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Medicine year 3- EOCP > Opthalmology core conditions 2 > Flashcards

Opthalmology core conditions 2 Flashcards

1
Q

Definition of glaucoma

A

Progressive optic neuropathy causing specific optic nerve abnormalities (optic disc cupping) and field defects (arcuate field defects). It is most commonly associated with raised intra-ocular pressure.

Glaucoma causes a loss of retinal nerve fibers, the nerve fibers in the inferior part of the optic disc are the first to be lost.

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2
Q

Glaucoma triad

A

Disc cupping, field defects and intra-ocular pressure

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3
Q

Glaucoma- disc cupping

A

Cup gets bigger due to loosing retinal nerve fibers as the neuro-retinal rim shrinks. The normal ration is <0.5 but people who are short sighted have a larger sup disc ration, if the cupping is symmetrical between both eyes then its likely to be normal

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4
Q

Glaucoma- field defects

A

The most common field defect is an arcuate field loss caused by the loss of either inferior or superior nerve fibers, normally the patient is not aware till its severe. The inferior disc margin is normally the first to be damaged. The inferior retina corresponds to the superior part of the visual field

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5
Q

Normal intra-ocular pressure

A

14-22 mmHg

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6
Q

Raised intra-ocular pressure pathologies

A

• Raised intra-ocular pressure can lead to damage to the nerve fibre layer and optic disc causing visual field defects which we call Glaucoma.
• Raised intra-ocular pressure can exist without there being any glaucomatous damage. This is called Ocular Hypertension
• Damage to the nerve fibre layer and optic nerve with corresponding field defects can occur with a normal intra-ocular pressure. This is called Normal Tension Glaucoma

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7
Q

Movement of aqueous humour

A

• Aqueous humour is formed by the ciliary body to provide nutrients the lens and cornea
• It flows into the anterior segment, in front of the lens and through the pupil
• Drains via the trabecular meshwork into schlemms canal through the episcleral veins into the venous circulation

The angle= the irido-corneal angle, determines the type of glaucoma the patient has.

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8
Q

Diagosing glaucoma

A

Due to the presence of disc cupping and corresponding visual field defects. Acute angle closure glaucoma and acute rubeotic glaucoma are the exception as the IOP rises acutely causing severe pain so there is no time for progressive optic neuropathy

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9
Q

Different types of glaucoma

A

• Normal Tension Glaucoma (NTG)
• Ocular Hypertension (OHT)
Primary Angle Closure Glaucoma (PACG)
• Acute Angle Closure Glaucoma (AACG)
• Congenital glaucoma
• Secondary glaucoma
• Primary open angle glaucoma

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10
Q

Primary open angle glaucoma- risk factors

A

• Seen in older people, risk increases with age
• African Caribbean people are at greater risk and those with first degree relatives who have glaucoma
• History of very gradual loss of visual field over many years

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11
Q

Normal tension glaucoma

A

• When optic disc cupping and corresponding field defects occur without the rise in IOP
• Earlier onset then POAG
• Associated with a history of migraines or Raynauds disease
• More common in women
• Vascular cause
• As the IOP is not raised, it is often missed by opticians until there are significant optic disc changes and field loss. As before patients are usually asymptomatic.

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12
Q

Ocular hypertension

A

Have a high IOP without developing glaucoma. If the IOP goes above 28, then the risk of retinal vascular occlusions increases so require the same treatment as patients with POAG. These patients have a 10% chance of developing POAG so are kept under review

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13
Q

Primary angle closure glaucoma

A

• Contact between the iris and trabecular meshwork, IOP is raised. The irido-corneal angle appears closed
• Risk factors- shallow anterior chamber, genetic susceptibility, age, Asian ethnicity

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14
Q

Treatment for primary angle closure glaucoma

A

• Laser iridotomy (opens up the angle)
• Cataract surgery- opens up the angle as removing the lens creates more room
• Topical pressure lowering drugs

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15
Q

Acute angle closure glaucoma

A

• AACG is a small subset of primary angle closure glaucoma (PACG)
• The anterior chambers are very narrow
• Patients are normally hypermetropes (long sighted) as their eyes are shorter (from back to front) than normal.
• When the pupil dilates, the iris blocks the aqueous from entering the anterior chamber and the drainage angle, causes an acute rise in pressure
• Acutely painful red eye- the patient often feel systemically unwell and their vision deteriorates
• Its precipitated by dilation of the pupil
• Causes corneal oedema which untreated leads to nerve fibre death

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16
Q

Treatment for acute angle closure glaucoma

A

• IV Diamox (a carbonic anhydrase inhibitor)- reduces the production of aqueous
• Pilocarpine drops- constrict the pupil which then allows the normal flow of aqueous
• Laser treatment- creates a small hole in the peripheral iris diverting the flow of aqueous so it cant happen again

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17
Q

Congenital glaucoma

A

• Presents in the first year of life- patients have abnormal drainage angles
• Eye initially expands developing ‘bubpthalamos’, cornea gets cloudy as aqueous enters the cornea
• The baby suffers from intense photophobia, blepharospasm and watering eye
• Treatment is difficult involving surgery and medicine, visual outcome is poor

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18
Q

Secondary glaucoma

A
  • Rubeosis
  • Trauma (either penetrating or blunt) can cause damage to the drainage angle causing the IOP to go up.
  • Cataract can lead to acute angle closure glaucoma.
  • Uveitis can cause glaucoma by the inflammatory cells blocking aqueous drainage.
  • Steroid drops or injections given to the eye cause a pressure rise in the eye of about 10% of patients. If steroids are continued then glaucoma develops. This glaucoma is very difficult to manage.
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19
Q

Secondary glaucoma- Rubeosis

A

Rubeosis (new vessels on the iris) can develop in proliferative diabetic retinopathy or secondary to the ischaemia caused by retinal vein occlusion. New vessels can block the drainage angle causing an acute pressure rise. Causes intense pain and reduced vision. Rubeotic glaucoma requires pan retinal photocoagulation to reduce the neovascularisation and allow aqueous to drain again.

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20
Q

Primary open angle glaucoma- history

A

• Any visual problems?
• Past Ocular history: surgery, trauma, uveitis?
• Refractive error: myopic (short sighted) people may be more likely to have POAG
• Prolonged use of steroid eye drops
• Family History of glaucoma
• Ethnic origin

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21
Q

Primary open angle glaucoma- Examination

A

• Visual acuity- using a Snellen chart
• Measurement of IOP- Goldmann tonometer or hand held tonometers (not as accurate)
• Measurement of Corneal thickness- measured when assessing IOP as the pressure needed to flatten the cornea will vary with corneal thickness), measured using a handheld ultrasound probe
• Inspection of drainage angle- a gonioscope allows the slit lamp to view the angle
• Assessment of disc cupping and nerve fibre layer
• Visual field assessment- using automated visual field test machines, needs to be adjusted to account for age
• Thickness of the cornea- imaging and OCT may be used
• Optic disc- fundoscopy or OCP (Optical coherence tomography)

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22
Q

Other causes of optic disc cupping/sectoral pallor of optic nerve

A

• physiological disc cupping
• congenital abnormalities of the optic nerve
• retinal vascular occlusions

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23
Q

Other causes of peripheral field loss

A

• congenital abnormalities of the optic disc
• retinal vascular occlusions
• bitemporal hemianopia (optic chiasm compression)
• retinitis pigmentosa

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24
Q

Prognosis for POAG

A

• No cure-you just try and slow the progression of optic neuropathy
• Need to control intraocular pressure
• Without treatment sight loss can progress to involve the central visual field causing severe sight impairment

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25
Q

Topical treatment for POAG

A

• Prostaglandin analogues i.e. latanoprost- improves drainage
• Beta blockers i.e. timolol- reduces aqueous production, cant be given with respiratory and cardiac disease
• Carbonic anhydrase inhibitors i.e. brinzolamide- reduce aqueous production
• Sympathomimetics i.e. brimonidine- improves drainage and reduces aqueous production
• Miotics i.e. pilocarpine- improves drainage

26
Q

Systemic treatment for POAG

A

Carbonic anhydrase inhibitor i.e. Acetozolamide which reduces aqueous production.

27
Q

Laser treatment for glaucoma

A

• Selective laser trabeculectomy- targets melanin pigment in the trabecular meshwork increasing the drainage capacity
• Argon laser trabeculoplasty (ALT)- uses laser to burn holes in the trabecular meshwork to increase drainage of aqueous humour, repeated treatments aren’t an option
• Trabeculectomy- a small tunnel is created in the scleral surface of the limbus, taking a chunk of the trabecular meshwork into the anterior chamber, fluid can then drain
• Insertion of a drainage shunt- a tube is inserted through the sclera and into the anterior chamber, allowing the aqueous humour to drain under the conjunctiva

28
Q

How do most people find they have glaucoma

A

Glaucoma is often asymptomatic as visual loss is slow and painless, most patients are referred by opticians who have seen suspicious changes

29
Q

Retinal detachment

A

The separation of the neuro-retina from the retinal pigment epithelium (RPE)

30
Q

Risk factors for retinal detachment

A

• Myopes ( short sighted people) are at greater risk of detachment as their retina is thinner (their eyes are larger) and is more prone to developing holes or tears.
• Post cataract surgery (1% within 5 years)
• Ocular Trauma
• Acceleration/deceleration injuries
• Male> Female
• Increasing age
• Trauma- ocular, head injury, bungee jumping
• Cataract surgery
• Chinese and East Asians> Indians and South Asians>Caucasians> Black Africans

31
Q

What are the symptoms of retinal detachment

A

• sudden onset of flashes of light
• sudden onset of floaters, often black
• cobwebs
• shadows in vision, often inferiorly
• sudden loss of visual acuity

32
Q

Examination for retinal detachment

A

• Visual acuity
• Slit lamp examination
• Intra-ocular pressure
• Relative afferent pupil defect
• ‘Tobacco dust’ may be seen in the anterior vitreous
• Fundoscopy
• Fields to confrontation

33
Q

Differentials for retinal detachment

A

• Acute posterior vitreous detachment
• Migraine
• Posterior uveitis
• Vitreous haemorrhage

34
Q

Acute posterior vitreous detachment

A

The vitreous becomes more liquid and contracts away from the retinal surface. This can lead to retinal detachment but normally stops there. Causes flashes and floaters

35
Q

Rhegmatogenous retinal detachment

A

• Most common form
• The vitreous fills the posterior chamber of the eye, as we age it becomes more liquid and shrinks away from the retinal surface, the tension can cause the retina to tear. The fluid can then get behind the retina causing a retinal detachment
• Retinal detachment separates the retina photoreceptor layer and the retinal pigment epithelium layer

36
Q

What normally stops the retina from detaching

A

• The vitreous and vitreous fluid push the retina against the choroid.
• The retinal pigment epithelium (RPE) continually pumps fluid from the potential sub-retinal space into the choroid, creating a force that keeps the retina attached to the RPE.

37
Q

Tractional retinal detachments

A

• Most commonly in end stage proliferative diabetic retinopathy
• Neo-vascularisation occurs in response to ischaemia, the new vessels fibrose, shrinking in size and pulling on the retina, lifting it from the retinal pigment epithelial layer. This shortens the retina so it cannot remain attached

38
Q

Exudative retinal detachment

A

• Fluid/exudate forms underneath the retina pushing it forward
• The RPE pump cannot cope with this extra fluid.
• This can be caused by tumours, inflammatory conditions, retinal vein occlusions and systemic problems such as renal failure and malignant hypertension.

39
Q

Retinal detachment surgery

A

• The only option to treat retinal detachment
• The aim is to re-attach the neuro-retina to the retinal pigment epithelium and to seal the retinal break to prevent re-detachment
• You will then need drainage of the subretinal fluid

40
Q

Different types of retinal detachment surgery

A

• External approach- a plastic explant or buckle is sutured over the retinal break, indenting the sclera/choroid/RPE so that contact is made with the detached retina
• Internal approach- most common, a virectomy (removal of the vitreous) is performed its then replaced with saline. A gas bubble or oil is injected into the eye to reattach the neuro-retina to the RPE, allowing the RPE to begin pumping, closing the potential space.

41
Q

Sealing of the retinal tear

A

Preventing fluid from leaking behind the retina again. Can be sealed using a ring of laser burns, causing an inflammatory reaction sealing the tear. If the tear is far out in the periphery cryotherapy may be used. This freezes the tear, precipitating an inflammatory response in the RPE and retina sealing the tear.

42
Q

Timing of surgery

A

• Macula on- need urgent surgery to prevent extension of the detachment
• Macula off- very urgent if the macula is just involved that day but if it has been several weeks then there is no hurry. If delayed the photoreceptors have less chance of recovery

43
Q

Retinal detachment- post operative care

A

• Analgesia
• Topical antibiotics- reduce infection
• Topical steroids- reduce inflammation

44
Q

Post operative vision-retinal detachment

A

• External buckles- can create astigmatism or increase the axial length of the eye making the eye more myopic
• Injection of gas or oil- significantly affects the patients vision, the gas will eventually disappear with time. Oil changes the patients refractive error, the patient can either get new lasses or wait for the oil to be changed for saline a few months later
• It is advised that no patients fly for at least 2 weeks if they have had oil placed in their eye, and for up to 8-12 weeks if they have had gas injected in their eye as part of their surgery.

45
Q

Complications of retinal detachment surgery

A

• Endophthalmitis- painful red eye with visual loss, treatment with IV antibiotics. Risk loosing the eye
• Cataracts
Uveitis
• Glaucoma
• Vitreous haemorrhage
• Re-detachment
• Double vision

46
Q

Prognosis for retinal detachment

A

Majority of patients have an anatomically successful surgery, visual success is more variable and depends on whether the macular was on or off prior to surgery. If the macula has been off a long time the photoreceptors may have died.

47
Q

Direct ophthalmoscopy

A

• Best in dark room with dilated pupil (tropicamide)
• Can be used for anterior segment and fundus
• Remember magnification is high, therefore only small area seen at one time
• Right eye for right eye and vice versa
• Ask patient to look in the direction of what you are trying to see, and approach from the opposite direction

48
Q

Conditions which cause chronic loss of vision

A

• Cataracts
• Age related macular degeneration
• Diabetes
• Glaucoma

49
Q

Acute painless loss of vision

A

• Central retinal artery occlusion (CRAO)- immediate
• Central retinal vein occlusion (CRVO)- urgent
• Anterior ischaemic optic neuropathy (AION)- immediate
• Optic neuritis- urgent
• Central serous retinopathy (CSR)
• Vitreous haemorrhage- urgent
• Retinal detachment- immediate
• Wet ARMD (Ae related macula degeneration)- immediate

50
Q

Acute painful loss of vision

A

• Acute angle closure glaucoma- immediate
• Trauma- immediate
• Uveitis- urgent
• Bacterial keratitis- immediate

51
Q

Non painful red eye

A

Subconjunctival haemorrhage. Check INR, BP and lubricants

52
Q

Non painful red eye with segmental redness

A

• Episcleritis- self limiting, NSAIDS, steroids
• Marginal ulcer- topical steroids, with or without antibiotics

53
Q

Non painful red eye, no segmental redness and discharge present

A

• Bacterial (sticky)- chloramphenicol, lid hygiene
• Chlamydia (sticky, big follicles)- babies and sexually active- erythromycin, azithromycin, doxycycline
• Viral (watery)- lubricants, steroids if they develop keratitis
• Allergic (watery)- remove allergen, give oral antihistamine i.e. olopatadine

54
Q

Non painful red eye, no segmental redness, no discharge

A

Meibomianitis/Belepharitis- lid hygiene, omega 3 fish oil, doxycycline if Rosaecea

55
Q

Painful red eye with trauma

A

• Foreign body- high speed, dilate to check if Intraocular foreign body, chloramphenicol. If corneal/scleral laceration or intraocular foreign body you will need surgery
• Blunt- abrasion, uveitis, hyphaema, angle recession, cataracts, retinal detachment, scleral rupture. Treat with lubricants, chloro steroids, anti-glaucoma, surgery etc
• ARC eye (UV)- lubricants
• Chemical- is it an acid or alkali, can cause ischaemia. Treat with Diphoterine, irrigation, antibiotics, lubricants, cyclo, steroids, vit C, Na citrate, doxycycline

56
Q

Painful red eye with corneal ulcer

A

• Hepatic ulcer- dendritic is treated with ganiclover. Geographric/Diciform ulcer is treated with ganciclovir and steroids later.
• Bacterial ulcer- central, round white >1mm, uveitis. Common with contact lens’s. You need an urgent corneal scrape and gram stain. Need to admit intensive antibiotics (cyclopegia) and later steroids

57
Q

Painful red eye with a big pupil and hazy cornea

A

Acute angle closure glaucoma- Hypermetropia/cataracts. Lots of pain, vomiting, blurred vision and rainbow haloes. Admit IV Diamox, analgesia, antiemetics, pilocarpine and steroids

58
Q

Painful red eye with small pupil and photophobia

A

• Uveitis- circumcorneal redness, anterior chamber ccells, flare, KP (keratic precipate), hypopyon (accumulation of leukocytes in the anterior chamber), increased IOP, posterior activity. Investigate if recurrent and treat with steroids, cyclopegia and IOP lowering
• Endophthalmitis- consider if post op, ‘golden hour’ vit tap. Treat with vancomycin, ceftazidime with or without dexamethasone

58
Q

Painful red eye with small pupil and photophobia

A

• Uveitis- circumcorneal redness, anterior chamber ccells, flare, KP (keratic precipate), hypopyon (accumulation of leukocytes in the anterior chamber), increased IOP, posterior activity. Investigate if recurrent and treat with steroids, cyclopegia and IOP lowering
• Endophthalmitis- consider if post op, ‘golden hour’ vit tap. Treat with vancomycin, ceftazidime with or without dexamethasone

59
Q

Painful red eye with no other symptoms

A

Scleritis, rare, with people on NSAIDS and immunosuppressed.

Medicine year 3- EOCP (27 decks)

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