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BMB > Exam 3 > Flashcards

Exam 3 Flashcards

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
Q

2 theories for sound localization (horizontal)

A
  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
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26
Q

Audible frequency range

Human voice frequency range

A
  • 20 to 20,000 Hz

- 250 to 7500 Hz

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27
Q

dB SPL vs. dB HL vs. dB SL

A

dB SPL - absolute

dB HL - human specific

dB SL - individual specific

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28
Q

Describe the auditory brainstem response test.

ECOLI

A

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)
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29
Q

Good test to assess Meniere’s disease?

A

ECoG - check cochlear response

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30
Q

Describe otoacoustic emissions test (OAE)

A
  • 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
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31
Q

Profound hearing loss at what level?

A

> 90 dB HL -> non-auditory communication

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32
Q

Describe the aspects of conductive lesion

A
  1. Air/bone gap
  2. normal word recognition
  3. abnormal tympanogram
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33
Q

Describe aspects of a cochlear lesion

A
  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
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34
Q

Describe aspects of a auditory nerve lesion

A
  1. Abnormal ABR
  2. word recognition to hearing loss disproportionate
  3. probs w/ acoustic reflex/decay
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35
Q

Describe Weber test

A
  • 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
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36
Q

Describe Rinne test

A
  • Compare air to bone conduction
  • Air – in front of ear
  • Mastoid process – bone
  • If conductive problem – bone conduction > air conduction
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37
Q

Motor unit defintion

A

Alpha motor neuron and all the muscle fibers it innervates

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38
Q

Small vs large motor unit

A

Small

  • less force
  • fine control
  • smother contractions

Large
-more powerful, coarse contractions

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39
Q

Purpose of stretch reflex?

A

Prevent muscle from being overstretched

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40
Q

Static vs dynamic stretch receptors

A

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)
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41
Q

Reflexes - muscles, nerves and CNS level

  1. Biceps
  2. Triceps
  3. Brachioradialis
  4. Knee
  5. Ankle (gastroc)
  6. Jaw jerk
A
  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
Q

Steps through which tone is generated

A

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
Q

Brainstem LMN

A

Midbrain - III and IV

Pons - VI, V, VII

Medulla - IX, X, XII

44
Q

List differences between early and late signs of LMN injury

A

LATE
Add
-atrophy (denervation type)
-fibrillations (spontaneous contractions of INDIVIDUAL muscle fibers)

Subtract
-fasciculations (except with ALS)

45
Q

What’s pathognomonic for a LMN injury

A

Fibrillations

46
Q

Brainstem reflexes

  1. Pupillary light reflex
  2. Corneal and Jaw jerk reflexes
  3. Gag
  4. VOR
A
  1. Midbrain
  2. Pons
  3. Medulla
  4. Medulla, pons and midbrain

Bilateral responses to stimulation on one side

47
Q

What’s responsible for tonic stimulation of extensor gamma motor neurons for tone?

A

Vestibulospinal tract

48
Q

Signs of isolated vestibular lesions

A
  • abnormal nystagmus
  • vertigo
  • swaying or falling
  • can be permanent
49
Q

Signs of isolated reticular nuclei and/or red nucleus lesions

A
  • difficulty w/ postural adjustments during whole body movements
  • usually temporary
50
Q

Difference b/w Broca’s and transcortical aphasia

A

lose ability of repeat a phrase with Broca’s

51
Q

Describe alternating hemiplegia

A

Same side face (LMN) / opposite side limb (UMN) deficit from a single lesion

52
Q

Describe a hemiplegic and diplegic gait

A

Hemiplegic

  • arm flexed at elbow
  • wrist/fingers flexed
  • extension at knee
  • plantar flexion
  • hip rotated out

Diplegic
-scissoring of legs

53
Q

Describe decorticate posturing

-level of lesion

A

-Elbow flexed and knee extended

ABOVE THE RED NUCLEUS
-rubrospinal and vestibulospinal systems intact

54
Q

Describe decerebrate posturing

-level of lesion

A
  • elbow extension/knee extension
  • antigravitational muscles uninhibited

BELOW THE RED NUCLEUS and ABOVE THE VESTIBULAR NUCLEUS
-rubrospinal system lost

55
Q

List the branchial motor nerves

A

V, VII, IX, X, XI

56
Q

Define central pattern generators

  • controller

- trigger

A

Preprogrammed circuit that causes rhythmic or oscillating movements

  • controller -> cerebral cortex
  • trigger -> brainstem
57
Q

Max deficit time seen w/ Guillain-Barre?

A

2 weeks

58
Q

3 most common causes of death with Guillain-Barre

A
  • resp failure
  • DVT
  • Cardiac arrythmias
59
Q

How to assess risk of resp failure

A

Check forced vital capacity

60
Q

Length dependent peripheral neuropathy

  • onset
  • time course
  • associated with (most common cause)
  • serology to rule out
  • Tx
A

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
Q

Differences b/w CIPD and Guillain-Barre

A

CIPD

  • active beyond 8 weeks
  • no resp failure
  • responds to prednisone
  • atypical pattern
62
Q

Paraneoplastic pure sensory neuropathy

  • presentation
  • etiology and pathogenesis
A

PRESENTATION

  • diffuse numbness
  • painful paresthesias
  • sensory ataxia

ETIOLOGY
-cancer -> commonly small cell lung

PATH
-Anti-Hu Abs attack DRG (sensory neuron selectivity)

63
Q

Charcot Marie Tooth Disease

  • etiology
  • progression
  • CMT-1 vs CMT-2
A

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
Q

List 4 mononeuropathies and which one does NOT have motor sxs

A
  1. Median @ wrist -> CTS (SENSORY ONLY)
  2. Ulnar @ elbow
  3. Fibular @ fibular head
  4. Radial in spiral groove
65
Q

Risk factors for carpal tunnel

A

DM, thyroid disease, pregnancy

66
Q

Dermatomes and myotomes for

  • C5
  • C7
  • L5
  • S1
A

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
Q

Myasthenia gravis associated with?

Pathology

A

Thymus pathology (e.g. thymoma)

Abs against nicotinic Ach receptors

68
Q

Signs and sxs of LEMS

Pathology

Common cause

Treatment

A

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
Q

ALS

  • signs (including lab tests)
  • Treatment
A

SIGNS

  • progressive weakness and wasting
  • spastic (slow) dysarthria
  • EMG -> fibrillations and fasciculations

Tx
-Riluzole -> glutamate antagonist

70
Q

Lab value elevated with myopathies?

A

creatine kinase

71
Q

Dystrophies vs myositis

  • times course
  • tx
A

DYSTROPHIES

  • Slowly progressive and hereditary
  • At present, disappointing Rx

Myositis

  • weeks to months
  • responsive to immunosuppression
72
Q

Myopathies have (proximal/distal) muscle weakness?

Exception?

A
  1. Proximal

2. Exception -> Myotonic dystrophy

73
Q

Which myositis has SLOW progression

A 
Inclusion body (very slow)
-unresponsive to steroids
74
Q

Fxal divisions of cerebellar cortex

A
  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
Q

Purkinje cells are (excitatory/inhibitory) on to deep cerebellar nuclei

A

Inhibitory

76
Q

Climbing vs mossy fibers

A

Climbing

  • from ION
  • synapse on PC dendrites

Mossy

  • not from ION
  • synapse onto granule cells

Both are excitatory inputs

77
Q

Dorsal vs ventral spinocerebellar tracts

A

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
Q

Which part of red nucleus do the following pathways go through?

  • From interposed nuclei (spinocerebellum-paravermal cortex)
  • From dentate nuclei (corticocerebellum)
A
  1. magnocellular -> forms rubrospinal tract

2. Parvocellular

79
Q

Medulloblastoma can cause damage to which cerebellar structure/pathway?

What effects are seen?

A
  • 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
Q

Intention tremor results for damage to?

Disruption of what?

A
  • Damage to lateral cerebellar lobe, dentate nucleus, or SCP

- Disruption of viscoelastic freeze arrangement

81
Q

In unilateral cerebellar lesions, the fast phase of nystagmus is toward the side of the lesion or away?

A

Toward

82
Q

Anterior lobe syndrome

  • cause
  • structures damaged
  • manifestations
A

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
Q

Posterior lobe syndrome

  • cause
  • manifestations
A

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
Q

Flocconodular lobe syndrome

A
  • 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
Q

Major breakdown product of DA which can be used to measure DA system activity

A

HVA - homovanillic acid

86
Q

Describe 4 CNS dopaminergic pathways

A
  1. Nigrostriatal
    - substantia nigra -> striatum (caudate+putamen)
    - Parkinson destroys this

2/3. Mesolimbic + Mesocortical

  • VTA -> nucleus accumbens + frontal cortex
  • antipsychotics act here
  1. Hypothalamic
    - arcuate nuc -> median eminence
    - reg of PRL release for pituitary
    - tuberoinfundibular
87
Q

Highest brain [NE]?

[DA]?

A

NE -> LC

DA -> SN/ST

88
Q

Effect of Desiparmine in DA vs NE neurons

A

NE -> inhibits reuptake

DA -> does not

89
Q

Death from cocaine overdose is due to what?

A

Inc HR and Inc BP due to vasoconstriction

Peripheral effect

90
Q

Why does L-dopa tx become less efficacious as time under tx goes on?

A

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
Q

Output neurons of the striatum are?

What NT?

A
  • medium spiny neurons

- GABAergic

92
Q

Relate GPi/m output to movement

A

Increased output - less movement

Decreased output - increased movement

93
Q

Define hemiballism and what causes it

A
  • ballistic movements
  • damage to subthalamic nucleus contralateral to affected side
  • proximal musculature affected
94
Q

Tx for essential tremor

A
  1. Drugs
    - primidone
    - propanolol (peripheral Beta-2 blockade)
    - alcohol
  2. Thalamotomy
  3. Vim thalamic stimulation (DBS)
95
Q

Tx of huntington’s disease associated chorea

A

GABA agonists

  • valproate
  • clonazepam

Presynaptic DA depletes

  • reserpine
  • Alpha-methylparatyrosine
  • Tetrabenazine

DA receptor blockers

96
Q

Head of caudate nucleus is vascularized by

A

Recurrent artery of Heubner.

Branch off the anteromedial group of striate arteries

97
Q

Superior part of internal capsule vascularized by

A

Lenticulostriate arteries

Anterolateral group - MCA + ACA

98
Q

What does the anterior choroidal artery supply?

A
  • Optic tract
  • Medial temporal cortex - Parahippocampal gyrus
  • Amygdala
  • Posterior limb of internal capsule
  • -Inferior
  • -Sublenticular
  • -Retrolenticular
99
Q

Summarize blood supply to internal capsule

A

Superior part - lenticulostriate arteries

Inferior part

  • posterior limb - anterior choroidal
  • anterior limb + genu - medial striate arteries
100
Q

2 important branches of ACA and structure(s) they supply

A
  • Pericallosal – inferior to cingulate gyrus
  • Callosomarginal – superior to cingulate gyrus
  • They go to the paracentral lobule and supplementary motor cortex
101
Q

The venous angle is landmark for?

formed from?

A
  • interventricular foramen

- jx of thalamostriate vein and internal cerebral vein

BMB (15 decks)

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