PLAB 1 Short Notes ENT

  • Otitis Externa 

Aetiology & Pathology

Acute inflammation of the skin of the meatus

Anaerobes such as pseudomonas


Minimal discharge


Ear pain 

Tragal tenderness 

Topical gentamicin or Topical gentamicin with hydrocortisone. Both are correct. An example is which contains both gentamicin and hydrocortisone appropriate for most bacteria including anaerobes such as pseudomonas which commonly affect the external ear.


Topical gentamicin ( Aminoglycoside)

Topical gentamicin with hydrocortisone ( Gentisone-HC) – effective against anaerobes( pseudomonas)

Acetic acid 2% 1 spray tds for 7 days as (first line – Public Health England)

Neomycin sulphate with corticosteroid 3 drops tds for 7-14 days as (second line-  Public Health England

Combinations of topical acetic acid, topical aminoglycoside ( Gentamycin) topical corticosteroids

Otitis externa + suspected tympanic membrane perforation- ciprofloxacin drops(not currently licensed)

        (Aminoglycosides ear drops are ototoxic)

  • Malignant ottitis externa

Aeriology & Pathology

An aggressive infection rather than a malignancy, or cancer

Infection can spread to the outer ear and surrounding tissue, including the bones of the jaw and face

Risk factors  – Diabetes / Immune deficiency 


It is rare.

Conductive hearing loss 

foul-smelling purulent otorrhoea

Without treatment, malignant otitis externa can be fatal with a 50% mortality rate.


Need an urgent referral to ENT.

  • Furuncle in ear canal (boils)

Aetiology & Pathology

Infected hair follicle. 

Staphylococcus aureus is the most common cause.

Diabetics/immunosuppressive drugs  predisposed to furuncles

It may be  a complication of otitis externa.


It is seen as an abscess of skin overlying the ear canal cartilage. 

Furuncles are typically  hard, tender, red nodules surrounding a hair follicle 

Enlarges over a few days.


Most furuncles in the ear canal resolve spontaneously 

 Some require flucloxicillin. 

Only very few of the furuncles grow larger require incision and drainage.

  • Foreign body in ear 

Magnetic material – Removed by a magnet

Insect – 2% lidocaine -> Olive oil

Uncooperative child – Remova under General Anesthesia 

Ear wax – Olive oil 

Adhesive- Removed manually within 1-2 days once desquamation has occurred

Seeds/ organic matter/ soft objects – Suction with a small catheter

                     Irrigation with water is contra-indicated 

                    (May swell and increase the level of pain and difficulty to remove if exposed to water).

Referral to an ENT specialist if

  • If the patient requires sedation
  • If there is any difficulty in removing the foreign body
  • If the patient is unco-operative.
  • If the tympanic membrane has been perforated.
  • If an adhesive is in contact with the tympanic membrane.
  • Batteries that are stuck in the auditory canal. ( need to be taken out within 24 hours.)
  • Insect in ear 

2% lidocaine

Insects should be killed prior to removal, using 2% lidocaine.

Olive oil can also be used to float the insect out by pouring olive oil into the ear.

  • Seed/ organic matter in ear 

Suction with a small catheter

  • Ear wax

Ear wax softening drops are the first thing to try for a buildup of earwax. 

Sodium bicarbonate 5%, sodium chloride 0.9%, olive oil, or almond oil drops can be used

Prescribe ear drops for 3–5 days initially, to soften wax and aid removal. 

If symptoms persist, consider ear irrigation

If irrigation is unsuccessful, there are three options:

• Advise the person to use ear drops for a further 3–5 days and then return for further irrigation.

• Instill water into the ear. After 15 minutes irrigate the ear again.

• Refer to an Ear Nose and Throat specialist for removal of wax.

NICE CKS have not recommended irrigation without prior use of a softening agent

     Extra force may be needed which is more likely to cause trauma.

Advise people against inserting anything in the ear. Cotton buds, matchsticks, and hair pins can cause the wax to become impacted by pushing it further into the canal.

  • Ear drum perforation


Temporary conductive hearing loss



Discharge of blood or mucus or both from the ear. 

Nausea and vomiting may also occur. 


Examination with otoscopy


Most small perforations heal on their own 

Larger perforations may need a referral to an ENT specialist.

  • Tympanosclerosis


Has characteristic chalky white patches seen on inspection of the eardrum. 

If eardrum is viewed as normal, it is unlikely to be tympanosclerosis.

  • Rinne’s and Weber’s test

Performing both Rinne’s and Weber’s test allows differentiation of conductive and sensorineural deafness.

Rinne’s test

A tuning fork is placed over the mastoid process until the sound is no longer heard, followed by repositioning just over external acoustic meatus

• Note that air conduction (AC) is normally better than bone conduction (BC) (Positive Rinne’s test)

• If BC > AC, then the patient has conductive deafness (Negative Rinne’s test)

• (Abnormal Rinne’s test)

Note that the words positive and negative are used in a somewhat confusing fashion here, as compared to their normal use in medical tests. 

Positive or negative in this case means that a certain parameter that was evaluated was present or not.

Thus, a “positive” result indicates the healthy state, in contrast to many other medical tests. 

Therefore, some prefer to avoid using the term ‘positive’ or ‘negative’, and simply state if the test was normal or abnormal 

e.g. ‘Rinne’s test was abnormal in the right ear, with bone conduction greater than air conduction’.

Weber’s test

A tuning fork is placed in the middle of the forehead equidistant from the patient’s ears. 

The patient is then asked which side is loudest

• If sound is localized to the unaffected side, then this is unilateral sensorineural deafness

• If sound is localized to the affected side, then this is unilateral conductive deafness


If Weber’s test localises to the right side. It can either be right conductive deafness OR left sensorineural deafness. 

A Rinne’s test would be able to confirm if it is a right conductive deafness.

  • Otosclerosis

Aetiology & Pathology

Pathological increased bony turnover

This leads to sclerosis and failure of the sound conduction mechanism. 

This is due to ankylosis of the stapes footplate in the fenestra ovalis of the cochlea. 

This reduces normal sound transmission resulting in a conductive deafness.

Female gender – otosclerosis usually occurs in females (2:1 female:male ratio)

Pregnancy – pregnancy accelerates the progression of osteosclerosis

Genetic factors are involved, so the condition often (but not always) runs in families. 

The family history is especially important to note as it is commonly given in the stem if the question writers want you to pick otosclerosis.


Otosclerosis is the commonest cause of progressive deafness in young adults.

 It usually presents between 15 and 45 years of age.

Key features for otosclerosis:

Main symptoms are progressive hearing loss and tinnitus

Majority of the time it is bilateral

Conductive hearing loss (where the cochlea is involved there may be a mixed conductive/sensory pattern of hearing loss)

               Better hearing when in noisy environments

A family history of hearing loss

It is bilateral in 80% of cases, although it is not uncommon for one ear to be worse than the other.

Untreated, the deafness gradually worsens. Other symptoms of otosclerosis include tinnitus and vertigo


Flamingo pink tympanic membrane ( Schwartz sign)


There is no curative treatment at the moment. 

The management involves either surgery (stapedectomy or stapedotomy, with the insertin of a prosthesis) or bilateral hearing aids for those not fit for surgery.

  • Acute otitis media

Aetiology and Pathology

Acute otitis media is acute inflammation of the middle ear and may be caused by bacteria or viruses.

The most common bacterial pathogens are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis and Streptococcus pyogenes of which amoxicillin would be suitable. 

The most common viral pathogens are respiratory syncytial virus (RSV) and rhinovirus.



• Rapid onset of pain (younger children may pull at the ear)

• Fever

• Irritability

• Coryza

• Vomiting

• Often after a viral upper respiratory infection

• A red, yellow or cloudy tympanic membrane or bulging of the tympanic membrane.

• An air-fluid level behind the tympanic membrane

    Discharge in the auditory canal secondary to perforation of the tympanic membrane

• Perforation of the eardrum often relieves pain. This is because bulging of the tympanic membrane causes the pain.


The diagnosis can be seen with otoscopy

Tympanic membrane is Red /bulging ( Light reflex is lost) /cartwheel appearance of vessels

   (light reflex/cone of light)=cone shaped reflection in anterior inferior quadrant of tympanic membrane. 

    The absence of the light reflex occurs when there is a distortion of the shape of the tympanic      

     Eg- bulging membrane due to an increase of inner ear pressure seen in otitis media.


 Usually conservative as aetiology is usually viral

• If bacterial aetiology is suspected, prescribe oral amoxicillin ( 5 days)

children who are allergic to penicillin, prescribe a five-day course of erythromycin or clarithromycin. 

  • Otitis media with effusion ( Glue ear)

Aetiology & Pathology

An important risk factor for otitis media with effusion is parental smoking.


Otitis media with effusion (Also known as glue ear)  is common with the majority of children having at least one episode during childhood

• Hearing loss is usually the presenting feature 

(glue ear is the commonest cause of conductive hearing loss in childhood). 

May present a Listening to the TV at excessively high volumes 

Needing things to be repeated.

Lack of concentration, withdrawal especially in school

• Secondary problems – speech & language delay, behavioural/ balance problems may also be seen

• Rarely complains of ear pain

• May have prior history of infections (especially upper respiratory tract) or oversized adenoids


• Retracted or bulging drum. It can look dull, grey, or yellow. 

There may be bubbles or a fluid level


Audiograms: conductive defects.( mild conductive hearing loss.)

Tympanogram would show a hearing loss between 20 to 40 dB.

• Impedance audiometry: flat tympanogram


Tell parents to stop smoking

• Observation first because may resolve, monitor every 3 months

if a scenario is given with a recent diagnosis of otitis media with effusion, and the question is asking for the SINGLE best management → “Reassure and review in 3 months” would be the best choice.

• Surgery: If persistent bilateral OME over 3 months → insert grommets

• Hearing aids: Reserve for persistent bilateral OME and hearing loss if surgery is not accepted.

  • Acquired cholesteatoma

Aetiology & Pathology

Occurs following repeated ear infections 

Destructive expanding growth consisting of keratinising squamous epithelium in the middle ear and/or mastoid process

An  abnormal collection of skin cells inside your ear that left untreated can continue to grow and damage the bones of the middle ear (ossicles)

cholesteatoma is a misnomer as it is actually neither cholesterol nor a tumour


Small lesions are associated with a progressive conductive hearing loss 

As the lesion grows and erodes into adjacent structures, there may be additional features such as vertigo, headache and facial nerve palsy

Frequent painless otorrhoea which may be foul-smelling

• Progressive, unilateral conductive hearing loss

• Tympanic membrane perforation is seen in around 90% of cases or retracted tympanum


Signs on otoscopic exam:

A retraction pocket in attic or posterosuperior quadrant of tympanic membrane

Granular tissue

White mass behind the eardrum

Purulent drainage

in 90% of cases of acquired cholesteatoma, the tympanic membrane is perforated.


usually poorly responsive to antibiotic treatment

  • Congenital cholesteatoma

Perforation is seen less commonly with congenital cholesteatoma 

There is often no history of recurrent suppurative ear disease unlike acquired cholesteatoma.


• Presents in childhood (6 months to 5 years) but may occasionally present much later, in adulthood

• Often no history of recurrent suppurative ear disease, previous ear surgery or tympanic membrane perforation

• May be an incidental finding on routine otoscopy of an asymptomatic child


• Seen as a pearly white mass behind an intact tympanic membrane

• Signs on otoscopic exam:

Spherical white mass behind intact membrane

  • Noise-induced hearing loss (NIHL) 

If at working place ( occupational hearing loss. )

Aetiology and Pathology

Loud noise ( at work place) force leads to cellular metabolic overload, and damage to hair cells in the inner ear


Bilateral hearing impairment( high-frequency sensorineural hearing loss. )


Should be referred to an audiologist who would be able to confirm a sensorineural hearing loss and provide hearing aids.

  • Presbycusis 
  • Vestibular Neuritis 


Vestibular neuritis follows a viral infection

Pathology is vestibular neuropathy ( not inflammation of the vestibular nerve)


Onset is usually very abrupt 

Recurrent vertigo attacks lasting hours or days (feel as if the room is rotating)

Unsteadiness, nausea and vomiting

Moving the head aggravates symptoms

There is no hearing loss with vestibular neuritis.

(Labyrinthitis is similar but ,with hearing symptoms (sensory  hearing loss or tinnitus). 

  • Labyrinthitis


Inflammation of both  vestibular nerve and the labyrinth.


Vertigo and nystagmus 

Hearing loss and tinnitus ( not a feature of vestibular neuritis.)

  • Presbyacusis (Age-related sensorineural hearing loss)

Aetiology & Pathology

Degenerative changes in the inner ear.


Usually occurs after age 50

Loss of ability to hear high-frequency sounds. 


Difficulty understanding speech, especially in noisy environments ( Speech has two components: vowels         

        which are low-frequencies and consonants which are high-frequencies. When the high-frequency

          sounds are lost, consonants are lost, which results in difficulty in understanding speech)

Usually brought in by the family to clinics as the patient woiuld not think his/her hearing is impaired

    (Don’t shout, I’m not deaf!’ is a common phrase used by elderly patients suffering from presbyacusis)

Shouting words to them would only increase the low-frequency sounds and not the high-frequency sounds.


Using hearing aids that increase the high-frequency sound. 

In the UK, the NHS uses bilateral digital hearing aids.

  • Meniere’s disease.


20-60 years old

Female more affected than  male 




Increased feeling of pressure in the ear.

Vertigo is usually the prominent symptom

Episodes last minutes to hours

Typically symptoms are unilateral

But bilateral symptoms may develop after a number of years


MRI is normal


Nausea and vertigo in menniers disease is relieved by





Acute attacks: buccal or intramuscular prochlorperazine

                            Admission is sometimes required

  • Acoustic Neuroma ( Vestibular schwannomas)

Aetiology & Pathology


It causes problems by having local pressure and behaving as a space-occupying lesion.


5% of intracranial tumours are schwannomas

90 % of cerebellopontine angle tumours are schwannomas 

Symptoms are caused by Involvement of cranial nerve

Cranial nerve 5: absent corneal reflex

Cranial Nerve 6 – 

Cranial nerve 7: facial palsy

Cranial Nerve 8 – hearing loss (sensorineural deafness), vertigo, tinnitus

Bilateral acoustic neuromas are seen in neurofibromatosis type 2


• MRI of the cerebellopontine angle is the investigation of choice.


  • Benign paroxysmal positional vertigo ( BPPV)


Characterised by the sudden onset of dizziness and vertigo triggered by changes in head position.

• Vertigo usually occurs on turning over in bed or lying down (basically any acceleration of the head)

(the room spinning around patient)

• Each episode typically lasts 10-20 seconds but can last a few minutes

• Nausea during episodes


• Hallpike’s Manoeuvre positive

  • A Dix-Hallpike test would help provide the diagnosis> The Dix-Hallpike manoeuvre would be positive if the patient reports reproductin of vertigo and nystagmus is seen.

Whilst standing and lying blood pressure is also important in clinical practice to perform to exclude orthostatic hypotension


• Mostly spontaneous resolution with exacerbations

• Epley’s manoeuvre

A repositioning technique used to reposition otoliths back into the utricles from the posterior semicircular canals

Hearing Assessment in children 

Hearing screening is offered to all babies in England within 4 to 5 weeks of birth. 

Babies who were born in hospital are given a newborn hearing test before they are discharged otherwise it would be done in the first few weeks of life by a health visitor.

The hearing screening programme offers 2 types of test:

• Automated otoacoustic emission (AOAE)

• Automated auditory brainstem response

Automated otoacoustic emission (AOAE) test takes a few minutes

A soft-tipped earpiece is placed in the newborn’s ear and clicking sounds are played. 

Vibration of the hair cells in response to noise generates acoustic energy which is detected by a microphone in the external meatus. 

If AOAE test is performed and there is no clear response in one or both eares, then the automated auditory brainstem response (AABR) test is performed.

The AABR test involves placing 3 electrodes on the infant’s forehead and neck. 

Clicking sounds are then played. 

The electrodes would measure brain wave activity in response to the clicks.

Given that AOAE test is not even an option in this question, the next most appropriate answer would be the AABR test. 

AABR also has the benefit of detecting auditory neuropathy in children who are deaf but have normal otoacoustic emissions (i.e. in those who have a normal cochlea).

The Newborn Hearing Screening Programme was introduced in the UK in the early 2000’s

Even if a newborn passes this test, they could still develop hearing loss later on in their development.

 Hearing loss could be ‘missed’ during assessment due to the subjective nature of the test.

If baby’s motor and verbal milestones are normal, the next best step would be to refer this child for a hearing assessment.

Symptoms of hearing loss include, but are not limited to:

• Inattentive, not reacting when called

• Talking too loudly, listening to TV at high volume

• Unsettled at school

When should we refer for a hearing assessment?

• Any parental or professional concern

• Bacterial meningitis

• Temporal bone fracture

• Severe unconjugated hyperbilirubinaemia

• Children with delayed speech and language milestones.

Any parents who express concerns about hearing despite previous screening should always be referred for a hearing assessment.

Hearing tests in the children:

• < 6 months

o Otoacoustic emissions (OAE):

▪ Vibration of the hair cells in response to noise generates acoustic energy which is detected by a microphone in the external meatus.

o Audiological brainstem responses (ABR):

The ears are covered with earphones that emit a series of soft clicks. Electrodes on the infant’s forehead and neck measure brain wave activity in response to the clicks.

• 6-18 months:

o Distraction testing:

▪ As the child sits on parent’s lap, an assistant in front attracts the child’s attention while a tester attempts to distract by making noises behind and beside child, eg with a rattle, conversational voice.

• 2-4 years:

o Conditioned response audiometry:

▪ The child is trained to put pegs into holes or give toys to a parent on a particular auditory cue.

o Speech discrimination:

▪ The child touches selected objects cued by acoustically similar phrases, eg key/tree.

• 5 years:

o Pure tone audiogram

▪ Each ear is tested individually. The child presses a button when he hears a tone.

  • Nasal Polyps

Aetiology & Pathology

• Lesions arising from the nasal mucosa, occurring at any site in the nasal cavity or paranasal sinuses.


Nasal obstruction

• Rhinorrhoea

• Anosmia (loss of smell

Note that nasal polyps tend to be bilateral.

Associated with  Asthma & Aspirin sensitivity

Samter’s triad- Nasal polyps + Asthma + Aspirin sensitivity 

  • Nasopharyngeal carcinoma


Smoking and alcohol can increase the risk of nasopharyngeal carcinoma

Infection with the Epstein-Barr virus.


The first symptom of nasopharyngeal carcinoma is often a painless swelling or lump in the upper neck. This is often due to a swollen lymph node. 

Other symptoms include nasal obstruction, epistaxis and otitis media from eustachian tube obstruction. Hearing loss (conductive deafness) in one ear and tinnitus are also symptoms seen in nasopharyngeal carcinoma.

  • Paranasal sinus carcinoma

Paranasal sinus tumours (maxillary, ethmoid, frontal, sphenoid) are commonly welldifferentiated squamous cell carcinoma. 

They present with signs and symptoms similar to this stem which include with local swelling, pain, and ocular symptoms if the orbit is involved.

 Pain particularly in the upper cheek, nasal obstruction, blood in nasal discharge point towards a likely diagnosis of paranasal sinus carcinoma.

  • Sinusitis 

Aetiology & Pathology

Caused by inflammation of the membranous lining of  sinuses.

It happens when there is a build-up of pressure inside the sinuses and the small opening from the sinuses to the nose becomes blocked. 

The pressure builds up and causes pain behind the face and head. 

Upper respiratory tract infections are one of the predisposing factors


Headache that worsens on bending his head forward

     ( There are two types of headaches which can worsen on bending. Sinus headaches and migraines). Sinusiti is not associated with nausea/ vomiting. 

      (Migraines are often accompanied by nausea, vomiting and sensitivity to light).

Pain is a dull, throbbing pain 

  In the upper face especially in the area of the cheeks (maxillary sinus)

  Bridge of the nose (ethmoid sinus)

  Above the eyes (frontal sinus). 

It is usually on one side and tends to be worse first thing in the morning. 

The pain may get worse when you move your head, strain or bend forward. 

It is usually accompanied by a stuffy nose. 

Examination of the facial area may reveal local tenderness, redness, swelling, and the presence of clear or discolored nasal discharge.

  • Maxillary sinusitis 

Aetiology & Pathology

The maxillary sinus is innervated by the infraorbital nerve and anterior, middle and posterior superior alveolar nerves. 

Hence, pathology here may be felt as referred pain and described as upper jaw pain, toothache or pain directly at the skin of the cheek.

Caused by inflammation of the membranous lining of  sinuses.

It happens when there is a build-up of pressure inside the sinuses and the small opening from the sinuses to the nose becomes blocked. 

The pressure builds up and causes pain behind the face and head. 

Upper respiratory tract infections are one of the predisposing factors


Tenderness at the anterior wall below the inferior orbital margin can be found in maxillary sinusitis.

  • Epistaxis


If haemodynamically compromised

• Arrange immediate transfer to A and E. 

Use first aid measures to control bleeding e.g. Lean forward, open mouth. 

Pinch cartilaginous (soft) part of nose firmly and hold for 10 to 15 minutes without releasing the pressure, whilst breathing through their mouth.

If haemodynamically stable

• just use first aid measures to control bleeding ( Lean forward, open mouth and pinch cartilaginous part of nose firmly)

• If bleeding does not stop after 10 – 15 minutes of nasal pressure, (and still haemodynamically stable), then do NASAL CAUTERY (using silver nitrate). If cautery is ineffective or bleeding point cannot be seen, then NASAL PACKING.

  • Nasal Septal Abcess

Aetiology & Pathology

Nasal septal abscess is where there is a collection of pus between the mucoperichondrium and septal cartilage.

 It results from a bacterial infection of a nasal septal haematoma. 


Temperature and general malaise. 


To prevent Abcess formation Incision and drain septal haematoma 

  • Temporomandibular joint disorder:

The term temporomandibular disorders (TMDs) refers to a group of disorders affecting the temporomandibular joint (TMJ), masticatory muscles and the associated structures.

Aetiology & Pathology

Contributing factors – muscle overactivity which include bruxism (grinding of teeth) 


Facial pain, restricted jaw function and joint noise. 

The pain is around the temporomandibular joint but is often referred to the head, neck and ear.

  • Leukoplakia 

Aetiology & Pathology



• Seen as white thickening of the oral mucosa

(white patch that adheres to oral mucosa cannot be removed by rubbing)


• These should be biopsied as it is premalignant


  • Parotitis


Painful and tender mass at the angle of the jaw.

  • Acute Sialadenitis

Aetiology & Pathology –  Acute sialadenitis  

Acute inflammation of a salivary gland. 

Inflammation caused by bacteria or virus infection.

The infection is often the result of dehydration with overgrowth of the oral flora. 

 A common scenario would be postoperative dehydration. 

Presentation – Acute sialadenitis

Patients typically present acutely in A and E with erythema over the area, pain, tenderness upon palpation, and swelling. 

Purulent material may be observed.

The swelling may become enormously enlarged, sometimes even reaching the size of an orange, with overlying inflamed reddened skin and edema.

Mild pain and swelling are usually common before and during meals. 

Fluctuation test may be positive in the swelling if it is filled with fluid. 

Other symptoms of sialadenitis include a foul taste in the mouth

 decreased mobility in the jaw, dry mouth, skin changes, weight loss, shortness of breath, keratitis, dental pain, skin discharge and lymphadenopathy. 

The patient may run fever with rigors and chills along with malaise and generalized weakness as a result of septicemia. 

In severe cases, pus can often be secreted from the duct by compressing the affected gland. 

The duct orifice is reddened with reduced flow. 

There may or may not be a visible or palpable stone.

  • Chronic Sialadenitis

Aetiology & Pathology – chronic sialadenitis

Chronic inflammation of salivary gland

Can be infective or autoimmune.

The chronic form of the disease is associated with conditions linked to decreased salivary flow, rather than dehydration. 

These conditions include calculi (sialolithiasis).

Presentation- Chronic sialadenitis

Chronic sialadenitis, in contrast, is typically less painful and is associated with recurrent enlargement of the gland (often following meals) typically without erythema. 

  • Benign mixed parotid tumour ( Pleomorphic adenoma )

Aetiology & Pathology

Benign parotid tumour


Mobile mass 

Most common tumour of the parotid gland and 

Causes over 1/3 of submandibular tumours

The most common salivary gland tumour


• Presents around middle age

• Slow-growing and asymptomatic

• Solitory

• Painless

• Usually mobile

• Firm single nodular mass

Have the capacity to undergo malignant transformation.



Removing by superficial parotidectomy or enucleation

  • Submandibular Neuplasm


Submandibular neoplasms often appear with diffuse enlargement of the gland. 


Any masses of this sort need to be investigated. 

In fact, any salivary gland swelling that is present for more than 1 month needs to be investigated or removed. 

Ultrasound-guided fine needle aspiration (FNA) cytology is used to obtain cytological confirmation.

  • Mandibular tumour

Not mobile

  • Acute Tonsillitis 

Aetiology & Pathology 

Tonsillitis is usually caused by a viral infection

Less commonly  bacterial infection-Streptococcal infection). 


Pain in the throat is sometimes severe and may last more than 48 hours, along with pain on swallowing.

Pain may be referred to the ears.


The throat is reddened, the tonsils are swollen and may be coated or have white flecks of pus on them.

• Possibly a high temperature.

• Swollen regional lymph glands.

• Classical streptococcal tonsillitis has an acute onset, headache, abdominal pain and dysphagia.

• Examination shows intense erythema of tonsils and pharynx, yellow exudate and tender, enlarged anterior cervical glands.

If the sore throat is due to a viral infection the symptoms are usually milder and often related to the common cold.

In streptococcal infection the tonsils often swell and become coated and the throat is sore. 

The patient has a temperature, foul-smelling breath and may feel quite ill. 

The differences are variable and it is impossible to tell on inspection if the infection is viral or bacterial in real life. 

Signs of bacterial tonsilitis rather than a viral tonsilitis.

4 signs:

•High temperature

• White pus-filled spots on the tonsils

• No cough

• Swollen and tender lymph nodes (glands)


Antipyretic analgesics 

    paracetamol ,  ibuprofen are recommended for relief of fever, headache and throat pain 


Surgery is not a treatment for the acute condition 

But aimed at reducing the incidence of recurrent infections.

The indications for tonsillectomy are controversial.

Referral for tonsillectomy is indicated in children with no other explanation for recurrent symptoms provided the frequency of symptoms is:

• More than 7 episodes per year for one year

• More than 5 per year for 2 years

• More than 3 per year for 3 years

  • Peritonsillar Abcess ( quinsy)

Aetiology & Pathology

A complication of acute tonsillitis

Pus is trapped between the tonsillar capsule and the lateral pharyngeal wall


Difficulty in swallowing can result in drooling.

Typically preceded by a sore throat for several days

Sore throat


Pain localized to one side of the throat

Peritonsillar bulge

Uvular deviation → Bulging tonsil pushes the uvula away from the affected side


Trismus (difficulty opening the mouth)

Altered voice quality (‘hot potato voice’) due to pharyngeal oedema and trismus


Incision & drainage of aspiration in combination with intravenous antibiotics ( usually IV benzylpenicillin)

The changes in microbiology of the causative orgainsm and their resistance is the primary reason antibiotics alone is not sufficient as treatment. 

Needle aspiration, incision and drainage and quinsy tonsillectomy are all considered acceptable surgical management for acute peritonsillar abscess.

  • Tonsillar carcinoma

Aetiology & Pathology

Carcinoma of the tonsil is a type of squamous cell carcinoma. 

Risk factors include smoking, regular alcohol intake and HPV infection. 


The most important sign is a palpable lump in the neck, which this patient does not have.

Not mobile

  • Infectious Mononucleosis ( Glandular fever)

Aetiology & Pathology

Epstein Barr viral infection


Affects teenagers most often. 

Patients are unwell with very large and purulent tonsils and a long-lasting lethargy. 

An enlarged spleen is classically described.

  • Thyroglossal cyst

Aetiology & Pathology

most common congenital anomaly of the neck

They form along the embryological tract of the thyroid


Account for 2-4% of all neck masses.. 

They usually present as fluctuant swellings in the midline of the neck along the line of thyroid descent. These cyst tend to move upwards on tongue protrusion 

  • because they are attached to thyroglossal tract which attaches to larynx by  peritracheal fascia.

They are painless and mobile but can become painful if infected.

  • Laryngeal Carcinoma

Risk factors

• Smoking is the main avoidable risk factor for laryngeal cancer

Linked to an estimated 79% of laryngeal cancer cases in the UK.

• Certain occupational exposures (asbestos, formaldehyde, nickel, isopropyl alcohol and sulphuric acid mist) can also cause laryngeal cancer.

• Insufficient fruit and vegetables intake is linked to an estimated 45% of laryngeal cancer cases in the UK.

• Human papillomavirus type 16 (HPV16) seropositivity is associated with an increased risk of oral, pharyngeal and laryngeal cancer.


• Chronic hoarseness is the most common early symptom.

• Other symptoms of laryngeal cancer include pain, dysphagia, a lump in the neck, sore throat, earache or a persistent cough.

• Patients may also describe breathlessness, aspiration, haemoptysis, fatigue and weakness, or weight loss

Chronic hoarseness is the most common early symptom of laryngeal cancer. The typical

patient would be an elderly male patient who smokes and presents with progressive

hoarseness, then stridor, difficulty or pain on swallowing. Later with haemoptysis and

ear pain if the pharynx is involved.

  • Laryngeal Candidiasis

Aeriology & Pathology

Steroids predispose to fungal infection and can cause laryngeal candidiasis 


 Hoarseness of voice 

  • Oesophageal candidiasis


• Dysphagia

Odynophagia (pain on swallowing) food or fluids

  • Functional Dysphonia

Aetiology & Pathology

Voice disturbance that occurs in the absence of any structural abnormality of the larynx or any cord paralysis. 

It is a diagnosis of exclusion

There may be various interacting causes, such as heavy demands on the voice, poor vocal technique and stress.


Symptoms include vocal fatigue (voice becoming worse with use) and laryngeal discomfort. 

24 Comments on “PLAB 1 Short Notes ENT”

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