Opthamology

Question 1

What is the sympathetic innervation of the pupil?

Answer 1

Efferent innervation to the radial muscle of the iris

Contraction dilates the pupil

Sympathetic dysfunction results in a miotic pupil that is poorly responsive to the dark; anisocoria is greater in the dark

Question 2

What is the parasympathetic innervation of the pupil?

Answer 2

Efferent innervation to the sphincter muscle of the iris; contraction causes pupillary constriction

Parasympathetic results in a mydriatic (tonic) pupil that is poorly responsive to the light; anisocoria is greater in the light

Question 3

Horner syndrome

Answer 3

Disruption of sympathetic fibers resutling in ptosis, miosis, and anhydrosis

Anisocoria is greater in the dark with normal pupillary response to light and dilation lag of the miotic pupil

Horner + eye pain is suggestive of carotid dissection

Question 4

Pupillary findings associated with sympathetic dysfunction

Answer 4

Anisocoria greater in the dark; both pupils have normal light response

The smaller pupil is abnormal

Question 5

Pupillary findings associated with parasympathetic dysfunction

Answer 5

Anisocoria is greater in the light and the larger pupil has a poor response to light; the larger pupil is abnormal

May also see:

Light-near dissociation - better pupillary constriction to a near target than to light

Tonic dilation to a distant target

Segmental palsy - partial constriction of the iris sphincter in some areas only

Question 6

Anisocoria greater in light - DDX

Answer 6

Parasympathetic dysfunction
Structural damage to the iris
3rd nerve palsy

Question 7

What are characteristics of neurologic visual field disturbances?

Answer 7

One or more of the following:

The defect respects vertical and/or horizontal meridians

The defect is homonymous - it involves the same area of the visual field in each eye

Remember the reverse retinotopy of the visual field mapping to the visual cortex

Question 8

Signs and symptoms of optic nerve injury

Answer 8

Symptoms: Monocular vision loss, decreased brightness, impaired color vision

Signs: Loss of vision (acuity, field, or both), afferent pupillary defect, color vision loss, abnormal optic nerve

Question 9

Afferent pupillary defect (APD)

Answer 9

Decreased pupillary constriction of both eyes when light is shone in the affected eye vs. the non-affected eye; indicates that less light is being sensed by the affected eye

Question 10

Binocular diplopia

Answer 10

Double vision that is present only when both eyes are open, and goes away when either eye is closed

Due to ocular misalignment

Question 11

Localization of ocular misalignment

Answer 11

N - Nerve (3, 4, 5)
E - Eye (displaced)
J - Neuromuscular junction
M - Muscle (thyroid associated opthalmopathy, rare myopathies)

Question 12

What questions do you ask to evaluate diplopia?

Answer 12

Binocular vs. mono-ocular
Horizontal vs. vertical
Worse with any position of gaze?
Worse with near or distance viewing?

Question 13

3 types of nystagmus, by phase

Answer 13

1. Pendular (slow-slow)
2. Jerk (fast-slow)
3. Mixed (slow-slow + fast-slow)

Question 14

Downbeat nystagmus

Answer 14

Localizes to the cervicomedullary junction; caused by compression of the cerebellar flocculus, often due to Chiari malformation

The flocculus normally inhibits the anterior semicircular canals, which stimulate the eyes to move upward; when these anterior semicircular canals are disinhibited, the eyes will drift upward and then a rapid “corrective” downbeat occurs

Question 15

Oscillopsia

Answer 15

The appearance of movement of the visual world due to eye movement disturbance

Most often due to nystagmus; characterized by the speed of the oscillatory phases:

Pendular (slow-slow)
Jerk (Fast-slow)
Mixed

Question 16

What do alpha-1 receptors do in the eye?

Answer 16

alpha-1 receptors contract the radial muscle, causing pupillary dilation

alpha-1 also constricts blood vessels

Question 17

What do beta-2 receptors do in the eye?

Answer 17

beta-2 receptors in the ciliary body increase aqueous humor production

Question 18

What do alpha-2 receptors do in the eye?

Answer 18

alpha-2 receptors in the ciliary body decrease aqueous humor

Question 19

What do muscarinic receptors do in the eye?

Answer 19

Muscarinic receptors in the circular muscle cause pupillary constriction

Muscarinic receptors in the lens cause accomodation for near vision

Question 20

Role of prostaglandins in treating glaucoma

Answer 20

First line for open angle glaucoma; increases aqueous humor outflow

Side effects: Brown discoloration of iris, eyelash lengthening and darkening, ocular irritation; almost no systemic side effects

Question 21

Second line agents for open angle glaucoma

Answer 21

Beta blocker

Carbonic anhydrase inhibitor

Selective alpha-2 agonist

Question 22

Role of alpha adrenergic agonists in glaucoma treatment

Answer 22

Selective alpha-2 adrenergic agonists increase aqueous humor outflow and inhibit secretion of aqueous humor

Side effects: Red eye, ocular irritation, CNS depression (hypotension,, somnolence)

Question 23

Role of cholinergic agonists in glaucoma treatment

Answer 23

Cause muscarinic-induced contraction of the ciliary muscle, which facilitates aqueous outflow

Side effects: Risk of cataract development, ciliary spasm leading to headaches, myopia, dim vision

Question 24

Role of Beta Blockers in treatment of glaucoma

Answer 24

Non-selective, block B-2 receptors in the eye; decreases ocular blood flow, which reduces ultrafiltration required for aqueous humor production

Side effects: bradycardia, heart block, asthma

Question 25

Role of carbonic anhydrase inhibitors in glaucoma treatment

Answer 25

Inhibit formation of carbonic anhydrase in the ciliary body epithelium, reducing formation of bicarbonate ions which reduces fluid transport and IOP Side effects: Bitter taste

Question 26

Pathophysiology of closed angle glaucoma

Answer 26

Mechanical blockage of the trabecular meshwork by the peripheral iris, preventing outflow of IOP; blockage occurs acutely and intermittently, resulting in extreme fluctuations of IOP

Question 27

Topical treatments for closed angle glaucoma

Answer 27

Pilocarpine - induces miosis (contraction of the ciliary muscle) which frees the entrance to the trabecular space at the canal of Schlemm from blockage by iris tissue + Apraclonidine + Timolol

Question 28

Systemic treatments for closed angle glaucoma

Answer 28

Acetazolamide - blocks formation of aqueous humor Mannitol - osmotor diuretic; produces intraocular dehydration

Question 29

Definitive treatment for closed angle glaucoma

Answer 29

Laser peripheral iridotomy Avoid anti-cholinergic drugs, which can precipitate an attack of closed angle glaucoma

Question 30

Bacterial conjunctivitis - clinical course & common organisms

Answer 30

Usually self-limiting, but treatment shortens clinical course and reduces spread Most common pathogens are S. aureus, S. pneumoniae, and H. influenzae

Question 31

Bacterial conjunctivitis - Empirical treatment

Answer 31

Erythromycin (Azithromycin in kids) Fluoroquinolones

Question 32

Bacterial keratitis - Treatment

Answer 32

Mild, small, peripheral infections are treated empirically the same way as bacterial conjunctivitis: Erythromycin/Azithromycin or Fluoroquinolone Severe, central, larger infections are treated more aggressively with Fluoroquinolones, aminoglycoside, or vancomycin

Question 33

HSV Keratitis - Treatment

Answer 33

Oral acyclovir or topical trifluridine Avoid topical steroids

Question 34

Viral Conjunctivitis - Treatment

Answer 34

Adenovirus is the most common causative agent Self-limiting with no specific antiviral treatment Symptomatic relief with OTC antihistamine or decongestant drops

Question 35

Physiologic anisocoria

Answer 35

Seen in 15-20% of people < 1mm difference between the two pupils; remains the same in light and dark

Question 36

Blow out orbital fracture

Answer 36

Caused by backwards displacement of the orbit by a traumatic force; force is transmitted to the retro-orbital sinuses, blowing out the medial wall and floor of the orbit

Question 37

Entrapped orbital fracture

Answer 37

Orbital fracture with entrapment of soft tissue (i.e. extraocular muscle) within the suture lines, causing paralysis of the eye

Question 38

Thyroid eye disease - Pathophysiology

Answer 38

Primary inflammatory disease of the orbital soft tissue. associated with autoimmune thyroid disease (most commonly Graves) Orbital fibroblasts express TSH-R which binds pathological stimulatory thyroid auto-antibodies, stimulating fibroblast secretion of pro-inflammatory cytokines and recruitment of inflammatory cells into the orbital soft tissue Production of GAGs, swelling of EOMs due to lymphocytic proliferation, and orbital fibroblast proliferation contributes to 'bulging' appearance of the eye and retracted lid

Question 39

Phases and treatment of thyroid eye disease

Answer 39

Dynamic phase - can occur before or after onset of autoimmune thyroid disease; treated with steroids Active phase - typically lasts 18-36 months Static/quiescent phase - treated surgically

Question 40

Nasolacrimal duct obstruction (NLDO)

Answer 40

Caused by blockage of the lacrimal duct, below the lacrimal sac - due to stones or inflammation Presents with epiphora - unilateral overflow of tears onto the face; may also present with dacrocystitis (inflammation of the lacrimal sac)

Question 41

Presbyopia

Answer 41

Progressive loss of ability to focus on near objects, occurring as a result of the natural loss of flexibility of the lens with aging

Question 42

Iritis

Answer 42

Inflammation of the iris - may be idiopathic (single occurrence) or manifestation of systemic autoimmune condition Presents with ocular pain, photophobia, blurred vision, redness, and irregularly shaped pupil Treated with topical steroid eye drops

Question 43

Corneal abrasion

Answer 43

Presents with severe eye pain or foreign body sensation with acute onset of tearing, blurred vision, and redness Fluorescein stain can be used with a blue light to visualize the epithelial defect Treated with artificial tears and topical antibiotic ointment to prevent secondary infection

Question 44

Corneal ulcer

Answer 44

Infection of the corneal stroma; occurs secondary to trauma or contact lens wear Presents as acute onset of pain, redness, decreased vision, and eyelid swelling with a white infiltrate seen in the cornea Small ulcers are treated empirically with fluoroquinolones; larger ulcers require culture and may leave a corneal scar with permanent vision loss, indicating a corneal transplant

Question 45

Herpes Keratitis

Answer 45

Viral infection of the corneal epithelium with HSV-1 Presets with unilateral redness, pain, photophobia, decreased vision, tearing Fluorescein stain under blue light shows dendritic epithelial ulcer in branching pattern with terminal bulbs Treated with oral acyclovir and topical trifluridine

Question 46

Herpes Zoster Opthalmicus

Answer 46

Reactivation of VZV causing ocular manifestations Presents with a clinical prodrome of fatigue, fever, and unilateral rash on forehead, eyelid, and nose; presents with unilateral eye pain, redness, decreased vision, photophobia Treated with oral acyclovir or valacyclovir

Question 47

Pterygium

Answer 47

UV induced benign fibrous overgrowth of conjunctiva onto the cornea Treated with artificial tears, sunglasses, vasoconstrictors (short term), or surgical removal

Question 48

Subconjunctival hemorrhage

Answer 48

Rupture of a blood vessel under the conjunctiva Usually asymptomatic and resolves within 1 week; no specific treatment is indicated

Question 49

Chronic dry eye

Answer 49

Inadequate tear production due to systemic conditions (rheumatoid arthritis, lupus, Grave's) or medications (anti-histamines, pain medications, anti-depressants) Presents as bilateral foreign body sensation, redness, blurred vision, reflex tearing worse toward the end of the day Treated with artificial tears, flax seed, Omega 3, medicated eye drops to improve tear production (Restasis)

Question 50

Allergic conjunctivitis

Answer 50

Irritation of the conjunctiva by an allergen Presents as bilateral itching, eyelid swelling, redness, watery discharge; more common in people with a history of allergies, asthma, and eczema (atopic triad) Treated with antihistamines/mast cell stabilizers and/or topical steroids

Question 51

Cataracts

Answer 51

Gradual clouding of the lens of the eye causing progressive decline in visual acuity; normally develops with age as lens proteins break down Causes in younger patients: poorly controlled DM, steroids, trauma, radiation

Question 52

Macula vs. Fovea

Answer 52

Macula - central region of the retina, location of highest visual acuity Fovea - region of the macula containing only cones; location of most sensitive color discrimination

Question 53

What is the blood supply to the retina?

Answer 53

The main blood supply of the central 2/3 retina is the opthalmic artery, a branch of the internal carotid The choroid is a vascular layer underneath the RPE that supplies blood to the outer 1/3

Question 54

Diabetic retinopathy - Pathophysiology

Answer 54

Microvascular injury to small retinal capillaries with loss of pericytes and loosening of tight junctions causing hemorrhage and leakage; eventually loss of capillaries occurs (ischemia) followed by attempted neovascularization

Question 55

Nonproliferative diabetic retinopathy

Answer 55

Earliest stage of diabetic retinopathy Microvascular damage to retinal capillaries causes flame and dot-blot hemorrhages, venous beading and dilation, deposition of hard exudates (lipoprotein), and macular edema

Question 56

Proliferative diabetic retinopathy

Answer 56

More advanced stage of diabetic retinopathy involving neovascularization of the optic disc and retina; complications include: Hemorrhage of neoproliferative vessels Obstruction of the trabecular meshwork, causing neovascular glaucoma Fibrovascular proliferation causing retinal detachment

Question 57

Treatment of proliferative diabetic retinopathy

Answer 57

Prophylactic: Glycemic control, BP control, screening eye exams Symptomatic - photocoagulation of leaky vessels to treat/prevent further macular edema; intravitreal injection of anti-VEGF monoclonal antibodies prevents neovascularization and decreases capillary leakiness

Question 58

Central retinal vein occlusion

Answer 58

Blockage of the main vein carrying blood from the retina, causing swelling of the optic nerve, intraretinal hemorrhage, and macular edema

Question 59

Hypertensive retinopathy

Answer 59

Chronic hypertension leading to vasoconstriction and arteriosclerosis of the retinal arteries; causes retinal hemorrhage, macular edema, and optic edema (papilledema)

Question 60

Age-related macular degeneration

Answer 60

#1 cause of blindness > 50 years old 90% nonexudative (dry), caused by lipoprotein deposits (Drusen) on the surface of the retinal epithelium causing photoreceptor atrophy Treated with AREDS vitamins

Question 61

Exudative (wet) age related macular degeneration (AMD)

Answer 61

10% of patients with dry AMD will develop wet AMD Involves choroidal neovascularization (CNV) into the retinal epithelium, causing macular edema and hemorrhage with epithelial detachment and scarring Treated with Anti-VEGF injections

Question 62

Arteritic anterior ischemic optic neuropathy (AION)

Answer 62

Infarction of the optic disc related to giant cell arteritis; presents with HA, fatigue, jaw claudication, scalp tenderness, vision loss, and optic disc edema Diagnosed by temporal artery biopsy with elevated ESR and/or CRP Treated with steroids

Question 63

Smooth pursuit

Answer 63

Tracking to keep an object on the fovea | Max speed 50 degrees/sec

Question 64

Saccades

Answer 64

Rapid movements of the eye that bring an object onto the fovea by bringing the eye to a predetermined position Max speed up to 700 degrees/second; occur at a rate of 3/second during normal viewing of the world Visual perception is shut down during a saccade

Question 65

Convergence vs. Divergence

Answer 65

Convergence - moving the fovea to a closer object Divergence - moving the fovea to a more distant object

Question 66

Near Reflex (Accomodation)

Answer 66

Both medial recti contract to turn eyes nasally (convergence) Pupils constrict to increase depth of field Ciliary muscles contract, allowing the lens to change shape to become fatter

Question 67

What are the control centers for saccade generation?

Answer 67

Frontal eye field of motor cortex projects directly to the PPRF and to the PPRF via the superior colliculus Permanent loss of the ability to make saccades requires damage to both the frontal eye field AND the PPRF

Question 68

Where is the pattern generator for horizontal saccades?

Answer 68

The paramedial pontine reticular formation (PPRF), in the reticular formation near the abducens nucleus

Question 69

What is the blind sight response?

Answer 69

Individuals with a stroke in the visual cortex causing blindness will still foveate toward a bright light flashed in a dark room; the retinal input to the superior colliculus directly drives the saccadic eye movement

Question 70

How does the vestibuloocular reflex work?

Answer 70

Turning the head to the right excites hair cells in the right horizontal canal, which project to the right vesibular nuclei; cells in the vestibular nuclei project by way of the MLF to excite left lateral rectus motor neurons in the abducens nucleus as well as internuclear interneurons that cross over and acsend in the MLF to excite right medial rectus motor neurons

Question 71

Internuclear opthalmoplegia

Answer 71

Caused by MLF damage occurring between CN VI and CN III nuclei; often seen in MS due to demyelination of long tract axon Causes discoordination of medial and lateral recti during horizontal gaze so that the affected eye cannot deviated medially with contralateral gaze; presents as binocular diplopia

Question 72

CN III Palsy

Answer 72

Ptosis Pupillary dilation Unilateral "down and out" gaze

Question 73

Afferent pupillary defect

Answer 73

Presents as relative dilation when light is swung from the non-affected side to the affected side in a dark room; this occurs because the direct response of the affected eye to light (constriction) is weaker than the consensual response of affected eye to dark (dilation)

Question 74

Physiology of aqueous humor

Answer 74

Continuously produced by the cells of the epithelium covering the ciliary body; maintains an ocular pressure 10-15 mmHg above atmospheric pressure Aqueous humor drains into the canal of Schlemm