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ENT Flashcards

1
Q

HEARING LOSS

What are the two types of hearing loss and briefly explain them?

A
  • Conductive = sound is not conducted to the inner ear due to problem of external or middle ear
  • Sensorineural = sound is conducted to inner ear but issue at the sensory organ (cochlear) or vestibulocochlear nerve
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2
Q

HEARING LOSS

What are the causes of conductive hearing loss?

A
  • Wax impaction
  • Otitis media with effusion
  • Perforated tympanic membrane
  • Otosclerosis
  • Cholesteatoma
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3
Q

HEARING LOSS

What are the causes of sensorineural hearing loss?

A
  • Presbycusis = most common (age-related), gradual + insidious (symmetrical high frequency hearing loss)
  • Meniere’s disease
  • Congenital infections = rubella, CMV
  • Acoustic neuroma
  • Drugs = loop diuretics, aminoglycosides
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4
Q 
HEARING LOSS
Explain the axis of an audiogram
What is normal?
What indicates sensorineural hearing loss?
What indicates conductive hearing loss?
What indicates mixed hearing loss?
A
  • X-axis is frequency (Hz) going low to high, Y-axis is volume (dB) with top quiet to bottom loud
  • Anything <20dB line
  • BOTH air + bone conduction impaired (>20dB)
  • ONLY air conduction >20dB, bone is normal
  • BOTH air + bone impaired but AIR WORSE by >15dB
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5
Q

HEARING LOSS

What two bedside tests would you do in hearing loss and briefly explain them?

A
  • Rinne’s = place tuning fork on mastoid then external acoustic meatus
  • Weber’s = place tuning fork on forehead in midline
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6
Q

HEARING LOSS

What are you looking for in Rinne’s test?

A
  • Normal = louder at EAM
  • Conductive = louder at mastoid
  • Sensorineural = both decreased
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7
Q

HEARING LOSS

What are you looking for in Weber’s test?

A
  • Normal = vibrations equal in both ears
  • Conductive = louder in ABNORMAL ear
  • Sensorineural = louder in NORMAL ear
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8
Q

HEARING LOSS

What is the management of hearing loss?

A
  • Conductive = resolve issue (e.g., syringe ears, treat infection)
  • Sensorineural = hearing aids, cochlear implants if profound hearing loss >95dB
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9
Q

OTOSCLEROSIS

What is the pathophysiology of otosclerosis?

A
  • Autosomal dominant condition with replacement of normal bone by vascular spongy bone mainly affecting base of stapes where it attaches to oval window causing stiffening preventing it from transmitting sound
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10
Q

OTOSCLEROSIS

What is the clinical presentation of otosclerosis?

A
  • Progressive conductive deafness at 20–40y
  • Tinnitus
  • Audiometry = Carhart’s notch (false depression of bone conduction at 2000Hz)
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11
Q

OTOSCLEROSIS

What is the management of otosclerosis?

A
  • Hearing aid

- Stapedectomy

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12
Q

SSNHL
What is sudden sensorineural hearing loss (SSNHL)?
What is the most common cause?
What are some other causes?

A
  • Sensorineural hearing loss over <72h
  • Idiopathic
  • Meniere’s disease, ototoxic meds, MS, stroke, acoustic neuroma
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13
Q

SSNHL

How do you manage SSNHL?

A
  • URGENT ENT referral
  • Audiometry to establish Dx
  • CT/MRI head if ?stroke/acoustic neuroma
  • ALL cases receive high dose PO corticosteroids
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14
Q

OTITIS MEDIA
What is otitis media?
What are some causes?

A
  • Acute infection of middle ear, v common in paeds

- Mostly bacterial = strep pneumoniae #1, H. influenzae, moraxella catarrhalis

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15
Q

OTITIS MEDIA
What is the clinical presentation of otitis media?
What would you find on examination?

A
  • Recent viral URTI Sx
  • Otalgia = tugging/rubbing ear in paeds
  • Conductive hearing loss
  • Otoscopy = bright red + bulging tympanic membrane (loss of light reflex)
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16
Q

OTITIS MEDIA

What are the potential sequelae of otitis media?

A
  • Otitis media with perforation
  • Otitis media with effusion
  • Labyrinthitis
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17
Q

OTITIS MEDIA
How does otitis media with perforation present?
What can happen if unresolved?

A
  • Purulent otorrhoea clinically + on otoscopy

- Chronic suppurative otitis media = perforation of tympanic membrane with otorrhoea for >6w

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18
Q

OTITIS MEDIA

What are some complications of otitis media?

A
  • Mastoiditis
  • Meningitis
  • Brain abscess
  • Facial nerve paralysis
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19
Q

OTITIS MEDIA
What is the first line management of otitis media?
What might be considered afterwards?

A
  • Supportive management with analgesia, safety net to seek help if no improvement after 3d
  • First line Abx = amoxicillin 5–7d (erythromycin if pen allergic/pregnant)
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20
Q

OTITIS MEDIA

When would you consider immediate antibiotic prescription?

A
  • Sx ≥4d + not improving
  • Systemically unwell
  • Immunocompromised
  • <2y and bilateral
  • Otitis media with perforation
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21
Q

OME
What is otitis media with effusion (OME)?
What are some risk factors for OME?

A
  • Fluid collection within the middle ear space without signs of acute infection.
  • Male, siblings with glue ear, trisomy 21, parental smoking
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22
Q

OME

What is the clinical presentation of OME?

A
  • # 1 cause of conductive hearing loss in paeds
  • May have secondary problems such as speech + language delay
  • Otoscopy = dull + retracted TM with visible fluid level
  • Audiometry = flat tympanogram
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23
Q

OME

What is the management of OME?

A
  • Watchful waiting for 3m
  • Grommet insertion to allow fluid to drain
  • Adenoidectomy
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24
Q

OTITIS EXTERNA
What is otitis externa?
What are some risk factors?

A
  • Infection of outer ear

- Increased water contact (swimming), cotton buds, hearing aids, DM

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25
Q

OTITIS EXTERNA
What is the most common cause of otitis externa?
What are some other causes?

A
  • Bacterial = pseudomonas aeruginosa #1, staph. aureus

- Derm = seborrhoeic dermatitis, contact dermatitis

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26
Q

OTITIS EXTERNA

What is the clinical presentation of otitis externa?

A
  • Otalgia (esp. on tragus palpation), otorrhoea, itch

- Otoscopy = red, swollen, eczematous canal with discharge

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27
Q

OTITIS EXTERNA

What is a key complication of otitis externa?

A
  • Malignant otitis externa = infection spreads to bones surrounding the ear canal + skull + can progress to osteomyelitis of the temporal bone
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28
Q

OTITIS EXTERNA
What patients are susceptible to malignant otitis externa?
How does it present?
What are some potential complications?

A
  • Immunocompromised (DM, HIV)
  • Severe otalgia, otorrhoea, temporal headaches
  • Facial nerve palsy, meningitis, death
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29
Q

OTITIS EXTERNA

What is the management of malignant otitis externa?

A
  • Non-resolving otitis externa with worsening pain = URGENT ENT REFERRAL
  • CT scan
  • IV Abx to cover pseudomonas (ciprofloxacin)
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30
Q

OTITIS EXTERNA
What is the first line management of otitis externa?
What if it doesn’t respond?
What is the second line management of otitis externa?

A
  • Topical Abx ± steroid (may need delivery via pope wick)
  • ENT referral
  • PO flucloxacillin if infection spreading, ?swab, ?antifungal
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31
Q

CHOLESTEATOMA

What is cholesteatoma?

A
  • Hyperproliferative non-malignant growth of keratinising squamous epithelial cells of the middle ear causing local destruction
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32
Q

CHOLESTEATOMA

What is the epidemiology of cholesteatoma?

A
  • Most common patients 10–20y

- Majorly associated with cleft palate

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33
Q

CHOLESTEATOMA

What is the clinical presentation of cholesteatoma?

A
  • Painless, foul-smelling, brown, non-resolving otorrhoea
  • Unilateral hearing loss (classically conductive) + tinnitus
  • Local invasion > vertigo (semi-circular canals), facial nerve palsy
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34
Q

CHOLESTEATOMA

What investigations would you do in cholesteatoma?

A
  • Otoscopy = white attic crust seen in uppermost part of ear drum
  • CT head (temporal bone) to confirm diagnosis + plan for surgery
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35
Q

CHOLESTEATOMA
When would you emergency admit someone with cholesteatoma?
What is the general management?

A
  • Local invasion or neuro Sx

- ENT referral for surgical removal

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36
Q

BPPV
What causes benign positional paroxysmal vertigo (BPPV)?
What is the pathophysiology?

A
  • Canaliths (crystals) in the semi-circular canals
  • Normally found in utricle of inner ear but can dislodge into semi-circular canals due to age, infection, head trauma or DM
  • On movement, crystals cause abnormal movement of endolymph in canal > vertigo
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37
Q

BPPV

What is the clinical presentation of BPPV?

A
  • Vertigo which is triggered by change in head position ± nausea
  • Episodes last for up to 1 minute
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38
Q

BPPV

How is BPPV diagnosed?

A
  • Dix-Hallpike Manoeuvre
  • Pt sits upright, head turned 45º to test side, lie down rapidly with head overhanging edge of bed for 1m whilst observing eyes
  • Positive = vertigo + rotatory nystagmus
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39
Q

BPPV

How is BPPV managed?

A
  • Epley manoeuvre

- Teach patients exercises = vestibular rehabilitation (Brandt-Daroff exercises)

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40
Q

BPPV

Describe the Epley manoeuvre

A
  • Dix-Hallpike then remain 1m
  • Rotate head 90º other side for 1m
  • Roll onto shoulder head is facing, rotate head so looking to floor for 1m
  • Slowly sit up, tilt head down tucking chin into chest for 1m
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41
Q

MENIERE’S DISEASE
What is the pathophysiology of Meniere’s disease?
What age group does it classically affect?

A
  • Excessive pressure + progressive dilation of the endolymphatic system in the labyrinth of the inner ear
  • More common in middle-age adults
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42
Q

MENIERE’S DISEASE

What is the classic triad for clinical presentation of Meniere’s disease?

A
  • Triad of UNILATERAL recurrent vertigo, tinnitus + (low freq) sensorineural hearing loss
  • Episodes last mins–hours + often occur in clusters
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43
Q

MENIERE’S DISEASE

Other than the classic triad, what else might occur in Meniere’s disease?

A
  • Sensation of aural fullness
  • Nystagmus
  • Positive Romberg’s
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44
Q

MENIERE’S DISEASE
How is Meniere’s disease diagnosed and what should you tell patients?
What is the acute management of Meniere’s disease?
What is the prophylactic management of Meniere’s disease?

A
  • ENT referral to confirm, tell them to inform DVLA + stop driving until good symptom control
  • Buccal/IM prochlorperazine
  • Betahistine + vestibular rehabilitation exercises
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45
Q

VESTIBULAR NEURONITIS
What is vestibular neuronitis?
What is it associated with?

A
  • Inflammation of the vestibular nerve

- Viral URTI

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46
Q

VESTIBULAR NEURONITIS
How does vestibular neuronitis present?
What does it importantly not present with?

A
  • Recurrent vertigo attacks lasting hours–days
  • N+V, horizontal nystagmus
  • NO hearing loss or tinnitus
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47
Q

VESTIBULAR NEURONITIS

What key exam sign is positive in vestibular neuronitis and explain it?

A
  • +ve head impulse test (sign of peripheral vertigo)
  • Pt focuses on examiner’s nose entire time, head rapidly jerked in 1 direction
  • Normal vestibular system or CENTRAL vertigo = eyes fixed on nose
  • Abnormal = eyes saccade (rapidly move back/forth) then fix back
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48
Q

VESTIBULAR NEURONITIS

What is the management of acute and chronic vestibular neuronitis?

A
  • Rapid relief = buccal/IM prochlorperazine if severe, short PO prochlorperazine or antihistamine (cyclizine) if less severe
  • Chronic Sx = vestibular rehabilitation exercises preferred
49
Q

VIRAL LABYRINTHITIS

What is viral labyrinthitis?

A
  • Inflammation of the labyrinth, affecting both vestibular + cochlear end organs
50
Q

VIRAL LABYRINTHITIS
What is the clinical presentation of viral labyrinthitis?
How is this differentiated from vestibular neuronitis?

A
  • Acute onset (often post viral URTI)
  • Vertigo, N+V, nystagmus (horizontal)
  • Gait disturbances = may fall towards affected side
  • Sensorineural hearing loss AND tinnitus in labyrinthitis
51
Q

VIRAL LABYRINTHITIS
What exam finding is positive in viral labyrinthitis?
What is the management of viral labyrinthitis?

A
  • +ve head impulse test (impaired vestibulo-ocular reflex)

- Prochlorperazine or antihistamines to reduce vertigo

52
Q

ACOUSTIC NEUROMA

What is an acoustic neuroma/vestibular schwannoma?

A
  • Cerebellopontine angle tumour of the vestibulocochlear nerve schwann cells, often slow growing + benign
53
Q

ACOUSTIC NEUROMA

What is the clinical presentation of acoustic neuroma and why?

A

Cranial nerves affected –

  • CNV = absent corneal reflex
  • CNVII = facial palsy (forehead NOT spared)
  • CNVIII = vertigo, unilateral SN hearing loss + tinnitus
54
Q

ACOUSTIC NEUROMA

What is a key association with bilateral acoustic neuromas?

A
  • Neurofibromatosis type 2
55
Q

ACOUSTIC NEUROMA

What is the management of acoustic neuroma?

A
  • Urgent ENT referral = MRI cerebellopontine angle #1, audiometry
  • Treatment with observation, surgery or radiotherapy
56
Q

RAMSAY HUNT SYNDROME

What is Ramsay Hunt syndrome?

A
  • Herpes zoster oticus = reactivation of the VZV in the geniculate ganglion of CNVII
57
Q

RAMSAY HUNT SYNDROME

What is the clinical presentation of Ramsay Hunt syndrome?

A
  • Auricular pain can be 1st sign
  • Facial nerve palsy
  • Painful vesicular rash around ear
  • May have vertigo + tinnitus
58
Q

RAMSAY HUNT SYNDROME

What is the management of Ramsay Hunt syndrome?

A
  • PO aciclovir AND PO prednisolone
59
Q

AURICULAR HAEMATOMA
What are auricular haematomas associated with?
What is the management?

A
  • Rugby or boxing injuries
  • Same-day ENT assessment to avoid cauliflower ear deformity
  • Incision + drainage superior to needle aspiration
60
Q

TMJ DYSFUNCTION

What is the clinical presentation of temporomandibular joint (TMJ) dysfunction?

A
  • Earache (referred from auriculotemporal nerve)
  • Facial pain, joint clicking or popping on jaw movement
  • Teeth-grinding
61
Q

TMJ DYSFUNCTION

How is TMJ dysfunction managed?

A
  • Conservative with jaw rest, soft diet

- If chronic = ENT referral

62
Q

MASTOIDITIS
What is mastoiditis?
What is a key complication of mastoiditis?

A
  • Extension of AOM into mastoid air cells with abscess formation + bone necrosis
  • Meningitis, also facial nerve palsy + hearing loss
63
Q

MASTOIDITIS

What is the clinical presentation of mastoiditis?

A
  • Fever + systemically unwell
  • Persistent throbbing pain
  • Pinna pushed down + forward
  • Mastoid tenderness, erythema + swelling
64
Q

MASTOIDITIS

What is the management of mastoiditis?

A
  • CT
  • IV Abx
  • Surgery if subperiosteal abscess
65
Q

RHINOSINUSITIS
What is rhinosinusitis?
What are the causes?

A
  • Inflammation of the mucosal lining of the nose + paranasal sinuses
  • Infectious or allergic
66
Q

RHINOSINUSITIS
What causes infectious rhinosinusitis?
What causes allergic rhinitis?

A
  • Mostly viral (rhinovirus), can be bacterial (S. pneumoniae)
  • Type 1 IgE mediated hypersensitivity reaction
67
Q

RHINOSINUSITIS
How is allergic rhinitis sub-categorised?
What are some triggers?

A
  • Season, perennial (year-round) or occupational

- Smoke, pollen, house dust mite, exercise

68
Q

RHINOSINUSITIS

What is the clinical presentation of rhinosinusitis?

A
  • Rhinorrhoea + nasal congestion
  • Post-nasal drip = foul taste
  • Sinus facial pain, worse on bending forward = cheeks (maxillary), between eyes (ethmoidal), deep headache (sphenoidal)
69
Q

RHINOSINUSITIS

What investigations would you consider in rhinosinusitis and when would you?

A
  • Nasal endoscopy ± CT if persistent symptoms despite treatment
70
Q

RHINOSINUSITIS

What are some potential complications of rhinosinusitis?

A
  • Chronic rhinitis > nasal polyps
  • Intra-cranial infection = meningitis, cerebral abscess
  • Osteomyelitis of frontal bone
  • Orbital cellulitis/abscess
  • “Double-sickening” viral > bacterial
71
Q

RHINOSINUSITIS

What is the management of infective rhinosinusitis?

A
  • Analgesia + nasal decongestants, Abx (phenoxymethylpenicillin) if purulent discharge
  • Chronic/recurrent (>10d) = intranasal corticosteroids (fluticasone)
72
Q

RHINOSINUSITIS

What is the management of allergic rhinitis?

A
  • First line (mild-mod) = PO/intranasal antihistamines + allergen avoidance
  • Second line (mod-sev) = intranasal steroids
  • ?Role of short course nasal decongestants
73
Q

RHINOSINUSITIS

What is an important note about nasal decongestants?

A
  • Short courses only as increasing doses required to achieve same effect (tachyphylaxis)
  • Can lead to rebound hypertrophy of nasal mucosa (rhinitis medicamentosa) upon withdrawal
74
Q

NASAL POLYPS
What are nasal polyps?
What is the epidemiology?
What are some associations?

A
  • Growths of nasal mucosa
  • More common in men, not often seen in paeds/elderly
  • Samter’s triad (asthma, aspirin sensitivity + nasal polyposis), chronic rhinitis, congenital (CF, kartagener’s syndrome)
75
Q

NASAL POLYPS
What is the clinical presentation of nasal polyps?
What is a worrying sign?

A
  • Watery rhinorrhoea + nasal obstruction
  • Poor sense of taste/smell
  • Unilateral Sx or bleeding = ENT referral as RED flag
76
Q

NASAL POLYPS

What is the management of nasal polyps?

A
  • All referred to ENT for full exam
  • First line = intranasal topical corticosteroids to shrink polyps
  • If fail = endoscopic polypectomy
77
Q

NASAL FRACTURE

What is the clinical presentation of nasal fracture?

A
  • Bruising + tenderness over nose
  • Mobility + deformity of the nose
  • Epistaxis
78
Q

NASAL FRACTURE
What is a major complication of nasal fractures?
How does it present?

A
  • Septal haematoma = bilateral haematoma between perichondrium (skin) + septal cartilage
  • Soft/boggy swelling, sense of nasal obstruction, pain
79
Q

NASAL FRACTURE
What is the management of septal haematoma?
Why is this important?

A
  • Incision + drainage and IV Abx

- Prevents septal necrosis (risk of saddle-nose deformity) + abscess

80
Q

NASAL FRACTURE

What is the management of nasal fracture?

A
  • Only correct if cosmetic deformity or septal haematoma
81
Q

EPISTAXIS

What are the two locations of epistaxis and which is most common?

A
  • 90% anterior plexus bleed = Kiesselbach’s plexus/little’s area
  • Posterior plexus bleed = originate from deeper structures
82
Q

EPISTAXIS

What is to note about posterior plexus bleeds?

A
  • More profuse, more in older patients

- Higher aspiration risk + airway compromise

83
Q

EPISTAXIS

What are the causes of epistaxis?

A
  • Most benign + self-limiting = nose picking/blowing
  • Trauma to nose or foreign body insertion
  • Bleeding disorders = haemophilia, vWD, anticoagulants
  • Cocaine use
84
Q

EPISTAXIS

What is the stepwise management of epistaxis?

A
  • ABCDE approach initially
  • Pinch cartilaginous area of nose firmly, lean forward, 10–15m
  • Cautery with silver nitrate stick IF source of bleed visible (topical anaesthetic 1st)
  • Nose packing if cautery not viable or bleeding point not visible (posterior packing requires catheter)
  • Sphenopalatine ligation
85
Q

EPISTAXIS

What management is considered after first aid measures?

A
  • Consider topical antiseptic Naseptin (chlorhexidine + neomycin) to reduce crusting + risk of vestibulitis
  • Avoid blowing/picking nose, heavy lifting, exercise, alcohol
86
Q

EPISTAXIS

What is a caution with naseptin?

A
  • Peanut or soy allergies
87
Q

TONSILLITIS

What are the causes of tonsillitis?

A
  • Viral #1 = adenovirus, influenza, rhinovirus

- Bacterial = group A beta-haemolytic streptococcus pyogenes

88
Q

TONSILLITIS

What scoring systems are used in tonsillitis that link to the clinical presentation?

A
  • FeverPAIN = Fever, Purulence, Attends <3d, severely Inflamed tonsils, No cough/coryza
  • CENTOR = tonsillar exudate, fever, tender anterior cervical lymphadenopathy + absent cough
89
Q

TONSILLITIS

What are some potential complications of tonsillitis?

A
  • Post-strep glomerulonephritis
  • Rheumatic fever
  • Scarlet fever
  • Otitis media
  • Peritonsillar abscess (quinsy)
90
Q

TONSILLITIS
What is quinsy?
What are the features?

A
  • Rare but severe complication of bacterial tonsillitis

- Sore throat, dysphagia, trismus, peritonsillar bulge, uvular deviation (away from quinsy), muffled ‘hot potato’ voice

91
Q

TONSILLITIS

What is the management of quinsy?

A
  • IV Abx + aspiration preferred to previous incision + drainage
92
Q

TONSILLITIS

What is the management of tonsillitis?

A
  • Most self-resolve, paracetamol + ibuprofen
  • CENTOR ≥3, FeverPAIN ≥4 (2-3=delayed) for Abx
  • Phenoxymethylpenicillin or clarithromycin/erythromycin if pen allergic
93
Q

TONSILLITIS

What is the criteria for tonsillectomy?

A
  • ≥7 episodes in 1 year OR 5 per year for 2 years OR 3 per year for 3 years
  • Recurrent quinsy (≥2 episodes)
  • Enlarged tonsils causing breathing issues/stridor, dysphagia, snoring
94
Q

TONSILLITIS
What are some complications with a tonsillectomy?
What’s the management?

A
  • Pain
  • Haemorrhage = primary 6-8h due to inadequate haemostasis, secondary 5–10d due to infection
  • All haemorrhage > ENT, if primary back to theatre, if secondary/infection admit + Abx
95
Q

EPIGLOTTITIS
What is epiglottitis?
What causes it?

A
  • Acute infection of supraglottic tissue with risk of airway occlusion
  • Haemophilus influenzae type B
96
Q

EPIGLOTTITIS

What is the clinical presentation of epiglottitis?

A
  • Rapid onset 3Ds = Drooling, Distressed, Dysphagia
  • Soft inspiratory stridor in very systemically unwell child
  • Tripoding = optimise airway by leaning forward + extending neck
97
Q

EPIGLOTTITIS
How do you diagnose epiglottitis?
What investigation might you do?

A
  • Clinically via direct visualisation by specialist

- Lateral C-spine XR = epiglottis swelling (thumb sign)

98
Q

EPIGLOTTITIS
What is the prophylaxis for epiglottitis?
How do you manage epiglottitis?

A
  • Prevention with HiB vaccine, give household contacts rifampicin
  • Urgent anaesthetist/ENT input + DO NOT EXAMINE THROAT
  • Secure airway (may require ET intubation), IV cefotaxime or ceftriaxone
99
Q

HEAD AND NECK CANCERS
What is the most common histological type for head and neck cancers?
Where does it spread to?
Why is early recognition crucial?

A
  • Squamous cell carcinoma
  • Lymph nodes
  • Risk of affecting ability to breathe, swallow + talk
100
Q

HEAD AND NECK CANCERS
What are the two main risk factors for head and neck cancers?
What are the main locations for head and neck cancers?

A
  • Smoking + alcohol

- Nasopharynx, oral cavity, pharynx, larynx

101
Q

HEAD AND NECK CANCERS
What are red flag features of nasopharynx cancer?
What are some key risk factors?

A
  • Otalgia, hearing loss (CN palsies), changes to sense of smell, unilateral serous otitis media
  • Asian + EBV
102
Q

HEAD AND NECK CANCERS
What are red flag features of oral cavity cancer?
What are some key risk factors?

A
  • Ulcer for >3w, persistent + unexplained neck lump, erythro(leuko)plakia
  • Recurrent dental infections, sun exposure (lips)
103
Q

HEAD AND NECK CANCERS
What are red flag features of pharynx cancer?
What is a key risk factors?

A
  • Persistent neck lump, dysphagia, otalgia

- HPV

104
Q

HEAD AND NECK CANCERS
What are red flag features of larynx cancer?
What is a key risk factors?

A
  • Hoarse voice, persistent neck lump, dysphagia, stridor

- Smoking ++

105
Q

HEAD AND NECK CANCERS

What is the management of head and neck cancers?

A
  • Full ENT exam + flexible nasoendoscopy
  • Fine needle aspiration if mass found
  • Options = chemo, radiotherapy or surgery
106
Q

NECK LUMPS

Give 8 differentials for neck lumps and note their location

A
  • Reactive lymphadenopathy = #1
  • Thyroid swelling
  • Thyroglossal cyst, midline
  • Anterior triangle = branchial cyst, carotid aneurysm
  • Posterior triangle = pharyngeal pouch (Zencker’s diverticulum), cystic hygroma, cervical rib
107
Q

NECK LUMPS
What are some differentiating features of…

i) reactive lymphadenopathy?
ii) thyroid swelling?

A

i) Recent local/generalised infection

ii) Moves upwards on swallowing but NOT tongue protrusion

108
Q

NECK LUMPS
What is a thyroglossal cyst?
How does it present?
How is it managed?

A
  • Persistent thyroglossal duct in paeds
  • Fluctuant, midline mass which MOVES UP with tongue protrusion
  • Excise cyst + thyroglossal duct
109
Q

NECK LUMPS

What is a pharyngeal pouch?

A
  • Outpouching of pharyngeal lining through a weakness in the pharyngeal wall muscles (Killian’s dehiscence)
110
Q

NECK LUMPS

What is the presentation of pharyngeal pouch?

A
  • Dysphagia
  • Regurgitation
  • Chronic cough
  • Halitosis
  • Older men
  • Neck mass on L that may gurgle on palpitation
111
Q

NECK LUMPS
How is a pharyngeal pouch investigated?
What is the management?

A
  • Diagnostic = barium swallow
  • Avoid endoscopy as perforation risk
  • Excise
112
Q

NECK LUMPS
What is a cystic hygroma?
How does it present?
What is the management?

A
  • Congenital lymphatic lesion often on L side (posterior triangle)
  • Most evident at birth, SNT, transilluminates, increased size when coughs/cries
  • Excise
113
Q

NECK LUMPS
What causes a branchial cyst?
How does it present?
How is it managed?

A
  • Failure of obliteration of second branchial cleft in embryology
  • SNT + fluctuant mass anterior to sternocleidomastoid (anterior triangle)
  • Early adulthood
  • Excise
114
Q

NECK LUMPS
Who is a cervical rib more commonly seen in?
What can it lead to?

A
  • Adult females

- Thoracic outlet syndrome = compression of brachial plexus, subclavian artery/vein at site of thoracic outlet

115
Q

NECK LUMPS

How does thoracic outlet syndrome present?

A
  • Neurogenic #1 = weak hand muscles, paraesthesia

- Vascular = painful arm swelling + distended veins

116
Q

NECK LUMPS

How does a carotid aneurysm present?

A
  • Pulsatile lateral neck mass which does NOT move on swallowing
117
Q

LUDWIG’S ANGINA

What is Ludwig’s angina?

A
  • Progressive cellulitis that invades the floor of the mouth + soft tissues of the neck often 2º to odontogenic infections which spread to submandibular space
118
Q

LUDWIG’S ANGINA

What is the clinical presentation of Ludwig’s angina?

A
  • Fever, neck swelling + dysphagia

- Seen in immunocompromised with poor dentition

119
Q

LUDWIG’S ANGINA

What is the management of Ludwig’s angina?

A
  • Life-threatening emergency as airway obstruction can occur rapidly
  • Immediate admission with airway management + IV Abx

FINALS (20 decks)

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