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Neuro & Special Senses > Ear > Flashcards

Ear Flashcards

1
Q

What is the sensory supply to the pinna?

A

Upper lateral surface - CN V3 auriculotemporal
Lower lateral/medial - C3 - greater auricular
Superior medial - C2/C3 lesser occipital nerve
External auditory meatus - auricular branch of vagus

So can perform regional nerve blocks

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2
Q

What is the anatomy of the external ear?

A

Auricle/pinna and external acoustic meatus

Lateral third of external acoustic meatus is cartilage, medial two thirds are bony from temporal bone
Contains keratinised squamous epithelium

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3
Q

What is the vascular supply to the auricle?

A

External carotid artery, superficial temporal, occipital

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4
Q

What is the innervation of the external acoustic meatus?

A

Auriculotemporal nerve branch of trigeminal

Auricular nerve - branch of vagus CN X

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5
Q

What is the tympanic membrane?

A

Middle layer of connective tissue
Oblique angle to maximise sound localisation
At centre - umbo attaches to handle of malleus

Transmits sound waves from external ear to ossicles of the middle ear

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6
Q

What is the innervation of the middle ear?

A

Vagus nerve and glossopharyngeal nerve

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7
Q

What is the anatomy of the middle ear?

A

Auditory ossicles - malleus, incus, stapes form oval window and transmit and amplify sound vibrations

Tensor tympani, stapedius muscles

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8
Q

What is the function of the Eustachian tube?

A

Aerates the middle ear to equalise pressure

For optimum movement of the tympanic membrane

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9
Q

What is the anatomy of the inner ear?

A

Vestibulocochlear organs, receives sound waves to convert into electrical signals

Bony labyrinth - vestibule, three semi circular canals and the cochlea. Vestibule contains saccule and utricle to detect linear motion.

Semicircular canals - rotatory movements
Cochlear contains organ of corti containing epithelial cells converting sound waves to electrical impulses

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10
Q

What is ear trauma commonly related to?

A

Sports injuries

Violence

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11
Q

How severe is ear trauma normally?

A

Normally uncomplicated and treatable under local anaesthetic

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12
Q

How should a laceration with exposed cartilage be managed?

A

Cover any exposed cartilage with skin

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13
Q

What may be done if there is skin loss or a skin laceration can’t be closed by primary closure?

A

Plastic reconstructive surgery

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14
Q

What is the main risks with bites to the ear?

A

Infection from skin commensal or oral commensal of offending creature/person
Staph epidermis and S hominid are most prevalent coagulase negative commensals

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15
Q

How would you manage a patient with an ear bite?

A

Take a good history - work out likely organism

Leave wound open

Irrigate wound thoroughly

Antibiotics

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16
Q

Why are pinna haematoma’s dangerous?

A

Disrupt blood supply to cartilage as it normally obtains nutrients via diffusion from vessels in the perichondrium.

Can lead to avascular necrosis

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17
Q

What is cauliflower ear?

A

Cartilage undergoes avascular necrosis which stimulates the formation of new cartilage but it grows asymmetrically

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18
Q

What can cause a tympanic membrane perforation?

A

Blunt force - trauma to side of head
Penetrating trauma - e.g. cotton bud
Otitis media
Barotrauma - explosion/scuba diving

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19
Q

How does a tympanic membrane perforation present?

A

Pain
Conductive hearing loss (possibly)

Can get tinnitus and serosanguineous discharge

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20
Q

How can tympanic membrane perforation be managed?

A

Most heal within 8 weeks- monitoring
Antibiotics if contamination
Keep clean and cry

Not healing after 6 months or hearing loss/recurrent infection - myringoplasty

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21
Q

What can cause haemotympanum?

A

Basal skull fracture - most common
Nasal packing
Bleeding disorders/anticoagulants
Recurrent ear infections

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22
Q

How does haemotympanum present?

A

Seen through tympanic membrane

Associated with conductive hearing loss

Sense of fullness in ear

Pain

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23
Q

How is haemotympanum managed?

A

Treat conservatively but follow up to ensure no residual hearing loss

However commonly associated with other issues - head trauma

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24
Q

What is otitis externa and causes?

A

Inflammation of the skin of the external ear canal
Acute - less than three weeks, chronic >3
Swimmer’s ear - water causes inflammation in ear

Bacterial infection, fungal, eczema, seborrhoeic dermatitis, contact dermatitis

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25
Q

When is it important to think about fungal infection as a cause for otitis externa?

A

Patients who have had multiple courses of topical antibiotics - kills friendly bacteria that have protective function against fungal infections

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26
Q

What are the two most common bacterial causes of otitis externa?

A

Pseudomonas aeruginosa - gram neg aerobic rod shaped bacteria, grows in moist oxygenated environments e.g. CF

Staphylococcus aureus

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27
Q

What is the presentation of otitis externa?

A

Ear pain, discharge, itchiness, conductive hearing loss if becomes blocked

On examination - erythema, swelling, tenderness of canal
Pus or discharge, lymphadenopathy

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28
Q

What is the management of otitis externa?

A

Mild - acetic acid 2% antifungal and antibacterial
(Otomize ear spray)

Moderate - topical antibiotic and steroid e.g.
Neomycin, dexamethasone, acetic acid
Neomycin and bethamethasone

Fungal infections with - clotrimazole ear drops

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29
Q

What is it important to exclude before prescribing aminoglycosides?

A

e.g. gentamicin or neomycin
Potentially ototoxic, if get past tympanic membrane

So exclude perforated tympanic membrane

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30
Q

What is malignant otitis externa?

A

Severe and life threatening form of otitis externa
Infection spreads to bones of ear canal
Progresses to osteomyelitis of temporal bone

Risk factors e.g. diabetes, immunosuppressants, HIV

Causes persistent headache, severe pain and fever
Granulation tissue at junction between bone and cartilage

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31
Q

What is the treatment for malignant otitis externa?

A

Admission to hospital, ENT treatment
IV antibiotics
Imaging - CT or MRI head

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32
Q

What complications can malignant otitis externa lead to?

A 
Facial nerve damage and palsy
Other cranial nerve involvement 
Meningitis
Intracranial thrombosis
Death
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33
Q

What is otitis media?

A

Infection of middle ear, often preceded by viral upper respiratory tract infection

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34
Q

What is the cause of otitis media?

A

Strep pneumoniae most common cause

Haemophilus influenzae
Moraxella catarrhalis
Staph aureus

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35
Q

What is the presentation of otitis media?

A

Ear pain
Reduced hearing in affected ear
Generally feeling unwell, symptoms of upper airway infection
Can cause issues in balance and vertigo if affecting vestibular system
Discharge if tympanic membrane perforated

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36
Q

What is seen on examination of the ear in otitis media?

A

Bulging red inflamed looking membrane (as opposed to pearly grey translucent and shiny)
If perforation, may see discharge and hole in membrane

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37
Q

What is the management of otitis media?

A

Most cases resolve without antibiotics after 3 days-wk
Simple analgesia for pain and fever

Immediate abx if significant co-morbidities, systematically unwell or immunocompromised.

Delayed prescription - collected after 3 days if still bad
Amoxicillin for 5-7 days, clarithromycin if allergic, erythromycin in penicillin allergic women

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38
Q

What are the complications of otitis media?

A 
Otitis media with effusion
Temporary hearing loss
Perforated tympanic membrane 
Labyrinthitis, mastoiditis, abscess
Facial nerve palsy
Meningitis
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39
Q

What is chronic suppurative otitis media?

A

Chronic inflammation of the middle ear and mastoid

Presents with recurrent ear discharges through a tympanic perforation

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40
Q

What are the causes of chronic suppurative otitis media?

A 
Pseudomonas aerugonisa
Staph aureus
Proteus species
Aspergillus
Candida albicans
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41
Q

What are the risk factors for chronic suppurative otitis media?

A 
Younger age - under five
Allergy/atopy
URTI
Acute or recurrent otitis media
Exposure to second hand smoke
Social deprivation
Snoring
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42
Q

What is the management of chronic suppurative otitis media?

A

Appropriate antibiotic given topically - careful use of aminoglycosides
Intensive microsuction to remove debris
Control of granulation tissue

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43
Q

What are the types of chronic otitis media?

A

Active or inactive depending on whether the ear is discharging or not
Can be subdivided into mucosal disease or squamous

Active - chronic discharge from the middle ear through a tympanic perforation
Inactive mucosal disease - tympanic perforation

Inactive mucosal - dry perforation
Inactive squamous - retraction pocket which has potential to become active with retained debris (keratin)
Active mucosal - wet perforation with inflamed middle ear mucosa and discharge
Active squamous - cholesteatoma

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44
Q

What is active squamous disease in chronic otitis media?

A

Cholesteatoma

If this is present, surgery is required

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45
Q

What is otitis media with effusion?

A

Middle ear effusion without the signs of infection

Glue ear

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46
Q

What are the causes of OME?

A

Eustachian tube dysfunction - in children smaller and more horizontal, impairing middle ear ventilation
Cleft palate

Beware of nasopharyngeal tumours in adults which can block drainage

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47
Q

What is the presentation of OME?

A

Conductive hearing loss, behavioural changes
May be asymptomatic in an infant
Poor speech development
Otoscopy - tympanic membrane is dull, visible fluid level

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48
Q

What are the investigations for OME?

A

Pure tone audiogram - conductive hearing loss
Tympanometry will show flat trace due to reduced compliance of the tympanic membrane - type b curve
In an adult with unilateral effusion, flexible nasoendoscopy FNE to rule out nasopharyngeal tumour

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49
Q

What is the treatment for OME?

A

Antibiotics have no benefit
Watch and wait - 50% of OME will resolve spontaneously within 3 months
Hearing aids may be useful while waiting to resolve
Myringotomy and ventilation tube insertion - grommets that will self extrude after 9 months

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50
Q

What common bacterial pathogens can cause an infection/ottorhoea?

A 
Pseudomonas aeruginosa
Staph aureus
Proteus spp.
Strep pneumonia
Haemophilus influenza
Moraxella catarrhalis
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51
Q

What are the differentials for otorrhoea?

A

Fungal otitis externa - itchy ear canal, fluffy white discharge/coating of the canal

Acute otitis media +- perforation - recent URTI, deep severe ear pain, mucoid ear discahrge

Otitis externa - thin watery discharge

Necrotising otitis externa/malignant - foul smelling discharge, cranial nerve palsies, unilateral severe pain

Cholesteatoma - ear drum retraction, perforation, keratin accumulation, unilateral chronic offensive smelling ear

CSF otorrhoea - clear watery discharge, history of trauma or skull base injury

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52
Q

What is otosclerosis?

A

Remodelling of the small bones of the middle ear
Leads to conductive hearing loss
Usually presents before age 40

Base of stapes attaches to oval window, causing stiffening and fixation and preventing it from transmitting sound correctly

Autosomal dominant

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53
Q

What is the presentation of otosclerosis?

A

Patient under 40
Unilateral or bilateral hearing loss, or tinnitus
Tends to affect hearing of lower pitched sounds more than higher pitched sounds
There is intact sensory hearing, so patient can experience voice being loud - talks quietly

54
Q

What is seen on examination of otosclerosis?

A

Otoscopy is normal

Weber’s - normal if otosclerosis is bilateral
Unilateral - sound louder in the more affected ear

Rinne’s - conductive hearing loss

55
Q

What are the investigations for otosclerosis?

A

Audiometry - conductive hearing loss
Bone conduction readings will be normal
Hearing loss greater at lower frequencies

Tympanometry will show generally reduced admittance (absorption) of sound
Tympanic membrane stiff, non compliant, non-absorbant reflects the sound back

High resolution CT can detect boney changes

56
Q

What is the management of otosclerosis?

A

Conservative - use of hearing aids

Surgery - successful, can restore to normal
Lift tympanic membrane and surrounding skin out of the way to access middle ear through ear canal:

Stapedectomy - remove entire stapes and replace with prosthesis

Stapedotomy - remove part of stapes bone, leave the base (footplate) attached to oval window
Small hole made in base for prosthesis to attach

57
Q

What is vertigo?

A

Sensation that there is movement between the patient and their environment, a problem with the vestibular system (peripheral) or brainstem/cerebellum (central)

Vision, proprioception and signals from the vestibular system are responsible for maintaining balance and posture

58
Q

What are the peripheral/vestibular causes of vertigo?

A

Benign paroxysmal positional vertigo
Meniere’s disease
Vestibular neuronitis
Labyrinthitis

Trauma to vestibular nerve
Vestibular nerve tumours - acoustic neuroma
Otosclerosis
Hyperviscosity syndromes
Herpes zoster infection - RH syndrome
59
Q

What are central causes of vertigo?

A

Posterior circulation infarction - stroke
Tumour - gradual onset
Multiple sclerosis - relapsing and remitting
Vestibular migraine - triggered by e.g. stress, bright lights, strong smells, certain foods, dehydration

60
Q

What are the differences in presentation between peripheral and central vertigo?

A

Peripheral - sudden onset, short duration, hearing loss or tinnitus often present, coordination in tact, bad nausea

Central - gradual onset, persistent duration, hearing not usually impaired, coordination impaired, mild nausea

61
Q

What are key features that may point to a specific cause of vertigo?

A

Recent viral illness - labyrinthitis or vestibular neuronitis
Headache - vestibular migraine, cerebrovascular accident, brain tumour
Ear symptoms e.g. pain, discharge - infection
Acute onset neurological symptoms - stroke

62
Q

What should be examined in a patient presenting with vertigo?

A

Ear examination - any infection or pathology
Neurological examination - assess for central causes of vertigo e.g. stroke, or MS
Cardiovascular examination - assess for cardiovascular causes of dizziness e.g. arrhythmias or valve disease

Special tests:
Romberg’s test
Dix-Hallpike manoevre
HINTS examination to distinguish between central and peripheral vertigo

63
Q

What is the HINTS examination?

A

HI - head impulse test
Patient sitting upright and fixing gaze on examiner’s nose
Examiner holds head then rapidly jerks it 10-20 degrees in one direction whilst still looking at nose
Then move back to centre and repeat in opposite direction

Patient with abnormally functioning vestibular system - eyes will saccade (rapidly move back and forth)

N - Nystagmus
Patient look left and right, eyes will saccade
Few beats can be normal, unilateral more likely a peripheral cause

Test of skew - alterative cover test
Patient focuses on examiners nose
Cover one eye at a time, eyes should remain fixed on nose with no deviation
If there is vertical correction when eye uncovered - drifted up or down - central cause of vertigo

64
Q

What is the management of a patient presenting with vertigo?

A

Suspected central vertigo - referral for further investigation e.g. CT or MRI head for cause
Peripheral vertigo - prochlorperazine, antihistamines

Betahistine reduced attacks in Meniere’s
Epley manoevre for BPPV
Triptans, propranolol, amitriptyline for migraines
DVLA guide

65
Q

What is the cause of BPPV?

A

Due to calcium carbonate crystals displaced in semicircular canals
May be displaced due to viral infection, trauma, ageing

Disrupts flow of endolymph
Head movement creates flow of endolymph triggering episodes of vertigo

66
Q

What is the presentation of BPPV?

A

Head movements trigger episodes, e.g. turning over in bed
Symptoms settle after 20-60 seconds
Asymptomatic between attacks
Occur over several weeks, resolve, then recur

Does not cause hearing loss or tinnitus

67
Q

What is the Dix-Hallpike manoeuvre?

A

Sit upright, head turned 45 degrees to one side - to right to test right ear and vice versa
Support head to stay at 45 degrees whilst lowering patient backwards until head hanging off cough
Then extend head back 20-30 degrees below couch
Watch eyes for 30-60 seconds, look for nystagmus
Repeat on other side

68
Q

What is the Epley manoeuvre?

A

To treat BPPV move crystals so does not disrupt endolymph
Follow steps of Dix Hallpike
Rotate head 90 degrees past central position
Roll onto side so head rotates further 90 degrees
Patient sit up sideways with legs off the cough
Position head in central position, chin to chest
Support head in place for 30 seconds
Look for nystagmus

69
Q

What is the treatment for BPPV?

A

Epley’s curative 90% of the time
Brandt-Daroff exercises - sit on end of bide and lyinh sideways from one side to the other
Surgical management is rare

70
Q

What is Meniere’s?

A

Long term inner ear disorder
Excessive build up of endolymph causing higher than normal pressure
Endolymphatic hydrops

71
Q

What is the presentation of Meniere’s?

A

40-50 years old
Unilateral episodes of vertigo, hearing loss, tinnitus
Vertigo comes and goes in episodes, 20 mins, settles
Can come in clusters, then prolonged periods is better

Hearing loss fluctuates, then becomes more permanent
Sensorineural hearing loss, unilateral

Fullness in the ear, drop attacks, imbalance

72
Q

What is the management of Meniere’s?

A

For acute attacks - prochlorperazine, antihistamines
Prophylaxis with betahistine

Pressure reducing therapies
e.g. low salt diet
medications e.g. betahistine, diuretics
Intratympanic injection of steroid or gentamicin
Decompression, labyrinthectomy, vestibular nerve section

73
Q

What is vestibular neuronitis?

A

Inflammation of the vestibular nerve

Usually transmits signals from vestibular system to brain for balance, along with cochlear nerve for cochlea for hearing = 8th cranial nerve, vestibulocochlear

74
Q

What is the presentation of vestibular neuronitis?

A

Recent history of viral upper respiratory tract infection
Symptoms most severe for first few days

Acute onset of vertigo
Initially constant, then triggered/worsened with head movement
Nausea and vomiting, balance problems

Hearing loss and tinnitus not features of neuronitis - consider labyrinthitis or Meniere’s

75
Q

What medical interventions are used in Meniere’s disease?

A

Thiazides - bendroflumathiazide
Betahistine (antivertigo)
Antiemetic - prochlorperazine

76
Q

What surgical interventions are used in Meniere’s disease?

A 
Grommets
Dexamethasone middle ear injection
Endolymph sac decompression
Vestibular destruction using middle ear gentamicin injection
Surgical labyrinthectomy (rare)
77
Q

How is an acute vestibular neuritis investigated?

A

MRI to exclude acoustic neuroma
Excludes lesion along central auditory pathway

Pure tone audiogram

Head impulse test - eyes will saccade when fixed on examiners nose

78
Q

What is the management of vestibular neuronitis?

A

Steroids - normally orally, can be injected into middle ear
Anti-virals
Other treatments e.g. hyperbaric oxygen, carbogen

79
Q

What is labyrinthitis?

A

Inflammation of the bony labyrinth of the inner ear
includes semi-circular canals, vestibule, cochlea
Usually following upper respiratory tract infection

80
Q

What is the presentation of labyrinthitis?

A

Acute onset vertigo
Hearing loss
Tinnitus

Symptoms associated with causative virus - cough, sore throat, blocked nose

81
Q

How can labyrinthitis be diagnosed?

A

Clinical diagnosis, examination, head impulse test

82
Q

What is the management of labyrinthitis?

A

Supportive care, short term use of medication
Prochlorperazine
Antihistamines e.g. cyclizine

Antibiotics for bacterial labyrinthitis
Underlying infection e.g. otitis media or meningitis needs appropriate treatment - hearing loss key complication of meningitis, hence offered audiology assessment

83
Q

What are causes of sensorineural hearing loss?

A

Sudden sensorineural hearing loss over 72 hours
Presbycusis - age related
Noise exposure
Meniere’s
Labyrinthitis
Acoustic neuroma
Neurological conditions e.g. stroke, MS, brain tumours
Infections
Medications - loop diuretics, aminoglycoside abx e.g. gentamicin, chemo drugs e.g. cisplatin

84
Q

What are causes of conductive hearing loss?

A 
Ear wax or foreign object
Infection
Fluid in middle ear
Eustachian tube dysfunction
Perforated tympanic membrane
Otosclerosis
Cholesteatoma
Exostoses
Tumours
85
Q

What are acoustic neuromas?

A

Benign tumours of the schwann cells surrounding the auditory nerve innervating the inner ear
Usually unilateral, benign - neurofibromatosis type II

Occur at the cerebellopontine angle

86
Q

What is the presentation of acoustic neuroma?

A 
40-60 years, gradual onset
Unilateral sensorineural hearing loss - first symptom
Unilateral tinnitus
Dizziness or imbalance
Sensation or fullness in the ear

Can grow large enough that they can cause facial nerve palsy if compress facial nerve
Fore head not spared - lower motor neurone lesion

87
Q

What are the investigations for an acoustic neuroma?

A

Sensorineural pattern of hearing loss on audiometry

Brain imaging MRI/CT to establish tumour

88
Q

What is the management for an acoustic neuroma?

A

Conservative if no symptoms or tx inappropriate
Surgery - partial or total removal
Radiotherapy to reduce growth

Risk of vestibulocochlear nerve injury - permanent hearing loss or dizziness
Facial nerve injury - facial weakness

89
Q

What is a cholesteatoma?

A

Abnormal collection of squamous epithelial cells in the middle ear, non-cancerous but can invade

90
Q

What is the pathophysiology of a cholesteatoma?

A

Negative pressure in the middle ear
due to eustachian tube dysfunction
causes pocket of tympanic membrane to retract
Squamous epithelial cells proliferate out of this pocket
Can damage the ossicles and cause hearing loss

91
Q

What is the presentation of a cholesteatoma?

A

Foul discharge from the ear
Unilateral conductive hearing loss

Infection, pain, vertigo, facial nerve palsy as continues to grow

Otoscopy shows build up of white debris
crust in the tympanic membrane

92
Q

What is the management of a cholesteatoma?

A

CT head to confirm diagnosis, plan for surgery
MRI assess invasion, damage to local soft tissues
Surgical removal

93
Q

Two muscles are involved in the Acoustic Reflex. What is this and name the muscles involved.

A

Protective muscles contract in response to loud noises

Tensor Tympani and Stapedius

94
Q

What is the difference between Vestibular Neuritis and Labyrinthitis?

A

Vestibular Neuritis only affect vestibular nerve
Labyrinthitis affects vestibular nerve and labyrinth

Vestibular Neuritis will not alter hearing

95
Q

What causes Vestibular Neuritis?

A

Reactivation of latent type 1 HSV in Vestibular Ganglion

Commonly preceded by URTI

96
Q

What causes Labyrinthitis?

A

Usually viral in origin
Bacterial is dangerous (passes between anatomical connections)
May be associated with systemic disease

97
Q

Name three clinical investigations you could do for suspected Labyrinthitis/VN

A

Head Impulse Test
Nystagmus (consistent and unilateral)
Skew

98
Q

Name five investigations for Menieres

A 
Full Neurological exam
Pure tone audiometry
MRI IAM
Video Head Impulse testing 
ECG
99
Q

What is an important management step in Menieres?

A

Inform DVLA

100
Q

Name four risk factors for BPPV

A

Older Age
Women
Menieres (co diagnosis in 30%)
Anxiety Disorders

101
Q

What does the direction of Nystagmus in BPPV indicate about the canals?

A

Vertical and Rotary - Posterior Canal

Horizontal - Horizontal canal

102
Q

BPPV is self limiting over a number of weeks but can reoccur. What should you advise the patient?

A

Notify DVLA
Get out of bed slowly
Epleys Manouvre (Dix Hallpike but wait for Nystagmus to subside then rotate 90 degrees and sit patient up)

103
Q

Give a differential diagnosis for BPPV

A

Vestibular Migraine

104
Q

Otosclerosis is caused by the pathological increased bone turnover. Give four risk factors

A

Genetics (Autosomal Dominant)
Oestrogen
Viral
Lack of fluoride

105
Q

There are two types of tinnitus: Pulsatile and Non Pulsatile.

What is Pulsatile tinnitus?

What is Non Pulsatile tinnitus?

A

Synchronous with heartbeat due to turbulent flow reaching cochlea

Causes: Carotid Atherosclerosis, AV Malformation, Pagets, Otosclerosis

Non-pulsatile Buzzing/high pitched/clicking

Causes: Presbyacusis, Menieres, Drugs

106
Q

Name three drugs associated with Tinnitus

A

Loop Diuretics
NSAIDs
Salicyclates

107
Q

How is Tinnitus investigated?

A

MRI (if unilateral to exclude Acoustic Neuroma)
Pulsatile - CT/MR Angiography
Tinnitus Functional Index

108
Q

Aside from Webers and Rinnes, Pure Tone Audiometry is used to investigate reduced hearing. What is this?

A

Evaluates the quietest sound that can be heard in each ear

Must exclude wax/infection beforehand

109
Q

Describe the difference in audiometry graphs between Presbyacusis and Menieres

A

Menieres - hearing loss at a lower frequency

Presbyacusis - hearing loss at a higher frequency

110
Q

Describe four surgical management options for reduced hearing loss

A

Bone anchored hearing aid
Cochlea Implant
Stapedectomy and Prosthesis
Tympanoplasty

111
Q

Give three management options for excess wax

A

Topical Olive Oil/Sodium Bicarbonate
Microsuction
Syringing

112
Q

Name three congenital and two acquired causes of childhood deafness

A

Congenital - Rubella, Ear Atresia, Ossicular Abnormalities

Acquired - Hypoxia, Jaundice, Meningitis, Head Injury

113
Q

What is Ramsey Hunt Syndrome?

A

Reactivation of Herpes Zoster in geniculate ganglion

114
Q

What are the motor branches of the facial nerve?

A

Within facial canal - Nerve to Stapedius

Prior to Parotid - Posterior Auricular, Nerve to Digastic, Nerve to Omohyoid

Within Parotid - Temporal, Zygomatic, Buccal, Mandibular, Cervical

115
Q

Name five clinical features of Ramsay Hunt Syndrome

A
  • Vesicular rash on ipsilateral ear/hard palate/ anterior 2/3 of tongue
  • Hearing loss
  • Ipsilateral facial weakness
  • Drooling
  • Hyperacusis
116
Q

How is facial paralysis graded?

A

House Brackmann (I - IV)

117
Q

Ramsey Hunt Syndrome is a clinical diagnosis. What features would point towards an alternative?

A

Systemic Illness
Hearing abnormalities
Forehead sparing

118
Q

What are the main management points for Ramsey Hunt Syndrome?

A

Analgesia
Steroids +PPI
Aciclovir

Eye care

119
Q

What particular things would you want to note in a child with reduced hearing?

A 
Age of first word
Milestones
Vocab extent 
Pain/Discharge
Imbalance
DH
120
Q

Name three syndromes that include deafness

A

Waadenberg (+Heterochromia and wide nasal bridge)

Jervell Lange Nielson

CHARGE

121
Q

Why do Electronic Hearing Aids work better for conductive hearing loss?

A

Sensorineural causes recruitment - loud sounds are heard exceptionally loudly

122
Q

Name three conditions to avoid in someone who has to lip read

A

Poor background lighting
Beard and Moustache
Covering face with hand

123
Q

What is a contraindication to Cochlear Implant?

A

Middle ear infection

124
Q

Give four otological causes of Otalgia

A

Otitis Externa
Furunculosis
Otitis Media
Acute Ototic Barotrauma

125
Q

Name a non otological cause of Otalgia

A

Referred pain (Tonsillitis, Teeth, TMJ)

126
Q

Name two causes of watery otorrhoea

A

Eczema of external ear

CSF

127
Q

Name two causes of purulent otorrhoea

A

AOM

Furunculosis

128
Q

Name two causes of bloody otorrhoea

A

Trauma

AOM

129
Q

Name a cause of foul smelling otorrhoea

A

Cholesteotoma

130
Q

The causes of vertigo can be diagnosed based on time frame. Give two causes of vertigo lasting ‘hours to days’

A

Ototoxicity

Central vestibular disease

131
Q

What would investigations of Otosclerosis show?

A

Tympanogram - normal type A

Pure Tone Audiometry - Carhart notch (dip at 2kHz)

132
Q

How are audiograms plotted?

A

Document volume at which patient can hear different tones

Frequency in Hz on x axis
Volume in dB on y axis

X - left sided air conduction
] - left sided bone
O - right sided air
[ - right sided bone

Neuro & Special Senses (12 decks)

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