Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GLOCKTOMETRY > PEG > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Glauc treatment

A

MEDS, LASER, SURGERY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Beta adrenergic blocking agents

A

First line glauc therapy
Decrease AH production
CI: lung/heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cholinergic agents

A

Pilocarpine:
Increase AH outflow via miosis
CI: neovasc, 2ACG
SE: Accom spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Carbonic Anhydrase Inhibitors, types and mech

A

Topical (Dorzolamide, Brinzolamide) and acetazolamide (most powerful for IOP reduction)
Decrease AH production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Simbrinza

A

Brinzolamide, brimonidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Cosopt

A

Timolol and dorzolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Glauc surgery indications

A

> 30mmhg

Signif IOP fluctuations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Trabeculectomy

A

Penetrating glauc surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Non penetrating glaucoma surgery

A

deep sclerectomy

viscocanalostomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PACG treatment

A

pilocarpine, emergency referral

laser periphery iridotomy
monitor reg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Secondary Glaucoma types

A 
pigmentary
pseudo-exfoliative
inflammatory    LINKS W RD
neovascular    LINKS W RD
post-traumatic
steroid induced   LINKS W RD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Glaucoma assoc with RD

A

Neovasc, inflam, scarring, surgery, treatment with steroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Congenital Glaucoma

A

Posner schlossman syndrome

neovascular glauc

trabeculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Prevention of secondary Glaucoma

A 
Early detection and management
Education
Good management of eye conditions inducing 
Secondary glauc
Diabetes control
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Optic Neuritis, what is it?, sx, signs, treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Signs of ON dysfunction

A

reduced VA, RAPD, impaired CV, VF defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Optic nerve VS Macular Disease

A

OND: RAPD, severe dyschromatopsia, reduced brightness

MD: No RAPD, mild dyschromatopsia, augmented brightness,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Optic Neuropathy types

A

inflam, ischaemia, compressive, toxic, traumatic, congenital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Anterior ischaemic optic neuropathy types

A

PCA occlusion

1) arteritic ION - giant cell arteritis
2) non arteritic - caused by ACS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Arteritic AION, what is it?, sx, signs, management

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Non-arteritic AION (sx and signs)

A 
no sx, 
visual loss sudden (not severe), 
altitudinal hemianopia, 
reduced CV, 
ONH pale and oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Compressive optic neuropathies

A

ON glioma and meningioma (tumours between brain and spine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Toxic Neuropathy, who does it affect? sx and signs

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Traumatic Optic Neuropathy (mech, sx, signs)

A

compression,
Impact to head,
vasospasm,
ischaemia

sx - vision and visual field loss
signs - RAPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lebers Hereditary Optic Neuropathy, who and signs

A

9 Men:1 teenagers
rapid unilateral visual loss, pseudo oedema of disc.
H/S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Papilloedema, symptoms, mechanical and vascular signs

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Papilloedema grading, and cause

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Pseudotumour Cerebri, who?, risk, sx, signs, management

A

young overweight women, idiopathic

risk - anaemia,
symptoms - headaches, vision blur, diplopia
signs - papilloedema
management - emergency referral and steroids, weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Chiasmal syndrome, cause, sx (ocular, systemic), DD, management

A

Chiasmal lesions.
sx - ocular -> VF loss
sx - systemic -> headache, body changes

DD - R Disease
management - VF testing, neuroimaging, lumbar puncture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Monocular transient visual loss

& binocular, time frame and meaning

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Post traumatic glaucoma

A

Blunt trauma, after: (penetrating, chemical injuries & radiation therapy)
May have previous trauma, eg cataract, ret breaks, RD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is non organic visual loss?

A

visual complaint not explained by tests

types - conversion reaction, hysterical blindness and malingering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Conversion reaction, cause and symptoms

A

<35 yrs, symptoms are a result of repressed emotional stress.
sx - weakness, paralysis, urinary retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Ocular Hysteria, what is it?, and symptoms

A

blindness with fluctuating VA, and VF defects (ring scotoma).
diplopia, blepharospasm, colour blindness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Malingering, what is it?, indications, tests

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Causes of binocular diplopia and sx

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

RAPD, conditions leading to it

A
  • Unilateral ON - Optic Neuritis, asym glaucoma, ON tumour

- Unilateral Retinal Diseases - RD, severe AMD, tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Efferent Pupillary Abnormalities, categories, examples and which is the abnormal?

A
  • 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Horners syndrome, who, what, when?

A

Congenital or acquired
ptosis on small pupil side, if on other, 3CN lesion
miosis, anhydrosis
aniscoria greater in dark

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tonic Pupil, what is it?, who?, reason

A

Pupil reacts badly to light, but well to accom, so will eventually constrict on near

near response is tonic

unilateral and women

3CN ganglion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Argyll Robertson Pupil, what is it and what is it linked with?

A

Both pupils small and irregular,

linked with neurosyphillis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Nystagmus, what is it, categories, common types?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Cerebellar Jerk nystagmus, what is it, when does it increase, what else to do?

A

jerky, large amplitude, low frequency
increases when look in direction of fast phase

Scan for cerebellar signs: headache, limb weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Down beat nystagmus, what is it?, when is it bigger, cause?

A

In primary position, fast phase downwards.

bigger when looking laterally

cause: Stroke, MS, alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

See-saw Nystagmus, what is it, what does it indicate?

A

torsional nystagmus - one eye elevated and intorts the other is depressed and extorts.

Chiasmal lesion, examine VF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Congenital Pendular Nystagmus, when does it increase, what to examine

A

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,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Managing a child with congenital nystagmus

A

establish cause, improve vision, prisms for convergence, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Congenital CNIII Palsy, cause, characteristics

A

Cause - FOH, traumatic birth.

characteristics -
XOT, HYPOT, HYPERT, intorsion Ptosis,
limitation of elevation, depression, adduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Acquired CNIII Palsy, cause, symptoms, characteristics

A

Causes - tumours, trauma, inflammation of vascular lesions of brain

Sx - unilateral ptosis, ocular pain, headache, diplopia

Characteristics - partial, complete. Ptosis, elevation, depression, abduction limited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

CN4 Palsy, features

A

features: vertical diplopia, head tilt to opposite side, hypertropia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Congenital CN6 Palsy, syndrome

A

Duanes syndrome - congential absence of 6TH CN

Mobius syndrome - Blateral palsy of 6TH AND 7TH CN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Acquired CN6 Palsy, cause, symptoms, signs

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Blood Supply to ONH, anatomy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Glaucomatous OD,

what to look for and rules?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

OD size & what haemorrhage indicates, and how

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Vascular changes

A 
Kinking
nasal migration
bowing
baring
sharpen vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

RNFL - retinal never fibre layer, what to look for?

A
  • Red free, brightness
  • visibility of peripapillary RV, striation
  • look for diffused and localized loss
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Peripapillary atrophy, what is it

A

Alpha zone - hypo/hyper pigmentation region around, like shadow
beta zone -
if large - thin nrr, - shows glaucomic progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

NRR size and how to examine and indications?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Non - glaucomatous cupping, signs of non glaucoma

A

congenital, coloboma, AION,
traumatic/shock optic neuropathy,
radiation compression
syphillis

rim pallor, <50 yrs
central VF loss

72
Q

Autosomal dominant optic atrophy, signs

A

early onset, central scotoma, colour blindness, cupping

73
Q

OD Hypoplasia

A

abnormal development of OD,

small and irregular, wedge shape defects

74
Q

Optic Disc Pit, what is it, sx

A

uncommon congenital, pit in disc

sx - enlarged blind spot, vf defect, enlargement of disc

75
Q

Optic disc coloboma, what is it?

A

white excavation within disc, central and empty

no significant peripapillary pigmentation

76
Q

Neuroimaging, who for?

A

Loss of central VA, VF
hemianopic VF loss
acute onset vision loss
neuroretinal rim pallor

77
Q

Disc damage, full function

A

congenital, prefunctional

78
Q

Functional Loss, little damage

A

VF test error, observational error

79
Q

SOAPF

A

Subjective - px’s observations
Objective - optoms observations and tests
Analysis - optom understanding of problem
Plan - advice, treatment, interventionist action
Followup

80
Q

Px Red eye, h/s, as

A
  • 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
Q

Acute Dacryiocystitis

A

Inflammation of Lacrimal sac, assoc w obstruction of naso-lacrimal duct

82
Q

Sudden loss of vision conditions, H/S check

A

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
Q

Causes of sudden visual loss

A 
CRAO, BRAO
CRVO, BRVO
VIT HAEM, RD
Ischaemic Optic Neuropathy, inc giant cell arteritis
Optic neuritis
84
Q

Px with blurred vision, what to do

A

VF,
reaction to light,
dilate w tropicamide and fundus exam

85
Q

Ocular trauma types

A

Chem,
Blunt,
Open eye,
FB

86
Q

Chemical burn trauma, what is it, sx, signs, management

A

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
Q

Blunt Trauma, presentation and examination

A

P - Black, painful, reduced and double vision
E - corneal abrasion, hyphaemia, dilated

posterior examination difficult due to swelling

88
Q

Open eye trauma, presentation, examination and management.

A

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
Q

Ruptured globe, causes, sx , signs, management

A

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
Q

Ocular foreign body, cause, sx, signs, examination, management

A

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
Q

Structure of eye

A

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
Q

Diagnostic Process

A
  • 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
Q

OCT

A
  • cuts 2D optical sections, 3D image formed
  • based on interferometry
  • digital manipulation
  • safe quick and easy
  • hospital
94
Q

Hospital- Based imaging

A

-AF,RF,IR
different retinal layers, lipofuscin

-Fluorescence angiography
vascular integrity, fluorescein, indocyanine green

OCT angiography
High res OCT
polarisation sensitive OCT

95
Q

Types of headaches and sx

A
  • 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
Q

Types of Neuralgia, what is it, cause, treatment

A

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
Q

Types of tumour, what is it, diagnosis, treatment

A

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
Q

Stroke, what is it, rf, sx

A

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
Q

Epilepsy, what is it, types, DD, diagnosis, what to do, after seizure?

A

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
Q

MS, what is it, early sx, sx that occur later, DD, diagnosis, treatment

A

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
Q

Myasthenia Gravis, what is it?, types, who, sx, diagnosis, treatment, myastheic crisis

A
  • 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
Q

Facial nerve palsy, cause, sx, management, coma n what to do?

A

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
Q

Vitreous, contents

A
  • h2o, collagen, hyaluronic acid

- vitreous attached to vitreous base, which straddles ora serrata

104
Q

Vitreous opacities

A
  • floaters - persistent hyaloid remnants
  • asteroid hyalosis
  • pigment - melanin granules from ret tears
  • cells - vit haem, malignant
105
Q

Vitreous degen

A
  • 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
Q

Posterior Vitreous Detachment, what is it, sx, signs, risks, management

A
  • 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
Q

Retinal breaks, tears and holes. AND TREATMENT.

A
  • periph are hard to see, use 3 mirror
  • can cause retinal detachment

Treatment

  • uncomplicated PVD - explanation
  • retinal break - laser cryotherapy
108
Q

Retinal Detachment, types, how, sx, management, who, treatment

A

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
Q

Epiretinal membrane, sx, sign, investigation, management

A
  • 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
Q

Macular hole, what is it, who/how, sx, signs, investigation, management, treatment

A
  • 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
Q

Retinal vein occlusion mechanism.
Origin or C and B and when each one occurs
Atherosclerosis, risk factors, medical investigations, management, treatment, long term conseq

A

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
Q

CRVO, sx, VA, Types, complications. cystic macula oedema

A
  • 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
Q

BRVO, signs

A
  • Same signs as CRVO but depend on retinal quadrant affected, superotemporal quadrant most common
  • occlusion at AV crossing
114
Q

Cystoid macular oedema, ft, cause

A

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
Q

Neovascularization, what is it and its role in RVO

A

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
Q

Retinopathy of prematurity - (ROP), RF, management, treatment

A
  • 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
Q

Retinal Microcirculation, Microangiopathy

A
  • 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
Q

Retinal haemorrhages types and cotton wool spots

A

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
Q

Microaneurysms, retinal oedema, exudates

A

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
Q

Arrhythmias, ventricular arrhythmia, Tachycardia, Bradycardia, Atrial fibrilation

A

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
Q

Coronary heart disease, Heart angina, Heart attack, ocular manifestation of arteriosclerosis

A

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
Q

Coronary Artery Disease and the eye.

A

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
Q

Cardiac drugs

A

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
Q

Eye drops and cardiovascular side effects

A

Absorbed into systemic circulation, via conjuc vessels.
Can cause toxicity

Atropine - tachycardia
Tropicamide - vasomotor collapse
Pilocarpine - arrhythmia
Beta - blockers - bradycardia

125
Q

Blood pressure measurement, hypertension, retinopathy, hypertensive vs diabetic, referral

A

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
Q

Hypotension, types

A

1) Acute
2) Constitutional
3) Postural

sx - fatigue, headache, vertigo

treatment - salt, avoid alcohol, water
important risk for glauc

127
Q

Ocular Blood supply and circulation

A

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
Q

Retinal circulation, microcirculation

A

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
Q

Investigation of ocular disease

A

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
Q

Congenital retinal blood vessel anomalies

A
  • 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
Q

Vascular disease, RF, Hypertensive retinopathy

A
  • 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
Q

Accelerated hypertension = malignant hypertension, Retinal macroaneurysm, Amaurosis Fugax

A

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
Q

Anterior ischaemic optic neuropathy AION, CF, FT

Giant Cell arteritis - temporal arteritis

A

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
Q

Retinal artery emboli, Retinal arterial occlusion, rf, ft, management

A

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
Q

Diabetic eye disease, types, classification. treatment, P0, P1, U, management

A
  • 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
Q

R1 - Background Diabetic Retinopathy, ft

A 
Microaneurysms
Haemorrhage - Dots and Blots
Oedema
CWS
Excudates
DOESNT AFFECT VISION

R1 - ANNUAL REF

137
Q

M1 - Diabetic maculopathy, how, ft, detection

A

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
Q

R2 - Pre proliferative diabetic retinopathy

A

multiple haemorrhage, CWS,
venous iregularities - beading and omega loops

before proliferative
sight threatening

R2 if present - ROUTINE REF

139
Q

R3A & S - Proliferative retinopathy, subhyaloid haemorrhage, vitreous haemorrhage

A

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
Q

Advanced diabetic eye disease

A 
end stage, severe vision loss
persistent vit haemorrhage, 
fibrovasular proliferation
tractional RD
neovasc
BLIND EYE
141
Q

Haemoglobinopathies - other causes of microvascular retinopathy, sickle cell

A

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
Q

Endocrine system

A

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
Q

Diabetes Mellulitis

A
  • 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
Q

Acute complications

A
  • 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
Q

Chronic complications

A
  • 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
Q

RPE, where is it, fx, age

A

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
Q

Drusen

A

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
Q

AMD, types, classification, RF

A

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
Q

Pigment epithelial detachment (PED). Types

A

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
Q

Choroidal Neovascularization, causes, what is it, location, macular choroidal neovasc

A

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
Q

Management of AMD, Charles Bonnet Syndrome

A

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
Q

RPE & CHOROID

A

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
Q

Coloboma, etc

A

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
Q

Acquired disorders, Uveitis

A

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
Q

Oncology definitions

A
  • 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
Q

More pigmented lesions

A
  • 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
Q

Hearing impairment

A

Techniques to communicate -

interpreter, amplifying device, some can lip read, sensitive to non verbal behaviour,

158
Q

Additional px needs

A

1) Intellectual,
2) hearing,
3) multiple impairments,
4) stroke/head injury

159
Q

Intellectual needs

A

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
Q

Multiple impairments

A

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
Q

The respiratory system

A

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
Q

Lung diseases

A

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
Q

ENT disorders and the eye

A
  • 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
Q

Genetics

A

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
Q

Genetics and the eye

A

Rare - RP AND STARGARDT
Chromosomal - Trisomy 21 down syndrome
Mitochondrial - Kearns - Sayre

Common
multifactorial - AMD, MYOPIA, POAG, CATARACT

166
Q

Sickle cell haemoglobinopathy

A

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
Q

Albinism

A
  • 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
Q

Retinal and macular dystrophies

A 
Photoreceptors - 
retinitis pigmentosa, cone dystrophies. 
RPE - 
Stargardts disease, fundus flavimaculatus, Bests vitelliform macular dystrophy
Bruch's - 
dominant drusen
Choroid - 
Choroideremia

Retinoblastoma

169
Q

Degenerative myopia

A

> 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
Q

Dystrophies, RETINITIS PIGMENTOSA

A

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
Q

Cone dystrophies

A

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
Q

Stargardts

A

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
Q

Best vitelliform macular dystrophy

A

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
Q

RPE dystrophy: dominant drusen

A
  • 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
Q

Retinoblastoma

A

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
Q

STroke handout

A

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

GLOCKTOMETRY (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions