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Block 6 > Week 2 > Flashcards

Week 2 Flashcards

1
Q

What cranial nerves are found on the pons? (4- rule of 4s)

A
  1. V - trigeminal
  2. VI - abducens
  3. VII - facial
  4. VIII - vestibulocochlear
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2
Q

What cranial nerves are found above the pons? (4- rule of 4s)

A
  1. I - olfactory
  2. II - optic
  3. III - oculomotor
  4. IV - trochlear
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3
Q

What cranial nerves are found on the medulla? (4- rule of 4s)

A
  1. IX - glossopharyngeal
  2. X - vagus
  3. XI - accessory
  4. XII - hypoglossal
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4
Q

What cranial nerve moves eyes up, down, medially; raises upper eyelid, constricts pupil, adjusts the shape of the lens of the eye?

A

Oculomotor (III)

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5
Q

What happens to eye if oculomotor nerve (III) is injured or affected?

A

Eye turned down and out, ptosis, pupil dilation (mydriasis), loss of accommodation

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6
Q

What CN moves eye medially and down?

A

CN IV - trochlear (controls superior oblique muscle)

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7
Q

What CN has the function to abduct eye (lateral rectus)

A

CN VI (abducens)

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8
Q

What CN is important for facial expression, closing eye, tears, salivation, taste?

A

CN VII (facial)

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9
Q

Olfactory - CN I
1. Central connection in brain?

A
  1. olfactory bulb

nerve itself starts in the olfactory epithelium of nasal concha

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10
Q

Optic - CN II
1. Central connection in brain? (2)

A
  1. Lateral Geniculate Nuclei (for vision)
  2. Pretectal Nuclei (mediating non-conscious behavioral responses to acute changes in light. - projects to EW nuclei)

Nerve itself starts in the retinal ganglion of the retinal bipolar cells

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11
Q

Vestibularcochlear - CN VIII
1. Central connection in brain for balance and VOR reflex?

but nerve starts in vestibular ganglion of semic ducts+utricle, saccule

A
  1. vestibular nuclei

nerve itself starts in the spiral ganglion of spiral organ

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12
Q

Vestibularcochlear - CN VIII
1. Central connection in brain for hearing?

A
  1. Cochlear nuclei
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13
Q

Where is the origin of the CN III (oculomotor) -> to coordinate eye movements and elevation of eyelid?

A

Oculomotor nucleus

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14
Q

Where is the origin of the CN III (oculomotor) -> to coordinate pupillary constriction and accomodation?

A

Edinger-Westphal nucleus

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15
Q

Where is the origin of the CN IV (Trochlear) -> to coordinate eye movements?

A

Trochlear nucleus (contralateral)

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16
Q

Where is the origin of the CN VI (abducens) -> to coordinate eye movements?

A

abducens nucleus

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17
Q

Where is the origin of the CN V (trigeminal) -> to coordinate mastication and dampening tympanic membrane?

A

Motor trigeminal nucleus

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18
Q
  1. Where is the origin of the CN V (trigeminal) -> to coordinate sensations?
  2. After this where does it project to?
A
  1. Trigeminal ganglion (aka gasserian)
  2. Principal or main spinal trigeminal nuclei
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19
Q
  1. Where is the origin of the CN V (trigeminal) -> to coordinate proprioceptive reflexes?
  2. After this where does it project to?
A
  1. mesencephalic trigeminal nucleus
  2. Motor trigeminal nucleus

reflexes like jaw reflex, lacrimal reflex, etc

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20
Q

Where is the origin of the CN VII (facial) -> to coordinate facial expression and dampening of stapes?

A

facial nucleus

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21
Q

Where is the origin of the CN VII (facial) -> to coordinate lacrimal glands, nasal glands, sublingual glands, submandibular glands?

A

superior salivatory nucleus

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22
Q
  1. Where is the origin of the CN VII (facial) -> to coordinate taste?
  2. After this where does it project to?
A
  1. geniculate ganglion
  2. Nucleus of solitary tract (solitary nucleus)
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23
Q
  1. Where is the origin of the CN IX (glossopharyngeal) -> to coordinate pharynx elevation during swallowing?
A
  1. nucleus ambiguus
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24
Q
  1. Where is the origin of the CN IX (glossopharyngeal) -> to coordinate salivation from parotid gland?
A
  1. inferior salivatory nucleus
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25
Q
  1. Where is the origin (cell bodies) of the CN IX (glossopharyngeal) -> to coordinate taste?
  2. Then where does it project to?
A
  1. inferior (petrosal) ganglion
  2. solitary nucleus (nucleus of solitary tract)
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26
Q
  1. Where is the origin (cell bodies) of the CN IX (glossopharyngeal) -> to coordinate general sensations?
  2. Then where does it project to?
A
  1. superior and inferior ganglia
  2. spinal trigeminal nucleus
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27
Q
  1. Where is the origin (cell bodies) of the CN IX (glossopharyngeal) -> to coordinate chemoreceptor and baroreceptor reflexes?
  2. Then where does it project to?
A
  1. inferior ganglion
  2. solitary nucleus
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28
Q
  1. Where is the origin (cell bodies) of the CN IX (glossopharyngeal) -> to coordinate swallowing and vocalizaiton?
A
  1. nucleus ambiguus
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29
Q
  1. Where is the origin (cell bodies) of the CN XI (accessory) -> to coordinate head and shoulder movement?
A
  1. spinal accessory nucleus in C1-C5 or C6
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30
Q

Peripheral distribution including:
many eye muscles (MR, SR, IR, IO), superior palpebral levator, ciliary ganglion
-> is for what CN?

A

CN III

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31
Q

The CN that has peripheral distribution to:
1. masseter, temporalis, pterygoids, mylohyoid, tensor palatini, anterior belly of digastric, tensory tympani (motor control)
8. face, anterior scalp, oral and nasal cavities, orbit (sensations)
9. muscles of mastication, periodontal membrane, TMJ (reflexes)

A

CN V

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32
Q

The CN that has peripheral distribution to:
1. Facial muscles, stylohyoid, post. belly of digastric, stapedius (motor control)
2. pterygopalatine ganglion -> lacrimal, nasal glands AND submandibular ganglion -> submandibular, sublingual glands (secretory control)
3. taste buds in anterior 2/3 of tongue (taste)

A

Facial nerve

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33
Q

The CN that has peripheral distribution to:
1. stylopharyngeus and superior pharyngeal constrictor (motor control)
2. otic ganglion -> secretion of parotid gland (secretory control)
3. posterior 1/3 of tongue (taste)
4. posterior oral canal, tonsilar region, auditory tube, middle ear (general sensations)
5. carotid bulb and sinus (chemoreceptor and baroreceptor reflexes)

A
  1. Glossopharyngeal (IX)
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34
Q

The CN that has peripheral distribution to:
1. pharyngeal and vocal muscles + sternomastoid and trap muscles (motor control)

A
  1. Accessory (XI)
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35
Q

The CN that has peripheral distribution to:
1. tongue muscles (motor control)

A
  1. hypoglossal (XII)
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36
Q

What CN nuclei are midline in the brainstem?

A

rule of 4
those that 12 can be divided by are in the middle. (ignore the ones that do not have nuclei in the brainstem - CN I and CN II)
1. CN XII, CN VI, CN IV, CN III

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37
Q

What are the 4 midline columns in the brainstem?

A
  1. Motor nucleus
  2. Motor pathway
  3. MLF
  4. Medial Lemniscus

All begin with “M”

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38
Q

What are the 4 lateral columns in the brainstem?

A
  1. Sympathetic
  2. Spinothalamic
  3. Sensory nucleus of CN 5
  4. Spinocerebellar

All start with S (“side”)

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39
Q

If you have injury to motor pathway (midline structure/column) what deficit do you show?

A
  1. contralateral weakness

Motor pathway (corticospinal tract)

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40
Q

If you have injury to medial lemniscus (midline structure/column) what deficit do you show?

A
  1. loss of contralateral proprioception/vibration
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41
Q

If you have injury to medial longitudinal fasciculus (midline structure/column) what deficit do you show?

A
  1. Ipsialteral internuclear ophthalmoplegia (unable to move one eye to a cetain direction - left or right)
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42
Q

If you have injury to motor nucleus and nerve (midline structure/column) what deficit do you show?

A
  1. ipsilateral CN motor loss (3,4,6,12 - midline CN)
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43
Q

If you have injury to spinocerebellar pathway (lateral structure/column) what deficit do you show?

A
  1. ipsilateral ataxia
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44
Q

If you have injury to spinothalamic (lateral structure/column) what deficit do you show?

A
  1. contralateral pain/temp sensory loss
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45
Q

If you have injury to sensory nucleus of CN5 (lateral structure/column) what deficit do you show?

A
  1. ipsilateral pain/temp loss in face

localize to lateral tract - not just the pons since its a large nerve

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46
Q

If you have injury to sympathetic pathway (lateral structure/column) what deficit do you show?

A
  1. Ipsilateral Horner’s Syndrome
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47
Q

what sx should and should not let you localize the injury to CN VIII in the pons?

A
  1. hearing loss - localize to CN VIII in the pons
  2. vestibular signs - these can be medulla and pons
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48
Q

What major artery supplies the midbrain?

A

PCA

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49
Q

What major artery supplies the pons?

A
  1. Lateral - AICA
  2. Medial - Basilar
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50
Q

What major artery supplies the medulla?

A
  1. Lateral - PICA
  2. Medial - ASA (anterior spinal artery)
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51
Q

Locked in Syndrome
1. What is it
2. what causes it

A
  1. Complete paralysis of all voluntary muscles except for the ones that control the movements of the eyes.
  2. Infarct affecting the base of the rostral pons OR infarct in the ventral pons affecting corticospinal tracts and corticobulbar tracts bilaterally (spinal cord and CN recieve no info from cortex
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52
Q

Webers syndrome
1. Can occur with an infarct to … (2)
2. Affects what region of brainstem?

A
  1. Branches of PCA and top of basilar artery
  2. midbrain basis
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53
Q

Benedikt’s syndrome
1. Can occur with an infarct to … (2)
2. Affects what region of brainstem?

A
  1. Branches of PCA and top of basilar artery
  2. Midbrain basis and tegmentum
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54
Q

AICA syndrome
1. What causes it?
2. Affects what region of brainstem?

A
  1. Stroke/infarct
  2. lateral pons
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55
Q

Medial Medullary Syndrome
1. Can occur with an infarct to …

A
  1. Paramedian branches of vertebral and spinal arteries
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56
Q

Wallenberg’s Syndrome
1. Can occur with an infarct to …
2. Affects what part of the brainstem

A
  1. vertebral artery
  2. lateral medulla

Although major a. is PICA, vertebral artery more commonly has infarct

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57
Q

What Meibomian glands?

A
  1. sebaceous glands in the eyelid
  2. Their secretions slow evaporation of tears (arrow)
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58
Q

What is the structure found in the space between the arrowheads?

A

Iris - muscle that contracts to regulate amount of light entering
- covered with melanin to give eye color and reduce light scattering

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59
Q
  1. What is the purpose of the ciliary body?
  2. What does it secrete?
A
  1. stretch the lens - it is attached to the lens by zonula fibers
  2. Secretes aqueous humor to nourish cornea/lens and help maintain eye pressure
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60
Q

Where is the anterior chamber of the eye found between?

A
  1. space between the cornea and the iris
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61
Q

What is the purpose of the canal of Schlemm?

A
  1. collects aqueous humor form anterior chamber and delivers it into the episcleral blood vessels
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62
Q

What structure is considered your blind spot?

A

optic disc bc the optic nerve forms under the optic nerve

optic disc rep start of CN II, where axons of ret. gangl. cells combine

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63
Q

What is the ora serrata?

A

The peripheral termination of the retina wehre there are no more photoreceptors

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64
Q
  1. What is the outermost layer of the retina? (on side of lens)
  2. Purpose:
A
  1. **Retinal pigment epithelium **
  2. Heavily pigment to prevent light scattering
    * holds ends of rods/cones in place
    * metabolic support for rods/cones
    * tight junctions protect retina from blood (immune)
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65
Q
  1. What is the innermost layer of the retina? (on side of optic nerve)
  2. Purpose:
A
  1. inner limiting membrane
  2. contains basal lamina (thin ECM btwn connective tissue and basolateral side of cells) of mueller cells (principal glial cells of retina)
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66
Q
  1. Identify the layer that contains the rods and cones
  2. Name of the layer
A
  1. image
  2. Photoreceptor layer
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67
Q

Rods vs Cones
1. which see black and white vs color

A
  1. Rods see black and white
  2. Cones see color
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68
Q

Rods vs cones
1. What proteins are they assocaited with?

A
  1. Rods - rhodopsin
  2. Cones- iodopsin
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69
Q

What are the three types of cones and what color does each see?

A
  1. I cones -red
  2. M cones- green
  3. S cones - blue
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70
Q

Rods vs Cones
1. One has multiple (rods/cones) that synapse on one ganglion cell
2. One has one (rods/cones) that synpase on one ganglion cell (1:1)

A
  1. Multiple RODS synapse on one ganglion cell
  2. one CONE synpases on one ganglion cell
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71
Q

What is the fovea

A

A small depression in the center of the macula that contains only cones and constitutes the area of maximum visual acuity

fovea is part of macula

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72
Q

What is the macula

A

part of the retina that processes sharp, clear, straight ahead vision

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73
Q
  1. Identify the layer that contains the outer boundary of muller’s cell cytoplasm
  2. Name of the layer
A
  1. outer limiting membrane

“external limiting membrane”

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74
Q
  1. Identify the layer that contains the nuclei of photoreceptor cells
  2. Name of the layer
A
  1. outer nuclear layer
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75
Q
  1. Identify the layer that contains the processes of photoreceptor cells and bipolar cells (synapsing on bipolar cells)
  2. Name of the layer
A
  1. outer plexiform layer
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76
Q
  1. Identify the layer that contains nuclei of muller, bipolar, amacrine, and horizontal cells
  2. Name of the layer
A
  1. inner nuclear layer
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77
Q
  1. Identify the layer that contains axons of bipolar cells and the dendrites of ganglion cells (synapsing on ganglion)
  2. Name of the layer
A
  1. inner plexiform layer
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78
Q
  1. Identify the layer that contains ganglion cell bodies
  2. Name of the layer
A
  1. ganglion cell layer
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79
Q
  1. Identify the layer that contains the efferent axons from ganglion cells
  2. Name of the layer
A
  1. nerve fiber layer
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80
Q

In absence of light [hyperpolarization/depolarization] occurs in rod

A

depolarization - glutamate is released constantly

similar in cone

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81
Q

In presence of light [hyperpolarization/depolarization] occurs in rod

A
  1. membrane is hyperpolarized - glutamate release is halted
  2. leads to reduced release of NT to bipolar cells

similar in cone

82
Q

How does retina transmit visual info to the brain
1. Light - stops release of NT glutamate
2. (Blank A)
3. (Blank B)

A
  1. less glutamate causes bipolar cells to open voltage gated Ca2+ channels which depolarizes bipolar cells
  2. Bipolar cells trigger ganglion cell depolarization -> AP moves through optic nerve and eventually to brain
83
Q

Differentiate between open angle and closed angle glaucom?

A
  1. open angle - drainage angle remains open but trabecular meshwork at the drainage point is blocked so fluid cannot circulate
  2. closed angle - iris pushes forward onto cornea and closes off the drainage of fluid through the canal of schlem (increasing fluid and pressure)
84
Q

Pilocarpine
1. MOA and how it helps glaucoma

A
  1. (M3) muscarinic agonist - mimics ACh to activate M3 -> causes contraction of iris smooth muscle to open the anterior chamber angle more and drain aquous humor
85
Q
  1. What drug is used to reduce fluid formation in open angle glaucoma?
A
  1. Carbonic anhydrase inhibitors ending in -zolamide
86
Q

Two drug names that are alpha 2 agonists -> inhibit (aqueous humor) fluid secretion in eye

A
  1. brimonidine
  2. apraclonidine

glaucoma

87
Q

Drug name of a beta 1 antagonist -> inhibit fluid secretion

glaucoma

A

Timolol

It’s non-selective B blocker - but its effect on beta 1 is what matters

88
Q

Drug name of a non-selective alpha and beta agonist -> inhibit fluid secretion

A

Dipivefrin

89
Q

What is first line treatment for glaucoma (2)

A
  1. Beta blockers (Timolol)
  2. Prostaglandin analogs (Latanoprost or Travoprost)
90
Q
  1. What drugs used for glaucoma are prostaglandin analogs?
  2. MOA
A
  1. Latanoprost or Travoprost
  2. Agonist on prostanoid receptors - induce synthesis of prostaglandins and MMP-1 to cause remodeling of ciliary body and increase outflow
91
Q

2nd line treatment of glaucoma (2)

A
  1. alpha agonists (brimonidine, apraclonidine)
  2. CA inhibits (-zolamide)
92
Q

3rd line treatment for glaucoma (1)

A
  1. Cholinergic agonists (pilocarpine)
93
Q

Common fixed combination of meds for glaucoma
1. Beta blocker (Blank A) + CA inhibitor (Blank B)

A
  1. Timolol (Blank A)
  2. Dorzolamide (Blank B)
94
Q

Common fixed combination of meds for glaucoma
1. Beta blocker (Blank A) + Alpha 2 agonist (Blank B)

A
  1. Timolol
  2. Brimonidine
95
Q

Common fixed combination of meds for glaucoma
1. CA inhibitor (Blank A) + Alpha 2 agonist (Blank B)

A
  1. Brinzolamide
  2. Brimonidine
96
Q

What glaucoma drug is contraindicated for patients with hepatic cirrhosis?

A

CA inhibitors

97
Q

What glaucoma drug is contraindicated for patients with Asthma or COPD?

A

Beta blockers - Timolol

98
Q
  1. What is proptosis?
  2. What are some causes
  3. Treatment?
A
  1. the bulging of one or both or your eyes from their natural position
    Causes
  2. Inflammatory processes (thyroid orbitopathy, idiopathic orbital inflammation, etc)
  3. Neoplastic (primary tumors that are benign or malignant, mets)
  4. variety of things depending on cause: meds, sx, radiation, chemo, etc
99
Q

Myopia
1. What is wrong with focal point?
2. What things can cause this (think structure of eye parts)
3. is far or near sight hard?

A
  1. Focal point is in front of the retina
  2. Either eye is too long or cornea has too much curvature
  3. Can’t focus on objects far away (nearsightedness)
100
Q

Myopia
1. What lense helps with myopia?

A
  1. A negative lens
101
Q

Hyperopia
1. What is wrong with focal point?
2. What things can cause this (think structure of eye parts)
3. is far or near sight hard?

A
  1. Focal point is behind the retina
  2. Eye is too short or cornea has too little curvature
  3. Can’t focus on objects nearby (farsighted)
102
Q

Hyperopia
1. What lense helps with Hyperopia?

A

A positive lens (like magnifying glass)

103
Q

Astigmatism
1. What is wrong with focal point?
2. What things can cause this (think structure of eye parts)
3. is far or near sight hard?

A
  1. There are multiple focal points
  2. uneven curvature of cornea
  3. objects appear blurry
104
Q

What is presbyopia?

A

Lens harden with age and are unable to chnage shape - causes farsightedness

105
Q

What are the 4 overarching causes of conjunctivitis (inflammation of white part of eye)

A
  1. Bacterial (S. pneumo, S. Aureus, etc) - purulent discharge
  2. Viral (adenovirus, HSV-1, measles) - watery discharge
  3. Allergic (this presents as both eyes affected)
  4. Immune (SJS, reactive arthritis)
105
Q

What can increase risk for cataracts in adults? (5)

A
  1. older age
  2. smoking and alcohol
  3. excessive sunlight
  4. Trauma, infection
  5. Increased glucose (diabetes) or galactose (aldose reductase acts on these and creates substances that increase lens osmolarity -> cataracts)
106
Q

What can cause cataracts in infants or young adults? (3)

A
  1. Classic galactosemia (increases galactose)
  2. Galactokinase deficiency (increases galactose - mild form than #1)
  3. TORCH infections (for ex: congenital rubella syndrome)
107
Q
  1. What is sympathetic ophthalmia?
  2. What causes this/starts this?
  3. What type of reaction occurs?
A
  1. a rare type of uveitis that causes small abnormal clumps of cells (granulomas) to form
  2. Penetrating eye injury that allows lymphatics to have acces to retinal antigens
  3. this leads to Type IV hypersensitivity reaction to injured and non-injured eyes -> eventually see granulomas form
108
Q

What is included in the uvea?

A
  1. iris, ciliary body, and choroid
109
Q

Differentiate non-rhegmatogenous retinal detachment from Rhegmatogenous retinal detachment?

A
  1. non-rhegmatogenous retinal detachment: no retinal break
  2. rhegmatogenous retinal detachment: retinal break
110
Q

What is diabetic retinopathy?

A
  1. Damage to retina caused by damage to retinal blood vessels
111
Q

What is Non-proliferative diabetic retinopathy?

A
  1. Structural changes within the retina such as microaneurysms, retinal hemorrhoages, macular edema, exudates
112
Q

What is proliferative diabetic retinopathy?

A
  1. appearance of new vessels that sprout (due to VEGF) from existing vessels
  2. These new cells have hemorrhage and can cause scarring
113
Q
  1. What is copper wire or silver wire change in retina?
  2. What disorder does this occur with?
A
  1. where the walls of the arterioles become thickened and sclerosed causing reflection of light
  2. Hypertensive retinopathy
114
Q
  1. What is A/V nicking in eye?
  2. What disorder does this appear with?
A
  1. On exam, a small artery is seen crossing a small vein - results in compression of vein due to arteriosclerosis of arteries
  2. hypertensive retinopathy
115
Q

What is central retina vein occlusion (CVRO)

A

Blockage of venous drainage from the retinal veins -> leads to increased pressure and causes hemorrhage and edema

116
Q

What condition of the eye is this an image of?

A

central retinal vein occlusion

117
Q
  1. What is central artery occlusion?
  2. What indicators are found on retina?
A
  1. total occlusion of central retinal artery which causes difuse infarct of retina
  2. chery red spot, retina is opaque + sudden loss of vision
118
Q
  1. What is retinitis pigmentosa?
  2. What causes it?
  3. What is seen on the retina?
A
  1. loss of rods, cones, and retinal pigment epithelium.
  2. Inherited gene mutations affecting rods, cones, and RPE
  3. constricted retinal vessels and optic atrophy (waxy pallor), pigment change
119
Q

What is age-related macular degeneration?

A
  1. deterioration of the macula that can be either wet or dry
120
Q

differentiate dry vs wet age related macular degeneration?

A
  1. Dry- Atrophic/non-neovascular -> diffuse discrete deposits (bruising), gradual visual loss
  2. Wet - Exudative/neovascular -> rapid and severe visual impairment with choroidal neo-vascularization
121
Q

How is wet age related macular degeneration treated?

A

given anti-VEGF agents, laser, or photodynamic therapy

122
Q

Is this wet or dry age related macular degeneration?

A

Wet - pointin at neo-vascularization

123
Q

Is this wet or dry age related macular degeneration?

A

dry - this is “bruising” or the discrete deposits

124
Q

What is the pathophysiology of papilledema?

A
  1. Increased ICP can cause venous stasis and stasis of axoplasmic transport (optic nerve) -> leads to optic nerve edema
125
Q
  1. What signs are evident on the retina that has papilledema
  2. What sx may pt have
A
  1. blurred disc margins, enlarged blind spot bc retina can be displaced laterally
  2. headache and transient visual black outs
126
Q
  1. What is pathophysiology of anterior ischemic optic neuropathy?
  2. what are the two types?
A
  1. acute ischemia to the optic nerve head
  2. Non-arteritic vs arteritic
127
Q

Differentiate non-arteritic vs arteritic anterior ischemic optic neuropathy?

A
  1. Non-arteritic -> (more common) due to transient hypoperfusion of the optic nerve -pt usually ahs CV disease
  2. Arteritic - due to giant cell arteritis (inflammatory disease affecting the large blood vessels)
128
Q
  1. What would you see in the eyes of a patient with anterior ischemic optic neuropathy?
  2. sx for the patient
A
  1. blurred disc margin and disc pallor
  2. Amaurosis fugax (transient vision loss), Pain in the temples, Pain when chewing, General fatigue,
129
Q
  1. What is the pathophysiology of optic neuritis?
  2. What do you see in the eye?
  3. Pt sx?
A
  1. inflammation of the optic nerve - most commonly due to autoimmune inflammatory demyelination
  2. disc margin is blurred and elevated optic disc
  3. pain with eye movement, vision loss, impaired color vision
130
Q

What is the most common primary malignant intraocular tumor in children?

A

Retinoblastoma

131
Q

Retinoblastoma
1. Mutation in what allele(s)?
2. Clinical presentation?
3. Where is the mass found?

A
  1. mutation in both alleles of Rb gene
  2. Leukocoria (white pupil), Strabismus (miss alignment of the eyes/crossed eyes), Pseudohypopyon (image)
  3. occupies vitreous cavity
132
Q

What does histology show of the retinoblastoma tumor?

A
  1. island of blue cells in sea of pink necrosis
133
Q

What is the most common primary malignant intraocular tumor in adults?

A

Uveal melanoma

134
Q

Uveal Melanoma
1. Pathophysiology
2. Mode of spread
3. shape of tumor in eye

A
  1. cancer that begins in the melanin of the eye (part of the iris which is part of the uvea)
  2. Spread hematogenously (via blood) to liver. Lymphatic spread is rare
  3. tumore is dome shaped or mushroom shaped
135
Q

Histological features of uveal melanoma?

A
  1. spindle shaped cells/formation
  2. Epithelioid cell - cells that are derivatives of activated macrophages resembling epithelial cells
136
Q

What is the most common malignant intraocular tumor in general?

A

metastases to the eye

137
Q

Signals from retina go to what part of the thalamus?

A

LGN

138
Q

After visual inputs go into the LGN (of thalamus) -> it proceeds into occipital lobe and then 2 different parts of cortex. What are they

A
  1. Meyer’s Loop (temporal lobe)
  2. Parietal lobe
139
Q
  1. What is anopia?
  2. What is a common cause of this
A
  1. complete vision loss in one eyeball due to optic nerve or retina of one eye being defected
  2. optic neuritis
140
Q
  1. What is amaurosis fugax? (type of anopia)
  2. Usually a cause of what
A
  1. fleeting darkness - painless, transient vision loss in one eye due to damage to optic nerve or retina
  2. TIA (transient ischemic attack), embolism
141
Q

Bitemporal Hemianopsia
1. How does this present in pt?
2. Lesion to what part of visual pathway
3. Caused by what

A
  1. unable to see lateral fields of both eyes
  2. optic chiasm - since lateral fields are right in the middle of the optic chiasm
  3. something compressing optic chiasm like pitutiary tumor or aneurysm
142
Q

Homonymoous Hemianopsia
1. How does this present in pt?
2. Lesion to what part of visual pathway
3. Caused by what

A
  1. loss of same visual field (either left or right)
  2. Lesion to the optic tract or parietal lobe on either side (injury behind optic chiasm)
  3. potentially a PCA stroke (PCA supplies occipital lobe)
143
Q

Quadrantic Anopia
1. How does this present in pt?
2. Lesion to what part of visual pathway
3. Caused by what

A
  1. when one quadrant of the visual field is lost
  2. Lesion to nerve fibers going from LGN to posterior lobe
  3. either temporal or parietal lobe damage
144
Q

Quadrantic Anopia
1. What does it mean if the lost quadrant of vision is the upper left/right quadrant
2. What does it mean if the lost quadrant of vision is the lower left/right quadrant

A
  1. temporal lobe damage
  2. parietal lobe damage
145
Q

Constriction of pupil
1. Is this parasympathetic or sympathetic control?

A
  1. parasympathetic control
146
Q

Constriction of pupil
1.What is the two neuron pathway for this action? (2)

A
  1. Start at Edinger-Westphal nucleus in the midbrain
  2. Nerve fibers from here enter orbit ALONG WITH CN III
  3. Synapse on ciliary ganglion behind eye (1st neuron)
  4. Ciliary ganglion signals sphincter pupillae (2nd neuron) -> activates Muscarinic receptor via ACh

ciliary ganglion has parasympathetic nerve fibers that come from CN III

147
Q

Dilation of pupil
1. Is this under parasympathetic or sympathetic control?

A
  1. sympathethic control
148
Q

Dilation of pupil
1. Describe the pathway to cause this action (3)

A
  1. Start at hypothalamus - nerve fiber goes to the spinal cord at Ciliospinal center of budge (C8-T12) (1st neuron)
  2. 2nd neuron exits spinal cord at T1 and travels with cervical sympathetic chain up to superior cervical ganglion (2nd neuron)
  3. 3rd neuron exits this ganglion and courses along ICA, through cavernous sinus, to **dilator pupillae muscle ** (3rd neuron)
149
Q

What three things happen during the accommodation reflex?

A
  1. convergence - eyes move medially to track object
  2. ciliary muscle changes shape of lens
  3. miosis - pupillary constriction to block divergent light rays from near object
150
Q
  1. What is afferent pupillary defect? (APD)
  2. What defect or issue can cause this
A
  1. when light shone in 1 eye produces less constriction when compared to the other eye (uneven level of constriction) - there is a problem picking up light in one eye
  2. issue in afferent aspects of pupillary constriction pathway. This can be due issues in optic nerve (optic neuritis), retinal defect, or even retinal artery occlusion
151
Q

Adie’s Tonic Pupil
1. How does it present
2. What is the pathophysiology?

A
  1. Dilated pupil on one side. Constriction still occurs (accomodation) when fixating on near object but when fixating on distant object it slowly dilates (after having been constricted when looking at nearby object)
  2. Due to parasympathetic innervation to one eye is blocked -> thus inhibiting constriction.

Most cases are idiopathic but can be due to harm of ciliary ganglion

152
Q

Third Nerve Palsy
1. How does it present (3)
2. What is the pathophysiology?

A
  1. persons affected eye is looking down and out, pupil is typically dilated, ptosis
  2. CN III is no longer functioning -> which controls many rectus muscles of the eye (leaving LR and SO unopposed - causing movement of eye), pupillae sphincter (thus unable to constrict), and levator palpebrae muscle (causes ptosis)
153
Q

When there is a lesion of CN III a person will have eye down and out but pupil can be dilated or not
1. Pupil dilation
2. Absence of pupil dilation
What does this mean

A
  1. This means parasympathethic nerves are impacted. Parasympathetic nerves run on outside of CN III and can be easily compressed by mass like Pcomm aneurysm
  2. This means there is CN III ischemic nerve damage - spares superficial parasympathetic nerves
154
Q

Horner Syndrome
1. How does it present
2. What is the pathophysiology?

A
  1. small pupils (miosis), ptosis, anhidrosis
  2. disruption of sympathetic chain connection to face.
    - Pupils are constriction (loss of sympathetic control of dilation), ptosis (lack of sympathetic control over superior tarsal muscle), anhidrosis (sweating is under sympathetic control)

many causes to this bc sympathetic chain is long and passes many things

155
Q

What is the cocaine dx test for horner’s syndrome

A
  1. Cocaine can cause pupillary dilation in normal eye but if it’s horner syndrome there will be no dilation even with cocain applied to eye
156
Q

What is the Apraclonidine dx test for horner’s syndrome

A
  1. apraclonidine is an alpha agonist that leads to pupillary dilation.
  2. If pupil dilates this indicates MUSCLE WORKS its just missing sympathetic innervation -> Horner’s syndrome
157
Q

Argyll-Roberston Pupil
1. How does this present as?
2. What is the pathophysiology?
3. What is strongly associated with? (disease)

A
  1. bilateral small pupils - no constriction to light but there is constriction to accomodation
  2. Tertiary syphilis affects the pretectal nucleus which signals constriction in response to light. BUT this is process is not involved in accomodation reflex
  3. tertiary syphilis
158
Q

CN IV/Trochlear Palsy
1. What does patient present with?
2. pathophysiology?
3. How does pt compensate

A
  1. affected eye turns up and outwards, diplopia, unable to look down while reading or going down stairs
  2. injury or defect in CN IV - (Remeber SO4)
  3. PT will tilt their head away from affected side to normalize/straighten affected eye
159
Q

CN VI/Abducens Palsy
1. What does patient present with?
2. pathophysiology?

A
  1. Affected eye is pulled medially at rest and when looking laterally affected eye won’t move because LR is affected
  2. Remember LR6
160
Q

Calroic Reflex Testing
1. What reflex does this test
2. How to do it (2 ways) and what results mean

A
  1. Vestibulo-ocular reflex
  2. Horizontal testing: COWS - cold, opposite; meaning eye move toward ear with cold water and then go away/opposite. Then with warm water, eye moves away from ear with warm water and then comes back/same (in normal responses)
  3. For vertical testing: For cold water both eyes go down and for warm eyes deviate upward in normal responses
161
Q

What is the Oculocephalic Reflex

A

Keeping the line of sight stable in space while head is moving

162
Q

What is the VOR reflex

A

This reflex keeps us steady and balanced even though our eyes and head are continuously moving when we perform most actions

163
Q

What does cavernous sinus syndrome present with (4)

A
  1. presents with variable ophthalmoplegia (paralysis of eye muscles)
  2. decreased corneal sensation
  3. Horner syndrome
  4. occasional decreased maxillary sensation

but also -> proptosis, headache, decreased facial sensation

164
Q

What is cavernous sinus sinus due to?

A
  1. 2° to pituitary tumor mass effect
  2. carotid-cavernous fistula
  3. cavernous sinus thrombosis related to infection.
165
Q
  1. What CN are involved in superior orbital fissure syndrome
  2. What sx are seen due to the CN affected
A
  1. CN III, IV, V (V1 part), and VI
  2. ptosis, proptosis, fixed dilated pupil, lacrimation, hyposecretion, loss of corneal reflex, opthalmoplegia
166
Q

Ocular Myasthenia Gravis
1. What does pt present with (4)

A
  1. Eyelid fatigueability
  2. Cogan’s lid twitch (after downgaze, upgaze produces affected lid to overshoot up and then it comes down again)
  3. Curtain sign (passively lifting a ptotic lid may cause the opposite lid to fall)
  4. Peek sign (fatigue in orbicularis oculi can cause involuntary opening of the eyes/less burying of the eyelashes as the patient tries tight shuting eyes)
167
Q

Ocular Myasthenia Gravis
1. pathophysiology

A
  1. A form of myasthenia gravis (MG)
  2. The muscles that move the eyes and control eyelids are easily fatigued and weakened. Due to antibodies attacking postsynpatic ACh receptor
168
Q

Vertical Gaze
1. Where in the brain is it controlled?
2. Lesions to what part of this brain can cause a vertical gaze palsy

A
  1. midbrain
  2. riMLF (rostral interstitial nucleus of medial longitudinal fasciculus) or interstitial nucleus of caja
169
Q

Internuclear Ophthalmoplegia (INO)
1. What kind of palsy is this? (vertical or horizontal)
2. What does the patient present with?

A
  1. horizontal
  2. Weak ADDUCTION (MEDIAL MOVEMENT) of one eye. While the other eye develops nystaglus since it recognizes eyes are not aligned.
170
Q

Internuclear Ophthalmoplegia (INO)
1. What is the lesion for this issue?
2. What disorder most often leads to this?

A
  1. Medial Longitudinal Fasciculus
  2. MS affecting myelination of MLF
171
Q

Ipsilateral Gaze Palsy
1. How does the patient present
2. What lesion(s) causes this

A
  1. Paralysis of gaze to the side of lesion for both eyes (can’t look to side of lesion)
  2. Medial pons lesion -> PPRF is located here
  3. If lesion is in Abducens (VI) nucleus then this is the same
172
Q

One and a Half Syndrome
1. What does patient present with (ex: patient tries to look to left)
2. What lesion/damage is this due to

A

Ex: patient tries to look to left
1. Patient cannot look left when trying to look left. Patient cannot turn left eye to right when trying to look right.
2. Lesion to PPRF and MLF from same affected side as PPRF

173
Q

Skew deviation
1. How does patient present?
2. Pathophysiology?

A
  1. vertical misalignment of the eyes
  2. Abnormal prenuclear vestibular input (info on change in position, direction, or movement of head) to the ocular (CN III) motor nuclei
    –> this is most commonly due to brainstem or cerebellar stroke. Other causes include multiple sclerosis and head trauma.
174
Q

Parinaud Syndrome
1. vertical or horizontal palsy?
2. How does patient present (4)

A

-> vertical gaze palsy
1. Difficulty looking up (paralysis of up gaze)
2. Light-near dissociation/Pseudo Argyll Roberston Pupil (Pupillary light reaction is impaired while the accomodative response remains intact)
3. Convergence-retraction nystagmus (irregular, oscillating movements of eyes- particularly with upward gaze and saccades upward)
4. Collier’s Sign (eyelid retraction)

175
Q

Parinaud Syndrome
1. Where is lesion found?

A
  1. posterior midbrain (superior colliculus and pretectal area) -> these areas coordinate upward gaze
176
Q

CN III
1. Somatic motor function ->
2. Parasympathetic function ->

A
177
Q

CN V
1. General somatic sensory function ->
2. Branchial motor function ->

A
178
Q

CN VII
1. Branchial motor function ->
2. Parasympathetic function ->
3. Visceral senosry (special) function ->
4. General somatic sensory function ->

A
179
Q

Which three CN have special somatic sensory functions

A
  1. CN I - smell
  2. CN II - vision
  3. CN VIII - hearing and vestibular sensation
180
Q

CN IX
1. Branchial motor function
2. Parasympathetic function
3. General somatic sensory function
4. Visceral sensory (special) function
5. Visceral sensory (general) function

A
181
Q

CN X
1. Branchial motor function
2. General somatic sensory function
3. Visceral sensory (special) function
4. Visceral sensory (general) function

A
182
Q

What are branchial motor fibers compared to somatic motor fibers?

A

branchial motor fibers are just fibers that innervate structures derived from the pharyngeal arches

183
Q

Tests for swallowing, phonation, elevation of the palate, and gag reflex are all to test what two CN?

A
  1. CN IX and X
184
Q

What is anosmia

A

loss of sense of smell

185
Q

What is the function of the nucleus solitarius (nucleus in the medulla)

A

Taste afferent from (VII, IX, and X) and visceral afferent of CN IX and X

186
Q

Function of the Nucleus ambiguus

A

location of cell bodies of motor nerves that innervate the ipsilateral muscles of the soft palate, pharynx, larynx and upper esophagus and are mainly responsible for swallowing and speaking

187
Q

What CN are purely motor?

A
  1. III, IV, VI, XI, and XII
188
Q

What CN are purely sensory?

A
  1. I, II, VIII
189
Q

What CN are both sensory and motor?

A
  1. V, VII, IX, X
190
Q
  1. What is nervus intermedius?
  2. Where is it located
A
  1. Part of facial nerve that carries sympathethic and sensory fibers.
  2. Between motor component of CN V and CN VIII
191
Q
  1. What causes a stye
  2. What causes a chalazion
A
  1. painful inflammation of sebaceious gland of the eyelash
  2. PAINLESS - inflammation of the tarsal gland
192
Q

Primary open angle vs 2ndary open angle glaucoma

A
  1. primary - an open, normal appearing anterior chamber angle and raised intraocular pressure (IOP), with no other underlying disease
  2. Secondary - when there is an identifiable underlying cause for raised IOP, this is termed secondary glaucoma. (still showing open angle)
193
Q

Primary closed angle vs 2ndary closed angle glaucoma

A
  1. closed angle due to pupillary block (image)
  2. due to a secondary disease
194
Q

Optic nerve cupping

A
  1. This occurs in glaucoma - increased intraocular pressure
195
Q

What changes occur to the lens in cataract formation?

A

Age-related nuclear sclerosis of the lens.
1. This change causes opacification because of compression of the lens fibers in the central (nuclear) portion of the lens.
2. As the yellow color of the lens increases, patients may notice a subjective difference in their evaluation of colors.

196
Q

What is the best drug to treat open angle glaucoma

A

Bimatoprost is the most effective drug to date in the treatment of open-angle glaucoma. It increases both the trabecular and uveoscleral outflow. (prostaglandin analog)

197
Q

What is a central scotoma

A

A central scotoma is a grey, black, blurry or blind spot in the middle of one’s vision. This central blind spot can be due to geographic atrophy (advanced dry macular degeneration) or to the damage of photoreceptor cells from choroidal neovascularization (leaking blood vessels).

198
Q

Giant cell arteritis
1. How does this affect retinal artery?
2. sx presentation

A
  1. granulomatous inflammation in the central retinal artery
  2. headache, tenderness to palpation over temple, jaw claudication, fatigue, vision loss + afferent pupillary defect,
  3. Retinal whitening with cherry red spot
199
Q

What is the function of the retinal pigment epithelium?

A
  1. Process of retinal pigment regeneration
  2. it regulates the transport of nutrients and waste products to and from the retina, it contributes to outer segment renewal by ingesting and degrading the spent tips of photoreceptor outer segments, it protects the outer retina from excessive high-energy light and light-generated oxygen reactive species and maintains retinal homeostasis through the release of diffusible factors
200
Q
  1. How does the superior oblique move the eye?
  2. How does the inferior oblique move the eye?
  3. How does the superior rectus move the eye?
  4. How does the inferior rectus move the eye?
A
  1. down and out
  2. up and out
  3. up and in
  4. down and in

Block 6 (9 decks)

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