Notes _ Notes - Ophthalmology.pdf

Notes & Notes For MRCP part 1 & 11 By Dr. Yousif Abdallah Hamad

Ophthalmology

Contains:

1/ Passmedicine 2015 (white & black fields) 2/ on examination 2015 (green fields) 3/ pastest 2015 (yellow fields)

Notes & Notes for mrcp

Dr.Yousif Abdallah Hamad

Preface ‘How do I get started?’ ‘Which books should I read?’ ‘Which are the best Self-assessm Self-assessment ent questions bank?’ ‘Passmedicine alone? Is it enough?’ or should I add other source? Should I add on-examination or pastest? These are the usual questions asked by the MRCP candidates. For all these questions, and depending on thorough follow up of a lot of candidates results , feedbacks and comments, rather than my personal experience, and after consultations of a wide range of mrcp experts, I decide to create a very concise notes collected from the most popular three mrcp sources : - Passmedicine 2015 (in black & white fields) - Onexamination 2015 (in green fields) And pastest 2015 (in yellow fields) Occasionally, I add a few facts from previous exams, last guidelines and uptodate source. How to use this ''notes & notes''? I recommend candidates to follow these steps: - First off all go carefully through this notes 2 times aiming to build a bulky knowledge of mrcp syllabus. - then start to practice questions from Passmedicine Passmedicine , onexam and pastest , you will find it very easy to answer , and if you face any difficult question you have to open your ''notes & notes'' and read the topic again before returns to question banks , this is crustily helpful to fix the idea. - In the last few days before your exam, return to this notes and read it once again. You will find some information written by red or big font, those are the answers of questions, which are tested in above sources and previous exams. I hope this collection will be enough to help you get through mrcp part 1 and give you a good grip before interring interring part 11.

Dr. Yousif Abdallah Hamad



Preface ‘How do I get started?’ ‘Which books should I read?’ ‘Which are the best Self-assessm Self-assessment ent questions bank?’ ‘Passmedicine alone? Is it enough?’ or should I add other source? Should I add on-examination or pastest? These are the usual questions asked by the MRCP candidates. For all these questions, and depending on thorough follow up of a lot of candidates results , feedbacks and comments, rather than my personal experience, and after consultations of a wide range of mrcp experts, I decide to create a very concise notes collected from the most popular three mrcp sources : - Passmedicine 2015 (in black & white fields) - Onexamination 2015 (in green fields) And pastest 2015 (in yellow fields) Occasionally, I add a few facts from previous exams, last guidelines and uptodate source. How to use this ''notes & notes''? I recommend candidates to follow these steps: - First off all go carefully through this notes 2 times aiming to build a bulky knowledge of mrcp syllabus. - then start to practice questions from Passmedicine Passmedicine , onexam and pastest , you will find it very easy to answer , and if you face any difficult question you have to open your ''notes & notes'' and read the topic again before returns to question banks , this is crustily helpful to fix the idea. - In the last few days before your exam, return to this notes and read it once again. You will find some information written by red or big font, those are the answers of questions, which are tested in above sources and previous exams. I hope this collection will be enough to help you get through mrcp part 1 and give you a good grip before interring interring part 11.

Dr. Yousif Abdallah Hamad



Acute angle closure glaucoma Acute angle closure glaucoma is associated with hypermet h ypermetropia. ropia. Primary open-angle glaucoma is associated with myopia

Glaucoma is a group disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa In acute angle closure glaucoma (AACG) there is a rise in IOP secondary to an impairment of aqueous outflow.



Factors predisposing to AACG include:   

hypermetropia (long-sightedness) pupillary dilatation lens growth associated with age

Features      

 

severe pain: may be ocular or headache decreased visual acuity symptoms worse with mydriasis (e.g. watching TV in a dark room) hard, red eye haloes around lights semi-dilated non-reacting pupil.The oval shape is due to the iris sphincter ischaemia from the high intraocular pressure. corneal oedema results in dull or hazy cornea systemic upset may be seen, such as nausea and vomiting and even abdominal pain

Management  

urgent referral to an ophthalmologist management options include reducing aqueous secretions with acetazolamide and inducing pupillary constriction with topical pilocarpine

Treatment of acute glaucoma - acetazolamide + pilocarpine

____________________________________________________________

Primary open-angle glaucoma Glaucoma is a group disorders characterised by optic neuropathy due, in the majority of patients, to raised intraocular pressure (IOP). It is now recognised that a minority of patients with raised IOP do not have glaucoma and vice versa Primary open-angle glaucoma (POAG), is the most common type of glaucoma. Primary open-angle glaucoma (POAG, also referred to as chronic simple glaucoma) is present in around 2% of people older than 40 years. Other than age, risk factors include:

    

family history black patients myopia hypertension diabetes mellitus



POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include

  

peripheral visual field loss - nasal scotomas progressing to 'tunnel vision' decreased visual acuity ophthalmoscopic exam  optic disc cupping

Primary open-angle glaucoma: management The majority of patients with primary open-angle glaucoma are managed with eye drops. These aim to lower intra-ocular pressure which in turn has been shown to prevent progressive loss of visual field.

Medication

Mode of action

Notes

Prostaglandin analogues (e.g. Latanoprost)

Increases uveoscleral outflow

Once daily administration Adverse effects include brown pigmentation of the iris

Beta-blockers (e.g. Timolol)

Reduces aqueous production

Should be avoided in asthmatics and patients with heart block

Sympathomimetics (e.g. brimonidine, an alpha2adrenoceptor agonist)

Reduces aqueous production and increases outflow

Avoid if taking MAOI or tricyclic antidepressants Adverse effects include hyperaemia

Carbonic anhydrase inhibitors (e.g. Dorzolamide)

Reduces aqueous production

Systemic absorption may cause sulphonamide-like reactions

Miotics (e.g. pilocarpine, a muscarinic receptor agonist)

Increases uveoscleral outflow

Adverse effects included a constricted pupil, headache and blurred vision

Surgery in the form of a trabeculectomy may be considered in refractory cases.

____________________________________________________________ Notes & Notes for mrcp


Age related macular degeneration Age related macular degeneration is the most common cause of blindness in the UK. Degeneration of the central retina (macula) is the key feature with changes usually bilateral. Traditionally two forms of macular degeneration are seen: 



dry (geographic atrophy) macular degeneration: characterised by drusen - yellow round spots in Bruch's membrane wet (exudative, neovascular) macular degeneration: characterised by choroidal neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis

Recently there has been a move to a more updated classification: 



early age related macular degeneration (non-exudative, age related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE) late age related macular degeneration (neovascularisation, exudative)

Risk factors      

age: most patients are over 60 years of age smoking family history more common in Caucasians high cumulative sunlight exposure female sex

Features

  

reduced visual acuity: 'blurred', 'distorted' vision, central vision is affected first central scotomas fundoscopy: drusen, pigmentary changes

Investigation and diagnosis



 

optical coherence tomography: provide cross sectional views of the macula if neovascularisation is present fluorescein angiography is performed

General management  

stop smoking high dose of beta-carotene, vitamins C and E, and zinc may help to slow down visual loss for patients with established macular degeneration. Supplements should be avoided in smokers due to an increased risk of lung cancer

Dry macular degeneration - no current medical treatments Wet macular degeneration

  

photocoagulation photodynamic therapy anti-vascular endothelial growth factor (anti-VEGF) treatments: intravitreal ranibizumab

____________________________________________________________

Cataracts

Majority  

age related UV light



Systemic    



diabetes mellitus steroids (Inhaled steroids can cause cataracts ) infection (congenital rubella) metabolic (hypocalcaemia, galactosaemia) (but if the galactosaemia is treated, the cataract is reversible). myotonic dystrophy, Down's syndrome

Ocular    

trauma uveitis high myopia topical steroids

Classification    

Nuclear: change lens refractive index, common in old age Polar: localized, commonly inherited, lie in the visual axis Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy

____________________________________________________________

Diabetic retinopathy

Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old.



About 80% of patients with type I diabetes will have retinopathy 10 years after presentation. By contrast, in type II diabetes, where the time of onset is uncertain, up to 25% of patients will have retinopathy at the time of diagnosis. Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes Endothelial dysfunction leads to increased vascular permeability which causes the characteristic exudates seen on fundoscopy. Pericyte dysfunction predisposes to the formation of microaneurysms. Neovasculization is thought to be caused by the production of growth factors in response to retinal ischaemia.

The earliest sign of diabetic retinopathy is the presence of microaneurysms on

fluorescein angiography. In exams you are most likely to be asked about the characteristic features of the various stages/types of diabetic retinopathy. Recently a new classification system has been proposed, dividing patients into those with non-proliferative diabetic retinopathy (NPDR) and those with proliferative retinopathy (PDR): Traditional classification

New classification

Background retinopathy

Mild NPDR

  

microaneurysms (dots) blot haemorrhages (<=3) hard exudates



1 or more microaneurysm

Moderate NPDR Pre-proliferative retinopathy   

  



cotton wool spots (soft exudates; ischaemic nerve fibres) > 3 blot haemorrhages venous beading/looping deep/dark cluster haemorrhages more common in Type I DM, treat with laser photocoagulation

 

Severe NPDR   


microaneurysms blot haemorrhages hard exudates cotton wool spots, venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

blot haemorrhages and microaneurysms in 4 quadrants venous beading in at least 2 quadrants IRMA in at least 1 quadrant


Proliferative retinopathy→ (urgent referral to an ophthalmologist for panretinal photocoagulation)   

retinal neovascularisation - may lead to vitrous haemorrhage fibrous tissue forming anterior to retinal disc more common in Type I DM, 50% blind in 5 years

Maculopathy

     

 

based on location rather than severity, anything is potentially serious hard exudates and other 'background' changes on macula check visual acuity more common in Type II DM Maculopathy can be indicated by the presence of hard exudates at the macula. The exudates can be arranged in a ring (circinate exudates) surrounding a point of capillary leakage. This can be shown on fluorescein angiography responds to laser treatment at the point of leakage.

Prognosis The approximate percentage of eyes that will lose useful vision irretrievably within 5 years if not treated :    

3% in those with background retinopathy 20% for those with exudative 30% for those with pre-proliferative, 50% for those with proliferative retinopathy.

Asymmetric diabetic retinopathy should always raise the suspicion that there is some other cause of ocular ischaemia on the worst-affected side, such as unilateral or asymmetrical carotid artery disease  do Carotid Doppler Asymmetric DM Retinopathy → suspect ocular ischemia (carotid artery disease)

____________________________________________________________

Angioid retinal streaks Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from the optic nerve head. They are caused by degeneration, calcification and breaks in Bruch's membrane . Causes 



Pseudoxanthoma elasticum (skin laxity with angioid streaks) is also known as GrönbladStrandberg syndrome. Ehler-Danlos syndrome



  

Paget's disease sickle-cell anaemia acromegaly

____________________________________________________________

Mydriasis Causes of mydriasis (large pupil)     

third nerve palsy Holmes-Adie pupil traumatic iridoplegia phaeochromocytoma congenital

Drug causes of mydriasis   

topical mydriatics: tropicamide, atropine sympathomimetic drugs: amphetamines, cocaine anticholinergic drugs: tricyclic antidepressants

____________________________________________________________

Holmes-Adie pupil Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil. Overview

   

unilateral in 80% of cases dilated pupil once the pupil has constricted it remains small for an abnormally long time slowly reactive to accommodation but very poorly (if at all) to light

Holmes-Adie syndrome



association of Holmes-Adie pupil with absent ankle/knee reflexes

Abnormally dilated pupil (mydriasis) which does not constrict in response to light, loss of deep tendon reflexes, and abnormalities of sweating.







characterized by a tonically dilated pupil that reacts slowly to light but shows a more definite response to accommodation (i.e., light-near dissociation) frequently seen in females with absent knee or ankle jerks and impaired sweating

pathophysiology





 

-

Viral or bacterial infection causes  damage to neurons in the ciliary ganglion , located in the posterior orbit , that provides parasympathetic control of eye constriction.

-

Additionally, patients with Holmes-Adie Syndrome can also experience problems with autonomic control of the body caused by damage to the dorsal root ganglia of the spinal cord.

Diagnosis testing with low dose (1/8%) pilocarpine may constrict the t onic pupil due to cholinergic denervation supersensitivity. A normal pupil will not constrict with the dilute dose of pilocarpine. The affected pupil is usually larger than the other but may constrict with time. The cause of the associated arreflexia is unknown.

____________________________________________________________

Optic atrophy Optic atrophy is seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision*. Causes may be acquired or congenital Acquired causes       

multiple sclerosis papilloedema (longstanding) raised intraocular pressure (e.g. glaucoma, tumour) retinal damage (e.g. choroiditis, retinitis pigmentosa) ischaemia toxins: tobacco amblyopia, quinine, methanol, arsenic, lead nutritional: vitamin B1, B2, B6 and B12 deficiency

Congenital causes   

Friedreich's ataxia mitochondrial disorders e.g. Leber's optic atrophy DIDMOAD - the association of cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness (also known as Wolfram's syndrome)

*strictly speaking optic atrophy is a descriptive term, it is the optic neuropathy that results in visual loss



Optic neuritis Causes   

multiple sclerosis diabetes syphilis

Features      

 

unilateral decrease in visual acuity over hours or days poor discrimination of colours, 'red desaturation' pain worse on eye movement relative afferent pupillary defect central scotoma Most cases of optic neuritis are retrobulbar and hence there are no abnormalities on fundoscopy. MRI with gadolinium of the brain will likely show  enhancement of the optic nerve Abnormal visual evoked potentials (VEP)

Management  

high-dose steroids recovery usually takes 4-6 weeks

Prognosis 

MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is c. 50%

____________________________________________________________

Retrobulbar neuritis the patient sees nothing and the doctor sees nothing' 

in retrobulbar neuritis it is said that 'the patient sees nothing and the doctor sees nothing'. As the inflammation is behind the optic nerve head (ie retrobulbar)

Symptoms andsigns of retrobulbar neuritis -

-

visual acuity will be reduced to a very variable degree, afferent pupillary defect will be apparent during the 'swinging flashlight test'. Colour vision will be reduced Red desaturation – ie when red looks paler to one eye than the other - is a sensitive sign of optic nerve dysfunction. Visual field defects will occur, typically a central scotoma, but the type of defect varies.







Retrobulbar neuritis has the same systemic implications as optic neuritis, in that an episode of optic or retrobulbar neuritis can contribute to a diagnosis of multiple sclerosis The retrobulbar neuritis seen with ethambutol may be unilateral or bilateral; as such unilateral symptoms do not preclude the diagnosis.

____________________________________________________________

Herpes simplex keratitis Herpes simplex keratitis most commonly presents with a dendritic corneal ulcer The herpes simplex virus may lie dormant in the trigeminal ganglion, reactivation can occur giving rise to eyelid and periorbital vesicles. Features  

    

red, painful eye photophobia epiphora visual acuity may be decreased fluorescein staining may show an epithelial ulcer

Eczema herpeticum In patients with atopic dermatitis or eczema herpes simplex infection can cause eczema herpeticum, which may be further complicated by secondary staphylococcal infection. This is treated by adding oral antibiotics, for example, flucloxacillin 500 mg q.i.d. Eczema herpeticum is a serious and potentially life-threatening condition which may require medical and dermatology input.

Management  

immediate referral to an ophthalmologist topical aciclovir

____________________________________________________________

Herpes zoster ophthalmicus Herpes zoster ophthalmicus (HZO) describes the reactivation of the varicella zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles. Features  

vesicular rash around the eye, which may or may not involve the actual eye itself Hutchinson's sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement



Management 





oral antiviral treatment for 7-10 days, ideally started within 72 hours. Topical antiviral treatment is not given in HZO oral corticosteroids may reduce the duration of pain but do not reduce the incidence of postherpetic neuralgia ocular involvement requires urgent ophthalmology review

Complications   

ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis ptosis post-herpetic neuralgia

____________________________________________________________

Blepharitis Blepharitis is inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis). Blepharitis is also more common in patients with rosacea The meibomian glands secrete oil on to the eye surface to prevent rapid evaporation of the tear film. Any problem affecting the meibomian glands (as in blepharitis) can hence cause drying of the eyes which in turns leads to irritation Features      

symptoms are usually bilateral grittiness and discomfort, particularly around the eyelid margins eyes may be sticky in the morning eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis styes and chalazions are more common in patients with blepharitis secondary conjunctivitis may occur

Management  



softening of the lid margin using hot compresses twice a day mechanical removal of the debris from lid margins - cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used* artificial tears may be given for symptom relief in people with dry eyes or an abnormal tear film

*an alternative is sodium bicarbonate, a teaspoonful in a cup of cooled water that has recently been boiled



Keratitis 

  

 

Keratitis refers to inflammation of one or more of the three corneal layers, the most common of which is epithelial keratitis. This is characterised by dendritic ulcers . Rarer forms involve the stroma or endothelium. Pseudomonas aeruginosa is commonly associated with contact lens related infections. first line treatment of corneal ulcer Levofloxacin hourly The management must also include advising the patient to discontinue wearing contact lenses and referral to a specialist ophthalmic unit. Keratitis describes inflammation of the cornea. There are a variety of causes. Recurrence is common.

Features     

red eye: pain and erythema ( sharp ocular pain) photophobia epiphora, and blurred vision (in many cases). foreign body, gritty sensation hypopyon may be seen

Infective 



Viral: herpes simplex keratitis Treated with topical antivirals, e.g. aciclovir 5 times per day. Topical steroids or oral antivirals can be used in some cases. bacterial: typically Staphylococcus aureus. Pseudomonas aeruginosa is seen in contact lens wearers Microbial keratitis, causing a white corneal infiltrate , is more likely if there is a history of contact lens wear or trauma, such as a corneal abrasion or a corneal foreign body.

  

fungal amoebic: acanthamoebic keratitis parasitic: onchocercal keratitis ('river blindness')

Enviromental   

photokeratitis: e.g. welder's arc eye exposure keratitis contact lens acute red eye (CLARE)



A c a n t h a m o e b a keratitis  





is a rare and serious keratitis associated with contact lens (CL) wear. Risk factors for Acanthamoeba keratitis are exposure of CL to contaminated water, for example, using tap water to clean CL or swimming in lenses. Clinical features of Acanthamoeba keratitis include pain out of proportion to clinical signs, ring infiltrates and radial keratoneuritis. Brolene drops is used in the management of Acanthamoeba keratitis,

Marginal keratitis  





Marginal keratitis is areas of peripheral corneal infiltrates/ulcers associated with blepharitis. It classically causes an infiltrate near the limbal edge with an area of clear cornea. There may be limbal vessels growing towards the lesion(s). It is thought to be caused by a hypersensitivity reaction to staphylococcal exotoxins fromStaphylococcus aureus present on the lid margins in blepharitis. Treatment involves topical steroids for the keratitis and lid hygiene advice and topical antibiotics to treat the underlying blepharitis. In severe cases oral doxycycline can also be used.

____________________________________________________________

Lacrimal duct problems Dacryocystitis is infection of the lacrimal sac Features

 

watering eye (epiphora) swelling and erythema at the inner canthus of the eye

Management is with systemic antibiotics. Intravenous antibiotics are indicated if there is associated periorbital cellulitis Congenital lacrimal duct obstruction affects around 5-10% of newborns. It is bilateral in around 20% of cases Features

 

watering eye (even if not crying) secondary infection may occur

Symptoms resolve in 99% of cases by 12 months of age



Red eye There are many possible causes of a red eye. It is important to be able to recognise the causes which require urgent referral to an ophthalmologist. Below is a brief summary of the key distinguishing features

Acute angle closure glaucoma

   

severe pain (may be ocular or headache) decreased visual acuity, patient sees haloes semi-dilated pupil hazy cornea

Anterior uveitis

    

acute onset pain blurred vision and photophobia small, fixed oval pupil, ciliary flush sign on ocular examination Hypopyon (While a hypopyon usually implies infective endophthalmitis (eg following cataract surgery), a sterile hypopyon can occur in cases of severe iritis (eg Behcet's disease).

Iritis is associated with conditions such as: - Reiter's -

Behcet's

-

Psoriatic arthropathy (about 20%)

-

and inflammatory bowel disease.

A chronic iritis is rarely described in association with Lyme disease.

Signs of anterior uveitis





   

Keratic precipitates: (opaque aggregates of inflammatory cells deposited on the endothelium in anterior uveitis. They are typically located inferiorly.

Cells +/- flare +/- fibrin in the anterior chamber Ciliary injection - localised conjunctival injection (redness) around the limbus Posterior synechiae - where part of the pupil margin becomes stuck to the lens Hypopyon (in severe anterior uveitis).Hypopyon is refers to a collection of inflammatory material in the anterior chamber resulting in an opaque fluid level visible inferiorly. It occurs in severe cases of anterior uveitis or endophthalmitis.

Scleritis    



 

Scleritis : inflammation that occurs throughout the entire thickness of the sclera, severe pain (may be worse on movement) and tenderness 50% of cases are bilateral. Pain often radiates to the forehead, brow and jaw. This pain worsens with movement of the eye, and is classically worse at night. There is associated watering, photophobia and a gradual decrease in vision (sometimes with diplopia). Systemic symptoms such as fever, headache and vomiting can occur. may be underlying autoimmune disease e.g. rheumatoid arthritis

Around 50% of patients with scleritis have an underlying disease, of which the majority are connective tissue disorders. Rheumatoid arthritis is the most common.  





On examination the globe is tender, and the sclera can have a bluish tinge. Application of topical phenylephrine 2.5% leads to blanching of episcleral vessels in episcleritis but not in scleritis. Management ultimately depends on the underlying cause, but includes NSAIDs and prednisolone. The patient should be referred urgently to the ophthalmology clinic

Conjunctivitis 

purulent discharge if bacterial, clear discharge if viral



Viral conjunctivitis -

causes redness, soreness and watering.

-

In severe cases it can cause a keratitis which may affect vision.

-

It is highly contagious so patients should be advised to practise strict hand hygiene, to avoid sharing towels and to take time off work.



-

It is a self-limiting disease which may take several weeks to resolve.

-

Patients are treated with topical lubricants and some ophthalmologists give topical chloramphenicol to protect against secondary bacterial infections.

Subconjunctival haemorrhage 

history of trauma or coughing bouts

____________________________________________________________

Posterior uveitis    

Posterior uveitis describes inflammation of the choroid, which can involve the retinal vessels. It presents with gradual visual loss and floaters, which is often bilateral. Discomfort and erythema are rare. Slit light examination can demonstrate inflammatory lesions on the retina or choroid, with inflammation of the retinal vessels and oedema of the optic nerve.

____________________________________________________________ CMV Retinitis: causes hemorrhage at the edge of the area of retinal necrosis

____________________________________________________________

Relative afferent pupillary defect Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the 'swinging light test'. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina



Causes  

retina: detachment optic nerve: optic neuritis e.g. multiple sclerosis

Pathway of pupillary light reflex  

afferent: retina → optic nerve → lateral geniculate body → midbrain efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve

____________________________________________________________

Retinitis pigmentosa Retinitis pigmentosa primarily affects the peripheral retina resulting in funnel vision Features

  

night blindness is often the initial sign funnel vision (the preferred term for tunnel vision) fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

Associated diseases

      

Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis Usher syndrome abetalipoproteinemia Lawrence-Moon-Biedl syndrome Kearns-Sayre syndrome Alport's syndrome mitochondrial myopathy



Fundus showing changes secondary to retinitis pigmentosa



CHRPE - congenital hypertrophy of the retinal pigment epithelium.  



These can be typical' or 'atypical'. Typical CHRPE are grey or black, with depigmented lacunas, and are found in one quadrant of one eye.They do not affect vision. Atypical CHRPE have a white fishtail and are bilateral. They do not affect vision, but if there are more than four atypical CHRPE in each eye, then familial adenosis polyposis or Gardner syndrome might be suspected as an association. Colonoscopy and examination of all family members would therefore be appropriate. A referral to gastroenterology is the best next step.

____________________________________________________________

Sudden painless loss of vision An elderly patient with acute visual loss has giant cell arteritis until proved otherwise

The most common causes of a sudden painless loss of vision are as follows:

    

ischaemic optic neuropathy (e.g. temporal arteritis or atherosclerosis) occlusion of central retinal vein occlusion of central retinal artery vitreous haemorrhage retinal detachment

Ischaemic optic neuropathy 

 

may be due to arteritis (e.g. temporal arteritis) or atherosclerosis (e.g. hypertensive, diabetic older patient) due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve altitudinal field defects are seen

Central retinal vein occlusion   

incidence increases with age, more common than arterial occlusion causes: glaucoma, polycythaemia, hypertension severe retinal haemorrhages are usually seen on fundoscopy

Central retinal artery occlusion  

due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis) features include afferent pupillary defect, 'cherry red' spot on a pale retina



Vitreous haemorrhage 



causes: diabetes, bleeding disorders. the most likely source of bleeding in a diabetic patient is fragile neovascular tissue (Proliferative retinopathy) features may include sudden visual loss, dark spots

Retinal detachment 

features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters (see below)

Differentiating posterior vitreous detachment, retinal detachment and vitreous haemorrhage Posterior vitreous detachment

♦ Flashes of light (photopsia) - in the peripheral field of vision ♦ Floaters, often on the temporal side of the central vision

Retinal detachment

Vitreous haemorrhage

♦ Dense shadow that starts peripherally progresses towards the central vision ♦ A veil or curtain over the field of vision ♦ Straight lines appear curved Central visual loss

♦ Large bleeds cause sudden visual loss ♦ Moderate bleeds may be described as numerous dark spots ♦ Small bleeds may cause floaters

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Tunnel vision Tunnel vision is the concentric diminution of the visual fields Causes      

papilloedema glaucoma retinitis pigmentosa choroidoretinitis optic atrophy secondary to tabes dorsalis hysteria



Keratoconus Keratoconus, meaning "cone shaped," describes a condition in which the cornea (the clear front window of the eye) becomes thin and protrudes. This abnormal shape can cause serious distortion of visual images.

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Rheumatoid arthritis: ocular manifestations Ocular manifestations of rheumatoid arthritis are common, with 25% of patients having eye problems Ocular manifestations Scleritis is painful, episcleritis is not painful

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keratoconjunctivitis sicca (most common)

dry eyes - do Tear-film integrity - A reflex response to irritation of the corneal surface is epiphora, or watering. - Symptoms will be worse when tear-film evaporation is greater, episcleritis (erythema) scleritis (erythema and pain) corneal ulceration keratitis

Iatrogenic 

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steroid-induced cataracts

'steroid cataract' is typically posterior subcapsular, and causes constant and gradually progressive blur. Steroids can cause raised blood glucose levels. Fluctuating blood sugar levels can cause osmotic swelling of the lens in the eye, resulting in fluctuations in vision. However, diabetic retinopathy will not affect vision unless maculopathy occurs or vitreous haemorrhage occurs. Steroids  raised intraocular pressure, chloroquine retinopathy



Episcleritis    

Results in ocular irritation with nodules. It is acute in onset, with mild pain or discomfort / grittiness. It can be unilateral or bilateral, with localised or diffuse red eye. There may be mild photophobia and watering. The lack of photophobia and discharge, and normal vision, makes episcleritis the most likely option

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Retinoblastoma  

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The incidence is 1 in 16,000 live births. Genetic predisposition occurs in 20% of patients with unilateral disease, and 30% of patients with bilateral disease. The gene has been localised to 13q and the inherited form is associated with an increased risk of malignancy such as osteosarcoma and pineal tumours. It may be inherited as autosomal dominant. The commonest presentation is leucocoria (yellowish white pupil reflex), and there may be diminished or absent vision or strabismus. Late symptoms are: - pupil irregularity - hyphema - pain - proptosis - signs of raised intracranial pressure. The tumours have rarely metastasised before they are detected.

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Ectopia lentis Ectopia lentis/subluxation of the lens is associated with:    

Ehlers-Danlos syndrome Marfan's syndrome Weill-Marchesani syndrome (short stature, skeletal abnormalities and ectopia lentis), and Refsum's disease.



Chronic progressive external ophthalmoplegia (CPEO) 

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CPEO is an eye movement disorder which is often associated with mitochondrial disease. Although it typically presents in young adults, it can affect all ages. Classically the initial sign is bilateral ptosis, which is often unnoticed by the patient until the lid droops to the point of producing a visual field defect. Ophthalmoplegia then develops, which is symmetrical and again therefore unnoticed until ocular motility limits peripheral vision. All directions of gaze are affected, but downward gaze often less so. Weakness of extraocular muscle groups, such as orbicularis oculi and facial muscles, can be present in 25% of patients. Visual acuity is affected in 95% of patients, but the deficit is usually mild. CPEO is diagnosed via muscle biopsy, which shows an accumulation of enlarged mitochrondria. PCR can also determine a mutation of mitochondrial DNA. There are no specific treatments currently, but surgery can be used to correct ptosis and prisms can be used to help with ophthalmoplegia.

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Kearns-Sayre syndrome 

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This is a mitochondrial inherited disease, and as such is only passed on by mothers to offspring. It is a slowly progressive neuromuscular disorder associated with progressive external ophthalmoplegia and heart conduction defect. Ocular manifestations include ptosis and peripheral retinal bony spiculed appearances.

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F u n d o s c o p i c f ea tu r e s 

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(CMV) retinitis Cytomegalovirus -

secondary to human immunodeficiency virus (HIV)

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Fundoscopy of the left eye revealed an extensive 'brushfire-like' lesion in the major superior temporal arcade with a large patch of white fluffy lesion mixed with extensive retinal haemorrhages.

Ocular histoplasmosis and syphilitic choroiditis would give a fundus picture of multiple whitish lesions . Syphilitic neuroretinitis would normally give a picture of a macular star exudation. Tuberculous periphlebitis gives a picture of perivenous sheathing and minimal retinal haemorrhages.



____________________________________________________________ Bilateral internal carotid artery displacement can cause binasal incongruous hemianopia if the optic nerves are compressed.

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Anisocoria is a condition characterized by an unequal size of the eyes' pupils. Affecting 20% of the population, it can be an entirely harmless condition or a symptom of more serious medical problems The history of anisocoria, with headaches and diplopia should ring alarm bells, in that a lifethreatening posterior communicating artery aneurysm /berry aneurysm needs to be excluded urgently.

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Eye signs in Systemic diseases 

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Lisch nodules of the iris are golden nodules occurring bilaterally in the teenage years onwards in Neurofibromatosis type 1 (NF-1). Axillary freckles appear at 10 years of age, while cafe au lait spots increase in size and number throughout childhood. Brushfield spots of the iris are found in people with Down syndrome. Kayser-Fleischer rings are due to copper deposition in Descemet's membrane of the cornea. Band keratopathy is caused by calcium deposition in Bowman's layer of the cornea. Patients who present with band keratopathy should have a serum calcium and phosphate level Ectopia lentis with aortic regurgitation Marfan syndrome (Lens dislocation (classically upwards)). Inferior dislocated lens consistent with a diagnosis of homocytinstinuria.

Roth's spots haemorrhages in the retina

associated with subacute bacterial

endocarditis.

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Immune reconstitution uveitis associated with recovery of the CD4 count in HIV . In this condition a granulomatous uveitis appears as the immune system recovers as a result of autoimmune mechanisms.



Hyphaema 

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Occurs when bleeding from iris vessels fills the anterior chamber with blood and if there is enough blood the main risk in the acute stage is of raised intraocular pressure (IOP).

Intravenous carbonic anhydrase inhibitors is the most appropriate treatment Strict rest is vital if a hyphaema is present, as there is an increased risk of a second bleed in the initial period. avoid drops that dilate the pupil (such as anticholinergics) the iris remains stable and a second bleed is therefore less likely.

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Acute corneal hydrops 

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Acute corneal hydrops occurs in advanced keratoconus, which is the most common cause of corneal ectasia. The cornea is made of three main layers: - Epithelium - Stroma - Endothelium The transparency of the cornea is maintained by the endothelium which constantly pumps water out from the stroma. Descemet's membrane is a specialised basement membrane which lies between the endothelium and stroma, which helps to provide structural integrity to the cornea. In acute corneal hydrops the endothelium and Descemet's membrane split which allows aqueous to enter the corneal stroma. Stromal and epithelial oedema results in corneal opacification and formation of epithelial bullae. Patient present with painful loss of vision cornea is opaque and appears to be protruding Keratoconus is associated with atopic conditions (for example, asthma, hay fever, eczema) and Down syndrome.

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Subtarsal foreign body  

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history of 'gritty pain' in the eye with pain on blinking. The appropriate management would be to examine underneath the lid to search for and remove a foreign body. Further management would involve topical chloramphenicol ointment three to four times a day for five days.



Notes _ Notes - Ophthalmology.pdf

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