Chapters 1-3 Flashcards
list the effects of aging on the eye
chronic dry eye due to loss of accessory lacrimal glands and smaller tear lake
increased crystalline lens leading to crowding of the anterior chamber (glaucoma)
vitreous humour develops liquefied pockets–> separation of the vitreous and its attachments to the retina and optic disc leading to posterior vitreous detachment (PVD)
atherosclerosis predisposes to vasculopathy–> CN III, IV, VI palsies, retinal artery/vein occlusions, anterior ischemic optic neuropathy
age delays regeneration of rhodopsin–> relative difficulty with night vision
what is accommodation
ability of the ciliary muscle to contract and lens to become more convex
what is the loss of accommodation called
presbyopia
associated with aging
what do you do if the patient cannot see the largest snellen chart
- reduce distance between patient and chart
- if unable to see chart at 3 feet, hold up 1 hand and extend two fingers (CF 1 ft)–> at least a CF 4 ft is near total blindness
- if cannot count fingers, determine if can detect hand movement
- if cannot detect hand movement, determine if can detect light
in what cases should dilation of pupils not be done
- anterior chamber assessment suggests shallow chamber and narrow angle
- patient is undergoing neuro observation
- patient has to read or drive shortly after
what muscles are responsible for the following eye movement:
up and right
right eye: SR
left eye: IO
what muscles are responsible for the following eye movement:
right
right eye: LR
left eye: MR
what muscles are responsible for the following eye movement:
right and down
right eye: IR
left eye: SO
what muscles are responsible for the following eye movement:
left and up
right eye: IO
left eye: SR
what muscles are responsible for the following eye movement:
left
right eye: MR
left eye: LR
what muscles are responsible for the following eye movement:
left and down
right eye: SO
left eye: IO
list patients that should be referred to ophtho
- patient with visual acuity less than 20/20 in 1 or both eyes with visual sx present
- visual acuity less than 20/40 in BOTH eyes in absence of complaints
- asymmetry in visual acuity of 2 lines or more–> refer PROMPTLY even if one is above 20/40
- presbyopia–> benefit for prescription of corrective lenses
- fundus changes accompanied by acute or chronic visual complaints or in a patient with systemic disease known to have ocular involvement
- patient with shallow anterior chamber depth should be referred
what history should you obtain on a patient with acute vision loss
- age and medical condition
- is loss transient, persistent or progressive
- monocular or binocular loss
- how severe
- tempo of loss–> abruptly or over hours/days/weeks
- did the patient have normal vision (with glasses if needed) in the past
- was there pain associated with vision loss
what is the most important physical exam technique in the setting of vision loss
ophthalmoscopy
what does ophthalmoscopy evaluate
fundus
refractive media
red reflex
what does tonometry measure
intraocular pressure
what physical exams should be done in the setting of vision loss
ophthalmoscopy and tonometry
list conditions associated with vision loss
- media opacities
- corneal edema
- hyphema
- cataract
- vitreous hemorrhage
what symptoms does media opacities cause
BLURRED vision
what would you find on physical exam in a patient with media opacities
reduction of visual acuity
darkening of the red reflex
does NOT cause RAPD but reflexes may be altered
acute loss of visual acuity–> conditions that cause rapid changes to the transparency
what does corneal edema cause
sudden opacification of the cornea
what causes corneal edema
increased IOP
what causes the vision loss associated with an attack of angle closure glaucoma
corneal edema
what can mimic corneal edema
any acute infection or inflammation of the cornea
how do you recognize corneal edema
sudden opacification of the cornea
recognized as dulling of the normally crisp reflection of incidence of light off the cornea
cornea takes on GROUND GLASS appearance
what is a hyphema
blood in anterior chamber
how do you recognize a complete hyphema
any significant hyphema causes reduced vision
a complete hyphema has light perception only
what causes hyphema
mostly due to blunt trauma
abnormal iris vessels (tumours, DM, surgery, inflammation) predisposes to hyphema and can occur spontaneously
how might a cataract cause acute vision loss
changes in lens hydration cause large fluctuations in refractive error that can be interpreted by patients as visual loss
how does vitreous hemorrhage reduce vision and what causes them
same way hyphema does
large hemorrhages occur after trauma and in any condition with neovascularization
retinal tears may present with vitreous hemorrhage
may accompany subarachnoid hemorrhage
how do retinal detachment, macular disease and retinal vascular occlusion all present
with SUDDEN visual loss
acute visual loss may develop in any inflammatory process that affects the retina (infectious chorioretinitis, vasculitides and idiopathic inflammation)
what are the symptoms patients complain of in retinal detachment
flashing lights (photopsia)
floaters
shade over vision in ONE EYE
what might you find on exam of a person with retinal detachment
RAPD if detachment is extensive enough to reduce visual acuity in the affected eye
retina will be elevated with or without folds and the choroidal background will be indistinct
how do you manage retinal detachment
EMERGENCY consultation if suspected
how does macular disease present
sudden visual loss or metamorphopsia
due to bleeding from neovascular net
reduces visual acuity but may not cause RAPD
management of macular disease
medication or laser surgery to cause regression of the neovascularization
what is another name for transient retinal vascular occlusion
amaurosis fugax
what should you do for a patient who is over 50 presenting with visual loss I one eye lasting minutes
investigate ipsilateral carotid circulation for a suspected atheroma causing amaurosis fugax/occlusion
should you refer a patient with amaurosis fugax
refer to ophtho, neuro or vascular surgeon depending on the results of the workup
what is a hollenhorst plaque
a cholesterol embolus which may lead to retinal vascular occlusion at arterial branch points
what is a central retinal arter occlusion (CRAO)
a prolonger interruption of retinal arterial blood causes permanent damage to the ganglion cells
how does CRAO present
sudden, PAINLESS, SEVERE vision loss
what are the findings of a CRAO within minutes to hours
vascular stasis–> narrowing of arterial blood columns and interruption of venous blood columns with appearance of BOXCARRING as rows of corpuscles separated by clear intervals
what are the findings of CRAO after hours
inner layer of the retina becomes opalescent
loss of normal transparency is the most obvious around the fovea
pallor of the perifoveal retina in contrast with the normal fovea (which gets its blood supply elsewhere) causes CHERRY SPOTS
optic disc does not swell unless the occlusion is in the ophthalmic or carotid artery
retina edema slowly resolves and the death of the ganglion cells and axons leads to optic atrophy
how quickly should you react to a CRAO
it is severe and urgent
what is a characteristic marker of CRAO other than boxcarring and cherry red spots
a pale disc in a blind eye
how do you manage CRAO
TRUE OPHTHO EMERGENCY
immediate treatment is necessary unless circulation spontaneously is restored
must have restoration of blood flow as this may preserve vision if done within a few hours
PCP can provide repetitive ophthalmic massage in attempts to dislodge the embolus
how acute is a branch retinal artery occlusion
subacute
how does a BRAO present
section of retina opacities–> PARTIAL loss of vision
patient is often able to describe the exact outline of the missing vision
most likely embolus and source should be investigated
should try to dislodge embolus if visual acuity is affected
how acute is a central retinal vein occlusion
chronic
how does a central retinal vein occlusion present
disc swelling, venous engorgement and COTTON WOOL SPOTS
also has diffuse retinal hemorrhages–> BLOOD AND THUNDER
vision loss can be severe but is usually subacute
is a central retinal vein occlusion a true ophtho emergency
no–> requires general follow up with ophtho to prevent later complications
acute hemorrhages and disc swelling resolve over time
who often presents with eh central retinal vein occlusion
older patients with HTN and atherosclerotic vascular disease
what is ischemic optic neuropathy
swelling of the optic disc + vision loss–> VASCULAR event rather than inflammation (which is what neuritis is)
how does ischemic optic neuropathy present
pale, swollen disc with SPLINTER hemorrhages and loss of visual acuity and visual field
also can have flame shaped hemorrhages
field loss is superior and infeior field (ALTITUDINAL)
what are common clinical complaints associated with giant cell arteritis
temporal headache/tenderness
scalp tenderness with hair brushing
anterior neck discomfort
fatigue or pain in tongue or jaw with chewing
episodes of transient diplopia or visual loss
may also have anorexia, weight loss, general malaise, aching/fatigue of upper arms and legs
how do you manage giant cell arteritis
take ESR and CRP immediately
high ESR or other symptoms must be treated with high dose corticosteroids
IMMEDIATE REFERRAL TO OPHTHO is indicated if giant cell arteritis is suspected/high possibility
how do you manage a traumatic optic neuropathy
can be treated with high dose IV corticosteroids or surgical decompression of the optic canal
what are two ways in which disruption of the visual pathway can lead to reduced visual acuity
hemianopia or cortical blindness
what is a hemianopia
a certain part of the visual field is lost
what often causes a homonymous hemianopia
may be from occlusion of the PCA–> infarction of the occipital lobe
what should you do for any patient with a hemianopia
MRI/CT
what is cortical blindness
extensive damage to the cerebral visual pathways resulting in complete vision loss
patient has NORMAL PUPILLARY REFLEXES and NORMAL FUNDOSCOPY but cannot see
what is a functional disorder causing visual loss? in which patients should you suspect this?
when there is visual loss without an organic basis
patient who reports complete blindness in one eye and normal vision in the other but has normal stereopsis and no RAPD should be suspected for a functional disorder
how does the optic nerve act/appear in optic nerve disease
the optic nerve may or may not appear normal but usually pupillary responses will be abnormal
how do optic nerve diseases differ from ischemic optic neuropathies
the ischemic processes are VASCULAR whereas the optic nerve diseases are inflammatory
what is optic neuritis
inflammation of the optic nerve
how does optic neuritis present
reduced visual acuity and RAPD–> generally SUDDEN
colours appear washed out or desaturated and everything is darker in the affected eye
what are findings on exam in optic neuritis
optic disc appears hyperemic and swollen–> margin are blurred with no discrete edge
what is the prognosis of optic neuritis
good after single attack
should be referred to ophtho for further follow up
certain patients may benefit from high dose IV corticosteroids (oral contraindicated)
what population usually present with retrobulbar optic neuritis
young adults
how does retrobulbar optic neuritis present
monocular, stepwise, progressive loss of vision developing over hours to days
PAIN ON MOVEMENT
NO abnormalities on fundoscopy
vision usually poor with a RAPD present
how do you investigate a retrobulbar optic neuritis
CT/MRI will ID the compressive lesion and these lesions are usually treatable with surgery
define papillitis
inflammation of the optic disc
what is papilledema
swelling of the optic disc from increased ICP–> BOTH discs are affected
visual acuity and pupillary reflexes are normal
does papillitis present with RAPD
yes
how can you distinguish papilledema from papillitis clinically
papillitis has an RAPD and papilledema doesnt
what are the similarities on exam in papillitis and papilledema
fundus exam shows blurred optic disc margins and optic disc cupping is obliterated
how does the optic disc appearance differ between papillitis and ischemic optic neuropathy
hyperemic in papillitis rather than pale in ischemic optic neuropathy
what is the main cause of visual loss in the western population over 50
age related macular degeneration (AMD)
what % of people who are blind are over 50
82%
what is the number one cause of blindness in african americans
glaucoma
what are the risk factors for glaucoma
age
race (if african american, get 2 points)
family history of glaucoma
last complete eye exam
level of risk:
if 4 or more–> risk is high and referral is advisable
if 3–> moderate and referral is advised
if 2 or less–> risk low
how do patients with early glaucoma present
most are asymptomatic early on
many lack pain, ocular inflammation or halos
significant peripheral vision can be lost before the patient notices
describe the visual deficits associated with glaucoma
characterized by SCOTOMAS which are areas of reduced or absent vision
contraction of the peripheral field that usually SPARES CENTRAL VISION
what is the hallmark of glaucoma
elevation of the intraocular pressure (IOP)
long elevation of IOP leads to optic nerve damage
in many cases glaucomatous nerve changes are evident despite apparently normal pressure
what is normal IOP
10-21 mmHg
is measurement if IOP a good way to screen for glaucoma
no–> it has a low sensitivity and specificity
how do you screen for glaucoma
visual field testing and exam of the optic nerve plus evaluation of risk factors
what generates IOP
aqueous humour produced by the ciliary body flows through the pupil into the anterior chamber and drains throught he trabecular meshwork to Schlemm’s canal
because of resistance to flow of aqueous humour through the meshwork and Schlemm’s canal, there is some pressure always present in the eye (normal 10-21 mmHg)
pressure is determined by the ease of flow through the meshwork/canal
define open angle glaucoma
common, insidious form
define acute angle closure glaucoma
due to trabcular meshwork becoming suddenly occluded by iris tissue
OCULAR EMERGENCY
how does acute angle closure glaucoma present
abrupt rise in pressure causes:
pain
nausea
coloured rainbows and halos around light
produced red, teary eye with HAZY CORNEA and FIXED, MID DILATED PUPIL
eye feels firm to palpation
define chronic angle closure glaucoma
caused by gradual scarring of the drainage angle resulting in elevated IOP
how does chronic angle closure glaucoma present
intermittent, low grade symptoms of headache, blurred vision (especially in situation in which the pupil is dilated, like low light)
what is congenital glaucoma
presents with tearing and sensitivity to light secondary to corneal edema
what is the blood supply to the optic nerve
branches of the ophthalmic artery (branches from the internal carotid)
what are the two types of factors that influence the development of glaucoma
IOP dependent and IOP independent factors
define glaucoma
progressive optic neuropathy that can lead to blindness if untreated
how often should you examine for glaucoma
every 2-4 years for patients over 40
how often should african americans be screened for glaucoma
every 3-5 years from ages 20-39 in addition to every 2-4 years after 40
what is the gold standard to evaluating IOP in the setting of glaucoma
goldmann applanation tonometry with slit lamp
ophthalmologist will also do gonioscopy (using speical contact lenses)
what is an independent risk factor for development of glaucoma
corneal thickness
what is a normal optic disc exam? what would suggest glaucoma?
normal:
optic disc should appear symmetrical between the eyes with a cup:disc ration of less than 0.5
cup:disc ration of greater than 0.5 or disc hemorrhages raise suspicion of glaucoma
when should you refer someone with suspected glaucoma
with one or more of the following:
- symptoms of acute glaucoma (refer immediately)
- optic cup diameter of of one half or more of the cup diameter
- cup:disc asymmetry of more than 0.1 between the two eyes
what is the most common cause of decreased vision
cataracts–mostly age related
when are cataracts mature
when the lens it totally opacified
define a cataract
any opacity or discolouration of the lens that impacts visual acuity
name the zones of opacity a cataract can affect
subcapsular
cortical
nuclear
location can be anterior or posterior
what do patients complain of when they are suffering from cataracts
images blurring
degree of impairment is related to where the cataract is
what do patients with posterior subcapsular cataracts complain os
relatively rapid decrease in vision with glare and image blur and distortion
what conditions/habits are associated with posterior subcapsular cataracts
corticosteroid use and metabolic causes
when should a referral for cataracts be made
based on whether or not the cataract prevents the patient from doing what they want to do
what is the leading cause of reversible central vision loss in people over 50
macular degeneration
where is the macula located
between the temporal vascular arcades–> the center is the fovea
what is the macula composed of
rods and cones
this is responsible for fine, central vision
what is the fovea composed of
is it partly avascular
appears darker and has a high density of cones but no rods
what changes/findings are associated with AMD
drusen
degenerative changes in the retinal pigment epithelium
choroidal neovascular membranes
where are age related macular changes usually found
usually confined to the posterior pole of the eye
what kinds of visual changes are associated with AMD
patient may have poor central vision but retain functional peripheral vision
(this is opposite to glaucoma which perserves central vision but affects peripheral vision)
what are drusen
hyaline nodules deposited in Brunch’s membrane which separates the retinal pigment epithelium from the inner choroidal vessels
patients with drusen alone tend to have normal or near normal vision with minimal metamorphopsia
what conditions are associated with drusen
increased age
retinal/choroidal degeneration
as a primary dystrophy
do degenerative changes always involve drusen
no–changes can occur without drusen
how do macular degenerative changes manifest
clumps of hyperpigmentation or depigmented atrophic areas
effect of visual acuity is variable
what % of AMD involves choroidal neovascularization
“wet” AMD
20%
what is the process of choroidal neovascularization
extension of vessels from inner choroid layer into the sub-pigment epithelial space and eventually into the sub retinal space via Brunch’s membrane
what other findings are associated with choroidal neovascularization in AMD
sub retinal hemorrhages (may result in acute visual loss)
exudates
may or may not have fibrosis
how do you ID choroidal neovascularization in AMD
fluorescein angiography
-or-
ocular coherence tomography
*the larger the membrane and the closer to the centre of the fovea, the worse the prognosis for good central vision
how do you diagnose AMD
amsler grid testing–> useful for evaluating function of the fovea
done with patients best near correction
areas of the grid that do not appear straight may indicate a scotoma
what ophthalmoscopy findings are associated with AMD
drusen
areas of decreased or increased pigment
sub retinal exudate
haemorrhage
absence of foveal reflex and mottled underlying pigment epithelium are early signs
who should you refer for AMD
any patient with one or more of the following:
recent onset of decreased visual acuity
recent onset of metamorphopsia (central vision distorsion)
recent onset of a scotoma
any ophthalmoscopic abnormalities in the appearance of the macula such as druse, degenerative changes in the RPE, exudate or blood
how do you treat AMD
anti-vascular endothelial growth factors (anti-VEGF) are helpful–i.e ranibuzumab and bevacizumab –> only effective with acute symptoms
anti-oxidant supplements are also encouraged (leafy greens, yellow veggies, daily vitamin)
smoking worsens AMD
should be referred to ophtho to qualify for low vision services
