Ophthalmology Flashcards
1
Q
Eyelids
A
- Protects the cornea
- Tarsal plates ⇒ dense CT plates
- Movement controlled by orbicularis oculi muscle (CN VII)
2
Q
Tear Film
A
- 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
3
Q
Extraocular Muscles
A
- 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
4
Q
Conjunctiva
A
Clear tissue overlying the sclera and lining the inner surfaces of the eyelids
5
Q
Cornea
A
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
6
Q
Layers of the Globe
A
Sclera, Uvea, Retina
7
Q
Sclera
A
- Outer white collagenous layer
- Covers posterior 4/5 of globe
- Anterior opening for cornea
- Posterior opening for optic nerve
8
Q
Uvea
A
- Middle vascular layer
- Provides blood flow to ocular structures
- Anterior eye ⇒ Iris and ciliary body
- Posterior eye ⇒ Choroid
9
Q
Retina
A
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
10
Q
Anterior Chamber
A
- 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
11
Q
Crystalline Lens
A
- Optically clear structure
- Provides ~ 1/3 of refractive power of the eye
- Suspended behind iris by zonular fibers
12
Q
Posterior Segment
A
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
- Exits back of the eye at the optic disc
13
Q
Refractive Error
A
Caused by light being focused in front of or behind the retina
Refractive power of eye comes from tear film, cornea, and lens
14
Q
Myopia
A
When light is focused in front of the retina
Corrected by “minus” or divergent/concave lens
15
Q
Hyperopia
A
When light is focused behind the retina
Corrected by “plus” or convergent/convex lens
16
Q
Astigmatism
A
When eye is ovoid
Light focuses in two planes instead of one point
17
Q
Chronic Conditions
A
- Cataracts
- Diabetic retinopathy
- Primary open angle glaucoma
- Age-related macular degeneration
18
Q
Cataract
A
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
19
Q
Diabetic Retinopathy
A
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
- Retinal neovascularization
-
Treatment:
- Blood glucose control
- Laser (panretinal photocoagulation)
- Iintravitreal injections of anti-VEGF medications
- Surgery
20
Q
Primary Open Angle Glaucoma
A
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
21
Q
Age-related Macular Degeneration
(AMD)
A
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
35
Q
Central Retinal Artery Occlusion
(CRAO)
A
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)
36
Q
Central Retinal Vein Occlusion
(CRVO)
A
- 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
37
Q
Acute Angle Closure Glaucoma
A
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
38
Q
Retinal Detachment
A
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
39
Q
Hypertensive Retinopathy
A
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
40
Q
Uveitis
A
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
-
Systemic inflammatory diseases
- Treated with topical steroids ± systemic treatment for underlying etiology
41
Q
Papilledema
A
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
42
Q
Optic Neuritis
A
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
43
Q
Arteritic Ischemic Optic Neuropathy (AION)
or
Giant Cell Arteritis (GCA)
A
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!
44
Q
HIV-Related Conditions
A
-
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
46
Q
Uveal Melanoma
A
- 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
47
Q
Retinoblastoma
A
-
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
