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VSAQ Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the usual inheritance pattern of cone dystrophy?

A

AD - Most cases are sporadic but of the inherited cases, it is usually AD.

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2
Q

What is the inheritance of Stargardts?

A

AR

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3
Q

Describe Mizuo phenomenon.

A

MIZUO PHENOMENON: change in fundus colour between light and dark adapted state in Oguchi’s disease (ie. disappearance of the abnormal shiny yellow-grey fundus colour with prolonged dark adaptation).
OGUCHI’S DISEASE: rare AR type of CSNB with non-progressive night blindness from birth characterised by Mizuo phenomenon.

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4
Q

What is the electrophysiological test used in Best’s disease?

A

EOG - Defective chloride channel results in low Arden Index (LP/DT) < 1.5 - 1.8

Normal ERG

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5
Q

How do you create cone response in ERG?

A

Flicker

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6
Q

What structures produce B wave?

A

Bipolar cells and Muller cells

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7
Q

In juvenile retinoschisis: (1) What layer is the schisis? (2) What is the inheritance?

A

(1) Between NFL and GCL

2) X-Linked recessive (retinoschisin gene

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8
Q

Systemic associations of angioid streaks.

A

PEPSI Common:
Pseudoxanthoma elasticum, Ehler-Danlos syndrome, Paget’s disease of bone, Sickle cell disease and other hemoglobinopathies, Idiopathic
LITE Less common:
Lead poisoning, Increased Ca or Phosphate, Tuberous sclerosis and NF, epilepsy

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9
Q

ICG – what wavelength is used?

A

800 nm absorption
830 nm emission
Penetrates through RPE

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10
Q

What is the most common non-ocular systemic association of RP that is associated with a syndrome?

A

Hearing loss

Part of Usher syndrome

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11
Q

Conditions associated with retinal dysplasia.

A

Norrie disease
Incontinentia pigmenti
Warburg syndrome

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12
Q

Causes of bull’s eye maculopathy in 26 year old man with minor difficulties in reading?

A

DYSTROPHIES: Cone and cone-rod dystrophies, Stargardts, benign concentric annular macular dystrophy
DRUGS: Hydroxychloroquine, chloroquine

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13
Q

Give 2 ocular and 1 nonocular features of Kearns Sayre?

A

OCULAR: Bilateral ptosis, chronic progressive external ophthalmoplegia, pigmentary retinopathy

NON-OCULAR: Cerebella ataxia, cardiac conduction defects, endocrine dysfunction (diabetes or hypogonadism), deafness, proximal myopathy

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14
Q

(1) What is the pattern of inheritance of hereditary juvenile retinoschisis? (2) Why is it associated with poor central visual acuity?

A

(1) X-linked recessive (retinoschisin gene)

(2) Central - foveal schisis with atrophic maculopathy; Peripheral - vitreous haemorrhage and retinal detachments

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15
Q

Indication for treatment of maculopathy in BRVO.

A

Macula oedema and visual acuity of 6/12 or worse at 3 months (BVOS) - grid laser
Macula oedema CMT > 250 μm and visual acuity of 6/12 or worse (BRAVO) - ranibizumab

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16
Q

What are the 2 wavelengths produced by the argon laser?

A

Argon Blue-Green laser: green 514nm and blue 488 nm

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17
Q

State the two major mechanisms of action of anti-VEGF treatment of AMD subretinal neovascularisation by agents such as Lucentis (ranibizumab) and Avastin (bevacizumab).

A

(1) Anti-angiogenesis

(2) Reduction in vascular permeability.

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18
Q

List the 2 most commonly recognised ocular paraneoplastic retinopathies.

A

(1) Cancer-associated retinopathy

(2) Melanoma-associated retinopathy

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19
Q

Give 4 causes of visual loss in BRVO.

A

(1) Macula oedema (2) Macula ischaemia

(3) Neovascularisation causing VH or RD (4) Rubeotic glaucoma

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20
Q

List 3 systemic associations of Von-Hippel Lindau.

A

(1) CNS hemangioblastomas - cerebellum, brainstem and spinal cord (2) Phaeochromocytoma (3) Renal cell carcinoma.

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21
Q

List 4 fundus findings indicating ischaemia in non-proliferative DR

A

(1) Cotton wool spots (2) Venous beading (3) IRMA

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22
Q

List 3 fluorescein angiographic signs of ocular ischaemic syndrome.

A

(1) Delayed arm to choroid filling time > 5 secs (2) Delayed arteriovenous transit time > 11 secs (3) Late staining of retinal vessel walls (arterioles > venules) (4) Patchy filling of the choroid (5) Intraretinal leakage at macula (6) Capillary non-perfusion

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23
Q

List 4 causes of hard exudates.

A

(1) DR (2) Hypertensive retinopathy (3) Retinal vein occlusion (4) Retinal macroaneurysm (5) CNVM (6) Retinal telangiectasia

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24
Q

Differential diagnosis of 34 yo male noted on routine eye exam to have CWS in one eye.

A

(1) DR (2) Hypertensive (3) Ischaemic - retinal vein occlusion or severe anaemia (4) Infectious - HIV, bartonella (5) Neoplastic - lymphoma/leukaemia

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25
Q

List 3 fundus findings in cone dystrophy.

A

(1) Bull’s eye maculopathy (2) Diffuse pigment granularity of posterior pole (3) Progressive RPE atrophy with geographic atrophy (4) Golden sheen in X-linked cone dystrophy

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26
Q

List 4 risks of laser for treatment of subretinal CNVM.

A

(1) Scotoma and scar extension (2) Risk of recurrence (3) Foveal burn (4) Subretinal haemorrhage

27
Q

Give 4 systemic conditions which may influence the severity of diabetic retinopathy.

A

(1) Hypertension (2) Dyslipidaemia (3) Impaired renal function (both marker of disease severity but can affect DR progression) (4) Anaemia (5) Pregnancy

28
Q

List 5 causes of choroidal folds

A

(1) Hypermetropia (2) Orbital mass/retrobulbar tumour (including thyroid eye disease) (3) Hypotony (4) Posterior scleritis (5) Chronic papilloedema (6) Scleral buckle

29
Q

Four weeks after macular laser treatment in a diabetic there is a sudden drop in acuity from 6/6 to 6/24. Give two macular causes for this.

A

(1) Increased macula oedema (2) CNVM

30
Q

Name 3 clinical features associated with a poor visual prognosis in diabetic maculopathy.

A

(1) Macula ischaemia (2) Hard exudates involving fovea (lipid dump) (3) Chronic oedema with lamella hole formation (4) Diffuse vs focal macula oedema

31
Q

Give 2 causes of visual loss with retinitis pigmentosa.

A

(1) Cystoid macula oedema (2) PSCC (3) Retinal degeneration involving macula (4) Macula hole or ERM

32
Q

Give 4 clinical signs of AMPPE.

A

(1) Multiple creamy-yellow placoid lesions at level of RPE or choriocapillaris concentrated in posterior pole (2) Old lesions - geographic RPE changes (3) FFA - initial blockage with late hyperfluorescence (4) Minimal AC or vitreous cells
Less commonly: (5) Disc edema (6) Vascular sheathing (7) Rarely get CME (cf birdshot)

33
Q

Give 4 clinical manifestations of ocular ischaemic syndrome.

A

(1) Light induced visual loss (delayed recovery) (2) Iris neovascularisation (3) Irregular venous dilatation (4) Mid-peripheral retinal haemorrhages (5) Optic disc pallor or disc oedema (6) NVD (and NVE less common)

34
Q

How did the ETDRS define ‘clinically significant macular oedema’?

A

(1) Retinal oedema < 500 μm from fovea (2) Hard exudates < 500 μm from fovea with adjacent retinal thickening (3) Retinal oedema > 1DD, any part of which is within 1DD from fovea

35
Q

List 4 features of Bardet-Biedl syndrome.

A

OCULAR: (1) Progressive rod-cone dystrophy with pigmentary retinopathy
NON-OCULAR: (1) Obesity (2) Polydactyly (3) Polycystic kidneys (4) Hypogonadism and hypogenitalism (5) Cognitive impairment
MNEMONIC: “Short, fat, thick, no dick”

36
Q

List 3 findings on FFA in a patient with cystoid macular oedema.

A

(1) Progressive hyperfluorescence at macula (2) Late accumulation in parafoveal cystic spaces in petaloid pattern (3) Mild disc leakage (4) Small hyperfluorescent spots due to early leaking in AV phase

37
Q

List 3 systemic risk factors for ARMD.

A

SYSTEMIC: (1) Smoking (2) HTN (3) Increased BMI (4) Cardiovascular disease (5) Dyslipidemia
DEMOGRAPHIC: (1) Increasing age (2) Caucasian (3) Family history/genetic

38
Q

Give 4 features that may indicate the presence of a subretinal CNVM.

A

(1) Subretinal fluid (2) Subretinal haemorrhage (3) Grey-coloured subretinal membrane (4) PED (5) Sub-retinal lipid deposits

39
Q

What are the 4 characteristic clinical features of Coats disease?

A

(1) Retinal telangiectasia (2) Intraretinal and subretinal exudates (3) Exudative detachment
(4) Male > female (5) Usually presents in 1st decade of life (6) Unilateral (7) Progressive (8) Leukocoria

40
Q

Give 3 features which correlated with poor prognosis in the CVOS study.

A

(1) Initial visual acuity <6/60 (2) Amount of non-perfusion on FFA (3) Moderate to severe venous tortuosity

41
Q

List the three most important ways of measuring the response of AMD subretinal neovascularisation to treatment.

A

(1) Visual acuity (2) OCT thickness (3) Presence or absence of subretinal haemorrhage?

42
Q

Give 2 treatments for gyrate atrophy.

A

(1) Vitamin B6 (300mg/day oral) reduces serum ornithine levels in a small proportion of patients (2) Dietary arginine restriction with low protein diet

43
Q

List 2 vitreous changes associated with retinitis pigmentosa.

A

(1) Mild vitritis (2) PVD

44
Q

What is the risk of development of FTMH in the other eye in idiopathic macular hole?

A

10 - 15% 5 year risk (much lower if already has PVD)

45
Q

What laser settings would you use for a macular grid?

A

(1) 50 - 100 μm spot size (2) 0.05 - 0.1s duration (3) Start at 60mW for very mild blanching (4) Space 1 burn-width apart (5) Apply 20 - 100 burns

46
Q

How close to the centre of the fovea can you laser according to macular photocoagulation study?

A

300 μm

200 μm for MPS retreatment study.

47
Q

In CVOS what percentage of perfused CRVO went on to become non-perfused in 3 yrs?

A

34% (conversion most rapid in first 4 months)

48
Q

Define severe NPDR.

A

4 quadrants of retinal haemorrhage, or 2 quadrants of venous beading, or 1 quadrant of IRMA.

49
Q

What characteristics were identified in the ETDRS as high risk for the development of proliferative retinopathy?

A

4 quadrants of retinal haemorrhage, or 2 quadrants of venous beading, or 1 quadrant of IRMA.

50
Q

CASE: 64 year old woman with unilateral superior-temporal BRVO, now 3/12 after onset. What would be the indication for laser treatment?

A

VA of < 6/12 which is due to macular edema (FFA should show no macular non-perfusion) AND be within 3-18 months post BRVO onset

51
Q

CASE: 75 year old man with subretinal CNVM due to ARMD. What is the risk of developing CNV in the fellow eye?

A

7 - 10% per year

52
Q

What is the degree of stenosis which would require carotid endarterectomy surgery?

A 
If symptomatic (eg. TIA or minor strokes), stenosis > 60%
If asymptomatic, stenosis > 70%
53
Q

What is Purtscher’s retinopathy?

A

SIGNS: Visual loss (VA or VF) and fundus appearance of microvascular angiopathy with multiple areas of retinal whitening (Purtscher’s flecken), CWS and minimal pre-retinal/retinal haemorrhages mainly at posterior pole. Should have no visible emboli. Unilateral or bilateral.
CAUSE: Head trauma (but without direct ocular injury), crush injury, orthopaedic surgery, long bone fracture or acute pancreatitis.

54
Q

Give 2 ocular manifestations of hepatitis C virus infection that are best supported by the literature.

A

(1) Xerophthalmia (dry eye syndrome similar to Sjögren)

2) Ischaemic retinopathy caused by HCV vasculitis (or due to interferon treatment

55
Q

What gene causes Stargardt’s disease?

A

Typically: ABCA4 (autosomal recessive) - ATP binding cassette transporter - transport molecules including retinoid across cellular membranes in photoreceptors

56
Q

Describe the acute and chronic fundus changes seen in malignant hypertension.

A

ACUTE: retinal arteriolar spasm, superficial retinal haemorrhages, retinal oedema, CWS, serous retinal detachment, disc swelling, Elschnig spots
CHRONIC: AV nipping, copper or silver wiring, broadening of arteriolar reflex, generalised arteriolar narrowing

57
Q

What information gives the most accurate prediction of the progression of RP?

A

Later age of onset which correlates with autosomal dominant form has better prognosis (compared to X-linked)

58
Q

List 4 ocular manifestations of hypertension (not including the changes in the vessels such as copper wiring and A/V nipping).

A

(1) CWS (2) Hard exudates (3) retinal haemorrhages (4) Elschnig spots (5) Disc swelling

59
Q

Give 2 classes of drugs causing pigmentary retinopathy

A

(1) Quinoline antimalarials (eg. chloroquine)
(2) Phenothiazine antipsychotics (eg. thioridazine)
(3) Iron chelators (eg. deferoxamine)

60
Q

(1) Describe the retinal lesions in Familial Adenomatous Polyposis. (2) What is its inheritance?

A

(1) Atypical CHRPE: multiple, bilateral, widely separated, oval or spindle-shaped with hypo-pigmentation. Bilateral lesions and lesions with a depigmented halo were the hallmarks of CHRPE associated with FAP. (2) AD

61
Q

What is the inheritance of Bests disease.

A

AD (but variable penetrance and expression)

62
Q

A young male patient is slightly obese, has a small appendage at the base of his little finger, and complains of difficulty with night vision. What is the most likely diagnosis?

A

Bardet-Biedl syndrome (rod-cone dystrophy)

63
Q

What role does vitamin A supplementation play in your management of a patient with retinitis pigmentosa?

A

Indication: Typical RP
Study: RCT 1990s
Dose: 15,000 IU Vitamin A palmitate
Benefit: Slow decline in ERG by 20%/year if started before age 30 (i.e. modest benefit only)
SE: Liver toxic, teratogenic! (C/I in pregnancy)

64
Q

What is tritanopia?

A

Deficiency in BLUE (short) wavelength sensitivity cones. Very rare 1:13,000. Difficulty with blue-yellow.

Medical Retina (2 decks)

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