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Nervous System III > Opthamology > Flashcards

Opthamology Flashcards

1
Q

What is the sympathetic innervation of the pupil?

A

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

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2
Q

What is the parasympathetic innervation of the pupil?

A

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

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3
Q

Horner syndrome

A

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

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4
Q

Pupillary findings associated with sympathetic dysfunction

A

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

The smaller pupil is abnormal

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5
Q

Pupillary findings associated with parasympathetic dysfunction

A

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

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6
Q

Anisocoria greater in light - DDX

A

Parasympathetic dysfunction
Structural damage to the iris
3rd nerve palsy

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7
Q

What are characteristics of neurologic visual field disturbances?

A

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

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8
Q

Signs and symptoms of optic nerve injury

A

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

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9
Q

Afferent pupillary defect (APD)

A

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

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10
Q

Binocular diplopia

A

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

Due to ocular misalignment

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11
Q

Localization of ocular misalignment

A

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

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12
Q

What questions do you ask to evaluate diplopia?

A

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

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13
Q

3 types of nystagmus, by phase

A
  1. Pendular (slow-slow)
  2. Jerk (fast-slow)
  3. Mixed (slow-slow + fast-slow)
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14
Q

Downbeat nystagmus

A

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

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15
Q

Oscillopsia

A

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

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16
Q

What do alpha-1 receptors do in the eye?

A

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

alpha-1 also constricts blood vessels

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17
Q

What do beta-2 receptors do in the eye?

A

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

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18
Q

What do alpha-2 receptors do in the eye?

A

alpha-2 receptors in the ciliary body decrease aqueous humor

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19
Q

What do muscarinic receptors do in the eye?

A

Muscarinic receptors in the circular muscle cause pupillary constriction

Muscarinic receptors in the lens cause accomodation for near vision

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20
Q

Role of prostaglandins in treating glaucoma

A

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

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21
Q

Second line agents for open angle glaucoma

A

Beta blocker

Carbonic anhydrase inhibitor

Selective alpha-2 agonist

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22
Q

Role of alpha adrenergic agonists in glaucoma treatment

A

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)

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23
Q

Role of cholinergic agonists in glaucoma treatment

A

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

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24
Q

Role of Beta Blockers in treatment of glaucoma

A

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

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25
Q

Role of carbonic anhydrase inhibitors in glaucoma treatment

A

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

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26
Q

Pathophysiology of closed angle glaucoma

A

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

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27
Q

Topical treatments for closed angle glaucoma

A

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

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28
Q

Systemic treatments for closed angle glaucoma

A

Acetazolamide - blocks formation of aqueous humor

Mannitol - osmotor diuretic; produces intraocular dehydration

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29
Q

Definitive treatment for closed angle glaucoma

A

Laser peripheral iridotomy

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

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30
Q

Bacterial conjunctivitis - clinical course & common organisms

A

Usually self-limiting, but treatment shortens clinical course and reduces spread

Most common pathogens are S. aureus, S. pneumoniae, and H. influenzae

31
Q

Bacterial conjunctivitis - Empirical treatment

A

Erythromycin (Azithromycin in kids)

Fluoroquinolones

32
Q

Bacterial keratitis - Treatment

A

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

33
Q

HSV Keratitis - Treatment

A

Oral acyclovir or topical trifluridine

Avoid topical steroids

34
Q

Viral Conjunctivitis - Treatment

A

Adenovirus is the most common causative agent

Self-limiting with no specific antiviral treatment

Symptomatic relief with OTC antihistamine or decongestant drops

35
Q

Physiologic anisocoria

A

Seen in 15-20% of people

< 1mm difference between the two pupils; remains the same in light and dark

36
Q

Blow out orbital fracture

A

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

37
Q

Entrapped orbital fracture

A

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

38
Q

Thyroid eye disease - Pathophysiology

A

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

39
Q

Phases and treatment of thyroid eye disease

A

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

40
Q

Nasolacrimal duct obstruction (NLDO)

A

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)

41
Q

Presbyopia

A

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

42
Q

Iritis

A

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

43
Q

Corneal abrasion

A

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

44
Q

Corneal ulcer

A

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

45
Q

Herpes Keratitis

A

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

46
Q

Herpes Zoster Opthalmicus

A

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

47
Q

Pterygium

A

UV induced benign fibrous overgrowth of conjunctiva onto the cornea

Treated with artificial tears, sunglasses, vasoconstrictors (short term), or surgical removal

48
Q

Subconjunctival hemorrhage

A

Rupture of a blood vessel under the conjunctiva

Usually asymptomatic and resolves within 1 week; no specific treatment is indicated

49
Q

Chronic dry eye

A

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)

50
Q

Allergic conjunctivitis

A

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

51
Q

Cataracts

A

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

52
Q

Macula vs. Fovea

A

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

53
Q

What is the blood supply to the retina?

A

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

54
Q

Diabetic retinopathy - Pathophysiology

A

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

55
Q

Nonproliferative diabetic retinopathy

A

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

56
Q

Proliferative diabetic retinopathy

A

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

57
Q

Treatment of proliferative diabetic retinopathy

A

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

58
Q

Central retinal vein occlusion

A

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

59
Q

Hypertensive retinopathy

A

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

60
Q

Age-related macular degeneration

A

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

61
Q

Exudative (wet) age related macular degeneration (AMD)

A

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

62
Q

Arteritic anterior ischemic optic neuropathy (AION)

A

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

63
Q

Smooth pursuit

A

Tracking to keep an object on the fovea

Max speed 50 degrees/sec

64
Q

Saccades

A

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

65
Q

Convergence vs. Divergence

A

Convergence - moving the fovea to a closer object

Divergence - moving the fovea to a more distant object

66
Q

Near Reflex (Accomodation)

A

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

67
Q

What are the control centers for saccade generation?

A

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

68
Q

Where is the pattern generator for horizontal saccades?

A

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

69
Q

What is the blind sight response?

A

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

70
Q

How does the vestibuloocular reflex work?

A

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

71
Q

Internuclear opthalmoplegia

A

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

72
Q

CN III Palsy

A

Ptosis
Pupillary dilation
Unilateral “down and out” gaze

73
Q

Afferent pupillary defect

A

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)

74
Q

Physiology of aqueous humor

A

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

Nervous System III (9 decks)

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