Brainscape's Knowledge GenomeTM

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


See full index

ophtho > Chapters 7-9 > Flashcards

Chapters 7-9 Flashcards

1
Q

what % of fibres in the anterior visual pathway serve central vision

A

90%

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

what makes up the anterior visual pathway

A

optic nerve

chiasm

tracts

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

what is a finding in many diseases of the optic nerve and anterior pathway

A

will cause red hues to become desaturated

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

what is an acceptable difference in pupil size?

A

less than 1mm is normal variation in 20% of the population

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

what is anisocoria

A

a difference in pupil size

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

what does a difference in pupil size (anisocoria) in DIM light indicate?

A

dilation SNS dysfunction–> HORNERS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what does a difference in pupil size (anisocoria) in BRIGHT light indicate?

A

abnormal constriction, PNS dysfunction–> 3rd NERVE PALSY, ADIE TONIC PUPIL

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

what does an RAPD almost always indicate

A

a leson in the optic nerve on the affected side or widespread/central retinal disorder (subtle)

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

do cataracts/vitreous hemorrhage affect pupillary reaction

A

no

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

does RAPD ever cause anisocoria

A

no, never

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

can RAPD ever be bilateral

A

no

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

what causes an RAPD

A

one optic nerve is less sensitive to light than the other

thus, the brain thinks the light to the normal eye is brighter than the light to the affected eye

when light is switched from the normal eye to the affected eye, the brain senses relatively less light in the affected eye and the affected pupil will DILATE

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

what is a mydriatic pupil

A

dilated pupil

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

with does a mydriatic pupil indicate

A

LOSS of PNS input to the iris sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what can cause loss of PNS input to the iris sphincter (and thus cause a mydriatic pupil)

A
  1. oculomotor nerve paresis –> check with MRI
  2. benign ciliary ganglionopathy (adie tonic pupil)
  3. trauma to the orbital parasympathetic system (traumatic mydriasis)–> check with CT
  4. dorsal midbrain syndrome–> MRI
  5. prior iris damage/surgery
  6. pharmacologic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what does CN III do

A

controls pupillary sphincter muscles and some of the muscles of ocular movements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what happens when CN III is compromised

A

third nerve palsy

causes eyelid proptosis, pupil dilated and poorly reactive, eye loses ability to elevate, depress or move nasally

eye is turned OUTWARD and SLIGHTLY DOWNWARD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what direction does the eye point in a third nerve palsy

A

outward and slightly downward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how should you manage a new onset third nerve palsy

A

must undergo immediate, urgent MRI, CV imaging to rule out neural compression

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

what is the most common cause of third nerve palsy

A

circle of willis aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what usually causes a dilated fixed pupil in an otherwise healthy individual with normal ocular motility

A

usually benign and may be due to migraine, adie tonic pupil, dilating agents or secondary to previous ocular trauma

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

what is perinaud syndrome

A

dorsal midbrain syndrome

damage/compression to the upper brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what causes dorsal midbrain syndrome/perinaud syndrome

A

can be caused by:

hydrocephalus

compressive lesion of the midbrain

MS

stroke

midbrain hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the symptoms of dorsal midbrain syndrome/perinaud syndrome

A

loss of UPGAZE

convergence-retraction nystagmus

light-near dissociation of the pupils

eyelid retraction (collier sign)

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

what is collier sign

A

eyelid retraction

sign of dorsal midbrain syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how should you manage suspected dorsal midbrain syndrome

A

urgen MRI

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

what is adie tonic pupil

A

benign, idiopathic, (usually) dilated pupil

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

what % of adie tonic pupil are unilateral

A

80%

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

what population is usually associated with adie tonic pupil

A

young women

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

how does adie tonic pupil present

A

tonic pupil is usually larger than the uninvolved pupil

reaction to light is diminished to absent

reaction to accomodation remains intact

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

what is a “small pupil”

A

a small pupil with normal reactivity with no ocular abnormalities

is of no neurological significance–> especially if difference is less than 1mm

must consider Horners syndrome and tertiary syphillis

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

what are the symptoms of Horner’s syndrome

A

small pupil + ptosis

due to loss of SNS tone from Horner’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what causes Horner’s

A

dysfunction of the extensive SNS pathways

can be caused by carotid dissection, cavernous carotid aneurysm, apical lung tumour

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

how do you confirm Horner’s

A

pharmacologic testing–> eye drops (APRACLONIDINE) will cause significant elevation of the eyelid and dilation of the pupil in an eye with Horner’s

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

what eye drop is used to test for Horner’s

A

apraclonidine–> will cause elevation of eyelid and dilation of pupil

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

how should you manage a horner’s syndrome

A

should have MRI

majority are idiopathic

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

what is a argyll robertson pupil

A

associated with tertiary syphilis

results in small, irregular pupils that demonstrate light-near dissociation

both pupils are usually involved but can be asymmetric

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

why does tertiary syphilis cause argyll robertson pupils

A

it can affect the fibres of the midbrain and pupillary light reflex

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

how should you manage argyll robertson pupil

A

should have serological testing for syphilis and MRI of brainstem

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

what nerve innervates the superior oblique muscle of the eye

A

CN IV

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

how does a complete paralysis of CN IV present (complete CN IV palsy)

A

vertical diplopia when down-gaze and contralateral side-gaze

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

what is the most common cause of CN IV palsy

A

microvascular disease–HTN, DM

trauma also common since CN IV is very thin

common congenital anomaly that presents in adulthood

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

what is the caused of a BILATERAL CN IV palsy

A

closed head trauma

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

what nerve supplies the lateral rectus muscles of the eye

A

CN VI

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

how does a complete paralysis of CN VI present? (CN VI palsy)

A

produces loss of ABDUCTION resulting in horizontal diplopia worse when gaze is towards affected side

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

what is the most common cause of CN VI palsy

A

microvascular disease (HTN, DM, smoking, hyperlipidemia)

98% spontaneously recover within 3-4 months

can also be caused by tumour (20%) or increased ICP which can lead to compression (CN VI is the most susceptible to this)

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

how do you manage a CN VI palsy

A

98% spontaneously recover within 3-4 months so treatment is initial watchful waiting period of 4 months

if no recovery or gets other symptoms, MRI

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

what is the most common cause if CN VI palsy in kids

A

trauma

can also be post infectious or inflammation of the petrous ridge from severe otitis media

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

where is the lesion in an INO

A

in the MLF

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

how does an INO present

A

slow and weak adduction of one eye and nystagmus of the abducting eye in lateral gaze

may be unilateral or bilateral

eyes may be straight or have exotropia

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

what is the usual cause of an INO in adults

A

microvascular disease–recovers in weeks or months

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

what is the usual cause of an INO in a young adult

A

commonly due to demyelinating disease, brainstem hemorrhage or trauma

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

what is the usual cause of an INO in a child

A

pontine glioma

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

how should you manage an INO

A

MRI and myasthenia gravis should be considered

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

how does a patient with convergence insufficiency present

A

double vision when viewing near but not at a distance

patients have normal eye movement and alignment in primary gaze but have exotropia in far vision

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

how does a patient with divergence insufficiency present

A

double vision at a distance but not when reading

normal motility–measures near their eyes are straight but crossed at a distance

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

what is myasthenia gravis

A

chronic autoimmune condition that interferes with neuromuscular transmission at skeletal muscles

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

what are the presenting complaints in MG in 50% of patients

A

ptosis and double vision

for those with ocular MG, half go on to develop weakness of other skeletal muscles within 2 years

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

what are the symptoms of MG besides ptosis and double vision

A

fatigability of muscle function with sustained effort

does NOT affect the pupil

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

how do you diagnose MG

A

serology for Ach receptor antibodies, electromyography and ice pack test

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

define nystagmus

A

spontaneous, rhythmic back and forth movement of one or both eyes

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

what are the three most common forms of nystagmus

A

are BENIGN

  1. extremes of lateral gaze (3/4 of horizontal nystagmus)
  2. nystagmogenic meds (anti-epileptics, barbituates, sedatives)
  3. searching/pendular nystagmus (most common… congenital)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

what are the three types of acquired nystagmus

A

cause oscillipsia and vertigo

  1. vestibular
  2. cerebellar
  3. brainstem dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

what kinds of processes can cause an acquired nystagmus

A

peripheral vestibular disease

trauma

MS

brain tumours

degeneration of CNS

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

how do you manage an acquired nystagmus

A

MRI (only for acquired)

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

where can you usually visualize pathological nystagmuses

A

in the primary eye position (straight ahead)

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

how do you ID an optic disc elevation

A

via fundoscopy

seen as an indistinct disc margin, elevation of the optic disc, vascular tortuosity and absence of the central cup (disc edema)

presence of capillary hyperemia and haemorrhage on or around the disc is a sign of active disc edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

how does a congenital optic disc elevation present

A

normal varient

may have bright yellow, proteinacious material within the disc itself (drusen)

because of deceptive appearance, referred to as pseudopapilledema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

list the characteristics of papilledema

A
  1. hyperemia of the disc
  2. tortuosity of the being and capillaries
  3. blurring and elevation of the margins of the disc
  4. obscuration of retinal vessels near the nerve
  5. haemorrhages on and surrounding the nerve head
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is papilledema

A

passive swelling of the optic disc secondary to increased ICP

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

is papilledema usually uni or bilateral

A

usually bilateral tho can be asymmetric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

what symptoms would you expect to see with papilledema

A

vision may not be affected initially

blurring, flickering or second-long obstruction may occur

sx of increased ICP–headaches, nausea, vomiting, double vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what causes increased ICP and thus papilledema

A

tumours

idiopathic intracranial HTN

cerebral trauma/haemorrhage

meningitis/encephalitis

dural sinus thrombosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

how do you manage papilledema

A

requires immediate MRI or CT scan

LP if mass and venous thrombosis ruled out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what is pseudotumour cerebri

A

idiopathic intracranial HTN

increased fluid pressure around the brain in absence of brain tumour, thrombosis or CSF abnormality

76
Q

in which patients is pseudotumour cerebri most common

A

women aged 20-40

77
Q

what are symptoms of pseudotumour cerebri

A

chronic papilledema may result in ischemia leading to vision loss

headache

transient blurred vision

pain with eye movement

pulsatile tinnitus

horizontal double vision

neck stiffness

papilledema with or without CN VI palsy

neuro exam usually NORMAL

78
Q

what exposures may lead you to think of a dx of pseudotumour cerebri

A

steroids

excessive vitamin A

retinoic acid

tetracycline and lithium

79
Q

how do you manage pseudotumour cerebri

A

brain MRI plus LP for opening pressure and CSF profile

80
Q

what is papillitis

A

inflammatory edema of the disc

may be indistinguishable from papilledema but is clinically distinct

81
Q

how can you try and distinguish between papillitis and papilledema

A

papillitis is more commonly unilateral and associated with decreased visual acuity, impaired colour, visual field defects and afferent pupillary defect

82
Q

what can cause papillitis

A

may result from demyelination ischemia, infiltration, compression or infection

83
Q

what is optic neuritis

A

inflammation and demyelination of the optic nerve

84
Q

what should you think of when someone presents with sudden, painful loss of vision

A

optic neuritis

85
Q

in which population is optic neuritis most common

A

women aged 15-45

86
Q

what are the symptoms of optic neuritis

A

acute or subacute VISION LOSS associated with periocular pain

pain is exacerbated with eye movement and preceeds vision decline

87
Q

how does anterior optic neuritis present

A

it is a form of papillitis

results in disc edema but swelling is usually mild

majority of optic neuritis occurs behind the eye so the optic disc appears normal

88
Q

what condition is most commonly associated with optic neuritis

A

MS–> 50% of patients who present with optic neuritis go on to develop MS

89
Q

what is the course of optic neuritis

A

most resolves spontaneously within weeks without treatment

may be faster with IV corticosteroids

90
Q

how do you manage optic neuritis

A

all patients should have an MRI with and without contrast

91
Q

what causes optic neuritis

A

may be idiopathic, post viral, systemic condition related (syphilis, sarcoidosis, collagen vascular disease)

92
Q

should you refer patients with optic neuritis

A

yes–all should be followed up by ophtho

93
Q

what should you think when someone presents with sudden, painless, unilateral loss of vision

A

ischemic optic neuropathy

94
Q

what causes ischemic optic neuropathy

A

sudden microvascular infarction of optic nerve

95
Q

which portion of the optic nerve is most vulnerable to ischemic optic neuropathy

A

anterior portion where it joins the eye

this is termed anterior ischemic optic neuropathy (AION)

this is non arteritic

96
Q

how does posterior ischemic optic neuropathy present

A

less common

results in sudden, severe, unilateral or bilateral vision loss in the setting of SYSTEMIC HTN (or cranial surgery, zoster, vasculitis)

optic disc is swollen or normal

97
Q

what is the most common form of ischemic optic neuropathy

A

non arteritic ischemic optic neuropathy (NAION)

98
Q

which patient population is associated with non arteritic ischemic optic neuropathy

A

patients over 40 with atherosclerotic risk factors (HTN, diabetes, hyperlipidemia, smoking, sleep apnea, obesity)

99
Q

when does non arteritic ischemic optic neuropathy happen?

A

DURING SLEEP

presents with unilateral vision loss first noticed WHEN WAKING

100
Q

which visual fields are lost with non arteritic ischemic optic neuropathy

A

upper or lower half of vision affected (altitudinal)

101
Q

what is always present in non arteritic ischemic optic neuropathy

A

RAPD

also disc edema

variable visual acuity effects

102
Q

how do you manage non arteritic ischemic optic neuropathy

A

there are no treatments are there is little to no recovery

test with CRP and ESR to rule out temporal arteritis

103
Q

how does arteritic anterior ischemic optic neuropathy present

A

sudden, painless, catastrophic visual loss in patients over 60

it is a cardinal feature og GIANT CELL/TEMPORAL ARTERITIS

accompanied by jaw claudication, new onset headache, visual abnormalities, elevated CRP, ESR

104
Q

how do you diagnose arteritic anterior ischemic optic neuropathy/giant cell arteritis

A

biopsy

105
Q

do all patients with visual loss and giant cell arteritis have sx

A

no, 1/5 do not

106
Q

how do you treat arteritic anterior ischemic optic neuropathy/giant cell arteritis

A

IV corticosteroids ASAP to spare the other eye

107
Q

what should you think of if someone has temporary painless vision loss in one eye

A

amaurosis fugax

108
Q

what may be found on fundoscopy for someone who had amaurosis fugax

A

hollenhorst plaque (intra-arterial plaque) at the retinal-arterial bifurcation

109
Q

what should you do to work up amaurosis fugax

A

evaluate for stenosis of the ipsilateral carotid, embolic sources from cardiac, temporal arteritis

ESR, CRP, carotid U/S, transesophageal echo

110
Q

what should you think of if patient has transient visual loss lasting 20-40 minutes and is associated with photopsias and/or headache

A

migraine

111
Q

define optic atrophy

A

morphological and physiological changes of the optic nerve as a result of damage to the ganglion cells

most easily observed as changes in the optic disc

112
Q

what causes optic atrophy

A

result of progressive change in appearance of axons and glial tissue–may become pale and cup may enlarge

disc may appear white after extensive damage

113
Q

how do you diagnose optic atrophy

A

should not dx unless concomitant, demonstrable optic nerve dysfunction

workup should include orbital MRI with contrast and serology

114
Q

define scotoma

A

area of abnormal or absent vision within an otherwise intact visual field

115
Q

define hemianopia

A

loss of half of visual field

116
Q

define homonymous hemianopia

A

loss of either right or left half of visual field in both eyes

117
Q

define bitemporal hemianopia

A

loss of the temporal half of the visual field in both eyes

118
Q

what are some possible causes of bitemporal hemianopia

A

pituitary adenoma, craniopharyngioma or parasellar meningioma

119
Q

what is a junctional scotoma

A

loss of central field in one eye and temporal visual defect in the other

120
Q

where is the lesion of the presenting complaint is a scotoma or altitudinal hemianopia with accompanying pupillary defect

A

anterior to the chiasm

i.e optic neuritis/papillitis
optic nerve glioma
meningioma
ischemic optic neuropathy

121
Q

where is the lesion if it produces a homonymous hemianopia

A

behind the chiasm

most commonly caused by stroke, trauma, mass lesion

122
Q

what ocular abnormality is associated with a PCA stroke

A

a neurologically isolated homonymous hemianopia

123
Q

what is charles bonnet syndrome

A

characterized by release hallucinations that occur in cognitively intact individuals with bilaterally decreased vision

solely see visual hallucinations that are sporadic and not associated with other neuro or cognitive defects

typically see colourful patterns, faces, animals, flowers or people

seen in 15% of people with vision worse than 20/80

124
Q

treatment of charles bonnet syndrome

A

increased lighting and more social interaction

125
Q

what ocular changes are associated with diabetes

A

refractive changes

RETINOPATHY

cataract formation

after 20 years, 50% of T1DM have severe subtype or proliferative diabetic retinopathy

126
Q

what can cause diabetic retinopathy

A

may be secondary to macular edema, haemorrhage from new vessels and retinal detachment from neovascular glaucoma

majority of patients have no sx until late in disease making screening important

127
Q

what are the two types of diabetic retinopathy

A

proliferative and non-proliferative

128
Q

describe the pathogenesis of diabetic retinopathy

A

multifactorial

primarily caused by metabolic effects of chronic hyperglycemia –> leads to vascular changes and retinal injury/ischemia

caused by impaired autoregulation of retinal blood flow, accumulation of SORBITOL within retinal cells and accumulation of advanced glycosylation end products in the extracellular fluid

tight BP control is as important as glycemic control in preventing developments and progression of diabetes

129
Q

what HbA1c is considered low risk for development of diabetic retinopathy

A

uncommon in patients with HbA1c below 7%

130
Q

what is the first manifestation of nonproliferative diabetic retinopathy

A

microaneurysm formation –>

capillaries leak and eventually become occluded

131
Q

what are the retinal findings in nonproliferative diabetic retinopathy

A

DOT AND BLOT hemorrhages

hard exudate

cotton wool spots

macular edema

132
Q

what is the most common visual impairment associated wtih nonproliferative diabetic retinopathy

A

macular edema

133
Q

what are the signs and characteristics of proliferative diabetic retinopathy

A

more severe progression of disease

marked by increased vascular tortuosity and haemorrhage, venous bleeding and microvascular abnormalities

because of ischemia, some new blood vessels grow over the optic disc or over the iris (causing glaucoma)

134
Q

what is the leading cause of blindness in diabetics

A

proliferative diabetic retinopathy

135
Q

how does proliferative diabetic retinopathy cause retinal detachment

A

neovascularization can cause bleeding into the vitreous with can cause traction and cause retinal detachment

136
Q

when should T1DM patients be screened for retinopathy

A

screened by ophtho if have had DM for equal to or more than 5 years

137
Q

when should T2DM patients be screened for retinopathy

A

at time of diagnosis

138
Q

what condition in women can exacerbate diabetic retinopahy

A

pregnancy

139
Q

what sign is associated with arteriolar sclerosis

A

COPPER WIRE ARTERIOLES–> when the light reflex becomes completely obscured you get SILVER WIRE arterioles

can get A/V crossing changes–> vein may be elevated or depressed by the arteriole which causes AV NICKING

140
Q

how do you ID arteriolar sclerosis

A

increase in light reflex of arteriolar sclerosis depends on severity and duration of the HTN

141
Q

what underlying condition causes arteriolar sclerosis

A

HTN

causes thickening of the walls and central light reflex increases in width

142
Q

what condition is associated with AV nicking?

A

arteriolar sclerosis

143
Q

what conditions can result due to AV Nicking

A

severe AV nicking can lead to branch retinal vein occlusion (BRVO)–> appears as diffuse retinal hemorrhage and cotton wool spots in the retina that is drained by the affected vein

may also have macular edema, central vision acuity decrease and may need laser therapy

144
Q

what ocular changes are associated with an acute rise in BP

A

constriction of arterioles–>

rise greater than 120 mmHg and a systolic over 200 mmHg causes FIBRINOID NECROSIS of the vessel wall

results in exudates, cotton wool spots, flame shaped hemorrhages and sub retinal fluid

145
Q

what ocular signs are associated with malignant HTN

A

swelling resembles papilledema and exudates assume a stellate configuration–> MACULAR STAR

146
Q

how are HTN ocular changes classified

A

Grade 0–> no changes

Grade 1–> barely detectable arterial narrowing

Grade 2–> obvious arterial narrowing with focal irregularities

Grade 3–> Grade 2 plus retinal hemorrhage and/or exudates

Grade 4–> grade 3 plus disc swelling

147
Q

what is the management of the ocular manifestations of HTN

A

managing the BP

148
Q

what ocular changes are associated with pregnancy

A

lowering of IOP

decreased corneal sensitivity

transient loss of accomodation

increased incidence of central serious chorioretinopathy and uveal melanomas, and pregnancy induced HTN

149
Q

how should you manage a woman who is diabetic and pregnancy from an ocular perspective

A

ophtho should see once a trimester

women with gestational diabetes are not at risk for retinopathy

150
Q

which patients with sickle cell are more likely to have ocular involvement

A

sickle hemoglobin SC and sickle cell thalassemia are more likely than those with SS disease

151
Q

what is the result of sickle cell on the eyes

A

intravascular sickling, hemolysis, hemostasis and thrombosis lead to occlusion followed by non-perfusion

retinal neovascularization can lead to vitreous haemorrhage and retinal detachment

patients with sickle cell should have baseline ophtho eval

152
Q

what thyroid disease is associated with ocular manifestations

A

graves–> thyroid related orbitopathy

153
Q

what is thyroid related orbitopathy

A

due to graves

due to autoantibody mediated enlargement of the extraocular muscles, orbital fat and lacrimal glands

the eyelid edema and conjunctiva vascular congestion that accompanies it do not require therapy

154
Q

what is a common presentation of thyroid related orbitopathy/graves

A

retraction of upper and lower eyelid with upper lid lag on down gaze

diplopia is common and may require surgery –> this requires ophtho care

155
Q

what is the most common cause of unilateral/bilateral protrusion of globes (exophthalmos)

A

thyroid related orbitopathy

results in corneal exposure and drying

156
Q

how is sarcoidosis characterized histologically

A

focal noncaseating granulomas

157
Q

in which patients is sarcoidosis most common

A

african american women between ages 20-40

158
Q

how do you dx sarcoidosis

A

biopsy from conjunctiva or lacrimal gland

159
Q

which disease are you testing for with a biopsy from the conjunctiva or lacrimal gland

A

sarcoidosis

160
Q

describe the ramifications of sarcoidosis from an ocular perspective

A

may be asymptomatic

can cause anterior or posterior UVEITIS
anterior is inflammation of the iris and ciliary body
posterior is inflammation of the choroid

suspected patients require complete ophtho evaluation

161
Q

what ocular manifestations can arise from autoimmune conditions like SLE, polyarteritis nodosa and Wegener granulomatosis

A

sclerokeratitis

uveitis

optic neuropathy

retinal vasculitis –> multiple cotton wool spots

162
Q

what ocular manifestations are associated with juvenile rheumatoid arthritis

A

asymptomatic iritis in 10% of cases

iritis more common in paciarticular form than the polyarticular form

requires visit to ophtho every 3 MONTHS since the iritis is asymptomatic

the iritis can lead to cataracts, glaucoma, corneal opacification

163
Q

what systemic conditions are associated with dry eye

A

many rheumatoid conditions–> causes keratitis sicca

most common are sjogrens, SLE, RA

treatment is artificial tears, lubricating ointment at night

164
Q

what ocular manifestations may indicate rheumatoid arthritis

A

severe dry eyes leading to risk of corneal melting, infection, possible perforation

for severe cases, ophtho can perform punctal occlusion to retain tears

165
Q

what effects can cancer treatment radiation have on the eyes

A

can lead to cataracts or delayed retinal vasculopathy (diabetic retinopathy type thing) and optic neuropathy

many chemo drugs also have ocular problems such as superficial keratitis

166
Q

what is a common finding on autopsy of kids with leukemia

A

there is infiltration in 75% of kids who die of leukemia resulting in ocular adnexal mets being found on autopsy

167
Q

what are the ocular manifestations of AIDS

A

cotton wool spots–> AIDS retinopathy

CMV retinitis

kaposi sarcoma of eyelids

less common–> shingles, herpes simplex keratitis, conjunctival microangiopathy, toxoplasma uveitis and retinitis, visual field defects or oculomotor dysfunction via CNS

168
Q

why do people with AIDS get cotton wool spots

A

due to focal occlusions of pre-capillary retinal arterioles that results in stasis

intra retinal hemorrhages may also be found

169
Q

what are the signs of CMV retinitis

A

characterized by SECTORAL hemorrhagic NECROSIS of the retina–> typically along a RETINAL VESSEL

170
Q

what should you do when you diagnose someone with HIV

A

refer to ophtho

patients who can sustain a higher CD4 count are less likely to develop CMV retinitis

171
Q

why is it important to treat syphilis early

A

late diagnosis can lead to permanent vision loss which is avoided with early treatment

172
Q

what are the ocular manifestations of syphilis

A

acute interstitial KERATITIS and keratouveitis occurs with congenital syphilis between 5-25 years

bilateral if congenital, unilateral if acquired

173
Q

what are the symptoms of ocular syphilis

A

intense pain

photophobia

opaque cornea

reduced vision

circular area of chorioretinal whitening may indicate CSF involvement (at RISK of neurosyphilis)

174
Q

what finding on ocular exam of the patient with syphilis would suggest risk of neurosyphilis

A

circular area of chorioretinal whitening may indicate CSF involvement

175
Q

how should you manage patients with syphilitic uveitis

A

get CSF tested for possible neurosyphilis

176
Q

how might secondary syphilis present

A

iritis

retinitis

choroiditis

or papillitis

177
Q

how might latent syphilis present

A

blurred vision

178
Q

how do you treat syphilis

A

systemic penicillin is curative

179
Q

what are the ocular manifestations of candida

A

fluffy, white-yellow superficial retinal infiltrate that may lead to vitreous haze and vitritis

rarely can cause inflammation of anterior chamber

180
Q

how do you treat ocular candidiasis

A

amphotericin B with or without intravitreal amphotericin or voriconazole

181
Q

what is herpes zoster ophthalmicus

A

varicella zoster infection involving CN V

182
Q

what is Hutchinson sign

A

lesion on the tip of the nose from extension of herpes zoster ophthalmicus

183
Q

why do we care about herpes zoster ophthalmicus

A

can lead to corneal infiltration

patients with anterior uveitis and keratitis (which is a serious vision threatening defect) require immediate ophtho referral

patients without skin lesions can still develop herpetic uveitis

can develop ACUTE RETINAL NECROSIS which is an OCULAR EMERGENCY requiring emergent systemic acyclovir

184
Q

how do you manage acute retinal necrosis from herpes zoster ophthalmicus

A

OCULAR EMERGENCY

requires emergent systemic acyvlovir

185
Q

what should you do if you have a patient with an autoimmune disorder or systemic infection that presents with a red eye, decreased vision, photophobia or floaters?

A

refer to ophtho

ophtho (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions