PEG Flashcards
1
Q
Categories of treatment for Glaucoma
A
1st choice: initial therapy by practitioner
1st line: approved drug for lowering iop
Therapeutic trial: topical in one eye at a time
Effective treatment: equal to effect on average population
2
Q
Glauc treatment
A
MEDS, LASER, SURGERY
3
Q
PROSTAGLANDIN
A
First line glauc treatment
Increase uveoscleral outflow
SE: irritation
CN: not effective in congential glauc or angle closure, Dont give to inflam or CMO
4
Q
Beta adrenergic blocking agents
A
First line glauc therapy
Decrease AH production
CI: lung/heart disease
5
Q
Cholinergic agents
A
Pilocarpine:
Increase AH outflow via miosis
CI: neovasc, 2ACG
SE: Accom spasm
6
Q
Carbonic Anhydrase Inhibitors, types and mech
A
Topical (Dorzolamide, Brinzolamide) and acetazolamide (most powerful for IOP reduction)
Decrease AH production
7
Q
Adrenergic agonists types and SE
A
Third Line
Apraclonidine: Decreasing AH prod, causes dry mouth, allergic conjunct
Brimonidine: Decreasing AH production and inc Uveoscleral outflow, causes dry mouth and fatigue
8
Q
Simbrinza
A
Brinzolamide, brimonidine
9
Q
Cosopt
A
Timolol and dorzolamide
10
Q
Glauc surgery indications
A
> 30mmhg
Signif IOP fluctuations
11
Q
Trabeculectomy
A
Penetrating glauc surgery
12
Q
Non penetrating glaucoma surgery
A
deep sclerectomy
viscocanalostomy
13
Q
PACG treatment
A
pilocarpine, emergency referral
laser periphery iridotomy
monitor reg
14
Q
Secondary Glaucoma types
A
pigmentary pseudo-exfoliative inflammatory LINKS W RD neovascular LINKS W RD post-traumatic steroid induced LINKS W RD
15
Q
Pigmentary Glauc
A
- Pigmentary dispersion syndrome assoc with GON
- open angle
Rubbing between lens zonule and iris pigment epithelium, so pigment released,
younger white, myopic
CF - iris transillumination, wide open, Sampaolesi’s line, fluctuation IOP, haloes
antiglauc drops
laser trabeculoplasty
laser iriditomy
trabeculectomy
16
Q
Pseudoexfoliative Glauc treatment
A
1) Pseudoexfoliative syndrome with GON,
2) ocular manifestation of secondary disorder,
3) lakes and sheets of material on anterior seg
Greek 50-70, start unilateral
CF - translucent disc like deposit , nuclear cataract, IOP higher than other glauc, SEVERE VF LOSS
anti glauc drops
Laser trabeculoplasty
Trabeculectomy
17
Q
Inflammatory Glaucoma
A
Repeated uveitis, inflam of cells, scarring, posterior synchiae eventually results in angle closure
likely to have herpetic uveitis, toxoplasmosis
presentation - red, painful, photophobic
CF - AC inflam, red eye, iris bombe
anti-inflamm, NO PILOCARPINE
cycloplegia
surgery
18
Q
Neovascular glaucoma treatment
A
Prolonged hypoxia, diab ret, crvo
new vessels around pupillary margin, then iris
fibrovascular tissue proliferation onto chamber angle
DD - High IOP, corneal oedema, AACG
anti glaucoma drops
pan retinal photocoagulation
19
Q
Steroid induced glaucoma
A
History of corticosteroid use, should be used with caution if FH of glaucoma, take baseline IOP before
surgery
withdraw STED, Medical treatment
20
Q
Glaucoma assoc with RD
A
Neovasc, inflam, scarring, surgery, treatment with steroid
21
Q
Lens induced glaucoma
A
Becomes swollen by injury, leakage of lens material
Phacomorphic lens (swollen) blocks pupil
Can result in lens displacement
Red eye, inflam
22
Q
Congenital Glaucoma
A
Posner schlossman syndrome
neovascular glauc
trabeculitis
23
Q
Glaucoma assoc with eye surgery
A
Cataract surgery - AC lens, foreign material, , injured angle and uveitis
Laser treatment - Pigment dispersion, injured angle, uveitis
Penetrating keratoplasty - angle damage,, steroids
RD surgery - silicon oil, steroids
24
Q
Secondary glauc causes
A
Trabeculitis Obstruction of the intertrabecular spaces Medication Trauma Increases in episcleral venous pressure
1) Synechial angle closure - abnormal vessels/inflam
2) Non synechial - abnormal lens/swelling
25
Prevention of secondary Glaucoma
```
Early detection and management
Education
Good management of eye conditions inducing
Secondary glauc
Diabetes control
```
26
Optic Neuritis, what is it?, sx, signs, treatment
Inflammation, demyelinating of ON
Manifestation of MS
sx) loss of vision in 1 eye, caused by heat/ exercise
signs) RAPD, drop in VA, blurred disc margin
treatment) steroids and urgent referral
27
Signs of ON dysfunction
reduced VA, RAPD, impaired CV, VF defect
28
Optic nerve VS Macular Disease
OND: RAPD, severe dyschromatopsia, reduced brightness
MD: No RAPD, mild dyschromatopsia, augmented brightness,
29
Optic Neuropathy types
inflam, ischaemia, compressive, toxic, traumatic, congenital
30
Anterior ischaemic optic neuropathy types
PCA occlusion
1) arteritic ION - giant cell arteritis
2) non arteritic - caused by ACS
31
Arteritic AION, what is it?, sx, signs, management
assoc with giant cell arteritis
sx) headache, pain in temple, scalp tenderness, pain while chewing
signs) sudden visual loss (permanent) then amaurosis fugax attacks
fundus swollen and pale OD, cupping
thick and pulseless temporal artery
emergency referral and steroids
32
Non-arteritic AION (sx and signs)
```
no sx,
visual loss sudden (not severe),
altitudinal hemianopia,
reduced CV,
ONH pale and oedema
```
33
Compressive optic neuropathies
ON glioma and meningioma (tumours between brain and spine)
34
Toxic Neuropathy, who does it affect? sx and signs
Heavy drinkers and smokers, ingest antifreeze
Vit B1, B12 deficiency
meds used for TB
sx and signs - progressive loss of vision,
depressed vision extended from blindspot
35
Traumatic Optic Neuropathy (mech, sx, signs)
compression,
Impact to head,
vasospasm,
ischaemia
sx - vision and visual field loss
signs - RAPD
36
Lebers Hereditary Optic Neuropathy, who and signs
9 Men:1 teenagers
rapid unilateral visual loss, pseudo oedema of disc.
H/S
37
Papilloedema, symptoms, mechanical and vascular signs
swollen OD due to intercranial pressure
sx - headache, vision blanking for seconds
signs
mechanical - ONH elevation, blurring of OD margins, cupping, choroidal folds
vascular - hyperaemia of disc, CWS, hard exudates, peripapillary haemorrhages.
38
Papilloedema grading, and cause
1 - early, blurring of OD margin, C halo of oedema round disc
2 - halo surrounds OD
3 - oedema covers blood vessels as they leave disc
4 - oedema covers disc
Cause - brain tumour, meningioma, hydrocephalus, pseudotumour cerebri
39
Pseudotumour Cerebri, who?, risk, sx, signs, management
young overweight women, idiopathic
risk - anaemia,
symptoms - headaches, vision blur, diplopia
signs - papilloedema
management - emergency referral and steroids, weight loss
40
Chiasmal syndrome, cause, sx (ocular, systemic), DD, management
Chiasmal lesions.
sx - ocular -> VF loss
sx - systemic -> headache, body changes
DD - R Disease
management - VF testing, neuroimaging, lumbar puncture
41
Monocular transient visual loss
| & binocular, time frame and meaning
cause - anterior to chiasm
if its evoked by gaze - lesions of orbit, meningioma of the ON sheath
Lasting seconds/minutes - amaurosis fugax
Lasting hours - thrombi, carotid stenosis, migraine
Binoc - posterior to chiasm, migraine, AV malformation, emboli
42
Post traumatic glaucoma
Blunt trauma, after: (penetrating, chemical injuries & radiation therapy)
May have previous trauma, eg cataract, ret breaks, RD
43
What is non organic visual loss?
visual complaint not explained by tests
types - conversion reaction, hysterical blindness and malingering
44
Conversion reaction, cause and symptoms
<35 yrs, symptoms are a result of repressed emotional stress.
sx - weakness, paralysis, urinary retention
45
Ocular Hysteria, what is it?, and symptoms
blindness with fluctuating VA, and VF defects (ring scotoma).
diplopia, blepharospasm, colour blindness
46
Malingering, what is it?, indications, tests
Don't want to do duties for a particular reason
indic:
1) maybe referred by solicitor,
2) sx way beyond objective findings
3) does not cooperate with treatment
4) personality disorder
Tests:
pref looking, flinch test (approaching to make blink), increase illumination and watch how they enter the room.
Check for RAPD, and stereoscopic testing
VF, ERG, and ask them to come back for another examination
47
Causes of binocular diplopia and sx
Orbits- trauma, tumour, thyroid infection disease
Ocular muscles- thyroid disease, injury, dystrophy
CN palises
Brain - tumour, injury, stroke
4CN - vertical diplopia better with head tilt
6CN - horizontal diplopia and worse D
48
RAPD, conditions leading to it
- Unilateral ON - Optic Neuritis, asym glaucoma, ON tumour
| - Unilateral Retinal Diseases - RD, severe AMD, tumours
49
Efferent Pupillary Abnormalities, categories, examples and which is the abnormal?
- Anisocoria- difference in pupil size
1) physiological- less than 1mm difference, both eyes constrict to light and equally promptly, may switch sides
2) pathological - horners, 3CN, Adies pupil, Argyll robertson, RAPD
Abnormal does not respond to bright light - unilateral pharmacological miosis
50
Horners syndrome, who, what, when?
Congenital or acquired
ptosis on small pupil side, if on other, 3CN lesion
miosis, anhydrosis
aniscoria greater in dark
51
Tonic Pupil, what is it?, who?, reason
Pupil reacts badly to light, but well to accom, so will eventually constrict on near
near response is tonic
unilateral and women
3CN ganglion
52
Argyll Robertson Pupil, what is it and what is it linked with?
Both pupils small and irregular,
| linked with neurosyphillis
53
Nystagmus, what is it, categories, common types?
oscillation of eyes
symmetrical - same speed in both eyes (pendular nystagmus)
Asymmetrical - Speed different between eyes (Jerky nystagmus)
Cerebellar Jerk, Down-beat, see-saw, congenital pendular
54
Cerebellar Jerk nystagmus, what is it, when does it increase, what else to do?
jerky, large amplitude, low frequency
increases when look in direction of fast phase
Scan for cerebellar signs: headache, limb weakness
55
Down beat nystagmus, what is it?, when is it bigger, cause?
In primary position, fast phase downwards.
bigger when looking laterally
cause: Stroke, MS, alcohol
56
See-saw Nystagmus, what is it, what does it indicate?
torsional nystagmus - one eye elevated and intorts the other is depressed and extorts.
Chiasmal lesion, examine VF
57
Congenital Pendular Nystagmus, when does it increase, what to examine
Nystag decreases on convergence, but increases on covering of an eye.
abnormal head posture
Examine ASegment for: congenital cataract, aphakia, aniridia
Examine PSegment for: ON hypoplasia,
58
Managing a child with congenital nystagmus
establish cause, improve vision, prisms for convergence, surgery
59
Congenital CNIII Palsy, cause, characteristics
Cause - FOH, traumatic birth.
characteristics -
XOT, HYPOT, HYPERT, intorsion Ptosis,
limitation of elevation, depression, adduction
60
Acquired CNIII Palsy, cause, symptoms, characteristics
Causes - tumours, trauma, inflammation of vascular lesions of brain
Sx - unilateral ptosis, ocular pain, headache, diplopia
Characteristics - partial, complete. Ptosis, elevation, depression, abduction limited.
61
CN4 Palsy, features
features: vertical diplopia, head tilt to opposite side, hypertropia
62
Congenital CN6 Palsy, syndrome
Duanes syndrome - congential absence of 6TH CN
| Mobius syndrome - Blateral palsy of 6TH AND 7TH CN
63
Acquired CN6 Palsy, cause, symptoms, signs
cause - tumour, trauma, inflammation of vascular regions of brain
sx - horizontal diplopia, headache
signs -
esodeviation increases when gazing on the same side and greater at D
abnormal head position.
64
Blood Supply to ONH, anatomy
1) Superficial NFL - capillaries originating from Retinal Arteries
2) Prelaminar region - short PCA from recurrent choroidal arterioles
3) Laminar region - short PCA
4) Retrolaminar -
branches of pial arteries and by the short PCA
CRA - contributes small branches
65
Glaucomatous OD,
| what to look for and rules?
what to look for?
1) Vertical cup elongation
2) thin NRR
3) notching haemorrhage
4) vascular changes
5) peripapillary atrophy
Rules to assess
1) observe scleral ring to show limits and OD size
2) size of rim
3) look for haemorrhage
4) examine RNFL
4) examine peripapillary atrophy
66
OD size & what haemorrhage indicates, and how
race dependant
pink is bad sign
Small OD - <1.2mm - small changes if glaucomatous, VF defects can present despite looking normal. LOOK FOR PARIPAPILLARY ATROPHY
Large OD - >1.8mm - cup shape and changes in NRR
Haemorrhages
- risk of glauc
- transient/recurring
- comes before notching
67
Vascular changes
```
Kinking
nasal migration
bowing
baring
sharpen vessels
```
68
RNFL - retinal never fibre layer, what to look for?
- Red free, brightness
- visibility of peripapillary RV, striation
- look for diffused and localized loss
69
Peripapillary atrophy, what is it
Alpha zone - hypo/hyper pigmentation region around, like shadow
beta zone -
if large - thin nrr, - shows glaucomic progression
70
NRR size and how to examine and indications?
1.33 - 2.66mm
NRR
1) Loss of tissue from edges, CARDINAL SIGN OF GON
2) ISNT rule
3) GON signs - notching, haemorrhage across rim, abnormally thin in 2 sectors
71
Non - glaucomatous cupping, signs of non glaucoma
congenital, coloboma, AION,
traumatic/shock optic neuropathy,
radiation compression
syphillis
rim pallor, <50 yrs
central VF loss
72
Autosomal dominant optic atrophy, signs
early onset, central scotoma, colour blindness, cupping
73
OD Hypoplasia
abnormal development of OD,
| small and irregular, wedge shape defects
74
Optic Disc Pit, what is it, sx
uncommon congenital, pit in disc
| sx - enlarged blind spot, vf defect, enlargement of disc
75
Optic disc coloboma, what is it?
white excavation within disc, central and empty
| no significant peripapillary pigmentation
76
Neuroimaging, who for?
Loss of central VA, VF
hemianopic VF loss
acute onset vision loss
neuroretinal rim pallor
77
Disc damage, full function
congenital, prefunctional
78
Functional Loss, little damage
VF test error, observational error
79
SOAPF
Subjective - px's observations
Objective - optoms observations and tests
Analysis - optom understanding of problem
Plan - advice, treatment, interventionist action
Followup
80
Px Red eye, h/s, as
- H/S - CL (ulcer), sticky discharge (infective conjunct), iritis (reoccurrence), itching (allergic conjunct)
- AS - lid swelling (acute dacriocystitis), cillary injection, ulcer/FB, reaction to light
- Fluorescein
- Lid eversion
DD -
with pain - AACG, Uveitis
without - Conjuct
81
Acute Dacryiocystitis
Inflammation of Lacrimal sac, assoc w obstruction of naso-lacrimal duct
82
Sudden loss of vision conditions, H/S check
Unilateral painless - CRAO, ION, RD, VIT HAEM,
Unilateral painful - AACG, Optic neuritis
Bilateral - Papilledema, malignant hypertension
H/S -
transient visual loss (curtain) - amaurosis fugax
Visual loss, flashes, floaters - RD, vit haem
Poorly controlled diab - diabetes mellitus and laser to retina
Headache - Giant cell arteritis
Pain on eye movement (young) - optic neuritis
83
Causes of sudden visual loss
```
CRAO, BRAO
CRVO, BRVO
VIT HAEM, RD
Ischaemic Optic Neuropathy, inc giant cell arteritis
Optic neuritis
```
84
Px with blurred vision, what to do
VF,
reaction to light,
dilate w tropicamide and fundus exam
85
Ocular trauma types
Chem,
Blunt,
Open eye,
FB
86
Chemical burn trauma, what is it, sx, signs, management
Exposure to chem
sx - pain, redness, photophobia, blurred
signs - epith loss, chemosis, corneal clouding, limbal ischaemia
mng -
wash with water,
If severe blepharospasm - topical anaesthesia aswel
industrial burn - eye casualty
assess severity by degree of cornea whiteness around cornea
87
Blunt Trauma, presentation and examination
P - Black, painful, reduced and double vision
E - corneal abrasion, hyphaemia, dilated
posterior examination difficult due to swelling
88
Open eye trauma, presentation, examination and management.
P - children who play with sharp objects, shattered wind screen, high velocity missiles at work place
E - VA reduced, displacement of iris
M - immediate eye casualty
89
Ruptured globe, causes, sx , signs, management
Cause - high velocity injury, blunt or sharp object
Sx - severe pain and loss of vision
Signs - subconjunctival haemorrhage, prolapse of intraocular contents
Mngmt - tetanus prophylaxis, x ray, plastic shield, urgent referral -
- -->primary - restores globe integrity
- -->secondary - attempt to restore
90
Ocular foreign body, cause, sx, signs, examination, management
c - high velocity object
sx - mild to moderate pain, red and watery
signs - May not be obvious
exam - VA, eversion
mngemnt - remove, refer in 24 hrs if cannot be removed. If intraocular, should be referred immediately.
91
Structure of eye
1) Posterior segment
- vitreous cavity
- Fundus of eye - ret, choroid, ON, interior surface of eye
2) Retina
- neurosensory retina
- retinal pigment
- subretinal space
- choroid
- sclera
3) Macular
5. 5mm, 18-20 degrees of field
- fovea - 1.5mm, 5 degrees, central depression.
- high cone density for va
4) Ora Serrata
- Between retina and cillary body
- transitional zone between non photosensitive region to complex photosensitive
- site of vitreous base
- CI - vitreous detachment and retinal break formation
5) Vitreous cavity
- 98% h2o, collagen fibrills, hyaluronic acid
- firmly attached to base which straddles ora serrata
- less attached to macula and vessels
- abnormal vitreoretinal adhesions
92
Diagnostic Process
- History - Elicit sx
- Visual fx, VA, Rx, amsler, VF
- examination - red reflex, slit lamp, dilation
- Investigating -Fundus photo, scanning laser ophthalmoscopy SLO, wide field SLO, OCT, hospital based tests
93
OCT
- cuts 2D optical sections, 3D image formed
- based on interferometry
- digital manipulation
- safe quick and easy
- hospital
94
Hospital- Based imaging
-AF,RF,IR
different retinal layers, lipofuscin
-Fluorescence angiography
vascular integrity, fluorescein, indocyanine green
OCT angiography
High res OCT
polarisation sensitive OCT
95
Types of headaches and sx
- Tension - non pulsating, bilateral. 30mins to 7 days
- Cluster - unilateral, supraorbital, deep intense, 15 mins to 3 hrs. associated with nasal congestion
- Migraine - unilateral,
due to broken sleep/depression,
if aura - visual, speech, motor. 4hrs to 3 days
- Eyestrain - eye-aches, decomp phoria, strabismus, after intense eye use
- High intercranial pressure - tumours, trauma, inflam, worse when lying down
- Giant cell arteritis
- Neuralgia - pain caused by lesions or dysfunction of nervous system.
Inflam and trauma, burning and shooting
96
Types of Neuralgia, what is it, cause, treatment
Trigeminal - most severe pain. stabbing pain in the nerve, triggered by day to day activity, ms/trauma/tumour, carbamazapine /surgery
Occipital - head trauma, muscle contraction, arthiritis
Postherpetic - after acute herpes zoster attack, stabbing pain, >1 month after herpes zoster, triggered by lightest touch,
med, electric nerve stim, hypnosis
97
Types of tumour, what is it, diagnosis, treatment
Benign - dont spread, only life threatening if causing too much pressure
Primary Malignant brain tumour - spreads to other parts of brain only, mental changes, loss of vision, hearing loss, speech difficulty
Lumbar puncture, MRI, x ray
chemo, surgery, radiation
98
Stroke, what is it, rf, sx
Blood flow to brain stops, ischaemic or haemorrhage,
RF - high bp, smoking, heart disease, diabetes
```
sx -
e - eyes dev or lose vision
f - facial numbness or weakness
a - sudden arm/ leg weakness on one side
s - slurred speech or difficulty speaking
t - time to call 999
```
99
Epilepsy, what is it, types, DD, diagnosis, what to do, after seizure?
recurring seizures, disrupting nervous system, mental and physical dysfunction
Partial - jerk movements/ tingling
General - grand mal
Absence - petit mal
DD - alcohol withdrawal, drug overdose, panic attack, stroke
diagnosis - EEG AND CT SCAN
what to do - 999, objects away, crowds away, do not restrain
after seizure - rotate and wipe away saliva, reassurance and minimalize embarrassment
100
MS, what is it, early sx, sx that occur later, DD, diagnosis, treatment
autoimmune
sx early - fatigue, poor coordination, elec sensation that runs down legs
sx late - imbalance tremors, mood swing, difficulty swallowing
DD- stroke, alcohol, emotional disorders
Diagnosis - MRI, lumbar puncture
treatment - interferon, steroids
101
Myasthenia Gravis, what is it?, types, who, sx, diagnosis, treatment, myastheic crisis
- Autoimmune, destroy communicate between nerves n muscles
- ocular and generalized
- women>men
-ptosis, lid fluttering, diplopia, difficulty: swallowing, talking, chewing, moving
diagnosis - mri, ct, muscle biopsy
treatment - prisms, surgery, diet
refer to neurologist
crisis - respiratory failure, stress, anxiety, tachycardia
CALL 999
102
Facial nerve palsy, cause, sx, management, coma n what to do?
innervates facial expression muscle
infection, inflam, tumour, trauma
idiopathic facial nerve palsy - bells palsy
sx - paralysis on one side of face, decreased taste, hard to close eye, dry eye
mngmnt - treat de, corneal problems
coma - get px on side, face turned jaw pointing up, loosen clothes, 999
103
Vitreous, contents
- h2o, collagen, hyaluronic acid
| - vitreous attached to vitreous base, which straddles ora serrata
104
Vitreous opacities
- floaters - persistent hyaloid remnants
- asteroid hyalosis
- pigment - melanin granules from ret tears
- cells - vit haem, malignant
105
Vitreous degen
- volume decreases with age, fragmentation of framework, lacunae formation - liquid pockets of gel
```
- Posterior Vitreous Degeneration
partial or
complete:
• Detachment of posterior hyaloid membrane
• Weiss ring
```
106
Posterior Vitreous Detachment, what is it, sx, signs, risks, management
- vit traction, haemorrhage and tear
- floaters, photopsia (golden arc of light) if persistent and retinal traction
- SL dilated - posterior hyaloid face, pigment
- ophthalmoscopy - weiss ring, retinal tear
- risks - retinal tear, vit haemorrhage, myope
- management
sx resolved and >6weeks, low risk, routine referral
acute <1week, NO LOSS OF VISION, soon referral
IF LOST, URGENT REFERRAL
107
Retinal breaks, tears and holes. AND TREATMENT.
- periph are hard to see, use 3 mirror
- can cause retinal detachment
Treatment
- uncomplicated PVD - explanation
- retinal break - laser cryotherapy
108
Retinal Detachment, types, how, sx, management, who, treatment
Separation of neurosensory retina and rpe.
4 types:
1) - Rhegmatogenous - PVD assoc,
-aqueous flows into subretinal space via hole.
hazy vision, dark curtain
-rheg rd - no red reflex, retinal folds
-Inform and immediate referral, macula on or off
-FH, myopic, injury and surgery
-Retinoplexy laser, treat vitrectomy, flatten and cryotherapy
2) - Exudative - inflam, reverse polarity of RPE
- rapid onset blurred central vision, unilateral
- NO RAPD
- OCT
- should resolve 2-6 months
3) - Tractional - fibrovascular proliferation
-forces pull neurosensory and RPE apart, severe diab retinopathy
- Partial posterior vitreous detachment
- Mechanical anterior traction, distortion, oedema
reduced va, metamorphsia
macular disturbance subtle
OCT
4) - Solid - tumour
- haemorrhage: traumatic, surgery
109
Epiretinal membrane, sx, sign, investigation, management
- thin fibrous tissue developing on macula, assoc w pvd
- secondary to retinal breaks and tears
- metamorphsia, reduced va
- pseudomacular hole
- OCT
- explain, routine referral
- vitreoretinal surgery if bad
110
Macular hole, what is it, who/how, sx, signs, investigation, management, treatment
- full thickness loss of macular tissue at centre. majority F
- trauma, high myopia, vit traction
- central distortion painless, vision no better than 6/60
- reduced va, central scotoma, no rapd
- OCT, fundus photography
- recent onset, soon within 2 weeks referral
- long standing, routine referral
- long standing then no treatment
- vitreoretinal surgery
111
Retinal vein occlusion mechanism.
Origin or C and B and when each one occurs
Atherosclerosis, risk factors, medical investigations, management, treatment, long term conseq
1) Occlusion sufficient to cause retinal damage.
2) likely to form thrombus (blood clot)
3) compression from adjacent artery
- central RVO at lamina cribrosa
- branched RVO at AV crossings
1) Atherosclerosis and arteriolosclerosis - can be caused by other compressions like glauc
2) Venous hypertension - retinal haemorrhage, oedema, reduced flow
3) Ischaemia and inner cell death
- CRVO Hemi retinal vein occlusion - hemispheric, Primary splitting CRV
- BRVO 5x more common than CRVO
Secondary to diabetic retinopathy as a vascular cause of reduced VA
RF
- age, diab, obesity, smoking, hypertension, contraceptive pill
- ocular venous compressions: glauc, thyroid disease
- other vascular disease: vasculitis
MI
- exclude systemic causes
- Blood pressure, urinalysis, blood test
Management
- VA, IOP, gonioscopy, dilated fundus exam
- OCT, fundus photog, fluorescence angiography
Treatment
- Anti VEGF
- photocoagulation
- cyclodestruction
- symptomatic relief
Long term consequences
- haemorrhage
- laser scars
- VF defects
112
CRVO, sx, VA, Types, complications. cystic macula oedema
- sx - sudden loss of vision, whole field, painless/ache in eye
- VA: 6/36
- signs - red reflex darker, asym IOP, fundus appearance
Ischaemic - worse than 6/36, dark blot haemorrhage, CWS
non - 6/36, less dramatic fundus, less CWS
cystoid macular oedema, neovasc, vit haem, BLIND PAINFUL EYE
113
BRVO, signs
- Same signs as CRVO but depend on retinal quadrant affected, superotemporal quadrant most common
- occlusion at AV crossing
114
Cystoid macular oedema, ft, cause
final common pathway
- fluid accumulation in OPL, in fluid filled spaces called the cystoid
- localised to central macula,
F/T - reduced VA, metamorphsia, CS, CV ophthalmoscopy(cyctic spaces), OCT
causes - cataract surgery, RVO, adrenaline, prostaglandin, isolated
LASER PHOTOCOAG, CRYOTHERAPY
115
Neovascularization, what is it and its role in RVO
A response to tissue damage in an attempt to repair.
can be fragile and leaky in eye - haemorrhage
RVO
cws - capillary shut down
happens in retina, OD, iris and drainage angle
can lead to neovascular glaucoma
116
Retinopathy of prematurity - (ROP), RF, management, treatment
- Retinal fibrovascular proliferation at infants
potentially blinding,
- RF - low birthweight
- Pathophysiology
- at birth, retina completely vascularized
- abnormal proliferation of blood vessels
Management
- fundus photography
Treatment
- anti VEGF, laser photocoagulation, cyrotherapy
117
Retinal Microcirculation, Microangiopathy
- selectively permeable
- thick basement membrane
- form inner blood retinal barrier
Microangiopathy
- capillaries become thick and weak when they bleed, they leak protein as a result and slow the blood flow
- breakdown of inner blood retinal barrier: oedema, excudates, haemorrhage
118
Retinal haemorrhages types and cotton wool spots
Dot -
leaky microaneurysms
venous end capillaries
Blot -
larger, capillary leakage, assoc with ischaemia
Flame -
superficial precapillary arterioles
CWS-
focal retinal ischaemia
discrete RNFL swelling
fluffy and white
119
Microaneurysms, retinal oedema, exudates
1) Dilations of retinal capillaries, thin wall so can leak and rupture. Forms dot haemorrhage and oedema
2) Extracellular/exudative
- from leaky blood vessels, breakdown of inner blood retinal barrier
- from damaged capillaries
- difficult to see
3) dehydrated extracellular oedema, precipitation of lipids, deposited around a leaking point, yellowish and hard,
120
Arrhythmias, ventricular arrhythmia, Tachycardia, Bradycardia, Atrial fibrilation
1) irregular beat rhythm,
sx - palpitations
causes - stress, caffeine, alcohol, lil sleep
2) ->ventricular arrhythmia
sudden death, tachycardia
sx- fatigue, breath shortness, fainting, palpitation
3) >100bpm
supreventricular and ventricular
sx (venticular) - dizziness, pounding heart, passing out
treatment - meds, defib, surgery
4) <60bpm
sx - faint feeling, dizziness
treatment - pacemaker
5) Atrial fibrilation
atria irregular depolarization pattern
sx - palpitations, chest pain,
causes - congenital
121
Coronary heart disease, Heart angina, Heart attack, ocular manifestation of arteriosclerosis
1) - one or more coronary arteries becomes narrowed or blocked
sx -chest pressure with increased activity, heartburn, sweating
RF - smoking, fatty diet, FH, high BP
treatment - meds, surgery
2) - oxygen to area of heart does not reach the demand
cause - arteriosclerosis - thickening and stiffening
sx - pain, squeezing, heartburn, weakness, sweating
diagnosis - ECG
management - when occurs Nitroglycerin tablet. Normally, beta blockers
3) myocardial infarction - death of a heart muscle from blockage
cause - atherosclerosis - build up of plaque so, less flow
RF - high BP, smoking, diab, high cholestrol FOH
sx - pain, squeezing, shortness of breath, sweating
- BEGIN CPR
4)changes in retinal vessels, ischaemia and emboli
122
Coronary Artery Disease and the eye.
Narrowing/blocking of vessels due to fats
1) Hypertensive changes - CRAO CRVO BRAO BRVO, ischaemic neuropathy, glaucoma
sx - reduced vision, CV changes, conjunc vessels change
123
Cardiac drugs
1)Anti - anginal agents
Reduce cardiac work and improve circulation
SE - headaches, blurring vision
```
2)Antiarrhythmic agents
Class 1 - Quinidine, block Na+ channel.
- may interfere with neuromuscular function,
diplopia, uveitis
- may induce lupus, ACG attacks
```
Class 2 - Propranolol, beta adrenergic blockade
- reduce rate and force of heart contraction
- se - dry eye, decrease in IOP
Class 3 - amiodarone, prolong repolarisation
- se - lens opacities, optic neuropathy
- management - careful slit lamp exam every 6 months
Class 4 - verapamil, ca2+ antagonist
- no side effects
3)Drugs for cardiac failure
- heart isnt pumping with enough force
sx - fatigue, shortness of breath, weight gain
treatment - meds, heart surgery
-digoxin to increase heart efficiency, dry eye se
124
Eye drops and cardiovascular side effects
Absorbed into systemic circulation, via conjuc vessels.
Can cause toxicity
Atropine - tachycardia
Tropicamide - vasomotor collapse
Pilocarpine - arrhythmia
Beta - blockers - bradycardia
125
Blood pressure measurement, hypertension, retinopathy, hypertensive vs diabetic, referral
1) relaxed, arm horizontal at heart level, 3 measurements 5 mins apart
2) Hypertension - > 140mmhg pressure
3)
Hypertensive
few haemorrhage, rare oedema, rare exudative, multiple CWS, flame haemorrhage
Diabetic
multiple haemorrhage, extensive oedema, few CWS, rare flame haemorrhage
grade 1+2 - non-urgent
grade 3 - more urgent
grade 4 - emergency
126
Hypotension, types
1) Acute
2) Constitutional
3) Postural
sx - fatigue, headache, vertigo
treatment - salt, avoid alcohol, water
important risk for glauc
127
Ocular Blood supply and circulation
1) Internal carotid artery
ophthalmic artery
posterior cillary artery
central retinal artery
2) CRA and cillary artery
- CRA supplies retina, outer plexiform layer,
- susceptible to damage
-CA - uvea (RPE, photoreceptors) robust
-Posterior + Anterior CA supply - uvea, outer retina
-short posterior CA supply - posterior uvea,
anterior optic nerve
128
Retinal circulation, microcirculation
CRA divides - ST, IT, IN, SN
- retinal nerve fibre layer and ganglions
- arterioles cross over veins, share outer coat, hence BRVO
Capillaries, 1 cell thick, thick basement membrane
129
Investigation of ocular disease
1) Fundus photography -
Retinal vasculature, Haemorrhage, Exudates / CWS
2) Fluorescein angiography -
integrity of vessels and circulation, indocyanine green
3) OCT -
oedema and macula
4) OCT angiography -
retinal circulation
130
Congenital retinal blood vessel anomalies
- Congenital Tortuosity
- Anomalous BV's
- Bermeisters Papilla - Hyaloid artery at OD
- cillioretinal arteries grow from PCA
- Telangiectasia - abnormal dilation of a blood vessel
- Congenital retinal telangiectasia
- Idiopathic juxtafoveal retinal telangiectasia
- Coat’s disease - abnormal BV development
- rare, children, reduced VA, squint
131
Vascular disease, RF, Hypertensive retinopathy
- In the lumen
- Haemodynamic:
- Thrombosis - blood clot
- embolus - abnormal mass
- Vascular wall
- thinning - haemorrhage, oedema
-Thickening -
- Arteriosclerosis, - thickening of walls,
- Atherosclerosis, - fat deposits in walls,
thrombosis
Spasm, Inflammation
-Dilatation - tortousity
- External to Vessel
- Compression, IOP, glaucoma
RF - smoking, hypertension, diab, age, obesity
HR
140 bmp,
arteriolosclerosis - arteriovenous crossing changes, silver light reflex
132
Accelerated hypertension = malignant hypertension, Retinal macroaneurysm, Amaurosis Fugax
1) elevation in BP, assoc with organ damage: CNS
emergency - damage of arteries, arterioles and capillaries
flame haemorrhage, macular star (excudates), CWS
2) pathological BV dilation, leakage, exudates
3)transient ischaemic attack, fleeting loss of vision, due to a lack of blood flow to retina
lasts for a few secs/mins.
- indic - giant cell arteritis, systemic vascular disease
increased risk of CRAO AND BRAO
133
Anterior ischaemic optic neuropathy AION, CF, FT
| Giant Cell arteritis - temporal arteritis
1) Occlusion of posterior ciliary arteries
-arteritic - inflam of posterior cillary artery
bilateral and treatable (vasculitis), recovery rare
sx - GCA
-non arteritic - thrombotic occlusion
unilateral and untreatable. Small recov
FT - preceded by amaurosis fugax, starts unilateral, VF loss, pale swollen OD
2)occlusion and inflam of head, headache, jaw tenderness
diagnosis - blood test, biopsy
treatment - high dose steroids, risk of bilateral blindness if untreated (arteritic AION)
134
Retinal artery emboli, Retinal arterial occlusion, rf, ft, management
1) particle travelling through blood capable of blocking vessel. Anywhere between heart and eye.
- may be short duration or permanent, difficult to see but amaurosis fugax can present as a result.
2) No blood flow in vessel, can cause inner retinal ischaemia
CRA - thrombosis
BRA - emboli
cilio retinal arteries, can occlude emboli, so may protect against effects of CRAO, central sparring
RF - age, smoking, diab, obesity, amaurosis fugax, high bp, GCA, cardiovasc disease
FT - cherry spot, no recov
painless loss of vision:
CRAO - whole field, APD
BRAO - part field, RAPD
```
Management
immediate referral, re-establish circulation
rebreathing CO2 from bag
lower IOP
treat underlying disorders
```
135
Diabetic eye disease, types, classification. treatment, P0, P1, U, management
- microangiopathy - capillary damage
- inadequate diab control
- chronic
- progressive
Type 1
RF - duration of diabetes (since young) , glycaemic control, hypertension
Type 2
RF - preg, metabolic control, duration, hypertension, kidney disease, smoking, age, can progress quickly
1) Background Diabetic Retinopathy
2) Diabetic maculopathy - oedema
3) Pre-proliferative -
4) Proliferative
5) Advanced diabetic disease
Treatment
- diabetes control, elimination rf like BP/smoking
treatment of disorders like cataracts
photocoagulation -
Focal - seal leaking aneurysms,
Grid - diffuse non ischaemic oedema
Panretinal - kill ischaemia by releasing angiogenic factor
Anti - VEGF,
vitrectomy (vitreous haem),
retinoplexy (rd),
filtration surgery (neovasc),
P0 - NO PHOTOCOAG ANNUAL REF
P1 - PHOTOCOAG SCARS ROUTINE REF
U - UNGRADEABLE REFERRAL HES
136
R1 - Background Diabetic Retinopathy, ft
```
Microaneurysms
Haemorrhage - Dots and Blots
Oedema
CWS
Excudates
DOESNT AFFECT VISION
```
R1 - ANNUAL REF
137
M1 - Diabetic maculopathy, how, ft, detection
Same cause as background
increased permeability:
1) leakage,
2) diab oedema,
3) focal and diffuse diab maculopathy
Occlusion of vasculature - ischaemic diabetic maculopathy
How - loss of central vision, macular oedema
thickening and exudates within 500um
Detection - fundus, and fluorescein angiography, OCT
M1 if present - ROUTINE REF
138
R2 - Pre proliferative diabetic retinopathy
multiple haemorrhage, CWS,
venous iregularities - beading and omega loops
before proliferative
sight threatening
R2 if present - ROUTINE REF
139
R3A & S - Proliferative retinopathy, subhyaloid haemorrhage, vitreous haemorrhage
capillary shut down
retinal ischaemia
neovasc
tractional RD
subhyaloid haemorrhage
blood accumulates in front of retina
Vitreous haemorrhage
prolif DR, breaks out of neovasc vessles
blobls, complete loss of vision
URGENT referral if new
ACTIVE R3A - URGENT REF
STABLE/TREATED R3S - ROUTINE
140
Advanced diabetic eye disease
```
end stage, severe vision loss
persistent vit haemorrhage,
fibrovasular proliferation
tractional RD
neovasc
BLIND EYE
```
141
Haemoglobinopathies - other causes of microvascular retinopathy, sickle cell
Haemoglobin - 4 peptide chains, 2 alpha, 2 BETA
Abnormal chain production -Thalassaemia
```
1 alpha and beta from each parent
HbAS - sickle cell trait
HbSS - Sickle cell disease
HbSC - sickle cell C disease
HbSTYal - sickle thalasaemia
```
systemic ft - painful joints, abdominal pain, kidney disease
retinopathy - occlusive vasc disease, NVE, salmon patch Hge
sunburst patches- hyper plastic RPE
Treatment - lesions may spontaneously dissolve
Laser PRP/ antivegf - neovasc
vitreoretinal surgery - tractional RD, vit haemorrhage
Sickle cell disease - inherited blood supply
sickle shape, obstruct small vessels
142
Endocrine system
Acts through hormones influencing growth and metabolic activity.
diseases effecting -
-> cushing syndrome - excess glucocorticosteroids
- hypersecretion, upper body obesity, high BP, high
sugar, blurry vision, sleep disorder, fatigue,
emotional instability
- ocular ft - cataract, glauc
- > diabetes mellitus
- > thyretoxicosis(hyperthyroidism, graves)
143
Diabetes Mellulitis
- group of metabolic diseases w high blood sugar,
due to insulin defects
- classification - pre diabetes -high sugar but dont
meet diab req
type 1 - destruction of pancreatic cells,
autoimmune
type 2 - impaired insulin action, obese, 40+
-screening - 3p, blurred vision, dry itchy skin,
repeated yeast infection, impotence
- Elevated plasma glucose >200mg/dL
(11.2mmmol/L)
- Classical symptoms
- Fasting plasma glucose >126mg/dL (7mmol/L)
- GTT values at 2h>200mg/dL
144
Acute complications
- Diabetic ketoacidosis - not enough insulin to
neutralize glucose levels. Body breaks fat for
energy,
high amount of fatty acids (KETONES)
ft - hot skinned, blurred vision, difficulty to wake, fruity breath
EMERGENCY
- Hypoglycaemia - px not eaten enough after insulin
injection,
ft - sweating, intense hunger, trembling, weakness
management - sugar immediately
145
Chronic complications
- Accelerated Vascular Disease (micro and
macroangiopathy) -
in DM - eyes, kidney, nerves, heart, brain, heart
disease, stroke
other ft - candida infections, diabetic thick skin ,
yellow nails
- Other complications:
> Refraction - changes in lens thickness so
changes, reassess px on another day
> Colour vision - tritan, may affect ability to check
blood glucose levels
> Corneal changes - reduced sensitivity, tear ab,
higher risk for infections, use high o2 CL's
>Diabetic cataract - at any age, can progress
rapidly
>Diabetic papillopathy - bilat, loss of vision but
disappears in 6 months
>AION in diab - VA loss perm, IMMED REFERRAL
>Glaucoma and diabetes - assoc w POAG, check
for neovasc glaucoma, (BV close to margin)
>CN palsy in diab:
7 (lagophtalmos)
6 (x siplopia, head turn to involved eye)
3 (head pain, diverged eye, ipsilateral ptosis)
4 (y diplopia, head turn to good side)
- Neurological deficits
-miosis, reduced amb of accom, dilate tropicamide
1% and phenylepherine 2.5%
- asteroid hyalosis - calcium deposits on fundus
- hyperthyroidism - removes iodine from blood, and
used to produce regulatory hormones, Could be
due to graves disease
- Graves disease - hered women,
triggered by: stress, smoking, radiation to neck,
diagnosis - thyroid scan, hormonal levels
sx - sweating, heat intolerance, tremor, fast heart,
weight loss, fatigue
treatment - betablockers, anti thyroid drugs,
surgery
- Degenerative
146
RPE, where is it, fx, age
Retinal Pigment Epithelium -
Interface between neuroretina and choroicapillaris
Fx -
- Transport of nutrients, ions and water
- light absorbtion
- protection against photooxidation
- phagocytosis of photoreceptor outer segment membrane
- maintenance of ionic environment
- immune response and ocular immune privilege
Age
- cumulative effects of oxidative stress and inflammation
- accumulation of waste: lipofuscin, immune relevant proteins
- reduction in RPE fx
- Bruch's membrane - can thicken, or thin and break, reduced permeability, disordered transport
metabolic photoreceptor stress
147
Drusen
Abnormal material on Bruch's membrane, calcification
Materials: lipids, Apolipoproteins, oxidized proteins, compliment components
Distribution: symmetric, posterior pole of fundus
Common 60-70yrs
- Size - indicates risk of progression to AMD
- Small - hard well defined white/yellow
- Intermediate - fairly yellowish
- large - soft - less distinct edges, local elevation of
RPE
```
Consequences -
- loss of photoreceptors
- Toxic / immunological / inflammatory effect of
accumulated debris
- Dry AMD
```
148
AMD, types, classification, RF
DRY - non-exudative age related macular
degeneration
- Intermediate-size drusen - inc number n size
- RPE changes: hypopigmentation, hyperpigmentation.
- Geographic atrophy: sharply defined areas RPE
loss of retina and choriocapillaris
- Enlargement of atrophy: larger choroidal vessels, drusen
Sx - loss of central vision, vision better in brighter light
WET - exudative = neovascular AMD
- Macular oedema/haemorrhage/choroidal neovasc
sx - CV disturbance, reduced VA, metamorphsia, central scotoma
1) - No apparent ageing changes: No drusen or pigmentary abnormalities
2) - Normal ageing changes: Only drupelets, no pigmentary abnormalities, no effect on vision
3) - Early AMD: Medium drusen, no pigmentary abnormalities, minimal effect on vision
4) - intermediate AMD: Large drusen, pigmentary abnormalities, some effect on vision
5) - Late AMD: Neovascular AMD, geographic atrophy, severe effect on vision
RF - age, smoking, hypertension, ethnicity, diet
149
Pigment epithelial detachment (PED). Types
Retinal pigment epithelial detachment:
- Detachment of REP from the inner collagenous
layer of Bruch membrane.
- may have tear following laser or intravenous injection
- Persistence and progressive vision loss
- sudden deterioration in vision, shown by OCT
Types
1) Drusenoid - build up of soft drusen, no fluid, progressive visual loss as in dAMD, Scalloped edged, Fundal appearance, OCT.
```
2) Serous - Disruption of the physiological forces maintaining adhesion
Blurred central vision
Orange dome-shaped elevation in mac
Persistence and progressive vision loss
choroidal neovasc in 2 yrs
OCT, FUNDUS
```
RPE tear - following laser, sudden drop in vision,
3) Choroidal neovascularization - Haemorrhage, fibrovascular
pathological response to: new blood vessels:
from: choriocapillaris
going through: Bruch’s membrane
going into : Sub-RPE space (type 1), Subretinal space (type 2)
150
Choroidal Neovascularization, causes, what is it, location, macular choroidal neovasc
Causes -
1) degen amd
2) congenital - myopia, retinal dystrophys
3) trauma - accidental - choroidal rupture
- surgical - laser photocoagulation
4) inflam - toxoplasmosis, sarcoidosis
5) tumours - melanomas, nevi
Abnormal Bruchs membrane:
macrophage and cytokines:
1) promoting NV proliferation - VEGF
2) inhibiting NV proliferation - Pigment epithelium derived factor, complement factor H
Could be anywhere, macular most important to vision. Could be due to metabolic turnover, macular anatomy
Macular Choroidal Neovascularization
- sx - metamorphsia, positive scotoma, painless, uniocular initially.
- signs - co existing eye disease, subretinal fluid, greeny grey patch, haemorrhage
- Diagnosis
- Fluorescence angiography - ICG used, goes through haemorrhage, useful if diagnosis cant be found elsewhere.
- OCT - Hyporeflective=fluid. Hyperreflective=tissue
Defines - Sub RPE fluid, intraretinal neovascularization, RPE tear,
Later ft - Haemorrhage - Sub-RPE, Intraretinal, vitreous,
Exudates - lipid deposition,
Subretinal fibrosis - disciform scar
151
Management of AMD, Charles Bonnet Syndrome
1) - prophylaxis
- treatment to prevent disease: quit smoking, sun protect, diet (leafy greens), antioxidants
vitamin A (BETA CAROTENE FORM), C, E, Zn, Cu
- No benefit in normal eyes, beta carotene potentially toxic.
- Lutein and Zeaxanthin instead of B carotene
- Carotenoids (plant derived)- xanthophyll pigments: lutein, zeaxanthin, mesozeaxnthin
- exercises
2) - awareness,
Know FOH risk, their current condition ie drusen, warning signs. Early signs if FOH (sudden change, VA drop, metamorphsia)
3) - Early recog
clinics - NHS, referral protocols, OCT, FFA, ICG, same day treatment, tech
4) - Anti - VEGF A,
- Binds to and inactivates VEGF,
- prevents VEGF attaching to endothelial receptors Fusion protein
- inhibits VEGF A/B, reverse vessel growth
Intravitreal injection for wet amd
- Risks - RD, uveitis, lens damage RPE
- Drugs -
(Lucentis) - Licensed, small molec, expensive, 1x injection 4 weeks
(Avastin) - Unlicensed, large molec, cheap,
Aflibercept - 1x injection 6-8 weeks
5) - Management of low vision
Low vision aids
Certificate of visual impairment
Advice - optoms, macula society, local services
focal laser, PDT, surgery
- Charles Bonnet syndrome
Hallucinations with impaired vision.
Elderly, signif visual loss, no treatment, recog and reassure.
152
RPE & CHOROID
RPE ft
- Monolayer - hexagonal array
- Pigmented - Melanin, Lipofuscin
- Multifunction - support photoreceptor fx, light absorbtion
Choroid ft
- Choriocapillaris - capillary net
- Vascular layer - outer large vessels
- Connective tissue - melanocytes, immune cells
- Multifx - light absorbtion, immune, metabolic ret support
153
Coloboma, etc
Failure of choroidal fissure closure
iris (key hole), disc or choroidal
Variations in fundus pigmentation:
Diffuse - Relative to skin colour, alibinotic
Focal - Tigroid, around OD
Myelinated retinal Fibres
common, asymp,
white feather shape
Congenital hypertrophy of RPE
congen, increase in size of normal cells
flat oval lesions on fundus with halo
bear track pigment (black circles)
Gardner's syndrome
Familial adenomatous, polyposis (FAP) plus extracolonic manifestation
FAP - autosomal dominant
can become cancerous
Congenital intrauterine infection (ToRCH)
Maternal infection - signif effect on unborn child
Protozoal - Toxoplasma
Viral - Rubella, cytomeglovirus, Herpes Simplex
Bacterial - syphillis
- Congenital Rubella syndrome
German measles, maternal infection, spontaneous abortion, high risk of fetal infection
eg, brain, deaf, heart, retinopathy, cataract, glaucoma, microphthalmos
- Congenital Toxoplasmosis
protozoan parasite, can be from cats/other humans
Maternal infection
Effects - intrauterine death, choroidalretinal scars from birth and can reactivate later online in life
154
Acquired disorders, Uveitis
RPE - limited regen, disordered growth, abnormal pigmentation
Choroid - Vascular, immune, inflam, scar formation
- Trauma
blunt - choroidal rupture
penetrating - perforating
- Surgical
depends on intervention, incision, photocoagulation, cryotherapy, radiotherapy
- pigmentation
post CSCR
- Pos seg inflam
intermediate uveitis - (inflam of cillary body and periph ret). Bilateral, young px,
sx - chronic, blurred, floaters, no pain
signs - snowballs, white eye
- Posterior uveitis -
can involve all ret layers
unifocal - eg toxplasmosis,
multifocal - eg, ocular histoplasmosis syndrom
geographic - cytomegalovirus neuroretinitis
sx - blurred, floaters,
signs - vitritis, choroiditis, retinitis, vasculitis
- Non congenital posterior uveitis
reactivation of congenital infection:
toxoplasmosis, Toxocariasis, herpes zoster, fungi, CMV, histoplasmosis
systemic infections - AIDS, TB
non infections - Behcets, sarcoidosis
WHite Dot syndrome - multiple idiopathic white dots
WHAT TO DO FOR POS EYE INFLAM
refer, if severe visual loss then Urgent and if lesions seen
treatment - topical or systemic
155
Oncology definitions
- Tumour - abnormal mass of cells
- Neoplasm - Lesion of cells which have lost growth restraining mechanisms
- Benign neoplasm - abnormal cells, cohesive cells, growing expansively, doesnt threaten life
- malignant neoplasm - genetically transformed abnormal cells. fast uncontrollable growth, no cohesion, infiltrate surrounding tissues, spread through blood
156
More pigmented lesions
- Choroidal Naevi
benign proliferation of choroidal melanocytes
Dont grow after puberty
signs - slate grey lesions, oval. diffuse edges
harmless
asymptomatic
- Choroidal Melanomas
malignant proliferation of choroidal melanocytes`
above 30 yrs, common in lighter skin
spreads out of eye by metastasis (liver)
better if found early with no spread and small size
sx - asymp, reduced vision, VF defect
signs - abnormal mass, oval circular, darker colour, orange pigment, excudative RD, haemorrhage, break through bruchs membrane
Naevus or melanoma
suspicious naevi - flashes, floater, >5mm, elevation, near disc, orange fundus colour, distinct margin
What to do?
assess RF
photograph review in 12 months and compare size
refer - to be safe
OTHER INTRAOCULAR NEOPLASMS
Secondary - most common, women breast, male lungs
rare ones - lymphoma, retinoblastoma, Medulloepithelioma
157
Hearing impairment
Techniques to communicate -
| interpreter, amplifying device, some can lip read, sensitive to non verbal behaviour,
158
Additional px needs
1) Intellectual,
2) hearing,
3) multiple impairments,
4) stroke/head injury
159
Intellectual needs
Cause - chromosome ab, trauma, hypoxia, prenatal infection, prematurity, metabolic diseases, neurological diseases
Assoc with - optic atrophy, high myopia, cataracts, ret disease, anisometropia
Unusual behaviour - lack of eye contact, lack of commun, loud if so, high emotions
160
Multiple impairments
Greatest challenge
Eg - intellectual, mobility, communication, hearing, low vision, behavioural
Use gestures, address px directly
Stroke/head injury - memory/attention deficit, language impairment
visual fx of stroke - CN palsy, nystagmus, squint, diplopia, reduced stereopsis, reduced convergence, accom insuf, loss of vision, VF defects, ptosis, difficulty reading, abnormal hand eye coordination
Techniques - written info, closed q, address directly and patience
Other specific areas -
1) Cerebral palsy
- permanent brain damage,
- risk - infection, prematurity, trauma
- systemic findings - seizure, hearing difficulties
Ocular - amblyopia, strabis, RX, nystag, accom insuf
Examining - extra time and space, privacy
Initially assessment - observe head position, look for how to communicate, accurate H/S, involve px and carer, use diagrams or illustrations, give breaks
Post exam - discuss w carers, provide carer with report, give in written, send copy to go
2) Down's syndrome
- chromosome ab, mental disability, seizure, heart defect, leukaemic
- Physical ft - small head, short stature, depressed nasal bridge,
- neurological - seizure, delayed speech, delayed motor ability, increased risk of autism
- assoc systemic conditions - hypothyroidism, heart defects, leukaemia, decreased fertility
Anterior segment -
spots on iris periph, cataract, keratoconus
Posterior segment -
glauc, pseudopapilloedema
Others -
RX, hyperopia, hyperopia, myopia, astig, accom def, amblyopia, strabismus, nystagmus, congenital ectropion
```
3) Autism
lack of social interaction,
abnormal communication,
aspergers syndrome,
retts disorder,
risk - genetic factors
```
ocular fx - atypical gaze, tunnel vision, strabismus, refractive error, eye pressing
exam - history from parent and carer, ask carer to for help, warn px before touching
snellen - used in some px, single letters are better, pictures
near VA - important as they control life through schedules
pref looking - if cant communicate
test motility, binoc, eye tracking, fixation
BE CAREFUL WITH ILL
4) Dementia
161
The respiratory system
Inspiration, expiration, O2 &CO2 exchanged
```
sx-
Dyspnoea - Shortness of breath
Apnoea - respiratory arrest
Tachypnoea - increased breathing rate
Bradypnoea - slow respiratory rate
coughing
```
- Asthma - Chronic inflammation of airways
triggers - allergy, infections, exercise, weather change, smoking
sx - wheezing when breathing out
Effects on eye - High IOP in attack, Beta blockers used, corticosteroid used,
Glauc attack after albuterol treatment
Properly pos mask, specs, inhaler: can reduce deposition of inhaled meds
```
- Obstructive sleep apnoea syndrome
Snoring, Closing of upper airways,
1)soft tissue collapses on upper airway back wall
2)tongue falls back
3)no air can enter lungs
```
sx - snoring, obesity, anxiety, depression, morning headaches
Diagnosis and management - refer to specialist, weight loss, stop alcohol, sleep on one side, respiratory devices.
OSA - floppy eyelid syndrome
- sx eyelid laxity, ocular irritation keratitis
- history - multiple drops without any effect
- treatment - artificial tears, mild steds and surgery
- sleep opp side, air humidifier
linked to Glaucoma, Dry Eye, lacrimal gland prolapse, keratoconus, non arteritic ION
162
Lung diseases
Gen comfort, breathing and noises, colour of px face and nails, pos of px
- Coughing with blood(haemoptysis)
nose, mouth, throat, airways leading to lungs origin
```
- TB
Pulmonary disease by mycobacterium tuberculosis
transmits between people
sx - coughing, weight loss, fever, night
Diagnosis - x ray, sputum culture
```
TB In eye,
- Uveitis, rare,
- Conjunctivitis
- Keratoconjunctivitis
- Interstitial keratitis
- scleritis
- optic neuropathy
- Sarcoidosis
inflam disease not contagious, can attack any organ, here the lung
sx - glanulomas present
- In the eye
Conjunctival sarcoidosis, lacrimal gland infiltration, uveitis, choroidal granulomas
- Respiratory emergencies
Respiratory arrest
choking
allergic reaction
999 & CPR
163
ENT disorders and the eye
- Nasolacrimal duct obstruction
Congenital - watery eye, discharge, infection
acquired - watery eye
- Horners syndrome
sx - enophthalmos, ptosis, miosis
- Sinus inflammation -
Sinusitis
Acute bacterial sinisitis in infection. Preceded by a cold, allergy, irritation.
sx - pain, nasal discharge, fever, headache, pain in upper teeth
Treatment - Nasal decongestants, surgery
Cavernous sinus thrombosis -
Impairment of oculomotor nerves, Horners, sensory loss in trigeminal
Throat, sinus, face, orbit
sensory loss, oedema of eye lids, pain
signs - threat to vision and life, proptosis
px - ill, dilates, exophthalmos, papilloedema
Tumours of paranasal sinuses
disturbed orbit, pain, diplopia
Trauma
restricted eyemovement, pain, oedema, double vision
Cogan syndrome
inflam, autoimmune, affects eyes and ears
ft - epsicleritis, scleritis, interstitial keratitis, uveitis
164
Genetics
22 pairs, 1 pair of sex chromosomes
non chromosomal DNA - mitochondria
Genes - functional DNA
Cell division
Mitosis - identical 2 cell produce
Meiosis - exchange of alleles between homologous chromosomes, produces 4 cells. Used for gamete formation
Fertilization - union of haploid gametes, produce diploid zygote, then mitosis
Genotype - genetic code of an individual
Phenotype - manifestation of the genotype (physical)
Mutation - change in heritable DNA, changing genetic code
Mendelian - single gene inheritance
Autosomal Dominant - mutation of one copy of a pair of genes affecting the phenotype
Autosomal recessive - mutation of both gene pairs required to affect phenotyoe
X linked - mutation of x chromosome, manifests in males, female carriers
Polygenetic inheritance - multiple genes, environmental interaction and familial tendency
Chromosomal abnormalities -
whole (DOWN syndrome)
part
Mitochondrial inheritance - some forms of RP
Genetic testing - biochemical tests, chromosome analysis, molecular gene tests
Genetic counselling - establish inheritance
Treatment - symptomatic, stem cell, gene replacement
165
Genetics and the eye
Rare - RP AND STARGARDT
Chromosomal - Trisomy 21 down syndrome
Mitochondrial - Kearns - Sayre
Common
multifactorial - AMD, MYOPIA, POAG, CATARACT
166
Sickle cell haemoglobinopathy
1 x Alpha, 1 x Beta from each parent
4 chained molecule
mutation on B
HbAA - normal
HbAS - sickle cell trait
HbSS - Sickle cell
```
Central african
sickling shape at low O2 saturations
these obstruct the small vessels, cause ischaemia
The trait affects the eyes more but still not severe.
Sickle retinopathy -
- Vascular occlusions
- Neovascularization
- Retinal haemorrhages
```
167
Albinism
- At least 10 different inherited disorders.
- autosomal recessive, melanin defect
- eyes, skin, hair effected
- Ocular involvement only
FT - reduced VA, photophobia, Nystagmus, iris transillumination, hypopigmented fundus,
168
Retinal and macular dystrophies
```
Photoreceptors -
retinitis pigmentosa, cone dystrophies.
RPE -
Stargardts disease, fundus flavimaculatus, Bests vitelliform macular dystrophy
Bruch's -
dominant drusen
Choroid -
Choroideremia
```
Retinoblastoma
169
Degenerative myopia
>6D, progressive choroidal degen
polygenic inheritance
ft - inc in axial length, scleral expansion, staphyloma formation
signs - ,yopia, choroidal retinal degen, Break in Bruchs membrane, choroidal neovasc
assoc - cataract, RD, glauc
170
Dystrophies, RETINITIS PIGMENTOSA
tissue degen, molecular defect, fx and structural changes
Photoreceptor type
Mutation of Rhodopsin or rod disc stabilization
Retinitis pigmentosa RP
rhodopsin, visual cycle, membrane stability based
sx - night blindness, VF defect, loss of acuity
signs - pigmentation of retina, arteriololar narrowing, retinal atrophy, VF ring scotoma
ft - cataracts, cystoid macular oedema, keratoconus, glauc, myopia
Diagnosis
OCT - loss of photo receptor layers
Electrodiagnosis - ERG, reduced elec response in RP
Variations
Isolated - only ocular ft
Systemic assoc -
Ushers syndrome - congen deafness
Management - reg review, rx, tinted specs, identification of :glauc, cataracts
genetic counselling
171
Cone dystrophies
CFx - opposite to RP
sx - teens, day blindness, loss of VA and CV, nystagmus common
signs - Bulls eye maculopathy, late geographic atrophy
Investigations -
VF - central scotoma
OCT - loss of macular photoreceptors
Electrodiagnosis - loss of cones, some preservation of rods
- Bulls eye Maculopathy
also linked w stargardts
acq - geographic AMD, drug toxicity to chloroquine
- Juvenile macular dystrophy
cone dystrophy, stargardt disease, dominant drusen, sorsby fundus dystrophy
172
Stargardts
Mutation - ABCA4, PROM1, ELOVL4
sx - before 20
Macular dystrophy -
Loss of central vision (6/60 - 3/60), metamorphsia, central scotoma, glare, impaired CV,
signs -
Periph retinal & macular yellowish flecks
Foveal mottling, oval macular
Prognosis -
High lipofuscin conc
- Autofluorescence
OCT
- photoreceptor loss
- Hyper reflective - abnormalities
- Atrophy of all macular layers
173
Best vitelliform macular dystrophy
Genotype:
- VMD2 - Bestrophin
- RDS - Peripherin
```
Bestrophinopathies
Phenotype
- sx variable - loss of VA
- signs - Maculopathy, stages of progression
- Diagnosis - electrophysiological
```
Prognosis - loss of central vison in the 40's
174
RPE dystrophy: dominant drusen
- Doyne honeycomb macular degeneration
- Phenotype similar to AMD
- Genotype:
- EFEMP1
- Fibulin 3
Choroideremia
X linked - Males
Genotype - CHM genes, effects vesicle formation
Phenotype -
sx - in first 10 yrs, Nyctalopia, Progressive visual loss
Central vision retained until 60s
signs - Progressive, advancing macular, macular sparring
Female carrier - mild RPE changes
175
Retinoblastoma
Malignant embryonal retinal cells
- autosomal dominant, RB1 gene, tumour suppressor gene
- Mortality - 10% with treatment
100% without treatment
depends on tumour size, type and spread
CF- 3 yrs+, leukokocria, squint, orbital inflam
Exam - anaesthetic, no red reflex, Intraocular tumour, MRI
Treatment - radiotherapy, chemotherapy, enucleation, genetic counselling
176
STroke handout
Deprivation of blood to areas of brain via blockage
Transient ischaemic attack comes 1 day stoke (amaurosis fugax)
sx - hemianopia, limb weakness, hearing loss, hemipariesis
Monoc assoc with GiantCellArteritis, ClosedAngleGlauc
- Carotid artery disease
occlusion of carotid arteries via atherosclerosis, could also be C/BRAO
- CRAO - cherry red spot, white retina, painless, RAPD
- BRAO - Focal visual loss, white retina in occluded arteriole section
- AION - painless monocular visual loss, oedema, haemorrhage
- Systemic arterial hypertension is main cause:
can also cause kidney failure
wider retinal veins, higher chance of stroke,
- Hypertensive retinopathy characterized by arteriovenous nicking,
- Hypoperfusion of the retina and choroid -
TVL after looking at bright light, induced AHP
- Ocular Ischaemic Syndrome - gradual VA loss, could be sudden, increases IOP
Painful, better when supine
Cataract, vit haem, dot blot, microaneurysm, neovasc
AMD - Higher risk of stroke, common risk factors,
ANTI-VEGF - Increase chance of stroke
Diabetic retinopathy - doubles risk of stroke, poor glycaemic control increases the risk
- During Stroke
Eyes: Conjugate ocular deviation towards the affected
hemisphere.
• Face: Ask the patient to smile and assess the asymmetry of the
face.
• Arms: Ask the patient to raise both arms and observe
weakness.
• Speech: Slurring when asked to repeat a simple phrase.
• Time: Call 999 immediately if any of the above occur.
```
- After stroke
visual disability
- head tilt
- closing 1 eye
- Hemianopia
- lack of commun, so look for ways to improve, ie loud, clear, simple
```
