Visit 1 – Notes & CC’s
1.2.3. Discusses with the patient the importance of systemic disease and its ocular impact, its treatment,
and the possible ocular side effects of medication
(APR – screen sharing record with assessor px taking meds for systemic disease)
Indicators:
Takes a thorough history from the px to include meds, control & disease duration
Demonstrates a thorough understanding of the disease process for diabetes, inflammatory disease
etc
Provides a layman’s explanation of the disease
Patient encounter:
Patient taking medication for systemic disease e.g. cardiovascular disease, diabetes.
Diabetes
Record: type/duration/control
o Control – compliant with meds, up to date with GP
o Poor control = fluctuating refraction
o Lens hydration impacts Rx, lens may swell and bulge, causing myopic shift
o Proliferative = hyperopic shift
If no med name (if the px does not know)– assessor will ask for examples
Screening
All diabetic px over 12 invited annually (T1 & T2)
Offered because DR doesn’t tend to cause symptoms in early stages
Screening based primarily on digital fundus images (nurses, technicians)
Images graded, 3 levels of grading
o Stage 1 – background
o Stage 2 – pre proliferative
o Stage 3 – proliferative
Any images with signs of retinopathy will be sent to level 2 and 3 grading
Images that may require referral will be graded by at least two graders
Referred from DRS to HES if proliferative and/or severe maculopathy
Frequency of screening
If your last 2 screening results showed any signs of retinopathy – recall 12/12
If your last 2 screening tests found no retinopathy – recall 24/12
If you’ve only been screened once before, you'll be screened every year. You'll usually be moved
over to 2-yearly screening if you receive 2 screening results where no retinopathy is found.
Diabetic screening depends on area
Can be done in high street practices with DRS contract
Pxs may go to HES if higher risk category i.e. poor compliance
Glasgow - remote screening teams in health centres etc
Number on NHS inform site
Explaining diabetes
, This is a conditions where the amount of sugar (glucose) in the blood is too high because the body
can’t use it properly. This is usually caused by your body not having enough insulin or having poor
insulin which does not work properly. Insulin is the chemical that helps your body absorb sugar.
Ocular impact – DM/DMO
1. Diabetic retinopathy
Background: microaneurysms, dot/blot haems, exudates >2DD from fovea
Pre-proliferative: cotton wool spots, venous beading, deep retinal haemorrhages, exudates <2DD
from fovea
Proliferative: pre-retinal haemorrhages, exudates <1DD from fovea, disc & retinal
neovascularisation – NVD or NVE
Advanced: traction/fluid RD, vitreous haemorrhage, neovascular glaucoma
Pathogenesis of diabetic retinopathy
DR is predominantly a microangiopathy in which small BVs (capillaries) are particularly vulnerable
to damage from high glucose levels
Affects both type 1&2, more prevalent among T1
High blood sugar promotes oxidative stress as there is an imbalance between free radicals and
antioxidants in the body; the excessive amounts of oxygen-derived free radicals damage blood
vessels
In the early stages, weaker areas in the small blood vessels form microaneurysms
which can result in intraretinal leakages i.e. haemorrhages and exudates
Main concern at this point is a large number of leakages or leakage near the macula
Capillaries can also become blocked and the bloody/oxygen supply compromised causing hypoxia
VEGF is stimulated in response to this oxygen deprivation resulting in the formation of new leaky
blood vessels eventually resulting in more bleeding and scaring
For a hypoxic retina, treatment options include
o Anti VEGF injections – intravitreal ranibizumab/lucentis
o Diuretics
o PRP (lessens the amount of retina that needs oxygen by killing off peripheral cells in order to
reduce VEGF), 2000-4000 laser burns
Explaining diabetic retinopathy (DR prevalence Scotland: 5.9%)
DR is a complication of diabetes caused by high blood sugar levels damaging the retina The retina is the
light sensitive layer at the back of the eye that coverts light into electrical signals. These signals are then
sent to the brain which allows us to see. The retina needs a constant blood supply in order to do so.
Overtime, it is these blood vessels that can become damaged if blood sugar levels are persistently too high.
DR can lead to blindness if it is left undiagnosed and untreated. However, it usually takes several years for
diabetic retinopathy to reach a stage where it threatens your sight. To minimise risk, people with diabetes
should ensure they control their blood sugar, BP and cholesterol as well as attending their regular diabetic
screenings. Would also advise px to contact practice immediately is the experience gradual worsening of
vision, sudden vision loss, shapes floating in vision, blurred or patchy vision, eye pain or redness. Px should
not wait till screening/routine test.
2. Corneal neuropathy
Reduction in corneal nerve density causing corneal desensitization
, Starts with DED symptoms, progresses to breakdown of epithelium, corneal oedema & ulcers
3. Delayed healing of corneal epithelium
Increased risk of infection & persistent defects
4. Cataract
Age related cataracts (NS/CO/PSC) occur earlier/may progress quicker
Young diabetics may develop ‘diabetic cataract’ = snowflake opacities
Medication and side effects
Insulin - may cause hypoglycaemia which causes dizzy spells; in rare cases may cause presbyopia
when first starting treatment due to shifting fluids which affect the lens; generally stabilises
o Novorapid – ingredient insulin aspart, fast-acting and works rapidly to normalise blood sugar
levels, begins working after 10-20mins, lasts 3-5 hours
o Levemir – ingredient insulin detemir long acting, subcutaneous injection only, up to 24-hour
duration of action
Metformin (biguanide) (T2) – dry eye and increase risk of angle closure
Gliclazide – lens changes, refractive error shifts
High Blood Pressure
Pathogenesis
Hypertension is a medical condition where the pressure inside the arteries is persistently elevated
The initial response of retinal arterioles to systemic hypertension is vasoconstriction
Prolonged HBP can lead to hardening of vessel walls, AV nipping and eventually increased vascular
permeability
Side effects of HBP on the eye can include a blockage in the blood vessels of the retina (CRAO or
CRVO), loss of vision due to a loss of blood supply to the optic nerve (NAAION), loss of peripheral
vision due to stroke, or a transient loss of vision that comes & goes (amaurosis fugax)
May also cause cotton wool spots, retinal haemorrhages, retinal ischaemia and neovascularisation
Explaining to a px
High blood pressure (hypertension) is a condition where the pressure of the blood inside the
arteries is higher than it should be, and so the heart has to work harder than normal to pump blood
around the body
The consequences of uncontrolled HBP can be severe i.e. loss of vision due to a blockage in the
blood supply to the retina or optic nerve, loss of peripheral vision due to stroke or episodes of
vision loss which come and go.
The condition can be improved by lifestyle changes such as improving diet, avoiding excess alcohol
consumption, stopping smoking and increasing exercise, as well as medications such as beta-
blockers, calcium channel blockers and vaso-dilators.
Medications & ocular side effects
Beta blocker - Propranolol = dry eye
ACE inhibitors - Lisinopril & ramipril = may cause ciliary body oedema which leads to reduced
accommodation and angle closure
Calcium channel blockers – losartan
, Other conditions
Autoimmune conditions - rheumatoid arthritis, spondylosis, IBS, Crohns, sarcoidosis
o Increase likelihood of conditions such as
Episcleritis
Scleritis
Uveitis
Sjogren’s syndrome
Retinal vasculitis
Glaucoma – when inflammation disrupts drainage
Rheumatoid arthritis medications
o Disease modifying anti-rheumatic drugs
o Hydroxychloroquine
Central scotoma
Bulls eye maculopathy
Keratopathy
o Pxs should be on 12/12 recall to monitor these changes
Hyper & hypothyroidism
o TED can occur when the thyroid is both overactive or underactive
o Ocular impact = swelling of EOMs
o Levothyroxine
MS
o Optic neuritis – retrobulbar
Hyperlipidaemia
1.2.3. Discusses with the patient the importance of systemic disease and its ocular impact, its treatment,
and the possible ocular side effects of medication
(APR – screen sharing record with assessor px taking meds for systemic disease)
Indicators:
Takes a thorough history from the px to include meds, control & disease duration
Demonstrates a thorough understanding of the disease process for diabetes, inflammatory disease
etc
Provides a layman’s explanation of the disease
Patient encounter:
Patient taking medication for systemic disease e.g. cardiovascular disease, diabetes.
Diabetes
Record: type/duration/control
o Control – compliant with meds, up to date with GP
o Poor control = fluctuating refraction
o Lens hydration impacts Rx, lens may swell and bulge, causing myopic shift
o Proliferative = hyperopic shift
If no med name (if the px does not know)– assessor will ask for examples
Screening
All diabetic px over 12 invited annually (T1 & T2)
Offered because DR doesn’t tend to cause symptoms in early stages
Screening based primarily on digital fundus images (nurses, technicians)
Images graded, 3 levels of grading
o Stage 1 – background
o Stage 2 – pre proliferative
o Stage 3 – proliferative
Any images with signs of retinopathy will be sent to level 2 and 3 grading
Images that may require referral will be graded by at least two graders
Referred from DRS to HES if proliferative and/or severe maculopathy
Frequency of screening
If your last 2 screening results showed any signs of retinopathy – recall 12/12
If your last 2 screening tests found no retinopathy – recall 24/12
If you’ve only been screened once before, you'll be screened every year. You'll usually be moved
over to 2-yearly screening if you receive 2 screening results where no retinopathy is found.
Diabetic screening depends on area
Can be done in high street practices with DRS contract
Pxs may go to HES if higher risk category i.e. poor compliance
Glasgow - remote screening teams in health centres etc
Number on NHS inform site
Explaining diabetes
, This is a conditions where the amount of sugar (glucose) in the blood is too high because the body
can’t use it properly. This is usually caused by your body not having enough insulin or having poor
insulin which does not work properly. Insulin is the chemical that helps your body absorb sugar.
Ocular impact – DM/DMO
1. Diabetic retinopathy
Background: microaneurysms, dot/blot haems, exudates >2DD from fovea
Pre-proliferative: cotton wool spots, venous beading, deep retinal haemorrhages, exudates <2DD
from fovea
Proliferative: pre-retinal haemorrhages, exudates <1DD from fovea, disc & retinal
neovascularisation – NVD or NVE
Advanced: traction/fluid RD, vitreous haemorrhage, neovascular glaucoma
Pathogenesis of diabetic retinopathy
DR is predominantly a microangiopathy in which small BVs (capillaries) are particularly vulnerable
to damage from high glucose levels
Affects both type 1&2, more prevalent among T1
High blood sugar promotes oxidative stress as there is an imbalance between free radicals and
antioxidants in the body; the excessive amounts of oxygen-derived free radicals damage blood
vessels
In the early stages, weaker areas in the small blood vessels form microaneurysms
which can result in intraretinal leakages i.e. haemorrhages and exudates
Main concern at this point is a large number of leakages or leakage near the macula
Capillaries can also become blocked and the bloody/oxygen supply compromised causing hypoxia
VEGF is stimulated in response to this oxygen deprivation resulting in the formation of new leaky
blood vessels eventually resulting in more bleeding and scaring
For a hypoxic retina, treatment options include
o Anti VEGF injections – intravitreal ranibizumab/lucentis
o Diuretics
o PRP (lessens the amount of retina that needs oxygen by killing off peripheral cells in order to
reduce VEGF), 2000-4000 laser burns
Explaining diabetic retinopathy (DR prevalence Scotland: 5.9%)
DR is a complication of diabetes caused by high blood sugar levels damaging the retina The retina is the
light sensitive layer at the back of the eye that coverts light into electrical signals. These signals are then
sent to the brain which allows us to see. The retina needs a constant blood supply in order to do so.
Overtime, it is these blood vessels that can become damaged if blood sugar levels are persistently too high.
DR can lead to blindness if it is left undiagnosed and untreated. However, it usually takes several years for
diabetic retinopathy to reach a stage where it threatens your sight. To minimise risk, people with diabetes
should ensure they control their blood sugar, BP and cholesterol as well as attending their regular diabetic
screenings. Would also advise px to contact practice immediately is the experience gradual worsening of
vision, sudden vision loss, shapes floating in vision, blurred or patchy vision, eye pain or redness. Px should
not wait till screening/routine test.
2. Corneal neuropathy
Reduction in corneal nerve density causing corneal desensitization
, Starts with DED symptoms, progresses to breakdown of epithelium, corneal oedema & ulcers
3. Delayed healing of corneal epithelium
Increased risk of infection & persistent defects
4. Cataract
Age related cataracts (NS/CO/PSC) occur earlier/may progress quicker
Young diabetics may develop ‘diabetic cataract’ = snowflake opacities
Medication and side effects
Insulin - may cause hypoglycaemia which causes dizzy spells; in rare cases may cause presbyopia
when first starting treatment due to shifting fluids which affect the lens; generally stabilises
o Novorapid – ingredient insulin aspart, fast-acting and works rapidly to normalise blood sugar
levels, begins working after 10-20mins, lasts 3-5 hours
o Levemir – ingredient insulin detemir long acting, subcutaneous injection only, up to 24-hour
duration of action
Metformin (biguanide) (T2) – dry eye and increase risk of angle closure
Gliclazide – lens changes, refractive error shifts
High Blood Pressure
Pathogenesis
Hypertension is a medical condition where the pressure inside the arteries is persistently elevated
The initial response of retinal arterioles to systemic hypertension is vasoconstriction
Prolonged HBP can lead to hardening of vessel walls, AV nipping and eventually increased vascular
permeability
Side effects of HBP on the eye can include a blockage in the blood vessels of the retina (CRAO or
CRVO), loss of vision due to a loss of blood supply to the optic nerve (NAAION), loss of peripheral
vision due to stroke, or a transient loss of vision that comes & goes (amaurosis fugax)
May also cause cotton wool spots, retinal haemorrhages, retinal ischaemia and neovascularisation
Explaining to a px
High blood pressure (hypertension) is a condition where the pressure of the blood inside the
arteries is higher than it should be, and so the heart has to work harder than normal to pump blood
around the body
The consequences of uncontrolled HBP can be severe i.e. loss of vision due to a blockage in the
blood supply to the retina or optic nerve, loss of peripheral vision due to stroke or episodes of
vision loss which come and go.
The condition can be improved by lifestyle changes such as improving diet, avoiding excess alcohol
consumption, stopping smoking and increasing exercise, as well as medications such as beta-
blockers, calcium channel blockers and vaso-dilators.
Medications & ocular side effects
Beta blocker - Propranolol = dry eye
ACE inhibitors - Lisinopril & ramipril = may cause ciliary body oedema which leads to reduced
accommodation and angle closure
Calcium channel blockers – losartan
, Other conditions
Autoimmune conditions - rheumatoid arthritis, spondylosis, IBS, Crohns, sarcoidosis
o Increase likelihood of conditions such as
Episcleritis
Scleritis
Uveitis
Sjogren’s syndrome
Retinal vasculitis
Glaucoma – when inflammation disrupts drainage
Rheumatoid arthritis medications
o Disease modifying anti-rheumatic drugs
o Hydroxychloroquine
Central scotoma
Bulls eye maculopathy
Keratopathy
o Pxs should be on 12/12 recall to monitor these changes
Hyper & hypothyroidism
o TED can occur when the thyroid is both overactive or underactive
o Ocular impact = swelling of EOMs
o Levothyroxine
MS
o Optic neuritis – retrobulbar
Hyperlipidaemia
