Ophthalmology

Question 1

Aqueous humor

Answer 1

produced by non pigmented epithelium on ciliary body

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

Question 2

Path of aqueous humor

Answer 2

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)

Question 3

Uveoscleral outflow

Answer 3

Drainage into uvea and sclera increase with prostaglandin agonists

Question 4

Hyperopia

Answer 4

Light focuses in front of retina (eye too short)

Question 5

Myopia

Answer 5

Light focuses behind retina (eye too long)

Question 6

Astigmatism

Answer 6

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

Question 7

Presbyopia

Answer 7

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

Question 8

Cataract- defn

Answer 8

Painless, often bilateral, opacification of the lens

Question 9

Cataract- RFs

Answer 9

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

Question 10

Glaucoma- defn

Answer 10

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

Question 11

Glaucoma- tx

Answer 11

pharmacologic or surgical IOP lowering

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

Question 12

Open-angle glaucoma- RFs

Answer 12

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)

Question 13

Closed-angle glaucoma (aka narrow-angle)

Answer 13

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

Question 14

Closed-angle glaucoma: chronic vs. acute

Answer 14

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

Question 15

Conjunctivities

Answer 15

Red eye; inflammation of conjunctiva

Causes can be allergic, bacterial, viral

Question 16

Uveitis

Answer 16

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)

Question 17

Age-related macular degeneration

Answer 17

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)

Question 18

Diabetic retinopathy

Answer 18

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

Question 19

Retinal vein occlusion

Answer 19

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

Causes retinal hemorrhage and venous engorgement

Question 20

Retinal detachment

Answer 20

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

Question 21

Central retinal artery occlusion

Answer 21

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)

Question 22

Retinitis pigmentosa

Answer 22

Inherited retinal degeneration

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

Bone spicule-shaped deposits around macula

Question 23

Retinitis

Answer 23

Retinal edema and necrosis leading to a scar

Often viral, but can also be bacterial or parasitic

Consider when patient is immunosuppressed

Question 24

Papilledema

Answer 24

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

Question 25

Pupillary control- constriction/ myosis

Answer 25

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

Question 26

Pupillary light reflex

Answer 26

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

Question 27

Pupillary control- dilation/ mydriasis

Answer 27

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

Question 28

Horner syndrome

Answer 28

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)

Question 29

Marcus Gunn pupil

Answer 29

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

Question 30

Internuclear ophthalmoplegia

Answer 30

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

Question 31

CN III damage

Answer 31

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

Question 32

CN IV damage

Answer 32

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

Question 33

CN VI damage

Answer 33

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

Question 34

Comparison between CN VI damage vs. MLF damage

Answer 34

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

Question 35

Visual field defects

Answer 35

for all of the following examples assume injury to RIGHT side remember N comes before T (optic nerve --> chasm --> tract)

Question 36

Right optic NERVE

Answer 36

Right anoxia (loss of entire right visual field)

Question 37

Right optic chiasm

Answer 37

Bitemporal hemianopia (loss of peripheral vision bilaterally)

Question 38

Right optic TRACT

Answer 38

Left homonymous hemianopia (on both eyes) Loss of left visual field (peripheral vision of left side and central/ medial vision of right side)

Question 39

Right Meyer loop- inferior retina (temporal lobe)

Answer 39

Left upper quadrantic anopia (on both eyes) Can be caused by right temporal lesion or MCA damage

Question 40

Right dorsal optic radiation- superior retina (parietal lobe)

Answer 40

Left lower quadrantic anopia (on both eyes) Can be caused by right parietal lobe lesion or MCA damage

Question 41

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

Answer 41

Left homonymous hemianopia WITH MACULAR SPARING (bilateral)

Question 42

Macular degeneration

Answer 42

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