Diabetic Retinopathy

DIABETIC RETINOPATHY

Q. 1

Earliest feature of Diabetic Retinopathy is?

 A Microaneurysms
 B

Cotton Wool spots

 C Dot-&-Blot haemorrhages
 D

Hard Exudates

Q. 1

Earliest feature of Diabetic Retinopathy is?

 A Microaneurysms
 B

Cotton Wool spots

 C Dot-&-Blot haemorrhages
 D

Hard Exudates

Ans. A

Explanation:

Microaneurysms REF: Yanoff 2nd edition page 878

Microaneurysms are the first ophthalmoscopically detectable change in diabetic retinopathy


Q. 2

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with Macular grid photocoagulation. The patient still has vitreo macular traction. What is the preferred treatment?

 A >Intravitreal btvacizumab
 B >Pars plana vitrectomy
 C >Repeat macular grid photocoagulation
 D >Augmented macula photocoagulation
Q. 2

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with Macular grid photocoagulation. The patient still has vitreo macular traction. What is the preferred treatment?

 A >Intravitreal btvacizumab
 B >Pars plana vitrectomy
 C >Repeat macular grid photocoagulation
 D >Augmented macula photocoagulation
Ans. B

Explanation:

Pars plana vitrectomy [Ref: http://wtvw.hopkinsguides.com/hopkins/ub/citation/1594222Nitrectomy_for_diabeticjnacular_traction_and_edema_ associatedwith_posterior_hyaloidal_tractionj

Vitrectomy is the treatment of choice for vitreo macular traction which if left would lead to retinal detachment. It involves removing the cloudy vitreous and replacing it with a silicone oil.

Bevacizumab is anti-VEGF antibody. Blocking Vascular endothelial growth factor (VEGF) prevents angiogenesis, but has no role in treating macular traction.

Laser photocoagulation uses the heat from the laser to seal or destroy abnormal, leaking blood vessels in the retina. It is not effective to treat macular traction.


Q. 3

A 60 yr old man has both HTN and DM for 10 yrs. There is reduced vision in one eye. On fundus examination there is a central bleed and the fellow eye is normal. The diagnosis is

 A

Retinal tear

 B

Optic neuritis

 C

Diabetic retinopathy

 D

Hypertensive retinopathy

Q. 3

A 60 yr old man has both HTN and DM for 10 yrs. There is reduced vision in one eye. On fundus examination there is a central bleed and the fellow eye is normal. The diagnosis is

 A

Retinal tear

 B

Optic neuritis

 C

Diabetic retinopathy

 D

Hypertensive retinopathy

Ans. C

Explanation:

Diabetic retinopathy [Ref-Parson 21/e p304, 305; Yanoff Ophthalmology 3/e p584, 613, 716, 964] Extensively discussed with 2 Ophthalmologists

Central bleed implies bleed in macula. This is what is leading to reduced vision in the involved eye. Diabetic retinopathy is the obvious choice due to following reasons:

Diabetic retinopathy

Among the given options macular bleed can be seen in DR only.

Though DR is usually bilateral, but can be unilateral or assymetrical.

Microaneurysms are the first ophthalmoscopically detectable change in diabetic retinopathy, seen as small red dots in the middle retinal layers. When these microaneurysms rupture it may give rise to an intraretinal haemorrhages.

Optic neuritis

Optic neuritis can be ruled out as

–  Vision loss is usually abrupt

–  Mild periorbital pain (exacerbated by eye movement) is present in about 90% cases.

–  Usually seen in young patients

–  Fundus picture is not matching. Retinal haemorrhages are uncommon. Macular bleed is never seen. Fundus examination is normal in retrobulabar type of optic neuritis (which is the much more common type of optic neuritis). In the less common papillitis type of optic neuritis, optic disc swelling is present.

Funduscopic features of optic disc swelling include elevation of the optic nerve head, disk hyperemia, blurring of the disc margins, and edema of the nerve fibre layer. Optic disc hemorrhages are uncommon.

Retinal tear

Retinal tear are usually peripheral and typically occur in the equatorial and ora serrata regions of the retina. Peripheral retinal breaks alone do not cause loss of vision, but the associated conditions of vitreous hemorrhage and rhegmatogenous retinal detachment can result in severe visual loss. Even if retinal tear is central, will not cause macular bleed.

Retinal tear can be of 2 types: traumatic and non-traumatic.

Non traumatic can occur because of lattice degeneration or due to vitreous traction. Vitreous traction will lead to symptoms of flashes and associated haemorrhages would cause floaters.

Hypertensive retinopathy

Hypertensive retinopathy can be of 2 types- Chronic hypertensive retinopathty and Malignant acute hypertensive retinopathy.

Chronic hypertensive retinopathy is usually asymptomatic. Fundus picture is – focal constriction and dilatation of the retinal arterioles, tortuosity of the retinal arterioles, an increase in the arteriolar light reflex, and loss of transparency of the intra-arterial blood column, arteriovenous nicking (arteriovenous nicking is a highly specific .finding and the hallmark of chronic hypertensive retinopathy), retinal hemorrhages, macular edema, and cotton-wool spots.

Malignant hypertensive retinopathy is due to acutely elevated blood pressure in a patient with relatively young arterioles undefended by sclerosis. Vision loss is acute and severe. The fundus picture is dominated by edema. The entire retina may be clouded by a generalized edema which may be particularly accentuated at the disc, resulting in a marked degree of disc edema with multiple cotton wool patches, hard exudates and retinal haemorrhages.

Diabetic retinopathy and age:

Diabetic retinopathy affects both young and old, as it is the diabetic age and not the chronological age that is important.

The best predictor of diabetic retinopathy is the duration of the disease.

First 5 yrs of type 1 diabetes – very low risk

5-10 yrs of type 1 diahete        – 27% develop diabetic retinopathy

> 10 yrs                                        – 71 to 90 % develop diabetic retinopathy

> 20-30 yrs                                  – 95% develop DR.

(In type II diabetes, the time of onset and therefore the duration of disease are difficult to determine precisely)


Q. 4 Diabetic retinopathy is related to:
 A Duration of disease
 B Severity of disease
 C Family history
 D Control of diabetes
Q. 4 Diabetic retinopathy is related to:
 A Duration of disease
 B Severity of disease
 C Family history
 D Control of diabetes
Ans. A

Explanation:

Duration of disease


Q. 5

The screening strategy for prevention of blindness from diabetic retinopathy according to the NPCB involves:

 A

Opportunistic screening

 B

High Risk Screening

 C

Mass screening

 D

Screening by Primary Care Physician

Q. 5

The screening strategy for prevention of blindness from diabetic retinopathy according to the NPCB involves:

 A

Opportunistic screening

 B

High Risk Screening

 C

Mass screening

 D

Screening by Primary Care Physician

Ans. B

Explanation:

According to the National Programme for Control of Blindness, the screening strategy followed for prevention of blindness secondary to diabetic retinopathy involves screening of those individuals who are at high risk.
These high risk groups are identified using ophthalmoscopy and fundus photography.
 
Ref: Ophthalmology By Khurana, Pages 426-433; Concise Textbook Of Ophthalmology By Sharma, Pages 208-211; Park Textbook of Social and Preventive Medicine, 19th Edition, Pages 360-362.

Q. 6

Which of following is not a feature in diabetic retinopathy on fundus examination:

 A

Microaneurysms

 B

Retinal hemorrhages

 C

Arteriolar dilatation

 D

Neovascularisation

Q. 6

Which of following is not a feature in diabetic retinopathy on fundus examination:

 A

Microaneurysms

 B

Retinal hemorrhages

 C

Arteriolar dilatation

 D

Neovascularisation

Ans. C

Explanation:

Arteriolar dilation does not occur in diabetic retinopathy.

 
Ref: Clinical Ophthalmology By Kanski, 3rd Edition, Page 359 and 4th Edition, Pages 465-6 ; Comprehensive Ophthalmology By A K Khurana, 4th Edition, Page 259-62

Q. 7

Treatment of Advanced Proliferative Diabetic Retinopathy with extensive vitreoretinal fibrosis and fractional retinal detachment involves all of the following, EXCEPT:

 A

Reattachment of detached or torn retina

 B

Removal of epiretinal membrane

 C

Vitrectomy

 D

Exophotocoagulation

Q. 7

Treatment of Advanced Proliferative Diabetic Retinopathy with extensive vitreoretinal fibrosis and fractional retinal detachment involves all of the following, EXCEPT:

 A

Reattachment of detached or torn retina

 B

Removal of epiretinal membrane

 C

Vitrectomy

 D

Exophotocoagulation

Ans. D

Explanation:

There is no role of Exophotocoagulation in the management of advanced proliferative diabetic retinopathy with complications such as fractional RD and extensive vitreoretinal fibrosis. Endophotocoagulation may be used in conjunction with vitrectomy.

Ref: Oxford Textbook of Medicine 4th /350; Current Geriatric Diagnosis and Treatment (2004)/127


Q. 8

All of the following are implicated in the pathogenesis of macular oedema in diabetic retinopathy, EXCEPT:

 A

Retinal pigment epithelium dysfunction

 B

Oxidative stress

 C

VEGF (vascular endothelial growth factor)

 D

Increased protein kinase-C

Q. 8

All of the following are implicated in the pathogenesis of macular oedema in diabetic retinopathy, EXCEPT:

 A

Retinal pigment epithelium dysfunction

 B

Oxidative stress

 C

VEGF (vascular endothelial growth factor)

 D

Increased protein kinase-C

Ans. A

Explanation:

Diabetic macular edema (DME) / Can develop at any stage of retinopathy. Now the leading cause of vision loss in persons with diabetes. Increased vascular permeability causes plasma leaks from the macular vessels, leading to swelling and formation of hard exudates at the central retina.

Incidence over 10 years
 (1)   20% in persons with type 1 DM
 (2)   25% in persons with type 2 DM who require insulin
 (3)   14% in persons with type 2 DM who do not require insulin
Very Important
VEGF (vascular endothelial growth factor) is one of the many cytokines that plays an important role in diabetic retinopathy. VEGF is a marker for oxidative stress and induces hyperpermeability of macular capillaries, contributing to macular oedema. 
The molecular mechanisms involved in endothelial damage and macular ischemia are complex and involves sorbitol pathway, AGE formation (advanced glycation end products), protein kinase C, renin-angiotensin system, inflammation, oxidation and alterations in gene expression. 
Ref: Diabetic Retinopathy, By David J. Browning, Page 205, Springer, 2010.

Q. 9

In maturity onset diabetes mellitus, screening for diabetic retinopathy should be done at:

 A

Immediately

 B

After 5 years

 C

After 10 years

 D

After 15 years

Q. 9

In maturity onset diabetes mellitus, screening for diabetic retinopathy should be done at:

 A

Immediately

 B

After 5 years

 C

After 10 years

 D

After 15 years

Ans. A

Explanation:

Screening for diabetic retinopathy should be performed within 3 years from diagnosis in type I diabetes, on diagnosis in type II diabetes, and annually thereafter in both types. Digital fundal photography has been proven to be an effective and sensitive method for screening. Seven-field photography is the gold standard, but two 45° fields, one centered on the macula and the other centered on the disk, are becoming the method of choice in most screening programs.
 
Ref: Fletcher E.C., Chong N., Augsburger J.J., Corrêa Z.M. (2011). Chapter 10. Retina. In P. Riordan-Eva, E.T. Cunningham, Jr. (Eds), Vaughan & Asbury’s General Ophthalmology, 18e.

Q. 10

Cotton wool spots in diabetic retinopathy are due to:

 A

Retinal edema

 B

Retinal holes

 C

Retinal haemorrhage

 D

Macular degeneration

Q. 10

Cotton wool spots in diabetic retinopathy are due to:

 A

Retinal edema

 B

Retinal holes

 C

Retinal haemorrhage

 D

Macular degeneration

Ans. A

Explanation:

Cotton wools spots are nerve fiber layer infarcts that appear as superficial retinal whitening, typically less than one fourth disc area in size and may be found as single or multiples. They develop after retinal ischemia with secondary axoplasmic damming. They are usually found in the distribution of the radial peripapillary capillaries or along the retinal vascular arcades. 
  • Features of non proliferative retinopathy:  dilation of veins, microaneurysms, retinal hemorrhages, retinal edema, and hard exudates.
  • Maculopathy manifests as edema, exudates, or ischemia involving the macula.
  • Proliferative retinopathy is characterized by neovascularization, arising from either the optic disk or the major vascular arcades.
Ref: Riordan-Eva P. (2013). Chapter 7. Disorders of the Eyes & Lids. In M.A. Papadakis, S.J. McPhee, M.W. Rabow, T.G. Berger (Eds), CURRENT Medical Diagnosis & Treatment 2014.

Q. 11

Which of the following factor is related to diabetic retinopathy?

 A

Duration of disease

 B

Severity of disease

 C

Family history

 D

Control of diabetes

Q. 11

Which of the following factor is related to diabetic retinopathy?

 A

Duration of disease

 B

Severity of disease

 C

Family history

 D

Control of diabetes

Ans. A

Explanation:

Duration of DM and degree of glycemic control are the best predictors of the development of retinopathy; hypertension is also a risk factor. Nonproliferative retinopathy is found in many individuals who have had DM for >20 years (25% incidence with 5 years, and 80% incidence with 15 years of type 1 DM). Although there is genetic susceptibility for retinopathy, it confers less influence than either the duration of DM or the degree of glycemic control.
 
Ref: Powers A.C. (2012). Chapter 344. Diabetes Mellitus. In D.L. Longo, A.S. Fauci, D.L. Kasper, S.L. Hauser, J.L. Jameson, J. Loscalzo (Eds), Harrison’s Principles of Internal Medicine, 18e.

Q. 12

The screening strategy for prevention of blindness from diabetic retinopathy according to the NPCB involves –

 A

Opportunistic screening

 B

High risk screening

 C

Mass screening

 D

Screening by Primary Care Physician

Q. 12

The screening strategy for prevention of blindness from diabetic retinopathy according to the NPCB involves –

 A

Opportunistic screening

 B

High risk screening

 C

Mass screening

 D

Screening by Primary Care Physician

Ans. B

Explanation:

Ans. is ‘b’ i.e., High risk screening

  • High risk screening is applied to the group which has increased risk of developing certain disease/cancer.
  • Diabetic retinopathy patients are at increased risk of developing blindness. Therefore, screening strategy for prevention of blindness from diabetic retinopathy is high risk screening.

Q. 13

Which one of the following is not a target disease under ‘Vision 2020: The Right to Sight’

 A

Refractive error

 B

Trachoma

 C

Corneal blindness

 D

Diabetic retinopathy

Q. 13

Which one of the following is not a target disease under ‘Vision 2020: The Right to Sight’

 A

Refractive error

 B

Trachoma

 C

Corneal blindness

 D

Diabetic retinopathy

Ans. D

Explanation:

Ans. is `d’ i.e., Diebitic retinopathy 


Q. 14

ETDRS vision chart study is done in patients with diabetic retinopathy. ETDRS stands for:

 A

Extended therapy for diabetic retinopathy & its study

 B

Emergency treatment for diabetic retinopathy and study

 C

Eye testing or rotatory drum & its study

 D

Early treatment for diabetic retinopathy study

Q. 14

ETDRS vision chart study is done in patients with diabetic retinopathy. ETDRS stands for:

 A

Extended therapy for diabetic retinopathy & its study

 B

Emergency treatment for diabetic retinopathy and study

 C

Eye testing or rotatory drum & its study

 D

Early treatment for diabetic retinopathy study

Ans. D

Explanation:

D i.e. Early treatment for diabetic retinopathy study

The ETDRS chartQ is similar to the LogMAR scale, and is used for early detection of diabetic retinopathy. And ETDRS stands for early treatment for diabetic retinopathy studyQ.

The visual acuity in adults is usually measured by:

  1. Snellen’s Fraction (in Metres): As 6/6, 6/9, 6/12, 6/18, 6/24, 6/36, 6/60… depending on the no. of lines that the patient could read at 1m. Each alphabet subtends an angle of 5min at the nodal point at respective distance.
  2. Snellen’s Fraction (in Feet): The same as above, only that in the US its converted to feet, so recorded as 20/20, 20/200…
  3. Decimal Acuity: Snellen’s fraction is reduced to a decimal no. and a higher acuity is represented by a larger no., which is reverse in Snellen’s grading.
  4. LogMAR Scale Q: Based on the Minimum Angle of resolution. Here each row has 5 alphabets each in a ratio of 5:4, with each row in geometric progression i.e. each subsequent row has alphabets smaller in size by a factor of Logio10.
  5. ETDRS Q: Similar to LogMAR, having 10 alphabets in ratio 5:5.

Q. 15

Diabetic retinopathy, most likely present with

 A

IDDM with 2 years duration

 B

NIDDM with 2 years duration

 C

Juvenile diabetes

 D

Gestational diabetes

Q. 15

Diabetic retinopathy, most likely present with

 A

IDDM with 2 years duration

 B

NIDDM with 2 years duration

 C

Juvenile diabetes

 D

Gestational diabetes

Ans. B

Explanation:

B i.e. NIDDM with 2 years duration

  • Diabetic Retinopathy (DR) is commoner in type 1 or IDDM (40%) than in type 2 (NIDDM) diabetes mellitus (20%)

Duration of diabetes is most important risk factor Q for DR. DR rarely develops within 5 years of the onset of diabetes or before puberty, but about 5% of type 2 (NIDDM) diabetics have DR at presentation.


Q. 16

Degree of diabetic retinopathy depends on

 A

Type of disease

 B

Duration of disease

 C

Severity of disease

 D

Retinal involvement

Q. 16

Degree of diabetic retinopathy depends on

 A

Type of disease

 B

Duration of disease

 C

Severity of disease

 D

Retinal involvement

Ans. B

Explanation:

B i.e. Duration of disease

  • The presence & degree of diabetic retinopathy is more closely related to the duration of disease than to its severityQ.
  • Duration of disease is the most important and best predictor Q of diabetic retinopathy.

In diabetic retinopathy arteriolar changes consist of narrowing Q (not dilation) silver-wiring and obliteration resembling branch retinal artery occlusion. And venous changes are bending, looping and sausage like segmentation.


Q. 17

Development of Diabetic retinopathy depends on

 A

Intensity of disease

 B

Age of onset

 C

Duration of disease

 D

Any of the above

Q. 17

Development of Diabetic retinopathy depends on

 A

Intensity of disease

 B

Age of onset

 C

Duration of disease

 D

Any of the above

Ans. D

Explanation:

D i.e. Any of the above

Though duration of disease is the most important and best predictor Q of diabetic retinopathy, all the options mentioned here are, infact risk factors for DR, so, its best to go for Option D.


Q. 18

A 29 years old man with IDDM for the last 14 years develops sudden vision loss, has non-proliferating diabetic retinopathy, cause is

 A

Macular oedema

 B

Vitreous haemorrhage

 C

Subretinal haemorrhage

 D

Retinal traction

Q. 18

A 29 years old man with IDDM for the last 14 years develops sudden vision loss, has non-proliferating diabetic retinopathy, cause is

 A

Macular oedema

 B

Vitreous haemorrhage

 C

Subretinal haemorrhage

 D

Retinal traction

Ans. A

Explanation:

A i.e. Macular edema

Bleeding from newly formed vessels (neovscularization) is the commonest cause of spontaneous vitreous haeomorrhage in diabetic adultsQ.

MaculopathyQ is m.c. cause of visual loss among the patients with NPDR.

Involvement of fovea by edema & hard exudates or ischemia (diabetic maculopathy) is the most common cause of visual impairment in diabetic patients particularly those with type 2 diabetes (NIDDM)

Type I diabetics (IDDM) are at particular risk of developing PDR. And vitreous haemorrhage is most common cause of visual loss in patients with PDRQ.

Almost all type I diabetic patients develop retionapathy in about 15 years. In those with type II diabetes, the risk of diabetic retinopathy increases with the duration of diabetes (most important-risk factor), accompanying hypertension & smoking. Diabetic retinopathy is more common in type I diabetes than in type 2. Non proliferative DR is more common than proliferative DR; type 1 diabetics are at particular risk of developing PDR. It appears that duration is stronger predictor for proliferative disease than for maculopathy.

In NP DR, macular edema (most common)Q, exudates and capillary occlusions often cause blindness but affected patients usually maintain at least ambulatory vision. On the other hand, PDR may result in severe vitreous haemorrhage or retinal detachment, with hand movement vision or worst. Macular edema or retinal thickening (d/t fluid coming from leaking microaneurysm or diffuse capillary incompetence) Is an important manifestation of NPDR (early) and represents the leading cause of legal blindness in diabetics.

Proliferative new leaking vessels usually arise from retinal veins and grow along the route of least resistance (eg disc b/o absence of true internal limiting membrane or shallowly detached posterior vitreous). It has long been assumed that sudden vitreous contractions tear the fragile new vessels, causing vitreous haemorrhage. However, most diabetic vitreous haemorrhages occur during sleep, probably b/o an increase in blood pressur secondary to early morning hypoglycemia or to REM sleepQ. Because so few haemorrhags occur during exercise, it is not necessary to restrict the activity of patients, with proliferative DR. Haemorrhage (RBC) behind posterior vitreous face settle quickly to the bottom of eye & are absorbed. Whereas when RBCs break into vitreous body, they adhere to get & clearing may take months or years.


Q. 19

Earliest manifestation of diabetic retinopathy is

 A

Soft exudates/Cotton wool spot

 B

Dot haemorrhage

 C

Hard exudates

 D

Microaneurysm

Q. 19

Earliest manifestation of diabetic retinopathy is

 A

Soft exudates/Cotton wool spot

 B

Dot haemorrhage

 C

Hard exudates

 D

Microaneurysm

Ans. D

Explanation:

D i.e. Microaneurysm

Microaneurysms are located in the inner nuclear layer and are the earliest and most characteristic ocular lesion Q of diabetic retinopathy.


Q. 20

Diabetic retinopathy is characterized by:

 A

Hard exudates, dot haemorrhages and microaneurysm

 B

Flame shaped haemorrhages, soft exudates

 C

Deep haemorrhage only

 D

a and b

Q. 20

Diabetic retinopathy is characterized by:

 A

Hard exudates, dot haemorrhages and microaneurysm

 B

Flame shaped haemorrhages, soft exudates

 C

Deep haemorrhage only

 D

a and b

Ans. D

Explanation:

A i.e. Hard exudates, dot haemorrhages and microaneurysm; B i.e. Flame shaped haemorrhages soft exudates

–         Non-proliferative diabetic retinopathy (NPDR) is characterized by microaneurysms, retinal haemorrhages, exudates, cotton wool spot/soft exudatesQ (any or all of these in mild NPDR); Significant venous bleeding

VB 1 quadrant), mild intraretinal microvascular abnormalities (IRMA) or severe retinal haemorrhages (about 20 medium-large per quadrant in 1-3 quadrants) and CWS (commonly present) – in moderate NPDR. Severe NPDR may show one or more of -severe haemorrhages in all 4 quadrants, VB 2 and moderate IRMA in 1 or more quadrant. Very severe NPDR presents with two or more of the criteria for severe disease.

–         NPDR may present with retinal Haemorrhages, Exudates, Micro-Aneurysms, IRMA, Soft-exduates or Cotton wool spots and Venous bleedingQ (Mn-HEMA IS Very Nonproliferative”). Neovascularization (new vessels on disc = NVD or new vessels elsewhere = NVE) is seen in proliferative DR.


Q. 21

Which of following is not a feature in diabetic retinopathy on fundus examination

 A

Microaneurysms

 B

Retinal hemorrhages

 C

Arteriolar dilatation

 D

Neovascularisation

Q. 21

Which of following is not a feature in diabetic retinopathy on fundus examination

 A

Microaneurysms

 B

Retinal hemorrhages

 C

Arteriolar dilatation

 D

Neovascularisation

Ans. C

Explanation:

C i.e. Arteriolar dilatation

In diabetic retinopathy arteriolar changes consist of narrowing Q (not dilation) silver-wiring and

obliteration resembling branch retinal artery occlusion. And venous changes are bending, looping and sausage like segmentation.


Q. 22

First retinal abnormality in diabetic retinopathy:

 A

Microaneurysm

 B

Hard exudates

 C

Soft exudates

 D

Cotton wool spots

Q. 22

First retinal abnormality in diabetic retinopathy:

 A

Microaneurysm

 B

Hard exudates

 C

Soft exudates

 D

Cotton wool spots

Ans. A

Explanation:

A i.e. Microaneurysm


Q. 23

All of the following take part in the pathogenesis of CME in diabetic retinopathy except:

 A

Retinal Pigment Epithelial (RPE) dysfunction

 B

Oxidative stress

 C

VEGF

 D

Increased protein kinase c

Q. 23

All of the following take part in the pathogenesis of CME in diabetic retinopathy except:

 A

Retinal Pigment Epithelial (RPE) dysfunction

 B

Oxidative stress

 C

VEGF

 D

Increased protein kinase c

Ans. A

Explanation:

A i.e., Retinal pigment epithelial (RPE) dysfunction


Q. 24

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with Macular grid photocoagulation. The patient still has vitreo macular traction. What is the preferred treatment?

 A

Intravitreal bevacizumab

 B

Pars plana vitrectomy

 C

Repeat macular grid photocoagulation

 D

Augmented macula photocoagulation

Q. 24

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with Macular grid photocoagulation. The patient still has vitreo macular traction. What is the preferred treatment?

 A

Intravitreal bevacizumab

 B

Pars plana vitrectomy

 C

Repeat macular grid photocoagulation

 D

Augmented macula photocoagulation

Ans. B

Explanation:

B i.e. Pars plana vitrectomy

Pars plana vitrectomy plays a vital role in management of severe complications of diabetic retinopathy. The major indications are non-clearing vitreous hemorrhage, macular involving or macular threatening traction retinal detachment and combined traction-rhegmatogenous retinal detachmentQ.

In general, unless the macula becomes involved, observation is the best therapy for tractional retinal detachment patients because, in most cases, the detachment does not progress into the macula. However, vitrectomy becomes an urgent procedure when macular vision is suddenly lostQ.


Q. 25

Treatment of diabetic retinopathy neovascularisation is /are :

 A

Retinal laser photocoagulation

 B

Pars plana vitrectomy

 C

Phacoemulsion

 D

a and b

Q. 25

Treatment of diabetic retinopathy neovascularisation is /are :

 A

Retinal laser photocoagulation

 B

Pars plana vitrectomy

 C

Phacoemulsion

 D

a and b

Ans. D

Explanation:

A, B,  i.e. Retinal laser photocoagulation; Pars plana vitrectomy


Q. 26

Treatment of diabetic retinopathy

 A

Phacoemulsification

 B

Retina laser photocoagulation

 C

LASIK

 D

None

Q. 26

Treatment of diabetic retinopathy

 A

Phacoemulsification

 B

Retina laser photocoagulation

 C

LASIK

 D

None

Ans. B

Explanation:

B i.e. Retina laser photocoagulation


Q. 27

Diabetic retinopathy is treated by:

 A

Strict glycemic control

 B

Panphotococagulation

 C

Antihypertensive

 D

All

Q. 27

Diabetic retinopathy is treated by:

 A

Strict glycemic control

 B

Panphotococagulation

 C

Antihypertensive

 D

All

Ans. D

Explanation:

A i.e. Strict glycemic control; B i.e. Panphotocoagulation; C i.e. Antihypertensive

Diabetic retinopathy is treated by – strict glycemic & hypertensive control, antioxidants, photocoagulation (pan retinal, focal argon laser or grid pattern laser burns), intravitreal steroids and anti-VGF (vascular endothelial growth factor)Q and continuous screening.

LASIK is refractory surgery for high myopia and phacoemulsification is used for cataract surgery.

General measures

  • Strict control of blood glucose Q may delay the onset
  • Control of hypertension Q when associated is essential
  • Antioxidants Q are also
    useful for diabetics
  • Aspirin- an antiplatelet factor has no role
  • Pars plana vitrectomy is indicated for dense persistent vitreous hemorrhage, tractional retinal detachment and epiretinal membranes. Retinal detachment also requires surgery in DR. PDR= Proliferative Diabetic Retinopathy

NPDR = Non-PDR

Screening

Yearly

Till there is no-DR or

there is mild NP-DR

6 monthly

In moderate NPDR

3 monthly

In severe NPDR

2 monthly

In PDR with no high

risk characteristic

Pan retinal

photocoagulation

Focal argon laser burn

Grid pattern

laser burns

•   It consists of 1200-1600 spots, each 500 pm in

It is applied to

It is

size and 0.1 sec duration

individual

applied in

•   It is applied 2-3 disc areas from the centre of

microvascular

macular

macula extending peripherally to equator

formations in the

area for

 

centre of hard

diffuse

•   It is indicated in PDR (proliferative diabetic

exudates’ ring in focal

macular

retinopathy) with one of the high risk

exudative

edema

characteristic

maculopathy

 

Photocoagulation


Q. 28

Treatment of Advanced Proliferative Diabetic Retinopathy with extensive vitreoretinal fibrosis and tractional retinal detachment involves all of the following except.

 A

Reattachment of detached or torn retina

 B

Removal of epiretinal membrane

 C

Vitrectomy

 D

Exophotocoagulation

Q. 28

Treatment of Advanced Proliferative Diabetic Retinopathy with extensive vitreoretinal fibrosis and tractional retinal detachment involves all of the following except.

 A

Reattachment of detached or torn retina

 B

Removal of epiretinal membrane

 C

Vitrectomy

 D

Exophotocoagulation

Ans. D

Explanation:

D i.e. Exophotocoagulation

Treatment of advanced proliferative diabetic retinopathy with vitreoretinal fibrosis and tractional rectinal detachment involves previtrectomy pan retinal endophoto coagulation (not exophotocoagulation)Q, vitrectomy (pars plana or posterior route), reattachment of detached or torn retina and removal of epiretinal membraneQ.

In most cases it is preferable to attempt panretinal photocoagulation, because the more laser a patient has previtrectomy the better he or she usually does after vitrectomy. An uncommon and unfortunate complication of panretinal photocoagulation, particularly in patients with vitreous hemorrhage & preexisting fibrosis, is acceleration or production of a tractional detachment by the laser treatment. Vitrectomy removes the scaffolding & possible stimuli (disintegrated blood products) for neovascular growth.

Endophotocoagulation is used exclusively during a vitrectomy procedureQ. The endophotocoagulation probe may have a laser fiber ± an aspirating port to help remove subretinal fluid. To best treat retinal tears by endophotocoagulation, it is important that all subretinal fluids be removed from under the retina for the laser to take. If all traction is removed from the tear, once the fluid is removed from under the retina, it usually does not accumulate.

Epiretinal membrane is a thin sheet of abnormal scar tissue that grows over the retina and causes distortion of vision due to macular puckering (s/t contracted epiretinal membrane), detachment (secondary to localized retinal traction) and opacification of membrane.


Q. 29

Cotton wool spot is /are seen in:

 A

DR (Diabetic retinopathy)

 B

Hypertensive retinopathy

 C

AIDS

 D

All

Q. 29

Cotton wool spot is /are seen in:

 A

DR (Diabetic retinopathy)

 B

Hypertensive retinopathy

 C

AIDS

 D

All

Ans. D

Explanation:

A, B, C i.e. Diabetic retinopathy, Hypertensive retinopathy; AIDS

Cotton wool spots (or soft exudates) are seen in vascular retinopathies such as diabetic retinopathy, hypertensive retinopathy, retinopathy in toxaemia of pregnancy and /or pheochromocytoma and lupus erythematosus retinopathy. AIDS, CMV and radiation retinopathy are other causes.

Cotton Wool Spots (Soft Exudates)

 

– These are soft exudates seen as white fluffy superficial deposits in retina with indistinct (ill defined) margins giving the appearance of cloud like soft aggregates.

–   They are commonly small (but may be large), disappear rapidly and frequently change their shape.

– They are formed by the arrest of axoplasmic flow at the edge of an ischemic area where nerve fibers cross the boundary. Causes include.

Cotton Wool Spots in AIDS

  • The most common abnormal fundoscopic findings in AIDS
  • Represent areas of reinal ishchemia secondary to microvascular disease
  • At times, may be associated with small areas of haemorrhage making it difficult to distinguish from CMV retinitis. In contrast to CMV retinitis, however, cotton wool spots are

– Not associated with visual loss

– Tend to remain stable or improve over time

  1. Diabetic retinopathyQ
  2. Hypertensive retinopathyQ
  3. Retinopathy in toxaemia of pregnancyQ
  4. Retinopathy in pheochromocytoma
  5. AIDS, CMV retinitisQ
  6. Collagen Vascular diseases eg SLE (lupus) retinopathyQ DLE, Scleroderma, PAN etc
  7. Anemic conditions eg hypotensive retinopathy, carotid ligation, severe blood loss, cardiac embolic disease, leukemia, sickle cell retinopathy (±)
  8. CRVO (ischemic type)
  9. Radiation retinopathy

* Sickle cell retinopathy shows sea fan configuration (of sprouting new vessels) and sunburst spots.


Q. 30

Diabetic retinopathy is essentially an angiopathy affecting retinal:

 A

Precapillary arterioles

 B

Capillaries

 C

Venules

 D

All of the above

Q. 30

Diabetic retinopathy is essentially an angiopathy affecting retinal:

 A

Precapillary arterioles

 B

Capillaries

 C

Venules

 D

All of the above

Ans. D

Explanation:

Ans. All of the above


Q. 31

Spontaneous regression of proliferative retinopathy may occur in:

 A

Diabetic retinopathy

 B

Proliferative sickle retinopathy

 C

Retinopathy of prematurity

 D

All of the above

Q. 31

Spontaneous regression of proliferative retinopathy may occur in:

 A

Diabetic retinopathy

 B

Proliferative sickle retinopathy

 C

Retinopathy of prematurity

 D

All of the above

Ans. D

Explanation:

Ans. All of the above


Q. 32

Visual loss in diabetic retinopathy is due to all except:

 A

Cataract formation

 B

Background diabetic retinopathy

 C

Ischaemic maculopathy

 D

Vitreous hemorrhage

Q. 32

Visual loss in diabetic retinopathy is due to all except:

 A

Cataract formation

 B

Background diabetic retinopathy

 C

Ischaemic maculopathy

 D

Vitreous hemorrhage

Ans. B

Explanation:

Ans. Background diabetic retinopathy


Q. 33

Earliest change in diabetic retinopathy is:

 A

Hard exudate

 B

Soft exudate

 C

Dot haemorrhage

 D

Microaneurysm

Q. 33

Earliest change in diabetic retinopathy is:

 A

Hard exudate

 B

Soft exudate

 C

Dot haemorrhage

 D

Microaneurysm

Ans. D

Explanation:

Ans. Microaneurysm


Q. 34

Commonest cause of loss of vision in non-proliferative diabetic retinopathy is:

 A

Vitreous haemorrhage

 B

Macular edema

 C

Detachment of retina

 D

Subretinal haemorrhage

Q. 34

Commonest cause of loss of vision in non-proliferative diabetic retinopathy is:

 A

Vitreous haemorrhage

 B

Macular edema

 C

Detachment of retina

 D

Subretinal haemorrhage

Ans. B

Explanation:

Ans. Macular edema


Q. 35

Sudden loss of vision in patient with diabetic retinopathy is due to:

 A

Cataract

 B

Glaucoma

 C

Vitreous defects

 D

Papilloedema

Q. 35

Sudden loss of vision in patient with diabetic retinopathy is due to:

 A

Cataract

 B

Glaucoma

 C

Vitreous defects

 D

Papilloedema

Ans. C

Explanation:

Ans. Vitreous defects


Q. 36

All of the following take part in the pathogenesis of macular edema in diabetic retinopathy except:

 A

Retinal pigment epithelium dysfunction

 B

Oxidative stress

 C

VEGF

 D

Increased protein kinase-C

Q. 36

All of the following take part in the pathogenesis of macular edema in diabetic retinopathy except:

 A

Retinal pigment epithelium dysfunction

 B

Oxidative stress

 C

VEGF

 D

Increased protein kinase-C

Ans. A

Explanation:

Ans. Retinal pigment epithelium dysfunction


Q. 37

Vitreous haemorrhage in diabetic retinopathy

 A

Non-proliferative diabetic retinopathy

 B

Prolifertive diabetic retinopathy

 C

Both

 D

None

Q. 37

Vitreous haemorrhage in diabetic retinopathy

 A

Non-proliferative diabetic retinopathy

 B

Prolifertive diabetic retinopathy

 C

Both

 D

None

Ans. B

Explanation:

Ans. Prolifertive diabetic retinopathy


Q. 38

Panretinal photocoagulation is indicated in:

 A

Macular edema

 B

Retinal breaks

 C

Proliferative diabetic retinopathy

 D

Tractional retinal detachment

Q. 38

Panretinal photocoagulation is indicated in:

 A

Macular edema

 B

Retinal breaks

 C

Proliferative diabetic retinopathy

 D

Tractional retinal detachment

Ans. C

Explanation:

Ans. Proliferative diabetic retinopathy


Q. 39

Treatment of diabetic retinopathy neovascula­risation is/are:

 A

Retinal laser photocoagulation

 B

Pars plana vitrectomy

 C

Phacoemulsion

 D

LASIK

Q. 39

Treatment of diabetic retinopathy neovascula­risation is/are:

 A

Retinal laser photocoagulation

 B

Pars plana vitrectomy

 C

Phacoemulsion

 D

LASIK

Ans. A

Explanation:

Ans. Retinal laser photocoagulation


Q. 40

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with non-progressive diabetic retinopathy was treated with Macular grid photocoagulation.The patient still has vitreo macular traction. What is the preferred treatment?

 A

Intravitreal bevacizumab

 B

Pars plana vitrectomy

 C

Repeat macular grid photocoagulation

 D

Augmented macular photocoagulation

Q. 40

A patient with clinically significant diabetic macular edema with non progressive diabetic retinopathy was treated with non-progressive diabetic retinopathy was treated with Macular grid photocoagulation.The patient still has vitreo macular traction. What is the preferred treatment?

 A

Intravitreal bevacizumab

 B

Pars plana vitrectomy

 C

Repeat macular grid photocoagulation

 D

Augmented macular photocoagulation

Ans. B

Explanation:

Ans. Pars plana vitrectomy


Q. 41

All of the following are indications of pan retinal photocoagulation except:

 A

Pre-proliferative diabetic retinopathy

 B

Proliferative diabetic retinopathy

 C

Ischaemic central retinal vein occlusion

 D

Central retinal artery occlusion

Q. 41

All of the following are indications of pan retinal photocoagulation except:

 A

Pre-proliferative diabetic retinopathy

 B

Proliferative diabetic retinopathy

 C

Ischaemic central retinal vein occlusion

 D

Central retinal artery occlusion

Ans. D

Explanation:

Ans. Central retinal artery occlusion


Q. 42

Capillary microaneurysms is an earliest sign of:

March 2013

 A

Vitreous hemorrhage

 B

Non-proliferative diabetic retinopathy

 C

Trauma

 D

Hypertensive retinopathy

Q. 42

Capillary microaneurysms is an earliest sign of:

March 2013

 A

Vitreous hemorrhage

 B

Non-proliferative diabetic retinopathy

 C

Trauma

 D

Hypertensive retinopathy

Ans. B

Explanation:

Ans. B i.e. Non-proliferative diabetic retinopathy

Diabetic retinopathy

  • Fundus examination in DM:

–         NIDDM: As early as possible

–         IDDM: 5 years after diagnosis of DM

  • Incidence of diabetic retinopathy increases with disease duration

Q. 43

Characteristic feature of diabetic retinopathy:

September 2005, 2010 March 2007

 A

Hard exudate

 B

Soft exudate

 C

Ambylopia

 D

Microaneurysm

Q. 43

Characteristic feature of diabetic retinopathy:

September 2005, 2010 March 2007

 A

Hard exudate

 B

Soft exudate

 C

Ambylopia

 D

Microaneurysm

Ans. D

Explanation:

Ans. D: Microaneurysm

Diabetic retinopathy is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more.

Diabetic retinopathy often has no early warning signs. As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy, they can bleed (hemorrhage) and blur vision.

On fundoscopic exam, one can see cotton-wool spots, flame hemorrhages, and dot-blot hemorrhages.

Diabetic retinopathy is the result of microvascular retinal changes.

Hyperglycemia-induced pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls. The initial loss of pericytes leads to the formation of the dilatations of the vessels seen as microaneurysms and breakdown of the blood-retinal barrier making the retinal blood vessels more permeable.

Small blood vessels in the eye are especially vulnerable to poor blood sugar control. An over accumulation of glucose and/or fructose damages the tiny blood vessels in the retina. During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision.

Some people develop macular edema. It occurs when the damaged blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us see detail. The fluid makes the macula swell, which blurs vision.

As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage. The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina.

Fibrovascular proliferation can also cause tractional retinal detachment. The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.

Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages.

Diabetic retinopathy is detected during an eye examination that includes:

  • Visual acuity test:
  • Ophthalmoscopy: Note that hand-held ophthalmoscopy is insufficient to rule out significant and treatable diabetic retinopathy.

Ocular Coherence Tomography or OCT: This is a scan similar to an ultrasound which is used to measure the thickness of the retina.

Digital Retinal Screening Programs: This involves digital image capture and transmission of the images to a digital reading center for evaluation and treatment referral.

Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs for the early detection of diabetic retinopathy using slit-lamp biomicroscopy.

Early signs of the disease (over retina):

  • Leaking blood vessels,
  • Retinal swelling, such as macular edema,
  • Pale, fatty deposits on the retina (exudates) – signs of leaking blood vessels,
  • Damaged nerve tissue (neuropathy), and
  • Any changes in the blood vessels.

Panretinal photocoagulation, or PRP (also called scatter laser treatment), is used to treat proliferative diabetic retinopathy (PDR).Rather than focus the light on a single spot, hundreds of small laser burns are made away from the center of the retina, a procedure called scatter laser treatment or panretinal photocoagulation. The treatment shrinks the abnormal blood vessels.


Q. 44

Which is the most common early feature of diabetic retinopathy:        

September 2011

 A

Dot and blot hemorrhages

 B

Oedema

 C

Hard exudates

 D

Neovascularization

Q. 44

Which is the most common early feature of diabetic retinopathy:        

September 2011

 A

Dot and blot hemorrhages

 B

Oedema

 C

Hard exudates

 D

Neovascularization

Ans. A

Explanation:

Ans. A: Dot and blot hemorrhages

Ophthalmoscopically, the earliest change of background diabetic retinopathy characteristically affects the smaller blood vessels.

Small dot and blot haemorrhages are common

Diabetic retinopathy

  • It is retinopathy (damage to the retina) caused by complications of diabetes mellitus, which can eventually lead to blindness.
  • It is an ocular manifestation of systemic disease which affects up to 80% of all patients who have had diabetes for 10 years or more.

Signs and symptoms

  • Diabetic retinopathy often has no early warning signs.
  • As new blood vessels form at the back of the eye as a part of proliferative diabetic retinopathy (PDR), they can bleed (ocular hemorrhage) and blur vision.
  • In most cases, it will leave just a few specks of blood, or spots, floating in a person’s visual field, though the spots often go away after a few hours.
  • On funduscopic exam, one see cotton wool spots, flame hemorrhages (similar lesions are also caused by the alpha-toxin of Clostridium novyi), and dot-blot hemorrhages.
  • Elevation of blood-glucose levels can also cause edema (swelling) of the crystalline lens (hyperphacosorbitomyopicosis) as a result of sorbitol (sugar alcohol) accumulating in the lens.
  • This edema often causes temporary myopia (nearsightedness).
  • A common sign of hyperphacosorbitomyopicosis is blurring of distance vision while near vision remains adequate. Pathogenesis
  • Diabetic retinopathy is the result of microvascular retinal changes.
  • Hyperglycemia-induced intramural pericyte death and thickening of the basement membrane lead to incompetence of the vascular walls.
  • These damages change the formation of the blood-retinal barrier and also make the retinal blood vessels become more permeable.
  • During the initial stage, called nonproliferative diabetic retinopathy (NPDR), most people do not notice any change in their vision.
  • Early changes that are reversible and do not threaten central vision are sometimes termed simplex retinopathy or background retinopathy.
  • Some people develop macular edema.
  • It occurs when the damaged blood vessels leak fluid and lipids onto the macula.
  • The fluid makes the macula swell, which blurs vision.

Proliferative diabetic retinopathy (PDR) (or PDRP)

  • As the disease progresses, severe nonproliferative diabetic retinopathy enters an advanced, or proliferative, stage when blood vessels proliferate (i.e. grow).
  • The lack of oxygen in the retina causes fragile, new, blood vessels to grow along the retina and in the clear, gel-like vitreous humour that fills the inside of the eye.
  • Without timely treatment, these new blood vessels can bleed, cloud vision, and destroy the retina.
  • Fibrovascular proliferation can also cause tractional retinal detachment.
  • The new blood vessels can also grow into the angle of the anterior chamber of the eye and cause neovascular glaucoma.
  • Nonproliferative diabetic retinopathy shows up as cotton wool spots, or microvascular abnormalities or as superficial retinal hemorrhages.

Risk factors

All people with diabetes mellitus are at risk – those with Type I diabetes (juvenile onset) and those with Type II diabetes (adult onset).

  • The longer a person has diabetes, the higher the risk of developing some ocular problem.
  • People with Down’s syndrome, who have three copies of chromosome 21, almost never acquire diabetic retinopathy.
  • This protection appears to be due to the elevated levels of endostatin, an anti-angiogenic protein, derived from collagen XVIII.

The collagen XVIII gene is located on chromosome 21.

Management

There are three major treatments for diabetic retinopathy, which are very effective in reducing vision loss from this disease.

  • These three treatments are laser surgery, injection of triamcinolone into the eye, and vitrectomy.
  • Although these treatments are very successful (in slowing or stopping further vision loss), they do not cure diabetic retinopathy.

Laser photocoagulation

  • It is widely used for early stages of proliferative retinopathy.

Panretinal photocoagulation

  • Panretinal photocoagulation, or PRP (also called scatter laser treatment), is used to treat proliferative diabetic retinopathy (PDR).
  • The goal is to create 1,600 – 2,000 burns in the retina with the hope of reducing the retina’s oxygen demand, and hence the possibility of ischemia.

Intravitreal triamcinolone acetonide

  • Triamcinolone is a long acting steroid preparation.
  • When injected in the vitreous cavity, it decreases the macular edema (thickening of the retina at the macula) caused due to diabetic maculopathy, and results in an increase in visual acuity.
  • The effect of triamcinolone is transient, lasting up to three months, which necessitates repeated injections for maintaining the beneficial effect.
  • Complications of intravitreal injection of triamcinolone include cataract, steroid-induced glaucoma and endophthalmitis.

Vitrectomy

  • Instead of laser surgery, some people require a vitrectomy to restore vision.
  • A vitrectomy is performed when there is a lot of blood in the vitreous.
  • It involves removing the cloudy vitreous and replacing it with a saline solution.

Q. 45

Which of the following is characteristically associated with proliferative diabetic retinopathy:

September 2011

 A

Cotton wool spots

 B

Papilloedema

 C

Soft exudates

 D

Neovascularization

Q. 45

Which of the following is characteristically associated with proliferative diabetic retinopathy:

September 2011

 A

Cotton wool spots

 B

Papilloedema

 C

Soft exudates

 D

Neovascularization

Ans. D

Explanation:

Ans. D: Neovascularization

In proliferative diabetic retinopathy, the neovascularization arises from the optic nerve head; there is neovascularization of the disc and along the large vessels, as well as neovascularization elsewhere


Q. 46

Most important risk factor in development of diabetic retinopathy is ‑

 A

Duration of type II diabetes mellitus

 B

Type of diabetes mellitus

 C

Severity of disease

 D

Duration of treatment taken

Q. 46

Most important risk factor in development of diabetic retinopathy is ‑

 A

Duration of type II diabetes mellitus

 B

Type of diabetes mellitus

 C

Severity of disease

 D

Duration of treatment taken

Ans. A

Explanation:

Ans. is ‘a’ i.e., Duration of type II diabetes mellitus

Risk factors for development of diabetic retinopathv in diabetic patients

Risk factors associated with diabetic retinopathy arc :-

i) Duration of disease :- It is the most important risk factor. It is worth noting that it is the duration of disease after the onset of puberity, which acts as risk factor. For example, the risk of retinopathy is roughly same for two 25 years old patients, of whom one developed DM at 12 years (onset of puberty) and other at the age of 6 years because both have same duration (13 yrs) of disease after the onset of puberty. The risk of retinopathy in children diagnosed prior to the age of 2 years have a negligible risk of retinopathy for the first 10 years. So, age of onset also acts as a risk factor. However, after onset of puberty, age of onset is not a risk factor.

ii) Sex :- Incidence is more in females

iii) Poor glycemic control

iv) Accompanying factors :- Hypertension, smoking, poor renal status, obesity, hyperlipidemia

v) Pregnancy :- May accelerate the changes of diabetic retinopathy.


Q. 47

Most common cause of ruheosis iridis ‑

 A

Tumor

 B

CRAO

 C

Radiation retinopathy

 D

Diabetic retinopathy

Q. 47

Most common cause of ruheosis iridis ‑

 A

Tumor

 B

CRAO

 C

Radiation retinopathy

 D

Diabetic retinopathy

Ans. D

Explanation:

Ans. is ‘d’ i.e., Diabetic retinopathy 

Causes of rubeosis iridis (neovascularization of iris)

  • Common :- Diabetic retinopathy (most common cause), central retinal vein occlusion, Eale’s disease, sickle-cell retinopathy.
  • Rare causes :- Long standing retinal detachment, central retinal artery occlusion, intraocular inflammation (uveitis), intraocular tumors (choroidal melanoma, retinoblastoma), radiation retinopathy, ocular ischemic syndrome (carotid artery disease, carotid-cavernous fistula).

Q. 48

All are seen in non-proliferative diabetic retinopathy except ‑

 A

Microaneurysm

 B

Neovascularization

 C

Hard exudates

 D

Macular edema

Q. 48

All are seen in non-proliferative diabetic retinopathy except ‑

 A

Microaneurysm

 B

Neovascularization

 C

Hard exudates

 D

Macular edema

Ans. B

Explanation:

Ans. is ‘b’ i.e., Neovascularization

Classification of Diabetic retinopathy 

Nonproliferative

Proliferative

Background retinopathy

  1. Microaneurysm
  2. Dot and blot hemorrhage (deep hemorrhage)
  3. Hard exudate
  4. Macular edema

B) Preproliferative retinopathy

  1. Cotton-wool spots (soft exudates)
  2. Venous beading
  3. Extensive hemorrhage
  4. lntraretinal intrava scul ar abn ormalities (IRMA

Neovasculorization of the disc (NVD)

  1. Neovasculaization elsewhere in the retina (NVE)
  2. Viffeous hemorrhage
  3. Fibrovascular proli feration
  4. Trsction retinsl detachment
  5.  Iris surface neovascularization (rubeosis iridis or

neovascular glaacoma)



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