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MRCP I > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Macular degeneration - Dry macular degeneration

A

characterized by Drusen - yellow round spots in Bruch’s membrane

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2
Q

W et (exudative, neovascular) macular degeneration:

A

characterized by choroidal
neovascularisation. Leakage of serous fluid and blood can subsequently result in a rapid loss of vision. Carries worst prognosis

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3
Q

Risk factors - Macular degeneration

A

Age: most patients are over 60 years of age
* Family history
* Smoking
* More common in caucasians
* ♀sex
* High cumulative sunlight exposure

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4
Q

Features Macular degeneration

A
  • ↓ visual acuity: ‘blurred’, ‘distorted’ vision, central vision is affected first
  • Central scotomas
  • Fundoscopy: drusen, pigmentary changes
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5
Q

Dry macular degeneration -

A

no current medical treatments

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6
Q

Wet macular degeneration treatment

A

Photocoagulation
* Photodynamic therapy
* anti-vascular endothelial growth factor (anti-VEGF) treatments: intravitreal ranibizumab

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7
Q

Sudden Painless Loss of Vision:

A

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

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8
Q

Amaurosis fugax

A

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.

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9
Q

Ischemic optic neuropathy

A

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

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10
Q

Central retinal vein occlusion

A

Incidence ↑ with age, more common than arterial occlusion
* Causes: glaucoma, polycythemia, hypertension

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11
Q

central retinal Artery occlusion

A

Due to thromboembolism (from
atherosclerosis) or arteritis (e.g. Temporal
arteritis)
* Features include Afferent pupillary defect,
‘cherry red’ spot on a pale retin

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12
Q

Vitreous hemorrhage

A

Causes: diabetes, bleeding disorders
* Features may include sudden visual loss,
dark spots

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13
Q

Retinal detachment symtoms

A

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

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14
Q

Posterior vitreous detachment

A

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

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15
Q

Retinal detachment

A

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

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16
Q

Relative afferent pupillary defect

A

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

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17
Q

auses of Mydriasis (large pupil)

A
  • 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
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18
Q

Holmes-ADIe pupil

A

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

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19
Q

Angioid retinal streaks are seen on fundoscopy as irregular dark red streaks radiating from
the optic nerve head.

A

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

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20
Q

Optic atrophy

A

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

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21
Q

Optic atrophy causes

A

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)

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22
Q

Cataract: cause s

A
  • 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
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23
Q

Retinitis pigmentosa

A

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)

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24
Q

Associated diseases Retinitis pigmentosa

A

Refsum disease: cerebellar ataxia, peripheral
neuropathy, deafness, ichthyosis
* Usher syndrome
* Abetalipoproteinemia
* Lawrence-Moon-Biedl syndrome
* Kearns-Sayre syndrome
* Alport’s syndrome

25
Q

tunnel vision is the concentric diminution of the visual fields Causes:

A
  • Papilledema * Retinitis pigmentosa
  • Glaucoma * Choroidoretinitis
  • Optic atrophy secondary to tabes dorsalis
  • Hysteria
26
Q

Congenital Hypertrophy of the Retinal Pigment Epithelium (CHRPE):

A

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.

27
Q

acute angle closure glaucoma RF

A

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

28
Q

Drugs which may precipitate acute glaucoma

A

anticholinergics and tricyclic antidepressants.
Mydriatic drops

29
Q

acute glaucoma features

A

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

30
Q

Treatment of acute glaucoma

A

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

31
Q

Primary open-angle glaucoma (POAG) RF

A

Family history
* Black patients * Myopia
* Hypertension
* Diabetes mellitus

32
Q

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

A

Peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
* ↓ visual acuity
* Optic disc cupping

33
Q

Prostaglandin analogues (e.g. Latanoprost)

A

Increase uveoscleral outflow
Once daily administration
Adverse effects include brown pigmentation of the iris

34
Q

β-blockers (e.g. Timolol

A

↓ aqueous production
Should be avoided in asthmatics and patients with heart block

35
Q

Sympathomimetics (e.g. Brimonidine, an α2-adrenoceptor agonist)

A

↓ aqueous production and ↑ outflow
Avoid if taking MAOI or tricyclic antidepressants
Adverse effects include hyperemia

36
Q

Carbonic anhydrase inhibitors (e.g. Dorzolamide)

A

↓ aqueous production Systemic absorption may cause sulphonamide-like reactions

37
Q

Miotics (e.g. Pilocarpine)

A

Miotics (e.g. Pilocarpine)
↑ uveoscleral outflow
Adverse effects included a constricted pupil, headache and blurred vision

38
Q

Red eye - glaucoma or uveitis?

A
  • Glaucoma: severe pain, haloes, ‘semi-dilated’ pupil
  • Uveitis: small, fixed oval pupil, ciliary flush
39
Q

Scleritis

A

Severe pain (may be worse on movement) and tenderness
* May be underlying autoimmune disease e.g. Rheumatoid arthritis

40
Q

Anterior uveitis

A

Acute onset * Pain
* Blurred vision and photophobia
* Small, fixed oval pupil, ciliary flush

41
Q

Dacryocystitis

A

Watering eye (epiphora)
* Swelling and erythema at the inner canthus of the eye

Management is with systemic antibiotics

42
Q

Congenital lacrimal duct obstruction

A

Features:
* Watering eye (even if not crying)
* Secondary infection may occur
* Symptoms resolve in 99% of cases by 12 months of age

43
Q

Blepharitis

A

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

44
Q

Blepharitis

A

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

45
Q

Ocular manifestations RA

A

Keratoconjunctivitis sicca (most common)
* Episcleritis (erythema)
* Scleritis (erythema and pain)
* Corneal ulceration

  • Keratitis → associated with acns rosacea
46
Q

Thyroid eye disease

A

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

47
Q

Herpes Zoster Ophthalmicus (HZO) features

A

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

48
Q

Herpes Zoster Ophthalmicus (HZO) features treatment

A
  • 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
49
Q

Herpes Simplex Keratiti

A

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

50
Q

and keratopathy

A

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.

51
Q

Diabetic Retinopathy path

A

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

52
Q

Diabetic Retinopathy stages

A

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

53
Q

Proliferative retinopathy

A

(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

54
Q

earlist sign of DM Nephropathy

A

Microaneurysm on fluorescein angiography

55
Q

Maculopathy

A

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

56
Q

Screening DM Nephropathy

A
  • 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
57
Q

Optic Neuritis:

A

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
58
Q

Retrobulbar Neuritis:

A

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

59
Q

Trochlear Nerve Palsy:

A

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.

MRCP I (21 decks)

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