EAR

 Theories on cholesteatoma formation

o Invagination of the tympanic membrane (retraction pocket cholesteatoma)
 Retraction pockets of the pars flaccida deepen because of negative middle ear pressure
and possibly repeated inflammation
 As the retraction pocket deepens, desquamated keratin cannot be cleared from the recess,
and a cholesteatoma results
 Origin of such retraction pocket cholesteatomas is thought to be eustachian tube
dysfunction (or OME) with resultant negative middle ear pressure (ex vacuo theory)
o Basal cell hyperplasia
 Epithelial cells (prickle cells) of the pars flaccida could invade the subepithelial tissue by
means of proliferating columns of epithelial cells
o Epithelial ingrowth through a perforation (the migration theory)
 Keratinizing squamous epithelium from the surface of the tympanic membrane invades or
migrates into the middle ear from a perforation in the tympanic membrane
o Squamous metaplasia of middle ear epithelium
 Simple squamous or cuboidal epithelium of the middle ear cleft could undergo a
metaplastic transformation into keratinizing epithelium
 An area of keratinizing epithelium within the middle ear would enlarge because of
accumulated debris and contact with the tympanic membrane
 With intercurrent infection and inflammation, the cholesteatoma would lead to lysis of the
tympanic membrane
and perforation,
resulting in the typical
appearance of an attic
cholesteatoma

 TM and parts
 Boundaries of the middle ear
o Lateral: TM
o Medial: Oval window, vestibular complex, Impression of the chorda tympani and promontory
o Superior: Tegmen tympani
o Inferior: Jugular bulb
o Anterior: Tensor tympani, Carotid Artery, Maxillary bone where the ET is located
o Posterior: Mastoid antrum
 Layers
o Outer – Squamous epithelium
o Middle – Fibrous layer
o Inner – Simple cuboidal epithelium
 Outer and inner hair cell diff.
o inner hair cells are the actual sensory receptors, and 95% of the fibers of the auditory nerve that
project to the brain arise from this subpopulation. The terminations on the outer hair cells are
almost all from efferent axons that arise from cells in the brain
 Tonotopic organization
o The cochlea is organized spatially according to frequency, that is, tonotopic arrangement
o For every frequency there is a highly specific place on the basilar membrane where hair cells are
maximally sensitive to that frequency
 Basal end for high frequencies
 Apical end for low frequencies
o Frequency-selective neurons transmit the neural code from the hair cells through the auditory
system
o For multiple frequencies (complex sound), there are several points of traveling wave maxima, and
the cochlear apparatus constantly tunes itself for best reception and encoding of each component
frequency. The auditory mechanism’s superb frequency resolution is mostly secondary to the highly
tuned hair cell response rather than on processing at higher auditory centers.
 Sound transduction physiology
o Sound waves from the tympanic membrane travel along the ossicular chain, which comprise three
bones (the malleus, incus, and stapes), to the oval window. The displacement of the ossicular
chain varies as a function of the frequency and intensity of the sound.
o The malleus and incus weigh approximately the same, but the stapes is about one-fourth the mass
of the other ossicles. This difference facilitates the transmission of high frequencies.
o The tympanic membrane and ossicular chain most efficiently transmit sound between 500 and
3000 Hz. Thus, the ear has greatest sensitivity at those frequencies most important to
understanding speech.
o The middle ear transforms acoustic energy from the medium of air to the medium of liquid. It is an
impedance-matching system that ensures energy is not lost. This impedance matching is
accomplished by the following four factors:
 Area effect of the tympanic membrane
 Lever action of the ossicular chain
  The natural resonance and efficiency of the outer and middle ears
 The phase difference between the oval window and the round window
 Tuning fork exams
o Rinne test
 Compares a patient’s air and bone conduction hearing
o Weber
 Test of lateralization
o Schwabach
 Compares the patient’s bone conduction hearing to that of a normal listener (usually the
examiner)
o Bing test
 Examines the occlusion effect
 Unplugged audiometry
o 1st layer: tests air-bone gap
o 2nd layer: tests decibel loss
 Types of nystagmus
o Physiologic: end-point nystagmus noted on lateral gaze > 30 degree
o Spontaneous: nystagmus present without positional or other labyrinthine stimulation
o Induced: nystagmus elicited by stimulation, that is, caloric, rotation, etc.
o Positional: nystagmus elicited by assuming a specific position
 CSOM
o is a perforated tympanic membrane with persistent drainage from the middle ear (ie, lasting >6-12
wk)
LBEN
 Glottic SCCA Staging
o Stage 0
 “Carcinoma in-situ.” Abnormal, but non-invasive cells found in the top layer of tissue.
o Stage I
 Tumor is confined to the vocal cords (glottis), and the vocal cords can move normally.
o Stage Ia
 Tumor is located in only one vocal cord.
o Stage Ib
 Tumor spread to both vocal cords.
o Stage II
 Tumor has spread to the supraglottis or subglottis, and/or the vocal cords are unable to
move normally.
o Stage III
 Tumor is confined to the larynx AND: the tumor has caused a vocal cord to stop moving,
AND/OR the tumor has spread to the space between the glottis and thyroid cartilage
AND/OR the tumor has spread to the outer layer of the thyroid cartilage OR the cancer
has spread to one single lymph node on the same side of the neck that is 3 cm or less in
diameter.
o Stage IVa
 Tumor has grown through the thyroid cartilage and/or spread to tissues beyond the larynx
(i.e. thyroid gland, esophagus, trachea, neck muscles, or tongue muscles). Tumor may or
may not have spread to a single lymph node on the same side of the neck that is 3 cm or
less in diameter OR
 Cancer has spread to: a single lymph node on same side of the neck that is between 3 cm
and 6 cm in diameter, or multiple lymph nodes on same side of the neck that are less than
6 cm in diameter, or multiple lymph nodes on opposite or both sides of the neck that are
less than 6 cm in diameter.
o Stage IVb
 Tumor has grown into the tissue in front of the spine, has surrounded the carotid artery, or
has invaded the tissues around the trachea close to the lungs. Tumor may or may not
have spread to any number of lymph nodes in any location OR cancer has spread to a
single lymph node that is more than 6 cm in diameter
o Stage IVc
 Cancer has spread to distant organs or parts of the body, most often the lungs, liver, or
bones.
 Subunits of the larynx and structures involved
o Supraglottic portion: epiglottis (lingual and laryngeal aspects), false vocal cords (ventricular bands),
aryepiglottic folds (laryngeal aspect), arytenoid cartilages and ventricles
o Glottic portion: true vocal cords (superior and inferior surfaces) and anterior and posterior
commissures
 o Subglottic portion: between lower border of true vocal cords and first tracheal cartilage (or lower
margin of cricoid cartilage)
 Thyroid hormone synthesis
1. Iodide transported into the thyrocyte at the basal cell membrane by the symporter (NIS) travels down its
electrochemical gradient to the apical surface
2. Polypeptide chain of thyroglobulin (Tg) is synthesized on the surface of the endoplasmic reticulum, then
translocated into its lumen. Synthesis of carbohydrate units begins, and conformational changes transform
the polypeptide chains into stable dimers
3. Tg enters the Golgi where carbohydrate units are completed
4. Uniodinated Tg travels to the apical surface in small vesicles (AV)
5. Tg is iodinated, and iodotyrosyls are coupled to form T4 and T3 by thyroperoxidase in the presence of H2O2
o (1) the oxidation of iodide
o (2) its subsequent transfer to thyrosyl residues on thyroglobulin, producing monoiodotyrosine (MIT)
and di-iodotyrosine (DIT)
o (3) coupling of two iodotyrosine molecules, either one each of MIT and DIT to form T3 or two of DIT
to form T4
6. Tg, retrieved by micropinocytosis, enters the endosome-lysosomal pathway, where proteolysis and hormone
release occurs
7. Alternatively, Tg, retrieved by macropinocytosis, travels to lysosomes in colloid droplets (CD)
8. Thyroid hormones and precursors leave the lysosomes, and T4 and T3 enter the bloodstream
9. MIT and DIT are deiodinated, and released iodide is recirculated

 Half life
o PTH – 5 minutes, T4 – 1 week, T3 – 1 day, TSH – 1 hour
 UTZ findings of a malignant thyroid mass
o Hypoechoic solid
o Presence of microacalcifications
o Local invasion of surrounding structures
o Taller than it is wide
o Large size: cut off is often taken as 10mm to warrant a FNA
o Suspicious neck lymph nodes suggesting metastatic disease
o Intranodular blood flow
 RLN Course
o Originates from the vagus nerve (CN X) and descends the cervical region along the carotid artery
sheath into the mediastinum
o Right: exits anteriorly to the subclavian artery and travels inferiorly and posteriorly under the artery
before ascending through the neck between the trachea and the esophagus
o Left: exits at the aortic arch level and courses posteromedially beneath it before looping through the
aorticopulmonary window, posterior to the ligamentum arteriosum; the nerve then has an
ascending vertical path through the superior mediastinum until reaching the trachea-esophageal
groove
RAOS
 Polysomnography and components
o Overnight polysomnography in a sleep laboratory is the “gold standard” method for diagnosing
childhood OSAS
o Respiratory events:
 Obstructive apnea – cessation of airflow for at least 10 seconds with persistent respiratory
effort
 Central apnea – cessation of airflow for at least 10 seconds with no respiratory effort
 Mixed apnea – begins as central apnea and ends as obstructive apnea
 Hypopnea – 30% or greater decrease in flow lasting at least 10 seconds and associated
with a 4% or greater oxyhemogloin desaturation OR 50% or greater reduction in flow
lasting at least 10 seconds and associated with either a 3% or greater oxyhemoglobin
desaturation or an arousal
o The apnea-hypopnea index (AHI) is derived from the total number of apneas and hypopneas
divided by the total sleep time. Most sleep centers use a cutoff of 5-10 episodes per hour
o Recommendations: 5-15 episodes/hour for mild, 15-30 episodes/hour for moderate and >30
episodes/hour for severe
o 7 components:
 Nasal-oral thermistor
 Chest wall movement
 Abdominal wall movement
 Expired CO2
 End-tidal CO2
 ECG
 SpO2
 Tonsils
o Anatomy
 Lymphoid tissue with germinal centers containing 6 to 20 epithelial lined crypts. Capsule
over deep surface is separated from the superior constrictor by thin areolar tissue.
Lymphoid tissue of the palatine tonsil is contiguous with that of the lingual tonsil.
o Layers
 Tonsil
 Tonsillar capsule
 Loose areolar tissue with paratonsillar area
 Sup. Constrictor muscle
 Buccopharyngeal fascia/ Pharyngobasilar fascia
 Midal pterygoid muscle
o Blood supply
(a) Facial  Tonsillar branch  tonsil (main branch)
(b) Facial  Ascending palatine  tonsil
(c) Lingual  Dorsal lingual  tonsil
 (d) Ascending pharyngeal  tonsil
(e) Maxillary  Lesser descending palatine  tonsil
 Absolute and relative indications for tonsillectomy
o Absolute
 Enlarged tonsils that cause upper airway obstruction, severe dysphagia, sleep disorders,
or cardiopulmonary complications
 Peritonsillar abscess that is unresponsive to medical management and drainage
documented by surgeon, unless surgery is performed during the acute stage
 Tonsillitis resulting in febrile convulsions
 Tonsils requiring biopsy to define tissue pathology or suspicion of malignancy
o Relative
 Three or more tonsil infections per year despite adequate medical therapy
 Persistent foul taste or breath due to chronic tonsillitis that is not responding to medical
therapy
 Chronic or recurrent tonsillitis in a streptococcal carrier not responding to beta-lactamase-
resistant antibiotics
 Unilateral tonsil hypertrophy that is presumed to be neoplastic
o Paradise Criteria
 Minimum frequency of sore throat episodes
 7 or more in the preceding year or
 5 or more episodes in each of the preceding 2 years
 3 or more in each of the preceding 3 years
 Clinical features (sore throat plus the presence of one or more qualifies as a counting
episode)
 T >38.3 deg C
 CLAD (>2 cm)
 Tonsillar exudate
 Positive culture for GABS
 Crypts of Lieberkuhn
o Tubular glands that lie between the finger-like projections of the inner surface of the small intestine
o Cells of these glands (called Paneth cells) secrete intestinal juice as they gradually migrate along
the side of the crypt and villus
 How are tonsilloliths formed
o Arise from retained material and bacterial growth in the tonsillar or adenoid crypts and may exist in
patients with or without a history of inflammatory disorders in either the tonsils or adenoids
 (1) Agger-nasi cells, (2) Onodi cells, (3) Haler cells
o (1) Mound or prominence on the lateral wall just anterior to the middle turbinate insertion
o (2) a.k.a. Sphenoethmoidal cells are posterior ethmoid cells with superolateral pneumatization into
the sphenoid sinus, creating a horizontal septation
o (3) a.k.a. Infraorbital cells are ethmoid air cells that extend along the medial roof of the maxillary
sinus
 Structures of the OMC
o The ostiomeatal unit is a functional, rather than an anatomic designation, identifying the drainage
pathway of the maxillary sinus, frontal sinus, and anterior ethmoid sinus
o Hiatus semilunaris
o Uncinate process
o Maxillary ostium
o Infundibulum
o Middle meatus
o Bulla ethmoidalis
o Anterior ethmoid
 Classification of polyps

 Keros classification
o Keros described three types of formation of the ethmoid roof based on the vertical height of the
lateral lamella:
 Keros Type I: 1- to 3-mm depth to the olfactory fossa
 Keros Type II: 4- to 7-mm depth to the olfactory fossa
 Keros Type III: 8- to 16-mm depth to the olfactory fossa
 Frontal cell types according to Kuhn Classification
o Kuhn type I: One (1) Frontal ethmoid cell rests immediately superior to the agger nasi cell
o Kuhn type II: >1 Frontal ethmoid cell sits atop the agger nasi cell
o Kuhn type III: Significant pneumatisation of a frontal ethmoid cell and it extends beyond the frontal
recess into the frontal sinus
o Kuhn type IV: Air cell that is isolated within the frontal sinus
o Intersinus septal cell or a medial frontal ethmoidal cell – can be visualized by pushing into the
frontal recess medially
 Frontal cell types according to IFAC
TRAUMA
 Overjet and overbite
o Overjet - horizontal overlap of the maxillary central incisors over the mandibular central incisors,
normal overjet is considered to be 2-3 mm
o Overbite - vertical overlap of the maxillary central incisors over the mandibular central incisors,
normal is considered to be 2-3 mm, or approximately 20–30% of the height of the mandibular
incisors
 Buttresses of the face
o Vertical
 Nasomaxillary
 Zygomaticomaxillary
 Pterygomaxillary
 Vertical mandible
o Horizontal
 Frontal
 Infraorbital rim and nasal bone
 Hard palate and maxillary alveolus
 Horizontal mandible
 Zinggs Classification
o A – incomplete fracture, in the zygomatic pillar
 A1 – isolated frontozygomatic fracture
 A2 – lateral orbital wall fracture
 A3 – infraorbital rim fracture
o B – complete monofragment zygomati bone fracture (tetrapod)
o C – multifragment zygomatic fracture, same as type B but with fragmentation including the body of
the zygoma
 Bone healing
o When a bone breaks, blood flows from any vessel torn by the fracture. These vessels could be in
the periosteum, osteons, and/or medullary cavity. The blood begins to clot, and about six to eight
hours after the fracture, the clotting blood has formed a fracture hematoma. The disruption of blood
flow to the bone results in the death of bone cells around the fracture.
o Within about 48 hours after the fracture, chondrocytes from the endosteum have created an
internal callus (plural = calli) by secreting a fibrocartilaginous matrix between the two ends of the
broken bone, while the periosteal chondrocytes and osteoblasts create an external callus of hyaline
cartilage and bone, respectively, around the outside of the break. This stabilizes the fracture.
o Over the next several weeks, osteoclasts resorb the dead bone; osteogenic cells become active,
divide, and differentiate into osteoblasts. The cartilage in the calli is replaced by trabecular bone via
endochondral ossification.
o Eventually, the internal and external calli unite, compact bone replaces spongy bone at the outer
margins of the fracture, and healing is complete. A slight swelling may remain on the outer surface
 of the bone, but quite often, that region undergoes remodeling, and no external evidence of the
fracture remains.
 Different crumple zones of the face
o Orbital wall
o Orbital floor
o Maxillary and ethmoid sinuses
o Condylar neck of the mandible
 Forces of the mandible and where they work on
o Tension – superior border
o Compression – inferior border
o Torsion
HEAD AND NECK
 Course of the facial nerve
o Intracranial
o Meatal via fundus of the IAC until meatal foramen
o Labyrinthine
o Tympanic or horizontal
o Mastoid or vertical – gives rise to nerve to stapedius muscle, chorda tympani, nerve for auricular
branch of the vagus
o Extratemporal
 Types of BCCA
o Nodular basal cell carcinoma
o Cystic BCC
o Sclerodermiform (Morpheiform) BCC
o Infiltrated basal cell carcinoma
o Micronodular basal cell carcinoma
o Superficial basal cell carcinoma
o Pigment basal cell carcinoma
o Fibroepithelioma of Pinkus
 Facial prominences
o Frontonasal prominence (1)
o Maxillary (2)
o Mandibular (2)
 Topodiagnostic tests for facial nerve
o Schirmer's test
o Submandibular flow test
o Stapedial reflex test
 Ranula and plunging ranula
o Cystic lesion in anterolateral oor o mouth.
o Due to obstruction o sublingual gland.
o Plunging ranula: extends below mylohyoid muscle.
 Different salivary glands
o Saliva is a complex mixture of electrolytes and macromolecules secreted from three pairs of major
and numerous minor salivary glands.
o Major salivary glands consist of the parotid, submandibular, and sublingual glands
o Minor salivary glands line the mucosa of the lip, tongue, palate, and pharynx
 Different salivary fluids
 Which is more prone to salivary stone formation
o Submandibular gland
 Orientation – oriented superomedially draining lateral to the frenulum
 Law of gravity
 Composition
 What is ameloblastoma and pathogenesis
o The ameloblastoma is a neoplasm of the enamel organ that recapitulates the cells necessary for
tooth crown development.
o Intraosseous ameloblastomas arise from the lining of an odontogenic cyst, reduced enamel
epithelium, or odontogenic rests. In the soft tissues of the oral cavity, specifically the gingiva or
alveolar mucosa, they may arise from the basal cell layer.
o Those that arise from the overlying soft tissue are called peripheral ameloblastomas and are
covered separately.
o Three clinical types of ameloblastoma are unicystic ameloblastoma, peripheral ameloblastoma, and
ameloblastoma.
o Here the modifiers of multicystic or solid are not used. They are not separated here because they
are treated the same. Of these three, unicystic and peripheral have a much better clinical outcome
after a conservative removal and assured margins. For clarification, I use the term intraosseous
ameloblastoma to clarify that the lesion discussed is not peripheral.
 Different odontogenic tumors/cysts
RECON
 Cleft lift and palate embryology
o @ 4th wk = facial prominences form, formed by 1st pharyngeal arch from neural crest cells
 Maxillary prominence – forms lat to stomodeum, the primordial mouth
 Mandibular prominence – forms caudal (below) to stomodeum
 Frontonasal prominence – is a growth of mesenchyme that makes the upper border of the
stomodeum = forehead, orbital area
 On both sides of frontonasal prominences, there are forming 2 lateral thickenings of
surface ectoderm = nasal placodes
o @ 5th wk = nasal cavity and nasal projection begins to form (nose)
 nasal placodes fold inwards (“invaginate”) to form nasal pits
 around nasal pit, there is a ridge of tissue = nasal prominences.
 *Picture a bowl – the actual bowl is nasal pit, and the rim of the bowl is the nasal
prominences
 The nasal prominences are split into lat & medial nasal prominences
o @ 6th-7th wk = Maxillary prominences grow
 the future cheeks/zygomatic areas are growing, this pushes the medial nasal prominences
towards each other
 maxillary prominences & med. nasal prominences fuses
 This forms the upper lip
 lower lip & jaw = mandibular prominences
 Nose is formed by 5 areas:
 frontal part of frontonasal prominence = bridge of nose
 2 medial nasal prominences = crest of nose, tip
 2 lateral nasal prominences = sides, ala of nose
o The degree of clefting noted clinically is a consequence of the point in fetal development when the
fusion process is interrupted.
 Other ways to classify CLP
o Morphological Classification
 Davies and Ritchie (1922)
 Veau (1931)
o Embryological
 Kernahan & Stark (1958)
 Spina (1974)
 Muscles of the tongue
o intrinsic muscles of the tongue which do not have attachments outside the tongue and who's action
is to alter the shape of the tongue:
 superior longitudinal muscle of the tongue
 inferior longitudinal muscle of the tongue
 transverse muscle of the tongue
 vertical muscle of the tongue
o extrinsic muscles of the tongue (mnemonic) which have attachments outside the tongue and
therefore their actions alter the position of the tongue:
 genioglossus muscle: the majority of the tongue
 hyoglossus muscle
 styloglossus muscle
 palatoglossus muscle: supplied by the vagus nerve (CN X) via the pharyngeal plexus
 Bethesda class