Clinical Medicine and Surgery I · Exam 3

How to use this guide

Dr. Carter’s Clin Med Pro Study Tip (Hypotension deck, slide 7) lists what to learn for every condition. Each card below answers those ten fields:

Name of Condition
Definition
Etiology (cause)
Epidemiology (who)
Risk Factors
Pathology
Clinical Manifestation
Diagnosis
Treatment/Therapy
Mortality ★

Every field comes from the lecture slides only. Where a deck is silent the card says Not covered in the lecture rather than filling the gap from elsewhere (451 of 1420 fields in this exam; Mortality alone: 103 of 142). Slide numbers follow each field. Cards open closed; tap one to read it.

Lecture 15 · Disorders of the External and Middle Ear

Prof. Hugh Griffenkranz · 18 conditions · source: Disorders External and Middle Ear 9-2026.pptx

Eustachian tube dysfunction4 not covered

Name of Condition: Eustachian tube dysfunction Slides 6, 8
Definition: Not covered in the lecture
Etiology (cause): Most commonly edema of the tissue lining the tube secondary to upper respiratory infection or allergy; often transient (days to weeks) Slide 8
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Eustachian tube connects the middle ear to the nasopharynx, is closed except during swallowing or yawning, and passes air to equalize pressure (can also let fluid into the middle ear); edema of its lining blocks it Slides 7, 8
Clinical Manifestation: Sensation of ear fullness; mild-moderate hearing impairment; crackling/popping with yawning or swallowing (indicates partial blockage of the tube) Slide 8
Diagnosis: Physical exam: retraction of the tympanic membrane; decreased mobility with insufflation Slide 9
Treatment/Therapy: Systemic or intranasal decongestants; intranasal corticosteroids; forced exhalation against resistance (caution with active nasal discharge: may force fluid into the middle ear and trigger acute otitis media); education: avoid air travel or other altitude/pressure changes until symptoms resolve Slide 10
Mortality ★: Not covered in the lecture

Acute otitis media2 not covered

Name of Condition: Acute otitis media (AOM); suppurative otitis media (discharge into the external canal through a tympanic membrane perforation); recurrent AOM Slides 12, 13
Definition: Rapid-onset inflammation of the middle ear; recurrent AOM = 3 or more episodes in 6 months or >4 episodes in 12 months, with complete resolution between episodes Slide 13
Etiology (cause): Most often follows upper respiratory illness; eustachian tube dysfunction (inflammation from respiratory illness or allergies; obstruction by adenoid hypertrophy or other masses); most common bacteria Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis Slides 13, 14
Epidemiology (who): Otitis media is most common in the pediatric population, peak incidence around 2 years of age; adults are 3-15% of acute otitis media diagnoses Slide 12
Risk Factors: Not covered in the lecture
Pathology: Eustachian tube dysfunction leads to middle ear inflammation with purulent effusion; if the tympanic membrane perforates, discharge drains into the external canal (suppurative otitis media) Slides 13, 14, 16
Clinical Manifestation: Otalgia; fever; hearing loss; complications: tympanic membrane perforation, mastoiditis (infection spreads to the mastoid air cells), labyrinthitis (infection spreads to the labyrinth), meningitis/encephalitis (rare) Slides 15, 19
Diagnosis: Clinical diagnosis; exam (varies with degree of infection): erythematous and/or bulging tympanic membrane, purulent effusion often visible, decreased mobility on pneumatic otoscopy, possible cervical lymphadenopathy; tympanometry optional (quantitative tympanic membrane mobility) Slides 16, 17
Treatment/Therapy: Most episodes resolve spontaneously; antibiotics for bacterial involvement (e.g., amoxicillin); analgesics and antipyretics for otalgia and fever; consider tympanostomy tubes for refractory/recurrent episodes or complications (ENT (ear, nose, and throat specialist)) Slide 18
Mortality ★: Not covered in the lecture

Otitis media with effusion2 not covered

Name of Condition: Otitis media with effusion (OME); serous otitis media (serous effusion) Slide 13
Definition: Inflammation of the middle ear space with an effusion present Slide 13
Etiology (cause): Eustachian tube dysfunction trapping fluid in the middle ear space; effusion often present after bacterial acute otitis media resolves Slide 14
Epidemiology (who): Otitis media overall is most common in the pediatric population, peak incidence around 2 years of age (stated for otitis media as a group) Slide 12
Risk Factors: Not covered in the lecture
Pathology: Fluid effusion trapped in the middle ear by eustachian tube dysfunction; may be serous (serous otitis media) Slides 13, 14
Clinical Manifestation: Often asymptomatic (may be an incidental otoscopy finding); hearing loss; sensation of ear fullness; complications: temporary conductive hearing loss (speech/language delay in children), acquired cholesteatoma Slides 15, 19
Diagnosis: Clinical diagnosis; exam: dull tympanic membrane, air/fluid level often visible, decreased mobility on pneumatic otoscopy, possible cervical lymphadenopathy with recent respiratory illness or resolved acute otitis media; tympanometry optional Slides 16, 17
Treatment/Therapy: Most episodes resolve spontaneously; management depends on duration of fluid, degree of hearing loss, and effect on speech/language development; tympanostomy tubes (ENT (ear, nose, and throat specialist)); consider adenoidectomy if adenoid hypertrophy obstructs the eustachian tubes (ENT) Slide 18
Mortality ★: Not covered in the lecture

Chronic otitis media3 not covered

Name of Condition: Chronic otitis media (COM); subtypes: benign COM, COM with effusion (chronic serous otitis media), chronic suppurative otitis media (CSOM) Slide 20
Definition: Recurrent infections with a non-healing perforation of the tympanic membrane Slide 20
Etiology (cause): Not covered in the lecture
Epidemiology (who): Otitis media overall is most common in the pediatric population, peak incidence around 2 years of age (stated for otitis media as a group) Slide 12
Risk Factors: Not covered in the lecture
Pathology: Non-healing tympanic membrane perforation; benign COM = dry perforation with no active infection; COM with effusion = continuous serous drainage through the perforation; CSOM = persistent purulent drainage through the perforation Slide 20
Clinical Manifestation: Recurrent infections; serous or purulent drainage through the perforation depending on subtype (dry in benign COM) Slide 20
Diagnosis: Duration required for diagnosis is controversial (varies from weeks to months) Slide 20
Treatment/Therapy: Refer to ENT (ear, nose, and throat specialist) Slide 20
Mortality ★: Not covered in the lecture

Barotrauma3 not covered

Name of Condition: Barotrauma Slides 21, 22
Definition: Not covered in the lecture
Etiology (cause): Inability to equalize pressure in the middle ear; seen during air travel, rapid altitude changes, SCUBA (self-contained underwater breathing apparatus) diving Slide 22
Epidemiology (who): Not covered in the lecture
Risk Factors: Pressure changes while respiratory illness or allergy exacerbation is present; frequent flying (recurrent episodes) Slides 24, 25
Pathology: Can rupture the tympanic membrane or cause middle ear hemorrhage; severe cases involve the inner ear with rupture of the round or oval window Slides 22, 23
Clinical Manifestation: Otalgia; conductive hearing loss; inner ear complications: tinnitus, sensorineural hearing loss, vertigo, nausea and vomiting Slides 22, 23
Diagnosis: Exam: decreased tympanic membrane (TM) mobility on insufflation; hemotympanum (visible blood in the middle ear) if hemorrhage; visible perforation if present Slide 23
Treatment/Therapy: Equalize by swallowing, yawning, exhaling through the nose against resistance; oral/intranasal decongestants; myringotomy gives instant relief (reserved for severe otalgia and hearing loss with intact membranes, ENT (ear, nose, and throat specialist)); tympanostomy tubes for recurrent episodes in frequent flyers (ENT); prevention: avoid pressure changes when ill, or equalize and take decongestants beforehand Slides 24, 25
Mortality ★: Not covered in the lecture

Cerumen impaction3 not covered

Name of Condition: Cerumen impaction Slides 26, 27
Definition: Cerumen (protective, thick, oily/waxy secretion of the outer third of the external ear canal) fully or partially obstructing the canal, which is usually self-cleansing Slides 27, 28
Etiology (cause): Most commonly self-induced: attempts to clean the ear canal push cerumen deeper into the canal Slide 27
Epidemiology (who): Not covered in the lecture
Risk Factors: Inserting objects into the external canal (prevention: insert nothing; wipe the canal opening with a washcloth over the index finger) Slides 27, 28
Pathology: Not covered in the lecture
Clinical Manifestation: May be asymptomatic; pruritus; sensation of fullness; conductive hearing loss Slide 27
Diagnosis: Exam: visible cerumen fully or partially obstructing the external canal; may appear wet/sticky, dry/flaky, or dark Slide 28
Treatment/Therapy: OTC (over-the-counter) otic preparations soften cerumen and speed evacuation; clinic irrigation (body-temperature water, ONLY if the tympanic membrane (TM) is intact) or suction; curette removal (best for soft cerumen and compliant patients, painful if done incorrectly); with tympanostomy tubes or TM perforation, removal by ENT (ear, nose, and throat specialist) Slide 29
Mortality ★: Not covered in the lecture

Cholesteatoma1 not covered

Name of Condition: Cholesteatoma (keratinoma); acquired (primary, secondary) or congenital Slides 31, 32
Definition: Collection of keratinized squamous epithelium in the middle ear or mastoid; has no cholesterol components and is not a neoplasm Slide 31
Etiology (cause): Primary acquired: forms from tympanic membrane (TM) retraction, commonly the pars flaccida (may involve the pars tensa); secondary acquired: epithelial migration from the TM or after surgery; congenital: forms without TM retraction or perforation; acquired cholesteatoma is a complication of otitis media with effusion Slides 19, 32
Epidemiology (who): Primary is the most common type; congenital is the least common Slide 32
Risk Factors: Eustachian tube dysfunction; chronic middle ear inflammation Slide 33
Pathology: Squamous epithelium and keratin debris accumulate in a TM retraction or behind the TM; can erode bone and the ossicles Slides 34, 36
Clinical Manifestation: May be asymptomatic; tinnitus; recurrent otorrhea without otitis externa; hearing loss can be a late finding in primary cholesteatoma; rarely vertigo/dysequilibrium; complications: bone erosion, otorrhea, increased infection risk if middle ear and eustachian tube function are compromised Slides 33, 36
Diagnosis: Usually clinical; exam: TM retraction containing squamous epithelium and keratin debris and/or debris visible behind the TM (congenital: white lesion behind a normal TM), possibly purulent otorrhea, granulation tissue, ossicular erosion; audiometry for hearing loss; CT (computed tomography) for extent of severe cases, useful in secondary acquired disease if the TM is opaque Slides 34, 35, 36
Treatment/Therapy: Refer to ENT (ear, nose, and throat specialist); remove canal debris; antibiotics for infection; surgical removal, usually with tympanoplasty (reconstruction of the TM and ossicles if necessary); mastoidectomy if it extends into the mastoid with bony erosion Slide 37
Mortality ★: Not covered in the lecture

Hematoma of the external ear3 not covered

Name of Condition: Hematoma of the external ear Slide 39
Definition: Pooling of blood in the sub-perichondrial space Slide 39
Etiology (cause): Usually blunt trauma Slide 40
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Accumulated blood keeps oxygen and nutrients from the cartilage, risking tissue necrosis and deformity from necrosis/chronic scarring; granulation tissue forms after 7 days Slides 39, 40, 41
Clinical Manifestation: May develop hours after an injury; complications: recurrent/chronic hematoma, cauliflower ear (cosmetic deformity of the auricle) Slides 39, 42
Diagnosis: Early diagnosis essential; exam: edema and ecchymosis of the auricle, loss of cartilaginous landmarks; follow up 12-24 hours after the initial evaluation Slides 39, 40
Treatment/Therapy: Immediate drainage by incision or large-needle aspiration (harder after 7 days); then irrigation with topical antibiotics and/or systemic antibiotics; ear splinting (cotton bolsters, plaster molds, silicone putty, thermoplastic splints) improves cosmetic outcome and prevents recurrence; recurrent/chronic hematoma needs surgical debridement Slides 41, 42
Mortality ★: Not covered in the lecture

Lacerations and avulsion of the ear7 not covered

Name of Condition: Lacerations/avulsion of the ear Slide 43
Definition: Not covered in the lecture
Etiology (cause): Blunt or sharp trauma Slide 43
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Prompt repair and infection prevention are critical; simple lacerations closed with sutures; complex lacerations/avulsions may need debridement before closure; tissue grafts if tissue lost; recovered avulsed tissue can often be reattached; cover repairs with a pressure dressing to prevent hematoma Slide 43
Mortality ★: Not covered in the lecture

Tympanic membrane perforation4 not covered

Name of Condition: Tympanic membrane (TM) perforation; central or marginal Slides 44, 46
Definition: Disruption in the TM: central (does not extend to the margin) or marginal (involves the margin) Slide 46
Etiology (cause): Impact injury; explosive acoustic trauma; barotrauma; severe acute otitis media Slides 19, 45
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Symptoms vary with cause; generally not painful after the initial rupture; conductive hearing loss; complications: disruption of the ossicles if traumatic, risk of infection Slides 45, 47
Diagnosis: Exam: visible disruption in the TM; drainage through the perforation may be present if associated with acute otitis media Slides 46, 47
Treatment/Therapy: Most resolve spontaneously over several weeks (as little as 48-72 hours if associated with acute otitis media); surgical TM reconstruction for larger or long-standing perforations (ENT (ear, nose, and throat specialist)) Slide 46
Mortality ★: Not covered in the lecture

Foreign body of the ear canal5 not covered

Name of Condition: Foreign body of the external ear canal Slide 49
Definition: Not covered in the lecture
Etiology (cause): Anything that fits into the external canal: beads, popcorn, crayons, insects, pencil erasers, paper, etc. Slide 49
Epidemiology (who): More common in children than adults, but may occur at any age Slide 49
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Otalgia varying with the object's shape/structure; bloody discharge if the canal lining is damaged; sensation of fullness or foreign body Slide 49
Diagnosis: Not covered in the lecture
Treatment/Therapy: Do not push the object deeper; ENT (ear, nose, and throat specialist) referral for removal under microscopy may be warranted; firm objects: loop or hook; soft objects: alligator forceps; irrigation with caution (organic objects swell when wet) and only if the tympanic membrane (TM) is known intact; immobilize insects by filling the canal with lidocaine first (only if TM intact) Slide 50
Mortality ★: Not covered in the lecture

Foreign body of the auricle3 not covered

Name of Condition: Foreign body of the auricle (embedded piercing) Slide 51
Definition: Piercing embedded in the earlobe or another part of the auricle Slide 51
Etiology (cause): Ear piercings Slide 51
Epidemiology (who): Most common in girls and young adolescents with pierced ears, but may occur at any age Slide 51
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Pain, erythema, and edema of the affected area; possible purulent drainage from the piercing site Slide 51
Diagnosis: Exam: pain on palpation of the affected area; foreign body may be palpable Slide 51
Treatment/Therapy: Removal of the object under local anesthetic; younger or non-compliant patients may need sedation; infection is the biggest concern Slide 52
Mortality ★: Not covered in the lecture

Otitis externa2 not covered

Name of Condition: Otitis externa (OE); acute and chronic OE Slides 53, 58
Definition: Inflammation and infection of the external canal Slide 54
Etiology (cause): Most commonly Pseudomonas aeruginosa (38%), Staphylococcus epidermidis (9%), Staphylococcus aureus (8%); also other bacteria and fungi (otomycosis) Slide 54
Epidemiology (who): Affects 10% of people in their lifetime; all age groups, most common in children and early adolescence; most common in summer months Slide 54
Risk Factors: Moisture (swimming/water exposure); epithelial damage (aggressive cleaning/scratching); foreign bodies (cotton swab particles, paper); canal occlusion (hearing aids, headphones); auricular dermatitis (hygiene products, metal jewelry, psoriasis, atopic dermatitis); radiation therapy Slide 56
Pathology: Not covered in the lecture
Clinical Manifestation: Varies with duration and degree; otalgia worse with touch or movement of the auricle/tragus; otorrhea; pruritus; fullness; decreased hearing; complication: malignant (necrotizing) external otitis Slides 57, 61
Diagnosis: Clinical diagnosis; exam: tenderness, canal discharge, canal erythema/edema (erythema common in chronic OE), periauricular and anterior cervical lymphadenopathy, skin thickening in chronic OE; cultures only if severe, chronic, recurrent, immunosuppressed, postoperative, or treatment failure; differential: otomycosis, suppurative otitis media, contact dermatitis, psoriasis, ear canal carcinoma (rare) Slides 55, 58
Treatment/Therapy: Debris removal; otic drops: antiseptic (e.g., boric acid, aluminum acetate, alcohol), antibiotic (e.g., ofloxacin, ciprofloxacin, neomycin, polymyxin B), acidifying (acetic acid), combinations with steroids to reduce pain/inflammation; ear wick if canal stenosis; avoid acidifying and aminoglycoside drops if the tympanic membrane may not be intact Slides 59, 60
Mortality ★: Not covered in the lecture

Malignant otitis externa

Name of Condition: Malignant external otitis; necrotizing external otitis Slide 61
Definition: Severe infection of the bone/marrow spaces of the skull base and the soft tissue/cartilage of the temporal region; a complication of otitis externa Slide 61
Etiology (cause): Most commonly spread of Pseudomonas aeruginosa from otitis externa (>95%) Slide 61
Epidemiology (who): Elderly patients with diabetes and immunocompromised patients are most at risk Slide 61
Risk Factors: Diabetes in the elderly; immunocompromise; preceding otitis externa Slide 61
Pathology: Infection spreads from the external canal into skull-base bone and marrow and temporal soft tissue/cartilage; may cause visible necrosis of the ear canal Slide 61
Clinical Manifestation: Severe otalgia out of proportion to exam findings; copious otorrhea; possible visible ear canal necrosis; facial nerve weakness Slide 61
Diagnosis: MRI (magnetic resonance imaging) or CT (computed tomography) shows infection in bony structures Slide 61
Treatment/Therapy: Antipseudomonal antibiotics (e.g., ciprofloxacin) Slide 61
Mortality ★: Potentially fatal Slide 61

Otomycosis3 not covered

Name of Condition: Otomycosis (fungal otitis externa) Slides 62, 63
Definition: Fungal infection of the external canal Slide 62
Etiology (cause): Most commonly Aspergillus niger and Candida Slide 62
Epidemiology (who): 9% of ear canal infections; varies with climate Slide 62
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Pruritus; discomfort (less painful than bacterial otitis externa); otorrhea; foreign body sensation Slide 62
Diagnosis: Exam: Aspergillus shows visible fungal spores/filaments ("wet newspaper" appearance); Candida shows white fluffy/curd-like material; mild-moderate edema; on the otitis externa differential Slides 55, 63
Treatment/Therapy: Debris removal; topical antifungals Slide 63
Mortality ★: Not covered in the lecture

Otosclerosis4 not covered

Name of Condition: Otosclerosis Slides 64, 65
Definition: Bony overgrowth affecting the stapes, leading to eventual fixation and hearing loss Slide 65
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Bony overgrowth at the stapes causes stapes fixation and conductive hearing loss Slide 65
Clinical Manifestation: Gradually progressive conductive hearing loss, bilateral and asymmetric (70%) or unilateral (30%); hears better with background noise; tinnitus Slide 65
Diagnosis: Otoscopy normal (excludes other conductive causes such as foreign body, cerumen); Weber (lateralizes to the affected ear, or the more affected ear if bilateral) and Rinne (bone conduction ≥ air conduction) consistent with conductive loss; audiometry for extent; CT (computed tomography) is the initial imaging of choice; differential: tympanic membrane perforation, tympanosclerosis, otitis media with effusion, cholesteatoma, ossicular discontinuity, middle ear tumor Slides 66, 67
Treatment/Therapy: Observation if unilateral or not bothered; hearing aids; elective surgery one ear at a time: stapes replacement with a prosthesis or cochlear implant (ENT (ear, nose, and throat specialist)); sodium fluoride and bisphosphonates under investigation, use varies (ENT) Slide 67
Mortality ★: Not covered in the lecture

Keloid of the ear5 not covered

Name of Condition: Keloid of the ear (benign neoplasm of the ear) Slides 68, 69
Definition: Hypertrophic scars (deck's wording), a benign neoplasm of the ear Slide 69
Etiology (cause): Result from trauma Slide 69
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Pictured as large rounded scar masses on the earlobe and auricle Slide 69
Diagnosis: Not covered in the lecture
Treatment/Therapy: Avoid trauma; intralesional steroid injection; corticosteroid tape; excision; radiation therapy in adults, NEVER in children; follow closely for recurrence Slide 70
Mortality ★: Not covered in the lecture

Carcinoma of the ear canal4 not covered

Name of Condition: Carcinoma of the ear canal (malignant neoplasm of the ear) Slide 71
Definition: Malignant neoplasm of the ear canal Slide 71
Etiology (cause): Not covered in the lecture
Epidemiology (who): Very rare Slide 71
Risk Factors: Not covered in the lecture
Pathology: Aggressive malignant growth in the ear canal Slide 71
Clinical Manifestation: Abnormal growth in the ear canal; bloody otorrhea; friable ear canal; failure to respond to treatment for external otitis; late findings: hearing loss and facial paralysis Slide 71
Diagnosis: Definitive diagnosis by biopsy; often misdiagnosed as external otitis; on the otitis externa differential Slides 55, 71
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Lecture 16 · Disorders of the Inner Ear, Balance and Hearing Loss

Prof. Monique Jaquith · 30 conditions · source: 16. Disorders of Inner Ear 2026 - Dr. Jaquith.pptx

Note: Mastoiditis is listed in the instructional objectives (slide 2) but is not taught anywhere in this deck. Cholesteatoma, foreign body, tympanic membrane perforation, and multiple sclerosis appear only as names in cause lists.

Conductive hearing loss★ Professor emphasized2 not covered

★ Speaker notes on slide 11 (conductive causes list) mark it 'IMPORTANT'

Name of Condition: Conductive hearing loss (CHL) Slide 10
Definition: Hearing loss from dysfunction of the external/middle ear that impairs conduction of sound vibration to the inner ear Slide 10
Etiology (cause): Obstruction (cerumen); mass loading (effusion); stiffness (otosclerosis); discontinuity (ossicular disruption); causes: cerumen impaction and eustachian tube dysfunction (most common in adults), otitis media, tympanic membrane (TM) perforation, otosclerosis, foreign body, mass lesions (cholesteatoma, exostosis, glomus tumors), ossicular chain discontinuity Slides 10, 11
Epidemiology (who): Most common onset in childhood and young adulthood, up to age 40 (loss from cerumen impaction can occur beyond 40) Slide 42
Risk Factors: Not covered in the lecture
Pathology: External or middle ear disorder impairs sound conduction to the inner ear; inner ear and cochlear nerve intact Slides 10, 42
Clinical Manifestation: Ear canal/TM abnormality usually visible (except otosclerosis); little effect on sound; hearing seems to improve in noisy environments; voice remains soft Slide 42
Diagnosis: Weber: lateralizes to the impaired ear; Rinne: bone conduction (BC) = air conduction (AC) or BC > AC; tympanometry assesses middle ear/TM mobility and ossicular continuity Slides 39, 41, 42, 22
Treatment/Therapy: Often correctable Slide 10
Mortality ★: Not covered in the lecture

Cerumen impaction6 not covered

Name of Condition: Cerumen impaction Slides 10, 11
Definition: Obstruction of the ear canal by cerumen, a cause of conductive hearing loss Slide 10
Etiology (cause): Obstruction by cerumen Slide 10
Epidemiology (who): One of the most common causes of conductive hearing loss in adults; can occur beyond age 40 Slides 11, 42
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Otitis media (with effusion)6 not covered

Name of Condition: Otitis media; otitis media with effusion Slides 10, 11
Definition: Middle ear fluid accumulation (effusion) causing conductive hearing loss by mass loading of the eardrum Slide 10
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Mass loading: fluid adds weight to the tympanic membrane, altering acoustic properties and dampening sound conduction; stiff middle ear system Slides 10, 26
Clinical Manifestation: Not covered in the lecture
Diagnosis: Tympanogram type B (little or no point of maximum mobility, reduced compliance; flat curve) Slide 26
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Otosclerosis★ Professor emphasized5 not covered

★ Speaker notes on slide 28 (type As tympanogram in otosclerosis) mark it 'IMPORTANT'

Name of Condition: Otosclerosis Slides 10, 11
Definition: Abnormal bone growth in the middle ear that fixes the stapes in place, preventing it from vibrating Slide 10
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Stiffness effect: fixed stapes/ossicular chain cannot vibrate, causing progressive conductive hearing loss Slide 10
Clinical Manifestation: Progressive conductive hearing loss; ear canal and tympanic membrane (TM) usually look normal (exception among conductive causes) Slides 10, 42
Diagnosis: Tympanogram type As (normal middle ear pressure with a reduced compliance peak, from ossicular chain fixation) Slide 28
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Ossicular chain discontinuity6 not covered

Name of Condition: Ossicular chain discontinuity (ossicular chain disruption) Slides 10, 11
Definition: Separation or dislocation of the malleus, incus, and stapes, stopping sound from traveling correctly to the inner ear Slide 10
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Discontinuity of the ossicular chain interrupts sound conduction (conductive hearing loss) Slide 10
Clinical Manifestation: Not covered in the lecture
Diagnosis: Tympanogram type Ad (normal middle ear pressure with hypermobility; flaccid tympanic membrane from ossicular disarticulation); tympanometry estimates ossicular chain continuity Slides 29, 22
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Eustachian tube dysfunction★ Professor emphasized6 not covered

★ Speaker notes on slide 11 mark it 'IMPORTANT' (followed by the ETD note); slide 27 notes mark type C 'IMPORTANT'

Name of Condition: Eustachian tube dysfunction (ETD) Slide 11
Definition: Not covered in the lecture
Etiology (cause): Transient ETD secondary to upper respiratory infection; inflammation, infection, or mass lesion Slides 11, 22
Epidemiology (who): One of the most common causes of conductive hearing loss in adults Slide 11
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: A negative tympanogram pressure peak almost invariably indicates ETD; type C tympanogram (maximal compliance at significant negative middle ear pressure; treatment-significant when more negative than -200 mm H2O) Slides 22, 27
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Sensorineural hearing loss★ Professor emphasized2 not covered

★ Speaker notes on slide 14 (SNHL causes list) mark it 'IMPORTANT'

Name of Condition: Sensorineural hearing loss (SNHL); sensory and neural hearing loss grouped together Slide 12
Definition: Sensory: deterioration of the cochlea and loss of hair cells; neural: lesions of cranial nerve 8, auditory nuclei, ascending tracts, or auditory cortex Slide 12
Etiology (cause): Presbycusis (most common), noise, head trauma, Ménière's disease, ototoxicity, developmental/hereditary, multiple sclerosis, idiopathic, labyrinthitis, perilymphatic fistula, vascular (hypercoagulation, diabetes mellitus), syphilis, autoimmune disorders, acoustic neuroma Slide 14
Epidemiology (who): Most common onset in middle or later years Slide 42
Risk Factors: Not covered in the lecture
Pathology: Inner ear disorder involving the cochlear nerve and neuronal impulse transmission to the brain Slide 42
Clinical Manifestation: Trouble hearing on the phone, in groups/crowded rooms, the TV, doorbell, phone ring; 'people seem to mumble'; higher registers lost so sound may be distorted; worse in noise; voice may be loud; ear canal/tympanic membrane normal Slides 37, 38, 42
Diagnosis: Weber: lateralizes to the good ear; Rinne: air conduction > bone conduction; type A tympanogram; labs usually unnecessary except syphilis testing; vestibular testing an adjunct in selected patients; MRI (magnetic resonance imaging) with gadolinium for suspected retrocochlear loss Slides 39, 41, 42, 25, 35, 36, 31, 75
Treatment/Therapy: Usually not correctable; may be stabilized; some types preventable; acute-onset sensory loss may respond to corticosteroids in the first weeks Slide 13
Mortality ★: Not covered in the lecture

Tinnitus4 not covered

Name of Condition: Tinnitus Slide 43
Definition: Hearing a sound (ringing, buzzing, roaring) when no external sound is present Slide 43
Etiology (cause): Can be associated with any type of hearing loss Slide 44
Epidemiology (who): Not covered in the lecture
Risk Factors: Low tolerance for normal 'head' noise with depression, neurosis, stress, fatigue (fatigue a significant contributing risk factor) Slide 45
Pathology: Not covered in the lecture
Clinical Manifestation: Ringing, buzzing, humming, hissing, motor running, insects; often the first symptom of hearing loss; usually subjective, occasionally objective (heard by the examiner too); red flag: unilateral, pulsatile Slides 44, 45
Diagnosis: Not covered in the lecture
Treatment/Therapy: No drug more effective than placebo; biofeedback, masking noises; avoid loud noise and stimulants, check lead level, daily exercise, adequate rest, learn to ignore the noise Slides 45, 46
Mortality ★: Not covered in the lecture

Exostosis3 not covered

Name of Condition: Exostosis (surfer's ear) Slides 48, 49
Definition: Bony growth in the external ear canal Slides 48, 11
Etiology (cause): Repetitive exposure to cold water Slide 48
Epidemiology (who): Divers, surfers Slide 48
Risk Factors: Repetitive cold water exposure (diving, surfing) Slide 48
Pathology: Benign bony growth projecting from the bone surface; bilaterally symmetrical Slides 11, 48
Clinical Manifestation: Can block the canal or collect debris; conductive hearing loss Slide 48
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Glomus tumor6 not covered

Name of Condition: Glomus tumor Slide 50
Definition: Benign, highly vascular tumor derived from normal glomus formations of the middle ear and jugular bulb Slide 50
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Middle ear mass effect; may cause bony destruction of the skull Slide 50
Clinical Manifestation: Conductive hearing loss; pulsatile tinnitus; can present with spontaneous hemorrhage and paralysis of cranial nerves IX, X, XI Slide 50
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Ototoxicity3 not covered

Name of Condition: Ototoxicity (drug toxicity) Slide 52
Definition: Drug-induced damage to hearing (and balance) Slide 52
Etiology (cause): Aminoglycosides (most ototoxic and common), furosemide/loop diuretics, aspirin/salicylates, platinum-based chemotherapy, alcohol; many other agents Slides 52, 53, 97
Epidemiology (who): Not covered in the lecture
Risk Factors: Ototoxic drugs are often also nephrotoxic and vice versa (including nonsteroidal anti-inflammatory drugs) Slide 53
Pathology: Not covered in the lecture
Clinical Manifestation: Bilateral sensorineural hearing loss; peripheral vertigo of insidious or acute onset with nausea, vomiting; tinnitus may be present Slides 53, 97
Diagnosis: Not covered in the lecture
Treatment/Therapy: Monitor aminoglycoside peak levels Slide 52
Mortality ★: Prognosis: may or may not be reversible; partial adaptation occurs Slide 97

Noise-induced hearing loss2 not covered

Name of Condition: Noise-induced sensorineural hearing loss (SNHL) Slide 54
Definition: SNHL from noise exposure, temporary or permanent Slides 54, 55
Etiology (cause): Loud or repeated noise exposure; rarely, extremely intense impulse noise perforates the tympanic membrane (conductive hearing loss) Slides 54, 55
Epidemiology (who): One of the most common occupationally induced disabilities; exposure regulated by OSHA (Occupational Safety and Health Administration) Slide 54
Risk Factors: Noise level high enough or repeated often enough; damage possible after 2 hours at 80-85 dB (decibels), under 5 minutes at 105-110 dB Slides 55, 6
Pathology: Temporary threshold shift (TTS: temporary SNHL after acute exposure); permanent threshold shift (PTS: permanent loss after high or repeated exposure) Slides 54, 55
Clinical Manifestation: Ear feels full, 'crickets' after acute exposure Slide 55
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Prognosis: most acute exposures recover in 24-48 hours; high-level or repeated exposure causes permanent loss Slides 54, 55

Traumatic hearing loss (acoustic, head, penetrating)4 not covered

Name of Condition: Traumatic hearing loss: acoustic trauma; blows to the head; penetrating injuries Slide 56
Definition: Hearing loss from a single loud noise (acoustic trauma), head blows, or penetrating ear injury Slide 56
Etiology (cause): Single loud noise; tympanic membrane perforation; blows to the head (labyrinthine injury); penetrating injuries (stapes subluxation) Slide 56
Epidemiology (who): Penetrating injuries are rare Slide 56
Risk Factors: Not covered in the lecture
Pathology: Head blows can cause labyrinthine injury with sensorineural hearing loss (SNHL); penetrating injury usually subluxates the stapes, causing profound SNHL Slide 56
Clinical Manifestation: Immediate hearing loss after acoustic trauma; may mimic noise-induced loss or be complete loss of auditory and vestibular function Slides 56, 57
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Barotrauma4 not covered

Name of Condition: Barotrauma Slide 58
Definition: Injury of the tympanic membrane (TM) and middle ear caused by unequalized pressure Slide 58
Etiology (cause): Unequalized pressure during flying or underwater diving Slide 58
Epidemiology (who): Not covered in the lecture
Risk Factors: Flying; underwater diving Slide 58
Pathology: Pressure injury to TM/middle ear; may be followed by hemotympanum (blood in the middle ear) or transudative middle ear effusion Slides 58, 59
Clinical Manifestation: Pain, hyperemia, TM perforation, edema, ecchymosis; may result in conductive hearing loss Slide 58
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Presbycusis★ Professor emphasized2 not covered

★ Speaker notes on slide 14 (which define presbycusis, marked most common) mark it 'IMPORTANT'

Name of Condition: Presbycusis Slide 15
Definition: Gradual, progressive, age-related hearing loss in both ears Slides 15, 14
Etiology (cause): Aging Slide 60
Epidemiology (who): Most common cause of sensorineural hearing loss; age is the strongest predictor of hearing loss Slides 14, 8
Risk Factors: Age Slides 8, 60
Pathology: Deterioration/loss of hair cells in the organ of Corti and cochlear nerve degeneration; sensorineural Slides 15, 60, 61
Clinical Manifestation: Bilateral, symmetric, gradual loss; high frequencies first, progressing to mid-low; can hear speech but can't make out words; misses doorbell/phone; may have tinnitus; lip reads Slides 60, 61, 62
Diagnosis: Audiogram: sloping high-frequency hearing loss Slides 19, 62
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Perilymphatic fistula2 not covered

Name of Condition: Perilymphatic fistula Slide 63
Definition: Pathologic communication between the perilymphatic space of the inner ear and the middle ear, at the round or oval window Slide 63
Etiology (cause): Congenital or acquired; acquired from barotrauma, temporal bone trauma, or stapedectomy complication Slides 63, 64
Epidemiology (who): Rare cause of vertigo and sensorineural hearing loss Slide 63
Risk Factors: Head injury, barotrauma, heavy lifting and straining, stapedectomy Slide 64
Pathology: Fistula at the round or oval window Slide 63
Clinical Manifestation: Sudden sensorineural hearing loss and vertigo after head injury, barotrauma, or straining; sometimes an audible 'pop' Slide 64
Diagnosis: Not covered in the lecture
Treatment/Therapy: Treat symptomatically and refer to ENT (ear, nose, and throat specialist) Slide 64
Mortality ★: Not covered in the lecture

Autoimmune sensorineural hearing loss5 not covered

Name of Condition: Autoimmune sensorineural hearing loss (SNHL) Slide 65
Definition: SNHL from systemic autoimmune disorders Slide 65
Etiology (cause): Uncommon: Cogan's syndrome, polyarteritis nodosa, relapsing polychondritis, granulomatosis with polyangiitis (Wegener's); rarer: scleroderma, temporal arteritis, systemic lupus erythematosus, sarcoidosis Slide 66
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Most often bilateral and progressive SNHL with periods of deterioration and stabilization; may have vestibular dysfunction Slide 65
Diagnosis: Routine screening for autoimmune disorders does not appear warranted Slide 36
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

AIDS-related sensorineural hearing loss4 not covered

Name of Condition: AIDS (acquired immunodeficiency syndrome)-related sensorineural hearing loss (SNHL) Slide 67
Definition: SNHL as one of the many neurologic manifestations of AIDS Slide 67
Etiology (cause): Infectious complication (cryptococcal meningitis, syphilis) or primary neurologic manifestation Slide 67
Epidemiology (who): Not covered in the lecture
Risk Factors: Consider when AIDS risk factors are present Slide 67
Pathology: Not covered in the lecture
Clinical Manifestation: Unexplained SNHL Slide 67
Diagnosis: Consider AIDS in unexplained SNHL if risk factors present Slide 67
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Syphilitic sensorineural hearing loss2 not covered

Name of Condition: Syphilitic sensorineural hearing loss (SNHL) Slide 68
Definition: Congenital or acquired SNHL from syphilis Slide 68
Etiology (cause): Syphilis (Treponema pallidum), congenital or acquired Slide 68
Epidemiology (who): Hearing loss up to 80% in symptomatic neurosyphilis; not associated with primary acquired syphilis Slide 68
Risk Factors: Symptomatic neurosyphilis Slide 68
Pathology: Not covered in the lecture
Clinical Manifestation: Often indistinguishable from Ménière's: fluctuating SNHL, tinnitus, aural fullness, episodic vertigo Slide 68
Diagnosis: FTA-ABS (fluorescent treponemal antibody absorption) and MHA-TP (microhemagglutination test for Treponema pallidum) should be obtained; VDRL (Venereal Disease Research Laboratory) not helpful Slide 35
Treatment/Therapy: Antibiotic plus systemic corticosteroids; important to manage as a potentially treatable cause of SNHL Slides 68, 35
Mortality ★: Not covered in the lecture

Ménière's disease7 not covered

Name of Condition: Ménière's disease Slide 69
Definition: Peripheral vestibular disorder of episodic vertigo with fluctuating low-frequency sensorineural hearing loss (SNHL), tinnitus, and aural fullness Slides 69, 70, 97
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Episodic spontaneous severe spinning vertigo lasting hours (often presenting complaint), with nausea, vomiting, diaphoresis, nystagmus; fluctuating then progressive low-frequency SNHL; low-tone 'blowing' tinnitus; unilateral ear fullness Slides 69, 70, 89, 97
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Hereditary sensorineural hearing loss7 not covered

Name of Condition: Hereditary sensorineural hearing loss (SNHL) Slide 71
Definition: Inherited SNHL, nonsyndromic or syndromic Slide 71
Etiology (cause): Nonsyndromic hereditary hearing loss; Waardenburg's syndrome; Alport syndrome; Usher's syndrome Slide 71
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Acoustic neuroma★ Professor emphasized2 not covered

★ Speaker notes on slide 74 mark 'IMPORTANT - Slow growing'

Name of Condition: Acoustic neuroma Slide 72
Definition: Rare, slow-growing benign tumor of cranial nerve (CN) VIII, arising from sheath cells of its vestibular component Slide 72
Etiology (cause): Not covered in the lecture
Epidemiology (who): Rare; most often unilateral Slide 72
Risk Factors: Not covered in the lecture
Pathology: Benign, slow-growing tumor from sheath cells of the vestibular branch of CN VIII; causes CN VIII compression; may involve CN V and VII Slides 72, 97
Clinical Manifestation: Unilateral hearing loss (may be sudden); poor speech discrimination for the degree of tone loss; disequilibrium; tinnitus Slides 74, 97
Diagnosis: MRI (magnetic resonance imaging) with gadolinium is the gold standard for retrocochlear loss; electronystagmography is the gold standard for one-ear disorders; ipsilateral vestibular hypofunction with unilateral progressive SNHL (sensorineural hearing loss) suggests retrocochlear lesion Slides 75, 76, 32, 31
Treatment/Therapy: Observation (annual MRI), surgery, or radiation Slide 75
Mortality ★: Prognosis: progression may not be so 'benign' Slide 74

Vertebrobasilar insufficiency/occlusion4 not covered

Name of Condition: Vertebrobasilar arterial insufficiency/occlusion (vertebrobasilar artery disease) Slides 77, 86
Definition: Not covered in the lecture
Etiology (cause): Thrombotic or embolic occlusion; atherosclerosis or cervical arthritis Slides 77, 86
Epidemiology (who): Common cause of vertigo in elderly patients Slide 77
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Acute vertigo, nausea/vomiting, facial paralysis, tinnitus, ipsilateral gaze paralysis, ipsilateral facial and contralateral trunk/limb loss of pain and temperature, ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis) Slide 77
Diagnosis: MRA (magnetic resonance angiography) Slide 87
Treatment/Therapy: Not covered in the lecture
Mortality ★: Complications: can lead to TIAs (transient ischemic attacks) and CVAs (cerebral vascular accidents) Slide 86

Isolated cerebellar infarction7 not covered

Name of Condition: Isolated cerebellar infarction Slide 78
Definition: Not covered in the lecture
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Vertigo, facial pain or numbness, headache, or ataxia Slide 78
Diagnosis: Not covered in the lecture
Treatment/Therapy: Refer for evaluation (don't miss something bigger than the hearing loss) Slide 78
Mortality ★: Not covered in the lecture

Sudden sensorineural hearing loss5 not covered

Name of Condition: Sudden sensorineural hearing loss (SNHL) Slide 79
Definition: Unilateral sudden SNHL; a syndrome, not a disease Slide 79
Etiology (cause): Viral or vascular; exact etiology rarely certain; rarely retrocochlear pathology Slide 79
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Unilateral sudden hearing loss Slide 79
Diagnosis: Not covered in the lecture
Treatment/Therapy: Prompt referral to ENT (ear, nose, and throat specialist); acute-onset sensory loss may respond to corticosteroids in the first weeks Slides 79, 13
Mortality ★: Not covered in the lecture

Functional hearing loss7 not covered

Name of Condition: Functional hearing loss Slide 80
Definition: Not covered in the lecture
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Inconsistencies, complaints, and exaggerated listening effort on history; claimed bilateral significant loss with normal voice level and articulation Slide 80
Diagnosis: History and voice/speech quality; suspect functional behavior when claimed bilateral loss coexists with normal voice and articulation Slide 80
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Vascular disorders (small vessel ischemic disease)3 not covered

Name of Condition: Vascular disorders causing dizziness: small vessel ischemic disease; carotid artery stenosis Slides 85, 86
Definition: Most common non-vestibular cause of dizziness and balance loss in the elderly Slide 85
Etiology (cause): Small vessel ischemic disease (atherosclerosis) most common; carotid artery stenosis Slides 85, 86
Epidemiology (who): Elderly; carotid stenosis common, frequently with other peripheral vascular disorders Slides 85, 86
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Increased reflex time; difficulty processing complex tasks, balance, and locomotion; syncope Slide 85
Diagnosis: MRA (magnetic resonance angiography), showing small white lesions in small vessel disease; noninvasive carotid studies (Doppler) Slide 87
Treatment/Therapy: Not covered in the lecture
Mortality ★: Complications: can lead to TIAs (transient ischemic attacks) and CVAs (cerebral vascular accidents) Slide 86

Benign paroxysmal positional vertigo2 not covered

Name of Condition: Benign paroxysmal positional vertigo (BPPV) Slide 90
Definition: Severe vertigo associated with a change in head position Slide 90
Etiology (cause): Most cases have no identifiable cause; canalithiasis of the posterior semicircular canal thought most frequent (deck labels it 'cupulolithiasis theory') Slide 92
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Displaced otoliths in the semicircular canal (posterior canal most frequent) Slides 92, 93
Clinical Manifestation: Vertigo after 10-15 second latency lasting 10-60 seconds (>1 minute: consider another diagnosis) when rolling over, getting in/out of bed, looking up, tilting head back; specific side; clustered bouts; imbalance, worse on awakening; nausea, vomiting, nystagmus; hearing and tinnitus unaffected Slides 90, 91, 92, 97
Diagnosis: Classic eye movements on Dix-Hallpike maneuver (positional test provoking nystagmus) plus suggestive history; electronystagmography may be used Slides 93, 32
Treatment/Therapy: Epley maneuver (repositions otoliths in the semicircular canal) Slide 93
Mortality ★: Prognosis: bouts separated by remissions of months or more; episodes last a few weeks and may recur Slides 91, 97

Labyrinthitis4 not covered

Name of Condition: Labyrinthitis Slide 95
Definition: Inflammation of the membranous labyrinth of the inner ear Slide 95
Etiology (cause): Evidence supports viral cause; could be bacterial infection or systemic autoimmune disease; exact cause rarely certain Slide 95
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Inflammation of the membranous labyrinth Slide 95
Clinical Manifestation: Relatively sudden onset of sensorineural hearing loss and acute vertigo lasting several days to weeks; fever if bacterial Slides 95, 89
Diagnosis: Not covered in the lecture
Treatment/Therapy: Symptomatic; antibiotics if bacterial infection signs (fever); oral corticosteroids; oral diazepam or meclizine during acute vertigo Slide 95
Mortality ★: Not covered in the lecture

Vestibular neuronitis2 not covered

Name of Condition: Vestibular neuronitis (vestibular neuritis) Slide 96
Definition: Inflammation of the vestibular portion of cranial nerve 8 Slide 96
Etiology (cause): Likely viral; exact cause unknown Slide 96
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Inflammation of the vestibular portion of cranial nerve 8 Slide 96
Clinical Manifestation: Dramatic sudden vertigo, nausea, vomiting, nystagmus, gait imbalance; dizziness lasts days with gradual improvement; balance symptoms for months; no hearing change, tinnitus, or focal neurologic complaints Slides 96, 97
Diagnosis: Clinical diagnosis; electronystagmography is the gold standard for one-ear disorders Slides 96, 32
Treatment/Therapy: Symptomatic: oral diazepam or meclizine during acute vertigo; antiemetics; oral corticosteroids (deck marks with '?') Slide 96
Mortality ★: Prognosis: considered benign, self-limiting; may recur over 12-18 months Slides 96, 97

Lecture 17 · Disorders of the Nose and Paranasal Sinuses

Prof. Hugh Griffenkranz · 17 conditions · source: hughie Nose & Paranasal Sinuses fall 2026.pptx

Acute sinusitis (acute rhinosinusitis)1 not covered

Name of Condition: Acute sinusitis; acute rhinosinusitis (preferred term, because rhinitis and sinusitis usually coexist) Slide 9
Definition: Symptomatic inflammation of one or more paranasal sinuses lasting <4 weeks, from impaired drainage and retained secretions, with obstruction, facial pain/pressure/fullness, or both Slide 9
Etiology (cause): Infectious and noninfectious causes that obstruct the sinus ostia and retain mucus; viral in 90–98% (rhinovirus, parainfluenza virus, influenza virus); bacterial less often; fungal (Rhizopus, Mucor, occasionally Aspergillus) in immunocompromised patients; noninfectious: allergic rhinitis, barotrauma, chemical irritants Slides 10, 11, 12, 13
Epidemiology (who): Affects 1 in 8 adults (>30 million diagnosed with rhinosinusitis in the US each year); sinuses most often infected: maxillary > ethmoid > frontal > sphenoid Slides 3, 10
Risk Factors: Chronic allergies; smoking; immunocompromise; anatomical defect Slide 14
Pathology: Allergy/infection/inflammation → structural abnormality or mucosal congestion → obstruction of the ostiomeatal complex or sinus ostia → sinus hypoxia, mucosal edema, reduced mucociliary clearance, pooled secretions; maxillary sinuses most infected because their ostia are accessible to the outside Slides 4, 15
Clinical Manifestation: Nasal drainage/congestion (rhinorrhea, postnasal drip), facial pain or pressure, headache; associated retro-orbital pain, otalgia, hyposmia, halitosis, chronic cough; viral cause gives a viral syndrome; urgent: visual disturbance (especially diplopia), periorbital swelling or erythema, altered mental status Slides 17, 18, 19
Diagnosis: Clinical; tests not routinely recommended and none separate viral from bacterial; ≥3 clinical findings match imaging accuracy, so routine sinus radiography is discouraged; limited coronal CT (computed tomography) for recurrence or treatment failure; sinus CT if extrasinus involvement suspected Slide 21
Treatment/Therapy: Most improve without antibiotics; symptomatic: decongestants, NSAIDs (nonsteroidal anti-inflammatory drugs), nasal/sinus saline irrigation (neti pot, saline sprays), intranasal steroids; oseltamivir if influenza (age >13); ENT (ear, nose, and throat) referral for surgery if medical treatment fails; educate on diagnosis, cause, device/medication use, referral Slides 22, 24, 27
Mortality ★: Not covered in the lecture

Acute bacterial sinusitis1 not covered

Name of Condition: Acute bacterial sinusitis; acute bacterial rhinosinusitis Slides 10, 16
Definition: Acute sinusitis caused by bacterial infection of stagnant sinus secretions, often a bacterial superinfection of viral rhinosinusitis Slides 10, 15
Etiology (cause): Streptococcus pneumoniae, nontypable Haemophilus influenzae, and (in children) Moraxella catarrhalis; nosocomial cases often polymicrobial with Staphylococcus aureus and gram-negative bacilli Slides 11, 12
Epidemiology (who): Bacterial superinfection in 0.5–2% of viral rhinosinusitis episodes; diagnosis is the fifth leading reason for prescribing antibiotics Slide 10
Risk Factors: Chronic allergies, smoking, immunocompromise, anatomical defect (acute sinusitis); antibiotic exposure within 30 days or >30% local penicillin-resistant Streptococcus pneumoniae changes antibiotic choice Slides 14, 23
Pathology: Ostial obstruction → pooled, stagnant secretions → bacterial infection; if unresolved it can become chronic sinusitis Slide 15
Clinical Manifestation: Worsening >5–6 days after initial improvement; symptoms ≥10 days; persistent purulent discharge; unilateral upper tooth/facial pain; unilateral maxillary tenderness; fever (>100.4 F) and severe pain reproducible on palpation, worse bending over or supine; tooth pain, halitosis, tearing, odynophagia; yellow and putrid discharge; rust-colored discharge suggests Streptococcus pneumoniae Slides 16, 18, 19
Diagnosis: Clinical (no test separates viral from bacterial); confirm fever is not masked by antipyretics; CT (computed tomography) for recurrence, treatment failure, or suspected extrasinus involvement Slides 19, 21
Treatment/Therapy: Symptomatic care + antibiotics: amoxicillin/clavulanate; penicillin allergy: doxycycline or an antipneumococcal fluoroquinolone (moxifloxacin); recent antibiotics or resistance risk: extended-release amoxicillin/clavulanate, doxycycline, or fluoroquinolone; treatment failure: extended-release amoxicillin/clavulanate or fluoroquinolone; ENT (ear, nose, and throat) referral for surgery if medical treatment fails Slides 23, 24
Mortality ★: Not covered in the lecture

Allergic sinusitis5 not covered

Name of Condition: Allergic sinusitis Slides 13, 26
Definition: Allergy-driven sinus symptoms: allergies do not cause inflammation (-itis) per se but create the environment for infection; many patients who believe they have sinusitis actually have allergic sinusitis Slide 13
Etiology (cause): Allergic rhinitis (a noninfectious cause of sinusitis) Slide 13
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Multiple pathophysiology pathways Slide 26
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: 80% of patients use 2 or more allergy medications: non-drowsy oral antihistamine (loratadine, fexofenadine, cetirizine, levocetirizine; drowsy ones at night); leukotriene inhibitor at night (zafirlukast, montelukast); intranasal steroid (fluticasone; caution with chronic use); intranasal ipratropium; immunotherapy; decongestants (caution with chronic use and high blood pressure); local honey Slides 24, 26
Mortality ★: Not covered in the lecture

Chronic bacterial sinusitis3 not covered

Name of Condition: Chronic sinusitis; chronic bacterial sinusitis Slide 28
Definition: Sinusitis lasting >12 weeks Slide 28
Etiology (cause): Commonly associated with bacterial or fungal infection Slide 28
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Impaired mucociliary clearance → repeated infections rather than one persistent infection; unresolved obstruction/infection progresses to chronic sinusitis Slides 15, 28
Clinical Manifestation: Constant nasal congestion and sinus pressure with periods of increased severity Slide 28
Diagnosis: Sinus CT (computed tomography) defines extent, detects an anatomic defect or obstruction, and tracks response; endoscopic tissue samples for histology and culture; consider CBC (complete blood count) with differential and IgE (immunoglobulin E); allergy skin testing referral Slides 21, 28, 29
Treatment/Therapy: Repeated antibiotic courses (often 3–4 weeks at a time); intranasal glucocorticoids, sinus irrigation; oral steroids plus two weeks of amoxicillin/clavulanate; ENT (ear, nose, and throat) referral for surgical evaluation Slides 28, 29
Mortality ★: Not covered in the lecture

Chronic fungal sinusitis3 not covered

Name of Condition: Chronic fungal sinusitis; mycetoma (fungus ball) form Slide 30
Definition: Noninvasive chronic fungal sinus disease in immunocompetent hosts Slide 30
Etiology (cause): Typically Aspergillus and dematiaceous molds Slide 30
Epidemiology (who): Immunocompetent hosts Slide 30
Risk Factors: Not covered in the lecture
Pathology: Noninvasive; may form a mycetoma (fungus ball) in a sinus, which can erode bone Slide 30
Clinical Manifestation: Usually mild and indolent; mycetoma presents as unilateral disease Slide 30
Diagnosis: Not covered in the lecture
Treatment/Therapy: Mild indolent disease: endoscopic surgery, usually without antifungals; mycetoma: surgery, plus antifungals if bony erosion; recurrence is common Slide 30
Mortality ★: Not covered in the lecture

Allergic fungal sinusitis5 not covered

Name of Condition: Allergic fungal sinusitis (AFS) Slide 30
Definition: Allergic form of chronic fungal sinusitis presenting as pansinusitis with thick eosinophil-laden mucus Slide 30
Etiology (cause): Not covered in the lecture
Epidemiology (who): Seen in patients with nasal polyps and asthma; nasal polyps occur in 85% of patients with AFS (allergic fungal sinusitis) Slides 30, 63
Risk Factors: Not covered in the lecture
Pathology: Thick, eosinophil-laden mucus Slide 30
Clinical Manifestation: Pansinusitis with mucus the consistency of peanut butter; multiple nasal polyps (including in children) Slides 30, 60
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Deviated septum3 not covered

Name of Condition: Deviated (nasal) septum Slide 32
Definition: Nasal septum significantly displaced to one side, making one nasal air passage smaller than the other Slide 32
Etiology (cause): Congenital or traumatic Slide 32
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Displacement narrows one airway and can block the sinus ostia Slide 32
Clinical Manifestation: Congestion (ostial blockage) up to anosmia; severe forms: obstructive sleep apnea, snoring, facial pain, recurrent nosebleeds Slide 32
Diagnosis: Seen on coronal CT (computed tomography) and nasal endoscopy (labeled images) Slide 36
Treatment/Therapy: Surgery: septoplasty by an otorhinolaryngologist Slide 32
Mortality ★: Not covered in the lecture

Perforated septum4 not covered

Name of Condition: Perforated (nasal) septum; septal perforation Slide 37
Definition: Perforation through the nasal septum Slide 37
Etiology (cause): Congenital or traumatic; often intranasal steroid use or cocaine use; rarely Wegener's granulomatosis (a vascular autoimmune disease); rarely secondary syphilis Slide 37
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Chronic ischemia of the septum (intranasal steroids, cocaine) Slide 37
Clinical Manifestation: Not covered in the lecture
Diagnosis: Physical examination, possibly CT (computed tomography) Slide 40
Treatment/Therapy: Treat the underlying cause (septum may heal); otherwise surgery (septoplasty); ENT (ear, nose, and throat) referral Slide 40
Mortality ★: Not covered in the lecture

Septal hematoma4 not covered

Name of Condition: Septal hematoma Slide 41
Definition: Hematoma between the nasal septum and the perichondrium/mucosal epithelium Slide 41
Etiology (cause): Usually trauma; also bleeding disorders, cocaine, foreign body, medications Slide 41
Epidemiology (who): Not covered in the lecture
Risk Factors: Nasal fracture (associated with septal hematomas) Slide 56
Pathology: Blood collects between septal cartilage and perichondrium Slides 41, 42
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Drainage via intranasal incision under general anesthesia (illustrated incision, evacuation, and packing) Slides 41, 43
Mortality ★: Not covered in the lecture

Epistaxis, anterior1 not covered

Name of Condition: Anterior epistaxis (anterior nosebleed) Slide 46
Definition: Nosebleed from an anterior source; by far the most common type Slide 46
Etiology (cause): Most common: trauma from the patient's finger; 90% arise in Kiesselbach's plexus (vascular watershed area of the anterior septum) Slides 45, 46
Epidemiology (who): Common emergency department complaint; most cases before age 10 or at 45–65 years; winter predominance Slide 45
Risk Factors: Chronic dry nose; anticoagulant use; hemophilia; coagulation disorders; tumors; recent trauma or surgery; medications (aspirin, warfarin, clopidogrel, intranasal glucocorticoids); cirrhosis; HIV (human immunodeficiency virus); intranasal cocaine Slides 45, 48
Pathology: Cracked mucosa with damaged vessels in Kiesselbach's plexus Slides 46, 47
Clinical Manifestation: Nasal bleeding; symptoms of blood loss (chest discomfort, dyspnea, lightheadedness) and worsening of coronary artery disease or COPD (chronic obstructive pulmonary disease) Slide 48
Diagnosis: ABC (airway, breathing, circulation) first; normal appearance, vital signs, and respiratory function are reassuring; determine anterior vs posterior; history of timing, frequency, severity, predisposing conditions; PT (prothrombin time)/INR (international normalized ratio) only if anticoagulated; hematocrit and type and crossmatch if massive or prolonged Slides 45, 48, 49
Treatment/Therapy: Blow nose to clear clots, oxymetazoline spray, pinch alae against septum continuously 10 minutes; sit leaning forward, cotton pledget (± antibiotic ointment), spit out blood, cold compress to bridge (teach for home); then nasal tampons, gauze packing, balloon catheters, thrombogenic foams/gels; do not blow nose; ENT (ear, nose, and throat) referral Slides 49, 50, 51
Mortality ★: Not covered in the lecture

Epistaxis, posterior

Name of Condition: Posterior epistaxis (posterior nosebleed) Slide 46
Definition: Nosebleed from a posterior source, most often the posterolateral branches of the sphenopalatine artery, sometimes carotid branches Slide 46
Etiology (cause): Posterolateral branches of the sphenopalatine artery; branches of the carotid artery Slide 46
Epidemiology (who): Less common than anterior bleeds; epistaxis overall peaks before age 10 and at 45–65 years, in winter Slides 45, 46
Risk Factors: Chronic dry nose; anticoagulant use; hemophilia; coagulation disorders; tumors; recent trauma or surgery; medications (aspirin, warfarin, clopidogrel, intranasal glucocorticoids); cirrhosis; HIV (human immunodeficiency virus); intranasal cocaine Slides 45, 48
Pathology: Arterial bleeding that can produce significant hemorrhage Slide 46
Clinical Manifestation: Significant hemorrhage; symptoms of blood loss (chest discomfort, dyspnea, lightheadedness) Slides 46, 48
Diagnosis: ABC (airway, breathing, circulation) first; normal appearance, vital signs, and respiratory function are reassuring; determine anterior vs posterior; history of timing, frequency, severity, predisposing conditions; PT (prothrombin time)/INR (international normalized ratio) only if anticoagulated; hematocrit and type and crossmatch if massive or prolonged Slides 45, 48, 49
Treatment/Therapy: Initial tamponade (clear clots, oxymetazoline, 10 minutes of pressure); nasal packing for severe nosebleeds, balloon catheters, thrombogenic foams/gels; two large-bore IV (intravenous) lines if massive; do not blow nose; ENT (ear, nose, and throat) referral Slides 49, 51, 52
Mortality ★: Prognosis: higher-risk bleed: aspiration risk, possible infection, significant hemorrhage Slides 45, 46

Nasal foreign body4 not covered

Name of Condition: Nasal foreign body (FB) Slides 53, 54
Definition: Not covered in the lecture
Etiology (cause): Not covered in the lecture
Epidemiology (who): Most common in young children Slide 54
Risk Factors: Not covered in the lecture
Pathology: Usually on the nasal floor just under the inferior turbinate, or superiorly just in front of the middle turbinate Slide 54
Clinical Manifestation: Unilateral purulent, foul-smelling nasal discharge in a young child strongly suggests it Slide 54
Diagnosis: Visualization of the FB (foreign body) establishes the diagnosis; imaging rarely needed Slide 54
Treatment/Therapy: Removal: Tobey or bayonet forceps for graspable objects (paper, toy part, cotton, foam); wire loop, right-angle hook, curette, or suction tip for nongraspable round/smooth objects (bead, bean, magnet, battery); get help, ENT (ear, nose, and throat) referral Slides 54, 55
Mortality ★: Not covered in the lecture

Nasal fracture4 not covered

Name of Condition: Nasal fracture (nasal bridge fracture) Slide 56
Definition: Not covered in the lecture
Etiology (cause): Trauma Slide 56
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Nasal bridge is the most common site; associated with septal hematomas; may accompany orbital or midface fractures Slide 56
Clinical Manifestation: Contusion/tenderness over the nasal bridge (= fracture); tenderness, crepitus, abnormal movement Slide 56
Diagnosis: Palpation and inspection with a nasal speculum; suspect orbital/midface fractures; no x-ray needed if tenderness/swelling isolated to the bony bridge, breathing through each naris, nose straight, and no septal hematoma; otherwise plain nasal x-rays Slides 56, 57
Treatment/Therapy: Ice and head-of-bed elevation; if displaced, ENT (ear, nose, and throat) within 8 hours to reset, though waiting 3–4 days for swelling is common Slide 56
Mortality ★: Not covered in the lecture

Nasal polyps2 not covered

Name of Condition: Nasal polyps (nasal polyposis) Slide 59
Definition: Abnormal gray, glistening masses filled with inflammatory material in the nasal cavity or paranasal sinuses Slide 59
Etiology (cause): Not covered in the lecture
Epidemiology (who): Asthma in 20–50% and aspirin intolerance in 8–26% of polyp patients; polyps in 6–44% of CF (cystic fibrosis), 85% of allergic fungal sinusitis, 50% of Churg-Strauss syndrome, 20% of NARES (nonallergic rhinitis with eosinophilia syndrome); multiple polyps can occur in children with chronic sinusitis, allergic rhinitis, CF, or allergic fungal sinusitis Slides 60, 63
Risk Factors: Chronic rhinosinusitis, asthma, aspirin sensitivity (AERD, aspirin-exacerbated respiratory disease), allergic rhinitis, CF, allergic fungal sinusitis, primary ciliary dyskinesia, alcohol intolerance, Churg-Strauss syndrome, Young syndrome (chronic sinusitis, nasal polyposis, azoospermia), NARES Slides 59, 60, 63
Pathology: Inflammatory masses, typically seen under the middle turbinate Slides 59, 62
Clinical Manifestation: Large or extensive polyps: nasal congestion or blockage, thick discharge, anosmia Slide 60
Diagnosis: Characteristic appearance with nasal speculum or rhinoscope; CT (computed tomography) for extent/surgical planning; sweat chloride test if CF concern; CBC (complete blood count) with differential, IgE (immunoglobulin E), IgA (immunoglobulin A); consider nasal smear for eosinophils; evaluate all children with multiple polyps for CF and asthma Slides 59, 61, 64
Treatment/Therapy: Non-drowsy antihistamine (loratadine, fexofenadine, cetirizine, levocetirizine), leukotriene inhibitor at night (zafirlukast, montelukast), intranasal or oral steroids by extent, intranasal ipratropium, immunotherapy, decongestants (caution); surgery gives temporary relief, polyps often recur in months to years Slides 60, 65
Mortality ★: Not covered in the lecture

Allergic rhinitis2 not covered

Name of Condition: Allergic rhinitis Slide 66
Definition: Rhinorrhea secondary to an allergy Slide 66
Etiology (cause): Allergen (antigen) exposure recognized as foreign Slide 66
Epidemiology (who): Extremely common and, like all allergy issues, on the rise Slide 66
Risk Factors: Not covered in the lecture
Pathology: Allergen recognized as foreign → chemokine release → mucus hyperproduction → rhinorrhea Slide 66
Clinical Manifestation: Clear discharge from each nostril; bluish, edematous nasal mucosa; ± nasal polyps Slide 67
Diagnosis: Clinical, mostly patient history, with the exam findings above Slides 66, 67
Treatment/Therapy: Often 2 or more medications: non-drowsy antihistamine (loratadine, fexofenadine, cetirizine, levocetirizine; drowsy ones at night), leukotriene inhibitor at night (zafirlukast, montelukast), intranasal steroids (caution chronic use), intranasal ipratropium, immunotherapy, decongestants (caution chronic use and high blood pressure) Slide 68
Mortality ★: Not covered in the lecture

Nasopharyngeal carcinoma3 not covered

Name of Condition: Nasopharyngeal carcinoma (malignant lesion of the nose) Slide 69
Definition: The predominant tumor type arising in the nasopharynx Slide 69
Etiology (cause): Associated with EBV (Epstein-Barr virus) and HPV (human papillomavirus) Slide 69
Epidemiology (who): Rare in the US and Western Europe; endemic in Southern China (including Hong Kong), Southeast Asia, North Africa, the Middle East, and the Arctic; 2–3 times more common in males Slide 69
Risk Factors: Smoking; high-salt diet; Chinese herbs; rancid butter and sheep fat (butyric acid) Slide 69
Pathology: Not covered in the lecture
Clinical Manifestation: Headache, diplopia, facial numbness, neck mass Slide 70
Diagnosis: ENT (ear, nose, and throat) referral; endoscopic-guided biopsy of the primary tumor Slide 70
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Benign nasal neoplasms8 not covered

Name of Condition: Benign neoplasms of the nose Slide 71
Definition: Same benign lesions as skin (see dermatology lectures): warts, freckles, hemangioma, port wine stain, among others Slide 71
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Lecture 18 · Neoplasms and Neck Masses

Prof. Chand Shah · 34 conditions · source: CMS I Neoplasms and Neck Masses - Shah Fallsv-2.pptx

Note: Several conditions appear only as names in the KITTENS differential (slides 16-17) or the primary neoplasm table (slide 38) and are not taught: syphilis, sebaceous cyst, deep neck abscess, hematoma, thyroid hyperplasia, aberrant thyroid tissue, parathyroid cyst, salivary gland tumors, neurogenic tumors, lipoma, sarcomas, Ludwig angina, sialadenitis, melanoma. Thyroid staging (slide 43): the notes say it need not be memorized.

Branchial cleft cyst2 not covered

Name of Condition: Branchial cleft cyst (spelled "brachial" on slide 16 and in the slide 22 notes) Slides 22, 16
Definition: Congenital lateral neck cyst at the anterior border of the SCM (sternocleidomastoid) muscle Slides 22, 17
Etiology (cause): Failure of the pharyngobranchial ducts to obliterate during fetal development Slide 22
Epidemiology (who): Presents in late childhood or early adulthood Slide 22
Risk Factors: Becomes apparent when infected, usually after a URI (upper respiratory infection) Slide 22
Pathology: Not covered in the lecture
Clinical Manifestation: Tender, inflammatory mass at the anterior border of the SCM (sternocleidomastoid) muscle; overlying erythema and swelling if infected Slide 22
Diagnosis: Rule out HPV (human papillomavirus)-associated SCC (squamous cell carcinoma) before confirming a congenital mass, since it can present as a cystic neck mass in an adult Slide 22
Treatment/Therapy: Control infection first (antibiotics), then surgical excision of cyst and tract (definitive); avoid I&D (incision and drainage) unless acute abscess (needle aspiration/decompression preferred) because I&D makes definitive excision harder Slide 22
Mortality ★: Not covered in the lecture

Thyroglossal duct cyst3 not covered

Name of Condition: Thyroglossal duct cyst Slide 23
Definition: Congenital midline mass of the anterior neck, intimately related to the hyoid bone Slides 23, 17
Etiology (cause): Not covered in the lecture
Epidemiology (who): About one third of all congenital neck masses Slide 23
Risk Factors: Often appears only when infected, usually after a URI (upper respiratory infection) Slide 23
Pathology: Not covered in the lecture
Clinical Manifestation: Midline anterior neck mass, may be asymptomatic; location variable (can be lateral or as low as the thyroid gland), off-midline ones hard to tell from branchial cleft cyst; erythema and edema if infected Slide 23
Diagnosis: Pathognomonic sign: vertical motion of the mass with swallowing or tongue protrusion (shows its attachment to the hyoid bone); histopathology of every excised cyst to rule out thyroid carcinoma Slide 23
Treatment/Therapy: Antibiotics if infected; Sistrunk operation (standard; cyst excised with a cuff of tissue including the center of the hyoid bone), avoiding injury to the hypoglossal nerves Slide 23
Mortality ★: Not covered in the lecture

Laryngocele4 not covered

Name of Condition: Laryngocele (external laryngocele); infected form: laryngopyocele Slides 24, 16
Definition: Abnormal dilation or herniation of the saccule of the larynx Slide 24
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Dilated/herniated laryngeal saccule; secondary infection produces a laryngopyocele Slide 24
Clinical Manifestation: Cough, hoarseness, dyspnea, dysphagia, foreign body sensation, or any combination Slide 24
Diagnosis: Laryngoscopy (smooth dilation at the level of the false cord); CT (computed tomography) confirms the diagnosis and details the extent Slide 24
Treatment/Therapy: Treat if symptomatic: laryngoscopic decompression (small), external surgical excision (large; protect the superior laryngeal nerve), or laser endoscopy Slide 24
Mortality ★: Not covered in the lecture

Plunging ranula4 not covered

Name of Condition: Plunging ranula Slide 25
Definition: Mucocele or retention cyst of the floor of the mouth, called plunging when it extends through the mylohyoid muscle into the neck Slide 25
Etiology (cause): Arises from the sublingual gland Slide 25
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Sublingual gland mucocele/retention cyst extending through the mylohyoid muscle into the neck Slide 25
Clinical Manifestation: Slow-growing, painless submental mass Slide 25
Diagnosis: Not covered in the lecture
Treatment/Therapy: Excision of the sublingual gland Slide 25
Mortality ★: Not covered in the lecture

Lymphangioma4 not covered

Name of Condition: Lymphangioma Slide 26
Definition: Congenital malformation of the lymphatic channels Slide 26
Etiology (cause): Failure of the lymph spaces to connect to the rest of the lymphatic system Slide 26
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Soft, doughy, smooth, nontender, compressible mass; positive transillumination ("positive illumination" on the slide) Slide 26
Diagnosis: CT (computed tomography) and MRI (magnetic resonance imaging) to confirm extent and define associated abnormalities such as hemangiomas Slide 26
Treatment/Therapy: Surgical excision vs debulking (removing as much as possible) depending on infiltration; sclerotherapy (injected agent shrinks the vessels over time) Slide 26
Mortality ★: Not covered in the lecture

Hemangioma2 not covered

Name of Condition: Hemangioma Slide 27
Definition: Malformation of vascular tissue Slide 27
Etiology (cause): Not covered in the lecture
Epidemiology (who): Presents in the first few months of life Slide 27
Risk Factors: Not covered in the lecture
Pathology: Grows rapidly during the first year, then slowly involutes from 18 to 24 months of age Slide 27
Clinical Manifestation: Red or bluish soft, compressible mass that enlarges with straining or crying; with or without bruits Slide 27
Diagnosis: CT (computed tomography), MRI (magnetic resonance imaging) Slide 27
Treatment/Therapy: Observation alone for most; intervene for airway compromise, skin ulceration, dysphagia, thrombocytopenia, or cardiac failure: first line propranolol (if no contraindication); second line systemic corticosteroids, interferon alpha, surgical laser excision Slide 27
Mortality ★: Prognosis: 90% self-resolve without therapy Slide 27

Teratoma2 not covered

Name of Condition: Teratoma Slide 28
Definition: Rare germ cell tumor that may contain immature or fully formed tissue (including hair, teeth, muscle) Slide 28
Etiology (cause): Originates from pluripotent cells Slide 28
Epidemiology (who): Head and neck teratomas are 3.5% of all teratomas; most noted at birth or within the first year of life Slide 28
Risk Factors: Not covered in the lecture
Pathology: Pluripotent-cell tumor containing immature or fully formed tissues Slide 28
Clinical Manifestation: Firm neck mass; when large, respiratory compromise or dysphagia Slide 28
Diagnosis: CT (computed tomography) and MRI (magnetic resonance imaging) show calcifications; caution with CT radiation in young children, who may need sedation Slide 28
Treatment/Therapy: Surgical excision Slide 28
Mortality ★: Not covered in the lecture

Dermoid cyst5 not covered

Name of Condition: Dermoid cyst Slide 29
Definition: Congenital cyst from epithelium entrapped in deeper tissue Slide 29
Etiology (cause): Epithelium entrapped in deeper tissue during embryogenesis or by traumatic implantation Slide 29
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Midline, nontender, mobile neck mass in the submental region Slide 29
Diagnosis: Not covered in the lecture
Treatment/Therapy: Surgical excision (mainstay) Slide 29
Mortality ★: Not covered in the lecture

Thymic cyst5 not covered

Name of Condition: Thymic cyst Slide 29
Definition: Congenital neck mass (listed under Endocrine in the KITTENS differential) Slides 29, 16
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Slow-growing, asymptomatic mass; may be painful if infected Slide 29
Diagnosis: MRI (magnetic resonance imaging) and CT (computed tomography) useful for the differential; definitive diagnosis by biopsy (Hassall corpuscles present) Slide 29
Treatment/Therapy: Surgical excision Slide 29
Mortality ★: Not covered in the lecture

Sternocleidomastoid tumor of infancy3 not covered

Name of Condition: Sternocleidomastoid (SCM) tumor of infancy Slide 29
Definition: Benign mass within the SCM (sternocleidomastoid) muscle in infants, related to congenital torticollis (head turned to one side by the neck muscles) Slide 29
Etiology (cause): Not covered in the lecture
Epidemiology (who): Infants Slide 29
Risk Factors: Not covered in the lecture
Pathology: Slowly enlarges for 2-3 months, then regresses over 4-8 months Slide 29
Clinical Manifestation: Firm, painless, discrete mass within the SCM (sternocleidomastoid) muscle Slide 29
Diagnosis: Not covered in the lecture
Treatment/Therapy: Physical therapy to prevent restrictive torticollis; surgical excision only for persistent cases Slide 29
Mortality ★: Prognosis: 80% resolve spontaneously Slide 29

Reactive viral lymphadenopathy2 not covered

Name of Condition: Reactive viral lymphadenopathy (viral lymphadenitis) Slides 31, 16
Definition: Reactive cervical lymph node enlargement with a viral URI (upper respiratory infection) Slide 31
Etiology (cause): Adenovirus, rhinovirus, enterovirus (most common); associated with an underlying URI Slide 31
Epidemiology (who): Most common cause of cervical lymphadenopathy in children Slide 31
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Cervical lymphadenopathy with URI (upper respiratory infection) symptoms Slide 31
Diagnosis: A node larger than 1 cm is abnormal and needs further workup (biopsy for fungal, granulomatous, neoplastic causes) if it persists more than 4-6 weeks or enlarges Slide 31
Treatment/Therapy: Observation Slide 31
Mortality ★: Prognosis: nodes regress in 1-2 weeks Slide 31

Infectious mononucleosis (EBV) lymphadenopathy3 not covered

Name of Condition: Epstein-Barr virus (EBV) / mononucleosis lymphadenopathy Slide 31
Definition: Cervical lymphadenopathy caused by EBV (Epstein-Barr virus) mononucleosis Slide 31
Etiology (cause): EBV (Epstein-Barr virus) Slide 31
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Lymphadenopathy with tonsil and adenoid enlargement, fever, pharyngitis; palpate liver and spleen Slides 31, 15
Diagnosis: EBV (Epstein-Barr virus) monospot Slide 19
Treatment/Therapy: Supportive Slide 31
Mortality ★: Prognosis: adenopathy lasts 4-6 weeks Slide 31

HIV-associated cervical adenopathy2 not covered

Name of Condition: HIV (human immunodeficiency virus)-associated cervical adenopathy Slide 32
Definition: Cervical lymph node enlargement in patients with HIV (human immunodeficiency virus) Slide 32
Etiology (cause): Idiopathic follicular hyperplasia is the most common cause Slide 32
Epidemiology (who): Present in 12%-45% of patients with HIV Slide 32
Risk Factors: Not covered in the lecture
Pathology: Idiopathic follicular hyperplasia (most common) Slide 32
Clinical Manifestation: Cervical adenopathy Slide 32
Diagnosis: Rule out Mycobacterium tuberculosis, Pneumocystis carinii, lymphoma, Kaposi sarcoma; HIV testing among neck mass labs Slides 32, 19
Treatment/Therapy: Treat the HIV Slide 32
Mortality ★: Not covered in the lecture

Persistent generalized lymphadenopathy4 not covered

Name of Condition: Persistent generalized lymphadenopathy Slides 32, 16
Definition: Lymphadenopathy without an identifiable infectious or neoplastic cause Slide 32
Etiology (cause): Not covered in the lecture
Epidemiology (who): Commonly seen in patients with HIV (human immunodeficiency virus) Slide 32
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Generalized lymphadenopathy; the neck is the most common site Slide 32
Diagnosis: Diagnosis made when no infectious or neoplastic cause can be determined Slide 32
Treatment/Therapy: Treat the HIV (human immunodeficiency virus) Slide 32
Mortality ★: Not covered in the lecture

Suppurative bacterial lymphadenopathy5 not covered

Name of Condition: Suppurative (bacterial) lymphadenopathy Slide 33
Definition: Bacterial infection of cervical lymph nodes Slide 33
Etiology (cause): Most commonly Staphylococcus aureus and group A B-Streptococcus (as written on the slide) Slide 33
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Neck mass usually in the submandibular or jugulodigastric region, with sore throat, skin lesions, URI (upper respiratory infection) symptoms Slide 33
Diagnosis: Not covered in the lecture
Treatment/Therapy: Empirical antibiotics against anaerobic and gram-positive organisms; FNA (fine needle aspiration) or I&D (incision and drainage) if antibiotics fail Slide 33
Mortality ★: Not covered in the lecture

Toxoplasmosis3 not covered

Name of Condition: Toxoplasmosis Slide 33
Definition: Infectious cause of neck lymphadenopathy due to Toxoplasma gondii Slide 33
Etiology (cause): Toxoplasma gondii; contracted through poorly cooked meat or ingestion of "oocytes" (as written on the slide) in cat feces Slide 33
Epidemiology (who): Not covered in the lecture
Risk Factors: Poorly cooked meat; exposure to cat feces Slide 33
Pathology: Not covered in the lecture
Clinical Manifestation: Fever, malaise, sore throat, myalgias Slide 33
Diagnosis: Serologic testing (immunoglobulin; toxoplasmosis titers) Slides 33, 19
Treatment/Therapy: Sulfonamides or pyrimethamine Slide 33
Mortality ★: Not covered in the lecture

Tularemia3 not covered

Name of Condition: Tularemia Slide 33
Definition: Infectious cause of neck lymphadenopathy due to Francisella tularensis Slide 33
Etiology (cause): Francisella tularensis; transmitted by rabbits, ticks, contaminated water Slide 33
Epidemiology (who): Not covered in the lecture
Risk Factors: Exposure to rabbits, ticks, contaminated water Slide 33
Pathology: Not covered in the lecture
Clinical Manifestation: Tonsillitis, painful adenopathy, fever, chills, headache, fatigue Slide 33
Diagnosis: Serologic testing and cultures Slide 33
Treatment/Therapy: Streptomycin Slide 33
Mortality ★: Not covered in the lecture

Brucellosis2 not covered

Name of Condition: Brucellosis Slide 33
Definition: Infectious cause of lymphadenopathy due to Brucella Slide 33
Etiology (cause): Brucella; transmitted by ingestion of unpasteurized milk Slide 33
Epidemiology (who): Transmitted most commonly to children Slide 33
Risk Factors: Unpasteurized milk Slide 33
Pathology: Not covered in the lecture
Clinical Manifestation: Total body lymphadenopathy, fever, fatigue, malaise Slide 33
Diagnosis: Serology and cultures Slide 33
Treatment/Therapy: Trimethoprim-sulfamethoxazole or tetracycline Slide 33
Mortality ★: Not covered in the lecture

Cat scratch disease

Name of Condition: Cat scratch disease (cat-scratch fever) Slides 34, 16
Definition: Granulomatous infection causing neck lymphadenopathy after cat contact Slide 34
Etiology (cause): Bartonella henselae Slide 34
Epidemiology (who): Common in patients younger than 20 years Slide 34
Risk Factors: Contact with cats Slide 34
Pathology: Granulomatous disease (specific tissue pattern on biopsy from cell injury) Slide 34
Clinical Manifestation: Lymphadenopathy (commonly preauricular and submandibular), fever, malaise Slide 34
Diagnosis: Serologic testing with indirect fluorescent antibodies; cat scratch antigen titers Slides 34, 19
Treatment/Therapy: Self-limiting vs azithromycin Slide 34
Mortality ★: Prognosis: self-limiting Slide 34

Actinomycosis3 not covered

Name of Condition: Actinomycosis Slide 34
Definition: Granulomatous infection presenting as a neck mass Slide 34
Etiology (cause): Actinomyces Slide 17
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Granulomatous disease (specific tissue pattern on biopsy from cell injury) Slide 34
Clinical Manifestation: Painless, fluctuant neck mass in the submandibular or upper digastric region Slide 34
Diagnosis: Clinical and biopsy Slide 34
Treatment/Therapy: Penicillin Slide 34
Mortality ★: Not covered in the lecture

Atypical mycobacterial adenitis2 not covered

Name of Condition: Atypical mycobacteria (atypical mycobacterial infection) Slides 34, 16
Definition: Granulomatous mycobacterial infection of the neck in children Slide 34
Etiology (cause): Atypical mycobacteria Slide 34
Epidemiology (who): Pediatric population Slide 34
Risk Factors: Not covered in the lecture
Pathology: Granulomatous disease (specific tissue pattern on biopsy from cell injury) Slide 34
Clinical Manifestation: Unilateral neck mass in the anterior triangle or parotid gland; brawny (reddish-brown) skin, induration, pain Slide 34
Diagnosis: Stain or culture for acid-fast bacilli; skin testing Slide 34
Treatment/Therapy: Surgical excision vs I&D (incision and drainage) plus antibiotics Slide 34
Mortality ★: Not covered in the lecture

Tuberculous cervical adenitis (scrofula)1 not covered

Name of Condition: Tuberculosis (TB) of the neck; cervical TB is called scrofula Slides 34, 17
Definition: Cervical lymphadenitis caused by Mycobacterium tuberculosis Slide 34
Etiology (cause): Mycobacterium tuberculosis Slide 34
Epidemiology (who): Adults more than children Slide 34
Risk Factors: Recent travel, exposure to TB (tuberculosis) Slide 14
Pathology: Granulomatous disease (specific tissue pattern on biopsy from cell injury) Slide 34
Clinical Manifestation: Lymphadenopathy more diffuse and bilateral than atypical mycobacteria Slide 34
Diagnosis: TB (tuberculosis) skin test (PPD, purified protein derivative; notes contrast QuantiFERON gold); stain and culture for acid-fast bacilli Slides 34, 19
Treatment/Therapy: Isoniazid, rifampin, rifabutin, rifapentine, pyrazinamide, ethambutol; traditionally RIPE (rifampin, isoniazid, pyrazinamide, ethambutol) Slide 34
Mortality ★: Not covered in the lecture

Fungal neck infection3 not covered

Name of Condition: Fungal infection (of the neck) Slide 35
Definition: Fungal infectious inflammatory neck disorder Slide 35
Etiology (cause): Most common organisms: Candida, Histoplasma, Aspergillus Slide 35
Epidemiology (who): Immunocompromised patients particularly susceptible Slide 35
Risk Factors: Immunocompromise Slide 35
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Fungal cultures and serology required Slide 35
Treatment/Therapy: Amphotericin B; treat aggressively and early Slide 35
Mortality ★: Not covered in the lecture

Noninfectious inflammatory neck disorders5 not covered

Name of Condition: Noninfectious inflammatory disorders (e.g., Sjogren syndrome, sarcoidosis, IgG4 (immunoglobulin G4)-related sialadenitis, Kawasaki disease) Slide 35
Definition: Inflammatory neck masses without an infectious cause Slide 35
Etiology (cause): Generally autoimmune Slide 35
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Many patients have specific symptoms that point to the underlying disorder Slide 35
Diagnosis: ESR (erythrocyte sedimentation rate), CRP (C-reactive protein), autoimmune panel Slide 19
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Neck neoplasm (general)2 not covered

Name of Condition: Neck neoplasm / neoplastic neck mass Slides 37, 39
Definition: Benign tumors arise from neck soft tissue (fat, salivary tissue, lymph nodes, blood vessels, nerves); malignant tumors represent metastatic disease Slide 37
Etiology (cause): Not covered in the lecture
Epidemiology (who): Neck masses under 40 are mostly inflammatory (exception: Hodgkin lymphoma); high risk of malignancy in adults Slides 13, 14
Risk Factors: Age over 40; tobacco and alcohol use; family or previous history of cancer; previous skin/scalp lesion excision; radiation; immunocompromise/HIV (human immunodeficiency virus) Slides 13, 14
Pathology: Malignant: sarcomas, malignant peripheral nerve sheath tumors, lymphoma, metastasis (mucosal head and neck, salivary, skin); benign: paragangliomas, arteriovenous malformations, schwannomas, neurofibromas, neuromas, lipomas Slide 38
Clinical Manifestation: Hoarseness, dysphagia, odynophagia; asymptomatic, slowly progressive, firm; malignant clues: no infectious origin, over 2 weeks, over 1.5 cm, firm, noncystic, nontender, little mobility, ulceration Slides 37, 39, 13
Diagnosis: Presume malignant until proven otherwise; complete head and neck exam; fiberoptic laryngoscopy for occult primary; US (ultrasound), CT (computed tomography) with contrast, MRI (magnetic resonance imaging), PET (positron emission tomography); FNA (fine needle aspiration) biopsy Slides 39, 37
Treatment/Therapy: Refer to specialists early if suspicious or persisting after treatment; early and aggressive treatment needed in some neoplastic conditions Slide 19
Mortality ★: Not covered in the lecture

Metastatic squamous cell carcinoma to the neck4 not covered

Name of Condition: Metastatic squamous cell carcinoma (SCC) of the neck Slide 39
Definition: Most common metastatic lesion to the neck; malignant neck tumors mostly represent metastatic SCC from skin or upper aerodigestive tract Slides 39, 37
Etiology (cause): Spread from SCC (squamous cell carcinoma) of the skin or upper aerodigestive tract (head and neck primary); HPV (human papillomavirus)-associated SCC Slides 37, 22
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Asymptomatic, slowly progressive, firm neck mass; HPV (human papillomavirus)-associated SCC may present as a cystic neck mass in an adult Slides 39, 22
Diagnosis: FNA (fine needle aspiration) biopsy, not excisional (avoids spillage and complicated definitive treatment); then examine all head and neck mucosa, thyroid, salivary glands, skin (usually finds the primary in office); panendoscopy-guided biopsy with possible tonsillectomy; CT (computed tomography), MRI (magnetic resonance imaging), PET (positron emission tomography) Slides 39, 20
Treatment/Therapy: Primary found: treat primary tumor and neck; no primary found: radiation and neck dissection Slide 20
Mortality ★: Not covered in the lecture

Paraganglioma4 not covered

Name of Condition: Paraganglioma (carotid body, vagal, jugulotympanic) Slide 38
Definition: Benign vascular neoplasm of the neck Slide 38
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Benign vascular neoplasm; types: carotid body, vagal, jugulotympanic Slide 38
Clinical Manifestation: Pulsatile neck mass (pulsatile or bruit means vascular) Slides 20, 13
Diagnosis: CT (computed tomography), MRI (magnetic resonance imaging), or MRA (magnetic resonance angiography) angiogram confirms; CTA (computed tomography angiography) for pulsatile masses Slides 20, 19
Treatment/Therapy: Excise tumor or XRT (radiation therapy) Slide 20
Mortality ★: Not covered in the lecture

Lymphoma presenting as a neck mass4 not covered

Name of Condition: Lymphoma (cervical nodal) Slides 17, 20
Definition: Primary neoplastic cause of a neck mass Slides 17, 38
Etiology (cause): Not covered in the lecture
Epidemiology (who): Hodgkin lymphoma is the exception to inflammatory masses in patients under 40 Slide 13
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Rapidly growing mass without infectious symptoms; check liver and spleen Slides 13, 15
Diagnosis: FNA (fine needle aspiration) separates carcinoma from lymphoma; node biopsy with staging Slides 18, 20
Treatment/Therapy: Chemotherapy and XRT (radiation therapy) Slide 20
Mortality ★: Not covered in the lecture

Thyroid nodule / thyroid mass2 not covered

Name of Condition: Thyroid mass / thyroid nodule Slides 40, 41
Definition: Thyroid nodule or mass; the main cause of anterior neck masses Slide 40
Etiology (cause): Not covered in the lecture
Epidemiology (who): Main cause of anterior neck masses and lumps Slide 40
Risk Factors: Age (adults under 30 or over 60); childhood head and neck irradiation; full-body irradiation for bone marrow transplant; family history of thyroid cancer; MEN-2 (multiple endocrine neoplasia type 2) Slide 40
Pathology: Not covered in the lecture
Clinical Manifestation: Immobile midline neck mass that elevates with swallowing; recent growth, dysphagia, obstruction; incidental nodules over 1 cm on imaging need evaluation Slide 40
Diagnosis: US (ultrasound) with FNA (fine needle aspiration), TSH (thyroid-stimulating hormone), T3/T4; FNA is the procedure of choice after labs; low TSH: technetium radionuclide scan first, hot (hyperfunctioning) needs no FNA, cold/warm needs FNA; avoid iodine CT contrast if cancer suspected Slides 40, 41, 18
Treatment/Therapy: Hot nodule: treat hyperthyroidism; FNA benign: follow; malignant: surgery; indeterminate: consider molecular testing and surgery; inadequate: repeat FNA, then surgery if still inadequate and suspicious Slide 41
Mortality ★: Prognosis: hot (hyperfunctioning) nodule: low risk for malignancy Slide 41

Papillary thyroid carcinoma3 not covered

Name of Condition: Papillary thyroid carcinoma (PTC) Slides 42, 43
Definition: Most common thyroid cancer (75%) Slide 42
Etiology (cause): Not covered in the lecture
Epidemiology (who): 75% of thyroid cancers; most common in young females Slide 42
Risk Factors: Not covered in the lecture
Pathology: Involves thyroid epithelial cells Slide 42
Clinical Manifestation: Not covered in the lecture
Diagnosis: FNA (fine needle aspiration); staging differs by age: 45 or younger, stage I in thyroid or local nodes and stage II distant spread; 45 or older, stages I-IVC by size and spread Slides 41, 43
Treatment/Therapy: Lobectomy vs thyroidectomy, with or without neck dissection, with or without ablation, and surveillance Slide 44
Mortality ★: Prognosis: best prognosis of the thyroid cancers Slide 42

Follicular thyroid carcinoma3 not covered

Name of Condition: Follicular thyroid carcinoma (FTC); Hurthle cell variant Slides 42, 43
Definition: Second most common thyroid cancer (16%) Slide 42
Etiology (cause): Not covered in the lecture
Epidemiology (who): 16% of thyroid cancers Slide 42
Risk Factors: Not covered in the lecture
Pathology: Involves thyroid epithelial cells; spreads to local lymph nodes or by blood to bone and lungs Slide 42
Clinical Manifestation: Not covered in the lecture
Diagnosis: FNA (fine needle aspiration); staged with papillary cancer (age 45 cutoff, stages I-IVC by size and spread) Slides 41, 43
Treatment/Therapy: Lobectomy vs thyroidectomy, with or without neck dissection, with or without ablation, and surveillance Slide 44
Mortality ★: Prognosis: hurthle cell variant is more aggressive, with higher risk of metastases and recurrence Slide 42

Medullary thyroid carcinoma1 not covered

Name of Condition: Medullary thyroid carcinoma (MTC) Slides 42, 43
Definition: Thyroid cancer of the parafollicular (C) cells, about 5% Slide 42
Etiology (cause): Not covered in the lecture
Epidemiology (who): About 5% of thyroid cancers Slide 42
Risk Factors: MEN-2 (multiple endocrine neoplasia type 2) is listed as a thyroid-mass risk factor; family members of medullary patients are screened for MEN Slides 40, 44
Pathology: Disorder of parafollicular or C cells (produce calcitonin); insidious, most likely to metastasize Slide 42
Clinical Manifestation: Insidious; may go undiagnosed until a metastasis is found Slide 42
Diagnosis: FNA (fine needle aspiration); own staging table, stages I-IVC (stage I: only in thyroid, 2 cm or smaller) Slides 41, 43
Treatment/Therapy: Thyroidectomy and monitoring for recurrence (screening labs), with or without external beam radiation for nodal disease; screen family members for MEN (multiple endocrine neoplasia) Slide 44
Mortality ★: Prognosis: most likely thyroid cancer to metastasize Slide 42

Anaplastic thyroid carcinoma3 not covered

Name of Condition: Anaplastic (undifferentiated) thyroid carcinoma Slide 42
Definition: Most aggressive thyroid cancer, about 1% Slide 42
Etiology (cause): Not covered in the lecture
Epidemiology (who): 1% of thyroid cancers; commonly elderly patients Slide 42
Risk Factors: Not covered in the lecture
Pathology: Small cell, giant cell, spindle cell carcinoma; aggressive growth, often found after it has spread Slides 42, 43
Clinical Manifestation: Not covered in the lecture
Diagnosis: Staged only IVA-IVC (IVA in thyroid; IVB just outside thyroid; IVC distant, e.g., lungs) Slide 43
Treatment/Therapy: Resistant to all treatment modalities; slide 44 lists anaplastic with the exceptions to thyroidectomy ("needs an isthmectomy") Slides 42, 44
Mortality ★: Death in 6-36 months Slide 42

Primary thyroid lymphoma4 not covered

Name of Condition: Primary lymphoma of the thyroid Slide 45
Definition: Lymphoma arising in the thyroid, most commonly non-Hodgkin B cell tumors Slide 45
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Hashimoto thyroiditis Slide 45
Pathology: Most commonly non-Hodgkin B cell tumor Slide 45
Clinical Manifestation: Not covered in the lecture
Diagnosis: Hard to distinguish from Hashimoto thyroiditis by FNA (fine needle aspiration) alone; biopsy to confirm plus lymphoma staging Slide 45
Treatment/Therapy: Chemotherapy and radiation Slide 45
Mortality ★: Not covered in the lecture

Lecture 19 · Disorders of the Oral Cavity, Salivary Glands and Neck

Prof. Chand Shah · 43 conditions · source: CMS I Disorders of the Oral Cavity, Salivary Glands - Shah Fall UPDATEDsv.pptx

Leukoedema6 not covered

Name of Condition: Leukoedema (normal variant of the oral mucosa) Slide 9
Definition: Common, benign mucosal change; a normal variant Slide 9
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Accumulation of fluid within the epithelial cells of the buccal mucosa Slide 9
Clinical Manifestation: Asymptomatic, bilateral, grayish-white, semitransparent mucosal alteration that typically disappears when the mucosa is stretched Slide 9
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Fordyce granules5 not covered

Name of Condition: Fordyce granules (Fordyce spots) Slide 10
Definition: Normal variant: ectopic sebaceous glands (normal tissue cells in an abnormal location) Slide 10
Etiology (cause): Not covered in the lecture
Epidemiology (who): Found in about 90% of the adult population Slide 10
Risk Factors: Not covered in the lecture
Pathology: Ectopic sebaceous glands in the oral mucosa Slide 10
Clinical Manifestation: White to yellow, 1-2 mm discrete papules, symmetrically distributed on the buccal mucosa and vermilion border of the lips Slide 10
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Physiologic pigmentation5 not covered

Name of Condition: Physiologic oral pigmentation Slide 11
Definition: Normal variant of the oral mucosa with brown-gray pigmentation Slides 8, 11
Etiology (cause): Not covered in the lecture
Epidemiology (who): Commonly seen in individuals with darker skin types Slide 11
Risk Factors: Not covered in the lecture
Pathology: Increased melanocyte activity and melanin production Slide 11
Clinical Manifestation: Typically bilateral brown-gray band on the gingiva; patches may be seen on the tongue, floor of mouth and buccal mucosa Slide 11
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Stomatitis7 not covered

Name of Condition: Stomatitis Slide 13
Definition: Inflammation of the mouth and lips; any inflammatory process of the oral and lip mucous membranes, with or without ulceration Slide 13
Etiology (cause): Trauma (ill-fitting dentures or braces, biting cheek/tongue/lips), surgery, chemotherapy/radiation, viral infection (herpes, coxsackievirus), candidiasis, xerostomia (dry mouth), smoking/chewing tobacco, zinc or iron deficiency, allergic reactions, idiopathic (aphthous ulcers) Slide 13
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Aphthous stomatitis (canker sores)

Name of Condition: Aphthous stomatitis (canker sores); recurrent form = Sutton disease Slides 15, 17
Definition: Painful oral ulcers on freely moving, nonkeratinized mucosa; recurrent aphthous stomatitis is called Sutton disease Slides 15, 17
Etiology (cause): Cause unknown; human herpesvirus 6 (HHV-6) has been suggested Slide 15
Epidemiology (who): Most common cause of acute recurrent oral ulcers in adolescents and young adults Slide 15
Risk Factors: Trauma to the oral mucosa (cheek biting, dental procedures) exacerbates; stress predisposes Slide 15
Pathology: Found on freely moving, nonkeratinized mucosa (buccal and labial mucosa, nonattached gingiva, palate); minor (<1 cm), major (>1 cm, multiple, scarring) and herpetiform (numerous 1-3 mm ulcers, scarring) forms Slides 15, 16
Clinical Manifestation: Painful round ulcers with yellow-gray fibrinoid centers and red halos; minor: burning/tingling before ulcer, lasts 7-10 days; major and herpetiform: last over 1 month Slides 16, 17
Diagnosis: Clinical Slide 17
Treatment/Therapy: Observation (self-limiting); consider anti-inflammatories, antibiotics, antivirals, oral/topical corticosteroids (triamcinolone, fluocinonide), silver nitrate cauterization, Lactobacillus capsules, Kanka, dilute water rinses Slide 17
Mortality ★: Prognosis: self-limiting disorder; major and herpetiform ulcers carry a risk of scarring Slides 16, 17

Behcet syndrome5 not covered

Name of Condition: Behcet syndrome Slide 19
Definition: Inflammatory multisystem disorder with vascular, articular, gastrointestinal, neurologic, urogenital, pulmonary and cardiac involvement Slide 19
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Oral ulcers are the most common feature (up to 100% of patients); genital ulcers in about 75%, resembling oral aphthae Slide 19
Diagnosis: Clinical: recurrent aphthous ulcers plus characteristic systemic manifestations Slide 19
Treatment/Therapy: No cure; corticosteroids, IVIG (intravenous immunoglobulin), immunosuppressants (colchicine, azathioprine, cyclosporine, interferon alfa, cyclophosphamide) Slide 19
Mortality ★: Not covered in the lecture

Oral lichen planus3 not covered

Name of Condition: Oral lichen planus; types: reticular, plaque, atrophic, erosive/bullous, ulcerative, annular Slides 20, 21
Definition: Common chronic inflammatory autoimmune disorder in which activated lymphocytes destroy the basal layer Slide 20
Etiology (cause): May be familial or medication-induced (penicillamine, methyldopa, phenothiazines, antimalarials) Slide 20
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Activated lymphocytes destroy the epithelial basal layer; Koebner (isomorphic) phenomenon (new lesions provoked by physical trauma such as scratching) Slide 20
Clinical Manifestation: Recurrent purple, polygonal, pruritic papules on flexor surfaces and trunk; 60-70% involve lips, oral mucosa, eyelids; Wickham striae (lacy white lines) on buccal mucosa in reticular type; erosive/ulcerative types painful Slides 20, 21
Diagnosis: Not covered in the lecture
Treatment/Therapy: Aimed at pain relief; remove reversible factors (medications, dental restorations, improve oral hygiene, avoid tobacco/alcohol); topical or oral corticosteroids; lidocaine, tacrolimus, cyclosporine; close follow-up Slide 22
Mortality ★: Prognosis: 1-4% progress to squamous cell carcinoma, higher risk with ulcerative lesions Slide 22

Systemic lupus erythematosus (oral)5 not covered

Name of Condition: Systemic lupus erythematosus (SLE), oral involvement Slide 23
Definition: Mucous membrane (oral) involvement in SLE (systemic lupus erythematosus) Slide 23
Etiology (cause): Not covered in the lecture
Epidemiology (who): 40% of patients with SLE (systemic lupus erythematosus) have mucous membrane involvement Slide 23
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Oral lesions may be the first sign; painful or painless; no correlation with systemic activity; cheilitis, erythematous and honeycomb patches, white plaques, discoid and punched-out ulcers with surrounding erythema on lips, soft and buccal mucosa Slide 23
Diagnosis: Not covered in the lecture
Treatment/Therapy: Photoprotection; topical or intralesional corticosteroids, topical calcineurin inhibitors, systemic glucocorticoids; systemic antimalarials (hydroxychloroquine, chloroquine) Slide 24
Mortality ★: Not covered in the lecture

Herpes simplex ulcers

Name of Condition: Herpes simplex ulcers; herpetic gingivostomatitis (primary) Slide 25
Definition: Oral/perioral ulcers caused by HSV (herpes simplex virus) type 1 and 2 Slide 25
Etiology (cause): HSV-1 and HSV-2 (herpes simplex virus types 1 and 2) Slide 25
Epidemiology (who): Primary infection most common in seronegative children; herpetic gingivostomatitis is the most common primary manifestation in children and young adults Slide 25
Risk Factors: Recurrence triggered by stress, trauma (including dental treatment), immunosuppression, ultraviolet light/sunlight, menstruation Slides 25, 26
Pathology: Secondary disease is reactivation of virus dormant in the trigeminal ganglion, migrating along the axonal sheath Slide 25
Clinical Manifestation: Prodrome of burning, tingling, pain about 24 hours before; small painful lesions ulcerate to an erythematous base with gray cover; odynophagia, fever, malaise, cervical lymphadenopathy; heals without scar in 1-2 weeks Slides 25, 26
Diagnosis: Clinical when characteristic lesions present; confirm with HSV DNA PCR (polymerase chain reaction; most sensitive and specific); IgG (immunoglobulin G)/IgM (immunoglobulin M) serology distinguishes HSV-1 from HSV-2; viral culture is definitive; Tzanck smear (multinucleated giant cells, also seen with varicella zoster) Slide 27
Treatment/Therapy: Oral acyclovir for treatment and prophylaxis Slide 27
Mortality ★: Prognosis: resolves in 1-2 weeks, heals without a scar Slide 26

Acute suppurative sialadenitis

Name of Condition: Acute suppurative sialadenitis Slides 34, 35
Definition: Bacterial infection of the salivary glands Slide 34
Etiology (cause): Staphylococcus aureus (most common), then Streptococcus viridans, Haemophilus influenzae, Streptococcus pyogenes, Escherichia coli; Klebsiella, Enterobacter, Pseudomonas, Candida in chronically ill hospitalized patients Slide 35
Epidemiology (who): Postoperative patients, elderly patients with chronic medical conditions, children younger than 2 months Slide 35
Risk Factors: Dehydration, trauma, immunosuppression, debilitation, chemotherapy/radiation, age over 50, HIV (human immunodeficiency virus), xerostomia, sialolithiasis, anorexia/bulimia Slide 35
Pathology: Salivary stasis from duct stricture/obstruction reduces antibacterial activity; bacteria thought to ascend the parotid duct then spread hematogenously Slide 34
Clinical Manifestation: Usually unilateral parotid swelling (parotid most affected), firm and diffusely tender; overlying erythema; trismus, purulent ductal discharge (can be massaged from the duct), induration, fever, chills Slide 36
Diagnosis: Usually clinical; if uncertain: culture (fine-needle aspiration not required), ultrasound, CT (computed tomography) or MRI (magnetic resonance imaging) to check for stones, abscess, gland inflammation Slide 37
Treatment/Therapy: Rehydration; IV (intravenous) penicillinase-resistant gram-positive coverage (nafcillin or cefazolin) then oral dicloxacillin or clindamycin; warm compresses, massage, sialogogues (lemon drops, vitamin C lozenges), oral hygiene; no improvement in 48 hours suggests abscess: incision and drainage or image-guided aspiration Slide 38
Mortality ★: Most respond to medical therapy; mortality is higher with coexisting medical conditions; can progress to abscess Slide 39

Chronic granulomatous sialadenitis5 not covered

Name of Condition: Chronic granulomatous sialadenitis Slide 34
Definition: Chronic unilateral or bilateral salivary gland swelling with minimal pain Slide 34
Etiology (cause): Consider primary tuberculosis if risk factors present; differential includes cat scratch disease, sarcoidosis, actinomycosis, granulomatosis with polyangiitis (Wegener granulomatosis), syphilis Slide 34
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Chronic unilateral or bilateral salivary gland swelling with minimal pain Slide 34
Diagnosis: Fine-needle aspiration biopsy of the gland Slide 34
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Sialolithiasis1 not covered

Name of Condition: Sialolithiasis (salivary calculi, salivary stones) Slide 40
Definition: Salivary gland stones causing obstruction Slide 40
Etiology (cause): Change in saliva viscosity, ductal epithelial injury, salivary stagnation (dehydration) cause calcium phosphate/carbonate precipitation Slide 40
Epidemiology (who): 80-90% submandibular gland, 10-20% parotid, very few sublingual/minor glands; more common in men Slides 40, 41
Risk Factors: Long illnesses with dehydration, gout, diabetes, hypertension Slide 41
Pathology: Submandibular predominance from longer duct, more mucin, alkaline saliva, high calcium/phosphate; submandibular stones are calcium phosphate and hydroxyapatite and radiopaque Slides 40, 41
Clinical Manifestation: Recurrent submandibular swelling and pain worse with eating (salivary colic); infection with prolonged obstruction; xerostomia; gritty sand-like particles in mouth; stone palpable in anterior two thirds of submandibular duct Slide 42
Diagnosis: Usually clinical; confirm with x-ray, ultrasound (echogenic structure with acoustic shadow), CT (most sensitive), digital subtraction sialography (most accurate) Slides 41, 42
Treatment/Therapy: Conservative: hydration, hot compresses, gland massage, NSAIDs (nonsteroidal anti-inflammatory drugs), lozenges; removal by size/location: intraoral extraction (anterior duct), sialoendoscopy +/- open sialolithotomy, gland excision for hilum/body stones, interventional radiology, lithotripsy Slide 43
Mortality ★: Not covered in the lecture

Parotitis5 not covered

Name of Condition: Parotitis Slide 44
Definition: Painful swelling of the parotid gland Slide 44
Etiology (cause): Viral: mumps (paramyxovirus), herpes, Epstein-Barr virus; other: bacterial infection, diabetes, tumors, stones, dental problems Slide 44
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Swelling or inflammation of the parotid gland in response to the cause Slide 44
Clinical Manifestation: Painful swelling of the parotid gland Slide 44
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Vocal cord nodules1 not covered

Name of Condition: Vocal cord nodules; screamer's nodules (children); singer's nodules Slide 46
Definition: Smooth, paired lesions at the junction of the anterior one third and posterior two thirds of the vocal folds Slide 46
Etiology (cause): Vocal abuse Slide 46
Epidemiology (who): Most common cause of persistent dysphonia in children; frequent cause of voice deterioration in professional singers Slide 46
Risk Factors: Vocal abuse (screaming children, professional singers) Slide 46
Pathology: Paired lesions at the junction of the anterior one third and posterior two thirds of the vocal folds Slide 46
Clinical Manifestation: Hoarseness; persistent dysphonia Slide 46
Diagnosis: Laryngoscopy: small, well-defined, whitish, bilateral and symmetric vocal cord lesions Slide 47
Treatment/Therapy: Speech therapy is first line in adults and children (photodocumentation tracks progress); microlaryngoscopy Slide 47
Mortality ★: Not covered in the lecture

Vocal cord polyps3 not covered

Name of Condition: Vocal cord polyps Slide 48
Definition: Unilateral fluid-filled masses of gelatinous material within the superficial lamina propria of the vocal fold Slide 48
Etiology (cause): Not covered in the lecture
Epidemiology (who): More common in men Slide 48
Risk Factors: Vocal abuse and heavy smoking Slide 48
Pathology: Pedunculated, unilateral, fluid-filled gelatinous lesions in the superficial lamina propria at the point of maximal vibration (junction of anterior and middle thirds); may show vascular markings Slide 48
Clinical Manifestation: Not covered in the lecture
Diagnosis: Microlaryngoscopic examination with excision confirms diagnosis and excludes other pathology; a large polyp may conceal an early laryngeal squamous cell carcinoma Slide 48
Treatment/Therapy: Microlaryngoscopic excision; vocal rest and smoking cessation Slide 48
Mortality ★: Not covered in the lecture

Vocal cord papillomatosis2 not covered

Name of Condition: Vocal cord papillomatosis; recurrent respiratory papillomatosis (RRP) Slide 49
Definition: Benign, noncontagious, rare condition with exophytic warty lesions, usually in the larynx (also nose, pharynx, trachea) Slide 49
Etiology (cause): HPV (human papillomavirus) subtypes 6 and 11, rarely 16 Slide 49
Epidemiology (who): Bimodal: juvenile at 2-4 years; adult peak in the 30s Slide 49
Risk Factors: Not covered in the lecture
Pathology: Multiple friable irregular warty growths on true and false cords, at areas of airway constriction with turbulence, mucosal drying/cooling, and ciliary-to-squamous epithelial junctions Slide 50
Clinical Manifestation: Glottic lesions: dysphonia; supraglottic: stridor; hoarseness, airway obstruction; less often chronic cough, pneumonia, failure to thrive, dyspnea Slide 51
Diagnosis: Not covered in the lecture
Treatment/Therapy: No cure for HPV (human papillomavirus); remove symptomatic lesions (carbon dioxide laser, cold steel dissection, microdebrider); avoid tracheostomy (new squamociliary junction); adjuvant intralesional cidofovir (off-label); HPV vaccine (Gardasil, Gardasil 9) may prevent Slide 52
Mortality ★: Prognosis: spontaneous remission occurs but recurrence may come years later; 3-7% risk of malignancy Slide 52

Vocal cord paralysis2 not covered

Name of Condition: Vocal cord paralysis Slide 53
Definition: Voice disorder in which one or both vocal folds do not open or close properly Slide 53
Etiology (cause): Surgical injury (thyroid/parathyroid, esophagus, neck, chest), neck/chest trauma, tumors, infections (Lyme disease, Epstein-Barr virus, herpes, possibly COVID-19), neurologic (stroke, multiple sclerosis, Parkinson disease) Slide 53
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Recurrent laryngeal nerve or vagus nerve injury; unilateral or bilateral Slide 53
Clinical Manifestation: Unilateral: hoarse breathy dysphonia, aspiration, dysphagia, short phonation time, vocal fatigue, stridor in children, or asymptomatic; bilateral: inspiratory or biphasic stridor, weak cry, aspiration, hoarseness Slide 54
Diagnosis: Mirror laryngoscopy or flexible nasolaryngoscopy; full neurologic exam; laryngeal electromyography for prognosis Slides 54, 56
Treatment/Therapy: Determine if self-limiting or permanent; observation with voice therapy; surgical medialization of the affected fold (implant), thyroplasty Slide 55
Mortality ★: Prognosis: transected nerve or malignant infiltration will not recover; bruised or stretched nerve may recover in 6 months to 1 year Slide 56

Acute laryngitis4 not covered

Name of Condition: Acute laryngitis Slide 57
Definition: Most common cause of hoarseness; persists about a week after upper respiratory infection symptoms clear Slide 57
Etiology (cause): Viral (rhinovirus most common; parainfluenza, respiratory syncytial virus, adenovirus, influenza, pertussis), bacterial, fungal, acid reflux, smoking, toxic inhalation, cough, vocal abuse, direct injury, allergy Slide 57
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Dysphonia, hoarseness, low-grade fever, cough, rhinitis, postnasal drip Slide 57
Diagnosis: Clinical Slide 57
Treatment/Therapy: Conservative: hydration, antipyretics, voice rest, decongestants, humidification, smoking cessation; antibiotics only if secondary bacterial infection suspected Slide 57
Mortality ★: Not covered in the lecture

Chronic laryngitis6 not covered

Name of Condition: Chronic laryngitis Slide 58
Definition: Voice disturbance lasting more than 2 weeks; not a true diagnosis Slide 58
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Voice disturbance lasting more than 2 weeks Slide 58
Diagnosis: Always work up underlying cause (consider laryngeal cancer, vocal cord polyps); refer to ENT (ear, nose and throat) for laryngoscopy Slide 58
Treatment/Therapy: Not covered in the lecture
Mortality ★: Not covered in the lecture

Epiglottitis (supraglottitis)1 not covered

Name of Condition: Epiglottitis; supraglottitis (more correct term) Slide 60
Definition: ENT (ear, nose and throat) emergency: cellulitis of multiple areas of the supraglottis Slide 60
Etiology (cause): Hib (Haemophilus influenzae type b), most common in children; Streptococcus pneumoniae, Staphylococcus aureus, beta-hemolytic Streptococcus Slide 60
Epidemiology (who): Children 2-6 years, but any age including adults; rare; incidence down over 90% since Hib vaccine Slide 60
Risk Factors: Not covered in the lecture
Pathology: Cellulitis of the supraglottis with edema and erythema Slides 60, 66
Clinical Manifestation: Children, sudden rapid onset, 4 Ds: drooling, dysphagia, dysphonia (hot potato voice), distress; tripod position (sitting, leaning forward) with sniffing position (neck hyperextended, chin thrust forward); adults, slower: severe sore throat, odynophagia, fever, dyspnea; inspiratory stridor is late Slides 61, 62
Diagnosis: Avoid anxiety-provoking exams (can obstruct airway); lateral neck x-ray thumbprint sign (swollen epiglottis), not needed for diagnosis; CT (computed tomography) similar; laryngoscopy is gold standard Slides 63, 64
Treatment/Therapy: Airway first; children: operating room (rigid bronchoscopy, emergency tracheotomy), inhalation anesthesia to inspect and confirm, endotracheal intubation, cultures, parenteral antibiotics; adults: observe, intubation/tracheostomy if obstructed, humidification, glucocorticoids, IV (intravenous) antibiotics, nebulized epinephrine; ceftriaxone/cefotaxime + vancomycin (allergy: vancomycin + quinolone or carbapenem); consult ID (infectious disease specialist) Slides 65, 66, 67
Mortality ★: High mortality if not diagnosed and treated promptly; responds rapidly to treatment, extubation often possible in 48-72 hours Slides 60, 66

Viral pharyngitis4 not covered

Name of Condition: Viral pharyngitis (tonsillitis if tonsils affected; pharyngotonsillitis if both) Slides 69, 72
Definition: Viral infection causing inflammation of the throat (pharyngitis) and/or tonsils (tonsillitis) Slide 69
Etiology (cause): Viral causes are 70% of pharyngitis: adenovirus, Epstein-Barr virus, herpes simplex virus, HIV (human immunodeficiency virus), influenza, parainfluenza, rhinovirus, coronavirus, echovirus, enteroviruses, coxsackievirus Slide 70
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Sore throat, earache/headache, cough, rhinitis, laryngitis, hoarseness, fever, conjunctivitis, lymphadenopathy, herpangina (ulcerative vesicles over the tonsils) Slide 72
Diagnosis: Clinical; no further testing Slide 72
Treatment/Therapy: Supportive: hydration, antipyretics, pain relievers Slide 72
Mortality ★: Not covered in the lecture

Bacterial pharyngitis (GABHS)2 not covered

Name of Condition: Bacterial pharyngitis; strep throat; GABHS (group A beta-hemolytic Streptococcus) pharyngitis Slide 73
Definition: Bacterial infection of the pharynx/tonsils, most commonly GABHS (group A beta-hemolytic Streptococcus) Slides 69, 73
Etiology (cause): Bacteria are 30% of pharyngitis; most common GABHS; others group C/G streptococci, Neisseria gonorrhoeae, Mycoplasma pneumoniae, Chlamydia trachomatis, Corynebacterium diphtheriae Slides 70, 73
Epidemiology (who): Children and adolescents (not younger than 3); peaks in winter and spring; droplet spread; incubation 2-5 days Slide 73
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Fever over 100.4 F, sore throat, cervical lymphadenopathy, dysphagia, odynophagia, no cough, abdominal pain; tonsillar/pharyngeal erythema with purulent exudate Slide 73
Diagnosis: Rapid antigen test; confirm a negative with throat culture in children and adolescents (slide: always); ASO (antistreptolysin O) titer shows recent past infection, as in rheumatic fever, and does not diagnose acute pharyngitis (slide calls it definitive); Centor criteria: fever, exudate, tender anterior nodes, no cough, age 3-14 (+1), 45 or older (-1) Slides 74, 75, 76
Treatment/Therapy: Supportive care; penicillin VK for 10 days or amoxicillin; IM (intramuscular) penicillin G if compliance concern; mild allergy: cephalexin, cefadroxil; severe allergy: erythromycin, clarithromycin, clindamycin Slide 77
Mortality ★: Complications: untreated GABHS (group A beta-hemolytic Streptococcus) can lead to rheumatic fever (rare) and peritonsillar abscess Slides 78, 96

Rheumatic fever1 not covered

Name of Condition: Rheumatic fever Slides 78, 79
Definition: Rare sequela of untreated GABHS (group A beta-hemolytic Streptococcus) pharyngitis; inflammatory disease of joints, heart, skin and nervous system Slides 78, 79
Etiology (cause): Untreated GABHS (group A beta-hemolytic Streptococcus) infection Slide 78
Epidemiology (who): Peak ages 5-15; rare before 4 and after 40 Slide 78
Risk Factors: Untreated streptococcal pharyngitis Slide 78
Pathology: Cross-reactive antibodies to streptococcal infection affect the heart (endocarditis, myocarditis, pericarditis) Slide 78
Clinical Manifestation: Onset about 2-3 weeks after infection (range 1-5); JONES major: polyarthritis, carditis, nodules, erythema marginatum, Sydenham chorea; minor: arthralgia, fever, prolonged PR interval, elevated ESR (erythrocyte sedimentation rate)/CRP (C-reactive protein) Slides 78, 79
Diagnosis: JONES criteria: 2 major, or 1 major and 2 minor, with evidence of recent group A strep infection Slide 79
Treatment/Therapy: Not covered in the lecture
Mortality ★: Prognosis: typically resolves after about 6 weeks Slide 78

Chronic pharyngitis4 not covered

Name of Condition: Chronic pharyngitis Slide 80
Definition: Persistent pharyngeal inflammation from ongoing irritants or underlying disease Slide 80
Etiology (cause): Postnasal drip (chronic rhinosinusitis), irritants (dust, dry heat, chemicals, smoking, alcohol), chronic mouth breathing, voice abuse, allergy, granulomatous disease, connective tissue disorder, malignancy Slide 80
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Constant throat clearing, dry throat, odynophagia, thickened granular pharyngeal wall, pharyngeal crusting Slide 80
Diagnosis: Clinical; culture and biopsy if therapy fails Slide 80
Treatment/Therapy: Address underlying disorder, avoid precipitating factors, symptomatic treatment Slide 80
Mortality ★: Not covered in the lecture

Infectious mononucleosis2 not covered

Name of Condition: Infectious mononucleosis (mono) Slide 81
Definition: Highly contagious viral disease Slide 81
Etiology (cause): EBV (Epstein-Barr virus) 90%; CMV (cytomegalovirus) and other viruses 10% Slide 81
Epidemiology (who): Ages 15-24; 90-95% of adults are EBV (Epstein-Barr virus) seropositive; spread by oral contact or infected saliva Slide 81
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Prodrome of malaise, headache, low-grade fever (may be asymptomatic under age 10); triad: fever, tonsillar pharyngitis +/- exudate, cervical lymphadenopathy; palatal petechiae, hepatosplenomegaly, rash in 5%; penicillin (for example, amoxicillin) can trigger a rash (exanthem) Slides 82, 83, 87
Diagnosis: WBC (white blood cell count) with differential and heterophile (Monospot) test; positive confirms; negative suggests CMV (cytomegalovirus), confirm with EBV serology, IgM (immunoglobulin M) = current and IgG (immunoglobulin G) = past infection; PCR (polymerase chain reaction) for viral load in transplant Slides 84, 85
Treatment/Therapy: Supportive (fluids, NSAIDs (nonsteroidal anti-inflammatory drugs), acetaminophen, rest), no antiviral; corticosteroids for severe respiratory compromise; no heavy lifting/contact sports about 1 month until spleen normal on ultrasound Slide 86
Mortality ★: Complication: splenic rupture risk with contact sports or heavy lifting while splenomegaly persists Slide 86

Oral candidiasis (thrush)2 not covered

Name of Condition: Oral candidiasis; thrush Slide 88
Definition: Oral yeast infection Slide 88
Etiology (cause): Candida albicans; Aspergillus may also be cultured Slide 88
Epidemiology (who): Common in infants and immunosuppressed patients such as HIV (human immunodeficiency virus) Slide 88
Risk Factors: Dentures, debilitation with poor oral hygiene, diabetes mellitus, anemia, chemotherapy or local irradiation, oral or systemic corticosteroids, broad-spectrum antibiotics, elderly, HIV/immunocompromise Slide 88
Pathology: Not covered in the lecture
Clinical Manifestation: Painful, granular, creamy white curd-like patches on an erythematous base on buccal mucosa and tongue that rub off (unlike leukoplakia or lichen planus); fever, lymphadenopathy, odynophagia, taste changes Slide 89
Diagnosis: Clinical; KOH (potassium hydroxide) prep shows spores and pseudohyphae Slide 90
Treatment/Therapy: Saline and peroxide rinses; antifungals: nystatin oral suspension, clotrimazole, ketoconazole, fluconazole (longer in HIV); refractory: itraconazole or voriconazole Slide 90
Mortality ★: Not covered in the lecture

Cervical adenitis3 not covered

Name of Condition: Cervical adenitis (cervical lymphadenitis) Slide 91
Definition: Inflammation of a cervical lymph node (often used as a synonym for lymphadenopathy, which is a sign, not a diagnosis) Slide 91
Etiology (cause): About 70% beta-hemolytic strep, 20% staphylococci including MRSA (methicillin-resistant Staphylococcus aureus), 10% viruses, atypical mycobacteria, Bartonella henselae (cat scratch fever); also toxoplasmosis, TB (tuberculosis), brucellosis, herpes simplex, syphilis, CMV (cytomegalovirus), HIV (human immunodeficiency virus), histoplasmosis, varicella; inflammatory, degenerative, neoplastic Slides 91, 92
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Local ear, nose and throat infections involve regional nodes and can form abscesses; nodes may stay palpable if scarred Slides 91, 92
Clinical Manifestation: Typically a unilateral, solitary, anterior cervical node Slide 92
Diagnosis: Response to antibiotics; describe size, shape, mobility (immobile suggests malignancy), consistency, tenderness (tender = inflammatory); FNA (fine-needle aspiration) biopsy if persistent or enlarging (possible lymphoma) Slide 93
Treatment/Therapy: Treat the underlying cause; incision and drainage if abscess Slide 94
Mortality ★: Not covered in the lecture

Peritonsillar abscess (quinsy)1 not covered

Name of Condition: Peritonsillar abscess; quinsy Slide 96
Definition: Collection of pus between the palatine tonsil capsule and the pharyngeal muscles Slide 96
Etiology (cause): Complication of untreated strep throat or tonsillitis; aerobes: GABHS (group A beta-hemolytic Streptococcus), Staphylococcus aureus, Haemophilus influenzae; anaerobes: Prevotella, Porphyromonas, Fusobacterium, Streptococcus Slide 96
Epidemiology (who): Most common deep head and neck infection, especially young adults, adolescents and children; more common in males Slide 96
Risk Factors: Untreated strep throat or tonsillitis Slide 96
Pathology: Pus collects between the tonsil capsule and pharyngeal muscles; edema pushes the soft palate and peritonsillar fold medially, deviating the uvula Slides 96, 99
Clinical Manifestation: Severe sore throat, fever, odynophagia, dysphagia, hot potato voice; triad: trismus (inability to open jaw; most reliable), uvular deviation away from the involved side, dysphonia Slides 98, 99, 102
Diagnosis: Clinical; confirmed by pus at drainage; CT (computed tomography) with contrast shows extent; ultrasound distinguishes abscess from cellulitis and guides aspiration Slide 100
Treatment/Therapy: Secure airway first; needle aspiration or incision and drainage; parenteral amoxicillin-clavulanate or clindamycin, adding MRSA (methicillin-resistant Staphylococcus aureus) coverage if severe; oral if mild; tonsillectomy for recurrence, usually after infection resolves Slides 101, 102
Mortality ★: Not covered in the lecture

Retropharyngeal abscess

Name of Condition: Retropharyngeal abscess Slide 103
Definition: Abscess of the retropharyngeal space (skull base to posterior mediastinum) Slide 103
Etiology (cause): Spread from peritonsillar abscess or retropharyngeal node infection (adenitis to abscess); GABHS (group A beta-hemolytic Streptococcus), Staphylococcus aureus, Haemophilus influenzae, mixed flora Slide 103
Epidemiology (who): More common in children under 5 after upper respiratory infection, otitis media, sinusitis; adults: intraoral procedures, trauma, foreign bodies (fishbone), immunocompromise, odontogenic spread Slide 103
Risk Factors: Children: upper respiratory infection, otitis media, sinusitis; adults: intraoral procedures, trauma, foreign body, immunocompromise, dental infection Slide 103
Pathology: Infection of retropharyngeal space nodes progresses to abscess; can spread into the danger and prevertebral spaces toward the mediastinum Slides 103, 107
Clinical Manifestation: Early: fever, sore throat, pharyngeal erythema, dysphagia, odynophagia, neck stiffness, trismus; later: ill appearance, drooling, leaning forward with neck extended, respiratory distress Slide 104
Diagnosis: Labs; lateral neck x-ray: widened retropharyngeal (prevertebral soft tissue) space; CT (gold standard): rim-enhancing hypodense collection; distinguish abscess from adenitis Slide 105
Treatment/Therapy: Surgical emergency; protect airway; antibiotics covering streptococci, anaerobes, S. aureus: ampicillin-sulbactam or clindamycin + ceftriaxone; vancomycin or linezolid if no improvement; then oral amoxicillin-clavulanate or clindamycin Slide 106
Mortality ★: Complications: mediastinitis (50% mortality), respiratory distress, rupture with aspiration pneumonia, spread to danger and prevertebral spaces Slide 107

Ludwig angina1 not covered

Name of Condition: Ludwig angina Slide 108
Definition: Emergency: severe infection (cellulitis) of the floor of mouth and submental, sublingual and submandibular spaces Slides 108, 109
Etiology (cause): Streptococci, staphylococci, Bacteroides, Fusobacterium, Klebsiella (usually in diabetes with other flora); offending tooth or teeth Slides 108, 111
Epidemiology (who): Not covered in the lecture
Risk Factors: Diabetes (more aggressive course) Slide 108
Pathology: Posterior spread of cellulitis displaces tongue up and back; pus coalesces in the floor of mouth and can occlude the airway Slide 110
Clinical Manifestation: Edema and erythema of upper neck under the chin and floor of mouth; tongue displaced up and back; pus in floor of mouth Slide 110
Diagnosis: CT (computed tomography) with contrast: separates inflammation/phlegmon from abscess and shows extent Slide 110
Treatment/Therapy: Antibiotics: penicillin + metronidazole, ampicillin-sulbactam, clindamycin, selected cephalosporins; external drainage via bilateral submental incision if airway threatened or medical therapy fails; dental consultation Slide 111
Mortality ★: Complications: can rapidly compromise upper airway, requiring a surgical airway Slide 108

Diphtheria2 not covered

Name of Condition: Diphtheria; nasal, laryngeal, pharyngeal (most common) and cutaneous forms Slide 112
Definition: Acute Corynebacterium diphtheriae infection, usually of respiratory tract, also mucous membranes or skin wounds Slide 112
Etiology (cause): Corynebacterium diphtheriae, spread by respiratory secretions Slide 112
Epidemiology (who): Common in nonimmunized children older than 6 Slide 112
Risk Factors: Lack of immunization Slide 112
Pathology: Not covered in the lecture
Clinical Manifestation: Pharyngeal: tenacious gray membrane over tonsils and pharynx, mild sore throat, fever, malaise, toxemia, prostration; nasal discharge; laryngeal airway obstruction; myocarditis (arrhythmia, heart block, heart failure); cranial neuropathy (diplopia, slurred speech, dysphagia) Slide 112
Diagnosis: Clinical, confirmed by culture; differentiate from strep pharyngitis, mononucleosis, adenovirus, herpes simplex, candidiasis Slide 113
Treatment/Therapy: Laryngoscopy or bronchoscopy for airway; antitoxin from CDC (Centers for Disease Control and Prevention) to all; penicillin or erythromycin for 14 days; isolate until 3 negative cultures; treat contacts with erythromycin; prevent with childhood immunization, adult tetanus boosters, Tdap (tetanus, diphtheria and acellular pertussis vaccine) each pregnancy (27-36 weeks) Slides 113, 114
Mortality ★: Not covered in the lecture

Dental abscess5 not covered

Name of Condition: Dental abscess; types: periapical, gingival, periodontal, pericoronal Slide 116
Definition: Buildup of pus inside the teeth or gums Slide 116
Etiology (cause): Bacterial infection accumulated in the soft pulp of the tooth Slide 116
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Periapical at root tip; gingival between gum and tooth; periodontal in periodontal pocket; pericoronal around impacted/partly erupted tooth Slide 116
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Antibiotics (amoxicillin, ampicillin-sulbactam, amoxicillin-clavulanate, azithromycin, clindamycin, erythromycin, cephalexin, metronidazole, penicillin VK, ticarcillin-clavulanate); incision and drainage; root canal if restorable, else extraction with apical curettage Slide 117
Mortality ★: Not covered in the lecture

Gingivitis and periodontitis1 not covered

Name of Condition: Diseases of the gingiva: gingivitis (mildest) and periodontitis (periodontal/gum disease) Slides 118, 121
Definition: Gingivitis: plaque-driven gingival inflammation; periodontitis: untreated gingivitis with periodontal ligament/bone destruction and pockets Slides 118, 121
Etiology (cause): Bacterial plaque, inadequate oral hygiene; gram-negative bacteria (A. actinomycetemcomitans, P. gingivalis, P. intermedia, B. forsythus, C. rectus, E. nodatum, P. micros, S. intermedius, Treponema) Slides 118, 120, 121
Epidemiology (who): With dental caries, a primary cause of tooth loss Slide 118
Risk Factors: Diabetes, smoking, aging, genetics, systemic disorders, stress, poor nutrition, puberty, hormone changes, pregnancy, substance abuse, HIV (human immunodeficiency virus), certain medications Slides 120, 122
Pathology: Plaque at gum line causes hyperemia (gingivitis); spreads below gum line, bacterial toxins drive chronic inflammation; gums separate, pockets deepen, ligament and bone destroyed, teeth loosen and fall out Slides 118, 121, 122
Clinical Manifestation: Gingivitis: erythematous, edematous gums that bleed easily with little to no discomfort; periodontitis: pockets, loosening and loss of teeth Slide 121
Diagnosis: Not covered in the lecture
Treatment/Therapy: Gingivitis reversible with professional treatment and good home care; prevention: brushing, flossing, mouthwash, know your risk Slides 121, 122
Mortality ★: Associated conditions: heart disease/stroke (endocarditis risk), pneumonia, osteoporosis, kidney, pancreatic and blood cancers in men Slide 119

Dental caries, pulpitis and periapical abscess4 not covered

Name of Condition: Dental caries (cavities), pulpitis and periapical abscess Slides 123, 124
Definition: Pulpitis: inflammation of the tooth pulp; periapical abscess: pus pocket at the root of the tooth Slide 124
Etiology (cause): Tooth decay (most common), then injury Slide 124
Epidemiology (who): Dental caries and periodontal disease are primary causes of tooth loss Slide 118
Risk Factors: Not covered in the lecture
Pathology: Mild inflammation may resolve without permanent pulp damage; severe inflammation may kill the pulp; infection forms a periapical abscess at the root Slide 124
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Not covered in the lecture
Mortality ★: Complications: if untreated, infection may spread to the jaw or other sites (brain, sinus) Slide 124

Impacted teeth4 not covered

Name of Condition: Impacted teeth Slide 125
Definition: Tooth unable to emerge because of insufficient room Slide 125
Etiology (cause): Overcrowding of teeth with insufficient room for the new tooth Slide 125
Epidemiology (who): Wisdom teeth are usually impacted (last permanent teeth to erupt) Slide 125
Risk Factors: Not covered in the lecture
Pathology: Not covered in the lecture
Clinical Manifestation: Not covered in the lecture
Diagnosis: Not covered in the lecture
Treatment/Therapy: Usually removed (little use in chewing) Slide 125
Mortality ★: Complication: more likely to become infected Slide 125

Malocclusion4 not covered

Name of Condition: Malocclusion Slide 126
Definition: Abnormal alignment of the teeth and how upper and lower teeth fit together Slide 126
Etiology (cause): Jaw-tooth size mismatch, thumb sucking or tongue thrusting, lost teeth, birth defects Slide 126
Epidemiology (who): Not covered in the lecture
Risk Factors: Not covered in the lecture
Pathology: Unequal distribution of chewing (about 150 lb) and clenching (about 250 lb) forces wears teeth, causing fractures and loosening Slide 126
Clinical Manifestation: Worn teeth, fractures, loose teeth Slide 126
Diagnosis: Not covered in the lecture
Treatment/Therapy: Braces, aligners, tooth removal, surgery Slide 126
Mortality ★: Not covered in the lecture

Temporomandibular joint disorders

Name of Condition: Temporomandibular joint (TMJ) disorders; TMD (temporomandibular disorders); categories: myofascial pain, internal derangement, arthritis Slides 128, 129
Definition: Disorders of the TMJ (temporomandibular joint), masticatory muscles or both; second most common musculoskeletal cause of pain and disability Slide 128
Etiology (cause): Predisposing: trauma (blow to jaw, whiplash), stress (nocturnal bruxism); perpetuating: stress, poor coping, clenching/grinding, poor posture Slide 128
Epidemiology (who): Common in women of childbearing age (possible sex hormone link) Slide 128
Risk Factors: Trauma, stress, clenching/grinding, poor coping, poor posture Slide 128
Pathology: Myofascial pain (jaw muscles), internal derangement (displaced disc, dislocation, condyle injury), arthritis (degenerative or inflammatory) Slide 129
Clinical Manifestation: Jaw/face/head pain; limited opening, catching, locking; clicking, popping, grating; headache, neck/shoulder pain; tinnitus, ear fullness, hearing loss, dizziness; abnormal tooth wear, sensitivity Slide 130
Diagnosis: Clinical; CT (computed tomography)/MRI (magnetic resonance imaging) if abnormal pain or dysfunction not responding to short-term therapy; differentiate articular vs muscle disorders Slides 130, 131
Treatment/Therapy: Self-care; NSAIDs (nonsteroidal anti-inflammatory drugs), cyclobenzaprine, low-dose tricyclics (amitriptyline, desipramine, nortriptyline), oral methylprednisolone if synovitis; physical therapy, TENS (transcutaneous electrical nerve stimulation), acupuncture, mouth guards, arthrocentesis, arthroscopy, surgery Slide 131
Mortality ★: Prognosis: not life threatening, but major impact on quality of life Slide 128

Oral leukoplakia1 not covered

Name of Condition: Oral leukoplakia Slide 133
Definition: Premalignant white oral lesion that cannot be scraped off (unlike candidiasis) and cannot be attributed to another lesion Slide 133
Etiology (cause): Chronic irritation, smoking, infection Slide 134
Epidemiology (who): Not covered in the lecture
Risk Factors: Smoking and chewing tobacco, alcohol, chronic irritation Slide 134
Pathology: Altered squamous epithelium with increased risk of SCC (squamous cell carcinoma) Slide 133
Clinical Manifestation: White lesion of the oral mucosa that cannot be scraped off Slide 133
Diagnosis: Excisional biopsy to rule out malignancy Slide 134
Treatment/Therapy: Complete intraoral exam and node palpation; remove carcinogenic irritants (tobacco, alcohol); observation with serial biopsies and excisions Slide 134
Mortality ★: Prognosis: 5-20% progress to SCC (squamous cell carcinoma) Slide 133

Erythroplakia2 not covered

Name of Condition: Erythroplakia Slides 133, 135
Definition: Premalignant lesion like leukoplakia but with an erythematous (red) component Slides 133, 135
Etiology (cause): Not covered in the lecture
Epidemiology (who): Not covered in the lecture
Risk Factors: Alcohol and tobacco (major) Slide 135
Pathology: 90% are dysplastic or carcinoma Slide 135
Clinical Manifestation: Leukoplakia-like lesion with a red component Slides 133, 135
Diagnosis: As for leukoplakia: excisional biopsy Slides 134, 135
Treatment/Therapy: As for leukoplakia: remove irritants, observation with serial biopsies and excisions Slides 134, 135
Mortality ★: Prognosis: higher malignancy risk than leukoplakia (25%) Slide 133

Hairy leukoplakia1 not covered

Name of Condition: Hairy leukoplakia Slide 136
Definition: Benign mucosal hyperplasia Slide 136
Etiology (cause): EBV (Epstein-Barr virus); long-term systemic corticosteroids, solid organ transplant Slide 136
Epidemiology (who): Strongly associated with HIV (human immunodeficiency virus); common early finding in HIV Slide 136
Risk Factors: HIV, long-term systemic corticosteroids, solid organ transplant Slide 136
Pathology: Benign mucosal hyperplasia Slide 136
Clinical Manifestation: Painless lateral tongue lesions that wax and wane Slide 136
Diagnosis: Clinical and biopsy Slide 136
Treatment/Therapy: Observation; acyclovir, valacyclovir, famciclovir give temporary resolution Slide 136
Mortality ★: Not covered in the lecture

Salivary gland neoplasm, benign2 not covered

Name of Condition: Benign salivary gland neoplasm; pleomorphic adenoma, basal cell adenoma Slide 140
Definition: Benign tumor of the salivary glands; most parotid benign tumors are epithelial Slide 140
Etiology (cause): Not covered in the lecture
Epidemiology (who): 64-80% of salivary tumors are parotid (75-80% benign); submandibular 7-15% (50-60% benign); sublingual 1%; minor glands about 15% (35% benign) Slide 139
Risk Factors: Not covered in the lecture
Pathology: Parotid: mostly epithelial tumors; minor glands: pleomorphic adenoma most common, then basal cell adenoma Slide 140
Clinical Manifestation: Slow-growing painless mass, often at the tail of the parotid Slide 141
Diagnosis: FNA (fine-needle aspiration), less accurate than for other tumors but helps separate benign from malignant; diffusion-weighted MRI (magnetic resonance imaging)/CT (computed tomography) for deep lobe tumors Slide 141
Treatment/Therapy: Complete surgical excision; no radiation Slide 142
Mortality ★: Excellent prognosis and rare recurrence after removal; recurrence with positive margins; facial numbness or paralysis after surgery Slide 142

Salivary gland neoplasm, malignant1 not covered

Name of Condition: Malignant salivary gland neoplasm; mucoepidermoid carcinoma, adenoid cystic carcinoma, adenocarcinoma Slide 140
Definition: Malignant tumor of the salivary glands Slide 140
Etiology (cause): Not covered in the lecture
Epidemiology (who): 3-4% of head and neck malignancies and under 0.5% of all cancers; parotid most often affected Slide 140
Risk Factors: No specific risk factors known Slide 140
Pathology: Parotid: mucoepidermoid carcinoma most common; minor glands: adenoid cystic carcinoma and adenocarcinoma Slide 140
Clinical Manifestation: Painless mass Slide 141
Diagnosis: FNA (fine-needle aspiration) helps separate malignant from benign but is less accurate than for other tumors; diffusion-weighted MRI (magnetic resonance imaging)/CT (computed tomography) Slide 141
Treatment/Therapy: Surgical removal; radiation for certain stages (T1 and T2); chemotherapy as palliation Slide 143
Mortality ★: Poor prognosis with pain, facial or other nerve involvement, high-grade histology, skin/tissue invasion, recurrence Slide 143

Oral cavity and oropharyngeal cancer1 not covered

Name of Condition: Oral cavity and oropharyngeal neoplasm (cancer) Slide 144
Definition: Cancer of the anterior two thirds of the tongue, buccal mucosa, floor of mouth, hard palate, gingiva, retromolar trigone (oral cavity), or posterior tongue, palatine tonsil, soft palate, posterior pharyngeal wall (oropharynx) Slide 144
Etiology (cause): Oropharyngeal: 60-80% from HPV (human papillomavirus); lip: 90% from chronic sun exposure Slide 144
Epidemiology (who): Males 2-4 times (oral cavity) and 3-5 times (oropharynx) more than females; rises with age, mean 62 Slide 144
Risk Factors: Tobacco (chewing and smoking), alcohol, betel nut, poor oral hygiene, immunosuppression, HPV (oropharynx) Slides 144, 145
Pathology: Most common is SCC (squamous cell carcinoma); lymphoma second in tonsillar fossa; minor glands: adenocarcinoma, adenoid cystic, mucoepidermoid, polymorphous low-grade Slide 145
Clinical Manifestation: Nonhealing ulcer, bleeding, pain, ill-fitting dentures, vague discomfort, foreign body sensation; advanced: dysarthria, dysphagia, neck mass, referred otalgia; tonsillar: odynophagia, trismus Slide 146
Diagnosis: CBC (complete blood count), CMP (comprehensive metabolic panel), high-risk HPV test, in situ hybridization; CT (computed tomography)/MRI (magnetic resonance imaging) for primary and nodes; chest x-ray and PET (positron emission tomography) for metastases; fiberoptic endoscopy; biopsy; dental evaluation Slide 147
Treatment/Therapy: Oral cavity: surgical resection; oropharynx: resection + radiotherapy (better function); prevention: tobacco and alcohol cessation Slide 148
Mortality ★: Not covered in the lecture