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ENT Flashcards

1
Q

what is the external acoustic metatus made up of

A

outer 1/3 = cartilage

inner 2/3 = temporal bone

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2
Q

2 parts of the external ear

A

auricle/pinna

external acoustic meatus

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3
Q

which muscles contract in response to loud noise

A

tensor tympani and strapedius

inhibit vibrations of malleus, incus and stapes

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4
Q

how to position ear to straighten canal in adults vs children

A

adults = posteriorly and superiorly

children = posteriorly and inferiorly

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5
Q

tuning fork Hertz for rinne’s test

A

512 Hz

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6
Q

Utenberger’s test

A

patient marches on the spot with closed eye

if vestibular dysfunction will turn towards the lesion

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7
Q

decibels that a patient can hear at different distances

A

whisper at arm’s length (60cm) = >30 decibels

whisper at 15cm or conversational voice at 60 then can hear between 30-70 dB

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8
Q

Rinne negative

A

if sound is louder on the mastoid process

= conductive deafness

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9
Q

normal hearing

A

Normal = between 0-20dB in all frequencies - 20 and 20,000Hz

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10
Q

audiometry

A

present a pure tone at an audible level
decrease by 10 till can’t hear
then increase by 5 till they hear

To check for accuracy, should decrease 10 dB one more time to check for no response, then increase by 5 dB increments until the patient responds again to the signal

both a bone conduction threshold and air conduction is tested

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11
Q

presbycusis on an audiometry graph

A

Presbycusis usually affects the high frequencies more than the low

will show tailing off of both air and bone conduction at higher frequencies

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12
Q

Noise induced hearing loss on an audiometry graph

A

shows a sharp dropping off as you reach higher frequencies
if a hearing loss is noise induced you would expect that the sounds have to be made louder before they are heard at 4KHz than at any other frequency. This leads to a dip in the graph

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13
Q

symmetrical hearing loss

A

We consider a hearing loss to be symmetrical if the points for each ear occur within 10dB of each other

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14
Q

what does impedance audiometry encompass

A

tympanometry - measures pressure in the middle ear

measuring the reflex of the strapedius

eustachian tube funciton test

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15
Q

cause of a flat line on tympanometry waveform

A

middle ear effusion - EAC volume is normal
tympanic membrane
perforation or patent gromet- EAC volume >1cm3

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16
Q

peak on tympanometry occurs at negative pressure causes

A

eustacian tube dysfunction

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17
Q

uses of impedence audimetry

A

Is mainly used to determine the cause for conductive hearing loss

  • presence of infectious fluids in the middle ear
  • otitis media with effusion – glue ear
  • checking the patency of a grommet
  • to check for microscopic perforation of tympanic membrane
  • hypertrophy of adenoids or tonsils
  • Eustachian tube dysfunction
  • otosclerosis
  • ossicular chain fracture
  • facial palsy
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18
Q

external ear causes of ear pain

A 
chondritis (inflammation of the cartilage of the pinna - typically occuring after trauma/a cut - Psueodomans, staph or strep) 
pericondritis (inflammation of the pericondrium - a layer of CT which surrounds the cartilage) 
otitis externa
foreign body
trauma
herpes zoster
neoplasm
impacted cerumen (earwax)
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19
Q

referred causes of otalgia

A

salivary glands - calculi or infection
temporal arteritis
cranial nerve referred pain e.g. with trigeminal neuralgia (5) or Ramsay Hunt syndrome (7)
TMJ dysfunction

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20
Q

management of cerumen impaction

A

flush it out with a syringe filled with water or saline (the wax can be softened first with oil or bicarbonate drops - give for 2-3 days then put in water then suck all out)
or manual removal e.g. with alligator forceps

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21
Q

treatment of chrondritis or perichondritis

A

drain pus from an abscess if present

antibiotics like levofloxacin

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22
Q

external ear otorrhea

A

e.g. otitis externa

will only produce a small amount of discharge compared to middle or inner because there are no mucinous glands

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23
Q

types of discharge with middle ear otorrhea

A

serosanguinous suggests a granular mucosa of chronic otitis media

offensive discharge = choleastoma

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24
Q

inner ear otorrhea

A

CSF otorrhea may follow discharge

suspect if you see the halo sign on filter paper

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25
Q

conductive hearing loss causes

A
  • Wax production
  • Eardrum perforation
  • Middle ear effusion
  • Nasopharyngeal tumours blocking the Eustachian tube
  • Otosclerosis
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26
Q

pysiology of presbycusis

A

o Progressive loss of hair cells in the cochlea

o Start losing higher frequencies first as outer hair cells are most exposed to damage

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27
Q

sensorineural causes of hearing loss

A 
presbycusis
sudden (idiopathic) hearing loss - thought to be ischaemia or viral
noise exposure 
ototoxicity with drugs
acoustic tumour
dysacusis 
inflammatory diseases - measles, mumps, meningitis, syphilis, chronic middle ear infection
perilymph fistula
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28
Q

what decibels require protection against

A

> 90

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29
Q

dysacusis

A

despite having normal hearing, some patients are unable to hear well in noisy environemnts

presumed due to a choclear abnormality

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30
Q

ototoxic drugs

A

aminoglycosides e.g. gentamicin
loop diuretics
spironolactone
aspirin

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31
Q

character of tinnitus

A

Ringing, hissing or buzzing sounds suggest an inner ear or central cause.

Popping or clicking suggests an external or middle ear cause or the palate

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32
Q

subjective vs objective tinnitus

A

Subjective if the sound can only be heard by the affected individual. Most commonly caused by things causing sensorineural hearing loss e.g. presbycusis. Ototoxic drugs cause bilateral tinnitus with associated hearing loss.

Objective if the sound can also be heard by the examiner. This is rare and occurs due to rare things, like rare vascular disorders, carotid pathology, or in high output cardiac states.

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33
Q

subjective unilateral tinnitus and sensorineural hearing loss

A

Meniere’s disease - episodes of tinnitus associated with hearing loss + vertigo lasting 15 mins –>24 hours

acoustic neruoma - especially if associated with unilateral hearing loss

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34
Q

subjective bilateral tinnitus and sensorineural hearing loss

A

age-related hearing loss
noise-induced hearing loss
drug-induced ototoxicity (aspirin, NSAIDs, Abx, loop diuretics, cytotoxic drugs)

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35
Q

subjective unilatearl or bilateral tinnitus and conductive hearing loss

A

impacted wax, otitis media, cholesteatoma

otosclerosis - especially if there is a family hisotry

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36
Q

secondary causes of tinnitus

A

secondary to head or neck injury, multiple sclerosis, diabetes, or thyroid disease

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37
Q

acoustic neruoma

A

a benign intracranial tumour

are misnomers as they most commonly arise from the vestibular nerve Schwann cells - a schwannoma

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38
Q

symptoms of acoustic neuroma

A

progressive ipsilateral tinnitus +/- sensorineural deafness (cochlear nerve compression)
dizziness

any patient presenting with unilateral tinnitus = acoustic neuroma until proven otherwise

other: large tumours might give unilateral cerebellar signs or raised ICP signs. balance problems and unsteadiness. if compresses trigeminal nerve then may cause a numb face or tingling

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39
Q

management options for tinnitus

A

Try having continuous, low-level, unobtrusive sound in the background
Hearing aids. If hearing loss >35Db, a hearing aid that improves perception of background noise makes tinnitus less apparent.
Psychological support
CBT
Relaxation techniques may also be useful

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40
Q

diagnosis of acoustic neuroma

A

audiogram - will show a sensorinureal pattern of hearing loss
MRI

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41
Q

treatment of acoustic neuroma

A

observation if there is no tumour growth

focused radiation (stereotactic radiotherapy) or surgery

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42
Q

vertigo define

A

vertigo is a symptom - it is the illusion of movement of the patient’s surroundings, typically rotatory

vertigo is always worsened by dizziness

associated symptoms: 
o Difficulty walking or standing (pt may even fall) 
o Nystagmus – principle sign 
o Relief on lying or sitting still 
o Nausea/vomiting/pallor/sweating
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43
Q

2 divisions of causes of vertigo

A

peripheral/vestibular - i.e. affecting the vestibular nerve or semi-circular canals

central - rare. affecting the visual-vestibular centres of the brainstem e.g. infarct or drugs. acoustic neuroma could be a central cause

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44
Q

benign paroxysmal vertigo (BPPV) symptoms

A

most common cause of peripheral vertigo
attacks of sudden rotational vertigo >30 seconds that is provoked by head turning
nausea is often associated

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45
Q

cause of benign paroxysmal vertigo (BPPV)

A

Most cases are primary/idiopathic:
canalolithiasis (canalith particles)

debris in the semi-circular canal which are disturbed by head movements, resettles and causes vertigo for a few seconds after the movement

or can be secondary to head trauma, viral labyrinthitis, Meniere’s disease, migraine, ear surgery

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46
Q

diagnosis of benign paroxysmal positional vertigo

A

nystagmus when performing the Dix-Hallpike manoevre is diagnostic

turn head to side. patients are lowered quickly to a supine position with the neck extended around 30 degrees below horizontal (hanging off the bed) - will experience vertigo and see nystagmus

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47
Q

treatment of benign paroxysmal positional vertigo

A

epley manoervures
- clears the debris form the semi-circular canals

generally is self- limiting and treatment is only necessary if persistant

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48
Q

Meniere’s disease symptoms and definition

A

dilation of the endolymphatic spaces by hydrops (excess fluid) - causes distension and rupture of Reissner’s membrane –> release of endolymph into perilymphatic space and causes injury to the sensory and neural elements of the inner ear

typically one ear affected but over time both

causing recurrent attakcs of vertigo lasting >20 mins +/- episodes of N+V

flutuating sensorineural loss and tinnitus

associated fullness of the ear

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49
Q

epidemiology of Meniere’s disease

A

can affect any age
40s and 50s more likely to experience it
considered to be chronic

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50
Q

acute labyrinthitis vs vestibular neuronitis

A

o Vestibular neuronitis is thought to be due to inflammation of the vestibular nerve and often occurs after a viral infection.
o Labyrinthitis is a different diagnosis that involves inflammation of the labyrinth.

Hearing loss is a feature of labyrinthitis, but hearing is not affected in vestibular neuronitis

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51
Q

5 vestibular causes of vertigo

A

benign paroxysmal positional vertigo - seconds -minutes

meniere’s disease - 30 mins - 30 hours

acute labyrinthisis or vestibular neuronitis - 30h-week

trauma

ototoxicty by aminoglycosides or loop diuretics

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52
Q

cholesteatoma

A

a destructive and expanding growth consisting of keratinizing sqamous epithelium in the middle ear and/or mastoid process

the keratinizing epithelium exhibits independent growth leading to expansion and resporption of underlying bone

are not classified as tumours or cancers

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53
Q

symptoms of cholesteatoma

A 
foul smelling discharge 
may have conductive hearing loss
tinnitus may be present
headache
pain
  • facial paralysis and vertigo indicate central CNS complications.
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54
Q

management of vestibular neuronitis / acute labyrinthitis

A

o Reassure the person that symptoms will usually settle over several weeks – even if no treatment is given
o Advise that factors such as alcohol, tiredness, or intercurrent illness may have a greater than usual effect on their balance
o Advise that bed rest may be necessary but that activity should be resumed as soon as possible (even if vertigo becomes more prominent during movement).
o Advise the person not to drive when they are dizzy, or if they are likely to experience an episode of vertigo while driving.
o the person should inform their employer if their vertigo poses a risk in the workplace
o offer person written information
o if symptoms are severe, offer short-term symptomatic drug treatment
 vestibular suppressant medications (for example antihistamines and antiemetics)

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55
Q

management of cholesteatoma

A

1st line is surgery - a type of mastoidectomy

56
Q

malignant otitis externa

A

spread of otitis externa into the bone surrounding the ear canal

57
Q

diffuse vs localised otitis externa

A

diffuse = widespread inflammation of the skin and subdermis of the ear canal

localised = infection of a hair follicle that can progress to become a boil in the ear canal

58
Q

causes of otitis externa

A

most commonly bacterial - pseudomonas aeruginosa and staph aureaus

precipitating facotrs include ear trauma, excessive moisture or dermatitis

59
Q

diagnosis of acute otitis externa

A

based on examination and symptoms

ear pain (made worse when the tragus or pinaa is moved or when an otoscope is inserted), itch, discharge, hearing loss

swelling of the ear canal or redness
this can progress to the swelling containing a white or yellow filled centre

60
Q

appearance of chronic otitis externa

A

lack of earwax, dry hypertrophic skin, pain, constant itch

61
Q

appearance of malignant otitiis externa

A

granulation tissue at bone-cartilage junction of ear canal ; exposed bone in the ear canal

facial nerve palsy

temp >39 degrees

hearing loss, vertigo, pain

62
Q

differentials for otitis externa

A

acute otitis media - otitis externa can be secondary to otorrhea from otitis media

foreign body

impacted earwax

cholesteatoma - causes discharge

neoplasm - if there is a swelling in the ear canal that bleeds easily on contact

63
Q

management of localised otitis externa

A

treat with analgesia and application of local heat

oral Abx are rarely indicated

can drain pus if necessary but again this is rarely required

64
Q

management of diffuse otitis externa

A

investigations are rarely needed - tympanometry can show that the tympanic membrane is intact if unsure

consider taking an ear swab to determine the causative organism if treatment fails or otitis externa is recurrent or chronic

analgesia

consider prescribing a topical Abx with or without a topical csteroid - consider cleaning canal of debris and wax if it blocks medication getting in

oral Abx rarely indicated

consider inserting an ear wick soaked in the treatment if there is extensive swelling of the canal

65
Q

prognosis of malignant otitis externa

A

Without treatment, this can be a fatal condition — osteomyelitis will progressively involve the mastoid, temporal, and basal skull bones, and the infection will spread to cerebrospinal fluid causing meningitis.
With treatment, the mortality rate is less than 15%

66
Q

main cause of malignant (aka necrotrizing) otitis externa

A

pseudomonas aeruginosa = 95%

67
Q

otitis media vs otitis media with effusion

A

otitis medial with effusion is characterised by fluid in the middle ear but is not associated with symptoms and signs of an acute ear infection aka glue ear

whereas otitis media is inflammation with an effusion AND symptoms and signs of an ear infection

68
Q

causes of otitis media

A

bacterial - Haemophilus influenzae, strep pnuemoniae, streptococcus pyogenes…

viral – respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza, parainfluenza virus

69
Q

presentation of otitis media

A

earache - due to pressure on the TM. if perforation occurs, the pain lessens and hearing improves

tympanic membrane will be red yellow or cloudy and may be bulging. may be an air-fluid level behind the tympanic membrane

younger children may hold or rub their ear or have more non-specific symptoms like fever, crying, restlessness

70
Q

management of otitis media

A

Pain and fever managed with paracetamol or ibuprofen
Advise that the usual course of acute otitis media is about 3 days, but can be up to 1 week
Many people will not require Abx because symptoms usually resolve spontaneously within a few days
Abx are required when:
oSystemically very unwell
oHigh risk of complications

5-7-day course of amoxicillin is recommended first-line

Can give back-up prescription if symptoms do not start to improve within 3 days or worsen significantly or rapidly at any time

Take account of evidence that acute complications such as mastoiditis are rare with or without antibiotics, and the possible adverse effects of antibiotics

71
Q

complications of otitis media

A
  • Recurrence of infection
  • Hearing loss
  • Tympanic membrane perforation
  • Rarely – mastoiditis, meningitis, intracranial abscess, sinus thrombosis and facial nerve paralysis

Mastoiditis - the mastoid air cells will be filled with pus. Boggy red swelling observable behind the ear. This pus pushes the ear outwards

72
Q

glue ear cause

A

uncertain but over 50% of cases are thought to follow an episode of acute otitis media

persistence of OME may be caused by impaired eustachian tube function, low-grade viral or bacterial infection, local inflammaotry reaction, adenoidal infection

73
Q

presentation and diagnosis of glue ear

A

may be associated with significant hearing loss - usually resolves over several weeks or months

mild ear pain with fullness or popping may occur

diagnosis is based on suspected hearing loss - there are usually no signs on examination other than effusion

refer to audiometry and tympanometry where appropriate if uncertain

74
Q

management of glue ear

A
  • Spontaneous resolution of OME is common, so for most children a period of active observation over 6–12 weeks is appropriate
  • During this period, it is essential to re-evaluate signs and symptoms of the effusion and concerns regarding the child’s hearing or language development
75
Q

symptoms of a perforated eardrum

A

may feel a sharp pain or an earache that you’ve had for a while may suddenly go away

conductive hearing loss - usually temporary

other symptoms may include tinnitus, vertigo, otorrhoea

76
Q

causes of a perforated eardrum

A

otitis media - pressure builds up and pushes against the eardrum

foreign object - cotton swab or pin

less commonly: loud noise or surgery

77
Q

treatment of perforated eardrum

A

may heal in a few weeks or may take up to a few months

some require intervention e.g. a paper patch to promote healing or surgery (tympanoplasty)

78
Q

facial nerve - muscle supplied and taste supplied

A

facial nerve supplies stapedius – paralysis results in hyperacusis

supplies taste sensation to the anterior two-thirds of the tongue

79
Q

causes of facial nerve damage

A

Between the brainstem and middle ear
o Tumours – meningioma or astrocytoma
o Temporal bone trauma
o Acoustic neuroma
In the middle ear
o AOM – acute otitis media (oedema pressing on)
o Cholesteatoma
Neck or face
o Parotid tumours
o Facial lacerations
Global
o Ramsay hunt (herpes zoster of facial nerve)
o Lyme disease (Borrelia bacterium which is spread by ticks –> erythema migrans appears at site of tick bite)
o Bell’s palsy (15% undergo Wallerian degeneration of nerve (regrowth is 1mm per day, takes about 3 months to return to function)

80
Q

score to assess the degree of facial nerve damage

A

House-brachman score

  • I – normal
  • II – slight-mild weakness. Only on close inspection
  • III – moderate – facial asymmetry and weakness but eye closes. Asymmetrical mouth, may not be able to lift eyebrow
  • IV – moderately severe – total facial asymmetry and weakness with incomplete closure of the eye and inability to lift brow
  • V – severe – barely detectable movement. Slight movement of corner of mouth
  • VI – total – no facial function. Loss of tone
81
Q

UMN vs LMN facial nerve damage

A

UMN damage = forehead is spared

LMN = whole side is affected

82
Q

what structures open into the nasal cavity

A

paranasal sinuses
nasolacrimal duct - drains tears
eustachian tube - equalises pressure

83
Q

isolated nasal bone fracutre diagnosis

A

is clinical - will not need an X ray

84
Q

septal haematoma

A

causes - broken nose, injury, surgery

presents with pain, nasal obstruction with a boggy swelling

septal cartilage has no blood supply and recieves all nutrients from perichondrium so an untreated septal haematoma may lead to necrosis and a saddle nose deformity

treatment is incision and drainage

85
Q

window of opportunity for manipulation with a nasal fracture

A

swelling often interferes with adequate examination so patients should be reassesed after 5-7 days (so after initial A+E appointment then book in an OPD ENT appointment - in meanwhile advise ice pack and painkillers)

at 3 weeks nasal bones heals and fixate so manipulation would be near impossible

so around 7-21- day window

86
Q

how is nasal reduction performed followed nasal fracture

A

Manual reduction under anaesthesia

  • But if patient is happy to live with a minor deformity then nothing further needs to be done
  • is done under LA or GA

or referral for rhinoplasty in 3-6 months:
o Septoplasty
 Or surgery can be done to straight both the bone and cartilage
o Septorhinoplasty

87
Q

nose blood supply

A

the internal carotid (via the ethmoidal arteries) supplies the region above the middle turbinate - remaining areas are supplied by branches of the external carotid

L- superior labial artery
E - anterior ethmoidal
G- greater palatine artery
S - sphenopalatine artery

88
Q

recommended antibiotic for otitis media

A

5-day course of amoxicillin is first line if given (not always needed)

89
Q

if the tympanic membrane, how does this impact Abx treatment for otitis media

A

If the tympanic membrane is perforated, aminoglycosides are traditionally not used

90
Q

causes of epistaxis

A

trauma - e.g. nose picking of foreign body
inflammation - chronic sinusitus, allergic rhinosinusitis or nasal polyps
topical drugs - cocaine, steroids, decongestants
vascular - hereditary haemorrhagic telangiectasia or Wegener’s granulomatosis
poster-op bleeding
tumour - angiofibroma (benign) or SCC
nasal oxygen therapy

more general causes - HTN, atherosclerosis, increased venous pressure form mitral stenosis, haematological disorders

91
Q

site of majority of epistaxis

A

Little’s area on the anterior nasal septum, which contains the Kiesselbach plexus of vessels

Less commonly, epistaxis originates from branches of the sphenopalatine artery in the posterior nasal cavity.
o Posterior nosebleeds usually occur in older people, are more profuse, result in bleeding from both nostrils, and the bleeding site cannot be identified on examination

92
Q

assessment of epistaxis

A

A-E
if haemoydnamically unstable then try quantify the amount of blood loss via rough cups
ask if a temporary pack has been used before seeking help - this could push up foreign bodies further
examine both nasal passages with good lighting and a speculum
look for a small red dot when doing this - this will be the bleeding point

Suspect a posterior bleed if bleeding is profuse, from both nostrils, the bleeding site cannot be identified on speculum examination, and/or if bleeding first started down the throat

93
Q

general first aid measures for epistaxis

A

sit with their body tilted forward and mouth open to decrease swallowing of blood - avoid lying down unless feeling faint
pinch the cartilaginous part of the nose firmly for 10-15 mins without releasing pressure

94
Q

if epistaxis stops with first aid measures alone then consider applying….

A

a topical antiseptic (naseptin (chlorehxidine + neomycin) to reduce crusting and vestibulitits

naseptin (chlorhexidine and neomycin) cream to be applied to the nostrils 4x daily for 10 days

95
Q

what to do if epistaxis does not stop

A

nasal cautery if the bleeding point can be seen and the procedure can be tolerated
- use a local anaesthetic spray preferably with a vasoconstrictor like lidocaine with phenylephrine then wait 3-4 mins. apply silver nitrate stick to bleeding point for 3-10 secs. then apply a topical antiseptic to area (naseptin (chlorhexidine + neomycin)

nasal packing if cautery is ineffective or bleeding point cannot be seen

  • first anaesthetise (same as above)
  • admit to hospital if nasal pack has been inserted in primary care
96
Q

nasal packing options

A

nasal tampons e.g. Merocel
inflatable packs e.g. rapid-rhino - may be easier and more comfortable to insert and remove
ribbon gauze impregnated with vaseline - if left in for >48 hours then Abx should be started to prevent toxic shock syndrome

97
Q

secondary care measures for epistaxis

A

resuscitation - this may include transfusion to replace blood volume
formal packing - may be under GA
endoscopic assessmnet and electrocautery
examination under anaesthesia and surgical intervention (such as diathermy, septal surgery, arterial ligation + laser)
radiological arterial embolization
IV or oral tranexamic acid

98
Q

management of episatxis from posterior area

A

admit to hostpial
may require either balloon insertion (foley catheter or Brighton balloon) or a formal posterior pack (usually done under GA)

99
Q

rhinosinusitis define

A

inflammation of the nose and paranasal sinuses with >2 symptoms - one of which must be

  • nasal blockage/obstruction/congestion
  • nasal discharge
  • +/- facial pain or pressure
  • reduction or loss of smell
  • and either endoscopic or CT signs

NB the term rhinosinusitis is preferred over sinusitis because inflammation of the sinuses is almost always accompanied by inflammation of the nasal cavities

100
Q

acute vs chronic rhinosinusitis

A

acute <12 weeks
chronic >12 weeks

if chronic, patient may develop polyps due to inflammatory environment

101
Q

diagnosis of acute rhinosinusitis

A

diagnosed by presence of nasal blockage or discharge with facial pain/pressure and/or reduction of sense of smell
palpate the maxiofacial area to elict swelling or tenderness
perform anterior rhinoscopy to look for nasal inflammation, mucosal oedema and purulent nasal discharge
record pulse, BP and temp if person is systemicall unwell

102
Q

treatment of acute rhinosinusitis

A

refer to hospital if unwell of complications like periorbital oedema or cellulitis, reduced visual acuity, double vision, signs of meningitis…

offer written advice
analgesia
some people may want to do a trial of nasal saline or decongestants (although evidence is lacking to support their use)
adivise that is s usually caused by a virus and is only complicated by bacterial infection in about 2 in 100 cases. It takes 2–3 weeks to resolve, and most people will get better without antibiotics

103
Q

treatment of acute rhinosinusitis that persists >10 days

A

consider a high-dose nasal corticosteriod for 14 days

consider antibioitc prescription keeping in mind that evidence has shown they make little difference to how long symptoms last + withoulding is unlikely to lead to complications

104
Q

when should you suspect acute bacterial rhinosinusitis

A

symptoms >10 days
purulent discharge with unilateral predominance
severe local pain with unilateral predominance
fever >38 degrees C
A marked deterioration after an initial milder form of the illness (so-called ‘double-sickening’).
Elevated ESR/CRP

105
Q

causes of acute bacterial rhinosinusitis

A

s pneumoniae
h influenza
s aureus

106
Q

investigations for acute bacterial rhinosinusitus

A

diagnosis is clinical, by examining the nose and looking for mucosal inflammation, oedema, discharge etc.
In recurrent rhinosinusitis, a CT can be performed to assess for anatomical variation

107
Q

antibiotic treatment for acute bacterial rhinosinusitis

A

amoxicillin or doxycyline

108
Q

complications from bacterial rhinosinusitis

A

orbital cellulitis can occur, which is severe and life/sight threatening.
We can also see spread, leading to encephalomeningitis. In the same way, we can see osteomyelitis.
Mucocoeles (esp. frontal sinus) – we see pus filling the frontal cavity.

109
Q

types of allergic rhinitis

A
  • Can be seasonal
  • Perennial (occurring throughout the year, typically due to allergens from the house like dust mites)
  • Intermittent (<4 days a week or less than 4 consecutive weeks)
  • Persistent (more than 4 days a week AND >4 consecutive weeks)
  • Occupational
110
Q

management of allergic rhinitis

A
  • Sources of information and support.
  • Possible use of nasal irrigation with saline.
  • Allergen avoidance
  • The use of an as-needed intranasal antihistamine or non-sedating oral antihistamine, or an intranasal chromone,
  • The use of a regular intranasal corticosteroid during periods of allergen exposure for moderate-to-severe persistent symptoms, or if initial drug treatment is ineffective.
111
Q

chronic rhinosinusitis with nasal polyps symptoms + investigations

A

watery anterior rhinorrhoea, sneezing, purulent postnasal drip, nasal obstruction, sinusitis, mouth-breathing, snoring, headaches

investigate with anterior rhinoscopy or nasal endoscopy - polyps are pale, mobile and insensitive to gentle palpation

112
Q

treatment of chronic rhinosinusitis with polyps

A

medical polypectomy - topical steroids shrink the polyps e.g. betamethasone or a course of 5 days 40mg prednisolone. consider adding long term Abx. this process is known as a medical polypectomy. douching with saline also helps

endoscopic sinus surgery (ESS)/ endoscopic nasal polypectomy - consider if max medical treatment fails + ongoing severe symptoms

always important to rule out neoplams - if unilateral single polyp then refer to ENT

113
Q

CSF rhinorrhea

A

occurs when there is a fistula between the dura and skull base

due to basilar skull fracture or pituitary adenoma, ethmoid fracture or tumour

other signs of this include CSF otorrhea (drainage of CSF through the ear)

114
Q

investigations for CSF rhinorrhea

A

nasal CSF discharge test - positive for glucose

and nasal CSF uniquely containts beta-2 (tau) transferrin = gold standard diagnostic test

115
Q

management of CSF rhinorrhea

A

If traumatic, conservative management has high spontaneous resolution: 7-10 days bedrest (head elevated at 15-30 degrees) + lumbar drain
Leaks often stop spontaneously
If this does not occur, then neurosurgical closure is necessary to prevent the spread of infection to the meninges
CSF fistulae persisting for > 7 days had a significantly increased risk of developing meningitis
Avoid coughing, sneezing, nose blowing etc.
Cover with antibiotics and pneumococcal vaccine

116
Q

management of foreign body in child’s nose

A

Ask the child to blow their nose or ask parent to perform a ‘parental kiss’ – make the parent blow into the child’s mouth while occluding other nostril. 70% success rate.
Crocodile forceps may be used if the child is cooperative

117
Q

management of septal perforation

A

if aymptomatic can be managed with observation (although none will spontaneously close)
saline nasal irrigation, petroleum jelly applied to the edge of the perforation to promote healing

surgical closure via placement of a septal prosthesis - but only half of patients find this tolerable (can be botherseom)

118
Q

presentation of nasopharyngeal cancer

A

lymphadenopathy (main symptom is neck lump; 90%)
blocked nose
epistaxis
tinnitus
deafness
cranial nerve involvement due to base of skull extensions

119
Q

investigations for nasopharyngeal cancer

A

endoscopy + biopsy

MRI for staging

120
Q

when to suspect cancer of the paranasal sinuses

A

when chronic sinusitis presents for the first time later in life

blood-stained nasal discharge and nasal obstruction /masses

121
Q

histology of paranasal sinuses and investigations

A

50% squamous cell, 10% lymphoma, adenocarcinoma

investigate with MRI/CT + biopsy

122
Q

tonsils

A

pharyngeal/adenoi at the top
then 2 tubal tonsils
then 2 palatine tonsils
then one lingual at the bottom (posterior 1/3 of the tongue)

123
Q

salivary glands

A

parotid - serous - most tumours (mostly pleomorphic adenomas)

submandibular - mixed - most sontes

sublingual - mucous

124
Q

types of stridor

A

inspiratory - larynx
expiratory - lower respiratory tract i.e. asthma
biphasic - trachea

125
Q

2 clinical descriptions of acute sore throat

A

acute pharyngitis = inflammation of the part of the throat behind the soft palate (oropharynx)

tonsillitis = inflammation of the tonsils

126
Q

causes of sore throat

A

usually viral or bacterial
e.g. common cold, influexa, strep, infectious mononucleosis
acute herpetic pharyngitis - suggested by vesicles and shallow ulcers on the palate

physical irritation from GORD
chronic cigarette smoke
hayfever
oral mucositis secondary to radiotherapy or chemo
leukaemia - ulceration and haemorrhage of the mucus membrane of the pharynx may occur

127
Q

scores to determine the liklihood of strep infection (and therefore the need for Abx)

A

FeverPAIN score and centor criteria

strep infection is suggested by fever >38.5, exudate on the pharynx/tonsils, anterior neck lymphadenopathy and absence of cough

128
Q

FeverPAIN score

A
  • Fever over 38°C.
  • Purulence (pharyngeal/tonsillar exudate).
  • Attend rapidly (3 days or less)
  • Severely Inflamed tonsils
  • No cough or coryza

max score = 5 points

129
Q

simple advice for sore throat

A

o Regular use of paracetamol or ibuprofen to relieve pain and fever
o Adequate fluid intake to avoid dehydration until the discomfort and swelling subside
o Salt water gargling, medicated lozenges (containing a local anaesthetic and NSAID or an antiseptic agent) may provide temporary relief from throat pain

130
Q

first line antibiotic for strep pharyngitis

A

phenoxymethylpenicillin

131
Q

who might benefit from tonseillectomy

A

a frequency of more than 7 episodes per year for one year, 5 per year for 2 years, or 3 per year for 3 years

132
Q

complications of acute pharyngitis

A

scarlet fever - due to group A strep
otitis media - most common
peri-tonsillar abscess (quinsy) - risk of airway comprimse
parapharyngeal abscess

133
Q

most common organism to cause acute bacterial tonsillitis

A

strep pyogenes - over half

134
Q

acute tonsillitis symptoms

A

the tonsils will often meet in the midline and may be covered in a membrane
pharyngitis, fever, malaise and lymphadenopathy
tonsils are typically oedematous and yellow or white pustules may be present

135
Q

treatment of acute bacterial tonsillits if due to group A beta-haemolytic strep

A

with penicillin type antibiotics

phenoxymethylpenicillin or benzylpenicillin or amoxicillin

136
Q

when should quinsy be suspected (peri-tonsillar abscess)

A

with unilateral swelling and fever – surgical drainage usually produces prompt resolution of symptoms

137
Q

causes of odynophagia

A

infection of mouth, tonsils, throat, epilgottis or oesophagus e.g. URTI, cadidiasis, HIV, EBV

foreign object

non-infectious e.g. sores, ulcers, tumours, oesophageal disorders, acid reflux, injury

oesophageal cancer

spc (5 decks)

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