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Neuro > Exam 3, week 2 > Flashcards

Exam 3, week 2 Flashcards

1
Q

What are the basal ganglia disorders?

A

Tremor (resting)
Hypokinetic (Rigidity, Bradykinesia)
Hyperkinetic (Chorea, Athetosis, Akathisia)

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2
Q

What are the cerebellar disorders?

A 
Synergy (3 D's: Dysmetria, Dysdiadochokinesia, Decomposition of Movement)
Equilibrium (Dysequilibrium)
Tone (hypotonia)
Tremor (usually action)
Nystagmus
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3
Q

What are the 3 patterns of pathologically increased tone

A

Rigidity
Spasticity
Gegenhalten - paratonia; pt actively opposes any passive motion

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4
Q

What is rebound?

A

Increased range of movement with lack of normal recoil to original position. Seen in cerebellar diseases

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5
Q

What is positive Romberg?

A

Impaired proprioception, vestibular function, and cerebelar function

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6
Q

Pronator Drift is caused by?

A

Pyramidal tract dysfunction
Cerebellar dysfunction
Parietal Lobe Dysfunction

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7
Q

4 types of eye movements

A
  1. Smooth Pursuit - Tracking
  2. Saccades - Jumps of eyes
  3. OKN; VOR
  4. Vergence
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8
Q

4 functions of the optic n.

A

Pupillary light reflex (aferent CNII)
Visual acuity
Visual Field
Color vision

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9
Q

What are Lewy Bodies?

A

Spherical eosinophilic intraneuronal cytoplasmic inclusions

Filaments composed of synuclein

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10
Q

CN VI controls which muscle?

A

Lateral Rectus (ipsilateral)

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11
Q

Who coordinates voluntary saccadic eye movement?

A

PPRS

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12
Q

Damage to Vestibular ocular reflex (specifically MLF) causes?

A

Internuclear Opthalmoplegia (INO). Associated with MS because MLF is very long and vulnerable to demylination (source of double vision), deficit in medial rectus movement

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13
Q

On the opthalmoscope, which light would you use to visualize vasculature?

A

Green Light (red free)

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14
Q

What do the numbers on the wheel of the opthalmoscope?

A

Ability of the lens to bend light.
Red lenses gets more powerful at bending light
Green lenses gets less powerful

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15
Q

When testing for brainstem death, ice water can be placed in the ear to?

A

Inhibits the ipsilateral vestibular nuclei. See the eyes drift towards the irrigated ear because the contralateral nuclei is pushing the eye medially (loss of the opposing muscle).
Need negative response on both sides to say that the brainstem is dead. Loss on one side = focal lesion

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16
Q

What is a sign of a CNVI lesion

A

Loss of Lateral movement of the ipsilateral eye

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17
Q

Symptoms of CNIII palsy?

A

Closure of the upper lid (levator labii)
Affected eye is stuck laterally (CNVI is intact pulling laterally without opposition)
See rotation of the eye - CNIV is intact

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18
Q

Superior oblique controls (CNIV)

A

Downward movement of the medially deviated eye

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19
Q

Inferior oblique controls (CNIII)

A

Upward movement of the medially deviated eye

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20
Q

Nystagmus is named based on the?

A

Direction of the saccadic movement

Downward, upward etc

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21
Q

What is Horner’s syndrome?

A

Pupils may look even in the light, but in the dark the affected eye is unable to fully dilate (CNIII lesion)

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22
Q

What is diffuse lewy body disease?

A

Similar to PD but has more Lewy Body distribution in the brain
Associated with dementia (DLB if within a year, PDD if 10+ years following PD onset)
Often coexists with AD plaque (neurofibrillary tangles

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23
Q

What is Progressive Supranuclear Palsy

A

Tau + neurofibrillary tangles in the pallidum, subthalamic nucleus, substantia nigra, or pons
May have frontotemporal cortical atrophy (neuron, glial loss)
Tau inclusions, “4R” Tau

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24
Q

Pathophysiology of Progressive supranuclear Palsy?

A

Degeneration of migrostriatal system, paramedian brain stem, cerebellar “roof” nuclei
Degenerating neurons have “globose” Tau neurofibrillary tangles

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25
Q

What is corticobasal degeneration?

A

Tau (“4R” Tau), “astrocytic plaques”
Cerebral cortical atrophy, Tau inclusions in substantia migra
Tau inclusions associated with the four microtubule binding domains

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26
Q

What is multiple systems atrophy?

A

Glial (esp. oligodendroglial) alpha synuclein-immunoreactive inclusions
Striatonigral degeneration -> putamenal atrophy (grey green discoloration), loss of white matter tracts

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27
Q

Multiple system Atrophy affects which regions?

A

Striatoniagram degeneration
Pontocerebellar atrophy
cerebellar atrophy
olivocerebellar atrophy
Interomediolateral column degeneration (Shy-Drager syndrome)
Hallmark: argyrophilic glial cytoplasmic inclusions are alpha-synuclein immunoreactive

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28
Q

Describe Huntington Disease

A

AD CAG repeats Chr 4
Caudate atrophy - “medium spiney neurons”
Dementia, frontal lobe degeneration

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29
Q

What is degenerative ataxia?

A

Hereditary degenerative ataxias:
Spinocerebellar ataxia (SCA1-36)
Freidreich ataxis
Also non-hereditary ataxias

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30
Q

What are the “generic” patterns of degeneration in ataxias

A

“Primary” cerebellar cortical degeneration with olivocerebellar and spinocerebellar tract degeneration.
Olivopontocerebellar

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31
Q

What is cerebellar cortical degeneration?

A

Primary or secondary
Atrophy of cerebellar folia involving cortex and white matter
Bergmann gliosis
Loss of Purkinje cells (empty baskets, torpedoes)

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32
Q

What is Friedreich’s Ataxia?

A

about half of all ataxias
ar, Chr 9q (frataxin) GAA
Affect neurons in DRG (sensory neuropathy, “nodules of Nageotte”) and degenernation of peripheral sensory fibers and dorsal columns
Secondary degeneration of cuneate and gracile nuclei, cerebellar efferents

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33
Q

The cerebral cortex is the outter layer of the brain and is made up by?

A

The neocortex (six layers)

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34
Q

The hippocampus is phylogentically older and is made up by the

A

allocortex (three layers)

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35
Q

What is the makeup of the cortical macroconnectivity?

A

Cortical areas are linked by white matter tracts with adjacent corticies and subcortical structures

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36
Q

What are the 2 main categories of cortical disorders?

A
  1. Diffuse - Degenerative (AD), metabolic (hypoxia)

2. Focal - vascular (stroke), traumatic (contusion), neoplastic (tumor)

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37
Q

Lesions of the cortex can be divided into 4 groups

A

Frontal
Temporal
Parietal
Occipital

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38
Q

How did we discover the corticical functions?

A

By studying the cognitive deficits from strokes (the lesion method). Especially MCA strokes since they have the largest distribution

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39
Q

What are the types of damage seen in TBI cases?

A

Contusion
Bleeding (intraparenchymal, subdural, epidural)
White matter damage - DAI
All except DAI can be seen on imaging

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40
Q

Differences between benign and malignant brain tumors

A

Benign - compressive
Malignant - infiltrative
Also diffuse effects (edema, mass effect)

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41
Q

Functions of the Frontal lobe?

A 
Voluntary movement
Language production (left)
Motor prosody (right)
Comportment
Executive function
Motivation
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42
Q

Functions of the Temporal lobe

A 
Audition
Language comprehension (L)
Sensory prosody (R)
Memory 
Emotion
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43
Q

Functions of the Parietal lobe

A 
Tactile sensation
Visuospatial function (R)
Attention (R)
Reading, Writing (L)
Calculation (L)
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44
Q

Functions of the Occipital lobe

A

Vision
Visual perception
Visual receognition

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45
Q

Symptoms of Frontal lobe lesions

A

Deficit in motor function (UMN), language, prosody, and neuropsychiatric disorders
Neurobehavioral effects are florid and persistant with bilateral lesions

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46
Q

Broca’s aphasia was discovered on a patient that had lesions where?

A

Large cerebral infarct in the left frontal lobe -> Right hemiparesis and impaired speech

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47
Q

What is prosody?

A

The emotional content of language (right hemisphere)

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48
Q

What is motor aprosody and where would you find the lesion?

A

Failure to inflect speech with emotion.

Lesion of the right inferior frontal gyrus

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49
Q

What are the 3 main frontal lobe syndromes and where are the lesions?

A

Disinhibition - orbitofrontal cortices
Executive dysfunction - dorsolateral prefrontal cortices
Apathy - medial frontal cortices

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50
Q

What is comportment?

A

Capacity to maintain an appropriate behavioral repertoire in the face of social situation where limbic drives are influential and impulse control is critical.

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51
Q

What is disinhibition?

A

Disturbance in comportment. Pt’s are irritable, loss of empathy, impusivity, hypersexual, hyperphagia, and violence

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52
Q

Propensity for violence is associated with damage to

A

The frontal lobes. Vietnam study

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53
Q

What is executive dysfunction?

A

Implies frontal lobe damage

Perseveration (impairment to shift responses). Evaluate with alternating sequences test

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54
Q

Where does motivation come from?

A

medial frontal cortices, incl. anterior cingulate gyrus

Damage -> apathy, abulia, akinetic mutism

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55
Q

What are the symptoms of temporal lobe lesions?

A

Minor effect on audition

Major effect on language, prosody, memory, emotion (associated with irritative lesions of the cortex -> epilepsy)

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56
Q

What is Wernicke’s Aphasia?

A

Fluent, paraphasic speech with impaired auditory comprehension, repetition, and naming

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57
Q

What is sensory aprosody?

A

Inability to comprehend the prosody of others

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58
Q

Describe how emotion is developed by the temporal lobe

A 
Highly complex
Limbic system (incl. Papez circuit) provides basic emotions (fight-flight, appetite, sexual reproduction)
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59
Q

Limbic lesions often disrupt?

A

emotional function

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60
Q

What is temporal lobe epilepsy (TLE)?

A

common form of epilepsy
Focal cortical lesions in the temporal lobe producing complex partial seizures
Many behavioral phenomena
Today, concerned with interictal state of pt’s

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61
Q

How does TLE influence personality?

A

TLE -> long lasting behavioral changes due to rewiring of temporolimbic circuitry
Deepened emotionality, hyperreligiosity, philosophical interests, hypergraphia

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62
Q

What are the symptoms of parietal lobe lesions?

A

Deficits in tactile sensation, cognition (visuspatial, inattention to contralateral space)
Reading, writing, calculation (L side lesion)
Major emphasis: Hemineglect

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63
Q

What is hemineglect?

A

Right hemisphere lesions -> inattention to the left side of space
Clock drawing

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64
Q

What is the pathophysiology of neglect?

A

R hemisphere -> both sides of space
L hemisphere -> only contralateral space
So, R parietal lesion -> only permit surveillance of R hemisphere (loss of L side)
L hemineglect is more severe

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65
Q

Occipital lobe lesions produce?

A

Visual field deficits. Usually hemianopia, quadrantanopia

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66
Q

What is visual agnosia?

A

Failure to recognize objects despite intact vision

Recognition requires -> dorsal, ventral visual association cortices

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67
Q

What is prosopagnosia?

A

Right occipitotemporal lesion
Inability to recognize faces
Can be caused by tumors

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68
Q

What is cerebral Disconnection?

A

What matter lesions -> neurobehavioral sequelae

I.e. conduction aphasia -> arcuate fasciculus is damaged

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69
Q

What is conduction aphasia?

A

Type of cerebral disconnection

Arcuate fasciculus is damaged disconnecting Wernicke’s and Broca’s area

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70
Q

What is pure alexia (no agraphia) and where is the lesion?

A

Lesion of L Occipital lobe and splenium of corpus callosum. Disconnects the visual system from the L angular gyrus
Reading is lost, but still able to write

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71
Q

What is hemispheric disconnection?

A

Corpus callosum is severed (relief of epilepsy) but disconnects the cerebral hemispheres
Mild effects -> left hand anomia, agraphia, apraxia can be seen

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72
Q

What are distributed neural networks?

A

Higher functions
widespread networks of gray matter structure between hemispheres. Form functional ensembles dedicated to specific cognitive and emotional domains

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73
Q

Distributed neural networks facilitate?

A 
Memory encoding
Language
Spatial attention
Executive function
Memory retrieval
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74
Q

What is the wavelength of visible light?

A

400-700 nm
400 - blue
700 - red

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75
Q

The amplitude of light is seen as?

A

Brightness

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76
Q

The wavelength of light is seen as?

A

Color

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77
Q

What are the 3 properties of light?

A

Reflection
Absorption
Refraction

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78
Q

2 types of photoreceptors

A

Rods - night vision

Cones - color

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79
Q

Our blindspot is created by the?

A

Optic disk

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80
Q

What does receptor density refer to?

A

The receptor field size is about 100x larger in peripheral vision than in central

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81
Q

By daylight, only the central fovea can see

A

Clearly and in color

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82
Q

On dark night the periphery can see

A

in black and white with poor resolution

Fovea is blind

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83
Q

About how many photoreceptors are in the retina?

A

Rods ~ 100 million

Cones ~ 8 million

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84
Q

Phototransduction relies on rhodopsin which consists of?

A

Rhodopsin = opsin + retinal
opsin - 7 transmembrane spanning protein
Retinal - light sensitve molecule

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85
Q

What are the steps of phototransduction

A

Light -> rhodopsin -> activates Transducin (G-protein) -> activates cGMP phosphodiesterase -> hydrolizes cGMP
Light -> reduces [cGMP]

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86
Q

How do the photoreceptors orient in the retina?

A

Cones and Rods -> distal from the entry of light
Horizontal, bipolar, and amacrine cells are in the middle
Ganglion cell -> proximal to the entry of light
Ganglia come together to form the optic n.

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87
Q

What is the “rebound” response of retinal ganglion cell responses?

A

After light is turned off -> light was the inhibitory part of the receptive field

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88
Q

The Lateral Geniculate nucleus segregates the two main cell types:

A

Magnocellular

Parvocellular

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89
Q

what is the parvocellular system?

A 
Object vision - color, form, detail
High acuity (detail)
Small receptive field
Not responsive to motion
Color vision (cones)
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90
Q

What is the magnocellular system?

A 
Spatial vision - Motion, depth
Low acuity (crude form)
Large receptive fields
Responsive to motion
No color vision (rods)
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91
Q

What is the hierarchial organization of complex cell receptive field?

A

Converging cortical neurons with simple-cell receptive fields

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92
Q

What are the two parallel pathways in vision?

A

Dorsal - spatial vision (MT)

Ventral - object recognition (V4)

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93
Q

What are Refractive errors

A

Near-sightedness
Far-sightedness
Astigmatism
Presbyopia

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94
Q

What is near sightedness?

A

When the optical power of the eye is too large -> light focuses in front of the retina

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95
Q

What is far-sightedness

A

Optical power is too small -> light focuses behind the retina

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96
Q

What is an astigmatism?

A

Describes the shape of the cornea

Light will focus in front or behind the retina

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97
Q

When light is not focused on the retina properly?

A

Causes blurred vision and difficulty performing daily activities

98
Q

What can happen in uncorrected refractive error?

A

Visual impairment from blurring to legal blindness

99
Q

What is presbyopia?

A

Eye progressively losses its ability to focus on near objects.
Natural aging = lens becomes less flexible
Onset 40-50
Treat with magnifying lens or bifocals

100
Q

Parts of the basic eye exam

A

Visual Acuity
Visual Fields
Ocular Motility
Pupils
External exam (eyelid, conjunctiva, cornea)
Fundoscopic exam (red reflex, disc, retina)

101
Q

How to examine visual fields?

A

Pt looks at your nose and covers one eye
Hold fingers in periphery asking pt to identify the number of fingers
Repeat for other eye

102
Q

How to examine ocular motility?

A

Follow finger L, R, Up, Down looking for deficits

103
Q

How do you examine the pupils?

A

Round
Reactive to light
Equal
Afferent pupil defect

104
Q

What is the external eye exam?

A

Perform with a light pen

Eyelids, conjunctiva, cornea, anterior chamber

105
Q

What is the fundoscopic exam?

A

Opthalmoscope

Check Red reflex, optic n., retina

106
Q

Causes of unilateral red eye

A 
Viral/bacterial conjunctivitis
Iritis
Corneal abrasion
Corneal ulcer
Herpes
Herpes zoster ophthalmicus
Subconjunctival Hemorrhage
107
Q

Causes of bilateral red eye

A

Dry eyes

Allergic conjunctivitis

108
Q

What is conjunctivitis?

A

“pink eye”
viral or bacterial
Days
Pain, discharge, blurred vision, mattering of eyelids in the morning

109
Q

What is unique to viral conjunctivitis?

A

More common than bacterial
Usually follows a URI
Adenovirus most common
Moderate inflammation (pink), watery discharge, pre-auricular lymph node enlargement

110
Q

How do you treat viral conjunctivitis?

A

Hand hygiene
Cool compress, artificial tears
Severe cases -> steroid drops

111
Q

What is unique to bacterial conjunctivits?

A

Staph aureus, Strep pneumoniae
More severe inflammation (red)
Thick, purulent discharge
Swollen eyelid

112
Q

How do you treat bacterial conjunctivitis?

A

Antibiotic eye drops 1 wk, 3rd or 4th gen fluoroquinolone (Ciloxan, Ocuflox), Sulfacetamide, Tobramycin

113
Q

What is iritis?

A 
Uveitis with inflammation of the iris
~20-40 yrs, can be acute
Ocular/periorbital pain, photophobia, blurred or cloudy vision
Redness near limbus
Can have an irregularly shaped pupil
114
Q

How do you treat iritis?

A

Topical steroid drops
Dilating eye drops
Topical glaucoma drops PRN

115
Q

If a patient has a second bout or Iritis, do a work up for?

A

Rheumatology (Ankylosing spondylitis, RA, Bechet’s, Crohn’s, Sarcoidosis)
Syphilis, TB

116
Q

What is corneal abrasion?

A

Very painful scratch involving the cornea
Trauma, exposure to UV light
severe pain or foreign body sensation with acute onset
Tearing, blurred vision, redness
Fluorescein

117
Q

What is the treatment of corneal abrasion?

A

Mild -> artificial tears, antibiotic ointment
Large -> antibiotic ointment, patching of the eye, po pain med
NO topical anesthetic drops -> delay healing
Heal quickly, check for secondary infections
Risk of future abrasions

118
Q

What is a corneal ulcer?

A

Infection of the corneal stroma
Bacterial (Staph aureus, pseudomonas), fungal (fusarium), protozoa (Acanthamoeba)
Trauma with vegetative mater (incl contacts)
Acute onset -> severe pain, redness, decreased vision, eyelid swelling

119
Q

Exam findings for corneal ulcer

A

white infiltrate in cornea
Thinning of the cornea at site of infiltrate
Hypopyon inside the anterior chamber (sometimes)

120
Q

Treatment for corneal ulcer?

A 
4th gen fluoroquinolone
culture large ulcers
Slow healing
Can scar with permanent vision impairment
Corneal transplant if severe
121
Q

What is the cause of corneal foreign body

A

Any foreign material on the corneal surface
Metal, glass, organic material
Minor trauma but ask what they were doing
Suspicious for penetrating injury

122
Q

Symptoms of corneal foreign body

A

Pts complain of pain, redness, foreign body sensation, tearing
see foreign body with pen light
Check under the eyelids

123
Q

How do you treat corneal foreign bodies?

A

Superficial -> saline irrigation
More imbedded -> 30g needle, anesthesia
Couple of days -> rust ring, need to use a diamond burr
TOP antibiotics 1-2 weeks

124
Q

What is Dry Eye

A

Disorder of the tear film, usually bilateral
Foreign body sensation, blurred vision reflex tearing
Worse at the end of the day
Environmental influence

125
Q

Causes of dry eye?

A

Lack of tears due to systemic dz (RA, SLE,) or medications (anti-histamine, pain med)
Low production of tears or evaporate quickly (computers, fans)

126
Q

How do you diagnose and treat dry eye?

A

Symptoms alone
Schirmer’s test
Corneal staining pattern
Artificial tears, flax seed oil, omega 3s

127
Q

what is allergic conjunctivitis and how do you treat?

A

Conjunctiva is irritated by allergen. Bilateral, seasonal
Hx of allergies, asthma, eczema
Tx: avoid allergen, TOP antihistamine

128
Q

What is red eye due to herpes simplex

A

Herpatic keratitis, INF of corneal epithelium by HSV1
Most frequent cause of permanent vision loss
Unilateral eye redness (usually)
Fluorescin stain shows dendritic epithelial ulcer
Tx -> acyclovir
Can have a corneal scar

129
Q

What is red eye due to herpes zoster?

A

Reactivation of VZV
C1 distribution with derm involvement
Fatigue, low fever, unilateral forehead rash
Unilateral eye pain, redness, decreased vision
Fluorescin -> swollen lesions on corneal surface
Tx -> Acyclovir, risk for chronic dry eye following event

130
Q

What is pterygium?

A

“wing”, benign fibrocascular tumor induced by UV

Tx -> artificial tears, sunglasses, vasoconstrictors. Conjunctival autograft

131
Q

What is subconjuntival heme?

A

Subconjunctival hemorrhage due to ruptured vessel under the conjunctiva
Can occur without trauma
Asymptomatic
RFs -> sneezing, coughing, eye rubbing, trauma
No Tx necessary

132
Q

What is angle closure glaucoma?

A

Mid-dilated pupil, conjunctival injection, hazy cornea, shallow anterior chamber. Palpating the eye may feel hard
60-70 yrs
Unilateral severe eye pain, blurred vision, halos
Tx -> laser peripheral iridotomy allowing aqueous to gain entry to the anterior chamber and open trabecular meshwork

133
Q

What is open angle glaucoma?

A

Progressive optic n. dz associated with elevated intraocular pressure
RF’s -> age, ethnicity, Family Hx, myopia
Pt’s dont report symptoms, slowly causes damage to their peripheral vision
high IOP -> damages optic n. -> optic n. enlargement

134
Q

What are cataracts?

A

Gradual clouding of the lens
Progressive decline in vision
Develops with age, DM, steroid use, trauma or radiation
Tx -> if cannot be corrected with glasses -> phacoemulsification.

135
Q

What is the purpose of the lens?

A

Focus light on the retina

136
Q

What is phacoemulsification

A

Remove the natural lens using an U/S probe through a small incision. Replace cataract with artificial lens

137
Q

What are the 3 layers of the posterior chamber of the eye?

A

Sclera - outer
choroid - middle
retina - inner

138
Q

What is the retina?

A

Light sensitive tissue that captures the image
“visible” part of the brain, embryologically grows out from the brain during development
neuroectoderm

139
Q

What is the choroid?

A

Vascular layer that provides nutritional and metabolic support
Posterior uvea

140
Q

What is the sclera?

A

“white” part of the eye, fibrous covering

141
Q

What is the uvea?

A

iris, ciliary body, choroid

142
Q

What are the parts of the retina?

A

Macula (fovea, foveola)
Peripheral retina - peripheral and night vision, ora serrata (ant termination of retina), pars plana (posterior ciliary body)

143
Q

What are the layers of the retina?

A

Neurosensory retina - inner layer, light sensitive cells

Retinal pigment epithelium - outer layer, provides metabolic support

144
Q

What are the neurosensory cells of the retina?

A

Photoreceptors - rods, cones
Bipolar cells/ supporting glial cells - connecting cells
Ganglion cells - long axons forming the optic n. and terminate in the brain

145
Q

What is the function of the retinal pigment epithelium (RPE)?

A

Photoreceptor metabolism
Outer blood-retina barrier
Potential space

146
Q

What is the vasculature of the retina?

A

Central retinal artery - branch of opthalmic (ICA), inner 2/3 of retina
Central retinal vein
Capillaries - inner blood-retina barrier

147
Q

Think of eye pathology in colors

A

Red - Hemorrhage
Yellow - lipid/exudate
White - ischemia, inflammation, infection
Brown/black - pigment deposition, scars, neoplasms

148
Q

Where can hemorrhages occur?

A

Subretinal - dark, retinal vessels overlie
Dot-blot - small, middle layer of retina, DM
Flame/splinter - thin, follows nerve fiber layer, HTN
Preretinal - boat-shaped, obscures retinal vessels
Vitreous - diffuse bleeding, DM

149
Q

What are the causes of lipid/exudate in the retina (yellow)

A

Hard exudate - lipid leak from retinal vessels, DM
Drusen - yellow subretinal deposits in macula, cell waste accumulation
Cholesterol embolus - Hollenhorst plaque, plaque lodges at arteriole bifurcation

150
Q

What is the hallmark pathology for macular degeneration?

A

Drusen, yellow subretinal deposits in the macula. Accumulation of cell waste

151
Q

What is the cause of the ischemia, inflammation, infection in the retina (white)?

A

Cotton wool spot -“Fluffy” white areas, Capillary ischemia, DM, HTN
Branch retinal a. occlusion - larger area of sectoral infarction

152
Q

What is the cause of pigment deposition, neoplasms, and scaring in the retina (brown)?

A

Choroidal nevus - benign pigmented neoplasm, asymptomatic

153
Q

What is the cause of pigment deposition, neoplasms, and scaring in the retina (black)?

A

Macular scar - result of old inflammation

154
Q

What is diabetic retinopathy?

A

1 cause of blindness in working age adults

RF - diabetes, glycemic
Microvascular injury, retinal hemorrhage, capillary leakage, ischemia, neovascularization

155
Q

What are the 2 classes of diabetic retinopathy

A
  1. Non-proliferative diabetic retinopathy - may be asymptomatic
  2. Proliferative diabetic retinopathy - more severe, vision threatening
156
Q

Symptoms of Non-proliferative Diabetic Retinopathy (NPDR)?

A 
Microaneurysms
Flame hemorrhages
Dot-blot hemorrhages
Diabetic macular edema
Hard exudates
157
Q

Proliferative Diabetic Retinopathy (PDR) is?

A

Neovascularization - optic disc, retina
Fibrovascular proliferation
Complications - Vitreous hemorrhage, tractional retinal detachment, neovascularization of iris -> neovascular glaucoma

158
Q

How do you manage Diabetic Retinopathy?

A 
Glycemic and blood pressure control
Screening eye exams
Laser photocoagulation
Anti-Vascular Endothelial Growth Factor (VEGF)
Pars Plana Vitrectomy
159
Q

Hypertensive Retinopathy is?

A 
Vasoconstriction - arteriole narrowing
Arteriosclerosis - Cu2+, Ag 
Retinal hemorrhage
Macular edema and exudate
Optic disc edema (papilledema)
160
Q

What is age-related Macular Degeneration (AMD)?

A 
#1 cause of blindness > 50 y/o
RF - age, race (caucasian), gender (females), tobacco
161
Q

What is dry age-related Macular Degeneration (AMD)?

A

Dry - drusen, RPE changes, Geographic atrophy

TX -> antioxidant vitamins

162
Q

What is wet age-related Macular Degeneration (AMD)?

A

More vision loss
10% of AMD
Choroidal neovascularization (CNV) into RPE
Tx -> anti-VEGF intravitreal injections

163
Q

What is the vitreous?

A

80% of the eyes volume
Water, Hyaluronic acid, type II collagen
Attachements -> ora serrata, Macula, Optic n.

164
Q

What are the 3 pathologies associated with the choroid?

A 
Uveitis (idiopathic, autoimmune, or infections)
Choroidal nevus (benign pigmented spot)
Tumors (metastasis, melanoma)
165
Q

What is the optic n.?

A

CN II, afferent pupilary reflex

Synapses @ Lateral geniculate nucleus, midbrain (pupil and accomodation)

166
Q

What is the optic disc?

A

Neural rim : Central cup ~ 0.3
Symmetrical
Normal if ration

167
Q

What is Glaucoma?

A

1 optic neuropathy

injury to nerve fiber layer and optic disc
Visual field loss
RF -> age, elevated IOP, Black, Family Hx

168
Q

What PE findings suggest glaucoma and how do you treat??

A 
Elevated IOP
Enlarged Cup:Disc or asymmetry
Optic disc hemorrhage
Visual field defects
Tx -> meds, laser, surgery
169
Q

What is papilledema?

A

Bilateral optic disc swelling due to increased ICP

Blurring of disc margin, sometimes associated with surrounding hemorrhage

170
Q

what is Anisocoria?

A

Unequal size of the pupils

171
Q

What are the two types of pupillary disturbances?

A
  1. ABN reaction to light of dark

2. Aniscoria

172
Q

Parasympathetic input on the pupil leads to?

A

Constriction

173
Q

Sympathetic input on the pupil leads to?

A

Dilation

174
Q

A small pupil with poor reaction to the dark has a defect in which system?

A

Sympathetic dysfunction. Dilation lag, ptosis, anhidrosis = Horner syndrome

175
Q

A large pupil with poor reaction to light can have two causes

A
  1. ABN structure = iris damage

2. Parasympatheic dysfunction

176
Q

What are the sources of parasympathetic dysfunction in a large pupil with poor reaction to light?

A
  1. Tonic dilation, segmental palsy, light-near dissociation = Tonic
  2. ptosis, EOM paresis = CN III palsy
177
Q

What is the presentation of Horner’s syndrome?

A

Normal light response

anisocoria worse in the dark

178
Q

What is Tonic pupil?

A 
Aniscoria worse in light (poor response to light), dilated pupil
Segmental palsy ("portion isn't wired up to light reaction)
179
Q

Symptoms of optic n. damage

A
  1. Monocular vision loss (blurred, missing, dim)
  2. Decreased brightness or color vision impaired
    Exam findings -> vision loss (acuity, field), Afferent pupillary defect (APD), color vision loss, ABN optic n.
180
Q

What is afferent pupillary defect?

A

Hallmark of optic n. or tract disturbance

Afferent - prior to synapse in LGN

181
Q

What is diplopia?

A

Double vision. If bilateral think misalignment

182
Q

How do you determine where the misalignment occurs in diplopia?

A 
NEJM
Nerve (III, IV, VI)
Eye (displaced
Junction, neuromuscular (myasthenia)
Muscle (thyroid associated ophthalmopathy, rare myopathies)
183
Q

What is Oscillopsia?

A

Appears that the world is moving, when it isn’t

Nystagmus

184
Q

What are the types and directions of nystagmus?

A
  1. Pendular (slow-slow)
  2. Jerk (Fast-slow)
  3. Mixed
    Direction - horizontal, vertical, torsional, mixed
185
Q

What is the source of downbeat nystagmus and how is it treated?

A

Cervical-medullary junction
Not congenital
Surgical decompression

186
Q

D1 receptor is coupled to which Gprotein?

A

Gs

187
Q

D2 is coupled to which G protein?

A

Gi/0

188
Q

Haloperidol is a?

A

D1, D2 Antagonist

189
Q

Bromocriptine is a?

A

D2 Agonist

190
Q

Clozapine is a?

A

D4 antagonist (Gi/o)

191
Q

The direct pathway of the thalmus to the cortex?

A

Increases excitatory outflow (D1 increases)

192
Q

The indirect pathway of the thalmus to the cortex?

A

Decreases excitatory outflow (D2 decreases)

193
Q

Loss of substantia nigra neurons leads to?

A

Decreased DA release -> Decreased D1, D2 activation, loss of “go” signal -> decrease in motor function

194
Q

What are the steps in DA biosynthesis

A

Tyrosine (Tyrosine hydroxylase) -> Dihydoxyphenylalanine (Dopa) (AADC) -> DA (degraded by MAO, COMT)

195
Q

In the eye, a1 controls

A

Dilator muscle

196
Q

In the eye, M3 controls

A

Constrictor muscle, accommodation for near vision

197
Q

In the eye, B2 controls?

A

Aqueous humor production

198
Q

What are the symptoms and RF’s for open angle glaucoma?

A

Most common preventable cause of blindness

RF’s - IOP, Family Hx of glaucoma, Black

199
Q

How do you treat open angle glaucoma?

A

Prophylactic reduction of IOP

Reduce baseline IOP by 30%

200
Q

What drugs are used in open angle glaucoma

A
  1. Prostaglandins - increase outflow
  2. Beta-blockers, a2 agonist, Carbonic anhydrase inhibitor - decrease secretion
  3. cholinomimetics - increase outflow (in place of prostaglandins)
201
Q

Avoid beta antagonists in patients with?

A

asthma, bradycardia COPD

202
Q

Closed angle glaucoma is caused by?

A

Mechanical blockage of trabecular meshwork by peripheral iris

203
Q

Treatment options for closed angle glaucoma?

A

TOP:
Pilocarpine - induce miosis, remove trabecular block
Apraclonidine - decrease production
Systemic:
Acetazolamide - decrease production
Mannitol - intraocular dehydration until surgery

204
Q

What should be avoided by closed angle glaucoma patients while waiting for surgery?

A

Decongestants

Anticholinergics

205
Q

Treatments for bacterial conjunctivitis

A

Erythromycin - empiric
Azithromycin
Fluoroquinolones
Avoide aminoglycosides

206
Q

How do you treat corneal ulcers

A

Associated with contact use
Fluoroquinolones, tobramycin
Vanco

207
Q

Treatments for HSV Keratitis?

A

Acyclovir (po)

Trifluridine (TOP)

208
Q

Treatments for Viral Conjunctivitis?

A

OTC antihistamine

OTC drops

209
Q

Bulbar Palsy and Bulbar signs is associated with?

A

LMN

210
Q

The corticobulbar pathways and pseudobulbar pasly is associated with?

A

UMN

211
Q

Impairments in CNI lead to?

A

Unilateral - sensorineural

Bilateral - conductive (failure of odorants to reach olfactory mucosa)

212
Q

Impairmeents in CN II leads to deficits in?

A

Visual Acuity
Visual Fields
Direct Opthalmoscopy (red reflex, optic fundus)
Pupillary Exam

213
Q

What is the purpose of the swinging flashlight test?

A

Side to side differences in optic n. function, can detect small differences

214
Q

What is orthophoric?

A

Eyes are aligned in all directions of gaze

215
Q

What is herotropia?

A

Misalignment of the eyes at rest

216
Q

What is herophoria?

A

Latent tendency of the ye to malalign when stimulus to fixation is removed or fails

217
Q

spinal trimgeminal nucleus relays?

A

Pain and temperature information

218
Q

What is ageusia/dysgeusia?

A

Lost sense of taste or altered perception of taste

219
Q

What is parosmia?

Phantosmia?

A

parosmia - altered perception of an odor, usually unpleasant
phantosmia - perception of smell without an odor present

220
Q

Which senses are involved in the chemosensory systems?

A

Taste
Smell
Chemesthesis (V)

221
Q

The anterior 2/3 of the tongue is innervated by?

A

Facial n.

222
Q

The posterior 1/3 of the tongue is innervated by?

A

Glossopharyngeal n.

223
Q

Which taste sensations are facilitated by an ion channel?

A

Sour, salty

224
Q

Which taste sensations are facilitated by Gprotein coupled receptors?

A

Sweet, Bitter, Umami

GPCR -> amplification of PLCbeta2, IP3R3 and TrpM5 (channel) -> ATP release

225
Q

The LGN projects to which layer of the cortex?

A

IV

V and VI project back to the LGN

226
Q

Anterior nuclei of the thalamus relays?

A

Limbic information

227
Q

VA/VL nuclei of the thalmus relay?

A

Motor information

228
Q

VPL/VPM nuclei of the thalamus relay?

A

Somatosensory

229
Q

The LGN relays?

A

Visual information

230
Q

MGN relays?

A

Auditory information

231
Q

What are the association nuclei of the thalamus?

A

Dorsomedian (frontal cortex)

Pulvinar (visual)

232
Q

What are the other nuclei in the thalamus?

A

Centromedian N. (motor)

Reticular N. (inhibitory interneurons with connections to all the other nuclei)

233
Q

What are the 3 major circuit systems of the forebrain?

A
  1. Thalamocortical
  2. Lentiform Nuc./Basal Ganglia
  3. Limbic system (Hippocampus, Hypothalamus-amygdala)
234
Q

Role of the hypothalmus?

A

Homeostasis and control of body temperature

Emotional behavior

235
Q

What is the Papez circuit?

A

Hippocampus -> fornix -> mammillary body -> anterior n. -> cingulate gyrus -> hippocampus

236
Q

What does the Hypothalamus do?

A

Collects contextual information (cortex, amygdala) and sensory inputs (visceral, somatic) to create:
Visceral motor, somatic motor, neuroendocrine, and behavioral responses

237
Q

How does the hypothalamus regulate the autonomic and somatic motor systems?

A

Efferent projections to:

  1. Autonomic centers and preganglionic neurons
  2. Motor nuclei in brainstem
238
Q

How does the hypothalamus regulate the endocrine system?

A

Direct - oxytocin, vasopressin

Indirect - releasing and inhibiting factors

239
Q

What are the neural inputs to the hypothalamus?

A

Direct input from retina
Processed sensory information from limbic areas
Visceral sensation via nucleus of the solitary tract

240
Q

What are the humoral inputs to the hypothalamus?

A

Humoral afferents: temperature, osmolality, glucose, peripheral hormones

241
Q

They hypothalmus regulates body temperature. Which lesions would be problematic?

A

Anterior lesion - hyperthermia

Posterior lesion - hypothermia

Neuro (4 decks)

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