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General practice > Ophthal > Flashcards

Ophthal Flashcards

1
Q

Types of conjunctivitis

A

Bacterial
Viral
Allergic

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2
Q

Conjunctivitis presentation

A 
Unilateral or bilateral
Red eyes
Bloodshot
Itchy or gritty sensation
Discharge from the eye

Does not cause pain

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3
Q

How does bacterial conjunctivitis usually present

A

A purulent discharge and an inflamed conjunctiva. It is typically worse in the morning when the eyes may be stuck together. It usually starts in one eye and then can spread to the other. It is highly contagious.

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4
Q

How does viral conjunctivitis usually present

A

Is common and usually presents with a clear discharge. It is often associated with other symptoms of a viral infection such as dry cough, sore throat and blocked nose. You may find tender preauricular lymph nodes (in front of the ears). It is also contagious.

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5
Q

Management of conjunctivitis

A

usually resolves without treatment after 1-2 weeks.

Advise on good hygiene to avoid spreading (e.g. avoid sharing towels or rubbing eyes and regularly washing hands) and avoiding the use of contact lenses. Cleaning the eyes with cooled boiled water and cotton wool can help clear the discharge.

If bacterial conjunctivitis is suspected then antibiotic eye drops can be considered, however bear in mind it will often get better without treatment. Chloramphenicol and fuscidic acid eye drops are both options.

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6
Q

Why is it important to refer patients under 1 month with conjunctivitis

A

Neonatal conjunctivitis can be associated gonococcal infection and can cause loss of sight and more severe complications such as pneumonia

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7
Q

Management of allergic conjunctivitis

A

Antihistamines (oral or topical) can be used to reduce symptoms.

Topical mast-cell stabilisers can be used in patients with chronic seasonal symptoms. They work by preventing mast cells releasing histamine. These require use for several weeks before showing any benefit.

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8
Q

Lesion location in left homonymous hemianopia

A

Visual field defect to the left –> lesion of the right optic tract

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9
Q

Congruous vs incongruous visual defects

A

A congruous visual field defect is identical between the two eyes, whereas an incongruous defect differs in appearance between the eyes.

Congruous defects are complete whereas incongruous defects are incomplete

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10
Q

Which lesions cause incongruous visual defects

A

Optic tract lesions

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11
Q

Which lesions cause congruous defects

A

Optic radiation lesion or occipital cortex

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12
Q

Which lesions cause homonymous hemianopia

A

incongruous defects: lesion of optic tract

congruous defects: lesion of optic radiation or occipital cortex

macula sparing: lesion of occipital cortex

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13
Q

Which lesions cause superior homonymous quadrantanopias

A

superior: lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

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14
Q

Which lesions cause inferior homonymous quadrantanopias

A

inferior: lesion of the superior optic radiations in the parietal lobe

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

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15
Q

Which lesions cause bitemporal hemianopia

A

lesion of optic chiasm
upper quadrant defect >

lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour

lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

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16
Q

What is glaucoma

A

Refers to the optic nerve damage that is caused by a significant rise in intraocular pressure.

The raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.

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17
Q

What is aqueous humour produced by

A

Ciliary body

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18
Q

Normal intraocular pressure

A

10-21 mmHg

The pressure is created by the resistance to flow through the trabecular meshwork into the canal of scheme

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19
Q

Pathophys of open-angle glaucoma

A

There is a gradual increase in resistance through the trabecular meshwork.

This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye.

Therefore the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.

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20
Q

Pathophys of acute angle-closure glaucoma

A

The iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away.

This leads to a continual build-up of pressure. This is an ophthalmology emergency.

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21
Q

Effect of increased intraocular pressure on the optic disc

A

Increased pressure in the eye causes cupping of the optic disc. In the centre of a normal optic disc is the optic cup.

This is a small indent in the optic disc. It is usually less than half the size of the optic disc.

When there is raised intraocular pressure, this indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper.

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22
Q

Abnormal optic cup size

A

An optic cup greater than 0.5 the size of the optic disc is abnormal.

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23
Q

Risk factors for open-angle glaucoma

A

Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)

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24
Q

Presentation of open-angle glaucoma

A

Asymptomatic

Peripheral vision affected first until it closes in to result in tunnel vision

Gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time

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25
Q

Diagnosis of open-angle glaucoma

A

Goldmann applanation tonometry can be used to check the intraocular pressure.

Fundoscopy assessment to check for optic disc cupping and optic nerve health.

Visual field assessment to check for peripheral vision loss.

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26
Q

When is treatment for open-angle glaucoma usually started

A

Treatment is usually started at an intraocular pressure of 24 mmHg or above. Patients are followed up closely to assess the response to treatment.

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27
Q

1st line mx for open-angle glaucoma

A

Prostaglandin analogue eye drops (e.g. latanoprost) are first line. These increase uveoscleral outflow.

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28
Q

Notable side effects of prostaglandin analogue eye drops

A

Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).

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29
Q

Other options of management of open-angle glaucoma

A

Beta-blockers (e.g. timolol) reduce the production of aqueous humour

Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour

Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow

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30
Q

Surgical intervention for glaucoma

A

Trabeculectomy surgery may be required where eye drops are ineffective.

This involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva.

It causes a “bleb” under the conjunctiva where the aqueous humour drains.

It is then reabsorbed from this bleb into the general circulation.

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31
Q

Risk factors for acute angle-closure glaucoma

A

Increasing age
Females are affected around 4 times more often than males
Family history
Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
Shallow anterior chamber

32
Q

Medications which can precipitate acute angle-closure glaucoma

A

Adrenergic medications such as noradrenalin

Anticholinergic medications such as oxybutynin and solifenacin

Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects

33
Q

Presentation of acute angle-closure glaucoma

A

Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

34
Q

Examination findings in acute angle closure glaucoma

A 
Red-eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation
35
Q

Initial management of acute angle closure glaucoma

A

same-day assessment by an ophthalmologist
Lie patient on their back without a pillow
Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
Give acetazolamide 500 mg orally
Given analgesia and an antiemetic if required

36
Q

How does pilocarpine work

A

Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil.

Therefore it is a miotic agent. It also causes ciliary muscle contraction. These two effects cause the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork to open up.

37
Q

How does acetazolamide work

A

Acetazolamide is a carbonic anhydrase inhibitor. This reduces the production of aqueous humour.

38
Q

Secondary care management of acute angle-closure glaucoma

A 
Pilocarpine
Acetazolamide (oral or IV)
Hyperosmotic agents such as glycerol or mannitol
Timolol 
Dorzolamide 
Brimonidine
39
Q

Purpose of hyper osmotic agents in acute angle closure glaucoma

A

Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye

40
Q

Use of beta-blockers in acute angle closure glaucoma

A

Beta-blockers reduce production of aqueous humour

41
Q

Use of brimodine in acute angle closure glaucoma

A

Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow

42
Q

Definitive treatment for acute angle-closure glaucoma

A

Laser iridotomy - involves using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves pressure that was pushing the iris against the cornea and allows the humour the drain.

43
Q

What is posterior vitreous detachment

A

Posterior vitreous detachment is the separation of the vitreous membrane from the retina.

This occurs due to natural changes to the vitreous fluid of the eye with ageing.

44
Q

Risk factors for posterior vitreous detachment

A

As people age, the vitreous fluid in the eye becomes less viscous, and thus, does not hold its shape as well. Therefore, it pulls the vitreous membrane away from the retina towards the centre of the eye.

Highly myopic (near-sighted) patients are also at increased risk of developing posterior vitreous detachment earlier in life. This is because the myopic eye has a longer axial length than an emmetropic eye.

45
Q

Symptoms of posterior vitreous detachment

A

The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision)
Flashes of light in vision
Blurred vision
Cobweb across vision
The appearance of a dark curtain descending down vision (means that there is also retinal detachment)

46
Q

Signs of posterior vitreous detachment

A

Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).

47
Q

IX for suspected vitreous detachment

A

All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.

48
Q

Mx of posterior vitreous detachment

A

Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.

If there is an associated retinal tear or detachment the patient will require surgery to fix this.

49
Q

What is retinal detachment

A

Retinal detachment occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.

It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.

50
Q

Risk factors for retinal detachment

A

Age
Previous surgery for cataracts (accelerates posterior vitreous detachment)
Myopia
Eye trauma (consider boxing)
Family history
Previous history of retinal break/detachment in either eye

51
Q

Symptoms of retinal detachment

A

New onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively.

Sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment.

If the macula is involved, central visual acuity and visual outcomes become much worse.

52
Q

Examination findings in retinal detachment

A

Peripheral visual fields may be reduced, and central acuity may be reduced to hand movements if the macula is detached.

Relative afferent pupillary defect if the optic nerve is involved.

On fundoscopy, the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms. If the break is small, however, it may appear normal.

53
Q

Management of retinal tears

A

Management of retinal tears aims to create adhesions between the retina and the choroid to prevent detachment. This can be done using:

Laser therapy
Cryotherapy

54
Q

Surgical options for retinal detachment

A

Vitrectomy involves removing the relevant parts of the vitreous body and replacing it with oil or gas.

Scleral buckling involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and into contact with the detached retina.

Pneumatic retinopexy involves injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.

55
Q

What is anterior uveitis

A

inflammation in the anterior part of the uvea. The uvea involves the iris, ciliary body and choroid

56
Q

Conditions associated with acute anterior uveitis

A

HLA B27 related conditions:

Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis

57
Q

Conditions associated with chronic anterior uveitis

A 
Sarcoidosis
Syphilis
Lyme disease
Tuberculosis
Herpes virus
58
Q

Acute anterior uveitis presentation

A 
Unilateral 
Dull,aching,painful red eye 
Ciliary flush 
Miosis 
Photophobia 
Floaters and flashes
59
Q

Tear production acute anterior uveitis

A

Increased

60
Q

What is a hypoyon

A

Collection of white blood cells in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level. seen in acute anterior uveitis

61
Q

Mx of acute anterior uveitis

A

Steroids
Cylopegic-mydriatic meds(atropine)
Immunsuppressants(DMARDS)
Laser therapy

62
Q

Conditions associated with episcleritis

A

Rheumatoid arthritis

IBD

63
Q

Presentation of episcleritis

A 
Mild pain(no pain typically) 
Segmental redness(patch)
Foreign body sensation 
Dilated episcleral vessels 
Watering of eye
64
Q

Mx of episcleritis

A

Self-limiting - recovery in 1-4 weeks
Lubricating eye drops
Analgesia
Cold compress

65
Q

Complications of scleritis

A

Necrotising scleritis

Perforation of sclera

66
Q

Systemic conditions associated with scleritis

A

RA
SLE
IBD
Sarcoidosis

67
Q

Presentation of scleritis

A 
Severe pain 
Pain with eye movement 
Photophobia 
Eye watering 
Reduced visual acuity 
Abnormal pupil reaction to light
68
Q

Mx of scleritis

A

Same day assessment by ophthalmologist

Consider underlying systemic condition
NSAIDS
Steroids
Immunosuppression

69
Q

What is keratitis

A

Inflammation of the cornea

70
Q

Most common cause of keratitis

A

Herpes simplex infection

71
Q

Other causes of keratitis

A

Bacterial infection - pseudomonas or staph

Fungal - Candida

Contact lens acute red eye(CLARE)

72
Q

Complications of herpes keratitis

A

Can lead to stromal keratitis(inflammation of layer between epithelium and endothelium) –> stromal necrosis, vascularisation and scarring and can lead to corneal blindness

73
Q

Presentation of herpes keratitis

A 
Painful red eye
Photophobia
Vesicles around the eye
Foreign body sensation
Watering eye
Reduced visual acuity
74
Q

Diagnosis of herpes keratitis

A

Staining with fluorescein will show a dendritic corneal ulcer

Slit-lamp examination

Corneal swabs/scrapings

75
Q

Mx of herpes keratitis

A

Aciclovir (topical or oral)
Ganciclovir eye gel
Topical steroids may be used alongside antivirals to treat stromal keratitis

Corneal transplant if scarring caused by stromal keratitis

General practice (26 decks)

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