENT HYPERPLASTIC PRIMARY VITREOUS AND IS THE FAILURE OF THE FETAL HYALOID VASCULATURE TO REGERSS

CONDITION IS ASSOCIATED WITH PREMATURITY AND DEVELOPMENT OF CATARACT AND RETINAL DETACHMENT

PATIENTS PRESENT WITHIN THE 2 WEEKS OF LIFE WITH UNILATERAL LEUKOCORIA, MICRO-OPTHALMIA AND CATARACT (MITTENDORF DOT)

143
Q

What is retinopathy of prematurity?

A

BLOOD VESSELS GROW FROM THE OPTIC DISC TOWARDS THE PERIPHERY OF THE RETINA IN UTERO AND THIS GROWTH IS DRIVEN THROUGH A RELATIVE HYPOXIC STATE

MAIN RISK FACTOR FOR DEVELOPMENT OF ROP IS BRING BORN PREMATURELY

144
Q

Why is the periphery the most affected area in Retinopathy of prematurity?

A

RETINAL VESSELS REACH THE NASAL ORA SERRATA (JUNCTION BETWEEN RETINA AND PARS PLANA) AT 32 WEEKS GESTATION AND THE TEMPORAL AT 40 WEEKS

145
Q

What are the risk factors for retinopathy if prematurity?

A

PREAMTURELY BORN INFANT (< 32 WEEKS GESTATION)

WEIGHT LESS THAN 1500G

EXTENDED OXYGEN TREATMENT: FOR EXAMPLE IN NEONATAL RESPIRATORY DITRESS SYNDROME

146
Q

Describe the locations of retinopathy of prematurity

A

ZONE I: A CIRCLE WITH RADIUS OF TWICE THE DISTANCE FROM THE DISC TO FOVEA WITH THE OPTIC DISC BEING THE CENTRE

ZONE II: EDGE OF ZONE I TO NASAL ORA SERRATA

ZONE III: FROM ZONE II TO THE REMAINING RETINA

147
Q

Describe the stages of retinopathy of prematurity

A

WHITE DEMARCATION LINE SEPARATING VASCULAR FROM AVASCULAR AREAS

RIDGE: ELEVATED AND THICKENED DEMARCATION LINE

EXTRARETINAL FIBROVASCULAR PROLIFERATION OR NEOVASCULARISATION INFILTRATING THE VITREOUS

PARTIAL RETINAL DETACHMENT (A – EXTRAFOVEAL; B – FOVAL)

TOTAL RETINAL DETACHMENT (MOST COMMONLY TRACTIONAL)

148
Q

What is plus disease?

A

retinopathy of prematurity ADDITIONAL SIGNS OF INCREASED VENOUS DILATATION AND/OR ARTERIOLAR TORTUOSITY OF THE POSTERIOR RETINAL VESSELS CAN INCREASE THE SEVERITY OF THE CONDITION

149
Q

How is retinopathy of prematuriy screened for?

A

HIGH RISK CHILDREN SHOULD BE SCREENED VIA AN INDIRECT OPHTHALMOSCOPE WITH 28D LENS, COMPLICATIONS AND PERMANENT VISUAL LOSS CAN OCCUR IF THE DISEASE IS NOT TREATED EARLY

UK ROP SCREENING RECOMMENDATIONS (11) INCLUDE

ALL INFANTS BORN AT LESS THAN 32 WEEKS GESTATION AND / OR WEIGHING LESS THAN 1501G SHOULD BE SCREENED

  • IF BORN < 27 WEEKS GESTATION, SCREEN AT 30-31 WEEKS POSTMENSTRUAL AGE
  • IF BORN > 27 WEEKS AND < 32 WEEKS GESTATION OR BORN > 32 WEEKS GESTATIONAL AGE BUT WEIGH < 1501 G, SCREEN AFTER 4-5 WEEKS POSTNATAL AGE
  • SCREEN WEEKLY IF STAGE 3 DISEASE PLUS DISEASE OR IF VESSELS END AT ZONE 1 OR POSTERIOR ZONE 2
  • OTHERWISE SCREEN EVERY 2 WEEKS
150
Q

Describe the management of prematurity of retinopathy

A

TREATMENT WITHIN 48 HOURS WITH TRANSPUPILLARY DIODE LASER

TREAT IF:

  • ZONE 1, ANY STAGE PLUS DISEASE
  • ZONE 2: STAGE 3 PLUS DISEASE
  • ZONE 1: STAGE WITHOUT PLUS DISEASE
151
Q

What is coats disease?

A

UNILATERAL CONDITION OF UNKNOWN AETIOLOGY THAT IS CHARACTERISED BY THE TELANGIECTASIA AND NEOVASCULARISATION

COMMONNLY AFFECTS YOUNG BOYS

152
Q

What are the features of coats disease?

A

DVA, STRABISMUS AND LEUKOCORIA

RETINAL TELANGIECTASIA AND MICROANEURYSMS

INTRA/SUBRETINAL EXUDATION

COMPLICATIONS: EXUDATIVE RETINAL DETACHMENT AND NVG

153
Q

What is von-Hippel-Lindau disease?

A

AD CONDITION AFFECTING THE VHL GENE ON THE SHORT ARM OF CHROMOSOME 3

THIS CONDITION AFFECTS MULTIPLE ORGANS INCLUDING THE BRAIN, SPINAL CORD, RETINA, KIDNEYS, ADRENAL GLANDS AND PANCREAS

154
Q

What are the features of von hippel lindau disease?

A

RETINAL CAPILLARY HAEMANGIOMA WITH TORTUOUS FEEDER VESSELS

RENAL CELL CARCINOMA

PHAEOCHROMOCYTOMA

CNA HAEMANGIOBLASTOMA

155
Q

What is choroidal melanoma?

A

UVEAL TRACT MALIGNANT MELANOMAS ARISE FROM MELANOCYTES IN EITHER THE IRIS, CILIARY BODY OR CHOROID

CHOROIDAL MELANOMA IS THE MOST COMMON

156
Q

Describe a choroidal melanoma

A

USUALLY UNILATERAL IN PRESENTATION

CAN BE ASYMPTOMATIC OR CAUSE dVA AND EXUDAIVE RETINAL DETACHMENT

THEY CAN APPEAR PIGMENTED WITH A ‘COLLAR-STUD’ CONFIGURATION IF BRUCH’S MEMBRANE IS RUPTURED

METASTATIC SPREAD IF USUALLY TO THE LIVER

CHROMOSOME 3 MONOSOMY IS AN INDICATORY OF POOR PROGNOSIS

157
Q

Describe the management of central retinal vein occlusion

A

NON-ISCHAEMIC

  • IF VA IS 6/96 OR BETTER AND THERE IS EVIDENCE OF MACULAR OEDEMA ON OCT
  • COMMENCE INTRAVITREAL ANTI-VEGF OR OZURDEX (DEXAMETHASON) IMPLANT
  • BOTH TREATMENTS ARE FIRST LINE, ALTHOUGH YOUNGER PHAKIC PATIENTS OR WITH HISTORY OF GLAUCOMA SHOULD BE STARTED ON ANTI-VEGF
  • PATIENTS WITH HIGH CARDIOVASCULAR PROFILE SHOULD BE STARTED ON OZURDEX IMPLANT

ISCHAEMIC

  • NO NEOVASCULARISATION AND OPEN ANGLE: MONITOR FOR NEOVASCULARISATION AND GLAUCOMA
  • NEOVASCULARISATION PRESENT: URGENT PRP +/- CYCLODIODE LASER THERAPY IF ANGLE CLOSURE

Duke Elder 2020 (9 decks)

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