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Neurology > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Aqueous humor

A

produced by non pigmented epithelium on ciliary body

decreased production by beta blockers and carbonic anhydrase inhibitors, increased outflow by alpha-2 agonists

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2
Q

Path of aqueous humor

A

Produced by ciliary body –> travels around gap between iris and lens –> gets drained via trabecular meshwork, canal of Schlemm and episcleral vasculature (drainage increased with M1 agonist)

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3
Q

Uveoscleral outflow

A

Drainage into uvea and sclera increase with prostaglandin agonists

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4
Q

Hyperopia

A

Light focuses in front of retina (eye too short)

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5
Q

Myopia

A

Light focuses behind retina (eye too long)

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6
Q

Astigmatism

A

Abnormal curvature of cornea –> different refractive power at different axes

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7
Q

Presbyopia

A

Age-related changes in accommodation (difficulty focusing on near object (image focuses behind retina)

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8
Q

Cataract- defn

A

Painless, often bilateral, opacification of the lens

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9
Q

Cataract- RFs

A

increased age, smoking, excessive alcohol use, excessive sunlight, prolonged corticosteroid use, diabetes mellitus, trauma, infection

congenital risk factors: NF type II (juvenille cataracts), Marfan (subluxation of lens), homocystineuria, galactosemia, galactokinase deficiency (mild condn other than cataract formation), trisomies, ToRCHES (e.g. rubella), Alport (type IV collagen defect), myotonic dystrophy

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10
Q

Glaucoma- defn

A

Optic disc atrophy with cupping (thinning of outer rim of optic nerve head)

Usually associated with elevated intraocular pressure (IOP)

Progressive visual field loss if untreated

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11
Q

Glaucoma- tx

A

pharmacologic or surgical IOP lowering

Carbonic anhydrase inhibitors, a2 agonists, beta blockers, prostaglandins, M1 agonists

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12
Q

Open-angle glaucoma- RFs

A

Associated with increased age, AA race, FH

Primary- cause unclear
Secondary- Obstruction: WBCs block trabecular meshwork (e.g. uveitis), RBCs (vitreous hemorrhage), retinal elements (retinal detachment)

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13
Q

Closed-angle glaucoma (aka narrow-angle)

A

Primary: enlargement or forward movement of the lens against iris –> obstruction of normal aqueous flow –> fluid builds up behind the iris –> pushes iris against cornea –> impedes flow of aqueous humor outside through trabecular meshwork

Secondary: hypoxia from retinal disease (e.g. diabetes, venous occlusion) –> induces vasoproliferation in iris that contracts the angle

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14
Q

Closed-angle glaucoma: chronic vs. acute

A

Chronic: often asymptomatic with damage to optic nerve and peripheral vision

Acute: Ophthalmic EMERGENCY, increased IOP pushes iris forward and angle closes abruptly
S&S: very painful, red eye, halos around lights, rock hard eye, frontal headache
DO NOT GIVE EPINEPHRINE- mydriatic effect that will make this worse

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15
Q

Conjunctivities

A

Red eye; inflammation of conjunctiva

Causes can be allergic, bacterial, viral

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16
Q

Uveitis

A

Inflammation of urea (comprised of the iris (iritis), choroid (choroiditis) and ciliary body (pars planitis))

May have hypopyon (accumulation of pus in the anterior chamber)

Associated with systemic inflammatory disorders (sarcoidosis, RA, juvenille idiopathic arthritis, HLA-B27-associated conditions)

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17
Q

Age-related macular degeneration

A

Degeneration of macula (central area of retina)

Causes distortion and eventual loss of central vision

Dry/ nonexudative- yellow material deposited; prevent progression with multivitamin and antioxidants

Wet/ exudative- rapid loss of vision due to bleeding secondary to choroid revascularization; tx with anti-VEGF injections (ranibizumab)

18
Q

Diabetic retinopathy

A

Retinal damage due to chronic HYPERglycemia

Non proliferative: HEMORRHAGE; damaged capillaries leak blood which seeps into renal and causes hemorrhages and macular edema; tx with blood sugar control

Proliferative: HYPOXIA; chronic hypoxia results in new blood vessel formation with resultant traction on retina; tx: peripheral retinal photocoagulation, surgery, ant-VEGF

19
Q

Retinal vein occlusion

A

Blocked central or branch of retinal vein (from nearby arterial atherosclerosis)

Causes retinal hemorrhage and venous engorgement

20
Q

Retinal detachment

A

Separation of photoreceptor layer with rod and cones (neurosensory layer) from the pigmented epithelium (which normally shield excess light)

Causes degeneration of photoreceptors and subsequent vision loss

Visualized as crinkling of retinal tissue and changes in vessel direction

Surgical emergency

21
Q

Central retinal artery occlusion

A

Acute, painless monocular vision loss

Retine cloudy with “cherry-red” spot at fovea (center of macula)

Evaluate for embolism (pathway: internal carotid –> ophthalmic –> retinal artery)

22
Q

Retinitis pigmentosa

A

Inherited retinal degeneration

Painless, progressive vision loss- beginning with night blindness (rods affected first)

Bone spicule-shaped deposits around macula

23
Q

Retinitis

A

Retinal edema and necrosis leading to a scar

Often viral, but can also be bacterial or parasitic

Consider when patient is immunosuppressed

24
Q

Papilledema

A

Optic disc swelling (usually bilateral) due to increased ICP (e.g. secondary to mass effect)

Enlarged blind spot and elevated optic disk with blurred margins

25
Q

Pupillary control- constriction/ myosis

A

Constriction: parasympathetic (e.g. CN III)- pupillary sphincter muscles

26
Q

Pupillary light reflex

A

Light sends signal via CN II –> activates bilateral Edinger-Westphal nuclei –> causes bilateral contraction (consensual)

27
Q

Pupillary control- dilation/ mydriasis

A

Dilation: sympathetic- pupillary dilator muscles (travels via/ near the internal carotid artery);

Note: the sympathetic fibers (of the superior cervical ganglion) that innervate smooth muscle of the eyelids and sweat glands of the forehead and face also innervated the pupillary dilator muscles

28
Q

Horner syndrome

A

Sympathetic denervation of the face causing:
Ptosis (baby- vs. CN III causes big mama ptosis)
Anhidrosis (absence of sweating)
Miosis (pupillary constriction)

Caused by lesions above T1 (e.g. Pancoast, Brown-Sequard, late-stage syringomyelia)

29
Q

Marcus Gunn pupil

A

Afferent pupillary defect- due to optic nerve damage or severe retinal injury

Decreased bilateral pupillary constriction (light shone in affected eye will not cause or only cause mild constriction of both eyes; as opposed to light shown in the unaffected eye- which will cause both eyes to constrict)

Breaking down the term, this makes sense because AFFERENT pupillary defect implies that the affected eye is not able to sense and relay the AFFERENT light signal

30
Q

Internuclear ophthalmoplegia

A

MLF lesion: IPSILATERAL medial rectus is damaged/ paralyzed

MLF- normally allows crosstalk between CN VI and III (when left lateral rectus (VI) moves laterally, MLF goes to the contralateral medial rectus (III) and tells the right eye to move medially)

If damaged, the left eye will still move laterally, but the right eye will remain facing straight (so the lesion is IPSILATERAL to the MLF that is damaged- because the MLF is termed after it crosses to the contralateral side)

To restate this in a different way: RIGHT vs. LEFT INO refers to the side of the eye that is paralyzed (during lateral movement of the contralateral eye); so a right INO indicates that the right middle rectus muscle is not activated (remains paralyzed) when the left lateral rectus moves laterally

Convergence is unaffected

31
Q

CN III damage

A

Characteristic “down, out, and dilated gaze” on affected eye/ nerve

Has motor and parasympathetic components

Motor: MR, IR, SR + IO; so deficit would allow only the SO (IV- down and slightly in) and LR (VI- out) to work –> so gaze will be down and (mostly) out;

Parasympathetic: normal senses light and constricts; so deficit would prevent eye from constricting

32
Q

CN IV damage

A

Affected eye looks up (head tilt TOWARD the side of the lesion)

SO is damaged, so affected cannot move down and in- so even when the unaffected eye looks laterally and down, the affected eye will not be able to look down- it can look medially because the medial rectus is undamaged

33
Q

CN VI damage

A

Eye that cannot move laterally

When unaffected eye moves medial, affected eye remains looking ahead (cannot move laterally)

NOT to be confused with the MLF damage when affected eye (and ipsilateral MLF) do not move medially, while the unaffected eye moves laterally

34
Q

Comparison between CN VI damage vs. MLF damage

A

CN VI damage: medial motion seen, lateral motion not seen (in affected eye); convergence is normal

INO/ MLF damage: lateral motion seen, medial motion not seen (in affected eye); convergence is normal

35
Q

Visual field defects

A

for all of the following examples assume injury to RIGHT side

remember N comes before T (optic nerve –> chasm –> tract)

36
Q

Right optic NERVE

A

Right anoxia (loss of entire right visual field)

37
Q

Right optic chiasm

A

Bitemporal hemianopia (loss of peripheral vision bilaterally)

38
Q

Right optic TRACT

A

Left homonymous hemianopia (on both eyes)

Loss of left visual field (peripheral vision of left side and central/ medial vision of right side)

39
Q

Right Meyer loop- inferior retina (temporal lobe)

A

Left upper quadrantic anopia (on both eyes)

Can be caused by right temporal lesion or MCA damage

40
Q

Right dorsal optic radiation- superior retina (parietal lobe)

A

Left lower quadrantic anopia (on both eyes)

Can be caused by right parietal lobe lesion or MCA damage

41
Q

PCA infarct (causing damage to right occipital lobe/ visual cortex)

A

Left homonymous hemianopia WITH MACULAR SPARING (bilateral)

42
Q

Macular degeneration

A

Loss of central vision; macula affected, but circumference not affected

Neurology (5 decks)

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