Ophthalmology Flashcards
Macular degeneration - Dry macular degeneration
characterized by Drusen - yellow round spots in Bruch’s membrane
W et (exudative, neovascular) macular degeneration:
characterized by choroidal
neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis
Risk factors - Macular degeneration
Age: most patients are over 60 years of age
* Family history
* Smoking
* More common in caucasians
* ♀sex
* High cumulative sunlight exposure
Features Macular degeneration
- ↓ visual acuity: ‘blurred’, ‘distorted’ vision, central vision is affected first
- Central scotomas
- Fundoscopy: drusen, pigmentary changes
Dry macular degeneration -
no current medical treatments
Wet macular degeneration treatment
Photocoagulation
* Photodynamic therapy
* anti-vascular endothelial growth factor (anti-VEGF) treatments: intravitreal ranibizumab
Sudden Painless Loss of Vision:
The most common causes of a sudden painless loss of vision are as follows:
* Ischemic optic neuropathy (e.g. Temporal arteritis or atherosclerosis)
* Occlusion of central retinal vein
* Occlusion of central retinal artery
* Vitreous hemorrhage
* Retinal detachment
Amaurosis fugax
classically described as a transient monocular vision loss that appears as a “curtain coming down vertically into the field of vision in one eye”. Sometimes it occurs as episodes, caused by epsilateral carotid artery diease.
Ischemic optic neuropathy
May be due to arteritis (e.g. Temporal arteritis) or atherosclerosis (e.g. HTN, DM, old patient)
* Due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve
* Altitudinal field defects are seen → loss of vision above or below the horizontal level
Central retinal vein occlusion
Incidence ↑ with age, more common than arterial occlusion
* Causes: glaucoma, polycythemia, hypertension
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 retin
Vitreous hemorrhage
Causes: diabetes, bleeding disorders
* Features may include sudden visual loss,
dark spots
Retinal detachment symtoms
Features of vitreous detachment, which may precede retinal detachment, include flashes of light or floaters (see below)
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
Dense shadow that starts peripherally progresses towards the central vision
* A veil or curtain over the field of vision
* Straight lines appear curved (positive Amsler grid test)
* Central visual loss
Relative afferent pupillary defect
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
auses of Mydriasis (large pupil)
- Third nerve palsy
- Holmes-adie pupil
- Traumatic iridoplegia
- Pheochromocytoma
- Congenital
Drug causes of mydriasis - Topical mydriatics: tropicamide, atropine
- Sympathomimetic drugs: amphetamines
- Anticholinergic drugs: tricyclic antidepressants
Holmes-ADIe 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
Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from
the optic nerve head.
he elastic layer of Bruch’s membrane is characteristically thickened and calcified
Causes
* Pseudoxanthoma elasticum
* Ehler-danlos syndrome
* Paget’s disease
* Sickle-cell anemia
* Acromegaly
Optic atrophy
pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision*. Causes may be acquired or congenital
Optic atrophy causes
Acquired causes
* Multiple sclerosis
* papilledema (longstanding)
* raised intraocular pressure (e.g. glaucoma, tumour)
* retinal damage (e.g. choroiditis, retinitis pigmentosa)
* ischemia
* 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)
Cataract: cause s
- Age related
- UV light
Systemic - DM
- Steroids
- Infection (congenital rubella)
- Metabolic (hypocalcemia,
galactosemia) - Myotonic dystrophy, Down’s
syndrome
Ocular - Trauma
- Uveitis
- High myopia
- Topical steroids
Retinitis pigmentosa
rimarily affects the peripheral retina resulting in tunnel vision
Features
* Night blindness is often the initial sign
* Funnel vision (the preferred term for tunnel vision)
Associated diseases Retinitis pigmentosa
Refsum disease: cerebellar ataxia, peripheral
neuropathy, deafness, ichthyosis
* Usher syndrome
* Abetalipoproteinemia
* Lawrence-Moon-Biedl syndrome
* Kearns-Sayre syndrome
* Alport’s syndrome
tunnel vision is the concentric diminution of the visual fields Causes:
- Papilledema * Retinitis pigmentosa
- Glaucoma * Choroidoretinitis
- Optic atrophy secondary to tabes dorsalis
- Hysteria
Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE):
Typical CHRPE:
* Gray or black depigmented lacunae
* Found in 1 quadrant of eye
* Do not affect vision
Atypical CHRPE:
* White fish tail shaped bilaterally
* Affect the vision when there are > 4 in each eye
* Associated with Adenosis polyposis and Gardner’s syndrome → do colonoscopy.
acute angle closure glaucoma RF
here 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
Drugs which may precipitate acute glaucoma
anticholinergics and tricyclic antidepressants.
Mydriatic drops
acute glaucoma features
Features
* Severe pain: may be ocular or headache
* ↓ 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
* Corneal edema results in dull or hazy cornea
* Systemic upset may be seen, such as nausea and vomiting and even abdominal pain
Treatment of acute glaucoma
anagement
* Urgent referral to an ophthalmologist
* Management options include reducing aqueous secretion with acetazolamide and pupillary
constriction with topical pilocarpine
Treatment of acute glaucoma - acetazolamide + pilocarpine
Primary open-angle glaucoma (POAG) RF
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’
* ↓ visual acuity
* Optic disc cupping
Prostaglandin analogues (e.g. Latanoprost)
Increase uveoscleral outflow
Once daily administration
Adverse effects include brown pigmentation of the iris
β-blockers (e.g. Timolol
↓ aqueous production
Should be avoided in asthmatics and patients with heart block
Sympathomimetics (e.g. Brimonidine, an α2-adrenoceptor agonist)
↓ aqueous production and ↑ outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperemia
Carbonic anhydrase inhibitors (e.g. Dorzolamide)
↓ aqueous production Systemic absorption may cause sulphonamide-like reactions
Miotics (e.g. Pilocarpine)
Miotics (e.g. Pilocarpine)
↑ uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision
Red eye - glaucoma or uveitis?
- Glaucoma: severe pain, haloes, ‘semi-dilated’ pupil
- Uveitis: small, fixed oval pupil, ciliary flush
Scleritis
Severe pain (may be worse on movement) and tenderness
* May be underlying autoimmune disease e.g. Rheumatoid arthritis
Anterior uveitis
Acute onset * Pain
* Blurred vision and photophobia
* Small, fixed oval pupil, ciliary flush
Dacryocystitis
Watering eye (epiphora)
* Swelling and erythema at the inner canthus of the eye
Management is with systemic antibiotics
Congenital lacrimal duct obstruction
Features:
* Watering eye (even if not crying)
* Secondary infection may occur
* Symptoms resolve in 99% of cases by 12 months of age
Blepharitis
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
Blepharitis
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
Ocular manifestations RA
Keratoconjunctivitis sicca (most common)
* Episcleritis (erythema)
* Scleritis (erythema and pain)
* Corneal ulceration
- Keratitis → associated with acns rosacea
Thyroid eye disease
25-50% of patients with Graves’ disease. It is thought to be due to an autoimmune response against an autoantigen, possibly the TSH receptor, causing retro- orbital inflammation. The patient may be eu-, hypo- or hyperthyroid at the time of presentation
Features
* Exophthalmos
* Conjunctival edema
* Papilledema
* Ophthalmoplegia
* Inability to close the eye lids may lead to sore, dry eyes. If severe
and untreated patients can be at risk of exposure keratopathy
Herpes Zoster Ophthalmicus (HZO) features
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
Herpes Zoster Ophthalmicus (HZO) features treatment
- 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 post- herpetic neuralgia
- Ocular involvement requires urgent ophthalmology review
Herpes Simplex Keratiti
Features
* Red, painful eye
* Photophobia
* Epiphora
* Visual acuity may be ↓
* Fluorescein staining may show an epithelial ulcer, dendritic
pattern of staining.
Management
* Immediate referral to an ophthalmologist
* Topical acyclovi
and keratopathy
corneal disease derived from the appearance of calcium on the central cornea caused by calcium deposition in Bowman’s layer.
Treatment: the calcium can be scraped off the cornea or removed with a laser. This can restore sight, but it can take a number of months for normal vision to return as the cornea will be damaged during the operation. This cannot be repeated too many times as it would make the cornea thinner and thinner.
Diabetic Retinopathy path
Hyperglycemia is thought to cause ↑ retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage to endothelial cells and pericytes.
Endothelial dysfunction leads to ↑ 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 ischemia
Diabetic Retinopathy stages
Mild NPDR
* 1 or more microaneurysm
Moderate NPDR
* Microaneurysms
* Blot hemorrhages
* Hard exudates
* Cotton wool spots, venous beading/looping and
intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR
Severe
* Blot hemorrhages 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 hemorrhage
* Fibrous tissue forming anterior to retinal disc
* More common in type I DM, 50% blind in 5 years
earlist sign of DM Nephropathy
Microaneurysm on fluorescein angiography
Maculopathy
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
Screening DM Nephropathy
- T1DM
o Newly diagnosed DM → after 5 years o From 5-10 years → anuual
o More than 10 years DM → 6 monthly - T2DM
o Anually
Optic Neuritis:
Features
* Diabetes
* Syphilis
- Unilateral ↓ in visual acuity over hours or days
- Poor discrimination of colors, ‘red desaturation’
- Pain worse on eye movement
- Relative afferent pupillary defect
- Central scotoma
Retrobulbar Neuritis:
nflammation behind the optic nerve head, the optic disc is normal. Patient sees nothing, Doctor sees nothing
Features:
* Visual acuity loss
* Afferent pupillary defect during swinging flashing light
* Color vision will be reduced (red looks pallo
Trochlear Nerve Palsy:
cause torsional diplopia, Torsion is a normal response to tilting the head sideways. The eyes automatically rotate in an equal and opposite direction, so that the orientation of the environment remains unchanged – vertical things remain vertical.
