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STEP 1 (3) > Neurology-Ophthamalogy > Flashcards

Neurology-Ophthamalogy Flashcards

1
Q

The blood vessels include the central retinal vein and artery

A
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2
Q

What are the main refractive errors (common causes of impaired vision, correctable with glasses)?

A

Hyperopia

Myopia

Astigmatism

Presbyopia

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3
Q

What is Hyperopia?

A

aka farsightedness.

When the eye is too short for the refractive power of the cornea and lens resulting in light being focused behind the retina

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4
Q

What is myopia?

A

aka nearsightedness.

When the eye is too long for the refractive power of the cornea and lens causing light to focus in front of the retina

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5
Q

What is astigmatism?

A

abnormal curvature of the cornea causing different refractive power at different axes

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6
Q

What is presbyopia?

A

Age-related impaired accommodation (focusing on near objects), possibly due to decreased lens elasticity. Often necessitates ‘reading glasses’

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7
Q

What is this?

A

A cataract, a painless, often bilateral, opacification of the lens causing impaired vision

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8
Q

What are the risk factors for cataracts?

A

age, smoking, alcohol, sunlight, prolonged corticosteroid use

classic galactosemia

galactokinase deficiency

diabetes mellitus (sorbitol)

trauma, infection

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9
Q

What is glaucoma?

A

optic disc atrophy with characteristic cupping (thinning of the outer rim of the optic nerve head) (below)

usually with elevated intraocular pressure (IOP) and progressive peripheral visual field loss

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10
Q

What is open angle glaucoma?

A

associated with increased age, AA race, fam hx. Painless, and more common in the U.S.

Primary- cause unclear

Secondary- blocked trabecular meshwork from WBCs (e.g uveitis), RBCs (e.g. vitreous hemorrhage), and retinal elements (e.g. retinal detachment)

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11
Q

What is primary closed/narrow angle glaucoma caused by?

A

Primary- enlargement or forward movement of the lens against the central iris (pupil margin) causing obstruction of normal aqueous flow through the pupil resulting in fluid buildup behind the iris, pushing the peripheral iris against the cornea and impeding flow through the tabecular meshwork

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12
Q

What is secondary closed/narrow angle glaucoma caused by?

A

hypoxia from retinal disease (e.g. DM, vein occlusion) induces vasoproliferation in iris that causes angle contraction

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13
Q

What is the difference between chronic closure of the glaucoma angle and acute closure?

A

chronic closure is often asymptomatic with damage to the optic nerve and peripheral vision, while acute closure is a true ophthalmic emergency caused by increased IOP pushing the iris forward (very painful, red eye, sudden vision loss, halos around light, frontal headache)

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14
Q

What is uveitis?

A

inflammation of the uvea (e.g. iritis aka anterior uveitis, choroiditis aka posterior uveitis). May have hypopyon (accumulation of pus in the anterior chamber) (below) or conjunctival redness

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15
Q

What are the associations of uveitis?

A

systemic inflammatory disorders (e.g. sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27 diseases)

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16
Q

What is most likely happening here?

A

age-related macular (central area of the retina) degeneration that causes distortion (metamorphopsia) and eventual loss of central vision (scotoma)

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17
Q

What are the types of macular degeneration?

A

dry and wet

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18
Q

Describe dry (nonexudative, 80+%) MD?

A

marked by deposition of yellowish extracellular material in and beneath the Bruch membrane and retinal pigment epithelium (‘drusen’) with gradual loss of vision

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19
Q

How can dry (nonexudative, 80+%) MD be prevented?

A

multivitamins and antioxidants

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20
Q

Describe wet (exudative, 10-15%) MD

A

rapid loss of vision due to bleeding secondary to choroidal neovascularization

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21
Q

Normal fundoscopy

A
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22
Q

How should wet MD be tx?

A

anti-VEGF injections (e.g. ranibizumab) or laser therapy

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23
Q

What are the types of diabetic retinopathy?

A

nonproliferative and proliferative

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24
Q

Describe nonproliferative DR

A

damaged capillaries leak blood causing lipids and fluid to seep into the retina resulting in hemorrhages and macular edema

tx: BG control and macular laser therapy

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25
Q

Describe proliferative DR

A

chronic hypoxia results in new blood vessel formation with resultant traction on retina

tx: peripheral retinal photocoagulation and anti-VEGF (e.g. bevacizumab)

26
Q

What is this likely showing?

A

retinal vein occlusion (commonly due to compression from nearby arterial atherosclerosis) resulting in retinal hemorrhage and venous engorgement and edema in the affected areas

27
Q

What is this?

A

Retinal detachment

28
Q

What is retinal detachment?

A

seperation of neurosensory layer of the retina (photoreceptor layer with rods and cones) from the outermost pigmented epithelium (normally shields excess light, supports the retina) causing degeneration of photoreceptors and vision loss

29
Q

Retinal detachment may be 2ndary to what?

A

retinal breaks, diabetic traction, and inflammatory effusions

30
Q

Retinal detachment is more common in what pts?

A

those with high myopia

31
Q

Retinal detachment is often preceded by what?

A

posterior vitreous detachment (flashes and floaters) and evntual monocular loss of vision like a ‘curtain drawn down”- surgical emergency

32
Q

What is this?

A

central retinal artery occlusion resulting in acute, painless monocular vision loss and a clasic “cherry-red” spot at the fovea (front)

33
Q

What is retinitis pigmentosa?

A

an inherited retinal degeneration that causes painless, progressive vision loss beginning with blind nightness

Front: Bone spicule-shaped deposits around the macula

34
Q

What part of the eye is affected first in retinitis pigmentosa?

A

the rods

35
Q

What is this?

A

Retinitis-retinal edema and necrosis leading to scar formation

36
Q

What are the major causes of retinitis?

A

often viral (CMV, HSV, and HZV)

associated with immunosuppression

37
Q

What is this?

A

Papilledema- optic disc swelling (usually bilateral) due to increased ICP (e.g. 2ndary to mass effect

Enlarged blind spot and elevated optic disc with blurred margins

38
Q

What controls pupil constriction (miosis)?

A

parasympathetics

1st neuron: Edinger-Westphal nucleus to ciliary ganglionvia CN III

2nd neuron: short ciliary nerves to the pupillary sphincter muscles

39
Q

How does the pupillary light reflex work?

A

light in either retina sends a signal via CN II to pretectal nuclei in the midbrain that activates bilateral Edinger-Westphal nuclei causing the pupils to contract bilaterally

40
Q

What mediates pupil dilation?

A

sympathetics

1st neuron: hypothalamus to ciliospinal center of Bidge (C8-T2)

2nd neuron: exit at T1 to superior cervical ganglion (travels along the cervical sympathetic chain near the lung apex, subclavian vessels)

3rd neuron: plexus along the internal carotid, through cavernous sinus; enters obit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of the eyelids (minor retractors) and sweat glands of the forehead and face

41
Q

What is a Marcus Gunn pupil?

A

an afferent pupillary defect due to optic nerve damage or severe retinal injury resulting in decreased bilateral pupillary constriction when light is shone in the affected eye relative to the unaffected eye

tested with ‘swinging flashlight’ test

42
Q

What is Horner syndrome?

A

sympathetic denervation of the face resulting in:

  • ptosis (superior tarsal muscle)
  • anhidrosis (absence of sweating) and flushing on affected side of face
  • miosis
43
Q

What causes Horner syndrome?

A

associated with spinal cord lesions above T1 (e.g. Pancoast tumor, Brown-Sequard syndrome, late-stage syringomyelia)

44
Q

Ocular muscles

Innervation: LR6SO4R3

A
45
Q

How would a CN III nerve lesion present?

A

CN III has both motor (central) and parasympathetic (peripheral) components

Motor output to ocular muscles affected primarily by vascular disease (e.g. DM due to sorbitol) due to decreased diffusion of oxygen and nutrients to the interior fibers (presents as a ‘down and out’ eye) (below)

Parasympathetic output-fibers on the periphery are 1st affected by cimporession (e.g. PCom aneurysm, uncal herniation) Signs: diminished or absent pupillary reflex

46
Q

How would a CN IV lesion present?

A

eyes move upward particularly with a contralateral gaze and head tilt toward the side of the lesion (problems going down stairs, may present with compensatory head tilt in the opposite direction)

47
Q

How would a CN VI lesion present?

A

medially directed eye that cannot abduct

48
Q
A
49
Q

How would lesion of the right optic nerve present?

A

Right anopia- complete blindness in the right eye with normal left eye

50
Q

How would lesion of the optic chiasm (e.g. pituitary enlargement) present?

A

bitemporal/bipolar hemianopia- lateral fields impaired in both eyes

51
Q

How would lesion to the right optic tract present?

A

left homonymous hemianopia- loss of the left hemispheres of vision in BOTH eyes

52
Q

What could cause left upper quadrantic anopia?

A

lesion of the right Meyer loop (temporal lobe)

right temporal lesion, MCA

53
Q

What could cause left lower quadrantic anopia?

A

lesion of the right dorsal optic radiation from the lateral geniculate body

right parietal lesion, MCA

54
Q

What could cause a left hemianopia with macular sparing?

A

lesion of all projections from the lateral geniculate body if a PCA infarct

55
Q

What could cause this (central scotoma)?

A

macular degeneration

56
Q

Paths from the lateral geniculate body:

Meyer loop- inferior retina; loops around the inferior horn of the lateral ventricle

Dorsal optic radiation- superior retina; takes the shortest path via the internal capsule

A

NOTE: When an image hits the primary visual cortex in the occipital lobe, it is upside down and left-right reversed

57
Q

What is Internuclear ophthalmoplegia (INO)?

A

A disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus.

Additionally, the divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will “see double” when looking to the left, seeing two images side-by-side. Convergence is generally preserved

58
Q

What is the medial longitudinal faciculus (MLF)?

A

a pair of tracts that allow for crosstalk between CN VI and CN III nuclei. Coordinates both eyes to move in the same horizontal direction.

HIGHLY myelinated (so the eyes move together)

Lesions may be unilateral or bilateral

59
Q

Bilateral lesions to the medial longitudinal faciculus (MLF) is classic in what disease?

A

MS

60
Q

Lesion to the MLF causes internuclear ophthalmoplegia (INO), a conjugate horizontal gaze palsy caused by a lack of communication such that when CN VI nucleus activates the ipsilateral lateral rectus, the contralateral CN III nucleus does not stimulate the medial rectus to fire .

A

The abducting eye gets nystagmus due to the CN VI overfiring to try to stimulate CN III

Convergence is normal

NOTE: “right” INO would indicate that the right CN III is paralyzed (ie. which side cant adduct)

STEP 1 (3) (16 decks)

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