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Neuro and special senses > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is glaucoma

A

Optic nerve damage due to significant rise in intraocular pressure

Rise in pressure due to blockage of flow of aqueous humour

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2
Q

What are the 2 types of glaucoma

A

Open angle

Closed angle

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3
Q

What are the anterior and posterior chambers of the eye

A

Anterior chamber: between cornea and iris

Posterior chamber: between lens and iris

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4
Q

Describe the path of flow of aqueous humour in the eye

A

Ciliary body (production) –> around lens –> under iris –> through anterior chamber –> through trabecular meshwork –> into canal of Schlemm –> into general circulation

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5
Q

What is normal intraocular pressure

A

10 - 21 mmHg

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6
Q

Explain the pathophysiology of open angle glaucoma

A

Gradual increase in resistance through trabecular meshwork (more difficult for humour to exit eye)

Slow, chronic onset

Increased pressure causes cupping of optic disc (central indentation becomes larger, cup > 0.5 size of disc is abnormal)

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7
Q

What are the risk factors for open angle glaucoma

A

Increasing age

Family history

Black ethnicity

Nearsigntedness (myopia)

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8
Q

How might open angle glaucoma present

A

Often asymptomatic (spotted on routine screening)

Peripheral vision affected first (get tunnel vision)

Fluctuating symptoms (pain, headache, blurred vision, halos around lights)

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9
Q

What are the investigations for open angle glaucoma

A

Non-contact tonometry (puff of air into cornea, measure pressure, not very accurate but useful for screening)

Goldmann applanation tonometry (gold standard, apply pressure directly to cornea)

Fundoscopy (optic disc cupping, general optic nerve health)

Visual field assessment (look for peripheral vision loss)

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10
Q

What is the management for open angle glaucoma

A

Aim to reduce intraocular pressure

Start treatment if pressure > 24 mmHg

Prostaglandin analogue eye drops (latanoprost, increases uveoscleral outflow, side effects: eyelash growth, eyelid/iris pigmentation)

Beta blockers (timolol, reduces aqueous humour production)

Carbonic anhydrase inhibitors (dorzolamide, reduces aqueous humour production)

Sympathomimetics (brimonidine, reduces production, increases flow)

Surgery (trabeculectomy - create new channel for flow)

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11
Q

Explain the pathophysiology of acute angle-closure glaucoma

A

Intraocular pressure very high

Iris bulges forward, seals off trabecular meshwork from anterior chamber

Aqueous humour not drained away

Very high pressure behind iris worsens closure of angle

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12
Q

What are the risk factors for acute angle-closure glaucoma

A

Increasing age

F>M

Family history

East asian ethnicity

Shallow anterior chamber

Medications (anticholinergics, adrenergics, tricyclic antibiotics)

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13
Q

How might acute angle-closure glaucoma present

A

Patient appears unwell

Short history

Severely painful red eye

Blurred vision

Halos around lights

Headaches

Nausea, vomiting

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14
Q

How might the eye appear on examination in acute angle-closure glaucoma

A

Red eye

Teary

Hazy cornea

Decreased visual acuity

Dilated pupil

Fixed pupil size

Firm eyeball on palpation

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15
Q

What is the initial management for acute angle-closure glaucoma

A

Lie on back without pillow

Pilocarpine eye drops (cause pupillary constriction and ciliary muscle contraction - opening up angle)

Oral acetazolamide (reduces aqueous fluid production)

Analgesia

Antiemetics

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16
Q

What is the secondary care management for acute angle-closure glaucoma

A

Pilocarpine (opens up pathway for flow of fluid)

Acetazolamide (reduces production of fluid)

Hyperosmotic agents (increase osmotic gradient between blood and eye)

Timolol (reduces production of fluid)

Dorzolamide (reduces production of fluid)

Brimonidine (reduces production of fluid, opens up angle)

Laser iridotomy (definitive management, make hole in iris for flow of fluid)

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17
Q

What is age-related macular degeneration

A

Degeneration of macula causes progressive deterioration in vision

Most common cause of blindness in the UK

2 types (wet, dry)

See drusen on fundoscopy

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18
Q

Explain wet age-related macular degeneration

A

Associated features: atrophy of retinal pigment layer, degeneration of photoreceptors

Development of new vessels from choroid layer (due to VEGF, leak fluid and blood, get oedema, rapid loss of vision)

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19
Q

What are the layers of the macula (bottom to top)

A

Choroid (contains blood vessels)

Bruch’s membrane

Retinal pigment epithelium

Photoreceptors

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20
Q

What are drusen

A

Yellow deposits of protein and lipids

Between retinal pigment epithelium and Bruch’s membrane

Abnormal if large and numerous

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21
Q

What are the risk factors for age-related macular degeneration

A

Age

Smoking

White/east asian ethnicity

Family history

Cardiovascular disease

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22
Q

How might age-related macular degeneration present

A

Gradual central visual field loss

Reduced visual acuity

Crooked or wavy appearance to straight lines

Wet: more acute, loss of vision over days, full vision loss in 2-3 years, can be bilateral

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23
Q

What are the investigations for age-related macular degeneration

A

Reduces visual acuity on Snellen chart

Scotoma (central patch of vision loss)

Ambler grid test (assess distortion of straight lines)

Fundoscopy (see drusen)

Slit-lamp biomicroscopic fundus examination (get cross-sectional view of retina)

Fluorescein angiography (get detailed picture of oedema and neovascularisation)

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24
Q

What is the management for age-related macular degeneration

A

Refer to ophthalmology

Dry: no specific treatment, lifestyle improvement to slow progression

Wet: anti-VEGF medications (injected directly into vitreous chamber once a month)

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25
Q

What is diabetic retinopathy

A

Blood vessels in retina damaged due to prolonged exposure to high blood sugars

Progressive deterioration in health of retina

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26
Q

Explain the pathophysiology of diabetic retinopathy

A

Increased vascular permeability (get leaky blood vessels, blot haemorrhages, formation of hard exudates)

Microaneurysms (weakness in vessel walls, get small bulges)

Venous beading (walls of vessels not straight)

Cotton wool spots (due to damage to nerve fibres, fluffy white patches on retina)

Intraretinal microvascular abnormalities (dilated and tortuous capillaries in retina, act as shunts)

Neurovascularisation

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27
Q

What are the classifications of diabetic retinopathy

A

Based on fundoscopy

Non-proliferative:

  • No new blood vessel development
  • Can become proliferative
  • Mild, moderate, or severe

Proliferative:

  • New blood vessel development
  • Vitreous haemorrhages

Diabetic maculopathy:

  • Macular oedema
  • Ischaemic maculopathy
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28
Q

What is the management for diabetic retinopathy

A

Laser photocoagulation

Anti-VEGF medications

Viteoretinal surgery (for severe disease)

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29
Q

What are the complications of diabetic retinopathy

A

Retinal detachment

Vitreous haemorrhage (bleeding into vitreous fluid)

Rubeosis iridis (new blood vessel formation in iris)

Optic neuropathy

Cataracts

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30
Q

What is hypertensive retinopathy

A

Damage to small blood vessels due to systemic hypertension (systemic or malignant)

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31
Q

What are the fundoscopy signs of hypertensive retinopathy

A

Silver wiring/copper wiring (walls of arterioles thickened and sclerosed, get increased refraction)

Arteriovenous nipping (arterioles cause compression of veins that they cross)

Cotton wool spots (due to ischaemia and infarction of retina)

Hard exudates (due to damaged vessels leaking lipids into retina)

Retinal haemorrhage (release of blood into retina)

Papilloedema (optic disc swelling, blurring of optic disc margins)

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32
Q

What is the Keith-Wagner classification of hypertensive retinopathy

A

Stage 1 - mild narrowing of arterioles

Stage 2 - focal constriction of blood vessels and AV nicking

Stage 3 - cotton wool spots, exudates, haemorrhages

Stage 4 - papilloedema

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33
Q

What is the management for hypertensive retinopathy

A

Control blood pressure

Control lipid levels

Stop smoking

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34
Q

What are cataracts

A

Lens becomes cloudy and opaque

Reduced visual acuity (less light entering eye)

Most in older age

Can be congenital (screen for red reflex in neonatal examination)

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35
Q

What are the risk factors for cataracts

A

Increasing age

Smoking

Alcohol

Diabetes

Steroid (especially eye drops)

Hypercalcaemia

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36
Q

How might cataracts present

A

Usually asymmetrical

Very slow reduction in vision

Progressive blurring of vision

Changes in colour vision (colours become more brown/yellow)

‘Starbursts’ around lights (especially at night)

Loss of red reflex (lens grey/white)

Glare

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37
Q

What is the management for cataracts

A

Is manageable, no intervention needed

Surgery (drill, break lens into pieces, remove pieces, implant artificial lens)

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38
Q

What are the complications of cataracts

A

Endophthalmitis:

  • Complication of eye surgery
  • Inflammation of inner contents of eye
  • Usually due to infection
  • Treat with intravitreal antibiotics
  • Can lead to loss of vision/eye

Posterior capsule opacification:

  • Build-up of debris on capsule
  • Treated with lasers
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39
Q

What are the causes of abnormal pupil shape

A

Trauma to sphincter muscles

Anterior uveitis

Acute angle-closure glaucoma

Rubeosis iridis (neurovascularisation of iris)

Coloboma (congenital malformation of eye)

Tadpole pupil (usually temporary, associated with migraines)

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40
Q

What are the features of 3rd nerve palsy

A

Ptosis

Dilated, non-reactive pupil

Divergent strabismus (squint)

‘Down and out’ position

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41
Q

Which eye muscles does CN 3 supply

A

All extraocular muscles except LR and SO

Levator palpebrae superioris (lifts eyelid)

Sphincter muscles of iris

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42
Q

What are the causes of 3rd nerve palsy

A

Idiopathic

If pupil spared, usually microvascular cause

If full 3rd nerve palsy: compression of nerve (idiopathic, tumour, trauma, aneurysms, raised ICP)

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43
Q

What are the features of Horner syndrome

A

Ptosis

Miosis

Anhidrosis

May have enopthalmos (sunken eyes)

Light and accommodation reflexes normal

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44
Q

What are the causes of Horner syndrome

A

Central lesions (stroke, multiple sclerosis, tumours)

Pre-ganglionic (tumours, trauma, thyroidectomy, cervical rib)

Post-ganglionic (carotid aneurysms, cluster headaches)

Congenital (associated with heterochromia)

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45
Q

What is the management for pupil disorders due to Horner syndrome

A

Cocaine eye drops (stop noradrenaline re-uptake)

Low concentration adrenaline eye drops

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46
Q

What is a Holmes Adie pupil

A

Unilateral dilated pupil

Sluggish to react to light

Slow dilation following constriction

Pupil gets smaller over time

Also have absent ankle and knee reflexes

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47
Q

What is a Argyll-Robertson pupil

A

Specific to neurosyphilis

Constricted pupil that accommodates when focussing on near objects, but no reaction to light

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48
Q

Give an overview of blepharitis

A

Inflammation of eyelid margin

Gritty, itchy, dry eye

Associated with dysfunction of Meibomian glands

Can get styes or chalazions

Management: hot compress, gentle cleaning, lubricating eye drops (hypromellose, polyvinyl alcohol, carbomer)

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49
Q

Give an overview of styes

A

Hordeolum externum: infection of glands of Zeis/Mill (at base of eyelashes), tender red lump, may point outwards

Hordeolum internum: infection of Meibomian glands (deep), painful, may point inwards

Management: hot compresses, analgesia, consider topical antibiotics (if persistent/have conjunctivitis)

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50
Q

Give an overview of chalazion

A

When Meibomian glands become blocked and swell up

Swollen eyelid

Not tender

Red

Management: hot compress, analgesia, consider topical antibiotics (if inflamed), may need surgical drainage

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51
Q

Give an overview of entropion

A

Eyelid turned inwards

Lashes against eyeball

Pain

Can get corneal damage/ulceration

Management: tape eyelid down, lubricating eye drops, surgery (definitive)

Same-day ophthal referral if risk to sight

52
Q

Give an overview of ectropion

A

Eyelid turned outwards

Inner part of eyelid exposed

Can get exposure keratopathy

Management: none for mild cases, lubricating eye drops, may need surgery

Same-day ophthal referral if risk to sight

53
Q

Give an overview of trichiasis

A

Inward growth of eyelashes

Pain

Can get corneal damage/ulceration

Management: remove eyelashes (epilation), electrolysis, cryotherapy, laser treatment

Same-day ophthal referral if risk to sight

54
Q

Give an overview of periorbital cellulitis

A

Eyelid and skin infection in front of orbital septum

Swelling

Redness

Hot skin around eyelid/eye

Use CT to differentiate from orbital cellulitis

Management: systemic antibiotics, admit vulnerable patients (may develop orbital cellulitis)

55
Q

Give an overview of orbital cellulitis

A

Infection around eyeball

Involves tissues behind orbital septum

Pain on eye movement

Reduced eye movements

Changes in vision

Abnormal pupil reaction

Proptosis (eyeball sitting forward)

A medical emergency

Admit, give IV antibiotics

May need surgical drainage (if abscess forms)

56
Q

What is conjunctivitis

A

Inflammation of the conjunctiva (thin layer of tissue covering inside of eyelid and sclera)

May be bacterial, viral, or allergic

57
Q

How might conjunctivitis present in general

A

Unilateral or bilateral

Red eyes

Bloodshot

Itchy/gritty sensation

Discharge from eye

Not painful

No photophobia

No changes to visual acuity

58
Q

How might bacterial conjunctivitis present

A

Purulent discharge

Inflamed conjunctiva

Worse in morning (eye stuck together)

Starts in one eye, may spread to the other

Highly contagious

59
Q

How might viral conjunctivitis present

A

Clear discharge

Associated with other symptoms of viral infection

Pre-auricular lymph nodes may be tender

Contagious

60
Q

What are the painless red eye conditions

A

Conjunctivitis

Episcleritis

Subconjunctival haemorrhage

61
Q

What are the painful eye conditions

A

Glaucoma

Anterior uveitis

Scleritis

Corneal abrasions and ulceration

Keratitis

Foreign body

Traumatic/chemical injury

62
Q

What is the management for conjunctivitis

A

Usually spontaneously resolves in 2 weeks

Advise on good hygiene

If bacterial, consider antibacterial eye drops

Babies < 1 month: urgent ophthalmology review, neonatal conjunctivitis associated with gonococcal infection can cause loss of sight

63
Q

What is allergic conjunctivitis

A

Due to exposure to allergens

Swelling of conjunctival sac and eyelid

Significant watery discharge and itching

Management: antihistamines (topical/oral)

64
Q

What is anterior uveitis

A

Inflammation of interior part of uvea

Uvea involves: iris, ciliary body, choroid

Get inflammation and immune cells in anterior chamber

Causes: autoimmune, infection, trauma, ischaemia, malignancy

Get ‘floaters’ in vision (due to immune cells)

65
Q

What conditions are associated with acute anterior uveitis

A

Ankylosing spondylitis

Inflammatory bowel disease

Reactive arthritis

66
Q

What conditions are associated with chronic anterior uveitis

A

Sarcoidosis

Syphilis

Lyme disease

TB

Herpes

More macrophages, less severe, > 3 months

67
Q

How might anterior uveitis present

A

Unilateral

Spontaneous onset

Dull, aching, painful red eye

Ciliary flush (ring of red spreading out from cornea)

Reduced visual acuity

Floaters, flashes

Miosis

Photophobia

Pain on eye movements

Abnormal pupil shape

Hypopyon (yellow fluid in front of iris)

68
Q

What is the management for anterior uveitis

A

Refer for same day ophthalmology review

Steroids

Cycloplegic-mydriatic medications (antimuscarinics - block iris sphincters and ciliary body)

Immunosuppressants (DMARDs, TNF inhibitors)

Laser therapy

Cryotherapy

Surgery

69
Q

What is episcleritis

A

Benign and self-limiting inflammation of episclera

Episclera: outermost layer of sclera

Common in young and middle-aged adults

Usually due to inflammatory disorders (rheumatoid arthritis, inflammatory bowel disease)

70
Q

How might episcleritis present

A

Acute onset

Unilateral

Usually not painful

Segmental redness (patch of redness in lateral sclera)

Foreign body sensation

Dilated episcleral vessels

Watery eye

No discharge

71
Q

What is the management for episcleritis

A

If in doubt, refer to ophthalmology

Usually self-limiting (resolves in 1-4 weeks)

Lubricating eye drops

Simple analgesia

Cold compress

Severe cases: systemic NSAIDs, topical steroid eye drops

72
Q

What is scleritis

A

Inflammation of full thickness of sclera

Not usually due to infection

73
Q

What is necrotising scleritis

A

Severe form of scleritis

Have visual impairment

No pain

Can get perforation of sclera

Significant complication

74
Q

What conditions are associated with scleritis

A

Rheumatoid arthritis

SLE

Inflammatory bowel disease

Sarcoidosis

Glanulomatosis with polyangiitis

75
Q

How might scleritis present

A

Acute onset

Can be unilateral/bilateral

Severe pain

Pain with eye movements

Photophobia

Eye watering

Reduced visual acuity

Abnormal pupil reaction to light

Tenderness on palpation of eye

76
Q

What is the management for scleritis

A

Refer for same-day ophthalmology review

Manage underlying condition

NSAIDs

Steroids

Immunosuppressants

77
Q

What is a corneal abrasion

A

Scratch or damage to cornea

Chemical abrasions can cause severe damage and loss of vision

78
Q

What are the common causes of corneal abrasions

A

Contact lenses

Foreign bodies

Fingernails

Eyelashes

Entropion (inward turning eyelid)

79
Q

How might corneal abrasions present

A

History of contact lenses/foreign body

Painful red eye

Foreign body sensation

Watery eye

Blurred vision

Photophobia

80
Q

What are the investigations for corneal abrasion

A

Fluorescein stain (collects in abrasions/ulcers)

Slit lamp examination (for significant abrasions)

81
Q

What is the management for corneal abrasions

A

If significant, refer for ophthalmology review

Remove foreign body

Simple analgesia

Lubricating eye drops

Antibiotic eye drops

Follow-up after 24 hours

Cyclopentolate eye drops (dilate pupil, help relieve symptoms)

Chemical abrasions: immediate irrigation for 20-30 mins, urgent ophthalmology referral

If uncomplicated, usually heal over 2-3 days

82
Q

What is keratitis

A

Inflammation of cornea

Causes: herpes (most common), bacterial, fungal, contact lenses, exposure keratitis

83
Q

What is stromal keratitis

A

Herpes keratitis that is affecting the stromal layer

Associated with: stromal necrosis, vascularisation, scarring, corneal blindness

84
Q

How might keratitis present

A

Painful red eye

Photophobia

Vesicles around eye

Foreign body sensation

Watery eye

Reduced visual acuity

85
Q

What are the investigations for keratitis

A

Fluorescein staining (show dendritic corneal ulcers)

Slit lamp examination (for diagnosis of keratitis)

Corneal swab/scraping (isolate causative virus)

86
Q

What is the management for keratitis

A

Refer for urgent ophthalmology review

Aciclovir

Ganciclovir eye gel

Topical steroids

If have significant corneal scarring: corneal transplant

87
Q

What is a subconjunctival haemorrhage

A

Relatively common

Rupture of small blood vessel in conjunctiva

Release of blood into space between sclera and conjunctiva

Due to: strenuous exercise, heavy coughing, weight lifting, straining, trauma

88
Q

How might a subconjunctival haemorrhage present

A

Bright red blood covering white of the eye

Painless

Does not affect vision

History of precipitating event

89
Q

What is the management for subconjunctival haemorrhage

A

Resolve spontaneously in 2 weeks

If foreign body sensation, lubricating eye drops

90
Q

What is posterior vitreous detachment

A

Vitreous body comes away from retina

Very common (especially in elderly)

91
Q

How might a posterior vitreous detachment present

A

Painless

Spots of vision loss

Floaters

Flashing lights

92
Q

What is the management for posterior vitreous detachment

A

No treatment needed (symptoms improve as brain adjusts)

Can predispose to: retinal tears, retinal detachment

93
Q

What is retinal detachment

A

Retina separates from choroid

Usually due to retinal tears (vitreous fluid gets under retina)

Sight-threatening emergency (outer retina relies on blood vessels from choroid for blood supply)

94
Q

What are the risk factors for retinal detachment

A

Posterior vitreous detachment

Diabetic retinopathy

Trauma to eye

Retinal malignancy

Older age

Family history

95
Q

How might retinal detachment present

A

Painless

Peripheral vision loss (often sudden, like ‘shadow coming across eye’)

Blurred/distorted vision

Floaters

Flashing

96
Q

What is the management for retinal detachment

A

Immediate referral to ophthalmology

Manage retinal tears: laser, cryotherapy

Manage retinal detachment: aim to reattach retina, vitrectomy (remove part of vitreous body), scleral buckling (use silicone buckles to put pressure on outside of eye), pneumatic retinopexy (injection of gas bubble into vitreous body)

97
Q

What is retinal vein occlusion

A

Thrombus in retinal vein, blocking drainage of blood from retina

Pooling of blood in retina

Leakage of blood and fluid (macular oedema, retinal haemorrhage, damage to retinal tissue, loss of vision, release of VEGF)

98
Q

How might retinal vein occlusion present

A

Sudden, painless loss of vision

99
Q

What are the risk factors for retinal vein occlusion

A

Hypertension

High cholesterol

Diabetes

Smoking

Glaucoma

Systemic inflammatory conditions

100
Q

What are the investigations for retinal vein occlusion

A

Fundoscopy (flame/blot haemorrhages, optic disc oedema, macular oedema)

Look for causes of retinal vein occlusion (bloods, glucose, blood pressure)

101
Q

What is the management for retinal vein occlusion

A

Immediate referral to ophthalmology

Aim to treat macular oedema and prevent complications for neovascularisation

Laser photocoagulation

Intravitreal steroids

Anti-VEGF therapy

102
Q

What is central retinal artery occlusion

A

Central retinal artery: branch of ophthalmic artery (branch of internal carotid), supplies blood to retina

Common causes of occlusion: atherosclerosis, giant cell arteritis, vasculitis

103
Q

What are the risk factors for central retinal artery occlusion

A

Older age

Family history

Smoking

Alcohol consumption

Hypertension

Diabetes

Poor diet

Inactivity

Obesity

104
Q

How might central retinal artery occlusion present

A

Sudden, painless loss of vision

Relative afferent pupillary defect (pupil more sensitive to light)

105
Q

What are the fundoscopy findings in central retinal artery occlusion

A

Pale retina with cherry-red spots

Pale due to lack of perfusion

Spots due to macula showing up more

106
Q

What is the management for central retinal artery occlusion

A

Immediate referral to ophthalmology

Immediate: attempt to dislodge thrombus (ocular massage, remove fluid from anterior chamber, inhaled carbogen, sublingual isosorbide dinitrate)

Long-term: treat reversible risk factors, secondary prevention of cardiovascular disease

107
Q

What is retinitis pigmentosa

A

Congenital inherited condition

Degeneration of rods and cones in retina

Usually have more rod degeneration

Night blindness

108
Q

How might retinitis pigmentosa present

A

Night blindness

Peripheral vision lost before central vision

109
Q

What might you see on fundoscopy in retinitis pigmentosa

A

Pigmentation (‘bone-spicules’, mostly in mid-peripheral area of retina)

Narrowing of arterioles

Waxy/pale optic disc

110
Q

What is the management for retinitis pigmentosa

A

Refer to ophthalmology for assessment and diagnosis

Genetic counselling

Vision aids

Sunglasses (prevent retina from accelerated damage)

Driving limitations

Regular follow ups

Vitamin/anti-oxidant supplements

Oral acetazolamide

Steroid injections

Anti-VEGF injections

Gene therapy may be possible in the future

111
Q

What is the ophthalmology management for facial nerve palsy

A

Acute eye protection (lubricating eye drops, cross-taping)

112
Q

Which causes of an acute red eye are associated with itching/scratchiness/burning

A

Allergy

Conjunctivitis

Corneal disorders

Foreign body

Trichiasis

Dry eye

113
Q

Which causes of an acute red eye are associated with localised eyelid tenderness

A

Hordeolum

Chalazion

114
Q

Which causes of an acute red eye are associated with deep intense pain

A

Corneal abrasion

Scleritis

Iritis

Acute glaucoma

Sinusitis

115
Q

Which causes of an acute red eye are associated with photophobia

A

Corneal abrasion

Iritis

Acute glaucoma

116
Q

Which causes of an acute red eye are associated with halo vision

A

Corneal oedema (acute glaucoma, over-wearing contacts)

117
Q

How do you test low vision

A

Count fingers

Hand movements

Perception of light

No perception of light

118
Q

Give an overview of 3rd nerve palsy related to eye position

A

Down and out

CN3 supplies:

  • Superior branch: SR
  • Inferior branch: MR, IR, IO

Classic features: ptosis, dilated and unreactive pupil, diplopia

119
Q

Give an overview of 4th nerve palsy related to eye position

A

Up and in

Often have a head tilt

CN4 supplies SO

120
Q

Give an overview of 6th nerve palsy related to eye position

A

Eye facing in

CN6 supplies LR

121
Q

Give an overview of beta blockers as a method of reducing intraocular pressure

A

Timolol, carteolol

Reduce production of aqueous fluid

122
Q

Give an overview of alpha agonists as a method of reducing intraocular pressure

A

Aorackinidine, brimonidine

Reduce production of aqueous fluid

Increase drainage of aqueous fluid

123
Q

Give an overview of prostaglandin analogues as a method of reducing intraocular pressure

A

Latanoprost, bimatoprost

Increase uveoscleral outflow of aqueous fluid

124
Q

Give an overview of carbonic anhydrase inhibitors as a method of reducing intraocular pressure

A

Dorzolamide, brinzolamide

Reduce production of aqueous fluid

125
Q

Give an overview of parasympathomimetics as a method of reducing intraocular pressure

A

Pilocarpine

Increase outflow of aqueous fluid (ciliary muscles contract, opening up trabecular meshwork)

Neuro and special senses (4 decks)

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