 The peripheral system includes: external ear, middle ear (tympanic cavity+ tympanic membrane+

eustachian tube), inner ear

 The tympanic membrane has 3 layers: outer epidermal (reflects light), middle (connective fibers:
radial and circular), internal (mucosal). Anatomical elements: umbo, polizer triangle (?). The pars
tensa of the membranic tympane has 3 layers
 Tubo-tympanic effusion symptoms and signs: tympanic aspiration, mobile liquid bubbles in the
tympanic cavity and thickened secretions that determine the level of the liquid-glue ear
 Tubal-tympanic catarrh is characterized by: autofonie, low frequency hearing noises
 -The epithympanic recess is the higher floor of tympanic cavity, ; situated above the tympanic
membrane, contains ear ossicles with their ligaments, communicates with mastoid air cells.
-The mesothympanitis is the floor of tympanic membrane, contains oral and round window
-The hypothimpanum is located inferior to tympanic membrane. Presents tympanic cells
communicating witg mostoid cells system
 The footplate of the stapes connects with: perilymphatic space, tympanic cavity (?); the hammer
articulates with incus
 The functions of vestibular system are: fixation of an optical horizon (for space orientation in case
of rapid movements of the head) and maintining balance
 An otohaematoma is a sero-hematical collection of auricle (pinna), it’s an external ear trauma
 An external ear canal furuncle (boil) can cause: the swelling of the external ear canal, local pain,
slight hearing loss. It’s typically caused by S.Aureus. DD with other otitis. Treatment: antibiotics and
anti-infiammatory drugs: oxacillin.
 Fungal ear infection can cause: cotton-like appearance of the round mass in the external ear canal.
Otomycosis, caused by Apergillus nigger, pain, felling of fullness and foreign body in the ear.
Treatment with PIMAFUCIN, clorotrimazole.
 The patency of Eustachian tube is assessed through Politzer’s maneuver and Valsalva’s. Eustachian
Tube connects tympanic cavity and nasopharynx. The role is maintain equal pressure on both sides
of the tympanic membrane
 The facial nerve has 6 segments
 The ear wax is: brownish colour in the external auditory canal, hypersecretion ceruminous glands
of external ear
 Treatment pericondrities: local and general antiflmmatory drugs and general package with Rivanol
solution (if necessary:surgical intervention, incision and drainage)
 Othosclerosis: the osteopathy evolves in 3 stages: congestive (osteoclasts, capillary dilatations,
ostheopongiosis) when the bone becomes spongious through the increased bone absorption and
apprearance of osteoclasts, with reduction of osteoblats, otosclerosis (when compact bone is
formed, with decrease of osteoblasts). Symptoms: low frequencies are affected and paraacusia
Willis is present
 Bacterial acute otitis media is caused by eustachian tube dysinfunction, rhinopharyngeal
inflammations, sysyemic viral infections, external traumatism of TM with TM perforation. The
classification of an acute otitis media is done by nature of the Pathogens: pneumococcus,
staphylococcus, apprearance of perforation: before/after perforation and the way disease evolves.
Symptoms: fever, pain, autophonia, hearing loss, tinnitus with low frequencies; by othoscopy:
congestive stage (intense vascular drawing) and catharral stage (retracted TM, no light reflex
(polizer bright triangle), reduction of mobility of TM.
if there’s effusion we define it acute suppurated otitis media, regards all compartments of the
middle ear, there’s hyperplasia of the middle ear mucosa, it’s an evolution of a catharallis otitis
media, where secretion from serous and mucous becomes purulent. Deleted bright reflex,
congestion, hyperemia of tympanic membrane, transmission hearing loss, leukocytosis
 Symptoms: ear pain, pulsation in the ear with irradiation on the dental arch, fever 39-40.
We can distinguish between after evolution and after perforation. The treatment last 10-14 days.
Complications: meningitis with cerebral abscess and cavernous sinus thrombosis, labyrinthitis,
mastoiditis, becomes cronic
In children is frequent,bilateral, unobservedevery fever stages needs an otologycal exam!
 Myringitis: viral infection just in TM and not in the middle ear
 Acute suppurative otomastoiditis: middle earsuppurative process, trasmitted to the mastoid.
Symptoms: pain on mastoid palpation, intense congested and bulging TM, perforation of TM with
pus leaking, trasmission hearing loss, gelle fistula, veiling of mastoid air cell (?). 2 clinical forms:
supraacute (middle ear+ mastoid) and subacatute: headache, purulent otorrhea, minimal changes
of TM and major changes of the mastoid. In children (nasal infections, poor hygiene, prematurity,
Eustachian Tube conformation) 2 clinical forms: latent (hidden): appears as a toxicosis form
(dehydratation, digestive and nervous syndrome) and manifested. Symptoms: insomnia, fever,
agitation. Digestive disorders (endocranial complications). Treatment: drainage, antibiotics,
tympanotomy, antromastoidectomy.
 Otitis media: chronic inflammatory process of the middle ear and mastoid, polymicrobial
pathology. Etiology: Damage to the TM (perforation), mucosal lesions(cellular infiltration,
microcystic fomration, granulated polyps), bone lesions (vascular thrombosisbone necrosis)
Symptoms: chronic recurrent aural discharge with reduced hearing, otoscopy: central defect of TM
(scaring, polyps).
 Baro traumatism: symptoms: epytympanic congestion, diffuse congestion with TM retraction,
linear break of TM, hearinjg loss by unilateral compression or bilateral decompression. Causes:
Baro traumatism to aviators, blast (explsion or deflagration), supersonic bang (short action time),
acute acoustic trauma (loud noise over 2 hours-7 days), treatment vasodilation and vitamin,
electrical traumatism (electrocution, directly primary lesions of MT, late secondary lesions)
 Gardenigo syndrome: cefalea, paralysis VI, chronbic otitis media
 Otogenic meningitis is the complication of: acute or chronic otitis media, chronic otitis media
chronic cholesteatomatous otitis media
 The middle ear include: middle caviry, tympanic membrane
 What does the tympanometry show in a chronic serous otitis media: type B tympanogram
 Atticitis: inflammation of the tympanic cavity
 Cholesteatomatous otitis media: cronical otitis, when perforation is large, the epithelium goes to
the middle cavity: the cholesteatom is a pseudotumor that occupies the middle cavity.
Symptopms: otoragy, hearing loss trasmission, fetid suppurated otorrhea, blocked ear, otoree
insensitive to local and general treatment. The positive diagnosis of cholesteatoma is made by:
audiometry, CT mastoid
 Acustic trauma can cause: neurosensorial hearing loss with a notch at 4000 Hz
 Sudden onset hearing loss is: it has a sudden onset and the hearing loss is greater than 30 dB
(problem inner ear). Etiology vascular, infection, traumatic, tumors, neuro, etc. Symptoms: tinnitus,
headache, nausea, vomit, ear fullness, phonophobia, sensorz’ neuralz hypoxia
 Respiratory sleep disorders can be classified as: central or mixed apnea syndrome, obstructive
sleep apnoea syndrome, sleep hypoventilation syndrome (oxygen desaturation or increased
PaCO2>10 mmHg). Snoringyearsapnoea. Appear: patient with tonsillar hyperthrophy,
voluminous tongue, long and wide uvula; overweight patients, men with poor sleep hygiene
Diagnosis OSAS: respiratory events> 15/hour; sleep disturbance symptoms >5/h.
Polyspleepography=gold standard, evaluation of anatomical factors: changes in the nasal and
oropharynx, (lingual cystis, macroglossia), involved laryngeal disorders (vocal cord paralysis, edema,
atresia, compression), nasal and sinus disease (septum deviation, rhinitis, polyposis), facial and
 cervical changes (micrognathia, retrognathia).
Treatment: uvulopalatopharyngoplastica, laser, radiofrequency
 Muller’s manoeuvre: forced inhalation with the mouth closed and the nose held in between the
fingers, free exhalation
 The nasal cavity consists of nasal septum, nasal turbinates, nasal meatal, posterior nasal apertures
(choanae)
 Ethmoidal cells are a labyrinth made up of air cells, cavities found between the middle nasal
turbinate (horn), orbit (Lateraly delimitation: lamina orbitalis), sphenoidal sinus. The posterior
ethmoid cells: relation with optic nerve. The anterior with riddled ethmoid blade.
 The anterior wall of sphenoid sinus has: 3 segments: ethmoidal, nasal, septal.
Tge sphenoidal sinuses are pneumatic cubical cavities, inthe sphenoid bone body. They have 5
walls: anterior (nasal), posterior (skull base), upperwall (skull base, 3 zones: optical, pituitary and
olphactory), inferior, external (cavernous sinus, arteries lie carotid, nerves III, IV, VI)
 The blood supply of the nasal cavity is provided by: anterior and posterior ethmoidal artery (from
ophtalmic artery, indirectly internal carotid artery), sphenopalatine artery (from maxillary artery).
The nose vascularity is made by facial artery (from external carotid) and oftalmic artery (from
internalncarotid artery)
 The ethmoidal bulla is located in the middle nasal meatus (ethmoid?)
 Ostiomeatal complex: uncinate process, semilunar hiatu, frontal recess, ethmoidal bulla, etmoidal
infundibulum, maxillary sinus opening ostium
 The function of the nose: breathing, phonation, olfaction, warming up the air that we inhale,
humidification of the air that we inhale
 Defense function of nasal mucosa are: non specific defensive mechanism, specific mechanism,
humoral reaction
 The nasal pyrmaid consists of: 2 nasal rectangular bone, triangular and lateral cartilages (alar)
 Bilateral nasal obstruction is specific for: nasal polyposis, allergic rhinosinusitis
 Nasal trauma can be classified in: closed traumatic lesion, open traumatic lesion, nasal fractures
 Syntomatology of nasal fractures: sudden and localized pain, epistaxis,, nasal obstruction, paleness
of the face. Nasal fractures are classified: without/with displacement, nasal bones, nasalm septum.
Treatment: fixation and fracture reduction, stop nosebleeds, late intervention 3-4 days, medication
 Positive diagnosis of cerebro-spinal rhinorrhea is: spontaneous CSF leak through the nose, CSF
leak after jugular vein compression,CT
 Fronto-basal fractures can be classified as: Type I, II, III, IV
 Symptoms of nasal contusion: spontaneous pain, epistaxis, faintness (dizziness),. Treatment:
antinflammatory and local cold compress. It’s closed traumatic injury.
 Clinical signs of a nasal furuncle: erithematous inflammation of the region, inflammation of the
upper lip, fever, pain= is the only local sign of furuncule/folliculitis
 Nasal erysipelas is an infection caused by Group A beta haemolytic streptococc. Treatment:
Penicillin C endovenous
 Clinical symptoms of acute rhinitis: irritated bose, sneezing nose, nasal obstruction
 Respiratory epithelium is: ciliated cylindrical epithelium. Other epitelium of nasal cavities:
multilayered (un/)keratinized squamous epithelium, unciliated cylindrical epithelium.
 Major symptoms in ACUTE RHINOSINUSITIS are: anterior or posterior rhinorrhea, nasal
obstruction, fever. COMPLICATIONS: pharyngitis, otic, tracheo-bronchite, tonsillitis, (sinusitis?)
 Treatment of rhinitis chronic allergic: intranasal cortisone (+ surgical drainage+ oral
corticotherapy)
 Rhinosinusitis is classified in: acute, recurrent acute, subacute, chronic
 Bent and Kuhn criteria for allergo-fungal rhinosinusitis: nasal polyposis+ allergic mucine presence+
chronic sinusitis at CT scan+ positive fungicrops+ anamnesis of hyper-sensivity+ skin tests and
positive serology
 Acute rhinopharyngitis of the child treatment: antipyretic drugs, nasal decongestants, vitamins
 Acute odonthogenic rhinosinusitis is: unilateral with fetid rhinorrea (pain in dental arcade, imaging
tooth damage ?)
 Nasal polyposis we have groups: 4: allergic, inflammatory, distorting and recurrent in child, killian
solitary
 Sinus secretion collection: under endoscopic control+ middle meatus+ superior or sphenoethmoid
recess
 Rinomanometria anteriore: valutazione flusso aereo+ valutazione resistenze nasali
 Treatment of acute sinusitis: drenage, aerating by endoscopy/open surgery. Adult:
vasoconstrictive+ topical corticotherapy+ antibiotics. Child: expectorans+ nasal desobstructors+
antinlammatory drugs+ intravenous antibiotics
 Symptoms of acute sphenoidal rhinosinusitis are: posterior rhinorrhoea, retro ocular pain
 Complication of acute adenoiditis of the newborn: laringo-traheo-bronchitis, acute suppurative
otitis, bronchopneumonia (NO WEIGHT LOSS). In adult: pharyngitis, sinusitis, tracheitis, tonsillitis
 Otoscopy adenoiditis: transmission hearing loss+ retraction of tympanic membrane+ decrease of
light reflex
 Nasal basal cell carcinoma is: ulcerated+ pearl tumor+ isolated+ vegetant
 Widal triade: nasal polyposis, asthma, aspirine intollerance
 Simple acute adenoiditis of the child is characterised by: pharynx hyperaemia, sudden onset
 Topographic anatomical regions of larynx: supraglottic, subglottic, glottis
 Functions of larynx: protection, respiratory, phonation
 Acute laryngitis: multifactorial acute inflammation of the laryngeal mucosa of polymorphic
etiology.evolution 10 days, hoarseness, sore throat, pain to speek, dysphagia, cough, dyspnea,
aphonia, fever Classification by etiology and age (?)
-Etiology of acute catarrhal laryngitis: appears due to vocal abuse, some sort of trauma, certain
climatic conditions.Sudden onset, dysphonia, dryness of the throat. Positive diagnosis by: flexible
laryngoscopy or rigid 90 degree endoscopic examination. Evolution 10-14 days. Complications:
edema, pericondritis, phlegmon or abscess. Treatment: cortizonic antiinfiammatory
(anticough,antistaminic, wet inhalation, rest)
-Acute edematous laryngitis: can cause inspiratory dyspnea, irritative cough, anxiety, dysphagia,
fever. Primary or secondary after allergies, rhinosinusitis
-Subglottic odematous laryngitis: small children, inhaler dyspnea, wheezing, edema
-Supraglottic laryngitis= Epiglottitis is: a supraglottic laryngitis, acute inflammation of epiglottis.
Dyspnoe, dysphonia, fever, fast onset. H.Influenzae.
-Acute laringo-traheo-bronchitis: children <5 y, slow onset and evolution, viral, strepto,staphilo,
pneumococcus. Fibrinous or membranous; Spasmodic croup: sudden onset, wheezing, stridour,
dry cough, dyspnoea, no infection, children 3-4 y
 Chronic laryngitis can be classified as:
-red chronic laryngitis: Catharal, Red Laryngeal Pachidermitis, Pseudomixomatous chronic laryngitis,
chronic hypertrophic laryngitis;
-white: keratosis, acanthosis or white pachidermia, corneous papyloma, leucoplasia
-chronic laryngitis in the gastro-esophagian reflux= GER. Gastric secretion without vomitis and
regurgitation (nexium, zantac); specific chronic laryngitis (tubercolosis, fungal); precancerous
stages: dysplasia (simple hyperplasia or several dysplasia in situ carcinoma)
Treatment: vocal therapy, reducing irritative agents, smoking cessation, vit A oil
 LARYNGEAL TUMOR
-BENIGN: POLYPS, NODE ,GRANULOMA, CONTACT ULCUS ; LARYNGEAL PAYLOMA ;CYSTS,
PSEUDCYSTS TUMORS ; RARELY TUMORS, LIPOMA, CONDROMA, HEMANGIOMA, ADENOMA
-MALIGN: MALIGN EPITHELLIUM TUMORS, NEURO ENDOCRINE TUMORS, SOFT TISSUE TUMORS
BONES AND CARTILAGENOUS TUMORS
 Adult laryngeal papillomatosis is: benign disease with malignant potential, benign disease
considered precancerous
 The following don’t characterize acute edematous subloggtic laryngitis: constant fever,
pharyngeal pain
 Leukoplakia: a benign laryngeal tumor with the potential to turn malignant (precancerous) whitish
 Vocal cord polyps: benign laryngeal tumor, possible cause of dysphonia
 Laryngeal papillomatosis: benign disease with the potential to turn malignant
 Reinke’s edema is: a diffuse, chronic inflammation of the vocal cords caused by the accumulation
of a gelatinouse substance in Reinke’s space, a benign vocal cord tumor, a possible cause of
dysphonia and dyspnoea
 The initial symptoms of esophageal foreign body: sialorrhea, severe pain, dysphagia for solid food,
dysphagia for liquids, sensation of foreign body, pressur in thorax (epigastric region), aphonia.
Investigation: (Barium swallow) radiology, esophagnoscopic, anamnesis and clinical exam.
Treatment: extraction of the foreign body with esophagoscopy, extraction in a natural way
 Symptoms in secondary phase of airway foreign bodies are: chest pain, stridor, later symptoms:
primary and secondary esophageal perforations
 Early complications of foreign bodies in the airways are: pulmonary abscess, simple bronchitis
 Angina can cause: foul breath, pain upon swallowing, dysphonia (?), fever.
Treatment: antibiotics, antypiretic, pain killers, liquid diet (?)
 Acute unspecific angina is characterized by: salivation, dyspnea, trismus (NOT halena!). Pain in
acute angina causes trismus
 Severe form of acute tonsillitis is characterized by: enlarged tonsils, saburral tongue
 Acute suppurative tonsillitis can cause: fever, whitish deposits on the palatine tonsils,
odynophagia, uvula edema
 The forms of chronic tonsillitis are: hypertrophy,atrophic, crypts, retntion cyst, lithiasis, chronic
with acute phase
 Complication of chronic tonsillitis: Peritonsillar phlegmon + upper airway infection + lymphatic
tissue infection + gastrointestinal disorders +ulcerous tonsillitis
 Non specific lab exams for infections: ERS+ ASLO+ PCR+ fibrinogen
 Peritonsillar phlegmon examination: Anterior papillar tumefaction + soft palate bulge + pushed
toward the healthy part
 About precancerous lesions the following are true: in chronic laryngitis there’re modifications to
the vocal cord epithelium that precede cancer, the morphologic changes to the laryngeal mucosa
are determined by local irritans
 Treatment of acute suppurative tonsillitis: metronidazole, penicillin
 Clinical symptoms of gastro-esophageal reflux disease: pirosis, dysphagia