Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Eye Disease > Diabetic Eye Disease 2-Management Part 1 + 2 > Flashcards

Diabetic Eye Disease 2-Management Part 1 + 2 Flashcards

1
Q

what are the referral guidelines for all stages of DR/M/ P?

A

go look at the first diab brainscape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How would we class AND manage this fundus?
Also list characteristics

A

R1 + M0- annual review
few scattered dot haemorrhages and possible microaneurysms, all well away from the macular area.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

how would we class AND manage this fundus?
Also list characteristics

A

R1 + M1
Management-refer, to be seen soon (within 4 weeks)
Characteristics: a retina with definite intraretinal haemorrhage and exudate changes with a few within a disc diameter of the fovea.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what further tests can be conducted for suspect diab maculopathy?

A

visual acuities and amsler

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How would we class AND manage this fundus?
Also list characteristics?

A

R2 + M1
Management - refer to be seen soon (within 4 weeks)
Extensive non proliferation changes throughout retina inc within 1 DD of fovea- presence of multiple blot haemorrhages= R2 also significant Cotton wool spots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How could we class AND manage this fundus? Also list characteristics

A

R3A- refer as emergency - call hospital to arrange this- evident haemorrhages that can lead to tractional ret detachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How could we class AND manage this fundus? Also list characteristics

A

R3: Refer urgently to be seen within 1 week
NVD- Can’t see macula in this though so unsure if any M changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How could we class AND manage this fundus? Also list characteristics

A

R3A- emergency same day even phone HES to send px
-tractional Retinal Detachment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

as well as standard referral pathway, where else should we refer the px?

A

To the GP especially if undiagnosed- Diabetes mellitus need to be diagnosed, managed and controlled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are 4 modifiable risk factors in diab retinopathy?

A
  • blood sugar levels
  • lipid levels- Research into statins to help DR going on
  • blood pressure
  • smoking- this isn’t a defined risk factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the ‘legacy effect’?

A

where good glycaemic control can protect against future DR progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how does blood pressure control have an influence on DR?

A

-Potential for reduced microaneurysm, reduced hard exudates and cotton-wool spots and was aasociated with less need for photocoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does lipid lowering affect DR?

A

Reduces risk of macular oedema and exudation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does reducing lipid levels impact in DR progression?

A

reduces risk or progession of macular oedema and exudation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what type of DM is smoking a risk association with?

A

T1 DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main treatment (laser) for DR?

A

argon laser photocoagulation (focal and scatter)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What treatment is available to treat clinically significant macular oedema?

A

focal laser therapy (ALSO REDUCES RETINAL THICKENING)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when should scatter laser treatment be considered?

A

in eyes with severe non proliferative OR early proliferative DR (esp if T2 DM) and all eyes with severe proliferative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how much does early treatment reduce the risk of blindness caused by DR by?

A

Reduced risk of blindness in 5 years from 50% to 5% in people with proliferative DR.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

list three studies done in order to see the effective treatments for DR?

A
  • DCCT study (Investigates T1)
  • ETDRS
  • UKPDS (Investigates early T2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

does aspirin cause a risk in DR?

A

No affect on progression of DR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Should we consider a vitrectomy in advanced active DR?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what was the ETDRS ? ( NOT talking about VI test chart)

A

4- year RCT evaluating argon laser photocoagulation + asprin treatment for non-proliferative & early proliferative DR assessing risk & benefits of this in 1989

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what can be defined as ‘clinically significant macular oedema’ (CSMO)

A

-Retinal thickening at or within 500µm of the centre of the macula
-Hard exudates at or within 500µm of the centre of the macula, if associated with thickening of the adjacent retina
-Retinal thickening of one disc area or larger any part of which is within one disc diameter of the centre of the macula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

when do we use early laser treatment ( focal laser photocoagulation )for CSMO?

A

if bvs are leaking as it seals off the bvs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what laser treatment do we use in the case of diffuse leakage from capillaries in macula (diffuse diabetic macular oedema) ?

A

laser grid photocoagulation-places numerous coagulations around the fovea in to restore the blood–retinal barrier.
prevents futher deterioration BUT HARDLY ANY IMPACT in restoring VA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Can laser grid photocoagulation have an impact on restoring vA?

A

No

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how can we minimise damage to the fundus with laser?

A

by using low energy laser burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what growth factors can laser have an effect on?

A

laser can
-upregulate biochmeical mediators with antiangiogenic activity eg PEDF (pigment epithelium derived growth factor)
-stimulates increase of angiotensin 2-inhibiting VEGF induced angiogenesis/VEGF
-less VEGF= less vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

do exudates always get reabsorbed after laser treatment?

A

not always- gradually absorb but Extensive exudates within fovea causes irreversible damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

can focal laser coagulation improve vision?

A

yes-can actually improve vision by 2 lines in in 35% of patients at 2 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the growth factor promoting new vesselgrowth?

A

VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

List the 2 Anti-VEGF Injections available for DR treatment

A
  • Ranibizumab (Lucentis)
  • Aflibercept (eylea)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is Ranibizumab?

A

a monoclonal antibody fragment, which binds to and inactivates all isoforms of VEGF-A.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is bevacizumab?

A

not licensed for use in the eye, but cheaper, so used widely globally (rarely prescribed by the NHS).

36
Q

what is the recommended retinal thickness when treating with Ranibizumab?

A

400 microns or more

36
Q

what is the recommended retinal thickness when treating with Ranibizumab?

A

400 microns or more

37
Q

At what retinal thickness should we start treating with Ranibizumab?

A

400 microns or more

38
Q

what Anti-VEGF treatment is available for CSMO and how does it work?

A

-aflibercept (EYLEA)
a recombinant fusion protein that acts as a soluble decoy receptor and binds to VEGF-A, VEGF-B and placental growth factor (PlGF)

39
Q

is the recommended retinal thickness for CSMO using Eylea also 400 microns or above?

A

Yes (NICE, 2015)

40
Q

What is a disadvantage of laser photocoagulation?

A

retinal scarring- can become more of a risk if fovea involved (scotoma risk)

41
Q

disadvantages of laser therapyfor macular oedema?

A

-can stabilise but not improve VA
-laser scar expansion an lead to a scotoma

42
Q

what two treatments can be used in combination for CSMO?

A

Ranibizumab (Reduces risk of prolif DR developing) and laser treatment

43
Q

what is another therapy for CSMO which can be used in ‘resistant’ cases when focal laser and anti-VEGF injections not working?
+ give two examples of the medication used

A

intraviteral steroid therapy:

  • Triamcinolone injections
  • long-acting fluocinolone acetonide (FA).
44
Q

state 2 disadvanatges of intravitreal steroid injections when treating CSMO?

A
  • Raised IOPS
  • Cataract formation
45
Q

general referral pathway for R2 pre-prolif diab ret?

A
  • refer to GP for blood tests (HbA1c, blood pressure, lipids.),
  • refer to ophthalmologist- can consider prophylactic laser photocoagulation depnding: on severity, risk of progressiona and symptoms
46
Q

Management for R3 prolif diab ret?

A

refer to ophthalmologist

Following will be considered:

  • Pan retinal photocoagulation (PRP) recommended for patients with active proliferative DR
  • Intravitreal anti-VEGF injections to stabilise retinopathy, before cataract or vitrectomy
  • Vitrectomy for px with vitreous haemorrhage (especially if non clearing haemorrhage or associated with RD/ ghost cell glau/ tractional RD)
47
Q

what is pan retinal photocoagulation?

A

laser burns to peripheral retina

48
Q

why is pan retinal photocaogulation used in DR and how does it work?

A

Reduced outer retinal oxygen consumption , so now oxygen from the choroid can reach the inner retina where it doesn’t normally
Reduced hypoxia 🡪 reduced VEGF production 🡪 reduced neovascularisation.
May also work by killing ischaemic retina, so reducing VEGF production

49
Q

does pan retinal photocoagulation improve vision

A

NO- just stabilises it - although halves risk of severe visual loss

50
Q

6 disadvantages of pan retinal photocoagulation?

A
  • collateral damage to retinal tissue
  • macular oedema (decrease in VA)
  • colour vision defects
  • generalised field restriction
  • difficulty adjusting to changes in light levels
  • can be painful
51
Q

name an alternative to pan retinal photocoagulation?

A

cryotherapy

52
Q

what do we want the fundus to appear as post pan retinal photocaogulation?

A

we want paler areas not white as white can indicate disruption of neurosensory retina.
Strong white patches indicate full thickness burns and visibility of sclera.

53
Q

What 4 types of glaucoma are associated with diabetes mellitus?

A

-neovascular glaucoma (caused by rubeosis iridis)
-Open angle glaucoma (not conclusive association)
-Narrow / Closed angle glaucoma
-Secondary glaucoma

54
Q

what is neovasc glauc?

A

growth of vessels on iris/trabec meshwork-ocular emergency

55
Q

what treatments for diab may make a px predisposed to glaucoma?

A
  • steroid treatment
  • panretinal photocoagulation,
  • scleral buckling to treat RD
  • Silicone oil to treat RD
  • intraocular gas to treat RD
56
Q

how do we treat neovasc glauc?

A

treated with panretinal photocoagulation (to reduce hypoxia) + medical treatments e.g. atropine to reduce congestion, steroids to reduce inflammation, anti-glaucoma drugs + surgical treatment e.g. trabeculectomy in advanced cases.

57
Q

how are diab px more at risk of developing cataracts earlier?

A
  • glucose reduces to surbitol (an alcohol) & cannot pass through membranes
  • accumulation of this in the lens = osmotic imbalance stress (water draw into lens)
  • then lens fibres can rupture + burst = cataract
58
Q

what is a diabetic cataract?

A

increaed free radicals float around and less antioxidants, and in the case of diab lenses advanced glycation end products in lens may be linked to diabetic cataracts.

59
Q

what 2 risk factos can make a px with DM more prone to cataract?

A

poor blood sugar control, increased duration DM.

60
Q

what is another word for true diabetic cataract

A

snowflake cataract

61
Q

what is true diabetic cataract?

A

Multiple white anterior and posterior subcapsular and cortical opacities seen. (also vacuoles- this is all why they’ere called SNOWFLAKE)

62
Q

is true diab cataract uni or bilateral?

A

bilateral

63
Q

is true diab cataract rare

A

yes

64
Q

what type of DM can be a risk facotr for true diab cataract?

A

Related to very high serum glucose levels in young type I diabetic Px.

65
Q

what two types of age related cataract occur in DM px?

A
  • Cortical
  • Posterior Subcapsular
66
Q

how much earlier can age related catarcat occur in Diabetic px than non diabetics?

A

May appear ~10 years earlier than in non-diabetic Px.

67
Q

what two optic nerve conditions can be associated with diabetes?

A
  • AION
  • diabetic papillopathy (disc oedema, mild visual loss)
68
Q

What palsies are associated with DM?

A

3rd, 4th and 6th nerve (we won’t forget this after OSCE)

69
Q

WHAT IS THE RISK PERCENTAGE OF DIAB PXS GETTING CRANIAL NERVE PALSIES

A

25-30% in over 45s (acute OM palsy)

70
Q

Does diab 3rd nerve palsy spare the pupils?

A

yes

71
Q

what 4 corneal conditions occur in DM px

A
  • Reduced corneal sensitivity due to corneal neuropathy
  • Aqueous tear deficiency (Dry Eye Syndrome)
  • Corneal endothelial dysfunction
  • diab epitheliopathy
72
Q

when do we consider diabetes and the cornea

A

when fitting cls or refractive surgery

73
Q

what occurs in diabetic epitheliopathy?

A
  • recurrent erosions
  • Corneal abrasions
  • Persistent epithelial defects
74
Q

do we dilate all diab pxs?

A

no, esp if they are on the diab screening programme-You should dilate any patient with DM who has not been screened within the past 12 months.

75
Q

recall for px on diab screening programme

A

routine recall-often 2 years

76
Q

Recall for px NOT on diab screening programme

A

recall 12 months-encourage px to attnd, and should dilate any px who hasnt been in pastn 12 months

77
Q

typical H+S for diab px?

A
  • What type of DM?
  • What age of onset?
  • Ask about risk factors- well controlled diab? Hyperlipidamiea? High cholesterol?? Ht? smoking?
  • When were you last seen by the DESP?
  • Any problems with vision at distance or near? Any flashers or floaters? Diplopia?
  • Plus usual detailed H&S.
78
Q

Name the sx associated with M1, R3, CAG, fluctuating blood sugar, Cataract and nerve palsy.
(these are all associations of DR)

A
  • M1: reduce VA
  • R3: haemorrhage –> sudden vision loss, dark floaters
    tractional RD –> sudden loss of vision, flashes, curtain/veil
  • CAG: haloes, hazy vision, pain, redness
  • Fluctuating blood sugar: fluctuating rx + blurred vision
  • Cataract: decrease in vision + CS
  • Nerve palsy: diplopia
79
Q

Relevant clinical tests for diab px?

A
  • VAs
  • CS
  • colour vision
  • VFs
  • IOPs
  • Oculomotor status and pupils
  • indirect ophthalmoscopy
  • Fundus photography
  • OCT
  • Anterior eye / anterior chamber / vitreous
  • Retinal vasculature (Fluorescein angiography) moreso hes
80
Q

what Clinical test is commonly used in hes for DR?

A

Fluorescein angiography-leaky bvs fluoresce

81
Q

How do microaneurysms appear on fluoroscien angiography?

A

LITTLE WHITE SPOTS

82
Q

do leaky bvs appear as hyper or hypo fluorescing on fluoroscien angiography?

A

hyperfluorescent region
on the other hand, Dark patches (hypofluorescent) where capillaries are non perfused . Pale splotches = laser burns

83
Q

why is fluorscien angiography a good clinical test to do?

A

can notice wispy or development of new bvs even with obscuring vit haem on normal fundus photo

84
Q

how is an OCT used for DM pxs? (3 points)

A
  • management of diabetic maculopathy
  • measure thickness + observe oedema thickness
  • assess pre-post treatment change

Eye Disease (48 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions