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Medicine year 4 ACE > Core conditions 4 > Flashcards

Core conditions 4 Flashcards

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1
Q

Cataracts management surgery

A

Surgery is the only effective treatment for cataracts. This involves replacing the lens with an artificial one. Referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery. Prior to cataract surgery, patients should be provided with information on the refractive implications of various types of intraocular lenses. After cataract surgery, patients should be advised on the use of eye drops and eyewear, what to do if vision changes and the management of other ocular problems. Cataract surgery has a high success rate with 85-90% of patients achieving 6/12 corrected vision (on a Snellen chart) postoperatively.

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2
Q

Cataracts: complications following surgery

A
  • Posterior capsule opacification: thickening of the lens capsule
  • Retinal detachment
  • Posterior capsule rupture
  • Endophthalmitis: inflammation of aqueous and/or vitreous humour
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3
Q

The lens

A

Responsible for refraction of light and when young accommodation. It has a central nucleus surrounded by cortical fibres, and is encapsulated by a basement membrane made mostly of type IV collagen. It is suspended by a ring of elastin fibres, the Zonules of Zinn, from the ciliary body. Cortical fibres are continually made causing the lens to increase in size throughout life.

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4
Q

Age related cataracts; three main types

A
  • Nuclear sclerosis: old lens fibres are compressed by new lens fibres, causing cloudiness and yellowing, causes myopic shift. Vision can be corrected by changing glasses.
  • Cortical: Changes in the water content of the cortical lens fibres case cortical lens opacities resulting in glare and occasionally monocular diplopia
  • Posterior sub-capsular: in the posterior layer of the cortex just in front of the lens capsule, cause significant visual loss early as its the focal point of the eye. Significant problems with glare. Fastest developing type of age related cataracts.
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5
Q

Non age related cataracts

A
  • Congenital: screened in post natal baby checks. main causes are hypoglycaemia, trisomy (Down’s, Edward and Patau), myotonic dystrophy, infectious disease (toxoplasmosis, rubella, cytomegalovirus and herpes simplex) and prematurity
  • Related to systemic or primary ocular disease:
  • Traumatic: penetrating, blunt, chemical injury, radiation, electric shock, UV light. iatrogenic (surgery for retinal detachment or glaucoma or intra-vitreal injections)
  • Surgery and rehabilitation is complex as the eye is growing and the refraction changes rapidly. Risk of amblyopia especially in unilateral cataracts
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6
Q

Conditions that cause non age related cataracts

A
  • Any disease requiring regular use of corticosteroids
  • Diabetes Mellitus
  • Myotonic dystrophy
  • Atopic dermatitis
  • Neurofibromatosis type 2
  • Wilson’s disease
  • Ocular disease: chronic uveitis, Pseudo-exfoliation syndrome, very high myopia, retinitis pigmentosa. retinal detachment, ARMD (secondary to anti-VEGF injections)
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7
Q

Cataracts: fitness to drive

A
  • No problem with driving when colourblind
  • You must be able to read a car number plate from 2001 or later from a distance of 20 meters
  • Lorry drivers must have a corrected vision of at least 6/7.5 in one eye
  • Can still drive if you have one eye
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8
Q

Self management for cataracts

A
  • Keeping spectacles up to date
  • Using brighter lights, or sitting near windows to read
  • Wearing sunglasses to reduce glare
  • Using a magnifying lens for reading small print
  • Using large print books or increasing font size on electronic gadgets/ computers
  • Exercise and healthy diet, stop smoking
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9
Q

Cataracts: co morbidities that affect whether you can have cataract surgery

A
  • uncontrolled BP > 200/100
  • uncontrolled diabetes BM>20
  • patients unable to lie relatively flat, eg those with severe kyphosis or orthopnoea present significant difficulties for surgeons
  • significant dementia
  • Surgery can be performed at any age if medically stable. May be appropriate if they have a few months left to improve QoL
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10
Q

Glaucoma

A

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

Glaucoma triad: optic disc cupping, field defects and intra ocular pressure

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11
Q

Glaucoma: field defects and pressure

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

Normal intra-ocular pressure= 14-22mmHg

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12
Q

Raised intra-ocular 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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13
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
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14
Q

The angle and diagnosing glaucoma

A

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

Diagnosing glaucoma- 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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15
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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16
Q

Primary open angle glaucoma

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
  • Normal drainage angle but blockage in trabecular meshwork or Schlemm canal causes IOP to rise
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17
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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18
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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19
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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20
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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21
Q

Acute angle closure glaucoma (aacg) 1

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
22
Q

AACG

A
  • Acutely painful red eye- the patient often feel systemically unwell and their vision deteriorates
  • Its precipitated by dilation of the pupil i.e. antidepressants and anti-psychotics
  • Causes corneal oedema which untreated leads to nerve fibre death
23
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
24
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
25
Q

Secondary glaucoma

A

Can develop secondary to other conditions or medication: Rubeosis, trauma, cataracts, uveitis, steroids and rare congenital problems
- Trauma can damage the drainage angle
-Uveitis can cause glaucoma by the inflammatory cells blocking aqueous drainage
- Steroid drops cause a pressure rise of 10%

26
Q

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.

27
Q

POAG: 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
28
Q

POAG: symptoms

A
  • Gradual reduction in peripheral vision (tunnel vision)
  • Painless
  • Patient may walk into objects
  • Haloes surrounding light
  • Blurred vision
  • Headaches
29
Q

POAG: risk factors and co-morbidities

A

Risk factors: increasing age, family history, black ethnic origin, near sightedness (myopia), female, diabetes, hypertension, obstructive sleep apnoea, smoking

Co-morbidities: falls, depression

30
Q

POAG: examination

A
  • Visual acuity- using a Snellen chart, normally fine in glaucoma
  • 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
  • Visual field assessment- using automated visual field test machines, needs to be adjusted to account for age. Not very accurate
  • Fundoscopy- checks optic disc cupping and optic nerve health
  • OCT- assess disc cupping and nerve fibre layer, helps monitor glaucoma progression
31
Q

Glaucoma: unsure of diagnosis

A

Glaucoma is a progressive disease so if you are unsure about diagnosis you can wait 6 months then try again

32
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
33
Q

Other causes of peripheral field loss

A
  • congenital abnormalities of the optic disc
  • retinal vascular occlusions
  • bitemporal hemianopia (optic chiasm compression)
  • retinitis pigmentosa
34
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
  • Prognosis depends on: age at onset, level of loss at diagnosis, starting IOP, type of glaucoma, response to treatment, ethnic origin
  • Annual follow up
35
Q

Topical treatment for POAG

A
  • Prostaglandin analogues i.e. latanoprost- improves drainage. Side effects: eye colour change and eyelash growth
  • 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
36
Q

Systemic treatment for POAG

A

Carbonic anhydrase inhibitor i.e. Acetozolamide which reduces aqueous production. Can cause eye discomfort and altered taste

37
Q

Laser treatment for glaucoma 1

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
38
Q

Laser treatment for glaucoma 2

A
  • 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
39
Q

When is glaucoma picked up and DVLA

A

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

Required by law to contact the DVLA

40
Q

Glaucoma: conservative management

A
  • Eye clinic liaison officers: help sign post patient to support services
  • Using a white cane
  • Can register as sight impaired or severely sight impaired: increased access to benefits
41
Q

Age related macular degeneration

A

Age related macular degeneration is the most common cause of sight loss in the UK. Characterised by degeneration of retinal photoreceptors that result in formation of drusen which can be seen on fundoscopy. More common with age and in females

42
Q

Risk factors for ARMD

A
  • Age
  • Smokers
  • Family history
  • Women, Caucasions
  • Hypertension, dyslipidaemia, obese and diabetes mellitus
43
Q

Classification of ARMD

A
  • Dry macular degeneration: majority of cases (90%), also known as atrophic. Characterised by drusen- yellow round spots in Bruch’s membrane
  • Wet macular degeneration: also known as exudative or neovascular macular degeneration. Characterised by choroidal neovascularisation. Leakage of serous fluid and blood can cause loss of vision, carries worst prognosis
44
Q

Clinical features of ARMD

A
  • A reduction in visual acuity especially in near field: gradual in dry ARMD, subacute in wet ARMD
  • Difficulties in dark adaption with deterioration in vision at night
  • Photopsia (perception of flickering or flashing light) and glare around objects
  • Visual hallucination: Charles-Bonnet syndrome
45
Q

Signs of ARMD

A
  • distortion of line perception may be noted onAmsler grid testing
  • fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
  • in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
46
Q

Investigations of ARMD

A
  • slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina. Also do a colour fundus photography to provide a baseline against which changes can be identified over time.
  • fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
  • ocular coherence tomography
47
Q

Management of ARMD

A
  • Zinc with anti-oxidant vitamin A,C and E
  • anti- VEGF- vascular endothelial growth factors i.e. Ranibizumab usually given by 4 weekly injections. Used in wet ARMD. Injected in the vitreous causing regression of new vessels and prevents new ones. Risk of developing endophthalmitis and losing your vision, treatment needed ASAP
  • Laser photocoagulation: only when there is new vessel formation. Risk of acute visual loss after treatment so anti-VEGF is preferred. Involves using Verteporfin which is injected into the circulation and activated by specific wavelengths of light causing selective damage. Don’t use in the fovea as damages retinal tissue
  • Surgery: if there is a large sub-retinal haemorrhage, can be used to displace it from the macula
48
Q

Conservative management of ARMD

A
  • Mediterranean diet,
  • Vitamin supplements (C, E, copper, zinc, lutein and zeaxanthin)- only if intermediated AMD in both eyes or advanced in one eye aiming to delay progression
  • Stop smoking
  • Support: Low vision services, Eye liaison officers (sign post to local services, supporting ear), Registering as blind
49
Q

Who should anti-VEGF be offered to

A
  • Treatment should be offered within 2 weeks
  • Treatment should be offered to those with VA> 6/96
  • Loading dose of 3 injections (4 week intervals)
  • Treat and extend regimen after this
  • Monitoring for at least 2 years after successful treatment as 40% will reactivate
50
Q

Drusen

A
  • The retinal pigment epithelium (RPE) deal with the buy products of phototransduction
  • With age RPE becomes slower and more lipid and protein build creating drusen deposits
  • The larger the drusen and the softer they appear the more serious the degeneration

Medicine year 4 ACE (9 decks)

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