OPHTHAL - clinical Flashcards

Question

Why is acute angle-closure glaucoma an ophthalmological emergency?

Answer 1

It requires rapid treatment to prevent permanent vision loss due to sustained high intraocular pressure damaging the optic nerve

Answer 2

- Increasing age - Family history - Female sex (4× more likely than males) - Chinese & East Asian ethnic origin - Shallow anterior chamber

Answer 3

- Open-angle glaucoma is more common in Black individuals, whereas angle-closure glaucoma is rare in this group and more common in Chinese and East Asian populations (Ethnic origin is an important risk factor to consider in exam questions)

Answer 4

- Adrenergic medications (e.g., noradrenaline) - *causes mydriasis (blocks outflow of aqueous humour), ciliary muscle relaxation (can cause anterior displacement of lens-iris diaphragm), and increased aqueous humour production (but it cannot drain properly)* - Anticholinergic medications (e.g., oxybutynin and solifenacin) - *causes mydriasis (pupil dilation), which can lead to pupillary block, and closure of the iridocorneal angle* - Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects - *causes mydriasis (pupil dilation), which can lead to pupillary block, and closure of the iridocorneal angle* . (particularly an issue in people with anatomically narrow iridocorneal angles as they are more vulnerable)

Answer 5

Typical symptoms: - Severely painful red eye - Blurred vision - Halos around lights - Associated headache, nausea and vomiting . Signs O/E: - Red eye - Hazy cornea - Decreased visual acuity - Fixed, dilated pupil - Hard eyeball on gentle palpation

Answer 6

- Lay patient on their back without a pillow - Pilocarpine eye drops (2% for blue eyes, 4% for brown eyes) - Acetazolamide 500 mg orally - Analgesia and antiemetics as needed - Urgent ophthalmology admission

Answer 7

- It is a miotic agent (constricts the pupil) --> *acts on muscarinic receptors in the sphincter muscles in the iris* - it also causes ciliary muscle contraction . These two effects open up the drainage pathway for aqueous humour

Answer 8

It is a carbonic anhydrase inhibitor --> *reduces aqueous humour production*

Answer 9

- Pilocarpine eye drops - Acetazolamide (oral/IV) - Hyperosmotic agents (e.g. IV mannitol) - *increase osmotic gradient between blood and eye* - Timolol (beta-blocker) - *reduces aqueous humour production* - Dorzolamide (carbonic anhydrase inhibitor) - *reduces aqueous humour production* - Brimonidine (sympathomimetic) - *reduces aqueous humour production and increases uveoscleral outflow*

Answer 10

Laser iridotomy - *laser creates hole in iris, allowing aqueous humour to flow directly from posterior chamber to anterior chamber, this relieves the pressure pushing iris forward against the cornea and opens up the pathway for the aqueous humour to drain*

Answer 11

Due to dilation of the pupils, which further reduces the iridocorneal angle --> worsening symptoms

Answer 12

A progressive condition affecting the macula --> *it is the most common cause of blindness in the UK* - Often unilateral, but can be bilateral

Answer 13

- Dry (non-neovascular) AMD - *90% of cases* - Wet (neovascular) AMD - *10% of cases*

Answer 14

The macula is responsible for high-definition colour vision in the central visual field. . Its four layers are: - Choroid layer (at the base) - *contains the blood vessels that supply the macula* - Bruch's membrane - Retinal pigment epithelium - Photoreceptors

Answer 15

Drusen are yellowish deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane - a few small Drusen is normal in older patients, but frequent and larger drusen can be an early sign of macular degeneration . Other features: - Atrophy of retinal pigment epithelium - Degeneration of the photoreceptors

Answer 16

Wet AMD is characterised by neovascularisation from the choroid layer (blood vessels grow into retina) - these vessels can leak fluid or blood, causing oedema and faster vision loss

Answer 17

Vascular endothelial growth factor (VEGF) stimulates neovascularisation in wet AMD - Anti-VEGF medications target this factor to slow disease progression

Answer 18

- Older age - Smoking - Family history - Cardiovascular disease (e.g., hypertension) - Obesity - Poor diet (low in vitamins and high in fat)

Answer 19

- Gradual loss of central vision - Reduced visual acuity - Metamorphopsia (wavy or crooked appearance of straight lines) - Difficulty reading small text

Answer 20

Wet AMD presents more acutely than dry AMD, with vision loss developing over days and potentially leading to complete blindness within 2-3 years - often progresses to bilateral disease

Answer 21

- Glaucoma --> Peripheral vision loss + Halos around lights - AMD --> Central vision loss + Wavy appearance of straight lines (metamorphopsia)

Answer 22

- Reduced visual acuity - *using a Snellen chart* - Scotoma (an enlarged central area of vision loss) - Amsler grid test - *shows distortion of straight lines (metamorphosis)* - Drusen - *on fundoscopy*

Answer 23

- Slit lamp examination - *gives detailed view of retina and macula* - Optical coherence tomography (OCT) - *gives cross-sectional view of layers of retina, can be used to diagnose AND monitor AMD* - Fluorescein angiography (fluorescein contrast given and retina is photographed to assess blood supply) - *identifies oedema and neovascularization in wet AMD*

Answer 24

- No specific treatment available - Lifestyle modifications - *avoid smoking, control BP, consider vitamin supplementation to slow progression*

Answer 25

Anti-VEGF injections (e.g., ranibizumab, aflibercept, bevacizumab) --> *block VEGF and slow development of new vessels* . (they are injected directly into the vitreous chamber (intravitreal), usually once a month)

Answer 26

damage to the retinal blood vessels due to prolonged high blood sugar levels

Answer 27

- Hyperglycaemia --> *damages retinal blood vessels + endothelial cells* - Increased vascular permeability (leaking blood vessels) --> *blot hemorrhages + hard exudates* - Blood vessel wall damage --> *microaneurysms + venous beading* - Damage to nerve fibres in retina --> *cotton wool spots (fluffy, white patches on retina)* - Intraretinal microvascular abnormalities (IRMA) --> *dilated and torturous capillaries in the retina* - Neovascularisation --> *growth of new blood vessels, due to release of growth factors in the retina*

Answer 28

Neovascularisation (new blood vessel formation) is the key feature of proliferative diabetic retinopathy

Answer 29

- Background - *microaneurysms, retinal haemorrhages, hard exudates , and cotton wool spots* - Pre-proliferative - *venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA)* - Proliferative - *neovascularisation, vitreous haemorrhage* . Diabetic maculopathy exists separately and involves: - exudates within the macula - macular oedema

Answer 30

- Drusen --> *yellow deposits of proteins and lipids, located between retinal pigment epithelium and Bruch's membrane (seen in AMD)* . - Hard exudates --> *yellow-white deposits of lipids and proteins, located in the retinal layers due to leaky blood vessels (seen in diabetic retinopathy*

Answer 31

- Vision loss - Retinal detachment - Vitreous haemorrhage (bleeding into the vitreous humour) - Rubeosis iridis (new blood vessel formation in the iris) --> *can lead to neovascular glaucoma* - Optic neuropathy - Cataracts

Answer 32

Non-proliferative --> *close monitoring and strict diabetic control* . Proliferative: - Pan-retinal photocoagulation (PRP) --> *laser treatment across the retina to suppress new vessels* - Intravitreal anti-VEGF injections - Surgery (e.g. vitrectomy) - *for severe cases* . Macular oedema --> *intravitreal dexamethasone implant*

Answer 33

To be able to see the retina on fundoscopy more clearly and therefore monitor diabetic retinopathy changes (cataracts obscure fundoscopy view)

Answer 34

Damage to the retinal blood vessels due to hypertension, which can develop slowly with chronic hypertension or rapidly in malignant hypertension

Answer 35

- Silver wiring/copper wiring - *walls of arterioles become thickened and sclerosed reflecting more light O/E* - Arteriovenous (AV) nipping - *arterioles compress veins at crossings (due to sclerosis and hardening of arterioles)* - Cotton wool spots - *caused by ischaemia and infarction of retina, causing damage to nerve fibres* - Hard exudates - *caused by damaged vessels leaking lipids onto retina* - Retinal haemorrhages - *caused by damaged vessels rupturing and releasing blood in the retina (dot/blot occur deeper, flame haemorrhages occur in nerve fibre layer)* - Papilloedema - *caused by ischaemia of optic nerve, resulting in optic nerve swelling (oedema)*

Answer 36

- Stage 1: Mild narrowing of arterioles - Stage 2: Focal constriction of blood vessels and AV nipping - Stage 3: Cotton-wool spots, haemorrhages, and exudates - Stage 4: Papilloedema (malignant hypertension)

Answer 37

BP control and management of CVD risk factors (eg. smoking cessation and lipid control)

Answer 38

A progressively opaque lens that reduces the light entering the eye and visual acuity

Answer 39

To focus light on the retina - *it is held in place by the suspensory ligaments attached to the ciliary body, which changes its shape to adjust focus* . (note: the lens has no blood supply and is nourished by the aqueous humour)

Answer 40

- Contracts --> suspensory ligaments loosen --> lens thickens (near vision). - Relaxes --> suspensory ligaments tighten --> lens narrows (distance vision)

Answer 41

The red reflex

Answer 42

- Increasing age - Smoking - Alcohol - Diabetes - Steroids - Hypocalcaemia

Answer 43

Symptoms are usually asymmetrical: - Slow reduction in visual acuity - Progressive blurring of the vision - Colours becoming more faded, brown, or yellow - Starbursts can appear around lights (particularly at night)

Answer 44

Loss of the red reflex, with the lens also appearing grey/white on ophthalmoscopy

Answer 45

- No intervention if symptoms are manageable . Cataract surgery (day case with good results): - Breaking up and removing the lens - Implanting an artificial lens . (note: cataracts can prevent the detection of other pathology (eg. AMD or diabetic retinopathy), which can become apparent after surgery if the patient still has visual symptoms)

Answer 46

Endophthalmitis - *inflammation of inner eye, usually caused by infections, can lead to vision loss* - Treated with intravitreal antibiotics injected directly into the eye

Answer 47

- Nuclear - affects central nucleus of lens - Posterior subcapsular - affects back surface of lens - Cortical - affects outer edge (cortex) of lens

Answer 48

To rule out a tumour - *commonly associated with retinoblastoma*

Answer 49

Leukocoria (aka. white pupillary reflex) - *retinoblastoma (malignant tumour of retina)* . (congenital cataract is also a cause)

Answer 50

Circular muscles in the iris (sphincter pupillae), innervated by the parasympathetic nervous system, using acetylcholine as a neurotransmitter - parasympathetic fibres travel along the oculomotor nerve (CN III)

Answer 51

- Trauma to the sphincter muscles in the iris --> *e.g. during cataract surgery* - Anterior uveitis --> *can cause adhesions (scar tissue) in the iris* - Acute angle-closure glaucoma --> *can cause ischaemic damage to muscles of iris (usually a vertical oval)* - Rubeosis iridis --> *neovascularisation in the iris (usually due to poorly controlled diabetes and diabetic retinopathy)* - Coloboma --> *congenital hole in the iris + irregular pupil shape*

Answer 52

Dilator muscles in the iris (dilator pupillae), innervated by the sympathetic nervous system, using adrenalin as a neurotransmitter

Answer 53

Temporary, misshapen pupil due to muscle spasm in part of the dilator muscle - may be associated with migraines and Horner syndrome

Answer 54

- Congenital - Stimulants (e.g. cocaine) - Anticholinergics (e.g. oxybutynin) - Trauma - Third nerve palsy - Holmes-Adie syndrome - Raised intracranial pressure - Acute angle-closure glaucoma

Answer 55

- Ptosis (drooping upper eyelid) - *due to paralysis of the levator palpebrae superioris* -Dilated non-reactive pupil - *due to paralysis of sphincter pupillae* - Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye - *due to unopposed lateral rectus and superior oblique*

Answer 56

- Horner syndrome - Cluster headaches - Argyll-Robertson pupil (neurosyphilis) - Opiates - Nicotine - Pilocarpine

Answer 57

Pupil-sparing --> *suggests a microvascular cause*: - diabetes - hypertension - ischaemia . Pupil-involving --> *suggests nerve compression*: - tumour - trauma - cavernous sinus thrombosis - posterior communicating artery aneurysm - raised ICP . (pupillary fibres are located at the periphery of the nerve, microvascular causes lead to infarct of central nerve fibres first)

Answer 58

- The oculomotor nerve (CN III) travels directly from the brainstem to the eye in a straight line - it passes through the cavernous sinus and runs close to the posterior communicating artery (PCOM) --> *making it susceptible to compression from cavernous sinus thrombosis or a PCOM aneurysm*

Answer 59

- Ptosis (drooping eyelid) - Miosis (constricted pupil) - Anhidrosis (loss of sweating) . (enopthalmos (sunken eye) may be present, light/accommodation reflexes are not affected)

Answer 60

Damage to the sympathetic nervous system supplying the face

Answer 61

First order neurons (central neurons): - originate in hypothalamus - descend through brainstem to spinal cord (C8-T2) . Second-order neurons (pre-ganglionic neurons): - exit spinal cord and travel to superior cervical ganglion - pass through apex of lung (note: sympathetic chain runs along each side of the spinal cord) . Third-order neurons (post-ganglionic neurons): - travel from superior cervical ganglion along internal carotid artery to the eye

Answer 62

- Central (first-order) lesions --> *anhidrosis of the arm, trunk, and face* - Pre-ganglionic (second-order) lesions --> *anhidrosis of the face* - Post-ganglionic (third-order) lesions --> *no anhidrosis (due to the sweat gland fibres have already branched off with the external carotid artery before the lesion occur)*

Answer 63

Central lesions (4Ss): - S - Stroke - S - Multiple Sclerosis - S - Swelling (tumours) - S - Synringomyelia (cyst in spinal cord) . Pre-ganglionic (4Ts): - T - Tumour (Pancoast tumour) - T - Trauma - T - Thyroidectomy - T - Top rib (a cervical rib growing above first rib and clavicle) . Post-ganglionic (4Cs): - C - Carotid aneurysm - C - Carotid artery dissection - C - Cavernous sinus thrombosis - C - Cluster headache

Answer 64

Heterochromia (difference in iris colour on the affected side)

Answer 65

- Cocaine eye drops --> *normal pupil dilates, Horner pupil does not* . In Horner syndrome, the nerves are not releasing noradrenaline, so blocking re-uptake makes no difference, and there is no pupil change) . - Low-dose adrenaline (0.1%) --> *dilates Horner pupil, but not normal pupil*

Answer 66

- Cocaine blocks the reuptake of noradrenaline (or norepinephrine) at the NMJ, which leads to increased noradrenaline in the synaptic cleft, and consequently pupil dilation (noradrenaline stimulates dilator muscles of the iris) . - Normal pupil --> *pupil dilates* - Horner pupil --> *pupil does not dilate effectively (sympathetic pathway is impaired, preventing normal adrenergic response)*

Answer 67

- Adrenaline (epinephrine) is a sympathomimetic drug that normally causes pupil dilation (mydriasis) by stimulating alpha-1 adrenergic receptors on the iris dilator muscle - In Horner syndrome, due to disruption of the sympathetic pathway, the affected pupil becomes hypersensitive to adrenergic stimuli, this occurs because of upregulatoin of alpha-1 receptors (denervation hypersensitivity) on the dilator muscle - When a low dose (0.1%) of adrenaline is applied to the eye, the pupil in someone with Horner syndrome will show a dilation response due to this hypersensitivity (however, a normal pupil with normal sensitivity will not dilate with such a low dose) . (note: post-ganglionic lesions will show the most prominent response)

Answer 68

- Dilated pupil - Sluggish light response - Normal accommodation response - Slow redilation after constriction ("tonic" pupil)

Answer 69

Holmes-Adie syndrome, which also features absent ankle and knee reflexes.

Answer 70

Neurosyphilis - *commonly called a “prostitute’s pupil” due to its relation to neurosyphilis and because “it accommodates but does not react”*

Answer 71

- Constricted pupil - Accommodates on near object, but does not react to light ("prostitute’s pupil") - Irregularly shaped

Answer 72

Blepharitis is inflammation of the eyelid margins, causing a gritty, itchy, dry sensation in the eyes

Answer 73

Dysfunction of the Meibomian glands (which secrete meibum (oil) onto the surface of the eye)

Answer 74

Styes and chalazions

Answer 75

Warm compresses and gentle cleaning of the eyelid margins to remove debris - *e.g. with a cotton bud and baby shampoo*

Answer 76

A stye that results from infection of the Meibomian glands, which are deeper and often more painful

Answer 77

An infection of the glands of Zeis (sebaceous glands) or glands of Moll (sweat glands) at the base of the eyelashes, presenting as a tender, red lump

Answer 78

A blocked and swollen Meibomian gland, also called a Meibomian cyst

Answer 79

1. Warm compresses and analgesia 2. Topical antibiotics (e.g., chloramphenicol) may be considered if conjunctivitis is present or symptoms persist

Answer 80

Warm compresses and gentle massage towards the eyelashes to encourage drainage (rarely, surgical drainage may be required)

Answer 81

A swelling in the eyelid that is usually not tender, but can occasionally be red and painful

Answer 82

Inward turning of the eyelid, causing the lashes to press against the eye

Answer 83

Corneal damage and ulceration

Answer 84

1. Initial management involves taping the eyelid down (to prevent it from turning inwards) 2. Definitive treatment is surgical --> *same-day referral to ophthalmology is required if there is a risk to sight*

Answer 85

Lubricating eye drops to prevent the eye from drying out

Answer 86

Outward turning of the eyelid, exposing the inner surface

Answer 87

Exposure keratopathy - *as the eyeball is inadequately lubricated and protected*

Answer 88

- Mild cases --> *regular lubricating eye drops* - Severe cases --> *surgical correction* (note: same-day ophthalmology referral if there is a risk to sight)

Answer 89

Inward growth of the eyelashes

Answer 90

Pain, corneal damage, and ulceration

Answer 91

- Removal of affected eyelashes - Recurrent cases may need electrolysis, cryotherapy, or laser treatment (to prevent eyelashes from regrowing) (same-day ophthalmology referral if there is a risk to sight)

Answer 92

An infection of the eyelid and skin in front of the orbital septum (anterior to orbital septum)

Answer 93

Swollen, red, hot skin around the eyelid and eye (no visual changes/eye pain)

Answer 94

Orbital cellulitis is a sight- and life-threatening emergency (CT scan can help distinguish them)

Answer 95

- Urgent ophthalmology referral - Systemic antibiotics (oral or IV) - Severe cases or vulnerable patients (e.g., children) may require admission - *due to risk of developing into orbital cellulitis*

Answer 96

An infection behind the orbital septum (posterior to orbital septum) affecting the tissues around the eye

Answer 97

Similar appearance to periorbital cellulitis, but with additional symptoms: - Pain with eye movement - Reduced eye movements - Vision changes - Abnormal pupil reactions - Proptosis (bulging eye)

Answer 98

- Emergency admission under ophthalmology - IV antibiotics - Surgical drainage if an abscess forms

Answer 99

Inflammation of the conjunctiva, the thin tissue covering the inside of the eyelids and the sclera - can be bacterial, viral, or allergic - can be unilateral or bilateral . (conjunctiva protects and lubricates the eye)

Answer 100

- Red, bloodshot eye - Itchy or gritty sensation - Discharge . There is NO pain, photophobia, or reduced visual acuity . *(discharge covering the eye may cause blurry vision, but this should return to normal when the discharge is cleared)*

Answer 101

- Purulent discharge - Worse in the morning (eyes stuck together) - Typically starts in one eye and spreads to the other (highly contagious)

Answer 102

- Clear discharge - Associated with viral symptoms (dry cough, sore throat, blocked nose) - Tender pre-auricular lymph nodes . *(viral conjunctivitis is also contagious)*

Answer 103

- Acute angle-closure glaucoma - Anterior uveitis - Scleritis - Corneal abrasions or ulceration -Keratitis - Foreign body - Traumatic or chemical injury

Answer 104

- Conjunctivitis - Episcleritis - Subconjunctival haemorrhage

Answer 105

Conditions that cause pain or reduced visual acuity

Answer 106

No, it usually resolves in 1–2 weeks without treatment (even bacterial cases)

Answer 107

- Avoid sharing towels - Avoid close contact - Regular hand washing - Clean the eyes with cooled boiled water and cotton wool (can help clear the discharge)

Answer 108

Chloramphenicol or fusidic acid eye drops

Answer 109

It could be gonococcal conjunctivitis, which can cause permanent vision loss

Answer 110

- Swelling of the conjunctival sac and eyelid - Itching - Watery discharge

Answer 111

1. Antihistamines (oral or topical) 2. Topical mast-cell stabilisers (for chronic seasonal symptoms) - *work by preventing mast cells from releasing histamine*

Answer 112

Inflammation of the anterior uvea - *which includes the iris, ciliary body, and choroid*

Answer 113

The anterior chamber - *where inflammatory cells (neutrophils, lymphocytes, macrophages) accumulate*

Answer 114

A fluid collection of inflammatory cells seen at the bottom of the anterior chamber

Answer 115

Autoimmune disease . Other factors - *infection, trauma, ischaemia, or malignancy*

Answer 116

- Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis) - *HLA-B27 associated* - Inflammatory bowel disease - Sarcoidosis - Behçet’s disease

Answer 117

- Ciliary flush - *ring of red spreading from the cornea outwards* - Miosis - *constricted pupil due to sphincter muscle contraction* - Abnormally shaped pupil - *due to posterior synechiae (adhesions) pulling the iris into abnormal shapes* - Hypopyon - *inflammatory cells collected as a white fluid in the anterior chamber*

Answer 118

- Painful red eye (dull, aching pain) - Reduced visual acuity - Photophobia (due to ciliary muscle spasm) - Excessive lacrimation (tear production)

Answer 119

- Urgent referral to ophthalmology . 1. Steroids (eye drops, oral, or IV) 2. Cycloplegics (e.g., cyclopentolate, atropine) - *dilate pupil and reduce pain by paralysing the ciliary muscles (reducing ciliary spasm)*

Answer 120

They dilate the pupil and reduce pain by paralysing the ciliary muscles (reducing ciliary spasm) - cyclopentolate and atropine are antimuscarinic drugs that reduce the action of the iris sphincter muscles and ciliary muscles

Answer 121

DMARDs or anti-TNF medications

Answer 122

Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera beneath the conjunctiva

Answer 123

Inflammatory disorders --> RA, inflammatory bowel disease (it is not usually caused by an infection)

Answer 124

- No photophobia - No discharge - Normal visual acuity

Answer 125

Acute-onset unilateral features: - Localised or diffuse redness (often in the lateral sclera) - No pain (or mild pain) - Dilated episcleral vessels

Answer 126

Phenylephrine eye drop test --> *causes blanching of episcleral vessels (redness disappears in episcleritis but remains in scleritis)*

Answer 127

- Self-limiting --> *usually resolves in 1-2 weeks* - Mild cases --> *no treatment needed* - Symptom relief --> *analgesia (e.g. ibuprofen) and lubricating eye drops* - Severe cases --> *may require steroid eye drops*

Answer 128

Inflammation of the sclera, the outer connective tissue layer surrounding most of the eye (excluding the cornea) - it forms the visible white part of the eye

Answer 129

Necrotising scleritis --> *can lead to perforation of the sclera* (perforation of sclera can lead to infection, vision loss (due to damage to cornea or retina), and sometimes loss of the eye)

Answer 130

1. Idiopathic (no clear cause) 2. Underlying systemic inflammatory conditions 3. Less commonly, infection (e.g., Pseudomonas or Staphylococcus aureus) . - more common in women

Answer 131

- Rheumatoid arthritis - Vasculitis (particularly granulomatosis with polyangiitis)

Answer 132

The connective tissue of the sclera is similar to joint connective tissue, so it may be affected by rheumatoid arthritis

Answer 133

- Scleritis --> *associated with rheumatoid arthritis & vasculitis* - Anterior uveitis --> *associated with seronegative spondyloarthropathies (e.g. ankylosing spondylitis)*

Answer 134

- Red, inflamed sclera (localised or diffuse) - Congested vessels - Severe "boring" pain - Pain with eye movement - Photophobia - Epiphora (excessive tear production) - Reduced visual acuity - Tenderness to palpation of the eye

Answer 135

- Urgent referral to ophthalmology - Screening for an underlying systemic condition (eg. RA or vasculitis) . Treatments: - NSAIDs (oral) - Steroids (topical or systemic) - Immunosuppression (appropriate to underlying systemic condition) --> *eg. methotrexate for RA*

Answer 136

Antimicrobial treatment appropriate to the infecting organism

Answer 137

A scratch or damage to the cornea --> *causes a red, painful eye and photophobia*

Answer 138

- Damaged contact lenses - Fingernails - Foreign bodies (e.g., metal fragments) - Tree branches - Makeup brushes - Entropion (inward-turning eyelid)

Answer 139

Herpes keratitis, which requires antiviral treatment

Answer 140

They may be associated with Pseudomonas infection, which can cause serious corneal damage

Answer 141

- Immediate, extensive irrigation - Urgent ophthalmology referral - *can cause severe damage and vision loss*

Answer 142

A history of trauma followed by: - Painful red eye - Photophobia - Foreign body sensation - Epiphora (excessive tear production) - Blurred vision

Answer 143

- Fluorescein staining - *yellow-orange dye collects in abrasions or ulcers, highlighting them* - Cobalt blue light - *used to enhance the fluorescein stain*

Answer 144

Usually heal over 2-3 days. - Foreign body removal (if present) - Simple analgesia (eg. paracetamol) - Lubricating eye drops - Antibiotic eye drops (e.g., chloramphenicol) - Close follow-up

Answer 145

If the abrasion is: - complicated - not healing - associated with contact lens use, chemical injury, or infection

Answer 146

- Hypromellose drops - *least viscous (lasts ~10 min)* - Polyvinyl alcohol drops - *medium viscosity* - Carbomer drops - *most viscous (lasts 30-60 min)*

Answer 147

1. Anaesthesia 2. Foreign body removal - (irrigation OR needle technique OR Jeweller's forceps OR Alger brush (if residual rust rings or iron deposits)* 3. Post-removal care - *antibx prophylaxis +/- cycloplegics +/- analgesia +/- tetanus prophylaxis* 4. Pain relief - *lubricant drops +/- oral analgesia* 5. Follow-up -*24-48hrs post-procedure*

Answer 148

Inflammation of the cornea (also referred to as a corneal ulcer)

Answer 149

- Viral infection (e.g. herpes simplex) - Bacterial infection (e.g., Pseudomonas or Staphylococcus) - Fungal infection (e.g., Candida or Aspergillus) - Contact lens-induced acute red eye (CLARE) - Exposure keratitis - *caused by inadequate eyelid coverage (e.g., ectropion)*

Answer 150

Contact lens wearer - *due to natural barrier of eye being disrupted (especially if lens hygiene is poor/wear lenses overnight)* - Pseduomonas aeruginosa

Answer 151

Herpes simplex virus (HSV) infection, also called herpes simplex keratitis - most commonly affects epithelial layer of cornea

Answer 152

- Primary infection - *often mild, may present as blepharoconjunctivitis* - Recurrent infection - *due to reactivation of latent virus in the trigeminal ganglion*

Answer 153

Trigeminal ganglion

Answer 154

Inflammation of the stromal layer of the cornea (between epithelium and endothelium), leading to: - Stromal necrosis - Vascularisation - Scarring - Risk of corneal blindness (due to above)

Answer 155

Mild symptoms of blepharoconjunctivitis (inflammation of eyelid margins and conjunctiva)

Answer 156

- Painful red eye - Photophobia - Vesicles (fluid-filled blisters) - Foreign body sensation - Watery discharge - Reduced visual acuity

Answer 157

Dendritic corneal ulcer (branching appearance)

Answer 158

- Initial management step --> *Urgent opthalmology referral* - Main treatment --> *Topical/oral antivirals (eg. aciclovir or ganciclovir)*

Answer 159

Topical steroids --> *increases herpes load and worsens condition* (eg. risk of corneal perforation)

Answer 160

Corneal scrapings for viral testing

Answer 161

Corneal transplant

Answer 162

- Hypertension - Bleeding disorders (e.g., thrombocytopenia) - Whooping cough - Medications (e.g., antiplatelets, DOACs or warfarin) - Non-accidental injury (NAI)

Answer 163

A small blood vessel within the conjunctiva ruptures, releasing blood into the space between the sclera and conjunctiva . Common triggers: - Strenuous activity (e.g. heavy coughing, weightlifting, straining from constipation) - Trauma to the eye

Answer 164

A bright red patch underneath the conjunctiva, covering the white of the eye

Answer 165

- Painless - No impact on vision - Possible history of precipitating event (e.g., coughing, heavy lifting)

Answer 166

Clinical diagnosis based on history and examination . - Check BP - *for hypertension* - Check INR - *in patients taking Warfarin*

Answer 167

No treatment required --> *it resolves spontaneously in ~2 weeks* - Lubricating eye drops can be used for mild irritation

Answer 168

when the vitreous body comes away from the retina

Answer 169

The vitreous humour becomes less firm, making it unable to maintain its shape and adhesion to the retina . (the vitreous humour is the gel inside the vitreous chamber of the eye, it maintains the structure of the eyeball and keeps the retina pressed on the choroid)

Answer 170

PVD is painless and may be asymptomatic, but can present with key symptoms such as: - Floaters - Flashing lights - Blurred vision

Answer 171

No treatment is needed - *symptoms improve as the brain adjusts*

Answer 172

PVD can predispose patients to these conditions, which can present with flashes, floaters, and vision loss (a thorough assessment of the retina should be done in these cases)

Answer 173

Separation of the neurosensory retina (photoreceptors and nerves) from the retinal pigment epithelium (base layer attached to the choroid)

Answer 174

A tear allows vitreous fluid to enter between the neurosensory retina and the retinal pigment epithelium, separating them

Answer 175

- The neurosensory retina relies on the choroid for its blood supply - Detachment can disrupt blood flow, leading to permanent photoreceptor damage

Answer 176

- Lattice degeneration (thinning of the retina) - Posterior vitreous detachment - Trauma - Diabetic retinopathy - Retinal malignancy - Family history

Answer 177

Painless condition, but key symptoms are: - Peripheral vision loss (described as a shadow coming across the vision) - Blurred or distorted vision - Flashes and floaters

Answer 178

A detailed retinal assessment to check for retinal tears or detachment --> *any suspicion of retinal detachment requires immediate ophthalmology referral*

Answer 179

Aims to create adhesions between the retina and the choroid: - Laser therapy - Cryotherapy

Answer 180

(aim is to reattach retina and reduce any traction/pressure that may cause it to detach again) 1. Vitrectomy - *removes vitreous fluid, fixes the tear, and inserts gas or oil to hold the retina in place* 2. Scleral buckle - *a silicone band is placed around the eye to push the sclera inward, reconnecting the retina (acts like a corset, squeezing the eye contents together)* 3. Pneumatic retinopexy - *a gas bubble is injected into the vitreous body to press the retina back into place (head must be positioned in a specific way for an amount of time to ensure the bubble is pressing the separated layer back into place)*

Answer 181

- Blood clot (thrombus) forms in a retinal vein - *blocking venous drainage from the retina* - Hardened arteries (atherosclerosis) can press on nearby veins, particularly where they cross - *leading to vein narrowing and potential blockage*

Answer 182

1. Central retinal vein occlusion (CRVO) - *affects the whole retina* 2. Branch retinal vein occlusion (BRVO) - *affects the area drained by the blocked branch vein* . These can further be classified as being either ischaemic or non-ischaemic: - Retinal ischaemia --> *leads to release of VEGF, resulting in new vessel development (neovascularisation)*

Answer 183

Branch retinal veins drain into the central retinal vein, which runs through the optic nerve to drain into either the superior ophthalmic vein or cavernous sinus

Answer 184

The arteries can compress the veins, leading to narrowing and increased risk of clot formation (atherosclerosis is the main cause of this)

Answer 185

1. Venous congestion in the retina 2. Increased pressure in retinal veins 3. Fluid and blood leak into retina --> *causing macular oedema and retinal haemorrhages* 4. This results in retinal damage and vision loss

Answer 186

Retinal ischaemia triggers VEGF release, leading to neovascularisation (new blood vessel growth)

Answer 187

- Hypertension - High cholesterol - Diabetes - Smoking - High plasma viscosity (e.g., myeloma) - Myeloproliferative disorders - Inflammatory conditions (e.g., SLE)

Answer 188

Painless blurred vision or vision loss

Answer 189

- BRVO --> *vision loss corresponds to the affected branch vein area* - CRVO --> *widespread vision loss* - Macular involvement (ie. branch draining macula) --> *loss of central vision*

Answer 190

"Stormy sunset": - Dilated tortuous retinal veins - Flame and blot haemorrhages - Retinal oedema - -Cotton wool spots Hard exudates

Answer 191

- Immediate referral to an ophthalmologist . Management in secondary care aims to treat macular oedema and prevent neovascularisation: 1. Anti-VEGF therapies (e.g., ranibizumab, aflibercept) --> *to reduce macular oedema* 2. Dexamethasone intravitreal implant --> *to treat macular oedema* 3. Laser photocoagulation --> *to treat neovascularisation*

Answer 192

There is an obstruction to blood flow through the central retinal artery --> *leading to ischaemia of the retina*

Answer 193

The ophthalmic artery, which is a branch of the internal carotid artery

Answer 194

- Atherosclerosis (most common) - Giant cell arteritis (GCA) - *vasculitis affecting the ophthalmic or central retinal artery reduces blood flow*

Answer 195

- Cardiovascular disease risk factors (smoking, hypertension, diabetes and raised cholesterol) --> *increases risk of atherosclerosis* - GCA risk factors - *white ethnicity, older age, female and polymyalgia rheumatica*

Answer 196

Sudden painless loss of vision, often described as a "curtain coming down" over vision

Answer 197

Relative afferent pupillary defect (RAPD) - *the affected pupil constricts less when light is shone directly in it compared to when light is shone in the unaffected eye*

Answer 198

- Pale retina - *due to ischaemia and lack of perfusion* - Cherry red spot - *at the fovea, where the thinner surface allows the red choroid to be seen*

Answer 199

Temporary loss of vision due temporary interuption to the blood supply - *usually caused by an embolus or due to carotid artery disease)*

Answer 200

- Retinal detachment - Central retinal artery occlusion - Central retinal vein occlusion - Vitreous haemorrhage (e.g., due to diabetic retinopathy)

Answer 201

GCA is a potentially reversible cause: - Investigations - *ESR blood test (inflammation) and temporal artery biopsy* . - Treatment - *high-dose systemic steroids (eg. prednisolone), to prevent further vision loss*

Answer 202

Immediate referral to ophthalmology, as it is a vision-threatening emergency

Answer 203

- Ocular massage - *to move the embolus* - Anterior chamber paracentesis - *removing fluid from the anterior chamber to reduce the IOP* - Inhaled carbogen (5% CO₂, 95% O₂) - *to dilate the artery* - Sublingual isosorbide dinitrate - *to dilate the artery* - Oral pentoxifylline - *to dilate the artery* - IV acetazolamide - *to reduce IOP* - IV mannitol - *to reduce IOP* - Topical timolol - *to reduce IOP*

Answer 204

- Identify and treat reversible risk factors - Secondary prevention of cardiovascular disease --> *e.g. managing BP, lipids, and diabetes*

Answer 205

A genetic condition causing progressive degeneration of the photoreceptors in the retina - *rods are affected more than cones*

Answer 206

- Rods are responsible for night vision and peripheral vision --> *degeneration leads to night blindness and peripheral vision loss*

Answer 207

- It can occur in isolation or as part of systemic diseases - Different genetic mutations affect the age of onset and disease progression

Answer 208

- Night blindness (often the first symptom) - Peripheral vision loss (before central vision is affected) --> *progressing to tunnel vision and potentially total blindness*

Answer 209

Currently there are no treatment options to slow the disease process. . - Ophthalmology referral for assessment and follow-up - Genetic counselling - Vision aids - Sunglasses to reduce retinal damage - Driving limitations - *patients should inform the DVLA*

Answer 210

- Bone-spicule pigmentation (sharp, pointed pigment resembling bone matrix) - Mid-peripheral pigment deposits - Narrowing of arterioles - Waxy or pale optic disc

Answer 211

- Usher syndrome - *associated with hearing loss* - Bassen-Kornzweig syndrome - *associated with progressive neurological impairments* - Refsum disease - *associated with peripheral neuropathy, hearing loss, and ichthyosis (scaly skin)*

Answer 212

Double vision - *the images on the retina do not match*

Answer 213

- The brain suppresses signals from the less dominant eye --> *leading to a “lazy eye" (ie. person has one dominant eye they use to see, and one eye they ignore)* - If untreated, the "lazy eye" becomes progressively more disconnected from the brain and over time the problem becomes worse --> *this is called amblyopia*

Answer 214

- Concomitant squint - *due to differences in the control of the extra-ocular muscles (severity of squint can vary)* - Paralytic squint (rare) - *due to paralysis in one or more of the extra ocular muscles*

Answer 215

Misalignment of the eyes

Answer 216

the affected eye becomes passive and has reduced function compared to the other dominant eye

Answer 217

- Esotropia - *eye deviates inward (towards the nose)* - Exotropia - *eye deviates outward (towards the ear)* - Hypertropia - *eye deviates upward* - Hypotropia - *eye deviates downward*

Answer 218

- Idiopathic (most common in healthy children) - Neurological conditions (e.g., hydrocephalus, cerebral palsy) - Space-occupying lesions (e.g., retinoblastoma) - Trauma

Answer 219

- Shine a pen-torch at the patient from 1 metre away - Observe the corneal light reflex . - Central and symmetrical reflection = normal - Deviation from centre = indicates a squint

Answer 220

1. Cover one eye while the patient fixates on an object in front of them 2. Move the cover to the opposite eye and observe the previously covered eye: - Moves inward --> *had drifted outward when covered (exotropia)* - Moves outward --> *had drifted inward when covered (esotropia)*

Answer 221

The visual fields are still developing --> *early intervention prevents permanent squint*

Answer 222

1. 1st-line --> Occlusive patch over the good eye to force weaker eye to develop 2. Atropine eye drops in good/dominant eye --> causes blurred vision (dilates eye), again forcing the weaker eye to develop . other things to consider: - treat underlying pathology (eg. cataracts) - corrective lenses for refractive errors

Answer 223

- Manifest squint (heterotropia) - *where the eyes are visibly misaligned when the eyes are open and being used* - Latent squint (heterophoria) - *eyes are misaligned when eyes are closed or covered, but appear normal when open*

Answer 224

- distant objects seen more clearly than near ones - *because light focuses behind the retina rather than directly on it* - the eye is too short, or the cornea/lens is too flat, leading to insufficient focusing power

Answer 225

- near objects are seen more clearly than distant ones - *because light focuses in front of the retina* - eye is too long, or the cornea/lens is too steep, leading to excessive focusing power

Answer 226

Glasses OR Contact lenses: - Hyperopia - Convex (plus) lenses are used to help focus light onto the retina - Myopia - Concave (minus) lenses are used to diverge light, allowing it to focus on the retina . (Surgery: LASIK reshapes cornea to increase (hyperopia) or decrease (myopia) curvature

Answer 227

Hypermetropic eyes often have a shallow anterior chamber and narrow drainage angles, increasing the likelihood of angle closure.

Answer 228

- A pseudosquint (also known as pseudostrabismus) refers to the appearance of a squint (strabismus) when the eyes are actually properly aligned - This condition is typically caused by facial or structural features around the eyes rather than an actual misalignment - It is common in children and does not require treatment. . - causes: wide nasal bridge (this is why corneal light reflex is an important test for strabismus (squint)

OPHTHAL - clinical Flashcards

(252 cards)