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ENT OSCE Disease Chart

Physical Diagnosis 2 · ENT OSCE · Class of 2028

127 conditions — 55 routine, 54 urgent, 18 emergent

Use the Download as PDF button, top right, to keep this offline — it prints landscape with every row intact.

This is the run-sheet’s companion. The ENT OSCE Run-Sheet tells you the order of the station; this tells you what to do once you have a diagnosis in mind. Same 127 diseases as the CMS comparison chart, turned ninety degrees: that one answers what is this, this one answers what do I do about it.

Ordered least urgent first, deliberately. Routine sits at the top because the station will almost always be a routine complaint, so the rows you are most likely to need are the ones you reach without scrolling. Urgent follows — still a clinic referral, but in days rather than weeks. Emergent sits at the bottom as the must-never-miss tail, and every row there is a diagnosis whose whole teaching point is that it gets mistaken for something in the blocks above it.

Every test names its finding. “Order a computed tomography” is worth nothing in a station if you cannot say what makes it positive, so the tests column reads investigation → what you would see, and it is split: what confirms this diagnosis, and what would send you to one of the three differentials instead.

The differentials are the top three only. Not the complete list — the three you would actually be asked to defend, each with the single feature that separates it from the row it sits in.

Inspection findings, treatment and patient education are pulled live from the CMS chart rather than rewritten here, so the two pages cannot drift apart. Those three columns carry their lecture and slide citation in the first column.

Routine55 conditions

Managed in clinic, on a normal timescale. This is what the station is most likely to be, and it is the block to know cold.

Condition How the patient describes it
the words they actually use		 What you see on inspection Physical exams to rule it in or out
the maneuvers, not the findings		 Top 3 differentials
and what separates each one		 Tests — and what a positive looks like Treatment & referral Patient education
Hereditary sensorineural lossEarL16 · slide 71“It runs in my family — my father and my brother both went deaf young.” Or a newborn fails the hearing screen.Nonsyndromic hereditary hearing loss, plus the named syndromes: Waardenburg's, Alport and Usher's.Otoscopy is normal. Audiometry. Draw a three-generation family tree. Look for syndromic features: white forelock and different-colored eyes (Waardenburg), goiter (Pendred), retinitis pigmentosa (Usher), renal disease (Alport).
  1. Congenital infectionCytomegalovirus or rubella — acquired, not inherited
  2. PresbycusisLate onset without a family pattern
  3. Noise-induced lossAn exposure history and a characteristic notch
Rules it INAudiometry → a sensorineural loss, often symmetric. Genetic testing → a causative variant, connexin 26 being the commonest. Imaging → inner ear malformation such as an enlarged vestibular aqueduct.Rules the differentials OUTPositive congenital infection screening redirects the cause; an exposure history with a 4000 hertz notch means noise; a negative family history does not exclude a recessive cause.Amplification and the associated systemic disease.RoutineThe syndromic names carry the other organ involved — kidney in Alport, vision in Usher.
Noise-induced hearing lossEarL16 · slide 54–55“After the concert my ears rang for a day.” Or, at work, “I’ve been on the factory floor for twenty years.”One of the most common occupationally induced disabilities; exposure is regulated by OSHA. Most acute exposures produce temporary sensorineural loss recovering in 24–48 hours — a temporary threshold shift, with the ear feeling full and “crickets”. If the level is high enough or repeated often enough the loss becomes permanent — a permanent threshold shift. Rarely, extremely intense impulse exposure perforates the drum, giving a conductive loss instead.Otoscopy is normal. Weber and Rinne showing sensorineural loss. Take a detailed exposure history — occupational, recreational, firearms — and ask about hearing protection.
  1. PresbycusisSloping high-frequency loss WITHOUT a notch, and no exposure history
  2. Acoustic traumaA single blast rather than cumulative exposure
  3. OtotoxicityDrug-related and typically progressing with dose
Rules it INAudiometry → a notch at 3000 to 6000 hertz, classically 4000, with RECOVERY at 8000 hertz. That recovery is what separates the notch from presbycusis, which keeps falling.Rules the differentials OUTA continuously sloping curve without recovery at 8000 hertz is presbycusis; asymmetry suggests another cause; an air-bone gap means a conductive component.Remove the exposure and protect hearing. The permanent component is not recoverable.RoutineThe temporary shift is the warning shot — recovering by the next day does not mean no damage is accumulating.
ExostosisEarL16 · slide 48“I’ve been a cold-water surfer for years and my ears keep getting blocked and infected.”Bony growth in the external canal, bilaterally symmetrical, related to repetitive cold water exposure — divers and surfers. Can block the canal or collect debris.Otoscopy showing multiple, bilateral, broad-based bony swellings in the deep bony canal. Assess how much canal remains and whether the drum can be seen. Tuning forks if hearing is down.
  1. OsteomaSolitary, unilateral and pedunculated — the direct contrast
  2. Cerumen impactionWax rather than bone; it can be cleared
  3. Ear canal carcinomaFriable, bleeding and painful rather than smooth and bony
Rules it INOtoscopy → smooth, hard, skin-covered bony mounds. Computed tomography if surgery is planned → the extent of bony narrowing.Rules the differentials OUTA single pedunculated lesion is an osteoma; wax that clears excludes it; friable bleeding tissue needs biopsy for carcinoma.Address obstruction and trapped debris; surgical removal if the canal is occluded.RoutineEarplugs in cold water are the prevention; the growths themselves are slow and painless.
OtosclerosisEarL15 · slide 65–67“My hearing has been slipping for years — my mother went the same way. Oddly I hear better in a noisy room.”Bony overgrowth affecting the stapes, which eventually fixes and causes hearing loss. Gradual conductive loss, bilateral and asymmetric in 70%, unilateral in 30%. The patient reports that hearing is better with background noise. Tinnitus.Otoscopy is NORMAL, which is the point — occasionally a faint pink blush on the promontory. Weber lateralizes TOWARD the worse ear; Rinne is negative on that side. Ask about family history and about worsening in pregnancy.
  1. Otitis media with effusionA conductive loss too, but the drum is abnormal and tympanometry is flat
  2. Cerumen impactionSame conductive pattern, resolved instantly by clearing the canal
  3. CholesteatomaConductive loss with discharge, a retraction pocket and keratin
Rules it INAudiometry → a conductive loss with a Carhart notch, a dip in bone conduction around 2000 hertz. Tympanometry → type As, normal pressure with REDUCED compliance from the fixed stapes. Acoustic reflexes absent.Rules the differentials OUTA flat type B tympanogram means fluid, not fixation; an abnormal drum on otoscopy excludes it; clearing wax and restoring hearing excludes it.Observation if unilateral or the patient is untroubled. Hearing aids. Surgery is elective, generally one ear at a time, replacing the stapes with a prosthesis or placing a cochlear implant (ENT). Non-surgical options under investigation — sodium fluoride, bisphosphonates — with recommendations varying widely (ENT).RoutineA conductive loss with a normal-looking drum is the pattern; improved hearing in noise is the sentence patients volunteer.
Tympanic membrane perforationEarL15 · slide 45–47“Something popped in my ear and now there’s a bit of blood and my hearing is down.”Follows impact injury, explosive acoustic trauma, barotrauma or severe acute otitis media. Symptoms vary with cause but it is generally not painful once the membrane has ruptured. Conductive hearing loss. Otoscopy distinguishes central (does not reach the margin) from marginal (involves the margin); drainage through the perforation if it followed acute otitis media.Otoscopy to size and site the perforation. Weber toward the affected ear with a negative Rinne. Keep the ear dry — do not irrigate. Look for vertigo, which would suggest inner ear injury.
  1. Otitis media with effusionFluid behind an INTACT drum; tympanometry separates them
  2. CholesteatomaA marginal perforation with keratin debris rather than a clean tear
  3. Perilymphatic fistulaVertigo and sensorineural loss after the same event
Rules it INOtoscopy → a visible defect. Tympanometry → a flat trace with a LARGE canal volume, which is what distinguishes a perforation from an effusion. Audiometry → a conductive loss proportional to the size of the hole.Rules the differentials OUTA normal canal volume on tympanometry means an intact drum with effusion; a sensorineural loss or vertigo redirects to inner ear injury.Most resolve spontaneously over several weeks — and as little as 48–72 hours when it followed acute otitis media. Surgical reconstruction for large perforations or ones present a long time (ENT).RoutineKeep the ear dry while it heals. Report worsening hearing or dizziness — trauma can disrupt the ossicles as well.
Eustachian tube dysfunctionEarL15 · slide 6–10“My ear feels blocked since my cold, and it crackles when I swallow.”Edema of the tube lining after an upper respiratory infection or allergy stops the tube equalizing pressure. Fullness, mild to moderate hearing impairment, and crackling or popping with yawning or swallowing, which indicates the blockage is only partial. Usually transient — days to weeks.Otoscopy for a retracted drum, then pneumatic otoscopy — reduced mobility on insufflation is the finding. Check the nose for the cause. Weber and Rinne to prove any loss is conductive.
  1. Otitis media with effusionAmber fluid or a visible level behind the drum, not just retraction
  2. Cerumen impactionWax occludes the canal; the drum cannot be seen at all
  3. Acute otitis mediaBulging, red and painful rather than retracted and merely full
Rules it INPneumatic otoscopy → a retracted drum that moves poorly or not at all. Tympanometry → a type C tracing, the peak shifted to negative middle ear pressure.Rules the differentials OUTA type A tympanogram excludes it. Clearing wax and finding a normal mobile drum excludes both wax and effusion; a bulging red drum redirects to acute otitis media.Systemic or intranasal decongestants and intranasal corticosteroids. Forced exhalation against resistance. Caution with active nasal discharge — that maneuver can force infected fluid into the middle ear and trigger acute otitis media.RoutineAvoid air travel and other pressure changes until symptoms resolve. It is the commonest single reason an ear will not clear on a plane.
Otitis externaEarL15 · slide 54–59“My ear is really sore, especially if I touch it — I’ve been swimming a lot.”Inflammation and infection of the external canal, affecting 10% of people in their lifetime, all ages but commonest in children and early adolescence and in summer. Organisms: P. aeruginosa 38%, S. epidermidis 9%, S. aureus 8%; other bacteria and fungi possible. Risk factors: moisture and swimming, epithelial damage from aggressive cleaning, foreign bodies such as cotton swab fibers, occlusion by hearing aids or headphones, dermatitis of the auricle, radiation. Symptoms: otalgia exacerbated by touching or moving the auricle or tragus, otorrhea, pruritus, fullness, reduced hearing.Pain on tragal pressure or pulling the pinna — the defining maneuver. Otoscopy for a swollen, erythematous canal with debris; try to see the drum, which should be normal. Palpate the mastoid and check cranial nerve VII to exclude the malignant form. Check for diabetes.
  1. Acute otitis mediaNo tragal tenderness; the drum bulges and the canal is normal
  2. OtomycosisItch predominates, with visible hyphae or a wet-newspaper appearance
  3. Malignant otitis externaGranulation at the bony-cartilaginous junction, night pain, cranial neuropathy
Rules it INClinical → tragal tenderness with a swollen inflamed canal. Culture if it fails to settle → usually Pseudomonas or Staphylococcus.Rules the differentials OUTA bulging drum with no tragal tenderness redirects to otitis media; failure to respond in a diabetic patient means imaging for the malignant form; hyphae on examination mean otomycosis.Remove debris, then otic drops: antiseptic (boric acid, ichthammol, phenol, aluminum acetate, gentian violet, thymol, cresylate, alcohol), antibiotic (ofloxacin, ciprofloxacin, colistin, polymyxin B, neomycin, chloramphenicol, gentamicin, tobramycin) or acidifying (acetic acid). Combination drops with a steroid reduce pain and inflammation. An ear wick if the canal is stenosed.RoutineKeep the ear dry, stop cleaning it, and use the drops for the full course — the pain settles well before the infection does.
OtomycosisEarL15 · slide 62–63“My ear itches constantly and there’s a strange discharge — the drops the doctor gave me made it worse.”Fungal infection of the external canal, 9% of ear canal infections and varying with climate. Commonest organisms Aspergillus niger and Candida. Pruritus, discomfort that is less painful than bacterial otitis externa, otorrhea, foreign body sensation.Otoscopy for fluffy white hyphae with black or gray spores (Aspergillus) or a curd-like white debris (Candida). Assess tragal tenderness — usually much less than bacterial disease. Check the drum is intact before any drops.
  1. Bacterial otitis externaPain rather than itch; no hyphae; improves on antibiotic drops
  2. Chronic otitis media with dischargeDischarge comes through a perforation, not from the canal
  3. Eczematous otitis externaDry scaling skin and itch without fungal elements
Rules it INOtoscopy → visible fungal elements. Microscopy of debris with potassium hydroxide → hyphae or budding yeast.Rules the differentials OUTAbsence of fungal elements with a good antibiotic response means bacterial disease; a visible perforation with discharge redirects to chronic otitis media.Debris removal and topical antifungals.RoutineIt is treated by cleaning the canal as much as by the drops; the itch outlasting the pain is the clue that it is fungal.
Conductive hearing lossEarL16 · slide 10–11, 42“Sounds are muffled, like my ear is plugged — but my own voice sounds loud.”An external or middle ear disorder impairing sound conduction to the inner ear. Four mechanisms: obstruction (cerumen), mass loading (effusion), stiffness (otosclerosis) and discontinuity (ossicular disruption). Onset is typically childhood to age 40. The abnormality is usually visible on otoscopy — except in otosclerosis. Hearing seems to improve in a noisy environment and the voice stays soft, because the inner ear and cochlear nerve are intact. Causes: cerumen impaction*, eustachian tube dysfunction*, otitis media, perforation, otosclerosis, foreign body, cholesteatoma, exostosis, glomus tumor, ossicular discontinuity (*commonest in adults).Otoscopy of canal and drum — the cause is usually visible. Weber lateralizes TOWARD the affected ear; Rinne is negative (bone better than air) on that side. Pneumatic otoscopy.
  1. Sensorineural lossWeber lateralizes AWAY and Rinne stays positive — the opposite pattern
  2. Mixed lossBoth an air-bone gap AND reduced bone conduction
  3. Functional lossTuning forks and audiometry contradict each other and the behavior
Rules it INAudiometry → an air-bone gap with normal bone conduction — that gap IS the definition. Tympanometry → type B for fluid or perforation, type C for negative pressure, type As for fixation.Rules the differentials OUTAbsent air-bone gap excludes it; depressed bone conduction means a sensorineural or mixed loss; inconsistent responses suggest a functional loss.Treat the cause. Often correctable — which is the headline difference from sensorineural loss.RoutineThe reassuring half of the pair: most conductive loss has a fixable mechanical cause.
PresbycusisEarL16 · slide 15, 60–61“Everyone mumbles these days, and restaurants are impossible.” Often the family raises it before the patient does.The commonest sensorineural hearing loss. Progressive age-related loss from hair cell loss in the organ of Corti and cochlear nerve degeneration. Bilateral, symmetrical, gradual. High frequencies go first, progressing to mid and low. Patients hear speech but cannot make out the words, miss the doorbell and the phone, may have tinnitus, and lip-read more than they realize. It is common enough that primary care screens everyone aged 65 and over for it as a matter of routine. The prevalence percentages on the slide are explicitly not to be memorized — “you don’t have to memorize these statistics”.Otoscopy — clear wax first, since impaction is common and reversible. Weber and Rinne showing a sensorineural pattern. Check symmetry; presbycusis should be symmetric.
  1. Noise-induced lossA notch at 4000 hertz with recovery at 8000, and an exposure history
  2. Cerumen impactionConductive and immediately reversible — always excluded first
  3. Acoustic neuromaAsymmetric, which presbycusis is not
Rules it INAudiometry → a bilateral, symmetric, gradually sloping high-frequency sensorineural loss, with speech discrimination falling in noise.Rules the differentials OUTAsymmetry mandates imaging rather than a hearing aid; a 4000 hertz notch means noise damage; an air-bone gap means something conductive is also present.Amplification and communication strategy. Not correctable.RoutineFace the patient, do not shout — volume is not the problem, discrimination is.
Benign paroxysmal positional vertigoEarL16 · slide 89–93, 97“When I roll over in bed or look up, the room spins for about half a minute, then stops.”Severe vertigo with change in head position — rolling over, getting into bed, standing up, bending, looking up to reach an object, tilting the head back to shave, a haircut, turning rapidly. A specific side is typically described. Symptoms come on after a short latency of 10–15 seconds and last only 10–60 seconds; more than a minute should prompt an alternative diagnosis. Bouts cluster in time with remissions of months or more. Between attacks there may be constant lightheadedness worse with head movement, and imbalance for hours after an episode.Dix-Hallpike maneuver — the diagnostic test. Look for upbeating torsional nystagmus after a latency of a few seconds, lasting under a minute and fatiguing on repetition. Supine roll test for the horizontal canal. Otoscopy and hearing are normal; check cerebellar signs.
  1. Meniere diseaseHours of vertigo with hearing loss and fullness, not seconds
  2. Vestibular neuronitisContinuous for days rather than provoked and brief
  3. Central positional vertigoNystagmus WITHOUT latency, non-fatiguing, direction-changing
Rules it INDix-Hallpike → latency, torsional upbeating nystagmus, brief duration, fatigability. All four features together confirm it; no imaging is required.Rules the differentials OUTNystagmus that is immediate, sustained and non-fatiguing is CENTRAL and needs imaging; hearing loss excludes it; continuous vertigo redirects to neuronitis.The Epley maneuver, which repositions the otoliths in the semicircular canal.RoutineHearing is not affected and there is no tinnitus — those two absences are what place it against Ménière's.
Keloid of the earEarL15 · slide 69–70“A lump grew where I had my ear pierced and it keeps getting bigger.”Benign neoplasm of the ear: keloid and hypertrophic scars resulting from trauma.Inspect and palpate a firm, rubbery nodule extending BEYOND the original wound margin. Note the site and skin type. Examine the canal, which is normal.
  1. Hypertrophic scarStays WITHIN the wound boundary and often regresses — the key distinction
  2. Epidermoid cystSofter, with a central punctum, and may discharge keratin
  3. Chondrodermatitis nodularisPainful, on the helix, in older patients
Rules it INClinical → a firm scar growing beyond the original injury. Biopsy only if the diagnosis is in doubt.Rules the differentials OUTGrowth confined to the scar line means hypertrophic scar; a punctum means a cyst; marked tenderness on the helix means chondrodermatitis.Avoid further trauma. Intralesional steroid injection, corticosteroid tape, excision. Radiation therapy in adults, NEVER in children. Follow closely for recurrence.RoutineRecurrence is the rule rather than the exception, which is why follow-up is part of the treatment.
Functional hearing lossEarL16 · slide 80“I can’t hear anything at all in that ear” — yet the patient responds to conversation from that side.Suspected when the history contains inconsistencies, complaints and exaggerated listening effort. The patient's voice and speech quality provide important information: someone claiming significant bilateral loss while speaking at a normal level with normal articulation should be suspected of functional behavior.Otoscopy is normal. Watch for internal inconsistency: responding to speech at levels the claimed threshold would not permit. Weber and Rinne that do not fit the claimed loss — a total unilateral loss should lateralize away, and often does not. Stenger test.
  1. True sensorineural lossTuning forks, audiometry and behavior all agree
  2. Conductive lossA visible cause with a matching air-bone gap
  3. Auditory processing disorderConsistent thresholds with difficulty only in noise
Rules it INObjective testing — otoacoustic emissions → present, proving cochlear function; auditory brainstem response → normal thresholds. Both contradict the claimed loss. Stenger test → positive in a feigned unilateral loss.Rules the differentials OUTAbsent emissions with an abnormal brainstem response mean the loss is REAL; consistent behavioral results across sessions argue against it. Approach without accusation — there may be a genuine psychological cause.Address the underlying reason rather than the audiogram.RoutineA genuinely deaf voice changes. That is the observation the diagnosis rests on.
Acute otitis mediaEarL15 · slide 12–19“My ear has been throbbing since last night and I feel feverish.” A toddler tugs at the ear and will not settle.Rapid-onset middle ear inflammation, most often following an upper respiratory illness. Commonest in children, peak incidence around age 2; adults are only 3–15% of diagnoses. Otalgia, fever, hearing loss. Suppurative form discharges into the canal through a perforation. Recurrent means 3 or more episodes in 6 months, or more than 4 in 12 months, with complete resolution between.Otoscopy for a bulging, erythematous drum with loss of the light reflex and landmarks. Pneumatic otoscopy — immobility is the single most useful sign. Palpate the mastoid for tenderness. Tuning forks.
  1. Otitis media with effusionFluid WITHOUT pain, fever or bulging — the distinction that decides antibiotics
  2. Otitis externaPain on tragal traction with a swollen canal; the drum is normal if seen
  3. MastoiditisPostauricular tenderness with a protruding auricle — the complication to exclude
Rules it INPneumatic otoscopy → a bulging immobile drum. Tympanometry → a flat type B tracing with normal canal volume. Diagnosis is clinical; no imaging is needed.Rules the differentials OUTA mobile, non-bulging drum excludes it; a normal drum with tragal tenderness redirects to otitis externa; a normal postauricular area excludes mastoiditis.Most episodes resolve spontaneously. Antibiotics for bacterial involvement — amoxicillin. Analgesics and antipyretics for the pain and fever. Tympanostomy tubes for refractory or recurrent episodes, or when complications are present (ENT).RoutineExplain that most cases settle on their own, so a wait-and-see period is not neglect — most of these are viral. Return if pain worsens or discharge appears.
Chronic otitis mediaEarL15 · slide 20“My ear has been draining on and off for years and the hearing on that side is poor.”Recurrent infection with a non-healing perforation of the tympanic membrane. Duration required for diagnosis is controversial — weeks to months. Three subtypes: benign (dry perforation, no active infection); with effusion, also called chronic serous otitis media (continuous serous drainage through the perforation); and chronic suppurative (persistent purulent drainage).Otoscopy for a perforation and discharge; note whether the perforation is central or marginal. Look for keratin debris or a retraction pocket, which would mean cholesteatoma. Tuning forks. Facial nerve examination.
  1. CholesteatomaA marginal or attic perforation with white keratin debris and a foul smell
  2. Chronic otitis externaCanal is inflamed but the drum is intact
  3. Ear canal carcinomaFriable and bleeding rather than simply discharging
Rules it INOtoscopy → a persistent perforation with drainage. Audiometry → a conductive loss. Culture of the discharge → the organism guiding topical therapy. Computed tomography of the temporal bone → ossicular erosion or a soft tissue mass.Rules the differentials OUTAn intact drum excludes it; absent keratin and a central perforation argue against cholesteatoma; biopsy excludes carcinoma if tissue is friable.Refer to ENT.RoutineThe perforation is the disease, not just its aftermath — water precautions and follow-up matter because it will not close on its own.
Otitis media with effusionEarL15 · slide 13–19“My hearing is muffled and my ear feels full — but it doesn’t hurt.” In a child, “he keeps turning the television up.”Middle ear inflammation with an effusion but without acute infection. Follows eustachian tube dysfunction trapping fluid, and often persists after a bacterial acute otitis media has resolved. Often asymptomatic and picked up incidentally on otoscopy; otherwise hearing loss and fullness.Otoscopy for an amber or dull drum, an air-fluid level or bubbles. Pneumatic otoscopy. Weber lateralizes TOWARD the affected ear and Rinne becomes negative on that side — the conductive pattern. In an adult with a unilateral effusion, examine the nasopharynx.
  1. Eustachian tube dysfunctionRetraction without fluid; the earlier point on the same spectrum
  2. Acute otitis mediaPain, fever and bulging, which this lacks
  3. Nasopharyngeal carcinomaThe reason a unilateral adult effusion is never dismissed
Rules it INTympanometry → a flat type B curve with NORMAL canal volume (a large volume would mean a perforation instead). Audiometry → a conductive loss, typically 20 to 30 decibels.Rules the differentials OUTA type A tympanogram excludes it; fever with a bulging drum redirects to acute otitis media; nasopharyngoscopy excludes a tumor in the unilateral adult case.Most resolve spontaneously. The decision to intervene turns on how long the fluid has been there, the degree of hearing loss, and the effect on speech and language development. Tympanostomy tubes (ENT); adenoidectomy if hypertrophy is obstructing the tubes (ENT).RoutineIn a child the risk is not the ear but the speech and language delay from months of muffled hearing — which is why duration matters more than the appearance.
BarotraumaEarL15 · slide 22–25“My ear has been blocked and painful since the flight landed.”Inability to equalize middle ear pressure, seen with air travel, rapid altitude change and SCUBA diving. May rupture the tympanic membrane or bleed into the middle ear. Otalgia and conductive hearing loss.Otoscopy for a retracted drum, hemorrhage within the drum, or fluid. Check the drum is intact. Tuning forks. Ask about diving depth and about vertigo, which suggests inner ear involvement.
  1. Eustachian tube dysfunctionSame mechanism without the acute pressure event or hemorrhage
  2. Perilymphatic fistulaVertigo and sensorineural loss after the same barotrauma — far more serious
  3. Acute otitis mediaFever and a bulging drum with an infective prodrome
Rules it INOtoscopy → retraction, a hemotympanum, or a traumatic perforation. Audiometry → a conductive loss; a SENSORINEURAL loss instead points to a fistula.Rules the differentials OUTA sensorineural pattern on audiometry excludes simple barotrauma; a normal mobile drum excludes it; fever with bulging redirects to infection.Equalize by swallowing, yawning, exhaling through the nose against resistance. Oral or intranasal decongestants may help. Myringotomy gives instant relief and is reserved for severe otalgia and hearing loss with an intact membrane (ENT). Recurrent episodes in frequent flyers may justify tympanostomy tubes (ENT).RoutineAvoid pressure changes while a respiratory illness or allergy flare is active. If flying is unavoidable, take a decongestant beforehand and equalize on descent.
Cerumen impactionEarL15 · slide 27–29“My hearing went suddenly on that side — it started after I used a cotton bud.”Cerumen is a protective, thick, oily secretion of the outer third of the canal, and the canal is normally self-cleansing. Impaction is most commonly self-induced by cleaning attempts that push wax deeper. May be asymptomatic, or cause pruritus, fullness and conductive hearing loss.Otoscopy showing wax occluding the canal. Weber lateralizes TOWARD the blocked ear, Rinne is negative on that side. Re-examine the drum AFTER removal — that is the step people skip.
  1. Otitis externaPain on tragal traction; the canal is edematous rather than merely full of wax
  2. Otitis media with effusionA conductive loss with a clear canal and fluid behind the drum
  3. Sudden sensorineural hearing lossWeber would lateralize AWAY — the reason tuning forks matter
Rules it INOtoscopy → obstructing cerumen, and normal hearing once it is removed. That resolution IS the confirmation.Rules the differentials OUTIf hearing does not return after clearance, the wax was not the cause — audiometry then, and Weber lateralizing away means a sensorineural cause.Over-the-counter otic preparations to soften it. Irrigation or suction in clinic — irrigation uses body-temperature water and ONLY if the drum is intact. Curette removal suits soft wax and a compliant patient. If tympanostomy tubes or a perforation are present, removal must be done by ENT.RoutineDo not insert anything into the canal. If cleaning is wanted, a washcloth over the index finger at the opening is the whole technique.
TinnitusEarL16 · slide 44–46“There’s a ringing in my ears that never stops — it’s worst at night.”Can accompany any type of hearing loss and is often the first symptom of it. Described as ringing, buzzing, humming, hissing, a motor running, insects. Usually subjective; occasionally objective, meaning the examiner can hear it too. Everyone hears normal head noise in silence; low tolerance for it is associated with depression, neurosis, stress and fatigue.Establish whether it is pulsatile, which changes everything. Auscultate the ear, neck and skull for a bruit. Otoscopy — look for a red mass behind the drum. Tuning forks. Review medications.
  1. Glomus tumorPulsatile, with a red retrotympanic mass and a positive Brown sign
  2. OtotoxicityBilateral, follows a culprit drug, often with hearing loss
  3. Noise-induced or age-related lossNon-pulsatile tinnitus accompanying the loss itself
Rules it INAudiometry → the accompanying hearing loss that usually drives it. If PULSATILE, imaging with vascular study → a vascular tumor or a dural fistula.Rules the differentials OUTNon-pulsatile bilateral tinnitus with symmetric loss needs no imaging; a normal otoscopy excludes a glomus tumor; stopping a culprit drug with improvement points to ototoxicity.No drug has been more effective than placebo. Biofeedback and masking noises may work.RoutineAvoid loud noise, get the lead level checked, avoid stimulants, exercise daily, get adequate rest, and learn to treat the noise as an annoyance rather than a threat.
Benign nasal neoplasmsNose & sinusesL17 · slide 71“One side of my nose has been blocked for months and it bleeds now and then.”The lecture defers to the dermatology block: warts, freckles, hemangioma, port-wine stain and the rest behave on the nose as they do elsewhere.Anterior rhinoscopy and endoscopy, noting that the lesion is UNILATERAL. Assess for facial numbness, eye signs and proptosis. Palpate the neck. In an adolescent boy with recurrent bleeding, do NOT biopsy — consider angiofibroma and image first.
  1. Nasal polypsBilateral, pale and insensate; unilateral disease is the alarm
  2. Inverted papillomaUnilateral, locally aggressive, and carries a risk of carcinoma
  3. Sinonasal malignancyBone destruction, pain, numbness or an orbital or neck sign
Rules it INEndoscopy → a unilateral mass. Computed tomography and magnetic resonance → extent and whether bone is remodelled (benign) or destroyed (malignant). Biopsy → the histological diagnosis — except where imaging suggests a vascular lesion.Rules the differentials OUTBilateral pale mobile masses are polyps; a strongly enhancing mass in a teenage boy means angiofibroma and blind biopsy is contraindicated; benign histology with bone remodelling excludes carcinoma.As for the equivalent skin lesion — see the dermatology lectures.RoutineWorth knowing only as the counterpart to the malignant list; the detail lives in the dermatology material.
Allergic rhinitisNose & sinusesL17 · slide 13, 26, 66–68“My nose runs and itches, I sneeze in fits, and my eyes water — it’s worst in spring.”Rhinorrhea secondary to allergy: the body treats the allergen as foreign and releases chemokines causing hypermucosal production. Extremely common and rising.Anterior rhinoscopy for pale, bluish, boggy turbinates with clear discharge. Look for the allergic salute crease, allergic shiners and Dennie-Morgan lines. Examine the conjunctivae. Check for polyps and assess for asthma and eczema.
  1. Viral rhinitisDays rather than a season, with sore throat and no itch
  2. Vasomotor rhinitisTriggered by temperature, odors and food; no itch or sneezing fits
  3. Nasal polypsObstruction and anosmia with visible pale masses
Rules it INClinical → itch, sneezing, clear rhinorrhea and boggy pale turbinates with a trigger pattern. Skin prick testing or specific immunoglobulin E → sensitization to the suspected allergen, which guides avoidance and immunotherapy.Rules the differentials OUTPurulent discharge with facial pain redirects to sinusitis; negative allergy testing with trigger-related symptoms suggests vasomotor rhinitis; a short self-limiting course is viral.80% of patients end up on two or more allergy medicines. Non-drowsy oral antihistamine by day and a drowsy one at night if needed; leukotriene inhibitor at night; intranasal steroids with caution in chronic use; immunotherapy; intranasal ipratropium; decongestants with caution in chronic use and in high blood pressure.RoutineAllergy does not cause “-itis” itself — it creates the perfect environment for infection. Many patients who think they have sinusitis have allergic disease.
Deviated septumNose & sinusesL17 · slide 32–36“I’ve never been able to breathe through this side, and it’s worse at night.”The nasal septum is significantly displaced to one side, making one air passage smaller. Congenital or traumatic. Ranges from congestion — through blockage of the ostia — to anosmia. In severe forms: obstructive sleep apnea, snoring, facial pain and recurrent nosebleeds.Anterior rhinoscopy with a speculum, looking at both sides and comparing. Occlude one nostril at a time and test airflow. Look for a septal spur. Check the external nasal pyramid for deformity.
  1. Turbinate hypertrophyObstruction from swollen turbinates that shrink with a decongestant
  2. Nasal polypsPale mobile masses; the septum itself is straight
  3. Allergic rhinitisBilateral and fluctuating, with itch and sneezing
Rules it INAnterior rhinoscopy → visible septal deviation narrowing one side, with reduced airflow on that side. Decongestant challenge → obstruction PERSISTS, since bone and cartilage do not shrink; that is the key discriminator.Rules the differentials OUTObstruction relieved by a decongestant means turbinate hypertrophy, not the septum; visible polyps redirect; a straight septum excludes it.Surgery — septoplasty, by an otorhinolaryngologist.RoutineThe recurrent nosebleeds and the snoring are what usually bring the patient in, not the deviation itself.
Perforated septumNose & sinusesL17 · slide 37–40“My nose whistles when I breathe, it crusts, and it bleeds a bit.”A perforation through the nasal septum. Congenital or traumatic, but many are from intranasal steroid use or cocaine use, both by chronic ischemia. Rarely granulomatosis with polyangiitis (Wegener’s), a vascular autoimmune disease, may cause nasal deformity. Rarely, secondary syphilis — seldom seen now.Anterior rhinoscopy — shine a light in one nostril and look for it through the other. Measure and site the perforation. Take a history of cocaine use, nose picking, prior surgery and vasculitis symptoms.
  1. Granulomatosis with polyangiitisPerforation with crusting PLUS systemic and renal disease
  2. Cocaine-induced perforationOften large and progressive, with a use history
  3. Postsurgical or traumaticA history that explains it, and it does not progress
Rules it INRhinoscopy → a through-and-through defect. Antineutrophil cytoplasmic antibody, inflammatory markers, urinalysis → positive in vasculitis. Biopsy of the edge → granulomatous inflammation or malignancy.Rules the differentials OUTNegative vasculitis serology with normal urinalysis excludes granulomatosis; a benign biopsy excludes malignancy; a clear surgical history explains a stable perforation.Treat the underlying cause and it may grow back; otherwise septoplasty.RoutineThe drug history is the diagnosis here — ask about both prescribed nasal steroids and cocaine.
Acute sinusitis (rhinosinusitis)Nose & sinusesL17 · slide 9–27“My face aches and my nose is blocked — it started as a cold about four days ago.”Symptomatic inflammation of one or more paranasal sinuses lasting under four weeks, from impaired drainage and retained secretions, with obstruction and/or facial pain, pressure or fullness. “Rhinosinusitis” is the preferred term because rhinitis and sinusitis usually coexist. Affects 1 in 8 adults — over 30 million a year in the United States — and is the fifth leading reason antibiotics are prescribed. Nasal drainage and congestion, rhinorrhea, postnasal drip, headache. Pain localizes to the involved sinus and is worse bending over or lying flat.Palpate and percuss over the frontal and maxillary sinuses. Anterior rhinoscopy for mucosal edema and discharge. Transillumination. Examine the eyes and mental state to exclude the complications — that is the part that changes management.
  1. Viral upper respiratory infectionUnder 10 days, improving, without the bacterial features
  2. Allergic rhinitisItch and sneezing with clear discharge and pale boggy turbinates
  3. Dental infectionUnilateral maxillary pain with a tender tooth on percussion
Rules it INClinical → congestion, purulent discharge and facial pain or pressure. Imaging is NOT indicated in uncomplicated disease — opacity is common in simple colds and does not distinguish viral from bacterial.Rules the differentials OUTFull painless eye movements with normal vision and mental state exclude the complications; improvement by day 10 argues against bacterial disease; a tender tooth redirects to dental origin.Most improve WITHOUT antibiotics. Symptomatic: decongestants, non-steroidal anti-inflammatories, nasal or sinus lavage, intranasal steroids, neti pot, saline sprays. If bacterial: amoxicillin/clavulanate. Penicillin allergy: doxycycline, or an antipneumococcal fluoroquinolone such as moxifloxacin. If influenza, oseltamivir for five days in anyone over 13. Medical treatment fails → ENT referral for surgery.RoutineTell the patient what they have, how they got it, how to use the medicine or device, and — if referring — to which specialty. Most cases are viral and settle without antibiotics.
Bacterial sinusitis — the features that suggest itNose & sinusesL17 · slide 16–19, 23“I was getting better after a week and then it came back worse with a fever.”Only 0.5–2% of viral episodes develop a bacterial superinfection, so these features are what raise the possibility: worsening after 5–6 days of initial improvement; persistent symptoms for 10 days or more; persistent purulent discharge; UNILATERAL upper tooth or facial pain; unilateral maxillary tenderness; fever; altered mental status.The same sinus examination, but the diagnosis is made from the time course: symptoms persisting beyond 10 days without improvement, severe symptoms with fever for 3 to 4 days at onset, or double worsening after initial improvement. Check for complications.
  1. Viral rhinosinusitisPeaks at days 3 to 6 and improves — no double worsening
  2. Allergic rhinitisItch, sneezing, clear discharge, and it is seasonal or exposure-linked
  3. Complicated sinusitisEye or neurological signs; the tier above this one
Rules it INClinical → one of the three time-course patterns above. Computed tomography only if complications or failure of therapy → air-fluid levels with mucosal thickening.Rules the differentials OUTSteady improvement within 10 days excludes it; purulence ALONE does not confirm it, since viral infection turns purulent too; normal eye examination excludes orbital spread.Symptomatic treatment plus antibiotics — amoxicillin/clavulanate first line.RoutineThe color of the discharge is the thing patients most expect to be diagnostic, and it is the thing that matters least.
Branchial cleft cystNeckL18 · slide 22“There’s a soft lump on the side of my neck — it swells up whenever I get a cold.”Failure of the pharyngobranchial ducts to obliterate in fetal development. Presents in late childhood or early adulthood, usually when the cyst becomes infected after an upper respiratory infection: a tender, inflammatory mass at the anterior border of the sternocleidomastoid, with overlying erythema and swelling if infected.Palpate a smooth, fluctuant, non-tender mass ANTERIOR to the sternocleidomastoid, usually in the upper third. It does NOT move with swallowing or tongue protrusion — that is how it is separated from a thyroglossal cyst. Look for a skin pit or sinus opening. Transilluminate.
  1. Thyroglossal duct cystMIDLINE and rises with tongue protrusion
  2. Cystic metastatic nodeIn an adult over 40 this must be excluded — a cystic node can look identical
  3. LymphangiomaSofter, multiloculated, transilluminates brightly, present in infancy
Rules it INUltrasound → a well-defined anechoic cystic lesion anterior to the sternocleidomastoid. Computed tomography or magnetic resonance → extent and its relation to the great vessels. Fine needle aspiration in any adult → benign cyst fluid rather than malignant cells.Rules the differentials OUTMidline position with elevation on swallowing means thyroglossal; malignant cells on aspiration mean a cystic metastasis, and in an adult that possibility must be closed before excision is planned.Control the infection first, then surgical excision of the cyst and its tract. Avoid incision and drainage unless there is frank abscess — and even then needle aspiration is preferred, because I&D makes the definitive excision harder.RoutineThe cyst was always there; the infection is what made it visible. Excision has to take the whole tract or it recurs.
Dermoid cystNeckL18 · slide 29“There’s a firm lump in the middle of my neck under my chin.”Arises from epithelium entrapped in deeper tissue during embryogenesis, or by traumatic implantation. Presents as a midline, non-tender, mobile mass in the submental region.Palpate a midline, doughy, non-tender mass. Ask for tongue protrusion — it does NOT rise, unlike a thyroglossal cyst. Bimanual examination of the floor of the mouth to see whether it sits above or below mylohyoid.
  1. Thyroglossal duct cystRises with tongue protrusion — the single distinguishing test
  2. Plunging ranulaBluish, translucent, arising from the floor of the mouth
  3. Submental lymphadenopathyMultiple, tender, with an infective source in the mouth or lip
Rules it INUltrasound or magnetic resonance → a well-defined midline lesion with fat content and the sack-of-marbles appearance of keratin debris. It does not connect to the hyoid.Rules the differentials OUTElevation on tongue protrusion with a tract to the hyoid means thyroglossal; a translucent bluish floor-of-mouth swelling means ranula; tender multiple nodes with a dental source mean adenopathy.Surgical excision is the mainstay.RoutineOne of the midline masses — thyroglossal duct cyst is the other, and that one moves with the tongue.
HemangiomaNeckL18 · slide 27“It wasn’t there at birth, then it appeared and grew fast for months — now it’s fading.”A malformation of vascular tissue. Present in the first few months of life, grows rapidly through the first year, then begins to involute at 18 to 24 months. A red or bluish soft mass, compressible, that increases in size with straining or crying, with or without a bruit.Inspect color and depth — superficial lesions are bright red, deep ones bluish. Compress it — it blanches and refills. Note the growth phase. Check for airway involvement if it is in a beard distribution, and look for multiple lesions.
  1. Vascular malformationPresent AT birth and grows proportionately — it never involutes
  2. LymphangiomaTransilluminates, does not blanch, and is not red
  3. Pyogenic granulomaA small friable bleeding papule appearing rapidly at one point
Rules it INClinical → the proliferate-then-involute history with a blanching vascular lesion. Ultrasound with Doppler → a high-flow soft tissue mass. Magnetic resonance → extent, and airway involvement in segmental lesions.Rules the differentials OUTA lesion present at birth that grows only with the child is a malformation, not a hemangioma; absence of blanching excludes it; low flow on Doppler suggests a venous malformation.90% resolve without any therapy — observation alone. Intervene only for airway compromise, skin ulceration, dysphagia, thrombocytopenia or cardiac failure. First line: propranolol. Second line: systemic corticosteroids, interferon alpha, or surgical laser excision.RoutineParents need the growth-then-involution curve explained, or the rapid first year reads as failure of treatment.
LaryngoceleNeckL18 · slide 24“A lump comes up in my neck when I blow hard, and my voice goes husky.” Often a wind player or glassblower.An abnormal dilation or herniation of the saccule of the larynx. Cough, hoarseness, dyspnea, dysphagia or a foreign body sensation, in any combination. Secondary infection of one is called a laryngopyocele.Ask the patient to perform a Valsalva maneuver — the mass enlarges. That reducibility is the finding. Palpate for a compressible mass at the thyrohyoid membrane. Auscultate for a hiss on decompression. Examine the larynx.
  1. Branchial cleft cystDoes not change with Valsalva
  2. Laryngeal carcinomaCan OBSTRUCT the saccule and cause a secondary laryngocele — must be excluded
  3. Thyroid noduleMoves with swallowing rather than with Valsalva
Rules it INComputed tomography → an air-filled or fluid-filled sac continuous with the laryngeal ventricle. Laryngoscopy → the saccular opening, and it excludes a tumor at the same time.Rules the differentials OUTA mass that does not change with Valsalva is not a laryngocele; a normal larynx on endoscopy excludes an obstructing carcinoma, which is the reason endoscopy is done at all.Symptomatic disease only: laryngoscopic decompression for small lesions; surgical excision by an external approach for larger ones, taking care not to injure the superior laryngeal nerve; or laser endoscopy.RoutineThe airway symptoms are what force the operation, not the size.
Lymphangioma (cystic hygroma)NeckL18 · slide 26A parent says “she was born with a soft swelling in her neck and it’s getting bigger.”A congenital malformation of the lymphatic channels, arising because the lymph spaces fail to connect to the rest of the lymphatic system. The mass is soft, doughy, smooth, non-tender and compressible, and transilluminates.Palpate a soft, compressible, ill-defined mass, usually in the posterior triangle. Transilluminate — it glows brightly, which is the classic finding. Assess airway and feeding. Watch for sudden enlargement after an infection or bleed.
  1. HemangiomaRed or blue, blanches, and follows proliferate-then-involute growth
  2. Branchial cleft cystDiscrete and unilocular, anterior rather than posterior triangle
  3. TeratomaContains solid elements and calcification; does not transilluminate uniformly
Rules it INUltrasound → a multiloculated cystic mass with thin septa. Magnetic resonance → extent and airway relationship, which is what surgery is planned from. Fluid levels suggest previous hemorrhage.Rules the differentials OUTBright uniform transillumination with multiloculated cysts excludes a solid tumor; a blanching vascular lesion is a hemangioma; solid components with calcification mean teratoma.Surgical excision or debulking depending on how far it infiltrates. Sclerotherapy is the alternative.RoutinePositive transillumination is the bedside finding that separates it from the solid masses.
Plunging ranulaNeckL18 · slide 25“I had a swelling under my tongue and now there’s a soft lump in my neck.”A mucocele or retention cyst of the floor of the mouth, presenting as a slow-growing, painless submental mass. It arises from the sublingual gland and is called plunging when it extends through the mylohyoid muscle into the neck.Bimanual examination — one hand in the floor of the mouth, one on the neck. Look for a bluish translucent swelling in the floor of the mouth. Palpate the submandibular gland and check Wharton duct.
  1. Simple ranulaConfined to the floor of the mouth, not extending through mylohyoid
  2. Dermoid cyst of the floor of mouthDoughy, midline, without the bluish translucent quality
  3. Submandibular sialadenitisPainful gland with pus at the duct, worse with meals
Rules it INMagnetic resonance or computed tomography → a unilocular cystic lesion extending THROUGH the mylohyoid muscle into the neck — that transit is what makes it plunging. Aspiration → thick, mucoid, saliva-like fluid.Rules the differentials OUTA cyst confined above mylohyoid is a simple ranula; pus from Wharton duct with meal-related pain means sialadenitis or a stone.Excision of the sublingual gland — the gland is the source, so removing the cyst alone leaves it to recur.Routine"Plunging" is an anatomical statement: it has gone through mylohyoid.
Sternocleidomastoid tumor of infancyNeckL18 · slide 29“There’s a hard lump in the baby’s neck and she always turns her head to one side.”Related to congenital torticollis. A firm, painless, discrete mass within the sternocleidomastoid muscle that enlarges for 2 to 3 months and then regresses over 4 to 8 months.Palpate a firm, fusiform mass WITHIN the sternocleidomastoid muscle — it moves with the muscle, not independently. Assess head posture: the head tilts TOWARD and the chin turns AWAY from the affected side. Test passive neck rotation. Examine the hips — dysplasia is associated.
  1. Cervical lymphadenopathyNodes are separate from the muscle and often multiple
  2. Branchial cleft cystCystic and anterior to the muscle rather than inside it
  3. Cervical spine anomalyTorticollis with restricted movement but no muscle mass
Rules it INClinical → a mass within the muscle with the characteristic head posture and a birth history of difficult delivery. Ultrasound → fusiform thickening of the muscle itself, no discrete node. Hip ultrasound → associated dysplasia.Rules the differentials OUTA mass separate from the muscle is a node; cervical spine imaging → excludes a bony anomaly if movement stays restricted; a normal muscle on ultrasound excludes it.80% resolve spontaneously and need only physical therapy to prevent restrictive torticollis. Surgical excision is reserved for persistent cases.RoutineThe natural history is the treatment plan: it gets bigger before it gets better.
Thymic cystNeckL18 · slide 29“There’s a painless lump low in my child’s neck.” Usually found incidentally.Presents as a slow-growing, asymptomatic mass that may become painful if it is infected.Palpate a soft cystic mass in the LOWER lateral neck, often left-sided, sometimes extending toward the chest. Check whether it changes with position or Valsalva. Assess for airway or vascular compression.
  1. Branchial cleft cystUpper third of the neck rather than the lower
  2. LymphangiomaMultiloculated, transilluminates, posterior triangle
  3. Mediastinal extension of any cystThe reason chest imaging is part of the workup
Rules it INUltrasound → a cystic lower neck lesion. Computed tomography or magnetic resonance including the CHEST → continuity with the thymus or extension into the mediastinum, which changes the operation.Rules the differentials OUTAn upper-neck cyst anterior to the sternocleidomastoid is branchial; imaging showing no mediastinal connection excludes extension; multiloculated cysts suggest lymphangioma.Surgical excision.RoutineThe histology is the diagnosis; imaging only narrows the list.
Thyroglossal duct cystNeckL18 · slide 23“There’s a lump in the middle of my neck.” A parent may report it appearing after a sore throat.About one third of all congenital neck masses. A midline anterior neck mass, often asymptomatic until it becomes infected after an upper respiratory infection. Location varies — some sit lateral or as low as the thyroid, and those are hard to tell from a branchial cleft cyst.Palpate a MIDLINE mass, usually at or just below the hyoid. Ask the patient to swallow and then to protrude the tongue — it rises with both. That elevation is the diagnostic maneuver. Palpate the thyroid gland itself.
  1. Branchial cleft cystLateral, anterior to the sternocleidomastoid, and does not elevate
  2. Dermoid cystAlso midline, but it does NOT move with tongue protrusion
  3. Ectopic thyroid tissueMay be the patient's ONLY thyroid — excising it would leave them athyreotic
Rules it INUltrasound → a midline cystic lesion, AND confirmation that a normal thyroid gland is present in its usual place — that second finding is the one that must never be skipped. Thyroid function tests.Rules the differentials OUTAbsence of movement on tongue protrusion suggests a dermoid; a lateral position means branchial cleft; ultrasound showing no orthotopic thyroid means the mass is ectopic thyroid, not a cyst.Antibiotics if infected. Sistrunk operation is the standard: the cyst is excised with a cuff of tissue including the center of the hyoid bone, taking care not to injure the hypoglossal nerves.RoutineTaking the middle of the hyoid out is not overtreatment — leaving it behind is why these recur.
ActinomycosisNeckL18 · slide 34“My jaw has been swollen and lumpy for months and it’s started draining through the skin.”Presents as a painless, fluctuant neck mass in the submandibular or upper digastric region.Palpate a firm, indurated, woody mass, usually at the angle of the jaw. Look for sinus tracts discharging sulfur granules. Examine the dentition — poor dental hygiene or a recent extraction is the usual portal. Note that it crosses tissue planes, which infections usually do not.
  1. Tuberculous adenitisMatted nodes that fistulate too, but without sulfur granules
  2. Osteomyelitis of the mandibleBone pain with sequestra on imaging
  3. MalignancyHard, fixed, progressive — and it is why tissue is obtained
Rules it INAnaerobic culture, held for prolonged incubation → Actinomyces israelii. Microscopy of pus or granules → sulfur granules with branching filamentous gram-positive rods. Histology → the same granules in tissue.Rules the differentials OUTAcid-fast bacilli redirect to tuberculosis; malignant cells on histology change the diagnosis; absence of granules with a routine pyogenic organism means ordinary infection.Penicillin.RoutinePainless and fluctuant together is the combination that points here.
BrucellosisNeckL18 · slide 33“I’ve had fevers that come and go, sweats and aching joints — I drink unpasteurized milk.”Brucella, transmitted by ingestion of unpasteurized milk, most commonly in children. Total body lymphadenopathy with fever, fatigue and malaise.Palpate cervical nodes, liver and spleen. Take temperature over time to show the undulant pattern. Examine joints and the spine. Occupational and dietary history: farm work, abattoirs, unpasteurized dairy, travel.
  1. TuberculosisAlso chronic with fever and sweats; nodes matt and fistulate
  2. LymphomaFever, sweats and weight loss without an exposure history
  3. Infectious mononucleosisAcute, self-limiting, with a positive monospot
Rules it INBlood cultures held for prolonged incubation → Brucella species; warn the laboratory. Serum agglutination titres → a raised or rising titre. Bone marrow culture has a higher yield when blood cultures are negative.Rules the differentials OUTNegative serology with negative prolonged cultures excludes it; acid-fast bacilli redirect to tuberculosis; node biopsy showing lymphoma changes the diagnosis entirely.Trimethoprim-sulfamethoxazole or tetracycline.RoutineGeneralized rather than regional adenopathy is what sets it apart from the others on this slide.
Cat scratch diseaseNeckL18 · slide 34“My kitten scratched me and about two weeks later the glands in my neck came up.”Bartonella henselae, with a history of contact with cats. Common under 20 years of age. Lymphadenopathy — commonly preauricular and submandibular — with fever and malaise.Find the inoculation papule or pustule at the scratch, then palpate the draining regional nodes, which are tender and may suppurate. Examine the eyes — conjunctivitis with preauricular nodes is Parinaud oculoglandular syndrome. Palpate liver and spleen.
  1. TularemiaThe same ulcer-plus-node pattern with rabbit or tick exposure
  2. Atypical mycobacterial adenitisViolaceous overlying skin in a young child, no scratch history
  3. LymphomaPainless progressive nodes with constitutional symptoms and no inoculation site
Rules it INBartonella henselae serology → raised immunoglobulin G or M titres. Polymerase chain reaction of node aspirate → the organism. Node histology → stellate granulomas with necrosis, if biopsied.Rules the differentials OUTNegative Bartonella serology excludes it; tularemia serology covers the other zoonosis; acid-fast staining excludes mycobacterial disease; most cases resolve in 2 to 4 months, and failure to do so prompts a rethink.Self-limiting, or azithromycin.RoutineSelf-limiting is the headline; azithromycin shortens it rather than being required.
Reactive viral lymphadenopathyNeckL18 · slide 31“I got some sore lumps in my neck when I had that cold.”The commonest cause of cervical lymphadenopathy in children, associated with an underlying upper respiratory infection. Commonest pathogens are adenovirus, rhinovirus and enterovirus. Nodes regress in 1 to 2 weeks.Palpate multiple, small, soft, MOBILE, mildly tender nodes. Note size and site. Examine the pharynx, ears, teeth and scalp for the source. Palpate other nodal basins and the spleen — generalized adenopathy means something different.
  1. Bacterial suppurative adenitisA single large, hot, fluctuant, very tender node
  2. Infectious mononucleosisPosterior cervical nodes, marked fatigue, splenomegaly
  3. LymphomaPainless, rubbery, progressive, WITHOUT an infective source and with night sweats
Rules it INClinical → small mobile tender nodes with an identified infective source, regressing within 2 to 4 weeks. That regression is the confirmation. Investigate only if it persists.Rules the differentials OUTAny node persisting beyond 4 to 6 weeks, over 1.5 centimeters, hard, fixed, or supraclavicular gets fine needle aspiration → malignant cells would redirect entirely; a positive monospot means mononucleosis; fluctuance means suppuration.Observation.RoutineThe two numbers that matter are 1 cm and 4 to 6 weeks; past either, it stops being reactive.
ToxoplasmosisNeckL18 · slide 33“I’ve had swollen glands in my neck for weeks and I feel tired” — often with a cat at home or a taste for undercooked meat.Toxoplasma gondii, contracted through poorly cooked meat or ingestion of oocytes in cat feces. Fever, malaise, sore throat and myalgias with the adenopathy.Palpate painless or minimally tender posterior cervical nodes. Look for splenomegaly and a rash. Take an exposure history: cats, litter trays, undercooked meat. Fundoscopy if vision is affected. Pregnancy status matters enormously.
  1. Infectious mononucleosisThe closest mimic — both give posterior nodes and fatigue
  2. Cat scratch diseaseA papule at the scratch with regional nodes, also cat-associated
  3. LymphomaProgressive painless nodes with night sweats and weight loss
Rules it INToxoplasma serology, immunoglobulin M and G with avidity testing → acute infection; avidity distinguishes recent from remote. Node histology if biopsied → a characteristic reactive pattern.Rules the differentials OUTA positive monospot with atypical lymphocytes means mononucleosis; negative toxoplasma serology excludes it; Bartonella serology identifies cat scratch disease instead.Sulfonamides or pyrimethamine.RoutineOne of four exposure histories on the same slide — cat feces here, cat scratch for Bartonella.
Chronic pharyngitisThroat & larynxL19 · slide 80“My throat feels scratchy and irritated all the time — it’s been like this for months.”Causes: postnasal drip from chronic rhinosinusitis, irritants (dust, dry heat, chemicals, smoking, alcohol), chronic mouth breathing, voice abuse, allergy, granulomatous disease, connective tissue disorder, malignancy. Constant throat clearing, dry throat, odynophagia, a thickened and granular pharyngeal wall, and pharyngeal crusting.Inspect the pharynx for diffuse erythema, granularity or cobblestoning of the posterior wall. Look for the driver: postnasal drip, reflux, smoking, mouth breathing, dry environment. Examine the nose. Palpate the neck. Ask about the red flags — weight loss, otalgia, dysphagia, a neck mass.
  1. Laryngopharyngeal refluxPosterior laryngeal erythema and edema with throat clearing
  2. Allergic rhinitis with postnasal dripNasal itch, sneezing, boggy turbinates
  3. Oropharyngeal carcinomaThe red-flag diagnosis — a persistent unilateral lesion or ulcer
Rules it INClinical → persistent symptoms with a diffusely irritated pharynx and an identifiable irritant. Nasal endoscopy or laryngoscopy if it persists or red flags appear → the underlying source, and it excludes a tumor.Rules the differentials OUTAny persistent unilateral lesion or ulcer goes to biopsy; response to antireflux measures supports reflux; treating rhinitis and seeing the throat settle confirms postnasal drip.Address the underlying disorder, avoid precipitants, treat symptoms.RoutineMalignancy is on the causes list, so failed therapy earns a biopsy rather than another course of something.
Viral pharyngitisThroat & larynxL19 · slide 70, 72“My throat is sore, I’ve got a cough and a runny nose.”70% of pharyngitis. Adenovirus, Epstein-Barr virus, herpes simplex, HIV, influenza, parainfluenza, rhinovirus, coronavirus, echovirus, enteroviruses, coxsackievirus. Sore throat with earache or headache, cough, rhinitis, laryngitis, hoarseness, fever, conjunctivitis, lymphadenopathy. Herpangina is ulcerative vesicles over the tonsils.Inspect the pharynx for diffuse erythema, usually WITHOUT exudate. Palpate anterior cervical nodes. Check for fever. Note the presence of cough, rhinorrhea and hoarseness — these point AWAY from streptococcal infection. Palpate the spleen if fatigue is prominent.
  1. Streptococcal pharyngitisExudate, tender anterior nodes, fever, and NO cough
  2. Infectious mononucleosisPosterior nodes, marked fatigue, splenomegaly, palatal petechiae
  3. Peritonsillar abscessUnilateral with trismus and uvular deviation
Rules it INClinical → sore throat with cough and coryza, and a low Centor score. Rapid antigen test if streptococcal disease is plausible → negative supports viral etiology.Rules the differentials OUTCentor criteria — fever, tonsillar exudate, tender anterior nodes, ABSENCE of cough — score the likelihood; a positive rapid antigen or throat culture redirects to bacterial disease; a positive monospot with atypical lymphocytes means mononucleosis.Supportive: hydration, antipyretics, analgesia.RoutineThe presence of cough and coryza is what argues against streptococcal disease, and it is a Centor point.
Acute laryngitisThroat & larynxL19 · slide 57“I lost my voice with this cold — it’s been a few days.”The commonest cause of hoarseness, persisting about a week after upper respiratory symptoms have cleared. Viral (rhinovirus commonest, parainfluenza, respiratory syncytial virus, adenovirus, influenza, pertussis), bacterial or fungal; also acid reflux, smoking, toxic inhalation, cough, vocal abuse, direct injury and allergy. Dysphonia, low-grade fever, hoarseness, cough, rhinitis and postnasal drip.Assess voice and listen for stridor, which would mean something more serious. Examine the pharynx. Check for fever and lower respiratory signs. Note the duration — under three weeks is the point.
  1. Chronic laryngitisBeyond three weeks, and it requires visualization
  2. EpiglottitisSevere odynophagia, drooling, toxicity — the emergency to exclude
  3. Laryngeal carcinomaPersistent hoarseness with risk factors; excluded by time course here
Rules it INClinical → hoarseness with an upper respiratory infection, resolving within one to three weeks. No investigation is needed if it settles. Laryngoscopy if it does not.Rules the differentials OUTDrooling and severe odynophagia redirect urgently to supraglottitis; hoarseness persisting beyond three weeks means laryngoscopy, which is what excludes carcinoma; stridor changes the priority to the airway.Conservative: hydration, antipyretics, voice rest, decongestants, humidification, smoking cessation. Antibiotics are not indicated unless a secondary bacterial infection is suspected.RoutineVoice rest is the treatment patients most often skip and most need.
Vocal cord nodulesThroat & larynxL19 · slide 46–47“I’m a teacher and my voice is hoarse by the end of every day — it’s been months.”Smooth, paired lesions at the junction of the anterior one third and posterior two thirds of the vocal folds, from vocal abuse. The commonest cause of persistent dysphonia in children — screamers' nodules, and a frequent cause of voice deterioration in professional singers — singers' nodules.Listen to voice quality and how it changes with use. Ask about vocal demand and abuse: shouting, singing, professional voice use, smoking, reflux. Palpate the neck. Any hoarseness beyond two to three weeks gets the larynx VISUALIZED — that rule is what the station is testing.
  1. Vocal cord polypUsually UNILATERAL and often follows a single vocal injury
  2. Laryngeal carcinomaThe reason hoarseness is never watched indefinitely — smoker, weight loss, otalgia
  3. Reflux laryngitisDiffuse posterior erythema and edema without discrete lesions
Rules it INLaryngoscopy, flexible or with videostroboscopy → BILATERAL, symmetric lesions at the junction of the anterior and middle thirds of the cords — that symmetry and site name them. Stroboscopy shows the mucosal wave impairment.Rules the differentials OUTA unilateral lesion is a polyp or a tumor, not a nodule; an irregular, ulcerated or fixed cord goes to biopsy; improvement with voice therapy alone supports the diagnosis.Speech therapy is first line in adults and children. Photodocumentation in the voice clinic tracks progress; microlaryngoscopy if needed.RoutineBilateral and symmetric is the finding that separates nodules from a polyp, which is unilateral.
Gingivitis and periodontitisMouth & salivaryL19 · slide 118–122“My gums bleed when I brush and my breath is bad.” Later, “my teeth feel loose.”Chronic infection of the gingiva beginning with bacterial plaque at the gum line. Gingivitis is the mildest form: erythematous, edematous gums that bleed easily, with little or no discomfort, caused by inadequate oral hygiene — and reversible with professional treatment and good home care. Untreated it becomes periodontitis: plaque spreads below the gum line, bacterial toxins provoke a chronic inflammatory response in which the body turns on itself, gums separate from teeth, pockets form and become infected, the periodontal ligament and bone are destroyed, and teeth loosen and fall out. Risk: diabetes, smoking, aging, genetics, stress, poor nutrition, puberty, pregnancy, substance abuse, HIV and certain medications. Gram-negative organisms.Inspect gingivae for erythema, edema and bleeding on gentle probing. Assess tooth MOBILITY and look for gingival recession — those separate periodontitis from gingivitis. Note plaque and calculus. Ask about diabetes, smoking and medications such as phenytoin and calcium channel blockers.
  1. Necrotising ulcerative gingivitisPunched-out interdental papillae with severe pain and fetor
  2. Leukemic gingival infiltrationBoggy hypertrophied gums with bruising and systemic illness
  3. Drug-induced gingival hyperplasiaOvergrowth linked to a specific medication
Rules it INClinical with periodontal probing → gingivitis is inflammation with NO attachment loss and is REVERSIBLE; periodontitis shows pocket depths over 3 millimeters with attachment loss and is NOT. Dental radiographs → alveolar bone loss confirming periodontitis. Blood glucose and HbA1c.Rules the differentials OUTAbsence of pocketing and bone loss means gingivitis alone; full blood count → excludes leukemia if the gums are boggy and the patient is unwell; a medication review explains drug-induced overgrowth.Professional cleaning and oral hygiene — brushing, flossing, mouthwash — and modifying risk.RoutinePeriodontal disease and dental caries are the primary causes of tooth loss. The slides also link gum disease to endocarditis risk, pneumonia, osteoporosis and, in men, kidney, pancreatic and blood cancers.
Impacted teethMouth & salivaryL19 · slide 125“My back gum is sore and swollen and I can’t open my mouth properly” — typically a young adult with wisdom teeth.Impaction is usually caused by overcrowding and insufficient room for a new tooth to emerge. Wisdom teeth are the usual culprits, being the last permanent teeth to erupt into a jaw that may not accommodate them. Impacted teeth are more likely to become infected.Inspect the retromolar area for an operculum — a flap of gum over a partially erupted tooth — with erythema and pus. Measure mouth opening. Palpate for swelling and cervical nodes. Assess the floor of mouth and the airway if swelling is significant.
  1. PericoronitisInfection around the operculum — the usual complication
  2. Dental abscessArises from a carious tooth with apical rather than pericoronal swelling
  3. Dentigerous cystA painless expanding radiolucency around an unerupted crown
Rules it INPanoramic radiograph → the impacted tooth, its angulation, and its relation to the inferior alveolar canal — that relation is what the surgeon plans around. It also shows any associated cyst.Rules the differentials OUTAn apical radiolucency on a carious tooth means a periapical abscess instead; a well-defined pericoronal radiolucency over 3 millimeters suggests a dentigerous cyst; trismus with a raised floor of mouth means spread and changes urgency.Usually removed — they are of little use in chewing.RoutineA pericoronal abscess is the complication that links this row to the dental abscess row.
MalocclusionMouth & salivaryL19 · slide 126“My teeth don’t meet properly and it’s hard to chew” — or the concern is entirely about appearance.Abnormal alignment of the teeth and the way upper and lower teeth fit together. Normal chewing produces about 150 lb of force on the molars, and about 250 lb when clenching during sleep; if that force is unevenly distributed, teeth wear, fracture or loosen. Causes: size mismatch between jaw and teeth, thumb sucking or tongue thrusting, lost teeth, birth defects. Slide 126 illustrates Class I normal occlusion, Class II distal occlusion and Class III mesial occlusion.Ask the patient to bite together and inspect the relationship of the molars and incisors. Note overjet, overbite, crossbite and crowding. Assess jaw opening and listen for temporomandibular joint clicking. Check for mouth breathing and tongue thrust. Examine facial symmetry.
  1. Temporomandibular joint disorderPain, clicking and limited opening; often coexists
  2. Skeletal jaw discrepancyThe mismatch is in the bones, not just the teeth — it changes the treatment
  3. Acquired malocclusion after fractureA traumatic history with a sudden change in bite
Rules it INClinical bite assessment → the Angle classification: class I normal molar relationship, class II retrognathic, class III prognathic. Panoramic and cephalometric radiographs → whether the discrepancy is dental or skeletal, which decides braces versus surgery. Study models.Rules the differentials OUTA SUDDEN change in bite after trauma means a mandibular or maxillary fracture and needs computed tomography, not an orthodontic referral; cephalometric analysis separates skeletal from dental causes; joint imaging addresses the temporomandibular component.Braces or aligners, removal of teeth, or surgery.RoutineThe force numbers are the reason a bite problem becomes a structural one.
Temporomandibular joint disordersMouth & salivaryL19 · slide 128–131“My jaw clicks and aches, especially in the morning, and sometimes it locks.”Disorders affecting the temporomandibular joint, the masticatory muscles, or both. The second commonest musculoskeletal condition causing pain and disability. Common in women of childbearing age, with a possible link to female sex hormones. Predisposing: trauma — a blow to the jaw or whiplash — and stress, which disrupts sleep and increases nocturnal bruxism. Perpetuated by stress, poor coping, clenching and grinding, and poor posture. Three categories: myofascial pain, internal derangement (displaced disc, dislocated jaw, condylar injury), and arthritis. Jaw, face and head pain; limited opening, catching or locking; clicking, popping or grating; headache, neck and shoulder pain; tinnitus, ear fullness, hearing loss, dizziness; abnormal tooth wear and sensitivity.Palpate the joint just anterior to the tragus while the patient opens and closes, and palpate the masseter and temporalis for tenderness. Measure maximal opening — under about 40 millimeters is restricted. Note clicking, crepitus and deviation of the jaw on opening. Examine the bite and check for bruxism wear facets. Examine the ear, which is normal — this is a common cause of referred otalgia.
  1. Otitis media or externaEar pain with an ABNORMAL ear examination; here the ear is normal
  2. Dental pathologyA percussion-tender tooth localizes the pain
  3. Giant cell arteritisJaw CLAUDICATION on chewing in an older patient, with scalp tenderness
Rules it INClinical → joint or muscle tenderness with clicking, deviation and restricted opening. Imaging is not routine; magnetic resonance if it persists → disc displacement; computed tomography → degenerative or bony change.Rules the differentials OUTAn abnormal ear examination redirects to ear disease; a percussion-tender tooth means dental pain; in a patient over 50 with jaw pain on chewing, inflammatory markers to exclude giant cell arteritis — missing that costs vision.Eliminate pain and restore function: self care; non-steroidal anti-inflammatories, muscle relaxants (cyclobenzaprine), low-dose tricyclics (amitriptyline, desipramine, nortriptyline); oral steroids if there is synovitis; physical therapy, transcutaneous electrical nerve stimulation, acupuncture, local anesthesia, mouth guards, arthrocentesis, arthroscopy, surgery.RoutineThe ear symptoms are the trap — tinnitus, fullness and dizziness send these patients to an ear examination that is normal.
Oral candidiasis (thrush)Mouth & salivaryL19 · slide 88–90“I’ve got white patches in my mouth and things taste odd” — often after antibiotics or in an inhaler user.Candida albicans; Aspergillus may also be cultured. Common in infants and the immunosuppressed. Risk factors: dentures, poor oral hygiene, diabetes, anemia, chemotherapy or local irradiation, corticosteroids, broad-spectrum antibiotics, age, HIV. Creamy white curd-like patches on an erythematous base, painful, granular, usually on buccal mucosa and tongue, with fever, lymphadenopathy, odynophagia and taste change.Inspect for creamy white plaques. SCRAPE one with a tongue depressor — it comes off, leaving an erythematous, sometimes bleeding base. That is the diagnostic maneuver. Examine denture-bearing areas and the angles of the mouth. Ask why: inhaled steroids, antibiotics, diabetes, immunosuppression.
  1. LeukoplakiaDoes NOT scrape off — and it is premalignant
  2. Lichen planusLacy striae that do not wipe away
  3. Hairy leukoplakiaOn the LATERAL TONGUE, does not scrape off, marks immunosuppression
Rules it INClinical → plaques that wipe off with an erythematous base. Potassium hydroxide preparation or a swab → budding yeasts and pseudohyphae. Blood glucose and HIV testing if there is no obvious cause → the underlying reason.Rules the differentials OUTA plaque that will not scrape off is leukoplakia and needs biopsy; lacy striae mean lichen planus; unexplained thrush in an adult is a reason to look for immunosuppression, not just to prescribe an antifungal.Saline and peroxide washes; topical antifungals — nystatin suspension, clotrimazole, ketoconazole, fluconazole. HIV patients may need longer fluconazole; refractory disease needs itraconazole or voriconazole.RoutineThe patches rub off with a tongue depressor. Leukoplakia and lichen planus do not — that single maneuver separates three diagnoses.
Fordyce granulesMouth & salivaryL19 · slide 10“There are little yellow spots inside my lip and cheek — are they normal?”Normal variants — ectopic sebaceous glands in a site where sebaceous glands are not expected. Small yellow-white papules on the vermilion of the lip and the buccal mucosa.Inspect for multiple small yellow-white papules on the buccal mucosa and vermilion border. They are painless, symmetric and do not ulcerate. Palpate to confirm they are soft and superficial.
  1. Oral candidiasisWipes off; white rather than yellow, and often symptomatic
  2. Lichen planusLacy striae rather than discrete papules
  3. Sebaceous hyperplasia or a small lipomaDiscrete solitary lesion rather than a scattered field
Rules it INClinical → ectopic sebaceous glands, a normal variant present in most adults. No investigation and no treatment are needed.Rules the differentials OUTA lesion that wipes off is candida; anything ulcerating, growing or solitary is not a Fordyce granule and needs a closer look.None — reassurance.RoutinePatients find them alarming because they appear suddenly to the person looking; they have always been there.
LeukoedemaMouth & salivaryL19 · slide 9“The inside of my cheeks looks grayish-white” — usually noticed by a dentist, not the patient.A common, benign mucosal change and a normal variant, caused by accumulation of fluid within the epithelial cells. Diffuse grayish-white appearance of the buccal mucosa.Inspect the buccal mucosa bilaterally for a diffuse gray-white filmy appearance. STRETCH the mucosa — the whiteness DISAPPEARS. That single maneuver makes the diagnosis. Note that it is bilateral and symmetric.
  1. LeukoplakiaDoes NOT disappear on stretching, and cannot be wiped off — and it is premalignant
  2. Oral candidiasisWipes off leaving an erythematous base
  3. Lichen planusLacy white striae in a defined pattern, often with erosions
Rules it INClinical → the whiteness resolving on stretching, bilateral and symmetric. No biopsy is required. It is a normal variant, commonest in darker-skinned individuals.Rules the differentials OUTPersistence on stretching means leukoplakia and warrants biopsy; a plaque that wipes off means candidiasis; unilateral or localized lesions are not leukoedema.None — reassurance.RoutineNaming it as a variant is the whole job; it needs no biopsy and no follow-up.
Physiologic pigmentationMouth & salivaryL19 · slide 11“My gums have brown patches” — usually long-standing and asymptomatic.Physiologic oral pigmentation is commonly seen and is a normal variant, from melanin.Inspect for symmetric brown pigmentation, most often on the attached gingiva. Confirm it is long-standing and stable — that history does most of the work. Check for pigmentation elsewhere and review medications. Note any single, growing or irregular lesion separately.
  1. Oral melanomaA single, irregular, growing pigmented lesion — rare but the reason to look carefully
  2. Smoker's melanosisRelated to smoking and improves on cessation
  3. Addison disease or drug-induced pigmentationNew, generalized, with systemic features or a culprit drug
Rules it INClinical → symmetric, stable, long-standing pigmentation, commonest in darker-skinned individuals. Biopsy any lesion that is solitary, asymmetric, growing or newly appeared → the histological diagnosis.Rules the differentials OUTMorning cortisol and electrolytes → excludes Addison disease if pigmentation is new and generalized; a medication review explains drug-induced change; benign histology excludes melanoma.None — reassurance.RoutineThe reason it matters is the differential it sits in, not the lesion itself.
Aphthous stomatitis (canker sores)Mouth & salivaryL19 · slide 15–17“I keep getting painful ulcers in my mouth — they come and go and last about a week.”The commonest cause of acute recurrent oral ulcers in adolescents and young adults. Found on freely moving, non-keratinized mucosa — buccal and labial mucosa, non-attached gingiva, palate. Trauma (cheek biting, a dental procedure) and stress are exacerbating factors; the cause is unknown, though human herpesvirus 6 has been suggested. Minor (<1 cm) are commonest, burn and tingle first, and last 7–10 days. Major (>1 cm) are more painful, multiple, scar, and last over a month. Herpetiform are numerous 1–3 mm ulcers, scar, and last over a month.Inspect for shallow, round or oval ulcers with a gray-yellow base and an erythematous halo, on NON-KERATINIZED mucosa — buccal, labial, floor of mouth, not the hard palate or gingiva. Count and size them. Look for genital ulcers and eye inflammation before calling them simple.
  1. Herpes simplexVesicles first, on KERATINIZED mucosa, clustered rather than solitary
  2. Behcet syndromeOral ulcers PLUS genital ulcers and uveitis — the reason to ask
  3. Squamous cell carcinomaA single ulcer that does NOT heal in two weeks, with induration
Rules it INClinical → recurrent painful ulcers on non-keratinized mucosa healing within 7 to 14 days without scarring. Full blood count, ferritin, folate, vitamin B12 and celiac serology if severe or frequent → a treatable deficiency or celiac disease.Rules the differentials OUTAny ulcer persisting beyond two weeks is biopsied to exclude carcinoma. Vesicles on keratinized mucosa mean herpes; genital ulceration and eye disease redirect to Behcet syndrome.Observation — it is self-limiting. Anti-inflammatories, antibiotics, antivirals, oral and topical corticosteroids (triamcinolone, fluocinonide), cauterization with silver nitrate, Lactobacillus capsules, dilute water rinses.RoutineRecurrent aphthous stomatitis is called Sutton disease. Non-keratinized mucosa is the location rule that separates it from herpes.
Herpes simplex ulcersMouth & salivaryL19 · slide 25–27“I got a tingle first, then blisters that broke into ulcers — it happens whenever I’m run down.”Herpes simplex virus 1 and 2. Herpetic gingivostomatitis is the commonest manifestation of primary infection in children and young adults, with fever, malaise and cervical lymphadenopathy. Secondary disease is recurrence of dormant virus from the trigeminal ganglion, triggered by stress, trauma, immunosuppression or ultraviolet light. Small painful lesions that ulcerate, leaving an erythematous base with a gray cover; heals without a scar; resolves in 1–2 weeks.Inspect for clustered vesicles that rupture into shallow ulcers on KERATINIZED mucosa — hard palate, attached gingiva, vermilion border. Primary infection gives a gingivostomatitis with fever; recurrences are localized. Palpate for tender nodes. Check immune status if severe.
  1. Aphthous ulcersNON-keratinized mucosa, no vesicles, no prodrome
  2. Herpangina or hand-foot-and-mouthPosterior oropharynx, in children, with a different pattern
  3. Erythema multiformeTarget lesions on the skin with widespread mucosal erosions
Rules it INClinical → the prodrome, vesicles and site. Polymerase chain reaction of a swab from a deroofed vesicle → herpes simplex virus, and it is the most sensitive test. Tzanck smear → multinucleated giant cells, but it does not distinguish herpes simplex from varicella zoster.Rules the differentials OUTA negative polymerase chain reaction from a fresh vesicle excludes it; ulcers on non-keratinized mucosa without vesicles are aphthous; target lesions redirect to erythema multiforme.Oral acyclovir for treatment and prophylaxis.RoutineThe 24-hour prodrome is the window in which treatment works best, so patients are taught to recognize it.
ParotitisMouth & salivaryL19 · slide 44“Both sides of my face are swollen in front of my ears and it hurts to chew.”Painful swelling of the parotid gland. Causes: viral — mumps (paramyxovirus), herpes, Epstein-Barr virus — and also bacterial infection, diabetes, tumors, stones and dental problems.Inspect for swelling that obscures the angle of the mandible and lifts the earlobe outward and upward — that is what makes it parotid rather than nodal. Palpate for tenderness. Milk Stensen duct. Check cranial nerve VII. Ask about immunization and contacts, and examine the testes in a male.
  1. Suppurative parotitisUnilateral with PUS from the duct
  2. Cervical lymphadenopathyDiscrete nodes that do not lift the earlobe or obscure the mandibular angle
  3. Parotid neoplasmA discrete firm mass rather than diffuse gland swelling
Rules it INClinical → diffuse bilateral parotid swelling with the earlobe lifted. Mumps polymerase chain reaction on a buccal swab, with immunoglobulin M serology → confirms mumps. Serum amylase → raised from salivary origin. Ultrasound → distinguishes diffuse gland inflammation from a discrete mass or abscess.Rules the differentials OUTPus on milking the duct means bacterial infection; a discrete mass on ultrasound needs aspiration for tumor; facial nerve weakness is never inflammatory parotitis and points to malignancy.Directed at the cause.RoutineIt is a presentation, not a single disease — the work is deciding which of the causes it is.
SialolithiasisMouth & salivaryL19 · slide 40–43“Whenever I start to eat, my gland under the jaw swells up and aches — then it goes down again.”Salivary calculi. Change in saliva viscosity, ductal injury or stagnation causes calcium phosphate and calcium carbonate to precipitate. 80–90% occur in the submandibular gland — the duct runs a longer course, and the saliva has higher mucin, alkaline content, calcium and phosphate. 10–20% parotid. Commoner in men. Risk: long illness with dehydration, gout, diabetes, hypertension.Bimanual palpation along the floor of the mouth, back to front, to feel a stone in Wharton duct. Milk the duct and observe the saliva — reduced or absent flow rather than pus. Note the meal-related pattern. Palpate the gland for size and tenderness.
  1. Acute suppurative sialadenitisConstant pain with PUS at the duct, not meal-related swelling
  2. Salivary neoplasmPainless, persistent, progressive — it does not fluctuate with meals
  3. Duct strictureThe same obstructive pattern without a palpable stone
Rules it INUltrasound → an echogenic focus with acoustic shadowing, the first-line test. Non-contrast computed tomography → a radiopaque calculus; about 80% of submandibular stones are radiopaque. Sialendoscopy → direct visualization, and it can treat at the same time.Rules the differentials OUTPus at the duct redirects to acute infection; a persistent mass with no stone on imaging needs cytology for neoplasm; a stricture on sialendoscopy explains obstruction without a stone.By location and size: intraoral extraction if palpable or visible anteriorly; gland excision for large stones in the hilum or body; sialoendoscopy, the minimally invasive option that can avoid removing the gland; lithotripsy. Conservative: hydration, hot compresses, massage, non-steroidal anti-inflammatories, lozenges.RoutinePain that arrives with the first mouthful and settles afterwards is the history that makes this diagnosis without any test.

Urgent54 conditions

Still a referral rather than an emergency, but measured in days, not weeks. The commonest way to get one of these wrong is to manage it correctly and too slowly.

Condition How the patient describes it
the words they actually use		 What you see on inspection Physical exams to rule it in or out
the maneuvers, not the findings		 Top 3 differentials
and what separates each one		 Tests — and what a positive looks like Treatment & referral Patient education
AIDS-related sensorineural lossEarL16 · slide 67“My hearing has got worse” — in a patient known to be, or at risk of being, immunocompromised.Sensorineural loss is among the numerous neurological manifestations of AIDS. It may come from an infectious complication — cryptococcal meningitis or syphilis — or be a primary neurological manifestation.Otoscopy — look for opportunistic infection and Kaposi lesions. Audiometry. Review antiretroviral and antimicrobial drugs for ototoxicity, which is often the real cause. Full cranial nerve examination.
  1. OtotoxicityFrom the treatment rather than the disease — commonly the actual mechanism
  2. Opportunistic central nervous system infectionFocal neurological signs alongside the hearing loss
  3. Otitis media with effusionA conductive loss, more common in this group too
Rules it INAudiometry → a sensorineural loss. Human immunodeficiency virus serology and CD4 count → the diagnosis and degree of immunosuppression. Imaging if focal signs → an opportunistic lesion.Rules the differentials OUTA conductive pattern redirects to middle ear disease; improvement after stopping a culprit drug points to ototoxicity; normal imaging excludes a central lesion.Treat the underlying cause.UrgentIt is on the list so that unexplained loss prompts a risk-factor history rather than an audiogram alone.
Acoustic traumaEarL16 · slide 56–57“A firework went off next to me and that ear has been ringing and muffled ever since.”A single loud noise creating immediate hearing loss, and it may perforate the tympanic membrane. Blows to the head can cause labyrinthine injury with resulting sensorineural loss. Penetrating injuries are rare but usually involve subluxation of the stapes, causing profound sensorineural loss.Otoscopy — look for a perforation, since blast can do both. Weber and Rinne; the pattern may be mixed. Assess for vertigo.
  1. Noise-induced hearing lossCumulative exposure rather than one event
  2. Tympanic membrane perforationConductive loss from the blast; the drum shows the tear
  3. Perilymphatic fistulaVertigo with sensorineural loss and pressure sensitivity
Rules it INAudiometry → a sensorineural loss, often with tinnitus, from a single event; a mixed pattern if the drum is also perforated.Rules the differentials OUTA pure conductive loss with a visible perforation is the drum alone; persistent vertigo raises a fistula; a gradual course excludes acute trauma.Supportive; ENT for perforation or suspected ossicular injury.UrgentOne event can do what years of exposure does — and a penetrating injury threatens balance as well as hearing.
Autoimmune sensorineural lossEarL16 · slide 65–66“My hearing has dropped in both ears over a few weeks — and my joints have been sore.”Sensorineural loss that is most often bilateral and progressive, with periods of deterioration and stabilization, and may be accompanied by vestibular dysfunction. Uncommon: Cogan's syndrome, polyarteritis nodosa, relapsing polychondritis, granulomatosis with polyangiitis. Even less common: scleroderma, temporal arteritis, systemic lupus erythematosus, sarcoidosis.Otoscopy is normal. Serial tuning forks and audiometry to show progression. Look for systemic autoimmune disease — joints, skin, eyes (interstitial keratitis suggests Cogan syndrome), kidneys.
  1. Sudden sensorineural hearing lossSudden and usually unilateral rather than progressive and bilateral
  2. Meniere diseaseEpisodic vertigo with fullness and fluctuating low-frequency loss
  3. Syphilitic lossCan mimic it exactly — which is why serology is sent
Rules it INSerial audiometry → a rapidly progressive bilateral asymmetric sensorineural loss over weeks to months. Autoimmune screen (antinuclear antibody, inflammatory markers) and a trial of corticosteroids → improvement supports the diagnosis.Rules the differentials OUTNegative treponemal serology excludes syphilis; a stable audiogram over months excludes it; no steroid response argues against it.Treat the underlying disease.UrgentThe stepwise pattern — worse, then stable, then worse — is what distinguishes it from a steady decline.
OtotoxicityEarL16 · slide 52–53“Since I started that new medication my ears ring and my hearing is worse.”Aminoglycosides are the most ototoxic and the most common — monitor peak levels. Also furosemide, aspirin and platinum-based chemotherapy. Many other agents have potential ototoxicity, and drugs that are ototoxic are frequently also nephrotoxic and vice versa, including the non-steroidal anti-inflammatories. Produces bilateral sensorineural hearing loss.Review every medication and the cumulative dose — this is the examination that matters. Otoscopy is normal. Weber and Rinne give a sensorineural pattern. Assess gait and do the head impulse test, since some agents hit balance rather than hearing.
  1. PresbycusisAge-related and gradual, with no temporal link to a drug
  2. Noise-induced lossA 4000 hertz notch and an exposure history
  3. Meniere diseaseEpisodic vertigo with fluctuating LOW-frequency loss and fullness
Rules it INSerial audiometry → a bilateral, symmetric, HIGH-frequency sensorineural loss that progresses with dosing. Drug levels where relevant → troughs above target. Loop diuretic loss may be reversible; aminoglycoside loss usually is not.Rules the differentials OUTA loss that predates the drug excludes it; asymmetry points elsewhere and needs imaging; low-frequency fluctuating loss redirects to Meniere disease.Stop or change the agent where possible; the loss is often not reversible.UrgentIf a drug is ototoxic, ask about the kidneys too — the two toxicities travel together.
Perilymphatic fistulaEarL16 · slide 63–64“Since the dive, when I strain or hear a loud noise the room tilts.”A pathological communication between the perilymphatic space of the inner ear and the middle ear, at the round or oval window. Congenital or acquired. Acquired causes: barotrauma, temporal bone trauma, or a complication of stapedectomy. Presents as sudden sensorineural loss and vertigo after head injury, barotrauma, or heavy lifting and straining, sometimes with an audible “pop”. A rare cause of vertigo and sensorineural loss.Fistula test — pressure on the tragus provokes vertigo or nystagmus. Ask about symptoms on straining, coughing or lifting. Otoscopy. Weber and Rinne. Assess gait.
  1. Meniere diseaseSpontaneous episodic vertigo, not provoked by pressure or sound
  2. BarotraumaConductive loss from the same event, without vertigo or sensorineural loss
  3. Superior canal dehiscenceSound-induced vertigo too, but with autophony and a bony defect on imaging
Rules it INAudiometry → a fluctuating sensorineural loss. High-resolution computed tomography of the temporal bone → a bony defect or pneumolabyrinth. Exploratory tympanotomy → visible perilymph leak, which is definitive.Rules the differentials OUTA negative fistula test with a purely conductive loss points to simple barotrauma; a dehiscent superior canal on fine-cut imaging redirects the diagnosis.Treat symptomatically and refer to ENT.UrgentThe trigger is the diagnosis: sudden hearing loss and vertigo that began with a strain, a dive or a blow.
Syphilitic sensorineural lossEarL16 · slide 35, 68“My hearing and balance have both been going.” — the history may include nothing obvious.Congenital or acquired. Hearing loss is not associated with primary acquired syphilis, but reaches as high as 80% in symptomatic neurosyphilis. Presentation is often indistinguishable from Ménière's: fluctuating sensorineural loss, tinnitus, aural fullness and episodic vertigo.Otoscopy is normal. Audiometry and tuning forks. Look for systemic signs and take a sexual history. Ophthalmic examination for interstitial keratitis. Fistula test may be positive without a fistula (Hennebert sign).
  1. Autoimmune sensorineural lossThe clinical twin — separated only by serology
  2. Meniere diseaseEpisodic, with the classic triad, and no systemic features
  3. Acoustic neuromaUnilateral and progressive, with imaging findings
Rules it INTreponemal serology (fluorescent treponemal antibody absorption or equivalent) → reactive. Lumbar puncture if neurosyphilis is suspected → reactive cerebrospinal fluid with pleocytosis. Audiometry → a fluctuating or progressive sensorineural loss.Rules the differentials OUTNon-reactive treponemal serology excludes it and redirects to the autoimmune workup; normal imaging excludes a schwannoma.Antibiotic with the addition of systemic corticosteroids.UrgentIt is tested for precisely because it is a potentially treatable cause of sensorineural loss hiding behind a Ménière's picture.
Glomus tumorEarL16 · slide 50“I hear my own heartbeat whooshing in my ear all the time, in time with my pulse — and my hearing on that side is going.”Benign but highly vascular tumor derived from the normal glomus formations of the middle ear and jugular bulb. Produces a middle ear mass effect, can present with spontaneous hemorrhage and paralysis of cranial nerves IX, X and XI, and may erode the skull base.Otoscopy for a red or blue pulsatile mass behind the drum. Brown sign — the mass blanches on positive pressure with the pneumatic otoscope. Auscultate for a bruit. Cranial nerves VII and IX to XII. Never biopsy it in clinic.
  1. High-riding jugular bulbA vascular variant, also blue behind the drum, but not a tumor
  2. Aberrant internal carotid arteryPulsatile too — and biopsy would be catastrophic
  3. HemotympanumBlood behind the drum after trauma; not pulsatile
Rules it INComputed tomography and magnetic resonance with angiography → an intensely enhancing mass with a salt and pepper pattern of flow voids and bone erosion. Urinary catecholamines if it is secreting.Rules the differentials OUTImaging is what excludes the vascular variants — and it must come BEFORE any instrument touches the mass; a trauma history with a non-pulsatile blue drum is hemotympanum.ENT and skull base management.UrgentPulsatile tinnitus with a mass behind the drum is not reassured away.
Hematoma of the external earEarL15 · slide 39–42“I got hit in the ear wrestling and it’s swollen up.”Blood pooling in the sub-perichondrial space, usually after blunt trauma. The collection keeps oxygen and nutrients from the cartilage, which is what risks necrosis. May develop hours after the injury, so patients are re-checked at 12–24 hours. Examination: edema and ecchymosis of the auricle with loss of the cartilaginous landmarks.Inspect for loss of the normal cartilaginous contours. Palpate for fluctuance. Check the canal and drum are intact. Look for other head injury.
  1. PerichondritisInfected, hot, exquisitely tender, and it spares the lobule
  2. Simple contusionBruising WITHOUT a fluctuant collection lifting the perichondrium
  3. Relapsing polychondritisRecurrent, bilateral, non-traumatic, also sparing the lobule
Rules it INClinical → a fluctuant swelling obscuring the contours; aspiration or incision → blood, which both confirms and treats.Rules the differentials OUTNo fluctuance means contusion, not hematoma; hot, spreading erythema means perichondritis and needs antibiotics; bilateral non-traumatic disease suggests polychondritis.Drain it — incision or large-needle aspiration — and do it early. After 7 days granulation tissue makes drainage much harder. Follow with irrigation and topical and/or systemic antibiotics. Ear splinting improves the cosmetic result and prevents re-accumulation: cotton bolsters, plaster molds, silicone putty, thermoplastic splints.UrgentEarly diagnosis and drainage is what prevents cauliflower ear. Come back at 12–24 hours even if it looks minor, because the hematoma can appear late.
Lacerations and avulsionEarL15 · slide 43“I caught my ear and it’s torn open and bleeding — will it heal straight?” The cosmetic worry is usually as prominent as the pain.Blunt or sharp trauma to the auricle. Prompt repair and infection prevention are critical. Simple lacerations close with sutures; complex ones and avulsions may need debridement first; tissue grafts if there is tissue loss. If avulsed tissue is recovered, reattachment is often successful.Assess the wound for cartilage exposure. Examine the canal and drum. Check facial nerve function and look for other injuries. Tetanus status.
  1. Simple skin lacerationCartilage NOT exposed; a far simpler repair
  2. Auricular hematomaClosed injury with fluctuance rather than a break in the skin
  3. Avulsion with vascular compromiseA pale, cold segment needing specialist salvage
Rules it INDirect inspection → whether cartilage is exposed and whether the segment is perfused, which determines who repairs it.Rules the differentials OUTIntact perfusion with skin-only injury excludes the complex repairs; an intact drum excludes middle ear injury.Repair as above, then cover with a pressure dressing to prevent a hematoma forming under the repair.UrgentBring any avulsed tissue — reattachment often works.
Foreign body of the auricleEarL15 · slide 51–52“My piercing has gone into the skin” or “there’s something stuck in the outer part of my ear.”Piercings becoming embedded in the earlobe or elsewhere on the auricle. Most common in girls and young adolescents with pierced ears. Pain, erythema and edema; may have purulent drainage from the piercing site. Examination: pain on palpation, and the foreign body may be palpable.Inspect for an embedded object and any cartilage involvement. Palpate for fluctuance and look for spreading erythema. Examine the canal too.
  1. PerichondritisInfection of cartilage, hot and tender, sparing the lobule
  2. Auricular hematomaFluctuant collection without a retained object
  3. KeloidA firm overgrowth at an old piercing site rather than an acute problem
Rules it INInspection → the object and whether cartilage is breached; cartilage involvement is what raises the stakes.Rules the differentials OUTAbsent erythema and tenderness excludes perichondritis; a chronic firm nodule at a piercing is a keloid, not a foreign body.Removal under local anesthetic; younger or non-compliant patients may need sedation.UrgentInfection is the biggest concern, not the object itself.
Foreign body of the canalEarL15 · slide 49–50“There’s something in my ear” — or a parent noticed a child pushing something in. An insect gives “I can hear it moving.”Commoner in children but possible at any age, and can be anything that fits — beads, popcorn, crayons, insects, pencil erasers, paper. Otalgia varies with the shape of the object; bloody discharge if the canal lining is damaged; fullness and foreign body sensation.Otoscopy to identify the object and see past it to the drum. Note whether it is organic (must not be irrigated, it swells) or a button battery (immediate removal). Re-examine the canal and drum after removal.
  1. Cerumen impactionWax rather than an object; irrigation is safe
  2. Otitis externaDiffuse canal edema and tragal tenderness with no object
  3. OtomycosisFungal debris that can look like material but shows hyphae
Rules it INOtoscopy → direct visualization of the object, and an intact drum after removal.Rules the differentials OUTSeeing wax only excludes a foreign body; persistent pain and discharge after removal means secondary otitis externa, not a retained object — unless the canal cannot be fully seen.CAUTION — do not push the object deeper. Firm objects come out with a loop or hook, soft ones with alligator forceps. Irrigation only if the drum is known to be intact, and with care: organic objects swell when wet and lodge harder. Insects are immobilized first by filling the canal with lidocaine — again only if the drum is intact. Refer to ENT for removal under microscopy where warranted.UrgentNothing goes into the ear at home to fetch it out; attempts are what turn a simple removal into a referral.
Sensorineural hearing lossEarL16 · slide 12–14, 42“I can hear that people are talking but I can’t make out the words, especially in a crowd.”Sensory (deterioration of the cochlea and loss of hair cells) and neural (lesions of the eighth nerve, auditory nuclei, ascending tracts, auditory cortex) are difficult to separate clinically and are grouped together. Onset in middle or later years; the ear canal and drum look normal. Higher registers are lost so sound is distorted, hearing worsens in a noisy environment, and the voice may be loud because hearing is difficult.Otoscopy is normal. Weber lateralizes AWAY to the better ear; Rinne remains positive bilaterally. Cranial nerves and cerebellar signs. Establish whether onset was sudden — that changes it into an emergency.
  1. Conductive lossWeber toward, Rinne negative, and usually a visible cause
  2. Acoustic neuromaAsymmetric, with speech discrimination worse than the pure tone loss predicts
  3. PresbycusisBilateral, symmetric, gradual, high-frequency — the commonest cause
Rules it INAudiometry → reduced air AND bone conduction together with no air-bone gap. Magnetic resonance with gadolinium if asymmetric → an enhancing internal auditory canal lesion.Rules the differentials OUTAn air-bone gap excludes it; symmetric high-frequency loss in an older patient is presbycusis, not a tumor; normal imaging excludes a schwannoma.Usually not correctable, but may be stabilized and some types prevented. Acute-onset sensory loss may respond to corticosteroids in the first weeks.UrgentThe window for steroids in sudden loss is short, which is why new one-sided hearing loss is not a wait-and-see problem.
LabyrinthitisEarL16 · slide 95, 97“The spinning has been constant for two days and my hearing has dropped on that side.”Inflammation of the membranous labyrinth of the inner ear. Relatively sudden onset of sensorineural hearing loss AND acute vertigo. Exact etiology rarely certain; evidence supports a viral cause, and it may be associated with bacterial infection or systemic autoimmune disease. Also listed as a complication of acute otitis media.Otoscopy — look for otitis media as a source. Weber and Rinne: hearing loss is what separates this from neuronitis. Head impulse test, nystagmus direction, truncal stability and cerebellar signs.
  1. Vestibular neuronitisIdentical vertigo but hearing is PRESERVED
  2. Cerebellar infarctionCannot sit unsupported, direction-changing nystagmus, headache
  3. Meniere diseaseRecurrent discrete attacks rather than one sustained illness
Rules it INClinical → sustained vertigo with unidirectional nystagmus, an abnormal head impulse test, plus hearing loss. Audiometry → a sensorineural loss on the affected side. Imaging only if central features appear.Rules the differentials OUTNormal hearing means vestibular neuronitis; direction-changing nystagmus or truncal instability means a central cause and needs urgent imaging; brief positional attacks mean positional vertigo.Symptomatic. Antibiotics if bacterial symptoms such as fever are present. Oral corticosteroids. Oral diazepam or meclizine during the acute vertigo.UrgentThe difference from vestibular neuronitis is one word: labyrinthitis affects hearing.
Ménière's diseaseEarL16 · slide 69–70, 89, 97“It comes in attacks — the room spins for hours, my ear feels full and roars, and my hearing goes down and then comes back.”Fluctuating LOW-frequency sensorineural hearing loss that may fluctuate at first then progress. Low-tone, “blowing” tinnitus. Unilateral fullness in the ear. Episodes of vertigo, often the presenting complaint. Typical attack: episodic, spontaneous, severe spinning vertigo lasting several hours, frequently with nausea, vomiting and diaphoresis.Otoscopy is normal. Weber lateralizes AWAY, Rinne positive. Dix-Hallpike, which should be negative — that is how positional vertigo is excluded. Head impulse test, nystagmus, gait, cerebellar signs and cranial nerves.
  1. Benign paroxysmal positional vertigoSECONDS, positional, no hearing loss or fullness
  2. Vestibular neuronitisA single sustained attack over days with NO hearing loss
  3. Acoustic neuromaProgressive unilateral loss with imbalance rather than discrete attacks
Rules it INAudiometry during or between attacks → a fluctuating LOW-frequency sensorineural loss, which is the signature. Magnetic resonance → normal, done to exclude a schwannoma rather than to confirm this.Rules the differentials OUTA positive Dix-Hallpike with fatigable nystagmus means positional vertigo; normal hearing throughout excludes Meniere disease; an enhancing internal auditory canal lesion redirects to acoustic neuroma.Symptomatic control of the attacks and the underlying management.UrgentThe tetrad is vertigo, fluctuating hearing loss, tinnitus and fullness — and unlike the other peripheral causes, hearing is affected.
Vestibular neuronitisEarL16 · slide 96–97“I woke up two days ago and the room has been spinning ever since — but my hearing is fine.”Inflammation of the vestibular portion of cranial nerve VIII, likely viral though the cause is unknown. Considered benign and self-limiting. Dramatic, sudden vertigo with nausea and gait imbalance. Dizziness lasts days with gradual improvement; balance symptoms may persist for months. Not associated with any change in hearing or focal neurological complaints.Head impulse test — a corrective saccade toward the affected side. Nystagmus should be unidirectional and horizontal, beating away from the lesion. Test truncal stability — the patient can sit. Full cerebellar and cranial nerve examination. Otoscopy and hearing are normal.
  1. LabyrinthitisThe same picture PLUS hearing loss
  2. Cerebellar infarctionNormal head impulse test, direction-changing nystagmus, cannot sit
  3. Meniere diseaseRecurrent episodes with fullness and fluctuating hearing
Rules it INClinical → the three-part peripheral pattern: abnormal head impulse test, unidirectional nystagmus, no skew deviation, with normal hearing.Rules the differentials OUTA NORMAL head impulse test in a persistently vertiginous patient is a red flag for a central cause; hearing loss makes it labyrinthitis; imaging excludes infarction where doubt exists.Symptomatic. Oral diazepam or meclizine during the acute phase, antiemetics, and oral corticosteroids are questioned in the deck rather than asserted.UrgentNormal hearing and no focal neurology is what makes it benign — either of those being abnormal moves the diagnosis.
CholesteatomaEarL15 · slide 31–37“There is a foul smell from my ear, it keeps draining, and my hearing is getting worse.”A collection of keratinized squamous epithelium in the middle ear or mastoid. No cholesterol in it and not a neoplasm, despite the name. Primary is commonest and forms from retraction of the tympanic membrane, usually the pars flaccida; secondary follows epithelial migration or surgery; congenital is least common and forms with no retraction or perforation. Risk factors are eustachian tube dysfunction and chronic middle ear inflammation. May be asymptomatic; otherwise tinnitus, recurrent otorrhea in the absence of otitis externa, and hearing loss as a late finding.Otoscopy for a retraction pocket in the attic or pars flaccida with white keratin debris and granulation. Cranial nerve VII. Fistula test — pressure on the tragus producing vertigo or nystagmus suggests erosion into the labyrinth. Tuning forks.
  1. Chronic suppurative otitis mediaA central perforation with discharge but no keratin or bone erosion
  2. Chronic otitis externaThe canal is the problem; the drum is intact
  3. Ear canal carcinomaFriable and bleeding, with pain out of proportion
Rules it INOtoscopy → keratin debris in a retraction pocket. Computed tomography of the temporal bone → a soft tissue mass with bony erosion of the scutum or ossicles — the erosion is what makes it a cholesteatoma rather than debris.Rules the differentials OUTNo bone erosion on computed tomography with a central perforation means chronic otitis media instead; a positive fistula test raises labyrinthine erosion and changes urgency.Refer to ENT. Remove canal debris, treat infection with antibiotics, then surgical removal, usually with tympanoplasty. Mastoidectomy if it extends into the mastoid with bony erosion.UrgentIt erodes bone, so it is removed rather than watched — the discharge is a symptom of that, not a simple infection.
MastoiditisEarL15 · slide 19“My ear infection got better and then came back, and now behind my ear is swollen and sore.”Spread of acute otitis media infection into the mastoid air cells. Listed with tympanic membrane perforation, labyrinthitis and the rare meningitis or encephalitis as the complications of acute otitis media.Inspect from BEHIND and ABOVE for the auricle pushed forward and outward. Palpate the mastoid for tenderness, swelling and fluctuance. Otoscopy. Cranial nerve VII and signs of meningism, since spread is the danger.
  1. Acute otitis mediaEar pain without postauricular swelling or auricular protrusion
  2. Postauricular lymphadenitisA discrete mobile node; the auricle is not displaced
  3. Severe otitis externaTragal tenderness with a swollen canal, no mastoid air cell involvement
Rules it INContrast computed tomography of the temporal bone → opacified mastoid air cells with coalescence — loss of the bony septa, which is what separates true mastoiditis from the incidental fluid seen in ordinary otitis media. Raised white cell count and inflammatory markers.Rules the differentials OUTFluid in the air cells with INTACT septa is not mastoiditis; a mobile tender node with a normal scan is adenitis; normal imaging excludes intracranial extension.Treat as a complicated acute otitis media — ENT involvement.UrgentIt is the reason acute otitis media that is not settling gets re-examined rather than simply re-prescribed.
Acoustic neuromaEarL16 · slide 72–75, 97“My hearing has slowly gone in one ear, it rings, and I feel unsteady — lately my face feels a bit numb.”Benign tumor of cranial nerve VIII, rare, and most often unilateral. Symptoms: unilateral hearing loss, which may be sudden; poor speech discrimination compared with what the tone loss would predict; often disequilibrium. Progression may not be so “benign”. May involve cranial nerves V and VII.Otoscopy is normal. Weber lateralizes AWAY, Rinne positive. Cranial nerves V and VII — corneal reflex is an early loss. Gait and cerebellar testing. Note that facial weakness is a LATE sign, so its absence proves nothing.
  1. PresbycusisBilateral and symmetric; asymmetry is what triggers imaging
  2. Meniere diseaseEpisodic vertigo with fullness and low-frequency fluctuating loss
  3. Sudden sensorineural hearing lossAbrupt rather than slowly progressive
Rules it INMagnetic resonance imaging with gadolinium → an enhancing mass in the internal auditory canal or cerebellopontine angle — the gold standard. Audiometry → an asymmetric sensorineural loss with speech discrimination disproportionately poor for the pure tone thresholds.Rules the differentials OUTNormal magnetic resonance imaging excludes it; symmetric loss makes presbycusis far more likely; fluctuating low-frequency loss with fullness redirects to Meniere disease.Observation with annual MRI, surgery, or radiation.UrgentThe discriminating symptom is not the volume of the loss but the disproportionately poor word understanding on the affected side.
Epistaxis — anteriorNose & sinusesL17 · slide 45–51“My nose started bleeding and I can’t get it to stop.”A common emergency department complaint, most cases before age 10 or between 45 and 65, with a winter predominance. The commonest cause is trauma — from the patient’s finger. Chronic dry nose is a risk factor. Anterior bleeds are by far the commonest: 90% arise in the vascular watershed of the nasal septum — Kiesselbach’s plexus.Have the patient blow out clots, then anterior rhinoscopy with good light to find the bleeding point on Kiesselbach plexus. Pinch the soft part of the nose for 10 to 15 minutes, leaning FORWARD — forward, not back, so blood is not swallowed. Check circulation and look in the throat for a posterior source.
  1. Posterior epistaxisNo visible anterior point; blood running down the pharynx
  2. Bleeding disorder or anticoagulationRecurrent, bilateral, with bruising elsewhere
  3. Sinonasal or nasopharyngeal tumorRecurrent unilateral bleeding with obstruction or a neck mass
Rules it INAnterior rhinoscopy → a visible anterior septal bleeding point that stops with pressure. That IS the confirmation — 90% of nosebleeds are anterior.Rules the differentials OUTBleeding continuing with no visible point, and blood in the pharynx, means a posterior source; full blood count and coagulation studies → thrombocytopenia or a raised international normalized ratio if recurrent; endoscopy excludes a tumor.Initial tamponade, and patients can do it themselves: blow the nose to clear clots → spray with oxymetazoline → pinch the alae against the septum continuously for 10 minutes. Also: sit up and lean forward at the waist so blood is not swallowed, a cotton pledget in the nostril, spit out blood in the pharynx, cold compress on the bridge. Then nasal tampons, gauze packing, balloon catheters, thrombogenic foams and gels.UrgentTeach these maneuvers for use at home. And DO NOT BLOW THE NOSE afterwards.
Nasal foreign bodyNose & sinusesL17 · slide 53–55A parent says “she’s had a smelly discharge from one side of her nose for a week.” The insertion is usually unwitnessed.Commonest in young children. Most often on the floor of the nasal passage just under the inferior turbinate, or superiorly just in front of the middle turbinate. Unilateral purulent and foul-smelling nasal discharge in a young child strongly suggests it.Unilateral foul purulent discharge in a child IS a foreign body until proven otherwise. Anterior rhinoscopy with good light and suction. Examine the other nostril and both ears too — children rarely stop at one. Identify a button battery, which is an emergency.
  1. Unilateral sinusitisDischarge without an object; far less common at this age
  2. Choanal atresiaCongenital, present from birth, with clear rather than foul discharge
  3. RhinolithA calcified mass around a long-retained object
Rules it INAnterior rhinoscopy → direct visualization of the object. Imaging only if a battery or magnet is suspected and not seen → the object with its characteristic outline.Rules the differentials OUTA clear nasal cavity on both sides excludes it; bilateral clear discharge suggests rhinitis; resolution of the discharge after removal confirms the cause.Removal — instrument chosen by what the object is: forceps for graspable objects, a wire loop, right-angle hook or curette for round smooth ones, suction for smooth or free-floating beads, beans, magnets or batteries. Get help — refer to ENT.UrgentA one-sided smelly discharge in a toddler is a foreign body until proven otherwise, not sinusitis.
Nasal fractureNose & sinusesL17 · slide 56–58“I took a blow to the nose, it bled, and now it looks crooked.”From trauma. Suspect other injuries — orbital and midface fractures. Associated with septal hematoma. The nasal bridge is the commonest site. Examination: palpate for tenderness, crepitus and abnormal movement, and inspect with a nasal speculum.Inspect for deformity from the front and from ABOVE. Palpate for crepitus and step-off. Anterior rhinoscopy for a septal hematoma — mandatory. Test airflow each side. Check for clear rhinorrhea, which could be cerebrospinal fluid. Examine eye movements and vision.
  1. Septal hematomaThe complication that must be found now, not at follow-up
  2. Orbital floor fractureDiplopia, restricted upgaze and infraorbital numbness
  3. Soft tissue injury aloneSwelling and bruising with no bony step or deformity
Rules it INClinical → deformity, crepitus and epistaxis. Plain films are NOT routinely useful. Computed tomography if other facial fractures are suspected → the fracture pattern and orbital involvement.Rules the differentials OUTAbsence of a septal swelling on rhinoscopy excludes hematoma; full painless eye movements exclude orbital entrapment; testing clear rhinorrhea for beta-2 transferrin excludes a cerebrospinal fluid leak.Initial treatment is ice and head of bed elevated.UrgentThe four criteria are the useful thing to carry — they decide imaging at the bedside.
Nasal polypsNose & sinusesL17 · slide 59–65“Both sides of my nose are blocked, it’s been going on for months, and I can’t smell anything.”Abnormal, gray, glistening masses filled with inflammatory material in the nasal cavity or paranasal sinuses. Large or extensive polyps cause congestion or blockage, thick discharge and ANOSMIA. Frequently associated with chronic rhinosinusitis, asthma and aspirin sensitivity — aspirin-exacerbated respiratory disease. In children they occur with chronic sinusitis, allergic rhinitis, cystic fibrosis or allergic fungal sinusitis. From the slide that is an image of a list: associated conditions include bronchial asthma 20–50%, cystic fibrosis 5–44%, allergic fungal sinusitis 85%, aspirin intolerance 8–20%, alcohol intolerance 50%, Churg-Strauss 50%, primary ciliary dyskinesia, Young syndrome and NARES 20%.Anterior rhinoscopy for pale, gray, grape-like, MOBILE and INSENSATE masses — touching them does not hurt, which distinguishes them from turbinates. Assess smell. Ask about asthma and aspirin sensitivity. In a child, think cystic fibrosis; unilateral polyps in an adult mean imaging and biopsy.
  1. Hypertrophied turbinatePink, sensitive to touch, and it shrinks with a decongestant
  2. Inverted papillomaUnilateral, may harbor carcinoma — the reason unilateral is never assumed benign
  3. Sinonasal malignancyUnilateral with bleeding, pain or facial numbness
Rules it INEndoscopy → polyps in the middle meatus. Computed tomography → polypoid soft tissue opacifying the sinuses. Sweat chloride test in a child → raised in cystic fibrosis. Biopsy of a unilateral polyp → excludes papilloma and carcinoma.Rules the differentials OUTA pink tender structure that shrinks with a decongestant is a turbinate; benign histology excludes malignancy; bone destruction on imaging redirects to tumor.Medical: non-drowsy oral antihistamine (loratadine, fexofenadine, cetirizine, levocetirizine), leukotriene inhibitor at night (montelukast, zafirlukast), intranasal or oral steroids, intranasal ipratropium, immunotherapy, decongestants with caution. Surgery gives only temporary relief — they recur within months to years.UrgentEvaluate EVERY child with benign multiple nasal polyposis for cystic fibrosis and asthma. The deck gives that its own slide.
Septal hematomaNose & sinusesL17 · slide 41–43“I broke my nose and now I can’t breathe through either side.”A hematoma between the nasal septum and the perichondrium or mucosal epithelium. Usually secondary to trauma; other causes are bleeding disorders, cocaine, foreign body and medications. Associated with nasal fracture — look for it in every nasal injury.Anterior rhinoscopy in EVERY nasal trauma — this is the reason the examination is mandatory. Look for a bluish, boggy swelling of the septum, usually bilateral. Palpate with a cotton applicator — it is fluctuant and compressible, unlike a deviated septum.
  1. Deviated septumFirm, not compressible, and asymmetric rather than bilateral
  2. Nasal fracture with swellingSoft tissue swelling outside; the septum itself is normal
  3. Septal abscessThe same swelling with fever and pain — the sequel if it is missed
Rules it INAnterior rhinoscopy with palpation → a compressible bilateral septal swelling. Needle aspiration → blood, which confirms it. Left alone it destroys the cartilage and produces a saddle nose deformity.Rules the differentials OUTA firm non-compressible septum is a deviation; fever with purulent aspirate means abscess; clear rhinoscopy excludes it.Drainage via intranasal incision under general anesthesia.UrgentThe same lesson as the auricular hematoma in Lecture 15: cartilage separated from its blood supply does not survive.
Chronic bacterial sinusitisNose & sinusesL17 · slide 28–29“My nose has been blocked and running for months and I’ve lost my sense of smell.”Sinusitis lasting more than twelve weeks. The mechanism is impaired mucociliary clearance causing REPEATED infections rather than one persistent infection. Constant nasal congestion and sinus pressure, with periods of increased severity.Anterior rhinoscopy for polyps, edema and purulence. Assess smell. Palpate the sinuses. Look for the underlying cause: allergy, a deviated septum, dental disease, immune deficiency.
  1. Nasal polypsPale, insensate, mobile grape-like masses; often coexist
  2. Allergic rhinitisItch and sneezing dominate; symptoms fluctuate with exposure
  3. Sinonasal neoplasmUnilateral obstruction with bleeding or facial numbness
Rules it INSymptoms lasting 12 weeks or more PLUS objective evidence: nasal endoscopy → purulence, edema or polyps in the middle meatus; computed tomography of the sinuses → mucosal thickening and sinus opacification. Symptoms alone are not enough.Rules the differentials OUTA normal endoscopy and normal scan exclude it despite the symptoms; unilateral disease with bleeding demands biopsy to exclude tumor; allergy testing identifies a treatable driver.Repeated antibiotic courses, often 3–4 weeks at a time — oral steroids plus two weeks of amoxicillin/clavulanate is the stated regimen. Adjuncts: intranasal glucocorticoids, sinus irrigation. Refer to ENT for surgical evaluation and to allergy for skin testing.UrgentIt is a drainage problem as much as an infection, which is why it keeps coming back and why surgery enters the conversation.
Chronic fungal sinusitisNose & sinusesL17 · slide 30“One side of my nose has been blocked for ages and the treatments haven’t worked.”Noninvasive disease in immunocompetent hosts, typically Aspergillus and dematiaceous molds. Recurrence is common. The allergic form is seen in patients with nasal polyps and asthma and presents as pansinusitis with thick, eosinophil-laden mucus the consistency of peanut butter.Anterior rhinoscopy and endoscopy, particularly for unilateral disease. Assess immune status and glycemic control — that determines whether this is the indolent form or the invasive one. In the immunocompromised, look for black necrotic mucosa, which is an emergency.
  1. Chronic bacterial sinusitisUsually bilateral and responds to antibiotics
  2. Sinonasal neoplasmUnilateral too, with bleeding and bone destruction
  3. Invasive fungal sinusitisNecrotic eschar with rapid progression in an immunocompromised patient
Rules it INComputed tomography → unilateral opacification, often with hyperdense material and calcification within the sinus. Endoscopy with biopsy and fungal culture → fungal elements; tissue invasion on histology is what defines the invasive form.Rules the differentials OUTHistology showing no tissue invasion means the non-invasive form and a very different urgency; biopsy excludes carcinoma; a normal scan excludes it.Mild indolent disease is cured by endoscopic surgery WITHOUT antifungals. A fungus ball is treated surgically — and with antifungals only if bony erosion has occurred.UrgentThe surprise here is that most of it is treated surgically rather than with drugs.
TeratomaNeckL18 · slide 28“The baby was born with a large firm mass in the neck” — often detected before birth on scan.Head and neck teratomas account for 3.5% of all teratomas. They originate from pluripotent cells and present as firm neck masses, most commonly noted at birth or within the first year. A large one can cause respiratory compromise or dysphagia.Palpate a firm, irregular mass containing both solid and cystic parts. Assess the airway immediately — that is the priority. Look for tracheal deviation and check feeding. Examine the thyroid.
  1. LymphangiomaSoft, compressible and transilluminates; purely cystic
  2. GoiterMoves with swallowing and is thyroid in origin
  3. NeuroblastomaFirm, may be associated with Horner syndrome and raised urinary catecholamines
Rules it INUltrasound and magnetic resonance → a heterogeneous mass with fat, cystic areas and CALCIFICATION — that mixed tissue content is what names it. Alpha-fetoprotein → a baseline, since a rise suggests a malignant germ cell component.Rules the differentials OUTA uniformly cystic transilluminating lesion is a lymphangioma; a mass moving with swallowing is thyroid; raised urinary catecholamines redirect to neuroblastoma.Surgical excision.UrgentSize is the whole problem here: it is a benign lesion that can obstruct an airway.
Cervical adenitisNeckL19 · slide 91–94“My child has a fever and a swollen, tender lump on the side of the neck.”Inflammation of a lymph node, often used synonymously with lymphadenopathy. Cervical lymphadenopathy is a sign, not a diagnosis. Infectious causes include toxoplasmosis, tuberculosis, brucellosis, primary herpes simplex, syphilis, cytomegalovirus, HIV, histoplasmosis and chickenpox; also inflammatory, degenerative and neoplastic causes. The typical case is a unilateral, solitary, anterior cervical node: about 70% beta-hemolytic streptococcus, 20% staphylococcus including MRSA, 10% viruses, atypical mycobacteria and Bartonella henselae.Palpate for size, tenderness, warmth, mobility and FLUCTUANCE. Search for the primary source: teeth, tonsils, ears, scalp, skin. Assess trismus, torticollis, drooling and the airway — those signal deep neck extension. Palpate other nodal groups and the spleen.
  1. Deep neck space abscessTrismus, torticollis, toxicity — the escalation to exclude
  2. Reactive viral adenopathyMultiple small mobile nodes, minimal tenderness, no fever
  3. MalignancyHard, fixed, painless, progressive, or supraclavicular
Rules it INClinical → a tender enlarged node with an identified source. Ultrasound → a solid inflamed node versus a hypoechoic collection, which is the decision that matters. Contrast computed tomography if deep extension is suspected → a rim-enhancing abscess. Full blood count and inflammatory markers.Rules the differentials OUTA solid node without a collection is treated with antibiotics rather than drained; a node that fails to settle in 4 to 6 weeks, or is hard and fixed, goes to aspiration or biopsy for malignancy; mycobacterial studies if it becomes chronic.Treat the underlying cause. Incision and drainage if there is an abscess.UrgentScarred nodes may stay palpable long after the infection has gone, which is not failure.
Atypical mycobacteriaNeckL18 · slide 34A parent says “he has a lump in his neck that isn’t sore, and the skin over it has gone purple.” Typically a well child under five.A pediatric infection. A unilateral neck mass in the anterior triangle or the parotid gland, with brawny (reddish-brown) skin, induration and pain.Palpate a non-tender node with VIOLACEOUS thinning skin over it. Note that the child is systemically WELL. Examine the chest. Ask about tuberculosis contacts and travel, since the differential is what matters. Check immune status.
  1. Tuberculous adenitisSystemic symptoms, positive contact history and a positive interferon test
  2. Suppurative bacterial adenitisHot, painful, red rather than cool and violaceous, with fever
  3. LymphomaProgressive, firm, with constitutional symptoms
Rules it INMycobacterial culture and polymerase chain reaction of aspirate or excised node → a non-tuberculous species. Interferon gamma release assay → NEGATIVE, which is what separates it from tuberculosis. Chest radiograph → normal.Rules the differentials OUTA positive interferon assay with an abnormal chest film means tuberculosis, a different treatment entirely; a hot painful node with fever means pyogenic adenitis. Incision and drainage is avoided — it produces a chronic sinus; complete excision is preferred.Surgical excision, or incision and drainage with antibiotics.UrgentUnilateral and pediatric here; tuberculous adenitis is more diffuse and bilateral.
Fungal neck infectionNeckL18 · slide 35“These neck glands have been up for weeks and haven’t responded to antibiotics” — usually in an immunocompromised patient.Immunocompromised patients are particularly susceptible. The commonest organisms are Candida, Histoplasma and Aspergillus.Palpate the nodes and note induration or fistulation. Assess immune status carefully — it determines both likelihood and severity. Examine the mouth for candidiasis, the chest, and the skin. Take a travel and exposure history for endemic fungi.
  1. Tuberculous adenitisThe main mimic — chronic nodes in the same population
  2. ActinomycosisWoody induration with sulfur granules
  3. LymphomaProgressive painless nodes with constitutional symptoms
Rules it INFungal culture and staining of aspirate or biopsy → the organism. Histology with special stains → fungal elements in tissue. Serology or antigen testing for endemic fungi → positive. Assess the immune deficiency itself.Rules the differentials OUTAcid-fast bacilli redirect to mycobacterial disease; sulfur granules mean actinomycosis; malignant cells mean lymphoma. Failure of antibacterial therapy is the trigger to send fungal studies, not to escalate antibiotics again.Amphotericin B, treated aggressively.UrgentNon-infectious inflammatory causes sit on the same slide: Sjögren syndrome, sarcoidosis, IgG4-related sialadenitis and Kawasaki disease.
HIV-associated cervical adenopathyNeckL18 · slide 32“I’ve had swollen glands for months, along with night sweats and weight loss.”Cervical adenopathy is present in 12% to 45% of patients with HIV. Idiopathic follicular hyperplasia is the commonest cause. Persistent generalized lymphadenopathy — lymphadenopathy with no identifiable infectious or neoplastic cause — is also common, and the neck is its commonest site.Palpate persistent, generalized, symmetric adenopathy in two or more sites. Examine the mouth for candidiasis, hairy leukoplakia and Kaposi sarcoma. Palpate liver and spleen. Take a risk history.
  1. LymphomaAsymmetric, progressive, and much more likely in this same population
  2. Tuberculous adenitisMatted nodes that may fistulate; also commoner here
  3. Reactive adenopathyFollows an acute infection and resolves
Rules it INHuman immunodeficiency virus serology with confirmatory testing → positive, and CD4 count with viral load → degree of immunosuppression. Excisional node biopsy if a node is dominant or growing → distinguishes reactive hyperplasia from lymphoma or mycobacterial disease.Rules the differentials OUTReactive hyperplasia on biopsy excludes lymphoma; acid-fast staining and culture exclude tuberculosis; resolution with treatment argues against malignancy. A dominant enlarging node in a patient with the virus is biopsied, not watched.Treat the HIV.UrgentThe adenopathy is a marker of control, not a separate problem to excise.
Suppurative bacterial lymphadenopathyNeckL18 · slide 33“This lump in my neck is hot, red and really painful, and I’ve got a fever.”Most commonly Staphylococcus aureus and group A beta-hemolytic Streptococcus. Masses develop in the submandibular or jugulodigastric regions, with sore throat, skin lesions and upper respiratory symptoms.Palpate a single, large, hot, erythematous, exquisitely tender node; test for FLUCTUANCE — that is what decides drainage. Find the source: teeth, tonsils, scalp, skin. Assess the airway and for deep neck extension.
  1. Reactive viral adenopathyMultiple small mobile nodes, mildly tender, no fluctuance
  2. Deep neck abscessTrismus, dysphagia and toxicity; the escalation to exclude
  3. Infected congenital cystA pre-existing lump that has become infected
Rules it INClinical → a hot, tender, fluctuant node with fever. Ultrasound → a hypoechoic collection with debris rather than a solid node — abscess versus cellulitis. Contrast computed tomography if deep extension is suspected → a rim-enhancing collection. Aspiration culture → the organism.Rules the differentials OUTA solid node without a collection on ultrasound is treated medically, not drained; trismus and airway compromise redirect to a deep neck space infection; a long-standing lump suggests an infected congenital cyst.Empirical antibiotics against anaerobes and gram-positive organisms. Fine needle aspiration or incision and drainage if antibiotics fail.UrgentFailure of antibiotics is the trigger to drain, not the starting point.
Tuberculous adenitis (scrofula)NeckL18 · slide 34“I’ve had swollen glands in my neck for months with fevers and night sweats, and I’ve lost weight.”Mycobacterium tuberculosis. Cervical tuberculosis is called scrofula. Adults are affected more than children, and the lymphadenopathy is more diffuse and bilateral than in atypical mycobacterial disease.Palpate MATTED, firm nodes, classically in the posterior triangle, which may fistulate to the skin. Examine the chest. Take a contact, travel and immune-status history. Look for adenopathy elsewhere.
  1. Atypical mycobacterial adenitisA well young child, violaceous skin, negative interferon assay
  2. LymphomaRubbery discrete nodes rather than matted, with the same constitutional symptoms
  3. Metastatic carcinomaHard and fixed, with a mucosal primary to be found
Rules it INInterferon gamma release assay or tuberculin skin test → positive. Node aspirate or biopsy for acid-fast staining, culture and polymerase chain reaction → Mycobacterium tuberculosis; histology shows caseating granulomas. Chest radiograph → active or old pulmonary disease.Rules the differentials OUTA negative interferon assay with a non-tuberculous species on culture means atypical mycobacteria; non-caseating granulomas suggest sarcoidosis; malignant cells redirect to lymphoma or carcinoma.Isoniazid, rifampin, rifabutin, rifapentine, pyrazinamide, ethambutol — traditionally RIPE: rifampin, isoniazid, pyrazinamide, ethambutol.UrgentBilateral and diffuse versus unilateral and brawny is the whole distinction from atypical mycobacteria.
TularemiaNeckL18 · slide 33“I got a sore on my hand after skinning rabbits, and now my glands are up and I have a fever.”Francisella tularensis, transmitted by rabbits, ticks and contaminated water. Tonsillitis, painful adenopathy, fever, chills, headache and fatigue.Look for an ulcer at the inoculation site with regional adenopathy — the ulceroglandular pattern. Palpate the draining nodes for fluctuance. Take the exposure history: rabbits, ticks, deerflies. Examine the chest and eyes.
  1. Cat scratch diseaseA papule with regional nodes but a cat rather than a rabbit or tick
  2. Suppurative bacterial adenitisHot fluctuant node without an inoculation ulcer
  3. Plague or anthraxOther zoonoses with a similar pattern and different exposures
Rules it INSerology, acute and convalescent → a fourfold rise in titre. Culture is possible but the laboratory must be warned, since it is a hazard to staff. Polymerase chain reaction on tissue → the organism.Rules the differentials OUTNegative serology on paired samples excludes it; Bartonella serology redirects to cat scratch; routine culture growing a common pyogenic organism means ordinary adenitis.Streptomycin.UrgentThe exposure history is the question: rabbits and ticks.
Follicular thyroid carcinomaThyroidL18 · slide 42, 44“I’ve had this lump for a while” — or the presentation is a bone or lung metastasis in an older patient.16% of thyroid cancers, involving thyroid epithelial cells. Spreads to local lymph nodes or by blood to bone and lungs. The Hürthle cell variant is more aggressive, with a higher risk of metastases and recurrence.Palpate the nodule with swallowing. Cervical nodes are often NEGATIVE, because spread is hematogenous — a normal neck does not reassure here. Check the voice. Examine for bone tenderness and take a respiratory history.
  1. Follicular adenomaCytologically IDENTICAL — only capsular or vascular invasion separates them
  2. Papillary carcinomaNodal spread with diagnostic nuclear features on aspiration
  3. Multinodular goiterMultiple nodules, benign cytology, stable over years
Rules it INFine needle aspiration → a follicular neoplasm — which CANNOT distinguish carcinoma from adenoma. Surgical excision with histology → capsular and vascular invasion, which is the only thing that makes it a carcinoma. Imaging of chest and bone for metastases.Rules the differentials OUTHistology without invasion means an adenoma; papillary nuclear features on cytology redirect; raised calcitonin means medullary disease. A follicular result on aspiration always goes to surgery — repeat aspiration cannot settle it.As for papillary: lobectomy or thyroidectomy with or without neck dissection and ablation.UrgentHematogenous spread is what separates it from papillary.
Medullary thyroid carcinomaThyroidL18 · slide 42, 44“There’s a lump in my thyroid” — sometimes with diarrhea or flushing, and sometimes a known family history.About 5%. A disorder of the parafollicular or C cells, which produce calcitonin. More insidious, most likely to metastasise, and can go undiagnosed until a metastasis is found.Palpate the thyroid and the cervical nodes. Take a family history for multiple endocrine neoplasia — and examine for its other components: check blood pressure and ask about episodic sweating and palpitations for phaeochromocytoma, and look for mucosal neuromas and a marfanoid habitus.
  1. Papillary carcinomaCommoner, with nodal spread and characteristic cytology
  2. Anaplastic carcinomaRapid growth in an older patient with compressive symptoms
  3. Parathyroid adenomaHypercalcemia rather than raised calcitonin
Rules it INSerum calcitonin → markedly raised, and it is the tumor marker for follow-up. Carcinoembryonic antigen → also raised. Fine needle aspiration → amyloid stroma with spindle cells. RET proto-oncogene testing → a germline mutation, which triggers family screening.Rules the differentials OUTNormal calcitonin excludes it; plasma metanephrines must be checked and a phaeochromocytoma excluded BEFORE any thyroid surgery — operating first can be fatal. A negative RET test means sporadic disease.Thyroidectomy with monitoring for recurrence on screening labs, with or without external beam radiation for nodal disease. Screen family members for multiple endocrine neoplasia.UrgentThe only one of the four with a familial syndrome to chase in the relatives.
Papillary thyroid carcinomaThyroidL18 · slide 42, 44“There’s a painless lump in my neck” — often noticed by someone else, in a younger patient.The commonest thyroid cancer at 75%, with the best prognosis, commonest in young females. Involves thyroid epithelial cells.Palpate the nodule during swallowing; note firmness and mobility. Palpate the cervical nodes carefully — it spreads by lymphatics and a node may be the presenting sign. Assess the voice. Ask about childhood radiation exposure and family history.
  1. Benign colloid noduleSoft, unchanging, benign cytology
  2. Follicular carcinomaSpreads by BLOOD rather than lymphatics, and cytology cannot call it
  3. Medullary carcinomaRaised calcitonin, with a familial syndrome to consider
Rules it INFine needle aspiration → the nuclear features that make this the one thyroid cancer cytology can diagnose confidently: Orphan Annie nuclei, nuclear grooves and psammoma bodies. Ultrasound of neck and nodes → the primary and nodal spread.Rules the differentials OUTBenign cytology with a reassuring ultrasound excludes it; a follicular pattern on cytology cannot be resolved without surgery; raised calcitonin redirects to medullary carcinoma.Lobectomy or thyroidectomy, with or without neck dissection, ablation and surveillance. Almost all thyroid cancers need thyroidectomy, except a well-differentiated cancer localized to one lobe with no metastasis.UrgentCommonest and kindest — the pairing is the exam point.
Primary thyroid lymphomaThyroidL18 · slide 45“My thyroid has grown quickly over a few weeks and it feels tight” — often an older woman with known Hashimoto thyroiditis.Most commonly non-Hodgkin B cell tumors, associated with Hashimoto thyroiditis.Palpate a rapidly enlarging, firm, diffuse goiter. Assess for stridor, tracheal deviation and compressive symptoms. Palpate other nodal basins and the spleen. Check for hypothyroidism from the underlying thyroiditis.
  1. Anaplastic carcinomaThe critical distinction — same rapid growth, utterly different treatment
  2. Hashimoto thyroiditisThe background condition; firm goiter but not rapidly growing
  3. Riedel thyroiditisWoody, fixed, fibrotic gland invading surrounding tissue
Rules it INCORE or OPEN biopsy → lymphoma with immunohistochemistry to type it. Fine needle aspiration is often insufficient, because architecture matters. Thyroid peroxidase antibodies → raised, reflecting the Hashimoto background. Staging imaging.Rules the differentials OUTAnaplastic cytology on aspiration redirects to a very different pathway; this distinction matters because lymphoma responds to chemotherapy and radiotherapy rather than surgery; a stable goiter over years excludes it.Chemotherapy and radiation — not primarily surgical, unlike the carcinomas above.UrgentThe one thyroid malignancy where the answer is not an operation.
Thyroid nodule and massThyroidL18 · slide 40–41“I noticed a lump in the front of my neck” — or it was found incidentally on a scan done for something else.The main cause of anterior neck masses and lumps. An immobile midline neck mass that elevates with swallowing is likely thyroid. Risk factors: age under 30 or over 60, childhood head and neck irradiation, full body irradiation for bone marrow transplant, family history of thyroid cancer, and multiple endocrine neoplasia type 2. Recent growth, dysphagia or obstruction are the concerning symptoms.Stand BEHIND the patient to palpate the thyroid, and ask them to swallow — thyroid masses rise. Assess size, consistency, mobility and whether it is single or multinodular. Palpate cervical nodes, listen to the voice, and check for tracheal deviation and stridor. Look for signs of over- or underactivity.
  1. Multinodular goiterSeveral nodules in a diffusely enlarged gland; far lower risk
  2. Thyroid carcinomaHard, fixed, growing, with hoarseness or nodes — the point of the workup
  3. Thyroglossal duct cystMidline, rises with TONGUE protrusion as well as swallowing
Rules it INThyroid stimulating hormone FIRST → if SUPPRESSED, a radionuclide scan showing a hot nodule, which is almost never malignant and does not need aspiration. If normal or raised, ultrasound → suspicious features (microcalcification, taller-than-wide shape, irregular margins, hypoechogenicity) and then fine needle aspiration → the cytological diagnosis.Rules the differentials OUTA hot nodule on scintigraphy effectively excludes cancer; benign cytology with reassuring ultrasound allows surveillance; elevation on tongue protrusion redirects to a thyroglossal cyst.Determined by the biopsy. Fine needle aspiration is the diagnostic procedure of choice once primary thyroid disease has been excluded on labs.UrgentIf thyroid cancer is suspected, avoid iodine-contrast computed tomography — it compromises radioiodine treatment afterwards.
Bacterial pharyngitis (GABHS)Throat & larynxL19 · slide 73–77“My throat is agony to swallow, I’ve got a fever, and I have NO cough.”30% of pharyngitis; the commonest bacterial cause is group A beta-hemolytic Streptococcus. Common in adolescents and children but not under 3 years. Peaks in winter and spring; droplet spread; incubation 2–5 days. Fever above 100.4 °F, sore throat, cervical lymphadenopathy, dysphagia, odynophagia, LACK OF COUGH, abdominal pain. Tonsillar and pharyngeal erythema with purulent exudate.Inspect for tonsillar erythema with exudate and palatal petechiae. Palpate tender ANTERIOR cervical nodes. Measure temperature. Apply the Centor criteria. Check for trismus and uvular deviation, which would mean an abscess. Look for a scarlatiniform rash.
  1. Viral pharyngitisCough, coryza and hoarseness present; low Centor score
  2. Infectious mononucleosisPOSTERIOR nodes and splenomegaly; giving amoxicillin causes a rash
  3. Peritonsillar abscessUnilateral, with trismus, uvular deviation and a muffled voice
Rules it INRapid antigen detection test → positive confirms it; a NEGATIVE test in a child is backed up by throat culture, which is the gold standard. Centor score of 3 or 4 supports testing and treating.Rules the differentials OUTA positive monospot with atypical lymphocytes means mononucleosis — and this matters because aminopenicillins cause a florid rash there; cough and coryza suggest viral disease; trismus with uvular deviation redirects to quinsy.Symptomatic care plus antibiotics: penicillin VK for 10 days, or amoxicillin. Intramuscular penicillin G if compliance or oral intake is a concern. Mild penicillin allergy: cephalexin or cefadroxil. Severe allergy: macrolides or clindamycin.UrgentTreatment is as much about preventing rheumatic fever as about the sore throat.
Infectious mononucleosisThroat & larynxL19 · slide 81–87“I’ve had a sore throat for two weeks and I’m exhausted — I can barely get out of bed.”Highly contagious; 90–95% of adults are Epstein-Barr virus seropositive. Commonly 15 to 24 years. Spread by oral contact or infected saliva. Epstein-Barr virus in 90%, cytomegalovirus and others in 10%. Prodrome of malaise, headache and low-grade fever — or asymptomatic under 10 years. Triad of fever, tonsillar pharyngitis with or without exudate, and cervical lymphadenopathy. Also palatal petechiae, hepatomegaly, splenomegaly, and a maculopapular rash in 5%.Inspect for large tonsils with exudate and palatal petechiae. Palpate POSTERIOR cervical nodes — the distribution is a real discriminator. Palpate for splenomegaly, gently. Check for hepatomegaly, jaundice and a rash. Assess the airway if the tonsils are very large.
  1. Streptococcal pharyngitisAnterior nodes, no splenomegaly, shorter course
  2. Cytomegalovirus infectionA very similar illness with a NEGATIVE monospot
  3. Acute HIV seroconversionAlso mononucleosis-like — and it must be considered
Rules it INMonospot (heterophile antibody) → positive, though often falsely negative in the first week and in young children. Full blood count with film → lymphocytosis with atypical lymphocytes. Epstein-Barr specific serology → confirms when the monospot is negative. Liver function tests → raised transaminases.Rules the differentials OUTA negative monospot with a compatible illness means sending Epstein-Barr serology, cytomegalovirus testing and HIV testing; a positive rapid streptococcal test explains a different illness. Avoid aminopenicillins — they cause a florid rash here.Supportive — there is no antiviral therapy. Corticosteroids for severe respiratory compromise. Avoid heavy lifting and contact sports for about a month, until the splenomegaly has resolved, to prevent splenic rupture.UrgentGiving penicillin triggers an exanthem — the classic sequence is a sore throat treated as strep, a rash, and then the real diagnosis.
Rheumatic feverThroat & larynxL19 · slide 78–79“A few weeks after a bad sore throat, my joints started hurting and moving from one to another, and I get short of breath.”A rare complication of untreated group A beta-hemolytic streptococcal infection, from cross-reactive antibodies produced against the streptococcus that attack heart muscle — endocarditis, myocarditis or pericarditis. Signs appear 2 to 3 weeks after the infection, sometimes as early as one week or as late as five. Peak incidence between 5 and 15 years; rare before 4 and after 40. Typically resolves after about six weeks.Auscultate the heart carefully for a NEW murmur and a rub — carditis is what causes lasting harm. Examine joints for a MIGRATORY arthritis. Look for subcutaneous nodules over extensor surfaces and erythema marginatum on the trunk. Observe for Sydenham chorea.
  1. Septic arthritisOne hot joint that does not migrate; aspiration settles it
  2. Juvenile idiopathic arthritisPersistent rather than migratory, without the preceding sore throat
  3. Reactive arthritisFollows a gastrointestinal or genitourinary infection instead
Rules it INJones criteria → two major, or one major plus two minor, WITH evidence of preceding streptococcal infection: raised or rising antistreptolysin O titre or a positive culture. Echocardiography → valvular regurgitation, most often mitral. Electrocardiogram → a prolonged PR interval. Inflammatory markers → raised.Rules the differentials OUTNo evidence of preceding streptococcal infection makes the diagnosis untenable — that requirement is what excludes the mimics; joint aspiration excludes sepsis; a normal echocardiogram excludes carditis but not the diagnosis.Treat and eradicate the streptococcal infection; manage the carditis.UrgentThis is the reason a sore throat gets an antibiotic at all — the throat would settle without one.
Chronic laryngitisThroat & larynxL19 · slide 58“My voice has been rough for a couple of months — I smoke and I get a lot of heartburn.”Voice disturbance lasting more than two weeks. Not a true diagnosis — always work up the underlying condition.Assess voice quality. Take the risk factor history: smoking, alcohol, reflux, vocal abuse, inhaled corticosteroids. Palpate the neck for nodes and ask about otalgia, weight loss and dysphagia. Visualize the larynx — this is not optional at this duration.
  1. Laryngeal carcinomaThe diagnosis this workup exists to exclude, in exactly this patient
  2. Reflux laryngitisPosterior erythema, edema and granuloma with reflux symptoms
  3. Vocal cord lesionsDiscrete nodules or polyps rather than diffuse inflammation
Rules it INLaryngoscopy → diffuse erythema and edema WITHOUT a discrete mass, ulceration or cord fixation. Biopsy of any suspicious area → the histology, which is what settles it. Consider reflux testing.Rules the differentials OUTA mass, ulcer or immobile cord means carcinoma until biopsy says otherwise; discrete bilateral lesions at the anterior third mean nodules; improvement on antireflux therapy supports reflux laryngitis.Treat what the laryngoscopy finds.UrgentTwo weeks of hoarseness is the threshold at which a smoker gets scoped, not reassured.
Vocal cord papillomatosisThroat & larynxL19 · slide 49–52A parent says “his voice has been hoarse for months and now he makes a noise when he breathes.” In adults, persistent hoarseness.Recurrent respiratory papillomatosis: benign, non-contagious, rare, with exophytic warty lesions usually in the larynx but also nose, pharynx and trachea. Human papillomavirus subtypes 6 and 11, rarely 16. Bimodal: juvenile between 2 and 4 years, adult peaking in the 30s. Multiple friable irregular warty growths affecting true and false cords, at points of air turbulence and at the change from ciliary to squamous epithelium. Glottic lesions cause dysphonia; supraglottic lesions cause stridor.Assess voice and listen for STRIDOR — airway obstruction is the danger. Visualize the larynx. Note that it recurs after removal. Ask about maternal history in a child.
  1. Vocal cord nodulesSmooth and symmetric; no airway compromise or recurrence
  2. Laryngeal carcinomaIn adults, and papillomatosis can undergo malignant transformation
  3. CroupAcute, with a barking cough, rather than months of hoarseness
Rules it INLaryngoscopy → exophytic, wart-like, cauliflower lesions on the cords and supraglottis. Biopsy with human papillomavirus typing → types 6 and 11 most often, and it excludes carcinoma.Rules the differentials OUTA smooth symmetric pair of lesions means nodules; dysplasia or invasion on histology means malignant transformation and changes management; an acute barking cough is croup, not this.No curative measure for the virus — the aim is removing symptomatic lesions with minimal morbidity: carbon dioxide laser resection, cold steel dissection, laryngeal microdebrider. Avoid tracheostomy, which introduces another squamociliary junction the papillomas favor. Adjuvant intralaryngeal cidofovir is off-label.Urgent3–7% risk of malignant transformation. Gardasil and Gardasil 9 offer eventual prevention.
Vocal cord paralysisThroat & larynxL19 · slide 53–56“My voice is breathy and weak, and I cough when I drink.” — often after neck or chest surgery.One or both folds fail to open or close properly. Causes: injury during surgery to thyroid, parathyroid, esophagus, neck or chest; neck or chest injury; tumors; infections (Lyme disease, Epstein-Barr virus, herpes); neurological disease (stroke, multiple sclerosis, Parkinson disease). Unilateral gives hoarse breathy dysphonia, aspiration, dysphagia, vocal fatigue — and may be asymptomatic. Bilateral gives inspiratory or biphasic stridor, weak cry, aspiration.Assess voice and test the cough — a weak, breathy cough suggests glottic incompetence. Watch for aspiration on swallowing. Listen for stridor, which means BILATERAL paralysis and an airway emergency. Full cranial nerve examination. Palpate thyroid and neck; look for surgical scars.
  1. Laryngeal carcinomaFixes the cord mechanically rather than by nerve injury
  2. Cricoarytenoid joint fixationCord immobile from the joint, not the nerve — separated at endoscopy
  3. Functional dysphoniaNormal cord movement on examination despite an abnormal voice
Rules it INLaryngoscopy → an immobile cord, and whether it is unilateral or bilateral. Computed tomography from SKULL BASE to MEDIASTINUM → a lesion anywhere along the recurrent laryngeal nerve; the left nerve loops under the aortic arch, so the chest must be included. Thyroid ultrasound and function tests.Rules the differentials OUTNormal cord movement excludes paralysis and suggests a functional cause; palpation of the arytenoid at endoscopy separates fixation from paralysis; a normal scan along the whole nerve course means idiopathic or postviral paralysis.Decide whether it is self-limiting or permanent. Observation with voice therapy; surgical medialisation of the affected fold, or thyroplasty.UrgentLaryngeal electromyography predicts recovery: a transected or tumor-infiltrated nerve will not recover, while a bruised or stretched one may return over 6 months to a year.
Vocal cord polypsThroat & larynxL19 · slide 48“My voice went hoarse after I screamed at a match and it hasn’t come back.”Unilateral masses forming within the superficial lamina propria of the vocal fold, commoner in men with a history of vocal abuse and heavy smoking. Fluid-filled and gelatinous, pedunculated, sometimes with visible vascular markings, at the point of maximal vibration.Assess voice quality — often breathy and rough. Take the history of a single vocal event, smoking and reflux. Visualize the larynx. Palpate the neck for nodes.
  1. Vocal cord nodulesBilateral and symmetric, from chronic rather than single abuse
  2. Laryngeal carcinomaIrregular, ulcerated, may fix the cord — must be excluded
  3. Reinke edemaDiffuse fusiform swelling of both cords in a smoker, not a discrete polyp
Rules it INLaryngoscopy with stroboscopy → a UNILATERAL, often pedunculated lesion on the free edge of the cord. Histology after excision → benign, and it excludes carcinoma at the same time.Rules the differentials OUTBilateral symmetric lesions mean nodules; diffuse cord swelling in a smoker means Reinke edema; benign histology is what formally excludes malignancy, which clinical appearance alone cannot do.Excision of the polyp, with continued vocal rest and smoking cessation.UrgentA large polyp may conceal an occult early laryngeal squamous cell carcinoma, which is why it is excised rather than watched.
Dental abscessMouth & salivaryL19 · slide 116–117“This tooth has been killing me and now my face is swollen.”A build-up of pus inside the teeth or gums, from bacterial infection accumulating in the soft pulp of the tooth. Slide 116 divides them into periapical (at the root tip), gingival (in the space between gum and tooth), periodontal (in a periodontal pocket) and pericoronal (around an impacted or partially erupted tooth).Percuss the suspect tooth — exquisite tenderness localizes it. Inspect for gingival swelling, a sinus tract, and caries. Assess the floor of mouth, trismus, and the airway — spread is the danger. Palpate cervical nodes. Check temperature.
  1. Ludwig anginaBilateral firm floor-of-mouth elevation with tongue displacement — the emergency
  2. Periodontal abscessArises from the periodontal pocket, tooth usually still vital
  3. SialadenitisGland swelling with pus at the duct, not tooth-related
Rules it INClinical → a percussion-tender tooth with localized swelling. Periapical or panoramic radiograph → a radiolucency at the tooth apex. Contrast computed tomography if there is facial swelling or trismus → the extent of spread and any deep space collection.Rules the differentials OUTRaised, firm floor of mouth means Ludwig angina and a different urgency entirely; pus from a salivary duct redirects to sialadenitis; a vital tooth with a pocket suggests periodontal rather than periapical origin.Antibiotics — amoxicillin, ampicillin-sulbactam, amoxicillin-clavulanate, azithromycin, clindamycin, erythromycin, cephalexin, metronidazole, penicillin VK. Incision and drainage. Root canal if the tooth can be restored; extraction with curettage of apical tissue if it cannot.UrgentUntreated, infection from a tooth can spread to the jaw, the brain or the sinus — and Ludwig angina is the neck version of that spread.
Dental caries, pulpitis and periapical abscessMouth & salivaryL19 · slide 123–124Early: “it’s sensitive to cold but it settles quickly.” Later: “it throbs at night and keeps me awake.”Common teeth diseases are cavities, pulpitis, periapical abscess, impacted teeth and malocclusion. The commonest cause of pulpitis and periapical abscess is tooth decay, and the second commonest is injury. Mild inflammation, if relieved, may not damage the pulp permanently; severe inflammation kills it. Pulpitis can lead to a pocket of pus at the root — a periapical abscess.Inspect teeth for cavitation and discoloration. Percussion tenderness and thermal testing — reversible pulpitis settles within seconds of removing the stimulus; irreversible pulpitis lingers and throbs. Assess mobility, swelling and any sinus tract. Check trismus and the airway.
  1. Reversible pulpitisBrief pain on stimulus only — the tooth is savable with a filling
  2. Irreversible pulpitisLingering spontaneous pain — needs root canal treatment or extraction
  3. Periapical abscessPercussion tenderness with swelling and an apical radiolucency
Rules it INThermal and percussion testing → which stage it is, and therefore which treatment. Periapical radiograph → the carious lesion's depth and an apical radiolucency once an abscess has formed. Vitality testing → a non-vital tooth.Rules the differentials OUTA tooth responding briefly and normally to cold is reversible pulpitis, not an abscess; no apical radiolucency argues against a periapical collection; facial swelling with trismus means imaging for spread rather than another radiograph.Dental treatment of the decay; root canal or extraction as for dental abscess.UrgentUntreated, infection from a tooth can spread to the jaw or beyond — brain or sinus.
Salivary gland neoplasmMouth & salivaryL19 · slide 139–143“There’s a painless lump in front of my ear that’s been slowly growing.”64–80% arise in the parotid, and 75–80% of those are benign. 7–15% submandibular, 50–60% benign. 1% sublingual. About 15% are minor salivary gland, and only 35% of those are benign. Most benign parotid tumors are epithelial; in minor glands the commonest is pleomorphic adenoma, then basal cell adenoma. Malignant disease is 3–4% of head and neck malignancy; mucoepidermoid carcinoma is the commonest, and in minor glands adenoid cystic carcinoma and adenocarcinoma. No specific risk factors are known. Benign parotid tumors are slow-growing painless masses often at the tail of the parotid.Palpate the mass for size, consistency, mobility and FIXATION. Test cranial nerve VII — facial weakness means malignancy until proven otherwise. Palpate cervical nodes. Examine the mouth and the parapharyngeal space bimanually. Note pain, which also suggests malignancy. Remember the rule: the SMALLER the gland, the HIGHER the chance the tumor is malignant.
  1. Pleomorphic adenomaThe commonest, benign, mobile and painless — but it can transform
  2. Warthin tumorBenign, often bilateral, in older male smokers
  3. Mucoepidermoid or adenoid cystic carcinomaFixed, painful, with facial weakness or nodes
Rules it INUltrasound → a solid mass and its position relative to the facial nerve plane. Fine needle aspiration → the cell type. Magnetic resonance → deep lobe extension and perineural spread — adenoid cystic carcinoma spreads along nerves. Definitive histology comes from excision.Rules the differentials OUTIncisional biopsy is avoided in the parotid — it seeds tumor and risks the facial nerve; benign cytology with a mobile painless mass and normal facial nerve function supports an adenoma; facial weakness, fixation or nodes mean malignancy regardless of what cytology says.Benign: complete surgical excision, no radiation. Malignant: surgical removal, radiotherapy for T1 and T2, palliative chemotherapy. Complications include recurrence with positive margins and transient or permanent facial paralysis.UrgentPrognosis is poor with pain, facial or other nerve involvement, high-grade histology, skin or tissue invasion, or recurrent disease.
Hairy leukoplakiaMouth & salivaryL19 · slide 136“The side of my tongue has gone white and ridged” — painless, and in a patient who may not know they are immunocompromised.Benign mucosal hyperplasia associated with Epstein-Barr virus, long-term systemic corticosteroids and solid organ transplantation. Strongly associated with HIV and a common early finding in HIV infection. Painless lateral tongue lesions that wax and wane over time.Inspect the LATERAL border of the tongue for white corrugated or hairy vertical folds. Attempt to scrape — it does NOT come off, unlike candida. Examine for other markers of immunosuppression: candidiasis, Kaposi sarcoma, adenopathy, wasting. Take a risk history.
  1. Oral candidiasisWipes off; may coexist on top of it
  2. LeukoplakiaAny site, and it is premalignant — hairy leukoplakia is not
  3. Lichen planusLacy striae, usually bilateral buccal, with a different appearance
Rules it INClinical appearance and site → strongly suggestive. Biopsy with Epstein-Barr virus testing → the virus in epithelial cells, confirming it. HIV testing with CD4 count → the underlying immunosuppression, which is the real finding.Rules the differentials OUTA plaque that wipes off is candida; the essential next step is not treating the tongue but testing for immunosuppression — hairy leukoplakia is a marker, not a disease in its own right; it is not premalignant, which separates it from leukoplakia.Observation. Acyclovir, valacyclovir or famciclovir produce temporary resolution.UrgentThe lesion itself is benign; its value is as a pointer to undiagnosed HIV.
Oral leukoplakiaMouth & salivaryL19 · slide 133–134“There’s a white patch in my mouth” — usually painless and often found by a dentist.A premalignant squamous lesion: altered epithelium at increased risk of progression to squamous cell carcinoma, 5–20%. Defined as a white lesion of the oral mucosa that cannot be scraped off and cannot be attributed to another definable lesion. Causes include chronic irritation, smoking and infection.Inspect and palpate the lesion — induration is worrying. Attempt to scrape it: it does NOT come off, which is the definitional feature. Note site — floor of mouth and ventral tongue carry the highest risk. Note whether it is homogeneous or SPECKLED, the speckled form being far more dangerous. Take a tobacco and alcohol history and palpate the neck.
  1. CandidiasisWipes off, leaving an erythematous base
  2. Lichen planusLacy striae rather than a homogeneous patch
  3. Squamous cell carcinomaInduration, ulceration or a mass — what the biopsy is looking for
Rules it INClinical definition → a white patch that cannot be wiped off and cannot be given another diagnosis — it is a diagnosis of EXCLUSION. BIOPSY → hyperkeratosis, dysplasia, or invasive carcinoma; the degree of dysplasia is what determines management.Rules the differentials OUTA patch that wipes off with yeasts on microscopy is candidiasis — and a trial of antifungal treatment is a reasonable first step, but persistence means biopsy; lacy striae mean lichen planus; benign hyperkeratosis excludes malignancy for now but not surveillance.Observation after eliminating carcinogenic irritants — smoking, chewing tobacco, alcohol — with serial biopsies and excisions.UrgentThe scrape test is the bedside discriminator: candidiasis wipes off, leukoplakia does not.
Behcet syndromeMouth & salivaryL19 · slide 19“I get mouth ulcers over and over, and I’ve had sores on my genitals and trouble with my eyes.”An inflammatory, multisystem disorder with vascular, articular, gastrointestinal, neurologic, urogenital, pulmonary and cardiac involvement. Oral ulcers are the commonest feature, affecting up to 100% of patients. Genital ulcers occur in about 75% and look like oral aphthae.Inspect oral ulcers, then examine the genitals and refer for a slit lamp examination of the eyes. Look for skin lesions — erythema nodosum and pustules. Examine joints and the nervous system.
  1. Recurrent aphthous stomatitisOral ulcers ALONE, with no genital, ocular or systemic disease
  2. Inflammatory bowel diseaseOral ulcers with bowel symptoms rather than genital ulcers and uveitis
  3. Herpes simplexVesicular, clustered, and it responds to antivirals
Rules it INClinical → recurrent aphthous ulceration in the context of the characteristic systemic manifestations; genital ulcers, similar in appearance to oral aphthae, occur in about 75%. Slit lamp → uveitis. Inflammatory markers → raised. There is no single confirmatory blood test.Rules the differentials OUTIsolated oral ulcers with no other system involved mean simple aphthous stomatitis; a positive viral swab means herpes; bowel investigation identifies inflammatory bowel disease instead.No cure. Corticosteroids, intravenous immunoglobulin, immunosuppressives — colchicine, azathioprine, cyclosporine-A, interferon alpha, cyclophosphamide.UrgentThe oral ulcers look ordinary; it is the genital ulcers and the systemic features that make the diagnosis.
Oral lichen planusMouth & salivaryL19 · slide 20–22“There are white lacy lines inside my cheeks, and lately eating spicy food burns.”A common chronic inflammatory autoimmune disorder in which the basal layer is destroyed by activated lymphocytes. May be familial or drug-induced (penicillamine, methyldopa, phenothiazine, antimalarials). Classically purple, polygonal, pruritic papules on flexor surfaces and trunk; 60–70% affect lips, oral mucosa and eyelids, and the oral lesions are more chronic. Kobner isomorphic phenomenon — lesions provoked by physical trauma. Types: reticular (lacy white Wickham striae), plaque (looks like leukoplakia), atrophic, erosive and bullous, ulcerative, annular.Inspect for Wickham striae — lacy white lines, usually BILATERAL on the buccal mucosa. Note whether it is reticular (asymptomatic) or erosive (painful, and the form that carries malignant risk). Examine skin, nails, scalp and genitals. Review medications for a lichenoid reaction.
  1. LeukoplakiaA homogeneous white patch without striae; also premalignant
  2. CandidiasisWipes off; may also be superimposed on lichen planus
  3. Lichenoid drug reactionLooks identical — the medication history is what separates them
Rules it INBiopsy → a band-like lymphocytic infiltrate at the basement membrane with basal cell degeneration. Direct immunofluorescence helps exclude the blistering diseases. Reticular disease with classic striae may be diagnosed clinically.Rules the differentials OUTA plaque that wipes off with hyphae on microscopy is candida; resolution after stopping a drug means a lichenoid reaction; dysplasia on biopsy changes it from a chronic condition to a premalignant one and mandates surveillance.Aimed at pain relief. Identify reversible contributors — medications, dental restorations, oral hygiene, tobacco and alcohol. Topical or oral corticosteroids; lidocaine, tacrolimus, cyclosporine.Urgent1–4% progress to squamous cell carcinoma, and the risk is higher with ulcerative lesions — which is why close follow-up is the point of the diagnosis.
Systemic lupus erythematosus — oralMouth & salivaryL19 · slide 23–24“I have ulcers on the roof of my mouth that don’t hurt, and I’ve been tired with sore joints and a rash.”40% of patients with systemic lupus erythematosus have mucous membrane involvement, and oral lesions may be the first sign of lupus. Painful or painless, with no correlation to systemic activity. Lesions: cheilitis, erythematous patches, honeycomb patches, discoid and discrete ulcers. White plaques, erythematous areas and punched-out erosions with surrounding erythema on the soft and buccal mucosa.Inspect for painless ulcers, characteristically on the HARD PALATE — the painless quality and the palatal site are both unusual. Look for a malar rash and photosensitivity. Examine joints. Check blood pressure and look for signs of renal disease.
  1. Aphthous ulcersPAINFUL and on non-keratinized mucosa — the opposite on both counts
  2. Lichen planusLacy striae with a different distribution
  3. Herpes simplexVesicular and painful, on keratinized mucosa
Rules it INAntinuclear antibody → positive, the screening test. Anti-double-stranded DNA and anti-Smith → specific for lupus. Complement C3 and C4 → low in active disease. Full blood count → cytopenias. Urinalysis → protein and casts in renal involvement.Rules the differentials OUTA negative antinuclear antibody makes lupus very unlikely; painful ulcers on non-keratinized mucosa with no systemic features mean aphthous stomatitis; a positive viral swab means herpes.Photoprotection plus medication: topical or intralesional corticosteroids, topical calcineurin inhibitors, systemic glucocorticoids, and systemic antimalarials — hydroxychloroquine or chloroquine.UrgentThe oral ulcers do not track disease activity, so they cannot be used to judge control.
Acute suppurative sialadenitisMouth & salivaryL19 · slide 34–39“My cheek swelled up quickly, it’s hot and painful, and there’s a foul taste in my mouth.” Often an elderly, dehydrated or postoperative patient.Bacterial infection of a salivary gland, beginning with stasis of salivary flow. Occurs in post-operative patients, elderly patients with chronic conditions, and children under 2 months. Risk factors: dehydration, trauma, immunosuppression, chemotherapy or radiation, age over 50, HIV, xerostomia, sialolithiasis, anorexia and bulimia. Staphylococcus aureus is the commonest pathogen. The parotid is most commonly affected: unilateral, firm, diffusely tender, with overlying erythema, trismus, purulent ductal discharge, induration, fever and chills.Palpate the gland for a tender, warm, indurated swelling. Milk the duct — Stensen duct opposite the second upper molar for parotid, Wharton duct in the floor of mouth for submandibular — and look for PUS at the orifice. That expressed pus is the finding. Assess hydration, trismus and the airway. Check cranial nerve VII.
  1. SialolithiasisSwelling that comes on WITH MEALS and settles between them, without pus
  2. Mumps parotitisBilateral, viral, in an unvaccinated patient, with no purulent discharge
  3. Parotid neoplasmPainless, firm, progressive — and facial weakness means malignancy
Rules it INMilking the duct → frank pus, which confirms it. Culture → usually Staphylococcus aureus. Ultrasound or contrast computed tomography → an abscess needing drainage, or a stone. Avoid sialography in acute infection.Rules the differentials OUTClear saliva on milking with meal-related swelling means a stone; bilateral swelling without pus suggests mumps — viral serology or polymerase chain reaction confirms it; a painless progressive mass needs imaging and cytology for tumor.Rehydration plus intravenous antibiotics with penicillinase-resistant gram-positive cover (nafcillin or cefazolin), then oral (dicloxacillin, clindamycin). Warm compresses, massage, sialogogues (lemon drops or vitamin C lozenges), oral hygiene. No improvement in 48 hours means presume an abscess.UrgentSubmandibular disease that fails treatment can mimic Ludwig angina, which threatens the airway.

Emergent18 conditions

These do not wait for a clinic appointment. If the station gives you one of these, the answer to “what is your plan” begins with where the patient goes now, not with which test you would order.

Condition How the patient describes it
the words they actually use		 What you see on inspection Physical exams to rule it in or out
the maneuvers, not the findings		 Top 3 differentials
and what separates each one		 Tests — and what a positive looks like Treatment & referral Patient education
Sudden sensorineural hearing lossEarL16 · slide 13, 79“I woke up and one ear just wasn’t working.”Unilateral. Described explicitly as a syndrome, not a disease. Viral or vascular etiology; rarely retrocochlear pathology — horses not zebras. The exact cause is rarely certain.Otoscopy must be normal. Weber lateralizes AWAY to the good ear and Rinne stays normal (air over bone) in both — that pair is what proves it is sensorineural. Check cranial nerves and balance.
  1. Cerumen impactionWax visible; Weber would lateralize TOWARD the blocked ear
  2. Otitis media with effusionAmber drum with reduced mobility; conductive pattern
  3. Acoustic neuromaGradual rather than sudden, with speech discrimination out of proportion
Rules it INPure tone audiometry → a sensorineural loss with NO air-bone gap, by definition at least 30 decibels across three contiguous frequencies. Magnetic resonance with gadolinium → an enhancing lesion in the internal auditory canal if a schwannoma is the cause.Rules the differentials OUTA normal otoscopy excludes wax and effusion; a normal tympanogram excludes a middle ear cause; normal imaging excludes a schwannoma.Demands prompt referral to ENT. Acute sensory loss may respond to corticosteroids within the first weeks.EmergentSpeed is the whole management. This is the one hearing complaint that is seen the same day.
Malignant otitis externaEarL15 · slide 61“My ear has been running for weeks and the pain keeps me awake — the drops did nothing.”Also called necrotizing external otitis. A severe and potentially fatal infection of the bone and marrow spaces of the skull base and the soft tissue and cartilage of the temporal region. Elderly diabetics and immunocompromised patients are most at risk. Over 95% is spread of P. aeruginosa from an otitis externa. Symptoms: severe otalgia out of proportion to the physical findings, copious otorrhea, sometimes visible necrosis of the canal and evidence of facial nerve weakness.Otoscopy looking for granulation tissue at the bony-cartilaginous junction. Palpate the mastoid and TMJ. Test all cranial nerves, especially VII — a facial palsy marks skull base spread. Check glucose and immune status.
  1. Ordinary otitis externaResponds to drops within days and has no granulation or night pain
  2. OtomycosisItch dominates, visible hyphae or curd, no bone involvement
  3. Ear canal carcinomaAlso treatment-resistant, but bleeds and is friable rather than granulating at one point
Rules it INComputed tomography or magnetic resonance of the temporal bone → bony erosion of the skull base. Erythrocyte sedimentation rate → markedly raised, and it is what treatment response is tracked against. Canal culture → Pseudomonas aeruginosa.Rules the differentials OUTNormal imaging and prompt response to topical therapy exclude it; biopsy of friable tissue excludes carcinoma; fungal culture excludes otomycosis.Antipseudomonal antibiotics — for example ciprofloxacin.EmergentThe complaint that matters is pain far worse than the ear looks, in a diabetic or immunocompromised patient. That combination is not treated as a routine swimmer's ear.
Carcinoma of the ear canalEarL15 · slide 71“It has been discharging for months, now there is blood in it and a deep ache.”Very rare and aggressive. Presents with an abnormal growth in the ear canal, bloody otorrhea, a friable ear canal and failure to respond to treatment for external otitis. Late findings are hearing loss and facial paralysis. Often misdiagnosed as otitis externa.Otoscopy for friable tissue and bloody otorrhea. Palpate for parotid and cervical nodes. Cranial nerve examination, particularly VII.
  1. Malignant otitis externaDiabetic or immunocompromised, granulation rather than a friable mass
  2. Chronic suppurative otitis mediaPainless discharge through a perforation, no bleeding
  3. CholesteatomaWhite keratin behind a retraction pocket, foul but not bloody
Rules it INBiopsy of the canal lesion → squamous cell carcinoma on histology. Computed tomography of the temporal bone → bony erosion where infection alone would not.Rules the differentials OUTImaging for bone involvement separates it from the infections; a normal biopsy with Pseudomonas on culture points back to necrotising otitis externa.Biopsy first, then oncological management (ENT).EmergentThe teaching point is the misdiagnosis: an otitis externa that does not respond, especially with blood, gets looked at again rather than re-treated.
Isolated cerebellar infarctionEarL16 · slide 78“Everything is spinning and I cannot sit up without falling over.”Symptoms include vertigo, facial pain or numbness, headache, or ataxia. The deck's instruction is explicit: “Don't miss something bigger than the hearing loss” — look for signs of a more sinister acute problem.Truncal stability — can they sit unsupported? A peripheral patient usually can. Look for direction-changing nystagmus, limb ataxia, and any focal deficit. Ask about headache.
  1. Vestibular neuronitisUnidirectional nystagmus, can still sit, no headache
  2. LabyrinthitisSame as neuronitis but with hearing loss; still no central signs
  3. Positional vertigoBrief and positional; the patient is well between episodes
Rules it INMagnetic resonance imaging with diffusion weighting → restricted diffusion in a cerebellar hemisphere. Computed tomography is often NORMAL early, so a normal scan does not exclude it.Rules the differentials OUTUnidirectional fatigable nystagmus with intact truncal stability and no headache points peripheral; normal imaging excludes infarction.Refer for evaluation.EmergentIt is in a hearing lecture as a warning, not as an ear disease.
Vertebrobasilar insufficiency or occlusionEarL16 · slide 77, 85–87“The room spins and my speech goes funny, and sometimes I see double.”A common cause of vertigo in elderly patients. Occlusion may be thrombotic or embolic. Symptoms: acute vertigo, nausea and vomiting, facial paralysis, tinnitus, ipsilateral gaze paralysis, ipsilateral loss of pain and temperature on the face, contralateral partial loss of pain and temperature on the trunk and limbs, and ipsilateral Horner's syndrome. Vascular disease is the commonest non-vestibular cause of dizziness and balance loss in the elderly.Full cranial nerve and cerebellar examination — the point is to find the signs that are NOT ear. Gait, finger-nose, heel-shin. Blood pressure in both arms; listen for carotid bruits; check rhythm for atrial fibrillation.
  1. Vestibular neuronitisSustained vertigo but NO other neurological sign and normal hearing
  2. Meniere diseaseEpisodic vertigo with fluctuating low-frequency loss and fullness
  3. Positional vertigoSeconds only, provoked by position, fatigable nystagmus
Rules it INMagnetic resonance imaging and angiography of the posterior circulation → stenosis or occlusion of the vertebral or basilar artery, with infarction in its territory.Rules the differentials OUTThe presence of diplopia, dysarthria or limb signs is itself what excludes the peripheral causes; a normal Dix-Hallpike excludes positional vertigo.Vascular and stroke management.EmergentVertigo with any crossed sensory finding, facial weakness or gaze palsy is a brainstem problem until proven otherwise.
Epistaxis — posteriorNose & sinusesL17 · slide 45–46“It won’t stop, and I keep swallowing blood.”Arises most commonly from the posterolateral branches of the sphenopalatine artery, but may arise from branches of the carotid. Results in significant hemorrhage.Assess circulation first — pulse, blood pressure, conscious level. Then anterior rhinoscopy: if no bleeding point is visible and blood runs down the pharynx, it is posterior. Look in the throat.
  1. Anterior epistaxis90% of cases; a visible spot on Kiesselbach plexus, stops with pressure
  2. Nasal foreign bodyUnilateral foul purulent discharge, usually a young child
  3. Nasopharyngeal tumorRecurrent bleeding with obstruction, a neck mass or cranial nerve signs
Rules it INNasal endoscopy → a bleeding point posterior to the middle turbinate, with no anterior source — often the only way to see it. Full blood count → the hematocrit, and type and crossmatch → blood ready if it continues. Coagulation studies → a raised international normalized ratio or low platelets driving it.Rules the differentials OUTA visible anterior bleeding point that stops with ten minutes of pressure excludes a posterior source; endoscopy excludes a tumor.As for anterior bleeding, escalating to packing and ENT involvement.EmergentPosterior bleeds carry a higher risk because of ASPIRATION and subsequent infection — that is why the distinction is made.
Nasopharyngeal carcinomaNose & sinusesL17 · slide 69–70“I found a lump in my neck, and lately I’ve had double vision and my cheek feels numb.”The predominant tumor arising in the nasopharynx. Rare in the United States and Western Europe; endemic in Southern China including Hong Kong, Southeast Asia, North Africa, the Middle East and the Arctic. Two- to threefold more common in males. Associated with Epstein-Barr virus, human papillomavirus and smoking, and with high-salt diets, Chinese herbs, rancid butter and sheep fat.Palpate the neck systematically. Cranial nerve examination — especially VI for diplopia and V for facial numbness. Otoscopy for a middle ear effusion, which is often the first sign. Anterior rhinoscopy.
  1. Chronic sinusitisCongestion and discharge without a neck mass or cranial nerve deficit
  2. Reactive lymphadenopathyFollows an infection and regresses within two weeks
  3. LymphomaRapid painless nodal growth with night sweats and weight loss
Rules it INEndoscopic guided biopsy → carcinoma of the nasopharynx. Magnetic resonance imaging → a nasopharyngeal mass with skull base involvement. Epstein-Barr titres are supportive, not diagnostic.Rules the differentials OUTA normal nasopharynx on endoscopy excludes it; a node that regresses excludes malignancy; Epstein-Barr serology supports rather than confirms.Oncological management following biopsy (ENT).EmergentThe combination that should prompt referral is a neck mass with cranial nerve symptoms, not nasal symptoms alone.
Sinusitis with urgent featuresNose & sinusesL17 · slide 17, 21“My sinuses have been bad for a week and now my eye is swollen and I’m seeing double.”The lecture names these separately as symptoms requiring urgent attention in a patient with sinusitis: visual disturbance, especially diplopia; periorbital swelling or erythema; altered mental status.Eye movements and pain on movement, visual acuity, pupils for a relative afferent defect, and look for proptosis. Assess mental state. Palpate sinus tenderness.
  1. Uncomplicated bacterial sinusitisFacial pain and purulence WITHOUT eye or neurological signs
  2. Pre-septal cellulitisLid swelling but the eye is white, movements full and painless
  3. Allergic rhinitisBilateral clear discharge with itch and a bluish boggy mucosa
Rules it INContrast computed tomography of orbits and sinuses → opacified sinuses PLUS fat stranding, a subperiosteal collection or proptosis — sinus opacity alone is present in ordinary sinusitis and proves nothing.Rules the differentials OUTFull painless eye movements with normal vision exclude orbital involvement; normal mental state and no headache argue against intracranial spread.Urgent evaluation and imaging rather than another course of symptomatic treatment.EmergentThe orbit sits next door to the ethmoid sinus. Eye signs in a sinusitis patient are the ones that change the plan.
Ludwig anginaNeckL19 · slide 108–111“My tooth was killing me and now my whole neck under the chin is swollen and I can’t swallow.”A severe infection of the floor of the mouth and the submental, sublingual and submandibular spaces. Can rapidly compromise the upper airway and force a surgical airway. Streptococci, staphylococci, Bacteroides, Fusobacterium, Klebsiella — the last usually in patients with diabetes, who have a more aggressive course. Edema and erythema of the upper neck under the chin and the floor of the mouth; the tongue is displaced upwards and backwards by posterior spread of cellulitis; pus coalescing at the floor of the mouth.Inspect and palpate the floor of the mouth — is it raised and firm? Look for tongue displacement upward and backward. Assess airway and voice. Examine the dentition for the offending tooth.
  1. Submandibular sialadenitisSwelling of the gland itself, pus from the duct, no floor elevation
  2. Dental abscessLocalized to one tooth without spread across the floor of the mouth
  3. Peritonsillar abscessIntraoral and unilateral with trismus and uvular deviation
Rules it INContrast computed tomography of the neck → diffuse cellulitis and phlegmon of the submandibular and sublingual spaces, with or without a rim-enhancing collection; airway narrowing is the finding that decides the next hour.Rules the differentials OUTA soft floor of mouth with a normally positioned tongue excludes it; pus expressible from Wharton duct points to sialadenitis.Antibiotics: penicillin with metronidazole, ampicillin-sulbactam, clindamycin, or selected cephalosporins. External drainage via bilateral submental incision if the airway is threatened or medical therapy fails. Dental consultation to deal with the offending tooth.EmergentIt is usually odontogenic, which is why the dental referral is part of the treatment rather than an afterthought.
Peritonsillar abscess (quinsy)NeckL19 · slide 96–101“My throat is agony on one side, I can’t open my mouth properly and I sound strange.”Purulence between the capsule of the palatine tonsil and the pharyngeal muscles, beginning as a complication of untreated strep throat or tonsillitis. The commonest deep infection of the head and neck, especially in young adults, adolescents and children; commoner in males. Aerobes: group A beta-hemolytic streptococcus, Staphylococcus aureus, Haemophilus influenzae. Anaerobes: Prevotella, Porphyromonas, Fusobacterium, Streptococcus. Severe sore throat, fever, odynophagia, medial deviation of the soft palate and peritonsillar fold, uvular deviation, hot potato voice, trismus, dysphagia.Measure mouth opening — trismus is the most reliable sign. Inspect for uvular deviation and medial displacement of the soft palate. Listen for the hot potato voice. Palpate cervical nodes.
  1. Severe tonsillitisBilateral and symmetric with no palatal deviation or trismus
  2. Retropharyngeal abscessNeck stiffness and a widened prevertebral space; younger child
  3. EpiglottitisDrooling with tripod posture; the mouth cannot safely be examined
Rules it INNeedle aspiration → frank pus, which both confirms and treats. Ultrasound → a discrete hypoechoic collection rather than diffuse cellulitis. Contrast computed tomography → a rim-enhancing peritonsillar collection.Rules the differentials OUTSymmetric tonsils with a midline uvula exclude it; a normal lateral neck film excludes a retropharyngeal collection.Secure the airway first if needed. Needle aspiration and incision and drainage. Antibiotics: parenteral amoxicillin-clavulanate or clindamycin, adding MRSA cover if severe; oral if tolerated. Tonsillectomy for recurrent tonsillitis and recurrent abscesses, usually after the acute infection settles — quinsy tonsillectomy during infection is occasional.EmergentTrismus is the most reliable symptom; the dysphonia comes from vagus nerve involvement failing to elevate the palate.
Retropharyngeal abscessNeckL19 · slide 103–107A parent says “she won’t eat, she’s drooling and she holds her neck stiff.”An abscess in the retropharyngeal space, running from the base of skull to the posterior mediastinum. May spread from a peritonsillar abscess or from a node in that space. Commoner in children under 5 after upper respiratory infection, otitis media or sinusitis; in adults it follows intraoral procedures, trauma, foreign bodies such as fishbone, immunocompromise or odontogenic spread. Group A beta-hemolytic streptococcus, Staphylococcus aureus, Haemophilus influenzae, mixed flora. Early: fever, sore throat, pharyngeal erythema, dysphagia, odynophagia, neck stiffness, trismus. Late: ill appearance, drooling, leaning forward with the neck extended, respiratory distress.Observe posture and drooling. Test neck movement — stiffness and refusal to extend is the pointer. Assess the airway. Avoid vigorous pharyngeal examination.
  1. EpiglottitisSame drooling and posture but a much faster onset and no neck stiffness
  2. Peritonsillar abscessTrismus with uvular deviation; older patient
  3. MeningitisNeck stiffness with photophobia and altered consciousness rather than dysphagia
Rules it INLateral neck radiograph → a widened prevertebral soft tissue space, taken in full inspiration with the neck extended or it falsely appears widened. Contrast computed tomography of the neck, the gold standard → a rim-enhancing collection in the retropharyngeal space, which is what separates a drainable abscess from cellulitis.Rules the differentials OUTA normal prevertebral space excludes it; computed tomography separates abscess from adenitis, which is the decision that matters.Protect the airway. Surgical emergency. Antibiotics covering streptococci, anaerobes and Staphylococcus aureus: ampicillin-sulbactam, or clindamycin with ceftriaxone; vancomycin or linezolid if not improving; switch to oral on clinical improvement.EmergentMediastinitis carries 50% mortality. Other complications: respiratory distress, rupture with aspiration pneumonia, and spread into the danger space, which is continuous left to right and leads directly to the thorax.
Neck neoplasm — generalNeckL18 · slide 37, 39“There’s a lump in my neck that hasn’t gone away.”Benign tumors arise from the soft tissue of the neck — fat, salivary tissue, lymph nodes, blood vessels, nerves. Malignant ones are usually metastatic squamous cell carcinoma from skin or the upper aerodigestive tract. Hoarseness, dysphagia and odynophagia are the symptoms; the lesion itself is asymptomatic, slowly progressive and firm.Characterize the mass: site, size, consistency, mobility and tenderness. Then the complete head and neck examination — visualize every mucosal surface and palpate the oral and pharyngeal surfaces. Palpate thyroid, other nodal basins, liver and spleen. Auscultate for a bruit.
  1. Reactive lymphadenopathyInfective context, tender, regresses within two weeks
  2. Congenital cystPresent for years, fluctuant, lateral or midline by type
  3. LymphomaRapid growth WITHOUT infective symptoms, with night sweats and weight loss
Rules it INFine needle aspiration, minimum four passes → malignant cells, and which kind: squamous carcinoma against lymphoma. Contrast computed tomography → a solid, irregular, centrally necrotic node rather than a smooth cystic one.Rules the differentials OUTAn identified infective source with resolution excludes malignancy; aspiration separates carcinoma from lymphoma; imaging separates solid from cystic.Directed by the primary once it is found. Once the diagnosis is confirmed, all mucosal surfaces of the head and neck, the thyroid, the salivary glands and the skin are examined — the office examination usually finds the primary.EmergentThe malignancy features from slide 13: no infectious origin, duration over 2 weeks, size over 1.5 cm, firm and non-tender with little mobility, age over 40, tobacco and alcohol, and ulceration.
Primary neck tumors — the listNeckL18 · slide 38Not a presentation — a reference list of what a primary neck tumor can be.Malignant: sarcomas (rhabdomyosarcoma, fibrosarcoma, malignant fibrous histiocytoma, liposarcoma, leiomyosarcoma); malignant peripheral nerve sheath tumors; lymphoma; and metastasis — mucosal cancer from head and neck, salivary malignancies, skin malignancies. Benign: vascular neoplasms, chiefly paragangliomas (carotid body, vagal, jugulotympanic); arteriovenous malformations; peripheral nerve neoplasms (schwannomas, neurofibromas, neuromas); and lipomas.As for any neck mass: characterize the lump, then a complete head and neck examination, and auscultate for a bruit before any needle is used.
  1. Metastatic squamous carcinomaFar commoner than any primary neck tumor
  2. LymphomaRubbery, multiple, with constitutional symptoms
  3. ParagangliomaPulsatile with a bruit — must not be biopsied blindly
Rules it INFine needle aspiration → the cell type, for solid masses only. Computed tomography angiography FIRST if it pulsates → an intensely enhancing mass splaying the carotid bifurcation, which is a paraganglioma and must not be needled.Rules the differentials OUTA bruit or pulsation excludes a safe blind biopsy and redirects to angiography.By tumor type.EmergentA pulsatile mass or a bruit means vascular, and paraganglioma heads that list.
Anaplastic thyroid carcinomaThyroidL18 · slide 42, 44“This lump in my throat has grown in a matter of weeks and now my voice has gone.”1% of thyroid cancers, commonly in elderly patients. Small cell, giant cell and spindle cell types. The most aggressive form — death in 6 to 36 months — and resistant to all treatment modalities.Palpate the thyroid while the patient swallows — it should elevate. Assess for stridor and tracheal deviation. Listen to the voice; check for cervical nodes.
  1. Papillary carcinomaSlow-growing in a younger patient with a far better outlook
  2. Primary thyroid lymphomaAlso rapid in an older patient, but on a Hashimoto background
  3. Multinodular goiterLong-standing, soft, no hoarseness or compressive symptoms
Rules it INFine needle aspiration → undifferentiated small, giant and spindle cells. Computed tomography → a large infiltrative mass with tracheal compression.Rules the differentials OUTCytology separates it from lymphoma, which needs an open biopsy; a long history with a stable gland excludes it.Isthmectomy rather than thyroidectomy.EmergentThe one thyroid cancer where the prognosis is measured in months.
Epiglottitis (supraglottitis)Throat & larynxL19 · slide 60–67“It hurts so much to swallow I can’t even manage my own spit.” A child may say nothing and simply sit forward.More correctly supraglottitis: cellulitis involving multiple areas of the supraglottis. Acute disease presents in children aged 2 to 6, though any age can be affected. Commonest pathogen is Haemophilus influenzae type B — incidence has fallen over 90% since the vaccine. Others: Streptococcus pneumoniae, Staphylococcus aureus, beta-hemolytic streptococci. Children: the 4 Ds. Adults: severe sore throat, dysphagia, odynophagia, fever, dyspnea, cough; muffled voice, stridor and drooling in under 10%. Sudden onset progressing over hours in children, more slowly in adults. Classic picture is an irritable patient sitting or leaning forward, neck hyperextended, chin thrust forward. Inspiratory stridor is a LATE finding — the airway is nearly obstructed.Look, do not touch. Observe posture (tripod, neck extended, chin forward), drooling, voice quality and work of breathing. Do NOT perform an intraoral examination or venipuncture — either can complete the obstruction.
  1. Peritonsillar abscessTrismus with uvular deviation; the mouth CAN be examined
  2. Retropharyngeal abscessNeck stiffness with a widened prevertebral space on X-ray
  3. CroupBarking cough with a slower onset and a well-looking child
Rules it INMirror or fiberoptic laryngoscopy, the gold standard → a cherry-red, swollen epiglottis, performed only where the airway can be secured. Lateral neck radiograph → the thumbprint sign, a swollen epiglottis in profile — supportive, but a normal film does NOT exclude it, so it is never the reason to stand down.Rules the differentials OUTDirect visualization of a normal supraglottis excludes it; a lateral neck film showing a widened prevertebral space redirects to retropharyngeal abscess.Airway, antibiotics, prevention. Pediatric: to theater for rigid bronchoscopy and emergency tracheotomy standby; inhalation anesthesia, confirm the diagnosis, secure the airway by intubation; blood cultures and supraglottic swab; parenteral antibiotics — extubation is often possible within 48 to 72 hours. Adult: observation, intubation or tracheostomy if the airway obstructs, humidification, glucocorticoids, intravenous antibiotics, nebulized adrenaline. Third-generation cephalosporin plus an antistaphylococcal agent — ceftriaxone or cefotaxime with vancomycin for 7–10 days.EmergentThe mortality is what justifies the caution: rare, but high if it is not recognized and treated promptly.
DiphtheriaThroat & larynxL19 · slide 112–114“My throat is a bit sore but I feel dreadful.” — the malaise is out of proportion to the sore throat.Corynebacterium diphtheriae, attacking the respiratory tract and sometimes mucous membrane or skin wounds, spread by respiratory secretions. Nasal, laryngeal, pharyngeal (commonest) and cutaneous forms. Common in unimmunized children over 6 years. Nasal: discharge. Laryngeal: upper airway and bronchial obstruction. Pharyngeal: a tenacious gray membrane covering tonsils and pharynx, with mild sore throat, fever, malaise, toxemia and prostration. Complications: myocarditis (arrhythmia, heart block, failure) and neuropathy involving cranial nerves first — diplopia, slurred speech, difficulty swallowing.Inspect the pharynx for a tenacious gray membrane that bleeds when disturbed. Palpate for a bull neck. Cardiac and cranial nerve examination, since the toxin causes myocarditis and neuropathy. Check immunization status.
  1. Streptococcal pharyngitisExudate wipes away and does not bleed; no toxemia
  2. Infectious mononucleosisPalatal petechiae with splenomegaly and marked fatigue
  3. CandidiasisCreamy patches that wipe off leaving an erythematous base
Rules it INThroat swab and culture on tellurite medium → Corynebacterium diphtheriae. Electrocardiogram → heart block or arrhythmia from toxin-induced myocarditis.Rules the differentials OUTAn exudate that wipes off without bleeding excludes it; a positive monospot points to mononucleosis; potassium hydroxide preparation confirms candida.Laryngoscopy or bronchoscopy to prevent or relieve obstruction. Antitoxin for all — obtained from the Centers for Disease Control. Penicillin 250 mg four times daily or erythromycin 500 mg four times daily for 14 days. Isolate until three consecutive cultures after therapy are negative. Treat contacts with erythromycin for 7 days.EmergentPrevention is immunization: childhood schedule plus boosters, and Tdap in every pregnancy between 27 and 36 weeks.
Oral cavity and oropharyngeal cancerMouth & salivaryL19 · slide 144–148“This ulcer hasn’t healed for weeks, and my ear aches on that side.”Oral cavity means the anterior two thirds of tongue, buccal mucosa, floor of mouth, hard palate, upper and lower gingiva and retromolar trigone — the lip is no longer part of the oral cavity under the 8th staging system. Oropharynx means posterior third of tongue, palatine tonsil, soft palate and posterior pharyngeal wall. Males are 2–4 times more likely for oral cavity and 3–5 times for oropharyngeal. 60–80% of oropharyngeal cancer is human papillomavirus related; 90% of oral cavity cases relate to chronic sun exposure. Mean age 62. Risks: tobacco chewed and smoked, alcohol, betel nut, poor oral hygiene, immunosuppression. Squamous cell carcinoma is commonest; lymphoma is the second commonest tumor of the tonsillar fossa. Non-healing ulcers, bleeding, pain, ill-fitting dentures; advanced: dysarthria, dysphagia, neck mass, referred otalgia from cranial nerve involvement; tonsillar lesions give odynophagia and trismus.Inspect and palpate every oral surface, including the floor of mouth and tongue base. Assess tongue mobility and trismus. Palpate cervical nodes. Examine the ear — it will be normal despite the pain.
  1. Traumatic ulcerResolves once the denture or sharp tooth is corrected
  2. Aphthous ulcerHeals in 7 to 10 days; on non-keratinized mucosa
  3. Erythroplakia or leukoplakiaA patch rather than an ulcer, though either may harbor carcinoma
Rules it INBiopsy → squamous cell carcinoma. p16 immunohistochemistry or in situ hybridization → positive in human papillomavirus related oropharyngeal disease, which carries a better prognosis. Computed tomography or magnetic resonance → the primary and any nodal spread.Rules the differentials OUTHealing within two weeks after removing an irritant excludes malignancy; a normal ear examination with persistent otalgia is itself a pointer TOWARD it.Surgical resection alone for oral cavity; resection plus radiotherapy for oropharyngeal, where radiotherapy gives better functional outcomes.EmergentPrevention is tobacco and alcohol cessation. An ulcer that has not healed is the symptom that should never be watched.
ErythroplakiaMouth & salivaryL19 · slide 133, 135“There’s a red patch in my mouth that won’t go.” — often asymptomatic and found incidentally.As leukoplakia but with an erythematous component. 90% are either dysplastic or already carcinoma, and the risk of malignancy is around 25% — substantially higher than leukoplakia. Alcohol and tobacco are the major risk factors.Inspect every mucosal surface with a good light. Attempt to scrape the lesion — it does not come off. Palpate the lesion and the neck nodes. Ask about tobacco and alcohol.
  1. LeukoplakiaWhite rather than red, and far less likely to be malignant
  2. Erythematous candidiasisPainful, denture-related, responds to antifungals
  3. Lichen planusLacy white striae, often bilateral and symmetric
Rules it INExcisional biopsy → dysplasia or frank carcinoma in about 90%, which is the figure that makes this urgent.Rules the differentials OUTA lesion that wipes off is candidiasis; resolution on antifungal therapy excludes it; biopsy settles the rest.As for leukoplakia, but the threshold for excision is lower.EmergentRed is worse than white. If one lesion on the slide deck earns urgency, it is this one.