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Phase 3b > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

describe the location of damage to create
1. total right eye vision loss
2. bitemporal hemianopia
3. lest nasal hemianopia
4. right homonymous hemianopia
5. left homonymous hemianopia with macular sparing

A
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2
Q

pathophysiology of acute angle-closure glaucoma

A
  • iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining
  • continual buildup of pressure causing acute symptoms – emergency
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3
Q

risk factors for acute glaucoma

A
  • Increasing age
  • Family history
  • Female (four times more likely than males)
  • Chinese and East Asian ethnic origin
  • Shallow anterior chamber
  • Certain drugs – TCA, anticholinergics, adrenergics
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4
Q

presentation of acute glaucoma

A
  • Generally unwell with a short history of severely painful red eye, blurred vision, halos around light, headache, n+v
  • On examination:
    o Red eye
    o Hazy cornea
    o Decreased visual acuity
    o Mid-dilated pupil
    o Fixed-size pupil
    o Hard eyeball on gentle palpation
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5
Q

management of acute glaucoma

A
  • Laser iridotomy usually required for definitive treatment (makes holes in iris for humour to flow from posterior chamber directly to anterior
  • Pilocarpine eye drops – causes pupil constriction
  • Acetazolamide (oral or intravenous) – carbonic anhydrase inhibitor
  • Hyperosmotic agents (e.g., intravenous mannitol) increase the osmotic gradient between the blood and the eye
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6
Q

chronic/acute angle glaucoma

A
  • Glaucoma = optic nerve damage caused by a rise in intraocular pressure
  • Raised intraocular pressure is caused by blockage in aqueous humour trying to escape the eye
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7
Q

physiology of anterior/posterior chambers of eye

A

Anterior chamber of the eye is between the cornea and iris, posterior is between the lens and the iris – both are filled with aqueous humour (supplies nutrients, made by the ciliary body, drains through the trabecular meshwork to the canal of Schlemm then into general circulation)

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8
Q

pathophysiology of chronic/acute angle glaucoma

A

gradual increase in resistance through the trabecular network causing an increase in pressure
* Raised intraocular pressure causes cupping of the optic disc – optic cup is normally <50% of the size of the optic disk

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9
Q

risk factors of a chronic/acute-angle glaucoma

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Myopia (nearsightedness)
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10
Q

presentation of chronic/acute angle glaucoma

A
  • gradual onset peripheral vision loss
  • pain, headaches, blurred vision, halos around light
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11
Q

management of chronic/acute angle glaucoma

A
  • 360° selective laser trabeculoplasty
  • Prostaglandin analogue eye drops
  • Trabeculectomy surgery if other treatments ineffective
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12
Q

cataracts

A
  • Progressively opaque eye lens which reduces the light entry and visual acuity.
  • Can be congenital and tested for with the red light reflex during NIPE
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13
Q

presentation of cataracts

A
  • Slow reduction in visual acuity
  • Progressive blurring of the vision
  • Colours becoming more faded, brown or yellow
  • Starbursts can appear around lights, particularly at night
  • Loss of red light reflex
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14
Q

management of cataracts

A

surgery for new lens

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15
Q

blepharitis

A
  • Inflammation of the eyelid margins
  • Gritty, itchy, dry eyes
  • Can be caused by dysfunction of the meibomian glands
  • Can lead to styes and chalazions
  • Warm compress and gentle cleaning
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16
Q

stye

A
  • Hordeolum externum = infection of the glans of Zeis (sebaceous glands) or glands of Moll (sweat glands)
  • Hordeolum internum = infection of the Meibomian glands – more painfull and deeper
  • Hot compress and analgesia – topical abx if associated with conjunctivitis
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17
Q

chalazion

A
  • Forms when a blocked Meibomian gland swells – often called a Meibomian cyst
  • Swelling in eye lid – usually non-tender
  • Warm compress, gentle massage towards eyelashes
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18
Q

entropion

A
  • When the eyelid turns inwards – can cause pain, corneal damage and ulceration
  • Tape eye lid down to prevent recurrence – need eye drops if eye stays open
  • Definitive management is surgical
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19
Q

ectropion

A
  • Eyelid turns outwards - can result in exposure keratopathy when eyeball exposed and not adequately lubricated
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20
Q

trichiasis

A
  • Inward growth of eye lashes
  • Cause pain, can lea to corneal damage and ulceration
  • Remove affected eyelashes
21
Q

periorbital cellulitis

A
  • Eyelid and skin infection infront of the eye
  • Swollen, red, hot skin of eyelid
  • Systemic abx – need to prevent development into orbital cellulitis
22
Q

orbital cellulitis

A
  • Infection around the eye including tissue behind the orbital septum
  • Pain with eye movement, vision changes, abnormal pupil reactions, proptosis (eye bulging)
  • Emergency admission under ophthalmology
  • IV abx, may need surgical drainage if abscess forms
23
Q

conjunctivitis

A
  • Inflammation of the conjunctive (thin layer of tissue that covers the inside of the eyelids and the sclera)
  • May be bacterial, viral or allergic
  • Unilateral or bilateral
24
Q

presentation of conjunctivitis

A
  • Red, bloodshot eye
  • Itchy or gritty sensation
  • Discharge
  • Doesn’t cause pain, photophobia or reduced visual acuity
  • Bacterial – purulent discharge – worse in morning
  • Viral – clear discharge, coryzal symptoms
25
Q

causes of an acute painful red eye

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury
26
Q

causes of an acute painless red eye

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
27
Q

pathophysiology of diabetic eye disease/retinopathy

A
  • Increased vascular permeability = leaking blood vessels, blot haemorrhages, hard exudates (yellow/white lipid and protein deposits in retina)
  • Microaneurysms and venous beading (walls of veins appear like a string of beads)
  • Damage to nerve fibres in retina – cotton wool spots/fluffy white patches on retina
  • Intraretinal microvascular abnormalities (IRMA) refer to dilated and tortuous capillaries in the retina. These can act as a shunt between the arterial and venous vessels in the retina.
  • Neovascularisation involves the release of growth factors in the retina, stimulating new blood vessel development.
28
Q

grading of diabetic eye disease

A
  • pre-proliferative
  • proliferative (neovascularisation)
29
Q

management of proliferative diabetic retinopathy

A

pan-retinal photocoagulation, anti-VEGF meds (intravitreal injection) or surgery

30
Q

what is keratitis

A

inflammation of the cornea

31
Q

causes of keratitis

A
  • Viral infection (e.g., herpes simplex)
  • Bacterial infection (e.g., Pseudomonas or Staphylococcus)
  • Fungal infection (e.g., Candida or Aspergillus)
  • Contact lens-induced acute red eye (CLARE
32
Q

HSV keratitis

A
  • Most common cause
  • Can be primary or recurrent
  • Usually affects only the epithelial layer of cornea.
  • Inflammation of the stroma (layer between epithelium and endothelium) can lead to stromal necrosis, vascularisation and scarring
33
Q

presentation of keratitis

A
  • Painful red eye
  • Photophobia
  • Vesicles (fluid-filled blisters)
  • Foreign body sensation
  • Watery discharge
  • Reduced visual acuity
  • Fluorescein staining shows a dendritic (branching) ulcer
34
Q

management of keratitis

A

urgent referral, may need topical or systemic treatment and corneal transplant if scarring

35
Q

macular degeneration

A
  • Age-related MD is a progressive condition affecting the macula
  • Most common cause of blindness in UK
  • 90% non-neovascular/dry and 10% neovascular/wet
36
Q

what does the macula do and what are the 4 layers

A
  • Macula is in centre of retina and generated high-definition colour vision
  • Has 4 layers:
    o Choroid layer (at the base), which contains the blood vessels that supply the macula
    o Bruch’s membrane
    o Retinal pigment epithelium
    o Photoreceptors (towards the surface)
37
Q

pathophysiology of macula degeneration

A
  • Drusen = yellow deposits of protein/lipids between retinal pigment epithelium and Bruch’s membrane in AMD
  • Other features: Atrophy of the retinal pigment epithelium, Degeneration of the photoreceptors
38
Q

pathophysiology of wet macula degeneration

A

new vessels develop from choroid layer and grow into retina, they leak and cause oedema and faster vision loss. A key chemical causing vessel development is vascular endothelial growth factor (VEGF).

39
Q

presentation of macula degeneration

A
  • Unilateral vision loss with:
    o Gradual loss of central vision
    o Reduced visual acuity
    o Crooked or wavy appearance to straight lines (metamorphopsia)
  • wet AMD presents more acutely with complete vision loss in 3 years
40
Q

management of macula degeneration

A
  • Specialist
  • Dry AMD = monitoring and reducing risk of progression
  • Wet AMD = anti-VEGF meds (ranibizumab) into vitreous chamber monthly
41
Q

scleritis

A
  • Inflammation of the sclera
  • Sclera = outer layer of connective tissue around eye (except cornea) – white part of eye
  • Most severe type = necrotising scleritis which can lead to perforation
  • Most are idiopathic or related to a systemic inflammatory condition (RA, vasculitis)
  • Less commonly due to infection
42
Q

presentation of scleritis

A
  • Gradual onset
  • Red, inflamed sclera (localised or diffuse)
  • Congested vessels
  • Severe pain (typically a boring pain)
  • Pain with eye movement
  • Photophobia
  • Epiphora (excessive tear production)
  • Reduced visual acuity
  • Tenderness to palpation of the eye
43
Q

management of scleritis

A

refer, NSAIDs, steroids, immunosuppression, antimicrobials

44
Q

uveitis

A
  • Anterior uveitis involves inflammation of the anterior uvea causing hypopyon (fluid collection containing inflammatory cells)
  • anterior most common
45
Q

causes of uveitis

A
  • An autoimmune process usually causes it, but it can be due to infection, trauma, ischaemia or malignancy.
  • Associations – seronegative spondyloarthropathies, inflammatory bowel disease, sarcoidosis, Behcets disease
46
Q

presentation of uveitis

A
  • Painful red eye (typically a dull, aching pain)
  • Reduced visual acuity
  • Photophobia (due to ciliary muscle spasm)
  • Excessive lacrimation (tear production)
47
Q

examination findings of uveitis

A
  • Ciliary flush (a ring of red spreading from the cornea outwards)
  • Miosis (a constricted pupil due to sphincter muscle contraction)
  • Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes
  • Hypopyon
48
Q

management of uveitis

A
  • Refer
  • Steroids (eye drops, oral or intravenous)
  • Cycloplegics (e.g., cyclopentolate or atropine eye drops)
  • May need DMARDs or anti-TNF drugs
49
Q
A

Phase 3b (5 decks)

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