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Pleno Pemicu 4 Kelompok 2

• Tutor : dr. Sari & dr. Eni


• Ketua : Erri Pratama
• Sekretaris : Josephine Angelia S.
• Penulis : Imelda Jarisa Arisal
• Anggota :
1. Yovita Valencia
2. Mercy Tania
3. Ignatius Bayu Hermawan
4. Petrus Mario Tromp Ipsan
5. Elita Syaravina
6. Stefanus Andrew Susanto
7. Cindy Claudia
8. Dila Nur Fitriani
Bagai Terombang-ambing di Tengah Lautan
Seorang perempuan berusia 38 tahun datttang ke IGD RS dengan keluhan pusing
berputar hebat disertai rasa mual. Pasien merasa dirinya seperti diombang-ambing di atas
kapal kecil di tengah ombak yang besar, sehingga untuk berdiri pun dia harus bertumpu.
Pada mulanya, dia merasakan telinga kanannya terasa tertutup dan berdengung hebat
ketika bangun tidur tadi pagi, kira-kira 5 jam yang lalu. Dia lalu pergi ke dokter praktik di
dekat rumah dan diberi obat. Tetapi belum sempat dia meminum obat, dia merasakan
keluhan ini bertambah hebat, hingga akhhirnya keluarganya memutuskan untuk
membawanya ke IGD RS.
Pasien mengatakan keluhan pusing berputar dusertai mual dan muntah pernah
dialamnya ketika berpergian dengan obil ke luar kota dan bisa diatasinya dengan minum
obat anti mabuk. Tapi keadaan yang seperti ini, baru kali ini dialaminya.
Selain itu, selama 3 bulan terakhir, pasien juga mengalami telinga kiri berdengung,
mimisan dan hidung yang semakin buntu. Sebelum terakhir dia menemukan adanya
benjolan di leher samping kiri. Dia usdah pernah berberapa kali berobat ke dokter untuk
keluhannya ini, tetapi belum membaik.
Dokter juga menanyaan riwayat penyakit yang pernah dideritanya dan pasien
mengatakan dia pernah menderita cacar ular tapi tidak mengetahui untuk penyakit yang
lain.
Dokter kemudian melakukan pemeriksaan tanda-tanda vital, pemeriksaan THT.
Dokter juga melakukan palpasi pada kelenjar getah bening di leher kanan dan kiri.
setelah pemeriksaan selesai, dokter memutuskan untuk merawat inap pasien
tersebut dan melakukan pemeriksaan penunjang.
Apa yang dapat saudara pelajari dari kasus tersebut?
I. Unfamiliar Terms
1. Berdengung : persepsi mendengar suatu suara di telinga
2. Cacar ular : herpes zooster penyebabnya varicella zooster (lesi membentuk alur di
tubuh)

II. Rumusan Masalah


Pusing berputar disertai rasa mual.
1. Apa saja kelainan yang mempunyai keluhan tersebut?
2. Mengapa dapat timbul keluhan tersebut?
3. Apa saja penyebabnya?
Merasa terombang-ambing, berdiri harus bertumpu.
4. Mengapa?
5. Apa saja kelainan yang memiliki keluhan tersebut?
Telinga kanan terasa tertutup dan berdengung hebat ketika bangun tidur.
6. Apa saja kelainan yang memiliki keluhan tersebut?
7. Bagaimana hubungan keluhan ps dng berdengung hebat ketika bangun tidur?
Keluhan bertambah hebat
8. Apa penyebabnya?
II. Rumusan Masalah
Pusing berputar, mual, muntah, saat berpergian ke luar kota dengan mobil, diatasi dengan
obat anti mabuk.
9. Apa penyebabnya?
10. Bagaimana hubungan antara keluah ini dengan keluhan sekarang?
Telinga kiri bedengung, mimisan, hidung semakin buntu.
11. Apa penyebabnya?
12. Bagaimana hubungan antara keluhan pada telinga kanan dan telinga kiri?
13. Bagaimana hubungan antara telinga kiri berdengung & mimisan dengan hidung
semakin buntu?
Benjolan di leher samping kiri 1 bulan yang lalu, sudah berobat belum membaik.
14. Apa penyebabnya?
15. Mengapa belum membaik setelah berobat?
16. Bagaimana hubungan antara benjolan di leher kiri dengan mimisan?
Riwayat penyakit : cacar ular
17. Bagaimana hubungan antara keluhan ps dengan riwayat cacar ular?
Dokter lakukan TTV, pemeriksaan THT, palpasi KGB leher kanan & kiri  dokter putuskan
untuk rawat inap ps & lakukan PP.
18. Mengapa dokter lakukan pemeriksaan tersebut?
III. Curah Pendapat
1. Vestibular (gangguan keseimbangan) : persepsi visual dan gerakan.
vestibular neuritis, Meniere disease,
10. Berhubungan, apabila pasien memiliki
BPPV, dizziness, hipotensi ortostatik,
BPPV  berikan efek pada keluhan.
kelainan sistemik (hipoglikemik), anemia,
labirintis, motion sickness. 11. Telinga berdengung  tinnitus (akibat
penimbunan cairan endolimfatikus,
2. Gangguan sistem vestibular  input
reflex membrane tympani  tuli
saraf otonom  memicu mual muntah.
konduktif), hidung tersumbat & mimisan
3. Infeksi telinga dalam, infeksi virus, ( infeksi, benda asing, polip pada
tumor. konka, ca nasofaring, hipertensi,
rinosinusitis).
4. Gangguan keseimbangan sudah hebat
sehingga perlu bertumpu. 12. Tinitus (telinga berdenging).
5. Idem no 1. 13. Skip
6. Meniere disease, labirintis, otosklerosis. 14. Pembesaran KBG karena infeksi,
metastasis ca.
7. Perubahan posisi kepala  Perubahan
cairan endolymph di labirin karena 15. Keganasan  metastasis ca nasofaring.
perpundahan ion kalium di organ otolit.
16. Karena adanya infeksi bersifat laten dari
8. Perubahan posisi terus-menerus  herpes zoster  otosklerosis, vertigo.
stimulus semakin banyak  keluhan
17. Menyingkirkan DD.
semakin berat.
9. Stimulus vestibular ↑ dan berulang,
IV. Mind Map
Hindung tersumbat,
Keganasan
mimisan, 3 bulan yang lalu

Terombang- Mual & pusing - TD


ambing + motion Sistemik TTV
berputar - GD
sickness
Tuli sensorik
Gangguan Gangguan
keseimbangan pendengaran
Tuli konduktif
Tinnitus
Infeksi
Gangguan
Sentral Perifer
telinga dalam
Keganasan
IV. Learning Issues
1. MM patomekanisme herpes zoster ke arah telinga
2. MM fisiologi pendengaran dan keseimbangan
3. MM gangguan dan infeksi telinga dalam
4. MM gangguan pendegaran (tuli kongenital, tuli konduktif,
tuli perseptif, trauma akustik akut)
5. MM gangguan keseimbangan (vertigo, vestibular neuritis)
6. MM keganasan pada THT
LI 1 : MM patomekanisme herpes
zoster ke arah telinga
Pathophysiology Herpes Zoster
• VZV infection of the head and neck that involves the facial nerve, often the
seventh cranial nerve (CN VII)
• Other cranial nerves (CN) might be also involved  CN VIII, IX, V, and VI (in
order of frequency)
• This infection gives rise to vesiculation and ulceration of the external ear and
ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral
facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy
• VZV remain latent in neurons of cranial nerve and dorsal root ganglia 
Subsequent reactivation of latent VZV  result in localized vesicular rash,
known as herpes zoster
• VZV infection or reactivation involving the geniculate ganglion of CN VII within
the temporal bone
• Diminished level of VZV-specific cell-mediated immunity may lead to
reactivation of this virus
• Hearing loss and vertigo  are thought to occur as a result of transmission of
the virus via direct proximity of cranial nerve (CN) VIII to CN VII at the
cerebellopontine angle or via vasa vasorum that travel from CN VII to other
nearby cranial nerves
LI 2 : 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 3 : MM gangguan dan infeksi
telinga dalam
Bacterial labyrinthitis
• May develop through a dissemination of • Vertigo with malaise
infection from the middle ear space • Fever in association with an URTI
• Can be associated with otitis media or as • Frequntly: signs of acute otitis
a result of bacterial spread through a media or suppurative otitis media
bony fistula in px with cholesteatoma
• Bacterial invasion into the labyrinth
and chronic otitis media
though the oval and round windowds 
• 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  auditory and vestibular functional loss
labyrinth • Neuronal loss due to retrograde
• Either the foraminae chribrosa of degeneration
the fundus
• Px with meningitis, esp. children 
• The vestibular sensory regions should always be evaluated otologically
• The cochlear aqueduct
• Bacterial labyrinthitis classified into
Opens into the basal region of the scala three stages:
tympani (inside the round window membrane)
• Serous or toxic labyrinthitis
• Clinical Picture: • Suppurative otogenic labyrinthitis
• Acute or subacute onset of hearing • Suppurative meningogenic
loss labyrinthitis
Serous labyrinthitis Acute suppurative otogenic labyrinthitis
• Irritation of the labyrinth caused by • Caused by bacterial invasion into the inner ear 
invasion of bacterial toxins either vertigo and hearing loss
from • Bacteria invasion  accumulation of PMN  local
• Acute or chronic otitis media precipitate formed in the perilymph and eventually
• Perilymphatic fistula or in the endolymph  endolymphatic hydrops
meningitis • Followed by necrosis of the membranous
• Leading to: veritgo and labyrinth often with spread to the meninges
sensorineural hearing loss  life threatening condition
• Less severe form: inner ear function • May be followed by healing, fibrosis and new bone
is generally restored formation (labyrinthitis ossificans)
• Severe cases  partial or complete • Usually leads to profound loss of auditory and
loss of hearing or vestibular function vestibular function
• Loss of hair cells • Chronic form: complication of chronic
• Cochlea > vestibular system tympanomastoiditis  slowly progressive osteolytic
• May occur during the course of destruction of the bony labyrinth with invasion of
acute or chronic otitis media granulation tissue  degeneration of the auditoy
• Through toxins reaching the and vestibular sensory organs
inner ear via the round or oval • If not arrested  intracranial complications
windows
• Common microorganisms: Β-Haemolytic
• May also result from meningitis Streptococci, Pneumococci, Staphylococci,
• Perilymph shows a stainable Haemophilus influenza, Proteus vulgaris,
precipitate 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 • Terdapat resorpsi tulang
bersifat lokal yg mmpengaruhi tulang endochondral dengan p’mbesaran
endochondral ( yg ditandai dengan ruang perivascular diikuti deposisi
adany gg resorpsi & deposisi tulang) dari tulang yg imatur
• Lesi otoscleroticterdiri dari area • Resopsi tulang dimediasi oleh
resorpsi tulang,p’tukan tulang osteoklas & p’tukan tlg baru oleh
baru,proliferasi vaskular & stroma jar osteoblas
ikat • Proliferasi dari p darah pd active
otosclerosis
• Otosklerosis berkatian dgn lesi yg
melibatkan tulang stapes & • Focus otosklerotik jg trdpt stroma
manifestasinya berupa : tuli konduktif jar ikat ( tersusun atas fibroblast &
histiosit)
• HISTOPA OF OTOSCLEROSIS
• Tdk ada sel2 inflammasi
• Lesi terdiri dari resorpsi area
• Fokus otosklerotik mnunjukkan area
tulang,p’tukan tulang yg
baru,proliferasi vaskular,stroma yg aktif ditandai dgn pe+ selular &
vaskularisasi bersama dgn resorpsi
jaringan ikat
tulang & p’tulang baru
• Tanda per1 otosclerosis adalah blue
mantle ( mrupakann area dari otic • Fokus otosklerotik daerah yg
capsule yg berwarna lbh basofilik inaktifdense mineralized bone
dari normal)
Otosclerosis
• Distribusi lesi otosclerosis: fibrovaskular (adanya
• Area anterior oval window (80-95%) hipertrofi,deposisi dari jar ikat &
• Round window ( 30%) pningkatan vaskularisasi)
• Stapes footplate (12%) • Disebabkan krn adanya respon
sitokin,faktor angiogenik,dan
• Posterior oval window ( 5-10%) mediator kimia lainnya
• Pathology of Conductive hearing • Pningkatan vaskularisasi
Impairment mukosa pd fokus sklerotik dkat
• Keterlibatan stapes gg dgn oval window tmpak ada
pendengaran konduktif mulai dari 5- bercak kemerahan dpt dilihat
60 dB dgn otoskop ( Schwarze Sign)
• Penyebaran fokus otosklerotik dari • Pathology of sensorineural hearing
fokus anterior ke oval window impairment
diduga krn adanya “fiksasi fibrosa” • dapat terjdi jika fokus otosklerotik
dari footplate stapes mncapai endosteum koklea
• Adanya progresi dari • Jika fokus tsb sdh mncapai
otosklerosismnyebabkan fiksasi endosteum sering terjdai atrofi
tulang dari footplate anterior yg dari ligamentum spiral ,perusakan
mnyebabkan gg p’dengaran fibrosit & digantikan dgn suatu
konduktif substansi eosinofilik disebut
• Mukosa telinga tengah krn fokus “hyalinisasi” ligamentum spiral
otosklerotikproliferasi
Otosclerosis
• Ligamentum spiral pnting untuk fungsi • Pathology of Vestibular symptoms
dari koklea • Tidak seimbang,dizziness
• Fibrosit dri ligamentum /serangan berulang vertigo
merupakan sel yg menempel 1 • Etiologi :
sama lain ( gap junction system)
trdpt connexin (yg mmbentuk • Predisposisi genetik : gen tersebut
channel untuk aliran ion & berkaitan dgn regulasi
metabolit antar sel ) kolagen,kartilago & homeostasis
tulang & supresi pertumbuhan
• Fibrosit jg mengandung
enzim,protein,dan sitokin • Expresi dari COL1A1 ,gen
mmpengaruhi homeostasis di kolagen tipe 1 berhub kuat
koklea dgn osteogenesis imperfekta
& osteoporosis
• Remodeling tulang dipengaruhi
oleh sitokin2 inflammasi dimana • Measles virus : pd fokus
sitokin yg dilepaskan oleh tlg yg otosklerosis ditemukan partikel
mengalami remodelin pd fokus virus,antigen & RNA (active
otosklerosis dpt berdifusi ke osteosclerosis foci) ( titer IgG
ligamentum spiral mngganggu spesifik measles mengalami
homesotasis cairan & ion di koklea elevasi dan ditemukan di perilim
gg pendengaran sensorineural pd ps dgn otosklerosis)
Otosclerosis
• Tanda & Gejala : sakit
• Gg pendengaran konduktif progresif • Timpanogram : depressed/normal
• lbh mudah berbicara /memahami • HRCT & MRI
p’mbicaraan pd lingkungan yg berisik
• Treatment :
• Tinnitus , Gg vestibular
• fluoride therapy for clinical
• Gg pendengaran sensorineural otosclerosis has been stimulated by
• PF : reports of a lower incidence of
otosclerosis in areas that have high
• Kanal auditori eksterna & membran
natural water levels of fluoride
timpani tampak normal
• Conventional hearing aids
• Schwartze sign : warna kemerahan
pada promontorium krn ↑ • Bone-anchored hearing aids (BAHA)
vaskularisasi tulang • Surgery
• PP : • Complications :
• Air bone gap : melebar pda frekuensi • Postoperative conductive hearing
rendah impairment, Sensorineural hearing
• Carhart notch : mrupakan karakteristik damage, Facial nerve injury,
dari otosklerosis & gg pendengaran Perilymphatic fistula, Vertigo,
sensorineural skitar 2 kHz Reparative granuloma, Discomfort to
loud noise, Alteration in taste,
• Tes rinne : konduksi tulang lbh baik
Cholesteatoma, Meningitis
dari konduksi udara & tes weber
mnunjukkan ada lateralisasi pd sisi yg
LI 4 : 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
Acquired Causes
• Congenital CMV : mrupakan pnyebab • Meningitis mrupakan
tersering ( non herediter sensorineural permanent childhood
hearing loss) ,hearing loss dapat :
delayed & atau progresif impairment yg paling sering
,resiko terjdinya gg pendengaran
• Congenital rubella syndrome:
nongenetic congenitally acquired
sensorineural stlh meningitis
hearing loss bakterial 10%
• Terjadi jika adanya infeksi maternal • Rehabilitation can be
o/ virus rubella 1st trimester initiated ( after meningitis)
deafness ,ocular defect (
catarct),KV anomalies ( patent
• If cochlear implantation
ductus arteriosus, pulmonary artery necessary should be done
stenosis),CNS ,prubahan kulit with minimal delay ( as
• Syphilis : bakteri Treponema pallidum( ossification of cochelar duct
infeksi tersering)(transmisi tersering can make implantation
melalui kontak seksual ,tetapi sifilis dpt difficult )
ditransmisikan dari ibu yg terinfeksi ke
anak ( congenital sifilis)(can oocur any • Measles
stage of the pregnancy & if occurs in 1st
/2nd trimester untreated
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 • outer hair cell (OHC) plasma
reduction in auditory acuity associated with membrane fluidity, the role of
noise exposure glucocorticoid receptors &
oxidative stress
• Predisposing factors : interaction between
noise-induced hearing loss and age-related • Structural mechanisms :
hearing loss, smoking, diabetes & CVD • Changes to the micromechanical
structures within the cochlea 
• Pathology :
depolymerization of actin filaments
• Metabolic mechanisms : in stereocilia may be a substrate of
• Acoustic overstimulation  TTS
excessive release of • changes to nonsensory elements of
neurotransmitters (glutamate) the cochlea, such as swelling of the
associated with the transduction stria vascularis, afferent nerve
function of the cochlea  endings & of supporting cells
noiseinduced hearing loss
• Apoptosis & necrosis
(glutamate receptor antagonists
may reduce TTS) • Apoptotic changes in chinchilla
OHC (specifically nuclear
• stimulation with sound of
condensation and cell body
moderate intensity  ↑ cochlear
shrinkage) have been detected five
blood flow, & with sound of high
minutes after exposure to impulse
intensity ↓ cochlear blood flow
noise, whereas necrotic change
(this being a potential mechanism
(nuclear swelling) appeared 30
for cochlear dysfunction associated
minutes following exposure
with noise 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 5 : 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 • migraine-associated vertigo 
lingkungan yg berputar menit ke jam
• Melibatkan angular motion • penyakit Meniere  beberapa
sensing system (semicircular jam
canals & their central projections) • neuritis vestibular akut dan
 dpt terjadi dari labirin sampai stroke batang otak 
ke korteks vestibular  u/ beberapa hari
mengetahui letak lesi • Vertigo presentations :
membutuhkan gejala tambahan • Single vertigo episode
• Hearing loss & tinitus  • Recurrent (or episodic) vertigo
keterlibatan labirin / N.VIII & • Chronic dizziness
gejala batang otak gejala seperti
frank diplopia, mati
rasa/kelemahan pd wajah dan
disartria
• Vertigo akut:
• BPPV  < 1menit
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, & • Horizontal/horizontal-torsional
aural fullness nystagmus, beats towards the
• Pathophysiology : Overproduction affected ear (last < 1 hour)
/malabsorption of endolymph  • Paretic phase
endolymphatic hypertension  gross • Nystagmus beats away from the
enlargement of the membranous
affected ear (several hours – 1
labyrinth (hydrops)  periodic rupture or 2 days)
of membranous labyrinth  leakage
potassium-rich endolymph into •  peripheral hypofunction 
perilymph  meniere attacks spontaneous neural activity in
the right vestibular nucleus is <
• Clinical manifestations  nystagmus beats toward the
• Reccurrent attacks of spontaneous left ear
vertigo, nause, vomitng • Recovery phase
• Lateralized low-frequency hearing • Nystagmus beats towards the
loss, tinnitus, aural fullness affected ear again (last like the
• Later stage of the disease  drop 2nd phase)
attacks (Patient simply drop to the
ground without warning  fracture
& serious injury)
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 6 : MM keganasan pada THT
Nasopharyngeal Carcinoma
• The result of a complex interplay of genetic products are consistently found in
factors, early latent infection by EBV & its both differentiated & undifferentiated
reactivation and exposure to types of NPC
environmental carcinogen • The EBV DNA has the characteristic of
• In endemic areas, the rate can be as much being homogenous & is likely to be
as 50 times higher than that in other due to clonal cellular proliferation
countries • Clinical features :
• The highest age-standardized incidence • An early tumour may cause no
rate occurs in southern China amongst the symptoms
Cantonese population of the Guangdong • Presence of an upper neck swelling
Province
• Cervical lymphadenopathy
• Other Southeast Asian races, including • Nasal symptoms : bloodstained nasal
Malays, Indonesians, Thais, Vietnamese discharge, nasal obstruction, post-
and Filipinos, as well as Eskimos (in nasal drip, frank epistaxis
Canada, Alaska and Greenland) are also
• Headache or cranial nerve symptoms
noted for a high prevalence of NPC
• Trismus
• Three times as common in men as women
• Ophthalmoplegia, accompanied by
• Below the age of 50, the incidence of NPC proptosis
is higher than any other cancer
• Pathogenesis :
• The EBV genome & latent gene
Nasopharyngeal Carcinoma
• Treatment : III, & 20–40 % for stage IVA-B
• Megavoltage external radiotherapy • For disseminated disease (stage
(ERT) IVC), the median survival is only 6
• Chemotherapy months
• Salvage treatment • For all patients with
nondisseminated disease, the
• Surgery
overall control rate of 60 % at five
• Prognosis : years can be expected
• Poor prognostic factors including old • Complications :
age, male gender, cranial nerve
• major and minor salivary glands are
palsy, level and fixity of lymph nodes
well within the field of irradiation
• The average five-year survival
achieved by conventional • Xerostomia occurs in all patients and
radiotherapy alone is excellent for usually develops following the first
few doses of irradiation
early disease  approximately 80–
90 % for stage I & 70–80 % for stage • Symptoms of oropharyngeal
II mucositis
• The average five-year survival • altered taste sensation
achieved by conventional • dermatitis
radiotherapy alone for locally • alopecia of the irradiated area
advanced nondisseminated disease
is approximately 40–60 % for stage
Juvenile Angiofibroma
• Juvenile angiofibroma is an uncommon, sustained bleeding
benign & extremely vascular tumour that • The stromal compartment is made up
arises in the tissues within the of plump cells that can be spindle or
sphenopalatine foramen stellate in shape and give rise to
• It develops almost exclusively in adolescent varying amounts of collagen 
males, though there are reports of this tumours very hard or firm, while
tumour being found in children, the others may be relatively soft
elderly, young & even pregnant women • Almost exclusively found in adolescent
boys  sex-hormone receptors 
• The tumour extends into the nasopharynx,
androgen receptors are present in at
paranasal sinuses, pterygopalatine &
least 75% of tumours, receptors being
infratemporal fossa. Larger tumours can
present in both the vascular & stromal
involve the orbit and cavernous sinus
elements
• Pathogenesis : • VEGF localized on both endothelial &
• Present as well-defined, lobulated stromal cells  tumour development
tumours that are covered by • Overexpression of IGFII
nasopharyngeal mucosa
• Germline mutations in the APC gene
• The tumour consists of proliferating, on chromosome 5q This gene
irregular vascular channels within a regulates the beta-catenin pathway
fibrous stroma which influences cell to cell adhesion
• Tumour blood vessels : lack smooth  Mutations of beta-catenin 
muscle and elastic fibres  development of these neoplasms
contributing to its reputation for
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
Kesimpulan dan Saran
• Kesimpulan
• Kami telah mempelajari fisiologi dari pendengaran dan
keseimbangan, serta kelainan yang berkaitan dengan
gangguan dan infeksi pada telinga tengah, ganguan
pendengaran, gangguan keseimbangan, dan keganasan
pada THT.
• Saran
• Pada pasien disarankan untuk melakukan pemeriksaan
lebih lanjut untuk menyingkirkan kemungkinan
diagnosis.
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