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ophtho > Chapters 1-3 > Flashcards

Chapters 1-3 Flashcards

1
Q

list the effects of aging on the eye

A

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

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2
Q

what is accommodation

A

ability of the ciliary muscle to contract and lens to become more convex

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3
Q

what is the loss of accommodation called

A

presbyopia

associated with aging

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4
Q

what do you do if the patient cannot see the largest snellen chart

A
  1. reduce distance between patient and chart
  2. 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
  3. if cannot count fingers, determine if can detect hand movement
  4. if cannot detect hand movement, determine if can detect light
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5
Q

in what cases should dilation of pupils not be done

A
  1. anterior chamber assessment suggests shallow chamber and narrow angle
  2. patient is undergoing neuro observation
  3. patient has to read or drive shortly after
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6
Q

what muscles are responsible for the following eye movement:

up and right

A

right eye: SR

left eye: IO

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7
Q

what muscles are responsible for the following eye movement:

right

A

right eye: LR

left eye: MR

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8
Q

what muscles are responsible for the following eye movement:

right and down

A

right eye: IR

left eye: SO

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9
Q

what muscles are responsible for the following eye movement:

left and up

A

right eye: IO

left eye: SR

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10
Q

what muscles are responsible for the following eye movement:

left

A

right eye: MR

left eye: LR

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11
Q

what muscles are responsible for the following eye movement:

left and down

A

right eye: SO

left eye: IO

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12
Q

list patients that should be referred to ophtho

A
  1. patient with visual acuity less than 20/20 in 1 or both eyes with visual sx present
  2. visual acuity less than 20/40 in BOTH eyes in absence of complaints
  3. asymmetry in visual acuity of 2 lines or more–> refer PROMPTLY even if one is above 20/40
  4. presbyopia–> benefit for prescription of corrective lenses
  5. fundus changes accompanied by acute or chronic visual complaints or in a patient with systemic disease known to have ocular involvement
  6. patient with shallow anterior chamber depth should be referred
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13
Q

what history should you obtain on a patient with acute vision loss

A
  1. age and medical condition
  2. is loss transient, persistent or progressive
  3. monocular or binocular loss
  4. how severe
  5. tempo of loss–> abruptly or over hours/days/weeks
  6. did the patient have normal vision (with glasses if needed) in the past
  7. was there pain associated with vision loss
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14
Q

what is the most important physical exam technique in the setting of vision loss

A

ophthalmoscopy

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15
Q

what does ophthalmoscopy evaluate

A

fundus

refractive media

red reflex

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16
Q

what does tonometry measure

A

intraocular pressure

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17
Q

what physical exams should be done in the setting of vision loss

A

ophthalmoscopy and tonometry

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18
Q

list conditions associated with vision loss

A
  1. media opacities
  2. corneal edema
  3. hyphema
  4. cataract
  5. vitreous hemorrhage
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19
Q

what symptoms does media opacities cause

A

BLURRED vision

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20
Q

what would you find on physical exam in a patient with media opacities

A

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

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21
Q

what does corneal edema cause

A

sudden opacification of the cornea

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22
Q

what causes corneal edema

A

increased IOP

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23
Q

what causes the vision loss associated with an attack of angle closure glaucoma

A

corneal edema

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24
Q

what can mimic corneal edema

A

any acute infection or inflammation of the cornea

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25
Q

how do you recognize corneal edema

A

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

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26
Q

what is a hyphema

A

blood in anterior chamber

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27
Q

how do you recognize a complete hyphema

A

any significant hyphema causes reduced vision

a complete hyphema has light perception only

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28
Q

what causes hyphema

A

mostly due to blunt trauma

abnormal iris vessels (tumours, DM, surgery, inflammation) predisposes to hyphema and can occur spontaneously

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29
Q

how might a cataract cause acute vision loss

A

changes in lens hydration cause large fluctuations in refractive error that can be interpreted by patients as visual loss

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30
Q

how does vitreous hemorrhage reduce vision and what causes them

A

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

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31
Q

how do retinal detachment, macular disease and retinal vascular occlusion all present

A

with SUDDEN visual loss

acute visual loss may develop in any inflammatory process that affects the retina (infectious chorioretinitis, vasculitides and idiopathic inflammation)

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32
Q

what are the symptoms patients complain of in retinal detachment

A

flashing lights (photopsia)

floaters

shade over vision in ONE EYE

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33
Q

what might you find on exam of a person with retinal detachment

A

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

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34
Q

how do you manage retinal detachment

A

EMERGENCY consultation if suspected

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35
Q

how does macular disease present

A

sudden visual loss or metamorphopsia

due to bleeding from neovascular net

reduces visual acuity but may not cause RAPD

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36
Q

management of macular disease

A

medication or laser surgery to cause regression of the neovascularization

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37
Q

what is another name for transient retinal vascular occlusion

A

amaurosis fugax

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38
Q

what should you do for a patient who is over 50 presenting with visual loss I one eye lasting minutes

A

investigate ipsilateral carotid circulation for a suspected atheroma causing amaurosis fugax/occlusion

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39
Q

should you refer a patient with amaurosis fugax

A

refer to ophtho, neuro or vascular surgeon depending on the results of the workup

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40
Q

what is a hollenhorst plaque

A

a cholesterol embolus which may lead to retinal vascular occlusion at arterial branch points

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41
Q

what is a central retinal arter occlusion (CRAO)

A

a prolonger interruption of retinal arterial blood causes permanent damage to the ganglion cells

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42
Q

how does CRAO present

A

sudden, PAINLESS, SEVERE vision loss

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43
Q

what are the findings of a CRAO within minutes to hours

A

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

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44
Q

what are the findings of CRAO after hours

A

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

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45
Q

how quickly should you react to a CRAO

A

it is severe and urgent

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46
Q

what is a characteristic marker of CRAO other than boxcarring and cherry red spots

A

a pale disc in a blind eye

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47
Q

how do you manage CRAO

A

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

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48
Q

how acute is a branch retinal artery occlusion

A

subacute

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49
Q

how does a BRAO present

A

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

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50
Q

how acute is a central retinal vein occlusion

A

chronic

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51
Q

how does a central retinal vein occlusion present

A

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

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52
Q

is a central retinal vein occlusion a true ophtho emergency

A

no–> requires general follow up with ophtho to prevent later complications

acute hemorrhages and disc swelling resolve over time

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53
Q

who often presents with eh central retinal vein occlusion

A

older patients with HTN and atherosclerotic vascular disease

54
Q

what is ischemic optic neuropathy

A

swelling of the optic disc + vision loss–> VASCULAR event rather than inflammation (which is what neuritis is)

55
Q

how does ischemic optic neuropathy present

A

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)

56
Q

what are common clinical complaints associated with giant cell arteritis

A

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

57
Q

how do you manage giant cell arteritis

A

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

58
Q

how do you manage a traumatic optic neuropathy

A

can be treated with high dose IV corticosteroids or surgical decompression of the optic canal

59
Q

what are two ways in which disruption of the visual pathway can lead to reduced visual acuity

A

hemianopia or cortical blindness

60
Q

what is a hemianopia

A

a certain part of the visual field is lost

61
Q

what often causes a homonymous hemianopia

A

may be from occlusion of the PCA–> infarction of the occipital lobe

62
Q

what should you do for any patient with a hemianopia

A

MRI/CT

63
Q

what is cortical blindness

A

extensive damage to the cerebral visual pathways resulting in complete vision loss

patient has NORMAL PUPILLARY REFLEXES and NORMAL FUNDOSCOPY but cannot see

64
Q

what is a functional disorder causing visual loss? in which patients should you suspect this?

A

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

65
Q

how does the optic nerve act/appear in optic nerve disease

A

the optic nerve may or may not appear normal but usually pupillary responses will be abnormal

66
Q

how do optic nerve diseases differ from ischemic optic neuropathies

A

the ischemic processes are VASCULAR whereas the optic nerve diseases are inflammatory

67
Q

what is optic neuritis

A

inflammation of the optic nerve

68
Q

how does optic neuritis present

A

reduced visual acuity and RAPD–> generally SUDDEN

colours appear washed out or desaturated and everything is darker in the affected eye

69
Q

what are findings on exam in optic neuritis

A

optic disc appears hyperemic and swollen–> margin are blurred with no discrete edge

70
Q

what is the prognosis of optic neuritis

A

good after single attack

should be referred to ophtho for further follow up

certain patients may benefit from high dose IV corticosteroids (oral contraindicated)

71
Q

what population usually present with retrobulbar optic neuritis

A

young adults

72
Q

how does retrobulbar optic neuritis present

A

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

73
Q

how do you investigate a retrobulbar optic neuritis

A

CT/MRI will ID the compressive lesion and these lesions are usually treatable with surgery

74
Q

define papillitis

A

inflammation of the optic disc

75
Q

what is papilledema

A

swelling of the optic disc from increased ICP–> BOTH discs are affected

visual acuity and pupillary reflexes are normal

76
Q

does papillitis present with RAPD

A

yes

77
Q

how can you distinguish papilledema from papillitis clinically

A

papillitis has an RAPD and papilledema doesnt

78
Q

what are the similarities on exam in papillitis and papilledema

A

fundus exam shows blurred optic disc margins and optic disc cupping is obliterated

79
Q

how does the optic disc appearance differ between papillitis and ischemic optic neuropathy

A

hyperemic in papillitis rather than pale in ischemic optic neuropathy

80
Q

what is the main cause of visual loss in the western population over 50

A

age related macular degeneration (AMD)

81
Q

what % of people who are blind are over 50

A

82%

82
Q

what is the number one cause of blindness in african americans

A

glaucoma

83
Q

what are the risk factors for glaucoma

A

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

84
Q

how do patients with early glaucoma present

A

most are asymptomatic early on

many lack pain, ocular inflammation or halos

significant peripheral vision can be lost before the patient notices

85
Q

describe the visual deficits associated with glaucoma

A

characterized by SCOTOMAS which are areas of reduced or absent vision

contraction of the peripheral field that usually SPARES CENTRAL VISION

86
Q

what is the hallmark of glaucoma

A

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

87
Q

what is normal IOP

A

10-21 mmHg

88
Q

is measurement if IOP a good way to screen for glaucoma

A

no–> it has a low sensitivity and specificity

89
Q

how do you screen for glaucoma

A

visual field testing and exam of the optic nerve plus evaluation of risk factors

90
Q

what generates IOP

A

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

91
Q

define open angle glaucoma

A

common, insidious form

92
Q

define acute angle closure glaucoma

A

due to trabcular meshwork becoming suddenly occluded by iris tissue

OCULAR EMERGENCY

93
Q

how does acute angle closure glaucoma present

A

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

94
Q

define chronic angle closure glaucoma

A

caused by gradual scarring of the drainage angle resulting in elevated IOP

95
Q

how does chronic angle closure glaucoma present

A

intermittent, low grade symptoms of headache, blurred vision (especially in situation in which the pupil is dilated, like low light)

96
Q

what is congenital glaucoma

A

presents with tearing and sensitivity to light secondary to corneal edema

97
Q

what is the blood supply to the optic nerve

A

branches of the ophthalmic artery (branches from the internal carotid)

98
Q

what are the two types of factors that influence the development of glaucoma

A

IOP dependent and IOP independent factors

99
Q

define glaucoma

A

progressive optic neuropathy that can lead to blindness if untreated

100
Q

how often should you examine for glaucoma

A

every 2-4 years for patients over 40

101
Q

how often should african americans be screened for glaucoma

A

every 3-5 years from ages 20-39 in addition to every 2-4 years after 40

102
Q

what is the gold standard to evaluating IOP in the setting of glaucoma

A

goldmann applanation tonometry with slit lamp

ophthalmologist will also do gonioscopy (using speical contact lenses)

103
Q

what is an independent risk factor for development of glaucoma

A

corneal thickness

104
Q

what is a normal optic disc exam? what would suggest glaucoma?

A

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

105
Q

when should you refer someone with suspected glaucoma

A

with one or more of the following:

  1. symptoms of acute glaucoma (refer immediately)
  2. optic cup diameter of of one half or more of the cup diameter
  3. cup:disc asymmetry of more than 0.1 between the two eyes
106
Q

what is the most common cause of decreased vision

A

cataracts–mostly age related

107
Q

when are cataracts mature

A

when the lens it totally opacified

108
Q

define a cataract

A

any opacity or discolouration of the lens that impacts visual acuity

109
Q

name the zones of opacity a cataract can affect

A

subcapsular

cortical

nuclear

location can be anterior or posterior

110
Q

what do patients complain of when they are suffering from cataracts

A

images blurring

degree of impairment is related to where the cataract is

111
Q

what do patients with posterior subcapsular cataracts complain os

A

relatively rapid decrease in vision with glare and image blur and distortion

112
Q

what conditions/habits are associated with posterior subcapsular cataracts

A

corticosteroid use and metabolic causes

113
Q

when should a referral for cataracts be made

A

based on whether or not the cataract prevents the patient from doing what they want to do

114
Q

what is the leading cause of reversible central vision loss in people over 50

A

macular degeneration

115
Q

where is the macula located

A

between the temporal vascular arcades–> the center is the fovea

116
Q

what is the macula composed of

A

rods and cones

this is responsible for fine, central vision

117
Q

what is the fovea composed of

A

is it partly avascular

appears darker and has a high density of cones but no rods

118
Q

what changes/findings are associated with AMD

A

drusen

degenerative changes in the retinal pigment epithelium

choroidal neovascular membranes

119
Q

where are age related macular changes usually found

A

usually confined to the posterior pole of the eye

120
Q

what kinds of visual changes are associated with AMD

A

patient may have poor central vision but retain functional peripheral vision

(this is opposite to glaucoma which perserves central vision but affects peripheral vision)

121
Q

what are drusen

A

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

122
Q

what conditions are associated with drusen

A

increased age

retinal/choroidal degeneration

as a primary dystrophy

123
Q

do degenerative changes always involve drusen

A

no–changes can occur without drusen

124
Q

how do macular degenerative changes manifest

A

clumps of hyperpigmentation or depigmented atrophic areas

effect of visual acuity is variable

125
Q

what % of AMD involves choroidal neovascularization

A

“wet” AMD

20%

126
Q

what is the process of choroidal neovascularization

A

extension of vessels from inner choroid layer into the sub-pigment epithelial space and eventually into the sub retinal space via Brunch’s membrane

127
Q

what other findings are associated with choroidal neovascularization in AMD

A

sub retinal hemorrhages (may result in acute visual loss)

exudates

may or may not have fibrosis

128
Q

how do you ID choroidal neovascularization in AMD

A

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

129
Q

how do you diagnose AMD

A

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

130
Q

what ophthalmoscopy findings are associated with AMD

A

drusen

areas of decreased or increased pigment

sub retinal exudate

haemorrhage

absence of foveal reflex and mottled underlying pigment epithelium are early signs

131
Q

who should you refer for AMD

A

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

132
Q

how do you treat AMD

A

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

ophtho (5 decks)

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