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ENT Flashcards

1
Q

Hearing aid vs cochlear implant

A

Hearing aids amplify sounds, whereas cochlear implants bypass the outer and middle ear to directly stimulate the auditory nerve.

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2
Q

List the differentials for dizziness/vertigo

A
  • Ménière’s disease.
  • Benign paroxysmal positional vertigo (BPPV).
  • Postural hypotension.
  • Vestibular neuritis.
  • Labyrinthitis.
  • Acoustic neuroma.
  • Posterior circulation stroke syndrome (POCS).
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3
Q

What are the 2 main causes of hearing loss?

A
  • Conductive hearing loss: problem with sound travelling from the environment to the inner ear.
  • Sensorineural hearing loss: problem with the sensory system or vestibulocochlear nerve in the inner ear.
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4
Q

Name the 3 sections of the ear

A
  • Outer ear
  • Middle ear
  • Inner ear
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5
Q

Function of semicircular canals?

A

Sense head movement (the vestibular system)

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6
Q

What is the function of the cochlea?

A

Converts the sound vibration into a nervous signal, to be transmitted by the vestibulocochlear nerve.

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7
Q

Name the 3 bones of the middle ear

A

Malleus, incus and stapes

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8
Q

Sudden onset hearing loss (< 72 hours) requires what?

A

A thorough assessment to establish cause.

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9
Q

Describe some symptoms which may occur alongside hearing loss

A
  • Tinnitus.
  • Vertigo (the sensation that the room is spinning).
  • Pain (may indicate infection).
  • Discharge (may indicate an outer or middle ear infection).
  • Neurological symptoms.
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10
Q

Which tests are used to differentiate between sensorineural and conductive hearing loss?

A

Weber’s test and Rinne’s test

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11
Q

Describe Weber’s test

A

To perform Weber’s test:

  • Strike the tuning fork to make it vibrate and hum.
  • Place it in the centre of the patient’s forehead.
  • Ask the patient if they can hear the sound and which ear it is loudest in.

Normal: patient hears the sound equally in both ears.

Sensorineural hearing loss: sound louder in the normal ear (quieter in the affected ear). The normal ear is better at sensing the sound.

Conductive hearing loss: sound louder in the affected ear. This is because the affected ear ‘turns up the volume’ and becomes more sensitive, as sound has not been reaching that side as well due to the conduction problem. When the tuning fork’s vibration is transmitted directly to the cochlea, rather than having to be conducted, the increased sensitivity makes it sound louder in the affected ear.

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12
Q

Describe Rinne’s test

A

To perform Rinne’s test:

  • Strike the tuning fork to make it vibrate and hum.
  • Place the flat end on the mastoid process.
  • Ask the patient to tell you when they can no longer hear the humming noise.
  • When they can no longer hear the noise, remove the tuning fork (still vibrating) and hover it 1cm from the same ear.
  • Ask the patient if they can hear the sound now.
  • Repeat on the other side.

Normal: AC > BC. ‘Rinne’s positive’.

Sensorineural hearing loss: AC > BC.

Conductive hearing loss: BC > AC. ‘Rinne’s negative’.

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13
Q

Outline the causes of sensorineural hearing loss

A
  • Sudden sensorineural hearing loss.
  • Presbycusis (age-related hearing loss).
  • Noise exposure.
  • Ménière’s disease.
  • Labyrinthitis.
  • Acoustic neuroma.
  • Neurological conditions (e.g. stroke, multiple sclerosis or brain tumours).
  • Infections (e.g. meningitis).
  • Medications: loop diuretics (e.g. furosemide), aminoglycosides (e.g. gentamicin), chemotherapy (e.g. cisplatin).
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14
Q

Outline the causes of conductive hearing loss

A
  • Ear wax.
  • Infection (e.g. otitis media or otitis externa).
  • Fluid in the middle ear (effusion).
  • Eustachian tube dysfunction.
  • Perforated tympanic membrane.
  • Otosclerosis.
  • Cholesteatoma.
  • Exostoses.
  • Tumours.
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15
Q

What is audiometry and audiograms?

A
  • It involves testing a patient’s hearing by playing a variety of tones and volumes using headphones (air conduction) and a bone conduction device (oscillator).
  • Audiometry results are recorded on an audiogram.
  • Audiograms can help identify and differentiate conductive and sensorineural hearing loss.
  • Hearing is tested to establish the quietest volume (dB) at which a patient can hear each frequency (Hz).
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16
Q

What is the medical term for age-related hearing loss?

A

Presbycusis

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17
Q

What type of hearing loss is presbycusis?

A

Sensorineural

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18
Q

Which sound pitch does presbycusis mostly affect?

A

High-pitched sounds

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19
Q

What are the causes of presbycusis?

A
  • Loss of hair cells in the cochlea.
  • Loss of neurones in the cochlea.
  • Atrophy of the stria vascularis.
  • Reduced endolymphatic potential.
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20
Q

What is a key risk factor for presbycusis?

A

Exposure to loud noise over time.

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21
Q

Describe the presentation of presbycusis

A
  • Gradual, insidious and bilateral hearing loss.
  • Loss of high-pitched sounds e.g. speech.
  • May be associated tinnitus.
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22
Q

How would you diagnose presbycusis?

A

Audiometry

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23
Q

Describe the management of presbycusis

A
  • Hearing aids.
  • Cochlear implants (in patients where hearing aids are not sufficient).
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24
Q

Define sudden sensorineural hearing loss (SSNHL)

A

Hearing loss over less than 72 hours. It is most often unilateral and permanent or resolve over days to weeks.

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25
Q

Outline the causes of SSNHL

A
  • Idiopathic (most common).
  • Infection (e.g., meningitis, HIV and mumps).
  • Ménière’s disease.
  • Ototoxic medications.
  • Multiple sclerosis.
  • Migraine.
  • Stroke.
  • Acoustic neuroma.
  • Cogan’s syndrome (a rare autoimmune condition causing inflammation of the eyes and inner ear).
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26
Q

What is the criteria to diagnose SSNHL?

A

Audiometry with a loss of at least 30 decibels in three consecutive frequencies on an audiogram.

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27
Q

Management for SSNHL

A
  • Immediate referral to ENT for assessment within 24 hours.
  • Idiopathic SSNHL: steroids (oral or intra-tympanic).
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28
Q

What is the role of the Eustachian tube?

A

To equalise the air pressure in the middle ear and drain fluid from the middle ear.

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29
Q

Describe the presentation of Eustachian tube dysfunction

A
  • Reduced or altered hearing.
  • Popping noises or sensations in the ear.
  • A fullness sensation in the ear.
  • Pain or discomfort.
  • Tinnitus.
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30
Q

Outline the investigations for Eustachian tube dysfunction

A

If associated with a clear cause (e.g. recent viral URTI or hay fever) no investigations are required.

In persistent, problematic or severe symptoms, investigations to help establish the diagnosis and cause include:

  • Tympanometry (tube dysfunction may show peak admittance (most sound absorbed) with negative ear canal pressures).
  • Audiometry.
  • Nasopharyngoscopy.
  • CT scan to assess for structural pathology.
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31
Q

Management for Eustachian tube dysfunction

A
  • No treatment, waiting for it to resolve spontaneously (e.g., recovering from the viral URTI).
  • Valsalva manoeuvre (holding the nose and blowing into it to inflate the Eustachian tube).
  • Otovent to clear blockages and equalise pressure.
  • Decongestant nasal sprays (short term only).
  • Antihistamines and a steroid nasal spray for allergies or rhinitis.
  • Surgery may be required in severe or persistent cases (adenoidectomy, grommets, balloon dilatation Eustachian tuboplasty).
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32
Q

Name the condition where there is remodelling of the small bones in the middle ear leading to conductive hearing loss

A

Otosclerosis

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33
Q

What is the inheritance pattern of otosclerosis?

A

Autosomal dominant

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34
Q

Describe the pathophysiology of otosclerosis

A

Abnormal bone remodelling and formation, mainly affecting the base of the stapes, where it attaches to the oval window, causing stiffening and fixation and preventing it from transmitting sound effectively.

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35
Q

Describe the typical presentation of otosclerosis

A

Patient under 40 years presenting with unilateral or bilateral hearing loss and tinnitus, affecting lower pitched sounds.

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36
Q

How would you investigate for suspected otosclerosis?

A
  • Audiometry: bone conduction readings will be normal (between 0 and 20 dB). However, air conduction readings will be greater than 20 dB, plotted below the 20 dB line on the chart. Hearing loss tends to be greater at lower frequencies.
  • Tympanometry: reduced admittance (absorption) of sound.
  • High-resolution CT scan.
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37
Q

What are the management options for otosclerosis?

A
  • Conservative: hearing aids.
  • Surgical: stapedectomy or stapedotomy.
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38
Q

Define otitis externa

A

Inflammation of the external auditory canal.

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39
Q

What is another name of otitis externa?

A

Swimmers ear

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40
Q

Outline the risk factors for otitis externa

A
  • Swimming
  • Trauma
  • Removal of ear wax
  • Diabetes
  • Young age
  • Eczema, psoriasis
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41
Q

Name 2 bacteria and 2 fungi that cause otitis externa

A
  • Bacteria: Pseudomonas aeruginosa, Staphylococcus aureus.
  • Fungi: Candida albicans, Aspergillus.
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42
Q

Describe the features of otitis externa

A
  • Ear pain
  • Discharge
  • Itchiness
  • Conductive hearing loss (if the ear becomes blocked)
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43
Q

What is the management for otitis externa?

A
  • Mild cases: acetic acid 2% (EarCalm) - can also be used prophylactically in swimmers.
  • Moderate cases: topical antibiotic and steroid e.g. neomycin, dexamethasone and acetic acid (Otomize spray) - aminoglycosides should not be used if there’s a perforated tympanic membrane due to the risk of ototoxicity.
  • Severe cases: discuss with ENT.
  • Fungal: clotrimazole ear drops.
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44
Q

What is malignant otitis externa?

A

When the infection spreads from the external auditory canal to the skull base, progressing to osteomyelitis of the temporal bone.

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45
Q

Which patients does malignant otitis externa most commonly affect?

A

Elderly, diabetic, immunocompromised or HIV.

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46
Q

What is the most common causative organism in malignant otitis externa?

A

Pseudomonas aeruginosa

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47
Q

Describe the features of malignant otitis externa

A
  • Severe ear pain
  • Discharge
  • Headache
  • Fever
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48
Q

What finding indicates malignant otitis externa?

A

Granulation tissue at the junction between the bone and cartilage in the ear canal.

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49
Q

Describe the management plan for malignant otitis externa

A
  • Admission to hospital under the ENT team.
  • IV antibiotics.
  • Imaging (e.g. CT or MRI head) to assess the extent of the infection.
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50
Q

What complications can arise from malignant otitis externa?

A
  • Facial nerve palsy.
  • Other cranial nerve involvement (e.g. glossopharyngeal, vagus or accessory nerves).
  • Meningitis.
  • Intracranial thrombosis.
  • Death.
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51
Q

Medical term for ear wax?

A

Cerumen

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52
Q

What is ear wax made from and what is its function?

A
  • Made from secretions and dead skin cells.
  • It prevents infection in the ear canal.
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53
Q

What can impacted ear wax result in?

A
  • Conductive hearing loss
  • Discomfort in the ear
  • A feeling of fullness
  • Pain
  • Tinnitus
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54
Q

What are the 3 main methods for removing ear wax?

A
  • Ear drops – usually olive oil or sodium bicarbonate 5%.
  • Ear irrigation – squirting water in the ears to clean away the wax.
  • Microsuction – using a tiny suction device to suck out the wax.
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55
Q

Outline the causes of primary and secondary tinnitus

A

Primary tinnitus has no identifiable cause and often occurs with sensorineural hearing loss.

Secondary tinnitus refers to tinnitus with an identifiable cause. Causes include:

  • Impacted ear wax
  • Ear infection
  • Ménière’s disease
  • Noise exposure
  • Medications (e.g. loop diuretics, gentamicin and chemotherapy drugs such as cisplatin)
  • Acoustic neuroma
  • Multiple sclerosis
  • Trauma
  • Depression

Tinnitus may also be associated with systemic conditions:

  • Anaemia
  • Diabetes
  • Hypothyroidism or hyperthyroidism
  • Hyperlipidaemia
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56
Q

What are the red flags that could indicate a serious underlying cause of tinnitus and the need for specialist assessment?

A
  • Unilateral tinnitus.
  • Pulsatile tinnitus.
  • Hyperacusis (hypersensitivity, pain or distress with environmental sounds).
  • Associated unilateral hearing loss.
  • Associated sudden onset hearing loss.
  • Associated vertigo or dizziness.
  • Headaches or visual symptoms.
  • Associated neurological symptoms or signs (e.g. facial nerve palsy or signs of stroke).
  • Suicidal ideation related to the tinnitus.
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57
Q

Management for tinnitus

A
  • It tends to improve or resolve over time without any interventions.
  • Underlying causes of tinnitus can be treated, such as impacted ear wax or infection.
  • Improve symptoms: hearing aids, sound therapy (adding background noise to mask the tinnitus), or CBT.
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58
Q

Which sensory inputs are responsible for maintaining balance and posture?

A
  • Vision
  • Proprioception
  • Signals from the vestibular system
59
Q

Describe the function of the vestibular system

A

The vestibular system is the most important sensory system to understand when learning about vertigo. The vestibular apparatus is located in the inner ear. It consists of three loops called the semicircular canals that are filled with a fluid called endolymph. These semicircular canals are oriented in different directions to detect various movements of the head. As the head turns, the fluid shifts inside the canals. This fluid shift is detected by tiny hairs called stereocilia found in a section of the canal called the ampulla. This sensory input of shifting fluid is transmitted to the brain by the vestibular nerve and lets the brain know that the head is moving in a particular direction.

The vestibular nerve carries signals from the vestibular apparatus to the vestibular nucleus in the brainstem and the cerebellum. The vestibular nucleus then sends signals to the oculomotor, trochlear and abducens nuclei that control eye movements and the thalamus, spinal cord and cerebellum. The cerebellum is responsible for coordinating movement throughout the body. Therefore, the vestibular signals help the central nervous system coordinate eye movements and other movements throughout the body.

60
Q

Outline the four most common causes of peripheral (vestibular) vertigo

A
  • Benign paroxysmal positional vertigo (BPPV): caused by calcium carbonate crystals (otoconia) that become displaced into the semicircular canals and disrupt the vestibular system function. The attacks of vertigo are triggered by movement and last around one minute. The Dix-Hallpike manoeuvre diagnoses BPPV.
  • Ménière’s disease: caused bye excessive build up of endolymph in the semicircular canals, disrupting the sensory signals. It causes attacks of tinnitus, hearing loss, vertigo and feeling of fullness in the ear. Not associated with movement. Spontaneous nystagmus during attacks.
  • Vestibular neuronitis: inflammation of vestibular nerve, due to a viral infection.
  • Labyrinthitis: inflammation of labyrinthitis, due to a viral infection. Can also cause hearing loss.
61
Q

Name 2 other causes of peripheral vertigo

A
  • Trauma to vestibular nerve.
  • Acoustic neuromas.
62
Q

Outline the four most common causes of central (cerebellum or brainstem) vertigo

A
  • Posterior circulation stroke: sudden onset and may be associated with ataxia, diplopia, cranial nerve defects or limb symptoms.
  • Tumour: gradual onset with associated symptoms of cerebellar or brainstem dysfunction.
  • Multiple sclerosis: relapsing and remitting symptoms, associated with optic neuritis or transverse myelitis.
  • Vestibular migraine: last mins-hours, often associated with visual aura and headache.
63
Q

What questions would you ask a patient with dizziness?

A
  • Vertigo (room is spinning) or lightheadedness (feeling faint)?
  • Onset: sudden (peripheral) or gradual (central - executive stroke),
  • Duration: short (peripheral) or persistent (central).
  • Hearing loss or tinnitus: present (peripheral - except BPPV) or absent (central).
  • Coordination: intact (peripheral) or impaired (central).
  • Nausea: severe (peripheral) or mild (central).
  • Recent viral illness (labyrinthitis or vestibular neuronitis).
  • Headache (vestibular migraine, cerebrovascular accident or brain tumour).
  • Typical triggers (vestibular migraine).
  • Ear symptoms, such as pain or discharge (infection).
  • Acute onset neurological symptoms (stroke).
64
Q

How would you examine a patient with vertigo?

A
  • Ear examination: look for signs of infection or other pathology.
  • Neurological examination: assess for central causes of vertigo.
  • CV examination: assess for cardiac causes of dizziness (e.g. arrhythmias or valve disease).
  • Special tests: Romberg’s test (screens for problems with proprioception or vestibular function), Dix-Hallpike manoeuvre (to diagnose BPPV) and HINTS examination (to distinguish between central and peripheral vertigo).
65
Q

Outline the HINTS examination

A
  • HI – Head Impulse test: diagnose peripheral causes of vertigo (eyes will saccade), but test will be normal if the patient has no current symptoms or a central cause of vertigo.
    N – Nystagmus: demonstrated by having the patient look left and right, the eyes will then rapidly saccade or oscillate. Unilateral horizontal nystagmus is more likely to be a peripheral cause. Bilateral or vertical nystagmus suggests a central cause.
    TS – Test of Skew: if there is a vertical correction when an eye is uncovered, this indicates a central cause of vertigo.
66
Q

Management of central vertigo

A

Further investigation with CT or MRI to establish cause.

67
Q

Management of peripheral vertigo

A
  • Short-term symptom relief: prochlorperazine or antihistamines (e.g., cyclizine, cinnarizine and promethazine).
  • Betahistine - Ménière’s disease.
  • Epley manoeuvre - BPPV.
  • Avoid triggers, lifestyle changes, triptans (acute symptoms) and propranolol, topiramate or amitriptyline (prophylactic) - vestibular migraine.
  • Inform DVLA.
68
Q

Describe the pathophysiology of BPPV

A
  • Calcium carbonate crystals (otoconia) become displaced in the semicircular canals causing abnormal motion of the endolymph and the feeling of vertigo.
  • Attacks are triggered by head movement.
69
Q

What are the symptoms of BPPV?

A
  • Short episodes of positional vertigo typically lasting < 1 minute.
  • Triggered by head movements or positional changes, e.g. turning over in bed.
  • Hearing loss and tinnitus are NOT associated.
70
Q

How is BPPV diagnosed?

A

The Dix-Hallpike manoeuvre:

  • The patient sits upright on a flat examination couch with their head turned 45 degrees to one side (turned to the right to test the right ear and left to test the left ear).
  • Support the patient’s head to stay in the 45 degree position while rapidly lowering the patient backwards until their head is hanging off the end of the couch, extended 20-30 degrees.
  • Hold the patient’s head still, turned 45 degrees to one side and extended 20-30 degrees below the level of the couch.
  • Watch the eyes closely for 30-60 seconds, looking for nystagmus.
  • Repeat the test with the head turned 45 degrees in the other direction.

In patients with BPPV, the Dix-Hallpike manoeuvre will trigger rotational nystagmus and symptoms of vertigo.

71
Q

How is BPPV treated?

A

The Epley manoeuvre:

  • Follow the steps of the Dix-Hallpike manoeuvre, having the patient go from an upright position with their head rotated 45 degrees (to the affected side) down to a lying position with their head extended off the end of the bed, still rotated 45 degrees.
  • Rotate the patient’s head 90 degrees past the central position.
  • Have the patient roll onto their side so their head rotates a further 90 degrees in the same direction.
  • Have the patient sit up sideways with the legs off the side of the couch.
  • Position the head in the central position with the neck flexed 45 degrees, with the chin towards the chest.
  • At each stage, support the patient’s head in place for 30 seconds and wait for any nystagmus or dizziness to settle.
72
Q

Describe the function of the semicircular canals and otolith organs

A
  • The semicircular canals detect rotation of the head.
  • The otolith organs detect gravity and linear acceleration.
73
Q

Describe the features of vestibular neuronitis

A
  • Recent viral URTI.
  • Acute onset vertigo.
  • N+V.
  • Balance problems.
  • NO hearing loss.
74
Q

Management of vestibular neuronitis?

A
  • Prochlorperazine
  • Antihistamines (e.g. cyclizine, cinnarizine and promethazine)
75
Q

Which condition may occur following vestibular neuronitis?

A

BPPV

76
Q

Define labyrinthitis

A

Inflammation of the bony labyrinth of the inner ear, including the semicircular canals, vestibule and cochlea, due to viral URTI.

77
Q

How can bacterial labyrinthitis occur?

A

Secondary to otitis media or meningitis (rare - mostly viral).

78
Q

Describe the presentation of labyrinthitis

A
  • Acute onset vertigo
  • Hearing loss
  • Tinnitus
79
Q

Outline the management of labyrinthitis

A
  • Short-term (3 days) of anti-emetics: Prochlorperazine or Antihistamines.
  • Antibiotics for bacterial labyrinthitis.
80
Q

What is a key complication of meningitis?

A

Hearing loss

81
Q

Describe the typical triad of symptoms in Ménière’s disease

A
  • Hearing loss
  • Vertigo
  • Tinnitus

(+ feeling of fullness in the ear)

82
Q

Outline the pathophysiology of Ménière’s disease

A

Excessive buildup of endolymph in the labyrinth of the inner ear (endolymphatic hydrops), disrupting the sensory signals.

83
Q

Describe the typical presentation of Ménière’s disease

A

40-50 year old presenting with unilateral episodes of vertigo (episodic attacks, NOT triggered by movement), hearing loss (sensorineural, affecting low frequencies), and tinnitus. Spontaneous nystagmus may be seen during an acute attack. This is usually in one direction (unidirectional).

84
Q

Outline the management of Ménière’s disease

A
  • Acute attacks: prochlorperazine and antihistamines.
  • Prophylaxis: betahistine (histamine analogue - improves circulation of the inner ear).
85
Q

What is the other name for an acoustic neuroma?

A

Vestibular schwannoma

86
Q

What is an acoustic neuroma?

A

A benign tumour of the Schwann cells surrounding the auditory nerve (vestibulocochlear nerve).

87
Q

In what part of the brain do acoustic neuromas occur?

A

At the cerebellopontine angle

88
Q

Unilateral vs bilateral acoustic neuromas

A
  • Acoustic neuromas are usually unilateral.
  • Bilateral acoustic neuromas are associated with neurofibromatosis type II.
89
Q

Describe the typical presentation of an acoustic neuroma

A

40-60 year old presenting with a gradual onset of:

  • Unilateral sensorineural hearing loss (often the first symptom).
  • Unilateral tinnitus.
  • Dizziness or imbalance.
  • A sensation of fullness in the ear.

They can also be associated with a facial nerve palsy (LMN - no forehead sparing).

90
Q

Investigations for an acoustic neuroma

A
  • Audiometry
  • Brain MRI
91
Q

What are the management options for an acoustic neuroma?

A
  • Conservative if no symptoms or treatment inappropriate.
  • Surgical removal (risks: vestibulocochlear or facial nerve injury).
  • Radiotherapy to reduce growth.
92
Q

Define cholesteatoma

A

An abnormal collection of squamous epithelial cells in the middle ear.

93
Q

Describe the typical presenting symptoms of a cholesteatoma

A
  • Foul discharge from the ear (recurrent infections).
  • Unilateral conductive hearing loss.
  • White debris on upper tympanic membrane (otoscopy).
94
Q

Outline the management plan for a cholesteatoma

A
  • CT head to confirm diagnosis.
  • Surgical removal.
95
Q

Where does epistaxis usually originate from?

A

Kiesselbach’s plexus, located in Little’s area.

96
Q

List the triggers for epistaxis

A
  • Nose picking (common)
  • Colds
  • Sinusitis
  • Vigorous nose-blowing
  • Trauma
  • Changes in the weather
  • Coagulation disorders (e.g. thrombocytopenia or Von Willebrand disease)
  • Anticoagulant medication (e.g. aspirin, DOACs or warfarin)
  • Snorting cocaine
  • Tumours (e.g. squamous cell carcinoma)
97
Q

Is epistaxis usually unilateral or bilateral?

A

Unilateral.

However, bilateral bleeding may indicate bleeding posteriorly, which presents a greater risk of blood aspiration.

98
Q

How would you advise patients on how to manage a nosebleed?

A
  • Sit up and tilt the head forwards (tilting the head backwards is not advised as blood will flow towards the airway).
  • Squeeze the soft part of the nostrils together for 10-15 minutes.
  • Spit out any blood in the mouth, rather than swallowing.
99
Q

Outline the management for severe epistaxis

A
  • Nasal packing using nasal tampons or inflatable packs.
  • Nasal cautery using silver nitrate sticks (first line)
100
Q

What would you prescribe after treating an acute nosebleed?

A
  • Naseptin nasal cream (chlorhexidine and neomycin) four times daily for 10 days to reduce any crusting, inflammation and infection.
  • This is contraindicated in peanut or soya allergy.
101
Q

Which major arteries supply the nose?

A

Internal and external carotid arteries.

102
Q

Define sinusitis and rhinosinusitis

A
  • Sinusitis: inflammation of the paranasal sinuses.
  • Rhinosinusitis: inflammation of sinuses and the nasal cavity.

Acute < 12 weeks; chronic > 12 weeks.

103
Q

What are the sinuses function?

A

Secrete mucus to protect against infection and humidify air.

104
Q

Name the 4 paranasal sinuses

A
  • Frontal
  • Maxillary
  • Ethmoid
  • Sphenoid
105
Q

What can causes inflammation of the sinuses?

A
  • Infection, particularly following viral URTI.
  • Allergies, such as hayfever (allergic rhinitis).
  • Obstruction of drainage e.g. due to a foreign body, trauma or polyps.
  • Smoking.
106
Q

Describe the presentation of acute sinusitis

A
  • Recent viral URTI.
  • Nasal congestion and discharge.
  • Facial pain or headache.
  • Facial pressure worse on bending forward.
  • Facial swelling over sinuses.
  • Loss of smell.
  • O/E: tenderness to palpation of affected areas, inflammation of nasal mucosa, fever.
107
Q

Chronic sinusitis may be associated with …

A

Nasal polyps

108
Q

Investigations for persistent sinusitis

A
  • Nasal endoscopy
  • CT sinuses
109
Q

Outline the management of acute sinusitis

A
  • Most cases resolve within 2-3 weeks (viral), therefore do not offer antibiotics to patients with symptoms for up to 10 days.
  • If symptoms don’t improve after 10 days: high dose steroid nasal spray (mometasone) for 2 weeks, delayed antibiotic prescription (phenoxymethylpenicillin).
110
Q

Outline the management options for chronic sinusitis

A
  • Saline nasal irrigation
  • Steroid nasal sprays or drops (e.g., mometasone or fluticasone)
  • Functional endoscopic sinus surgery (FESS)
111
Q

Describe the nasal spray technique

A
  • Tilting the head slightly forward.
  • Using the left hand to spray into the right nostril, and vice versa (this directs the spray slightly away from the septum).
  • NOT sniffing hard during the spray.
  • Very gently inhaling through the nose after the spray.
112
Q

What is the medical term for hayfever?

A

Allergic rhinitis

113
Q

What is the pathophysiology of allergic rhinitis?

A

IgE-mediated inflammation of the nasal mucosa.

114
Q

List the triggers for allergic rhinitis

A

Grass, tree pollen, house dust mites.

115
Q

Describe the common presentation of allergic rhinitis

A

Sneezing, runny nose (rhinorrhoea), nasal obstruction, itching, and cough.

116
Q

Outline the management of allergic rhinitis

A
  • Intranasal antihistamines (e.g. azelastine).
  • Oral antihistamines: sedating (e.g. chlorphenamine) or non-sedating (loratadine, cetirizine).
  • Intranasal sodium cromoglicate (inhibits mast cell degranulation).
  • Intranasal corticosteroids (e.g. mometasone furoate, beclometasone, fluticasone).
117
Q

Acute-phase vs late-phase response in allergic rhinitis

A

Acute: sneezing and increase in nasal secretion follows shortly afterwards.
Late: characterised by nasal obstruction.

118
Q

What is the first-line treatment for allergic rhinitis?

A

Nasal antihistamine - azelastine.

119
Q

What further treatment can be used for allergic rhinitis?

A
  • For sneezing: oral antihistamine.
  • For nasal blockage: intranasal corticosteroid.
  • Sodium cromoglicate can be used as an alternative or add on treatment.
120
Q

What is the MOA of azelastine?

A

H1 receptor antagonist - blocks the effect of histamine, therefore preventing itching, vasodilation, mucus secretion and bronchoconstriction.

121
Q

Which drug does azelastine interact with?

A

MOA inhibitors

122
Q

What are the indications for cetirizine?

A

Urticaria, dermatitis, allergic rhinitis

123
Q

What is the MOA of Fluticasone?

A

Corticosteroid - inhibits mast cells, eosinophils and basophils - anti-inflammatory effect.

124
Q

List the potential side effects from fluticasone

A
  • Raised IOP
  • Headache
  • Nasal septal perforation
  • Nasal irritation
  • Throat irritation/taste disturbance
  • Hypersensitivity reactions/bronchospasm
  • Psychological effects in children
125
Q

What is the MOA of sodium cromoglicate?

A

Mast cell stabiliser, inhibiting mast cell degranulation.

126
Q

Why are unilateral nasal polyps a red flag?

A

They are concerning for malignancy and require a specialist referral for assessment.

127
Q

Describe the management of nasal polyps

A
  • Medical: intranasal topical steroid drops or spray.
  • Surgical: intranasal polypectomy or endoscopic nasal polypectomy.
128
Q

What is the most common cause of tonsillitis?

A

Viral

129
Q

What is the most common cause of bacterial tonsillitis?

A

Group A streptococcus (Streptococcus pyogenes)

130
Q

Which tonsils are typically enlarged in tonsillitis?

A

Palatine tonsils

131
Q

Describe the typical presentation of tonsillitis

A
  • Sore throat
  • Fever (>38°C)
  • Pain on swallowing
132
Q

What is the purpose of the centor criteria?

A

It is used to estimate the probability that tonsillitis is due to bacterial infection and will benefit from antibiotics.

133
Q

Outline the centor criteria

A
  • Fever >38ºC
  • Tonsillar exudates
  • Absence of cough
  • Tender anterior cervical lymph nodes (lymphadenopathy)

Score >=3 gives a 40-60 % probability of bacterial tonsillitis.

134
Q

Outline the management of tonsillitis

A
  • Viral: safety net to return if pain hasn’t settled after 3 days or fever rises, simple analgesia for pain and fever, fluids, delayed prescription.
  • Bacterial: Penicillin V (phenoxymethylpenicillin) for a 10-day course (first-line) or Clarithromycin (penicillin allergy).
135
Q

List the complications of tonsillitis

A
  • Peritonsillar abscess (quinsy)
  • Otitis media
  • Scarlet fever
  • Rheumatic fever
  • Post-streptococcal glomerulonephritis
  • Post-streptococcal reactive arthritis
136
Q

What is the criteria for NHS funded tonsillectomy?

A
  • Malignancy is suspected.
  • > 1 episode of quinsy or airway obstruction.
  • Recurrent sore throat with disabling episodes preventing normal function, due to tonsillitis (>=7 episodes in the last year or 5 in each of the last two years or 3 in each of the preceding three years).
  • Obstructive sleep apnea.
137
Q

What is quinsy?

A

Peritonsillar abscess due to bacterial infection with trapped pus and is a complication of untreated tonsillitis.

138
Q

What additional symptoms might you expect with quinsy compared to tonsillitis?

A
  • Trismus (unable to open their mouth).
  • Change in voice due to the pharyngeal swelling - a “hot potato voice”.
  • Swelling and erythema in the area beside the tonsils.
139
Q

Outline the management of quinsy

A
  • ENT referral for needle aspiration or incision and drainage.
  • Broad spectrum antibiotics e.g. co-amoxiclav.
  • Dexamethasone.
140
Q

What is the main significant complication of a tonsillectomy?

A

Post-tonsillectomy bleeding - managed with hydrogen peroxide gargle, adrenaline swabs or surgery.

141
Q

What are the features of a pharyngeal pouch?

A
  • Dysphagia.
  • Regurgitation.
  • Halitosis.
  • Globus.
  • Weight loss.
  • Hoarseness.
  • Chronic cough.
142
Q

What is the gold standard investigation for a pharyngeal pouch?

A

Barium swallow

143
Q

What is the management for a pharyngeal pouch?

A
  • Asymptomatic or small pouches (i.e. < 1cm): no specific treatment.
  • Symptomatic or larger pouches: surgery or endoscopy.
144
Q

Name one complication from a pharyngeal pouch

A

Aspiration pneumonia

Child Health (9 decks)

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