Pemicu 4

Eko Siswanto
405150087
LI 1 : MM fisiologi pendengaran
dan keseimbangan
• 2 aspek pendengaran : identifikasi suara &
lokalisasi
• Gelombang suara  getaran udara yg
merambat

Nada (telinga manusia 20-20.000 Hz)

Suara Intensitas / kekuatan
Warna suara / kualitas

• Gel. Suara  auricula  meatus acusticus

externus  membran timpani bergetar 
osikulus memindahkan getaran ke cairan
telinga dalam, melalui jendela oval
• Permukaan membran timpani > jendela
oval
• Peran sel rambut dalam :
Mengubah gaya mekanis
suara menjadi impuls listrik
pendengaran

• Peran sel rambut luar :

elektromotilitas
LI 2 : MM gangguan dan infeksi
telinga dalam
Bacterial labyrinthitis
• May develop through a dissemination of
infection from the middle ear space
• Can be associated with otitis media or as
a result of bacterial spread through a
bony fistula in px with cholesteatoma
and chronic otitis media
• May also develop as a result of the sread inflammation and tissue destruction
of bacteria from the subarachnoid space (necrosis) with a fibro-osseous reaction
into the perilymphatic fluid of the
labyrinth
• Either the foraminae chribrosa of
the fundus
• The vestibular sensory regions
• The cochlear aqueduct
Opens into the basal region of the scala
tympani (inside the round window membrane)
• Clinical Picture:
• Acute or subacute onset of hearing
loss
• Vertigo with malaise
• Fever in association with an URTI
• Frequntly: signs of acute otitis
media or suppurative otitis media
• Bacterial invasion into the labyrinth
though the oval and round windowds 
 auditory and vestibular functional loss
• Neuronal loss due to retrograde
degeneration
• Px with meningitis, esp. children 
should always be evaluated otologically
• Bacterial labyrinthitis classified into
three stages:
• Serous or toxic labyrinthitis
• Suppurative otogenic labyrinthitis
• Suppurative meningogenic
labyrinthitis
Serous labyrinthitis
• Irritation of the labyrinth caused by
invasion of bacterial toxins either
from
• Acute or chronic otitis media
• Perilymphatic fistula or
meningitis
• Leading to: veritgo and
sensorineural hearing loss
• Less severe form: inner ear function
is generally restored
• Severe cases  partial or complete
loss of hearing or vestibular function
• Loss of hair cells
• Cochlea > vestibular system
• May occur during the course of
acute or chronic otitis media
• Through toxins reaching the
inner ear via the round or oval
windows
• May also result from meningitis
• Perilymph shows a stainable
precipitate
Acute suppurative otogenic labyrinthitis
• Caused by bacterial invasion into the inner ear 
vertigo and hearing loss
• Bacteria invasion  accumulation of PMN  local
precipitate formed in the perilymph and eventually
in the endolymph  endolymphatic hydrops
• Followed by necrosis of the membranous
labyrinth often with spread to the meninges
 life threatening condition
• May be followed by healing, fibrosis and new bone
formation (labyrinthitis ossificans)
• Usually leads to profound loss of auditory and
vestibular function
• Chronic form: complication of chronic
tympanomastoiditis  slowly progressive osteolytic
destruction of the bony labyrinth with invasion of
granulation tissue  degeneration of the auditoy
and vestibular sensory organs
• If not arrested  intracranial complications
• Common microorganisms: Β-Haemolytic
Streptococci, Pneumococci, Staphylococci,
Haemophilus influenza, Proteus vulgaris,
Pseudomonas aeruginosa
Suppurative meningogenic labyrinthitis
• Spread of bacteria from the subarachnoid space  labyrinth
• Usually via the cochlear aqueduct, internal auditory canal
Viral labyrinthitis
• Believed to be the most common cause • Sometimes through viraemia or direct
of delayed endolymphatic hydrops/ spread via the subarachnoid space
Menière’s disease infection
• Clinical picture: • Histological findings : Different
• URTI + acute disturbance of auditory degeneration of the organ corti
and vestibular function with: vertigo • Early encapsulation of the tectorial
and nystagmus (for 3-5 days) membrane
• Varying degrees of permanent • Degeneration of the stria vascularis
hearing loss • Round cell infiltration of the
• Recovery from vestibular symptoms: modiolus and contents of the
gradual and depends on activation internal auditory canal
of vestibular compensatory • All cases: degenerated saccule with
mechanism sloughing of the otolithic membrane
• May involve either the peripheral end • Vestibular labyrinths involved to
organs of the peripheral nerve trunk varying degrees
• Affecting one or both ears
Otosclerosis
• Merupakan kelainan herediter yg
bersifat lokal yg mmpengaruhi tulang
endochondral ( yg ditandai dengan
adany gg resorpsi & deposisi tulang)
• Lesi otoscleroticterdiri dari area
resorpsi tulang,p’tukan tulang
baru,proliferasi vaskular & stroma jar
ikat
• Otosklerosis berkatian dgn lesi yg
melibatkan tulang stapes &
manifestasinya berupa : tuli konduktif
• HISTOPA OF OTOSCLEROSIS
• Lesi terdiri dari resorpsi area
tulang,p’tukan tulang yg
baru,proliferasi vaskular,stroma
jaringan ikat
• Tanda per1 otosclerosis adalah blue
mantle ( mrupakann area dari otic
capsule yg berwarna lbh basofilik
dari normal)
• Terdapat resorpsi tulang
endochondral dengan p’mbesaran
ruang perivascular diikuti deposisi
dari tulang yg imatur
• Resopsi tulang dimediasi oleh
osteoklas & p’tukan tlg baru oleh
osteoblas
• Proliferasi dari p darah pd active
otosclerosis
• Focus otosklerotik jg trdpt stroma
jar ikat ( tersusun atas fibroblast &
histiosit)
• Tdk ada sel2 inflammasi
• Fokus otosklerotik mnunjukkan area
yg aktif ditandai dgn pe+ selular &
vaskularisasi bersama dgn resorpsi
tulang & p’tulang baru
• Fokus otosklerotik daerah yg
inaktifdense mineralized bone
Otosclerosis
• Distribusi lesi otosclerosis:
• Area anterior oval window (80-95%)
• Round window ( 30%)
• Stapes footplate (12%)
• Posterior oval window ( 5-10%)
• Pathology of Conductive hearing
Impairment
• Keterlibatan stapes gg
pendengaran konduktif mulai dari 5-
60 dB
• Penyebaran fokus otosklerotik dari • Pathology of sensorineural hearing
fokus anterior ke oval window
diduga krn adanya “fiksasi fibrosa”
dari footplate stapes
• Adanya progresi dari
otosklerosismnyebabkan fiksasi
tulang dari footplate anterior yg
mnyebabkan gg p’dengaran
konduktif
• Mukosa telinga tengah krn fokus
otosklerotikproliferasi
fibrovaskular (adanya
hipertrofi,deposisi dari jar ikat &
pningkatan vaskularisasi)
• Disebabkan krn adanya respon
sitokin,faktor angiogenik,dan
mediator kimia lainnya
• Pningkatan vaskularisasi
mukosa pd fokus sklerotik dkat
dgn oval window tmpak ada
bercak kemerahan dpt dilihat
dgn otoskop ( Schwarze Sign)
impairment
• dapat terjdi jika fokus otosklerotik
mncapai endosteum koklea
• Jika fokus tsb sdh mncapai
endosteum sering terjdai atrofi
dari ligamentum spiral ,perusakan
fibrosit & digantikan dgn suatu
substansi eosinofilik disebut
“hyalinisasi” ligamentum spiral
Otosclerosis
• Ligamentum spiral pnting untuk fungsi • Pathology of Vestibular symptoms
dari koklea
• Fibrosit dri ligamentum
merupakan sel yg menempel 1
sama lain ( gap junction system)
trdpt connexin (yg mmbentuk
channel untuk aliran ion &
metabolit antar sel )
• Fibrosit jg mengandung
enzim,protein,dan sitokin
mmpengaruhi homeostasis di
koklea
• Remodeling tulang dipengaruhi
oleh sitokin2 inflammasi dimana
sitokin yg dilepaskan oleh tlg yg
mengalami remodelin pd fokus
otosklerosis dpt berdifusi ke
ligamentum spiral mngganggu
homesotasis cairan & ion di koklea
gg pendengaran sensorineural
• Tidak seimbang,dizziness
/serangan berulang vertigo
• Etiologi :
• Predisposisi genetik : gen tersebut
berkaitan dgn regulasi
kolagen,kartilago & homeostasis
tulang & supresi pertumbuhan
• Expresi dari COL1A1 ,gen
kolagen tipe 1 berhub kuat
dgn osteogenesis imperfekta
& osteoporosis
• Measles virus : pd fokus
otosklerosis ditemukan partikel
virus,antigen & RNA (active
osteosclerosis foci) ( titer IgG
spesifik measles mengalami
elevasi dan ditemukan di perilim
pd ps dgn otosklerosis)
Otosclerosis
• Tanda & Gejala :
• Gg pendengaran konduktif progresif
• lbh mudah berbicara /memahami
p’mbicaraan pd lingkungan yg berisik
• Treatment :
• Tinnitus , Gg vestibular
• Gg pendengaran sensorineural
• PF :
• Kanal auditori eksterna & membran
timpani tampak normal
• Schwartze sign : warna kemerahan
pada promontorium krn ↑
vaskularisasi tulang
• PP :
• Air bone gap : melebar pda frekuensi
rendah
• Carhart notch : mrupakan karakteristik
dari otosklerosis & gg pendengaran
sensorineural skitar 2 kHz
• Tes rinne : konduksi tulang lbh baik
dari konduksi udara & tes weber
mnunjukkan ada lateralisasi pd sisi yg
sakit
• Timpanogram : depressed/normal
• HRCT & MRI
• fluoride therapy for clinical
otosclerosis has been stimulated by
reports of a lower incidence of
otosclerosis in areas that have high
natural water levels of fluoride
• Conventional hearing aids
• Bone-anchored hearing aids (BAHA)
• Surgery
• Complications :
• Postoperative conductive hearing
impairment, Sensorineural hearing
damage, Facial nerve injury,
Perilymphatic fistula, Vertigo,
Reparative granuloma, Discomfort to
loud noise, Alteration in taste,
Cholesteatoma, Meningitis
LI 3 : MM gangguan pendegaran
Tuli Kongenital
• Kebanyakan anak yg mnderita gg
pendengaran permanent :
sensorineural hearing loss
• Pnyebab gg pendengaran konduktif:
COM & bbrp kondisi kongenital yg
jarang ( bilateral aural atresia)
• Faktor risiko :
• Kondisi yang menyebabkan
perawatan di NICU atau SCBU
lebih dari 48 jam
• Sindrom yang di dalamnya
termasuk tuli
• Riwayat keluarga menderita tuli
sejak kecil
• Anomali kranio-fasial (co: cleft
palate)
• Infeksi in utero
Tuli Kongenital
Maternal Infections
• Congenital CMV : mrupakan pnyebab
tersering ( non herediter sensorineural
hearing loss) ,hearing loss dapat :
delayed & atau progresif
• Congenital rubella syndrome:
nongenetic congenitally acquired
hearing loss
• Terjadi jika adanya infeksi maternal
o/ virus rubella 1st trimester
deafness ,ocular defect (
catarct),KV anomalies ( patent
ductus arteriosus, pulmonary artery
stenosis),CNS ,prubahan kulit
• Syphilis : bakteri Treponema pallidum(
infeksi tersering)(transmisi tersering
melalui kontak seksual ,tetapi sifilis dpt
ditransmisikan dari ibu yg terinfeksi ke
anak ( congenital sifilis)(can oocur any
stage of the pregnancy & if occurs in 1st
/2nd trimester untreated
Acquired Causes
• Meningitis mrupakan
permanent childhood
impairment yg paling sering
,resiko terjdinya gg pendengaran
sensorineural stlh meningitis
bakterial 10%
• Rehabilitation can be
initiated ( after meningitis)
• If cochlear implantation
necessary should be done
with minimal delay ( as
ossification of cochelar duct
can make implantation
difficult )
• Measles
Tuli Kongenital
• Skrining
• Tes elektropsikologik (0-6 bulan): OAE, AABR, CERA
• Behaviouraal Observation Audiometry (BOA) (0-6 bulan)
• Visual Reinforcement Audiometry (6-36 bulan)
• Performance Testing (2-5 tahun)
• Pure Tone Audiometry (3++)
• Auditory Speech Discrimination Tests
• The co-operative test (18-30 bulan)
• Toy discrimination tests (30 bulan ++)
• Consonant discrimination tests (6++)
• Tatalaksana
• Behind the ear (BTE) air conduction hearing aids with a soft mould
• Bone anchored hearing aid
• Cochlear implantation
• Inclusive education and least restrictive environment
Noise-Induced Hearing Loss (Trauma Akustik)
• The term noise-induced hearing loss refers to
reduction in auditory acuity associated with
noise exposure
• Predisposing factors : interaction between
noise-induced hearing loss and age-related
hearing loss, smoking, diabetes & CVD
• Pathology :
• Metabolic mechanisms :
• Acoustic overstimulation 
excessive release of
neurotransmitters (glutamate)
associated with the transduction
function of the cochlea  noise
induced hearing loss (glutamate
receptor antagonists may reduce
TTS)
• stimulation with sound of
moderate intensity  ↑ cochlear
blood flow, & with sound of high
intensity ↓ cochlear blood flow
(this being a potential mechanism
for cochlear dysfunction associated
with noise exposure)
• outer hair cell (OHC) plasma
membrane fluidity, the role of
glucocorticoid receptors &
oxidative stress
• Structural mechanisms :
• Changes to the micromechanical
structures within the cochlea 
depolymerization of actin filaments
in stereocilia may be a substrate of
TTS
• changes to nonsensory elements of
the cochlea, such as swelling of the
stria vascularis, afferent nerve
endings & of supporting cells
• Apoptosis & necrosis
• Apoptotic changes in chinchilla
OHC (specifically nuclear
condensation and cell body
shrinkage) have been detected five
minutes after exposure to impulse
noise, whereas necrotic change
(nuclear swelling) appeared 30
minutes following exposure
Noise-Induced Hearing Loss (Trauma Akustik)
• Examination : • Prevention :
• otological examination will be • further noise exposure should be
normal kept away from as far as possible
• tone audiogram, with both air and • avoiding the excessive noise
bone conduction to identify any altogether or, if this is not
conductive hearing loss possible, by the use of ear
• Tympanometry is helpful to protection in the form of earplugs
confirm normal middle ear or earmuffs
functioning
• Cortically evoked reflex
audiometry may be required to
provide a more objective measure
of hearing thresholds
• MRI may be required to exclude a
vestibular schwannoma
• Loudness discomfort levels are a
useful measure of the presence of
hyperacusis
• Management : binaural hearing aids,
tinnitus retraining therapy (tinnitus)
Age-related Sensorineural Hearing Impairment
• Age-related hearing loss may be defined as • otological examination will be normal
mid- to late adult onset, bilateral, • tone audiogram
progressive sensorineural hearing loss,
where underlying causes have been
excluded
• Age-related hearing loss excludes hearing
loss caused by primary factors including
loud noise exposure, underlying medical
conditions (e.g. atherosclerosis, diabetes,
hypertension, Paget’s disease of bone,
myxoedema), intrinsic otological disease
(e.g. otosclerosis, chronic otitis media &
Menie`re’s disease), head injury & ototoxic
drug therapies
• Symptoms : difficulty in hearing
conversation, patients may complain of a
more obvious hearing problem &
frequently having to ask others to repeat
themselves, tinnitus
• Examination :
• patient will be older, at least in their
fifties
Age-related Sensorineural Hearing Impairment
• Management :
• Non-specific management :
• advice regarding the optimization of their acoustic
environment  the reduction of background noise (as far as
possible), face-to-face conversation to maximize exposure to
nonverbal communication cues & an explanation of the
problem to allow the legitimization of their hearing loss
• Practical measures for individuals with a more severe hearing
loss  infrared headphones for use with their television,
volume controllable telephones, louder doorbells, often with
an alternative alerting system such as a flashing light or
vibrating pager system
• Hearing dogs can take on such a role as well as providing a
valuable source of companionship in the elderly
• Lip-reading classes can be extremely valuable.
• Specific management :
• Hearing aids  additional, 10 dB sensory advantage
LI 4 : MM gangguan keseimbangan
Motion Sickness
• Merupakan sindrom yg terjadi pada buruk, ps sbaiknya duduk ditmpt yg
seseorang jika orang tersebut mengalami gerakan rotasi & vertikal nya kurang)
gerakan2 tertentu, biasanya saat sedang • Synchronize the visual system with
berpergian , dengan gangguan berupa the motion : small study that
mual focusing on the true horizone
• Etiologi minimize symptoms of motion
• konflik antara sistem vestibular, sickness
visual & proprioseptif • Actively synchronize the body with
the motion
• Gejala Klinis
• Frequent consumption of light ,soft
• 1st recognized symptom: nausea ,low fat & low acid food minimize
• Sensasi penuh pada epigastrium symtpom of motion sickness
• Malaise
• Drowsiness
• Iritabilitas
• Behavioral Intervention : prevention of
motion sickness
• Minimize vestibular motion
(sebaiknya psien disarankan untuk
mnghindari berpergian jika cuaca yg
Vertigo
• Vertigo : ilusi baik diri sendiri atau
lingkungan yg berputar
• Melibatkan angular motion
sensing system (semicircular
canals & their central projections)
 dpt terjadi dari labirin sampai
ke korteks vestibular  u/
mengetahui letak lesi
membutuhkan gejala tambahan
• Hearing loss & tinitus 
keterlibatan labirin / N.VIII &
gejala batang otak gejala seperti
frank diplopia, mati
rasa/kelemahan pd wajah dan
disartria
• Vertigo akut:
• BPPV  < 1menit
• migraine-associated vertigo 
menit ke jam
• penyakit Meniere  beberapa
jam
• neuritis vestibular akut dan
stroke batang otak 
beberapa hari
• Vertigo presentations :
• Single vertigo episode
• Recurrent (or episodic) vertigo
• Chronic dizziness
BPPV (Benign Paroxysmal Positional Vertigo)
• Disorder characterized by brief attacks • May accompanied by nausea &
of vertigo, with associated nystagmus, vomiting
precipitated by certain changes in head • nystagmus following a Dix–
position with respect to gravity Hallpike manoeuvre
• Etiology : • nystagmus typically less than 30
• inappropriate stimulation of SCC seconds
hair cells, in response to changes • DD/
in head position by sequestered • Migrainous vertigo
otoconia
• posterior fossa tumour
• may occur as a complication of
head trauma or vestibular neuritis • Management
• Epidemiology • Epley manoeuvre
• Women > men • surgical occlusion of the posterior
SCC can be highly effective in
• Most common in elderly relieving symptoms
• Clinical Manifestation
• brief recurrent episodes of vertigo
 following changes in head
position with respect to gravity
• Vertigo  lasts 10–20 seconds
Meniere’s Disease
• Disorder characterized by spontaneous • Phase of the attacks
attacks of vertigo, associated fluctuating • Irrritative phase
sensorinerual hearing loss, tinnitus, &
aural fullness
• Pathophysiology : Overproduction
/malabsorption of endolymph 
endolymphatic hypertension  gross
enlargement of the membranous
labyrinth (hydrops)  periodic rupture
of membranous labyrinth  leakage
potassium-rich endolymph into
perilymph  meniere attacks
• Clinical manifestations
• Reccurrent attacks of spontaneous
vertigo, nause, vomitng
• Lateralized low-frequency hearing
loss, tinnitus, aural fullness
• Later stage of the disease  drop
attacks (Patient simply drop to the
ground without warning  fracture
& serious injury)
• Horizontal/horizontal-torsional
nystagmus, beats towards the
affected ear (last < 1 hour)
• Paretic phase
• Nystagmus beats away from the
affected ear (several hours – 1
or 2 days)
•  peripheral hypofunction 
spontaneous neural activity in
the right vestibular nucleus is <
 nystagmus beats toward the
left ear
• Recovery phase
• Nystagmus beats towards the
affected ear again (last like the
2nd phase)
Meniere’s Disease
• Etiologi : • Hearing <<  hearing aids by
• idiopathic cochlear implantation
• endolymphatic hydrops • Systemic aminoglycosides
(streptomycin & gentamycin)
• DD/ :
• vestibular neuritis • Complications
• migrainous vertigo • Continue to have vertigo
attacks
• Management
• < production of endolymph
• Strict sodium restriction
(urinary sodium
<50mmol/day)
• Diuretics
• Surgery
• Endolymphatic sac surgery
• Vestibular neurectomy
• Labyrinthectomy
Vestibular Neuritis
• Sudden, spontaneous, isolated, total or • Acute phase : spontaneous horizontal-
subtotal loss of afferent vestibular input from torsional nystagmus
one labyrinth
• Diagnosis
• Etiology : viral infection of the vestibular • Fukuda or Unterberger test
nerve
• subjective visual horizontal (SVH) test
• Clinical Manifestation : • Electronystagmography adds little to
• acute spontaneous vertigo with clinical observation with Frenzel lenses
associated nausea, vomiting and
• DD/ :
postural imbalance.  aggravated by
head movement • Cerebellar infarction
• unsteady and may veer towards the side • Management
of the affected labyrinth • corticosteroid & antiviral treatments
LI 5 : MM keganasan pada THT
Nasopharyngeal Carcinoma
• The result of a complex interplay of genetic
factors, early latent infection by EBV & its
reactivation and exposure to
environmental carcinogen
• In endemic areas, the rate can be as much
as 50 times higher than that in other
countries • Clinical features :
• The highest age-standardized incidence
rate occurs in southern China amongst the
Cantonese population of the Guangdong
Province
• Other Southeast Asian races, including
Malays, Indonesians, Thais, Vietnamese
and Filipinos, as well as Eskimos (in
Canada, Alaska and Greenland) are also
noted for a high prevalence of NPC
• Three times as common in men as women
• Below the age of 50, the incidence of NPC
is higher than any other cancer
• Pathogenesis :
• The EBV genome & latent gene
products are consistently found in
both differentiated & undifferentiated
types of NPC
• The EBV DNA has the characteristic of
being homogenous & is likely to be
due to clonal cellular proliferation
• An early tumour may cause no
symptoms
• Presence of an upper neck swelling
• Cervical lymphadenopathy
• Nasal symptoms : bloodstained nasal
discharge, nasal obstruction, post-
nasal drip, frank epistaxis
• Headache or cranial nerve symptoms
• Trismus
• Ophthalmoplegia, accompanied by
proptosis
Nasopharyngeal Carcinoma
• Treatment :
• Megavoltage external radiotherapy
(ERT)
• Chemotherapy
• Salvage treatment
• Surgery
• Prognosis :
• Poor prognostic factors including old • Complications :
age, male gender, cranial nerve
palsy, level and fixity of lymph nodes
• The average five-year survival
achieved by conventional
radiotherapy alone is excellent for
early disease  approximately 80–
90 % for stage I & 70–80 % for stage
II
• The average five-year survival
achieved by conventional
radiotherapy alone for locally
advanced nondisseminated disease
is approximately 40–60 % for stage
III, & 20–40 % for stage IVA-B
• For disseminated disease (stage
IVC), the median survival is only 6
months
• For all patients with
nondisseminated disease, the
overall control rate of 60 % at five
years can be expected
• major and minor salivary glands are
well within the field of irradiation
• Xerostomia occurs in all patients and
usually develops following the first
few doses of irradiation
• Symptoms of oropharyngeal
mucositis
• altered taste sensation
• dermatitis
• alopecia of the irradiated area
Juvenile Angiofibroma
• Juvenile angiofibroma is an uncommon,
benign & extremely vascular tumour that
arises in the tissues within the
sphenopalatine foramen
• It develops almost exclusively in adolescent
males, though there are reports of this
tumour being found in children, the
elderly, young & even pregnant women
• The tumour extends into the nasopharynx,
paranasal sinuses, pterygopalatine &
infratemporal fossa. Larger tumours can
involve the orbit and cavernous sinus
• Pathogenesis :
• Present as well-defined, lobulated
tumours that are covered by
nasopharyngeal mucosa
• The tumour consists of proliferating,
irregular vascular channels within a
fibrous stroma
• Tumour blood vessels : lack smooth
muscle and elastic fibres 
contributing to its reputation for
sustained bleeding
• The stromal compartment is made up
of plump cells that can be spindle or
stellate in shape and give rise to
varying amounts of collagen 
tumours very hard or firm, while
others may be relatively soft
• Almost exclusively found in adolescent
boys  sex-hormone receptors 
androgen receptors are present in at
least 75% of tumours, receptors being
present in both the vascular & stromal
elements
• VEGF localized on both endothelial &
stromal cells  tumour development
• Overexpression of IGFII
• Germline mutations in the APC gene
on chromosome 5q This gene
regulates the beta-catenin pathway
which influences cell to cell adhesion
 Mutations of beta-catenin 
development of these neoplasms
Juvenile Angiofibroma
• Presentation : • Treatment : removed the tumour
• Recurrent severe epistaxes & through a midline, nosesplitting incision,
progressive nasal obstruction radiotherapy (gamma-knife therapy)
• These tumours do not grow fast • Complications : recurrence, surgically
• In most, there is a delay of at least 6 induced infraorbital nerve sensory
/ 7months between the onset of deficits, prolonged nasal crusting
symptoms & presentation (ozaena), ocular problems, radiotherapy
effects (Growth retardation,
• Signs and symptoms of tumour
panhypopituitarism, temporal lobe
growth & extension  swelling of
necrosis, cataracts, radiation
the cheek, trismus, hearing loss
keratopathy, thyroid & nasopharyngeal
secondary to Eustachian tube
malignancies)
obstruction, anosmia & a nasal
intonation or plummy quality to the
voice
• More extensive tumour growth with
invasion of the orbit and cavernous
sinus  proptosis, diplopia, visual
loss, facial pain & headache
• Anterior rhinoscopy : confirm the
presence of abundant mucopurulent
secretions in the nasal cavity
Resep Obat
R/ Dimenhidrinate tab 50 mg No. VI
S 2 dd 1 tab p.c.
------------------------------------------------ Ꙅ
R/ flunarizin tab 5 mg No. III
S 1 dd 1 tab
------------------------------------------------ Ꙅ
Daftar Pustaka
• Sherwood L. Human physiology: from cell to systems.
7th ed. Canada: Thomson Publishing Inc; 2010.
• George G. Browning, Burton J. Martin, Clarke Ray,
Hibbert John, Jones S. Nicholas, Lund J Valerie. Scott
Brown’s Otorhinolaryngology, Head and Neck Surgery.
Volume 3. London: Edward Arnold Ltd, 2008.
• Gleeson M, Browning GG, Burtin MJ, Clarke R, Hibbert
J, Jones NS et al, editors. Scott-Brown’s Otolaryngology,
7th ed.
• ANDREW BRAINARD, MD, MPH, CHIP GRESHAM, MD,
Middlemore Hospital, Auckland, New Zealand,
http://www.aafp.org/afp/2014/0701/p41.pdf