Common diseases Flashcards

1
Q

List the aetiological causes of cataracts (7)

A
Age related
Traumatic
Metabolic
Toxic
Secondary 
Maternal infection/drug ingestion
Hereditary
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2
Q

What are the 3 types of age-related cataracts?

What does each look like?

A

Subcapsular (ant/posterior*) → granular deposits
Nuclear sclerotic → opaque cloudiness
Cortical → radial spokes

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3
Q

What kinds of traumatic injuries can cause cataracts?

A
Penetrating eye injury
Blunt injury
Glass blowers (infrared radiation)
Ionising radiation
Electric shock
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4
Q

What are the metabolic causes of cataracts (7)

A
Diabetic (age related earlier + true diabetic (osmotic over hydration))
Galactosaemia
Mannodisosis
Hypocalcaemic syndromes
Fabry's
Wilson's
Lowe's
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5
Q

What are the toxic causes of cataracts? (3)

A

Corticosteroids
Chlorpromazine
Chemo

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6
Q

List some secondary causes of cataracts (4)

A

Anterior uveitis
Hereditary (retinitis pigmentosa, gyrate atrophy, stickler’s)
High myopia
Glaucomflecken

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7
Q

What maternal infections can cause neonatal cataracts?

A

Rubella (50%)
Toxoplasmosis
CMV

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8
Q

What maternal drug ingestion can cause neonatal cataracts? (2)

A

Corticosteroids

Thalidomide

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9
Q

What are some causes of presenile cataracts? (2) + 2 presentations/features of each

A

Myotonic dystrophy - cortical polyhchromatic, post subcapsular stellate
Atopic dermatitis - posterior stellate, dermatitis/no lashes

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10
Q

What are some syndromes associated with cataracts? (4)

A

Downs
Alports
Werner’s
Rothmund’s

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11
Q

What are the 3 classifications of cataracts?

A

Immature
Mature (lens totally opaque)
Hypermature (lens wrinkled)

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12
Q

What are the management options for cataracts? (2)

A
Biometry
Surgical (phecoemulsification)
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13
Q

What other factors must be considered when deciding cataract management? (4)

What is NOT a contraindication for surgery
What is an indication/criteria for surgery

A

Effect on pt’s life (job, ADLs)
General health
Co-existing ocular pathology
Best visual acuity correction

Age not contraindication
Must be mature

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14
Q

What are some possible complications of cataract surgery? (4) + relative incidences

A
Posterior capsule opacification (20%)
Vitreous loss (4%)
Retinal detachment (1%)
Endophthalmitis (0.1%)
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15
Q

What are the clinical features of acute bacterial endophthalmitis? (5)

What are the common pathogens

A
Pain
Marked vision loss
Absent/poor red reflex
Corneal haze
Hypopyon/exudates

Staph epidermidis, s.Aureus, pseudomonas

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16
Q

What Ix can be done for cataracts? + why would Ix have to be done?

A

Ocular B scan (USS)

If suspect posterior pole pathology (but view obscured by dense cataract)

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17
Q

What happens in dry AMD? (physiology)

A
Soft thickenings (Drusens) of Bruch's membrane
→ atrophy / death of photoreceptors (from RPE → inner choroid)
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18
Q

What happens in wet AMD

A
Choroidal neovascularisation (inner choroid)
These vessels bleed/leak → scarring
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19
Q

What are some RFs for age-related macular degeneration? (5)

A
Age
Smoking
CVD (hypertension/lipidaemia)
DM
Low anti-oxidants in blood
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20
Q

What age group does AMD affect?

How does it present?

A

> 50s

Blind spots in central vision + visual distortion

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21
Q

What are some of the social effects of AMD? (4)

A

High falls risk
Difficulty with ADLs
Distress/depression
High use of healthcare/community services

22
Q

How is AMD treated?

A
No cure only low-vision aids
Wet AMD (CNV): 
Laser photocoag (not for foveal lesions) (prevent progression + leakage recurs in 50%)
Photodynamic therapy
Anti-VEGF
23
Q

Describe the basic pathophysiology behind diabetic retinopathy

And what happens specifically in proliferative?

A

Retinal vasculopathy of small vessels → leakage +/or closure and seqeulae (VEGF etc released)

Retinal ischaemia → new vessels on optic disc or retinal surface

24
Q

List the RFs for diabetic retinopathy (8)

A
Duration of DM
Poor DM control
Age
Smoking
Hypertension
Hyperlipidaemia
Renal impairment
Pregnancy
25
Q

What are the clinical manifestations of Non-Proliferative (Background retinopathy) (6)

A
Microaneurysms
Retinal haemorrhages (dots/flames)
Exudates
Cotton wool spots
Vascular dilations (beading) - severe
Intra-retinal anastomoses - severe
26
Q

What happens structurally regarding neovascularisation in PDR

A

Originate from veins
Initially flat but raise into vitreous
Fragile/bleed → Vitreous haemorrhage

27
Q

What are some late changes of proliferative retinopathy? (3)

A

Retinal detachment / fibrosis
Rubeosis iridis
Neovascular glaucoma

28
Q

What are the 3 subtypes of proliferative diabetic retinopathy?
And what can be seen on fundoscopy in each?

A

Focal (retinal thickenings + exudates)
Diffuse (oedema + haemorrhages but no exudates)
Ischaemic (perifoveal capillary network closure → oedema + dark haemorrhages)

29
Q

What can be used to Dx ischaemic retinopathy

A

Fluorescin angiography

30
Q

What are some other effects of DM in the eye? (5)

A
Higher incidence of infections
Delayed healing of infections + corneal abrasions/ulcers
Higher incidence of cataracts
More severe post-op ocular inflamm
Cranial nerve palsies (3/4/6)
31
Q

How is diabetic retinopathy managed?

A

Control diabetes + RFs
PDR: laser photocoag (focals/ grid-diffuse / cannot use in ischaemic)
Anti-VEGF

32
Q

What are some of the modern treatments for age-related macular degeneration? (2)
+ what are their drawbacks

A

Anti-VEGF: neuroprotective + injections wear off 4-6wks + v expensive
Long-acting steroids (triamcinolone): cause cataracts + raise IOP

33
Q

What are the main factors affecting IOP ?

Describe the pathology b/wn IOP and glaucoma

A
Aqeuous production (from ciliary body)
Resistance of drainage (trab mesh)

Raised IOP ± vascular factors → optic disc cupping + death/atrophy of retinal nerve fibres

34
Q

What are the 3 main symptoms of primary open angle glaucoma?

A

Usually asymp as chronic/slow-progressive
Visual field defects
Tunnel vision
Blindness

35
Q

What will be seen O/E in primary open angle glaucoma? (3)

+ what investigations can be done? (3)

A

IOP > 21
Optic disc atrophy (blurring of borders)
Cup:disc ISNT thickness rule lost

IOP (tonometer)
Visual fields
Fundoscopy

36
Q

What are some RFs for Primary Open Angle Glaucoma (5)

A
Raised IOP
FH**
Black race
Diabetes
Myopia
37
Q

Describe the pathophysiology behind primary angle closure glaucoma

A

Lens gradually grows with age → pushes iris closer to trabecular meshwork (+ cuts off at critical point)

38
Q

What are some RFs for primary angle closure glaucoma?(3)

A

Narrow angle (smaller lens / shallow anterior chamber) i.e. smaller globes
Hypermetropia (linked to above)
FH

39
Q

What are the symptoms / signs of acute angle closure glaucoma (6)

In what time scale do symptoms present??

A

PAIN (eyes + headache)
Blurred vision
Red eye
Vomiting (severe)

Corneal oedema
Fixed mid-dilated pupil

Symps may be present for wks before attack (going to bed helps as pupil dilates + pulls away)

40
Q

How is acute angle closure glaucoma managed?
Urgent management (3)
Long-term management

A

Urgent IV carbonic anhydrase inhibitor (acetazolamide)
(Analgesia + anti-emetics)
Wait 1hr
Pilocarpine eye drops (every 5mins)

Laser iridotomy
Trabeculectomy

41
Q

What are some secondary causes of glaucoma? (3)

III Advanced

A

Neovascular: central vv occlusion / DR (→ rubeosis iridis)
Uveitic: inflamm/steroids
Traumatic: blunt/penetrating

Injury/Inflamm/Iatrogenic
Advanced cataracts/diabetes

42
Q

List the medical management options of glaucoma (mainly POAG) (5)

How does each lower IOP

A
Prostaglandin analogues (latanaprost)
Beta-blockers (timolol)
Carbonic anhydrase inhibs (drops/p.o.) (dorzolamide)
Alpha agonist (brimonidine)
Cholinergic (pilocarpine)
43
Q

List the SEs of each medical treatment of glaucoma (5)

A

Prostaglandins - thick lashes, pigmentation
Beta - cardiac/resp effects
Carbonic anhydrase inhibs - taste probs, acidosis
Alpha - dizziness, syncope, allergy
Cholinergic - eye ache + poorest compliance

44
Q

What is done in a laser iridotomy (trabeculoplasty)?

Who is it done in?

A

Shots around trabecular meshwork

All age groups (primary treatment) + with open-angle

45
Q

What is done in a trabeculectomy?

What are its main disadvantages? (2)

A

Creates controlled fistula where aqueous leaks out under conjunctiva

Open pathway for infection
Treatment failure (when conjunctival tissue activates/scars)
46
Q

What are the RFs for a trabeculectomy failing? (5) (PMH/DH)

A
Previous eye surgery
Black race
Diabetes (esp w. retinopathy)
Long-term topical medications (e.g. pilocarpine)
Coexisting/past uveitis
47
Q

What are the obvious features of intraocular foreign body?
+ important things to check

What Ix are done

A

Sudden onset irritation + photophobia (±vision loss)
NB ask exact mechanism + check under eyelid

X-Ray/CT

48
Q

How is ocular chemical injury managed? (4)

A

Urgently irrigate w. saline (litres)
Determine substance type
Compare pH for both eyes (alkaline worse)
Abx/VitC/Steroids/Mydriatics

49
Q

List some complications of blunt ocular trauma? (8)

A

Peri-orbital haematoma
Sub-conjunctival haemorrhage
Hyphaema (+ acute glaucoma)

Traumatic cataracts
Lens dislocation (zonule rupture)

Retinal tear/detachment
Extensive retinal haemorrhage - v v severe
Vitreous haemorrhage- v v severe

50
Q

What is a blow out fracture + what features would present? (2)
List a complications

A

Weak orbital floor fracture + eye thru floor into maxillary sinus

Restriction of eye movements
Periorbital swelling

Inferior rectus can get trapped/ischaemic if not released

51
Q

What investigations are done in a blow-out fracture (2)

A

X-Ray (checking opacification of sinus) (not Dx)

CT (for conclusive)