ENT

Question 1

Approach to dizziness (to arrive at 11 ddx inc differentiating two spont cont)

Answer 1

Continuous or episodic?

If episodic triggered or spontaneous? Triggered do DH test -> positive then BPPV, negative assess for orthostatic hypotension and consider subclavian steal (provoked by turning head to opposite side or using arms, may be >15mmHg diff between arms, may have pain or numb/tingle in arm, may have syncope or hearing loss or tinnitus)
Meanwhile if spontaneous most common (esp if headache, other sx, time course match) is vestibular migraine, but hearing loss may be menieres, depending on mental state may also be panic attack or psych disease/functional or TIA

If continuous is there a trigger (toxin eg ototoxic meds or damage eg barotrauma)? If no then do HINTS exam. Normal skew, horizontal unilateral nystagmus and saccade present means peripheral means vestibular neuritis (may be preceding sx of viral illness), abnormal skew with no saccade and nystagmus dominated by vertical, torsional, or bidirectional gaze evoked suggests central cause (stroke, TIA, MS, NMO)

Question 2

dizziness and vertigo- what % of over 65s, four common ddx, what rarely causes isolated vertigo, most likely cause if lasts seconds, x2 likely if last minutes

Answer 2

Patients use ‘dizziness’ to describe many sensations. Recurrent ‘dizzy spells’ affect approximately 30% of those over 65 years and can be due to postural hypotension, cerebrovascular disease, cardiac arrhythmia or hyperventilation induced by anxiety and panic. Vertigo (the illusion of movement) specifically indicates a problem in the vestibular apparatus (peripheral) or, much less commonly, the brain (central)

TIA and stroke rarely if ever cause isolated vertigo

As a guide, recurrent episodes of vertigo lasting a few seconds are most likely to be due to BPPV; vertigo lasting minutes or hours may be caused by Ménière’s disease (with associated symptoms including hearing loss, tinnitus, nausea and vomiting) or migrainous vertigo (with or without headache)

Question 3

vertigo diffs: BPPV vs menieres vs vestib neuritis (labyrinth) vs vestib migraine - onset and hearing loss in all 4, test for BPPV, for menieres what freq of hearing affected, what precedes vertigo and how long attack lasrs; for vest neuritis lasts how long and how long to recover (labyrinthitis extra feature), vestibulat migraine lasts how long and 4 associated features

Answer 3

Once you have established that the symptom is that of true vertigo, it is imperative to ascertain the duration and frequency of attacks, as this is the key to reaching the correct diagnosis and determining if the disorder is most likely peripheral (pertaining to the ear) or central (brain). There are 3 common causes of vertigo originating from the labyrinth itself: Benign Paroxysmal Positional Vertigo (BPPV)- most common cause of true vertigo with typical age of onset 40-60 years Vestibular neuronitis Meniere’s Disease

Another common condition that is seen is vestibular migraine

BPPV sudden w no hearing loss, vestibular neuritis sudden or gradual with no hearing loss, menieres gradual with fluctuating hearing loss, vestibular migaine sudden or gradual and may have hearing loss so can be hard to tell from menieres

BPPV- Dix-Hallpike test positive. Rotatory vertigo on moving head

Meniere’s – Rotatory vertigo associated with fluctuating hearing loss often with low frequency thresholds affected. Tinnitus usually gets worse during an attack. Patients classically get an aural fullness before onset of vertigo. attacks last minutes-hours

Vestibular neuritis – Rotatory vertigo that is continuous for over 24 hours often associated with nausea and vomiting. Classically they are confined to bed and it takes several days to weeks to recover. labyrinthitis is similar but also has hearing loss

Vestibular migraine – Rotatory vertigo can last minutes to hours to days. Classically associated with headaches/photophobia/visual disturbance\phonophobia but these are not always present

Question 4

vertigo two key examinations, imaging if asym sensorineural hearing loss accompanies and what you’re looking for, what is vHiT and what is it used for, short and long term mx for BPPV and what if resistant, 2 general mx for vestib neuro + specific drug for mild and severe; underlying pathology for menieres, 3 initial mx, 5 later options, what to relieve sx, who to tell; how to mx vestib migraines x2

Answer 4

Full neurological examination
Dix-Hallpike test

MRI of internal auditory meatus may be appropriate with asymmetrical sensorineural loss to exclude an acoustic neuroma

Video head impulse testing (vHiT) – this is performed using specialist equipment and can be used to assess the function of the semi-circular canals by measuring visual ocular reflex (VOR) function. It takes around 15minutes to perform and is a quick and sensitive measure of labrythine function

Treatment
BPPV - Epley’s manoeuvre can be curative in up to 90% by repositioning of the displaced otoconia crystals. In persistent cases, Brandt-Daroff exercises may be advised. Surgical management is rarely required but posterior semi-circular canal occlusion is useful in resistant cases.

Vestibular neuronitis – Treatment is expectant with anti-emetics during the acute phase; chronic symptoms needs vestibular rehab exercises, short course of prochlorperazine or antihistamine can alleviate less severe cases and more severe buccal/im prochlor

Meniere’s Disease – There is a hierarchy of treatments depending on the severity of the disease and response to previous treatments. The underlying pathophysiology is thought to be endolymphatic hydrops. Therefore “pressure reducing” therapies include low salt diet, medications such as betahistine and diuretics although the evidence for these treatments is weak. Intratympanic injection of steroid or gentamicin is used for those that fail conservative management. Other treatment options include saccus decompression, labyrinthectomy and vestibular nerve section.
prochlor to relieve attacks; vestib rehab; dvla should be told and dont drive until symptoms controlled

Vestibular migraine – Common trigger factors include dehydration, foods (classically chocolate, cheese), anxiety and a poor sleep pattern. A symptom diary can help identify these. In those that do not respond to avoidance measures, there are a variety of migraine-preventative medications

Question 5

dizziness (verty vs non verty, what duration tells you(4 durations 1:2:2:2), what supports otological vs neural cause)

Answer 5

vertiginous (spinning, like being drunk or getting off ride, everything at an angle) or non verty (light headed, woozy, spaced out, floaty); q to help - does it feel like you may fall over or pass out? does it feel as though youve been spinning around or stood up too quickly? do surroundings appear to be moving or do you think youll lose awareness of them?
duration most important factor to find cause - second BPPV, minutes to hour migraine or TIA, several hours menieres disease or TIA, several days vestibular neuritis, demyelination
a vertiginous pt will try to keep head still
focal migraine suggested by unprovoked (ie not related to position change) vertigo without hearing loss or tinnitus, usually lasting around 1hr; fh or pmh of migraine favours this, also triggers like menstruation, stress, altered sleep
cerebellar tia/stroke - look at risk factors, unlikely if not also some of diplopia, dysarthria, or ataxia; short history of bilat hearing loss with each ep lasting minutes could be due to tias in this territory and support diagnosis; absence of nystagmus or it being atypical eg vertical points to vascular cause, otological causes have horizontal nystagmus
vestibular schwannoma - progressive unilat hearing loss or tinnitus, slow growth allows compensation so often not vertigo but vague imbalance; rarely may cause acute hearing loss
otological cause also supported if no other neuro symptoms

Question 6

Nystagmus 13 causes; also diff central from peripheral x2

Answer 6

Involuntary eye movement; Nystagmus may be caused by congenital disorder or sleep deprivation, toxicity (wernickes, overdose inc pharmaceutical drugs), alcohol, or rotational movement, stroke; tumour, MS, brain (cerebellar) abscess, cerebellar ataxia, vestib pathology (BPPV, labyrinthitis, menieres), chiari malform

Vertical nystagmus is only seen if the cause is central. Nystagmus due to central causes may be horizontal, rotational or vertical, and does not disappear on fixing the gaze. Nystagmus in the peripheral type disappears with fixation of the gaze

Question 7

ear anatomy

Answer 7

outer ear consists of the pinna, external auditory canal, and tympanic membrane and is responsible for the transmission of sound waves from the external environment

middle ear is an air-filled space containing the three ossicles (malleus, incus, and stapes), bones responsible for transmitting vibrations from the tympanic membrane to the inner ear.

inner ear is located within the bony labyrinth of the temporal bone and contains the cochlea, semicircular canals, utricle, and saccule

cochlea contains cala vestibuli, scala media (also referred to as the cochlear duct), and scala tympani. The scala vestibuli and scala tympani both contain perilymph and surround the scala media, which contains endolymph. The endolymph within the scala media originates from cerebrospinal fluid (CSF)

Endolymph is rich in potassium and low in sodium and calcium, whereas perilymph is rich in sodium and low in potassium and calcium. This difference in concentration allows for a positive endocochlear potential

hearing: Vibrations are transmitted from the malleus through the incus to the stapes, which are in contact with the cochlear oval window; Vibrations across the oval window initiate a perilymph wave that propagates along the scala vestibuli, with high frequency sounds dissipating earlier at the base of the cochlea and low-frequency sounds dissipating later towards the apex of the cochlea. The perilymphatic wave terminates at the round window, another point at which the middle ear communicates with the inner ear; As vibration transmits across the oval window, perilymph gets pushed towards the cochlear apex, which causes the scala media to become compressed; this causes the tectorial membrane to change the position of cells within the organ of Corti; contains 15000 inner and outer hair cells arranged tonotopically throughout the cochlea to help distinguish between sounds of varying frequencies. The hair cells have projections known as stereocilia and kinocilia that are in contact with the tectorial membrane. Vibrations transmitted to the tectorial membrane cause displacement of stereocilia, leading to the displacement of the adjacent kinocilia. Movement of the kinocilia triggers depolarization of the hair cell, leading to an influx of calcium and the release of specific neurotransmitters that act at the cochlear ganglion

balance:
semicircular canals, including their ampullas, are responsible for angular acceleration (rotational movement of the head), whereas the utricle and saccule are involved in linear acceleration

muscles:
stapedius serves to decrease the vibration of the stapes, thereby dampening the sound energy that reaches the cochlea; damage gives hyperacusis
tensor tympani tenses the tympanic membrane to prevent loud sounds from damaging the inner ear; innervated by CNV and activated during talking, chewing, coughing, and laughing

Middle ear myoclonus (MEM), one of many causes of pulsatile tinnitus, is due to dysfunction of either the tensor tympani or stapedius muscle. It is often characterized as a clicking sound with the involvement of the tensor tympani and as a buzzing sound when due to the dysfunctional movement of the stapedius. It is also described as a tapping, throbbing, fluttering, or whooshing sound. The tinnitus is usually objective and, therefore, can be heard by the examiner

dev:
week 4 ectoderm forms auditory placode which invaginates towards mesoderm; cochlear ducts and endolymph accumulation by week 5; hair cells differentiate at 10-12 weeks

Question 8

development of the ear

Answer 8

internal ear is derived from ectoderm, and it is the first of the three anatomic parts of the ear to form; begins as otic placode around 4th week which invaginates to form otic pit and then elongates giving a ventral duct that forms the cochlea by the 6th week; ganglion cells from CN VIII migrate into cochlear to innervate hair cells and surrounding mesenchyme is induced to form a cartilaginous capsule that ossifies by 23rd week to form bony labyrinth

middle ear derived from endoderm, from extension of 1st pharyngeal pouch called tubotympanic sulcus; during dev endoderm and ectoderm approach with thin mesoderm between such that tympanic membrane contains all three layers; cartilaginous ossicles derived from neural crest cells from 1st/2nd arches condense around week 6 and undergo endochondral ossification; the two muscles derive from mesoderm; Eustachian tube is formed from the proximal portion of the tubotympanic sulcus

external ear first develops in the lower cervical region, but it gradually moves posterolaterally during development to reach its typical location; auricle develops from the mesenchymal proliferation of the first and second pharyngeal arches at the end of the fourth week of development. Six prominences, or auricular hillocks, form around the external auditory meatus and eventually fuse to form the auricle. Three auricular hillocks, hillocks 1 to 3, arise from the first pharyngeal arch to form the tragus, helix, and cymba concha; and three auricular hillocks, hillocks 4 to 6, arise from the second pharyngeal arch to form the concha, antihelix, and antitragus; meatus first develops as an invagination of ectoderm between the first and second pharyngeal arches that extends toward the developing middle ear structures; by 18 weeks, the external auditory meatus is completely patent

Question 9

development of the ear - pathophys

Answer 9

Neonatal hearing loss is sometimes due to developmental anomalies of the neurosensory components of the internal ear. The most common cause, Enlarged Vestibular Aqueduct Syndrome (EVA), is an autosomal recessive condition in which there is a bilateral enlargement of the endolymphatic duct and vestibular aqueduct; Maternal infection with rubella is another source of neonatal hearing loss that may hinder the development of the organ of Corti in the fourth week of development, resulting in its malformation. Similarly, maternal infection with cytomegalovirus is another potential cause of congenital sensorineural hearing loss; there are other common congenital genetic and dysplastic causes too

Congenital anomalies of the middle ear are relatively rare and include congenital fixation of one or more of the ossicles, a rare primary bone dysplasia called familial expansile osteolysis, and a cyst-like abnormal accumulation of skin cells called cholesteatoma

Given the role of the pharyngeal arches in the development of the external ear, anomalies of the external ear are associated with other pharyngeal arch anomalies and a variety of chromosomal disorders; Preauricular tags, or simply ear tags, are common and usually benign findings in neonates, accessory auricular hillocks sometimes produce auricular appendages, preauricular tags, or an accessory auricle, occasionally associated with cr or pharyngeal arch problems

Microtia is a developmental anomaly of the external ear involving an under-development of the typical mesenchymal proliferations that form the external ear. This condition presents at birth as an unusually small and sometimes misshapen external ear and is highly variable in its degree of severity; Bilateral microtia is a classic indicator of Treacher-Collins Syndrome

Cryptotia is a malformation of the cartilage of the external ear that involves part of the external ear, usually the superior portion, being buried under the adjacent skin

atresia of the external acoustic meatus has been associated with various pharyngeal arch malformations

Common conditions that can cause low-set and unusually formed ears include:

Down syndrome
Turner syndrome
Digeorge syndrome
Beckwith-Wiedemann syndrome
Potter syndrome
Rubinstein-Taybi syndrome
Smith-Lemli-Opitz syndrome
Treacher Collins syndrome
Trisomy 13
Trisomy 18

Question 10

hearing loss diffs (5 conductive inc appearance (and for last diff age range, inheritance, TM buzzword); 1 ix for sudden onset sensorineural + 1 mx and 1 referral, most common cause; 6 sensorineural inc 3 ototoxic drugs)

Answer 10

conductive

earwax (see on otoscopy, may feel blocked)
OME (may have popping/clicking/feel pressure, see dull TM or fluid level)
TM perf (see on otoscopy, if active infection may have discharge)
cholesteatoma (chronic smelly discharge, observe in attic, may see retraction pocket, refer to ent)
otosclerosis (20-40yo, uni or bilat, may have no visible signs, PTA shows raised threshold, autosom dom, maybe tinnitus, sometimes flamingo tinge hyperaemic tymp mem)

sudden onset sensorineural hearing loss needs urgent referral to ENT, MRI to exclude acoustic neuroma, and high dose oral corticosteroids; majority of cases idiopathic

sensorineural
presbycusis (bilat, gradual onset)
noise induced (oft have tinnitus)
acoustic neuroma (asymmetric, needs MRI - if bilat consider NF2)
menieres
complication of meningitis, esp kids
also consider drug ototoxicity (aminoglycosides, furosemide, aspirin)

Question 11

tinnitus two main ix (three times when imaging is required and two scans depending on type)

Answer 11

audiological assessment to detect underlying hearing loss

imaging- not all patients will require imaging. Generally, non-pulsatile tinnitus does not require imaging unless it is unilateral or there are other neurological or ontological signs.

MRI of the internal auditory meatuses (IAM) is first-line
pulsatile tinnitus generally requires imaging as there may be an underlying vascular cause. Magnetic resonance angiography (MRA) is often used to investigate pulsatile tinnitus

Question 12

AOM - how common in kids; preceding thing, 3 bacti causes, 6sx/findings, general mx x2, 5 indications for abx (and what given), 8 comps

Answer 12

extremely common in young children, with around half of children having three or more episodes by the age of 3 years.

Pathophysiology
whilst viral upper respiratory tract infections (URTIs) typically precede otitis media, most infections are secondary to bacteria, particularly Streptococcus pneumonaie, Haemophilus influenzae and Moraxella catarrhalis
viral URTIs are thought to disturb the normal nasopharyngeal microbiome, allowing bacteria to infect the middle ear via the Eustachian tub

Whilst guidelines vary, the majority use the following criteria to diagnose otitis media:
acute onset of symptoms
otalgia or ear tugging
presence of a middle ear effusion
bulging of the tympanic membrane otorrhoea
inflammation of the tympanic membrane i.e. erythema

generally a self-limiting condition that does not require an antibiotic prescription. There are however some exceptions listed below. Analgesia should be given to relieve otalgia. Parents should be advised to seek medical help if the symptoms worsen or do not improve after 3 days.

Antibiotics should be prescribed immediately if:
Symptoms lasting more than 4 days or not improving
Systemically unwell but not requiring admission
Immunocompromise or high risk of complications secondary to significant heart, lung, kidney, liver, or neuromuscular disease
Younger than 2 years with bilateral otitis media
Otitis media with perforation and/or discharge in the canal

If an antibiotic is given, a 5-7 day course of amoxicillin is first-line. In patients with penicillin allergy, erythromycin or clarithromycin should be given.
complications: perf -> otorrhoea; dev into chron supp; hearing loss, labyrinthitis, mastoiditis, meningitis, brain abscess, facial nerve paralysis

Question 13

cochlear implant - suitability in children determined by what 2 things? what must adults do and for how long; causes of profound hearing loss in kids x6 and adults x5; 3 contraindications

Answer 13

Suitability for a cochlear implant is determined by:
In children, audiological assessment and/or difficulty developing basic auditory skills.
In adults, patients should have completed a trial of appropriate hearing aids for at least 3 months which they have been objectively demonstrated to receive limited or no benefit from.

Causes of severe-to-profound hearing loss:

In children
Genetic (accounts for up to 50% of cases).
Congenital e.g. following maternal cytomegalovirus, rubella or varicella infection.
Idiopathic (accounts for up to 30% of childhood deafness).
Infectious e.g. post meningitis.

In adults
Viral-induced sudden hearing loss.
Ototoxicity e.g. following administration of aminoglycoside antibiotics or loop diuretics.
Otosclerosis
Ménière disease
Trauma

Prior to an assessment for the cochlear implant, patients should have exhausted all medical therapies

Contraindications to consideration for cochlear implant:
Lesions of cranial nerve VIII or in the brain stem causing deafness
Chronic infective otitis media or tympanic membrane perforation
Cochlear aplasia

Question 14

chronic otitis media (mucosal vs squamous and what dry vs wet form of each is, how to treat infection x2 and how to prevent recurrent AOM, 4mx of suspected cholesteatoma)

Answer 14

two types of chronic otitis media: Mucosal: A tympanic membrane perforation in the presence of recurrent or persistent ear infection. Squamous: Gross retraction of the tympanic membrane with formation of a keratin collection. (cholesteatoma)

The disease may be active (infection present) or inactive (no infection present): Inactive mucosal: Dry perforation Inactive squamous: Retraction pocket, which has the potential to become active with retained debris (keratin) Active mucosal: Wet perforation with inflamed middle ear mucosa and discharge Active squamous: Cholesteatoma

if infection then antibiotc + steroid ear drops
tympanoplasty to prevent recurrent aom

For all people with suspected cholesteatoma, arrange semi-urgent referral to an ear, nose, and throat specialist.
Investigations carried out in secondary care will include an audiology assessment and a CT scan.
Prior to surgical treatment, aural discharge may be treated with topical antibiotics.

Question 15

audiograms (diagnosis is high freq loss, higher freqs but prominently around 4kHz, low freq, cookie bite inc what freq centered on usually), 2x conductive causes in younger ppl esp and tympanometry appearance for first of these, (and vest migraine vs menieres inc attack length and hearing)

Answer 15

high freq loss is presbycusis, high freq but most prominent ~4kHz is noise exposure hearing loss, low freq is menieres; cookie bite looks like a bite mark centered on the mid range freqs (1000kHz) is often due to congenital hearing loss

conductive could be glue ear, earwax etc

tympanometry for glue ear: should look like upright chevron centered over 0, if shifted left TM is retracted, and if a flat line then glue ear

(menieres and vest migraine v similar but former attacks v rarely occur for longer than 24 hrs whereas latter might, also former will (after repeated attacks) eventually get low freq hearing loss whereas latter wont)

Question 16

causes of deafness in children - 3:(6:4:4) inc commonest overall and 3 things it’s linked to

Answer 16

conductive - otitis media with effusion (glue ear) commonest cause in children, may be linked to AOM, cleft palata, down syndrome); others inc wax build-up, foreign body

sensorineural - prenatal causes inc TORCH, maternal aminoglycosides, structural brain problems, AD or AR inherited, mucopolysac, or syndromes; perinatal causes incprematurity, low birth weight, aspyhixa, kernicterus; postnatal inc infection (mumps, mening, enceph), ototoxic drugs, head injury, lead poisoning

Question 17

5 causes of chronic ear discharge

Answer 17

chronic suppurative, chronic otitis externa, cholesteatoma, hitiocytosis X, rhabdomyosarcoma

Question 18

tympanograms - three general steps, when most compliant, what if max compliance at neg pressure, two causes of flat one

Answer 18

probe seals off EAM then range of pressures introduced to EAM, compliance of TM measured by reflecting sound off it, then plot compliance curve on graph

TM most compliant when pressures either side of it are equalised, normally around EAM pressure of 0

hypermobile ear drum is >3ml compliance peak at 0, poorly compliant <2ml peak at 0; if max complicance/peak is at neg pressure suggests eust tube blocked (so air resorbed in middle ear giving neg pressure); flat due to either perf ear drum or completely fluid filled middle ear meaning not compliant

Question 19

otitis media in children (acute eight sx, four TM appearance, five ddx, four reasons to admit, two steps if persists, what if recurrent, three reasons for 2ww, what ix if rec + grommet)

Answer 19

three kinds: acute AOM, glue ear aka with effusion OME, and chronic suppurative CSOM

acute - earache, tugging etc; maybe fever, crying, poor feeding, cough, rhinorrhoea, maybe vomit; red/cloudy TM that is bulging; may have perforated; if not bulging this not likely; consider also glue ear (no bulge, air/fluid level etc), chronic suppurative, otitis externa, referred pain, mastoiditis; admit if mening/mastoid/ nerve involvement / intracran abscess; fails to improve reassess for differentials, prescribe antibiotic (if had amoxi then coamoxiclav); if recurrent refer to ent, 2ww if glue ear symptoms between episodes, cervical lymphadenopathy, or epistaxis/nasal obstruction; if rec with grommet swab for c&s

Question 20

otitis media in children - CSOM and OME (chron supp three sx and five things maybe in history, five ddx, three things to see impact on and two mx; glue ear four sx, assess impact on what, four TM appearance, good test, five crit to refer, ENT two ix and two mx; how long to follow up for, how many need rereferral; reason for semi-urgent referral)

Answer 20

chron supp - ear discharge for 2wks+ w/ no pain/fever, hearing loss in affected ear, history of AOM, glue ear, grommet; history of urti, atopy; may see middle ear inflam or TM perf; consider otitis externa, AOM, glue ear, cholesteatoma, impacted wax; explore effects on language dev, daily life, school etc, hearing loss, advise they keep it dry, refer to ent

glue ear - hearing loss oft presenting symptom or mishearing, difficulty communicating in groups etc; mild ear pain or fullness; recurrent urti or aom; asses impact on life and school, language dev, balance; TM may be normal, may have air/fluid level, retracted or pacified drum, loss of light reflex; tympanometry good sens and spec for diagnosing; audiometry; active observation over 6-12wks as oft spont resolves; immediately refer to ent if down syndrome or cleft palate, or if not resolved after observation period, or if affecting language dev or getting complications; ent do tympanometry, audiometry x2 3mo apart; grommets, if surgery not acceptable then hearing aids instead; follow up until grommets extruded (10mo), 1/3 need reinsertion within 5yrs so if come back with OME then rerefer; semiurgent referral if persistent foul smelling discharge (maybe cholesteatoma)

Question 21

paeds hearing tests- newborn x1 (how works, what looking for); follow up if first test abnormal; three further tests and age when done

Answer 21

Newborn
Otoacoustic emission test
All newborns should be tested as part of the Newborn Hearing Screening Programme. A computer-generated click is played through a small earpiece. The presence of a soft echo indicates a healthy cochlea

Newborn & infants
Auditory Brainstem Response test
May be done if otoacoustic emission test is abnormal

6-9 months
Distraction test
Performed by a health visitor, requires two trained staff

18 months -
2.5 years
Recognition of familiar objects
Uses familiar objects e.g. teddy, cup. Ask child simple questions - e.g. ‘where is the teddy?’

> 3 years
Pure tone audiometry
Done at school entry in most areas of the UK

Question 22

otalgia diffs 4 diffs (one ant to tragus) including their typical pt (+7 sources of ref)

Answer 22

child, severe, preceding urti, erythema and bulging drum, febrile - AOM
severe, often preceding itch and after contact with water - otitis externa
elderly and severe pain + immunosup/DM - malignant otitis externa
pain ant to tragus and worse on eating, misaligned/clicking bite - tmj dysfunction
mod/severe intermittent pain with normal eardrum - referred, beware red flags; causes of referred can be tmj dysfunction, salivary gland path, dental abscess, sinusitis, peritonsillar abscess, tonsilitis, oropharyngeal carcinoma, laryngeal cancer, cervical spine disease eg cervical spondylosis

Question 23

otitis externa (three causes + recent trigger (and three sub-causes for first), three sx and three appearance, two initial mx + if dont respond; malignant oe 2 risk factors, 6x sx, one imaging, two mx inc to cover what)

Answer 23

Causes of otitis externa include:
infection: bacterial (Staphylococcus aureus, Pseudomonas aeruginosa) or fungal
seborrhoeic dermatitis
contact dermatitis (allergic and irritant)
recent swimming is a common trigger of otitis externa

Features
ear pain, itch, discharge
otoscopy: red, swollen, or eczematous canal

The recommended initial management of otitis externa is:
topical antibiotic or a combined topical antibiotic with a steroid
if the tympanic membrane is perforated aminoglycosides are traditionally not used*
if there is canal debris then consider removal
If a patient fails to respond to topical antibiotics then the patient should be referred to ENT.

malignant oe:
Diabetes (90%) or immunosuppression (illness or treatment-related)
Severe, unrelenting, deep-seated otalgia
Temporal headaches
Purulent otorrhea
Possibly dysphagia, hoarseness, and/or facial nerve dysfunction

Diagnosis
urgent ct scan needed

Treatment
non-resolving otitis externa with worsening pain should be referred urgently to ENT
Intravenous antibiotics that cover pseudomonal infections

Question 24

epistaxis diffs (ant v post bleeds location and severity, causes 1:5:1:1:1:2:1

Answer 24

split into anterior and posterior bleeds, whereby the former often has a visible source of bleeding and usually occurs due to an insult to the network of capillaries that form Kiesselbach’s Plexus aka littles area. Posterior haemorrhages, on the other hand, tend to be more profuse and originate from deeper structures. They occur more frequently in older patients and confer a higher risk of aspiration and airway compromise

most common cause is trauma to the nose- this can range from the insertion of foreign bodies, nose picking and nose blowing. Bleeding can also indicate platelet function disorders such as thrombocytopenia, splenomegaly, leukaemia, Waldenstrom’s macroglobulinaemia and ITP. In adolescent males, juvenile angiofibroma is a benign tumour that may bleed as it is highly vascularised. If the nasal septum looks abraded or atrophied, inquire about drug use. This is because inhaled cocaine is a powerful vasoconstrictor and repeated use may result in obliteration of the septum. In the elderly, hereditary haemorrhagic telangiectasia may cause prolonged nasal bleeding. Granulomatosis with polyangiitis and pyogenic granuloma may also present with nosebleeds,as might hypertension

Question 25

epistaxis mx - first mx (inc follow ups x2 and which to choose, what if recurrent), 3 reasons you might admit, then choose cautery or packing when, 2 reqs for packing; what to give after cautery

Answer 25

If the patient is haemodynamically stable, bleeding can be controlled with first aid measures. This involves:
Asking the patient to sit with their torso forward and their mouth open- avoid lying down unless they feel faint. This decreases blood flow to the nasopharynx and allows the patient to spit out any blood in their mouth. It also reduces the risk of aspirating blood.
Pinch the cartilaginous (soft) area of the nose firmly and consistently for at least 20 minutes and ask the patient to breathe through their mouth.

If first aid measures are successful, consider using a topical antiseptic such as Naseptin (chlorhexidine and neomycin) to reduce crusting and the risk of vestibulitis. Cautions to this include patients that have peanut, soy or neomycin allergies, and Mupirocin is a viable alternative. for around 2 weeks, check BNF/NICE (newer naseptin doesnt have arachis oil so may not provoke peanut allergy but old formulations are about); if recurrent refer to ENT clinic

Admission and follow up care may be considered in patients if a comorbidity (e.g. coronary artery disease, or severe hypertension) is present, an underlying cause is suspected or if they are aged under 2 years (as underlying causes such as haemophilia or leukaemia are more likely in this age group).

If bleeding does not stop after 10-15 minutes of continuous pressure on the nose, consider cautery or packing. Cautery should be used initially if the source of the bleed is visible and cautery is tolerated- it is not so well-tolerated in younger children! Packing may be used if cautery is not viable (inc young kids) or the bleeding point cannot be visualised, also don’t do cautery on both sides due to risk of damaging septum; ENT can come and pack, and admit if packing, and consider surgical mx if severe or not responding; give abx after cautery as you would after first aid

Question 26

nasal polyps (inc 6 associations and what is samter’s triad, 3 usual features and 2 unusual, 2 mx), septal haematoma consequence of what, 3 sx, exam finding and how to tell from septum, mx x2, 2 consequences of not treating; commonest cause of polyps in kids

Answer 26

Around 1% of adults in the UK have nasal polyps. They are around 2-4 times more common in men and are not commonly seen in children or the elderly.

Associations
asthma (particularly late-onset asthma)
aspirin sensitivity
infective sinusitis/chronic rhinosinusitis*
cystic fibrosis
Kartagener’s syndrome
Churg-Strauss syndrome (eGPA)

The association of asthma, aspirin sensitivity and nasal polyposis is known as Samter’s triad.

Features
nasal obstruction
rhinorrhoea, sneezing
poor sense of taste and smell

Unusual features which always require further investigation include unilateral symptoms or bleeding.

Management
all patients with suspected nasal polyps should be referred to ENT for a full examination
topical corticosteroids shrink polyp size in around 80% of patients

Nasal septal haematoma is an important complication of nasal trauma which should always be looked for.

may be precipitated by relatively minor trauma
the sensation of nasal obstruction is the most common symptom
pain and rhinorrhoea are also seen
on examination, classically a bilateral, red swelling arising from the nasal septum
this may be differentiated from a deviated septum by gently probing the swelling. Nasal septal haematomas are typically boggy whereas septums will be firm

Management
surgical drainage
intravenous antibiotics

If untreated irreversible septal necrosis may develop within 3-4 days and may result in saddle nose deformity

cystic fibrosis most common cause in children -> consider testing

Question 27

nasopharyngeal carcinoma (viral assoc, 5 sx/comps, 2 ix and firstline mx)

Answer 27

SCC, associated with EBV
cervical lymphad, otalgia, unilat serous otitis media, nasal obstruction/discharge/epistaxis, palsy of eg CN3/4/5/6
CT and MRI, radiotherapy first line mx

Question 28

rhinitis and rhinosinusitis manifestation (4 things); allergic rhinitis mx (mild, mod, role for decongestants, investigation)

Answer 28

‘rhinitis’ describes inflammation of the lining (mucous membranes) of the nose, characterized by nasal congestion, a runny nose, sneezing, itching and post-nasal drip. It can be usually divided into allergic and non-allergic causes. The term ‘rhinosinusitis’ describes inflammation of the lining of the nose and paranasal sinuses. It has a number of manifestations, the commonest symptoms being anterior or posterior rhinorrhea (runny nose or post-nasal drip), nasal blockage/congestion or obstruction, and facial headache or reduction in sense of smell

allergic rhinitis mx:
allergen avoidance
if the person has mild-to-moderate intermittent, or mild persistent symptoms:
oral or intranasal antihistamines
if the person has moderate-to-severe persistent symptoms, or initial drug treatment is ineffective
intranasal corticosteroids
a short course of oral corticosteroids are occasionally needed to cover important life events
there may be a role for short courses of topical nasal decongestants (e.g. oxymetazoline). They should not be used for prolonged periods as increasing doses are required to achieve the same effect (tachyphylaxis) and rebound hypertrophy of the nasal mucosa (rhinitis medicamentosa) may occur upon withdrawal
mainstay of investigation is the skin-prick allergy test (SPT); can do RAST in eg kids who wont tolerate SPT

Question 29

rhinosinusitis (how common, lasts how long, 5 predisposing factors, 4 features, 3 mx, 3 red flags)

Answer 29

affects up to 1 in 10 people. It is generally defined as an inflammatory disorder of the paranasal sinuses and linings of the nasal passages that lasts 12 weeks or longer.

Predisposing factors include:
atopy: hay fever, asthma
nasal obstruction e.g. Septal deviation or nasal polyps
recent local infection e.g. Rhinitis or dental extraction
swimming/diving
smoking

Features
facial pain: typically frontal pressure pain which is worse on bending forward
nasal discharge: usually clear if allergic or vasomotor. Thicker, purulent discharge suggests secondary infection
nasal obstruction: e.g. ‘mouth breathing’
post-nasal drip: may produce chronic cough

Management of recurrent or chronic sinusitis
avoid allergen
intranasal corticosteroids
nasal irrigation with saline solution

Red flags symptoms
unilateral symptoms
persistent symptoms despite compliance with 3 months of treatment
epistaxis

Question 30

allergic rhinitis

Answer 30

Allergic rhinitis is common in children and adults and is a significant cause of
morbidity.
* Classified as intermittent or persistent (rather than seasonal or perennial)
* Patients must be evaluated for asthma symptoms. 75% of children with asthma
suffer from AR and AR increases the risk of hospitalisation in children with
asthma
* Patients must be asked about eczema and pollen food syndrome.
* Patients must demonstrate their nasal spray technique regularly and
adherence to therapy should be established before stepping up therapy

Classic symptoms: Rhinorrhoea, pruritus (nose, throat, mouth), nasal
congestion (mouth breathing, snoring), sneezing

Mild if all of the following:
1. Normal sleep
2. No impairment of daily activities
3. No impairment of work/school
4. Symptoms present but not
troublesome

Mod-severe if one or more of:
1. Disturbed sleep
2. Impairment of daily activities
3. No impairment of work/school
4. Troublesome Symptoms

Persistent if >4 days a week for >4 weeks, otherwise intermittent

Red flags for ENT:
Unilateral symptoms including blockage, clear
rhinorrhoea and facial pain
* Serosanguinous discharge
* Visual and neurological signs (considering sinonasal
malignancy)
* Failure of 3 months maximum medical therapy,
particularly where nasal blockage and anosmia
remain significant symptoms

Step 1: allergen avoidance and nasal douching
Step 2: (start here if mod-sev sx): antihistamine (oral cetirizine or an intranasal one) if pruritus dominant (and generally preferred in kids) or nasal corticosteroid (mometasone, fluticasone, beclometasone) if congestion dominant
Step 3: r/v after 2-4 weeks, increase to intranasal antihistamine and intranasal steroid
Step 4:Regular nasal antihistamine, nasal
corticosteroid and oral antihistamine
Step 5: Refer to allergy clinic for skin prick or RAST, desensitisation etc - if asthma too they may start montelukast (reasons to refer earlier than this stage inc multisystem allergy eg with food/eczema/etc)

For seasonal rhinitis, start nasal spray 1-2
weeks before onset of appropriate pollen
season
2. Nasal steroids unlikely to work if there is nasal blockage due to secretions. Try topical
decongestant drops for 5 days
3. Aim to step down rx once control gained, trying every 2-4 weeks

If eye symptoms present consider:
* Olopatadine eye drops age 3+
* Sodium cromoglicate eye drops

In ppl >12yo intranasal anticholinergics can be used for persistent runny nose despite above

For people allergic to:
House dust mite and/or pets in the home — symptoms are usually present throughout the year, requiring ongoing treatment.
Tree pollens — treatment is usually required from early to late spring.
Grass pollens — treatment is usually required from late spring to early summer.
Weed pollens — treatment is usually required from early spring to late autumn.
If there are recurrent episodes of symptoms controlled by intranasal corticosteroids, advise the person to restart treatment two weeks before re-exposure to causative allergens. (or several weeks before likely start if not sure when eg pollen season will start)

Question 31

acute sinusitis (3 common inf agents, 4 predisposing factors, 3 sx, 4 mx)

Answer 31

inflammation of the mucous membranes of the paranasal sinuses. The sinuses are usually sterile - the most common infectious agents seen in acute sinusitis are Streptococcus pneumoniae, Haemophilus influenzae and rhinoviruses.

Predisposing factors include:
nasal obstruction e.g. septal deviation or nasal polyps
recent local infection e.g. rhinitis or dental extraction
swimming/diving
smoking

Features
facial pain
typically frontal pressure pain which is worse on bending forward
nasal discharge: usually thick and purulent
nasal obstruction

Management of acute sinusitis
analgesia
intranasal decongestants or nasal saline may be considered but the evidence supporting these is limited
NICE CKS recommend that intranasal corticosteroids may be considered if the symptoms have been present for more than 10 days
oral antibiotics are not normally required but may be given for severe presentations.
The BNF recommends phenoxymethylpenicillin first-line, co-amoxiclav if ‘systemically very unwell, signs and symptoms of a more serious illness, or at high-risk of complications’
‘double-sickening’ may sometimes be seen, where an initial viral sinusitis worsens due to secondary bacterial infection

Question 32

Pott puffy tumour (what it is/results from; most common cause, 2nd most common; 4 risk factors; why more commonly seen in kids and what age most common/why; 4 sx and 6 problems with extension; 2ix, 2mx, 2 ppl to consult

Answer 32

forehead oedema resulting from osteomyelitis of the frontal bone with associated subperiosteal abscess (tumour used here in its old sense of swelling rather than any neoplasm)

most common cause is a rare complication of acute or chronic frontal or ethmoid sinusitis
Head trauma, especially to the frontal area, is the second most common cause. PPT occurs by direct extension of wound infection
Risk factors that affect the normal immune response and can influence the development of PPT include diabetes mellitus, chronic renal failure, and aplastic anemia, as well as other causes of immunosuppression

more commonly seen in the pediatric and young adolescent population, as the frontal sinuses may be relatively hypoplastic because the pneumatization process of the frontal and ethmoid sinus starts in early childhood, but can vary, and may not be fully pneumatized until 15 to 18 years old (most commonly presents in the adolescent period because it is when the peak of vascularity in the diploic circulation is reached during the pneumatization process)

forehead swelling, headache, fever, and rhinorrhea; intracranial extension gives subdural or extradural empyema, meningitis or encepahlitis, venous sinus thrombosis, orbital cellulitis

CTH or MRI needed

systemic antibiotics and surgical treatment to drain abscesses, debride devitalized tissue, and restore sinus drainage -> ENT and neurosurgery should be consulted

Question 33

obstructive sleep apnoea (4 predisposing (big __ x3 + ctd (+3 causes of one of the big ones)), 3x consequences, 3 assessment, diagnostic test, 3x mx)

Answer 33

Predisposing factors
obesity
macroglossia: acromegaly, hypothyroidism, amyloidosis
large tonsils - may see in kids having apnoeas while asleep
Marfan’s syndrome

The partner often complains of excessive snoring and may report periods of apnoea.

Consequence
daytime somnolence
compensated respiratory acidosis
hypertension

Assessment of sleepiness
Epworth Sleepiness Scale - questionnaire completed by patient +/- partner
STOP-Bang (use to suggest likelihood in any consultation)
Multiple Sleep Latency Test (MSLT) - measures the time to fall asleep in a dark room (using EEG criteria)

Diagnostic tests
sleep studies (polysomnography) - ranging from monitoring of pulse oximetry at night to full polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry

Management
weight loss
continuous positive airway pressure (CPAP) is first line for moderate or severe OSAHS
intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
the DVLA should be informed if OSAHS is causing excessive daytime sleepiness
limited evidence to support use of pharmacological agents

Question 34

adenoids

Answer 34

Adenoids are small glands at the back of the nose, above the roof of the mouth. In younger
children adenoids form part of the immune system. A child’s adenoids can become swollen or enlarged following a bacterial or viral infection, or an allergic reaction. Swollen adenoids often cause mild discomfort and treatment is not needed. As children get older the adenoids shrink and the immune system can fight infections without them.
Some children can experience severe discomfort, which can interfere with daily life. Swollen adenoids can block the nose, which can affect breathing and can cause snoring at night. They can also block the Eustachian tubes causing hearing loss and ear infections (OME - adenoids may compress or obstruct the Eustachian tube ostium, thereby causing middle ear underpressure and subsequent effusion formation).

adenoids may be graded based on percentage of posterior choana occluded

adenoidectomy may be performed if failure to thrive due to difficulty in eating solid foods, strong clinical history suggestive of sleep apnoea, problems with OME, significant impact on quality of life e.g., loud and persistent noisy / mouth breathing leading to social difficulties, difficulty eating solid foods that creates unreasonably slow eating, difficulty exercising, or assessed to be at significant risk of choking/airway obstruction whilst eating

Question 35

odynophagia (7)

Answer 35

pain on swallowing, oft worse when drinking a hot liquid, may be indicative of oesophageal ulceration or oesophagitis from GORD, or oesophageal candidiasis

cancer less likely as implies mucosal sensation is intact - dont dismiss this tho

may be urti, pharyngitis, epiglotitis

Question 36

tonsillitis (most common causes, second most common cause)(5sx,4signs)(4 complications, timecourse, 7 ix, 4mx things, centor criteria and what abx to use (+ why inc type of reaction), 4 crit for tonsillectomy, 2 prim comps of that, two sec comps, mx of post-ton h+, how to manage prim h+ and how to man sec h+ (when it happens/commonly why?)

Answer 36

infection of the palatine tonsils. It may be bacterial or viral.

Acute tonsillitis is most common in children and young adults. The causative agents are mostly viral (70%) and to a lesser extent bacterial (30%). As a result, antibiotics are typically not efficacious in the majority of cases. Group A beta hemolytic streptococci is the most common cause of bacterial tonsillitis

Sore throat Odynophagia (painful swallowing) and dysphagia Earache Systemic upset: Malaise and headache Viral tonsillitis may present with milder symptoms

Signs Pyrexia Swollen tonsils +/- exudate Thick or ‘hot potato’ voice with enlarged tonsils
bilat cervical lymphadenopathy

resolves after 5-7 days, may recur
complications: peritonsillar abscess, paraphayng/retropharyng abscess with non-resolving sore throat, systemic upset, neck stiffness/tenderness
consider FBCs/U&Es/LFTs, glandular fever screen, ASOT, CRP, cultures if pyrexial

Regular IV/PO analgesia e.g. paracetamol and ibuprofen
Topical Analgesia e.g. Benzdyamine (Difflam)
Fluid resuscitation (important, these patients are often dehydrated from not drinking adequate fluid) Antibiotics Use the Centor or fever-pain Criteria to guide this decision. There is a 50% chance of the tonsillitis being bacterial if: Pus on tonsils (tonsillar exudate) Pyrexia No cough Tender cervical lymph nodes Antibiotics should be given to those who meet 3 or 4 criteria. Penicillin V (phenoxymethypenicllin), 500mg QDS for 10 days. Erythromycin is an alternative in penicillin allergic patients. Avoid amoxicillin- this causes a rash if the patient has glandular fever due to type IV hypersensitivity.

indications for tonsillectomy are controversial. NICE recommend that surgery should be considered only if the person meets all of the following criteria
sore throats are due to tonsillitis (i.e. not recurrent upper respiratory tract infections)
the person has five or more episodes of sore throat per year
symptoms have been occurring for at least a year
the episodes of sore throat are disabling and prevent normal functioning

Complications of tonsillectomy
primary (< 24 hours): haemorrhage in 2-3% (most commonly due to inadequate haemostasis), pain
secondary (24 hours to 10 days): haemorrhage (most commonly due to infection), pain
All post-tonsillectomy haemorrhages should be assessed by ENT.

Primary, or reactionary haemorrhage most commonly occurs in the first 6-8 hours following surgery. It is managed by immediate return to theatre.

Secondary haemorrhage occurs between 5 and 10 days after surgery and is often associated with a wound infection. Treatment is usually with admission and antibiotics. Severe bleeding may require surgery.

Question 37

peritonsillar abscess (4sx, 2mx + consider what)

Answer 37

aka quinsy
peritonsillar abscess typically develops as a complication of bacterial tonsillitis.

Features include:
severe throat pain, which lateralises to one side
deviation of the uvula to the unaffected side
trismus (difficulty opening the mouth)
reduced neck mobility

Patients need urgent review by an ENT specialist.

Management
needle aspiration or incision & drainage + intravenous antibiotics
tonsillectomy should be considered to prevent recurrence

Question 38

infectious mono (most commonly what + 2 alternatives; 3 ways carried; 2 main cell types infected; sx triad + 6 other sx, 3 linked malignancies; 3ix, 4mx, admission crit x3

Answer 38

90% due to EBV, can be CMV, HHV6
Saliva, semen, blood
Infects epithelial cells and B cells

Classic triad
Sore throat
Fever
Lymphadenopathy

Other clinical features
Splenomegaly: 50% patients. Avoid contact sports for 8 weeks!
Palatal petechiae
Hepatitis: ALT derangement
Lymphocytosis
Haemolytic anaemia: cold agglutinins (IgM)
99% develop maculopapular pruritic rash on taking amoxicillin

Malignancy: Burkitt’s, nasopharyngeal carcinoma, lymphoma

Diagnosis
Heterophile antibody (monospot, paul bunnell) test: infected B cells produce polyclonal IgM which agglutinate RBCs, needs to be in second week of illness (if negative repeat in 5-7 days + get serology, if 2nd negative then test for CMV, toxoplasmosis, HIV)
Serology: EBV IgM and IgG (IgM is most useful for telling acute infection) - note may only be positive once unwell for 7 days +
EBV PCR only if immunocomp or unwell in PICU

Management
Supportive: fluids, analgesia, safety-net, sporting advice
admit if stridor, dehydrated, or complication (splenic rupture, meningitis, carditis etc)

Question 39

salivary gland enlargement - where are most tumours, where most stones; tumour 80% rule x3; 6 features suggesting malignant; 3 features of commonest tumour and mx + risk; 3 features of second most common tumour; 2 features of stone, complication if infected, 2 ix, 1mx; 6 other ddx

Answer 39

parotid (serous) - most tumours
submandibular (mixed) - most stones
sublingual (mucous)

tumours: 80% parotid, 80% of these = pleomorphic adenomas, 80% superficial lobe
malignant rare: short hx, painful, hot skin, hard, fixation, CN VII involvement

Pleomorphic adenomas (benign, ‘mixed parotid tumour’, 80%)
middle age
slow growing, painless lump
superficial parotidectomy; risk = CN VII damage

Warthin’s tumour (benign, ‘adenolymphomas’, 10%)
males, middle age
softer, more mobile and fluctuant (although difficult to differentiate)

Stones
recurrent unilateral pain & swelling on eating
may become infected → Ludwig’s angina
80% are submandibular
plain x-rays; sialography
surgical removal

Other causes of enlargement
acute viral infection e.g. mumps, HIV
bacterial infection staph, TB, syphillis
sicca syndrome and Sjogren’s (e.g. RA)
sarcoidosis (in this and sjogrens see bilat, nontender, maybe xerostomia)
GPA
1st branchial cleft cyst

nearly all tumours need surgical resection, for benign disease this will usually consist of a superficial parotidectomy. For malignant disease a radical or extended radical parotidectomy is performed. The facial nerve is included in the resection if involved. The need for neck dissection is determined by the potential for nodal involvement

Question 40

submandibular gland disease (what percent of stones in this gland and what percent of those radio-opaque; usual composition; 2 sx; main ix; 2 mx depending on location; commonest cause of gland inflam, appearance x2, complication; what percent of submand tumours are malignant, 3ix, mx)

Answer 40

Sialolithiasis
80% of all salivary gland calculi occur in the submandibular gland
70% of these calculi are radio-opaque
Stones are usually composed of calcium phosphate or calcium carbonate
Patients typically develop colicky pain and post prandial swelling of the gland
Investigation involves sialography to demonstrate the site of obstruction and associated other stones
Stones impacted in the distal aspect of Wharton’s duct may be removed orally, other stones and chronic inflammation will usually require gland excision

Sialadenitis
Usually occurs as a result of Staphylococcus aureus infection
Pus may be seen leaking from the duct, erythema may also be noted
Development of a sub mandibular abscess is a serious complication as it may spread through the other deep fascial spaces and occlude the airway (ludwigs angina)

Submandibular tumours
Only 8% of salivary gland tumours affect the sub mandibular gland
Of these 50% are malignant (usually adenoid cystic carcinoma)
Diagnosis usually involves fine needle aspiration cytology
Imaging is with CT and MRI
In view of the high prevalence of malignancy, all masses of the submandibular glands should generally be excised

Question 41

ludwigs angina (3 features, 2 mx)

Answer 41

type of progressive cellulitis that invades the floor of the mouth and soft tissues of the neck. Most cases result from odontogenic infections which spread into the submandibular space.

Features
neck swelling
dysphagia
fever

It is a life-threatening emergency as airway obstruction can occur rapidly as a result.

Management
airway management
intravenous antibiotics

Question 42

mumps (diagnosis x2 steps; how long for gland to swell and how often b/l; 6 sx, 5 complications, 3 reasons unlikely; 10 ddx; lasts how long; how long to stay off school/work; 4mx; 2mx if contacted someone with mumps (2 reasons can’t do first step); 2 compications to admit and 2 mx for male complication)

Answer 42

clinical diagnosis confirmed by saliva sample ->IgM mumps antibody

consider if pt has parotitis - reaches full size in 2-3 days, usually other gland follows but 25% cases unilat; may be tender, have earache, problems pronouncing words; viral signs, anorexia, headache

watch for epididymoorchitis, oophoritis (N&v, lower abdo pain), viral meningitis (fever, headache, vomiting, neck stiffness, tiredness peaking over 2 days and resolving in a week), mild/transient pancreatitis, temp deafness

unlikely if had both doses of mmr, under 1yo, or previously had

consider EBV, parainfluenza, flu, adenovirus, parvovirus b19 etc; acute suppurative parotis (staph aureus, mycobaceteria), parotid duct obstruction, sarcoidosis, sjogrens, wegeners (GPA)

notify local health protection unit; self limiting over 1-2 wks, drink lots of fluid and use paracetamol/ibuprofen, warm/cold packs; stay off school/work for 5 days
consider 1 wk follow up, seek medical advise if epidoorchitis or meningitis symptoms

if contacted possible mumps: mmr vaccine if not had both doses, seek advice if get symptoms - cant give mmr if pregnant, nor if immunocompromised
epididymoorchitis treat in similar way + bed rest, unlikely to impact fertility but if severe/bilat or pt worried offer semen analysis 3mo later
admit if meningitis/encephalitis

Question 43

parotitis and sialadenitis - gland details, common causes

Answer 43

Parotid Gland
Largest of the glands
Stensen duct travels parallel to the zygoma, ~1cm inferior to it, and exist opposite the 2nd mandibular molar
Produces two-thirds of stimulated salivation.
Lower rate of secretion.
Produces primarily serous, watery saliva
More likely to become inflamed due to infectious and autoimmune reasons.
Submandibular Gland
2nd largest of the glands
Wharton duct exits the floor of the mouth near the frenulum of the tongue.
Produces two-thirds of the constant salivation.
Produced mixture of mucinous and watery saliva.
Mucinous saliva aids in lubrication, mastication, and swallowing.
More likely to become inflamed by obstructive processes, like stones.
Sublingular Glands
Multiple smaller glands.
Have very small ducts without a dominant duct.
Minor Salivary Glands
Scattered in the oral cavity and oral pharynx

causes of enlargement/inflam:
Infectious
Viral
Mumps
Vaccination has made this much less common, but outbreaks do occur.
Systemic illness… so look for other systems that may be involved.
EBV
HIV (Can cause bilateral involvement (think of this with bilateral parotitis - often non-tender)
Parainfluenza
Parvovirus
Influenza
Adenovrius
Coxsackievirus
Bacterial
Staph, Strep, H. flu, E. coli, Bacteroides
Most commonly occurs in the Parotid Gland.
TB is a rare cause

Immunologic
Sjogren Syndrome
IgA deficiency
Juvenile rheumatoid arthritis
Ankylosing spondylitis
Sarcoidosis
Ulcerative colitis
GPA
Bulimia Nervosa Sialadenosis (unclear etiology, but may be first presentation)

Trauma:
Local obstruction from stones
Relatively uncommon in children.
Submandibular gland involved in majority of cases (higher amount of mucoid saliva production).
Penetrating injuries
Blunt injuries
Radiation injury

Question 44

parotitis and sialadenititis

Answer 44

Swelling, pain, fever, and erythema of the affected gland.
Trismus and pain with mastication
Purulence may be expressed from the associated duct.
Inspissated mucus may also mimic purulence.

Juvenile Recurrent Parotitis is a common cause.
True incidence is unknown, but thought to be the second most common cause of salivary disease in children worldwide (after Mumps)

Has two peaks in age of presentation: ages 2-6 years and at age of puberty.
Self-limited and resolves spontaneous after puberty

general mx: analgesia, hydration, warm massage, send any pus for culture and start abx if could be infected (fluclox + metro)
if recurrent, not responding, or complicated (stone, abscess) then get USS of the gland
recurrent merits ENT referral ?juvenile recurrent parotitis, which will need surgery or steroid injection to duct

also for acute and chronic give advice for contributing risk factors: Manage underlying risk factors with good hydration, avoid dry
mouth (sialogogues like sour candy or lemon is good for this), good oral hygiene and consider use of chewing gum to stimulate saliva flow

Question 45

kawasaki disease- what it is, age range, commonest ethnicity, peak incidence; which group should you always assess for this; 7 main symptoms and 6 others; incomplete criteria x4 (+4 suggestive bloods), 6 internal organ manifestations; 10 ddx, 7 ix, 8 mx

Answer 45

idiopathic self limiting vasculitis in children 6mo-5yo, mainly in east asian people but also affects other races; peak incidence 18-24mo
assess any children with fever for 5days+ for this, ask about symptoms not just now but also from when fever started as may have resolved by presentation (ie from below don’t need to have the sx concurrently, just to have had them)

abrupt onset fever (39deg+), often irritable out of prop with fever; must also have 4+ of: oropharyngeal inflam (cracked lips, strawberry tongue, inflamed mucosa), erythema/oedema or desquam of extremities, bilat dry conjunctivitis, widespread non-vescicular rash (often start with erythema of palms/soles/perineum, itchy and takes various forms), cervical lymphadenopathy; also maybe lethargy, diarrhoea, vomiting, urethritis, myalgia, arthralgia

atypical/incomplete if fever >5 days, 2/3 clinical criteria, raised CRP/ESR, and 3 other blood/urine tests suggestive (thrombocytopenia, raised WCC, abnormal LFTs, hypoalbuminemia, sterile pyuria); these children should also get early echo; note also you might catch it early, so if features suggestive but fever <5 days monitor and if fever >5 days then mx as kawasaki, likewise if features not consistent with kawasaki otherwise but fever continues to persist

risk of coronary artery aneurysms, MI, pancarditis, aortic or mitral incompetence
aseptic meningitis and sterile pyuria may occur; gallbladder may be distended

ddx: EBV, measles, URTI, scarlet fever, TSS, scalded skin syndrome, systemic JIA, SJS, leptospirosis, drug reaction

FBCs, LFTs, CRP/ESR, trop, ECG, urinalysis; echo is essential to assess for aneurysms and heart function

inpatient bed rest during acute 2 week due to risk of cardiac events; aspirin (yes really, high dose follow BNFC, until fever settles then low dose until repeat echo) and IVIg (2g/kg over 12 hours, 24hrs if cardiovasc compromise) to protect heart and reduce fever; follow up echo in 6-8 weeks; discuss with cardiology if any cardiac lesion or myocarditis urgently, discuss anyway to plan follow up with them vs locally in 6-8 weeks; if aneurysms present, fever not settling, hypoalb, or <1yo then methylpred; rheum or ID may suggest infliximab, ciclosporin if not responding; if recurs at any time then refer to rheum/ID

Question 46

complement and angioedema - absence of which enzyme, what they present with, 2 times replacement enzyme given, what test to perform

Answer 46

absence of C1 esterase inhibitor causes intermittent angioedema in response to minor triggers, such as viral infections or stress, or without any
clear trigger at all
Patients can be treated with intravenous C-1 esterase inhibitor as prophylaxis before dental or surgical procedures or in response to acute
attacks of angioedema.

A key test for hereditary angioedema (C1 esterase inhibitor deficiency) is to check the levels of C4 (compliment 4). C4 levels will be low
in the condition. The exam question describe a patient with episodes of unexplained lip swelling and ask what test to perform. The answer is C4 levels

Question 47

Anterior triangle of the neck - borders (sup/lat/med/top/bot), and 4 subdivisions (inc contents 4:1:4:4)

Answer 47

Superiorly – inferior border of the mandible (jawbone).
Laterally – anterior border of the sternocleidomastoid.
Medially – sagittal line down the midline of the neck.
Investing fascia covers the roof of the triangle, while visceral fascia covers the floor

carotid triangle of the neck has the following boundaries:
Superior – posterior belly of the digastric muscle.
Lateral – medial border of the sternocleidomastoid muscle.
Inferior – superior belly of the omohyoid muscle.
The main contents of the carotid triangle are the common carotid artery (which bifurcates within the carotid triangle into the external and internal carotid arteries), the internal jugular vein, and the hypoglossal and vagus nerves.

submental triangle in the neck is situated underneath the chin. It contains the submental lymph nodes, which filter lymph draining from the floor of the mouth and parts of the tongue.
It is bounded:
Inferiorly – hyoid bone.
Medially – midline of the neck.
Laterally – anterior belly of the digastric

submandibular triangle is located underneath the body of the mandible. It contains the submandibular gland (salivary), and lymph nodes. The facial artery and vein also pass through this area.
The boundaries of the submandibular triangle are:
Superiorly – body of the mandible.
Anteriorly – anterior belly of the digastric muscle.
Posteriorly – posterior belly of the digastric muscle.

muscular triangle is situated more inferiorly than the subdivisions. It is a slightly ‘dubious’ triangle, in reality having four boundaries. The muscular triangle contains some muscles and organs – the infrahyoid muscles, the pharynx, and the thyroid, parathyroid glands.
The boundaries of the muscular triangle are:
Superiorly – hyoid bone.
Medially – imaginary midline of the neck.
Supero-laterally – superior belly of the omohyoid muscle.
Infero-laterally – inferior portion of the sternocleidomastoid muscle

Question 48

Posterior triangle of the neck - borders (ant/post/inf, floor and ceiling) and 6 contents

Answer 48

Anterior – posterior border of the sternocleidomastoid.
Posterior – anterior border of the trapezius muscle.
Inferior – middle 1/3 of the clavicle.
The posterior triangle of the neck is covered by the investing layer of fascia, and the floor is formed by the prevertebral fascia

significant muscle in the posterior triangle region is the omohyoid muscle. It is split into two bellies by a tendon. The inferior belly crosses the posterior triangle, travelling in an supero-medial direction, and splitting the triangle into two. The muscle then crosses underneath the SCM to enter the anterior triangle
EJV lies superficially and drains into sup clavicle vein which is accessed here; floor has cervical plexus and trunks of brachial plexus, CNXI also lies superficially in this triangle

Question 49

COVID19 - prodrome how long; 15 sx, which three most common; how many ppl show no sx vs critical sx; mild mx x1; mod/sev x3

Answer 49

prodrome (pre-illness phase) lasts between 2–10 days.

symptoms are fever, a new and continuous cough, shortness of breath, fatigue, loss of appetite, anosmia (loss of smell), ageusia (loss of taste), headache, muscle pain, sore throat, nasal congestion, chest pain, nausea and vomiting, diarrhoea, skin rashes

3 most common: Headache.
Runny nose.
Sore throat.

81% develop only mild to moderate symptoms (up to mild pneumonia), while 14% develop severe symptoms (dyspnea, hypoxia, or more than 50% lung involvement on imaging) and 5% of patients suffer critical symptoms (respiratory failure, shock, or multiorgan dysfunction)

at least ⅓ may show no symptoms; some people – over half of a cohort of home-isolated young adults– continue to experience a range of effects, such as fatigue, for months after recovery, a condition called long COVID; long-term damage to organs has been observed

Mild sx: supportive care includes medication such as paracetamol or NSAIDs to relieve symptoms
Mod sx: People with more severe cases may need treatment in hospital. In those on supplemental O2, use of the glucocorticoid dexamethasone is strongly recommended, as it can reduce the risk of death; NIV or ventilation and consider monoclonals

Question 50

neck lump - how common is cervical lymphadenopathy in kids, abnormal size is what, usual cause; what if tender and fluctuant (+ix when?), widespread lymphadenopathy suggests what 2 things; features of ddx: parotitis (4), SCM pseudotumour (4, 2ix, 1mx), thyroglossal duct cyst (6, 1ix), branchial cleft abnorms (3 types, ix, which triangle in); 5 tumours; cystic hygroma (3 features, which triangle in, ix); in summary 5 reasons to USS neck mass

Answer 50

90% of kids 4-8yrs have cervical lymphadenopathy at some point;

abnormal if >1.5cm in short axis (in adults abnormal if >1cm)

usually self resolving due to some viral or other cause, and other investigations not needed (pea sized nodes common and need no action unless grow to malteaser size +)

if tender and fluctuant may be cervical lymphadenitis, imaging not needed unless suspect abscess in which case USS may be helpful

widespread lympadenopathy may indicate leukaemia, or systemic/autoimmune disease

parotitis - fever, malaise, myalgia, tender swelling at angle of mandible

sternocleidomastoid pseudotumour - first 7-28 days of life, firm mass, associated with torticollis and dev dys hip; USS spec and sens, physio to treat + uss of hip to check for DDH

thyroglossal duct cyst - midline, mobile, usually below hyoid - if above still can be but more likely lymph node or dermoid cyst; inc in size over time, elevate with tongue protrusion; may be infected and form sinus tract; uss

cyst, sinus, or fistula from branchial cleft abnorms; if palpable lump, USS; generally ant triangle

in infants and young children may have rhabdomyosarcoma or neuroblastoma, in older kids lymphoma (thyroid, salivary gland tumours also poss but rare)

cystic hygroma - large, soft, painless mass within post triangle; uss first choice imaging modality

in summary: uss for focal neck mass >1.5cm, midline lump, any palpable lump if <6mo, suspected congen lesion, any lymphadenitis not responding to medical therapy - esp if inc pain, or redness over lump (assess abscess ie need for surgical incision/drainage)

Question 51

paediatric lymphadenopathy and lymphadenitis

Answer 51

Most lymphadenopathy is due to benign self-limited disease, such as viral or bacterial
infection
 Lymph nodes < 1cm are normal in children aged < 12 years. Axillary nodes up to 1 cm
and inguinal nodes up to 1.5 cm also usually normal. Ix likely not needed initially if <2cm and well
Supraclavicular nodes of any size at any age warrant further investigation

acute <2 weeks, chronic >6, sub-acute 2-6 weeks (likely secondary to infection but must consider malignancy and get bloods + CXR - if unexplained then co-amox for 2 weeks then review)

acute unilat: lymphadnitis, kawasaki, malignancy, langerhans cell histiocytosis
acute bilat: viral URTI, EBV, GAS (>3yo), CMV, malignancy, LCH
chronic unilat: non tuberculous mycoplasma, cat scratch disease, lymphoma/leukaemia, TB, toxoplasmosis, LCH
chronic bilat: EBV, CMV, lymphoma/leukaemia, toxoplasmosis, HIV, TB, LCH

Observation and reassurance without investigation is usually appropriate for the well
appearing child with cervical lymphadenopathy and lymph nodes <2cm.

normal/reactive node -> do nothing
if abnormal and features suggest a cause above then do confirmatory testing and treat
if abnormal with no features of above diagnoses or confirmatory testing negative (ie unexplained) then FBC with film, CRP, LFT, LDH, ESR, monospot
Serology: EBV, CMV, ASOT and save serum
CXR (if ?TB or ?malignancy)
Consider USS of node if ?abscess

if above NAD then trial 2 weeks co-amox and review, if no improvement discuss ?biopsy the node; always safety net for malignancy – rapid growth, systemic upset or signs of SVC obstruction

if strong possibility of malignancy then same day consultant review + organise biopsy (>2cm with: systemic features, splenomegaly, bone pain or swelling, node hard or non-mobile, present in multiple sites around body, increasing in size over 2 week period or not getting smaller after 4-6 weeks, not baseline after 8-12 weeks (note that baseline might be <1cm and mobile and rather than new node a normal once that had just been felt for the first time), abnormal CXR/bloods, supraclavicular node)

Ultrasound cannot reliably differentiate between reactive and malignant
lymph nodes and must not be used as a screening tool to ‘exclude
malignancy’

if confirmed lymphadenitis then oral co-amox with GP review in 2 days, if fever not resolved after 48 hours may not be penetrating well into lymph node -> admit for IV abx
if severe (massive, abscess present, unwell with fever and vomiting) then admit for IV co-amox, USS if not already got, and refer to surgeons/ENT to drain abscess
note if LN near jaw check carefully for dental infection and ?discuss with max-fax

Question 52

inhaled foreign bodies: 3sx, 2 ways to attempt to remove, how to remove if partial obstruction; 4sx if in lower bronchus, 1ix, 1mx; swallowed foreign body 4sx, serious consequence, 2 ix and 1 mx

Answer 52

inhaled - coughing, choking, may present as unconscious w/ cardiorespiratory arrest; open airway, visualise, remove with forceps; alternating backblows and chest thrusts and try to remove; if however obstruction only partial then seat child however they are most comfortable, and arrange urgent surgical removal

if in lower bronchus may have wheeze, cough, unexplained fever/dyspnoea, and maybe but not always a history of choking, coughing, or wheezing while eating or playing; CXR, surgery

swallowed - oft witnessed, sometimes present with gagging, vomiting, obstruction, rectal bleeding (dep on site where lodges); perf of oesophagus or gut is possible
if radioopqaue then plain AXR; CT another option, and can do endoscopy w/ removal

Question 53

thyroid cancer - 3 types, which common and in young females, which best prognosis, which secretes calcitonin + what associated with; 2 mx and 1 f/u; 4 sx, 3ix

Answer 53

Papillary 70% Often young females - excellent prognosis
Follicular 20%
Medullary 5% Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2

total thyroidectomy
followed by radioiodine (I-131) to kill residual cells
yearly thyroglobulin levels to detect early recurrence

firm enlarging lump, lymphadenopathy, hoarse voice, difficulty swallowing/breathing
if thyroid nodule: TFTs, USS, maybe scintigraphy

Question 54

9 neck lumps diffs (commonest inc 2 preceding features; rubbery and painless ddx + 3 features; 2 ddx move upwards with tongue protrusion + when painful; if gurgles on palpation, 4 sx; cystic hygroma is what, which side, what age normally; mobile mass between SCM and pharynx, cause, where diff types seen, when normally seen, complication; pulsatile mass; one other ddx, commoner in what gender, what potential risk)

Answer 54

Reactive lymphadenopathy By far the most common cause of neck swellings. There may be a history of local infection or a generalised viral illness

Lymphoma Rubbery, painless lymphadenopathy
The phenomenon of pain whilst drinking alcohol is very uncommon
There may be associated night sweats and splenomegaly

Thyroid swelling May be hypo-, eu- or hyperthyroid symptomatically
Moves upwards on swallowing
Thyroglossal cyst More common in patients < 20 years old
Usually midline, between the isthmus of the thyroid and the hyoid bone
Moves upwards with protrusion of the tongue
May be painful if infected

Pharyngeal pouch More common in older men
Represents a posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
Usually not seen but if large then a midline lump in the neck that gurgles on palpation
Typical symptoms are dysphagia, regurgitation, aspiration and chronic cough

Cystic hygroma A congenital lymphatic lesion (lymphangioma) typically found in the neck, classically on the left side
Most are evident at birth, around 90% present before 2 years of age

Branchial cyst An oval, mobile cystic mass that develops between the sternocleidomastoid muscle and the pharynx
Develop due to failure of obliteration of the second branchial cleft in embryonic development most commonly but may be 1st, 3rd, or v rarely 4th (3rd overlies SCM, 4th just below, 1st preauricular)
Usually present in early adulthood
May form fistula or become infected, needing MRI and surgical mx

Cervical rib More common in adult females, around 10% develop thoracic outlet syndrome

Carotid aneurysm Pulsatile lateral neck mass which doesn’t move on swallowing

Question 55

thyroid masses (first line ix inc 4 suspicious features, U2-5 grading means?, what happens with suspicious nodules?)

Answer 55

commonest presentation of thyroid disease is the presence of a thyroid mass. These can also cause compressive symptoms such as dyspnoea or dysphagia.

First line imaging is ultrasound of the neck to risk stratify thyroid lesions and look for malignant cervical lymphadenopathy. This can distinguish whether a patient has a solitary thyroid nodule or a suspicious nodule within a multinodular goitre. Suspicious features on ultrasound include solid hypoechogenic nodules with microcalcifications, irregular margins, taller than wider, and lymphadenopathy. Ultrasound scans are graded U2 (benign) to U5 (malignant); U3 and U4 are equivocal and need further investigation with ultrasound guided FNAC (fine needle aspiration cytology).

Question 56

sore throat approach - is there much difference between bacti and viral; what % is viral (3 common viruses), 6 bacti that cause inc commonest, another organism that causes; most likely age range for strep throat; 3 general ix if bad; 3 general mx; abx choice and length

Answer 56

no evidence that bacterial sore throats are more severe than viral ones or that the duration
of the illness is significantly different in either case. The precise diagnosis may be of academic interest, or possibly clinically relevant in more severe cases. Between 50 to 80% of infective sore throat is of viral cause, including influenza and primary herpes simplex. An additional 1-10% of cases are caused by Epstein-Barr virus (glandular fever). The most common bacterial organism identified is group A beta-haemolytic streptococcus (GABHS), which causes 5-36% of infections. Other organisms include Chlamydia pneumonia, Mycoplasma pneumonia, Haemophilus influenza, Candida, Neisseria meningitides and Neisseria gonorrhoeae

Streptococcal infection is most likely in the 5–15 year old age group and
gets progressively less likely in younger or older patients

ix if bad can include throat swab for culture, bloods for glandular fever + ASOT

paracetamol or ibuprofen, ensure hydration maintained, difflam spray another option to control pain

oral penicillin V (phenoxymethylpenicillin) for 5-10 days

Question 57

viral URTI in children - 8 families of virus involved, 5 infections included in umbrella term and how often do kids get in winter, 3 main non-suppurative complications after GAS infection and how their incidence impacts choice of whether to give abx, how many kids get what 3 sx on abx (hence risk/benefit analysis)

Answer 57

symptom complex usually caused by several families of virus; these are the rhinovirus (picornavirus), coronavirus, parainfluenza, respiratory syncytial virus (RSV), adenovirus, human metapneumovirus and influenza. Occasionally the enterovirus is implicated in summer

“URTI” is probably a misnomer as it incorrectly implies an absence of lower respiratory tract symptoms; URTI includes common cold, acute pharyngitis and tonsillitis, acute sinusitis and acute otitis media (AOM); in winter kids get colds on a monthly basis

rarity of nonsuppurative complications (post-strep glomerulonephritis, rheumatic fever, arthritis) after GAS infection in current UK general
practice means that any risk reduction as a result of presumptive antibiotic treatment for pharyngitis and tonsillitis is difficult to assess
but is likely to be very low.
1 in 24 children will develop diarrhoea, vomiting or rash following antibiotic treatment leaving the risk/benefit analysis finely balanced

Question 58

URTI in children: 2 most important bacti causes, general 4 features of commonest bacti cause and most important consequence of not treating it; pertussis risk highest when, why are teens/adults suseptible, how presents in adults x2, when to give empiric macrolide to infant (2 criteria)

Answer 58

two most important causes of pharyngitis requiring antibiotics are diphtheria and Streptococcus pyogenes (GAS). Fortunately diphtheria is extremely rare but can occur where public immunisation programmes have waned.

Pharyngitis due to S pyogenes may be easy to recognise, as it manifests as a febrile, purulent pharyngitis without rhinitis or cough. However, milder cases can be confused with viral URTI. The most important consequence of not treating pharyngitis is rheumatic fever

for pertussis, infants are especially at risk until all three primary doses of vaccine have been given at 6, 10 and 14 weeks. Adolescents and adults are susceptible to pertussis due to waning immunity. A useful clinical case definition for adults is an acute cough illness lasting at least seven days, especially if associated with posttussive vomiting or gagging beyond two weeks. Any infant with URTI symptoms and in contact with an adult or adolescent fulfilling the case definition of pertussis should receive a macrolide antibiotic

Question 59

viral urti in children - sx, signs, causes

Answer 59

common cold: exclusively urti viruses but predisposes to AOM and bacti sinusitiis; rhinorrhoea, sneezing, sore throat, fever for 2–3 days at start, some cervical LN, resolve in 10-14 days

tonsillitis/pharyngitis: URTI viruses, EBV (prolonged, anterior lymphadenopathy, check spleen), CMV, GAS, diphtheria, mycoplasma/chlamydia; sore throat. N&V, headache, coughing (may sound more fruity but not very productive), myalgia, cervical LN, flushed face, fever, conjunctivitis - be careful to look at tongue and chest/neck/upper body for scarlett fever (facial flush with perioral sparing and sandpaper rash in skin creases), 7-10 days, watch out for mastoiditis, peritonsillar or lymphoid abscess aka lypmhadenitis, or post-strep complications like rheum fever, HSP or post-strep GN, reactive arthritis

red flags ?admission for abx: <3 month old with fever >38
- Toxic appearance, signs of sepsis
- Respiratory distress, stridor, voice changes,
trismus, drooling, torticollis, neck swelling,
inadequate oral hydration
- Severe suppurative complication
(also check to see if dehydrated with examination and ideally urine dip)

low threshold for abx if previous rheumatic fever, immunosuppressed, or chronic disease; otherwise give abx if suspect GAS

Question 60

urti in children - cold caused exclusively by what, incs risk of 2 things, may be followed by what immune phenomena, 5 sx and lasts how long; tonsillitis/pharyngitis 7 causes, 9 sx, 2 places to examine for what ddx, lasts how long, 3 places abscess may form, 4 post-strep complications and how to tell if had strep, which penicillin best choice and why, what is in difflam spray; bacti sinusitis 5 bugs, 2 ways to tell started, 2 sx, lasts how long; AOM 6 causes, lasts how long

Answer 60

common cold: exclusively urti viruses but predisposes to AOM and bacti sinusitis, rarely followed by HSP; rhinorrhoea, sneezing, sore throat, fever for 2–3 days at start, some cervical LN, resolve in 10-14 days

tonsillitis/pharyngitis: URTI viruses, EBV, CMV, GAS, diphtheria, mycoplasma/chlamydia; sore throat. N&V, headache, coughing (may sound more fruity but not very productive), myalgia, cervical LN, flushed face, fever, conjunctivitis - be careful to look at tongue and chest/neck/upper body for scarlett fever (looking for flushed face with perioral sparing, sandpaper rash can be all over but esp skin folds and chest), 7-10 days, watch out for mastoiditis, peritonsillar or lymphoid abscess aka lymphadenitits, or post-strep complications like rheum fever, HSP or post-strep GN, reactive arthritis; ASOT to tell if recent GAS infection; fever-pain or centor score for abx decision (and note strep throat is v uncommon if <3yo so don’t test for it routinely); abx decrease length of illness by <1 day, main benefit is reducing risk of complications

PenV for 10 days better than amox as may cause rash if EBV, if can’t swallow then will need IV ceftriaxone; difflam spray available otc and in hospitals, has LA benzydamine (NSAID) and relieves pain of sore throat, good esp to ensure oral intake or if v painful; also available as mouthwash, can be used for sore throat of eg common cold; so strat is regular paracetamol +/- ibuprofen, add on difflam spray, regular oral fluids and safety net; abx if suspect GAS or have risk factors as per other card, single dose of IV/oral dex if severe sx; admit if red flags or dehydrated

acute bacti sinusitis: from pneumococcus, HiB, GAS, moraxella, anaerobes persistent or worsening nasal discharge 10 days after cold starts, or purulent discharge; persistent cough, facial tenderness/headache; 14-21 days

AOM: URTI viruses and CMV, pneumococcus, HiB, GAS, moraxella; lasts for 4-5 days usually

Question 61

lemierre syndrome - complication of what, 4 stages, most commonly responsible bacti, what can create better conditions for it to grow; what is normally in history at start of illness; 2 clues to presence of illness + the cord sign and what follows; 4ix; 2mx + controversial 3rd inc 3 reasons you might

Answer 61

rare complication of bacterial pharyngitis/tonsillitis and involves an extension of the infection into the lateral pharyngeal spaces of the neck with subsequent septic thrombophlebitis of the internal jugular vein; release of septic emboli into the systemic circulation results in widespread dissemination of bacti into the lung, pleura, joints, bones, muscles, spleen, liver, kidney etc and also sepsis

most commonly responsible bacteria are Fusobacterium necrophorum, an obligate anaerobic, gram-negative bacilli and Fusobacterium nucleatum. These bacteria can cause invasive disease secondary to multiple virulence factors including endotoxins and exotoxins. Other organisms such as Streptococcus species., Bacteroides species., Staphylococcus aureus, Klebsiella etc also reported

EBV and strep throat etc can also create better conditions for fusobacterium to grow; it is a normal part of the throat and GI flora

Over two-thirds of patients recount a pharyngeal infection at the onset of the illness, but rarely the illness has been described in the setting of parotitis, otitis media, mastoiditis, sinusitis, and dental infections. Patients with confirmed Epstein-Barr infections may also develop LS

persistence of fever and worsening of sx at 1 week can be a clue; neck tenderness and swelling may be an early clinical sign that pharyngitis has extended beyond the oropharynx. Unilateral tenderness and swelling at the mandibular angle, known as the “cord sign,” indicates internal jugular thrombosis; then develop signs of septic emboli and sepsis

CXR if resp signs; blood cultures and other parts of septic workup; CT neck with contrast, can consider USS or MRI as alternatives

abx, surgery if abscess or thrombus extension, anticoag controversial but consider if clots large, b/l, or extending into venous sinuses

Question 62

plummer-vinson syndrome (triad, commonly in who and associated with what x5; 3mx; 9 ddx

Answer 62

condition characterized by the classic triad of dysphagia, iron-deficiency anemia, and esophageal webbing

more common in middle-aged women and is associated with an increased risk of developing squamous cell carcinoma of the pharynx and proximal esophagus. Other disorders associated with Plummer-Vinson syndrome include celiac disease, Crohn disease, rheumatoid arthritis, and thyroid disease, raising the possibility that immune dysregulation may be involved in its pathogenesis

Medical management of Plummer-Vinson syndrome includes iron supplementation. Occult or overt blood loss is generally ruled out, along with any underlying malignancies or iron malabsorption

Dysphagia in many patients resolves with just iron supplementation however those with advanced and long-standing dysphagia typically require mechanical dilation

Other causes of dysphagia are much more common than Plummer-Vinson syndrome; even the presence of iron deficiency anemia or an esophageal web should not lead to a diagnosis of PVS. Tracheoesophageal fistula in neonates, injuries to the esophagus like blunt trauma or penetrating injuries, gastroesophageal reflux disease (GERD), vascular rings, and diverticula are some of the conditions which can present with similar dysphagia and spectrum of symptoms. Motility disorders like scleroderma, achalasia and diffuse esophageal spasm may present with the esophageal web and dysphagia. Benign and malignant tumors of the esophagus can have a similar presentation.

Question 63

thoracic outlet syndrome - when happens, 3 structures compressed, 5 general sx (inc 6 places pain might be felt), 6 risk factors and thus classic patient; 5 features of vTOS and pain vs nTOS; 2 features of aTOS; in general think TOS when x2; 3 things to examine and 1 thing in obs; 3 ix, mx strats x2

Answer 63

when a disorder causes compression of the neurovascular bundle exiting the thoracic outlet

structures include the brachial plexus, subclavian artery, and subclavian vein. Compression of this area causes a constellation of distinct symptoms, which can include upper extremity pallor, paresthesia, weakness, muscle atrophy, and pain (in neck, trapezius, ears, occiput, upper pecs, outer part of arm)

congenitally anomalous anatomy such as aberrant scalene musculature, cervical ribs, and connective tissue may compress and entrap nerve roots as may acquired variation eg scarring from injury such as whiplash or repetitive strain, more rarely tumours inc pancoast; thus nTOS is often seen in young, active individuals who participate in athletic activities that involve repetitive overhead upper extremity motion and heavy lifting

vTOS in similar individuals, and may have heaviness, cyanosis, pain, and raynauds like episodes; venous thrombosis can occur, in contrast to pain exacerbated by overhead upper arm positioning in nTOS, the symptomatology of venous thrombosis is stable

aTOS rare, may be cervical rib or compression by humeral head or pec minor ligament in athletic individuals; limb ischaemia, or if effects vertebral artery maybe TIA

think TOS when confronted with a patient suffering from upper extremity pain and supporting physical exam findings; low threshold for imaging

examine shoulder, arm, and c-spine (looking for asymmetry in posture and muscle bulk) and may have sysBP variation >20mmHg between arms in vascular TOS

nerve conduction and EMG if suspect nTOS, CT/MRI for all; rehab first for nTOS + simple and neuropathic analgesia, if refractory or v/aTOS then surgery

Question 64

anatomy of the palate

Answer 64

anterior immobile hard bony segment and a posterior mobile soft palate that does not contain bone. The superior aspect of the palate forms the floor of the nasal cavities and has a lining of ciliated pseudostratified columnar epithelium (respiratory epithelium). The inferior aspect of the palate forms the roof of the oral cavity and is lined with stratified squamous epithelium (oral mucosa) that contains secretory salivary glands.

The hard palate comprises about two-thirds of the total palate surface area, and its underlying bony structure consists of the palatine processes of the maxilla and the horizontal plates of the palatine bones. The soft palate is comprised of muscle fibers covered by a mucus membrane, specifically five muscles which have a functional role in breathing and swallowing:

Levator veli palatini muscle: elevates the soft palate and is involved in swallowing.
Musculus uvulae muscle: functions to shorten the uvula.
Palatoglossus muscle: pulls the soft palate towards the tongue and is involved in swallowing.
Palatopharyngeus muscle: tenses the soft palate and draws the pharynx anteriorly, involved in breathing.
Tensor veli palatini muscle: tenses the soft palate and is involved in swallowing.

all are innervated by the pharyngeal plexus of CN X, except for the tensor veli palatini muscle, which receives innervation from a branch of the trigeminal nerve called the medial pterygoid nerve; sensory innervation of the palate originates from the maxillary branch of the trigeminal nerve

swallowing:
tongue elevates to move the bolus posteriorly into the oropharynx
pharyngeal phase, the first irreversible step in the swallowing mechanism, begins when the bolus reaches the palatoglossal arch. Afferent sensory fibers from CN IX, X, and XI in the oropharynx transmit the stimulus to the solitary tract nucleus in the brainstem
Efferent muscle fibers then travel to innervate the muscles of the larynx, pharynx, and esophagus to coordinate a reflex response

begins with soft palate elevation via the tensor palatini and levator palatini to seal the nasopharynx to prevent pressure escape into the nasal cavity
primary mechanism of airway protection is the closure of the vocal folds. The posterior cricoarytenoid, contracted at rest, is inhibited, and the lateral cricoarytenoids are stimulated to adduct the cords. The oblique and transverse arytenoid muscles bring the arytenoid cartilage together, aiding in glottic closure. Concurrently, the arytenoids are tilted forward to make contact with the epiglottis to assist in opening the passage towards the esophagus
pharynx becomes elevated and pulled anteriorly by contraction of the suprahyoid muscles, which helps to open the pharyngeal-esophageal transition
bolus is moved inferiorly by a peristaltic-like sequential contraction of the superior, middle, and inferior pharyngeal constrictor muscles in a top to bottom fashion
end of the pharyngeal phase involves the food bolus descending through a patent UES into the esophagus

bolus is propagated inferiorly by a wave of peristalsis once it reaches the esophagus

Question 65

cleft palate - lip and palate embryology, associated syndromes, and risk factors

Answer 65

primordial mouth, or stomodeum, begins to form around week four. The five facial prominences arise around the mouth: frontonasal prominence in the median, bilateral maxillary prominences, and bilateral mandibular prominences. The frontonasal prominence develops into medial and lateral nasal prominences. Over the next week, the two maxillary prominences grow toward the nasal prominences, meeting the lateral nasal prominences to develop into the nasolabial region and the medial nasal prominences to create the lip. The failure to merge around the end of week five yields a unilateral or bilateral cleft lip.

At this time, the development of the palate begins and is complete around week twelve. The medial nasal prominences fuse at the midline to form the median palatine process or the primary palate. The medial portions of the maxillary processes rotate from a vertical to a lateral position around week seven to form the lateral palatine processes, which fuse at the midline from anterior to posterior to form the secondary palate. Failure of midline fusion results in cleft palate

found in over 200 different congenital syndromes. The most commonly discussed are CHARGE (coloboma, heart defects, atresia choanae, growth retardation, genital abnormalities, and ear abnormalities) syndrome and velocardiofacial or DiGeorge syndrome (22q11.2 deletion). Cleft palate alone is more commonly associated with other congenital anomalies, about 50%, than CL/P, about 15%. The most commonly discussed anomaly associated with isolated cleft palate is the Pierre Robin sequence of micro/retrognathia, glossoptosis, and cleft palate. This sequence is most commonly seen in Stickler syndrome but is also found with Treacher Collins, Nager’s, DiGeorge, and fetal alcohol syndromes

Material risk factors for malformation including smoking, diabetes mellitus, and gestational diabetes, and teratogen exposure (valproic acid, phenytoin, retinoic acid, dioxin, thalidomide). There is a clear familial association also

Question 66

cleft palate

Answer 66

Prenatal diagnosis is made by ultrasound around 18 weeks gestational age. However, it is highly dependent on ultrasound technician experience and skill. With traditional 2D ultrasound, cleft lip is more accurately detected than cleft palate

After birth, cleft palate is easily diagnosed on examination of the neonate. Patient history will include respiratory distress and reflux during feeding. Feeding time is generally prolonged due to this with infant fatigue. Most infants will have difficulty with an adequate latch as well. On examination, there will be a visible palatal defect, except in cases of a submucosal cleft. These are felt on palpation as a midline defect

difficult to form seal and generate negative pressure/protect nasopharynx so risk of reflux through nose, poor intake, taking in lots of air - specialist nurse to advise on feeding and weaning, may need to use EBM and specially shaped feeding nozzle, sometimes will need to be fed via NGT until surgery done

need to be evaluated for glue ear as at higher risk; may need grommets or even hearing aids

SALT monitoring for speech dev, can refer for further ix on palate function or guide speech development as needed

A typical care plan timetable for cleft lip and palate is:

birth to 6 weeks – feeding assistance, support for parents, hearing tests and paediatric assessment
3 to 6 months – surgery to repair a cleft lip
6 to 12 months – surgery to repair a cleft palate
18 months – speech assessment
3 years – speech assessment
5 years – speech assessment
8 to 12 years – bone graft to repair a cleft in the gum area
12 to 15 years – orthodontic treatment and monitoring jaw growth

regular outpatient appointments at a cleft centre until around 21yo when growth stopped

Question 67

submucous cleft palate

Answer 67

In a structurally normal palate, the muscles which lift the palate run from side to side. An SMCP is where the palate may look normal, but the muscles run from front to back, rather than side to side. This may affect how well the palate can lift and close against the back wall of the throat. When the palate is not able to close against the back wall of the throat, this is known as velopharyngeal dysfunction

not always easy to see, but some of the signs may include:

A double uvula (the ‘dangly’ flap of soft tissue that hangs down at the back of the throat may appear ‘split’ or in 2 parts)
A translucent line running through the middle of the palate
A v-shaped notch at the back of the hard palate (usually only detected by a clinician feeling inside the roof of the mouth)

Signs of VPD may include one or more of the following:

Hypernasal speech (too much air in the nose during speech, resulting in a nasal tone)
Audible escape of air through the nose during speech, either as a ‘puff’ of air (emission) or ‘rumbling’ sound (turbulence)
Weak production of oral speech sounds
A lack of oral sounds in speech
Oral sounds replaced with nasal sounds (e.g. “daddy” becomes “nanny” or “baby” becomes “may-me”)
Food or liquids leaking through the nose when eating or drinking

Question 68

dental abscess

Answer 68

pain, may be acute onset and throbbing, may wake at night
might see fever, bad taste in mouth, trismus, dysphagia, lethargy, lack of appetite (especially in children)

may see:
Facial swelling, with or without cellulitis.
Regional lymphadenopathy.
Altered tooth appearance: the affected tooth may be elevated, broken, or show signs of decay.
Gum swelling.
Purulent drainage: may be intra- or extra-oral.

Palpation may reveal:
Tooth: increased mobility and tenderness.
Gum: tenderness, warmth, and a purulent exudate.

needs admission if airway compromise, ludwigs angina, septic, significant swelling (eg cant open eye), any orbital cellulitis, focal neurological signs, or dehydration

needs to see a dentist ASAP
soft foods and eat on other side of mouth, avoid food that is too hot or cold, ibuprofen as first line analgesic

Antibiotics are generally not indicated for otherwise healthy people at low risk of complications when there are no signs of spreading infection. In the absence of immediate attention by a dentist, only prescribe an antibiotic:
For people who are systemically unwell or if there are signs of severe infection (for example fever, lymphadenopathy, cellulitis, diffuse swelling).
For high-risk individuals to reduce the risk of complications (for example people who are immunocompromised or have diabetes).

Can give penv or amox

Question 69

dental injuries

Answer 69

Two complete sets of teeth
-primary (deciduous) (milk teeth): erupt between 6/12-2years
-permanent teeth begin to replace milk teeth at around 6 years
Anatomically there are four quadrants, with 8 permanent teeth per quadrant

injured tooth can be described accurately by the quadrant it is in and its position
from the midline e.g. Upper L2 would mean the 2nd incisor in the left upper quadrant

Broken tooth:
do you know where broken piece is? ? Has it been aspirated? CXR to look for FB
and / or ball-valve effect if history of choking or if unconscious

Bleeding tooth socket:
Achieve haemostasis with pressure or if the child can, ask them to bite into wet
gauze, soaked with adrenaline if necessary; call Max Fax

Intrusion:
This term describes when incisor teeth have been pushed proximally into the
gum after a trauma e.g. knocking upper incisors on a hard floor during a fall
forwards
Is there any other injury e.g. head or facial injury or intra/extraoral laceration?
Management depends on degree of intrusion, also intrusion of
milk teeth often requires no immediate treatment: consult Max
Fax on call, they may want an OPG

avulsed tooth:
Primary (milk) teeth need not be replaced
Permanent teeth should be re-implanted quickly, it is therefore important to ask the parent or guardian if this was a permanent
tooth: the prognosis for a re- implanted tooth worsens after 15mins, and it should therefore be replaced into the socket as soon as possible and held in the mouth by biting down onto a wad of gauze until Max Fax arrive

If immediate re-implantation is not possible (child can’t co-operate), preserve tooth in cold milk or saliva, and refer to Max Fax as a priority.

tooth pain:
Refer to dentist / Maxfax depending on severity (caries vs abscess).
Emergency dentist can be contacted via 111 service.
Max Fax need to know if tooth is tender to percussion; facial swelling, fever,
trismus, or dysphagia

many dental injury cases have safeguarding element, so always be vigilant in these cases

Question 70

larynx anatomy

Answer 70

primary function of the larynx in humans and other vertebrates is to protect the lower respiratory tract from aspirating food into the trachea while breathing. It also contains the vocal cords and functions as a voice box for producing sounds,

location of the larynx is at the level of the C3 to C7 vertebrae and is held into position by muscles and ligaments. The superior-most region of the larynx is the epiglottis, which is attached to the hyoid bone connected to the inferior part of the pharynx. In children, epiglottis is more anterior and superior with a more oblique angle to the trachea and the subglottis being narrower than the glottis, and it is more pliant too - all of which combine to ensure it gives a ball-valve effect in oedema, hence why epiglottitis in kids is such a big threat to the airway

larynx is a cartilaginous skeleton, some ligaments and muscles that move and stabilize it, and a mucous membrane

laryngeal skeleton has nine cartilages: the thyroid cartilage, cricoid cartilage, epiglottis, arytenoid cartilage, corniculate cartilage, and cuneiform cartilage. The first three are unpaired cartilages, and the latter three are paired cartilages

epiglottis is an elastic cartilaginous leaf-shaped flap covering the opening of the larynx. It is attached to the internal surface of the thyroid cartilage and projects over the pharynx, allowing the passage of air into the larynx, trachea, and lungs. As the hyoid bone rises, it draws the larynx upwards during swallowing to allow food or drink into the esophagus and to prevent food from entering the trachea

vocal cords are four folds of fibro-elastic tissue, two superior and two inferior ones, anteriorly inserted into the thyroid cartilage and posteriorly in the arytenoid cartilage. The superior vocal cords are thin, ribbon-shaped, and have no muscle elements, while inferior vocal cords are wider and have a muscular fascicle covering their entire length. The space between the superior vocal cords is larger than the space between the inferior vocal cords, and viewed from above, four vocal cords are present in the larynx space

receives both motor and sensory innervation via branches of the vagus nerve:

Recurrent laryngeal nerve – provides sensory innervation to the infraglottis, and motor innervation to all the internal muscles of larynx (except the cricothyroid).
Superior laryngeal nerve – the internal branch provides sensory innervation to the supraglottis, and the external branch provides motor innervation to the cricothyroid muscle.

interior surface of the larynx is lined by pseudostratified ciliated columnar epithelium. An important exception to this is the true vocal cords, which are lined by a stratified squamous epithelium

The difference between the neonatal epiglottis and that of an adult is that it is proportionally longer, narrower, larger, less flexible, and often omega-shaped. In the condition known as laryngomalacia (LM), a combination of an omega-shaped epiglottis, short aryepiglottic folds, and/or redundant supra-arytenoid tissue and cuneiform cartilages, causes a collapse of the supraglottic structures into the glottis during inspiration

Question 71

Laryngomalacia

Answer 71

Laryngomalacia presents with inspiratory stridor that typically worsens with feeding,
crying, supine positioning and agitation. The symptoms begin at birth or within the first
few weeks of life, peak at 6 to 8 months, and typically resolve by 12 to 24 months

Most forms of laryngomalacia are minor (70—90%). These minor forms do not have any consequences on the infant’s growth and simply require surveillance by the paediatrician or general practitioner to detect any signs of severity.
Only severe forms of laryngomalacia require therapeutic intervention.

Parents should be advised on positional therapy (feeding in upright position),
feeding interventions (thickening formula or breast feed) and for treatment for
reflux where appropriate (assess all for signs of GOR)

Signs of severity are:
poor weight gain (probably the most contributive element);
* dyspnoea with permanent and severe intercostal orxyphoid retraction;
* episodes of respiratory distress;
* obstructive sleep apnoea;
* episodes of suffocation while feeding or feeding difficulties

Endoscopy under general anaesthesia must be systematically performed in these severe forms to confirm the diagnosis and exclude an associated respiratory tract lesion, such as laryngeal dyskinesia, vocal cord paralysis, subglottic stenosis, tracheomalacia. Thus these patients need admission under paeds with urgent ENT referral and airway management, supplementaloxygen
and nasogastric feed as required

Most of the new surgical techniques used in this disease, called supraglottoplasties, are designed to reduce the excess tissues on supraglottic structures responsible for collapse; an example procedure would be resection of the aryepiglottic folds

Question 72

hereditary angioedema

Answer 72

characterized by recurrent episodes of angioedema without urticaria, usually affecting the skin or mucosa of the upper respiratory and gastrointestinal tracts (causing pain and diarrhoea). Laryngeal attacks are rare but a
medical emergency and may cause fatal airway obstruction - indeed bowel wall oedema with resultant abdominal pain and swelling of extremities are the most frequently reported initial symptoms
can exhibit prodromal symptoms of erythema marginatum, an evanescent, nonpruritic macular rash, but no urticaria/pruritus usually; sx protracted if not treated, lasting 2-5 days, unlike allergy/histamine induced forms

lack of a clinical response to treatment with antihistamines, corticosteroids, or epinephrine should raise suspicion of HAE

get C1NH level and function tests + C4 level to confirm; low C4 and C1-INH functional levels are clinically diagnostic, genetic mutation analysis is the ultimate confirmatory step; however, this last step is usually cost-prohibitive; normal C4 during an attack makes the diagnosis highly unlikely

Some paediatric patients will carry a letter from the Immunology department
regarding their treatment however as attacks often do not present until puberty,
some patients may present to ED with their first attack. If this is a first presentation,
the patient should be referred to immunology on discharge

emergency treatment with C1 esterase inhibitor is effective

peripheral and gastrointestinal attacks can be very painful: Give effective analgesia.
Following successful emergency treatment, paediatric patients should be admitted to
CSSU for observation and can usually be discharged after 6-12h if no evidence of
wheeze, stridor or other signs of airway compromise

In the rare patients with signs of airway compromise (such as stridor, dyspnoea,
hoarseness or reduced SpO2), early fibreoptic airway examination should be
considered. Once the decision to intubate has been made, the procedure should be
undertaken jointly by an experienced anaesthetist and ENT surgeon. Failed
intubation attempts or other instrumentation may worsen airway compromise and
staff need to be ready to proceed to a surgical airway