Optho part tressss Flashcards

1
Q

Anatomy of lens

A
  1. Intraocular location of lens behind the iris plane – contained within the lens capsule
    2. Optical clarity of the normal lens – typically the lens is optically clear at birth, but with aging it slowly becomes opaque, generally advancing from yellow, to brown to white. When the lens becomes opacified it is referred to as a cataract.
    3. Suspension of normal lens in retroiridic position by zonules – this allows the lens to change shape in response to changes in the ciliary body.
    Why do we have a lens? What is its function?
    4. Presbyopia - a condition where the eye exhibits a progressively diminished ability to focus on near objects with age. Presbyopia’s exact mechanisms are not known with certainty; the research evidence most strongly supports a loss of elasticity of the crystalline lens, although changes in the lens’s curvature from continual growth and loss of power of the ciliary muscles (the muscles that bend and straighten the lens) have also been postulated as its cause. Like gray hair and wrinkles, presbyopia is a symptom caused by the natural course of aging. The first signs of presbyopia – eyestrain, difficulty seeing in dim light, problems focusing on small objects and/or fine print – are usually first noticed between the ages of 40 and 50.
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2
Q

Symptoms attributable to cataract

A
  1. Slowly progressive blurring of vision
    2. Painless progressive loss of vision – most often noticed at night. One of the earliest symptoms is the presence of increased glare from point sources of light (headlights on cars).C. Examination of lens by direct ophthalmoscopy
    1. Evaluation of the red reflex
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3
Q

Examination of lens by direct ophthalmoscopy

A
  1. Evaluation of the red reflex
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4
Q

Abnormal lens feat General

A

a. loss of normal red reflex – this is often discovered by the primary care provider, this is usually a sign of an advanced cataract.
b. Dark spots in red reflex – often a sign of a moderate nuclear cataract where the red reflex appears “missing” centrally (like a donut).
c. Abnormal color of red reflex – can appear more orange or yellow in one or both eyes.

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5
Q

Lens abnormalities found in important systemic diseases :Marfan’s syndrome

A

due to mutations in the fibrillin gene, the lens is frequently displaced. The condition is bilateral, symmetric and non-progressive. Often good functional vision is intact, however when vision is impaired an artificial intraocular lens implant may prove beneficial.

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6
Q

Lens abnormalities found in important systemic diseases: Implantation of artificial intraocular lens

A

most lens based abnormalities (primarily cataracts) are treated by phacoemulsification (using ultrasound to break up and remove the lens) with intraocular lens implantation. Most modern lenses are placed in the same position as the physiologic lens inside the lens capsule. When the lens capsule is damaged or un healthy an intraocular lens can be placed in the sulcus between the lens capsule and posterior iris or in the anterior chamber resting on the anterior surface of the iris.

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7
Q

Neuro-Ophthalmology Anatomy

A

Afferent visual pathways – retina -> Optic nerve -> chiasm -> optic tract -> optic striations -> occipital lobe

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8
Q

Neuro-Ophthalmology Anatomy: Trigeminal nerve

A

Cranial nerve V, provides sensory innervation to the cornea and eyelids, clinically relevant in Herpes Zoster Ophthalmicus

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9
Q

Neuro-Ophthalmology Anatomy: Facial nerve

A

provides motor innervation to the orbicularis oculi, important for adequate lid closure and clinically relevant in Bell’s Palsy

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10
Q

Ocular autonomic pathways: sympathetic pathways

A

– important for pupil dilation, travels a circuitous route involving the superior cervical ganglion, this is the pathway that is disrupted in Horner’s syndrome

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11
Q

Ocular autonomic pathways: : parasympathetic pathways

A

important for pupils constriction, travel with the third cranial nerve, this pathway can be disrupted by an aneurysm in the circle of Willis (specifically the posterior communicating artery). It is important to understand this anatomy in the evaluation of a third nerve palsy.

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12
Q

pupillary pathways

A

– the light reflex consists of four neurons. The first connects the retina to the pre-tectal nucleus (these decussate in the chiasm). The second connects the pre-tectal nucleus to both Edinger – Westphal nuclei. The third connect the Edinger-westfal nucleus to the ciliary ganglion. Fourth from the ciliary ganglion to the pupil.

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13
Q
  1. Pupillary disorders: Dilated pupil
A

Unilateral – concern for third nerve palsy

Bilateral - pharmacological

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14
Q

Pupillary disorders: Adie’s tonic pupil

A

caused by denervation of the postganglionic supply to the sphincter pupillae and the ciliary muscle, thought to be caused by a viral illness. It typically affects young adults, and is almost always unilateral. The affected pupil is generally large and regular, and the light reflex is absent. It can be associated with diminished deep tendon reflexes or autonomic nerve dysfunction.

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15
Q

Pupillary disorders: Relative afferent pupillary defect

A

a condition in which the optic nerves conduct in an asymmetric fashion, most likely due to pathology affecting one optic nerve. Generally detected by the swinging flashlight test.

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16
Q

Pupillary disorders: Unilateral small pupil (Horner’s syndrome)

A

typical triad is unilateral ptosis, miosis and anhydrosis. It is a palsy of the oculosympathetic input. The mild ptosis is about 2mm in magnitude and due to weakness of the meuller muscle (not the levator). Lack of innervation to the pupillary sphincter results in miosis, but the pupil still generally responds to both light and accommodation. Horner’s can arise from an interruption of the hypothalamospinal tract in the lateral funiculus above T1, preganglionic neurons projecting to the superior cervical ganglia, or post-ganglionic neurons projecting from the superior cervical ganglia. Treatment of Horner’s syndrome involves treating the underlying cause. Acute Horner’s Syndrome requires urgent work-up, including imaging of the sympathetic nervous system. Frequent causes of Horner’s are vertebrobasilar artery infarction, tumors, multiple sclerosis, and internal carotid artery dissection. Chronic or congenital Horner’s syndrome workup is less urgent and does not immediately threaten ocular health.

17
Q

Cranial nerve palsies: III nerve

A

innervates medial rectus, superior rectus, inferior rectus, inferior oblique, levator palpebrae and carries parasympathetic fiber to the pupillary sphincter muscle. A third nerve palsy can result in ocular misalignment, ptosis and possibly mydriasis

				- pupil not involved, vasculopathic, not urgent
				- pupil involved, compressive, URGENT! (aneurysim of the posterior communicating artery in the circle of Willis)
18
Q

Cranial nerve palsies: IV nerve

A

provides innervation to the superior oblique muscle, frequently affected by microvascular disease

19
Q

Cranial nerve palsies: VI nerve

A

– innervates the lateral rectus, is very sensitive to increased intracranial pressure

20
Q

Cranial nerve palsies: V cranial nerve

A

provides corneal sensation, frequently the source of herpes zoster ophthalmicus

21
Q

Cranial nerve palsies: VII cranial nerve

A

“Bell’s Palsy”, can result in lagopthalmos and exposure, “crocodile tears”

22
Q

Myasthenia gravis

A

– frequently the extraocular muscles are the first affected by myasthenia. General presents as diplopia that gets worse as the day progresses, and exhibits fatiguability.

23
Q

Nystagmus

A

a repetitive, involuntary to and fro oscillation of the eyes. The plane of oscillation may be horizontal, vertical, torsional or non-specific. Can occur congenitally with no other problems, may result from intoxication, poor visual function, or central nervous system disease.