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Pre Reg > Unit 6 ocular disease > Flashcards

Unit 6 ocular disease Flashcards

1
Q

DR risk factors

A

Type 1 more common (40%), Type 2 (20%)
Duration of Disease
Before 30yrs – 50% risk after 10 years
After 30yrs – 90% risk after 10 years
Poor Metabolic Control
Pregnancy
Hypertension (most will have both conditions)
Obesity

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2
Q

what is hypertension

A

 Hypertension is a medical condition where the pressure inside the arteries is persistently elevated
 The initial response of retinal arterioles to systemic hypertension is vasoconstriction
 Prolonged HBP can lead to hardening of vessel walls, AV nipping and eventually increased vascular permeability

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3
Q

hypertensive retinopathy grading

A

 Grade 1 – arteriolar narrowing – 2:1 - GP
 Grade 2 – arteriolar narrowing / nipping – 1:3 - GP
 Grade 3 – narrowing, nipping, haemorrhages, exudates and Cotton wool spots – HES
 Grade 4 – narrowing, haems, exudates, Cotton wool spots, disc swelling, macular star - HES
in severe cases swollen disc, macular oedema as well

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4
Q

CRAO

A

 Sudden painless monocular loss in vision
 VA < CF, complete loss – generally all areas of the VF (Unless a cilioretinal artery supplying a critical macular area preserves vision)
 RAPD
 White, oedematous retina; cherry ret spot at fovea; Attenuation of arteries and vein

Referral emergency same day if <24hrs
Urgent if >24hrs

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5
Q

BRAO

A

 Sudden painless altitudinal or sectoral visual field loss; vision may be unaffected
 Signs confined to the region of the retina supplied by the affected branch
 VA is variable; RAPD often present
 Fundus signs may be subtle; whiteish, oedematous SECTOR of the retina (area of ischaemia)
 Altitudinal or sectoral VF defect – which may become permanent if left untreated

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6
Q

ischaemic CRVO

A
  • VA poor
  • RAPD
  • Dilation/tortuosity, flame shaped & dot-blot haem, cotton wool spots
     Rubeosis develops in 50% of eyes – 100 day glaucoma, new vessels at disc and elsewhere - poss vitreous haem as complication
     Macula may develop atrophic retinal and RPE changes, ERM and chronic CMO
     Urgent referral to HES (same day referral to GP for blood workup)
     Emergency referral if IOPs > 40mmHg
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7
Q

ACE inhibitors - Lisinopril & ramipril side effect

A

may cause ciliary body oedema which leads to reduced accommodation and angle closure

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8
Q

hyperthyroidism

A

 Thyroid eye disease / Graves
 WET phase (myogenic) - EOMs (recti; IR affected first) swell up to 8-10x normal size (2-3 years)
 DRY phase (mechanical) - Fibrosis & secondary muscle contracture
 Connective tissue inflammation; redness, discomfort, peri-orbital swelling
 Corneal exposure; gritty/redness
 Diplopia and proptosis
 May cause visual loss due to ONH compression

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9
Q

Marfans syndrome

A

 Autosomal dominant connective tissue disorder
 Tall, thin stature with long limbs
 Myopia, corneal abnormalities, ectopia lentis – dislocation of lens, retinal detachment

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10
Q

rheumatoid arthritis

A

 Dry eye disease / Sjogrens syndrome
 Iritis – 2nd episode; refer for systemic work up
 Episcleritis / scleritis – refer for systemic work up at 3rd episode

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11
Q

multiple sclerosis

A

 Demyelinating disease affecting CNS
 Optic neuritis; mostly commonly retrobulbar

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12
Q

ocular manifestations of high cholesterol

A

o Arcus
o Xanthalesma
o Retinal emboli – Hollenhorst plaque
o CRAO
o CRVO

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13
Q

what is the primary response of the retinal arterioles to systemic HBP?

A

HBP is vasoconstriction
* Arteriolosclerosis refers to hardening and loss of elasticity of small vessel walls
o Manifested most obviously by AV nipping at crossing points
o Mild AV changes may be seen in the absence of HBP
* In sustained HBP the inner blood-retinal barrier is disrupted, increased vascular permeability leading to flame-shaped haemorrhages and oedema
* Increased venular tortuosity can be associated with chronic hypertension and pre-hypertension, though evidence on tortuosity is conflicting
* CRVO

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14
Q

Ankylosing Spondylitis

A

ocular manifestations
o Acute anterior uveitis, occurs in about 25% of pxs
o Episcleritis
o Scleritis
o Keratitis
o Mechanical ptosis
o Cataract

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15
Q

asthma ocular manifestations

A

o Dry eye
o Cataract
o Glaucoma
o CSR – due to steroid inhalers

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16
Q

RVO risk factors

A

o Increasing age (>65)
o HBP
o Hyperlipidaemia
o Diabetes
o Glaucoma
o Oral contraceptive pill
o Smoking

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17
Q

CRAO cause

A

Central retinal artery occlusion (CRAO) is caused by a blockage in the central retinal artery, usually by a blood clot or cholesterol deposit

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18
Q

what is non ischaemic CRVO

A

Where the outer retinal layers are still perfused as choroidal circulation remains
intact
* 30% will progress onto ischaemic

Sudden onset, unilateral blurred vision (6/36-6/60). Main concern: conversion to ischaemic

Signs
* Tortuous dilated veins in all 4 quadrants of the retina
* Round/Blot and flame haemorrhages
* Occasional CWS
* Mild Possible macula and disc oedema
* Mild/absent RAPD

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19
Q

residual signs of cRVO

A
  • Disc collaterals
  • Epiretinal Gliosis
  • Pigmentary changes at the macula
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20
Q

Tx CRVO

A

Treatment – Laser PRP for neovascularisation, Intravitreal Anti-VEGF and steroids for
neovascularisation and macula oedema

Investigation – Investigate underlying cause and blood work up. Assess whether
ischaemic or non-ischaemic.

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21
Q

risk factors CRAO

A

Aged 70-80yrs
* Carotid artery occlusive disease
* systemic hypertension
* high cholesterol
* smoking
* diabetes
* history of stroke or TIA
* Amaurosis Fugax attack (sudden blanking of vision lasting a few seconds)

sudden painless loss of vision

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22
Q

later developments of CRAO

A
  • Atrophy of inner retinal layers and optic nerve
  • Neovascularisation at the disc and iris
  • Vessels remain attenuated and cherry red spot reduces over weeks
23
Q

management CRAO

A
  • Massage the globe with px laying down
  • REBREATHE CO2.
  • Nd-YAG laser of embolus if visible
  • Acetazolamide (Carbonic Anhydrase inhibitors): Decreases IOP by decreasing
    Aqueous Humour production
  • Sublingual Isosorbide dinitrate: Causes vasodilation, can help move a clot
  • Anti-coagulants (e.g. Warfarin) as risk of stroke/ischaemic heart disease is high.
24
Q

symptoms of TIA

A
  • Weakness
  • Numbness down one side of body
  • Vertigo
  • Diplopia
  • Slurred speech and loss of balance/co-ordination
  • Transient vision loss (amaurosis fugax):
    o Curtain coming down on vision, can be total or sectorial, resolves
    completely (centrally first)
    o Most common cause: embolism
    o High risk of impending CRAO or vision loss through AION.
    Urgent referral to GP and Ophthalmology for MRI and bloods.
25
Q

AAION symptoms

A
  • Sudden unilateral vision loss
  • Preceeding amaurosis fugax
  • Possible periocular pain
  • Headache, neck or temple pain
  • Scalp tenderness
  • Jaw claudication
  • Weight loss
  • Fatigue
  • Muscle pain/stiffness
  • Protruding temporal artery – pulseless, tender, doesn’t compress
26
Q

signs AAION

A

Signs
* VA <6/60
* RAPD
* Swollen optic disc
* Possible CWS
* Possible flame haemorrhages
* Arcuate VF defect

AAION can also lead to:
* CRAO
* 3rd and 4th nerve palsy

27
Q

what is NAION

A

Infarction of the optic nerve head due to PCA occlusion as a result of atherosclerosis. No
preceding amaurosis fugax.

Can be due to:
* hypertension
* diabetes
* heart disease
* carotid artery disease

28
Q

signs of NAION

A

Signs:
* Normal – severe reduction in VA
* RAPD
* Dyschromatopsia
* Altitudinal VF defect
* ONH signs:
o Diffuse or sectorial oedema
o Pale or mild hyperaemia
o Possible flame haemorrhages
Emergency referral

29
Q

Cataract cause

A

Cataract – Caused by denaturation of protein fibrils within the lens due to oxidative
stress, increasing age and metabolic disturbance

30
Q

causes of posterior subcapuslar

A

Diabetes
* High Myopia
* Steroids
* Age
* Male
* Thyroid Hormone Use

31
Q

OCT scan layers

A
32
Q

ERM cause and tx

A

causes:
pvd, surgery, retinal conditions like DR, RD, inflammation

tx - vitrectomy

An epiretinal membrane is a thin sheet of fibrous tissue that develops on the surface of the macula and can cause problems with central vision.

33
Q

anatomy of aqueous humour

A

 IOP is the fluid pressure inside the eye which gives structural integrity & support to refractive structures and intraocular contents
 IOP is determined by the balance of secretion and drainage of aqueous humour
 Aqueous humour is produced in the ciliary body (2-3 microlitres per minute) and secreted into the posterior chamber
 Posterior chamber is between the anterior lens surface and posterior iris surface
 The aqueous humour travels between the iris and lens into the anterior chamber via the pupil
 It then drains from the AC via the trabecular meshwork into Schlemm’s canal situated in the anterior chamber angle
 Schlemm’ s canal situated in the anterior chamber angle and drains into the episcleral circulation

34
Q

peripheral iridotomy

A

A hole created to allow drainage of aqueous humour through a different channel,
allowing for the push back of the iris that may lead to iris bombe/anterior synechiae
and ultimately pupil block in ACG. Normally used for ACG or those with narrow
angles.

35
Q

selective Laser trabeculoplasty (SLT)

A

Laser triggers the regeneration of cells in the trabecular meshwork to increase and
improve the outflow of aqueous humour in patients with OAG. Lowers IOP by
approx. 30%. Procedure can be repeated as it wears off over time.

36
Q

Trabeculectomy

A

A bleb is created, usually at the superior part of the sclera to allow fluid to drain out
into the sub-conjunctival space. After reaching this part, it either filters into the
tearfilm, get absorbed by vascular or perivascular conjunctival tissue or through
lymphatic vessels to be drained through aqueous veins

37
Q

Filtration tubes/aqueous shunt

A

In cases where other treatment methods have not worked. The tube creates a new
channel for aqueous humour to drain out underneath the conjunctiva. A bleb is also
created

38
Q

pathogenesis of DR

A
  1. Damage to the endothelium
  2. Loss of pericytes)
  3. Breakdown of blood-retinal barrier
  4. Thickening of capillary basement membrane
  5. VEGF release
39
Q

what are Flame Haemorrhages:

A

Flame Haemorrhages: originate from pre-capillary arterioles in the nerve fibre layer.

40
Q

what are dot blot haemorrhages

A

: arise from the venous end of capillaries (aka. Intra-retinal haemorrhage) in the Inner Plexiform and Inner nuclear layer.

41
Q

what are exudates

A

: Lipid laden neuronal breakdown products that have left leaky vessels with the
blood plasma and accumulate in the outer plexiform layer

42
Q

what are cotton wool spots

A

accumulations of neuronal debris within the nerve fibre layer as a
result of interruption of normal axoplasmic flow. This debris accumulates in the ganglion
cell nerve axons.

43
Q

what are microaneurysms

A

Weakening of the capillary walls due to a loss of pericytes resulting in
an outpouching (typically in the INL)

44
Q

why doess venous beading happen

A

assoicated with ischaemia

45
Q

why do drusen happen

A

Abnormal deposits of lipid material generated by the photoreceptors that
accumulate between the RPE and Bruch’s.

46
Q

risk factors DR

A
  • Longer Duration of Diabetes
  • Poor glycaemic control
  • Pregnancy
  • Smoking
  • High Blood Pressure
  • High Blood Sugar
  • High Cholesterol
  • Black, Native American or Hispanic Ancestry
47
Q

treatments - steroid injection

A

Dexamethasone or iLuven (Fluocinolone) (steroid) injections for Diabetic Macula Oedema: Steroids reduce the inflammation of vessels which causes the
breakdown of capillaries and pericyte loss

48
Q

types of secondary glaucoma

A

 Pseudoexfoliation (open angle)
o PXF = grey-white fibrillary amyloid-material
o Symptoms worsen following exercise

 Pigment dispersion (open angle)
o Young, white, myopic males
o Pigment is deposited on corneal endothelium Krukenberg spindle

 Hyphaemia (open angle)
o Blood in AC caused by trauma

 Phacomorphic (closed angle)
o Lens size increases and blocks drainage

 Rubeosis iridis may lead to neovascular glaucoma
o Pxs with ischaemic CRVO / DR are at risk of developing this
o Iris forms membrane onto TM and new vessels grow within the angle

49
Q

sign guidelines referral

A

Glaucoma (SIGN GUIDELINES) for routine referral

 Optic disc signs consistent with glaucoma
 Reproduceable VF defect in either eye
 Risk of angle closure (VG G1 / gonio > 270deg TM not visible)
 OHT IOP >25mmHg, irrespective of CCT
 OHT - IOP <26mmHg and CCT <555
o OHT meaning IOP >21mmHg
 Emergency / same day for IOP >40mmHg / red eye / angle closure

50
Q

DR grading

A

R0 – no retinopathy

R1 – mild background retinopathy
 At least one of the following features anywhere: dot haemorrhage, cotton wool spot, blot haemorrhage, flame shaped haemorrhage
 Rescreen in 12 months for DRS

R2 – moderate background
 4 or more haemorrhages in one hemi-field only
 Rescreen in 6 months

R3 – severe background / pre-proliferative
 4 or more haems
 Venous beading / IRMA routine referral

R4 – proliferative
 Active new vessels
 Pre-retinal haemorrhage
 Retinal neovasc NVD, NVE
urgent referral

M0 – no maculopathy

M1 – early
 Exudates >1 but <2DD from fovea

M2 – advanced
 Haemorrhages or exudates within 1DD from fovea
urgent referral

 Emergency referral
- Pre-retinal haemorrhage
- Traction retinal detachment
- Rubeosis

51
Q

risks for different races

A

Caucasian = ARMD
Afro – Caribbean = Glaucoma (POAG)
South East Asian (Chinese) = Glaucoma (PCAG)*
Japanese = Normal Tension Glaucoma (NTG)
Asian = Diabetes/HBP

52
Q

what type of glaucoma are myopes at a greater risk of
what type of glaucoma are hyperopes at a greater risk of

A

High Myopia = POAG and RDs
High Hyperopia = PCAG

53
Q

hydroxycholoquine ocular risks

A

Hydroxychloroquine
Decreases pain/swelling of arthritis and prevention of joint damage
Used for RA, Lupus, other autoimmune diseases

Risks:
Usually pxs on long term treatment
Drug is slowly secreted and becomes concentrated in melanin structures (choroid/RPE)

Bulls Eye Maculopathy and central scotomas (detected best with Red Amsler)

54
Q

ocular ADRs for
- amitrptyline
- steroids
- warfarin
- chlorpromazine
- amiodarone

A

Amitrptyline :
Antidepressants
Reduced Accommodation

Steroids :
Anti-inflammatory & Immunosuppressive
PSCC
Glaucoma
Increased IOPs

Warfarin :
Anti- Coagulant
Subconj Haemorrhage

Chlorpromazine :
Sedative for psychotic illness
Yellow/brown deposits on endothelium and anterior lens
Pigmentary changes and clumping at Retinal Layers

Amiodarone :
Anti-Arrhythemia Drug
Vortex Keratopathy
Optic Neuropathy
Subcapsular deposits

Pre Reg (7 decks)

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