Exam 3 Flashcards

(101 cards)

1
Q

Tympanic membrane

  • concave or convex relative to lateral side?
  • most depressed part called?
A
  • concave

- umbo

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2
Q

Innervation of tympanic membrane + surrounding structures

A

Outer surface TM + external auditory canal:
CN V, VII, X (GSA)

Mucosa lining TM + auditory tube + mastoid air cells: 
CN IX (GVA)
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3
Q

Child has a middle ear infection. Otoscopic exam will show?

A

Dull or absent light reflex from the eardrum

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4
Q

Groove for cartilaginous part of auditory tube is found b/w what 2 bones?

A

b/w petrous part and temporal part of sphenoid bone (base of skull)

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5
Q

Tensor tympanic muscle

  • location
  • innervation
  • action
A
  • just above auditory tube
  • CN V3
  • attenuation reflex
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6
Q

Middle ear communicates w/ mastoid air cells by way of the?

A

Auditus -> mastoid antrum

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7
Q

The tympanic plexus is located where?
Formed from?
Gives rise to which nerve?

A
  • promontory - basal turn of cochlea
  • CN IX
  • lesser petrosal nerve - preganglionic parasympathetic destined to the otic ganglion which supplies the parotid gland
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8
Q

Stapedius muscle housed in?

Innv by?

A
  • pyramid (pyramidal eminence)

- nerve to stapedius (CN VII)

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9
Q

The facial nerve innervates all the glands of the head except the:

A

parotid (lesser petrosal nerve) and integumentary gland

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10
Q

Describe the path of the chorda tympani nerve

function?

A

comes off CN VII -> passes above tensor tympani muscle -> passes through petrotympanic fissure -> submandibular ganglion

taste from anterior 2/3 of tongue
secretomotor innervation to glands

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11
Q

Greater petrosal nerve

  • branch of
  • what type of fibers?
A
  • CN VII

- GVE -> preganglionic parasympathetics

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12
Q

Rheumatoid fixation

A

Fibrous ankylosis (fixation) of synovial joint in rheumatoid arthritis

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13
Q

OTOSCLEROSIS

A

A bony ankylosis (knee) knits the bone of the middle ear to the stapes, preventing normal transmission of sound from the eardrum into the inner ear.

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14
Q

Hyperacusis

  • define
  • cause
A

Abnormal sensitivity to everyday sound levels or
noises, often sensitivity to higher pitched sounds, in the presence of essentially normal hearing.

Nerve to stapedius damage

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15
Q

Congenital absence of stria vascularis is due to failure of what? Consequence?

A

Neural crest cell migration

No endolymph production

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16
Q

Antibiotic induced ototoxicity mech?

A

destroy outer hair cells - loss of cochlear amplification

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17
Q

Structure responsible for calculating interaural INTENSITY differences

A

Trapezoid body in caudal pons

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18
Q

Structure responsible for calculating interaural SOUND differences

A

Superior olivary nucleus

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19
Q

Ear embryo
-otic vesicle filled with? form?

  • vestibular and spiral ganglia formed from?
  • mesenchyme develops into?
A
  • endolymph/membranous components of inner ear
  • statoacoustic ganglia
  • cartilage, perilymphatic space and bone
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20
Q

Derivations from which arch?

  • tensor tympani (malleus and incus)
  • stapedius (Stapes)
A
  • 1st arch (CN V)

- 2nd arch (CN VII)

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21
Q

Chromosomal and 1st arch syndromes commonly present w/ what clinical sign?

A

low set ears

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22
Q

duplication of what may form auricular pits?

A

first pharyngeal cleft

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23
Q

Movement of hair stereocilia:

  • depolarized (opening of channel)
  • repolarized (closing of channel)
A
  • outwards

- inwards

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24
Q

2 theories for encoding sound frequency

A
  1. Placement theory – mapping of individual fibers
  2. Phase locking in an auditory nerve fiber
    • Pattern of AP matches frequency of sound wave
    o This doesn’t explain high frequency sound waves b/c can’t fire APs fast enough to keep up
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25
2 theories for sound localization (horizontal)
1. Intensity difference due to head being an obstacle is detected by lateral superior olive o Only works for shorter wavelength sounds b/c head is not obstacle for longer wavelength sounds o Best for high frequency 2. Comparing phase differences o Peak of sound waves gets to opposite ear at a later time o Best for low frequency
26
Audible frequency range Human voice frequency range
- 20 to 20,000 Hz | - 250 to 7500 Hz
27
dB SPL vs. dB HL vs. dB SL
dB SPL - absolute dB HL - human specific dB SL - individual specific
28
Describe the auditory brainstem response test. ECOLI
Way to assess neural component of middle ear ``` E - Eighth nerve (Waves I and II) C - cochlear nucleus (Wave III) O - olivary complex (Wave IV) L - lateral lemniscus (Wave V) I - inferior colliculus (Wave VI) ```
29
Good test to assess Meniere's disease?
ECoG - check cochlear response
30
Describe otoacoustic emissions test (OAE)
* Measure sounds created converting mechanical to electrical energy for signal transport * Absent if hearing loss exceeds 30 dB HL * All infants get screening of this at birth
31
Profound hearing loss at what level?
>90 dB HL -> non-auditory communication
32
Describe the aspects of conductive lesion
1. Air/bone gap 2. normal word recognition 3. abnormal tympanogram
33
Describe aspects of a cochlear lesion
1. loss of loudness 2. word discrimination reduced proportional to degree of hearing loss 3. presence of auditory recruitment 4. normal tympanogram 5. Absent OAE 6. Normal ABR 7. Acoustic reflex and decay okay
34
Describe aspects of a auditory nerve lesion
1. Abnormal ABR 2. word recognition to hearing loss disproportionate 3. probs w/ acoustic reflex/decay
35
Describe Weber test
* Put tuning fork in midline of head * Patient should hear it symmetrically * If problem – tuning fork will lateralize * Conductive loss – to side of loss * If sensorineural – to opposite side of lesion
36
Describe Rinne test
* Compare air to bone conduction * Air – in front of ear * Mastoid process – bone * If conductive problem – bone conduction > air conduction
37
Motor unit defintion
Alpha motor neuron and all the muscle fibers it innervates
38
Small vs large motor unit
Small - less force - fine control - smother contractions Large -more powerful, coarse contractions
39
Purpose of stretch reflex?
Prevent muscle from being overstretched
40
Static vs dynamic stretch receptors
Static receptors - slow and smooth response; non-adapting - Stretch afferent fibers = II - muscle tone and smooth movements Dynamic receptors - fast response and rapidly adapting - Ia stretch afferent fibers - clinical stretch reflex (DTR)
41
Reflexes - muscles, nerves and CNS level 1. Biceps 2. Triceps 3. Brachioradialis 4. Knee 5. Ankle (gastroc) 6. Jaw jerk
1. Musculocutaneous nerve (C5,6) 2. Radial nerve (C6-7) 3. Radial nerve (C5,6) 4. Femoral nerve (L2-4) 5. Tibial nerve (S1) 6. C.N. V (Pons)
42
Steps through which tone is generated
brainstem motor centers -> gamma motor neurons -> contraction of IFF fibrils -> inc tension on static stretch receptors -> inc firing of group II stretch afferents -> low level firing of alpha motor neurons GAMMA LOOP
43
Brainstem LMN
Midbrain - III and IV Pons - VI, V, VII Medulla - IX, X, XII
44
List differences between early and late signs of LMN injury
LATE Add -atrophy (denervation type) -fibrillations (spontaneous contractions of INDIVIDUAL muscle fibers) Subtract -fasciculations (except with ALS)
45
What's pathognomonic for a LMN injury
Fibrillations
46
Brainstem reflexes 1. Pupillary light reflex 2. Corneal and Jaw jerk reflexes 3. Gag 4. VOR
1. Midbrain 2. Pons 3. Medulla 4. Medulla, pons and midbrain Bilateral responses to stimulation on one side
47
What's responsible for tonic stimulation of extensor gamma motor neurons for tone?
Vestibulospinal tract
48
Signs of isolated vestibular lesions
- abnormal nystagmus - vertigo - swaying or falling - can be permanent
49
Signs of isolated reticular nuclei and/or red nucleus lesions
- difficulty w/ postural adjustments during whole body movements - usually temporary
50
Difference b/w Broca's and transcortical aphasia
lose ability of repeat a phrase with Broca’s
51
Describe alternating hemiplegia
Same side face (LMN) / opposite side limb (UMN) deficit from a single lesion
52
Describe a hemiplegic and diplegic gait
Hemiplegic - arm flexed at elbow - wrist/fingers flexed - extension at knee - plantar flexion - hip rotated out Diplegic -scissoring of legs
53
Describe decorticate posturing | -level of lesion
-Elbow flexed and knee extended ABOVE THE RED NUCLEUS -rubrospinal and vestibulospinal systems intact
54
Describe decerebrate posturing | -level of lesion
- elbow extension/knee extension - antigravitational muscles uninhibited BELOW THE RED NUCLEUS and ABOVE THE VESTIBULAR NUCLEUS -rubrospinal system lost
55
List the branchial motor nerves
V, VII, IX, X, XI
56
# Define central pattern generators - controller | - trigger
Preprogrammed circuit that causes rhythmic or oscillating movements - controller -> cerebral cortex - trigger -> brainstem
57
Max deficit time seen w/ Guillain-Barre?
2 weeks
58
3 most common causes of death with Guillain-Barre
- resp failure - DVT - Cardiac arrythmias
59
How to assess risk of resp failure
Check forced vital capacity
60
Length dependent peripheral neuropathy - onset - time course - associated with (most common cause) - serology to rule out - Tx
o Onset w/ numb or tingling of toes and feet o Develops over years o Check diabetes (most common), B-12, SPEP, IFE o Also check thyroid and serology for syphilis o Tx the cause if you can find it – primary goal o Tx the sxs if can’t find cause •Amitriptyline – tricyclic antidepressant -This is a more effective drug •Duloxetine – SSRI -Much more expensive ``` •Gabapentin -Anticonvulsant class of med ```
61
Differences b/w CIPD and Guillain-Barre
CIPD - active beyond 8 weeks - no resp failure - responds to prednisone - atypical pattern
62
Paraneoplastic pure sensory neuropathy - presentation - etiology and pathogenesis
PRESENTATION - diffuse numbness - painful paresthesias - sensory ataxia ETIOLOGY -cancer -> commonly small cell lung PATH -Anti-Hu Abs attack DRG (sensory neuron selectivity)
63
Charcot Marie Tooth Disease - etiology - progression - CMT-1 vs CMT-2
ETIOLOGY -hereditary PN PROGRESSION - onset in teens - no pain and slow development CMT-1 - dysmyelinating - PMP-22 duplication (myelin protein) ``` CMT-2 normal velocity (axonal) ```
64
List 4 mononeuropathies and which one does NOT have motor sxs
1. Median @ wrist -> CTS (SENSORY ONLY) 2. Ulnar @ elbow 3. Fibular @ fibular head 4. Radial in spiral groove
65
Risk factors for carpal tunnel
DM, thyroid disease, pregnancy
66
Dermatomes and myotomes for - C5 - C7 - L5 - S1
a) C5 D -> just below clavicles and back of neck M -> shoulder muscles and biceps b) C7 D -> down back of arm and digits 2+3 M -> extensor muscles or arm and forearm c) L5 D -> lateral thigh and front of leg down to the dorsal aspect of the feet M -> glutes and leg muscles d) S1 D -> posterolateral region of thigh and leg + outside area of butt M -> glutes + posterior leg muscles + intrinsic foot muscles
67
Myasthenia gravis associated with? Pathology
Thymus pathology (e.g. thymoma) Abs against nicotinic Ach receptors
68
Signs and sxs of LEMS Pathology Common cause Treatment
SIGNS AND SXS • Lower leg weakness developing over months • Dry mouth + absent reflexes • EMG -> Greater response w/ exercise PATHOLOGY • Abs against VG Ca2+ channels CAUSE • Small cell lung cancer most common cause Tx • Diaminopyridine – blocks VG K+ channel -More time to open Ca2+ channels -Wider AP b/c membrane repolarizes slower
69
ALS - signs (including lab tests) - Treatment
SIGNS - progressive weakness and wasting - spastic (slow) dysarthria - EMG -> fibrillations and fasciculations Tx -Riluzole -> glutamate antagonist
70
Lab value elevated with myopathies?
creatine kinase
71
Dystrophies vs myositis - times course - tx
DYSTROPHIES - Slowly progressive and hereditary - At present, disappointing Rx Myositis - weeks to months - responsive to immunosuppression
72
Myopathies have (proximal/distal) muscle weakness? Exception?
1. Proximal | 2. Exception -> Myotonic dystrophy
73
Which myositis has SLOW progression
``` Inclusion body (very slow) -unresponsive to steroids ```
74
Fxal divisions of cerebellar cortex
1. Vestibulocerebellum - flocculonodular lobe - balance and coordinating head/eye movements 2. Spinocerebellum - vermis + paravermal area - anterior lobe included - spinal cord input - Control of posture, muscle tone and stereotyped movements (CPGs) 3. Cerebrocerebellum - connections with cerebral CTX via pontine nuclei - planning and initiation of movement coordination
75
Purkinje cells are (excitatory/inhibitory) on to deep cerebellar nuclei
Inhibitory
76
Climbing vs mossy fibers
Climbing - from ION - synapse on PC dendrites Mossy - not from ION - synapse onto granule cells Both are excitatory inputs
77
Dorsal vs ventral spinocerebellar tracts
Information about the position and status of muscles, tendons, joints and descending motor commands to the spinal cord. Dorsal -> inferior cerebellar peduncle Ventral -> superior
78
Which part of red nucleus do the following pathways go through? - From interposed nuclei (spinocerebellum-paravermal cortex) - From dentate nuclei (corticocerebellum)
1. magnocellular -> forms rubrospinal tract | 2. Parvocellular
79
Medulloblastoma can cause damage to which cerebellar structure/pathway? What effects are seen?
- Damage to cerebellar vermis - path to vestibular nucleus leading to malfunction of lateral vestibulospinal tract - TRUNCAL ATAXIA - unable to stand upright w/out support Cerebellar vermis - Results in defective anticipatory function by the cerebellum - Failure to counter the effect of gravity displacement produced by movement of a body part
80
Intention tremor results for damage to? | Disruption of what?
- Damage to lateral cerebellar lobe, dentate nucleus, or SCP | - Disruption of viscoelastic freeze arrangement
81
In unilateral cerebellar lesions, the fast phase of nystagmus is toward the side of the lesion or away?
Toward
82
Anterior lobe syndrome - cause - structures damaged - manifestations
CAUSE -malnutrition usually related to chronic alcoholism STRUCTURES DAMAGED - Purkinje cell death - shrinking of cerebellar cortex MANIFESTATIONS -Loss of coordination chiefly in lower limbs -Depressed tendon reflexes • Loss of tonic stimulation of gamma motor neurons via the reticulospinal tract -Heel to shin test fail
83
Posterior lobe syndrome - cause - manifestations
CAUSE -Commonly results from cerebral vascular accidents, tumor, trauma, or degenerative diseases MANIFESTATIONS - Loss of coordination of voluntary movements (ataxia) and hypotonia - Rate, range, and force of movements are abnormal - Intention tremor present
84
Flocconodular lobe syndrome
* Disturbance of balance manifested primarily as truncal ataxia * Patients may not beable to sit or stand without falling * Most often seen in children with medulloblastomas
85
Major breakdown product of DA which can be used to measure DA system activity
HVA - homovanillic acid
86
Describe 4 CNS dopaminergic pathways
1. Nigrostriatal - substantia nigra -> striatum (caudate+putamen) - Parkinson destroys this 2/3. Mesolimbic + Mesocortical - VTA -> nucleus accumbens + frontal cortex - antipsychotics act here 4. Hypothalamic - arcuate nuc -> median eminence - reg of PRL release for pituitary - tuberoinfundibular
87
Highest brain [NE]? [DA]?
NE -> LC DA -> SN/ST
88
Effect of Desiparmine in DA vs NE neurons
NE -> inhibits reuptake DA -> does not
89
Death from cocaine overdose is due to what?
Inc HR and Inc BP due to vasoconstriction Peripheral effect
90
Why does L-dopa tx become less efficacious as time under tx goes on?
Continued destruction of DA neurons and NS path Smaller window b/w off state of the drug and the dose at which patient experience dyskinesia during the on state
91
Output neurons of the striatum are? | What NT?
- medium spiny neurons | - GABAergic
92
Relate GPi/m output to movement
Increased output - less movement Decreased output - increased movement
93
Define hemiballism and what causes it
- ballistic movements - damage to subthalamic nucleus contralateral to affected side - proximal musculature affected
94
Tx for essential tremor
1. Drugs - primidone - propanolol (peripheral Beta-2 blockade) - alcohol 2. Thalamotomy 3. Vim thalamic stimulation (DBS)
95
Tx of huntington's disease associated chorea
GABA agonists - valproate - clonazepam Presynaptic DA depletes - reserpine - Alpha-methylparatyrosine - Tetrabenazine DA receptor blockers
96
Head of caudate nucleus is vascularized by
Recurrent artery of Heubner. Branch off the anteromedial group of striate arteries
97
Superior part of internal capsule vascularized by
Lenticulostriate arteries Anterolateral group - MCA + ACA
98
What does the anterior choroidal artery supply?
* Optic tract * Medial temporal cortex - Parahippocampal gyrus * Amygdala * Posterior limb of internal capsule * -Inferior * -Sublenticular * -Retrolenticular
99
Summarize blood supply to internal capsule
Superior part - lenticulostriate arteries Inferior part - posterior limb - anterior choroidal - anterior limb + genu - medial striate arteries
100
2 important branches of ACA and structure(s) they supply
* Pericallosal – inferior to cingulate gyrus * Callosomarginal – superior to cingulate gyrus * They go to the paracentral lobule and supplementary motor cortex
101
The venous angle is landmark for? | formed from?
- interventricular foramen | - jx of thalamostriate vein and internal cerebral vein