Ophthalmology

Question 1

Eyelids

Answer 1

• Protects the cornea
• Tarsal plates ⇒ dense CT plates
• Movement controlled by orbicularis oculi muscle (CN VII)

Question 2

Tear Film

Answer 2

• Tear film consists of aqueous, mucin, and lipid components
• Meibomian glands and glands of Zeis produce lipid for tear film
  
  • Blockage and inflammation of glands can cause a “stye”
• Lacrimal gland produces aqueous component
• Lacrimal drainage system drains into nasal cavity
  
  • Canaliculi ⇒ nasolacrimal sac ⇒ nasolacrimal duct ⇒ nasal cavity

Question 3

Extraocular Muscles

Answer 3

• Four rectus muscles ⇒ superior, inferior, medial, lateral
• Two oblique muscles ⇒ superior and inferior
• All controlled by oculomotor nerve (CN III) except for:
  
  • Superior oblique ⇒ trochlear nerve/CN IV
  • Lateral rectus ⇒ abducens nerve/CN VI

Question 4

Conjunctiva

Answer 4

Clear tissue overlying the sclera and lining the inner surfaces of the eyelids

Question 5

Cornea

Answer 5

Clear collagenous structure

Provides ⅔ of the eye’s refractive power

• Composed of 3 cell layers:
  
  • Surface epithelium with underlying Bowman layer
  • Stroma ⇒ keratocytes and collagen fibrils
    
    • Middle and largest layer
  • Endothelium ⇒ single cell layer on inner surface of cornea
    
    • Makes Descemet’s membrane (true basement membrane)
• Must remain optically clear:
  
  • Endothelial Na⁺/K⁺ pump and carbonic anhydrase ⇒ maintain dehydration of cornea
  • Corneal edema reduces optical clarity
• Eyelid and lacrimal system protect and lubricate the cornea

Question 6

Layers of the Globe

Answer 6

Sclera, Uvea, Retina

Question 7

Sclera

Answer 7

• Outer white collagenous layer
• Covers posterior 4/5 of globe
• Anterior opening for cornea
• Posterior opening for optic nerve

Question 8

Uvea

Answer 8

• Middle vascular layer
• Provides blood flow to ocular structures
• Anterior eye ⇒ Iris and ciliary body
• Posterior eye ⇒ Choroid

Question 9

Retina

Answer 9

Neurosensory layer

• Where light perceived and translated to neuronal signals
• Composed of neural, glial, and vascular elements
• Light ⇒ photochemical rxn in rods and cones
• Visual cascade from photoreceptor cells to ganglion cells
• Axons of ganglion cells form retinal nerve fiber layer ⇒ becomes the optic nerve
• Macula ⇒ central area of the retina encircled by vascular arcades
• Fovea ⇒ area of macula with primarily cone photoreceptors
  
  • Higest visual acuity and fine discrimination

Question 10

Anterior Chamber

Answer 10

• Contains aqueous humor produced by ciliary body
• Trabecular meshwork
  
  • In anterior chamber “angle”
  • Drains aqueous fluid
    
    • Blockage or reduced function ⇒ ↑ intraocular pressure and glaucoma
  • Visualized with gonioscopy

Question 11

Crystalline Lens

Answer 11

• Optically clear structure
• Provides ~ 1/3 of refractive power of the eye
• Suspended behind iris by zonular fibers

Question 12

Posterior Segment

Answer 12

Structures posterior to lens

Includes vitreous body, retina, choroid, optic nerve

• Vitreous humor ⇒ gel=like substance that fills that back of the globe
• Optic nerve ⇒ carries neurosensory signals from retina to brain
  
  • Exits back of the eye at the optic disc
    
    • Causes physiologic blind spot

Question 13

Refractive Error

Answer 13

Caused by light being focused in front of or behind the retina

Refractive power of eye comes from tear film, cornea, and lens

Question 14

Myopia

Answer 14

When light is focused in front of the retina

Corrected by “minus” or divergent/concave lens

Question 15

Hyperopia

Answer 15

When light is focused behind the retina

Corrected by “plus” or convergent/convex lens

Question 16

Astigmatism

Answer 16

When eye is ovoid

Light focuses in two planes instead of one point

Question 17

Chronic Conditions

Answer 17

• Cataracts
• Diabetic retinopathy
• Primary open angle glaucoma
• Age-related macular degeneration

Question 18

Cataract

Answer 18

Clouding of crystalline lens

• Caused by age, medications (corticosteroids), diabetes, trauma, congenital
• Results in reduced best-corrected visual acuity and/or glare
• Treatment is cataract extraction with intraocular lens implantation

Question 19

Diabetic Retinopathy

Answer 19

Caused by microvascular damage due to elevated blood glucose

• Non-proliferative/Background DR:
  
  • Dot-blot hemorrhages
  • Microaneurysms
  • Hard exudates
  • Cotton wool spots
  • May have macular edema
• Proliferative DR:
  
  • Retinal neovascularization
    
    • Caused by prolonged ischemia and VEGF release
    • Abnormal vessels can bleed ⇒ retinal or vitreous hemorrhage & retinal detachment
• Treatment:
  
  • Blood glucose control
  • Laser (panretinal photocoagulation)
  • Iintravitreal injections of anti-VEGF medications
  • Surgery

Question 20

Primary Open Angle Glaucoma

Answer 20

Progressive damage of retinal nerve fiber layer

• Usually associated with ↑ intraocular pressure
• ↑ “cup-to-disc ratio” on optic nerve exam
• Results in loss of peripheral vision & eventually blindness
• ↑ risk in African American population & those with a family history
• Treated with laser, surgery, or medications to lower intraocular pressure
  
  • β-blockers ⇒ ↓ production of aqueous humor @ ciliary body
  • α₂-selective agonists ⇒ ↓ production of aqueous humor & ↑ outflow via uveosclera pathway
  • Carbonic anhydrase inhibitors ⇒ ↓ production of aqueous humor @ ciliary body
  • Prostaglandin analogues ⇒ ↑ outflow via uveosclera pathway
  • Cholineric agents ⇒ induce miosis & ↑ outflow via trabecular meshwork

Question 21

Age-related Macular Degeneration

(AMD)

Answer 21

Degeneration of outer retinal layers in macula

• Dry AMD:
  
  • Deposition of degenerative material in yellow spots called “drusen” in Bruch’s membrane
  • Atrophy of retinal pigment epithelium and photoreceptor cells dt abnormal choriocapillaris layer
  • Results in ↓ visual acuity, color vision, contrast sensitivity
  • No treatment, more preventative
    
    • AREDS vitamins may reduce risk of progression
  • Monitor with Amsler grid for progression to wet AMD
• Wet AMD:
  
  • Choroidal neovascularization that breaks through Bruch’s membrane
  • Causes edema, hemorrhage and scarring of retina and subretinal space
  • Treated with intravitreal injections of anti-VEGF medications

Question 22

Acute Conditions

Answer 22

• Traumatic/Toxic:
  
  • Corneal abrasion and Infectious keratitis
  • Subconjunctival hemorrhage
  • Hyphema
  • Chemical injury
  • Eyelid laceration
  • Open globe injury
• Other acute conditions:
  
  • Conjunctivitis
  • Central retinal artery occlusion
  • Central rretinal vein occlusion
  • Acute angle closure glaucoma
  • Retinal detachment

Question 23

Corneal Abrasion

Answer 23

Defect in epithelial layer of cornea

• Sx include acute-onset pain, photophobia, tearing and redness
• Dx by fluorescein stain with cobalt blue light
• Cornea re-epithelializes within days
• Tx is supportive
• Abx prophylaxis if large abrasion or dirty mechanism of injury

Question 24

Infectious Keratitis

Answer 24

“Corneal ulcer”

Microbial infection of corneal stroma with overlying epithelial defect

• Sx include pain, photophobia, red eye
• Often occurs post-trauma
• High risk in contact lens wearers with poor hygiene practices
• Risk of corneal thinning and perforation
• Requires culture, aggressive abx therapy, and monitoring by ophthalmologist

Question 25

Subconjunctival Hemorrhage

Answer 25

Hemorrhage accumulating between sclera and conjunctiva

• May be due to Valsalva maneuver, coagulopathy, systemic conditions like DM or HTN, trauma, or idiopathic
• Requires eye exam to r/o other etiology
• Supportive tx only for simple subconjunctival hemorrhage

Question 26

Hyphema

Answer 26

Hemorrhage in anterior chamber of eye

• May be due to trauma, coagulopathy, neovascularization of the iris or angle, and anterior segment tumors
• Requires evaluation and treatment with ophthalmologist
• Patients with sickle cell disease have higher risk of secondary glaucoma and re-bleed

Question 27

Chemical Injury

Answer 27

• Ophthalmic emergency ⇒ requires immediate irrigation of chemical from the eye
• Acid injuries
  
  • Causes coagulation necrosis
  • Less risk of corneal perforation
• Alkali injuries
  
  • Causes saponification necrosis
  • Can rapidly lead to corneal perforation
• Both can result in anterior segment ischemia, corneal scarring/opacification, glaucoma, and other blinding conditions

Question 28

Eyelid Laceration

Answer 28

Simple lacs can be repaired at the bedside

Complex cases involving canaliculus or orbital septum require OR repair

Question 29

Open Globe Injury

Answer 29

• May be subtle
• Peaked pupil, iris, or uveal prolapse from laceration
• Ophthalmic emergency requiring repair in operating room
• High risk of infectious endophthalmitis
  
  • Treat with IV abx
• Rule out intraocular or orbital foreign body
  
  • History (mechanism of injury) is crucial
  • Imaging can be helpful (CT scan or X-ray, not MRI if suspect metallic FB)

Question 30

Conjunctivitis

Overview

Answer 30

Inflammation of the conjunctiva resulting in redness, tearing and/or mucous discharge, and mild discomfort.

Bacterial, viral, and allergic causes.

Question 31

Bacterial

Conjunctivitis

Answer 31

• Usually more purulent and unilateral
• May have hx consistent with source of inoculation
• Tx with topical abx

Question 32

Viral

Conjunctivitis

Answer 32

• May have hx of viral prodrome
• More often bilateral
• Usually more watery and occasionally itchy
• No abx indicated

Question 33

Allergic

Conjunctivitis

Answer 33

• Prominent itching and watering
• Tx is avoidance of allergen, topical antihistamines and anti-allergy medications

Question 34

Gonococcal

Conjunctivitis

Answer 34

Special case of bacterial conjunctivitis:

• Hyperacute, severe purulent discharge
• Risk of corneal involvement with perforation within 24 hours
• Requires ophthalmic consult, systemic treatment with ceftriaxone and concurrent treatment for chlamydia (azithromycin)

Question 35

Central Retinal Artery Occlusion

(CRAO)

Answer 35

Acute blockage of central retinal artery ⇒ acute ischemia of retina ⇒ “stroke of the eye”

• Often d/t an embolus
• Causes diffuse retinal pallor except at fovea ⇒ “cherry red spot” on fundus exam
• Usually results in severe vision loss
• No treatment ⇒ poor prognosis
• Systemic workup for etiology of embolus (ECHO, carotid studies, hypercoagulable work-up)

Question 36

Central Retinal Vein Occlusion

(CRVO)

Answer 36

• Often caused by compression of central retinal vein at optic nerve d/t HTN or anatomy
• Fundoscopic findings:
  
  • “Blood and thunder” fundus
  • Dilated and tortuous vessels
  • ± Macular edema
• Clincal manifestations:
  
  • Acute vision loss, usu. worse if severe macular edema or severe retinal ischemia
  • Severe ischemia ⇒ ± neovascularization of retina/iris ⇒ neovascular glaucoma
• Treatment:
  
  • No acute treatment
  • Chronic treatment with laser and/or anti-VEGF injections to treat neovascularization

Question 37

Acute Angle Closure Glaucoma

Answer 37

Acute rise in intraocular pressure caused by occlusion of outflow pathways for aqueous humor in the anterior chamber

• Very elevated intraocular pressure (40-60)
  
  • Can result in optic neuropathy and blindness in hours if untreated
• Clinical manifestations:
  
  • Acute-onset severe eye pain and redness
  • Blurred vision with rainbows or haloes around lights
  • Headache
  • ± Nausea/vomiting
• Exam findings:
  
  • Fixed mid-dilated pupil
  • Conjunctival injection
  • Corneal edema/haze
  • Closed angle on gonioscopy
• Requires urgent lowering of IOP with medications and ultimately usually requires laser iridotomy

Question 38

Retinal Detachment

Answer 38

Separation of retinal layer from underlying choroidal layer

• Most common type is rhegmatogenous retinal detachment
  
  • Caused by tear or hole in retina that allows fluid to separate retina from choroid
• Signs/symptoms include floaters, flashing lights, curtain/veil over vision
• Dx with B-scan US and dilated fundus exam
• Visual acuity depends on whether macula is attached or detached:
  
  • Macula-on RD (good vision) ⇒ requires emergent surgical repair
  • Macula-off RD ⇒ requires urgent but not emergent repair
• Retinal tear/hole may require barrier laser to prevent RD

Question 39

Hypertensive Retinopathy

Answer 39

Retinal vascular changes due to elevated blood pressure

Thickening of arteriolar walls ⇒ copper wiring and silver wiring

Grading system:

• Grade I: Arteriolar attenuation
• Grade II: A-V nicking
• Grade III: Flame-shaped retinal hemorrhages, cotton wool spots, retinal exudates
• Grade IV: Above + optic disc edema

Question 40

Uveitis

Answer 40

Inflammation of the uveal tissue

May be due to systemic inflammatory/autoimmune conditions or infections.

• Anterior uveitis: iritis or iridocyclitis
  
  • Sx include pain, red eye, photophobia, ± blurred vision
  • May see synechiae of iris to lens or keratic precipitates (white spots on back of cornea)
  • Requires slit lamp dx by visualization of WBCs in anterior chamber aqueous humor
• Posterior uveitis: choroid/vitreous involvement
  
  • Less specific symptoms
  • May have floaters and blurred vision
• Multiple etiologies including:
  
  • Systemic inflammatory diseases
    
    • SLE, sarcoidosis, rheumatoid arthritis, inflammatory bowel disease, Behcet disease
  • Infections
    
    • Syphilis, Lyme disease, CMV, herpetic infections, tuberculosis
• Treated with topical steroids ± systemic treatment for underlying etiology

Question 41

Papilledema

Answer 41

Optic disc edema secondary to ↑ intracranial pressure

• Etiologies: tumors, hydrocephalus, pseudotumor cerebri, ICH, AV malformations, brain abscess, encephalitis, cerebral venous sinus thrombosis
• May have headache, transient vision obscurations (position-dependent)
  
  • Esp. when returing to upright position from laying flat
• Fundoscopic findings:
  
  • Optic nerve head is elevated and hyperemic
  • Disc margins blurred
  • May see hemorrhages on or around the disc
• Treat underlying etiology

Question 42

Optic Neuritis

Answer 42

Acute optic nerve inflammation often associated with multiple sclerosis

• Unilateral reduced vision, reduced color vision, pain with extraocular movements
• Optic nerve appearance normal in 2/3 of cases
• Pulse-dose IV steroids over three days with PO taper
• MRI recommended especially if no prior diagnosis of MS
  
  • Can help assess risk of progression to MS over time
• Vision usually recovers over 4-6 weeks

Question 43

Arteritic Ischemic Optic Neuropathy (AION)

or

Giant Cell Arteritis (GCA)

Answer 43

Giant cell or temporal arteritis ⇒ ± inflammation in ophthalmic artery and ischemia of optic nerve ⇒ sudden vision loss

• Presentation:
  
  • Usually patients over 55,
  • Severely reduced visual acuity
  • Jaw claudication, tenderness of scalp over temporal artery
  • May have symptoms of polymyalgia rheumatica
• Check ESR, CRP, platelets ⇒ will all be elevated in GCA/AION
• Tx w/ Pulse dose IV steroids with PO taper
  
  • Critical to prevent involvement of contralateral eye
• Temporal artery biopsy for diagnosis (granulomatous inflammation) – do not delay treatment for biopsy!

Question 44

HIV-Related Conditions

Answer 44

• HIV Retinopathy:
  
  • Retinal hemorrhage, microaneurysms, cotton wool spots (microangiopathy)
• CMV retinitis:
  
  • “Pizza pie fundus”
  • Treated with IV ganciclovir or foscarnet
    
    • May do intravitreal ganciclovir
  • Risk higher when CD₄ count is ≤ 50
• Progressive Outer Retinal Necrosis (PORN):
  
  • Herpes virus-related retinal inflammation and necrosis
  • Requires IV antiviral (acyclovir) treatment
  • High risk of retinal detachment
• Other infectious retinochoroiditis:
  
  • Toxoplasma gondii, pneumocystis jirovecii, Cryptococcus neoformans, syphilis
• Tumors:
  
  • Kaposi sarcoma of conjunctiva or eyelid
  • Intraocular or periocular lymphoma
  • Conjunctival squamous cell carcinoma

Question 45

Acute Conjunctival Injection

Differentials

Answer 45

• Pupils as a clue:
  
  • PERRL ⇒ conjunctivitis, corneal abrasion or keratitis, subconjunctival hemorrhage
  • Small pupil that does not react normally ⇒ suspect acute ritis or anterior uveitis
  • Large pupil that does not react normally ⇒ suspect acute angle closure glaucoma
• Symptoms as a clue:
  
  • Pain and/or photophobia ⇒ corneal abrasion or keratitis, acute iritis/uveitis, acute angle closure galucoma
  • Painless ⇒ most types of conjunctivitis, subconjunctival hemorrhage

Question 46

Uveal Melanoma

Answer 46

• Most common primary intraocular tumor in adults
• May occur at iris, ciliary body, choroid
  
  • Choroidal melanoma ⇒ ± mushroom configuration if breaks through Bruch’s membrane
  • Spindle cell has best prognosis, epithelioid worst prognosis
• Propensity for hematogenous metastasis to liver
• Treatment may include radiation, plaque brachytherapy, enucleation, others

Question 47

Retinoblastoma

Answer 47

• Most common primary intraocular malignant tumor in children
  
  • Usually dx at age 3 or younger
• RB1 tumor suppressor gene mutation – “two-hit” hypothesis
  
  • Germline mutation results in bilateral disease
  • 45% of offspring affected
• 95% of cases are sporadic mutations
• Symptoms include leukocoria, strabismus, reduced vision
• Risk of metastasis low if does not extend outside the eye
  
  • May invade optic nerve, orbit, brain
  • Metastatic sites usually include bones, central nervous system, lymph nodes, abdominal viscera
• Treatment: chemo, radiation; enucleation is definitive therapy for tumors without extraocular extension
  
  • Good prognosis in developed countries (95% survival rates)
  • Patients with bilateral disease have higher risk of certain extraocular tumors later in life