ENT Flashcards
1
Q
Describe the sensory supply to the external ear
A
Upper lateral= CN V3 (auriculotemporal)
Lower lateral and medial= C3 (greater auricular nerve)
Superior medial= C2/3 (lesser occipital)
External auditory meatus= auricular branch of vagus nerve
These nerves can be blocked with local for various procedures
2
Q
What is important to asses in lacerations of the external ear?
A
that all the cartilage is covered with skin. if significant skin loss where primary closure will not be possible, plastic surgery reconstruction may be needed
3
Q
How should bites to the external ear be managed?
A
- significant risk of infection from skin and oral commensals
- wound left open
- irrigate wound
- prophylactic/ abx for infection
4
Q
How should pinna haematomas be managed?
A
Drainage and pressure dressing application (prevents reaccumulation)
5
Q
How should traumatic (direct or indirect) tympanic membrane perforations be managed?
A
Most will heal by themselves- watch and wait.
If hasnt healed after 6 months, myringoplasty to repair tymp membrane if its causing problems.
6
Q
How should haemotymapnum be managed?
A
- may be associated with temporal bone fracture (head CT) and conductive hearing loss
- treat conservatively as will settle with time but follow up to ensure no residual hearing loss from damage to ossicles
7
Q
How does otitis externa present?
A
- painful discharging ear
- swelling to external ear canal
- often history of swimming
8
Q
How is otitis externa managed?
A
- topical ear drops (neomycin)
- can get mixed antibacterial + antifungal drops
- swab if resistant
- microscution of pus/ debris may be needed to help get drops to source of infection
- a wick can be helpful to hold ear canal open to allow topical treatment to diffuse through if infection is severe
- advise: avoid swimming for 7-10 days while being treated, ear plugs for showers/ baths, dry ears after swimming with hair dryer on low heat, OTC aceitic acid drops after swimming/ bathing,
9
Q
What is malignant otitis externa? how is it managed?
A
- aggressive infection usually seen in diabetic or immunocompromised pts
- spreads from soft tissue into the bone
- presents with chronic ear discharge despoite dopical treatment, deep seated severe ear pain and sometimes CNVII palsies
- treat w/ IV abc + extended topical treatment
10
Q
What organisms commonly cause acute otitis media and how does it present?
A
- strep pneumonia and H. influenza
- eat pain (child pulling ear) which improved but then ear starts discharging (as tymp membrane ruptures) and fever
- Otoscopic exam: A distinctly red, yellow, or cloudy tympanic membrane. Moderate to severe bulging of the tympanic membrane, with loss of normal landmarks and an air-fluid level behind the tympanic membrane (indicates a middle ear effusion). Perforation of the tympanic membrane and/or discharge in the external auditory canal.
11
Q
How is acute otitis media managed?
A
- most conservativley with analgesia, severe or persistent cases need abx (amoxicillin)
- surgery for grommet if recurrent
12
Q
How can chronic otitis media (conductive hearing loss + discharge for >6/52) be classified? (2 ways)
A
Active (discharging) vs inactive (not)
Squamous (cholestaetoma if active, retraction pocket if inactive) vs Mucosal (chronic discharge into middle ear- active if discharging through perforation, often develops from AOM where membrane fails to heal)
13
Q
How does active squamous chronic otitis media develop?
A
kertinised squamous cells introduced into middle ear from retraction pocket or perforation
14
Q
What feature is reassuring if seen in squamous COM?
A
if anterioinferior part of tymp membrane as carries low risk of cholesteatoma
15
Q
What needs to be arranged if suspect cholesteatoma and why?
A
CT scan of petrous temoral bone to assess invasion before removal (wont metastasise but local invasion can cause significant damage)
16
Q
How can most chronic otitis media be managed?
A
- aural toileting
- topical abx and steroid treatments until symptoms resolve
- if >6 weeks go to specialist - myringoplasty or tympanoplasty can be done to close large or troublesome perforations
17
Q
How does otitis media with effusion present?
A
- usually in children and due to eustachian tube dysfunction (if adult be away of post nasal space tumours)
- conductive hearing loss (may be speech/ lang delay or school problems) and middle ear effusion on otoscopy
- not painful in itself but can lead to AOM which is
18
Q
How should otitis media with effusion be investigated and what findings would you expect?
A
- do tympanogram (flat (type B) tracing with normal canal volume)
- pure tone audiogram showing conductive hearing loss
19
Q
How is otitis media with effusion managed?
A
- conservative 1st line- most will resolve in 3 months
- hearing aids
- grommets +/- adenoidectomy
20
Q
how does otosclerosis present?
A
- in elderly, F>M
- progressive conductive hearing loss
- which is improved in noisy surroundings during early stages of the disease
- often tinnitus and fhx
21
Q
How should otosclerosis be investigated and what results would you expect?
A
- tympanogram shows normal type A tracing
- pure tone audiogram shows conductive hearingloss with characteristic carhart notch at 2kHz
22
Q
How can otosclerosis be managed?
A
- hearing aids
- surgically with stapedectomy
23
Q
What is the difference between the cochlear and the vestibular system?
A
cochlear is for hearing- stapes taps on window and moves hair cells.
Vestible is for balance- 3 of semicircular canals at 90degrees to eachother so movement in different planes causes movement of perilymph within them. The utricle has hair cells sticking up to detect horizonal movement. The saccule has hair cells sticking out so detects verticle movements
24
Q
What contributes to good balance?
A
- vestibular system
- proprioception
- vision
integrated centrally by - vestibular nerve
- peripheral nerves and dorsal column
- cranial nerves
- brain/ brainstem/ cerebellum
25
Describe the differences in signs and symptoms of central and peripheral vertigo
```
Central:
- gradual onset
- constant and milder
- unaffected by head position and movement
- N+V less predictable
- motor function, gait instability and ataxia common
Peripheral:
- sudden onset
- intermittent but severe symptoms
- affected by head position and movement
- N+V severe and more frequent
- motor function, gait and coordination usually intact
```
26
Give 3 central causes of vertigo?
- stroke
- migraine
- neoplasms
- demyelination eg MS
- drugs (gent, loop diuretics, chemo, amlodipine, SSRIs, anti epileptics, diazepams)
27
Give 3 peripheral causes of vertigo
- BPPV
- Menieres
- Vestibular neuritis
- labyrinthitis
28
What causes BPPV?
otoliths (crystals) in semicircular canals (most commonly posterior) causing abnormal stimulation of hair cells causing hallucination of movement when disturbed
29
How is BPPV diagnosed and treated?
diagnosis is with dix hallpike test and treatment is with epley manoruvre or brandt daroff exercises
30
What is thought to cause menieres disease?
- endolyphatic hydrops (increased fluid in endolymphatic compartment)
- not sure why exactly though
31
How does menieres present?
- tinnitus in affected ear
- episodic vertigo lasting mins-hrs with N+V
- fluctuating sensorineural hearing loss which becomes more apparent overtime
- aural fullness feeling
- initially well between attacks but feel unsteady and get sensorinueral hearing loss in between attacks as it progresses
- disease burns out overtime so dont have acute vertigo but have reduced hearing and generally poor balance (good ear can compensate to improve balance but takes time esp in elderly)
32
How can menieres be managed?
- reduce salt, chocolate, alcohol, caffeine, chinese food
- thiazides, betahistines and vestibular sedatives eg prochlorperazine (for acute attacks only) can help
- surgical options inc grommet, dexamethasone injections into middle ear, endolymphatic sac decompression, vestibular destruction w/ gent injection and surgical labyrinthectomy (rare)
33
What is vestibular neuronitis and how does it present?
- inflammation of inner ear canal causing severe incapacitating vertigo and N+V lasting several days, often preceeded by URTI
- No hearing loss
- during attacks they can get horizontal nystagmus but otherwise normal neuro exam
34
how should vestibular neuronitis be managed?
- treat acute attacks with vestibular sedatives (dont use after) and IV fluids if necessary
- can get long term vestible deficit after causing generalised unsteadiness for several weeks as brain compensates
- vestibular rehab with cawthorne- cooksey exercises can help recovery
35
How does labrynthitis present? (how is it different to vestibular neuronitis)
inflammation of vestibule AND cochlear so presents with severe sudden vertigo AND sensorineural hearing loss and N+V.
Often preceeded by URTI. manage same as vestibular neuronitis
36
How should sudden onset sensorineural hearingloss be managed?
Send in as emergency- needs pure tone audiogram and MRI so exclude other causes the management with steroids IV or into middle ear and anti virals. Other treatment such as carbogen and hyperbaric chambers are used but not widely practiced.
37
How may an acoustic neuroma present? How is it managed?
- unilateral progressive sensorineural hearing loss
- may or may not have associated vertigo
- MRI (to confirm and exclude brain stem ischaemia/ SOSNHL) and then microsurgery/ stereotactic surgery
38
Give 5 causes of conductive hearing loss
- cerumen impaction
- cholesteatoma
- tymp membrane perf
- foreign body
- AOE/ OME
- otosclerosis
39
Give 5 cause of sensorineural hearing loss
- acute vestibular/ brainstem ischaemia
- acoustic neuroma
- unilateral sudden onset sensorineural hearing loss
- noise induced hearing loss (overlaps with otosclerosis)
- ototoxic hearing loss
- presbyacusis
- menieres (++ vertigo)
- lebyrinthitis (++ vertigo)
40
What kinda tuning folk do you use for weber and rennies test?
- 256hz or 512 hz folk
41
What is a pure tone audiogram? what is considered normal?
- Asses how loud a sound or varying pitches as to be in order for the pt to hear it
- Anything above 20dB is considered normal
- The noise is played through air to test conduction and then through bone to test sensorineural function- often if conduction is normal they wont test sensorineural
42
What does a tympanogram measure and what do the three tracing types indicate?
- Measures compliance of tympanic membrane
- Type A: normal (peak at 0 daPa on x axis)
- Type B: flat, suggests middle ear effusion or perforation
- Type C: peak at <0 daPa (negative pressure), eustachian tube dysfunction
43
give 3 local and 3 systemic causes of epistaxis
Local: idiopathic (85%), trauma, iatrogenic, foreign body, inflammation (rhinitis, polyp), neoplasm
Systemic: hypertension, coagulopathies, anticoagulants, vasculopathies, hereditary haemorrhagic telangiectasia
44
How should epistaxis be managed?
- ABC
- Pinch soft part of nose, hold head forward, split out blood in mouth
- locate bleeding source
- Cautery with silver nitrate or bipolar diathermy, if anterior, by anterior rhinoscopy, if posterior by rigid endoscope. Topical adrenaline may help control bleeding prior to cautery
- Nasal packing if this fails- anterior pack initially, if bleeding continues into oropharynx then anterior & posterior pack
- Surgical ligation or embolization of sphenopalatine
- Anterior ethmoid cant be embolised because it comes from the internal carotid
- Can ligate external carotid as last resort
45
How should nasal trauma be assessed and managed?
- check for septal haematoma
- check for signs of basilar skull fracture and get CT is suspect
- ABC- epistaxis normally self limiting
- No XR usually required
- if deviated nose, consider manipulation under anaesthetic within 2 weeks of injury
46
Give 2 complications of sinus surgery
- orbit damage
- anterior skull base lies just above the sphenoid and ethmoid sinuses, if breaches during surgery it can cause a CSF leak
47
Define rhinosinusitis
inflammation of nose and paranasal sinuses characterised by two or more of the symptoms:
•Nasal blockage/ obstruction/ congestion/ discharge
•Anterior/ posterior nasal drip
•Facial pain or pressure
•Reduction or loss of smell
•Endoscopic signs of polyps, mucopurulent discharge or odema in middle meatus and/ or
•CT changes- mucosal changes within the osteomeatal complex or sinuses
48
What is the difference between acute and chronic rhinosinusitis
```
Acute= <12 weeks- viral or non viral
Chronic= >12 weeks, can be with or without nasal polyps
```
49
What causes acute rhinosinusitits?
Viral= rhinovirus or influenza virus, usually resolves within 5 days
Bacterial= step P, h influenza, persists longer than 5 days
Allergy and ciliary impairment can predispose to it
50
How is acute rhinosinusitis managed?
analgesia, nasal decongestants
| Topical nasal steroids and abx (phenoxymethylpen) (if persists > 10 days)
51
What predispose to chronic rhinosinusitis?
- allergy/ atopy
- ciliary impairments
- immunocompromised, hormonal
- foreign body
- trauma
- smoking
- dust fumes
- hormonal (pregnancy, hypothyroid)
- polyps (if bilateral dont need histological diagnosis)
52
How is chronic rhinosinusitis managed?
- avoid allergens
- nasal douching
- antihistamines, topical nasal steroids, oral steroids/ abx
- nasal polypectomy, functional endoscopic sinus surgery (improves ventilation/ drainage of sinus), septoplasy or reduction in inferior turbinates
53
What is the difference between intermittent and persistent and mild and mod- severe allergic rhinitis?
Intermittent= symptoms <4 days per week and for <4 weeks
persistent= >4 days p/w and >4 weeks
Mild= normal daily activites and sleep
Mod- severe= not
54
How should allergic rhinitis be investigated?
- skin prick test
| - RAST blood test if SPT not possible
55
How should allergic rhinitis be managed?
- allergen avoidadance (avoid drying washing outside, close windows, dont go out early or late when pollen count high, wash hair after pollen exposure, wood better than carpet, wash sheets at high temp)
- nasal douching
- mild: PRN antihistamines (nasal or systemic)
- mod/ sevre : + regular topical nasal steroids, short term decongestants (nasal ephedrine)
- runny nose: intranasal ipratroprium bromide
- immunotherapy and oral pred if very severe
56
Describe the clinical features of a retropharyngeal abscess
- commonly in child and after URTI
- Neck held rigid and upright with reluctance to move
- systemically unwell
- airway compromise
- dysphagia, odynophagia
- widening of retropharyngeal space on xray
- associated mortality due to airway problems and mediastinitis
57
How should a retropharyngeal abscess, parapharyngeal abcesses, ludwidgs angina and peritonsillar abscesses be managed?
- ct neck
- bloods for sepsis
- secure airway if any concerns
- IV abx
- surgery- incision and drainage
58
What is ludwigs angina and how does it present?
- infection of the space between the floor of the mouth and mylohyoid
- commonly associated with dental infection
presents with:
- swelling of floor of mouth
- painful mouth
- protruding tongue
- airway compromise
- drooling
59
What is a parapharyngeal abscess?
- abscess in potential space posterolateral to the oropharynx and nasopharynx which is divided by the styloid process
- presents in child, fever, odynophagia, trismus, reduced neck movements, neck swelling, drooling, medial diaplacement of lateral pharyngeal wall
- the pharyngeal space contains the carotid sheath so risk of severe complications
60
give 10 differentials for neck lumps
- infective: reactive lymph node, atypical mycobacterium
- neoplasm: lymphoma, H/N ca mets, lung/ breast mets, lipoma, sarcoma
- vascular: carotid body tumour,aneurysm, glomus jugulare
- inflammatory: sarcoidosis
- trauma: haematoma
- autoimmune: thyroid disease
- congenital: cystic hygroma, thyroglossal cyst, branchial cyst, dermoid cyst, teratoma
61
How are neck lumps investigated?
- all get USS, oral and neck exam and most get nasolaryncoscopy
- suspicious lesions will get FNA or core biopsy
62
Give 3 features of a reactive lymph node
- mobile
- regular/ soft/ round
- <1cm
63
Describe the possible clinical features and RFs of a head and neck ca?
- Dysphonia (laryngeal malignancy causes hoarseness)
- Dysphagia/ odynophagia
- Dsypnoea
- Neck mass
- Pain from site of pathology or reffered (neck pain often refered to ear)
- Neck mass
- Bleeding from nose or mouth
- Nasal blockage- usually unilateral, progressive
- Men > women
- Risk factors: alcohol, tobacco, beetle nut chewing, Chinese ethnic origin for nasopharyngeal malignancy, HPV infection esp for tonsillar malignancy
64
Describe how head and neck cancers are investigated and staged
- CT neck for tumour size and neck node mets
- EUA to look for and biopsy primaries as well as secondaries
- FNA or CNB- FNA usually find for SCC but not for TB or lymphoma
- open biopsies carry risk of seeding so rarely done
65
breifly describe the management of head and neck cancer
- palliation is common and may involve chemo or radio and occasionaly surgery
- surgery to primaru +/- neck node dissection is often followed by or preceeded by radiotherapy to primary +/- neck +/- chemo
66
What is the commonest cause of obstructive sleep apnoea in children?
adenotonsillar hypertrophy
67
describe the blood supply and drainage to the thyroid gland
- Blood supply is via superior and inferior thyroid arteries
| - Drainage via superior, middle and inferior thyroid veins
68
What are the three major risks associated with surgery to the thryoid gland?
- Recurrent laryngeal nerve runs just below it and so at risk in thyroidectomy- this supplies muscles of larynx except cricothyroid so can cause hoarseness or airway obstruction if nerves severed or bruised on both sides
- Parathyroid glands are closely related and so another post op complication is hypocalaemia
- post op haemorrhage (bad in neck)
69
How should thyroid nodules be assessed?
- need to check TFTs to check not hyperfunctioning
- USS
- need to check not neoplastic with FNA
- If FNA not conclusive and concerning features do hemithyroidectomy for definitive diagnosis (lumpectomy not done as hard to get correct margins and revision surgerys are difficult)
- FNA doesnt differentiate between follicular adenoma (benign) and follicular carcinoma so these need hemi also
70
What are the common types of thyroid neoplasms?
- benign: adenoma, usually follicular
- malignant: 70% papillary adenocarcinoma (younger pts or radiation to neck), 20% follicular carcincoma (mets to bone and lungs), 5% medullary carcinoma (often seen in MEN)
- anaplastic tumours are the worst, seen in older pts and only live weeks- months
71
How are thyroid adenomas and carcinomas managed?
Adenoma: nothing needed after diagnostic hemithyroidectomy
Carcinoma: total thyroidectomy +/- radioiodine therapy after
72
Which salivary glands are neoplasms most common in?
- the parotid gland - however 80% of parotid neoplasms are benign (pleomorphic adenomas)
- 50% of submandibular gland neoplasms are benign
73
What is acute sialadenitis? What causes it?
- red hot swollen painful salivary gland
- viral: paramyxovirus (mumps), coxsackie virus, echovirus, HIV
- Bacterial: staph- usually if dehydrated or immunocompromised
- chronic: v rare, usually TB, sarcoid, HIV or syphilis
74
How is acute sialadenitis managed?
analgesia, artificial saliva, abx if bacterial cause suspected, abscesses may form and need incision and draniage
75
What is sialolithiasis and what are the major RFs?
- stones in salivary duct causing obstruction and leading to pain, swelling
- stones are calcium phosphate
RFs:
- meds (diuretics, anticholinergics)
- dehydration
- gout
- smoking
- peridontal disease
- hyperparathyroidism
76
How is sialolithiasis investigated and managed?
- USS or sialogram
M:
- most will settle on own so just give analgesia and encourage hydration
- sialogogues encourage saliva secretion so may help (lemon juice)
- some may need radiological or surgical removal (can be intraoral if palpable or remove whole gland)
- complications: sialadenitis or abscess formation
77
What is sjogrens?
- autoimmune cause of lymphocytic infiltration into ductal tissue of sailivary and lacrimal glands
- causes dry eyes and mouth
- may be primary or secondary to CT disease (usually RA)
- diagnosis from hx, exam, autoantibody bloods and gland biopsy
78
Give 4 complications of acute otitis media
- mastoiditis
- intra cranial abcess
- meningitis
- facial nerve palsy
- chronic otitis media
- venous sinus thrombosis
79
Give 3 complications of grommmets
- fibrosis
- tympanosclerosis
- bleeding
- cholesteatoma
- ottorrhoea (abx and reffer if problematic)
- infection (AOM)
80
How is tonsilitis and recurrent tonsilitis managed?
- fluids and paracetamol
- abx (phenxoymethylpen) if likely bacterial (high feverpain/ centur score)
- if EBV: monitor LFTs and stop contact sport for 3 mo
- assess for peritonsilar abscess
- tonsilectomy if: >7 p/yr for 1 yr, 5p/yr for 2 yrs and 3 p/ yr for 3 yrs
81
Give 3 complications of adenotonsillectomy?
- velopharyngeal insufficiency (nasal speech, swallow difficulty)
- teeth/ soft palate/ uvula trauma
- primary or secondary post op haemorrhage (rare but can be life threatening)
- dehydration secondary to pain or n+v post op
- nasopharyngeal stenosis
- death
- infections
- resp compromise
82
What imaging is most sensitive for an ondontogenic abcess? (abcess as a result of dental surgery- requires urgent abx and drainage as can cause ludwigs angina)
orthopantomogram (OPG) radiograph
