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STEP > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

Open Angle Glaucoma

A
  • Increased intraocular pressure due to decreased outflow of aqueous humor
  • Can be blocked by WBCs (uveitis), RBCs ( vitreous hemorrhage) or retinal elements (retinal detachment).
  • Leads to optic neuropathy and causes loss of ganglion cell axons
  • Visualized on exam as pale optic disc and enlarged optic cup
  • Leads to loss of peripheral vision
  • Associated with increased age, african-american race, family history
  • Usually painless
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2
Q

What is the preferred first line treatment for open angle glaucoma?

A

Latanoprost

  • First line prostaglandin applied topically
  • Converted to active form by esterases in the cornea
  • Decreases collagen content in the uveoscleral outflow pathway and increase outflow of aqueous humor
  • May cause increased pigmentation in eyelids
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3
Q

Which cells secrete aqueous humor?

A
  • Non pigmented epithelial cells in the ciliary body.
  • It enters the posterior chamber.
  • It is decreased by beta blockers, alpha 2 agonists and carbonic anhydrase inhibitors
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4
Q

What is the Schlemms canal?

A

Scleral venous sinus that drains aqueous humor

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5
Q

What is conjunctivitis?

A
  • Inflammation of the conjunctiva
  • Produces a red eye
  • Allergic: bilateral itchy eyes
  • Bacterial: may secrete pus, treat with antibiotics
  • Viral: Most common, caused by adenovirus, sparse mucus discharge, swollen preauricular node; self limited disease
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6
Q

What are the 4 refractory errors and how are they usually treated?

A
  1. Hyperopia
  2. Myopia
  3. Astigmatism
  4. Presbyopia
    All are correctable with glasses
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7
Q

Hyperopia

A
  • Farsightedness
  • Eye is too short for refractive power of cornea and lens
  • Light is focused behind the retina
  • Correct with a convex (converging) lens
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8
Q

Myopia

A
  • Nearsightedness
  • Eye is too long for refractive power of cornea and lens
  • Light is focused in front of the retina
  • Correct with a concave (diverging) lens
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9
Q

Astigmatism

A
  • Abnormal curvature of the cornea
  • Different refractive power at different axes
  • Correct with a cylindrical lens
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10
Q

Presbyopia

A
  • Aging-related impaired accommodation (focusing on near objects)
  • Primarily due to decreased lens elasticity, change in curvature or decreased strength of the ciliary muscle
  • Patients often need reading glasses (magnifiers)
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11
Q

What are cataracts?

A
  • Painless often bilateral, opacification of lens
  • Often result in decreased vision
  • Risk factors: Increased age, smoking, excessive alcohol use, excessive sunlight, prolonged corticosteroid use, diabetes mellitus, trauma, infection
  • Congenital risk factors: classic galactosemia, galactokinase deficiency, trisomies (13,18,21), ToRCHeS (rubella), Marfan syndrome, Alport syndrome, myotonic dystrophy, neurofibromatosis 2
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12
Q

Where does 90% of the aqueous humor drain?

A 
Trabecular outflow
- Through the trabecular meshwork
- Into the canal of schlemm
- Into the episcleral vasculature
This is increased with M3 agonists
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13
Q

Where does the other 10% of the aqueous humor drain?

A

Uveoscleral outflow
- Drain into the uvea and sclera
Increased with prostaglandin agonists

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14
Q

Iris

A

Consists of two muscles

  • Dilator muscle is regulated by alpha 1 receptors, causes pupil to dilate,
  • Phenylephrine targets dilator muscle
  • Darkness dilates the pupil
  • Sphincter muscle is regulated by M3 receptors, causes pupil to constrict
  • Pilocarpine targets sphicter muscle
  • Bright light constricts the pupils
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15
Q

What is closed angle glaucoma?

A

Primary
- Enlargement/forward movement of lens against the central iris (pupil)
- Leads to obstruction of the normal aqueous flow through the pupil
- Fluid builds up behind the iris
- Pushes the peripheral iris against the cornea
- Impedes flow through the trabecular meshwork
Secondary
- Hypoxia from retinal disease such as DM or vein occlusion
- Induces vasoproliferation in iris that contracts the angle
-Can be acute or chronic

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16
Q

Chronic angle closure glaucoma

A

Asymptomatic with damage to the optic nerve and to peripheral vision

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17
Q

Acute angle closure glaucoma

A
  • True opthalmic emergency
  • Increase in Intraocular pressure pushes the iris forward
  • The angle closes abruptly
  • Very painful, red eye, sudden vision loss, halos around lights, frontal headache, fixed and mid dilated pupil
  • Do not give epinephrine due to mydriatic effect (dilation)
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18
Q

What is intraocular hypertension?

A
  • Any situation in which intraocular pressure is greater than 21 mmHg
  • Measured by applanation tonometry on two or more occasions
  • Absence of glaucomatous defects on visual field testing
  • Normal appearance of optic disc and nerve fiber layer
  • Normal open angles on gonioscopy
  • Absence of ocular conditions contributing to the elevation of pressure such as narrow angles, neovascular conditions and uveitis
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19
Q

What is diabetic retinopathy?

A
  • Damage to the endothelial lining of the small blood vessels of the eye
  • Leads to progressive occlusion on a microscopic level
  • The occlusion leads to obstruction and increased pressure
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20
Q

What is non proliferative retinopathy?

A
  • Background retinopathy

- Characterized by dilation of veins, micro aneurysms, retina edema and retinal hemorrhages (do not obstruct sight).

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21
Q

What is proliferative retinopathy?

A
  • More advanced form of disease
  • Progresses more rapidly to blindness
  • Vessels secrete angiogenesis factor because they are not providing sufficient nutrition to the retina
  • Neovascularization leads to optic nerve getting covered with abnormal new vessels
  • Hemorrhages protrude into the vitreous chamber
  • Vitreal hemorrhages are much more serious than micro aneurysms or intraretinal hemorrhages because they obstruct sight
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22
Q

How does diabetic retinopathy present?

A
  • Highly variable
  • Patients may be asymptomatic with advanced disease
  • Vision may decrease slowly or rapidly
  • Vitreal hemorrhages may develop suddenly and patients may complain of floaters.
23
Q

How is diabetic retinopathy diagnosed?

A
  • Screened on an annual basis
  • Fluorescein helps identify which vessels should undergo laser photocoagulation
  • Laser coagulation destroys focal areas of the retina and diminishes the production of the angiogenesis factor
24
Q

How is diabetic retinopathy treated?

A
  • Tight control of glucose, as close to normal as possible.
  • Blood pressure should be controlled to a level of <130/80 mm Hg.
  • Lipid levels should be < 100 mg/dL
  • Proliferative retinopathy requires immediate laser photocoagulation
  • Anti-VEGF can be used
25
Q

What is retinal detachment?

A
  • Separation of neurosensory layer (photoreceptor layer with rods and cones) of the retina from the outermost pigmented epithelium (supports the retina).
  • Leads to degeneration of photoreceptors and vision loss
  • Usually spontaneous but may result from trauma.
  • Predisposing factors are myopia and surgical extraction of cataracts
  • Traction on the retina can also occur from proliferative retinopathy from diabetes, retinal vein occlusion and age related macular degeneration leading to detachment
26
Q

How does retinal detachment present clinically?

A
  • Blurry vision developing in one eye without pain or redness
  • Patient may complain of floaters as well as flashes in the periphery of vision
  • It is sometimes described as the curtain coming down as the retina falls off the sclera behind it.
  • Fundoscopy shows a crinkling of retinal tissue and changes in vessel direction.
27
Q

How is retinal detachment treated?

A
  • Try to reatach the retina
  • Lean head back in hopes that retina falls back into place
  • Retina can be mechanically reattached to the sclera surgically, by laser photocoagulation, cryotherapy or by injection of expansile gas into the vitreal cavity.
  • A buckle or belt can be placed around the sclera to push it forward so it comes in contact with the retina
  • If all methods fail, vitreous can be removed and the retina can be surgically attached to sclera
  • 80% are cured with one operation, 15% require a second opertaion
28
Q

What is age related macular degenaration?

A
  • Degeneration of the macula (central area of the retina)
  • Causes distortion (metamorphopsia) and eventual loss of central vision (scotoma)
  • Most common cause of legal blindness in older persons
  • There is two types, dry and wet ARMD
29
Q

Dry Age Related Macular Degeneration

A
  • Dry (nonexudative) deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium (Drusen) with slow, gradual decrease in vision
  • Accounts for more than 80% of cases
30
Q

Wet Age Related Macular Degeneration

A
  • Wet (exudative), rapid loss of vision due to bleeding secondary to choroidal neovascularization.
  • There is abnormal growth of vessels from choroidal circulation into the subretinal space
  • The vessels leak, leading to subretinal fluid and localized exudative retinal detachment
31
Q

How is Age Related Macular Degeneration diagnosed?

A
  • Dry ARMD is confirmed by finding Drusen (small granular, subretinal deposits) on dilated eye exam (tropicamide)
  • Wet ARMD is diagnosed by fluoroscein angiography
32
Q

How is ARMD treated?

A

Dry ARMD is treated with zinc and antioxidant supplements (C, E and beta-carotene).
- Wet ARMD is treated with VEGF injections (ranibizumab)

33
Q

What is central retinal artery occlusion?

A
  • Due to carotid artery embolic disease, temporal arteritis, cardiac thrombi or myxoma or any causes of thrombophilia such as factor V leiden (evaluate for embolic source)
  • Acute painless, monocular vision loss
  • No redness of the eye
  • ## Exam reveals pale retina with overly diminished perfusion and a cherry red spot at the fovea
34
Q

How should a patient with central retinal artery occlusion be worked up?

A

Should undergo evaluation with carotid artery imaging, echocardiography and evaluation for thrombophilia

35
Q

How is central retinal artery occlusion treated?

A
  • The same as a CVA or TIA
  • Lay the patient flat
  • Supply oxygen
  • Occular massage in an attempt to unobstruct the vessel
  • Can use acetazolamide and thrombolytics
  • Anterior chamber paracentesis can be used to decompress the pressure in the eye and dislodge the embolus
36
Q

What is central retinal vein occlusion?

A
  • Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis
  • Patient are at high risk for developing glaucoma
  • Young patient should be worked up for inherited causes of thrombophilia, factor V mutation, protein C deficiency and antiphospholipid syndromes
37
Q

Presentation of central retinal vein occlusion?

A
  • Similar to those with retinal artery occlusion
  • Sudden loss of vision without pain, redness or abnormality in pupillary dilation
  • Occular exam by funduscopy reveals disk swelling, venous dilation, tortuosity (wiggles) and retinal hemorrhages
38
Q

How is a central retinal vein occlusion distinguished from a retinal arterial occlusion?

A
  • Hemorrhages
  • You cant have a hemorrhage in the retina if you dont have blood getting into the eye
  • Therefore you rule out arterial occlusion because blood is passing through the arterials
39
Q

Which medications can precipitate acute angle closure glaucoma?

A
  • Anticholinergics such as ipratropium bromide

- Tricyclic antidepressants

40
Q

Epinephrine (alpha1)

  • MOA in glaucoma
  • Side effects
A

MOA: Alpha agonist, decrease aqueous humor synthesis via vasoconstriction
Side effects: Mydriasis (dilation) do not use in closed angle glaucoma

41
Q

Brimonidine (alpha2)

  • MOA in glaucoma
  • Side effects
A

MOA: Alpha agonist, decrease aqueous humor synthesis

Side effects: Blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, ocular pruritis

42
Q

Timolol, betaxolol, carteolol

  • MOA in glaucoma
  • Side effects
A

MOA: Beta blockers, decrease aqueos humor synthesis

Side effects: No pupillary or vision chnages

43
Q

Acetazolamide

  • MOA in glaucoma
  • Side effects
A

MOA: Diuretic, decrease aqueous humor synthesis via inhibition of carbonic anhydrase
Side effects: No pupillary or vision changess

44
Q

Pilocarpine, carbachol
Physostigmine, achothiophate
- MOA in glaucoma
- Side effects

A

Direct cholinomimetics
Indirect cholinomimetics
MOA: Increase outflow of aqueous humor via contraction of ciliary muscle and opening of trabecular meshwork
- Pilocarpine is used in emergencies, very effective at opening canal of Schlemn
Side effects: Miosis (contraction) and cyclospasm (contraction of ciliary muscle)

45
Q

Bimatoprost, latanoprost

  • MOA in glaucoma
  • Side effects
A

MOA: Increase outflow of aqueous humor via decreased resistance of flow through uveoscleral pathway
Side effects: Darkens the color of the iris (browning), eyelash growth

46
Q

What is uveitis?

A

Inflammation of the uvea (the choroid, iris and ciliary body)

  • Anterior uveitis is also iritis
  • Posterior uveitis is also choroiditis/retinitis
  • May have hypopyon (pus in anterior chamber) or conjunctival redness
  • Associated with inflammatory disorders such as sarcoidosis, rheumatoid arthritis, juvenile idiopathic arthritis, HLA-B27 associated conditions
47
Q

What is retinitis pigmentosa?

A
  • Inherited retinal degeneration
  • Painless, progressive vision loss beginning with night blindness (rods affected first)
  • Bone spicule-shaped deposits around the macula
48
Q

What is retinitis?

A
  • Retinal edema and necrosis leading to scar
  • Often viral (CMV, HSV, VZV) but can be bacterial or parasitic
  • May be associated with immunosuppresion
49
Q

What is papilledema?

A
  • Optic disc swelling (usually bilateral)
  • Due to increased intracranial pressure secondary to mass effect
  • Enlarged blind spot and elevated optic sic with blurred margins
50
Q

Miosis

A
  • Constriction of the pupil
  • Parasympathetic mediated
  • 1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
  • 2nd neuron: Short ciliary nerves to sphincter pupillae muscles
51
Q

Mydriasis

A
  • Dilation of pupil
  • Sympathethic mediated
  • 1st neuron: Hypothalamus to ciliospinal center of Budge (C8-T2)
  • 2nd neuron: Exit at T1 to superior cervical ganglion(travels along cervical sympathetic chain near lung apex, subclavian vessels)
  • 3rd neuron: Plexus along internal carotid, through cavernous sinus, enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face
52
Q

What is Horner Syndrome?

A

Ptosis, Anhydrosis and Miosis

- Due to lesion of the spinal cord above T1

53
Q

Retinal Artery Occlusion

  • Signs
  • Causes
  • Pathway of clot
A
  • Causes acute, painless, monocular vision loss
  • Due to thromboembolic complications of atherosclerosis
  • Clot travels from internal carotid artery, through the ophthalmic artery and into the retinal artery
54
Q

Diabetic CN III mononeuropathy

A
  • Most common
  • Presents with acute onset diplopia in one eye only
  • Affected eye assumes down and out position due to unopposed pull by superior oblique (CNIV) and lateral rectus (CN VI)
  • All other ocular muscles are supplied by CN III and are paralyzed
  • Ptosis occurs due to paralysis of the levator palpebrae which is also supplied by the oculomotor nerve
  • Caused by ischemic nerve damage to the core of CN III, which contains the somatic component that innervates the extraoculor muscles
  • The autonomic component is located in the peripheral aspect of the nerve and is spared, therefore pupillary constriction and accommodation is normal

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