Opthalmology Flashcards

1
Q

Myopia?

Ass with?

A

Short sightness

Increased risk of retinal detachment

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2
Q

Hypermetropia?

Ass with?

A

Long sightness

Increased risk of angle-closure glaucoma

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3
Q

Amblyopia

  1. def
  2. occurrence at which age group
  3. causes (5)
  4. treatment
A
  1. Lazy eye, defective visual acuity in one eye (or rarely, both eyes) which persists after correction of refractive error and removal of any pathological obstacle to vision
  2. Can only develop during the critical period 
(upto approx. 8yrs old)
    3.
    Strabismic – manifest squint
    Anisometropic - unequal refractive error
    Stimulus deprivation. e.g. ptosis, cataract
    Meridional – astigmatism
    Ammetropic - bilateral high refractive error
  3. eye patch the healthy eye for certain hours each day
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4
Q

History

4 visual disturbances?
3 relavent FHx?
2 relavent SHx?

A
  • Floaters
  • Flashing light
  • Shadows
  • Glare
  • Diabetes
  • Hypertension
  • Vascular disorder
  • Smoking
  • Alcohol
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5
Q

Diplopia

def?
treatment?

A

double vision

  1. Covering or closing one eye
  2. Head posture (repositioning head to avoid looking in the direction of double vision)
  3. Stick-on Prisms
    Can only really help with diplopia occurring looking straight ahead
    Small prisms can be incorporated into glasses prescription if symptoms stabilise
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6
Q

Examination

A
  1. Central vision

I. Snellen chart (both aided and unaided)
- test of visual acuity
- normally carried out at 6m
- results given as a fraction, nominator is the distance from the chart, and denominator is distance at which a person with normal visual acuity sees it (6/10: patient 6m away, can only lead the 10m line)
II. if not count fingers (CF)
III. if not see hand move (HM)
IV. if not perceive light (PL)

  1. Peripheral vision

confrontational field testing

  1. Look

I. Eyelids
- Should be examined for malposition (entropion, ectropion, ptosis)
- Eversion of the upper eyelid - to look for follicles, lumps, and foreign bodies
- Lash line
II. Conjunctiva, Cornea and Sclera
- use fluorescein staining - this causes yellow staining of an epithelial defect such as an ulcer or abrasion which is more apparent under a blue light
- Corneal sensation (mediated by the trigeminal nerve) - tested by touching a fine wisp of cotton wool on the cornea and checking for a blink reflex (mediated by the facial nerve)
III. anterior chamber
- Check for blood and pus
IV. Pupil
- Abnormal pupil shape
- Anisocoria (>4mm difference in pupil size)

  1. Reflexes

I. Direct light reflex
II. Consensual light reflex
III. Swinging Torchlight test
- tests for relative afferent papillary defect (RAPD): stronger consensual reflex than direct
IV. accommodation reflex: stare at distant, then focus on my finger

  1. Ocular move
  2. Lateral rectus CNVI
  3. Medial rectus CNIII
  4. Superior rectus CNIII
  5. Inferior rectus CNIII
  6. Superior Oblique CNIV (nasal-inferior move)
  7. Inferior Oblique CNIII (nasal-superior move)
  8. Levator palpebrae superioris CNIII
  9. opthalmoscopy
    - The pupils need to be dilated using Tropicamide 1%. This can be combined with Phenylephrine 2.5% for a larger pupil dilatation and better peripheral retinal examination.
    - red reflex at 15cm
    - the right eye of the examiner is used to view the right eye of the patient and vice versa.
    - disc
    - macula
    - peripheral fundus
  10. Colour vision
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7
Q

Causes of a RAPD:

A
  1. Optic neuritis
  2. Optic atrophy
  3. Papillitis
  4. Retinal detachments
  5. Central retinal artery occlusion
  6. Widespread retinal disease
  7. Optic nerve compression
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8
Q

Opthalmoscopy exam

A
I. The Disc 
is examined for:
- Size
- Colour
- Swelling
- Cupping - cup:disc ratio
II. The Macula
- is situated 2 disc diameters temporal to the optic disc. - In young individuals it has a bright foveal light reflex. 
It should be examined for:
-Haemorrhage
- Exudate
- Pigment stippling
- Loss of the foveal light reflex
III. The Peripheral fundus 
Should be examined for:
- Haemorrhage
- Exudates
- Pigmentation
- Calibre of blood vessels
- New Vessels
- Lesions etc.
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9
Q

Entropion
Ectropion
Ptosis

A

lower eyelid folding inwards
lower eyelid folding outwards
upper eyelid droopy

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10
Q

Differentials for red eye (7)

A
  1. Lids
    - Blepharitis
    - Chalazion
    - Malposition
  2. Conjunctiva
    - Conjunctivitis
  3. Sclera
    - Episcleritis
    - Scleritis
  4. Cornea
    - Keratitis
  5. Uveal Tract
    - Uveitis
  6. Trabecular Meshwork
    - Acute Glaucoma
  7. Periorbital Skin
    - Preseptal cellulitis
    - Orbital cellulitis
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11
Q

Lid disorders

I. Blepharitis

  1. cause?
  2. history findings? (3)
  3. examination findings? 2

II. Chalazion

  1. def
  2. cause
  3. occurs most commonly in?
  4. treatment? 3

III. Entropion

  1. Def?
  2. Causes

IV. Ectropion

  1. def?
  2. causes?
A

I. Blepharitis

  1. It is usually a combination of:
    - Infection of the lid margins by staphylococcal bacteria
    - Overproduction of sebum by the glands at the lid margin
  2. Patients present with a history of:
    - Chronic ocular irritation
    - Watery eye
    - Red eye
  3. On examination there is:
    - crusting and scaling of the lash line
    - careful examination can demonstrate plugs of sebum in the meibomian gland orifices.
    —————————————–
    II. Chalazion
  4. Chalazion - a meibomian cyst (lipogranuloma)
  5. . caused by meibomian gland dysfunction.
  6. . It occurs with increased frequency in patients with acne rosacea and seborrhoeic dermatitis.
  7. ## . initially with hot spoon bathing and antibiotics but often chalazia require surgical incision and curettage.III. Entropion
  8. Turning inwards of the lid margin, can affect the upper or lower eyelid , leading to eyelashes causing corneal abrasions
    • Ageing (involuntional)
    • Conjunctival scarring (cicatricial)
        • Trachoma
        • Stevens-Johnson syndrome
        • Ocular pemphigoid
    • ## Acute spastic entropion - spasm of orbicularis muscleIV. Ectropion
  9. Turning outwards of the lid margins, almost always affects the lower eyelid, exposed conjunctiva may become inflamed, scarred and keratinised.
    • Ageing (involuntional)
    • Conjunctival scarring (cicatricial)
    • Paralytic - Facial nerve palsy
    • Mechanical - caused by large lower lid tumours
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12
Q

I. Sebum?

II. Meibum?

A

I.

  • Microscopic exocrine glands in the skin secrete an oily or waxy matter, called sebum,
  • to lubricate and waterproof the skin and hair of mammals

II.

  • gland at the rim of the eyelids inside the tarsal plate, supply meibum,
  • an oily substance that prevents evaporation of the eye’s tear film.
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13
Q

Conjunctiva

I. Bacterial conjunctivitis

  1. Symptoms (4)
  2. Pathogens (3)
  3. Management? (2)

II. Viral Conjunctivitis

  1. Symptoms (4)
  2. Examination (3)
  3. Pathogens (2)
  4. Management? (4)

III. Adult inclusion conjunctivitis

  1. Symptoms (1)
  2. Examination (3)
  3. Treatment (2)

IV. Allergic Conjunctivitis

  1. 2 types
  2. Symptoms (4)
  3. Examination (4)
  4. treatments (5)

V. Vernal keratoconjunctivitis

  1. age
  2. course
  3. ass with
  4. Sx
  5. treatment

VI. Atopic keratoconjunctivitis

  1. age
  2. ass with
  3. Sx
  4. treatment

VII. Neonatal Conjunctivitis (Ophthalmia Neonatorum)

  1. age
  2. secondary to?

VIII. Iatrogenic conjunctivitis

A

I. Bacterial Conjunctivitis

  1. Sx:
    - Red eye
    - Eyelids stuck together
    - Minimal pain
    - Purulent discharge
    • staphylococcal aureus
    • staphylococcal epidermidis
    • streptococcus pneumoniae.
  2. Management
    - although often a spontaneously resolving condition
    - is usually via broad spectrum topical antibiotics such as chloramphenicol or fucithalmic acid.
    - ————————————

II. Viral Conjunctivitis

  1. Sx:
    - Red eye
    - Watery discharge
    - Usually bilateral
    - Often preceding coryzal symptoms
  2. Ex
    - Conjunctival follicles
    - preauricular lymph nodes
    - Keratitis
    • Adenovirus (different serotypes)
    • Herpes Simplex Virus (HSV-1)
    • resolves over 2 weeks, although symptoms of irritation and discomfort may persist for months.
    • Lubricants - can be used for comfort
    • Antibiotics (chloramphenicol) - to prevent secondary bacterial infection
    • Topical Aciclovir (Zovirax) drops - if HSV-1 has been isolated
    • ## Topical steroid drops - should only be used under ophthalmological supervision, and only if the inflammation is very severe.III. Adult inclusion conjunctivitis
  3. Sx
    - Unilateral mucopurulent discharge
  4. Ex:
    - Large conjunctival follicles
    - Preauricular lymphadenopathy
    - Subepithelial corneal deposits
  5. Treatment:
    - Topical erythromycin ointment - 2 weeks
    - Referral to GUM clinic for one of the following systemic antibiotic treatment:
    - - - Azithromycin single dose
    - - - Doxycycline
    ——————————————-
    IV.Allergic Conjunctivitis
    • Seasonal allergic rhinoconjunctivitis (allergen most commonly pollen with onset of ‘hayfever’ in summer months)
    • Perennial allergic rhinoconjunctivitis (allergen such as house dust mite may cause symptoms throughout year)
  6. Sx
    - Rapid onset
    - Itching
    - Red eye
    - Often in children following exposure to an allergen usually pollen
  7. Ex
    - Usually bilateral
    - Conjunctival papillae (Giant cobblestone papillae)
    - Conjunctival Chemosis (Oedema)
    - Preauricular lymphadenopathy
  8. treatment:
    - Topical Antihistamine - e.g: levocabastine
    - Topical Mast Cell Stabiliser - e.g: Sodium cromoglycate
    - Combination of both antihistamine & mast cell stabiliser - e.g. olopatadine
    - Systemic antihistamines
    - Topcial steroid use under ophthalmological supervision
    - —————————————-

V. Vernal keratoconjunctivitis

  1. occurs in children
  2. seasonal (warm months)
  3. associated with family history of atopy (asthma, rhinitis, dermatitis)
  4. bilateral, ulceration and infiltration of upper cornea
  5. Treatment:
    Chronic conjunctivitis treatment is similar to that of acute conjunctivitis, but the use of topical and oral steroids is required more often.
    ——————————————-
    VI. Atopic keratoconjunctivitis
  6. occurs in adults
  7. associated with atopy
  8. bilateral, can also cause corneal ulceration and scarring
  9. Treatment:
    Chronic conjunctivitis treatment is similar to that of acute conjunctivitis, but the use of topical and oral steroids is required more often.
    ——————————————
    VII. Neonatal Conjunctivitis (Ophthalmia Neonatorum)

Occurs in newborns
Usually infectious secondary to N. gonorrhoeae or Chlamydia. trachomatis
—————————————
VIII. Iatrogenic conjunctivitis

It should always be remembered that that the drops prescribed to patients can cause ocular irritation and red eye, which may necessitate cessation of the medication.

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14
Q

Chlamydial Conjunctivits serotypes and what they cause

A
  • Serotypes A-C cause Trachoma (a chronic conjunctivitis, endemic to Africa and Asia)
  • Serotypes D-K cause Adult inclusion conjunctivitis
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15
Q

Follicles vs papillae?

Main causes?

A

Follicles

  • Significant diagnostic importance
  • Hyperplasia of lymphoid tissue
  • Translucent avascular mounds of plasma cells and lymphocytes
  • Each follicle is encircled by a small blood vessel
  • Main causes include:
  • –Viral infections including HSV
  • –Chlamydial infections

Papillae

  • Non-specific and of less diagnostic value
  • Hyperplastic conjunctival epithelium thrown into numerous folds
  • Central vascular tuft
  • Can be large - cobblestone or giant
  • Main causes include:
  • —Non-specific: can be seen in any conjunctival irritation or conjunctivitis
  • —Allergic conjunctivitis
  • —Bacterial infection
  • —Contact lens related problems
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16
Q

2 types of chronic conjunctivitis

A

Chronic Conjunctivitis

  • Both ‘vernal’ and ‘atopic’ keratoconjunctivitis are within a spectrum of chronic allergic conjunctivitis.
  • Both result from repeated exposure to an allergen. Symptoms include itching, burning as well as red eye.
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17
Q

Episcleritis

  1. pattern
  2. Sx (2)
  3. Ex (1)
  4. Treatment (3)
A
  1. The condition of episcleritits is common, self-limiting, frequently recurrent and occasionally there is an underlying systemic disorder.
  2. Sx:
    - Mild discomfort
    - Epiphora (watering)
  3. Ex
    - Unilateral redness
  4. Treatment:
    - Observation
    - Simple lubricants - usually sufficient for most cases
    - Oral NSAIDS
    - Topical steroids - may be required in persistent cases
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18
Q

Scleritis

  1. epi
  2. Sx 2
  3. def
  4. aetology (-)
  5. sign (1)
  6. treatment (2)
A
  1. Scleritis is much less common than episcleritis but is far more serious.
    • extremely painful and often wakes the patient at night.
    • Localised or Generalised redness
      3.
    • It is characterised by cellular infiltration of the entire thickness of the sclera.
    • Scleritis is frequently part of a general inflammatory reaction associated with a system immune-mediated collagen vascular disease.
    • Inflammation of the sclera can progress to ischaemic and necrosis, eventually leading to scleral thinning and perforation of the globe.
    • It covers a spectrum of disease, ranging from self-limiting episodes of inflammation to necrotisation of the sclera and potential loss of vision.
  2. Aetiology:
    - Systemic associations
    - Wegeners Granulomatosis
    - Rheumatoid Arthritis
    - Polyarteritis Nodosa
    - Infections
    - Secondary to corneal ulcers - often pseudomonas aeruginosa
    - Post ocular surgery
  3. sign
    Scleral necrosis and thinning
  4. treatment
    - Oral Prednisolone
    - Immunosuppressive agents, e.g. mycophenolate mofetil (cellcept) or azathioprine
19
Q

Keratitis

  1. Def?

I. Bacterial keratitis

  1. RFs?
  2. Symptoms? (2)
  3. Examination (2)
  4. Pathogens? (4)
  5. Treatment (4)

II. Viral Keratitis (HERPES SIMPLEX VIRUS)

  1. course
  2. Symptoms & signs 3

III. Viral Keratitis (HERPES ZOSTER OPHTHALMICUS)

  1. cause
  2. complications
  3. sequel
  4. management 2

IV. Viral Keratitis (ADENOVIRUS)

  1. adenospots
  2. symptoms
  3. treatment

V. Fungal keratitis

  1. pathogens (2)
  2. symptoms (4)
  3. examination (5)
A

I. Bacterial keratitis

  1. Risk Factors:
    - Contact lens wear
    - Trauma
    - Compromised ocular surface, e.g. dry eye or blepharitis
    - Corneal exposure, e.g. facial nerve palsy
    - Immunosuppresion, e.g. topical steroid use
  2. Sx
    - Purulent conjunctivitis
    - Reduced vision
  3. Ex
    - Corneal ulcer / opacity
    - Hypopyon (white cells in the anterior chamber)
  4. Common causative organisms:
    - Pseudomonas aeruginosa - causes aggressive infections
    - Staphylococcus epidermidis
    - Sterptococcos pneumoniae
    - Haemophilus influenzae
  5. Treatment:
    - Corneal Scrape - should always be taken and sent for M,C & S
    - Broad spectrum topical Antibiotics, e.g: Ofloxacin. - initially every hour day and night.
    - Topical Steroid therapy - should only be undertaken under ophthalmological supervision. Can be given to help with scarring and necrosis.
    - ——————————————

II. Viral Keratitis (HERPES SIMPLEX VIRUS)

    • Primary infection usually occurs in childhood.
    • It is caused by direct transmission of virus through infected HSV secretions.
    • Primary infection is usually subclinical.
    • Following initial infection, the HSV virus lies dormant within the trigeminal ganglion.
    • A recurrent epithelial keratitis is then caused by reactivation of the latent virus and invasion of the corneal epithelium.
    • Painful red eye
    • Dendritic ulcer - which may develop into a Geographic ulcer
    • Decreased corneal sensation

III. HERPES ZOSTER OPHTHALMICUS

    • AKA Shingles
    • caused by the varicella-zoster virus (VZV).
    • Herpes Zoster Ophthalmicus (HZO) accounts for approximately 10% of shingles with infection of the T10 (umbilical) dermatome being more common.
    • Primary infection usually occurs in childhood in the form of chicken pox.
    • Secondary infection (shingles) is caused by reactivation of latent VZV within the trigeminal ganglion. - It usually affects the skin causing a cellulitis but may also result in infection of any ocular structure.
  1. Ocular complications:
    - Conjunctivitis
    - Keratitis
    - Iritis
    - Scleritis
    - Secondary glaucoma
    - Cranial nerve palsies
    - Retinitis
  2. Sequelae:
    - Post herpetic neuralgia
    - Recurrent Keratitis
  3. Management:
    - Oral Aciclovir (zovirax) - reduces duration & severity of disease as well as post herpetic neuralgia
    - Topical Steroids - often used for ocular inflammation
    - —————————————

IV. ADENOVIRUS

  1. a keratitis can develop which consists of multiple faint subepithelial white deposits (Adenospots).
  2. Sx
    - blurring of vision
    - glare
    - the lesions may persist following resolution of the conjunctivitis.
  3. treatment
    - The Adenospots often spontaneously resolve
    - but occasionally topical steroids can be utilised to speed up resolution.
    - —————————

V. Fungal keratitis

  1. Common pathogens:
    - Filamentous fungi - e.g: Aspergillus, Fusarium
    - Candida Albicans
  2. Symptoms:
    - Red eye
    - Photophobia
    - Blurred vision
    - Discharge
  3. Signs:
    - Filamentous fungi
    - Greyish stromal infiltrate
    - Surrounding satellite infiltrates
    - Hypopyon
    - Candida
    - ——–Yellow-white ulcer similar to a bacterial keratitis picture
  4. Management:
    - Topical antifungal agents e.g: Natamycin, Amphotericin
    - Corneal graft - in unresponsive cases
20
Q

Acanthamoeba keratitis

  1. caused by? where is it found?
  2. signs?
A
  1. Acanthamoeba is a hardy protozoan organism which is ubiquitous within the environment, particularly in water.
  2. signs
    - Red eye
    - Dendritiform epithelial lesions
    - Non-suppurative ring with variable epithelial breakdown (established cases)
21
Q

Uveitis

  1. def
  2. classification (3)
  3. Aetiology (5)
  4. Sx? (4)
  5. Examination (3)
  6. treatment (2)
A
  1. defined as inflammation of the uveal tract which includes the iris, ciliary body and the choroids.
  2. Uveitis can be sub-classfied into:
    - — Anterior Uveitis (Iritis) - inflammation of the iris and anterior chamber
    - — Intermediate Uveitis - inflammation localised to the vitreous and peripheral retina
    - — Posterior Uveitis - inflammation of the posterior part of the uveal tract and overlying retina
  3. Aetiology
  4. Idiopathic
  5. HLA-B27 associated arthropathies
  6. Infectious
    - Syphilis
    - Tuberculosis
    - Herpes Simplex / Zoster
  7. Sarcoidosis
  8. Juvenile Idiopathic Arthritis
  9. Sx
    - Photophobia
    - Red eye
    - Pain
    - Blurred vision
  10. Ex
    - Circumcorneal injection (redness)
    - Keratic precipitates (KPs) - clumps of cells on the corneal endothelium
    - Posterior synechiae - adhesions between the lens and iris
    - flare(dusty beam projector)
  11. Treatment:
    - Topical steroid drops - e.g: Prednisolone
    - Dilating drop (mydriatic) - e.g: Cyclopentolate (to try and prevent posterior synechiae formation and ease pain by inhibiting accommodation)
22
Q

HLA-B27 related causes?

A

(remember the pneumonic PUBCAR):

Psoriatic Arthritis

Ulcerative Colitis

Behcets

Crohn’s disease

Ankylosing Spondylitis

Reiter Syndrome

23
Q

Glaucoma

  1. Cause/pathology
  2. RFs?
  3. Prodrome?
  4. Sx?
  5. signs?
  6. treatment
A
    • Within an anatomically normal eye, aqueous humour is produced by the ciliary body. It then bathes the lens and passes through the pupil and drains via the trabecular meshwork.
    • Angle closure glaucoma is caused by the obstruction of aqueous outflow with a subsequent acute rise in intraocular pressure (40-80mmHg).
    • As we get older, the globe becomes smaller and the lens enlarges.
    • In certain individuals this leads to apposition of the lens to the back of the iris, thus preventing flow of aqueous humour from the posterior to the anterior chamber.
    • Aqueous then collects behind the iris and pushes it onto the trabecular meshwork preventing drainage of aqueous from the eye.
  1. Risk Factors:
    - Elderly
    - Female
    - Hypermetropic
    - Family History
  2. Prodrome:
    - Haloes
    - Red eye
    - Nausea
    - Eye pain
  3. And subsequently:
    - Vomiting
    - Photophobia
    - Visual loss
  4. Signs:
    - Red eye
    - Corneal oedema (hazy)
    - Fixed semi-dilated pupil
    - Shallow anterior chamber
    - Visual loss
  5. Treatment:
    I. Medical - lower intraocular pressure
    - IV acetazolamide (diamox)
    - Beta Blockers (topical)
    - Pilocarpine (topical) - to both eyes to try and prevent an attack in the fellow eye.
    II. Surgical - reverse pathology
    - Laser iridotomy
    - Trabeculectomy
24
Q

Periorbital Skin

I. ORBITAL CELLULITIS

  1. Sx
  2. sign
  3. on admition

II. PRESEPTAL CELLULITIS

  1. Sx
  2. sign
  3. Treatment
A

Orbital cellulitis is usually associated with infection of the paranasal sinuses.

I. ORBITAL CELLULITIS

  1. Sx:
    - Decreased Vision
    - Unwell patient
  2. Signs:
    - Unilateral swollen eyelids
    - Decreased Eye Movements (Ophthalmoplegia)
    - Proptosis
    Admission
    - CT scan
    - Intravenous antibiotics
    ————————————
    II. PRESEPTAL CELLULITIS
  3. Sx?
    - Swelling
    - No Decreased Vision
  4. signs?
    - Proptosis
    - Decrease in eye movements
  5. Treatment:
    Broad spectrum oral antibiotics
25
Q

Retinal Vein Occlusion

  1. which veins?
  2. sx?
  3. signs?
  4. complication?
  5. aetiology?
  6. treatment
A
  1. Vein occlusions can affect the central retinal vein (CRVO) or a branch (BRVO). They are caused by a thrombosis within the vessel lumen.
    2.symptoms
    - Painless loss of vision (varying from 6/9 to hand movements, depending on amount of retina involved)
  2. Signs:
    - Possible RAPD
    - Fundoscopy:
    - Dot/Blot haemorrhages
    - Cotton Wool Spots
    - Swollen optic disc
    - Macular oedema
    Note: in a BRVO signs are confined to the area of retina served by the blocked vein.
  3. complication
    - Macular oedema
    - Neovascularisation (new vessels) of the iris and retina
  4. Aetiology:
    -Idiopathic
    -Hypertension - artery compresses vein at arteriovenous crossing
    -Inflammatory causes:
    —-Sarcoidosis
    —-Lyme disease
    - Thrombophilic tendency (clotting tendency)
    —-Hyperviscosity states, e.g: Protein S def, Protein C def.
    —-Smoking
    —-Oral contraceptive pill
    —-Pregnancy
    —-Tumours
  5. Treatment:
    - Macular oedema: - laser treatment to reduce oedema can be successful
    - Neovascularisation: - laser of ischaemic areas can reverse new vessel formation
26
Q

Retinal Artery Occlusion

  1. which arteries?
  2. aetiology
  3. symps and signs?
  4. Rfs?
  5. treatment?
A

As with vein occlusions, artery occlusions can affect the central retinal artery (CRAO) or a branch (BRAO).
2. embolisation from the carotid artery. If the embolus passes through the retinal vasculature, the patient may only complain of transient loss of vision - Amaurosis Fugax.
3.
- Painless loss of vision
- possible RAPD
- Fundoscopy:
—-Retinal pallor
—-Cherry red spot - a red spot may be seen at the macular where the retina is thinner and the unaffected choroidal vasculature is seen.
—Emboli - may be seen
Note: in a BRAO signs are confined to the area of retina served by the blocked vein.
4.RF?
- Diabetes
- ischaemic heart disease
- peripheral vascular disease
- a history of smoking
- giant cell (temporal) arteritis should always be ruled out.
5. Treatment:
- Patients are often prescribed low dose Aspirin and sent for a carotid ultrasound.
- Although there is no proven treatment to restore vision, clinicians often attempt to acutely drop the intraocular pressure within the first 2 hours to attempt to reverse the occlusive event. This is attempted using ocular massage, anterior chamber paracentesis and/or intravenous acetazolamide.

27
Q

Amaurosis Fugax.

A

transient loss of vision

28
Q

Visual field defects

I. Homonymous Hemianopia
II. Quadrantanopia
III. Bitemporal hemianopia
1.  def
2. causes
IV. Altitudinal visual field defects
1. def
2. aetiology
A

I. Homonymous Hemianopia

  • loss of vision on the same side in both eyes
  • Lesion of the optic radiation e.g: stroke as it approaches the occipital cortex can lead to homonymous hemianopia.

II. Quadrantanopia

III. Bitemporal hemianopia

  1. Bilateral hemianopia is a loss of temporal field vision in both eyes, which is caused by a lesion that affects the optic chiasm and damages fibres from the nasal halves of the retina as they decussate.
  2. The most common causes are:
    - Pituitary tumour
    - Craniopharyngioma
    - ————————————–

IV. Altitudinal visual field defects

  1. A visual field that shows loss of all or part of the superior half or the inferior half of the visual field of one or both eyes, and which respects the horizontal meridian.
  2. Aetiology:
    - Retinal causes - BRVO, BRAO
    - Optic nerve causes - Arteritic/Non-arteritic ischaemic optic neuropathy, Papilloedema
    - Lesions in the cerebral cortex
29
Q

2 factors responsible for loss of visual acuity with ageing?

A

cataract and macular degeneration

30
Q

Types of cataracts?

A
  1. Nucleosclerotic
  2. Cortical
  3. Posterior sub-capsular (this affects driving at night, and reading)

(see anatomy of lens)

31
Q

2 types of glycauma?

Triad of symptoms?

A
  1. primary open angle
  2. secondary angle closure
  • Increased IOP (>21mmHg)
  • increased cup:disc ratio
  • loss of visual field
32
Q

Why ageing increases the susceptibility to Glaucoma?

How open angle glaucoma is turned into close angle?

A
  • Within an anatomically normal eye, aqueous humour is produced by the ciliary body. It then bathes the lens and passes through the pupil and drains via the trabecular meshwork.
  • Angle closure glaucoma is caused by the obstruction of aqueous outflow with a subsequent acute rise in intraocular pressure (40-80mmHg).
  • As we get older, the globe becomes smaller and the lens enlarges.
  • In certain individuals this leads to apposition of the lens to the back of the iris, thus preventing flow of aqueous humour from the posterior to the anterior chamber.
  • Aqueous then collects behind the iris and pushes it onto the trabecular meshwork preventing drainage of aqueous from the eye.
33
Q

A patient presents with a red eye that is not reactive to light:

a. pupil is dilated
b. pupil is constricted

What is the likely diagnosis?

A

a. close angle glaucoma

b. iritis

34
Q

Age related macular degeneration (AMRD)

  1. 2 types
  2. Pathology
  3. 2 types of dry?
  4. what makes wet? how treated?
A
1. 
I.DRY ARMD
Progresses slowly
Moderate visual loss
Not treatable
II. WET ARMD
Progresses quickly
Severe visual loss
Sometimes treatable
  1. hyaline deposit between Bruch’s membrane and choroid prevents blood supply to fovea
  2. I. Drusen:
    - vision 6/12

II. Atrophy:

  • vision 6/60
  • either central or geographical
    • neovascularisation
    • anti-VEGF medication (ranibizumab)
    • pan photo-coagulation
35
Q

How to tell if someone is short or long sighted from their glasses?

A
  • magnified eyes in long-sighted

- smaller eyes in short

36
Q

Hyphaema?

A

pooling or collection of blood inside the anterior chamber of the eye (the space between the cornea and the iris)

37
Q

Papilloedema

A

optic disc swelling in presence of raised intracranial pressure

38
Q

Causes of floaters/flashes?

A
  1. Posterior vitrous detachment (PVD)
    Common in trauma/myopia
    can lead to retinal detatchment
  2. Retinal detachment
    treated with virterectomy (elderly) and scleral buckle (younger)
39
Q

LR6 SO4

A

lesion in lateral rectus -> CNVI
lesion on superior oblique -> CNIV
lesion in everything else -> CNIII

40
Q

Diabetic retinopathy

  1. pathology?
  2. classification
  3. investigation
  4. treatment?
A
1. 
increased glucose -> ROS -> increased viscosity and reduced red cell deformity -> basement membrane thickening -> EC proliferation/bleeding
2. 
I. Background
- micro-aneurysm 
- Exudate
- Dot haemorrhage
II. Pre-proliferative 
 More extensive ischaemic changes
- venous dilatation 
- venous bleeding
- multiple cotton wool spots (>5) (micro infarcts of retina)
III. Proliferative
- new vessel on the optic disc (NVD)
- new vessels elsewhere (NVE)
- rubeosis iridis: neovascularisation of the iris. May obstruct drainage of aqueous humour resulting in 'neovascular glaucoma
- needs pan photocoagulation, if not treated tractional retinal detachment

—> note : all can be with or without maculopathy

  1. Fluorescein Angiography
    - assessing ischaemia
    - localising leakage
  2. Laser to solve:
    a. maculopathy - closure of leaking vessels (stimulation of RPE pump activity – reducing oedema)
    b. proliferative disease - destroy ischaemic retina, decrease angiogenic growth factors
41
Q

Micro and macrovascular complications of diabetes?

A
Micro:
- eye 
- kidneys
Macro:
- peripheral neuropathy
- cardiac problems
- ulcers
42
Q

Maculopathy

  • Def
  • 3 different types (complication of diabetic retinopathy)
A
  • Clinically Significant Macular Oedema
  1. Focal maculopathy.
    - There is focal leakage from a microaneurysm or dilated capillaries.
    - Exudates are seen, often in rings around the leaking microvasculature (circinate exudates).
  2. Diffuse maculopthy
    - refers to diffuse retinal oedema as a result of leakage from microvasculature at the posterior pole of the eye
  3. Ischaemic maculopathy
    - results from closure of the perifoveal microvasculature.
    - It is confirmed with fluorescein angiography.
43
Q

3 different types of laser for diabetic retinopathy?

A

absorbtion of high energy light by RPE produces thermal burn to RPE and retina

  1. Focal
  2. Grid
  3. Panretinal photocoagulation (PRP)
44
Q

Squint

  1. aka?
  2. 2 main types
  3. directions
  4. test for presence of manifest squint
  5. test for presence of latent squint
  6. most common cause in children
  7. 4 causes in adults
A
  1. strabismus
  2. I. (hyper/hypo/exo/eso) -tropia:
    - constant or manifest squint
    - present in one eye
    II. (hyper/hypo/exo/eso) -phoria:
    - aka latent
    - not always obvious, but present in both eyes
    - more apparent on dissociation of the eys
    - can become manifest at times
  3. hyper/hypo/exo/eso
    exo: temporal (aka diverge)
    eso: nasal (aka converge)
    • shine a light directly, if the reflection is not central abnormal
    • cover the eye, then uncover, if squint present the eye moves slightly
  4. alternate cover test: cover one eye and then the other while holding a pen in front of patient to focus on. If latent squint, uncovering the eye makes it move
  5. refractive error (long/short sightedness)
    (others FHx, intraocular problems (cataract, optic n problems, etc), neurological problems, etc)
  6. Hypertension
    Stroke
    Diabetes
    Myasthenia Gravis