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ENT Flashcards

1
Q

which nerve supplies the upper lateral surface of the external ear

A

auriculotemporal nerve

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2
Q

what nerve is the auriculotemporal nerve a branch of

A

mandibular branch of the trigeminal

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3
Q

which nerve supplies the superior medial surface of the external ear

A

lesser occipital nerve

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4
Q

which nerve supplies the lower lateral surface of the external ear

A

greater auricular nerve

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5
Q

which nerve supplies the external auditory meatus

A

auricular branch of the vagus nerve

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6
Q

what is the management of a laceration of the external ear

A

clean wound and insert sutures, making sure cartilage is all covered with skin. if closure not possible or significant skin loss - seek opinion from a a plastic reconstructive surgeon

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7
Q

what is the management for bites to the external ear

A

leave open and irrigate thoroughly. commence abx

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8
Q

what can haematoma of the pinna of the ear lead to, and how

A

disruption of the blood to cartilage of the ear, as the cartilage obtains nutrients from the diffusion of vessels in the perichondrium.
disruption can lead to avascular necrosis, and deformity cauliflower ear

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9
Q

what is the management for haematoma of the pinna of the ear

A

urgent drainage and pressure dressing to prevent reaccumulation of haematoma

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10
Q

what is the management for tympanic membrane perforation

A

most heal by themselves - “watch and wait”

if it hasn’t healed by itself after 6 months, myringoplasty is performed to repair the tympanic membrane

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11
Q

what are the symptoms of tympanic membrane perforation

A

pain, conductive hearing loss

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12
Q

what is the management of haemotympanum

A

conservative - as it usually resolves itself

should be followed up to ensure no residual hearing loss from damage to ossicles

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13
Q

what are the risk factors for otitis externa

A

hot humid climates, swimming, older age, immunocompromise, diabetes, narrow external auditory meatus

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14
Q

what are the common organisms causing otitis externa

A

skin commensals - s. aureus
also Pseudomonas aeruginosa
some are fungal e..g aspergillus spp

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15
Q

what is the presentation for otitis externa

A

painful discharging ear, may be itchy. erythema, may be hearing loss

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16
Q

what is malignant otitis externa

A

aggressive infection mainly seen in immunocompromised and diabetics. the infection spreads from the ear canal and into the bone
signficant mortality rate even with treatment

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17
Q

how does malignant otitis externa present

A

chronic ear discharge despite topical treatment
seated severe ear pain and sometimes CN palsies
can cause skull base osteomyelitis

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18
Q

what is the management of otitis externa

A
  • topical ear drops e.g. gentamicin given empirically
  • swab dc if resistant to treatment
  • topical antifungals if fungal
  • microsuction of pus/debris to enable drops to get to source of infection
  • wick may be used in severe infection to hold canal open and allow topical treatment to diffuse through
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19
Q

how is malignant otitis externa managed

A

aggressive treatment with IV abx and topical treatment at the same time for extended periods of time

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20
Q

what are the different types of otitis media

A
  • acute

- chronic - mucosal and squamous types which can be active or inactive

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21
Q

what type of epithelium lines the middle ear

A

pseudostratified squamous (same as the respiratory tract)

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22
Q

what are the common pathogens causing acute otitis media

A
  • s pnuemoniae
  • h influenzae
  • moraxella species
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23
Q

what are the symptoms of acute otitis media

A

ear pain
ear pulling in your children
discharge if tympanic membrane rupture
fever

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24
Q

what is the management for acute otitis media

A
  • conservative: analgesia
  • medical: amoxicillin/clarithromycin if pen allergic in severe/persistent cases
  • surgery: grommets if recurrent
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25
Q

what is otitis media with effusion associated with

A

eustachian tube dysfunction

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26
Q

is otitis media with effusion painful

A

no - but can become painful if it becomes infected

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27
Q

what are the clinical features on examination of a patient’s tympanic membrane and hearing with otitis media with effusion

A
  • tympanic membrane shows middle ear effusion

- hearing: conductive hearing loss, type B tymapnogram

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28
Q

what audiogram result do you get with tympanogram otitis media with effusion

A

type B

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29
Q

how can otitis media with effusion affect a child’s development

A

inability to hear properly can lead to speech delay/problems at school

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30
Q

what is the management for otitis media with effusion

A
  • conservative: leave for 3 months, hearing aid

- surgery: grommets +/- adenoidectomy

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31
Q

what is the difference between active and inactive types of chronic otitis media

A 
active = dc present
inactive = no dc
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32
Q

what type of chronic otitis media is cholesteatoma

A

active squamous type COM

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33
Q

what is inactive squamous type COM

A

retraction pocket which may potentially develop into active squamous type (cholesteatoma)

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34
Q

what is active mucosal type of COM

A

where there is chronic dc from the middle ear through a tympanic membrane perforation and often a conductive hearing loss
assoc with spread to temporal lobe/intracranially

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35
Q

what is cholesteatoma

A

A destructive expanding growth consisting of keratinising squamous epithelium. Can erode through the bone and cause destruction

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36
Q

how is cholesteatoma treated

A

surgical removal +/- mastoidectomy

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37
Q

how can cholesteatoma progress

A

grow from the middle ear into the mastoid bone

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38
Q

how is mucosal COM treated

A

topical antibiotics and aural toilet
if fails - surgery to look for cholesteatomy and repair a perforated eardrum
ensure good ventilation

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39
Q

what are the branches of the facial nerve from proximal to distal (motor and sensory root)

A
  • greater petrosal nerve
  • nerve to stapedius
  • chorda tympani
  • terminal motor branches
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40
Q

what does the greater petrosal nerve supply

A

lacrimal gland

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41
Q

what does the chorda tympani supply

A

taste buds of anterior tongue

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42
Q

is otosclerosis inherited

A

yes - can follow what appears to be an autosomal dominant pattern

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43
Q

what is the pathological process of otosclerosis

A

mature bone is gradually replaced with woven bone and stapes footplate becomes fixed to the oval window - symptoms develop

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44
Q

what is the history of someone with otosclerosis

A

progressive hearing loss, tinnitus, improved hearing in noisy environments in early stages of disease

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45
Q

what is schwartze’s sign

A

a pinkish hue of the tympanic membrane o/e of someone with otosclerosis

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46
Q

what are the investigations you would do for someone with otosclerosis

A
  • tympanogram - normal type a trace

- pure tone audiogram - conductive hearing loss

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47
Q

what is the characteristic appearance of otosclerosis on pure tone audiogram

A

carhart notch at 2 KHz

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48
Q

what is the management of otosclerosis

A
  • conservative - hearing aid

- surgery - stapedectomy and replacement with prosthesis

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49
Q

in which bone is the inner ear situated

A

petrous part of the temporal bone

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50
Q

what are the part of the inner ear

A
  • cochlea

- vestibule and semicircular canals

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51
Q

what is the structure of the membranous labyrinth

A

filled with endolymph and contained in bony labyrinth

the membranous labyrinth itself is suspended in in perilymph

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52
Q

what structure connects the perilymphatic system with the oval with the subarachnoid space

A

cochlear duct

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53
Q

how is sound transmitted in the ear

A

stapes -> oval window -> movement of perilymph -> vibrations transmitted through endolymph -> tectorial membrane -> movement of hair cells -> depolarisation of neuronal fibres -> cochlear nerve
low frequency sounds detected at apex of cochlea whereas high frequency at base

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54
Q

describ the components of the vestibular system

A
  • 3 semicircular canals at 90deg to each other which detect rotatory movement
  • Utricle: hairs point Up and detect linear/horizontal movement
  • Saccule: hairs point to the Side and detect vertical movements
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55
Q

define vertigo

A

hallucination of movement, caused by central or peripheral vestibular pathology affecting the vestibular system

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56
Q

what are some of the central causes affecting the central system causing vertigo

A

stroke, migraine, neoplasms, dehydration

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57
Q

what are some of the peripheral causes affecting the central system causing vertigo

A

bppv, meniere’s, vestibular neuronitis

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58
Q

what is BPPV

A

vertigo which occurs with particular head movement, which is benign in nature and lasts a short period of time.

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59
Q

what is the cause of BPPV

A

otholiths in semicircular canals causing abnormal stimulation of hair cells - gives hallucination of movmeents

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60
Q

describe the manouevre performed to diagnose BPPV

A

dix hallpike - turn head 45 deg towards the affected side and quickly lie patient down from sitting, with the neck extended 30 degrees. watch the eyes for nystgamus (rotatory?)

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61
Q

which maneouvre is performed to treat BPPV

A

Epley maneouvre

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62
Q

what is the aetiology of Meniere’s disease

A

precise aetiology unknown - there i increased endolymph in the endolymph compartment

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63
Q

what are the clinical features of Meniere’s disease

A
  • tinnitus in affected ear
  • episodic vertigo with nausea and vomiting
  • fluctuating sensorineural hearing loss which over time become permament
  • aural fullness
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64
Q

describe the progression of Meniere’s disease

A

Initally between attacks patients are well, however as the disease progresses, there is progressive sensorineural hearing loss and reduced vestibular function on affected side.
Disease burns itself out, but persisting reduced hearing and generally unbalanced (if other ear normal - can compensate)

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65
Q

what is the general management of Meniere’s disease

A
  • general: reduce salt, chocolate, alcohol, caffeine, chinese food
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66
Q

what is the medical management of meniere’s

A
  • medical: thiazides, betahistine, prochlorperazine (vestibular sedative)
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67
Q

what is the surgical management of meniere’s

A
  • surgical: grommets, middle ear injection of dexamethasone, endolypmhatic sac decompression, vestibular injection using middle ear injection of gentamicin
    rarely: surgical labyrinthectomy
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68
Q

what is vestibular neuronitis

A

inflammation of the inner ear causing severe incapacitating vertigo lasting several days with N+V

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69
Q

what are the clinical features of a vestibular neruonitis attack o/e

A

vertical nystagmus, but otherwise normal on exam

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70
Q

what is the treatment during an acute attack of vestibular neuronitis

A

vestibular sedatives, fluids

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71
Q

what is the progression of vestibular neuronitis

A

often long term vestibular deficit after the acute episode which can lead to a generalised unsteadiness, which takes a few weeks for the brain to recover from

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72
Q

how can patients with long term poor balance due to vestibular neuronitis be managed

A

vestibular rehab exercises - cawthorne-cooksey

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73
Q

what are the investigations you would do on a patient with sudden onset sensorineural loss (emergency)

A
  • pure tone audiogram

- mri (acoustic neuroma)

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74
Q

what is the management for sudden onset sensorineural loss

A
  • steroids (po/injected into middle ear)

- antivirals

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75
Q

describe the weber test

A
  • tuning fork made to vibrate
  • placed on centre of patient’s forehead
  • bone conduction occurs via base of skull to both cochlear
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76
Q

what would be the result of a weber test with sensorineural hearing loss

A

tone will be heard louder on opposite side to hearing loss

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77
Q

what would be the result of a weber test with conductive hearing loss

A

tone will be heard louder on the same side as the hearing loss (conductive hearing loss blocks out background noise, so relative to the other ear the tone will sound louder)

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78
Q

describe the Rinne’s test

A
  • tuning fork made to vibrate

- place on mastoid for a few minutes then when its stops ringing, place lateral to the external auditory meatus

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79
Q

what is Rinne’s positive

A

when sound is heard louder when tuning fork lateral to the external auditory meatus (normal)

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80
Q

what is Rinne’s negative

A

when sound is heard louder when tuning fork is placed over mastoid process (i.e. conductive hearing loss)

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81
Q

what result would you get with a Rinne’s test where you have sensorineural hearing loss (if they retain some hearing)

A

rinne’s positive

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82
Q

what are the axes on a pure tone audiogram

A 
x = frequency (Hz) of sound
y = decibel (loudness)
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83
Q

what is the threshold for normal hearin gon a pure tone audiogram

A

anything above 20db

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84
Q

how should you investigate asymmetrical hearing loss

A

mri

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85
Q

what does presbyacusis appear like on pure tone audiogram

A

as frequency increases, decibels increases in magnitude as well (therefore higher frequencies require more voume in order for it to be heard by patient)
on PTA looks like it “drops off”

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86
Q

how do you know someone has a conductive hearing loss with pure tone audiogram

A

you plot on a PTA air and bone conduction in each each, and look for a discrepancy between the two lines (air line lower than bone = conductive hearing loss)

87
Q

what does a tympanogram measure

A

compliance of the tympanic membrane

88
Q

what is on the x and the y axis of a tympanogram graph

A 
x = pressure (decpascals)
y = compliance (ml)
89
Q

what are the three different types of tympanogram charts

A

type A = normal (peak at 0 decapascals)
type B = perforation (line higher) or fluid in middle ear (line lower)
type C = peak below 0 (negative pressure) i.e. -200, or -400 etc, which means eustachian tube dysfunction

90
Q

name the vessels that supply kiesselbachs triangle

A
  • posterior ethmoidal
  • anterior ethmoidal
  • sphenopalatine
  • greater palatine
  • superior labial
91
Q

what is it important in the patient’s history to ask about when presenting with a nosebleed

A

htn
anticoag
inherited thrombophilias
vasculopathies

92
Q

list some of the causes of epistaxis

A
  • idiopathic mainly
  • trauma
  • iatrogenic
  • foreignn body
  • inflammation e.g. rhinitis, polyps
  • neoplastic (should exclude)
93
Q

what is the management of epistaxis

A
  • a-e assessment
  • pinch soft part of nose tilting head forward and spit out any blood in the mouth
  • locate source of bleed and cauterise with silver nitrate/bipolar diathermy
  • anterior pack
  • posterior pack if continues bleeding
  • surgical vessel ligation/ radiological embolisation if nothing is working
94
Q

what are the serious complications of nasal fractures

A
  • septal haematoma

- basal skull fracture and csf leak

95
Q

what is the management of nasal trauma

A

a-e/epistaxis management
examine for septal haematoma
if deviated nose, consider manipulation under anaesthesia within 2 weeks
(no xr required)

96
Q

what is the lamina papiracea

A

thin plate of bone of ethmoid bone that forms the medial wall of the orbit (air/blood can track up from nose into eye through this)

97
Q

where does the sphenoid sinus drain

A

sphenoethmoidal recess

98
Q

where do the posterior ethmoidal cells drain

A

superior meatus

99
Q

which structures drain into the middle meatus

A

anterior ethmoidal cells
maxillary sinus
frontal sinus

100
Q

what are the complications of sinus surgery

A

damage to the orbit and its contents

csf leak and brain damage in sphenoid and frontal sinus breach

101
Q

what are the complications to the eye that can result from rhinosinusitis

A

infection can spread to the orbit and cause peri-orbital sinusitis which is sight threatening

102
Q

what are the complications to the brain that can result from rhinosinusitis

A

meningitis, intracranial brain abscess

103
Q

list the symptoms of rhinosinusitis

A
  • nasal blockage/obstruction/discharge
  • anterior/posterior nasal drip
  • facial pain/pressure
  • reduction in sense of smell
104
Q

how is rhinosinusitis diagnosed

A
  • endoscopic signs of polyps, mucopurulent discharge, oedema of middle meatus
  • ct showing mucosal changes within the osteomeatal complex or sinuses
105
Q

what is the difference between acute and chronic rhinosinusitis

A
  • acute: less than 12 weeks, complete reoslution of symptoms

- chronic: more than 12 weeks, without complete resolution of symptoms

106
Q

what are the subdivisions of chronic rhinosinusitis

A

with or without nasal polyps

107
Q

list the viruses commonly causing acute rhinosinusitis

A

rhinovirus, influenza virus

resolution of symptoms within 5 days

108
Q

what is considered as causative agents of acute rhinosinusitis is symptoms do not resolve in 5 days

A

bacterias e.g. strep pneumoniae, h influenzae, m catarrhalis

109
Q

what conditions can predispose patients to acute rhinosinusitis episodes

A

allergy

cilliary impairment

110
Q

what is the management of acute rhinosinusitis

A
  • analgesia
  • nasal decongestants
  • topical nasal steroids
  • po abx if lasts over 5 days
111
Q

list some of the predisposing factors for chronic rhinosinusitis

A
  • allergy/atopy
  • infections e.g. s aureus
  • ciliary impairment e.g. cf
  • anatomical abnormalities e.g. septal deviation
  • immunocompromise
  • aspirin hypersensitivity
  • swimming/diving
112
Q

are polyps usually unilateral or bilateral

A

bilat

113
Q

when would a polyp require biopsy for histology

A

worrying history/examination

unilateral

114
Q

what are the investigations for nasal polyps apart from examination

A
  • skin prick test if allergy suspected
  • ct sinuses if surgery planned
  • some need biopsy
115
Q

what is the management for polyps

A
  • conservative: nasal douching, avoid allergens
  • medical: antihistamines, nasal/po steroids if severe
  • antibiotics if infected
  • surgery: polypectomy - endoscopically, correcting anatomical abnormalities
116
Q

what is ARIA

A

allergic rhinitis according to its impact on asthma

117
Q

list the different fascial layers that make up the neck

A

1) superficial investing layer
2) pretracheal fascia
3) fascia of infrahyoid muscles
4) carotid sheath
5) prevertebral fascia

118
Q

what are the borders of the anterior triangle of the neck

A

midline of the neck, anterior border of scm, lower border of mandible

119
Q

what are the borders of the posterior triangle of the neck

A

posterior border of the scm, anterior edge of the trapezius, middle 1/3rd of the clavicle

120
Q

which nerves run in the posterior triangle of the neck

A

cnXI

vagus nerve

121
Q

what is the anatomical site where a retropharyngeal abscess develops

A

anterior to the prevertebral fascia, behind the pharynx

122
Q

where does the retropharyngeal space extend to

A

base of the skull to mediastinum

123
Q

what are the clinical features of a retropharyngeal space abscess

A
  • rigid head and neck
  • systemically unwell
  • airway compromise
  • dysphagia/odynophagia
124
Q

what are the investigations you would do in a retropharyngeal abscess

A 
ct neck
lateral cxr (may show widening of retropharyngeal space)
125
Q

what is the management of retropharyngeal abscess

A
  • secure airway
  • iv abx
  • surgery - incision and drainage
126
Q

what is ludwig’s angina

A

infection of the space between the floor of the mouth and the myelohyoid

127
Q

what is ludwigs angina usually caused by

A

dental infection

128
Q

what are the clinical features of ludwigs angina

A
  • swelling of the floor of the mouth
  • painful mouth
  • protruding tongue
  • airway compromise
  • drooling
129
Q

where is parapharyngeal abscess located anatomically

A

potential space posterolateral to the pharynx

130
Q

what are the clinical features of parapharyngeal abscess

A
  • odynophagia
  • trismus
  • reduced neck movement
  • neck swelling at upper part of scm
131
Q

what is the treatment for parapharyngeal abscess

A
  • secure airway
  • iv abx
  • surgical drainage
132
Q

what is the main causative organism for epiglottitis

A

h influenzae

133
Q

what is the presentation of epiglottitis

A

stridor, choking, pyrexia

134
Q

what is the management of epiglottitis

A

secure airway,
dont examine, keep clam
theatre for intubation by paeds anaesthetist
iv abx - cephalosporins

135
Q

where are jugulodigastric lumps located typically

A

angle of the mandible

136
Q

where are thyroglossal cysts located

A

in the midline between the hyoid bone and thyroid gland

137
Q

where is a branchial cyst located

A

anterior border of the scm

138
Q

what is the gold standard investigation you would perform on any patient presenting with a neck lump

A

us-guided fna

unless pulsatile!

139
Q

name the 4 muscles that make up the pharynx

A

superior, middle and inferior constrictors, and the cricopharyngeus

140
Q

where does the killian’s dehisence, which is vulnerable to herniation, lie

A

between inferior constrictor and cricopharyngeus muscle

141
Q

what are some of the symptoms of pharyngeal pouches

A

dysphagia, regurgitation, recurrent chest infections from aspiration in some, halitosis

142
Q

list the 3 muscles that cause depression and elevation of the pharynx

A
  • stylopharyngeus
  • salpingopharyngeus
  • palatopharyngeus
143
Q

what are the commonest causes of OSA in children and adults respectively

A

children - adenoid hypertrophy

adults - obesity

144
Q

what are the investigations you would perform on a patient with OSA

A
  • weight/bmi
  • tfts
  • cxr (signs of obstructive lung disease)
  • ecg (signs of rvf)
  • sleep study
145
Q

what is the management of OSA

A
  • advice and lifestyle changes about weight loss, not drinking alcohol before bed etc
  • cpap
  • mandibular positioning devices
146
Q

list the bacteria that can cause tonsillitis

A
  • beta haemolytic streptococci
  • staphylococci
  • s pneumoniae
  • h influenza
  • e coli
147
Q

list the viral causes of tonsillitis

A
  • rhinovirus
  • adenovirus
  • enterovirus
  • ebv
148
Q

where may tonsilitis pain be referred to

A

ear - otalgia

149
Q

what is trismus

A

spasm of the jaw muscles leading to reduced opening of the jaw

150
Q

what are some of the clinical features/presentations of head and neck cancers

A
  • dysphonia
  • dysphagia
  • dyspnoea
  • neck mass
  • pain from site, referred pain to ear
  • bleeding from nose or mouth
  • nasal blockage
    often unilateral
151
Q

what histological type are the majority of head and neck cancers

A

squamous cell carcinomas

152
Q

list the risk factors for head and neck cancer

A
  • alcohol
  • tobacco
  • beetle nut chewing (oral cavity ca)
  • chinese ethnic origin for nasopharyngeal malignancy
153
Q

what are the types of examination under anaesthetic you can perform on head and neck cancer patients

A

panendoscopy or laryngooesophagoscopy

154
Q

when is ct performed in patients with head and neck cancer

A

lymphadenopathy present with a proven scc - presumed 2ndary spread

155
Q

why is an fna performed in head and neck cancers and a direct biopsy avoided

A

direct biopsy can lead to seeding of the cancer onto the surface of the skin

156
Q

what investigation can be performed to look for secondary mets in head and neck cancer

A

ct chest - done routinely

157
Q

what is the palliative management of head and neck cancer

A

chemo, radio, occassional surgery

158
Q

what is the curative management of head and neck cancer

A

radiotherapy to primary site, and often the neck too
chemotherapy
surgery - endoscopic laser resection, open surgery to site/neck

159
Q

what is the blood supply to the thyroid gland

A

superior and inferior thyroid arteries from the external carotid artery and thyrocervical trunk respectively

160
Q

what is the venous drainage of the thyroid gland

A

superior, middle and inferior thyroid veins

161
Q

where does the recurrent laryngeal nerve run with relation to the thyroid gland

A

tracheo-oesophgeal groove

162
Q

what do the recurrent laryngeal nerve supply

A

muscles of the larynx except the cricothyroid muscle, vocal cords, sensation below vocal cord

163
Q

what are the investigations for thyroid gland cancers

A
  • tft’s, thyroid antibodies
  • us guided fna
  • hemithyroidectomy + histology if any diagnostic doubt
164
Q

list some non neoplastic nodules

A
  • single nodule: colloid, cystic

- multinodular: goitre

165
Q

list some thyroid neoplasms

A
  • benign: adenoma

- malignancy: different types

166
Q

list the different types of malignant thyroid cancers

A
  • papillary
  • follicular
  • medullary
  • anaplastic
  • hurthe cell
  • lymphoma
167
Q

what is the management for non neoplastic thyroid nodules

A

conservative unless diagnostic uncertainty

surgery: compressive symptoms, cosmesis (try to only do hemithyroiedectomy)

168
Q

what is the management for thyroid adenoma

A

diagnostic hemithyroidectomy, then no further treatment

169
Q

what is the management for thyroid carcinoma

A

total thyroidectomy for papillary, follicular and medullary thyroid cancers
anaplastic disease is often too far advanced for curative surgery
radioiodine for papillary and follicular thyroid cancer

170
Q

list some of the complications of thyroid cancer surgery

A

post op haemorrhage
airway obstruction
vocal cord palsy
hypocalcaemia due to parathyroid gland damage/removal

171
Q

what consistency of saliva do each of the salivary glands produce

A
  • parotid: serous
  • submad: mixed mucous and serous
  • subling: mucous
172
Q

which nerve runs through the parotid gland to split it into deep and superficial lobes

A

facial nerve

173
Q

what is the path of the parotid duct

A

pierces the buccinator muscle and buccal mucosa to open opposite the 2nd molar tooth

174
Q

which is the most common gland for salivary duct neoplasms

A

parotid gland (80%)

175
Q

what proportion of parotid gland tumours are benign

A

80%

176
Q

what is the main type of parotid gland tumour

A

pleomorphic adenoma

177
Q

which muscle is the submandibular gland superior to

A

diagastric

178
Q

where does the submandibular duct open

A

close to the frenulum of the tongue

179
Q

which nerves run medial to the submandibular gland

A

hypoglossal and lingual nerves

180
Q

what proportion of submand neoplasms are malignant

A

50%

181
Q

what can cause a submandibular abscess to form

A

sialolithiasis

sialadenitis

182
Q

what is sialadenitis

A

inflammation of a salivary gland

183
Q

what are the common viral causes of sialadenitis

A
  • mumps
  • coxsackie virus
  • echovirus
  • hiv
184
Q

which bacteria typically causes sialadenitis

A

staph aureus

185
Q

what are some of the causes of chronic sialadenitis (rare)

A

tb, hiv, sarcoidosis, syphillis

186
Q

what are sialithiesis

A

stones in salivary duct causing obstruction, pain and swelling - worse during meals

187
Q

what are the investigations you would do for sialadenitis

A

uss, sialogram

188
Q

what is a sialogram

A

contrast medium is injected into gland duct

189
Q

what is the management of sialolithiesis

A

conservative: analgesia, hydration
meds: sialologues (promote saliva excretion)
removal surgery

190
Q

what are the complications of sialolithiesis

A

sialadenitis, abscess

191
Q

what is the pathophsyiology of sjogren’s syndrome

A

lymphocytic infiltration into ductal tissue of secretory glands

192
Q

what are the signs and symptoms of sjogrens

A

xerostomia, xerophthalmia, enlarged salivary glands

193
Q

which cancer is associated with sjogrens

A

increased risk of lymphoma

194
Q

what are the investigations you would do for sjogrens syndrome

A

anti-ro/-la

biopsy of salivary glands and inner lip

195
Q

what are the generic treatments for thyroid cancer

A
  • radioiodine
  • thyroidectomy
  • LN excision, neck dissection
  • levothyroxine replacement
  • chemotherapy for palliation (esp in anaplastic thyroid cancer)
196
Q

what are the symptoms of laryngeal and pharyngeal cancers

A
  • hoarseness, voice changes
  • lump in neck
  • sore throat/feelings something stuck in throat
  • persistent cough
  • stridor
  • hallitosis
  • referred ear ache
  • dysphagia
197
Q

what is a glottis T2 in the classification of laryngeal cancers

A

extends to supraglottis +/- subglottis +/- impaired vocal cord motility

198
Q

what biological agent can be used in oropharyngeal cancer

A

cetuximab

199
Q

what are important questions to ask in the history of someone presenting with hoarseness

A
  • duration and nature
  • occupation
  • voice misuse
  • smoking, alcohol
  • dysphagia, reflux
  • chest problems, infections, operations
  • thyroid disease
  • weight loss
200
Q

what are the investigations you would perform in someone presenting with hoarseness of voice

A
  • endoscopic evaluation of larynx, microlaryngoscopy
  • biopsy
  • cxr
  • uss thyroid
  • ct neck and chest
  • mri
201
Q

list some of the causes of hoarseness

A
  • vocal nodules
  • muscle tension
  • vocal polyp
  • reinke’s oedema
  • vocal cord palsy
202
Q

what is the treatment for vocal nodules due to chronic voice abuse

A

speech therapy

203
Q

what is the treatment for muscle tension causing hoarseness of voice

A

reassurance and speech therapy

204
Q

what is reinke’s oedema

A

mucosal oedema of the cords

205
Q

who is reinke’s oedema more common in

A

smokers, hypothyroid

206
Q

when would you refer for visualisation of the vocal cords in a patient with hoarseness

A

if it lasts 3 or more weeks

207
Q

what are the risk factors for bell’s palsy

A

dm, urti

208
Q

what may be some other more sinister causes of facial droop if not bell’s palsy

A

brain tumour, stroke, ramsay hunt syndrome, lyme disease

209
Q

what is ramsay hunt syndrome

A

reactivation of herpes zoster in the lateral geniculate ganglion - can present as LMN of facial nerve (hence differential for bell’s)

210
Q

what is the prognosis of bells palsy

A

should start improving at 14 days, and recovered completely by 6 months

211
Q

what is the management of bell’s palsy

A

corticosteroids, antivirals (HSV1), eye drops

212
Q

which muscle is paralysed to cause eyelids being unable to close with bell’s palsy

A

obicularis oculi

213
Q

what is the bell’s phenomenon

A

when attempt is made to close the eyes, the eye drifts upwards and out (this is a protective mechanism)

Special Senses (2 decks)

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