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Medicine year 3- EOCP > Ophthalmology core conditions > Flashcards

Ophthalmology core conditions Flashcards

1
Q

Diabetic retinopathy

A

When the blood vessels in the retina are damaged due to prolonged exposure to high blood sugar. Increased vascular permeability causes blot haemorrhages and the formation of hard exudate. Damage to the blood vessel wall causes microaneurysms and venous beading. There can be vascular occlusion leading to ischaemia. Vascular leaking and occlusion can cause VEGF production leading to neovascularisation which can cause haemorrhage

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2
Q

Symptoms of Diabetic retinopathy

A
  • Painless gradual reduction of central vision
  • Haemorrhages give the appearance of dark floater
  • If the haemorrhage is large it can result in sudden visual loss
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3
Q

Fundoscopy- proliferative diabetic retinopathy

A
  • Cotton wool spots
  • Microaneurysms
  • Hard exudate
  • Blot haemorrhages
  • Neovascularisation
  • Macular oedema
  • Ischaemic maculopathy
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4
Q

Fundoscopy non-proliferative diabetic retinopathy

A
  • Mild- microaneurysms
  • Moderate: microaneurysms, blot haemorrhage, hard exudate, cotton wool spots and venous beading
  • Severe: blot haemorrhage, microaneurysms in 4 quadrants, venous beading in 2 quadrates, intraretinal microvascular abnormalities in any quadrant
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5
Q

Complications of diabetic retinopathy

A
  • Retinal detachment
  • Vitreous haemorrhage
  • Rebeosis iridis
  • Optic neuropathy
  • Cataracts
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6
Q

Management of diabetic retinopathy

A
  • Laser photocoagulation
  • Anti-VEGF medication such as ranibizumab and bevacizumab
  • Vitreoretinal surgery in severe disease
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7
Q

Risk factors for diabetic retinopathy

A
  • Poor glucose control
  • Poor blood pressure control
  • Poor renal function
  • High lipids
  • Obesity
  • Anaemia
  • Pregnancy
  • Smoking
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8
Q

The three stages of diabetic retinopathy

A

Background, Pre-proliferative, Proliferative

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9
Q

Symptoms of Hypertensive retinopathy

A
  • Silver wiring or copper wiring is where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
  • Arteriovenous nipping is where the arterioles cause compression of the veins where they cross. This is due to sclerosis and hardening of the arterioles.
  • Cotton wool spots are caused by ischaemia and infarction in the retina causing damage to nerve fibres.
  • Hard exudates are caused by damaged vessels leaking lipids into the retina.
  • Retinal haemorrhages are caused by damaged vessels rupturing and releasing blood into the retina.
  • Papilloedema is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
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10
Q

Hypertensive retinopathy grading= Keith- Wagener fundoscopy findings

A
  • Grade 1 = generalised alveolar narrowing caused by vessel sclerosis - leading to silver/copper wiring appearance
  • Grade 2 = focal narrowing and AV nipping i.e. venous compression where the arteriole crosses the venule
  • Grade 3 = retinal haemorrhages i.e. flame haemorrhages, hard exudates and cotton wool spots
  • Grade 4 = papilloedema and loss of sight - blurring of the optic disc

The first two stages tend to be seen in chronic hypertension whilst the last two are the acute changes of more severe hypertension

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11
Q

Management of diabetic retinopathy

A

Focussed on controlling blood pressure and other risk factors such as smoking and blood lipid levels

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12
Q

Acute angle glaucoma

A
  • Caused by an anatomically narrow angle between the iris and the cornea
  • This pushes the iris against the trabecular meshwork and seals it
  • Therefore, the aqueous humour cant drain and intraocular pressure rapidly increases
  • Opthalmic emergency as it can lead to blindness
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13
Q

Symptoms of acute angle glaucoma

A
  • More common in hypermetropia
  • Seen in acutely painful red eye, cloudy cornea and a mid dilated fixed pupil
  • Patients are systemically unwell with nausea and headaches
  • Blurred vision, halos around light
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14
Q

Medications pre-disposing to closed angle glaucoma

A
  • Adrenergic i.e. noradrenaline
  • Anticholinergics i.e. oxybutynin
  • Tricyclics i.e. amitriptyline
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15
Q

Risk factors for closed angle glaucoma

A
  • Increasing age
  • Females are affected around 4 times more often than males
  • Family history
  • Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
  • Shallow anterior chamber
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16
Q

Investigations into glaucoma

A
  • Cupping of the optic disc - most important feature
  • The cupping is of >0.5 disc:cup ratio
  • Increased vertical cup to disk ratio
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17
Q

Examination of glaucoma

A
  • Red-eye
  • Teary
  • Hazy cornea
  • Decreased visual acuity
  • Dilatation of the affected pupil
  • Fixed pupil size
  • Firm eyeball on palpation
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18
Q

Management of glaucoma- Primary care

A
  • Lie patient on their back without a pillow
  • Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
  • Give acetazolamide 500 mg orally
  • Given analgesia and an antiemetic if required
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19
Q

Management of glaucoma- secondary care

A
  • Pilocarpine
  • Acetazolamide (oral or IV)
  • Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye
  • Timolol is a beta-blocker that reduces the production of aqueous humour
  • Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
  • Brimonidine reduces the production of aqueous fluid and increase uveoscleral outflow
  • Laser iridotomy is a definitive treatment
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20
Q

Open angle glaucoma

A

Most common form of glaucoma. The drainage through the trabecular meshwork is reduced due to a gradual increase in resistance

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21
Q

Symptoms of open angle glaucoma

A
  • Gradual reduction in peripheral vision (tunnel vision)
  • Painless
  • Patient may walk into objects
  • Haloes surrounding light
  • Headaches
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22
Q

Risk factors for open angle glaucoma

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Near sightedness (myopia)
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23
Q

Investigations into open angle glaucoma

A
  • Non-contact tonometry estimates intraocular pressure by shooting a puff of air at the cornea and measuring the response
  • Goldmann applanation tonometry, applies different pressures to the cornea to get an accurate measurement of the intraocular pressure
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24
Q

Examinations into open angle glaucoma

A
  • Goldmann applanation tonometry can be used to check the intraocular pressure.
  • Fundoscopy assessment to check for optic disc cupping and optic nerve health.
  • Visual field assessment to check for peripheral vision loss.
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25
Q

Management of open angle glaucoma

A
  • Treatment is usually started at an intraocular pressure of 24mmHG or above
  • Prostaglandin analogue eye drops (i.e. latanoprost). These increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).
  • Trabeculectomy surgery- if eye drops are ineffective, makes a new channel in the anterior chamber
26
Q

Risk factors for retinal detachment

A
  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Trauma to the eye
  • Retinal malignancy
  • Older age
  • Family history
27
Q

Symptoms of retinal detachment

A
  • Peripheral vision loss
  • Blurred or distorted vision
  • Flashes and floaters
28
Q

Rhematogenous retinal detachment

A
  • most common type
  • ageing is the most common cause
  • when the vitreous pulls on the retina and causes a small tear
  • also due to trauma
29
Q

Tractional retinal detachment

A

Scar tissue on the retina pulls the retina away from the back of the eye, common in diabetic retinopathy

30
Q

Exudative retinal detachment

A

Fluid builds up behind the retina but there is no tear, the fluid pushes the retina away from the back of the eye and causes it to detach

31
Q

Investigations into retinal detachment

A
  • With a slit lamp test/ tonometry
  • B-scan ultrasound of the orbit helps determine if the retina is detached
32
Q

Examination- retinal detachment

A
  • Pigmented cells in the anterior vitreous
  • Potential vitreous haemorrhage
  • Retinal tear or hole
33
Q

Management of retinal detachment

A
  • Vitrectomy
  • Scleral buckling
  • Pneumatic retinopexy
34
Q

Management of retinal tears

A

Laser therapy, cryotherapy. Helps create adhesion between the retina and the choroid to prevent detachmeny

35
Q

Diabetic retinopathy- microaneurysms

A

Persistent hyperglycaemia shunts excess glucose into the aldose reductase pathway converting glucose into sorbitol. This sorbitol damages the endothelial pericytes of the retinal capillaries. This leads to the formation of microaneurysms, which can either burst and bleed or leak causing oedema and exudates.

36
Q

Diabetic retinopathy- vascular occlusion

A

Increased red blood cells and platelet aggregation and increased RBC rigidity leads to sluggish circulation and endothelial cell damage, focal capillary occlusion, ischaemia, hypoxia and infarction. You get the development of cotton wool spots, venous changes and neovascularisation

37
Q

Diabetic retinopathy- VEGF

A

Produced in response to ischaemia, hypoxia and inflammation. It alters capillary permeability (vascular leakage causing oedema) and causes proliferation and migration of endothelial cells to form new vessels (neovascularisation).

38
Q

Diabetic retinopathy- Neovascularisation

A

The new vessels are fragile. They can bleed causing sub-hyaloid and vitreous haemorrhage, having bled they may fibrose and cause retinal detachment. New vessels in the iris can block the drainage angle causing a rise in intraocular pressure, known as rubeotic glaucoma.

39
Q

Symptoms of background retinopathy

A

• Microaneurysms
• Dot and Blot haemorrhage
• Oedema
• Exudate
• Slow progression, not a big concern. No treatment is needed

40
Q

Symptoms of pre-proliferative diabetic retinopathy

A

• Larger blot haemorrhages
• Venous dilation, beading and loops
• Cotton Wool Spots- formed from the waste products of axonal transport, when there is ischaemic damage to the nerve fibre layer
• IRMAs ( Intra-Retinal Microvascular Abnormalities)- collateral vessels which are formed in response to vascular occlusion

41
Q

IRMA

A

The formation of collateral vessels between the arterial and venous system, unlike neovascularisation these are healthy vessels which don’t bleed or leak. Can differentiate by performing an IVFA, with IRMA’s there will be no leakage.

42
Q

Proliferative diabetic retinopathy

A

• This is characterised by the presence of neovascularisation on the disc (NVD), else where (NVE) in the retina and on the iris (rubeosis iridis).
• If left untreated these can lead to vitreous haemorrhage and tractional retinal detachment
• Can still have normal vision if no background changes in the foveal region

43
Q

Diabetic retinopathy- haemorrhage

A

Sub-hyaloid haemorrhage- the new vessels which grow are very friable and can leak. Can leak into the space between the retina and the vitreous, the sub-hyaloid space.

Vitreous haemorrhage- the new vessels can grow directly into the vitreous. If the patient moves suddenly then the Proliferative diabetic retinopathy movement of the vitreous may tear the new vessels causing a haemorrhage into the vitreous.

44
Q

Diabetic retinopathy- Rubeosis iridis and tractional retinal detachment

A

Rubeosis iridis- new vessels can grow on the iris, they can grow across the iris and into the drainage angle of the eye

Tractional retinal detachment- happens when the new vessels become so extensive they fibrose. Can lead to irreparable visual loss.

45
Q

Complication diabetic retinopathy

A

1) Sub-hyaloid haemorrhage
2) Vitreous haemorrhage
3) Rubeosis iridis
4) Tractional retinal detachment

46
Q

Pan retinal photocoagulation

A

Treatment for diabetic retinopathy. Involves lasering the peripheral retina, reducing the area of tissue requiring oxygen by creating burns which destroy retinal tissue. Causes the new vessels to shrink away. You don’t laser the macular region as it will cause central visual loss. You lose peripheral vision which can affect your ability to drive

47
Q

Diabetic retinopathy- treatment of vitreous haemorrhage

A

Most resolve by themselves. PRP cannot be performed through haemorrhage. If haemorrhage does not clear you can perform a vitrectomy to remove the vitreous surgically and replace it with fluid. The vitreous also acts as a reservoir for VEGF, so the VEGF is also removed.

48
Q

Maculopathy

A

Background retinopathy changes occurring in the macular region, this reduces the patients vision. Not all patients develop maculopathy

49
Q

Diabetic maculopathy signs on fundoscopy

A

• Dot and blot haemorhage
• Microaneurysms
• Cotton wool spot
• Ring of exudate
• Oedema
• Gradual deterioration of visual acuity, central blurriness

50
Q

Treatment of maculopathy

A

• If background diabetic retinopathy occurs close to the fovea then treatment is needed to control the leakage from microaneurysms to prevent visual loss
• Focal laser- seals the microaneurysms, preventing oedema and exudation
• Anti- VEGF= reduces oedema and exudation, doesn’t cause any scarring so can be used in patient where laser could cause irreversible sight loss
• Intra-vitreal steroids- treat macular oedema. Reduce inflammation, VEGF and thus vascular leakage. Long acting implants are injected into the eye
• Diabetic control

51
Q

Cons of anti-VEGF

A

• Carries risk of endophthalmitis, a sight threatening infection
• Need lots of injections, laser is one off
• Expensive

52
Q

Investigations into diabetic retinopathy

A

• Intra-venous Fluorescein Angiography (IVFA)- a fluorescein dye is injected and enters the choroidal and retinal vessels, the blood vessels at the back of the eye can be visualised
• Optical coherence tomography (OCT)- non-invasive with no harmful radiation

53
Q

Factors which contribute to diabetic retinopathy

A

• Glucose control
• Blood pressure- 130/80 is the recommended blood pressure for diabetics with diabetic retinopathy
• Anaemia, renal failure, high cholesterol, obesity and smoking
• Pregnancy

54
Q

Diabetic retinopathy screening

A

• Screening is offered every year to people with diabetes aged 12 and over
• Visual acuity test
• Mydriatic agent applied to dilate the pupil
• Digital photographs taken of both retinas
• Images graded for signs of diabetic retinopathy and maculopathy using the RxMx grading system

55
Q

Hypertensive retinopathy

A

• More prevalent in African Caribbeans than Caucasians, in women more than men. Smoking contributes to the disease, and it is worse in those with co-existing renal disease.
• Retinal vessels undergo constriction, the sclerosis and later exudation occurs
• Flame shaped haemorrhages
• Cotton wool spots
• Exudation happens later then in diabetic retinopathy

56
Q

Malignant hypertension

A

Occurs with a severely raised BP, and may present with headaches and visual loss. Swollen optic discs (not papilloedema) and exudation alongside the other changes may be seen.

57
Q

Treatment for hypertensive retinopathy

A

• Blood pressure control
• Anti-VEGF, intra-vitreal steroids and pan retinal photocoagulation are needed for venous occlusions to prevent macular oedema and neo-vascularisation

58
Q

Pathology of Hypertensive retinopathy

A

• Hypertension leads to the constriction of arterioles
• Thickening of the arteriole walls causing the appearance of copper and silver wiring and AV nipping
• Leads to ischaemia and hypoxia, increased capillary permeability, retinal oedema, retinal haemorrhage, cotton wool spots and exudate

59
Q

Main features differenting diabetic and hypertensive retinopathy

A

Microaneurysms are only found in diabetic retinopathy so exudates feature extensively whilst cotton wool spots are a major feature of hypertensive retinopathy

60
Q

Diabetic retinopathy vs Hypertensive retinopathy

A

• Diabetic retinopathy= micro-aneurysms, oedema, exudate, dot and blot haemorrhage, cotton wool spots
• Hypertensive retinopathy= Cotton wool spots, flame haemorrhage, arteriole constriction, venous dilation, silver and copper wiring, exudation and disc swelling much later

Medicine year 3- EOCP (27 decks)

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