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Neurological Medicine > Block 3: Eyes and Ears > Flashcards

Block 3: Eyes and Ears Flashcards

1
Q

What muscles and their respective receptors/NTs regulate eyelid position?

A
  • striated muscles, OO and LPS (ACh, nicotinic)

- smooth muscle, ST (NE, a1 adrenergic)

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2
Q

What are the functions of blinking?

A
  • Corneal lubrication
  • Eye protection
  • Visual information processing (brain pieces together visual field when blink)
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3
Q

Spontaneous blinking originates in the premotor brainstem structures that are highly influenced by _____________ activity. What are the expected blinking rates of persons affected by Parkinson Disease, Schizophrenia, and Huntington’s disease?

A

Dopaminergic

PD – decreased
Schizophrenia, Huntington’s – increased

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4
Q

What initiates the blink reflex?

A
  • Touch of the cornea (CN V1 afferents)

- Bright light/rapidly approaching objects (CN II afferents)

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5
Q

What is the composition of tears?

A
  • lipids (from oil glands)
  • aqueous-based solution (from lacrimal gland)
  • mucous (from conjunctiva)
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6
Q

What is refraction of the eye determined by?

A
  • Cornea and the lens

- Refraction is defined by the bending of the light to focus on the retina

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7
Q

Draw out the visual pathway - nasal and temporal fields.

A
  • temporal fields remain ipsilateral – outside, not crossed

- nasal fields cross (contralateral) – middle is crossed

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8
Q

How does the eye perform the act of accommodation?

A
  • Sympathetic NS is activated; results in relaxation of ciliary muscle through activation of B2 receptors
  • Parasympathetic function occurs in relaxed state; results in contraction of the ciliary muscle through activation of muscarinic receptors
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9
Q

Define hyperopia. How is this condition corrected?

A

Farsightedness (image is focused behind the retina)

- Corrected by using convex lens to increase the refractive power (positive diopters)

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10
Q

Define myopia. How is this condition corrected?

A

Nearsightedness (image is focused in front of the retina)

- Corrected by using concave lens (negative diopters)

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11
Q

Define presbyopia. What population commonly has this condition?

A

Presbyopia occurs when a person’s lens becomes less flexible which results in a decrease in accommodation.
- Occurs is virtually everyone in middle age; they wear reading glasses to correct this condition.

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12
Q

Define astigmatism.

A

Astigmatism is an unevenness in the lens which results in part of the visual field being out of focus.

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13
Q

Define cataracts.

A

Cataracts result due to the cloudiness/opaqueness in the lens

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14
Q

Light intensity is regulated by the pupillary light reflex, which has both parasympathetic and sympathetic controls. Describe the parasympathetic portion of this system.

A
  • Parasympathetic system causes bilateral miosis (pupil constriction)
    • Light enters the left eye and interacts with the photoreceptors which cause the ganglion cells of the optic nerve tract to generate a potential
    • The optic tract then goes to the thalamus and the pretectal nucleus found in the midbrain
    • From the pretectal nucleus there are two pre-ganglionic nerve fibers given off to interact with the Edinger-Westphal nucleus of CN III on both the right and left sides which eventually synapse in the ciliary ganglion
    • From the ciliary ganglion, the post-synaptic parasympathetic neurons go to the sphincter pupillae muscles causing them to constrict
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15
Q

In the pupillary light reflex, ________ as a result of parasympathetic stimulation of the ________ ________ muscles (muscarinic receptors). ____________ results from sympathetic stimulation (α1 receptors) that activates the _________ _________ .

A

miosis (pupil constriction); sphincter pupillae

mydriasis (pupil dilation); dilator pupillae

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16
Q

Regulation of the inflow and outflow of eye fluid is accomplished through the sympathetic and parasympathetic systems, respectively. What receptors are a part of each system and what is their effect on flow?

A

• Inflow (sympathetics):
o β2 increases flow; α 1 decreases flow (work on cAMP)
o Cl- secretion drives water secretion due to osmosis
- Cl- secretion is regulated by HClO3- which is influenced by carbonic anhydrase (CA)
• Outflow (parasympathetics):
o Canal of Schlemm: regulated by the sphincter pupillae
- if contract the sphincter, this increases flow
o Uveosclerosis system: reabsorption of fluid through the ciliary muscle
o Both PGs and parasympathetics regulate outflow

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17
Q

What is the circuitry for the visual system?

A
  1. Stimulus: light enters the eye and interacts with photoreceptors in the back of the retina
  2. Photoreceptors generate receptor potential and carry out signal transduction
  3. Bipolar cells code the signal using a graded potential
  4. Ganglion cells generate the AP
    o Other cell types (amacrine and horizontal cells) are responsible for lateral inhibition within the retina
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18
Q

Light is defined by its frequency and intensity. Define both frequency and intensity in relation to light.

A
  • Frequency: defining color (see color due to object absorbing all other wavelengths and the color being seen is reflected to your eye)
  • Intensity: describes brightness
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19
Q

Rods are responsible for __________ vision (the monochromatic vision that occurs in ____ light). The three types of cones (blue, green and red; or Short, Medium and Long wavelength, respectively) have better temporal and spatial resolution than rods, making _________ vision better for discrimination of surfaces and movement under ________ light conditions.

A

scotopic, low

photopic, bright

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20
Q

Phototransduction occurs in four different steps and is used to amplify the light signal. What are the four steps in the activation of rods?

A
  1. Activate the receptor protein (rhodopsin) –> G protein (transducin)
  2. Transducin converts GTP to GDP –> activates phosphodiesterase (PDE)
  3. PDE –> destroys cGMP
  4. decreased amounts of cGMP –> closing of Na+ channels (hyperpolarizing the cell)
21
Q

What are the fundamental steps in the visual cycle for rods?

A
  1. light hits pigment and splits it into its components (opsin and all-trans-retinal)
  2. Bleaching the pigment (= the split)
  3. Pumping of all-trans-retinol into the RPE
  4. All-trans-retinol is made into 11-cis-retinal is then pumped back into the rod or it can combined with the opsin and can be made into rhodopsin (reason why rods are slow)

Note, cones go through a similar cycle, but do so within the cone itself which allows for faster processing

22
Q

What is the cause of dry macular degeneration?

A

Dry macular degeneration develops due to atrophy of retinal pigment epithelia (RPE).

23
Q

What is the cause of wet macular degeneration?

A

Wet macular degeneration develops in deep retinal layers and is caused by growth of blood vessels within the retina resulting in edema and hemorrhage which eventually leads to fibrosis and scarring.

24
Q

What clinical stage of diabetic retinopathy is observed when a patient presents with these fundoscopic findings: blot hemorrhages, cotton wool spots, microaneurysm, macular edema, hard exudates?

A

Nonproliferative diabetic retinopathy (NPDR)

25
Q

What clinical stage of diabetic retinopathy is observed when a patient presents with these fundoscopic findings: intraretinal vasular abnormalities and venous beading?

A

Preproliferative diabetic retinopathy (PPDR)

26
Q

What clinical stage of diabetic retinopathy is observed when a patient presents with these fundoscopic findings: boat hemorrhage (can become floaters in eye), neovascular vitreoretinopathy, vitreous hemorrhage?

A

Proliferative diabetic retinopathy (PDR)

27
Q

Hypertensive retinopathy is caused by narrowing or sclerosis of the arterioles within the eye. This results in what findings upon fundoscopic exam?

A

flame hemorrhages, cotton wool spots, optic nerve edema (severe cases), arteriovenous nicking, “silver wiring”

28
Q

Amaurosis fugax is characterized by sudden loss of vision in one eye which generally lasts only minutes and is painless. Fundoscopic exam reveals what hallmark?

A

Hollenhorst plaque = embolic material (cholesterol) within retinal arteriole

  • Emboli are non-occlusive, are a warning sign for future vascular system disaster, require a carotid US and echocardiogram
29
Q

Patients with ophthalmic migrane present with or without headache (cephalgic and acephalgic, respectively) and claim that they can “see jagged, colorful lines.” What is the hallmark of this condition?

A

Scintillating scotoma whic is painless and temporary (at least 20-30 minutes) and involves both eyes causing temporary hemianopsia. It is treated with migrane medications (triptans) and reassurance.

30
Q

Retinal detachment occurs when the retina is displaced from the back of the eye resulting in what clinical findings?

A

painless, partial vision loss; may be progressive and is sustained (does NOT resolve spontaneously); often accompanied by floaters and photopsias

  • Frequently found in people with myopia
31
Q

What is the hallmark of Retinal Arterial Occlusion (CRAO)?

A

Cherry Red Spot, which indicates acute central retinal artery occlusion, occurs because the rest of retina is pale/swollen/opacified and fovea is not as thick so you can see intact choroidal circulation beneath retina

32
Q

What are some treatments for Retinal Arterial Occlusion (CRAO)?

A
  • Rebreathing CO2: causes arterial dilation within the retina
  • Timolol or levobunolol, 0.5% (lowers IOP)
  • IV acetazolamide, 500 mg (lowers IOP)
  • Massage globe with lids closed: alternating high and low pressure during massage
    • By pushing embolic material to the periphery it can minimize extent of retinal infarction
33
Q

What is the fundoscopic finding upon a diagnosis for Retinal Vein Occlusion (CRVO or BRVO)?

A

“squashed tomato” which denotes diffuse red spots throughout the retina

34
Q

Temporal arteritis (giant cell arteritis) has two causes of vision loss. What are they?

A

Vision loss:
• secondary to retinal arteriolar occlusion or optic nerve infarction
• can be severe involving one or both eyes (may result in total blindness)

35
Q

What deficits are expected in a CN III palsy?

A

Results in ptosis, dilated pupil, eye down and out

36
Q

What deficits are expected in a CN IV palsy?

A

results in paralysis of SO muscle, vertical diplopia, subtle findings

37
Q

What deficits are expected in a CN VI palsy?

A

results in paralysis of LR muscle, affected eye is esotropic (turned in) causing horizontal diplopia

  • May be associated with IOP, often idiopathic
38
Q

What are the eight common causes of red eye?

A
  • Corneal abrasion
  • Corneal laceration
  • Narrow angle glaucoma
  • Subconjunctival hemorrhage
  • Anterior Uveitis (Iritis)
  • Adult conjunctivitis
  • Hyphema
  • Chemical injury
39
Q

Action of phenylephrine?

A

acts on a1 adrenergic receptors and dilates the pupil for a short duration of time

40
Q

Action of epinephrine?

A

Increases aqueous humor outflow and inhibits its formation. Acts on a1, a2, b1, and b2 receptors; a1 dilate pupil

41
Q

Action of nicotine?

A

It indirectly releases NE as it activates nicotinic receptors on the post-g cell.

Also, activates parasympathetics to produce miosis (this is the more common reaction.)

42
Q

Action of cocaine?

A

Cocaine blocks the axoplasmic pump which increase [NE] in the synaptic cleft by preventing NE retuptake.

Will dilate the eye if sympathetic nerves are intact and releasing NE (no effect if have a nerve problem)

43
Q

Action of amphetamine?

A

Amphetamine reverses the axoplasmic pump causing NE to be released from the pre-g cell resulting in more NE in synaptic cleft.

If post-g nerve is present, then there will be pupil dilation in response to amphetamine.

44
Q

Action of atropine?

A

Atropine is an inhibitor of the parasympathetic NS

45
Q

Action of pilocarpine?

A

Will produce miosis. If pilocarpine is active (produces miosis) then the defect MUST be in the nerve.

It is a muscarinic agonist.

46
Q

Action of physotigmine and ecothiophate?

A

These drugs are anitcholinesterases (AChE) –> allow ACh to be in the cleft longer allowing for a parasympathetic response.

47
Q

Action of Terazosin?

A

Terazosin is an a1 antagonist which treats eye disease.

48
Q

Action of reserpine?

A

Reserpine is a NE depleting agent. It blocks granule pump within pre-g allow MAOs to degrade NE within the pre-g terminal.

Can cause miosis and ptosis.

49
Q

Explain how to tell the difference between nerve and eye damage when a person has eye dysfunction.

A

First, test the eyes with light. If they do not respond, test with cocaine to see if the nerve is intact since cocaine needs to have intact pre-g and post-g nerves to elicit the desired response of pupil dilation. If there is not a response, test with amphetamine since it only needs to have the post-g nerve intact to elicit the desired response of pupil dilation. By this method one can deduce if the post-g or pre-g nerve is affected. If these are good, then the eye has a defect.

Neurological Medicine (5 decks)

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