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Basics of Retina
Gross anatomy of retina
Retinal area = 266 mm2; thickest at peripapillary re
gionQ (.56 mm) and thinnest at ora serrataQ (0.1 mm).
After death retina appears white opaqueQ.
Optic disc about 1.5 mm dia; light falling on optic disc
gives rise to NO visual sensation called blind spot
(of Mariotte); Optic nerve contains about 1.2 million
nerve fibresQ which originate in retinal ganglion cells.
Macula lutea (yellow spot) about 5.5 mm dia, situated
temporal to optic disc.
Fovea centralis is the central depressed part of the
macula about 1.5 mm dia, corresponds to central 5
degrees of visual field and is most sensitive part of the
Foveola (0.35 mm dia) forms the floor of the fovea and
is located about 2 disc diametersQ (3 mm) away from
the temporal edge of the optic disc and about 1 mm
below the horizontal meridian; at foveola only cones
are found.
Foveal avascular zone (FAZ) = 0.4-0.6 mm dia; FAZ is
located inside the fovea but outside the foveola.
Umbo is a tiny depression in the centre of foveola
which corresponds to foveolar reflex.
Parafovea = 0.5 mm width surrounding the fovea;
Perifovea 1.5 mm in width surrounding the peri
Ora serrata here the retina ends and ciliary body
starts; here the sensory retina is firmly adherent to the
vitreous base and the retinal pigment epithelium.

2 Quick Review of Ophthalmology

Microscopic anatomy of Retina
Retina: consists of ten layers. From outside (choroid side)
inwards, they are:

Retinal pigment
epithelium (RPE)


Inner nuclear layer


Layer of rods and



Inner plexiform layer


External limiting


Ganglion cell layer


Outer nuclear layer


Nerve fibre layer


Outer plexiform layer


Internal limiting membrane

The RPE consist of a single layer of hexagonal cells;

at the fovea, the RPE cells are taller and contain more
Adhesion between the RPE and the sensory retina is
weaker than between the RPE and Bruchs membrane.
The potential space between the RPE and the sensory
retina is the subretinal space.
The RPE cells with their zonula occludens constitute
the outer blood retinal barrierQ.
The IPM (Interphotoreceptor matrix) is the strongest
mechanism for binding the retina to the RPEQ.
Other mechanisms of retinal adhesion = vitreous gel
pressure, intraocular pressure and RPE water trans
GlycoconjugatesQ, including glycolipids, glycopro
teins, and proteoglycans, are present in the plasma
membrane of photoreceptor cells and in the interpho
toreceptor matrix.
Fluorescein Angiography
Fluorescein molecule is
relatively small; hence
fluorescein freely crosses
the choroidal vessel wall
and settles in retinal
vessels - This makes
FA primarily a study of
retinal vasculature

Indocyanine Green
Angiography (ICGA)
ICG is a larger molecule,
typically protein (albumin)
bound it is retained in
choroidal vessels since
choroidal vessel wall is
impermeable to larger
molecules - This makes
ICGA primarily a study of
choroidal vasculature

Retina 3
method of choice for
detecting Classic CNVM

method of choice for detecting

Occult CNVM

FA is useful for delineating

vessels in retina, iris and
Flower petal pattern
on FA seen in cystoid
macular edema
Smoke stack and
ink blot pattern on FA
seen in central serous

ICGA is superior to FA in:

Occult CNVM
Polypoidal choroidal
Chronic central serous
Lacquer cracks in myopic eyes
Angioid streaks


Electroculogram (EOG)

a wave =
photoreceptor (rods and
cones) activity;

Reflects the activity of the

retinal pigment epithelium and

b wave = response of
bipolar cells;

Measures the standing potential

between the electrically positive
cornea and the electrically
negative back of the eye;
Performed in both light and dark
adapted states

c wave = generated
by retinal pigment
epithelium and related
to retinal metabolism.

Arden ratio = light peak/dark

trough = 1.85 or 185% (Normal

Normal ERG is biphasic.

Subnormal EOG is confirmatory

in Best disease (autosomal
dominant); ERG is norma

Extinguished ERG:
advanced RP, CRAO,
complete old RD,
advanced siderosis
Subnormal ERG: early
RP, large area of retina
is not functioning
Negative ERG: Gross
disturbances of retinal
Pattern ERG: indicates
activity of central
macular region

4 Quick Review of Ophthalmology

Multifocal ERG: for
disorders of central




CAttle trucking appearance


Blood and thunder fundus

3. Hypermetropia

Silk shot retina (pseudoneuritis)

4. Myopia

Tesselated background, posterior

staphyloma, temporal crescent, lattice
degeneration MC

5. Sickle cell

Sea fan retinopathy, Rising sun


6. Pars Planitis


7. Sarcoidosis

Candle wax drippings, Landers sign

8. Salt and
Pepper fundus

Congenital syphilis
Lebers amaurosis
Congenital Rubella

9. Purtshcers

Bilateral multiple cotton wool spots and/

or superficial hemorrhages around optic
nerve; By definition, seen in severe head
and chest injury; pseudo Purthschers
retinopathy = embolism (fat, air, amniotic
fluid), acute pancreatitis, SLE, lymphoma,
TTP, after BMT

10. Uyemuras

Xerophthalmic fundus

11. Mizuo

Oguchis disease (congenital stationary

night blindness)

12. Angioid

Pseudoxanthoma elasticum (MC), EhlersDanlos syndrome, Pagets disease, Sickle

cell disease, Idiopathic; Hypercalcemia,
Acromegaly, Lead poisoning; {PEPSI,

13. Angioid

Orange peel or peau de orange

appearance of retina

14. Terson

Intraocular hemorrhage (intraretinal and

vitreous hemorrhage) + subarachnoid

Retina 5
15. Shaken Baby

Multilayered hemorrhages (pre, intra and

sub-retinal) hemorrhages

16. Morning glory


mesodermal defect with lamina cribrosa


17. Sturge Weber


Tomato catsup fundus (Diffuse choroidal


18. Tuberous

Mulberry tumor (retinal astrocytoma)

19. Best disease

Scrambled egg/Eg Yolk and

pseudohyopyon maculopathy

20. End stage


Cracked Mud appearance (Progressive

Outer Retinal Necrosis)

21. Acute retinal


Swiss cheese pattern

22. CMV retinitis

Cottage cheese and ketchup; tomato

ketchup/pizza pie retinopathy

23. VKH syndrome

"Sunset Glow" fundus, chronic/recovery


24. Toxoplamosis

"Headlight in fog" appaearance choroiditis seen through vitreous haze

Cotton wool spots (CWS)

Acute obstruction of precapillary retinal arteriole
causing blockage of axoplasmic flow and buildup of
axoplasmic debris in the nerve fibre layer - seen as
cotton wool spot (CWS).
Note: Even a single CSW is abnormal; in absence
of DM, HTN or a retinal vein occlusion, a systemic
workup should be performed.
DM is MC cause; Also seen in acute or chronic HTN;
CRVO, BRVO; HIV retinopathy; Giant cell arteritis;
collagen vascular disease (SLE - MC, Wegener's PAN,
scleroderma etc...); Infections (toxoplasmosis, Lyme,
leptospirosis, orbital mucormycosis, onchocerciasis,
subacute bacterial endocarditis); Purtscher retinopathy;
radiation retinopathy; interferon therapy; Cancers
(metastatic carcinoma, leukemia, lymphoma); Hypercoagu
lable states; Others (migraine, hypoetension; IV drug abuse;
papilledema, papillitis, sickle cell anemia, acute blood loss).

6 Quick Review of Ophthalmology

Diabetic Retinopathy (Dr)

Duration of diabetes is the most important determining
factor. Longer duration of diabetes, more is the risk for
Good metabolic control of diabetes will NOT prevent
DR, although it delays its development by a few years.
Systemic factors which have an adverse effect on DR
includepregnancy; hypertension, renal disease, obesity,
hyperlipidemia, smoking, anaemia.
Microvascular occlusion
1. Capillary changesthickening of basement membrane,
endothelial cell damage and proliferation.
2. Deformation of RBCsoxygen transport.
3. Changes in plateletsstickiness and aggregation.
(1), (2), (3) Retinal capillary nonperfusion
retinal ischaemia retinal hypoxia.
Retinal hypoxia:

Arteriovenous (AV) shunts that run from arterioles

to venules (IRMAintraretinal microvascular abnor
Neovascularisaionhallmark of PDR; hypoxic retinal
tissue attempts to revascularise hypoxic areas through
growth factors (importantly vascular endothelial
growth factor, VEGF)
Microvascular leakage
Cellular elements of retinal capillaries consist of
endothelial cells and pericytes (blood retinal barrier).
Pericytes are wrapped around the capillaries (one
pericyte per endothelial cell) and are responsible for
structural integrity of vessel wall.
In DM, there is in the number of pericytes
distension of capillary walls breakdown of blood
retinal barrier leakage of plasma constituents into
the retina retinal edema, hard exudates, haemorrhage.

Retina 7
Capillary distension saccular pouches of the
vessel wall (microaneurysms) either leak or become
Classification of DR
Non proliferative DR (NPDR): Ophthalmoscopic features
of NPDR include:
Microaneurysms in macular area (earliest clinically
detectable lesion).
Retinal haemorrhages, both superficial (flame shaped)
and deep (dot blot haemorrhages).
Hard exudatesyellowish white, waxy, patches
arranged in clumps or in circinate pattern around
macula (circinate retinopathy).
Retinal edema characterized by retinal thickening.
Cotton wool spots (if > 8, high risk of developing
Venous abnormalities, beading, looping, dilation.
Intraretinal microvascular abnormalities (IRMA).
Dark-blot haemorrhages representing retinal infarcts.
Mild NPDR: few microneurysms, retinal haemorrhages
and hard exudates in one or two quadrants.
Moderate NPDR: above findings seen in two or three
Severe NPDR: above findings in all four quadrants and at
least one of the following plus signs:
Cotton-wool spots
Venous beading in > 2 quadrants
IRMA in > one quadrant
Very severe NPDR: same as above except that atleast 2 or 3
plus signs of severe NPDR are present.
Diabetic Maculopathy:
Focal, Diffuse, Ischaemic or Mixed
Clinically significant macular edema (CSME)

Retinal edema within 500 of centre of fovea.

Hard exudates within 500 of centre of fovea +
adjacent area of retinal thickening

Retinal edema > 1 disc diameter, any part of which
lies within 1 DD of centre of fovea.

8 Quick Review of Ophthalmology

Proliferative DR (PDR)
NVD (Neovascularisation at
NVE (Neovascularisation
Preretinal haemorrhage
Vitreous haemorrhage
Tractional RD
Neovascularisation of iris
and or angle.

High-risk Characteristics in
NVD up to 1 disc diameter
>1/4 disc area
Less extensive NVD +
preretinal/vitreous haemorrhage
NVE >1/2 disc area +
preretinal/vitreous haemorrhage

Management of DR
General: Control of blood glucose, control of hypertension,
anaemia should be promptly treated, drugs for decreasing
platelet adhesiveness; hypolipidemic drugs.
Specific Treatment:
1. Mild NPDR: Periodic examination as outlined above.
2. Moderate to severe NPDR: Here again, patient should
be followed up very closely. However treatment is
warranted in following conditionsuniocular pa
tient, pregnancy, renal/cardiac failure, and poor com
pliance for follow-up, uncontrolled blood sugar, prior
to cataract extraction/YAG capsulotomy.
3. Diabetic maculopathy:

Focal maculopathy: focal argon laser photocoagu
lation required around the microaneurysms or
leaking vessels.

Diffuse maculopathy: macular-grid photocoagula
tion required, but avoid the fovea.

Ischaemic maculopathy: Photocoagulation will not
improve vision; follow up is necessary as about
30% will develop PDR within 2 years.
4. PDR: The treatment of choice is argon laser Pan
Retinal Photocoagulation (PRP). Aim of treatment is to
convert the hypoxic area to anoxic area, and thereby,
to induce involution of new vessels, and to prevent
recurrent vitreous haemorrhage. PRP is performed in
two or more sessions because, if done in one session
only, it causes more serious complications. The new
vessels usually take 4-8 weeks time to regress after
adequate PRP.

Retina 9
Diabetes Type

Time of First


Type 1

3-5 years after

onset (in all patients
> 9 yrs of age)


Type 2

At time of diagnosis


Prior to pregnancy
or during
pregnancy (type 1
or type 2)

Prior to conception
or early in the first

Every 3 months
until delivery

Diabetic Retinopathy Studies

Diabetic Retinopathy Study (DRS)

Early Treatment Diabetic Retinopathy Study (ETDRS)
United Kingdom Prospective Diabetes Study (UKPDS)
Diabetes Control and Complications Trial (DCCT)
Diabetic Retinopathy Vitrectomy Study (DRVS)
Retinopathy Type

Follow-up (Months)

1. Normal or minimal NPDR


2. Mild to moderate NPDR

6-12 (3 months if CSME present)

3. Severe or very severe


4. Non-high-risk PDR

5. High-risk PDR

6. High-risk PDR
not amenable to
photocoagulation (e.g.,
media opacities)


Other ocular signs in diabetes mellitus

Transient variations in refraction:

Hyperglycemia increased refractive
index of lens myopic shift

Hypoglycemia decreased refractive
index of lens hypermetropic shift.

Diplopia in ophthalmoplegia caused by neuropathy

Photopsia and diplopia in cerebral hypoglycemia.

10 Quick Review of Ophthalmology

Diminished vision in cataract, maculopathy and

vitreous haemorrhage.
Complete blindness from tractional RD, massive
vitreous proliferation and neovascular glaucoma.
Sudden onset of muscle palsies (third nerve, sixth
Pupil sparing third nerve palsy: The parasympathetic
pupillomotor fibres are located superficially in the
third nerve and derive their blood supply from
the pial blood vessels whereas the main trunk of
the nerve is supplied by the vasa nervorum. The
microangio-pathy associated with medical lesions
(diabetes, hypertension) involves the vasa nervorum,
causing neural infarction of the main trunk of the
nerve, but sparing the superficial pupillary fibres.
Painful ophthalmoplegia.
Increased incidence of stye and hordeolum internum.
Xanthelasma (due to associated hyperlipidemia).
Tortuous and constricted blood vessels.
Sludging of blood.
Delayed epithelial healing due to abnormality in
epithelial basement membrane.
Punctate keratopathy.
Delayed healing of infective keratitis due to hyper
Wrinkling of Descemets membrane.
Decreased corneal sensation (due to trigeminal neuro
Hydrops of pigment epithelium (due to transient
glycogen storage), release of pigment into AC dur
ing surgery or simply even after dilation of pupil.
Rubeosis iridis.
Variation in refractive power (during hyperglycemia) increased glucose content (sorbitol) of
the lens cortex imbibition of water lens
becomes thicker induced myopia.

Retina 11

Snowflake cataract.
Posterior cortical cataract.
Early onset of senile cataract.
Vitreous haemorrhage.
Fibrovascular proliferation in the vitreous.
Diabetic retinopathy (as discussed already).
Lipemia retinalis (due to associated triglyceridemia,
in keto-acidosis).
10. IOP
Increased incidence of POAG.
Neovascular glaucoma: In DM, if posterior capsule
rupture occurs during cataract surgery, there
is higher chance of neovascularisation of iris/
angle since the vasogenic growth factors from the
posterior chamber gain access to the AC.
IOP decreased in diabetic ketoacidosis (due to increased
plasma bicarbonate level).

Retinal Vessel Occlusions

Central Retinal Artery Occlusion (CRAO)

Thrombosis is MC cause of CRVO

(hypercoagulable states), embolism (MC due to
carotid atherosclerosis; or it may be cardiac
in origin) and retinal arteritis with obliteration
(giant cell arteritis, polyarteritis nodosa,


Amaurosis fugax (transient sudden visual loss

lasting for few minutes due to occlusion by minute
emboli) may be a premonitory Sudden painless
loss of vision, RAPD, white retina, cherry red
spot in macula, attenuated retinal arterioles,
sludging of blood in the veins called as cattle
trucking appearance, after a week or so the
retina resumes its normal ophthalmoscopic
appearance leaving behind atrophic white optic
disc and thread like retinal arteries. Susac
syndrome: triad of CRAO, sensorineural
deafness, encephalopathy.

12 Quick Review of Ophthalmology


Treatment: lie flat, ocular digital massage for 15

minutes (to dislodge emboli, lower IOP), anterior
chamber paracentesis, IV acetazolamide/

Variants of CRAO
Branch Retinal Artery Occlsuion: Acute and severe
altitudinal visual field defect. BRAO follows lod
gement of cholesterol embolus at arteriolar bifurcation
(Hollenhorst plaque); white retina in the area with
obstructed blood flow, permanent sectorial visual field
Cilioretinal artery occlusion: Cilioretinal artery
perfuses retina but is derived from posterior ciliary
circulation, present in 30% of individuals; here pallor
is localized to posterior pole.
Ophthalmic artery occlusion: Causes include orbital
disease, retrobulbar anaesthesia, cardiovascular di
sease similar to that associated with CRAO. Signs
Total afferent papillary defect; severe loss of VA (PL
negative); Intense retinal whitening (both retinal and
choroidal circulation are simultaneously involved).
Ocular causes

Lysosomal storage disorders


Central Retinal Artery

Occlusion (CRAO)

Tay-Sachs disease
(virtually ALL cases
Kenneth Wrights Pediatric
Ophthalmology, 2nd/799; MC
metabolic causeQ)

Berlins edema of the

macula (commotio retinae)

Niemann Picks diseaseQ (less

common than in Tay Sachs)

Macular hole with

surrounding retinal

Sandhoffs disease (GM2

gangliosidosis type 2)

Quinine toxicity

Generalized GM1
gangliosidosis type 1

Ocular Ischemic

Sialodosis types 1,2

(Cherryred spot-myoclonus

Retina 13

Farbers disease

Infantile Metachromatic

Batten Mayou disease

Goldbergs syndrome

?? Gauchers disease ??

Hurlers syndrome
B-galactosidase deficiency
Hallevorden Spatz

Note: Gauchers disease is NOT COMMONLY GIVEN as

a cause of cherry red spot in standard textbooks of medi
cine and ophthalmology except in DukerYanoffs Oph
thalmology book best option to choose if the question
sayscherry red spot is seen in all except.
Pathogenesis of cherry red spot

Thickening and loss of transparency of retina at posterior

pole (in various conditions given above)

Fovea is the thinnest part of the retina and devoid of

ganglion cells retains relative transparency

Underlying orange-red hue of choroidal vasculature is

transmitted and seen as cherry red spot

In sphingolipidoses, progressive accumulation of

glycolipids and phospholipids in the ganglion cell layer of
the retina gives the retina a white appearance; as ganglion
cells are absent at foveola, this area remains

Predisposing factors:
Systemic: Increasing age (sixth and seventh deca
des); systemic hypertension and diabetes mellitus;
hyperviscosity syndromes (chronic leukemia,
polycythemia, Waldenstroms macroglobulinemia,
sickle cell disease), periphlebitis (sarcoidosis,
Behcets disease); elevated ESR (only in women);

14 Quick Review of Ophthalmology

Ocular: Raised IOP (POAG), hypermetropia, head

trauma, optic disc drusen, congenital anomaly of
the CRV.
Mechanism: The vein is compressed by a thickened
artery where the two share a common adventitia (i.e.
at A-V crossings in the retina and just behind the
lamina cribrosa).

Central Retinal Vein Occlusion (CRVO)

Non-Ischaemic CRVO


More common (75% of cases)

Less common

Moderate loss of VA

Severe loss of VA (< 6/60 or


Slight RAPD (Marcus Gunn


Marked RAPD

Mild tortuosity and dilation of

all branches of the CRV

Marked tortuosity and

engorgement of retinal veins

Mild to moderate retinal

haemorrhages (dot-blot
and flame shaped) in all 4
quadrants and most numerous
in the periphery

Extensive retinal
haemorrhages involving both
peripheral retina and posterior
pole (Blood and Thunder

Few cotton wool spots

Numerous cotton wool spots

Mild optic disc edema and

macular edema

Severe optic disc edema and


FFA: venous stasis but good

retinal capillary perfusion

FFA: masking of retinal

vascular bed by retinal
haemorrhages and extensive
areas of capillary nonperfusion

Prognosis: Good return of

VA to near normal in 50%
of patients. Main cause for
persistent poor VA is chronic
cystoid macular edema

Prognosis: VA is permanently
impaired due to macular
ischaemia. Rubeosis iridis
develops in about 50% of
eyes at 3 months (the 100
day glaucoma), neovascular
glaucoma, vitreous
ERG is subnormal

Treatment: Treat predisposing


Treatment: PRP or
cryoapplication if media is hazy

Retina 15
Central Retinal Vein Occlusion (CRVO) and Ocular
Ischemic Syndrome (OIS)


Dilated retinal veins

Venous tortuosity

Retinal edema

Hard exudate

Retinal arterial pulsations


Optic disc edema

Arterial pulsations with

light pressure

Delayed choroidal filling


N to high


Retinal artery
pressure (measured by

Branch Retinal Vein Occlusion (BRVO)

Three times more common than CRVO.
Clinical features: Sudden onset of blurred vision and
metamorphopsia or a relative visual field defect; a
peripheral vein occlusion may have no effect on visual
function. Dilated and tortuous veins, flame-shaped/
dot-blot haemorrhages, retinal edema, cotton-wool
spots absorption of haemorrhage and beginning
of hard exudates formation. Signs of old occlusion are
vascular sheathing and collaterals.
Complications: Neovascularisation, Chronic macular
edema (MC cause of persistent poor VA after BRVO).
Treatment: Wait 8-12 weeks for retinal haemorrhages
to clear and spontaneous visual improvement to occur.
If VA continues to be 6/12 or worse after 3 months,
Argon laser photocoagulation should be considered.
Recent advances in CRVO/BRVO treatment:

Ozurdex is a dexamethasone intravitreal implant
(0.7 mg) approved for treatment of
Macular edema following CRVO or BRVO
Noninfectious posterior uveitis

16 Quick Review of Ophthalmology

It is in a biodegradable polymer form and slowly

releases the drug over a 6 months period.
See under anti-VEGFs in Ophthalmology below for
more about Intravitreal Avastin.

Retinal Detachment (RD)


1. RD is separation of the neurosensory retina from the

retinal pigment epithelium (RPE), (which represent
the two layers of the primary optic vesicle), by subre
tinal fluid (SRF).
Retinoschisis is the splitting of the sensory retina
into two layers.
Retinal break is a full thickness defect or discon
tinuity in the sensory retina.
Tears are caused by dynamic vitreoretinal traction;
they have a prediliction for the upper temporal
fundus, more dangerous than hole.
Holes are caused by chronic atrophy of the sensory
retina; they have a prediliction for the upper
temporal fundus; less dangerous than tears.
Primary break is defined as the one responsible for
the RD.
Secondary break is not responsible for the RD or
forms after RD has occurred.
The upper temporal quadrant is the MC for retinal
break formation. About 50% of eyes with RD have
more than one break and in most eyes these are
located within 90o of each other.
2. Syneresis is the contraction of vitreous gel that sepa
rates from solid components.
3. Synchisis is the liquefaction of vitreous gel.
4. Choroidal detachment is an effusion into the suprachoroidal space.

Peripheral Retinal Degenerations

About 60% of all retinal breaks develop in peripheral
retina that shows degenerative changes that may
be associated with spontaneous hole formation or
predispose to retinal tears.

Retina 17
Predisposing degenerations


Lattice degenerationpresent in 8%
of general population and in 40% of
eyes with RD; important cause of
RD in young myopes; characterized
by white arborising lines, arranged
in lattice pattern occurring in upper
temporal peripheral fundus between
the equator and posterior border of
vitreous base with long axis parallel
to ora serrata. Lattice also seen in
Marfan synd.; Ehler Danlos synd.

Snow flakes
(micro cystoid)

Atypical lattice: Is characterized

by radial lesions, which appear
continuous with the peripheral blood
vessels; seen in Stickler syndrome.
Snail track degeneration
White with pressure; White without
Focal pigment clumps

Classification of RD

MC type; Due to tear/break in retina

which permits SRF derived from the
synchitic (fluid vitreous) to gain access
into the subretinal space
MC in myopes due to frequent lattice
Photopsia/flahses (more temporally)
and floaters present.
Loss of vision like a curtain coming
across field of vision.
Schaffers sign - Tobacco dust in
vitreous (anterior vitreous pigments)
Features of Chronic RD = pigmented
demarcation lide, intraretnal cysts, fixed
folds, white dots underneath the retina
(subretinal precupitates), relative visual
field defect.
Treatment options for rhegmatogenous
RD: laser photocoagulation;
cryotherapy,; pneumatic retinopexy;
vitrectomy, scleral buckle or a
combination of these with endolaser

18 Quick Review of Ophthalmology

Tractional RD

(2nd MC type) Due to proliferative

vitreoretinopathy sensory retina
is pulled away from the RPE by
contracting vitreoretinal membranes;
the source of SRF is unknown; MC in

Exudative RD

NO tear/break; SRF derived from the

choroids gains access to subretinal
space through damaged RPE
Causes are choroidal melanoma,
toxemia of pregnancy, malignant
hypertension, Haradas disease.
NO photopsiae/floaters
Shifting of subretinal fluid is the
D/D of Bilateral Exudative RD
Ca metastasis to choroid, Uveal
effusion syndrome, Posterior scleritis,
Eclamspia, Central serous retinopathy,

Vitreous substitutes and agents for retinal tamponade

The definition of retinal detachment is the separation
of the neurosensory retina from the retinal pigment
epithelium (RPE), (which represent the two layers of
the primary optic vesicle), by subretinal fluid (SRF).
Hence retinal tamponade is used in retinal detachment
treatment and aims to ensure adhesion of the detached
neurosensory retina to the retinal pigment epithelium.
Agents used for retinal tamponade are

Gases: SF6 (sulfur hexafluoride); C3F8 (perfluoro
propane); C2F6 (perfluoroethane); air

Oil: Silicone oil

Liquid: PFCL (Perfluorocarbon liquid).

Retinitis Pigmentosa (RP)

Typical RP is a diffuse bilaterally symmetrical retinal
dystrophy predominantly affecting rods.
Inheritance: Sporadic; AD (MC, best prognosis); AR;
XLR (least common, worst prognosis, female carriers
have normal fundi or show golden-metallic tapetal
reflex temporal to the macula which is virtually
pathognomonic); uncertain (6%).

Retina 19

Clinical features:
Symptoms include defective dark adaptation
(night blindness, nyctalopia), progressive visual
field defect.
Classic triad of RP: (1) arteriolar attenuation (2)
bone-spicule pigmentation that is perivascular and
more in equatorial region (3) Waxy pallor of optic
disc that is least reliable sign of the triad.
Unmasking of larger choroidal vessels (due to
pigment migration) gives the fundus a tessellated
Three types of maculopathy that may be seen are:
atrophic, cellophane, cystoid macular edema.
Associated ocular features: optic disc drusen, openangle glaucoma (3%), posterior subcapsular
cataracts, keratoconus, myopia, posterior vitreous
ERGreduced amplitude of scoptopic and photopic
b-wave, delay in time between the flash of light and
peak of b-wave (delayed implicit time).
EOG: absence of light rise.
Visual field: initially annular/ring scotoma, later
progressive constriction of visual field.
Atypical RP:
Retinitis punctata albescens: scattered white dots
most numerous between posterior pole and equa
Sector RP: Involvement of only one quadrant
(usually nasal) or one half (usually inferior) of the
fundus; slow progression and many cases remain
Pericentric RP: Similar to typical RP, except that pig
mentary changes are confined to pericentral retina
RP with exudative vasculopathy: Coats-like telan
giectatic vascular abnormalities, lipid deposition in
peripheral retina and exudative RD
Note: Epiretinal and subretinal microchip implants
have been used with modest success in RP

20 Quick Review of Ophthalmology

RP like fundus picture is seen in:

End stage chloroquine retinopathy

End stage syphilitic retinopathy

Cancer related retinopathy
Syndromes Associated With Retinitis Pigmentosa (RP)
Syndromes (All AR)

Features in addition to RP

Bassen-Kornzweig syn.

Acanthocytosis, fat
malabsorption, ataxia; jejunal
biopsy is diagnostic

Refsums syn.

Due to defective metabolism

of phytanic acid that
accumulates. Peripheral
neuropathy, cerebellar ataxia,
elevated CSF proteins,
deafness, icthyosis, cardiac

Bardet-Biedl syn.

Mental retardation, polydactyly,

obesity, hypogonadism; (coned
rod dystrophy causing Bulls
eye maculopathy is typically
a/w Bardet Biedl syndrome)

Ushers syn.

Sensorineural deafness.

Kearns-Sayre syn.

Chronic progressive external

ophthalmoplegia, heart block.

Cockaynes syn.

Bird-like facies, dwarfism,

flexion contracture of limbs,
mental retardation, ataxia and
premature aging.

Cohen syn.

Facial dysmorphism,
prominent incisors, mental
deficit, muscle hypotonia,
truncal obsesity

Friedrich ataxia

Ataxia, nystagmus

HARP syn. a.k.a.


acanthocytosis, RP, Pallidal
degeneration (Progressive
extrapyramidal dysfunction
and dementia)

NARP syn.

Neuropathy, Ataxia, RP

Retina 21

Age Related Macular Degeneration (ARMD)

Also called senile macular degeneration, a bilateral
disease that is a leading cause of blindness in the
western world.

Earliest clinically detectable feature of ARMD are
drusen, which are, yellow-white spots at the pos
terior pole associated with subsequent develop
ment of ARMD.

Drusen consist of focal aggregations of hyaline
material located between the basal lamina of
the RPE and inner collagenous layer of Bruchs

Drusen may be hard, soft, diffuse, or calcified.
Types of ARMD
Non-exudative (dry, atrophic)

Exudative (wet,
neovascular) ARMD

MC type90% of cases;
causes mild to moderate
gradual loss of vision over many

Less common, but a/w

rapidly progressive
loss of vision, all
central vision may be
lost within a few weeks.

Clinically appears as sharp

circumscribed areas of RPE
atrophy with varying degrees of
loss of choriocapillaries.

Two important features

of exudative ARMD are
detachment of the
RPE and choroidal
(subretinal or
choroidal neovascular
membranes, SRNVM
or CNVM).

Treatment: There is no effective

treatment except for provision of
low visual aids.

Sequelae of exudative
detachment of the RPE
detachment of the
neurosensory retina
Vitreous haemorrhage
Disciform scarring at the
Exudative RD

22 Quick Review of Ophthalmology

Antioxidants: As per AREDS
study (Age Related Eye Disease
Study) vitamin C, beta carotene,
zinc, cupric oxide is useful

Argon laser
may be effective in
obliterating extrafoveal
SRNVMs outside the
foveal avascular zone
For never treatments
see below

Anti VEGFS in Ophthalmology (Recent Advances)

Vascular endothelial Grwoth Factor (VEGF) promotes
angiogenesis, increases vascular permeability and has
proinflammatory action.
In the human eye, increased levels of VEGF correlate
with retinal ischemia associated neovascularisation
in diabetic retinopathy, retinal venous occlusion and
retiniopathy of pematurity; also VEGF levels are
elevated in wet AMD.
Hence anti-VEGF agents are developed to use in these
conditions; all are used intravitreally.
Currently available anti VEGFs are
Pegaptanib sodium

First FDA approved anti-VEGF;

it is a pegylated aptamer
which binds with high affinity
to the major pathologic VEGF
isoform, VEGF165 thereby
inhibiting it from binding to its

Bevacizumab (Avastin)

Humanised monoclonal
antibody against VEGF; binds
all the isofrms of VEGF and
its biologically active cleavage
products; currently FDA
approved for IV treatment
of colorectal cancer; ocular
uses are off-label but found
safe and effective worldwide.

Retina 23
Ranibizumab (Lucentis)

Second FDA approved antiVEGF; Humanised monoclonal

antibody against VEGF; binds
all the isofrms of VEGF and
its biologically active cleavage


Anti-VEGF fusion protein that

binds all isoforms of VEGF-A
and placental growth factor

Indications of anti-VEGFs
Wet ARMD (choroidal neovascular membrane,
Diabetic retinopathy (for macular edema)
Retinal Venous occlusive disease (for macular edema)
Other Angiostatic drugs
Anecortave Acetate

An angiostatic cortisone
which lacks glucocorticoid
activity (hence ocular
hypertension and cataracts are
avoided); Used for wet AMD

Squalamine lactate

Systemically administered anti

angiogenic compound; was
discontinued since it was not
better than ranibizumab.

PDT (Photodynamic therapy)

Photodynamic therapy is used in the treatment of
wet ARMD (age related macular degeneration).
Verteporfin dye and diode laser is used. Less popular
now due to availability and efficacy of anti-VEGFs.
Choroidal Neovascular Membrane

Grey-green membrane or blood seen deep to retina.

More common: ARMD, high myopia, IPCV (idio
pathic polypoidal choroidal vasculopathy), an
gioid streaks, choroidal rupture (trauma), ocular

24 Quick Review of Ophthalmology

Less common: drusen of optic nerve, tumours,

retinal scarring after laser photocoagulation, idio


Hypertensive retinopathy
The fundus picture of hypertensive retinopathy is charac
terized by
1. Vasoconstriction generalized and focal arteriolar
narrowingQ; obstruction of precapillary arterioles
cotton wool spots. (reflects severity of HTNQ)
2. Leakagecaused by abnormal vascular permeability
flame shaped haemorrhagesQ, hard exudates and retinal
edema. Hard exudates around the fovea in Henles
layer macular starQ.
3. Arteriosclerosis thickening of vessel wall
clinically seen is the presence of marked changes at
AV crossings (AV nipping which also indicates that
hypertension has been present for a long time reflects
duration of HTNQ)
Grading of hypertensive retinopathy
(Keith Wagner Barker gradingQ)
Grade Imild generalized arteriolar attenuation
with broadening of arteriolar light reflex and vein
Grade IImore severe generalized and focal
arteriolar constriction associated with deflection of
veins at AV crossings (Salus sign).
Grade IIIcopper-wiring of arterioles, banking of
veins distal to AV crossings (Bonnet sign), tapering of
veins on either side of crossings (Gunn sign). Flame
shaped haemorrhages, cotton wool spots, and hard
exudates are also present.
Grade IVall grade 3 changes + silver wiring + disc
edemaQ (malignant hypertension) + macular star
a/w renal insufficiencyQ.
Other ocular manifestations of hypertension include
CRVO, BRVO, CRAO, anterior ischaemic optic neuropathy,

Retina 25
retinal artery macroaneurysm, ocular motor nerve palsies.
Acute hypertension as seen in eclampsia may cause
choroidal ischaemia and exudative/serous RD. Uncontrolled
systemic hypertension also has an adverse effect on diabetic
Hypertensive Choroidopathy: Rare, but may occur as
a result of acute HTN crisis (accelerated HTN) in young
Elschnigs spotsQ: Small black spots surrounded by
yellow halo represent choroidal infarcts.
Seigrist streaksQ: Flecks arranged linearly along cho
roidal vessels indicates fibrinoid necrosis
Exudative RDQ: Sometimes bilateral occurs in
toxemia of pregnancy.
Central Serous Retinopathy

Localised serous detachment of retina at

macula due to RPE pump failure
Affects young males with type A
personality, hypertensives, aggravated by
systemic steroid usage; may be a/w optic
disc pit


Moderately blurred vision correctable with

weak plus lens (acquired hypermetropia),
central positive scotoma (something
blocking vision), micropsia, ring reflex at
macula, foeval reflex absent or disotorted


Diagnosed by fluorescein angiogram

shows MC smoke-stack pattern or ink-blot
Usually resolves spontaneously in 80-90%
Laser photocoagulation is indicated in
following cases:
Long-standing CSR (>4 months) with
marked loss of vision.
Recurrent CSR with visual loss.
If vision in fellow eye is permanently
reduced to previous attacks of CSR.

26 Quick Review of Ophthalmology

Causes of Bulls Eye Maculopathy
In adults

In children

Chloroquine maculopathy

Bardet Biedl syndrome

Advanced Stargdardts

Hallervorden Spatz disease

Fenestrated sheen macular


Leber congenital

Benign concentric annular

macular dystrophy


Clofazimine retinopathy

AD cerebellar ataxia

Sielmeyer Vogt syndrome

Juxtafoveal Retinal Telangiectasia

Definition: Idiopathic juxtafoveal retinal telangiectasia
is a retinal vascular anomaly characterized by irregular
dialation and incompetence of the retinal vessels involves
the juxtafoveal area.
Gass and Blodis classification:

Always unilateralQ ; Affects Males

Temporal macula is involved
Exudation present minimal or massive;
Thought of as a variant of Coats disease
Involved area 2 DD (disc diameters); Visual
acuity is rarely affected

Group 1B

Same as above except that Involved area < 2 DD

Group 2

Bilateral symmetric; Temporal macula is

Retinal venules that drain the telangiectatic
capillaries at right angles key findingQ
NO lipid exudates; Crystalline deposists, RPE
hyperplasia, CNV may be present
Vision dependant on presence of atrophy and

Group 3

Always bilateral; Progressive visual loss will

occur over time
Perifoveal telangiectasias with retinal capillary
A/w CNS vasculopathyQ

Retina 27
Persistent hyperplastic primary vitreous
Early in embryonic life the lens is surrounded by
embryonic vascular tissue (tunica vasculosa lentis),
which in turn merges with the primary vitreous
containing fibrovascular mesodermal tissue
Regression of this tissue may fail leaving proliferating
fibrovascular remnants, either
Behind the lens (Anterior

On the inner surface of the

peripapillary retina (Posterior

Presents as a retrolental

It represents persistent
hyaloid vasculature on the
optic disc.

Mittendorf dot is the mildest

manifestation and appears
as a small white axial nodule

Bergmeisters papilla
is an isolated white mass
containing hyaloid artery
remnants on the optic disc.

More severe variants appear

as large plaques that span
the posterior surface of the
lens, and draw in the ciliary
processes centripetally
retrolental fibroplasia

Epiretinal membranes,
falciform folds, tractional
retinal detachment

Ultimately angle closure

glaucoma ensues

Optic nerve hypoplasia

may be seen

PHPV is usually unilateral; Both anterior and pos
terior PHPV can occur simultaneously.
Hallmark features of PHPV are leucocoria, centripetal
traction of the ciliary processes, and microphthalmia.
Idiopathic Polypoidal Choroidal vasculopathy (IPCV)
Also called Poserior uveal bleeding syndrome; MC
in females of Asian or African descent and in HTN
Subretinal red-orange polyp-like lesions of choroidal
ICG angiography ,may confirm the vessels arising
from inner choroidal circulation with terminal
aneurysmal dilatations (popcorn lesions).

28 Quick Review of Ophthalmology

Ocular hsitoplasmosis
Yellow white punched out round spots usually < 1
mm deep to the retina in any fundus location (hsitospots).
A macular CNV appearing as a gray-green patch
beneath the retina
Peripapillary atrophy or scarring.
Leber's congenital amaurosis
Autosomal Recessive; MC genetic cause of congenital
blindness in children.
Fundus - pigmentary retinopathy; vision loss within a
few months of birth, infantile nystagmuc, photphobia,
paradoxic pupillary response, oculodigital sign (eye
poking) and markedly reduced or flat ERG.; A/w
Gene therapy targeting RPE65 gene has shown success
in human trials.
Causes of night blindness (nyctalopia)
1. Retinitis pigmentosa (RP)
2. Gyrtae atrophy of choroid: First decade of life;
plasma ornithine levels is 10-20 times normal; lysine
is decreased; scalloped RPE and choriocapillaris in the
retina; constriction of visual fields and nonrecordable
ERG. AR. Arginine restricted diet needed; supplemen
tal vitamin B6 (pyridoxine).
3. Choroideremia: Males in firstd ecade of life; loss of
peripheral vision early > late los of central vision. NO
bony spicules; reduced ERG; XLR.
4. Vitamin A deficiency: Uyemura's fundus; small yellow
white well demarcated spots deep in the retina. (see
conrea chapter for rest)
5. Zinc deficiency: Abnormal dark adapatation; zinc
needed for vitamin A metabolism.
6. Congenital Staionary Night Blindness (CNSB): Night
blindness from birth, normal visual fields, not pro
gressive; one variant is Oguchi disease in which Mizuo
phenomenon occurs (fundus has a tapetum appearance
in light adapted state but appears normally colored
when dark adapted - takes about 12 hours).

Retina 29
7. Undercorrected myopia: Maybe the MC cause of poor
night vision.
Note: Cone dystrophy causes photpohobia and vision
worse during daytime (hemeralopia) rather than night.

30 Quick Review of Ophthalmology

Retina - Questions
1. True about Optic disc:
A. About 3 mm diameter
B. gives rise to blind spot in visual field
C. Contain 10 million nerve fibre
D. Fovea centralis is nasal to it
2. The average distance of the fovea from the temporal
margin of the optic disc is:
A. 1 disc diameter
B. 2 disc diameter
C. 3 disc diameter
D. 4 disc diameter
3. Regarding fovea, which of the following statements
is false:
A. Has the lowest threshold for light
B. Contains only cones
C. Contains only rods
D. Maximum visual acuity
4. Most sensitive part of retina is
A. Macula
B. Fovea-centralis
C. Optic disc
D. Ora serrata
5. Strongest force of bonding b/w retina an RPE
A. Vitreous gel pressure
B. Intraocular fluid pressure
C. RPE water transport
6. Which of the following is not seen in inter
photoreceptor matrix?
A. Glycoproteins
B. Metalloproteinase
C. Proteglycans
D. Glycolipids
7. The retina receive its blood supply from all, except:
A. Posterior ciliary artery
B. Central retinal artery
C. Retinal arteries
D. Plexus of Zinn and Haller arteries

Retina 31
8. True about FFA are all except
A. Fluorescein sodium injected into forearm vein
B. Most Useful for studying choroidal circulation
C. Flower petal pattern seen in cystoid macular
D. Smoke stack pattern on central serous retinopathy
9. True about ICG angiography
A. ICG injected into brachial artery
B. Most Useful for studying choroidal circulation
C. Flower petal pattern seen in cystoid macular
D. Smoke stack pattern on central serous retinopathy
10. Salt and pepper fundus is seen in
A. Multiple sclerosis
B. Cystinosis
C. Well Marchaesani syndrome
D. Congenital syphilis
11. Salt and pepper fundus occurs in all except
A. Lebers amaurosis
B. Cong. syphilis
C. Rubella
D. Ehlers Danlos syndrome
12. Cottage cheese and tomato ketchup retinpathy /Pizza
pie retinopathy is seen in
A. Tuberculous chrordoiditis
B. CMV retinitis
C. Eales disease
13. Blood and thunder fundus is seen in
14. Pseudopapillitis fundus picture is seen in
A. Hypermetropia
B. Presbyopia
C. Myopia
D. Astigmatism
15. Uyemuras fundus is a feature of deficiency of
A. Vitamin A
B. Vitamin C
C. Vitamin D
D. Vitamin E

32 Quick Review of Ophthalmology

16. Mizuo phenomenon is seen in
A. Oguchis disease
B. Best disease
C. VKH syndrome
D. Myopia
17. Angiod streaks in the eyes are seen in
A. Pseudoxanthoma elasticum
B. Tendinous xanthoma
C. Xanthelasma
D. Eruptive xanthoma
18. In NIDDM, fundus examination is done:
A. At the time of diagnosis
B. 5 years after diagnosis
C. At diagnosis & 5 years after diagnosis
D. At 2 years
19. Diabetic retinopathy, most likely present with
A. IDDM with 2 years duration
B. NIDDM with 2 years duration
C. Pheochromocytoma
D. Gestational diabetes
20. In maturity onset diabetes mellitus, opthalmoscopy
should be done at
A. Immediately
B. After 5 years
C. After 10 years
D. After 15 years
21. Degree of diabetic retinopathy depends on
A. Type of disease
B. Duration of disease
C. Severity of disease
D. Retinal involvment
22. Diabetes mellitus can lead to all except
A. Vitreous haemorrhage
B. Retinal detachment
C. III, IV and VI nerve palsy
D. Hypermetropia
23. A 35 year old insulin dependent diabetes mellitus
(IDDM) patient on Insulin for the past 10 years
complains of gradually progressive painless loss of
vision. Most likely he has:
A. Cataract
B. Vitreous haemorrhage
C. Total rhegmatogenous retinal detachment
D. Tractional retinal detachment not involving the

Retina 33
24. Earliest manifestation of diabetic retinpathy
A. Soft exudates / Cotton wool spot
B. Dot haemorrhage
C. Hard excudates
D. Microaneurysm
25. Diabetes mellitus is associated with all except:
A. Hard exudates
B. Neovascularisation
C. Glaucoma
D. Sunflower Cataract
26. Diabetic retinopathy is characterized by:
A. Hard exudates, dot haemorrhages and micoraneurysm
B. Macular star with papilledema
C. Deep haemorrhage only
D. Hard exudates only
27. Which of the following is not a feature in diabetic
retinopathy on fundus examination?
A. Microaneurysms
B. Retinal haemorrhages
C. Arteriolar dilatation
D. Neovascularisation
28. In a young patient presenting with recurrent vitreous
hemorrhage, diagnosis is:
A. Eales disease
C. Proliferative retinopathy
D. Coats disease
29. All are used to treat CME except
A. Bevacuzumab
B. Triamcinolone acetonide
C. Laser photocoagulation
D. Timolol maleate
30. Treatment of rubeosis iridis in diabetic retinopathy
A. Pan Retinal laser photocoagulation
B. Pars plana vitrectomy
C. Phacoemulsification
D. Anti VEGFs
31. Treatment of Advanced Prolifrerative Diabetic
Retinopathy with extensive vitreoretinal fibrosis
and traction retinal detachment involves all of the
following except

34 Quick Review of Ophthalmology


Reattachment of detached or torn retina

Removal of epiretial membrane

32. A young patient with sudden painless loss of vision

with systolic murmur over chest, ocular examination
reveals- cherry red spot in macula with clear AC.
With perception of light, diagnosis
A. Central retinal artery occlusion
B. Central retinal vein occlusion
C. Macular choroiditis with infective endocarditis
D. Central serrous retinopathy
33. On fundoscopic examination of a patient of giant cell
arteritis who has had history of sudden & painless
loss of vision two days back the surgeon finds orange
reflex. He also notices segmentation of blood column
in vessels. These vessels are _____& patient had
suffered from _______
A. Retina arterires & Central Retinal Artery occlusion
B. Retinal veins & CRAO
C. Retinal veins & CRVO
D. Retinal arteries & CRVO
34. Following are seen in CRA occlusion except
A. Gradual loss of vision
B. Cherry red spot
C. Sudden loss of vision
D. Pale retina
35. All of the following may be used to differentiate
Central Retinal Venous Occlusion (CRVO) from
Occular Ischemic Syndrome due to Carotid Artery
Stenosis, Except
A. Dilated Retinal Vein
B. Tortuous Retinal Vein
C. Retinal Artery Pressure
D. Opthalmodynamometry
36. Retinal neovacularization is seen inA/E
A. Diabetic retinopathy
B. Eales disease
C. Retintis pigmentosa
D. Retinopathy of prematurity

Retina 35
37. Chorodial neovacularization Membrane (CNV) are
associated with all except
A. Trauma
B. Myopia
C. Angioid streaks
D. Hypermetropia
38. Cotton wool spots are seen in all except:
C. Hypertension
D. Central serous retinopathy
39. Hard exudates are seen in all except
A. Daibetic retinopathy
B. Retinitis pigmentosa
C. Eales disease
D. Retinal artery macroaneysm
40. Clinically Retinal Detachment is best diagnosed by:
A. + 90 D lens
B. 3 mirror contact lens
C. Direct ophthalmoscopy
D. Indirect ophthalmoscopy
41. Cause of exudative retinal detachment are all except
A. Scleritis
B. Toxamia of pregnancy
C. Dysthyroid eye disease
D. Central serious retinopathy
42. Risk factors for retinal Detachment are all except :
A. Diabetic retinopathy
B. Myopia
C. Hypermetropia
D. Retinopathy of prematurity
43. Cause of exudative retinal detachment
A. Central retinal artery occlusion
B. Diabetic retinopathy
C. Haradas syndrome
D. Best disease
44. Tractional Retinal detachment is seen in:
A. Myopia
B. Retinitis pigmentosa
C. Diabetes
D. Hypertension

36 Quick Review of Ophthalmology

45. A patient with detachment of retina with photopsia
with floaters in the eye. Diagnosis is
A. Vitreous
B. Exudative retinal detachment
C. Rhegmetogenous retinal detachment
D. Tractional retinal detachment
46. Features in retinal detachment all except
A. Field defect
B. Retinal tears
C. Always a/w vitreous haemorrhage
D. Defective vision
47. A 35 year old insulin dependent diabetes mellitus
(IDDM) patient on Insulin for the past 10 yrs
complains of gradually progressive painless loss of
vision. Most likely he has
A. Catract
B. Vitreous haemorrhage
C. Total rhegmatogenous retinal detachment
D. Tractional retinal detachment not involving the
48. A 60 year old male patient operated for cataract 6
months back now complains of floaters and sudden
loss of vision. The diagnosis
A. Vitreous hemorrhage
B. Retinal detachment
C. Central retina artery occlusion
D. Cystoid macular edema
49. Primary aim of retinal detachment surgery
A. Removal of vitreous
B. Drainage of subretinal fluid
C. Vitrectomy
D. Encirclage
50. Which enzyme is defective in Refsums disease?
A. Phytanic acid oxidase
B. Succinate thiokinase
C. Malonate dehydrogenase
D. Thiophorase
51. Retinits Pigmentosa is associated with all except
A. Usher Syndrome
B. Marfans Syndrome
C. Kerans-Sayre Syndrome
D. Bassen Kornzweig Syndrome

Retina 37
52. All are true about retinite pigmentosa except
A. Genetic inheritance (X-linked)
B. Early diagnosis and treatment prevents
C. Visual acuity not diminished till late in course
D. Associated with systemic abnormalities
53. A patient presented with peripheral field loss and
fundus examinations shows waxy exudates & pale
disc with pigmentation around retinal vessels
diagnosis is
A. Behcets syndrome
B. Choriorentitis
C. Open angle glaucoma
D. Retinitis pigmentosa
54. Ring scotoma is a feature of:
A. Blue dot cataract
B. Diabetic retinopathy
C. Nuclear cataract
D. Retinitis pigmentosa
55. Ring scotoma is a seen in all except
A. Retinitis pigmentosa
B. Pan retinal photocoagulation
C. Myopic chorioretinal atrophy
D. Retinal detachment
56. In Retinitis pigmentosa, following are true except
A. Pigment Present
B. Pale waxy disc
C. Narrowing of vessels
D. ERG normal
57. Retinitis pigmentosa like fundus is seen in all except
A. End stage chloroquine retinopathy
B. End stage syphilitic retinopathy
C. Cancer related retinopathy
D. Sickle cell retinopathy
58. All are examples of anti-VEGFs except
A. Bevacizumab
B. Infliximab
C. Ranibizumab
D. Pegaptanib sodium

38 Quick Review of Ophthalmology

59. Indications for intravitreal Avastin (bevacizumab)
are all except
A. Diabetic macular edema
B. CRVO associated macular edema
C. Choroidal neovascular membrane
D. Second episode of central serous retinopathy
60. PDT (photodynamic therapy) is used in treatment of
A. Wet AMD
B. Dry AMD
61. Most common cause of blindness in western world is
A. Cataract
B. Uncorrected Refractive error
C. CMV retinitis
D. Age related macular degenration
62. A 30 year old patient with history of recurrent
headache was sent for fundus evaluation. He was
found to be having generalized arterial attenuation
with multiple cotton wool spots and flame shaped
haemorrhages in both eyes. The most likely cause is:
A. Diabetic retinopathy
B. Hypertensive retinopathy
C. Central retinal artery occlusion
D. Temporal arteritis
63. All the following changes are caused in the retina by
benign hypertension except
A. Narrowing of arterioles
B. Exudates
C. Cotton wool spots
D. Retinal hemorrhage
64. Keith Wagner classification is used for
A. Diabetic retinopathy
B. Hypertensive retinopathy
C. Angle closure glaucoma stages
D. Uveitis
65. A 25 years old executive presents with metamorphopia
in his right eye. On examination the fundus show a
shallow detachment at the macula . The fluorescein

Retina 39
angiography shows a smoke stack. Which of the
following management should be given
A. Topical antibiotic corticosteriod combination
B. Systematic corticosteroid for two weeks and then
C. Pulse Methyl Predenisolone for three days and
then taper
D. Wait and watch for spontaneous recovery
66. A young adult male presented with sudden painless
diminished vision. He recovered spontaneously
within 3 months. Most likely cause of his problem is
A. Central serous retinopathy
B. Macular hole
C. Myopic cresent
D. Vitreous haemorrhage
67. All are ocular emergencies except
A. Acute Angle closure glaucoma
B. Central serous retinopathy
C. Retinal detachment
D. Central retinal arterial occluaion
68. Enlarging dot sign in fundus fluroscein scanning is
seen in
A. Cystoid macular edema
B. Central serous retinopathy
C. Significant macular edema
D. Coats deisease
69. Last part of retina to be vascularised during develop
ment is
A. Upper temporal retina
B. Upper nasal retina
C. Lower temporal retina
D. Lower nasal retina
70. Retinopathy in neonate is due to
A. Prematurity <1500gm
B. O2 toxicity
C. Trauma
D. Diabetes
Which of the following will cause Bulls eye
B. Chloroquine
C. Ethambutol
D. Steroids

40 Quick Review of Ophthalmology

72. All the following are true of Eales disease except
A. Occurs in the young
B. Vitreous hemorrhage is present
C. Retinal detachment
D. Optic neuritis