Opthamology Flashcards
Where is aqeuous humor produced
Ciliary body - travels through the anterior chamber, trabecular meshwork and into the canal of schlemm before reaching general circulation
Pathophys of open-angle gluacoma
Gradual increase in resistance through the trabecular meshwork makes it more difficult for aqeuous humor to flow through the meshwork + exit the eye therefore the pressure slowly builds up within the eye
Pathophys of closed-angle glaucoma
The iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing any aqueous humor from draining away = opthamological emergency (continuous build up of pressure)
What opthalmoscopy finding suggests increased pressure
Cupping of the optic discs
Open-angle glaucoma
Sx;
* Often diagnosed by routine screening as remains asymptomatic for a long while
* Gradual loss of peripheral vision / blurred vision
* Fluctuating pain / headaches
* Halo’s appear around lights particularly at nightime
Invx;
1. Gold standard = Goldmann applanation tonometry (measures intraocular pressure)
2. Fundoscopy - optic disc cupping
Management;
–> commence when intraocular pressure is 24mmHg +
1. Prostaglandin analogue eye drops (latanoprost)
2. Beta-blockers (to reduce production of aqueous humor)
3. Carboic anhydrase inhibitors (dorzolamide)
Surgery = trabeculectomy (when eyedrops become ineffective)
Side effects of latanoprost
Eyelash growth
Eyelid pigmentation
Iris browning
Closed-angle glaucoma
Risk factors = Age / Long-sightedness (hypermetropia) / Pupil dilation / female / FHx / Chinese / Shallow anterior chamber / Medications (e.g TCAs & anticholingerics)
Sx; Rapid onset of
* severely painful red eye
* blurred vision
* Decreased visual acuity
* Halo’s around lights & symptoms worsened with mydriasis
* Associated headache & nausea & vomitting
O/E - the eye will be red & teary with a **hazy cornea + fixed dilated pupil. Eyeball is firm to touch. **
Diagnosis = Both Tanometry + Gonioscopy (slit lamp) are needed
Management;
* same day referral to opthamology
* **Lie patient on back + Pilocarpine eye drops (Inc dose for brown eyes) + Acetazolamide
**
Definitive management = Laser iridotomy
How does Pilocarpine help in close-angle glaucoma
= Cholingeric agonsit
It causes miosis (constriction) which therefore contracts the ciliary muscles - opens the trabecular meshwork + increases outflow of aqueous humor
Other uses = Sjogren’s syndrome & Radiotherapy induced dry mouth
Macular degeneration
Most common cause of blindness in UK. Common in pts over 75yrs.
2 types;
1. Wet - 10% - worse prognosis and more acute & have development of new vessels (can bleed) stimulated by VEFG.
2. Dry - 90% - characterised by drusen
RF = Age / Smoking / White or Chinese / Fhx / CVD
Presentation;
* Difficulties in dark adaptation
* Gradual worsening of central vision loss
* Reduced visual acuity
* Crooked or wavy appearance to straight lines.
O/E = Reduced visual acuity + scotoma.
* Amsler grid test = distortion of straight lines
* Fundoscopy = Drusen
Diagnosis = slit-lamp fundus examination + optical coherence tomography (1st line for Wet AMD)+/- Fluroscein angiography (2nd line to diagnosed wet AMD)
Management;
–> Refer to opthamology
Dry AMD = conservative management
Wet = Anti-VEGF medication (Ranibizumab, bevacizumab) - *needs to be commenced <3months in to be effective *
Layers of the macula
- Choroid layer - contains the blood vessels which supply blood to the macula
- Bruchs membrane
- Retinal pigment epithelium
- Photoreceptors
What are drusen
Yellow deposits of proteins/lipids between the retinal epithelium + photoreceptors. Normally they are small and hard but get bigger and more of them in macular degeneration.
What is the most common cause of blindness among 35-65yr olds
Diabetic retinopathy
How does Diabetes cause retinopathy
Prolonged hyperglycemia causes damage to small vessels in the retina + endothelium. It increases vascular permeability which causes leakage to blood from blood vessels (blot haemorrhages) and lipid deposits (hard exudates)
Damage to blood vessel walls causes **microaneurysms + venous bleeding. **
Damage to retinal nerve fibres causes Cotton wool spots
As the disease progresses there is neovascularisation (Due to VEGF)
Features/Staging of non-proliferative diabetic retinopathy
Mild = microaneurysms
Moderate = microaneurysms + Blot haemorrhages + Hard exudates + cotton-wool spots
Severe = Microaneurysm/blot haemorrhage in 4 quadrants + cotton-wool spots in 2
Management = Generally just observe + prevent it getting worse. if severe = laser photocoagulation.
Proliferative Diabetic retinopathy
Presence of Neovascularisation (may lead to vitreous haemorrhage)
May have macular oedema
Management = Panretinal laser photocoagulation
Consider Anti-VEGF (e.g ranibizumab)
If vitreous haemorrhage = vitreoretinal surgery
Keith-Wagner classification of Hypertensive retinopathy
Stage 1 = Silver-wiring
Stage 2 = AV nipping
Stage 3 = Flame/blot haemorrhages (macular star) + Cotton-wool spots + hard exudates
Stage 4 = Papillodema
Cataracts
When the lens becomes cloudy + opaque thus reducing visual acuity by reducing the light entering the eye.
RF = age / Smoking / Alcohol / DM / Steroids / Hypocalcemia (hypoparaythyroidism)
Presentation;
* Usually unilateral / asymmetrical
* Very slow reduction in visual acuity
* Change of colour vision - colours may appear more browny/yellow
* “Starbursts” may appear around lights - particularly at night
O/E = loss of the red reflex.
Management = surgical replacement
Endopthalmitis
= complication of cataract surgery where inner eye contents become inflammaed due to infection.
(treat with intravitreal Abx)
Unilateral Mydriasis which is sluggish to react to light
+ associated absent ankle/knee reflexes
Holmes-Adie syndrome
- usually caused by viral infection causing damage to post-ganglionic parasympathetic fibres
Miotic, irregularly shaped pupil which accomodates but does NOT react to light
Argyll-robertson pupil (“prostitutes pupil”)
- specific finding in neurosyphillis.
Blepharitis
Inflammation of eye margins
Causes a gritty, dry & itchy sensation in the eyes + may cause styes / chalazions.
Management = conservative (hot compresses/cleaning) + Lubricating eye drops (hypromellose, carbomer etc)
Ectropion
Where the eyelid turns outwards exposing the inner aspect of eyelid.
Can result in **exposure keratopathy **
Management = Lubricating eyedrops.
Peri-orbital cellulitis
Skin infection in front of the orbital septum
Presentation;
* Swelling of eyelids
* Erythema + hot skin on eyelid
*note - it is important to differentiate this from orbital cellulitis which is a site + life threatening emergency (CT scan needed)
Management = Oral Abx (IV if systemically unwell or vulnerable)
Orbital cellulitis
Infection around the eyeball involving tissues behind the orbital septum.
Key features (which differentiates it from peri-orbital)
* Pain on eye movement
* Reduced eye movement
* Changes in vision
* Abnormal pupil reactions
* Proptosis
Management = Medical emergency!!! IV antibiotics needed and may need surgical drainage if abscess occurs.
Conjunctivitis
Unilateral/bilateral red, itchy or gritty eyes.
Can be purulent or non-purulent.
*NOTE - does not cause pain or reduced visual acuity (vision may be blurry due to discharge)
Management = conservative (should clear up in 1-2wks)
If bacterial -** give Chloramphenicol/Fusidic acid eye drops**
**If age <1 month = Urgent opthamology referall **
Anterior uveitis
= Inflammation of the uvea (the anterior chamber becomes infiltrated by neutrophils, lymphocytes + macrophages)
Sx;
* Unilateral
* Dull, achey painful red eye - WORSE ON MOVEMENT
* May have floaters / flashers
* Miosis + Hypopyon
* Lacrimation
* Ciliary flush (redness around cornea)
*NOTE - Acute uveitis is associated with HLA-B27 (IBD, AS, reactive arthritis & psoriatic arthritis)
Chronic - is associated with Sarcoidosis + Syphillis + TB + Lyme disease + Herpes
Management = Same day referall.
1. Steroids
2. Mydriatic meds e.g Atropin/cyclopenolate eye drops
3. Immunosupressants if HLA-B27
Scleritis
= Inflammation of the full thickness of the sclera. Can be necrotising.
Presentation;
* Severe pain on movement of eye + on palpation of eye
* Photophobia
* Reduced visual acuity
* Eye watering
* Abnormal reaction to light
*Note - associated with RA, SLE, Sarcoidosis, Wegners.
Management = same day referral.
Consider underlying condition
NSAIDs + Steroids + Immunosupressants
Corneal abrasians
= Scratches or damage to the cornea
Presentation;
* History of lens/foreign body in eye
* Painful red eye
* Blurred vision/photophobia
Diagnosis = flourescein stain - highlights abrasians
Keratitis
Inflammation of the cornea - commonly caused by contact lenses or viral infection (herpes)
Diagnosis = Fluorescein stain - shows dendritic ulcer
Slit lamp may be diagnostic.
If herpes related = oral aciclovir. Abx if contacts
Posterior vitreous detachment
Clasically presents with Photopsia (flashes of light in periphery) + Floaters (often on temporal side of ventral vision)
Harmless + associated with age
Retinal detachment
Dense shadow that starts peripherally and comes in (like a curtain closing)
Central vision loss
Straight lines appear curved / Spider webs, flashers, floaters
Painless
Management = Sight-threatening emergency, urgent referall!
Can have a vicrectomy, scleral bucling or retinoplexy
Sudden painless loss of vision. O/E there are flame/blot haemorrhages / macula oedema and optic disc oedema
Retinal vein occlusion
RF = HTN / DM / smoking etc
Management = urgent referal. Laser photocoagulation/anti-VEGF
Sudden painless loss of vision + Relative afferent pupillary defect. O/E there is a pale retina with cherry-red spot
Central retinal artery occlusion
Most common cause = atherosclerosis or Giant cell arteritis (temporal arteritis - RF women >50yrs with polymyalgia)
Manageemnt = immediate referall.
ESR / Temporal artery biopsy should be done (to find giant cell)
High dose prednisolone
Retinitis pigmentosa
= Congenital autisomal condition
Presentation;
* Night blindness (due to rod degeneration)
* Tunnel vision loss (initially peripheral then central later)
* V slow onset (usually diagnosed aged 25-40)
Fundoscopy = Bone-spicule black pigmentation in peripheral retina & Mottling of retina epithelium.
Associated conditions;
1. Usher’s syndrome = this + hearing loss
2. Refsum disease = this + Cerebellar ataxia + Peripheral neuropathy + deafness + skin changes
3. Alport’s syndrome
Management;
–> Refer to opthamology. Also genetic counselling + Vision aids.
Wear sunglasses to protect from further damage
Driving limitations + must inform DVLA
To slow disease progression consider acetazolamide + Steroids + Anti-VEGF (e.g ravicuzumab)
Causes of Amaurosis fugax
- Ischemic / Vascular (e.g arterial disease, TIA, ischemic optic neuropathy, retinal artery/vein occlusion etc)
- Vitreous haemorrhage
- Retinal detachment
- Retinal migraine
Ancanthamoeba infection
Associated with contact lens wearing.
Presents with watery, gritty, painful eye + hypopyons
Horner’s syndrome + Causes
Triad of;
1. Ptosis
2. Miosis
3. Anhidrosis
+/- enopthalmus
Central lesions (4 Ss) = Head + Arm + Trunk anhidrosis
1. Stroke
2. MS
3. Swelling/tumours
4. Syringomyelia
Pre-ganglionic (4 Ts) = Anhidrosis confined to the face
1. Tumour (pancoast)
2. Trauma
3. Thyroidectomy
4. Top rib growth
Post-ganglionic (4 Cs) = No anhidrosis
1. Carotid aneurysm
2. carotid artery dissection
3. cavernous sinus thrombosis
4. cluster headache
How should you manage a contact lens wearer presenting with acute painful red eye
Urgent referall to opthamology
- to exclude microbial keratitis
Marcus Gunn Pupil
Relative afferent pupillary defect
Associated with MS (optic neuritis)
Diagnosed on swinging light test - The pupil will abnormally dilate when light is shone into it and on the swinging test as the light is moved from good - bad eye both will dilate (instead of both constricting)
Accomodation will be normal
Risk factors for retinal detachment
- Myopia
- Posterior vitreous detachment
- Old age
- Trauma e.g boxing
- Diabetes
- previous cataract surgery
Most common cause of keratitis in contact lens wearers
Pseudomonas
